Boies Text PDF
Boies Text PDF
Boies Text PDF
ADAMS
BOIES
HILGER
BOIE
FUND
OF
OTOLARYNG
THROAT DISEASES
GEORGE L. ADAMS, M.D.
Department of Otolaryngology,
University of Minnesota Hospital and Clinic,
Minneapolis, Minnesota
Sixth Edition
1989
W. B. SAUNDERS COMPANY
Harcourt Brace Jovanovich, Inc.
Singapore 238884
Boies: Fundamentals of Otolaryngology: A Textbook of Ear, Nose and Throat Disease 6/e
Adams
Copy Right 1997, 1989 by W.B. Saunders Company, Philadephia, PA
Fundamentals of otolaryngology.
Boies fundamentals of otolaryngology: a textbook of ear, nose and throat
disease.^41 ed./George L. Adams, Lawrence R. Boies, Jr., Peter A. Hilger.
p. cm.
Rev. ed. of: Boies’s fundinentals of otolaryngology. 5th ed. 1978.
Includes bibliographies and index.
ISBN 0-8089-2045-6
1. Otolaryngology. I. Boies, Lawrence R., 1898-1987. II. Adams, George L.
(George Linton), 1941- IH. Boies, Lawrence R., 1932- IV. Hilger,
Peter A , 1948- V. Title.
[DNLM: 1. Otorhinolaryngologic Diseases. WV 100F981]
RF46.F96 1989
617’.51 -del 9
DNLM/DLC
for Librarv of Congress 88-39685
CIP
This Edition First Published in the Philippines 1997 Philippines Reprint ISBN#0-8089-2045-6
All right reserved. No part of this publication may be reproduced or transmitted in any form or by any means,
electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without
V' > - : \\
permission in writihg front the original publisher, W.B. SAUNDERS COMPANY, A Division of Harcourt Brace &
Company, The Curtis Center, Independence Square West, Philadelphia, PA 10106.
Published in the Philippines by Harcourt Brace & COMPANY ASIA PTE LTD under special arrangement with W.B.
Saunders Company, USA. This edition is the only authorized complete and unabridged reproduction of the latest
American Edition, published and priced for the sales in the Philippines.
Eleven years have passed since publication of the Fifth Edition of Boies
Fundamentals of Otolaryngology. The original text, printed more than 40
years ago, provided clinical information on the management and care of
patients with otolaryngology disorders. Each subsequent edition has included
more basic science information. We recognize that there are now three- and
four-volume texts available in the field of otolaryngology-head and neck
surgery, and we have endeavored to limit this text to the basic principles of
diagnosis, recognition of causative factors, and management of the more
common problems. The new Sixth Edition stresses basic science principles
of anatomy, embryology, and physiology and correlates this information
with the clinical findings to assist in understanding the management of
disorders of the ears, nose, throat, head, and neck. The textbook, in a
sense, has been entirely rewritten and not just updated. The illustrations,
for the most part, have been replaced with better quality artwork. The
textbook has been expanded to keep pace with the expanding scope of our
specialty. The added sections on wound healing and wound repair provide
basic information for repair of minor defects.
The current authors are teachers at the University of Minnesota who
lecture to the sophomore class sessions in otolaryngology. Chapters outside
the normal scope of otolaryngology have been written by experts in those
areas in order to provide a more thorough presentation of the material.
While the text is aimed primarily at medical students at the beginning of
their clinical years, the material will be of value to family physicians and
first-year residents in family practice and otolaryngology. Those who plan to
specialize in head and neck surgery are provided with references in which
more complex procedures are described in greater detail.
The format for the Sixth Edition has changed significantly to comply
with today’s medical school curricula. Besides the emphasis on pathophysi¬
ology, there is a greater emphasis on basic principles. In the margins of each
chapter, specific major points are highlighted or re-emphasized. This method
indexes important facts for the student to recall. The editors of the Sixth
Edition have tried to provide the basic information necessary in the most
concise, easily understood manner for a medical student on a busy otolar¬
yngology-head and neck surgery rotation.
The current editors wish to acknowledge material originally prepared
by authors of the Fifth Edition whose chapters have been expanded and
revised by the current faculty. Special thanks for past contributions to
Doctors Mary Jayne Capps, Anderson C. Hilding, Robert H. Mathog, Kurt
Poliak, Cedric A. Quick, Melvin E. Sigel, Ms. Carol Berman, Mr. Richard
L. Hoel, and Ms. Elaine LaBenz.
George L. Adams
Peter A. Hilger
CONTENTS
PART ONE
1
The Head and Neck History and Examination . 3
Leighton G. Siegel
PART TWO
THE EAR
2
Embryology, Anatomy, and Physiology of the Ear . 27
Stephen L. Liston and Arndt J. Duvall, 111
3
The Vestibular System .... 39
John H. Anderson and Samuel C. Levine
4
Audiology .... 46
Frank M. Lassman, Samuel C. Levine, and Donna G. Greenfield
5
Diseases of the External Ear ... 77
Lawrence R. Boies, Jr.
6
Diseases of the Middle Ear and Mastoid . 90
Michael M. Paparella, George L. Adams, and Samuel C. Levine
7
Diseases of the Inner Ear ... 123
Samuel C. Levine
8
Disorders of the Facial Nerve ....... 142
Robert H. Maisel and Samuel C. Levine
9
Facial Pain, Headache, and Otalgia ......... 157
Lawrence R. Boies, Jr.
ix
CONTENTS
PART THREE
10
Applied Anatomy and Physiology of the Nose . 177
Peter A. Hilger
11
Allergic Conditions in Otolaryngology Patients . 196
Malcolm N. Blumenthal
12
Diseases of the Nose ... 206
Peter A. Hilger
13
Diseases of the Paranasal Sinuses . 249
Peter A. Hilger
PART FOUR
14
Embryology, Anatomy, and Physiology of the Oral Cavity,
Pharynx, Esophagus, and Neck . 273
Stephen L. Liston
15
Diseases of the Oral Cavity . 282
Robert J. Gorlin
16
Disorders of the Salivary Glands ... 317
George L. Adams
17
Diseases of the Nasopharynx and Oropharynx .. 332
George L. Adams
18
Infections in the Immunocompromised Host. 370
Norman T. Berlinger
PART FIVE
THE LARYNX
19
Anatomy and Physiology of the Larynx . . .. .,383
James I. Cohen
CONTENTS xl
20
Benign Laryngeal Disorders . 392
John D. Banovetz
21
Speech and Language Disorders . 412
Virginia Wigginton, Meredith Gerdin, and Frank M. Lassman
PART SIX
22
Benign Neck Masses . 429
James I. Cohen
23
Malignant Tumors of the Head and Neck . 443
George L. Adams
PART SEVEN
24
Diseases of the Lower Air Passages, Esophagus, and Mediastinum:
Endoscopic Considerations . 471
Leighton G. Siegel
25
Tracheostomy . 490
Robert H. Maisel
PART EIGHT
26
Facial Plastic Surgery . 505
Peter A. Hilger
27
Maxillofacial Trauma . 526
Kent S. Wilson
Index 541
i»ART ONE
HISTORY AND
EXAMINATION
1
THE HEAD AND NECK
HISTORY AND EXAMINATION
by Leighton G. Siegel, M.D
The Ear
Patient History
The minimal history should include an inquiry about hearing impairment,
head noises (tinnitus), dizziness (vertigo) or imbalance, discharge from the
ear, and earache. If any of these complaints are found, they should be
characterized in detail. The following outline is a practical guide for inquiry
into these complaints.
Hearing Impairment
Typical complaints produced by hearing loss are: “I can hear when there
is one person but not when I am with a group of people or when it’s noisy.”
“Everyone mumbles nowadays.” “My child only hears what he wants to
hear.” “My child is over one year old and isn’t talking.” “My wife (for some
reason it’s frequently a wife) says I am not paying attention and she wants
my hearing checked.”
Specific questions that might be asked include:
1. Was onset sudden or gradual? Duration?
2. Which ear is affected, or are both involved?
3. Does the hearing get alternately better and worse?
4. Do things merely sound quiet, or is understanding also a problem and
under what circumstances?
5. Was the onset associated with other illness, trauma, noise exposure,
or the use of medication, including aspirin?
6. Is there a family history of hearing impairment?
7. Was there any prenatal or postnatal difficulty or disease or difficulty
with delivery?
8. Has there been any past ear disease or surgery?
9. Was there occupational, military, recreational, or other noise
exposure?
10. Is there a history of measles, mumps, influenza, meningitis, syphilis,
severe viral illness, or use of ototoxic drugs such as kanamycin,
streptomycin, gentamicin, or certain diuretics?
11. What social, occupational, or educational handicap does the hearing
loss produce?
Head Noises
1. What is the nature of the noise? Can it be described as ringing, high-
pitched, roaring, humming, hissing (sound of escaping steam), or
pulsating (synchronous with pulse)?
2. Is the noise heard all the time or only in a very quiet room?
3. Is it heard after noise exposure at work or elsewhere?
Dizziness
1. Does the patient describe the symptom as lightheadedness, imbalance,
spinning, or a tendency to fall? Toward which direction? Is the dizziness
affected by head position? Is it present when lying down? Is onset
related to getting up quickly?
2. What are the frequency and duration of attacks?
3. Is the dizziness continuous or episodic?
4. Have the patient describe the first attack. How long is the interval
between episodes?
1—THE HEAD AND NECK HISTORY AND EXAMINATION 5
Earache
1. Characterize the pain.
2. Is this a recurrent problem? If so, how often does it occur?
3. Is the pain just in the ear or does it spread to or come from another
place?
4. Does anything seem to trigger the pain such as chewing, biting down,
coughing, or swallowing. (Many locations in the head and neck will
refer pain to the ear.)
5. Are there any other head or neck symptoms?
Helix v
Crus of
helix
External
..-auditory
Concha
' Anti -
tragus
Helix
Lobule
6 PART ONE—HISTORY AND EXAMINATION
FIGURE 1-2. A, Normal tympanic membrane. B, Early stage of acute purulent otitis media.
C, Later stage of acute otitis media. D, Serous otitis media. £, Bubbles In the middle ear
are seen in serous otitis media after inflammation. (Courtesy of Dr. Richard A. Buckingham
and Dr. George E. Shambaugh, Jr.)
examination, grasp the pinna and retract it backward and upward in adults
and downward in infants. The appearance of the normal ear and right
tympanic membrane is illustrated in Figures 1-1 and 1-2.
The hand-held aural speculum is used in conjunction with a head mirror
and light source. It is thin-walled and funnel-shaped, should have a non-
reflective surface, and is available in a selection of sizes (Fig. 1-3). The
1—THE HEAD AND NECK HISTORY AND EXAMINATION 7
Cerumen spoon
examiner chooses the largest one that comfortably fits the external ear canal.
Since the opening is small, the speculum must be swiveled within the ear
canal to visualize the entire tympanic membrane. All specula are held in the Only part of the ear is seen
through a speculum.
left hand so that the right, or dominant, hand is free to position the patient
or manipulate instruments. Left-handed examiners may make compensatory
adjustments. The hand-held speculum is best when manipulations, such as
wax removal, need to be done (Fig. 1-4).
Battery-powered otoscopes are commonly used. The most useful of these
have fiberoptic illumination, give a magnified view of the tympanic mem¬
brane, and are provided with a sealed head and pneumatic bulb attachment.
Manipulation (as in removing wax) is much more difficult than with a head
mirror and hand-held speculum (Fig. 1-5). An “operating” or open head is
also available for the battery-powered otoscope. Manipulation through the
open operating head is somewhat easier than with a sealed head, but
unfortunately the great advantage of pneumatic inspection is not possible.
As with the hand-held speculum, the largest size fitting the ear canal is used It must be moved to scan the
entire ear.
and must be swiveled within the ear canal to visualize the entire tympanic
FIGURE 1-5. A hand-held battery-powered otoscope with a sealed system allows for
pneumatic otoscopy. Only gentle pressure is required to move a normal tympanic membrane.
FIGURE 1-6. The Siegle pneumatic otoscope permits determination of tympanic membrane
mobility. The special speculum allow a tight seal of the external ear canal.
1—THE HEAD AND NECK HISTORY AND EXAMINATION 9
a small amount of pressure in the external ear canal while observing the
tympanic membrane. If a perforation is present, the tympanic membrane
will have no movement. Movement will be abnormal in the presence of
fluid. A shifting meniscus will distinguish an air-filled level in the middle ear
from a scar on the tympanic membrane.
Cleansing of the External Ear Canal. The external ear canal may be
blocked with cerumen or a purulent discharge. Cleansing of the ear canal
should be done gently, causing the patient little or no pain. Wax may be
removed through the aural speculum with a cerumen spoon or with an To remove wax or foreign mate-
alligator forceps. If there is moisture in the external ear canal, a suction or 'f^'yjnvfitdeeper''
cotton-tipped metal applicator may be used for cleaning (Fig. 1-7). If the
tympanic membrane has no perforation, the ear may also be cleaned by
irrigation with water that is approximately body temperature. If other
temperatures are used, vertigo and/or discomfort will be produced (Fig. 1-
8).
Screening audiometric testing and vestibular testing are essential for the
evaluation of ear and vestibular disorders and should be available in the
primary care setting. These subjects are discussed in detail in Chapter 2.
FIGURE 1-9. Rinne test. This test is used to compare the duration or Done conduction with
that of air conduction for the ear being tested. A fork of 512 Hz struck a moderate blow and
is held by the stem firmly against the mastoid bone [A). When the patient signals that he no
longer hears the vibrating fork, the duration of bone conduction is noted and the fork is
immediately transferred to position (B) so that the prongs are about one-half inch away and
broadside to the external auditory meatus. When the patient no longer hears by air the sound
of the vibrating fork, note the air conduction. In a normal ear, the fork is heard approximately
twice as long by air conduction as by bone.
1—THE HEAD AND NECK HISTORY AND EXAMINATION 11
FIGURE l-iu. Weber test. This test determines whether monaural impairment is of conductive
or neural origin by comparing the bone conduction of both'eats. A 512 Hz tuning fork can
be 'placed on the forehead or the teeth. A, Normal response. £S,The fork is heard on the right
side. If the right ear is the diseased ear, then the loss is of the conductive type. If the left ear
is the diseased ear, then the hearing loss is of the sensorineural type.
majority of patients with nasal or sinus disease have one or more of the
following symptoms: discharge, nasal obstruction, colds, headache or other Only a small percentage of pa¬
pain, epistaxis, sneezing attacks, occasional external swelling, loss of or tients with sinus complaints will
change in smell, and allergy. If any of these complaints are found, they causes of their symptoms.
should be characterized in detail. The following is a practical guide for
inquiry into these complaints. Further information to be considered in the
history can be found in the chapters dealing with the nose and paranasal
sinuses.
Patient History
Discharge
1. Is one side or are both sides involved?
2. Duration? Continual or intermittent, and how so? Age at onset?
3. Is the discharge watery or thick? Purulent or bloody?
4. Does it occur with environmental or seasonal changes?
Obstruction
1. Is one side or are both sides involved?
2. Duration? Continual or intermittent, and how so? Age at onset?
3. Is there a history of injury?
4. Is there a history of nasal or other otolaryngologic surgery?
5. Is there a history of allergic disorders, especially those associated with
seasonal variation? If suggestive, a complete allergic history is indicated.
6. Does the patient use nasal sprays or medications?
Bleeding
1. What is the duration? Frequency? How long ago was the last episode?
2. Is the bleeding unilateral or bilateral?
3. Does bleeding originate from the anterior or posterior nares or both?
4. Does it occur only in winter?
5. Is there a history of trauma?
6. Does the patient have a bleeding tendency?
7. Does the patient use any medications?
8. Is hypertension present?
12 PART ONE—HISTORY AND EXAMINATION
order to better judge the pressure being applied to the nose. The examiner’s
right hand is placed on top of the patient’s head so that it can be tilted and
moved. The left forefinger is stabilized on the side of the patient’s nose and
the speculum opened in an up-and-down direction in the nasal vestibule. It
is often helpful to gently grasp the ala of the nose between the forefinger
and the speculum and apply slight traction toward the examiner. This avoids
discomfort and provides the best view. The speculum remains in the same
hand when inspecting the opposite nasal cavity.
The intranasal examination begins with inspection of the nasal vestibule.
Folliculitis of the vibrissae may occur in this area. The nasal mucosa is
examined, and the septum is visualized as well as inspected carefully for
purulent discharge or polyps that may be coming from the sinuses. Topical
vasoconstrictors, such as 0.5 per cent phenylephrine (Neo-Synephrine),
applied in a spray or on cotton placed intranasally, will decongest the mucosa
to improve the view in patients with obstructive mucosal swelling. The floor
of the nose should be seen all the way back to the soft palate. The patient
is asked to say “k k k k,” and if no obstruction is present, the soft palate is
seen to rise with each vocalization.
A battery-powered otoscope is frequently used to examine the interior of
the nose at the bedside. This examination is inadequate and of limited
usefulness.
Other Methods of Nasal and Sinus Examination. Palpation and percussion
over the frontal and maxillary sinuses or the teeth may produce pain in some
cases of sinusitis. Transillumination is useful but is not a substitute for
radiographs in the evaluation of sinus disease. Cultures and sensitivity tests
are needed when infection is present, and smears for eosinophils are indicated
in cases of allergy. Endoscopic techniques using flexible and rigid instruments
are of increasing usefulness in evaluating pathology in portions of the nasal
cavity and nasopharnyx that are difficult to visualize with traditional methods.
Paranasal sinus radiographs are required to fully evaluate the absence or
presence and extent of sinus disease. Indeed, only a presumptive diagnosis
of sinus disease can be made without them. The four most useful views are
the lateral, Waters, Caldwell, and base of the skull.
Sore Throat
1. Frequency?
2. What is the duration of each episode?
3. Is the sore throat accompanied by fever, discharge, expectoration,
difficulty in swallowing, difficulty breathing, voice change, or cough?
4. Location and duration of external swelling?
5. Is there any referred pain, such as earache? If so, which side?
6. What treatment has been given in the past?
7. Has the patient been a smoker? How much?
fIGURE 1-12. The use of two tongue depressors and the head light allows one tongue
blade to push the lip to the side and the second tongue blade to push the tongue aside.
This permits adequate visualization of the retromolar trigone, gingiva, and floor of the
mouth.
16 PART ONE—HISTORY AND EXAMINATION
Bimanual palpation is very Palpation. All areas in the oral cavity and pharynx appearing unusual or
useful producing symptoms must be palpated. Tumors and cysts lying deep within
oral tissues can be found only by palpation. Calculi in the submaxillary ducts
can frequently be detected in this manner (Fig. 1-13). Salivary glands, except
for ptotic submaxillary glands in the elderly, are normally not palpable. The
temporomandibular joints can easily be palpated by placing the fingertips in
the external ear canals and asking the patient to open and close the mouth.
The Nasopharynx
The nasopharynx can often partially be seen directly through the nares
when the interior of the nose is examined. A more complete examination of
the nasopharynx is done with the No. 0 nasopharyngeal mirror (Fig. 1-14).
The mirror is warmed, usually over an alcohol lamp, so that the patient’s
breath will not fog it and obscure the view. The examiner checks the
temperature of the mirror by placing it against the back of the hand before
inserting it into the patient’s mouth. The tongue is depressed as for the
pharyngeal examination, and the mirror is positioned in the pharynx. The
posterior third of the tongue should not be touched to reduce the likelihood
of stimulating the gag reflex. The posterior pharyngeal wall is less sensitive
than the tongue, and the soft palate is least sensitive. While the mirror is in
the oropharynx, the patient is told, “Think about breathing through your
nose. The soft palate will then drop, and the nasopharynx can be scanned
with the mirror (Fig. 1-15).
Only a small portion of the nasopharynx can be seen at one time. The
examiner must mentally put the images together while rotating the mirror
to view the entire area (Fig. 1-16). It is generally easiest to orient initially
the posterior margin of the nasal septum and choana. The mirror then can
1—THE HEAD AND NECK HISTORY AND EXAMINATION 17
be rotated laterally to reveal the superior ana middle turbinates, mtv tot ua,
and the eustachian tube orifices.
The nasopharynx can also be examined with a nasal endoscope. This is a
telescope-like device that gives a magnified view of the nasopharynx. It is
introduced through the nose after the area has been anesthetized. The It is possible to palpate the na-
nasopharynx can be directly visualized through the mouth by retracting the sopharynx.
soft palate. Several mechanical devices are available for this. One simple
way consists of passing a soft catheter through the nose until it can be seen
in the pharynx. A hemostat is used to grasp this end and pull it out the
mouth. Pulling gently on both ends of the catheter will retract the soft palate
and allow direct visualization of the nasopharynx. Even better visualization
can be obtained by simultaneously using two catheters, one through each
nostril. Adequate topical anesthesia should be used during this manipulation.
Hoarseness
1. Duration (weeks, months, or years)?
2. Was the onset sudden or gradual?
3. Was the voice completely gone at any time? If so, for how long?
4. Has the patient ever been hoarse before? If so, when and how often?
5. Was the hoarseness preceded by a head cold or sore throat?
6. Is there any discomfort in the region of the larynx?
7. Does the patient cough? Can the patient raise much phlegm?
1—THE HEAD AND NECK HISTORY AND EXAMINATION 19
8. Is there any pain related to the use of the voice? Is there discomfort in
breathing?
9. Is there a history of excessive alcohol ingestion or smoking?
Cough
1. Duration (weeks, months, or years)?
2. In what part of the throat does the cough seem to start?
3. What is coughed up?
4. Are there situations in which the cough is worse, such as during
exposure to cold air, smoke, dust, or other irritants? Is it worse at
night when lying down or during exercising?
5. Has the patient lost weight? If so, how much?
6. Is there any loss of appetite or strength?
7. Is hemoptysis present?
8. Is there a history of smoking?
Med. glosso¬
epiglottic. plica*
Vent, of larg
allecula
FIGURE 1—17. Indirect laryngoscopy re¬
quires a mirror of the proper size
warmed so that it will not steam on the
patient’s exhalation. Gentle tension
should be made on the patient’s tongue,
Circum-
using a strip of gauze to grasp the vallate
tongue and gently pull it out. The under papilla
Incorrect
FIGURE 1-18. Proper positioning for examination c the larynx, pharynx, oral cavity, and neck. The
patient sits upright, bent forward at the waist with the ead slightly projected. Note that the light source
is at the same level as the patient’s eyes.
and systemic). The examiner should be aware that different types of light
(incandescent, fluorescent, or daylight) will each give the skin a slightly
different color. Percussion over the sinuses and teeth may elicit pain or
tenderness. Auscultation of the neck will help evaluate the carotid arteries
and over the skull will help identify vascular tumors or arteriovenous
malformations or shunts.
Cranial nerve and otoneurologic testing can easily be done as part of the
otolaryngologic examination. Much is automatically done, such as observing
vocal cord and pharyngeal motion as an indication of the function of cranial
nerves IX and X. A brief outline of specific functions follows.
The olfactory nerve is checked by presenting familiar odors such as
chocolate or vanilla to one nostril while the other is held closed. Standard
scratch and sniff odors may be used.
The optic nerve can be roughly checked with visual acuity and visual field
tests. The fundus should be inspected as part of every general examination.
Oculomotor, trochlear, and abducens nerves are evaluated when pupillary
reflexes are elicited and range of motion of the eyes is checked. The examiner
should ask specifically about diplopia.
The trigeminal nerve supplies sensation to the face which is easily evalu¬
ated. Absence of the corneal reflex is often found with enlarging acoustic
neuromas. Blinking occurs when the cornea is touched with a wisp of cotton
but not when the sclera is touched.
The facial nerve controls the muscles of facial expression which are easily
observed during the neck and face examination. Facial paralysis is an
interesting and important topic, which is covered in detail in Chapter 8 in
this text.
The cochleovestibular nerve mediates hearing and balance. These func¬
tions are discussed in detail throughout this text. A gross assessment of
hearing followed by tuning fork and audiometric testing will evaluate hearing
function. The evaluation of vestibular function and vertigo is discussed in
Chapter 3. Nystagmus, past-pointing, gait, Romberg, and tandem standing
abnormalities often occur with vestibular disorders and should be checked.
Central nervous system diseases that produce changes in proprioception and
coordination may mimic vestibular disease. These functions should be
evaluated, since they are not affected by primary vestibular disease.
The glossopharyngeal nerve supplies sensation to the pharynx and is
responsible for the gag reflex. The gag reflex should be checked on both
sides of the pharynx with the tongue blade when the pharynx is inspected.
The vagus nerve innervates the muscles of the palate, pharynx, and larynx.
Symmetrical motion of these structures is observed normally as part of the
pharyngeal and laryngeal examination.
The accessory nerve is tested by having the patient shrug both shoulders
against resistance, and the sternocleidomastoid is palpated while the head is
turned against resistance.
The hypoglossal nerve supplies motor innervation to the tongue. Unilateral
atrophy or fasciculation or the inability to protrude the tongue in the midline
indicates a hypoglossal lesion.
This is only a brief sketch of basic neurologic evaluation as related to
otolaryngology. Malignancies arising in the pharynx and nasopharynx have
direct access to the foramina in the base of the skull and can present as
cranial nerve palsy mimicking neurologic disease. The differential diagnosis
of sensorineural hearing loss, particularly when unilateral, and of all patients
22 PART ONE—HISTORY AND EXAMINATION
with vertigo must include a systematic and thorough cranial nerve and
general neurologic evaluation.
Palpation of the neck and face should be done in a systematic manner.
Cervical and metastatic nodes are often located in the anterior triangle of
the neck. This area must be carefully inspected, particularly deep to the
Develop a routine or mental sternocleidomastoid muscle and along the course of the carotid sheath.
checklist tor palpating the neck, structures that normally can and should be palpated are the hyoid bone, the
thyroid and cricoid cartilages and the thyrohyoid and cricothyroid spaces,
tracheal rings, the sternocleidomastoid muscle, the carotid arteries, and the
clavicles and supraclavicular spaces. Crepitation of the thyroid cartilage
against the cervical vertebrae is normally present. All the soft tissues of the
neck can be examined and described by anatomic triangles (Fig. 1-19).
The thyroid gland is normally not palpable. Examination is easiest when
standing behind the patient with the thumb behind the fingers in front of
the lower portion of the sternocleidomastoid muscle. The patient is asked
to swallow while this area is palpated. Thyroglossal duct cysts occur on or
near the midline in the upper half of the neck. They slide upward when the
tongue is protruded. Branchial cleft cysts may be beneath the anterior
portion of the sternocleidomastoid muscle anywhere along its course. A
node over the cricothyroid membrane is often metastatic from the larynx or
thyroid gland. The trachea may deviate from the midline in the presence of
mediastinal or pulmonary disease. Subcutaneous emphysema usually indi¬
cates a ruptured esophagus or airway. This is, of course, only a small list of
possible findings.
Biopsy
The examiner should not hesitate to perform a biopsy of any nonvascular
mucosal or cutaneous lesion for which the diagnosis is not immediately
apparent. Biopsy of deeper structures should be made only after a thorough
examination fails to reveal their origin or nature. Do not biopsy nasal polyps
in young males, as the highly vascular angiofibroma may have the appearance
of a polyp.
Special Studies
Specimens are easily obtained for cytologic studies from all mucosal
surfaces, both directly and via endoscopy. Culture, sensitivity tests, and
smears are indicated when infection is present in these areas. Endoscopic Fine needle biopsy is generally
procedures, including nasopharyngoscopy, direct laryngoscopy, bronchos¬ a safe and rewarding evaluation
technique.
copy, and esophagoscopy, are extremely useful in the diagnosis of head and
neck, tracheobronchial, or esophageal disease. Other useful special tech¬
niques and studies are described in appropriate chapters of this text.
PART TWO
THE EAR
EMBRYOLOGY, ANATOMY,
AND PHYSIOLOGY OF THE EAR
by Stephen L. Liston, M.D., and Arndt J. Duvall, III, M.D.
The embryology, anatomy, and physiology of the ear are the means to
understand function, and, therefore, pathology and treatment. To correlate
the basic knowledge within these disciplines is to better understand ultimately
the treatment of problems in hearing and balance. Our equilibrium is more
basic, and more important, than hearing. An organism can- exist Without
hearing but cannot exist without being in balance with its environment.
Therefore, the vestibular mechanism, as a part of the organism’s orientation
to its environment, phylogenetically arose before hearing. The ear contains
the vestibular portion of balance, but our orientation to the environment is
also determined by our eyes and by our deep tendon sense. The ear is the
organ of hearing and of balance.
Anatomically, the ear is divided into three parts—the external, middle, The external canal is one-half
and inner ear. The external and middle ear develop from the ^branchial cartilaginous and two-thirds
bong.
apparatus. The inner ear develops entirely separately from the oticplacode.
Thus a congenital abnormality can occur in one part, while the other parts
may develop normally.
External Ear
The external ear canal is derived from the^gfodermal first branchial cleft.
The tympanic membrane represents the closing membrane of the first
branchial cleft. During one stage of its development, the external ear canal
actually is closed completely by a meatal plug of tissue but reopens again, Sensation from the posterosu-
and this may be a factor in some cases of atresia or stenosis of this structure. perior portion of the external
canal is transmitted by the
The^pinna is derived from the margins of the first branchial cleft and the seventh cranial nerve.
first and second branchial arches. The pinna is supplied by the auriculotem¬
poral branch of thejnandibular nerve and by thejesser occipital and,greafer
auricular nerves, which are branches of the cervical plexus.
Middle Ear
The middle ear cavity is derived from the^endodermal first branchial cleft.
This air-containing structure expands into the tubotympahTc recess (Fig. 2-
1), which continues to expand around the bones and nerves of the middle
ear (Fig. 2-2) and extends more or less into the mastoid region. The^essicles
are derived from the cartilage of the^branchial arches. To simplify this
28 PART TWO—THE EAR
Tubo tympanic
FIGURE 2—1. Floor of the pharynx of an embryo showing the formation of the tubotympanic
recess. The recess arises as a lateral expansion of the pharyngeal lumen at the level of the
first three internal pharyngeal grooves and pouches. The external auditory meatus is shown
as a solid “meatal plug” of ectoderm growing deeply into the mesoderm from the upper end
of the first external pharyngeal groove to make contact with the tubotympanic recess, the
“drum" being formed at the area of contact. (From Davies J: In Paparella MM, Shumrick DA
(eds): Otolaryngology. Vol 1: Basic Sciences and Related Disciplines. Philadelphia, WB Saunders
Co, 1973, p 172.)
Inner tar
The ectodermal otic placode is located on the lateral surface of the head
of the embryo. This placode sinks to form an otic pit and is eventually
Petrosquamosal
buried beneath the surface as the otic vesicle (Fig. 2-3). This vesicle comes
to lie close to the developing hindbrain and to a collection of neurons known
as the acousticofacial ganglion. This ganglion is important in the development
of the facial, acoustic, and vestibular nerves. The auditory vesicle forms a
diverticulum that comes to lie close to the developing neural tube and that
will become the endolymphatic duct. Then the otic vesicle constricts, forming
a superior utricle and inferior saccule. Three flange-like projections develop
from the utricle. The membranous lining away from the periphery of these
flanges resorbs, leaving three semicircular canals at the periphery of the
flanges. The saccule gives off a spiral cochlear duct. Specialized end-organs
phylogenetically derived from the naked neuromast develop in the semicir¬
cular canals to form cristae, in the utricle and saccule to form maculae, and
in the cochlea to form the organ of Corti. These end-organs come into
connection with the neurons of the acousticofacial ganglion. These neurons
form the ganglia of the vestibular nerve and the spiral ganglia of the cochlear
nerve.
The mesenchyme around the otic ganglion condenses into a cartilaginous
capsule around the membranous derivatives of the otic vesicle. This cartilage
resorbs in certain areas around what is now the membranous labyrinth,
leaving a space that communicates via the cochlear aqueduct with the space
containing CSF and forms the perilymphatic spaces of the bony labyrinth.
The membranous labyrinth contains endolymph. The bone derived from the
cartilaginous capsule of the otic vesicle is a special type of bone known as
endochondral bone.
Petrous c
portion '“iy
; Petrosquamous;
suture FIGURE 2-4. The temporal bone at birth and in the adult.
NEWBORN
ADULT
Mastoid_2 y
portion
Tympanic portion
ring. The styloid process is derived from thd^econd branchial cartilage. The
squamous portion develops inxartilage. The petrous portion is derived from
the&artilaginous capsule of otic vesicle. There are suture lines between these
various portions visible on the definitive temporal bone. The mastoid (breast¬
The facial nerve of an infant is like) process is'not present at birth, and this means that the infant’s'facial
not as protected by the mastoid
nerve is very superficial. The air-containing derivatives of the tubotympanic
process.
recess extend from the middle ear via the aditus to the antrum, an air-
containing region in the mastoid bone. However, how far the pneumatization
of the rest of the mastoid process extends varies. Some bones are poorly
pneumatized or sclerotic, some are moderately pneumatized or diploic, while
frequently the mastoid and much of the petrous and even squamous temporal
bone is filled by air cells (Fig. 2-5).
every effort should be made to preserve this structure. The skin can be
stripped off the underlying cartilage by hematoma or pus and the necrosis The skin of the external canal
of the underlying cartilage leads to a cosmetic deformity of the pinna lies directly over bone. Even
slight inflammation is very tender
(cauliflower ear). for there is no room for exoan-
The external ear canal ls^artilaginous laterally but/bony medially. There sion.
is often a narrowing of the external ear canal at the bone-cartilage junction.
TheTemporomandibular joint and'parotid gland are anterior to the external
ear canal, while the'mastoid process is posterior to the ear canal. The facial
nerve exits the'stylomastoid foramen and passes lateral to the styloid process
posteroinferior to the external ear canal and then runs beneath the external
ear canal to enter the parotid gland. The cartilage of the external ear canal
is one of the surgical landmarks used to find the facial nerve; the tympano¬
mastoid suture is another such landmark.
The superior wall of the middle ear abuts the floor of the middle cranial
fossa. The posterior wall superiorly contains the aditus to the antrum of the
mastoid, and below this is the facial nerve. The stapedius muscle arises in
the region of the facial nerve, and the tendon passes through a bony pyramid
to the neck of the stapes. The chorda tympani nerve arises from the facial
nerve below the stapedius and passes forward lateral to the incus but medial
to the malleus to exit the middle ear via the petrotympanic suture. The
chorda tympani nerve joins the lingual nerve and carries secretomotor fibers
to thfe submandibular ganglion and taste fibers from the anterior two thirds
of the tongue.
The floor of the middle ear is the roof of the jugular bulb, which
superolaterally is the sigmoid sinus and then more centrally the transverse
sinus. This is the major venous outflow of the cranial cavity. The auricular
branch of the vagus nerve enters the middle ear via the floor. The anterior
wall inferiorly is the wall of the carotid canal. Above this the eustachian
tube opens and the tensor tympani muscle occupies the area superior to the
eustachian tube and passes back to hook around the cochleariform process
and insert into the neck of the malleus.
The lateral wall of the middle ear is the bony wall of the epitympanum
above, the tympanic membrane, and the bony wall of the hypotympanum
below.
The most prominent feature of the medial wall is the bony promontory
2—EMBRYOLOGY, ANATOMY, AND PHYSIOLOGY OF THE EAR 33
7empora//obe of brain
Lateral Wall
Anterior Wall
Eustachian tube
Bu/b of in t.
Juyu/ar vein
Medial Wall
Posterior Wall
Prominence oflat. semicirc. canal
Prominence of facial canal
Aditus to antrum
Fossula of round window
Pyramidal eminence
Stapes closinq oval window
Aperture for chorda tymp.
Promontory
Facial nerve
TZochleariform process
Lateral Wall
Ant. Wall
Cana! for
Insertion of tens.-
tens. tymp.
tymp. mus.
mus.
Chorda tymp.
Eustachian
Tymp. memb tube
FIGURE 2-7. A diagrammatic scheme of the shape and relationships of the middle ear
structures.
covering the first turn of the cochlea. The tympanic nerve runs across the
promontory. The opening of the round window is located posteroinferior to
the promontory. The footplate of the stapes is located in the oval window
on the posterosuperior margin of the promontory. The bony fallopian canal
containing the facial nerve runs above the oval window from the cochleari-
form process anteriorly to the stapedial pyramid posteriorly.
The mastoid cavity is shaped like a three-sided pyramid, the apex pointed
caudally. The roof of the mastoid is the middle cranial fossa. The medial
wall is the lateral wall of the posterior cranial fossa. The sigmoid sinus flows
beneath the dura mater of this region. The anterior wall contains the aditus
and antrum. The bulge of the lateral semicircular canal projects into the
antrum. Below these two landmarks, the facial nerve runs in its bony canal
to exit the temporal bone at the stylomastoid foramen, which is located at
the anterior end of a ridge formed by the insertion of the digastric muscle.
The lateral wall of the mastoid is subcutaneous bone easily palpable posterior
to the pinna.
34 PART TWO—THE EAR
FIGURE 2—8. The relative size and the topography of the eustachian tube are depicted in this
drawing by Brodel.
2—EMBRYOLOGY, ANATOMY, AND PHYSIOLOGY OF THE EAR 35
The nerve fibers then run through a bony shelf, the osseous spiral lamina,
to reach the sensory cells of the organ of Corti (Fig. 2-9). The bony cavity
of the cochlea is divided into three portions by the endolyfnph-contaming,
35 mm long cochlear duct. The upper scala vestibuli contains perilymph and
is divided from the cochlear duct by the thin Reissner’^ membrane. The
lower scala tympani contains perilymph and is divided from the cochlear
duct by the osseous spiral lamina and the basilar membrane. The perilymph
of these two scalae communicates at the apex of the spiral cochlea past the
blind end of the cochlear duct, through a small opening called the helico-
trema. The basilar membrane is narrow at the base (high tones) and wide
at the apex (low tones).
Sitting upon the basilar membrane, from the base to the apex, is the organ
of Corti, which contains the essential organelles of the peripheral neural
mechanism of hearing. The organ of Corti contains one row of inner hair
cells (3,000) and three rows of outer hair cells (12,000). They are suspended
through holes on the horizontal arm of a teeter-totter formed by supporting
cells (Fig. 2-10). Afferent and efferent nerve-ending boutons attach to the
lower ends of the hair cells. From the superior surface of the hair cells
project stereocilia that are attached to a gelatinous, acellular, overlying,
rather flat mantle called the tectorial membrane. This tectorial membrane is
secreted and supported by a medially placed platform called the limbus.
The vestibular part of the inner ear is made up of the saccule, utricle, and
semicircular canals. The utricle and saccule both contain a macula that is
covered with hair cells. Overlying these hair cells is a gelatinous layer into
which the cilia project, and within this gelatinous layer are calcium-containing
otoliths, which have a heavier density than the endolymph. These otoliths
are pulled on by gravity, and this shearing force bends the cilia of the hair
cells and stimulates the receptors.
The saccule communicates with the utricle via a narrow duct that is also
the passage leading to the endolymphatic sac. The utricular macula is on a
plane perpendicular to the saccular macula. The three semicircular canals
open into the utricle. Each semicircular canal has one end which is dilated
into an ampulla that contains the hair cells of the crista. The hair cells
project into a gelatinous cupula. Movements of the endolymph within the
semicircular canal will move the cupula, which will bend the cilia of the hair
cells of the crista and stimulate the receptors (see Chapter 3).
The pinna is, to some extent, a “collector” pf sound. The external auditory
canal, because of its shape and dimension, greatly amplifies the sounds in
the region of 2 to 4 kHz; it will amplify these frequencies by 10 to 15 dB.
Thus, sounds in this frequency range are most hazardous from the standpoint
of acoustic trauma.
The middle ear contains the malleus, incus, and stapes (Fig. 2-11). The
handle of the malleus is embedded in the tympanic membrane. The tensor
tympani muscle inserts into the neck of the malleus. The head of the malleus
articulates with the anterior surface of the body of the incus within the
epitympanum. The incus has a short process that projects backwards and a
long process that passes down to articulate with the head of the stapes.
The natural axis of rotation of the malleus and incus is along a line from
the short process of the incus to the region of the neck of the malleus. The
stapes is a stirrup-shaped bone. The contractions of the stapedius muscle
can be measured by using impedance audiometry, and these measurements
are an important clinical tool. The middle earjs an impedance-matching
device between air (our environment) and liquid (inner ear), When sound
waves transmitted through air reach fluid, 99.9 per cent of the energy is
reflected. Only 0.1 per cent is transmitted (a loss of 30 dB). The middle ear
compensates for the loss primarily because the tympanic membrane has an
area 17 times greater than that of the stapedial footplate. The ossicular chain
contributes a levered gain of 1.2/1. Thus, a middle ear is unnecessary in
creatures that live in water.
The vibrations of sound are transmitted through the external auditory
canal and middle ear to the inner ear via the stapes, causing a travelling
wave to be created along the basilar membrane and its organ of Corti. The
peak of the travelling wave along the 35 mm long basilar membrane is
determined by the frequency of the sound wave. This results in bending of
the stereocilia by shearing action with the tectorial membrane, thus depolar¬
izing the hair cells and creating action potentials in the attached auditory
nerve fibers. It is here that the mechanical sound waves are converted to the
electrochemical energy for transmission through the eighth cranial nerve. At
least some frequency analysis occurs at the organ of Corti level. The electrical
event in the organ of Corti can be measured and is called the cochlear
2—EMBRYOLOGY, ANATOMY, AND PHYSIOLOGY OF THE EAR 37
Squar
Teqmen tympani
Incus V-O I 1 v
Aditus to
' tv antrum
Suspensory
liqamerft <
mal leus
Mai leus
Mastoid
Attic Vj, antrum
(epitym- L0
panum)
Tympanic
membrane
Auditory tube -
neuron derives from many outer hair cells and each outer hair cell is
innervated from many different afferent neurons.
There are also about 500 efferent nerve fibers reaching each cochlea.
These also branch extensively, such that each outer hair cell has many
efferent nerve endings. Any one outer hair cell’s efferent nerve endings are
not all derived from one efferent neural fiber.
The neural fibers of the cochlear nerve (Fig. 2-12) pass to the dorsal and
ventral cochlear nuclei. Most fibers from the nuclei cross the midline and
ascend to the contralateral inferior colliculus, but some ascend ipsilaterally.
There are further crossovers at the nuclei of the lateral lemniscus and inferior
colliculi. From the inferior colliculi, the auditory pathway runs to the medial
geniculate body and then to the auditory cortex of the temporal lobe.
Because of the frequent crossing over of nerve fibers, central lesions of the
auditory pathways almost never cause a unilateral hearing loss.
The neural fibers of the vestibular nerve pass to one of the four vestibular
nuclei and from there are widely distributed, with pathways to the spinal
cord, cerebellum, and other parts of the central nervous system.
References
Anson BJ, Donaldson JA: Surgical Anatomy of the Temporal Bone and Ear. Philadelphia,
WB Saunders, 1981.
Schuknecht HF, Gulya AJ: Anatomy of the Temporal Bone with Surgical Implications
Philadelphia, Lea & Febiger, 1986.
Shambaugh GE, Glasscock ME: Surgery of the Ear. Philadelphia, WB Saunders, 1980.
3
THE VESTIBULAR SYSTEM
by John H. Anderson, M.D., Ph.D., and Samuel C. Levine, M.D.
PHYSIOLOGY
Sensory signals coming from the inner ear, the retina of the eye, and the
musculoskeletal system are integrated in the central nervous system (CNS)
in order to control gaze and the position and movement of the body in
space. In this section we briefly describe the equilibrium receptors and Adequate stimulus: accelera¬
tion, a change in velocity per
discuss their role. When we refer to the "vestibular system,” we mean not
unit of time.
only the receptors but also the pathways in the CNS which are involved in
processing the afferent signals and which activate motoneurons.
The receptors are hair cells located in the cristae of the semicircular canals
and the maculae of the otolith organs. Functionally there are two types.
Those of the semicircular canals are sensitive to rotation, specifically to
angular acceleration (which is a change in angular velocity), and those of
the otolith organs are sensitive to linear motion, specifically to linear
acceleration, and to changes in head position relative to gravity. This
difference in sensitivity to linear versus angular acceleration is due to the
geometry of the canals and otolith organs and the physical characteristics of
the structures overlying the hair cells.
Hair Cells. Morphologically, the individual hair cells of the canals and
otolith organs are very similar. Each has a structural polarization that is
defined by the positions of the stereocilia relative to the kinocilium (see Fig. Polarization of hair cells: struc¬
tural and functional.
3-1). Corresponding to this, there is a functional polarization in the response
of the hair cells (see Fig. 3-2). If a movement causes the stereocilia to be
bent toward the kinocilium, then the hair cells are excited. If the movement
is in the opposite direction and causes a bending away from the kinocilium,
then the hair cells are inhibited. In the absence of any movement, there is
some release of transmitter from the hair cells which causes the afferent
nerve fibers to have a spontaneous or resting firing rate. This makes it
possible for the afferents to be either excited or inhibited, depending on the
direction of the movement.
Semicircular Canals. In any one canal the polarization is the same for all
the hair cells, and during a rotation they are all either excited or inhibited. Canal pairs: excitation and inhi¬
bition.
The three canals are approximately perpendicular to each other, and each
canal of one ear is approximately coplanar with a canal from the other ear.
Thus, there are three pairs: left horizontal-right horizontal, left anterior-
right posterior, and left posterior-right anterior. During a rotation one canal
of a pair will be excited while the other will be inhibited. For example, if
the head is in a normal, upright position and there is an acceleration in the
horizontal plane causing a rotation to the right, then the afferents of the
right horizontal canal will be excited and those of the left canal will be
inhibited. If the rotation is in the vertical plane, causing a forward rotation,
39
40 PART TWO -THE EAR
then the anterior canals of both sides will be excited and the posterior canals
inhibited.
It should be noted that angular acceleration is the adequate stimulus for
Canal stimulus: angular acceler- the semicircular canal afferents. A constant velocity rotation will not excite
ation. them. Of course, in order to reach a given velocity, there must be an
acceleration and the effects of this will decay to zero over time, up to a few
minutes. This time lag is due to CNS processing of the afferent activity and
to the inertia of the cupula and the viscosity of the endolymph, which cause
the displacement of the cupula to lag behind the change in the angular
velocity of the head. For example, consider the effect of suddenly coming
to a stop after rotating to the right, in a clockwise direction. This deceleration
to zero velocity is equivalent to an acceleration in the opposite direction, to
the left. Therefore, the afferents of the left canal will be excited and those
of the right inhibited. If this is done in complete darkness, then the subject
will have the perception that he is rotating to the left. As the cupula of each
canal returns to its resting position, the subject will perceive that he comes
to a stop.
Otolith Organs. There are two otolith organs: the utriculus, which is
located approximately in the horizontal plane of the head, and the sacculus,
which is located approximately in the vertical plane. In contrast to the
semicircular canals, the hair cells of a given otolith organ do not all have
the same polarization. In the utricular macula, the kinocilium is located on
the side of the hair cell located closest to the central region, the striola.
Thus, during a given head tilt or linear acceleration, some of the afferents Otolith stimulus: linear acceler¬
ation and gravity.
will be excited and others will be inhibited. However, this does not mean
that there will be a cancellation of the responses in the CNS. The afferents
with a given polarization may project to different neurons in the vestibular
nuclei and may subserve different functions. Also, because there are different
polarizations within each macula, the CNS has information about linear
motion in three dimensions, even though there are only two maculae.
Vestibular Reflexes. The afferents go the CNS and^synapse on neurons in
the vestibular nuclei in the brain stem. Neurons in the vestibular nuclei then
project to other parts of the brain; some go directly to the motoneurons
innervating the extraocular muscles and to spinal motoneurons and others
go to the brain stem reticular formation, cerebellum, and other structures.
Direct connections between the vestibular nuclei and the extraocular
motoneurons constitute one important pathway by which eye movements
and the vestibulo-ocular reflex (VOR) are controlled. The VOR is an eye Nystagmus: slow phase (com¬
pensatory) alternating with fast
movement that has a “slow” component opposite to the head rotation and phase (in opposite direction).
a “fast” component in the same direction as the head rotation. The slow
component compensates for the head movement and serves to stabilize an
image on the retina. The fast component serves to redirect gaze to another
part of the visual field. This alteration in the direction of the eye movement
during vestibular stimulation is one example of a normal nystagmus.
EYES IN
'ry0 ■ NEUTRAL
POSITION
L y/®CI8*
EYES
SWING EYES
TO RIGHT SWING
TO LEFT
measured for constant accelerations, and the phase and gain are measured
for sinusoidal rotations.
Another paradigm involves the subject himself moving his head back and
forth. In this case there is stimulation of both the vestibular receptors and
the receptors in the neck muscles. The latter may play an important role in
compensating for the loss of vestibular function. Although this is a Active head movement and high
complicating factor, the paradigm has the advantage that very rapid head frequency stimulation.
movements with large amplitudes can be attained so that the vestibular
labyrinth (together with the neck muscle receptors) can be very strongly
44 PART TWO—THE EAR
inputs detect no motion while in fact the body is swaying back and forth. In
normal subjects, the vestibular system provides an inertial reference to
resolve this conflict and posture is maintained. The vestibular-deficient
subjects, however, cannot do this.
SUMMARY
References
Black FO: Vestibulospinal function assessment by moving platform posturography. Am J
Otolaryngol 6:39-46, 1985.
Fineberg R, O’Leary DP, Davis LL: Use of active head movements for computerized vestibular
testing. Arch Otolaryngol Head Neck Surg 113:1063-1065, 1987.
Honrubia V, Baloh RW, Yee RD, Jenkins HA: Identification of the location of vestibular
lesions on the basis of vestibulo-ocular reflex measurements. Am J Otolaryngol 1(41:291-
301, 1980.
Honrubia V, Jenkins HA, Baloh RW, et al: Vestibulo-ocular reflexes in peripheral labyrinthine
lesions: I. Unilateral dysfunction. Am J Otolaryngol 5:15-26, 1984.
Hudspeth AJ: Transduction and tuning by vertebrate hair cells. Trends Neurosci, Sept 1983,
pp 366-369.
Leigh RJ, Zee DS: The Neurology of Eye Movement. Philadelphia, FA Davis, 1983.
Miles FA, Lisberger SG: Plasticity in the vestibulo-ocular reflex: A new hypothesis. Annu Rev
Neurosci 4:273-300, 1981.
Robinson DA: The use of control systems analysis in the neurophysiology of eye movements.
Annu Rev Neurosci 4:463-503, 1981.
Takahashi M, Uemura T, Fuyishiro T: Compensatory eye movement and gaze fixation during
active head rotation in patients with labyrinthine disorders. Ann Otol 90:241-245, 1981.
4
AUDIOLOGY
by Frank M Lassman, Ph.D., Samuel C. Levine, M.D., and
Donna G. Greenfield, MS.
Purposes of Audiology
Audiology, which is the science of hearing, involves the evaluation of
hearing and the rehabilitation of individuals with communication problems
related to hearing impairment. There are two reasons for evaluation: (1)
medical diagnosis of the location and type of disease and (2) assessment of
the impact of hearing impairment upon learning, social interaction, and
vocation.
Hearing measurements can add precision to diagnose the locus of patho¬
logic involvement and specific disease entities. Patients with different diseases
within the same area (e.g., noise deafness and Meniere’s syndrome both
involve the cochlea) report very different hearing experiences and will have
potentially different audiometric findings. Likewise, the qualities of the
impaired hearing experience will limit attention skills, language development,
speech precision, and general communication effectiveness in ways specific
to the degree and type of impairment. Plans for special education and
rehabilitation should be influenced and guided by the hearing measurement
along with other important variables such as intelligence, motivation, and
family support. The physician is forced to look at the integrity of the middle
ear somewhat indirectly and is totally unable to examine the cochlea and
the auditory nervous system except by studying the way they function in
response to sound.
problems are due to disorders of the external or middle ear. Sensorineural Types of hearing impairment:
(II conductive, (2) sensori¬
hearing problems are secondary to disturbance of the cochlea, eighth nerve,
neural (cochlear and retrococh¬
or central auditory channels. Earlier terms such as “nerve” loss and “per¬ lear), (3) mixed.
ceptive” loss have been discarded because most so-called nerve diseases
were found in or had originated in the cochlea, whereas “perceptive”
suggested a psychological dynamic. The distinction between “cochlear” and
“retrocochlear” is considered by some to be useful when the test battery is
sufficiently sophisticated. Mixed or combined hearing loss involves distur¬
bances of both conductive and sensorineural mechanisms.
Testing Models
Air conduction (AC) utilizes the external and middle ear in the transmis¬
sion of sound to the cochlea and beyond. It is thought to be the usual avenue
of sound transmission. In bone conduction (BC), the skull is set into vibration
by direct contact with a periodically oscillating body, such as a tuning fork.
The bone-conducted stimulus is thought to set the cochlear fluids into
motion, bypassing the external and middle ear. Bekesy (1932) has shown
that the vibrating patterns of the cochlea are the same regardless of whether
sound has been introduced by air conduction or bone conduction.
The bone conduction test has been traditionally treated as a measure of
the integrity of the cochlea and beyond. Normal bone conduction hearing
strongly suggests normal cochlear, nerve, and brain stem function. If the
sensorineural component (BC) is normal, while the total system (AC) is
impaired (BC>AC), the impairment is judged to have resulted from damage
to the remaining portion of the system, i.e., the middle ear and/or external
ear, not measured by the normal bone conduction finding. On the other
hand, if the bone conduction measurement is no more sensitive than the air
conduction (BC=£AC), the total impairment is judged to have resulted from
damage or change in the cochlear or retrocochlear mechanism. But many
investigators led by Tonndorf have challenged this traditional interpretation
of the absent air/bone gap. They demonstrate some elevation of bone
conduction threshold secondary to middle ear disturbances.
A set of tuning forks sampling the auditory range from low to high
frequencies makes a survey of hearing sensitivity easy for the physician. The
usual set samples some of the C notes of the musical scale, i.e., 128, 256,
512, 1024, 2048, 4096, and 8192 Hz. Hz is the abbreviation for hertz, which
is the contemporary designation for “cycles per second,” the unit of fre¬
quency. The higher the frequency, the higher .the pitch. Limiting the survey
to the so-called speech frequencies—512, 1024, and 2048 Hz—is usually
sufficient.
Threshold
The tuning fork is held by the. stem, and one of the tines is struck against
a firm but resilient surface, such as the heel of the hand or the elbow. Care
48 PART TWO—THE EAR
should be taken not to strike the fork against the edge of a table or some
other unyielding object that will produce overtones, some of which are
With care, forks canprovide iin- audible at some distance from the fork, and may even cause permanent
portant diagnostic information. alteration in the vibratory pattern of the fork. The fork is held close to the
ear, and the patient is asked to report when the sound is no longer audible.
At that report, the fork is placed next to the examiner’s ear and the interval
between that time and the time at which the sound is no longer audible to
the examiner is measured. The procedure not only provides a rough estimate
of relative hearing sensitivity but, if forks are available in various frequencies,
offers a pitch sensitivity pattern.
Schwabach Test
The Schwabach test compares the patient’s bone conduction to that of the
examiner. While the stem of the vibrating fork is held against the mastoid,
Schwabach: mastoid to mastoid, the patient reports when the sound becomes inaudible. At that moment, the
examiner applies the fork stem to his own mastoid and measures the time
(in seconds) the examiner can still perceive the sound.
A normal Schwabach is obtained when the patient and examiner have
approximately equal bone conduction. A prolonged or increased Schwabach
is assigned when the patient’s bone conduction is appreciably longer than
the examiner’s, as in the instance of conductive hearing impairment. When
the examiner can hear the fork well after the patient, suggesting a sensori¬
neural hearing impairment, the term diminished Schwabach is applied. The
interpretations of the Schwabach test are shown in Table 4-1.
Rinne Test
The Rinne test compares the patient’s hearing by bone conduction against
that by air conduction. The hilt of the vibrating fork is held against the
Rinne: compares bone conduc- patient’s mastoid (bone conduction) until sound is no longer heard; the tines
tion to air conduction are then piaced close to the same ear (air conduction). The normal ear will
resume hearing the fork by air conduction, a finding called the positive
Rinne (AOBC). These results are explained by an impedance mismatch.
The patient with sensorineural hearing impairment will also yield a positive
Rinne, if the fork is audible at all, since the sensorineural disturbance should
affect both air conduction and bone conduction routes equally (AOBC).
The term negative Rinne is applied when the patient cannot resume
hearing by air conduction after the fork is no longer audible by bone
conduction (AC<BC). Rinne test interpretations are summarized in Table
4-2.
Weber Test
The Weber test extends the familiar experience of hearing one’s own voice
louder when an ear is blocked. The stem of the vibrating fork is held to the
midline of the forehead, and the patient is asked to report whether the
sound is heard in the left, right, or both ears.
In general, the patient perceives the sound of the fork in the ear with
better bone cqaduction or greater conductive component. If the tone is
heard in the reportedly poorer ear, a conductive hearing loss should be
suspected for that ear. If heard in the better'ear, sensorineural loss is
suspected for the poorer ear. The fact that the patient lateralizes the
perception to the conduction-impaired ear rather than to the better ear may
seem incongruous to the patient and sometimes to the examiner.
The Weber test is most useful in instances of unilateral impairment, but
ambiguity may"develop when one ear has both conductive and sensorineural
(combined) involvement or when a tuning fork of only one frequency is
available. The clinician should use the Weber test only in conjunction with
other tests and should not interpret the test by itself.
Bing Test
The Bing test is an application of the so-called occlusion effect, in which
the fork is heard louder as the normal ear is occluded. If the auditory meatus
is alternately occluded and left open, as the vibrating fork is held to the
mastoid, an increase and decrease in loudness will be perceived by the
normal ear (positive Bing). A similar result will occur with sensorineural
hearing impairment, but the patient in whom the conductive mechanism is
already modified, as in otitis media or otosclerosis, should not notice any
loudness changes (negative Bing).
A common error in the Rinne and Schwabach tests arises from the nature
of bone conduction. A vibrating fork applied to the right mastoid vibrates
But diagnostic “power" will in¬ not only the right temporal bone but the entire head; thus, the left ear is
crease when forks are coupled being stimulated simultaneously. Attenuation across the head is minimal. In
with the other audiometric tests
in the diagnostic battery. the Rinne test the response to a bone-conducted stimulus will reflect the ear
with better bone conduction, regardless of which ear it may be. Hence, it is
possible to obtain the bone conduction response of the left ear when testing
the right ear. And if bone conduction is greater than air conduction, the
result is a false-negative Rinne.
Similarly, an increased or prolonged Schwabach for the right ear may
actually be a response of the left ear in which bone conduction is better than
in the right ear. The incidence of the false-negative Rinne and the false
increased Schwabach may be reduced by a request for localization from the
patient. It may also be controlled by the introduction of a masking noise
into the nontested ear from a masking device such as a “Barany buzzer.”
This should be done with some caution, since the high-intensity masking
noise may itself be lateralized across the skull and back to the tested ear.
Because of these problems of validity and reliability, it is wise to use a
battery of tuning fork tests, affording an opportunity for comparison among
test indications, rather than to depend upon one test. This also partly
accounts for the development of electrical audiometry.
Threshold
The objective of the measurement is to determine the lowest intensity
level in decibels that can be heard for each frequency and thus the threshold
of audibility for that sound.
FREQUENCY (Hz)
AC A 1
UnmaskedV-/ ^
AC l 1
Masked 4A
HEARING LEVEL IN dB (ANSI-69)
BC
Mastoid/
Unmasked'
BC
Mastoid Q
Masked
BC
Forehead “]
Masked
Both
BC
Forehead
Unmasked
Sound Field
j
s
Examples of No
Response Symbols
75>
SRT SPEECH DISCRIM.%
RT L RT L 7 *
FIGURE 4—1. Audiogram and key showing standard symbols.
Threshold Determination
1. Test the better ear first utilizing the following sequence of frequency
presentation: 1000 Hz, 2000 Hz, 4000 Hz, 8000 Hz, 1000 Hz (repeat),
500 Hz, 250 Hz. With the exception of the 1000 Hz repetition, the
4—AUDIOLOGY 53
Validity
Comparison of air conduction and bone conduction thresholds continues
to be an important determinant in the decision-making process related to
medical and surgical management of otologic diseases. The difference
between the air and bone thresholds is called the air-bone gap.
Masking
Masking is the obscuring of one sound by another, or the elevation in the
threshold of one signal produced by the introduction of a second signal.
Although the most efficient masker of a pure tone is another tone of the
same frequency, there is an obvious problem in differentiating the masked
signal from the masker. Narrow band noise is the most efficient masker of
pure tones. This consists of energy in a limited band of frequencies whose
center frequency is the same as the pure tone signal being tested. Getting
just the right level of masking is difficult. Too little masking results in
hearing in the nontest ear. Too much will give a wrong threshold.
Hood (1962) outlined the fundamental methods of masking:
1. Establish the air conduction audiogram of both ears in the normal way
of masking, if necessary, of the nontest ear, i.e., when the difference
in the hearing loss between the two ears exceeds 50 dB.
2. Find the bone conduction threshold with the bone conductor applied
to the mastoid of the test ear without masking of the nontest ear.
3. Apply the masking of the appropriate band to the nontest ear by means
of an insert receiver and find a bone conduction threshold reading.
4. Apply the “shadowing” procedure thus: Increase the level of the
masking noise by 10 dB above threshold and retest the bone conduction
threshold. If the bone conduction threshold is raised by 10 dB, increase
the masking intensity by another 10 dB and repeat. Continue this
procedure until the point is reached at which the bone conduction
remains constant with further additional incremented steps of 10 dB of
the masking noise. This is the “change over” point and gives the true
bone conduction threshold of the test ear.
criterion regarding when to mask for pure tone testing is applicable when
doing speech audiometry; i.e., when presentation level of the signal exceeds
the bone conduction threshold of the nontest ear by 45 dB, masking should
be used. The examiner must pay particular attention to this relationship
when testing for speech discrimination, since the words are being presented
at suprathreshold levels.
Although narrow bands of noise are preferred when masking pure tones,
their frequency responses are too limited to mask the broad spectrum of
speech. The preferred maskers are either white noise or speech noise, which
is a white noise shaped by filters to resemble the frequency spectrum of
speech.
Regardless of which noise is utilized, effective masking levels must be
established for the particular audiometer being used. This can be accom¬
plished by averaging the effective levels at 500, 1000, and 2000 Hz or through
measurements on a group of individuals with normal hearing. The noise and
speech can be mixed into the same earphone and speech thresholds deter¬
mined when several noise levels are used. This tells the examiner the dial
setting required to obtain the desired threshold shift in the masked ear.
Classic Interpretation
Audiograms may be interpreted according to degree of loss, configuration Audiogram interpretation and
or pattern of loss, and air conduction-bone conduction relationships. the air/bone gap.
A “pure” conductive loss may show any degree of impairment up to
approximately 70 dB hearing level (HL). Losses greater than 70 dB HL
must include some sensorineural component. Sensorineural losses may be of
any degree, from the mildest to the most profound.
By far the most important contribution to audiogram interpretation is
found in the relationships between air conduction and bone conduction
thresholds, that is, the presence or absence of the air-bone gap. These
relationships may be described generally as follows:
1. When bone conduction thresholds are better (more sensitive) than air
conduction thresholds by 10 dB or more and are normal, the loss is
conductive (Fig. 4-3).
2. When bone conduction thresholds are the same as air conduction
thresholds and neither is normal, the loss is sensorineural (Fig. 4-4).
3. When bone conduction thresholds are reduced but are still better than
air conductions by 10 dB or more, the loss is mixed or combined (Fig.
4-5).
56 PART TWO—THE EAR
FREQUENCY (Hz)
- lO
o -<c
. , -<-
10
20 -c \ N
-
30 ^ -i r
J Kp -1 7-
FIGURE 4-3. The reduced air conduction and normal bone
40 conduction (air-bone gap) thresholds typical of a conductive
hearing impairment.
50
60
70
80
90
1O0
FREQUENCY (Hz)
IIO
125 250 500 lOOO 2000 4000 8000
SRT SPEECH DISCRIM.%
RT L RT l
-lO •—--
CD 10 -€ s
<v
20 ■ V
z
<. 30
CQ
tJ 40
<
FIGURE 4-4. Equally reduced air and bone conduction thresh¬
olds typical of a sensorineural hearing impairment.
z
50
)—<a
—I —
UJ
> 60
UJ
_j
70
O
2
O' 80
<
UJ
X 90-
100
O
<
(ANSI-69)
10
20
"X 'v
/ I
/
30
\
LEVEL IN dB
40 \
\
50 ■-d ) v
->
60 ——^i
FIGURE 4—5. Unequally reduced air and bone conduction
70 V /- thresholds with retention of air-bone gap typical of mixed
HEARING
y--1
or combined hearing impairment.
80
90
lOO
IIO
When the air/bone gap is present there is some alteration of the conductive-
transforming mechanism of the external or middle ear. An absent air-bone
gap is seen as an index of sensorineural involvement. But the “Carhart
notch” in otosclerosis is recognized as a bone conduction threshold elevation
by a middle ear pathology, and others see a high frequency loss of bone
conduction secondary to otitis media. So caution should be exercised with a
strict interpretation of the absent air/bone gap.
More examples of typical audiograms are shown on pp 64-66.
Tympanometry
Impedance audiometry has assumed an increasingly important role in the
audiologic assessment battery. Tympanometry is an indirect measure of the
compliance (mobility) of the tympanic membrane and ossicular system under
conditions of positive, normal, and negative pressure. High acoustic energy
is introduced into the ear by a probe tube; some is absorbed, and the
remainder is reflected back out the canal and collected by a second channel
of the probe tube. In the normal ear, a measuring device shows the reflected
energy to be less than the incident energy. On the other hand, when the ear
is filled with fluid, the drum is thickened, or the ossicular system is stiffened,
the energy reflected is greater than that in the normal ear. The amount of
reflected energy is more equivalent to the incident energy. This relationship
is used as a measure of compliance.
The tympanogram is a graphic representation of relative compliance in
the tympano-ossicular system while air pressure changes are produced in the
external meatus. Maximum compliance will be obtained at normal air
pressure, while compliance is reduced as air pressure is increased or de¬
creased from normal. Persons with normal hearing and with sensorineural
hearing impairments will demonstrate a normal tympano-ossicular system.
Tympanogram types
Liden (1969) and Jerger (1970) developed a classification of tympano-
grams. The classification types, which are illustrated in Figure 4-6, are as
follows:
Type A (Normal Tympanogram). Maximum compliance occurs at or near
ambient air pressure, suggesting normal middle ear pressure.
Type As. Maximum compliance occurs at or near ambient air pressure,
but compliance is lower than in type A. Fixation or stiffening of the ossicular
system is often associated with type As.
Type Ad. Very high maximum compliance occurs at ambient pressure,
with extremely rapid increase in compliance as pressures are reduced toward
normal ambient pressure. Type AD is associated with ossicular discontinuity
or a monomeric tympanic membrane.
Type B. The tympanogram is relatively “flat” or “dome shaped,” showing
little change in the reflective quality of the tympano-ossicular system as air
pressures change in the external canal. The type B tympanogram is associated
with middle ear fluid, thickened drum, or impacted cerumen. The impedance
characteristics of the tympano-ossicular system are dominated by the
incompressible nature of the abnormality present. Small pressure changes
have little effect.
58 PART TWO—THE EAR
COMPLIANCE
Acoustic Immittance
Acoustic immittance measurements have developed with appropriate tech¬
nology to quantify the ease with which acoustic energy enters the ear. In
addition or in place of patterns A, As, AD, B, and C, acoustic immitance
describes and quantifies primary physical parameters of those patterns. These
include: (1) static admittance or tympanogram peak height; (2) equivalent
canal volume or acoustic admittance with +200 decapascals of ear canal
pressure; (3) tympanometric peak pressure (TPP), or the pressure at which
maximum admittance obtains; and (4) the gradient (GR) or tympanometric
width where there is 50 per cent reduction in the maximum admittance.
Whether immittance introduces new fundamentals or is a more precise
expression of the Jerger/Liden graphics may be argued. Nevertheless, a
clearer separation of measures may be correlated with ear disorders. The
advantage of a tympanogram type (A, etc.) is its broad-stroked description,
which can be eye-balled and communicated easily among professionals. The
admittance parameters have the potential for greater differentiation with a
profile of three to four parameters rather than any single measure.
Table 4-3 shows means and 90 per cent ranges for four admittance
parameters derived with the Welch Allyn Microtymp by Margolis and Heller
(1987) for children and adults. The parameters include peak admittance for
226 Hz (Peak Ya), equivalent ear canal volume ( + 200 Vec), tympanometric
peak pressure (TPP), and tympanometric gradient (GR).
The future direction for immittance testing exploits the differential ballis¬
tics and diaphragm physics made available by using Luscher frequency
stimuli. The potential here is to expose the presence of eardrum calcified
4—AUDIOLOGY 59
plaques, adhesions of the drum and ossicles, stapedial fixation, and other
middle ear aberrations not presently discernible with the conventional 220
Hz stimulus.
Acoustic Reflex
The acoustic reflex arc contains a direct pathway of three to four neurons.
It connects the auditory nerve to both stapedial motor neurons. The reflex
occurs bilaterally even though the eliciting signal is introduced to only one
ear. Contraction of the stapedial muscle, inserting in the head of the stapes,
produces a stiffening effect on the tympano-ossicular system. The result is
increased impedance, which manifests itself as an increase of the reflected
energy of the tone being presented to the probe tube ear. Signal strength to
elicit the reflex in subjects with normal hearing ranges from 70 to 90 dB HL
with a pure tone stimulus.
A mild to moderate unilateral conductive hearing loss (30 to 40 dB HL)
can elevate the acoustic reflex threshold by the amount of the conductive
component when the stimulus is presented to the impaired ear. Elevated
reflex thresholds have also been noted when cochlear losses exceed 60 to 65
dB HL on the stimulated ear.
The absence of the acoustic reflex can be attributed to various factors,
including a significant sensorineural hearing loss in the ear being stimulated,
a retrocochlear lesion in the stimulated ear, facial nerve involvement on the
probe ear side, congenital absence of the stapedius muscle, surgical removal
of the stapes, and a moderate or greater conductive hearing loss in the
stimulated ear.
The acoustic reflex may occur but not be a recordable event. For example,
the slight increase in tension caused by the contraction of the stapedius will
not significantly change the existing stiffness of the tympano-ossicular dis¬
continuity, since the contraction of the stapedius muscle cannot affect the
stiffness of the system.
Elevated acoustic reflex thresholds occur when stimulating the affected
ears of patients with extra-axial brain stem lesions and patients with multiple
sclerosis. In both classes of patients, there tends to be a high incidence of
acoustic reflex decay (continuous stimulation 10 seconds) with a reflex half-
life as short as 3 seconds in some individuals. Abnormal reflex decay can be
a sign of an eighth nerve tumor. The acoustic reflex is of value in assessing
peripheral facial nerve function. The acoustic reflex can be used in assessing
the hearing of neonates and other children too young to cooperate and as a
part of a test battery for functional hearing loss. Its accuracy is sufficient for
60 PART TWO—THE EAR
SPEECH AUDIOMETRY
or more between the SRT and the pure tone average. The patient may
misunderstand the directions, become uncooperative, or sometimes exagger¬
ate a hearing loss for personal gain.
Speech Discrimination
The assessment of a patient’s ability to recognize speech provides much
information. It is useful in diagnosis and treatment. A number of lists have
been developed which are phonetically balanced, i.e., reflecting the relative
incidence of the various speech sounds in the English language. Lists are Retrocochlear lesions may be
also balanced for vocabulary familiarity. The word lists are presented to the identified on discrimination
tests.
patient at a level 30 dB or 40 dB above his SRT. The patient responds
verbally. The speech discrimination score is a percentage based on the
number of words the patient repeats correctly.
The maximum speech discrimination score can generally be achieved when
the word lists are presented at 35 to 40 dB above the SRT of patients with
normal hearing, with conductive hearing loss, and frequently with mild
sensorineural losses. The expected score presented at this level may approach
94 to 100 per cent. For severe hearing impairments, in which threshold
approaches the output limits of the audiometer, test of discrimination is
often accomplished at the patient’s most comfortable level of loudness.
It may be necessary to present the word lists at several intensity levels in
order to demonstrate the top score. For some of these patients the max may
be no better than 50 to 60 per cent, and instead of a better score resulting
from greater intensity of the stimulus words, the score may actually deteri¬
orate. This phenomenon is called “rollover.” The most dramatic speech
discrimination losses occur when the patient has an eighth nerve lesion, such
as an acoustic neuroma; scores of 20 per cent or less can occur even with
relatively mild hearing levels.
The diagnostic power of discrimination tests may be enhanced by degrading
the stimulus or its environment. For example, word lists with filtering of
information above 500 Hz may be difficult to recognize through the ear
opposite the temporal lobe tumor or the temporal lobe epileptic focus.
Competing messages in the same ear with word lists will degrade performance
in the ear with the “bottleneck” problem of the acoustic tumor.
Problems
The nature of the recorded word lists will determine the discrimination
score. Variables such as precision of articulation, syllabic rate, and familiarity
are standardized within a given set of word lists but not among the sets.
Different sets yield different scores on the same ear.
Electrical potentials evoked by sound from the brain (scalp) have been
the subject of study by clinicians for three-quarters of this century. Various
response components including late responses, middle latency responses,
electrocochleography, and fast responses have attracted attention. Auditory
brain stem evoked response testing (ABR) has become more important over
62 PART TWO—THE EAR
the last 20 years and its clinical use has become widespread. ABR as we
know it was not really performed until 1968. Testing equipment was advanced
rapidly, and by 1971, Jewett had established definitive descriptions of what
the ABR looked like. Advancing this technology has been the rapid decline
in price and size of computer components that are essential to the operation
of ABR measurement apparatus.
Technique
ABR’s represent the electrical response of the eighth nerve and some
portion of the brain stem which occurs in the first 10 to 12 msec after an
auditory stimulus is sensed by the inner ear. By presenting a series of clicks
to the ear, synchronous firing from high frequency auditory fibers is elicited.
Unfortunately, it is difficult to read a single electrical response. In order to
clearly see this pattern, an averaging scheme must be used to make each of
the waves or stimulation sites apparent. Current standards present a click
stimulus at 75 dB or 80 dB above the threshold. This click repeats at a fixed
repetition rate, e.g., 11/sec or 33/sec, until 1500 or 2000 click responses have
been “averaged.” Electrodes placed over the mastoids are compared with
the midforehead, creating an EEG. By averaging these waves of the EEG,
a pattern emerges. These wave forms, which were described by Jewett in
1971, are labelled I through VII. It is clear now that waves I and II arise
from the area of the eighth cranial nerve and that later waves are generated
higher in the brain stem (Fig. 4-7).
Variables concerning the intensity and polarity of the click can be con¬
trolled. Patient conditions such as body temperature and medications can
affect the recording, but under most circumstances they are not a significant
problem in obtaining a reliable wave pattern.
The results of this test are then mapped out showing the relative time of
waves I through V. This time period is referred to as the latency of each
wave and the inter-wave latency intervals. It is also possible to describe
amplitudes and a general morphology.
Clinical Use
Clinically, the ABR is useful in several situations. First, it is helpful in the
diagnosis of cerebellopontine angle tumors. Second, it may be helpful in
I II III iv v
I_i_I_I_I_L__I_I_i
0123456 78
milliseconds
4—AUDIOLOGY 63
i i i i l_I-1-1-1
012345678
milliseconds
Meniere’s Disease
In evaluating patients with Meniere’s disease, it is important to look for
retrocochlear causes of pathology, such as acoustic tumors. Additionally, it
is important to ascertain that the problem is in fact in the cochlea itself.
ABR is an accurate indicator of this process. Apparently, cochlear lesions
have little effect on the latencies and conduction times in the pathway once
the cochlear delay has been removed. As the intensity of the stimulus
increases, the delay declines dramatically. This decline is nonlinear and is
indicative of the loudness recruitment seen in Meniere’s disease.
Threshold Evaluation
Patients who are uncooperative, or patients who cannot cooperate because
of age or mental status, can have their hearing evaluated using ABR. It is
difficult to obtain an absolute threshold, but it is possible to get close to a
threshold using ABR. It is often used in neonatal intensive care situations,
in which infants are particularly prone to sensorineural hearing loss. ABR
thresholds with clicks correlate well with pure tone thresholds of 2 KHz and
4 KHz. They correlate less well with 500 Hz, although recent work with
special filters and other strategies may help with this problem.
patients have ABR’s that are difficult to reproduce. They have frequently
changing ABR patterns that can be normal at one time and unrecognizable
or distorted the next. It provides a way of documenting and, in some cases,
diagnosing multiple sclerosis.
Coupled with the electric responses of later time frames to form an electric
response battery, the ABR can help to describe the integrity of the entire
auditory nervous system and address such considerations as auditory proc¬
essing disorders and attention deficits.
PEDIATRIC AUDIOMETRY
FREQUENCY (Hz)
-IO-
-< ( _ / -^
o -<-<-£-«-<-
\
io-
HEARING LEVEL !N dB (ANSI-69)
-6 V
20 ---—sQ
)—( r )-^c
80-
90-
lOO —-
11O ------
FREQUENCY (Hz)
«;
-10
O / / /
\
I
50 ( X-
y
)^-(
60
70
80
90
100
110
FREQUENCY (Hz)
SRT SPEECH DISCRIM.%
125 250 500 1000 2000 4000 8000
Rl30dB RT 52-68
FREQUENCY (Hz)
FREQUENCY (Hz!
o Z /
N /
10
FIGURE 4—14. The progressive nature of otosclerosis requires
at least two or three audiograms before the complete audio¬ 20
80
90
FREQUENCY (Hz)
125 250 500 1000 2000 4000 8000 SRT SPEECH DISCRIM.%
RT 35dB RT 94-100
Newborn to 24 Months
A number of clinical tests have given way to ABR testing in this area.
Behavioral tests were often difficult to evaluate, were sometimes inconsistent,
and required more experienced examiners. Most neonatal units use ABR to
screen any child thought to be at risk for hearing loss. Current recommen¬
dations include:
Speech Audiometry
Using speech to measure hearing has impressive face validity. When the
child can repeat words, point to the proper object, or perform the requested
action, the examiner has sampled a considerable portion of the nervous
system, but there are problems. The language chosen must be appropriate
for the child’s age and cultural environment. The intrinsic limitation on
language development imposed by the hearing impairment will limit the
range of vocabulary, sentence complexity, and so on. Nevertheless, certain
practices in speech audiometry are useful.
Three-year-old and some two-year-old children can be taught to repeat
familiar words or point to familiar objects. A speech reception threshold
can be obtained if these words are spoken or played through a calibrated
speech audiometer.
Discrimination scores can be accomplished with single syllable word lists
at a kindergarten level (PB-K). A number of auditory discrimination tests
(the DIP, the WIPI, and the G-F-W) have been standardized as picture
identification tasks for young children.
68 PART TWO—THE EAR
For the child who is adventitiously hearing impaired, the physician ought
to be able to obtain speech reception thresholds and discrimination estimates
similar to those obtained in adults, but the language restrictions of the
congenitally hearing impaired child will seriously limit applications without
considerable listening training.
