Handout

ANATOMY OF THE ORAL CAVITY,
PHARYNX, LARYNX & NECK

1. ORAL CAVITY i
- extends from the lips and cheeks externally to the anterior pillars of the fauces
internally, where it continues into the oropharynx.
= SECTIONS
*ORAL VESTIBULE - is the part of the mouth outside the teeth bounded laterally by the °-»
mucosa of the lips and cheeks and the lateral aspect of the mandibular and maxillary
alveoli. It is the region between the internal mucosa of the cheek and the teeth.
MUSCLES
*ORBICULARIS ORIS MUSCLE - is a muscle of facial expression that is oriented
circumorally around the opening of the mouth. It helps to close the lips and keeps the
mouth closed. It helps to compress the cheeks against the teeth and helps during
chewing. Its origin and insertion is entirely into the skin and mucosa of the lips and
surrounding skin of the face. It continues laterally to the buccinator muscle.
™BUCCINATOR MUSCLE- arises from the maxilla and mandible medially and the
pterygomandibular raphe posteriorly.
™LEVATOR ANGULI ORIS, LEVATOR LABII SUPERIORIS ALAEQUE NASI, LEVATOR
LABII MUSCLES - also contribute to the musculature of the oral cavity superiorly.
™DEPRESSOR ANGULI ORIS, DEPRESSOR LABII INFERIORIS AND STRIPS OF THE
RESORIUS AND PLATYSMA MUSCLES - contribute to the musculature of the oral cavity
inferiorly.
Corrugator supercd
Mamtaizs (cut)
*ORAL CAVITY PROPER - is the space behind the teeth, between the medial surfaces of
the maxillary and mandibular alveoli, It is the area of the mouth that extends from the lips
to the anterior tonsillar pillar. It contains the lips, gums, tongue, inner lining of the cheeks,
the tissue underneath the tongue between the point of attachment of the tongue and the
mandible (floor of the mouth).
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- the mucosal lining of the oral cavity and pharynx is lubricated by the salivary glands.
The cranial border of the oral cavity proper is the hard and soft palate. It separates the
oral and nasal cavities.
- the oral cavity opens through the oropharyngeal isthmus into the oropharynx. The
anterior 2/3 of the tongue belongs to the oral cavity proper. The posterior 1/3 of the tongue
is present in the oropharynx. It is connected by the frenulum on the floor of the oral cavity.
- the openings of Wharton’s ducts are located on each side of the frenulum. They
transport a large amount of saliva which is produced by both submandibular glands.
Adjacent to the ducts are the sublingual glands. They give the floor of the mouth the
cobble-stoned surface. The parotid gland orifice opens opposite the maxillary second
molar on either side, and the orifices of the submandibular duct open on either side of
the midline of the floor of the mouth anteriorly. The openings of the submandibular glands
are called the caruncles. Deep to the mucosa of the floor of the mouth are the sublingual
salivary glands, each of which has multiple ducts draining into the oral cavity.
= SALIVARY GLANDS
*MAJOR SALIVARY GLANDS
™» SUBMANDIBULAR GLANDS - are the second largest salivary glands in the human body
and they lie beneath the floor of the mouth, beneath the mandible. These paired salivary
glands lie below the lateral part of the body of the mandible and fill the major portion of
the submandibular triangle. There are two lobes, larger superficial and smaller deep. Both
lobes are continuous around the posterior margin of the mylohyoid muscle. The
superficial lobe lies on the mylohyoid muscle, while the deep lobe lies on the hyoglossus
muscle and terminate in an excretory duct. Its excretory Wharton’s duct emerges from
the deep lobe and drains into the floor of the mouth at the sublingual papilla lateral to the
tongue frenulum. The secretions from this gland are mixed seromucinous, with viscosity
intermediate between those of the sublingual and parotid glands.
sINNERVATION
i. Facial nerve (CN VIl) ii.Lingual nerve (sensory nerve)
iii. Hypoglosssal nerve (CN XIl)
=BLOOD SUPPLY - Facial artery
™»PAROTID GLAND - is the largest of the 3 major salivary glands. It is located anterior to
the mastoid process and EAC. It extends as deep as the pharyngeal wall. The inferior tail
of the parotid is between the ramus of the mandible and sternocleidomastoid muscle.
Superficial (80%) and deep (20%) portions of the parotid gland are divided by the facial
nerve (CN VII). An accessory lobe superior to the parotid duct is present in some cases.
It secretes saliva through Stensen’s ducts into the oral cavity. The parotid duct (Stensen’s
duct) passes over the masseter muscle and can be palpated just in front of a clenched
masseter muscle. It goes into the oral cavity through the bucccinator muscle and opens
in the buccal mucosa opposite the second molar tooth.
“STRUCTURES THAT PASS THROUGH THE PAROTID GLAND
i. Facial nerve ii. Retromandibular vein lll. External carotid artery
=LYMPHATIC DRAINAGE - there are numerous lymph nodes within the parotid gland.
These lymph nodes drain into the preauricular or parotid lymph nodes, which ultimately
drain into the deep cervical chain
=BLOOD SUPPLY - External carotid artery
=» SUBLINGUAL GLANDS - the smallest of the major salivary glands. Unlike the parotid
and submandibular glands, no actual capsule surrounds the sublingual glands.
- these paired salivary glands are present in the anterior part of the floor of the mouth.
They are situated between the mucosa, mylohyoid muscle and anterior part of the body
of the mandible. They have multiple excretory ducts which open either directly into the

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floor of the mouth or drain into the Wharton’s duct of the submandibular gland. The
secretions of the glands are primarily mucinous, and are therefore more viscous than
saliva produced by the submandibular and parotid glands.
"BLOOD SUPPLY
i. Sublingual branch of the lingual artery _ii. Submental branch of the facial artery
*MINOR SALIVARY GLANDS - there are about 450 minor salivary glands in the oral cavity
situated in the mucosa of the lips, cheeks, palate (250 on hard palate, 100 on soft palate
and 10 on uvula), floor of mouth and retromolar region. They have mucous secreting
acini and contribute to 10% of total salivary secretion.
BLOOD SUPPLY OF THE ORAL CAVITY MUSCULATURE - perforating branches of the anterior
and inferior labial arteries that are terminal branches of the external facial artery.
SENSORY INNERVATION - the maxillary division of the trigeminal nerve innervates the
buccal mucosa and the mucosa of the lips.
MOTOR INNERVATION - is from the facial nerve.
= BOUNDARIES
*SUPERIORLY - hard and soft palates *INFERIORLY - tongue
*BELOW - floor of the mouth *LATERALLY - cheeks
ePOSTERIORLY - anterior pillars
“BUCCAL MUCOSA - consists of all mucous membranes of the inner surface of the cheek
and lips and extends between the superior and inferior gingivobuccal sulcus. It extends
posteriorly up to the pterygomandibular raphe and anteriorly to the meeting line of lips,
It covers the parotid duct, minor salivary glands, buccinator muscles and upper and
lower alveoli.
LYMPHATIC DRAINAGE - buccal mucosa drains into submental and submandibular nodes
and from there to the deep cervical lymph nodes.
ALVEOLI AND GINGIVAE - gums (gingivae) surround the teeth and cover the upper and
lower alveolar ridges.
*UPPER ALVEOLAR RIDGE - jaw ridge on the roof of the mouth between the upper teeth
and hard palate. It includes the alveolar process of the maxilla and its mucosa from the
upper gingival gutter to the junction of the-hard palate.
LYMPHATIC DRAINAGE
BUCCAL ASPECT OF MUCOSA - drains to the submandibular lymph nodes

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*» LINGUAL ASPECT - drains either directly to the upper deep cervical or through the
lateral retropharyngeal nodes.
*LOWER ALVEOLAR RIDGE - jaw ridge on the bottom of the mouth behind the teeth. It
includes the alveolar process of the mandible and its mucosa from the buccal gutter to
the floor of the mouth.
LYMPHATIC DRAINAGE - the central part of both buccal and lingual surfaces of mucosa
drains to the submental nodes whereas the lateral parts drain into the submandibular
nodes.
FLOOR OF THE MOUTH - is semilunar in shape encompassing the area from the inner
border of the lower alveolar ridge to the undersurface of the tongue. It is divided by the
frenulum anteriorly and contains the sublingual and part of the submandibular salivary
glands. It is highly vascular with rapid absorption of sublingual medications. There are
few minor salivary glands in the floor of the mouth. Its posterior boundary is the base of
the anterior tonsillar wall.
*CONTENTS
*» Ducts of the submandibular glands » Ducts of the sublingual glands
» Extrinsic musculature of the tongue
MYLOHYOID MUSCLES - constitute the muscular floor of the mouth and arise from the body
of the mandible and insert into the median raphe that extends from the posterior surface
of the mandible to the anterior surface of the hyoid bone. The firmness of this muscular
floor encourages edema of the floor of the mouth to project upward rather than
downward. It helps to elevate the hyoid.
*LYMPHATIC DRAINAGE
® ANTERIOR PORTION OF THE FLOOR OF THE MOUTH - drains into the submental and
submandibular nodes (Level |). Lymphatics from this area cross the midline.
* POSTERIOR PORTION - drains into the upper deep cervical nodes (Level Il and Ill).
< HARD PALATE - is the bony plate that forms a partition between the nasal passages and
the mouth. It extends from the inner border of the superior alveolar ridge to the posterior
boundary of the palatine bone. It forms the roof of the oral cavity and floor of the nasal
cavity. It contains a high number of minor salivary glands. It offers support to the floor of
the nose and is covered by the dense mucosa firmly adherent to the underlying
periosteum. The hard palate is included in the oral cavity whereas the soft palate is part
of the oropharynx.
ANTERIOR 2/3 OF THE TONGUE - the mobile portion of the tongue which extends
anteriorly from the circumvallate papilla to the undersurface of the tongue.
= LIPS - are two fleshy folds surrounding the oral orifice which form the anterior boundary
of the oral cavity. They are the muscular folds surrounding the mouth. They are covered
externally by the skin and internally by mucous membranes. In between these layers are
the muscles of the lips, especially the orbicularis oris muscle, and the superior and
inferior labial arteries. Within their submucosa are many minor serous and mucinous
salivary glands that lubricate the mucosa and initiate digestion. The two surfaces of the
lip, skin and mucosal, become continuous with one another round its red margin which
is called vermilion.
- the line of contact between the lips, the oral fissure, lies just above the incisal edges of
the anterior maxillary teeth. On each side, a labial commissure forms the angle (corner)
of the mouth, usually near the first premolar tooth.
*PHILTRUM - is a shallow vertical groove in the central region of the upper lip which is
limited above by its attachment to the columella of the nose, and ends below in a slight
tubercle limited by lateral ridges. The lower lip shows a small depression in the midline
that corresponds to the tubercle.

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*CUPID’S BOW - the junction between the external, hair-bearing skin and the red,
hairless surface of the upper lip almost invariably takes the form of a double-curved bow.
VERMILION BORDER - is the transition from skin to lip mucosa. It is the site along which
the two lips meet with one another marked by a line that indicates transition from a dry
vermilion to a moist vermilion. It is devoid of sweat and sebaceous glands and requires
frequent moistening.
®DRY VERMILION - with a pattern of wrinkles has a clear cut boundary line between it
and the skin proper, patterned with Cupid’s bow in upper lip and central fullness in the
lower lip.
®»SMOOTH WET VERMILION - merges without obvious surface change with mucosa
lining of lip. Mucosal surface has mucous glands and supporting tissue within the muscle
and mucosa.
eEPITHELIUM - the lip is covered with non-keratinized stratified squamous epithelium
which is transparent and contains no hairs, sebaceous glands, or pigments so it appears
red. On the vermilion border the mucosa is closely applied to the orbicularis muscle and
the distance between the epithelium and muscle is just 2 mm.
*BLOOD SUPPLY - small submental arteries and inferior and superior labial arteries which
are branches of the facial artery supply to lips.
eLYMPHATIC DRAINAGE
LOWER LIP - medial portion of lower lip drains into the submental (Level !) and lateral
portion to the submandibular nodes. (Level I).
™UPPER LIP - it drains into the preauricular, infraparotid and submandibular lymph
nodes.
Upper lip (lablum) <a Frenulum of upper lip:
Superlor__/ A Se ae Gingiva covering the
vestibule # ‘a > maxiliary alveolar
process.
Hard palate Fauces
Soft palate Palatine tonsil
Uvula Tongue
Frenulum of tongue
Opening of
submandibular duct
Ginglva covering the
mandibular alveolar
process
Incisors Frenulum of lower lip
Inferior vestibule Lower llp (lablum)

a
Il. TONGUE 6
- it is a highly mobile muscular organ that can vary greatly in shape. The anterior 2/3 of
the tongue is part of the oral cavity while the posterior 1/3 of the tongue is included in the
oropharynx. The posterior 1/3 (base of tongue) is situated behind the circumvallate
Papillae and foms the anterior wall of the oropharynx.
=PARTS
*Root *Body ‘Tip
- the tongue is situated partly in the mouth and partly in the oropharynx. It is mainly
composed of muscles and is covered by a mucous membrane on its dorsum, tip, and
side. The anterior 2/3 of the tongue, except for the muscles, is derived from the first
branchial arch and the posterior 1/3 from the third arch. The anterior 2/3 can be moved,
while the base is fixed. The muscles are derived from the mesodermal tissues, which are
not part of the first arch. The base of the tongue is covered by lymphoid tissue, the lingual
tonsil.
- the tongue is concerned with mastication, taste, deglutition (swallowing), articulation
(speech), and oral cleansing, but its main functions are squeezing food into the pharynx
when swallowing and forming words during speaking.
TONGUE MUSCLES
*EXTRINSIC MUSCLES - originate from the mandible, styloid process, and the hyoid
process, and are thus enabled to pull the tongue in different directions. They cause
depression, retraction, and elevation.
™ Genioglossus ™®Hyoglossus
™»Styloglossus ®Palatoglossus
eINTRINSIC MUSCLES (wholly within the tongue) - because of their orientation they
impart a great diversity in movement to the tongue. They offer the possibility to change
the shape of the tongue.
® Inferior longitudinal ® Superior longitudinal
*»Intercalated transverse longitudinal
TERMINAL SULCUS - is a prominent V-shaped groove in the mucous membrane of the
dorsum of the tongue at the anterior margin of the circumvallate papillae, with the apex
directed posteriorly and approximately separating the anterior 2/3 from the posterior
1/3. The posterior part of the tongue has no papillae, but is covered with the lymphoid
tissue of the lingual tonsils.
FORAMEN CECUM - marks the origin of the thyroglossal duct at the apex of the sulcus.
FRENULUM - attaches to the anterior inferior aspect of the tongue to the floor of the mouth.
TYPES OF TONGUE PAPILLA - the anterior 2/3 of the tongue is covered by a non-keratinized
stratified squamous epithelium overlying a lamina propia that is organized into
projections known as papillae. Most papillae are filiform, having tapered tips.
eVALLATE (CIRCUMVALLATE) PAPILLAE - about 7-12 vallate papillae are arranged in
the V-shaped groove over the posterior 1/3 of the tongue just in front of the terminal
sulcus. These papillae are circular and relatively large (2-5 mm in diameter). They are
commonly elevated from the lingual surface, with the taste buds lying in the papillary and
contra-papillary crypt surfaces.They appear like flat-topped, short cylinders sunken into
the mucosa and surrounded by a deep trench. The walls of this trench are studded with
taste buds. They and their taste buds are innervated by the glossopharyngeal nerve (CN
IX). The papillae also contain specialized pressure, tactile and temperature receptors.
*FUNGIFORM PAPILLAE - are red, circular- and small, varying from 1 to 4 mm in
diameter. These papillae are slightly elevated above the lingual surface, and are
surrounded by smaller, more numerous, spiny-like papillae, the filiform papillae. They
are mushroom-like, globular, highly vascular, located primarily along the sides and tip,

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and contain 1 to 8 taste buds each on their superior surfaces. They may also contain
specialized pressure, tactile and temperature receptors. Their nerve supply comes from
the chorda tympani (CN VII). There are over a hundred on each side of the anterior tongue.
They frequently appear deeper red in hue than the filiform papillae.
*FILIFORM PAPILLAE - are small, slender, cone-shaped and found mostly on the dorsum
of the anterior 2/3 of the tongue. They serve a tactile function but do not contain taste
buds. These projections provide an abrasive surface that helps break down food against
the hard palate during mastication.
*FOLIATE PAPILLAE - are peg-shaped papillae that form ridges on the posterior and
lateral parts of the tongue and are studded with taste buds. They too lie in a “moat” and
are innervated by the chorda tympani and CN IX.
*PALATAL PAPILLAE - are over the palate and house taste buds opening directly into the
oral cavity. 4
These 5-20 papillae are mainly centered at the hard/soft palate junction. They are
innervated by both the glossopharyngeal and vagus nerves. The taste buds in these
papillae are mainly single and surrounded by small salivary glands.
- papillae and taste buds may occur in other oral and pharyngeal locations, including the
lips, inner surface of the lingual mucosa, epiglottis, various pharyngeal regions and the
upper 1/3 of the esophagus as well as the pharynx.
VON EBNER'S GLANDS (SEROUS) - open into the bottom of some of the trenches that
surround the papillae, particularly the vallate.
- both the number of papillae and buds per papilla decline with age.
BLOOD SUPPLY OF THE TONGUE - is from the lingual branch of the external carotid artery.
BRANCHES OF THE LINGUAL ARTERY
¢Dorsal lingual artery eSublingual artery ¢Deep lingual arteries
VENOUS DRAINAGE - is to the lingual vein and the facial vein.
= LYMPHATIC DRAINAGE OF THE TONGUE - is ipsilateral and contralateral.
TIP OF TONGUE - drains to the submental and deep jugular cervical chain.
eSUBLINGUAL SURFACE - drains to the submandibular nodes.
*REST OF THE ANTERIOR 2/3 OF THE TONGUE - drains to the deep jugular chain of
lymph nodes. These level Ill nodes are situated between the digastric and omohyoid
muscles.
eCENTRAL PORTION AND BASE - drain into deep cervical nodes of both sides.
= INNERVATION OF THE TONGUE
*MOTOR NERVE- is the hypoglossal nerve (CN XIl), which after descending in the neck,
turns forward above the greater cornu of the hyoid bone and runs on the outer surface of
the hyoglossus muscle accompanied by the lingual vein.
*SENSORY NERVES
=» GLOSSOPHARYNGEAL NERVES (CN IX) - pass around the posterior border and lateral
surface of the stylopharyngeal muscle to supply the posterior 2/3 of the tongue deep to
the hyoglossus muscle. They supply both general sensation and taste from the vallate
papillae to the epiglottic valleculae.
™»LINGUAL NERVES (CN V) - are branches of the mandibular division of the CN V and
also receive the chorda tympani from the facial nerve.
- the 2 lingual nerves supply the mucosa of the anterior 2/3 of the tongue. CN V provides
general sensation and some of the facial fibers to the taste buds

Rot <
Body’ «
TH. DHARYNX
- it is a 12-14 cm long fibromuscular conical tube lined with epithelium which forms the
upper part of the air and food passages. It extends from the base of the skull superiorly
to the level of the sixth cervical vertebra. Inferiorly, it becomes continuous with the
esophagus through the pharyngoesophageal junction (1.5 cm width), which is the
narrowest part of the GIT apart from the appendix. It is the area of the throat that extends
from the tonsillar pillar to the posterior pharyngeal wall.
*PHARYNGEAL WALL - from within outwards, it consists of four layers:
MUCOUS MEMBRANE - the pharyngeal mucosa is continuous with the mucous
membrane of the eustachian tubes, nasal cavities, mouth, larynx and esophagus. There
are numerous mucous glands. The lining epithelium is of the stratified squamous type,
except in the nasopharynx where columnar ciliated epithelium is found.
» PHARYNGEAL APONEUROSIS - consists of the pharyngobasilar fascia.
™®MUSCULAR COAT - consists of two layers of muscles
sEXTERNAL LAYER - consists of 3 horizontal circular muscles - superior, middle and
inferior constrictor muscles
BINTERNAL LAYER - consists of 3 vertical muscles - stylopharyngeus,
salpingopharyngeus and palatopharyngeus muscles.
%»BUCCOPHARYNGEAL FASCIA
A. DIVISIONS
1. MASOPHARYNX - is the portion of the pharynx that extends from the base of the
skull to the level of the hard palate. It is the uppermost part of the pharynx and lies behind
the nasal cavities. It is related posteriorly.to the base of the skull.
- it contains adenoid tissue and the orifices of the eustachian tubes which connect the
nasopharynx with the middle ear cavities and are lined by columnar ciliated epithelium in
continuity with that of the nasopharynx.

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- anteriorly, the nasopharynx communicates with the nasal cavities through the
posterior nares. This area is not accessible to direct inspection and must be examined
by mirrors or optical instruments.
- the nasopharyngeal epithelium anteriorly is ciliated, pseudostratified respiratory in type
with goblet cells. The ducts of mucosal and submucosal seromucous glands open on to
its surface. Posteriorly, the respiratory epithelium changes to non-keratinized stratified
squamous epithelium which continues into the oropharynx and laryngopharynx.
BOUNDARIES
*ROOF
® Body of the sphenoid »Basilar process of the occipital bone
eANTERIOR WALL
»Choanae » Soft palate
*POSTERIOR WALL - Cervical vertebrae
eINFERIORLY
» Oropharynx ™» Soft palate
*LATERAL WALL
™»PHARYNGEAL OPENING OF THE EUSTACHIAN TUBE - is situated 10-12 mm behind
and alittle below the level of the posterior end of the inferior turbinate. The tubal aperture
is approximately triangular in shape, and is bounded above and behind by the torus
tubarius.
eustachian
™TORUS TUBARIUS - is an elevation, which is raised by the cartilage of the
tube
between
FOSSA OF ROSSENMULLER - is a variable depression in the lateral wall, located
the posterior wall of the nasopharynx and the salpingopharyngeal fold.
=ADENOID OR NASOPHARYNGEAL TONSIL - is a median mass of mucosa-associated
lymphoid tissue situated in the roof and posterior wall of the nasopharynx.. At its maximal
a
size (during the early years of life), it is shaped like a truncated pyramid, often with
vertically orientated median cleft.
- the free surface of the adenod is marked by folds that radiate forwards and laterally from
a median blind recess, the pharyngeal bursa (bursa of Luschka), which extends
backwards and up. The recess is present in the fetus and the young but only occasionally
present in the adult, and marks the rostral end of the embryological notochord. The
number and position of the folds and of the deep fissures that separate them vary. A
median fold may pass forwards from the pharyngeal bursa towards the nasal septum, or
instead a fissure may extend forwards from the bursa, dividing the nasopharyngeal tonsil
into two distinct halves that reflect its paired developmental origins.
- the nasopharyngeal epithelium lines a series of mucosal folds around which the
lymphoid parenchyma is organized into follicles and extrafollicular areas. Internally, the
tonsil is subdivided into 4-6 lobes by connective tissue septa, which arise from the
hemicapsule and penetrate the lymphoid parenchyma. Seromucous glands lie within the
connective tissue, and their ducts extend through the parenchyma to reach the
nasopharyngeal surface.
- the distribution of adenoid tissue in the nasopharynx is chiefly on the superior and
posterior walls, though it may extend to the Fossa of Rossenmuller and to the orifices of
the eustachian tubes. The adenoid acts as a peripherally placed lymph node, from which
efferent ducts pass to the nearest node in the cervical chain. Mucous glands are
frequently found at the base of the adenoid.It has no crypts and capsule
- after birth, it intitially grows rapidly. It increases in size up to the age of 6 years and then
tends to regress and almost completely disappears by 20 years of age. Itt usually
undergoes a degree of involution and atrophy from the age of 8-10 years (although

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hypoplasia may still occur in adults up to the seventh decade). Relative to the volume
of the nasopharynx, the size of the adenoid is largest at 5 years, which may account for
the frequency of nasal breathing problems in preschool children, and the incidence of
adenoidectomy in this age group.
*NASOPHARYNGEAL BURSA- this epithelial-lined median recess, which is seen within
the adenoid mass, extends from the pharyngeal mucosa to the periosteum of the
basiocciput.
*RATHKE’S POUCH - this dimple above the adenoid (junction of nasal septum and roof
of the nasopharynx) is the remnant of the buccal mucosal invagination, which forms the
anterior lobe of the pituitary.
*FOLLICLES OR "GERM CENTERS" OF GOODSIR - are groups of specially differentiated
lymphoid cells in the form of more or less rounded or oval-shaped areas, having pale
centers and darker margins.
- the pseudostratified ciliated columnar epithlium completely covers the free surface of
the adenoid, dips down into its crypts, and is continuous with that of the adjacent
nasopharynx. The epithelium covering the adenoid has no submucosa, as the latter
passes directly beneath the base of the adenoid.
*BLOOD SUPPLY - the following branches of the external carotid artery supply to the
adenoids
» Ascending palatine branch of facial artery
® Ascending pharyngeal artery
»Pharyngeal branch of the 3% part of the maxillary artery
*VENOUS DRAINAGE - is to the pharyngeal plexus.
*LYMPHATICS - drain into the upper deep jugular nodes directly or through the
retropharyngeal and parapharyngeal lymph nodes.
«SENSORY NERVE SUPPLY - is from the trigeminal nerve.
2. OROPHARYNX - extends from below the soft palate to the upper border of the
epiglottis. It opens into the mouth through the oropharyngeal isthmus, demarcated by the
palatoglossal arch, and faces the pharyngeal aspect of the tongue. Its lateral wall consists
of the palatopharyngeal arch and palatine tonsil. It is lined with stratified squamous
epithelium. It is that portion which is visible via the mouth. The free edge of the soft
palate forms the palatine arch which separates the oral cavity from the pharynx. From its
center the uvula hangs downwards, and from the arch, on either side, run two folds of
mucous membrane, raised up by bands of muscle fibers of the palatoglossus and
palatopharyngeus muscles to form the palatoglossal and palatopharyngeal arches, or
anterior and posterior pillars of the fauces.
= BOUNDARIES
*POSTERIOR WALL - retropharyngeal space that lies opposite the axis and upper part of
the 3 cervical vertebra.
*ANTERIOR WALL - the upper part of the anterior wall communicates with the oral cavity
through the oropharyngeal isthmus. The structures present in the lower part are the base
of tongue, lingual tonsils and valleculae.
»OROPHARYNGEAL ISTHMUS - is bounded by the following structures:
=ABOVE - soft palate
s|NFERIOR - dorsal surface of tongue
=LATERAL - on either side, by palatoglossal_arch (anterior tonsillar pillar)
*BASE OF TONGUE - lies posterior to circumvallate papillae and insertion of
palato glossa l muscle
» LINGUAL TONSILS - are situated in the base of the tongue

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™VALLECULAE (EPIGLOTTIC VALLECULA) - pockets/depressions in between the
median glossoepiglottic fold and the lateral glossoepiglottic fold, anterior to the
epiglottis. These cup-shaped spaces, one on each side, lie between the base of the
tongue and anterior surface of the epiglottis. The median glossoepiglottic fold separates
the two valleculae. Laterally, they are bounded by the pharyngoepiglottic fold that is the
upper limit of the pyriform sinus of the laryngopharynx. They are “spit-traps” and saliva
is temporarily held there.
*LATERAL WALL - both anterior and posterior tonsillar pillars emerge from the soft palate
and enclose the tonsillar fossa, in which is situated the palatine tonsil. The structures
present in the lateral wall include:
™» PALATINE OR FAUCIAL TONSIL
» ANTERIOR PILLAR OR PALATOGLOSSAL ARCH - the palatoglossus muscle is present
in this fold
»POSTERIOR PILLAR OR PALATOPHARYNGEAL ARCH - the palatopharyngeus muscle
lies in this fold.
*SUPERIOR WALL - anteriorly, the soft palate makes the roof of the oropharynx.
Posteriorly, it communicates with the nasopharynx through the nasopharyngeal isthmus
at the plane of the hard palate and atlas vertebra.
eINFERIOR WALL - it communicates with the laryngopharynx at the plane of the upper
border of the epiglottis and the pharyngoepiglottic folds and 3" cervical vertebra.
- the posterior and lateral walls are formed by the superior and middle pharyngeal
constrictors. It is continuous with the mouth through the oropharyngeal isthmus formed
by the palatoglossal muscles on each side. The anterior border is the posterior third of
the tongue especially the circumvallate papillae.
HARD PALATE - is formed by the two palatal processes of the maxilla and the horizontal
processes of the palatine bones. The anteriorly positioned incisive fossa and the greater
and lesser palatine foramina posteriorly allow the passage of the nasopalatine and
palatine arteries and nerves. It has transverse ridges (rugae) to retain the food bolus. It
forms the roof of the oral cavity and floor of the nasal cavity. It contains a high number
of minor salivary glands.
«BLOOD SUPPLY OF THE PALATE - is from the ascending branches of the facial artery
as well as from the branch of the maxillary artery. The palatine vessels and nerves pass
through the palatine canal.
*INNERVATION OF THE HARD PALATE - by branches of the maxillary division of the
trigeminal nerve, the greater palatine nerve, and the nasopalatine nerve.
«LYMPHATIC DRAINAGE
® ANTERIOR PART - drains to the submandibular nodes.
POSTERIOR PART - drains either directly to the upper deep cervical or via lateral
retropharyngeal nodes.
*=VELUM PALATI OR SOFT PALATE - is a mobile flap suspended from the posterior border
of the hard palate, sloping down and back between the oral and nasal parts of the
pharynx. The boundary between the hard and soft palate is readily palpable and may be
distinguished by a change in colour, the soft palate being a darker red with a yellowish
tint. The soft palate is a thick fold of mucosa enclosing an aponeurosis, muscular tissue,
vessels, nerves, lymphoid tissue and mucous glands; almost half its thickness is
represented by numerous mucous glands that lie between the muscles and the oral
surface of the soft palate. The latter*is covered by a stratified squamous
epithelium, composed of muscle and connective tissue while the nasal surface is covered
with a ciliated columnar epithelium. Taste buds are found on the oral aspect of the soft
palate.. It does not contain bone. It separates the mouth from the pharynx. It contains the

12
palatine tonsils. When the soft palate is elevated, it creates a vacuum in the oral cavity
and keeps food out of the nasal cavity.
eit plays a role in
» Swallowing » Sucking * Speech and articulation
*MUSCLES
™TENSOR VELI PALATINE MUSCLE - tenses the palatine velum and opens the
eustachian tube by swallowing
™LEVATOR VELI PALATINE MUSCLE - rises by a small tendon from a quadrilateral
roughened area on the medial end of the inferior surface of the petrous part of the
temporal bone, in front of the lower opening of the carotid canal. Additional fibres arise
from the inferior aspect of the cartilaginous part of the pharyngotympanic tube and from
the vaginal process of the sphenoid bone. At its origin, the muscle is inferior rather than
medial to the pharyngotympanic tube and only crosses medial to it at the level of the
medial pterygoid plate. It passes medial to the upper margin of the superior constrictor
and anterior to salpingopharyngeus. Its fibres spread in the medial third of the soft palate
between the two strands of palatopharyngeus to attach to the upper surface of the
palatine aponeurosis as far as the midline, where they interlace with those of the
contralateral muscle. Thus, the two levator muscles form a sling above and just behind
the palatine aponeuro is the elevator of the soft palate which arises from the temporal
bone and attaches to the palatine aponeurosis at the upper part. It is divided into parts
by a median raphe and consists of muscle fibers supported by fibrous tissue covered by
an outer mucous membrane.
- the soft palate is quite mobile, and in conjunction with the pharyngeal musculature,
seals off the nasopharynx to prevent nasal regurgitation during deglutition and nasal air
emission during speech. Within the lamina propia of both hard and soft palates are
numerous minor salivary glands.
*MOTOR INNERVATION OF THE SOFT PALATE MUSCLES - is carried by branches of the
vagus and glossopharyngeal nerves, except the tensor veli palatine, which is innervated
by the mandibular division of the trigeminal nerve.
eSENSORY INNERVAT ION OF THE SOFT PALATE - is carried by the lesser palatine nerve.
- the lateral margins of the palate, on each side, divide into the:
*ANTERIOR PILLAR (PALATOGLOSSAL ARCH, ANTERIOR FOLD) - runs from the soft
palate to the side of the tongue and contains the palatoglossus muscle.
*POSTERIOR PILLAR (PALATOPHARYNGEAL FOLD, POSTERIOR FOLD) - projects more
medially and passes from the soft palate to merge with the lateral wall of the pharynx; it
contains the palatopharyngeus muscle.
“UVULA - is the cone-shaped central projection. It is a free, inferior border of the soft
palate, projected in variable lengths.
© PASSAVANT'S PAD - is a prominence produced by contraction of the upper fibers of the
superior constrictor muscle which can be seen when the palate is elevated during
swallowing.
© PLICA TRIANGULARIS - is a mucosal fold, stretching backward from the palatoglossal arch
down to the tongue and covering a portion of the anterior surface of the tonsil during
young adult life. It is infiltrated by lymphoid tissue and frequently represents the most
prominent (anteroinferior) portion of the tonsil. It rarely persists into middle age.
- it has no muscular tissue and should be removed with the tonsil during tonsillectomy
because it may form a pocket or pouch where food and other debris collect.
<PLICA SEMILUNARIS - is the upper fold of mucous membrane which unites the 2 pillars
at their junction.

13
SUPRATONSILLAR FOSSA — is a triangular tonsillar fossa (tonsillar sinus) Ithat ies on
each side of the oropharynx between the diverging palatopharyngeal and palatoglossal
arches, and contains the palatine tonsil.
ANTERIOR TONSILLAR SPACE - is a space enclosed in a_ triangular fold of mucous
membrane which extends from the anterior pillar to the anteroinferior part of the tonsil at
the lower pole which is attached to the tongue.
= LINGUAL TONSIL - is a sessile structure situated at the base of the tongue between the
faucial tonsils, and extends anteroposteriorly from the foramen cecum to the epiglottis.
It is covered by squamous epithelium and is separated from the musculature of the
tongue by a layer of fibrous tissue. It is divided in the midline by the median
glossoepiglottic ligament. The tonsil consists of numerous rounded or circular crater-
like elevations of lymphoid tissue, surrounded at their periphery by connective tissue. In
the center of each crater the duct of a mucous gland opens. The size of the lingual tonsils
may vary among individuals.
VENOUS DRAINAGE - a venous plexus is found at the base of the tongue.
*ARTERIAL SUPPLY - is from the external carotid through the dorsal lingual branch of
the lingual artery.
*LYMPHATIC DRAINAGE - the lymphatic system of the lingual tonsils aids in forming
wbc and filtering out bacteria.
»® Suprahyoid »Submaxillary Deep cervical lymph nodes
*NERVE SUPPLYG
»>CN IX ® Superior laryngeal branch of CN X
—WALDEYER'S RING - is a circumpharyngeal ring of mucosa-associated lymphoid tissue
that surrounds the openings into the digestive and respiratory tracts. It is made up
anteroinferiorly by the lingual tonsil, laterally by the palatine and tubal tonsils, and
posterosuperiorly by the pharyngeal tonsil and smaller collections of lymphoid tissue in
the intertonsillar intervals.
- this tissue is primarily involved in inducing secretory immunity and regulating
immunoglobulin production. The cells are organized in lymphoid follicles similarto lymph
nodes, but have specialized endothelium-covered channels that facilitate antigen uptake
directly into the tissue, similar to Peyer patches in the colon. The independence of this
system from lymphatic drainage is a unique advantage for antigen acquisition. The
location of Waldeyer’s tonsillar ring and its design allow direct exposure of the
immunologically active cells to foreign antigens entering the upper aerodigestive tract,
which maximizes the development of immunologic memory.
- Waldeyer’s ring grows throughout childhood until the age of about 11 years old and
after that decreases spontaneously. These tissues are most active from the ages of 4 to
10 and tend to involute after puberty. After their involution, the secretory immune function
of these tissues remains, but not at the same level as previously.
- its greatest importance is probably in the first few years of life and removal of the
adenoids and tonsils should be done in the few years of life only with clear and pressing
necessity.
COMPONENTS OF WALDEYER'S RING
» Adenoids or nasopha ryngeal tonsil »Palatine tonsils
» Lingual tonsils »Lateral pharyngeal bands
»SCATTERED LYMPHOID NODULES - located in Rossenmuller's fossa beneath the
mucous membrane of the posterior pharyngeal wall.
»GERLACH'S TONSIL - adenoid tissue found around the orifice of the eustachian tube.

. . 14
- this collection of lymphoid tissue is the first to sample and react to antigens in the
air and food entering the body, and serves as a defense against infection and p_ Ilays an
important role in the development of the immune system.
= PALATINE TONSILS - are ovoid masses of lymphoid tissue situated in the lateral wall of
the oropharynx. Size varies according to age, individuality and pathological status
(tonsils may be hypertrophied and/or inflamed). It is therefore difficult to define the
normal appearance of the palatine tonsil. At birth, they are of insignificant size, but they
enlarge during early childhood, especially between the 3% and 6" years of age. They
usually reach a maximum at puberty, when they average 20-25 mm in vertical, and 10-
15mm in transverse, diameters and they project conspicuously into the oropharynx.
Between the ages of1 and 11 years, the tonsil and adenoid grow proportionally to the
lower facial skeleton . Tonsillar involution begins at puberty, when the reactive lymphoid
tissue begins to atrophy, and by old age only a little tonsillar lymphoid tissue remains.
- its medial, free, surface usually presents a pitted appearance. The pits, 10—20 in number,
lead into a system of blind-ending, often highly branching, crypts that extend through the
whole thickness of the tonsil and almost reach the connective tissue hemicapsule. In a
healthy tonsil, the openings of the crypts are fissure-like and the walls of the crypt lumina
are collapsed so that they are in contact with each other. The human tonsil is polycryptic.
The branching crypt system reaches its maximum size and complexity during childhood.
- the mouth of a deep tonsillar cleft (intratonsillar cleft, recessus palatinus) opens in the
upper part of the medial surface of the tonsil.
- after the age of 5 years, this embedded part of the tonsil diminishes in size. There is a
tendency for the whole tonsil to involute from the age of 14 years, and for the tonsillar
bed to flatten out. During young adult life, a mucosal fold, the plica triangularis, stretches
back from the palatoglossal arch down to the tongue. It is infiltrated by lymphoid tissue
and frequently represents the most prominent (anteroinferior) portion of the tonsil. It
rarely persists into middle age.
- they are the largest component of the ring and have a specialized histologic structure.
The matrix is lymphoid tissue with crypts, which shows a deep extension into the tissue.
The cells are organized in lymphoid follicles, so they maximize the surface which comes
in contact with antigens. The lymphoid tissue is adherent to a capsule, so inflammation
of the tonsils is limited.
- the location of the tonsils and their design allow direct exposure of the immunologically
active cells with the antigens entering the upper aerodigestive tract. The tissue is
involved in the production of immunoglobulin and inducing secretory immunity.
- the tissue is more active in childhood between the ages of 4 and 10 years and maximizes
the immunologic memory in this way. After puberty the lymphoid tissue starts to involute.
- there are four lymphoid compartments in the palatine tonsils. Lymphoid follicles many
with germinal centres, are arranged in rows roughly parallel to neighbouring connective
tissue septa. Their size and cellular content varies in proportion to the immunological
activity of the tonsil.
eSURFACES AND POLES -a tonsil has two surfaces, medial and lateral, and two poles,
upper and lower. The surface epithelium of the tonsil is continuous with the epithelium
of the oropharynx. The tonsillar crypts are tube-like invaginations from the surface
epithelium.
- the medial or free surface is covered,by a closely adherent stratified squamous
epithelial membrane extending into the blind pouches or crypts, which have their
openings on the surface of the tonsil. The epithelium lining the crypts is thin and offers
poor protection to bacterial infection.

135
- the lateral or outer aspect of the tonsil is loosely attached to the superior constrictor
muscle of the pharynx which subjects the tonsil to compression during the act of
deglutition. The contraction of the palatoglossus and palatopharyngeus muscles of the
pillars also compress the tonsil.
*ARTERIAL BLOOD SUPPLY - the main artery of the tonsil is the tonsillar branch of the
facial artery, which arises from the external carotid artery. The other blood vessels which
supply the tonsil include:
»SUPERIOR POLE
=Branch of the ascending pharyngeal artery
=Lesser palatine artery
» INFERIOR POLE
#Tonsillar branch of the dorsal lingual artery
=Ascending palatine artery from the facial artery
®Tonsillar branch of the facial artery is the main blood supply
*VENOUS DRAINAGE- veins from the tonsils drain into the paratonsillar vein, which are
present on the lateral surface of the tonsil and drain into the common facial vein and
pharyngeal venous plexus.
™®LINGUAL VEINS - main venous drainage
PHARYNGEAL VEINS
*NERVE SUPPLY
™TONSILLAR BRANCHES OF THE GLOSSOPHARYNGEAL NERVE - main nerve supply.
Because the glossopharyngeal nerve also has a tympanic branch, severe tonsillitis
frequently presents wit-h referred pain to the ear.
™» DESCENDING BRANCHES OF THE LESSER PALATINE NERVES
eLYMPHATIC DRAINAGE - palatine tonsils drain into the jugulodigastric (tonsillar) nodes
of the upper deep cervical group, which are situated below the angle of the mandible.
®TONSILLAR LYMPH NODES
»UPPER JUGULAR DIGASTRIC LYMPH NODES
*CAPSULE - is a white fibrous sheath, the pharyngeal fascia surrounding the tonsil
except on the free surface which sends out trabeculae which pass into the parenchyma
and carry with them the blood vessels, nerves, and efferent lymphatics.
- it is separated from the muscles of the tonsillar bed by loose connective tissue which
allows easy dissection in this plane during tonsillectomy. It may become adherent to the
muscle after repeated attacks of infection.
*BED OF THE TONSIL - the superior constrictor, glossopharyngeal nerve and
styloglossus muscle form the bed of the tonsil.
*ELEMENTS OF THE TONSILS
CONNECTIVE TISSUE - the trabecula or reticulum, acts as a supporting framework to
the tonsil substance proper and carries blood vessels, nerves, and lymphatics.
™®GERMINATING FOLLICLES - are the centers wherein the large mother cells of the
leukocytic group undergo karyokinesis and f orm young lymphoid cells.
*INTERFOLLICULAR TISSUE - is made up of lymphoid cells in various stages of
development, and of different sizes and shapes.
eTONSILLAR CRYPTS -8 to 10 in number, are lined with stratified squamous epithelium.
They are usually tubular and compound and extend deep into the substance of the tonsil.
Those opening in the supratonsillar fossa usually extend downward and outward,
whereas in the lower portion of the tonsil their direction is outward. They are usually
comparatively straight, though they may be tortuous in their course. Though they
maximize the exposure of tissue to surface antigen, they can also harbor debris and
bacteria and may be the reason that tonsils are so commonly infected. Clinically, the

16
crypts seem to be the source of the greatest amount of local and constitutional
disturbances, as they often become filled with food debris, tissue debris, and bacteria.
*SECONDARY CRYPTS - arise from the main crypts within the substance of the tonsil.
The crypts may be filled with cheesy material, which consists of epithelial cells, bacteria
and food debris and can be expressed out with pressure over the anterior tonsillar pillar.
*TONSILLAR FOSSA (SINUS TONSILLARIS) - is formed by three thin pharyngeal
muscles. The palatoglossus muscle forms the anterior tonsillar pillar while the
palatopharyngeus muscle forms the posterior tonsillar pillar.
- the pillars meet superiorly and unite with the soft palate. Inferiorly, they divide to enter
the tissues at the lateral portion of the base of the tongue and the lateral wall of the
pharynx.
- laterally, the superior constrictor muscle completes the sinus. Under this thin muscle
lies the glossopharyngeal nerve; the neurovascular structures of the carotid sheath are
found more deeply beneath. With deep dissection or with sutures placed beyond the
tonsillar capsule, these vital structures can be damaged inadvertently.
®PALATOGLOSSUS MUSCLE - has a fan-shaped origin in the oral surface of the soft
palate and terminates in the lateral side of the tongue.
»PALATOPHARYNGEUS MUSCLE - is a vertically arranged muscle attached above to
the soft palate, the eustachian tube and the base of the skull. It extends downward to the
upper esophageal wall and is of greater importance than the palatoglossus.
™® SUPERIOR CONSTRICTOR MUSCLE - has transversely disposed fibers and originates
from the:
"Lower portion of the internal pterygoid plate =Mandible
=Pterygomandibular ligament =Hamularprocess
MUSCLES OF THE SOFT PALATE
eAzygos uvulae *Levator palati ¢Tensor palati
*Palatoglossus ¢Palatopharyngeus
= LYMPHATIC DRAINAGE OF THE OROPHARYNX
*UPPER JUGULAR CHAIN - particularly the jugilodigastric (tonsillar) node
*RETROPHARYNGEAL AND PARAPHARYNGEAL NODES - soft palate, lateral and
posterior pharyngeal walls and the base of the tongue.
*POSTERIOR CERVICAL GROUP
3. LARYNEOPHARYNX (HYPOPHARYNX) - is situated behind the entire length of the
larynx (known clinically as the hypopharynx) and extends from the superior border of the
epiglottis, where it is delineated from the oropharynx by the lateral glossoepiglottic folds,
to the inferior border of the cricoid cartilage, where it becomes continuous with the
esophagus. The laryngeal inlet lies in the upper p art of its incomplete anterior wall, and
the posterior surfaces of the arytenoid and cricoid cartilages lie below this opening.
-it extends superiorly from the level of the hyoid bone to the upper end of the esophagus.
It is partially separated from the oropharynx by the pharyngoepiglottic fold, which
extends from the epiglottis to the side of the pharynx. It is the lowest part of the pharynx;
it lies behind and partly lateral to the larynx. Posteriorly, it lies on the 3, 4th, 5th, 6th
cervical vertebrae. It is the part of the throat that connects to the esophagus. It is divided
into 3 sites:
*PIRIFORM SINUS OR RECESS - lateral to the larynx are two mucosal pouches whose
medial borders are the lateral walls of the larynx and form lateral channels for food during
deglutition. The two pyriform sinuses lead to the opening of the upper end of the
esophagus which is situated behind the cricoid cartilage - the postcricoid region.
Foreign bodies may lodge here. If this area is injured (e.g., by a fish bone), it can cause a
globus sensation or feeling that something is still stuck in the throat.

7
- the obliquely sloping inlet of the larynx lies in the anterior part of the laryngopharynx
and is bounded above by the epiglottis, below by the arytenoid cartilages of the larynx,
and laterally by the aryepiglottic folds. Below the inlet, the anterior wall of the
laryngopharynx is formed by the posterior surface of the cricoid cartilage.
*POSTCRICOID AREA - this anterior wall of the laryngopharynx (pharyngoesophageal
junction) extends between the level of the arytenoids and lower border of the cricoid
lamina.
*POSTERIOR PHARYNGEAL WALL - extends from the superior level of hyoid bone to the
level of the inferior border of the cricoid cartilage and between the apices of the pyriform
fossa. It is lined by mucosa, and is enclosed within the three constrictor muscles of the
pharynx - superior, middle and inferior. The mucous membrane of the laryngopharynx
is covered with pseudostratified ciliated columnar epithelium except over the laryngeal
surface of the epiglottis, the anterior surface of the arytenoids, and the free edges of the
true vocal cords where stratified squamous epithelium is found. Many mucous glands
and much lymphoid tissue, collected into follicles, are found.
- the posterior and lateral walls are formed by the middle and inferior pharyngeal
constrictors. It extends inferiorly to the cricopharyngeus, where the pharynx empties into
the cervical esophagus.
- anteriorly, it extends from the valleculae and contains the epiglottis and the larynx. The
vallecula is a recess between the tongue and the anterior surface of the epiglottis.
- the aryepiglottic folds run from the epiglottis to the arytenoid cartilages to form the walls
of the entrance to the larynx. The posterior aspect of the hypopharynx contains the
posterior pharyngeal wall and post-cricoid mucosa.
LYMPHATIC DRAINAGE
*PYRIFORM SINUS - drains into the upper jugular chain through the thyrohyoid
membrane
ePOSTERIOR PHARYNGEAL™ WALL - lateral pharyngeal or parapharyngeal nodes and
then to deep cervical lymph nodes
*POSTCRICOID REGION - parapharyngeal nodes and nodes of the supraclavicular and
paratracheal chain.
MUSCLES OF THE LARYNGOPHARYNX
*CONSTRICTORS
» SUPERIOR CONSTRICTOR
®MIDDLE CONSTRICTOR - is attached to the greater cornua of the hyoid bone which
gives stability to the hypopharynx.
»® INFERIOR CONSTRICTOR - is attached to the oblique line of the thyroid cartilage to a
fibrous band bridging the cricothyroid space lateral to the cricothyroid cartilage. The
lowermost fibers of the inferior constrictor arise from the cricoid to form the
cricopharyngeus, which serves as the upper esophageal sphincter.
paratracheal chain.
eSTYLOPHARYNGEUS ePALATOPHARYNGEUS
= PHARYNGEAL TISSUE SPACES
ePERIPHARYNGEAL SPACE - is formed by the submandibular and submental spaces,
posteriorly by the retropharyngeal space and laterally by the parapharyngeal spaces.
eRETROPHARYNGEAL SPACE - is an area of loose connective tissue that lies behind the
pharynx and anterior to the prevertebral fascia, extending upwards to the base of the
skull and downwards to the retrovisceral space in the infrahyoid part of the neck.
- each parapharyngeal space passes laterally around the pharynx and is continuous with
the retropharyngeal space. However, unlike the retropharyngeal space, it is a space that

. . 18
is restricted to the suprahyoid region.The parapharyngeal space is divided into an
anterior, or prestyloid, compartment and a posterior, or retrostyloid, compartment
™PRESTYLOID SPACE - contains the retromandibular portion of the parotid gland, fat
and lymph nodes.
®RETROSTYLOID SPACEN - contains the internal carotid artery, the internal jugular
vein, the glossopharyngeal, vagus, accessory and hypoglossal nerves, the sympathetic
chain, fat and lymph nodes.
BLOOD SUPPLY OF THE PHARYNX
eARTERIES
» ASCENDING PHARYNGEAL - supplies posterolateral part
®SUPERIOR THYROID - lower pharynx
»INFERIOR THYROID - lower pharynx
®VIDIAN ARTERY - from maxillary artery
»TONSILLAR ARTERIES
eVEINS
™» POSTERIOR WALL PLEXUS - communicates with pterygoid plexus above and superior
thyroid below
™»BATSON’S PLEXUS - in mucosa of pharynx, communicates with superior laryngeal and
esophageal veins
NERVE SUPPLY OF THE PHARYNX
PHARYNGEAL PLEXUS - made up of CN IX and X
*GLOSSOPHARYNGEAL NERVE - sensory
*PHARYNGEAL BRANCH OF VAGUS - motor except to:
=» TENSOR VELI PALATINI - n. V3
™»STYLOPHARYNGEUS - CN IX
» LOWER INFERIOR CONSTRICTOR - superior laryngeal nerve branches
MUSCLES OF THE PHARYNX - all innervated by CN X except for the stylopharyngeus which
is innervated by CN IX.
= LYMPHATICS
®»ROOF AND POSTERIOR WALL - to lateral pharyngeal node
™®TONSILLAR REGION - deep cervical
=» LARYNGOPHARYNX - pierce the thyrohyoid to reach deep cervicals
Iv. LARYNX
- it occupies the central compartment of the neck. It is located within the hypopharynx.
It is located more superiorly in the child than in the adult.
- the cricoid cartilage in the child is at the level of the fourth cervical vertebral body in
contrast to that in the adult, which is at the level of the sixth vertebral body.
- the larynx lies in the middle and anterior part of the neck at the level of the C3-C6
vertebrae in an adult, and in a child, it is at the level of the C2-C3 vertebrae and descends
as the child grows. It connects the hypopharynx to the trachea.
- during swallowing and phonation, the larynx moves in a vertical as well as
anteroposterior direction. The passive side to side movement of the larynx produces a
grating sensation called laryngeal crepitus.
= COMPARTMENTS
*SUPRAGLOTTIC LARYNX - extends from the tip of the epiglottis and vallecula superiorly
to the ventricle and undersurface of the "false" cords inferiorly. It is the area above the
vocal cords.
» Arytenoid cartilages » Aryepiglottic folds
» False vocal cords »Epiglottis

19
*GLOTTIC LARYNX - it encompasses the “true” vocal cords, extending from the
ventricle between the true and false cords to 0.5 cm below the free edge of the true cords,
including the anterior commissure and interarytenoid area.
*SUBGLOTTIC LARYNX - it extends from the inferior portion of the glottis down to the
inferior edge of the cricoid cartilage.
= CARTILAGES - the larynx has 3 single (thyroid, cricoid and epiglottis) and 3 paired
cartilages (arytenoid, corniculate and cuneiform).
*HYALINE CARTILAGES - undergo ossification which begins first in the thyroid at the age
of 25 years and later in the cricoid and arytenoids, and is complete by 65 years.
Thyroid cartilage *»Cricoid cartilage
»Arytenoid cartilages, except its tip
*ELASTIC CARTILAGES - are fibroelastic and do not ossify.
»Epiglottis »Corniculate cartilage of Santorini
*Tip of the arytenoids Cuneiform cartilage of Wrisberg
= SUPPORTING STRUCTURES
*HYOID BONE - consists of:
»Central body »2 Greater cornua ™»2 Lesser cornua
- it is only attached to other bones by muscles or ligaments. It helps with tongue
movement and swallowing. 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. Inferior to the hyoid bone, and suspended by the thyrohyoid ligament, are
the 2 alae, or wings, of the thyroid cartilage. It is the only bone within the airway and is
the only radiopaque structure within the larynx.
- the posterior superior surface of the hyoid serves for the attachment of the hyo-
epiglottic and thyrohyoid membranes and forms the anterosuperior boundary of the pre-
epiglottic space with the valleculae immediately above.
-the attachments of the hyoid bone to the mandible and skull by the stylohyoid ligament
and the digastric, stylohyoid, mylohyoid, hyoglossus and geniohyoid muscles serve to
maintain the larynx in position in the neck and to raise the larynx during deglutition and
phonation.
- the attachments of the sternohyoid and omohyoid muscles to the hyoid are important
in inferior movement of the larynx. It is connected to the thyroid cartilage by the
thyrohyoid membrane.
‘THYROID CARTILAGE -- is the largest of the laryngeal cartilages, consisting of 2
flattened laminae, fused at the midline after birth. It encloses the larynx anteriorly and
laterally. It serves to protect the vocal cords, which are located directly behind it. The
angle between the two laminae is an expression of sexual dimorphism in the adult,
diverging at an average angle of 75-90 degrees in men and 90-110 degrees in women. The
alae join in the midline at an angle that is more acute in the male, producing the
“Adam’s apple.” On the posterior border of each ala are the superior and inferior cornua.
The inferior cornua articulates with the cricoid cartilage, allowing a small amount of
gliding and rocking between the thyroid and cricoid cartilages.
- anteriorly and superiorly, the thyroid laminae are unfused, resulting in the thyroid notch.
At the lateral and posterior extent of the laminae are the paired superior greater cornua
and the inferior lesser cornua.
SUPERIOR CORNUA - forms a point of attachment to the greater cornua of the hyoid
bone by means of a thick fibrous band, the thyrohyoid ligament.
» INFERIOR CORNUA - articulates with the cricoid cartilage, forming a synovial joint, the
cricothyroid joint, which alters the angle between the thyroid and cricoid cartilages.

20
- superior attachments of the thyroid cartilage to the hyoid bone are completed by the
thyrohyoid membrane.
- inferiorly, the thyroid cartilage is attached to the cricoid cartilage by means of the
» Cricothyroid joint * Cricothyroid muscle
*Cricothyroid membrane and ligament
OBLIQUE UNE - is a faint ridge visible or palpable along the posterior 3/4 of the laminae,
forming a landmark. It is the attachment for a series of extrinsic laryngeal muscles that
move the larynx relative to adjacent anatomic structures
*»Omohyoid muscle ™* Sternothyroid muscle
Inferior constrictor muscle
- internally, the thyroid laminae are lined with mucoperichondrium except at the anterior
commissure, the internal portion of the angle.
- at this point are the attachments for 5 ligaments forming the structural supports for the
5 LARYNGEAL FOLDS:
=®» MEDIAN THYROEPIGLOTTIC LIGAMENT (Median thyrohyoid fold)
*BILATERAL VESTIBULAR LIGAMENTS (Vestibular folds) (False vocal cords)
®»BILATERAL VOCAL LIGAMENTS (Vocal folds) (True vocal cords)
- the attachments of these ligaments penetrate the inner mucoperichondrium and
cartilage at the anterior commissure and insert into the outer perichondrium forming a
structure called Broyle’s ligament. This ligament contains blood vessels and lymphatics
and constitutes an important route of spread of vocal cord tumors.
eCRICOID CARTILAGE - is the only circumferentially complete cartilaginous ring in the
airway, so it is unable to expand. It is the first ring of the trachea. It is directly below the
thyroid cartilage. It is anatomically related to the thyroid gland. The isthmus is inferior
to the cricoid cartilage. The lobes of the thyroid gland extend superiorly on each side.
- the posterior surface, or lamina, of the cricoid is quite wide, giving this cartilage the
appearance of a signet ring. Prolonged endotracheal intubation is often damaging to the
mucosal lining within the ring and may lead to acquired subglottic stenosis.
™»SUPERIORLY - it supports the vocal cords tethered anteriorly by the thyroid cartilage
and the cricothyroid joint and posteriorly by the arytenoid cartilages and the
cricoarytenoid articulation.
»INFERIORLY - the first tracheal cartilage attaches to the cricoid by an inter-cartilaginous
ligament.
- “nferiorly, it supports the trachea by means of ligamentous and muscular attachments.
The thyroid and cricoid cartilages are joined in the midline by a median cricothyroid
ligament.
-
the posterior midline of the cricoid cartilage is marked by a ridge dividing the 2 laminae,
which receives the longitudinal fibers of the esophagus and separates the posterior
cricoarytenoid muscles. The superior margin of the cricoid cartilage slopes downward
anteriorly and in reference to the inferior margin of the thyroid cartilage defines the
cricothyroid angle, or visor angle. The significance of this angle is that it is constant
during deglutition and respiration, but closed during phonation.
- the superior-posterior margin of the cricoid laminae bilaterally has 2 articular surfaces
that constitute the inferior half of the important cricoarytenoid joint.
*EPIGLOTTIS - is a single, leaflike structure, composed primarily of elastic fibrocartilage.
The inferior portion is intralaryngeal and the superior portion is directed
posterosuperiorly across the airway at the baSe of the tongue. By virtue of its shape and
location, it performs an important protective function for the laryngeal aditus during
deglutition. It functions as a keel, forcing swallowed food to the side of the laryngeal

21
airway. The thin inferior portion of the cartilage, or petiole, is attached to the posterior
portion of the angle of thyroid cartilage by way of the thyroepiglottic ligament.
- the anterior portion of the epiglottis conveys 3 mucosal folds to the attachments on the
posterior portion of the tongue
Median glossoepiglottic fold ® Paired lateral glossoepiglottic folds
VALLECULA - is the depression formed on each side of the medial fold.
- in adults, the epiglottis is mildly concave posteriorly. In children and some adults, it is
markedly curved and is called an omega, or juvenile epiglottis.
*ARYTENOID CARTILAGES - are paired, pyramidal-shaped structures that serve as
supports for the posterior laryngeal folds. They sit on top of the posterior portion of the
cricothyroid cartilage. On the base of each pyramid is a concave-shaped facet for
articulation with the cricoid cartilage in the complex cricoarytenoid joint. They have a
particularly significant role in phonation as the intrinsic muscles of the larynx and the
vocal folds are attached to these cartilages. They are important because they influence
the position and tension of the vocal cords.
PROCESSES
» ANTERIOR VOCAL PROCESS - is directed anteriorly and differs from the body in that it
is formed by elastic cartilage. Extending anteriorly from each vocal process and inserting
into the thyroid cartilage in the midline is a vocal ligament.
- the vocal process makes up the posterior 2/5 of the vocal cord, while the vocal ligament
forms the remaining membranous, or vibratory, portion of the cord. The vocal process is
attached to the inner surface of the hyoid cartilage by the vocal ligament. Some of the
intrinsic muscles are attached to the vocal ligament.
™»LATERAL MUSCULAR PROCESS - is directed in a posterolateral direction.
ARYEPIGLOTTIC FOLD - attaches to the apex of the pyramid with the vestibular ligament and
fold inserting inferior to this attachment. It is a fold of mucosa that connects the epiglottis
with the arytenoid cartilages.
TRUE VOCAL FOLD (TRUE VOCAL CORD) - is actually the superior free border of the
cricothyroid ligament.
- this ligament is attached posteriorly to the vocal process of the arytenoid cartilage and
anteriorly to the thyroid cartilage, leaving a free and thickened lateral edge that is covered
with mucosa, which comprises the vocal fold. It attaches to the medial portion of the base,
and the inter-arytenoid and thyrorytenoid muscles attach to the posterior surface.
- the lateral projection of the base gives rise to the muscular process, which contains the
at\itachment for the posterior and lateral cricoarytenoid muscles.
- movement of the arytenoids results in rapid and diverse changes in the aryepiglottic,
vestibular and vocal folds. The medially directed apex of the arytenoid cartilage
articulates or fuses with the small corniculate cartilages of Santorini.
*CORNICULATE CARTILAGES OF SANTORINI - are small conical nodules in the
posterior portion of the aryepiglottic fold. They are paired on top of the arytenoids. They
articulate with the apex of the arytenoid cartilage.
*CUNEIFORM CARTILAGES OF WRISBERG - are composed of fibroelastic cartilage
embedded farther anteriorly along the aryepiglottic fold. They are paired and are lateral
to the corniculates on the aryepiglottic folds.
- the corniculate and cuneiform cartilages may provide a stiffening and elastic recoil
function for the posterior aryepiglottic folds.

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LIGAMENTS AND MEMBRANES
EXTRINSIC
*THYROHYOID MEMBRANE - spans the distance between the superior margin of the
hyoid bone and its greater cornua and the superior margin of the thyroid cartilage. It is
pierced by the neurovascular bundle of the superior laryngeal vessels and internal
laryngeal nerve, and connects the thyroid cartilage to the hyoid bone. A bursa exists
along the posterior surface of the hyoid bone to facilitate its movement during deglutition.
*HYOEPIGLOTTIC LIGAMENT - attaches the anterior surface of the epiglottis to the body
of the hyoid bone. It divides the epiglottis into two parts suprahyoid and infrahyoid. It
joins the anterior surface of the epiglottis and the posterior surface of the hyoid to form
the roof of the pre-epiglottic space and the floor of the valleculae.
*CRICOTRACHEAL MEMBRANE - connects the cricoid cartilage to the first tracheal ring.
INTRINSIC
*CRICOVOCAL MEMBRANE .- is a triangular fibroelastic membrane arising from the
superior margin of the arch of the cricoid cartilage to join the vocal ligament on each side.
It has a free upper border (vocal ligament), which stretches between the middle of the
thyroid angle to the vocal process of the arytenoids. The lower border is attached to the
arch of the cricoid cartilage. Anteriorly, itis attached to the inferior margin of the thyroid
cartilage and the superior margin of the cricoid cartilage, where it is thickened and
constitutes the cricothyroid ligament.
™» CONUS ELASTICUS- is formed by the 2 sides of the cricovocal membranes. Subglottic
foreign bodies sometimes get impacted in this region.
*»CRICOTHYROID MEMBRANE - the anterior part of the conus elasticus is thick and
forms the cricothyroid membrane, which connects the thyroid cartilage to the cricoid
cartilage.
* CRICOTHYROID LIGAMENT - is a flat band of tissue joining the cricoid and thyroid
cartilages. bem
*QUADRANGULAR MEMBRANE - extends from the lateral margins of the epiglottis to
connective tissue termed the fibroelastic membrane. It is separated from the inferior
component by the laryngeal ventricle or sinus of Morgagni.
- this connective tissue system is the principal support for the laryngeal mucous
membranes. Inferiorly, the membrane extends into the vestibular cord (false vocal cord).

- itis the dividing wall between the larynx and the pyriform sinus, and its superior
border is called the aryepiglottic fold.
- the quadrangular membrane and the aryepiglottic fold form a common wall between
the upper pyriform fossa and the laryngeal vestibule, a deep lateral recess closed by the
thyroid cartilage and open posteriorly into the postcricoid esophagus.
Greater iglottic cartilage
Lesser horn
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SPACES
ePRE-EPIGLOTTIC SPACE OF BOYER - comprises a space filled with fat and loose
areolar tissue and is a common site of invasion of epiglottic tumors through the small
glandular perforations in the epiglottic cartilage.
- it separates the anterior surface of the infrahyoid epiglottis from the thyrohyoid
membrane and thyroid cartilage. It may be invaded by carcinoma of the supraglottic
larynx or the base of the tongue.
» ANTERIORLY
®Thyroid cartilage =#Thyrohyoid membrane
» SUPERIORLY
=Median thyroepiglottic ligament #Vallecula
®POSTERIORLY - anterior surface of the epiglottic cartilage
»INFERIORLY - petiole of the epiglottis
®»LATERALLY - continuous with the paraglottic space
*PARAGLOTTIC SPACE - communicates with the pre-epiglottic space.
» ANTEROLATERALLY
«Inner perichondrium of the thyroid cartilage
=Conus elasticus #Quadrangular membrane
» MEDIALLY - ventricle
» POSTERIORLY - reflection of the pyriform sinus
eSUBGLOTTIC SPACE
» SUPERIORLY - vocal cord fms
» SUPEROLATERALLY - conus elasticus
®INFERIORLY - inner surface of the cricoid membrane
- it communicates with the trachea
*REINKE’S SPACE - this potential space has a scanty subepithelial connective tissue and
lies under the epithelium of the vocal cords.

24
CAVITY OF THE LARYNX - superiorly, the laryngeal cavity communicates with the
laryngopharynx through the laryngeal inlet. The larynx ends at the lower border of the
cricoid cartilage (level of lower border of VI cervical vertebra) and becomes continuous
with the trachea. The vestibular and vocal cords divide the laryngeal cavity into 3 parts:
VESTIBULE - this region lies between the laryngeal inlet and vestibular folds.
*VENTRICLE (SINUS OF THE LARYNX) - this deep elliptical space lies between the
vestibular and vocal folds.
*SUBGLOTTIC REGION (INFRAGLOTTIC LARYNX) - extends from below the vocal cords
to the lower border of the cricoid cartilage.
INLET OF THE LARYNX - during swallowing, the aryepiglottic folds, tubercle of the epiglottis
and arytenoids approximate and close the laryngeal inlet completely.
= LARYNGEAL SUSPENSION - the larynx is suspended in the anterior midline of the neck by
virtue of its elastic attachments to the hyoid bone.
*THYROID CARTILAGE - is suspended from the hyoid bone by means of the thyrohyoid
membrane anteriorly and the stylopharyngeus muscle posteriorly, arising on the styloid
process of the temporal bone and inserting on the posterior margin of the thyroid lamina.
*CRICOID CARTILAGE - is suspended from the thyroid cartilage by the articulating
cricothyroid joint, the cricothyroid ligament and membrane (anteriorly), and the conus
elasticus (cricovocal membrane). Inferior to the cricoid, the cricotracheal membrane
suspends the trachea from the larynx, forming a continuous elastic membrane that can
be traced to the two main bronchi and their successive divisions.
MUSCLE S OF THE LARYNX
*EXTRINSIC MUSCLES - are involved in the movement of the larynx as a whole. They
connect the larynx to the surrounding structures, the extrinsic muscles, the strap
muscles and constrictors, help with laryngeal elevation and pharyngeal constriction.
Origin is located outside the larynx and insertion is inside the larynx.
»INFRAHYOID GROUP (DEPRESSORS) (STRAP MUSCLES) - these muscles originate
from the hyoid bone superiorly and the sternum and scapula inferiorly. They are
antagonistic to the elastic suspensory ligaments and elevators of the larynx, and the
concerted action of all three groups determine the position of the larynx in the upper
aerodigestive tract. These muscles are innervated by means of the descendens
hypoglossi portion of the ansa hypoglossi, derived from C1-C3 roots.
=Sternothyroid =Sternohyoid sOmohyoid
™ SUPRAHYOID GROUP (ELEVATO RS) - these muscles are attached to the hyoid bone.
They comprise the musculature of the floor of the mouth.
- they are innervated by the ansa hypoglossi (C1 to C3) and the CN V, CN VII, and CN IX.
They are all elevators of the larynx relative to the base of the tongue. The thyrohyoid is
considered a strap muscle but functions mainly as an elevator. The digastric, geniohyoid,
and mylohyoid muscles form the floor of the mouth.
=PRIMARY ELEVATORS - are attached to the thyroid cartilage and include the vertical
pharyngeal muscles (stylopharyngeus, salpingopharyngeus, palatopharyngeus) and an
infrahyoid muscle (thyrohyoid).
"SECONDARY ELEVATORS - are attached to the hyoid bone and include the suprahyoid
muscles:
i. Digastric ii. Stylohyoid =x, iii. Geniohyoid
iv. Mylohyoid v. Genioglossus vi. Hyoglossus
™»PHARYNGEAL CONSTRICTORS - the inferior and middle pharyngeal constrictors, not
considered primarily laryngeal elevators, do secondarily perform this function by virtue
of their attachments to the greater cornua of the hyoid bone and the oblique line of the
thyroid cartilage and the cricothyroid muscle.

25
*INTRINSIC MUSCLES - are involved with vocal cord mobility.They connect the
laryngeal cartilages to each other. These muscles insert on the arytenoid cartilage and
can alter the position of the vocal cords.
- all of the intrinsic muscles cause the true vocal cords to move toward the midline
(adduct) except for one muscle, the cricoarytenoid muscle, which causes the vocal cords
to separate (abduct). Origin and insertion are located within the larynx.
- the motor innervation of all the intrinsic laryngeal muscles is through the terminal
branch of the recurrent laryngeal nerve, the inferior laryngeal nerve, except the
cricothyroid muscle which is innervated by the external branch of the superior laryngeal
nerve, which is also a branch of the vagus nerve and all are paired except for the
transverse arytenoid muscle (interarytenoid),.
»®» ADDUCTORS OF THE VOCAL CORDS - closing muscles or constrictors.
#LATERAL CRICOARYTENOID - most powerful adductor. It is a small muscle whose
fibers arise from the lateral and superior border of the arch of the cricoid cartilage
and pass obliquely posteriorly and superiorly to insert on the anterior surface of the
muscular process of the arytenoid. It rotates the arytenoid medially, causing adduction.
Contraction pulls the muscular process away from each other and brings the vocal
processes (and the vocal cords) together. Because this mechanism initiates speech
production, this muscle is also called the muscle of phonation.
=THYROARYTENOID (internal tensor) - together with the conus elasticus makes up the
bulk of the true vocal cords. It originates from the thyroid cartilage and inserts into the
muscular process of the arytenoids. It has the same action as the lateral cricoarytenoids.
It is a component of acommon muscular sheet that arises on the midline of the posterior
surface of the thyroid cartilage to the vocal processes of the arytenoid cartilage.
Contraction of the muscle decreases the thyroid-arytenoid distance and therefore
decreases vocal cord tension. It is considered a strong adductor of the vocal cords
because its action glides the arytenoid bodies and the vocal processes together in the
midline.
- while the cricothyroid contracts to lengthen the cords, the thyroarytenoid
simultaneously contracts to oppose lengthening so that the cords become tense.
- itis also an adductor. Its action is to increase the size of the laryngeal introitus by virtue
of its action on the free margin of the aryepiglottic fold.
=TRANSVERSE ARYTENOID - unites the 2 arytenoid cartilages. Contraction causes
similar action as the above and in addition causes the arytenoids to glide toward the
midline. It is the sole unpaired muscle in the larynx and receives bilateral innervation from
the recurrent laryngeal nerves and therefore is not paralyzed by unilateral recurrent
laryngeal nerve disease. It may also receive motor supply from the superior laryngeal
nerves. The fibers of this muscle have their origins and insertions on the muscular
processes and lateral border of the arytenoid cartilage bilaterally, spanning the
arytenoids. This muscle approximates the arytenoids, thus acting as a vocal cord
adductor.
"OBLIQUE ARYTENOID - paired, intertwines with fibers of the transverse arytenoid
muscle. Together with the transverse arytenoid, the group is called interarytenoid
muscle. They arise from the posterior surface of each arytenoid and pass obliquely
across the midline to insert on the apical region of the opposite arytenoid, forming an X.
Superiorly, some of the fibers of this muscle continue laterally into the aryepiglottic fold
to constitute the bilaterally paired aryepiglottic muscle.
- this muscle provides a sphincteric action for the aryepiglottic folds and the laryngeal
aditus by adducting the cords and approximating the arytenoids to the tubercle of the
epiglottis.

26
™ ABDUCTOR OF THE VOCAL CORDS - POSTERIOR CRICOARYTENOID - opens up
the larynx. It is the most powerful of all laryngeal intrinsic muscles. It originates from the
posterior surface of cricoid lamina and inserts into the muscular process of arytenoid.
It is the most important respiratory muscle of the larynx; the only muscle that opens the
glottis. It is the sole abductor of the vocal cords. On contraction, it pulls the arytenoid
muscular processes together and brings the vocal processes and the vocal cords apart
(rotates arytenoid cartilage laterally). It rotates the arytenoid outward, abducting the vocal
cord.
- this muscle is secondarily important during phonation, where it serves as an antagonist
to the thyroarytenoid in stabilizing the vocal process of the arytenoid cartilage thus
contributing to vocal cord tension.
MAIN ANTAGONIST - lateral cricoarytenoid
®TENSORS OF THE VOCAL CORDS
#CRICOTHYROID (external tensor) - fan-shaped; originates from the anterior surface of
the cricoid arch and inserts laterally on the thyroid alae. It is the only laryngeal muscle
that attaches to the external surface of the larynx. On contraction, it pulls the thyroid
cartilage downward and forward, thereby stretching the cord.
- it also be considered both an intrinsic and extrinsic muscle of the larynx.
i. EXTRINSIC - in the sense that it acts to change the distance between 2 laryngeal
cartilages - - the thyroid and the cricoid.
ii. INTRINSIC - in the sense that it affects vocal cord tension. It is the only muscle
innervated by the external branch of the superior laryngeal nerve.
2 MUSCLE HEADS
i. PARS RECTA - which arises on the lateral thyroid lamina and inserts on the anterior
arch of the cricoid cartilage. Its fibers are positioned to close the visor angle.
ii. PARS OBLIQUA - follows a more horizontal course from the anterior surface of the
inferior horn of the thyroid to the anterior arch of the cricoid cartilage.
- its fibers are positioned to subluxate or rock the cricothyroid joint. This muscle plays
an important role in phonation and in increasing vocal cord tension at the extreme range
of pitch.
- it functions synergistically with the posterior cricoarytenoid muscle in producing vocal
fold tension. Contraction of the cricothyroid muscle draws the anterior arch of the cricoid
superiorly toward the inferior margin of the thyroid cartilage and results in vocal cord
tension only if the posterior cricoarytenoid muscle is intact and contracting to stabilize
the arytenoid cartilages relative to the cricoid cartilages.
- thus, unilateral posterior cricoarytenoid muscle paralysis imparts a rotatory motion to
the posterior commissure toward the side of the paralysis at high pitch, because of the
contraction of the intact contralateral posterior cricoarytenoid muscle.
BTHYROARYTENOID (internal tensor) - while the cricothyroid contracts to lengthen
cords, the thyroarytenoid simultaneously contracts to oppose lengthening so that the
cords become tense. It is also an adductor.
- it is a component of a common muscular sheet that arises on the midline of the posterior
surface of the thyroid cartilage to the vocal processes of the arytenoid cartilage. Together
with the conus elasticus, it makes up the bulk of the true vocal cords. It has the same
action as the lateral cricoarytenoids. Contraction of the muscle decreases the thyroid-
arytenoid distance and therefore decreases:vocal cord tension.
- it is considered a strong adductor of the vocal cords because its action glides the
arytenoid bodies and vocal processes together in the midline. Its action is to increase the
size of the laryngeal introitus by virtue of its action on the free margin of the aryepiglottic
fold.

27
#VOCALIS (internal tensor) - most medial and superior fibers of thyroarytenoid.
- in older individuals, the vocalis and thyroarytenoid muscles may lose some tone; the
cord becomes bowed outwards and the voice becomes weak and hoarse.
= INNERVATION - all of the larynx is innervated by branches of the vagus nerve (CN X) on
each side. The motor neurons arise from the nucleus ambiguous of the medulla. The
vagus nerve exits through the jugular foramen and then travels within the carotid sheath
in the neck. Two pairs of nerves supply the larynx with both sensory and motor
innervation.
*SUPERIOR LARYNGEAL NERVE - leaves the vagal trunk just below the nodose ganglion,
curves anteriorly and medially beneath the internal and external carotid arteries and
divides before reaching the thyrohyoid membrane into 2 branches:
® INTERNAL LARYNGEAL NERVE - pierces the thyrohyoid membrane along with the
superior laryngeal vessels and supplies sensory innervation to the mucosa of the
supraglotic larynx and hypopharynx.
- it provides the sensory innervation for the vallecula, epiglottis, pyriform sinus, and all
the internal laryngeal mucosa superior to the free margin of the true cords. It is sensory
to the larynx.
»EXTERNAL LARYNGEAL NERVE - travels in relation with the superior thyroid artery
and supplies the cricothyroid muscle. The cricothyroid is the only intrinsic laryngeal
muscle that is innervated by the superior laryngeal nerve and not by the recurrent
laryngeal nerve. Each external branch is the motor supply for just one muscle, the
cricothyroid.
- the superior laryngeal nerve branches form the nodose ganglion soon after the vagus
nerve exits the skull base through the jugular foramen. It is the motor supply of the
cricothyroid. It may or may not send additional motor fibers to arytenoid group.
*RECURRENT LARYNGEAL NERVE (RLN) (INFERIOR LARYNGEAL NERVE) - supplies
motor function and sensation to the larynx. It is called the “recurrent” laryngeal nerve
because the branches of the nerve descend into the thorax before rising up between the
trachea and esophagus to reach the neck.
- it ascends in a groove between the trachea and esophagus, enters the larynx just behind
the cricothyroid articulation, and provides the motor supply to all the intrinsic laryngeal
muscles except the cricothyroid. It is sensory to the undersurface of the true cords (the
subglottic region) and the superior trachea.
- the inferior laryngeal nerves loop around respective associated arteries, travel through
the tracheo-esophageal groove, and enter the larynx just behind the cricothyroid
articulation.
®RIGHT RECURRENT LARYNGEAL NERVE - hooks around the subclavian artery or
aorta. It arises from the vagus at the level of the subclavian artery and loops around the
subclavian artery and then ascends in the tracheoesophageal gutter. It does not have an
intrathoracic course.
»LEFT RECURRENT LARYNGEAL NERVE - loops under the arch of the aorta. It has an
intrathoracic course and arises from the vagus in the mediastinum at the level of the arch
of the aorta.
- it loops around the aortic arch and ascends into the neck in the tracheoesophageal
gutter. 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.
MOTOR SUPPLY - all the intrinsic muscles of the larynx are supplied by the recurrent
laryngeal nerve except the cricothyroid muscle, which is supplied by the external
laryngeal nerve, a branch of the superior laryngeal nerve. Both recurrent and superior

28
laryngeal nerves are the branches of the vagus nerve (CN X), which carry the fibers of
the cranial part of the accessory nerve (CN XI).
SENSORY SUPPLY - the larynx above the vocal cords is supplied by the internal laryngeal
nerve (branch of the superior laryngeal). The larynx below the vocal cords Is supplied by
the internal branch of the recurrent laryngeal nerve.
= ARTERIAL SUPPLY - is from branches of the superior and inferior thyroid arteries.
*SUPRAGLOTTIC AREA
»®» SUPERIOR LARYNGEAL ARTERY -a branch of the superior thyroid artery which is the
first branch of the external carotid artery. It pierces the thyrohyoid membrane, along with
the superior laryngeal vein, nerve, and lymphatics.
- occasionally a small branch of the ascending portion of the superior thyroid artery, the
cricothyroid artery, pierces the cricothyroid membrane singularly or in multiple
perforators to anastomose with the superior laryngeal artery.
SUPERIOR THYROID ARTERY - arises from the external carotid artery as the first branch,
although it sometimes has its origin from the carotid bifurcation or the common carotid
artery. It courses superoanteriorly to send off a small infrahyoid artery near the greater
cornu of the hyoid bone.
- it continues inferiorly and branches in the vicinity of the superior cornu of the thyroid
cartilage to give off a superior laryngeal branch and continues along the inferior
constrictors to terminate on the superior lobe of the thyroid gland and anterior surface
of the sternocleidomastoid.
CRICOTHYROID ARTERY - passes inferiorly in association with the external branch of the
superior laryngeal nerve.
™»LINGUAL ARTERY - second branch of the external carotid artery
*INFRAGLOTTIC AREA - supplied by inferior laryngeal artery which is a branch of the
inferior thyroid artery.
INFERIOR THYROID ARTERY - a branch of the thyrocervical trunk, ascends in the tracheo-
esophageal groove accompanied by the recurrent laryngeal nerve. It gives rise to the
inferior laryngeal artery as it is crossing the recurrent laryngeal nerve.
- in concert with the recurrent nerve, the inferior laryngeal artery enters the larynx below
the inferior margin of the inferior constrictor muscle.
VENOUS SYSTEM - the venous return from the larynx is carried by the superior laryngeal
vein and the superior and middle thyroid veins, all of which enter the internal jugular vein.
= LYMPHATIC DRAINAGE - with the exception of the vocal cords, the larynx is richly supplied
with lymphatic drainage; particularly the supraglottic larynx. The cords themselves have
a poor lymphatic supply. There are 2 separate drainage systems, superior and inferior,
with the dividing line being the true vocal cord. There is a lack of communication between
the laryngeal lymph nodes and the mediastinal lymph nodes sequestering laryngeal
metastases to the neck for extended periods. Laryngeal lymphatics drain in to the
infrahyoid, superior deep cervical, prelaryngeal, pretracheal, and paratracheal lymph
nodes.
*GLOTTIC AREA - practically devoid of lymphatics; tumors originating in this area remain
localized for long periods.
*SUPRAGLOTTIC AREA - the lymphatics drain into the upper deep cervical nodes
through the thyrohyoid membrane. They largely follow the superior laryngeal artery after
collecting at the anterior portion of the aryepiglottic fold and passing along the pyriform
sinus to exit the larynx through the superior neurovascular bundle, piercing the
thyrohyoid membrane. They then communicate to some degree with the pharyngeal
lymphatics and drain to the first-echelon lymph nodes in the superior and middle jugular
groups

29
*INFRAGLOTTIC AREA - the subglottic drainage is more diverse, going to the
pretracheal nodes, the lower deep cervical nodes, the supraclavicular node, and even the
superior mediastinal nodes. They drain into the prelaryngeal (Delphian node) and
pretracheal nodes (through the cricothyroid membrane) and then to the lower deep
cervical and mediastinal nodes. Some lymphatics pierce the cricotracheal membrane
and drain into the lower deep cervical nodes.
- infraglottic lymph channels have a greater potential for contralateral spread because of
the crossing of the lymphatic channels in the area of the cricoid cartilage and the
cricothyroid membrane.
» ANTERIOR LYMPHATIC TRUNK - Delphian or pretracheal node - Supraclavicular nodes
»POSTEROLATERAL LYMPHATIC TRUNKS - Paratracheal nodes - Superior mediastinal
nodes
- laryngeal tumors drain to ipsilateral groups of lymph nodes and the group of lymph
nodes may be determined by the position of the primary tumor in the supraglottic and
infraglottic larynx.
JOINTS
*CRICOTHYROID JOINTS - are small synovial joints between the inferior cornua of
the thyroid cartilage and the posterior portions of the cricoid cartilage. Each cricoid joint
surface is a slightly raised area with a small central depression which fits the slightly
convex surface of the thyroid portion of the joint. Each joint is supported by 3 ligaments
- anterior, inferior and posterior cricothyroid ligaments. Joint motion is a rotatory motion
in the sagittal plane only. The joint is the fulcrum on which the cricothyroid muscle
functions. Therefore, destruction or fixation of the joint will lessen the effect of the
cricothyroid muscle on the tension of the vocal cords.
*CRICOARYTENOID JOINT - each arytenoid cartilage articulates with an elliptical facet
on the posterosuperior margin of the cricoid lamina. The articulating facet of the
arytenoid is saddle-shaped and positioned at right angles to the cricoid facet.
- the joint is supported by a joint capsule lined by synovium and the capsule is
strengthened posteriorly by a strong cricoarytenoid ligament.
- the joint structure permits 2 types of movement
™»ROTATORY MOVEMENT - occurs at a vertical axis and abducts or adducts the vocal
cord
»GLIDING MOVEMENT - the arytenoids glide laterally and medially and help in closing
or opening the posterior part of the glottis.
= INTERIOR OF THE LARYNX
*EPIGLOTTIS - is the first structure noted on mirror examination. from which 3 mucosal
bands extend to the tongue - 1 median and 2 lateral glossoepiglottic folds.
- these produce 2 valleculae on either side. The inferior 2/3 of the epiglottis separates the
vestibule from the pre-epiglottic space.
*VALLECULA - is a small pocket between the median and each lateral band. 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 pyriform sinus between the
aryepiglottic folds and the thyroid cartilage.
ePYRIFORM SINUSES - are the lateral pharyngeal recesses on each side of the larynx.
They are the primary route for food passage into the cervical esophagus. More inferiorly
are the muscles of the cricoid lamina, and below this the opening of the esophagus.
MEDIAL WALL - is the quadrangular cartilage above and the arytenoid with its attached
lateral musculature below.
™»LATERAL WALL - is the internal surface of the thyroid ala.
POSTERIORLY - the pyriform sinus is continuous with the hypopharynx.

. ; 30
-the pyriform sinuses and pharynx converge inferiorly into the esophageal introitus,
which is encompassed by the strong cricopharyngeal muscle.
ARCO TIC FOLD - is a fold of mucosa connecting the epiglottis with the arytenoid
cartilages.
*ARYTENOIDS - can be seen below the free margin of the epiglottis, appearing as 2 small
mounds connected by the thin interarytenoid muscle. It is pyramidal in shape.
®BASE- articulates with the cricoid cartilage
* MUSCULAR PROCESS - this lateral process provides attachment to the intrinsic
laryngeal muscles.
»VOCAL PROCESS - this anterior process provides attachment to the vocal ligament or
the vocal cord.
» APEX - superiorly, it supports the corniculate cartilage in the aryepiglottic fold.
- within the larynx itself, 2 pairs of horizontal bands arise from the arytenoids and insert
into the center of the thyroid cartilage anteriorly. The superior bands are the false
cords or ventricular bands, and they are lateral to the true cords.
™ TRUE VOCAL CORDS (VOCAL FOLDS) - these pearly-white sharp bands, one on each
side, extend between the middle of the thyroid angle and vocal processes of the
arytenoids.The vocal cord consists of a ligament (upper edge of the cricovocal
membrane), which is covered with mucous membrane that has scanty subepithelal
connective tissue.
- it extends from the floor of the ventricle of Morgagni inferiorly to the cricoid cartilage, a
distance of 1.5 to 2 cm, although the bulk of the cord is above the inferior margin of the
thyroid cartilage. Because the superior surface of the vocal cord is flat, the mucosa
reflects light and appears white on indirect laryngoscopy. The true vocal cords are a
maximum 2.4 cm in length in the adult male and 1.7 cm in length in the adult female. The
true vocal cords are formed by a membranous anterior 2/3 and a cartilaginous posterior
1/3.
=MEMBRANOUS PORTION - is formed by the conus elasticus and the laterally placed
thyroarytenoid muscles. The vocal ligaments are merely the thickened superior margins
of the conus elasticus.
i. ANTERIORLY - the membranous cords meet to form a V-shaped commissure and
are attached to the thyroid cartilage by the vocal tendon of Broyle’s.
ii. POSTERI ORLY - the membranous cords are attached to the vocal
processes.
=CARTILAGINOUS PORTION - is formed by the vocal processes and the inferior body of
the arytenoid. The vocal cords are separated by a variable possible
cartilaginous
commissure.
» VESTIBULAR FOLDS (FALSE VOCAL CORDS) - these folds of mucous membrane, one
on each side, contain the vestibular ligament, fibers of the thyroarytenoid muscle and
mucous glands. They are situated anteroposteriorly across the laryngeal cavity.
- they are another set of vocal cords immediately superior to the ventricle which are
more round, blunted protrusions located on a plane superior to the true vocal cords.
They contain minimal musculature but are rich in glandular structures. The false cords
are formed by the inferior free margin of the quadrangular membrane. They are fleshy
masses which are attached anteriorly to the epiglottis near the petiole and posteriorly,
they blend into the mucosa over the arytendids.
eCONUS ELASTICUS - is a tough, fibrous band extending from the vocal ligament to the
inferior border of the cricoid cartilage.
*LARYNGEAL VENTRICLE (VENTRICLE OF MORGAGNI) - is a laterally directed sulcus
separating the true and false vocal cords. The structure is approximately 2 cm long in the

31
adult male. It extends laterally almost to the thyroid ala from which it is separated
by mucosa and muscle fibers. The floor is formed by the flat superior surface of the true
vocal cord. As the ventricle extends laterally, it also extends vertically lateral to the
quadrangular membrane.
- near the anterior end of the roof of the ventricle is an opening to a vertical extension,
the laryngeal saccule (sacculus or appendix), which extends further into the aryepiglottic
fold. It harbors the mucous glands thought to lubricate the cords.
*SACCULE - this diverticulum of mucous membrane starts from the the anterior part of
the ventricle and extends superiorly between the vestibular folds and thyroid lamina. The
secretions of mucous glands in the saccule provide lubrication for the vocal cords.
*PYRIFORM FOSSA - are usually considered part of the hypopharynx for clinical
purposes, but they are also an anatomic part of the larynx. Each fossa lies lateral to the
vestibule of the larynx. It lies between the thyrohyoid membrane and the thyroid ala
laterally and aryepiglottic fold, arytenoid and superior cricoid cartilage medially.
®» SUPERIOR BOUNDARY -is marked by the lateral glossoepiglottic fold.
»® INFERIOR BOUNDARY - is less well defined because of the manner in which the fossa
blends into the upper esophagus.
™APEX - is usually at the level of the upper level of the cricoid although there is
considerable individual variation.
POSTERIOR BOUNDARY - is marked medially by the arytenoid cartilage and laterally
by a line drawn parallel to the vocal cord in the abducted position and projected to
the lateral pharyngeal wall.
*VESTIBULE - is that part above the vocal cords.
®LATERALLY -the aryepiglottic folds separate the laryngeal vestibule from the pyriform
fossae.
®POSTERIORLY - the arytenoid cartilages and the interarytenoid muscle form the
partition between the vestibule and hypopharynx.
*SUPRAGLOTTTIS - is the area superior to the inferior margins of the false vocal cords.
» ANTERIOR WALL - is formed by the epiglottis which tapers inferiorly.
=» LOWER END - is marked by a prominence, the tuberculum impar epiglotticum, which is
about 1 to 1.5 cm superior to the anterior commissure.
*GLOTTIS (RIMA GLOTTIDIS) - this narrowest part of an adult laryngeal cavity lies
between the vocal cords and arytenoids of the two sides. The size and shape of the glottis
varies with the activities of the vocal cords. The anterior 2/3 of the glottis is formed by
the membranous vocal cords while the posterior 1/3 by the vocal processes of the
arytenoids. The anteroposterior length of the glottis is more in men (24 mm) than in
women (16 mm).
*INFRAGLOTTIS - is the area below the glottis. This division is made because of the
different lymphatic supply of the 2 areas.
= BOUNDARIES
eSUPERIOR BOUNDARY OF THE LARYNX
Free edge of the epiglottis » Aryepiglottic folds
™ Corniculate cartilages ® Superior margin of the interarytenoid area
*INFERIOR BOUNDARY - is the inferior border of the cricoid cartilage
- HISTOLOGY sn
*CILIATED PSEUDOSTRATIFIED COLUMNAR EPITHELIUM - covers the laryngeal
musculature and cartilage.
»Ventricles »Infraglottic area
Inferior portions of the false vocal cords

32
FREE EDGE OF THE TRUE VOCAL CORDS - is covered by stratified epithelium, 8-10 cells
layers thick, although this epithelium tends to be thinner over the vocal processes.
*NONKERATINIZING SQUAMOUS EPITHELIUM - these areas usually represent the points
of the larynx that have frequent physical contact with either food particles or another
portion of the larynx.
»Tip of the epiglottis » Aryepiglottic folds » Pyriform fossae
- the anatomy of the vibratory margin includes not only the epithelium but also 3 layers
of lamina propia and the intrinsic laryngeal muscle.
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34
SURFACE ANATOMY LANDMARKS - are important for neck examination as well as for
planning the surgical incision.
*MASTOID - provides insertion to the sternocleidomastoid (SCM). The parotid gland is
present between the mastoid and angle and ramus of the mandible.
*MANDIBLE - the submandibular gland can be palpated just below the ramus of the
mandible.
*HYOID - the swellings of the thyroglossal cyst and subhyoid bursitis are seen close to
the hyoid and move up on protruding out the tongue.
*THYROID CARTILAGE - Adam's apple is more prominent in males than females.
*CRICOID CARTILAGE - lies at the level of the 6'" cervical vertebra and forms the lower
limit of the larynx and laryngopharynx.
* TRACHEA - the cervical trachea can be shifted to either side due to thyroid and superior
mediastinal tumors.
*THYROID GLAND - the thyroid isthmus can be palpated below the cricoid cartilage over
the 2"* to 4" tracheal rings. The normal thyroid lobules lie deep to the SCM and are not
palpable.
*STERNOCLEIDOMASTOID MUSCLE - divides the anterolateral quadrangular part of the
neck into anterior and posterior triangles.
*TRAPEZIUS MUSCLE - this large muscle makes the posterior boundary of the posterior
triangle and elevates the shoulder.
*CAROTID ARTERIES - the common carotid artery (CCA) is best palpated at the level of
the greater cornu of the hyoid bone in the carotid triangle where it bifurcates into the
internal (ICA) and external carotid arteries (ECA).
eINTERNAL JUGULAR VEIN - extends from the lobule of the ear to the medial end of the
clavicle deep to the SCM in the carotid sheath.
*CHASSAIGNAC’S TRIANGLE - is formed by the longus colli, scalenus anterior and
subclavian artery.
TRIANGLES OF THE NECK - the SCM divides the anterolateral quandrangular part of the
neck into the anterior and posterior triangles. The digastric and omohyoid muscles divide
these triangles into further sub-triangles.
eANTERIOR TRIANGLE - is bound by the SCM, inferior border of the mandible and
cervical midline. The anterior and posterior bellies of the digastric and superior belly of
the omohyoid divide the anterior triangle into 4 triangles.
» SUBMENTAL - contains lymph nodes.
™ SUBMANDIBULAR - contains submandibular salivary gland, lymph nodes, facial
vessels, and marginal branch of the facial nerve.
™ CAROTID - contains the carotid sheath and bifurcation of the CCA and lymph nodes.
™» MUSCULAR - contains the infrahyoid strap muscles and structures that lie deep to them
in the central compartment like the thyroid and parathyroids, larynx and trachea,
laryngopharynx and cervical esophagus and carotid sheath.
*POSTERIOR TRIANGLE - is bounded by the SCM, clavicle and anterior border of the
trapezius. The inferior belly of the omohyoid divides the posterior triangle into 2 triangles.
* OCCIPITAL - contains the accessory nerve, lymph nodes, fibrofatty tissue and nerves
of the cervical plexus. =
®SUPRACLAVICULAR - contains fibrofatty tissue, brachial plexus, subclavian vessels,
thyrocervical trunk, Sibson’s subpleural fascia and cervical pleura.
LYMPH NODES OF THE HEAD AND NECK
*SUBMENTAL NODES - 2 to 9 in number, lie in the mylohyoid muscle in the submental
triangle.
eSUBMANDIBULAR NODES - lie in the submandibular triangle.

35
*PAROTID NODES - lie in relation to the parotid gland.
*POST-AURICULAR NODES (MASTOID NODES) - lie behind the auricle.
OCCIPITAL NODES - at the apex of the posterior triangle are situated both superficial
and deep into the splenius capitus muscle.
*FACIAL NODES - lie along the facial vessels.
*MALAR NODES - lie near the outer canthus.
*SUPERFICIAL GROUP OF LATERAL CERVICAL NODES - lies along the external jugular
vein.
*DEEP GROUP - which consists of 3 chains: internal jugular, spinal accessory and
transverse, lie deep to the SCM and in the posterior triangle.
®INTERNAL JUGULAR CHAIN
#Upper group(Jugulodigastric node) =Middle group =Lower group
™®SPINAL ACCESSORY CHAIN
™TRANSVERSE CERVICAL CHAIN (SUPRACLAVICULAR NODES)
SCALENE NODES - medial group of supraclavicular nodes.
*ANTERIOR CERVICAL NODES - which lie between the 2 carotids and below the level of
the hyoid bone.
» ANTERIOR JUGULAR CHAIN
=» JUXTAVISCERAL CHAIN
=Prelaryngeal node (Delphian node) =Pretracheal nodes =Paratracheal nodes
*LYMPH NODES NOT PALPABLE CLINICALLY
™»RETROPHARYNGEAL NODES
=Lateral group =Medial group
» SUBLINGUAL NODES
LEVELS OF CERVICAL LYMPH NODES - the cervical lymph nodes are divided into different
levels, which is very important in cases of head and neck malignancies.
*LEVEL | - SUBMENTAL NODES AND SUBMANDIBULAR NODES
™LEVEL IA - submental nodes
™LEVEL IB - submandibular nodes
eLEVEL Il - UPPER JUGULAR (between skull base and hyoid bone)
™LEVEL IIA - inferomedial to accessory nerve
LEVEL IIB - superolateral to accessory nerve
eLEVEL III - MIDDLE JUGULAR (between hyoid bone and upper border of cricoid cartilage)
LEVEL IV - LOWER JUGULAR (between upper border of cricoid cartilage and clavicle)
eLEVEL V - posterior triangle group subdivided into upper, middle and lower,
corresponding to planes of levels Il, Ill and IV.
LEVEL VA - spinal accessory nodes above the level of the cricoid cartilage
LEVEL VB - transverse cervical chains and supraclavicular nodes below the level of the
cricoid cartilage.
*LEVEL VI - anterior compartment nodes: prelaryngeal (precricoid or delphian),
perithyroidal, pretracheal, paratracheal)
LEVEL VII - superior mediastinal nodes

36
= CERVICAL F**ASCIA
*SUPERFICIAL CERVICAL FASCIA - the thin cervicocephalic superficial fascia lies
immediately beneath the skin and invests platysma and muscles of facial expression.
- the space between the superficial fascia and investing layer of deep cervical fascia
contain the following structures.
» ADIPOSE TISSUE
» SENSORY NERVES
™» SUPERFICIAL LYMPHATICS
»® VESSELS: EXTERNAL AND ANTERIOR JUGULAR VEINS
*DEEP CERVICAL FASCIA - has 3 layers and at certain places these layers coalesce and
cannot be separated from each other.
» SUPERFICIAL INVESTING LAYER
*» MIDDLE VISCERAL (PRETRACHEAL) LAYER
» DEEP PREVERTEBRAL LAYER
CAROTID SHEATH - all the 3 layers contribute in its formation.

PHYSIOLOGY OF THE
PHARYNX AND LARYNX
I. FUNCTIONS OF THE NASOPHARYRX
*RESPIRATION - its chief function is to serve as a rigid open tube for the respired air
on its way to the larynx and trachea. The nasopharynx is completely separated from the
oropharynx by elevation of the palate against the posterior wall of the oropharynx during
®»Swallowing »Vomiting
»Belching ™» Gagging
eVENTILATION
Channel for ventilation and equalization of air pressure on both sides of the TM
Channel for drainage from the nose and paranasal sinuses.
*VOICE RESONANCE - it is part of the resonating chamber for voice production.
*DRAINAGE - it is a drainage channel for nasal and nasopharyngeal mucus secretions.
NASOPHARYNGEAL ISTHMUS - cuts off the nasopharynx from the oropharynx during
swallowing, vomiting, gagging and speech.
FUNCTIONS OF TONSILS AND ADENOIDS
eIMMUNOLOGY AND HOST DEFENSES - T-lymphocytes in the parafollicular region
provide cell-mediated immunity against various viruses, bacteria and fungi. Once the
pathogens enter into the lymphoid aggregations, they are dealt with by IgM and IgG
antibodies, which are produced by plasma cells.
*SENTINELS AT THE PORTAL OF THE AERODIGESTIVE TRACT - oropharyngeal
subepithelial masses of lymphoid tissues, which form part of Waldeyer’s ring, act as
protective sentinels against harmful intruders into the air and food passages. The crypts
in the tonsils increase the surface area for contact with foreign substances.
eANTIBODY PRODUCTION - especially secretory IgA; B lymphocytes in the germinal
centers of these lymphoid follicles produce antibodies IgA.
Il. FUNCTIONS OF THE ORAL CAVITY AND OROPHARYNX

FOOD INGESTION - the lips are the entrance of the aerodigestive tract and help to close
the mouth during chewing, so that the food stays in the oral cavity.
eMASTICATION - masticatory movements comprise exceedingly complex and
coordinated neuromuscular events. They include not only mandibular elevation and
depression but also opposing tooth alignment and accurate regulation of masticatory
forces. Mastication is characterized not only by simple straight opening and closing of
the jaw but also retrusive, protrusive and lateral jaw movements. The process involves:
BITING - the strength of closing the mandible with biting can be rather substantial,
being measured at more than 200 pounds per square inch. A maximum force of about 150
kg can be developed between the molar teeth of a dentate patient. The maximum force
occurs between the first molars, and falls off by about 10 kg in the incisor region. During
normal function, a force of 7-15 kg occurs during swallowing and chewing.
7 MONTHS OF AGE - the act of biting is first developed.
™ CHEWING - the teeth are important during chewing, especially the molars, with a high
molar occlusal force.
- itis a series of forward, backward, and/or lateral rhythmic motions of the mandible. The
tongue and cheek muscles keep the food between the biting surfaces of the teeth.

