Ent LQ1

EARS, NOSE & THROAT (ENT)
Topic: Ear Anatomy, Physiology, Embryology and Congenital Anomalies

Lecturer: Dr. Cruz, Melanie Grace
ANATOMY AND PHYSIOLOGY OF THE EAR Internal Auditory Canal:

Ear:  Also known as the internal
 Organ of hearing and balance acoustic meatus
 Related to the temporal bone  It lies on the temporal bone
The temporal bone is located at the lateral and exists between the inner
portion of the skull as depicted in the image ear and posterior cranial fossa
on the left in green.  CN VIII is composed of cochlear
and vestibular nerve
 CN VII and CN VIII enter and
Parts of the Temporal Bone: exit the internal auditory canal
ANATOMIC SUBDIVISIONS:
1. Squamous
o It forms the lateral wall of the skull and is the biggest part
2. Mastoid
o Located posteriorly and contains air cells
3. Tympanic
o Forms the bony ear canal
4. Styloid
o The elongated portion (based on the image above)
5. Petrous
o Not shown in the image above
o It contains many vital structures and is best seen in the
medial side
Development of the Mastoid Bone:

 The mastoid process is absent at birth and
the facial nerve is still superficial
o The facial nerve is therefore Lecture Discussion:
vulnerable to injuries during The ear is subdivided into the outer, middle and inner portion
delivery using obstetric forceps  Outer ear is from the auricle up to the tympanic membrane
 The mastoid tip elongates by the SCM  Middle ear is from the tympanic membrane up to the oval
(sternocleidomastoid) pull when the infant window
begins to hold up the head  Inner ear includes the labyrinth
 Pneumatization begins in infancy and up to
around 4-6 years old External Ear - Pinna
 The largest and most consistent air cell is Landmarks:
the Antrum  Helix and Anti Helix
 Tragus and Anti-tragus
3 Degrees of Temporal Bone Pneumatization:  Conchae Cavum and
Cymba
 Lobule
Lecture Discussion:
The most protuberant portion of the ear is the Pinna. It is comprised of
cartilage and skin EXCEPT for the lobule which is composed of skin and fat.
The structure of the pinna is intricate comprising of several elevations and
depressions.
 Helix – outermost rim of the auricle
Lecture Discussion:
 Conchae – deepest depression of the ear
A well pneumatized or well aerated mastoid will have numerous air cells as
represented here as the honeycomb-like appearance. Black representing air,
while the White septations as bone.
A diploic bone is partially pneumatized
A sclerotic bone is dense and has no air cells
#GrindNation Page 1 of 7
Strength in knowledge
External Ear – Ear Canal Innervation of the External Ear and Tympanic
 EAC length: 2.5 cm Membrane:
 Lateral or Outer 1/3 is  VII – Sensory cutaneous branches
Cartilaginous  V – Auriculotemporal nerve
o Has cerumen  X – Arnold’s Nerve
glands and hair  C3 – GAN
follicles  C2, C3 – Lesser occipital nerve
 Medial 2/3 is Bony
o No cerumen glands or hair follicles Lecture Discussion:
 Isthmus – Junction It just shows that the External Ear and the Tympanic
Membrane have similar nerve innervation
o This is an anatomical constriction
External Ear – Tympanic Membrane

 8 mm (wide) x 9 mm (high) x 0.1  ALDERMAN’S NERVE/ARNOLD’S NERVE - Irritation of the Auricular
mm (thickness) branch of CN X may cause reflex coughing, vomiting or sneezing
 Pearly white in color
 Parts divided by malleolar folds: Middle Ear
1) Pars Flaccida  Wedge-shaped cavity with six walls
 Shrapnell’s  The space is very narrow from side-
membrane to-side
 Located superiorly
2) Pars Tensa Middle Ear Boundaries:
 Located inferior to the malleus 1. Roof – tegmental wall
 It has a great surface area 2. Floor – jugular wall
3. Posterior – mastoid wall
Tympanic Membrane Layers: 4. Anterior – carotid wall
1. Outer Ectoderm – continuous with the skin of the external ear 5. Lateral – membranous wall (represents the tympanic membrane)
2. Middle Mesoderm – fibrous (inner circular and outer radial) 6. Medial – labyrinthine wall
containing the handle of the malleus o This wall separates the middle ear from the inner ear
3. Inner Endoderm – continuous with the mucosal membrane of the (labyrinths)
middle ear
Notch of Rivinus
Annulus Fibrosus
 Fibrocartilaginous ring supporting
the Tympanic Membrane
 Lies in the tympanic sulcus (groove
in the tympanic bone)
 Deficient superiorly at the NOTCH
OF RIVINUS
Annulus Fibrosus
Pars Flaccida
 Retracts readily if there is any absorption of air when Eustachian tube
is blocked and it bulges if there is fluid or inflammatory swelling Additional Information: Middle Ear Boundaries
 Superior - TEGMEN TYMPANI (epitympanum)
within the middle ear cavity
 Inferior - JUGULAR BULB (hypotympanum)
 When the ear drum retracts, the short process of the malleus
 Medial - PROMONTORY, OVAL WINDOW, ROUND WINDOW,
becomes prominent LATERAL SEMICIRCULAR CANAL
 When it bulges, the landmarks are obliterated  The footpiece of the stapes seals off the oval window.
 Lateral - EAR DRUM, Scutum
Retracted Pars Flaccida Bulged Pars Flaccida  Anterior - TENSOR TYMPANI, internal carotid artery, EUSTACHIAN
TUBE
 Posterior – FACIAL CANAL and aditus ad antrum
Middle Ear Contents:

 Ossicles – malleus, incus and stapes
 Branches of Facial Nerve – nerve to stapedius and chorda tympani
 Tympanic Plexus – sensory to middle ear over the promontory
 Middle Ear Muscles – tensor tympani and stapedius
Ossicles Nerve Supply of the Middle Ear:

 Suspended in the middle ear cavity forming a chain for conduction of  Auriculotemporal branch of CN V
vibrations from the drum to the oval window  Auricular branch of CN X (Arnold’s nerve)
Maleus Head, neck and handle  Tympanic Branch of CN IX (Jacobsen’s nerve)
Body, short process, long process or lentiform
Incus
process Inner Ear
Head, anterior and posterior crus, foorplate; seals 2 Main Parts of the Inner Ear:
Stapes
off the oval window in a piston like fashion 1. Bony Labyrinth (Osseus Labyrinth) – the outer shell
2. Membranous Labyrinth – suspended within the bony labyrinth
Middle Ear Joints

Diarthrodial Joint Syndesmotic Joint
 Malleoincudal  Stapes
 Incudostapedial  Oval window Osseus Labyrinth
 One of hardest bone in the body
Branches of the Facial Nerve (Mastoid Segment)  Contains the organ for hearing and balance
 Nerve to the stapedius which is attached to the stapes  Specifically it contains the:
 Chorda tympani which is responsible for taste sensation to the 1) Bony cochlea
anterior 2/3 of the tongue 2) Bony vestibule
3) Bony semicircular canals
Middle Ear Muscles  3 canals lie at right angle to one another
Muscle TENSOR TYMPANI STAPEDIUS
ORIGIN Cochleariform Process Pyramidal Eminence  Contains perilymph – it is the fluid within the labyrinth
ATTACHMENT Malleus Stapes
Nerve to the Stapedius 3 Types of Semicircular Canals:
NERVE SUPPLY CN V-C3 which is a branch of  Superior or anterior semicircular canal
CN VII  Lateral or horizontal semicircular canal
Pulls the handle of the Pulls the stapes away  Posterior semicircular canal
malleus medially from the oval window
ACTION
3 Openings of the Cochlear Canal:
Pulls the tympanic Pulls the stapes
 Round window – fenestra cochlea
membrane inward outward
 Oval window – fenestra vestibule
Function of Middle Ear Muscles:  Cochlear Aqueduct - opens into a tiny canal from the basal turn of
 Contract in response to high intensity sound or anticipation to the cochlea through the temporal bone to the subarachnoid cavity
vocalization by stiffening the ossicular chain to protect the inner ear
against overstimulation Membranous Labyrinth
3 Parts of Membranous Labyrinth:
 Dampening effect
1. Membranous Semicircular Canals
o 2 openings from the Lateral
Eustachain Tube
SCC
 The eustachain tube is lined by pseudostratified columnar ciliated
o 3 opening from the Superior
respiratory epithelium found in the nose, nasopharynx, and middle
SCC and Posterior SCC (joining
ear
at the crus communis)
 Main function: Equalize the pressure between the ear and the
o Ampulla – dilated ends
atmosphere
 2 Muscles that dilate the Eustachian Tube:
2. Membranous Vestibule
o Tensor Veli Palatini – innervated by the mandibular
o Utricle and saccule
branch of CN V from the Otic Ganglion
o Utricular duct (UD) & Saccular duct (SD)
o Levator Veli Palatini – innervated by pharyngeal branch
o Endolymphatic duct – fusion of the UD and SC
from CN X
3. Membranous Cochlea
Blood Supply of the Middle Ear:
o Scala media/cochlear duct
 Deeper auricular branches of the internal maxillary artery
o Ductus reuniens – connecting the cochlear duct and the
saccule
Tectorial Membrane
 The membranous labyrinth contains endolymph  Gelatinous structure which lies on top of OHC and IHC
Cochlea Pillars of Corti

 Lies horizontal in front of the vestibule  Structure in between OHC and IHC
 Resembles a snail shell of 2 ½ (2 ¾) turns
 Apex – lower frequency Perilymph vs. Endolymph
 Base – higher frequency Perilymph Endolymph
 Spiral lamina – attachment of the Basilar membrane Volume 78.3 cu.mm 2.76 cu.mm
 Spiral ganglion - average of 31,000 ganglion cells Sodium Content 310 mg/100 mL 15 mg/100 mL
 Cochlear Nerve Potassium Content 30 mg/100 mL <600 mg/100 mL
Protein Content 70-100 mg/100 mL 20-30 mg/100 mL
pH 7.2 7.5
Specific Gravity Lower Higher
Lecture Discussion: Perilymph vs. Endolymph

The most important to remember here is:
 Perilymph  Sodium content is higher compared to endolymph
 Endolymph  Potassium content is higher compared to
perilymph
AUDITORY SYSTEM
 The pinna collects
sound waves.
 The sound waves are
transferred to the ear
canal and into the ear
drum.
 The ear drum vibration
will cause ossicular
Different Parts of the Cochlea: vibration or coupling.
 SCALA VESTIBULI – above the  The ossicular vibration will have what is called impedance matching.
Cochlear Duct (Perilymph)  Impedance matching – efficient sound transmission
 SCALA TYMPANI – below the o Without this, sound will just bounce off the oval window
Cochlear duct (Perilymph)
 Vibration of ossicles ( malleus - incus - stapes)
 SCALA MEDIA – endolymph
 Footplate of stapes strikes the oval window
 Perilymphatic displacement leads to basilar membrane displacement
 Modiolus
which will cause endolyphatic compartment displacement
o Central Conical Axis
allows passage of
the auditory nerve fibers Area Ratio Lever Ratio
TM: footplate Malleus to Incus
 Helicotrema
17-20:1 1.31:1
o Apex of the modiolus
 Stria vascularis
Hair Cell Activity
o Blood supply of the cochlea
 Stereocilia moves towards kinocilium.
 There will be depolarization (180 spikes/sec).
Organ of Corti
 There will be opening of gated channels.
 Principal sensory
 There will be influx of potassium from the endolymph.
structure in cochlea
 The membrane potential will be positive once there is potassium
epithelial structure on
influx.
top of the basilar
membrane  The calcium channels will be activated.
 Calcium channel activation will cause calcium influx.
Hair Cells  Glutamate will be released into the nerve endings.
 Functions as receptor
cells that transduce mechanical movement into electrochemical Von Bekesy Travelling Wave Theory
signal  Wave from cochlear base transfers to apex
o Inner Hair Cells (IHC)  The motion of the basilar membrane takes the form of a traveling
 Single row wave, like the one that occurs when you flick a rope
 Most important sensory cells of hearing  The wave oscillates at the frequency of stimulation
o Outer Hair Cells (OHC)  For the Organ of Corti to be given maximal displacement, creating
 3 rows COCHLEAR MICROPHONICS which is a local electrical potential
 Acts as amplifiers
 It is important to note that the basilar membrane is narrow near the Blood Supply:
base of the cochlea and wide at the apex. It is also stiffer at the base  INTERNAL AUDITORY ARTERY (branch of anterior inferior cerebellar
than the apex  this is the reason why at the base, we can hear artery) – blood supply to the cochlea that enters into the internal
higher frequency sounds while at the apex, we can hear lower auditory canal
frequency sounds
EMBRYOLOGY AND CONGENITAL ANOMALIES
Auditory System: External Ear:
E Eight Nerve  The ear starts to develop at the 3rd-7th week of gestation
Lecture Discussion:
C Cochlear Nucleus This is the auditory pathway of  Modification of the surface ectoderm by which the skin is brought to
O Superior Olivary Nucleus how we are able to hear. From the functional relationships with the ossicles at the drum and the
L Lateral Lemniscus periphery, impulses will travel external canal
I Inferior Colliculus from the cochlear nerve which will
M Medial Geniculate Body go to the Eight Nerve all the way to
the Auditory Cortex
A Auditory Cortex
 BA 41 – Primary Auditory Cortex

 BA 42 – Secondary Auditory Cortex
Balance Apparatus
 3 Semicircular Canals – angular acceleration
 Vestibule – linear acceleration
o Utricle – horizontal Hillocks of His
o Saccule – vertical  6 Hillocks of His
 1st Branchial Arch
Semicircular Canals o 1 – Tragus
 Dilated ends at the vestibule called ampulla containing crista o 2 – Helical Root
ampullaris o 3 – Helix
 Cristae ampullaris contains hair cells (sensory)  2nd Branchial Arch
 On top of the hair cells is a gel- like structure called cupula where it o 4 – Anti helix
is suspended to the wall of the opposite ampulla o 5 – Anti tragus
 Coplanar o 6 - Lobule
o If one side is excitatory the other side is inhibitory  Pinna – 1st and 2nd BA
 Angular acceleration of the body causes movement of the endolymph
with the semicircular canal parallel to the rotation. ANOMALIES OF THE EXTERNAL EAR
 Due to inertia, movement of endolymph causes displacement of the  Maldevelopment of the 1st and 2nd arches
hair cells opposite to the direction of the acceleration stimulus.  Auricular deformities are the most prominent
 Torsional pendulum model  Most common is a LOP EAR deformity.
 MACROTIA – abnormally large ear
Utricle and Saccule  MICROTIA – abnormally small ear
 Linear acceleration in relation to  ANOTIA – absence of ear
gravity
 Ear Canal Atresia/Stenosis - Partial or complete stenosis of the ear
 Contains macula canal.
 Hair cells suspended in a  Rudimentary ear appendages
gelatinous matrix
 Failure to fuse of the Hillock of His leads to
 Otoliths (CaCO3) crystals are formation of pre-auricular sinus cyst
suspended on top of the otolithic
membrane
Vestibular Function:
 Vestibule-ocular reflex - stabilize eye gaze
 Vestibulocolic reflex – posture and gait
 Vestibulospinal reflex - posture and gait, extension of limbs
 ANS – adjust hemodynamic reflex maintaining cerebral perfusion
 Cerebellum – coordination and adaptation of vestibular reflex
 Cortex – perception of movement and orientation
Stimulation of the vestibular organs result in neural excitation that travels via
the vestibular nerve to the 4 vestibular nuclei in the brain
Nystagmus
 A Reflex Eye Movement elicited upon stimulation of the semicircular
canals
 Jerk Nystagmus: Slow and Fast Phases
1st Branchial Cleft/Groove ANOMALIES OF THE MIDDLE EAR

 Ectoderm  Involve the ossicles
 If forms the following:  Congenitally deformed, disrupted, or fixed.
o Meatal plug which  Common deformities include a missing part of the incus and fixation
hollows out of the stapes.
o External auditory  Isolated ossicular malformations may be correctible through ear
canal, glands and surgery.
hair  If the stapes is fixed, stapedectomy and prosthesis replacement will
o External layer of re-establish hearing.
the TM (tympanic
membrane) Development of the Inner Ear
 Develops as an ectodermal thickening on the lateral surface of the
1st Branchial Pouch head at the level of the 4th ventricle in embryos of 4 mm in size (9 –
 Endoderm 10days)
 It forms the following:  Otic placode (ectoderm) – forms the otic pit - pinches off to form otic
o Tubotympanic recess cyst/otic vesicle
o Middle ear space  Neural crest migrate to otic cyst - acousticofacial ganglion - geniculate
o Eustachian tube ganglion moves away from otic cyst leaving the - vestibulocochlear
o Mastoid air cells ganglion hair cell formation
Development of the External and Middle Ear Otic Vesicle