HEARING AIDS
Amplification Features
A hearing aid is a miniature public address system. It has a microphone,
an amplifier, a loudspeaker, and a battery as power source. It is further
adapted with gain control, tone control, and maximum power control.
Recently, automatic signal processing devices have been added in an effort
to improve the signal-to-noise ratio in background noise. These components
are “packaged” for wearing in the ear (ITE) (Fig. 4-16) behind the ear
(BTE) (Fig. 4-17), and on the body (Fig. 4-18). The smallest of the ITE
type are the “canal” aids with some components set deeper in the canal and
closer to the eardrum.
Ear Selection
Binaural hearing is strongly recommended whenever possible. The advan¬
tages of binaural amplification may include (1) improved speech discrimi¬
nation in background noise; (2) binaural summation, which results in a
loudness advantage compared with the loudness when listening to the same
signal monaurally; (3) the “squelch effect,” or suppression of background
noise when attending to a primary signal; (4) elimination of the head shadow
effect; (5) localization; and (6) judgments of naturalness.
For personal or for audiologic reasons, some patients may not be candi¬
dates for binaural amplification. Therefore, it becomes necessary to select
the one ear that can benefit most from amplification. Generally speaking,
the ear chosen is the ear with the better speech discrimination and widest
dynamic range. The dynamic range is the difference between the hearing
threshold level and the threshold of discomfort.
72 PART TWO—THE EAR
Unilateral Hearing Loss. If the unilateral hearing loss does not exceed 60
to 70 dB hearing loss, if speech discrimination is relatively good, and if
amplified sound is tolerated well, amplification can be used in the impaired
ear. This arrangement will provide the user with some binaural cues and will
minimize the head shadow effect.
If the impaired ear does not meet these criteria, a CROS (Contralateral
Routing of Signals) hearing aid can be used. The microphone is housed in
one hearing aid, and the amplifier and receiver are located in the second
hearing aid. This arrangement also can be built into eye glasses. The signal,
therefore, is delivered from the impaired ear to the ear with normal hearing.
A radio frequency circuit may be used to transmit sound from one side to
the other. Although the CROS hearing aid does little to improve localization,
it does occasionally prove helpful in certain noise listening conditions and
also minimizes the head shadow effect.
Variations of the CROS, namely, the Bi-CROS or the Multi-CROS, can
be used when a significant hearing loss exists in the better ear, and the
poorer ear is not deemed suitable for amplification. The Bi-CROS has a
microphone in each hearing aid and a single amplifier feeding sound into
the better ear.
Cochlear Implants
Some individuals receive little benefit from hearing aid use. Indeed, the
hearing aid may provide the individual with only vibrotactile stimulation and
not with improvement in speech discrimination.
For some of these individuals, the cochlear implant has been recom¬
mended. The cochlear implant is designed for patients with profound
sensorineural deafness. The functioning of the sensory hair cells is impaired
in these individuals, whereas the auditory nerve may still function adequately.
Several kinds of cochlear implants have been developed. All the devices
have four features in common: a microphone for picking up the sound, a
microelectronic processor for converting the sound into electrical signals, a
transmission system for relaying the signals to the implanted components,
4—AUDIOLOGY
and a long, slender electrode that the surgeon inserts into the scala tympani
to the inner reaches of the cochlea. This electrode is intended to deliver
electrical stimuli directly to the fibers of the auditory nerve in one or more
places. Some devices developed have only single-channel electrodes, whereas
others have multichannel electrodes.
Depending on the type of cochlear implant, it may provide information
regarding intensity, segmental features such as voiced/voiceless, consonants,
tempo and rhythm, intonation, and word stress. These auditory cues in
conjunction with lipreading may significantly improve speech discrimination
abilities. The multichannel devices seem to be assisting lipreading and, in a
few patients, seem to improve discrimination without lipreading. Work in
this area continues to be experimental, and clinical decisions should remain
conservative and realistic.
AURAL REHABILITATION
Preschool Programs
Because of the influence of the parents’ language input on the child’s early
linguistic maturation, parents are encouraged to assume a more active role
in the education and language training of their hearing-impaired preschool¬
ers. Many preschool programs offer descriptions and demonstrations of
techniques that the parents can use at home to assist the child in developing
lipreading and listening skills. The parents also receive instructionTegarding
hearing loss, language development, communication problems, hearing aid
maintenance, and child management. During the first three years, the parents
are the primary source of language stimulation. Most educators feel that as
the parents’ knowledge about communication increases, their effectiveness
as teachers will likewise increase.
When the child is enrolled in a nursery school program, the teacher
assumes a more dominant role in language training. The parents’ participa¬
tion, while not diminishing, is more closely related to the teacher’s lesson
plans in order to supplement and expand classroom activities at home. The
emphasis of the nursery school program is on language development,
expansion of vocabulary, improved communication skills, and socialization
with peers.
As a child prepares to leave the preschool program, placement recom¬
mendations are made based on his language and communication skills, social
maturity, and academic readiness. Placement options include a self-contained
class for hearing impaired in a day school setting, residential school for
hearing impaired, or full- or part-time integration (mainstreaming) in a
normal hearing class.
Integration (Mainstreaming)
Children who are integrated into normal classes generally have developed
good aural/oral communication skills. However, children whose primary
method of communication is sign language may attend normal classes with
the help of an interpreter.
Efforts should be made to provide <the necessary adaptations and services
to maintain the child in the regular classroom. The ambient noise level and
reverberation characteristics of typical classrooms tend to create difficulties
for the hearing-impaired student. Preferential seating near the teacher,
4—AUDIOLOGY 75
Methodology
The form of communication one should teach the hearing-impaired child
has been a matter of controversy for many years. Initially, the methods were
reduced to oralism vs. manualism (sign language), with many advocates and
variations on each theme.
There are several different methods used to develop oral language/speech
skills by deaf children. They emphasize lipreading and hearing in various
combinations from the extreme of amplified hearing exclusively and without
lipreading to almost the same emphasis on lipreading. As hearing aids of
greater strength and fidelity were developed, the child’s residual hearing
became a more important determinant of the educational method. The
development of auditory training devices with the teacher wearing a micro¬
phone/transmitter at a constant distance from her mouth afforded greater
speech precision and better speech/background noise relationships.
American Sign Language (Ameslan) is a system of handsigns in general
use in this country. Each gesture signifies a word, a phrase, or a concept.
Abstractions tend to be communicated in concrete terms. The main criticism
of Ameslan is its crude grammar. The syntactical structure does not mirror
spoken or written English nor are there markers for past tense or plurals.
The various shadings and subtle differences in words may come blurred in
Ameslan communication.
Finger spelling is a finger alphabet. It is usually used to augment rather
than replace Ameslan. Finger spelling is important when exact names and
numbers need to be communicated in an otherwise almost totally Ameslan
system. Ameslan and finger spelling were developed into variants, such as
Seeing Essential English (SEE), which answered some of the criticism of
Ameslan alone. The “combined approach” and the “Rochester method”
joined manual communication with speech.
More recently, Total Communication has emerged to become a leading
educational philosophy and practice. Its basic tenet is that every possible
means should be used to communicate with the hearing-impaired child. The
child is exposed to sign ^language, finger spelling, natural gestures, facial
expressions, lipreading, bodily movement, speech heard through a hearing
aid, and auditory training. Some critics question whether multimodal or
even bimodal stimulation can be facilitative or just confusing. Many believe
that the teacher’s bias determines the child’s eventual choice of communi¬
cation modality.
Whatever approach is best suited for the hearing-impaired child depends
upon a number of factors such as age of onset and of identification, severity
and type of hearing loss, auditory processing skills, home environment and
parental involvement, and age of hearing aid usage. In an enlightened
program, advocacy of a method does not occur. The unique talents and
needs of the individual child are considered by the professional along with
the family, and the educational method or approach is tailored to meet those
needs.
76 PART TWO—THE EAR
References
HronfrihntBOne fc°ndu,?ion: A rev'ew of the Present position with special reference to the
contributions of Dr. Georg von Bekesy. J Acoust Soc Am 24:1325-1332, 1962.
Jerger J. Chnic,a! experience with impedance audiometry. Arch Otolaryngol 92:311-324 1970
94 aSb-eorSr Aud,t°ry evoked far fields ^raged from the scalp of humans’ Brain
Katz J: Handbook of Clinical Audiology. 3rd ed. Baltimore, Williams & Wilkins, 1985.
1969° lhe SC°Pe 3nd appllcatlon of current audiometric tests. J Laryngol Otol 83:507-520,
M268197-208’ lg^ JW: Screening tympanometry criteria for medical referral. Audiology
References
Anderson TW, et al: The effect on winter illness of large doses of vitamin C. Can Med Assoc
1 111:31,1974.
Andrewes CH: Rhinoviruses and common colds. Ann Rev Med 17:361-370, 1966.
Barton RPE: Clinical manifestations of leprous rhinitis. Ann Otol Rhinol Laryngol 85 74-82
1976.
Bernstein L, et al: The nasal cavities. Otol Clin North Am 6:609-874, 1973.
Dykes, MH, Meier P: Ascorbic acid and the common cold. JAMA 231:1073, 1975.
Karlowski TR, et al: Ascorbic acid for the common cold. JAMA 231:1038, 1975.
Luke M, Mehrize A, Folger F, Rowe R: Chronic nasopharyngeal obstruction causing cor
pulmonale. Pediatrics 37:762-768, 1966.
McDonald TJ, DeRemee RA, Kern EB, Harrison EG: Nasal manifestations of Wegener’s
granulomatosis. Laryngoscope 84:2101-2112, 1974.
Meyer HM: The control of viral diseases. J Pediatr 73:653, 1968.
Ogura J, Togawa K, Dammkeohler D, et al: Nasal obstruction and the mechanics of breathing
Arch Otolaryngol 83:135-150, 1966.
Paoling L: Ascorbic acid and the common cold. Scott Med J 18:1-2, 1973.
Riggs RH: Some congenital nasal anomalies including dermoid cysts. J Louisiana State Med
Soc 118:1-4, 1966.
Schaeffer JP: The Nose, Paranasal Sinuses, Nasolacrimal Passageways and Olfactory Organ in
Man. New York, Blakiston, 1920.
Settipane GA: Allergic rhinitis—update. Otolaryngol Head Neck Surg 94:470-475, 1986.
Sooknundun M, Deka RC, Kacker SK, Kapila K: Congenital mid-line sinus of the dorsum of
the nose. Two case reports with a literature survey. J Laryngol Otol 100:1319-1322, 1986.
Stahl RH: Allergic disorders of the nose and paranasal sinuses. Otolaryngol Clin North Am
7:703-718, 1974.
Stoksted P, Neilsen J: Rhinometric measurements of the nasal passages. Ann Otol Rhinol
Laryngol 66:187-197, 1957.
5
DISEASES OF THE
EXTERNAL EAR
by Lawrence R. Boies, jr., M.D.
The external ear includes the auricle, or pinna, and the external auditory
canal. The canal has both a cartilaginous and a bony portion. As noted in
Chapter 2, the tympanic membrane divides the middle ear from the external
ear.
The external ear serves to collect and funnel sound waves to the middle
ear structures. Because of the unique anatomy of the auricle and the curved,
or spiral, configuration of the canal, the external ear protects the tympanic The external ear affords protec-
membrane from injury, foreign bodies, and thermal effects (see Fig. 1-1). Hon to the tympanic membrane.
The external auditory canal is roughly 2.5 cm long, extending from the
anterior lip of the concha to the tympanic membrane. The outer one third
is referred to as cartilaginous, while the inner two thirds is the bony portion
(Fig. 5-1). The narrowest area-of the canal is near the bone-cartilage
77
78 PART TWQ—
—THE EAR
junction. Only the outer one third, or cartilaginous portion, is mobile. When
The auricle is pulled posterolat- one inserts an otoscope, the auricle normally must be pulled posterolaterally
eraily to insert an otoscope. in order to view the bony canal and tympanic membrane. Together with the
outer layer of the tympanic membrane, the canal forms an epithelium-lined-
pouch that can trap moisture, making this area susceptible to infections
under certain conditions.
The skin lining the cartilaginous portion is thicker than that lining the
bony portion and contains hair follicles, the number of which varies among
individuals but which help afford a barrier in the canal. The anatomy of the
bony external auditory canal is unique in that it is the only place in the body
where there is skin directly overlying bone with no subcutaneous tissue.
Thus, this area is extremely sensitive and any swelling is very painful, as
there is no room for expansion.
One way the external ear provides protection is through the formation of
cerumen, or ear wax. Most of the glandular structures, the sebaceous and
apocrine glands that produce cerumen, are located in the cartilaginous
Cerumen has protective portion of the canal. The exfoliated cells of the stratum corneum also
qualities. contribute to the formation of this unusual substance, which provides a
protective, water-repellent coating to the canal wall. The pH of the combined
ingredients is around 6, an additional factor that acts to prevent infection.
Furthermore, migration of desquamated epithelial cells provides a self¬
cleansing mechanism from the tympanic membrane outward.
Infection and inflammation of the external ear canal are among the most
Ear canal infections are more common otolaryngologic problems, especially during warm, humid weather.
common in a warm, humid The more common presenting symptoms of conditions involving the auricle
environment.
and external auditory canal may include the following: pain (otalgia), itching,
swelling, bleeding, and a blocked sensation.
A careful examination of the ear and surrounding region will usually
reveal a specific problem. The importance of the remainder of the otolar¬
yngologic examination should be stressed. Points of interest in the patient’s
history might include past external ear infections, recent swimming, other
skin problems, allergies, trauma, and the use of ear jewelry, especially items
containing nickel.
CERUMEN
Cerumen is the product of both sebaceous and apocrine glands, which are
located in the cartilaginous portion of the external auditory canal. There are
two basic types, “wet” and “dry.” Their autosomal pattern of inheritance
was not widely recognized until 1962 when it was reported by Matsunaga.
The wet type is dominant. Caucasians have a greater than 80 per cent
probability of having a wet, sticky, honey-colored ear wax that may darken
on exposure to the elements. Blacks have an even greater predisposition
toward this type. In the Mongoloid races, including the American Indian,
the dry, scaly, “rice brand” phenotype is more frequently seen. Neither
variant has a clear association with inflammatory conditions involving the
external canal.
Cerumen is known to have protective qualities. It acts as ad/ehicle for the
removal of epithelial debris and contaminants away from the tympanic
membrane. It provides lubrication and prevents desiccation of the epidermis
Cerumen has bactericidal with its associated Assuring. Studies have demonstrated that wet and dry
properties, cerumen have quite'similar bactericidal effects. Although these studies were
carried out in vitro, it is probable that in vivo results would be comparable.
5—DISEASES OF THE EXTERNAL EAR 79
EXTERNAL OTITIS
The term external otitis has long been used to describe a variety of
conditions. The spectrum of infections and inflammations includes both acute
and chronic forms. Under infections one must consider bacterial, fungal,
and viral-agents. Noninfectious inflammations include the dermatoses, some
of which are primary conditions directly involving the external ear. Shapiro
has pointed out that the distinction between an external otitis that is primarily
a dermatosis and that which is of infectious origin is not always clear. A
dermatosis may become infected after a time, while a skin infection may
develop an eczematous reaction to the causal organism. Again, a careful
history and examination often will give a clue to the primary condition.
Emphasis here will be on the infections and inflammatory conditions of
the external ear which most frequently confront the physician.
Infections may occur as a result of certain predisposing factors, such as
the following:
Thymol/alcohol
Salicylic acid/alcohol Mainly fungal’organisms—may also be effective against
Boric acid/alcohol bacterial infections by lowering pH of canal, skin
Acetic acid/alcohol
M-cresyl acetate
Generally antiseptic
Aqueous merthiolate
82 PART TWO—THE EAR
obacter aerogenes. Lakes, oceans, and private pools are all potential sources
of this type of infection. Diagnostic features include:
1. Tragal tenderness
2. Severe pain
3. Canal wall swelling involving most of the canal
4. Scanty discharge
5. Normal or slightly diminished hearing
6. Absence of obvious fungal particles
7. Possible presence of tender regional ^denopathv
Diffuse otitis externa usually is The stroma overlying the bone of the inner third of the canal is very thin,
very painful. allowing minimal room for swelling. Thus, the subjective discomfort the
patient experiences is often out of proportion to the extent of the disease
visualized.
Because of the degree of circumferential canal wall edema often seen, a
wick may be required to bring medication into contact with most of the
canal wall. A short strip of gauze packing may be used for this purpose;
Use of an ear wick may be however, specially designed products, such as the Pope Otowick, are now
indicated. widely available and are generally preferred. An alligator-type ear forceps
is ideal for introduction of ear wicks, with the wick then kept saturated with
the selected otic solution. One has the choice of several different otic
medications for the treatment of diffuse external otitis (see Table 5-1).
Frequently used otic dr-ops include Cortisporin (polymyxin B, neomycin,
hydrocortisone), Coly-My.cin S (colistin, neomycin, hydrocortisone), Pyoci-
din (polymyxin B, hydrocortisone), VoSol HC (acetic acid—nonaqueous 2
per cent, hydrocortisone), and Chloromycetin (chloramphenicol).
Only in severe cases should systemic drugs be considered; bacterial
sensitivity studies are recommended. Systemic antibiotics are required es¬
pecially if perichondritis or chondritis of the ear cartilage is suspected.
Diffuse external otitis secondary to acute or chronic otitis media may be
encountered. Treatment then must be aimed primarily toward the middle
ear involvement in these cases.
(m-cres.yLace.tate), and Otic Domeboro (acetic acid 2 per cent) are of value
in most cases. Recently, there has been increasing acceptance of specific
topical fungicides such as nystatin-containing preparations (Mycostatin, My-
colog) and ^fotrimazole (Lotrimin), which are not available solely as otic
preparations.
Perichondritis
This condition develops when trauma or’ inflammation causes an effusion
of serum or pus between the layer of perichondrium and the cartilage of the
external ear. In most cases of trauma, the injury is in the form of aflaceration
or is the result of incidental damage during surgery on the ear. Occasionally,
it follows 'simple bruising without hematoma. An inadequately treated
furuncle provides a ready source of a potent causative agent, such as a
virulent type of micrococcus (!Staphylococcus), -Streptococcus, or Pseudo¬
monas-aeruginosa. The diagnosis is simple; the involved part of the auricle
swells, becomes'reddened, feels warm, and is very tender upon palpation
(Fig. 5-3).
Eczematous Dermatitis
The practicing otolaryngologist not infrequently encounters a lesion that
involves the external canal and adjacent portions of the'meatus and concha
^ Differentiation between a pri¬ and is characterized by 'redness, 'itching, 'swelling, and a'stage of watery
mary dermatosis and infection exudation followed by crusting. As implied earlier, the differentiation
may be difficult.
between primary-dermatosis and infection may be difficult. A seborrheic
dermatitis or a skin reaction related to neomycin sensitivity may present in
this fashion. The label of eczematous dermatitis is often used because of the
characteristic appearance of the lesion.
When a considerable portion of the auricle is involved and the lesion
seems to be spreading, wet dressings using a solution such as Bttrew’s may
be advisable for 24 to 48 hours, at which time fluoiinated steroid ointment
and solution are employed. Naturally, if an infection is suspected, topical
antibiotics may be required.
Mf the acute stage is not controlled, chronic changes characterized by
thickening of the skin, and even stenosis of the external canal, may develop.
The chronic stage may be troublesome because of periods of uncomfortable
itching and the tendency of the patient to resort to scratching, thus causing
further irritation. In such cases consultation with a dermatologist may be
beneficial.
Relapsing Polychondritis
This disease of unknown etiology leads to inflammation and destruction
of cartilage. While this is a generalized disorder of cartilage, involvement of
Involvement of both nasal and the nose and ears is seen in 80 to 90 per cent of cases. The auricular
aural cartilage is seen in up to deformity resembles an acute infectious perichondritis or an inflamed cauli¬
90 per cent of cases.
flower ear. The loss of cartilage may lead to “floppy” ears and saddle-nose
deformities. Alternation of the inflammation between the two ears (without
predisposing cause) or the presence of fever suggests this disorder. Tinnitus
and vertigo may be encountered as well as hearing loss due to collapse of
the external auditory meatus. When the larynx, trachea, and bronchi are
involved, hoarseness and even death due to collapse of laryngotracheal and
bronchial walls may result.
Disease activity fluctuates, and the disorder has an unpredictable prog¬
nosis. There may be a single occurrence or multiple recurrences over many
years. Treatment includes salicylates or corticosteroids for an acute attack,
although some controversy surrounds the use of the latter. Dapsone has
been used to prevent recurrent attacks. Affected structures should be
protected from trauma.
TRAUMA
Lacerations
The most common keerations of the ear occur as a result of the patient
digging in an ear with a finger or using an instrument such as a hairpin or
paper clip. A laceration of the canal wall may result in transient bleeding,
thus worrying the patient, who will usually then consult a physician. No
treatment other than keeping the ear dry is normally required. The patient
is reassured following examination to rale out tympanic membrane perfora¬
tion.
Severe lacerations involving the auricle should be explored for cartilagi¬
nous damage. The cartilage should be approximated carefully before plastic
repair of the skin is done. Such wounds should be. observed closely for the
development of infections of the perichondrium. Prophylactic antibiotics are
given if there has been gross contamination of the wound or exposed
cartilage.
Frostbite
Frostbite of the auricle can occur rapidly in environments with a low
temperature and a high wind chill factor. Because it is insidious, it is not
painful until rewarming occurs. Outcome depends on the depth of injury
and the duration of exposure. Injury is thought to occur by direct cellular
damage and by microvascular insult leading to local ischemia.
Rapid rewarming is the current therapeutic recommendation. The affected
Rapid rewarming in water be¬ ear should be bathed in water at a temperature between 100 and 108°F until
tween 100 and 108°F is recom¬
mended for frostbite.
there is objective evidence that thawing has occurred. Analgesia will be
required. The full extent of injury may not be apparent for several days, so
the patient who is sent home must be followed carefully.
Surgical debridement should be delayed. Clinically apparent infection
should be treated with antibiotics. Patients with very stiff cartilage of the
pinna probably had prior frostbite.
5—DISEASES OF THE EXTERNAL EAR 87
Hematoma
This condition is most frequently seen in wrestlers and boxers. Untreated,
it may result in the so-called cauliflower ear. Simple needle aspiration of the
hematoma has been used in the past, but most physicians now recommend
more vigorous treatment by incision and drainage of collected blood under
sterile conditions, followed by the application of a pressure dressing, partic¬
ularly in the conchal area. Localized pressure is better obtained by using
through and through sutures over dental rolls or other similar materials.
Treatment is best accomplished as soon as practical following injury, before
organization of the hematoma begins. Wrestlers should be reminded about
wearing protective headgear, even during practice.
MALFORMATIONS
free of cartilage, and are of first cleft origin only. Type II abnormalities
contain both epithelium of first cleft origin and cartilage from the first and
second arches. The sinus tract may be observed to drain intermittently and
occasionally become infected (Fig. 5-5). Usually a tract can be identified by
methylene blue injection and excised. In some patients, these tracts may
pass medially or lateral to the facial nerve; thus, the facial nerve must be
identified during the dissection.
NEOPLASMS
A variety of skin lesions, including neoplasms, may be encountered on
the auricle and in the external canal (Fig. 5-6). Few are peculiar to this
anatomic region. Somewhat unusual from the standpoint of appearance is
the osteoma, a benign tumor of the external canal wall which presents as a
single, firm, rounded growth attached by a smaller bony pedicle to the inner
third (or bony portion) of the canal wall. This tumor should be differentiated
from an exostosis, which is more common and which consists of a rounded
protuberance of hypertrophic canal bone (usually multiple and bilateral).
The cause of exostoses is not completely clear; it has been stated that these
growths occur more frequently in people who do a great deal of swimming
in cold waters. Exostoses usually require no treatment, although they may
result in more frequent canal blockage by cerumen in some individuals.
Osteomas are carefully chiseled from the canal wall with the aid of the
operating microscope. Benign polyps from the middle ear present in the
external canal. Careful removal under the operating microscope is indicated
if they are not responsive to medical treatment; in such cases they should
be examined histologically.
Squamous cell carcinoma, the most common malignancy of the external
auditory canal, is amenable to cure if diagnosed early and properly treated.
Chronic discharge, often serosanguinous, and free bleeding, pain, and
5—DISEASES OF THE EXTERNAL EAR 89
MISCELLANEOUS
Sebaceous cysts occur in the postauricular fold and are often multiple.
Large cysts may become inflamed intermittently and are more likely to be
cured by complete excision than by drainage alone.
Nodules involving the helix may represent localized areas of chondritis,
known as chondrodermatitis nodularis chronicis helicis (painful nodule).
They are more common in men and occur most often on the superior helix
or anthelix. While steroid injection is sometimes adequate treatment, local
excision provides both a cure and a pathologic diagnosis.
Gouty tophi may occur in the subcutaneous tissue or cartilage of the
auricle as whitish-yellow nodules containing urate or sodium biurate cystals.
Unsightly tophi may be excised.
Pain in the area of the auricle and external canal in the absence of physical
findings certainly deserves investigation. The subject of otalgia will be
discussed in Chapter 9.
References
Chai T-J, Chai TC: Bactericidal activity of cerumen. Antimicrob Agents Chemother 18:638-
641, 1980.
Chander JR: Malignant external otitis. Laryngoscope 78:1257-1294, 1968.
Corey JP, Levandowski RA, Panwalker AP: Prognostic implications of therapy for necrotizing
external otitis. Am J Otol 6:353-358, 1985.
Fairbanks DN (ed): Antimicrobial Therapy in Otolaryngology—Head and Neck Surgery. 4th
ed. Washington, DC, American Academy of Otolaryngology, 1987.
Goodman WS, Middleton WC: The management of chronic external otitis. J Otolaryngol
13:183-186, 1984.
Hyslop NE: Ear wax and host defense. N Engl J Med 284:1099-1100, 1971.
Lucente FE, Parisier SC, Som PM, Arnold LM: Malignant external otitis: A dangerous
misnomer? Otolaryngol Head Neck Surg 90:266-269, 1982.
Matsunaga E: The dimorphism in human normal cerumen. Ann Hum Genet 25:273-286, 1962.
Meyers BR, Mendelson MH, Parisier SC, Hirschman SZ: Malignant external otitis. Arch
Otolaryngol Head Neck Surg 113:974-978, 1987.
Naiberg J, Berger G, Hawke M: The pathologic features of keratosis obturans and cholesteatoma
of the external auditory canal. Arch Otolaryngol 110:690-693, 1984.
Neal GD, Gates GA: Invasive Pseudomonas osteitis of the temporal bone. Am J Otol 4:332-
337, 1983.
Senturia BH, Morris MD, Lucente FE: Diseases of the External Ear. 2nd ed. New York,
Grune & Stratton, Inc, 1980.
Sessions DG: Frostbite of the ear. Laryngoscope 81:1220-1232, 1971.
Shapiro SL: Some remarks on otitis externa. Eye Ear Nose Throat Mon., 52:61-68, 1973.
Shire JR, Donegan JO: Cholesteatoma of the external auditory canal and keratosis obturans.
Am J Otol 7:361-364, 1986.
Sismanis A, Huang CE, Adedi E, Williams GH: External ear canal cholesteatoma. Am J Otol
7:126-129, 1986.
Stone M, Fulghum RS: Bactericidal activity of wet cerumen. Ann Otol Rhinol Laryngol 93:183-
186, 1984.
Uri N, Kitzes R, Meyer W, Schuchman G: Necrotizing external otitis. The importance of
prolonged drug therapy. J Laryngol Otol 98:1083-1085, 1984.
6
DISEASES OF THE
MIDDLE EAR AND MASTOID
by Michael M. Paparella, M.D., George L. Adams, M.D., and
Samuel C. Levine, M.D.
Diseases of the middle ear and mastoid are common throughout the
United States and the world. For example, excluding the common cold,
several studies indicate otitis media to be the next most common problem
seen in a pediatric office. Inflammation of the middle ear cleft (eustachian
tube, middle ear, and mastoid) is especially prevalent in children and in
underserved areas such as ghettos, Indian reservations, and certain areas of
Alaska. It is also likely that genetics plays a role, as there is often a history
of ear disease in parents and siblings. Since the widespread use of antibiotics
for otitis media and mastoiditis in the mid-1930’s, the rates of mortality and
serious complications resulting from otitis media have been greatly reduced.
However, today, middle ear disease often presents in a chronic or insidious
form causing hearing loss and drainage. Morbidity usually means hearing
loss, which interferes with educational, social, or professional functions. In
school-age children middle ear fluid problems (for example, serous otitis
media) are quite common; the child may demonstrate a poor performance
in school until the problem is detected through screening and is then
diagnosed and treated.
by a perforation of the tympanic membrane. Such perforations may be tympanic membrane perforation
with intermittent or persistent
extremely small and difficult to see or quite large and obvious. These discharge.
perforations can be classified as four types, based on the site of pathologic
involvement: tubal, central, marginal, and pars flaccida. The first two are
generally safe; the last two usually are more serious (Fig. 6-1).
Myringitis refers to an inflammation of the tympanic membrane. As has
been indicated, inflammation of the tympanic membrane can accompany
middle ear inflammation or be associated with external otitis. However,
myringitis specifically pertains to inflammation in which the tympanic mem¬
brane is primarily involved. In hemorrhagic, or bullous, myringitis the most
notable finding is bleb formations (bullae) on the tympanic membrane and
adjacent canal wall. This clinical appearance can occur in children, in whom
it is associated with the common bacteria that cause acute suppurative otitis
media. These bullae contain serous fluid, blood, or both, and appear red or
purple. Differential diagnosis includes external otitis and herpes zoster oticus
(Ramsav Hunt syndrome). In adults hemorrhagic mvringitis is usual1'' a «-“1a
The eustachian tube connects the middle ear cavity with the nasopharynx
and is intimately related to diseases of both. The lateral third as it enters
the middle ear is bony, whereas the medial two thirds is fibrocartilaginous.
The infant eustachian tube differs from that of the adult. In the infant it is
short, wide, and horizontal in location, and this is one reason why inflam¬
mation of the eustachian tube is so common in infants, especially during the
period of bottle feeding. As the child grows, the eustachian tube elongates,
narrows, and develops a downward course medially. The tube is normally
Tensor veli palatini muscle closed and opens by active muscular contraction of the tensor veli palatini
function is essential for proper
muscle during swallowing and certain other times such as yawning or opening
eustachian tubal activity.
of the ja\\Sb-Eunctk>nsi*f the eustachian tube are (1) ventilation, (2) drainage,
and (3) pj$Jt^iion. of the middle ear from contamination by nasopharyngeal
sefiE&tions. Ventilation provides equalization of atmospheric pressure on
both sides of the tympanic membrane. The tube opens by muscular activity
when the pressure differential is 20 to 40 mm Hg. An intact tensor .veli
palatini, muscle is essential for this function.
Eustachian tube ventilation can be assessed in the office by looking for
lateral displacement of the tympanic membrane with an otoscope or, in the
presence of a perforation, listening through an auscultation tube while the
patient squeezes the nostrils and swallows (Toynbee maneuver) or squeezes
the nose and blows hard against the occluded nostrils, with a closed mouth,
allowing his ears to “pop” (Valsalva.maneuver). The middle ear can also be
inflated by politzerization, during which air is forced through the nose while
the nasopharynx is closed as the patient swallows. The air is introduced
through the nose with a Politzer bag with an olive tip. Direct eustachian
tube catheterization was a common procedure in the past but is seldom
performed today.
Secretions formed in the middle ear will drain into the nasopharynx
through a normally functioning eustachian tube. A vacuum will develop in
the middle ear during periods of eustachian tube obstruction. Prolonged
obstruction can lead to increased fluid production, perpetuating the problem.
When not relieved by medical management, the vacuum has to be interrupted
by myringotomy. Then drainage of the fluid can occur via the eustachian
tube.
Being normally closed, the eustachian tube protects the middle ear from
contaminated nasopharyngeal secretions and pathogenic organisms. The
normal protection can be interfered with by heavy nose blowing or continual
exaggerated sniffling, thus allowing passage of organisms into the middle
ear.
Disorders affecting the eustachian tube include an abnormally patent tube,
palatal myoclonus, obstruction, and cleft palate.
6—DISEASES OF THE MIDDLE EAR AND MASTOID 93
Palatal Myoclonus
Palatal myoclonus is a fairly rare condition in which the palatal muscles
undergo periodic rhythmic contractions. This results in a clicking sound in
the ear of the patient and may be heard by the examiner’s ear. Although
the exact cause of palatal myoclonus is unknown, it has been associated with
vascular lesions, multiple sclerosis, aneurysms of the vertebral artery, tumors,
and various other lesions of the brain stem or cerebellum. Usually no
treatment is needed; rarely, incision of the tensor tympani muscle of the
middle ear can be considered.
Cleft Palate
Cleft palate deformity results in eustachian tube dysfunction due to lack
of anchorage of the tensor palatini muscle. In the unrepaired cleft palate,
this prevents the muscle from exerting sufficient contraction on the eustachian
tube orifice to open it during swallowing. This inability of the tube to open
results in inadequate ventilation of the middle ear, and inflammation ensues.
Thus, the incidence of middle ear disease in children with cleft palate is
94 PART TWO—THE EAR
Barotrauma*
Barotrauma is damage to tissues caused by changes in barometric pressure
Boyle’s Law: volume of a gas which occur during diving or flying. Boyle’s Law states that a decrease or
varies inversely to pressure. increase in environmental pressure will expand or compress, respectively, a
given enclosed volume of a gas. If the gas is contained within a flexible
structure, that structure can be damaged by this expansion or compression.
Barotrauma can occur whenever the gas-filled spaces in the body (middle
ear, sinus, lung) become enclosed spaces through blockage of normal venting
pathways.
The middle ear is the most common site of barotrauma, primarily because
of the complexity of eustachian tube function. The eustachian tube is
normally closed but opens with swallowing, chewing, yawning, and the
Valsalva maneuver. Colds, allergic rhinitis, and individual anatomic variation
all predispose to eustachian tube dysfunction. Increasing pressure requires a
“clearing” action as described above to equalize pressure, but decreasing
pressure can usually be equalized passively. As environmental pressure
decreases, the air in the middle ear will expand and passively vent through
the eustachian tube. As environmental pressure increases, the air in the
middle ear and within the eustachian tube is compressed. This tends to
collapse the eustachian tube. Once the pressure difference between the
environment and the middle ear space becomes too great (about 90 to 100
mm Hg), the cartilaginous portion of the eustachian tube will firmly collapse.
If more air cannot be added through the eustachian tube to restore the
middle ear volume, structures of the middle ear and adjacent tissue can be
damaged as the pressure difference continues to grow. A predictable -se¬
quence of injury occurs as the relative vacuum develops within the middle
ear space. First the tympanic membrane is retracted inward. This stretches
the eardrum and causes rupture of small vessels to produce an injected
appearance and hemorrhagic blebs within the drum. As the pressure builds,
small vessels within the middle ear mucosa also dilate and rupture, causing
a hemotympanum. Occasionally the pressure will rupture the tympanic
membrane.
Middle ear barotrauma can occur in underwater diving or flying. The
change in pressure in the first 17 feet of water is equal to the pressure change
*The section on Barotrauma was written by Rick Odlund, M.D., former Navy Diving Medical
officer.
6—DISEASES OF THE MIDDLE EAR AND MASTOID 95
Congenital Problems
The ossicles can be congenitally deformed, disrupted, or fixed. Since they
derive from the first and second branchial arches, other developmental
anomalies of these arches (syndromes) often occur as well, such as Treacher
Collins syndrome, which is congenital stenosis of the ear plus maxillofacial
dysostoses. Ossicular deformities can also occur in isolation. Common
96 PART TWO—THE EAR
deformities include a missing portion of the incus and fixation of the stapes.
There are a variety of forms of congenital stenosis. These children may be
born without a pinna or with only a rudimentary one (microtia). The
deformity of the pinna can, in a general way, be correlated with the amount
of deformity to be expected below in the middle ear and tympanic membrane.
There can be complete lack of development of the external auditory canal,
or it can appear with a blind end or develop with a concentric narrowing.
The functional aspects of this problem (deafness) should be corrected before
consideration is paid to cosmetic repair of the pinna. Children with congenital
hearing loss require early identification and treatment. Hearing aids should
be used at the earliest possible time. Cosmetic correction of a microtia is
recommended before first grade to reduce peer pressure. Bone-anchored
hearing aids may assist the surgical aplasia procedures. Isolated ossicular
deformities are usually correctable through surgery. If the stapes is fixed, a
stapedectomy and prosthesis replacement will re-establish hearing.
As mentioned before, the ossicles can become fixed owing to tympano¬
sclerosis in patients who have previously had otitis media.
Otosclerosis
Otosclerosis is an autosomal A common cause of conductive hearing loss in adults is otosclerosis.
dominant trait. Otosclerosis is an autosomal dominant disorder, seen in both men and
women, that begins to cause progressive conductive deafness in early
adulthood. The patient develops symptoms in the late teens and early
twenties. While usually bilateral, it can occur unilaterally. Histologically,
otosclerosis is quite common, occurring in as much as 10 per cent of the
population. However, only a small percentage develop the clinical manifes¬
tations of hearing loss. This is a disease of the bony labyrinth, in which an
area of otospongiosis (soft bone) forms, especially in front of and adjacent
to the footplate, causing fixation of the footplate. Although conductive
deafness is the main problem, in time sensorineural hearing loss due to
cochlear otosclerosis can develop as well.
The patient usually complains of a hearing loss when a level of 40 dB or
greater is reached. The primary care physician’s most important diagnostic
tool is the 512 Hz tuning fork to demonstrate a negative Rinne test. Bone
conduction is heard louder than air conduction by the patient. The Weber
test is helpful and will be positive in the involved ear if unilateral otosclerosis
is present or in the ear with the greater conductive hearing loss. The
tympanic membrane is usually normal in appearance but occasionally will
have a pink or orange discoloration due to the vascular otospongiosis in the
middle ear as seen through the tympanic membrane (positive Schwartze’s
sign). Surgical procedures offer an excellent chance for restoring hearing,
depending mainly on cochlear function. The major postoperative complica¬
tion is sensorineural hearing loss, with an incidence of 2 to 3 per cent in
experienced hands. Patients must be assessed very carefully through audio¬
logic as well as otologic examination (Fig. 6-2).
Hippocrates said, “Acute pain of the ear with continued strong fever is to
be dreaded for there is danger that the man may become delirious and die.”
Acute otitis media and mastoiditis were major problems prior to the
introduction of antibiotic therapy in the mid 1930’s. Today patients with
uncomplicated acute otitis media are treated successfully by the pediatrician
or the family physician.
The middle ear is usually sterile, which is remarkable considering the flora
of organisms which exists in the nasopharynx and pharynx. The combined
physiologic action of cilia and mucus-secreting enzymes (for example, mur-
amidase) and antibodies acts as a defense mechanism when these microbial
contaminants are exposed to the middle ear space during the act of swallow-
ing. Acute otitis media results when this physiologic mechanism is disrupted.
In addition to the surface defense mechanism, an important subepithelial
capillary network provides humoral factors, polymorphonuclear leukocytes,
and other phagocytic cells. Obstruction of the eustachian tube is a basic
causative factor in acute otitis media. Thus, a major barrier against bacterial
6—DISEASES OF THE MIDDLE EAR AND MASTOID 99
invasion is lost, and bacterial species that may not ordinarily be pathogenic
are able to colonize the middle ear, invade tissue, and cause infection.
Although the majority of respiratory infections are caused by viral agents,
most acute otitis media infections are caused by pyogenic bacteria. The most
frequently recovered bacteria include Streptococcus pneumoniae, Haemo¬
philus influenzae, and beta-hemolytic streptococci (Table 6-1). Streptococcus
pneumoniae is by far the most common organism in all age groups. H.
influenzae is a frequent pathogen recovered from children under five years
of age, although it remains a significant pathogen in adolescents as well.
Classic symptoms of acute purulent otitis media include pain, fever,
malaise, and sometimes headache in addition to earache; in children partic¬
ularly, anorexia and sometimes nausea and vomiting are present. Fever may
be quite high in small children but can be absent in 30 per cent of cases.
The tympanic membrane typically is red and bulging either in part or in its
entirety (Fig. 6-3), and the vessels over the tympanic membrane and malleus
handle become injected and therefore more prominent. In short, there is an
abscess of the middle ear.
Because of the increasing incidence of ampicillin resistance, antibiotics are
combined with clavulanic acid and are effective against beta-lactamase
formers. Either a cephalosporin or ampicillin combined with clavulanic acid
has become the preferred medication for these resistant organisms. Sulfisox-
azole plus erythromycin is another effective substitute in penicillin-allergic
patients. All medications should be administered for at least 10 to 14 days,
and a follow-up examination is a must to assure complete resolution.
FIGURE 6—3. A, Early stage of acute purulent otitis media. B, Later stage of acute otitis media.
(Courtesy of Dr. Richard A. Buckingham and Dr. George E. Shambaugh, Jr.)
100 PART TWO—THE EAR
OtitiS'Prone Children
Otitis media is one of the most common infections in children. In some
studies it is estimated to occur in 25 per cent of children. It is more common
Otitis-prone child: in Native American and Eskimo children than in whites and least common
—male
in blacks. The majority of episodes occur in the first two years of life, with
—under age 2
—Native American, white a second peak incidence during the first year of school. Those who have had
—first episode usually under six or more episodes of otitis media before age six have been termed “otitis-
age 6 months
prone.” A study by Howie showed that an episode of S. pneumoniae
—S. pneumoniae episode
infection in the first year of life was associated with continuing incidence of
repeated episodes of acute otitis media. Boys are affected more than girls.
These children did not have an increased incidence of allergic conditions.
Eight serotypes of S. pneumoniae are responsible for more than 75 per cent
of episodes of acute otitis media. Thus, the development of a pneumococcal
vaccine could be an important step in controlling these repeated episodes.
Treatment of children with this high propensity to develop otitis media is
either medical or surgical. Medical management includes administration of
antibiotics in low dosage for periods of up to three months in the winter.
Another alternative is placement of ventilation tubes. The decision to
perform myringotomy is generally based on failure of medical prophylaxis
or the development of allergic reactions to commonly employed antimicro¬
bials, either the sulfa drug group or the penicillins.
FIGURE 6—4. A, Serous otitis media. B, Bubbles in the middle ear are seen in serous otitis
media after inflammation. (Courtesy of Dr. Richard A. Buckingham and Dr. George E.
Shambaugh, Jr.)
102 PART TWO—THE EAR
Fluid persisting after 3 months Persistence of fluid is an indication for surgical correction. This consists of a
of medical management with
myringotomy incision, removal of the fluid, and Often insertion of a pressure
hearing loss is an indication for
myringotomy. equalization tube. The pressure equalization tube acts as a vent to allow air
to enter the middle ear. This relieves the vacuum and lets the fluid drain or
be absorbed.
The decision to proceed to surgical intervention is not made on duration
alone. Severity of the hearing impairment and frequency and severity of
preceding problems are considered. The problem is most often bilateral, but
a child with a thin fluid, minimal hearing loss, or unilateral problem may be
treated for a longer period by a more conservative approach. On the other
Unilateral serous otitis media in hand, thinning of the tympanic membrane, deep retraction, significant
an adult requires investigation
hearing impairment, and poor school performance may be indications to
of the nasaopharynx for tumor.
proceed to myringotomy sooner.
The ventilation tubes are left in place until spontaneously extruded—
usually within a period of six months to one year (Fig. 6-5). Unfortunately,
because of recurrence of the fluid, some children require insertion of special
tubes designed to stay in for longer than one year. The disadvantage of
these longer-lasting tubes has been the persistence of a perforation after
extrusion. Ventilation tube insertions have provided immediate restoration
of hearing and correction of severely retracted tympanic membrane, espe¬
cially when there is persistent negative pressure.
The greatest disadvantage of ventilation tubes has been the need to keep
the middle ear dry. Various plugs have been devised for this purpose.
Myringotomy incision and tube placement have also been on rare occasion
associated with the development of a cholesteatoma. Drainage through the
tubes is not unusual and may be associated with upper respiratory infections
Persistent drainage through a or allowing water to enter the middle ear, and, in certain cases, can be a
ventilation tube requires cul¬
ture, systemic antibiotics, and
persistent, unexplained problem. In these instances, medical management
appropriate topical antibiotic with systemic antibiotics or antibiotic ear drops has to be continued for long
drops. periods of time, even while tubes are in place. Failure to respond to this
type of management necessitates mastoid radiographs and further evaluation.
The value of adenoidectomy for chronic serous otitis media is still contro¬
versial. Certainly in individuals with large adenoids causing nasal and
nasopharyngeal obstruction, there is a role for this procedure. The majority
of children do not fit this category. The value of adenoidectomy in children
with moderate adenoid tissue and recurrent problems is still being evaluated.
The most recent study (Gates) reports adenoidectomy is beneficial even
when the adenoid tissue is not obstructing.
B
FIGURE 6-5. A, Myringotomy incision. B, Aspiration of fluid. C, Insertion of ventilation tube. D, Ventilation
tube in place. E, Type I, standard ventilation tube (left) and type II, larger ventilation tube with larger inner
flange and opening for chronic, obstinate cases (right). Both tubes are made of silicone rubber. (A to D
from Paparella MM, Shumrick DA (eds): Otolaryngology, Vol 2. Philadelphia, WB Saunders Co, 1973, p 90.
£ from Paparella MM, Payne E: Otitis media. In Northern J (ed): Hearing Disorders. Boston, Little, Brown
and Company, 1976, Fig 10—2.)
04 PART TWO—THE EAR
FIGURE 6 6. Law position. The external canal, tympanic cavity, vestibule, and internal canal are
shown by an area of diminished density behind the mandibular condyle. The attic-aditus-antral
areas are obscured entirely. The pneumatic ceils of the mastoid process are well visualized. (From
Compere WE Jr: Conventional radiologic examination of the temporal bone. In Shambaugh GE |r
(ed): Surgery of the Ear, 2nd ed. Philadelphia, WB Saunders Co, 1967, p 103.)
Stenvers views (Figs. 6-6 to 6-10). Prior to the advent of antibiotics, the
Law view was of particular value in evaluating acute mastoiditis. This is a
nearly direct lateral view. Even today it is usually obtained prior to any
mastoid surgery to determine the position of major landmarks such as the
mastoid tegmen and sigmoid sinus as well as the general overall size of the
mastoid. The additional lateral elevation of the x-ray beam in the Schuller
view not only shows those structures seen in the Law position, but also
permits visualization of the attic or epitympanum. By angulation of the head
45 degrees, the Mayer position is obtained. This film demonstrates the region
of the antrum and the head of the malleus. By a modification of the direction
of the x-ray beam, it is also possible to demonstrate the incus and the area
of the epitympanum. The Owens view is similar to the modification of the
Mayer position, but less angulation of the beam provides a better
visualization of the ossicles and epitympanic recess as they are now visualized
above the petrous ridge. Another modification of an oblique view is known
as the Chausse III projection. It provides additional information about the
structures in the middle ear.
The Stenvers position views the long axis of the petrous pyramid to
demonstrate the internal auditory canal, the labyrinth, and the antrum. The
Towne view shows both petrous pyramids through the orbits, permitting
direct comparison of the petrous pyramids and internal auditory canals on
the same film. When the physician is most interested in structures of the
middle ear, the standard Schuller, modified Mayer, and Chausse III views
6—DISEASES OF THE MIDDLE EAR AND MASTOID 105
CT Scanning
Computed tomography has in most instances become the preferred method
of diagnosing middle ear, mastoid, and inner ear abnormalities (Fig. 6-11).
Initially used for determining the presence of acoustic neuromas, the more
refined CT scanners are capable of demonstrating ossicular discontinuity,
6—DISEASES OF THE MIDDLE EAR AND MASTOID 109
FIGURE 6-11. CT scans of a normal ear and mastoid. A, PAC, large petrous air cell; EAC, external auditory canal; SS,
sigmoid sinus; MAC, mastoid air cells. Arrow points to the basal turn of the cochlea. B, A series of small arrowheads
outlines the course of the facial nerve through the fallopian canal. The large arrow points to the malleus, showing how
the head of the malleus lies within the attic of the middle ear space.
of the causative organism. The usual responsible organisms are the same as
those that cause acute otitis media.
Treatment initially is a wide myringotomy, culture, and appropriate
intravenous antibiotics. When the radiologic examination shows loss of the-
trabecular pattern or there is progression of disease, an urgent, complete
mastoidectomy is mandatory to prevent serious complications such as pe¬
trositis, labyrinthitis, meningitis, and brain abscess.
Since the middle ear is connected to the mastoid, chronic otitis media is
accompanied by chronic mastoiditis. These inflammatory problems can be
considered active or inactive. Active refers to the presence of infection with
drainage from the ear or otorrhea resulting from underlying pathologic
changes such as cholesteatoma or granulation tissue. Inactive refers to the
sequelae from a previously active infection that has “burnt out”; thus
otorrhea is absent.
Patients with inactive chronic otitis media often complain of a hearing
loss. There may be other symptoms of vertigo, tinnitus, or a sense of fullness
as well. A dry perforation of the tympanic membrane is usually seen. Other
changes may indicate tympanosclerosis (white patches in the tympanic
membrane), loss of ossicles which is sometimes visible through the tympanic
membrane perforation, and fixation or disruption of ossicles from previous
infection. If there is sufficient disability and hearing loss, surgical correction
or tympanoplasty can be considered.
to blockage of secretion, exposure of dura or lateral sinus wall, or imminent Vertigo in a patient with chronic
brain abscess formation. Vertigo in a patient who has chronic middle ear middle ear disease suggests
erosion of the horizontal semi¬
suppuration is another serious symptom. This suggests the presence of a circular canal.
fistula, which means an erosion of the bony labyrinth, most commonly the
horizontal semicircular canal. This is a serious finding, since infection can
then pass from the middle ear and mastoid into the inner ear, thereby
causing labyrinthitis (complete deafness) and, from there, possibly menin¬
gitis. A fistula test should be performed in every case of chronic middle ear
suppuration when there is a history of vertigo. A fistula test requires Fistula test: positive pressure
application of both positive and negative pressure to the tympanic membrane applied by pneumatic otoscope
causes vertigo and nystagmus.
and thereby across the middle ear space. The pneumatic otoscope, if an
excellent seal can be obtained, may be suitable for this purpose. The test
should be routinely done in patients with chronic otitis media, since a fistula
may be present in the absence of vertigo (Fig. 6-12). A negative fistula test,
however, does not exclude the possibility of a fistula.
Tympanic membrane perforations may be marginal or central. If the
perforation is marginal or in the attic, cholesteatoma should be suspected.
Granulation tissue may be seen filling the perforation or, in some instances,
will form a sizable polyp extruding into the ear canal. Special care is required
when this polyp is removed under the microscope to avoid injury to the
ossicular chain. Multiple perforations in the tympanic membrane in adults
suggest the possibility of tuberculous infection of the middle ear.
Radiologic examination usually reveals a sclerotic-appearing mastoid,
often smaller and less pneumatized than the opposite or normal side. Bone
erosion, especially in the area of the attic (scutum missing), suggests
cholesteatoma.
Treatment
Conservative treatment for chronic otitis media consists essentially of
advising the patient to keep water out of the ear and cleansing in the office
with careful spot suctioning. Hydrogen peroxide or alcohol can be used for
cleansing with a soft cotton-tipped wire applicator for removal of diseased
tissue and inspissated suppuration. Local powders and ear drops, usually
containing antibiotics and steroids, can be applied. Attention is directed to
112 PART TWO—THE EAR
Surgery
Surgery is aimed at eradicating infection and obtaining a safe, dry ear
through a variety of tympanoplasty and mastoidectomy procedures. The
primary purpose of surgery is removal of disease and is achieved if proper
Conductive hearing loss can result from chronic otitis media. If a tympanic
membrane is intact, the middle ear contains air, and there is a disruption of
the ossicular chain, a maximum conductive hearing loss of 60 dB will result. The maximum conductive loss
occurs when there is ossicular
The magnitude of the conductive loss may not always correlate with the
discontinuity in the presence of
severity of the disease, since pathologic tissues can also conduct sound to an intact tympanic membrane.
the oval window. Sensorineural deafness can result from acute otitis media
as well as chronic otitis media. Any time there is an infection in the middle
ear space, especially under pressure, there is a possibility that the products
of infection will spread through the round window membrane into the inner
ear, causing sensorineural hearing loss. The infection is usually limited to
the basal turn of the cochlea, a portion that is not tested routinely when
hearing is measured. Over time, however, the hearing loss can spread until
it does become a problem later in life. This emphasizes the need for more
aggressive treatment to prevent possible permanent sensorineural loss from
developing in patients with acute otitis media who do not undergo resolution
within 48 hours with appropriate antibiotic therapy (Fig. 6-17).
Facial Nerve Paralysis. The facial nerve can be injured by either chronic
or acute otitis media. In the case of acute otitis, the nerve is affected by
purulent material directly in contact with the nerve. Because there may be
114 PART TWO—TH E EAR
Dural piafc
(Middle fossa)
Pos+,-sup. on
FIGURE 6—14. A, Simple mastoidectomy. The external auditory canal and middle ear are left intact while
the mastoid is exenterated of disease and cell structures. B, Mastoid surgery can also be approached
endaurally, as seen here. A larger opening (meatus) into the ear canal remains. C, Modified radical
mastoidectomy. In this operation the mastoid is exenterated and the posterior canal wall is removed. The
middle ear may be normal or nearly normal; however, often, tympanoplasty techniques need to accompany
the mastoid procedure. Postoperatively, one sees a mastoid cavity and a relatively normal appearing
tympanic membrane. D, Classic radical mastoidectomy indicates removal of all diseased tissues in the
middle ear and mastoid. The otologist usually attempts to preserve or restore hearing through tympano¬
plasty as well.
6—DISEASES OF THE MIDDLE EAR AND MASTOID 115
Anterior
FIGURE 6-15. Tympanoplasty types. Middle ear spaces (mainly mesotympanum) decrease in size from type I to type IV.
Assuming many other factors, the most common of which is good eustachian tube function, to be stable and under
control, hearing results are decreasingly good as one proceeds from type I through type IV tympanoplasty. Under
favorable conditions, type 1 tympanoplasty should result in normal or nearly normal restoration of conductive hearing,
whereas type IV should result in approximately a 30 db air-bone gap. A, Type I—graft rests on malleus. B, Type II—grafts
rests on incus. C, Type III—graft attaches to head of stapes. D, Type IV—graft attaches to footplate of stapes. £, Type Va—
fenestration of lateral semicircular canal (arrow). F, Type Vb—stapedectomy (arrow). (From Paparella MM, Shumrick DA
(eds): Otolaryngology, Vol 2. Philadelphia, WB Saunders Co, 1973, p 292.)
116 PART TWO—TH E EAR
B
118 PART TWO—THE EAR
Petrositis occurs in individuals of chronic petrositis is surgical, and during surgery for chronic ear infection
with pneumatized petrous petrous air cells are explored and diseased tissue is evacuated using a variety
apetic cells.
of techniques.
Lateral Sinus Thrombophlebitis. Infectious invasion of the sigmoid sinus,,
as it courses through the mastoid, results in thrombophlebitis of the lateral
sinus. Small fragments of the thrombus break off, creating a shower of
infectious emboli. Fever, unexplained by other findings, is the first sign of
this invasion. It tends to fluctuate considerably and, as the disease develops
fully, a septic or “picket fence” (spiking) pattern results. Chills often
accompany a rise in temperature; pain is isolated to the area of the mastoid
emissary vessels, which can become red and tender. This is called Griesinger’s
sign. The diagnosis is confirmed by magnetic resonance imaging (MRI) or
digital subtraction angiography. Blood cultures may be positive, particularly
if made at the time of the chill. Treatment is surgical and consists of removing
the focus of infection in the infected mastoid cells, necrotic lateral sinus
plate, or an infected and often necrotic lateral sinus wall. Drainage of the
sinus and evacuation of the infected clot are indicated. Ligation of the
internal jugular vein to prevent escape of the infected emboli into the lung
and to other parts of the body is performed.
Extradural abscess: Extradural Abscess. Extradural abscess represents a collection of pus
-pulsatile, purulent discharge
between the dura and the bone overlying either the mastoid cavity or the
—severe earache
—ipsilateral headache middle ear. It is most frequently assciated with chronic suppurative otitis
-low grade fever media with granulation tissue or cholesteatoma with erosion of the tegmen
—develops during episode of
in this region. Symptoms include severe earache and headache.
acute otitis media.
Subdural Abscess. A subdural abscess may develop as direct extension of
Subdural abscess: an extradural abscess or by extension of thrombophlebitis through the venous
—develops from chronic
channels. Symptoms include fever, headache, and the development of coma
otitis media
—headache in a patient with chronic suppurative otitis media. Multiple central nervous
—fever, restlessness system findings include seizures, hemiplegia, and a positive Kernig’s sign.
—focal seizures
While an extradural abscess is frequently drained through the mastoid cavity
—difficulty speaking
—coma at the time of radical mastoidectomy, a subdural abscess requires primary
—CSP may be normal, no neurosurgical drainage.
organisms.
Myringotomy
Myringotomy is the incision of the tympanic membrane, either to provide
ventilation to the middle ear, to permit drainage of middle ear fluid, or to
obtain cultures. The procedure is performed under the operating microscope
using general or local anesthesia. In the office setting, local anesthetic
appropriately injected into the external canal or iontophoresis using a 2 per
cent xylocaine solution placed in the ear canal provides sufficient anesthesia.
Local anesthesia is particularly useful in older children or adults with serous
otitis media but is less effective when the tympanic membrane is acutely
inflamed. It is not used in the presence of external otitis. A curvilinear
incision is made about 2 mm from the margin of the drumhead starting
below and continuing upward anteriorly or posteriorly. Incisions are made Myringotomy incisions are made
in the anterior interior or poste¬
in the anterior inferior or posterior inferior quadrant to avoid injury to the rior inferior quadrants.
ossicular chain. It is technically easier to make the incision in the posterior
inferior quadrant, and this area is less sensitive. The blade is never inserted
more than 2 mm in order to prevent touching the medial wall of the middle
ear, which can cause pain and bleeding. Further, there can be a dehiscence
or bulge of the jugular vein coming onto the floor of the middle ear.
Disruption of the ossicular chain is avoided by placing the incision in the
inferior quadrants. Damage to the round window is avoided by making an
incision only through the tympanic membrane and by limiting the depth of
the incision (Fig. 6-17).
Myringotomy is performed for treatment of complications of otitis media
such as mastoiditis or facial nerve paralysis developing during a course of
120 PART TWO—THE EAR
Primary Tumors
vascular tumor and can often be seen as a bulging purplish mass in the floor
of the middle ear through a semitransparent tympanic membrane. The
blanching that occurs by pressure from a pneumatic otoscope is called
Brown’s sign. The CT scan with contrast is the most useful diagnostic test.
In some instances angiography and retrograde jugular venography are
necessary to make the diagnosis and determine the blood supply and extent
of the tumor. Certainly a tissue diagnosis requires surgical exploration of
the site, and in most instances surgery is the preferred modality of treatment.
If the tumor is extensive, combined surgery and radiotherapy often are
indicated. Unresectable tumors do show response to radiation therapy.
Other benign tumors include neurofibroma of the facial nerve, hemangioma,
and osteoma.
Primary malignant tumors that can involve the middle ear space include
squamous cell carcinoma, rhabdomyosarcoma, adenoid cystic carcinoma,
and adenocarcinoma.
Rhabdomyosarcoma occurs in young children. This disease was once
considered universally fatal, whereas in recent years there have been reported
cures with combined radiotherapy and chemotherapy.
Many squamous cell carcinomas originate primarily from the ear canal
and then invade the middle ear and mastoid secondarily. It is especially When external otitis does not
important to suspect any lesion in the external canal which does not heal resolve with usual treatment, a
biopsy is indicated.
spontaneously or with appropriate medical treatment as representing a
possible malignancy. Persistent chronic external otitis is a definite indication
for biopsy of the external ear canal. If these tumors are found early, the
patient has a much better chance of being cured than if the lesion progresses,
necessitating total temporal bone resection and yielding a much lesser chance
for survival. Occasionally, tumors, especially with superimposed infection,
will present with symptoms of drainage, especially bloody drainage. Other
symptoms include pain, a sense of fullness, hearing loss, and if the vestibular
labyrinth is involved, vertigo. Facial nerve paralysis develops if the tumor Facial nerve paralysis is a late
erodes through the posterior canal wall and involves the facial nerve, but sign of malignancy of the tem¬
poral bone.
this generally occurs late in the course of the disease. The tumor will also
extend anteriorly through fissures into the region of the parotid gland and
pterygomaxillary fossa.
The most common malignant tumors of the middle ear in adults are
adenoid cystic carcinoma and adenocarcinoma. The most common malig¬
nancy to extend from the external canal to the middle ear is squamous cell
carcinoma. Other less common tumors capable of arising in the external
canal and then invading the middle ear are adenoid cystic carcinoma,
malignant melanoma, and neglected basal cell carcinoma.
Secondary Tumors
Tumors that arise from distant primary foci and metastasize to the middle
ear, mastoid, and temporal bone include adenocarcinoma of the prostate,
mammary carcinoma, hypernephroma or renal carcinoma, bronchogenic
carcinoma, gastrointestinal carcinoma, and melanoma.
In addition, the middle ear and mastoid can be invaded by tumors from
adjacent areas such as meningioma, acoustic neuroma, glioma, neurilemoma,
adenoid cystic and mucoepidermoid carcinoma of the parotid gland, and
nasopharyngeal cancers extending up the eustachian tubes.
Hematologic malignancies such as malignant lymphoma and leukemia
122 PART TWO—THE EAR
frequently involve the temporal bone, almost always involving the bone
marrow of the petrous apex, and can also cause infiltration of the middle
ear and eustachian tube, resulting in conductive hearing losses and effusions.
In terminal or severe leukemia, actual hemorrhage can take place in the
inner ear, causing sudden profound deafness as well as vestibular symptoms.
References
Bluestone CD, Stool SE: Pediatric Otolaryngology. Philadelphia, WB Saunders Co, 1983, p
16.
Draf W, Schulz P: Insertion of ventilation tubes into the middle ear: Results and complications
Ann Otol Rhinol Laryngol 89(Suppl 68):303, 1980.
Gates GA, Avery CA, Cooper JC, Prihoda TJ: Chronic secretory otitis media: Effects of
surgical management. Ann Otol Rhinol Laryngol 98(Suppl 138):1, Jan 1989.
Healy GB, Teele DW: The microbiology of chronic middle ear effusions in children. Laryn¬
goscope 87:1472, 1977.
Holm VA, Kunze L: Effects of chronic otitis media in language and speech development
Pediatrics 43:833-839, 1969.
Howie VM, Ploressard JH, Sloyer JL: The “otitis prone” condition. Am J Dis Child 129 678-
688, 1975.
Jokipii AMM, Karma P, Ojala K, et al: Anaerobic bacteria in chronic otitis media. Arch
Otolaryngol 103:278, 1977.
Klein JO: Microbiology of otitis media. Ann Otol Rhinol Laryngol 89(Suppl 68) 98 1980
Miglets AW, Saunders WH, Paparella MM: Atlas of Ear Surgery. St Louis, The CV Mosby
Co, 1986.
Moller P: Long-term otologic features of cleft palate patients. Arch Otolaryngol 101:605-607,
Paparella MM, Shumrick DA (eds): Otolaryngology. Vol 1: Basic Sciences and Related
Disciplines. Vol 2: Ear. Vol 3: Head and Neck. Philadelphia, WB Saunders Co, 1980.
Paradise JL, Bluestone CC, Taylor FH, et al: Adenoidectomy with or without tonsillectomy
for otitis media. Ann Otol Rhinol Laryngol 92(Suppl 107):36,1983.
“ugh GE Jr, Glasscock ME: Surgery of the Ear. 3rd ed. Philadelphia, WB Saunders Co,
Teele DW Klein JO, Rosner BA: Epidemiology of otitis media in children. Ann Otol Rhinol
Laryngol 89(Suppl 68):5, 1980.
DISEASES OF
THE INNER EAR
by Samuel C. Levine, M.D.
Patients who experience disease of the inner ear have symptoms of hearing
loss, tinnitus, and disequilibrium. The physiology of hearing and balance has
been covered in previous chapters. Here we discuss the clinical presentation
of these problems and review by disease process the disorders of the inner
ear. After discussing the clinical presentation of these problems in a general
way, the chapter is divided into two large sections. The first deals with
diseases that predominantly affect the cochlea and the later section deals
with diseases that primarily affect the vestibular system. Since the two
systems are physically interrelated, it is rare that a process involves only one
of the structures. For this reason, there is some repetition.
Clinical Issues
History. The history of hearing loss is often one of the most difficult to
ascertain. A frequently heard clinical complaint is “My hearing is fine. My
wife insisted that I come in and have my hearing tested.” Patients will also
have significant trouble describing when they first noticed that they had a
hearing problem. This is often associated with a time that they first were
unable to use a telephone or found that while they were in a car with
competing noise they had a problem with their hearing. It is important for
diagnostic reasons to ascertain whether the patient has fluctuation in his or
her hearing or a distinctly one-sided problem. Some factors in the history
may even suggest the type of hearing loss which a patient has experienced.
Patients who have high-tone sensorineural hearing loss will describe an
inability to hear a female speaker or may have problems with certain words
with high-tone consonants such as “f,” “s,” or “th.”
It is important to obtain a work and social history in any case related to
hearing loss. Patients who have had military exposure to noise often will
have high-frequency sensorineural hearing loss. Similarly, adults who have
worked for many years in loud work places will develop hearing problems.
Ototoxic drugs may cause similar complaints. Finally, certain families appear
to be prone to familial hearing loss. If this is not elicited in the history, it
can be easily overlooked.
Tinnitus. Tinnitus is defined as an abnormal ringing noise in the ear. It is Tinnitus is any abnormal noise
extremely common and is associated most frequently with sensorineural that the patient hears.
hearing loss. Anyone who complains of a pulsatile sound must be examined
for an anatomic source. Anatomic sources for the tinnitus include vascular
problems such as aberrant vessels or middle ear tumors. Patients who have
124 PART TWO—THE EAR
Physical Examination
away when the patient can see again is suggestive of labyrinthine pathology.
Patients should be examined for joint position sense and peripheral sensation.
Cerebellar function can be tested by finger-to-nose and rapid alternating
movements.
Laboratory Evaluation
Any patient who complains of hearing loss or tinnitus must have a thorough
audiologic evaluation. This includes hearing threshold evaluation in frequen- Any patient who complains of
cies from 250 Hz to 8 kHz. When appropriate, bone conduction, tympano- hearing loss or tinnitus must
11 1 j * have an audiosram
grams, and reflexes need to be examined. If the patient’s symptoms suggest
a vestibular etiology or the etiology of a patient’s dizziness cannot be
ascertained by history alone, an electronystagmography (ENG) examination
is necessary. Thorough ENG testing requires visual tracking, rapid deviation
of eye movement, and caloric testing; optionally the patient may have
bithermal caloric stimulation or rotational chair testing. ENG test equipment
and procedures vary widely. The person performing the test needs to have
experience in the operation and standardization of the equipment.
Laboratory tests may be obtained when it is considered appropriate. A
suggested battery might include a CBC, urinalysis, coagulation function,
glucose tolerance tests, thyroid and lipid testing, and an FTA-ABS test.
Metabolic causes of dizziness or hearing loss are few, but they represent
correctable causes for the patient’s symptoms.
2% X-Linked
126 PART TWO—THE EAR
Congenital Deafness
The list of genetic causes of hearing loss is extremely long. This is reviewed
in Table 7-2. The most common causes of sensorineural hearing loss in
children are reviewed in Table 7-3. Proctor reviewed these causes and
showed that eight leading causes account for almost half of all hereditary
hearing loss. Leading the list is diabetes. Hyperlipidemia is the second
leading cause and otosclerosis is third. The remaining five causes represent
less than 1 per cent each.
Chromosomal Abnormalities
The number of described genetic syndromes involving deafness is so large Any syndrome with renal disor¬
that a detailed discussion of each is impossible. Therefore, the more common ders, retinitis pigmentosa, facial
anomalies or cardiac problems
syndromes that may be encountered will be discussed. may have hearing loss as part
Alport’s Disease. This dominantly transmitted syndrome is a progressive of the clinical picture.
renal disease (glomerulonephritis) that usually begins in childhood. Kidney
degeneration is usually accompanied by a progressive sensorineural hearing
loss that increases as renal malfunction worsens. Hearing loss associated
with Alport’s syndrome is bilateral, symmetric, and greater in the high
frequencies. Response to caloric tests may be reduced. Males are affected
more frequently than females.
130 PA RT TWO—TH E EAR
FIGURE 7—3. Paget’s disease, vertical section through the temporal bone. C.C., Remants
of the old cochlear capsule. C.T., Cavum tympani. J.A.M., Internal auditory meatus. M.T.T.,
Tensor tympani muscle. N.B., Newly formed bone. N.VII, Facial nerve. (Photomicrograph
from Otological Research Laboratory, College of Physicians and Surgeons, Columbia
University.) (Reprinted from Jackson C, Jackson CL: Diseases of the Nose, Throat and Ear
(ed 2). Philadelphia, WB Saunders Co, 1959.)
7—DISEASES OF THE INNER EAR 131
patient’s life. Only FTA-ABS tests are reliable in the diagnosis of later
phases of syphilis.
Bullous Myringitis. This is an infectious process involving the middle
layer of the tympanic membrane. It is a painful process that has been
associated with high-tone sensorineural hearing loss.
Ototoxic Drugs
Table 7-4 presents an extensive list of drugs and chemicals that affect the
inner ear and hearing mechanism. As a general rule, any drug or chemical
that causes a renal toxic effect can and usually does cause some ototoxicity.
Each of the listed drugs can cause both vestibular and hearing symptoms.
Most of the medications listed are irreversible in their effects, although if
the effect is detected early enough and the drug discontinued some hearing
loss can be reversed. Drugs with ototoxic effects that are particularly
reversible include salicylates. Salicylate poisoning results in a 30- to 40-dB
flat hearing loss that is reversible when the drug is discontinued. Similarly,
erythromycin causes hearing loss only when given intravenously and in
relatively high doses. When this drug is withdrawn, the hearing loss is also
reversed. Medications such as dihydrostreptomycin have been banned in the
United States because of their long-term effects on the auditory system.
Even after dihydrostreptomycin is discontinued, effects on the hearing system
can occur as late as a month following discontinuation of the drug.
When using any ototoxic agent: In handling patients who are on potentially ototoxic drugs, the first rule
It) get baseline hearing levels,
12) test for balance, (3) warn
is that the patient must be warned about the potential side effects. If
the patient of the potential possible, baseline studies including balance and hearing tests should be
toxicity. performed before the drug is prescribed. At the first warning sign, a repeat
test need's to be done. Drug level monitoring will show toxic levels in some
cases prior to evidence of the drug’s toxic effect. Decisions to remove
ototoxic drugs from a therapeutic regimen must be weighed against the
potentially life-threatening disorders that they are treating.
Acoustic Tumors
The most common inner ear tumor causing hearing loss is an acoustic
neuroma. Acoustic neuromas are benign tumors of the Schwann cells
covering the eighth nerve. These schwannomas occur most often on the
balance portion of the eighth nerve. Other causes of hearing loss by tumors
in the internal auditory canal include seventh nerve neuromas, meningiomas,
hemangiomas, and aberrant vessels. Tumors in younger individuals or a
family history of acoustic neuromas may represent an early manifestation of
von Recklinghausen’s syndrome. Von Recklinghausen’s disease causes all
cases of bilateral acoustic neuromas. The usual course of an acoustic neuroma
is that the patient develops a unilateral sensorineural hearing loss. This is at
first mild, but as the tumor continues to grow, it slowly crushes the nerves
of the internal auditory canal. Rarely, patients complain of vestibular
symptoms. The hearing loss progresses slowly in most cases. Acoustic
neuromas can, however, cause sudden hearing loss or Meniere-like syn¬
dromes as well. Any unilateral or asymmetric hearing loss is an acoustic Any asymmetric hearing loss re-
neuroma until proved otherwise. Discovery of small acoustic neuromas is quires further work-up with ABR,
made by having a high degree of suspicion leading to ARR ("auditory CT’orM,ll‘
brainstem response) testing and radiologic confirmation. Acoustic tumors
are seen only on enhanced CT scans with high-resolution thin slices. MRI
also provides an excellent view of these tumors and is probably more
sensitive than CT scanning (Fig. 7-5).
Acoustic tumors may be removed surgically by three major routes. They
can be resected from the middle fossa, from the posterior fossa, or across
Trauma
Trauma to the inner ear can be divided into two primary forms. One is
acoustic energy and the second is mechanical energy. In injuries causing
mechanical trauma to the temporal bone, temporal bone fractures are
possible. Structurally, the temporal bone is made of some of the densest
bone in the human body. It is protected by its central location. When the
temporal bone fractures, it rarely does so without associated problems.
These can and usually do include loss of consciousness, subdural or epidural
hematoma, or concussion. Ultimately, this means that the patient’s hearing
is not a critical problem given (or requiring) acute treatment. These patients
often will need neurosurgical procedures.
Temporal bone fractures are divided into two general groups (Fig. 7-6).
Temporal bone fractures are 80 One is longitudinal fractures; the second is transverse fractures. Statistically,
per cent longitudinal, 20per gp per cent Qf tpc fractures are longitudinal and 20 per cent are transverse.
Longitudinal fractures begin at the foramen magnum and travel out to the
external auditory canal. The ear usually bleeds and there is a conductive
hearing loss. Transverse fractures account for a high proportion of injuries
to the labyrinth and facial nerve because the fracture line travels through
the petrous apex or the labyrinth. Labyrinthine injuries can be less severe,
causing a concussion phenomenon with recovery of balance and hearing, or
more severe, with total loss of hearing.
Blast injuries cause a concussion wave that does more damage to the
middle ear than to the inner ear, but high-tone sensorineural hearing loss
can result from this type of injury. Acoustic trauma is perhaps the most
common cause of sensorineural hearing loss. Sensorineural hearing loss is
caused by both loudness and length of exposure. The Occupational Safety
and Health Administration (OSHA) has established standards that are
believed to relate hearing loss to the exposure of workers to loud noises
over time in the work place. While levels of 80 dB for 8 hours are thought
to be safe, exposure to 110 dB noise over a relatively brief period of time is
considered dangerous to the long-term safety of the hearing mechanism.
Experience has shown that high-tone hearing loss occurs first, and this is
believed to be related to the acoustic energy and the natural frequency of
the inner ear hearing mechanism. Early on, noise exposure results in a
temporary threshold shift. These generally improve in less than two weeks.
Repeated trauma results in permanent threshold changes.
Presbycusis
Presbycusis is the loss of hearing over time due to the aging mechanism
in the inner ear. There are four pathologic types that have been classified
by Schuknecht. The first phenomenon is sensory presbycusis. In this form
of pathology hair cells are lost first. Later, this leads to a loss in cochlear
neurons. Usually this involves hair cell loss on the basal turn of the cochlea
and high-tone hearing loss. Neuropresbycusis, on the other hand, involves a
primary loss of cochlear neurons with relative preservation of the hair cells.
There is relatively greater loss of word discrimination in this case and only
a gradual loss of hair cells over time. Strial presbycusis leaves excellent word
discrimination scores after a degenerative process causes moderate to severe
hearing loss that is relatively flat in nature. Pathologically, the stria vascularis
appears to degenerate and shrink. Finally, cochlear-conductive hearing loss
leaves a normal neuronal and hair cell population without damage to the
stria vascularis but shows a hearing loss that is thought to be related to a
limitation of movement in the basilar membrane. The exact nature of the
pathologic process is not clear.
Treatment Concepts
Any patient suffering from a known etiology of hearing loss should first
have that etiology controlled. Any patient on ototoxic drugs should have the
drugs stopped if at all possible. Patients who are in noisy work places should
wear protection and should limit their exposure to loud noise. Once trauma
to the acoustic mechanism has occurred by whatever method, hearing loss
is usually permanent. Currently, treatment of hearing loss involves amplifi¬
cation using an external hearing aid. While implantable devices are consid¬
ered, the common application of such devices is not yet available. In severe
cases, cochlear implantation with an electrode array is possible at this time
Only the totally deaf patient is currently considered for implantation in this
manner.
Tinnitus poses one of the most complex problems to treatment. It is purely
a psychoacoustic phenomenon and, therefore, cannot be measured. It has
been estimated that 13 million people suffer with this problem. Perhaps one
million patients suffer severe or debilitating tinnitus. Often masking of the
tinnitus is the most practical alternative. Recommendations to patients
involve the use of masking with a fan or “pink” noise such as an FM radio
tuned off of the station. If these simple measures do not help and the patient
has a hearing loss, then treatment with an amplification method is recom¬
mended. In severe cases that have failed these methods, a tinnitus device or
instrument is prescribed. In these cases, producing the pitch or frequency of
the tinnitus can sometimes create a masking inhibition that persists even
7—DISEASES OF THE INNER EAR 137
after the device is turned off. A small number of patients respond to this
form of therapy. Other methods such as DC stimulation have been tried and
occasionally are of value. More often, patients respond well to biofeedback
or other psychologic methods to help them deal with their symptoms in a
better manner.
Balance depends upon four separate and interdependent systems. First, Balance comes from vestibular,
the vestibular system senses accelerating movement and perceives gravity. ocular, proprioceptive, and cen¬
tral (neural) sources.
Proprioceptive cues from joint position senses and muscle tone provides
information concerning the relationship of the head to the remainder of the
body. Third, vision gives perceptions of position sense, speed, and orienta¬
tion. Finally, all of these senses are integrated through the brain stem and
cerebellum.
A B
FIGURE 7—7. A, Microphotograph showing the early serofibrinous stage of meningitic labyrinthitis.
Serofibrinous exudate (E) has collected mainly in the middle coil. Pus cells have invaded the modiolus
but not the labyrinthine fluids. B, Microphotograph showing the diffuse purulent stage of meningitic
labyrinthitis. Pus cells are diffusely distributed throughout the cochlear spaces and the modiolus.
Destruction of the cochlear duct has already occurred in the basal coil. (From Jackson C, Jackson CL:
Diseases of the Nose, Throat and Ear (ed 2). Philadelphia, WB Saunders Co. 1959.)
difference. Toxic labyrinthitis usually resolves with some loss of hearing and
vestibular function. This is thought to be caused by toxic products from an
infection and not by viable organisms. Acute suppurative labyrinthitis occurs
with an acute bacterial infection that extends into the structures of the inner
ear. The chances of complete loss of hearing and vestibular function are
quite high. Finally, chronic changes can exist from any source and may lead
to endolymphatic hydrops or pathologic changes ultimately sclerosing the
labyrinth.
Meniere’s Disease (Fig. 7-8). Meniere’s disease is a disorder of swelling
in the endolymphatic space. This pathologic process is referred to as hydrops.