2
CHEWING CYCLE - bilateral chewing is far less common than unilateral chewing since one
side of the jaw is usually favored in mastication. Each chewing cycle lasts approximately
0.8-1.0 second.
=OPENING PHASE - during which there may be some lateral deviation. The opening
movement appears to be only just sufficient for the teeth to clear the bolus; tooth contact
with the bolus occurs soon after the beginning of the closing phase.
=CLOSING PHASE - which begins with a lateral component towards the working side.
There is also a lateral component back towards the centric occlusion in the final closing
phase, which is often guided by gliding tooth contacts. The temporalis muscle on the
working side is the first to become active, followed by both masseters and the temporalis
of the non-working side.
- during both the opening and beginning of the closing phases, the masticatory muscles
undergo isotonic contraction or relaxation.
BOCCLUSAL PHASE
10 -12 MONTHS OF AGE - chewing develops.
BITING AND CHEWING ARE FUNCTIONS OF THE
=Proprioceptive nerve endings from the muscles of mastication
=Mandibular movement
"Oral sensory receptors of the trigeminal nuclei
I. PHYSIOLOGY OF DEGLUTITION OR SWALLOWING

- swallowing involves a series of activities that occur within a matter of seconds.
Traditionally described as a reflex, the process is more properly regarded as a
programmed motor behavior. Swallowing is initiated when food or liquid stimulates
sensory nerves in the oropharynx. In a 24-hour period, an average person will swallow
between 600 and 1000 times but, of these, only some 150 will relate to feeding; the
remainder occur to clear continuously produced saliva and are less frequent at night.
DEGLUTITION OR SWALLOWING - is a very complex muscular action that involves several
activities all at the same time. In order for swallowing to work properly, these functions
need to work in a systematic order, without fail.
- the passage of the bolus from the mouth to the esophagus requires the interaction of
both the respiratory and digestive tracts, with swallowing providing for the propulsion of
the food from the oral cavity into the stomach, as well as providing a protective reflex for
the digestive and upper respiratory tracts.
As a protective reflex, deglutition has been evoked to assist in:
=» Removal of aspirated particles that have entered the larynx and lower respiratory tract
to be propelled by a cough, or other clearing gesture, back into the pharynx.
Removal of particles originally trapped in the nasopharynx.
Returning material influxed from the stomach into the esophagus and pharynx.
- it is elicited by the stimulation of either the superior laryngeal or glossopharyngeal
nerves. Swallowing in the human can be initiated voluntarily, but it is necessary to have
the capacity to develop a bolus. Voluntary “dry swallows” cannot be performed in
succession in the humans. After deglutition is initiated, it becomes a reflex-elicited event
that cannot be modified by any sensory input.
- swallowing occupies a dominant position over respiration in the arrangement
of pharyngeal function in the brainstem so that the initiation of the swallowing act results
in an inhibition of respiration.

® ACTIVE PHASES
#ORAL PREPARATORY PHASE OR MASTICATOR PHASE - begins with salivation at the
sight and smell of food, continuing when a food bolus is placed into the oral cavity. The
salivary glands produce 1,500 ml of saliva each day. Saliva is composed of 99% water
and 1% enzymes, proteins and salts. Salivary flow is critical for effective swallowing
function. The pH of saliva is 6.2-7.4.
LIQUIDS - are taken into the mouth and held there either on the floor of the mouth or
against the hard palate by the upward movement of the tongue. During swallowing, the
muscles that dilate the pharyngotympanic tube are activated during a pause in respiration
in the expiratory phase. Throughout this first phase, the soft palate is fully lowered by
contraction of palatoglossus and palatopharyngeus muscles. The posterior part of the
tongue is simultaneously elevated; the apposed soft palate and tongue form a tight seal
that helps to prevent premature leakage of the bolus into the oropharynx before the
airways are fully protected. Slight leakage of fluid does sometimes occur; the tendency
for there to be leakage because of imperfect sealing increases with age.
SOLIDS - when solid food is swallowed, the process is slightly different from that just
described for swallowing liquids. Food is mixed with saliva and reduced to smaller pieces
by the processes of chewing.
ORAL TRANSIT/TRANSFER PHASE - is under voluntary neuromuscular control. There
is the voluntary transfer of material from the mouth to the pharynx. it consists of chewing
as well as propulsion of the food bolus posteriorly into the pharynx
LIQUIDS - the liquid in the oral cavity is transported through the palatoglossal and
palatopharyngeal arches into the oropharynx. Genioglossus raises both the tongue tip
and the part of the tongue immediately behind the tip so that they come into contact with
the alveolar ridge. Orbicularis oris and buccinator remain contracted, keeping the lips
and cheeks taut and the liquid central in the oral cavity. The liquid is accommodated in a
shallow midline gutter that forms along the dorsum of the tongue, probably as a result of
the co-contraction of the styloglossi and the genioglossi, aided by the superior
longitudinal and transverse fibers of the intrinsic muscles. The mandible is elevated and
the mouth is closed. The floor of the mouth and the anterior and middle portions of the
tongue are elevated by co-contraction of the suprahyoid group of muscles (mylohyoid,
digastric, geniohyoid and stylohyoid); the effectiveness of the suprahyoid muscles is
increased as they contract against a fixed mandible (the mouth does not have to be
closed to swallow, but it is much harder to swallow if it is open). Contraction of stylohyoid
elevates the more posterior parts of the tongue and empties the longitudinal gutter. At
the same time, the tongue flattens. The elevated, flattened tongue pushes the liquid
against the hard palate, and the sides of the tongue seal against the maxillary alveolar
processes, helping to move the liquid further posteriorly. At the same time, the posterior
oral seal relaxes and the posterior tongue moves forwards;, sweeping or squeezing the
liquid towards the pillars of the fauces, finally delivering it to the oropharynx and initiating
the pharyngeal stage of swallowing, where the pharyngeal aperture is initially increased
and then closed.
SOLDS - when the food has been converted to a suitable consistency to be swallowed, it
is transferred to the oropharynx and valleculae, where it can be retained for a few seconds
prior to swallowing.
- the tongue helps during chewing to chop up the food bolus by various changes of its
shape and pressing the bolus against the teeth and hard palate. The bolus is mixed with
saliva. Chewing food and mixing it with saliva prepares the bolus for swallowing.

4
- the bolus is progressively augmented in one or more stages until a swallow is initiated
and the pharyngeal phase begins. In this part of the ‘oral phase for solid food’, the
essential action is chewing; the mandible is moved by the action of the jaw elevators and
depressors and the food is reduced by the grinding action of the teeth and simultaneously
mixed with saliva. The lips are maintained as a tight labial seal by the contraction of
orbicularis oris; buccinator performs a similar function for the cheeks. In this way, the
sulci are closed, the vestibule normally remains empty, and any food that enters the
vestibule is returned to the oral cavity proper. Buccinator keeps the cheeks taut, ensuring
that they are kept clear of the occlusal surfaces and that the food remains in place under
the occlusal surfaces of the molar teeth.
- it was thought that the soft palate was depressed throughout this phase. It is now
recognized that the posterior seal is not tight, and that the oral cavity and oropharynx
remain in communication, permitting addition of material to the bolus while chewing
continues. Spillage occurs because the soft palate is not in continuous contact with the
posterior part of the tongue, as was once thought,
- bolus formation appears to involve several cycles of transporting food from the anterior
to the posterior part of the tongue through the palatoglossal and palatopharyngeal arches
until a bolus accumulates on the oropharyngeal surface of the tongue (retrolingual
loading), the valleculae and within the oropharynx. Throughout this phase, the lateral and
rotatory tongue movements that deliver the food to the teeth for grinding and reduction
are crucial for normal bolus formation because they ensure that the food is positioned
under the occlusal surfaces of the teeth. If effective tongue movements do not occur,
chewing will be compromised. Movements of the tongue are also cyclical in phase with
the movements of the jaw and hyoid bone. As the jaw is depressed, the tongue is also
depressed and moves anteriorly. As the jaw is elevated, the tongue is retracted so that it
no longer lies under the anterior teeth as they as are brought together by jaw elevation.
These coordinated actions help to ensure that the tongue is not usually bitten during
chewing.
- chewing continues until all the food has been moved posteriorly, a process that can last
from less than 1 second to as much as 10 seconds. The oral preparatory, oral transport
and pharyngeal phases of swallowing therefore overlap when solid food is being
swallowed. As pieces of food are prepared in the mouth, they are moved to the posterior
part of the tongue or on into the oropharynx in a similar manner to that used to transport
liquids.
- after the bolus is formed and is on the dorsal surface of the tongue, the tip of the tongue
is placed on the anterior alveolar ridge just in front of the maxillary central incisors. The
soft palate is elevated to allow the bolus to pass through the faucial isthmus and, in its
final elevation, becomes triangular in shape and contacts the adjacent pharyngeal wall to
prevent penetration of the bolus into the nasopharynx.
- the end of this phase of swallowing is marked by the tongue propelling the prepared
bolus of food to the posterior part of the oral cavity and then on into the oropharynx to
initiate the swallow. Contact with either the posterior wall of the oropharynx or the
mucosa overlying the palatoglossal and palatopharyngeal arches was once thought to be
necessary to initiate a swallow; it is now known that there is a great degree of variability
in the position of the bolus at the time at which a swallow is initiated.
- the lips and cheeks contract followed by tongue contraction against the hard palate. The
tongue and hard palate come into contact and the soft palate elevates, drawing the food
bolus against the posterior pharyngeal wall. Normal movement of the anterior 2/3 of the
tongue is essential for carrying out this stage. The posterior 1/3 of the tongue is

6
important in the generation of force that propels a food bolus posteriorly toward the
pharynx. Without a functioning tongue base, tongue and soft palate contact cannot be
made. With impaired tongue to soft palate contact, the nasopharynx cannot be sealed
from the oral cavity. As a result food can enter into this space. The tongue forces the food
bolus through the oropharyngeal isthmus into the oropharynx. The palatoglossus
muscle then contracts to prevent reflux into the oral cavity
®PASSIVE OR INVOLUNTARY PHASES - are parts of a reflex arc that are initiated by
appropriate sensory stimuli through cranial nerves IX and X. Involuntary peristalsis then
occurs in conjunction with reflex laryngeal protective mechanisms to complete the
swallow cycle.
=™=PHARYNGEAL PHASE - the delivery of the bolus to the oropharynx triggers the
pharyngeal phase of the swallow. This phase, which is involuntary and is the most critical
stage of swallowing, involves the pharynx changing from being an air channel (between
the posterior nares and laryngeal inlet) to a food channel (from the fauces to the upper
end of the esophagus). The airway is protected from aspiration during swallowing by
hyolaryngeal elevation, and by resetting respiratory rhythm so that airflow ceases briefly
as the bolus passes through the hypopharynx; the total time that elapses from the bolus
triggering the pharyngeal phase to the re-establishment of the airway is barely 1 second.
- the nasopharynx is sealed off from the oropharynx by activation of the superior
pharyngeal constrictor and contraction of a subset of palatopharyngeal fibers to form a
variable, ridge-like structure (Passavant's ridge), against which the soft palate is elevated.
- the airway is sealed at the laryngeal inlet by closure of the glottis. The epiglottis is
retroflexed over the laryngeal aditus as a result of passive pressure from the base of the
tongue and active contraction of the aryepiglottic muscles. The sequence of events that
close the glottis may alter according to the type of swallow and consistency of the bolus.
To prevent aspiration of material, irrespective of its consistency, the hyoid bone and
larynx are raised and pulled anteriorly with precise timing by the suprahyoid muscles and
the longitudinal muscles of the pharynx. In this way, the laryngeal inlet is brought
forwards under the bulge of the posterior tongue, i.e. out of the path of the bolus. This
action helps expand the hypopharyngeal space and relax the upper esophageal
sphincter, which is also raised by several centimeterss. The bolus passes over the
reflected anterior surface of the epiglottis and is swept through the laryngopharynx to the
upper esophageal sphincter.
- breathing is suspended briefly during swallowing; the larynx is closed, the soft palate
is elevated and there is active neural inhibition of ventilation. Swallowing is normally
initiated during an expiration, which is then inhibited while swallowing occurs (typically
for a period of 0.5-1.5seconds). The resumption of expiration provides a degree of
protection against any residues of solid food that might remain uncleared within the
pharynx following the swallow being inhaled into the airway. The bolus is moved by
sequential contraction of the pharyngeal constrictor muscles superiorly behind the
bolus. The sequential contraction of the constrictor muscles is often assumed to be the
driving force that propels the bolus towards the esophagus. However, evidence that the
head of the bolus moves faster than the wave of pharyngeal contraction suggests that, at
least in some situations, the kinetic energy imparted to the bolus as it is expelled from
the mouth into the oropharynx may be sufficient to carry it through the pharynx. This
energy is generated by pressure gradients created within the pharynx by the:
i. TONGUE DRIVING FORCE - (tongue thrust pressure force) is a positive pressure that
squeezes the bolus towards the laryngopharynx. It is generated by the upward movement
of the tongue pressing the bolus against the contracting pharyngeal wall and requires a

6
tight nasopharyngeal seal (created by elevation of the soft palate). There is a view that
the tongue driving force is the most important factor responsible for moving the bolus
down the pharynx.
li HYPOPHARYNGEAL SUCTION PUMP - is caused by the elevation and anterior
movement of the hyoid and larynx, which creates a negative pressure in the
laryngopharynx, drawing the bolus towards the esophagus, aided by a more negative
pressure inside the esophagus.
tii. STRIPPING ACTION’ OF THE PHARYNGEAL CONSTRICTORS - the pharyngeal
constrictors generate a positive pressure wave behind the bolus. Their sequential
contraction may facilitate clearance (‘stripping’) of the pharyngeal walls and piriform
sinuses; if this is so, residues that remain in the valleculae must reflect inadequate
tongue force generation at the end of the oral phase of swallowing.
- at the end of this phase, the bolus is propelled towards the upper esophageal sphincter.
At rest, this sphincter is closed by active contraction. Cricopharyngeus relaxes prior to
the bolus arriving and the sphincter is then opened actively by the combined action of
the suprahyoid muscles in moving the larynx anteriorly and superiorly, and passively by
pressure from the arriving bolus. The upper esophageal sphincter thus differs in its action
of
from that of other sphincters where opening is generally passive and a consequence
pressures generated by the movements towards them of fluids or solids.
- the pharyngeal constrictors move upwards and forwards and begin propelling the bolus
through the pharynx with a sequential contraction. This engulfing action of deglutition
takes approximately 100 ms. The pharynx develops considerable force as it ejects the
the
food bolus into the esophagus with a velocity of 100 cm/s being reached about half of
velocity at which blood is ejected into the aorta from the heart.
- the bolus then enters either pyriform sinus and begins its descent into the cervical
enter the
esophagus. The relaxation of the cricopharyngeal sphincter allows the food to
the larynx
cervical esophagus and move inferiorly into the stomach. Simultaneously,
over the
rises and is pulled under the root of the tongue: the epiglottis folds down
the epiglottis tips
laryngeal opening. During this phase of pharyngeal constriction,
vestibule by
inferoposteriorly and the true and false vocal cords protect the laryngeal
to close off the
constricting the laryngeal aperture. There is true vocal fold adduction
protective mechanism that prevents
airway.This is the primary laryngopharyngeal
for elevating the
aspiration during swallowing. The suprahyoid muscles are responsible
contract to
hyoid bone and larynx. At the same time, the intrinsic laryngeal muscles
digastric) and the thyrohyoid
prevent aspiration. The oral floor muscles (mylohyoid and
thrusts and pharyngeal
muscles elevate the larynx. Through a combination of tongue
through the hypopharynx and into the
muscle contractions, the food is propelled
of the bolus through the piriform
esophagus. Thus, the epiglottis facilitates passage
fossae and into the esophagus.
bolus enters the cervical
- the final portion of the pharyngeal phase is when the food
the soft palate returns to its
esophagus. This pharyngeal phase is completed when
original position and the larynx is reopened for respiration.
variability, whereas the
- the oral phase of deglutition is subjected to marked individual muscular
Any lack of
pharyngeal swallowing movements are generally consistent.
resulting in aspiration.
coordination or sensation can significantly impair swallowing,
upper esophageal sphincter
=ESOPHAGEAL PHASE - begins after the relaxation of the
peristaltic movement, in that
has allowed the bolus to enter the esophagus. This is a true
behind the bolus
a muscular relaxation in front of the bolus and subsequent constriction

7
move it towards the stomach. The esophageal phase of swallowing is much more
variable than the other phases and lasts between 8 and 20 seconds
- it is the involuntary transport phase whereby the food passes along the esophagus
through a relaxed lower esophageal sphincter into the gastric cardia. The fastest
movement of the food bolus occurs in the upper 1/3 of the esophagus. When the food
bolus passes through the upper esophageal sphincter, a contraction is initiated in the
upper esophagus, which progresses distally to the lower esophagus. This is called
primary peristalsis. Secondary peristalsis is initiated by distension as a bolus is placed
directly within the esophagus. The peristaltic wave continues throughout the esophagus
propelling the food bolus to the lower esophageal sphincter, which relaxes and allows
the food bolus to enter the stomach.
- the lower esophageal sphincter has a tendency to relax periodically at times,
independent from swallowing. These periodic relaxations are called transient lower
esophageal sphincter relaxations. The cause is unknown but gastric distension may
play a role. These transient lower esophageal sphincter relaxations can allow for a small
amount of gastroesophageal reflux to occur. Upright posture and gravity are important
factors for facilitating lower esophageal transport.
FOOD PASSAGE DOWN THE ESOPHAGUS ASSISTED BY
i. Positive external pressure
ii. Peristaltic esophageal waves
iii. Negative pressure within the esophageal lumen
REQUIREMENTS FOR SWALLOWING
i. Development of a bolus
ii. Prevention of disbursal of the bolus during deglutition
iii. Development of differential pressures facilitating bolus propulsion
iv. Prevention of food or fluid entering the nasopharynx or larynx
v. Rapid transit of the bolus through the pharynx, minimizing the suspension of
respiration
vi. Prevention of gastric reflux during esophageal emptying
vii. Clearing of residual material from the pharyngo-esophageal tract
- a liquid bolus is usually split by the epiglottis, travelling on each side of the larynx
through the piriform recesses to rejoin behind the cricoid cartilage. The epiglottis acts
as a ledge, checking the descent of the bolus and obviating early closure of the larynx.
The larynx may be closed at any stage during deglutition, but is always closed when the
last of the bolus leaves the pharynx, at which point material entering the laryngeal
vestibule is squeezed out. The cover provided by the epiglottis bending over the laryngeal
entrance prevents the deposition of residue, and reinflation of the airway carries any
residue up into the vallecula. In the absence of epiglottic function, repeated swallowing
removes food from the laryngeal entrance prior to airway reinflation.
- pressure of the bolus through the esophagus requires the coordinated activity if the
esophageal inlet, the esophageal outlet and the body of the esophagus.
eSPEECH AND ARTICULATION - air expelled from the lungs causes the vocal cords to
vibrate and produce sound. It resonates in the upper pharynx, the paranasal sinus and
the nose. Articulation means to shape the sound into understandable words by the vocal
tract. Therefore, the coordinated movement of the tongue, teeth, lips and mouth is
necessary. Clear and distinct speech needs a competent oral cavity without congenital
anomalies or other abnormalities. The oral cavity and pharynx are critical to phonatory
activity. It is necessary for the nasal cavity to be relatively sealed from the oropharynx
and oral cavity.

*TASTE SENSATION - the tongue tastes 4 qualities, sweet, salty, bitter and sour, through
the taste receptors. The flavor recognition is a combination of olfactory sensations
through the nose, gustatory stimuli of the taste buds and mechanical and thermal
receptors. Three cranial nerves carry taste sensation of the oral cavity and the
oropharynx.
*ACCESSORY RESPIRATORY FUNCTION - mouth breathing is not the normal respiratory
way. It occurs in stress situations, during increased cardiovascular demands and in times
of nasal congestion, as in URTI. Air respired through the mouth is not humidified and
warmed as it is by normal nasal respiration. Oral respiration is not as physiologic as nasal
breathing.
1. PHYSIOLOGY OF TASTE
<TASTE BUDS - taste receptors are in the cell membranes of groups of about 30-50
modified epithelial cells arranged to form a barrel-shaped organ called a taste bud. A
pore at the top of the taste bud makes contact with the outside fluid environment in the
mouth and taste molecules are believed to bind with the hair-like cilia at or near the
opening.
- the taste cells are continually being replaced by mitotic division from the surrounding
epithelial cells, The life span of each taste cell is limited and a taste bud is actually
comprised of taste cells at various levels of maturity. The outer tips of the taste cells are
arranged around a minute taste pore. From the tip of each cell several microvilli (taste
hairs) protrude outwards into the taste pore towards the oral cavity. Interwoven among
the taste cells is a branched terminal network of several taste nerve fibers. There is
therefore an extremely intimate contact between the taste cells and the nerves. The taste
buds degenerate when the taste nerve fibers are destroyed. If subsequently, the taste
fibers regrow to the epithelial surface of the mouth, the local epithelial cells reform to a
new taste bud. Taste cells in a bud are not independently operating receptors, but make
contact with each other and share junctions between cells for common signaling
functions. They consist of taste, sustentacular and basal cells, and nerve fibers, which
be
arborize at the basal end of the taste (neurosensory) cells. Several taste buds can
innervated by the same fiber.
to 3
- from the oral end of the taste cell and projecting into the pores are microvilli of 2
ym. Adsorption onto the surfaces of the microvilli may be the mechanism initiating the
taste
electrophysiologic phenomenon of what is perceived as taste. The neurosensory
cells have a life span of about 10 days. New cells differentiate from the surrounding
nerves.
epithelium, migrate into the taste bud structure and make contact with sensory
Taste acuity declines with age.
papillae. These
- taste buds in the oral cavity are present in papillae, e.g. the fungiform
of the lingual nerve. Taste buds
papillae and buds are innervated by the chorda tympani
taste. The root of the
are also located on the soft palate, an important area for sensing
higher taste
tongue and upper part of the throat are also sensitive to tastes. People with
sensitivity tend to possess more taste buds.
their
- although all the taste buds are capable of responding to each taste quality,
of sensory
response characteristics are concentration dépendent. Thus, differentiation
in a
discrimination may be observed. Taste buds in fungiform papillae appear to respond
rather more uniform manner to low concentrations of both sweet and salty taste
a rather
substances, whereas the taste buds in the vallate papillae appear to respond in
uniform manner to low concentrations of sweet substances and only to higher

‘9
concentrations of salty, sour and bitter stimuli. Taste buds in the palatal papillae respond
in a uniform manner to both sour and bitter substances.
- taste buds compose 20-50 cells. The taste buds from the fungiform and palatal papillae
are relatively long and slender, whereas those from the vallate papillae are more globular.
The component cells all comprise cell processes that extend to the pore region of the
bud, and all the cells have desmosomal junctions with one another.
TASTE - is the detection and recognition of liquid phase stimuli. Taste or gustation is a
sensation that is developed well before birth. Initially, therefore, it may comprise part of
the monitoring system of the amniotic fluid. After birth, the complex process of taste may
be subdivided into a number of component aspects.
*PRENEURAL TASTE EVENTS - are assumed to be influenced by a variety of factors:
*» Stimulus characteristics ™»Taste support systems
» General taste bud characteristics ™ Specific taste bud receptor characteristics
®Mechanisms of stimulus-receptor binding
*NEURAL TASTE EVENTS - follow taste bud stimulation. It is influenced by a variety of
factors
® Transduction in the chemical binding energy to an electrically recognizable generator
potential -
Neural transmission of the generator potential
» Formation of the action potential and its axonal conduction
Transmission of the action potential in those brain centers involved with taste detection
and recognition
»CNS integration of the received signals
MECHANICS OF TASTE - the initial event in the process of taste presumably involves the
binding of the taste stimuli to the taste bud receptor on the exposed receptor membrane
of the taste bud. Such binding may be influenced by a variety of factors, including
interactions between taste stimuli, hormones, ganglionic blocking agents and proteolytic
enzymes.
- the membrane of the taste cells is negatively charged on the inside with respect to the
outside. Applications of a taste substance to the taste hairs results in partial loss of the
negative potential. Generally, the degree of depolarization of the cell membrane is
approximately proportional to the logarithm of the concentration of the stimulating
substance. Once the generator potential is formed, it is conducted by neural or modified
neural elements to the synapse where true depolarization occurs. Subsequently, these
signals are translated along the VIIth, IXth and Xth cranial nerve branches to the ipsilateral
nucleus of the tractus solitarius. From the tractus solitarius, a large number of impulses
are transmitted directly to the superior and inferior salivary nuclei. These, in turn, transmit
impulses to the major salivary glands to help to control the secretion of saliva during the
ingestion of food. Generally, the taste pathways closely parallel those of the somatic
pathways from the tongue.
TASTE STIMULI - present day dogma contends that taste stimuli represent 4 primary
qualities - sweet, sour, salty and bitter.
*THE SWEET TASTE - is not caused by any single class of chemicals but several,
including - sugars, glycerols, alcohols, aldehydes, ketones, etc. Most of the substances
that cause a sweet taste are therefore organic chemicals, and a slight molecular change
can cause a change in taste from sweet to bitter. Thus, the stimuli that produce a sweet
response are diverse, so that the simple view that carbohydrates are equivalent to sweet
cannot hold.

10
*THE SOUR TASTE - the best correlation between taste stimulus and taste response
concerns the sour taste for the hydrogen ion concentration and/or the degree of
dissociation of the acid. There are, however, exceptions to this general rule, in that all
acids are not sour.
*THE SALTY TASTE - is elicited by ionized salts. The quality of the taste varies between
one salt and another because the salts also elicit other taste sensations besides
saltiness.
*THE BITTER TASTE - is not caused by any single type of chemical. Bitter substances,
represented by alkaloids, ureas, and other long-chain organic substances containing
nitrogen, represent a diversity of sensory stimuli, although many anomalies exist.
-some substances have sweet taste on the front of the tongue, where taste buds with
special sensitivity to the sweet taste are principally located, and a bitter taste on the back
of the tongue, where the taste buds that are more sensitive to the bitter taste are located.
- the bitter taste, when it occurs in high intensity, usually results in a person rejecting a
particular food or medication. This is undoubtedly an important function of the bitter taste
sensation, since many of the deadly toxins found in poisonous plants are alkaloids, and
these all cause intensely bitter tastes.
- there are certain thresholds for stimulation of various taste sensations. The bitter taste
is much more sensitive compared to the other taste sensations: an important protective
function. Many patients are, however, taste blind for certain substances, especially for
different types of thiourea compounds.
=TASTE SUPPORT SYSTEMS
*Secretions of glands of the oral cavity which come into direct contact with the taste
system
*Physical structures that house the taste buds
- the salivary secretions are derived from both major and minor salivary glands and, with
the diminution of their functions, resulting either from radiotherapy or Sjogren’s
syndrome, taste acuity for all stimuli is either destroyed or markedly attenuated.
TASTE PREFERENCES - the phenomenon of taste preference almost certainly results from
some mechanism located in the CNS, although taste buds may become sensitized to the
needed nutrient. Thus previous experience with unpleasant or pleasant tastes plays a
major role in determining a patient’s likes and dislikes. This suggests that taste
preference reflects a central rather than peripheral mechanism.
TASTE SENSATION - the flavor of food is a combination of gustatory transduction through
the taste buds in combination with olfactory sensation through the nose.
CRANIAL NERVES - responsible for the sensation of taste in the oral cavity and oropharynx.
*FACIAL NERVE (CN VII) - carries the special visceral efferents for taste to the anterior
2/3 of the tongue via the chorda tympani nerve.
*GLOSSOPHARYNGEAL NERVE (CN IX) - innervates the posterior 1/3 of the tongue
VAGUS NERVE (CN X) - innervates several taste buds around the base of the epiglottis.
TY. LARYNGEAL PHYSIOLOGY

A. FUNCTIONS OF THE LARYNX
¢Protection of the lower respiratory tract =. *Respiration
*Provides sphincteric action for deglutition *Facilitates phonation
“AIRWAY PROTECTION - is done by the larynx during the act of swallowing. In infants, the
higher position of the larynx allows contact of the epiglottis with the posterior surface of
the soft palate so they are able to breathe while nursing without passage of food into the
airway. During deglutition, the epiglottis forms a continuous airway with the

nasopharynx, and liquid and solid materials are deflected laterally by the epiglottis into
the pyriform sinus.
- during growth, the epiglottis descends from its formerly high cervical position to a lower
position relative to the other structures of the upper airway, thus interrupting the
continuity of the upper airway. The airway is protected through a sequence of events
initiated when a bolus of food comes into contact with either the tip of the epiglottis or
the aryepiglottic folds.
SENSORY REFLEX ARCH - GLOSSOPHARYNGEAL NERVE (CN IX).
MOTOR ARCH - is mediated via the VAGUS NERVE.
- the initial occurrence with this stimulation is the inhibition of inspiration. The true vocal
cords then forcefully close, which secondarily causes closure of the false vocal cords.
Subsequent to this, the aryepiglottic folds are drawn medially, posteriorly displacing the
epiglottis.
- while these events are occurring with the intrinsic laryngeal musculature, the extrinsic
laryngeal muscles are also active. The suprahyoid extrinsic muscles are stimulated at
the same time that the infrahyoid extrinsic muscles are inhibited. This stimulation and
inhibition cause a superior-anterior vector force on the larynx as a unit, which displaces
it under the protective hood of the base of the tongue during the act of swallowing.
- these sequential events usually are sufficient for the subconscious passage of food
beyond the larynx and into the cervical esophagus, where it is transported to the stomach
with no danger to the airway.
TIERS OF PROTECTION
*FIRST TIER OF PROTECTION - contraction of the superior division of the thyroarytenoid
muscles contained in the aryepiglottic folds.
- during deglutition, the larynx in the adult is elevated and anteriorly displaced so that the
supraglottic portion projects toward the nasal cavity, positioning the shield-like epiglottis
and aryepiglottic folds into the position to deflect the food stream laterally. This
protective function of the epiglottis is enhanced by the ability of the superior portion to
fold posteriorly over the laryngeal aditus. The aryepiglottic folds are approximated by the
contraction of the superior division of the thyroarytenoid muscle. Concurrently with this
contraction, the pre-epiglottic fat pad is pressed against the thyroid cartilage and the
hyoid bone, pushing the base of the epiglottis toward the raised ventricular bands.
eSECOND TIER OF PROTECTION - contraction of the thyroarytenoid fibers in the false
cords.
- the vestibular folds are closed together under the strong contraction of the fibers of the
thyroarytenoid muscle that lie lateral to the folds.
eTHIRD TIER OF PROTECTION - contraction of the inferior division of the thyroarytenoid
at the level of the true vocal cord.
- this barrier to aspiration is the most significant one owing to the upturned border of
the cord margin. These folds are thick, with upturned margins. When tightly opposed,
pressure in the upper airway relative to the lower airway drives the edges more tightly
together. The inferior division of the thyroarytenoid muscle provides the bulk of the
cross-sectional area to the vocal cord.
COUGH REFLEX - the cough is an essential feature of airway protection and maintenance
in the clearance of debris from the lower respifatory tract. The explosive exit of air from
the lower airway requires that the glottis act as a valve as the lower airway pressure is
increased to very high levels. This involves effort closure of the glottis by the vestibular
and vocal folds secondary to the contractions of the superior and inferior divisions of the
thyroarytenoid muscle. The vestibular folds are directed inferiorly, whereas the vocal

12
folds are directed superiorly. As pressure in the ventricle is increased, the vestibular
vocal folds are forced together. The orientation of the vocal folds prevents the ingress
of air when they are closed.
- the laryngeal inlet is closed by the sphincteric action of the slips of the thyroarytenoid
muscle in the aryepiglottic folds and false cords in addition to the adduction of the true
vocal cords and arytenoids brought about by the other intrinsic muscles of the larynx.
- elevation of the larynx under the base of the 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. Respiration is inhibited during swallowing
owing to a reflex mediated by receptors present in the mucosa of the supraglottic area
preventing the inhalation of food or saliva.
= RESPIRATION - many factors influence glottic size during respiration.
- the intrinsic laryngeal musculature is subject to reflex central respiratory control
coordinating laryngeal and diaphragmatic function. The glottis widens several msec
before diaphragmatic descent because of the action of the posterior cricoarytenoid
muscle. This is a direct effect of the medullary respiratory center and occurs with
rhythmic bursts of activity.
- during inspiration, the larynx is displaced inferiorly away from the hyoid partly because
of tension in the trachea and partly because of phasic inspiratory activity in the extrinsic
laryngeal musculature. This causes the vestibular and vocal folds to become stretched
and displace the arytenoid cartilages laterally. The combination of these 2 effects causes
glottic widening and an increase in cross-sectional area of the glottis.
- the cricothyroid muscle while acting in concert with the posterior cricoarytenoid muscle
and the mechanical coupling effects, the muscle acts to increase the glottis cross-
sectional area because the vocal folds are lengthened and the posterior commissure is
displaced more posteriorly. This muscle is also modulated by the medullary respiratory
center.
- both muscles are driven in concert during respiration - the posterior cricoarytenoid
muscle increasing the lateral diameter and the cricothyroid muscle increasing the
anteroposterior diameter of the larynx.
- inspiration is marked by a stimulation of the recurrent laryngeal nerve, resulting in
vocal cord abduction just before phrenic nerve stimulation, which permits air flow into
the lungs.
<PHONATION- voice production is the most complex laryngeal function. It is believed
to result from an initial forceful closure of the vocal cords during the act of expiration.
Cord closure increases the intratracheal pressure with expiration. It ultimately results in
a pressure that is greater than the closing pressure of the vocal cords, thus forcing them
to open. However, the opening of the cords causes a rapid reduction of the intratracheal
pressure, permitting the vocal cords to close again an effectively pinch off a “puff” of air.
This alternating rise and fall of the intratracheal pressure causing the vocal cords to open
and close and pinch off boluses of air is responsible for phonation.
HOARSENESS - any pathologic processes altering the mass of vocal cords or their ability
to close will ultimately affect the quality of the voice.
- when an air column of sufficient pressure and duration reaches the larynx, the vocal
cords are approximated and a fundamental tone is produced by the passive vibration of
the vocal cords, according to the aerodynamic theory of sound production.

13
- although vibration is primarily determined by the passive effects of subglottic pressure,

physical properties of the vocal cords and mechanical stress caused by the extrinsic
laryngeal musculature play an important role. Mechanically, changes in vocal cord
morphology as modulated by thyroarytenoid and vocalis tension and elasticity and air
pressure as represented by subglottic pressure and glottic air particle velocity are
important determinants of voice quality.
- the fundamental frequency of vibration of the folds varies with age and sex and averages
125 Hz in the adult male and 250 Hz in the adult female.
DETERMINANTS OF THIS FREQUENCY AND INTENSITY:
«VIBRATORY MASS OF BOTH FOLDS
eTHEIR ANTEROPOSTERIOR TENSION
*FUNCTIONAL DUMPING AT HIGH PITCHES
*SUBGLOTTIC PRESSURE
- as pitch increases, the vocal cords lengthen and tense secondary to the action of the
cricothyroid muscle. Although cord lengthening alone might reduce pitch, this effect is
offset by fold thinning produced by thyroarytenoid action, which increases the internal
tension of the vocal cord. In general, the longer the vocal cords are, the lower the
fundamental frequency and the greater the vocal cord tension, the higher the frequency.
- in normal phonation, the fundamental frequency is the prime but not the sole
determinant of voice quality.
- itis 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 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.
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 - 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.

DISEASES OF THE MOUTH
i. CLEFT LIP/CLEFT PALATE DEFORMITIES
- constitute the most common congenital defects of the head.
= ANATOMY OF THE LIPS
*LIPS - the normal upper lip is divided into the:
®RED LIP - a mucous membrane
BWHITE LIP - a cutaneous structure.
VERMILION BORDER - mucocutaneous junction between the red and white lips which
is an important anatomic boundary that must be reconstructed meticulously in cleft fip
repair for a natural-looking result; failure to do so will draw attention to the irregularity at
the vermilion border and will create a poor cosmetic result.
®ORBICULARIS ORIS MUSCLE - in unaffected persons, it forms a complete sphincter
around the oral cavity and provides the substrate for proper form and function of the lips
and mouth; all patients with cleft lip deformities have muscular deficiencies and
irregularities of varying degrees that lead to the abnormal appearance and function of {ne
lip and mouth.
- for proper correction of cleft lip deformities, it is essential not only to create symmetry
of the lip superficially, at the skin level, but also to recreate the complete orbicula‘is
muscular sling for long-lasting cosmetic and functional results; complete mucosal
coverage must be reestablished to ensure optimal healing and to prevent distorting
wound contracture.
- the muscle fibers in cleft lip deformities run in an inferior-to-superior direction along ‘he
margins of the cleft; they insert into the columella medially and along the nasal aiae
laterally; these fibers must be detached from their insertions and reoriented in a
horizontal direction to bridge the cleft and create a complete muscular sling around the
entire circumference of the oral cavity.
- bilateral clefts also have abnormally oriented muscle fibers that run along the edges of
the lateral aspect of the cleft; the prolabial segment does not contain any useful muscle
but is filled with connective tissue; patients have premaxillary and alveolar protrusion
relative to the nasal septum; the premaxillary bony deformity may push the lip so far
anteriorly and superiorly toward the nasal tip that the columella is severely diminished in
strength and height and may even be obliterated completely; often, length to the medial
crura is inadequate, and consequently, columellar skin is insufficient.
= ANATOMICAL CHARACTERISTICS OF CLEFT LIP
*UNILATERAL CLEFT LIP NASAL DEFORMITIES
»Lip »Columella ®& Nostril
®Alar base =» Septum
- the nasal tip is deflected toward the noncleft side with a relatively short medial crus and
long lateral crus on the cleft side; the lateral crus of the lower lateral cartilage is caudaily
displaced on the cleft side; the columella is shorter than normal on the cleft side; tire
columella lies on the noncleft side because of the unopposed action of the intact
orbicularis oris muscle.
- the nostril on the cleft side is horizontally oriented rather than lying in the normal vertical
orientation; the nasal septum is deflected to the noncleft side; the alar base on the side
of the cleft is displaced laterally, inferiorly, and:posteriorly.
- there is a deficiency of maxillary bone on the cleft side, and the nasal floor is offen
absent

¢
ip 2
*BILATERAL CLEFT LIP NASAL DEFORMITY - differs from the unilateral deformity in
several aspects other than laterality; the degree of nasal deformity relates to the:
™® SEVERITY OF THE CLEFT LIP DEFORMITY - such as whether the cleft lip is complete
or incomplete
» DEGREE OF PREMAXILLARY PROTRUSION
- bilateral cleft lip nasal deformities are symmetric, which makes the repair of the nose
somewhat simpler with regard to achieving tip symmetry; the challenging aspect of the
bilateral cleft lip nasal deformity is the lack of adequate columellar tissue as a result of
deficient length of the lower lateral cartilages and a deficiency of skin that overlies these
shortened cartilages; the tip usually is broad and flat, and the alae are laterally displaced
with resultant horizontally oriented nostrils.
ANATOMY OF THE PALATE
*PALATE - consists of the hard and soft palate forming the roof of the mouth and the floor
of the nose.
INCISIVE FORAMEN - divides the palate into the:
® PRIMARY PALATE OR PREMAXILLA - has the incisive foramen as its posterior border,
a triangular area of the anterior hard palate extending from anterior to the incisive
foramen and to a point just lateral to each lateral incisor tooth; includes the alveolar ridge
containing the four incisor teeth.
BPREMAXILLA aLiIP =NASAL TIP =COLUMELLA.
=®SECONDARY PALATE - extends from the incisive foramen anteriorly to the uvula
posteriorly; develops after completion of development of the primary palate and extenc's
from the incisive foramen anteriorly to the uvula posteriorly.
EMBRYOLOGY
*FOURTH EMBRYONIC WEEK - at the end of this week, the neural crest-derived facial
prominences appear from the first pair of pharyngeal arches:
MAXILLARY PROMINENCES - found laterally
®FRONTONASAL PROMINENCES - formed by the proliferation of mesenchyme ventral
to the forebrain, form the upper border of the stomodeum; on either side of the
frontonasal prominences are local thickenings of surface ectoderm that form the nasal
placodes.
eFIFTH WEEK OF EMBRYONIC LIFE - the nasal placodes invaginate to form the nasal
pits; this invagination process creates a ridge of tissue around the pit, called the lateral
nasal prominence laterally and the medial nasal prominence medially.
¢SIXTH AND SEVENTH WEEK OF EMBRYONIC LIFE - the paired maxillary prominences
grow medially toward the paired medial nasal prominences; over time, fusion of the
paired medial nasal prominences and paired maxillary prominences occurs, thereby
forming the upper lip:
FUSION OF MEDIAL NASAL PROMINENCES
®Philtrum =Medial upper lip
®Nasal tip =Columella
=» MAXILLARY PROMINENCES - form the lateral aspects of the upper lip; the lateral nasal
prominences form the nose and are not involved in the formation of the upper lip.
PALATOGENESIS - begins at the end of the 5th week, and complete fusion occurs by 12
weeks of development.
*PRIMARY PALATE OR MEDIAN PALATINE PROCESS - forms at approximately 4-7 weeks
of intrauterine life and forms the initial separation between the oral and nasal cavities.
- as the maxillary prominences grow and push the medial nasal prominences medially,
the medial nasal prominences fuse not only at the surface, but also at deeper levels; thus,
the intermaxillary segment, or primary palate - which includes the central maxillary

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SS
alveolar arch that houses the four incisor teeth and the hard palate anterior to the incisive
foramen - formed by the deeper levels of fusion of the paired median prominences which
gives rise to the central upper lip, the central maxillary alveolar arch and associated
lateral and central incisors, and the hard palate anterior to the incisive foramen.
- embryologically, clefts of the lip are almost invariably associated with clefts of the
primary palate; cleft lip occurs very early in pregnancy - between the 4th and 7th week of
gestation, when the two separate sides of the upper lip fail to fuse properly.
- once the primary palate is completely developed, the secondary palate begins to
develop.
*SECONDARY PALATE - makes up the major portion of the palate; formed from the
palatine shelves, which are two outgrowths of the maxillary prominences.
- begins developing after the development of the primary palate is completed; formation
of the secondary palate occurs by inferior and medial growth and migration of the palaial
shelves; as the palatal shelves displace inferiorly, the developing nasal cavities expand
laterally and inferiorly.
- the paired palatal shelves are initially separated by the developing tongue; palatal fusion
occurs from anterior to posterior, beginning at the incisive foramen at 8 weeks of
gestation and reaching completion by week 12 with uvular fusion; the degree of clefting
noted clinically is a consequence of the point in fetal development at which the fusion
process is interrupted.
- interruption of the natural fusion of the secondary palate caused various degrees of
palatal clefting; growth of the mandible with associated anterior movement of the tongue
allows the palatal shelves to migrate inferiorly and to assume a more horizontal position;
if this process does not proceed normally, the paired palatal shelves cannot migrate
inferiorly and medially; lack of contact of these shelves creates palatal clefting.
- the pathogenesis of secondary cleft palate is failure of this fusion to occur; the primary
palate is anterior to the incisive foramen, and the secondary palate is posterior to the
incisive foramen.
®SIXTH WEEK OF EMBRYONIC LIFE - the palatine shelves are directed obliquely
downward on either side of the tongue
=» SEVENTH WEEK OF EMBRYONIC LIFE - the palatine shelves migrate inferomedially to
lie horizontally above the tongue; it is in this horizontal position that the palatine shelves
fuse in the midline to form the secondary palate; the palatine shelves fuse with the
previously formed primary palate anteriorly, and the nasal septum fuses with the newly
formed secondary and primary palate.
TE. CED LEP WITH OR WITHOUT CLEFT PALATE

- usually involve clefts of the primary palate anterior to the incisive foramen, occur due
to lack of fusion of the medial nasal process of the frontal nasal prominence with the
maxillary process; failure of either of these occurrences can result in clefts involving the
nose; this results in a cleft in the typical location between the premaxilla and the lateral
maxilla, on either one or both sides.
- although the primary palate and the secondary palate form at different stages of
embryonic development, cleft palate is most commonly seen in combination with cleft
lip; the alveolar portion of the cleft lies between the maxillary lateral incisor and canine
tooth roots; this results in malposition of the maxillary lateral incisor and cuspid in beth
the deciduous and permanent dentition; the maxillary lateral incisor on the cleft side is
absent in 80-90% of cleft patients; when present, it may be smaller than the contralateral
tooth or significantly dysmorphic; absence of other teeth is not uncommon, but it may be

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related to the surgery itself because adults who have not been operated on do not show
the same patterns of hypodontia.
- cleft lip with or without cleft palate must be distinguished from isolated cleft palate
deformities because of different embryologic, etiologic, and epidemiologic factors.
PREVALENCE - second most common congenital malformation (club foot is most
common).
*UNITED STATES
®CLEFT LIP = 1 in 1000 live births
=NATIVE AMERICANS = 3.6 in 1000 births - cleft lip deformities occur with the highest
incidence.
BASIAN AMERICANS = 2.1 in 1000 births
=NON-HISPANIC WHITES = 1 in 1000 births
AFRICAN AMERICANS = 0.41 in 1000 births - with the lowest incidence
= CLEFT PALATE = 0.5 in 1000 live births - does not differ among ethnic groups.
*CONSIDERING THE CLEFT DEFORMITIES OF ALL RACES GROUPED TOGETHER
®CLEF LIP AND PALATE = 50% ISOLATED CLEFT PALATE = 30-35%
® ISOLATED CLEFT LIP = 15-20% »CLE FT LIP AND ALVEOLUS = 5%
= CLSSIFICATION
*UNILATERAL OR BILATERAL
*RIGHT OR LEFT - unilateral clefts of the lip should designate which side is involved.
eCOMPLETE OR INCOMPLETE
COMPLETE CLEFT LIP - involves the entire vertical thickness of the upper lip and is
often associated with an alveolar cleft because the lip and primary palate share the sarie
embryologic origin.
=» INCOMPLETE CLEFT LIP- involves only a portion of the vertical height of the lip, with
a variable segment of continuity across the cleft region; the variable continuous segment
may present as a simple muscular diastasis with intact overlying skin or as a wide cicft
with only a thin band of skin that crosses the region of the cleft.
SIMONART BAND - is a bridge or bar of lip tissue of variable size that crosses the cleft gap;
it usually consists of skin only, although some histologic studies have shown that
muscle fibers may lie within the band.
®UNILATERAL CLEFT OF THE SECONDARY PALATE - is defined as one in which the
palatal process of the maxilla on one side is fused with the nasal septum.
BILATERAL COMPLETE CLEFT OF THE SECONDARY PALATE - has no point of fusisn
between the maxilla and the nasal septum.
COMPLETE CLEFT OF THE ENTIRE PALATE - involves both the primary and secondary
palate and includes one or both sides of the premaxilla/alveolar arch and frequenily
involves a cleft lip.
® ISOLATED CLEFT PALATE - usually involves only the secondary palate and has varying
degrees of severity.
= ETIOLOGY - both genetic and environmental factors contribute to cleft lip and/or palate;
eGENETICS - monozygotic twins demonstrate a 40-60% concordance in clefts; the lack of
100% concordance in monozygotic twins suggests that genetics alone does not determine
orofacial clefts.
® MULTIFACTORIAL INHERITANCE - plays the major role.
&® FAMILIAL INHERITANCE - occurs, but classic Mendelian inheritance is rare.
™ CHROMOSOMAL ABERRATIONS - such as Trisomy D and E have increased incidence
of clefts. Ds
*ENVIRONMENTAL FACTORS
Rubella virus ™» Thalidomide » Aminopterin

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»Phenytoin »Retimoic acid » Alcohol

Tobacco smoke
*SEX - overall males are more affected than females; cleft lip occurs more commonly in
males than in females, whereas cleft palate occurs more commonly in females than in
males; fusion of the palatine shelves 1 week later in females than in males is thought to
be responsible for the higher frequency of cleft palate in females.
»>ISOLATED CLEFT LIP AND CLEFT LIP AND PALATE - more common in males (2:1).
»ISOLATED CLEFT PALATE - more common in females (2:1); the reason for this
he is because embryologically the mechanism for cleft palate is different than for
cleft lip. ISOLATED CLEFT PALATE - more common in female (2:1); the reason for this difference is because embryologically the mechanism
for cleft palate is different that for cleft lip.
*RACE - highest in native Americans, then Orientals, and Whites, with lowest in Blacls.
*INCREASED PATERNAL AGE - associated with increased risk of clefts.
A. ISOLATED CLEFT PALATE - represents a failure of fusion; it appears to be a different
entity from cleft lip, with or without cleft palate and children with this condition commonly
have associated congenital anomalies; an isolated cleft palate usually involves the
secondary palate only and has varying degrees of severity.
- the normal embryologic course of events regarding palate development includes a
force that changes the direction of the palatal shelves from a vertical to a horizontal plane;
while this is occurring, the embryologic tongue is migrating in an anterior-inferior
direction away from the shelves; this movement provides room for the horizonial
realignment of the palatal shelves; the palatal shelves ultimately fuse.
- anything that interferes with this normal course of events, such as the proportions of
the skull base or the size and/or migration of the tongue or mandible, can have an
adverse effect and be associated with the development of an isolated cleft palate.
- in patients with cleft palate, the muscles of the soft palate may be hypoplastic in
addition to exhibiting misdirection and abnormal insertions into the posterior hard palets;
the mucosa that envelops these muscles is deficient, except in the case of a submuccus
cleft palate; if the cleft involves the hard palate, a midline bony deficiency of variable
degree will extend toward the incisive foramen; the vomer usually is unattached in
isolated cleft palate but may or may not be attached if a cleft lip is present.
- abnormal muscle insertions, combined with tissue absence or hypoplasia, lead to
palatal dysfunction; palatoplasty aims to restore function by reorienting the muscles aind
reconstructing the continuity of the tissues.
- in this defect, neither the lip nor the alveolar process is involved; the cleft may involve
only the soft palate or both the soft and hard palates but never the hard palate alone; the
cleft may extend forward from the uvula to varying degrees; in some cases, the cleft is
limited to the uvula or to the uvula and soft palate; in others, it may extend into the hard
palate; in the extreme form, the cleft palate may extend anteriorly as far as the
nasopalatine foramen, the incisal canal; when the cleft involves a considerable portion of
the hard palate, the nasal chambers are in direct communication with the oral cavity; in
most instances, the nasal septum is not attached to either palatal process throughout the
extent of the cleft.
INCIDENCE - the genetics of cleft lip and palate are not classical Mendelian, but siblings
of cleft patients are at greater risk; the risk is directly related to the frequency and severity
of the clefts.
- approximately 10% of patients with a cleft deformity will have other anomalies at birth;
it is more common in females (75%); 33% aré-associated with syndromes.
eWHITES = 1/2,500 births *BLACKS = 1/2,500 births
*ORIENTALS = more frequent

“—
= ASSOCIATED WITH
eIncreasing parental age Geographic location
*Occurrence of clefting in relatives ¢Maternal measles during gestation
= ENVIRONMENTAL FACTORS RESPONSIBLE FOR CLEFTING
¢Fetal alcohol exposure *Cigarette smoking
*Folic acid deficiency or antagonists *Phenytoin
*Retinoic acid derivatives *Amniotic band syndrome
*Maternal diabetes
= CLASSIFICATION
*BIFID UVULA - is the most common condition and smallest expression of clefting of the
soft palate; this occurs when there is lack of fusion of the uvular soft tissues and muscles.
*SUBMUCOUS CLEFT PALATE (SMCP) - is the least severe incomplete cleft palate: it
occurs when the palate has mucosal continuity but the underlying levator palatini muscle
is discontinuous across the midline and longitudinally oriented, similar to the muscle
anatomy in overt clefts of the palate; wth contraction of velar musculature, a distinct
midline muscle diastasis may be seen.
- the significance of a submucous cleft may be difficult to assess clinically; the child with
submucous cleft palate is often undiagnosed in infancy.
CALMAN’S CLASSIC TRIAD - is diagnostic of SMCP
»>BIFID UVULA
™ZONA PELLUCIDA -a bluish translucent zone in the midline of the soft palate
®PALPABLE NOTCH IN THE POSTERIOR HARD PALATE - as a result of the absence of
the posterior vomerine spine.
- the diagnosis of occult SMCP is made during nasoendoscopy for evaluation of
velopharyngeal insufficiency; the masculature is deficient and inappropriately oriented;
the clue is a slight speech disorder; it is diagnosed by palpation, which shows a bony
dehiscence under an intact palatal mucosa.
*INCOMPLETE CLEFT PALATE - involves the secondary palate only; occurs through the
entire soft palate and into a portion of the hard palate; the defect is below the incisive
foramen; the defect may be variable, from an opening in the posterior soft palate to a cleft
extending up to the incisive foramen; there is almost always a separation of the bony
shelves of the hard palate, which is variable but may extend anteriorly to the incisive
foramen; most commonly, dentition is normal and symmetric.
eUNILATERAL CLEFT - if on one side the palatal process of the maxilla is fused with the
nasal septum.
*BILATERAL CLEFT - is not attached to the nasal septum, and the septum is visible
through the cleft.
*COMPLETE PALATAL CLEFT - involves the primary and secondary palate; the defect is
up to the incisive foramen.
® UNILATERAL COMPLETE CLEFT PALATE - is characterized by direct communication
between the entire length of the nasal passage and oropharynx; it is a full-thickness
palatal defect of nasal mucosa, bony palate, velar musculature, and oral mucosa; ali of
these deficiencies must be addressed during the cleft palate repair or later at the time of
alveolar cleft bone grafting.
BILATERAL COMPLETE CLEFT LIP AND PALATE - the premaxillary segmertt,
containing the central and lateral incisor tooth rdots is discontinuous from the alveolar
arch; the lateral segments often collapse inward and lingually, resulting in “locking out”
of the premaxilla.
*ALVEOLAR CLEFT - defect involving alveolus, may be isolated or combined with a
palatal cleft.

a
= TREATMENT
°Repair at 10-14 months (after lip repair)
ePRESURGICAL CONSIDERATIONS - may require orthodontic treatment (NAM, Latham,
taping) to move premaxilla or to realign maxillary segments.
»LIP TAPING - application of tape across the cleft in order to narrow the cleft gap width;
may be helpful in patients with unilateral or bilateral complete or nearly complete cleft iip
with widened gap; effect of the taping allows mobilization of the lip segments and gradual
narrowing of the overall cleft gap, which in turn can help diminish overall tension on tip
closure and potentially lead to improved operative outcome.
™®NASOALVEOLAR MOLDING (NAM) - involves fabrication of a palatal appliance by a
trained orthodontist; the shape of the appliance is changed over time to narrow the width
of the palatal cleft gradually by guiding the palate segments closer together; once
appropriate narrowing has been achieved, small posts are added to the front of tne
appliance, coated with soft silastic cushion, and placed inside the nostril, to allow gentle
traction; this traction is then guided by weekly adjustments over a period of 2- 3 months;
in patients with unilateral cleft lip and asymmetric nostrils, NAM allows establishment of
better symmetry via gradual repositioning of the nasal tip and alar cartilages from a
lateral-posterior position into a more symmetric anterior-medial alignment in relation to
the contralateral nonaffected nostril; in the patient with bilateral cleft, the traction is
applied to both nostrils and allows elongation of the short columella; definitive surgical
repair of the cleft lip follows the NAM or to realign maxillary segments
- if NAM is not used, cleft lip repair is typically performed at 3-4 months of age; but the
timing varies among surgeons; some have suggested that lip repair be performed within
48 hours of the child's birth to prevent a separate hospitalization and to allow the parents
to leave the hospital with a healthy-appearing newborn.
eADVANTAGES OF DELAYED SURGERY:
® Availability of more tissue for the repair
= More time for parent-child bonding :
=™ More time for the parents to gain a better understanding and acceptance of the infant's
congenital deformity.
*TIMING OF PALATE REPAIR SURGERY - takes into account:
™ Speech development ® Maxillary growth
=» Associated syndromes » Other medical conditions
- repair prior to 1 year of age results in better speech outcomes; timing of surgical closure
depends on the width and not the length of the cleft space; hard palate clefts are
frequently closed simultaneously with the soft palate cleft; in some instances, surgical
closure of very wide hard palate clefts may need to be postponed until there is additional
palatal growth, which may be as late as 5 to 6 years of age; an obturator with a pharyngeal
extension (speech aid appliance) can be worn until the palate is closed.
*SUBMUCOUS CLEFT PALATE - an infant identified with SMCP need not routinely
undergo repair because a significant number of individuals will not develop
velopharyngeal insufficiency; these patients should be closely monitored with serial
speech evaluations and audiometric surveillance; corrective surgical technique for SMCP
is focused on anatomic correction of the velar muscle diastasis; although pharyngeal
flaps and sphincter pharyngoplasty have been proposed as primary means of
treatment, most surgeons focus on repair of the abnormal levator muscle position.
*GOALS OF PALATOPLASTY
® Separation of the nasal cavity from the oral:cavity
™ Creation of a competent velopharyngeal valve for both swallowing and speech
® Avoidance of injury to the growing maxilla

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™ Development of functional occlusion » Union of the cleft segments

» Reduction of nasal regurgitation ™ Preservation of midface growth
*Intelligible and pleasant speech - improved speech outcomes are seen when the soft
palate is repaired early; palate surgery during childhood may adversely affect facial
growth; case studies of adults with unrepaired clefts demonstrate normal midface
development.
- normal speech is the primary goal of cleft palate repair with a secondary goal of
minimizing effects on maxillary growth; normal speech requires velopharyngcal
competence to close the oral cavity off from the nasal cavity to produce pressure
consonants; this requires static physical separation of the two cavities in the region of
the hard palate and dynamic closure of the soft palate against the posterior pharyngeal
wall with a functioning levator veli palatini muscle; ina cleft palate, the levator veli palatini
muscle fibers are oriented abnormally along the cleft; all modern techniques of cleft
palate repair involve repair of the nasal lining and oral mucosa and reorientation and
repair of the levator veli palatini muscle; the primary measure of outcome of cleft palate
repair is normal speech.
«STAGED APPROACH - to preserve growth potential
Early repair of the soft palate
® Obturation of the hard palate
Later surgical closure of the hard palate
- others have not found a significant difference in maxillary development between
patients who have single-stage palatoplasty versus those who undergo a two-staye
repair.
*FEEDING/LACTATION - the immediate problem in an infant born with a cleft lip or palate
is feeding; some advocate the construction of a plastic obturator to assist in feedings,
most believe that with the use of soft artificial nipples with large openings, a squeezacie
bottle, and proper instruction, feeding of infants with clefts can be achieved.
®EVALUATE FEEDING ASSISTANCE
=Poor suction, lengthy feeds, inadequate intake, excessive air intake, nasal regurgitation,
poor airway protection
lf feeding >25-30 minutes consider feeding assistance because too much energy is
being expended and will cause failure to thrive
®SPECIAL NIPPLES - help with difficulty obtaining a seal
Preemie nipples =Mead-Johnson =McGovern’s cross-cut
sUNIDIRECTIONAL FEEDERS: Haberman, Pigeon
- frequent rests and burps, upright feeding with chin support, palatal
prosthesis/obdurator or preoperative nasoalveolar molding (PNAM)
*MULTIVITAMIN SUPPLEMENTS - have been shown to lower the risk for CLP and
possibly isolated CP; whether or not preconception folic acid supplementation alone can
reduce clefting is controversial.
*DENTAL
»Prostheses/molding »Latham appliance ® Orthodontic appliances
®Oral hygiene andcare Dental restoration :
*CLEFT PALATE REPAIR - because clefts of the palate vary considerably in size, shape,
and degree of deformity.
® CRITERIA FOR TIMING OF SURGICAL CORRECTION
eWidth of the cleft "Adequacy of the existing palatal segments
=aMorphology of the surrounding areas (width of the oropharynx)
=Neuromuscular function of the soft palate and pharyngeal walls

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COMPLICATIONS
»EARLY - bleeding, airway obstruction, dehiscence (reduce with soft or pourable liquid
diet ce) weeks postop, no pacifier, use of arm restraints, feeding by sippy-cup or
syringe
™LATE - fistulae (various types), velopharyngeal insufficiency, maxillary growth
disturbance
B. ISOLATED CLEFT LID - is not a fusion failure problem; it arises from the inability to
maintain an epithelial bridge in an area that is deficient in underlying mesoderm, which
is normally contributed by the maxillary and nasal processe; ultimately, a breakdown of
the epithelium occurs, and a cleft lip is present; clefts of the lip are more common in
males.
- most cleft lips occur at a typical location in the upper lip where one of the philtral
columns normally lies, and they extend into the nose; the deformity involves the mucosa,
orbicularis oris muscle, and skin; the nasal deformity is characterized by a slumped and
widened ala (nostril) that is posteriorly misplaced at its base; the nasal floor is
nonexistent in complete clefts and the nasal septum is deviated.
- the cleft lip can extend into the gum partially or completely through the alveolus,
creating a bony defect; the cleft lip deformity affects the nose as well as the lip, and
therefore both of these structures must be addressed in the reconstruction of the
deformity.
= EPIDEMIOLOGY - in males, cleft lips most commonly occur on the left side; there is a
0.1% overall risk of cleft lip with or without cleft palate in the general population.
“ASIANS = 2/1,000 «CAUCASIANS =1/2,000
*AFRICAN AMERICANS = 0.5/1,000
- 21% of patients with cleft lip have associated congenital malformations; cleft !ip
formation is most likely influenced by a patient’s genetic make-up but is multi-factoriai.
= RISK FACTORS
*Malnutrition during pregnancy * Phenytoin «Steroids
«Tobacco eAlcohol «Accutane
= PATHOPHYSIOLOGY - patients with cleft lips have altered anatomy, including a shart
philtrum with one or both of the philtral columns affected as well as an abnormal
orbicularis oris which is inserted into the cleft margin and alar wing; the patient will have
a predictable pattern of nasal deformities including a caudally dislocated nasal septum
separated from a displaced anterior nasal spine of the maxilla, a shortened columella,
attenuated flattened lower lateral nasal cartilage on the cleft side with the flared alar base,
and an inferiorly rotated upper later nasal cartilage; also, patients with cleft lips inherently
will have some degree of alveolar cleft with potential for collapse of the maxillary arc
and class III malocclusion (the maxillary teeth sit posterior to the mandibular teeth); these
hard and soft tissue anatomic changes translate to the various changes in appearance,
speech, and swallowing/feeding seen in cleft lip patients.
= CLASSIFICATION
*MICROFORM CLEFT OF THE UPPER LIP - occurs when the patient has incomplete
separation of the lip with distortion but not separation of the white roll/vermillion border,
dehiscence of the orbicularis oris muscle with minimal or no overt clefting of the
epidermis of the upper lip.
*INCOMPLETE CLEFT LIP - has lip separation through the white roll/vermillion borcer
and often a downward displacement of the ala but an intact nasal sill with a fibrous band
called a Simonart band; a complete cleft lip has complete separation of lip and nasal sill;
often associated with an alveolar cleft because the lip and primary palate share the same
embryologic origin; it involves a through-and-through defect of skin, muscle and mucosa

10
of the lower> aspect of the li P
but does not extend superiorly through the entire height of
Pp; an incomplete cleft lip involves only a portion of the vertical height of the lip,
the lip;
with
a variable segment of continuity across the cleft region; the variable
continuous segment
may present as a simple muscular diastasis with intact overlying skin or as
a wide claft
with only a thin band of skin that crosses the region of the cleft.
SIMONART BAND - a bridge or bar of lip tissue of variable size that bridges the cleft gzp;
usually consists of skin only, although some histologic studies have shown that some
muscle fibers lie within the band; unilateral clefts of the lip should include a designation
of whether the right or the left side is involved.
*COMPLETE CLEFT LIP - involves the entire vertical thickness of the upper lip; often
associated with an alveolar cleft because the lip and primary palate share the same
embryologic origin; the defect is up to the vestibule; a cleft of the alveolus is almest
always associated with complete clefting of the upper lip.
*UNILATERAL CLEFT LIP DEFECT - orbicularis oris muscle is directed superiorly in
complete cleft or is hypoplastic in incomplete cleft; floor of nose communicates with oral
cavity; maxilla is hypoplastic on cleft side; lower lateral cartilage is inferior on cleft side;
nasal ala is retrodisplaced on cleft side; nasal columella is displaced toward normal sic!z;
dome is lowered, horizontal nares on cleft side; cartilaginous nasal septum and nasal
Spine are deflected away from cleft; alveolar defect passes through developing dentition
- the cleft is more common on the left side (70%), although no more extensive.
*BILATERAL CLEFT LIP DEFECT - the floor of the nose communicates with the oral cavity
bilaterally; central part of alveolar arch is rotated forward and upward; prolabium skin for
the lip is underdeveloped; central lip has no muscle or vermilion; nasal columella is shcrt,
nasal tip is widened, cartilaginous nasal septum and nasal spine are deflected forward.
- if both sides of- lip development are cleft, prolabium often protruding.
- the primary difference between the unilateral and bilateral cleft deformities lies in the
position and characteristics of the medial segment of the cleft, namely the premaxilla and
prolabium; the lateral segments of the bilateral cleft lip deformity are similar to those of
the unilateral deformity.
- in bilateral deformities, the premaxilla is either partially or completely detached from
both maxillae; the premaxilla and prolabium protrude anteriorly and superiorly and
generally are unrelated to the maxilla itself; the columella is most often shorter than
normal and may not even be evident on surface inspection.
®INCOMPLETE BILATERAL CLEFT LIP - there is usually some skeletal continuity
between the lateral maxillary processes and the central premaxilla; there is often little or
no protrusion of the premaxilla.
& COMPLETE BILATERAL CLEFT LIP - the central premaxillais totally detached fram
each lateral maxillary process and may result in a “locked out” premaxilla.
TREATMENT - surgical decisions should be based on careful analysis of the defects; the
goals are restoring function such as lip closure, nasal airway, normal speech, eustachisn
tube function, and useful dental occlusion in addition to maximizing symmetry of the Sip,
nose, and midface.
*RULE OF TENS - primary lip repairs are done when the child meets the rule of tens.
™At least 10 wks of age - at 10 weeks, there is an increase in size of the lips and nose,
sufficient time for counseling and determination of other abnormalities; at 10 weeks,
there is an increase in size of the lips and nose, sufficient time for counseling and
determination of other abnormalities. ms
®Child of at least 10 Ibs - this is usually done at 3 months of age after the child shows
sufficient weight gain; this timing permits a potentially safer anesthetic administration.
® Minimum Hgb level of 10 gm/DI

tt
*GOALS OF THE REPAIRS - an anatomic reconstruction with minimal scarring and
normal function; in general, the skin around the cleft is cut into flaps that are brought
together in a way that will give adequate length to the lip and restore the continuity of the
orbicularis musculature.
*PREOPERATIVE EVALUATION
» Width of cleft and deficient lip elements » Extent of nasal deformity
®Columellar dimensions »Premaxillary protrusion
*SURGICAL/AESTHETIC SUCCESS IS DEPENDENT ON
® Extent of deficiencies of bone, cartilage and soft tissue
® Surgical skill and technique
» Attention to details, such as racial characteristics, biology of scar formation, parent
education, and cooperation in postoperative care.
*SURGICAL REPAIR - there are many techniques for repair of a cleft lip, but most are a
variation of the rotation-advancement repair; bilateral defects may be staged within
months; varying degrees of primary rhinoplasty can be performed at the time of primary
cleft lip repair.
®LIP ADHESION - produces an incomplete cleft, performed at 2-4 weeks for severe clefis;
reduces tension when definitive repair is performed (postponed to 4-6 months), scar band
may interfere with definitive repair.
®TENNISON-RANDALL’S TRIANGULAR TECHNIQUE
™MILLARD’S ROTATION-ADVANCEMENT TECHNIQUE - the most common technique for
cleft lip repair; it entails the downward and lateral rotation of the medial segment of the
cleft lip combined with the medial advancement of the lateral cleft segment into the
defect; all cleft lips have a discrepancy between the vertical height of the lip from ‘ne
Cupid's bow peak to the columellar base on the cleft and noncleft sides of the lip (philtral
ridge height).
FOLATE - has been found to be preventative for cleft lip formation.
C. CLEFT LiD-CLEFT PALATE - is the most common deformity, due to the earlier insult
to the lip; it is more common in males (75%); the more severe the defect, the more males
are affected; cleft defects are bilateral in 80% of patients and unilateral in 20%; about
85% of bilateral cleft lips and 70% of unilateral cleft lips are associated with cleft palate;
cleft defects are left-sided in 75% of cases and right-sided in 25%; cleft lip is not always
complete.
INCIDENCE - ethnic factors also affect the incidence of cleft lip and palate.
“ASIANS = 1/500 *NATIVE AMERICANS = 1/300
*BLACKS = 1 / 2,500
CLINICAL FEATURES - in infants, there is considerable difficulty in nursing, as it is not
possible to close the lips and shut off the palate; food escapes through the nose, and the
child tends to aspirate milk into the trachea.
- infections of the upper and lower airways occur due to disordered swallowing and
respiratory physiology; abnormal tubal function leads to serous otitis media, chronic
otitis media, and conductive deafness.
SPEECH DEFECTS:
*Rhinolalia aperta *Lisping
*Abnormal articulation *Velopharyngeal insufficiency
VELOPHARYNGEAL INSUFFICIENCY (VPI) - is a disorder resulting in the improper closing of
the velopharyngeal sphincter (soft palate muscle in the mouth) during speech, allowitig
air to escape through the nose instead; although clinical signs vary, the symptoms of
velopharyngeal dysfunction are similar to those of a cleft palate.

42
*®Hypernasal speech (especially noted in the articulation of pressure consonants such
as p, b, d, t, h, v, f, ands
*» Conspicuous constricting movement of the nares during speech
* Inability to whistle, gargle, blow out a candle, or inflate a balloon
*»Loss of liquid through the nose when drinking with the head down
» Otitis media ® Hearing loss
- during speech, the velopharyngeal sphincter must close off the nose to properly
pronounce pressure consonants.
- to close off the nose from the mouth during speech, several structures come together
to achieve velopharyngeal closure
*Velum (soft palate or roof of the mouth) » Lateral pharyngeal walls
» Posterior pharyngeal wall).
- if the velopharynx is not closed, snort sounds may be produced through the nose or
you may hear air coming out of the nose during speec; improper function of this structure
also produces a nasal tone in the voice.
- there are anomalies of occlusion and position of the teeth; the nose is almost always
involved,
= PATHOGENESIS - the cause is probably multifactorial.
*EMBRYONIC DAMAGE - is caused by:
™ Hypoxia »Embryopathy »>Toxins
™Vvirus infections in the mother »Genetic lesions
eFAMILIAL CLUSTERINGn- irregularly dominant.
= COMPLICATIONS
eABNORMAL MIDFACE DEVELOPMENT - clefts of the primary palate usually have
underdeveloped maxillary alveolar arches and facial growth is abnormal.
*VELOPHARYNGEAL INCOMPETENCE .- cleft patients have an _ incompetent
velopharyngeal valve, which results in nasal regurgitation while swallowing; even after
palate repair, velopharyngeal function may not return entirely to normal, and speech
therapy is often helpful.
*SPEECH DEFECTS - "typical cleft palate speech “ - nasal escape of air (heard as
snorting or grunting), a hypernasal quality, and difficulty with consonants; normal infants
begin to develop consonants in speech at age 9 months, which influences the timing of
operative repair of cleft palate.
eABNORMAL EUSTACHIAN TUBE FUNCTION’ - the cleft palate patients have a
"functional" obstruction of the tube at the nasopharyngeal end - as opposed to the
“mechanical” obstruction found in serous otitis patients.
TREATMENT - is a long-term commitment.
MEDICAL TREATMENT - will largely focus on requirements from any concomitant congeniial
abnormalities and based on nutritional needs.
*NAM (Nasoalveolar molding) - can be employed with assistance from an orthodontist
within the first few weeks to months of life; it involves the creation of an orthodontic
appliance that molds a protruding segment and alveolar process into a more favorable
position; this allows for repositioning of the alveolar segments, medialization of the ajar
base, and columellar lengthening, which allows for easier surgical repair of cleft lip 2d
nasal cleft deformity down the line; these require frequent adjustments by the
orthodontist.
*LIP TAPING - often performed in patients with less severe clefts
eLIP ADHESION - approximation of the cleft lip edges without changing lip landmarks or
disturbing tissue required for definitive closure, often used in patients with wide clefts
who are poor NAM candidates for social or geographic reasons.

13
SURGICAL TREATMENT - surgical intervention for initial cleft lip usually occurs at 3 to 5
months of age.
*SURGICAL TECHNIQUES FOR PRIMARY REPAIR OF CLEFT LIPS
® UNILATERAL CLEFT LIP
=Millard repair rotation advancement «Fisher repair =Mohler repair
» BILATERAL CLEFT LIPS - Mulliken repair
*COMMON GOALS IN ALL REPAIR
®To reestablish a competent orbicularis oris muscle
®Lengthen the philtrum and lip » Minimize visible scarring
*USUAL TREATMENT SEQUENCE
™Lip adhesion » Definitive lip surgery
® Hard and soft palate closure » Orthodontic expansion
“TIMING - in view of these complications, the reconstructive surgeon is faced with timing
the cleft repair so that hearing and speech are optimized, but effects on midface growth
are minimized; these are performed at specific times corresponding to the developmenial
stage of the patient:
LIP ADHESION - is done at 2-4 weeks of age, provided that there are no medical
contraindications.
™®CLEFT LIP REPAIR - if a lip adhesion is not indicated, cheiloplasty is performed when
the patient is as young as_ 6-8 weeks of age, assuming that the following conditions are
met:
EThere are no medical contraindications =Pediatric anesthesia expertise is available
eSurgical field magnification is available
- surgical closure of a cleft lip is usually performed by 3 mos of age, when the infant has
shown satisfactory weight gain and is free of any oral, respiratory, or systemic infectioz.
CLEFT PALATE REPAIR- is usually scheduled at approximately 8 to 12 months of age;
palate repair should be completed before the child is 2 years of age so that the child has
the structure to create normal sounds as he or she develops speech.
BSURGERY ON PALATE - best done after the deciduous molars are in proper occlusicn
#SURGERY FOR SMALL CLEFTS - done earlier at 12-18 months of age
aSURGERY ON LARGER CLEFTS - done at 18-24 months of age, with occasional deiay
to 30 months of age
nSURGERY ON ISOLATED SOFT PALATE CLEFT - done at 6-12 months of age
*ADDITIONAL SURGERY AFTER CLEFT REPAIR - when there has been unfavorable
healing of a cleft lip repair, secondary correction of the lip can be accomplished hy
re-creating the defect and closing it with a more satisfactory alignment; additicnal
procedures may be required for particularly severe cleft lip deformities; the initial repair
may be revised at 4 or 5 years of age.
™Z-PLASTY - some children born with a cleft palate will have nasal speech despite
closure of the palate; Z-plasty may be done to make the soft palate longer and decrease
nasal escape of speech sounds.
®PHARYNGEAL FLAP - involves raising a flap of tissue from the back wall of the threat
and attaching it to the soft palate; the flap deflects some of the air that used to leak out
the nose.
® TRANSPLANTING TISSUE FROM THE LOWER LIP TO THE UPPER LIP
*INDICATIONS FOR ADDITIONAL SURGERY
= Speech problems not resolved with speech therapy
™Improve the way the nose or lip look fon
™ Provide support for the teeth where the gum ridge is affected
*PLASTIC PROCEDURES TO IMPROVE SPEECH - plastic closure of the cleft is intended
i aa
A

W4
to improve the speech and articulation and is successful in 70% of cases; secondary
procedures may be needed for speech improvement in 15% of cases
*METHODS OF TREATMENT
» ADEQUATE FEEDING - is the first priority in managementt of the newborn with a cleft
lip/palate; infants with clefts of the primary palate only generally have little or no
difficulty with feeding; clefts of the secondary palate are associated with feeding
problems and may require special techniques and devices to achieve adequate feeding;
in general, the wider the palatal cleft, the more difficult feeding may be.
- infants with a cleft palate are limited in their ability to suck; the common cavity between
the nose and the mouth allows air to leak as the infant tries to suck; cleft lip alone usually
does not cause feeding problems.
- a number of strategies have been devised, and different feeders have been created for
feeding the infant with a cleft palate; generally, breast feeding is ineffective; alternately,
expressed (pumped) breast milk can be delivered using one of the specialized feeders.
MOST COMMONLY USED CLEFT PALATE FEEDERS
=aMead Johnson ®Dr. Brown's
"Haberman =Pigeon bottles
- each allows for parent-controlled delivery of the meal (expressed breast milk or
formula}; parents and caregivers need to be taught how to use the feeder properly and
should be observed for the first feeding to ensure proper use; trial and error may be
needed to discover the best technique and feeder for the infant.
- a variety of cleft palate nipples are available that allow for more posterior placement of
the milk and decrease the need for generating high negative pressures,
=Montgomery nipple =Preemie nipple
- the infant should be fed in the slightly upright position; children with cleft palate
generally swallow much more air during feeds; frequent burping often is necessary,
which should be explained to parents; attention should be paid to the child's growth;
following weight and length gains using standardized growth charts is very useful to
ensure that the infant stays on the appropriate growth curves.
® LIP ADHESION - is a preliminary procedure indicated in a patient with a wide unilateral
cleft lip in which performing a cheiloplasty could be done only under excessive tension;
if the child presents with a very wide cleft lip and palate, it will be advantageous to help
the cleft to become narrower, thereby facilitating the surgical outcome of the cleft lip
repair; the goal of a lip adhesion is to surgically convert a complete cleft lip into an
incomplete cleft lip, allowing the definitive lip repair to be performed with less tension.
®CHEILOPLASTY - is performed to close the opening in the lip caused by this birth
defect; if the cleft is bilateral, closure may be performed on both sides simultaneousiy,
or the surgeon may repair the lip one side at a time in separate surgeries.
»® CLEFT LIP RHINOPLASTY -is necessary in patients with cleft lip deformities of the nose
to improve nasal function and correct the distortion; in the case of a severe nasal
deformity, reconstructive rhinoplasty may be done in the child's early years.
- in other cases it is recommended that the operation be performed in the child's middle
teenage years, when the nose has attained its maximum growth; secondary surgery to
achieve optimum reconstruction is common,
- corrective surgery on the nose may be delayed until adolescence; nasal surgery can
also be performed at the time of the lip repair.
™PHARYNGOPLASTY - is performed with formation of a velopharyngeal flap; the soft
palate is brought into contact with the posterior pharyngeal wall using a soft tissue flap;
the principle of pharyngoplasty is to restore the function of the short, immobile,
insufficient soft palate to as near normal as possible.

1
=Autogenous or synthetic material is implanted to achieve protrusion of the posterior
wall of the pharynx, supplementing the Passavant’s pad by forming a prominence on the
posterior pharyngeal wall during contraction of the superior constrictor muscle.
=The soft palate is displaced posteriorly. .
=» PALATOPLASTY - methods for repairing a cleft palate may vary widely in terms of when
they are performed and what techniques are used; the repair of a complete cleft palate is
generally performed in two operations; many surgeons prefer to close the posterior
palate either at the time of lip repair or when the child is one year of age or older.
- approximately three to six months later, the entire palate is repaired by lengthening it to
close the defect and prepare it for speech; however, later revisions are often needed by
children because of scarring and impaired growth of the palate.
is a
- communication (fistula) between the oral cavity and the nose or maxillary sinus
sequela of cleft palate procedures and requires surgical closure; an additional operation,
a bone graft commonly from the skull, hip or rib, may be required to replace missing bone
in the roof of the mouth, or gums (alveoloplasty).
- cleft palate patients may also have abnormal movement of the speech mechanism in the
back of the throat; as they grow older and begin to speak, air may escape from the nostrils
in an abnormal way and cause hypernasality; a surgical procedure known as a
pharyngeal flap palatoplasty is done to correct this deformity and permit normal speech;
optimal speech develops when an intact palate is achieved by 12 months of age; fhe
goal is to repair both hard and soft palates in one operation by this time.
CRITICAL FACTORS
=PALATAL SHELF WIDTH - determines the amount of tissue available for cleft closure.
=BODY WEIGHT - 15 Ibs or greater being optimal
BABSENCE OF MEDICAL CONTRAINDICATIONS
- for complete secondary palate clefts with cleft lip, these conditions are met by the
time the patient is 9-12 months old; for infants with secondary palate clefts only,
palatoplasty is performed at a slightly earlier age, usually 8-12 months.
= RECURRENT RISK RATES FOR FUTURE OFFSPRING
CLEFT LIP +/- ISOLAYED
CLEFT PALATE CLEFT PALATE
Parents normal, one child affected 44% 2.5%
One parent, no affected children 3.2% 6.8%
One parent, one affected child 15.8% 14.9%
1. OSEER-RENDU-WEBER SYNDROME
(HEREDITARY HEMORRHAGIC TELANGIECTASIA- HHT)
- an autosomal dominant multisystem vascular disorder that causes variable cutaneous
and mucosal telangiectasia formation, as well as AV malformations in the lungs, brain,
and liver.
- there are multiple localized angiomata on the skin, particularly in the circumoral region,
and the skin of the cheek, fingers, the nasal orifice and the ear; it is characterized by the
appearance of multiple telangiectasias on the face, mouth, lips, tongue and other areas.
- it is transmitted as a non-sexlinked simple dominant Mendelian characteristic; lesions
may be presentin childhood but more often appear in puberty and become progressively
worse with increasing age.
- the typical lesion is a cherry-red, non-elevated macule that resembles a crushed spider;
the lesions blanch on pressure and regain their color when the pressure is removed;
the telangiectatic areas are nonpulsating; these often give rise to profuse hemorrhage
either spontaneously or as a result of trauma.

A®
- the oral lesions do not often bleed, but the bleeding may occur without any known or
apparent injury or irritation; severe oral hemorrhage may be experienced several times
a day for weeks; as the affected individual grows older, the bleeding episodes tend to
increase in frequency and intensity; most patients have a low hemoglobin as a
manifestation of the iron deficiency anemia caused by the hemorrhage.
TREATMENT - laser ablation of symptomatic lesions; supportive treatment includes
supplemental iron therapy for iron deficiency anemia.
TY. HERPES LABIALIS (ORAL HERPES SIMPLEX)

- 80-90% of persons over 50 years are seropositive for HSV-1, although 20-40% of the
population experience herpes simplex labialis: vesicular herpetic lesions on the lips or
around the mouth caused by type-1 virus.
DEFINITION - an infection caused by the herpes simplex virus, characterized by an
eruption of small and usually painful blisters on the skin of the lips, mouth, gums, or
the skin around the mouth.
CAUSES AND INCIDENCE - herpes labialis (cold sores, fever blister) is the most common
manifestation of recurrent HSV-1 infection; the most common site of herpes labialis is tne
vermilion border of the lip, although lesions sometimes occur on the nose, chin, cheek,
or oral mucosa.
- at least 1 out of 1,000 people may be affected with this virus; most people have been
affected with the type 1 virus by the age of 20; the incidence of primary infection is
greatest during childhood when 30-60% of under 20’s are exposed to the virus through
intimate contact with the infected secretions of a virus carrier.
- in most cases, initial infection occurs in childhood and has its manifestation in the oral
cavity; the initial infection may cause no symptoms or mouth ulcers; the virus remains in
the nerve tissue of the face; in some people, the virus reactivates and produces recurrent
cold sores that are usually in the same area but are not serious; herpes virus type 2
causes genital herpes and infection of babies at birth; both viruses are contagious;
contact can occur directly, or through contact with infected razors, towels, dishes, etc.;
the herpes virus can also infect the fetus and cause congenital abnormalities.
= PATHOGENESIS - primary infection with HSV-1 most commonly occurs by inoculation of
the oral mucosa; this epithelium is not protected by a full stratum corneum and loss of
mucosal integrity with opportunities for introduction of the virus occur frequently from
microtrauma associated with mastication; the primary infection may be asymptomatic or
a fulminant gingivostomatitis may ensue; the factors that determine the severity of t!:e
primary infection are unknown; the immune response to primary infection coud
determine the subsequent susceptibility of individuals to recurrent herpes labialis.
- recurrent herpetic disease is most likely to be the consequence of reactivation of virus
from sites of latency in neural ganglia and descent of virions through sensory nerve
axons to reinvade the peripheral epithelium; internal reinfection of the epidermis evolves
within a few hours to fully developed, vesicular herpes labialis lesions.
A. PRIMARY HERPES SIMPLEX DISEASE
1. PRIMARY HERPETIC GINGIVOSTOMATITIS - primary oral infection with HS\-1
usually occurs by viral inoculation of the oral mucosa, and may be asymptomatic or
present as fulminant gingivostomatitis; transmission is dependent on intimate, personal
contact with someone excreting HSV; gingivostomatitis and pharyngitis are the mest
frequent manifestations of first-episode HSV-1 infection; infection occurs mest
commonly in children between ages 1 and 5 years; it is rarely seen in adults.
- the incubation period is 3 to 12 days; although most cases are mild, some are severe;
sore throat and fever may precede the onset of painful vesicles occurring anywhere in

a
the oral cavity or on the face; the vesicles rapidly coalesce and erode with a white, then
yellow, superficial, purulent exudate; children are unable to swallow liquids because of
the edema, ulcerations, and pain; tender cervical lymphadenopathy develops; fever
subsides in 3 to 5 days, and oral pain and erosions are usually gone in 2 weeks; in severe
cases, they may last for 3 weeks.
- the virus must come in contact with mucosal surfaces or abraded skin, where it
replicates and initiates infection; HSV-1 is spread primarily via direct contact with
contaminated secretions or saliva.
SYMPTOMS - this first exposure to herpes virus results in a systemic illness; it starts
with small vesicles on an erythematous base on the tongue, gingival mucosa, and
anterior palate, and it progresses to painful ulcerations with a gray or white base;
perioral skin is often involved; it persists for 7-14 days although the fever persists for
only 2-6 days.
*SKIN LESION/RASH - located around the lips, mouth, and gums
*SMALL VESICLES (BLISTERS) - 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 about 2-4 mm in diameter, painful, covered
by a yellowish pseudomembrane, and surrounded by a red margin; the intact vesicie
rarely lasts for more than 24 hours; the vesicles quickly rupture leaving shallow, round
discrete ulcers surrounded by inflammation.
- as the disease progresses several lesions may coalesce, forming some large irreguiar
lesions; after 10-14 days, the primary infection subsides without scar formation.
eGENERALIZED ACUTE, MARGINAL GINGIVITIS - is an important diagnostic criteria in
this disease; several small gingival lesions are often present.
eINFLAMMATION OF THE POSTERIOR PHARYNX
*ENLARGED AND TENDER SUBMANDIBULAR AND CERVICAL LYMPH NODES
*FEVER - may precede appearance of blisters and ulcers by 1 or 2 days
*lrritability *Pain in the mouth ¢Drooling
«Dysphagia *Malaise Dehydration
*Nausea *Somnolence ¢Fetor
eConvulsions ¢Decreased food intake
TREATMENT - the virus cannot be eliminated; early treatment with antiviral medication
is necessary to decrease the viral load; treatment is usually symptomatic to relieve the
pain and maintain oral hygiene; if untreated, the symptoms will generally subside in 7-to
2 weeks; despite clinical resolution, viral shedding takes place and these individuals can
be a source of infection.
*ANALGESICS - e.g. paracetamol, ibuprofen
*LOCAL ANALGESICS - their duration of action is short-lived.
e.g. benzamine hydrochloride mouthwash, 5% lidocaine ointment
*CHLORHEXIDINE MOUTHWASH OR GEL - helps prevent bacterial superinfection of the
ulcerated areas
*ANTIVIRAL AGENTS - are given in severe cases, especially in adults and
immunocompromised patients; they may shorten the course of the symptoms and
decrease pain. Bi
® ACYCLOVIR = 15 mg/kg/dose up to 200 mg/dose 5x a day for 7-10 days, when started
within the first 72 hours, with decreased duration of symptoms and significantly
decreased time of viral shedding.
& CYTOSINE ARABINOSIDE (Ara-C) » ADENOSINE ARABINOSIDE (Ara -A)
»IDOXURIDINE (IUDR) »PENCICLOVIR »FAMCICLOVIR
PRIMARY INFECTION = 5 x 200 mg acyclovir per day orally is required.

18
REACTIVATED INFECTION - topical application of penciclovir or acyclovir is necessary; local
aseptic treatment to avoid bacterial infection is required.
*ENRICHED LIQUID DIET- a mostly liquid diet consisting of cool to cold, nonacidic drinks
should be provided while the child's mouth is very sore.
*SUPPORTIVE THERAPY
® Apply ice or a warm washcloth to the sores to help ease pain
®Wash the blister gently with antiseptic soap and water to help prevent spreading the
virus to other body areas
Rest » Gentle oral hygiene
=PROGNOSIS - the disease is self-limiting and does not often recur; however, certain
patients suffer from recurring infections; complications are a bacterial superinfection
with staphylococci or streptococci.
2. INCCULATION HERPES SIMPLEX - is not uncommon in physicians, dentists, and
dental hygienists; the virus in the saliva of a patient penetrating through an abrasion of
the skin.
B. SECONDARY HERPES SIMPLEX DISEASE
HERPES SIMPLEX LABIALIS (COLD SORES OR FEVER BLISTERS) - roughly 20-40% of the
population will experience labial or perioral outbreaks of vesicular herpetic lesions; the
frequency of these outbreaks is extremely variable, ranging, in some individuals, froin
rare episodes every 5-10 years, to monthly or more frequent outbreaks among a small
proportion of subjects; the severity of the illness is most often mild, although
uncomfortable and cosmetically disfiguring.
- oral HSV-1 infections recur more often than oral HSV-2 infections; recurrent oral herpes
simplex can appear as a localized cluster of small ulcers in the oral cavity, but the most
common manifestation consists of eruptions on the vermilion border of the lip; fever
(fever blisters), URTIs (cold sores), and exposure to UV light, among other things, may
precede the onset; the course of the disease in the oral-labial area is the same as itis in
other areas.
- immunosuppressed patients are at greater risk of developing lesions on the lips, in the
oral cavity, and on surrounding skin; lesions may also appear on the upper lip and chin;
many experience a decrease in the frequency of recurrences, but others experience an
increase; a history of recurrent herpes labialis is present in 38 of college students; the
prevalence of asymptomatic excretion of HSV following recurrence varies from 1-5% in
adults.
<= PRODROMAL SYMPTOMS (precede the local lesions by 1-2 days) - experienced by 46-60%
of patients; approximately 25%of herpes labialis outbreaks “abort” (i.e., they do not
progress beyond prodromal symptoms or the papule stage)
*WARNING SYMPTOMS
® Itching of the lips or skin around the mouth ® Burning near the lips or mouth area
® Tingling near the lips or mouth area
*BEFORE THE BLISTERS APPEAR
® Sore throat » Fever » Swollen glands
® Painful swallowing Malaise » Increased sensitivity
»Pain ™ Headache
= CLINICAL APPEARANCE - after a prodromal period, the lesion generally begins as a small
grouping of erythematous papules that over a few hours progress to create a small, thin-
walled vesicle; approximately 25% of episodes will have no prodromal stage and will
present directly as vesicles; within 48 hours the vesicles rupture and coalesce to leave
erosions; the vesicles may form shallow ulcers or become pustular; the short-lived ulcer
dries and develops a crusted scab; complete healing without scarring occurs with

19
reepithelialization of the ulcerated skin, usually within 7-10 days; some patients
experience local lymphadenopathy but no constitutional symptoms; the virus may
become latent, residing in the nerve cells, with recurrence at or near the original site
although the recurrence is usually milder.
- reactivation may also involve the oral mucosa (recurrent intraoral herpes) with vesiclos
developing which burst to leave a cluster of oral ulcers; their distribution tends to he
localized and unilateral.
- lesions usually develop on the lower lip, but can also occur at a variety of locations an
the face, such as upper lip, nose, or chin; and oral cavity, such as on the gingivae, tongue,
or buccal mucous membranes. ;
STAGES - the classical lesion develops through theses 8 stages over a period of 10 days.
*DEVELOPMENTAL STAGES
™Prodrome Erythema » Papule
*SIGNIFICANT STAGES - the time of greatest lesion severity is when the vesicle ruptures
and becomes an ulcer; decreases in severity occur with formation of the hard crust and
with loss of crust; during the hard crust stage, there is little change in lesion size, hut
lesion pain and virus shedding decline sharply.
Vesicle (blister) »>Ulcer »Crusting
*FINAL STAGES
=» Dry flaking ® Residual swelling
- the lesions of herpes labialis tend to occur on the outer 1/3 of the lips and the lower tip
is more frequently involved than the upper lip; 2/3 of labial lesions are on the vermilion
border, and the other third at the junction of the border with the skin.
- lesions are most often single and “secondary lesions”, those appearing one or more
days after the first sore, develop in 1/5 of cases.
- from episode to episode, lesions commonly cross the midline of the face or move from
one lip to the other if the patient suffers frequent episodes; whereas among those with
infrequent lesions, the lesion location generally remains the same.
= PRECIPITATING FACTORS
*MOST COMMON FACTORS - DESCENDING ORDER OF FREQUENCY
» Emotional stress Illness » Bright sunlight
Trauma Fatigue ™» Menstruation
®Chapped lips » Season of the year (extreme cold weather)
*OTHER FACTORS
»Immunosuppression Food =»Colds
® Psychosomatic factor » Fever
*HEALTH CARE PROCEDURE TRIGGERS
=Fever therapy ® Trigeminal ganglion surgery
® Oral trauma from dental manipulation
Epidural administration of morphine for analgesia
= IDENTIFICATION OF THE HERPES VIRUS (either the primary or recurrent form)
“VIRAL CULTURE VIRAL DNA TEST
*TZANCK TEST - to check for HSV eFLOURESCENT ANTIBODY EXAMINATION
*CYTOLOGIC STUDY (Giemsa smears)
<TREATMENT - a number of treatment modalities have been used for herpes on the
vermilion border; because lesion development occurs so rapidly, antiviral therapies
administered at clinical onset tend not to significantly effect lesion severity or frequency
of aborted lesions, unless used in the prodromal or erythema stages; herpetic stomatitis
is seldom treated with drugs, because the drugs are expensive and the condition usually

£0
eek away without treatment; if untreated, the symptoms will generally subside in 1 to 2
weeks.
*TOPICAL PENCICLOVIR 1% OR ACYCLOVIR 5% - must be started as soon as symptoins
begin, to be of any benefit; it can reduce the duration of the outbreak and reduce viral
shedding.
- the cream is applied frequently (e.g., every 2 hours while awake) at the first sign of
prodromal symptoms or erythema; these creams may shorten an episode of herpes
labialis by a few hours or a day and may not be worth the high cost; many patients believe
that these creams are effective and prefer them to oral medication.
*ORAL ANTIVIRALS - have a modest clinical benefit only if initiated very early after
recurrence; they may be of value in patients whose recurrences are associated with
protracted clinical illness; they may shorten the course of the symptoms and decrease
pain; they can alter the severity of sun-induced reactivation; short-term prophylactic
treatment may help patients who anticipate high-risk activity (e.g., intense sunlight
exposure); intermittent administration does not alter the frequency of subsequent
recurrences.
™® ORAL ACYCLOVIR - has been found to be effective in the treatment of herpes labialis,
albeit with a relatively small degree of clinical benefit. = 200 mg given 5 times a day if
herpes labialis develops near the eye.
®» FAMCICLOVIR *™VALACYCLOVIR
*COMBINATION TREATMENT - CORTICOSTEROIDS WITH ORAL ANTIVIRAL AGENT -
may be beneficial for episodic treatment of herpes labialis; Valacyclovir (500 mg two
times a day for 3 days) and topical fluocinonide (0.05% three times a day for 5 days)
significantly reduced lesion size and pain.
*The lips should be protected from sun exposure with an opaque cream such as zinc
oxide or with sun-blocking agents incorporated into a lip balm (e.g., ChapStick); a ccol
water or Burow’s solution compress decreases erythema and debrides crusts to promote
healing; lubricating creams may be applied if the lips become too dry.
*TOPICAL ANESTHETICS AND MOUTHWASHES - an oral topical anesthetic (viscous
lidocaine) is available for severe pain; it must be used with care as it masks all sensation
and may interfere with swallowing and allow the child to burn him- or herself on hot
liquids without knowing it; a few rare deaths have been reported from overdosage ad
misuse of lidocaine.
*AVOID HOT BEVERAGES, SPICY AND SALTY FOODS, AND CITRUS
= COMPLICATIONS
*HERPETIC KERATOCONJUNCTIVITIS - a secondary herpes infection in the eye, may
develop; herpes infection of the eye is a leading cause of blindness because it causes
scarring of the cornea.
*DEHYDRATION - may develop if the child refuses to eat and drink adequately because
of a sore mouth.
*SPREAD OF HERPES TO OTHER SKIN AREAS
*SECONDARY BACTERIAL SKIN INFECTIONS
*RECURRENCE OF HERPES LABIALIS
*GENERALIZED INFECTION - may be life threatening in immunosuppressed people,
including those with atopic dermatitis, cancer, HIV infections.
PREVENTION - it is estimated that approximately 80% of the population carry herpes
simplex virus; it is difficult to prevent children from picking up the virus at some tire
during their childhood.

21
*Avoid direct contact with herpes sores; children should strictly avoid close contact with
people with cold sores (such as kissing parents with active cold sores) and avoid other
children with herpetic stomatitis.
*Apply sunblock or lip balm containing zinc oxide to the lips before going outside.
*Apply a moisturizing balm to prevent the lips from becoming too dry.
*Wash items such as towels and linens in boiling water after each use.
*Do not share utensils, straws, glasses, food or other items with actively infected people.
*Avoid precipitating causes (especially sun exposure) if prone to oral herpes.
PATIENTS WITH SEVERE OR FREQUENT RECURRENCES - Acyclovir = 200 mg t.i.d. for 6-9
months.
TV. OROPHARYNGEAL SQUAMOUS CELL CARCINOMA (OPSSC)

- the oropharynx is a common site for the presentation of upper aerodigestive tract
malignancies, more than 90% of which are histopathologically squamous cell carcinoma;
it is a disease of increasing age with 95% of cases in people older than 40 years old; it
predominantly occurs in males with a ratio of 2:1, with an average age of 60 years.
ORAL CANCER - refers to cancer occurring between the vermilion border of the lips and the
junction of the hard and soft palates or the posterior 1/3 of the tongue.
- it arises in gingival tissue, buccal sulcus, floor of the mouth and other portions of the
buccal mucosa; the most common site for oral ca is the lip, the frequent intraoral site for
ca occurrence is the tongue; primary ca of the lip originates on the vermilion border,
although it may be secondarily involved from a. basal cell ca beginning on the adjacent
skin; by the time of definitive diagnosis and treatment, 50% of oral ca have already
exhibited lymph nodal and distant metastasis.
- it is an invasive epithelial neoplasm with varying degrees of squamous differentiation
and a propensity to early and extensive lymph node metastases; independent from the
gross appearance, histopathologic patterns of invasion demonstrate multiple variations
as well; severe dysplasia and CIS are common elements found in association with
invasive OPSCC but are mainly seen in patients with a history of tobacco and alcohol
consumption; these are rare in the presence of HPV-associated pathology; invasive
carcinoma eliminates the regular cellular architecture and can include invasion of the
lymphovascular space, neurotropism, and infiltration of other tissue components such
as muscle or cartilage, demonstrating the aggressive behavior of the tumor; . SCC can
vary from keratinizing (KSCC) to nonkeratinizing (NKSCC) and well-differentiated to
poorly differentiated.
- macroscopically, oral cancers can be exophytic growths, flat cancers with central
ulceration and indurated edges, or deeply infiltrating ulcers; verrucous carcinoma is an
exophytic lesion that is histologically well-differentiated and has a better prognosis than
other oral cancers.
- about 40% of intraoral squamous ca begin on the floor of the mouth or on the lateral
and ventral surfaces of the tongue; about 38% of all oral carcinomas occur on the lower
lip; these are usually solar-related cancers on the external surface.
- these tumors typically present in young to middle-aged, healthy, nonsmoking and
nondrinking Caucasian males; non-HPV-associated OPSCC occurs predominantly in
adults in the 5'" and 6" decades of life with a history of smoking and alcohol abuse;
= ETIOLOGY
*DECREASED IMMUNITY- the increasing incidence of oral ca is clearly age related, which
may reflect declining immune surveillance with age; it may occur in immunosuppressed
patients following organ and bone marrow transplantation; HIV/AIDS patients are at
increased risk of oral ca.

22
*SMOKELESS TOBACCO CHEWING - is a common habit, particularly in India, parts of
Southeast Asia, the Middle East, China, and Taiwan; it is a major risk factor for
oropharyngeal cancer in these parts of the world
- the tobacco is consumed without combustion, by being placed into contact with
mucous membrane, through which nicotine is absorbed.
*SMOKING (especially >2 packs/day) - tobacco smoke contains carbon monoxide which
is an important factor in the development of oral ca; sttudy shows that cigar and pipe
smoking increase the risk of cancer than cigarette smoking; pooling of carcinogens in
saliva gives rise to cancer in the floor of the mouth and ventral and lateral tongue;
smoking is more strongly associated with soft palate carcinoma than anterior sites.
*ALCOHOL - all forms of alcohol have been implicated in the etiology of oral ca; the
mechanism by which alcohol affects includes the dehydrating effect of alcohol on the
mucosa which increases mucosal permeability and the effects of carcinogens on the
mucosa.
- risk increases dramatically when alcohol use exceeds 6 oz of distilled liquor, 15 oz of
wine or 36 oz of beer/day; the combination of heavy smoking and alcohol abuse is
estimated to raise the risk 100x in women and 38x in men.
*IONIZING RADIATION - carcinoma of buccal mucosa may occur as a complication of long
term radiotherapy.
*TRAUMA - in combination with other factors like chronic cheek biting, denture use and
irregular teeth may act as co-carcinogen and may promote transformation of epithelial
cells.
eVIRUS
®HUMAN PAPILLOMA VIRUS (HPV) - high-risk HPV 16 is identified as the oncogenic
subtype in 90% of the HPV-associated OPSCCs, but other subtypes - such as 18, 31, and
33 - an also be present; the prevalence of HPV-associated OPSCC varies from 45- 90%
across different studies depending on the method of HPV detection.
- epidemiologic studies propose that having multiple sexual partners and engaging in
oral sexual behaviors is significantly associated with HPV infection and HPV-associated
OPSCC.
*INTRAORAL LESIONS
® Chronic ulceration and fissure »®Lichen planus
® Median rhomboid glossitis ®Leukoplakia
»Plummer-Vinson syndrome
*REVERSE SMOKING
*CHRONIC IRRITATION - dental caries, , chewing tobacco, use of
® Dental caries » Chewing tobacco
»Betel nut » Overuse of mouthwash
= PATHOLOGY
EPITHELIAL PRECURSOR LESIONS - in general, precursor lesions of the oropharynx
present clinically as:
®»LEUKOPLAKIA - white patches; most white lesions do not show dysplastic cells and
relate to hyperplasia; they rarely undergo malignant transformation and may even
regress after underlying etiologic factors have been eliminated.
- it is induced by the same factors (tobacco, alcohol) that cause carcinomas; the
malignant potential of leukoplakia corresponds to the degree of cellular dysplasia seen
on biopsy
®ERYTHRPLAKIA - red patches; they can often lead to malignancy; usually shows severe
cellular dysplasia and carries a 50% risk of malignant degeneration.