 The meatal plug and tubo-  Medial becomes endolymphatic diverticulum
tympanic recess meet to  Lateral becomes utriculosaccular chamber that becomes later the
form the tympanic ring utricle and saccule
 At birth - the ring is present o (DORSAL) Utricular chamber becomes the utricle and
but has not yet developed semicircular canals
into bony meatus. o (VENTRAL) Saccular chamber becomes the saccule and
 After birth - The tympanic cochlea
ring extends by  The endolymphatic duct is shifted down to form a connection
intramembranous between the utricle and saccule.
ossification, adding a new bone laterally forming the bony meatus  14 – 15 days (6 mm size) – endolymphatic ducts
 MIDDLE EAR – developmentally an air sinus and develops as an  37 days (15 mm size) – semicircular canal
outpouching of the pharynx  Macula (statoreceptors) reaches adult form by 14-16 weeks
 The ossicular chain – develops from the upper end of the first  Crista reaches adult form by 23 weeks
(mandibular) and second (hyoid) cartilages  Organ of corti reaches adult form by 25 weeks
 The ossicles develop outside the middle ear cavity and are  Cochlea – evolves parallel with the middle ear and ossicles
extramucosal and are secondarily incorporated to the M.E. by  The cartilagenous otic capsule conceals the inner ear and later
formation of attic recesses. becomes petrous bone.
1st and 2nd Branchial Arches: Development of the Otic Vesicle

1st Branchial Arch  A region of ectoderm overlying the Rhombencephalon thickens to
 Meckel’s cartilage form the otic placode which invaginates to form otic pits which will
 Mesoderm will develop into tensor veli palatine and tensor tympani eventually become the otic vesicle
 Neural crest will develop into maxilla, malleus and body of the incus
Development of the Inner, Middle, and External Ear
2nd Branchial Arch  ach otic vesicle will subdivide into dorsal and ventral compartments
 Reichert’s cartilage and then become the organs of the inner ear
 Styloid  The ossicles will emerge from the mesenchyme of the first and
 Stapedius second pharyngeal arches
 Lenticular process of the incus  Dorsal Compartment
 Stapes o Endolymphatic duct
o Utricle
o Semicircular canal
 Ventral Compartment
o Saccule
o Cochlear duct
 The auditory tubes surrounds the ossicles creating the tympanic
cavity of the middle ear
 The point of contact between the tympanic cavity and the external
ear becomes the tympanic membrane or ear drum
 The pharyngotympanic tube will dissociate to form the Eustachian
tube and the tympanic cavity
ANOMALIES OF THE INNER EAR C. NON-GENETIC

 Pregnancy exposure to rubella virus
A. CONGENITAL
especially vulnerable during the 1st
 No cochlear and labyrinthine development trimester
Michel’s Aplasia
 Complete aplasia  SNHL
 Partial aplasia Congenital Rubella
 Pathology shows aplasia of the saccule and
 1.5 cochlear turn (bony and membranous the Organ of Corti.
labyrinth affected)  Cardiac anomalies, blindness, and mental
Mondini’s Deformity  Flattened cochlea with development of retardation.
only the basal turn  Erythroblastosis faetalis results from RH
 Abnormally dilated vestibule and vestibular blood incompatibility of the parents
duct characterized by bilirubin deposition in the
 Autosomal recessive Kernicterus brain
 Cochleosaccular dysplasia (membranous  There’s jaundice, mental retardation,
Scheibe’s Deafness
labyrinth only) cerebral palsy, and deafness may be
 The bony labyrinth is fully developed present shortly after birth
 Aplasia of the Cochlear duct  Thyroid disease associated with deafness
 Organ of Corti and adjacent ganglion cells as in this condition is referred to as
Alexander’s Deafness
 The bony and membranous labyrinth are Cretinism endemic cretinism. Presenting with mixed
normal hearing loss having both conductive and
 Lateral displacement of the lacrimal points sensorineural component
and medial canthus
 Hyperplasia of eyebrows D. OTHER ABNORMALITIES
 Partial albinism in the form of a white  This disease begins in early childhood
Waardenburg’s Disease
forelock  Skeletal deformity, dwarfism, mental
 Flat nasal root Hurler’s Syndrome
retardation, blindness
 Mild to severe SNHL (sensorineural hearing  Profound SNHL
loss)
 Skeletal defects such as fusion of the
 Maybe autosomal dominant, recessive or cervical vertebra, spina bifida, scoliosis,
Albinism sex-linked, characterized by bilateral Klippel-feil Syndrome torticollis
severe to profound SNHL  Vestibular dysfunction and profound SNHL.
 Congenital male dystrophy  Autosomal recessive
Dominant Deafness  Congenital SNHL – high frequency  Obesity, DM, retinitis pigmentosa, and
Onychodystrophy (DDOD)  Small, short fingernails, toenails progressive deafness.
 Rare Alstrom’s Disease  Hearing loss starts at age 10 and slowly
 Retinitis pigmentosa progresses.
Usher’s Syndrome
 Moderate to severe SNHL  Inherited as an autosomal recessive trait
 Craniofacial dysostosis
 Premature closure of the cranial sutures,
B. CHROMOSOMAL short upper lip, protruding lower lip,
Trisomy 13-15 D underdevelopment of the midface,
Crouzon’s Disease
“Patau’s Trisomy” exophthalmos, hook nose
 Atresia of the external meatus and mixed
deafness.
 Autosomal dominant trait
 Low set ears, undifferentiated pinna,  Autosomal recessive
absence of external and middle ears  Mental deficiency
Richards-Rundle
 Cleft lip and palate, microphthalmia,  Ataxia
Syndrome
coloboma iridis, and aplasia of the optic  Hypogonadism
nerve  Severe SNHL at childhood
 Infants die within a short period of time  Autosomal recessive, X-linked
 Childhood progressive glomerulonephritis
Alport’s Disease  Progressive SNHL particularly on higher
frequencies.
 Type IV collagen defect
Trisomy 18 E
“Edward’s Syndrome”
 Malformed pinna, low set ears

 Flexion of the index finger over the 3rd
finger
 Micrognathia, a prominent occiput.
 Patients with this syndrome fail to
thrive and dies in infancy
Topic: Diseases of the External Ear, Middle Ear and Mastoid
Lecturer: Dr. Uy, Sidney
DISEASES OF THE EXTERNAL EAR  Predisposing Factors for Otitis Externa:

1.) Cerumen o Change from acidic to alkaline pH
 Product of both sebaceous & apocrine glands in the cartilaginous part o Increase in temperature & humidity
of the ear canal o Trauma
 WET TYPE of cerumen is more common than the dry type.  Examples are trauma due to :
 Has protective qualities:  Excessive cleaning
o Vehicle for removal of epithelial debris & dirt away from the  Swimming
ear drum
o Lubrication  Management of Otitis Externa:
o Prevents dryness of the skin of the external auditory canal o Careful cleaning of the ear canal either by suction or cotton
o Bactericidal effects swipes
o Evaluation of discharge, canal wall edema & ear drum
 Management of Impacted Cerumen: o Decide if an ear wick is to be used.
o Ceruminolytics  softens the ear wax o Selection of local medication
 Water
 Mineral oil Image showing How to use an Ear Wick in treating Otitis Externa
 H2O2 (Hydrogen Peroxide)
 Ex: Otosol, Audiclean, Auraglar
Generic name of these Otic/Ear drops is
Sodium Docusate
o If the impacted cerumen has already softened, removal can

already be done. Impacted cerumen can be removed by:
 Curette
 Water irrigation
 Suctioning
Images illustrating how removal of impacted cerumen is done:

Curette Suctioning
Lecture Discussion: How to Use an Ear Wick in treating Otitis Externa

Ear Wick  ensures that the otic drops would reach inside the ear canal.
Because if the external auditory canal is really swollen and is almost closed
up, the otic drops might not reach the inner part of the ear canal. We usually
use a sterile gauze or sterile cotton as an ear wick.
Water Irrigation
 There are 2 types of Otitis Externa:
1. Otitis Externa Circumscripta (Furunculosis)
2. Diffuse Otitis Externa (Swimmer’s Ear)
Otitis Externa Circumscripta (Furunculosis)

 Confined only on one side
 Confined to the fibrocartilagenous part of the
ear canal
 Usually begins in a pilosebaceous follicle
Lecture Discussion: Water Irrigation
 Usual agent: Staphylococcus aureus or S. albus
This can only be done if the patient’s ear wax is already softened. The only
 Ear can develop abscess if left untreated.
contraindication is if the patient has perforated tympanic membrane 
you cannot do aural irrigation  Pointing can occur.
 It resembles a pimple inside the ear canal
2.) Otitis Externa  Treatment:
 Another common disease of the external ear o Antibiotic otic drops
 It is an external infection of the ear. PND otic drops are usually used  Polymyxin B,
 Only the external auditory canal is affected. Neomycin, and Dexamethasone otic drops
 It is usually caused by BACTERIA, FUNGI or VIRUS.
o Analgesic
 It can be non-infectious such as in the case of NON-SKIN DERMATOSIS.
o Warm moist compress
o Drainage (if needed)
Diffuse Otitis Externa (Swimmer’s Ear) 4.) Herpes Zoster Oticus (Ramsay Hunt Disease)
 Swimmer’s ear  Viral infection of external ear
Usually affects patients that went swimming in a water that is  Manifestations:
dirty with ear trauma. o Facial nerve paralysis
o Otalgia or ear pain
 The whole ear canal is inflamed o Herpetic eruptions in the auricle and
 Occurs commonly during hot, humid weather  aggravating factor surrounding area
 Etiology is Pseudomonas aeruginosa
 Manifestations:  Treatment:
o Severe pain o Since it is a viral infection, its treatment is symptomatic.
o Tragal tenderness o It usually resolves on its own but it takes a long time.
o Swelling of canal  Self-limiting
o Patient may present with scanty discharge o Pain relievers can be given.
o Normal or slight hearing loss due to the swelling of ear canal o Steroids are given to accelerate the inflammation of the ear.
o Lymphadenopathy can be present in severe cases.
 Neck nodes or Cervical lymph nodes 5.) Perichondritis
 Effusion of serum or pus between the perichondrium
 Treatment: and the ear cartilage
o Ear wick is used since the ear canal is very inflamed and is  It has the appearance of “cauliflower ear” which is
almost closing. very common among boxers.
o Otic drops  It is due to regular trauma or inflammation
 Antibiotics & Steroids  Manifestations:
o Severity will determine if there is a need to give oral antibiotics o Red, tender, warm and swollen auricle
 Penicillins
 Macrolides – if allergic to penicillins  Management:
 Quinolones o Antibiotics are given either orally or parenterally
o Topical medications  if there are external lesions
3.) Otomycosis (Fungi) o Otic drops can be given.
 Fungal infection of the ear canal o Antibacterial ointments with steroids
 Common in o Evacuation of fluid through 2 big incisions then bolster packing
immunocompromised patients afterwards
 Also common in patients with o Excision of necrotic cartilage
poor hygiene
 Common etiologies are EAR MALFORMATIONS
Pityrosporum and Aspergillus Lop ears Excessively protruding ears
(A. niger and A. flavus) Anotia Congenitally absent ear
 Manifestations: Microtia Congenitally small ear
o Itchiness Macrotia Congenitally big ear
o Patient may sometimes present with ear blockage because the Atresia Ear did not form
molds of the fungus are embedded in the ear canal.
o Patient may present with dry ear.
o In physical examination with otoscopy:
 Blackish spores with hyphal elements can be seen.
 It has a “wet newspaper” appearance
 Management:
o Regular ear cleaning
o All the hyphal elements must be removed inside the ear canal
because the patient will not recover even if otic drops are given
but still there are hyphal elements left inside the ear canal.
o Otic drops are given once all the hyphal elements have been
removed.
o Antifungal otic drops given usually for 2 weeks
Candibec solution, Kenacomb otic  are brand names of GRADING OF EAR MALFORMATIONS
the antifungal otic drops Grade 1 Smaller than normal but the ear has mostly normal anatomy
Their generic name is Clotrimazole Part of the ear looks normal, usually the lower half
Grade 2
The canal may be normal, small or completely closed
o Acidification is done for easier eradication of the fungi Just a small remnant of peanut shaped skin and cartilage
Grade 3
There is no canal, which is called “aural atresia”
Complete absence of both external ear and ear canal
Grade 4
Also called “anotia”
Lecture Discussion: Ear Malformations

If the patient has already Grade 3 or 4 ear malformation  request for a
temporal bone CT scan to ensure if the patient has normal ossicles, external Lecture Discussion:
auditory canal, middle ear, and inner ear.
Treatment for Exostosis &
 If the patient has normal structures for the middle ear & inner ear
Osteoma is surgical excision. If
 you can now do surgery to create an external auditory canal
so that the patient can hear left untreated, it may cause
 If the patient has intact middle ear but inner ear (cochlea) has hearing loss because it might
problems  you can do surgery (cochlear implant) or bone block the external auditory canal
anchored hearing aids (blocking the sound entering
going into the ear drum). Also it
PRE-AURICULAR SINUS ANOMALIES might cause infections, irritation
 1st Branchial Cleft Anomalies (Pre-auricular sinus) or inflammation.
 Cyst or sinus tract involving pinna & ear canal
 Contains endodermal tissue only

Type I
 Free of cartilage
 Has both epithelium of 1st cleft and cartilages
from 1st and 2nd arches
Type II  Sinus tract drains intermittently & can be
infected
 It usually needs surgery
 Management:
o Usually, excision is done if not infected. Darwin’s Tubercle Keloid Scarring
o If infected, antibiotics (macrolides or beta lactams are given).
o If there is an abscess, drainage must be done. BENIGN SKIN LESIONS
o The whole sinus tract must be removed.  Sun damaged skin
Solar Keratosis
 Painless
Lecture Discussion: Management of Preauricular Sinus  Scaly
Proper treatment is surgical excision. If left untreated, a Type II Preauricular  “Cutaneous horn”
sinus would cause recurrent infections, and sometimes abscess. To prevent  No treatment is usually done
those from happening you have to tell the patient to undergo surgical  You can advise to undergo
excision. cryotherapy or excision of
the solar keratosis
ACCESSORY AURICLE (SKIN TAG)
 Nothing is done Seborrheic Keratosis
 It does not need surgery.  Round
 It can be removed through surgery (for  Dark
patients who are vain)  “liver spots”
 Sun damage
 No treatment is usually done
 You can advise to undergo
EXTERNAL EAR TUMORS cryotherapy or excision of
 Single, rounded growth with bony peduncle the seborrheic keratosis
to inner 3rd of the bony canal
Osteoma  If symptomatic and causes recurrent Tophi
infections, it can be removed.
 Due to gout
 Usually, no treatment is done.
 Painless, smooth, uric acid
 Dense
crystals subcutaneously
Exostosis  Rounded protuberance of hypertrophic canal
deposited
bone
 Can be resolved by treatment
 Resembles a pimple inside the ear canal
of the gout
 Can be big or small
Ear Polyps
 Can sometimes be infected
 Keloid Scarring
 Surgically removed
Darwin’s Tubercle  Thickening on the helix at the junction of the
upper and middle thirds
Carcinomas of the Ear  Basal cell carcinoma
 Squamous cell carcinoma
MALIGNANCIES OF THE AURICLE  Management:

Basal Cell Carcinoma o Hearing loss is associated with thickened and retracted ear
drum.
o For retracted ear drum, MYRINGOTOMY is done.
 Wide excision is advised. 1.) Perforation

 Margins at excision must be
Types of Perforation: Causes of Drum Perforation:
negative.
 Tubal  Sudden changes in pressure, as in
 Patient may be subjected to  Central barotrauma, blast injuries
chemo or radiotherapy after.  Marginal  Foreign bodies, pointed objects
 Pars Flaccida or Attic  Ear cleaning or manipulations
Squamous Cell Carcinoma
 There may be a need to

remove the whole ear
because it may distally
spread.
 Patient may be subjected to
chemo or radiotherapy after.
 Central perforation – most common type (90-95% of patients with

perforated ear drum)
FOREIGN BODIES IN THE EAR
 Very common especially in pediatric patients Clean Traumatic Perforations Contaminated Perforations
 Can be insects inside the ear  Heal spontaneously  Ear drops and systemic
 Usually put in by the patient  The ears must be kept dry. antibiotics are given.
 The foreign body must be removed.  Antibiotics may be given if with  Closure is done when infection
 If it is an insect, it must be killed first before it can be removed. pain & inflammation. resolves.
o Kill it with mineral oil or lidocaine spray  Closure is done through
 Usually removed with forceps or suction TYMPANOPLASTY.
 Management:
DISEASES OF THE TYMPANIC MEMBRANE
Tympanosclerosis o If it is an inactive type, there is no treatment done.
o Antibiotics are given for actively draining infections.
o Oral antibiotics may be given if it is severe
 Thickened ear drum 2.) Myringitis

 Inflammation of the ear drum
 Usually self-limiting
 Can cause bulging ear drum
Retracted drum
Bullous or Hemorrhagic Myringitis
o There are blebs or bullae in the ear drum
o Ear drum is not perforated.
 Ear drum is retracted o The ear drum may contain serous fluid, blood or both.
inwards o Ear drum may appear red or purple.
o Usually caused by Mycoplasma pneumoniae
 Management:
o Antibiotic ear drops (PND otic drop)
Bulging drum
o Pricking of blebs
 Fine needle or knife
 Swollen ear drum
 Can be due to tumor or
otitis media
EUSTACHIAN TUBE DISORDERS  Treatment:

Functions of Eustachian Tube: o Decongestants
 Ventilation o Cessation of diving
 Drainage  Precaution/Management:
 Protection of middle ear from nasopharyngeal contamination Barotrauma o Avoid flying/diving when + colds
(continued) o Equalize pressure
o Decongestants before flying/diving
Assessment of Eustachian Tube Function:
o Instruct the patient to do valsalva and
 Lateral displacement of the drum Toynbee to equalize pressure.
 Listening while patient does: o Instruct the patient to chew gums
o Toynbee – swallowing with nostrils pinched
o Vasalva – blowing hard with mouth & nose closed 3.) Otosclerosis
 Usually autosomal dominant
1.) Abnormally Patent Eustachian Tube  Affects both men & women
 The Eustachian tube is open all the time.  Progressive conductive hearing loss in early adulthood
 Air enters the middle ear with respiration.  Pathology:
 History: o Normal bone is replaced by soft bone (otospongiosis) in area
o Significant weight loss  loss of fatty tissue around ET opening of stapes footplate  fixation of footplate
 Manifestations:
o Otophony/Autophony – the patient hears his own respiration
o Sensation of ear fullness
o “plugged up” feeling
 Physical Examination:
o Drum is thin & atrophic
o Drum moves in & out with respiration
Schwartze Sign:
 Management:
o You do myringotomy
o Insertion of ventilation tube
To equalize the pressure between the middle ear and
external ear
2.) Eustachian Tube Obstruction

 Causes:
o Inflammation or congestion of ET
o Adenoiditis or nasopharyngitis
o Tumor in the ET or nasopharyngeal area blocking the ET o Red pulsating mass is seen inside the ear drum
opening o Drum is pink or orange due to vascular otospongiosis
o Foreign body in the ET
o Scarring due to extensive surgery  Physical Examination:
o Destruction or lack of anchorage of tensor veli palatini muscle o Drum is normal
o Schwartze’s sign: drum is pink or orange due to vascular
 Lack of anchorage of tensor veli palatini muscle otospongiosis
 There is no delineation between oro and nasopharynx.
 There will be middle ear infection because bacteria  Management:
Cleft Palate
can easily go into the middle ear. o Middle ear surgery
 Inadequate ventilation of the middle ear o Stapes is removed and malleus is directed into the footplate
 Inflammation
OTITIS MEDIA
 Damage to tissues caused by changes in barometric Natural History of Otitis Media:
pressure during diving or flying, with ET blockage
 Pressure difference between atmosphere & middle
ear reaches 90-100 mm Hg making the ET cartilaginous
part collapse
Barotrauma  Diving or flying, during descent
 Manifestations:
o Pain, ear fullness, hearing loss
 Physical Examination:
o Drum is congested
o Hemorrhagic blebs or hemotympanum
o Drum perforation
Otitis Media continued….. Serous & Mucoid Otitis Media continued…..