Pathologically, Meniere’s disease is caused by a swelling of the endolymphatic
compartment. When this process reaches a pinnacle, a Reissner’s membrane
ruptures, mixing endolymph and perilymph. This causes a temporary hearing
loss that resolves when the membrane reseals and the chemical composition
of the endolymph and perilymph returns to normal. Classically, the patient Meniere's disease is character¬
develops a low-tone sensorineural hearing loss followed by a symptom of ized by hearing loss, tinnitus,
dizziness, and pressure or full¬
low-pitched tinnitus. Patients describe aural fullness and then become acutely ness in one ear.
vertiginous. Attacks last between 15 minutes and several hours in duration.
This classic picture can be modified to involve only the vestibular portion of
the labyrinth when symptoms involve only changes in balance and aural
140 PART TWO—THE EAR
Perilymph Fistula
Patients who have sudden barotrauma in the area of the ear can experience
sensorineural hearing loss and dizziness. This is seen in divers, flyers, and
anyone who has a sudden change in pressure in the middle ear space. These
sudden changes can cause a disruption of the round or oval window
membrane, allowing perilymph to leak into the middle ear space. The role
of minor pressure changes such as sneezing has not been determined. Some
cases of perilymph fistula have developed without apparent pressure change.
The fistula can be repaired by sealing a leak with fat grafts. Resolution of
the symptoms of dizziness occurs in only a few cases. The rates of occurrence
and cure are still debatable.
7—DISEASES OF THE INNER EAR 141
Treatment
A majority of the diseases listed here cause a change in the vestibular
function. This means that neural firing from the nerves is still present, but
the data transmitted to the brain are unreliable. Treatment is directed toward
reducing the level of function of the vestibular nerve in the brain stem.
Vestibular suppressants include antihistamines and benzodiazepines. The
two primary drugs used for this are Antivert and Valium. Both drugs give
symptomatic relief but do not generally make symptoms completely disap¬
pear.
Severe and persistent cases of vestibular vertigo can be treated with
vestibular nerve sections through one of at least three routes. First, the
nerve can be sectioned through the middle fossa. This procedure is primarily
limited to patients under 60 years of age in good health and those willing to
accept a half-head shave. A second route involves the posterior fossa, where
a suboccipital craniectomy is performed and the nerve is identified in the
internal auditory canal. The procedure carries some risk to the facial nerve
as well as the cochlear nerve but can usually be accomplished without
significant difficulty. The degree of completeness of the section has been
under question in recent literature. The final route is a translabyrinthine
approach with removal or destruction of the entire vestibular system. In this
case, there is a high degree of success, but all patients will lose hearing in
the affected ear.
References
Hughes G: Clinical Otology. New York, Thieme, Inc., 1986.
Konigsmark BW, Gorlin RJ: Genetic and Metabolic Deafness. Philadelphia, WB Saunders
1976.
Schuknecht HF, Gulya AJ: Anatomy of the Temporal Bone. Philadelphia, Lea & Febiger,
DISORDERS OF
THE FACIAL NERVE
by Robert H. Maisel, M.D., and Samuel C. Levine, M.D.
LACRIMAL
FIGURE 8—1. Topographic anatomy of the facial nerve. Physiologic testing permits determination of the
site of the injury. Lesions medial to the geniculate ganglion will cause diminished tearing. A lesion within
the middle ear may cause absence of the stapedial reflex. Injury to the chorda tympani will diminish taste
and salivation.
and anastomoses with fibers that innervate the lacrimal apparatus. The facial
fibers make a sharp turn posteriorly at the geniculate ganglion and descend
through the labyrinthine segment to the tympanic segment of the nerve. The
nerve enters the tympanic segment and makes a second genu (or turn). It is
here, near the oval window, that the nerve can become exposed and may
be palpable in the middle ear. The nerve descends from the genu vertically
and gives a branch to the stapedius muscle. Below this level, a second branch
emerges and backtracks through the ear as the chorda tympani nerve. The
chorda carries fibers of touch, pain, temperature, and taste to the anterior
two thirds of the tongue. It also controls salivation from the submandibular
glands. It passes between the malleus and incus (Fig. 8-2) and exits the The bony covering overthefa-
temporal bone through the iter anterior. The major portion of the facial ciat nerve in the middle ear can
nerve carries motor fibers that exit from the stylomastoid foramen just dehiscent.
medial to the mastoid process. Seventy per cent of the fibers at this point
represent motor fibers to the face. The nerve subsequently turns anteriorly
and divides into five major branches—the temporal, zygomatic, buccal,
mandibular, and cervical. The branches may anastomose with one another
as the nerve passes through the parotid gland (Fig. 8-3).
Geniculate ganglion
Greater & Lesser sup.
petrosol n.
TYMPANIC..
Stylomastoid
foramen
Posterior
auricular n.
Digastric n.
Upper Division I
Forehead
Post, auricular n. Orbicularis of eye
^ .Lower
FIGURE 8—3. Peripheral distribution wy. ' . Division!
of the facial nerve. (From Sham¬
baugh GE, Clemis JD: Facial nerve ..Orbicularis
paralysis. In Paparella MM, Shum¬
/ of mouth
rick DA (eds): Otolaryngology. Vol
2, Philadelphia, WB Saunders Co,
1973, p 266.)
Platysma
S of neck
8—DISORDERS OF THE FACIAL NERVE 145
line transferase) are manufactured by the nerve cell body in the pons and
are transported along the nerve to the motor end plate through the micro¬
tubular systems. It is believed the neurometabolites are carried proximally
by similar transport mechanisms from each axon. The facial nerve has a
single motor neuron that is located within the central nervous system (CNS).
The sensory cell bipolar neurons have their nuclei outside of the central
nervous system, with one axon from the periphery to the cell body and
another from there to the central nervous system. The motor cell axon is
covered by Schwann cells, which form the neural tubule for nonmyelinated
nerves and which themselves lay down the insulating myelin for myelinated
nerves. A node of Ranvier, which represents the junction between Schwann
cells, is seen every millimeter. The basement membrane on the outside of
the Schwann cell is continuous so that the axon is never in contact with
extracellular spaces (even at the nodes of Ranvier). The axon receives its
oxygen from the Schwann cells and rejuvenates its axoplasm from the parent
neuron. The rate of axoplasmic metabolism as well as its rate of movement
appears to be about 1 mm a day. It progresses from the central nervous
system cell distally; this is the rate of regeneration of an axon where the
nerve is completely transected.
NEUROPHYSIOLOGY'NEUROPATHOLOGY OF INJURY
SECOND DEGREE
INJURY
B
FIGURE 8—4. A, First-degree injury. Nerve fiber is twisted or compressed in such a way as to distort
intraneural anatomy yet allow axoplasmic flow in both directions. Note that the myelin layer is also
maintained in these injuries. 6, Second-degree injury. With continued pressure, torsion, or both, axoplasmic
continuity is disrupted. The distal axon's trophic influence on myelin layer is lost, resulting in distal
degeneration of the myelin layer. Schwann cell and endoneurium, which together constitute the endoneurial
tube, remain intact. (From Johns ME, Crumley RL: Facial nerve injury, repair, and rehabilitation [a self-
instructional package], Washington, DC, American Academy of Otolaryngology, 1979, pp 19-20.)
146 PART TWO—THE EAR
The distance from the site of injury to the ceil body in the pons determines
to some degree the amount of injury to the entire nerve. If the injury occurs
in the internal auditory canal with axon disruption, long distances of
axoplasm are lost and the permanent damage is greater than when such an
injury occurs distally near the motor end plates. Younger people make a
more complete recovery from the same nerve injury (if repaired) than do
older people and people with chronic diseases (e.g., diabetes) or metabolic
disorders. If the amount of pressure on the nerve is sufficient to completely
block the movement of axoplasm past the site of injury over several days,
axonotmesis (second-degree injury) occurs with loss of axonal continuity
(Fig. 8-4B). This results in wallerian degeneration distally. The axons may
continue for several days being electrically responsive to external stimulation
(distally) but with no voluntary motor movement or electrical conductivity
across the site of injury. Histologically, the proximal nerve remains normal
but biochemical changes occur. Axonotmesis and neurotmesis have several
histologic correlates. The Schwann cells become swollen and phagocytic.
They then multiply until they fill the connective tissue tubule surrounding
each nerve fiber. The neuron deprived of nutrients normally brought back
through the axons loses Nissl substance with swelling of cytoplasm (chro¬
matolysis). The distant nerve continues to undergo changes, which are
usually not evident until three or four days after injury. The formation of
Biingner’s bands occurs. These are thought to provide a biochemical mode
of attraction for new nerves. When the nerve fiber is cut, repairing nerve
produces in its healing phase a growth cone at the proximal end of the axon.
It begins to grow toward the original distal end where the new motor end
plates are. There are multiple protoplasmic processes of the growth cone,
and a single regenerating axon will branch and enter Schwann cells of many
tubules, while similarly a single Schwann cell may be shared by many small
axons. Similarly, growth to another nerve may occur. Histochemical analysis
of a regenerating neuron shows increasing levels of RNA synthetase and
There is theoretical evidence to glucose-6-phosphate dehydrogenase, maximizing at about 21 days. Some
suggest that the repair ot a cut
facial nerve is more likely to be theorists have suggested, on the basis of this information, that cut nerves
effective if done 21 days after heal best if repaired at this time, but immediate repair is still the treatment
the injury. of choice. Delay is unwarranted owing to scarring and physical changes in
the wound.
Facial muscles are branchiomeric muscles, and greater muscle wasting is
seen in somatic muscle than in branchiomeric muscle after loss of motor
nerves. In humans it has been noted that there is a progressive but mild
decrease in facial muscle fiber size over the two weeks after complete
denervation. Observation has not shown complete degeneration of facial
muscle fibers following denervation. For these reasons, it is believed that
rehabilitation of the facial muscles by nerve transfer or reanastomosis of the
original injured nerve is reasonable for periods of at least 24 months after
injury. The facial nerve really goes through three stages after injury. Stage
1, which occurs up to 21 days, involves the physiologic events described
above, in which the cell body undergoes metabolic transformation and begins
to regenerate to create axoplasm that will inhabit the now empty neurotu¬
bules.
Stage 2, which lasts up to two years, is a period when the cell body and
the proximal segment can regenerate using the Biingner’s bands or reserved
endoneural tubes through which the regenerating axons can reach the facial
8—DISORDERS OF THE FACIAL NERVE 147
muscles. Therefore, certainly up to two years after an injury, it should be It is possible to repair the facial
considered plausible to reanastomose the severed nerve, interpose a cable nerve up to two years after the
injury.
graft between the two points of loss of continuity, or transfer another
functioning motor nerve to the distal nerve segments. Stage 3, which is
usually characterized by distal neural scarring and muscle degeneration,
obviously precludes consideration of restoring neuromuscular continuity.
DIAGNOSTIC TESTING
AUDIOLOGIC TESTING
Any patient who suffers a facial nerve palsy needs to have a complete
audiogram. Testing must include air conduction and bone conduction thresh¬
olds, as well as tympanometry and stapes reflexes. The function of the eighth
cranial nerve can be evaluated using auditory brain stem evoked response
(ABR) tests. This test is most helpful in detecting pathology in the internal
auditory canal. A conductive hearing loss suggests an abnormality in the
middle ear space, and in view of the exposure of the facial nerve in this area
infectious sources need to be considered. Reflex testing is much more
complex. A loud tone is presented, either to the ipsilateral or contralateral
ear, which evokes a reflex movement of the stapedius muscle. This changes If facial nerve paralysis devel¬
the tension on the tympanic membrane and results in a change in the ops during acute otitis media,
the nerve may be dehiscent in
impedance of the ossicular chain. If the tone is presented to the opposite, the middle ear.
normal-hearing ear and the reflex is elicited, the seventh nerve is thought to
be intact at this point. Absence of this reflex when either ear is stimulated
suggests an abnormality of the afferent seventh cranial nerve.
TEAR TESTS
By using a Schirmer test, the tearing function of the eye can be evaluated. The Schirmer test compares
These strips are commercially available and are placed over the lower lid tearing on both sides.
into the conjunctival sac on both sides (Fig. 8-5). After three minutes, the
length of the strip that is moist is compared to the opposite side. A difference Decreased tearing on the
of greater than 25 per cent suggests potential involvement of the seventh Schirmer test means injury to
the greater superficial petrosal
cranial nerve. The side of less tearing is interpreted to represent greater nerve or to the facial nerve
superficial petrosal nerve activity due to loss of action in the parasympathetic
nerve of Wrisberg (Table 8-1).
148 PART TWO—THE EAR
FIGURE 8-5. A Schirmer’s test demonstrating decreased lacrimation of the right eye in
comparison to the left eye.
TASTE
SALIVATION
CON
FIGURE 8-7. The facial nerve excitability test demonstrating stimulation of the lower
division of the facial nerve just anterior to the stylomastoid foramen.
the probe is pressed against the face in the area of the facial nerve. The
current is slowly increased to 5 ma, or until the patient has discomfort (Fig.
8-7). The forehead, eyebrow, periorbital area, cheek, nasal ala, and lower
lip are tested by gently sweeping the electrode. Any movement in the area
indicates a normal response. A small difference in response between the
paralyzed side and the normal side is considered to be a sign of recovery.
Marked decrease means that twitch on the paralyzed side occurs at 25 per
cent of the current used on the normal side. When compared at ten days,
92 per cent of the Bell’s palsy patients had some return of function. When
the electrical response was lost, 100 per cent had incomplete return of
function. In those patients in whom there was a marked decrease, 73 per
cent had incomplete return of facial function. The statistics suggest that the
most reliable form of testing is direct nerve function tests.
DIFFERENTIAL DIAGNOSIS
CONGENITAL LESIONS
Congenital causes of facial nerve paralysis are uncommon. One of the Mobius’ syndrome: (1) external
more common causes in this category is Mobius’ syndrome. In this case, the ZtZ^ofZTneJe!
facial nerve forms but it is a fibrotic tract. And while muscle development ^ |///r andXII.
may be present in some cases, it usually rapidly degenerates to fibrosis.
Unfortunately, these children have no response to any electrical testing at
birth and will not develop any form of facial movement because of the
abnormality.
More often, facial nerve paralysis is a result of childbirth trauma. During
the process of childbirth, fractures of the temporal bone can occur. The use
of forceps has been indicated as a potential cause of many of these lesions.
Any neonate identified with a seventh nerve paralysis should have tests as
soon as possible. Stimulation of the face after birth will differentiate
congenital causes from birth trauma. If the injury occurs in the birth process,
electrical stimulation will be possible for several days. This is an important
finding in both the diagnosis and prognosis of the facial palsy.
INFECTIONS
Infections occurring anywhere along the path of the facial nerve can lead
to paralysis. Rarely, meningitis will present with facial nerve palsy. Abscesses
in the parietal-cortex region can create a central paralysis. This is diagnosed
by the ability to move the forehead on the affected side but the inability to
move the remainder of the face on that side. Ramsay Hunt syndrome, or
herpes zoster oticus, involves the nerve and creates a rash in the external
auditory canal and pinna. Small pustules form in the external auditory canal
and are extremely tender (Fig. 8-8).
Bacterial infections of the middle ear can paralyze the face. Infections can
be acute or chronic. They can involve only inflammatory materials, or
cholesteatomas may also be present. An uncommon tick-borne illness called
Lyme disease can also cause paralysis of the facial nerve among other cranial
nerve palsies.
TRAUMA
Facial nerve evaluation should Trauma to the temporal bone is a common cause of facial palsy. Fractures
be performed immediately on can be both longitudinal and transverse (see Chapter 2). While longitudinal
any patient with a basilar skull
fracture. The prognosis is better fractures are much more common, transverse fractures injure the nerve
if the nerve functions partially, many times more frequently. The energy needed to cause a temporal bone
even if it is later found to fracture is substantial, and many of these palsies are not noticed until the
be paretic.
patient awakens from coma following a motor vehicle accident.
VASCULAR LESIONS
NEOPLASMS
IDIOPATHIC CAUSES
involvement affecting all five major branches. The onset is acute, with a
progressive course reaching the stage of greatest muscle weakness within
three weeks. Upper respiratory inflammation symptoms may precede the
onset of paralysis. Severe ear pain may occur early; dysacusis and other
signs such as dysgeusia relating to parasympathetic nerve paresis accompa¬
nying the facial motor hypofunction are consistent with the diagnosis.
Careful history-taking and physical examination including otoneurologic
work-up are necessary to exclude disorders that may, at first glance, mimic
a Bell’s palsy and, therefore, deserve their own diagnosis. Once the diagnosis
is secured by the absence of historic events such as a slowly progressive or
recurring facial paralysis and the absence of either active middle ear disease
or palpable masses in the parotid gland, a treatment plan should be derived
and explained to the patient.
TREATMENT
FIGURE 8-9. The prognosis for recovery follows the response to evoked electro¬
myography noted within the first 10 days. Prognosis is poor if the response to
evoked electromyography is lost within the first 5 days and is favorable, if the
response is maintained beyond 10 days, and especially 14 days. Early return of
voluntary motor unit action potentials noted by EMG within the first 14 days
indicates that the nerve is recovering and portends a favorable prognosis. (Reprinted
by permission from May M: Office medical management of acute facial palsies. In
May M (ed): The Facial Nerve. New York, Thieme Medical Publishers, inc 1986 p
334.1
FIGURE 8—11. Localization of the pathologic changes observed in the meatal and labyrinthine segments of
the facial nerve following total intratemporal exposure for Bell's palsy. Note that, in 8 of 11 cases, the
observed pathologic alteration of the facial nerve fibers was particularly evident in the distal part of the
internal auditory canal. (From Fisch U, Esslen E: Total intratemporal exposure of the facial nerve: Pathological
findings in Bell’s palsy. Arch Otolaryngol 95:337. Copyright 1972, American Medical Association.)
156 PART TWO—THE EAR
treatment a unilateral face lift to tense the skin on the paralyzed side
similarly makes a more pleasant presentation of the patient with paralysis
(Fig. 8-10).
Some clinicians recommend prednisone at a dose of 1 mg/kg/day for up
to 14 days as medical therapy for Bell’s palsy. There is little agreement in
the literature on the effect of steroids in preventing denervation, synkinesis,
autonomic mass movement, and crocodile tearing, and little evidence that
they alter the course of the paralysis or palsy. Steroids do stop the otalgia,
and for patients with severe otalgia this is a good medical treatment. All
other medications are unproven in this disease. From 1970 to 1985 the best
surgical treatment was either a transmastoid facial nerve decompression
from the geniculate ganglion distally to the level of the stylomastoid foramen
or a middle fossa decompression as advocated by Fisch. Figure 8-11 shows
the location of the surgical pathology in 12 cases of Bell’s palsy.
More otologists are at present reluctant to recommend transmastoid
surgery; when electrical tests and clinical evaluation suggest surgery, a neuro¬
otologic approach through the middle cranial fossa is often the treatment
undertaken.
References
Adour KK, Bell DM, Wingord J: Bell’s palsy: Dilemma of diabetes mellitus. Arch Otolaryngol
99:114-117, 1974.
Alford BR, Jerger JF, Coats AC, et al: Neurophysiology of facial nerve testing. Arch
Otolaryngol 97:214-219, 1973.
Cannon CR, Jahrsdoerfer RA: Temporal bone fractures, review of 90 cases. Arch Otolaryngol
109:285-288, 1983.
Fisch U: Surgery for Bell’s palsy. Arch Otolaryngol 107:1-11, 1981.
Harner SG, Daube JR, Ebersold MJ, Beatty CW: Improved preservation of facial nerve
function with use of electric monitoring during removal of acoustic neuromas. Laryngoscope
96:65-69, 1986.
Kettel K: Peripheral facial paralysis in fractures of the temporal bone. Arch Otolaryngol 51:25—
41, 1960.
Malone B, Maisel RH: Anatomy of the facial nerve. Am J Otolaryngol 9(6):497-504, 1988.
May M, Hughes GB: Facial nerve disorders, update 1987. Am J Otolaryngol 8:167-180, 1987.
9
FACIAL PAIN,
HEADACHE, AND OTALGIA
by Lawrence R. Boies, Jr., M.D.
CLASSIFICATION OF HEADACHE
In the early 1960’s a committee was formed to classify the causes of head
pain according to etiology so that the student and practicing physician might
approach the problem in a more organized manner.* The report distinguished
between migraine headaches, considering them vascular in nature, and
tension headaches, relegating them to the musculature. This classification
has been widely applied since that time; however, in the interim, there have
been significant questions raised concerning this dichotomy and the conse¬
quent treatment of these disorders. Rather than separate entities, the view
is currently being postulated that migraine, tension, and cluster headaches
are differing manifestations of central nervous system disturbances involving
the upper brain stem, limbic system, and/or hypothalamus. These distur-
*The Committee was composed of Drs. Arnold P. Friedman (chairman), Knox H. Finley,
John R. Graham, E. Charles Kunkle, Adrian M. Ostfeld, and Harold G. Wolf.
157
158 PART TWO—THE EAR
Major Categories
I. Vascular headache of migraine type
A. “Classic” migraine
B. “Common” migraine
C. “Cluster” headache
D. “Hemiplegic” and “ophthalmoplegic” migraine
E. “Lower-half” headache
II. Muscle-contraction headache
III. Combined headache: vascular and muscle-contraction
IV. Headache' of nasal vasomotor reaction
V. Headache of delusional, conversion, or hypochondriacal states
VI. Nonmigrainous vascular headaches
VII. Traction headache
VIII. Headache due to overt cranial inflammation
IX-XIII. Headache due to disease of ocular, aural, nasal and sinus, dental, or
other cranial or neck structures
XIV. Cranial neuritides
XV. Cranial neuralgias
Descriptions
I. Vascular Headaches of the Migraine Type. Recurrent attacks of headache,
widely varied in intensity, frequency, and duration. The attacks are commonly
unilateral in onset and are usually associated with anorexia and sometimes with
nausea and vomiting; some are preceded by, or associated with, conspicuous
sensory, motor, and mood disturbances; they are often familial.
Evidence supports the view that cranial arterial distention and dilatation are
importantly implicated in the pain phase but cause no permanent changes in
the involved vessel. Listed below are particular varieties of headache, each
sharing some, but not necessarily all of the mentioned features:
A. “Classic” Migraine. Vascular headache with sharply defined, transient
visual and other sensory or motor prodromes or both.
9—FACIAL PAIN, HEADACHE, AND OTALGIA
N.B.: So-called chronic post-traumatic headache may arise from any one of
several mechanisms. Such headache may represent sustained muscle contraction
(II), recurrent vascular dilatation (I, B), or rarely, local scalp or nuchal injury
(XIII) In some patients, the post-traumatic pain is part of a clinical disorder
characterized by delusional conversion or hypochondriacal reactions (V).
EVALUATION OF HEADACHE
History
Clinical Examination
Manifestations of systemic conditions mentioned in the headache classifi¬
cation should be searched for. A complete neurologic examination may be
indicated in certain cases. Specific points relating to the examination of the
head and neck might include the following:
Differential Diagnosis
Dorland’s Illustrated Medical Dictionary (27th Ed) defines headache or
cephalgia (cephalalgia) simply as pain in the head. Neuralgia, on the other
hand, is a paroxysmal pain that extends along the course of one or more
nerves. It is usually of a severe, stabbing character. Both primary and
secondary causes of neuralgia should be considered.
Head pain may be divided into acute and chronic (or chronic recurring)
types. Obviously, acute types may become chronic. Generally, one would
associate the term acute with head pain related to acute febrile states; acute
infections involving the ears, sinuses, or teeth; intracranial hemorrhage;
meningitis, cerebritis, and brain abscess; and with primary attacks of mi¬
graine, cluster headache, the cranial neuralgias, and glaucoma. The remain¬
der would be termed chronic.
Friedman has stated that most patients with headache as a major complaint
Cluster headache Behind or above one eye with Nasal congestion, lacrimation,
extension to temple or maxilla conjunctival injection; may occur at
night
Muscle-contraction headache “Hatband,” bitemporal, occipital, Chronic anxiety; in some cases may be
suboccipital related to occupational muscle fatigue
Nasal vasomotor reaction In and around nose, ethmoid, and Nasal obstruction and rhinorrhea often
maxillary areas; may radiate into occur
frontal area
Temporal arteritis In area of temporal (often bilateral) Ischemic optic neuritis
or other involved branches of
extracranial arteries
Acute sinusitis Pain in area of involved sinus; Fever, malaise, tenderness over
sphenoid sinusitis may cause involved sinus, nasal discharge and
retro-orbital, occipital, or congestion, associated upper
vertex pain respiratory tract infection
Chronic sinusitis Infrequently causes chronic head pain; Nasal polyposis, chronic suppurative
may be confused with vasomotor nasal discharge
reaction, since symptoms are in same
general area
Temporomandibular joint dysfunction In and around ear with radiation into Aural fullness; clicking in joint
neck or temporal area
Trigeminal neuralgia Face; any of the three divisions of the Usually associated trigger zones that
trigeminal nerve may be involved, respond to light contact
alone or in combination
Glossopharyngeal neuralgia Pharynx with radiation into ear Salivation; trigger zones in tonsillar
region
9—FACIAL PAIN, HEADACHE, AND OTALGIA 163
Cluster Headache
According to the classification presented earlier, cluster headache is now
considered a vascular headache of the migraine type. Previously used terms
for this condition are mentioned in the outline (I, C). The predominantly
unilateral facial and head pain occurs primarily in men, with sudden onset
and abrupt cessation. It is said to be the most excruciating of the vascular Cluster headaches are said to
headaches. There is no prodrome. Frequent attacks, one to three per day, be the most excruciating of the
vascular headaches.
of short duration, typically 45 minutes to one hour, tend to occur in clusters
or clumps during a period of up to three months. Periods of remission may
last from months to even years, averaging two years. The focus of pain is
usually centered behind one eye, with radiation to involve the entire side of The focus of pain is usually be-
the face and neck. The pain is often associated with flushing, sweating, hind one eye.
increased lacrimation, and rhinorrhea on the involved side. It is not unusual
for an attack to occur at night, awakening the patient from his sleep. An
attack may be precipitated by alcohol, histamine, and other vasodilators.
The mechanism involving dilatation of the extracranial and dural arteries is
generally accepted; however, the interrelationships and specific nature of
neurologic, humoral, and psychologic factors are not understood completely.
The main entities to consider in the differential diagnosis include trigeminal
neuralgia, acute glaucoma, intracranial aneurysm, and acute sinusitis, partic¬
ularly with sphenoid involvement. Features such as lack of trigger points,
unilateral lacrimation, lack of other eye findings, and the general pattern of
attacks help distinguish cluster headache in the differential diagnosis.
The following modes of treatment are available:
1. The inhalation of 100 per cent oxygen may abort an acute attack. Some
patients keep an oxygen tank at their bedside.
2. Ergotamine has been the most dependable drug. However, because of
gastroparesis, oral ergotomine is not always appropriate. Ergotomine
inhalation has been found to be suitably fast and effective. Also
available are sublingual, parenteral, and rectal forms.
3. Local application of anesthetic (lidocaine) nose drops has been reported
to be an effective abortive agent.
4. Methysergide has been used successfully as prophylactic treatment.
64 PART TWO—THE EAR
Muscle-Contraction Headache
Otolaryngologists frequently encounter headache originating in the mus¬
cles and fibrous structures about the head. The pain is often of a chronic
nature and is located in the frontal, temporal, occipital, and suboccipital
regions (Fig. 9-1). Tension is a common cause, although fatigue and
"Hat band” headaches are com- inflammatory disturbances may be factors. Fortunately, many tension head-
monly caused by tension. aches are Qf a miid character. The patient complains of the sensation of a
tight band (“hat band”) around the head, but it is not severe enough to
be painful. This sensation is produced by a mild, involuntary increase in
mast, m
Lev. auric, n.
scap. m
Trap, m.
FIGURE 9-1. There are numerous possibilities in the muscular, nervous, and vascular
structures in the posterior neck and occiput for the production of headache or neuralgia.
9—FACIAL PAIN, HEADACHE, AND OTALGIA 165
1. It is unilateral.
2. It responds favorably to simple analgesia.
3. It is modified by position or activity.
4. It is described in simple, accurate terms.
5. Despite chronicity, there are periods of clear-cut relief.
6. There is an element of progression.
entity but rather have viewed the reported pain as psychogenic in origin,
representing a manifestation of a reactive disorder. This conclusion was
supported by the lack of significant histopathology or laboratory and radio-
graphic changes. However, as criteria evolve to standardize the diagnosis of
this condition, its existence has gained a greater degree of credibility.
166 PART TWO—THE EAR
provided that one has ruled out allergic conditions, infections, and anatomic
deformities. Nasal sprays such as Afrin may be efficacious on a short-term
basis. Systemic decongestants have been used with good results in some
patients. In unyielding cases partial turbinectomy or electrocautery of the
turbinates may be performed. Vidian nerve section may be considered in
extreme cases.
“Lower-half” Headache
This term has been used in reference to lower facial pain. Included in this
grouping are atypical facial neuralgia, sphenopalatine ganglion neuralgia Atypical “lower-half" headaches
are currently thought to be of
(Sluder), and vidian neuralgia (Vail). Current thought is that, in general,
vascular origin.
most pain syndromes involving this area are vasodilating in origin and are
not due to neuropathic processes, unless one might implicate the autonomic
nervous system in specific cases. True neuralgias involving only the sensory
fibers of the maxillary division of the trigeminal nerve which pass through
the sphenopalatine ganglion may exist but probably are rare. Greater
involvement of the maxillary trunk should give a picture indistinguishable
from a second-division trigeminal neuralgia. However, these atypical lower
face pain syndromes have generally been more diffuse, deep-seated, and
poorly localized. They have occurred in a younger age group and have been
void of trigger zones. Few have been relieved by nerve section. Certainly a
careful intranasal examination (including sphenopalatine ganglion cocaini- A careful intranasal examination
is recommended.
zation) is recommended in such cases. Contacts between the nasal septum
and lateral wall should be considered as causes of this type of head pain;
however, treatment generally is directed toward a vasodilating etiology.
Temporal Arteritis
Temporal arteritis is a condition of unknown cause. Although originally
described as involving the temporal arteries, it is now referred to generally
as extracranial arteritis, since it may involve other branches of the external
carotid system. Moreover, arteries elsewhere in the body may be affected.
Classically, the arteritis is of the giant cell type.
The condition often causes constant, moderately severe head pain that
tends to be bilateral and is associated with tenderness in the area of the
involved arteries; it may mimic migraine, muscle-contraction, or cluster
headache. The pain is not influenced by cough or head movements. Most
commonly, temporal arteritis occurs in older individuals and may be accom¬
panied by generalized weakness and anemia. Diagnosis is made by biopsy Diagnosis is made by biopsy and
microscopic examination of a
and microscopic examination of a suspected vessel. The sedimentation rate
suspected vessel.
is often markedly increased. Blindness may occur owing to ischemic optic
neuritis; therefore, prompt treatment with high-dose, prolonged prednisone
is recommended to minimize or prevent this complication.
Sinusitis
Acute rhinosinusitis certainly can result in contacts within the nasal fossae
in addition to pressure or tension within a given sinus. Contact pain patterns
168 PART TWO—THE EAR
have been discussed. Individual sinus involvement will tend to produce the
following general pain locations:
1. Maxillary: anterior facial (cheek) with radiation into teeth, orbital, and
malar regions
2. Ethmoids: interocular with spread into frontal location
3. Frontal: forehead, interocular, and temporal areas
4. Sphenoid: retro-orbital, radiation toward vertex and occasionally the
mastoid areas
One must remember that several or all sinuses (pansinusitis) may be
involved on one or both sides.
When headache with chronic sinusitis is encountered, it is usually due to
pathologic conditions such as a mucocele or osteoma or is related to an
intercurrent acute flare-up. Certainly any chronic inflammatory process in
the nasal region can result in contact pain, as previously noted. Tumors,
although rare in this area, must be considered.
Diagnosis and treatment of sinusitis are discussed in Chapter 13.
Inflammation involving dental structures may mimic sinus pain and may
also actually cause maxillary sinusitis.
Otalgia
Otalgia, or ear pain, may be due to primary or secondary causes. In some
cases the term reflex or referred otalgia has been used for the secondary
type. Primary causes of otalgia are usually apparent on careful otologic
examination. Such conditions are outlined in the first portion of Table 9—2.
Often when a patient has ear pain, particularly when it is of a mild degree,
he or she is not able to identify the location of the pain more specifically
Source: Nelms CR. Paparella MM: Otalgia. Minn Med 52:955, June 1969.
than in the general area of the external ear and deeper. Therefore, when
there is no evidence of acute middle ear inflammation or disease in the
external ear, it is important to determine which lesions might be present in
the distribution of the sensory fibers of the several cranial nerves that supply
these structures but have ramifications in more distant areas.
The fifth, seventh, ninth, and tenth cranial nerves have sensory fibers in
some areas of the auricle, the external canal, and the tympanum, with
considerable overlap in the areas supplied. Also, the second and third
cervical nerves supply sensation to the postaural area, while the auriculotem¬
poral branch of the fifth nerve innervates some of the external ear and a
considerable area in front of the auricle and around the temporomandibular
170 PART TWO—THE EAR
joint. For the most part, in cases of secondary or referred otalgia, one cannot
Pharyngeal and laryngeal maiig- determine the nerve through which pain is being referred until a lesion is
nancies must be ruled out in found. The most important lesions that demand early detection are, of
cases o unexpame otagia. course) malignancies. The patient with a lesion on the rim of the larynx, in
the piriform sinus, or on the epiglottis may complain of earache on the
involved side. The reference is through the superior laryngeal branch of the
vagus nerve. Any lesion, including early carcinoma, in the area of the
palatine tonsils, the adjacent tongue, and lingual tonsils may cause earache
via the glossopharyngeal nerve. Otalgia that occurs following tonsillectomy
may be explained in the same manner (Fig. 9-3).
Dental disease may cause earache referred through a branch of the
trigeminal nerve. Molar impaction and dental infection are common causes.
CNS
«r|w
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w|lu|S
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MIDDLE EAR
ORAL Jiwl
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— — ——-
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ORAL CAVITY ^-
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9—FACIAL PAIN, HEADACHE, AND OTALGIA 171
initial treatment for these patients to disocclude the teeth and allow the
mandible to assume the normal position, thereby allowing the muscles of
mastication to relax and assume a more normal function. If the cause of the
joint dysfunction is related to the occlusion, then correction of the malocclu¬ Correction of malocclusion may
be necessary in some cases.
sion is extremely important. This may range from very minimal grinding of
the occlusal surface of the teeth, known as occlusal equilibration, to ortho-
172 PART TWO—THE EAR
Trigeminal Neuralgia
The diagnosis of primary trigeminal neuralgia (tic douloureux) is usually
The sharp, lancinating pain with not difficult because of the character of the pain. In this type of headache
trigger zones is characteristic
of trigeminal neuralgia. the pain is of sudden onset, sharp and lancinating, and initiated at trigger
zones about the face which react to light physical contact or drafts of air. It
usually occurs in persons beyond middle age and may involve one or more
of the divisions of the trigeminal nerve. The ophthalmic division is least
frequently affected. Attacks may occur every few seconds, with intervals of
freedom. Periods of recurrent attacks may last from a few days to a few
weeks. Remissions of months to years are seen. The disease is usually
unilateral and the cause is unknown.
In the secondary type of trigeminal neuralgia, the pain as a rule is of a
chronic nature, with longer episodes and less severe attacks. Trigger zones
are uncommon. The cause is found to be some lesion involving one of the
Specific causes must be ruled nerve roots. Tumors, both intra- and extracranial, must be ruled out. While
out before making the diagnosis
of a primary neuralgia. occasionally multiple sclerosis is found to be the cause, dental, nasal, and
sinus diseases are the more common causes. In actuality, the neurologic
disturbance associated with the aforementioned temporomandibular joint
dysfunction may involve a branch of the trigeminal nerve and, therefore,
technically would be considered a secondary form.
Drug treatment consists of use of phenytoin (Dilantin), baclofen, clona¬
zepam, valproic acid, or carbamazepine (Tegretol) alone or in combination.
When prescribing Tegretol in particular, the physician must be aware that
severe, sometimes irreversible, adverse reactions involving the hematopoietic
system can result. Early detection of hematologic change is important, since
in some patients the resultant aplastic anemia is reversible.
Patients unresponsive to the medical treatment described are managed by
alcohol injection or rhizotomy of the involved nerve or nerve root. Currently,
percutaneous radiofrequency rhizotomy seems to be the method of choice!
Other treatment possibilities include surgical ablation of the gasserian
ganglion or nerve decompression.
Glossopharyngeal Neuralgia
Primary glossopharyngeal neuralgia, a tic douloureaux of this nerve, is
relatively rare. The paroxysms of stabbing pain in the ear, with trigger zones
in the tonsillar area of the involved side, accompanied by salivation, provide
A common secondary form may
a picture in which the diagnosis is not difficult. A secondary form that is
he seen briefly after
tonsillectomy. common is seen in the earache following tonsillectomy or with any inflam¬
matory or neoplastic process involving the tonsillar area and adjacent areas
in the absence of middle ear disease. As previously discussed, one must
consider the many causes of referred otalgia when entertaining the diagnosis
of glossopharyngeal neuralgia.
PART THREE
ANATOMY
External Nose
The midline structure projecting outward from the plane of the cheeks
and upper lip, the external nose may be divided structurally into three
divisions: the bony vault, the most superior, is immobile; below it comes the
slightly movable cartilaginous vault; and lowest is the movable nasal lobule.
Considering the bony skeleton only, the lower half of the pyriform aperture
divides the internal from the external nose. Superiorly, the external nasal
skeletal structures include the ascending processes of the maxillae and the
two nasal bones, all supported by the nasal process of the frontal bone and
a portion of the perpendicular plate of the ethmoid bone. The anterior nasal
spine, representing the portions of the embryologic medial maxillary process
that engulfs the anterior premaxilla, may also be considered a part of the
external nose. The next division, the slightly movable cartilaginous vault, is
made up of the upper lateral cartilages, fused with each other in the midline
and also fused with the upper margin of the quadrangular septal cartilage.
The lowest third of the external nose, the nasal lobule, has its shape
maintained by the lower lateral cartilages. The lobule encloses the nasal
vestibule and is delineated medially by the columella, laterally by the alae
of the nose, and anterosuperiorly by the nasal tip (Fig. 10-1). Mobility of
the nasal lobule is necessary for facial expression, sniffing, and sneezing.
The subcutaneous muscles of expression over the nasal bones, anterior
cheeks, and upper lip assure this mobility. Subcutaneous connective tissue
177
178 PART THREE—THE NOSE AND PARANASAL SINUSES
Lower lateral
cartilage
Nares
Nasal septal
cartilage
Dorsunv
Anterior nasal
Alar groouo
Supratip spine
area External nares
Tip Nasolabial fold
Nasal bones
Frontal process
of maxilla
Upper lateral
cartilages
Nasal septal
FICURL 10—1. The external portion of the nose.
cartilage
Lower.lateral
cartilage
and skin complete the needed tissues of the external nose. The soft tissue
division between the internal and external nose has as its inferior margin the
pyriform crest with its skin cover, the nasal septum medially, and, as its
superior and lateral delineation, the lower margin of the upper lateral
The nasal valve is the narrowest cartilage. This narrowest structure of the entire upper respiratory tract is
structure in the upper respira¬ referred to by the anatomist as the limen nasi or the os internum, and by
tory tract.
the physiologist as the nasal valve of Mink. The designation “valve” is
appropriate because it moves with, and helps regulate, respiration.
Internal Nose
This structure extends from the os internum anteriorly to the posterior
choana, which divides the nasal cavity from the nasopharynx. The nasal
septum, a bony midline structure, anatomically divides the organ into two
noses. The internal lateral nasal walls are further structured by the turbinates
and the irregular air spaces between them—the inferior, middle, and superior
meati (Fig. 10-2). While the skeletal outlines appear to assure rigid diameters
of the air spaces, the soft tissue coverings of the internal nose tend to vary
greatly in thickness, altering the resistance, and, consequently, the pressures
and flow volumes of the inspiratory and expiratory air currents. The varying
diameters come about from strictly mucosal congestion and decongestion,
from changes in the vascular swell bodies of the turbinates and upper septum,
and from crusts and deposits or drainage of mucosal secretions.
10—APPLIED ANATOMY AND PHYSIOLOGY OF THE NOSE 179
The nasolacrimal duct empties into the inferior meatus anteriorly. The The frontal, maxillary, and ante¬
rior ethmoid sinuses open into
hiatus semilunaris of the middle meatus provides sinus ostia for the frontal,
the middle meatus.
anterior ethmoid, and maxillary sinuses. The posterior ethmoid sinus cells
drain into the superior meatus, and the sphenoid sinus drains into the
sphenoethmoid recess (Fig. 10-3).
FIGURE 10-3. The lateral wall shown without the turbinates. The ostia of the paranasal
sinuses as well as the nasolacrimal duct can be seen opening into the appropriate meatus.
180 PART THREE—THE NOSE AND PARANASAL SINUSES
The olfactory nerve endings occupy fairly small areas on the medial and
lateral internal nasal wall, high up in the nasal vault. Structural deformities,
as well as excessive mucosal thickening or edema, can prevent the inspired
air streams from reaching the olfactory area and, thus, severely interfere
with olfaction.
¥he skeletal portion of the septum is composed of the septal cartilage
(quadrangular) anteriorly, the perpendicular plate of the ethmoid above, the
vomer and rostrum of the sphenoid posteriorly, and a ridge below comprising
the crest of the maxillas and the crest of the palatines (Fig. 10-4). Ridges
and spurs, which sometimes require removal, occur not infrequently. Warp¬
ing of the septum, which may be due to growth factors or trauma, may be
so great that it interferes with the air flow and must be corrected surgically.
Minor septal deformities rarely The adjacent turbinates commonly compensate for irregularities in the
alter nasal air flow because of
turbinate compensation. septum (if they are not too great) by increasing in size on the concave side
and decreasing on the other side in such a way as to maintain the optimum
width of the air spaces. Thus, even though the septum is warped, air flow
may be even and normal. Areas of erectile tissue on both sides of the septum
serve to adjust its thickness under varying atmospheric conditions.
Paranasal Sinuses
Human beings have about 12 cavities along the roof and lateral aspects of
the nasal air space, varying in number, shape, size, and symmetry. These
sinuses are hollows within the several facial bones and are accordingly named
maxillary, sphenoid, frontal, and ethmoid sinuses (Figs. 10-3 and 10-5).
The latter usually consist of interconnected small groups of anterior and
posterior ethmoid cells, each group having an ostium draining into the nose.
All of the sinuses are lined with a modified respiratory epithelium capable
of producing mucus and, having cilia, of emptying secretions into the nasal
cavities. In health, the sinuses are essentially air-filled.
ID—APPLIED ANATOMY AND PHYSIOLOGY OF THE NOSE 181
Middle
turbinate
Orbital
cavity
Hiatus
Septum
semilunaris
Hiatus Ethmoid
air cells Inferior
semilunari:
turbinate Maxillary
Ostium of sinus
Maxillary sinus
Sphenoid
sinus
Nasal
Nasofrontal
septum
duct
Ethmoid
air cells
A rudimentary maxillary sinus, or antrum, is most consistently present at The maxillary sinus is the only
birth. The other paranasal sinuses appear in early childhood within the facial sinus routinely present at birth.
bones. These bones outgrow the cranium while supporting it. As their firm
centers are resorbed, nasal mucous membranes are drawn into the newly
forming cavities.
HISTOLOGY
epithelium and cilia uniform in length and spacing. The force of the air
currents passing through the various localities also influences the thickness
of the lamina propria and the number of glands in this mucosa. It is thin
where there is a low or gentle air flow and thick where the air streams are
strong. Secretion-producing glands and goblet cells, the sources of the
mucous blanket, are found in proportion to the thickness of the lamina
propria. The very viscous and sticky mucous blanket catches dust, inspirated
foreign bodies, and bacteria and, through the action of the cilia, carries
these substances to the pharynx, to be swallowed and destroyed in the
stomach. Lysozyme and immunoglobulin A (IgA) are found in the mucous
blanket and give further protection against pathogens. The mucous blanket
in the nose is renewed about three to four times an hour. The cilia—tiny,
hairlike structures—move in unison rapidly in the direction of the blanket’s
flow, then bend and recover much more slowly. Their stroke rate is 700 to
1000 cycles per minute.
Cilia
The cilia, about 5 to 7 microns in length, are located on the end plates of
the surface cells in the epithelium and number about 100 per square micron,
10—APPLIED ANATOMY AND PHYSIOLOGY OF THE NOSE 183
with about.,250 per cell in the upper respiratory tract. The cilia seem to work
almost automatically. For example, it is possible to tear a cell into small bits
without stopping ciliary movement; a single cilium will continue to stroke as
long as a tiny bit of cytoplasm containing its basal body remains attached to
it. All of the cilia in an area of epithelium are coordinated in a marvelous
manner. Each, as it strokes, moves metachronously with the surrounding
cilia. As one observes them stroking, the ranks bow in unison and the files
in sequence. Not only are the strokes of adjacent cilia coordinated as to
time, but the directions of untold millions in a sinus are so coordinated as
to be an important factor in carrying the mucus to the nasopharynx.
The structure of the cilia has been revealed by the transmission electron
microscope (Fig. 10-7). They are built up of two single central microtubules
surrounded by nine pairs of microtubules, all enclosed within the thin,
fragile, trilaminar cell membrane. Each cilium consists of a shaft, a tapered
tip, and a basal body. Not all microtubules extend completely to the tip.
The two central single microtubules do not extend below the level of the
cell surface. However, just below the level of the cell surface, each pair of
peripheral microtubules is joined by a third microtubule in the basal body,
a structure found in the apical cytoplasm. These triplets then continue to
descend further in the apical cytoplasm as rootlets, gradually tapering off.
In stroking, the individual cilia do not merely move back and forth like
wheat stalks in a grain field. Each stroke has a powerful, rapid phase in the
direction of flow with the cilium straight and stiff, followed by a slower
phase of recovery during which the cilium bends. The time relationship
between the effective phase and the phase of recovery has been worked out
experimentally, on the rat. The ratio is 1:3; i.e., the effective phase takes
one third the time of the phase of recovery. The stroke is not unlike the
arm stroke of a swimmer.
Cilium
Bridge
Subfiber A
Subfiber B
Radial spok«
Spoke head
^3STTt—'Central
>/Ok/ / microtubule
p/tSC
Doublet
microtubule
hw
Ciliary membrane
Dynein arms
FIGURE 10—7. Anatomic detail of a cilium.
184 PART THREE—THE NOSE AND PARANASAL SINUSES
Olfactory Area
Great interpersonal variations characterize the structure of the olfactory
region; these differences may be in the thickness of the mucosa (it is usually
about 60 microns thick), in the size of the cells, and in the olfactory vesicles.
The border between the respiratory and olfactory regions is generally very
sharply defined but irregular. In man the olfactory pseudostratified columnar
epithelium is composed of three cell types: (1) olfactory bipolar nerve cells;
(2) sustentacular, supporting cells, which are the most numerous; and (3) a
few, small basal cells, which are probably stem cells for the sustentacular
cells (Fig. 10-8).
Each olfactory cell is a bipolar neuron. In the epithelium they are evenly
distributed among the supporting cells. These olfactory sense cells constitute
The olfactory bipolar neurons the only portion of the central nervous system that reaches the surface of
niir^rTttemus^sUmihat the body- The distal end of such a cel1 is a modified dendrite that protrudes
reaches the body's surface, above the surface of the epithelium, forming the so-called olfactory vesicle.
On the surface of this vesicle are 10 to 15 nonmotile cilia. The proximal end
of each cell tapers to a thin process about 0.1 micron in diameter, which is
the axon. This axon joins with other similar axons to form the olfactory
nerves, which pass through the cribriform plate into the olfactory bulb,
where they form synapses with the dendrites of a second set of neurons. The
axons of this second set of neurons form the olfactory tract, which passes to
the brain to connect with numerous nuclei, fasciculi, and other tracts. The
central olfactory apparatus is highly complex.
The supporting sustentacular cells probably do more than just support; it
is postulated that the sustentacular cells provide lateral support and also
represent a means of intraepithelial ionic communication via their junctional
complexes with the olfactory bipolar neurons. They are supplied at the
Olfactory
bulb
Olfactory
tract
Glomerulus
Blood Supply
The sphenopalatine branch of the internal maxillary artery supplies the
conchae, meatus, and septum. The anterior and posterior ethmoidal branches
of the ophthalmic artery supply the ethmoidal and frontal sinuses and the
roof of the nose (Figs. 10-9 and 10-10). A branch of the superior labial The superior portions of the na¬
sal cavity are nourished by the
artery and the infraorbital and alveolar branches of the internal maxillary
ethmoid arteries, while the pos¬
artery supply the maxillary sinus, and the pharyngeal branch of the same terior and inferior portions are
artery is distributed to the sphenoid. The veins form a close cavernous plexus supplied by the maxillary artery.
under the mucous membrane. This plexus is especially well marked over the
middle and inferior conchae and the lower portion of the septum, where it
forms the erectile tissue, \4tpous drainage is accomplished principally
through the ophthalmic, anterior facial, and sphenopalatine veins.
Anterior
ethmoid Posterior
artery ethmoid
^artery
Spheno¬
palatine
FIGURE 10—9. The blood supply of the lateral nasal wall. The artery
ethmoid arteries are branches of the ophthalmic artery from
the internal carotid artery. The sphenopalatine and greater
palatine arteries are terminal branches of the external carotid
artery.
Nasal branch
Posterior of greater
palatine artery
ethmoid
arteries
Anterior
ethmoid artery
Kiesselbach's
FIGURE 10-10. The blood supply of the nasal
plexus
septum. In addition to the vessels supplying
the lateral nasal wall, branches from the supe¬
rior labial artery and palatine artery reach the
septum. Kiesselbach’s plexus is the most com¬
Posterior
mon area for epistaxis.
septal
nasal
Septal arteries
branch of
superior
Major palatine
labial artery
artery
186 PART THREE—THE NOSE AND PARANASAL SINUSES
Lymphatic System
The nose has a rich supply of lymphatics occurring in an anterior and a
posterior network. The anterior network of lymphatics is small and drains
along the facial vessels to the neck. They serve the most anterior portion of
the nose—the vestibule and the preturbinal area.
The posterior network serves the majority of the nasal anatomy, joining
three main channels in the posterior area of the nose—the superior, middle,
and inferior channels. The superior group, from the middle and superior
turbinates and that portion of the nasal wall, pass above the eustachian tube,
and empty into the retropharyngeal lymph nodes. The middle group, passing
below the eustachian tube, drain the inferior turbinate, inferior meatus, and
a portion of the floor and go to the jugular chain of lymph nodes. The
inferior group, from the septum and part of the floor of the nose, pass
through the lymph nodes along the internal jugular vessels (Fig. 10-11).
Nerve Supply
Directly involved are the first cranial nerve for olfaction, the ophthalmic
and maxillary divisions of the trigeminal nerve for all other sensory afferent
impulses, the facial nerve for movement of the respiratory muscles of the
external nose, and the autonomic nervous system. This last is mainly by way
of the sphenopalatine ganglion, to control the diameters of veins and arteries
in the nose as well as mucous production, thus modifying air flow conduc¬
tance, temperature, and moisture regulation of the air streams (Fig. 10-12).
FIGURE 10-12. The nerve supply of the nose. Olfaction Is mediated by the olfactory nerve located
high in the nasal vault. Autonomic control of nasal physiology is mediated primarily by sympathetic
and parasympathetic fibers that reach the nose by way of the sphenopalatine ganglion. Sensation is
from the ethmoid branches of the ophthalmic division of the fifth cranial nerve and the maxillary
division of the fifth nerve.
PHYSIOLOGY
Olfaction
Just as nasal anatomy makes inspection of the olfactory cleft with a nasal
speculum usually not possible, for the same reason inspiratory air flow curves
normally do not reach high enough into the cleft to allow us to detect an
odor, unless it is very strong. If we are to be successful at identifying a given
odor, we usually have to sniff, that is, create additional negative pressure to
pull the entering air currents up into the olfactory area. With pathologic
nasal airway obstruction a patient will often complain of anosmia before
mentioning that he has become a mouth breather. Moreover, since we A decrease in the sense of
characterize different foods by a combination of taste and smell, the patient’s smell is often perceived as a
decrease in taste.
presenting complaint may be that food does not “taste right” anymore.
Man’s sense of smell is rudimentary compared to other members of the
animal kingdom, yet the sensitivity of this organ is truly startling. McKenzie
states that vanillin is perceptible by us as a smell when it is present in
concentrations as low as 5 x 10-10 gm/L of air. The process by which odors
are perceived has not been determined with certainty, but there are two
theories that suggest chemical or undulation mechanisms. According to the
chemical theory, particles of odorous substances are distributed by diffusion
PART THREE—THE NOSE AND PARANASAL SINUSES
throughout the air and cause a chemical reaction when they reach the
olfactory epithelium. According to the undulation theory, waves of energy
similar to light impinge upon the olfactory nerve endings. Regardless of
mechanism, the olfactory sense is quickly exhausted.
It is still very difficult to standardize in a laboratory test descriptions of
different characteristics of various odors or measurements of comparative
odor concentrations. Amoore identified seven main categories of odors,
adequate to encompass and describe all the varieties perceived. Although
many investigators agree with his theory, his system is still not accepted in
routine clinical practice or as the basis for determining disability ratings.
Instead, for the most part, investigators try to distinguish between anosmia,
hyposmia, normal olfaction, and parosmia (perverted olfaction) by offering
an odoriferous substance, such as oil of clove, in various air dilutions to the
test subject.
The sinuses have no obvious physiologic function. Negus is of the opinion
that they serve the sense of smell by accommodating extension from the
ethmoturbinals, especially in the frontal and sphenoid sinuses. Ethmoturbin-
als covered with olfactory epithelium occur in some of the lower animals. In
man, the sinuses are empty and our sense of smell is far inferior to that of,
for instance, the dog or cat; man’s ethmoturbinals have apparently disap¬
peared during the process of evolution.
Airway Resistance
The human breath begins at the rim of the nostril. The act of breathing
conveys air through the upper and lower respiratory tract to the alveoli of
the lung in sufficient volume, with sufficient pressure, moisture, warmth,
and cleanliness, to assure optimal conditions for oxygen uptake, and in the
reverse process optimal elimination of carbon dioxide brought to the alveoli
by the blood stream (Fig. 10-13). The nose, with its many inspiratory and
expiratory baffles and the valvelike action of the erectile tissues in the Variations in nasal resistance
turbinates and septum, smoothes and shapes the air streams, regulates are due primarily to changes in
the erectile tissues of the turbi¬
volumes of passing air and pressure, and conducts most of the air-condition¬ nates.
ing activities (air filtration, control of temperature and humidity).
Changes in air pressure which take place inside the nose during the
respiratory cycle have been measured using rhinomanometry. During quiet
respiration air pressure changes inside the nose are minimal and normally
are not greater than 10 to 15 mm H20, with an air flow rate varying between
0 and 140 ml/min. At inspiration a drop in pressure occurs; air flows out of
the sinuses. During expiration there is a small increase in pressure; air flows
into the sinuses. Sinus air exchange is very minor on the whole, except
during the act of sniffing, the mechanism whereby air delivery to the olfactory
membranes lining the sinuses is increased.
A wide range in nasal airway resistance has been noted in normal
individuals. More than 50 per cent of the total respiratory resistance during The nose provides more than 50
normal respiration is due to the total nasal resistance. In striking contrast, per cent of normal respiratory
resistance.
only 20 per cent of total respiratory resistance is accounted for by the oral
passage during mouth breathing. In the majority of individuals there is a
change from nasal to oronasal breathing during exercise with its increased
air requirements. A wide variation normally exists, however, as to when this
transition occurs. Although oral breathing is demonstrably easier, individuals
will usually resort to it as their normal style of breathing only in the case of
uncompensated nasal stenosis or when poor pulmonary function cannot
overcome normal nasal resistance. With complete nasal obstruction and its
resultant necessary transoral respiration, an increase in Pco2 has been noted
by some investigators. This preference for nasal breathing is requisite during
the first six months of human life and continues to provide protection against
airborne hazards throughout life.
Several areas of the nose where the air passage narrows can be likened to
“valves.” In the vestibular segment of the nose there are two such narrow¬
ings. The more anterior narrowing is found between the posterior aspect of
the upper lateral cartilage and the nasal septum. Any deviations of the nasal
septum in this area often cause an increased narrowing with its resultant
symptomatic airway obstruction. Such deviations can result from trauma or
growth irregularities. The second narrowing is found at the bony piriform
aperture. These two areas can be considered highly significant clinically in
the greater preponderance of intranasal surgical corrections.
A normally occurring alternation in nasal resistance between the right and An alternating cyclic variation in
left nasal passages has been demonstrated through the use of rhinomanom¬ airway resistance exists be¬
tween the right and left nasal
etry. Respiration volumes in the two passages are altered through alternating
passages.
congestion and decongestion of the erectile tissue covering the nasal turbi¬
nates on opposite sides of the septum. Cycles in normal individuals have
been found to vary from 1 hour to 6 hours in length, with an average cycle
length of 2Vi hours. These fluctuations are not normally noted by most
individuals, since total nasal resistance tends to remain at a constant level.
Air Conditioning
During the brief time that air traverses the horizontal portion of the nasal
passage, 16 to 20 times a minute in normal respiration, the inspired air is
warmed (or cooled) to near body temperature and its relative humidity is
brought to near 100 per cent.
190 PART THREE—THE NOSE AND PARANASAL SINUSES
Air Purification
The hairs, or vibrissae, of the skin-lined nasal vestibule play a role in air
filtration. More prominent in males, it is not understood what role this sex
differentiation plays in air filtration needs.
The irregular internal anatomy of the nasal passages causes eddies in the
Mucociliary Function
The transport of foreign particles deposited from inspired air posteriorly
to the pharynx, where they are either swallowed or expectorated, is carried
out through action of cilia moving the mucous blanket with its entrapped
particles (Fig. 10-17). Nasal airflow turbulence provides extensive exposure
mucus.
192 PART THREE—THE NOSE AND PARANASAL SINUSES
of inspired air to the nasal epithelium with its mucous blanket, a highly
viscid, continuous sheet of secretion which extends into all of the spaces and
angles of the nose, sinuses, eustachian tubes, pharynx, and the entire
bronchial tree.
The upper layer of this exceedingly thin mucous blanket, which is rich in
glycoproteins, is the more viscid, with a tensile strength that allows the cilia’s
stiff forward motion to keep the blanket moving posteriorly in a continuous
stream. The lower,.periciliary layer is more serous, providing little hindrance
to the bending, ciliary recovery stroke. The mucous blanket is renewed by
the submucosal glands two to three times an hour.
Just as the ciliary movement of the bronchopulmonary lining propels the
mucous blanket toward the pharynx, so, too, do the cilia of the nose and
ears. A considerable negative pressure is created by the pulling action of the
cilia on the mucous blanket when any of these chambers is blocked by a
mucous plug. This may result in intense sinus pain as the plug clears the
ostium and, as the mucous plug moves down the auditory canal, may cause
atelectasis of the tympanic membrane.
Effective ciliary action has been shown to be compromised by extreme
drying of the air, as often occurs in many homes during the winter heating
months. It is also important to maintain the normally occurring neutral pH
of 7. Air pollution interferes with ciliary effectiveness in various ways.
Nitrogen dioxide and sulfur dioxide, frequent components of smog, compro¬
mise nasal health. Positively charged particulate matter can neutralize the
negative atmospheric ion count normally produced by solar irradiation.
Ciliary movement has been shown to be reduced and even to stop as the ion
count becomes more positive. As a result, although the patient may present
with a complaint of “sinusitis,” the real cause is impaired ciliary physiology.
Nasal mucus, in addition to its role in transporting particulate matter
deposited from inspired air, also transfers heat, normally warms inspired
and cools expired air, and humidifies the inspired air with more than a liter
of moisture each day. However, even this amount of moisture is often not
sufficient to humidify the highly desiccated air frequently encountered in
heated homes during northern winters. This may result in mucosal drying
with its many accompanying nasal problems. The degree of moisture in the
mucous blanket is determined by neural stimulation of the seromucous
submucosal glands in the nasal lining.
The anterior third of the nasal chamber changes in response to changes in
the physical properties of the inspired air. With a great deviation from the
norm the respiratory epithelium lining the anterior portion of the turbinates,
particularly the inferior turbinate, becomes transitional or squamous and no
cilia are observed. The mucous blanket in this region becomes more viscid
and movement is achieved only through the pulling transmitted along the
mucous blanket from still-ciliated areas located posteriorly. If there is a high
content of particles in the inspired air, as occurs in certain occupations,
crusting is observed around the vibrissae and the anterior turbinal ends.
The direction of mucous streaming in the nose is generally backward.
Since the cilia are more active in the protected inferior and middle meatus,
they tend to drag the mucous blanket from the common meatus into these
recesses. The direction of flow on the septum is back and somewhat
downward toward the floor. On the floor, the direction is back, with a
tendency to flow under the inferior turbinate into the inferior meatus. On
10—APPLIED ANATOMY AND PHYSIOLOGY OF THE NOSE 193
the medial aspect of the turbinates, the flow is back and downward, passing
under the inferior margin into the corresponding meatus. The drainage from
the nonciliated areas in the anterior third of the nose is practically all through
the meatus. This is the area that collects most of the airborne contaminants.
The direction of the flow in the sinuses is spiral, beginning, in humans, at
a point remote from the ostium. The rate increases progressively as the
ostium is approached, and in the ostium the mucous blanket passes out in
the form of a whirling tube at a rate of 15 to 20 mm/min.
The rate of mucous flow determined by ciliary action varies in different
portions of the nose; that of the anterior nasal segment may be only one
sixth that of the posterior, which is 1 to 20 mm/min. Mucociliary deficiencies,
either inherent or acquired, have been demonstrated to relate to significant
disease states.
The mucous blanket, in addition to trapping and removing inert particulate
matter, also presents a barrier to allergens, viruses, and bacteria. Although
viable organisms are readily cultured from the anterior nasal segment, it is
difficult to obtain a positive postnasal culture. Lysozyme, present in the
mucous blanket, is destructive to the walls of some bacteria. Active phago¬
cytosis in the nasal membrane provides subsurface protection. The respira¬
tory cell membrane also provides cellular-induced immunity.
Quantities of immunoglobulins are produced in the nasal mucosa, perhaps
in part by plasma cells normally found in the tissue. According to physiologic
need, IgG; IgA, and IgE have been observed. Allergic rhinitis occurs when
an inhaled allergen comes into contact with the IgE antibodies to that antigen
which are fixed to nasal mucosal and submucosal mast cells, generating and
releasing inflammatory mediators that produce characteristic nasal mucosal
changes.
Pulmonary Correlations
Normal pulmonary physiology is dependent upon nasal breathing. Bron¬ Pulmonary physiology is influ¬
chial tone is dependent upon nasopulmonary reflexes that also cause changes enced by the health of the nose.
in total pulmonary resistance and perfusion. Studies have reported instances
in which serious cardiorespiratory problems, ranging from moderate cardio-
megaly and right ventricular hypertrophy to severe right cardiac failure and
pulmonary edema, were caused by partial obstruction of the upper respira¬
tory tract. These changes were reversed after the airway was cleared.
However, these observations were made mainly in black children with
enlarged adenoids and were attributed to hypoxia and hypercapnia causing
a pulmonary vasoconstriction and elevated pulmonary arterial pressure. It is
therefore assumed that an individual susceptibility must be prerequisite for
these pathologies, since observation of these changes is very rare when
compared with the frequency of nasopharyngeal obstruction in children in
general.
Research has demonstrated a reflex transmitted from the nasal mucosa to
the homolateral lung. A decreased cardiac output and increased peripheral
vascular resistance have also been related to nasal membrane stimulation.
The peripheral vascular resistance, however, has not altered carotid flow.
This is a similar finding to that described in the “diving reflex,” which
selectively preserves cerebral blood flow.
194 PART THREE—THE NOSE AND PARANASAL SINUSES
SPEECH MODIFICATION
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Ironside F, Matthews J: Adenocarcinoma of the nose and paranasal sinuses in woodworkers in
the state of Victoria, Australia. Cancer 36:1115-1121, 1975.
Landahl HD: On the removal of airborne droplets by the human respiratory tract. II. The
nasal passages. Bull Math Biophys 12:161—169, 1950.
10—APPLIED ANATOMY AND PHYSIOLOGY OF THE NOSE 195
Landahl HD1, Herrmann RG: Retention of vapours and gases in the human nose and lung.
Arch Indust Hyg 1:36-45, 1950.
Lehmann G: The dust filtering efficiency of the human nose and its significance in the causation
of silicosis. J Indust Hyg 17:37-40, 1935.
Maurer H: Z Anat Entwicklungsgesch 105:359, 1936.
Maurer H: Z Anat Entwicklungsgesch 107:203, 1937.
McKenzie D: Aromatics and the Soul. New York, Hoeber, 1923, p 39.
Morrow PE: Some physical and physiological factors controlling the fate of inhaled substances.
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Negus VE: The function of the paranasal sinuses. Acta Otolaryngoal 44:408-426, 1954.
Negus VE: Biology of Respiration. London, E & S Livingston, Ltd, 1965.
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73:381-403, 1964.
Palm PE, McNerney JM, Hatch T: Respiratory dust retention in small animals: A comparison
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Proctor DF, Wagner HN Jr: Clearance of particles from the human nose. Arch Environ Health
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Proetz AW: Applied Physiology of the Nose. 2nd ed. St Louis, Annals Publishing Co, 1953.
Rasmussen AT: The Principal Nervous Pathways. New York, Macmillan Co, 1932, pp 48-50.
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bovine bacilli, and rate and pattern of tubercle development. J Exp Med 97:61-68, 1953.
Speizer FE, Frank NR: The uptake and release of S02 by the human nose. Arch Environ
Health 12:725-728, 1966.
Taylor M: The nasal vasomotor reaction. Otolaryngol Clin North Am 6:645-654, 1973.
Williams HL: The nose as form and function. Ann Otol Rhinol Laryngol 78:725-740, 1969.
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air-filled cavities. Ann Otol Rhinol Laryngol 79:513-518, 1970.
11
ALLERGIC CONDITIONS IN
OTOLARYNGOLOGY PATIENTS
by Malcolm N. Blumenthal, M.D.
Allergies are common conditions involving the nose and sinuses. They are
defined as adverse immune reactions. Atopy is a type of allergy which is
mediated by reagin-type antibodies. They include diseases such as seasonal
rhinitis, allergic asthma, and eczema. Although the IgE system is the main
immunoglobulin involved in the production of atopic conditions, other
immune mechanisms may play a role in the allergic reactions.
Immunoglobulin-Mediated Reactions
Antibody Cell-Associated Reactions (Reagin, Cytophilic, Anaphylactic
Antibodies). These reactions involve an antibody, usually IgE, attached by
the Fc portion to a cell containing mediators, or their precursors (mast cell,
basophil, eosinophil, macrophage). The Fab portion of these antibodies
interacts with the specific allergen (ragweed, mite, egg). Consequently there
is activation of several membrane-associated enzymes. Products of these
This process ernes immediate- enzymatic cleavages lead to the release of mediators (Table 11-1). These
rhinitis. mec^ators cause immediate-type reactions, occurring within seconds' to
minutes, such as edema, as well as late-phase reactions, occurring several
hours after the interaction. Late inflammatory reactions most likely result
from the release of mediators from the mast cells as well as from eosinophils,
macrophages, and platelets. Clinical examples are some cases of asthma,
anaphylaxis, and urticaria as well as seasonal rhinitis (Atkins and Zweiman;
Matthews; Plaut and Lichtenstein; Schwartz; Wasserman).
Antigen Cell-Associated Reactions (Cytotoxic, Blocking and Stimulating
Antibodies). These reactions involve an antibody, usually of the IgG and
IgM variety, interacting with an antigen that is part of or associated with the
cell wall. As a result these reactions, which are usually complement-
dependent, can cause damage, stimulation, or blockade. Those involving
damage to the cell are conditions such as Rh-positive and penicillin hemolytic
anemia and autoimmune thrombocytopenia. Stimulation from this type of
196
1 1 —ALLERGIC CONDITIONS IN OTOLARYNGOLOGY PATIENTS 197
Cell-Mediated Reactions
Antigen interacting with T lymphocytes leads to the release of various
mediators, resulting in the clinical picture. Antibodies may assist in the
selection of the lymphocyte to interact. Clinical examples are contact
dermatitis and some transplantation reactions.
ically mediated conditions (Geha; Welliver). IgE levels are more often
elevated than not with such atopic diseases as asthma, rhinitis, eczema, and
allergic bronchopulmonary aspergillosis. In addition, elevated levels are also
found with many other diseases (Table 11-3). There are a large number of IgE elevation is compatible with
commercial immunoassays for total serum IgE levels that use a variety of but not diagnostic of allergy.
assay techniques. Elevated IgE levels, like eosinophils, are compatible with
but not diagnostic of allergic reactions.
Many other laboratory procedures such as complement studies and ra¬
diography are available to provide information that the disease process is
compatible with an immunologically mediated disease. None of these tests
are sufficient for the diagnosis. Therefore, the next step is to identify the
allergen and determine how it is related to the symptom.
In Vitro Methods
Quantification of Specific IgE. After the IgE was characterized in
1968 it was possible to raise antisera against this immunoglobulin class. This
The RAST method is the most opened up the area of performing immunoassays (Emanuel; Gleich et al).
popular my to quantify IgE.
The most widely used version is the radioallergosorbent test (RAST), which
employs allergen insolubilized on a cellulose paper disc (allergosorbent) that
binds specific IgE (and other antibody classes) from serum during a first
incubation. The immunoglobulin-bound solid phase is then washed, and
1-125 isotope-labeled anti-IgE (fc) or enzyme-labeled anti-IgE (Fc) is incu¬
bated with the washed disc in a second incubation. After further washing
the radioactivity bound to the IgE on the disc is counted, or, in the case of
enzyme-labeled antibody, a substrate is incubated to produce a colored or
fluorescent product. The radioactivity bound to the disc or the quantity of
product generated by enzyme activity is related to the disc-bound IgE by a
The RAST results do not always reference serum source from which unknown specimens are interpolated. It
correlate with clinical allergy.
should be stressed that the scoring systems for all of these procedures have
not been well related to the clinical picture. In general, a high value will
include fewer nonallergic patients but will also exclude allergic subjects. A
low score will include more allergic subjects as well as nonallergic individuals.
All the results must be interpreted in relationship to the history. The
advantages and disadvantages of this assay are summarized in Table 11-4.
During the past several years modifications of the original RAST have
been marketed for the measurement of specific IgE in the human serum.
The relative performance of these newer systems is still largely unevaluated.
1 1 —ALLERGIC CONDITIONS IN OTOLARYNGOLOGY PATIENTS 201
In principle, most of the assays are of similar design to the RAST. They
differ mainly in the solid phase used to fix the allergen, the type of tracer
attached to the anti-IgE detection protein, and the instrument required to
read the final signal (Emanuel).
Measurement of the Release of Mediators. IgE can be measured
using assay systems of the release of mediating substances (Gleich et al).
The most common is the histamine release assay. This method involves using
peripheral leukocytes that contain basophils assumed to have attached IgE.
Increasing amounts of test allergen are added to the cells, and the release
of histamine is measured using a biologic, fluorometric, or immunoassay
system. The amount of histamine released is expressed as a percentage of
total histamine in the cells. These methods have been expensive and time-
consuming. New methodology may allow this procedure to be more econom¬
ical and easier to perform. The histamine release systems measure not only
IgE antibody but possibly other reaginic antibodies as well as their ability to
attach to cells and release mediating substances. Their other advantages and
disadvantages are summarized in Table 11-4.
Comparison of In Vivo and In Vitro Testing for Reaginic Anti¬
bodies. The clinical evaluation of immunologically mediated disease can be
performed using in vivo and in vitro methods. One of the major problems
with all these tests has been the variability of allergens from lot to lot and
from supplier to supplier. Another has been the lack of reliable information
on the relevant biologic potency of extracts. Better standardization proce¬
dures are resolving these problems (Blumenthal et al).
Generally a significant positive correlation is found between RAST tests,
skin tests, histamine release assays, and histories. The skin test is the most The skin test is the most sensi-
sensitive assay at the present time for IgE-mediated reactions. tive method.
Indications for performing the RAST and the histamine release assay are
(1) situations in which the patient cannot be skin tested such as the presence
of dermatographism, dependence on medication that interferes with skin
testing, extreme youth and age when skin testing is difficult to perform and
interpret, and previous extreme sensitivity to the test allergen, (2) the need
to confirm the significance of a positive skin test, and (3) a strong history of
allergen sensitivity but a negative skin test.
At the present time, skin testing is the initial method used to confirm the
presence of an IgE mechanism involving the suspected allergen. This is due
to the lower cost and greater sensitivity of this method. If RAST or the
histamine release assay is to be performed first, it is with the knowledge that
202 PART THREE—THE NOSE AND PARANASAL SINUSES
these methods are less sensitive and more expensive and skiri testing still
may have to be done if the in vitro tests are negative.
allergic rhinitis involves the reaginic antibody (IgE), skin testing for
immediate wheal/flare reactions and/or radioallergosorbent test (RAST) is Shin testing and/or RAST evalu¬
ation is recommended.
recommended.
Treatment. Therapy for allergic rhinitis, nasal polyps, and sinusitis falls
into five major areas.
Avoidance of the Causative Allergen. This may be accomplished
by isolating the patient from the allergen, placing a barrier between the
patient and the allergen, or removing the allergen from the patient.
Symptomatic Treatment with Drugs. Oral antihistamines are chem¬
ical compounds that antagonize the action of histamine through the compet¬
itive inhibition of histamine at the histamine-receptor sites. They should be
given in a rational way. Since patients exhibit marked variability in response
to various antihistamines, individualization of doses and frequency of admin¬
istration is important. Commonly used H, antihistamines are ethanolamines, Oral medications include a wide
variety of antihistamines and
ethylenediamine, alkylamines, phenothiazines, and miscellaneous agents decongestants.
such as cyproheptadine, hydroxyzine, and piperazine. Common side effects
seen with these antihistamines are sleepiness, loss of appetite, constipation,
anticholinergic effects such as drying of the mucous membranes, and difficulty
in urination. A new generation of H, antihistamine is under development.
As a group they lack any direct chemical relationship to histamine but have
a common structure of an^aromatic nitrogen in the form of a piperidine,
piperazine, or pyridine. Furthermore, these structuTes are more polar and
so their access into the central nervous system is limited, thereby reducing
or eliminating related side- effects. These include antihistamines such as
terfenadine, loratidine, and astemizole. They also promise to be longer
acting (Dockhorn and Shellenberger).
It has been suggested by some investigators that H2 antihistamines such
as cimetidine and ranitidine may be useful when given along with the Hj
antihistamines if there is significant nasal obstruction. Symptomatic use of
H, and H2 antihistamines has given disappointing results in the treatment of
nasal polyps (Havas et al).
A decongestant may be given either alone or in combination with an H,
antihistamine orally or locally for the treatment of allergic rhinitis. The oral
route is usually preferred. Chronic use of local antihistamines and deconges¬
tants is not routinely recommended. Some information suggests that local
antihistamines may be sensitizing. In addition, use of local decongestants
over a long period of time may cause irritation and a “rebound phenomenon”
such as rhinitis medicamentosum (Blue). Their use for nasal polyps has been
disappointing.
Cromolyn sodium may be given intranasally. This drug will decrease the
release of mediating substances. It is considered a preventive medication
that is given before the onset of symptoms. Side effects are minimal ahd Topical therapy includes cromo¬
lyn and corticosteroids.
have been mainly those of local irritation. Its use for nasal polyps has not
been well demonstrated (Norman, 1983).
Corticosteroids may be used for the treatment of allergic rhinitis. They
may be given systemically as well as intranasally with a poorly absorbed
corticosteroid such as beclomethasone or flunisolide. The local medications
are preferred because of their more direct action and lower risk'of side
effects. They usually take several days to weeks to become effective. These
agents also have been reported to decrease the size of nasal polyps (Norman,
1983).
204 PART THREE—THE NOSE AND PARANASAL SINUSES
SUMMARY
Three criteria should be satis¬ Before a physician can confidently diagnose and treat an allergy, the
fied before diagnosis and
following criteria should be satisfied: (1) The clinical picture is compatible
treatment.
with an allergic reaction. (2) The causative agent has been identified. (3)
The immune mechanism has been established. After these criteria have been
satisfied, treatment can be given to interfere with the various ongoing
processes that result in the final allergic clinical picture.
References
Atkins P, Zweiman B: The IgE-mediated late phase skin response—unraveling the enigma. J
Allergy Clin Immunol 79:12, 1987.
Belin H, Norman PS: Diagnostic tests in the skin and serum of workers sensitized to B. subtilis
enzymes. Clin Allergy 7:55, 1977.
Blue JA: Rhinitis medicamentosa. Ann Allergy 26:425, 1968.
I 1 —ALLERGIC CONDITIONS IN OTOLARYNGOLOGY PATIENTS 205
Blumenthal MN, Fish L. Morris R, et al: Adverse health effects from allergens Minn Med
70:278, 1987.
Cohen S, Ottesen E: The eosinophil, eosinophilia. and eosinophil related disorders. In
Middleton E, Reed C, Ellis E (eds): Allergy: Principles and Practice. St Louis, CV Mosby
Co, 1983, p 701.
Coombs RRC, Gell PGH: Classification of allergic reactions. In Gell RRA. Coombs PGH
(eds): Clinical Aspects of Immunology, 2nd ed. Oxford, Blackwell Scientific Publications
Ltd, 1968.
Dockhorn R, Shellenbergcr MK: Antihistamines: The new generation. Immunol Allergy Pract
9:124, 1987.
Emanuel I: Comparison of in vivo allergy diagnostic methods. Immunol Allergy Pract 7 483
1983.
Geha R: Fluman IgE. J Allergy Clin Immunol 74:109, 1984.
Giraldo B, Blumenthal M, Spink W: Aspirin intolerance and asthma: A clinical and immuno¬
logical study. Ann Intern Med 71:479, 1969.
Gleich G, Yunnginger J, Stobo J: Laboratory methods for studies of allergy. In Middleton E,
Reed C, Ellis E (eds): Allergy: Principles and Practice. St Louis, CV Mosbv Co, 1983, p
271.
Havas T, Cole P, Parker L, et al: The effect of combined H, and H; histamine antagonists on
alteration in nasal airflow resistance induced by topical histamine provocation. J Allergy Clin
Immunol 78:856, 1986.
Mathews K: Mediators of anaphylaxis, anaphylactoid reactions and rhinitis. Am J Rhinol 117
1987.
McDonald J, Mathison D, Stevenson D: Aspirin intolerance in asthma: Detection by oral
challenge. J Allergy Clin Immunol 50:198, 1972.
Norman PS: Review of nasal therapy: Update. J Allergy Clin Immunol 72:421, 1983.
Norman PS: Allergic rhinitis. J Allergy Clin Immunol 75:531, 1985.
Platts-Mills TAE, Heymann PW, et al: Cross-reacting and species-specific determinants on a
major allergen from Dermatophagoides pteronyssinus and D. farinae\ development of a
radioimmunoassay for antigen PI equivalent in house dust and dust mite extracts. J Allergv
Clin Immunol 78:398, 1986.