23
™MIXED VARIANTS - some lesions appear as mixed variants with white and red
components. '
- erythroplakia or mixed lesions frequently display dysplasia
*HYPERPLASIA - denotes increased cell counts in the spinous layer (acanthosis) or in
the basal/parabasal layers; the cells are free of atypia, and tissue architecture is regular.
“DYSPLASIA - the presence of changes in architecture and cellular atypia, , which is
characterized by a wide range of microscopic features.
®»MILD DYSPLASIA- is defined by cytologicand lateral borders of the tongue and lower
lip and less frequently the floor of the mouth, alveolar mucosa, palate and buccal mucosa.
- it may be solitary and multifocal; nodular or polypoid and pink to red and have at least
one ulcerated patch on their surface.
- the patient may present with an awareness of a mass in the mouth and neck; small
lesions are asymptomatic; large lesions may cause some pain or paresthesia and
swelling; patients complain of a persistent ulcer in the oral cavity.
- the clinical appearance of an ulcer is one of irregular shape, induration and raised
everted edges; it usually has a broad base and may be dome-like or nodular; the surface
may range from granular to pebbly to deeply creviced; in some cases, the surface may
be entirely necrotic and have a ragged whitish gray appearance; it may be completely red
or the red surface may be sprinkled with white necrotic or keratin areas.
- the base and borders are firm to palpate and the lesion may get fixed after infiltration
into underlying tissues.
- superficial and deep cervical nodes are usually affected; they become enlarged and are
firm to hard on palpation; the nodes are non-tender unless associated with secondary
infection or inflammatory response; fixation of nodesifferentiated squamous cell
carcinoma
¢Moderately-differentiated squamous cell carcinoma
¢Poorly-differentiated squamous cell carcinoma
+ DIAGNOSIS - will be established by a biopsy.
eA PERSISTENT "COLD SORE" - may be the early lesion.
*CRUSTING, PEELING OR MILD ULCERATION - may appear early.
eLEUKOPLAKIA - is present at times.
*PAINLESS INDURATION OF THE LESION - is a characteristic finding.
STAGING OF OPSCC
*TNM GROUPING FOR OROPHARYNX SQUAMOUS CELL CARCINOMA
From Amin MB, Edge SB, American Joint Committee on Cancer: AJCC Cancer Staging.
T and N Category
Non—Human Papillomavirus- Human Papillomavirus—Associated -

Associated (p16-Positive)
(p16-Negative)
TNM Clinical and Pathologic TNM Stage Clinical TNM Pathologic TNM
Stage Stage Stage
Stagel T1iNO TO-T2NO-N1 TO-T2NO-N1
Stage Il T2NO _ T0-T2N2 or T3NO- T3-T4NO-N1 or TO-
“ N2 T2N2
Stage Ill T3NO0 or T1-3N1 T4 or N3 T3-4N2
Stage IV NA Any M1 Any M1
$$

4
T and N Category
Non-Human Papillomavirus- Human Papillomavirus—Associated
Associated (p16-Positive)
(p16-Negative)
TNM Clinical and Pathologic TNM Stage Clinical TNM Pathologic TNM
Stage Stage Stage
Stage IVA T4aNO0-N2c or T1-T3N2a-2c NA NA
Stage IVB T4bNO0-N3 or T1-T3N3 NA NA
Stage IVC Any M1 NA NA
TNM , Tumor/node/metastasis.
= TREATMENT- surgical and radiologic modes of treatment
are successful; a “v"-shaped
incision is made so as to include all the growth with a generous margin of normal tissue;
the overall 5-year survival rate for oral SCC is approximately 40%.
PRIMARY CANCER
*SURGICAL EXCISION - is the treatment of choice for most oral cancers.
®LIP - cancers of the vermilion surface of the lip are best treated with full-thickness
excision of the lip with reconstruction to maximize postoperative function; when large
areas of the lip exhibit premalignant change, the lip can be surgically shaved, or a laser
can remove all affected mucosa; sunscreen application is recommended thereafter.
lateral margins of 5 mm of uninvolved lip are taken with the cancer.
=» ORAL CAVITY - small cancers can usually be excised through the open mouth taking
a margin of1 cm of normal-appearing tissue; small defects are closed by direct suture
or split-thickness skin grafts; larger cancers (>2 cm) require more extensive exposure,
resection, and subsequent reconstruction; for cancers involving bone, marginal or
segmental resection of the mandible is performed; a composite resection involves
resection of an oral cancer, resection of a portion of the mandible, and a neck dissection.
®TONGUE - surgery is usually the initial treatment, particularly for early stage disease;
selective neck dissection is indicated if the risk of nodal disease exceeds 15-20%.
*RADIATION THERAPY - is an alternative to surgery for oral cancers smaller than 4 cm in
diameter (T1 and 12 cancers); the side effects of mucositis, xerostomia, and
osteoradionecrosis of the mandible must be balanced against potential advantages.
- T3 and T4 cancers are usually treated with combined surgery and radiation therapy to
improve the rate of local control.
- routine surgical reconstruction is the key to reducing postoperative oral disabilities,
procedures range from local tissue flaps to free tissue transfers.
- speech and swallowing therapy may be required after significant resections;
chemotherapy is recommended as adjuvant therapy along with radiation in patients with
advanced nodal disease. ty
Vv. SYPHILIS
- it is a general infection of the blood and lymph streams caused by treponema pallidum;
it is the presence of the spirochetes in the perivascular spaces that excites the reaction,
which consists of an accumulation of mononuclear cells, chiefly lymphocytes and plasma
cells; it is a sexually-transmitted disease; transmission can occur during kissing or by

25
contact with objects such as mouth pieces of musical instruments and medical or dental
instruments; primary, secondary and tertiary syphilis may all occur in the oral cavity.
A. PRIMARY SYPHILIS — CHANCRE
- the chancre occurs at the site of entry of treponema pallidum which is most commonly
on the genitalia but can be elsewhere, the mouth being the second most common site;
although it may occur anytime from 9-90 days after exposure, the usual time is within 2-
4 weeks.
- asolitary painless chancre develops after an incubation period at the site of inoculation;
it begins as a papule before proceeding to ulceration and may vary in size from 5 mm to
several cm in diameter; it is the initial manifestation of the disease, and the lesion is a
slightly raised, ulcerated firm plaque, usually round, which is indurated with rolled edges;
it is usually painless unless superinfected; cervical lymph nodes are usually enlarged
and rubbery in consistency; the chancre is highly infectious and therefore should be
examined with caution; the lesions of primary syphilis usually resolve within 3-12 weeks
without scarring.
LOCATIONS OF CHANCRES
*LIPS - most of the male patients tend to develop lesions on the upper lip while most of
the female patients develop chancres in the lower lip; chancres of the lips may occur as
multiple lesions. ,
* TONGUE - lesions can be commonly seen on the lateral surface of the anterior 2/3 area
or on the dorsal surface and often there is enlargement of the foliate papillae.
eUVULA - appears red and swollen
*TONSILS - show edema, redness and surface erosions or ulcerations
*Oral mucosa *Gingiva
¢Pharyngeal region *Soft palate *Hard palate
B. SECONDARY SYPHILIS
- the secondary lesions usually appear within 3-6 weeks after the chancre; after
entering the body at the primary focus, the organisms proliferate and spread by way of
the bloodstream to produce lesions elsewhere; their location is not related to the site of
the primary lesion; the disease can be transmitted by contaminated salivary droplets.
- it is characterized by a macular or papular rash, febrile illness, malaise, headache,
generalized lymphadenopathy, and sore throat; the oral mucosa is involved in
approximately 1/3 of patients; oral ulceration, described as “snail track ulcer” develops.
lesions of secondary syphilis are infective but resolve within 2-6 weeks; = 30% of patients
with untreated secondary syphilis develop the latent form many years after the initial
infection.
TYPES OF MUCOUS MEMBRANE LESIONS
*MUCUS PATCHES - are found on the tongue, buccal mucosa, tonsils, pharyngeal
region and in the lips; they are the most infectious lesions of syphilis and appear as
flat, irregular, slightly raised, painless, white round lesions and surrounded by an
erythematous base and covered by a yellowish-gray slough; multiple mucus patches may
coalesce together to form snail tract-like ulcer; trauma results in a bleeding surface.
SNAIL TRACT ULCER - is formed by the confluence and coalescence of these glistening
mucus patches; it is often painless or mild to,moderately painful.
*SPLIT PAPULE - is a raised papular lesion developed at the commissure of the lip and
with a fissure separating the upper lip portion from the lower lip portion; they are double
papules which occur at the angle of the mouth; they are highly infectious.
*CONDYLOMATA LATA - are flat, silver gray wart-like papules sometimes having
ulcerated surfaces; they are painless; regional lymphadenopathy is uSually present.

26
C. TERTIARY SYDHILIS - GUMMA
- lesions of tertiary syphilis are now rarely seen due to the successful treatment of the
earlier stages; two oral lesions are recognized in the tertiary form of syphilis: gumma in
the palate and leukoplakia affecting the dorsal surface of the tongue.
- it may manifest anytime during 3-10 years after the primary infection; it is a localized,
indurated chronic granulomatous lesion with nodular or ulcerated surface.
- it is usually asymptomatic; the lesion may occur anywhere in the body including the
oral cavity; a gumma is a painless, well-defined ulcer; the lesions are found most
frequently on the hard and soft palate, tonsils, mandible, lips and tongue; it may also
involve the salivary glands and the jaw bones.
- gumma may manifest as a single, deep punched out mucosal ulcer; it usually starts as
a small, pale raised nodular mass in the midline of the palate which ulcerates and rapidly
progresses to the zone of necrosis; gummatous destruction of the palatal bones is a
common cause of perforation of the palate; healing with scar formation is possible.;
D. CONGENITAL SYPHILIS
- a pregnant patient with primary or secondary syphilis may infect the developing fetus,
resulting in characteristic congenital abnormalities (congenital syphilis); itis acquired by
the fetus "in utero" during its development from a mother who had active infection with
treponema pallidum; for the first 16 weeks of pregnancy the fetus is protected from
infection because the spirochetes from the maternal circulation are unable to penetrate
the placenta; however, after the 16th week the fetus becomes vulnerable to infection;
most fetal infections occur after the 6th month.
ORAL ASPECTS OF CONGENITAL SYPHILIS
*RHAGADES - are linear lesions found about the oral orifice or anal orifice; they result
from diffuse leutic involvement of the skin of these parts from the 3rd to 7th week after
birth; the lesions first appear as red or copper-colored linear areas covered with a soft
crust; they are seen most frequently on the lip near the angle of the mouth because of
the thinness of the epithelium covering the structure and its greater mobility; healed
syphilitic rhagades appear clinically as ordinary cicatrices, but histological study reveals
specific pathological changes; the linear scars are radially arranged and perpendicular
to the mucocutaneous junction; frequently, there is diminished coloring of the lip and a
lack of distinctness of the mucocutaneous border.
*HUTCHINSON'S TRIAD - the complete triad occurs in <1% of individuals with prenatal
syphilis.
*8th NERVE DEAFNESS _ ®INTERSTITIAL KERATITIS
® DENTAL ABNORMALITIES (HYPOPLASIA) - NOTCHED OR SCREW-DRIVER-SHAPED
INCISORS AND MULBERRY MOLARS - of the permanent incisors, the cuspid and the 1st
molars, since these teeth are being formed during the period of acute leutic infection;
there is a general constriction of the crown toward the incised edge because of the
hypodevelopment of the middle mamelon which produce the “screwdriver " and the"peg-
shaped" incisors, frequently associated with this disease.
= DIAGNOSIS
*SCREENING TESTS
»VDRL (VENEREAL DISEASE RESEARCH LABORATORY)
® RAPID PLASMA REAGIN (RPR) TEST fi
*CONFIRMATION - these tests are specific but more expensive
» TREPONEMA PALLIDUM HEMAGGLUTINATION (TPHA)
®» FLUORESCENT TREPONEMAL ANTIBODY ABSORPTION (FTA-ABS)

27
= TREATMENT
*BENZATHINE PENICILLIN G = 2.4 x 108 units IM biweekly or 1.2 x 108 units of Procaine
Penicillin per day IM for 15 days in primary, secondary and latent syphilis (duration of
infection more than one year).
*ALTERNATIVE THERAPY
=» DOXYCYCLINE = 200 mg per day
™® ERYTHROMYCIN = 2 gm per day for 2 weeks in penicillin-allergic patients
AZITHROMYCIN
TERTIARY AND LATENT SYPHILIS (duration of infection more than 1 year) = 2.4 x 10° units
IM of Benzathine Penicillin IM once a week for 3 weeks is recommended.; after therapy a
serologic test for syphilis needs to be performed.
VI. TASTE DISORDERS

- overall, gustatory dysfunction is rare; although the majority of the patients report taste
loss, most of them suffer from loss of olfactory sensitivity; it is the olfactory loss that
contributes to the loss of perception of flavor.
- the most common cause of a loss in smell or taste is aging; typically, age-associated
loss in the chemical senses appears progressively after the age of 60 years, and shows
large individual variation, greatly afflicting some and leaving others intact; they can
appear either abruptly or progressively.
TASTE LOSS - taste sensitivity is robust compared with smell sensitivity; not only are
there 3 types of papillae and 3 cranial nerves on each side involved in mediating taste,
but there is also the taste constancy that contributes to the robustness; this constancy
is believed to be based on inhibitory feedback loops among the cranial nerves, so that
damage to one taste nerve releases inhibition on others, resulting in intensification of
sensations from other regions of the oral cavity; despite this, taste loss can result from
damage to any location of the neural gustatory pathway, from the taste buds via the
peripheral and central nervous system.
= DEFINITIONS
eAGEUSIA - describes a complete loss of taste
*HYPOGEUSIA - is a diminished sense of taste
*HYPERGEUSIA - refers to an enhanced gustatory sensitivity
*DYSGEUSIA - relates to a distorted taste perception, which is by far the most common
complaint.
MAJOR CAUSES
*HEAD TRAUMA - is thought to produce lesions that involve the processing of gustatory
sensations; recovery is possible.
eINFECTIONS OF THE URT - may involve the taste buds, the nerves innervating the taste
buds, or the central structures of the brain.
*DRUGS -a large number of drugs have been implicated in the etiology of taste disorders
but little is known about the mechanisms that underlie these disorders.
*TOXIC EXPOSURE eWORKING CONDITIONS eLIFESTYLE
*BURNING-MOUTH SYNDROME .- is an intraoral pain disorder that is frequently
associated with dysgeusia and often described as the persistent presence of a metallic
or bitter taste; other symptoms include dry mouth and thirst.
- frequently, burning increases throughout the day; it is most prevalent in post-
menopausal women; partial spontaneous remission may occur in approximately half of
these patients within 6 years of onset.

28
POSSIBLE CAUSES OF BURNING-MOUTH SYNDROME
» PSYCHOLOGICAL
=Anxiety «Depression
®»HORMONAL - estrogen-related changes
NUTRITIONAL
#Vitamin B1,Bzand Bs deficiency =Zinc deficiency
™® EXPOSURE TO TOXIC SUBSTANCES
®» IATROGENIC CAUSES
=Dental procedures Radiation
AGE-RELATED TASTE LOSS - is less prominent than age-related smell loss.
Vil. ACUTE MONOCYTIC LEUKEMIA - HYPERPLASIA OF THE GUMS

- monocytic leukemia which is a very rare form of leukemia produces oral lesions most
frequently of all leukemias; it is thought to be due to the invasion of leukemic cells into
the gingival tissues; it is a relatively uncommon sign, seen mostly in acute myelogenous
leukemia, but even so only in about 3-5% of cases.
INTRAORAL LESIONS
*MARKED GINGIVAL ENLARGEMENT, WITH OR WITHOUT ASSOCIATED AREAS OF
NECROSIS - the hypertrophic tissue frequently reaches the occlusal surface of the teeth;
the gingival enlargement in some forms of the disease may cover the surface of the teeth;
bleeding from the gingiva following tooth extraction may be the initial symptom and
spontaneous and persistent hemorrhage occurs frequently; submucosal hemorrhage
may or may not be present.
- this type of gingivitis is characterized frequently by pronounced gingival enlargement
caused by the infiltration of the gingival tissues by neoplastic blood cells, which
produces a peculiar thickening of the gingival margins, which have a tendency to stand
away from the teeth; the color may be bluish-red to pink; the tissues are generally soft
and spongy; regional lymphadenopathy may be present.
*PULPAL ABSCESSES IN CLINICALLY SOUND TEETH - liquefaction of the pulp may
develop in noncarious teeth; fistulas may be present in the periapical areas; the leukemic
cellular infiltration in the periodontal membrane results in varying degrees of looseness
and mobility of the teeth.
*ULCERATIONS OF THE CHEEKS, TONSILS OR THE PHARYNX
VIII. GIANT CELL EDULIS (DERIDHERAL GIANT CELE GRANULOMA)

- it is the formation ofa granular cell myoblastoma, a benign neoplasm, commonly located
on the edge of the oral mucosa on the alveolar and maxillary processes; classically, it is
a swelling with a deep-red color (although older lesions tend to be paler) that often arises
interdentally, but only anterior to the permanent molars.
- most patients are in the 4'"- 6" decades; females are affected 2x as often as males; it is
predominant in white persons.
“ETIOLOGY - it probably arises because chronic irritation triggers a reactionary
hyperplasia of mucoperiosteum and excessive production of granulation tissue; it is an
unusual response of tissue to injury.
- the trauma may be caused by tooth extraction and dental irritation; it can occur in
chronic infections; it may appear under the stimulus of increased circulating
parathormone.
CLINICAL FEATURES - it occurs on the gingiva and alveolar mucosa, most frequently
anterior to the molars; it is more common on the mandible than on the maxilla; in the
early stage, it appears as discoloration and slight swelling of the buccal aspect of the

29
gingiva; later the lesion increases in size, becomes rounded and often pedunculated; the
color of the lesion is usually dark red or maroon color; it may be pink or bluish in color,
it may feel soft to hard; the lesions vary in size from 0.5 to 1.5 cm in diameter; itis vascular
or hemorrhagic and sometimes ulceration is also present; there may be tenderness on
palpation.
- itis shown as a light-red neoplasm on the oral mucosa and can lead to difficulties during
food ingestion; it usually occurs near an infected tooth root that has caused an area of
localized osteomyelitis; x-rays show erosion of the bony alveolar processes.
- this granuloma is a small, pedunculated, hemorrhagic nodule that occurs most
frequently on the gingiva and has a strong tendency to recur following simple excision;
the fact that they are closely related to the gingival margins suggests that calculus
and overhanging margins of dental restorations are important irritants that should be
eliminated when the lesion is excised.
- identical lesions of the same histological structure occur in association with the
florid gingivitis and periodontitis that may complicate pregnancy; the increased
prevalence of pregnancy epulides toward the end of pregnancy when levels of
circulating estrogens are highest, the tendency for these lesions to shrink after delivery
indicate a definite role for these hormones in the etiology of the lesion.
TREATMENT - involves the extraction of the infected tooth and surgical excision of the
epulis, including the periosteum; excision with borders of normal tissue, with the entire
base of the lesion to avoid recurrence; elimination of chronic irritants; they tend to return.
- removal of epulis during pregnancy is deferred until after delivery because removal
during pregnancy is marked by a high recurrence rate; clindamycin is an acceptable
antibiotic alternative, especially for penicillin-resistant anaerobic infections.
IX. MOTTILED ENAMEL

- it is an acquired form of enamel hypoplasia resulting from drinking water that contains
in excess of 1 PPM fluoride; it is due to disturbance in tooth formation during the
formative period of dentition; it may be mild to severe in character.
- dental fluorosis is an impairment of mineral acquisition into the enamel during the long-
lasting and complex process of maturation; this results in increasing enamel porosity
along the entire tooth surface.
- there is only a risk of developing dental fluorosis when the dentitions are developing;
the risk for developing dental fluorosis that is visible on the permanent incisors is
greatest during the first three years of life.
- there is a linear dose-response relationship between fluoride ingestion and dental
fluorosis; the effect of fluoride in teeth is cumulative, meaning that the longer the teeth
undergo mineralization, the more likely that severe dental fluorosis will appear following
aconstant dose of fluoride; posterior teeth are therefore more severely attacked by dental
fluorosis than anterior teeth.
*MILD CHANGES - it is manifested by white, opaque areas involving more of the tooth
surface.
*MODERATE TO SEVERE CHANGES - changes showing pitting and brownish staining of
the surface and sometimes even corroded appearance.
= CLINICAL FEATURES - the appearance can vary between “minute white flecks, yellow or
brown spots or areas, scattered irregularly over the surface of a tooth, or it may be a
condition where the entire tooth surface is of a dead paper-white color.
- dental fluorosis in primary dentition is less severe as compared to permanent dentition;
it often becomes stained as unsightly yellow to brown color, which is caused by coloring
agents from food, medicine and by disintegration of the increased protein contained in

30
the hypomineralized parts of the enamel; sometimes, white patches in enamel may
become Striated, pitted and mottled; the mottling of the enamel is most prominent on the
anterior teeth, but may also be found on the other teeth of the arch; in particularly severe
cases, hypoplasia of the enamel may develop.
TREATMENT - since the staining of the teeth results from the entry of pigmentations into
immature enamel (and is therefore actually extrinsically stained), the discoloration can
be removed with strong abrasive agent or the application of 30% hydrogen peroxide
solution to the teeth.
X. PLUMBISM
- lead is a cumulative poison, it remains accumulatether factors promoting release of
stored lead: acidosis, fever, sweating, consumption of alcohol and exposure or sunlight.
-toxication from lead may occur acutely or over a long period of time; evidence of lead
absorption is found in the typical rbc changes with anemia; lead lines at the epiphyseal
ends of growing bone can be demonstrated radiologically; chronic lead poisoning results
from daily intake of 1-2 mg of lead.
- oral tissues are exposed to lead through direct contact with ingested lead and through
secretion of lead in the saliva; there is a metallic taste which is accompanied by excessive
salivation and dysphagia.
- when exposure to lead is very high and oral hygiene is very poor, a thin gray-blue line
known as “Burton line” is seen along the gingival margin at the base of the teeth; it is
seen to be composed of numerous distinct small dark granules; pressure on the gingiva
will accentuate the lead line by causing ischemia of th tissues.
= CAUSES
eINGESTION OR INHALATION OF LEAD PAINT DUST - inhalation of lead dust and fumes
by makers of white lead, lead paints, plumbers, glass polishers, printers and glass
blowers.
- lead paint dust is the most common source of lead exposure for children; children < 3
years are at the greatest risk for lead poisoning as they are more likely to put things
containing lead into their mouths and their brains are rapidly developing.
*Drinking water stored in lead cisterns
eTinned food contaminated with lead from solder
*Use of hair dyes and cosmetics containing lead
*Percutaneous absorption of tetraethyl lead in persons who handle petrol and gasoline.
*Absorption of vermilion dye applied to the scalp.
TREATMENT - lead can be removed from the body by a chelating agent such as calcium
edetate (EDTA) or penicillamine.
XI. DEUTZ-JEGHERS SYNDROME

-- it is characterized by autosomal dominant inheritance, benign intestinal polyposis, and
pigmented mucosal and cutaneous lesions; it is found in equal frequency in both sexes;
there is also abnormal melanin pigmentation of the circumoral area of the face; the
interdigital areas of the hand may be involved; the areas about the eyes, lips and nostrils
are 1-10 mm in size and usually have a clearly demarcated margin; there is no known
physiological basis for the location of pigmented areas which in themselves are harmless
and require no treatment; polyposis of the uterlis and nasal mucosa may be associated
with similar abnormal pigmentation.

31
XH. RECURRENT APHTHOUS STOMATITIS (RAS)
- it is the most common painful oral disease, affecting = 20% of the population;
characteristic oral ulcerations initially present in the first and second decades of life;
while the frequency of episodes often diminishes sharply during the third decade,
patients are always at risk for developing recurrent lesions.
- several subtypes are included within the RAS group; episodic recurrences are its main
characteristic feature; aphthae are recurrent oral ulcerations, generally small with an
erythematous base; when recurrent (i.e., at least three attacks within the last 3 years), it
is termed recurrent aphthous stomatitis (RAS).
PATHOPHYSIOLOGY - idiopathic, may be immunologic, infectious, hormonal, stress-
induced, traumatic, or nutritional
- it is an inflammatory ulcerative disease of unknown etiology; a chronic inflammatory
condition with heavy infiltration with lymphocytes in the submucosa of the ulcers occurs.
- is unknown; many suggestions have been made; an autoimmune or
“ETIOLOGY
hypersensitivity mechanism is widely considered possible but RAS is not typical of either
disease type; most reports indicate that RAS is an abnormality of the immunologic
response to oral bacteria.
- a higher prevalence has been found in the higher socioeconomic groups, in females,
and amongst individuals under "stress" such as students at the time of examinations.
- there is also a genetic predisposition but the condition does not follow a simple
inheritance pattern; it appears to be at least 2x as prevalent among professional school
student personnel as among the general populace.
- 20-60 % of the population have had aphthous ulcers at some time in their lives; the first
episodes most frequently begin during the 2"4 decade of life; people most frequently get
them between the ages of 10 and 40 and they are often recurrent.
= TRIGGER FACTORS
eTrauma to the oral mucosa due to local anesthetic injections, sharp tooth, dental
treatments, and tooth brushing injury
*Stress may induce or predispose the patient to have habits such as lip or cheek biting
and this may result in ulceration.
Nutritional deficiencies (vitamin B12, folate, iron)
*Hormonal alterations
elmmunological abnormal eLack of sleep
elliness *Certain toothpastes
*FOODS - particularly chocolate, coffee, peanuts, eggs, cereals, almonds, strawberries,
cheese, walnuts, pineapple and tomatoes
MICROORGANISMS IMPLICATED
*ORAL BACTERIA - have been implicated to play a role in the pathogenesis of these
lesions. Ex. Streptococcus sanguis
*HELICOBACTER PYLORI
*VARIOUS VIRUSES - including the Epstein-Barr virus (EBV) have been implicated in
RAS.
= CONTRIBUTING FACTORS
FAMILIAL AND GENETIC BASIS
*eLOCAL IMMUNE RESPONSE - it has been suggested that it represents a form of
autoimmunity, since autoantibodies to oral mucosal homogenates are found in 70-80%
of those with recurrent aphthous stomatitis as opposed to 10% of controls.
*VITAMIN DEFICIENCIES - several nutritional deficiencies have been associated with RAS
- Vitamin B complex, folic acid and iron are commonly deficient.
eHORMONAL CHANGES -i.e., menstruation

32
*SYSTEMIC CONDITIONS -i.e., HIV, Behcet’s syndrome, Crohn’s disease, Celiac disease
= PROTECTIVE FACTORS - for unknown reasons
*Oral contraceptives Pregnancy
*Tobacco, including smokeless tobacco and nicotine containing tablets
= CLASSIFICATION OF RAS-TYPES
*MINOR APHTHOUS STOMATITIS (MIKULICZ DISEASE) - is the most common form
(85%); there is burning and tingling before ulcer formation; they are <8 mm (typically 2-3
mm) and last 7-10 days; they heal without scarring.
*MAJOR APHTHOUS STOMATITIS (SUTTON DISEASE) - is less common (10%);
appearing after puberty, the prodrome is more intense and the ulcers are multiple, more
painful, deeper, larger, and longer lasting than minor aphthae; fever, dysphagia, malaise,
and scarring may occur.
*HERPETIFORM APHTHOUS STOMATITIS (morphologically resembling but unrelated to
herpes virus); they begin as multiple (up to 100), small crops of small, painful clusters of
ulcers on an erythematous base; they coalesce to form larger ulcers that last 2 weeks.
- they tend to occur in women and ata later age of onset than do other forms of RAS; they
account for 5% of cases; the ulcers are not as deep as major aphthous ulcers but there
is the risk of scar formation.
- minor and major RAS usually begin in childhood or early adolescence and have a
tendency to resolve naturally later in life; herpetiform ulcers appear later than minor and
major RAS, usually in the 3 decade.
MAJOR RAS
HERPETIFORM RAS
80-90% of patients 10-12 % of patients 8-10 % of patients
@Less than1 cmin @Greater than 1 cm 1-3 mm in diameter and
diameter (usually 1-3 cm) occurs in various sized
Lesions are often HiLesions are often crops
solitary multiple Mi May have contiguous
Ulceration may be areas of ulceration
deeper HiLesions resemble a
herpes simplex lesion
HiLesions are not caused
by
the herpes virus
Hit is not contagious
They are usually very
painful
Generally affects: Generally affects: Generally affects:
Labial mucosa Lips HGingiva
@ Buccal mucosa Soft palate WHard palate
Lateral and ventral HMTongue es, Vermillion border of the
tongue @Tonsillar pillar lips
HIFloor of mouth Alveolar ridges
M@Pharynx

33
Healing: Healing: Healing:
Usually in 7-10 days Usually lasts 20-30 days Usually within 2-3 weeks
Leaves no scar but can last longer Mi May leave a scar
formation MMay leave a scar
Usually 1-5 ulcers may be Usually 1-10 ulcers Often occur in groups of
present at any one time 5-100
Round or oval shape Round or oval shape, and Round or oval shape,
tend to have irregular coalesce to form large,
edges irregular areas of ulceration
Usually not very painful Prolonged and more May be very painful
painful ulceration.
May present patient with
great problems - eating
may become difficult
Peak onset in children or | Peak onsetin children or | Peak onset in adolescence
adolescents adolescents or early adulthood
DIAGNOSIS - is based almost exclusively on the history and clinical findings; clinical
examination is helpful in differentiating subtypes and excluding other disorders; in all
ulcer types there is a yellow or white slough in the early stage; the ulcer margin is well-
defined with a rim of marginal erythema but shape may become slightly irregular or less
well-defined as the ulcer heals.
- ulceration may follow minor trauma such as a knock with a toothbrush or a bite; some
patients experience prodromal symptoms of tingling or pain before ulceration appears
and this is a useful sign to start treatment.
CLINICAL ASPECTS - after a tingling or burning sensation in the affected mucosa
during the prodromal stage 2-48 hours before an ulcer appears, the mucosa becomes
focally erythematous and necrotic; within hours, a small white papule forms which
ulcerates and gradually enlarges during the next 48-72 hours with the formation of single
or multiple round to oval ulcerations usually 2-3 mm in diameter, with about 10% being
larger than 1 cm; the ulcer is covered by a grayish white fibrous exudate and
surrounded by a bright red halo; most patients experience 2-6 lesions/episode occurring
several times a year.
- they appear as recurrent ulcers with circumscribed margins with erythematous halos
and gray or yellowish floors; they affect the nonkeratinized or poorly keratinized mucosa
of the mouth and oropharynx; multiple spherical, flat craterlike lesions form in the mobile
mucosa of the oral cavity; the lesions are confined to the intraoral mucosa and consist
of 2-6 round, symmetric, shallow ulcers not preceded by vesicles.
- the main "problem" caused by aphthous ulcers is pain, which varies considerably
among patients from slight to severe; the acute painful phase lasts 3 to 4 days with
complete healing in 7 to 10 days.
< SYMPTOMS - may occur at the time of ulceration or may exist prior to the presence of the
lesions.
*Pain and difficulty eating and drinking relatéd to the pain
*Tingling Burning
+ PHYSICAL EXAMINATION
May be tender to palpation
*Usually round or oval, ulcerative appearing lesion(s) with central clearing and well
circumscribed margins; may be surrounded by an erythematous halo.

34
°Solitary or multiple ulcers may be present
= PRINCIPLES OF TREATMENT - there is no definitive curative treatment for RAS; treatment
is primarily aimed at pain relief and the promotion of healing to reduce the duration of the
disease or rate of recurrence; a variety of topical and systemic therapies have been tried;
no single treatment has been determined to be the one treatment for all patients;
individual drugs appear to work better for some than others.
*GENERAL - it will be evident from the fact that so many treatments exist that none is
highly effective in all patients; patients with severe ulceration should be informed that:
They may need to try several treatments before they find one which works well for them.
*Treatments are not completely effective, they should only be expected to reduce the
number of ulcers, reduce pain and sometimes reduce frequency.
*Although a good response may be obtained in the most severe cases the aim of
treatment for most people should be to make the ulcers bearable.
*REASSURANCE
™RAS is a very common condition - up to 25% of the population suffer it at some time.
™® Underlying conditions have been considered and excluded as a cause.
®RAS is not a serious condition but will be an inconvenience.
®RAS is not malignant.
®RAS is not contagious or infectious.
»Patients’ children may develop ulcers but the disease is not inherited in a simple
fashion.
*NO TREATMENT - if reassurance is effective no treatment may be required; this should
be the clinician’s aim for infrequent ulcers which heal in the typical 7-10 days.
- most patients will accept this provided the effectiveness and any risks of treatment are
realistically explained.
«THE FOLLOWING MAY HELP REDUCE PAIN WHEN ULCERS ARE PRESENT:
® Avoid spicy foods and acidic fruit juices or carbonated drinks
™® Drink through a straw to bypass the mouth
® Avoid sharp foods such as crisps
® Avoid stress if possible which may exacerbate ulcers or trigger a series of ulcers
= TREATMENT
GENERAL
»PAIN RELIEVERS
MAPHTHASOL (amlexanox oropharyngeal) 5% ORAL PASTE - apply as soon as possible
after symptom onset; apply 0.25 inch 4x a day (following oral hygiene after meals and at
bedtime) up to 10 days.
BIORABASE or ZILACTIN (benzocaine) OROPHARYNGEAL LIQUID OR GEL - use as
needed; it can relieve pain, itching, and burning associated with these lesions; it can
significantly reduce the size and duration of the outbreak; the liquid form is nonfilm-
forming; the gel provides an occlusive film over the lesion(s) (which can last up to 6
hours.
MXYLOCAINE OINTMENT (5 %) - is effective in reducing discomfort.
WANALGESICS - ibuprofen or acetaminophen may help reduce the pain.
» ANTI-INFLAMMATORY >
MKENALOG (triamcinolone acetonide) OROPHARYNGEAL 0.1% PASTE (also called
Kenalog in Orabase)

33
MILIDEX (fluocinonide) 0.05% TOPICAL OINTMENT - apply 0.25 inch every night; can
apply 2-3x a day after meals if more severe lesions exist; up to 7 days.
® ANTIVIRAL
MIZOVIRAX (acyclovir) TOPICAL 5% OINTMENT - apply 6x per day x 7 days
ZOVIRAX (acyclovir) TOPICAL 5% CREAM
MXERESE (acyclovir/hydrocortisone) TOPICAL 5% OR 1% CREAM - apply 5x per day *
5 days
*» TOPICAL TETRACYCLINE = dissolve 250 mg of chlortetracycline into 50 ml of water
and hold in the mouth for 20 minutes 4-6x/day.
® SILVER NITRATE - is applied to the ulceration base.
*FOR SYMPTOMATIC TREATMENT OF MILD ULCERATION
*®BENZYDAMINE HYDROCHLORIDE (Diflam) MOUTHWASH
™® CHLORHEXIDINE GLUCONATE (Corsodyl) MOUTHWASH
™®» CARBOXYMETHYLCELLULOSE PASTE (Orabase; Carmellose sodium)
*MILD RAS (Defined as RAS minor with ulcer free period of one month or more)
® HYDROCORTISONE SODIUM SUCCINATE (Corlan) = 2.5 mg q.i.d. during attack, b.i.d.
between attacks for at least 6 weeks before reducing to use during attacks only.
®TRIAMCINOLONE 0.1% IN CARBOXYMETHYLCELLULOSE PASTE (Adcortyl in
Orabase) - applied q.i.d. to dried areas around ulcers with moistened finger.
*MODERATELY SEVERE RAS (defined as RAS minor with ulcer free period 2-4 weeks
approximately; it is also considered if pain, duration or number of ulcers is more severe
than is typical.
®BETAMETHASONE SODIUM PHOSPHATE (Betnesol mouthwash) = one 0.5 mg tablet
dissolved in 5-10 ml of water used as a mouthwash q.i.d. during ulcer attacks.
® BECLOMETHASONE DIPROPIONATE AEROSOL (Beconase spray) = 2 puffs (100
micrograms) sprayed onto affected mucosa to a maximum of 8 puffs per day.
*SEVERE RAS (defined as ulcer-free period less than 2 weeks, continuous ulceration, all
cases of RAS major); cases of moderate severity refractory to above treatments.
TRY THESE IN THE FOLLOWING ORDER UNLESS SEVERE CONTINUOUS ULCERATION
MAKES AN IMMEDIATE TRIAL OF PREDNISOLONE NECESSARY.
® COLCHICINE = 500 micrograms daily; monitoring for adverse effects essential.
®PREDNISOLONE = 40 mg for 5 days, reducing by 5 mg every 2 days to 5 mg, then
reducing by 1 mg per day until drug withdrawn; monitor severity during withdrawal of last
15 mg and select maintenance dose to maintain remission before ulcers reappear; a
suitable maintenance dose is usually 5 mg daily or on alternate days for the first month;
monitor for adverse effects.
® AZATHIOPRINE = 50-100 mg daily may be required in addition, primarily as a steroid
sparing agent during the maintenance phase of treatment.
®MONTELUKAST SODIUM = 10 mg/day has been reported as potentially effective with
fewer adverse effects than steroids.
™ CLOFAZIMINE - has shown efficacy in some trials in reducing the frequency of lesions
and symptoms in patients who continue to experience lesions
™ THALIDOMIDE - is the only FDA approved for the treatment if major aphthae in
individuals with HIV infection ;
*HERPETIFORM ULCERATION “s
™TETRACYCLINE = 250 mg capsule dissolved in 10 ml of water and used as a
mouthwash; hold in the mouth for 3 mins and spit out.

36
- herpetiform ulcers are often unresponsive to steroids which form a second line of
treatment if tetracyclines fail.
MANAGEMENT OF CHILDREN WITH RAS - children who are affected severely by any form of
oral ulcers can experience weight loss, time off school, difficulty in speaking and eating
and dehydration; in many cases the parents are more worried than the child and many
children can accept quite severe ulceration.
PRINCIPLES OF TREATMENT IN CHILDREN
» Ensure that the diagnosis is correct. .
*»Ensure that the underlying conditions are detected and effectively treated if present.
*Reassure parents and child and explain limitations of treatment; usually another family
member will suffer from RAS and this experience may aid reassurance.
» Avoid over-medicating the condition - consider no intervention. .
®Parents should monitor eating and hydration during attacks; dietary supplementation
is not usually required but nutritional support may be considered in small children who
refuse to eat for the entire duration of ulceration. . .
Children under the age of six cannot usually rinse and expectorate effectively; avoid
preparations which should not be swallowed in young children unless you have seen
them rinse effectively; in practice, RAS does not affect this age group except in the most
severely affected cases.
® Avoid tetracycline preparations even as mouth rinses until age 12 years.
Try benzydamine and local anaesthetic preparations as a first line symptomatic
treatment.
In more severe cases therapeutic intervention may be necessary.
BTRIAMCINOLONE 0.1% IN CARBOXYMETHYL CELLULOSE PASTE (Adcortyl in
Orabase) - can be managed only by older children.
sHYDROCORTISONE SODIUM SUCCINATE (Corlan) = 2.5mg tablets are safe in children
because of their low steroid potency and may be used as for adults.
Xi. GLOSSODYNIA (BURNING MOUTH SYNDROME)

- it is a chronic, idiopathic intraoral mucosal pain condition that is not generally
accompanied by clinical lesions or systemic disease; the condition may be a
multifactorial disorder, which makes evaluation and treatment difficult.
© ETIOLOGY - the precise etiology and pathogenesis of BMS is unknown; it is unclear as
to why, but this condition usually affects postmenopausal women.
POTENTIAL CAUSES
*There may be a neuropathic origin.
*Nutritional deficiencies may play a role.
*BMS symptoms can occur after radiation and chemotherapy.
*Anxiety is suggested to be associated with BMS.
*Certain medications may cause or aggravate: ACE-inhibitors (ACEI), angiotension
receptor blockers (ARB), and/or antiretrovirals (for the treatment of HIV infection)
*Other causes can include overuse of mouth rinses, irritation from toothpaste or oral
products, and alcohol or tobacco use.
MICROORGANISMS IMPLICATED - microbial infections with or without visible lesions as a
cause of BMS have been suggested.
= SYMPTOMS - can be intermittent or continuous and may gradually increase throughout
the day; symptoms may be aggravated by spicy and/or acidic foods; typically bilateral
and may involve the following: anterior 2/3 of the tongue; tip of tongue; anterior hard
palate; lower lip; during periods of increased stress or anxiety, the patient may report an
exacerbation of symptoms

37
*BURNING, SCALDING, OR TINGLING
*ORAL PAIN *XEROSTOMIA - dry mouth
*DYSGEUSIA - taste disturbances. usually described as bitter and/or metallic in quality.
= PHYSICAL EXAMINATION - a thorough examination of the tongue and the mouth is of
paramount importance; examination may reveal no visual abnormalitie; if abnormalities
are present, there may be erythema, edema or swelling of the tongue, papillary atrophy,
and/or surface ulceration.
«TREATMENT - no single treatment has been determined to be the one treatment for all
patients; individual drugs may work better for some than others.
*ANTIFUNGAL 13
®» MYCELEX (clotrimazole troches)
™NYSTATIN = 100,000 units/mL
eANTI-INFLAMMATORY
KENALOG (triamcinolone acetonide) OROPHARYNGEAL 0.1% PASTE
®>LIDEX (fluocinonide) 0.05% TOPICAL OINTMENT
*INCREASES SALIVARY GLAND SECRETION (helps with xerostomia)
®CEVIMELINE
»SALAGEN (pilocarpine)
®NEUTRASAL
*NEUROLOGICALS
*SSRI (Selective Serotonin Reuptake Inhibitor) *GABAPENTIN
®ANTIANXIETY (Benzodiazepine) ®TCA (Tricyclic Antidepressant)
XIV. LEUKOPLANIA
- oral leukoplakia is the most serious commonly occurring lesion of the oral mucosa; the
lesion is predominantly found in the 4th to the 6th decade; however, numerous lesions
are found in the 3rd decade and even a few in teenage patients; the prevalence of
leukoplakia varies from 0.2% to 4%.
- "hairy" leukoplakia of the mouth is an unusual form of leukoplakia that is seen only in
AIDS and HIV positive individuals; it consists of fuzzy (hairy) white patches on the tongue
and less frequently elsewhere in the mouth; hairy leukoplakia may be one of the first
signs of infection with the HIV virus.
- leukoplakias are whitish hyperkeratotic lesions of the oral mucosa; they usually develop
on the tongue, but they may appear on the insides of the cheek; they are usually
harmless, and lesions usually clear in a few weeks or months after the source of irritation
is removed; some of these lesions because of their pathology are potentially
precancerous or in fact already malignant; the risk of malignant transformation is difficult
to estimate in any individual case; lesions in the floor of the mouth and ventral tongue,
and those showing evidence of epithelial dysplasia or carcinoma in situ, are considered
to be at high risk; pararadoxically, the risk of malignant transformation is greater in non-
smokers than in smokers; it is very rare in non-smokers; the regression of leukoplakia
in smokers following cessation suggests that a proportion of the lesions are reactive,
whereas leukoplakia in non-smokers may reflecta local cellular genetic change that tends
to be progressive; they are important lesions*because a small proportion have a higher
risk of turning malignant than does normal mucosa; it is therefore important to identify
the “high-risk’ leukoplakias. —
-less than 10% of cases can transform into small cell carcinoma (SCC); leukoplakias are
very unpredictable; they may improve, remain stable, or progress to SCC; there are no
validated clinical and/or biological factors that can predict malignant transformation; if
they do progress to SCC, it may take a few months or many years; therefore, it is

38
important to first exclude other known diseases or disorders (e.g., lichen planus and
candidiasis) that carry little or no risk of cancer; then if the lesion(s) persist, a biopsy is
warranted to rule out malignancy; even if the biopsy is negative for malignancy, it is
important to maintain a close follow-up of these patients and continue to rebiopsy if the
lesion persists over time, despite removing the suspected irritant.
HISTOLOGY
*HOMOGENOUS LEUKOPLAKIAS - are plaque-like lesions with a uniform smooth or
wrinkled surface; there is less risk of malignant transformation.
*NON-HOMOGENOUS LEUKOPLAKIAS - tend to be less circumscribed and show a
greater range of appearances; they may show variations in the surface contour; they may
be nodular or spiky; the lesions may show variations in color with red areas interspersed
with white areas; the risk of malignant transformation is greater; often these lesions are
multifocal.
= SITES WITH HIGH RISK OF MALIGNANT CHANGE
*Ventrolateral surface of the tongue *Floor of the mouth
*Maxillary retromolar area *Soft palate
RISK FACTORS
*Tobacco *Betel nut chewing
eAlcohol eCandidal infection
*Chronic trauma from sharp or broken tooth
= ETIOLOGY
eSYSTEMIC
» POSSIBLE NUTRITIONAL FACTORS
aVitamin A hyponutrition
#Vitamin B complex hyponutrition
®POSSIBLE CONSTITUTIONAL CHARACTERISTICS
» POSSIBLE ENDOCRINE FACTORS - Gonadal disturbance
*»POSSIBLE RELATION TO SYSTEMIC DISEASE - Ex. Syphilis
- syphilis is found more often in patients with leukoplakia of the tongue.
*LOCAL - chronic irritation of all types
= MECHANICAL TRAUMA - chronic local irritative factors appear to be more important in
the development of leukoplakia; it is believed that if a low-grade irritant is allowed to
continue over a long period in a susceptible host, dysplastic changes have a tendency to
occur.
=Sharp edges of teeth on tooth roots
Irritation from mal-opposed teeth or dentures, fillings and crowns
«Unconscious habit of biting oral tissues
CHEMICAL TRAUMA - Ex. alcohol, nicotine including smokeless products
- it may also result from chronic smoking or other tobacco use (smoker's keratosis) pipe
smoking involves a high risk for development of leukoplakia, as does chewing tobacco
or snuff in the mouth for a prolonged period of time.
» THERMAL TRAUMA
*» BACTERIAL
=Poor oral hygiene =Periodontal diseasé”
SIGNS AND SYMPTOMS - a white patch that has developed slowly over weeks to months;
the lesion may eventually become rough textured and may become sensitive to touch,
heat, spicy foods, or other irritation; a biopsy of the lesion confirms the diagnosis and an
examination of the biopsy specimen occasionally shows changes that indicate oral
cancer.

39
-a typical feature of leukoplakia of the tongue is lack of papilla at the site of the lesion;
this will assist in differentiating this lesion from BMG and lichen planus; the clinical lesion
of leukoplakia may vary from a small localized area of hyperkeratosis to an extrinsic
hyperkeratotic involvement of large areas of the oral mucosa.
of oral
- the usual lack of painful symptoms is one of the characteristic features
and
leukoplakia; it can be considered as a callus of the oral mucosa; loss of pliability
symptom noted by
flexibility of the yellowish white area is frequently the first and only
the patient especially when the tongue is involved. ;
rarely any
- the margins of the hyperkeratotic areas usually are well defined and there is
seen on the
gross inflammatory reaction adjacent to the lesion; a white plaque is often
vermilion border of the lip in smokers.
PHYSICAL EXAMINATION
plaque or lesion that cannot be removed off the surface by
‘White, well-demarcated
rubbing; the surface texture can vary from a smooth thin surface to a leathery appearance
with surface fissures. .
*Leukoplakia lesion(s) may or may not be present in association with erythroplakia
MOST COMMON LOCATIONS
eLip (vermilion) ¢Buccal mucosa
¢Mandibular gingiva *Tongue
¢Floor of mouth (FOM) ¢Hard and soft palate
¢ Maxillary gingiva
<TREATMENT - the goal of treatment is to eliminate the lesion; removal of the source of
irritation is the primary treatment for leukoplakia; dental causes (rough teeth, irregular
surface on dentures or filling, etc.) should be treated as soon as possible; smoking or
other tobacco use should be stopped.
- surgical excision of small lesions with a knife or with a CO2 or KTP laser may be
indicated if removal of the source of irritation is ineffective in reducing leukoplakia; the
lesion is usually removed in the office under local anesthesia; laser excision has a lower
recurrence rate plus the advantages of better precision, bloodless field, excellent tissue
healing, and less pain and discomfort.
Xv. GLOSSITIS
- it is an inflammation of the tongue that can lead to loss of filiform papillae; changes in
the appearance of the tongue may be a primary tongue disorder or may be a symptom of
other disorders; glossitis causes the tongue to swell and change color; papillae are lost,
causing the tongue to appear smooth; occasionally, glossitis can be inherited.
= EPIDEMIOLOGY - it is seen more frequently in patients of lower socioeconomic status,
malnourished patients, alcoholics, smokers, elderly patients, immunocompromised
patients and patients with dentures.
- ETIOLOGY
«LOCAL CAUSES
*» NUTRITIONAL DEFICIENCIES - Vitamin E, riboflavin, niacin, Vitamin B12, iron
® INFECTIONS - viral, bacterial, candidiasis, yeast
™® TRAUMA - rough edges of teeth, or poorly fitting dentures
IRRITATION OF THE TONGUE - from toothpaste, medications, alcohol, tobacco, hot
food, spices, or citrus
» SENSITIZATION (Allergic reaction) - from toothpaste, mouthwash, breath fresheners,
dyes in candy, plastic in dentures or retainers, ACE inhibitors
*» DRY MOUTH - Sjogren syndrome
® MECHANICAL IRRIRATION OR INJURY FROM BURNS

™» NEOPLASMS
* TOBACCO, ALCOHOL. HOT FOOODS, SPICES OR OTHER IRRITANTS
“SYSTEMIC CAUSES
*»Aphthous ulcers » Syphilis Tuberculosis
Erythema multiforme » Oral lichen planus » Pemphigus vulgaris
= PREVENTION
*GOOD ORAL HYGIENE - thorough tooth brushing and flossing and regular professional
cleaning and examination may be helpful to prevent these disorders.
*Minimize injury in the mouth when possible
*Avoidance of primary irritants such as hot foods, spices, tobacco, and alcohol
= SIGNS AND SYMPTOMS
*Pain and swelling of the tongue may be present when glossitis is associated with
infections, trauma, or lichen planus
«Red, smooth appearance of the tongue due to loss of filiform papillae
«Pale tongue if caused by pernicious anemia
*Ulcerations may be present in patients with herpetic glossitis, pemphigus, or
streptococcal infection
“Excessive use of mouthwash may result in a “hairy” appearance of the tongue
*Sore and tender tongue
Tongue color usually dark "beefy" red
¢Difficulty with chewing, swallowing, or speaking
TREATMENT - varies with the etiology of the glossitis; the goal of treatment is to reduce
inflammation; it usually does not require hospitalization unless tongue swelling is severe.
*MALNUTRITION WITH AVITAMINOSIS - multivitamins
*CANDIDIASIS
FLUCONAZOLE = 200 mg on day 1, then 100 mg/day for at least 2 weeks
®NYSTATIN = 400,000 U suspension q.i.d. for 10 days or 200,000 pastilles dissolved
slowly in the mouth 4-5x q.i.d. for 10-14 days
¢PAINFUL ORAL LESIONS
2% LIDOCAINE VISCOUS = 1-2 tbsps q 4 hrs prn to rinse the mouth
=» TRIAMCINOLONE 0.1% - applied to painful ulcers prn for symptomatic relief
*LIFESTYLE CHANGES - with elimination of tobacco, alcohol, and other primary irritants
*DENTAL EVALUATION - for correction of ill-fitting dentures
eCORRECTION OF ASSOCIATED METABOLIC ABNORMALITIES - such as
hyperglycemia from DM
«GOOD ORAL HYGIENE
*CORTICOSTEROIDS - such as prednisone may be given to reduce the inflammation of
glossitis; for mild cases, topical applications (such as prednisone suspension that is
used as a mouth rinse but not swallowed) may be recommended to avoid the side effects
of systemic (swallowed or injected) corticosteroids.
“ANTIBIOTICS
*TREATMENT OF ANEMIA AND NUTRITIONAL DEFICIENCIES - often by dietary changes
or other supplements. “~
PROGNOSIS - glossitis usually responds well to treatment if the cause of inflammation
is removed or treated; this disorder may be painless or may cause tongue and mouth
discomfort; in some cases, glossitis may result in severe tongue swelling that blocks the
airway.
= COMPLICATIONS
*Airway blockage
*Difficulties with speaking, chewing, or swallowing

41
XVI. MEDIAN RHOMBOID GLOSSITIS

- it is an inflammatory or infectious condition of the dorsum of the tongue; it is an
uncommon condition; the estimated prevalence in adults is < 1%; although in the past it
was considered a developmental failure of the branchial arches to cover the tuberculum
impar, over the past 20 years, evidence of an associated candidiasis has provided a more
likely pathogenesis; in the majority of cases, Candida organisms can be cultured from
the lesion and clinical resolution occurs following systemic antifungal therapy; histologic
examination reveals hyphae penetrating the superficial epithelium of the tongue, with
focal neutrophil microabscesses.
- it is found predominantly in men (3:1) and it is usually recognized by the 4th decade.
the
= CLINICAL FEATURES - it presents as a smooth well-demarcated area of erythema at
junction of the anterior 2/3 and posterior 1/3 of the tongue.
- it consists of the presence of a red, smooth diamond-shaped area in the midline of the
tongue just anterior to the inverted "v" formed by the presence of the circumvallate
papillae; this area is depapillated, slightly raised, sometimes tufted, or at times slightly
lobulated.
-it frequently has a diffuse red color, which is in contrast with the lighter pink or white
color of the surrounding tissue; the absence of papillae permits the underlying blood
vessels to shine through the mucosa, and the tongue looks red and slick; it has the same
muscular consistency as the rest of the tongue but it is devoid of the usual papillary
coating.
- it is usually asymptomatic and recognized mainly during the course of P.E. or because
of painful symptoms arising from mild inflammation in the fissured area; when pain is an
accompanying symptom, the concern about developing ca is ever present.
DIAGNOSIS - can be made relatively easily from the clinical appearance.
< TREATMENT - the use of systemic antifungal agents, such as Fluconazole and Iconazole,
has produced encouraging results.
XVII. BENIGN MIGRATORY GLOSSITIS (GEOGRAPHIC TONGUE)

- a descriptive term applied to a map-like appearance of the tongue resulting from
irregular denuded patches on its surface; it is caused by a desquamation of the filiform
papillae in different regions of the tongue; the tongue has characteristic irregular-shaped
white and red spots; the fields move along the tongue; the different colors and patterns
give the surface a “map-like” look; the pattern on the surface of the tongue may change
very rapidly; the pattern results from the loss of tongue papillae, giving areas of the
tongue flat spots, and the subsequent geographic appearance; these areas of papillae
loss are called denuded and they may persist for more than a month; occasionally, mild
irritation of the tongue is reported.
ETIOLOGY - its exact etiology has not been established, although it has been suggested
that it is related to a decrease in the keratinase enzyme; it is recognized more frequently
in children and young adults.
*May be associated with stress
*May be exacerbated by menses i
*Individuals with an allergic background more likely to develop this abnormality.
Some clinicians have reported a hereditary tendency to this condition.
*A psychosomatic background has also been suggested.
eLocal irritation of a small portion of the tongue from hot or spicy foods, alcohol, tobacco,
or other local irritants.

cs
42
CLINICAL FEATURES - this condition is characterized by the appearance of irregular
depapillated, erythematous areas surrounded by pale well-demarcated margins on the
dorsal surface and lateral margins of tongue such areas appear and regress relatively
quickly over a period of a few days; rarely, similar-appearing lesions can be found on
other mucosal surfaces; the condition is relatively common and can affect any age group,
including young children; patients are often unaware of the presence of geographic
tongue, although some individuals complain of discomfort on eating, especially hot or
spicy foods.
¢Map-like appearance to the surface of the tongue
¢Patches and lesions on the tongue
*Sore and burning pain (in some cases)
*Beefy red and smooth tongue
eLocation changing from day to day
*Gustatory relay or loss
- the lesions are usually multiple and consist of irregular depapillated areas which
appear as pink to red macular spots; areas of the dorsal surface of the tongue are
depapillated exposing the underlying thin epithelium, revealing the reddish areas of the
tongue musculature, which gives the appearance of inflammation; these papillae
undergo alternating regeneration and desquamation, causing the shiny area to change
location - thus the term migratory.
-the characteristic feature of the lesions is that they vary their position from day to day;
the duration of a lesion in any particular area of the tongue varies from 3-7 days; the
joining of one or more of the irregular depapillated areas produces a mapled
appearance on the dorsum of the tongue giving rise to the common name.
- the lesions of BMG are seldom recognized by the patient unless there is burning of
the affected areas; the pain and burning sensation is usually aggravated by ingestion of
highly seasoned food, salad dressing, carbonated or alcoholic beverages and by
smoking.
TREATMENT - the patient should be reassured about the benign nature of the condition;
nutritional deficiency should be excluded in all patients with symptomatic geographic
tongue; BMG requires no specific treatment because the condition is usually self-limiting;
as the individual gets older, the disease tends to be less severe.
*VITAMIN A
*ZINC SULFATE = 125 mg dissolved in water and used as a mouthwash for approximately
2-3 minutes every 8 hours over 3 months.
PREVENTION - avoid local irritation (hot/spicy food, alcohol, tobacco, and so on) if you
are prone to geographic tongue.
XVII. FISSURED TONGUE (SCROTAL TONGUE)

- itis the most common developmental anomaly of the tongue; there seems to bea linear
progression in the prevalence of this entity with age, being seen in 1% of infants and
approximately 2.5% of children and in 4% of young adults; it follows an autosomal
dominant inheritance pattern. Goon
em
= ETIOLOGY
eCONGENITAL OR INHERITED - it is seen in Down’s syndrome or Melkersson-Rosenthal
syndrome; it is considered to be a familial disorder, but it is not always congenital.
eINFECTION eMALNUTRITION
¢VITAMIN A DEFICIENCY *TRAUMA

43
= SIGNS AND SYMPTOMS - fissured tongue is an asymptomatic condition, unless food
particles and debris lodging in the depths of the fissures cause a mild glossitis; this
condition is characterized by tongue papillae divided into groups and clumps of small
fissures which may not be apparent until the tongue is folded; the fissures may also be
interconnected; the pattern of the fissuring varies widely from the haphazard
arrangement to the symmetrical pattern similar to the veins of a leaf; the groove pattern
on the dorsum of the tongue, as well as the length, the number and the depth of the
grooves is variable; these changes are of no pathological significance except for the
mild and painful sores that may occur; these are associated with the inflammation of the
fissures resulting from the collection of food debris in the depths of the fissured areas.
TREATMENT - is not necessary for a fissured tongue except for any infections caused
by trapped food.
*ORAL HYGIENE - the mild inflammatory symptoms may be treated with the usual
procedures for improvement of oral hygiene and assurance to the patient that these
inflamed "cracks" will not predispose to oral ca.
*HYDROGEN PEROXIDE - when the fissured areas become painful as the result of
seconary infection, the lateral edges of the tongue shall be rolled downward when the
tongue is protruded; then the exposed fissured areas can be swabbed gently with a 3%
hydrogen peroxide solution to remove the decomposing food debris.
*WARM MOUTHWASH - or an occasional coating of the tongue with unflavored milk of
magnesia will relieve the painful symptoms; these agents are not curative but tend to
relieve the painful symptoms.
XIX. BLACK HAIRY TONGUE

-itis characterized by elongation of the filiform papillae (3 mm or longer) and the growth
of a black pigment-producing fungus on the papillae; the tongue can also appear brown,
white, green, pink or any variety of hues depending on the specific etiology and
secondary factors (i.e., use of colored mouthwashes, breath mints, candies); yeast
organisms have been seen within the keratin of these elongated filiform papillae; the
surface epithelium is usually inflamed.
= ETIOLOGY - it is caused by a filamentous hyperkeratosis of the filiform papillae, which
look like hairs on the tongue’s surface; the elongation of papillae is caused either by a
loss of desquamation or by an increased production of keratin; the hyperkeratosis is
triggered by
*Antibiotic therapy ¢Chronic mucosal irritation
*Nicotine abuse eMetabolic imbalance
eTherapeutic radiation of the head and neck
SYMPTOMS - various colorations of the tongue from brown to black may result from the
overgrowth of various pigment-producing organisms.
= PATHOLOGY - the tips of the filiform papillae are elongated and usually composed of
normally short tufts of cornified cell material, but in this case may project overall 2-4 mm
outward; they are usually gathered toward the posterior portion of the tongue.
= TREATMENT - it is harmless and usually disappears spontaneously.
*SURGICAL REMOVAL OF THE EXCESSIVELY LONG PAPILLAE - by _ using
electrodesiccation, carbon dioxide laser or even scissors.
*TOPICAL ANTIFUNGAL MEDICATIONS - when symptomatic and candida albicans is
present
*ANTIFUNGAL AGENTS - cotrimazole, nystatin, ketoconazole, fluconazole
ePROPER HYGIENE - the patient should brush the dorsum of the tongue 2-3x/day
eDISCONTINUE ORAL ANTIBIOTICS IF POSSIBLE

44
*APPLYING OXIDIZING SOLUTIONS - it has been found that a lower ph of the surface of
the tongue is more resistant to the development of black hairy tongue.
XX. LINGUAL VARICOSE VEINS (CAVIAR TONGUE)

- they appear as bluish bulges under the mucosa; varicose veins can develop on the
ventral surface of the tongue; the lingual veins onthe undersurface of the tongue are
usually present.
- in the later years of life, they may become prominent, tortuous and present well-
developed varicosities; they are also noted in the valleculae and sometimes over the
surface of the tongue base.
- patients with these lesions are usually >40 years old with little sex predilection; many
patients with these lesions develop a fear of malignancy or uncontrollable hemorrhage.
XXI. HUNTER’S GLOSSITIS (DERNICIOUS ANEMIA)

- itis achronic disease which results from a deficiency of intrinsic factor, a substance
secreted by the parietal cells of the fundus of the stomach which is necessary for the
absorption of vitamin B12 which takes place in the ileum.
- the disease can affect all racial groups, but the incidence is higher among people of
Scandinavian or Northern European descent.
- pernicious anemia usually does not appear before the age of 30, although a juvenile
form of the disease can occur in children; juvenile or congenital pernicious anemia is
evident before the child is 3 years old; the incidence is 1 out of 1,000 people.
ETIOLOGY - it is due to a deficiency of vitamin B12, which is necessary for DNA synthesis
of rapidly dividing cells, such as those found in the bone marrow; the primary cause of
pernicious anemia is autoimmune-mediated destruction of gastric parietal cells that
produce intrinsic factor which binds to vitamin Bizin the stomach and is responsible for
intestinal absorption of the vitamin.
= RISK FACTORS
*History of autoimmune endocrine disorders
*A family history of pernicious anemia
«Scandinavian or Northern European descen
= CLINICAL FEATURES - patients have clinical signs and symptoms of anemia including
weakness, lethargy, fatigue, shortness of breath, and pallor; in severe cases there are
central neurological manifestations including peripheral neuropathies, headache,
dizziness, and tinnitus; within the mouth the dorsum of the tongue is erythematous,
painful, and depapillated.
SYMPTOMS - the tongue shows an atrophic inflammation; associated symptoms are
burning of the tongue combined with paresthesia and dry mouth; the surface of the
tongue is atrophic and glazed, sometimes with a flushed appearance.
-the tongue symptoms and changes are prominent and common and a painful glossitis
and glossopyrosis may be early symptoms of this disease; the glossitis is characterized
by its fiery red color and its usual distribution to the tip and the margins of the tongue,
with papillary atrophy of the affected area; in advanced disease there is diminution of the
papillary anatomy of the entire tongue, with a loss of the normal muscle tone; some
patients also complain of a loss of taste sensation; there are spontaneous remissions
and exacerbations of the glossitis. ”
DIAGNOSIS - to diagnose the cause of glossitis, the serum level of vitamin Biz must be
measured.
TREATMENT - the condition is managed by parenteral injections of vitamin B12, first ona
weekly basis then subsequently at 1- or 3-monthly intervals for life; the oral symptoms of

45
pernicious anemia resolve rapidly after the correction of the deficiency; response to this
therapy is usually seen within 48 to 72 hours, so there is usually no need for blood
transfusions as a treatment for very low blood counts.
- oral vitamin Biz is not recommended because it will not produce the desired response
(the problem is an inability to absorb vitamin B12, not a lack of the vitamin in the diet).
- a well-balanced diet is essential to provide other components for healthy blood cell
development such as folic acid, iron, and vitamin C.
XX. TUBERCULOSIS OF THE TONGUE

- primary infection of oral mucosa is rare; these lesions are observed more often in
patients having advanced TB, but they develop at times in patients without other
demonstrated symptoms of the disease; although lesions may develop as the result of
contact of the tissues with infected material by direct extension of a tuberculous process
or by hematogenous seeding or lymphatic spread, they are most often associated with
pulmonary TB and result from contact of the oral tissues with infected sputum.
-the tongue is the most frequent site of oral lesions, but the cheeks, the lips and the
palate also are involved; tongue lesions develop commonly where the lateral margin of
the tongue rests against rough, sharp or broken down teeth, or at the site of other
irritants; deep central ulcers of the tongue are usually typical in appearance with a thick
mucous material in the base of the ulcer; the method of inoculation is undetermined in
most oral lesions; however, patients with oral lesions often give a history of pre-existing
trauma.
- any area of chronic irritation or inflammatory response may furnish a favorable site for
localization of organisms; oral lesions are characterized by severe, unremitting, and
progressive pain, which interferes seriously with proper nutrition and rest.
TREATMENT - local palliative treatment of oral lesions is supplemental to the systemic
treatment; the establishment of good oral hygiene and the elimination of all source of
irritation should be the first phase of treatment; the elimination of traumatic irritation of
the mucosa and the tongue minimizes the possibility of the development of oral mucosal
lesions.
XXII. HEMANGIOMA
- it is usually congenital, and 90% affect girls; the sites of predilection are the tongue,
cheek, and parotid regions; the tumor may be so large that it becomes life-threatening
due to recurrent bleeding, airway obstruction, or obstruction of eating; these tumors
often resolve spontaneously within the first 2 years of life, and surgical removal should
therefore be delayed if possible until age 3 or 4.
- it is a tumor-like malformation composed of seemingly disorganized masses of
endothelial lined vessels that are filled with blood and connected to the main vascular
system; these are congenital malformations and tend to decrease in size at puberty.
- larger ones tend to persist through adult life; such lesions characteristically bleed
profusely when traumatized; many hemangiomas are evident at birth, and they frequently
increase in size with general bodily growth; filling of previously empty vascular channels
also accounts for an increase in size of these lesions, such changes sometimes occurring
very rapidly following trauma; hemangiomas of the tongue and gingiva are often caused
by unusually rugose epithelium. :
Es
—TYPES
*CAPILLARY HEMANGIOMAS (STRAWBERRY HEMANGIOMAS) - consist of a mass of
small, fine capillary vessels that project into the skin so that a macular, pink to red skin
abnormality is noted; they may occur anywhere in the oral cavity, although the lips,

46
tongue and buccal mucosa are most frequently affected; they appear as well-
circumscribed, flat or raised lesions with a blue discoloration; they may be found in as
many as 2.5% of all newborns, but as many as 50-70% spontaneously involute by age 7.
*CAVERNOUS HEMANGIOMA - contains large, thin-walled vascular spaces; the masses
occur typically in the head, neck, lips, tongue, and larynx; symptoms result from the
deforming effect of the mass; a mixed type can occur.
DIAGNOSIS - blanching of the lesion when pressure is applied to it using a glass slide can
confirm the presence of a cavernous hemangioma.
TREATMENT - majority of cases of hemangioma do not require active treatment;
however, prominent or nodular regions can become progressively traumatized and give
rise to hemorrhage.
the
- if the tumor is growing quickly, embolization of the feeding vessel arising from
external carotid artery may be attempted or diethylstilbestrol can be given for a limited
period.
- if symptoms persist, small, localized lesions can be surgically excised or treated with
cryotherapy; more extensive or deep lesions require specialist management including
surgery and the possible use of sclerosing agents or embolization.
XXIV. RANULA
- it is a mucin-filled cystic or pseudo-cystic transilluminable swelling in the floor of the
mouth; blockage of the submandibular or sublingual gland duct may cause a large
mucocele in the floor of the mouth, with external swelling; the oral lesion consists of a
bluish discoloration and dome-shaped swelling of the mucosa in part of the floor of the
mouth; pressure upwards on the cervical swelling makes the oral lesion more prominent
and demonstrates their essential continuity; it is compressible and usually located
unilaterally in the vicinity of one of the submandibular ducts; it has a tendency to recur.
- there may be a history of repeated bursting of the ranula into the mouth with discharge
of a little watery fluid followed by healing.
TREATMENT - aspiration or incision and drainage may not prevent a recurrence; a
complete extirpation of the cyst is preferable either through the mouth or if the cyst is
large and has burrowed inferiorly it may be removed through the neck; it is essential to
remove that part of the floor of the mouth which contains the leaking duct; if the cervical
part of the swelling occupies the submandibular salivary gland region, itis very likely that
the duct concerned is the submandibular duct; the submandibular salivary gland should
be removed from the neck at the same operation.
XXV. DERMOID CYST

- it develops from a misplaced fetal inclusion that takes an activity and forms a cyst;
dermoids commence shortly after birth, but on the account of their slow and painless
growth attract little attention until their size gives annoyance; they project into the floor
of the mouth or into the neck behind the chin or both places; at times, they attain the size
of an orange.
-the round or oval dermoid cyst has a thick wall lined with stratified epithelium; it
usually contains hair or other skin appendages and certain fatty bodies and fatty acid
crystals; it probably results from incorporation of ectoderm at the time of closure of
embryonic fissures during the 3rd and 4th weeks:in utero.
- oral dermoid cysts most commonly arise in the floor of the mouth and have been
classified into median and lateral dermoid cysts; they probably originate above the
mylohyoid muscle, although they may penetrate through a developmental hiatus; they
usually become evident between 12-25 years old.

41
A. SUBLINGUAL OR GENIOGLOSSAL DERMOID CYST - the cyst is located above the
geniohyoid muscle and causes elevation and displacement of the tongue, producing
difficulty in speaking, eating, and even breathing due to pressure exerted upon the
epiglottis.
B. SUBMENTAL OR GENIOHYOID DERMOID CYST - the cyst is deeper, between the
geniohyoid and mylohyoid muscles and may bulge into the submental area; it 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 cause a bulge in
the oral floor; the cyst varies in size but may approach several centimeters in diameter;
it usually feels doughy but may be more fluctuant.
- microscopically, the lining of the cyst is a keratinized stratified squamous epithelium;
one or more skin appendages such as hair follicles, sweat glands, or sebaceous glands
are present; in the absence of skin appendages, it is not considered a dermoid cyst but
an epidermoid cyst.
XXVI. TORUS PALATINUS

- it is a bony exostosis of varying size and shape located in the midportion of the hard
palate, which is covered by the palatal epithelium; the mass is usually solitary and located
in the midline; there is no increased potential for malignant degeneration.
- Clinically, it may interfere with proper fitting of dentures and require surgical removal; it
must be distinguished from tumors of the minor salivary glands and fissural cysts of the
palate
TREATMENT - excision is advisable only when it is necessary for proper fitting of a
maxillary denture.
¢Surgical removal by drilling
¢Surgical removal by chisels
XXVIII. TORUS MANDICULARIS

- itis a bony exostosis usually situated on the lingual surface of the mandible adjacent to
the cuspid and first bicuspid teeth; it is asymptomatic until an attempt is made at fitting
a denture.
TREAMENT - is only required if
*Lower dentures no longer fit
*Exostosis has recurrent infections
*Ulceration
*Neoplasm
XXXVI. ANKYLOGLOSSIA (TONGUE-TIE)

- it is a congenital anomaly characterized by an abnormally short, thick lingual frenulum,
which affects movement of the tongue; ankyloglossia may cause breastfeeding, tongue
mobility and speech difficulties; however, there are no standard guidelines or criteria for
the management of ankyloglossia. It is a cofitroversial subject and it also remains
controversial which tongue ties need to be managed surgically and which can be left for
observation.
~ during the first 4 to 5 years of life, the oral cavity changes significantly in shape and
size; ankyloglossia can be significant at birth, but usually the functional effects tend to
decrease with time and oral growth.
- therefore, as the child grows, the severity of the ankyloglossia can become less
apparent and the initial restrictions of lingual frenulum movement are usually diminished.

48
- despite this information, there is evidence to suggest that in some cases surgical
measures to release the frenulum can aid in breastfeeding and speech problems.
- partial ankyloglossia is manifested by an abnormally short and thick lingual frenulum;
various degrees of ankyloglossia occur, ranging from mild restriction with only a mucous
membrane band to those in which both the frenulum and the underlying fibers of the
genioglossus muscle are markedly fibrosed; rarely, complete ankyloglossia with fusion
of the tongue to the floor of the mouth may be encountered.
= RESULTS OF LIMITATION OF MOVEMENT OF THE TONGUE TIP
eMalocclusion with an anterior "open bite" deformity,
eEarly prognathism
¢Swallowing and speech difficulties
quire
TREATMENT - children with severe ankyloglossia meeting any of these criteria re
¢«Frenulectomy
eGenioglossus myotomy
«Mucous membrane closure with multiple Z-plasties
INDICATIONS
*Persistent lactation difficulties despite efforts and instruction by a lactation specialist
*Speech impairment accompanied with ankyloglossia;in however, other causes of
speech problems should be considered and fully assessed by a speech-language
pathologist.
PROCEDURE
FRENULECTOMY (also called frenotomy, frenectomy, and frenuloplasty) is the main surgical
treatment to release or remove an ankyloglossia; in an infant, a lingual frenulectomy can
be done in the office with no anesthetics; the procedure takes less than a minute to
perform; the frenulum is divided with scissors and since the frenulum is so thin, it
generally requires no sutures; tongue mobility is usually adequate enough to prevent
adhesions from forming.
- however, in older children, a frenulectomy usually requires a trip to the operating room
for general anesthesia to ensure adequate cooperation from the patient.
- a lactation specialist often refers infants for evaluation if the infant is having trouble
breastfeeding; although ankyloglossia is a common cause of breastfeeding difficulties, it
is not the only cause; it is important to emphasize to the mother that breastfeeding
difficulties may or may not be improved post frenulectomy; if a short frenulum was the
contributing cause of the breastfeeding difficulties, then post frenulectomy, the mother
should see less compression of the nipple by the tongue, better attachment, increased
milk transfer, and less maternal pain; if a short frenulum was the contributing cause
associated with articulation problems, then post frenulectomy the child with
ankyloglossia should see improvement with tongue mobility and speech.

DISEASES OF THE NASOPHARYNX,
OROPHARYNX & NECK
1. SYMPTOMS OF DHARYNGEAL DISEASE . .
°PAIN - is the most common complaint; tonsil pain is made worse by swallowing and is
typically referred to the ear since the Vth CN supplies both sites; pain that is present all
the time and causes trismus suggests either a quinsy or a spread of an oropharyngeal
tumor to the pterygoid muscles.
*DYSPHAGIA
TYPES
®TRUE DYSPHAGIA - is a real difficulty in swallowing food, resulting in food coming
back into the mouth, slow eating and loss of weight; it means the presence of a cancer of
the hypopharynx or esophagus until proven otherwise and is usually progressive.
®A FEELING OF A LUMP IN THE THROAT - may be the early symptom of a cancer but is
usually due to a spasm of the cricopharyngeus secondary to stress, reflux esophagitis,
pharyngeal pouch or pressure from a big thyroid or cervical osteophytes.
®DIFFICULTY INSWALLOWING DUE TO PAIN -is seen in pyriform sinus tumors but is
most commonly a symptom of tonsillar infection.
*SPEECH PROBLEMS - muffled speech can occur in hypopharyngeal and oropharyngeal
tumors of some size, and hyponasality is heard if a big nasopharyngeal mass blocks the
posterior choanae and pushes the palate down.
*REGURGITATION OF RECENTLY EATEN FOOD - signifying a pharyngeal pouch
*NASAL SYMPTOMS - epistaxis and nasal obstruction - from nasopharyngeal lesions.
*LUMPS IN THE NECK - enlarged neck nodes are common in both infections and tumors.
- the whole larynx may also enlarge in pyriform sinus tumors.
Hl. EXAMINATION
eNASOPHARYNX
=® POSTERIOR RHINOSCOPY - the nasopharynx is examined with a tongue depressor and
nasopharyngeal mirror; it takes several attempts to view the whole nasopharynx and it is
often necessary to spray the soft palate and base of tongue with lignocaine to stop
gagging.
™®NASAL ENDOSCOPY - to view both eustachian tubes, the adjacent fossae of
Rosenmuller, the roof of the nasopharynx and the choanae.
*OROPHARYNX - can be easily seen by depressing the tongue with a tongue depressor;
the examination should be orderly, looking at each of the areas in turn - the tonsils and
fauces, the soft palate and the posterior pharyngeal wall; to see the floor of the
oropharynx, i.e. the base of tongue and valleculae, the tongue should be pulled forwards
and a laryngeal mirror used; the lateral walls and base of tongue should always be
palpated if a tumor is suspected: the lateral walls to examine for fixation and the tongue
base because tumors in this region start deep and come to the surface late.
*HYPOPHARYNX - is examined with a laryngeal mirror and it may be necessary to
anesthetize the area with a local anesthetic ‘to stop gagging; the examination should be
orderly and both pyriform sinuses should be clearly seen, in addition to the arytenoids
and the posterior wall; the use of the flexible endoscope helps in the patient who cannot
tolerate a mirror.
*NECK - should be palpated; it is necessary to record exactly the position, number, size
and fixation of any nodes; the distribution is helpful; posterior triangle nodes are often

2
found in viral infections and supraclavicular nodes are seen in gastro-esophageal and
lung lesions; it is important to palpate the thyroid and to assess the mobility of the larynx.
i. RADIOLOGY
PLAIN FILM - in nasopharyngeal disease a simple lateral view gives an indication of the
size of the mass; base of skull views show evidence of erosion of the skull base; it is of
little value in oropharyngeal disease, but in hypopharyngeal lesions a simple lateral film
of the neck may show an increase in the soft-tissue shadow in the postcricoid space.
*CONTRAST FILMS - the most useful film is barium swallow which will demonstrate a
pharyngeal pouch, an esophageal web, a hypopharyngeal tumor or pressure from without
by a thyroid swelling or cervical osteophytes.
*CT SCANS - are essential in the evaluation of all nasopharyngeal lesions to assess
whether or not there is intracranial spread; in oropharyngeal lesions a CT scan will
demonstrate spread to the parapharyngeal space; in hypopharygeal lesions scans are
especially helpful if extraesophageal spread is suspected at the thoracic inlet.
iV. ACUTE ADENOIDITIS

- the adenoid tissue may chronically harbor infection or become acutely infected during
respiratory tract infections or sinusitis.
= SYMPTOMS
*Nasal obstruction ¢Purulent nasal discharge °Fever eEar pain
*Hyponasal speech ¢Postnasal drip *Throat pain
= EXAMINATION - may reveal inflamed, exudative adenoid tissue
= TREATMENT - Penicillin is the drug of choice; broad-spectum antibiotics can be given.
VY. ADENOID HYPERTROPHY (Al)

- is a common cause of upper airway obstruction in children that has a wide range of
clinical manifestations and complications; adenoids, or nasopharyngeal tonsils, are
located in the roof of the nasopharynx.
- they rapidly enlarge after birth and start to become prominent by 2- 3 years old, reach
a maximum size between 7-10 years old, often filling the entire nasopharynx and
extending into the posterior choanae; thereafter they progressively decrease in size
through adulthood; spontaneous resolution is expected.
- regression starts in early adolescence and continues into later life; most people have
little if any identifiable adenoidal tissue by 30 to 40 years of age; however, normal
adenoids can occasionally be identified in patients 50 to 60 years old; males are more
commonly involved (70%) than females.
- if no adenoidal tissue is seen in a young child, the possibility of an immune deficiency
syndrome or immunosuppression should be considered; prominent adenoidal tissue in
adults should raise the possibility of HIV disease.
TRIAD OF HIV INFECTION
Increased adenoidal tissue ® Parotid cysts (lymphoepithelial cysts)
® Diffuse cervical lymph adenopathy
- since the advent of effective chemotherapy, the prominent adenoids and cervical
adenopathy need not be present in these patients.
ETIOLOGY - the common causes of adenoid hypertrophy in adults are chronic infection
and allergy; pollution and smoking are also important predisposing factors; also
associated with sinonasal malignancy, lymphoma, and HIV infection
*RECURRENT URI -is the chief cause of enlargement of the adenoid due to the irritation
and inflammation which occur in the nasopharynx.

3
*EUSTACHIAN TUBE DYSFUNCTION - with the resultant serous otitis media as well as
repeated episodes of acute otitis media.
¢Heredity *Chronic nasal congestion
¢Persistent allergy *Insufficient aeration
eInefficient nasal breathing elrritants
«GERD *Attending day care
SIGNS AND SYMPTOMS - are largely those resulting from the obstruction of the nose at
the posterior choanae end of the eustachian tubes; enlarged adenoids can become
nearly the size of ping-pong balls and completely block airflow through the nasal
passages; infants present with difficulty in feeding, whereas older children present with
symptoms of nasal obstruction, such as mouth breathing and snoring; otitis media may
result from encroachment on the orifice of the eustachian tube; hypertrophic adenoids
appear as a homogeneous fullness of the nasopharyngeal mucosal space, which
obliterates the fossae of Rosenmiiller and obstruction of the pharyngeal encroaches on
the nasopharyngeal airway.
“TRIAD
®CHRONIC MOUTH BREATHING
®SNORING - occurs because the mouth is open, especially at night, for the sake of
adequate airway.
™®HYPONASAL SPEECH - the difference in voice quality occurs because obstruction can
interfere with nasal breathing.
eCHRONIC RHINORRHEA INABILITY TO BLOW THE NOSE
ADENOID FACIES
Open mouth ®Long face » Dark circles around eyes
® Highly arched palate ® Vacant expression
®UPTURNED UPPER LIP - the patient may develop the habit of elevating the upper lip
to improve the ease of ingress of air.
*CHRONIC OR RECURRENT NASAL OBSTRUCTION
*RECURRENT EPISODES OF DEAFNESS - follow obstruction of the eustachian tubes;
in the beginning, the deafness is due to retraction of the TM; but if unrelieved, the
obstruction leads first to serous otitis media and second (with superimposed infection)
to suppurative otitis media.
*DIFFERENCE IN VOICE QUALITY - occurs because obstruction can _ interfere with
nasal breathing.
eCOR PULMONALE OR SLEEP APNEA-TYPE SYNDROMES - can develop in children
who are < 2 years old with adenoid hypertrophy.
¢Changes in dental structure and malocclusion Cough
*Conductive hearing loss *Recurrent AOM *Halitosis
= DIAGNOSIS - best diagnosed by clinical history and physical examination.
CHILDREN - further assessment can be done by pinching the nose and asking them to say
“baseball” or “Mickey Mouse” with the nose pinched and unpinched. Assess the degree
of change and muffled (nasal) appearing sounds during speech.
eNASAL ENDOSCOPY - is the ‘gold standard’ in assessing posterior choanal obstruction
although mirror examination is still widely used; the degree of choanal obstruction
caused by adenoidal hypertrophy was significantly higher when assessed by rigid
nasoendoscopy than when assessed by trans-oral mirror examination; nasoendoscopy
gives a more physiological view of the posterior choanae without disturbing the position
of the soft palate; it is the key diagnostic tool to detect both adenoid hypertrophy and
adenoiditis; it is difficult to do a mirror exam in children.
*LATERAL SOFT TISSUE X-RAY OF THE NECK - reveals a large adenoid shadow
impinging on the nasal airway; a lateral radiograph should be obtained during inspiration

4
through the nose, with the mouth closed; the adenoid-to-nasopharyngeal ratio may aid in
diagnosing prominent, clinically significant adenoids; in a symptomatic patient,
adenoidal hypertrophy can be suspected when the nasopharyngeal airway is narrowed
on lateral plain film; because tremendous variation in adenoidal size exists in the normal
pediatric patient, any measurement should be used with caution and clinical symptoms
must always be considered.
POLYSOMNOGRAPHY - may help confirm or establish the diagnosis and determine the
severity of sleep apnea, useful to assess the severity of the sleep-disordered breathing.
= ASSOCIATED CONDITIONS RELATED TO ADENOID HYPERTROPHY
Obstructive Sleep Apnea (OSA)
*Adenoiditis (Allergic or Infectious)
*Chronic otitis media or effusion associated with eustachian tube dysfunction
TREATMENT - management of patients with adenoidal hypertrophy depends in part on
the severity and the duration of the obstruction
*MEDICAL TREATMENT -- in milder cases of short duration or in patients with intermittent
symptoms, careful monitoring; treatment of atopy with intranasal steroids, when present;
or institution of a 2- to 4-week course of antimicrobial therapy with a B-lactamase-stable
agent may result in significant shrinkage of hypertrophied adenoidal tissues.
- a trial of nasal corticosteroids is indicated prior to surgical intervention. Intranasal
corticosteroids may significantly improve nasal obstruction symptoms in children with
moderate to severe adenoidal hypertrophy; this improvement may be associated with a
reduction in adenoid size.
eSURGICAL PROCEDURES -a recurrently obstructing hypertrophic adenoid should be
surgically removed during a period of health.
®TRADITIONAL ADENOIDECTOMY - is performed under general anesthesia, using the
blade of an adenotome or adenoid curette; this gross removal of tissue is usually followed
by bipolar electrocautery for hemostasis; the morbidity of this procedure is fairly low,
with minimal pain and a low incidence of postoperative bleeding, halitosis, or neck pain;
complete removal of all adenoid tissue is not possible because the adenoids are not
encapsulated like the tonsil so recurrent infection and hypertrophy are possible.
ADENOID CURETTE- has a sharp edge and is the most standard and conventional
successful method of removal; the adenoids are removed with the curette by feel after
placing it in position in the nasopharynx; various sizes of curettes are available to
accommodate the various sizes of nasopharynges. Hemostasis is controlled with packing
and electrocautery.
POWER ASSISTED MICRODEBRIDEMENT - can be performed either transnasally or
transorally; the adenoid is removed by using an ossillating blade, shaver, under direct
vision with a defogged endoscope which enables the surgeons to perform surgery faster
than a curette technique; to sculpt the tissue as they desire, with minimal bleeding and
similar efficacy; it has been advocated for removing adenoid tissue that is difficult to
reach using other techniques.
SUCTION ELECTROCAUTERY - the adenoids are removed by a combination of
coagulation and suction; it has been used to thermally ablate the tissue layer by layer.
- these surgeons contend that the controlled removal of the adenoids makes both
nasopharyngeal stenosis and velopharyngeal insufficiency less likely to occur; the
procedure is complete when the posterior choanae are clearly visible.
*INDICATIONS FOR ADENOIDECTOMY
® NASAL OBSTRUCTION
®Chronic mouth breathing
=Sleep apnea, excessive snoring, other sleep disturbances, enuresis

5
#Adenoid hypertrophy resulting in craniofacial growth abnormalities, cor pulmonale, or
attention deficit hyperactivity disorder (ADHD)
» INFECTION
BAdenoid hypertrophy associated with chronic sinusitis, unresponsive to medical
therapy
®Chronic purulent nasopharyngitis despite adequate medical management
®Chronic adenoiditis or adenoid hypertrophy associated with production and persistence
of middle ear effusions (serous otitis media or mucoid otitis media).
#Recurrent acute suppurative otitis media that has not responded to medical treatment
with prophylactic antibiotics
"Certain cases of chronic suppurative otitis media in children with associated adenoid
hypertrophy
=Purulent adenoiditis - many organisms can induce the inflammation in Waldeyer’s ring
and most infections are polymicrobial, working synergistically, causing mixed infections;
hyperplastic or even normal size adenoids might be a source of recurrent infection;
recent reviews show biofilms in adenoid tissue as the main reservoir of resistant bacteria
in children with URIs, what is generally associated with inadequate antibacterial
treatment.
SUSPICION OF A NASOPHARYNGEAL MALIGNANCY (biopsy only)
eCONTRAINDICATIONS
»Cleft palate Blood dyscrasias
®Submucous clefts ® Medical contraindications
Recent pharyngeal infection
VI. ACUTE DHARYNGITES

- pharyngitis is an inflammatory disease of the mucosal and submucosal structures of
the throat; it is a painful inflammation of the pharynx that is usually accompanied by acute
rhinitis, though the pharynx may be involved to a greater extent than the nose or larynx;
infection of the tonsils and larynx may occur simultaneously.
- itis prevalent during the cold season; it occurs in outbreaks during winter and early
spring, predominantly involving children 5 to 15 years of age; Group A B-Hemolytic
Streptococcus (GABHS) is uncommon in preschool-age children and in adults; it is more
common in children than in adults after the age of 6 months; as the maternal immunity
fades, children become more susceptible to URI.
- an increased rate can be expected f ,the child attends day care; in children < 3 years,
the predominance of a viral cause is even higher than in school-age children; children
may experience 6-8 URIs per year, with approximately 50% of them associated with
pharyngitis; Group C &-Hemolytic streptococcus pharyngitis occurs mainly in college
students and young adults.
- PATHOGENESIS - primarily infectious, may be secondary to:
¢Sinonasal disease ¢Caustic injury *Chronic allergy
*GERD ¢Smoking *Endotracheal intubation
Neoplasia ¢Pollution .
ETIOLOGY ™
*VIRAL CAUSES OF PHARYNGITIS (30-60%) - viruses are the most common cause of
acute pharyngitis; it may start as a sore throat or be preceded by colds and conjunctivitis.
RHINOVIRUS OR ADENOVIRUS - most common, usually associated with conjunctivitis
and higher fever.
*® EPSTEIN BARR VIRUS (EBV) OR CYTOMEGALOVIRUS(CMV)
HERPES SIMPLEX VIRUS - pyrexic patient, tachycardic with tender lymph nodes with
vesicular lesions on the mucous membranes, occasionally the oropharynx.

6
® INFLUENZA TYPES A and B OR PARAINFLUENZA VIRUS - associated with cold or
croup symptoms.
®CORONAVIRUS - associated with common cold symptoms.
®ENTEROVIRUS - usually small vesicles are present on the tonsils, tonsillar pillars,
uvula, or soft palate on examination
® RESPIRATORY SYNCYTIAL VIRUS - usually accompanied with LRT symptoms.
»ECHOVIRUS »®»REOVIRUS
® HUMAN IMMMUNODEFICIENCY VIRUS »COXSAKIE VIRUS
«BACTERIAL CAUSES OF PHARYNGITIS- it may be complicated by a secondary bacterial
infection; the posterior pharynx is congested with mucopus and enlarged lymphoid
tissues.
® GABHS (Streptococcus pyogenes) - is the most common bacterial cause of pharyngitis
(especially in children); up to 37% of all cases of pharyngitis in children and 5-15% in
adults; Streptococcal pharyngitis is relatively uncommon before 2-3 yrs of age, quite
common among children 5-15 yrs old, and declines in frequency in late adolescence and
adulthood; illness occurs throughout the year but is most prevalent in winter and spring;
it is readily spread among siblings and schoolmates; GABHS causes 15-30% of
pharyngitis in school-age children.
INCUBATION PERIOD OF GABHS - lasts from 12 hours to 4 days.
®» NEISSERIA GONORRHEA
®FUSOBACTERIUM NECROPHORUNM - 10% of pharyngitis: highest incidence in
patients aged 15-30 years old.
OTHER ORGANISMS
®&STAPHYLOCOCCUS AUREUS ® ARCANOBACTERIUM HAEMOLYTICUM
CORYNEBACTERIUM DIPHTHERIAE ® CHLAMYDOPHILA PNEUMONIAE
® HAEMOPHILUS INFLUENZAE ® MYCOPLASMA PNEUMONIAE
‘FUNGAL CAUSES OF PHARYNGITIS - the most common isolated organism is Candida
albicans, but other organisms - C. glabrata, C . tropicalis, C .dubliniensis, C. rugose,
andC.krusei are now emerging as causative agents, especially in immuno-
compromised patients and in those that have received previous radiotherapy.
- because C albicansis a normal commensal of the oral cavity, oropharyngeal
candidiasis (OPC) is considered an opportunistic infection and is now the most frequent
opportunistic infection.
= PATHOLOGY - the pharynx is often the first site of infection because viruses and bacteria
often settle in this part of the body after a person inhales dust or water vapor containing
the microorganisms; infection can also arise when a person touches their nose or mouth
after having touched an object shared with another person with the disease; the foreign
invader reproduces rapidly after settling on the body tissue.
= SIGNS AND SYMPTOMS OF PHARYNGITIS
*BACTERIAL INFECTION - patients with severe sore throats accompanied by fever are
more likely to have infections of bacterial origin; sometimes children will have an
associated scarlatinal rash and may also complain of gastrointestinal upset and
headache; pharyngeal erythema and possibly even an exudate will be found; edema of
the soft palate and uvula with tender upper jugular adenopathy is occasionally present. —
- in infants, it may present with refusal to’ feed, drooling, fever and diarrhea; most
suggestive of bacterial pharyngitis are diffuse redness of the throat and the tonsillar
pillars with petechial mottling of the soft palate, absence of URI symptoms, and vomiting.
GONOCOCCAL PHARYNGIMS - is usually asymptomatic but may present with a high fever
and gingivostomatitis.
*VIRAL INFECTIONS - are more common in patients who have moderate pharyngitis;
they begin gradually, cause less intense inflammation, produce a milder degree of illness,

3rd or 4th 7
last a shorter period and produce fewer complications than the bacterial infection; viral
infections manifest with fever, refusal to feed, general malaise, headache and moderate
throat pain; acute onset and high fever from onset suggest viral etiology; the fever is
highest on the 3 or 4‘ day; throat pain may be absent in the beginning; in some cases,
it appears early but rarely as severe as in bacterial pharyngitis; clustering of cases in the
family or neighborhood would suggest a viral etiology.
- URI-associated pharyngitis is usually mild and preceded by other symptoms, such as
rhinorrhea and congestion, followed by mild to moderate sore throat, dysphagia,
hoarseness, and low-grade fever; severe throat pain is atypical; exam will reveal
oropharyngeal erythema and/or tonsillar hypertrophy without exudate.
- patients with pharyngitis due to adenovirus may have higher fevers and conjunctivitis.
STRONGLY SUGGESTIVE OF VIRAL PHARYNGIMS
Conjunctivitis ® Rhinorrhea Cough
™»Coryza Viral exanthema
Discrete ulcerative keratitis ® Diarrhea
™»HOARSENESS - is more commonly seen in this group of patients and is consistent with
a viral infection
- the cervical lymph nodes are moderately enlarged and may not be tender.
- the throat and tonsils are moderately red with or without follicular exudate on the throat,
the tonsils, or both; unlike that of bacterial pharyngitis, the exudate in the viral pharyngitis
never joins to form one whole patch; the pharyngitis is often associated with enlarged
tonsils.
*FUNGAL INFECTION - in those on long term antibiotic treatment; the patient complains
of oral discomfort, burning, altered taste sensation, and dysphagia; white
pseudomembranes that consist of desquamated epithelial cells, fibrin, and fungal hyphae
can be scraped off to expose the underlying mucosa, which appears erythematous; other
areas that can be involved in addition to the oropharynx include the buccal mucosa, hard
palate, soft palate, tongue, larynx, hypopharynx, and esophagus; clinical symptoms and
findings are not significantly different if it is caused by C. albicans or another variety.
RISK FACTORS FOR FUNGAL PHARYNGITIS
®»HIV POSITIVE - symptomatic patients
® RADIATION FOR HEAD AND NECK CANCER - candida can be isolated in 73% of
patients and can cause infection in 27%.
®XEROSTOMIA - either because of prior radiation to the head and neck, from Sj6gren
syndrome, or as a side effect from medications
®STEROID INHALERS ®BROAD-SPECTRUM ANTIBIOTICS
® |MMUNOSUPPRESSED INDIVIDUALS ®DIABETES MELLITUS
® CUSHING SYNDROME ® TERMINAL ILLNESS
® HIGH-CARBOHYDRATE DIET
SIGNS AND SYMPTOMS OF GABHS PHARYNGITIS - colonization of the pharynx by GABHS
can result in either asymptomatic carriage or acute infection; after an incubation period
of 2-5 days, pharyngeal infection with GABHS classically presents as rapid onset of
significant sore throat and fever.
- acute streptococcal pharyngitis is a disease of childhood and adolescence with a peak
incidence at 5 to 6 years of age; outbreaks may arise in institutional settings; it is rare in
children <3 years of age, and it may be difficult to diagnose due to an atypical
presentation such as mucopurulent rhinorrhea and excoriated nares without significant
pharyngitis.
*COMMON SYMPTOMS OF ACUTE STREPTOCOCCAL PHARYNGITIS:
Sudden onset of sore throat Fever >38° C (100.4° F) » Odynophagia
*ASSOCIATED SIGNS AND SYMPTOMS

» Malaise » Dysphagia » Otalgia
Headache » Nausea/vomiting Abdominal pain
» Tonsillopharyngeal inflammation »Scarlatiniform rash
» Anterior cervical adenitis History of exposure to Step pharyngitis
Palatal petechiae ™» Patchy tonsillopharyngeal exudates
®The surface of the tongue can resemble a strawberry when the papillae are inflamed
and prominent (“strawberry tongue”); initially, the tongue is often coated white, and with
the swollen papillae;it is called a “white strawberry tongue;” when the white coating is
gone after a few days, the tongue is often quite red, and is called a “red strawberry
tongue.”
= EXAMINATION - shows dry and erythematous pharyngeal mucosa, sometimes encrusted;
palatal and pharyngeal mucosa are dry with a glazed surface; mucus is produced which
is initially colorless but later tenacious and yellow; deep red solitary follicles are usually
Prominent, and there is a regional lymphadenopathy with swelling and tenderness,
especially in children.
- lymphoid follicles on the pharyngeal wall swell and appear as little pink nodes; anterior
cervical lymphadenopathy is common; whitish deposits are seen throughout the oral
cavity and pharyngeal mucosal surfaces; a white to grayish pseudomembrane forms over
the buccal, tongue, and tonsil mucosa in discrete or confluent specks and can be readily
removed leading to raw or bleeding surfaces.
< DIAGNOSIS - throat culture and rapid antigen-detection tests (RADTs) are the diagnostic
tests for GABHS available in routine clinical care; there are both false-negative cultures
as a consequence of sampling errors or prior antibiotic treatment and false-positive
cultures as a consequence of misidentification of other bacteria as GABHS; some
laboratories prefer nucleic acid testing that is specific for GABHS and no longer use
culture to confirm the diagnosis.
- a child who is chronically colonized with GABHS (streptococcal carrier) can have a
positive culture if it is obtained when the child is evaluated for pharyngitis that is actually
caused by a viral infection.
- rapid identification and treatment of patients with GABHS pharyngitis can reduce the
risk of spread, allowing the patient to return to school or work sooner, and can reduce
the acute associated morbidity. :
*THROAT CULTURE - is the diagnostic test of choice for GABHS infection; optimally
obtained and processed, a single throat culture is 90-97% sensitive and 90% specific for
GABHS growth; results can take 18-48 hours to obtain, and this time delay can affect
follow-up treatment.
- it should be obtained before beginning antibiotic therapy, because even a single dose
can cause the culture to be negative; testing for bacteria other than GABHS is performed
infrequently, and should be reserved for patients with persistent symptoms and
symptoms suggestive of a specific non-GABHS bacterial pharyngitis, for example, when
there is concern for gonococcal infection or sexual abuse.
- culture of a throat swab on a sheep blood agar plate has been the “gold standard” for
the documentation of the presence of GABHS pharyngitis in the URT and for the
confirmation of the clinical diagnosis of acute streptococcal pharyngitis.
*RAPID ANTIGEN DETECTION TESTS (RADTs) - several tests have been developed to
detect streptococcal group A carbohydrate-from swabbed material; although the RADTs
are highly specific, they are not as sensitive as routine throat culture; American
guidelines suggest that all children and adolescents who have a negative RADT result
should undergo throat culture; in addition, these patients should also have a monospot
and CBC to evaluate for other causes of pharyngitis.

9
- a major disadvantage of throat cultures is the delay in obtaining results; RADTs have
been developed for the identification of a Streptococcal infection in the clinic and helps
to decide whether to prescribe antibiotics to the patient with pharyngitis; they have very
high specificity, generally 295%, so when a RADT is positive it is assumed to be accurate
and a throat culture is unnecessary.
- swabbing the throat and testing for GABHS pharyngitis by RADT and/or culture should
be performed because the clinical features alone do not reliably discriminate between
GABHS and viral pharyngitis except when overt viral features like rhinorrhea, cough, oral
ulcers, and/or hoarseness are present; in children and adolescents, negative RADT tests
should be backed up by a throat culture.
- routine use of back-up throat cultures for those with a negative RADT is not necessary
for adults in usual circumstances, because of the low incidence of GABHS pharyngitis in
adults and the risk of subsequent acute rheumatic fever is generally exceptionally low in
adults with acute pharyngitis
- anti-streptococcal antibody titers are not recommended in the routine diagnosis of acute
pharyngitis as they reflect past but not current events.
- testing for GABHS pharyngitis usually is not recommended for children or adults with
acute pharyngitis with clinical and epidemiological features that strongly suggest a viral
etiology (eg, cough, rhinorrhea, hoarseness, and oral ulcers).
- diagnostic studies for GABHS pharyngitis are not indicated for children <3 years old
because acute rheumatic fever is rare in children <3 years old and the incidence of
streptococcal pharyngitis and the classic presentation of streptococcal pharyngitis are
uncommon in this age group; selected children <3 years old who have other risk factors,
such as an older sibling with GABHS infection, may be considered for testing.
- follow-up posttreatment throat cultures or RADT are not recommended routinely but
may be considered in special circumstances; diagnostic testing or empiric treatment of
asymptomatic household contacts of patients with acute streptococcal pharyngitis is not
routinely recommended.
- cultures alone cannot differentiate the acute and carrier states of GABHS; an estimated
20% of school-age children are chronic carriers, and up to 25% of household contacts of
symptomatic GABHS patients are carriers.
- recent guidelines advise that patients with frequent sore throat and positive studies for
GABHS may either have frequent GABHS or are GABHS carriers with frequent viral
pharyngitis.
GUIDELINES FOR SCREENING FOR ASYMPTOMATIC CARRIERS
®In patients with a history or family history of rheumatic fever
During a community outbreak of rheumatic fever, poststreptococcal
glomerulonephritis, or invasive GABHS infection
®When tonsillectomy is being considered
When symptomatic GABHS spreads among household members
- although both have positive throat culture results, true infections are distinguished from
the carrier state by the addition of:
»A rise in the antistreptolysin-O titer of 20.2 log 10 between the acute and convalescent
phase (2-4 weeks after presentation)
Relevant history of symptoms and signs during episode
*» Documented response to antibiotics “
*GABHS SCORING SYSTEMS - GABHS tonsillopharyngitis is difficult to accurately diagnose
solely based on symptoms or signs, because significant overlap is seen with findings
common to other causes of pharyngitis; because of this diagnostic difficulty, scoring
systems have been developed for predicting the likelihood of GABHS on clinical grounds
alone.