 Very common especially in pediatric patients  Causative Factors:
 There is infection of the middle ear via the Eustachian tube (fever). o Eustachian tube dysfunction (ETD)
 A patient with otitis media usually has had cough or colds a week before o Adenoidal hypertrophy
which is left untreated. o Chronic adenoiditis
 There is mucosal edema in the middle ear and ET. o Cleft palate
 There is hyperemia of the tympanic membrane and purulent middle ear o Nasopharyngeal tumors
effusion which leads to bulging tympanic membrane. o Barotrauma
 If left untreated, it leads to pressure necrosis of tympanic membrane o Pharyngitis/sinusitis
resulting in perforation. o Radiation therapy
 Mucopurulent discharge comes out o Immunologic/metabolic deficiency
1.) Acute Purulent Otitis Media  Physical Examination:

 There is obstruction of ET o Immobile drum on pneumatic otoscopy
 “Abscess in the middle ear” o Amber or yellow color drum (serous OM)
 Most common Etiologies: o Dull & opaque drum (mucoid OM)
o Pyogenic bacteria o Malleus appears short, retracted & chalky white
 Strep pneumoniae (most common)
 H. influenzae (children & adolescent)  Treatment:
 Beta Hemolytic Strep o You treat the cause of the otitis media
o Antibiotic, decongestants, ET ventilation exercises (Toynbee,
 Manifestations: valsalva), allergy hyposensitization
o Pain o Allergic rhinitis should be treated because the infection can go
o Fever into the ear since there is nasal congestion in these patients.
o Malaise o Allergic rhinitis is treated to relieve pressure in the middle ear.
o Headache o Surgery: Myringotomy, ventilation tube insertion, removal of
o Earache fluid
o Anorexia in children Surgery is usually the last resort after 4-6 months of
o Nausea and vomiting in children medical management without any known improvements.
Lecture Discussion: MASTOID

The main difference between the ear pain of otitis externa from 1.) Acute Coalescent Mastoiditis
otitis media would be the tragal tenderness.  Found in untreated/inadequately treated otitis media patients
 When the patient has otitis externa  pain is on the  Etiology is same as otitis media
external side and when the tragus is examined, there is  Manifestations:
pain. o Pain, fever, hearing loss
 When the patient has otitis media  the pain is inside of o Post-auricular swelling
the ear. Even if you manipulate the external ear or auricle, o Sagging of posterior canal wall
tragus, there is no pain because the pain is inside the ear. o Mastoid tenderness
 Physical Examination:  Management:

o Drum is red & bulging, with blood vessels injected & prominent o Wide myringotomy
o Wide incision to evacuate all the pus inside
 Treatment: o Antibiotics, after Culture/Sensitivity test
o Antibiotics given for 10-14 days o Surgery (mastoidectomy)
o Amoxicillin 80 mg/kg/day - drug of choice
o Ampicillin 2.) Chronic Otitis Media & Mastoiditis
o Coamoxiclav Active Inactive
o Cephalosporins  Presence of infection  Previous active infection which has
o Sulfisuxonate & Erythromycin (macrolides for penicillin allergic  Draining ear due to “burn out”
patients) granulation tissue or  No otorrhea
cholesteatoma  Hearing loss, vertigo, ear fullness,
2.) Serous & Mucoid Otitis Media (Otorrhea) tinnitus
 Transudation of plasma from the blood  Dry perforation
Serous Otitis Media vessels in the middle ear due to hydrostatic  Tympanoslerosis, ossicular disruption
pressure differences
 Active secretion from glands & cysts in the
Mucoid Otitis Media
middle ear lining mucosa
Chronic Otitis Media & Mastoiditis continued….. TUMORS OF THE MIDDLE EAR
Manifestations:  Originates from the glomus bodies that
relate to the jugular bulb in the floor of the
 Otorrhea Glomus Jugulare or
middle ear, or from nerve distributions from
o Purulent Glomus Tympanicum
the middle ear
o Mucoid (active secretory glands)
 Highly vascular tumor, bulging purplish
o Foul-smelling, putrid & dirty yellow (cholesteatoma) mass (Brown’s sign)
o Thin, watery (TB)  It sometimes extends out of the ear.
 Due to ear drum perforation, patient has conductive hearing loss. Carcinoma of the Ear  Most common malignant tumors of the
 Pain may be rare but may indicate complication. middle ear are adenoid cystic CA and
 Vertigo – erosion of semicircular canals adenocarcinoma.
 Perforation
o Marginal & attic (cholesteatoma) Management:
o Multiple (TB)  Surgery
 Chemotherapy
 Management:
o Conservative
 Keep water out of the ear.
 Cleaning with hydrogen peroxide or alcohol
 Antibiotic drops
Usually what is given is quinolone otic
drops/ofloxacin otic drops. Sometimes you can
also give oral antibiotics – quinolones
(ciprofloxacin/levofloxacin)
o Surgery
 Tympanoplasty – to restore hearing
You are creating a new ear drum
 Mastoidectomy – to produce safe & dry ear

This is done especially if the patient already has
cholesteatoma. When you are doing
mastoidectomy, you are also doing
tympanoplasty, the difference is that here, you
drill out all the affected tissue inside the mastoid
bone
3.) Cholesteatoma
 Found in chronic otitis media & chronic mastoiditis
 Keratinizing squamous epithelium (skin) entrapped in the middle ear &
mastoid
 Increases in size and erodes the bone
 Damage the ossicles
 Press on the facial nerve
 Treated by mastoidectomy
Complications of Chronic Otitis Media & Chronic Mastoiditis:

 Hearing loss – conductive, sensorineural
 Facial nerve paralysis
 Labyrinthitis
 Petrositis – CN V, CN VI
 Lateral sinus thrombophlebitis
 Brain abscess
 Meningitis
Topic: Diseases of the Inner Ear
Lecturer: Dr. Caluag, Jim
Introduction:  Deafness can be assessed by tuning fork testing

If an infection involves the external ear, the common term that we use is  Headache, pain and fever may be absent.
otitis externa  A stiff neck accompanied by elevated spinal fluid pressure and an
If an infection involves the middle ear, it is known as otitis media increase in WBC count is not a good sign.
But if an infection involves the inner ear, it is called as labyrinthitis.
 A unilateral tympanogenic labyrinthitis produces more severe
 There is no such term as Otitis Interna
vestibular upset than a bilateral meningogenic labyrinthitis
LABYRINTHITIS This is because the patient is unable to adjust quickly enough to an
 Is an inflammatory process that involves both the auditory and acute labyrinthine failure
vestibular portions of the labyrinth giving rise to sensorineural hearing
loss and dizziness. Chronic Stage
 The inflammation may be localized to involve only the cochlea/auditory  ACUTE STAGE is followed by the CHRONIC STAGE or LATENT
labyrinth, which renders the patient to have hearing loss/deafness. LABYRINTHITIS characterized by FIBROBLASTIC PROLIFERATION within
 It may also localize to involve the vestibular labyrinth which will enable the inner ear fluid spaces.
the patient to complain of dizziness alone.  This chronic stage follows the initial stormy period and usually lasts
 The infection of the inner ear could come from other regions or other from 2-6 weeks.
structures.  By this time, the inner ear is already completely destroyed and deafness
 May spread from adjacent structures such as middle ear or mastoid is now complete.
(tympanogenic/otogenic labyrinthitis) or from meninges  Incapacitating vertigo has already subsided but a milder vestibular
(meningogenic labyrinthitis) upset and positional vertigo usually persist.
 Whether it is otogenic or meningogenic form, both disease entities  Audiologic, and vestibular studies revealed markedly reduced cochlear
involve the spread of infection first into the PERILYMPHATIC SPACES and vestibular function
causing extreme damage into the end organs of hearing and balance.  If bilateral meningogenic labyrinthitis has occurred, there will be
 Another way of the spread of the infection is through the bloodstream difficulty in ambulation, especially on soft surfaces
or HEMATOGENOUS spread and this is a special characteristic of viral
inflammations involving the inner ear. Healed Stage
Viral infection invades the labyrinth by the way of stria vascularis  This is followed by the third stage also known as the HEALED STAGE or
and the infection is called viral endolymphatic labyrinthitis giving COMPENSATED LABYRINTHITIS which is characterized by
rise to deafness resulting to damage to the end organs of hearing OSSIFICATION OF THE SO-CALLED LABYRINTHITIS OSSIFICANS.
 This period commences after 2-3 months or it takes years before
FORMS OF LABYRINTHITIS labyrinthitis ossificans will occur in the membranous labyrinth.
1.) Suppurative/Purulent Labyrinthitis  By this time, the patient has fully compensated the loss of auditory and
 Characterized by complete deafness or permanent hearing loss due to vestibular functions as per hearing and caloric testing
destruction of sensory areas of the labyrinth  Occasionally, positional vertigo may persist for some months during
 Consists of 3 Stages: this stage.
1. Acute Stage (Stormy Period)
 Characterized by the invasion of pus cells Management:
2. Chronic Stage (Latent Labyrinthitis)  Suppurative labyrinthitis must be actively treated during the ACUTE
 Characterized by fibroblastic proliferation within the STAGE with:
ear fluid spaces o Bedrest
3. Healed Stage (Compensated Labyrinthitis) o Intensive doses of Penicillin/Cephalosporins
 Characterized by ossification of the so called o Sulfa drugs and Quinolones
labyrinthitis ossificans o Rehabilitation in the Healed stage
Acute Stage:
 It starts with the ACUTE STAGE which is characterized by the invasion  If SNHL (sensorineural hearing loss) or vertigo is present, MODIFIED
of pus cells. RADICAL MASTOIDECTOMY must be done to eradicate Mastoid and
Middle Ear Diseases
 The acute stage is characterized by a stormy period lasting for 1-2
weeks wherein the vestibular symptoms peaks for the first few days
Complications:
then gradually subsides after a week.
 The most serious stage is the ACUTE STAGE because during this stage,
 When diffuse suppurative labyrinthitis occurs unilaterally, the patient
complications may occur by the spread of the infection to adjacent
has severe vertigo and the patient cannot stand or sit upright.
regions such as to the internal auditory canal along the nerves and the
 The patient must lie quietly on the side of the diseased ear which is
vessels or to the cochlear aquiduct.
completely deaf.
 Common complication is Septic Meningitis
 Slight head and body movements cause the patient to vomit.
o Extradural and cerebellar abscesses as well as sinus
 The surroundings seem to spin in the direction from the normal to the
thrombosis are possibilities
diseased side.
 The patient is very incapacitated to cooperate with tests that suggest a
diagnosis of the basic clinical picture.
 Caloric tests reveals impaired vestibular response
 Labyrinthitis should be differentiated from brain lesions
In labyrinthitis, labyrinthine nystagmus occurs for a few weeks and
then subsides whereas in a brain lesion nystagmus is noted for a
much longer duration
2.) Viral Labyrinthitis  Heavy metals (Gold, Lead, Mercury)

 It is usually seen in patients with measles, mumps and influenza.  Arsenic
 The virus gains entry to the endolymphatic spaces progressing via the  Aniline Dyes
3. Chemicals
stria vascularis and the condition is known as VIRAL ENDOLYMPHATIC  Alcohol
LABYRINTHITIS.  Tobacco
 Vestibular symptoms in VIRAL ENDOLYMPHATIC LABYRINTHITIS  Carbon Monoxide
usually is present during the onset but it subsides after about 2-3 days.  Bleomycin
4. Anti-cancer Drugs
 In viral labyrinthitis, deafness develops quickly and persists as a  Cisplatinum
permanent handicap.  Salicylates (Aspirin)
 Vestibular difficulty is not usually incapacitating for these viral disorders 5. Miscellaneous  Polybrene
so the patient usually does not consult to the doctor early in the course
Agents  Nitrogen mustard
 Quinine
of the disease necessitating a retrospective diagnosis after a time
relapse and the deafness of the patient has already become stable.
 There are certain drugs such as MANDELAMINE – induces tinnitus alone
 Since it is viral, treatment is supportive, symptomatic and non-specific.
 Streptomycin in large doses primarily destroys the Vestibular labyrinth
 It is a self-limiting condition and the patient will eventually recover.
sparing the Auditory Labyrinth although hearing will eventually
deteriorate
3.) Toxic (Serous) Labyrinthitis
It is important to monitor patients on streptomycin therapy for
 Also known as serous or irritative labyrinthitis
systemic diseases
 It is characterized by chemical changes in the inner ear fluid spaces but
there is no pus cell invasion.
Management:
 Serous labyrinthitis could occur after infection of bacterial toxins
 The most effective treatment for ototoxicity caused by drugs is to
involving the round and the oval window or after a meningeal infection.
withdraw from using the drug.
 It could also occur following an ear surgery
 The damage in ototoxicity is permanent.
 Spontaneous vertigo occurring in the presence of middle ear infection
 Hearing loss of the patient may be subjective but may not be supported
indicates serous labyrinthitis.
by clinical findings.
 If nystagmus is present – irritative type (the quick component is towards
 If upon examination, the patient complains of hearing loss bilaterally
the affected ear).
but upon inspection, both ears are normal, hearing loss may be
 There will be hearing impairment.
attributed to the use of such drugs mentioned above.
 Caloric Test – diminished vestibular response
 When vertigo or sensorineural hearing loss develops, erosion of the NEOPLASAMS OF THE INNER EAR
lateral semicircular canal or invasion of the round window membrane 1.) Malignant Lymphoma and Leukemia
is suspected.
 Only involves the temporal bone including the bone marrow of the
 Serous labyrinthitis causes less severe vertigo as compared to petrous apex as well as infiltrations involving the middle ear.
suppurative labyrinthitis in which the patient is severely incapacitated
by the rapid destruction of the end organs. 2.) Terminal Leukemia
 Management:  When leukemia becomes terminal, actual hemorrhage can occur
o Treatment involves administration of large doses of Penicillin involving the inner ear and complete deafness will result.
IV given in the meningitic dose of 2-3 million units per day.
o Symptomatic care which includes sedation and anti- 3.) Acoustic Neuromas
vertiginous drugs may help.
 Some of the most common tumors of the inner ear are tumors involving
o Surgery for more complicated cases
the CEREBELLO-PONTINE ANGLE such as ACOUSTIC NEUROMAS.
If granulation tissue is present in the M.E. or Mastoid, a
complete MASTOIDECTOMY must be done to alleviate the
Neoplasms
source of infection in the inner ear
 All patients complaining of dizziness, ringing of the ear, unilateral SNHL
and facial paralysis should have audiometric test for pure tone, a
OTOTOXICITY
careful caloric examination and radiologic examination of the
 Hearing loss (deafness and ringing of the ear) may result from
temporal bone including MRI and CT scan
detrimental effects of certain substances that involves the inner ear.
 The tumor can involve the vestibular nerve causing dysfunction
Agents Responsible for Causing Ototoxicity although true whirling vertigo is absent
 Aminoglycosides  There is generally a feeling of disequilibrium associated with other
 Chloramphenicol neurologic symptoms
 Ristocetin  Characteristic feature of an acoustic tumor – inability of the patient to
1. Antibiotics
 Macrolides understand speech (RECEPTIVE APHASIA)
 Pharmacetin  Once a tumor is suspected, a diagnostic test for auditory fatigue in
 Polymyxin B Sulfate
tumors of the internal auditory canal should be requested –
 Ethacrynic acid
CLIVOGRAM (Pantopaque Myelography) of the internal auditory canal
2. Diuretics  Furosemide
and posterior fossa
 Mannitol
Management:
 Removal of the tumor depends upon its biologic nature, location, size,
and symptom-causing disabilities
 Surgery varies from Middle Cranial fossae or Posterior Cranial fossae
approaches
TRAUMA SENSORINEURAL HERING LOSS