Plaut M, Lichtenstein L: Cellular and chemical basis of the allergic inflammatory response. In
Middleton E, Reed C, Ellis E (eds): Allergy: Principles and Practice. St Louis, CV Mosbv
Co, 1983, p 119.
Schwartz L: Mediators of human mast cells and human mast cell subsets. Ann Allergv 58 226
1987.
Smith JM: Epidemiology and natural history <5f asthma, allergic rhinitis and atopic dermatitis
(eczema). In Middleton E, Reed C, Ellis E (eds): Allergy: Principles and Practice. St Louis
CV Mosby Co, 1983, p 771.
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1327. f
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Welliver R: Allergy and the syndrome of chronic Epstein-Barr virus infection. J Allergy Clin
Immunol 78:278, 1986.
12
DISEASES OF THE NOSE
by Peter A. Hilger, M.D.
Although the nose sits in the center of the middle third of the face, it is a
structure often overlooked when human disease is discussed. Alterations of
nasal physiology create disturbances that run the gamut from temporary
inconvenience and mild illness, such as an upper respiratory infection, to
life-threatening disorders such as choanal atresia in the neonate. The effects
of altered nasal physiology can be seen locally, as in nasal allergy; regionally,
as in dental deformities and mouth breathing secondary to chronic nasal
obstruction; and systemically, such as cardiopulmonary failure secondary to
chronic nasal obstruction.
Examination by biopsy
FIGURE 12—2. Instruments necessary for the study of the nasal space.
CONGENITAL DISORDERS
a. b.
are always present, change with nasofacial growth, and may become more
troublesome as the child matures.
The nasal deformities include septal deflections that are often severe
enough to cause significant nasal obstruction. In addition, the lower lateral
cartilage and soft tissues of the nasal alae are asymmetric. This often results
in a nose with inadequate tip projection, an acute nasolabial angle, sagging
of the nasal ala on the cleft side, and irregularities in the position of the
nostril sills (Fig. 12-3). The tip deformities may also compromise the nasal
airway and compound the nasal obstruction due to septal deflection. Fistulas
may also persist through the palate or gingivobuccal sulcus, which will allow
the contents of the oral cavity to contaminate the nose, leading to mucosal
edema and further nasal obstruction. Reconstructive procedures can provide
major improvement of both the functional and aesthetic deformities.
Since it is inappropriate to discuss the oral problems in this section on
nasal disease, the interested student is referred to those chapters on oral
disease, embryology, and congenital syndromes.
nervous system, whereas gliomas are not (Fig. 12-4C and D). Treatment is
always excision; depending upon its location, a neurosurgical approach may
be necessary.
A glioma is usually a solid, noncompressible, nonpulsatile gray or purple
mass that does not transilluminate and does not produce a positive Fursten-
berg sign, i.e., no enlargement on compression of the jugular. Gliomas are
usually noticed at, or shortly after, birth. Approximately 60 per cent are
extranasal, usually occurring along the nasomaxillary suture or near the
midline, infrequently in the midline; 30 per cent are intranasal; and 10 per
cent have both components. The differential diagnosis most commonly
includes dermoid cysts and encephaloceles. CT scanning, NMR, and plain
film in three planes are recommended for diagnosis.
Encephaloceles are frequently associated with other midline fusion defects
such as cleft lip or palate as well as a high incidence of other central nervous
system anomalies. Because an encephalocele is by definition the extracranial
herniation of meninges and brain, a cranial defect is always present.
Encephaloceles are usually bluish, compressible, pulsatile, may be transil-
luminated, and produce a positive Furstenberg sign. The differential diag¬
nosis should include dermoid cysts, neurofibromas, and hemangiomas. They
are best delineated by CT, NMR scanning, and plain film in three planes.
Neurosurgical intervention is necessary.
212 PART THREE—THE NOSE AND PARANASAL SINUSES
Choanal Atresia
Choanal atresia will be discussed in the chapter dealing with diseases of
the nasopharynx (Chapter 17).
INFLAMMATORY DISEASES—RHINITIS
individuals. There is some indication that children up to age five are more
susceptible. The commonly cited experience that chilling, exposure to
moisture and cold winds, and fatigue enhance the development of cold
symptoms has not been corroborated in well-controlled laboratory studies'
on known virus-infected volunteers. Exposure to the outdoor elements alone
may increase the chances of allergic episodes. It has been postulated that
vasomotor changes brought about by hormonal influences similarly enhance
the incidence of colds. Conclusions that colds may be aborted by the
administration of vasodilators have not been shown to be justified.
Prophylaxis and Therapy. Many useful virus vaccines have been developed
since Jenner’s fight against smallpox in 1798. Because of the very large
number of different viruses involved, it has so far been impossible to develop
vaccines to cover even most possibilities of infection. Antibiotics have value
only in treating secondary bacterial infections. Chemotherapeutic agents
have, to this date, played a very minor role because none has a broad-
spectum effect.
Antihistamines, desensitization, and general antiallergic measures are
useful in treating the allergic disorders. Antihistamines used to treat colds,
coughs, and allergies are Hrblocking agents. Little evidence exists that
patients with colds experience clinical benefit from their administration.
While topical vasoconstrictors such as phenylephrine or oxymetazoline may
provide relief of watery rhinitic discharge, they must be used with caution
in infants and young children. Oral decongestants decrease some of the
profuse nasal discharge, making the patient more comfortable, but they will
not effect a cure.
Although cough suppressants are widely used, the Committee of Drugs of
the American Academy of Pediatrics has voiced this warning: “Symptomatic
treatment may mask serious underlying disease and may be hazardous,
particularly in infants whose small airways can be easily plugged with
tenacious mucus. ... When a valid indication exists for antitussive therapy,
such as a nonproductive cough that seriously disturbs sleep or school
attendance, either codeine or dextromethorphan, which appear to be
equiactive, should be recommended.” Because of the danger of Reye’s
syndrome, aspirin should be avoided. Analgesic-antipyretic preparations may
provide symptomatic relief, with acetaminophen being the antipyretic of
choice.
The best treatment of the uncomplicated viral cold is probably still bed
rest and isolation for approximately two days. Adequate hydration can be
ensured through the use of a cool mist humidifier, increased fluid intake,
and administration of saline nose drops. During the phase of secondary
bacterial infection, specific antibiotics may be administered.
In spite of all the advances in virology and tremendous efforts by clinicians
everywhere to prevent, control, and treat the common cold, little has been
accomplished and much needs to be done in the future.
In addition to the common cold, other viral illnesses encountered, some
of which may result in permanent anosmia, include:
Influenzal Rhinitis. Influenzal rhinitis is caused by viruses A, B, and C of
the orthomyxoviruses. The sneezing, watery nasal discharge, and stuffy nose
are comparable in severity to the common cold; however, secondary bacterial
infections and necrosis of the ciliated epithelium occur more frequently with
influenza. Vaccination is recommended for high-risk groups. Antibiotics are
effective only for secondary bacterial infections.
12—DISEASES OF THE NOSE 215
Rhinitis of Viral Exanthemas. Rhinitis is frequently a prodromal symptom Rhinitis is 2 frequent prodromal
syndrome ot measles, rubella,
of measles, rubella, and chickenpox, often preceding the exanthema by two
and chickenpox.
to three days. Secondary bacterial infections and complications are more
common than with a cold. Although chickenpox will be most frequently
encountered, measles and rubella are still a consideration for the clinician,
particularly in areas with a high noncompliance with MMR vaccinations.
Fungal
Bacterial
Nasal involvement in the following diseases is often just part of the
systemic disease.
Tuberculosis. While primary tuberculosis of the nose is rare in the United
States, involvement of the nose is occasionally seen among patients with
active pulmonary tuberculosis. Diagnosis begins with a chest radiograph. If
this is negative, smears and cultures of sputum and nasal discharge followed
by biopsy may be carried out. If these are positive for Mycobacterium
tuberculosis, an appropriate course of antituberculosis medication must be
carried out.
Leprosy. More common in tropical countries, leprosy is also found in the
United States, chiefly in Texas, Hawaii, California, Louisiana, Florida, and
New York. With a progression very similar to rhinoscleroma, the nose may
be the site of the primary infection or it may be part of the systemic disease.
Early symptoms include obstruction, crust formation, and bleeding. The
upper respiratory tract is more frequently involved in the lepromatous form
of leprosy than in the tuberculoid or dimorphous form of leprosy.
Mycobacterium leprae always involves the nose before spreading to the
pharynx and larynx.
Rhinoscleroma. Rhinoscleroma is a granulomatous disease of the nose
endemic to Central and Southern Europe and some areas of Asia. Previously
rarely seen in the United States, the incidence has been rising in the West
and Southwest. Caused by Klebsiella rhinoscleromatis, this disorder involves
the nose primarily but may later extend to involve any area of the upper
respiratory regions, including the larynx. A slowly progressing disease, it
begins with an early acute inflammatory reaction with a purulent, foul¬
smelling rhinorrhea. This is followed by nasal crusting and slow-growing,
hard, insensitive nodules that may eventually obstruct the nose. The lower
nose and upper lio become prominent if left untreated, causing extensive
disfigurement.
Diagnosis is based on the clinical course and pathological examination of
the specimen showing characteristic Mikulicz cells and rod-shaped bacteria
within the cytoplasm. Granuloma and fibrosis are present. Antibiotic therapy
is required. Surgical treatment may be indicated to correct the severe scarring
that results.
ALLERGIC RHINOSINUSITIS
Allergic disorders involving the nose occur much more frequently than
the lay person or the average physician suspects, affecting approximately 10 Allergic rhinitis affects 10 per
cent of the population.
per cent of the general population. The nose, as one of the prominent shock
organs of allergic disease, is plagued by primary allergic manifestations,
chronic rhinitis and sinusitis superimposed on allergic changes, complications
of relatively mild anatomic obstructions by edema, and, finally, the late
after-effects of chronic allergenic insults, such as mucosal hypertrophy and
polyposis. Nasal air flow may be compromised by the nasal congestion and
rhinorrhea that occur in allergic rhinitis, directly or indirectly. When con¬
fronted by nasal disease, the clinician needs a high index of suspicion and
the ability to diagnose and treat allergic disorders.
218 PART THREE—THE NOSE AND PARANASAL SINUSES
Diagnosis
This section is concerned specifically with allergy in relation to the tissues
of the nose and paranasal sinuses. The differential diagnosis of nasal allergy
includes nonallergic rhinitis, infectious rhinitis, and the common cold.
The symptoms of nasal allergy differ from those of infectious rhinitis. The
allergic response is usually characterized by sneezing, nasal congestion, and
profuse, watery rhinorrhea. No fever is present and the secretion does not
progress from thin to thick and purulent, as it does in infectious rhinitis.
There is a rapid onset of symptoms after allergen exposure, including watery,
itchy eyes or palate. A seasonal pattern or association with animal dander,
dust, smoke, or other inhalants can usually be elicited. Associated symptoms
such as nausea, belching, bloating, diarrhea, somnolence, or insomnia may
also suggest an ingested allergen and differentiate these patients from those
with viral rhinitis. Another important difference is that the duration of
allergic rhinitis is generally considerably longer than that of viral rhinitis. In
patients with allergic diatheses, a positive family history of allergy or asthma
is frequently present. As with viral rhinitis, acute bacterial sinusitis may
occur secondary to ostial compromise and pooling of the secretions.
The diagnosis of nasal allergy should be established by a systematic
investigation that will include a careful history and some or all of the
following: nasal examination, skin tests, and elimination regimens. An
elimination regimen may also be used as a treatment.
1 2—DISEASES OF THE NOSE 219
History
Inquiries begin with a history of any allergic diseases in the family. The
patient should also be questioned about allergic disorders other than those
of nasal origin, such as asthma, eczema, urticaria, or drug sensitivities. The
time of year in which the symptoms are prevalent is helpful in determining
seasonal allergies. Correlating onset of symptoms with environmental
changes at work or about the home is important. Are the living quarters in
a dusty or damp area? Do symptoms start with outdoor activities? Pets in
the household often are the cause of difficulties. It is important to obtain a
history of previous treatment, especially if hyposensitization was utilized.
What medications have been used in the past? Which drugs have been
helpful without causing side effects?
Symptoms of food allergy are less obvious and require a very detailed
history. The time of day of the onset of the symptoms is important, e.g.,
relationship to meals. Because the patient may be allergic to some of his
favorite foods, it may be difficult for him to associate the fact that symptoms
could be related to a frequently ingested substance. Cravings for food can
represent allergic symptoms. Specific food idiosyncrasies, on the other hand,
may point to allergy-producing ingestants.
Nasal Examination
The nasal mucosa in patients with allergy is generally moist, pale, and
grayish pink in color. The turbinates appear swollen (Fig. 12-7). If there is
an associated infection, the secretions range from thin and mucoid to thick
and purulent; at the same time the mucosa may become red and inflamed,
congested, or even dry. Polyps may develop in the maxillary antral and
ethmoid region and extend into the middle and superior meatus. In addition,
polypoid degenerative changes can occur throughout the nasal mucosa,
covering the lateral nasal walls; this classic appearance of the nasal mucosa
is not always seen, however. Radiography of the paranasal sinuses is
nonspecific but may show a thickened mucosal lining and occasional pooling
of secretions (Fig. 12-8). When the natural ostia become obstructed from
excessive swelling, an air-fluid level within the sinus cavities or even total
opacification may become apparent (Fig. 12-9).
FIGURE 12—7. A comparison of the anterior rhinoscopic views in the normal nose with
one in which the turbinates are swollen as in acute allergic rhinitis.
220 PART THREE—THE NOSE AND PARANASAL SINUSES
Nasal Smear
Treatment
Elimination of Allergens
Treatment of nasal allergy is dependent upon several factors. First, if
possible, the offending allergenic agent should be eliminated. In the case of
pollen allergy, the patient should make proper alterations in his/her environ¬
ment, such as preventing unnecessary exposure to ragweed pollen. Air-
conditioning of the car and home as well as utilization of electronic air filters
may be helpful. The patient sensitive to dust should live in as clean an
environment as possible, with every effort made to keep the rooms free of
dust-collecting items such as shag carpeting and draperies. A patient sensitive
to mold should avoid sleeping in damp areas, such as basement bedrooms.
Windows should be kept closed at night, as the cold night air frequently
contains molds. Patients sensitive to smoke should avoid smoke-filled rooms
and association with persons smoking in an enclosed area, such as an
automobile. Patients who are known to be sensitive to specific foods will
have to make every effort to eliminate those foods from their diet. This may
not be easy because processed foods frequently contain substances, infor¬
mation about which may not be immediately available to the consumer.
Medical Management
Local nasal treatment is directed at reducing swelling and formation of
secretions and increasing the airway. Temporary relief can be obtained from
local application of 0.5 per cent ephedrine sulfate, but this becomes less
effective with repeated use. Although 0.25 per cent Neo-Synephrine is an
effective topical vasoconstrictor, it may affect the nasal pH and reduce ciliary
activity. Another effective medication is 0.05 per cent oxymetazoline. Topical
application to the nasal mucosa generally provides progressively shorter
periods of temporary relief, becoming less and less effective with use, and
may lead to rhinitis medicamentosa.
Local injection of steroids, usually in the form of triamcinolone, into the
inferior turbinate has been utilized. Topical steroid therapy with beclome-
222 PART THREE—THE NOSE AND PARANASAL SINUSES
Surgical Treatment
Benign mucoid polyps of the nose are commonly associated with nasal
allergy. They can occur in children but are seen much more often in adults.
Because of nasal airway obstruction, polyps become annoying to the patient.
After an obstructing lesion is properly identified as a benign polyp, it may
be removed. The patient must be warned that, in the presence of allergies,
polyps recur, resulting in repeated polyp removal throughout life. However,
proper attention to the underlying allergic disorder tends to delay the rate
Most polyps originate in the of recurrence. Most polyps originate as an outpouching of the mucosa
sinuses. covering the maxillary or ethmoid sinuses. The ever-growing mucosal en¬
largement forms a rounded, soft, moist, often gelatinous, sometimes fleshy
mass or at times a serum-filled sac, fixed onto a gradually elongating narrow
pedicle that reaches from the sinus, through the ostium, into the nasal cavity.
Most polyps are amber or grayish blue but may at times become reddened
from local irritation or secondary infection. But what looks like a polyp is
not always a polyp! When all the polyps are on one side and none is on the
other, one should consider a unilateral, localized infection of the nose or
sinuses or even a foreign body in the nose. In the toddler and grade schooler,
mucoviscidosis and its nasal changes enter the differential diagnosis. The
nasal polyp, a pseudotumor, must be differentiated from a host of true
benign and malignant neoplasms; these are indeed rare but must not be
missed. The unsuspecting surgeon who uses a nasal snare to remove a
juvenile angiofibroma of the nasopharynx which looks like a polyp may set
off an exsanguinating hemorrhage. The most difficult lesions to distinguish
from the true benign nasal polyps are areas of mucosal polypoid degenera¬
tion, most frequently encountered in the anterior portion of the swollen
inferior and middle turbinates. Differentiation and identification are made
easier by using a decongestant spray in the nose, such as 1 per cent ephedrine
or a 0.25 per cent Neo-Synephrine solution. Even better is a 4 per cent
cocaine solution, which provides some anesthesia in addition to decongestant
action. A nasal suction tip may then be utilized, not only to aspirate
secretions for easier inspection but to palpate the soft tissue lesion. Although
somewhat movable, the polypoid mucosa has a sessile attachment to the
turbinate with the relatively firm bone in its center, while the true polyp
moves freely on its pedicle.
Prior to nasal polypectomy, adequate premedication and topical anesthesia
are applied. The snare wire is then looped around the stalk of the polyp
without complete tightening of the wire, and the polyp, its stalk, and the
Polypoid obstruction of sinus base of the pedicle are avulsed all in one piece (Fig. 12-10). Sinus infections,
ostia contributes to the develop¬
caused by the obstructive presence of the polyp stalk in the ostium, usually
ment of sinus infections.
clear up more readily after the polypectomy. If polyps recur and are related
to recurrent sinusitis, surgical correction of the sinus disease may be
indicated.
Hypertrophic turbinates may require cauterization, cryosurgery, or partial
resection to create an adequate airway. Such surgery should be conservative
to prevent atrophic rhinitis (Fig. 12-11).
12—DISEASES OF THE NOSE 223
Systemic Treatment
Methods of systemic treatment include medication and allergic desensiti¬
zation. Allergic rhinitis, whether perennial or seasonal, is most frequently
treated with combinations of decongestants and antihistamines. Many such
combination drugs are available. Patients with hypertension and those who
are taking monoamine oxidase inhibitors should not be given any drug
containing an ephedrine-like substance. Such patients can be treated with
antihistamine alone.
Rather than a single disorder of the nose, this term refers to a group of
conditions. Even though the presenting symptoms may be similar, careful
history and proper examination are necessary to fully define the given
condition so that proper treatment can be instituted. Beginning students in
this area of rhinology may be confused by the variety of terms with which
they are confronted by both patients and other physicians. Table 12-2 thus
outlines some of these terms and their recommended usage.
Vasomotor Rhinitis
This condition of the nasal mucosa results from two opposing forces:
Activity of the parasympathetic nerves causes engorgement of the vascular
bed with resultant congestion and increased mucous production, while
activity of the sympathetic nerves causes vasoconstriction with its resultant
nasal patency and decreased mucous production. Factors affecting this
balance will be the main subject of the following discussion.
The term vasomotor rhinitis has been applied rather widely; however, it
may be considered a misnomer. Vasomotor rhinitis, as it is currently
understood, is neither an allergic nor an inflammatory disorder, although,
in the strictest sense of the word, the latter implies an inflammatory state of
226 PART THREE—THE NOSE AND PARANASAL SINUSES
the involved anatomic structures. Factors responsible for the rhinopathia are
classified broadly as drug-induced, endocrine, vegetative, and psychoemo-
tional.
Drug-Induced Rhinitis
Antihypertensive drugs, sympathetic blocking agents, may cause nasal
congestion.
Rebound vasodilation, called rhinitis medicamentosa, can result from the
Rebound vasodilation and abuse of sympathomimetic decongestant nose drops and nasal spray. The
congestion are frequent conse- average individual suffering from nasal congestion can obtain immediate
quences ot prolonged use of .... 0
topical decongestants. mitial relief for a period of several hours by utilizing these topical nasal
preparations. However, prolonged use results in a chronic congestive state
wherein the nasal membrane is sensitive to any irritant, especially when
intermittently applied (Fig. 12-12). After an initial vasoconstriction, a
secondary vasodilatation occurs which can make the nasal obstruction even
worse than before. Moreover, the mucous cells may be unduly stimulated
and may increase nasal blockage by excess secretion. The application of
these topical drugs may also alter the ciliary action and interrupt the
protective mucous blanket present in the nasal cavity. Prolonged use of such
medication may result in a hypertrophic rhinitis, treatment of which requires
immediate discontinuation of topical nasal medication and a long discussion
with the patient about the cause of the problem, careful history-taking, and
physical examination to determine and treat the underlying problems that
led the patient to initiate the use of topical nasal medications. If the
underlying problem is allergy, topical steroids such as flunisolide, beclome-
thasone, or, rarely, an intraturbinal injection of a corticosteroid may be
used. Also recommended is the use of systemic sympathomimetics, e.g.,
pseudoephedrine.
Other drugs that have been implicated in vasomotor rhinitis include
rauwolfia serpentina, alcohol, tobacco, and hashish.
12—DISEASES OF THE NOSE 227
impaired movement
nf mucous debris
Injured cilia
✓ Cilia
Engorged goblet cells
Goblet cells
Basement membrane
Thickened basement
membrane
Blood vessel
Dilated and engorged
blood vessel
SUPERFICIAL LAYER
OF SUBMUCOSA J
Edema of stroma -
Mucous gland
Hypersecretion of
mucous gland
DEEP LAYER
OF
SUBMUCOSA <
Thickened deep loyer
'''■ Periosteum
Slightly thickened _
periosteum
Hormonal
Estrogens stimulate vascular congestion of the nasal membranes as well
as engorgement in the uterus, generally peaking in the immediate premen¬
strual phase when pelvic congestion is at its maximum, causing some women
to note nasal congestion at this time. During pregnancy, as the levels of
estrogen rise, symptoms of nasal congestion usually begin during the fourth
to fifth month and progress to term, paralleling the increased production of
estrogen. Symptoms disappear spontaneously at delivery in most patients.
In a similar manner, birth control medication may produce nasal engorge¬
ment.
Another endocrine cause of nasal engorgement is hypothyroidism, or
myxedema. Relief is obtained only with the use of thyroid extract. Con¬
versely, antithyroid drugs may produce congestion.
Temperature
In general, cold air causes vasoconstriction and warm air causes engorge¬
ment due to vasodilation. Sudden environmental temperature changes may
stimulate nasal congestion and/or rhinorrhea.
228 PART THREE—THE NOSE AND PARANASAL SINUSES
Emotional Causes
Studies have shown that the recollection of humiliating and frustrating
experiences results in nasal responses identical to those that occurred in
response to noxious stimuli. Generally speaking, fear and dejection result in
shrinkage and pallor of the nasal mucosa, while anxiety, conflict, frustration,
and resentment result in hyperemia, swelling, and hypersecretion.
Nonairflow Rhinitis
If, because of a laryngectomy or tracheostomy, the nose is no longer
exposed to the regular movements of air associated with breathing, the
mucous membranes become engorged and violaceous.
Hypertrophic Rhinitis
Vascular Atony
Chronic allergy and sinusitis causing stimulation of the vessels of the nose
over a long period of time may lead to permanent vascular atony with
continued nasal congestion, regardless of appropriate medical therapy.
Surgical resection of grossly obstructive tissue may be required to establish
an adequate airway. However, resection should be conservative to avoid
creating the equivalent of atrophic rhinitis.
most prominently involves the blood supply of the nasal lining, gradually
increasing the nasal space in all directions as the lining becomes thinner.
Mucous glands atrophy and disappear, while fibrosis of the subepithelial
tissues becomes gradually more generalized. Tissues surrounding the nasal
mucosa become affected, including cartilage, muscle, and bone of the nasal
skeleton. Eventually the dryness and crusting and irritation of the nasal
mucosa extend to the lining of the nasopharynx, hypopharynx, and larynx.
This can affect the patency of the eustachian tube, resulting in chronic
middle ear effusion, and can cause adverse changes in the lacrimal apparatus,
including keratitis sicca.
In the late changes of atrophic rhinitis, also referred to as ozena, extensive
crusting may be accompanied by a loathsome fetor. While others around
him cannot stand the odor, the patient is usually protected by anosmia. He
complains of loss of taste and inability to sleep well or tolerate cold air.
With his markedly widened airway he experiences progressively increased Sensory disturbance and air How
obstruction to his nasal breathing, mainly because the air baffles that regulate changes may cause symptoms
of obstruction in atrophic
nasal pressure changes and convey sensory messages from the nasal mucosa rhinitis.
to the central nervous system have moved farther and farther out of the
picture.
Multiple theories exist for the cause of atrophic rhinitis and related
degenerative disorders. Some authors emphasize hereditary factors. A causal
relationship between the direct and indirect effects of trauma and tissue
atrophy is almost universally recognized. The trauma may be accidental or
iatrogenic, namely, the late effect of surgery. Radiation therapy to the nose
most readily damages blood vessels and mucus-producing glands and almost
always leads to atrophic rhinitis. Neurovascular changes, such as blood vessel
deterioration mediated by insults to the autonomic nervous system, have
been documented. Various infections, such as acute exanthemas, scarlet
fever, diphtheria, and chronic infections, have been implicated as the cause
of injury to the submucosal blood vessels. Environmental causes have also
been suggested because of the increased incidence in lower socioeconomic
populations.
Ozena is much more common in the countries around the Mediterranean
Sea than in the United States. A drop in the incidence of measles, scarlet
fever, and diphtheria in southern Europe since World War II appears to
coincide with a similar sharp decline in the incidence of ozena.
To date, medical treatment of atrophic rhinitis has, at best, been palliative. Medical therapy in atrophic rhi¬
It includes irrigations and cleansing of crust formation; local and systemic nitis is palliative.
endocrine, steroid, and antibiotic therapy; vasodilators; the use of mild local
tissue irritants such as alcohol; and lubricating ointments. The major treat¬
ment emphasis is surgical, all efforts being directed at narrowing the nasal
passages again and by so doing improving the mucosal blood supply. Surgical
techniques are divided into two major categories: (1) implants, through
either an intra- or an extranasal approach and (2) operations, such as
narrowing of the nasal lobule or infracture of the nasal bones.
lesions in the upper and/or lower respiratory tracts, (2) systemic vascular
focal necrosis, and (3) focal necrotizing glomerulitis. Affecting men and
women equally, it is seen primarily in adults.
The patient will often present with a long-standing cold, recurrent sinusitis;
epistaxis, progressive nasal obstruction, chronic otitis media, and hearing
loss that are unresponsive to treatment. Although lesions may involve any
area of the respiratory tract, nasal crusting and friable nasal mucosa are the
norm, with eventual saddling a common sequela.
No specific laboratory test is diagnostic. A mild anemia is usually present,
with an elevated erythrocyte sedimentation rate, and urinary abnormalities
Multiple biopsies may be neces¬ if there is kidney involvement. Diagnosis is dependent upon biopsy of the
sary to identify this potentially involved tissues for demonstration of necrotizing granulomas and extensive
lethal disease.
vasculitis. Multiple samples may be necessary to demonstrate the diagnostic
lesion.
Differential diagnosis includes polymorphic reticulosis, infectious granu¬
lomas, fungal and tuberculous infections, sarcoidosis, and other vasculitides.
Therapy in acute patients involves treatment with corticosteroids and
cyclophosphamide. Some authors believe, however, that the addition of
steroids to the cytotoxic medications provides symptomatic improvement
without altering the course of the disease as when treated with cytotoxic
medications alone.
Polymorphic Reticulosis
Polymorphic reticulosis is a rare disease characterized by local inflamma¬
tion and destruction of the tissues of the midface. Fatal if untreated, it was
originally called lethal midline granuloma, a term no longer considered
appropriate.
The symptoms and clinical findings are very similar to those of Wegener’s
granulomatosis. Diagnosis is dependent upon a biopsy, with tissues charac¬
terized by a dense, mixed lymphoid infiltration. The absence of giant cells,
vasculitis, and systemic involvement differentiates it from Wegener’s granu¬
lomatosis, and the mixed population of cells differentiates it from lymphoma.
This differential diagnosis is critical, since the only therapy shown to be
effective is radiation therapy.
Relapsing Polychondritis
Relapsing polychondritis is a rare connective tissue disease of unknown
etiology causing episodic inflammation and subsequent destruction of the
cartilaginous structures of the body. Nasal involvement results in saddle-
nose deformity with no involvement of the mucosa. No specific laboratory
test is diagnostic; a biopsy helps provide the diagnosis. Corticosteroids have
been found useful in severe cases, but in the majority of symptomatic cases,
therapy with salicylates and nonsteroidal anti-inflammatory medications is
indicated.
Sarcoidosis
Nasal sarcoidosis is usually as¬ Nasal sarcoidosis is generally associated with the more common pulmonary
sociated with pulmonary mani¬ manifestations of this disease with world-wide distribution and unknown
festations.
etiology. A generalized granulomatous disorder primarily affecting young
12—DISEASES OF THE NOSE 231
adults, in the United States blacks are 10 times more likely to be affected
than are Caucasians. Nasal findings include crusting and thickened mucosa
on the inferior turbinate and septum.
A biopsy demonstrating noncaseating granulomas is characteristic, al¬
though not diagnostic. Other, systemic signs often include hypergammaglob¬
ulinemia and a reduction of serum albumin. Treatment Of the symptomatic
patient involves steroids, either systemically or in a topical nasal spray,
aimed at reducing both nasal stuffiness and crusting. Local treatment with
irrigation and moisturizing medication may also be helpful.
Osler-Weber-Rendu Syndrome
Also called hereditary hemorrhagic telangiectasia, this autosomally domi¬
nant syndrome is characterized by the formation of vascular lesions around
the lips, oral cavity, and nose. One of the most common presenting
manifestations is recurring epistaxis that requires multiple transfusions. Recurring epistaxis occurs fre¬
quently in Osler-Weber-Rendu
Septal dermoplasty is one method designed to control the repeated epistaxis. syndrome.
The operative procedure involves careful removal of the mucosa of the
anterior nasal septum, floor of the nose, and anterior portion of the inferior
turbinate and replacement of this mucosa with a split-thickness skin graft
(Fig. 12-13). The procedure is usually performed on one side only but may
be repeated later on the opposite side. While it creates crust formation in
the nose, it may be necessary in patients who have required multiple
transfusions. Hormonal therapy has provided improvement for some pa¬
tients, allowing them to avoid surgical intervention.
Sjogren’s Syndrome
This disorder, consisting of dry eyes, dry mouth and nasopharynx, and a
chronic arthritis, may also have some nasal manifestations. It is covered
more fully in Chapter 17.
EPISTAXIS
Nasal hemorrhage is such a common problem that every physician should Every physician should be able
to control most episodes of epi¬
be prepared to handle the majority of such episodes. The keystone to proper staxis.
treatment is the application of pressure to the bleeding vessel. Probably 90
per cent of episodes of anterior epistaxis are easily treated by firm, continuous
pressure applied to both sides of the nose just superior to the nasal alar
cartilages, with the patient sitting in an upright position. This position
reduces the vascular pressure, and the patient can more easily expectorate
any blood in the pharynx. However, when it becomes apparent that control
is not adequate, the patient’s physician needs immediately to try another
method. Only those methods available to the physician which can be applied
to the majority of persistent cases of epistaxis will be dealt with here in
detail. Other methods will be mentioned briefly.
Management
History
Proper management of epistaxis will depend on a careful history. Impor¬
tant items include the following:
Avoid cauterizing both sides of septum, an effort should be made not to cauterize the same area on both
the septum.
sides. Even with very shallow penetration of the cauterizing agent, the
surface area covered by cautery must be limited. Otherwise, as cilia are
destroyed and squamous epithelium overlying scar tissue replaces normal
respiratory mucosa, stowage points in the flow of the mucous blanket
develop. As the flow of mucus slows or stops in those areas of previous
cautery, crusts form on the septum. The patient then picks his nose to
remove the crusts, injuring the lining, setting off a new nosebleed, and
completing the vicious circle by returning to the doctor for another attempt
at cautery.
Shallow penetration is also obtained with silver nitrate, which is fairly
useful in children. Deeper penetration may be obtained with beads of
chromic acid and even electrocautery. During very active bleeding, no
method of cauterization of the nose is effective or safe. Repeated bleeding
from a blood vessel over the septum may be resolved by locally elevating
the mucosa and letting the tissues realign themselves or by reconstructing
the underlying septal deformity to relieve the localized atrophy and mucosal
tension spots.
With recurrent minor nosebleeds of unidentified nasal origin, the physician
must rule out nasopharyngeal or paranasal sinus tumors that erode blood
vessels. Chronic sinusitis is another possible cause. Finally, one should look
for distant pathologic disturbances such as renal disease and uremia or
systemic illness such as a coagulation disorder.
can be treated on an outpatient basis, being told to sit siill most of the day
and to slightly elevate the head at night. The pack may then be removed in
the office after two to three days. Elderly or debilitated patients should be
hospitalized.
FIGURE 12—18. Intranasal tampons. A, Compressed tampon in nose. B, Tampon expanded to control hemorrhage.
Posterior epistaxis is believed to exist when (1) the majority of the blood
loss is occurring into the pharynx, (2) an anterior pack fails to control the
hemorrhage, or (3) it is evident from nasal examination that the hemorrhage
is posterior and superior. This situation occurs commonly in elderly individ¬
uals who may have arteriosclerosis but may also occur in anyone after severe
nasal trauma.
Sphenopalatine Ganglion Block. In the presence of posterior epistaxis
some physicians recommend that a sphenopalatine block be given, which
can be both diagnostic and therapeutic. Careful injection of 0.5 ml of
Xylocaine. 1 per cent, with epinephrine, 1:100,000, into the greater palatine
canal will cause vasoconstriction of the sphenopalatine artery. In addition to
vasoconstriction, this injection provides anesthesia for the placement of a
posterior nasal pack. Should the blood loss be from a division of the
sphenopalatine artery, a decrease in the epistaxis will be noted within a few
minutes. This decrease in bleeding may last only a short time until the
Xylocaine is absorbed. Glycerin (2 per cent USP) and Xylocaine (2 per cent)
can be injected for a more prolonged effect. When no effect is obtained
from injection, the blood loss may be from the anterior or posterior ethmoid
arteries. Because of possible ocular complications, this method is better
reserved for the specialist.
Posterior Nasal Pack. A posterior pack placed through the mouth (Fig.
12-19) can be pulled by a catheter through the nose into the posterior
choana. A 4- x 4-inch sponge rolled tightly and tied with No. 1 silk sutures
makes an excellent pack. A topical antibiotic ointment is applied to reduce
the incidence of infection. Tamponade by various commercially available
preshaped nasal balloons passed anteriorly and then inflated is also possible.
12 —DISEASES OF THE NOSE 237
nose, the physician places the usual anterior pack between them and ties the
The strings of a posterior pack two strings snugly in a bow over a roll of gauze. Both strings should be
should not be tied across the brought out through the same nostril and not tied over the columella—this
columella.
can cause pressure necrosis of the soft tissues, a very unsightly deformity
that is difficult to correct.
Patients requiring a posterior pack are admitted to the hospital, with
Patients with a posterior pack elderly patients or patients with underlying medical diseases placed in the
are admitted to the hospital intensive care unit. Consideration should include the following items when
the patient is admitted:
1. Frequent monitoring of vital signs, including blood pressure, pulse,
and respiration
2. Electrocardiogram (in a patient with significant medical illness,
continuous monitoring with a cardiac monitor)
3. Use of oxygen as necessary (with caution in chronic obstructive lung
disease) because of the possibility of complications secondary to
sedation, acute blood loss, and a fall in arterial Po2 associated with
the pack
4. Monitoring of blood arterial gases
5. Hemoglobin and hematocrit at least every 12 hours
6. Studies (PT, PTT, platelet count) for any bleeding abnormality
7. All tests necessary to perform a sufficient medical evaluation of any
possible underlying cause of the occurrence of the epistaxis, such as
FBS, BUN, or creatinine
8. Intravenous fluids should be administered, as these patients will have
a poor oral intake.
9. Pain medication, usually meperidine hydrochloride (Demerol) or
codeine. (It is important to provide significant sedation and analgesia
without causing respiratory depression.)
10. Clear liquid diet
11. Examination of the pharynx for active bleeding
12. Head elevated 45 degrees
13. Prophylactic broad-spectrum antibiotics because of interrupted
drainage patterns from nose and sinuses
14. Type and cross-match for blood if significant blood loss has occurred
The posterior pack is generally kept in place for three to five days. During
this period of time, the patient will be uncomfortable and will require
sedatives and analgesics. Studies have shown that complete obstruction of
the nasal airway in certain individuals may lead to an elevation of the Pco2
Hypoxia and hypercapnia are and reduction of the Po2. This combination of events in a patient with a
common when a posterior pack history of significant cardiac or pulmonary disease can lead to significant
is present.
complications, e.g., myocardial infarction or cerebrovascular accident. It is
often advisable to loosen a traditional pack or deflate a balloon prior to
complete removal. If bleeding redevelops the tamponade can be re-estab¬
lished with less discomfort than if the packing needs to be replaced.
further dissection. Vessels are identified and metal clips placed on the
internal maxillary, sphenopalatine, and descending palatine arteries (Fig.
12-20). The wound is closed and the posterior nasal pack removed. A lesser
anterior nasal pack may still be required. If there is any evidence of an
infection or fear that infection may develop, a nasal antral window is created
embolization is an alternative to during the procedure. Selective catheterization with embolization of branches
ligation. of the externai carotid artery is another approach that achieves the same
objective as ligation.
Ligation of the Anterior Ethmoid Artery. Flemorrhage from terminal
branches of the ophthalmic artery occasionally requires ligation of the
anterior ethmoid artery. The vessel is approached through a curved incision
extending along the nose, midway between the dorsum and the medial
canthal area. This incision is carried directly down to the bone, with the
periosteum carefully elevated and the medial canthal ligament identified.
The anterior ethmoidal artery always lies in the suture line between the
ethmoid and frontal bone. A single ligature or hemostatic clip is applied to
the vessel (Fig. 12-21). Because of the close approximation to the optic
nerve, the ethmoid vessels are approached with care and gentle retraction
on the globe.
staxis begins again several hours later. It may, in fact, develop several days
later in a nonreduced fracture when the swelling begins to subside. The best
treatment in such circumstances is an immediate reduction of the nasal
fracture. Failure to control the hemorrhage after fracture reduction may
require any one of the various vessel ligation procedures previously de¬
scribed. If the septum has been fractured, the treating physician should
investigate the area to rule out a septal hematoma.
TRAUMA
Nasal fractures, along with other maxillofacial injuries, are discussed fully
in Chapter 26. However, it is important to note here that nasal trauma is a
frequent cause of nasal obstruction.
Although the patient may recall the incident leading to current obstructive Post-traumatic septal deformi¬
ties are common sources of na¬
symptoms, childhood injuries that are not remembered may have previously
sal obstruction.
created significant anatomic alteration and obstruction. Moreover, what may
have appeared to the patient or treating physician to be a “minor” injury
can create enough deformity to be functionally significant.
The most common structural disturbance causing airway obstruction is a
deflected or deviated nasal septum (Fig. 12-22). The normally straight
242 PART THREE—THE NOSE AND PARANASAL SINUSES
midline structure has, in almost all instances, been affected by trauma with
its direct and indirect sequelae. Injuries to an individual during growth and
development have more of an impact than similar insults suffered by an
Minor trauma can cause signifi- adult. The physiologic effect of the deformity depends not only on its relative
cant septal deformities, structural complexity but also on its location. Moreover, other nasal pathol¬
ogy such as allergies, infections, neoplasm, or metabolic disorders can
temporarily, recurrently, or permanently add to the severity of the obstruc¬
tive symptoms. The injury may create a septal hematoma due to the
collection of blood beneath the mucoperichondrium. The patient usually
complains of severe obstruction, and intranasal inspection reveals boggy
septal mucosa that does not shrink following application of topical decon¬
gestants. Immediate drainage is necessary, often followed by nasal packing
to avoid the development of a septal abscess, as mentioned earlier in this
chapter.
The structure of the external nose, both cartilaginous and bony portions,
may be likened to a “pyramid” or a “tent” with a central support, the
septum. Injuries may cause obstruction through one or more of the following
mechanisms:
1. Collapse of the side wall medially, thus narrowing one nasal fossa (Fig.
12-23A and B). The fracture of a nasal bone often carries the attached
upper lateral cartilage medially, resulting in obstruction.
2. Displacement of the septum. Unilateral displacement narrows one
passage and enlarges the other, causing unilateral obstruction. Bilateral
obstruction results if the septal fracture causes fragments to be displaced
into each nasal fossa.
3. Fracture and displacement of both the nasal vault and septum, deviating
the “pyramid.” The fractures apparent on magnitude of the obstruction
is dependent upon the degree of obstruction resulting from each
component of the injury (Fig. 12-23C).
NEOPLASMS
Neoplasms involving the nose and paranasal sinuses are discussed together
owing to the intimate relationship of these structures. As a result of the
diverse histologic make-up of the nose and paranasal sinuses, the variety of
neoplasms that may occur is great. However, because most are found very Nasal neoplasms occur infre-
infrequently, only those that are encountered with any regularity or are of deently.
special interest will be presented here. Malignant tumors are covered in
Chapter 23.
It is important for the physician to remember that the symptoms due to
244 PART THREE—THE NOSE AND PARANASAL SINUSES
neoplasms of the nose and paranasal sinuses are not striking, the most
common including nasal obstruction, epistaxis, and blood-tinged mucus. A
nasal speculum is used to provide adequate examination of the nasal cavity,
Symptoms of nasal neoplasms both before and after administration of either phenylephrine or a dilute
are nonspecific. cocaine solution. A mirror or other optical instrument is necessary to
visualize the posterior choanae and nasopharynx.
While these steps will provide the physician with the location of abnormal
tissue, imaging techniques such as radiographs, tomograms, computed to¬
mographic (CT) scans, and magnetic resonance imaging (MRI) help deter¬
mine the extent of the disease, whether surgery is a viable option, and, if
so, the appropriate surgical approach.
Squamous Papilloma
Possibly of viral etiology, epithelial changes in squamous papilloma may
range through various degrees of dyskeratosis. Lesions are often noted at
the mucocutaneous junction in the anterior nose, especially on the anterior
caudal margin of the septum. For both diagnosis and treatment the lesions
are excised under local anesthesia. As most of them are small, no sutures
are needed. Before closure of the larger ones, it is well to undermine skin
and mucosa for a short distance.
Inverted Papilloma
Extramedullary Plasmacytoma
Fibrous Dysplasia
Fibrous dysplasia refers to nonencapsulated fibro-osseous tumors involving
the facial bones with frequent impingement on the paranasal sinuses of the
nose (Fig. 12-24). The etiology is unknown.
A slow-growing tumor, it is rarely associated with pain and tends to
appear around the time of puberty, with the patient presenting for cosmetic
reasons due to facial asymmetry. Because growth of this tumor again slows
with age, the need for treatment is dependent upon the degree of deformity
or the presence of pain. Although complete resection is desirable owing to
the slow growth of the tumor, in the majority of patients only sufficient
tumor is removed to restore normal facial contours and function.
In a small proportion of patients malignant degeneration of the tumor has
been reported. The majority of these reports involved patients treated with
radiation for the fibrous dysplasia. It is imperative, therefore, that radiation
therapy be avoided unless there are no other alternatives and that patients
with fibrous dysplasia be followed closely to detect any changes.
MISCELLANEOUS
Septal Perforation
Until the advent of penicillin, tertiary lues was the most common cause
of perforations of the nasal septum. As the incidence of syphilis decreased,
the most common cause shifted to the large number of patients who had
had excessive septal injury. Other causes include acute as well as chronic
trauma like nose-picking; infected septal hematomas, tuberculosis, leprosy,
and other infections; and the illicit use of cocaine, with accompanying
frequent intranasal manipulation, mucous alterations, ischemia, and septal
necrosis.
The symptoms of nasal perforations can be annoying to the patient. There
may be a whistling sensation through the nose during speech. Small perfo¬
Nasal crusting and whistling are rations frequently tend to have more of a whistling sensation than very large
frequent symptoms of septal perforations. The edges of the perforations tend to crust, resulting in
perforations.
obstruction. As the crusts break off, bleeding occurs (Fig. 12-25). The
resultant epistaxis may be difficult to control and will require packing of
both sides to apply adequate pressure.
Repair of anything other than small perforation of the nose is difficult.
Surgical repair is difficult. Both homogeneous and autogenous tissues of various types have been
utilized to replace the absent cartilaginous support. The mainstay of the
repair requires development of mucoperichondrial flaps, which are then
swung to close the defect. A flap is developed on each side in such a manner
as not to expose cartilage in the same place on the opposite side. These flaps
are then sutured into position and held there by stents. Silastic prostheses
that obturate the defect are an alternative to surgery and are preferred by
some patients.
Foreign Bodies
Foreign bodies as a cause of nasal obstruction are practically always
encountered in children. Children at play tend to place small objects in the
nasal passages. Common foreign bodies found in children are beads, buttons,
erasers, marbles, peas, beans, stones, and nuts. Recently inserted objects
give little or no discomfort unless they are sharp or very large. The usual Foreign bodies often present as
unilateral obstruction and rhi-
symptoms are unilateral obstruction and discharge with odor. The majority
norrhea.
of foreign objects are found either in the anterior part of the vestibule or in
the inferior meatus along the floor of the nose. None should be allowed to
remain in the nasal passages because of the danger of producing necrosis
and secondary infection and the potential for aspiration into the lower
respiratory tract. Removal can be accomplished in the cooperative child in
the clinic after applying a topical anesthetic and vasoconstrictor, such as
cocaine. A blunt, bent hook inserted behind the object or a small alligator
forceps is helpful (Fig. 12-26). Occasionally, general anesthesia will be
needed.
Rhinoliths
Rhinoliths are considered to be a special type of foreign body usually
observed in adults. Insoluble salts of the nasal secretions form a calcareous
mass about any long-retained foreign body or blood clot. A chronic sinus
discharge may initiate such a mass to form in the nasal passages.
Rhinophyma
Rhinophyma is a red thickening of the nasal tip with hypertrophy of the
sebaceous glands associated with acne rosacea. Occurring most commonly
in men, its exact etiology has not yet been determined. Treatment becomes
necessary when the rhinophymatous tissue causes an obvious cosmetic
deformity or when the bulk of tissue compromises the airway. Surgical
correction can be performed under local anesthesia. One of the more
frequently used procedures is to carefully carve down the excessive tissue
with a sharp blade. Reduction via dermabrasion and laser excision are also
treatment options. Care is taken not to expose the underlying cartilage and
to leave sufficient epithelium to permit re-epithelialization and healing. In
severe cases relining with full-thickness or split-thickness skin grafts is
necessary.
248 PART THREE—THE NOSE AND PARANASAL SINUSES
References
Anderson TW, et al: The effect on winter illness of large doses of vitamin C. Can Med Assoc
J 111:31, 1974.
Andrewes CH: Rhinoviruses and common colds. Ann Rev Med 17:361-370, 1966.
Barton RPE: Clinical manifestations of leprous rhinitis. Ann Otol Rhinol Laryngol 85:74-82,
1976.
Bernstein L, et al: The nasal cavities. Otol Clin North Am 6:609-874, 1973.
Dykes, MH, Meier P: Ascorbic acid and the common cold. JAMA 231:1073, 1975.
Karlowski TR, et al: Ascorbic acid for the common cold. JAMA 231:1038, 1975.
Luke M, Mehrize A, Folger F, Rowe R: Chronic nasopharyngeal obstruction causing cor
pulmonale. Pediatrics 37:762-768, 1966.
McDonald TJ, DeRemee RA, Kern EB, Flarrison EG: Nasal manifestations of Wegener’s
granulomatosis. Laryngoscope 84:2101-2112, 1974.
Meyer HM: The control of viral diseases. J Pediatr 73:653, 1968.
Ogura J, Togawa K, Dammkeohler D, et al: Nasal obstruction and the mechanics of breathing.
Arch Otolaryngol 83:135-150, 1966.
Pauling L: Ascorbic acid and the common cold. Scott Med J 18:1-2, 1973.
Riggs RH: Some congenital nasal anomalies including dermoid cysts. J Louisiana State Med
Soc 118:1-4, 1966.
Schaeffer JP: The Nose, Paranasal Sinuses, Nasolacrimal Passageways and Olfactory Organ in
Man. New York, Blakiston, 1920.
Settipane GA: Allergic rhinitis—update. Otolaryngol Head Neck Surg 94:470-475, 1986.
Sooknundun M, Deka RC, Kacker SK, Kapila K: Congenital mid-line sinus of the dorsum of
the nose. Two case reports with a literature survey. J Laryngol Otol 100:1319-1322, 1986.
Stahl RH: Allergic disorders of the nose and paranasal sinuses. Otolaryngol Clin North Am
7:703-718, 1974.
Stoksted P, Neilsen J: Rhinometric measurements of the nasal passages. Ann Otol Rhinol
Laryngol 66:187-197, 1957.
13
DISEASES OF
THE PARANASAL SINUSES
by Peter A. Hilger, M.D.
For a physician one of the most common daily occurrences is the visit by
a patient who declares that he or she has “sinus problems.” The lay public
blames the paranasal sinuses for more symptoms than almost any other
single anatomic structure in the body. However, it is an undeniable fact that
sinus infection, as we know it today, is much less frequent than in the
preantibiotic era. Patients still attribute to dysfunction of the sinuses such
symptoms as headache, nasal obstruction, postnasal drainage, fatigue, hali¬
tosis, and dyspepsia. Sinus disease, however, produces a set of rather
characteristic symptoms which varies only with the severity of the disease
and its location. It is the purpose of this chapter to describe the usual clinical
picture of various acute and chronic diseases of the paranasal sinuses. The
information in this chapter and in the chapters on tumors of the nose and
sinuses and on diseases of the nose should clarify diagnosis of true sinus
disorders and indicate the appropriate management for each.
Infectious Sinusitis
General Considerations
The most important concept in dealing with sinus infection is to realize
that the nose and paranasal sinuses are only a part of the total respiratory
system. Diseases that can affect the bronchi and lung can also affect the
nose and paranasal sinuses. In relation to the infective process, therefore,
the whole of the respiratory tree with its anatomic extensions should be
considered as one entity. The infection may initially affect the entire
respiratory system, but in varying degrees, and the subsequent pathologic The sinobronchial syndrome re¬
fers to concurrent exacerbation
change or clinical condition is determined by the predominance of the of sinus and pulmonary disease.
infection in a particular area, leading to sinusitis, laryngitis, pneumonitis,
and so on. This relationship between the upper and lower respiratory tracts
is responsible for the so-called sinobronchial syndrome.
The anatomy of the sinuses is described in Chapter 10; however, it is
important to remember when the different sinuses develop during childhood
and adolescence and, therefore, when they become susceptible to infection.
The maxillary and ethmoid sinuses are present at birth and are usually the The maxillary and ethmoid si¬
nuses are the only sinuses pres¬
only sinuses that are involved in childhood sinusitis. The frontal sinuses start
ent at birth.
to develop from the anterior ethmoid sinuses at about 8 years of age and
249
1 3 —DISEASES OF THE PARANASAL SINUSES 251
are among the most common predisposing local factors. Maxillofacial defor¬
mity, particularly cleft palate, can cause considerable problems in children.
These children tend to suffer from chronic nasopharyngeal and sinus infec¬
tions at a much higher rate. Dental conditions account for approximately 10
per cent of all acute maxillary sinus infections.
The symptoms of acute maxillary sinus infection consist of fever, malaise,
and a vague headache that is usually relieved with simple analgesics such as
aspirin. There is a feeling of fullness in the face, and pain in the teeth may
be felt during sudden movements of the head, such as when going up and
down stairs. Often there is some degree of characteristic dull, throbbing
cheek pain with tenderness to pressure and percussion. Mucopurulent
secretions may emanate from the nose and are sometimes malodorous.
Frequently, an irritative, nonproductive cough is present. During acute
maxillary sinusitis, physical examination may reveal pus in the nose, usually
from the middle meatus, or pus or mucopurulent secretions in the naso¬
pharynx. There is tenderness upon palpation and percussion of the maxillary
sinuses. Transillumination is decreased if the sinus is full of fluid. The
radiologic appearance of acute maxillary sinusitis may be that of mucosal
thickening initially, followed by complete opacification of the sinus due to
severe mucosal swelling or to an accumulation of fluid filling the sinus (Fig.
13-L4). Finally, the characteristic air-fluid level due to accumulation of pus
is seen in the upright views of the maxillary sinus (Fig. 13-15). Therefore,
sinus radiographs should include the supine and upright views, the most
advantageous for detecting maxillary sinusitis. A-mode ultrasound screening
has also been mentioned as a safe, noninvasive diagnostic method. Further
investigations might require a complete blood count and nasal culture. A
strong word of caution must be issued with regard to interpretation of nasal
cultures. Cultures from the maxillary sinus would be valid; however, this
pus is loculated within a bony cavity. An anterior nasal culture, on the other
FIGURE 13—1. A, X-ray (Waters’ view) of maxillary sinus showing an opaque sinus and a grossly deviated bony
nasal septum. 6, An x-ray view (Waters-Waldron position) of a pansinusitis involving the right maxillary,
ethmoid, and frontal sinuses. There is a fluid level visible in the involved maxillary sinus.
252 PART THREE—THE NOSE AND PARANASAL SINUSES
Anterior nasal cultures are un¬ hand, will reveal all the organisms within the nasal vestibule, including the
reliable in sinusitis.
normal inhabitants, such as Staphylococcus and several other gram-positive
cocci, which bear no relationship to the bacteria that may be causing the
sinusitis. Therefore, the bacterial nasal culture taken from the anterior part
of the nose is of little value in interpreting the bacteria within the maxillary
sinus and may even give false information.
A culture from the posterior aspect of the nose or the nasopharynx would
be much more accurate but, technically, this is extremely difficult to obtain.
Specific cultures of the bacteria concerned with sinusitis are obtained using
maxillary irrigation. Most frequently, an appropriate antibiotic is given to
cover the more common organisms involved in this disease (Streptococcus
pneumoniae, Haemophilus influenzae, anaerobes, Branhamella catarrhalis).
Acute maxillary sinusitis is generally treated with a broad-spectrum anti¬
biotic such as amoxicillin, ampicillin or erythromycin plus sulfonimide, with
other alternatives being amoxicillin/clavulanate, cefaclor, cefuroxime, and
trimethoprim plus sulfonamide. Decongestants such as pseudoephedrine are
useful, and potent nose drops such as phenylephrine (Neo-Synephrine) or
oxymetazoline may be used during the first few days of the infection but
then should be discontinued. Hot packs to the face and analgesics such as
Radiologic changes lag oehind aspirin and acetaminophen are useful for symptomatic relief. The patient
clinical improvement.
usually shows some signs of improvement within two days, and the disease
process is often completely resolved within 10 days, although radiologic
confirmation of complete resolution may take two or more weeks. Failure
to resolve on active therapy would indicate either that the organisms are not
sensitive to the antibiotics or that the antibiotics are failing to reach the
loculated infection. In this instance, the sinus ostium may be so edematous
that the sinus cannot drain freely and a true abscess is formed. In this
instance, prompt antral irrigation is indicated. The route of insertion of the
trocar for maxillary antral irrigation is usually beneath the inferior turbinate
after initial cocainization of the mucous membrane (Fig. 13-2). An alternate
route is the sublabial approach, in which a needle is passed through the
gingival buccal sulcus through the incisive fossa (Fig. 13-3). Warm saline is
irrigated into the maxillary antrum via this route, and the pus is flushed out
through the natural ostium. Either method is acceptable, provided that the
clinician has the skill and experience necessary to perform the procedure.
Maxillary Sinusitis of Dental Origin. This particular form of maxillary Dental disease is responsible
dental disease is responsible for 10% of cases of sinusitis occurs following for 10 per cent of sinusitis
cases.
dental problems. The most common cause is the extraction of a molar tooth,
usually the first molar, during which a small piece of bone lying between the
apex of the tooth and the maxillary sinus is removed (Fig. 13-4). It was
Nathaniel Highmore in 1651 who described the thin membrane of bone that
separates the teeth from the sinus. He stated, “The bone which encloses the
maxillary antrum and which separates it from the socket of the teeth does
not much exceed a piece of wrapping paper in thickness.” The maxillary
antrum is frequently called the antrum of Highmore. Other dental infections
such as apical abscess or periodontal disease may cause a similar condition.
The bacteriologic picture of sinusitis of dental origin is predominantly that
of the gram-negative infection. This leads to a particularly foul-smelling pus
and, consequently, foul odor from the nose. Antibiotics, irrigation of the
sinus, and correction of the dental problem are the mainstays of therapy.
Predisposing Local Factors. Other local predisposing causes of acute
maxillary sinusitis are a foreign body in the nose and a deviated nasal
septum. Surgical removal of the foreign body is obviously mandatory, and
surgical correction of the deviated nasal septum is usually performed after
the acute phase has resolved completely. Since sinusitis may also follow
packing of the nose for epistaxis, it is common practice to prescribe a
prophylactic antibiotic in any nasal packing. Facial fractures can disturb the
normal physiologic drainage of the sinus and lead to infection. Barotrauma
causes mucosal edema and occlusion of the sinus ostium, leading to an
accumulation of sinus secretions and subsequent infection.
b.
Oroantral
fistula
254 PART THREE—THE NOSE AND PARANASAL SINUSES
Ethmoid Sinusitis
Isolated acute ethmoid sinusitis is more common in children, frequently
presenting as orbital cellulitis. In adults it often accompanies maxillary
sinusitis and must be regarded as an inevitable accompaniment of frontal
sinusitis. Symptoms include pain and tenderness between the eyes and over
the bridge of the nose, nasal drainage, and nasal obstruction. In children
the lateral wall of the ethmoid labyrinth, the lamina papyracea, is often
dehiscent, and orbital cellulitis is therefore more likely to occur (Fig. 13-5)
Treatment of ethmoid sinusitis involves the use of systemic antibiotics, nasal
decongestants, and topical vasoconstrictor sprays and drops. Development
o impending complications and inadequate improvement are indications for
an ethmoidectomy (Fig. 13-6).
Frontal Sinusitis
Acute frontal sinusitis is almost always associated with anterior ethmoid
infection. The frontal sinus develops from the anterior ethmoid air cells, and
the tortuous frontal nasal duct runs in close relationship to these cells.'The
predisposing factors of acute frontal sinus infection are similar to those for
other sinus infections. The disease is seen predominantly in adults and
apart from the usual general symptoms of any infection, frontal sinusitis is
b.
associated with a characteristic head pain. The pain is situated above the
eyebrows, is present usually in the morning, becomes worse by midday, and
then gradually lessens during the remainder of the waking hours. The patient
will usually state that the forehead is tender to the touch, and there may be
supraorbital swelling. The pathognomonic sign is excruciating tenderness to
pressure and percussion over the infected sinus. Transillumination may be
impaired, and sinus radiographs will confirm either periosteal thickening,
generalized opacity of the sinus, or an air-fluid level. The treatment consists
of appropriate antibiotics as described previously, decongestants, and vaso¬
constrictor nasal drops. Failure to resolve quickly or the onset of complica¬
tions would require drainage by frontal sinus trephine technique (Fig. 13-
7).
Sphenoid Sinusitis
Acute isolated sphenoid sinusitis is exceptionally rare. It is supposed to
be characterized by headache directed to the vertex of the skull. Much more
commonly, it forms part of a pansinusitis, and, therefore, its symptoms are
intermingled with those of other sinus infections. Sphenoid sinus trephination
was performed with some frequency in the preantibiotic era but now has
become almost an extinct procedure.
Chronic Sinusitis
By definition, chronic sinusitis lasts .several months or years. In acute
sinusitis, pathologic changes of the mucous membrane consist of polymor¬
phonuclear infiltrates, vascular congestion, and desquamation of the surface
epithelium, all reversible changes. The pathologic picture of chronic sinusitis
is complex and irreversible. The mucosa is generally thicker, thrown into
folds or pseudopolyps. The surface epithelium may show areas of desqua¬
mation, regeneration, metaplasia, or simple epithelium in varying amounts
on the same histologic section. Microabscess formation, granulation tissue,
and healing by scar tissue are intermingled. Overall, there is a round cell
and polymorphonuclear infiltrate in the submucosal layers.
The etiology and predisposing factors of chronic sinusitis are quite varied.
256 PART THREE—THE NOSE AND PARANASAL SINUSES
Pollution,
Chemicals
Allergy,
Immunologic
Deficiencies
I
Inadequate Treatment
A large piece of the medial wall of the inferior meatus is removed to allow
gravitational drainage and ventilation, and possibly, therefore, to allow
regeneration of healthy mucous membrane within the maxillary sinus. A
more radical procedure bears the name of two surgeons who popularized
it—the Caldwell-Luc operation (Fig. 13-11). In this surgical procedure, the
epithelium of the maxillary sinus cavity is removed completely and a drainage
antrostomy is performed at the termination of the procedure in a manner
similar to that described previously. The end result is satisfactory, since the
active diseased mucous membrane has been either replaced with normal
mucosa or filled with inert scar tissue.
FIGURE 13—11. Caldwell-Luc procedure. Irreversible maxillary sinus disease can be treated surgically by (A)
an incision in the canine fossa and (B) removing a portion of the bone of the anterior wall of the sinus. The
opening can be enlarged (C) with a biting forceps. An opening (D) into the inferior meatus similar to a
nasoantral window is made to replace the compromised natural ostium. Ventilation and drainage of the
sinus can then occur through (£) the inferior meatus or the natural ostium if resolution of the sinus disease
opens the natural ostium. The operation is completed by (F) closure of the oral incision.
13 —DISEASES OF THE PARANASAL SINUSES 259
FIGURE 13—13. Ethmoidectomy. Two methods to remove diseased ethmoid air cells are demon¬
strated. An external ethmoidectomy is performed through [A) an incision on the lateral side of the
nose. The soft tissues and periosteum, including the lacrimal sac and medial canthus, are elevated.
Biting forceps and curettes are used to (B) remove the diseased air cells. At the completion of the
procedure, the ethmoid air cells have been replaced by one large cell that opens into the nose
(C). An intranasal ethmoidectomy accomplishes the same objective but is performed with instru¬
ments that reach the ethmoid cells through the nares and middle meatus (D and £).
FIGURE 13-16. Frontal sinus obliteration. Chronic frontal sinus disease can be treated by
eliminating the sinuses altogether. The procedure can be performed through a brow incision or
a coronal incision. The anterior wall of the sinus is incised (A). The sinus mucosa is removed (8),
the nasofrontal ducts are plugged, and the sinus is filled with fat.
Sinusitis in Children
The ethmoid and maxillary sinuses are present at birth, with the remaining
sinuses developing during late childhood and adolescence. Until the second
decade of life the ethmoid and maxillary sinuses are the only clinically
important sinuses.
Children of all ages are particularly prone to upper respiratory tract viral
infections as well as allergies. Common sequelae of these conditions include
mucosal edema and loss of cilia with viral infections, resulting in occlusion
of the sinus ostia. Once the ostium is closed, the air within the sinus is
absorbed and replaced by an effusion that easily becomes infected secondarily
by bacteria.
Mechanical factors such as adenoid hypertrophy, foreign bodies, choanal
atresia, and stenosis may contribute significantly to poor airway physiology
and stasis of secretions.
Congenital immunologic defects, Kartagener’s syndrome, Down’s syn¬
drome, Hurler’s syndrome, and the various dysglobulinemias are associated
with sinusitis in children, as are the acquired immunodeficiencies of leukemia
and immunosuppression by drugs. Nasal polyps occur in approximately 50
per cent of children with cystic fibrosis. Sinusitis in these children is common.
1 3 —DISEASES OF THE PARANASAL SINUSES 263
COMPLICATIONS OF SINUSITIS
Computed tomography (CT) scans are a great asset in defining the extent
of the sinus disease and the extent of infection outside the sinuses—into the
orbit, soft tissues, and cranium. This type of investigation should be routine
in refractory, chronic, or complicated sinusitis.
Orbital Complications
The ethmoid sinuses are predominantly responsible for orbital complica¬
tions. Orbital swelling may also be the presenting sign of acute ethmoiditis;
however, both the frontal sinuses and the maxillary sinuses lie in close
proximity to the orbit and may also cause infection of the orbital contents.
There are five stages:
1. Mild inflammatory or reactionary edema (Fig. 13-17A). This can occur
in the orbital contents as a result of the proximity of infection in the
ethmoid sinuses. As stated previously, this is particularly seen in
children because the lamina papyracea that separates the orbit from
the ethmoid sinuses is frequently dehiscent in this group.
2. Orbital cellulitis. Edema is diffuse and bacteria have actively invaded
the orbital contents, but pus formation does not occur (Fig. 13-175).
264 PART THREE—THE NOSE AND PARANASAL SINUSES
Mucocele
A mucocele is a mucus-containing cyst found in the sinuses. These cysts
are most frequently seen in the maxillary sinus, are often referred to as
mucous retention cysts, and are quite innocuous. In the frontal, sphenoid,
and ethmoid sinuses these cysts may enlarge and, by pressure atrophy, erode
the surrounding structures. They may, therefore, present as swelling of the
forehead or nasal bridge or may displace the eye laterally. In the sphenoid
sinus they may cause diplopia and impairment of vision by pressure on the
neighboring nerves.
A pyocele is an infected mucocele. The symptoms of a pyocele are quite
similar to those of a mucocele, although more acute and more severe.
Surgical exploration of the sinus for removal of all diseased and infected
mucosa and re-establishment of good drainage or obliteration of the sinus
are the mainstays of treatment.
Intracranial Complications
Acute Meningitis. Apart from cavernous sinus thrombosis, which has
previously been described, one of the most severe complications of sinusitis
is acute meningitis. Infection from the paranasal sinuses may spread along
the preformed venous channels or directly from the neighboring sinuses,
such as through the posterior wall of the frontal sinus or through the
cribriform plate near the ethmoid air cell system (Fig. 13-20).
Contamination
throuqh vein wall
j>Cerebral cortex
Front, sinus-
Periosteum
Periorbital space fi J
Lamina papijracea--
1 w T C- >
exSonn72^Dia^mriC ruepre5entati°n °f the venous system « "highway” of
which brain H , °mu S'nUS mUCOSa to adioininS structures. Note the depth at
which brain abscess develops because of the venous anatomy of the cerebral cortex.
13 —DISEASES OF THE PARANASAL SINUSES 267
a CT scan. Prior to antibiotic use, this spread of infection into the calvarium
would elevate the pericranium and lead to the classic description of Pott’s
puffy tumor. Treatment of this complication includes large doses of anti¬
biotics given intravenously, followed by prompt incision of the periosteal
abscess and trephination of the frontal sinus to provide drainage. A drainage
tube or catheter is sutured into the sinus until the acute infection has
completely subsided and the frontonasal duct is functioning well. If the
frontonasal duct has been irreparably damaged by the process, a subsequent
procedure will be necessary to re-create a new frontonasal duct. In spreading
osteomyelitis of the calvarium, wide debridement and massive antibiotic
therapy are mandatory. Fortunately, this complication is now rare.
NONINFECTIOUS SINUSITIS
Barosinusitis
Paranasal sinus homeostasis is dependent upon ostial integrity. Any
pathologic condition that causes edema of the mucosa near a sinus ostium
Ostial compromise is a precur¬ predisposes a patient to the development of barosinusitis. As the environ¬
sor of barosinusitis. mental atmospheric pressure changes, the compromised ostium prevents
pressure equilibration in the adjacent sinus. When environmental alteration
produces significant negative intrasinus pressure, as noted in scuba diving or
the descent from altitude in an airplane, fluid transudation or hemorrhage
occurs in the sinus. Pain and pressure usually accompany the change and
occasionally mild epistaxis occurs. A sinus with an incompetent ostium and
fluid is an ideal environment for the development of acute suppurative
sinusitis. Radiography may reveal complete opacification or an air-fluid level.
Treatment includes the use of topical and systemic decongestants, antibiotics
in many cases, and the avoidance of environmental pressure changes until
sinus ostial function is re-established.
Allergic Sinusitis
The changes occurring in the sinuses are the same as those observed in
the nose. Polyps presenting in the nose usually originate in the sinuses and
may also fill the sinuses. Polypoid changes alter the normal homeostatic
mechanism of the sinuses and predispose the sinuses to acute and chronic
sinusitis, e.g., osteal obstruction, loss of normal ciliary epithelium. Acute
and chronic infections are treated as noted earlier in this chapter. Polypoid
changes may require medical therapy, as noted in the section on allergic
rhinitis, with steroids (topical and systemic), decongestants, and antihista¬
mines. Polyps need resection if they obstruct the nasal airway or sinus ostia.
Extensive or recurrent polypoid diseases are an indication for additional
sinus surgery, such as a nasal-antral window and, occasionally, frontal sinus
surgery. If the polypoid disease involves the turbinates, partial turbinectomy,
270 PART THREE—THE NOSE AND PARANASAL SINUSES
Benign tumors that are seen in the sinuses are the same as those noted in
the nose. They are discussed in Chapter 12.
One additional tumor that deserves mention is the osteoma, a benign
tumor that can develop within the sinuses—most frequently the frontal sinus.
Its clinical significance lies in the potential for the tumor to obstruct the
sinus ostium as it enlarges. This can then set the stage for the development
of sinusitis. When an osteoma encroaches upon the sinus ostium it should
be resected or the sinus obliterated if a frontal sinus is involved.
Malignant tumors are covered in Chapter 23.
References
Chandler JD, Langenbrunner DJ, Stevens ER: The pathogenesis of orbital complications in
acute sinusitis. Laryngoscope 80:1414-1428, 1970.
Dawes JDK: The management of frontal sinusitis and its complications. J Laryngol Otol 75:297-
344, 1961.
Eavey RD, Nadol JB, Holmes LB, et al: Kartagener’s syndrome. A blinded, controlled study
of cilia ultrastructure. Arch Otolaryngol Head Neck Surg 112:646-650, 1986.
Eliasson R, Mossberg B, Cammer P, et al: The immotile-cilia syndrome: A congenital ciliary
abnormality as an etiologic factor in chronic airway infections and male sterility. N Engl J
Med 297:1-6, 1977.
Fairbanks DNF: Antimicrobial Therapy in Otolaryngology—Head and Neck Surgery. American
Academy of Otolaryngology—Head and Neck Surgery Foundation, 1987.
Fearon B, Edmonds B, Bird R: Orbital facial complications of sinusitis in children. Laryngoscope
89:947-953, 1979.
Hawkins DB, Clark RW: Orbital involvement in acute sinusitis. Clin Pediatr 16:464-471, 1977.
Imbrie JD: Kartagener’s syndrome: A genetic defect affecting the function of cilia. Am J
Otolaryngol 2:215-222, 1981.
Jarsdoerfer R, Feldman P, Rubel E, et al: Otitis media and the immotile cilia syndrome.
Laryngoscope 89:769-777, 1979.
Kennedy DW, Zimreich SJ, Rosenbaum AE, Johns ME: Functional endoscopic sinus surgery.
Theory and diagnostic evaluation. Arch Otolaryngol 111:576-582, 1985.
Kennedy DW: Functional endoscopic sinus surgery: Technique. Arch Otolaryngol 111:643-649,
1985.
Quick CA, Payne E: Complicated acute sinusitis. Laryngoscope 82:1248-1263, 1972.
Schramm VL, Meyers EN, Kennerdell JS: Orbital complications of acute sinusitis: Evaluation,
management and outcome. ORL J Otorhinolaryngol Relat Spec 86:221-230, 1978.
Shahin J, Gullane PJ, Dayal VS: Orbital complications of acute sinusitis. J Otolaryngol 16:23-
27, 1987.
Shapiro ED, Wald ER, Brozanski BS: Periorbital cellulitis and paranasal sinusitis: A reappraisal.
Pediatr Infect Dis 1:91-94, 1982.
Stammberger H: Endoscopic endonasal surgery—Concepts in treatment of recurring rhinosi-
nusitis. Part I. Anatomic and pathophysiologic considerations. Head Neck Surg 94:143-147,
1986.
Stammberger H: Endoscopic endonasal surgery—Concepts in treatment of recurring rhinosi-
nusitis. Part II. Surgical technique. Head Neck Surg 94:147-156, 1986.
PART FOUR
THE ORAL
CAVITY AND
PHARYNX
14
EMBRYOLOGY, ANATOMY,
AND PHYSIOLOGY OF THE
ORAL CAVITY, PHARYNX,
ESOPHAGUS, AND NECK
by Stephen L. Liston, M.D.
EMBRYOLOGY
The oral cavity, pharynx, and esophagus are derived from the embryonic
foregut. The foregut also gives rise to the nasal cavity, teeth, salivary glands,
anterior pituitary, thyroid and larynx, trachea, bronchi, and alveoli of the
lungs. The mouth forms when the primitive stomodeum, a fusion of the
ectoderm and endoderm, breaks down. The upper lips are formed by
elements of the medial and lateral nasal processes and the maxillary proc¬
esses. Cleft lips are usually not midline but lateral to the medial nasal
process, which forms the premaxilla. The lower lip develops from elements
of the mandibular processes. The muscles of the lip are derived from the
second branchial region and supplied by the facial nerve. The vermilion
border of the lips has a characteristic bowed appearance; a notch in this bow
is a very noticeable cosmetic defect.
The teeth are derived from the dental lamina, which gives rise to the
cementum and enamel of the definitive teeth. The development of the human
dentition through the milk teeth to the final eruption of the adult third molar
corresponds to the age of the patient, and charts are available to follow the
normal eruption of the dentition. There are a variety of benign and malignant
cysts and tumors that derive from remnants of the dental lamina. The teeth
273
274 PART FOUR—THE ORAL CAVITY AND PHARYNX
are supplied by branches from the maxillary and mandibular branches of the
trigeminal nerve. In the upper jaw, there is some variation and overlap in
the regions of supply of the branches of the maxillary nerve.
The palate is formed in two parts: the premaxilla, containing the incisor
teeth and derived from the medial nasal process, and the posterior palate,
both hard and soft palate, formed by fusion of the palatal shelves. A cleft
palate, therefore, will be midline posteriorly but will swing to the side of the
premaxilla anteriorly. At one stage, the palatal plates are lateral to the
tongue and if the tongue does not descend, the palatal plates cannot fuse.
This is the basis of the cleft palate associated with the micrognathia of the
Pierre Robin syndrome.
The tongue is formed from several epithelial eminences in the floor of the
The lingual nerve provides gen¬ mouth. The anterior tongue is derived mainly from the first branchial region
eral sensation to the tongue;
and supplied by the lingual nerve, with the chorda tympani branch of the
the mental nerve, which trans-
verses the mandible and exits facial nerve supplying the taste buds and the secretomotor supply of the
through the mental foramen, submandibular gland. The glossopharyngeal nerve supplies all the sensation
provides sensation to the lower
to the posterior third of the tongue. The muscles of the tongue are derived
lip region.
from postbranchial myotomes that migrate forward, bringing with them the
hypoglossal nerve. This migration of the hypoglossal nerve is responsible for
its having a predictable relationship to branchial fistulas. The thyroid arises
from the foramen cecum in the posterior part of the tongue and migrates
along the thyroglossal duct into the neck. If this migration does not occur,
the result is a lingual thyroid. Remnants of the thyroglossal duct may persist,
and these may be tucked up behind the body of the hyoid bone.
The salivary glands grow as outpouchings of the epithelium of the mouth
and come to lie in close proximity to important nerves. The submandibular
duct is crossed by the lingual nerve. The facial nerve comes to be embedded
in the parotid gland.
ANATOMY
The oral cavity and the pharynx are somewhat arbitrarily divided into
regions. The oral cavity is anterior to the free margin of the soft palate, the
anterior tonsillar pillar, and the base of the tongue. The nasopharynx extends
Laryngo-or
Larynx hypopharynx
14—EMBRYOLOGY, ANATOMY, AND PHYSIOLOGY 275
from the base of the skull to the level of the soft palate. The oropharynx
extends from this level to the level of the epiglottis, while below this line is
the laryngopharynx, or hypopharynx (Fig. 14-1).
The Pharynx
Behind the mucosa of the posterior wall of the pharynx is the basisphenoid
and basiocciput superiorly, then the anterior portion of the atlas and the
bodies of the axis, and then the other cervical vertebrae. The nasopharynx
opens anteriorly into the nose via the posterior choanae. Superiorly, the
adenoid lies on the mucosa of the roof of the nasopharynx. Laterally, the
opening of the cartilaginous eustachian tube occupies a region anterior to a
recess called the fossa of Rosenmuller. Both these structures pass above the
276 PART FOUR—THE ORAL CAVITY AND PHARYNX
free border of the superior constrictor. The tensor veli palatini, the muscle
that tenses the palate and opens the eustachian tube, enters the pharynx via
this space. This muscle forms a tendon that hooks around the bony hamulus
to enter the soft palate. The tensor veli palatini is supplied by the mandibular
nerve via the otic ganglion (Fig. 14-2).
The oropharynx communicates anteriorly with the oral cavity. rfhe pha¬
ryngeal tonsil within its capsule lies on the mucosa on the lateral wall of the
oral cavity. Anterior to the tonsil, the anterior tonsillar pillar is composed
of palatoglossus muscle, and posteriorly the posterior tonsillar pillar is
composed of the palatopharyngeus. These muscles help close the posterior
oropharynx. They are innervated by the pharyngeal plexus of nerves.
The tonsil is composed of lymphoid tissue covered by squamous epithelium
containing many crypts (Fig. 14-3). There appears to be no documentable
Pharyngeal
tonsil
- Soft palate
Palatine
tonsil
Lingual tonsil
immune deficit caused by removing the tonsils (o,r adenoids). The cleft above
the tonsil represents the remnant of the endodermal opening of the second
branchial arch; this is where a second branchial fistula or internal sinus will
open. Infection may collect between the capsule of the tonsil and the loose
surrounding tissues and may track up toward the base of the soft palate as
a peritonsillar abscess.
The hypopharynx opens anteriorly into the introitus of the larynx (Fig.
14-4). The epiglottis is attached to the base of the tongue by two lateral and
one midline frenulum. These produce two valleculae on either side. Below
the valleculae is the laryngeal surface of the epiglottis. Below this is the
opening of the glottis medially, and laterally there is a space called the
piriform sinus between the aryepiglottic folds and the thyroid cartilage. More
inferiorly are the muscles of the cricoid lamina, and below this the opening
of the esophagus.
The cervical esophagus runs more or less in the midline of the neck behind
the trachea and anterior to the vertebral bodies. The recurrent laryngeal
nerves lie in the groove between the esophagus and trachea. The common
carotid artery and the contents of the carotid sheath lie lateral to the
esophagus. There is a triangular weakness in the muscular coat of the A Zenker's diverticulum devel¬
pharynx above the cricopharyngeus muscle which arises from the cricoid and ops through the posterior pha¬
ryngeal wall below the inferior
encircles the upper esophagus. A diverticulum, called Zenker’s diverticulum, constrictor and above the crico¬
can project through this weak area and interfere with swallowing. pharyngeus.