10
»>PROBABILITY GROUPS
=HIGH-PROBABILITY GROUPS - that should receive empiric antibiotic therapy
sINTERMEDIATE-PROBABILITY GROUPS - that should undergo further testing with a
rapid antigen test and/or throat culture
=LOW-PROBABILITY GROUPS - that require only symptomatic therapy and appropriate
follow-up.
® CLINICAL PREDICTION SCORING SYSTEMS -_ scoring systems based on features of
sore throat have been developed; these scoring systems should not be used in patients
who are immunocompromised, have complicated comorbidities, or have a history of
rheumatic fever; clinicians should also consider epidemiologic circumstances; for
example, these scoring systems should be avoided during an epidemic of acute
rheumatic fever, in parents with school-aged children, or for adults with occupations that
bring them into frequent contact with children.
=WALSH SCORING SYSTEM - uses an algorithm based on five items:
i. Temperature > 38.3 C (100.9 F) ii. Enlarged or tender cervical lymph nodes
iii. Pharyngeal or tonsillar exudates iv. Recent exposure to GABHS
v. Recent cough
=CENTOR SCORING SYSTEN - is based on four criteria taking signs and symptoms into
consideration; one point is given for each of the following if present.
CENTOR CRITERIA FOR DETERMINING GROUP A BETA-HEMOLYTIC STREPTOCOCCAL PHARYNGITIS
i. Fever ii. Tonsillar exudate
iii. Tender anterior cervical adenopathy iv. Absence of cough
- based on these signs and symptoms, the centor score is calculated by totaling all the
four criteria; a score of (0- 4) is given in Table 1.
TABLE 1: CENTOR STREPTOCOCCAL SCORE. CENTOR SCORE
0 No throat swab or culture & No Antibiotics
1 No throat swab or culture & No Antibiotics
2 Rapid test /throat swab & culture are done, antibiotics if positive
3 Rapid test /throat swab & culture are done, antibiotics given empirically
4 Culture all and Antibiotics are given empirically
- the Centor criteria have been endorsed by the Centers for Disease Control and
Prevention (CDC), the American Academy of Family Physicians, and the American
College of Physicians for use in clinical practice guidelines for treatment of acute
pharyngitis in adults.
BMCISAAC DECISION RULE (MODIFIED CENTOR CRITERIA) - is a modification of the
Centor criteria for diagnosing GABHS; Mclsaac allots points to specific criteria.
MODIFIED CENTOR CRITERIA FOR DETERMINING GROUP A BETA-HEMOLYTIC STREPTOCOCCAL
PHARYNGITIS
i. Fever ii. Tonsillar exudate
iii. Tender anterior cervical adenopathy iv. Absence of cough
v. 3 to 14 years old - add 1 point
vi. 15 to 44 years old — 0 point
vii. > 45 years old — subtract 1 point
- the number of points provides a predictive percent of the probability of having GABHS
SCORE vay
i. 0 POINTS = 2% to 3% of patients have GABHS
Il. 1 POINT = 4% to 6% incidence
iii. 2 points = 10% to 12% incidence
iv. 3 points = 27% to 28% incidence
v. 4 points = 38% to 63% incidence
SCORE < 2= no treatment is recommended

W
SCORE = 20r3 = cultures or OlAs are recommended
SCORE = 4or5 = treatment is the best option.
IDSA (INFECTIOUS DISEASES SOCIETY OF AMERICA) RECOMMENDATIONS FOR THE DIAGNOSIS OF
GABHS PHARYNGITIS -IDSA continues to support laboratory confirmation of clinically
suspected cases of GABHS pharyngitis in adults; the IDSA supports the use of RADTs
alone, without confirmation by throat culture, as an acceptable alternative diagnostic
strategy; even though several variables can affect the results, the IDSA still supports the
use of throat culture as the gold standard for documentation of the presence of GABHS
in the URT and for the confirmation of acute GABHS pharyngitis; for achieving maximal
sensitivity in diagnosis, some physicians still choose to use throat culture or to back up
a negative RADT with a culture.
- the American Heart Association also still recommends laboratory confirmation; in
considering the sensitivity (80% to 90%) and specificity (>95%) of the more recently
utilized RADTs, the low incidence of GABHS, and the very low risk of rheumatic fever in
the adult population.
= SEVEN DANGER SIGNS IN PATIENTS WITH SORE THROAT
*Persistence of symptoms longer than 1 wk without improvement
*Respiratory difficulty, particularly stridor
¢Difficulty in handling secretions
*Difficulty in swallowing
*Severe pain in the absence of erythema
*A palpable mass
*Blood, even in small amounts, in the pharynx or ear
= TREATMENT
eVIRAL PHARYNGITIS - mostly, pharyngitis is self-limiting and resolves in 3-4 days; viral
sore throats are only treated by controlling or relieving symptoms until the virus runs
its course.
™®ANALGESICS AND ANTIPYRETICS - for fever, throat painr and malaise; the drug of
choice is paracetamol.
®ANTIVIRAL AGENTS - are indicated only for herpes simplex virus 1 or 2 infection
(ACYCLOVIR x 10 days) and HIV infection; they do not decrease the length of illness and
are not used except in cases when the patient's immune system is compromised.
® OPTIMAL REST ® PLENTY OF ORAL FLUIDS
=» AVOIDANCE OF IRRITANTS ® THROAT LOZENGES OR SPRAYS
*BACTERIAL PHARYNGITIS - prompt antibiotic treatment reduces the duration of
symptoms (if treatment begins within 24 to 48 hours of symptom onset), reduces the
period of contagiousness to 24 hours after beginning treatment, and decreases the
incidence of suppurative complications; prevention of rheumatic fever is possible if
antibiotic therapy is started up to 10 days after the onset of symptoms; it is estimated
that 3,000 to 4,000 patients with GABHS must be treated for a single case of acute
rheumatic fever to be prevented; antibiotic treatment does not appear to affect the
incidence of acute poststreptococcal glomerulonephritis; other possible manifestations
include scarlet fever, toxic shock syndrome, necrotizing fasciitis, and bacteremic spread
of infection to distant sites. .
® ANTIBIOTICS - both Amoxicillin and Penicillin V are now drugs of choice, moving away
from the only Penicillin’ position of a few years ago.
- a 10-day course of penicillin or amoxicillin has traditionally been first-line treatment for
acute GABHS infection in most cases; for those who are penicillin allergic, a first-
generation cephalosporin, clindamycin, clarithromycin, or azithromycin are first-line
treatments; acetaminophen or NSAIDs are recommended for the management of

12
symptoms, aspirin should be avoided and steroids are not indicated; penicillin failure
occurs in 7-37% of cases.
THEORIES OF PENICILLIN FAILURE
=A protective effect for GABHS by f-lactamase-producing bacteria in the tonsil
#Lack of other bacteria that inhibit GABHS virulence
=Poor penetration of the pharyngeal tissues by penicillin
#Antimicrobial resistance to penicillin
- recent data suggest that macrolides and cephalosporins may be more effective as first-
line therapy and that cephalosporins, clindamycin, and amoxicillin/clavulanic acid are all
preferred for penicillin failures or allergies; macrolide resistance, because of the
hypervariable region of the GABHS M-protein gene, has also been reported. 2
GOALS OF ANTIBIOTIC THERAPY
=To eliminate nfections Avoid suppurative complications
=Hasten recovery =Prevent rheumatic fever
IDSA CLINICAL PRACTICE GUIDELINES FOR THE MANAGEMENT OF GABHS PHARYNGITIS
- patients with acute GABHS pharyngitis should be treated with an appropriate antibiotic
at an appropriate dose for a duration likely to eradicate the organism from the pharynx
(usually 10 days); based on their narrow spectrum of activity, infrequency of adverse
reactions, and modest cost, penicillin or amoxicillin is the recommended drug of choice
for those non-allergic to these agents.
=PENICILLIN V - Oral x 10 days
i.Children = 250 mg bid or tid
ii. Adolescents and adults = 250 mg qid or 500 mg bid
BAMOXICILLIN - Oral x 10 days
i. Amoxicillin = 50 mg/kg od (max = 1000 mg)
ii. Alternative = 25 mg/kg bid (max = 500 mg)
=BENZATHINE PENICILLIN G - IM Once
i. WEIGHT <27 kg = 600,000 U ii. WEIGHT 227 kg = 1.2 million U
PATIENTS WITH AN IgE-MEDIATED PENICILLIN ALLERGY - antibiotics that contain a beta-lactam
ring (cephalosporins, amoxicillin) should be used with caution; although cross-reactivity
between penicillin and cephalosporins is probably less than 10%, the risk of anaphylaxis
justifies the consideration of other viable agents.
BPATIENTS WITH NONANAPHYLACTIC REACTIONS TO PENICILLINS
DOSAGE - varies with agent chosen x 10 days
i. CEPHALEXIN ORAL = 20 mg/kg/dose bid (max = 500 mg/dose)
ii. CEFADROXIL ORAL = 30mg/kg od (max = 1g)
BPATIENTS WITH HISTORY OF SEVERE OR ANAPHYLACTIC REACTIONS TO
PENICILLIN - macrolides such as azithromycin, clarithromycin, and erythromycin may be
used, although resistance has been reported; clindamycin is also a reasonable alternative
in penicillin-allergic patients.
- mactolides are given for other bacterial agents, including Mycoplasma pneumoniae and
Chlamydia species which may account for a third of bacterial pharyngitis in adults; they
are also indicated if the patient is allergic to Penicillin
|. CLINDAMYCIN ORAL = 7mg/kg/dose tid (max= 300 mgdose)
li. AZITHROMYCIN ORAL = 12 mg/kg od x “5 days (max = 500 mg)
iii, CLARITHROMYCIN = 7.5 mg/kg/dose bid x 10 days (259 mg/dose)
BGONOCOCCAL PHARYNGITIS - occurs in 1-22 % of the sexually active population.
i. CEFTRIAXONE ii. CEFIXIME
=®NONASPIRIN ANTIPYRETICS AND ANALGESICS .
® CORTICOSTEROIDS - clinical trials have shown that corticosteroids can hasten pain
relief in patients with sore throat; single dose oral dexamethasone (10 mg in adults, 0.6

13
mg/kg for children) was the most common intervention and resulted in pain resolution
= 11 hours sooner than placebo.
» ADEQUATE FOOD INTAKE
® THROAT LOZENGES -are often used for short-term pain relief.
®SALTWATER GARGLE, WARM LIQUIDS, AND REST - may be helpful in relieving
symptoms.
RECURRENT PHARYNGITIS - true recurrent GABHS pharyngitis can occur for several
reasons:
*Reinfection with the same M type if type-specific antibody has not developed
*Poor compliance with oral antibiotic therapy
*Macrolide resistance if a macrolide was used for treatment
Infection with a new M type; unfortunately, determining the GABHS M type in an acute
infection is not available to the clinician.
- retreatment with an initial first-line agent (oral penicillin, benzathine penicillin, or a first-
generation cephalosporin) is reasonable; worth noting is the difficulty in differentiating
between viral pharyngitis with GABHS carriage and actual GABHS pharyngitis; this
becomes even more of an issue in patients with multiple recurrences; between 5-15% of
children are asymptomatic carriers during seasons when GABHS pharyngitis is most
prevalent; a positive test result during a time of wellness may indicate GABHS carriage.
GIVEN FOR 10 DAYS
®»CLINDAMYCIN ORAL = 20-30 mg/kg/day tid (max= 300 mgdose)
®PENICILLIN AND RIFAMPIN ORAL
®PENICILLIN V = 50 mg/kg/day qid (max = 2,000 mg/day)
=RIFAMPIN = 20 mg/kg/day od for the last 4 days of treatment (max = 600 mg/day)
®AMOXICILLIN-CLAVULANATE (AUGMENTIN) - AMOXICILLIN = 40 mg/kg/day tid
(max = 2,000 mg/day)
®BENZATHINE PENICILLIN G (IM) ANF RIFAMPIN (ORAL)
=PENICILLING BENZATHINE
i. <27 kg = 600,000 U ii. 227 kg = 1,200,000 U
=#RIFAMPIN = 20 mg/kg/day bid (max = 600 mg/day)
- treatment with intramuscular benzathine penicillin eliminates nonadherence to therapy;
apparent recurrences can represent pharyngitis of another cause in the presence of
streptococcal carriage; chronic GABHS carriage is particularly likely if the illnesses are
mild and otherwise atypical for GABHS pharyngitis; undocumented histories of recurrent
pharyngitis are an inadequate basis for recommending tonsillectomy; few children are so
severely affected and the limited clinical benefit of tonsillectomy for most must be
balanced against the risks of anesthesia and surgery.
eFUNGAL PHARYNGITIS - the diagnosis can be confirmed by KOH preparation and/or
positive culture; cultures can be obtained with an oral swab or a swish sample of 10 mL
normal saline instilled in the mouth for 10 seconds and then collected in a sterile
container.
- disease manifestations are usually local, but rarely they can become systemic and
cause significant morbidity and mortality; initial therapy for uncomplicated OPC includes
improving oral hygiene and use of topical antifungals.
- patients with a refractory or recurrent infection and those at high risk for systemic
disease should be treated with systemic antifungals.
i. FLUCONAZOLE - is the predominant medication used to treat OPC, because the
predominant organism, C. albicans, has consistently shown sensitivity to the drug, and
it is generally well-tolerated; with increased use, however, development of resistance to
fluconazole has become a growing concern; resistance is usually correlated to the degree

14
of immunosuppression and the total dose of the drug; systemic treatment is often
required and essential in patients with HIV/AIDS.
ii. ITRACONAZOLE - is an alternative effective antifungal and should be used for
fluconazole-resistant strains.
VII. CHRONIC DHARYNGITIS

- itis a chronic inflammation of the pharynx, usually with granular hypertrophy of the
posterior wall which occurs when the mucosa is irritated over a long period.
= ENIOLOGY - chronic inflammation may be caused by extrinsic or intrinsic factors.
*EXTRINSIC FACTORS - tobacco smoke and alcohol are particularly irritant to the
pharyngeal mucosa.
® Alcohol Nicotine »Dust
Dry heat » Allergens » Chemical inhalation irritants
*INTRINSIC FACTORS - may be all acute or chronic infections
® Chronic rhinosinusitis (Postnasal drip) Tonsillitis
Adenoid hypertrophy (Chronic mouth breathing) ® Bronchitis
® Granulomatous diseases Voice abuse
® Connective tissue disorders ® Malignancy
*MEDICATIONS
»Psychotrophic agents » Antidepressants
» Antiseptic throat lozenges Steroids
= PATHOGENESIS - the patient often has a constitutionally determined functional weakness
of the mucosa; the disease may be due to chronic exogenous damage from dust,
chemicals, heat, marked changes in temperature, and working in drafty and smoky
conditions; and dry or incorrectly air-conditioned atmosphere, marked nicotine and
alcohol abuse, mouth breathing, nasal obstruction, abuse of nose drops, chronic
sinusitis, and adenoidal hypertrophy.
= PATHOLOGY - the superficially located lymphoid nodules of the pharyngeal mucosa
are the primary site of hypertrophy and impart a granular appearance; in addition the
lateral pharyngeal bands may be much enlarged the pharynx
and the mucosa throughout
diffusely red.
=-FORMS
SIMPLE CHRONIC PHARYNGITIS - causes a globus sensation, constant throat clearing,
bouts of coughing, a feeling of dryness or phlegm in the throat, pain in the neck and on
swallowing of varying degree, and tenacious secretions; the course is intermittent, and
there is no generalized upset and no fever.
*CHRONIC HYPERPLASTIC PHARYNGITIS - with an erythematous mucosa and lymph
follicles; the mucosa of the posterior pharyngeal wall is thickened and granular with
prominent solitary follicles; it is smooth red to greyish-red in color, possibly with venous
telangiectasis and secretion of stringy colorless mucus; there is usually a very
disturbing, strange sensation in the pharynx with compulsive throat clearing and
swallowing, gagging, and even vomiting.
*CHRONIC ATROPHIC PHARYNGITIS - with white secretions and a thin layer of mucosa;
the posterior pharyngeal wall is dry, glazed often with dry, tough crusts of secretion; the
mucosa is smooth, pink, often very tender and transparent, but may also be red and
thickened; simultaneous atrophic rhinitis and laryngitis sicca may occur; the patient is
constantly obliged to spit out the stringy secretion; at night there is a feeling of choking
and disturbance of sleep; continuous clearing of the throat may produce slight mucosal
hemorrhage; the disease depends on climatic or temperature conditions, and the
symptoms resolve at the seaside but are worse in hot dry air; older people are more often
affected.

13
SIGNS AND SYMPTOMS
*Foreign body sensation *Odynophagia *Coughing
*Soreness of the throat *Hawking *Sense of dryness
eFrequent desire to clear the throat *Pharygeal crusting
eThickened and granular pharyngeal wall
*Secretions are dry, tenacious or, at a later stage, absent so that the posterior wall is dry
and glazed.
= TREATMENT
*Elimination of predisposing factors *Mucosal care
¢Restore the nasal airway *Antiallergic treatment
*Mandel's paint *Fluids
*Electrocautery of the granules *Gargles
°10% silver nitrate is applied weekly when the superficial lymphoid follicles or
lateral bands appear to be the seat of discomfort.
Vill. ATROPHIC PHARYNGITIS

- varying degrees of atrophy of the mucosal elements of the pharynx are frequently
encountered.
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; the blanket of
mucus, which is normally transparent, seems thicker and semitransparent; it may be
raised off the surface in spots.
ADVANCED FORM - the dryness is striking, the mucous coating is glue-like in its
consistency, and at times an actual crust is seen; when the secretion is removed, the
underlying mucous membrane has a dry, furrowed appearance; this advanced stage
has been termed "pharyngitis sicca" and is usually associated with "rhinitis sicca”.
= EMOLOGY - the cause 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 atrophic rhinitis.
- there are trophic changes in the mucosa which result in a hyposecretion of mucus and
which are influenced by some factor that is not understood.
=SYMPTOMS
eSENSE OF DRYNESS AND THICKNESS IN THE UPPER PHARYNX - main symptom
*HAWKING - the patient's attempt to dislodge the adherent secretion consists of
frequent attempts to clear the throat.
eMILD HOARSENESS - may accompany this disorder due to extension of the process
to the larynx and the irritation from frequent attempts to clear or cough out the sticky
secretion.
*SORENESS - varying degrees are not uncommon.
eFETOR
TREATMENT
eMANDEL’S PAINT - is applied to the pharynx to stimulate secretion.
*POTASSIUM IODIDE - an average dose is 10 drops of a saturated solution 3x/day with
meals.
*BREATHING OF WARM MOIST AIR - helps to moisten the inspissated secretion; this is
done 20-30 minutes once or twice a day. ee
IX. MEMBRANOUS DHARYNGITIS

A. VINCENT'S ANGINA TRENCH MOUTH, ULCEROMEMBRANOUS PHARYNGITIS)
- is a severe form of gingivitis that leads to ulceration and necrosis of the gingiva with
pain and bleeding of the gums; it is an acute necrotizing infection of the pharynx; it has

16
a slow, sometimes insidious onset; the disease is self-limiting but highly contagious; it
is caused by an overgrowth of normal oral bacteria as a consequence of poor oral hygiene
combined with other factors such as poor diet, overcrowded living conditions, smoking
and lowered resistance.
- it can occur at any age, but it is most common in adolescents and adults in their 20s to
40s; in developing countries where malnutrition is common and good oral hygiene
lacking, trench mouth occurs commonly in young children; it is an air-contact infection
with an incubation period of 1-3 days.
= ETIOLOGY
eA DEBILITATED STATE OF HEALTH
*LOCAL IRRITATIVE LESIONS IN THE MOUTH - favor the development of the disease.
®Decayed teeth ®Inflamed gums »Poor oral hygiene
=PREDISPOSING FACTORS
*Stress ¢Poor oral hygiene «Insufficient rest
*Nutritional deficiency «Smoking or chewing tobacco
*Throat, tooth, or mouth infections eA compromised immune system
ORGANISMS - it is an infection by 2 symbiotic organisms - a fusiform bacillus and a
spirochete (Borrelia vincentii); these organisms are found in the mouth of many healthy
people, suggesting that other factors, such as decreased resistance to infection due to
inadequate nutrition, immunodeficiency or poor oral hygiene, are required for
development of the disease
PATHOLOGY - the lesions commonly involve one tonsil, usually at its upper part, it may
spread to the soft palate, the other tonsil, the pharynx, or the gums; the membrane
covering the patches is a pseudomembrane, and is formed by the necrosis of the
superficial layers of the mucous membrane, not by exudation.
-the patches are of grayish-white color, surrounded by a red inflamed areola, but
separated from each other by healthy tissue; on removal of the pseudomembrane, which
is granular and cheesy in consistency, an ulcerative area is exposed, varying
in extent and depth; the ulcerated areas bleed freely, and are soon covered by a new
pseudomembrane; this ulcer heals in = 7-10 days.
SIGNS AND SYMPTOMS - often begin suddenly; it may be complicated with peritonsillar
abscess and jugular vein septic phlebitis.
eGINGIVAL ULCERS (rarely on buccal mucosa) - crater-like ulcers between the teeth filled
with plaque and food debris; ulcers become punched-out lesions after slight pressure or
irritation; it is characterized by punched-out erosions of the interdental papillae; the
process tends to spread and eventually involve all gingival margins, which become
covered by a necrotic pseudomembrane.
*PURULENT EXUDATE - which can easily be wiped off; it may extend to the palate, buccal
mucosa and gingiva.
*TONSILLAR ULCER - often deep on one tonsil, with a whitish exudate and the site of
predilection for this is the upper pole.
*Oral fetor *Feeling of foreign body in the throat
*Unilateral pain on swallowing or talking *Foul taste in the mouth
eIpsilateral swelling of the jugulodigastric nodes
*Profuse gum bleeding in response to any pressure or irritation
*Ipsilateral enlarged and tender submaxillary and cervical lymph nodes
PHYSICAL EXAMINATION - is significant for a unilateral deep ulcer on the upper pole of the
tonsil, which is covered by a white exudative membrane; one tonsil shows a white,
necrotizing exudative membrane sometimes combined with an ulcerative lesion; the
base of the ulcer is gray and bleeds easily when scraped with a swab; there may also
be an associated submandibular lymphadenopathy.

7
DIAGNOSIS - is confirmed by the presence of numerous fusiform bacteria seen with
Fontana stain; dental x-rays or x-rays of the face may be done to determine how severe
the infection is and how much tissue has been destroyed.
= TREATMENT
*ANTIBIOTICS
*Penicillin »Clindamycin
* Amoxicillin/Clavulanate » Ceftixozime
First generation cephalosporins Newer macrolides
PATIENTS ALLERGIC TO PENICILLIN
® Erythromycin » Tetracycline
*METRONIDAZOLE
°2-5% SILVER NITRATE - is applied topically
*REMOVAL OF DEVITALIZED TISSUE - with ultrasonic cavitron
*HYDROGEN PEROXIDE MOUTHWASH - is often recommended to remove dead or dying
gum tissues - hourly - equal amounts of hydrogen peroxide and warm water.
*GOOD ORAL HYGIENE - is vital to the treatment of trench mouth; brush and floss teeth
thoroughly at least twice a day and preferably after each meal and at bedtime.
*SALT WATER RINSES - (1/2 tsp of salt in 1 cup of water) may soothe sore gums.
*COATING AGENTS - may reduce pain, especially before eating.
*LIDOCAINE - may be applied to the gums for severe pain.
*Analgesics *Soft non-irritating diet
*Vitamin c *Rest
*Avoid irritants, including smoking and hot or spicy food
B. DIPHTHEREA - the incidence of Corynebacterium diphtheriae infection has declined
markedly since the introduction of diphtheria vaccination; this organism causes an early
exudative pharyngotonsillitis with a thick pharyngeal membrane and produces a lethal
exotoxin that can damage cells in distant organs; infection can spread to the throat,
tonsils, palate, ear, skin, and larynx with associated severe upper airway obstruction ina
minority of cases; the disease is still endemic in many developing countries and some
5000 cases of diphtheria are reported worldwide each year.
- C. diphtheriae is a gram-positive pleomorphic aerobic bacillus that can have a “Chinese
character” appearance on Gram stain; it is best identified by culture on tellurite media;
only toxigenic strains infected with a bacteriophage cause diphtheria disease; early
diagnosis and isolation of the patient is critical; mortality rates range from 5% to as high
as 20% in children <5 years old.
- it occurs more frequently in unimmunized or inadequately immunized persons; the
disease is transmitted by contact, droplets, or contamination by oral or nasal secretions;
while infection in the pharynx incites a mild local inflammatory reaction, the virulence of
the organism is caused by the production of an exotoxin by toxigenic strains; Diphtheriae
toxin causes local tissue necrosis and enters the systemic circulation, primarily affecting
the myocardium and peripheral nerves.
= CAUSATIVE AGENT - Corynebacterium diphtheria
- transmission occurs through infected secretions from the nose, throat, eyes, or skin
lesions; the organism initially remains localizéd to the mucosal surfaces of the URT; local
inflammation and toxin-mediated tissue necrosis causes formation of a fibrinous, patchy,
adherent, gray-black pseudomembrane; the location of pseudomembranes can be nasal,
tonsillar, pharyngeal, laryngeal, laryngotracheal, conjunctival, genital, or cutaneous;
more than one area can be affected, but the oropharynx is the most commonly involved
site; attempts to remove a pseudomembrane characteristically causes bleeding from the
underlying tissue; sore throat and low-grade fever usually begin 1-2 days prior to
developing the pseudomembrane; the severity of local symptoms is quite variable; they

18
may be mild and resolve with sloughing of the pseudomembrane in 7-10 days; if disease
extends into or primarily involves the larynx, or if the pseudomembrane is aspirated after
sloughing, symptoms may be severe and life threatening; patients typically develop a
“bull-neck” appearance caused by marked swelling of cervical lymph nodes and
extensive infiltration of the neck soft tissues; this can cause external compression on the
larynx with subsequent airway obstruction.
- toxin effects at distant sites cause myocarditis, neuritis, and acute tubular necrosis;
myocarditis is associated with delayed administration of antitoxin and typically
occurs
just as the local disease is improving at 2 weeks after onset; peripheral neuritis occurs
3- 7 weeks later, usually affects motor rather than sensory nerves, and commonly affects
the soft palate and pharyngeal muscles.
= INCUBATION PERIOD = 2-5 days
=RISK FACTORS
*Adults and children who don't have up-to-date immunizations
*People living in crowded or unsanitary conditions
*Undernourished people
*People who have a compromised immune system
PATHOGENESIS - the bacteria enter the nasopharynx; multiplication of organisms leads
to production of toxins which cause epithelial cell necrosis with collection of polymorphs
and fibrin leading to false membranous formation (because it consists of a necrotic layer
of mucosa, whereas a true membrane is superimposed over the intact mucosa); the
characteristic grayish-white membrane is composed of necrosed epithelial cells and
inflammatory exudates.
- the exotoxin is absorbed from the local site into circulation and binds to tissues,
particularly the heart and nervous tissue, leading to toxic degeneration; the liver, kidney
and adrenals may also be affected.
= CLINICAL FEATURES - the onset is insidious with fever of low to moderate degree,
malaise, anorexia, and headache; the child looks toxic, the degree varying with the
severity; rapid and shallow pulse, pallor, cold and clammy skin, delirium and circulatory
collapse may occur.
= SIGNS AND SYMPTOMS - there is a mild prodromal illness: the temperature is usually in
the region of 38°C and not more than 39°C.
*Odynophagia «Dysphagia *Fetid odor
*Nausea «Vomiting *Fever and chills
*Hoarseness ¢Nasal discharge ¢Malaise
*Cervical lymphadenopathy —°Very high pulse rate *Headache
- toxigenic strains are able to produce lethal diphtheria exotoxin; it may spread
systemically and lead to myocarditis, nephritis and encephalitis; 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.
EXAMINATION - the tonsils are moderately reddened and swollen with firm, adherent
white or grey velvety pseudomembranes which become confluent and extend beyond
the boundaries of the tonsils to the faucial pillars and the soft palate, and which are fixed
firmly to their bases; the membranes can be wiped off with difficulty and leave bleeding
surfaces behind; the jugulodigastric lymph nodes are very swollen, tender, and often
hard; there is a characteristic smell of acetone on the breath; 60% of cases are localized
to the pharynx including the tonsils, and in 8% the larynx is also involved.
DIAGNOSIS - culture of the tonsil is done on MacConkey’s or Klebs-Loffler’s medium to
show the “Chinese character” appearance of Corynebacterium diphtheriae; definitive
diagnosis is based on isolation of the organism; the pseudomembrane should be

19
cultured, and the laboratory should inoculate Loeffler coagulated serum, tellurite, and
blood agar media.
- finding GABHS does not rule out the Possibility of diphtheria, because this organism
can be cultured in 30% of cases; smears taken from organisms growing on Loeffler
medium characteristically show club-shaped organisms that form sharp angles with each
other; this morphology is reminiscent of a “Chinese character” appearance;
recovered
diphtheria should be tested for toxigenicity; this is performed using the
guinea pig
neutralization test or the Elek test, which is based ona commercially available antiserum
and tests whether a precipitin reaction forms when this antiserum is placed on growing
colonies.
SCHICK TEST - positive
= TREATMENT - has to start immediately; it consists of both the antitoxin and antibiotics;
OUTCOME DEPENDS ON:
The location and extent of the pseudomembrane
®The patient's immunization status
® How quickly the antitoxin is administered
*DAT (DIPHTHERIA ANTITOXIN) - should be administered as soon as possible
because
it can only inactivate toxin that has not already entered the cells; the antitoxin
is a
hyperimmune antiserum of equine origin, so tests for sensitivity to horse serum
should
be performed prior to administration; the recommended dose is dependent
on the
location of the disease and the duration of the illness; patients should
receive
antitoxin diluted in normal saline and administered slowly intravenously after a (-) skin
test within 48 hours of onset to be effective.
® MILD CASES = 20,000 IU
® MODERATE CASES = 40,000-80,000 IU
®LESS SEVERE SYMPTOMS = 20,000 to 40,000 IU
® NASOPHARYNGEAL DIPHTHERIA = 40,000 to 60,000 IU
® SEVERE SYMPTOMS = 80,000 to 100,000 IU
*ANTIBIOTICS - symptoms in patients who are treated early with penicillin are less
severe; antibiotics are needed to eradicate the organism, and the recommended
antibiotics are penicillin and erythromycin; alternatively, C. diphtheriae is also
sensitive
to tetracycline, clindamycin, and rifampin; supportive care is important, because most
patients have difficulty swallowing, and some patients require intubation or tracheostomy
to avoid upper airway obstruction; a booster vaccination should be given during the
recovery period, and serial electrocardiograms should be obtained for early detection of
cardiac complications; disease eradication should be documented by two negative
cultures after completion of the treatment.
- the patient's immunization history is important information in determining suspicion of
disease, because recent immunization or booster injection would make disease highly
unlikely; diphtheria toxoid booster injection is recommended every 10 years in adults;
this is especially important for people who travel to epidemic or endemic areas.;
immunized patients can still be carriers for the organism, because the vaccination is
directed solely against the toxin; when carriers are detected, treatment should consist of
a course of antibiotics and a toxoid booster injection, if none was administered during
the previous year.
PENICILLIN G = 50,000 IU/kg per day for 4 days and Penicillin V is required for the next
5 days.
®CLINDAMYCIN - is given in high doses.
® ERYTHROMYCIN - is given to eliminate the carrier state and for penicillin-allergic
patients

20
*PATIIENT ISOLATION - the patient is no longer infectious 2-4 days after adequate
therapy.
*REPEAT CULTURE - should be performed to make certain the patient is not harboring
the organism in the pharynx; in 2% of patients, bacteria cannot be eliminated, so they
have to undergo tonsillectomy to eradicate the focus; before discharge, patient needs to
be pathogen-free, evidenced by the throat culture of the last 3 weeks.
*BRONCHODILATORS
*TRACHEOSTOMY - may be required in the patient who develops an airway obstruction.
- the disease is preventable with vaccination of children with either the diphtheria-tetanus
toxoid or diphtheria-tetanus-pertussis vaccines.
= COMPLICATIONS
*Myocarditis with cardiac failure *Muscle paralysis *Otitis media
*Palatal paralysis due to polyneuritis eAirway obstruction
*Hemorrhagic nephritis or nephrosis ¢ General toxicity
*Peripheral neuritis «Pneumonia
X. INFECTIOUS MONONUCLEOSIS
- EBV is the causative agent of infectious mononucleosis (IM); pharyngitis associated
with EBV is typically transmitted by oral contact; EBV is especially common in
adolescents; younger children tend to be asymptomatic and to have chiefly abdominal
complaints; the mononucleosis syndrome consists of fever, general malaise, headache,
pharyngitis, dysphagia, and odynophagia.
- itis a viral infecton and there are 2 peaks of primary infection: at age 1-5 years and in
adolescence; transmission is via close contact, especially of the mucous membranes.
- it can be spread through contact with saliva, mucus from the nose and throat, and
sometimes tears; because the virus can be spread through kissing, it has earned the
nickname the "kissing disease."
= PATHOPHYSIOLOGY- transmission usually requires direct and prolonged contact with
infected oropharyngeal secretions with salivary exchange being the main mode of
transmission.
- the infection begins with viral replication in oropharyngeal epithelial cells and
then spreads to local B lymphocytes, which then disseminate throughout the
reticuloendothelial system; the atypical lymphocytes that are produced are T cells
directed against EBV infected B cells.
=INCIDENCE - most people become infected with the EBV at some point during their
lifetime; >95% of adults worldwide are infected; children can become infected with EBV
and have few, if any symptoms.
= INCUBATION PERIOD = 4-6 WEEKS
SIGNS AND SYMPTOMS - following a variable incubation period,
PRODROME = 3-5 days of generalized myalgia, headache, fever, chills, fatigue and malaise
occur followed by the onset of the triad of severe sore throat, lymphadenopathy, and
fever (380 to 390C) in 15-25 year olds; it is usually an acute, self-limited, benign
lymphoproliferative disease.
«PHARYNGITIS - is one of the hallmarks of infectious mononucleosis.
PAIN IN THE NECK WHEN SWALLOWING
*ENLARGED, ERYTHEMATOUS PALATNE TONSILS - with yellow-white exudate on the
surface and within the crypts.
*LYMPHADENOPATHY - posterior and anterior cervical, axillary and inguinal adenopathy
lasting up to 4 weeks
*HEPATOMEGALY = occurs in 30-50% of patients

21
*SPLENOMEGALY = occurs by the 2™ or 3 week of illness in about 50% of all cases:
(mild splenomegaly is present 50% of the time) even if not palpable on physical
examination rarely, splenic rupture can occur and may be fatal.
*JAUNDICE = 15% of patients
*MACULAR RASH = occurs in 40% of patients, especially if ampicillin is given.
*EXANTHEM - can occur at the junction of the hard and soft palates which can last for
less than 48 hours.
*ACUTE UPPER AIRWAY OBSTRUCTION - caused by marked hypertrophy of the tonsillar
and adenoid tissue; it may obstruct the nose and eustachian tubes, and postnasal space
«Enlargement and ulceration of the lymphoid tissue of the pharynx
*An irregular white pseudomembrane covers the tonsils
«FEVER AND MALAISE - the fever and pharyngitis generally subside within 2 weeks, while
adenopathy, organomegly, and malaise may last as long as 6 weeks.
¢MYALGIA AND ARTHRALGIA
=DIAGNOSIS - can usually be made on the basis of clinical presentation, the presence of
at least 10% atypical lymphocytes in the peripheral blood smear, and a positive heterophil
serology
LABORATORY DIAGNOSIS OF EPSTEIN-BARR VIRUS
®White blood cell counts typically range from 10,000 to 20,000/uL.
® Marked lymphocytosis and atypical lymphocytes.
Often elevated serum transaminase, alkaline phosphatase, and bilirubin levels.
® Diagnostic assay: heterophile agglutination test (monospot).
=Measures immunoglobulin M antibodies (not specific EBV to antigens, produced by
EBV-stimulated plasma B cells) 40-60% positive in first week; 80-90% positive at one
month after onset.
=Sensitivity of 81-95% for the commercial tests in a general population.
=Negative predictive value of 78-88% has been shown in children.
=EPV specific antibody ttters
®High positive predictive value, >95%.
® Confirmation of acute or convalescent EBV infection.
® Perform in children < 4 years of age and atypical or persistent symptoms with a negative
heterophile antibody.
- methods based on the polymerase chain reaction (PCR) have a high sensitivity for EBV
viral DNA but are expensive and used clinically only with suspected EBV-associated
encephalitis.
*PAUL BUNNELL TEST - demonstration of heterophile antibodies in the serum; a_ positive
titer is >1:28.
*BLOOD SMEAR - many of the lymphocytes demonstrate 10% “atypical” oval, kidney-
shaped, or slightly lobulated nuclei, and the cytoplasm may appear vacuolated; IM
causes an absolute lymphocytosis with >10% atypical lymphocytes; a vigorous cytotoxic
T-cell response to EBV accounts for the lymphocytosis and causes many of the
associated symptoms; finding atypical lymphocytes on a peripheral blood smear may be
consistent with a clinical impression of IM but is not specific for this illness;
toxoplasmosis, CMV, acute HIV infection, ‘hepatitis A, tularemia, and rubella can also be
associated with this finding; CMV can cause a mononucleosis-like illness, but typically
the sore throat is much less prominent; other serologic findings may include neutropenia
(50-80%), thrombocytopenia (25-50%).
TREATMENT - management of EBV mononucleosis is based on symptoms since the
disease is self-limiting; recovery may take weeks.
«ANTIVIRALS - are not beneficial in uncomplicated infections.

22
*ANTIBIOTICS - are indicated only for secondary bacterial infections; ampicillin or
amoxicillin should not be used, because they cause a maculopapular rash in 95% of
patients with IM; other B-lactam antibiotics can cause a rash in 40-60% of patients with
IM, So alternative antibiotics should be used.
- EBV-associated rash is classically a morbilliform rash, mainly involving the trunk and
Sparing the extremities, that resolves within 1-6 days.
*ORAL CORTICOSTEROID INDICATIONS
*Complications related to impending upper arway obstruction
Severe hemolytic anemia Severe thrombocytopenia
» Persistent severe disease
- when severe obstructive disease is present, oral steroid tapered over 5-6 days can be
helpful at reducing the swelling of the throat and tonsils; other airway interventions, such
as placement of a nasopharyngeal tube, endotracheal intubation, or tracheostomy are
rarely necessary
*ANALGESICS AND ANTIPYRETICS - pain control, primarily with nonsteroidal
antiinflammatory drugs (NSAIDs), is important.
*THROAT CULTURE - should be obtained because of the possibility of a co-existing
&-Hemolytic streptococcal pharyngitis.
*BED REST - until the fever has resolved, with a gradual return to physical activity;
patients with hepatosplenomegaly should avoid physical activity for about 3 months
because of the risk of splenic rupture; they should be advised to avoid contact sports
until examination and abdominal ultrasonography confirms resolution of splenomegaly.
*TONSILLECTOMY - may sometimes be indicated for severe local symptoms such as
respiratory obstruction and dysphagia, and persistent fever.
*THROAT LOZENGES OR SPRAYS elV FLUIDS
*AVOID FATTY FOODS *SALINE GARGLES
*AVOID COFFEE AND OTHER STIMULANTS, ALCOHOL AND TOBACCO
= COMPLICATIONS
*RUPTURED SPLEEN - the risk of splenic rupture is estimated at 0.1% and can occur
within the first 3 weeks of illness; therefore, it is reasonable to restrict athletic activities
for at least 3-4 weeks and until patients are asymptomatic; at that point, patients should
base their return to usual activities on their energy levels; it will cause worsening
abdominal symptoms or an acute abdomen.
«CNS SYMPTOMS - occur in 3% of patients as aseptic meningitis, cranial neuropathy and
transverse myelitis, encephalitis.
CRANIAL NERVE PARALYSIS - affecting the VII" and X"* cranial nerves
eGUILLIAN-BARRE ASCENDING PARALYSIS eMYOCARDITIS
*HEMOLYTIC ANEMIA *GIT HEMORRHAGE
*AiRWAY OBSTRUCTION *DANGER OF ASPHYXIA
Xi. ACUTE TONSILLITES

- itis an infection of the tonsils; spread is by droplet infection; it can occur at any age but
is most frequent in children <9 years old; in children <3 years old with acute tonsillitis,
15% of cases were found to be streptococcal; the remainder were probably viral; in older
children, up to 50% of cases are due to streptococcus pyogenes.
=TYPES
*ACUTE TONSILLITIS - the duration of the infection is < 3 weeks; it can either be bacterial
or viral (75%) in origin.
*SUBACUTE TONSILLITIS - can last between 3 weeks and 3 months
*CHRONIC TONSILLITIS - sore throat for at least 3 months accompanied by tonsillar
inflammation. which can last for long periods if not treated; it is almost always bacterial.

23
= PATHOLOGIC TYPES
*CATARRHAL TONSILLITIS - when the tonsils are inflamed as a result of generalized
infection of the oropharyngeal mucosa; there is no exudate on the tonsil.
*LACUNAR TONSILLITIS - yellow spots occur over the openings of the crypts.
*ACUTE PARENCHYMATOUS TYPE - when the whole tonsil is uniformly congested and
swollen.
*ACUTE FOLLICULAR TYPE - when the inflammatory exudate collects in the tonsillar
crypts, these present as multiple white spots on an inflamed tonsillar surface; yellow
spots corresponding to the lymphatic follicles can also form.
*MEMBRANOUS TONSILLITIS - when exudation from crypts coalesce to form a
membrane over the surface of the tonsil.
= ETIOLOGY
*MOST COMMON VIRAL PATHOGENS IN TONSILLITIS
® Adenovirus =» Coxsackievirus ® Parainfluenza
»Enteroviruses »>EBV »>HSV
Respiratory syncytial virus
*MOST COMMON BACTERIAL PATHOGENS IN TONSILLITIS
GROUPA &-HEMOLYTIC STREPTOCOCCUS (GABHS) - is the most common and
important pathogen; this infection most commonly presents in children aged 5-6 years.
® Staphylococcus aureus Haemophilus influenzae
® Moraxella catarrhalis »Pneumococcus
=PATHOLOGY - the tonsil is swollen and_ inflamed and the crypts contain an
accumulation of leukocytic and epithelial debris intermixed with bacteria; it is probable
that differences in the strains or the virulence of the organisms may account for the
following variations of pathologic phases:
°A simple inflammation of the tonsil area *Formation of exudate
*Cellulitis of the tonsil and its surrounding area *Formation of peritonsillar abscess
¢Tissue necrosis
= SIGNS AND SYMPTOMS - the onset is often sudden with the temperature rising to 40°C;
the acute symptoms rarely extend beyond the 5th or 7th day.
*TRISMUS- is common because of the inflammation ofthe internal pterygoid muscles.
eCOATED TONGUE - with a yellowish-brown "fur
*REFERRED OTALGIA - through reflex sources without actual inflammation in the
tympanum; ear pain occurs because of the common sensory innervation of the
pharyngeal and middle ear mucosa through the glossopharyngeal nerve.
*BILATERAL TENDER UPPER JUGULAR CERVICAL ADENOPATHY- the lymph node
under the angle of the jaw is usually swollen and tender; cervical adenopathy is rare in
viral illnesses.
*ABDOMINAL DISTRESS, NASAL DISCHARGE AND OBSTRUCTION - may be seen in
some children.
eOTITIS MEDIA - is occasionally a complication of the inflammation in the throat
¢Severe sore throat Dysphagia *Odynophagia
*Bad taste in the mouth *Fetid and offensive breath *Fever and chills
*Malaise ¢Tinnitus and slight deafness *Headache
= PHYSICAL EXAMINATION - the tonsils and pharyngeal mucosa are red and swollen and
may be covered with purulent exudate; the tongue may also become red ("strawberry
tongue”).
- the tonsils may sometimes have yellow or white spots; a yellowish exudate may
cover the crypt openings and there may be some palatal erythema and edema; the
patches are not true membranous products, but are the secretions and debris which

24
completely fill the crypts; occasionally a fibrinous exudate is admixed with debris, which
gives it some of the characteristics of an inflammatory membrane.
- lymphoid patches may also be inflamed, and exudate may also be present; there may
also be edema of the uvula and soft palate.
TREATMENT - should be from 7-10 days.
ANTIBIOTICS
PENICILLIN V x 10 days - is still the drug of choice unless the patient is sensitive.
*®BENZATHINE PENICILLIN - a single IM injection of 1.2 M units is also effective and is
preferred when there is doubt that the patient will complete the full course of antibiotic
therapy by mouth.
Cephalexin » Amoxicillin
FOR PATIENTS ALLERGIC TO PENICILLIN
» Erythromycin »® Clarithromycin ®Clindamycin
FOR RESISTANT ORGANISMS
®Clindamycin » Amoxicillin-clavulanate ® Dicloxacillin
*GARGLES - the patient should be instructed to use 3 glassfuls of the gargling solution
each time; the first glassful should be as warmas_ the patient can comfortably stand;
the second and the third glassfuls can be even warmer; instruct the patient to gargle
every 2 hours; the patient may use an isotonic saline solution for gargling (1/2 tsp table
salt in 8 oz. warm water).
TOPICAL ANESTHETICS - viscous lidocaine solutions are often prescribed for relief of
severe pain.
*THROAT LOZENGES - to relieve the pain.
Adequate fluid intake *Bed rest
*Light diet *Oral analgesics
= COMPLICATIONS
* Peritonsillar, parapharyngeal, and retropharyngeal abscess
*Airway obstruction *Deep neck infection *Septicemia
*Meningitis ¢Mediastenitis ¢Glomerulonephritis
*Acute rheumatic fever *Thrombophlebitis of the jugular vein
XH. CHRONIC/RECURRENT TONSILEEEIS

- chronic inflammatory changes in the tonsil are usually the result of recurrent acute
infections treated inadequately; recurrent infections lead to development of minute
abscesses within the lymphoid follicles; these become walled off by fibrous tissue and
surrounded by inflammatory cells.
- the most common and the most important cause of recurrent infection of the tonsils is
persistent or recurrent infection of the nose and paranasal sinuses; this leads to
postnasal discharge which then infects the tonsils as well.
- recurrent infections of the tonsils and peritonsillar tissue lead to permanent
inflammation in the tonsillar crypts and scarring of the tonsillar tissue; bacteria may grow
in the badly drained crypts; chronic infected factors are considered as a "focus" which
may activate other chronic inflammatory diseases in the body by spreading bacteria and
mediators; it may follow acute or subacute episodes of tonsillitis, especially in older
children this is more commonly seen in adults but can occur at any age.
= DEFINITION OF CHRONIC/RECURRENT TONSILLITIS
>7 episodes of acute tonsillitis in 1 year
>5 episodes per year for 2 consecutive years
>3 episodes per year for 3 consecutive years
ETIOLOGY - the organisms are usually a mixed flora of aerobic and anaerobic bacteria
in which B-Hemolytic Streptococcus predominate.

23
eH. INFLUENZAE - there is increasing evidence that it plays a major role in this disorder
as well as in the pathogenesis of tonsillar hypertrophy.
*Streptococci *Staphylococcus aureus *Actinomycetes
Chlamydia Mycoplasma *Anaerobes
PATHOGENESIS - poor drainage of the branching crypts leads to retention of cell debris
which forms a good culture medium for bacteria; from such crypt abscesses, the infection
extends via the epithelial defects of the reticular epithelium into the tonsillar parenchyma
to form a cryptic parenchymatous tonsillitis; alternatively, it penetrates into the
capillaries surrounding the crypts, allowing intermittent or continuous penetration of
toxins and organisms into the general circulation; in the long term, the tonsillar
parenchyma undergoes fibrosis and atrophy.
*TONSILLAR ENLARGEMENT - can occur because of hyperplasia of the parenchymal
structures or fibrinoid degeneration with obstruction of the tonsil crypts.
*CACAGUS - unpleasant taste
* Difficulty in swallowing *Change in the voice eCough
*Recurrent or persistent sore throat Dysphagia Anorexia
*Malodorous tonsillar concretions *Expulsion of tonsillar debris
*Recurrent odynophagia Halitosis ¢Malaise
*Cervical lymphadenitis *Joint pain eFatigue
*Jugulodigastric lymph nodes are often enlarged
= DIAGNOSIS
2 CLINICAL PICTURES
*HYPERTROPHIC TYPE - the tonsils may appear hypertrophic and protrudi
ng out of the
pillars; the tonsils are more or less fixed to their bed; the tonsillar surface
is fissured or
scarred; these are diffusely congested; mouths of Crypts appear open from
which
epithelial debris may be squeezed on pressure; the anterior pillars are hyperemic.
- the enlargement is caused by an increase in all the cellular elements comprisi
ng the
tonsil; the crypts seem partially stenosed, but a purulent exudate or greyish-
yellow
material may be pressed out of the opening of the crypts by a tongue depresso
r.
- some crypts may be enlarged and a "cheesy" or putty-like" material
can be expressed
from them; a chronic infection, usually low-grade is obvious.
*SMALL ATROPHIC AND RECESSED TONSIL - the tonsils appear atrophic
and scarred,
often with surrounding erythematous tonsillar tissue; the tonsil may
be small and
recessed with hyperemic margins and a small amount of thin, purulent secretio
n can be
expressed from the crypts; the tonsillar pillars may show some
signs of scarring or
chronic inflammation; in blood counts, the number of wbc as well as
the concentration
of antistreptolysin may increase; enlargement of the jugulodigastric
lymph nodes is an
important sign of tonsillar infection,
< TONSILLAR HYPERTROPHY GRADING SCALE
GRADE TONSIL % OF SPACE THE
DESCRIPTION TONSIL OCCUPIES
0 Surgically removed tonsil sen
1+ | Tonsils are hidden within the tonsil pillars 0-25%
2+ | Tonsils extend to the pillars 25-50%
3+ | Tonsils are beyond the pillars 50-75%
4+ | Tonsils extend to midline 75-100%
TYPES OF CHRONIC TONSILLIMIS
*CHRONIC FOLLICULAR TONSILLITIS - the tonsillar enlargement is associated with
the
Presence of prominent inflamed follicles; whitish material can be seen extruding from the
follicles when the anterior pillars are pressed with a tongue depressor.

26
*CHRONIC PARENCHYMATOUS TONSILLITIS - the tonsils are enlarged but the follicles
are not prominent; infection is found within the substance of the tonsil.
= TREATMENT
*MEDICAL
®ANALGESICS
» ANTIBIOTICS
BANTIBIOTICS WITH BETA-LACTAMASE COVERAGE - e.g. Cephalosporins,
Amoxicillin-clavulanate
®ANTIBIOTICS WITH ANAEROBIC COVERAGE - e.g. Clindamycin
® DAILY THROAT IRRIGATIONS - using a dental or oral irrigating device.
«SURGICAL
TONSILLECTOMY - can be performed to remove the tonsils in chronic/recurrent cases, or
in acute cases where the palatine tonsils become so swollen that swallowing is impaired;
patients whose tonsils have been removed are still protected from infection by the rest
of their immune system.
- tonsillectomy may be considered in the treatment of children with recurrent throat
infection; children with less severe or frequent disease are unlikely to have long-term
benefits from tonsillectomy; the indication for tonsillectomy in children <5 years old
should be considered very strictly because post-tonsillectomy hemorrhage in this age
group is life threatening.
» TECHNIQUES
=COLD TECHNIQUE BHOT TECHNIQUE
=SMONOPOLAR CAUTERY - the monopolar technique using coagulation is most
frequently used.
BCOBLATION TECHNIQUE - uses a bipolar current to create a plasma field, which can
then split tissue
- this is done under lower temperatures of 60-70°C which diminishes surrounding tissue
damage; it may offer a safer, alternative technique that affords decreased or similar
hemorrhage rates, as well as decreased pain.
PROCEDURES
ETRADITIONAL TONSILLECTOMY - usually consists of a subcapsular dissection with a
knife or electrocautery and total removal of the tonsils under general anesthesia; this
dissection can also be achieved with a harmonic scalpel or laser.
sSUBTOTAL (INTRACAPSULAR) TONSILLECTOMY - the tonsillar capsule as well as
some minor percentage of the tonsillar tissue lining the capsule is preserved; it may offer
a decreased rate of postoperative bleeding and should be considered for patients
undergoing tonsillar surgery for obstructive tonsillar hypertrophy.
i. CARBON DIOXIDE (CO2) LASER - was _ initially used for a subtotal reduction of the
hypertrophic tonsils in children with obstructive symptoms.
LASER TONSIL ABLATION (LTA)- is done using a hand-held COz or KTP laser to
vaporize and remove tonsil tissue; this technique reduces tonsil volume and eliminates
recesses in the tonsils that collect chronic and recurrent infections; this
procedure is recommended for chronic recurrent tonsillitis, chronic sore throats,
severe halitosis, or airway obstruction caused by enlarged tonsils.
ii, BIPOLAR RADIOFREQUENCY ABLATION - produces an ionized saline layer that
disrupts molecular bonds without using heat; as the energy is transferred to the
tissue, ionic dissociation occurs; this mechanism can be used to remove all or only part
of the tonsil; it is done under general anesthesia and can be used for enlarged tonsils
and chronic or recurrent infections; it has been claimed that this technique results in
less pain, faster healing, and less post-operative care; this technique has been criticized

27
for a higher than expected rate of bleeding presumably due to the low temperature which
may be insufficient to seal the divided blood vessels.
iii, POWERED TISSUE MICRODEBRIDER- the endoscopic microdebrider is used in
performing a partial tonsillectomy, by partially shaving the tonsils; this procedure entails
eliminating the obstructive portion of the tonsil while preserving the tonsillar capsule;
the procedure results in less post-operative pain, a more rapid recovery, and perhaps
fewer delayed complications.
=TONSILLOTOMY - means partial resection of hyperplastic tonsils; the anterior and
posterior pillars and the fibrous capsule of the tonsils are not removed; the obstructive
part of the tonsil is only resected; it is indicated in early childhood (<6 years old), when
snoring, respiratory obstruction, dysphagia and failure to grow exists, and no chronic or
acute infection of the tonsils is present; it may be a suitable method for treating tonsillar
hyperplasia in early childhood; complications such as secondary postoperative bleeding
are reduced because the capsule of the tonsils remains intact and the vessels of the
peritonsillar space are not exposed to saliva.
INDICATIONS FOR TONSILLOTOMY - only indicated in children or adults who have
hyperplasia of the palatine tonsils.
- it is contraindicated if there is a history of recurrent infections or abscess
® ABSOLUTE INDICATIONS FOR TONSILLECTOMY
"Hypertrophy resulting in obstructive sleep symptoms in adults or children that lead to
adverse pulmonary or cardiovascular conditions
BHypertrophy and airway obstruction leading to malformation of the facial bones or
malocclusion of the teeth requiring dental attention
#Hypertrophy resulting in dysphagia and poor weight gain
=Recurrent peritonsillar abscesses requiring drainage that fail to heal with appropriately
dosed medications
"Tonsillitis that spawns febrile convulsions
=Tonsils with suspicious growth oranatomic characteristics that may require biopsy for
the exclusion of malignancy
® RELATIVE INDICATIONS FOR TONSILLECTOMY
# 27 clearly documented (sore throat associated with fever >38.2°C, cervical
lymphadenopathy, tonsillar exudate or positive strep test) episodes of acute tonsillitis
within a year, 25 episodes per year over the last 2 years, or 23 per year over last 3 years.
- some clinicians recommend tonsillectomy in children who miss 22 weeks of school
annually because of tonsillar infections.
- children who undergo tonsillectomy for recurrent tonsillitis may have a higher risk
postoperative hemorrhage than those who undergo the procedure for obstructive
symptoms.
=Children with multiple antibiotic allergies or intolerance
"A history of aphthous stomatitis, pharyngitis and adenitis with fever (PFAPA), or a
history of peritonsillar abscess.
=Persistent episodes of a foul taste in the mouth or malodorous breath that do not clear
with appropriate medical therapy.
Chronic bouts of tonsillitis in a streptocaccal carrier that do not respond to beta
lactamase-resistant antibiotics.
"Nocturnal enuresis where upper airway obstructive sleep disorder also is present from
large tonsils and adenoids.
#Attention deficit hyperactivity disorder resistant to treatment with coexistent upper
airway obstructive sleep disorder

28
® INDICATIONS FOR TONSILLECTOMY IN| TREATMENT OF RECURRENT
STREPTOCOCCAL TONSILLITIS
= WELL-DOCUMENTED CLINICAL FEATURES FOR EACH EPISODE:
i. Sore throat associated with fever >38.3°C
ii. Cervical lymphadenopathy, tonsillar exudate, or GABHS positive testing
iii. Frequency of 27 episodes in the preceding year, 25 episodes in each of the preceding
2 years, 23 episodes in each of the preceding 3 years
="OTHER FACTORS FOR DECISION MAKING ABOUT SURGICAL INTERVENTION
i. How well infections have responded to medical therapy
ii. Quality-of-life issues (e.g., days of work/school missed)
iii. Children who have multiple antibiotic allergies or intolerance
iv. Periodic fever with aphthous stomatitis, pharyngitis, and adenitis
v. History of peritonsillar abscess
*®CLINICAL INDICATIONS FOR TONSILLECTOMY
CRITERION DEFINITION _
#1 Minimum frequency of sore throat— Documentation in the medical
episodes based on the Paradise record for each episode of a sore
Criteria for Tonsillectomy: throat should include at least one of
27 episodes in the past year, or the following:
Wi>5 episodes in each of the HTemperature >38.3°C
preceding 2 years, or HiCervical adenopathy
Wi23 episodes in each of the HiTonsillar exudate or erythema
preceding 3 years Hi\Positive test for GABHS
OR
#2 A history of recurrent throat Additional factors that favor a
infections not meeting criteria in #1 tonsillectomy that include (but are
not limited to) one or more of the
following:
ElMultiple antibiotic
allergy/intolerance
HIPFAPA syndrome (periodic fever,
aphthous stomatitis, pharyngitis,
and adenitis)
@Peritonsillar abscess
Hi Parapharyngeal abscess
OR
#3 A diagnosis of sleep disordered Documentation of all of the
breathing (SDB) can be made on the following:
basis of history and physical WTonsillar hypertrophy
examination alone and does not
require polysomnography Abnormalities of respiratory
pattern or the adequacy of
ventilation during sleep, including
but not limited to snoring, mouth
breathing, and pauses in breathing
@ A condition related to SDB

29
{including but not limited to growth
retardation, poor school
performance, enuresis, excessive
sleepiness, inattention, aggression,
depression, hyperactivity, and
behavioral problems) that is likely
to improve after tonsillectomy
OR
#4 A diagnosis of SDB for children | Documentation of all of the
<3 years of age following:
Behavioral issues related to SBD is WTonsillar hypertrophy
more difficult to identify in children
< 3 years of age fy SDB is chronic (> 3 months)
HChild’s parent or caregiver
reports regular episodes of
nocturnal choking, gasping, apnea,
or breath holding
OR
#5 A diagnosis of obstructive sleep | Documentation of all of the
apnea (OSA) Documentation of all of | following:
the following: BTonsillar hypertrophy
MTonsillar hypertrophy BA polysomnogram with an apnea—
BA polysomnogram with an apnea— hypopnea index (AHI) > 1.0
hypopnea
OR
#6 Suspicion of tonsillar_ malignancy
® CONTRAINDICATIONS’ TO TONSILLECTOMY
BSystemic or chronic infection =Repeated URI
"Fevers of unknown origin BAllergic rhinitis
=Poor muscular tone eAsthma
=Blood dyscrasias - leukemia "Sinusitis
=General inability or failure to thrive =Cleft palate
=Diabetes ®Pharyngitis sicca
#Enlarged tonsils without obstructive symptoms ®Tuberculosis
COMPLICATION OF TONSILLECTOMY
HEMORRHAGE - is main potential complication and may either be primary or secondary.
COMPLICATIONS OF TONSILLITIS - Group A B-Hemolytic Streptococcus may be
complicated by suppurative and nonsuppurative sequelae.
*SUPPURATIVE COMPLICATIONS
Cervical lymphadenitis ®Peritonsillar abscess ® Parapharyngeal abscess
*RHEUMATIC FEVER - generally follows a GABHS infection, presenting as polyarthritis,
carditis, Sydenham chorea, and a truncal rash; acute rheumatic fever is now a rarity, with
episodes occurring in >400/100,000 of streptococcal infection episodes in endemic
countries compared with <4/100,000 in nonendemic countries.
- patients with suspected rheumatic fever should be referred to a cardiologist for
complete workup and treatment, as untreated disease can lead to rheumatic heart
disease; penicillin prophylaxis is essential for the secondary prevention of rheumatic
fever, beginning at either 5 or 10 years of age with varying durations depending on the
presence of carditis or valvular disease.

30
*POSTSTREPTOCOCCAL GLOMERULONEPHRITIS - may be seen after pharyngeal or
Skin infections, with an annual incidence of 470,000 (<1% of GABHS infections); typically
an acute nephritic syndrome develops 1-2 weeks after a streptococcal infection; the
infection is secondary to the presence of a common antigen shared by the glomerulus
and the streptococcus; penicillin management may not decrease the attack rate, and
there is no evidence that antibiotic therapy affects the natural history of
glomerulonephritis.
*PEDIATRIC AUTOIMMUNE NEUROPSYCHIATRIC DISORDERS ASSOCIATED WITH
STREPTOCOCCAL INFECTIONS (PANDAS) - comprise a constellation of neurologic
symptoms after GABHS infection; other qualities that may help to differentiate PANDAS
from other obsessive-compulsive and/or tic disorders include a remission of
neuropsychiatric symptoms during antibiotic therapy, elevated streptococcal titers, a
history of tonsillectomies/adenoidectomies, and clumsiness as a presenting symptom.
XH. UNILATERAL TONSILLAR ENLARGEMENT

- during a routine examination, itis not uncommon for an unsymptomatic patient to have
a unilateral tonsillar hypertrophy; in most cases, the tonsil is situated medially in the
tonsillar fossa, giving the illusion of an enlarged tonsil.
- rarely is there an underlying malignancy causing unilateral tonsillar enlargement in the
pediatric population.
- most studies recommend watchful waiting unless there is heightened suspicion for
malignancy in the history or P.E., particularly in the presence of constitutional
symptoms.
XIY. LINGUAL TONSILLITES

- itis less common and the lingual tonsils are rarely acutely inflamed along with the
faucial tonsils; it is more common in tonsillectomized patients and in adults, especially
immunocompromised patients or patients with diabetes.
ETIOLOGY AND PATHOLOGY - are much the same as those of an acute inflammation of the
faucial tonsils.
=SIGNS AND SYMPTOMS
«DYSPHAGIA - is the main symptom *Sore throat
°A sense of a lump in the throat «Dyspnea
*Slight fever *Malaise
*Cervical adenopathy with tenderness *Abscess formation may occur
*Burning sensation in the region of the great cornu of the hyoid bone
EXAMINATION - inspection of the lingual tonsils with the aid of a laryngeal mirror
reveals a reddened, swollen lingual mass with whitish or yellowish spots dotting the
surface of the tonsil, similar to those seen in an acute tonsillitis involving the faucial
tonsils; movements of the tongue are painful and the tongue base is tender on palpation.
TREATMENT - culture followed by appropriate antibiotic therapy is required.
*CULTURE
*ANTIBIOTICS - Macrolides or Penicillin V for 10 days
*LINGUAL TONSILLECTOMY BY CO2 LASER - has been performed when medical
management has not been effective.
CHRONIC LINGUAL TONSILLITIS - chronic inflammation of the lingual tonsils may be
a problem after tonsillectomy when the lingual tonsils undergo compensatory
hypertrophy.
SYMPTOMS - the patient complains of discomfort in the throat, dysphagia and a thick
plummy voice.

31
= TREATMENT - most patients respond to medical treatment, avoiding irritant foods, and
application of local paints; sometime diathermy or cryosurgery may be needed to reduce
the size of the lingual tonsils.
XV. PERITONSILLAR ABSCESS (QUINSY)

- it consists of suppuration outside the tonsillar capsule, and the swelling can extend to
the soft palate and the tonsil may also be pushed medially; it is the most common space-
occupying infection seen in the head and neck; it is usually unilateral; the abscess
usually lies in the space between the tonsillar capsule and the surrounding pharyngeal
muscle bed.
- this infection occurs more frequently in teenagers and young adult males and is rare in
children, but they can develop at any age; the infection begins most commonly when
tonsillitis spreads beyond the boundary of the tonsillar capsule and invades the potential
space between the lateral aspect of the tonsillar capsule and the superior constrictor
muscle of the pharynx.
- typical localizations are the upper pole and along the palatoglossal arch.; usually the
Process Starts with an acute infection of the tonsils and cellulitis of the surrounding
tissues and progresses into an abscess beyond the tonsillar capsule; the abscess usually
occurs in patients with recurrent tonsillitis or those with chronic tonsillitis that has been
inadequately treated; it probably results from an infection of the crypts in the
supratonsillar fossa which are large, slit-like cavities with irregular outlines; the
absence of any history of tonsillitis is not uncommon; it may occur rapidly, with an early
onset of tonsillitis, or late in the course of an acute tonsillitis.
«ETIOLOGY - bacteriologic have revealed both aerobic and anaerobic organisms.
*FUSOBACTERIUM NECROPHORUM most common anaerobic bacteria
*STREPTOCOCCUS PYOGENS - most common aerobic bacteria
«Group A Streptococci *Bacteroides «Haemophilus
¢Staphylococcus aureus *Peptococcus
= PATHOLOGY - infection is thought to spread through the tonsillar crypts and capsule
into the peritonsillar space; the infection begins as a peritonsillar cellulitis and
progresses to an abscess, most commonly near the superior pole of the tonsil, that
extends beyond the tonsillar capsule; the abscess forms in the potential space between
the buccopharyngeal fascia and the capsule itself; abscess within the body of the tonsil
itself is rare.
-in the majority of cases, the pus finds its way into the supratonsillar fossa, which is
characterized by marked swelling and edema of the soft palate; this generally causes
deviation of the uvula to the normal side.
- it is unusual for this process to be bilateral; in other cases the pus burrows downward
and backward, displacing the tonsil forward with little if any swelling inthe supratonsillar
region; the posterior pillar bulges to a marked extent with abscess in this location.
- if the superior constrictor muscle is penetrated by the abscess, an infection in the
parapharyngeal space results; this penetration may take place directly or through the
veins.
= PREDISPOSNG FACTORS
«CHRONIC TONSILLITIS *DENTAL INFECTIONS
«SMOKING *INFECTIOUS MONONUCLEOSIS
«INCOMPLETE TONSILLECTOMY
SIGNS AND SYMPTOMS - the onset of the peritonsillar abscess is continuous from a
preceding acute infection; the disease is usually limited to one side; there is a unilateral
swelling of the palate and pillars on the side of the abscess: the tonsil is displaced

32
downwards and medially; the edematous uvula is pushed towards the opposite side with
its tip usually pointing to the side of the lesion.
*FEVER AND CHILLS - the temperature rarely exceeds 99° F, whereas in the early
stage of an acute tonsillitis it often rises to 103° F or higher.
*MUFFLED VOICE “HOT POTATO VOICE” - because the marked swelling interferes with
articulation.
*PAIN - progressively increases with the extension of the purulent accumulation until it
is almost unbearable
*DIFFICULTY OPENING THE MOUTH - because the muscles of mastication are
encroached upon by the abscess so it is difficult to open the mouth sufficiently wide to
permit an examination of the throat.
*DRIBBLING OF SALIVA - is one of the characteristic symptoms.
*THICK VISCID SECRETIONS FORM IN THE THROAT - itis with the greatest difficulty that
the patient succeeds in removing it.
* AIRWAY OBSTRUCTION - may occur because of the swollen mucous and submucous
tissue of the pharynx; the patient often has suffocative attacks during sleep which
awaken him.
*TRISMUS - because of spasm of the pterygoid muscles.
eRancid breath
*Referred ear pain on the side of the infection is not uncommon.
¢Extreme unilateral soreness of the throat *Odynophagia
«Cervical lymphadenopathy ¢Uvular deviation
«Heavily coated tongue *Difficulty in swallowing
¢Dehydration if the disease has been present for a period of time
<=EXAMINATION - can be limited by trismus; physical findings include inflamed and
erythematous oral mucosa, purulent tonsillar exudates that obscure the tonsil, and tender
cervical lymphadenopathy; it reveals a unilateral redness and swelling as both tonsils are
rarely affected at the same time; if both are affected, the second usually begins as the
first subsides; if both are affected at once, the suffocative symptoms are severe and
alarming.
- as the disease progresses, the redness, tenderness, pain, and swelling increase in
severity; if the abscess is in the tonsil, the tonsil itself is swollen without much
displacement of the palate and uvula; if the abscess is in the peritonsillar tissue, the
swelling often appears to be inthe region of the upper portion of the anterior pillar.
- the palate and uvula are pushed over to the opposite side of the throat; this is partly
due to the swollen tonsil but largely to the edema, cellulitis and pressure of the abscess
itself upon the tonsil; the soft palate and uvula, as well as the pharyngeal
mucous membrane, are red and edematous.
- the region of the tonsil is a deep, dusky red color; the crypts are often filled with a
pulp-like debris, which was probably the original source of the infection.
- the disease may run for 5-10 days when allowed to run its course, though it may extend
over a long period; the termination is marked by the spontaneous or artificial discharge
of the fetid pus.
- when the discharge is spontaneous, it usually takes place through the anterior pillar,
though it occasionally occurs through one ofthe crypts; in some instances, there is a
spontaneous resorption of the cellulitis without discharge of pus.
= DIAGNOSIS
*NEEDLE ASPIRATION - is diagnostic, although false-negative aspirations occur in = 10%
of cases, and another 10% may require repeated aspirations, and therapeutic.
*MICROBIOLOGIC EXAMINATION - shows a mixed infection with aerobic and
anaerobic bacteria.

«ULTRASOUND - may verify the diagnosis.
= TREATMENT
«MEDICAL TREATMENT
*® ANTIBIOTICS - effective against Staphylococcus aureus and oral anaerobes.
IV THERAPY
=PIPERACILLIN-TAZOBACTAM
®HIGH-DOSE CEFTRIAXONE PLUS METRONIDAZOLE.
"AMPICILLIN/SULBACTAM = 3 g every 6 hours
=CLINDAMYCIN = 900 mg every 8 hours
=PENICILLIN G = 10 million units every 6 hours plus METRONIDAZOLE = 500 mg every
6 hours
ORAL THERAPY
"AMOXICILLIN = 500 mg biid x 10 days plus METRONIDAZOLE = 500 mg tid x 10 days
#AMOXICILLIN-CLAVULANATE = 875mg bid x 10 days
=#CLINDAMYCIN = 600 mg bid or 300 mg qid x 14 days
=PENICILLIN V = 500 mg qid plus
=METRONIDAZOLE = 500 mg qid
® ANALGESICS AND ANTIPYRETICS
® CORTICOSTEROIDS - have been shown to speed recovery, reducing throat pain, time
in hospital, fever and trismus, with no increase in complications.
eSURGICAL TREATMENT
®» INDICATIONS FOR DRAINAGE
=Presence of a pointing abscess ®Clinical deterioration
®Failure to respond to IV antibiotics ®Evidence of an abscess on imaging
® SITES OF DRAINAGE
=The most prominent part of the swelling should be selected and drainage done.
=The intersection of an imaginary line drawn from the base of the uvula and another
imaginary line drawn along the anterior faucial pillar
=Through the supratonsillar crypt
™NEEDLE ASPIRATION - after spraying topical anesthesia, using a 10-mL syringe with
a 17 or 18-gauge needle, insert the needle in the fluctuant area of the abscess constantly
pulling back while advancing; use a three point method - do needle aspirations from the
superior, middle, and lower regions of the peritonsillar space.
- aspirate as much pus as possible; have Yankhauer suction ready in pus drains with
injection, so the patient does not aspirate the pus.
- if a large amount of pus is found and not adequately drained by this method, further
incision and drainage can be performed; significant resolution of swelling, dysphagia,
and odynophagia is usually apparent within 24 hours.
ADVANTAGES OF NEEDLE ASPIRATION
alt immediately relieves symptoms
sit is more cost-effective.
sit is easier to perform and uses equipment that is universally available.
alt can be done by physicians who are not head and neck specialists.
"lt is less painful than an incision and drainage and avoids the potential complication
of aspiration of the abscess contents. bs
® INCISION AND DRAINAGE - is indicated if fluctuation is present; the point of incision
is determined by the location of pouching or fluctuation; it is usually in front of the
anterior pillar on a level with the junction of the upper and middle thirds of the tonsil,
though it may be in the posterior pillar or through the tonsil.
-the pharynx is sprayed with a topical anesthesia like 10% xylocaine, then
2 cc's of xylocaine with adrenaline 1/100,000 are injected; using a No. 11 or 15 scalpel

34
blade, make a 1- to 1.5-cm incision in the mucous membrane parallel to the palatal arch
at the site with the largest bulge or area of maximal fluctuance; have Yankhauer suction
ready in case pus drains with injection, so the patient does not aspirate the pus; expect
bleeding because this is an inflamed and vascular area.
- using a hemostat, gently open the incision to break up the loculations and allow the pus
to flow freely out of the space; suction the incised area with a No. 9 or 10 Frazier suction
tip to aid in removal of the purulent material; allow the patient to gargle with saline or
diluted peroxide/saline solution.
- in older children and adults with severe trismus, surgical drainage may be performed
after the application of 4% xylocaine to the site of the incision and to the area of the
sphenopalatine ganglion in the nasal fossa; younger children require GA.
DISADVANTAGES OF INCISION AND DRAINAGE
=The expertise of a head and neck specialist is required.
=The procedure is extremely painful.
"The patient is placed at risk of aspirating the suddenly released abscess contents.
- in addition to surgical drainage, the patient is treated with antibiotics effective against
streptococcus, staphylococcus, and oral anaerobes, and warm saline irrigations.
-in individuals with repeated peritonsillar abscess or a history of repeated episodes
of pharyngitis, a tonsillectomy is performed either immediately or as_ interval
tonsillectomy 6 weeks later.
®ACUTE TONSILLECTOMY OR QUINSY TONSILLECTOMY - some advocate immediate
tonsillectomy since they feel that it is a safe procedure that supplies complete drainage
of the abscess when the tonsil is removed; it alleviates the need for a planned
tonsillectomy 6 weeks later, at which time there is frequently scarring and fibrosis
present and the tonsillar capsule is less easily identified.
ADVANTAGES OF ACUTE TONSILLECTOMY
=Complete abscess drainage without recurrence
=Greater technical simplicity with less hemorrhage
=Shorter and more comfortable convalescence
=Less severe illness =Rapid relief of symptoms
=Single hospitalization "Ease of surgical dissection
=Greater cost efficiency ®Less risk of infectious complication
INDICATIONS FOR IMMEDIATE TONSILLECTOMY
#Upper airway obstruction
eSepsis with cervical adenitis or deep neck abscess
BHistory of recurrent exudative pharyngitis
*SINTERVAL TONSILLECTOMY - in view of the painful nature of this condition and the
possible serious complications that may arise, tonsillectomy is advocated after 6-8
weeks, when the inflammation has subsided.
*»INCISION AND DRAINAGE FOLLOWED BY DELAYED OR INTERVAL TONSILLECTOMY
® NEEDLE ASPIRATION FOLLOWED BY DELAYED OR INTERVAL TONSILLECTOMY
XVI..INFECTION OF THE LATERAL BANDS

- this is a specific form of infection of the lateral pharyngeal bands especially in patients
who have had their tonsils removed; there is swelling, redness, and yellow spots around
the lateral bands, and also in the solitary follicles on the posterior pharyngeal wall.
TREATMENT - Penicillin
- if the disease recurs frequently, the area should be cauterized with 2-5% silver nitrate
solution; the cryoprobe may also be used carefully.

35
XVI. TONSILLOLITHS (CALCULUS OF THE TONSIL)
- concretions of varying size and consistency can form within the substance of the
tonsils; repeated episodes of inflammation may produce fibrosis at the openings of the
tonsillar crypts; normally, the content of tonsillar crypts is drained into the oral cavity;
food, epithelial and bacterial debris accumulate within these crypts and produce a
chronic inflammation.
- initially, these concretions are soft and cheesy, but with time, they calcify and become
hard calculi; calcification occurs subsequent to the deposition of inorganic salts, and
contributes to the gradual growth of the concretion; the resultant calculus may reach a
significant size and even ulcerate through the surface of the tonsil.
- this process may be facilitated by the oral flora and may include fungi and actinomyces-
like organisms; in deep or stenotic crypts, food and secretions may stagnate; this may
lead to bacterial overgrowth and a localized infection.
- itis not uncommon for patients to pick them with various sharp objects, such as crochet
needles, knitting needles, pencils, etc.
SYMPTOMS - more frequently there are no symptoms or simply a sensation of a foreign
body with the desire to swallow or cough to remove the sensation; sudden spontaneous
extrusion of the tonsillolith is often followed by bleeding of short duration.
- tonsilloliths may cause symptoms of recurrent sore throats, chronic cough or otalgia;
there is also a sensation of constant irritation and halitosis; patients invariably complain
about the foul smell that emanates from these cheesy concretions.
EXAMINATION - demonstrates whitish tonsilloliths within the tonsil; there may be local
inflammation and enlargement of the affected tonsil.
TREATMENT - includes the removal of these concretions from the tonsillar crypts when
possible, by the use of curettes and probes; larger calculi may require incision and
extraction.
- this also includes aggressive mouth care, which includes irrigation of the tonsils or
cleaning them with a cotton swab soaked in 3% hydrogen peroxide.
- with time, the cellular debris is often retained in the branching crypts and with recurrent
formation of focal bacterial abscesses in the tonsillar parenchyma, which later undergoes
fibrosis and scarring, local care may not control these symptoms; tonsillar surgery and
elimination of these cryptic structures may be needed to control these infections.
XVIII. DEED NECK INFECTIONS

- they develop in potential pharyngeal spaces; the source of infection may be of dental,
pharyngeal, or traumatic origin, in which there is perforation of the protecting mucous
membranes of the oral or pharyngeal cavity.
A. PARAPHARYNGEAL ABSCESS
- the parapharyngeal space lies laterally to the pharynx and starts superiorly at the skull
space and ends inferiorly at the level of the hyoid bone; the infections are usually related
to pharyngeal infection and are more common in children; a parapharyngeal abscess is
usually polymicrobial, emanating from odontogenic or pharyngotonsillar infections.
- most cases are secondary to severe tonsillitis, quinsy or a penetrating ingested foreign
body; as the carotid sheath passes through«this space into the anterior mediastinum,
infection can spread rapidly along the carotid sheath, causing mediastinitis; it is
potentially fatal if not promptly and adequately treated with IV antibiotics and surgical
drainage.
MEDIAL BOUNDARY - is the superior constrictor muscle.
LATERAL MARGIN - is the mandible, the parotid and pterygoid muscle.
COMPARTMENTS - each fossa is divided into 2 unequal compartments by the styloid
process and its attached muscles.

36
*ANTERIOR (PRESTYLOID) COMPARTMENT - is the larger one and it may become
involved in a suppurative process as a result of infected tonsils, some forms of
mastoiditis or petrositis, dental caries, and surgery; it contains connective tissue,
muscles, and lymph nodes and occasionally the external maxillary arteries.
*POSTERIOR (RETROSTYLOID) COMPARTMENT - is formed by the carotid sheath and
contains the:
Internal carotid artery Internal jugular vein
Ascending pharyngeal artery ™»Hypoglossal nerve
® Vagus nerve » Cervical sympathetic
® Glossopharyngeal nerve ™Spinal accessory nerve
ETIOLOGY - the parapharyngeal space may become infected
*By direct implantation from an operating needle.
*Through the vascular channels as would occur with an endophlebitis or thrombosis
*Through the lymphatics from suppuration of the deep cervical nodes or a lymphangitis.
¢From contiguous spread from deep neck space infections, parotitis, sinusitis, infected
neck tumors, infected branchial cleft cysts, suppurative lymphadenitis, chronic otitis with
cholesteatoma, mastoiditis.
*By iatrogenic introduction of organisms during a mandibular nerve block or anesthesia
for tonsillectomy, nasal intubation, or dental extraction
=SIGNS AND SYMPTOMS - usually develop within 4-7 days after the infection has been
introduced; odynophagia, pain, and swelling of the neck are the most common
complaints; a history of an antecedent sore throat may be elicited; torticollis caused by
irritation of the sternocleidomastoid muscle is also reported.
- the patient is usually a young child and there may be a severe general malaise.
- the maximal swelling is behind the posterior faucial pillar and there may be little edema
of the soft palate.
¢Odynophagia «Drooling ¢Pain of the throat and neck
¢Tender swelling of the neck, in the region of the angle of the mandible
*Trismus may be present due to inflammation and edema around the pterygoid
musculature; it is due to a splinting of the internal pterygoid muscle.
*A high continuous temperature is frequently present, especially if a lymphatic
involvement occurs.
°A tender swelling in the submaxillary region of the affected side, especially at the angle
of the mandible usually occurs before the end of the first week.
*Pain may be referred to the ear.
*Dysphagia is a characteristic complaint that gets increasingly worse.
eEdema of the uvula, pillars and palate occurs early.
*Adenitis of the lymph nodes is present and is usually overshadowed by the swelling in
that region.
*Displacement of the lateral pharyngeal wall usually occurs without swelling or
enlargement of the tonsil.
— PHYSICAL EXAMINATION - the classic physical findings of infection involving the anterior
compartment of the parapharyngeal space are medial tonsillar displacement and
posterolateral pharyngeal wall bulging; other findings include fever, trismus, caused by
irritation of the muscles of mastication, edetiia, and swelling at the angle of the mandible,
often seen in patients with an anterior parapharyngeal abscess; involvement of the
posterior space is associated with many of these same signs; if the anterior compartment
is spared, however, little or no trismus occurs; instead, posterior displacement of the
tonsillar pillar and retropharyngeal swelling may be present.
CT SCAN - aids in delineating the abscess.

37
= TREATMENT
*MEDICAL
* FIRST CHOICE
=PENICILLIN G = 25,000-400,000 unlts/kg/day
=CHLORAMPHENICOL = 50 mg/kg/day In 4 doses q 6 hrs
* SECOND CHOICE
=CEFOXITIN=1gm q 6 hrs "GENTAMICIN = 80 mg q 8 hrs
*SURGERY - is indicated by signs of abscess formation and the symptoms of increasing
sepsis; the safest approach to the parapharyngeal space is through a lateral cervical
approach; drainage is necessary for a period of 24-72 hours.
*INTRAORAL INCISION - is done if bulging into the pharynx is noted; a curved tonsillar
hemostat is inserted about 1/2 inch through the superior constrictor muscle into the
anterior compartment, and spread; the incision should be kept open until drainage stops.
™ EXTERNAL INCISION - if the abscess points externally or shows marked swelling,
drainage may be established by making a small incision over the fluctuant area or over
the most prominent portion of the swelling.
-a curved forceps is thrust into the cavity of the abscess, and the opening enlarged by
spreading the forceps; a cigarette drain extending to the bottom of the abscess
is sutured in place.
= COMPLICATIONS
eSEPTIC THROMBOPHLEBITIS OF THE JUGULAR VEIN - the most serious complications
of a pharyngomaxillary space infection involve the surrounding vasculature.
*SUDDEN MASSIVE HEMORRHAGE - from erosion of the internal carotid artery; because
of the variable position of the carotid artery within this abscess, incision and drainage
are performed through an external skin incision to improve exposure and complete
drainage of the abscess.
B. LUDWIG'S ANGINA (SUBMANDIBULAR ABSCESS)- Is a potentially fulminant
disease process that can lead to death within hours; this is a progressive cellulitis of the
connective tissues of the floor of the mouth and neck that begins in the submandibular
Space, comprised of the sublingual and submaxillary spaces, usually arising from a
dental infection.
= ETIOLOGY - it is most frequent in the young and in young adults; males are more often
attacked; it is most often related to dental extraction or trauma to the floor of the mouth.
*ODONTOGENIC - in 90% of cases and most commonly arises from the third lower
molars; dental caries especially of the molar and premolar teeth; periapical, pericoronal
or periodontal infections from mandibular molar teeth; after extraction of a tooth, hairline
fractures may occur in the lingual cortex of the mandible, providing microorganisms
ready access to the submaxillary space; an infected or recently extracted lower molar is
noted in most affected patients.
¢Trauma to floor of the mouth *Local mouth infection *Mandibular fracture
*Osteomyelitis of the jaw bone *Peritonsillar abscess *Tonsillitis
*Laceration in the floor of the mouth *Foreign body
- ORGANISMS - the responsible bacteria originate from oral flora, and a variety of aerobic
or anaerobic microorganisms have been implicated.
*ANAEROBES - the gas-producing organisms are usually predominant if the infection
is from the teeth.
*HEMOLYTIC STREPTOCOCCI - is the most frequent organism.
*STAPHYLOCOCCI *BACTEROIDES *FUSIFORM BACTERIA
PATHOLOGY - the condition has been attributed to a lymphadenitis and a
perilymphadenitis but itis essentially a cellulitis which spreads by continuity of tissue;
the accompanying edema usually finds its easiest route of exit superiorly and

38
posteriorly, encroaching on the airway; pus, if it forms, usually points within the mouth;
both the edema and pointing of the pus tend to be directed toward the mouth by the
mylohyoid muscle.
- the infection may spread to the submaxillary space and thence to the neck by direct
extension along the hyoglossus muscle; it usually develops as a result of a dental
infection, but it may develop from suppurative cervical lymph nodes in the submaxillary
space.
= CLINICAL FEATURES - the most common presentation in patients with Ludwig's angina
includes dysphagia, odynophagia, neck swelling, and neck pain; other symptoms and
signs include dysphonia, hot potato voice, dysarthria, drooling, tongue swelling, pain in
the floor of the mouth, restricted neck movement, and sore throat; patients should be
questioned regarding recent dental extraction and disease; the rapid development of
crepitus and unilateral pharyngitis in patients with a recent dental extraction should
suggest the diagnosis of Ludwig's angina.
- the duration of the infection may vary from a few days to 3-4 weeks; the condition is
always bilateral and the patient is often unable to open the mouth, speak or swallow
properly.
*lt produces a rapidly spreading, large, diffuse and board-like aggressive swelling that
involves the upper part of the neck and floor of the mouth bilaterally with brawny
induration.
*The swelling causes elevation of the tongue, which may be pushed up against the palate
and the patient often has a typical open mouthed appearance; patient cannot speak or
swallow because stiffness in movements of the tongue generally develops; there is
intense pain on tongue movement and the patient may be severely dehydrated.
*Pain in efforts to clear the throat
*There is considerable salivation, as the patient is unable to swallow and is unable to eat.
*The enlarged tongue may protrude outside the mouth and the condition is called woody
tongue.
*The displaced tongue and pharyngeal swelling may interfere with breathing and in later
stages produce asphyxia.
*Trismus occurs as the infection and inflammation spread to the internal pterygoid
muscle in the parapharyngeal space; it is present if the infection or cellulitis invades the
parapharyngeal space causing an irritative spasm of the internal pterygoid muscle.
“Usually, the patient is very toxic with high fever, chills, rapid pulse, dysphagia, sore
throat, drooling and fast respiration.
*The skin beneath the chin is erythematous and edematous, the edema can spread down
unto the skin of the anterior neck and descend into the chest wall; the swollen area of the
neck is firm, painful, non-fluctuant and does not pit upon pressure.
*In untreated cases, cellulitis may spread further and cause a massive swelling in the
neck above the hyoid bone; which is often known as bull neck.
*As the condition deteriorates further, there may be development of edema of the glottis,
which can result in death due to asphyxia.
*Three facial spaces are involved bilaterally, i.e. submandibular, submental, and
sublingual; if the involvement is not bilateral, the infection is not considered a typical
Ludwig’s angina.
DIAGNOSTIC PROCEDURES - the diagnosis is made clinically; soft tissue plain films of the
neck may confirm the diagnosis by identifying swelling of the affected area and airway
narrowing and gas collections but, in general, are not of value; CT and MRI can identify
deep space neck infections and airway compromise; ultrasonography is also useful in
diagnosing abscesses and edema in the setting of Ludwig's angina; CBC and_ bacterial
cultures are also done.

39
= TREATMENT - should be started as early as possible.
CONSERVATIVE TREATMENT
- sudden asphyxiation is the most common cause of death in patients with Ludwig's
angina; stridor, tachypnea, dyspnea, inability to handle secretions, and agitation all
suggest impending airway compromise; flexible endoscope-guided oral or nasal
intubation under sedation with topical anesthesia is the preferred method of airway
control; direct laryngoscopy can be particularly difficult because of the inability to retract
the tongue into the submandibular space and posterior and cephalad displacement of the
tongue by the infection; emergentcy tracheostomy may be necessary in patients with
Ludwig's angina if flexible endoscopic intubation cannot be accomplished.
* HIGH DOSE ANTIBIOTIC THERAPY - should be initialized as soon as possible to
prevent
the patient from having a Progressing infection with life-threatening complications;
whenever the therapy starts conservatively with IV antibiotics, the general rule is that
patients must respond within 18-24 hours; if they do not, a surgical exploration is
necessary to detect occult abscesses.
EMERGENT HIGH-DOSE IV ANTIBIOTIC REGIMENS
™>PIPERACILLIN-TAZOBACTAM »>TICARCILLIN-CLAVULANATE,
® HIGH DOSE PENICILLIN PLUS METRONDAZOLE CEPHALOSPORINS
™CLINDAMYCIN - can be used in penicillin- allergic patients
VANCOMYCIN - should be added if the initial Gram stain reveals gram-positive cocci.
*ANALGESIC ANTI-INFLAMMATORY DRUGS
*REMOVAL OF THE CAUSE OF DENTAL INFECTION
SURGICAL TREATMENT
*INDICATIONS
®If there is obvious abscess formation
™lf anaerobic bacteria are present, seen by gas within the soft tissues in the CT scans,
indicating an aggressive anaerobic fasciitis.
® If there is no improvement after conservative treatment
*EMERGENCY TRACHEOSTOMY OR NASOPHARYNGEAL INTUBATION - may be
necessary to control the airway; preparations should be done before incision and
drainage since intubation is not possible as the tongue obstructs the view ofthe larynx
and cannot be compressed by the laryngoscope.
*DRAINAGE BY SURGICAL INCISION AT THE ANTERIOR PART OF THE NECK - after the
airway has been established by intubation or tracheostomy, a horizontal incision is made
in the submental area and the fascial muscles and are separated in the midline, thus
interrupting the tightness that has formed in the floor of the mouth; incision and drainage
is recommended even without an abscess; upon opening the abscess cavity, one should
obtain bacterial cultures as well as biopsies in the case of edema to exclude neoplasm;
all loculated areas of the abscess must be opened and drained.
C. MASTICATOR ABSCESS - the masticator space contains the ramus of the mandible
and the temporalis muscle; abscesses may occur medial or lateral to the temporalis
muscle; this potential space is in close proximity to the pharyngomaxillary space which
includes the internal pterygoid muscle, masseter muscle, and ramus of the mandible.
- itis 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.
TREATMENT - if the infection fails to resolve after a week of intensive antibiotic therapy,
surgical drainage is required; drainage of the lateral portion is accomplished by hairline
incisions that extend through the temporalis fascia.
- a transverse cervical incision is made 2 fingerbreadths below the mandible and
carried down to the mandibular periosteum; blunt dissection is used to drain the abscess.

40
- it may be necessary to make a separate incision intraorally, thus draining the infection
into the mouth.
D. RETROPHARYGEAL ABSCESS - the retropharyngeal space lies in the midline and
extends from the base of the skull to the superior mediastinum (at about the level of T2);
retropharyngeal abscesses tend to occur laterally to the midline; the infection can easily
access the mediastinum, which allows the rapid spread of infection and life-threatening
complications.
= ETIOLOGY - retropharyngeal abscess is an uncommon condition that previously was a
disease of childhood, with 96% of cases occurring in patients <6 years; it occurs
primarily in infants and small children <2 years; in adult patients, who are now
increasingly affected, cellulitis develops in the retropharyngeal area; once the
retropharyngeal space is involved, the infection spreads rapidly and an abscess forms.
- usually polymicrobial, with a mixture of aerobes and anaerobes; B-Lactamase-
producing organisms are present in 2/3 of the cases.
- it is the most common cause of pyogenic vertebral osteomyelitis, leading to the
formation of retropharyngeal abscess; disseminated coccidioidomycosis may also cause
retropharyngeal abscess.
VARIOUS FACTORS LEADING TO RETROPHARYNGEAL ABSCESS
*Nasopharyngitis *Otitis media *Parotitis
*Tonsillitis *Peritonsillar abscess »°*Endoscopy
*Dental infections and procedures Ludwig's angina
eUpper airway instrumentation *Lateral pharyngeal space infection
eingestion of caustic substances Tuberculosis
*Hematologic spread from distant infection °Vertebral fractures
*Blunt and penetrating trauma (usually from foreign bodies, commonly fish bones)
*Suppuration in the retropharyngeal lymph nodes, perhaps following an acute bacterial
infection
- 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 instrumentation or intubation.
-in children there is an accumulation of pus between the posterior pharyngeal wall and
prevertebral fascia which results from a_ suppuration and breaking down of lymph nodes
in the retropharyngeal tissue; these nodes are immediately anterior to the second cervical
vertebra and are no longer present in older children.
SIGNS AND SYMPTOMS
*CHILDREN - it is frequently accompanied by severe general malaise, neck rigidity,
dysphagia, odynophagia, drooling, a croupy cough, an altered cry and marked dyspnea;
dyspnea may be the prominent symptom and may also be accompanied by febrile
convulsions and vomiting.
Neck pain ®Trismus
® Unexplained fever following an URI A loss of appetite
® Unilateral cervical adenitis ® Change in speech
™Stridor occurs when the abscess becomes larger or edema extends downward to
involve the larynx.
*ADULTS =
® Cough is usually present » Dysphagia »>Neck stiffness
® Pain on swallowing ® Airway obstruction Fever
® Drooling » Muffled voice
®DYSPHONIA - described as a duck quack ( cri du canard )
® Pain and swelling in the neck; as the abscess increases, as the parapharyngeal spaces
are usually simultaneously involved.

41
®A unilateral or predominantly unilateral adenitis on the affected side is almost always
observed.
= DIAGNOSIS
*EXAMINATION - shows a fluctuant mass at the posterior wall of the pharynx and edema
of the pharynx and larynx; the anterior longitudinal ligament may be affected, so the head
cannot be moved; patients have fever and malaise.
*LATERAL NECK X-RAY - may show abscess formation; true lateral films with the neck
fully extended during deep inspiration are the most reliable; other radiographic findings
include reversal of the normal lordosis of the cervical spine, air-fluid levels in th e abscess
cavity, foreign bodies, and vertebral body destruction.
- in the small infant the swelling of the pharyngeal wall may not be readily detected by
inspection or palpation; a lateral soft tissue radiograph of the neck may reveal a marked
increase in the soft tissue shadow between the pharyngeal airway and the bodies of the
cervical vertebrae; the larynx and trachea are demonstrated in a forward position.
*CT SCAN - most important evaluation - shows a hypodense retropharyngeal region with
a ring-form enhancement; the presence of air confirms the diagnosis.
MRI
eULTRASOUND - is useful for differentiating retropharyngeal cellulitis from
retropharyngeal abscess.
=TREATMENT - antibiotics in conjunction with operative incision and drainage by an
otolaryngologist; in select cases, retropharyngeal abscesses can be treated successfully
with antibiotics alone or in combination with needle aspiration.
- tuberculous (cold) abscesses should be drained only extraorally unless the patient is in
acute respiratory distress; consultation with an infectious disease specialist and
otolaryngologist is advised when tuberculosis or a fungal infection is suspected as the
causative agent.
- when a diagnosis of an actual abscess is confirmed, the abscess should be drained;
the head is lowered so that escaping pus will not be aspirated, and a small, pointed
scalpel blade is used to make a short vertical incision at the point of greatest swelling; if
pus does not escape, a small closed hemostat may be inserted into the wound, gently
pushed to a deeper level, and spread.
- high dose antibiotic treatment should include those covering staphylococcus,
streptococcus, and common oral anaerobes, including penicillin-resistant strains of
bacteroides.
= COMPLICATIONS
*ASPHYXIA - due to aspiration of septic debris; it may occur when a mouth gag is inserted
for examination and drainage or from sudden rupture of a large abscess.
*HEMORRHAGE - may require ligation of the internal carotid artery
E. COMPLICATIONS OF DEED HEAD AND NECK INFECTIONS
eAirway obstruction «Septicemia
Neuropathy ¢Carotid artery rupture
*Jugular vein thrombosis so «Mediastinitis
Rupture into pharynx “
XIX. AIDS
- 40 % of AIDS patients present with otolaryngological symptoms. - HIV type 1 infection
causes a mononucleosis-like syndrome in 40-90% of patients that starts days to weeks
of
after exposure; this febrile illness is called acute retroviral syndrome (ARS). Because
patients at risk for HIV are frequent ly not
the nonspecific signs and symptoms, even
s in any
promptly diagnosed; thus ARS should be included in the differential diagnosi
.
patient with a fever of unknown origin and risk factors for HIV exposure

42
=SIGNS AND SYMPTOMS
- the time course from mucosal breach to initial viremia is 4-11 days; symptoms related
to ARS are caused by the robust immune response to replicating virus; the most common
symptoms and signs include fever (median maximum temperature 38.9°C [102 °F]),
lethargy, skin rash, myalgia, headache, pharyngitis, cervical adenopathy, and arthralgia.
- pharyngitis occurs in 50-70% of patients and usually appears as hypertrophy of the
tissues of Waldeyers ring without exudates; other oral manifestations less commonly
observed include ulcers (29%) and candidiasis (17%).
= PRESENTATION
*Persistent cervical lymphadenopathy *Oral or pharyngeal candidiasis
*Persistent tonsillopharyngitis
*KAPOSI'S SARCOMA OF ORAL CAVITY - usually reddish raised lesions
*HAIRY LEUKOPLAKIA - white patches on tongue which regress and recur
= DIAGNOSIS - is dependent upon laboratory tests.
*COMPLETE BLOOD COUNT - may reveal lymphopenia or thrombocytopenia; atypical
lymphocytes and a decreased CD4 cell count are usually not observed at this time;
because antibodies to HIV appear 24 weeks after infection, enzyme-linked
immunosorbent assay (ELISA) and Western blot tests are also negative at this time; a
quantitative plasma HIV-1 RN tA level tested by PCR is necessary to make a timely
diagnosis; this level will be >50,000 copies/mL; the high viral titer associated with ARS is
reflective of the initial burst of viremia with wide dissemination of virus and seeding of
lymphatic organs; ifa quantitative plasma HIV-1 RNA level cannot be obtained, detection
of viral p24 antigen is an alternative test that can be used to make the diagnosis.
- the natural history of ARS is resolution of signs and symptoms, along with the viremia,
within 14 days after onset; disease progression to other HIV manifestations or acquired
immune deficiency syndrome (AIDS) ultimately occurs; although data are limited
regarding long-term benefits of early treatment, immediate and sustained therapy with
antiretroviral medications may limit the extent of viral dissemination, restrict damage to
the immune system, protect antigen-presenting cells, and reduce the chance of disease
progression; patient compliance with sustained treatment is important, because
inconsistent adherence can cause viral resistance that can limit future treatment options.
- in patients with AIDS, persistent ulcers in the oropharynx can be caused by herpes
simplex virus, cytomegalovirus (CMV), Cryptococcus , histoplasmosis, mycobacterial
organisms, and lymphoma; in many cases, however, no identifiable etiology is
determined after exhaustive microbiologic, serologic, and pathologic tests; the
pathogenesis of these ulcers is unclear but has been postulated to be immunogenic.
=TREATIMENT - injected and systemic steroids have shown success for treating these
AIDS-related ulcers; Friedman and colleagues showed that intralesional injections of
triamcinolone acetonide completely healed 51% of the 36 treated ulcers by 4 weeks and
72% by 8 weeks; for the 10 patients who did not have complete clinical resolution, six still
had marked symptomatic improvement; in other studies, preliminary data suggested that
thalidomide was effective, and a multicenter, double-blinded, randomized, placebo-
controlled study was subsequently performed: this study revealed complete healing in
55% of the patients in the thalidomide-treated group as opposed to 7% in the placebo
group, which was highly statistically significant; the median time to complete healing
was 3.5 weeks; most of the patients in the thalidomide group who did not show a
complete response had at least a partial response; quality-of-life measures were
performed on these patients and showed reduced pain and improved ability to eat.