 Hearing loss may result from several forms of trauma such as noise  Quite a common complaint
exposure, explosive blasts and blows to the head and the ears.  It is a permanent and progressive disorder although there are cases of
 The fact that noise exposure can produce hearing loss has been known sensorineural hearing loss that can be reversible if the disease is
for a long time as Boilmaker’s deafness but lately a significance has identified and treated early.
been given to minor degrees of such hearing losses.  Examples include endolymphatic hydrops or Meniere’s Disease, or
 In general, an 85 decibel of noise exposure is injurious. other types of fluctuant hearing losses due to allergies, vascular
 Hearing loss caused by noise exposure results in extreme damage problems, serous or toxic labyrinthitis and ototoxicity.
involving the organ of Corti.  Hearing loss may also result from syphilis and hypothyroidism and
 The documented time of exposure to 80 decibel of noise is 54 minutes. proper treatment for the systemic disease will eventually result to
 If the noise is concentrated at 50 decibels, earphones should be used hearing improvement.
for less than 2 hours.  In the case of syphilis, the disease process may be localized to involve
 If a person is exposed to a 50 decibel noise for 6 hours, there is a only the inner ear and a trial period of high doses of Penicillin therapy
residual effect in the acoustic nerve and noise induced hearing loss can given intravenously will lead to improvement of the hearing function.
develop.  The main hope in dealing with sensorineural deafness lies in prevention.
 Animal research indicates that exposure to high intensity sounds for  When permanent sensorineural hearing loss is found, it is important to
long periods causes varying degrees of degeneration from slight provide follow up to the patient in order to assess the progression of
changes in the hair cells to complete degeneration and destruction of the hearing loss.
the Organ of Corti.  Audiology may be helpful in providing rehabilitation to the patient in
relation to the patient’s problems at work or in any social situation.
Factors Affecting Noise-Induced Deafness:  Hearing can be improved through amplification following hearing aid
 Overall level of noise education.
 Frequency composition of the noise  Hearing aid must be recommended by a professional in order for the
 Daily distribution of the noise patient to have satisfactory results.
 Total time of exposure to the noise  It is also important to teach patients lip reading along with hearing
amplification in order for them to function normally in the society.
Management:
 The most effective method of treatment is to avoid noise. TINNITUS
 The second most effective method of treatment is to reduce noise  Also known as ringing of the ears
exposure by wearing ear defenders (ear muffs).  A sound experience perceived by the patient originating with himself
Ear defenders - generally provides only up to 35 decibels of  Tinnitus heard at the center of the head indicates that the origination
protection. If the sound is intense enough, it can still be injurious in the two ears is of the same pitch and the loudest of the experience
practically arises from the neural apparatus of the central nervous
FRACTURES OF THE TEMPORAL BONE system.
 Bleeding caused by fracture cannot be controlled or treated by
applying pressure. 1.) Objective Type
 Manifests as a profusely bleeding ear  The tinnitus is heard not only by the patient but also by the examiner
 Any form of instrumentation must not be done unless sterile upon auscultation of the external auditory canal and the examiner will
instruments will be used because the injury might be further hear a sound which is usually described as a bruit type of tinnitus.
contaminated.  Causes of Objective Tinnitus:
 Fractures of the temporal bone may give rise to hearing loss and o Altered sound conduction
dizziness. This is associated with obstruction to sound conduction
seen in impacted cerumen, a middle ear fluid or a simple
1.) Longitudinal Fracture otosclerotic fixation of the stapedial footplate described as
 Considered to be less severe in causing deafness as compared to the a hollow sea-shell type of a sound due to masking of a well-
horizontal type functioning cochlear neural apparatus from the covering
effect of ambient sound
 May give rise to a concussion fracture in the inner ear resulting to
sensorineural hearing loss and usually there is a delayed onset of facial
o Vascular pathology
paralysis that would occur at about 24-48 hours
When a middle ear pathology exceedingly vascular as in a
 It is managed conservatively with steroid therapy and rehabilitation.
carotid body-like tumor, a pulsing sound of blood flow can
be heard as a troublesome tinnitus with exceedingly
2.) Horizontal or Transverse Fracture vascular and extensive otosclerotic foci
 The fracture line will extend to involve the internal acoustic meatus
going into the bony labyrinth. o Clonic contraction of middle ear muscles
 The bony labyrinth cannot heal by primary intention so secondary When the tensor-tympani and the stapedius develops
inflammation arises in the inner ear which gives rise to a profound clonic contraction, the result is a flutter or a machine gun-
sensorineural hearing loss and a dizziness together with an abrupt onset like sound in the ear. Nervous tension, stress, and fatigue
of facial paralysis. plays a part
 It is radically managed by doing mastoidectomy under general
anesthesia on an indication of facial nerve decompression. o Cervico-cranial vibrating phenomena
Vibratory phenomena perceived as an unpleasant sound
experience if the loudness is above the reception threshold
of the cochlear neural apparatus
Causes of Objective Tinnitus continued….. VERTIGO

o Patent Eustachian Tube  A patient with dizziness oftentimes comes to the clinic complaining of
Produces rushing sounds of air during respiration and lightheadedness, giddiness, imbalance or disequilibrium.
perceived as autophony by the patient, rapid weight loss  Vertigo is described as a sensation or hallucination of a twirling
and use of birth control pills are frequent factors motion.
 It is important to determine the cause of dizziness in order to establish
treatment and diagnosis.
2.) Subjective Type
 Tinnitus is heard only by the patient and is the most frequent type. Causes of Vertigo
 Causes of Subjective Tinnitus:  Refraction errors  Anemia
o Pathologic alterations in the cells of the end organ of Corti  Acoustic neuroma  Pregnancy
Pathologic disturbance in the hair cells on the basal turn of  Glaucoma  Postural hypotension
the cochlea results to high-pitched tinnitus described by  Brain lesion (tumors, infection  Chronic otitis media
the patient sounding like a bell ringing or trauma)  Hypertension
 Locomotor ataxia  Labyrinthitis (any form)
o Physical distortion of the cochlear sensory system  Tabes dorsalis  Toxic exposure
Creates a discordant cacophonic sound experience which is  Chronic alcoholism  BPPV
exceedingly distressing occurring in Meniere’s disease in  Multiple sclerosis  Vertebra-basilar insufficiency
which hearing impairment occurs first as lack of  Diabetes mellitus  Labyrinthine concussion
discrimination as a result of frequency distortion  Migraine  Meniere’s disease
 Hypoglycemia  Temporal bone fractures
o Endolymphatic hypertension  Seizures (grand mal)  Vestibular neuronitis
Results from functional vascular change in the terminals of  Cerebello-pontine angle lesions  Dehydration
the cochlear vascular system usually occurring in patients  Intracranial space occupying  Electrolyte imbalances
with fundamental endocrine imbalance lesions
o CNS disorders  Any disorder that causes unilateral reduction in vestibular function may
A neural apparatus central to the cochlea can be the origin cause vertigo
of tinnitus. Cerebello-pontine angle lesion affecting the 8th  The best way to establish whether vestibular activity is reduced,
nerve trunk directly generates a minor high pitched tinnitus vestibular function is measured by Caloric Test done by tilting the
not usually localized to the ear patient’s head 60 degrees backward and irrigating the ear with cold
water, a horizontal nystagmus of 1-3 minutes duration occurs with fast
Treatment for Tinnitus: component towards the opposite side
 Correction for a known cause is the most effective positive treatment  Most patients have very active response and the characteristic of
since therapy can be aimed specifically. nystagmus must be noted
 A bedside clock radio, loudly ticking alarm clock or a fan provides There are 3 characteristic of nystagmus exhibited by the patient:
ambient noise to mask the ringing at bedtime. 1. Vertical nystagmus – indicates brain lesion
 Tranquilizers and sedatives may be initially used but should be 2. Horizontal nystagmus – indicates that there is
discontinued as the patient becomes more adjusted to the symptoms. labyrinthine lesion
 The patient should be informed that there are no miracle drugs or 3. Rotary nystagmus – means that the vertigo is systemic
surgical procedures for tinnitus. in origin
 If there is an accompanying hearing loss, wearing hearing aids will
increase ambient sound to mask the tinnitus.  Vertigo due to CENTRAL DISORDERS – central vertigo may be due to:
o Multiple sclerosis
o Acoustic neuromas
o Seizures
o Basilar insufficiency
o Vascular accidents
 Several conditions affect the vertebral basilar arterial system and may
cause vertigo
Cervical Spondylitis
 May cause compression on the Basilar Artery resulting to vertigo
 Another condition is insufficient blood supply to the basilar system
 Chronic ischemia of the vertebral basilar arterial system due to
Atherosclerosis produces vertigo
Benign Paroxysmal Vertigo (BPPV) Other Management of Meniere’s Disease:

 Condition usually seen in adults when the patient’s head is placed in a  If the patient has INCAPACITATING VERTIGO in spite of extended
certain provocative position medical treatment, LABYRINTHECTOMY is done in which the inner ear
 A patient with this problem has nystagmus towards the affected ear. contents are surgically removed and surgical drainage of the
 Most evidence to date locates the causative lesion to involve the utricle. Endolymphatic sac to reduce swelling
 May follow trauma or may appear spontaneously  Another is IV administration of high doses of streptomycin which will
 Hearing and Caloric Testing are Normal primarily destroy the vestibular labyrinth, although hearing function
should be well monitored
 Management:
o Reassurance that the condition is not serious
o Antiemetics and sedatives can help
Vestibular Neuronitis
 Also known as epidemic labyrinthitis because it sometimes seems to
occur in epidemic form
 Patient presents with intermittent vertigo.
 Examination shows normal hearing but with a reduced caloric reaction
 Thought to be due to a virus that attacks the ganglion of the vestibular
nerve but attacks the whole vestibular labyrinth
 Thought to be due to the activation of Human Herpes simplex virus
 Medications are supportive but not specific.
 A self-limiting
Vertigo caused by Tumors

 Hearing loss and vertigo can be caused by tumors affecting the middle
or inner ear.
 Tumors of the temporal bone may be classified as primary or
secondary.
Primary Tumors:
 Glomus jugulare tumor of the middle ear
 Chemodectomas
 Squamous cell carcinoma of the ear canal and the middle ear
 Acoustic neuromas
 Management:
o Treatment after an early diagnosis is preferably surgical.
o Radiotherapy is a useful pre and post-operative adjunct
therapy.
MENIERE’S DISEASE (ENDOLYMPHATIC HYDROPS)

 There is an excessive amount of endolymph being produced which
results to an increase in the volume of the endolymph resulting to
swelling of the membranous labyrinth that will eventually cause
dizziness and deafness (sensorineural hearing loss).
 The cause is probably related to a disturbance in the osmotic pressure
gradient at the blood-endolymph barrier.
 Triad Symptoms of Meniere’s Disease:
o Tinnitus (Subjective)
o Deafness (SNHL)
o Vertigo (Episodic)
 Management:
o Diuretics are given to reduce the swelling of the membranous
labyrinth.
o It has the same principle of management with glaucoma.
o Sedatives
o Central vasodilators
o Antiemetics
Topic: Basic Audiology
Lecturer: Dr. See, Nixon
AUDIOLOGY Tuning fork Tests:

 Is a subspecialty in the field of ENT-HNS that deals with the evaluation  Weber Test
of hearing and rehab of individuals with communication problems o Test of lateralization
 Reasons for Evaluation: o Result: if tone lateralize to:
o Medical diagnosis of the locations and type of diseases  Better ear – sensory loss
o Assessment of the impact of hearing problem  Poor ear – conductive loss
 Types of Hearing Evaluation:  Rinne’s Test

o Tuning fork – can test for: o Compares bone against air conduction
 Conductive hearing impairment o If the result is:
 Sensory hearing impairment  (+): AC > BC  normal or Sensory hearing loss
 EXCEPT FOR mix type  (-): BC > AC  conductive hearing loss
o Pure tone audiometry
o Speech audiometry  Schwabach’s Test
o Special tests: o Compares patient’s bone with the examiner (assuming the
 Impedance examiner is normal)
 BERA Comparing the patient’s ability to hear the tuning fork vs.
the examiner’s
TYPES OF HEARING IMPAIRMENT
 Conductive Type Hearing Loss o Result:
o Problem lies in the external and middle ear  Equal with examiner: Normal
 Sensory Neural Hearing Loss  Prolonged: conductive
o Problem lies in the inner ear and the whole auditory pathway  Diminished: sensory
o Auditory pathway: (COLIMA)
 Cochlea  Bing’s Test
 Superior Olives o “Occlusion test”
 Lateral lemniscus o Result:
 Inferior colliculus  Positive: increasing and decreasing hearing ; normal
 Medial geniculate body or sensory loss
 Auditory cortex  Negative: no change in variation or conductive loss
 Mixed Type
AUDIOMETRY
Lecture Discussion: Pure Tone Audiometry
 Audiometer – an electronic device w/c produces sound free of noise
Conductive and Sensorineural hearing loss can be diagnosed with a tuning
(sound energy or overtones)
fork EXCEPT for the third type (mixed type  combination of conductive and
sensorineural, it can only be determined by audiological evaluation)  Parts:
o Attenuator: variation of sound intensity; measured in decibels
TUNING FORK TESTS o Frequency oscillator: changes the frequency pitch; measured
 Measured in hertz (cycle per second) in hertz
 128, 256, 512, 1024, 2048, 4096 and 8192 Hz o Transducers: earphones and bone vibrators
512, 1024, 2048  these are part of your speech frequency.
 Lower than that (256, 128 Hz) we call it “low frequency tuning Lecture Discussion:
fork” Audiometer – has different parts similar to that of a radio
 Higher than that (4096, 8192 Hz) we call it “high frequency  Attenuator – similar to a volume regulator
tuning fork”  Frequency oscillatory – (comparing it to a radio) it could change the
different stations of the radio
 Transducers – (comparing to a radio) it would be the speakers
Figure Above: Figure Above: Basic Audiometer & Head Phone, Bone Vibrator
The low frequency tuning forks (C-128, C-256)  they have a rounded tip on Head phone – we use the headphone for air conduction testing
top which we call “Dampers,” these are there to prevent the production of Bone vibrator – we use it for bone conduction testing
overtones when you overstimulate the tuning fork by hitting it too much.
Below it are your “Tines or Prongs/Tongs,” then the “Body” and the “Stem
or Neck.”
Underneath is the “Hilt or Base”  part of the tuning fork that should touch
the patient’s head
 Interaural Attenuation:  Procedure: HUGHSON WESTLAKE TECHNIQUE

o Is the reduction of a signal’s intensity as it is transmitted from Your textbook have described a technique but fails to acknowledge
one ear to the other the author of that technique. In the textbook, it is the Hughson
o Estimates: Westlake Technique  it is the most universally accepted (even in
 In Bone conduction testing, 0 dB other countries). This is also known as the 5 up 10 down technique
 In Air conduction testing, 45 db
1. Test better ear always at 1KHz, 2KHz, 4KHz, 8KHz, 500Hz,
250Hz - Air Conduction
We give 1000 Hz  this is the amount of initial sound
chosen because the speech frequency is between 500-2000
Hz, so 1000 Hz is the mid-speech frequency, patient will be
able to easily identify this tone when it is presented
2. Starting at 0 dB level and ascend by 10 dB increment

3. Follow the 5 up 10 down rule
4. Successive ascent of 5 dB increment until a typical response is
obtained
Lecture Discussion: Interaural Attenuation 5. Enter appropriate symbol
If the air conduction testing, you stimulate the right ear with 50 dB, 5 dB can 6. Proceed to the next frequency 15-20dB below the previous
be heard on the left ear (the non-tested ear)  patient will capable of threshold
responding to it but it is a false positive response 7. Same procedure done with Bone testing
For bone conduction testing, since we are vibrating the right mastoid  the Lecture Discussion: 5 up 10 down rule
whole skull will vibrate as well as the non-tested ear (the left ear)  patient For example you give stimulus at 0 dB, the patient did not respond. Give
will also be responding to that = false positive result another 10 dB, the patient did not respond. And then when you give it 30 dB,
the patient responded  that is not yet the threshold of the patient. You
follow the 5 up 10 down rule:
 Cross Hearing:  So you decrease 30 dB to 20 dB, the patient did not respond. Add
o Patient respond to the test signal on the non-tested ear another 5 (=25 dB), if the patient did not respond then add another
To eliminate the cross hearing or interaural attenuation  5. If the patient responded again at 30 dB  that means that it
we give another sound that is complex (a hissing sound to would be the threshold of the patient at 1000 Hz by air conduction
distract the non-tested ear so that the patient will
concentrate in responding to the interrupted tone given on The next test would be at 2000 Hz then followed by 4000 Hz, 8000 Hz, then
the tested ear) go back to the low frequency (500 Hz, 256 Hz). After getting the result by Air
The stimulus on pure tone audiometry is a series of pure conduction, you proceed with the same technique by Bone conduction
tone (interrupted tone) testing. The results can be placed on an audiogram
 Masking:
o Obscuring one sound by another sound
The sound you hear here is like that of in the T.V. when
stations are off
o Elevation of one signal produced by introduction of a 2nd sound
Lecture Discussion: Masking