The pharynx is an area in which the air passages from the nose to the
larynx cross the food passages from the mouth to the esophagus. Hence,
any dysfunction of the pharyngeal musculature, mainly composed of the
three pharyngeal constrictors, will cause difficulty in swallowing and usually
also aspiration of saliva or food into the tracheobronchial tree.
The Neck
In the early embryo there is no well-defined neck separating the thorax
from the head. The neck is formed as the heart, which is originally below
the foregut, migrates into the thorax and the branchial apparatus develops
its final form. The migration of the heart is the reason why many of the
structures of the neck migrate caudally. In the early embryo there are ridges
along the side of the foregut which are also visible externally. These ridges
are the branchial apparatus.
Although there are phylogenetically six branchial arches, the fifth arch
never develops in man, and its only derivative is the ligamentum arteriosum.
Each of the four branchial Only four arches are ever visible externally. Each branchial arch has a
arches contains a cartilaginous
bar, an artery, a nerve, and
cartilaginous bar; associated with this bar is an arterial arch, a nerve, and
some mesenchyma that will some mesenchyma that will form muscle. Behind each arc is an external
form muscle. groove consisting of ectoderm and an internal pouch consisting of endoderm.
The area between the ectoderm and endoderm is known as the closing plate.
Parts of these structures named above develop into definitive adult
structures. Other parts that normally disappear may persist and form
abnormal structures in the adult. The normal derivatives of the branchial
apparatus are listed in Table 14—1. It should be noted that the ectodermal
cleft and endodermal pouch are located posterior to the cartilaginous arch,
artery, and nerve.
Abnormal persistence of parts of the branchial apparatus can lead to a
variety of cysts, sinuses, and fistulas. Persistence of the ectoderm of the first
branchial arch may result in a cyst or sinus lying parallel to and even
Excision of a first branchial cleft reduplicating the external ear canal. A different type of persistence may
cyst requires identification and lead to cysts, sinuses, or fistulas running in a line from deep in the external
dissection of the facial nerve. ear canal through the parotid gland to the angle of the mandible anterior to
laryngeal nerve. The pharyngeal lymphatic drainage may involve the retro¬
pharyngeal and lateral pharyngeal chains with subsequent passage into the
deep cervical nodes. Nasopharyngeal malignancies often metastasize into the
posterior cervical chain.
Deglutition
Disorders of swallowing are best Deglutition may be divided into three stages. The first is the voluntary
demonstrated on a modified movement of food from the mouth into the pharynx. The second stage, the
video esophagram.
transport of the food through the pharynx, and the third stage, the passage
of the bolus through the esophagus, are both involuntary. The actual steps
of deglutition are as follows: Following mastication food is positioned on the
middle third of the tongue. Elevation of both the tongue and soft palate
forces the bolus into the oropharynx. The suprahyoid muscles contract,
elevating the hyoid bone and larynx and thus opening the hypopharynx and
the piriform sinuses. Simultaneously the intrinsic laryngeal muscles contract
in a sphincter-like fashion to prevent aspiration. A strong motion of the
tongue posteriorly plunges the food interiorly through the oropharynx, a
movement aided by the contraction of the superior and middle pharyngeal
constrictors. The bolus is guided through the esophageal introitus when the
inferior pharyngeal constrictor contracts and the cricopharyngeus muscle
relaxes. Peristalsis, assisted by gravity, moves the food down the esophagus
and into the stomach.
Initially, abscesses are confined The fascial spaces of the head and neck are areas of loose connective
to potential spaces formed by
tissue that may be the sites of abscess formation as well as pathways by
cervical fascia.
which infection may spread. These spaces are surrounded by fascial sheaths,
which are layers of thickened connective tissue enclosing the muscles and
organs. The function of these sheaths is to offer some protection as well as
to allow the movement of the structures against one another.
The superficial cervical fascia encircles the scalp, face, and neck subcuta¬
neously to enclose the muscles of facial expression and the platysma. The
deep cervical fascia has been described as having two or three components,
and the nomenclature is often confusing. For practical purposes, there is a
superficial, a middle, and a deep component to the deep cervical fascia (Fig.
14-5). The superficial component is also called the investing layer; the
middle component is termed the pretracheal (or visceral) layer; and the deep
component is referred to as the vertebral (or prevertebral) layer. The
Fascial spaces are not com¬ superficial (investing) component of the deep fascia encircles the neck,
pletely closed spaces, and ab¬
scess can extend from one
attaching only to the nuchal ligament of the vertebrae posteriorly. It splits
space to the other and even to to enclose the trapezius and sternomastoid muscles but lies anterior to the
the opposite side of the neck. strap muscles. The pretracheal layer is limited to the anterior neck below
14—EMBRYOLOGY, ANATOMY, AND PHYSIOLOGY 281
FIGURE 14-5. Chief layers of the cervical fascia below the hyoid bone. Note the relations
of the various nerves. The fascias and fascial spaces are, of course, schematically shown
and exaggerated. (From Hollinshead WH: Anatomy for Surgeons. Vol. 1: The Head and
Neck. New York, Hoeber Medical Division, Harper 6. Row, 1982, p 271.)
the hyoid bone. It attaches to the superficial layer at the lateral border of
the strap muscles on each side, extends posterior to these muscles in front
of the larynx and trachea, and encircles the thyroid gland. From it arises a
thin fascial tissue that encircles the hypopharynx and esophagus and is
sometimes considered part of the pretracheal layer. Below, this layer is
continuous with the pericardium. The vertebral layer of the deep cervical
fascia, like the superficial layer, also attaches to the nuchal ligament and
encircles the neck, but at a deeper level. It covers the vertebral bodies and
the scalene muscles anteriorly and the paraspinous and deep neck muscles
laterally. Over the front of the vertebral bodies it splits to form two layers,
an alar part anteriorly and a true prevertebral part posteriorly. The space
between these two parts is considered a “danger space,” through which an
infection may spread downward to the chest. Between the prevertebral layer
and the pretracheal layer on each side is a tube of fascia encircling the
carotid artery, vagus nerve, and jugular vein called the carotid sheth. Above
the hyoid bone, the superficial and pretracheal layers change. The superficial
layer of the deep cervical fascia becomes external to the suprahyoid muscu¬
lature but then splits to enclose the mandible and muscles of mastication
and also forms the capsules of the submandibular and parotid glands. The
pretracheal layer extends above the hyoid bone posteriorly only as the layer
encircling the pharyngeal muscles. The vertebral layer is unchanged above
the level of the hyoid, but the carotid sheath at this level is less easily
identified.
Infections that can involve these potential spaces are discussed in Chap¬
ter 17.
References
Davies J: Embryology and anatomy of the head, neck, face, palate, nose, and paranasal sinuses.
In Paparella MM, Shumrick DA (eds): Otolaryngology, Ed 2, Vol 1. Philadelphia, WB
Saunders Co, 1980, pp 63-123.
Hollinshead JW: Anatomy for Surgeons, Vol I: The Head and Neck. New York, Harper &
Row, 1968.
15
DISEASES OF THE ORAL CAVITY
by Robert J. Gorlin, DDS, MS, DSc
Diseases of the oral cavity are of interest to both physicians and dentists.
These diseases may represent a localized disease entity or a manifestation
of a systemic illness. Diagnosis and treatment of oral lesions can be puzzling
to the medical student and primary care physician, who may have had
limited experience in this area. While it is not the intention of the authors
to catalogue the many and varied conditions that may present in the oral
cavity, it is believed that an overview of these conditions, including some
common dental disorders, will provide a framework for differential diagnosis
and management.
Oral Tori
Torus palatinus (Fig. 15-1) is characterized by a nodular or lobular bony
growth in the midline of the hard palate. Like its mandibular counterpart,
it is rare in infants and is usually not manifest until puberty. In the adult
population, it is noted in 25 per cent of females and 15 per cent of males.
Surgical removal may be indicated for maxillary denture construction.
Micrognathia
Micrognathia may be congenital or acquired (e.g., as a sequel to trauma,
infection, or juvenile rheumatoid arthritis). Although the term is rather
nonspecific in that it may refer to diminution in size of either jaw. common
usage has essentially limited it to the mandible.
Whatever the association, the ultimate diminution in size of the mandible
is due to a failure at the growth center in the condyle. Trauma or infection
of the area of the condyle, almost always unilateral, will produce unilateral
reduction of the mandible.
Mandibular micrognathia is usually an isolated polygenic trait but has
been noted in association with a plethora of syndromes. Maxillary micro¬
gnathia is seen in craniofacial dysostosis, in acrocephalosyndactyly, and in
trisomy 21. Mild occlusal deformities may be corrected by the orthodontist.
Surgical correction of severe maxillary or mandibular hypoplasia is usually
carried out by the maxillofacial or oral surgeon after growth of the jaws is
complete.
Robin Anomaly
The combination of cleft palate, micrognathia, and glossoptosis is nonspe- Pierre Robin: (1) micrognathia
cific, being seen as an isolated finding or in association with several syn- (mandibblar hypoplasia), (2)
dromes glossoptosis, (3) posterior cleft
T, . ' , , . palate.
ihis anomaly appears to represent arrested intrauterine development.
284 PART FOUR—THE ORAL CAVITY AND PHARYNX
During the tenth to twelfth week in utero, the maxilla grows rapidly, and
by the fourth to fifth month the disparity between the upper and lower jaws
is quite apparent.
The “Andy Gump” facies is quite distinctive. Dyspnea and periodic
cyanotic attacks associated with recession of the sternum and ribs are in
evidence during the inspiratory phase of respiration, especially when the
infant is in the supine position. The difficulty is usually noted at birth. If the
infant survives the initial period, mandibular growth subsequently catches
up so that a normal profile is achieved by four to six years of age.
The exact physiologic mechanism by which the syndrome is produced is
Airway is maintained by forward not known, but most investigators have suggested that the symmetric lack
traction on the tongue. of mandibular growth (micrognathia) prevents adequate support of lingual
musculature, allowing the tongue to fall downward and backward (glossop-
tosis). This obstructs the epiglottis, permitting egress of air but preventing
Patient is kept in prone position inhalation, much like a ball valve.
to keep tongue from falling back Treatment, in the mild case, consists of keeping the infant in a prone
and causing airway obstruction.
Tracheostomy is required in the position, at times suspending the head by means of a stocking cap. In the
more severe cases. severe case, the tongue tip is sutured to the anterior mandible or lower lip.
Prognathism
Enlargement or anterior placement of the lower jaw may be absolute or
relative and is a multifactorial hereditary trait. After the jaws have ceased
to grow (usually by 16 to 17 years), the patient is referred to an orthodontist
and oral or maxillofacial surgeon for correction. Many successful surgical
techniques are available.
Malocclusion
Various types of disturbed development of the face and jaws may result
in malocclusion. Underdevelopment of the maxilla or mandible or overde¬
velopment of the mandible may require special surgical procedures after
puberty. Incompatibility of tooth size and jaw size may result in spacing,
crowding, or irregularity of teeth. Prolonged retention of primary teeth may
result in delayed eruption of permanent teeth. Neglected primary or per¬
manent teeth may be lost prematurely. Early consultation with an orthodon¬
tist is indicated to resolve problems associated with malocclusion.
Macroglossia
An enlarged tongue may be relative or absolute and may result in abnormal
C02 and Yas laser surgery can speech. Most congenital cases are due to lymphangioma or hemangiolym-
be effective in removal of phangioma. Cystic hygroma may also be present. The tongue surface is most
limited lesions. often irregular or papillary, with 1- to 3-mm blister-type nodules. The most
successful treatment is a combination of sclerosing agents and corrective
surgery.
The tongue may also be enlarged in the macroglossia-omphalocele syn¬
drome. In the adult, macroglossia may be seen with primary amyloidosis.
15—DISEASES OF THE ORAL CAVITY 285
Clefts of the primary and secondary palates are among the more common
congenital anomalies. A vast amount of data has been gathered about facial
clefts, only a small portion of which can be presented here.
Clinically, there is great variability in the degree of cleft formation (Fig.
15-6). The minimal degrees of involvement include such anomalies as bifid
uvula, linear lip indentations, so-called intrauterine healed clefts, and sub¬
mucous cleft of the soft palate. A cleft may involve only the vermilion border
of the upper lip or may extend to involve the nostril and the hard and soft
palates. Isolated palatal clefts may be limited to the uvula (bifid uvula), or
they may be more extensive, cleaving the soft palate or both the soft and
hard palates.
287
Of all maxillofacial clefts, the combination of cleft lip and cleft palate
comprises about 50 per cent of the cases, with isolated cleft lip and isolated
cleft palate each accounting for about 25 per cent, irrespective of race.
Cleft lip, with or without cleft palate, occurs in about 1 (range, 0.6 to 1.3)
per 1000 white births. The incidence appears to be increasing, probably as
a result of declining postnatal mortality, decreasing operative mortality,
steadily improving operative results, and attendant increases in marriage and
childbearing. The prevalence is higher in Orientals (about 1.7 per 1000
births) and lower among blacks (approximately 1 per 2500 births).
Isolated cleft lip may be unilateral or bilateral (approximately 20 per cent).
When unilateral, the cleft is more common on the left side (about 70 per
cent of cases), although no more extensive. Lips are somewhat more
frequently cleft bilaterally (approximately 25 per cent) when combined with
cleft palate. Cleft lip-cleft palate is more common in males. About 85 per
cent of bilateral cleft lips and 70 per cent of unilateral cleft lips are associated
with cleft palate.
The development of isolated cleft palate appears to De quite separate from
that of cleft lip with or without cleft palate. It has been demonstrated that
siblings of patients with cleft lip, with or without cleft palate, have an
288 PART FOUR—THE ORAL CAVITY AND PHARYNX
increased frequency of the same anomaly but not of isolated cleft palate,
and vice versa. Children with isolated cleft palate not uncommonly (about
30 per cent) have associated congenital anomalies.
The incidence of isolated cleft palate among whites and blacks appears to
be 1 per 2000 and 1 per 2500 births, respectively, and may be somewhat
Complete clefts are more com¬ more frequent among Orientals. It is more common in females. Breakdown
mon in females. of cleft palate according to extent clearly indicates that whereas a 2:1 female
predilection exists for complete clefts of the hard and soft palates, the
male:female ratio approaches 1:1 for clefts of the soft palate or uvula only.
The recurrence risk for cleft lip with or without cleft palate, if both parents
are normal, is 3 to 4 per cent. The corresponding figure for cleft palate is
about 2 per cent. Essentially the same risk data can be applied to the
offspring of an affected person.
A cleft uvula can be a sign of a Cleft uvula appears to be an incomplete form of cleft palate. The incidence
submucosal cleft of the palate.
of cleft uvula is about 1 per 80 whites. The frequency of cleft uvula among
Adenoidectomy is contraindi¬
cated in the presence of a sub¬ various American Indian groups is quite high, ranging from 1 per 9 to 1 per
mucosal cleft. 14 individuals. In blacks it is comparatively rare (1 per 300 births).
Treatment
Treatment of cleft lip-cleft palate is complex and involves several disci¬
plines. The best treatment is provided by a “team approach.” The team
comprises a maxillofacial surgeon, otolaryngologist, pedodontist, orthodon¬
tist, prosthodontist, speech pathologist, human geneticist, psychologist, and
social worker. A considerable overlap of interest and concern for this clinical
problem related to structure, function, and well-being of the patient demands
the diagnostic and treatment skills of all these specialists for an extended
period of time.
The development of adequate speech and language skills is an important
Otitis media is almost universal concern. Speech and language are learned primarily through audition. Since
in infants under age two with
there is a relatively high incidence of ear disorders and consequent hearing
unrepaired clefts.
loss (primarily conductive) in the child with cleft palate, early identification
and treatment are important to ensure optimal hearing function during
speech and language developmental years.
Surgical closure of the lip is usually performed within the first few months
of life, whenever body weight exceeds 10 pqunds. The ideal time for surgical
closure of the palate has been debated, but in the United States at least 80
per cent of the surgeons prefer some time between the first and second years
of life. Various techniques have been used in lip closure, but those employing
angular rather than linear incision lines are preferred because of late
postoperative shortening of the upper lip on the operated side following the
linear techniques. In the case of bilateral clefts, lip closure is much more
difficult owing to anterior displacement of the primary palate and is often
accomplished in two stages.
Early closure of the palatal cleft provides a better mechanism with which
to produce speech. Surgical closure of the secondary palate can be performed
with a variety of techniques, most notably the bridge flap technique of von
Langenbeck and the pedicle flap technique of Veau. The primary goal of
surgery is to achieve complete closure of the hard and soft palates and to
provide a soft palate that has sufficient length and mobility. Lengthening of
the soft palate is ordinarily accomplished by a so-called push-back procedure.
1 5—DISEASES OF THE ORAL CAVITY 289
remains of the nasopalatine duct, which gives rise to the nasopalatine cyst.
Grouped as pseudocysts of the jaws are the aneurysmal bone cyst, static
bone cyst, and solitary bone cyst. None of these is epithelium-lined. The
static bone cyst appears to be a congenital bone defect; trauma has been
suggested as the etiologic agent in both the aneurysmal bone cyst and the
solitary bone cyst. Some of the more common cysts are considered separately.
Odontogenic Cysts
Dentigerous Cyst (Fig. 15-7). The dentigerous cyst surrounds the crown
of an unerupted tooth of either the regular (in approximately 95 per cent of
all cases) or the supernumerary dentition. It probably arises through
alteration of the reduced enamel epithelium after the crown has been
completely formed. Fluid accumulates either between layers of the enamel
epithelium or between the epithelium and the tooth crown. The cyst may
arise, however, from cystic degeneration of remnants of the dental lamina.
The teeth usually involved are the mandibular third molar, maxillary
canine, maxillary third molar, and second mandibular premolar, although
the cyst may occur about any unerupted tooth. The crown of the tooth
projects into the lumen of the cystic cavity. The cyst may be of any size,
ranging from a subtle dilatation of the pericoronal sac to a space occupying
the entire body and ramus of half the jaw. Possibly because of the anatomy
of the upper and lower jaws, the larger cysts involve the mandible. Although
the cyst develops in relationship to a single tooth, it may include the crowns
of several adjacent teeth as it enlarges. Furthermore, it may displace teeth
to positions remote from their normal sites, especially in the maxilla.
Dentigerous cysts are usually solitary. When multiple, however, possible
association with nevoid basal cell carcinoma.syndrome should be ruled out.
Eruption Cyst. The eruption cyst is an uncommon type of dentigerous
cyst associated with erupting deciduous or rarely permanent teeth. It
represents the accumulation of tissue fluid or blood in a dilated follicular
space about the crown of an erupting tooth. It may be unilateral or bilateral,
single or multiple, and may be present at birth.
Gingival and Palatal Cysts of Newborn Infants. Nearly all human fetuses
after their fourth month in utero and at least 80 per cent of newborn infants
have small nodules or cysts (Epstein's pearls, Bohn's nodules) at the junction
of the hard and soft palates near the median raphe. The nodules, usually
several, are white to yellowish white small epithelial inclusion cysts, probably
FIGURE 15-8. Radicular cyst. A, Caries involved the pulp, which caused a periapical abscess
surrounding the root of the maxillary lateral incisor. 6, Clinical appearance. Note swelling
extending to the palate. C, Observe extensive destruction of the crown.
294 PART FOUR—THE ORAL CAVITY AND PHARYNX
Nasoalveolar Cyst. The nasoalveolar (nasolabial) cyst has also been called
Klestadt’s cyst. It probably arises from epithelial rests located at the junction
of the globular, lateral nasal, and maxillary processes.
The cyst is situated at the attachment of the ala of the naris, i.e., near the
base of the nostril. It is not located within bone. The nasoalveolar cyst may
cause enough facial swelling to obliterate the nasolabial fold on the involved
side. Bilateral involvement is noted in about 10 per cent of the patients.
Ordinarily the cyst swells into the floor of the nasal vestibule, projecting
beneath the anterior end of the inferior turbinate. At times, this causes nasal
obstruction. Intermittent pain is experienced by about one third of the
patients. Blunt dissection of the cyst has indicated that it is attached to the
nasal mucosa. It can be clearly demonstrated with the use of a radiopaque
material.
The nasoalveolar cyst occurs predominantly (about 75 per cent of all
cases) in women and appears to occur more often in blacks.
Dermoid and Epidermoid Cysts. The term “dermoid cyst” will be used
here to denote a developmental cyst lined by epidermis and cutaneous
appendages. It probably results from incorporation of ectoderm at the time
of closure of embryonic fissures during the third and fourth weeks in utero.
Oral dermoid cysts most commonly arise in the floor of the mouth and
have been classified into median (midline) and lateral dermoid cysts. They
probably always originate above the mylohyoid muscle, although they may
penetrate through a developmental hiatus. They usually become evident
between 12 and 25 years of age.
The cyst, if located above the geniohyoid muscle (sublingual or
genioglossal dermoid cyst), causes elevation and displacement of the tongue,
producing difficulty in speaking, eating, and even breathing due to pressure
exerted upon the epiglottis. If the cyst is deeper (between the geniohyoid
and mylohyoid muscles), it may bulge into the submental area.
The submental or geniohyoid dermoid cyst is manifested by a slow painless
swelling in the submental region. It extends from the mandible to the hyoid
bone, giving the appearance of a double chin. As it enlarges, it may push
the larynx down and by upward growth causes a bulge in the oral floor. The
296 PART FOUR—THE ORAL CAVITY AND PHARYNX
enamel. It also progresses along dentinal tubules and especially in the young
may rapidly lead to exposure of the underlying pulp tissue.
Inflammatory processes in the tooth pulp may be infected or nonmfected.
Trauma to the tooth from a blow (which may or may not fracture the tooth),
from dental operations, or from excessive thermal changes may induce
inflammation. Since the rigid walls of the tooth do not permit expansion of
the inflamed pulp, the circulation may be cut off and the pulp may become
an infarct that is later replaced by fibrous connective tissue. Bacterial
infection is the common sequel to dental caries or to mechanical exposure
of the tooth pulp.
Pulpitis may be acute or chronic. In acute pulpitis pain is usually severe
and is increased by heat or cold. It is often aggravated by lying down
(increased vascular pressure) and may be accompanied by a mild fever and
leukocytosis. Characteristically, the purulent process spreads to involve the
entire pulp and, unless the tooth is opened to establish drainage, the
periapical tissues become involved in an acute alveolar abscess. Once the
tissues about the root apex become involved, the tooth becomes sensitive to
percussion.
Acute alveolar abscess is usually the result of suppurative infection
spreading from the tooth pulp through the root canals to the periodontal
ligament about the tooth root ends. The inflammation characteristically
follows the blood vessels into the bone marrow spaces. Suppuration follows
pathways determined by the location of the tooth roots and the characteristics
of adjacent structures. Usually the periosteum overlying the tooth root end
is destroyed, and eventually pus is drained through a fistula (gum boil). In
maxillary teeth, drainage may occur into the antrum or into the palate.
Occasionally the soft tissues are extensively involved, and, if they are not
treated, drainage to the surface of the skin of the face or neck may occur.
Osteomyelitis, cavernous sinus thrombosis, and Ludwig’s angina are serious
complications.
A much more common sequel to dental pulp infection is the dental
granuloma. Clinically this may be completely symptomless. Radiographic
examination frequently discloses an area of bone rarefaction about a tooth
root apex, with a chronically infected or partially obliterated root canal.
This area is usually spherical and well demarcated.
A granuloma represents a balance between the defense forces of the body
and a chronic area of necrotic tissue in the tooth root that is acting as an
infected sequestrum. If the tooth is extracted, the granulation tissue usually
disappears during the healing process. Occasionally a granuloma may persist
as an area of “residual infection” after the tooth is extracted. Common oral
organisms, chiefly Streptococcus and Staphylococcus, have been demon¬
strated in many dental granulomas, although some lesions appear to be
sterile.
episodes of acute suppuration may occur. The reactions in both cases consist
of a walling-off process with a marked chronic inflammatory cell infiltration.
In periodontal disease this represents an attempt to cover the surface of the
chronic ulcer that develops about the involved tooth root area.
The disease commonly begins as gingivitis. Plaque and calculus deposited
upon the tooth surfaces, impaction of food, decayed teeth, overhanging
margins of dental restorations, and ill-fitting dental appliances are among
the local causes. Once a “pocket” has been established below the gingival
margin, calcified deposits form on the tooth root surfaces and act as infected
foreign bodies, thus prolonging and promoting the inflammatory process
with progressive resorption of the fibrous and bony tooth-supporting struc¬
tures. Proliferation of epithelium that lines the pocket occurs concomitantly
with the loss of tissue. Periodontal disease is more common in older
individuals, and after middle age, it becomes the chief cause of tooth loss.
Patients with diabetes mellitus are especially susceptible to periodontal
disease, and an alert clinician should suspect this condition if there are oral
signs and symptoms.
Pregnancy, with its change in endocrine balance, frequently is accompanied
by gingivitis and hyperplastic inflammatory responses. Gingivitis may be
somewhat more frequent during puberty.
Necrotizing Ulcerative Gingivitis (Vincent’s Infection) (Fig. 15-11). This
condition is extremely rare in children, occurring far more commonly in
The oral mucous membranes, especially those of the gingiva and tongue,
are sites of round to oval, sharply demarcated, disseminated vesicles or
erosions. The individual lesions are 2 to 4 mm in diameter, painful, covered
by a yellowish pseudomembrane, and surrounded by a red margin. The
intact vesicle rarely lasts for more than 24 hours.
After about 10 to 14 days, the primary infection subsides without scar
formation. Following a latent period of varying length, often not until after
puberty, secondary or recurrent herpes simplex may develop. Immuno¬
compromised patients may suffer a severe primary infection.
Treatment consists largely of supportive therapy, topical anesthetics such
as 5 per cent Xylocaine (lidocaine) ointment, and enriched liquid diet.
Topical acyclovir (Zovirax) is of limited efficacy.
Inoculation herpes simplex is not uncommon among physicians, dentists,
and dental hygienists, the virus in the saliva of a patient penetrating through
an abrasion of the skin.
Regardless of whether the primary infection is clinical or subclinical,
recurrent herpetic lesions develop later in many persons, being precipitated
by many different factors. Not all individuals suffer from recurrent herpes
simplex. It has been estimated that from 70 to 90 per cent of the population
are carriers of the virus after 14 years of age.
Secondary (Recurrent) Herpes Simplex. The most common form of
herpetic infection, secondary herpes simplex, possibly affects 25 to 50 per
cent of the adult population. After a prodromal period of 24 to 48 hours,
marked by a burning, itching, or tingling sensation in the region of the
forming lesions, the eruption appears. This consists of groups of small clear
vesicles that soon become transformed into pustules or crusted confluent
erosions located most often on the vermilion or mucocutaneous junction of
the upper or lower lip. The infection generally recurs at the same sites.
Secondary herpes simplex may very rarely involve the oral cavity proper
where, in contrast to primary gingivostomatitis, it affects only circumscribed
areas such as the hard palate and fixed gingiva. They appear as grouped
small (1 to 2 mm) ulcers.
A variety of stimuli may precipitate recurrent herpes simplex. These
include fever, sunlight, food allergy, colds, menstruation, mechanical trauma,
and possibly even psychosomatic factors.
Subjective complaints extend from mild itching or burning to severe pain
in addition to the cosmetic inconveniences involved. After four to ten days,
the crusted lesions heal without scarring.
Identification of the herpes simplex virus in either the primary or recurrent
form can be done by viral isolation, fluorescent antibody examination, or
cytologic study (Giemsa smears).
Treatment is largely ineffective. The immunosuppressed patient should be
treated with oral or intravenous acyclovir.
Trauma may play some role, since typical aphthae may arise at the site of
injury (needle puncture, “cotton roll” stomatitis). It has been recently
suggested that recurrent aphthous stomatitis represents a form of autoim¬
munity, since autoantibodies to oral mucosal homogenates are found in 70
to 80 per cent of those with recurrent aphthous stomatitis as opposed to 10
per cent of controls. After a burning sensation in the affected mucosa during
the prodromal stage, the mucosa becomes focally erythematous and necrotic,
with formation of single or multiple, round to oval ulcerations usually 2 to
10 mm in diameter, with about 10 per cent being larger than 1 cm. The
ulcer is covered by a grayish white fibrinous exudate and surrounded by a
bright red halo. It usually persists for one or two weeks and heals without
scarring. Xylocaine ointment (5 per cent) is effective in reducing discomfort.
Tetracycline swish and swallow suspensions (250 mg/5 ml q.i.d) also offer
some relief.
Major Aphthae
Major aphthae (periadenitis mucosa necrotica recurrens, Sutton’s disease)
is a disease of unknown cause affecting the oral mucosa; it is characterized
by large (1 to 2 cm) single or multiple necrotic ulcerations of the lips, cheeks,
tongue, soft and hard palates, and anterior tonsillar pillars. Apparently, the
gingiva is rarely, if ever, involved. Ulceration also may occur on the
pharyngeal and laryngeal walls. The condition is recurrent, with multiple
episodes spaced over several years—in some cases, up to 15. After healing,
the ulcer leaves a fibrous retractile scar. Pain and systemic manifestations
are present during the acute state of the disease.
Females are slightly more frequently affected than males. The onset can
take place at any age but is more common around puberty.
Treatment is generally ineffective, but some relief is provided by the use
of 5 per cent Xylocaine ointment. Topically applied 0.05 per cent triamcin¬
olone acetonide or fluocinonide ointment, four to five times per day, is also
helpful.
Herpes Zoster
Herpes zoster is a recurrent neurotrophic manifestation of reactivated
chickenpox virus. Presumably, the virus persists in ganglion cells, becoming
reactivated when immunity has decreased through injuries such as local
trauma, stress, neoplasia, or massive new infection with chickenpox-zoster
virus.
After an incubation period of 4 to 20 days, the disorder appears with a
neuralgic prodromal phase. Within two to three days, grouped vesicles form
in the area innervated by the involved nerve. When the face is affected, as
in zoster ophthalmicus or zoster oticus (Ramsay Hunt syndrome), the pain
is especially severe, and general prodromal symptoms such as fever and
nausea are marked. With the appearance of the vesicles, rarely before, a
painful regional lymphadenitis develops. Herpes zoster occurs more com¬
monly in males than in females and principally affects individuals over 45
years of age.
In herpes zoster of the cranial nerves, several types can be distinguished:
(1) trigeminal type (attack of the gasserian ganglion with involvement of one
306 PART FOUR—THE ORAL CAVITY AND PHARYNX
or more branches), (2) zoster oticus (attack on the geniculate ganglion), (3)
zoster of the glossopharyngeal nerve, (4) zoster of the vagus nerve, and
other segmental types. Ophthalmic zoster is especially dangerous, since the
conjunctiva and cornea are often involved, and iritis, glaucoma, and even
panophthalmitis may occur.
On the oral mucosa, the lesions are more diffuse. The unilocular zoster
vesicle is especially short-lived. It rapidly changes into a painful aphtha
surrounded by a red halo. When the second trigeminal division is involved,
unilateral vesicles appear on the palate, uvula, maxillary gingiva, and upper
buccal and labial mucosa. Involvement of the lower lip, mandibular gingiva,
and oral floor is seen in third division zoster.
Postzoster neuralgias are extremely painful for months or even years,
especially in elderly persons. A combination of anesthesia or hypesthesia of
the affected segment, often with very severe neuralgia, is especially distress¬
ing. In addition, herpes zoster may simulate lancinating trigeminal neuralgia.
In the immunocompromised patient, intravenous acyclovir or vidarabine
affords help. However, in the immunocompetent patient, the disorder will
run its course and help is largely supportive.
Pemphigus
A bullous disease of autoimmune etiology, pemphigus can be subdivided
into many clinical types, all of which are histologically characterized by
intraepithelial vesicles or bullae. Immunofluorescent studies have demon¬
strated autoantibodies to the intercellular cement substance of the stratified
squamous epithelium of the oral mucosa and skin of patients with pemphigus.
Areas involved by pemphigus, The most severe type, pemphigus vulgaris, often resulted in rapid death
especially the larynx, can heal prior to the use of corticosteroids. It occurs almost exclusively in middle-
with cicatricial formation.
aged and elderly persons and has no sex predilection. Lesions start in the
mouth in 50 per cent of the patients, and there is oral involvement at some
stage in the disease in all patients. The pharynx, larynx, and nasal, anal,
and vaginal mucosae are also involved. Vesicles and bullae tend to arise on
relatively normal-appearing skin and may be precipitated by pressure or
friction (Nikolsky’s sign). They are ordinarily tense and round but do not
last long on a mucosal surface. They rupture, leaving peripheral epithelial
tags.
Microscopically, the vesicle is usually suprabasilar and contains acantho-
lytic cells as well as variable numbers of nonspecific inflammatory cells,
among which there is a moderate number of eosinophils.
Various immunosuppressive agents, alone or in combination, are successful
(prednisone, methotrexate, cyclophosphamide, azathioprine). A soft diet
and topical Xylocaine can be used until control is achieved.
occur most commonly during the seventh decade. There may be some female
predilection. The oral lesions frequently present as a desquamative gingivitis.
Minor trauma wipes away the epithelium, leaving a raw hemorrhagic surface.
The vesicles that occur on the buccal mucosa, tongue, or soft palate are
more stable than those of pemphigus, the split taking place at the basal
lamina. In contrast to pemphigus, there is no acantholysis and frequently
there is a moderate, chronic, inflammatory infiltrate in the subepithelial
connective tissue. Immunofluorescent studies show linear deposition of
complement and immunoglobulins in the basement membrane zone.
Ocular lesions appear late in the disease process. There is redness,
swelling, burning, tearing, and photophobia. The patient often complains of
a foreign body sensation. Fibrous adhesions develop between the palpebral
and bulbar conjunctivae. Scarring produces trichiasis, entropion, and corneal
damage with resultant blindness.
As in the case of pemphigus, various immunosuppressive agents such as
prednisone or azathioprine may be employed.
dorsum of £|a"USVA Note ^ lace"like striae on the buccal mucosa. B, Whitish plaques on th
dorsum of the tongue. Note striae on the lateral borders.
15—DISEASES OF THE ORAL CAVITY 309
the lesions originate in the posterior area and spread anteriorly. Generally,
they are asymptomatic, although a metallic taste or mild discomfort is
common. Superficial erosions, bullous lesions, and deep, chronic, painful
ulcerations occasionally occur.
Halitosis
Halitosis (fetor oris), or bad breath, is a common complaint. Offensive
mouth odor depends upon many factors such as decreased salivary flow rate
resulting in mucosal dryness (due to antihistamines, Sjogren’s syndrome,
astringent mouthwashes, radiation sialoadenitis); poor oral hygiene (food
remnants, unclean dentures); odoriferous foods (garlic, onion, fatty diet);
periodontal disorders, especially if there is marked tissue destruction (per¬
iodontitis, necrotizing ulcerative gingivitis); necrotic soft tissue lesions; and
heavy smoking.
Rarely a systemic cause can be implicated, such as the fetid odor of a
disorder of the respiratory system, the acetone breath of uncontrolled
diabetes mellitus, or the ammoniacal odor of uremia.
The efficacy of a mouthwash is only transient. The cause of the halitosis
must be eliminated.
ORAL TUMORS
Odontogenic Tumors
The more common odontogenic tumors will be discussed in this section
(Table 15-2).
From Gorlin RJ: In Anderson’s Pathology (JM Kissane, ed): Vol 2. 8th ed. St Louis, The CV Mosbv Co
1 5—DISEASES OF THE ORAL CAVITY 311
Ameloblastic Fibroma
The vast majority of patients with this tumor nave been between ages 5
and 20 years.
This tumor usually produces painless, asymptomatic, slow expansion of
the cortical plates of the premolar-molar area of the maxilla or, far more
frequently, the mandible. Radiographically, it is a smooth, outlined, cystlike
lesion that cannot be differentiated from the unilocular ameloblastoma.
Ameloblastic Odontoma
Ameloblastic odontoma is characterized by the simultaneous occurrence
of ameloblastoma and a complex or compound odontoma within the same
tumor.
With few exceptions, the tumor is found in children, over 90 per cent of
the patients being under age 15. It is more common in males and is found
somewhat more frequently in the maxilla.
Growth is slow and often is associated with swelling of the alveolar
process. Radiographs reveal areas of cystlike destruction.
Complex Odontoma
Complex odontoma differs from ameloblastic odontoma by the virtual
absence of ameloblastic tissue. In normal tooth development, degeneration
of the dental lamina occurs soon after hard tissue formation, and the complex
odontoma corresponds to this more complete stage of induction. At least 70
per cent occur in the second and third molar area and are somewhat more
common in the mandible. Usually they are asymptomatic and are found on
routine dental radiographic examination. They appear as irregular radiopac-
ities surrounded by a narrow radiolucent band.
Myxoma
The myxoma (myxofibroma) of the jaw is a locally aggressive, nonmetas¬
tasizing tumor of odontogenic origin, probably arising from the connective
tissue of the dental papilla.
Only rarely does the myxoma occur before the age of 10 years or after
age 50. Approximately 60 per cent arise within the second and third decades.
The tumor is slow-growing, and, on the average, it has been present for
about five years prior to therapy.
Radiographically, differentiation from other jaw radiolucencies is difficult,
if not impossible, and this lesion cannot easily be distinguished from fibrous
dysplasia, central giant cell granuloma, or ameloblastoma. The tumor is not
well defined but tends to be honeycombed, perforating the cortex of the jaw
only if it reaches great size. In the mandible, it involves the ramus and body
with equal frequency. Those tumors that arise in the maxilla may perforate
and invade the antrum, filling it completely and producing exophthalmos.
The antral walls are expanded but seldom are destroyed. The teeth are often
displaced.
Cementoma
Cementoma most commonly involves the periapical regions of the man¬
dibular anterior teeth. The frequency is roughly 2 to 3 per 1000 patients,
with 70 to 90 per cent occurring in females.
The average age at which the lesion is discovered is about 40 years. Only
rarely is it seen in persons under 25 years of age and almost never below
the age of 20 years. It is more common in blacks than in whites.
The teeth involved are nearly always mandibular. The lesions are often
multiple, and some individuals have as many as eight mandibular teeth
involved. Because of a lack of symptoms, diagnosis is usually made during
routine dental radiographic examination.
314 PART FOUR—THE ORAL CAVITY AND PHARYNX
Nonodontogenic Tumors
Numerous types of benign and malignant neoplasms may occur in the oral
regions. Two of the more fascinating benign tumors seen in infancy are the
melanotic neuroectodermal tumor of neural crest origin and the congenital
epulis, which is a granular cell myoblastoma.
Congenital Epulis
This benign tumor is present at birth; it is usually pedunculated and
located on the maxillary or mandibular gingiva, generally in the anterior
region. It is limited almost exclusively to females. Histologically, it is similar
to a granular cell myoblastoma (schwannoma) but without associated pseu-
doepitheliomatous hyperplasia. Treatment consists of simple surgical exci¬
sion.
FIGURE 15-23. Fibrous dysplasia. A, Asymmetry of the face with swelling beneath the left eye. B, Ground
glass appearance of the lesion in the patient shown in A.
Hemorrhage
Oral hemorrhage usually results from acute trauma. Rarely, unusual
bleeding may follow minor oral surgical procedures, such as tooth extraction.
All wounds are managed by examination and debridement of necrotic tissue
and foreign material. Primary closure or application of folded sterile gauze
pressure dressings for 15 to 45 minutes is usually sufficient. The mouth
should not be rinsed, since clots are easily dislodged from their moist
environment. The application of warm, moistened tea bags or absorbable
gelatin sponge cut to size and saturated with thrombin has also been used
for persistent bleeding.
316 PART FOUR—THE ORAL CAVITY AND PHARYNX
Tooth Fracture
If a tooth receives a severe, sharp blow, fracture often occurs. This fracture
may be visible and involve the clinical crown of the tooth, or it may not be
clinically demonstrable if it involves the invested or root portion. In either
instance, dental consultation should be immediate. It should be emphasized
that the physician should recommend that the child see the family dentist or
pedodontist within the shortest time possible.
Fractures of the crowns of teeth are treated by covering surfaces with a
protective, crown-shaped plastic or metallic cap. The cap is secured in
position by a mixture, such as zinc oxide and eugenol, which minimizes pulp
hyperemia and protects against irritation by thermal and chemical factors. If
fracture of the tooth crown involves the pulp portion, treatment consists of
pulp removal with sealing (ideally), pulpotomy (slightly less successful), or
extraction.
Root fractures, although rare in primary teeth, are immobilized in situ by
supportive wire ligation of affected and neighboring teeth.
It is worth emphasizing that early dentition performs a valuable space-
maintaining function for the subsequent permanent dentition. Early loss of
primary teeth adversely affects the development of a properly aligned
permanent dentition.
References
Gorlin RJ, Goldman HM: Thoma’s Oral Pathology. 6th ed. St Louis, The CV Mosby Co, 1970.
Gorlin RJ, Cohen MM Jr, Levin S: Syndromes of the Head and Neck. 3rd ed. New York,
Oxford University Press, 1989.
Shafer W, Hine M, Levy BM: Textbook of Oral Pathology. 4th ed. Philadelphia, WB Saunders
Co, 1983.
16
DISORDERS OF
THE SALIVARY GLANDS
by George L. Adams, M.D.
ANATOMY
The parotid gland is the largest of the major salivary glands and occupies
the space just anterior to the mastoid process and external auditory meatus.
Anteriorly, it lies lateral to the ascending ramus of the mandible and masseter
muscle. Inferiorly, it abuts on the sternocleidomastoid muscle and covers The facial nerve artificially di¬
the posterior belly of the digastric muscle. It is separated from the subman¬ vides the parotid gland into su¬
perficial and deep portions.
dibular gland by the stylomandibular ligament. The deep portion of the
parotid gland extends posteriorly and medial to the ascending ramus of the
mandible and is known as the retromandibular extension. It is this portion
of the gland which is in close contact with the parapharyngeal space.
The facial nerve leaves the skull through the stylomastoid foramen and
passes anteriorly just lateral to the styloid process. The nerve then enters
the substance of the parotid gland and divides into two major trunks, the
cervicofacial and the temporofacial. The temporofacial division then sepa¬
rates into the temporal and zygomatic branches, while the cervicofacial gives
off the cervical branches, marginal mandibular division, and buccal division,
which passes anteriorly just below the parotid duct. Passage of the facial
nerve through the substance of the parotid gland divides the gland, for
clinical purposes, into a superficial lobe and that portion medial to the facial The deep lobe of the parotid is
nerve known as the deep lobe. It is the deep lobe that lies in close contact in close proximity to both the
internal and external carotid
with the ninth, tenth, eleventh, and twelfth cranial nerves and the division
arteries.
of the external carotid artery into the superficial temporal and internal
maxillary arteries.
The parotid duct is approximately 6 cm long and arises from the anterior
portion of the gland. It crosses the masseter muscle and turns sharply over
the anterior border of the muscle to pierce the buccinator muscle. It then
continues for a short distance in the submucosal tissues of the mouth and
enters the oral cavity through a small papilla just opposite the crown of the
second upper molar tooth.
The submandibular (submaxillary) gland lies beneath the horizontal ramus
of the mandible and is enclosed by a thin layer of connective tissue. It lies
entirely within the digastric triangle formed by the anterior and posterior
bellies of the digastric muscle. Medially it is bordered by the styloglossus
and hyoglossus muscles, and anteriorly it is limited by the mylohyoid muscle.
317
318 PART FOUR—THE ORAL CAVITY AND PHARYNX
The more medial portion of the gland is closely associated with the floor of
the mouth. The submandibular duct (Wharton’s duct) is also 6 cm in length.
It passes between the mylohyoid and hyoglossus muscles just medial to the
sublingual gland and enters the mouth just lateral to the lingular frenulum.
The paired sublingual glands lie just beneath the anterior floor of the
mouth and are actually large collections of minor salivary glands. Secreted
saliva enters the floor of the mouth through multiple short ducts.
The sublingual and submandibular glands are mixed glands in that they
contain both serous and mucous glandular elements. The parotid gland
contains almost entirely serous elements. In the resting state the submandib¬
ular gland produces approximately two thirds of the saliva, and the parotid
glands supply approximately one third of the saliva.
Salivary response to stimulation is dependent upon neural reflexes carried
along the parasympathetic nervous system. The parasympathetic supply of
Jacobson’s nerve, a division of the parotid gland begins in the inferior salivatory nucleus. The fibers leave
the ninth cranial nerve, passes
across the promontory of the
the brain through the glossopharyngeal nerve and pass through the middle
middle ear. ear, crossing the promontory in Jacobson’s nerve. In the tympanic plexus,
they enter the lesser petrosal nerve and thereby reach the otic ganglion.
Postganglionic fibers from the otic ganglion reach the parotid gland through
the auricular temporal division of the fifth nerve. The parasympathetic
supply of the submandibular gland arises in the superior salivatory nucleus.
The fibers enter the nervus intermedius (nerve of Wrisberg) and follow the
facial nerve into its vertical portion in the mastoid. The fibers then leave the
seventh nerve in the chorda tympani, pass through the middle ear, and join
the lingual nerve. The fibers follow the lingual nerve to a small ganglion
closely associated with the submandibular gland. Postganglionic fibers leave
the submandibular ganglion to pass to the substance of the gland. Because
sectioning of the chorda tympani nerve and Jacobson’s nerve does not always
reduce salivary secretion, other pathways of parasympathetic nerve supply
to the glands must exist. It is suggested that these pathways involve the
hypoglossal and glossopharyngeal nerves. The sympathetic nerve supply to
the major salivary glands is from the superior cervical ganglion by way of
the arterial plexus. Sympathetic stimulation of the major salivary glands is
reported to cause an increased flow followed by a compensatory decrease in
flow. Since there are no muscle elements within the glands themselves, it is
believed that this increase in flow may be due to contraction of the
myoepithelial, or basket, cells associated with the striated ducts.
INFLAMMATORY DISORDERS
Acute Parotitis
The most common form of acute parotid swelling is mumps. Without a
history of exposure, the diagnosis may not be easy. The white blood cell
Mumps can cause sensorineural count may be low, and there may be a relative lymphocytosis. Serum amylase
hearing loss.
may be elevated. The mumps vaccine should reduce the incidence of this
disorder and its possible complications of orchitis, oophoritis, pancreatitis,
sensorineural hearing loss, and encephalitis. Another form of parotid swelling
which occurs in children is recurrent sialadenitis. This disorder may occur at
any time from the age of one month through late childhood and is charac-
16—DISORDERS OF THE SALIVARY GLANDS 319
Chronic Sialadenitis
the symptoms include recurrent swelling and pain over the parotid region.
A very viscous salivary secretion can be expressed from the duct by applying
pressure over the gland. Calculi are not present. Sialography performed in
the quiescent phase shows a characteristic picture with degenerative changes
in the tubular ducts suggestive of the bronchogram findings seen in bron¬
chiectasis. Symptoms and pathologic characteristics may vary from mild
initial changes to severe chronic changes, by which time the gland has
become firm and enlarged as a result of numerous repeated infections.
In certain situations when there are repeated episodes and the cause of
obstruction of the salivary gland is not evident, dilatation of the duct is
performed. After application of a local anesthetic, such as 4 per cent topical
cocaine or lidocaine (Xylocaine), lacrimal duct probes of increasing size are
16—DISORDERS OF THE SALIVARY GLANDS 321
introduced into the duct throught the papillae. The stricture in the duct may
be found and can be dilated. Occasionally there will be a sudden flow of
saliva from the gland when the obstruction is released. The procedure can
then be followed by a sialogram, introducing a small polyethylene tube into
the dilated duct orifice. A sialogram may help to further elicit the cause of
the recurrent obstruction.
When there is advanced chronic sialadenitis that no longer responds to Surgical treatment of chronic
medical management, it may become necessary to perform a parotidectomy. parotitis may include tympanic
neurectomy, parotid duct liga¬
Parotidectomy under such circumstances may be difficult, and the possibility tion, and parotidectomy.
of injury to the facial nerve is increased. Because of these risks, other
procedures have been developed in an effort to avoid parotidectomy. These
methods include ligation of the parotid duct (which is expected to cause
atrophy of the gland) and sectioning of Jacobson’s nerve on the promontory
of the middle ear through an endaural approach, thereby interrupting the
parasympathetic supply to the parotid gland.
Salivary gland calculi (sialolithiasis) occur far more commonly in the
submandibular gland than in the parotid gland. Ninety per cent of subman¬
dibular gland stones are radiopaque, while in the parotid gland, only 10 per
cent are identifiable on a scout film. There may be either a single large stone
or multiple small pieces of gravel. Symptoms include the sudden onset of
swelling and pain over the submandibular region, usually shortly after a
meal. Fever occurs when infection develops behind the obstruction. Treat¬
ment in the acute phase may require surgical removal of the salivary calculus
from the duct as it passes along the floor of the mouth. Occasionally the
stone may be milked out of the duct until it appears at the lingual papillae
adjacent to the frenulum. At other times, following administration of a local
anesthetic, an incision is made directly onto the stone for its removal.
Initially it may be necessary to obtain a culture, treat with antibiotics, and
wait until the acute phase subsides before any manipulation of the duct can
be attempted.
Recurrent sialadenitis of the submandibular gland is more frequently Surgical treatment of chronic
treated by surgical resection of the gland, and this is a less hazardous submandibular gland sialadeni¬
tis requires submandibular
procedure than parotidectomy under similar circumstances. Here, care is
gland resection including the
taken to preserve the marginal mandibular division of the facial nerve, the duct.
hypoglossal nerve, and the lingual nerve, all of which lie in close proximity
to the enlarged, chronically infected gland.
SYSTEMIC DISEASE
The parotid glands are the salivary glands most often involved in systemic
illnesses. The following are notable examples of systemic disease involving
salivary glands.
Sarcoidosis involving the parotid glands is referred to as Heerfordt’s
syndrome, or uveoparotid fever. The gland becomes diffusely swollen with
slight tenderness. Facial nerve paralysis can occur. The term uveoparotid
fever is used because of the possible coexistence of uveitis. Other systemic
manifestations of sarcoidosis such as hypercalcemia, enlarged liver and
spleen, enlarged cervical nodes, and enlarged hilar nodes as demonstrated
by chest radiographs may be present. Definitive diagnosis is made by biopsy.
The only treatment available at the present time consists of administration
of systemic steroids.
322 PART FOUR—THE ORAL CAVITY AND PHARYNX
SIALORRHEA
Radiosialographic Scanning
This technique depends on the increased concentration of iodine in saliva
compared to plasma. Radioactive technetium-99, like iodine, is secreted by
the intralobular ductal epithelium of major salivary glands. Both the parotid
and submandibular gland can be demonstrated using this nuclear medicine
technique. A normal gland appears symmetric and smooth, but a tumor
mass will show an area of decreased uptake, or in the case of Warthin’s
tumor, an area of increased concentration. Since it was later established that
increased uptake was not limited to Warthin’s tumor, but could occur in
pleomorphic adenoma and oncocytoma, the technique has become less
helpful.
Sialography
This technique requires injection of water- or oil-soluble contrast material
directly into the submandibular or parotid duct. After application of a topical
FIGURE 16-2. Instruments used for dilatation of Stensen’s duct or Wharton’s duct consist of
the set of lacrimal duct dilators, a catheter for insertion into the duct, and a syringe for instilling
contrast medium.
324 PART FOUR—THE ORAL CAVITY AND PHARYNX
anesthetic to the area of the duct, pressure is gently applied to the gland,
and the very fine orifice of the duct is identified by the saliva flow. The duct
orifice is dilated with lacrimal probes (Fig. 16-2 and 16-3). An 18-gauge
catheter, similar to the type used for administering intravenous fluids, or
polyethylene tubing is gently inserted about 2 cm into the duct. The catheter
is secured to the corner of the mouth. The technique is similar for both the
parotid gland and submandibular gland. Cannulating the submandibular
gland duct, however, may require more patience than dilation of the parotid
Always obtain a scout film be- duct. A scout x-ray film is obtained to make certain that there are no
fore injection of contrast, radiopaque substances, such as stones, in the gland. Between 1.5 and 2 ml
of contrast medium is injected gently through the catheter into the gland
until the patient feels pressure but never beyond the point when the patient
complains of pain. Appropriate lateral, oblique lateral, oblique, and antero¬
posterior films are obtained. When the catheter is removed, the patient may
be given a small amount of lemon juice. In 5 to 10 minutes a repeat film is
taken. Normally all contrast medium should have been expressed within that
time. Persistence of contrast medium within the gland 24 hours after this
test is definitely abnormal.
There are advantages and disadvantages to water-soluble and to lipid-
soluble contrast materials. Currently, Pantopaque and Lipiodol are the most
popular contrast materials.
Sialography is most useful in chronic disorders of the parotid gland such
as recurrent sialadenitis, Sjogren’s syndrome, or ductal obstruction such as
stricture. It is of no value in differentiating a benign from a malignant mass. Never inject contrast during an
It is contraindicated in the presence of a recent, acute inflammation of the acute exacerbation of inflamma¬
gland (Fig. 16-4). tion.
Computed Tomography
This is the single most useful radiologic diagnostic test of salivary gland
masses. It requires the intravenous injection of a contrast material, first as
a bolus and then with a continuous drip. Initially, this technique was
combined with standard sialography, but with newer, high-resolution scan¬
ners this is seldom necessary. The parotid gland will appear less dense than
surrounding structures and can be delineated from the masseter muscle. The
most common tumor mass, pleomorphic adenoma, may appear as a well-
defined, slightly enhancing mass. By this technique, it can be determined if
the mass extends into the deep lobe or parapharyngeal space. Since the CT
scan is not useful in differentiating benign from malignant lesions, biopsy
remains imperative. It is helpful, however, to have a preoperative assessment
of the size and location of any unusual mass or large mass, especially when
it is not certain if the mass actually began within the substance of the parotid
gland or is encroaching upon the parotid from adjacent areas.
MRI scanning will most likely replace the need for CT scan combined
with sialography in most incidences.
In Children
The most common benign gland tumor of children is the parotid gland
hemangioma. The skin overlying the mass may have a bluish discoloration,
and there may be fluctuation in the size of the mass when the child cries.
This tumor will show a gradual increase in size during the first four to six
months of life but should begin to show evidence of resolution by age two.
Similar to the hemangioma is the lymphangioma, which also arises in the
parotid gland region. Pleomorphic adenoma is the third most common
tumor, and the most common solid tumor, found in children. Other benign
tumors include neurofibroma and lipoma. Salivary gland tumors in children
most frequently involve the parotid gland, while the submandibular and
minor salivary gland areas are uncommon sites.
326 PART FOUR—THE ORAL CAVITY AND PHARYNX
FIGURE 16-4. A, Normal submandibular duct (Wharton's duct) and gland. B, Normal
parotid duct (Stensen’s duct) and gland.
16—DISORDERS OF THE SALIVARY GLANDS 327
In Adults
The pleomorphic adenoma (benign mixed tumor) accounts for 75 per cent Benign tumors of the parotid
gland outnumber malignant tu¬
of parotid gland tumors, both benign and malignant, in the adult. It is most mors 4:1. There is no method
common in the parotid region, where it appears as a painless swelling of short of excision to be certain a
long duration in the preauricular area or the region of the tail of the parotid lesion is benign. Skinny needle
biopsy is of benefit if positive
gland. There should be no pain or evidence of facial nerve weakness. In the but does not obviate the need
parotid area, although classified as benign, the tumor may continue to for surgery. Even diagnosis by
increase in size and become locally destructive. Complete surgical resection frozen section at surgery can be
difficult.
is the only treatment. Care should be taken to prevent injury to the facial
nerve, and the nerve is preserved even when immediately adjacent to the
tumor. The tumor may develop primarily in the deep lobe and extend into
the retromandibular region. In these circumstances the facial nerve is
carefully preserved and gently retracted so that the tumor can be removed
from its deep location extending into the parapharyngeal space.
Occasionally a deep lobe pleomorphic adenoma may present primarily
intraorally. It can be recognized by the deviation of the soft palate and
anterior tonsillar pillar toward the midline by a mass lateral to the tonsillar
area. Resection should be performed through the neck rather than intraor¬
ally.
When removing parotid tumors, the entire superficial lobe, or that portion
of the gland lateral to the facial nerve, is removed en bloc for biopsy
purposes, dissecting out and preserving the facial nerve. Pathologic exami¬
nation of the frozen section may not reveal the true nature of the tumor,
and more radical surgery may be required when permanent section results
are received. “Shelling out” a pleomorphic adenoma in the superficial lobe
of the parotid gland is not recommended because of the high likelihood of
recurrence. At the time of surgery the tumor mass appears encapsulated,
but pathologic examination will show extracapsular extension. The incidence
of recurrence when the entire tumor with a sufficient cuff of normal parotid
gland is resected is less than 8 per cent. Should a pleomorphic adenoma
recur, there is a high likelihood of injury to at least one of the divisions of
the facial nerve when the tumor is re-resected. Although this tumor is
considered benign, there have been cases of multiple recurrences with
relentless growth in which the tumor expands to involve the region of the
external canal and may actually extend into the oral cavity and paraphar¬
yngeal space. Recurrent tumors may undergo malignant degeneration, but
the incidence of this is less than 6 per cent. Irradiation therapy to a tumor
that has recurred and has become unresectable provides significant palliation.
Pleomorphic adenoma is also the most common tumor of the submandib¬
ular gland. Total surgical resection of the submandibular gland should
provide an adequate margin for removal of this tumor. Pleomorphic tumor
is also the most common benign tumor of the minor salivary glands. It
occurs most frequently on the palate near the midline at the junction of the
hard and soft palates. This location is also the most common for malignant
salivary gland tumors of the palate. A wide local resection of the tumor in
this location should be adequate.
Papillary adenocystoma lymphomatosum (Warthin’s tumor) is another Wartbin's tumor is the most
common tumor to occur
relatively common benign salivary gland tumor. It is most common in 50- to bilaterally.
60-year-old males. It is also the most common tumor to occur bilaterally.
Treatment consists of surgical resection with facial nerve preservation. The
tumor is encapsulated, and recurrence is unlikely.
328 PART FOUR—THE ORAL CAVITY AND PHARYNX
Other benign salivary gland tumors include the oxyphil adenoma (acido¬
philic cell), serous cell adenoma, and oncocytoma. Treatment is similar to
that for pleomorphic adenoma.
The parapharyngeal space may be the primary site of origin for benign
tumors. Most commonly these are salivary gland tumors that may have
arisen from the deep lobe of the parotid gland and extended into the
parapharyngeal space. Tumors of neurogenic origin such as schwannomas
may originate in this area from the vagus nerve or cervical sympathetic
chain. These tumors present as a smooth mass pressing the lateral pharyngeal
wall medially. These tumors should be approached through the neck rather
than intraorally because of the presence of major vessels and important
cranial nerves in this space. A preliminary arteriogram not only may
demonstrate the effect of the tumor on the location of the internal carotid
artery but also may be useful in detecting a chemodectoma or neurogenic
tumor within this space.
The most common tumor of the parapharyngeal space is a pleomorphic
adenoma. The second most common is a malignant adenocystic carcinoma.
The largest group of other tumors are of neurogenic origin, such as
schwannomas and neuromas. Any tumor of the parapharyngeal space should
be treated via an external, transcervical approach. This allows better control
of the major vessels in the area. It also prevents seeding of the tumor, which
can occur through a transoral approach. Because of the extensive postoper¬
ative edema that can occur, tracheostomy is often required.
•Significant local extension is defined as evidence of tumor involvement of skin, soft tissues, bone, or
the lingual or facial nerves.
From Beahrs OH, Myers MH (eds): Manual for Staging of Cancer. 2nd ed. Philadelphia, JB Lippincott
Co, 1983, p 50.
References
Batsakis JG: The pathology of head and neck tumors: The lymphoepithelial lesion of Sjogren’s
syndrome. Head Neck Surg 5:150-163, 1982.
Bernstein L, Nelson R: Surgical anatomy of the extraparotid: Distribution of the facial nerve.
Arch Otol 110:177-183, 1984.
Gates GA: Radiosialographic aspects of salivary gland disorders. Laryngoscope 82:115-130,
1972.
Goode RL, Smith RA: The surgical management of sialorrhea. Laryngoscope 80:1078-1089,
1970.
Hemenway W: Chronic punctate parotitis. Laryngoscope 81:485-509, 1971.
Johns M: Parotid cancer: A rational basis for treatment. Head Neck Surg 3:132-141, 1980.
Swartz JD, Saluk PH, Lansman A, et al: High resolution computerized tomography, part 2:
The salivary glands and oral cavity. Head Neck Surg 7:150-161, 1984.
Parotid Tumors
Conley JJ: Problems with reoperation of the parotid gland and facial nerve. Otolaryngol Head
Neck Surg 99:480-488, 1988.
Guillamondegui OM, et al: Aggressive surgery in the treatment for parotid cancer: The role of
adjunctive postoperative radiotherapy. AJR 123(1):49—54, 1975.
Matsuba HM, et al: High-grade malignancies of the parotid gland: Effective use of planned
combined surgery and irradiation. Laryngoscope 95:1059-1063, 1985.
Spiro RH, Armstrong J, Harrison L, et al: Carcinoma of major salivary glands. Arch Otolaryngol
115:316-321, 1989.
Radiological Assessment
Blatt IM, Rubin P, French AJ, et al: Secretory sialography in diseases of the major salivary
glands. Ann Otol Rhinol Laryngol 65:295-317, 1956.
Byrne MN, Spector JG, Garvin CF, Gado MH: Preoperative assessment of parotid masses: A
comparative evaluation of radiologic techniques to histopathologic diagnosis. Laryngoscope
90:284-292, 1989.
O’Hara AE: Sialography: Past, present and future. CRC Crit Rev Clin Radiol, Vol 4, 1973.
17
DISEASES OF THE
NASOPHARYNX AND
OROPHARYNX
by George L. Adams, M.D.
1. On the posterior wall extending toward the vault is the adenoid tissue.
2. There is lymphoid tissue on the lateral pharyngeal wall and in the
recessus pharyngeus, known as Rosenmuller’s fossa.
3. Torus tubarius—this reflection of pharyngeal mucosa over the rounded
protrusions of the cartilaginous portion of the eustachian tubes projects
as a thumblike intrusion into the lateral wall of the nasopharynx just
above the attachment of the soft palate.
4. The posterior choanae of the nasal cavity.
5. The cranial foramina, which are in close proximity and can be involved
by extension of nasopharyngeal disease, include the jugular foramina
through which pass the glossopharyngeal, vagal, and spinal accessory
cranial nerves.
6. Important vascular structures in the immediate proximity include the
inferior petrosal sinus, the internal jugular vein, the meningeal branches
from the occipital and ascending pharyngeal arteries, and the hypo¬
glossal foramen, through which passes the hypoglossal nerve.
7. The petrous portion of the temporal bone and foramen lacerum is in
proximity to the lateral portion of the roof of the nasopharynx.
8. The ostium of the sphenoid sinuses.
332
1 7—DISEASES OF THE NASOPHARYNX AND OROPHARYNX 333
The nasopharynx can be examined in one of three ways. With the patient
breathing through the mouth and with gentle downward pressure on the
middle one third of the tongue with tongue blades, a mirror is introduced
into the oropharynx. This examination differs from the laryngeal examination
because of the small size of the mirror used and because the mirror must be
rotated slightly from side to side to see the entire nasopharynx. Reflection
in an upward direction permits visualization of the torus tubari on each side,
the posterior choanae of the nasal cavity (Fig. 17-1), the posterior ends of
the inferior turbinates, and the vault and posterior wall of the nasopharynx.
Often patients require a topical anesthetic to decrease the “gag reflex” which
prevents adequate visualization. Gagging does not justify inadequate visu¬
alization of the nasopharynx in any patient suspected of having a problem
related to this area. If topical anesthesia alone does not permit adequate
examination, it is possible to pass a small catheter through the nasal cavity,
grasp it in the oropharynx, and direct it out through the mouth. This permits
retraction of the soft palate (Fig. 17-2). Of course, anesthesia to both the
nasal cavity and oropharynx is required.
An even better technique to visualize the nasopharynx is to pass a flexible A flexible nasopharyngoscope
nasopharyngoscope or a straight nonflexible nasopharyngoscope (Fig. 17-3) passed through the nasal cavity
directly through the nose into the nasopharynx. This provides not only the divides the best visualization
best visualization but also magnification.
In cases in which it is strongly suspected that there is an underlying
abnormality in the nasopharynx, general anesthesia in the operating room
with bilateral retraction of the soft palate provides an opportunity to palpate
the structures mentioned and obtain biopsies.
FIGURE 17-2. Adenoid mass as seen at operation and drawn directly Adenoid
from life. A retractor is shown pulling the soft palate and uvula upward tissue
to expose the lower portion of the adenoid vegetations. Note the
sharp inferior margin of the adenoid mass.
334 PART FOUR—THE ORAL CAVITY AND PHARYNX
Nasopharyngeal Bursitis
Naopharyngeal bursitis, or Thornwaldt’s disease, is a form of postnasal
discharge that is produced by mucoid drainage from a pocket in the
uppermost part of the posterior pharyngeal wall. The pocket is called the
pharyngeal bursa. This is an unusual cause of postnasal drainage, and it is
corrected by excision (Fig. 17-4).
full extent of such tumors; as they rarely remain limited to the nasopharynx,
but extend into the pterygomaxillary fossa, skull base, or sinuses. The Diagnosis is made by history,
diagnosis is so apparent by the very vascular appearance of the tumor and exam, CT, and arteriogram. A
biopsy is not necessary and is
the history of epistaxis in an adolescent male that a preoperative biopsy is hazardous.
not obtained, for it may lead to uncontrollable hemorrhage. The arteriogram
is sufficient to make the diagnosis.
Malignant Tumors
Management of malignant tumors is discusssed in Chapter 23. It is
important only to mention the presenting symptoms of unilateral serous
otitis media, cranial nerve paralysis (particularly the sixth nerve), and nasal
obstruction. The most common presenting sign of nasopharyngeal carcinoma A high posterior cervical lymph
is a posterior high cervical lymph node. Nasopharyngeal cancers are not node suggests a nasopharyn¬
geal source.
associated with smoking and can occur in young individuals. A particularly
high incidence in Chinese has been noted. Research is being conducted on There is an association between
the association of the Epstein-Barr virus and nasopharyngeal carcinoma. Ebstein-Barr virus and nasopha¬
ryngeal carcinoma.
Individuals with nasopharyngeal carcinoma have an elevated EB viral titer,
and elevation of the titer after initial treatment often heralds recurrence.
Adenoid Hypertrophy
The adenoids are an accumulation of lymphoid tissue along the posterior
wall of the nasopharynx above the level of the soft palate. They normally
hypertrophy during childhood, reaching their greatest size in the preschool
and early school-age years. Spontaneous resolution is expected, so that by
age 18 to 20 adenoid tissue will not usually be apparent on indirect
nasopharyngeal examination. The adenoids often transiently enlarge with
URI’s, and spontaneous regression obviates the need for aggressive treat¬
ment. Adenoid tissue is seldom mentioned unless it interferes with normal
function of one of the surrounding important structures. Hypertrophied
338 PART FOUR—THE ORAL CAVITY AND PHARYNX
FIGURE 17-6. Adenoid hypertrophy in this four-year-old child obstructs the nasopharynx.
The child presented with hyponasality to his voice, sleep disorders, and bilateral serous otitis
media.
1 7—DISEASES OF THE NASOPHARYNX AND OROPHARYNX 339
The most common and preferred treatment for chronic serous otitis media
that is refractory to medical management with antibiotics and other forms
of conservative treatment is the insertion of ventilation tubes through the
tympanic membrane. In children this is the most direct approach to alleviate
the fluid accumulation and improve hearing. However, the tubes may remain
in place only 6 to 12 months and the underlying problem is not always
corrected. It is appropriate to look at the opposite end of the eustach'an
tube to determine whether the enlarged adenoids play a direct or indirect Adenoidectomy is beneficial in
role in obstruction of this portion of the tube. Studies by Bluestone and some individuals with recurrent
serous otitis media.
others demonstrate that removal of enlarged adenoids can, in at least 50 per
cent of cases, be effective in alleviating repeated episodes of otitis media
and perhaps the need for ventilation tube insertion. These studies have not
been effective in determining which group of patients would most benefit
from adenoidectomy.
Adenoidectomy for speech problems should be undertaken with great
care. Speech pathologists should be consulted beforehand, for if a short
palate, submucous cleft, or velopharyngeal insufficiency should result from
the adenoidectomy, the voice may become hypernasal. In these situations
full radiologic evaluation as well as a flexible nasopharyngoscopic exam is
necessary.
Adenoidectomy should be avoided in cases of incipient velopharyngeal
insufficiency, which might be created by removal of the adenoids in a patient A bifid uvula serves as a "Hag"
with a very short soft palate or submucous cleft of the short or hard palate. to warn of possible submucous
palatal cleft.
It should certainly be avoided in patients with an obvious cleft palate. There
may, however, be unusual cases in which a limited adenoidectomy is
indicated for a patient with airway obstruction and a submucous cleft. In
this case the parents must be warned of the possibility of further deterioration
of voice quality if such an operative procedure is performed. There is no
evidence to suggest that adenoidectomy will reverse dental changes that
have already occurred, but removal can help prevent recurrence of maloc¬
clusion after orthodontia.
Because the adenoid tissue is not encompassed by a capsule like the
tonsils, complete removal of all adenoid tissue is nearly impossible and
recurrent hypertrophy or infection is possible.
340 PART FOUR—THE ORAL CAVITY AND PHARYNX
DISEASE FREQUENCY
Acute pharyngitis without membrane formation Very common at all ages
Acute tonsillitis Very common in children
Lingual tonsillitis Moderately common in adults
Peritonsillar abscess More common at ages 13-20
Acute pharyngitis with membrane formation or ulceration:
Vincent’s (Plaut’s) angina Common in young adults
Diphtheria Uncommon
Pharyngitis associated with hematologic disorders:
Infectious mononucleosis Common
Acute leukemia Uncommon
Acute Pharyngitis
Acute viral and bacterial pharyngitis are very common disorders. Numer¬
ous attempts have been made at classifications of an acute inflammation
involving the pharyngeal wall. It probably is most logical to group a number
of these infections under the relatively simple title of “acute pharyngitis.”
This includes acute pharyngitis occurring in the ordinary head cold, as a
result of acute infectious disorders such as the exanthemas or influenza, and
from the uncommon miscellaneous causes, such as herpetic manifestations
and thrush (Fig. 17-7).
Etiology and Pathology. The cause of acute pharyngitis may vary from an
organism producing a simple exudative or catarrhal change to one that
produces edema and even ulceration. The organisms found include various
streptococci, pneumococci, and the influenza bacillus, among others. In the
early stages, there is hyperemia, then edema and increased secretion. The
exudate is at first serous but becomes thicker or mucoid, and then tends to
become dry and may adhere to the pharyngeal wall. With the hyperemia,
the blood vessels of the pharyngeal wall become dilated. Small white, yellow,
or gray plugs form in the follicles or lymphoid tissue. In the absence of
tonsils, attention is usually focused on the pharynx, and it is observed that
lymphoid follicles or plaques on the posterior pharyngeal wall, or localized
more laterally, are inflamed and swollen. This lateral wall involvement,
when isolated, has been referred to as “lateral pharyngitis” (Fig. 17-8). It
is possible, of course, even in the presence of tonsils, for only the pharynx
to be involved.
In recent years, with progress in the identification of viruses, reports ot
clinical problems related to a viral causative agent have become numerous.
It is important to be aware of the probability of a viral etiology in acute
pharyngitis associated with adenopathy in the absence of follicular pharyngitis
membrane formation. Vesicle formation on the mucous membrane, as in
herpes, strongly suggests a viral etiology.
A number of viruses have been identified in adenoid tissue during
epidemics of acute pharyngitis (Table 17-1).
Symptoms and Signs. At the onset, the patient often complains of a
dryness or “scratchiness of the throat. Malaise and headache are common.
There is usually slight elevation of temperature. The exudate in the pharynx
invariably thickens. It may be dislodged with some difficulty, with a rasping,
hawking effort and cough. A certain amount of hoarseness is present if the
inflammatory process involves the larynx. In some cases, there may be
dysphagia chiefly as the result of pain, referred pain to the ear, cervical
adenopathy, and tenderness. The pharyngeal wall is reddened and may have
a dry, glazed appearance and a coating of mucoid secretion. The lymphoid
tissue usually appears red and swollen.
Acute Tonsillitis
Etiology. Acute suppurative bacterial tonsillitis is most often caused by
beta-hemolytic Streptococcus Group A, although pneumococci, staphy¬
lococci, and Haemophilus influenzae as well as viral pathogens can be
involved. Occasionally nonhemolytic streptococci or Streptococcus viridans
are cultured, usually in less severe cases. Nonhemolytic streptococci and
Streptococcus viridans may be cultured from the throats of healthy persons,
particularly in the winter months, and during epidemics of acute respiratory
infections, hemolytic streptococci can be found in the throats of apparently
healthy persons.
Pathology. There is a general inflammation and swelling of the tonsil
tissue with an accumulation of leukocytes, dead epithelial cells, and
pathologenic bacteria in the crypts. It is probable that differences in the
strains or the virulence of the organisms may account for the following
variations of pathologic phases:
Ungual Tonsillitis
The lingual tonsils do not have the complex crypt arrangement of the
faucial tonsils, nor are they as large. For these reasons, lingual tonsil
infections are much less common. Rarely are the lingual tonsils acutely
inflamed along with the faucial tonsils. Lingual tonsillitis is more common
in tonsillectomized patients and in adults.
The etiology and pathology are much the same as those of an acute
inflammation of the faucial tonsils. The symptoms usually are soreness on
swallowing, a sense of a lump in the throat, malaise, slight fever, and in
some cases cervical adenopathy with tenderness. Inspection of the lingual
tonsils with the aid of a laryngeal mirror and reflected light reveals a
reddened, swollen lingual mass with whitish spots dotting the surface of the
tonsil, similar to those seen in an acute tonsillitis involving the faucial tonsils.
344 PART FOUR—THE ORAL CAVITY AND PHARYNX
Membranous Pharyngitis
Membranous pharyngitis has been described by some as a clinical entity,
but membrane formation accompanies several forms of acute pharyngitis
which are distinct entities but which resemble one another clinically. These
diseases are Vincent’s infection, diphtheria, the throat involvement accom¬
panying certain blood disturbances, and the pseudomembranous character
of a variety of throat disorders.
Vincent’s (or Plaut’s) Angina. This infection of the pharynx and mouth is
often referred to as “Vincent’s infection” or “trench mouth.” It is caused
by fusiform bacilli and spirochetes normally present in the oral cavity. It is
more often encountered in a limited form without systemic reaction than in
the more severe form, and it may be associated with other throat
inflammations.
This form of membranous pharyngitis is commonly seen in young adults.
Besides sore throat there are generally a low-grade fever, tender cervical
adenopathy, and foul breath. Diagnosis is confirmed by the presence of
numerous fusiform bacteria seen with Fontana stain. Treatment consists of
supportive measures, sodium perborate or hydrogen peroxide mouthwash,
and specific penicillin therapy.
Diphtheria. While the overall incidence of diphtheria is steadily declining
in the United States, there is still an associated 10 per cent mortality rate.
The pharynx remains the most common site for this infection. The disease
occurs more frequently in unimmunized or inadequately immunized
individuals. Individuals who are adequately immunized have a protective
level of antitoxin for ten years or more. The most common initial complaint
is a sore throat. In addition, patients may complain of nausea, vomiting,
and dysphagia. The status of immunization has no effect on the presenting
complaint. Examination reveals a characteristic membrane present over the
tonsillar area with spread to adjacent structures. The membrane appears
dirty and dark green and may even obstruct the view of the tonsils. Bleeding
occurs with elevation of the membrane which is unlike other causes of
membranous pharyngitis. The diagnosis is usually made earlier and treatment
initiated sooner when it is known that an epidemic of diphtheria is present.
There is often a delay in diagnosis of sporadic cases and in small epidemics.
The causative organisms are toxigenic strains of Cory neb acterium
diphtheriae. Smears of the nasopharynx and tonsil are obtained and placed
in transport medium to be later cultured on MacConkey agar or Loeffler
medium. Suspicious strains are then tested for toxigenicity.
Treatment of the disease consists of two phases: (1) use of a specific
antitoxin and (2) elimination of the organism from the oropharynx. Before
the antitoxin is administered, the patient should be tested for sensitivity to
the serum. Patients should receive 40,000 to 80,000 units of antitoxin diluted
in normal saline and administered slowly intravenously. Antibiotic therapy
in the form of penicillin or erythromycin is initiated to eliminate the carrier
state. Repeat culture should be performed to make certain the patient is not
harboring the organism in the pharynx. Persistence of the organism requires
long-term treatment with erythromycin.
1 7—DISEASES OF THE NASOPHARYNX AND OROPHARYNX 345
Complications from diphtheria are common, and the patient who develops
an airway obstruction may require tracheostomy. Cardiac failure and muscle
paralysis may occur, and the inflammatory process may spread to the ears,
causing an otitis media, or to the lungs, causing pneumonia.
Atrophic Pharyngitis
A condition that is just the opposite of hypertrophic pharyngitis may
occur. Varying degrees of atrophy of the mucosal elements of the pharynx
are frequently encountered. In the mild cases, the mucosa appears thin and
glistening or glazed, with an absence of all but a few of the lymphoid
collections that are seen in an average pharynx. On careful inspection, one
can usually see that the blanket of mucus, which is normally transparent,
seems thicker and semitransparent. It may be raised off the surface in spots
In the advanced form of atrophic pharyngitis, the dryness is striking, the
mucous coating is gluelike in its consistency, and at times an actual crust is
seen. When this secretion is removed, the underlying mucous membrane has
a dry, furrowed appearance. This advanced stage of atrophic pharyngitis has
been termed “pharyngitis sicca” and is usually associated with an atrophic
rhinitis, or “rhinitis sicca.”
Etiology. The cause of atrophic pharyngitis is not definitely known. It has
been claimed that it is caused by the air not being sufficiently warmed and
humidified by the nasal mucosa, as would occur in chronic mouth breathing
and in the instances of atrophic rhinitis in which the air-conditioning role of
the nose is not functioning. There are apparently, however, trophic changes
in the mucosa which result in a hyposecretion of mucus and which are
influenced by some factor that is not understood.
Symptoms. The main symptom of atrophic pharyngitis is a sense of dryness
and thickness in the upper pharynx. The patient’s attempt to dislodge the
adherent secretion consists of frequent attempts to clear the throat, usually
by “hawking.” Varying degrees of soreness are not uncommon. Hoarseness
of a mild degree may accompany this disorder, owing to an extension of the
process to the larynx and the irritation from frequent attempts to clear or
cough out the sticky secretion. In some instances there is fetor.
Treatment. When an atrophic rhinitis is concurrently present, it should
also receive therapeutic attention. Local application of Mandl’s paint to the
pharynx is beneficial. The purpose of this medication is to stimulate secretion.