DISEASES OF THE LARYNX
I. EVALUATION OF VOICE FUNCTION
eCLINICAL EVALUATION OF DYSPHONIA
™ Cause of the voice disorder ® Degree of phonatory deficit
™® Prognosis for recovery of function
*THERAPEUTIC RECOMMENDATIONS - based on these assessments
» Behavioral » Medical » Surgical
- the most effective treatment plan often includes a multidisciplinary approach, using
complementary techniques; to optimize outcomes, preoperative voice therapy is often
used to provide education on vocal hygiene and resonant voice techniques.
INSPECTION - thyroid prominence normally seen in men; moves upward on swallowing;
absence of this movement indicates fixation of the larynx by infection or tumor.
- indrawing of the suprasternal notch on inspiration combined with inspiratory stridor
points to laryngotracheal obstruction by a foreign body, tumor, edema, etc.
=PALPATION - laryngeal skeleton and neighboring structures are palpated during
respiration and swallowing:
*Thyroid cartilage *Carotid artery with carotid bulb
*Cricothyroid membrane and cricoid cartilage
¢Thyroid gland lying inferior and lateral to the thyroid and cricoid cartilages
*Simultaneous movement of the larynx and thyroid gland on swallowing
= LARYNGOSCOPY
*eINDIRECT LARYNGOSCOPY .- visualization of the larynx and hypopharynx through
means other than a direct line of site; image obtained is viewed after ithas been
reflected and/or transmitted.
=Mirrors =Fiberoptic glass rods
=Glass prisms =Microchip cameras
=» ADVANTAGES
=Provides superior visualization of endolaryngeal structures
Requires less compliance ®Facilitates documentation
® USED TO ASSESS
=Vocal fold mucosa for general health (color, edema, erythema, thickness, atrophy, etc)
=Mechanical disturbances (immobility, hypomobility, tremor, spasmodic or muscle-
tension disorders)
=Glottis competence
=Presence of masses/lesions
™ PROCEDURE - tongue grasped with the thumb and middle finger of the left hand, thumb
lies on the tongue; index finger used to push back the upper lip.
- light from the mirror directed toward the uvula; vocal cords appear as whitish, flat,
ribbon-like bands extending from the angle of the thyroid cartilage to the vocal processes
of the arytenoids.
- mobility of the vocal cords is tested on asking the patient to phonate “E”; by tilting the
mirror, the pyriform fossae and a part of the posterior pharyngeal wall can be inspected.
® DIFFICULTIES IN INDIRECT LARYNGOSCOPY
alf the patient is not cooperative or is very sensitive, he may gag and thus makes the
examination difficult; local spraying with topical xylociane helps in such cases.
"ln a short neck, the larynx is placed high up.making laryngeal examination difficult.
=The tongue may rise on phonation obscuring the view of the endolarynx.
Blt is difficult in children

*® USES OF INDIRECT LARYNGOSCOPY
"Forms a part of the routine ENT examination =For taking a biopsy
#Diagnosis and evaluation of a laryngeal disease =Cauterization of ulcers
"Removal of small benign lesions
®Anesthetizing the larynx and trachea for direct laryngoscopy and bronchoscopy
*DIRECT LARYNGOSCOPY - larynx is directly examined with a rigid laryngoscope or
fiberoptic laryngoscope.
® PROCEDURE - performed with the neck flexed forward while the head is extended; the
tongue is displaced either laterally or anteriorly; this position affords a direct line-of-sight
for visuailization through an open mouth to the larynx.
- laryngeal endoscopy, using flexible or rigid endoscopes, is used to examine vocal fold
structure and gross function.
® TYPES OF ENDOCSOPES .
#RIGID ENDOSCOPES - provide higher resolution than flexible ones and provide brighter,
clearer pictures; contrast is excellent, the selection of viewing angles is large, and the
image is more accurately magnified than with a flexible endoscope; when applicable, it
offers image quality superior to that of any other modality, making it the best option for
documentation purposes.
- examination does not usually require topical anesthesia; its primary limitation is that
phonation is limited to sustained vowels, most commonly “ee,” which complicates
assessment of disorders that are more apparent in connected speech.
- itis difficult to accurately assess arytenoid motion; although it is performed more easily,
it still requires patient cooperation.
=#FLEXIBLE ENDOSCOPES - the primary advantage is the ability to view the larynx
dynamically during natural functions such as speech and singing; arytenoid mobility and
the glottal gap can be more accurately described, the velopharyngeal port can be
assessed during the same examination.
- fiberoptic laryngoccopy offers the advantage of being feasible in non-compliant
populations such as small children and seriously ill, demented or psychiatric patients.
- traditional scopes carry image through fiberoptics; newer devices (chip-tip or distal-
chip) have a digital sensor (chip) on the tip of the flexible component that sends the
image digitally to a video display, allows for higher resolution images.
USES
i. Preferred when the question is one of movement rather than structure or mucosal health
ii. Useful for disorders such as spasmodic dysphonia and muscle-tension dysphonia, in
which the voice problem is more obvious during speech than in sustained vowels.
DISADVANTAGES OF FLEXIBLE ENDOSCOPES
i. Light transport and magnification are inferior to rigid endoscope
ii. Distortion occurs at the periphery of the image
iii. A moiré or honeycomb effect can occur when the image is focused; the honeycomb
effect is not a concern with flexible endoscopes that contain a charged-coupled device
camera in the tip; quality of examinations not equal to that achieved with rigid endoscopy
iv. Many patients find it to be more invasive than the rigid examination
v. Carries the risks of nosebleed, reactions to the anesthetic, and vasovagal reaction.
*INDICATIONS FOR DIRECT LARYNGOSCOPY
"DIAGNOSTIC PURPOSES
i. When a lesion in the larynx, as seen in indirect laryngoscopy, needs further evaluation
to know its nature or extent, a direct view of the larynx is necessary.
ii. When indirect laryngoscopy is not possible as in children.

iii. lf an elongated incurled epiglottis obscures the view of the endolarynx
iv. To know about the pathological lesions in blind areas of the larynx.
®THERAPEUTIC PURPOSES
i. For intubation, administering general anesthesia and to have a control on the airway.
ii. For removal of foreign bodies, thickened secretions and crusts in the larynx.
iii, For operations like removal of cordal nodules, vocal polyps, cysts, taking a biopsy,etc
® CONTRAINDICATIONS FOR DIRECT LARYNGOSCOPY
"ln injuries and disease of the cervical spine
"Trismus, long incisor teeth, and a short and thick neck make the procedure difficult.
*MICROLARYNGOSCOPY - provides excellent illumination of the larynx, the upper
trachea, and the hypopharynx including all hidden areas.
- allows early detection of lesions, their extent; can take a biopsy from the properly
selected area; accurate surgical removal; areas of leukoplakia are also properly excised.
- proper excision of the lesions like vocal nodules and vocal polyps under magnification
prevents damage to the vocal cords and thus better functional results are obtained.
*RADIOGRAPHY OF THE LARYNX - is of considerable help in the diagnosis and
assessment of the laryngeal disorders such as the following:
Surgical emphysema Foreign bodies in the larynx
® Narrowing of the airway by edema or growth Fractures of the laryngeal cartilages
To note the position of the tracheostomy tube
To note the degree and extent of laryngotracheal stenosis
® Erosion of the laryngeal cartilage and to assess the extent of disease in malignancy
- usually the lateral view (x-ray of the soft tissues of the neck) is helpful.
*HIGH RESOLUTION CT - delineates the laryngotracheal air column and shows the
valleculae, epiglottis, ventricle and the subglottic region; it allows accurate assessment
of the site and extent of stenosis and tumors, and of any damage to local, laryngeal, and
neighboring structures; AAO-HNS guideline recommends first visualizing the larynx
before obtaining a CT or MRI to avoid unnecessary testing.
°MRI - soft tissue findings such as the extent of a tumor or any lymph node metastasis
*LARYNGEAL VIDEOSTROBOSCOPY - the vocal cords vibrate at 80-400x/sec; video-
stroboscopy uses a rapidly flashing strobe light that is synchronized with vocal cord
vibrations to evaluate vocal cord mucosal motion; the frequency of the strobe light is set
near the frequency of voice, allowing the examiner to view the vocal cords in “slow
motion”, identifying subtle changes in the mucosa or tension of the vocal cord that can
result in hoarseness; it allows viewing of the vibratory characteristics of the vocal cords,
as well as opening and closing gestures.
- stroboscopic analysis of irregular vibration, which is frequently observed in disordered
voice production, is limited; requires a long enough phonatory segment to trigger the
strobe light and cannot provide information about the phonation onset and offset,
because these are very short and irregular.
- stroboscopy has been shown to change the diagnosis in 30-47% of patients diagnosed
using flexible endoscopy; provides additional detail to the original diagnosis in an
additional 32%; ilt provides information about vocal fold structure and gross function.
USES
™To assess vocal fold vibration patterns, mucosal pliability, the underlying layered
structure of the vocal folds, and the undersurface of the vocal fold edges.
To diagnose and document voice and laryngeal disorders, plan treatment, make
longitudinal comparisons, educate patients, and provide biofeedback for voice and
breathing therapy

4
™To record the examination or to include still images in the documentation for routine
follow-up and for medicolegal reasons
® Characterizing stiffness, scar, or submucosal injury
*® Detecting small vocal fold lesions
®»Identifying asymmetric mass or tension
® Monitoring tissue healing after phonosurgery
*VIDEO KYMOGRAPHY - allows the observation of movements at a single horizontal line
from a laryngeal image, added together to represent the vibratory pattern.
*HIGH-SPEED DIGITAL IMAGING (HSDI) - captures thousands of frames (images) per
second; the video is then played in slow motion to examine mucosal wave.
- newer and more expensive than stroboscopy; complements endoscopy and
stroboscopy; details of short and aperiodic vibration can be observed, and the image
analysis allows quantification of vibratory details that is not otherwise possible.
- both HSDI and video kymography capture images much faster than the vibration rate
of the vocal folds so that detailed information of every vibration cycle is collected.
*NARROW-BAND IMAGING (NBI) - considered one of the “biologic endoscopy”
techniques; uses the absorption characteristics of light to enable a detailed analysis of
vascular patterns within and outside a lesion; in the larynx, it has been used to improve
identification of recurrent respiratory papillomatosis and to screen for malignancies by
identifying high-yield areas to sample for biopsy.
*ELECTROGLOTTOGRAPHY (EGG) - measures the conductance of a low-frequency
electric signal across the neck between two surface electrodes; the conductance of the
signal varies with the vibration of the vocal folds:
®VOCAL CORDS CONTACT EACH OTHER - conductance increases, and the slope of
the resultant EGG trace is positive
®VOCAL CORDS SEPARATE - conductance decreases, and slope is negative.
- the results are relative and do not measure glottal area or closure; the waveform's shape
is potentially meaningful for describing the pattern of vocal fold vibration.
*LARYNGEAL ELECTROMYOGRAPHY (LEMG) - if abnormalities are detected on EMG,
the diagnosis of a neural lesion is confirmed; a normal EMG supports, but does not
confirm mechanical fixation of the vocal fold.
USES
®To assess spontaneous and voluntary activity of laryngeal muscles.
®*lIts chief value is in assessing nerve integrity in vocal fold immobility to assess the
prognosis of recovery from a nerve injury
® Occasionally useful in the diagnosis of myasthenia, motor neuron disease, and
myopathy
To differentiate between a vagus nerve and recurrent laryngeal nerve (RLN) injury,
because cricothyroid function should be intact after RLN injury.
®To counsel the patient about the prognosis for recovery of function; laryngeal EMG can
more reliably identify when a vocal fold will not recover movement, rather than when it
will; when a nerve is completely severed, voluntary activation of the muscle is abolished;
after 3 weeks, fibrillation potentials and positive sharp waves may appear and indicate
denervation; in patients with evidence of denervation and poor motor unit recruitment,
recovery is extremely unlikely, and early surgical intervention is prudent.
*ACOUSTIC AND PERCEPTUAL MEASURES - perceptual assessment and acoustic
objective measures are also useful in documenting progress and success of treatment.

3
™» ACOUSTIC ANALYSIS - measures of fundamental frequency, pitch, period fluctuations

or jitter (normal = 0.40%), amplitude fluctuations or shimmer (normal = 0.50 dB), and
harmonic-to-noise ratio (normal = 11 dB). .
= PERCEPTUAL TESTING - rating of voice features by an expert listener, utilizes numeric
scoring system.
=GRBAS: (0 = normal to 3 = severe) - individually rates:
i. Grade ii, Roughness iii. Breathiness
iv. Asthenia _ v. Strain
=CAPE-V (Consensus Auditory-Perceptual Evaluation of Voice): visual analog scale that
individually rates overall severity, roughness, breathiness, strain, pitch, and loudness.
PERCEPTUAL VOICE ABNORMALITIES .
#ABNORMALLY HIGH FUNDAMENTAL FREQUENCY - may be due to tension producing
vocal fold mass, muscle tension phenomenon, protracted pubescence
=ABNORMALLY LOW FUNDAMENTAL FREQUENCY - consider load producing vocal fold
mass (Reinke’s edema, growths) or hypothyroidism (laryngeal myxedema)
"ABNORMALLY LOUD VOICE - may be secondary to sensorineural hearing loss,
hyperfunction (muscle tension dysphonia), excessive respiratory efforts, or psychogenic
disorder.
=#ABNORMALLY SOFT VOICE - may be secondary to conductive hearing loss, reduced
respiratory effort, glottic incompetence, vocal fold mass, vocal fold immobility, vocal fold
bowing defect, or psychogenic disorder.
B=DYSPHONIA - consider vocal fold mass, vocal fold immobility, vocal fold bowing defect,
muscle-tension abnormalities, vocal fold swelling, or psychogenic.
=DIPLOPHONIA - two simultaneous pitches, may be due to recruitment of false vocal
folds during phonation or the presence of an asymmetric mass (eg, unilateral vocal fold
polyp or cyst)
BHARSHNESS -- strained or strangled; may be from upper motor neuron dysarthria
(spastic), adductor spasmodic dysphonia, psychogenic, muscle-tension abnormalities,
or a compensatory result from an underlying vocal fold mass.
BTREMOR - suggests organic vocal tremor (extrapyramidal system), spasmodic
dysphonia, or psychogenic.
SBREATHINESS - excessive airflow from a longer “open phase” or incomplete
ADduction; may be from a glottal chink (mass effect), bowed deformity secondary to
vocal fold immobility, presbylaryngis, glottis lesions, muscle-tension dysfunction,
abductor spasmodic dysphonia, or a psychogenic disorder.
“ARREST OF PHONATION - sudden stops; consider spasmodic dysphonia, load-bearing
vocal fold mass, muscle-tension disorders, psychogenic.
®APHONIA - complete absence of phonated sound; often a functional disorder
(psychogenic), bilateral ADductor vocal fold immobility, mass that results in an open
glottis.
=STRIDOR - may be due to bilateral vocal fold immobility, obstructing vocal fold mass,
laryngospasm, paradoxical vocal fold motion disorder, or psychogenic.
BHYPERNASALITY - suggests velopharyngeal incompetence (flaccid or spastic
dysarthria, anatomic defects)
BHYPONASALITY - may be secondary to adenoid or tonsilar hyperplasia, sinonasal
disease, nasal obstruction (septal deformities, nasal masses), or nasopharyngeal mass.
*SPEECH AERODYNAMIC STUDIES - some measure of airflow or volume velocity is
useful in determining how rapidly the air passes through the glottis.

- they are measures of:
™»MEAN TRANSGLOTTAL AIRFLOW RATE (normal = 100 mL/sec)
™®GLOTTAL RESISTANCE (normal = 30-50 cm H2O/Ips)
®SUBGLOTTAL PRESSURE (normal = 6-8 cm H20)
Hl. STERTOR AND STRIDOR

STERTOR - can be used to describe noisy breathing from the vibration of tissues above
the level of the larynx.
STRIDOR - is the hallmark of any laryngeal obstruction; can be described as a high pitched,
musical, or harsh sound often mistaken for “wheezing.”
- Stridor and stertor can be heard on exam without auscultation and can be correlated
with phase of breathing, wakefulness, sleep, and feeding; on auscultation, noisy
breathing can be an indication of tracheal sources of turbulent airflow.
- it is noisy breathing heard when there is obstruction to the free flow of air through the
larynx or trachea; it may be inspiratory or expiratory; it is produced by a number of
conditions which cause narrowing of the larynx or trachea.
- it is mainly a problem of children, because the larynx is relatively small and laryngeal
tissues are sensitive, lax, flabby and susceptible to edema and spasm.
eWHEN THE OBSTRUCTION LIES MAINLY IN THE LARYNX - stridor is inspiratory
because a negative pressure develops below the site of obstruction and thus, laryngeal
structures tend to collapse inwards narrowing the airway and causing a noisy breathing,
while on expiration, these structures are forced apart.
WHEN THE OBSTRUCTION LIES BELOW THE VOCAL CORDS - stridor is either heard
both during inspiration and expiration or mainly during expiration depending on the
severity of the obstruction; the timing of the stridor with the respiratory phase gives an
idea about the site of obstruction; if the voice is hoarse, the lesion is likely at the level of
the cords; stridor with a clear voice indicates that the obstruction is not at glottis level.
LEVEL OF PHYSICAL FINDINGS

OBSTRUCTION
SUPRAGLOTTIC | Stridor is inspiratory and characterized by a low-pitched flutter.
Voice may be normal.
GLOTTIC Stridor is inspiratory and expiratory and exhibits a phonatory quality.
Dysphonia is present.
SUBGLOTTIC Stridor is mainly expiratory
Brassy, barking cough is characteristic.
Voice may be normal.
It. HOARSENESS
- it is defined as a disorder characterized by altered vocal quality, pitch, loudness, or
vocal effort that impairs communication or reduces voice-related quality of life;
hoarseness may affect newborns, infants, children, and adults of any age; individuals
with hoarseness have impaired communication with their family and peers, which may
result in depression, social isolation, missed work, lost wages, or reduced quality of life.
- most hoarseness is caused by benign or self-limiting conditions, but it may also be the
Presenting symptom of a more serious or ‘progressive condition requiring prompt
diagnosis and management.
- voice quality may be described as breathy, strained, rough, tremulous or weak; on
questioning, hoarseness may actually be increased vocal effort, vocal fatigue or cough;

7
changes in pitch or abnormal pitch range, particularly in singers, may be the primary
complaint.
- hoarseness affects approximately 20 million people in the U.S. at any given time, and
about one in three individuals will become hoarse at some point in their life; hoarseness
is more common in women (50% higher than men), children (peak range 8-14 years), the
elderly, and professional voice users (e.g., teachers, performers, telemarketers, aerobics
instructors. .
HISTORY - can yield important information that can focus the differential diagnosis in
these patients; in a patient with hoarseness and a history of tobacco use, head and neck
carcinoma is the first diagnosis to eliminate.
- an essential part of a thorough history is elucidating the patient’s pattern of voice use,
including an evaluation of the patient’s “voice personality” type with the amount and
style of voice use; an inquiry about recent vocal use (e.g. screaming) and environment
(e.g. noisy work place) should be made.
*IMPORTANT QUESTIONS TO DEFINE HOARSENESS
®How does your voice sound different to you?
® Does your voice consistently sound normal?
ls your voice worse at different times of the day?
®Does your voice fatigue with use?
eASSOCIATED SYMPTOMS
®Pain ® Dysphagia ™® Odynophagia
Cough ®Shortness of breath ® Aspiration
Weight loss ® Heartburn ® Hearing loss
- patient should be asked about tobacco and ethanol use, exposure to to airborne irritants
(e.g. chemicals in the workplace), previous surgery of the neck or chest or other
procedures that require intubation or manipulation of the upper airway.
= DEFINITIONS OF THE COMMON CAUSES OF HOARSENESS
HOARSENESS CAUSE DEFINITION
VOCAL CORD NODULES Callus formations on the vocal cords
VOCAL CORD PARALYSIS Vocal cord weakness or immobility
REINKE’S ED MA Accumulation of fluid in the vocal
cords; seen in patients who smoke,
are vocally abusive, and have reflux
laryngitis.
LARYNGEAL PAPILLOMA Growths on the larynx caused by
infection with human papilloma virus
SPASMODIC DYSPHONIA Condition that results in irregular
voice breaks and interruption with
phonation; this is a focal dystonia of
the laryngeal muscles
REFLUX LARYNGITIS linflammation of the larynx caused by
gastric acid reflux
MUSCLE TENSION DYSPHONIA | Voice disorder that results from
excessive 6r unequal tension of the
laryngeal muscles while speaking;
results from improper use of the
laryngeal muscles and occurs

commonly with reflux laryngitis or
after a severe URI
FUNCTIONAL DYSPHONIA Abnormal use of the vocal
mechanism despite normal anatomy;
Can be related to __ stress,
psychological disturbance, or
habituation of compensatory
techniques developed during an URI
= CHARACTERISTICS OF HOARSENESS
VOICE DIAGNOSIS
QUALITY
Low-pitched | Reinke’s edema, vocal abuse, reflux laryngitis, vocal cord paralysis
Breathy Vocal cord paralysis, abductor spasmodic dysphonia, functional
dysphonia, vocal cord lesion (e.g. nodule, cyst, polyp)
Fatigued Muscle tension dysphonia, vocal cord atrophy, vocal cord paralysis,
reflux laryngitis, vocal abuse, vocal cord lesion
Strained Adductor spasmodic dysphonia, muscle tension dysphonia, reflux
laryngitis
Tremulous Parkinson’s disease, essential tremor of th- head and neck, spasmodic
dysphonia, muscle tension dysphonia
Hoarse Vocal cord lesion, muscle-tension dysphonia, reflux laryngitis _|
=TREATMENT- treat the underlying cause when discovered
AAO-HNS CLINICAL PRACTICE GUIDELNES: HOARSENESS - intended to enhance diagnosis,
promote appropriate therapy, improve outcomes, and to expand counseling and
education
*Most, but not all, hoarseness is the result of benign underlying or self-limiting factors;
however, clinicians should consider the possibility of a serious underlying condition
(growth or tumor of the larynx) or medication side effects as a cause.
eLaryngoscopy is an office procedure to visualize the larynx (voice box and vocal cords)
that should be performed if hoarseness persists or if the cause is uncertain.
elmaging studies, such as a CT or MRI scans, should not be obtained for a primary
complaint of hoarseness prior to visualizing the larynx; laryngoscopy is the primary
diagnostic modality and should be done first.
*Anti-reflux medicines should not be prescribed for hoarseness unless there are
® Signs or symptoms of gastroesophageal reflex disease (GERD), such as heartburn or
regurgitation
® Signs of inflammation of the larynx seen during laryngoscopy.
*Steroids or antibiotics given by mouth are not recommended for hoarseness and should
not be used routinely.
*Voice therapy is a well-established intervention for hoarseness that can be performed at
any age; laryngoscopy should be performed prior to voice therapy and results
communicated to the speech-language pathologist; therapy for hoarseness usually
includes one to two sessions per week for four to eight weeks.
*Surgery is not the primary treatment for most hoarseness, but may be indicated for
suspected cancer, other tumors or growths, abnormal movement of the vocal cords, or
abnormal tone of the vocal cord muscles.

9
*The risk of hoarseness may be reduced by preventive measures such as staying well-
hydrated, avoiding irritants (especially tobacco smoke), voice training, and amplification
during heavy voice use.
TY. CONGENITAL MALFORMATIONS OF THE LARYNX

- they are generally a result of abnormal growth and maturation of the soft tissues lining
the larynx of the fetus; the most frequent source of abnormality is a failure of canalization
of the occluded larynx between the 8-10th week of fetal life; any condition that alters the
size of the laryngeal lumen has the potential to alter the infant’s cry or produce the
noises created during respiratory activity.
GROUPS OF SYMPTOMS
*RESPIRATORY STRIDOR - suggests a ventilatory disorder; upper airway patency
depends on active muscle contraction; pressure sensors in the larynx sense negative
airway pressures and stimulate active dilation of the larynx in preparation for inspiration;
because of the intrinsic structure of the larynx, at any given glottic aperture, the
resistance to airflow is greater in inspiration than in expiration.
- when the airway is narrowed, stridor results from the rapid, turbulent air flow through
that narrowed segment; often, the type of stridor will provide a clue for the clinician
concerning the site of the laryngeal abnormality.
- laryngomalacia accounts for 60% of cases of chronic laryngeal stridor.
®INSPIRATORY STRIDOR - usually associated with abnormality of supraglottic portion
®>EXPIRTORY STRIDOR
®BOTH INSPIRATORY AND EXPIRATORY STRIDOR - usually suggests some
compromise of the airway below the level of the vocal cords; cyanosis, indrawing and
restlessness are other common symptoms in this group.
*ABNORMALITIES OF PHONATION - occur with most laryngeal malformations.
®APHONIA - the cry may be completely absent.
®WEAKNESS OF CRY- if there is a weak “air-spilling” cry, the child may have a vocal
cord paralysis.
=» HOARSENESS
A. ATRESIA OF THE LARYNX - due toa failure of the epithelial primordium of the
vocal cords to split in a sagittal plane; may be limited to the supraglottic, glottic or
infraglottic levels or may involve all levels of the endolarynx.
CLINICAL PICTURE - depends on the severity of the lesion.
COMPLETE ATRESIA - glottis is closed at or above the vocal cords by a firm fibrous
membrane; the neonate is aphonic, tries vigorously to breathe, undergoes rapid
deterioration, becomes cyanotic despite continued respiratory efforts, and soon dies of
asphyxia unless immediate tracheotomy is performed; the condition is incompatible with
life unless an emergency tracheotomy is performed or there is an associated
tracheoesophageal or bronchoesophageal fistula; complete congenital atresia is
associated with tracheal and esophageal anomalies; the most severe type of congenital
laryngeal atresia presents as stillbirth and may not be recognized.
- it is the most extreme form of obstruction at this level and results in a desperate
emergency during the first moments of life; it is a life-threatening malformation, and in
the past, virtually all affected newborn died;.nowadays, antenatal ultrasound examination
allows diagnosis of the condition and an emergency tracheotomy is done in the DR.

10
= DIAGNOSIS
*PRENATAL ULTRASOUND - identifies the signs of congenital high airway obstruction
syndrome, such as hyperechogenic lungs, a flattened or inverted diaphragm, a dilated
and fluid-filled trachea, fetal hydrops, and polyhydramnios.
*FETAL MRI - correlates highly with prenatal ultrasound, can detect laryngeal atresia with
the advantage of having a capability to identify the level of obstruction in most cases.
= TREATMENT - an emergency tracheostomy is required immediately upon birth to secure
an airway; repair of laryngeal atresia requires laryngotracheal reconstruction.
B. BIRD EPIGLOTHIS - a rare anomaly defined as a cleft of the epiglottis that
encompasses at least 2/3 of its length; characterized by a division of the epiglottis into 2
equal and symmetrical halves which tend to be flaccid and may prolapse into the glottis.
- infants may be asymptomatic, but typically they present with stridor or aspiration.
= ASSOCIATED ANOMALIES
eMIDLINE DEFECTS - cleft palate, bifid uvula, micrognathia, and microglossia
*POLYDACTYLY - has been reported in approximately 75% of patients
*HYPOTHALAMIC-PITUITARY AXIS - is often disrupted in children with a bifid epiglottis
*PALLISTER-HALL SYNDROME (PHS)
«CONGENITAL HYPOTHALAMIC HAMARTOBLASTOMA SYNDROME
= DIAGNOSIS - is made on direct laryngoscopy
TREATMENT - supraglottaplasty may be performed if the epiglottis is lax and prolapses
into the laryngeal inlet.
C. CONGENITAL WERS OF THE LADYNX - are the result of failure of normal splitting of
the vocal cord primordium; they result from the failure of complete recanalization of the
laryngeal lumen during embryonic development.
- these lesions arise at about the 10° week of intrauterine life; as a result, fibrous
segments partially or totally occlude the laryngeal inlet; the patency of the laryngeal
lumen is deficient because of persistent attachment between the two halves of the larynx.
- the morphology of the webs varies widely - some are paper thin while others are quite
thick; they account for approximately 5% of congenital anomalies; they are uncommon
and have an estimated incidence of 1/10,000 births.
- most laryngeal webs are glottic with extension into the subglottic area; the webs usually
occur anteriorly and the lesions are often asymptomatic if they extend less than halfway
back along the cords; because the glottis area is triangular, these anteriorly placed webs
reduce the glottic area by 15-20% and are usually not sufficient to cause stridor; if the
web extends posteriorly, the symptoms may be marked; the stridor is primarily
inspiratory but also has an expiratory component; the infant's cry is hoarse and weak.
LOCATION OF CONGENITAL WEBS
*GLOTTIC = 7% *SUBGLOTTIC = 12% *SUPRAGLOTTIC = 2%
= COHEN’S CLASSIFICATION
*TYPE | - the true vocal folds are visible within the web; although there is usually no
airway obstruction, voice dysfunction is common.
*TYPE Il - the true vocal folds are usually visible within the web; voice disorder is the
common presenting symptom; however, airway compromise may occur with upper
respiratory tract infections.
*TYPE Ill - with anterior potentially cartilaginous subglottic extension; the anterior portion
of the web is solid and extends into the subglottis; most of the true vocal folds are visible
within the web; airway obstruction and voice disorder are moderately severe.
*TYPE IV - extends into the subglottic area with resulting subglottic stenosis; infants with
this type of web are aphonic with severe airway compromise.

GLOTTIC WEB CLASSIFICATION BY COHEN
SEVERITY | EXTENT OF | SUBGLOTTIC SYMPTOMS
GLOTTIC INVOLVEMENT
EXTENSION
Type 1 <35% None or thin anterior web Mild hoarseness
Type 2 | 35%-50% | Thin to moderately thick Hoarse, weak cry, stridor with
anterior web with minimal exertion
subglottic extension
Type 3 |50%-75% | Thick anterior web, extends to | Severe hoarseness, moderate
lower border of cricoid airway obstruction
Type 4 | 75%-90% | Uniformly thick web, extends to | Aphonic, severe airway
lower cricoid obstruction, requires
tracheotomy
CLINICAL MANIFESTATIONS - symptoms will vary with the site and degree of webbing;
they cause respiratory obstruction of variable degrees; signs and symptoms include
disorders of phonation, stridor, and airway obstruction.
GLOTTIC WEBS - most webs involving the anterior glottis are generally thin and associated
with mild hoarseness and minimal airway obstruction; with laryngoscopy the vocal folds
are visible.
®AIRWAY OBSTRUCTION - the patient’s voice may require emergency tracheostomy
immediately after birth.
®DYSPHONIA - marked by a weak, hoarse cry in infants; the patient’s voice may be
hoarse or may be totally aphonic.
®» DELAYED SPEECH DEVELOPMENT
»INSPIRATORY AND EXPIRATORY STRIDOR
SUBGLOTTIC WEBS - are infrequent
® STRIDOR - may have an expiratory component
®» OBSTRUCTION - usually some feeding difficulty when obstruction is fairly severe.
SUPRAGLOTTIC WEBS - are rare.
= DIAGNOSIS
*DIRECT LARYNGOSCOPY - may be performed without anesthesia in newborn infants.
*BRONCHOSCOPY- should be done to rule out the possibility of associated anomalies
beneath the area of the web.
*LARYNGOGRAMS
TREATMENT - small laryngeal webs causing dysphonia only may be left untreated until
the larynx is of more substantial size when the patient is 5-6 years old and voice and
speech become more important.
*THIN WEBS - endoscopic lysis of the web, with or without topical mitomycin treatment,
can be used to treat small (type 1 and some type 2) anterior laryngeal webs.
®™GLOTTIC LEVEL - a thin, transparent web may easily be swept away by the
bronchoscope, completely correcting the problem; they may respond to serial
laryngoscopic dilatation.
- thin anterior webs and glottic laryngeal webs may require endolaryngeal division of the
web with a knife or a CO 2 laser with or without temporary placement of a keel to prevent
readhesion.
*SUBGLOTTIC LEVEL - the anterior cricoid plate is usually abnormal; requires an
external approach with division of the web and the cricoid plate and the use of cartilage
grafting.

12
*THICK WEBS - approached through a precise midline thyrotomy; removal of excess

tissue using a fiberoptic laryngoscope, and placement of a mucosal graft fixated with
fibrin glue or stenting; require tracheostomy and insertion of a laryngeal keel until cordal
re-epithelialization occurs.
- the use of COzlaser is not recommended; the resulting voice is reportedly satisfactory,
- the more extensive webs require an open approach to address subglottic narrowing;
laryngotracheal reconstruction or laryngofissure with silastic keel are most commonly
used to correct the defect; decannulation may be achieved by either single-stage or two-
stage laryngotracheal reconstruction.
*REPEATED DILATATION *LARYNGEAL INSERTS
*LASER OR SURGICAL EXCISION - definitive repair should be carried out as soon as it
is feasible so that normal development of the larynx, laryngeal reflexes and speech are
permitted; surgical correction can usually be carried out by 1 year of age.
*TRACHEOSTOMY - is indicated in extensive webs of the larynx because of obstruction;
it is the treatment of choice if the child is dyspneic and unable to tolerate the web.
® TYPE | - observation or COz laser division with mucosal flap
- minor anterior vocal cord webs with minimal voice problems require no treatment; for
longer membranous webs with no airway compromise, endoscopic repair may be
delayed until pre-school age.
®TYPE Il - COz laser division with endoscopic keel; late repair is preferable as a silicon
keel is not well tolerated in an infant larynx without a tracheostomy; by the age of
4 years, surgical correction is easier as the larynx is larger.
® TYPE Ill - CO2 laser division with endoscopic keel or open surgery if a cartilaginous
component is present
®TYPE IV - tracheostomy, two stage PCTR (Partial Cricotracheal Resection) or LTR
(Laryngotracheal Reconstruction) with temporary stenting
D. LARYNGOMALACIA (LAA) - is usually a benign self-limited disorder; it may be an
isolated finding in the otherwise healthy infant, or it may be associated with other
neurologic disorders such as cerebral palsy.
¢Most common congenital laryngeal anomaly (50-75%)
¢Has been reported to be inherited in rare cases.
*Most common cause of stridor in neonates and infants and persistent stridor in children
*Occurs more frequently in term males with a normal birth weight, although recent
evidence suggests that it is equally common in females.
*Premature Hispanic infants and black infants of all gestational ages are at higher risk.
*Frequently associated with secondary airway lesions (eg, subglottic stenosis,
tracheomalacia) and with gastro-esophageal reflux.
¢Common in patients with neuromuscular disorders.
*A mechanically similar identity has been described in adults following
®» Head injury ® Laryngeal trauma
» Laryngeal surgery
*Tonsillectomy and adenoidectomy for sleep apnea
® EXERCISE-INDUCED - LM results when enough inspiratory force occurs during
exercise to draw the aryepiglottic folds into the larynx and partially obstruct the glottis;
in severe cases with redundant aryepiglottic folds, supraglottoplasty can be beneficial.
PATHOPHYSIOLOGY - involves laryngeal cartilages that have not yet developed the
resilience to provide rigid support of the airway; any inspiratory effort that creates
negative pressure through the larynx results in medial displacement of the laryngeal

13
tissue, which decreases the caliber of the airway lumen; as the rigidity of the cartilage
improves during the ensuing weeks, the child’s symptoms eventually disappear.
- the inspiratory stridor of LM results from collapse of the supraglottic larynx, which
creates a narrow airway and turbulent airflow; the etiology of this collapse has been
elusive, but it appears to be related to neuromuscular hypotonia; sensorimotor
integration of peripheral sensory afferent reflexes, brainstem function, and the motor
efferent response are responsible for laryngeal function and tone.
= PATHOGENESIS - abnormal calcium metabolism causes weakness in the supraglottic
laryngeal skeleton, particularly in the epiglottis.
= ETIOLOGY - the cause is unknown although the syndrome is more common in lower
socio-economic groups and poor nutritional status may be an etiologic factor; it is more
common among males than in females (2:1).
SCHOOLS OF THOUGHT
*STRUCTURAL ETIOLOGY - the anatomic findings of a tubular epiglottis, shortened
aryepiglottic folds and large arytenoids in these patients cause a narrowing of the
supraglottis and the resultant higher airway pressure forces collapse of these tissues
into the glottic opening; this theory is supported by histologic exams which demonstrate
normal cartilage in autopsy specimens.
*NEUROGENIC ETIOLOGY - neuromuscular immaturity, hypofunction or incoordination
is believed to cause flaccidity of the supraglottic structures; supporters of this theory
point to studies which show an association of other neurologic disorders including
central apnea, and hypothermia in some patients.
= CLINICAL MANIFESTATIONS
eINTERMITTENT HIGH PITCHED FLUTTERING INSPIRATORY STRIDOR -— hallmark of
laryngomalacia; develops within the first 2 weeks of life, which resolves slowly over
several months; the median time to spontaneous resolution of stridor is 7-9 mos, and the
vast majority will have no stridor by 18 months.
- the stridor of LM is high, but compared with the stridor of vocal cord paralysis, it is
relatively low in pitch and does not have a musical quality; it nearly always worsens with
feeding, often the infant will need to take breaks while feeding in order to breathe.
= MILD LM - the stridor often improves with crying, as tone in the pharynx is increased
® MODERATE TO SEVERE LM.- stridor will typically worsen with crying because of the
increased airflow through the severely collapsed larynx.
® SEVERE LM - infants have been found to have shorter aryepiglottoic folds.
- pathologic specimens of surgically resected supraarytenoid tissue have been found to
have nerve hypertrophy compared with controls, which supports the theory of neurologic
dysfunction as the etiology of LM.
- on each inspiration, the epiglottis is pulled towards the glottis thus producing narrowing
causing inspiratory stridor which is always present but becomes much more severe
during exertion and crying; while on expiration, the folds are forced apart, stridor is
inconstant and is sometimes extremely marked; the vocal folds are normal and the voice
of the patient is normal.
- the noise consists of a croaking sound accompanying inspiration, which rises to a high
pitched crow when a longer or more vigorous breath is taken; the stridor increases in
loudness during the first few months, gradually lessens and disappears during the
course of the second year; depending on the form of laryngomalacia, stridor may persist
for the first year of life or even up to several years.
- the stridor varies considerably with airflow’and posture; appears or worsens with supine
position; may improve in prone position; it is loudest with increased ventilation (e.g.

14
crying, agitation, feeding) and worsens during intercurrent respiratory tract infections; in
severe cases, it is accompanied by cyanosis; it is absent when the infant is asleep.
*SUPRASTERNAL RETRACTIONS - sucking in of the suprasternal notch immediately
above the breastbone; these patients require more frequent hospitalization and
intubation with URI than the average child; the natural history in most patients is for
Spontaneous recovery, however because of frank airway obstruction or other
complications, 10-15% of babies require surgical intervention to improve their airway.
*FEEDING DIFFICULTIES - are related to gastro-esophageal reflux in up to 80% of cases.
MODERATE TO SEVERE CASES
» Regurgitation » Recurrent vomiting
® Occasional coughing ® Choking .
® ASPIRATION - often due to incoordinated breathing and swallowing during deglutition
*POOR WEIGHT GAIN *FAILURE TO THRIVE
*OBSTRUCTIVE SLEEP APNEA - observed in older children and adults; similar to
neonates with LM, older children with sleep apnea and LM improve after
supraglottoplasty; neurologically impaired children (i.e., those with cerebral palsy) with
poor pharyngeal tone are particularly prone to LM.
= DIAGNOSIS — direct laryngocopy is indicated; the epiglottis is usually omega-shaped and
soft, and covers the laryngeal entrance on inspiration, although it can also be found in
otherwise normal infants with no airway obstruction.
- the shape and function of the vocal cords are normal; on inspiration, the structures
around the vestibule will be seen to invaginate with the synchronous production of the
stridorous sound; the stridor can be relieved by inserting the laryngoscope into the
vestibule of the larynx.
¢FIBEROPTIC FLEXIBLE LARYNGOSCOPY( FFL)
®IN THE SEDATED PATIENT - the topical lidocaine typically used can cause increased
collapse of the arytenoids and folding of the epiglottis during inspiration, which could
possibly lead to overestimation of the severity of LM.
=»IN THE AWAKE PATIENT - findings suggest that this is the optimal way to diagnose
LM, but it has been found to miss mild LM or lead to overdiagnosis in a normal airway.
BADVANTAGES OF AWAKE FFL
i. The ability to perform the examination expediently in the clinic setting with the parents
ii. The avoidance of sedation iii. Reduced medical expense
=DISADVANTAGE OF AWAKE FFL- in nearly all cases, the infant is crying during the
examination, which can alter the appearance of the supraglottic structures.
*FLEXIBLE NASOLARYNGOISCOPY - consistently accurate method of diagnosis.
*TRANSNASAL FIBEROPTIC LARYNGOSCOPY - only thing required for diagnostic
confirmation conducted in the OPD in mild cases seen in 80-90% of infants.
MOST COMMON LARYNGEAL FINDINGS
Inward collapse of aryepiglottic folds and arytenoid cartilage into laryngeal inlet during
inspiration
*Epiglottis collapses into laryngeal inlet during inspiration, short aryepiglottic folds
*AIRWAY FLUOROSCOPY - proposed as a screening tool for the infant with stridor;
although found to have a relatively high specificity, has a low sensitivity and is thus not
recommended if FFL is available.
*BRONCHOSCOPY [>
TREATMENT - usually self-limiting; generally begins to improve by 4-6 monthe of age
and resolves by 9-18 months; the cartilage becomes stiffer during the course of weeks
or months, and the symptoms gradually disappear.

15
- In most cases, apart from parental reassurance and support, no specific therapeutic
measures are needed; the condition usually subsides spontaneously as the cartilages
gain rigidity; feedings should be divided into fractions with a pause after every 2 or 3
swallows; in cases of respiratory distress, tube feeding is indicated; severe temporary
dyspnea should be managed in a neonatology ICU with continuous positive airway
pressure (CPAP) or intubation; tracheotomy is rarely required.
- approximately 10-31% of infants seen by a pediatric otolaryngologist require surgical
intervention for their LM.
*INDICATIONS FOR SURGERY - for severe LM resulting in these conditions, to prevent
worsening failure to thrive, cor pulmonale or cardiac failure.
Feeding difficulties ® Apnea ® Microaspiration
»Pectus excavatum »Cyanosis » Failure to thrive
*SURGICAL TREAMENT - the current standard treatment is supraglottoplasty
(aryepiglottoplasty).
=Carbon-dioxide (CO 2 ) laser "Laryngeal microscissors
"Sinus instruments =Microdébrider
™COz LASER SUPRAGLOTTOPLASTY TECHNIQUE - is currently popular, the
aryepiglottic folds are divided and the redundant arytenoid tissue is vaporized
® DIVISION OF SHORT ARYEPIGLOTTIC FOLDS - the simplest type of supraglottoplasty.
® REMOVAL OF VARIOUS PORTIONS OF THE PROLAPSING SUPRAGLOTTIS
"Tissue overlying the arytenoids BAryepiglottic folds
=Posterior portion of the epiglottis.
- it is important to preserve the interarytenoid mucosa to avoid postoperative stenosis.
® EPIGLOTTOPEXY - for the child with a severely omega-shaped epiglottis to unfurl the
epiglottis and open up the airway; the mucosa of the lingual surface of the epiglottis and
the corresponding mucosa of the base of the tongue are removed with the carbon-dioxide
laser, followed by suturing of the epiglottis to the tongue base; unilateral
supraglottoplasty has been advocated by some to reduce the risk of postoperative
supraglottic stenosis; however, most surgeons perform a bilateral procedure to obtain
the maximum benefit.
- the supraglottoplasty procedures are well tolerated by infants and typically require only
a short hospital stay of 1-3 days; the success of the various forms of supraglottoplasty-
epiglottopexy are high, and the vast majority of children obtain relief from their
obstruction; children with severe LM often have a lower-percentile weight on a
standardized growth curve, and improvement in growth curve percentile is substantial
after supraglottoplasty.
- following supraglottoplasty, the incidence of aspiration also improves significantly;
some children have ongoing aspiration for months after surgery and require thickening
of feedings or gastrostomy tube placement.
- sleep mechanics also improve as evidenced in studies that have compared preoperative
and postoperative PSG
- those children who do not improve with supraglottoplasty often have underlying
neurologic or syndromal abnormalities and may require a tracheotomy.
- complications from surgery are rare, the most concerning of which is supraglottic
Stenosis, which may occur in up to 4% of.,cases; c\hildren who do not improve
significantly with the initial surgery may require revision supraglottaplasty, which is more
commonly needed in children with comorbidities.
COMPLICATIONS OF LM - occur in severe cases; these patients require more frequent
hospitalization and intubation with URI than the average child.

16
*Feeding difficulties *Cor pulmonale ¢Bradycardia

*Obstructive sleep apnea *Failure to thrive
*PECTUS EXCAVATUNM - due to persistent retractions can all be seen in severe cases.
E. CONGENITAL CYSTS
*SUPRAGLOTTIC CYSTS - commonly located at the aryepiglottic folds or at the
epiglottis, are usually congenital.
*SUBGLOTTIC CYSTS - are usually acquired as a result of airway trauma.
GROSS APPEARANCE - determined by the point of origin in the larynx and the type of cyst;
the appearance varies widely; while some are covered by thin mucosa and are easy to
recognize, others appear as a submucosal mass.
- the cyst can be considered to be either external or internal to the larynx based on the
degree of compression by the cyst and the extent of disease within the larynx.
- cysts generally do not communicate with the interior of the larynx.
SACCULAR CYSTS (anterior or lateral) - are submucosal and do not communicate with the
lumen but the size of these cysts ranges from 0.5 to 0.8 cm, depending on the location.
- eversion and prolapse occur, further complicating the classification of cysts of the
larynx; the cysts are variably filled with thin serous fluid to tenacious, thick, mucinous,
gelatinous, or bloody fluid.
“ETIOLOGY - the appendix and ventricle are lined with respiratory epithelium which
contains many goblet cells as well as numerous sero-mucinous glands in the
submucosa.
MUGOCELE - a mucous-filled cyst may arise either from obstruction of the neck of the
appendix or from obstruction of the duct of the individual gland.
®False vocal cord ® Aryepiglottic fold
®Thyrohyoid membrane deep to the strap muscles, near the entrance of the internal
branch of the superior laryngeal nerve and artery.
- frequently, there is a fibrous pedicle extending through the thyrohyoid membrane from
the external cyst; less commonly, a mucocele may be present in both locations with the
parts connected through the thyrohyoid membrane, giving it a "dumb-bell" configuration.
- alaryngocele becomes a mucocele if its laryngeal opening becomes obstructed and
it fills with mucus.
RISK FACTORS
* PREMATURITY
eHISTORY OF PROLONGED INTUBATION DURING THE NEONATAL PERIOD
*HOARSENESS - usual symptom described as a change of voice by the patient.
¢"HOT POTATO” VOICE - seen in patients with larger lesions.
«INSPIRATORY STRIDOR - the most common presenting symptom in infants is airway
obstruction with inspiratory stridor; 40% of these infants will present with respiratory
distress in the first several hours of life.
FEEDING DIFFICULTIES
*PALPABLE CYSTIC MASS - is attached to the thyrohyoid membrane and moves on
swallowing.
=DIAGNOSIS - laryngeal examination discloses a unilateral mass of the false vocal fold
and aryepiglottic fold which bulges into the laryngeal aditus and the pyriform fossa.
- the true vocal cord on the side of the lesion is obscured from view; the entire glottis may
be obscured by a large cyst.
= TREATMENT
*ENDOSCOPIC EXCISION - the usual method of treatment.

w7
*MARSUPIALIZATION - wide opening of the walls of the cyst by using cold steel
instruments, COz laser or microdebrider.
*ASPIRATION - done when excision is not possible.
*TRACHEOTOMY - may have to be done.
*LASER EXCISION - the carbon dioxide laser is used.
F. CONGENITAL HEMANGIOMAS - are usually of the cavernous type and tend to occur
anteriorly in the subglottic region of the larynx; a cutaneous IH in the “beard distribution”
of the face is associated with an airway IH in over 50% of patients.
SUBGLOTTIC INFANTILE HEMANGIOMAS (IH) - are benign vascular malformations associated
with prematurity; they are twice as common in females as in males.
= PATHOLOGY - characterized by endothelial proliferation and uniform, strongly positive
staining for erythrocyte-type glucose transporter protein isoform 1 (GLUT-1).
= CLINICAL MANIFESTATIONS - the symptoms may be absent at birth and may first appear
in association with an URI; then they persist after the infection resolves; IH grows rapidly
in the first 6 months of life, stabilizes for approximately a year, then slowly involutes,
usually by the age of 3 years; to avoid total airway obstruction, medical or surgical
intervention is usually needed.
*STRIDOR - patients typically present in the first 6 months of life with inspiratory or
biphasic stridor that mimics the symptoms of subglottic stenosis.
*BARKING COUGH - may mimic the symptoms of nonresolving croup responds
temporarily to oral steroids
eDYSPNEA *HOARSENESS *SPONTANEOUS BLEEDING
eCYANOSIS eINDRAWING
= DIAGNOSIS
eDIRECT LARYNGOSCOPY AND MICROLARYNGOSCOPY - endoscopy shows a smooth,
compressible mass, often on the posterior or lateral wall.
*SOFT TISSUE ROENTGENOGRAMS OF THE LARYNX - help in delineating the size and
extent of the lesion, and calcium may be noted in lesions present for some time.
*COMPUTED TOMOGRAPHY (CT) MRI
= TREATMENT
*TRACHEOSTOMY - done to allow time for spontaneous regression; usually begins
within 8-10 months.
*LASER EXCISION - done if involution is not evident within a reasonable period of time.
eCRYOSURGERY
G. LARYNGOCELES - are abnormal dilations or herniations of the saccule that may be
internal, external, or acombination; they appear as air-containing rounded masses in the
neck or supraglottic region, sometimes with air-fluid levels.
- they are localized dilatations of the appendix or saccule of the laryngeal ventricle; they
are outpouchings of the laryngeal mucosa into the neck structures that usually exit the
endolarynx from the thyrohyoid membrane; the expansion of the saccule can be quite
marked; by definition, laryngoceles must communicate freely with the endolarynx and
be filled with air.
- they occur as a result of elongation and dilatation of the saccule of the laryngeal
ventricle they often form due to obstruction of the laryngeal saccule where it opens into
the laryngeal ventricle; sometimes a small cancer near the neck of the saccule may be
responsible and thus becomes Clinically manifest.
- laryngoceles can be associated with carcinoma: the percentage varies, but the literature
supports that 10-50% of laryngoceles in adults are associated with carcinoma; they are
found in 2% of healthy individuals and in 18% of patients with carcinoma of the larynx.

- they are rare; they may be bilateral; they develop in men who are usually in their fifties
more often than in women and they appear across all ages.
LARYNGOPYOCELE - infected pus-filled laryngocele
in
- saccular cysts and laryngoceles are unusual causes of respiratory obstruction
children; the anterior-superior portion of the laryngeal ventricle leads to a pouch of
mucous membrane called the saccule, which rises superiorly between the false vocal
fold, the base of the epiglottis, and the inner surface of the thyroid cartilage; scant muscle
surrounds the saccule and compresses it to express its secretions on the vocal folds.
or of the
SACCULAR CYST - results from the obstruction of the laryngeal saccule orifice
collecting ducts of the submucosal glands located around the ventricle.
eANTERIOR - protruding between the anterior and posterior vocal cords
*LATERAL - extending into the false vocal cord and aryepiglottic fold.
- laryngoceles produce intermittent upper airway obstruction and hoarseness because
of episodic filling with air, whereas saccular cysts produce constant symptoms because
of mucoid fluid within the cyst.
PATHOPHYSIOLOGY - congenital or acquired expansion from increased intraglottic
pressure of laryngeal saccule.
PATHOLOGY - laryngoceles are seen as outpouchings of the airway and are lined with
respiratory cells; long-standing inflammation results in the formation of metaplastic
squamous cells in the lining; squamous cell carcinoma can be present in laryngoceles
but itis not clear if the squamous carcinoma initiated the laryngocele.
=TYPES
eINTERNAL LARYNGOCELE - is confined to the interior of the larynx and extends
posterosuperiorly into the area of the false vocal fold and aryepiglottic fold; it consists of
an air-containing sac confined within the larynx and extends into the false vocal cord
and aryepiglottic fold and within the thyrohyoid membrane; it extends superiorly in the
paraglottic space and appears endoscopically as a submucosal supraglottic mass.
eEXTERNAL LARYNGOCELE - extends beyond the confines of the larynx through an
opening in the thyrohyoid membrane and manifests as a neck mass; it presents as a
cystic mass on the lateral surface of the thyrohyoid membrane which is connected to the
ventricle by a narrow patent tube.
-it may exist alone or in continuity with the internal component; it manifests clinically as
a soft swelling that is noted to one side of the midline over the thyroid ala.
eMIXED LARYNGOCELE - when a laryngocele causes dilatation within the larynx as well
as another dilatation outside the larynx; it consists of connected air-containing cavities
on both sides of the thyrohyoid membrane; the symptoms tend to fluctuate, increasing
with straining and disappearing at rest.
ETIOLOGY - laryngoceles can be congenital and present in infants, or they can be
acquired in adults; practices that can lead to the development of acquired laryngoceles
include instances where intralaryngeal air pressure is increased with open vocal folds
but where outward airflow is restricted, as would happen in:
*Straining «Coughing
¢Playing wind instruments eExcessive straining with voice use
“CLINICAL MANIFESTATIONS - can be asymptomatic when small; symptomatic as they
expand; the vast majority present with an internal unilateral mass; however, symptoms
may spontaneously resolve when the expelled air decompresses the mass.
*EXTERNAL LARYNGOCELE
® DYSPNEA AND DYSPHONIA » DYSPHAGIA
FOREIGN BODY IN THE THROAT

19
®COMPRESSIBLE, SPHERICAL MASS - over the thyrohyoid membrane which moves

with the larynx on swallowing; the mass may be absemt or vary widely in size with time.
®BRYCE’S SIGN - is characterized by a gurgling and hissing in the throat when the
neck mass is compressed.
»PERSISTENT, PRODUCTIVE COUGH - especially if infection is present.
*INTERNAL AND 9 FORMS
®HOARSENESS »STRIDOR ®» DYSPNEA
DIAGNOSIS -the masses in the false vocal cord and in the lateral neck are obvious on
clinical examination when the patient strains; the smooth swelling increases in size on
puffing, straining, and on playing wind instruments. .
- a laryngocele presents as a well-circumscribed, air- or fluid-filled structure extending
from the laryngeal ventricle into the paraglottic space or through the thyrohyoid
membrane into the soft tissues of the neck.
*DIRECT LARYNGOSCOPY - it is a fluid-filled dilation of the saccule (blind sac in
ventricle) without communication with the laryngeal lumen.
- it is indicated to rule out an underlying neoplasml the diagnosis can be suggested by
aspirating the mass with a large needle.
*CT AND MRI - delineate the mass precisely, which aids in planning surgical resection.
*MIRROR LARYNGOSCOPY *STROBOSCOPY
*SOFT TISSUE ROENTGENOGRA M OF THE NECK - during the valsalva maneuver will
disclose the presence of the air-containing cystic structures; if infection is present, an
air-fluid level may be noted on the roentgenogram.
= TREATMENT - not all laryngoceles need to be treated.
*SMALL ASYMPTOMATIC LARYNGOCELES - require no therapy and will seldom cause
any difficulty if causative factors are removed.
*SYMPTOMATIC LARYNGOCELES AND LARYNGOPYOCELES - should be excised using
an external approach and a temporary tracheostomy is done.
® INTERNAL LARYNGOCELES - can be excised endoscopically or they can be unroofed
widely and marsupialized.
®EXTERNAL OR MIXED LARYNGOCELES - often require an external approach to
completely remove the lesion.
SURGICAL MARSUPIALIZATION - is the treatment of choice for a laryngocele, most
commonly with the CO 2 laser to ablate the posterior wall of the cyst.
- posterior saccular cysts commonly recur after marsupialization and often necessitate
several endoscopic procedures; tracheotomy may be required, and subglottic stenosis
is a potential complication of the treatment; alternatively, the cyst may be excised via a
lateral cervical approach through the thyrohyoid membrane.
- benign cysts can be managed symptomatically, with aspiration or endoscopic removal
only as clinically necessary.
H. LARYNGOTRACHECESCPHAGEAL CLEFT (LTEC) - laryngeal clefts (LC) and
laryngotracheoesophageal clefts (LTECs) are rare congenital anomalities; there is the
absence of tissue between larynx/trachea an hypopharynx/esophagus; it is the result of
a failure of closure of the tracheoesophageal septum, thus creating a groove in the region
of the cricoid cartilage; it is a congenital midline defect of the posterior larynx and
trachea and the anterior wall of the esophagus:*
*LARYNGEAL CLEFT- is caused by failure of fusion of the posterior cricoid lamina, which
leads to abnormal communication between the posterior portion of the larynx and
esophagus.

20
*LARYNGOTRACHEOESOPHAGEAL CLEFT - results from extension of an LC to involve

incomplete development of the tracheoesophageal septum, leading to abnormal
communication between the trachea and esophagus.
with
*SUBMUCOUS LARYNGEAL CLEFT - consists of a posterior midline cartilage defect
intact soft tissue that includes mucosa and interarytenoid muscle; it is associated with
ion is
subglottic stenosis and typically is not identified unless a postmortem examinat
performed.
= BENJAMIN AND INGLIS CLASSIFICATION
eTYPE | - involves interarytenoid musculature
*TYPE Il - involves the cricoid only
°TYPE Ill - involves the proximal LTE
*TYPE IV - involves the thoracic tracheoesophageal septum
ETIOLOGY- LTEC is a rare disorder that occurs in less than 0.1% of the population; Evans
found an incidence of 0.4% in all patients with laryngeal abnormalities; there is a slight
however,
male preponderance; the pattern of inheritance is that of autosomal dominant;
most cases are sporadic; p0Orenatal hydramnios and prematurity are associated with
approximately 33% of all clefts.
ANOMALIES ASSOCIATED WITH LTEC
*TRACHEOESOPHAGEAL FISTULA - is the most common association that is seen in
approximately 20% of the LTEC and increased for Types Il through IV.
eG! TRACT ABNORMALITIES - overall are the most common anomalies.
» Anal atresia ® Meckel's diverticulum ® Hiatal hernia
®» Gastroesophageal reflux - commonly associated and causes significant morbidity when
coexisting with LTEC.
® Laryngomalacia Cleft lip and palate
® Bronchial and tracheal stenosis ® Cardiovascular defects
® Genitourinary abnormalities ®Tracheomalacia
MORTALITY RATES - LTEC is associated with a high mortality rate that is directly related to
the severity of the defect.
*TYPES I and Il- = 43% eTYPE Ill = 42% *TYPE IV = 93%
- of the patients who died, 67% had other serious congenital malformations; there are
very few patients in the literature with Type IV clefts that have survived.
SYMPTOMS - usually arise immediately after birth.
«ASPIRATION AND CYANOSIS WITH FEEDS - are the most common symptoms which are
nonspecific.
¢Persistent barking cough Choking *Excessive oral secretions
*Respiratory distress *Inspiratory stridor *Changes in the cry
*Recurrent aspiration pneumonia ¢Dysphonia or aphonia
DIAGNOSIS - proper and quick diagnosis is helpful to avoid continued damage to lungs
and esophagus.
*DIRECT LARYNGOSCOPY - should be performed in all patients suspected of having a
cleft, under general anesthesia and breathing spontaneously.
*CINERADIOGRAPHY - may be a useful study to help determine the position of the fistula.
*ENDOSCOPY *CHEST X-RAY
= TREATMENT
GOALS FOR TREATMENT be»
®To secure the airway ®To avoid chronic aspiration
=To prevent pulmonary complications from ongoing aspiration
®To ensure adequate nutrition; some centers recommend temporary NGT feedings.

21
eSTABILIZATION OF THE AIRWAY - if evaluations reveal a healthy patient with LTEC, the
patient may only need to be intubated and early repair may be possible; most patients
will require a tracheotomy prior to repair of the cleft.
®TYPE | CLEFTS - generally have an adequate airway and will not require tracheotomy.
TYPE Il TO IV CLEFTS - due to the high incidence of association with tracheomalacia
and other pulmonary anomalies, tracheotomy is usually required.
™TYPE IV CLEFTS - may need a double arm endotracheal tube that extends past the
carina into both the mainstem bronchi.
MEDICAL MANAGEMENT - is often adequate for type 1 LCs because aspiration will resolve
as they grow older.
=THICKENING OF LIQUIDS =UPRIGHT POSITIONING FOR DRINKING
lV FLUIDS - are given to treat the dehydration
*ANTIBIOTICS - to treat the pneumonia
*CONTROL OF GASTROESOPHAGEAL REFLUX - necessary to control it prior to repair;
simple medical management may be all that is indicated but the patient often requires
surgical intervention; insertion of a gastrostomy tube and fundoplication may be
performed to avoid continued aspiration and to decompress the stomach.
SURGICAL TREATMENT- in children with significant aspiration problems; surgical approach
depends on the type of cleft involved and the surgeon's preference; symptomatic type I-
Il and certain type Ill clefts can be repaired endoscopically, most type Ill and all type IV
require open repair.
B|INJECTION LARYNGOPLASTY
BENDOSCOPIC REPAIR OF THE CLEFT
- depending on the material used for the injection laryngoplasty, the procedure may need
to be repeated, or the patient may eventually require endoscopy of the cleft.
¥Y. LARYNGOPHARYNGEAL REFLUX (LPR)

- retrograde movement of gastric contents into the laryngopharynx; reflux of
gastroduodenal contents into the laryngopharyngeal region may cause inflammation and
symptoms resulting in chronic laryngitis.
- may involve a primary defect in the upper esophageal sphincter which relates to direct
contact of laryngeal tissues with pepsin and bile contents in an acidic pH.
GERD (GATROESOPHAGEAL REFLUX DISEASE) - retrograde transit of gastric contents into the
esophagus occurs with or without regurgitation to the pharynx or vomiting; it affects
7-10% of the population on a daily basis, and 40% on a monthly basis.
- gastric refluxate consists of hydrochloric acid, gastric pepsin, bacteria, bile salts, and/or
pancreatic digestive enzymes, which may have untoward effects on the esophageal and
airway mucosa.
= PATHOPHYSIOLOGY - the impact of reflux on the larynx is multifold and includes both
pathophysiologic and maladaptive behavioral changes; the direct effect of the acidic
refluxate causes an immediate inflammatory response; reflux contents of the stomach
also includes pepsin, which is a proteolytic enzyme (digests protein) that is activated in
an acidic environment; as a result, there is autodigestion of the laryngeal mucosa with
the effects of pepsin being considered to be more dangerous than the acid; pepsin
persists on the mucosa with the potential for activation when it is exposed to subsequent
episodes of reflux.
= RISKS
*Obesity *Alcohol abuse *Hiatal hernia

¢Pregnancy *Scleroderma *Feeding tube
SIGNS AND SYMPTOMS
*GERD - postprandial heartburn, supine reflux, choking spells at night, regurgitation,
hoarseness (worse in the morning), esophagitis, abnormal esophageal pH monitoring,
abnormal esophageal acid clearance/motility.
*LPR - chronic hoarseness (worse in the morning), globus sensation (often the primary
symptom), dysphagia, daytime (upright) reflux, mouth burning, halitosis, dry or itchy
throat discomfort, excessive throat clearing, chronic cough, recurrent respiratory
disease, laryngospasm, apnea, otalgia, torticollis (Sandifer syndrome: distinctive neck
posture in children that protects against acid reflux).
NOCTURNAL REFLUX - patients complain of awakening with a bad taste in the mouth and a
sensation of having an obstruction in the throat; this symptom is induced by too heavy
meals, taken too late in the evening and accompanied by alcohol consumption.
LARYNGEAL FINDINGS - can range from mild isolated edema and/or erythema of the area
of the arytenoid cartilages, to diffuse laryngeal edema and hyperemia with granuloma
formation and airway obstruction.
*PSEUDOSULCUS VOCALIS - a pattern of subglottic edema that extends from the
anterior commisure to the posterior part of the larynx; it appears like a groove or a sulcus
*VENTRICULAR OBLITERATION - may be identifed in up to 80% of patients with LPR;
swelling of the true and false vocal cords causes this space to become obliterated and
thus poorly visualized.
= DIAGNOSIS
*NASOPHARYNGOSCOPY - allows for visualization of characteristic findings as well as
complications (vocal fold granulomas)
*BARIUM SWALLOW - good initial screening test for demonstrating esophageal anatomy,
high false-negative rate (especially LPR), identifies hiatal hernias and strictures.
e24-HOUR DUAL-PH PROBE - most sensitive, “gold standard,” distal probe 5 cm above
LES and proximal probe 2 cm above UES, allows differentiation of GERD and LPR; triple
probe monitoring adds a nasopharyngeal probe.
<*TREATMENT
*BEHAVIOR MANAGEMENT
®Weight reduction if applicable ®Smoking cessation
® Avoidance of tight-fitting clothes » Avoid overeating, eating before sleep
® Elevation of the head of the bed (approximately 6 inches) while sleeping
Do not lie down 2 to 3 hours after eating.
®Abstain from caffeine, fatty foods, alcohol, mints, chocolate, citrus, spicy food,
carbonated beverages, spicy tomato based products, red wines, and late-night meals.
® Avoid aspirin, nitrates, and calcium channel blockers
*MEDICAL MANAGEMENT
™®PROTON-PUMP INHIBITORS (PPI - omeprazole, pantoprazole) - indicated as first-line
agents for complicated GERD and LPR or failed first-line regimens; it blocks the “proton
pump” responsible for acid secretion; recurrence of symptoms is common in patients
who require PPI therapy for initial treatment; if effectiveness of acid suppressive therapy
is uncertain, may consider 24-hour pH probe while on PPIs; typically, GERD requires
single-dose PPI and LPR requires double-dose PPI, take 1 hour before meals, avoid taking
with calcium.
- the AAOHNS (American Association of Head and Neck Surgery) indicates that treatment
for LPR must be more aggressive and prolonged than that for GERD, and depends on the
symptoms and severity of LPR and on the response to therapy; the AAOHNS advises that

at
patients with mild or intermittent symptoms of LPR can be treated with dietary and
lifestyle changes and with H2 antagonists, while the majority of patients require at least
twice-daily PPI therapy; some patients require therapy with both a PPI and an H2
antagonist, and the AAOHNS recommends the use of twice-daily PPI for a minimum of 6
months.
™®H2-BLOCKERS (cimetidine, famotidine, ranitidine) - a 4-6 weeks trial as first line of
medical management may be considered for uncomplicated GERD; it blocks histamine
interaction with its receptor; side effects include constipation, diarrhea, confusion, and
elevated liver enzymes.
™®PROKINETIC AGENTS (metoclopramid) - indicated for delayed gastric emptying, also
increases LES pressure; side effects include tardive dyskinesia, drowsiness, depression,
and confusion
*LIQUID ANTACIDS (calcium carbonate, hydroxides of aluminum and magnesium,
sodium bicarbonate) - may be firstline therapy for mild GERD, take after meals and before
sleep, overuse may result in acid-base and other metabolic disturbances.
™SUCRALFATE - nonsystemic oral medication, covers and protects exposed ulcerated
mucosal surfaces
*SURGICAL MANAGEMENT - indicated for failed medical regimen or those who require
continuous or increasing acid suppressive therapy (effectiveness of acid suppression
therapy should be the major criteria for predicting successful outcome of fundoplication
operation)
VI. INFECTIOUS DISEASES OF THE LARYNX

1. ACUTE SUBGLOTTIC LARYNGITIS - most common type of acute dyspneic laryngitis.
* ENOLOGY - basically caused by a viral infection with accompanying secondary bacterial
infection; cool, damp, and foggy weather in fall and winter appear to increase the
morbidity; recurrent infections in the nasopharynx and nasal obstruction due ot
chronically inflamed hypertrophied adenoids and tonsils are etiological factors.
*PARAINFLUENZA 14 VIRUS - most common cause
¢Parainfluenza 3 virus eMyxovirus *Rhinovirus
eAdenovirus eEchovirus
*RESPIRATORY SYNCYTIAL VIRUS - can also be found in babies.
« PATHOLOGY - there are only minor tissue changes in the larynx; 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; the supraglottic and glottic
areas are relatively noninflamed; however, erythema and edema of the subglottic larynx
can both result in airway compromise
- the trachea may have some secondary edema, but not as pronounced as the subglottic
inflammation; the edema involves the mucosa over the cricoid cartilage, which is
restricted by a circumferential, rigid cartilaginous structure; the area has no potential to
expand as do other areas of the airway.
- PATHOGENESIS - very serious acute disease of early infancy, most common between
1-5 years old; within a short time, life-threatenig narrowing of the child’s airway can
develop due to inflammatory mucosal swelling of the elastic cone in the subglottic space.
= CLINICAL MANIFESTATIONS - symptoms occur as a result of mucosal edema in the larynx,
trachea, and bronchi; it has a gradual onset and course; symptoms worse at night and
continuing for a few days; mild rhinitis and conjunctivitis are followed ina few days by:
*COUGH - harsh, dry and barking *STRIDOR - usually inspiratory ‘ey

24
*RESPIRATORY DISTRESS SYMPTOMS - retraction of the suprasternal notch and of the

intercostal spaces during inspiration, cyanosis, perioral pallor, and worsening of the
symptoms due to a fear of asphyxia in children.
*DYSPNEA - often occurs at night; inspiratory bradypnea and dyspnea are accompanied
by crowing. ,
- the severity of respiratory obstruction depends on the degree of mucosal swelling in the
subglottis; worsening symptoms on children lead to concern due to the impending threat
of airway obstruction; the voice is normal or slightly deeper; swallowing is normal;
temperature is moderate, around 38° C; the patient generally does not appear toxic.
- because it can be caused by many different viruses, it is not unusual for a child to have
more than one episode; each episode results in antibody production only to the specific
viral strain causing that particular infection; symptoms typically last between 3 and 5
days, although the child may be infectious for 2 weeks.
PHYSICAL EXAMINATION - auscultation reveals bilateral decreased breath sounds,
rhonchi, and scattered rales.
DIAGNOSIS - is based on history and physical examination, but it can be difficult
especially if the symptoms are severe and mimic the appearance of acute epiglottitis; if
the diagnosis is a possibility, the patient should be managed as if with epiglottitis.
ePLAIN X-RAY FILMS - can be very helpful and have a characteristic appearance.
AP VIEW - there is distention of the hypopharynx with symmetric subglottic narrowing
in the first 1-2 cm of the trachea; this is also known as the” STEEPLE SIGN”.
®LATERAL VIEW - may show subglottic narrowing or loss of the air shadow
*CBC - is generally unremarkable except for a lymphocytosis.
*BRONCHOSCOPY - would show mild subglottic.
TREATMENT - based on the severity of symptoms; should be started as soon as possible;
most children have self-limiting disease that is only mild or moderate in terms of airway
distress; mild illness can be easily treated at home with conscientious parental
monitoring, but specific instructions must be thoroughly discussed with the parents
including causes and symptoms of respiratory distress.
- a child who appears toxic or has progressive stridor, cyanosis, or mental status
changes, should be hospitalized; should not receive sedatives or opiates as these may
depress the respiratory drive; expectorants or bronchodilators as these may irritate the
airway and cause increased obstruction; antibiotics do not cure the disease as it is viral.
*HUMIDIFICATION - humidifier or other means; in cooler weather or at night, taking the
child outside may break the acute episode alone.
*ADEQUATE FLUIDS - either orally or intravenously.
*PULSE OXIMETRY OR ARTERIAL BLOOD GAS ANALYSIS (ABG) - if hospitalized,
monitoring for hypoxia is important.
“OXYGEN
*RACEMIC EPINEPHRINE - in patients with more severe symptoms, nebulized racemic
epinephrine produces a rapid improvement in symptoms by vasoconstriction and,
therefore, a reduction in mucosal edem; it may eliminate the need for intubation; the child
should be monitored for at least 6-10 hours after the last treatment because of the
possible risk of “rebound”, the child may improve for a few hours after treatment, but
actually deteriorate to a more severe state later.
*CORTICOSTEROIDS - both nebulized and systemic steroids have been demonstrated to
produce an improvement in the symptoms; consequently, there is a reduction in the
length of time spent in the hospital as well as a decreased need for other interventions
such as intubation; because the beneficial effects of steroids require several hours before

25
onset, the simultaneous administration of racemic epinephrine and steroids results in

both immediate and lasting symptom relief.
*ENDOTRACHEAL INTUBATION - indicated in a small number of cases (1.5%) who do not
respond to medical therapy and airway obstruction worsens, until the edema resolves;
most children can be extubated after a few days and have no permanent clinically
significant sequelae from either the disease or treatment.
*TRACHEOSTOMY - for severe obstruction and progressive sicca-type crust formation.
2. ACUTE SPASMODIC LARYNGITIS - characterized by acute attacks of inspiratory
stridor that occur at night and subside in a short time, only to recur in subsequent nights.
It is the least serious type.
= ETIOLOGY - the children are usually between 1- 3 years old. The cause is viral in most
instances, but reflux, allergy and psychologic factors appear to play important roles.
= SYMPTOMS - the child is awakened from sleep with marked stridor and a harsh, barky,
metallic cough with cyanosis; cold-like symptoms, if present, are extremely mild, and
fever is absent; acute spasm of the vocal cord adductors may be the cause, possibly
triggered by allergy, viral infection, or gastroesophageal reflux.
- spontaneously resolving within a few minutes, such a bout never exceeds 1 hour;
recurrent episodes during the night for several days is the general rule, but some nights
may be skipped between attacks; relapse is frequent.
= PHYSICAL EXAMINATION - the pharynx reveals only minimal, if any, edema.
=TREATMENT - at home, exposure to steam in the bathroom or to the cool night air is
sufficient to break the attack; the child often arrives in the ER with surprised parents
because the attack has been broken during the ride by the night air; racemic epinephrine
will break the attack if needed; parents need accurate information and reassurance before
discharging the patient home including written instructions.
3. SUPRAGLOTTIMIS (ACUTE EPEGLOTEITES) - is a fulminany infection of the entire
supraglottic airway; it may be involved, but the epiglottis and aryepiglottic folds are most
extensively involved.
- it primarily affects children and follows a bout of rhinopharyngitis, but it occurs
frequently in adults and is as potentially lethal as in children.
- the normally well-defined thin structures become edematous and enlarged; the edema
often encroaches on the vallecula and rarely may extend to the posterior pharyngealw
tall.
- the hypopharynx and piriform sinuses usually are mildly to moderately overdistended;.
the remainder of the airway is fairly normal, although at least 25% of children with
epiglottitis have subglottic narrowing; extensive manipulation of the patient should be
avoided because of the possibility of inducing glottic spasm
- itas a rapidly progressive, life-threatening airway emergency; as the epiglottis enlarges,
it curls posteriorly and inferiorly and limits the patency and ease of visualization of the
airway; with partial occlusion, additional mucus can easily lead to complete obstruction;
the area around the epiglottis is rich in lymphatic tissue and this makes it easy for
inflammation and infection to spread to the epiglottis.
- as acute supraglottitis has become a rarer entity in the pediatric population, it may be
less readily recognized; because of the high morbidity and mortality, rapid and accurate
diagnosis is essential.
= ETIOLOGY - in the past, the annual incidence of supraglottitis in the US was 5 per
100,000 children 5 years of age or younger, predominantly caused by Haemophilus
influenzae; after introduction of the conjugated H. influenzae type B (HIB) vaccine in the
1980s, there was a precipitous decline in cases of epiglottitis and other invasive

26
Haemophilus influenzae diseases; additionally, the median age of disease in children
shifted from 3 years to 6-12 years; a greater proportion of cases now occur in adults.
*CAUSATIVE ORGANISMS
»® Streptococcus pneumoniae ®S. pyogenes
® Staphylococcus aureus ®H. influenzae serotypes
*OTHER CAUSES
® Irritation from a foreign body or burn
®Tumors such as epiglottic cysts or neoplasms (e.g., lymphoma)
® Granulomatous disease (e.g., sarcoidosis, tuberculosis, Wegener granulomatosis)
® Angioneurotic edema ®Lack of immunization with HIB
® Failure of antibody production, especially in those with immunodeficiency.
- atypical cases may result from a vast range of infectious and noninfectious entities,
such as Kawasaki disease and posttransplant lymphoproliferative disorder.
- the incidence is higher in the winter, with some studies describing higher numbers in
the early winter and spring; regional differences in incidence occur as well, with the
incidence and springtime peak being lower in southern climates; for unexplained reasons
there is a higher incidence in Navaho Indians and Eskimos.
ADULTS - the infectious cause is more likely group A streptococcus.
= PATHOLOGY - there is asevere cellulitis of the tissues of the epiglottis and aryepiglottic
folds; there is profound edema and erythema ofall the supraglottic structures, especially
the epiglottis, aryepiglottic folds, and false vocal cords.
- the mucous membrane is bright red and edematous; excretions on or in the larynx tend
to be thick and inspissated; obstruction of the laryngeal vestibule prevents effective
cough and removal of secretions creating a second obstructive problem.
= CLINICAL MANIFESTATIONS - the clinical presentation of drooling, fever, and sore throat;
it is similar to that of viral laryngotracheobronchitis (croup) or retropharyngeal abscess;
lateral radiographs of the neck help to distinguish these entities.
*HALLMARK FEATURES - are rapid in onset and progressive over hours.
® DYSPHAGIA - is an important symptom and may be asign 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.
®DROOLING OF SALIVA - because of increased production and the reluctance to
swallow because of pain; the mouth falls open to allow the saliva that is too difficult to
swallow to dribble out.
® RESPIRATORY DISTRESS
*CHILD - refusal of food and liquid intake may lead to dehydration; child appears toxic
and anxious in appearance with clinical evidence of major upper airway obstruction
™SORE THROAT - disease starts with this, then quickly progresses to dysphagia and
extreme difficulty in breathing
» DYSPHAGIA ®» DROOLING OF SALIVA ®» DYSPNEA
®DYSPHONIA- speech is limited because of pain, and the voice may be muffled (“hot
potato speech) an
OTHER SYMPTOMS
®HIGH FEVER - usually marks the onset of the disease.
*STRIDOR - is not an outstanding feature and it is variably present as an inspiratory
and/or expiratory rattle; inspiratory stridor usually forces the patient to sit upright in
bed with the nose pointing upward in a “sniffing position (neck flexed and head
extended).

27
» INCREASING RESTLESSNESS, AGITATION AND DISORIENTATION - appears as the

respiratory distress is increasing.
SIGNS OF AIRWAY OBSTRUCTION - shallow respiration, inspiratory stridor, retraction
»CYANOSIS - as distress continues, the children develop a peculiar ashen gray color
which is a significant sign of impending respiratory arrest.
» COUGH » LETHARGY
CLASSIC POSITION - the child sits erect with the head forward, flexed at the waist, with the
chin forward, mouth open and the tongue protruding from the mouth - in order to lessen
the airway obstruction.
- activity is minimal, and the patient usually prefers to sit leaning forward or in the
“tripod” position (i.e., seated, with the hands braced against the bed and the head held in
the sniffing position to maximize airflow); sudden laryngospasm may occur with
aspiration of secretions into an already compromised airway, which results in respiratory
arrest.
- general reactions to increasing obstruction and dysphagia include dehydration,
hyperpyrexia, tachycardia, anxious facies and restlessness.
- the clinical course is characterized by rapid improvement to the point that often the
airway is much improved within 48 hours and the endotracheal tube is no longer
necessary; because the disease is bacterial in origin, involving primarily one genus, the
incidence of recurrence is negligible.
*ADULTS - there may be more protracted and less severe presentation than that seen in
children (more than 24 hours; prompt recognition of this acute airway emergency is
essential to prevent airway obstruction; it less commonly causes airway distress; the
clinical course appears to be less severe, with less seasonal variation .
®FEVER & SORE THROAT
®MUFFLED VOICE ™ DYSPHAGIA
®ODYNOPHAGIA - pain is severe and is worsened on swallowing; it is slower to develop
and to resolve than in children.
RESPIRATORY OBSTRUCTION - is less likely to occur, but may do so with a fatal result.
= DIAGNOSIS
eEXAMINATION - children with epiglottitis typically have a normal oral exam or pooling
of secretions, and the larynx may be tender to palpation.
- if epiglottitis is suspected, no further examination is recommended outside of a
controlled setting; the risk of complete obstruction is high and the airway has to be
secured; attempts to visualize the epiglottis, especially in children with moderate or
severe distress, should be done with extreme caution and in the OR.
eRADIOLOGY - lateral neck radiographs best show the changes of epiglottitis.
®Swollen epiglottis (“thumb print” sign)
® Thickening of the aryepiglottic folds
®The hypopharynx may distend as airway compromise progresses
- soft tissue x-rays of the neck will indicate the characteristic supraglottic swelling
impinging on the airway when it is not possible to see it over the base of the tongue.
- radiology should only be considered in patients with mild symptoms and no sign of
respiratory distress; the child should be accompanied by a physician with equipment
necessary to secure the airway; this study should be performed during inspiration.
- due to the upper airway obstruction, dilation of the hypopharynx occurs secondary to
airtrapping.
*DIRECT LARYNGOSCOPY - is rarely necessary for diagnostic reasons and is
contraindicated unless a bronchoscope or an endotracheal tube is immediately available

s
toy
28
since respiratory obstruction may be precipitated; an edematous, cherry red epiglottis

with inflammation of the surrounding supraglottis is seen.
*CT SCAN - thickening of the supraglottic tissues can be easily appreciated; patients
with supraglottitis have a tenuous airway, and the recumbent positioning may provoke
abrupt airway occlusion; conventional x-rays are preferred for the initial evaluation.
*CHEST X-RAY - is indicated since atelectasis and pneumonia may accompany this
disease; epiglottic swelling is visible on a lateral radiograph.
*CULTURE/SENSITIVITY TESTS - of the pharyngeal secretions should be done.
= TREATMENT
*CONTROL OF THE AIRWAY - airway management takes priority in these patients; it
begins in the ER where the child is observed at all times by a physician capable of
securing an airway; the child should be taken to the OR to secure the airway and the
otolaryngologist should be ready to perform a tracheotomy if needed; endotracheal
intubation is the method of choice as the supraglottic swelling is usually reversible in a
few days, unless complications occur.
- if good ICU observation is not available then tracheotomy is safer; aAfter the airway is
secured, a more thorough laryngoscopy may be performed and the supraglottitis
cultured; at the end of the procedure, the oral endotracheal tube may be changed to a
nasotracheal tube, which is more secure; after obtaining a secure airway the patient is
transferred to the ICU for close observation.
- the child should be kept sedated and some authors favor complete paralysis and
mechanical ventilation to prevent accidental extubation; criteria for extubation vary, with
some otolaryngologists performing a repeat laryngoscopy either directly or using a
fiberoptic scope; some authors extubate without laryngeal examination relying on the
presence of air leak and improved clinical picture; a number of reports have shown that
the period of intubation needed has been reduced to around 48 hours; extubation is
usually possible after 48-72 hours, at which time the edema has subsided sufficiently to
allow an air leak around the endotracheal tube.
*OXYGEN THERAPY - advisable so that more oxygen is available for alveolar ventilation.
*MUCOLYTIC AGENTS - may be nebulized to help liquefy secretions.
*BROAD SPECTRUM ANTIBIOTICS - should be instituted by IM or IV routes after a throat
culture has been obtained; most patients are treated with parenteral antibiotics for
around 5 to 7 days and then may be converted to oral antibiotics.
® SECOND-GENERATION CEPHALOSPORINS - Ceclor, Cefzil, Ceftin, etc
® THIRD-GENERATION CEPHALOSPORINS - Omnicef, Rocephin, etc
- they are given either alone or in combination with Ampicillin for ; coverage.
%»CLINDAMYCIN - if the patient is allergic to Penicillin
*STEROIDS eVAPORIZATION
ADULTS - conservative airway management in an intensive care setting is often
successful, and a tracheostomy is seldom required; conservative measures include
oxygenation, humidification, hydration, corticosteroids, and intravenous antibiotics.
DIFFERENTIATING CROUP FROM SUPRAGLOTTIINS mn

CROUP SUPRAGLOTTITIS
USUAL AGE 1-5 years “= | Any age
ONSET Gradual (days) Sudden (hours)
DYSPHAGIA No Yes
DROOLING Little, if any Yes

COUGH Yes No
VOICE Hoarse Muffled
PALPATE LARYNX/NECK Nontender Tender/painful
LARYNGOTRACHEOBRONHITIS (CROUP) - is an inflammation of the

4. ACUTE
typically occurs in young children and is the most common
subglottic larynx which
acute
infectious cause of stridor; it primarily involves the subglottic region; it is a severe
inflammatory disease of the larynx, trachea and bronchi.
play a part in
ETIOLOGY - atmospheric conditions (i.e. low humidity and cold) may
production of the disease.
eVIRUS - is probably the basic etiologic agent.
®»PARAINFLUENZAE VIRUS TYPE 1- most frequently isolated (75%)
» Respiratory syncytial virus (RSV)
®Parainfluenzae Type 3 » influenzae A and B
LESS COMMON
® Adenoviruses ® Rhinovirus »Coxsachieviruses
®Echovirus ® Measles virus
*BACTERIA - a secondary bacterial infection by organisms indigenous to the nose and
throat may develop.
® Haemophilus influenzae ® Streptococcus ® Staphylococcus
®Branhamella catarrhalis ®»Pneumococcus
*ALLERGIES eINHALED IRRITANTS
EPIDEMIOLOGY - croup is a very common disease; the incidence is highest in children
aged 6 months to 2 years; typical croup symptoms are rarely observed in children older
than 6 years of age, likely owing to the increase in airway diameter; the incidence is
higher in boys; in temperate climates the incidence typically peaks in late autumn and
winter; up to 15% of patients have a strong family history of croup.
— PATHOPHYSIOLOGY - bacterial superinfection following viral URI prodrome.
= PATHOLOGY - inflammatory edema and mucus production result in airway narrowing in
the subglotiic region, resulting in stridor; inflammation of the vocal cords results in
hoarseness, and sometimes aphonia; the most important feature is edematous swelling
in the region of the conus elasticus with the result that there is marked narrowing of the
already narrow infraglottic area; there is intense inflammatory reaction of the mucosa
with loss of epithelium and outpouring of a thick, viscid, mucoid secretion.
CLINICAL MANIFESTATIONS - the symptoms often start abruptly, and typically worsen
during nighttime; nonspecific coryzal symptoms frequently precede the illness
*PRODROMAL SYMPTOMS
®MILD URI - is the usual beginning of the disease.
®LOW-GRADE OR MODERATE FEVER
TYPICAL FEATURES
MILD INSPIRATORY STRIDOR - may also be present; the disease process may be self-
limited at this time but some children may continue to develop increasing respiratory
difficulty; when the child’s airway is significantly narrowed, he struggles to inhale air past
the obstruction and into the lung, producing the characteristic inspiratory stridor and
suprasternal retractions, and the classic barking or seal-like cough.
»“CROUPY”, BARKING, NON-PRODUCTIVE COUGH - develops over the space of 2-3
days; the onset of cough is usually at night.
® HOARSENESS

30
“OTHER SYMPTOMS
»®» HIGH FEVER
®INDRAWING IN THE SUPRACLAVICULAR, INTERCOSTAL AND SUBCOSTAL AREA - is
associated with increasing inspiratory stridor in the more severely ill patients.
» CHILD USUALLY WANTS TO LIE DOWN
=» MANIFESTATIONS OF AIR HUNGER AND HYPOXIA
Anxious facies =Restlessness
=Refusal to take food and drink =Refusal to talk
®»CYANOSIS - may appear in severe cases.
® STUPOR - the child lies quietly and develops a glazed facial expression.
®»SYMPTOMS OF HYPOXIA, HYPERCAPNIA AND ACIDOSIS
=Hyperpyrexia "Malaise ®=Tachycardia
=Dehydration =Restlessness =Disorientation
=Nausea and vomiting
®EVIDENCE OF EXHAUSTION AND IMPENDING RESPIRATORY FAILURE
=Ashen-gray color =Tachycardia =Lassitude
=Reduced entry to the lungs BLittle effort to cough
= DIAGNOSIS
*RADIOGRAPHY - radiographic studies are not indicated or obtained routinely in patients
with croup but are useful in confusing cases, primarily to exclude other causes of stridor;
the radiographic changes are caused by inflammatory edema that affects the larynx and
subglottic tissue.
®FRONTAL VIEW - is most helpful in the diagnosis; symmetric subglottic airway
narrowing or “pencilling” of the airway is the major radiographic finding; in contrast to
congenital subglottic stenosis, narrowing of the subglottic portion of the trachea is not
fixed and may improve on expiration.
®LATERAL VIEW OF THE NECK - appears less helpful, although the narrowing may be
noted; this projection shows hypopharyngeal airway distension, but more importantly, it
establishes that the epiglottis and aryepiglottic folds are normal.
«DIRECT LARYNGOSCOPY .- is indicated to rule out other obstructive conditions; a
smooth diffuse redness is noted in the infraglottic area and this may be associated with
an apparent increase in tissue mass; the supraglottic structures may be red but are
otherwise normal;ing require hospitalization.
eHUMIDIFIED AIR - the patient should be placed in a croupette; compressed air or
oxygen is used to nebulize the moisture.
*HYDRATION - systemic hydration is as important as hydration of the tracheobronchial
tree and appropriate amounts of parenteral fluids are indicated.
*OXYGEN - should be given in children with oxygen saturation below 92% in room air; it
should be given with care since CO2 narcosis may occur secondary to increased alveolar
oxygenation.
*PARENTERAL ANTIBIOTICS - should be given since steroids are usually used
c=horamphenicol or ampicillin may be used.
*CORTICOSTEROIDS- are beneficial in reducing the inflammatory response and edema
of the infraglottic tissues; hydrocortisone derivatives such as prednisolone and
methylprednisolone produce the best anti-itiflammatory response.
*NEBULIZED EPINEPHRINE - studies have shown it to have resulted in a considerable
reduction in the need for intubation or tracheostomy.
*TRACHEOSTOWY - indicated when obstruction with cyanosis, tachycardia, ashen-gray
pallor, marked decrease in pulmonary ventilation, inability to cough or collapse present.

31
Vi. ACUTE LARYNGITIS

- laryngitis is a general term that refers to any infectious, noninfectious, localized, or
systemic inflammatory process that involves the larynx; laryngitis in children is most
often caused by viral croup; laryngitis in adults is most often caused by viral URI,
smoking, or laryngopharyngeal reflux (LPR).
= ETIOLOGY
*VIRUSES - the cause of this is almost always a virus.
®RHINOVIRUS - most common
® Influenza A virus ® Adenoviruses ® Enterovirus »® Paramyxovirus
® Respiratory syncytial virus =» Coronavirus ® Parainfluenza virus
*BACTERIA
®» Staphylococcus ® Streptococcus pnuemoniae
»Pneumococcus
- it is more common in the winter months and is usually caused by acute coryza (common
cold)
®VIRAL - adult infection of the larynx is most often of viral origin, accompanied by
general malaise and/or fever.
=sHoarseness =Coughing "Sensation of globus
sLow-grade fever =Rhinitis =Postnasal drip
=Edema and erythema of the vocal fold mucosa
HERPETIC LARYNGITIS - which occurs most often in immunodepressed subjects is
characterized by vesicles or painful ulceration of the larynx.
®BACTERIAL - usual complication of a viral laryngitis; if the hoarseness persists for
more than several days, there is a possibility of a secondary bacterial invasion; the
laryngitis may be pseudomembranous, and if associated with tracheatis, mimics
diphtheria.
=»FUNGAL
=CANDIDIASIS (MONILIASIS) - edema, erythema, adherent, friable, cheesy, white
plaques; spread from oral cavity
BASPERGILLOSIS - allergic, noninvasive, or invasive; the severity of the attack depends
on immunocompetence; it may mimic a laryngeal carcinoma.
#BLASTOMYCOSIS - red laryngeal ulcers or miliary nodules on vocal cords, red granular
lesions, painful abscesses
®HISTOPLASMOSIS - ulcerative lesions in larynx (anterior larynx and epiglottis), may
have granulomas
=COCCIDIOMYCOSIS - nodular laryngeal mass
PATIENTS AT RISK
*Diabetics eImmunocompromised
«Previous radiation therapy *linhaled corticosteroid use
*Chronic corticosteroids *Posttransplant
*Poor nutrition *Debilitating illnesses
*Long-term antibiotics *HIV
SIGNS AND SYMPTOMS se
*Odynophagia *Mucositis *Dysphonia
*Cough *Dyspnea *Aspiration
DIAGNOSIS
“Endoscopy *Biopsy (may be confused with malignancy)

32
TREATMENT
*Establish airway *Antifungal regimen
®TUBERCULOSIS - laryngitis may be associated with pulmonary TB, infected secretions
from the lungs contaminate the larynx, or the bacterium may pass through the blood
system; the pulmonary infection may pass unnoticed.
PATHOGENESIS - almost always secondary to active pulmonaty TB; the infection is
transmitted to the larynx by bacilli contained in the sputum.
- the posterior part of the larynx, interarytenoid area, and epiglottis are most commonly
affected; there is a danger of perichondritis; monocorditis can be caused by a military
tuberculous deposit.
CLINICAL APPEARANCE
*Hyperimia eMonocorditis *Exudative edema of the vocal cords
*Uceration of the different parts of the larynx
DIAGNOSIS - made with biopsy of the edematous, erythematous, granular lesions in the
larynx; in fresh cases, microlaryngoscopy initially shows reddish-brown submucous
nodules, which are partly confluent; later, ulcerations or granulations develop.
- monocorditis is characterized by redness and thickening, occasionally with small
ulcerations of one vocal cord.
- if left untreated, tracheal stenosis may develop.
®SYPHILIS - the larynx can become involved in the later stages of systemic syphilis;
laryngeal localizations are both rare and highly polymorphic.
BSECONDARY STAGE - temporary mild edema, painless
BTERTIARY STAGE
APPEARANCE OF THE LARYNX - papules, edema, ulcers
&IMMUNOODEPRESSION OR AIDS - open the door to specific infections of the larynx,
incurring the return of both tuberculosis and syphilis.
- invasive forms involving neighboring organs, septicemia, bleeding and obstruction of
the larynx.
«AUTOIMMUNE
&® RHEUMATOID ARTHRITIS ®» AMYLOIDOSIS
& WEGENER’S GRANULOMATOSIS SARCOIDOSIS
®RELAPSING PERICHONDRITIS ®SYSTEMIC LUPUS ERYTHRMATOSIS
eINFLAMMATORY
=>LARYNGOPHARYNGEAL REFLUX - most common noninfectious cause of laryngitis
® ALLERGIC LARYNGITIS
&®ANGIOEDEMA OF THE LARYNX .- life-threatening inflammatory reaction due to
vascular dilation of the larynx
& CHEMICAL/THERMAL INJURY » RADIATION LARYNGITIS
PATHOLOGY - there is capillary dilatation and hyperemia associated with generalized
extracellular edema; a submucosal leukocytic infiltrate, mostly of mononuclear cells, is
present initially; later polymorphonuclear cells appear if a secondary bacterial infection
develops; the superficial mucosal layers usually slough and shallow ulcerations covered
by pseudomembranes may develop.
- the mucosa of the larynx becomes congested and may become edematous; a fibrinous
exudate may occur on the surface; sometimes infection involves the perichondrium of
the laryngeal cartilages producing perichondritis.
CLINICAL MANIFESTATIONS - the main complaint of the patient is the huskiness or
hoarseness of voice and discomfort in the throat particularly on swallowing.

33
*PRODROME
®LOW-GRADE FEVER » MALAISE
*SYMPTOMS
®SORE THROAT, PAIN IN THE LARYNX
®DRY IRRITATING COUGH AND COUGHING ATTACKS - may be a troublesome feature
™CHANGE IN VOICE - can vary from a breathy voice, usually due to the patient
protectively splinting the larynx, to a raspy hoarse voice secondary to a hemorrhagic
lesion on the cords.
- the usual symptoms are those of a common cold with associated hoarseness; the
laryngitis is almost always associated with acute rhinitis or nasopharyngitis; although
viral acute laryngitis can be seen in children, it is more common in adults; the onset of
infection may be associated with exposure to sudden temperature changes, dietary
deficiencies, malnutrition and lack of immunity.
- hoarseness or aphonia is usually constant in duration.
® RESPIRATORY DISTRESS - is rare with the exception of young infants; if it is diphtheria
is the cause, respiratory distress with airway compromise is quite marked secondary to
the pseudomembrane blocking the laryngeal inlet; complete obstruction and respiratory
arrest may occur.
™® DANGER OF AIRWAY OBSTRUCTION IN CHILDREN
® DYSPNEA - is present only in severe cases.
® LARYNGEAL SECRETIONS - early in the course of the disease they are scanty, later
they may become abundant but viscid and may be blood tinged; the process is usually
self-limited with spontaneous improvement.
= DIAGNOSIS - is made on the basis of history, general examination, and listening to the
voice; laryngeal inspection is not necessary to confirm the diagnosis.
INDIRECT LARYNGOSCOPY - reveals a diffuse congestion of the laryngeal mucosa; the vocal
cords look dull red and slightly edematous with stringy mucus between the cords; the
arytenoids, aryepiglottic folds and vestibular bands may show varying degrees of edema;
thick secretions appear on the surfacd of the laryngeal mucosa.
- vascular injection of the vocal cord mucosa is also commonly seen; the mucosa may
be granular with patchy superficial ulceration and areas of gray pseudomembrane
formation; vocal cord motion is normal although the margins of the cords may be red
and edematous and actually appear polypoid because of edema of Rienke's space;
excessive mucus may be evident; it is not unusual to see some component of erythema
in the supraglottic portion of the larynx, but it is most pronounced in the glottis.
= TREATMENT
*COMPLETE VOICE REST - to prevent further irritation of the inflamed vocal cords for at
at least 48 hours, followed by gentle voicing; It is important for Speedy recovery.
*EXPECTORANTS - to relieve dryness and tickle and to liquefy the secretions.
*SYSTEMIC HYDRATION - to avoid further inspissation of secretions.
*STEAM INHALATIONS - are soothing to the inflamed mucosa and also provide
humidification.
*BROAD SPECTRUM ANTIBIOTICS - to prevent secondary bacterial infection of the
ulcerated mucosa in the more severe cases.
® CEFUROXIME » AMOXICILLIN-CLAVULANATE
® MACROLIDES
"CLARITHROMYCIN = 500 mg by mouth bid for 5-7 days
"AZITHROMYCIN = 500 mg followed by 250 mg once daily for 4-5 days if the cause of
laryngitis is found to be Mycoplasma pneumoniae or Chlamydiophila pneumonia

34
eSTEROIDS - may be needed in severe cases.

eHUMIDIFICATION IN A COOL ROOM *BED REST
*ANALGESICS AND ANTIPYRETICS
*REMOVAL OF ALL IRRITANTS
Avoid alcohol and caffeine because of diuretic effect.
™» Avoid decongestants because of their drying effect
™®Guaifenesin may be a useful adjunct as a mucolytic agent.
®Smoking shoud be forbidden and chemicals such as certain dye stains
® Allergic toxins such as hair sprays, shellfish, amd crustacean should be eliminated
VIE. CHRONIC LARYNGITIS

- it occurs if the symptoms last more than 3 weeks; it is more common in males than
females; chronic inflammatory changes frequently involve the laryngeal mucosa,
producing a variety of clinical manifestations.
= ETIOLOGY - is unknown but one or more sources of persistent laryngeal irritation may
be significant in any single case.
*CHRONIC INFECTION - chronic laryngitis may be produced by a chronic inflammatory
focus in the tonsils, pharynx, teeth, gums or paranasal sinuses; the larynx is exposed to
infected material from these sites and gradually develops features of chronic
inflammation.
® Bronchiectasis ® Rhinosinusitis
*VOCAL ABUSE - is an important cause of chronic laryngitis; teachers, salesmen, public
speakers, lawyers, vendors, etc. whose occupations demand a constant use of voice
with strain and tension suffer more from this problem.
*SMOKING - tobacco has harmful effects on the laryngeal mucosa; inhalation of smoke
produces edema and chronic inflammatory changes in the mucosa which eventually lead
to hyperkeratosis and leukoplakia.
*ALCOHOL - produces chronic inflammatory changes in the pharyngeal mucosa and the
nearby laryngeal mucosa gets involved; alcohol drinking is often associated with
smoking and vocal abuse.
eIRRITANT FUMES - chronic irritation of the larynx may result from fumes inhaled in
factories and is likely to produce chronic laryngitis.
*PERSISTENT MOUTH BREATHING SECONDARY TO NASAL OBSTRUCTION - with
resulting inadequate humidification of inspired air causes laryngeal mucosal alterations.
GASTROESOPHAGEAL REFLUX (GERD), LARYNGOPHARYNGEAL REFLUX (LPR)- the
resulting chronic posterior laryngitis is related to reflux of acid into the pharynx and may
occur without the classic symptoms of GERD.
«DRUGS
Theophylline » Diazepam
»%Calcium-channel blockers ® Vasodilators
*LARGE MEALS *CHRONIC ALLERGIES
*DIETARY FACTORS
®» Caffeine ® Alcohol ® Mints
Chocolate »Fats ai
= PATHOPHYSIOLOGY AND PATHOLOGY - chronic laryngitis refers to an inflammatory
process that determines irreversible alterations of the laryngeal mucosa; reactive and
reparative processes of the larynx represent the main pathogenetic factor, which can
persist even when the causative stimulus ends.

36
- depending on the causes, the pattern of changes can be very different; inflammation,
edema, and infiltration and proliferation of the mucosa can represent different levels of
response to insults.
- the inflammatory process damages the ciliated epithelium of the larynx, particularly in
the posterior wall; this impairs the important function of moving the mucous flow out of
the tracheobronchial tree; when the ciliary beating motion of the epithelium is impaired,
the resultant mucous stasis on the posterior wall of the larynx and around the vocal cords
provokes a reactive cough; mucous across the vocal cords may manifest with
laryngospasm.
SIGNIFICANT CHANGES MAY ARISE IN THE VOCAL CORD EPITHELIUM :
eHyperkeratosis «Dyskeratosis *Parakeratosis
*Acanthosis ¢Cellular atypia
- the basic effect of laryngeal irritants is to produce vasodilatation and hyperemia; this
may, in turn, precipitate submucosal hemorrhages, interstitial edema and production of
an inflammatory exudate consisting mainly of mononuclear cells; eventually, the injured
area is invaded by fibroblasts, causing fibrosis and hyalinization with thickening and
deformity of structure; the pathologic changes in the larynx may be diffuse or localized;
most commonly they are localized to the true vocal cord.
- the ciliated respiratory epithelium of the supraglottic areas undergoes squamous
metaplasia; the areas of normal stratified squamous epithelium may show thickening due
to acanthosis, keratosis and parakeratosis.
- glandular structures undergo hypertrophy early in the course of the disease, but later
they may undergo complete atrophy ending in the sicca syndrome.
= CLINICAL MANIFESTAT IONS - these persists for weeks or months.
*HOARSENESS «GLOBUS SENSATION IN THE LARYNX
¢DEEPER VOICE «FEELING OF NEEDING TO CLEAR THE THROAT
¢«DYSPHONIA - hoarse voice which fatigues easily; voice quality and quantity may
fluctuate, although complete recovery never occurs.
*CHRONIC COUGH - is reportedly most marked at night; if gastroesophageal reflux
disease (GERD) is the causative factor, the cough can be described as either dry or
productive of small amounts of mucous, depending on the degree of involvement of the
posterior wall of the larynx.
eSTRIDOR - due to laryngospasm may occur if mucous strands cross the vocal cords.
«DYSPHAGIA AND OTALGIA - are identified when the pharynx is involved because of the
shared innervation between the throat and the pharynx.
*CHRONIC THROAT PAIN - there may be discomfort and a tendency to clear the throat.
DIAGNOSIS - the true vocal cords appear reddened or thickened with rough edges but
mobility is not affected since the changes are primarily mucosal and submucosal.
GERD4ANDUCED POSTERIOR LARYNGITIS
» Flexible endoscopy ® Barium esophagography
<TREATMENT - is often ineffective; voice therapy may be helpful in cases of faulty voi ce
production and referral to a singing teacher is of value to professional or amateur singers.
ELIMINATION OF EXOGENOUS TOXINS (such as tobacco) - is the mainstay of treatment.
¢VOICE REST - can be useful for a few days in case of acute exacerbations.
*CORRECTION OF A DEVIATED NASAL SEPTUM - to restore normal nasal respiration.
*ANTIBIOTICS - are only used when pathogenic bacteria are identified in a smear test
with culture/sensitivity test.
*STEROIDS, SALINE INHALATION, MUCOLYTIC AGENTS - are given for a period of
4 weeks

36
*REGULAR LARYNGOSCOPIC FOLLOW-UP EXAMINATIONS - are advisable in patients

with chronic laryngitis,because of the possibility of dysplasia.
*MICROLARYNGOSCOPY AND BIOPSY - should be performed in all doubtful cases to
detect malignancies early.
*SPEECH THERAPY - for re-educating vocal habits.
GERD-INDUCED POSTERIOR LARYNGIMIS - medical therapy includes dietary and lifestyle
changes with total acid suppression.
HISTAMINE Hz RECEPTOR ANTAGONISTS - cimetidine, ranitidine, famotidine,
nizatidine
®PROTON PUMP INHIBITORS - omeprazole, lansoprazole
IX . NEUROGENIC DISORDERS OF THE LARYNX

= CLINICAL FEATURES - if the symptoms are unilateral, there is squealing or a weak cry;
bilateral lesions cause inspiratory stridor.
=PATHOGENESIS - some cases are idiopathic, while some are due to congenital or
cardiovascular anomalies, or stretching of the neck during birth; dysphonia can appear
as the first sign of neurogenic disease while the other speech symptoms like dysarthria
may only become evident as the disease progresses; caution should be used in the
treatment of neurogenic voice symptoms until it can be assured that the laryngeal
disorder is focal and not part of a progressive neurodegeneartive disease.
= DIAGNOSIS - fiberoptic laryngopharyngoscopy or direct laryngoscopy, showing one or
both. vocal cords.
= CATEGORIES
*CONSISTENT NEUROGENIC VOICE DISORDERS - are characterized by constant vocal
quality, loudness or pitch deviations during speech and sustained vowels.
*SPASTIC DYSARTHRIA, INCLUDING DYSPHONIA - associated with upper motor neuron
disease involving the corticobulbar tracts.
*RHYTHMICALLY FLUCTUATING NEUROGENIC VOICE DISORDERS - include palate-
pharyngolaryngeal myoclonus and essential voice tremor.
*NONRHYTHMICALLY FLUCTUATING NEUROGENIC VOICE DISORDERS - are most
common; these are characterized by unpredictable, irregular variations in quality,
loudness and pitch in speech.
*NEUROGENIC VOICE DISORDERS - associated with loss of volitional control of voice
production, including apraxia of phonation, respiration or speech and akinetic mutism,
usually follow a cerebrovascular accident or cortical injury.
eFLUCTUATING VOCAL FOLD PARALYSIS - can occur in myasthenia gravis mimicking a
vocal fold paralysis.
=PARKINSON'S DISEASE - reduced loudness and breathy vocal quality, referred to as
hypophonia, are the hallmark of voice disorders in early Parkinson's disease; an essential
quality is a voice quality that fades into breathlessness in contextual speech.
- in later stages of the disease, the patient may be unable to produce phonation even with
instruction; in advanced disease, severe "on-off" drug related phenomena may occur,
during which patients may experienced breathy voice followed by periods of propulsive
speech with strained quality.
= PROGRESSIVE SUPRANUCLEAR PALSY - patients may have voice symptoms similar to those
in parkinsonism, with the possible exception of vocal tremor; dysphagia is a major
problem for these patients; hypophonia is present, with unilaterally reduced vocal range
and speed of movement; the associated dysarthria may include palilalia (uncontrolled
syllable repetition) and oral motor rigidity.