This is a schematic representation of a masking noise on the non-tested ear
Lecture Discussion: Audiogram
 Threshold: The usual practice here in the Philippines is that we separate from the right
o Lowest intensity/loudness (dB) that patient can hear in ear and the left ear. In other countries, they only give you a single graph
different frequencies (Hertz) where all the threshold are placed in one graph  this is quite confusing
o Air Conduction Testing sometimes
o Bone Conduction testing
 INTENSITY: loudness, sound intensity (db)
 FREQUENCY: audible sound cycles per second (Hertz)
 Sensory Neural Hearing Loss: both BC and AC are the same and neither
is normal
Lecture Discussion: Audiogram Key

But because we have internationally approved signs and symbols for right Lecture Discussion: If both bone conduction and air conduction thresholds
and the left ear by air conduction and by bone conduction, whether it is are abnormal, but without a gap of more than 10 dB patient will be
masked or unmasked, we could easily understand and interpret an diagnosed as sensory neural hearing loss
audiometric graph. Another widely accepted practice is to use a red pen for
the right ear and a blue pen for the left ear  Mixed Type Hearing Loss: both AC and BC thresholds are reduced, but
BC thresholds are still better than AC by 10 dB or more
 NORMAL: 0 – 20 dB
These are the normal threshold based on ANSI (American National
Standard Institute) but by WHO criteria  they allow 0-25 dB as
normal
 SPEECH FREQUENCY: 512 Hz, 1024 Hz, 2048 Hz
Interpretation:
 Normal: when bone conduction and air conduction thresholds are
between 0-20 dB
Lecture Discussion: If both AC and BC threshold are both abnormal but this
time there is a gap of more than 10 dB  a mixed type of hearing loss (you
cannot diagnose this by tuning fork test)
Degrees of hearing loss (according to ANSI):

 Mild 25-45 db
 Moderate 45 – 60 db
 Severe 55 – 70 db
 Profound 70-100 db
Lecture Discussion: Another international practice is that the bone
conduction threshold are joined by a dotted line. The air conduction
threshold are joined by a solid line. If both air conduction and bone
conduction results are between 0-20 dB  these represent a normal
tympanogram
 Conductive Type Hearing Loss: BC thresholds are normal and better

than AC by more than 10 dB
Lecture Discussion: If the bone conduction thresholds are within normal, and
the air conduction is below normal  this represent a conductive type
hearing loss
IMPEDANCE AUDIOMETRY Lecture Discussion: Type A

 Tympanometry The graph peaked at 0 pressure, meaning to say both external and middle
 Acoustic Reflex ear pressure are the same so the tympanic membrane will move very freely
 OAE – otoacoustic emission test
 Type Ad
RA 9709 Universal Newborn Hearing and Intervention Act of 2009: o Very highly compliance at ambient pressure
 OAE – Otoacoustic emission test o Seen in ossicular discontinuity
By Philippine law, it is now obligatory to test all newborn for
hearing screening 24 hrs. after birth. If a patient fails this test 
it can be repeated after 1 month. If it fails again, you have to do
other confirmatory tests
 AABR – Automated Auditory Brainstem Response Audiometry
Confirmatory Test
 ABR – Auditory Brainstem Evoked Response audiometry
 ASSR – Auditory Steady State Response Audiometry
Lecture Discussion: Type Ad
It has the same pressure on both external and middle ear but the tympanic
membrane will move very loosely at 0 pressure because there’s no limitation
or restriction on the movement by the ossicles. This can be seen on patient
with ossicular chain discontinuity
 Type As
o Very low compliance at ambient pressure
o Seen in ossicular fixation
Lecture Discussion:
This is a schematic diagram of impedance audiometry. The external ear is
totally sealed off, no sound or pressure or stimulus can get in without being
measured and no sounds or echoes can come out without being measured
as well
Lecture Discussion: Type As
1. Tympanometry Similar with the first two types, the movement of the tympanic membrane is
 Is an indirect measure of the compliance (mobility) of the tympanic seen on 0 pressure. But it is now limited or restricted. This are usually seen if
membrane under conditions of (+), (-) or normal pressures the ossicular chain has a problem like fixation because of recurrent middle
Lecture Discussion: ear infection.
If you have a middle ear fluid, the tympanic membrane is bulging or under
The tympanic membrane will be able to move freely if the pressure
pressure. For sure it will not be able to move either on positive or negative
in the external ear is the same as the pressure in the middle ear
pressure
because they are both open to the atmosphere
 Type B (Flat)
 Purpose:
o Little or no change in middle ear compliance
o TM mobility
o Impacted cerumen, perforated ear drum, with middle ear fluid,
o Middle ear pressure
TM perforation
o TM perforation
o Patency of the eustachian tube
 Procedure:
o Acoustic energy ( 45 db SPL) is introduced into the ear.
Some are absorbed, others are reflected back (echoes)
and measured by another channel
Tympanogram
 Type A (Normal)
o Maximum compliance of tympanic membrane at 0 pressure Lecture Discussion: Type B
Impacted cerumen, perforated ear drum, etc  all these situations there will
be no movement of the tympanic membrane at all. So when you try to do
tympanometry, the graph will be very flat
 Present – Normal hearing

 Absent – 8th cranial nerve lesion
unilateral conductive
bilateral conductive
disarticulation
facial paralysis
stapedial fixation
Lecture Discussion: Lecture Discussion:

If you have a retracted ear drum  the tympanic membrane is adherent Acoustic reflex is present in normal individuals. It will be absent for any
already on the medial wall of the middle ear. Negative pressure should be bilateral lesion, whether conductive or sensory neural hearing impairment. If
applied to the external ear to equalize the pressure in the middle ear for the it is unilateral, we could still do ipsilateral testing if it’s needed. It will be
tympanic membrane to go back to its normal position. absent in facial nerve paralysis or stapedial fixation
 Type C SPEECH AUDIOMETRY

o Maximum compliance at negative air pressure greater than  Ability to hear and understand speech
100 mmH2O  Speech is the stimulus itself
o Poor ET function  2 Parts of Speech Audiometry:
o Speech reception thresholds
2. Acoustic Reflex  Level in dB at which the patient can identify 50% of
 Contraction of stapedius muscle in response to stimulation of sound of test words (spoken words) correctly
sufficient intensity  Countercheck of pure tone audiometry
 70 – 100 dB stapedius muscle contract bilaterally and reflexibly  Threshold average of 500 Hz, 1000 Hz, 2000 Hz
If a sound (very loud sound) is forced into the external ear, pressure These reception thresholds is the average of the
will be transmitted to your tympanic membrane (ear drum)  threshold of pure tone audiometry in speech
overstimulating the ossicles (maleus, incus, stapes) and force it frequency
inside the oval window  could rupture the oval window and
render the patient very dizzy for a long time and be totally deaf for o Speech discrimination
life. But because of the acoustic reflex, this rarely happens  Aka: speech intelligibility test
 Words are presented 40 dB louder than the SRT
 Also called stapedial reflex (speech reception threshold); patient is instructed to
If we look closely to the location of the stapedius muscle, when it repeat each word
contracts, it limits the movement of the stapes inwards towards the Example:
oval window. That is why acoustic reflex is considered a very Speech reception threshold of the patient is at 30
important protective reflex dB. You increase the volume by 40 dB to stimulate
the patient so that would be at 70 dB  that is
 Basic Components: quite loud for the patient to hear and at the same
o Afferent Limb - auditory fibers from the cochlea time understand the words
o Reflex Center – Caudal portion of the Pons
o Efferent Limb – facial nerve  Percentage of response is recorded:
90 – 100% Normal
75 – 90% Slight difficulty
60 – 75% Moderate difficulty
Poor discrimination
50- 60%
Difficulty in conversation
below 50% Very poor discrimination
 If the speech discrimination is >80%  they are good

candidates to wear hearing aids
Lecture Discussion:
Since the acoustic reflex is reflexive and bilateral, then we can take
advantage of this characteristic. We can do acoustic reflex contralaterally or
ipsilaterally.
PEDIATRIC AUDIOMETRY
 Behavioral Audiometry
o Newborn to 24mos of age
o Difficult to handle and inconsistent
o replaced by BERA
 Play audiometry -2-4 years old
 Speech audiometry
 Objective audiometry
o Impendance Audiometry
o BERA
o Otoacoustic Emission test
ANATOMY AND DISORDERS OF THE FACIAL NERVE

Facial Nerve
Lecture Discussion: Hearing Aids

Hearing aids are very expensive so we have to identify which patients we
advise to buy hearing aids. Depending on the types and the value added to
it, then the cost would incrementally increase. You have different types of
hearing aids, you have:
 CIC – completely-in-the-ear hearing aids
 ITE – in-the-ear hearing aids
 ITC – in-the-canal hearing aids
 BTE – behind-the ear hearing aids
The smaller it is, the more expensive your hearing aid will be but not
necessarily they are the most with important features. Every features that
you add on the hearing aid will entail another expense on the price of the Picture Above:
hearing aid
This is the reason why we see patient with facial nerve problem as well
(besides hearing problems). As the facial nerve exits the brainstem it enters
AUDITORY BRAINSTEM EVOKED RESPONSE
the internal auditory canal that is already part of your temporal bone so 70%
 Also called ABR (Auditory Brainstem Reflex) or BERA (Brainstem Evoked of the peripheral fiber of the facial nerve is within ENT.
Response Audiometry)
 Represent electrical response of CN VIII and some portions of the brain After it has passed through the internal auditory canal, it gives a peripheral
to auditory stimulus after being sensed by the inner ear branch to your lacrimal gland thru the greater petrosal nerve to control
 80 dB above threshold click stimulus at fixed repetitions e.g. 11/sec or lacrimation. It turns back and down towards the middle ear giving a branch
33/sec until 2000 click response have been average to your stapedial muscle. Then again, it turns back going to the mastoid. The
 Electrodes on mastoid vs. forehead  EEG pattern circled portion in this diagram is part of your middle and your mastoid. Along
 Series of waves ( I-VIII) are produced I and II are from the cochlea the mastoid it will give another branch which is the chorda tympani towards
Results: latency of each wave and interwave your tongue and your submandibular and sublingual gland. Before it exits the
stylomastoid foramen and give the famous 5 peripheral muscular innervation
 Five main functions of facial nerve:

 Wave I – 1st order neuron
o Lacrimation
 II – cochlea
o Salivation
 III - superior olives
o Impedance regulation of sound
 IV – V- inferior colliculus
o Pain, touch and temperature
o Taste – on the anterior 2/3 of the tongue
 Clinical Uses:
o Cerebellopontine angle
tumors – 95%
o Menniere’s disease
o Hearing threshold in infants
Lecture Discussion:
What is important are the early waves because your ABR was designed to
diagnose Cerebellopontine angle tumors. If we look at the sensitivity and
specificity of this test, it is at 95%. It is a very reliable test. Likewise, this ABR
is used as a mandatory confirmatory test for hearing evaluation in infants
o Nerve Function Tests:

 EMG – Electromyography
 normal
 fibrillation
 denervation
 bizarre pattern
EMG is usually done by a neurologist or by rehab

medicine. In EMG, what we usually look for is the
fibrillation potential that would indicate a good
chance of recovery of facial nerve paralysis, but
this will only be present after the 3rd week, that
Picture Above: Upper and Lower Motor Neuron Lesions would be too long and too late to initiate
rehabilitation. The principle of rehabilitation is
This illustrates which facial nerve needs to be attended by a neurologist and that we have to start rehabilitation at the time of
which facial nerve paralysis need to be treated by an otolaryngologist. You injury that is why they developed another test
remember the differentiation of having UMN type paralysis and LMN type which is ENog.
paralysis. For all cranial nerve, the level of decussation of its fiber (crossing
of the fiber to the opposite side) is at the level of the nucleus. The nucleus of
 ENog – Electoneurography
the facial nerve is in the pons. So fibers of the facial nerve innervates the
opposite upper and lower face BUT it also receives an ipsilateral innervation  Can be done earlier than 3 weeks
to the lower face. Prognosticates the recovery of the
patient much earlier than EMG
Knowing this, if the patient has UMN paralysis  it will block both
innervation to the contralateral upper and lower face. But since it will have  Persistence of paralysis 90% compare to the
an ipsilateral innervation to the upper face, the upper face will remain intact. normal side in 10 days indicate poor
If the upper face is intact  then it will be purely neurological case. prognosis
In case the patient has LMN paralysis  blocking both upper and lower  Maximal Stimulation Test
contralateral face, it will receive the same innervation also on the ipsilateral Is a crude test. An electrode is placed on the cheek
upper face but since this will also be blocked, then the patient has a total and electrical stimulation is given. This is quite
paralysis on the opposite, it will be 70% ENT. painful to the patient
 DIAGNOSTIC PROCEDURES: DEGREE OF INJURY

o Audiologic Evaluation 1st Degree Neuropraxia - partial disruption of axonal activity
 Pure Tone Audiometry 2nd Degree Axonotmesis - wallerian degeneration
 BERA 3rd Degree Neurotmesis - aberrant regeneration can occur
 Tympanometry 4th Degree Perineural disruption – intraneural scarring
 Stapedial Reflex 5th Degree Complete Transection – no regeneration
o Schirmer’s Test
 Difference of 25% is Significant NEUROPATHOLOGY AND SPONTANEOUS RECOVERY OF FACIAL NERVE
In facial nerve localization, if the differentiation of INJURY
both eyes is >25%  that is considered significant,
meaning to say the lesion is at level of the greater DEGREE PATHOLOGY RECOVERY
petrosal nerve Compression: damming of axoplasm
1st 1 – 4 weeks
no morphologic changes
compression persist with increase
o Taste Sensation Stimulation 2nd 1 – 2 months
intraneural pressure, loss of axon
 Sweet and Sour – Tip
intraneural pressure increases
 Salt – Lateral 3rd 2 – 4 months
loss of myelin tubes
 Bitter – Base
above + disruption of perineurium
We do not use the bitter taste as a stimulus 4th 4-18 months
partial transection
because the facial nerve only access on the above + disruption of epineurium
anterior 2/3 of the tongue 5th Never
complete transection
To test for the salty sensation, you ask the patient
to protrude the tongue and place the salty
sensation or stimulus at the lateral part on one
side NOT on the center or on the tip. Do not ask
the patient to retract the tongue because the taste
stimulus will simply diffuse to the other side and
the patient can identify it. The same is true with
the sweet and sour taste.
o Salivation
 Cannulation of the Wharton’s Duct
 25% difference is significant
DISEASES OF THE FACIAL NERVE

1.) Congenital
 Mobius Syndrome – Fibrotic Facial nerve
 Traumatic Birth – more common than Mobius syndrome
The mastoid tip of a newborn is very superficial or nearly absent. So
the facial nerve is very superficial if you do not have the protection
of the mastoid. If a baby is delivered by high forceps  it could easily
injure the facial nerve of the baby
2.) Infections
 Herpes zoster Oticus
 Middle ear Infections
3.) Trauma
 Temporal Bone Fracture
o Longitudinal – parallel to the temporal bone
 Delayed complete paralysis
 Full recovery
o Transverse - perpendicular fracture
 25% full recovery
 Greater chance of permanent paralysis
4.) Neoplasm Involving the Facial Nerve

 Cerebellopontine Angle Tumors
o Acoustic Neuroma
o Meningioma
 Middle Ear Lesions (tumors):
o Glomus jugulare – a benign tumor on the floor of the middle ear
All benign tumors can slowly erode all surface (even bones)
o Histiocytosis – now classified as a variant of malignant lymphoma

o Rhabdomyosarcoma aggressive tumor in the head and
o Squamous cell carcinoma neck
5.) Idiopathic Cause

 Bell’s Palsy
o Treatment:
 Corneal Protection
 Steroids
 Fascial Slings
o Nerve Grafting:
 Spinal Accessory nerve
 Hypoglossal Nerve
o Muscle Slings:
 Temporalis Muscle
 Masseter Muscle
Lecture Discussion: Bell’s Palsy

If the paralysis has been there for a long time (6 months – 1 year) then facial
reanimation can be considered. Nerve grafting with the use of spinal
accessory nerve or hypoglossal nerve attaching to the orbicularis oris or oculi
muscles. Or Muscle slings, harvesting the temporalis muscle and joining it
with the orbicularis oculi or the masseter muscle, attaching it to your
orbicularis oris  you will have at least some facial animation
Topic: Anatomy of the Nose and Paranasal Sinuses
ANATOMY  The internal nose is not uniform, being:

A. Nose o Wider below
I. External Nose o A little bit narrow above.
 The upper portion of the nose is rigid  It is also wider in the middle, anteriorly and posteriorly.
 The lower portion of the nose is rubbery and flexible.
 The internal nose is largely filled with the nasal septum and the
turbinates.
Turbinates are also known as conchae
 Superiorly:
o The upper rigid part of the nose is composed of the frontal  The nasal septum and turbinates have regular spaces in between
process of the maxilla which is also known as the nasal them which form the so-called “flues” or the spaces for the flow of
pyramid or the bridge of the nose. air.
The nasal pyramid or the nose bridge is where  The horizontal spaces next to the nasal septum are known as the
glasses/spectacles are placed when a person is wearing one common meatuses which are straight and parallel with the surface.
Superior, Middle and Inferior Meatus
o Together with the frontal process of the maxilla which makes o Potential spaces lying between the superior, middle and
up the nasal pyramid are the nasal bone plates fused together. inferior turbinates
 Inferiorly: o The WIDEST portion is the INFERIOR MEATUS
o The lower part of the nose is formed by a group of cartilages o The combined volume of these spaces is approximately
15-20 cc.
consisting of the:
o The volume on either side is approximately 7-10 cc.
 Lateral nasal cartilage
o MIDDLE MEATUS – where the ostium of the frontal,
 Medial and lateral dura of the greater or major
maxillary and anterior ethmoid sinuses drains
alar cartilages o SUPERIOR MEATUS – is where the posterior ethmoids
 Free margin of the septal cartilage and sphenoid sinuses drains
 Connective tissue covering the whole nose. o INFERIOR MEATUS – where the nasolacrimal duct opens
o The septal cartilage is part of the nasal septum.
 The columella is formed by the: III. Septum
o Lower margins of the septal cartilage  Practically divides the nasal cavity into two nearly equal compartments
o Anterior nasal spine (covered with skin)  Also known as the internal nasal skeletal framework
o Medial portion of the two greater (major) alar cartilages  Composed of 6 structures: a single cartilage and 5 bones
Composition:
 The nostrils are formed by the two major (greater) alar cartilages which
o Quadrangular cartilage
are flexible plates bent in such a way that they tend to form the lateral o Perpendicular plate of the ethmoid bone
and medial walls of the nares o Vomer
o Rostrum of the sphenoid
II. Internal Nose o Crest of the palate
o Crest of the maxilla
 Majority of the nasal septum is made up of the QUADRANGULAR

CARTILAGE or the SEPTAL CARTILAGE.
 The quadrangular cartilage is in the anterior part of the nasal septum
and it is posteriorly fused to the VOMER.
 Superiorly and anteriorly, the vomer is supported by the
PERPENDICULAR PLATE OF THE ETHMOID BONE.
 Superiorly and posteriorly, the vomer is supported by the ROSTRUM OF
THE SPHENOID BONE.
 The internal nose is an air conditioning chamber that houses the  Inferiorly and anteriorly, a portion of the quadrangular cartilage which
septum and the turbinates. is fused with the vomer rests on top of the CREST OF THE MAXILLARY
 It is lined by thick, red and moist mucosae with rigid walls and floors BONE.
roughly measuring about 2 inches in height and 3 inches in length.  Inferiorly and posteriorly, the vomer rests on top of the CREST OF THE
 The internal nose posteriorly opens into the pharynx via the 2 PALATINE BONE.
choanae
Choanae – oval opening about ½ inch transverse diameter and
about 1 inch in height
IV. Turbinates  The sphenoid sinus occupies the sphenoid bone and
 Septal deviations due to abnormal growth that may interfere with the Sphenoid Sinus extends to the wings of the sphenoid, the clinoid
nasal airflow must be surgically corrected process and the lateral margin of the pterygoid plates
 The turbinates are areas of erectile tissue (cavernous venous spaces) on  Housed in the ethmoid labyrinth medially bounding
both sides of the nasal septum serving to adjust their size in varying the orbital cavity
Anterior
atmospheric conditions and they are also known as nasal radiators.  It is separated by a thin plate of bone known as the
and
 They have a rich blood supply. lamina papyracea which is normal dehiscent in the
Posterior
pediatric age group. That’s why in pediatric patient 
 The inferior and middle turbinates are long fleshy bodies that hang Ethmoids
they would orbital complications (e.g. orbital
downwards occupying the lateral nasal wall. They extend horizontally
cellulitis) if their ethmoid sinus infection would extend
to almost the full length of the lateral nasal wall. through the lamina papyracea
 They are supplied with erectile tissue or cavernous venous spaces that
serve to adjust their size.  Sinuses present at birth: Maxillary and Ethmoids
 They act as radiators of the nose and they are subserved with a rich  The frontal sinus is not yet developed and the sphenoid sinus is
blood supply. rudimentary
 The mucous membrane of the respiratory tract lines the nasal cavity,
sinuses, nasopharynx, Eustachian tubes, middle ear space, and mastoid
down to the respiratory bronchioles
 The pharynx- lined by squamous epithelium
 Pseudostratified columnar ciliated epithelium – lines the respiratory
epithelium composed of long columnar cells surmounted by cilia of
about 100 to a cell underlain with 3-4 layers of replacement cells
 Pseudostratified cuboidal epithelium – surfacely lines the paranasal
sinuses with only 1-2 layers of replacement cells
 The Cilia of the epithelium are uniform in length
 The glands and blood vessels in the stroma of the submucosae vary in
Hiatus Semilunaris number and in size in direct proportion of the air flow and they furnish
 In the middle meatus, the ostia of the frontal, maxillary and anterior the mucous blanket
ethmoids opens into the HIATUS SEMILUNARIS  These glands are tubular and racemose, containing serous and mucosal
cells
Ethmoidal Bullae
 A vestigial structure that arises from the fusion of the ethmo-
C. Olfactory Epithelium
turbinals that carry olfactory epithelium in lower animals but not in
 The olfactory epithelium is of high cylindrical type with distinct basal
man
cells in which the upper surface of the cell of the olfactory epithelium
 It is found in the upper margins of the hiatus semilunaris
appears different from that of the respiratory portion.
Ethmo-turbinals  3 types of cells makes up the olfactory epithelium:
 Well-developed in lower animals which carry olfactory epithelium 1. Cuboidal cells forming the basal layer
in which some lies within the frontal and sphenoidal sinuses 2. Tall cylindrical supporting cells
 Man has a relatively rudimentary sense of smell and the olfactory 3. Sense cells
epithelium is confined to the uppermost middle area of the nasal
septum Olfactory Sense Cells
 They are bipolar nerve cells that form a tract coming from the central
B. Paranasal Sinuses nervous system.
 The paranasal sinuses are irregularly shaped air spaces that lie adjacent  They are evenly distributed among the supporting cells.
to the nose.
 All sinuses vary in size, shape, configuration and symmetry. Olfactory Vesicle
 They are air cavities bounded by bones that are embedded within the  From the distal end of these olfactory sense cells, a modified dendrite
skull. will be protruding above the surface epithelium giving rise to the
OLFACTORY VESICLE.
 Lies between the outer and inner table of the frontal
bone with which the floor serves as the roof or ceiling  At the surface of the olfactory vesicle, there are 6-8 motile cilium and
Frontal Sinus at the proximal end the cilium tapers to a smooth thin filament which
of the orbit
 The superior wall of the orbit makes up its floor. is about 1 micron in diameter and this will make up the axon.
 Occupies majority of the maxillary bone  It will join with other similar axons giving rise to the OLFACTORY
 Extends from the orbit and serves as the orbit’s roof NERVES
or ceiling down to the apices of the molars in which  The axons are collected together to pass through the Cribriform plate
some of the molars protrude particularly the into the Olfactory bulb to form a synapse with the dendrites of the
premolars or the first and second molar tooth root mitral cells
Maxillary Sinus protrudes into the sinus cavity
(Antrum of  Axons of these mitral cells forms the Olfactory Tract going into the CNS
Highmore)
 Lies beneath the maxillary bone wherein the floor of to connect with numerous nuclei
the orbit makes up its roof and the apices of the
molars serve as its floor.
 Traumatic tooth extraction of 1st or 2nd upper molar
would lead to sinusitis due to a presence of oroantral
fistula
Cilia NERVE SUPPLY OF THE NOSE AND PARANSAL SINUSES

 The cilia are about 5-7 micron in length and they are located at the end  The nerve supply of the nose is derived from the:
plate of the surface epithelium in numbers of 100 cilia per square o Maxillary (V2)
micron. o Ophthalmic (V1) division of the trigeminal nerve (CN V)
 These cilia of the epithelium work in a coordinated manner and they
principally function for MUCOCILIARY TRANSPORT (CLEARANCE)
Mucous Blanket
 It is a highly elastic, viscid and continuous sheet of secretion extending
into all spaces of the respiratory tract, including the Eustachian tube,
the middle ear and the mastoid.
 It is very sticky that minute foreign particles coming in contact with it
adheres to it promptly so it further aids in filtering out minute foreign
particles within the inspired air.
 It has a pH of about 7.
 The mucous blanket in the nose and sinuses is moved to the pharynx by
ciliary motion and is renewed in the glands at least 2-3 times an hour.
BLOOD SUPPLY OF THE NOSE AND PARANASAL SINUSES Anteriorly
V1 (ophthalmic division of CN V) carry afferent
 The blood supply of the nose comes from the: and
sensory impulses
o INTERNAL MAXILLARY ARTERY Superiorly
It is a branch of the EXTERNAL CAROTID ARTERY V2 (maxillary division of CN V) receives
parasympathetic fibers from SUPERFICIAL
o OPHTHALMIC ARTERY PETROSAL NERVE coming from the GENICULATE
GANGLION OF THE FACIAL NERVE (CN VII)
It is a branch of the INTERNAL CAROTID ARTERY
V2 also receives sympathetic fibers coming from the
DEEP PETROSAL NERVE supplying the lower and
 The nasal septum, lateral nasal wall and the nasal cavity itself derives Posteriorly
posterior portion of the nasal mucosa through the
its blood supply from the SPHENOPALATINE BRANCH OF THE INTERNAL and
SPHENOPALATINE GANGLION  this position of the
MAXILLARY ARTERY. Inferiorly
sphenopalatine ganglion in the pterygopalatine
 The upper part of the nasal cavity, the roof of the nose, frontal sinus fossa close to the sphenopalatine foramen makes it
and anterior and posterior ethmoid sinuses derives its blood supply accessible for topical anesthetics in doing intranasal
from the ANTERIOR AND POSTERIOR ETHMOIDAL BRANCHES OF THE surgeries under local anesthesia. Your
OPHTHALMIC ARTERY. sphenopalatine foramen lies behind and above the
 The sphenoid sinus derives its blood supply from the PHARYNGEAL posterior tip of your middle turbinate
BRANCH OF THE INTERNAL MAXILLARY ARTERY.
 The maxillary sinus derives its blood supply from the: PHYSIOLOGY
o INFRAORBITAL ARTERY I. Olfaction
All are branches of the
o SUPERIOR LABIAL ARTERY  In olfaction, the sense of smell is relatively basic.
INTERNAL MAXILLARY
o ALVEOLAR ARTERY  Odoriferous particles are dissolved in solution and are brought by nasal
ARTERY
airflow to the nasal roof where the olfactory mucosa is found.
VENOUS DRAINAGE OF THE NOSE AND PARANASAL SINUSES  The olfactory bipolar neurons are stimulated and run through the
 The venous drainage is through the: olfactory nerves going into the central nervous system by way of the
o OPHTHALMIC VEINS CRIBRIFORM PLATE OF THE ETHMOID.
o ANTERIOR FACIAL VEINS  The central nervous system will interpret the character of the smell.
o SPHENOPALATINE VEIN
II. Respiration and Humidification
LYMPHATIC DRAINAGE OF THE NOST AND PARANASAL SINUSES
 In respiration, the nose concerns air conditioning that involves AIR
 The lymphatic drainage of the nose drains via an anterior and posterior
MOISTENING and AIR HUMIDIFICATION.
network.
 The nose acts as a rigid airway for inspiration and expiration.
 The ANTERIOR NETWORK is minute and they drain the anterior part of
 It is also responsible for filtering out minute particles within the inspired
the nose.
air.
o They drain along the facial vessels going into the submaxillary
 It plays a great role in HUMIDIFICATION, AIR MOISTENING and HEAT
tracts draining the anterior part of the nasal cavity, the nasal
EXCHANGE.
vestibule and the 3 turbinal areas.
 The nose produces 1 L of mucus per day which has an antibacterial
 The POSTERIOR NETWORK drains the major portion of the nose which
effect. It contains an enzyme Muramidase which helps in breakdown of
is joined into 3 main channels and they are divided into 3 main
bacterial cell walls and also contain IgA and IgE
subgroups:
 Also implicated in the Naso-pulmonary Reflex through the
drains the upper lateral nasal wall, superior and
Hypothalamus to influence nasal airway resistance
Superior Group middle turbinates drain to the Retropharyngeal
Lymph Nodes
passing below the E.T. the inferior turbinates and III. Phonation
Middle Group inferior meatus and nasal floor drains to the  The nose plays an important role in phonation since it adds RESONANCE
Jugular Lymph Nodes to voice production
drains the septum and anterior nasal floor drains
Inferior Group to the lymph nodes along the Internal Jugular
Vessels
EMBRYOLOGY Failure of the buco-nasal membrane to rupture before birth will give
A. Nose rise to a congenital condition known as congenital choanal atresia
 The nose forms BETWEEN THE 4TH and 8TH WEEK OF EMBRYONIC LIFE
(AOG) and continuously undergoes changes even in adulthood.  The ANTERIOR PORTION of the palate will undergo SPONTANEOUS
o During early embryonic development, there are 5 BRANCHIAL OSSIFICATION.
ARCHES in the UPPER END of the embryo that only exist for a  The POSTERIOR PORTION of the palate that did not undergo
period of 2 WEEKS before it starts to DEGENERATE. OSSIFICATION will develop to become the SOFT PALATE.
 The olfactory sac grows POSTERIORLY between the MEDIAN NASAL
PROCESS and FRONTO-NASAL PROCESS compressing a portion of the
FRONTO-NASAL PROCESS giving rise to the NASAL SEPTUM which
should undergo SPONTANEOUS FUSION with the PALATE.
B. Palate
 The development of the paranasal sinuses remain a mystery.
 As the face grows down and forward in a much more rapid rate than
cranium growth, the ossified materials in these bones are removed to
be used in forming the rapidly growing facial bones.
 As these ossified materials are being removed, the nasal mucous
 The region ANTERIOR TO THE FOREBRAIN develops to become the membrane is sucked into the resulting bony spaces resulting to BONY
FRONTO-NASAL PROCESS in which the ANTERIOR FACE, NOSE and RESORPTIONS taking place in the MAXILLA, FRONTAL, ETHMOID and
JAWS develop. SPHENOID BONES while simultaneously, the MUCOUS MEMBRANE
o At the LATERAL portion of the FRONTO-NASAL PROCESS, from the nose advances intending to occupy these areas.
secondary processes develop and they are the RIGHT and LEFT  As a result, the sinuses are irregular in size, shape, location, symmetry,
MEDIAN NASAL PROCESS. number, anatomic placement.
 They vary greatly in every individual.
 The sinuses on either side are assymetrical
Outgrowth of the middle meatus, largest paranasal

Maxillary Sinus
sinus with a volume of 15 cc per sinus
Develops during late childhood, arises from the
Frontal Sinus expansion of the anterior air cells from the ethmoids
with a volume 6-7 cc per sinus
Develops as an excavation into the sphenoid bone with
Sphenoid Sinus
a volume of 7.5 cc
A labyrinth of small air cells, develops as outpocketings
Ethmoid Sinus
of the middle meatus with a volume of 14 cc
 While the maxillary and mandibular processes grow MEDIALLY, from SPECIAL DIAGNOSTIC PROCEDURES FOR THE NOSE AND PARANASAL
the LATERAL MAXILLARY PROCESS, the LATERAL NASAL PROCESS SINUSES
arises. A. Radiographic Examinations
 Between the LATERAL and MEDIAN NASAL PROCESS, PITS form which I. Caldwell View
eventually develop as the ANTERIOR NARES.  Also known as FOREHEAD-NOSE VIEW
 The PREMAXILLA which is derived from the FRONTO-NASAL PROCESS  This view helps to further evaluate the status of
will eventually fuse with the MAXILLARY PROCESS and gives rise to the the MAXILLA, MAXILLARY and FRONTAL SINUS,
UPPER JAW and UPPER LIP. ETHMOID AIR CELLS, LAMINA PAPYRACEA and
 During the 7TH and 8TH WEEK AOG, most of the PALATE is formed by FRONTO-ZYGOMATIC SUTURE.
the MEDIAN and the LATERAL PALATINE PROCESS which is also derived
from the MAXILLARY PROCESS. II. Water’s View
 During the 8TH WEEK, the PREMAXILLA will eventually FUSE with the  Also known as CHIN-NOSE VIEW or OCCIPITO-
PALATE in which their fusion is INCOMPLETE and the separation MENTAL VIEW
between them develops to become the INCISIVE FORAMEN.  Requested to further evaluate the status of the
The premaxilla is the anatomical landmark that most surgeons use ORBIT, ORBITAL CAVITY, INFERIOR ORBITAL
to classify whether a cleft palate is complete or incomplete. RIM, FRONTAL PROCESS OF THE MAXILLA,
If a congenital cleft palate traverses the incisive foramen, it is NASAL BONES (NASAL PYRAMID), NASAL
labeled as complete cleft palate and its surgical procedure is SEPTUM, NASAL CAVITY, MAXILLA, ZYGOMA,
uranoplasty
ZYGOMATIC ARCH, SYMPHYSIS MENTI, ANGLE
If a congenital cleft palate do no traverse the incisive foraman, it is
OF THE MANDIBLE and CORONOID PROCESS OF
labeled as incomplete cleft palate and its surgical procedure is
THE MANDIBLE
called staphylorraphy
III. Basal View