Potassium iodide may be given internally for the same effect. An average
dose is 10 drops of a saturated solution three times daily with meals. A
combination of the local application of a throat paint and the internal
administration of the iodide is desirable. The breathing of warm moist air,
1 7—DISEASES OF THE NASOPHARYNX AND OROPHARYNX 349
such as can be accomplished by placing a hot, moist turkish towel across the
nose and mouth, helps to moisten the inspissated secretion. Twenty to 30
minutes of this once or twice a day is desirable. Attention should also be
given to matters of general health
Chronic Tonsillitis
Diagnosis. Chronic tonsillitis is undoubtedly the most common of all
recurring throat diseases. The clinical picture varies, and diagnosis depends
largely upon inspection. In general, there are two rather widely differing
pictures that seem to fit into the category of chronic tonsillitis. In one type
the tonsil is enlarged, with evident hypertrophy and scarring (Fig. 17-11).
The crypts seem partially stenosed, but an exudate, often purulent, can be
expressed from them. In some cases one or two crypts are enlarged, and a The size of the tonsils in
considerable amount of “cheesy” or “putty-like” material can be expressed chronic tonsillitis does not nec¬
essarily correlate with severity
from them. A chronic infection, usually low-grade, is obvious. The other
of the problem.
common clinical picture is that of the small tonsil, usually recessed and often
referred to as “buried,” in which the margins are hyperemic, and a small
amount of thin, purulent secretion can often be expressed from the crypts.
Cultures from tonsils with chronic disease usually show several organisms of
relatively low virulence and, in fact, rarely demonstrate beta-hemolytic
streptococci.
Treatment. The one certain cure for chronic tonsillitis is surgical removal
of the tonsils. This is reserved for those cases in which medical or more
conservative management has failed to alleviate the symptoms. Medical
management includes prolonged courses of penicillin, daily throat irrigations,
and efforts to cleanse the tonsillar crypts with a dental or oral irrigating
device. The size of tonsil tissue does not correlate with chronic or recurrent
infection.
TONSILLECTOMY
Indications
While there may be a variance in opinion on the exact indications for
tonsillectomy in children, there is less disagreement on the indications for
this procedure in adults. Tonsillectomy is commonly performed in young
adults who have suffered repeated episodes of documented tonsillitis, peri¬
tonsillar cellulitis, or peritonsillar abscess. Chronic tonsillitis can result in
extensive loss of time from work.
352 PART FOUR—THE ORAL CAVITY AND PHARYNX
Surgical Procedure
Preparation of the Patient
When the decision has been reached that tonsillectomy is to be performed,
it must be realized that this may be the young patient’s first surgical
procedure. A complete history and physical examination should be per¬ A history of a bleeding problem
formed with particular attention to existence of any familial or inherited is more accurate than any sin¬
gle preoperative screening test.
disorders and specifically any bleeding tendency. In addition, a history of
any relative who may have had difficulty with general anesthesia should be
sought in an effort to exclude the remote possibility of malignant hyperther¬
mia. The most commonly preferred screening tests for bleeding disorders
include partial thromboplastin time, prothrombin time, and platelet count.
The patient should not take any aspirin for two weeks before surgery. The
history remains the most valuable guideline for the possibility of a bleeding
tendency. Complete blood count and urinalysis are always required prior to
a general anesthetic. Chest radiograph and electrocardiogram are recom¬
mended in adults over age 40. There should be documentation on the chart
of the need and indication for the surgical procedure.
The physician should explain to the patient in terms the young child can
understand exactly what surgical procedure will be performed and that it is
being done in an effort to help the patient and to prevent repeated episodes
of infection or to improve hearing. It should be made clear that there may
354 PART FOUR—THE ORAL CAVITY AND PHARYNX
Technical Considerations
There is no substitute for proper training for the performance of these
procedures.
Important anatomical relationships must be appreciated by the surgeon
(Figure 17-12A) who performs tonsillectomy.
Surgical Anatomy
1. The structure of the two pillars—the palatoglossus muscle (anterior
pillar) and the palatopharyngeus muscle (posterior pillar)
2. The lateral boundary of the tonsillar fossa—the superior constrictor
muscle
3. The relationships of the plicae, particularly the plica triangularis
4. The blood supply, which is derived from five arteries—the dorsalis
linguae from the lingual artery; the ascending palatine and the tonsillar,
both from the external maxillary; the ascending pharyngeal from the
external carotid; and the descending palatine from the internal
maxillary.
Anomalous blood vessels in this area may offer certain difficulties in tonsil
surgery.
The main lymphatic drainage from the palatine tonsils leaves the fibrous
trabeculae of the tonsil to pass through the capsule to the superior constrictor
muscle of the pharynx. Several trunks form at this site, pierce the bucco¬
pharyngeal fascia, and enter glands of the deep cervical chain from which
drainage reaches the thoracic duct and then enters the general circulation.
There has been no proof that there are effective afferent lymphatic vessels
from the tonsils.
Such things as endotracheal anesthesia, nonexplosive anesthetics, intra¬
venous fluids, and suction cautery for hemostasis have aided the surgeon
technically. Local anesthesia for adults is safe and quite acceptable to the
patient (Figures 17-12B, 17-13, and 17-14).
Postoperative Bleeding. Postoperative bleeding is categorized into
immediate and delayed. Immediate persistent postoperative bleeding is
generally handled by reanesthetizing the patient and controlling by ligature
or suction electrocautery. Later bleeding of significance may be handled in
17—DISEASES OF THE NASOPHARYNX AND OROPHARYNX 355
Pharejnqeal
Tonsil
Soft palate
Palatine
FIGURE 17-12. A, The relationships of tonsil
the structures included in the orophar¬
ynx. The details of the structures sur¬
rounding the tonsils. (Redrawn from Lincjual tonsil
Hirsch.). 6, The principle of adenoidec-
tomy with LaForce adenotome requires
insertion of the opened adenotome in
the midline followed by additional inser¬
tion of the adenotome in lateral posi¬
tions on either side of the midline. The
advantage of this instrument is that it is
less traumatic than the curet, the depth
of incision is better controlled, and the
adenoid removed is safely caught in the
basket of the adenotome. After the ad¬
enoid is removed, or during phases of
its removal, there is value in holding a
sponge in the nasopharynx to control
the bleeding so that the site of removal
can be repeatedly inspected to ensure
thorough removal of the adenoid mass
and to visualize bleeding points on
which to apply a hemostat. This tech¬
nique is suitable only for the removal of
an ordinary hypertrophic adenoid.
Pharyngeal space infection: This potential space is funnel-shaped, with its base located at the base of
dental, oral cavity, tonsils, pa¬ the skull on each side close to the jugular foramen and its apex at the great
rotid gland, traumatic, mastoid.
horn of the hyoid bone. The inner boundary is the ascending ramus of the
mandible and its attached medial pterygoid muscle and the posterior portion
of the parotid gland. The dorsal boundary consists of the prevertebral
muscles. Each fossa is divided into two unequal compartments by the styloid
process and its attached muscles. The anterior (prestyloid) compartment is
the larger. It may become involved in a suppurative process as a result of
infected tonsils, some forms of mastoiditis or petrositis, dental caries, and
surgery. The smaller posterior compartment contains the internal carotid
artery, jugular vein, vagus, and sympathetic nerves. Only a thin layer of
fascia separates this compartment from the retropharyngeal space.
Infection can spread rapidly The fascial spaces of the neck have been previously described (Chapter
from one potential space to
14). Pharyngeal infections can extend into the potential spaces surrounded
another.
by these fascial planes. Because patients have generally been treated with
an antibiotic, the classic development of a fascial space deep neck infection
is less common today (Fig. 17-16). The physician should initially determine
which space is most likely involved as well as the probable causative
organism.
When infection extends from the pharynx into this space, the patient will
develop marked trismus. While the lateral pharyngeal wall may be pushed
medially, as in a peritonsillar abscess, this infection should always be drained
through a cervical incision. The neck becomes swollen near the angle of the
mandible. CT scan aids in delineating the abscess.
A transverse incision, two fingerbreadths below the mandible, gives access
to the anterior border of the sternocleidomastoid muscle (Fig. 17-17). The
submaxillary gland is identified as well as the posterior belly of the digastric
muscle. Blunt dissection toward the styloid process opens this space. Alter
pus is collected for both culture and Gram’s stain, drains are inserted into
the abscess. The skin is approximated loosely.
The most serious complications of a pharyngomaxillary space infection
involve the surrounding vasculature. Septic thrombophlebitis of the jugular
vein can occur. There can be sudden massive hemorrhage from erosion of
the internal carotid artery. An initial small hemorrhage (sentinel bleed)
suggests this complication. Identification of the internal carotid arteries is
mandatory when this complication is suspected and plans are made for
drainage of the abscess. Thus, if hemorrhage occurs when the abscess is
drained, immediate ligation of the internal carotid artery or common carotid
artery can be performed.
Ludwig’s Angina
Ludwig’s angina is a cellulitis or phlegmonous inflammation of the superior
compartment of the suprahyoid space. This potential space exists between
the muscles attaching the tongue to the hyoid bone and the mylohyoid
muscle. Inflammation of this space causes extreme firmness in the tissue of Free pus is not encountered
when a Ludwig’s infection is
the floor of the mouth and forces the tongue upward and posteriorly and drained. Tissue edema is re¬
thus can potentially obstruct the airway. Ludwig’s angina develops most leased by decompressing the
frequently as a result of infection of dental origin, but it may develop from submaxillary space.
Masticator Abscess
This potential space is in close proximity to the pharyngomaxillary space.
This space includes the internal pterygoid muscle, masseter muscle, and
ramus of the mandible. While infections in the adjacent pharyngomaxillary
space are primarily the result of infection in the pharynx, the masticator
space is most frequently involved secondary to infection of dental origin.
Swelling and tenderness occur over the ramus of the mandible as well as
firmness developing along the lateral floor of the mouth. It is not possible
to depress the tongue because of the swelling and edema in the floor of the
mouth. Infections in this space should be treated initially and vigorously
with appropriate antibiotics. If the infection fails to resolve after a week of
intensive antibiotic therapy, surgical drainage is required. A transverse
cervical incision is made two fingerbreadths below the mandible and carried
down to the mandibular periosteum. Blunt dissection is then used to drain
the abscess. It may also be necessary to make a separate incision intraorally,
thus draining the infection into the mouth.
Retropharyngeal Abscess
Etiology. This disease occurs primarily in infants or small children under
the age of two. In older children or adults it is almost always secondary to
spread from a parapharyngeal space abscess or traumatic interruption of the
posterior pharyngeal wall lining by trauma from a foreign object or during
1 7—DISEASES OF THE NASOPHARYNX AND OROPHARYNX 361
During the past ten years the effects of long-term upper airway obstruction
with development of sleep apnea syndrome or the cardiopulmonary syn¬
drome have received significant attention. The severity of these long-term
effects had not been previously appreciated. Sleep apnea and associated
snoring are no longer considered psychosocial problems. Their interrelation¬
ships with significant cardiac and pulmonary problems have been recognized.
Obstruction can occur anywhere The cardiopulmonary syndrome results from the efforts of the heart and
from the nasal cavity to the su-
praglottic larynx, or anyplace
lungs to compensate for long-term chronic obstruction (Table 17-4). Other
where the tissues are pliable findings associated with this syndrome include systemic hypertension (in 30
rather than fixed. to 50 per cent of individuals), polycythemia, and cardiac arrhythmias
(bradycardia and ventricular tachycardia).
Clinical Presentation:
Obstructive sleep-disordered breathing primarily affects adult males (95
per cent) and occurs in perhaps 1 to 3 per cent of the adult population. The
clinical syndrome is associated with snoring in all individuals, and the
‘Conrad Iber, M.D., and Robert Maisel, M.D., contributed to the section on Obstructive
Sleep Apnea.
Mechanisms
Obesity and increasing age are associated with an increased risk of sleep-
disordered breathing. Although prospective studies of adults with sleep
apnea demonstrate reduced pharyngeal size and increased compliance with
evidence of mild retrognathia, most adults do not have clinically evident
disease of the upper airway. Narrowing of any portion of the supraglottic
airway can contribute to pharyngeal collapse during sleep. Nasal obstruction
due to septal deviation, massive adenoidal hypertrophy, or other anatomic
or functional problems may produce sleep apnea. Most of the common
aerodigestive pathway (pharynx) is composed of soft tissues capable of
collapse and airway narrowing. Continuous muscle tone is required to
maintain patency at the level of the nasopharynx, tongue base, and supra¬
glottis. Sleeping in the supine position and relaxation of muscle tone, which
accompanies sleep, can create obstruction. Although loss of phasic pharyn¬
geal dilator activity was initially implicated in obstructive sleep apnea, recent
studies show phasic inspiratory activation of upper airway muscles more
commonly in patients than in normal subjects. Presumably the obstructive
sleep apnea patient requires greater upper airway muscle activation than
normal to maintain airway patency.
Coexisting anatomic obstruction of the upper airway combined with
functional relaxation of the muscle tone and the sphincters increase the
likelihood of pharyngeal collapse. Individuals with good daytime muscle
tone may demonstrate disturbances during sleep and frank obstructive sleep
apnea, with no apparent findings during waking hours. Obstruction may
result from redundant tissue in the superior hypopharynx, base of tongue,
or oropharyngeal areas. At night during both REM (rapid eye movement)
and non-REM sleep, there is loss of muscle tone, and obstructive apnea will
develop with continued inspiratory diaphragmatic and intercostal muscle
contraction.
Provocative factors in adults include anatomic derangements (lymphoma-
tous involvement of the nasopharynx, allergic rhinitis, and acquired retro¬
gnathia) as well as causes of pharyngeal collapse (alcohol, benzodiazepines,
androgens, hypothyroidism). Correction of congestive heart failure may
result in significant improvement or resolution of sleep apnea in some pa-
364 PART FOUR—THE ORAL CAVITY AND PHARYNX
Diagnosis
For a patient suspected of having obstructive sleep apnea, a careful
interview is held preferably in the presence of another household member.
Daytime somnolence often is Many patients deny or do not realize the symptoms are a result *of the
associated with sleep apnea.
disease. Apnea causes arousal from sleep with disruption of the normal sleep
cycle and subsequent symptoms of sleep deprivation—most notably daytime
somnolence. These patients, or more usually their families, complain about
significant or even heroic snoring. This may be so bad that a spouse has to
move out of the room or work and travel partners are unable to stay in the
same hotel room with the patient. Patients complain of morning headaches
and impotence; families report that in severe cases the patient does not
participate in family activities or decisions. Many of the patients are able to
function in the workplace but immediately come home, eat dinner, and fall
asleep. They may partake of meals with the family but may not participate
in any other activities. Despite what appears to be an excess of sleep, these
people are chronically sleep deprived from the recurrent awakenings asso¬
ciated with sleep-disordered breathing.
Physical examination of the head and neck may be quite normal, although
the physician should always look for obstructive lesions in the nose, naso¬
pharynx, oropharynx, and hypopharynx. Specific lesions sought in the
examination include nasal-septal deformity, nasal polyps, hypertrophic tur¬
binates, and adenoid hypertrophy. In some apnea patients, the uvula is
edematous and wrinkled, looking much like an earthworm. The soft palate
may appear long, although no relationship of these anatomic landmarks to
the degree of sleep apnea has been confirmed. Many patients are obese,
some by 50 to 100 per cent over normal body weight.
Obstructive sleep apnea is a disease that causes two significant problems.
The fragmentation of sleep disturbs the psychosocial activities of the patient,
disenchants the family, and destroys emotional relationships. And because
of excessive daytime sleepiness, the patient may be a hazard in the workplace
1 7—DISEASES OF THE NASOPHARYNX AND OROPHARYNX 365
C* ~ A,
°4 " *1
O, - O* --------
Airflow *. Vr
Ribcage ♦•r'' \ /\Y «/ \y
Abdomen y v Y
Airflow
Ribcage +
Abdomen
h- S 86c H
Treatment
Treatments of sleep apnea include bypassing the upper airway (tracheos¬
tomy), correcting identifiable anatomic abnormalities (uvulopalatopharyn-
366 PART FOUR—THE ORAL CAVITY AND PHARYNX
FIGURE 17-21. A, Anterior cervical skin incisions. B. Stoma after tracheocutaneous flap
approximation. (From Sahni R, Blakley B, Maisel RH: Flap tracheostomy in sleep apnea
patients. Laryngoscope 95:221-223, 1985.)
1 7—DISEASES OF THE NASOPHARYNX AND OROPHARYNX 367
FIGURE 17-22. Uyulopalatopharyngoplasty. a, Typical oropharynx in a patient with sleep apnea secondary
to oropharyngearobstruction. Note elongated, engorged uvula, and thick, redundant folds of tissue. The
tonsils are removed initially if this has not previously been done, b and c, Mucosal flaps based inferiorly,
extending to the midline, are elevated, d, Excessive redundant submucosal tissue is excised and the uvula
is partially amputated, e. Midline sutures are placed and reapproximated to the soft palate, f, Completion
of procedure. (Adapted from Fujita.)
References
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9(3):655—675, 1976.
Bierman CW, Furukawa CT: Medical management of serous otitis in children Pediatrics
61(5): 768-774, 1978.
Blakley BW, Maisel RH, Mahowald M, Ettinger M: Sleep parameters after surgery for
obstructive sleep apnea. Otolaryngol Head Neck Surg 95:23-28, 1986.
Bluestone CD: Eustachian tube function and allergy in otitis media. Pediatrics 61(1):753—760,
Bluestone CD, Beery QC: Adenoidectomy in relationship to otitis media. Ann Otol Rhinol
Laryngol 85(Suppl):280, 1976.
Christiansen TA, Duvall AJ, Rosenberg Z, Carley RB: Juvenile nasopharyngeal angiofibroma
Trans Am Acad Ophthalmol Otolaryngol 78:140, 1974.
1 7—DISEASES OF THE NASOPHARYNX AND OROPHARYNX 369
DeDio RM,-Tom LWC, McGowan KL, et al: Microbiology of the tonsils and adenoids in a
pediatric population. Arch Otolaryngol Head Neck Surg 114:763-765, 1988.
Donovan R, Southill JE: Immunological studies in children undergoing tonsillectomy Clin Exp
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Fairbanks DNF: Snoring: Surgical vs. nonsurgical management. Laryngoscope 94:1188-1192
1984.
Feinstein AR, Levitt M: The role of tonsils in predisposing to streptococcal infections and
recurrence of rheumatic fever. N Engl J Med 282:285, 1970.
Freeman AJ, et al: Previous tonsillectomy and the incidence of acute leukemia of childhood
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Fujita S, Conway W, Zorick F, Roth T: Surgical correction of anatomic abnormalities in
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Guilleminault C, Simmons FB, Motta J, et al: Obstructive sleep apnea syndrome and
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Manford RS, Orey HW, Brooks GF, Feldman RA: Diphtheria deaths in the United States
JAMA 229:1890, 1974.
Mawson GR, Adlington P, Evans M: A controlled study evaluation of adenotonsillectomy in
children. J Laryngol Otol 81:777-790, 1967.
McCurdy JA Jr: Peritonsillar abscess: A comparison of treatment by immediate tonsillectomy
and interval tonsillectomy. Arch Otolaryngol 103:414-415, 1977.
McKee WJE: A controlled study of the effects of “tonsillectomy and adenoidectomy ” Br J
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Chapters I, II, and III.
18
INFECTIONS IN THE
IMMUNOCOMPROMISED HOST
by Norman T. Berlinger, M.D., Ph.D.
weeks. Furthermore, the absolute neutrophil count may remain below 500/
cu mm for up to four or five weeks. It is during this neutropenic period of
profound immunosuppression that the marrow recipient is inordinately
susceptible to serious or fatal infections, often with unusual or unfamiliar
organisms. Even after recovery of normal or nearly normal numbers of
circulating neutrophils, neutrophil chemotaxis or intracellular killing of
organisms may remain abnormal.
Nonspecific immune mechanisms such as antibody-dependent cell-me¬
diated cytotoxicity and natural killing similarly recover rapidly with marrow
engraftment. Serum immunoglobulin levels can return to normal within
several months after engraftment. However, maturation of the humoral
immune system may be prolonged so that the production of antibody to
some antigens may be poor despite the ability to produce sufficient immu¬
noglobulin.
T cell and B cell levels may return to normal soon after engraftment, but
T cell subpopulations may remain abnormal for prolonged periods of time.
The occurrence of infection early during the course of marrow transplan¬
tation is directly related to the duration of the neutropenic period. The
occurrence of infection after engraftment is related to the rapidity of
maturation of the immune system and to the development of GVHD, which
itself is immunosuppressive and often must be treated with immunosuppres¬
sive drugs.
Early Infections
Confounding the prompt and accurate diagnosis of infectious complications
during this period of profound neutropenia is the fact that the usual signs Signs and symptoms of inflamma¬
and symptoms of inflammation are not likely to be evident. The clinical tion are less obvious with immu¬
nosuppression.
presentation of localized infection in neutropenic patients is often subtle.
Localized infections may elude diagnosis and be discovered only at autopsy.
In neutropenic patients, erythema and pain seem to be the only reliable
indicators of localized infection. The other classic signs of localized infections,
such as exudates, local warmth, edema and swelling, regional adenopathy,
cough, sputum production, sputum purulence, and radiographic air-fluid
levels, are all less prevalent. The degree of subtlety of these latter signs is
directly proportional to the degree of patient neutropenia, with a major
reduction of these signs and symptoms occurring with an absolute neutrophil
count of 0 to 100/cu mm.
Otitis Media
This is a relatively infrequent problem. Again, pain and erythema are the
only reliable clinical signs. Pain is sometimes misleading in patients who
have a concurrent oral or pharyngeal mucositis, which may cause referred
pain in the ear. Tympanic membrane retraction is minimal, and frank
effusion is seldom seen at the time of either otoscopy or myringotomy.
When otitis media is suspected in the presence of an otherwise unexplained
fever, the patient ought to undergo bilateral tympanocentesis with saline
lavage and aspiration of the middle ear clefts to obtain a Gram’s stain, a
KOH preparation, and cultures for aerobes, anaerobes, and fungi. A solution
of 90 per cent phenol can be applied to the myringotomy site for hemostasis
372 PART FOUR—THE ORAL CAVITY AND PHARYNX
Otomycosis
A fungal infection of the external auditory canal in an immunologically
normal patient is called an otomycosis and usually represents a harmless
saprophytic growth that often resolves without treatment. In the bone
marrow recipient, however, fungal infection of the external auditory canal
can persist and spread to involve the middle ear and mastoid. The fungi
invade the vasculature of the infected part of the ear and cause tissue
destruction by infarction and secondary necrosis. The facial nerve can be
involved directly by fungal invasion or indirectly by infarction to yield a
facial nerve paralysis. Aspergillus species seem to be the most common
pathogenic organisms, although infections with Scopulariopsis and Coccidi-
oides have occurred.
The usual presentation of a complicated otomycosis in a bone marrow
recipient is a dry, gangrenous involvement of the external auditory canal.
Some granulation tissue may be present, and there is often anesthesia of the
uninvolved portions of the ear canal. Middle ear or mastoid involvement
should be suspected in the presence of a tympanic membrane perforation.
In the presence of an intact tympanic membrane, hearing loss, facial nerve
paresis, or pain out of proportion to the physical findings should similarly
raise the suspicion of middle ear or mastoid involvement.
Prompt and aggressive surgical debridement of the external auditory canal
should be performed. When indicated, middle ear exploration or a mastoid-
otomy should be performed to obtain mucosal specimens for fungal cultures
and fungal stains. When mastoid involvement is proved, a radical or modified
radical mastoidectomy should be performed to allow aeration and inspection
of the entire mastoid cavity. Systemic antifungal agents and granulocyte
infusions are the usual medical adjuncts, as for any fungal infection in a
bone marrow recipient.
Sinusitis
The majority of cases are bacterial in origin, and the causative bacteria
usually are the ones encountered in a routine practice. The presentation of
Mucosal thickening is the usual sinusitis is almost always the radiographic detection of maxillary sinus
presentation of maxillary sinusi¬ mucosal thickening in a patient with an unexplained fever. Air-fluid levels
tis in the immunocompromised
host. are rarely seen. The clinical examination is usually unremarkable. If the
fever persists, surgical intervention is the treatment of choice when the
patient is expected to remain profoundly neutropenic for at least several
more days, surgical intervention in the form of nasoantral windows allows
representative cultures, prompt and effective treatment of the sinusitis, and
a biopsy of diseased mucosa for detection of any possible invasive fungal
elements. Thus, sinus lavage or aspiration is an insufficient treatment.
Aspergillus is the most common Fungal sinusitis is relatively infrequent but not rare. It is the most lethal
fungus causing sinusitis.
sinus infection, with the mortality rate for fulminant necrotizing aspergillosis
18—INFECTIONS IN THE IMMUNOCOMPROMISED HOST 373
being estimated as high as 80 per cent. Fusarium species are less common
pathogens but also cause a fulminant form of infection. Penicillium and
Alternaria are relatively uncommon fungal pathogens. These latter organisms
tend to cause indolent and less aggressive disease, although they invade local
blood vessels also.
Early diagnosis of fungal sinusitis requires a high index of suspicion and a
careful clinical examination. Early ethmoid sinusitis often presents as a black
necrotic patch of mucosa, which may be only several millimeters in diameter,
on the anterior end of the middle turbinate or as a slight erythema at the
medial canthal area. Early maxillary sinusitis presents as erythema or
tenderness over the cheek. In a neutropenic patient, fungal sinusitis can
demonstrate a unilateral opacified antrum, and this is usually not the case
with a bacterial pathogen.
Since Aspergillus and Fusarium species seem to be the most common
fungal pathogens, surgery is the treatment of choice to interrupt a potentially
fulminant infection that can rapidly spread to the orbit, facial soft tissues,
and central nervous system. The surgical treatment should be identical to
that for mucormycosis of the paranasal sinuses. The surgical treatment is
justified even though the specific fungus may not have been identified or
speciated at the time of surgery. A delay of even several days can allow
rapid local spread, aerosol dissemination to the lungs, and hematogenous
spread to distant organs.
Once engraftment occurs, adequate numbers of circulating neutrophils
halt local progression and dissemination so that the disease may become
indolent. Reactivation can occur later on in the sinuses previously affected
if the patient subsequently develops severe GVHD, requires immunosup¬
pressive agents, or again becomes severely neutropenic.
Rhinitis
Bacterial and fungal infections can occur on the nasal septum. It appears
that only the fungal infections assume any clinical importance, since, as in
fungal sinusitis, local tissue destruction can occur. The infection can spread
distally to the soft tissues of the face (Fig. 18-1) or can spread proximally
to the cribriform plate. The fungal infection of the septum can be detected
as a dry, dark or black patch of anesthetic mucosa, most commonly occurring
at the area of Kiesselbach’s plexus. A wide septectomy is usually indicated.
Laryngitis
Upper airway problems are usually due to the extension of infectious
problems in the mouth and nasopharynx. With the breakdown of mucosal
barriers, oral infections with Candida or herpes simplex virus are common.
Obstructive laryngitis can be caused by these organisms as well as by
Aspergillus. The respiratory obstruction is seldom due to airway edema, but
rather to marked mucosal ulceration resulting in the formation of obstructing
crusts, pseudomembranes, or casts caused by bleeding, serous exudation, or
the sloughing of necrotic tissue (Fig. 18-2). The performance of an urgent
tracheostomy can be especially treacherous, since the obstructing crusts can
extend well below the site of the tracheostomy. In such a situation, surgical
entry into the trachea can precipitate total acute airway obstruction, which
374 PART FOUR—THE ORAL CAVITY AND PHARYNX
Esophagitis
This is most frequently caused by Candida species and often results from
the swallowing of Candida-contaminated saliva. Some patients are asymp¬
tomatic, whereas others complain of dysphagia or burning retrosternal pain.
Cervical Cellulitis
LATE INFECTIONS
Sinusitis
Sinusitis is usually due to bacteria, and the pathogens tend to be the ones
encountered in a routine practice such as Haemophilus influenzae, Strepto¬
coccus pneumoniae, and Staphylococcus aureus. These infections are appro¬
priately treated with an antral lavage and antibiotics chosen according to
sensitivity testing. More unusual organisms such as Klebsiella and Gardnerella
18—INFECTIONS IN THE IMMUNOCOMPROMISED HOST 377
Children
In HIV-infected children, recurrent otitis media and chronic sinusitis can
be presenting illnesses before the onset of opportunistic infections or the
definitive diagnosis of AIDS. For children with these types of infections, it
is recommended that a careful history be taken for blood transfusions and
to assess whether the parents are at risk for AIDS.
Infections are a major source of morbidity in the patient with cancer and
often are the major cause of death. Cancer patients are susceptible to
infectious complications due to altered host defense mechanisms, which may
be deficient secondary to the malignancy itself or to its treatment.
Immunologic Milieu
A number of immune functions can be adversely affected by cancer
therapy.
Granulopoiesis, of course, can be inhibited by cytotoxic agents and gran-
378 PART FOUR—THE ORAL CAVITY AND PHARYNX
Infections
Sinusitis is frequent in the cancer patient undergoing chemotherapy. When
the symptoms appear chronic, the possibility of anaerobic bacteria must be
entertained and appropriate cultures obtained and antibiotics chosen. It
appears that anaerobic pathogens can be isolated in at least 50 per cent of
the cases of chronic maxillary sinusitis. Fungal sinusitis is common in the
cancer patient also. The incidence of Aspergillus infection seems to be
increasing, and one cancer treatment center has reported that 20 per cent of
adults with acute leukemia developed Aspergillus sinusitis during a five-year
period (Fig. 18-3).
Esophagitis is most commonly caused by Candida, but herpes simplex
virus and bacteria can also be etiologic agents.
In general, the greater the degree of neutropenia, the more likely the
infectious complications will resemble those in the bone marrow transplant
recipient, both in the types of etiologic organisms and in the subtlety of
clinical presentation.
The most common recurrent head and neck infections in children with
congenital immunodeficiency diseases are rhinitis, sinusitis, tonsillitis, and
suppurative otitis media. The majority of these children who present to the
otolaryngologist already have a known and proven diagnosis of the immu¬
nodeficiency disease.
Nevertheless, a small but significant number present with the basic
immunologic abnormality undiagnosed. To aid in the identification of pa¬
tients who deserve an immunologic evaluation, careful attention should be
paid to certain factors in the history and physical examination. These include
a family history suggestive of immune deficiencies, a history of other
recurrent infectious processes such as skin infections or recurrent pneumonias
18—INFECTIONS IN THE IMMUNOCOMPROMISED HOST 37y
FIGURE 18-3. Giemsa silver stain demonstrating Aspergillus organisms in the mastoid cavity of a patient
with acute leukemia.
References
Berkow RL, Wisman SJ, Provisor AJ, et al: Invasive aspergillosis of paranasal tissues in
children with malignancies. J Pediatr 103:49-53, 1983.
Berlinger NT: Sinusitis in immunodeficient and immunosuppressed patients. Laryngoscope
95:29-33, 1985.
Harris JP. South MS: Immunodeficiency diseases: Head and neck manifestations. Head Neck
Surg 5:114-124, 1983.
380 PART FOUR—THE ORAL CAVITY AND PHARYNX
Marcusen DC, Sooy CD: Otolaryngologic and head and neck manifestations of acquired
immunodeficiency syndrome (AIDS). Laryngoscope 95:401-405, 1985.
McGill TJ, Simpson G, Healy GB: Fulminant aspergillosis of the nose and paranasal sinuses:
A new clinical entity. Laryngoscope 90:748-754, 1980..
Shannon KM, Ammann AJ: Acquired immune deficiency syndrome in children J Pediatr
106:332-342, 1985.
Wong KK, Hirsch MS: Herpes virus infections in patients with neoplastic disease: Diagnosis
and therapy. Am J Med 76:464-478, 1984.
PART FIVE
THE LARYNX
19
ANATOMY AND
PHYSIOLOGY OF THE LARYNX
*>«/ lames I. Cohen, M.D., Ph.D.
Embryology
The pharynx, larynx, trachea, and lungs are derivatives of the embryonal
foregut, which appears at about 18 days after conception. Soon thereafter,
the median pharyngeal groove arises, containing the first indications of the
respiratory system and the anlage of the larynx. The laryngotracheal sulcus
or groove then becomes apparent at around 21 days of embryonic life (Fig.
19-1). Caudal expansion of this groove represents the pulmonary primor-
dium. It deepens and becomes saclike and then bilobed at 27 to 28 days.
The most proximal portions of this enlarging tube will become the larynx.
The arytenoid swellings and the epithelial lamina are recognizable by 33
days, and the cartilages and muscles, including vocal folds for the most part,
develop during the subsequent three to four weeks.
Only the cartilage of the epiglottis does not appear until midfetal life.
Since the development of the larynx is closely linked to the development of
the branchial arches of the embryo, many of the laryngeal structures are
derivatives of the branchial apparatus.
Arytenoid
swellings
383
384 PART FIVE—THE LARYNX
Incomplete closure of the cri- Defective development may result in a variety of abnormalities that can
fSSSS/S be dia8nosed by direct examination of the larynx. The larynx itself may be
small, or there may be a variable degree of webbing between the true vocal
cords. Rarely, the posterior arm of the T of the laryngotracheal sulcus may
persist, leaving an opened laryngeal cleft between the esophagus and trachea.
Laryngomalacia, an abnormal degree of flaccidity in the laryngeal framework
which allows it to collapse during respiration, is the most common congenital
laryngeal abnormality seen as a cause for stridor in the newborn. It is almost
always a benign self-limiting condition that will resolve with growth and
development. Developmental disorders of the larynx are discussed in Chapter
20; disorders of the esophagus and tracheobronchial tree are discussed in
Chapter 24.
Supporting Structures
The laryngeal skeletal structure is composed of one bone and several
paired and unpaired cartilages (Fig. 19-2). Superiorly is the hyoid bone, the
U-shaped structure that can be palpated both anteriorly on the neck and
transorally in the lateral pharyngeal wall. Extending from each side of the
central portion, or body, of the hyoid bone is a posteriorly directed long
process and a small, superiorly oriented short process. Attached to the
superior surface of the body and to both processes are tendons and muscles
from the tongue, mandible, and skull. During swallowing, contraction of
these muscles elevates the larynx. However, when the larynx is stabilized,
these muscles open the mouth and contribute to tongue motion. Inferior to
the hyoid bone, and suspended by the thyrohyoid ligament, are the two
alae, or wings, of the thyroid (shield) cartilage. The alae join in the midline
at an angle that is more acute in the male, producing the visible “Adam’s
apple. On the posterior border of each ala are the superior and inferior
cornua. The inferior cornu articulates with the cricoid cartilage, allowing a
small amount of gliding and rocking between the thyroid and cricoid
cartilages.
The cricoid cartilage, also easily palpable subcutaneously, is attached to
the thyroid cartilage by the cricothyroid ligament. Unlike all other supporting
Sup. cornu
Sup. rhqroid
not-ch
Comicu/ate Arytenoid FIGURE 19—2. The cartilages of the lar¬
cart. ' 1 ynx. (Redrawn from Turner.)
M Muscular
process Vocal process
_Th toroid artic¬
ular surface
Oblique line Inf. cornu Arch
Laryngeal Musculature
The laryngeal muscles may be divided into two groups (Fig. 19-3). The
extrinsic muscles act mainly on the larynx as a whole, whereas the intrinsic
muscles cause movements between the various laryngeal structures them¬
selves. The extrinsic muscles may be categorized by function. The depressors,
or strap muscles (omohyoid, sternothyroid, sternohyoid), originate inferiorly.
The elevators (mylohyoid, geniohyoid, genioglossus, hyoglossus, digastric,
stylohyoid) extend from the hyoid bone to the mandible, tongue, and styloid
process of the skull. The thyrohyoid, although considered a strap muscle,
functions mainly as an elevator. Attached to the hyoid bone and posterior
386 PART FIVE—THE LARYNX
Transverse arqtenoid m
Arqopfqlottic m.
Post, crico¬
ot rqtenoid m. FIGURE 19-3. The appearance of
the larynx and attached trachea
after removal of all but the muscular
and ligamentous structure, a, Side
view; b, posterior view; c, a dia¬
grammatic representation of the ar¬
Thqro-arqtenoid m. Thqroid cart. rangement of the intrinsic muscles;
d and e, position, attachments, and
Lat. crico-
arqtenoid m.
action of the cricothyroid muscle.
(Redrawn from Turner.)
Crico-
thqroid m
Arqtenoid m.
edge of the thyroid cartilage alae are the middle and inferior constrictors,
which encircle the pharynx posteriorly and function during swallowing. The
lowermost fibers of the inferior constrictor arise from the cricoid to form the
strong cricopharyngeus, which serves as the upper esophageal sphincter.
The anatomy of the intrinsic laryngeal musculature is best understood by
relating it to function. Extending between the two arytenoids are the
transverse and oblique fibers of the interarytenoid (or arytenoid) muscle.
When it contracts, the arytenoid cartilages glide toward the midline, ad¬
ducting the cords. The posterior cricoarytenoid muscle extends from the
posterior surface of the cricoid lamina to insert on the muscular process of
the arytenoid; it rotates the arytenoid outward, abducting the vocal cord. Its
main antagonist, the lateral cricoarytenoid, takes origin on the lateral cricoid
arch; it inserts also on the muscular process and rotates the arytenoid
medially, causing adduction. Making up the bulk of the vocal cords are the
barely separable vocalis and thyroarytenoid muscles, which contribute to
cord tension. In older individuals, the vocalis and thyroarytenoid muscles
may lose some tone; the cords appear bowed outward, and the voice becomes
weak and hoarse. The other major laryngeal muscles are the paired crico¬
thyroids, fan-shaped muscles that originate anteriorly from the cricoid arch
The cricothyroid muscle tenses and insert on the broad lateral surface of the thyroid alae. Contraction of
the vocal cords, this muscle pulls the thyroid cartilage forward, stretching and tensing the
cords. This also tends to passively rotate the arytenoid medially, so the
cricothyroid is also considered an adductor. In summary, then, there are
19—ANATOMY AND PHYSIOLOGY OF THE LARYNX 387
one abductor, three adductors, and three tensors, all of which are listed as
follows:
Because of the longer course of the left inferior nerve and its relationship
to the aorta, it is more vulnerable to injury than the right.
The superior laryngeal nerve, The arterial supply and venous drainage of the larynx closely parallel the
superior laryngeal artery, and
nerve supply. The superior laryngeal artery and vein are branches of the
vein enter the larynx laterally
between the hyoid bone and superior thyroid artery and vein, and they join the internal branch of
thyroid cartilage. the superior laryngeal nerve to form the superior neurovascular pedicle. The
inferior laryngeal artery and vein arise from the inferior thyroid vessels and
enter the larynx alongside the recurrent laryngeal nerve.
Knowledge of the lymphatic drainage of the larynx is important in cancer
therapy. There are two separate drainage systems, superior and inferior,
with the dividing line being the true vocal cord. The cords themselves have
a poor lymphatic supply. Superiorly, the flow accompanies the superior
neurovascular pedicle to join the upper lymph nodes of the deep cervical
chain at the level of the hyoid bone. The subglottic drainage is more diverse,
going to the pretracheal nodes (one in particular is just anterior to the cricoid
and is called the Delphian node), the lower deep cervical nodes, the
supraclavicular nodes, and even the superior mediastinal nodes.
Med. qioaao-
«pm»*t5c -pi*co*
Vent, of
‘allfCuks
t&opH,
intro-
- itus
19—ANATOMY AND PHYSIOLOGY OF THE LARYNX 389
Surrounding Structures
Anteriorly, the isthmus of the thyroid gland covers the first few tracheal
rings, while the thyroid lobes rest on the lateral tracheal wall and may even The thyroid isthmus is elevated
extend up onto the thyroid alae. The isthmus must be elevated, and or incised during tracheostomy.
occasionally incised, when placing a tracheostomy through the third tracheal
cartilaginous ring. The strap muscles cover the larynx and thyroid gland
except in the midline, where the median raphe places the laryngeal structures
in a subcutaneous position. The cricothyroid membrane is easily palpable
and, in an emergency, can be rapidly incised to establish an airway. Not
infrequently, the innominate artery passes anteriorly to the cervical trachea,
necessitating careful palpation during any tracheostomy procedure. Lateral
and posterior to the larynx are the carotid sheaths, each containing the
carotid artery, jugular vein, and vagus nerve.
Elevation of the larynx under the base of tongue further protects the larynx
as it serves to push the epiglottis and aryepiglottic folds down over the inlet.
These structures then divert food laterally away from the laryngeal inlet into
the pyriform sinuses and through the esophageal introitus. Simultaneous
relaxation of the cricopharyngeal muscle promotes the passage of food into
the esophagus rather than the larynx. In addition, respiration is inhibited
during swallowing owing to a reflex mediated by receptors present in the
mucosa of the supraglottic area. This prevents inhalation of food or saliva.
In animals such as the deer the epiglottis extends superiorly to contact the
nasal surface of the soft palate. This configuration allows simultaneous
breathing while eating so that the animal can still smell and thus protect
itself while grazing. Similarly, in infants, the higher position of the larynx
allows contact of the epiglottis with the posterior surface of the soft palate.
They are thus able to breathe while nursing without passage of food into the
airway.
During respiration, the intrathoracic pressure is controlled by varying the
degree of closure of the true vocal cords. This modulation of pressure assists
the cardiac system inasmuch as it affects pulmonary and cardiac filling and
emptying. In addition, the intrinsic design of the true and false vocal cords
allows the larynx to serve as a pressure valve that, when closed (Fig. 19-6),
allows the build-up of intrathoracic pressure necessary for straining acts such
as lifting or defecation. Sudden release of this pressure produces a cough,
which is useful in maintaining the expansion of the terminal alveoli of the
lungs and clearing any secretions or food particles that end up in the
laryngeal inlet despite all the other protective mechanisms mentioned above.
Voice production, however, is perhaps the most complex and certainly
the best studied of the laryngeal functions. The advent of fiberoptic viewing
systems and stroboscopes that can be coordinated with voice frequency has
helped a great deal in understanding this phenomenon. It is currently thought
that the adducted true vocal cords serve as a passive reed that vibrates as a
result of the air forced up between them by contraction of the expiratory
muscles. The fundamental tone that is produced can be modified in a number
of ways. The intrinsic muscles of the larynx (and the cricothyroid) play a
major role in the adjustment of pitch by changing the shape and mass of the
free edges of the true vocal cords and the tension in the cords themselves.
The extralaryngeal muscles may also play a role. Also, because of the lower
position of the larynx in humans, a large portion of the pharynx is available,
in addition to the nasal cavity and paranasal sinuses, for modulation of the
tone produced by the larynx. All of this is monitored by a feedback
mechanism consisting of the human ear and a system within the larynx itself
which is poorly understood. By contrast, the loudness of the voice is
essentially proportional only to the pressure in the subglottic airstream that
is setting the true vocal cords in motion. Whispering, on the other hand, is
believed to be due to escape of air through the posterior commissure between
the abducted arytenoids without vibration of the true vocal cords themselves.
Any disease that affects the action of the intrinsic and extrinsic muscles
of the larynx (nerve paralysis, trauma, surgery) or the mass of the true vocal
cords (i.e., vocal cord polyps or carcinoma) affects laryngeal function, and
disorders of either swallowing (i.e., aspiration) or voice will result. Such
disease processes will be discussed in detail in subsequent chapters.
References
Crelin ES: Development of the upper respiratory system. CIBA Clinical Symposia, Vol 29, No
4, 1977.
Fink RB, Demarest RJ: Laryngeal Biomechanics. Cambridge, MA, Harvard University Press,
1978.
Hollinshead HW: Anatomy for Surgeons, Vol 1: The Head and Neck. New York, Harper and
Row, 1968.
Kirchner JA: Physiology of the larynx. In Paparella MM, Shumrik DA (eds): Otolaryngology.
Philadelphia, WB Saunders Co, 1980, pp 377-388.
O’Rahilly R, Tucker JA: The early development of the larynx in staged human embryos. Ann
Otol Rhinol Laryngol 82 (Suppl 7):1—27, 1973.
Tucker HM: Monographs in Clinical Otolaryngology—-Surgery for Phonatory Disorders, Vol
3. New York, Churchill Livingstone, 1981, pp 6—11.
Van Alyea OE: The Embryology of the Ear, Nose, and Throat. Rochester, MN, American
Academy of Ophthalmology and Otolaryngology, 1944.
Wyke BD, Kirchner JA: Laryn-Neurology. In Hinchcliffe R, Harrison D (eds): Scientific
Foundations of Otolaryngology. Chicago, Year Book Medical Publishers, 1976, pp 546-573.
20
BENIGN
LARYNGEAL DISORDERS
by John D. Banovetz, M.D.
PATIENT COMPLAINTS
Incorrect
larynx. A chest film may also help localize stridor to upper or lower airway.
Computed tomography and magnetic resonance imaging are valuable in
evaluating masses because they accurately visualize laryngeal spaces and
detect changes in laryngeal cartilages not visible by other means. Esopha-
gograms, particularly those done with videoradiography, are also useful.
Voice recordings can also be diagnostic of the type of vocal disorder and
can be used to compare pre- and postoperative status.
CONGENITAL ANOMALIES
The normal infant larynx is situated higher in the neck than that of the
adult. The infant larynx is softer, less rigid, and more compressible by airway
pressures. In the infant, the larynx is at the level of C2 to C4, whereas in The infant larynx is located
the adult it lies anterior to C4 to C6. The size of the newborn larynx is more superiorly in the neck.
approximately 7 mm in the anteroposterior length and opens approximately
4 mm in a lateral direction. The symptoms that arise from disease here
concern respiratory obstruction, dysphagia, the quality of cry or noise
produced, and a failure to thrive. Airway obstruction may in itself lead to a
failure to thrive, which may be more obvious than the airway obstruction.
Laryngomalacia
There is no underlying pathologic or progressive disorder in laryngoma¬
lacia. Rather, it is an exaggeration of the soft, flabby state that is normal
for newborns. As the infant inhales, the soft larynx falls together, narrowing
the inlet, and stridor results. Swallowing is unaffected. The cry should be
normal. The weight gain and development of these infants are usually
normal. Stridor is the major symptom, and it may be constant or may occur
only with excitement. With the stridor may come retraction of the sternum Laryngomalacia is usually not
and chest; laryngomalacia has been named as a cause of pectus excavatum. apparent until a few weeks of
Usually infants are several weeks old when laryngomalacia begins, in contrast
to the respiratory distress syndrome of the newborn. On direct examination
the physician can see the larynx fall together with inhalation. The subglottic
394 PART FIVE—THE LARYNX
area is normal, and the stridor ceases if the larynx is held open with a
laryngoscope. The prognosis is good for this most common laryngeal anom¬
Laryngomalacia can be associ¬ aly, as the cartilages gain rigidity. Most infants cease to have the stridor by
ated with a second upper airway
the twelfth to fifteenth month. Twenty per cent of infants with laryngomalacia
abnormality.
have an additional cause of airway obstruction.
Tracheomalacia is a similar disorder of the trachea due to lack of rigidity
of the tracheal cartilages. Tracheomalacia and compression of the airway by
an anomalous great vessel are similar conditions and must be differentiated.
This can usually be done endoscopically. Arteriograms may be necessary to
effectively study the great vessels. Esophagograms also help delineate
vascular abnormalities, especially anomalous vascular rings.
Webs
Congenital webs may be glottic (75 per cent), subglottic (12 per cent), or
supraglottic (12 per cent). Usually both the airway and the cry or voice are
affected, with the symptoms beginning at birth. Webs must first be diagnosed
by endoscopic visualization. Then treatment, consisting of laser or surgical
excision, repeated dilatation, or tracheotomy and the use of laryngeal inserts,
can be accomplished. The long-term prognosis for congenital laryngeal webs
is favorable.
Congenital Cysts
Newborns who have congenital cysts usually have airway obstruction or
simply do not grow. The episodes of airway obstruction can be confusing
and may be thought to be due to a seizure disorder. Usually the voice and
swallowing are normal. The cyst may arise from the base of the tongue, the
aryepiglottic folds, or the false cords. Whenever possible, these cysts should
be excised, preferably endoscopically. If this is not possible, then aspiration
or marsupialization may be done. In an exceptional patient tracheotomy and
external surgery are necessary.
Hemangioma
Hemangioma of the subglottic area of the larynx is considered here
because it is a tumor that occurs primarily in infants under six months of
age. Half of the patients with laryngeal hemangiomas have an external
hemangioma on the head or neck. Stridor plus a visible hemangioma strongly
suggests this diagnosis. These tumors are not true neoplasms but rather
20—BENIGN LARYNGEAL DISORDERS 395
Laryngocele
Laryngocele is a special type of congenital cyst that develops as a residual
from a small appendix or saccus of the laryngeal ventricle. Like a thyroglossal
duct, it may present at any age, but its origin is congenital. As the cyst
begins, it first causes a bulging of the false vocal cord on that side. With
enlargement, the cyst dissects along the superior laryngeal nerve and vessels
to present as a mass in the neck. Since this cyst may communicate with the
airway, a radiograph may show an air-fluid level. These cysts do not
necessarily contain air but may be solid, containing only fluid. As they
enlarge, they encroach on the airway and may cause stridor and airway
obstruction. The diagnosis can be suggested by aspirating the mass with a
large needle. The only effective treatment for laryngocele is dissection of
the cyst, using an external approach. Usually this is accompanied by a
temporary tracheostomy.
Laryngotracheoesophageal Cleft
This rare congenital abnormality is a result of a failure of fusion of the
dorsal portions of the cricoid cartilages. There is an associated failure of
closure of the tracheoesophageal septum, thus creating a groove in the
region of the cricoid cartilage that resembles in many respects the more
common H-type tracheoesophageal fistula. The infant may have cyanosis,
respiratory distress, and recurrent episodes of pneumonia. In addition, there Clefts may not be apparent on
may be associated changes in the cry as well as inspiratory stridor. Direct routine direct laryngoscopy.
vocal cord dysfunction. Infants with unilateral vocal cord paralysis may show
varying symptoms. In many the cord is lateral enough to give a breathy poor
cry but no respiratory distress. Other infants may have the cord median
396 PART FIVE—THE LARYNX
Children with bilateral vocal enough so as to limit respiratory exchange. Stridor, especially with crying or
cord paraylsis can have a nor¬
mal cry.
activity, results. Infants with bilateral vocal cord paralysis have a good cry
but poor respiratory exchange and need prompt airway support. An endo¬
tracheal tube forced between the cords gives short-term relief, but trache¬
otomy is necessary eventually. Paralysis often recovers in 6 to 9 months but
may take up to 14 months. The tracheotomy is left until the airway enlarges
by growth, reinnervation, or a lateralization procedure.
LARYNGEAL TRAUMA
Laryngeal Fracture
Sharp compression of the larynx, hyoid, and upper trachea between the
cervical spine and the unyielding force of an automobile or motor bike can
cause a fracture. Hyoid fractures usually do not cause airway obstruction,
since the pharynx is very wide at this level. The greater cornu of the hyoid
does not normally unite to the body until age 35. This fact must be known
when radiographs of the hyoid are interpreted. Actual separation of the
greater cornu from the body must occur before a fracture can be diagnosed
here. The epiphyseal line is not a fracture line. Treatment of hyoid bone
fractures can usually be expectant.
Signs of laryngeal fracture: Fractures of the thyroid cartilage itself are common. These injuries are
hoarseness, stridor, hemopty¬
sis, subcutaneous emphysema. characterized by (1) a history of a blow to the neck, (2) hoarseness, (3)
inspiratory or expiratory stridor (or both), (4) hemoptysis, and (5) subcuta¬
neous emphysema. The most likely fracture runs in a vertical plane from the
bottom of the thyroid notch to the lower border of the cartilage. Avulsion
of the thyroid cartilage from the cricoid and trachea may also occur. Facial
pain, aphonia, and subcutaneous emphysema are the most common symp¬
toms. Airway obstruction may develop explosively. On palpation, the
cervical area is usually flat and there is loss of the prominence of the thyroid
When laryngotracheal separa¬ cartilage and cricoid. These patients, if not unconscious, are nearly impos¬
tion occurs, the trachea will re¬
tract into the lower neck. Emer¬ sible to examine with a mirror because their pain and hematoma are too
gency tracheostomy is required. great. If fracture is suspected and the thyroid cartilage is not palpated,
tracheostomy should be done. Intubation is hazardous in these patients,
since it may be impossible to do without compromising the little remaining
airway. Tracheostomy under local anesthesia is preferred in these injuries.
20—BENIGN LARYNGEAL DISORDERS 397
Scar tissue narrowing the airway is a sequela of disease or injury, and its
treatment is extremely difficult. Blunt or perforating trauma, high tracheot¬
omy, caustic ingestion, a gunshot wound, and irritation from an endotracheal
tube cuff are the more common causes of laryngeal stenosis. Usually patients
who require long-term endotracheal intubation with cuffed tubes are des¬
perately ill, and the laryngeal stenosis occurs as a result of the heroic therapy
they receive. Because of its more resilient cartilage, the child’s larynx is
more forgiving in long-term intubation than are those of adults. CT scans
can be used to delineate laryngeal and subglottic stenosis. Nevertheless,
cuffed endotracheal tubes should be used for as short a time as possible with
the cuff deflated intermittently. Low-pressure cuffs lessen but do not com¬
pletely prevent stenosis. Cuffed tubes should be made of new, nonirritating
plastic and should be free of sterilization gas contamination before being
used. Treatment of chronic laryngeal stenosis is very complicated and must
be individualized. Dilatation, excision, direct re-anastomosis, skin grafting
over a mold, and partial or total laryngectomy are all used.
Intubation Granuloma
Croup
Croup is a rapidly developing infection of the larynx resulting in stridor
and airway obstruction. Although it can develop at any age, even in adults,
croup is most common in children under six years of age.
Both the laryngeal surface of the epiglottis and the area just below the
vocal cords in the larynx contain loose areolar tissue that is prone to swell
when inflamed. Flence, croup can be divided into acute supraglottitis
(epiglottitis) and acute subglottic laryngitis. Although both can be rapid in
onset and severe, acute epiglottitis tends to be more explosive, often
terminating fatally in a few hours without treatment. Both disorders appear
clinically the same—with restlessness, apprehension, stridor, retraction, and
cyanosis—but there are some subtle differences. A child with epiglottitis
tends to sit up with mouth open and chin forward, is not hoarse, tends not
to have as croupy a cough, but is more likely to have dysphagia. Because it
is painful to swallow, the child may drool. Dysphagia in epiglottitis may be
a sign of impending collapse. It results from spread of inflammation into the
adjacent esophageal inlet and means that the inflammatory process has
swollen the epiglottis markedly.
Children with acute subglottic laryngitis are hoarse with a very croupy
cough and usually want to lie down. Other characteristics that differentiate
these two forms of croup are listed in Table 20-1.
These children must be rapidly treated without long delay in the radiology
or emergency department and must not be upset or agitated. A soft tissue
lateral radiograph of the neck may show narrowing of the subglottic area or
Arterial blood gas studies are of an enlarged epiglottis. A chest radiograph should be normal but is taken to
little value in acute upper air¬ rule out pneumonia, the presence of a foreign body, or asthma. Blood gas
way obstruction.
studies and the finding of leukocytosis are academically interesting, but in
the rapidly changing child results are not obtained in time to aid in planning
treatment. Depressing the tongue to see the epiglottis may force the swollen
epiglottis into the larynx like a cork and should not be done unless one is
equipped to pass a bronchoscope or endotracheal tube.*
Treatment must begin quickly. Intravenous fluid therapy is started in order
to prevent dehydration and drying of secretions. Cold, moist humidity,
Blood culture may isolate H. in¬ preferably with the smallest particulate size of water vapor, is necessary.
fluenzae. Antibiotic therapy to actual Haemophilus or Staphylococcus is initiated while
awaiting the culture results. Antibiotics should not be withheld because,
clinically, it may be difficult to distinguish between the types of croup, and
the course can be very rapid. While smears and cultures should be taken,
their results arrive too late to be of value. Steroids are given in large doses
to reduce inflammation. The patient must be carefully observed and consid¬
eration given to intubation or tracheostomy. The indication for airway
Onset hours Onset days 1-2 week period ol Rapid onset, usually
respiratory infection evening
with rapid deterioration
support is deterioration in spite of humidity, antibiotics, and steroids. To Acute epiglottitis can occur in
30-to 40-year-old adults.
evaluate the croup one must monitor pulse, respiratory rate, degree of
restlessness and apprehension, the use of accessory muscles of respiration,
the degree of cyanosis, the degree of retraction, and the overall fatigue of
the patient. If the patient can sleep, airway support is not necessary. On the
other hand, a respiratory rate over 40, a pulse rate greater than 160, and
increasing restlessness and retraction indicate the need for support.
Some authors recommend sedation for croup patients, but it is our belief In selecting an antibiotic for H.
that no sedation or narcotics should be given. The status of the patient influenzae supraglottitis, recog¬
nize that 20 per cent of organ¬
should be watched at all times. Croup is one of the few disorders that require isms are ampicillin resistant.
the physician to be in constant attendance at the bedside. Racemic epineph¬
rine given by inhalation has been valuable, especially in laryngotracheobron-
chitis, and has reduced the need for airway support. Intubation or trache¬
otomy can be used to maintain the airway. If the child collapses, an Ambu
respirator with positive pressure is used to force oxygen through the
edematous airway. ^lasal intubation can be accomplished and may remain
for days. Children’s larynges allow longer intubation than do adults’. When
it must be done, tracheotomy should be performed in an orderly manner in
an operating room over a tube. Most cases of croup resolve in 48 to 72
hours and the patient can be extubated. Chest radiography must be done
after tracheotomy because, especially in children, the pleura rises into the
neck. Its injury results in pneumothorax.
400 PART FIVE—THE LARYNX
Acute Laryngitis
Vocal abuse, toxic fume inhalation, and infection produce acute laryngitis.
Usually the infection is not limited to the larynx but is a paninfection
involving the sinus, ear, larynx, and bronchial tubes. The influenza virus,
adenoviruses, and streptococci are the most common causative organisms.
Diphtheria must always be suspected in laryngitis, particularly if there is any
evidence of a membrane or lack of immunization history. Mirror examination
usually shows a diffuse erythema of the larynx. Cultures of the throat should
be taken. Treatment consists of voice rest, antibiotics, increased humidity,
and cough suppressants. Medications whose side effect is to cause drying
should be avoided in laryngeal treatment. Singers and voice professionals
must be advised to let the inflammatory process subside before resuming
their careers. Attempting to sing during the infection may result in hemor¬
rhage in the larynx and the subsequent development of vocal cord nodules.
Rheumatoid Arthritis
Because the cricoarytenoid joint is a true joint, it may be involved by a
rheumatoid process. Pain radiating to the ear, dysphagia, and hoarseness
are symptoms of acute cricoarytenoid arthritis. On visualization the affected
arytenoid is edematous, erythematous, and immobile. In order to differen¬
tiate a vocal cord paralysis from rheumatoid fixation the joint must be
palpated directly. In vocal cord paralysis the joint should move passively,
whereas it is fixed in an arthritis. In addition to systemic rheumatoid
treatment, steroids may be injected directly in and about the cricoarytenoid
joint.
Hypothyroidism
Infiltrative Disorders
The lesions of sarcoid and amyloid may infiltrate the larynx. If localized,
they can be surgically removed. Only 1.5 per cent of patients with sarcoidosis
have laryngeal involvement. The supraglottic larynx is primarily involved as
the true cords are spared. Patients present with hoarseness and dysphagia.
Endoscopic findings show diffuse edema without ulceration of the supraglot¬
tic larynx. Biopsy demonstrates noncaseating granulomas with giant cells.
Treatment requires systemic steroids or direct intralesional injection of
steroids. Obstructing lesions may require tracheostomy.
Histoplasmosis can cause simultaneous mucosal ulceration in the larynx
and oral cavity. These nodular ulcerations may be the initial sign of the
disease an^re often confused with carcinoma or tuberculosis. Diagnosis
depends upon identifying the fungus or detecting a serologic change.
20—BENIGN LARYNGEAL DISORDERS 401
Pemphigus vulgaris may affect the larynx primarily or may be associated Treatment of laryngeal pemphi¬
with oral mucosal involvement. Typical blebs are not seen in the larynx, but gus requires dapsone and ste¬
roids. Even then, cicatricial ste¬
the laryngeal surfaces are ulcerated or covered with a whitish membrane. If
nosis can result.
the associated findings and history suggest pemphigus, treatment should be
begun.
Androgen Therapy
Vocal Nodules
A variety of clinical synonyms exist for the vocal nodular polyp, including
screamer’s nodules, singer’s nodes, or teacher’s nodes. Benign nodules may
Vocal cord nodules that do not be unilateral and result from prolonged or improper use of the vocal cords.
respond to conservative treat¬ Often when there is some coexisting inflammation, the vocal cords strike
ment are excised by micro¬
scopic laryngoscopy. firmly together, causing formation of a polyp or nodule. The nodule may
vary histologically from a soft, loosely edematous tumor to a firm, fibrous
growth or a vascular lesion with many small vessels as its most outstanding
feature. Some patients respond to vocal restraint and re-education, but many
require endoscopic surgery.
Contact Ulcer
The mechanical action of the vocal cords against each other is more likely
to form vocal nodules in women and children, whereas in men it is more
likely to form a contact ulcer. Men forcefully bring the arytenoid cartilages
together, and the resulting irritation forms a granuloma called a contact
ulcer. Characteristically the patient complains of pain and notices only a
slight vocal change. Contact ulcers heal slowly, usually over two to three
months. Speech therapy usually aids their resolution. Biopsy is of value to
reduce some of the excessive granulation tissue and to give assurance to the
patient that the granuloma is not malignant.
Juvenile Papilloma
Papilloma is the most common tumor of the larynx in children. The onset
of the papilloma usually occurs in children between 18 months and 7 years
20—BENIGN LARYNGEAL DISORDERS 403
of age, and involution often occurs at puberty. The duration of the disorder
can extend over 10 years with many recurrent papillomas. Many children
require multiple hospital admissions to maintain the voice and airway.
Hoarseness and abnormal cry are the initial symptoms. Occasionally croup
is suspected, but the papilloma is diagnosed when there is no response to
therapy. Papillomas can enlarge to cause airway obstruction and present as
an emergency requiring tracheostomy. Papillomas can be hormone-depen¬
dent, regressing with pregnancy and puberty. If they persist into adult life,
they tend to be less aggressive and slower to recur. Papillomas are considered
to have a viral etiology, although the virus has not yet been isolated.
With such a socially devastating disease, requiring dozens of hospital
admissions in some patients, many treatments have been proposed. Irradia¬
tion has been discarded because of the late development of carcinoma. The
most effective current therapy is precise surgical removal, often using a
microscope with a C02 laser. In some cases a tracheotomy must be main¬
tained for years. Repeated surgical excisions can lead to laryngeal scarring
or webbing. Other therapies include tetracycline, steroids, smallpox vaccine,
autologous vaccines, and alpha Nj interferon. Fortunately, papillomas are
not common. Malignant transformation in the absence of irradiation is rare
and usually occurs in older patients with a history of smoking or long¬
standing papilloma.
Chondroma
Chondromas are slow-growing tumors of hyaline cartilage arising from the
cricoid, thyroid, arytenoid, or epiglottic cartilages. Hoarseness related to
restriction of the vocal cord and dyspnea due to airway obstruction are the
main symptoms. Many of these tumors are calcified and can be suspected
from radiographic examination. The treatment is surgical, with the origin
and the extent of the tumor determining the surgical technique. Because
these tumors are slow-growing, they can sometimes be partially removed,
relieving the patient’s symptoms without sacrificing the larynx.
Leukoplakia or Erythroplakia
Persistent irritation of the larynx, particularly by smoking, may lead to
the development of whitish areas. Clinically the whitish area is termed
leukoplakia. Paradoxically, areas with the histology and clinical significance
may appear reddened (erythroplakia). Any area of the larynx may be
involved, but usually the vocal cords are most affected. Commonly hoarse¬
ness is the patient’s complaint. Biopsy of these areas shows hyperkeratosis,
carcinoma in situ, or frank carcinoma. Hyperkeratosis is found in most
biopsies. Its treatment requires total endoscopic removal and careful follow-
404 PART FIVE—THE LARYNX
the surgical procedures that could be done transorally. Thus the carbon
dioxide laser has reduced the necessity for operative procedures on the
larynx.
Figures 20—2 and 20—3 explain the mechanism of the laser, which is an
acronym for “light amplification of stimulated emissions of radiation.”
Rather than allowing the light source to illuminate and propagate in multiple
directions with multiple light frequencies, the radiation is made (1) coherent
(that is, in phase), (2) collimated (parallel directions), and (3) monochro¬
matic (one frequency only). This creates a high-power density at one focal
spot. Whether a COz (Table 20-2) or a YAG laser is used, the light
generation in an active medium is the same. The operating room and the
patient are protected from any stray laser beams. The surgeon, sitting at the
head of the table and using the operating microscope, directs the beam onto
the area of tissue that is to be removed for biopsy or vaporized. Currently
the laser is frequently employed for the treatment of subglottic stenosis,
subglottic hemangioma, and most particularly, for the removal of juvenile
laryngeal papillomas.
Large benign laryngeal tumors require an external approach. Usually a
I I
Pathology Paralysis of cricothyroid Paralysis of all intrinsic Paralysis of all intrinsic Vagus nerve lesion above
muscle; sensory loss muscles on that side muscles the superior laryngeal
in half of larynx nerve; may be unilateral
or bilateral
Effect Loss of pitch; aspiration Hoarse; good airway Good voice; poor airway, Similar to corresponding
except in small children; especially on exertion lesions of recurrent
breathy voice; poor paralysis; more likely to
cough aspirate
Examination Anterior commissure Cord in paramedian Vocal cords do not move Cord(s) are immobile but
looks tilted to side of position; no lateral laterally; some patients in intermediate position
lesion; arytenoid on motion adapt and exist with due to loss of adduction
that side tilts in decreased exercise by cricothyroid muscle
tolerance
408 PART FIVE—THE LARYNX
Because of the small size of the glottis, unilateral paralysis,in a child may
compromise the airway to result clinically in stridor. Many patients recover
their vocal cord function either because the nerve recovers and again moves
the cord or because the opposite vocal cord compensates by crossing the
midline to once again firmly abut against the paralyzed cord. This is possible
if the paralyzed cord is in a paramedian position. Before restorative proce¬
dures are done, 6 to 12 months should elapse to allow time for compensation.
If these mechanisms do not occur, Teflon paste can be injected lateral to
the true cord to increase its bulk and move it medially so that the normal
moving cord can approximate, producing a pleasing voice (Fig. 20-5).
Bilateral vocal cord paralysis (Fig. 20-6) presents a different problem.
Because both vocal cords are usually in a paramedian position, the voice is
less affected, yet the glottic chink is not wide enough to permit any exertion.
The patient may even be dyspneic at rest. Usually patients with bilateral
cordal paralysis have vocal cords that are nearly together, and the majority
of them require a tracheostomy to relieve their airway obstruction. Very
rarely does a patient with a bilateral vocal cord paralysis have the cords
widely separated. Such adducted cords do not result from neurogenic lesions
but can result from laryngeal trauma. In this case the airway is satisfactory,
but the voice is weak and breathy. More commonly in bilateral paralysis
from neurologic lesions, the vocal cords are adducted, and the patient has a
good voice with a very poor airway. These patients often require a trache¬
ostomy. A valve in the tracheostomy tube allows air to be inhaled through
the tube and then closes on expiration, diverting the air stream through the
vocal cords to produce a voice. Many patients do not accept valve tubes,
and a variety of surgical procedures are done to increase the airway while
sparing the voice. These operations all involve compromise; they trade vocal
Spastic Dysphonia
Spastic dysphonia is a strained, hoarse voice, often staccato-like, due to
hyperadduction of the true and false cords. This “tension larynx” usually
starts in young adults, who become very self-conscious and may change
occupation to avoid speech. Psychotherapy, drugs, biofeedback, voice ther¬
apy, and hypnosis have been of limited success. Surgical section of the right
recurrent laryngeal nerve has been the best therapy, although voices do not
return to complete normalcy and some redevelop the dysphonia in time.
The pathophysiology of the disorder is unknown.
Myasthenia Gravis
All ages can be affected by myasthenia, a disease that usually starts with
bulbar involvement. Characteristically muscles weaken with use and recover
after rest. Often the eye or facial muscles are involved, but speech and
swallowing dysfunction may cause the patient to seek medical help. A
diagnostic test can be done with Prostigmin, 15 mg orally (or 0.5 to 1.0 mg
IM); improvement should occur within 30 minutes.
Psychogenic Aphonia
The patient may complain of a total inability to talk, but on examination
the larynx looks and moves normally. Upon request the patient is able to
cough normally, and this is the key to the psychogenic etiology. Often there
is a history of emotional disturbance, particularly if the patient is questioned
directly.
Vocal Weakness
Many older patients complain of vocal weakness. Their voice lacks its
usual tone and vigor. Frequently the voice breaks or drops in pitch. On
examination the vocal cords appear slightly bowed. As the larynx ages, this
bowing occurs normally to a variable degree. The vocal change then is an
extension of a normal physiologic aging process.
When older patients are weakened after illness or surgery, their voices
suffer because of their overall debility and improve as they gain muscle
strength. Excessive emotional tension in the young also can produce a
functional weakness with a cracking, breaking voice. A feeling of dryness or
of a lump in the throat is often an accompanying symptom.
low in the neck to enter the trachea. The thyroid gland overlies the trachea,
and in a restaurant, entering the trachea can be both bloody and difficult.
The cricothyroid membrane is subcutaneous between the thyroid and cricoid
cartilages. There are no major vascular structures here and entry is much
easier. After the airway is secure, the foreign body can be removed in a
leisurely manner. If necessary, an orderly tracheostomy can be done later in
a hospital setting. In an emergency with poor facilities, a cricothyrotomy is
preferred over tracheostomy.
References
Bailey BJ, Biller HF: Surgery of the Larynx. Philadelphia, WB Saunders Co, 1985.
Cotton RT, Richardson MA: Congenital laryngeal anomalies. Otolaryngol Clin North Am
14:203-218, 1981.
DeSanto L, et al: Cysts of the larynx; classification. Laryngoscope 80:145-176, 1970.
Fried MP (ed): The larynx. Otolaryngol Clin North Am 17(1): February 1984.
Friedman ER, et al: Bacterial tracheitis—two-year experience. Laryngoscope 95:9-11, 1985.
Hodge KM, Ganzel TM: Diagnostic and therapeutic efficiency in croup and epiglottitis.
Laryngoscope 97:621-625, 1987.
Linscott MS, Horton WC: Management of upper airway obstruction. Otolaryngol Clin North
Am 12:351-373, 1979.
Nau TW, et al: Management of neonatal subglottic stenosis. Otolaryngol Clin North Am
2(1:153-162, 1986.
Simpson GT, Shapshay SM (eds): The use of lasers in otolaryngologic surgery. Otolaryngol
Clin North Am 16(4): November 1983.
Tucker JA: Obstruction of the major pediatric airway. Otolaryngol Clin North Am 12:329-
342, 1979.
21
SPEECH AND
LANGUAGE DISORDERS
by Virginia Wigginton, M.A., C.C.C.,
Meredith Gerdin, M.A., C.C.C., and
Frank M. Lassman. Ph D.
Definitions
Language is a system of symbols used for the understanding and expression
of ideas and feelings. Attributes of language include not only vocabulary
and grammar but also the abilities to remember, classify, order, and abstract.
In contrast, speech is one mode for conveying language. Among other
modes are writing, gesturing, and signing. Attributes of speech include pitch,
loudness, and quality of voice; vowels, consonants, diphthongs, and the
blending of these into syllables, words, and phrases; and rate, intonation,
and rhythm. “Language" and “speech” are distinguished here for purposes
of clarity. This is not meant as an argument that they are dynamically
separable. For example, there is a considerable amount of language infor¬
mation contained in intonation.
In defining speech and language disorders, there are three primary
considerations: (1) Can the language and speech be understood with little
or no difficulty? (2) Is the language usually appropriate to the substantive
requirements of the communication? (3) Does the manner of communicating
call attention to itself and divert attention from the message? When disorders
of speech or language are judged to exist, there is usually a problem in one
of these areas. With children, this possibility should follow a careful com¬
parison of the child’s performance against the general developmental descrip¬
tion that follows.
Prelinguistic Development
There are skills and knowledge learned in infancy which are necessary for
the development of language and communication. These primary skills are
412
21—SPEECH AND LANGUAGE DISORDERS 413
in the areas of cognition and social interaction. Cognitively, the infant must
learn to be aware of objects and events in his environment and to realize
their uniqueness. It is this knowledge base that is the subject of early
communications. Socially, the infant must learn that he can have a specific
effect on caregivers by what he does, to be both an initiator and responder Communication problems in
in interactions, to jointly attend to activities, and to interact with others for children may develop because
of disturbed social and cogni¬
a variety of reasons. Many children with communication problems have had
tive skills in infancy.
disturbances in the development of social and cognitive skills in infancy.
Linguistic Development
Language comprehension seems to precede language usage. Imitation may Language comprehension pre¬
occur without comprehension, but functional language for communication cedes language usage.
purposes appears to require prior comprehension. Even though there are
fairly predictable stages and ages for development, the range of normality is
great.
Receptive language is that which the child hears and must interpret. The
child progresses from simply alerting to a speaker to understanding meaning
based on grammatical construction within the first five years of life.
Expressive language is that which the child expresses to others. Speech
progresses from simple reflexive vocalization to complex sentences. Corre¬
spondingly, nonverbal communication progresses from unintentional behav¬
iors to refined, conventional gestures.
General guidelines for both receptive and expressive language are listed
in Table 21-1.
0-6 months Startles and turns to sound; Cooing and babbling for pleasure;
understands tone of voice (e.g., differential crying
angry vs. happy)
6-12 months Understands gestures; understands Use of vocalization with inflection;
some words and phrases may develop use of first word
12-18 months Understands common short and Use of single words, using that
simple sentences; points to some word to mean several things;
body parts; can identify familiar continues to use own jargon
picture (syllables with intonation)
18-24 months Understands a few prepositions Uses 2- and 3-word combinations;
and personal pronouns; listens to expresses negation by using
and understands simple stories; “no”
points to pictures when asked
2-3 years Can follow 3-part directions; 3- and 4-word sentences; uses
understands most adult some pronouns and prepositions;
sentences; understands concepts about 50% intelligible
like “one” and “many”
3-4 years Can identify object when given Mostly intelligible; 4- to 6-word
function; understands more sentences with various sentence
prepositions; understands types (interrogative, imperative,
information about more abstract negative)
events
4-5 years Except for vocabulary limitations, 90% of learning to talk completed;
understands most adult expression at a colloquial adult
communication level
414 PART FIVE—THE LARYNX
Physician’s Screening
Commonly, parents become concerned enough to bring a child who is not
talking or who uses only a few words to a physician at age 24 to 30 months.
An alert physician, however, may recognize problems even earlier. Children
not falling within accepted guidelines for language development should be
referred for consultation with an audiologist and speech pathologist. Speech
pathologists can determine whether behavior is outside acceptable limits and
thereby minimize long-term effects.
Hearing Loss
Failure to develop speech or The quality of speech and language reflects the ability to hear and perceive.
language requires evaluation tor There is usually a direct relationship between speech/language abilities and
hearing impairment.
the amount of residual hearing. Hearing loss, from the minimal to the
profound, negatively affects speech and language development.
The effects of profound deafness tend to be obvious. Vocabulary, word
order, and grammatical usage are faulty. Voice distortion, speech sound
errors, and rhythm deviations are characteristic, making speech very difficult
to understand.
The use of hearing aid amplification is important for reducing the effective
hearing impairment, enabling the child to hear others as well as himself.
The value of the hearing aid for maintaining speech skills is less obvious but
should not be underestimated.
The hearing aid is but one aspect of the habilitation process. Children
should not be expected to develop communication skills on the basis of
amplification alone. Remediation is further discussed in Chapter 4, which
deals with hearing impairment.
Age of onset is critical. Children who have normal hearing beyond age
two years, even for a short while, are likely to have significantly better
language/speech skills than those who are deaf at birth or very early in life.
Children with moderately severe hearing impairments usually have better
speech and language than those with more profound losses. Attention is
usually not drawn to the speech and language of those with mild hearing
impairment. Yet children with mild, chronic hearing impairment are at risk
A hearing loss of 20 dB may for reduction in language skills. A hearing loss of 20 dB in young children
affect speech. (three years old and under) has been shown to affect language/speech
21 —SPEECH AND LANGUAGE DISORDERS 415
250 500 1000 2000 4000 250 500 1000 2000 4 000
FIGURE 21-1. The audiogram (representing both ears) of the child with a hearing
impairment for the higher frequencies. Because of better hearing sensitivity for low
frequencies, the child often appears to have normal hearing to gross inspection. Speech/
language delay may be ascribed to other factors such as assumed intellectual retardation.
Voice Disorders
A common childhood voice disorder is hoarseness resulting from vocal
abuse. Unchecked, the condition of the vocal folds can progress from mild
irritation and edema to formation of nodules. Nodules respond to vocal rest
and often to a change in pitch. Group as well as individual therapy has been
successful in locating the causes of the abuse and helping the individual to
take responsibility for vocal output. Behavior modification—e.g., counting
uses of loud voice and timing total use of voice—has been effective.
416 PART FIVE—THE LARYNX
Cleft Palate
The child born with a cleft lip/cleft palate faces years of restorative
procedures and rehabilitation. Among the disciplines needed are pediatrics,
prosthodontics, pedodontics, nutrition, education, audiology and speech
pathology, otolaryngology, and maxillofacial surgery. Therefore, coordinated
management is essential.
Cleft palate deformity is often Vocal play helps the baby develop a perception of his oral structure and
associated with conductive
of the sounds he is producing. Cleft palate not only compromises oral
hearing loss.
sensation but also is frequently accompanied by hearing loss, impairing
auditory feedback and environmental stimulation.
In cases of cleft palate, the speech product is excessively nasal. Problems
related to nasal resonance are discussed later in the section on voice disorders
of adults. Of equal significance are the articulation problems that accompany
velopharyngeal insufficiency. That is, the precision of plosive (p-b-t-d-k-g),
fricative (s-z-f-v-th-sh-zh), and affricate (ch-dzh) consonants is reduced
through nasal escape. The child may grimace in an effort to occlude his
nares to prevent the escape of air. In the case of repaired cleft lip, sounds
likely to be affected are those requiring lip closure, rounding, and extension
(p-b-m-oo-ee).
Regardless of whether surgery, prosthesis, or both affect structural repair,
the child may still have inadequate velopharyngeal closure for speech.
Assistance with precise, rapid articulation of speech is necessary. Speech
outcome is one criterion for success of surgical/prosthetic management.
The cleft palate child is at risk for oral sensation deficits, feeding problems,
social/emotional problems, developmental delay, and speech and language
problems associated with hearing impairment.
Stuttering
Stuttering is a fluency disorder or an abnormality of speech rate or rhythm.
All speakers experience normal dysfluency, such as pauses or word repeti¬
tions. When the dysfluencies call attention to themselves or the speaker
struggles to avoid the dysfluency, the speaker is considered a stutterer. The
stutterer may repeat words or sounds, prolong sounds, or “block,” thus
producing no sound at all. In addition, these speech behaviors may be
accompanied by muscular tension and struggling. Secondary characteristics
may include head jerks, eye blinks, and facial contortions.