37
X. VOCAL CORD PARALYSIS

- it may result from lesions at the CNS or the main trunk of the vagus nerve and its two
laryngeal branches - inferior or recurrent laryngeal nerve and superior laryngeal nerve;
paralysis of one or both vocal cords may compromise breathing, swallowing and voicing.
- vocal cord paresis or paralysis can be unilateral or bilateral; when the vocal cords do
not move normally, it can result in a weak, breathy hoarse voice, and airway compromise
leading to reduced airway protection; vocal cord immobility is a physical finding and not
a diagnosis; it is important to determine the cause of the immobility, if able; with bilateral
vocal fold paralysis, the majority of the time, it is caused by surgical injury.
THEORIES
*SEMON AND ROSENBACK HYPOTHESIS - was used to explain the sequence of
paralytic conditions of the vocal cord; it stated that in the course ofa gradually advancing
organic lesion of the recurrent laryngeal nerve, abductor fibers are more vulnerable to
damage so the vocal cords approximate near the midline, the adduction is still possible
and it is only in the late stages that the adductor fibers get involved and the cords are
paralyzed in the intermediate position and the reverse happens during recovery.
- in a progressive lesion of the recurrent laryngeal nerve, the abductors are paralysed
before the adductors; in incomplete paralysis, the cord will be brought to the midline by
the adductors, but in complete paralysis it falls away to the paramedian position.
*WAGNER AND GROSSMAN THEORY - they postulated that median or paramedian
position of the paralyzed vocal cord in recurrent laryngeal nerve paralysis is due to intact
function of the cricothyroid muscle, which is innervated by the superior laryngeal nerve;
the intermediate position of the vocal cord is because of combined paralysis of the
recurrent laryngeal nerve and the superior laryngeal nerve, as now the cricothyroid
muscle also gets paralyzed.
= ETIOLOGY OF VOCAL CORD PARALYSIS IN ADULTS

TYPE OF PARALYSIS ETIOLOGY
UNILATERAL RECURRENT LARYNGEAL | Neoplasia, iatrogenic causes, trauma,
aneurysms
BILATERAL RECURRENT LARYNGEAL | Post-thyroid surgery, thyroid neoplasia
UNILATERAL VAGAL latrogenic causes, neurological cause, brain
stem infarction, neoplasia,
skull base osteomyelitis, idiopathic causes
BILATERAL VAGAL Neurological causes
= VOCAL CORD POSITIONS - it is not possible to predict the final position of the vocal cords
after damage to the superior and recurrent laryngeal nerves, as the nerves may recover
or partially preserve function; vice versa, the extent of neural injury cannot be deduced
from the position of the paralyze vocal cord.
os

38
POSITION VOCAL CORD OPENING

MEDIAN Both cords in midline - such as in phonation; it may occur in
recurrent laryngeal nerve (RLN) paralysis.
PARAMEDIAN 3-5 mm - such as in strong whisper; it may occur in RLN with
posterior cricoarytenoid paralysis.
INTERMEDIATE | 7 mm - this is the neutral position of the cricoarytenoid joint;
abduction and adduction take place from this position; it is most
often seen when the vagus nerve, including the superior and
inferior laryngeal nerves, are completely paralyzed, thus affecting
all of the internal and external laryngeal muscles.
SLIGHT 14 mm - such as during quiet respiration and paralysis of adductors.
ABDUCTION
FULL 18-19 mm - such as in deep inspiration.
ABDUCTION
= CAUSES OF LARYNGEAL PARALYSIS

*SUPRANUCLEAR (RARE) «NUCLEAR
*VAGAL *NEUROPATHIES
*NEUROMUSCULAR «MUSCULAR
*SUPERIOR LARYNGEAL *RECURRENT LARYNGEAL
CLINICAL MANIFESTATIONS - sudden interruption of the sensory supply to the larynx may
cause difficulty with deglutition and aspiration; when paralysis is unilateral, symptoms
are minimal and compensation is rapid; more difficulty may be encountered with bilateral
sensory paralysis, but complete compensation eventually develops.
SUPERIOR UNILATERAL BILATERAL COMPLETE

LARYNGEAL RECURRENT RECURRENT NERVE | PARALYSIS
NERVE NERVE PARALYSIS
PARALYSIS PARALYSIS
PATHOLOGY | Paralysis of Paralysis of all Paralysis of all Vagus nerve
cricothyroid intrinsic intrinsic muscles | lesion above the
muscle; muscles superior
Sensory loss laryngeal nerve
in half of may be
pharynx unilateral ot
bilateral
EFFECT Loss of pitch; | Hoarse; Good voice; Similar to
Aspiration Good airway; Poor airway corresponding
Breathy voice; especially on lesions of
Poor cough exertion RLN
paralysis;
More likely to
aSpirate

39
Anterior Cord in Vocal cords Cord(s) are

commissure paramedian do not move immobile but
looks tilted position; laterally in intermediate
to the side No lateral position due
of lesion; motion to loss of
Arytenoid on adduction
that side tilts in by cricothyroid
muscle
A. UNILATERAL SUPERIOR LARYNGEAL NERVE PARALYSIS - isolated lesions of

the superior laryngeal nerves are rare; they may result from injury to the main nerve
trunk or either of the terminal branches; they cause paralysis of the cricothyroid muscle
and ipsilateral anesthesia of the supraglottic larynx; laryngeal anesthesia and
paresthesia occur on the same side as the lesion.
ETIOLOGY - the involvement of the external laryngeal nerve (branch of superior laryngeal
nerve) in cases of thyroid surgery, tumors, neuritis or diphtheria cause cricothyroid
paralysis.
SURGICAL TRAUMA - is the most common cause of nerve injury below the nodose ganglion
and the most frequent injury is damage to the motor branch during thyroidectomy.
= CLINICAL FEATURES
*Askew position of the glottis
¢Shortening of vocal cord with loss of tension (wavy appearance of paralyzed vocal cord)
¢Flapping of paralyzed vocal cord (sags down during inspiration and bulges up during
expiration)
*TEMPORARY DIFFICULTY WITH ASPIRATION AND CHOKING SPELLS - because of the
laryngeal anesthesia particularly on drinking fluids; unilateral anesthesia of the larynx
may pass unnoticed.
*ALTERATIONS OF VOICE - are the main complaint of the patient; the patient has some
vocal weakness because of paralysis of the cricothyroid muscle; rapid compensation
occurs when the paralysis is unilateral but appears more slowly with bilateral paralysis;
the voice is weak, low-pitched, lacks resonance and becomes a monotone; raising the
pitch of the voice is almost impossible and air wasting causes a shortened phonation
time.
- the symptoms are explained by the lack of cord tension which allows the cord to balloon
superiorly during phonation, preventing effective glottic closure and producing a drop in
voice pitch which is especially noticeable in females; there may be some spontaneous
improvement of symptoms with time, but generally, they are persistent.
=DIAGNOSIS - indirect examination reveals an oblique glottis and deviation of the
posterior commissure to the sides of paralysis; there may be a level difference of the
cords as the affected cord lacks tension, because of cricothyroid paralysis; isolated
paralysis of one cricothyroid muscle presents a distinct picture when viewed by indirect
or direct laryngoscopy.
-the patient must be asked to phonate since the muscle is active only at this time; the
vocal cord on the paralyzed side appears béwed, short and bulky due to the unopposed
action of the thyroarytenoid muscle.
- the intact thyroarytenoid tends to pull the arytenoid forward and increase the
prominence of the tip of the vocal process on the side of paralysis; the vocal cord is

yf ta
40
usually at a lower level than that on the normal side due to the tilting of the cricoid and
to displacement of the hypotonic cord by inspiratory air currents.
- when the sensory branch is involved, anesthesia of the hemilarynx may be
demonstrated by palpation; the involved hemilarynx may appear injected secondary to
vasodilatation resulting from loss of sympathetic nerve supply, but simultaneous
destruction of the superior laryngeal artery prevents hyperemia.
- these physical findings are less marked or absent when superior laryngeal paralysis
is bilateral.
TREATMENT- correction of the vocal abnormalities is the main aim of therapy; however,
unlike unilateral paralysis of the recurrent nerve which may be compensated for by
overaction of the opposite vocal cord, the symptoms of unilateral cricothyroid paralysis
are made worse by overaction of the functioning cricothyroid muscle; therefore, voice
therapy is of no avail in these cases and may make the symptoms worse; a surgical
procedure to narrow the cricothyroid space may be of benefit if symptomatology is
severe; as a rule, no therapy is necessary once the situation is explained to the patient;
most patients will have a voice satisfactory for everyday needs and only a few demanding
improvement in voice will require surgery.
B. BILATERAL SUPERIOR LARYNGEAL NERVE PARALYSIS - uncommon condition,
both side cricothryroid muscles get paralyzed along with anesthesia of epilarynx.
= ETIOLOGY
¢Surgical or accidental trauma
¢Neuritis (mostly diphtherial)
«Pressure by enlarged cervical nodes or neoplasms
= CLINICAL FEATURES
Coughing and choking fits during swallowing
¢Weak and husky voice
«Inhalation of food and pharyngeal secretions
= TREATMENT
«Chronic and repeated aspiration needs management
*Neuritis cases may recover spontaneously
«Esophageal feeding tube
*EPIGLOTTOPEXY- (a reversible procedure) closes the laryngeal inlet and protects the
lungs from repeated aspiration.
C. UNILATERAL RECURRENT LARYNGEAL NERVE DARALYSIS - leads to ipsilateral
paralysis of all the intrinsic laryngeal muscles except the cricothyroid, which is supplied
by the external branch of the superior laryngeal nerve; the vocal cord may assume a
median or paramedian position and does not move laterally (abduction) on deep
inspiration.
- all internal laryngeal muscles are paralyzed on the affected side; if the external
cricothyroid muscle supplied by the external branch of thr superior laryngeal nerve is
still active, it stretches the paralyzed vocal cord and forces it into the paramedian
position; in incomplete paralysis of the adductors, the paresis of the single abductor of
the vocal folds is functionally predominant.
- it is usually associated with impaired abduction of the vocal cord or immobility in a
paramedian position; it results in immediate hoarseness and breathiness of voice;
inadequate glottis closure produces a breathy and rough voice with a weak cough
resulting from a failure of the mobile vocal fold to approximate the paralyzed fold during
adduction.

41
- it is most often of traumatic origin but may be a result of a toxic or infectious process;
unilateral left vocal cord paralysis is most common; fewer than 20% of cases are bilateral;
the left recurrent laryngeal nerve has a long course, extending down into the chest before
recurring around the arch of the aorta to return to the larynx; it is therefore more
susceptible to disease than the shorter right recurrent nerve
= ETIOLOGY
*CAUSES OF LEFT RECURRENT NERVE PARALYSIS IN THE CHEST
®» BRONCHOGENIC CARCINOMA - is a common cause; it leads to RLN paralysis.
» Carcinoma of the esophagus ® Malignant mediastinal nodes
» Cardiac and esophageal surgery Aortic aneurysm
*CAUSES OF PARALYSIS OF THE RIGHT OR LEFT RECURRENT NERVE IN THE NECK
®Thyroid surgery ® Carcinoma of the thyroid gland
Cervical spine surgery » Mediastinoscopy
» Penetrating wounds » Viral
® Carcinoma of the hypopharynx and esophagus
= CLINICAL FEATURES - often noted incidentally, the symptoms include moderate to severe
dysphonia in the acute phase; the voice may gradually improve due to compensation;
there is no appreciable respiratory obstruction except during severe physical activity; the
patients cannot sing high notes or raise his voice; about 1/3 of the patients remain
asymptomatic; no problems of aspiration or airway obstruction occur.
-at the onset, the patient usually experiences a severe voice disturbance which may
include temporary aphonia due to the intermediate position of the newly paralyzed cord
and lack of compensatory function by the normal cord.
- over a period of time, varying from weeks to months, the paralyzed vocal cord moves
to a paramedian or median position and the normal cord begins to compensate so that
the symptoms improve and the patient is misled into thinking the condition is regressing
spontaneously.
DIAGNOSIS - laryngoscopy shows an immobile vocal cord in the paramedian,
intermediate, or lateral position on one side; a careful search must be made for an
etiologic factor; thorough laryngologic, phoniatric, neurologic, and radiologic
examination are indicated in order to identify the cause; examination should include a
chest x-ray and x-ray of the skull and jugular foramen; blood tests should include CBC,
ESR, serology and blood sugar level; direct laryngoscopy is not usually indicated in a
case of recent acute paralysis but only in paralysis of many years duration.
PROGNOSIS - many patients with acute paralysis eventually have complete recovery
of function especially in those of inflammatory origin or of unknown etiology.
- in paralysis of traumatic origin, particularly following surgical trauma, the chances of
recovery are variable; paralysis associated with crushing laryngeal injuries is usually
permanent; evidence of spontaneous returning of function is usually present within 3
months after the onset of paralysis if function has not returned within 6 months, recovery
is unlikely.
MEDICAL TREATMENT - is indicated if the onset of the paresis has been acute.
*FOR VOICE IMPROVEMENT
™VOICE REST - is indicated forsome days «=
® ORAL STEROIDS
®NSAIDs
® ANTIVIRALS OR ANTIBIOTICS - if infection is suspected.
VOICE THERAPY - should be begun early as it will enhance compensation, especially
in patients in whom the paralysis is eventually permanent; if treatment of the causal

Dereeod
42
disease does not restore vocal cord mobility, the patient is given voice therapy to achieve
glottal closure by activating the remaining neuromuscular units on the paralytic side and
stimulating the mobile vocal cord on the other side; voice rehabilitation usually restores
vocal function within 2 to 3 months.
SURGICAL TREATMENT - for unilateral vocal cord palsy of a cause compatible with
survival, the operation of vocal cord medialization is available; a window is cut in the
thyroid cartilage and a block of silastic inserted to displace the cord towards the midline;
it has the advantage of being reversible if the cord palsy should recover.
- functional aphonia is usually self-limiting, or responds to explanation and
encouragement; the help of the speech therapist is valuable in persistent cases and some
patients may require psychiatric treatment.
*INDICATIONS FOR EARLY SURGICAL PROCEDURES
Paralysis secondary to minor neck trauma and a dislocation of the joint or a fracture
through the inferior thyroid cornu can be demonstrated
™When paralysis is immediately evident in a postoperative surgical patient and the
integrity of the nerve is unproven, exploration of the wound is indicated to remove any
ties which may be impinging on the nerve.
- when paralysis has been present 3-4 months, the chances of spontaneous recovery are
small and maximum compensation has usually occurred.
eSURGICAL INDICATIONS IN PROLONGED PARALYSIS ms
™When paralysis may have been due to a laxation or dislocation of the cricothyroid joint,
decompression of the laryngeal nerve should be done before 4 months.
®When paralysis is due to a lethal lesion, such as ca of the lung, and severe dysphonia
and aspiration occur because of glottic incompetence
When the problem of aspiration is severe and persistent, surgical repair of the glottic
function is indicated regardless of etiology.
D. BILDATERAL RECURRENT LARYNGEAL NERVE PARALYSIS - frequently leads to
functional glottis stenosis with the vocal folds in a fixed paramedian position; it is usually
of acute onset since the most frequent causes are trauma or acute neuritis; because the
cords lie near the midline, the airway is impc\caired and tracheostomy may be necessary.
ETIOLOGY- the most common causes are neuritis and thryroidectomy which is the most
common cause of bilateral vocal cord paralysis; commonly following surgery or
malignancy of the thyroid gland, but may be the result of pseudobulbar palsy
© CLINICAL FEATURES - the condition is often acute; the most common symptoms are
dyspnea and stridor which become worse on exertion or infection; they occur due to the
median or paramedian positions (due to unopposed action of cricothyroid muscles).
*DYSPNEA AND A DANGER OF ASPHYXIA - due to narrowing of the glottal chink.
Inspiratory stridor is noted during physical activity, sleep or when talking.
*DYSPHONIA - is present initially and lasts for a variable period - between 4-8 weeks,
depending on the cause, and with a weak and hoarse voice thereafter. Speech is
interrupted by long inspiratory phases.
*FEEBLE COUGHING
- the predominant symptom is airway compromise; this can range from unnoticeable to
mild dyspnea, inspiratory stridor and respiratory distress, even without exertion. Acute
airway obstruction resulting from bilateral vocal cord immobility (e.g. following
thyroidectomy) sometimes requires reintubation or tracheotomy.
- bilateral vocal cord paralysis is a potentially life-threatening condition that frequently
requires some kind of surgical intervention to prevent acute asphyxiation or pulmonary
consequences of chronic central airway obstruction; in contrast to unilateral vocal cord

43
paralysis, voice quality is not the primary concern in these patients; voice quality is
usually only mildly affected (if just the recurrent laryngeal nerves are involved.)
- a patient who presents with a bilateral recurrent laryngeal nerve palsy usually does so
in an emergency situation, following the development of stridor; the patient may have
been well previously, with an apparently normal voice, but developed airway
decompensation following an upper respiratory tract infection; because the vocal cords
are adducted, minimal swelling may precipitate stridor.
- initially, the vocal cords lie in a paramedian or intermediate position producing
symptoms ofa severe dysphonia with adequate airway; overa period of time, the vocal
cords gradually move toward the midline with a resulting improvement in voice and
increasing dyspnea; dyspnea and inspiratory stridor are made much worse by exertion;
acute laryngeal obstruction may occur in later stages when an URI is superimposed on
laryngeal paralysis.
= DIAGNOSIS - examination will disclose bilateral immobility of the vocal cords; cordal
position will vary with the length of time from the onset of paralysis; in cases of paralysis
of long duration, the only airway may be an elliptical slit between the membranous vocal
cords which widens on aspiration; in bilateral paralysis, the vocal cords are usually in
the paramedian position.
DIRECT LARYNGOSCOPY - is indicated to establish mobility of the cricoarytenoid joints for
prognostic purposes.
«PROGNOSIS - spontaneous recovery of function of one or both vocal cords is possible
in many cases of non-traumatic origin; spontaneous recovery is less likely after surgical
trauma or severe neck injuries; most patients with a bilateral paralysis will eventually
progress to a symptomatic stage of glottic obstruction unless one vocal cord recovers
the time required forthe appearance of severe dyspnea due to bilateral median
position may vary from a few days to 20 years.
< TREATMENT - will vary depending on the symptomatology, but it is mainly directed at
relief of dyspnea; patient is treated with either permanent tracheostomy with a speaking
valve or lateralization of the cord; many patients need emergency tracheostomy when
they suffer from URTI.
- relief of dyspnea will eventually necessitate a tracheostomy as an initial procedure;
further therapy will depend on the duration of the paralysis and the mobility of the
cricoarytenoid joints and the possibility of recovery.
*TRACHEOSTOMY - relieves stridor and preserves voice but it needs regular care;
tracheostomy and a cannula with a speaking valve are required only if dyspnea is severe;
many patients manage to stay without a tracheostomy by avoiding exertion as the
dyspnea is tolerable as long as they are at rest.
*LATERALIZATION OF THE CORD - vocal cord is moved and fixed in a lateral position;
though patient does not have tracheostomy but it is at the expense of a good voice.
*FOR AIRWAY IMPROVEMENT
®NASOTRACHEAL INTUBATION - for acute airway distress.
® HIGH DOSE INTRAVENOUS STEROIDS - are used in the early phase of the disease
NSAIDs
® ANTIVIRALS OR ANTIBIOTICS - if infection'is suspected.
MILD PHYSICAL TRAINING - once the patient has adjusted to the glottis narrowing.
*FOR DEGLUTITION DISORDERS
® FEEDING VIA NGT OR PEG
® MODIFICATIONS IN FOOD CONSISTENCY AND VISCOSITY
POSTURAL MANEUVERS - to modify the flow of the bolus.

® MODIFICATIONS IN VOLUME AND TEMPO OF FOOD PRESENTATION
™» SUPRAGLOTTIC SWALLOW
» EXERCISES TO INCREASE MUSCLE TONE AND TO IMPROVE COORDINATION
sINDICATIONS FOR GLOTTIS WIDENING SURGERY
»A lack of exercise tolerance
The potential risk to the patient from sporadic respiratory inflammations that may cause
swelling of the already tight glottis.
TREATMENT FOR PATIENTS WITH PERSISTENT BILATERAL PARALYSIS AND AN INADEQUATE
AIRWAY
eA PERMANENT TRACHEOSTOMY
Patients with a lethal disease » Elderly
™»Debilated patients who are unlikely to tolerate the necessarily incompetent glottis
produced by surgical correction.
eA PERMANENT TRACHEOSTOMY USING A VALVED TUBE
®Patients who require continued use of a good voice
Patients refusing surgery
™As a temporary measure, when recovery may still be anticipated
*NEUROLYSIS OF AN EXTERNAL LARYNGEAL NERVE - by dividing this nerve, it is
hoped that a cord in the median position will move laterally to the intermediate position
since opening of the glottis to this position is a passive movement. ;
*SURGICAL WIDENING OF THE GLOTTIS
™®The paralysis is 6-8 months old and no recovery is evident
The cause of paralysis leaves little possibility of recovery
®The cricoarytenoid joints are fixed
Temporary paralysis of a cricoarytenoid muscle does not produce an adequate airway
XE. LARYNGEAL TRAUMA

ETIOLOGY
*EXTRINSIC INJURIES
®AUTO ACCIDENTS - most frequent cause of injury
®Strangulation Other blunt injuries neck
*BURNS OF THE LARYNX
THERMAL
sIngestion of hot food or liquid Inhalation of hot air or gas
> CHEMICAL
sLye =Ammonia
=Sodium hypochlorite (Clorox) =Orthophenylphenol (Lysol)
*AUTOGENOUS TRAUMA - voice abuse
*IATROGENIC CAUSES
® Prolonged endotracheal intubation ® Laryngotomy
Inappropriate tracheotomy » Cricothyrotomy
Endoscopic procedures ®» Indwelling NGTS
*IRRADIATION INJURY
*FOREIGN BODIES ie
PATHOPHYSIOLOGY OF ACUTE LARYNGEAL INJURY - the distensibility of the submuco
sal
tissue of the larynx, particularly in the supraglottic portions, permits
the rapid
accumulation of fluid or blood; therefore, laryngeal edema or hematoma typically involve
the aryepiglottic folds and false vocal cords; since fluid or blood accumulation may be
rapid, symptoms of laryngeal obstruction may appear abruptly.

45
-the mucosal lining of the larynx and pharynx is easily torn by traumatic forces and
this may be followed by the rapid appearance of subcutaneous emphysema; healing of
laryngeal injuries is by granulation and eventual fibrosis.
- since the wounds are usually secondarily infected, epithelialization is often delayed
with the result that excessive granulation and fibrous tissue are laid down; Cicatrization
is followed by deformity and considerable permanent alteration in laryngeal function and
patency may develop secondary to relatively minor injuries.
= PATHOGENESIS
*EXTERNAL LARYNGEAL TRAUMA - blunt trauma occurs because of motor vehicle or
recreational accidents, assaults (including domestic violence), or strangulation; although
the neck is shielded from compressive injuries by the sternum and the mandible, injuries
can be substantial.
*PENETRATING NECK TRAUMA - usually results from stabbings or gunshot wounds; the
severity of a penetrating injury is determined by the mass and velocity of the missile; up
to 30% of patients will have multiple structures injured.
*INTUBATION INJURY - due to sophisticated ICUs, critically ill patients are being
sustained longer on ventilatory support with the potential long-term consequences of
affected speech and airway patency; complication rates of 4-19% have been reported
following prolonged intubation; therefore, converting an intubated patient to a
tracheotomy is often contemplated after 5-7 days.
- many factors determine the severity of intubation injury; anatomic variations predispose
some patients to a difficult or traumatic intubation; underlying illness, infection, and
reflux laryngitis may contribute to the injury.
- large diameter endotracheal tubes, excessive movement, over-inflated endotracheal
tube cuffs, and prolonged intubation increase the risk of damage; however, glottic edema
and superficial ulceration may be seen within just hours of intubation; the introduction
of high-volume, low-pressure systems and the frequent monitoring and maintenance of
cuff pressures below 20 mm Hg help to prevent this type of injury.
ACUTE INTUBATION INJURY - immediately or shortly after removal of the tube, patients
develop dysphonia, attacks of coughing, and hemoptysis; tthese factors lead to
myogenic or neurolgic paralysis; drying of the mucosa by the premedication can
exacerbate the mucosal injury; laryngeal complications can be expected after less than
48 hours of intubation in adults and after 3-7 days in young children, who tend to develop
subglottic mucosal injuries.
®DIAGNOSIS - laryngoscopy shows a subepithelial hematoma, superficial and deep
mucosal injuries, and rarely torn epithelium at the vocal fold or subluxation of the
arytenoid cartilage. Intubation granulomas are usually bilateral and located on the vocal
process.
TREATMENT - a hematoma or superficial mucosal or epithelial lesion can heal
spontaneously; subluxation of the arytenoid cartilage, which is usually connected with
paresis of the inferior larynheal nerve may require surgery.
CHRONIC INTUBATION INJURY - dysphonia or laryngeal dyspnea develop 2-8 weeks after
intubation anesthesia or prolonged intubation.
*Increasing airway obstruction with dyspnea and stridor *Cough
*Dysphonia or aphonia eHematemesis
*Neck pain and tenderness *Dysphagia
*Loss of the anterior thyroid prominence *Bony crepitus
*Subcutaneous emphysema eHemoptysis

46
eTenderness to palpation *Odynophagia

«Saliva leaking from an open wound *Bruising of the anterior neck
¢Deformities of the neck including alterations in contour and swelling
=DIAGNOSIS - the presence of any of the preceding clinical manifestations is a basis for
assuming a severe injury and is an indication for indirect and direct laryngoscopy and
bronchoscopy to determine the presence of edema, hematoma, mucosal tears, cartilage
displacement and vocal cord paralysis.
*CONVENTIONAL FILMS
Plain film x-rays of the chest » Soft-tissue neck films
- they must be obtained to detect
=Laryngeal fractures ®Tracheal injuries
"PNEUMOTHORAX - any abnormal air surrounding the trachea, mediastinum, or thorax
may be the first sign of impending tension pneumothorax and airway embarrassment.
*FIBEROPTIC NASOPHARYNGOSCOPY - is well-tolerated in a patient who is awake and
is a quick diagnostic test that allows a complete upper airway laryngeal evaluation; the
larynx should be evaluated carefully for vocal cord mobility and arytenoid symmetry.
*COMPUTERIZED TOMOGRAPHY (CT SCAN) - is the best radiographic tool available to
evaluate laryngeal trauma especially when the examination isi normal but there is a high
index of suspicion for occult laryngeal injury; it may reveal a subtle fracture that requires
fixation or it may obviate the need for rigid endoscopy if the scanned image is normal.
-it is not mandatory in patients with injuries that obviously require operative intervention
or in asymptomatic patients with an unremarkable physical examination; it may be
valuable in planning the procedure in a patient with a controlled and stable airway.
«RIGID ESOPHAGOSCOPY AND CONTRAST SWALLOW STUDIES - used often to rule out
concomitant esophageal perforation in penetrating trauma; when used together, the
sensitivity of these tests is approximately 90%.
*ANGIOGRAPHY - often used in the diagnostic evaluation of penetrating neck trauma; it
is the gold standard for evaluating vascular injury and is therapeutic when used with
interventional neuroradiology embolization.
= CLASSIFICATION OF LARYNGEAL INJURY
«CLASS | - Minor endolaryngeal hematoma without detectable fracture
*CLASS Il - Edema, hematoma, minor mucosal disruption without exposed cartilage,
nondisplaced fractures noted on computed tomographic scan
*CLASS Ill - Massive edema, mucosal tears, exposed cartilage, cord immobility
*CLASS IV - Class Ill injury with more than 2cm fractures or massive mucosal trauma
*CLASS V - Complete laryngeal separation
TREATMENT
eINITIAL MANAGEMENT
3 STEPS OF INITIAL RESUSCITATION
® SECURING THE AIRWAY - if the airway is compromised, absolute priority must be given
to establish an airway by the least traumatic means; if the airway has not been secured
and the patient is in respiratory distress, tracheostomy is preferable to blind intubation.
- intubation may be performed safely if the vocal cords are easily seen, there are no visible
injuries, and the smallest tube possible is «ised; but it can cause further injury to an
already tenuous airway, resulting in an emergent need for airway control.
- if the airway is stable, the first intervention should be a diagnostic flexible fiberoptic
laryngoscopy (FFL) to evaluate the extent of the intraluminal injury and the adequacy of
the airway; the status of the laryngeal mucosa and any submucosal injuries are noted,

thir
47
including hematomas; if possible, phonatory and respiratory examination is done to

assess arytenoid cartilage range of motion.
- surgical airway control such as a high tracheotomy or a cricothyroidotomy may be
necessary, but it should be converted to a formal tracheotomy as soon as possible to
prevent long-term sequelae (eg, subglottic stenosis).; further treatment depends on the
extent of laryngeal damage.
® OBTAINING HEMODYNAMIC STABILITY WHILE CONTROLLING THE ;ff
» IMMOBILIZING THE CERVICAL SPINE
*KEYS TO A SUCCESSFUL OUTCOME
»Prompt, early intervention
*Limited debridement
® Meticulous wound closure
CLASS | - patients are observed in a monitored setting for at least 24 hours with repeated
flexible fiberoptic examination of the airway every 8 hours; if the airway remains stable,
the patient can be discharged the next day without any further intervention.
CLASS II to CLASS V - are treated surgically.
"MEDICAL MANAGEMENT - is reserved for patients with a stable airway such as those
who present with minor mucosal lacerations, minor nonexpanding hematoma or a single
nondisplaced fracture of the thyroid cartilage with intact overlying mucosa.
® Close observation with continuous pulse oximetry
® Administration of humidified air
®Head of bed elevation over 45°
®Heliox (mixture of helium and 30 to 40% oxygen) can be used as a temporizing
measure while securing the airway.
Early administration of systemic corticosteroids may be advantageous although their
onset of action may take hours
Proton pump inhibitors or high dose Hz blockers can minimize further injury
*INDICATIONS FOR AN OPEN REPAIR OF AN OPEN FRACTURE
® Presence of a comminuted or displaced fracture
® Any fracture of the median and paramedian thyroid cartilage may result in aloss of
the AP dimension of the larynx
® Any injury resulting in vocal cord paralysis, airway compromise requiring intubation
or tracheostomy, or associated with an important injury to other areas of the neck
A. EDEMA AND HEMATOMA - are common to almost all laryngeal injuries; they will
resolve spontaneously and completely in the absence of any other injury.
TREATMENT
*Absolute voice rest *Corticosteroids
eHumidification of inspired air *Temporary tracheostomy
B. LARYNGEAL FRACTURE
1. HYOID BONE - the fracture usually occurs in the central body area because of the
resiliency of the cornua; the injury may occur as an isolated result of neck trauma or
in association with fractures of the other laryngeal cartilages; anisolated fracture is more
common in women.
*Pain and swelling over the upper anterior neck
*Bony crepitus is noted on palpation of the neck and on swallowing
*Grating of the fracture fragments *Odynophagia

48
DIAGNOSIS - the fracture can usually be seen on soft tissue roentgenograms of the
larynx; in indirect and direct laryngoscopic examinations are necessary to rule out an
associated avulsion of the epiglottis.
= TREATMENT
*TRACHEOSTONMY- if airway obstruction is present
*IMMOBILIZATION AND APPROXIMATION OF THE FRACTURE - by direct interosseus
wiring using no. 28 stainless steel wire.
*EXCISION OF THE AREA OF THE FRACTURE - to separate the fragments in cases of
symptomatic non-union.
2. THYROID AND CRICOID CARTILAGES
a. SUPROAGLOTTIC INJURY
= PATHOLOGY - the upper part of one or both thyroid alae is often fractured althoughto
thyroid fracture may be present; the important injury is an avulsion of the attachments
of the epiglottis and one or both false vocal cords from the thyroid cartilage; this allows
posterior displacement of the epiglottis which may obliterate the vestibular lumen.
- occasionally, an associated unilateral or bilateral vocal cord paralysis may be present
at the time of the acute injury; they are associated with contamination and infection and
healing begins with production of granulation tissue and ends with fibrosis and scar
contracture; the epiglottis becomes fixed in a posterior position by scarring and fixation
of the arytenoids may occur secondary to the healing process; the end result in an
untreated injury is supraglottic laryngeal stenosis.
Normal but muffled voice in the face of increasing airway obstruction
*Signs of coughing and aspiration on attempting to eat or swallow liquids
«Appearance of food or liquid at the tracheostomy opening without coughing or choking
is indicative of an extralaryngeal fistula
*Flattening of the upper neck contour and failure to palpate the thyroid notch
*Cervical emphysema *Airway obstruction
= DIAGNOSIS
*DIRECT LARYNGOSCOPY - may demonstrate soft tissue swelling, cartilage
displacement and vocal cord paralysis.
*LARYNGOGRAMS AND CINEFLUOROSCOPY - are often necessary to detect the
presence and site of a sinus or fistula.
b. GLOTTIC INJURIES
= PATHOLOGY - the thyroid cartilage is fractured in the region of attachment of the true
vocal cords; the fractures may be vertical or transverse and frequently there is
displacement of the fragments in their relation to each other; the vocal cords are
displaced or actually disrupted by the cartilage displacement.
- mucosal tears are common; vocal cord paralysis secondary to nerve damage or
disruption of the cricoarytenoid joint may be present primarily; healing in the untreated
case frequently results in glottic Stenosis.
= CLINICAL MANIFESTATIONS ORs
*Subcutaenous emphysema *Marked alteration of voice
*Palpation of the cartilage through the anterior neck = *Laryngeal obstruction
C. INFRAGLOTTIC INJURIES - are seen more frequently in males who have experienced blunt
trauma in an auto accident.
+ PATHOLOGY - there is a crushing injury of the cricoid cartilage and upper tracheal rings;
the anterior part of the cricoid may have one or two simple fractures or may be

ee
49
fragmented; in many cases, the cricoid injury is associated with crushing and separation
of the upper tracheal rings.
- occasionally, the injury is limited to the upper trachea which may be completely avulsed
from its attachment to the cricoid cartilage and retract into the upper mediastinum;
devascularized pieces of cartilage are produced and, as a result, perichondritis of the
cricoid cartilage is a common complication; because of infection, healing is delayed and
excessive granulation and fibrous tissues are produced.
- since the cricoid is a circular cartilage and is at the level of the narrowest point of the
laryngeal lumen, minor injuries frequently cause stenosis if untreated; vocal cord
paralysis, often bilateral, frequently accompanies this injury due to disturbance of the
cricothyroid joints and injury to the recurrent laryngeal nerves.
3. THYROID CARTILAGE FRACTURE - runs in a vertical line from the bottom of the
thyroid notch to the lower border of the cartilage.
*History of a blow to the neck *«Hoarseness
Inspiratory or expiratory stridor or both *Hemoptysis
*Subcutaneous emphysema
TREATMENT OF ACUTE LARYNGEAL FRACTURES
*TRACHEOSTOMY - inserted in the proper place below the second tracheal ring.
*SURGICAL EXPLORATION - is indicated in any neck injury with symptoms of stridor,
voice change, cartilage disruption and cervical emphysema.
*REDUCTION AND IMMOBILIZATION OF THE FRACTURE - must be carried out within
7-10 days to avoid chronic stenosis.
C. TRAUMATIC GRANULOMA OF THE LARYNX
“ETIOLOGY - it is a localized inflammatory response to mucosal loss caused by
endolaryngeal trauma.
*ENDOTRACHEAL INTUBATION - is the most common cause; it occurs most frequently
in women because the endotracheal tube tends to lie more posteriorly in the larynx due
to the size and configuration of the female larynx; the epithelium is also thinner in
females; the use of too large a tube, traumatic intubation and excessive movement of
the vocal cords against the indwelling tube are other etiologic factors.
*EXCESSIVE VOICE ABUSE
*BRONCHOSCOPY
*STRIPPING OF THE VOCAL CORDS
- mucosal loss is followed by ulceration and infection and then by overproduction of
reactive granulation tissue most frequently on the medial surfaces of the vocal processes
because of the increased susceptibility to trauma of the thin mucosa.
PATHOLOGY - the lesion begins as a mucosal ulceration which becomes secondarily
infected; re-epithelialization is prevented by irritation from continued laryngeal
function and infection; granulation tissue is formed but becomes excessive, producing
a sessile polypoid mass; as the lesion matures, epithelialization is completed and fibrosis
occurs, obliterating many vessels and causing the mass to shrink and become
pedunculated; eventually, the lesion may atrophy and disappear completely.
@ CLINICAL MANIFESTATIONS- the granuloma does not usually appear for 3 or more weeks
and is accompanied by: fim
*HOARSENESS - is often present immediately postoperatively and a small ulcer may be
seen on the vocal cords.
*A FEELING OF DISCOMFORT IN THE LARYNX
*EAR PAIN - occasionally

a?
50
- the laryngeal lesion is a dark red, edematous, sessile mass partially covered by exudate;
the mass is usually unilateral and is most frequent in the region of the vocal process; as
the lesion matures, it becomes more pedunculated and assumes a lighter color; the
symptoms tend to fluctuate more and periods of slight hoarseness may be interrupted by
episodes of aphonia when the polyp prolapses between the vocal cords; as time passes,
the mass shrinks in size, becomes pale and fibrotic and may disappear spontaneously.
= TREATMENT
COMPLETE VOICE REST - may result in healing and regression in the early stages.
*SURGICAL REMOVAL -is indicated when the mature pedunculated granuloma is present
and it is usually curative.
*ENDOSCOPIC SURGICAL REMOVAL - using the COz laser.

ENT EMERGENCIES
1. EAR
A. FOREIGN BODIES
of ways,
SIGNS AND SYMPTOMS - ear canal foreign bodies can present in a wide variety
they can be asymptomatic.
eEar pain *Purulent drainage ¢Decreased hearing
*Hyperacusis eItching eForeign body sensation
foreign
ETIOLOGY - most adults with normal mental status know the etiology of the
know
body; young pediatric patients and patients with altered mental status often do not
the etiology of the foreign body to the ear; considerations of what the foreign body of
unknown etiology might be may be elicited by history (ie, retained cotton swab after use
or live insect, particularly if given a history of the sensation of movement from within the
ear).
TREATMENT - an otoscope and a strong light source should be used to identify the
foreign body before any attempts at removal occur; topical anesthesia may be of utility
to assist in the extrication.
- examintion of the ear and removal of the foreign body from the EAC may provoke pain;
the duration of time that the foreign body has been in the ear may contribute to
inflammation, ulceration, and bleeding before any attempt at foreign body removal; it is
important to try to minimize serial examinations and attempts at removing the foreign
body; CT may be helpful if infection or erosion is suspected, particularly if the foreign
body has been present for a prolonged period.
*FOR SUCCESSFUL REMOVAL OF THE FOREIGN BODY
® Minimizing attempts at removal =» Pain management
® Suitable visualization of foreign body Proper equipment
® Cooperative patient » Dexterity
eFOREIGN BODY COMPOSITION AND APPROACH TO REMOVAL - consideration of the
material comprising the foreign body to be removed is important in facilitating successful
removal.
®SOLID, NONCOMPRESSIBLE FOREIGN BODY
=REMOVAL BY FORCEPS - insert the forceps along the periphery of the object between
the object and the EAC or grasp the diameter of the object. Ex. hair beads, toys, button
batteries, food products, and rocks.
BREMOVAL BY CERUMEN LOOP - if the object is small enough, pass the cerumen loop
between the object and the wall of the EAC; use the slightly angled part of the instrument
to get behind the object and pull it out of the ear; this technique may be particularly
useful with smooth or solid objects that are slick or slippery.
BREMOVAL BY FRAZIER SUCTION - connect a Frazier suction to a continuous low
suction and apply directly on to the object; occlude the insufflation port to suction out
the object; the strength of the suction may not be enough to remove the object.
=REMOVAL BY STERILE SWAB STICK WITH MEDICAL GLUE ADHESIVE - this technique
may be particularly useful in the removal of a round object that may be hard to grasp with
forceps; use a very small amount of medical adhesive glue on the back end of the stick
and carefully and gently place it directly on the objec; use great care not to advance the
foreign body farther into the EAC or misdirect the glued end inadvertently to the EAC
itself; after holding the glued end of the swab stick against the solid object for a few
seconds, the adhesive will have dried, which will allow manual removal of the foreign
body at the end of the glued stick and these will now be removed as one unit.

»COMPRESSIBLE FOREIGN BODY -
sREMOVAL BY SUCTION - avoid creating additional debris by inadvertent destruction of
the object during the removal process.
sREMOVAL BY WATER IRRIGATION - fill the syringe with warm water; attach the plastic
to the syringe; insert the angiocath next to or behind the foreign body (if
angiocath
possible); irrigate the ear by emptying the syringe through the angiocath; observe for the
foreign body to become dislodged; it will subsequently exit the canal with irrigation
- avoid this technique with objects that might expand (ie, food products) or button
batteries (to avoid battery current that may induce liquefaction necrosis)
Ex. retained tips of cotton swabs or pieces of paper that have been used in attempts at
cleaning the ear canal.
INSECTS - when a patient complains of “movement” or “fluttering” inside the ear along
with a foreign body sensation, the presence of an insect should be considered; a history
of recent camping activity or poor living conditions may prompt a concern for an insect
within the ear canal; in most cases, the insect is a cockroach
- light-avoiding insects (such as cockroaches) will often be stimulated to move when an
examiner's light is used to examine the ear; this may cause discomfort or provoke anxiety
to the patient.
- first, anesthetize and euthanize the insect; various success rates have been reported
with various used agents; efficacious formulations include lidocaine as a 10% spray or
less concentrated liquid, 2% lidocaine gel, mineral oil with 2% or 4% lidocaine, and
alcohol; given the viscosity of oil and gel, nonviscous agents will aid in maintaining a
good visual field for removal of the insect.
- instill nonviscous lidocaine into the ear and wait several minutes; once inactivity is
noted, proceed on to extraction; the Frazier suction may most efficiently extract the insect
intact and will avoid creating debris that can be caused by manual extraction.
& STYROFOAM - may be dissolved with acetone.
®CYANOACRYLATE GLUE - may be loosened/dissolved with acetone.
= WHEN NOT TO ATTEMPT FOREIGN BODY REMOVAL
*The foreign body is sharp and likely to cause more trauma on an attempt to remove
*Evidence of perforated TM on initial inspection
elmmunocompromised patient with evidence of infection; needs close outpatient follow-
up at minimum.
RISKS ASSOCIATED WITH REMOVAL OF FOREIGN BODIES IN THE EAR
*EAC bleeding *Otitis externa
*Unintentionally lodging the foreign body deeper in the EAC
«Incomplete removal «Perforation of the TM
= UNCOMMON COMPLICATIONS
*Damage to the ossicular chain ¢Sensorineural hearing loss
°Vertigo ¢Facial nerve paralysis «Meningitis
B. AURICULAR HEMATOMA - typically occurs as a sports-related injury, particularly
in wrestlers; simultaneous application of blunt and shearing forces to the pinna results
in disruption of perichondrial attachments to the underlying cartilage with subsequent
accumulation of blood in the subperichondrial space; the separation of cartilage from its
blood supply will lead to resorption or necrosis if left untreated, leaving potentially severe
scarring and a so-called cauliflower deformity.
TREATMENT (
*NEEDLE ASPIRATON
«INCISION AND DRAINAGE

3
*APPLICATION OF A SPLINT OR BOLSTER - no difference has been shown between

various methods of treatment, such as casting or bolstering; however, a recent
publication describes the successful use of mattress sutures in 18 ears with only one
hematoma recurrence.
- whatever the method, the splinting must be secure to ensure complete obliteration of
the subperichondrial space; recurrent hematoma or seroma that fails to respond to
seemingly appropriate evacuation and bolstering can also be treated with wider incision
and drainage followed by packing with thin iodoform gauze, until healing of the pocket
intention has occurred; if this method is used, it is usually possible to
by secondary
place the incision just under the helical rim.
eANTIBIOTIC THERAPY - a fluoroquinolone is prudent for injuries that involve cartilage;
in the ear, the rationale for fluoroquinolone use is related to the presence
of Pseudomonas aeruginosa and the excellent skin and soft tissue penetration with oral
administration rather than to some distinct cartilage-protecting characteristic of the drug.
- contaminated wounds may benefit from at least a single dose of levofloxacin or
ciprofloxacin, although there is no evidence to support a full treatment course in an
uninfected wound.
C. LACERATIONS - the prominent position of the ears over a firm underlying bony
surface leaves them particularly susceptible to lacerations, avulsions, and blunt trauma;
the unique and intricate detail of the ear's cartilaginous skeleton is virtually irreplaceable,
making it a fairly unforgiving structure with regard to revision of an unacceptable scar.
TREATMENT - full-thickness lacerations require accurate reapproximation of the cartilage
to maintain the original orientation, although the cartilage itself does not necessarily need
to be sutured; perichondrial and skin sutures are usually sufficient to close simple and
complex lacerations that involve cartilage; occasionally, anchoring sutures through
cartilage must be placed sparingly to bring wound edges together while maintaining the
original shape and prominence; in older patients, the cartilage is more brittle, and it is
difficult to place sutures solely in the cartilage that do not pull through.
D. AVULSIONS - traumatic loss of auricular tissue can be problematic.
* SMALL SEGMENTS OF DENUDED CARTILAGE - can be reliably covered with split- or
full-thickness skin grafts, as long as perichondrium is still present.
*SMALL OR MODERATELY SIZED COMPLEX OR COMPOSITE DEFECTS - those that
cannot be closed without distorting the ear, especially those that involve the helical rim,
can be dealt with in a staged manner; various techniques for composite grafting and local
flap reconstruction have been described and are performed in a delayed manner after
adequate cleaning, débridement, and local wound care.
*LARGER SEGMENTS OF COMPOSITE DEFECTS -a robust vascular supply frequently
allows partially avulsed auricular segments to survive, even large segments on a
relatively small pedicle.
*NEAR-TOTAL AVULSION INJURIES - replant the avulsed portion, leaving the pedicle
intact; management may then proceed as described earlier for other avulsions; some
debate surrounds the management of total and near-total avulsion injuries as it relates to
the cartilaginous framework of the ear.
®POCKET PRINCIPLE - some authors advocate deepithelialization of the avulsed
segment followed by burial in a postauricular subcutaneous pocket, whereas others
believe that the final result of a reconstructed auricle is more reliable with an autograft
than with banked cartilage, which often resorbs to some degree and is ultimately
distorted.
VARIATION OF THE POCKET PRINCIPLE - involves deepithelialization of only the
posterior aspect of the avulsed segment followed by fenestration of the exposed cartilage

4
at 1-cm intervals; the anterior skin edge of the avulsed segment may then be sutured to
a modest postauricular scalp flap elevated over the mastoid to provide a vascular supply;
the flap should be divided several weeks later, and a skin graft should be applied
posteriorly on the auricle; advocates of this technique cite preservation of the original
cartilaginous framework and overlying skin with reliable results.
- a temporoparietal fascia flap followed by split-thickness skin grafting also serves to
salvage an amputated auricle in an acute setting; in experienced hands, microvascular
replantation of an avulsed segment generally yields the best final outcome, even in cases
of venous insufficiency or inability to perform a venous anastomosis.
LEECH THERAPY AND ANTICOAGULATION PROTOCOLS - are acceptable adjuncts in
these cases and often have favorable results.
D. TRAUMATIC RUPTURE OF THE TYMPANIC MEMBRANE - the physician should
consider the possibility of more substantial injuries beyond the TM; patients with
perforations to the posterosuperior quadrant are at particular risk for fracturing the incus
or stapes; any patient who is vertiginous or dizzy after a traumatic TM perforation should
be explored urgently for the possibility of a traumatic subluxation of the stapes or a
perilymphatic fistula; emergency exploration is important if the inner ear has been
violated and the possibility of a persistent foreign body exists.
= ETIOLOGY
*PICKING THE EAR - secondary to probing with an object such as a cotton bud, metal
applicator, hair pin, needle or match stick while cleaning the ear; cotton bud injuries are
the most common type of direct mechanical trauma.
*EAR IRRIGATION - too forceful irrigation of the ear during removal of impacted cerumen
or foreign bodies.
*CONCUSSION - an explosion or hard slap on the ear can easily tear the tympanic
membrane, often resulting in severe pain and partial deafness; this is particularly
common in water-skiing or diving accidents; explosive blasts can produce more than
200 dB sound pressure level; tinnitus or vertigo may also be present.
*BAROTRAUMA
eSKULL FRACTURE - fractures through the base of the skull can tear the tympanic
membrane.
*HOT SLAG - welders sometimes have a red-hot piece of slag fly into the ear; there is
pain, followed by an infection that is difficult to treat; they carry a high rate of
tympanoplasty failure because of the cauterization effect of the slag injury along with
significant scar tissue that forms along the remaining TM.
SIGNS AND SYMPTOMS
*Sudden deafness, tinnitus or dizziness after the injury
¢Sudden pain *Bleeding
*Dislocation of the ossicles *Vertigo
*EAR DISCHARGE
® SEROPURULENT DISCHARGE - injuries caused by water may become rapidly infected.
™ SEROUS DISCHARGE - is present for a few days following injury if there is no infection.
PHYSICAL EXAMINATION - microscopic examination of the ear should be done within
24 hours after injury.
*INSPECTION OF THE TYMPANIC MEMBRANE AND MIDDLE EAR
*PALPATION OF THE OSSICULAR CHAIN
*MICROSCOPIC FINDINGS fe
Injected tympanic membrane » Ragged or stellate perforation
® Blood clot around or over the site of clearing ®» Hemotympanum

TREATMENT
*ASPIRATION OF BLOOD CLOTS *STERILE IRRIGATION
*LINEAR TEARS - most tears without tissue loss heal spontaneously. 90% of traumatic
perforations heal spontaneously in several days to weeks.
*CHEMICAL CAUTERY - cauterize edges with 10% silver nitrate or 50% trichloroacetic
acid.
eSTELLATE PERFORATION THAT CANNOT BE APPROXIMATED - the TM can be
approximated over a piece of sterile gelfoam placed in the middle ear.
*TYMPANOPLASTY - may be needed for large perforations or when there is poor healing;
cartilage grafting can be a useful tool to help support retracted eardrums; a technique
called fat myringoplasty can be done.
*ANTIBIOTICS - are given when there is an infection of the middle ear.
il. NOSE
A. FOREIGN BODIES - are most commonly seen in children, mentally challenged, and
psychiatric patients; they are most commonly located in or around the floor of the nose
just below the inferior turbinate or immediately anterior to the middle turbinate; if a
history is unable to be obtained, one must pay careful attention to signs and symptoms
exhibited by the patient, which may include unilateral nare obstruction, pain, nasal
discharge, epistaxis, sinus pain, or possibly aspiration of the foreign body if it dislodged
posteriorly from the nose and traveled down the airway without maintaining a high index
of suspicion, a misdiagnosis may occur that could result in sinusitis, inflammation, or
encrustation of the object within the sinus.
- the list of objects that have been reportedly removed from the nose is extensive and
limited seemingly only by the size of the nostril; because most people are right-handed,
most nasal foreign bodies are right-sided.
*FOREIGN BODY COMPOSITION - consideration of the material comprising the foreign
body to be removed will be useful in successfully removing it; objects are usually
inanimate or animate; the most commonly identified inanimate foreign bodies include
rubber erasers, paper wads, pebbles, beads, marbles, beans, safety pins, washers, nuts,
sponges, and chalk.
- myiasis of the nose is common in warm tropical climates of the southwestern United
States and the Far East, including India; the frequency of infestation is primarily related
to the poor hygiene of the inhabitants due to their living conditions; the most common of
all infestations is the fly maggot; “Texas” screwworms are serious pests to humans.
= DIAGNOSTICS - If the foreign body is visualized on physical examination, imaging may
not be necessary
PLAIN FILM X-RAY
® Patient is unable to provide a history
Placement of the object was unwitnessed
»® Suspicion for a button battery foreign body
*CT SCAN - if the foreign body is unable to be directly visualized.
*MRI - caution is advised in consideration of using it if there is any concern that the
foreign body may have a magnetic component; many facial body piercings use magnets,
making this etiology of foreign body even more worrisome for necrosis if tissue is caught
between the magnets or if MRI is used. a
APPROACHES TO REMOVAL - before attempting removal, the patient may benefit from
some combination of restraint, sedation, and pretreatment with vasoconstrictive agents
(eg, nebulized racemic epinephrine) and anesthetic (eg, benzocaine spray).

6
*POSITIVE PRESSURE TECHNIQUES - a quick burst of air into the mouth of the patient
with the unaffected nare occluded may result in spontaneous removal of the object; the
burst of air may be delivered by:
®A bag valve mask with the unaffected nare occluded
Having a breath delivered by a parent to their child as if they were going to give them a
kiss with the unaffected nare occluded; the “kiss” technique’s success rate of nearly
50%; was associated with additional advantages of decreased use of resources (eg, time,
anesthetics).
The patient taking a deep breath then blowing out through the nose with the unaffected
nare occluded
*SUCTION -a Frazier suction catheter to low wall suction may successfully remove an
object that appears to be loose within the nasal cavity or if organic matter is suspected
(to avoid further degradation of the material on removal.
«INSTRUMENTS
ALLIGATOR FORCEPS - may be used in removing solid, nonorganic, inanimate objects;
can be used to grab the object directly.
>A RIGHT-ANGLE BLUNT-TIPPED PROBE - may be used in removing solid, nonorganic,
inanimate objects; it may be able to go around the object and pull it out from the object’s
posterior side.
® PEDIATRIC FOLEY (5F OR 6F) - can be used by placing sterile lubricant or viscous
lidocaine to the distal end of the Foley and inserting it past the object; insufflate the Foley
balloon once it is to the posterior side of the object and then gently pull the Foley
anteriorly, thus pulling the object out of the nose.»
™® SNARE TECHNIQUE - is used to help dislodge an object that may be wedged in the
turbinate, making removal challenging; a 24-gauge wire “snare” loop can be created
using a 10-cm section with both ends in a clamp; this snare can then be inserted into the
nasal aperture and used to dissect a plane between the object and the septum, turbinate,
and nasal floor mucosa to free all sides of the object; use of oxymetazoline (0.05%) nasal
spray and a lidocaine with epinephrine before this will aid in vasoconstriction of the
mucosa and help minimize bleeding.
*MAGNET - this technique can be used for suspected metallic foreign bodies.
*MEDICAL ADHESIVE GLUE - cyanoacrylate tissue glue may be applied to the handle of
a cotton swab then directly applied to a clearly visualized object and held in place for =60
seconds; this will allow time for the glue to adhere to the object and the foreign body can
then be pulled out as the handle of the swab will have affixed itself to the object; great
care must be used so as not to have the glue contact healthy tissue instead of the foreign
body.
RISKS AND COMPLICATIONS
*Bleeding eInfection
*Dislodgement into the airway
- sedation is discouraged because it can increase complications by reducing the gag and
cough reflexes; foreign objects that have been forcefully inserted, have become
encrusted due to prolonged retention in the nasal cavity, or live and mobile animate
foreign bodies (ie, maggots, larvae) pose increased difficulty in removal.
B. EDISTAXIS - patients with nasal hemorrhage are commonly seen in the ER and
account for approximately 1 in 200 visits:“it is the most common otolaryngologic
emergency and affects up to 60% of the population in their lifetime, and 6% require
hospitalization.
- it occurs more frequently in the young (< 10 years) and old (70 to 79 years; males are
slightly more frequently affected than females until the age 50, but after 50 no difference

7
between sexes is reported; after the age of 50, severe epistaxis is more frequent, it usually
presents as a spontaneous unilateral bleeding from a discrete lesion; bilateral epistaxis
is more commonly due to trauma or a posterior source of bleeding; epistaxis from the
interior of the nose may be primary or secondary, spontaneous or induced and be located
posteriorly or anteriorly.
*ANTERIOR EPISTAXIS (90%) - the bleeding source can be visualized in the anterior
site,
portion of the nasopharynx; anterior rhinoscopy usually reveals the bleeding
prominent anterior septal vessels, and ulceration with or without crest.
LOCATION - Kiesselbach’s plexus area
*POSTERIOR EPISTAXIS (10%) - a bleeding source is not directly visible; bleeding
occurs beyond the middle turbinate or at the posterior and superior aspects of the nasal
cavity; blood also usually runs down the back of the throat; endoscopic examination (with
flexible or rigid endoscope) is helpful to attempt to identify the site; this is usually
performed bilaterally after applying decongestion and topical anesthesia.
most
- it can be life-threatening and is more common in patients >40 years of age; itis
disease; posterior bleeds may present with
commonly associated with arteriosclerotic
nausea, hematemesis, anemia, hemoptysis, or melena or may present with sudden
copious bleeding due to involvement of larger vessels.
LOCATION - the vessels most responsible for posterior epistaxis are branches of the
sphenopalatine artery and the anterior ethmoid artery; Woodruff’s plexus is a common
source of posterior bleeds.
*MIXED EPISTAXIS - mixed bleeds can be clinically suspected in patients who have brisk,
bilateral, nontraumatic bleeding that does not abate with anterior packing.
SOURCE OF BLEEDING
*LATERAL NASAL WALL- bleeding is usually seen from the region of the sphenopalatine
artery.
*SEPTUM - bleeding is usually from the anterior region.
=TYPES
*PRIMARY TYPE - no apparent organic pathology; primary causes account for 85% of
episodes and are idiopathic, spontaneous bleeds without any notable precipitant.
CONTRIBUTORY FACTORS
® FEBRILE STATE - vasodilation
» ALLERGIC RHINITIS - mucositis
® SEPTAL DEFLECTION - crusting on the deflected side
HYPERTENSION - increased intravascular pressure
® ARTERIOSCLEROSIS - vascular wall weakness
® DRUGS - particularly in the elderly when taking antiarthritic drugs.
®PREGNANCY - vasodilation
*SECONDARY TYPE - there is a clear and definite organic pathology:
»Trauma »URI ® Foreign bodies
® Malignancy ® Postoperative nose ® Sinus infections
BLOOD DISORDERS - ITTP, leukemia
- ETIOLOGY
*IDIOPATHIC - most common *TRAUMATIC - next most common
IATROGENIC *COAGULOPATHIC *NEOPLASTIC
*DRY NASAL MUCOSA (i.e., low-humidity environment such as in the desert or in a cold
climate where heating is used) - is a common cause of minor nosebleed.
MODERATE NOSEBLEED - is usually caused by nasal trauma.
SEVERE NOSEBLEED - is often a complication ofa medical condition such as a coagulopathy
caused by medications, cancer, or cirrhosis.

- epistaxis due to a general or constitutional factor is much less common etiologically
than those due to local factors; the exposed and unprotected state of the blood vessels
of the nasal mucosa renders them partially liable to rupture and thus hemorrhage; the
septal vessels are not well supported and protected from external insults by muscle
tissue, but rather lie closely adjacent to bone and cartilage, protected only by a thin
mucous membrane; once injured the blood vessel retracts poorly into the scant
submucosa; thus, apparently minor injuries and erosions cause vigorous nasal
hemorrhages.
area or
CHILDREN AND YOUNGER ADULTS - majority of epistaxis occur from Little’s
as to
Kiesselbach’s plexus; this area is exposed to the drying effect of inspiration as well
- for
the multiple small traumata of life; in other instances, the cause may be less obvious
ex. when there is a defect intrinsic in the blood vessel.
but more
ADULTS AND OLDER INDIVIDUALS - the site of bleeding may be located anteriorly
a
often is found to originate in the posterior part of the nose; the cause is usually
spontaneous rupture of a sclerotic vessel; the bleeding is made worse if the patient is
hypertensive.
«LOCAL IRRITATION
®INFECTION - chronic sinusitis, nasal diphtheria
® TRAUMA - is probably the most common cause of epistaxis.
sDIRECT TRAUMA TO THE NOSE WITHOUT FRACTURE - can cause epistaxis by its
shearing effect resulting in mucosal laceration.
=DIRECT TRAUMA TO THE NOSE WITH FRACTURES - causes nosebleeds by mucosal
laceration or arterial laceration due to the sharp, raw bone edges; can have epistaxis
with trauma to the sinuses, orbits, middle ear, and base of skull (can cause epistaxis if
it involves the anterior sphenoid sinus wall because it lacerates the posterior septal
branch of sphenopalatine artery).
BHABITUAL NOSE PICKING - especially in children, causes anterior septal nosebleeds;
chronic irritation of this area causes crusting and excoriation with formation of friable
granulation tissue that bleeds easily on further nose picking.
sSURGICAL PROCEDURES OF THE NOSE AND SINUSES - such as septoplasty,
rhinoplasty, turbinate and sinus surgery, as well as orbital floor procedures can cause
epistaxis usually from the mucosal incisions, but less frequently as a result of
complications such as transection of vessels and septal perforations.
=NOSE BLOWING
*ANATOMIC OR STRUCTURAL DEFORMITIES
®SEPTAL SPURS AND DEVIATIONS - involving the cartilaginous or bony septum, either
congenital or acquired, can cause epistaxis by interrupting the normal airflow pattern
inside the nasal cavity; eddy currents are produced that dry the adjacent nasal mucosa
and cause crusting; removal of the crust by a finger or by excessive nose blowing may
stimulate a bleed; if the removal of the crusts becomes habitual, continuous trauma may
cause a septal ulcer to form; this can result in a reduction of blood supply to that area of
septal cartilage and may result in a septal perforation, which can make bleeding more
regular; they disrupt the normal nasal airflow, leading to dryness and epistaxis.
=» SEPTAL PERFORATIONS DUE TO VARIOUS CAUSES - granulation and crusting occur
on the margins of the perforations which bleed easily; the mucus on the posterior edge
of the perforation dries and forms a crust and if it is removed or falls off, the underlying
raw mucosa is prone to bleed creating a further crust/blood clot.
=Septal surgery ®Nose picking =Trauma
"Granulomatous disease =Non-medical use of cocaine
eINFLAMMATORY CONDITIONS - usually manifest as congestion and blood-streaked

9
mucus, but can develop frank epistaxis; various local inflammatory reactions can alter
the normal mucosa, causing dryness and crusting, which allows introduction of bacteria
and subsequent formation of granulation tissue; increased vascularity and greater
friability of the vessels are characteristic of inflamed tissue; these inflammatory
conditions can lead to crusting and friable mucosa.
» URI » Allergic rhinitis » Low environmental humidity
» Sinusitis ® Nasal polyposis ®Vasomotor rhinitis
® Environmental irritants » Toxic chemicals
® Sarcoidosis ™»Wegener’s granulomatosis
- patients with recurrent epistaxis may have fibrinolytically active bacteria in the nasal
area
*FOREIGN BODIES - usually lodged in children, mentally retarded, and elderly
institutionalized patients; should be suspected with unilateral foul discharge; foreign
bodies that cause bleeding usually have
* Sharp edges Porosity » Irritating chemical properties
- bleeding occurs from the inflamed mucosa and granulation tissue around the foreign
body; intra-nasal parasites, including leeches, can lodge in the nose or nasopharynx and
cause epistaxis.
*TUMORS - benign and malignant tumors in the nasal cavities, nasopharynx, and sinuses
can present with epistaxis; cause bleeding indirectly from erosion into normal sino-nasal
structures or directly from tumors of high vascularity (i.e. hemangioma); bleeding usually
unilateral and can be intermittent or constant.
® Nasal polyps »Nasal hemangioma ® Nasopharyngeal carcnoms
®Inverted papilloma Squamous cellcarcinoma ™Melanoma
Adenocarcinoma *®E€Esthesioneuroblastoma ®Hemangiopericytoma
=» JUVENILE NASOPHARYNGEAL ANGIOFIBROMA - should be considered when a male
adolescent presents with nasal obstruction, epistaxis, and a nasal or nasopharyngeal
mass; it can cause severe spontaneous epistaxis.
eANEURYSMS - of the extradural or cavernous sinus portion of the internal carotid artery
can cause life-threatening epistaxis; often a history of cranial surgery or head trauma
with sudden onset unilateral blindness and cranial nerve deficits (anosmia and
involvement of CN II-VI); due to the inaccessibility of this area, often treated with arterial
embolization.
*MUCOSITIS - is the most common cause in children.
*SYSTEMIC DISORDERS
®»HYPERTENSION-ARTERIOSCLEROSIS - is the most common cause in adults.
® ACUTE INFECTIONS
®Influenzae Measles =Whooping cough
®Scarlet fever =Rheumatic fever =Typhoid fever
=Pneumonia =Erysipelas =Dengue =Malaria
*BLEEDING DISORDERS
™ Osler-Weber-Rendu disease ® Acute and chronic leukemia
Idiopathic thrombocytopenic purpura ® Aspirin overdose
Acute aplastic anemia ® Hemophilia
™»Polycythemia vera ®Pernicious anemia
*HEPATIC DISEASE
® Cirrhosis ® Hepatic failure a
*ENDOCRINE CAUSES
Pregnancy » Puberty ® Pheochromocytoma

10
*DRUGS
® Aspirin ® Phosphodiesterase-5 inhibitors
® ANTIPLATELE DRUGS - Clopidrogel, Dipyridamole
ANTICOAGULANTS - Wardarin, Phenprocoumon/Dabigatran, Rivaroxaban,
Fondaparinux
® TOPICAL STEROID SPRAYS - may induce intermittent epistaxis by the force of the spray
creating damage to the epithelium of the nasal septum; this epithelium may crust and
bleed when this crust is either removed or falls off; directing the spray away from the
septum may help reduce this problem.
*CHEMICAL NASAL IRRITANTS
» Cigarette smoke Cocaine abuse »® Sulfuric acid
» Ammonia » Gasoline » Phosporus
«IATROGENIC CAUSES
® Nasogastric and nasotracheal intubation » Surgical complications,
» Overzealous treatment of self-limited hemorrhage
SITE OF BLEEDING - the accurate location of the exact site of bleeding is important not
only for accurate placement of cautery or other form of local therapy, but also for
identifying the trunk blood vessel supplying this point; initially, one must note whether
the bleeding source is on the right or left side, in the front or the posterior part of the
nose, and above or below the middle meatus, which roughly divides the blood supply
from the 2 major contributors.
*INTERNAL CAROTID ARTERY - gives rise to the ophthalmic artery which gives rise to
® Anterior ethmoid artery Posterior ethmoid artery
«EXTERNAL CAROTID ARTERY - Sphenopaiatine artery.
- thus bleeding from above the anterior 1/2 of the middle turbinate comes from the anterior
ethmoid artery and bleeding from below the middle turbinate and more posteriorly in the
nose from the sphenopalatine artery.
® ANTERIOR PART OF THE NOSE - most nosebleeds start from the vascular network in
the anterior part of the nasal septum
KIESSELBACH'S PLEXUS ON THE SEPTUM (LITTLE’S AREA) - is located in the area of the
anterior caudal nasal septum where the sphenopalatine, greater palatine, anterior
ethmoid, and superior labial arteries anastomose; it is estimated that approximately 80-
90% of all epistaxis occurs in this area, especially in children and young adults.
POSTERIOR PART OF THE NOSE - posterior epistaxis is more serious and is frequently
associated with hypertension, diabetes, or major systemic vascular disorders.
WOODRUFF’S PLEXUS - is the most common site of posterior bleeding especially in older
adults and those with systemic illnesses; it is supplied by the lateral nasal branch of the
sphenopalatine artery; vessels in this area are branches of the internal maxillary artery
(external carotid); the anterior ethmoid artery, a branch of the ophthalmic artery (internal
carotid system) supplies the upper portion of the posterior part of the nose; bleeding
from this artery usually is seen high in the nose between the nasal septum and the middle
turbinate.
>OTHER SITES - sometimes blood oozes from the anterior end of the middle or inferior
turbinate; blood may come from the paranasal sinuses following severe head injury or in
the presence of a neoplasm; when a patient has a hereditary hemorrhagic telangiectasia
or a blood dyscrasia, virtually all of the nasal mucosa may bleed; however, patients with
blood dyscrasias do not bleed only from the nose; they also have skin petechiae,
ecchymoses, hematuria, or other manifestations of a generalized hematologic
disturbance; the nose usually bleeds only from one place at a time except in nasal
fractures or after instrumentation in the non-bleeding side.

- frequently, when bleeding is serious, blood passes behind the nasal septum and
appears in the unaffected side of the nose.
DIAGNOSIS OF THE SITE OF BLEEDING
ANTERIOR RHINOSCOPY - with a nasal speculum and a bright light (either a head mirror or
head lamp), the physician inspects the anterior part of the nose; the examination begins
at Kiesselbach’s plexus, moving superiorly and posteriorly along the nasal septum, and
concludes with the turbinates and lateral wall; it will commonly reveal a bleeding source
on the anterior nasal septum, evidence of anterior septal trauma (as after digital
manipulation), an eschar, a nasal septal perforation, or dilated vessels.
INTRANASAL ENDOSCOPY - is important in accurate diagnosis since the most important
factor in determining and effectively treating epistaxis is visualization of the offending
vessels.
PATIENT AND CLINICAL PREPARATION
*Obtain vital signs and address any significant vital sign abnormalities
*Gown and drape the patient appropriately to protect their clothing; the patient also can
be given an emesis basin.
*Ask the patient to sit upright in the sniffing position with the neck flexed and the head
extended; the base of the nose should remain parallel to the floor.
* After putting on a face shield, gown, and protective gloves, position yourself in front of
the patient, level with the patient's nose.
eHave the patient blow the nose to remove clots or suction the nasal passageway
carefully; this may temporarily increase bleeding but can aid in identifying the bleeding
site; suction from front to back along the nasal septum and then laterally.
*lf the bleeding is minimal, attempt to locate the specific bleeding source; if the bleeding
is too profuse for visualization of the source, administer a topical anesthetic and
vasoconstrictor.
- one method is to insert lidocaine with epinephrine-soaked cotton swabs into each nare;
ask the patient to clamp the nostrils to limit bleeding and promote contact with the
mucosa.
*If a discrete bleeding site is initially identified, an effective way to provide hemostasis
and anesthesia is to inject the mucosa at the base of the bleeder with 2% lidocaine with
epinephrine via a tuberculin needle and syringe device.
ANTERIOR EPISTAXIS - the blood exits almost entirely from the anterior portion of the nose.
™Kiesselbach’s plexus Posterior floor of the nasal cavity
® Junction of the anterior 1/3 and posterior 2/3 of the nasal septum
® High anterior septum
POSTERIOR EPISTAXIS - most of the bleeding occurs in the nasopharynx and mouth,
although some blood can exit through the anterior nose as well; it is often more severe
and difficult to control.
®Woodruff’s plexus situated on the posterior aspect of the lateral wall of the inferior
meatus
® Posterior part of the lateral nasal wall near the sphenopalatine foramen
Posterior end of the inferior turbinate
Middle turbinate and its medial surface
® Middle and posterior parts of the nasal septum
CRS

12
TREATMENT
ALGORITHM MANAGEMENT OF EPISTAXIS

NOSEBLEED
Controlled with Profuse, not controlled with

pressure pressure
Local mucosal therapy, Check vital signs, start IV in patients with

cautery or observation significant blood loss or hypovolemia
a _™
Bleeding site Bleeding site not
identified identified
Perform cauterization; bleeding

controlled?
No Place anterior pack;

———F bleeding controlled?
Replace with
anterior/posterior pack
Consider arterial
ligation _. NO
Consider angiography
and embolization
1. MEDICAL MANAGEMENT
*The first priority in the management of epistaxis is to address the airway, breathing, and
circulation (ABCs).
¢The bleeding quantity is estimated using clinical examination (pallor, tachycardia, pulse,
arterial tension, polypnea) and paraclinical signs ( CBCt, coagulation tests)
*Correct hypovolemia if needed (3:1 rule: for every 100 ml of blood loss, replace with 300
mL of crystalloid fluid); the degree, site, clinical state, and etiology of the nosebleed
dictates the initial treatment which measures should focus on immediate control of
hemorrhage and correction of hypovolemia; generally, NSS or LR are sufficient for fluid
management, but consider transfusion when volume loss is greater than 30% (1,500 ml
in adults) or if ongoing loss exceeds 100 ml/min.
*Vigilant hypertension control (antihypertensive agents)
*Address coagulopathy (fresh frozen plasma, platelets, cryoprecipitate)
*Apply vasoconstrictive agents (phenylephrine, oxymetazoline)
*May apply digital pressure over the anterior cartilaginous portion of the nose (just
superoposterior to alae).

13
‘If the bleeding does not stop or nasal compression leads to persistent uncontrolled
postnasal bleeding, nasal packing should be attempted.
*Once patient is stable or if patient presents with mild epistaxis, it is important to get a
good history and physical examination.
ANTERIOR EPISTAXIS ;
*APPLY ICE PACKS TO BRIDGE OF NOSE OR FOREHEAD - may also control bleeding;
or place a block of ice in the mouth to promote vasoconstriction and hence reduce blood
flow to the nose
*DIGITAL PRESSURE - most cases of anterior epistaxis can be controlled by applying
digital pressure at the anterior or cartilaginous part of the nose between the thumb and
index finger for a 15-20 mins without interruption to provide adequate tamponade of the
bleeding.
CRITICAL COMPONENTS o,
“No peeking” or fighting the temptation to release pressure before the allotted time is
up to check if bleeding has ceased; platelet plugs take up to 20 minutes to form and may
not be functional if not allowed time to mature.
POSITIONING - have the patient remain upright in the tilt-forward position (“chin-to-
chest”) because leaning the head back to prevent egress of blood out of the nares may
actually cause inadvertent swallowing (with subsequent vomiting) and aspiration of
blood; the patient should remain calm during this time; sometimes an ice pack over the
forehead and/or face is helpful.
TOPICAL DECONGESTANTS - oxymetazoline nasal spray has become the most readily
available topical vasoconstrictor used in the management of epistaxis; it has an
outstanding safety profile with limited systemic absorption and is relatively inexpensive;
a common strategy is to deliver oxymetazoline spray into the bleeding side(s) before
holding pressure with the head tilted forward; for the most part, the vasoconstriction
attained with topical agents is additive with holding pressure in achieving hemostasis.
- the use of oxymetazoline should be limited to 3 days or less to minimize the risk of
rhinitis medicamentosa.
*TRANEXAMIC ACID - there is some evidence suggesting that oral and/or topical
tranexamic acid may help in treating epistaxis.
°“SNIFFING,” OF AIR - an alternative strategy for management of slow-rate epistaxis is
through gentle nasal inspiration, much like sniffing; constant influx and efflux of air
creates a local drying effect over bleeding surfaces; patients are asked to sniff several
times per minute until the bleeding ceases; this is especially effective for patients
presenting with slow ooze epistaxis following nasal, septal, or sinus surgery, because
their nasal cavities tend to be more widely open following surgical treatment of sources
of obstruction, thereby introducing more laminar airflow; sometimes a large clot forms
and occludes the nasal airway, which decreases the effectiveness of this strategy.
*SUCTIONING - blood clots and fresh blood are aspirated from the nose.
eTOPICAL EPINEPHRINE (1:1,000) - is applied to a cotton ball, which is placed into the
bleeding nostril over the bleeding site; this is only short-acting and when the adrenaline
effect wears off after about 20 minutes, the bleeding may return in a greater quantity.
*LOCAL PRESSURE -- is easily supplied by inserting a clean dry cotton pack within the
nose against the bleeding vessel and leaving it in place for 3-4 hours; applying finger
pressure to the outside of the nose adds additional pressure.
*CAUTERY OF THE BLEEDING SITE - after an anterior source of bleeding is identified,
cautery may be used to achieve hemostasis; the nasal mucosa should be pre-
anesthetized with 4% lidocaine solution on a cotton pledget to reduce discomfort; the
principle of cautery is to injure the nasal mucosa and underlying vasculature, resulting

14
in immediate coagulation and vasoconstriction and immediate cessation of bleeding.

™» CHEMICAL CAUTERY- silver nitrate sticks may be used to cauterize but will not work
onan actively bleeding source; hemostasis must be achieved first; suction the nares and
keep a small Frazier suction catheter ready to suction excessive blood; for brisk bleeding
inject lidocaine with epinephrine at the base of the vessel with a tuberculin syringe;
attempt to dry the surrounding mucosa with a dry cotton swab; silver nitrate needs to be
applied to a dry area to be effective; drying the area will also minimize spread of silver
nitrate beyond the area.
- apply the silver nitrate stick with gentle pressure for 3-10 secs; do not use the stick for
>10 secs in any area, or septal cartilage may be damaged; do not cauterize an area greater
than 1 cm in diameter; do not cauterize both sides of the septum at the same location; it
causes a burning sensation, so the patient will appreciate having the anesthetic in place
for at least 15 mins; most patients sneeze after the application of silver nitrate; if bleeding
restarts, the initial cautery was insufficient and should be applied again; the cauterized
area immediately turns white or gray.
- after the successful procedure is completed, the patient is instructed to use saline spray
and antibiotic ointment in the nose 2x/day for 2 weeks and to avoid strenuous activities
for 7-10 days; if possible, the patient should not use any aspirin or NSAIDs products for
this duration of time.
#ADULTS - chemical cautery can be done without anesthesia.
=CHILDREN - if with recurrent, severe nosebleeds may be cauterized under general
anesthesia; this is more readily tolerated by young patients, than electrodessication or
electrocautery, but is less effective.
INDICATIONS
=Minor bleeding aObservable bleeding point
BEasily visualized regions (Kiesselbach’s plexus)
ADVANTAGES
=Minimal tissue damage =Simple
=Potential to avoid packing Quick
DISADVANTAGES
#Allows for coagulation of superficial vessel only
#High rate of rebleeding ®Risk of perichondrial exposure
COMPLICATIONS
=Nasal septum perforation (especially when performed on both sides at the same time)
#Local scars =Cartilage injury 8lntranasal mucosal adhesions
»ELECTROCAUTERY- has little advantage over chemical cautery with silver nitrate
sticks; since an actively bleeding vessel is virtually impossible to cauterize with AgNOs,
electrocautery with suction may be the next choice; the cautery tip is heated to a cherry
redness and the bleeding vessel lightly singed until the outlines of the vessel have
disappeared.
- it provides greater depth of penetration, but is also more likely to cause exposure of
cartilage and/or septal perforation.
- since electrocautery is more painful than AgNOs,, they may need injection with local
anesthetic; more severe epistaxis when nasal endoscopy is feasible, has to be treated
with endoscopic bipolar cautery. [
- either bipolar forceps or unipolar suction diathermy can be used; some of the bipolar
suction forceps now available help to remove the blood and smoke at the same time; the
bulbous head of the unipolar suction device allows cautery of a sizable vessel anywhere
in the nose, and its large suction channel is less likely to become blocked by congealed

15
blood; simultaneous bilateral cautery should be avoided to minimize the risk of causing
‘a septal perforation.
»ELECTRODESSICATION - is preferred because it affords better control; it is necessary
to have a nearly dry field and for this purpose a combination of a suction tip and an
electrode is convenient; the tip of the probe is held in light contact with the bleeding point
as the dessicating current is applied.
- after cautery, patients should be advised against nose blowing for about 10 days to
allow the area to heal; a greasy antiseptic barrier cream should be applied several times
daily for 2 weeks to prevent the eschar from drying and coming off, with a resulting
rebleed; the ointment should not be placed directly on the area treated but is best placed
inside the rim of the nostril on the tip of the finger and then “milked” upward by
massaging the nostril rims, and then it can be sniffed up; this advice can also be given
to patients with a crusted septal area from picking or excessive drying.
- if cauterization fails or bleeding recurs within 72 hours, consider the use of packing or
a balloon device.
*TOPICAL HEMOSTATIC AGENTS - provide a procoagulant effect; nasal saline spray
should be used for several days after placement to facilitate resorption.
® MOST COMMONLY USED TOPICAL HEMOSTATIC AGENTS:
&GELFOANM - is usually preferred.
=SURGICEL - may be better for stimulating coagulation but it is more expensive and may
delay healing; it is often reserved for when Gelfoam is not effective or available.
® OTHER TOPICAL HEMOSTATIC AGENTS
=Fibrin glue (Tisseel) ® Microfibrillar collagen (eg, Avitene, Davol)
=Human-derived thrombin in gelatin matrix (eg, Floseal)
- these dressings form a scaffold for the formation of a blood clot; they may be used as
a primary technique for discrete bleeding, as a bandage over a previously cauterized site,
or as amucosal sheet over an area of diffuse bleeding (e.g., coagulopathy) before packing
is applied; if these are in place before packing is removed, it may prevent the clot from
being dislodged
®&INDICATIONS
=Mild observable bleeding point
®|rritated focal area suspicious for recent bleed
=» ADVANTAGES
aLess damage than cautery Simple
=Potential to avoid packing Quick
®DISADVANTAGES - may rebleed if no packing placed
*NASAL PACKING - is generally reserved for those cases where external pressure and
_Cauterization fails to control the bleeding; first, try and effectively evacuate clots and
pooled blood from the nasal cavity with suction.
® INDICATIONS FOR NASAL PACKING
"Recurrent nosebleeds despite treatment
"Traumatic nosebleed with suspected nasal fracture
="Nosebleed associated with a septal perforation or other nasal abnormality
®Nosebleed ina frail patient ;
®Nosebleed in a patient with a high-risk medical condition
"Nosebleed lasting longer than 10 minutes despite pinching outer nasal tissue or
applying ice pack
"Acute or recurrent epistaxis after conservative management or cauterization

16
®CONTRAINDICATIONS (RELATIVE) TO NASAL PACKING

«Patients with advanced COPD or other advanced cardiac or pulmonary conditions (nasal
can induce the nasopulmonary reflex, causing the arterial oxygen pressure to
packing
drop by as much as 15 mm Hg).
=Untreated coagulopathy #A displaced fracture
"Osler-Weber-Rendu disease (nasal packing can disrupt friable tissue, especially
be
posterior packing, and should be done with caution in these patients; attempts should
made to normalize clotting factors, if possible, before instrumentation).
the
ANTERIOR NASAL PACKING - achieves hemostasis, prevents desiccation, and protects
area from trauma; improperly placed packing may further abrade the area, dislodge
prematurely, or migrate into the posterior pharyngeal area.
and
- anterior packing must be placed with adequate analgesia, proper visualization,
deliberate movements; before inserting the pack into the nasal cavity, coat the product
topical
with a topical antibiotic; consider spraying a topical vasoconstrictor with a
anesthetic (lidocaine) into the nasal cavity; keep packing in place for 3-5 days to allow
to
the vessel to develop a mature thrombus; provide antistaphylococcal antibiotics
prevent toxic shock syndrome, rhinosinusitis, and otitis media.
- easier-to-use commercial devices have largely supplanted traditional petrolatum gauze.
BLEEDING:
PRODUCTS THAT PROVIDE PRESSURE AGAINST THE NASAL MUCOSA TO TAMPONADE
bleeding.
®NASAL TAMPON - easily applied; a reasonable first choice for most anterior
=Lubricate the tampon generously with antibiotic ointment
#Trim the length and width carefully to minimize trauma to the nose
®Using bayonet forceps, advance the packing carefully along the floor of the nose; direct
it parallel to the floor, not upward toward the top of the nose.
eExpand it with 5-10 mL of saline, although contact with the moisture of the nose will
often cause it to swell spontaneously.
- sometimes necessary to place two tampons side by side before inserting them, to fill
the nasal cavity and provide better pressure on the areas of bleeding.
sObserve for 10 minutes after anterior packing to identify continued bleeding
ADVANTAGES
|. Rapid insertion ii. Little discomfort
iii.Ease of use even by inexperienced personnel
iv. Possible inhibition of bacterial growth
EXPANDABLE SPONGE
=Trim the sponge to a size and shape that appears consistent with the patient’s nasal
opening, usually about 4-6 cm in length; an exact fit is not required.
- if only a small sponge is available, then consider using two sponges side by side; when
cutting the sponge, make sure to avoid leaving any corners or other sharp edges.
«Coat all but the distal tip of the sponge in petroleum jelly to avoid premature softening
of the sponge; the use of an antibiotic ointment may decrease the risk of recurrence
insert the sponge in a smooth motion, entering in a near vertical direction, and then
rotating it to a horizontal direction; continue passing the sponge along the inferior nasal
floor until it is completely inside the nasal passage; when in place, the trailing tip of the
sponge should be visible inside the nostril but not protruding from it.
#Slowly drip about 2 mL of saline or tap water onto the tip to help the sponge expand
more quickly; it applies pressure over the-bleeding point.
® POLYVINYL ALCOHOL SPONGES (Merocel)
®» RESORBABLE PACKING (Nasopore)
®VASELINE STRIP GAUZE - traditional anterior nasal packing placed to posterior
choanae, controls most posterior bleeding; it is more difficult but may be considered if

WwW
the foregoing measures are unavailable or unsuccessful; the nose should be packed with
a sterile petrolatum ribbon gauze (0.5-1.0 inches wide) to which is added an antibacterial
ointment to prevent toxic shock syndrome.
alf time permits, a topical anesthetic (4% xylocaine) is necessary.
"Application of a procoagulant dressing prior to the insertion of the nasal packing may
be helpful
» Antibiotic-impregnated petrolatum jelly gauze should be placed with a bayonet forceps
in a pleated manner, beginning inferiorly along the floor of the nasal cavity and
progressing superiorly; the leading edge of the pack is inserted along the floor of the
nostril as far posteriorly as possible and another layer is placed on top sequentially and
so on until the nostril is totally packed.
- the anterior packing may be left in place 3-4 days if necessary, though there is danger
of obstructing the paranasal sinus ostia so that antibiotic treatment is necessary.
ADVANTAGES - simple, proper formal strip-gauze pack controls most posterior bleeding;
does not require inpatient monitoring
DISADVANTAGES - results in nasal obstruction; risk of pressure necrosis (nasal and septal
cartilage), hypoxia, rhinosinusitis, bacteremia, and epiphora; requires prophylactic
antibiotics.
- when compared with gauze packing, compression devices are easier to place, better
tolerated, and very successful; preformed nasal packing products are convenient
alternatives to anterior nasal packing.
RAPID RHINO - is an air-inflatable balloon coated with a hydrocolloid fabric, which
eases insertion and removal.
*SYSTENIC ANTIBIOTICS - patients with packing require antibiotics that cover common
nasal pathogens such as Staphylococcus aureus, Streptococcus pneumoniae, Moraxella
catarrhalis , and Haemophilus influenzae.
- all patients should be instructed to notify health care providers if increasing pain,
rebleeding not controlled with 15 minutes of nose pinching/ice application, or fever
occurs; patients should also receive instructions on how to keep the packing moist with
a humidifier at home and frequent applications of nasal saline drops; patients with
anterior packing should have the packing removed by an experienced health care
provider in 48-72 hours; if the patient is medically frail or had significant bleeding,
hospital admission may be indicated; patients needing posterior packing or insertion of
a Foley or posterior balloon device generally require admission to an intensive care unit
and specialist consultation.
POSTERION EDISTAXIS - is bleeding from sites in the nasal cavity not visualized from
the anterior approach; bleeding that begins with the sensation of blood in the posterior
pharynx or bleeding that cannot be localized anteriorly is considered posterior.
- it occurs in 10% of patients with epistaxis; it is more common in people older than 50
years old, and it is more likely to present with signs of hemodynamic instability.
*POSTERIOR SOURCE OF BLEEDING SUSPECTED WHEN:
&The majority of the blood is occurring into the pharynx
An anterior pack fails to control the hemorrhage
™ It is evident from nasal examination that the hemorrhage is posterior and superior.
*ENDOSCOPY - is mandatory because it offers a systematic and rigorous examination of
the nasal cavity to locate the bleeding source and immediate local treatment
(electrocauterization) can be applied; if the nose is packed before endoscopy is done,
this can complicate detection o the exact site of bleeding, because this often causes
mucosal trauma; endoscopic cauterization achieves hemostasis in >80% of patients with
posterior epistaxis at the first attempt and >90% after a second attempt.

18
COMPLICATIONS OF ENDOSCOPY
Palatal numbness from thermal damage to the greater palatine nerve
®Damage tothe lacrimal duct
*®Possible damage to the optic nerve when cautery is used in a patient who has already
had an ethmoidectomy.
- treatment requires the use of both anterior and posterior packing; some recommend
that a sphenopalatine block be given, which can be both diagnostic and therapeutic; a
decrease in the epistaxis is noted if it is coming from a division of the sphenopalatine
artery; when no effect is obtained, the bleeding may be from the ethmoid arteries.
*POSTERIOR PACKING
*®INFLATABLE BALLOON DEVICES - coat the tip of the device with petroleum jelly or
other lubricant; insert the catheter with the longer portion of the bevel toward the nasal
septum to prevent damage to the turbinates or mucosa.
FOLEY CATHETER - often used as a posterior pack because of its availability, ease of
use, and successful tamponading effect.
"Insert a 12-Fr Foley catheter through the bleeding naris into the posterior aspect of the
pharynx.
alnflate the balloon halfway with approximately 5 to 7 mL of normal saline or water.
“Slowly pull the Foley catheter into the posterior part of the nasopharynx and secure it
against the posterior aspect of the middle turbinate.
"Finish inflating the balloon with another 5 to 7 mL of normal saline or water.
- if pain or inferior displacement of the soft palate occurs, deflate the balloon until the
pain resolves. Ensure proper placement before completely inflating the balloon because
the balloon will remain too posterior in the nasopharynx and fail to achieve hemostasis.
BWhile maintaining constant gentle anterior tension on the Foley catheter, place anterior
nasal packing of layered petrolatum gauze.
=Pack the opposite nasal cavity to counteract septal deviation.
=Place a short section of plastic tubing over the catheter and secure it with a nasogastric
tube clamp or umbilical clamp; be careful to not exert undue pressure on the nasal alae
to avoid causing necrosis.
- if bleeding persists, it is likely due to an area high in the nasal cavity, where the balloon
does not reach; one solution is to deflate the balloon, leave it in place, and use anterior
petroleum gauze packing on top of it; the balloon can then be reinflated to seal the
packing in the upper portion of the anterior nasal cavity.
- persistent bleeding may also be due to a bowed septum; packing the contralateral side
may halt bleeding by correcting the bowing.
®DUAL BALLOON PACK - these devices have been a significant advance in the
treatment of epistaxis; it has a posterior balloon that inflates with =10 mL of air and an
anterior balloon that inflates with approximately 30mL of air; each device may vary
slightly.
sAfter appropriately anesthetizing the naris, place the lubricated pack along the floor of
the affected naris as far back as possible.
=Inflate the posterior balloon approximately halfway with air, and then, with traction, pull
the balloon into place up against the posterior aspect of the middle turbinate.
=Complete the inflation of the posterior balloon with air; some clinicians prefer to inflate
all balloons with saline instead of air because air may deflate slowly; inflate slowly, and
stop if pain is felt; this is usually an uncomfortable sensation to the patient; if the patient
complains of pain or if the posterior soft palate deviates downward, deflate the balloon
until the symptoms are relieved.

1g
«Maintain the position of the balloon and inflate the anterior balloon with up to 30 mL of
air; again, halt inflation if the patient experiences increasing pain or deviation of the nasal
septum.
- overinflating the balloons can cause severe pain, displacement of the soft palate,
interfere with swallowing, and cause tissue necrosis.
aSome authors suggest packing the opposite naris to prevent such lateral deviation
=Place a small piece of gauze between the nose and the external catheter hub to decrease
skin irritation.
- bilateral posterior nasal packs should be avoided, particularly in the elderly or they
should be hospitalized and closely monitored; large packs may also compress the
eustachian tube and cause ear symptoms.
® TRADITIONAL POSTERIOR NASAL PACKING - posterior nasal gauze pack is the classic
method of treating posterior epistaxis; balloon devices are easier to use and less
distressing to the patient, formal posterior nasal packing is less commonly used.
=Anesthetize the patient's nares and posterior pharynx with topical anesthetic.
=Prepare a roll of gauze with two silk ties (2-0) secured around the middle and extending
in opposite directions; one set of ends will be used to place the posterior pack and the
second will remain extruding from the oral cavity to remove the pack.
=Place 2 rubber catheters through the bleeding nostril.
=When they are seen in the posterior of the pharynx, grasp the tips with forceps and
guide out of the mouth.
®Attach it to one set of the ends of silk ties secured to the gauze pack
=Retract the rubber catheter, thus carrying the No. 2 silk tie through the nasopharynx and
out of the nose.
=Tie both ends of silk ties around the catheter.
=Pull the catheters back through the nose and snug the roll of gauze against the posterior
aspect of the choanal arch
BAttach the silk tie that remains in the oropharynx to the patient's cheek to aid in removal
or rescue of the posterior pack.
=Use the silk ties exiting the nostril to maintain the position of the posterior pack.
=Pack the anterior passage as described for anterior epistaxis.
=Secure the silk ties over a gauze pad or dental roll.
-in the past, patients with traditional posterior packing were often admitted to the hospital
for the duration of the posterior packing; administering humidified air or oxygen often
makes this pack more comfortable.
- these techniques are extremely uncomfortable, lower arterial oxygen saturation, and
may induce dysrhythmias or an acute myocardial infarction in patients with severe
cardiovascular disease; because toxic shock syndrome has been reported with the use
of nasal packs, patients are started on intravenous antibiotics; the packing is left in place
for 3-5 days.
- nasal packing fails to stop epistaxis in up to 25% of cases.
- if available, tranexamic acid can be considered.
- sinus endoscopes can be used to locate the site of bleeding and to cauterize it;
septoplasty or ligation of the anterior or posterior ethmoid, internal maxillary,
sphenopalatine, or external carotid artery may be necessary; arterial embolization is
another option. im
INDICATIONS
"Failed anterior packing =Skull base trauma
=Hemorrhage from a major branch of the sphenopalatine artery
ADVANTAGES - may be inserted for severe bleed in the emergency room or office.

DISADVANTAGES
®Risk of airway compromise
=Requires hospital monitoring, ICU if bilateral
=Requires patient cooperation (painful)
aMay require intubation or general anesthesia
sEustachian tube dysfunction (hearing loss)
=Risk of alar necrosis where the anterior aspect of the pack is secured
REMOVING PACKING - posterior packing should be removed by a specialist.
=Soften and rehydrate the dressing with saline, taking care not to use so much as to
cause the patient to aspirate; usually, 3 to 5 mL of saline is sufficient; give the fluid a few
minutes to diffuse through the material
=To remove the Rapid Rhino, first deflate the balloon.
®Follow universal precautions and protect the patient, furniture, and flooring from
potential blood spills.
#Have the patient sit up and lean forward, bracing himself or herself with arms grasping
a supporting surface.
\nstruct the patient to mouth breathe, to remain still, to not blow his or her nose or snort.
=With a basin in one hand, and bayonet forceps in the other, gently and smoothly remove
the packing.
=Inspect the nasal mucosa for residual bleeding and retained packing; if present, treat
appropriately; often there will be some mild drainage that is nasal mucus mixed with old
blood; this drainage rapidly subsides and does not require further treatment.
MAJOR COMPLICATIONS OF NASAL PACKING
=NASAL PULMONARY REFLEX - studies have shown that complete obstruction of the
nasal airway in certain individuals may lead to an elevation of the Pcoz and reduction of
the Po2,; continuous pulse oximetry and cardiac monitoring are mandatory as posterior
packing can cause hypoxemia, apnea, and cardiac dysrhythmia because of stimulation
of the nasopulmonary reflex.
eSEPTICEMIA "Cardiac dysrhythmias
BTOXIC SHOCK SYNDROME (TSS) - is caused by a toxin which is released by coagulase-
positive staphylococcus (Staphylococcus aureus) or group A_beta-hemolytic
Streptococcus
eMyocardial infarction =Death (posterior packing)
MINOR COMPLICATIONS OF NASAL PACKING
BAlar necrosis =Serous otitis media eSeptal perforation
sLocal infections sAcute sinusitis Ethmoid fracture
#Balloon migration ®Aspiration of the packing =Premature dislodgment
Dysphagia “Eustachian tu e dysfunction
=Displacement of airway with nasal obstruction
=Pressure necrosis of nasal mucosa
=Blood may exit the nasolacrimal duct and be noted in the eye
aAllergic reaction to materials or anesthetics
- rebleeding may also be seen with early pack removal; one series found that removal of
the packing within 48 hours increased the risk for rebleeding; most posterior packs are
left in place for 72 to 96 hours. om
- dysphagia from the packing can lead to poor oral intake and possibly necessitate
intravenous fluid hydration.
- a decrease in the arterial partial pressure of oxygen (Pa 02; 7.5 to 11mm Hg) and an
increase in the arterial partial pressure of carbon dioxide (Pa coz ; 7 to 13 mm Hg) can be
seen in patients with nasal packing who are treated with sedation; however, despite

21
traditional theoretical concerns, such altered pulmonary physiology cannot be attributed

to posterior packing alone; although it has been hypothesized that a posterior pack will
cause vagal stimulation and thereby result in varying degrees of bradycardia and
bronchoconstriction because of the so-called nasopulmonary reflex, studies have failed
to substantiate substantial physiologic changes attributed to posterior packing; observe
patients with significant cardiopulmonary disease and posterior nasal packs in a
monitored setting.
- tissue necrosis of the nasal ala, nasal mucosa, and soft palate secondary to improper
placement or padding has been described; protect the skin with gauze placed under the
device to reduce skin maceration; the risk for necrosis increases with the duration of the
packing, so all packing should be removed in 3-5 days.
- if the posterior pack becomes dislodged, it will fall into the oropharynx and place the
patient at risk for asphyxiation, vomiting, and aspiration; the patient and nursing
personnel need to be familiar with the technique for removing the pack; to remove the
pack, cut the anterior sutures that exit the naris from the gauze roll if they have not already
broken; grasp the sutures exiting the mouth and guide the packing out of the
nasopharynx; it may be necessary to extract the packing with forceps or digits.
*ENDOSCOPIC NASAL CAUTERIZATION OR LIGATION - is recommended as first-line
treatment in all cases of uncontrolled posterior epistaxis; it can be done under local or
general anesthesia; most of the time, it is done in the operating room under general
anesthesia; under endoscopic guidance, the anterior ethmoid artery is ligated if the
bleeding is anterior and high, and the sphenopalatine artery is ligated if the bleeding is
located; nasal packing is inserted after the procedure.
*TRANEXAMIC ACID (TXA) - is considered in cases of poorly controlled epistaxis; TXA
is an antifibrinolytic agent; a randomized control trial published by Zahed et al. compared
the application of topical tranexamic acid (a drug used for patients with hereditary
hemorrhagic telangiectasia) with the use of anterior packing for cases of anterior
epistaxis presenting to the emergency department.
*CRYOTHERAPY- is not frequently used, but can attempt control of severe posterior
epistaxis by use of cold water flowing through elastic catheters; it has a low complication
rate.
eWARM WATER IRRIGATION - is effective in epistaxis; study by Stangerup et al. showed
that warm water irrigation was more effective than nasal packing for the control of
posterior epistaxis (55% success rate compared to 44%, resp.).
«MOISTURING OR HUMIDIFYING AGENTS - the most common management to prevent
dessication in chronic recurrent epistaxis.
® Nasal saline mist » Nasal saline gel ® Irrigation
®Petrolatum based ointments Room humidifiers »Foam
eADJUNCTIVE TREATMENT
® Humidity in the home and workplace ® Sneezing with mouth open
Avoid nose-picking and nose-blowing ® Avoid straining
®Discontinuing medications (such as aspirin and anticoagulants)
2. SURGICAL TREATMENT - many otolaryngologists opt for early management of
posterior bleeds with endoscopic cautery under direct visualization in the OR, early
surgical control using arterial ligation, or referral to interventional radiology for selective
arterial embolization.
*ELEVATION OF THE SEPTAL MUCOPERICHONDRIUM - may be necessary for some
persistent or recurrent septal bleeding; the cicatrix which forms between the elevated
membrane and the subsequent cartilage obliterates the abnormal vessel; a more firm
cicatrix is formed if the cartilage is also removed so that the elevated membrane

22
is in contact with its fellow on the opposite side. ;

*SEPTOPLASTY - is helpful to manage epistaxis in selected cases with severe septal
deviation or septal mass ;
*LIGATION OF THE VASCULAR SUPPLY - may be required if bleeding fails to respond to
posterior packing or posterior endoscopic cauterization under general anesthesia;
endoscopic ligation is safer than embolization.
INDICATIONS
»® Uncontrolled epistaxis (typically posterior bleed)
* Identifiable bleeding site »Recalcitrant recurrent epistaxis
TECHNIQUES
™ENDOSCOPIC SPHENOPALATINE ARTERY LIGATION (ESPAL) - preferred operative
approach for intractable posterior epistaxis; dissection of the posterior middle turbinate
with ligation of the sphenopalatine artery; it has replaced the need for posterior nasal
packs, other than in emergency situations, to control profuse bleeding.
ENDOSCOPIC ANTERIOR AND POSTERIOR ETHMOID ARTERY LIGATION - preferred
operative approach for intractable anterior epistaxis; located at roof of ethmoid sinus.
» EXTERNAL ANTERIOR AND POSTERIOR ETHMOIDAL ARTERY LIGATION - for anterior
bleed; approach from a Lynch incision.
®TRANSANTRAL MAXILLARY ARTERY LIGATION - classic approach for intractable
posterior epistaxis (rarely used today); pterygopalatine fossa contents exposed via a
Caldwell-Luc (or transoral) approach allows ligation of the distal branches of the
maxillary artery (ascending pharyngeal, sphenopalatine, posterior nasal) .It is performed
under local anesthesia via transfemoral catheterization.
eBefore the procedure is done, angiography is performed to check for any unsafe
communications between the internal and external carotid systems.
eThe major advantage of this procedure is that if the patient is actively bleeding at the
time of the angiography, the embolization site can be targeted.
eClotting material is injected into the site of bleeding (if discovered) and this occludes
the artery.
aThe most serious complication of this procedure involves migration of the embolization
clotting material, which poses a risk of a stroke and ophthalmic artery occlusion, which
can lead to blindness.
aThe procedure can be repeated if hemorrhage recurs
INDICATIONS
®Intractable nasal hemorrhage (usually for posterior origin)
®Surgically inaccessible sites | »Nonoperative candidates
ADVANTAGES
® Diagnostic (defines bleeding site)
Therapeutic ™ May be repeated
™Can be done under local anesthesia
DISADVANTAGE - risk of embolic event (pulmonary emboli, stroke)
*EMBOLIZATION - angiographic embolisation uses coils, gel foam, or polyvinyl! alcohol
to embolise the bleeding vessel; this technique is found to have a success rate as high
as 87%; a catheter is placed in the internal maxillary artery and the bleeding vessel is
embolized; the success rate of this procedure is high, although not without risk; major
complications such as cerebrovascular accidents and blindness can occur in up to
4% of cases.