 Between the NASAL SPACE and the MOUTH, the PALATE will eventually
undergo SPONTANEOUS THINNING OUT forming the BUCO-NASAL  Also known as SUBMENTO-VERTICAL VIEW
MEMBRANE which will eventually RUPTURE BEFORE BIRTH giving rise  Evaluates the SPHENOID SINUS, POSTERIOR
to the PRIMARY CHOANAE. ETHMOIDS, MAXILLARY and FRONTAL SINUSES
 Also requested to view the ZYGOMATIC ARCH
IV. Soft Tissue Lateral View CONGENITAL ANOMALIES

 Same as LATERAL VIEW  Congenital anomalies of the nose are brought about by altered patterns
 In this view, emphasis is given on the SOFT of development because only humans have two skeletal portions of the
TISSUE to evaluate the degree of STEP DOWN external nose, namely the portion projecting from the anterior face.
or STEP UP DEFORMITIES exhibited by a  In the normal course of events, the size and shape of the adult nose are
NASAL BONE FRACTURE. determined by family and racial characteristics.
 This is quite useful in evaluating a greenstick  The possible aftereffects of a postnatal injury to any growing skeletal
fracture involving the nasal bone part of the body include a complete growth arrest, decelerated growth
or an accelerated growth rate.
 Congenital defects may result from maternal diseases particularly viral
B. Tomograms infections and maternal use of medications that is toxic to the
I. CT Scan developing fetus.
 This special diagnostic procedure uses a special scintillation detector  The growth of the face and nose takes place by elongation of several
that passes through a body section. ectodermal processes that extend DOWNWARDS from ABOVE and
 A digital computer is used to process this information. MEDIALLY from the SIDES.
 This allows sections of the body to be seen and evaluated separately or  The anterior nares are completely developed in the 7th week of
segmentally. embryonic life and the primitive septum lengthens backwards as the
mesenchyme surrounds each nasal cavity
 Useful in delineating the extent of a particular lesion be it secondary to
INFECTION, FRACTURE or TUMOR.  The vomeronasal organs of Jacobson appears in the medial wall of the
nasal cavity by the 5th week obtaining full growth by the 2nd trimester
II. MRI and then degenerates
 A non-invasive imaging technique with no known biological hazards  Special V-shaped cartilages supporting this organ may persist in adult
life as preseptal cartilages giving rise to obstructing nasal spurs in the
 It has certain advantages over the conventional X-Rays and CT scans due
adults
to its exquisite soft tissue contrast particularly for evaluating HEAD AND
NECK MALIGNANCIES  At birth, most of the septum are cartilaginous showing bones only in
the VOMER, ANTERIOR NASAL SPINE and PREMAXILLA and they have V-
C. Physical Examinations SHAPED GROOVES in the MIDLINE upon which the CARTILAGINOUS
SEPTUM rests on top of it.
I. Anterior Rhinoscopy  Any process interfering the growth rate of these bones will result in
 Physical examination of the nose buckling of the cartilages they support
 Done with a use of a nasal speculum for  The lower part of the premaxilla encloses the unerupted incisors and
initial screening of the nasal status, the upper part forming the 2 premaxillary wings constitutes the key
externally and internally structures supporting the external nose
 It is useful in evaluating presence of NASAL  This emphasizes that outward influences affecting the 2nd half of the 1st
OBSTRUCTION which can be secondary to trimester would severely affect the development and of the human
HYPERTROPHIC TURBINATES, TUMORS or nose
FOREIGN BODIES. Influences Affecting the Development of the Nose:
o Medications taken by the mother
II. Nasal Endoscopy o Mechanical intrauterine injuries
 Mandatory diagnostic procedure to all ENT o Maternal diseases
clinics o Incomplete abortion which results to localized or septic
 It is a rather invasive procedure. failures
 The examiner is aided by a 4 mm rigid or o Nutritional deficiencies of the developing individual
flexible telescope that is insinuated
endonasally giving the examiner access on
the status of the ANTERIOR and POSTERIOR
NASAL CAVITIES often attached to an
endocamera unit and recorded in a
computer for patient’s review
GENETIC DEFECTS SEEN AT BIRTH  Stenosis of the nostrils is due to failure of resolution of the
Hamartoma epithelium plug of the nostril occurring in the 6th fetal month
A benign, focal malformation that

resembles a neoplasm in the tissue of
its origin
Hemangioma
 If the preseptal cartilages fails to resolve in the 3rd trimester – results

A congenital benign tumor or to spurs, chondromas and impacting vomer ridges
vascular malformation  Some infants with seemingly well-developed noses displaced on 1
side actually represents a healed intrauterine fracture during the 3rd
trimester caused by accidental fall of the mother or by pressure of the
nose against the mother’s pelvic bone
 Majority of intrauterine nasal fractures heals to normal without
Rubinstein Taybi’s Syndrome
treatment
Contributing Factors Affecting Incidence of Birth Injuries:

Bird’s beak appearance or deformity  Intrauterine fetal position
of the nose  Intrauterine pressure
 Birth canal presentation
 Racial characteristics
Wardenburg’s Syndrome Factors Associated with Deformities of the Nose and Septum During the Active
Period of Growth:
 Dental misalignment especially those affecting the upper incisor teeth
 Deviations of the teeth from the midline associated with dental
Exhibits a wide and flat nose malocclusion
Meningoceles and Encephaloceles
A result of incomplete closure of the

CHONDROCRANIUM
Most Common Diseases in Pregnancy Affecting the Development of the Nose:

 Syphilis
 Measles
 Chickenpox
Medications Having Adverse Effects on the Development of the Nose When

Given to Pregnant Women:
 Reserpine
 Coumadin
 Untoward influences in the 1st trimester would result to congenital

defects such as absence of the nose at birth, which there is only one
lateral nasal process presenting as a tubular proboscis while the other
lateral nasal process fails to evolve
 Congenital Dermoid Cyst are epithelial structure persisting in the
fusion line of intranasal fissure explaining the frequently seen sinus
tract connecting the dermal cyst with the skin surface of the nasal
bones
 Injured development in the 4th fetal month results to bifid or cleft
noses or double noses with combination of cleft lips and palates
Topic: Diseases of the Nose and Paranasal Sinuses
Lecturer: Dr. Hernandez, Josefino
OUTLINE Lecture Discussion: Lateral Nasal Wall

I. Anatomy We can see here the different turbinates (also called concha). We have here
II. Diseases the:
A. External Nasal Diseases  Inferior turbinate  underneath it is the inferior meatus into
 Nasal Vestibulitis which the nasolacrimal canal drains through the valve of Hasner
 Nasal Furunculosis  Middle turbinate  underneath it is the middle meatus  it is a
B. Rhinitis space into which the frontal sinus, maxillary sinus and anterior
 Allergic Rhinitis ethmoids drain
 Viral Rhinitis  Superior turbinate  underneath it is the superior meatus where
 Non-Allergic Rhinitis the posterior ethmoids drain
 Atrophic Rhinitis
 Rhinitis Medicamentosa The inferior turbinate and middle turbinate can be visualized anteriorly
when examining the nasal cavity
C. Rhinosinusitis Superior turbinate can be visualized posteriorly
D. Tumors of the Nose and Paranasal Sinuses
 Nasal Polyps Sphenoid Sinus – seen more posteriorly than the superior turbinate. Has an
 Inverting Papilloma ostium at the sphenoethmoidal recess
 Carcinoma
AIRFLOW PATTERNS
NOSE
 Aside from contributing significantly on how we look, the nose
subserves the sense of smell, prepares inhaled air for use in the lungs,
furnishes the air resistance necessary for normal functioning of the
lungs, and exerts certain reflex effects upon the lungs
Nose
 Turbinates
Are bony structures attached to the lateral nasal wall
 Septum  You can see here that the cribriform plate separates the nasal cavity
Divides the nose into 2 from the orbit and through small openings, the olfactory nerve endings
 Mucosa pass through to reach the upper third of the nasal cavity which is the
With erectile tissue covered with Pseudostratified ciliated columnar olfactory area. As we sniff more air, it reaches that area so that we can
epithelium  significant for mucociliary clearance which propels smell the substance or particle we try to sniff
mucous from anterior going posteriorly into the nasopharynx
PARANASAL SINUSES
 Paired:
o Frontal
o Maxillary
o Ethmoids
 Anterior
 Posterior
o Sphenoid
 When breathing in normally, we can see here that air flow is

Maxillary and Ethmoid sinuses are present at birth concentrated inferiorly but some of the air will still reach the olfactory
area. So anything that would result or prevent the substance or particle
Lateral Nasal Wall from reaching the olfactory area, will result in anosmia or hyposmia.
This can be secondary to nasal congestion or masses or tumors that will
obstruct or prevent the substance/particle from reaching the olfactory
area
Ostium of sphenoid sinus

Sphenoidal sinus
 When we exhale we can note that the air flow is more turbulent
Ethmoidal Bulla, Endoscopy Mucociliary Clearance continued…..
 This is the mucociliary clearance involving the frontal sinus. So you can
have secretions moving up superiorly, medially and eventually going
lateral then medially, inferiorly and exits the natural ostium into the
 This is the image we see when we do endoscopy. From the front we can
frontal recess. But take note that some of the secretions will revert back
see here S – septum. Mt – middle turbinate that is attached superiorly
to the mucociliary pathway
to the cribriform plate. It – inferior turbinate. Between the two
turbinates is the space ~ middle meatus  where you find the UP –
Drainage:
unicinate process as well as the B – ethmoidal bulla which is part of the
 Inferior meatus
ethmoid air cells
o Nasolacrimal canal through the valve of Hasner
When a patient cries, some of the tears will enter the
Ethmoidal Infundibulum
punctum and nasolacrimal canal  exits into the nose
 Middle meatus
o Frontal sinus: 4-7 ml
o Maxillary sinus: 15 ml
o Anterior ethmoid air cells
 Superior meatus
o Posterior ethmoid air cells
 Sphenoethmoidal recess
o Sphenoid: 7 ml
NASAL PATENCY TEST

Glatzel’s mirror test
 A 3D space extending from HSL antero-inferiorly to the LNW, with the  Patient is allowed to exhale onto the mirror and misting is compared on
maxillary ostium in its floor each side
 Lateral to the uncinated process  Difference in misting may indicate obstruction
Lecture Discussion: Ethmoidal Infundibulum

This is a coronal image cut along the level of the maxillary ostium. So we have
here the orbit, maxillary sinus, natural ostium. Middle part is the nasal
septum attached superiorly to the cribriform plate. We also have the inferior
turbinate, middle turbinate  these are bony structures. Sometimes the
middle turbinate may have pneumatization called concha bullosa, the larger
the concha bullosa is, it is possible that it may cause the unicinate process to
pushed laterally resulting into the development of maxillary sinusitis
MUCOCILIARY CLEARANCE
Cottle’s Maneuver
 The cottle’s maneuver is a test in which the cheek on the side to be
evaluated is gently pulled laterally with one to two fingers to open the
valve. This test is used to determine if the most significant site of nasal
obstruction is at the valve or farther inside the nasal cavity
 So secretions develop at the floor which move up laterally, medially, and

superiorly and it always exits through the natural ostium  this is
genetically predetermined so the natural ostium should always be
patent, otherwise rhinosinusitis will develop
EXTERNAL DISEASES OF THE NOSE o It can also trigger asthma in asthmatic patients.
 Nasal Vestibulitis o If there is obstruction of the ostium, secretions cannot come
o Infection of the skin of the nasal out so there is impaired mucociliary clearance which will
vestibule eventually lead to bacterial overgrowth on the secretions
o Staphylococci is the most which will cause the patient to develop bacterial
common organism rhinosinusitis.
o Could be secondary to trauma or
frequent nasal manipulation Classification of Rhinitis:
Allergic Infectious Others
 Nasal Furunculosis  Can be intermittent  Can be acute or  Can be Non-allergic,
o Infection of the nasal hair follicle or persistent. chronic Non-infective,
oftentimes caused by Staphylococcus  Recurrent rhinitis idiopathic, NARES, etc
aureus due to an IgE
o Could be secondary to plucking of nasal mediated reaction
vibrissae (hair) of the nasal mucosa
to allergens
Infection of the external nose can progress to cellulitis or cavernous sinus
1. Allergic Rhinitis
thrombosis
 Allergic rhinitis is now classified as intermittent or persistent.
Treatment:  Intermittent allergic rhinitis
 Consists of analgesics, warm compress and antibiotics directed against o Involves having signs and symptoms less than 4 days per week
staphylococcus or less than 4 weeks.
o In intermittent type, either of the 2 given criteria is sufficient
to be able to diagnose a patient as having an intermittent type
RHINITIS
of allergic rhinitis.
 Simply means inflammation of the nose
 Inflammation of the lining mucosa of the nose characterized by one or
 Persistent allergic rhinitis
more of the following symptoms:
o Involves having signs and symptoms more than 4 days per
o Nasal congestion
These 4 are the cardinal signs week and more than 4 weeks.
o Rhinorrhea
and symptoms of rhinitis o For persistent allergic rhinitis, the 2 given criteria should both
o Sneezing
be present in order for a patient to be diagnosed as having
o Itchiness
persistent allergic rhinitis.
Nasal congestion must be differentiated from nasal obstruction.  Allergic rhinitis can be further classified as mild, moderate or severe.
o Nasal congestion may result to nasal obstruction but the  The infection will not affect the sleep as well as
problem is usually not permanent. Mild
daily activities (e.g. work or school) of the patient.
o Nasal obstruction is used to identify more permanent
 Will affect the daily activities of the patient
conditions such as nasal polyps and tumors as well as
 Sleep disturbance
septal deviation. Moderate
 Impairment of school or work
o Nasal congestion is applied to rhinitis and sinusitis.
 Troublesome symptoms
Rhinorrhea  nasal discharge that can be clear/watery or  Will affect the daily activities of the patient
mucopurulent  Sleep disturbance
o Clear/Watery  we attribute it to viral rhinitis, Severe
 Impairment of school or work
allergic rhinitis, non-allergic rhinitis
 Troublesome symptoms
o Mucopurulent  we attribute it to bacterial
infections (e.g. acute bacterial sinusitis)
 ARIA: The New Classification
 Rhinitis may appear to be a simple disorder, but it can lead to more
serious problems if overlooked and left untreated
 Sequelae of Rhinitis:
o If the rhinitis lasts longer than 10 days, the patient may
develop sinusitis.
o If the rhinitis persists, it may actually affect the Eustachian tube
connected to the middle ear so the patient will develop otitis
media.
There will be inflammation of the Eustachian tube mucosa
so air will not reach the middle ear and there will eventually
be fluid behind the middle ear prompting patient to
develop otitis media
Causes of Allergic Rhinitis:
o Mucopurulent discharge coming from the sinuses which  Allergic rhinitis can be provoked by exposure to allergens in the
contains bacteria can be propelled posteriorly and it will reach environment.
the oropharyngeal area and patient can develop  Examples of allergens are pollens (tree such as alder, hazel oak, elm and
tonsillopharyngitis. birch grass, weed), house and dust mites, animal danders, cockroaches
o This infection may further go down to develop laryngitis which and certain mold species.
presents with hoarseness.  These are the common causes of allergic rhinitis.
Signs and Symptoms of Allergic Rhinitis: Management of Allergic Rhinitis:

 Sneezing  Allergen avoidance
 Nasal itchiness  Pharmacotherapy – antihistamines, intranasal corticosteroids, topical,
 Clear, watery rhinorrhea nasal and systemic steroids, leukotriene receptor antagonist
 Nasal congestion (Montelukast)
 Pale and boggy turbinates  Decongestants may or may not be used depending on the severity of
 Redness of the eyes the congestion.
 Allergic shiners  Immunotherapy – if pharmacotherapy fails
o Infraorbital dark circles probably related to venous plexus
engorgement Pharmacologic Treatment of Allergic Rhinitis (ARIA Guidelines)
 Nasal salute
o Patient actually tries to take out the watery nasal discharge
 Linea nasalis
o Dorsal crease develops due to nasal salute
 Dennie’s line
o An accentuated line or atopic pleat of the lower eyelid  Take note: as an individual drug, the best medication is intranasal
corticosteroids followed by oral antihistamines
Pathogenesis of Allergic Rhinitis:
 For nasal obstruction – best drug is intranasal decongestant
 Sometimes may need more than 1 medication to improve their condition
 Initially, an allergic patient is sensitized.