The speech of many children It is important to know that many children have exaggerated dysfluencies
with dysfluencies at ages 3 and
4 will improve spontaneously.
at around three to four years of age. These interruptions are not associated
with any struggle or tension in speaking and usually disappear spontaneously.
Parents may need reassurance about normal dysfluencies. They should avoid
overreacting to the dysfluencies while responding positively to the sense of
21—SPEECH AND LANGUAGE DISORDERS 417
Behavioral/Emotional Disorders
Children with behavioral/emotional disorders often have associated lan¬
guage disorders, including mutism, disordered content of speech, compre¬
hension deficits, poor communicative interaction, and atypical vocal char¬
acteristics. The specific type of language disorder, e.g., neologisms, pronoun
reversals, echolalia, excessive talkativeness, is often useful in establishing a
differential diagnosis. Children with the most severe disturbances, autistic
disorder or schizophrenia, always exhibit extreme language disturbance.
There are some children whose emotional disturbance is thought to be a
primary “cause” of the language problem. Emotional disturbance can also
“result” from the inability to communicate. In either case, the communica¬
tion problem warrants evaluation by a speech pathologist.
Cerebral Palsy
The child with cerebral palsy requires a specialized orientation of the
speech pathologist and of the physician as well. Knowledge of body tone,
sensation, posture, and reflexes is essential.
Before speech can be acquired, the child needs an oral musculature that
can manage basic vegetative functions such as eating or swallowing. The
optimum posture for breath support to produce voice should be established.
The speech of the cerebral palsied child reflects his basic neurophysiologic
condition. Voice quality, speech sound articulation, respiration rate, and
rhythm are distorted by flaccidity, spasticity, rigidity, tremor, or athetosis.
The language of the physically disabled child is frequently affected by his
experiential limitations. Moreover, because by definition cerebral palsy
involves brain damage, the child may manifest many or all of the features
associated with language disability or organic mental retardation. In the case
of cerebral palsy related to Rh incompatibility and kernicterus, sensorineural
hearing loss with the resultant speech and language difficulties may occur.
The ability to communicate is more crucial than the ability to speak. When
a child has severe motor speech limitations, alternate or supplementary
communication systems (e.g., word or symbol boards or computer-assisted
communication) may be necessary.
Coordinated rehabilitation services including those of the physician and
occupational and physical therapists, social worker, speech pathologist, and
others are necessary.
Mental Retardation
In contrast to children with specific language disorder or emotional
disturbance, retarded children are retarded generally. They are delayed in
socioemotional, intellectual, and perceptual-motor development as well as
in language. The greater the severity of general retardation, the greater the
language delay. The profoundly retarded child may not talk at all.
Articulation Disorders
The child who has defective speech articulation may have difficulty with
the precision or sequencing of speech sounds. At any given age, certain
articulation errors fall within normal developmental expectations (Table
21-2).
Parents are sometimes concerned that a child’s speech problem is related
to being “tongue-tied” when, in fact, a lingual frenum would need to be
In the rare incidence that a extremely restricted to account for an articulation disorder. Almost all
tight lingual frenum affects
children compensate for “tongue-tie,” and, in many cases, the restriction
speech, a simple “l" plasty can
be performed. lessens over time.
The most prevalent type ot articulation disorder is called functional
misarticulation. There are four types: substitution, omission, distortion, and
addition. Functional articulation disorders (the largest single disorder cate¬
gory) are common among young school-aged children.
Two other types of articulation disorders are associated with physiological
problems. Children with dysarthria have imprecise speech for reasons of
paralysis, weakness, or lack of coordination of the speech mechanism. When
the difficulty involves the selection, programming, or sequencing of sounds,
2 p, h, n, b, k, f
2Vi m, g
3 w, d, y, v
yh s
4 sh
4‘/2 t, ng, ch, r, 1, z, th
*By 50% of children in all positions of a word. Source: Olmsted D: Out of the Mouths of Babes. The
Hague, Mouton, 1971.
21 —SPEECH AND LANGUAGE DISORDERS 419
it is called apraxia of speech. Dysarthria and apraxia can severely limit the
child’s ability to develop fluent speech.
Voice uisorder*
Voice is an acoustical end-product of a smooth, balanced, dynamic,
interrelated system involving respiration, phonation, and resonance. A
subglottic pressure of air from the lungs, compressed by abdominal and
thoracic musculature, is addressed against the vocal folds. Sound is produced
by rapid opening and closing of the cords, set into vibration by a smooth
combination of muscular tension and rapid air pressure changes. The pitch
is largely determined by the frequency of cord vibration.
Sound produced at the glottis is amplified and is supplied with characteristic
quality (resonance) as it moves through supraglottic passages, especially the
pharynx. Disturbance of this system can result in voice disorder.
Voice problems have been estimated to occur in 1 per cent of all people
in the United States. Reported incidence of voice disorders in school children
ranges from 6 to 23.4 per cent.
Voice Therapy
Following medical examination, the speech and language pathologist can
utilize several techniques that may help the voice patient achieve a more
normal voice. The first step is to increase the patient’s ability to monitor his
own vocal production and to increase awareness of situations in which vocal
abuse can occur. Other treatment goals may include (1) educating the patient
regarding normal anatomy and physiology of the vocal mechanism; (2)
eliminating faulty speaking habits; (3) reducing vocal abuse; (4) decreasing
musculoskeletal tension; and (5) counseling.
Prior to surgical intervention, the patient should receive a trial period of
voice therapy. Therapy for non-life-threatening disorders can often alleviate
the need for surgery. Then the physician, with input from the speech and
language pathologist, can determine the best course of action for the patient.
Post-surgical patients, if not referred to the speech and language pathol¬
ogist prior to surgery, can benefit from therapeutic intervention to reduce
trauma to the vocal folds. A brief period of voice rest, no more than a few
days, may help patients recovering from vocal fold surgery. However, there
is no evidence that voice rest is of benefit to patients in general, and it may
be harmful to those with psychogenic disorders.
Alaryngeal Speech
A person who has undergone laryngectomy must make many adjustments
afterward. One of the most difficult is that of learning to communicate again.
“ball of air” into the throat. Certain consonant sounds (e.g., p., t, and k)
serve to drive air into the esophagus. This is called “consonant injection.”
The laryngectomee who is able to use consonant injection has a built-in
“pumping action,” so that in connected speech, he is continually “recharg¬
ing.”
Inhalation of air into the esoph- During inhalation, the patient maintains a patent airway between the nose
agus is possible if there is re- or iips ancj the esophagus. As he inhales through the stoma, there is increased
laxation of the nasopharynx. negative pressure in the esophagus, creating a partial vacuum. If the
pharyngoesophageal segment is relaxed, the higher pressure in the mouth
and hypopharynx pushes air into the esophagus. The inhalation method has
the advantage of being very natural, since pulmonary and phonatory air are
in synchrony. It is quite possible for a laryngectomee to use a combination
of methods.
Course of Treatment
Rehabilitation should begin, whenever possible, before surgery. A pre- A presurgical visit and discus-
surgical visit to the patient by a speech pathologist and, when indicated, by ston about rehabilitation is es-
a successful laryngectomized speaker informs him that help will be available.
Some laryngectomized patients have reported after surgery that they were
Croup Support
Laryngectomees help each other, providing information and encourage¬
ment to the new patient. The patient should be made aware of the
International Association of Laryngectomees, in care of the American
Cancer Society, 90 Park Avenue, New York, New York 10016.
ORAL DYSFUNCTION/DYSPHAGIA
The clinician may change the patient’s position or use special techniques to
facilitate the swallow during the study. Information gained from the modified
barium swallow, particularly the presence or absence of aspiration, is
necessary for making decisions regarding oral feeding and treatment proce¬
dures.
References
Aronson AE: Clinical Voice Disorders. 2nd ed. New York, Thieme, Inc, 1985.
Gabbard SA: References for communication disorders related to otitis media. Semin Speech
Lang Hear 3:351, 1982.
Hall P, Tomblin J: A follow-up study of children with articulation and language disorders. J
Speech Hear Disord 43:227-241, 1978.
Logemann J: Evaluation and Treatment of Swallowing Disorders. San Diego, College Hill, Inc,
1983.
McClean J, Snyder-McClean L: A Transactional Approach to Early Language Training.
Columbus, OH, Charles E. Merrill, 1978.
McClowry D. Guilford A. Richardson S: Infant Communication: Development, Assessment,
and Intervention. New York, Grune and Stratton, Inc, 1982.
Milisen R: The incidence of speech disorders. In Travis L (ed): Handbook of Speech Pathology
and Audiology. New York, Appleton-Century-Crofts, 1970.
Salmon S: Factors that may interfere with acquiring esophageal speech. In Keith R, Darby F:
Laryngectomee Rehabilitation. 2nd ed. San Diego, College Hill Press, Inc, 1986.
Senturia B, Wilson F: Otorhinolaryngologic findings in children with voice deviations. Prelim¬
inary report. Ann Otolaryngol Rhinol Laryngol 22:1027-1042, 1968.
Shames G, Florance C: Disorders of Fluency. In Shames G, Wiig E (eds): Human Communi¬
cation Disorders. Columbus, OH, Charles E. Merrill, 1982.
Silverman E, Zimmer C: Incidence of chronic hoarseness among school-aged children. J Speech
Hear Disord 40:211-215, 1975.
Singer EM, Blom E: An endoscopic technique for restoration of voice after laryngectomy. Ann
Otolaryngol Rhinol Laryngol 90:529-533, 1980.
Wiig E-, Semel E: Language Assessment and Intervention for the Learning Disabled. 2nd ed.
Columbus, OH, Charles E. Merrill, 1984.
NEOPLASMS OF THE
HEAD AND NECK
22
BENIGN NECK MASSES
by James I. Cohen, M.D., Ph.D.
ANATOMIC CONSIDERATIONS
The anatomic boundaries of the neck are as follows: superiorly the lower
border of the mandible, the mastoid tips, and the superior nuchal line;
inferiorly the suprasternal notch, the clavicles, and a horizontal line through
the spinous process of the seventh cervical vertebra (Fig. 22—1). For The sternocleidomastoid muscle
descriptive purposes, the neck is divided into two halves by the vertical divides each side of the neck
midline, and each side is further divided into an anterior and posterior mt0 two tnaneles‘
triangle by the sternocleidomastoid muscle. Most masses appear in the
anterior cervical triangle.
The surface landmarks of the neck, which are normally palpable, include
the mandible, the submandibular glands, the tail of the parotid glands, the
hyoid bone, the larynx, the thyroid, the trachea, the sternocleidomastoid
muscles, the clavicles, and the cervical vertebrae (Fig. 22—1). These structures
are therefore used to further define a number of regions in the neck (Fig.
22-2), which are important in describing the position of a lump in the neck.
DIAGNOSTIC EVALUATION
The evaluation of any neck mass begins with a careful history. A logical
series of questions can quickly narrow down the diagnostic possibilities and
streamline subsequent investigations and management (Table 22-1). These
questions and their significance are listed below:
1. What is the age of the patient? Congenital lesions are far more common The older the patient, the more
in younger individuals, whereas malignant lesions are more likely in likely the neck mass is malig-
the elderly. nant-
2. Is the mass growing rapidly? In the absence of signs of infection,
malignant lesions (lymphoma, metastatic cancer) are far more likely to
experience rapid growth than benign ones.
429
430 PART SIX—NEOPLASMS OF THE HEAD AND NECK
muscle
Posterior Anterior
cervical cervical
triangle triangle
FIGURE 22-3. A, CT scan of a neck mass. A large mass is seen adjacent to the hyoid bone and deep to
the sternocleidomastoid muscle. B, MRI scan of a neck mass. A large mass is seen deep to the
sternocleidomastoid muscle. The carotid artery and internal jugular vein are seen deep to the mass.
Interpretation of a fine needle attached to a syringe into the mass to obtain sufficient cells for cytologic
aspirate requires experience, examination (Fig. 22-4). This procedure is generally well tolerated by
patients and is both safe and accurate in experienced hands. Hence it is the
preferred method at present. By contrast, large-bore needle biopsy methods
(which obtain a “core” of tissue) (Fig. 22-4) and operative “open” biopsy
techniques are more invasive and have a higher risk of “seeding” the
malignancy and complicating future management.
By appropriate work-up most neck masses can be classified into one of
the categories listed in Table 22-3. These will each be discussed separately
below
1st ist
Internal
Foramen
carotid External
Foramen caecum
area
Cystic Hygroma
A cystic hygroma is a lymphangioma that arises from vestigial lymph
channels in the neck. It may present as a relatively simple thin-walled cyst
in the floor of the mouth or may involve all the tissues from the floor of the
Enlarged lymph nodes are by far the most common type of neck masses
encountered. The cervical lymphatic system consists of interconnected groups
or “chains” of nodes which parallel the major neurovascular structures in
the head and neck (Fig. 22-9). The skin and mucosal surfaces of the head
and neck all have specific and predictable nodes associated with them. Thus,
the location of an enlarged lymph node is an important clue to the position
of the primary disease.
There are general guidelines that may be helpful in the assessment of a
Transverse or
Supraclavicular chain
22—BENIGN NECK MASSES 437
neck node. Tender neck nodes are more likely to be infectious in origin, Consider an enlarging cervical
whereas painless nodes are more likely to contain metastatic disease. Multiple lymph node in an individual over
60 years of age as malignant
regions of enlarged lymph nodes usually represent systemic disease such as until proven otherwise.
lymphomas, tuberculosis, or infectious mononucleosis, whereas solitary
nodes are more often metastatic. Low neck nodes are more likely to contain
metastatic disease from a source other than the head and neck, whereas
upper cervical nodes are more likely secondary to a head and neck source.
Open biopsy is the last step in the work-up of a neck mass. Prior to biopsy ,
direct examination of the nasopharynx, larynx, hypopharynx, and esophagus
under anesthesia should be performed to rule out small lesions that are
difficult to see with the patient awake. Only when all of these examinations
fail to reveal a source of disease should an open biopsy be considered.
Where possible, node biopsies should be excisional without violation of the
mass itself. Vital structures must be preserved until a definitive diagnosis of When a lymph node is excised
cancer has been established. Skin incisions should be oriented in such a for diagnosis, the incision
should be planned for possible
manner that they can be extended for the performance of a neck dissection, later incorporation for a radical
should it prove necessary. neck dissection.
Chronic Infections
Chronic infections that involve cervical lymph nodes include tuberculosis,
fungal disease, syphilis, sarcoidosis, cat scratch fever, and AIDS (acquired
immunodeficiency syndrome). Owing to their chronicity, these lymph node
infections are easily confused with neoplasms, especially the lymphomas.
While biopsy is occasionally necessary for diagnosis, skin tests and serologic
study are often more useful. Treatment of all of these conditions is primarily
medical, with surgery reserved for residual sinus tracts or other complica¬
tions.
Malignant Lymphoma
Cervical adenopathy is one of the most common presenting symptoms in
patients with Hodgkin’s and non-Hodgkin’s lymphoma. The nodes them¬
selves tend to be softer, smoother, more elastic, and more mobile than
nodes with metastatic carcinoma. Rapid growth is not unusual, particularly
with non-Hodgkin’s lymphoma. Extranodal sites, particularly Waldeyer’s
ring, are often involved in non-Hodgkin’s lymphoma, and enlargement in Lymphoma can present as rapid
giywth of any area of Waldeyer’s
this area may provide a clue to the diagnosis of this disease. Complete ring.
diagnosis requires an excisional biopsy of an intact lymph node. Fine needle
aspiration alone is not enough. Treatment involves the use of radiation
therapy and/or chemotherapy depending upon the pathologic type and
clinical stage of the disease.
438 PART SIX—NEOPLASMS OF THE HEAD AND NECK
METASTATIC DISEASE
Metastatic Adenocarcinoma
Adenocarcinoma in a cervical node most frequently represents metastatic
disease from the thyroid gland, salivary glands, or gastrointestinal tract.
Thus, this situation also requires a thorough search for the primary tumor
through endoscopic and radiologic study of the bronchopulmonary, gastroin¬
testinal, and genitourinary tracts, salivary glands, and thyroid. In women,
breast and pelvic tumors must also be considered.
Neurogenic Tumors
The large number of nerves in the head and neck make the area susceptible
to tumors of neurogenic origin. Neurilemmomas (schwannomas) and neu¬
rofibromas, which are the most common types seen, are quite similar. Both
arise from the neurilemmal (Schwann) cell of myelinated nerves and both
usually present as painless, slowly growing masses in the lateral neck.
Differentiation between these two types of tumor can be accomplished only
by histologic examination. Owing to their potential for malignant degener- Paralysis of the involved nerve
ation and their slow but progressive growth, surgical resection is indicated, usually nsults when a neuroma
This, however, may involve resection of the involved nerve(s), particularly
with neurofibromas, which tend to be more invasive and less encapsulated
than neurilemmomas.
THYROID MASSES
Diagnostic Approach
Unless there is a concern that thyroid cancer may be present, thyroid
swellings are often treated by medical therapy rather than surgery. Hence,
it becomes extremely important when considering any thyroid mass to
identify those thyroid lumps that might contain malignancy. This discussion
will focus on this issue.
For any individual with a thyroid swelling, clues to the presence of
malignancy are initially sought in the history and physical examination. The
history should specifically ask about prior radiation exposure. Even though
thyroid cancer is relatively uncommon in the general population (1 per cent
440 PART SIX—NEOPLASMS OF THE HEAD AND NECK
4 4
22—BENIGN NECK MASSES 441
#.*-
+ i
L+- CJaV
R.VC
at i ""’ n
4
* ”
-S^Motc^
4^0 iV
FIGURE 22-12. A, A thyroid scan with a “hot"—hyperfunctioning—area that corresponds clinically to the
position of a palpable thyroid nodule. B, A thyroid scan with a “cold” thyroid nodule. There is decreased
uptake seen in the left inferior pole of the thyroid which corresponds clinically with the position of the
palpable nodule in the thyroid.
Thyroid Nodules
If physical examination and thyroid scans suggest a discrete thyroid nodule,
then the diagnostic approaches somewhat different from that used for diffuse
disease. Most nodules are benign. However, those that are truly solitary,
firm or hard, growing rapidly, or nonfunctional (“cold”) on scan are more
likely to be malignant. Similarly, if a nodule appears in either a young male,
a pregnant female, or an individual with a history of irradiation or family
history of thyroid cancer, the chances of malignancy are higher.
Fine needle aspiration of thyroid nodules properly done or interpreted
has proven helpful in determining the presence or absence of malignancy
within a thyroid nodule. An aspiration that is positive or suspicious for the
presence of malignancy suggests the need for surgery, whereas those nodules
that are histologically benign and disappear with aspiration can often be
treated with thyroid suppression and observation.
Hyperfunctioning (“hot”) nodules and those in which the suspicion of
malignancy is extremely low can be treated with a trial of thyroid hormone
replacement therapy to see whether this will make the mass disappear.
However, if this is ineffective or signs of malignancy appear, then surgery is
necessary.
Surgery for thyroid nodules involves an excisional biopsy consisting of
total lobectomy and not enucleation alone. More extensive surgery is
performed if the frozen section of the resected specimen reveals carcinoma.
References
Allard RHB: The thyroglossal duct cyst. Head Neck Surg 5:134-146, 1982.
Bonnadonna G, Molinari R, Banfi A: Hodgkin’s and non-Hodgkin’s lymphoma presenting in
the head and neck. In Suen JY, Myers EN (eds): Cancer of the Head and Neck. New York,
Churchill Livingston, 1981, pp 699-717.
Bumstead RM: Thyroid disease: A guide for head and neck surgeons. Ann Otol Rhinol
Laryngol 89(Suppl):72, 1980.
Chandler JR, Mitchell B: Branchial cleft cysts, sinuses and fistulas. Otolaryngol Clin North Am
14:175-186, 1981.
Hamaker RC, Singer MI, DeRossi RV, Shockley WW: Role of needle biopsy in thyroid
nodules. Arch Otolaryngol 109:225-228, 1983.
Holt GR, Mattox DE, Gates GA: Decision Making in Otolaryngology. St. Louis, CV Mosby
Co, 1984, pp 40-41, 88-89, 114-115.
Knight PK, Mulne AF, Vassay LE: When is lymph node biopsy indicated in children with
enlarged peripheral nodes? Pediatrics 69:391-396, 1982.
Lai KK, Stottmeier KD, Sherman IH, McCabe WR: Mycobacterial cervical lympadenopathy.
JAMA 251:1286-1288, 1984.
Lindberg R: Distribution of cervical lymph node metastases from squamous cell carcinoma of
the upper respiratory and digestive tracts. Cancer 28:1446-1449, 1972.
Spiro RHM, DeRose G, Strong EW: Cervical node metastasis of occult origin. Am J Surg
146:441-446, 1983.
Stal S, Hamilton S, Spira M: Hemangiomas, lymphangiomas, and vascular malformations of
the head and neck. Otolaryngol Clin North Am 19:769-796, 1986.
23
MALIGNANT TUMORS
OF THE HEAD AND NECK
by George L. Adams, M.D.
In spite of the lay media’s constant urging of the public to seek medical
Hoarseness is the earliest sign care early, it is not infrequent for a patient to present with laryngeal
of laryngeal cancer.
obstruction from a large cancer rather than the early symptom of hoarseness.
Similarly, a patient with a pharyngeal tumor may ignore the early symptoms
of pain and dysphagia only to present when pharyngeal or esophageal
obstruction has developed. Thus, a great advancement in the control of head
Persistent hoarseness requires and neck malignancy would be education of the public to obtain early
a mirror or fiberoptic exam of
examination. (The physician is obligated to ensure a thorough evaluation of
the larynx.
the patient’s symptoms, including indirect mirror or flexible fiberoptic scope
examination—see Chapter 1.)
23—MALIGNANT TUMORS OF THE HEAD AND NECK 445
ETIOLOGY
Squamous cell carcinoma comprises 90 per cent of head and neck malig¬ Squamous cell carcinoma com¬
nancies. Adenocarcinoma, which usually develops in a major or minor prises 90 per cent ot head and
neck cancer.
salivary gland, is the next most common type. All other pathologic varieties
comprise less than 1 per cent. Tobacco is the etiologic agent most frequently
cited in development of squamous cell carcinoma. However, heavy alcohol
ingestion is often associated with heavy smoking and is incriminated as an
etiologic factor, particularly in tumors of the oral cavity, tonsillar area, and
piriform sinus. Poor oral hygiene has also been implicated. On rare occasions,
an elderly individual without any of these habits develops floor of mouth or
tongue cancer without explanation. While most head and neck malignancy
develops in the 50- to 70-year-old age group, carcinoma of the oral cavity
has been recognized in individuals in their twenties. Alcohol and tobacco
use does not seem to be implicated in many of these younger individuals.
A viral etiology, specifically the Epstein-Barr virus, has been associated Epstein-Barr virus has been as¬
with the development of nasopharyngeal carcinoma. Cantonese Chinese sociated with nasopharyngeal
carcinoma.
have a high incidence of nasopharyngeal cancer, suggesting a racial predilec¬
tion. Although the incidence is extremely high in Chinese living in their
homeland, the incidence remains high in Chinese born and raised in the
United States. Adenocarcinoma arising high in the nasal vault and ethmoid
sinuses is prevalent among hardwood furniture workers in certain areas of
Great Britain, suggesting environmental factors. Workers exposed to chro¬
mium and nickel have also been demonstrated to have a higher incidence of
paranasal sinus malignancies (Table 23-1).
Patients with head and neck malignancies are prone to develop a second
tumor at an incidence rate of approximately 4 per cent per year for the first
five years after discovery of the original cancer. Most of these second primary
malignancies are in the upper aerodigestive tract. A second primary tumor
in the lung is particularly common. Thus, the patient ostensibly cured of his
original cancer should remain under constant surveillance for the rest of his
life, not only for the development of metastases from that tumor but also
for detection of a new malignancy.
PATHOLOGY
Squamous cell carcinoma develops as an ulcerative lesion with necrotic Squamous cell carcinoma is far
edges, usually surrounded by some inflammatory response. While the tumor more common in men. Adeno¬
carcinoma occurs equally in
may remain an ulcerative lesion, it is often surrounded by areas of leuko¬
men and women.
plakia of the premalignant type. The tumor initially spreads along the
mucosal surface, eventually extending into the underlying soft tissue. Path¬
ologically, these tumors are graded on the basis of histologic appearance
related to the clinical course. Simply put, all classifications range from well-
1. Lymphocyte predominance
2. Nodular sclerosis
3. Mixed cellularity
4. Lymphocyte depletion
METASTATIC TUMORS
Metastases to the head and neck from primary tumors elsewhere can
occur. Hypernephroma is the most common tumor to metastasize to the
paranasal sinuses. A mass in the supraclavicular fossa may represent metas¬
tases from a primary tumor of the lung, kidney (renal cell carcinoma),
bladder, prostate, breast, or gastrointestinal tract. Tumors that tend to
metastasize to bone can present in the mandible, maxilla, sphenoid sinus, or
petrous portion of the temporal bone. Even metastatic carcinoma to the
tonsil has been described.
Malignant Melanoma
Melanoma is classified according to size, location, and depth of invasion
determined histologically (Table 23-3).
23 —MALIGNANT TUMORS OF THE HEAD AND NECK 449
From Beahrs OH, Mvers MH (cds): Manual for Staging of Cancer. 2nd ed. Philadelphia. JB Lippincott
Co. 1983. p 118.
Head and neck malignancies may occur in all age groups. However, the
age of the patient is useful in arousing suspicion of a particular type of
tumor. For example, rhabdomyosarcoma and lymphoma would be more
likely in children, whereas adenocarcinoma occurs in all ages. In the 40- to Squamous cell carcinoma:
70-year age range, tumors are most frequently the squamous cell type, with male, age BO, heavy smoker,
drinking history.
a high male predominance, and the history usually elicits heavy smoking or
450 PART SIX—NEOPLASMS OF THE HEAD AND NECK
The concept ot "panendoscopy" In the operating room, thorough endoscopic evaluation is made not only
developed because of the 5 to 8 of the patient’s known or suspected tumor but also of other suspicious areas.
per cent incidence of a second
head and neck cancer. Thus, leukoplakia beyond the primary tumor area must also be biopsied.
The tongue and upper pharynx are carefully palpated. The nasopharynx is
directly visualized and palpated. The laryngopharynx is carefully inspecied
using a laryngoscope, carefully lifting the arytenoid area to examine the
postcricoid and hypopharyngeal regions. The tumor mass is carefully defined
and outlined and an appropriate drawing made in the patient’s chart. Exact
knowledge of the extent of the tumor is imperative. Tattooing the margins
of accessible tumors with India ink is helpful for follow-up examinations.
Presence or absence of palpable neck nodes must be documented, and
palpation is repeated when the patient is under anesthesia. Whether these
nodes are fixed to underlying structures and whether they are present
unilaterally or on the ipsilateral or contralateral side are important. Knowl¬
edge of the extent of the primary tumor and the status of regional metastases
is required in order to plan definitive care and stage the tumor.
23 —MALIGNANT TUMORS OF THE HEAD AND NECK 451
Classification
From Beahrs OH. Myers Mil (eds): Manual for Staging of Cancer. 2nd ed. Philadelphia, JB Lippincott
Co, 1983, pp 44, 50.
MODALITIES OF TREATMENT
There are at present five specific methods available for treatment of head
and neck malignancies:
1. Radiation therapy
2. En bloc surgical excision
3. Laser excision
4. Chemotherapy
5. Combination of modalities
In an effort to improve survival rates, it has been common in the past ten
years to combine two or more of these modalities. Prior to initiation of any
form of treatment, a thorough evaluation is made of the patient’s general
452 PART SIX—NEOPLASMS OF THE HEAD AND NECK
health, likelihood of responsible follow-up, and extent of the tumor and its
metastases. Then, after the options are discussed with the radiation therapist,
family, and others who may be involved in the patient’s care, a treatment
plan is derived. Although a small tumor may be treated adequately by either
radiation therapy or surgery, larger tumors are usually treated by surgery,
with radiation given either pre- or postoperatively. Recurrent tumors not
amenable to additional surgery or irradiation are treated by chemotherapy,
often as part of a research protocol. The role of each of these major
modalities is discussed below.
Radiation Therapy*
Radiation plays an important part in the management of head and neck
malignancies and can be employed as the sole method of treatment for
certain tumors. The radiotherapist, employing x-rays and gamma-rays, must
know the quantity and quality of the radiation in the particular beam being
used. The quantity, or dose, of radiation designates the amount administered,
and the quality, or penetration ability, determines the percentage of radiation
that will reach a lesion at a given depth below the body surface. When the
patient is exposed to x- or gamma-irradiation, a portion of the photons pass
through unchanged, but a certain fraction is absorbed by the interaction
with the atoms of the body. The absorbed photons, if sufficiently energetic,
liberate photoelectrons, recoil electrons, and negatron-positron pairs that
ionize other atoms nearby. In other words, the absorbed energy causes
ionization that is primarily responsible for the therapeutic effects of pene¬
trating radiation.
Definitions
In measuring radiation absorbed, the ideal method would be to calculate
the number of ergs of energy absorbed in the irradiated tissue by the ionizing
radiation. This method requires sophisticated apparatus. Early attempts to
quantify the amounts of radiation absorbed involved exposure of photo¬
graphic film to determine the degree of darkening produced by radiation
exposure or observation of acute changes on the irradiated skin after a given
dose of radiation was administered. This was termed erythema dose.
In 1908, it was suggested that radiation be quantified by measuring the
ionization produced in air or some other gas by a standard radiation
exposure, and hence the roentgen unit was created. The modern definition
of a roentgen is very precise, but essentially it defines a certain amount of
ionization occurring in a specific quantity of air under standard conditions.
However, this measurement does not indicate the dose absorbed by a patient
exposed to a particular beam of radiation. Therefore, an absorbed dose must
also be defined. The amount of energy absorbed in tissues exposed to one
roentgen depends on the type of radiation and the material irradiated.
Hence, in 1953, the Seventh International Congress of Radiology adopted
the rad (radiation absorbed dose) as the unit of absorbed dose. The rad is
independent of the type of radiation and represents an absorbed dose of 100
ergs per gram of any material irradiated. The amount of radiation given to
a patient is ordinarily expressed clinically in tissue rads.
An additional unit of interest is the rem (roentgen-equivalent-man). This
Goals
The use of radiation therapy for treatment of head and neck carcinoma
has attained greater prominence in recent years. This was made possible by
technological improvements of the machines that produce ionizing radiation,
greater understanding of radiobiologic principles, and increased precision in
radiation measurement and delivery.
The radiotherapist employs several techniques for administering ionizing
radiation. Superficial lesions such as skin carcinoma are best treated by low-
voltage x-ray apparatus. More deep-seated lesions, like those of the tongue
or lymph nodes, require greater penetration, such as that provided by the
cobalt or electron beam. Interstitial irradiation (direct implantation) tech¬
niques utilizing radioactive materials such as radium, gold, or iridium provide
additional methods of treatment. Direct implantation of radioactive materials
results in high local irradiation with the least adverse effects beyond the
immediate area.
The application of a particular technique to a given patient depends on
many factors. It is necessary to know the site and extent of the primary
tumor but also the areas of definite or suspected metastases. A careful
drawing, showing the extent of tumor involvement, is made in the chart and
on the patient’s tumor record. The tumor should be staged according to the
TNM classification system for future reference. The age and general physical
condition of the patient are important factors. It should be decided initially,
before treatment, whether the patient will receive full-course or only pre- or
postoperative irradiation. It is important to know if the patient has had any
previous radiation therapy, including the dosage and specific area.
The use of irradiation as either a preoperative or postoperative technique
is designed to overcome the deficiencies of each modality when used alone.
In the more advanced lesions surgery is effective in removing the bulk of
the tumor in the primary site and metastatic neck nodes but may fail to cure
the patient because of microscopic seeding of unresected tissues by malignant
cells. Conversely, irradiation is effective in eradicating small nests of tumor Postoperative radiation therapy
cells at the periphery of the primary tumor and in metastatic neck nodes but is administered when there is
extra capsular extension of the
frequently fails to control the bulky, poorly oxygenated primary tumor.
cancer.
It has been demonstrated that 5000 rads of gamma radiation given over
five weeks can control 90 per cent of subclinical (i.e., microscopic) squamous
cell carcinoma. On the other hand, 7000 to 8000 rads of gamma radiation
may not control large bulky deposits of squamous carcinoma in the primary
site or lymph nodes. Hence, the rationale of combination therapy is to
achieve the sterilization of microscopic deposits of tumor cells in the treated
454 PART SIX—NEOPLASMS OF THE HEAD AND NECK
Laryngeal Lesions
Irradiation alone can be used for treatment of less advanced laryngeal
lesions, thus permitting preservation of voice. With careful follow-up,
surgical resection can be performed later should the carcinoma persist or
recur. This approach is particularly applicable in true vocal cord lesions.
Here, an 80 per cent rate of primary control is attained with irradiation
alone and the surgical salvage rate for those lesions not controlled is likewise
high.
In order to achieve a homogeneous dose distribution throughout the tumor
volume, two or more separate beam portals are used to deliver the radiation.
As an example, in treatment of an early true vocal cord lesion, both right
and left lateral portals would be employed to irradiate a volume of tissue
such as that seen in Figure 23-1. Here, the portal size is quite small, since
these lesions are of limited extent and their potential for nodal metastasis is
minimal.
Nasopharyngeal Carcinoma
In contrast, as seen in Figure 23-2, the portals used in the treatment of a
nasopharyngeal carcinoma are much more extensive, as the potential for
nodal metastasis in such cancers is great. Again, both right and left lateral
portals would be used in order to achieve a homogeneous dose.
TREATMENT GOALS —
Include : Exclude :
1. Primary 1. All nodes
23—MALIGNANT TUMORS OF THE HEAD AND NECK 455
Borders
Superior : approx. 1cm. above upper
border of zygoma
Inferior : at level of thyroid notch
Anterior : orbital margin to mandible
avoiding major part of the
larynx
Posterior ; include spinal accessory
chain
Block
1,. top 2 cm. above zygoma
2. to post, margin of EAC and base
of mastoid process (floor of EAC)
3. orbital contents
TREATMENT GOALS —
Include :
1. retropharyngeal nodes
2. anterior cervical chains
3. spinal accessory chains
4. posterior cervical triangles
5. supraclavicular fossae
FIGURE 23-2. Treatment portal used in treatment of nasopharyngeal carcinoma. In
addition to this portal, an additional anterior beam is used to treat the lower neck (EAC
= external auditory canal).
as the opposite eye. Figure 23-3 illustrates a treatment plan for a carcinoma
involving the left maxillary antrum. The connecting lines drawn within the
outline of a transverse section through the maxillary sinus represent isodose
lines and connect points of equal dose within the treatment volume. With
FIGURE 23—3. Contour drawn through maxillary sinus, illustrating beam directions,
important anatomic structures, tumor volume, and isodose curves. Note that beam I is
an open, unwedged beam but that beam II passes through a lead wedge filter in order
to achieve a homogeneous dose distribution.
•456 PART SIX—NEOPLASMS OF THE HEAD AND NECK
the proper arrangement of portals to cover the volume of the tumor and
simultaneously avoid uninvolved and sensitive structures, an acceptable
treatment plan may be constructed. Because of the highly complex calcula¬
tions involved in designing such a plan, a computer is necessary in order to
achieve precision in a reasonable period of time. Also, a radiation physicist
and other ancillary personnel are required for the proper operation and
application of these complex functions.
Complications
The difficulties associated with the> administration of radiation therapy
may be divided into early and late complications. Early problems include
the following:
Surgical Treatment
The objective of surgical treatment is total resection of the cancer with a
margin or cuff of normal tissue of at least 2 cm. In addition, surgery on the
primary malignancy is often combined with a cervical lymphadenectomy
(radical neck dissection). The neck specimen is left attached to the primary
area, for example, the larynx* so that the entire region is removed “en
bloc.” This basic surgical principle is applied wherever possible, with certain
exceptions such as the nose, where an “en bloc” neck dissection would not
be reasonable. Resection of the primary tumor combined with the neck
dissection often creates a large soft tissue defect. Regional flaps consisting
of the pectoralis major myocutaneous muscle flap, the forehead flap, the
regional tongue flap, or flaps of cervical skin are then used to repair the
defect.
The second objective of surgical resection is to restore the functional
23—MALIGNANT TUMORS OF THE HEAD AND NECK 457
Nasopharyngeal Carcinoma
The nasopharynx is a primary site for squamous cell carcinoma, undiffer¬
entiated carcinoma, adenocarcinoma, and primary lymphoma. Lymphoepi-
thelioma, which may involve the nasopharynx in younger individuals, rep¬
resents a squamous cell carcinoma combined with elements of lymphatic
458 PART SIX—NEOPLASMS OF THE HEAD AND NECK
tissue. Malignant tumors in the nasopharynx may remain silent until they
involve surrounding structures. Fifth cranial nerve involvement can cause
local and facial pain or numbness. When the tumor spreads superiorly it
Unilateral serous otitis media in may produce diplopia by involving the sixth and then third cranial nerves.
an adult suggests the possibility
Anterior extension results in nasal obstruction. Lateral extension to involve
of a nasopharyngeal neoplasm.
the eustachian tube produces unilateral serous otitis media with a conductive
hearing loss. Metastases are to the retropharyngeal, deep jugular, and spinal
A high posterior cervical node is accessory nodes. A solitary enlarged lymph node located posteriorly and
often the presenting sign of a
high in the neck is often the presenting sign.
nasopharyngeal carcinoma.
The palpable cervical metastasis does not represent the primary nodal
drainage because the retropharyngeal nodes are usually involved first.
Therefore, surgery is rarely indicated. Irradiation is the primary treatment
for both the primary lesion and the cervical metastases. A radical neck
dissection is done when the primary lesion and retropharyngeal lymph nodes
have been sterilized but a cervical metastasis persists.
FIGURE 23-4. A, Frontal view of the skull showing possible pathways or extension of a maxillary sinus
cancer. B, Side view of areas of possible extension that should be considered in determining resectability.
(From McQuarrie D, Adams G, Schons A, Browne G (eds): Head and Neck Cancer: Clinical Decisions and
Management Principles. Chicago, Year Book Medical Publishers, 1985, p 319.)
particularly when they arise on the hard palate. These minor salivary gland
tumors are initially nonulcerating, slightly tender, submucosal masses. Squa¬
mous cell carcinoma, on the other hand, ulcerates early and is tender because
of secondary surrounding inflammation.
Treatment of early oral cavity lesions is often successful with either
irradiation or nonradical surgical procedures. Larger tumors are treated by
a composite procedure, which includes an incontinuity neck dissection. When
possible, especially in lesions originating in the anterior tongue and floor of
the mouth, preservation of a rim of the mandible allows removal of the
primary tumor by a “pull through” into the neck. This may avoid functional
and cosmetic defects if the tongue is not bound down by the closure.
T Primary tumor
Tis Carcinoma in situ
Tl Greatest diameter of primary tumor 2 cm or less
T2 Greatest diameter of primary tumor more than 2 cm but not more than 4 cm
T3 Greatest diameter of primary tumor more than 4 cm
T4 Massive tumor more than 4 cm in diameter with deep invasion to involve antrum,
pterygoid muscles, base of tongue, skin of neck
N Regional lymph nodes
NO No clinically positive node
N1 Single clinically positive homolateral node 3 cm or less in diameter
N2 Single clinically positive homolateral node more than 3 cm but not more than 6 cm
in diameter or multiple clinically positive homolateral nodes, none more than 6
cm in diameter
N2a Single clinically positive homolateral node more than 3 cm but not more than 6 cm
in diameter
N2b Multiple clinically positive homolateral nodes, none more than 6 cm in diameter
N3 Massive homolateral node(s). bilateral node(s), or contralateral node(s)
N3a Clinically positive homolateral node(s). one more than 6 cm in diameter
N3b Bilateral clinically positive nodes (in this situation, each side of the neck should be
staged separately: i.e.. N3b; right. N2a; left, Nl)
N3c Contralateral clinically positive node(s) only
M Distant metastasis
MO No evidence of distant metastasis
Ml Distant metastasis present
Specify _
From Beahrs OH, Myers MH (eds): Manual for Staging of Cancer. 2nd ed. Philadelphia, JB Lippincott
Co, 1983, p 27.
The occult primary condition exists when a metastatic carcinoma, usually An occult or "unknown”primary
squamous cell carcinoma or malignant melanoma, is found in a cervical cancer occurs when a malig¬
nant cervical lymph node is di¬
lymph node other than the supraclavicular nodes. The site of the primary agnosed and no primary site in
tumor in the upper respiratory tract or food passage is not evident, even the head and neck can be
with careful endoscopic examination including “directed” biopsies of all found.
Another technique involves swinging a muscle pedicle flap from the levator
scapulae muscle to protect the carotid artery. When the pectoralis major
myocutaneous flap is used to reconstruct the pharynx or oral cavity, the
muscle adds bulk to the site of the neck dissection and protection of the
carotid artery.
An additional factor that must be recognized when planning a radical neck
dissection is the associated weakness on elevation of the ipsilateral arm due
to the loss of innervation of the trapezius muscle. The accessory nerve may
have to be excised because of its intimate association with the spinal accessory
chain in the upper neck.
A modification of the standard radical neck dissection which involves
Supraomohyoid neck dissection resection of the jugular, submandibular, and subdigastric nodal areas above
can be performed for tumors of
the omohyoid is known as a supraomohyoid neck dissection. Indications for
the oral cavity. Midline tumors
may require bilateral supra¬ this procedure include tumors of the anterior oral cavity and lip. In cases of
omohyoid neck dissections. tumors of the pharynx, base of the tongue, or larynx in which bilateral nodal
metastases are palpable, another option is to perform the ipsilateral neck
dissection at the time of resection of the primary tumor, followed in six
weeks by neck dissection on the opposite side. This two-stage, or “split,”
procedure is associated with considerably less morbidity than a bilateral
simultaneous radical neck dissection. If it is possible to preserve one jugular
vein without jeopardizing adequate tumor resection, postoperative morbidity
is considerably less.
The Bocca modification of a standard neck dissection offers yet another
alternative to radical neck dissection. Since the lymph nodes lie within the
fascial plane of the neck, it is possible to perform a careful dissection of the
layers of the superficial deep cervical fascia and its contents while preserving
the sternocleidomastoid muscle, jugular vein, and accessory nerve.
This modified neck dissection is then often followed with postoperative
irradiation therapy. The Bocca neck dissection is not done when (1) there
are large or multiple metastases, (2) there is radiation failure, (3) there is
extension into the muscles, (4) there are “fixed” metastases, or (5) there is
involvement of the accessory chain or posterior group of lymph nodes.
Because it is technically more difficult to perform a modified neck dissection
than a classic radical neck dissection, it should be undertaken only by those
doing the procedure frequently.
INVESTIGATIONAL PROTOCOLS
Induction chemotherapy 3 weeks Surgery 4-8 weeks Postoperative radiation
1-3 cycles
Chemotherapy
Solid tumors of the head and neck area have been generally resistant to
present chemotherapeutic agents. However, experimental and research pro¬
tocols have demonstrated initial response rates to certain combination Chemotherapy alone or in com¬
regimens. As exciting as these response rates have been, however, the bination with radiation therapy
can produce significant re¬
ultimate survival rate has not been appreciably altered. Chemotherapy thus sponse rates.
plays an adjuvant role in a research protocol setting. Some of the methods
in which chemotherapy has been employed are shown in Table 23-7.
The most common chemotherapy products currently used for squamous
cell carcinoma include methotrexate (MTX), 5-fluorouracil (5FU), and
cisplatin (Table 23-8). These drugs (except MTX) are administered by
intravenous infusion. Doxorubicin (Adriamycin) is often the control drug
used for sarcoma and may be combined with methotrexate. Mithramycin
has been used advantageously when hypercalcemia is associated with meta¬
static carcinoma.
The role of chemotherapy in the adjuvant setting is still to be defined.
Some studies have demonstrated a 70 per cent response rate for advanced
squamous cell carcinoma when two or three courses of chemotherapy are
administered preoperatively. This has not altered surgical wound healing,
but some patients have then refused surgery. Recurrence of tumor is then
always the result, and this time the tumor may not be operable. Chemo¬
therapy for recurrence of tumor in the previously operated, previously
irradiated site of the surgery has been much less effective.
Suggested Readings
It is not possible to cover the subject of head and neck cancer in this text. Selected additional
articles are suggested for more extensive reading on each of the subjects discussed in this
chapter.
General
McQuarrie D, Adams G, Schons A, Browne G (eds): Head and Neck Cancer: Clinical
Decisions and Management Principles. Chicago, Year Book Medical Publishers, 1985.
466 PART SIX—NEOPLASMS OF THE HEAD AND NECK
Million R, Cassisi NJ: Management of Head and Neck Cancer: A Multidisciplinary Approach.
New York, JB Lippincott Co, 1984.
Segren SL: Recent advances in radiation therapy of head and neck cancer. Head Neck Surg
4:227-232, 1982.
Silver CE: Surgery for Cancer of the Larynx and Related Structures. London, Churchill,
Livingstone, 1981.
Snow JB, Belber RD, Kramer S, et al: Randomized preoperative and postoperative radiation
therapy for patients with carcinoma of the head and neck: Preliminary report. Laryngoscope
90:930-945, 1980.
Suen JY, Myers EN (eds): Cancer of the Head and Neck. New York, Churchill Livingstone,
1981.
Vraebec DA, Heffron TJ: Hypothyroidism following treatment for head and neck cancer. Ann
Otol Rhinol Laryngol 90:449, 1981.
Neck Dissection
Bocca E, Pignataro O: A conservation technique in radical neck dissection. Ann Otol Rhinol
Laryngol 76:975-987, 1967.
Fletcher GH, Jesse RH: The place of irradiation in the management of the primary lesion in
head and neck cancer. Cancer 39:862-867, 1977.
Jesse RH, Ballantyne AJ, Larson D: Radical or modified neck dissection: A therapeutic
dilemma. Am J Surg 136:516-519, 1978.
Jesse RH, Fletcher GH: Treatment of the neck in patients with squamous cell carcinoma of
the head and neck. Cancer 39:868-872, 1977.
Johnson JT, Barnes EL, Myers EN, et al: The extracapsular spread of tumors in cervical node
metastasis. Arch Otolaryngol 107:725-729, 1981.
Medina JE, Byers RM: Supraomohyoid neck dissection. Head Neck Surg 11:111-122, 1989.
Schuller DE, et al: Analysis of disability resulting from treatment including radical neck
dissection or modified radical neck dissection. Head Neck Surg 6:551-558, 1983.
White D, Byers RM: What is the preferred initial method of treatment for squamous carcinoma
of the tongue? Am J Surg 140:553-555, 1980.
Maisel RH, Vermeersch H: Panendoscopy for second primary tumors in head and neck cancer
patients. Ann Otol Rhinol Laryngol 90:460-464, 1981.
McQuirt UF: Panendoscopy as a screening examination for simultaneous tumors in head and
neck cancer. Laryngoscope 92:569-576, 1982.
Vraebec D: Multiple primary malignancies of the upper aerodigestive system. Ann Otol Rhinol
Laryngol 88:846-854, 1979.
Adams GL, Duvall AJ: Adenocarcinoma of the head and neck. Arch Otolaryngol 93:261, 1971.
Eneroth CM: Salivary gland tumors in the parotid gland, submandibular gland and the palate
region. Cancer 27:1415-1418, 1971.
Frazell RL: Observations in the management of salivary gland tumors. Cancer 18:235-241
1968.
Johns ME: Parotid cancer: A rational basis for treatment. Head Neck Surg 3:132-144, 1980.
Sarcomas
Batsakis JG: The pathology of head and neck tumors: Nasal cavity and paranasal sinus. Head
Neck Surg 2:410-419, 1980.
Frazell E, Lewis J: Cancer of the nasal cavity and accessory sinuses. Cancer 16:1293, 1963.
Goefert H, Guillinondequi OM, Jesse RH, et al: Squamous cell carcinoma of the nasal
vestibule. Arch Otolaryngol 100:8-10, 1974.
Ketcham AS, Wilkins JM, Van Buren JM, et al: A combined intracranial facial resection for
tumors of the paranasal sinuses. Am J Surg 106:698, 1963.
23—MALIGNANT TUMORS OF THE HEAD AND NECK 467
Mendenhall NP, Parsons JT, Cassisi NJ, Million RR: Carcinoma of the nasal vestibule treated
with radiation therapy. Laryngoscope 97:626-632, 1987.
Myers EN, Schramm VL, Barnes EL: Management of inverted papilloma of the nose and
paranasal sinuses. Laryngoscope 91:2071-2084, 1981.
Session GA: Symposium: Treatment of malignancies of the paranasal sinuses. Laryngoscope
80:945, 1970.
Skolnik EM, Massari FS, Tenta LT: Olfactory neuroepithelioma. Arch Otolaryngol 81:644-
653, 1966.
Snow EB, Van Der Esch EP, Slotten EA: Mucosal melanomas of the head and neck. Head
Neck Surg 1:24-30, 1978.
Barrs DM, DeSanto LW, O’Fallon WM: Squamous cell carcinoma of the tonsil and tongue
base region. Arch Otolaryngol 105:479-485, 1979.
Harold CC: Management of cancer of the floor of the mouth. Am J Surg 122:487-493, 1971.
Jesse RH, Sugarbaker EV: Squamous cell carcinoma of the oropharynx: Why we fail. Am J
Surg 132:435-438, 1976.
Marks JE, Lee F, Smith PG, et al: Floor of mouth cancer: Patient selection and treatment
results. Laryngoscope 93:475-480, 1983.
Matz G, Shumrick DA, Aron BS: Carcinoma of the tonsil: Results of combined treatment.
Laryngoscope 84:2172-2180, 1974.
Parsons JT, Million RR, Cassisi NJ: Carcinoma of the base of the tongue: Results of radical
irradiation with surgery reserved for irradiation failure. Laryngoscope 92:689-696, 1982.
Strong EW: Carcinoma of the tongue. Otolaryngol Clin North Am 12:107-114, 1979.
DeSanto LW: The options in early laryngeal carcinomas. N Engl J Med 306:910, 1982.
Ogura JH, Bell JA: Laryngectomy and radical neck dissection for carcinoma of the larynx.
Laryngoscope 62:1, 1952.
Kirchner J, Som ML: Clinical significance of fixed vocal cord. Laryngoscope 81:1029, 1971.
Som ML: Conservation surgery for carcinoma of the supraglottis. J Laryngol Otol 84:655, 1970.
Strong MS: Laser excision of carcinoma of the larynx. Laryngoscope 85:1286, 1975.
Wang CC: Treatment of glottic carcinoma by megavoltage radiation therapy and results. AJR
120:157, 1974.
Adams GL, Paparella MM, Elfiky FM: Primary and metastatic tumors of the temporal bone.
Laryngoscope 82:1273-1285, 1971.
Conley JJ, Schuller D: Malignancies of the ear. Laryngoscope 86:1147-1163, 1976.
Lederman M: Malignant tumors of the ear. J Laryngol Otol 79:85, 1965.
Reconstruction
Baek S, Lawson W, Biller HF: An analysis of 133 pectoralis major myocutaneous flaps. Plast
Reconstr Surg 69:460-467, 1982.
Bakamjian VY: A two stage method for pharyngoesophageal reconstruction. Plast Reconstr
Surg 36:173-184, 1965.
Gluckman JL, et al: The free jejunal graft in head and neck reconstruction. Laryngoscope
91:1887-1894, 1981.
Schechter GL, Sly DE, Roger AL, et al: Set-back tongue flap for carcinoma of the tongue
base. Arch Otolaryngol 106:668-674, 1980.
Panje W: Prosthetic voice rehabilitation following laryngectomy. Ann Otol Rhinol Laryngol
90:116-120, 1981.
Singer MI, Blom ED: An endoscopic technique for restoration of voice after laryngectomy.
Ann Otol Rhinol Laryngol 89:52, 1980.
PART SEV
DISEASES OF THE
TRACHEA AND
CERVICAL
ESOPHAGUS
24
DISEASES OF THE LOWER
AIR PASSAGES, ESOPHAGUS,
AND MEDIASTINUM:
Endoscopic Considerations
by Leighton G. Siegel, M.D.
THE ESOPHAGUS
Esophageal Disorders
The most common esophageal disorders are probably related to motor The most common esophageal
function. They are generally classified as those of hypomotility or hyper- those of
motility or occasionally a combination of the two.
Functional dysphagia or dysrhythmia is a disorder of hypomotility. It
generally occurs in the older patient and produces the sensation of food
sticking substernally. On radiography the peristaltic waves seem to end in
the midportion of the esophagus, and swallowing is not completed until the
second dry swallow is made. Esophageal achalasia, sometimes called cardio¬
spasm, is a neuromuscular disorder. Failure of the esophagogastric junction
to relax with deglutition results in a proximal dilatation of the esophagus
with an absence of peristalsis. In achalasia the patient feels a need to force
or push food down with water or other beverages to complete swallowing.
There is a sensation of substernal fullness, and regurgitation is common. On
radiography there is a significant retention of barium in the esophagus, with
evident difficulty in passage from the esophagus into the stomach. In all
cases of achalasia esophagoscopy should be performed to rule out malignant
obstruction (Fig. 24-1).
Diffuse spasm of the esophagus is a disorder of hypermotility. Pain is the
primary symptom. This is associated with diffuse spasm of the lower part of
the esophagus and is usually precipitated by swallowing. These attacks are
intermittent, and between attacks the patient may swallow without difficulty.
471
472 PART SEVEN—DISEASES OF THE TRACHEA AND CERVICAL ESOPHAGUS
FIGURE. 24—1. Barium swallow demonstrating (A) corrosive esophagitis from chemical
ingestion, and (B) cardiospasm.
They may also occur without swallowing and may even awaken the patient
from a sound sleep. There may be no radiographic evidence of abnormalities,
but intraluminal esophageal pressure measurements may be diagnostic.
Differentiation between diffuse spasm and cardiac pain is occasionally
difficult.
A hiatus hernia, in which a portion of the stomach has herniated into the
Cough and/or hoarseness may thoracic cavity, is common and may produce a pressure sensation or pain
be the presenting symptoms of
an esophageal disorder. behind the lower sternum. Cough, dysphagia, palpitation, and tachycardia
may also be present. The pain is generally relieved when the patient assumes
an upright position and is aggravated when the patient is recumbent.
Radiographic studies and esophagoscopy are generally diagnostic.
Schatski s contraction ring is a concentric ring-like narrowing at the level
of the inferior esophageal sphincter. It produces dysphagia and discomfort
with regurgitation if more than a small amount of food is swallowed at once.
Diverticuli usually arise in the cervical esophagus and may produce
regurgitation of undigested food and progressive dysphagia as more food is
eaten. Radiographic studies are generally diagnostic.
Many systemic diseases produce esophageal symptoms. Examples of these
are scleroderma, dermatomyositis, myasthenia gravis, and cirrhosis with
esophageal varices.
Inflammatory disorders of the esophagus include acute esophagitis and
reflux esophagitis. Less often seen are tuberculosis and monilial inflamma¬
tions. Metabolic, degenerative, and neurogenic disturbances of the esophagus
may also occur. Benign and malignant neoplasia may arise from both the
esophageal wall and the mucosa or may originate in the stomach or
laryngopharynx and extend into the esophagus. Dysphagia, pain, and weight
loss are the most common initial symptoms of malignant disease, although
they may not occur early! Treatment depends upon size and location of the
neoplasm and consists of surgery/irradiation, or both.
24—DISEASES OF THE LOWER AIR PASSAGES, ESOPHAGUS, AND MEDIASTINUM 473
A great number of congenital anomalies of the esophagus exist. Some Anomalies that compress the
involve the esophagus alone. Others involve the esophagus and trachea. Still esophagus commonly compress
others are anomalies of adjacent structures that impinge on the esophagus. airPassa8esalso-
Esophageal absence is rare. A congenital duplicate esophagus may exist as
either a tube of a cystlike structure adjacent to the esophagus. Simple webs
are rare. Stenosis may be fibrotic or due to a failure of epithelialization of a
section of the esophagus. Congenital esophageal stenosis occurring at the
junction of the middle and proximal third may first become evident when
the infant begins taking solid foods. Several types of tracheoesophageal
fistulas exist, all of which require surgical therapy. Atresia without tracheo¬
esophageal fistula may require repeated bronchoscopic aspirations prior to
surgery. Vascular rings and other cardiovascular anomalies may produce
varying degrees of obstruction because of extrinsic pressure on the lumen of
the esophagus.
Caustic Ingestion
Corrosive esophagitis is most commonly produced by ingestion of house¬
hold cleaning agents, usually by children. The most destructive is sodium
hydroxide, or lye, which causes lysis of tissue and often deep penetration of
the esophageal wall. Liquid drain cleaners may damage the esophagus or
produce similar gastric lesions. Certain agents not only are caustic to the
esophagus but have severe systemic effects, such as renal failure.
If there is a history of possible ingestion of caustic agents, it is imperative
that the presence or absence of esophageal involvement be established. The When caustic ingestion is sus¬
presence or absence of oral pharyngeal ulcerations is of no help in deciding pected it is up to the physician
to prove or disprove that it has
if there is an esophageal burn. This can be established only by esophagos- occurred.
copy, which may be safely done provided that the scope is not passed beyond
the first visible esophageal injury. Esophagoscopy is generally performed 24
to 48 hours after ingestion. If the caustic agent produces an early severe
necrosis, perforation and resultant mediastinitis can occur. More commonly,
perforation does not occur, but in the healing process a scar circumferentially
constricts the esophagus, producing an esophageal stenosis (Table 24-1).
When large quantities of lye are ingested, as in adult suicide attempts,
emergency total esophagogastrectomy may be required. If perforation is
likely, steroids are not given. The use of steroids can mask a developing
peritonitis or mediastinitis. In such cases all efforts are directed at the
The most common site for lodgment is at the entrance to the esophagus
at the level of the cricopharyngeus muscle. Other common sites are where
the esophagus is indented by the arch of the aorta and the left main bronchus
and at the entrance to the stomach. Pathologic lesions of the esophagus may
produce partial obstruction and cause the lodgment of foreign bodies that
otherwise would pass through quite easily. Children account for nearly 70
per cent of foreign body ingestion. They tend to carry coins, pins, toys, and
other objects in their mouths, with subsequent accidental ingestion.
A foreign body that lodges in the esophagus produces both difficulty in Dysphagia and odynophagia are
swallowing and discomfort. The position of a foreign body in the esophagus common symptoms.
can often be accurately localized by the patient. If the foreign body has
lodged in the cervical esophagus, pressure against the back of the larynx and
trachea may produce hoarseness, cough, and dyspnea. Saliva may flow out
of the esophagus and into the larynx.
Radiopaque foreign bodies may be seen easily on posteroanterior and
lateral chest radiographs. Radiographs should include all areas from the
nose to the anus. Often more than one foreign body has been ingested, and
unless complete studies are made, additional objects, such as a needle that
has passed into the colon, could be missed. More commonly, the foreign
body is radiolucent and is not seen on plain roentgenogram. Thin metallic P.A. and lateral x-rays are
foreign bodies can be seen only if radiographed on edge. For this reason needed. Avoid large swallows of
barium.
both posteroanterior and lateral films are indicated. An esophagogram and
associated fluoroscopy should then be done. A large swallow of barium
should not be given, as it coats the walls of the esophagus with a thick white
paste that makes subsequent esophagoscopy very difficult. It is better to
have the patient swallow a bit of cotton or marshmallow with contrast
medium in it. Cotton fibers may catch on the foreign body for a moment or
two during deglutition, thereby revealing its presence through fluoroscopy.
Knowledge of the orientation of the foreign body in the esophagus is very
helpful in planning endoscopic removal (Fig. 24-2).
Symptoms associated with the ingestion of foreign bodies occur in three
stages. In the first stage of initial symptoms, there is a violent paroxysm of First stage
coughing or gagging. This occurs when the foreign body is first swallowed. Second stage
Third stage
The second stage is a symptomless interval. The foreign body has lodged,
and symptoms are no longer produced. This stage may last only a moment
or two. The third stage consists of the symptoms produced by complications.
There may be discomfort, dysphagia, obstruction, or perforation of the
esophagus with resultant mediastinitis.
Unless complete airway obstruction exists, first aid during the stage of What not to do.
initial symptoms should consist of resisting the urge to “do something.”
Slapping the patient on the back, hanging the child by the heels, putting a
finger down the patient’s throat, or attempting blind removal may convert a
simple, uncomplicated foreign body into a complicated obstructing one (Fig.
24-3). A more complete discussion on the management of acute airway
obstruction is found later in this chapter under Foreign Body Aspiration.
Esophageal foreign bodies generally require more urgent treatment than Prompt removal of esophageal
those in the tracheobronchial tree because of the danger of perforation of foreign bodies is more impor¬
tant than prompt removal of for¬
the thin esophageal wall and resultant mediastinitis. Therefore, ingested eign bodies in the tracheobron¬
foreign bodies with sharp edges or points should be removed on any chial tree.
emergency basis. Blunt esophageal foreign bodies, such as coins, may be
trapped initially by esophageal spasm. Coins and other disc-shaped objects
476 PART SEVEN—DISEASES OF THE TRACHEA AND CERVICAL ESOPHAGUS
FIGURE 24—2. Common types of esophageal foreign bodies in children. A, Coin at the
cervical narrowing ("upper pinchcock”); 6, safety pin arrested at the same site as in A; C,
campaign button arrested temporarily in the lower third of the esophagus.
FIGURE 24—3. Possible methods of impaction of a foreign body by ill-advised first aid. (From
Tucker GF Jr: Minutes Report of the Committee for the Prevention of Foreign Body Accidents.
Trans Am Bronchoesophagol Assoc 49:181 — 183, 1969.)
Physical Examination
Physical examinations for esophageal disease should begin with an assess¬
Remember to examine the lar¬ ment of the patient’s voice and speech. Careful palpation of the neck may
ynx and neck when esophageal
reveal evidence of metastatic malignant disease or an enlarged or abnormal
symptoms exist.
thyroid gland. The larynx and trachea normally lie in the midline and should
be checked for deviation. There should not be tenderness over the cricopha-
ryngeus muscle. Intraoral examination may reveal abnormal weakness of the
tongue, soft palate, or pharyngeal walls or deviation of the uvula in the
presence of neurologic disease. Vagal paralysis may produce asymmetric
movement of the posterior pharyngeal wall. Mirror examination of the
hypopharynx and the larynx may similarly reveal a vocal cord paralysis or
abnormal puddling of secretions or saliva in the piriform sinuses. This
puddling is a particularly important sign that may indicate an esophageal
obstruction such as a foreign body or tumor.
Esophagoscopy
Esophagoscopy is indicated after careful history, physical examination,
and radiographic studies are completed. Esophagoscopy is advised when any
question remains about the diagnosis or if therapy may be instituted via
esophagoscopy. A negative radiographic study does not eliminate the need
for esophagoscopy, since many small mucosal lesions, nonradiopaque foreign
bodies, and nonspecific inflammatory changes can be diagnosed only in this
manner. Esophagoscopy is contraindicated in the presence of an aortic
aneurysm (Fig. 24-5).
Two basic types of esophagoscopes exist. One type is a rigid metal tube
with an oval lumen which contains a light carrier and a channel for aspiration
24—DISEASES OF THE LOWER AIR PASSAGES, ESOPHAGUS, AND MEDIASTINUM 479
FIGURE 24—6. Approximate distance of the esophageal anatomic landmarks from the
upper incisor teeth as seen by the endoscopist, (Adapted from Jackson C, Jackson CL:
Bronchoesophagology. Philadelphia, WB Saunders Co, 1950, p 229.)
FIGURE 24-7. Obstructive emphysema in a 3'/2-year-old child with a foreign body (peanut)
in the right main bronchus, a, On inspiration, the bronchus enlarges and air passes around
the foreign body to inflate the right lung, b, On expiration, the air escapes normally from
the left lung, but the right bronchus closes tightly around the foreign body, keeping the
air trapped on the right side. There is a mediastinal shift to the left.
FIGURE 24-8. Top, Anatomic landmarks in the bronchial tree (inverted, as presenting to
the bronchoscopist). Arrows indicate directions of bronchoscopic views. (From Norris CM:
Bronchology. In English GM [ed]: Otolaryngology. Vol. IV. New York, Harper &. Row, 1976,
Ch 30.)
Bronchi are designated by simple descriptive names and numbers, according to the
Jackson-Huber nomenclature. These designations are shown in the bronchoscopic report
form. (Adapted from Jackson and Huber, Overholt, and Boyden.)
24—DISEASES OF THE LOWER AIR PASSAGES, ESOPHAGUS, AND MEDIASTINUM 483
Tracheobronchial Disorders
Tracheobronchial congenital anomalies are not uncommon and generally
produce respiratory obstruction at birth or soon after. A clear voice distin¬
guishes tracheal from laryngeal obstruction. Tracheal atresia and agenesis
are obviously incompatible with life. Membranous tracheal webs may be
dilated with the tip of a bronchoscope. Longer webs may require more
extensive treatment. Tracheomalacia or flaccid trqcheal cartilages may be
seen on videofluoroscopy and may produce symptoms of dyspnea. Tracheo
esophageal fistulas are generally amenable to surgical correction. Supernu¬
merary bronchial lobes and fissures are occasionally seen.
Metabolic, allergic, and degenerative disorders include asthma, bronchiec¬
tasis, emphysema, and chronic obstructive lung disease. Aspiration or
retention of thickened secretions, especially in children and debilitated or
postoperative patients, may result in atelectasis or pneumonia. This is a
common problem that may be prevented or treated via bronchoscopy.
Culture for identification of infection, including tuberculosis, may require
bronchoscopy. The diagnosis of tracheobronchial and pulmonary malignan¬
cies requires bronchoscopic examination. Often a direct biopsy may be made
or washings for cytologic study can be obtained via the bronchoscope. Benign
tumors are diagnosed in a similar fashion. Blunt and penetrating trauma to
the chest may involve the tracheobronchial tree, requiring endoscopic
evaluation.
How much time do you have to If a complete obstruction has occurred, the foreign body must be disim-
dislodge a total airway obstruc¬ pacted or an alternate airway established within four minutes. Hypoxia
tion?
beyond this time limit results in permanent brain damage. Someone should
immediately be sent to obtain a sharp knife so that a tracheostomy or-
cricothyrotomy may be attempted if measures to disimpact the foreign body
fail. The measures described in the preceding paragraph may be attempted.
An attempt may also be made to forcibly expel any air remaining in the
lung. This is generally done by grasping the patient just below the sternum
and forcibly squeezing the upper abdomen. This is the so-called Heimlich
hug taught in standard cardiopulmonary resuscitation courses. If successful,
the diaphragm will be elevated, compressing the lungs. The foreign body
will be blown out of the airway so that the patient may breathe again.
Another method that may be attempted is mouth-to-mouth resuscitation,
either to force the object further down into the tracheobronchial tree so that
it is not completely obstructive or to draw it out. If all these measures fail
to establish an airway, an emergency tracheostomy or cricothyrotomy must
be attempted. This procedure is described in Chapter 25.
The second stage is symptom¬ The second stage is the symptomless interval when the foreign body
less. becomes lodged in one position. This stage may last only an instant or may
extend over a number of years.
The third stage is complication. The third stage is the stage of complications. Obstruction, erosion with
infection, hemorrhage, or perforation may again draw attention to the
foreign body. The foreign body lodged in the larynx or the cervical esophagus
produces discomfort, hoarseness, cough, and perhaps dyspnea. Foreign
bodies in the trachea may move back and forth between the carina and the
bottom of the glottis with respiration, producing an audible slap and a
palpable thud. Traumatic laryngeal edema in this situation may result in
hoarseness and later airway obstruction.
Three types of bronchial ob¬ If the foreign body is in the bronchus, three physiologic possibilities exist
struction exist: complete, in terms of obstruction to air flow. If the object completely obstructs a
check-valve, and nonobstruc¬
tive.
bronchus, peripheral atelectasis results as air is absorbed from the distal
lung into the blood. If the object is nonobstructive, allowing air to flow
around it on both inspiration and expiration, all that may result is an asthma¬
like localized wheezing. Many foreign bodies have been thus misdiagnosed
as asthma. The third possibility, and the one most commonly found, is a
partial obstruction with the foreign body acting as a check-valve. The
bronchus expands on inspiration, allowing air to flow past it into the distal
lung. The bronchus contracts around the foreign body during expiration,
trapping air in the distal lung. This produces an emphysema peripheral to
the foreign body. If the foreign body is left in place, pneumonia, abscess,
or hemorrhage may occur. The possibility of a foreign body is one reason
for bronchoscopy in the presence of persistent or recurrent pneumonia,
localized wheezing, or hemoptysis.
Physical examination should give careful attention to auscultation for
findings compatible with atelectasis, emphysema, or wheezing. Mirror ex¬
amination of the larynx and hypopharynx may reveal foreign bodies present
in this area.
X-rays for a foreign body in the A radiograph, particularly in children, should include the entire area from
thoracic area should include the the top of the nose to the rectum. This is because children often have
neck and abdomen.
aspirated or ingested more than one foreign body. In such cases it is possible
to be looking for a toy in the trachea and miss another object that has
24—DISEASES OF THE LOWER AIR PASSAGES, ESOPHAGUS, AND MEDIASTINUM 485
migrated to the colon or has been coughed into the nasopharynx. Postero-
anterior and lateral chest radiographs are needed. In addition, and perhaps
most important, radiographs at the height of inspiration and at the end of
expiration are required. If these inspiratory and expiratory films are ne¬ Inspiratory and expiratory chest
glected, the presence of a foreign body may be missed. A film taken only at x-rays are helpful.
the height of inspiration may not show a check-valve emphysema. A film
taken only on expiration will miss an obstructive atelectasis. Fluoroscopy
during inspiration and expiration may also be valuable. The mediastinum Look for mediastinal movement.
moves toward the side of the foreign body on inspiration if there is a check
valve and when there is a complete obstruction. A radiopaque nonobstructing
foreign body may not be visible on chest radiograph (Fig. 24-7).
If a foreign body is suspected, the patient should be requested to obtain Instruct the patient /parent to
a duplicate of it so that the endoscopist can more accurately determine which bring a duplicate foreign body if
possible.
forceps and approach to use. The patient should be instructed to eat and
drink nothing, to reduce the risk of vomiting and subsequent aspiration at
the time of endoscopy. A foreign body lodged in the tracheobronchial tree,
not totally occluding the airway, is not as great an emergency as one that is
lodged in the esophagus unless it has sharp edges or is an uncooked or Uncooked or dehydrated vege¬
dehydrated vegetable, which can absorb fluids and swell within the lumen. tables are a special problem.
Patient History
Patients with presenting symptoms suggesting disease of the tracheobron¬
chial tree or lung should have a careful history with the following symptoms
and problems characterized:
Bronchoscopy
Bronchoscopy is indicated when the diagnosis of tracheobronchial or
pulmonary symptoms is not clearly established by radiography or when
therapy necessitates direct access to the tracheobronchial tree (Fig. 24-8).
Two basic types of bronchoscopes exist. One is a rigid metal tube with a
light source at the distal end and the capability of ventilating, the patient
during the procedure. The rigid bronchoscope gives a direct view of the
tracheobronchial tree and has the greatest latitude in terms of aspiration of
secretions, manipulation with forceps, and removal of foreign bodies. Bron-
choscopic telescopes may be placed through these to allow magnified direct
and angled visualization of the more peripheral bronchi. A wide variety of
foreign body and biopsy forceps are available for rigid bronchoscopes, many
having a built-in telescope for magnified viewing and manipulation.
The second type is the flexible fiberoptic bronchoscope (Fig. 24-9). The
larger of these bronchoscopes have small channels for aspiration of secretions
and insertion of a slender forceps for biopsy or foreign body removal as well
as a directable mobile tip. A small brush may be passed through the channel
to obtain brushing samples, under fluoroscopic control, from peripheral lung
lesions for histologic examination. The fiberoptic bronchoscope allows ex¬
amination and biopsy of bronchial segments more peripheral than can be
done through the rigid scope, particularly in the upper lobe branches.
Although the usual flexible bronchoscopes have a smaller diameter than the
comparable adult rigid scope, they are usually too large for use in infants
and children. Flexible fiberoptic bronchoscopes designed for children have a
smaller diameter but may lack a channel for suction or instrumentation and
may not have a directable tip. They normally cannot be used for anything
except diagnostic visualization and are not suitable for foreign body removal.
Bronchoscopy may be done under local or general anesthesia. The choice
FIGURE 24-9. Olympus flexible fiberoptic bronchoscope. Inset shows closeup views of
the brush (utilized for obtaining cells from peripheral lesions) and biopsy cups.
24—DISEASES OF THE LOWER AIR PASSAGES, ESOPHAGUS, AND MEDIASTINUM 487
MEDIASTINOSCOPY
FIGURE 24-10. Access to the paratracheal and parabronchial area is direct. Arteries
intervene between veins and tracheobronchial tree. The Zeiss Operating Microscope
offers superior light and magnification and enables photography. (From Paparella MM,
Shumrick DA [eds]: Otolaryngology. Vol. 3. Philadelphia, WB Saunders Co, 1973, p 734.)
488 PART SEVEN—DISEASES OF THE TRACHEA AND CERVICAL ESOPHAGUS
References
Becker W, Buckingham RA, Holinger PH, et al: Atlas of Ear, Nose and Throat Diseases. 2nd
ed. Philadelphia, WB Saunders Co, 1984.
Heimlich HJ: A life-saving maneuver to prevent food-choking. JAMA 234:398-401, 1975.
Harris CS, Baker SP. Smith GA, Harris RM: Childhood asphyxiation by food. A national
analysis and overview. JAMA 251:2231-2235, 1984.
Jackson C, Jackson CL: Bronchoesophagology. Philadelphia, WB Saunders Co, 1950.
Paparella MM, Shumrick DA (eds); Otolaryngology. Vol 3: Head and Neck. Philadelphia, WB
Saunders Co, 1980.
Ritter FN: Questionable methods of foreign body treatment. Ann Otol 83:729-733, 1974.
Rothmann BF, Boeckman CR: Foreign bodies in the larynx and tracheobronchial tree in
children. A review of 225 cases. Ann Otol 89:434-436, 1980.
25
TRACHEOSTOMY
by Robert H. Maisel, M.D.
HISTORY
This surgical procedure has a long and, until recently, maligned reputation.
McClelland believed that five periods in the development and acceptance of
tracheostomy were discernible. The earliest recorded tracheostomy is buried
in legend. The sacred Hindu book Rig Veda, written between 2000 and 1000
bc, mentions “the bountiful one who can cause the windpipe to reunite
when the cervical cartilages are cut across.” Historians, however, consider
Asclepiades, born about 124 bc, the first to carry out the operation. No
surgeon’s account appears before Brasavola (1500-1570) described his suc¬
cessful surgical management of Ludwig’s angina in 1546. In the second era,
from 1546 to 1833, such surgical attempts were feared, and only 28 successful
tracheostomies were reported in this three-century period.
Trousseau and Bretonneau popularized the operation in France, using it
for treatment of diphtheria with a 25 per cent rate of success (a high cure
rate for the time). This third era of tracheostomy was highlighted in 1921
when Chevalier Jackson described the modern techniques and warned against
incising the cricoid cartilage or first tracheal ring. This admonition, when
followed, reduced the high complication rate from iatrogenic subglottic
stenosis. During this era, the indication for such surgery was almost exclu¬
sively upper airway obstruction.
The fourth era began in 1932, with Wilson’s suggestion that airway toilet
could be managed in difficult cases of respiratory paralysis, specifically
poliomyelitis. Galloway also led the thinking of this era, using tracheostomy
for indications such as head injury, severe chest injury, barbiturate intoxi¬
cation, and postsurgical airway control. This was the period of enthusiasm.
During these years the aphorism “if you think about doing a tracheostomy,
do it” was bora, and this adage is still followed by many to prevent crisis
tracheostomy.
490
25—TRACHEOSTOMY 491
Prolonged Intubation
Since the early 1960s the firm trend to use tracheostomy to bypass
obstruction and to manage accumulated secretions or ventilatory failure has
begun to be challenged. Endotracheal intubation has become more compet¬ Careful endotracheal Intubation
itive, with better nursing care, including frequent suctioning of the trachea, has altered the indications for
“emergency" tracheostomy.
and the use of humidified air and new tubes made of improved plastics that
decrease the amount of crusting, thus no longer necessitating frequent
exchange of the tube. The speed of intubation and the ease of extubation,
as well as the avoidance of the complications of tracheostomy, make the
technique attractive.
Prolonged intubation has significant complications, with morbidity and
some mortality. These include acute sinusitis; nasal, mucosal, and cartilage
destruction; serous otitis media; and laryngeal and subglottic problems. The
laryngeal problems can be more difficult to treat than tracheal stenosis posed
by tracheostomy because the larynx is a functional muscular organ and not
just a hollow tube to conduct air. Reconstruction can be difficult, and
rehabilitation is occasionally unsatisfactory.
At present, many centers intubate patients in emergency situations or if
removal of the tube is expected within one week. After 72 hours, if the tube
is still needed, the tracheostomy is done. Few complications at the laryngeal
and subglottic regions have occurred following this protocol. Prolonged adult
intubation does increase the risks and severity of complications.
In children and infants more prolonged intubation has been successful. It Prolonged intubation is better
may be maintained for up to six days, as shown by clinical studies. Infants tolerated in infants and new¬
borns than in adults.
have been managed for longer periods because of the great difficulty in
performing and caring for tracheostomies in these patients. In neonatbs,
intubation up to six months has been reported with success. However,
occasional laryngeal complications have been seen after prolonged intubation
in children.
The frequency of subglottic stenosis may increase as more infants with
various respiratory distress syndromes are managed this way, and caution is
urged before yielding to the temptation to insert a tube. The more recent
adage, “if you think of doing a tracheostomy, intubate and think again,”
has some merit but must be tempered by the realization that intubation is a
temporary measure and must be either discontinued or replaced by a
tracheostomy tube.
The argument over intubation versus tracheostomy is still unsettled.
However, if intubation is elected, conversion to tracheostomy after six days
in children and after 72 to 96 hours in adults at present appears to be most
satisfactory.
PRESENT INDICATIONS
ANATOMY
The trachea is a hollow tube supported by (elastic) cartilage rings that are
incomplete posteriorly. It begins below the signet ring-shaped cricoid carti¬
lage and extends directly anterior to the esophagus, descending into the
thorax, where it divides into the two main bronchi at the carina. The great
vessels of the neck parallel the trachea laterally and are encapsulated by the
carotid sheath. The thyroid gland lies over the trachea anteriorly and
25—TRACHEOSTOMY 493
laterally, and the isthmus crosses it anteriorly, usually at the level of the
second to fifth tracheal ring. The recurrent laryngeal nerves lie in the
tracheoesophageal groove. Deep to the subcutaneous tissues and anteriorly
overlying the trachea are the suprasternal strap muscles, which attach to the
thyroid and hyoid.