HH. AAXILE OFACIAL TRAUMA
BASIC CONSIDERATIONS
eAIRWAY CONTROL AND RESPIRATORY MANAGEMENT
*ASSESSMENT OF CIRCULATORY STATUS AND HEMORRHAGE CONTROL
«ASSESSMENT OF NEUROLOGICAL STATUS (DISABILITY)
*EVALUATION AND THERAPY OF ANY ABDOMINAL OR THORACIC INJURY
*TREATMENT OF SOFT TISSUE, FACIAL, AND EXTREMITY TRAUMA
*REDUCTION AND FIXATION OF BOTH FACIAL AND EXTREMITY FRACTURE
A. AIRWAY CONTROL AND RESPIRATORY MANAGEMENT - the first priority in the
treatment of the trauma patient is assessment of airway patency, adequate oxygenation,
ventilation, and protection from aspiration; the upper airway may be obstructed by the
tongue or dislodged teeth.
- maintenance of the airway in the setting of significant maxillofacial injuries is
mandatory; death may occur from early airway obstruction, particularly in patients with
mandibular fracture or combined maxillary, mandibular, and nasal fracture; when the
patient is in the supine position, the “horseshoe” configuration of the mandible suspends
the tongue; loss of this suspensory arch causes the tongue to fall posteriorly and
completely obstruct the airway.
- in addition, soft-tissue swelling around injured oronasal structures, especially when
combined with decreased mentation, can result in loss of airway patency; nasotracheal
intubation is contraindicated because of possible midface instability and the potential
that the tube will be inserted into the brain through the cranium; swelling and hemorrhage
within the hypopharynx may rarely make endotracheal intubation impossible; under
these circumstance a surgical airway should be created to prevent asphyxia.
- position patient on abdomen or side to prevent aspiration (caution: cervical fracture); in
unconscious patients, the tongue may have to be pulled forward to prevent airway
obstruction; conscious patients with compromised airways will often show signs of
agitation and will not want to lie supine as this causes the tongue to fall back into the
airway; there may be stridor present and signs of increased respiratory effort.
*CLEAR DEBRIS FROM THE AIRWAY - suctioning of the oral or nasal cavity to remove
blood, vomitus or other debris.
*POSTURE- in the absence of associated spinal injuries, itis appropriate to sit the patient
up; patients with grossly displaced mandibular injuries, such as those from gunshot
wounds, should be allowed to sit leaning forward so that the tongue and any debris from
the oral cavity is allowed to fall away from the airway.
- neck extension and jaw thrust also helps to clear the airway, although neck extension is
not permitted in the case of suspected injuries to the cervical spine.
*ORAL AIRWAY - can be used to help maintain the airway temporarily in a patient with
reduced consciousness or a patient with a mandibular fracture which has resulted in
instability of the floor of the mouth with prolapse of the tongue into the pharynx; in
complex injuries, it is very important to note any blunt trauma to the larynx because a
laryngeal fracture or tear can cause rapid development of total obstruction.
- the majority of these patients will need a definitive airway, like an endotracheal tube, in
which there is a tracheal cuff to prevent debris escaping into the lungs.
- oral airway placement can cause retching and vomiting in the semiconscious patient.
*BAG-VALVE MASK (BVM) - is the most commonly used device for supporting
ventilation; BVM ventilation is extremely effective, but requires careful attention to
maintain a tight mask seal, airway patency, and delivery of adequate tidal volumes.
*ENDOTRACHEAL INTUBATION - is the method of choice when tracheal ventilation is
necessary; patients with an unstable or marginal airway require endotracheal tube
insertion or tracheostomy, depending on the potential for a continuing increase in edema

24
of the face, oral cavity, or oropharynx; orotracheal intubation should be attempted only
after it has been determined that there is no injury to the cervical spine or when there is
minimal distortion of the upper airway structures from edema, bleeding or laryngeal
trauma.
- nasotracheal intubation should not be performed in patients with trauma to the midface
or with suspected basilar fracture because of the risk of inadvertently introducing the
endotracheal tube into the cranium; under these circumstances, tracheostomy or
emergency cricothyrotomy should be performed.
*EMERGENCY SURGICAL AIRWAY
®» NEEDLE CRICOTHYROIDOTOMY - provides a temporary surgical airway; it supplies the
patient with oxygen, but without a definitive surgical airway there is an invitable build-up
of COz which limits the usefulness of this technique.
®SURGICAL CRICOTHYROIDOTOMY - provides a definitive surgical airway; it is a
procedure that can be performed extremely rapidly and, in an emergency, any rigid tube
with a hollow lumen can be used; specially designed cricothyroidotomy tubes are
available.
*EMERGENCY TRACHEOSTOMY - should be resorted to only if all other measures have
failed or if laryngeal injury is suspected; if several days are required to stabilize the
patient, a tracheostomy should be preferred to minimize the sequelae of prolonged
intubation; definitive management of facial injuries often produces additional edema,
making early extubation dangerous; hence, tracheostomy is often performed
perioperatively.
*MAJOR PATHOLOGICAL CONDITIONS AFFECTING VENTILATION
®Tension pneumothorax ® Open pneumothorax
®Massive hemothorax »Flail chest
«SIGNS OF HYPOXIA
® Agitated patient » Varying levels of consciousness
®Inappropriate behavior ® Signs of airway compromise
® Combination of these points
B. ASSESSMENT OF CIRCULATORY STATUS AND HEMORRHAGE CONTROL
- after proper airway control and respiratory management, initial assessment of the
circulatory status is required; the initial diagnosis of shock is based on clinical signs, not
laboratory data; signs of hypoperfusion lead to immediate investigation into the source
of blood loss; most trauma patients in shock are experiencing bleeding resulting in
hypovolemia; hemorrhage is therefore the most common cause of shock in trauma
patients; life-threatening bleeding following maxillofacial trauma is rarely related
exclusively to facial injuries; the occurrence of severe bleeding from facial trauma is
found in 1-11% of patients; the origin of bleeding is complex because the vascular supply
of the face involves branches of both internal and external carotid arteries.
- traumatic facial bleeding originates from both hard-soft-tissue sources, adding to the
difficulty of determining the exact source of bleeding; the origin of bleeding in
maxillofacial trauma is usually the internal maxillary artery and its intraosseous
branches; the course of the maxillary artery passes within the borders of common
complex facial fractures.
- different methods for the control of bleeding of maxillofacial in origin have been
described; rapid resuscitation followed by posterior nasal packing is sufficient to control
most bleeding; immediate reduction of fracture is mandatory to control bleeding.
- usually bleeding from the head and neck can be controlled by
*PRESSURE *PACKING
BLOOD AND FLUID VOLUME - must be replaced before any further evaluation of the facial
injury can be completed.

25
C. ASSESSMENT OF NEUROLOGICAL STATUS (DISABILITY)
- a rapid neurological assessment is performed - level of consciousness, pupillary size
and reactivity, and motor response are evaluated; alcohol and other drugs may impact
on the sensorium; injury to the CNS must be excluded as a primary reason for
neurological changes concurrent with the restoration of oxygenation and circulation.
- patients with severe head injury (GCS <9) should undergo immediate intubation with
mechanical ventilation irrespective of respiratory status at that time; extreme caution
must be used in positioning and manipulating these patients.
*X-RAY VIEWS OF THE CERVICAL SPINE AND APL PROJECTIONS - are required in any
severe head injury.
*SKULL X-RAYS - may show fractures.
°CT SCAN - may detect early intracranial bleeding; a brain CT Scan is mandatory in every
patient with known loss of consciousness, a GCS score of <15, or evidence of injury
above the clavicles; the incidence of brain injury in patients with maxillofacial trauma
varies from 15-48%; the risk of serious brain injury is particularly high with upper facial
injury.
eEVALUATION OF THE FOLLOWING:
®Level of consciousness » Amnesia
® Neurologic signs and symptoms
D. EVALUATION AND TREATMENT OF ANY ABDOMINAL OR THORACIC INJURY
- abdominal ultrasound has proved to be very sensitive in determining intraperitoneal as
well as intrapericardiac fluid and has almost replaced the diagnostic peritoneal lavage;
cervical spine injuries occur in 1.5-3.0% of blunt trauma victims, 25-75% of which are
unstable; patients with clinically significant head trauma may have a greater risk of
cervical spine injury, and the incidence increases to 7.8% in trauma victims with a GCS
score of <8.
- maxillofacial trauma is often associated with cervical spine injury; spinal injuries
associated with mandibular fractures typically involve the first or second cervical
vertebra, whereas middle or upper facial trauma typically is associated with injuries of
the lower cervical spine.
REASONS WHY DIAGNOSIS OF CERVICAL SPINE INJURY IN PATIENTS WITH MAXILLOFACIAL
TRAUMA IS IMPERATIVE:
*The presence of cervical trauma in association with maxillofacial injury makes airway
management more difficult
*Alterations in management related to the care of specific cervical-spine fractures and
associated neurological compromise.
®Fractured ribs, penetrating wounds, and splenic or hepatic rupture must be excluded.
E. TREATMENT OF SOFT TISSUE, FACIAL OR EXTREMITY TRAUMA
- facial trauma may or may not involve facial fractures; one must not overlook any soft
tissue injuries in patients with bony trauma.
*PALPATION - it is important to palpate the rims of the orbit, the zygomatic arch, the
fullness of the maxilla and alveolar ridge, and the full course of the mandible; intraoral
palpation is mandatory in the diagnosis of facial fractures.
°X-RAYS
® Skull x-rays ® Nasal bone x-ray
=»PNS x-rays » Orbital x-rays
® X-rays of the mandible and zygoma
*CT SCANS- are helpful in fractures of the face, particularly in complex injuries.
*MANAGEMENT OF FACIAL WOUNDS - facial lacerations do not require immediate
management; therefore a delay of up to 24 hours can be allowed to establish diagnosis
and patient stability.

26
RULES IN THE CLOSURE OF FACIAL WOUNDS:
® All bony and cartilaginous supporting structures must be replaced as close as possible
onto the original site, no matter how torn or comminuted; this tissue may be
indispensable in secondary cosmetic repair of extensive lacerations or bony loss.
Closure of facial lacerations requires meticulous layered closure of muscles,
subcutaneous tissue, and skin with fine sutures under atraumatic conditions to obtain
the best result.
The physician must be cognizant of injuries to the CN VII, the parotid duct, lacrimal
apparatus, and other areas prior to the closure of facial wounds.
IV. FACIAL BONE FRACTURES

SIGNS OF BRUISING RAISING SUSPICION OF AN UNDERLYING FRACTURE
*BATTLE’S SIGN - bruising over the skin of the mastoid bone can indicate a base of skull
fracture
*RACCOON EYES- bilateral periorbital swelling can indicate a fracture of the base of the
skull, naso-ethmoid region, frontal sinus, or Le Fort Il/IIl fracture
*BILATERAL INNER CANTHUS BRUISING - can indicate a nasal bone fracture
*BRUSING OVERLYING THE LOWER BORDER OF THE MANDIBLE - can indicate a
mandibular fracture.
= COMMON SYMPTOMS OF FACIAL BONE FRACTURES
*DEFORMITY OF THE FACIAL CONTOUR
®EVIDENCE OF DEFORMITY IN THE FRONTAL AND NASO-ETHMOID AREA
=FRONTAL BONE DEFORMITY - this is most commonly seen in patients with fractures
of the anterior wall of the frontal sinus; the appearance is of a midline depression in the
area immediately above the supraorbital ridge.
=NASO-ETHMOIDAL DEFORMITY - this is often associated with frontal deformity; the
classic appearance includes telecanthus, depression of the nasal bridge and elevation of
the nasal tip.
NASAL BONE DEFORMITY - the nose is frequently disrupted in facial injuries;
anatomically, only the upper third of the nose is bony; nasal fractures often present with
deviation of the nose.
® EVIDENCE OF ZYGOMATIC ARCH DEFORMITY
eIN-FRACTURE OF THE ARCH OF THE ZYGOMA - may be an isolated fracture of the arch
or may be associated with an extremely rotated zygomatic fracture.
®OUT-FRACTURE OF THE ARCH OF THE ZYGOMA - seen as bowing of the zygomatic
arch; often associated with posterior displacement and an internally rotated zygomatic
fracture; this is an important clinical sign as bowing is hard to correct surgically and if |
«BONY CREPITUS *EDEMA OF THE ADJACENT SOFT TISSUES
*ECCHYMOSIS *SUBCUTANEOUS EMPHYSEMA
*FACIAL SWELLING - its presence should be noted but it correlates poorly with the
severity of the underlying bony injury; swelling often masks underlying bony deformity.
*EPISTAXIS - is frequent if the nasal bones and ethmoid sinus are involved.
A. NASAL BONE FRACTURE
- EPIDEMIOLOGY - the prominence and delicate structure of the nose make it vulnerable
to a broad spectrum of injury, which accounts for why it is the most frequently fractured
facial bone. -
- males are affected ~2x as often as females in both the adult and pediatric populations,
with a peak incidence during the second and third decades of life.
- fracture of the nasal bones is generally considered the most common site-specific bony
injury of the facial skeleton; unfavorable changes in nasal appearance and function may
occur where there is a loss of structural integrity; therefore, the managing physician

27
should render appropriate and timely treatment based on the nature and extent of the
injury.
-a high incidence of nasal fractures is well reported in both the pediatric and adult patient
populations; retrospective studies of maxillofacial trauma report that nasal bone
fractures comprise 14-50% of all facial fractures.
*ADULTS - the highest rates of incidence are found among males, with a 2:1
predominance over cases reported in females; nasal bone fractures commonly result
from a “right cross" that smashes both nasal bones to one side; a frontal blow that
depresses the nasal bones; or various injuries that cause misalignment of the septum,
with or without nasal bone fracture; usually nasal fractures are simple, or comminuted,
rather than compound.
MALES - nasal fracture is most often associated with intentional trauma and is clearly
more common in the 15-30 year old age group.
®FEMALES - there was noted a bimodal distribution with a peak in the 15-25 year age
group and a second rise in the elderly; nasal trauma is usually the result of personal
injury, most commonly the result of falls.
- when considered collectively, most adult nasal fractures can be attributed to
altercations and sporting injuries, with a lesser number resulting from motor vehicle
accidents, falls, and miscellaneous causes. ‘
- the number of fractures from a specific etiology varies according to the makeup and
locality of the study population, with alcohol often having a contributory role.
eCHILDREN - a clear gender predilection for injury is less likely, although cases are more
often reported in males; also, more cases of nasal trauma in children are the result of
accidental injury related to sports and play rather than physical confrontation; it is
important to note, however, that anywhere from 30-50% of all pediatric victims of abuse
present with maxillofacial injury, particularly when evaluating the possibility of fracture
concealed by the presence of facial edema.
*INFANTS - occasionally, during birth the nose is fractured in the birth canal; such
fracture is usually of the greenstick type, and the nose inclines a little to one side.
PATHOGENESIS - because of its prominent position, central location, and the low
breaking strength of its skeletal support, the nose is particularly susceptible to fracture;
the pattern and extent of the fracture varies as a function of the site, direction, and
intensity of the impact, as well as nasal bone density.
PATHOPHYSIOLOGY - variables such as force, impact direction, nature of the striking
object, patient age, and other factors will influence the pattern of injury to both the bony
and cartilaginous components of the nose; younger adults often suffer the dislocation of
major segments, whereas older individuals tend to have more comminution of brittle,
osteopenic nasal bones.
- children, on the other hand, have more cartilaginous injuries and greenstick fractures
because of the greater proportion of nasal cartilage and the incomplete ossification of
nasal bones.
“combination of the projection of the nose and its relatively fragile supporting structures
compared with other facial bones make it particularly susceptible to fracture; the thinner
nasal bone below the intercanthal line, which projects more prominently from the face, is
fractured much more easily than the thicker bone of the nasal root above the line; lateral
forces may produce an ipsilateral depressed fracture, or they may outfracture the
opposite nasal bone, thereby resulting in significant deviation of the entire nose; athough
lateral forces are a more frequent cause of nasal injuries, deviated fractures can occur
from either frontal or laterally directed impacts as well.
- the cartilaginous portions of the external nose are able to absorb a greater amount of
force without fracture compared with the bony components, but they are still susceptible

28
to injury given their greater exposure; avulsion and dislocation of the upper lateral
cartilage (ULC) from the nasal bone and septum will result in a hollowed-out appearance
of the midportion of the nose; this injury may also tear the external nasal artery as it exits
between the nasal bone and ULC, thereby causing a dorsal hematoma; In cases of severe
frontal trauma, reduction of nasal projection and increased nasal tip rotation are
indicative of fracture and of telescoping of the cartilaginous portions of the anterior nose
and caudal septum.
= STRUCTURES INVOLVED IN INJURIES TO THE NOSE
*Frontal process of the superior maxilla «Nasal bones «Septum
MAIN CAUSES - isolated nasal bone fractures are usually the result of low-velocity
trauma; alcohol consumption being an important contributing factor in many cases
*ASSAULT - most common
*PERSONAL ACCIDENTS - falls
*SPORTS INJURIES *ROAD MISHAPS
SIGNS OF NASAL BONE FRACTURE - all external manifestations may be masked by severe
soft tissue edema especially in a patient seen a few hours after injury.
*SWELLING OF THE NOSE - continues to evolve and increases over the next 24 to 48
hours after injury.
*STEPDOWN DEFORMITY - depression or displacement of the nasal bones
*NASAL PAIN, TENDERNESS AND AIR FLUCTUATION
*DISPLACEMENT OF THE BONY DORSUM TO THE RIGHT WITH DEPRESSION OF THE
LEFT NASAL BONE (secondary to a "right hook" fist cuff injury)
*PERIORBITAL EDEMA *ECCHYMOSIS
*LACERATION OF THE DORSUM
<TYPES OF NASAL BONE FRACTURES
*CLASS | FRACTURE - fracture along the quadrilateral cartilage and the distal thin portion
of the nasal bone; usually caused by low-velocity trauma directed from a frontal or
frontolateral direction.
*CLASS II FRACTURE - fracture line involves the nasal bones, the frontal process of the
maxilla as well as the structures involved in a class | fracture; usually the result of a
medium velocity trauma directed laterally.
*CLASS III FRACTURE - fracture lines extend through the ethmoid labyrinth with resultant
telescoping inward of the nasal skeleton giving a "pig-nose" appearance.
TYPES OF SEPTAL CARTILAGE FRACTURES
*FRACTURE OF JARJAVAY - runs in a horizontal direction parallel with the maxillary crest
from the maxillary spine to the vomer and results from trauma directed onto the dorsum
of the nose.
*FRACTURE OF CHEVALLET - runs from the maxillary spine to the nasal bones and
results from lateral trauma.
- fractures and dislocations of the septum may occur independently or concomitantly
with fractures of the distal nasal bone framework; most commonly, the two injuries occur
together, but frontal impact nasal fractures carry the worst prognosis regarding
preservation of nasal height with closed reduction techniques; because of the intimate
association of the bones of the nose with the nasal cartilages and bony nasal septum, it
is unusual to observe fractures of either structure without damage to the other; in
particular, the caudal or cartilaginous portion of the septum is almost always injured in
nasal fractures.
- septal injury is one of the most crucial elements of nasal deformity and dysfunction; the
thinnest portions of the septum that tend to fracture most readily are located around the
superior septal angle, the central dorsal area of the quadrangular cartilage, and the
posterior portion of the perpendicular ethmoid plate; cadaver studies found that both

29
frontal and lateral forcos produced a consistent C-shaped fracture through tho
cartilaginous septum and perpendicular plate.
- failure to reduce these septal fractures has been shown to be responsible for many
cases of decreased nasal projection and lateral deviation found after unsuccessful
attempts at closed reduction.
- transmitted impact forces from the nasal bones and ULCs can also result in septal
dislocation of the maxillary crest, thus further destabilizing overlying structures and
aggravating airway obstruction; incomplete fracture of the septal cartilage was
hypothesized by Fry to cause the release of “interlocked stress” within the cartilage,
which leads to further deformity.
- a broad method of categorization is based on the direction of the impact force; lateral
type injuries, which are more common, tend to have less severe damage and a better
prognosis than the frontal types; lateral forces account for the majority of nasal fractures
and produce a wide variation of deformities, depending on the age of the patient, intensity
and vector of force; younger patients tend to have fracture dislocations of larger
segments, whereas older patients with more dense, brittle bone often exhibit
comminution.
- Stranc and Robertson developed a classification system using these two main groups,
with further breakdown of the frontal type into three different planes determined by the
depth of injury from the nasal tip; each successive plane is associated with a higher
likelihood of residual deformity after reduction.
- anteroposterior blows result in posterior displacement of the nose into the nasal cavity
and may occur with or without lateral impact; they also occur in three degrees of severity.
with any nasal fracture of significance, the septum “telescopes”, losing height, and the
nasal bridge drops; violent blows result in multiple fractures of the nasal bones, frontal
processes of the maxilla, lacrimal bones, septal cartilages, and the ethmoidal areas.
PLANE 1 INJURY - where the distal portion of the nasal bones are involved; a direct
force of moderate intensity from the lateral side may fracture only one nasal bone with
displacement into the nasal cavity; it includes damage to the anterior nasal spine, the
anterior septum, or the lower ends of the nasal bones; dislocation and telescoping of the
ULCs and septum may also be found.
¢PLANE 2 INJURY - where the entire nasal bones and dorsal septum are involved; when
forces are of increased intensity, some displacement of the contralateral nasal bone
occurs and the fracture may be incomplete or greensticked requiring completion of the
contralateral fracture to centralize the nasal processes; it results in more extensive
damage to the nasal bones and ascending maxillary process but does not involve the
orbital rims; the septum has a significant amount of deviation and may lack stability to
support the nasal dorsum.
*PLANE 3 INJURY- where the comminution extends beyond the nose into the frontal
processes of the maxilla; again, the latter injuries are true nasoethmoidal-orbital
fractures.
- in more severe frontal impact injuries, the frontal process of the maxilla may begin to
fracture and may be depressed posteriorly on one side; this depression first arises at the
pyriform aperture inferiorly and then involves the entire structure of the frontal process
of the maxilla, and is in effect the first stage of a heminasoethmoidal fracture, displaced
inferiorly and posteriorly; these fractures are “greensticked” or almost undisplaced at the
internal angular process of the frontal bone; the sidewall of the nose drops on one side,
the septum telescopes and displaces, and the nasal airway is effectively closed on the
ipsilateral side by the sidewall and turbinate impacting toward the septum blocking the
airway; in stronger blows, the septum begins to collapse from an anteroposterior
perspective as the comminution increases; patients with this injury are usually found to

30
have other midface and cranial base fractures, and the nasal bones and septum are
severely comminuted and overlapped.
- surgery for plane 3 injuries often is unable to fully restore the preexisting nasal
appearance and function, particularly if the orbital-ethmoid complex components of the
injury are not recognized and treated prooerly.
*PHYSICAL EXAMINATION - grasping the dorsum between two fingers and rocking the
pyramid back and forth aids in assessing the mobility of nasal bones; internal structures
should be evaluated by using a headlight and nasal speculum; clotted blood is removed
by suction, and assessment of hematoma, mucosal tears and active bleeding is
performed; bimanual palpation of the septum helps to differentiate septal swelling from
hematoma.
*RADIOLOGY
Soft tissue lateral »Water’s view »Caldwell’s view
*THREE-DIMENSIONAL CT - is recommended for extensive injuries involving the nasal-
orbital-ethmoidal complex.
= TREATMENT - nasal fractures are reduced by closed reduction; in moderate or severe
frontal impact fractures where loss of nasal height and length occur (plane II or plane Ill
nasoethmoidal orbital fractures), open reduction and primary bone or cartilage grafting
may be the only way to restore the support of the nose and return it to its original volume
and shape, filling the soft tissue envelope with new cartilage support and preventing soft
tissue contracture.
- in severe nasal injury (i.e. plane II nasal injury), open reduction with bone or cartilage
grafting to restore nasal height may be required; semi-closed reductions with limited
incisions using K wires to attempt to stabilize the nasal bones are less effective and
accurate; internal splinting of the septum should be part of the treatment plan (Doyle
splints); some nasal fractures are sufficiently dislocated that they can only be stabilized
with an open rhinoplasty reduction and bone or cartilage grafts.
- the nasal septum should be straightened and repositioned as soon after the injury as
possible; fractures of the nasal bones and septum frequently occur simultaneously, and
it is important to ensure that at the time of reduction the nasal bones and septum
fragments can be freely deviated in both lateral directions to ensure completion of partial
or “greensticked” fractures; incomplete fractures create early recurrence of
displacement by causing the nasal bones and septum to “spring” back toward their
original deviated position; when nasal bones are reduced, their intimate relationship with
the upper and lower lateral cartilages tends to reduce the upper septal cartilage as well
unless the cartilages are torn or avulsed from their attachments; displacement of the
cartilaginous septum out of the vomerine groove will not be reduced with nasal bone
reduction alone and must be done manually with an Asch forcep, and the septal
fragments maintained in position with an intranasal (Doyle) splint; in cases where the
septum has been dislocated from the anterior nasal spine, the septum should be reunited
by suture or wire fixation to the spine; septal hematomas should be aspirated and
minimized by transfixation sutures through and through the mucosa.
- when nasal fractures are treated late after the injury, it may not be possible to obtain the
desired result with a closed reduction or with a single operation; healing may make the
reduction of the displaced or overlapped fragments impossible without osteotomy at
each area of previous fracture by open rhinoplasty, septal resection and repositioning,
and/or bone or cartilage grafting; some advocate acute septal open reductions, where
telescoped portions of the septum are resected creating additional mucosal and cartilage
injury and causing further loss of nasal height; septal reconstruction procedures are
generally best performed secondarily; all patients with nasal fractures should be warned
that a late rhinoplasty is expected for correcting deviation, irregularity, loss of nasal

31
height, or nasal airway obstruction.
*TREATMENT OF BLEEDING
*NON-DISPLACED FRACTURES - should be treated with observation alone.
*REDUCTION - the aims of reduction of nasal fractures are to obtaina satisfactory airway
and to restore the original appearance of the nose.
®TIMING OF REDUCTION - fibrous connective tissue within the fracture line develops
around 10 days to 2 weeks after injury; manipulation should be performed before this
point; a short delay period of 2-3 days is also recommended to allow for diminishment of
swelling.
™CLOSED REDUCTION - may be best performed before edema prevents accurate
palpation and visual inspection to confirm the reduction, and before partial healing or
fibrosis limits the effectiveness of reduction; in practice, closed reduction of most nasal
fractures is frequently deferred 5-7 days until the edema has partially subsided and the
accuracy of the reduction may again be confirmed by visual inspection and palpation;
after two weeks, it becomes more difficult to reduce a nasal fracture, as partial healing in
malalignment has occurred; the soft tissue shrinks to accommodate the reduced skeletal
volume, making anatomic reduction more difficult; it must be done either under local or
general anesthesia; it is the best choice for
"Fractures that are non-comminuted =Unilateral
"Mild to moderate medial displacement =Recent fracture
- 70-90% of patients are satisfied after closed reduction of the nasal fracture; 3% require
secondary corrective treatment.
LOCAL ANESTHESIA - topical anesthesia with cotton pledgets soaked with 4% cocaine or
0.05% oxymetazoline combined with 4% lidocaine should be applied for 5-10 mins; local
anesthesia should also be injected (1% lidocaine and 1:100,000 epinephrine) along the
septum, lateral walls and floor of the nasal cavity.
PROCEDURE - the nasal bones are grasped between 2 fingers, and pressure is applied
laterally in the opposite direction of the deviation; in the case of a significant medial
collapse, a nasal elevator is used to elevate the nasal bone; outward pressure against the
bone moves it into position; a finger on the outer surface of the nose directs and controls
the positioning of the fragment; forceful thumb pressure is applied to the deflected nasal
pyramid until the deviated nose is returned to the midline.
- an Asche forcep is used to straighten the deviated septum; closed septal reduction can
be done by introducing both legs of an Asche forcep on both sides of the nasal septum;
the deviation is grasped and the septum is lifted using the arms of the forceps to push
the pieces back into realignment; it may be necessary to reduce severely impacted nasal
bones with a Walsham’s forceps, one blade placed intranasally and the other
extranasally.
- in children, the facial skeleton heals so fast that fracture must be reduced within 4-5
days to avoid malunion; if treated within 5-6 days after injury, a nasal fracture can be
reduced easily, thereafter reduction may be difficult.
CORRECTED IF
sHear bony click =aSymmetrical =Functional
®OPEN REDUCTION AND INTERNAL FIXATION
#Comminuted fractures =Bilateral
"Failed closed reduction =Depressed fracture
DELAYED REDUCTION (6 months or more)- of persistent deformities using standard
techniques of rhinoplasty.
*NASAL PACKING - should be placed for 3-5 days to prevent collapse of the post
reduction framework.
*SEPTUM SPLINTS - are recommended in comminuted septal fractures with severe

32
mucosal lesions.
*EXTERNAL NASAL SPLINTS - are applied for 10 days to either protect the nose or
maintain reduction or both; the external dressing may be prefabricated of aluminum or
from thermolabile plastic, plaster of Paris, or dental stent material.
NASAL SALINE SPRAYS - prevent crusting.
SYSTEMIC ANTIBIOTICS
Gross tissue disruption ® Open reduction
» Prolonged internal nasal dressing » Septal splints
= COMPLICATIONS
*SEPTAL HEMATOMA - is a collection of blood beneath the mucoperichondrium or
mucoperiosteum of the septum as a result of trauma; while uncommon, may result in
subperichondrial fibrosis and thickening with partial nasal airway obstruction; the
septum in these cases may be as thick as 1 cm in areas and may require trimming; in the
case of repeated trauma, the cartilages of the septum may be largely replaced with
calcified or chondrified material; submucous resection of thickened portions of the nasal
septum may be required, and in many patients turbinate outfracture, or partial resection
of enlarged turbinates, may simultaneously be advisable.
*SYNECHIAE - may form between the septum and the turbinates in areas where soft
tissue lacerations occur and the tissues are in contact; these may be treated by division
and placement of a Doyle splint between the cut surfaces for a period of 10-14 days.
*OBSTRUCTION OF THE NASAL VESTIBULE - may occur as a result of malunited
fractures of the pyriform margin, especially if displaced and telescoped medially, or from
overlap or lateral displacement of the nasal septum into the ipsilateral airway; osteotomy
of the bone fragments can correct displaced fractures; however, contracture due to
shrinkage or loss of soft tissue lining may require excision of the scar and replacement
with mucosal or composite grafts within the nasal vestibule or in some cases flap
reconstruction.
*RESIDUAL OSTEITIS OR INFECTION OF THE BONE OR CARTILAGE - is occasionally
seen in compound fractures of the nose; these conditions are usually treated by repeated
conservative debridements until the infected focus is completely removed; secondary
soft tissue grafting may restore absent tissue; chronic pain is infrequent and usually
affects the external nasal branches of the trigeminal nerve.
*MALUNION OF NASAL FRACTURES - is common after closed reductions, since the
exact anatomic position of the bone fragments is difficult to confirm or achieve by
palpation alone, and the presence of closed splinting may not prevent recurrent deviation
owing to the release of “interlocked stresses” in cartilage; any external or internal
deformity of significance may require a corrective rhinoplasty.
eSEPTAL ABSCESS *SADDLE NOSE DEFORMITY
*SEPTAL DEVIATION - especially along the nasal floor, produces varying degrees of
nasal obstruction depending upon the severity of deflection into the nasal cavity; the
caudal end of the septum may be deflected into the nasal vestibule, causing obstruction
or external deformity; nasal septoplasty through a caudal submucoperichondrial incision
is used to reconstruct and straighten the septum.
*SEPTAL PERFORATION - secondary to fracture of the cribriform plate, the roof of the
ethmoid sinus, the posterior table of the frontal sinus, or the sphenoid sinus; septal
perforations are repaired only if:
»%Complicated by persistent epistaxis ® Crusting with nasal obstruction
®Whistling
*CSF LEAK - fractures of the nasal bones, nasoethmoidal region, and frontal region may
occur in association with a dural defect and cerebrospinal fluid rhinorrhea; this provides
a potential route for ascending infection and meningitis; the dural defect may

33
communicate with the nasal cavity via the ethmoidal, frontal, or sphenoidal sinuses or
the cribriform plate; a basilar skull fracture with an intact tympanic membrane may also
present with cerebrospinal fluid rhinorrhea.
- the diagnosis should be suspected upon finding watery rhinorrhea with an increased
glucose content and may be confirmed by thin-section coronal CT following
subarachnoid instillation of metrizamide by intrathecal injection.
™TREATMENT - acute posttraumatic CSF rhinorrhea is treated conservatively with bed
rest in the semisitting position, fluid restriction, lumbar drainage, and diuretics for 5-7
days; the patient should avoid straining, blowing the nose, sneezing, or vigorous
coughing.
» INDICATIONS FOR SURGERY
=Persistent CSF leakage of more than 6 weeks duration
=Recurrent meningitis
=Pneumoencephalos or intermittent leak
<= COMMON ERRORS IN TREATMENT
*The physical attempts to set a nose that was fractured many years previously; the patient
becomes aware of the deformity only when new trauma calls attention to the nose.
X-ray films or a CT scan may reveal no fracture, when there actually is one present; the
clinical judgment is much more important.
*The patient waits too long to reduce the fracture.
*The physician regards an easy-to-reduce fracture too seriously (gives general
anesthesia) or a severe fracture too lightly (treats in the office rather than in the hospital).
*Secondary injuries to the septum may be overlooked.
B. MANDIBULAR FRACTURE
- it is the 2nd most common fracture of the facial skeleton and the 10th most fractured
bone in the whole body; it most commonly occurs due to motor vehicle accidents and
physical confrontations; they are often multiple.
- the area of the mandible that fractures is determined by the interaction of the nature of
the external force and the anatomic predisposition of the mandible to fracture at specific
locations; a fracture may occur directly under the point of impact, or the force may be
transmitted indirectly across the mandible to create a contralateral fracture; a blow to the
body usually will cause an ipsilateral body fracture through the mental foramen (a
naturally weak area) and either a contralateral angle fracture or a subcondylar fracture.
- the presence of a tooth at the angle seems to favor a fracture of the angle, and an
unerupted third molar creates an even more favorable condition for fracture to occur;
ramus fractures occur much less frequently than condylar, angle, and body fractures,
most likely because of the reinforcing ridges that naturally transmit forces through the
ramus to the condylar neck and also because of the muscle sling that envelopes the
ramus and cushions direct blows; impacts centered over the lower anterior alveolar ridge
may cause alveolar fractures, leaving the lower incisors floating in the fragment of bone;
posterior alveolar fractures are less common because of the longer, more stable posterior
tooth roots and because of the increased amount of spongy bone in the posterior
alveolus to absorb fracture forces.
- loss of tongue support and significant swelling of the floor of the mouth may occur in
patients with bilateral (“bucket handle”) or comminuted fractures of the mandible.
- the mechanism of injury often determines the site of potential fracture in patients with
trauma to the mandible; motor vehicle collisions and falls tend to cause fractures of the
condyles and symphysis because the force is directed towards the chin, whereas
assaults tend to produce injuries to the body or angle of the mandible at the point of
impact; patients with parasymphyseal fractures resulting from falls, often have an
associated fracture in the opposite subcondylar region.

34
*VELOCITY - of the impact force also is a factor.
LOW VELOCITY BLOW - to the mandibular body usually causes a body fracture with
little or no displacement at the point of contact and a contralateral subcondylar fracture.
®HIGH VELOCITY BLOW - may cause a displaced, comminuted fracture at the point of
impact but not a contralateral fracture.
*MODERATE BLOW - to the symphysis may cause a parasymphaseal fracture or bilateral
condylar fractures.
*VIOLENT BLOW - to the chin may create a flail mandible with a fracture of the
symphyseal or parasymphyseal area combined with either bilateral angle or subcondylar
fractures; this type of condylar fracture actually is a safety mechanism that prevents the
condylar head from being driven into the middle cranial fossa or through the tympanic
plate into the external auditory canal.
*DISPLACEMENT OF THE MANDIBULAR FRAGMENTS -also is influenced greatly by two
closely related factors.
Muscle pull Direction of angulation of the fracture line.
MECHANISM OF INJURY
*DIRECT BLOW TO THE BODY 3 IPSILATERAL BODY FRACTURE AND
CONTRALATERAL ANGLE OR SUBCONDYLAR FRACTURE
SYMPHYSIS > PARASYMPHYSEAL OR BILATERAL CONDYLE
CONDYLAR FRACTURES - protective mechanism to prevent condyle from being driven
into the middle cranial fossa
*ALVEOLAR FRACTURE - very light blows to lower anterior alveolar ridge
SITES COMMONLY FRACTURED
*ANGLE - junction of the thin ramus and thick body
«NECK OF THE CONDYLE
*BODY/ALVEOLAR RIDGE (weak) - alveolar portion
= CLASSIFICATION OF MANDIBULAR FRACTURES
1. ACCORDING TO CHARACTERISTICS
SIMPLE - when both the external skin and oral mucosa are intact
eCOMPOUND (OPEN) - when a laceration in the skin or intraoral mucosa is present.
*GREENSTICK FRACTURE - if the fracture is incomplete and involves only one cortex.
*COMMINUTED MANDIBULAR FRACTURE - is one with several fragments of bone
2. ACCORDUNG TO ANATOMIC LOCATION
*SYMPHYSEAL - at the midline of the mandible
*PARASYMPHYSEAL - on either side of the midline proximal to the mental foramen
*BODY - at the junction of the body and ramus
*CORONOID PROCESS -a fracture above the base of the sigmoid notch affecting the
coronoid process
*CONDYLAR AREA
*BODY *ANGLE
*SUBCONDYLAR *CORONAL PROCESS
- fractures of the coronoid and condylar processes often must be diagnosed from a
palpable localized hematoma or point tenderness; fractures of the body, angle, and
symphysis account for approximately 60% of mandibular fractures.
3. ACCORDING TO DENTITION
*DENTULOUS
*EDENTULOUS - the accuracy in approximation is not as critical ina jaw without teeth as
in the exacting task of establishing the preinjury occlusion of the dentulous mandible;
a denture can compensate for minor irregularities in the edentulous jaw.
*PEDIATRIC - is important because of the vulnerability of the unerupted dentition and the
conical shape of the teeth, which do not hold a wire ligature well.

35
4. ACCORDING TO THE STABILITY OF THE FRACTURE
FAVORABLE - muscles attached to the mandible tend to draw the broken fragments
toward one another helping to keep them in proper alignment.
*UNFAVORABLE - when the muscles attached to the mandible tend to pull the fragments
away from each other; unfavorable fractures need definitive open reduction more
commonly than favorable fractures.
SIGNS AND SYMPTOMS
*MALOCCLUSION - open bite deformity
eHYPOSTHESIA OF LOWER LIP AND GINGIVA - damaged inferior alveolar nerve
*ASSYMETRY OF MANDIBULAR ARCH (Step-Discontinuity)
PAIN AND TENDERNESS OVER THE FRACTURE - this pain is intensified by mandibular
movement.
*EAR PAIN - as a result of the mandibular condyles traumatizing the anterior wall of the
ear canal with the transmission of the force from an inferior to a superior direction when
there has been an inferior blow to the mandible.
*AIRWAY OBSTRUCTION - due to hemorrhage either from the floor of the mouth or from
a disruption in the bony support structure for the tongue.
*TRISMUS *LOOSE DENTITION
eINTRAORAL LACERATIONS OVER MANDIBLE *SUBLINGUAL HEMATOMA
*MUCOSAL DISRUPTION *BONE DEFORMITY
eLIMITATION OF MOTION eCREPITUS
*UNDUE MOBILITY OF THE FRACTURE SEGMENT
- careful intraoral inspection and palpation are important; initial evaluation includes
examination for fractures of the teeth and assessment both by inquiry and by direct
examination of the patient's dental occlusion.
= DIAGNOSIS
eORAL EXAMINATION - is mandatory since clinical signs indicating fractures of the
maxilla and mandible are often reflected in intraoral changes that are not obscured by
general facial swelling.
®COLEMAN’S SIGN - sublingual hematoma is highly suggestive of a mandibular fracture
® GINGIVAL LACERATION
BLOWER JAW- is suggestive of a mandibular fracture
sUPPER JAW - is suggestive of a segmental maxillary fracture.
®PALATAL BRUISING - indicates either a split palate or Le Fort fracture
®GROSS DEFORMITY OF THE MANDIBLE
® DISORDERS OF OCCLUSION
FANTERIOR OPEN BITE - either bilateral mandibular condyle fracture or a posteriorly
displaced Le Fort fracture
#LATERAL OPEN BITE - the patient’s teeth meet normally on one side, but on the
opposite side there is no contact; the most common cause for this is a mandibular
condylar fracture on the contralateral side to the open bite.
*ACTIVE RANGE OF MOVEMENT - normal mandibular opening is 35-45 mm; reduced
mandibular opening is not a reliable indicator of mandibular fracture, since it can be
secondary to soft tissue injuries and effusions of the temporomandibular joint; a more
accurate clinical sign is the amount of protrusion of the mandible.
*OBLIQUE VIEW - provides the exposure. needed to evaluate the symphyseal and
parasymphyseal regions.
*MODIFIED TOWN’S VIEW
*MANDIBULAR PANOREX RADIOGRAPHS - provide excellent views of all portions of the
mandible except the symphyseal and parasymphyseal regions.
*COMPUTED TOMOGRAPHY - for evaluating the position of facial bones in patients with

36
multiple facial fractures.
= TREATMENT- mandibular fractures can be treated conservatively if they are undisplaced:
patients have to be compliant and able to tolerate a strictly liquid/soft diet for 4 weeks.
- they need careful monitoring to check for failure of treatment that is usually heralded
by a change in occlusion or increasing pain.
eINDICATIONS FOR TREATMENT
® Displaced fracture with abnormal occlusion
®Unresolving pain from undisplaced fracture
*GOALS OF MANAGEMENT
® Restore preinjury occlusion
®Immobilize the mandible for sufficient period of time for healing
®% Maintain adequate nutrition
*AVOID INFECTION, MALUNION OR NONUNION -- it is essential to re-establish the
patient's dental occlusion, mastication, speech, and facial form.
*CLOSED REDUCTION - involves the application of Erich arch bars to teeth and applying
elastic bands for intermaxillary fixation; fixation lasts 5-8 weeks.
® Minimally displaced fracture » Favorable fracture
®Condylar fracture ®» Alveolar fracture
®For temporizing prior to definitive management
*OPEN REDUCTION - use of arch bars and elastic bands is coordinated with open
reduction and interosseus wiring; fracture segments immobilized using circumferential
wiring or metal plates; for edentulous patients an occlusal splint is applied.
- it is essential that there is adequate reduction of the bony fragments particularly at the
level of the teeth so that a normal occlusion is returned; small discrepancies in bony
reduction can be tolerated but even small discrepancies in the dental occlusion should
not be accepted.
® Unfavorable fracture Incomplete or poor dentition
®Laceration near fracture line » Failure of closed reduction
® Multiple fracture/comminuted
Fractures that are unstable, unfavorably aligned, or free floating
eANTIBIOTICS - penicillin being the drug of choice, should be given to nearly all
mandibular fracture patients because the mandibular mucoperiosteum is so closely
applied to the mandible that 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.
*ELASTIC FIGURE-OF-EIGHT BANDAGE ABOUT THE HEAD
®To support the mandible ® Reduce pain
® Stabilize the fractured fragments
*PROPER ALIMENTATION *ORAL HYGIENE
= COMPLICATIONS
*Excessive mobility *Nonunion
*Poor approximation of the fracture eMalocclusion
*Ankylosis or damage to the TMJ
C. ZYGOMATIC FRACTURE -a fracture of the zygomatic arch alone is common; the
zygoma is a major buttress of the midfacial skeleton; it forms the malar eminence, giving
prominence to the cheek, and forms the lateral and inferior portions of the orbit; the
zygomatic bone has a quadrilateral shape with several processes that extend to reach
the frontal bone, the maxilla, the temporal bone (zygomatic arch), and orbital processes.
- it is the third most frequently occurring fracture of the facial bone, with 85% of fractures
occurring in men; the zygoma may be injured independently or together with a maxillary
fracture; injuries that produce zygoma fractures usually involve a blow to the body of the

37
zygoma or "malar" prominence.
- although the zygoma is a sturdy bone, it is frequently injured because of its prominent
location; moderately severe blows are absorbed at the malar eminence and transferred
to its buttresses; severe blows may cause separation of the zygomatic body at its
articulating surfaces; these high-energy injuries dramatically increase the width of the
midface; as the zygoma is disrupted, it is usually displaced in a downward, medial, and
posterior direction, whereas high-energy injuries displace the zygoma in a posterior and
lateral direction because of disruption of the ligaments in addition to the fractures; the
direction of displacement varies with the direction of the injuring force and with the pull
of the muscles, such as that of the masseter.
- periorbital and subconjunctival hematomas are the most accurate physical signs of the
orbital fracture always associated with a complete zygoma fracture; numbness of the
infraorbital nerve is a common symptom as well; the infraorbital nerve runs in a groove
in the posterior portion of the orbit and enters a canal in the anterior third of the orbit,
behind the infraorbital rim; it may be crushed in a rim fracture with medial displacement,
as the fracture occurs in the weak area of bone penetrated by the infraorbital foramen;
direct force to the lateral face may result in isolated fractures of the temporal extension
of the zygoma (zygomatic arch) and the zygomatic process of the temporal bone in the
absence of a fracture of the remainder of the zygoma and its articulations.
- medial displacement of an isolated arch fracture is usually observed and may impinge
against the temporalis muscle and coronoid process of the mandible resulting in
restricted mandibular motion; fractures in the posterior portion of the zygomatic arch
may enter the glenoid fossa and produce stiffness or a change in occlusion because of
the swelling in the joint or muscles.
= TYPES
*TYPE 1 - simple fracture of the arch
*TYPE 2 - trimalar or tripod fracture - involves all 3 suture lines, all three arms are
fractured and the areas depressed.
ePALPABLE DEFORMITY (STEP DEFORMITY) Of THE INFRAORBITAL RIM
eDIPLOPIA ON UPWARD GAZE
*ANESTHESIA-HYPOSTHESIA - may be secondary to injury of
™® Zygomaticotemporal branch of CN V ®Infraorbital nerve
*FLATTENING OF THE LATERAL ASPECT OF THE CHEEK - occasionally only the
zygomatic arch is fractured with a depression of the lateral temporal region.
*TRISMUS
Fractured zygoma impinges on the coronoid process of the mandible
® Entrapment of the temporalis muscle
*LOCALIZED PAIN *PERIORBITAL ECCHYMOSIS
eUNILATERAL EPISTAXIS e*UNILATERAL SUBCONJUNCTIVAL HEMORRHAGE
*INFERIOR DISPLACEMENT OF THE OCULAR GLOBE
TREATMENT - if the fracture is undisplaced, there is no cosmetic problem and if the
infraorbital nerve is undamaged, no further active treatment is required.
- repair of fractures of the zygoma may be delayed for 5-7 days to allow for resolution of
edema, which facilitates the necessary exposures of fracture lines, as will the use of
preoperative steroids to reduce intraoperative edema; the repair should not be delayed
more than 10 days because the masseter muscle begins to shorten after this time, making
elevation of the zygoma more difficult; if extreme difficulty is encountered in mobilizing
the zygoma to its correct position even with the extended access approaches, the
masseter muscle can be detached from the zygoma and the arch; this often is necessary
in those patients not treated within the recommended 5-7 days.

38
- this maneuver should not have long-term effects on jaw mobility or masticatory function
but the additional soft-tissue trauma and subsequent scarring may cause accentuation
of the prominence of the reconstructed arch: accurate draping of the soft tissues over
the reconstructed arch helps to lessen this; simultaneous upward traction on the skin
flap and incised temporal fascia allows for a tight closure that holds the periosteum in
correct position over the arch and zygoma.
REDUCTION TECHNIQUES
*GILLIS TECHNIQUE - make a small incision above the fracture (and 1 cm above the
hairline) to insert an elevator under the temporalis fascia and pry the depressed fragment
upward.
*LATERAL ORBITAL APPROACH - incision is deep to the temporalis fascia with insertion
pnder the zygoma; unstable fractures may require wire fixation of the lateral orbit and rim
racture.
*KEENE INCISION - an intraoral incision can be made and the zygomatic arch is elevated
inferiorly through the mouth; zygomatic arch fractures often snap into position, and only
infrequently is packing necessary to hold the fragments laterally.
= PITFALLS IN THE MANAGEMENT OF ZYGOMATIC FRACTURES
*Failure to diagnose because of ecchymosis and edema
*Failure to appreciate fractures of the maxilla or floor of the orbit.
D. ORBITAL FLOOR FRACTURE (BLOWOUT FRACTURE)
- it is usually the result of direct frontal trauma; it may result from blunt trauma to the
orbit; it is characterized by dehiscence of the bone, herniation of orbital contents and,
possibly, entrapment of the muscles; the weakest part of the bony orbit is found in the
posterior ‘% of the floor, immediately anterior to the orbital fissure; included in the
downward herniation usually are the inferior rectus and inferior oblique muscles, and if
the periorbita is torn, orbital fat escapes into the maxillary sinus as well; within the
maxillary sinus, blood, bone fragments and orbital contents are found.
<= MECHANISM OF INJURY - it results from a force striking the soft tissues; the impact of the
force is on the lids and globe, and the orbital contents are retropulsed; with the sudden
increase in the intraorbital pressure, the thin portion of the orbital floor and/or medial wall
is fractured; if the rim of the orbit is spared, then this is a pure blowout fracture.
- following the application of non-penetrating trauma to the orbit there may be sufficiently
increased intraorbital pressure to cause a herniation of the orbital contents downward
through the fractured bony orbital floor into the maxillary sinus.
*DIPLOPIA - may result from incarceration of the inferior rectus in the fracture line, but
the vision is little affected by the injury.
*ENOPHTHALMOS - because of the 2 muscles involved (inferior rectus and the inferior
oblique), vertical rotation of the eye is greatly impeded and varying degrees of
enophthalmos are noted.
«LIMITATION OF EOM - upward gaze
*INFRAORBITAL HYPOSTHESIA - anesthesia or hyposthesia of the area supplied by the
infraorbital nerve suggests an injury to the nerve as it passes through the infraorbital
canal.
*PUPILLARY MISALIGNMENT *PERIORBITAL ECCHYMOSIS
*ORBITAL EMPHYSEMA *EPISTAXIS
*STEPLADDER DEFORMITY
= X-RAYS
*WATER'S VIEW - may show the downward herniation of the orbital contents.
*CALDWELL'S VIEW - usually shows a cloudy maxillary sinus because of hematoma.
TEARDROP SIGN - herniation of fat into the maxillary sinus; later there is haziness due to

39
bleeding into the sinus.
= INDICATIONS FOR SURGERY
*ENOPHTHALMOS *DIPLOPIA
X-RAY EVIDENCE OF FRACTURE
MANAGEMENT - OPEN REDUCTION
- correction of this requires exploration of the orbit and reconstitution of the floor, usually
with silastic to prevent a recurrence of the herniation; if this is not achieved, early
necrosis of the fat occurs with permanent enophthalmos; if there is entrapment of the
intraorbital muscles, the inferior rectus muscle is physically grasped and rotated.
*LOW LID INCISION - lift up periosteum and orbital fat; if there is a big gap, a sheet of
silastic or the septal cartilage is placed after lifting up the orbital contents.
eCALDWELL-LUC APPROACH - a pack, balloon or thin silastic implant is placed in the
maxillary sinus to support the orbital floor.
E. MAXILLARY FRACTURE
- it usually results from severe direct trauma; in the Philippines, fractures of the midface
are usually the result of a violent force to the face during fistfights or brawls rather than
automobile accidents; the history of the injury and direction of the blow are helpful in
evaluation the force required to fracture the maxilla and pterygoid plates of the sphenoid,
which are the two fractured bones common to all Le Fort fractures, is considerable; the
degree and direction of fracture displacement depends upon the degree, direction and
point of impact of forces.
= CLASSIFICATION
LE FORTS CLASSIFICATION OF MAXILLARY FRACTURES - resulted from Le Fort's observation
that the facial skeleton fractures in a stereotypical pattern when low velocity blows are
sustained.
*LE FORT | FRACTURE (ALVEOLAR FRACTURE, HORIZONTAL MAXILLARY
FRACTURE), GUERIN FRACTURE - occurs above the level of the maxillary dentition,
separating the alveoli and teeth from the remaining craniofacial skeleton; it crosses the
nasal septum, and posteriorly it completes the fractures through the posterior maxillary
walls and pterygoid plates.
- dental malocclusion is usually present; the fracture extends through the lateral nasal
wall and pyriform aperture, across the maxillary alveolus and antral walls to the pterygoid
plates; these injuries generally result from anterior forces directed to the lower midface.
- it results from forces directed horizontally and low into the anterior face of the maxilla
above the dentition; this results in a horizontal maxillary fracture above the dentition; it
separates the lower alveolar and palatal regions from the upper maxilla, which results in
a mobile palate, but a stable upper midface; the palate is separated from the rest of the
maxilla (horizontal separation); it is quite uncommon to sustain this fracture alone.
eLE FORT Il FRACTURE (PYRAMIDAL FRACTURE) - is the result of more severe trauma;-
it starts on one side at the zygomaticomaxillary buttress and crosses the face in a
superomedial direction; it fractures the inferior orbital rim and orbital floor, traverses the
medial orbit, crosses the midline at the nasal root or through the nasal bones, and then
travels inferolaterally across the contralateral side of the facial skeleton, creating a
pyramid-shaped inferior facial segment separated from the remaining craniofacial
skeleton is
- like the Le Fort I, it fractures the nasal septum, the posterior maxillary walls, and the
pterygoid plates.
- it is a triangular fracture to the palate and middle 3rd of the face, including the nasal
bone but excluding the zygoma; the palate with the maxilla is separated from the zygoma
and the ethmoids (midfacial fracture); all Le Fort Il fractures cross the nasal septum and
pterygoid plates.

40
- it is the most common of maxillary fractures; it is characterized by mobility of the palate
and nose as well as significant epistaxis
*LE FORT Ill FRACTURE (CRANIOFACIAL DYSJUNCTION, COMPLETE CRANIOFACIAL
SEPARATION) - occurs at the level of the skull base, separating the zygomas from the
temporal bones and frontal bones, crossing the lateral orbits and medial orbits, and
reaching the midline at the nasofrontal junction, also violating the nasal septum and
pterygoid plates.
- itis the result of severe frontal violence and is often fatal; it results in separation of the
mid and lower face from the rest of the cranium; it is usually the result of forces to the
nasal bridge or upper maxilla; they separate the zygoma from the temporal and frontal
bones, extending through the lateral and medial orbital walls, and crosses the nasion or
nasal bones to the contralateral side.
- itis the most severe Injury and involves complete disruption of the attachments of the
facial skeleton (the maxilla, nasal bone, and zygoma) to the cranium; the zygoma are
Separated from the cranium passing through the fronto-ethmoid and the frontozygomatic
sutures; the entire zygomaticomaxillary complex may be mobile and displaced.
= DIAGNOSIS - may be difficult; in clinical practice, Le Fort fractures are commonly found
in combination; edema rapidly obscures all visual landmarks, the face may be elongated,
and occlusion may be disrupted by the trauma; there is often extensive ecchymosis about
the eyes.
X- RAY VIEWS
«Waters view °Caldwell view
eSubmental vertex view eLateral view
- X-rays of the mandible should be taken if there is any doubt because mandibular
fractures are sometimes associated with maxillary fractures.
LE FORT!
*Malocclusion and an anterior open-bite deformity
*Hematomas and parietal fractures in maxillary sinuses
*Airway compromise can occur if the palate retrusion is severe
LE FORT I
Moderate dislocation *Midfacial depression °CSF leakage
LE FORT II
¢lmmediately after trauma, typical symptoms of facial tumefaction
*Hematoma *Bleeding Shock
*Commotion or cerebral contusion
*Loss of vision secondary to intraorbital hemorrhage or to direct optic nerve lesion.
*Complete craniofacial dislocations, often associated with neurosurgical injuries
*CSF leakage *Significant orbital trauma
= TREATMENT - surgical repair after stabilization of the patient.
eLE FORT |
> INTERMAXILLARY FIXATION
=Direct wiring to the pyriform aperture
#Suspension with circumzygomatic wires
®REATTACHMENT OF THE ALVEOLUS 5,
®Interdental wiring =Dentures =Plating
eLE FORT Il
® Exploration of the intraorbital rim
® Stabilization of any rim fracture
- this is best accomplished using gauge-26 wire ligatures; wiring of the infraorbital rim,
stabilization of the nose, and interdental fixation to stabilize the maxilla are required; in

41
the absence of dentures, dental splints may be required.
eLE FORT Ill
®Interosseus wiring of the frontal zygomatic fracture as well as the infraorbital rim
fracture
®The inferior maxilla must be suspended by means of the unfractured portion of the
frontal bone near the frontozygomatic suture line using a pullout wire coming through
the skin
™»The zygoma must be suspended from the frontal bones by wiring or plating into
position
®The alveolus is supported by fixation to the cranium by suspension wires or plates.
- the use of mini plates has frequently replaced suspension devices; these plates tend to
solidify the maxillary fracture segments and obviate the need for suspension; Kirschner
wires can be used to fix the upper jaw to a solid zygoma, or the maxilla can be suspended
by subcutaneous wires attached to the orbital rim or frontal bone; temporary dentures
attached to the palate or mandible can be wired to one another to maintain reduction.
SYSTEMIC ANTIBIOTICS - with penicillin as the drug of choice is necessary because most
maxillary fractures are compound.
F. FRONTAL SINUS FRACTURES - are relatively uncommon; direct frontal trauma of
adequate force may depress the outer table; if this is an isolated fracture with no other
involvement and no consequent frontal sinusitis, the fragments may be left alone; direct
inspection is usually necessary to adequately assess the posterior wall or inner table of
the sinus; the importance of adequate reduction of the broken fragments in this area is
prevention of CSF fluid leakage and subsequent meningitis.
Vv. DHARYNGEAL FOREIEN BODIES

- foreign bodies in the airway are commonly seen in the pediatric population; one case
series over a 20-year period reported that 75% of patients with foreign bodies to the
airway were younger than 9 years; peak incidence of aspiration is in the second year of
life, with a dramatic decline after age 3; the peak incidence of aspiration in adults occurs
in the elderly population.
*MOST COMMON FOREIGN BODIES IN THE MOUTH AND PHARYNX
®Fish bones Bone spicules Toothbrush bristles
®Pieces of toothpick Pieces of metal » Opercula of snails
® Fractured, broken, avulsed teeth
® Dental apparatus
®ITEMS INTENDED FOR THE GASTROINTESTINAL SYSTEM
=Meats Medications
®ITEMS THAT WERE TEMPORARILY PLACED AND HELD IN THE PATIENT’S MOUTH
=Pins =Needles
eJewelry "Thermometers
ITEMS BEING EXPLORED BY YOUNG TODDLERS
=#Small toys
®FOOD
i. Hot dogs (17%) ii. Candy (10%)
iii. Nuts (9%) iv. Grapes (8%)
= COMMON SITES
*COMMON LOCATIONS OF SMALL FOREIGN BODIES
»Tonsil » Base of the tongue
»Vallecular, or lateral wall of the pharynx
Ex. small pointed foreign bodies such as splinters of bone, fish bones, bristles from a
toothbrush, needles, nails, or bits of wood and glass

42
*COMMON LOCATIONS OF LARGER FOREIGN BODIES
Piriform sinus ® Hypopharynx
- thet often impact in these locations before entering the esophagus.
Ex. bits of toys, flat bones, coins, buttons, large fish bones, bits of false teeth
*SMOOTH ROUND OR OVOID OBJECTS
» Opening to the esophagus ® Cricopharyngeus muscle
*IRREGULAR FOREIGN BODIES
® Lingual or palatine tonsils » Base of the tongue
»Pyriform sinuses »Vallecul6a
= SIGNS AND SYPTOMS
*PAIN - is of varying severity, which is worse on swallowing, and swallowing may be
completely obstructed
*DYSPHAGIA *ODYNOPHAGIA *APHAGIA
*DROOLING - is a characteristic sign in a young child or infant.
WHEN THERE IS COMPRESSION OF THE LARYNX OR TRACHEA
DYSPNEA WHEEZING » PERSISTENT COUGH
- foreign bodies to the throat may present acutely with respiratory distress; the fact that
the incidence peaks in the very young and very old may help explain delays in diagnosis
for subacute cases, as specific and reliable indicators of airway foreign body presence
are often elusive; patients with foreign bodies to the throat may present acutely with the
need for immediate airway stabilization; those patients who are stable likely have a partial
airway obstruction and great care must be taken to avoid converting a patent airway to a
complete obstruction with diagnostic or therapeutic maneuvers.
ESOPHAGUS IS PENETRATED BY A SHARP OBJECT - such as a pin or fish bone, subcutaneous
emphysema can be palpated in the neck; foreign bodies lodging more distally in the
esophagus such as at the level of the aortic arch, left main bronchus, or
gastroesophageal junction generally do not produce early symptoms.
= DIAGNOSIS
CHEST X-RAY
*RADIOGR APHY - a swallow is performed with a contrast medium using a colorless
medium, not barium, which will not influence assessment of the mucosa at subsequent
endoscopy.
eAP AND LATERAL NECK FILMS «DIRECT INSPECTION *ENDOSCOPY
*INDIRECT LARYNGOSCOPY - should be done if not found by direct inspection.
*DIRECT LARYNGOSCOPY - may be necessary sometimes.
*X-RAY STUDIES - are mandatory if no foreign body is found and the patient still
complains of foreign body sensation in the throat when he swallows.
TREATMENT - instrumental extraction of the foreign body is performed as quickly as
possible, due to the danger of pressure necrosis or mucosal injury, causing abscess or
mediastinitis; foreign bodies of the palatine and lingual tonsils are removed directly with
a curved hemostat; objects located in the hypopharynx or esophagus require direct
laryngoscopy or esophagoscopy under general anesthesia.
- foreign bodies to the throat can be approached in various ways depending on various
factors.
FACTORS TO CONSIDER: fs
*ls the patient is stable or unstable?
*What is the anatomic location of the object (proximal or distal airway)?
¢What are the possible etiologies of the foreign body (based on age pediatric or elderly)?
*Airway: stable or unstable

43
VI. TRACHEOSTOMY
- it consists of making an opening in the anterior wall of the trachea for purposes of
establishing an airway to the lungs, bypassing the upper airway.
TRACHEOTOMY - refers to the incision made in the trachea.
= INDICATIONS
*Conditions causing upper airway obstruction
*Conditions necessitating protection of the tracheobronchial tree
Conditions causing respiratory failure.
— CRITERIA FOR PERFORMING TRACHEOSTOMY - tracheostomy should be carried out as an
elective procedure and not as a desperate last resort; there are degrees of urgency:
*lf the patient has life-threatening airway obstruction when first seen, it is obvious that
urgent treatment is required; if endotracheal intubation fails, tracheostomy must be done
at once; if there is no time for sterility - with the left hand, hold the trachea on either side
to immobilize it, make a vertical incision through the tissues of the neck into the trachea
and twist the blade through 90° to open up the trachea; there will be copious dark
bleeding but the patient will gasp air through the opening; using the index finger of the
left hand as a guide in the wound, try to insert some sort of tube into the trachea.
- the blood should then be sucked out by whatever means are available; once an airway
is established, the tracheostomy can be tidied up under more controlled conditions.
«In patients with airway obstruction of more gradual onset, do not allow the situation to
deteriorate to that described above; stridor, recession and tachycardia denote the need
for intervention, and cyanosis and bradycardia indicate that you are running out of time.
- the ideal is to carry out tracheostomy under general anaesthesia with endotracheal
intubation; once a tube has been inserted, the airway is safe and the tracheostomy can
be performed calmly and carefully with full sterile precautions; if the anaesthetist is
unable to intubate the patient, it will be necessary to perform the operation under local
anaesthesia using infiltration with lignocaine; the anaesthetist meanwhile will administer
oxygen through a face-mask.
*Elective tracheostomy should be carried out before deterioration occurs in non-
obstructive cases as listed above and patients who have previously been intubated
because of obstruction or for ventilation but who cannot be extubated safely; such
elective tracheostomy cases are ideal for trainees to learn the technique of the operation
safely under supervision and every such opportunity should be taken.
= INDICATIONS
*Elective tracheostomy may be necessary when respiratory problems are anticipated in
the postoperative period in patients being subjected to major head and neck thoracic
operations or in patients with chronic pulmonary insufficiency.
*Rarely, it may be indicated in patients in whom orotracheal intubation is difficult or
impossible for purposes of inducing general anesthesia.
*Tracheostomy should also be performed as a preliminary measure in operations for
oropharyngeal or laryngeal neoplasms to avoid unnecessary manipulation of the tumor.
°A tracheotomy should be considered for airway control whenever prolonged airway
intubation is anticipated.
*Therapeutic tracheostomy is indicated inzany case of respiratory insufficiency due to
alveolar hypoventilation in order to bypass obstruction, to remove secretions or to
provide for the use of mechanical artificial respiration.
*Patients with a decreased ability to clear secretions, ineffective ventilation or both.
= CONTRAINDICATION - in patients with obstructing carcinoma of the larynx because there
is some evidence that tracheostomy performed more than 48 hours before a definitive
surgical procedure leads to an increased incidence of stomal recurrence.
<TECHNIQUE - whenever possible, endotracheal intubation should be performed before

44
therapeutic tracheostomy.
*POSITION - the patient is positioned on his back with a pillow well under the shoulders
to allow maximal extension of the neck.
*ANESTHESIA - is unnecessary in unconscious patients; a local anesthetic is usually all
that is necessary in conscious patients, including children; local anesthesia is obtained
by infiltrating the skin in the line of the incision and depositing the agent in the deeper
midline tissues to the level of the anterior tracheal wall; lidocaine (xylocaine) 1%, with
epinephrine 1:150,000 is a satisfactory agent.
- the subcutaneous tissue is infiltrated with lidocaine and 1:100,000- epinephrine.
*INCISION - a horizontal skin incision should be used whenever possible; the incision is
made 5 cm long, approximately 2 finger-breadths above the sternal notch; it is at least 2
inches long and reaches the medial border of each sternocleidomastoid muscle; once
the skin incision is through the platysma muscle, the dissectlon is done vertically, staying
in the midline, using sharp blunt dissection with scissors and hemostat.
- the tracheal incision should never extend above the second tracheal ring to prevent the
tracheostomy tube from impinging on the cricoid cartilage and producing perichondritis;
in the average adult female, size No. 6 or No. 7 tube suffices, and in the male No.7 or No.
8 tubes are used.

y
OF L
NEOP S
HEA
THEA D M NECK
AND S
1. BENIGN TUMORS OF THE EXTERNAL EAR .
A. ACTINIC KERATOSIS (AK) (SOLAR KERATOSIS, SENILE KERATOSIS) - is a sun-
induced premalignant lesion. It appears as an erythematous patch of skin thay is often
raised from the surrounding healthy skin. It tends to have a flat top with a sandpaper
texture. .
- they are the most common epithelial precancerous lesions. Although lesions typically
appear in persons over age 50, it may occur in the twenties or thirties in patients who live
in areas of high solar irradiation and have fair skin. Patients have a propensity for the
development of nonmelanoma cutaneous malignancies.
- they are most often found in fair-skinned individuals, but can be seen in all races. Over
80% of AKs occur in sites with the most cumulative sun exposure, e.g. the bald scalp,
superior helices of the ears, face, dorsal hands, extensor forearms
- they have historically been characterized as being “precancerous” or “premalignant”
because the atypical keratinocytes within these lesions are confined to the epidermis.
There is no risk of metastasis until these lesions evolve into invasive carcinoma. The
likelihood of an invasive SCC evolving from a given AK has been estimated to occur at a
rate of 0.075-0.096% per lesion per year.
RISK FACTORS
¢Skin phototypes | and II «Increasing age
*Significant cumulative sun exposure *lmmunosuppression
¢Prior history of AKs *Male gender
= ETIOLOGY - cumulative exposure to sunlight appears to be important in the etiology.
Intermittent, intense ultraviolet (UV) exposure in childhood, manifest as sunburn, is also
strongly associated with the prevalence of actinic keratoses. It has been regarded as an
occupational and environmental disorder. It can also develop in lesions of vitiligo. Work
has demonstrated that Betapapillomavirus infection in combination with key risk factors
increases the risk of actinic keratoses. Abnormalities in DNA synthesis in keratinocytes
in the skin around the lesion suggest that there is a gradual stepwise progression from
sun-damaged epidermis to clinically obvious keratoses and eventually to squamous cell
carcinoma.
CLINICAL MANIFESTATIONS - the primary lesion is a rough erythematous papule with
white to yellow scale. Patients may report tenderness. AKs can range in size from a few
millimeters to large confluent patches several centimeters in diameter, especially in
patients with severe photodamage.
- one of the earliest signs is slight erythema with almost imperceptible scale, although
some lesions are devoid of visible erythema and present only as slight scale with
indistinct borders. A clue to their presence’ is background photodamage, i.e.
dyspigmentation, telangiectasia and solar elastosis.
- advanced lesions are typically thicker and well-defined with more visible hyperkeratosis
and erythema. Lesions typically are clustered in areas of highest cumulative sun
exposure, such as the superior helices of the ears, upper forehead, supraorbital ridge,
nasal bridge, malar eminences, dorsal hands, extensor forearms, shins, and the bald
scalp.
- AK may remit, or remain unchanged for many years. It has been stated that 8-20%
gradually transform into SCC if left untreated. The hyperplastic variant appears to have a
relatively high rate of malignant transformation, with a risk of up to 0.53% per lesion in
patients with non-melanoma skin cancer.

2
of single lesions after
- clinically, AKS may spontaneously regress. Rates of regression
1 year range from 15 to 63%, but a portion of these regressed lesions recur 1 year after.
lesion has
- tenderness on palpation should alert the clinician to the possibility that the
evolved into carcinoma.
CLINICAL SUBTYPES OF AKS
* HYPERTROPHIC OR HYPERKERATOTIC - papules and plaques with scale or scale-crust
and an erythematous base which often extends beyond the overlying hyperkeratosis. The
hyperkeratotic scale can become white or yellow-brown over \ime. Due to their thickness,
patients often find these lesions to be bothersome. ;
*PIGMENTED - often lacks associated erythema and has a hyperpigmented or reticulated
appearance.
*LICHENOID - is characterized histopathologically by the presence of a dense band-like
inflammatory infiltrate. Clinically, this lesion is similar to the classic form of AK but has
more erythema surrounding the base of the lesion. Patients may relate pruritus or
tenderness that coincides with the onset of the lichenoid infiltrate in a pre-existing AK.
*ATROPHIC - usually have minimal surface change but are appreciated as pink to red,
slightly scaly macules or patches that are found by histopathologic examination to have
an atrophic epidermis.
*ACTINIC CHEILITIS - used to describe the characteristic changes that occur on the lower
vermilion lip of individuals with moderate to severe photodamage. It may resemble the
classic form of AK, with well-demarcated, erythematous papules or thin plaques with
scales. In other patients, the erythema and especially the scale is more diffuse and
caninvolve the entire lower vermilion lip; areas of leukoplakia may also be present. The
potential for evolving into invasive SCC is higher for actinic cheilitis than for classic AKs.
*BOWENOID - when small foci of full-thickness atypia occur within a lesion that otherwise
has the characteristic features of an AK.
<= TREATMENT- because some percentage of actinic keratoses will progress to NMSC, their
treatment is indicated. There are many effective therapeutic modalities.
*CRYOTHERAPY WITH LIQUID NITROGEN - is by far the most commonly employed
therapeutic modality because it can be performed quickly and effectively in the office
setting. It is most effective and practical when there are a limited number of lesions.
™COTTON-TPPPED APPLICATOR METHOD - the liquid nitrogen into which the
applicator is dipped should be used for only one patient, because there is a risk of cross-
contamination from one patient to another. Infectious agents are not killed by freezing.
® HANDHELD NITROGEN SPRAY DEVICE - use a small-opening tip with continuous
bursts of nitrogen spray in a circular motion, depending on the size of the lesion,
attempting an even frosting. Only the lesion should be frosted, and the duration of
cryotherapy must be carefully controlled. A long freeze that results in significant
epidermal-dermal injury produces white scars, which are easily seen on the fair skin of
those at risk for actinic keratoses.
- when correctly performed, healing usually occurs within 1 week on the face. It is better
on the first visit to “undertreat” until the tolerance of a patient's skin to cryotherapy is
known. Application of 0.5% 5-FU for 1 week before cryotherapy improves the response.
@FREEZE TIME IS < 5SECS = 39% complete response rate
=FREEZE TIME IS > 5 SECS = 69% response rate
=FREEZE TIME IS > 20 SECS = 83% response rate
- with 20-sec freeze times, there is considerably more hypopigmentation as sequelae.
Therefore freeze times should be based upon size and thickness of the lesion as well as
location.
*TOPICAL AGENTS - individual lesions may be poorly defined and involve large,
contiguous areas requiring field treatment with topical agents.

ADVANTAGES OF TOPICAL APPROACHES
» Patient-administered » Non-invasive
» Carry little risk of scarring or pigmentary change
»Can be used for anatomically difficult or cosmetically sensitive areas.
panied by
- these agents require adequate patient compliance and are often accom
prolonged erythema lasting several weeks. .
TOPICAL CHEMOTHERAPY - recommended tor extensive, broad, or numerous lesions. Any
lesion that could represent an NMSC should be biopsied before beginning topical
chemotherapy or photodynamic therapy (PDT) for actinic keratoses. The most commonly
used topical agents are 5-FU cream and Imiquinod cream.
- topical tretinoin and adapalene do not have the efficacy of these two agents but can be
used for prolonged periods and represent an option for patients with a few early lesions.
They are also useful for pretreatment of hyperkeratotic lesions before a course of 5-FU.
3% diclofenac in 2.5% hyaluronan gel can be effective when used for 60 days.
- topical resiquimod and ingenol mebutate are newer topical therapeutic options and
trichloracetic acid peels may still be useful in some patients. The inflammatory reaction
with these agents parallels efficacy, but some data suggest a trend toward less irritation
without diminished efficacy if dimethicone lotion is applied before ingenol mebutate.
- the frequency and duration of treatment are determined by the individual's reaction and
the anatomic site of application
»5-FLUOROURACIL (5-FU) CREAM 0.5%-5% - is applied once daily in most cases. For
the face, 0.5% 5-FU gives a slightly less severe response than that produced by the 1%—
5% concentrations. Some patients prefer the stronger concentration for a briefer period,
while others favor a slower onset of the reaction and a more prolonged course. For the
5% cream, treatment duration rarely needs to exceed 2-3 weeks. For the 0.5% cream, the
treatment course is typically 3-6 weeks. Usually, the central face will respond more
briskly than the temples and forehead, which may require a longer duration of treatment.
- treatment is stopped when a peak response occurs, characterized by a change in color
from bright to dusky red, reepithelialization, and crust formation. Healing usually occurs
within another 2 weeks of stopping treatment, depending on the treatment site.
- pretreatment with tretinoin for 2-3 weeks can improve efficacy and shorten the duration
of subsequent 5-FU treatment. It has been observed that 5-FU “seeks out” lesions that
may not be clinically apparent. The use of topical 5-FU to the face can also reverse
photoaging. Clinically inapparent BCCs may be detected during or on completion of the
treatment.
®IMIQUIMOD 5% CREAM - has recently been shown to have high rates of treatment
success with durable results and has become an accepted first-line therapy. It is an
interferon (IFN) inducer and eradicates actinic keratoses by producing a local
immunologic reaction against the lesions.
- about 80% of patients respond to imiquimod, and 20% may not respond at all, perhaps
because that they lack some genetic component required to induce an inflammatory
cascade when imiquimod is applied. If it is applied three times a week, patients develop
an inflammatory reaction similar to that seen with daily application of 5-FU.
- the median percentage reduction in actinic keratoses is 83.3% with this treatment
protocol. Overall, although the reaction is less predictable with imiquimod, it is also
typically less severe than with high-concentration 5-FU.
- another regimen is to apply imiquimod for long periods at a reduced frequency, once or
twice weekly. Applications can be in alternating 1-month cycles or continuous for many
months. This may allow management of some patients who require treatment but cannot
tolerate any significant changes in appearance. Ultimately, the choice between topical 5-

4
FU and imiquimod will be based on patient preference, prior physician and patient
experience with the modalities, and the cost.
- Imiquimod is significantly more expensive per gram than any form of 5-FU. A meta-
analysis comparing efficacy studies of the two agents dosed in various concentrations
and regimens suggested imiquimod may have higher efficacy for actinic keratosis onthe
face and scalp. A recent Cochrane review concluded that 5-FU, imiquimod, ingenol
mebutate, and diclofenac are similarly efficacious but have different adverse events and
cosmetic outcomes.
*|INGENOL MEBUTATE - novel agent derived from the Euphorbia peplus plant has been
approved as an additional topical agent for the field treatment of AKs.
*PHOTODYNAMIC THERAPY (PDT) WITH AMINOLEVULINIC ACID (ALA) OR METHYL
AMINOLEVULINATe (MAL) - has continued to become more widespread, given its proven
therapeutic results and excellent cosmetic outcome. PDT offers a physician-administered
approach to field treatment with shorter periods of inflammation and erythema than
several topical agents, and thus many studies indicate higher patient satisfaction.
Variations in the light dose, light source, sensitizing agent and its application time, and
frequency of treatments may improve efficacy
- recently, there has been a growing trend towards combination therapy , such as topical
agents either before or after cryotherapy, or sequential use of multiple topical modalities
with varying mechanisms of action.
*OTHER APPROACHES - may be considered in certain situations when lesions have
failed the above treatments, or if severe photodamage is present.
®LASER RESURFACING »DERMABRASION
®CHEMICAL PEELS - 30% trichloroacetic acid
*RECALCITRANT OR HYPERKERATOTIC LESIONS
®» CURETTAGE » EXCISION
PREVENTION - is an important aspect of management This has been shown to prevent
the development of new AKs and reduce the incidence of non-melanoma skin cancers.
eSUN AVOIDANCE LOW FAT DIET
*DILIGENT USE OF BROAD SPECTRUM SUNSCREENS AND SUN BLOCKING AGENTS
B. KERATOACANTHOMAS (KAs) - are considered by some to be a variant of SCC and
by others to represent benign tumors (i.e. pseudomalignancy). It is a rapidly growing
tumor that can grow from a 1-mm flesh-colored papule to a 2.5-cm nodule with a keratin-
filled central crater in 3 to 8 weeks. Rapid growth with involution within 2 to 6 months
is
the hallmark of this lesion. Not all KAs will involute, however, and the
duration of
involution is unpredictable. Involution may take up to a year and may
produce scarring,
so observation is rarely suggested anymore. Most lesions occur on the head
and neck or
in sun-exposed areas of the extremities, with or without symptoms of pain
or tenderness.
Approximately 10% of these tumors appear on the pinna.
= PATHOGENESIS - the exact pathogenesis is unknown; however, the tumor has a
keratinocyte derived cell origin. There is more evidence for the keratinocytes
derived
from hair follicle epitheqdlium as the primary cells responsible
for the formation of this
tumor. They have an increased incidence in patients with chronic
ultraviolet exposure
and in the chronically immunosuppressed. This peculiar tumor of keratinocytes has
follicular features, and its growth pattern may indicate an evolution from hair follicles,
although a viral etiology is the most accepted theory.
- the reason that some of these tumors Ghdergo autoinvolution
is unknown.
There is
evidence to suggest that the tumors, like hair follicles,
are under a preset growth and
invoution control system.
= ETIOLOGY - is unknown, but likely results from
sun damage. Men are more commonly
affected than women, and fair-skinned individuals are
at greater risk than those with dark

5
es of life. These tumors are
skin. The peak age of onset is in the fifth to sixth decad
more common in the Caucasian population. .
clinical present ations The stage of
CLINICAL PRESENTATION - there are several distinct several months. The
up to
rapid proliferation is followed by a plateau period lasting .
occur.
incidence of local or regional metastasis is quite low, but can
exposures, immunosuppression,
- multiple KAs have been associated with chemical
.
BRAF inhibitors, and HPV infection.
flesh-co lored papule that rapidly
- the classic solitary keratoacanthoma starts as a small,
over
enlarges to form a crateriform nodule with a central keratin plug. It grows rapidly
to a month, culminating in an exophytic nodule that on
the course of a few weeks
maximum size in one
appearance may simulate squamous cell carcinoma. It grows to its
to two months. Some patients complain of pruritus within the lesion. Most will only cause
local destruction, but there are few that behave more aggressively.
within
- itis sharply demarcated from the surrounding skin and may have telangiectasias
cm and multiple keratoa canthom as are not
the lesion. They range in size from 1-2.5
The tumor is unique in that, if left alone, the keratoacanthoma will
uncommon
spontaneously involute within 6 months leaving an atrophic scar. Grouped KAs may
resolve more slowly than solitary KAs, while subungual KAs have been associated with
underlying bony destruction.
- the non-classic form does not spontaneously resolve, and it is not advisable to leave
these tumors alone, because a high percentage will continue to enlarge. If left alone, these
tumors can behave aggressively, with local invasion as well as distant metastasis. The
most common area of metastasis is the regional lymph nodes.
= TREATMENT
*COMPLETE SURGICAL EXCISION - the rapid growth can mimic invasive SCC, so
removal of this lesion with adequate depth for histopathologic review is the
recommended treatment. It is done after the keratoacanthoma has been biopsied. This
can be done with a standard elliptical excision or with Mohs micrographic surgery, which
should be considered for tissue sparing and margin control. In a very small percentage
of cases, keratoacanthoma may recur
eINTRALESIONAL 5-FLUORURACIL (0.2 to 0.3mL of 50 mg/MI - weekly for 6 weeks is
effective treatment. Methotrexate and bleomycin are alternatives. These may cause
complete resolution or may just decrease the size of the lesion for easier excision.
eELECTRODESSICATION AND CURETTAGE - may be used for smaller tumors if the site
is not of cosmetic concern.
eINTRALESIONAL METHOTHOTREXATE AND ORAL RETINOIDS - have been used in
refractory cases and in individuals who cannot tolerate surgery. The familial forms of
keratoacanthomas often require long-term retinoid therapy to keep the tumors at bay.
eORAL METHOTREXATE - a single dose of oral methotrexate 0.5 mg/kg may be effective
for patients with multiple KAs.
*RADIATION THERAPY - is efficacious with cosmetic outcome for poor surgical
candidates.
*CRYOTHERAPY
C. OSTEOMAS - are benign neoplasms of bone that occur along the medial bony EAC.
They occur as single large growths and have a smooth appearance. They are often
pedunculated and have a vascular core. They are located at suture lines and result in
lesser degrees of EAC obstruction. They are more common in males.
- they arise from cancellous bone of the EAC’and present as a single, smooth, bony, hard
peduculated tumor. They usually arise from the posterior meatal wall near the outer end
of the bony EAC. They can also occur in other areas where bone is present, such as the
mastoid or middle ear space.

6
h to occlude
SYMPTOMS - they are typically asymptomatic but if they are large enoug
ally removed. A conductive
the ear canal or cause trapping of debris, they can be surgic
betwee n the osteoma and tympanic
hearing loss due to accumulation of keratin and wax
membrane, and recurrent otitis externa.
DIAGNOSIS . .
overlying
*PALPATION - reveals a hard bony mass which is quite tender due to the thin
skin attachments. It is a solitary bony mass covered by normal skin. ;
*CT SCAN - shows the extension of the mass. They have bone marrow on high resolution
Ct imaging. This can distinguish them from exostosis, which have similar bony growths
but do not contain bone marrow.
TREATMENT - surgical removal by drill, avoiding injury to the tympanic membrane,
ossicles and temporomandibular joint. As much skin as possible should be saved.
D. EXOSTOSES - is also called “surfer’s ear.” They are areas of localized new bone
growth in the osseus part of the EAC, usually multiple and bilateral. They are firm, bony,
broad-based lesions composed of lamellar bone originating from the anterior and
posterior canal walls. They are formed by reactive bone formation and have been
associated with thermal irritation. They are the most common tumors of the EAC.
- they look like pearly white, round, or sometimes irregularly shaped growths. They are
very tender to touch during microscopic evaluation. Otherwise, the patient is usually
asymptomatic. There may be multiple growths in the EAC, which can occlude the ear
canal and lead to cerumen impaction and conductive hearing loss. Many times they occur
in clusters. They range from partially occlusive to completely occlusive. As these bony
growths enlarge, they occlude the lumen and can cause trapping of debris and ultimately
hearing loss if large enough to block the lumen of the ear canal entirely.
= ETIOLOGY - they occur with high prevalence in patients with repetitive exposure to cold-
water and cold-wind activities such as swimming,diving, boating and surfing. Typically
occurring after cold water exposure, they can present in the late teenage years in surfers
or cold water swimmers. Exposure to cold temperature is thought to produce a
periosteitis, which seems to cause new bone growth.
=DIAGNOSIS - they appear as discrete, round or ovoid bony tumors, sometimes
pedunculated, or as diffuse bulges of bone covered by very thin, normal skin.
<=SYMPTOMS - most patients are unaware of the lesions until they are incidentally
discovered during otologic examination. While most exostoses are asymptomatic,
occlusion of the EAC with an enlarged lesion may lead to cerumen impaction and external
otitis. Conductive hearing loss may occur secondary to cerumen impaction, or the
accumulation of debris, or a completely obstructing lesion.
TREATMENT - most cases of exostoses require no intervention. However, if there are
multiple lesions impacting hearing capability, surgical excision of the growth is indicated.
A postauricular approach can be employed, depending on the size of the lesions. The
transcanal technique is reserved for smaller exostoses with the TM in clear view. The
preservation of skin flaps speeds healing. A small skin graft may be required to cover the
bone after removal of the exostoses.
- caution must be taken in their removal as part of the exostosis can grow medial to the
TM and come within close approximation to the facial nerve and ossicles.
= COMPLICATIONS OF REMOVAL
*Facial paralysis ¢TM perforation
¢SNHL from the drill contacting the ossicular chain during removal
= PREVENTION - avoiding exposure to cold water may prevent the formation of exostoses.
E. AURAL POLYPS - may arise from the EAC or the middle ear and generally consist of
granulation tissue. Polyps composed of granulation tissue are usually covered by
squamous epithelium, but they still look redder and bleed much more easily than do

7
mucosal polyps. Polyp formation indicates chronicity of infection. Polyps arising from
the EAC heal rapidly after treatment because there is generally no underlying bone
disease. Polyps arising from the middle ear are often secondary to chronic mastoiditis
or chronic otitis media.
SYMPTOMS
*Foul, purulent discharge «Bleeding
«Decreased hearing
= TREATMENT
*REMOVAL OF THE POLYP - is done near its base with a small cup forceps or wire snare
followed by the application of 25-50% silver nitrate.
*ANTIBIOTIC EARDROPS
HE. BENIGN TUMORS OF THE MIDDLE EAR

PARAGANGLIOMA (GLOMUS JUGULARE TUMOR) AND GLOMUS TYMPANICUM -
are very vascular neoplasms that usually arise from the jugular bulb and tympanic plexus,
respectively. Both tumors spread into the middle ear and mastoid. They invade and
destroy the temporal bone, traveling along nerves, arteries and veins. Often, they will
invade through the skull base and have an intracranial intradural invasion.
- the natural history of these tumors is one of slow, progressive growth and gradual
invasion of the jugular foramen and its nerves (CNs IX, X, XI) as well as CNs VII, XII, and
Vill. Glomus jugulare tumors originate from the superior vagal ganglion, while glomus
tympanicum tumors arise from the auricular branch of the vagus nerve. The overall
incidence of CNS invasion is less than 20%. They are the most common tumors arising
in the middle ear.
- glomus tumors are slow-growing in nature and are often large before becoming clinically
evident. There is an average of 3-6 years from time of first symptom to diagnosis.
EPIDEMIOLOGY - they are rare tumors, but they are the second most common tumor
involving the temporal bone, and the most common tumor involving the middle ear.
Glomus tumors most commonly become symptomatic in the fourth decade of life, but
can arise throughout a wide age range. Most occur in Caucasian adults and are 3-6x more
common in women. Approximately 10% of patients will have tumors in multiple locations.
Bilateral glomus jugulare tumors are found in approximately 2% of patients.
HISTOLOGY - the glomus jugulare tumor usually arises in the hypotympanum at the site
of entrance of Jacobson's nerve or from the glomus bodies located in the adventitia of
the dome of the jugular bulb. It is called glomus tympanicum when found on the medial
wall of the middle ear, attached to a tiny arteriole.
*GLOMUS JUGULARE TUMOR
PULSATILE TINNITUS - is the most common presenting symptom.
*» JUGULAR FORAMEN SYNDROME - CNs IX, X, Xl
» Conductive hearing loss »lsolated facial nerve paralysis
® Lower nerve palsies ® Multiple cranial nerve paralysis
*GLOMUS TYMPANICUM
» Pulsatile tinnitus Conductive hearing loss
Facial weakness (CN VII/VIII deficits) ™Vertigo
» Violaceous retrotympanic mass( » Ear fullness
Throbbing pulsating discomfort » Otalgia
& Discharge due to secondary infection Bleeding especially when manipulated
- specific clinical symptoms depend upon the exact location of the tumor, the structures
it invades, and the size. The most common presentation is gradual onset of unilateral
hearing loss, which can be conductive or sensorineural in nature. Patients with hearing

8
loss often also experience dizziness. Pulsatile tinnitus may be present in highly vascular
difficulty
tumors. Lower cranial nerve involvement produces symptoms of hoarseness,
and fasciculation. Cranial
swallowing, aspiration, shoulder weakness, tongue atrophy,
nerve paresis is seen in up to 35% of patients. CN X is invaded most commonly (61%)
followed by CN VII (54%), CN XI (52%), CN IX (48%), and the least commonly CN XIl. Larger
tumors can produce facial weakness and Horner’s syndrome. ;
DIAGNOSIS - examination in the early stages reveals a reddish swelling behind the TM
which, with magnification, may be seen to pulsate. As the tumor enlarges, it causes the
inferior portion of the TM to bulge and finally breaks through to form a smooth dark red
polypoid mass which bleeds easily on manipulation.
*BROWN’S TEST - application of pressure with a pneumatic otoscope causes the tumor
to increase in pulsation as the pressure is raised until sudden blanching occurs after the
systolic pressure is exceeded.
*RADIOGRAPHIC EXAMINATION - is of little value in early cases but as the tumor
advances will reveal the extent of bony destruction.
*CT SCAN WITH CONTRAST - thin-section, high-resolution CT scanning is used to
delineate the extent of involvement of the temporal bone by the tumor. It is the most
useful diagnostic test.
*GADOLINIUM-ENHANCED MRI - helps to characterize the vascular nature of the tumor
which is often heterogenous.
«ANGIOGRAPHY - is used for preoperative assessment of tumors requiring embolization.
In advanced tumors, external carotid angiography and retrograde jugular venography are
helpful in delineating the extent of involvement and determining its blood supply.
= TREATMENT
«CONSERVATIVE TREATMENT
NO TREATMENT - for asymptomatic patients.
RADIOTHERAPY - proposed to slow or stop growth of large lesions when the morbidity
and mortality of the surgical tumor resection would exceed the risk of the tumor itself,
especially in the elderly and individuals in poor health. Unresectable tumors show some
response to radiation therapy.
*SURGERY- is the best modality of treatment.
® Patients who desire complete removal and immediate cure of tumor
® Large and giant tumors
Tumors with brainstem compression or significant intracranial extension
®Tumors with severe vascular encasement
SURGICAL APPROACHES
®TRANSCANAL APPROACH - indicated for glomus tympanicum.
» MASTOID-EXTENDED FACIAL RECESS APPROACH
»INFRATEMPORAL FOSSA APPROACH
*RADIOSURGERY - may have indications for residual tumors after surgical resection, and
for elderly patients with small tumors.
- for extensive tumors, combined surgery and radiotherapy often are indicated.
Radiotherapy causes tumor shrinkage but not eradication and is best combined with
surgical excision of the tumor.
Hl. MALIGNANT TUMORS OF THE EXTERNAL AND MIDDLE EAR

- malignant neoplasms of the auricle are cofmmon. This can be attributed to frequent sun
exposure, particularly in men. The most common malignancies that initially form along
the sun exposed areas of the auricle and then extend into the ear canal. The EAC does
have potential pathways for cancer to spread into adjacent sites. The Fissures of

gland. The
Santorini act as a potential route for cancer to spread inferiorly to the parotid
to the TMJ.
Foramen of Huschke is a medial potential pathway for spread of a tumor
A. CARCINOMA
- carcinoma of the auricle most often has its onset in the 6th or 7th decade
ETIOLOGY
ted
with about 80% occurring in males. Carcinoma of the EAC and middle ear is associa
in 75% with chronic otorrhea.
*Chronic exposure of the skin *Chronic eczema ePrevious radiation of the ear
HISTOLOGIC TYPES
1. SQUAMOUS CELL CARCINOMA (SSS) (EPIDERMOID CARCINOMA) - is a
cutaneous malignancy with the capacity for local destruction along with metastatic
spread. It is the most frequent primary malignant tumor of the temporal bone, accounting
for 60-80% of all malignancies arising from the skin of the EAC or the middle ear cleft. It
is the second most common malignant tumor arising from the sun-exposed sites in older
people, exceeded only by basal cell carcinoma.This type is more common in the
Caucasian population and in older individuals. It is more prevalent in the fifth to eight
decades of life. The incidence of SCC increases with each decade of life. It is definitely
linked to the amount of sun exposure one has had over one’s lifetime. Fair-skinned
individuals are most commonly affected.
- the demographics of SCC are similar to those of AKs, with the majority of SCC occurring
on the head, neck, upper extremities , or shins. In light-skinned populations, the degree
of UV exposure is related to SCC development while chronic irritation or injury can play
a role in all populations. SCC is found more frequently in men (3: 1 male : female) and the
incidence increases significantly after age 60 years . The incidence of SCC has been
rising worldwide in all age groups over the last several decades at an estimated 3-10%
per year. The incidence is about 1:1,000,000. The increase in the incidence of squamous
cell carcinomas is consistent with increased UV exposure. Keratin pearls and prickle
cells are the main differentiation from basal cell carcinoma.
- SCC-associated mortality is higher in whites and older persons, and men have a 3:1
greater SCC mortality rate as compared with women. SCCs located on the ear, lip and
genitalia appear to have a higher risk of death. While melanoma among whites is
responsible for 90% of skin cancer deaths before 50 years of age, in adults over 85 years
of age, the majority of skin cancer deaths are attributable to SCC.
- it may come from the skin of the auricle or may arise in the epithelium of the ear
canal, middle ear, or mastoid. It grows more rapidly and becomes ulcerated. It is
frequently associated with chronic otorrhea. Metastasis is more common than with basal
cell carcinoma.
*PREDISPOSING FACTORS
® Sun exposure Fair skin » Pre-existing lesions
®/mmunosuppression Previous radiation ®Scars and burns
*ETIOLOGIC FACTORS
Local and chronic trauma » Ultraviolet B radiation ®lonizing radiation
=» Chemical exposure ® Chronic ear discharge »® Chronic eczema
® Psoriasis Lupus ™»Tobacco abuse
ePREVENTION
» Protective clothing »UVB-Protective sunscreens
» Avoiding the sun between 10:00 AM and 3:00 P.M.
*PATHOGENESIS - SCC is related to cumulative UV exposure.
eCLINICAL FINDINGS - the appearance of these tumors is variable and includes plaques,
nodules, and ulcerations. These lesions are painless, ulcerative growths that are friable
and prone to bleeding.

10
ePREFERRED LOCALIZATIONS
» Margin of the helix Triangular fossa » Entrance of the EAC
*SYMPTOMS
» Otorrhea » Aural fullness » Bleeding
Itching » Otalgia » Hearing loss
»®»FACIAL PALSY - due to invasion of the Fallopian canal
SYMPTOMS RESULTING FROM TUMOR SPREAD
»Trismus Impairment of mouth opening »Imbalance
»Vertigo » Lower cranial nerve palsy » Headache
«DIAGNOSIS
»OTOSCOPY - presence of a swelling, polyp or papilomatous and ulcerated tumor that
tends to be necrotic and bleeding to touch.
®PUNCH BIOPSY
™»PALPATION OF THE PAROTID GLAND AND CERVICAL LYMPH NODES
CT SCAN AND MRI - may be used to evaluate advanced disease with tumor metastasis
to the adjacent temporal bone and soft-tissue structures of the head and neck.
*TREATMENT- the key to treatment ultimately lies in the prevention of metastasis.
Complete surgical resection with negative margins have dramrticallty improved the
Prognosis, whereas incomplete resection or positive margins portend a much
diminished chance of cure.
™SCC IN SITU
eElectrodessication and curettage =Simple elliptical excision
=5-FU CREAM - is also effective but leads to a higher rate of recurrence than the
traditional surgical methods.
BMOHS SURGICAL TECHNIQUE - is used to treat large areas of SCC
® INVASIVE SCC - should be treated surgically with Mohs surgery.
SMALL, WELL-DIFFERENTIATED SCCs - have been treated successfully with
electrodessication and curettage.
& METASTATIC SCC OF THE SKIN
sAdjunctive radiotherapy =Chemotherapy
HIGHER RISK FOR THE DEVELOPMENT OF METASTATIC DISEASE
*Recurrent SCCs Those larger than 2 cm in diameter
®Those developing in patients taking chronic immunosuppressive medications
CONSERVATIVE THERAPY - radiotherapy may be used in palliative care of patients with
extensive and aggressive tumors. In most cases radiotherapy is used postoperatively.
SURGERY
®»LATERAL TEMPORAL BONE RESECTION - where the EAC is removed “en bloc” with
the tympanic membrane and ossicular chain and tissue lateral to the facial nerve may be
adopted in T1 tumors of the EAC and perhaps T2 tumors in the elderly.
EXTENDED TEMPORAL BONE RESECTION WITH A PAROTIDECTOMY AND A
SUPRAMYOHYOID NECK DISSECTION AND EITHER FREE FLAP OR LOCAL ROTATION
FLAP REPAIR WITH A FULL COURSE OF POSTOPERATIVE RADIOTHERAPY - is the
recommended treatment for squamous cell carcinoma of the temporal bone. An excision
of the pinna and a wide oval of skin around it should be included in the resection. This is
indicated for the management of T2 to T4 EAC lesions and T1 to T4 middle ear cleft
tumors.
LOCAL EXCISION - 95% of squamous cell carcinomas <2cm in size can be
successfully treated with local excision with a surgical margin of at least 6 mm. Auricular
reconstruction may be required for large defects.
LOCAL EXCISION AND POSTOPERATIVE RADIOTHERAPY - for larger lesions radiation
therapy has a role as an adjunctive therapy combined with complete surgical resections.

11
™MOHS SURGICAL TECHNIQUE - refers to complete micrographic excision of the
tumor using intraoperative histopathology to assess for positive margins. This technique
is particularly useful for recurrent lesions, those >2 cm, or those with an aggressive
histology.
COMPLICATIONS .
Cervical lymph nodes invasion » Metastasis » Intracranial extension
*PROGNOSIS - in addition to the patient's age and overall immune status, the prognosis
for squamous cell carcinoma is dependent on the histologic subtype, the size, and the
location of the tumor. A better prognosis is associated with a well-differentiated
histology. The 5-year cure rate for squamous cell carcinomas ranges from 75% to 92%.
2. BASAL CELE CARCINOMA (RODENT ULCER) - is a neoplasm of the non-keratinizing
cells of the basal layer of the epidermis. It arises from the skin of the auricle or from the
external portion of the EAC and comprises 20% of the malignancies of the ear. It is the
least aggressive skin malignancy. It has an extremely low incidence of metastasis, below
0.1%.
- BCC is the most common skin cancer. Men generally have higher rates of BCC than
women (1.5-2:1) and they typically occur later in life. They have a tendency to occur in
fair-skinned persons wiith a history of significant long-term sun exposure. They are most
frequently seen on the sun-exposed areas of the head and neck, most often occurring on
skin with hair. One of the most common sites of occurrence is the periauricular area. They
do not always occur on sun-exposed skin.
- over the last 30 years, it is estimated that incidence rates have risen between 20% and
80%. In the US, a disproportionate increase has been observed in young women. Similar
increases in incidence rates have been noted. Incidence rates for BCC also increase with
age and the median age at diagnosis is 68 years.
- mortality from BCC is quite rare and occurs primarily in imnmunocompromised patients.
Cases of metastatic BCC are more likely from tumors with aggressive histopathologic
patterns (morpheaform, infiltrating, metatypical, basosquamous). Perineural growth, also
referred to as perineural invasion, may be an indicator of aggressive disease . Metastases
often involve regional lymph nodes, lungs, bone, and skin. The mean age at the time of
death is higher than with SCC, and the age-adjusted mortality rate for BCC has been
estimated at 0.12 per 100 000. Mortality risk is related to increasing age, Caucasian race,
and male gender (>2* compared with women).
- basal cell ca of the EAC is rarely the primary site of origin, more frequently the EAC is
invaded by a lesion originating from the auricle. Howeevr, basal cell carcinomas arising
from this area are associated with a worse prognosis, higher rates of mortality from the
disease compared to other locations. Despite aggressive wide local excision, local
recurrences are common.
- usually its appearance is a pigmented nodular lesion, but ulcerative lesions are also
common and difficult to differentiate from squamous cell carcinomaz.It is characterized by
a pearly appearance to the skin lesion with telangiectasias and rolled borders. It is
composed of cords and masses of cells with deeply basophilic nuclei. It usually has an
indolent course, existing for many months before a change in the lesion brings the patient
to the doctor. At this time, the tumor usually will have modified into a squamous cell
tumor.
- they are characterized by their slow-growing locally infiltrative nature and involve the
skin and the subcutaneous adnexal tissue. They extend wide and deep if left untreated,
but rarely metastasize.
- advanced lesions are often present as invasive and ulcerative lesions. Certain
biologically aggressive basal cell carcinomas can be very destructive and involve the
external canal, the auricular cartilage, and even the temporal bone.