 If the patient is not allergic, even if he is exposed to the allergen the
patient will not develop the infection.
 When the patient is exposed, the allergen combines with the IgE and
this combination will result in mast cell degranulation.
o When the mast cell degranulates, it will release the pro-
inflammatory mediators (histamine, leukotrienes, LTRA*  in particular, in patients with asthma
prostaglandin) and this will affect the eyes and the nose
resulting in immediate allergic reaction.  For mild intermittent, antihistamines can simple be given.
 In the early phase reaction, there is involvement of the eyes (itchiness,  For moderate severe intermittent up to moderate severe persistent,
redness) and nasal symptoms (itchiness, watery nasal discharge, intranasal corticosteroids may be given.
sneezing and congestion. o Intranasal corticosteroids are usually given together with
o This is an immediate allergic or early phase reaction. antihistamines.
 Few hours later, the patient will develop late phase reaction.  Allergen avoidance should always be discussed with the patient.
o It develops 2-4 hours after the exposure to allergens.  If medical management fails, patient can be referred for
o There will now be involvement of eosinophils. immunotherapy for desensitization.
o These eosinophils will go to the site of allergic reaction and the  Antihistamines are a mainstay in the treatment of allergic rhinitis.
major complaint of the patient will be chronic nasal blocking. o Antihistamines are inverse agonist since they occupy histamine
o There will be nasal obstruction. receptors.
Diagnosis is done by getting a good history and definitive diagnosis can be

achieved by skin testing  less expensive, more sensitive, technically easier to
perform, and results can be interpreted immediately
Effects of Antihistamines Effects of Nasal Steroids Comparison of Common Colds and Allergic Rhinitis:
 Relieve pruritus  Degree of inhibition of early phase
 Prevent sneezing reaction
 Decrease thin secretions  Primary effect on suppression of late
 Does not improve phase reaction
congestion  Reduction of non-specific activity
 Inhibition of effects of cytokines
Side Effects of Glucocorticoids

 Growth retardation in children and adolescent
 Suppression of HPA- axis
 Osteoporosis
 Aseptic necrosis of the bone
 Hypertension
 Peptic ulcer
 Centripetal obesity
 Glaucoma
 Cataract 3. Non-allergic and Non-Infective Rhinitis
 Diminished immune response  This also presents with recurrent rhinitis.
 Impaired wound healing  It is not governed by allergic mechanisms.
 Diabetes mellitus  It is not IgE mediated.
 Mental disturbance  It may be idiopathic.
 Proximal myopathy
 Non-allergic rhinitis with eosinophilia (NARES)
 Cushing’s syndrome
 Occupational rhinitis – people working in chemical factories develop
rhinitis upon exposure to various chemicals.
Differential Diagnosis of Allergic Rhinitis:
 Hormonal rhinitis – common among pregnant women where estrogen
1. Acute Rhinitis
is elevated and this triggers development of rhinitis
Viral Rhinitis Bacterial Rhinitis
 Drug induced rhinitis
 Common colds  Presents with mucopurulent
 Food
 Peaks on the 2nd day and gradually discharge
improves in 7-10 days  Streptococcus pneumoniae  Emotional
 Clear watery discharge 7-10 days  H. influenzae  Primary atrophic rhinitis
in duration
 Presents with nasal congestion, 4. Idiopathic Rhinitis
clear watery to mucoid nasal  Better term than vasomotor rhinitis.
discharge and may have mild sore  Non-allergic and non-infective rhinitis
throat and low grade fever  Presents with nasal hyperresponsiveness to non-specific triggers such
 Commonly caused by a cold virus as strong smells (perfumes, bleach, solvents), irritants (such as tobacco
which is well over a hundred smoke an exhaust fumes) and changes in environmental temperature
rhinoviruses
and humidity.
 Most cases are caused by
 When a person develops rhinitis during cold weather, it falls under non-
Rhinoviruses (comprising about
allergic rhinitis.
40% of the incidence)
 Respiratory Syncytial virus  The exact mechanism is unknown.
 Influenza virus  Definitely, antihistamine is not the drug of choice for this case.
 Adenoviruses  Common causes of non-allergic rhinitis are changes in the temperature,
 Treatment: supportive – tobacco smoke, perfumes and pollution.
decongestants, analgesics  Management: Intranasal corticosteroid, decongestants
2. Chronic 5. Atrophic Rhinitis

 Mycobacterium tuberculosis  There is atrophy of the nasal mucosa.
 Mycobacterium leprae  The patient will still complain of nasal obstruction.
 Klebsiella rhinoscleroma  It is a chronic inflammation of the nose characterized by a progressive
 Treponema pallidum atrophy of the nasal mucosa and the turbinates resulting in widened
 Fungi nasal passages, excessive crusting and a foul odor (ozena and anosmia).
 Incidence is quite rare  It is usually idiopathic.
 The cause is unknown.
 Common organisms implicated are Coccobacillus foetidus ozaena and
Klebsiella ozaena.
 It presents with nasal obstruction, atrophied turbinates, excessive
crusting and widened nasal cavity.
 Although there is good airway exchange the patient will still complain
of nasal obstruction.
 Therapy consists of buffered nasal saline irrigation twice daily and
vitamin A
6. Rhinitis Medicamentosa Findings:

 A form of idiopathic rhinitis characterized by worsening rebound  Paranasal sinus series or CT Scan of the PNS may reveal haziness, an air-
congestion following prolonged use of topical decongestants. fluid level or total opacification of the sinuses, but imaging studies are
 Medicamentosa means it is related to use of medications. NOT recommended for the routine diagnosis of ABRS
 Topical decongestants are advised continuous use not longer than 10 Treatment:
days.  Therapy would include appropriate antibiotics (7-10 days).
 If patients use topical decongestants for more than 10 days, instead of  Decongestants can be given if there is severe congestion.
the congestion being relieved by the medications, there will be more
 If the discharge is quite thick, mucolytics can be given.
development of congestion.
 Nasal saline irrigation will be of help.
 Rhinoscopy reveals congested and swollen turbinates.
 Intranasal corticosteroids can be used
 It is treated by discontinuing the use of nasal decongestants.
 Antihistamines are NOT INDICATED in the management of acute
 A shift to topical nasal steroids and systemic decongestants is bacterial rhinosinusitis.
necessary
Recommended Antibiotic Therapy for ABRS:
2. Rhinosinusitis  First-line antimicrobial regimen:
 Is an inflammatory condition involving the paranasal sinuses, as well as o Amoxicillin-clavulinic acid 625 mg q 8
the lining of the nasal passages o Amoxicillin 500 mg q 8
 Bacterial infection complicates only 0.5 to 2 % of viral URTIs, bacteria is  Use if patient is Penicillin allergic:
present in only 60% ARS cases and in most instances resolve o Doxycycline (among adults)
spontaneously o Levofloxacin (among adults)
o Azithromycin, Clarithromycin
1. Acute Rhinosinusitis  Cefuroxime remains an option in ABRS treatment
 The most important factor in the pathogenesis of rhinosinusitis appears
to be impaired mucociliary clearance and narrowing or obstruction of If unresponsive to medical management, CT scan of the paranasal sinuses
the sinus ostium. could be requested, patient may warrant Endoscopic sinus surgery
 Viral infection results in the loss of cilia and ciliated cells, reaching a
maximum around 1 week after the infection. 2. Chronic Rhinosinusitis
 Ciliary action is the most effective natural defense against acute  If signs and symptoms of acute rhinosinusitis persists longer than 3
rhinosinusitis months, it is already chronic rhinosinusitis.
Inflammation of the nasal cavity and paranasal sinuses and/or
Diagnosis: underlying bone that has been present for at least 12 weeks
 In general, a diagnosis of acute bacterial rhinosinusitis (ABRS) may be
made in adults with symptoms of a viral UTRI that has not improved  The most common predisposing factor is an untreated or poorly treated
after 10 days or worsened after 5 to 7 days lasting up to 4 weeks acute rhinosinusitis usually of more than 3 months duration.
 Other predisposing factors include trauma, structural deformities of the
Microorganisms of Acute Rhinosinusitis: nose, allergy and presence of nasal polyps.
Bacteria Viral  The signs and symptoms of chronic rhinosinusitis is more or less similar
Strep. pneumonia 31% Rhinovirus to the symptoms of acute rhinosinusitis except that the signs and
H. influenza 21% Influenza virus symptoms for chronic rhinosinusitis are LESS SEVERE
M. catarrhalis 2% Parainfluenza virus CRS can be divided to:
Anaerobes 6%  CRS without nasal polyps
Staph. Aureus 4%
 CRS with nasal polyps
Staph. Pyogenes 2%
Diagnosis of CRS:
Signs and Symptoms:  Based on the following criteria:
 Mucopurulent nasal and postnasal discharge o Presence of two or more of the following symptoms, one of
 For viral rhinitis, the discharge is watery to mucoid. which should be either:
 For bacterial rhinosinusitis, the discharge is mucopurulent yellowish to a) Nasal blockage/obstruction/congestion or
greenish nasal discharge. b) Nasal discharge (anterior/posterior nasal drip)’
 Usually, the discharge goes posteriorly hence the term post nasal drip. c) Facial pain/pressure; and
 Secretions will only come out of the nose if the patient blows his nose. d) Reduction or loss of smell
 Congestion o AND presence of any of the following:
 Pain a) Mucopurulent discharge
 Pressure b) Nasal polyps
c) Edema/Mucosal obstruction
 Heaviness and tenderness over the sinuses
d) Radiographic imaging showing mucosal changes
 Fever higher than 38.3 degrees
within ostiomeatal complex/sinuses
 Maxillary dental pain
 Hyposmia/Anosmia  A distinction should be made if there is acute exacerbation of CRS
 Fever The signs and symptoms are similar to the signs and symptoms of
 Rhinoscopy and endoscopy reveal purulent nasal discharge coating acute bacterial rhinosinusitis BUT the signs and symptoms of CRS
congested nasal mucosa are less severe. If the signs and symptoms will worsen again (fever,
mucopurulent discharge, tenderness on pressure)  indicates
exacerbation
Management: Signs and Symptoms:

 CRS with and without Nasal Polyps, being an inflammatory disease  Patients present with nasal obstruction because polyps can obstruct the
should be primarily treated with intranasal corticosteroids airway.
 Nasal saline irrigation is recommended  They may also present with discharge.
 CRS in acute exacerbation should be treated with short term antibiotics  Polyps can obstruct the ostium and sinusitis may develop.
 Surgical management is recommended if there is failure of medical  Patients also present with anosmia.
management of 1-3 months  The particles inhaled does not reach the olfactory epithelium.
 Multi-slice high resolution CT scan is done for patients who failed  Rhinoscopy reveals presence of translucent, grayish white cystic
medical management masses.
 Plain sinus X-rays have a limited role in the diagnosis of CRS and is not Management:
recommended
 If the polyps reach the oropharyngeal area, it warrants surgery.
 Most polyps are initially managed medically by giving intranasal
Management Key points:
corticosteroids for about 4-6 weeks.
 Drug of choice is intranasal corticosteroids combined with nasal
 It is a spectrum between medical and surgical management with the
saline irrigation.
ultimate aim of making the patient symptom free (no nasal obstruction
 Antibiotics are only given if there is exacerbation of the signs and
symptoms. and no mucopurulent nasal discharge).
 Intranasal corticosteroids are given at 2 sprays twice a day.  If the polyps regress through medical management, even if there are
 If patients present with thick discharge, mucolytics can be given. still small polyps left, it will not warrant any surgery as long as it does
 Referral to an otorhinolaryngologist can be done if the problem is not cause obstruction.
not adequately controlled.  It will only warrant surgery if there is nasal obstruction and there is
 Endoscopic sinus surgery can be done if indicated. mucopurulent discharge after about 4-6 weeks of medical
 On CT scan, the maxillary sinus should present as a dark area but if management.
there is an opacified area in CT scan, it could indicate that there is  A combination of topical as well as short term oral steroids can improve
mucopurulent discharge in that area. the signs and symptoms thereby surgery is not anymore needed.
 Mucopurulent discharge can lead to opacification  Antibiotics, mucolytics and decongestants may be given when there is
exacerbation of the signs and symptoms.
TUMORS OF THE NOSE AND PARANASAL SINUSES
1. Inverting Papilloma MALIGNANT TUMORS OF THE NOSE AND SINUSES
 A unilateral bulky deep red to gray lateral nasal wall lesion which may  Carcinoma of the nose can present with nasal obstruction and nasal
appear like a polyp with gross translucency. discharge
 Patients present with unilateral nasal obstruction, epistaxis and post  It can be mistaken for rhinosinusitis.
nasal drip.  Carcinoma of the paranasal sinuses presents with one or more of the
 If the lesion is unilateral, malignancy must be considered. following:
o Unilateral nasal obstruction
 Malignant transformation is considered to be less than 2% of all cases.
o Epistaxis
 It usually develops into squamous cell carcinoma.
o Nasal mass
 Histology shows epithelium of the lesion inverting into the underlying
o Maxillary bulge
stroma.
o Loose teeth
 It can also affect the maxillary sinus
o Bulging palate
 Three characteristics make this tumor very different from other
o Diplopia and blurring of vision
sinonasal tumors:
 A patient presenting with unilateral nasal obstruction, epistaxis and is
a) A relatively strong potential for local destruction
elderly must be screened to rule out the possibility of malignancy or
b) High rate of recurrence
inverting papillomas.
c) A risk of carcinomatous evolution
 An early case may progress to a late case of CA thus the management
will be more difficult.
Management:
 If the lesion involves the anterior maxillary wall, there could be
 Management involves complete excision via endoscopic sinus surgery
maxillary bulge.
or lateral rhinotomy with medial maxillectomy
 If it involves the gingiva, there might be loosening of the teeth.
 Diplopia, bulging palate and blurring of vision happens when the lesion
2. Nasal Polyps
affects the floor of the orbit which is the roof of the maxillary sinus.
 The most common mass in the nasal cavity
 Maxillary carcinoma is the most common.
 No definite etiology exists.
 Radiographs will reveal radioopacity of the nose and sinus as well as
 Certain risk factors are associated with the condition.
bone destruction.
 Usually bilateral
 The most common histopathologic feature is squamous cell carcinoma.
Risk Factors:
Diagnosis:
 Chronic infection – infection causes inflammation of the nasal mucosa
 CT scan of the paranasal sinuses – presents with bone destruction
prompting the patient to develop nasal polyps in the future.
 Malignant tumors invade the bone while benign tumors push the bone
 Allergies
away.
 Trauma
 Biopsy: incisional via gingiva-buccal approach or biopsy of nasal
 Metabolic disease
extension
 Aspirin intolerance
Management:
 Wide excision of the carcinoma or maxillectomy
 There must be a margin
 We want to catch patients with malignancy early. Early diagnosis should
result in better prognosis
 Modalities of treatment:
o Surgery
o Radiotherapy
o Chemotherapy
Surgery and postoperative radiation therapy may result in improved
local control, absolute survival, and complications when compared
with radiation therapy alone
SUMMARY
 Disorders of the Nose and Paranasal Sinuses result in congestion and
obstruction of the nasal cavity which can result in problems in olfaction

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EARS, NOSE & THROAT (ENT)

Topic: Ear Anatomy, Physiology, Embryology and Congenital Anomalies

ANATOMY AND PHYSIOLOGY OF THE EAR Internal Auditory Canal:

Development of the Mastoid Bone:

External Ear – Tympanic Membrane

Middle Ear Contents:

Ossicles Nerve Supply of the Middle Ear:

Middle Ear Joints

Cochlea Pillars of Corti

Lecture Discussion: Perilymph vs. Endolymph

 BA 41 – Primary Auditory Cortex

1st Branchial Cleft/Groove ANOMALIES OF THE MIDDLE EAR

Development of the External and Middle Ear Otic Vesicle

1st and 2nd Branchial Arches: Development of the Otic Vesicle

ANOMALIES OF THE INNER EAR C. NON-GENETIC

 Malformed pinna, low set ears

DISEASES OF THE EXTERNAL EAR  Predisposing Factors for Otitis Externa:

o If the impacted cerumen has already softened, removal can

Images illustrating how removal of impacted cerumen is done:

Lecture Discussion: How to Use an Ear Wick in treating Otitis Externa

Otitis Externa Circumscripta (Furunculosis)

Lecture Discussion: Ear Malformations

 Contains endodermal tissue only

MALIGNANCIES OF THE AURICLE  Management:

 Wide excision is advised. 1.) Perforation

Squamous Cell Carcinoma

 There may be a need to

 Central perforation – most common type (90-95% of patients with

 Thickened ear drum 2.) Myringitis

EUSTACHIAN TUBE DISORDERS  Treatment:

2.) Eustachian Tube Obstruction

Otitis Media continued….. Serous & Mucoid Otitis Media continued…..

1.) Acute Purulent Otitis Media  Physical Examination:

Lecture Discussion: MASTOID

 Physical Examination:  Management:

 Mastoidectomy – to produce safe & dry ear

Complications of Chronic Otitis Media & Chronic Mastoiditis:

Introduction:  Deafness can be assessed by tuning fork testing

2.) Viral Labyrinthitis  Heavy metals (Gold, Lead, Mercury)

TRAUMA SENSORINEURAL HERING LOSS

Causes of Objective Tinnitus continued….. VERTIGO

Benign Paroxysmal Vertigo (BPPV) Other Management of Meniere’s Disease:

Vertigo caused by Tumors

MENIERE’S DISEASE (ENDOLYMPHATIC HYDROPS)

AUDIOLOGY Tuning fork Tests:

 Types of Hearing Evaluation:  Rinne’s Test

 Interaural Attenuation:  Procedure: HUGHSON WESTLAKE TECHNIQUE

2. Starting at 0 dB level and ascend by 10 dB increment

o Elevation of one signal produced by introduction of a 2nd sound

Lecture Discussion: Masking

Lecture Discussion: Audiogram Key

 SPEECH FREQUENCY: 512 Hz, 1024 Hz, 2048 Hz

Degrees of hearing loss (according to ANSI):

 Conductive Type Hearing Loss: BC thresholds are normal and better

IMPEDANCE AUDIOMETRY Lecture Discussion: Type A

 AABR – Automated Auditory Brainstem Response Audiometry

 Present – Normal hearing

Lecture Discussion: Lecture Discussion:

 Type C SPEECH AUDIOMETRY

 If the speech discrimination is >80%  they are good

ANATOMY AND DISORDERS OF THE FACIAL NERVE

Lecture Discussion: Hearing Aids