SURGICAL TECHNIQUE
OD ID OD ID OD ID Size
ACE SIZE (mm) (mm) (mm) (French)
at this point, and the umbilical tape that binds the tracheostomy tube around
the neck is tied firmly while flexing the head. The skin incision is not sutured
(Fig. 25-1).
Cuffed tubes are low pressure The cuff, which should be compliant, is then inflated. Cuffs that have
(compliant) to prevent scarring. 5een correctly manufactured to provide sufficient compliance are available;
if these are not used, cuffs can be prestretched by the method of Geffin.
Tracheostomy in Children
When performing elective tracheostomy in children and infants, the smaller
the patient, the greater the importance of controlled ventilation by a mask
or tube. When the airway is controlled, a horizontal incision is cosmetically
more satisfactory, and meticulous midline dissection is crucial because of the
close proximity of the great vessels. Palpation of the endotracheal tube or
bronchoscope facilitates this. The pleural cupulae ascend into the neck on
inspiration, particularly under positive pressure respiration, and these must
be avoided during dissection, since they may overlie the trachea. Nicking
the cupula will cause pneumothorax. Needle aspiration of the trachea is an
accepted procedure in children to ensure that a major arterial vessel is not
Silk sutures placed at surgery mistaken for the airway. Silk sutures are placed anterolaterally on each side
are used as guides should acci¬ of the midline through two tracheal rings before a vertical incision in the
dental decannulation occur.
second and third (and sometimes fourth) rings is made. Again, the cricoid
and first ring are not to be violated. No tracheal tissue is excised in children.
The tube size appropriate to the tracheal lumen is used.
Emergency surgical control of the airway is gained by cricothyrotomy or
tracheostomy. A vertical skin incision causes less hemorrhage, and the
procedure is quickly performed, staying in the midline. No cartilage is
25—TRACHEOSTOMY 495
excised before the airway is controlled and cannulated. The cricoid and first
ring should be avoided. If cricothyrotomy is urgently elected, it can be done
by using a Mosher trocar or scalpel blade, extending the neck, identifying Cricothyrotomy is avoided in in-
the thyroid and cricoid cartilages, and incising the cricothyroid membrane. ,lints■
The airway is maintained with retractors or, if available, an appropriately
sized endotracheal or tracheostomy tube. The cricothyrotomy procedure
allows immediate access to the airway safely below the true vocal cord in a
relatively bloodless field; it is converted to a usual tracheostomy as soon as
possible under controlled conditions. Similarly, an emergency tracheostomy
496 PART SEVEN—DISEASES OF THE TRACHEA AND CERVICAL ESOPHAGUS
flow. This airstream goes through the larynx and creates a quiet but
comprehensible voice.
An alternative to tracheostomy in the neonate who has developed acquired Anterior cricoid split offers an
subglottic stenosis is the anterior cricoid split. The cricoid cartilage, the alternative to tracheostomy in a
select group of children with
upper two tracheal rings, and the inferior portion of the thyroid cartilage subglottic stenosis.
are divided in the midline over an endotracheal tube. The child is placed in
a pediatric intensive care unit while intubated for ten days. Precautions are
taken to avoid excessive head motion, and antibiotics are administered to
prevent infections with hospital-acquired Staphylococcus or Pseudomonas
species. At day ten, the endotracheal tube is withdrawn.
The rationale for such a procedure is that acquired subglottic stenosis is
FIGURE 25—5. Silicone tracheal cannula designed to be used in place of a tracheotomy tube.
A, The cannula extends only to the inner surface of the anterior tracheal wall, eliminating foreign
body projecting into trachea. B, Cannula, wing-shaped faceplate, plug, and ring washer. The
groove along the cannula’s long axis assists in drainage of secretions and serves to identify the
inferior aspect of the cannula. The first three rings adjacent to flange are triangular to assist in
fixing the cannula in place and make it difficult to displace anteriorly. The remaining grooves
serve to secure faceplate or ring washer in place. The plug has a head to prevent introduction
too far into the lumen of the cannula. C, Silicone tracheal cannula for long-term use shown with
two washers and a plug. The surface adjacent to the intraluminal junction is smooth to permit
and encourage growth of epithelium from both trachea and skin. (From Montgomery WW,
Montgomery SK: Manual for use of Montgomery laryngeal, tracheal, and esophageal prostheses.
Ann Otol Rhinol Laryngol (Suppl 125) 95(4): 1 — 16, 1986.)
always soft in its initial stages. This is due to the formation of granulation
tissue in the subglottic space. This granulation tissue, in large part, has an
edematous component, and the anterior cricoid split is a decompressive
procedure to allow the escape of edema from the otherwise intact cricoid
ring. In this manner, the inexorable process of granulation tissue leading to
firm cicatrix is interrupted.
Although the procedure was introduced approximately six years ago,
enough experience has been gained to show that its success rate is now
approximately 75 per cent. Thus, a large number of neonates with acquired
subglottic stenosis are able to be extubated and not have a need for artificial
airway in the form of a tracheostomy. At present, the procedure is reserved
for those children who are under three years of age and whose subglottic
stenosis is still in the soft granulation tissue stage. Since the procedure is a
decompressive one, it would not succeed when the subglottic stenosis has
progressed to a firm, dense cicatrix. The child must be otherwise extubatable
by all other parameters and not have any glottic pathology that would require
airway bypass (tracheostomy).
25—TRACHEOSTOMY 499
The upper airway has been bypassed, and its functions of warming of the
inspired air to 36°C, humidification, and removal of particulate matter have The tracheostomy incision is not
been lost. The cilia of the trachea lose function, and the cough is ineffective. sutured closed.
Early care of the stoma requires auscultation of the chest, and an immediate
chest radiograph is necessary in all children to check tube position so it is
not beyond the carina where it would enter the right bronchus and occlude
the left bronchus, and to assure that no pneumothorax has occurred. The
radiograph should be examined by the surgeon upon completion of the
procedure. Mediastinal emphysema is frequent on chest radiograph, and
repeat films at 48 hours should show no extension of the emphysema. A
humidity collar passing cool water-saturated air or oxygen is placed over the
stoma. A bedside tray with a tracheostomy set and a tube for replacement,
scissors, and full suction apparatus should be available, as should a bell for
summoning help.
Tracheal secretions are copious during the first 24 to 48 hours after
surgery, regardless of the primary disease requiring tracheostomy. The
bronchorrhea must be cleared, for these secretions will inspissate and
produce atelectasis, pneumonia, and pulmonary vascular shunting. The
cough is insufficient, and aspiration of the secretions through the tube is
necessary. This is done as frequently as needed and at least every 15 minutes A loose gauze dressing is
for the first several hours. The frequency thereafter is individually deter¬ placed around the tracheal
stoma.
mined, based on the amount of secretions, auscultation of the chest, and
listening to the patient. A gurgling patient with a tracheostomy is at great
risk and must be suctioned. The technique is performed under sterile
conditions, using a new disposable catheter every time, with the operator
wearing gloves and washing hands between patients.
Secretions tend to accumulate in the trachea often just below the tube.
Bronchial aspiration is also necessary and is achieved by this suctioning
technique. The catheter is attached by a V connector (Fig. 25-6) to a vacuum
line. No negative pressure is supplied to the line unless the V is occluded.
The method of choice is to insert the catheter through the tracheostomy
tube lumen with no negative suction pressure. In tracheostomy tubes with
an inner cannula, the cannula is removed before this is done. After the
suction catheter resists further penetration into the bronchus, it is withdrawn
slowly and completely by rotating the wrist while a fingertip occludes the V.
This is repeated for the other bronchus after a rest period. The rest is needed
because vacuum suction removes air from the lung and if repeated at
frequent intervals will reduce the residual lung volume. Resuctioning of the
same side is continued until auscultation is clear or gurgling respiration from
the tracheostomy tube has ceased.
Tubes with an inner cannula require frequent removal and cleaning of the
cannula. PVC and Silastic tubes are of one piece construction and do not
accumulate crusts or mucus as much as metal tubes. They should be removed
and inspected 48 hours after surgery, replaced, and reinspected at weekly
intervals to ensure that a circumferential bolus of mucus does not occlude
the lumen. The plastic tubes are now constructed to be most malleable at
body temperature. This further decreases resistance to conformity to the
trachea size and direction, which is a problem of metal tubes.
Low-pressure plastic cuffs are now available for the tracheostomy tubes.
These are designed to keep the pressure against the trachea at less than 25
500 PART SEVEN—DISEASES OF THE TRACHEA AND CERVICAL ESOPHAGUS
cm H20. This has reduced the incidence of tracheal cuff stenosis. One of
the low-pressure tubes is shown in Figure 25-7.
The alert, intelligent adult can be taught complete care of the stoma, and
in children over six months old the tracheostomy can be cared for at home.
Great caution and careful thought should precede discharging from the
hospital a child younger than six months of age while the child is wearing a
tracheostomy tube.
Complications
Surgical Complications. Complications during surgery can arise frequently,
but the alert surgeon recognizes, prevents, and overcomes them. Hemorrhage
is prevented by elective midline dissection with ligature of all vessels and
careful examination of all oozing surfaces. Pneumothorax, a problem of
tracheostomy in children due to the pleural position, is prevented as
25—TRACHEOSTOMY 501
FIGURE 25—7. Three frequently used commercially available tracheostomy tubes. A, No. 6
Shiley tube (also available with nondetachable cuff). B, Lanz tube No. GTI8 with controlled
pressure cuff to keep pressure on tracheal wall below 26 mm Hg. C, Jackson metal tube.
Cuff of rubber is attached by user. Not supplied by Pilling with cuff.
References
Bryant LR, Trinkle JK, Dubilier L: Reappraisal of tracheal injuries from cuffed tracheostomy
tubes: Experiments in dogs. JAMA 215:625-628, 1971.
Cavo J, et al: Low resistance in tracheotomy tubes. Ann Otol Rhinol Laryngol 82:827-830,
1973.
Chew JOY, Cantrell RW: Tracheostomy: Complications and their management. Arch Otol
96:583-645, 1972.
Cotton RT, Myer CM, Bratcher GO, Fitton CM: Anterior cricoid split, 1977-1987. Arch
Otolaryngol Head Neck Surg 114:1300-1302, 1988.
Cotton RT, Seid AB: Management of the extubation problem in the premature child: Anterior
cricoid split as an alternative to tracheotomy. Ann Otol Rhinol Laryngol 89:508-511, 1980.
Fearon B, Cotton R: Surgical correction of subglottic stenosis of the larynx in infants and
children. Ann Otol Rhinol Laryngol 84:231-235, 1974.
Goodall EW: The story of tracheotomy. Br J Child Dis 31:167-252, 1934.
Grillo HC, Cooper JD, Geffin B, Pontoppian H: A low pressure cuff for tracheostomy tubes
to minimize tracheal injury. J Thorac Cardiovasc Surg 62:898-907, 1971.
Jackson C: High tracheotomy and other errors: The chief causes of chronic laryngeal stenosis.
Surg Gynecol Obstet 32:392-397, 1921.
Mathog RH, Kenan PD, Hudson WR: Delayed massive hemorrhage following tracheostomy.
Laryngoscope 81:107-119, 1971.
McClelland RMA: Tracheostomy: Its management and alternatives. Proc R Soc Med 65:401-
403, 1972.
Montgomery WW, Montgomery SK: Manual for use of Montgomery laryngeal, tracheal, and
esophageal prostheses. [Supplement 125] 95(4):1—16, 1986.
Sahni R, Blakley BW, Maisel RH: Flap tracheostomy in sleep apnea patients. Laryngoscope
95(2):221-223, 1985.
Schuller DE, Birck HG: The safety of intubation in croup and epiglottitis: An eight year follow
up. Laryngoscope 85:33-46, 1975.
Snow JB, Preston WJ: Dry, aseptic method of tracheotomy care. Arch Otol 92:191-194, 1970.
Szachowicz E, Walsh J, Maisel RH: TALC tracheostomy tube: Normal laryngeal speech while
on a ventilator. Otolaryngol Head Neck Surg 89:221, 1981.
PART EIGHT
PLASTIC AND
RECONSTRUCTIVE
SURGERY
26
FACIAL PLASTIC SURGERY
by Peter A. Hilger, M.D.
GENERAL PRINCIPLES
505
506 PART EIGHT—PLASTIC AND RECONSTRUCTIVE SURGERY
Keloid and hypertrophic scars The processes of synthesis and lysis are in a delicate balance and, if
are due to abnormal collagen disturbed, disorders such as keloid or hypertrophic scar formation can occur.
metabolism. vitamin c and OXygen are essential cofactors for the rapid production of
Epithelialization
Basal epithelial cells begin to migrate across a wound within hours of
injury and produce collagen lytic enzymes that allow the cells to cleave
through collagen at the junction of eschar and viable tissue. Eschar, fibrin,
Epithelialization occurs more and old cellular debris impede epithelialization. If a wound is kept moist
rapidly if the wound surface is ancj protected so that no eschar forms, optimal epithelialization occurs if
moist' there is sufficient oxygenation.
It is important to remember that suture tracts are microwounds and, as
such, epithelial cells follow sutures into the wound to produce a cyst or a
sinus tract. To minimize these disfiguring complications early suture removal
and replacement or substitution by suture tape is recommended (Fig. 26-1).
Wound Contraction
Myofibroblasts cause wound Wound contraction is not the exact equivalent of contracture. Myofibro-
contraction. blasts are responsible for wound contraction; causing the wound bed to
contract decreases its surface area, which occasionally may be unfavorable.
While a smaller wound requires less time to heal, the contraction may distort
normal adjacent structures, e.g., ectropion, “trap-door” deformity. Corti¬
costeroids inhibit this process and may be useful clinically. In an open wound
this process can also be inhibited by stenting the edges during the contraction
phase or by applying a full-thickness skin graft.
Incisions
Surgery of the face requires careful planning of operative incisions. Surgical
scars may be camouflaged by placing the incision along favorable lines and
approximating wound edges without tension.
Incisions are less apparent if they are concealed in natural crease lines
and into shadows (Fig. 26-2). Usually the crease lines* are the lines of least
tension and, in such areas, the tendency for widening of the scar is minimal.
“Lines of least tension and crease lines should not be confused with Langer’s lines, which
are related to lines of least tension only in the cadaver. In the living subject these lines of least
tension may change as they are affected by the adjoining dynamic forces of the tissues.
Major exceptions are noted in the glabella area, where the lines of least skin
tension are horizontal rather than vertical, and in the lateral eyelid, where
they are horizontal rather than slanted upward. Concealment of scars can
also be achieved by placing incisions within hair-bearing areas, behind the
ears, and in shadows, such as at the side of the nose and beneath the lower
lip.
Incisions on the face are usually made with a small knife blade, i.e., Bard-
Parker No. 15. The incision is initiated using the belly of the blade, with the
physician holding tension on the skin in the direction of the incision line
(Fig. 26—3). The blade is rotated through the skin and to a more vertical
position to create a perpendicular cut and then rotated back to the original
position so that the belly is used to create the major portion of the incision.
The end of the incision is also cut in a perpendicular plane.
It is desirable to make this incision in a way that will minimize skin tension
at the surface. The skin is then undermined in all directions for approximately
1 cm, a maneuver that tends to reduce the traction from underlying structures
and provides for the advancement of skin during wound closure. Gentle use
of sharp hooks avoids trauma to the skin edges. Hemostasis is achieved with
cauterization of small vessels.
*No prophylactic immunization is required if the patient has had a booster within the previous year.
Note. With different preparations of toxoid, the volume of a single booster dose should be modified as stated on the package label.
Source: American College of Physicians and Surgeons. Committee on Trauma: Early Care of the Injured Patient Philadelphia WB
Saunders Co. 1972. p. 39.
510 PART EIGHT—PLASTIC AND RECONSTRUCTIVE SURGERY
a. Horizontal b. Vertical
interrupted mattress interrupted mattress
Local Flaps
Rotation, transposition, and advancement flaps are used primarily in the
repair of facial defects. A rotation flap rotates on a pivot point (Fig. 26-8),
a transposition flap is transposed over adjacent skin (Fig. 26-9), and
advancement flaps are advanced in a straight line. Local flaps can be safely
designed with up to a 4:1 length:width ratio (Figs. 26-6 and 26-7).
Ac.ancement flap
Rotation flap
a. b.
FIGURE 26-8. Rotation flap, a. Tissue is rotated about a pivot point to close a
wedge-shaped defect, b, Result after closure.
Transposition flap
Rhomboid flap
FIGURE 26—10. Rhomboid flap, a. The defect to be closed resembles two equilateral triangles placed base
to base, b, A flap of similar size is created with its base at one of the two 60-degree angles, c, Transposition
of the flap, d, The flap closes the recipient site, and the donor site is closed directly. The direction of
tension of the wound is shown and should be oriented in a relaxed skin tension line.
514 PART EIGHT—PLASTIC AND RECONSTRUCTIVE SURGERY
M-Plasty 2.
b.
The radial forearm flap is a good example of this type of flap. The lateral
half of the radius and the thin overlying skin can be transferred to reconstruct
a portion of the mandible and the adjacent intraoral lining or overlying skin.
Crafts
Skin gratts are classified according to the thickness of the transplanted
tissue (Fig. 26-12). Thin, split-thickness grafts are taken at approximately
the superficial dermis (about 0.012 inch), while the thick, split-thickness
grafts are excised to a deeper level of the dermis. Preferred donor sites are
the thighs, upper arms, buttocks, scalp, and abdomen.
Special instruments are available to obtain these grafts. Small grafts are
probably best removed with a small battery-operated dermatome. Larger
grafts may be taken with an electric, air-driven or hand-operated dermatome
(Fig. 26-13).
FIGURE 26-13. Brown electric driven (left) and Padgett manual (right) dermatomes.
516 PART EIGHT—PLASTIC AND RECONSTRUCTIVE SURGERY
Bolster
a. b.
FIGURE 26-14. Bolster to secure a
Cotton skin graft, a, A skin graft is sutured to'
bolster a defect; several sutures are left long.
b, A cotton bolster is then placed
over the graft and secured with the
sutures. The pressure keeps the graft
Skin
stabilized on the donor site, permit¬
graft ting nourishment and vascular in¬
growth.
Trap door
Graft techniques usually require the immediate transfer of the graft to the
recipient site. The graft should be immobilized by sutures and a tie-over
bolus pressure dressing (Fig. 26-14). Stab wounds or “darts” within the graft
may help to provide drainage of blood and serum. Donor sites are managed
by occlusal dressings, open dry technique, or coverage with an adherent
semipermeable membrane dressing. The donor site heals by epithelial
migration from skin appendages that remain in the bed of the donor site.
Full-thickness grafts, as the name implies, involve the excision of the
entire thickness of skin. The skin is usually excised in the form of an ellipse
from the supraclavicular or postauricular area and cleaned of subcutaneous
fat. The donor site is undermined and closed primarily. Transplanted full¬
thickness grafts are sutured to the recipient site and immobilized by pressure
dressings similar to those used in the management of split-thickness grafts.
Problem Solution
a Anterior
view FIGURE 26-15. Trap door defect. A
narrow flap of tissue may heai with an
elevated contour or trap door defor¬
mity. This can be treated by undermin¬
ing the tissues around the flap, which
Cross allows a sheet of scar tissue to form
sectional that matures with less flap elevation.
view
Sagittal
view
26—FACIAL PLASTIC SURGERY 517
Keloid
The incidence of keloid formation increases with increased pigmentation
of the skin. Keloids occur between the ears and waist and tend to spread
beyond the original wound; the overlying epithelium of the keloid is darker
than the surrounding skin. The rates of both collagen synthesis and lysis in
the keloid are greater than normally observed. Formation of keloids may be
related to melanocyte-stimulating hormone, which is suppressed by steroids.
Treatment consists of intralesional corticosteroids, subtotal excision, and/or
pressure for four to six months. Rarely, low-dose radiation therapy is
applicable.
Hypertrophic Scars
Hypertrophic scars, which are frequently difficult to differentiate from
keloids, usually stay within the boundaries of the wound and occur more
frequently in areas of motion or skin tension. Tension on wounds increases
collagen formation and may explain the occurrence of this problem. Treat¬
ment consists of intralesional corticosteroids, the therapeutic application of
pressure (22 mm Hg), and Z-plasty or graft if the scar is in an area of
tension.
Unsightly Scars
Although most abrasions, contusions, and lacerations of the face heal with
minimal scarring, a small group of individuals develop a significant deformity.
Scars that are wide, red, long, or oriented in an unfavorable direction or
have skin edges at different levels are more noticeable. Erythema, often
seen in immature scars, usually decreases over four to six months. However,
if the scar is under tension the erythema persists for a longer period of time.
Scar revision should be consid¬
Treatment consists of broken line scar revision, dermabrasion, or injectable ered after scar maturation.
lling substances. In most cases treatment consists of revision of the scar
tissue, timed to coincide with the maturation of wound healing. The
techniques of scar revision are listed in Table 26-2.
FIGURE 26-16. Z-plasty. A technique to lengthen and change the direction of a scar is shown.
FIGURE 26—17. Large scar of temple areas, distorting the eyebrow, and appearance after
excision with Z-plasty technique. (From Mathog, R. H.: Scar revision. Minnesota Med
5731-36, 1974.)
26—FACIAL PLASTIC SURGERY 519
FIGURE 26-19. A large, wide scar of the cheek caused by a dog bite, and the result of
treatment by zigzagplasty technique.
520 PART EIGHT—PLASTIC AND RECONSTRUCTIVE SURGERY
FIGURE 26—21. Rhytidectomy or face lift, a, Preoperative view demonstrating incisions in the
hair and preauricularly as well as the area to be undermined, b, Skin elevation, c. Excision of
redundant skin and skin closure, d, Postoperative result.
"\
26— FACIAL PLASTIC SURGERY 523
technique is not applicable in areas where the skin is very thin, such as the
eyelid.
Contour irregularities that are the result of aging or scar can also often be
improved with the injection of filling substances such as injectable collagen.
Recently, autologous fat injections have been advocated for this purpose,
but the ability of this technique to maintain improvement is unproven. No
permanent injectable filling substance is yet available with FDA approval.
Its prominent position in the center of the face makes the nose very
important to facial aesthetics. Because heredity or trauma may produce a
functionally or aesthetically unacceptable appearance, rhinoplasty is one of
the most commonly performed aesthetic procedures. The results of this
surgery can be very gratifying to both the patient and the physician and,
unlike some other cosmetic procedures such as surgery for the aging face,
the improvement is influenced very little by the passage of time.
Nasal correction requires both a functional and a cosmetic evaluation;
nasal obstruction is just as important as deformity of the external appearance.
A detailed history, examination of the interior of the nose, and evaluation
of the paranasal sinuses is essential to the diagnosis and correction of the
many conditions that cause nasal obstruction (discussed in Chapter 12).
Evaluation of the external nose requires a concept of beauty. The overall
proportion of the nose and general balance in relationship to the face should
be considered; that is, a small chin may give the appearance of an unusually
FIGURE 26-24. Technique of rhinoplasty, involving isolation of the bony and cartilaginous
skeleton, trimming of appropriate portions, and repositioning under controlled conditions.
524 PART EIGHT—PLASTIC AND RECONSTRUCTIVE SURGERY
large nose. In most cases it is desirable to have a narrow and straight (or
slightly curved) dorsum, a straight (nonretracted) columella, slight “supratip”
depression, and accentuation of the alar rim.
Rhinoplasty is designed to correct the' external appearance of the nose.
Often this procedure may be combined with a septoplasty, which is used to
correct internal, functional deformities (see Chapter 12). Essentially, the
rhinoplasty technique requires isolation of the bony and cartilaginous skel¬
eton and trimming and repositioning of the structures under controlled
conditions (Fig. 26-24).
In cases of deformities caused by loss of skeletal support, cartilage, bone,
or synthetic materials are implanted into the defect. During the healing
process the nose is immobilized and protected with external and internal
splints. Postoperative swelling may be observed for six months or more.
MENTOPLASTY
The chin, the nose, and the forehead have a usual balancing relationship
in the facial profile, and, in cases in which the chin is too large or too small,
mentoplasty is performed. Aberrant maxillary, mandibular, and dental
relationships may require surgical correction; it is important to evaluate the
entire facial skeletal contour before planning a surgical procedure that
26—FACIAL PLASTIC SURGERY 525
addresses only a small chin. A better functional and cosmetic result may be
produced by orthognathic surgery.
Mentoplasty can be done alone or in conjunction with rhinoplasty.
Enhancement of the chin may be accompanied by sliding the lower portion
of the bone of the chin forward (advancement genioplasty) or by implanting
some material, usually Silastic, in front of the chin (augmentation mento¬
plasty).
References
American College of Surgeons. Committee on Trauma: Early Care of the Injured Patient
Philadelphia. WB Saunders Co. 1972, pp 37-41.
Bernstein L: Z-plasty in head and neck surgery. Arch Otolaryngol 89:574-584, 1969.
Borges AF: Elective Incisions and Scar Revision. Boston, Little, Brown and Co, 1973, p 1014.
^9™269 272 ^973^ Reattachment of a totally amputated auricle. Arch Otolaryngol
Converse JM. et al: The aging face. In Converse JM (ed): Reconstructive Plastic Surgery 2nd
ed. Vol II, Philadelphia, WB Saunders Co, 1976.
Creelv JJ, Peterson JD: Carcinoma of the lip. Southern Med J 57:799-784, 1974.
Crikelair GF: Surgical approach to facial scarring. JAMA 172:160-162, 1960.
Farrior RT: A method of otoplasty. Arch Otolaryngol 69:400-408, 1959.
Fernandez AO, Ronis ML: The Treacher-Collins syndrome. Arch Otolaryngol 80:505-520,
Rutledge RT: The Pierre Robin syndrome. A surgical emergency in the neonatal period Br J
Plastic Surg 13:204-209. 1960. "
S™'hL JW' Chnical experience with the vermilion bordered lip flap. Plastic Reconstr Surg
27.527-543, 1961.
S^ CRt Surgical technique helpful in obtaining fine scars. Plastic Reconstr Surg 2:21-
Initial Care
Initial care is dependent upon the severity of injury. Maxillofacial and
laryngeal injury may range from the simplest nasal fracture without significant
epistaxis and only minor nasal deformity to the most massive facial crush
injury with extensive involvement of the entire head and neck. The initial
care involves rapid general evaluation of the patient’s vital signs and the
institution of basic life-support measures if appropriate.
Airway maintenance is the first Maintenance of the airway is the first priority and may involve suctioning
priority. Qf the orai or nasai cavity to remove blood or other debris. If the patient is
comatose or if mandibular fracture has resulted in instability of the floor of
the mouth with prolapse of the tongue into the pharynx, an oral airway may
be required. If, for whatever reason, an oral airway is unsatisfactory and
tracheal ventilation is necessary, endotracheal intubation is the method of
choice. Emergency tracheostomy is to be avoided if at all possible, since the
526
27—MAXILLOFACIAL TRAUMA 527
should be palpated for the presence of free air, which suggests rupture of
the tracheobronchial tree, and for crepitation or tenderness over the larynx
suggestive of fracture.
Cervical spine injury, such as fracture or dislocation, may be suggested by
nuchal muscle spasm, but this not a constant finding. It is advised that
severely injured patients be immobilized as though a cervical spine injury
had occurred until it is radiographically and clinically demonstrated that the
cervical spine is normal.
Radiographic Examination
Radiographic examinations and other tests may be helpful in arriving at
an accurate diagnosis following the history and physical examination. Frac¬
tures of the nose are usually best demonstrated in lateral radiographs, while
fractures of the middle third of the face and paranasal sinuses are best
demonstrated in the Waters projection. Laminagraphic evaluation may be
very helpful in attempting to determine whether fractures of the orbital floor
or anterior cranial fossa have occurred. Fractures of the mandible are best
demonstrated with oblique views of this bone or preferably with a panoramic
radiograph (Fig. 27-1). Computer-assisted tomographic scanning may be
extremely helpful in the diagnosis of facial bone and laryngeal injuries.
Reconstructions, as demonstrated in Figure 27-2, may be quite helpful in
treatment planning. Severe lacerations of the cheek may be evaluated by
sialography to determine whether the parotid duct is intact. This procedure
FIGURE 17—2. This CT reconstruction gives a three-dimensional view of the fractured right
maxilla.
Treatment Priorities
Very definite priorities have evolved in the care of the trauma patient
following initial resuscitative measures that are designed to stabilize the
airway and maintain cardiac output. The order of these priorities is as
follows: (1) evaluation and therapy of any central nervous system injury, (2)
evaluation and therapy of any abdominal or thoracic injury, (3) treatment The facial injury must not dis-
of soft tissue, facial, and extremity trauma, and (4) reduction and fixation tract systemic evaluation.
of both facial and extremity fractures. These guidelines, when applied to
facial trauma, dictate that soft tissue wounds be closed in the first four to
eight hours after injury.
If possible, fracture reduction should be done at that time. However, if
other injuries preclude reduction and fixation of facial fractures in the early
post-trauma period, this task is usually best postponed until the fourth to
sixth day after trauma when facial edema has largely resolved. Under nearly
all circumstances, facial fractures should be reduced within the first two
weeks to avoid the problems of malunion from rapid healing or nonunion
because of delayed reduction and fixation.
530 PART EIGHT—PLASTIC AND RECONSTRUCTIVE SURGERY
TYPES OF FRACTURES
Nasal Fracture
The most common bone injury involving the face is fracture of the nose.
It must be remembered that the nose is composed of not only bone but also
cartilage and soft tissue and that any or all of these tissues may be disrupted
by an injury. The usual signs of nasal fracture are (1) depression or
displacement of the nasal bones (Fig. 27-3), (2) edema of the nose, (3)
epistaxis, and (4) fracture of the septal cartilage with displacement or
All nasal injuries should be mobility. The patient must always be examined for hematoma of the septum
evaluated for septal hematoma, resulting from fracture, which, if undetected and untreated, may progress to
abscess formation with resorption of the septal cartilage and severe saddle-
nose deformity. Management of a septal hematoma includes incision and
drainage of the hematoma, placement of a temporary drain, application of
intranasal dressings to compress the septal mucosa and minimize the risk of
re-formation of the hematoma, and initiation of antibiotic therapy to decrease
the risk of infection.
Repair of nasal fractures can usually be carried out under local anesthesia
following the resolution of edema. The topical application of 4 per cent
cocaine on cotton pledgets, followed by infiltration of lidocaine, is usually
satisfactory. Not more than 5 ml of 4 per cent cocaine should be used in the
27—MAXILLOFACIAL TRAUMA 531
adult, and cocaine probably should not be used in children. Children usually
require general anesthesia for the reduction of nasal fractures.
The most common type of fracture involves depression of one nasal bone,
with displacement of the nasal pyramid to the opposite side. Elevation of
the depressed nasal bone with a flat elevator followed by displacement of
the pyramid to its pre-injury position usually may be accomplished without
great difficulty (Fig. 27-4). If closed reduction techniques do not yield a
satisfactory configuration, then open reduction techniques involving wide
exposure of the nasal septum and portions of the nasal bones may be
required. Severe injuries may require not only open reduction but also a
variety of fixation techniques such a direct wiring, external suspension, or
even transfixation with stainless steel wire and the application of lead plates.
Internal and external nasal dressings are useful following the reduction of
most nasal fractures. A satisfactory internal dressing consists of V2- to 1-inch
packing gauze impregnated with antibiotic ointment. External dressings are
applied to either protect the nose or maintain reduction or both. The external
532 PART EIGHT—PLASTIC AND RECONSTRUCTIVE SURGERY
FIGURE 27—4. Reduction of a depressed and dislocated nasal bone fracture. This reduction is
accomplished in two steps following anesthesia by first elevating the depressed nasal bone
as illustrated and then manually displacing the pyramid to the midline.
Mandibular Fracture
Fracture of the mandible is the second most common fracture of the facial
skeleton. Signs and symptoms suggestive or diagnostic of mandibular fracture
include (1) malocclusion of the teeth, (2) tooth mobility, (3) intraoral
lacerations, (4) pain on mastication, and (5) bone deformity. Initial evalua¬
tion includes examination for fractures of the teeth and assessment both by
inquiry and by direct examination of the patient’s dental occlusion. Most
patients can state quite accurately whether their teeth fit normally, and
examination may suggest improper alignment of the upper or lower dental
arches. Intraoral examination may show lacerations over the mandible and
there may be palpable or visible deformity of the mandible, both of which
suggest fracture. The most frequently fractured regions of the mandible are
the condyle and the angle (Fig. 27-5).
Repair of a mandibular fracture employs the general principle of splinting
the mandible with its intact dentition against the maxilla with its intact
dentition. The upper and lower dental arches are usually bound together by
ligating arch bars to the upper and lower dental arches with wire. These
arch bars have small hooks that accept either elastic or wire loops which
bind the upper to the lower dental arch (Fig. 27-6). More complex types of
27—MAXILLOFACIAL TRAUMA 533
mandibular fractures may require open reduction and the direct wiring or
plating of fragments to obtain stability in addition to intermaxillary fixation
with arch bars. Plating of facial fractures has become popular in the past
decade and provides excellent fracture immobilization and many times
eliminates the need to maintain fixation of the upper and lower dental
arches. This improves patient comfort, oral hygiene, speech, airway, and
alimentation. These open techniques may be required when severe commi¬
nution, gross displacement, or multiple fractures create a situation in which
closed reduction and intermaxillary fixation techniques are inadequate to
stabilize the fractured mandible. Antibiotics, penicillin being the drug of
choice, should be given to nearly all mandibular fracture patients because Most mandibular fractures are
the mandibular mucoperiosteum is so closely applied to the mandible that comP°und-
most mandibular fractures are compound. Antibiotics should be given from
the time of the fracture until the mucoperiosteum has healed and the fracture
has been stabilized.
FIGURE 27-6. Illustration of the principle of splinting one dental arch against
the other, employing arch bars that are affixed to the teeth and then joined
either with loops of wire or dental elastics.
534 PART EIGHT—PLASTIC AND RECONSTRUCTIVE SURGERY
FIGURE 27-7. Radiograph of "tripod" malar fracture. Arrows indicate fracture sites.
27—MAXILLOFACIAL TRAUMA 535
Injuries that produce zygoma fractures usually involve a blow to the .body
of the zygoma or “malar” prominence. The orbital floor may be fractured
in this process or may be “blown out” by an object such as a baseball or
tennis ball which occludes the orbit as it strikes the face (Fig. 27-8A and
B). Zygoma fractures may be characterized by (1) palpable deformity (step) Ophthalmologic examination
of the infraorbital rim, (2) diplopia on upward gaze, (3) hypesthesia of the should be part of the evaluation.
cheek, (4) flattening of the lateral aspect of the cheek, (5) periorbital
ecchymosis, or (6) inferior displacement of the ocular globe. Occasionally
only the zygomatic arch is fractured with a depression of the lateral temporal
region. Fractures of the orbital floor may be characterized only by restricted
upward gaze due to entrapment of the inferior rectus muscle. Hypesthesia
of the cheek is caused by contusion or laceration of the maxillary division
of the trigeminal nerve when the maxilla fractures. If Orbital floor fracture
is suspected, planigraphic or CT evaluation may be very helpful in determin¬
ing the degree of injury to the orbital floor.
Repair of these fractures may occasionally be carried out by closed
reduction techniques, but more often an open approach is required, espe¬
cially if an orbital floor fracture is significantly displaced. An open reduction
of the fractured zygoma usually involves a lateral brow incision to approach
the fractured frontozygomatic suture and a medial infraorbital incision to
approach the fractured zygomaticomaxillary region. Alternative approaches
include an intraoral incision to expose the lower portion of the zygoma and/
or subciliary, or conjunctival incisions to expose the orbital floor and orbital
rim. The orbital floor may be explored and reconstructed through this
infraorbital route. Orbital floor reconstruction is best done by realignment
of displaced bone fragments, but when this does not yield a stable floor, an
implant of transplanted bone or synthetic material may be required. When
the fractured zygoma has been reduced via these approaches, it is fixed in
place with stainless steel wire ligatures. Small metallic plates are also useful
and may be used in place of wire ligatures. Rarely, an injury of the zygoma
may be so severe that the bone must be affixed to external traction devices
to maintain its position. This general technique is referred to as external
fixation and usually involves a “halo” frame. When bone has been lost or
when the bone is extensively comminuted, immediate grafting with hip, rib,
or calvarial bone may be appropriate.
536 PART EIGHT—PLASTIC AND RECONSTRUCTIVE SURGERY
Maxillary Fractures
Fractures of the maxilla are among the most severe injuries involving the
face and are characterized by (1) mobility or displacement of the palate, (2)
mobility of the nose in association with the palate, (3) epistaxis, or (4)
mobility or displacement of the entire middle third of the face. Le Fort’s
classification of maxillary fractures is satisfactory for both diagnostic and
therapeutic purposes. It should be remembered, however, that any single
maxillary fracture may not precisely fit the classic descriptions of Le Fort
(Fig. 27-9A and B). This classification resulted from Le Fort’s observation
that the facial skeleton fractures in a stereotypical pattern when low-velocity
blows are sustained. The Le Fort I fracture is a low transverse fracture of
the maxilla involving the palate only and is characterized by mobility or
FIGURE 27—10. A, A severe maxillary fracture—Le Fort III, associated with a left mandibular
angle fracture. B, Repair employing intermaxillary fixation, open reduction, and interosseous
fixation with wire of the mandible and zygomaticomaxillary fractures and suspension-fixation
of the maxilla from the frontal processes.
538 PART EIGHT—PLASTIC AND RECONSTRUCTIVE SURGERY
Late Deformity
Late deformity of the face which results from untreated, inadequately
treated, or severe trauma usually may be improved surgically. Nearly all
unsightly scars may be improved by revision surgery employing camouflaging
techniques in combination with instruction in the judicious use of cosmetics.
Many late bone deformities may be improved by remobilization with reduc¬
tion and fixation in a more natural anatomic position. This is especially
applicable in the case of internal or external nasal deformity in which the
airway involvement or cosmetic results are not sufficiently apparent to cause
the patient to seek assistance until well after the traumatic episode. Bone
deformity that does not yield to mobilization often can be camouflaged by
implantation of autograft and/or homograft bone, or cartilage, or occasionally
synthetic material.
References
Dingman O, Natvig P: Surgery of Facial Fractures. Philadelphia, WB Saunders Co, 1964.
Foster A, Sherman JE: Surgery of Facial Bone Fractures. New York, Churchill Livingstone,
1987.
Mathog RH: Maxillofacial Trauma. Baltimore, Williams & Wilkins, 1984.
Rowe NL, Killey F1C: Fractures of the Facial Skeleton. 2nd ed. Edinburgh, E & S Livingstone,
1968.
Sisson GA, Tardy J: Plastic and Reconstructive Surgery of the Face and Neck: Proceedings of
the Second International Symposium. Vol 2: Rehabilitative Surgery. New York, Grune &
Stratton, 1977.
Zaydon J, Brown JB: Early Treatment of Facial Injuries. Philadelphia, Lea & Febiger, 1964.
INDEX
ii A
i
Chausse III projection, in middle ear evaluation, 104 Conduction, air, audiogram notation for, 51, 52
Cheek, lacerations of, evaluation of, 528-529 interaural attenuation in, and masking, 54
Chemical peel, for rhytide obliteration, 522-523 principles of, in audiometry, 50-51
Chemicals, ingestion of, 473-474 test models for, 47
Chemodectoma, 438, 439 thresholds in, in audiogram interpretation, 55-57, 56
Chemotherapy, agents for, 465, 465(t) validity of 53, 54
and associated infection, 378, 379 versus bone conduction, 47
for head and neck tumors, 464(t), 465, 465(t) bone, audiogram notation for, 51, 52
for squamous cell carcinoma, 464(t), 465(t) interaural attenuation in, 53-54
immune system effects of, 377-378 principles of, in audiometry, 50-51
Childbirth, trauma in, and facial nerve paralysis, 151 test models for, 47
Chin, deformities of, plastic surgery for, 524-525 thresholds in, validity of, 53, 54
Choanal atresia, in neonates, 209 versus air conduction, 47
Cholesteatoma, computed tomographic assessment of, 109 vibrator placement in, in pure tone audiometry, 51,
in chronic middle ear infection, 111, 112, 112 53
of external auditory canal, 80 Congenital anomalies, of lips, 286-291, 287
of mastoid, 107 of palate, 286-291, 287
Cholesterol granuloma, 112, 112 Congenital epulis, 314
Chondritis, in helix, 89 Continuous positive airway pressure (CPAP), for obstruc¬
Chondroma, of larynx, 403 tive sleep apnea, 366, 368
Chorda tympani nerve, anatomy of, 32 Contraction, in wound healing, 506
Chromosome(s), abnormalities of, and congenital deaf¬ Corniculate cartilage, anatomy of, 385
ness, 128 Cough, in laryngeal disease, 392
Cilia, respiratory, anatomy of, 183, 183 patient history in, 19
compromise of, 192 Cranial nerve(s), and herpes zoster, 305-306
function of, 191-193 eighth, acoustic reflex of, 59
histology of, 182-183 evaluation of, 21
Clark’s classification, of melanoma, 449(t) seventh, dysfunction of, 85. See also Facial nerve, paral¬
Cleft(s), laryngotracheoesophageal, 395 ysis of.
of face, 289-290 Craniofacial dysostosis, 290-291
of lips, 286-291,287 and micrognathia, 283
and associated developmental anomalies, 289-290 Cretinism, and congenital deafness, 129
formation of, 286, 287 Cricoid cartilage, anatomy of, 384, 384-385
treatment of, 288-289 split of, for subglottic stenosis, 497-498
and speech development, 288 Cricothyroid membrane, anatomy of, 389
of palate, 286-291, 287 Cricothyroid muscle, anatomy of, 386, 386
and associated developmental anomalies, 289-290 Cricothyrotomy, emergency, in children, 494-496
and eustachian tube dysfunction, 93-94 for foreign body aspiration, 410-411, 484
formation of, 286, 287 Cross hearing, in pure tone audiometry, 53
in children, and speech and language disorders, 416 Croup, clinical features of, 398, 399(t)
incidence of, 287-288 in laryngeal disease, 392
treatment of, 288-289 treatment of, 398-399
and speech development, 288 Crouzon syndrome, 290-291
Cleft lip. See Cleft(s), of lips. and congenital deafness, 131
Cleft palate. See Cleft(s), of palate. Cyst(s), congenital, of branchial cleft, 433, 433-434,
Cochlea, blood supply to, 34 434
computed tomographic assessment of, 109 of larynx, 394, 395
evaluation of, 47 dentigerous, 292, 292
ABR testing in, 63 dermoid, of nose, 210, 211
function of, 37-38 of oral cavity, 295-296
hair cells of, innervation of, 37-38, 38 epidermoid, 295-296
osseous, anatomy of, 34, 34-35, 35 eruption, 292
Cochlear duct, anatomy of, 35 fissural, 294-296, 295
Cochlear implants, 72-73 gingival, in newborns, 292-293
Cochlear microphonic, role in sound transmission, 36-37 incisive, 294, 295
Cochlear nerve, 38, 38 nasoalveolar, 295
Cochleovestibular nerve, evaluation of, 21 nasopalatine, 294, 295
Collagen, synthesis of, in wound healing, 505-506 nonodontogenic, 294-296, 295
Collagen injection, in facial plastic surgery, 523 odontogenic, 292, 292-294, 293
Common cold, 212-215 of branchial cleft, 22
clinical features of, 212-213 of hyoid bone, 434, 435
'treatment of, 213-214 of jaw, 291(t), 291-296, 292, 293, 295
Communication. See Speech', Language. of nose, 210, 211
Communitrach tube, 496-497 of oral cavity, 291(t), 291-296, 292, 293, 295
Compliance, in tympanometry, 57-58, 58 • of thyroglossal duct, 22
Computed tomography, of inner ear, 108-109, 109 palatal, of newborns, 292-293
of mastoid, 108-109,109 radicular, of oral cavity, 293, 293-294
of middle ear, 108-109, 109 retention type, 296
Conditioning, instrumental, in pediatric audiometry, 67 sebaceous, of external ear, 89
INDEX 545
Deafness. See also Hearing impairment; Hearing loss. Ear, anatomy of, 30-36
congenital, 125, 125-131, 126(t), 127(t) deformities of, plastic surgery for, 524
delayed, genetic, 129-131, 130 embryology of, 27-30
and associated abnormalities, 129-131, 130 examination of, 4-10
genetic, 126-128 patient history in, 4-5
and associated abnormalities, 127-128 external. See External ear.
chromosomal abnormalities in, 128 function of, 36-38
nongenetic, 128-129 inner. See Inner ear.
sensorineural, and otitis media, 113, 116 middle. See Middle ear.
cochlear implants for, 72 Ear wax. See Cerumen.
familial progressive, 129 Earache, patient history in, 5
unilateral, evaluation of, 68 Eardrum. See Tympanic membrane.
Debridement, of facial wounds, 508-509 Electromyography, for facial nerve evaluation, 149
Decongestant(s), complications from, 226, 227 Electroneuronography, 149
Deglutition, 280, 390 for facial nerve evaluation, 153, 154
muscles of, 384
Electronystagmography, for vestibular function evaluation
Dental caries, 296-297 42, 43, 125
Dental disorders, 296-301 Ellis-van Creveld syndrome, 300
Dental evaluation, in radiation therapy, 456 Emotional disorder(s), in children, and speech and lan¬
Dental replantation, in tooth trauma, 316 guage disorders, 417
Dental splinting, for mandibular fractures, 532-533, 533 Emphysema, mediastinal, after tracheostomy, 499
Dermabrasion, for acne scars, 519, 520 obstructive, in children, 482
for rhytide obliteration, 520, 522-523 Encephalocele, of nose, 210-211, 211
Dermatitis, eczematous, of external ear, 84 Endolymphatic hydrops, audiometric findings in, 66
Dermatomes, 515, 515-516 Endoscopy, for head and neck tumors, 450
Dermoplasty, septal, and epistaxis control, 241 for laryngeal tumor, 404
and Osler-Weber-Rendu syndrome treatment, 231, in chronic sinusitis treatment, 259, 259
231
in nasopharyngeal examination, 17
Diabetes, and gingivitis, 298 of nose, 207, 209
and necrotizing external otitis, 85
Endotracheal intubation, 491. See also Tracheostomy.
Diffuse otitis externa, 81-82
Enophthalmos, from orbital floor fracture, 534, 535
treatment of, 81(t), 82
Eosinophilia, interpretation of, 198, 198(t)
Dilantin, and gingival enlargement, 299, 300 Epiglottis, anatomy of, 385, 388, 388
Diphtheria, and acute sore throat, 340(t) function of, 390
in laryngitis, 400 Epiglottitis, in children, 398
treatment of, 344-345
Epistaxis, 231-241, 232, 233, 235-237, 239, 240
Diplacusis, evaluation of, 68 and frontal sinus fracture, 538
Diplopia, from zygoma fracture, 534
and juvenile nasopharyngeal angiofibroma, 336
Discharge, from ear, in chronic otitis media, 110 and leukemia, 241
patient history in, 5
and maxillary fracture, 536
from nose, 11
and nasal trauma, 240-241
in throat, 13-14
anterior, treatment of, 234-235, 235-237
Diverticuli, and dysphaarST472 / evaluation of, 232
Dizziness, 4-5. See alsvT VertigJ.
posterior, treatment of, 236-240, 237, 239, 240
differential diagnosisW_UJ4(t) complications of, 238
origin of, vestibular versus central, 124 hospitalization in, 238
patient history in, 124
nasal packing in, 236-238, 237
Doerfler Stewart test, 69
sphenopalatine ganglion block in, 236
Down’s syndrome, and micrognathia, 283
recurrent, and Osler-Weber-Rendu syndrome, 231, 241
and premature periodontal destruction, 301 cautery for, 233, 233-234
and scrotal tongue, 302
treatment of, cautery in, 233, 233-234
Drooling, treatment of, 322
patient history in, 233
Drug(s), ototoxic, 132(t), 132-133
principles of, 231-232
Drumhead, anatomy of, 32, 36
vessel ligation in, 238-240, 239, 240
examination of, 7. See also Tympanic membrane. Epithelialization, in wound healing, 506, 506
Dysarthria, 425
Epstein-Barr virus, and infectious mononucleosis, 345
in children, 418-419
and nasopharyngeal carcinoma, 337, 445
Dysfluency, in children, 416-417
Erythema dose, definition of, 452
Dysphagia, 471, 472
Erythema multiforme, of oral cavity, 307, 307-308
and airway obstruction, 492
Erythroblastosis fetalis, and congenital deafness, 128-129
arid croup, 398
Erythroplakia, of larynx, 403-404
and foreign body ingestion, 475 Esophagitis, 472
and speech and language disorders, 425-426 corrosive, 472, 473(t), 473-474
patient history in, 13, 13-14, 18 treatment of, 474
546 INDEX
Heimlich maneuver, for foreign body aspiration, 484 Immune system (Continued)
Hemangioma, of larynx, 394-395
development of, role of tonsils in, 351
of parotid gland, in children, 325
diseases of, congenital, 378-379
subglottic, laser microsurgery for, 405
evaluation of, 379
Hematoma, of external ear, 87
dysfunction of, from cancer therapy, 377-378
of nasal septum. 216, 531
infections of, 370-380
and nasal obstruction. 242
Immunosuppression, for organ transplantation, and infec¬
Hemilaryngectomy, for laryngeal carcinoma, 462 tion, 377
Hemorrhage, in tracheostomy, 500
from bone marrow transplantation, 370-371
of oral cavity, from trauma, 315
Incus, anatomy of, 31, 33
Hereditary hemorrhagic telangiectasia. See Osler-Weber- embryology of, 28
Rendu syndrome.
function of, 36
Herpes simplex, primary, inoculation, 303, 304
radiologic assessment of, 106, 107
of oral cavity, 303, 303-304
Infantile cortical hyperostosis, 315
secondary, 303, 304
Infection(s), acute, of external ear, 80-81, 81, 81(t) 83
Herpes zoster, of oral cavity, 305-306
of nose, 215, 215, 216
Herpes zoster oticus, 83, 91
and bone marrow transplantation, 371-376, 374
and facial nerve paralysis, 151
and facial nerve paralysis, 151
and otalgia, 168
bacterial, of nose, 217
Herpesvirus infection, after bone marrow transplantation,
chronic, and cervical lymph node involvement, 437
of external ear, 84-86, 85
of esophagus, in bone marrow recipient, 375
of mastoid, 110-113, 111, 112
of larynx, 373
of nose, 216-217
Hiatus hernia, 472
fungal, and cervical lymph node involvement, 437
and chronic nonspecific laryngitis, 401
in bone marrow recipient, 372
Histiocytoma, fibrous, chemotherapy for, 465(t)
of external ear, 82-83
treatment of, 447
of nose, 216
Histiocytosis X, 152
in cancer patients, 377-378
and premature periodontal destruction, 301
in immunocompromised patients, 370-380
Histoplasmosis, of larynx, 400-401
in tracheostomy, 501
Hoarseness, in laryngeal disease, 392, 444
of deep neck, 356-362, 357-361
in polychondritis, 86
of middle ear, 110-113, 111, 112
Hodgkin’s lymphoma, and cervical lymph node involve¬ of nasal septum, 374
ment, 437
of parapharyngeal space, 358, 358-359, 359
and tonsillectomy, 351
of trachea, 374
pathology of, 446-447
streptococcal, and tonsillectomy, 352
Horners syndrome, and vocal cord paralysis, 406
Inflammation, acute, of external ear, 80-84, 81, 81(t), 83
Human immunodeficiency virus (HIV), 376
chronic, of external ear, 84-86, 85
in children, 377
Inner ear, anatomy of, 34, 34-36
Hurler’s syndrome, and congenital deafness, 130
computed tomographic assessment of, 108-109, 109
Hydrocephalus, 119
diseases of, 123—141. See also Deafness; Hearing loss.
Hygroma, cystic, 435-436
and barotrauma, 95
and macroglossia, 284
ototoxic causes of, 132(t), 132-133
Hyoid bone, cyst of, 434, 435
embryology of, 28-29
fracture of, 396
evaluation of, 123-125
Hyperkeratosis, of larynx, 403
dizziness in, 124
Hypernasality, and speech and language disorders, 420
patient history in, 123
Hypernephroma, 448
physical examination in, 124-125
Hyperostosis, cortical, infantile. 315
tinnitus in, 123
Hyperpigmentation, and congenital deafness, 127-128 infections of, 131, 131-132
Hypertension, and obstructive sleep apnea, 362, 362(t)
complications of, 117
Hyperthyroidism, and thyroid disease, 440-442
innervation of, 34-35
Hyperventilation, and vertigo, 137
trauma to, 134, 134-135
Hypoglossal nerve, embryology of, 274
tumors of, 133, 133-134
evaluation of. 21
Internal auditory canal, radiologic assessment of, 102 104
Hypoglycemia, and vertigo. 137
108
Hyponasality, and speech and language disorders, 420 tumors of, 153
Hypopharyngectomy, for laryngeal carcinoma, 462
Internal nose, anatomy of, 178-180, 179
Hypopharynx, anatomy of, 19, 277, 277, 334-335
blood supply of, 185
diseases of, and obstructive sleep apnea, 364
Intranasal balloon, for epistaxis control, 234, 235, 236-237
examination of, 18-20, 20
Intubation, endotracheal, 491. See also Tracheostomy.
tumors of, malignant, treatment of, 462
Irrigation, antral, for maxillary sinusitis, 252, 252, 253
Hypopnea, and obstructive sleep apnea, 364
in cerumen removal, 79
Hypothyroidism, and chronic nonspecific laryngitis, 401 of external ear canal, 9, 10
and laryngeal involvement, 400
saline, for pharyngitis, 348
Papilloma (Continued)
Otitis media (Continued)
after bone marrow transplantation, 376 squamous, of nose, 244
Papillon-Lefevre syndrome, and premature periodontal de¬
and cleft palate, 288
and facial nerve paralysis, 147 struction, 301
Paralysis, congenital, of vocal cord, 395-396
and meningitis, 118
of cranial nerve, and nasopharyngeal tumors, 336, 337
and subdural abscess, 118
of facial nerve. See also Facial nerve, paralysis of.
chronic, 91, 110-113, 111, 112
and herpes zoster oticus, 83, 168
and labyrinthitis, 117
and otitis media, 113-117
fistula test in, 111, 111
and temporal bone malignancy, 121
treatment of, medical, 111-112
of recurrent nerve, in tracheostomy, 501
surgical, 112-113
Parapharyngeal space, infections of, 358, 358-359, 359
complications of, 113, 116, 117-120
from bone marrow transplantation, 371-372 complications of, 359
treatment of, 358-359, 359
in children, 100
recurrent, in HIV-positive children, 377 tumors of, 328
Parotid gland, anatomy of, 317
serous, 6, 100-102, 101
computed tomographic assessment of, 320
and adenoid hypertrophy, 338
hemangioma of, in children, 325
and chronic allergic rhinitis, 224
tumors of, benign, in adults, 327-328
and cleft palate, 94
and hearing loss, in children, 100 in children, 325
and nasopharyngeal tumors, 336, 337, 458 malignant, in children, 328-329, 329(t)
audiometric findings in, 64 treatment of, 327
chronic, adenoidectomy for, 339 ultrasonographic assessment of, 320
etiology of, 100 Parotitis, acute, 318-319
examination of, 101, 101 chronic, 322
in children, 100 suppurative, acute, 319
treatment of, medical, 101 Pectus excavatum, 393
surgical, 102, 103 Pediatric audiometry, 64-66, 64-68
Pemphigoid, of mucous membrane, 306-307
Otocyst, development of, 29
Otolaryngology, anesthesia in, 22-23 Pemphigus, of oral cavity, 306
biopsy in, 22-23 Pemphigus vulgaris, of larynx, 401
equipment for, 3 Pendred’s disease, and congenital deafness, 128
examination in, 3-23 Perichondritis, 83, 83-84
and headache, 161 Perilymph fistula, and vertigo, 140
and temporomandibular joint, 171 Periodontal disorders, 296-301
neurologic evaluation in, 21 destruction in, premature, 301
restraint in, 22-23 Periodontitis, 297-299
Otolith organs, evaluation of, 44 Peripheral nervous system, disorders of, evaluation of, 42
Otologic examination, in otosclerosis, 97 Petrositis, 117-118
Otomycosis, 82-83 Pharyngectomy, for hypopharyngeal tumors, 462
in bone marrow recipient, 372 Pharyngitis, acute, 340, 340-342, 341
Otosclerosis, 96 and acute sore throat, 340(t)
and congenital deafness, 129 diagnosis of, 342
assessment of, 96, 97 etiology of, 340-341, 341, 341(t)
audiometric findings in, 66 pathology of, 340-341
Carhart notch in, 57, 66 symptoms of, 341
Otoscope(s), battery powered, 7, 8 treatment of, 342
pneumatic, 8, 8 and tobacco use, 349
Siegle, 8, 8 atrophic, 347-348
Ototoxicity, causative agents of, 132(t), 132-133 treatment of, 348-349
Owens view, in middle ear evaluation, 104, 107 lateral, 341, 341
Ozena, 226(t), 228-229 membranous, 344-345
recurrent, adenotonsillectomy for, 350
viral, etiology of, 340-341, 341(t)
Pharynx, anatomy of, 274, 274-277, 276, 277
Paget’s disease, and congenital deafness, 130, 130 and otalgia, 169(t)
Palatal myoclonus, 93 blood supply of, 279
Palate, anatomy of, 275 embryology of, 273-274
clefts of, 286-291, 287. See also Cleft(s), of palate. examination of, 13-16
and encephalocele, 211 and otalgia, 161
and nasal deformities, 209-210, 210 equipment and technique in, 15, 15-16
embryology of, 274 patient history in, 13-14
fractures of. See Maxilla, fractures of function of, in voice production, 391
soft, evaluation of, 13 innervation of, 279-280
Palpation, in oral and pharyngeal examinations, 16,16 physiology of, 280
Papillary adenocystpma lymphomatosum, 327 Pierre Robin syndrome, 283-284
Papilloma, inverted, of nose, 244, 457 Piriform sinus, anatomy of, 389
juvenile, 402-403 Plasmacytoma, extramedullary, of nose, 244-245
laser microsurgery for, 405 Plastic surgery, facial, 505—525. See also Facial plastic sur¬
treatment of, 403 gery.
INDEX 555
Plate stabilization, for mandibular fractures, 533, 533 Radiation therapy (Continued)
for maxillary fractures, 537 preoperative versus postoperative, 453
for zygomatic fractures, 535 techniques of, 453-454
Plaut’s angina, 344 and tumor stage, 453
and acute sore throat, 340(t) Radical neck dissection, for head and neck carcinoma,
Play audiometry, 67 456-457, 463-464
Plummer-Vinson syndrome, and hypopharyngeal tumors, for occult tumors, 463
462 indications for, 463
Pneumomediastinum, in tracheostomy, 501 modifications of, 464
Pneumothorax, in tracheostomy, 501-502 Radiculopathy, cervical, and headache, 165
Poliomyelitis, incidence of, after tonsillectomy, 351 Radioallergosorbent test (RAST), 200-201, 201 (t)
Polychondritis, relapsing, nasal manifestations of, 230 Radiosialographic scanning, 323
of external ear, 86 Ramsay Hunt syndrome, 83, 91, 305
Polycythemia, and obstructive sleep apnea, 362 after bone marrow transplantation, 375
Polyp(s), antrochoanal, 256, 257 and facial nerve paralysis, 151, 151
nasal, 202-204 Rappaport classification, for non-Hodgkin’s lymphoma,
and aspirin sensitivity and asthma, 202, 225 447
and chronic ethmoid sinusitis, 259 Refsum’s disease, and Congenital deafness, 130
and obstructive sleep apnea, 364 Rem (roentgen-equivalent-man), definition of, 452-453
and sinusitis, 256 Renal dysfunction, and hearing loss, 129
clinical features of, 202 Respiratory tract, obstruction of, and associated disease,
differential diagnosis of, 222 193
treatment of, 203-204 Restlessness, in children, and airway obstruction, 492
complications of, 204 Restraint, in otolaryngologic examination, 22-23
surgical, 222, 223 Reticulosis, polymorphic, nasal manifestations of, 230
with hyposensitization, 204 Retraction, and airway obstruction, 492
versus inverted papilloma, 244 Rhabdomyosarcoma, 121, 152
of sinuses, 268-269 in children, 447-448
Polypectomy, nasal, 222, 223 Rheumatoid arthritis, and laryngeal disease, 400
Polyposis, nasal. See Polyp(s), nasal. Rhinitis, 212-217. See also Nasal allergy.
Positional tests, 44 allergic, 196, 202-204, 217-225, 219
Posturography, 44-45 and hyperplastic sinusitis, 224
Pregnancy, and gingivitis, 298 chronic, and nasal polyps and aspirin sensitivity, 225
Presbycusis, audiometric findings in, 65 and serous otitis media, 224
Prognathism, 284 diagnosis of, 202-203, 218-221
Pseudomonas aeruginosa, in tracheostomy, 501 differential diagnosis of, 204
Pulmonary disease, detection of, 22 incidence of, 202
Pulpitis, 297 pathogenesis of, 202
Pure tone audiometry, air conduction in, 50-51 treatment of, 203-204
audiogram in, and air-bone gap, 55, 56 allergen elimination in, 203
classic interpretation of, 55, 56, 57 medical, 203
notation for, 51, 52 surgical, 204
audiometric zero, and intensity range, 51 systemic, 223-224, 224(t)
bone conduction in, 50-51 with hyposensitization, 21
cross hearing in, 53-54 and temperature change, 227
interaural attenuation in, 53-54 and viral exanthemas, 215
masking in, 54-55, 55 atrophic, 226(t), 228-229
threshold determination in, 51-53 and atrophic pharyngitis, 348
patient preparation in, 51-52 treatment of, 229
procedures for, 52-53 hypertrophic, 226(t), 228
validity of, 53 and decongestant use, 226
versus speech audiometry, 60 in bone marrow recipient, 373, 374
Pyocele, and sinusitis, 265-266 infectious, versus nasal allergy, 218
influenzal, 214-215
nonallergic, chronic, 225-229, 226(t)
suppurative, 215
Rad (radiation absorbed dose), definition of, 452 vasomotor, 225-228, 226(t), 227
Radiation therapy, after neck dissection, 463 and drug usage, 226, 226(t), 227
complications of, 456 etiologic factors of, 226-228
for base of tongue tumors, 459 Rhinoliths, 247
for head and neck carcinoma, 452-456, 454, 455 Rhinophyma, 247
dosage definitions in, 452-453 Rhinoplasty, 523, 523
for laryngeal carcinoma, 454, 454, 461 Rhinoscleroma, 217
for nasal tumors, 457 Rhinoscopy, 207, 209
for nasopharyngeal carcinoma, 454, 455 for headache, 161
for sinus carcinoma, 454-456, 455 for nasal allergy, 219
for squamous cell carcinoma, 464(t) Rhytidectomy, 520, 521
for tonsillar tumors, 460 Rhytides, formation of, 520
immune system effects of, 377-378 obliteration of, 522-523
556 INDEX
Sinusitis (Continued)
Speech reception threshold (SRT), 60-61
sphenoid, acute, 255 Speechreading, 73
chronic, treatment of, 262
Splinting, for mandibular fractures, 532-533, 533
treatment of, 203-204, 204
Spondylosis, cervical, and headache, 165
versus impaired ciliary physiology, 192
Squamous cell carcinoma. See Carcinoma, squamous cell.
viral, 250
Stapes, anatomy of, 33, 33
Situs inversus, and Kartagener's syndrome, 269 embryology of, 28
Sjogren's syndrome, 322 function of, 36
and chronic parotitis, 322 Stenger test, 68
and sialography, 325 Stenosis, esophageal, 473, 473(t)
nasal manifestations of, 231 prevention of, 474
Skin tumors, malignant, 448-449, 449(t) laryngeal, 397
Skin flap(s). See also Flap(s). of external auditory canal, 84, 85
advancement, 512, 512 subglottic, 397
in tracheostomy, 496, 496, 49', congenital, 394
local, general considerations in, 512, 513 from intubation, 385
of face, 512-513, 512-514 in children, 491
rhomboid, 513, 513 treatment of, in neonates, 497-498
transposition, 512, 513 laser microsurgery for, 405
Skin grafts, classification of, 515, 515 tracheal, in tracheostomy, 502
general considerations in, 512 Stensen’s duct, dilatation of, 323
harvesting of, 515, 515-516, 516 sialographic assessment of, 326
Sleep apnea, obstructive, 362-368 Stenvers position, in middle ear evaluation, 104, 108
and cardiopulmonary syndrome, 362, 362(t) Stomatitis, aphthous, recurrent, 304-305
clinical presentation of, 362-363 Stridor, and airway obstruction, 492
diagnosis of, 364-365, 365 in laryngeal disease, 392
mechanisms of, 363-364 Stuttering, in children, 416-417
psychosocial effects of, 364-365 Sublingual glands, anatomy of, 318
treatment of, 365-368, 366, 367, 367(t), 368(t) Submandibular glands, anatomy of, 317-318
continuous positive airway pressure (CPAP) in, 368 sialographic assessment of, 323-325, 324, 326
genioplasty in, 366 tumors of, 327
medical, 367(t), 368 malignant, 331
surgical, 368(t)
Suctioning, in tracheostomy care, 499, 500
tracheostomy in, 366, 366 Supraclavicular fossa, mass of, 448
uvulopalatopharyngoplasty in, 366-367, 367, 368(t) Supraglottitis, clinical features of, 399(t)
Smell. See Olfaction. Sutton’s disease, 305
Snoring, 362-368. See also Sleep apnea, obstructive. Suture(s), absorbable, versus nonabsorbable, 510
Soft tissue, injury of, in maxillofacial trauma, 530 interrupted mattress, 510-511, 511
Sore throat. See also Pharyngitis-, Tonsillitis. running, 511, 511
acute, and associated diseases, 340, 340-350, 341 technique for, in facial plastic surgery, 509-511, 510
346(t). 347-349 511
patient history in, 13, 13-14 tracts of, 506, 506
Sound, transmission of, 36 Swallowing, stages of, 280
air conduction in, 47
Swimmer s ear, 81—82. See also Diffuse otitis externa.
Speculum, aural, 6-7, 7
Syphilis, and cervical lymph node involvement, 437
nasal, 12
and hearing loss, 131-132
Speech, after laryngectomy, 421-424
laryngeal involvement in, 401
and artificial larynx, 422, 422-423 Syringe, irrigating, 10
and voice prosthesis, 423, 423
methods for, 421-422
rehabilitation in, 423-424 Taste, innervation for, 275
support groups for, 424 Teeth, anatomy of, 275
definition of, 412
embryology of, 273-274
disorders of, 412-426
eruption of, disorders in, 300
adenoidectomy ii), 339 fractures of, 316
definition of, 412'
Teflon, injection of, for vocal cord paralysis, 408
in adults, 419-425, 422, 423
Temporal bone, anatomy of, 144
in children, 414-419, 415, 418(t) embryology of, 29-30, 30
screening tests for, 415 fractures of, 134,134
hypernasal, 194
radiologic assessment of, 102, 104-108, 104-108
hyponasal, 194
trauma to, and facial nerve paralysis, 152
rehabilition services in, 426
Temporomandibular joint, dysfunction of, 171-172
Speech audiometry, in children, 67-68 differential diagnosis of, 171
masking in, 54-55
features of, 162(t)
speech discrimination tests in, 61 treatment of, 171-172
speech reception threshold (SRT) test in, 60-61 examination of, and headache, 161
versus pure tone audiometry, 60 Tetanus, prophylaxis for, 509, 509(t)
Speech discrimination, 61 Tetracycline, dental side effects of, 300
Speech pathology services, 426
Thornwaldt’s disease, 335, 336
558 INDEX
Thrombophlebitis, and brain abscess formation, 266, 267 Torus mandibularis, 283, 283
of lateral sinus, 118 Torus palatinus, 282, 282
septic, and parapharyngeal space infection, 359 Total communication, 75
Thrombosis, of cavernous sinus, 264, 264, 265 Towne view, in middle ear evaluation, 104
Thyroglossal duct, anatomy of, 435 Toxic shock syndrome, and nasal packing, 215
cysts of, 434, 434, 435 Trachea, anatomy of, 386, 492-493
embryology of, 278-279 Aspergillus infection of, 374
hyroid gland, anatomy of, 389, 440 Tracheal atresia, 483
carcinoma of, from radiation therapy, 456 Tracheal cannula, 498
cysts of, 434, 435 Tracheitis, bacterial, 399(t)
diseases of, 439 Tracheobronchial tree, anatomy of, 482
diffuse, 440-442 disorders of, 483-485
examination of, 22, 22 congenital, 483
masses of, 439-442, 440, 441 evaluation of, 481, 482, 485-487
diagnosis of, 439-440 bronchoscopy in, 486, 486-487
thyroid scans in, 440, 440, 441 foreign bodies in, location of, 484-485
nodules of, evaluation of, 440, 441, 442 symptoms of, 483-484
Thyroid cartilage, anatomy of, 384-386, 384 Tracheomalacia, 394, 483
fracture of, 396 Tracheostomy, 389, 490-502
Thyroiditis, and diffuse thyroid disease, 440-442 alternatives to, in neonates, 497-498
diagnosis of, 441 complications of, delayed, 501-502
Thyrotoxicosis, 197 surgical, 500-501
Tic douloureux, 172, See also Neuralgia. definition of, 490
Tinnitus, audiologic evaluation of, 125 elective, in adults, 493-494, 494(t), 495
etiology of, 123-124 in children, 494
in polychondritis, 86 emergency, 494-496
treatment of, 136-137 in maxillofacial trauma, 526-527
Tissue expansion, in facial plastic surgery, M4 for bilateral vocal cord paralysis, 408, 408-409
TNM classification, for head and neck tumors, 451(t) for foreign body aspiration, 484
for laryngeal carcinoma, 461(t) for laryngeal fracture, 396
for oral cavity tumors, 460(t) for laryngitis, 373-374
Tobacco use, and chronic nonspecific laryngitis, 401 for Ludwig’s angina, 360
and pharyngitis, 349 for obstructive sleep apnea, 365-366, 366
and squamous cell carcinoma, 445 history of, 490-491
Tongue, anatomy of, 275 incisions for, 496, 497
base of, malignant tumors of, treatment of, 459-460 indications for, 491-492
embryology of, 274 modifications of, 496-498, 496-498
Tongue depressor, in oral and pharyngeal examination, postoperative care in, 499-500, 500
15, 15-16 surgical technique for, 493-502, 494(t), 495-498, 500,
Tongue tie, in children, 418 501
Tonsil(s), anatomy of, 276, 276-277, 334, 354, 355 tubes, postoperative care of, 499-500, 500
and immune system development, in children, 351 sizes of, for adults, 493, 494(t)
carcinoma of, 460 for children, 494(t)
hypertrophied, and lymphoma, 447 types of, 496-497, 501
Tonsillectomy, 350-356, 355, 356 versus endotracheal intubation, 491
and otalgia, 170 Tracheotomy, and laryngeal stenosis, 397
and poliomyelitis, 351 definition of, 490
anesthesia for, 354, 357 Transplantation, bone marrow. See Bone marrow trans¬
contraindications to, 353 plantation.
dissection technique in, 357 organ, and associated infections, 377
for obstructive sleep apnea, 366, 368(t) Trap door deformity, 513, 516, 516-517
hemostasis control in, 354-355, 357 Trauma, acoustic, 36
immediate, indications for, 347, 347(t) auricular defects from, 524
indications for, 351-353 during childbirth, and facial nerve paralysis, 151
instruments for, 356 to external ear, 86-87
outpatient versus inpatient, 356 to maxillofacial area, treatment of, 526-539. See also
patient preparation in, 353-354, Maxillofacial trauma.
postoperative bleeding in, 354-355 to nose, and epistaxis, 240-241
surgical anatomy for, 354, 355' to oral cavity, 315-316
technical considerations in, 354-356, 355 Treacher Collins syndrome, 95, 279, 291
with adenoidectomy, benefits of, 350-351 Trephination, for frontal sinusitis, 255
Tonsillitis, acute, 342-343 Trigeminal nerve, evaluation of, 21
and acute sore throat, 340(t) Trismus, and deep neck infection, 358
pathology of, 342 Trisomy 13-15 (D), and congenital deafness, 128
treatment of, 342-343 Trisomy 18 (E), and congenital deafness, 128
chronic, diagnosis of, 349-350, 350 Tuberculosis, and cervical lymph node involvement, 437
treatment of, 350 of esophagus, 472
etiology of, 352 of larynx, 401
lingual, 343-344 of middle ear. 111
and acute sore throat, 340(t) of nose, 217
INDEX 559
Tubotympanic recess, formation of, 27, 28 Ulcers, contact, of vocal cord, 402
Tumor(s), acoustic, 133, 133-134 Usher’s disease, and congenital deafness, 128
benign, of salivary glands, in adults, 327-328 Uveoparotid fever, 321
in children, 325 Uvulopalatopharyngoplasty, for obstructive sleep apnea,
carotid body, 438, 439 366-367, 367, 368(t)
malignant, connective tissue, 447-448
of head and neck, 443-467
treatment of, 451-465, 454, 455, 459, 460(t), 461(t),
464(t), 465(t)
chemotherapy in, 464(t), 465, 465(t) Vagus nerve, evaluation of, 21
radiation in, 452-456, 454, 455 Varicella-zoster virus infection, after bone marrow trans¬
surgical, 456-457 plantation, 375
of middle ear, 121 Vasoconstrictor(s), topical, in examination, 13
of nose, 457 Venous system, and sinusitis complications, 266,.266-267
of oral cavity, 458-459 Ventilation problems, chronic, versus airway obstruction,
of salivary glands, 329(t), 329-331 492
of sinuses, 458, 459 Ventilation tube(s), placement of, for serous otitis media,
of skin, 448-449, 449(t) 102, 103
metastatic, to head, 448 indications for, 120
to middle ear region, 121-122 Vertigo, 137-141
neuroectodermal, of neural crest origin, 314 and chronic otitis media, 111
neurogenic, 439 and inner ear disease, 117
nonodontogenic, 314 and tympanic membrane perforation, 98
occult, and cervical metastasis, 463 assessment of, fistula test in, 111, 111
odontogenic, 310(t), 310-313, 311, 313 benign paroxysmal positional, 137-138
adenomatoid, 311 diagnosis of, 44
epithelial, calcifying, 312 benign positional, 137-138
of cerebellopontine angle, 133, 152 causes of, nonvestibular, 137
of middle ear and mastoid, 120-122 vascular, 137
of oral cavity, 310(t), 310-314, 311, 313 vestibular, 137-140, 138(t), 139, 140
of parotid gland, 327 cervical, 137
of salivary glands, differentiation of, 328(t) differential diagnosis of, 124(t)
TNM classification of, 330(t) _ ** evalu.ation.of,(*41i<42
of skull base, and vocal cord paralysis, 406 in pblychondrifis>;86
of submandibular gland, 327 treatment ofj 144 (
malignant, 331 Vestibular function,' disorders of, 21
of tongue base, 459-460 evaluation of, 41-45, 43
Tuning fork, Riverbank 512 cycle, 9 caloric stimulation in, 42, 44
Tuning fork test(s), 9-10, 10, 11, 47-50. See also Hearing electronystagmography in, 42, 43
test(s). positional tests in, 44
Bing test, 49 posturography in, 44-45
reliability of, 49-50 rotation tests in, 42-44
Rinne test, 9, 11, 48, 49(t) vestibulo-ocular reflex in, 42
Schwabach test, 9, 48, 48(t) Vestibular nerve, pathways of, 38
threshold determination in, 47-48 Vestibular neuronitis, and vertigo, 138
validity of, 49-50 Vestibular reflex, pathways of, 41
Weber test, 9, 11, 49 Vestibular system, disorders of, 138(t)
Tympanic cavity, radiologic assessment of, 104 physiology of, 39-41
Tympanic membrane, anatomy of, 6, 31, 32, 33 Vestibule, of inner ear, anatomy of, 34, 35-36
appearance of, in acute otitis media, 99, 99 radiologic assessment of, 104
in disease, 90-91 Vestibulo-ocular reflex, evaluation of, 42
audiologic evaluation of, 57-58. See also Tympanome¬ pathways of, 41
try. Vincent’s angina, 344
diseases of, 90-92, 91 and acute sore throat, 340(t)
examination of, 5, 7, 7-8, 8 Vincent’s infection, 298, 298-299
inflammation of, 91-92 Virus(es), and hearing loss, 131
perforation of, 8-9, 91, 91, 96, 98, 111 respiratory, 213-215
and ossicular chain damage, 98 Vocal abuse, adductor hyperfunction and, 420
treatment of, 98 Vocal cord(s), anatomy of, 388, 389
Tympanocentesis, for otitis media, in bone marrow trans¬ contact ulcer of, in men, 402
plantation, 371 examination of, in chronic laryngitis, 402
Tympanogram, classification of, 57-58, 58 function of, 390, 390
of tympano-ossicular system, 57 leukoplakia of, 403
Tympanometry, 57-58 musculature of, 386-387
acoustic immittance in, 58-59, 59(t) nodules of, 400, 402
Tympano-ossicular system, tympanometry and, 57-58 paralysis of, 406-409, 407, 407(t), 408
Tympanoplasty, for chronic middle ear infection, 112-113, bilateral, 406, 407(t), 408, 408-409
115 causes of, 406-407
Tympanosclerosis, 110 congenital, 395-396
audiometric findings in, 65 cord designation in, 406, 406(t), 407
560 INDEX
Vocal cord(s) (Continued) Waldeyer’s ring, lymph nodes of, and non-Hodgkin’s lym¬
paralysis of, unilateral, 406, 407, 407(t) phoma, 437
in children, 407-408 lymphoma in, 447
treatment of, 408, 408 Warthin’s tumor, 327
Vocal weakness, 410 Waters’ view, 220
Voice, artificial larynx for, 422, 422-423 Weber test, 9, 11, 49
disorders of, and loudness, 419-420 Web(s), congenital, of larynx, 394
and pitch, 419 Wegener’s granulomatosis, nasal manifestations of, 229-
and vocal quality, 420 230
functional versus organic, 419 Wharton’s duct, dilatation of, 323
in adults, 419-421 sialographic assessment of, 326
in children, 415-416 Wheezing, and foreign body aspiration, 484
incidence of, 419 Wire stabilization, for mandibular fractures, 533, 533
psychologic factors in, 419 for maxillary fractures, 537, 537
therapy for, 421 Wound care, principles of, 503-512, 507, 508, 509(t), 510,
esophageal, and artificial larynx, 422-423 511. See also Facial plastic surgery; Facial wound(s).
methods for, 421-422 Wrinkles, formation of, 520
outcome factors in, 424 obliteration of, 522-523
production of, 390
prosthesis for, 423, 423
Von Recklinghausen’s disease, and acoustic neuroma, 133 Z-plasty, 517(t), 518, 518
and congenital deafness, 130 Zenker’s diverticulum, 277
and chronic nonspecific laryngitis, 401
Zigzag-plasty, 517(t), 518, 519
W-plasty, 517(t), 518, 519 Zygoma, fractures of, 534, 534-535, 535
Waardenburg’s disease, and congenital deafness, 127 repair of, 535