12
*RISK FACTORS
ULTRAVIOLET RADIATION - UV exposure is the predominant cause of BCC and
cutaneous SCC. There is, however, a difference in the type of UV exposure. For BCCs,
intermittent intense episodes of UV exposure and sunburns at any age appear to increase
risk, whereas cumulative long-term UV exposure and childhood sunburns increase the
risk for developing SCCs and AKs. .
- sun exposure early in life appears to have a greater influence on subsequent skin
cancer risk than at a later age. For example, individuals born in countries with high
ambient UV radiation such as Australia have significantly higher incidence rates of BCC
and SCC as compared to those with a similar genetic background (e.g. British, northern
Europeans) who migrated to these locales later in life from countries with lower ambient
UV radiation.
- several studies have demonstrated an increased risk for the development of BCCs and
SCCs in those who are exposed to artificial sources of UV radiation. Intentional tanning
has been shown to increase the risk of SCC development and Karagas etal.
demonstrated that any use of tanning devices was associated with odds ratios of 2.5 for
SCC and 1.5 for BCC, even after adjustment for history of sunburns, sunbathing, and sun
posure.
*® Prolonged sun exposure especially with history of sunburn in the past
® Fair pigmentation » Radiation therapy
» Arsenic exposure »Immunosuppression
*PREVENTION
Protective clothing »UVB-Protective sunscreens
® Avoiding the sun between 10:00 AM and 3:00 PM.
eCLINICAL FINDINGS - patients may initially present with ulceration and bleeding. Basal
cell carcinomas of the auricle typically occur on the posterior surface of the pinna and
in the preauricular area. The ulceration is usually hidden by a crust at the center of the
nodule with slightly raised and rolled margins.
eDIAGNOSIS
™»PUNCH BIOPSY
™CT SCAN AND MRI - may be used to evaluate advanced disease with tumor extension
to the adjacent temporal bone and soft-tissue structures of the head and neck.
*TREATMENT
® NONSURGICAL MEASURES
STOPICAL 5-FLUOROURACIL - treatment is employed for 4 weeks.
SRADIATION THERAPY - may be indicated for poor surgical candidates or for
unresectable lesions.
™» SURGICAL MEASURES
=CURETTAGE WITH ELECTRODISSECTION - this technique is operator dependent and is
typically used to excise nodular lesions and desiccate the base.
=CRYOSURGERY - is used for small basal cell carcinomas (<1 cm), with well-defined
borders.
=LOCAL EXCISION - 95% of basal cell carcinomas <2 cm in size can be successfully
treated with local excision with a surgical margin of 2-4 mm. Auricular reconstruction
may be required for large defects.
=MOHS SURGICAL TECHNIQUE - refers to complete micrographic excision of the tumor
using intraoperative histopathology to assess for positive margins. This technique is
particularly useful for recurrent basal cell carcinomas, those >2 cm, or those with an
aggressive histology.
“RADIATION THERAPY

13
*PROGNOSIS - in addition to the patient's age and overall immune status, the
prognosis for basal cell carcinoma is dependent on the histologic subtype, size, and
location of the tumor.
3. ADENOCARCINOMAS - arise from the skin appendages or glandular e lements of
the middle ear. These form masses of cells arranged in alveoli and ducts interspersed
with connective tissue. They grow rapidly and produce frequent metastases by both
lymphogenous and hematogenous routes. They appear to occur equally in men and
women.
«SYMPTOMS
* Hearing loss ® Tinnitus »Vertigo
«SUBTYPE TUMORS
» Low-grade primary adenocarcinoma
® High-grade or adenoid cysrtic casrcinoma of the temporal bone
DIAGNOSIS - the auricular lesion begins as a firm nodule which enlarges at a variable
rate. Erosion of the surface occurs with the formation of a superficial crusted ulcer with
hard rolled edges. Occasionally there will be a pre-existing papilloma or keratotic lesion
which will begin to enlarge and ulcerate. Carcinoma of the canal or middle ear is much
more difficult to diagnose early in its course. Usually associated with chronic infection,
the tumor has a rough red surface which may be mistaken for a granuloma or polyp. Any
case of nonresolving ear infection should be regarded with great suspicion. All
irregularities of the skin surface, granulomas, or polyps must be biopsied when present.
= TREATMENT
*AURICLE - the cure rate is 90%. The tumor is excised with a wide margin of normal
skin (at least 1 cm). The underlying cartilage is removed en bloc with the specimen.
Extensive tumors may require removal of the entire auricle with skin grafting of the
surgical defect. When associated with regional metastasis, resection of the ear is
accompanied by radical neck dissection.
*EXTERNAL AUDITORY CANAL - the cure rate is less than 35%. Wide excision of the
lesion dictates complete removal of the cartilaginous and bony auditory canal by means
of a mastoid approach which removes the canal en bloc without disturbance of the
involved tissue. The surgery is usually supplemented with postoperative radiation.
eMIDDLE EAR - carcinoma involving the middle ear and temporal bone has a poor
prognosis with a cure rate of less than 25 %.
=SURGICAL COMPLICATIONS
eIntracranial hemorrhage ¢Meningitis
¢Brain herniation «Wound infection
B. RHABDOMYOSARCOMA - is the most common tumor involving the EAC in children.
It is a relatively rare form of cancer. It is most common in children ages 1-5, and is also
seen in teenagers aged 15-19, although this is more rare. It is more prevalent around the
EAC, but may also arise from the middle ear. The external ear is thought to be involved
via lateral extension from a middle ear primary tumor in most cases. They appear to be
similar to polyps but cause extensive bony destruction and neurologic deficits, including
facial paralysis.
= SIGNS AND SYMPTOMS - it often appears insidiously with signs and symptoms that often
mimic chronic otitis media
Ear pain eHearing loss
eChronic ear discharge .2Aural polyp or granulation tissue
= DIAGNOSIS - is by biopsy of a hemorrhagic mass.
<=TREATMENT - all children are treated with multimodality therapy with systemic
chemotherapy, used in conjunction with either surgery, radiation therapy or both. Often
the tumor is beyond the bounds of surgical excision before the diagnosis is made.

14
- radiation therapy is made difficult by the surrounding bone which is often lost by
radionecrosis after treatment.
=PROGNOSIS - is poor because of the rapid progress of the lesion. Temporal bone
resection followed by radiation therapy seems to offer the best prognosis.
C. CYSTIC ADENCID EPITHELIOMA (BROOKE'S TUMOR) - is a special form of
carcinoma in which the cell type is thought to be derived from the germinal epithelium
of the hair follicles and/or sweat glands. The lesion is exceedingly rare but may involve
either the auricle or the EAC. Clinically this tumor appears after puberty and is more
common in females. .
—SYMPTOMS - they present as small, painless, slowly enlarging nodules which do not
ulcerate. Metastasis is rare.
= TREATMENT
- adequate surgical resection plus postoperative radiation is the preferred
treatment to date.
= PROGNOSIS - is poor because of insidious progress and recurrence despite seemingly
adequate treatment.
D. MALIGNANT MELANOMA - is one of the few types of cancers that has continued to
increase in incidence over the past century. However, the rate of mortality from melanoma
has dropped, probably as a result of early detection and surgical intervention. It is the
most common cancer in women aged 25 to 30 years.
- auricular melanoma accounts for 1% of all melanomas. The most common site of origin
is the helix (60%) followed by the lobule (25%). Melanomas occuring as a primary tumor
within the EAC are very rare. They often grow to significant thickness hidden within the
ear canal before they are noticed. Consequently, patients often present as an advanced
stage.The average age of presentation for a patient with malignant melanoma is 65-79.
The rate is lower in dark-skinned individuals. There is a lower incidence in women.
= PATHOGENESIS - there is no single gene defect that can explain the development of all
melanomas. The most plausible theory is that a melanocyte within the epidermis is
damaged by some external event, such as ultraviolet exposure, or by some internal event
such as the spontaneous mutation of a key gene in the regulation of cell proliferation or
apoptosis. After this event has occurred, the abnormal melanocyte proliferates with the
epidermis, starting as an in situ variant of melanoma. Approximately 10 % of melanomas
are considered to be an inherited familial form.
RISK FACTORS
¢Family history of melanoma *Prior melanoma or nonmelanoma skin cancer
«Inherited genetic susceptibility
*SUN EXPOSURE - the pattern of sun exposure may also be important; intermittent
intense exposure, rather than chronic sun exposure, may carry a higher risk..
*Artificial exposure to UV radiation by indoor tanning beds
¢Individuals with fair complexion, blond or red hair, blue eye color, and freckles, who
have a tendency to burn rather than tan.
‘Individuals with an increased number of typical or benign moles, atypical moles, or
dysplastic nevi. They are important precursor lesions of melanoma and serve as
markers
for increasing risk.
= PREVENTION - the avoidance of and protection from sun exposure are important in
preventing disease, as is early detection.
CLINICAL FINDINGS - may occur either onthe auricle or in the EAC being
more common
in the former location. Most melanomas involving the ear are present on the helix
and
antihelix.
- melanomas follow a characteristic growth pattern. The tumor
arises de novo from
previously normal skin in approximately 60% of cases and from preexisting
melanocytic

13
nevi in the remaining 40% of cases. There is no gender predilection. It is more common
in the Caucasian population.
- the thickness of the melanoma is critical for prognosis and curability. Therefore,
melanomas of the EAC are considered high risk lesions.
- melanoma has been described using the ABCDE mnemonic: .
A - Asymmetry B - irregular Border C - variation in Color
D - Diameter greater than 6 mm E - Evolving or changing
- these are rough guidelines and are not meant to be used to diagnose melanomas. Some
melanomas have all th ABCDE characteristics, and some have only one or two of them.
- diagnosis should be suspected with a pigmented lesion which begins to increase in
size or changes in color. These lesions may change in size, ulcerate, and bleed. On
presentation, these lesions are painless. A thorough head and neck examination requires
attention to enlarged lymph nodes that may occur with regional spread of disease.
=TYPES
*SUPERFICIAL SPREADING MELANOMA - is the most common variant seen in clinical
practice. It usually manifest as a slowly enlarging, irregularly shaped macule with
variegation in color. If not recognized and removed, it will continue to enlarge and will
eventually develop a vertical component that clinically represents the nodular form of
melanoma.
*NODULAR TYPE - some nodular forms can develop de novo without the preceding
superficial spreading type of melanoma as a precursor lesion. They are often large at the
time of diagnosis. It is believed that at this point it has developed the ability to
metastasize.
*LENTIGO MALIGNA MELANOMA - is most often seen on the face of patients in their fifth
to seventh decades of life, especially in those with a considerable sun exposure history.
This type is difficult to treat and has a propensity for local recurrence. The borders of the
melanoma are ill-defined, and it is often difficult to distinguish the background normal
sun-damaged melanocyte from the tumor cells.
*ACRAL LENTIGINOUS MELANOMA - has long been thought to portend a poor prognosis
because it is often diagnosed later in the course of its development. This form of
melanoma is more commonly seen in the African American population.
= DIAGNOSIS
*EXCISIONAL BIOPSY - is the method of choice.
*CHEST X-RAY - to rule out lung metastases.
e¢LIVER FUNCTION TESTS - to rule out liver metastases.
*CT SCAN AND MRI - have added sensitivity in detecting metastatic disease.
*RADIONUCLIDE BONE SCANS - can be used to diagnose bony metastases.
= TREATMENT
*NONSURGICAL MEASURES
™ ADJUNCTIVE RADIATION THERAPY - may have a role in palliation.
» IMMUNOCHEMOTHERAPY
*SURGICAL TREATMENT - is complete surgical resection when possible with negative
margins, commonly requiring a subtotal or toal temporal bone resection. The regional
lymph nodes should also be addressed with an appropriate level neck dissection.
Postoperative radiation therapy is also prudent in most cases due to the aggressive
nature of the cancer. ia
- the best method is excisional biopsy using a small (1-2 mm) margin of normal
surrounding skin. This allows for the diagnosis and an accurate measurement of the
Breslow depth.
BRESLOW DEPTH - is the distance from the granular cell layer to the base of the tumor. This
depth is considered to be the most important prognostatic indicator for melanoma.

16
® THERAPY IS BASED ON
=Breslow thickness "Presence of ulceration "Mitotic rate of the primary tumor
THE STANDARD OF CARE - is to perform a wide local incision with varying margins of
skin based on the above criteria .
MELANOMA IN SITU - is treated by wide local excision with 5-mm margins.
SENTINEL LYMPH NODE SAMPLING - is becoming routinely performed in the care of
these patients and aids in staging of the disease.
PATIENTS WITH METASTATIC DISEASE TO LOCAL LYMPH NODES ONLY - are offered
a localized lymph node dissection and adjunctive therapy with interferon. Those with
widedpread metastatic disease are given various chemotherapeutic regimens.
- the mortality rate for stage IV melanoma is very poor.
- the extent of excision, including surgical margins, is dependent on the histologic type
and stage of disease, and may include therapeutic and diagnostic regional lymph node
resection, including the resection of portions of the parotid gland and neck lymph nodes.
Since these lesions have a tendency to spread after surgical trauma, biopsy should be
avoided. If the lesion is of short duration, an en bloc excision with wide margins of
normal tissue should be done. If regional lymphatic spread is detected, radical neck
dissection offers a chance of cure in some cases.
=PROGNOSIS - since lymphatic metastasis occurs unpredictably and often early, the
prognosis should be guarded. Frequent follow-up examinations are needed to detect
spread at the earliest possibility.
Tv. BENIGN TUMOR OF THE INNER EAR

A. ACOUSTIC NEUROMA (VESTIBULAR SCHWANNOMA, CERERELLO-PCNTINE
ANGLE TUMOR) - refers to a benign schwannoma of the eighth cranial nerve. Acoustic
neurom-as arise principally from the vestibular division of the nerve. The superior and
inferior divisions are equally affected; intraoperatively, the nerve of origin usually is
difficult to determine. The 1992 National Institutes of Health Consensus Conference
made vestibular schwannoma the official term for these lesions.
- acoustic neuromas are slowly growing neoplasms that originate in the nerve sheath and
consist of schwannoma cells in a collagenous matrix. They typically are circumscribed
and grossly encroach on and displace neural structures without direct invasion.
Consistency varies and ranges from firm and dense to soft with large cystic spaces.
- these lesions usually arise within the internal auditory canal, but they occasionally
develop in the CPA medial to the porus acusticus. Because acoustic neuromas produce
symptoms by exerting pressure on surrounding neurovascular structures, auditory and
vestibular symptoms develop earlier with tumors of the internal auditory canal than with
tumors of the CPA.
- of the 2000 to 3000 acoustic neuromas diagnosed annually in the United States, more
than 95% occur as unilateral and nonhereditary lesions. The remaining acoustic
neuromas are manifestations of the neurofibromatoses, which consist of at least two
distinct genetic disorders.
*NEUROFIBROMATOSIS TYPE 1 (NF1), OR VON RECKLINGHAUSEN DISEASE, - is a
relatively common disorder of autosomal-dominant inheritance with variable penetrance
and an incidence of 1 in 4000 live births. NF1 neuromas occur throughout the body and
arise both intracranially and extracranially from the Schwann cells of any nerve; however,
acoustic neuromas develop in less than 5% of patients, and bilateral acoustic neuroma
is not a part of the syndrome.
*TYPE 2 NEUROFIBROMATOSIS (NF2) - is the central form of the disease, characterized
by bilateral acoustic neuromas in up to 96% of patients. Schwannomas of the other
cranial nerves, meningiomas, and ependymomas also are observed much more

7
commonly in patients with NF2. The precise frequency of NF2 is unknown, but it is far
less frequent than NF1. Acoustic neuromas in NF2 are characterized by an onset early in
life, often before the age of 21 years, as opposed to unilateral lesions, most of which are
diagnosed between the ages of 40 and 60 years. Thus acoustic neuromas that appear
before the age of 30 years mandate particularly close evaluation of the contralateral ear.
- although the acoustic neuromas in NF1 and NF2 resemble the lesions in nonhereditary
acoustic neuromas, they are technically more challenging to remove because of a
tendency to adhere to nearby structures. The clinical presentation of acoustic neuroma
in neurofibromatosis is identical to that of unilateral acoustic neuroma.
- malignant schwannomas may rarely occur. They often are associated with
neurofibromatosis, but they also may occur with solitary schwannomas. Another very
uncommon variant is a pigmented schwannoma.
+ ETIOLOGY/EPIDEMIOLOGY - these lesions are relatively common and account for 8% to
10% of all intracranial tumors and 80% of cerebellopontine angle tumors. They arise twice
as often from the vestibular division of CN Vill as from the auditory division. They develop
in 1/100,000 individuals yearly. Growth varies according to the patient's age. There is no
gender bias and the age of presentation is between 40 and 60 years of age. They are either
part of the familial disorder neurofibromatosis type 2 (5%) or sporadic tumors (95 %).
= NATIONAL HISTORY
- the growth rate of acoustic neuromas is extremely variable. These are generally slow-
growing tumors with average reported growth rates of 0.2cm per year; however, growth
rates in excess of 2cm per year have been documented. Untreated acoustic neuromas
are potentially lethal. Gradual enlargement can lead to indentation of the brainstem,
increased intracranial pressure, and death during a course of 5 to 15 years.
- growth of acoustic neuromas generally occurs in three phases with compression of the
eINTERNAL AUDITORY CANAL CISTERN *BRAINSTEM
- growth within the internal auditory canal results in acoustic and facial nerve
compression and attenuation. Displacement of the seventh cranial nerve, the acoustic
(eighth) nerve, and the anterior inferior cerebellar artery occurs just medial to the porus
acusticus (cisternal portion). Medial tumor growth augments the blood supply of the
tumor with bridging vessels from the brainstem surface. Fourth ventricle shift often
occurs when the CPA component reaches 2 to 3.cm, and total ventricle obstruction with
resulting hydrocephalus occurs with continued tumor growth. Trigeminal compression
occurs at approximately the 3-cm stage, which permits the superior portion of the tumor
to abut the fifth cranial nerve. Massive tumor growth with hydrocephalus, brainstem
compression, and cerebellar tonsil herniation may occur, and the otolaryngologist should
remain vigilant for signs and symptoms suggestive of retrocochlear pathology.
= SYMPTOMS
- sensorineural hearing loss (SNHL), tinnitus, dysequilibrium, and facial hypesthesia are,
in descending order, are the most common symptoms of acoustic neuroma. The
symptoms usually are slowly progressive, with a median duration of 2 years in one series.
*HEARING LOSS - up to 20% of affected patients experience sudden SNHL, although
complete recovery of hearing has been reported. Overall, only 1% of patients with sudden
SNHL are found to have acoustic neuroma, whereas up to 5% of patients with acoustic
neuroma have sudden hearing loss. Thus.any patient with asymmetric or sudden hearing
loss (even after total recovery) should be considered for further evaluation for a possible
retrocochlear lesion.
- although progressive unilateral SNHL is the most common symptom, loss of speech
discrimination is characteristic of retrocochlear dysfunction of the cochlear nerve,
presumably from pressure on the auditory nerve. The usual course of an acoustic
neuroma is that 90% of patients develop a unilateral sensorineural hearing loss which

usually progresses slowly. Any unilateral or asymmetric hearing loss is an acoustic
neuroma until proven otherwise. The hearing loss is generally characterized by a high-
frequency or flat type of loss. 5% will present with a sudden hearing loss. 5% of patients
have normal hearing at the first presentation.
*TINNITUS - is the first symptom in 80% of patients.
eVERTIGO - is unusual. o
*BALANCE DISORDERS - may develop as the tumor enlarges. The dysequilibrium
associated with acoustic nerve tumors usually is a mild balance disturbance, which often
is so minor that the patient does not mention it, and only careful questioning elicits it as
a symptom. Rotatory vertigo is far less common.
*FACIAL HYPESTHESIA - diminished facial sensation or corneal reflex results from
compression of the fifth cranial nerve, which is more likely with medium-sized and large
tumors. As large acoustic neuromas compress the fourth ventricle and brainstem, long
tract signs, ataxia, and findings of increased intracranial pressure (e.g., headaches,
nausea) are produced.
= DIAGNOSIS
*HALLPIKE CALORIC TESTING - commonly reveals canal paresis on the affected side.
*MRI WITH GADOLINIUM ENHANCEMENT - is the current standard for screening for
suspected vestibular schwannomas since it is more sensitive than CT scanning.
*CT SCAN - acoustic tumors are seen only on enhanced CT scans with high- resolution
thin slices.
TREATMENT - management of acoustic neuromas depends on the tumor's size and
growth rate, the patient's age, and the state and prognosis of bilateral hearing.
*CONSERVATIVE TREATMENT
® OBSERVATION (6-12 months) - for elderly patients and patients in good health with
slowly growing tumors.
™® RADIOTHERAPY - stereotactic radiosurgery (gamma knife) or fractionated stereotactic
radiotherapy may stop vestibular schwannoma growth mainly in small intracanalicular
and extracanalicular lesions.
™® ANNUAL IMAGING - is recommended for all patients being managed conservatively for
the rest of their life or until vestibular schwannoma growth is seen to a certain limit.
*SURGICAL TREATMENT
®TRANSLABYRINTHINE APPROACH - in patients with medium sized and large tumors
and in patients with small tumors with poor hearing,
®MIDDLE FOSSA APPROACH - in patients with intracanalicular or small tumors with
good hearing as an attempt to preserve residual hearing.
®RETROLABYRINTHINE OR RETROSIGMOID APPROACH -- in patients with large
extracanalicular vestibular schwannomas.
V. BENIGN TUMORS OF THE NOSE AND PARANASAL SINUSES

A. CYSTIC TUMORS
RETENTION CYSTS - are formed by enlargement of a gland in the sinus mucosal lining. The
blockage of the gland is either inflammatory or allergic in origin. They may either
resolve spontaneously or enlarge so as to fill the antrum and produce symptoms
requiring their removal.
1. MUCOCELES - are secreting cysts lined by sinus mucous membrane and enlarged by
usually clear, thick, and tenacious unless the mucocele has been converted toa pyocele
by the invasion of bacteria. The color and consistency of the contents of the pyocele
varies with the pathogenic organism.
a) FRONTAL SINUS MUCOCELES - develop following
«Blockage of the nasofrontal duct eChronic infection

19
*Surgery of the frontal sinus Trauma .
- the first manifestation of mucocele formation may be intermittent or persistent pain in
the supraorbital region as the mucocele expands. As the mucocele enlarges there isa
gradual thinning out of the walls of the frontal sinus.
-the expansion is inthe direction of least resistance which is usually the floor of the
frontal sinus. The orbital contents are displaced downward and laterally producing
proptosis and diplopia. Early, there is tenderness elicited by palpation of the roof of
the orbit. Later, a palpable mass becomes apparent in this region along with a defect in
the roof of the orbit. It may erode through the interfrontal septum to involve the contra-
lateral sinus. The mucocele may become infected, thus forming a pyocele which can lead
to serious intracranial and orbital complications.
= DIAGNOSIS
X-RAY - they appear as smooth, globular, punched-out areas of radiotranslucency. The
lateral view is valuable for determining extension into the anterior cranial fossa or
ethmoid sinus.
TREATMENT - the anterior osteoplastic approach has proven ideal for the treatment of
mucoceles and pyoceles of the frontal sinus, as a primary surgical procedure or following
other external frontal sinus operations. Usually the entire mucocele lining can be
removed. The inner cortical lining of the sinus is then removed and the sinus obliterated
with adipose tissue.
b) ETHMOID SINUS MUCOCELES - the direction of expansion is usually through the thin
lamina papyracea, thus displacing the orbital contents laterally or downward.
TREATMENT - is a complete external ethmoidectomy.
c) SPHENOID SINUS MUCOCELE - can cause empyema by obstructing the sinus ostium.
There may be destruction of the posterior wall and encroachment on the pituitary.
= ORBITAL COMPLICATIONS
*Orbital apex syndrome *Optic neuritis eEnophthalmos
TREATMENT - the surgical approach is by way of the external ethmosphenoidal approach.
d) MAXILLARY SINUS MUCOCELE - the clinical manifestations are produced by slow
expansion which causes pressure atrophy of the mucous membrane lining and also
absorption of the bony sinus walls.
*PROPTOSIS - due to upward displacement of the orbital contents.
*PTOSIS - produced by restriction of the upper half of the lid elevation.
*EPIPHORA - may accompany the proptosis.
*ENOPHTHALMOS - caused by aloss of the roof of the antrum.
*DIPLOPIA - resulting from an upward or downward displacement of the orbital contents.
This may be cured by simple removal of the mucocele employing the Caldwell-Luc
approach.
eSWELLING OF THE CHEEK - over the antrum
ePALPABLE DEFECT - occurring in the anterior wall of the antrum or of the infraorbital
rim.
eNASAL STUFFINESS OR OBSTRUCTION - resulting from a medial displacement of the
lateral wall of the nose
eA DEFECT IN THE FLOOR OF THE ANTRUM
2. DERMOID CYSTS - the most common site of onset of the dermoid cyst in relation to
the nose and paranasal sinuses is at the suture line between the nasal bones and the
nasal process of the frontal bone. This cyst is present at birth but may not manifest
itself until adolescence. It may extend into the nasal cavity, frontal sinus, ethmoid sinus,
or maxillary sinus. The dermoid cysts associated with the maxillary sinus usually have
their origin in the hard palate. They contain structures of the skin as glands, hair and
teeth.

20
TREATMENT- is complete surgical excision. The deformities resulting from this excision
should be repaired by reconstructive surgery.
B. SOLID TUMORS .
1. OSTEOMAS OF THE PARANASAL SINUSES - occur in the frontal and ethmoidal
sinuses. They are slow growing and cause few symptoms but may eventually call for
surgical removal. They are found in approximately 0.25% of routine roentgenographic
sinus examinations. They occur most frequently in the frontal sinus. They are more
common inmales and most frequently occur during puberty.
a) OSTEOMAS OF THE FRONTAL SINUS - may arise anywhere in the frontal sinus and are
usually covered by mucous membrane. The most frequent site of origin would seem to
be between the frontal and ethmoid bones.
SIGNS AND SYMPTOMS - osteomas of the frontal sinus usually are without signs and
symptoms. The direction taken by enlargement governs the character of the symptoms.
Increased intrasinus pressure produces frontal neuralgia and sensitiveness over the
growth. The most frequent direction of enlargement is toward the orbit which is the
direction of least resistance.
- diplopia results from a downward and outward displacement of the orbital contents
and proptosis may occur. The interfrontal septum may be displaced or destroyed by
pressure erosion. Most osteomas of the frontal sinuses have obtained considerable size
before producing the symptoms for their diagnosis.
TREATMENT - small osteomas not posing immediate surgical problems should have the
rate of growth observed by a periodic x-ray. As soon as there are symptoms secondary
to pressure, the treatment should be immediate removal. The radical Riedel operation has
been widely used for removal of the frontal sinus osteomas.
b) OSTEOMAS OF THE ETHMOID SINUS - may enlarge to involve the majority of the ethmoid
cells, to extend into the frontal sinus orbit, or sphenoid sinus. Extension of the osteoma
in the direction of the frontal sinus may encroach upon the nasofrontal passage and thus
be the precursor of chronic frontal sinus infection. Growth in the direction of the orbit
results in downward or outward displacement of the orbital contents.
TREATMENT - the external ethmoidectomy approach is the route of choice for removal of
osteomas of the ethmoids. If the osteoma is large, a considerable amount of the
ascending process of the maxilla and nasal bone may be necessary for adequate
exposure.
c) OSTEOMAS OF THE MAXILLARY SINUS - are rare and most often symptomless. When
complicated, they may be removed by the Caldwell-Luc approach.
2. SQUAMOUS PADILLOMA
—TYPES
a) INVERTED PAPILLOMA (SCHNEIDERIAN PAPILLOMA) - has a unique histological appearance
and arises from the membranes lining the nose and paranasal sinuses. The epithelium of
the tumor inverts into the underlying stroma. The most common site of origin is the lateral
nasal wall in the region of the middle meatus and ethmoid cells, and often (in 82% of
cases), it secondarily extends into one of the paranasal sinuses. It appears to be grossly
similar to a typical nasal polyp.
*MAXILLARY SINUS = 69% *SPHENOID SINUS = 11-20%
*FRONTAL SINUS = 11-16% [i
- isolated lesions of the sinuses without nasal involvement may occur. In approximately
8% of cases, the tumor may arise from the nasal septum. It may arise from multiple sites
in approximately 4% of cases. It is usually unilateral, but it has been reported to be
bilateral in up to 13% of cases. It can extend through the septum into the contralateral
nasal cavity.

21
- the incidence of this tumor is between 0.5% and 7.0% of all nasal tumors. It is most
usually encountered in the 5" to the 7"" decades, but the average age of onset is 52 years.
It is more commonly seen in males.
- whether because of multicentricity or incomplete excision, these neoplasms have a high
rate of recurrence with any procedure as high as 75%. Patients also have a 5-15% risk of
developing squamous cell carcinoma within the inverted papilloma.
ETIOLOGY - is unclear; however, there is an association with human papilloma virus
(HPV). Although histologically benign, it is treated like a premalignant tumor for 2
reasons
‘Locally invasive, at times it involves extensive bone erosion, and if conservatively
removed, shows a high incidence of local recurrence.
*Focal areas of squamous cell carcinoma are found within the papilloma in approximately
10% of the cases.
=SYMPTOMS
*NASAL OBSTRUCTION - most common symptom.
*Headache Unilateral epistaxis *Nasal discharge
*Facial pressure eAnosmia
=CLINICAL FINDINGS - on gross examination, there are no clear distinguishing
characteristics between an inverted papilloma and an inflammatory polyp, although an
inverted papilloma may be firmer and less translucent than an “average” polyp. It is
pliable, pink and tends to bleed quite easily.
= HISTOPATHOLOGIC EXAMINATION - one distinguishing feature of inverted papillomas is
the proliferation of the epithelium with fingerlike inversions into the underlying stroma. It
is covered by columnar or metaplastic squamous epithelium.
= TREATMENT - consists of total excision of the tumor with adequate margins.
*LATERAL RHINOTOMY ¢MIDFACIAL DEGLOVING
*MEDIAL MAXILLECTOMY
*TRANSNASAL ENDOSCOPIC MEDIAL MAXILLECTOMY
ADVANTAGES OF ENDOSCOPY
=» Superior magnification » Illumination
® Angled visualization ® Avoids external scarring
® Allows examination of the tumor bed Preserves the superstructure of the nose
b) HARD PAPILLOMA - is covered by stratified squamous epithelium which shows varying
degrees of cornification. It is more cauliflower-like than the soft papilloma and does not
bleed easily. Lesions are often noted at the mucocutaneous junction in the anterior,
especially on the anterior caudal margin of the septum.
TREATMENT - a simple papilloma may be removed by simple excision. Multiple papillomas
require wide excision by the lateral rhinotomy route. Any recurrence should be treated
by wide excision followed by radiation therapy.
3. NON-NEOPLASTIC TUMORS
a) NASAL POLYPS - are an edematous hypertrophy of the nasal mucosa resulting from a
chronic edematous inflammatory process. They may occur singly or in numbers and
may be pedunculated or sessile. They vary in their glandular component. The polyps may
become cystic as a result of glandular degeneration.
= DIAGNOSIS - is made by examination of the nose. Polyps are yellowish-grey or pink,
smooth and moist. They are pedunculated and move on probing.
“HISTOLOGY - nasal polyps consist of a loose edematous stroma infiltrated by
inflammatory lymphocytes and eosinophils and covered by respiratory epithelium.
= TREATMENT
«Nasal polyps may shrink with topical steroid therapy but will not usually disappear.

*Nasal polypectomy is performed under local or general anesthesia, the polyps being
removed with grasping forceps, snare, laser or by a powered microdebrider.
*FESS (FUNCTIONAL ENDOSCOPIC SINUS SURGERY) - may help patients with
primary and limited polyps by improving ventilation, drainage and by opening defined
anatomical narrow passages.
*Endoscopic ethmoidectomy may be required for recalcitrant cases.
*Short courses of oral steroids are useful in severe cases.
b) EOSINOPHILIC GRANULOMA - may occur in or around the paranasal sinuses. The
punched-out appearance of the x-ray and eosinophilia are suggestive of this diagnosis.
Radiation therapy is rarely necessary but is effective.
c) ANGIOMAS - cavernous hemangio-endothelioma of the nose is rare. It arises from the
ethmoid region in the lateral wall. It grows slowly by infiltration and is destructive to
surrounding tissues. It has a tendency to invade the sinuses, especially in the region of
the ethmoid, eventually filling the nose, sinuses and nasopharynx, producing in extreme
cases exophthalmos, nasal obstruction, or facial disfigurement. Hemangioma of the
nasal septum arises from the cartilage or cartilaginous vomer junction.
SYMPTOMS
*EPISTAXIS
*NASAL OBSTRUCTION - is proportionate to the size of the growth.
*REDUCIBLE AND PULSATING TUMOR - pressure upon the growth materially reduces its
size. The pulsation is greater when the tumor is attached to a large artery than if itis
attached to a vein. In the later event the pulsation is much less and the color is blue,
whereas if it is connected with both vein and artery the color will be dark red.
VI. MALIGNANT TUMORS OF THE NOSE AND PARANASAIL SINUSES

- sinonasal neoplasms constitute a rare group of tumors in Western society. They account
for only 0.2% to 0.8% of all malignancies and 2% to 3% of all head and neck cancers. The
overall incidence of sinonasal malignancies is 0.556 cases per 100,000 population per
year, with a male-female ratio of 1.8: 1.
“they are extremely rare in childhood, and the incidence increases with age beginning
around the fourth decade. The median age at diagnosis is 62 years in men and 72 years
in women. Originating from any histologic components of the sinonasal cavity, sinonasal
neoplasms have a variable histopathology. Accordingly, treatment options vary, surgery
being the mainstay in most of them.
- the most common histologies are squamous cell carcinoma (SCC), adenocarcinoma,
olfactory neuroblastoma (ON), and adenoid cystic carcinoma, whereas the most common
primary sites are the nasal cavity (43.9%) and maxillary sinus (35.9%).
- the intimate relationships between the nasal passages and sinuses allow tumors to
spread easily from one cavity to another. Most patients present with advanced disease,
which is correlated with a less favorable outcome. This problem is compounded by the
proximity of the orbit, brain, and cranial nerves.
= PATHOGENESIS - epidemiologic studies have shown associations between a variety of
environmental hazards and the development of paranasal sinus tumors.
eCIGARETTE SMOKING - the risk doubles among heavy or long-term smokers, and there
is a reduction in risk among long-term “quitters.” A significantly elevated risk of
paranasal sinus carcinoma was also found among nonsmokers whose spouses smoked.
A study examining the residual risk after cessation of smoking found a significant
decrease in risk of sinonasal cancer associated with increasing number of years since
cessation. Smoking has been associated with a higher risk for SCC, whereas no similar
statistically significant association has been observed for adenocarcinoma.
elncresed alcohol intake

23
*High consumption of salted or smoked foods
*Decreased intake of vegetables ;
*OCCUPATIONAL HAZARDS - the overall incidence of sinonasal neoplasms attributable
to occupational exposures ranges from 25% to 41%. In an analysis of European case-
control studies, occupation was associated with 39% of all sinonasal cancers in men and
with 11% in women.
OCCUPATIONAL HAZARDS ASSOCIATED WITH PARANASAL SINUS TUMORS

TUMOR TYPE OCCUPATIONAL SETTING SUSPECTED
CARCINOGEN
SQUAMOUS CELL Nickel refining Nickel compounds
CARCINOMA ;
Mustard gas manufacturing Dichlorodiethy|
sulfide
Isopropyl alcohol manufacturing Isopropyl alcohol
Watch painting Radium

ADENOCARCINOMA Woodworking Hardwood dusts
Chrome pigment manufacturing Chromium
compounds
Isopropyl alcohol manufacturing Isopropyl oil
- one of the earliest associations was made in nickel refining, in which a worker's relative
risk of developing paranasal sinus malignancy was more than 100 times that of the
general population.
- adenocarcinoma of the ethmoidal sinus is highly associated with exposure to hardwood
dust. Coexposure to pigment stains and formaldehyde can exert additional risk for
adeno-carcinoma.. Furniture makers and wood machinists in England have been shown
to have a 1000-fold higher incidence of adenocarcinoma of the ethmoid sinuses. A later
study showed a statistically significant reduction in the incidence of nasal
adenocarcinoma due to improvements in working conditions, including the reduction of
wood dust exposure.
- an increased expression of cyclooxygenase-2 (COX-2) was found in sinonasal
adenocarcinoma with wood dust exposure, suggesting a role for inflammatory
components in the carcinogenesis process. Leather dust exposure has been associated
mainly with adenocarcinoma as well.
- the development of paranasal sinus tumors has been linked with exposure to various
other agents, including chromium compounds, radium (used in watch dial painting),
dichlorodiethyl sulfide, isopropyl oil, textile dust, polyaromatic hydrocarbons (in gas
manufacturing), flour dust, and asbestos.
- there is a well-known association between paranasal sinus tumors and the Epstein-Barr
virus (EBV), especially with respect to T-cell non-Hodgkin's lymphoma.
A. MALIGNANT GRANULOMA - though’not truly neoplastic, it is a sinister condition
characterized by progressive ulceration of the nose and neighbouring structures.
TYPES
*STEWART TYPE - in which the lesion is limited to the skull and is characterized by a
pleomorphic histiocytic infiltration and which is a form of lymphoma.

24
*WEGENER TYPE - in which the kidneys, lungs and other tissues may show
periarteritis, the local nasal lesion containing multinucleated giant cells. It is probable
that Wegener’s granuloma is an auto-immune disease.
THERAPY - radiotherapy, steroids and cytotoxic agents are used in its treatment and
occasionally are successful.
B. SQUAMOUS CELL CARCINOMA - is the most common malignant tumor of the nose
and paranasal sinuses, accounting for approximately 60-80% of paranasal sinus tumors.
They occur twice as often in males as in females, and are most often diagnosed in
patients between 50 and 70 years old.
eMAXILLARY SINUSES = 60-70% *NASAL CAVITY = 20-30%
*FRONTAL OR SPHENOID SINUSES = < 5% *ETHMOID SINUSES = 10-15%
- industrial exposure to wood dust, nickel, leather, textile dust, chromium, formaldehyde
and asbestos have been implicated as causative factors.
SIGNS AND SYMPTOMS - squamous cell carcinomas arise from a silent location and grow
insidiously with little to no symptoms. At the time of diagnosis, these tumors are very
large and, therefore, patients with these tumors have a very poor prognosis.
- only when these neoplasms invade adjacent structures, causing symptoms of oral,
ocular, or facial involvement, are patients accurately diagnosed and treated. Tumors of
the nasal fossa and paranasal sinuses do not produce, for any particular lesion,
consistent clinical manifestations. Diagnosis of malignancy is often delayed because
the symptoms of early malignant tumors of the paranasal sinuses are identical to those
of the common benign chronic sinusitis. 19% of patients have a long-standing history of
chronic sinusitis before the development of malignancy.
«SENSATION OF PRESSURE, PAIN OR NO PAIN - pain, if present, is apt to be worse at
night or when the patient is recumbent. Persistent pain in the face develops if it erodes
into the periosteum of the posterior or lateral wall of the antrum. The pain may follow the
distribution of the second division of CNV.
eUNILATERAL NASAL OBSTRUCTION - should be considered a neoplasm until proven
otherwise.
*EXTERNAL SWELLINGS ABOVE THE FACE - such as the side of the nose and region of
the inner canthus, bulging of the cheek, swelling of the hard palate, soft palate, alveolar
ridge, or buccal fold may occur.
*NASAL DISCHARGE - may be serous, serosanguineous, or purulent.
eSINUS CONGESTION *HYPOSMIA
*HEADACHE
¢PARESTHESIA, ANESTHESIA, OR PARALYSIS OF CRANIAL NERVES
*ORBITAL MANIFESTATIONS
& Proptosis and enophthalmos » Diplopia
™ Nasolacrimal duct obstruction Interruption of the innervation of the EOMs
™ Bulging behind either the infraorbital rim or supraorbital rim
«Dentures may become ill-fitting and the maxillary teeth may become loosened if the
superior alveolar ridge is invaded.
*TRISMUS - represent extension of the disease into the pterygoid region.
eEUSTACHIAN TUBE OBSTRUCTION - -represents extension of disease into the
nasopharynx.
* HEMORRHAGE - may occur.
1. MAXILLARY SINUS - it is the most frequently involved of the paranasal sinuses with
malignant tumors. It occurs more frequently in men than in women and most often after
the age of 50 years. Cancers of the maxillary sinus can invade the hard palate and enter
the oral cavity. They can also invade the orbital floor, causing visual symptoms and
proptosis. Anterior invasion through the skin can occur.

- in advanced maxillary sinus cancers, cervical lymph node metastases can be the
initial manifestation. Cranial nerve symptoms result from invasion of the skull base.
= CUNICAL FEATURES
*EARLY - carcinoma of the maxillary antrum is seldom diagnosed until it has spread to
surrounding structures. In its earliest stages it will give rise to no symptoms.
* Blood-stained nasal discharge »Increasing unilateral nasal obstruction
*LATE
™® SWELLING OF THE CHEEK.
SWELLING OR ULCERATION OF THE BUCCO-ALVEOLAR SULCUS OR PALATE
™®EPIPHORA - owing to involvement of the nasal lacrimal duct.
™»PROPTOSIS AND DIPLOPIA - owing to involvement of the floor of the orbit.
™»PAIN - commonly in the distribution of the second division of the fifth nerve, but may
be referred via other branches to the ear, head or mandible.
= SPREAD - local extension beyond the bony confines of the antrum is not long delayed
and may involve the following: cheek, buccal sulcus, palate, nasal cavity and
nasolacrimal duct, infraorbital nerve, orbit and pterygopalatine fossa. Lymphatic spread
is to the submandibular and deep cervical nodes and occurs late. Distant metastases are
rare.
= DIAGNOSIS
°X-RAY - may indicate a neoplasm in the sinus.
*CT SCAN - is invaluable to assess the extent of invasion and bone erosion.
*MRI - will show the extent of soft tissue mass.
*BIOPSY - often the tumour will have spread into the nasal cavity, whence a biopsy is
easily obtained. If the tumour is still within the confines of the antrum, a specimen is
obtained via the antronasal wall. The interpretation of a biopsy obtained by way of the
Caldwell-Luc approach is conclusive.
= TREATMENT - for nearly all patients, the treatment is maxillectomy followed by radiation
therapy. Treatment with this combination of modalities has shown markedly improved
results compared to radiation therapy alone. The 5-year survival rate for patients with
maxillary sinus squamous cell carcinoma who are treated with combined surgery and
radiation therapy is 46-68% versus 9-19% for those patients treated with radiation therapy
alone.
*MAXILLECTOMY WITH EXENTERATION OF THE ORBIT- orbital exenteration is
necessary for maxillary cancers that invade the periorbital tissues. This results in
fenestration of the hard palate, for which a modified upper denture with an obturator is
provided. The fenestration allows drainage and access for inspection of the antral cavity.
*RADICAL RADIOTHERAPY COURSE - is given following maxillectomy. Radiation alone
is palliative.
- this aggressive combination of treatments is justified by the poor prognosis of the
disease if not treated adequately from the outset.
= PROGNOSIS - even with radical treatment, carcinoma of the antrum has a poor prognosis,
with only about 30% of patients surviving to 5 years.
2. FRONTAL SINUS - primary carcinoma is quite rare and is usually not diagnosed until
the time of surgery. bm
< SYMPTOMS - often there are no early symptoms. Nasal bleeding, pain, or even proptosis
may be the first symptom.
< TREATMENT - if the surgeon is suspicious of a tumor, a frozen section should be taken.
If this reveals carcinoma, the entire sinus should be removed without regard for
preservation of normal structures. The operation should be supplemented by radiation
therapy.
PROGNOSIS - is poor.

26
3. ENHMOID SINUS - carcinoma of the ethmoid sinus is usually secondary. The eye is
pushed outward, and shortly thereafter the skin near the inner canthus breaks down. CT
scan is necessary to localize the extent of these tumors. oo.
TREATMENT - irradiation and extensive external ethmoidectomy with en bloc excision, is
carried out both for diagnosis and adequate drainage. This is followed by radiation
therapy.
4. SPHENOID SINUS - primary malignancies of the sphenoid are also quite rare.
- the sphenoid is entered by way of the transethmoid route and total excision is done
both for the purpose of biopsy and to establish adequate drainage. This is subsequently
followed by radiation therapy.
B. ADENOCARCINOMAS - arise from the epithelial surface of the sinonasal mucosa and
occur more frequently than adenoid cystic carcinomas, which arise from the minor
salivary glands. Together, they represent the most common mucous gland malignant
neoplasms of the paranasal sinuses. As with other tumors of the paranasal sinuses, both
of these tumors often remain undiagnosed for a long time.
- adenoid cystic carcinomas tend to arise from the maxillary antrum and can infiltrate into
the surrounding tissue. They demonstrate perineural spread into the maxillary and
mandibular branches of the trigeminal nerve (CN V), with extension into the foramina
ovale and rotundum. Adenoid cystic carcinomas have a low incidence of regional
metastases but greater distant metastases.
- adenocarcinomas arise typically from the ethmoid sinuses. While there has been no
correlation with smoking in the development of adenocarcinomas, there has been a
documented association between woodworkers and these neoplasms. The incidence of
adenocarcinoma in woodworkers approaches that of lung cancer. There also has been
an increased prevalence of these tumors in leather workers. Several histological types
are seen with variability in mucin production and cellular differentiation. They are similar
to adenoid cystic carcinomas in their growth behavior.
TREATMENT - consists of multimodality therapy at the advanced stages of disease. For
maxillary sinus tumors, the treatment usually consists of a maxillectomy.
- an anterior craniofacial resection is often the recommended treatment for advanced
ethmoid cancers. Postoperative radiation therapy is frequently employed in treating
patients with all of these tumors.
C. OLFACTORY ESTHESIONEUROBLASTOMAS - arise from the olfactory epithelium
superior to the middle turbinate. These neoplasms account for only 1-5% of all malignant
tumors of the paranasal sinuses. They are initially unilateral and can grow into the
adjacent sinuses and the contralateral nasal cavity; they can spread to the orbit and the
brain.
TREATMENT - patients are best treated with combined modality therapy. The local tumor
contro! rate of combined therapy is 87% versus 51% for radiation alone, and 0% for
surgery alone. Surgical resection may involve either local resection or craniofacial
resection with radiation.
D. MALIGNANT MUCOSAL MELANOMAS - respiratory tract mucosal melanomas occur
in the nasal cavity and paranasal sinuses. They are exceedingly rare, with only 0.5-1.5%
of all melanomas occurring in the sinonasal cavity. These neoplasms originate from
melanocytes within the submucosa and from the mucosa of the paranasal sinuses. They
are located most frequently in the anterior septum, followed by the middle and inferior
turbinates. The maxillary sinus is the most common sinus cavity involved.
= CLINICAL FINDINGS - epistaxis appears to be the most frequent symptom, and nasal
obstruction is also common. On examination, the mass appears to be fleshy and
polypoid. Tumors in the nasal cavity tend to be smaller at the time of diagnosis than
tumors that arise within the sinuses. Nodal metastasis occurs in 10-20% of cases.

=TREATMENT - consists of surgical excision followed by postoperative radiation
therapy. As a result of this combined treatment approach, the 5-year disease-specific
survival rate for sinonasal mucosal melanomas is approximately 47%.
E. SINONASAL UNDIFFERENTIATED CARCINOMAS - are highly aggressive tumors of
the paranasal sinuses and often appear to be histologically similar to olfactory
esthesioneuroblastomas. Like inverted papillomas, sinonasal undifferentiated
carcinomas appear to arise from schneiderian mucosa. They grow rapidly, with extensive
local invasion into the sinuses, the orbit, and the brain.
TREATMENT - surgical resection with postoperative radiation therapy is the mainstay of
therapy, although this combined approach results in a very poor prognosis.
Vil. BENIGN TUMORS OF THE NASOPHARYNX AND DHARYNX

A. JUVENILE ANGIOFIROMA ( JUVENILE NASODHARYNGEAL ANGIOFIBROMA)
(JNA)) - is a benign neoplasm composed of an admixture of mature vascular and fibrous
tissue with locally destructive properties. Evidence suggests that this tumor does not
originate from the nasopharynx, but from a fibrovascular nidus in the posterolateral wall
of the nasal cavity and pterygopalatine fossa near the sphenopalatine foramen
secondarily extending into the nasopharynx and other adjacent anatomic sites.
- itis a relatively rare neoplasm, accounting for only 0.05 % of all head and neck tumors. It
occurs almost exclusively in males between 10 and 25 years of age; however, well-
documented cases in older patients are on record. They are uncommon over the age of
25 years. The great predilection for young males strongly suggests that this lesion is
androgen dependent, a theory confirmed by the fact that stromal and endothelial nuclear
immunostaining for androgen receptors is found in 75% of cases.
- the lesion has a pathognomonic epicenter of origin at the level of the pterygopalatine
fossa and subsequently grows through different pathways of spread that typically follow
foramina and fissures of the skull base.
The bone may be involved basically with two mechanisms:
*Resorption by pressure coming from subperiosteal growth
*Invasion of the cancellous component, initially at the level of the root of the pterygoid
process with subsequent expansion within the greater wing and erosion of the floor of
the middle cranial fossa.
- in its early phase, it through the sphenopalatine foramen into the nasopharynx and the
nasal cavity and along the vidian nerve into the floor of the sphenoid sinus. Lateral
extension through the pterygomaxillary fissure leads to invasion of the infratemporal
fossa, which in advanced lesions may be completely filled. When the lesion expands
anteriorly, the posterior wall of the maxillary sinus is progressively pushed forward.
Although benign, juvenile angiofibroma may extend intracranially through the orbit via
the inferior and superior orbital fissure or along the maxillary nerve to the parasellar
region. Encroachment upon the anterior skull base through the ethmoid is less commonly
observed. Regardless of the site and pattern of intracranial involvement, transdural
growth of the lesion is very rare.
- the rate of tumor growth is slow. The growth is hormonally influenced. These tumors
are thought to regress spontaneously as they are never seen in adults. This benign tumor
erodes bone and is known for its recurrence on incomplete removal.
*MOST COMMON SIGNS AND SYMPTOMS
#» EPISTAXIS — severe epistaxis occurs in 75% of cases.

28
PERSISTENT NASAL OBSTRUCTION - large tumors may extend anteriorly into the
nasal cavity, causing nasal obstruction and simulating a primary intranasal or paranasal
sinus
LATE SIGNS AND SYMPTOMS
» Facial swelling or deformity (swelling of the cheek)
»®Mucopurulent nasal discharge »Proptosis » Nasal speech
* Diplopia » Headache » Visual loss
» Sinusitis » Cranial nerve palsies »Anosmia
» Hearing deficits » Facial hypesthesia
» Pain in the face/sinus pressure » Eustachian tube obstruction
- typically, symptoms have been present for more than 1 year before diagnosis. The site
of occurrence is usually the posterolateral portion of the roof of the nasal cavity in the
area of the sphenopalatine foramen. Extension posteriorly may fill the nasopharynx and
extend into the oropharynx, causing displacement of the soft palate. Extension can occur
through the sphenopalatine foramen with involvement of the pterygomaxillary fossa and
infratemporal fossa, resulting in facial deformities. Extension into the middle cranial
fossa can occur if the tumor involves and destroys the pterygoid process.
= CLINICAL FINDINGS - - it mey appear as a sessile or lobulated mass but may occasionally
be polypoid or pedunculated and bleeds severely on manipulation and biopsy. It can
grow to occlude the involved nares completely. It may protrude below the free edge of
the soft palate, extend into the antrum, and grow to the external orifice of the nares,
posteriorly into the nasopharynx, or even into the orbit and cranial cavity.
- it is of very firm consistency, round or slightly nodular and of grayish or purplish red
color. It is benign histologically and does not metastasize but is highly destructive
locally. It may enlarge to occupy the nasopharynx completely and present in the
oropharynx. It may extend anteriorly and protrude through the nares.
= DIAGNOSIS - can be established radiographically without biopsy in most cases. Staging
and surgical planning should consider residual vascularity following embolization. CT
Scan and MRI may be used to confirm the diagnosis and outline the extent of the tumors.
Preoperative digital subtraction angiography and CT scanning should be performed to
evaluate the blood supply and the anatomic extent of the tumor.
*RADIOGRAPHY
HOLMAN-MILLER SIGN - refers to the anterior bowing of the posterior wall of the maxillary
antrum as seen on a lateral skull radiograph or cross-sectional imaging. This is a non-
specific sign that can be produced by any slowly-growing mass, whereas erosion of the
pterygoid lamina maybe pathognomonic for juvenile nasopharyngeal angiofibroma.
eCT SCAN - shows a homogenously enhancing mass in the posterior nasal cavity and
nasopharynx, with widening of the pterygopalatine fossa and anterior bowing of the
posterior maxillary wall.
eMRI - shows the interface of the tumor with soft tissues (orbit, masticator space, dura)
when there is bony erosion or extension of the tumor through the foramina. It can also
differentiate the tumor from obstruction of a sinus with retained secretions. Without MRI,
CT can be misleading, suggesting an aggressive neoplasm, such as a sarcoma.
eANGIOGRAPHY - arteriographic findings are usually diagnostic and include a tumor
with marked vascular hypertrophy and increased number of arteries without beading,
dilatation, segmental narrowing, or aneurysmal dilatation.
- it is not necessary in most cases but helps to confirm the diagnosis and demonstrates
the blood supply of the tumor. The blood supply is usually derived from branches of the
external carotid artery (internal maxillary and ascending pharyngeal arteries) and is often
bilateral in larger tumors. Advanced tumors also receive blood supply from the internal
carotid artery (ICA) via the vidian artery and cavernous branches. For advanced tumors

29
with skull base involvement and proximity to the ICA, angiography is important to
assess collateral intracranial circulation (competency of the circle of Willis).
*BIOPSY- is contraindicated.
MODIFIED (RADKOWSKI) STAGING OF NASOPHARYNGEAL ANGIOFIBROMA. ; ao
STAGE EXTENT OF DISEASE Aa io.
IA : Limited to posterior nares and/or nasopharyngeal vault

IB Tumor involving the posterior nares and/or nasopharyngeal vault with involvement of al
paranasal sinus
IIA Minimal lateral extension into pterygomaxillary fossa
IIB Full occupation of pterygomaxillary fossa with or without superior e!erosionn orbital bone
lic Extends into the infratemporal fossa or extension posterior to the pterygoid plates
IIA Erosion of base of skull (middle cranial fossalbase of pterygoids)—minimal i intracranial
IB Extensive intracranial extension with or without extension into cavernous sinus
TREATMENT - some large angiofibromas regress after puberty, especially after
incomplete surgical removal or radiation therapy. Spontaneous total regression,
however, is very rare. Therefore, in a patient with symptoms, treatment is indicated.
- there is controversy as to whether surgery or radiation is the treatment of choice, but
most writers favor surgical resection for early lesions. Preoperative embolization is used
in most cases to control intraoperative and perioperative bleeding
- radiation therapy or even chemotherapy may be necessary for more advanced and
aggressive tumors. Most post-therapy recurrences develop within the first
year. Meticulous removal of the angiofibroma is essential to prevent recurrence,
particularly the portion of the tumor which infiltrates the pterygoid canal and
basisphenoid. A multidisciplinary approach may be necessary to achieve cure
*SURGICAL EXCISION - is the primary treatment with endoscopic surgery replacing open
approaches for most tumors. The greatest challenge in surgery is bleeding caused by the
hypervascular nature of JNA. Treatment options for recurrent tumor include surgery or
radiation therapy (RT)
- vascular embolization usually precedes surgical intervention to control
bleeding. Recurrence rates vary from 6% to as high as 24%. High recurrence rates and
early recurrence may occur in nasopharyngeal angiofibromas involving the skull base.
Recurrences are more common in cases with intracranial extension. Tumor recurrence in
cases without intracranial extension usually occurs within 2 years of treatment.
- the choice of surgical approach depends on the stage of the tumor (extent and
vascularity). The choice of approach also depends on the characteristics of the patient
(age, size) and the experience of the surgeon with different approaches.
™» ENDOSCOPIC ENDONASAL - more popular for snall tumors.
™» TRANSVERSE PALATAL APPROACH - is the treatment of choice in uncomplicated
cases for those tumors which present posteriorly into the nasopharynx and posterior
nasal cavity.
®TRANSMAXILLARY APPROACH - for larger tumors with residual vascularity
®INFRATEMPORAL APPROACH - for tumors with lateral extension to the middle cranial
fossa or infratemporal area may benefit from a combined anterior and _ lateral
(infratemporal) approach.
® LATERAL RHINOTOMY - is used for those lesions which extend anteriorly into the nasal
cavity and paranasal sinuses.

30
*RADIATION THERAPY - is reserved for those patients with intracranial disease and
for those who refuse surgery.
*CRYOTHERAPY - may be used.
= PROGNOSIS - in general, the prognosis is excellent after surgical removal; mortality rates
range from 3% to 9%. Rarely, spontaneous regression may occur. Malignant
(Sarcomatous) transformation is a rare event and has been linked to treatment with
radiotherapy (postirradiation sarcoma). The recurrence is probably the result of
incomplete removal of tumor extensions.
B. PAPILLOMA OF THE PHARYNX - rarely occurs on the walls of the pharynx but is more
common in the faucial region. It is most frequently found on the uvula, the free borders
of the tonsillar pillars, and the tonsils themselves. They may be single or multiple,
sessile or pedunculated. They vary in size from that of a small pea to a large walnut and
frequently have a delicate mulberry appearance. Papilloma of the tonsils is more often
muliple than single. The growths usually give rise to no marked symptoms but do tend
to recur.
TREATMENT - Surgery
C. CRANIODHARYNGIOMA (RATHKE'S POUCH TUMOR) - is a benign, but
aggressively growing epithelial tumor originating from remnants of squamous cell
epithelium of the hypophyseal duct and/or Rathke’s pouch. It usually occurs between 10
and 20 years old. In the beginning, it is characterized by the syndrome of
*Endocrine disturbance (Hypopituitarism) *Failing vision
*Bilateral hemianopsia ¢Primary optic atrophy
*Supression of the sexual development and calcification of the subsellar portion of the
tumor.
*Enlargement of the sella turcica as the tumor extends beyond the sella, signs and
symptoms of increased intracranial pressure develop.
D. NASOPHARYNGEAL FIBROMA - is a very rare tumor resembling hyperplastic
adenoids clinically and a cavernous hemangioma histopathologically. It is usually single
although multiple growths have been reported. Softer varieties are called "polypoid
fibromas" or "fibromatous" myxoma.
- the true fibroma usually arises from the nasopharyngeal recess, less frequently from
the anterior sphenoid wall, base of the sphenoid, nasal process of the occipital bone,
nasal choanae, first cervical vertebrae, mouth of the eustachian tube, posterior palatine
surface and the pterygomaxillary recess. The softer fibromatous myxoma, or "polyp,"
usually arises in the nasal cavity and extends into the nasopharynx.
ETIOLOGY - it comprises 1% of all head and neck tumors. It usually occurs between 10
and 25 years of age in males. Two thirds of all cases occur between the age 13 and 17.
Hormonal factors seem to play a pathogenic role in the development of the disease,
hormonal disproportion between testosterone and estrogen. Spontaneous remission can
be expected after the age of 25.
PATHOLOGY - the surface of the tumor is covered by mucous membrane _ under which
are found large ramifying blood vessels. The mass is made up of dense fibrous tissue
and agglomerated cells. It contains large venous channels most abundant in the
peripheral portions. Fibromata may be sessile, but more often pedunculated. They often
attain large size.
- large fibromata are frequently attended ‘With inflammatory processes, hence adhesions
to the adjacent structures are common. Additional blood supply is derived through the
adhesions. They do not metastasize, but grow by extension. They may invade the orbit,
accessory sinuses, pterygoid and temporal fossae or the intracranial cavity.

31
=SYMPTOMS
*NASAL CONGESTION AND OBSTRUCTION - are early symptoms
*RECURRENT EPISTAXIS *HYPOSMIA
*THE VOICE BECOMES “FLAT” OR “DEAD” IN QUALITY
*RESPIRATION AND DEGLUTITION - are impeded as the process advances.
PAIN AND MUCOPURULENT DISCHARGE - at a later stage
e"FROG FACE "- becomes well marked when the growth has attained considerable
size. The maxillary bones are separated and exopthalmos becomes a prominent
symptom.
= EXAMINATION - shows the tumor to be a rounded mass, of a pinkish or dark purple color.
The veins are frequently varicosed, hence the examination by digital or instrumental aids
should be done carefully to avoid injuring them. The growth may project into the
posterior nares, or its direction may be toward the antrum and other sinuses. If
pedunculated, it is movable, unless it has become fixed by inflammatory adhesions.
-Ifitextends through the sphenomaxillary fissure, it may be felt under the zygoma. As
adhesions are usually present, its outline is difficult to distinguish.
=TREATMENT
*CONSERVATIVE TREATMENT
PRIMARY INOPERABILITY - periodic follow-up to detect spontaneous remission.
™®» PRIMARY INOPERABILITY WITH PROGRESSIVE TUMOR GROWTH - radiotherapy
*SURGICAL TREATMENT - complete resection via a transnasal or transmaxillary open or
endoscopic access. If necessary a midfacial degloving is performed.
E. FIBROMA OF THE TONSIL
ETIOLOGY - it occurs equally often in both sexes, more often in the young than in middle
and advanced life. It is a benign neoplasm next in frequency of occurrence to papilloma.
It rarely becomes malignant. Its growth is slow and is usually limited to one tonsil.
= PATHOLOGY - the fibroma is usually somewhat pedunculated, though it may be sessile.
The larger the fibroma, the larger the pedicle. Itis more often single than multiple. Usually
firm and scantily supplied with blood vessels. It is composed of white fibrous tissue, the
cells often being matted together, closely simulating embryonic connective tissue cells.
=SYMPTOMS - annoying symptoms are seldom present, except in the large
pedunculated type, in which it produces mechanical obstruction. Its presence is not
accompanied by discharge. It is characterized by symptoms similar to those of enlarged
hyperplastic tonsils.
TREATMENT- Surgery
F. ANGIOMAS
ETIOLOGY - angiomas of the nose, pharynx and larynx are rare. They are usually
congenital but may not manifest themselves for years.
= PATHOLOGY - angiomas are divided into hemangiomas and lymphangiomas. Angiomas
are sessile non-ulcerating with a nodular serpentine outline and usually are of a soft
consistency. Hemangiomas have a purplish-blue color. The lymphangiomas are
smoother and pale pink.
- a hemangioma may be associated with a similar process involving the skin. It is
frequently found at the base of the tonsil,gr tongue arising from a venous plexus.
eTYPES OF HEMANGIOMAS
® CAPILLARY HEMANGIOMAS - consist of loosely arranged tissue containing numerous
thin-walled blood vessels showing, at times, areas of thromboses, hyaline degeneration
and hemosiderin. The tumors are covered with normal stratified epithelium. Varices are
usually found on the posterior wall of the pharynx or on the base of the tongue. They
frequently occur in association with chronic pulmonary or circulatory disturbances.
Slight hemoptysis may occur at times.

32
®» CAVERNOUS HEMANGIOMAS - are thin-walled with an afferent artery and efferent
veins which do not communicate with the neighboring capillaries. They may occur singly
or in groups. Distended veins project above the surface and into the tissue beneath.
They may be compressed but refill at once when the pressure is removed. The tumors
are usually lobulated and dark purplish in color.
® HYPERTROPHIC » PSEUDOANGIOMAS
eTYPES OF LYMPHANGIOMAS
*»SIMPLE TYPE (LYMPHANGIOMA SIMPLEX) - is characterized by a new growth of
lymphatic vessels having a comparatively narrow lumen and more or less parallel walls.
™CAVERNOUS TYPE (LYMPHANGIOMA CAVERNOSUM) - is characterized by
irregularly shaped, intercommunicating lymph spaces of varying sizes.
HYPERTROPHIC TYPE (LYMPHANGIOMA HYPERTROPHICUM) - the lymphatic vessels
are lined with several layers of endothelium with at times a nodular or valvular growth of
endothelium into the lumen of the vessels.
®CYSTIC TYPE (LYMPHANGIOMA CYSTICUM) - is characterized by one or more large
lymphatic cysts in a new growth of lymph vessels.
SYMPTOMS - are variable, depending on the location and the size of the tumor. If the
tumor is large, slight or severe respiratory obstruction may be present. Hemoptysis may
occur without warning and may be severe. Pain is usually absent. They may be
pedunculated or more frequently they are attached by a broad base. They may be single
or multiple. Lymphangiomas are usually smoother and paler than hemangiomas.
= ETIOLOGY - the disease is transmitted as a dominant characteristic and is not sex bound.
The lesions are most frequently found in the nasal or oral mucous membrane, especially
the cartilaginous portion of the nasal septum, tongue, buccal regions, lips, and the floor
of the mouth. They vary in size from a small pin-head to large vascular networks and in
color from red to purple. The tissue covering the dilated vessels is extremely thin, permit-
ting frequent hemorrhages.
SYMPTOMS - bleeding varies from a mild loss of blood to a severe hemorrhage. It may
occur at long intervals or several times a day. Secondary anemia is common.
VII. MALIGNANT NEOPLASMS OF THE NASOPHARYNX AND PHARYNX

- comprise about 2 % of all malignant growths in the head and neck.
A. NASOPHARYNGEAL CARCINOMA (NPC) - is the most common type of
nasopharyngeal neoplasm. It is a tumor showing squamous differentiation is a unique
entity among carcinomas of the upper respiratoy and digestive tract, with distinct
geographical distribution and is strongly associated with Epstein Barr virus. The
nasopharynx is a primary site for squamous cell carcinoma, undifferentiated carcinoma,
adenocarcinoma, and primary lymphoma. Lymphoepithelioma, which may involve the
nasopharynx in younger individuals, represents a squamous cell carcinoma combined
with elements of lymphatic tissue.
PATHOGENESIS - the etiology is multifactorial, with race, genetics, environment, and EBV
all playing a role. Although uncommon in Caucasian populations, it is one of the most
frequent cancers in Southeast Asians and North Africans and has endemic clusters in
Indians and native Alaskans.
- NPC is primarily a tumor of adults with.a peak occurrence between 40 and 60 years,
although the tumor can occur in children. There is a strong male to female ratio of about
3:1, irrespective of geographic location. There is an association with dermatomyositis.
EBV is nearly always present in NPC, indicating an oncogenic role.
- the high incidence in people from southern China remains even after they immigrate to
non-endemic areas, but reduced incidence has been observed in second-generation
migrants. There is also a trend towards decreasing incidence the farther the population

33
has immigrated. These findings suggest that a combination of genetic, ethnic, and
environmental factors might affect nasopharyngeal carcinoma pathogenesis.
eGENETIC INFLUENCE - as in patients of southern Chinese origin
*EPSTEIN-BARR VIRUS - besides host genetics, EBV infection is perhaps the most
common causal agent of nasopharyngeal carcinoma.
*EXPOSURE OF THE NASOPHARYNX TO IRRITANTS - active and passive tobacco
inhalation and environmental factors such as sawdust and smoke inhalation.
*DIETARY FACTORS - consumption of preserved foods and alcohol ncluding salt-cured
fish.
*FAMILY HISTORY OF NPC
PATHOLOGY - boundaries between the categories and subtypes rely on sampling, with
considerable intra- and interobserver variability.
PATHOLOGIC SUBTYPES
*NONKERATINIZING SQUAMOUS CELL CARCINOMA - is the classic NPC
(lymphoepithelial carcinoma). It constitutes most cases in endemic areas (>95%) and is
predominantly associated with Epstein-Barr virus (EBV) infection.
® DIFFERENTIATED
®UNDIFFERENTIATED - the most common
*KERATINISING SQUAMOUS CELL CARCINOMA - accounts for less than 20% of cases
worldwide, and is relatively rare in endemic areas such as southern China.
*BASALOID SQUAMOUS CELL CARCINOMA - are exceptionally rare .
- Virtually all malignant tumours of the nasopharynx are squamous cell carcinoma, but
rarely lymphoma or adenoid cystic carcinoma may occur. NPC spreads_ locally to
invade the skull base and eustachian tube and metastasizes early to the upper deep
cervical lymph nodes. The lateral walls containing the Fossa of Rosenmuller are the most
common location of NPC and the posterior wall of the pharynx is only slightly less so.
The tumor spreads anteriorly into the nasal cavity, inferiorly into the oropharynx,
superiorly into the skull base, laterally into the parapharyngeal space and posteriorly
into the retropharyngeal space. It commonly spreads by lymphatics to the cervical lymph
nodes.
- lymphatics of the Fossa of Rossenmuller drain into the node of Rouvier within the
retropharyngeal space and subsequently to the upper deep cervical lymph nodes. This
explains why the neck lump is often the first presenting symptom of NPC. It may spread
through the bloodstream to distant sites such as the bone, lung and liver.
- less commonly a tumor is found on the roof and only rarely on the floor. Symptoms
are produced by the direction in which the tumor grows. It may extend through an orifice
adjacent to the site of origin or it may erode the bone by pressure necrosis. Malignant
tumors inthe nasopharynx may remain silent until they involve surrounding structures.
= SIGNS AND SYMPTOMS - the combination of unilateral deafness, enlarged cervical nodes
and cranial nerve palsies proclaims the diagnosis of nasopharyngeal cancer clearly.
*NECK LUMP - is the presenting symptom in more than 50% of the cases. A solitary
enlarged lymph node located posteriorly and high in the neck is often the presenting sign.
Such a node is typically wedged between the mastoid process and angle of the jaw. It
may be bilateral. The palpable cervical metastasis does not represent the primary nodal
drainage because the retropharyngeal nodes are usually involved first. It is inexcusable,
and dangerous, to biopsy such nodes until the nasopharynx has been examined and
biopsied.
«NASAL SYMPTOMS
®Blood stained nasal discharge » Nasal blockage
eAURAL SYMPTOMS
» Unilateral blocked ear » Pressure sensation in the ears

34
» Mild hearing loss »Tinnitus
*OPHTHALMO-NEUROLOGIC SYMPTOMS
* Unilateral facial numbness » Diplopia » Unilateral headache
*HOMOLATERAL HEAD PAIN - followed by nasal obstruction - next most common
symptom,
*NASAL OBSTRUCTION - as a result of extension anteriorly.
*RECURRENT EPISTAXIS
*UNILATERAL HEARING IMPAIRMENT - due to obstruction of the eustachian tube.
Lateral extension to involve the eustachian tube produces unilateral serous otitis media
with a conductive hearing loss.
*CRANIAL NERVE INVOLVEMENT - CN VI is the first one affected. This is followed by
CN V, CN IV, CN Ill. All of the cranial nerves may be involved. Pain may be referred to any
of the 3 divisions of the trigeminal nerve. CN V involvement can cause local and facial
pain or numbness. When the tumor spreads superiorly it may produce diplopia by
involving CN Vi and then CN III.
*PROPTOSIS AND BLINDNESS - invasion of the orbit
*SEROUS OTITIS MEDIA eREFERRED EAR PAIN
*HYPOSMIA eANOSMIA
=TNM STAGING CLASSIFICATION EIGHTH EDITION
TX Primary tumour cannot be assessed
TO No tumour identified, but there is EBV-positive cervical
node(s) involvement
T1 _Nasopharynx, oropharynx, or nasal cavity without
parapharyngeal extension
T2 Parapharyngeal extension, adjacent soft tissue
involvement (medial pterygoid, lateral pterygoid,
prevertebral muscles)
T3 Bony structures (skull base, cervical vertebra) and/or
paranasal sinuses
T4 Intracranial extension, cranial nerve, hypopharynx,
orbit, extensive soft tissue involvement (beyond the
lateral surface of the lateral pterygoid muscle, parotid
gland)
NX Regional lymph nodes cannot be assessed
NO No regional lymph node metastasis
N1 Unilateral cervical, unilateral, or bilateral
retropharyngeal lymph nodes, above the caudal border
of cricoid cartilage; <6 cm
N2 Bilateral metastasis in lymph node(s), $6 cm in greatest
dimension, above the caudal border of cricoid cartilage
N3a >6 cm and/or below caudal border of cricoid cartilage
(regardless of laterality)
N3b ..

35
Mo \No distant metastasis 7
M1 Distant metastasis
| §(T1NO MO
ll T2 NO-1 MO, TO-1 N1 MO
Il T3 NO-2 Mo, TO-2 N2 Mo
IVA T4 or N3 MO
IVB_ Any T, any N, M1
Ive
METASTASES - are to the retropharyngeal, deep jugular, and spinal accessory nodes.
DIAGNOSIS - currently is made by endoscopic examination followed by biopsy of the
suspected tumor. Diagnosis of NPC at the early stage would require detection of the
tumor prior to the appearance of metastatic lymph nodes in the neck or other local
extension.
*BIOPSY
*CT SCAN WITH BONE WINDOWS - to rule out cortical bone involvement
*MRI - of the head and neck.
*CHEST X-RAY - should be obtained to rule out metastatic disease.
*BONE SCAN - should be done in the setting of advanced disease to rule out metastatic
disease,
- MRI, CT, and F-fluorodeoxyglucose (F-FDG)-PET/CT are currently the most commonly
used imaging modalities for nasopharyngeal carcinoma staging and radiotherapy.
- with high soft-tissue resolution, MRI is better for evaluating primary tumour extension
and retropharyngeal lymph node metastasis than CT, while they share similar accuracy
in detecting cervical lymph node metastasis. F-FDG-PET/CT performs better than
conventional work-up (eg—chest radiography, abdominal ultrasound, — skeletal
scintigraphy) for diagnosing distant metastasis, and is also relatively more sensitive and
accurate for detecting small cervical lymph node metastases and local residual, recurrent
disease, or both. Therefore, MRI and F-FDG-PET/CT might be preferred for staging in
patients with high risk of distant metastasis.
- certainty is yielded only by biopsy. Delayed diagnosis remains a major issue. Although
NPC may be curable in the early stages, most patients present to the clinicians at late
stages. Owing to the hidden location of the tumor and their indirect manifestations,
diagnosis can be delayed for as much as 6 months in 70% of patients. Up to 13% of
patients may also present with neck lumps without a visible primary tumor (a situation
known as ‘occult primary’). Serial and multiple biopsies are sometimes necessary due
to submucosal disease, and false negative histopathological examination.
FINE NEEDLE ASPIRATION (FNA) - cytology of neck metastases at best has an accuracy of
82.6%. fismy
= TREATMENT
*RADIOTHERAPY - NPC is highly sensitive to ionising radiation; radiotherapy is the
mainstay treatment modality for non-metastatic disease. Over time, photon-based
radiotherapy techniques have progressed from conventional two-dimensional (2D)

36
radiotherapy to 3D conformal radlothorapy and then to intensity-modulated
radiotherapy (IMRT).
- currently, IMRT Is the most widely used technique. It has reduced the 5-year occurrence
rates of locoregional failure for newly diagnosed and non-metastatic nasopharyngeal
carcinoma to 7:4%,
- there is great interest in using proton or carbon ion radiotherapy for treating
nasopharyngeal carcinoma to improve the therapeutic ratio even further
*RADICAL NECK DISSECTION - is done once the primary site has been controlled, if there
mwere involved nodes at diagnosis or if any subsequently develop.
STAGE | and Il - Radiotherapy
STAGE Ill and IV - Induction chemotherapy followed by radiationy
RECURRENCE AND METASTASIS - Surgery/Radiotherapy/Chemotherapy
*CHEMOTHERAPY IN NON-METASTATIC NASOPHARYNGEAL CARCINOMA - while
early-stage nasopharyngeal carcinoma is treated with only radiotherapy as the main
curative treatment, locoregionally advanced disease requires more than radiotherapy.
Chemotherapy combined with radiotherapy is a crucial development for treating
locoregionally advanced disease. At present, the National Comprehensive Cancer
Network (NCCN) Guidelines recommend both concurrent chemoradiotherapy with
adjuvant chemotherapy or induction chemotherapy followed by concurrent
chemoradiation as level 2A evidence, and concurrent chemoradiotherapy alone as level
2B evidence for stage II-IVA nasopharyngeal carcinoma.
PROGNOSIS - is poor, but the earlier the diagnosis is made, the better the outlook.
B. CARCINOMA OF THE PHARYNX
=SYMPTOMS
*SORE THROAT - is the most common symptom of pharyngeal cancer.
«Dysphagia ¢Trismus *Globus sensation
eNeck mass *Ear mass
ADVANCED TUMORS
*Bleeding «Airway obstruction *Weight loss
DIAGNOSIS
*EXAMINATION - the head and neck region should be thoroughly examined to detect any
additional lesions, to detect any nodal spread and to document the tumor.
DOCUMENTATION
Tumors multidimensional size Location in the regions of the pharynx
® Mobility of the lesion Relationship to the prevertebral fascia
® Relationship to the larynx Vocal fold mobility
Invasion of surrounding structures
«CT SCAN AND MRI - can aid in evaluating the deep extent of the tumor and the tumor’s
relationship to the surrounding structures and in detecting small lymph nodes.
*ENDOSCOPY - will add to the evaluation of the primary tumor and permit biopsies to be
obtained. This will also aid in detecting second primary tumors.
= METASTATIC EVALUATION - should be reviewed once the tumor is staged.
*DISTANT METASTASIS - the chance for cure is minimal.
*NO METASTASIS PRESENT - the approach to treatment is dictated by the tumor’s
location and the patient’s choices
C. CARCINOMA OF THE TONSIL
- the tonsil is the most common site of squamous cell carcinoma in the oropharynx.
Tumors frequently present at advanced stages, and approximately 70% of patients
present with lymph node metastases. There is a male/female ratio of 4:1. The age of
predilection is 50-70 years. The history also often shows combined alcohol abuse and
smoking. 90% are Squamous cell carcinomas, and they are often well differentiated rather

37
than poorly differentiated. 60% of patients have lymph node metastases, of which 15%
are bilateral. 7% have distant metastasis affecting the lung, skeleton and liver.
- asymmetric tonsillar hypertrophy is a physical finding that should prompt the physician
to include neoplasms in the differential diagnosis. When this finding is accompanied by
a suspicious clinical course or history, a tonsillectomy should be performed for biopsy.
Lymphoma and squamous cell carcinoma are the most common primary tonsillar
neoplasms, but other malignant tumors may also present. Many primary malignant
neoplasms (eg, melanoma and renal cell, lung, breast, gastric and colon carcinomas)
have been reported to metastasize to the tonsil. Parapharyngeal space tumors are
important to consider as a diagnosis, since they may present with signs and symptoms
mimicking an asymmetric tonsillar hypertrophy or a tonsillar abscess.
- the predictive value of a malignant process is increased when tonsillar asymmetry is
associated with rapid enlargement, constitutional symptoms, atypical tonsillar
appearance, ipsilateral cervical lymphadenopathy, and a history of previous malignant
growths.
- in the absence of these risk factors, the likelihood of a malignant neoplasm is small.
Unilateral tonsillar enlargement in asymptomatic children is rarely of neoplastic etiology
and a true asymmetry of the tonsillar specimen is confirmed in fewer than half of cases.
However, the diagnosis of tonsillar lymphoma should be considered when unilateral
tonsillar enlargement is present either in an immunocompromised child or when acute
tonsillitis is asymmetric and unresponsive to medical therapy.
- it often metastasizes to the digastric triangle or the high jugular node known as the
tonsillar node. Such tumors extend inferiorly toward the base of the tongue and
superiorly onto the soft palate.
TREATMENT - T1 and T2 tonsil cancers can be treated with external beam radiation to the
primary site and neck with approximately 80% 5-year survival. If significant neck disease
is present, this is often combined with a planned neck dissection.
- surgery can be used as the primary treatment modality for T1 or T2 cancers in select
cases. Some tumors can be approached intraorally, but many will require complex
approaches with significant potential morbidity.
ADVANCED TONSIL CANCERS - can be treated with radiation alone, and more recently
attempts have been made to treat these tumors with chemo-radiation protocols. For
these tumors, the best cure rates can be obtained with combined therapy consisting of
surgery followed by radiation therapy. Prior to embarking on surgery the tumors
resectability must be assessed. Important areas or structures to evaluate for invasion by
cancer are the prevertebral fascia, carotid artery and skull base. If these areas are
involved, the tumor would be judged by most surgeons to be unresectable, and the
patient should be treated with radiation therapy.
- for resectable advanced tumors of the tonsils, the mandible should be evaluated. It
includes physically examining the tumor’s relation to the mandible to determine if it is
fixed. The tumor may also involve the mandible through tooth roots and these should
be inspected. If the mandible is invaded, the best approach is a composite resection with
a neck dissection.
- small tumors may be treated with irradiation, while larger tumors require surgical
resection, frequently accompanied by pre- or postoperative radiation therapy. Small
lesions with palpable metastases are usually treated by surgical resection and primary
closure.
- a lateral tongue, forehead, myocutaneous, or cervical flap can close a large defect.
Because of early metastases of moderate size lesions, neck dissection is usually
included in the surgical procedure.

38
IX. BENIGN TUMORS OF THE LARYNX
- benign tumours of the larynx cause persistent hoarseness.
MOST COMMON TUMORS
*PAPILLOMA - solitary or multiple
*HEMANGIOMA - almost exclusively in infants
*FIBROMA
A. VOCAL NODULES - are bilateral, chronic thickenings of the vocal cord epithelium,
usually located at the junction of the anterior third with the middle third. They are the
most common cause of persistent dysphonia in children. They are also a frequent cause
of deterioration in the voice quality of individuals who use their voices professionally,
particularly singers; these nodules are commonly referred to as "singers' nodules.”
=EMIOLOGY - persistent vocal abuse or hyperkinetic phonation is the single most
important precipitating factor. The lesions occur at the center of the membranous cord
because this area is the center of vibratory motion of the cord. Voice pitch is an important
factor as it is rare to see nodules in baritones or basses.
- they develop more frequently in women and male children, and in people with
occupations with highly demanding vocal activity (teachers, singers, salesmen). They are
also common in children with cleft palate.
- around 10-20% of patients with nodules have other vocal cord pathologic conditions,
that, if undetected, can be the reason for treatment failure.
PATHOPHYSIOLOGY AND PATHOLOGY - the genesis of vocal nodules is related to the
peculiar anatomy of the true vocal cords. At the free margin of the membranous vocal
cord is a subepithelial potential space (Rienke's space) which is limited superiorly and
inferiorly by the arcuate lines. This potential space is easily infiltrated by edema fluid or
blood. The lesions are located atthe midpoint of the free margin of the membranous or
vibrating vocal cord. They are usually bilateral but not always symmetrical.
- a forceful vibration causes trauma at the membranous portion of the vocal cord, leading
to edema of the submucosa. Persistent trauma during phonation may lead to thickening
of the epithelium and fibrosis at the level of Reinke’s space.
- nodules are closely related to voice misuse.
*YOUNG OR EARLY NODULE -- initially, the nodule is a soft light thickening at the
membranous portion of the vocal cord. It may be polypoid, soft, red and edematous. It is
covered by normal squamous epithelium and the underlying stroma may be edematous
and exhibit increased vascularity, dilated vessels and hemorrhage thus Producing the
polypoid and varix stages of nodule development.
*MORE MATURE NODULES - are small, pale, pointed and symmetrical and they are
precisely located directly opposite to each other and frequently a strand of mucus is seen
traversing the glottis between them. They are more firm and contain areas undergoing
fibrosis and hyalinization. The surface epithelium becomes thickened and keratosis,
acanthosis and parakeratosis may be present.
“VOICE "BREAKING" - in the higher tones and failure to maintain a tone. The lower tones
are least affected since the nodules are not in apposition when these tones are
produced.
*INCREASINGLY RAPID VOCAL FATIGUE, - usually develop before persistent, frank
hoarseness becomes apparent.
*HOARSENESS

39
= DIAGNOSIS
INDIRECT LARYNGOSCOPY OR FLEXIBLE NASOLARYNGOSCOPY - clearly shows the presence
of small, well-defined vocal cord lesions. Theso lesions are distinguishable from the
normal vocal fold by their whitish hue, are generally bilateral, and are most commonly
found at the junction of the anterior one third and posterior two thirds of the vocal fold.
*ACUTE NODULES - are usually edematous and transluscent
*CHRONIC NODULES - are white and fibrotic.
= TREATMENT
*ABSOLUTE VOICE REST - fresh, acute nodules will often disappear after a period of
enforced silence,
~ Professional singers with mature nodules who develop periodic hoarseness because
of episodic edema of the nodule will also respond well to voice rest.
*SPEECH THERAPY - should be utilized as a first-line treatment. It is the mainstay of
treatment in both children and adults. Photodocumentation of the nodules in voice clinics
indicates the treatment progress and aids patient compliance during speech therapy. The
Patient is taught how to use the voice appropriately, which often promotes regression of
the vocal cord nodules.
*CARBON DIOXIDE LASER EXCISION
*SURGICAL EXCISION - where dysphonia is not acceptable to the patient, or when the
nodules do not disappear after speech therapy.
*REMOVAL OF LARYNGEAL IRRITANTS - such as cigarette smoke and alcohol
B. VOCAL POLYPS - are benign lesions usually located the vocal edge of the vocal cord,
impending vocal cords meeting while adducting. They are usually larger than nodules,
with a wide or narrow pedicle and may have a contact lesion in the contralateral vocal
cord.
- they are most commonly found in adult males and vocal abuse and noisy environment
at work are risk factors.
OTHER FACTORS RELATED TO POLYPS
*Aspirin intake *Anxiety *Extroverted behavior
- with a history of voice abuse and heavy smoking.
= ETIOLOGY - the localized vocal polyp is the most common benign lesion of the larynx.
It is due mainly to trauma secondary to voice abuse. However, the trauma need not be of
long duration and frequently the onset of the lesion can be related to a single epiosode
of vocal strain. They may also develop acutely following an URI.
= PATHOLOGY - polyps are the consequence of a violent and short voice strength that
leads to the rupture of capillaries in the submucosa, with subsequent hemorrhage. If
after this hemorrhage, voice misuse continues the lesion can evolve into a hemorrhagic
polyp or after some time into a fibrotic polyp.
- the lesion consists of varying amounts of edematous stroma, dilated blood vessels,
fibrous tissue and hemorrhage. The early polyp is more vascular. As the lesion matures,
fibrosis and fibrinoid and hyaline degeneration become apparent in the stroma, old
hemorrhages and vessel walls.
*HOARSENESS - is the major complaint but it will vary according to size or location of
the polyp. The voice change may vary from_.almostno hoarseness to complete aphonia
when the polyp prolapses between the vocai cords.
*SENSATION OF SOMETHING IN THE THROAT - and a constant attempt to clear the
throat. It is unilateral and is situated at the same point on the vocal cord as a vocal nodule.
The lesion may be sessile and present on the upper surface of the edge of the vocal cord
but many are pedunculated and hang from a thin stalk which may allow them to prolapse
into or through the glottis.

40
- the color may range from a bright reddish-purple to a pale transluscent yellow. Polyps
may be bilateral but are most frequently localized to one vocal cord. .
TREATMENT - involves a microlaryngoscopic examination of the larynx plus excision of
the polyp both to confirm the diagnosis and exclude any other coexistent pathology. A
large polyp may conceal an occult, early laryngeal squamous cell carcinoma.
- excision is often performed using appropriate microsurgical instruments, but the vocal
cord polyp can be removed using laser. Patients can prevent recurrence by avoiding the
risk factors for disease, including smoking and vocal abuse.
C. DIFFUSE VOCAL POLYDOSIS (LOCALIZED HYPERTROPHIC LARYNGITIS)
“ETIOLOGY- persistent vocal abuse in hyperkinetic extroverted individuals is the main
etiologic factor. Smoking is the other most important inciting agent. The condition seems
to occur most frequently in middle-aged females.
= PATHOLOGY - the margins of the membranous true vocal cords are diffusely involved
by edematous tissue masses. On histologic examination, the edemais seen to be
confined to Rienke’s space which is markedly widened and filled with mucoid material
almost devoid of cells, fibrous tissue and blood vessels.
SEVERE HOARSENESS - is constant.
*VOICE PITCH - is low and tends to be a monotone which makes singing impossible.
*DYSPNEA AND STRIDOR - may occur when the polyps are large and emergency care
for obstruction may be necessary. Symmetrical pale, sausage-like masses will be seen
hanging from each membranous cord. They frequently are in approximation and
obliterate the anterior glottis so that the only airway is between the arytenoids. The
masses are usually a translucent grayish-pink color but inflammation may produce bright
redness. .
- TREATMENT - patients with lesser degrees of polyposis may get good regression from
removal of irritants and intensive vocal therapy alone. However, surgical stripping of the
cords must be performed in many cases. The treatment is most often surgical to confirm
the diagnosis, exclude any coexisting malignant neoplasms, and provide resolution;
conservative voice therapy is often not successful.
CONSIDERATIONS FOR SURGERY
*This lesion produces a characteristic vocal quality (low-pitched speaking fundamental
frequency with pitch instability), which some patients identify as an important and
desirable part of their persona. In those patients, then, to "cosmetically repair" the vocal
folds surgically may be contraindicated because the change in "vocal quality" would be
viewed by the patient as undesirable.
*There is a significant incidence of "occult" laryngeal carcinoma in smokers with Reinke's
edema. When the laryngologist suspects this possibility, a microlaryngeal examination,
with or without biopsy, or surgical repair may be indicated.
*Many patients with polypoid degeneration also have developed patterns of vocal misuse
and abuse. Therefore, before consideration of surgery, each patient should be evaluated,
counseled, and when indicated, treated by a speech pathologist trained in the
management of voice disorders. At the very least, the patient should be counseled
preoperatively to protect against abusive vocal behavior in the postoperative period.
D. LEUROPLARIA - refers to the flat, white, plaquelike lesion which may be seen on
any mucosal surface. The lesion tends to be smooth and well demarcated. Usually,
leukoplakia occurs on the superior surface of the true vocal cord but may occur
anywhere on the laryngeal mucosa.

41
-the lesions are usually small, discrete, irregular patches but sometimes they appear
as an extensive sheet. Leukoplakic patches may be present without evidence of other
laryngeal disease and have a peculiar "stuck-on" appearance. At other times, it occurs
in association with chronic inflammatory disease and malignancies.
X. CARCINOMA OF THE LARYNX AND LARYNGOPHARYNX

- represents the second most common cancer in the upper aerodigestive tract, preceded
in frequency only by cancer of the oral cavity. Squamous cell carcinoma accounts for
95% of laryngeal malignancies with the glottis being the most affected subsite.
FREQUENCY
*SUPRAGLOTTIC CA = 40%
*GLOTTIC CA = 59%
*SUBGLOTTIC CA =1%
+ENOLOGY - malignant tumors are more common in males by a ratio of 10:1, occurring
almost exclusively in smokers. The peak age incidence is 55-65 years, but it can occur in
young adults. Women are more likely to develop subglottic cancer than glottic ca.
- larynx cancer is also more prevalent among lower socioeconomic groups, for whom it
is typically not diagnosed until more advanced stages. It is directly linked to tobacco and
excessive alcohol use. Numerous studies have demonstrated that the relationship
between tobacco and laryngeal cancer seems to be a dose-dependent relationship.
RELATIVE RISKS
*For people who smoke up to half pack per day, the relative risk was calculated at 4.4
fold.
¢For people who smoke more than 2 packs per day, the relative risk is 10.4 fold.
- smoking cessation can decrease the risk for laryngeal ca.
= PATHOLOGY - 94% of cancers of the larynx and pharynx are of the squamous cell variety.
Adenoid cystic carcinoma and sarcoma may occur on rare occasions. The incidence of
nodal metastases from such a lesion varies according to primary site. Size is important
in determining the metastatic incidence and is a determining factor in deciding on the
neck dissection.
= CLASSIFICATION
*GLOTTIC CARCINOMA - refers to a tumor which is on the cord. It usually begins on the
superior surface of the true cord but may extend from the anterior commissure to and
including the vocal process. It may be unilateral or bilateral and may extend infraglotically
for a distance of 1 cm. Carcinoma of the true glottic region is one of the most common
head and neck malignancies.
- it tends to be well differentiated, to grow slowly, and to metastasize late. Because the
true cords have very limited lymphatic drainage, cervical lymph node metastases occur
in only 10% of cases. Cervical lymph node metastases usually occur when the cancer
infiltrates beyond the limits of the true cord.
- submucosal extension occurs early and can lead to involvement of the anterior
commissure and the contralateral vocal cord. The cancer can extend laterally, resulting
in cartilage destruction, or superiorly, with involvement of the false vocal cords and
aryepiglottic folds (transglottic carcinoma). Subglottic extension can also occur.
eSUBGLOTTIC CARCINOMA - refers to a tumor which extends to the lower border of the
cricoid. In general it is always more than 1 cm in size. Subglottic cancers or subglottic
extensions of a glottic cancer are associated with a high incidence of cervical lymph node
metastases.

42
*SUPRAGLOTTIC CARCINOMA - refers to a tumor which is confined from a zone on
the false cord up to the tip of the epiglottis but spares the margin of the aryepiglottic fold.
- the lymphatic drainage of the supraglottic larynx is abundant, and consequently
metastases appear early. 50% of these patients will present with cervical lymph node
metastases.
*TRANSGLOTTIC CANCER -is a tumor that crosses or involves the ventricle.
*HOARSENESS - the voice may be gravelly, change to a lower coarse volume and on to
one of near aphonia. The voice can be described as a "hot potato" voice when there is a
bulky lesion on the epiglottis or pyriform sinus.
*AIRWAY OBSTRUCTION - respiratory stridor can result. Usually involvement of one
arytenoid, or cord from fixation and partial paresis from any cause, or bilateral position
of the lesion above and below the glottis narrows the chink greatly and causes airway
obstruction.
*SORE THROAT - vague or real complaints of persistent sore throat are associated with
tumors of the pharyngeal region.
«DIET AND DEGLUTITION - a change can be made in the usual beverages enjoyed by the
patient.
*EAR PAIN *HEMOPTYSIS eA LUMP IN THE NECK
®GLOTTIC CARCINOMA - the prime symptom is hoarseness, which may persist as the
only symptom for many months. Only when spread from the cord has occurred will
earache, dysphagia and dyspnea supervene.
™SUPRAGLOTTIC CARCINOMA - as well as producing a change in the voice, may
metastasize early to the cervical nodes.
™SUBGLOTTIC CARCINOMA - produces less_ hoarseness but increasing airway
obstruction. It must not be mistaken for asthma or chronic bronchitis
SPREAD OF LARYNGEAL CARCINOMA - spread is local initially and proceeds:
¢Along the cord to the anterior commissure and onto the opposite cord
«Upwards onto the ventricular band and epiglottis
*Downwards to the subglottis
«Deeply into the laryngeal muscles, causing cord fixation.
LYMPHATIC SPREAD - from glottic lesions is late, but occurs readily from supraglottic and
subglottic sites to the deep cervical nodes.
- pulmonary metastases occur occasionally but other distant metastases are rare.
= DIAGNOSIS
*INDIRECT LARYNGOSCOPY - is the most important step in diagnosis. Every case of
hoarseness should be examined by indirect laryngoscopy; malignant growths are usually
seen easily.
*LARYNGOGRAMS - are of definite diagnostic importance.
«BIOPSY BY DIRECT LARYNGOSCOPY - is essential. Diagnosis is confirmed by
microlaryngoscopy and biopsy.
eCHEST X-RAY - must be done as bronchial carcinoma also may be present.
eCT SCAN OF THE LARYNxX - is often helpful in defining the extent of spread, and is
usually performed prior to deciding on treatment.
= TREATMENT
eRadiotherapy by external radiation is usually employed. In a small tumor limited to one
cord (the stage at which it should be diagnosed), the 5-year survival rate is 80-90% and
the patient retains a normal larynx.
«In very extensive disease or if there is recurrence following radiotherapy, total
laryngectomy is necessary. The patient obviously then has a permanent tracheostomy
and will need to develop esophageal speech. Good esophageal speech is attained by

A}
about 30% of patients; a further 30% develop reasonable voice but the remainder never
manage more than a mouthed whisper.
*Many patients are now provided with a tracheopharyngeal valve. A fistula Is formed
between the trachea and pharynx and a prosthatic valve fitted to the fistula, Occlusion by
the finger of the tracheostomy allows air to flow into the hypopharynx, while vibration of
the soft tissue produces phonation. This then allows fluent lung-powered voice for the
laryngectomee.
*Rehabilitation following laryngectomy concentrates on the development of speech with
help from the speech therapist, but also requires training in looking after the
tracheostomy, changing the tube as necessary and developing confidence socially after
mutilating surgery.
"EARLY STAGE LARYNGEAL CARCINOMA (Stages | and Il) - can be treated with either
Surgery or radiation in single-modality therapy. Because of the accumulated risk to
adjacent normal soft tissues, radiation can only be given once.
"ADVANCED STAGE LARYNGEAL CARCINOMA (Stages III and IV) - is treated with dual
modality therapy, traditionally surgery and radiation. Historically, fewer surgical
complications and possibly better survival has been found in performing surgery
followed by adjuvant radiation than by treating first with radiation and then with surgery.
The type of neck dissection chosen is guided by the extent of the neck disease.
- a preoperative consultation with a speech therapist is appropriate if significant voice or
swallowing changes are anticipated. These sessions help educate patients about the
speech and swallowing functions of the larynx and prepare the patient for postoperative
rehabilitation and therapy.
ADVANTAGES OF SURGERY vs RADIATION
=Shorter treatment period (compared with 6-7 weeks for radiation)
®The option of saving radiation for recurrence
=|mproved disease-free and overall survival
DISADVANTAGES OF SURGERY
=Greater risk "Poorer voice quality
Worse cosmetic outcome for external surgical approaches.
ADVANTAGES OF RADIATION
eBetter voice quality =Avoidance of surgical risks
SHORT TERM COMPLICATIONS OF RADIATION
=#Mucositis =Odynophagia
#_aryngeal edema even to the point of airway compromise.
LONG TERM COMPLICATIONS OF RADIATION
“Esophageal stricture =Xerostomia
= Laryngeal fibrosis =Radionecrosis
#Hypothyroidism =Delayed sarcoma
SURGICAL PROCEDURES
*VERTICAL HEMILARYNGECTOMY - removes the ipsilateral vocal cord and overlying
laryngeal cartilage. The procedure can be extended superiorly to include the ipsilateral
false cord or posteriorly to include the ipsilateral arytenoid cartilage. It is an appropriate
procedure for patients with reduced cord mobility due to cancer bulk.
- it is not for patients with reduced cord mobility due to invasion of the intrinsic
musculature, for slightly more advanced lesions with a mobile cord or when the tumor is
confined entirely to one side of the thyroid cartilage. Tracheostomy is maintained until
the swelling subsides and the airway is judged adequate.

44
*HORIZONTAL PARTIAL LARYNGECTOMY - is Indicated for patients with cancers
arising above the level of the true cords. All patients will have some degree of aspiration
following this procedure, but careful patient selection can minimize the long-term
consequences.
*TOTAL LARYNGECTOMY - is appropriate therapy for some patients with T3 laryngeal
cancers and for most patients with T4 cancers. In this situation, wide field laryngectomy
includes removal of the bilateral level Il, III, and IV cervical lymph nodes. Ipsilateral thyroid
lobectomy is performed to facilitate paratracheal lymph node dissection.
*LASER EXCISION - the carbon dioxide laser, used with direct laryngoscopy and
microscope guidance, is also a useful dissection tool, especially for supraglottic lesions.
Pathologic examination of margins is still necessary to assure that all tumor has been
excised, so an actual specimen is resected rather than vaporizing the tumor. The
advantage of this procedure is the single operative procedure, usually not requiring a
tracheostomy. The disadvantage is a poorer voice quality than in radiation.
*RADICAL OR MODIFIED NECK DISSECTION - the presence of cervical lymph node
metastases is an indication for radical or modified neck dissection. Elective neck
dissection or radiation therapy is not indicated for T1 and T2 glottic cancers but is
indicated for all supraglottic cancers and for T3 and T4 glottic cancers. If the primary
cancer is treated by surgery, an elective neck dissection is appropriate unless adjuvant
radiation therapy to the primary cancer site is planned. In that case, elective neck
radiation therapy can be given and the neck dissection deferred. If the primary cancer is
treated with radiation therapy, elective neck radiation therapy is appropriate and
operative dissection can be deferred.
*MICROLARYNGEAL SURGERY - the endoscopic removal of small T1 larynx cancers can
be achieved safely and effectively with use of the operating microscope and
microlaryngeal dissection instruments.
=PROGNOSIS - Glottic carcinoma diagnosed early and treated effectively is virtually a
curable disease.The later the diagnosis is made, the worse the prognosis. Never neglect
hoarseness. Supraglottic and subglottic tumours have a poorer prognosis owing to the
likelihood of rather later development of symptoms and early nodal spread. About 10%
of all patients successfully treated for laryngeal cancer will subsequently develop
carcinoma of the bronchus.

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ANATOMY OF THE ORAL CAVITY,

PHARYNX, LARYNX & NECK

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Thyroid carr. Cricoid curt. BIG sadam fren “Foreaar,

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Canilago, Hyold bona

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z.. 1 Palatine tonsil

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Il. FUNCTIONS OF THE ORAL CAVITY AND OROPHARYNX

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I. PHYSIOLOGY OF DEGLUTITION OR SWALLOWING

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TY. LARYNGEAL PHYSIOLOGY

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- although vibration is primarily determined by the passive effects of subglottic pressure,

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