OTORHINOLARYNGOLOGY

1 External otitis, foreign body of the external auditory meatus

Anatomy (External ear)

the external ear spans from the Auricle (pinna) to the tympanic membrane.
main parts include Helix x Antihelix, Tragus x antitragus, Concha, Lobule and External meatus.

the Ear canal is a narrow (0.7cm diameter in adults) canal rich in cerumen glands (modified
sweat glands producing antimicrobial wax - acidic), hair follicles and sebaceous glands that
ends on the tympanic membrane.

the Tympanic membrane is a fibroelastic layer of CT consisting of 2 parts:

• Flaccid part (2 layers)
• Tense part (3 layers)

it is separated into 4 quadrants (Anterior/Posterior, superior/inferior), with each having

distinct anatomical features.

It transmits sound waves onto the membrane→ middle ear bones (Malleus → Incus → Stapes)
which translate (mechanical movement) and amplify the signal.

Otitis Externa (Swimmer’s ear)

a common inflammation of the external auditory canal, MC due to infection (Pseudomonas, S. aureus, aspergillus) of the
skin of the canal. MC in children (7-14), and mostly during summer (swimming season).

Pathophysiology: change in the pH (due to humidity), Immunity, or break to skin (from device/trauma) → infection
RFs: swimming/moisture, obstruction (Wax, foreign object) or ear devices (plugs, aids, buds), narrow ear canal
• non-infectious causes: Mechanical (trauma), Systemic (DM, immunosuppression), Skin conditions
(Psoriasis/dermatitis)

Clinical presentation can be acute (<6w) or Chronic (>3m)

• Chronic: usually bilateral, painless, with thickened skin that’s easily traumatized → recurrence
• Acute: severe pain (more upon manipulation of ear*) and itch, sensation of “full ear/ear pressure” with some
hearing loss due to obstruction. systemic signs in severe cases (Fever, LAD)

diagnosis: CLINICAL
the auricle is red and swollen and painful on palpation (Tragus) or pulling (Pinna)*, and may drain pus.
otoscopy (if possible and not too swollen) →
• pus, narrowing/edema and redness, possible furuncles (Drain it)
• fungal infection shows fungal growths – gray/yellow dots surrounded by cotton-like material (hyphae)
• Culture may be taken if non-responsive to therapy

Therapy:
• Pain (Analgesia)
• Cleaning (remove debris)
• Acetate drops (fix pH) onto ear wick
• topical ear drops- Steroids and ATBs / Antiseptics –onto ear wick
o ATBs include: Ciprofloxacin (FQs) or AGs or Nystatin

Prevention (Swimmers): use ear plugs, avoid trauma, drain or dry (head tilt after shower/swim, blow dry)
Necrotizing OE / Malignant OE
A “deep” severe form of OE, usually seen in immunosuppressed patients (DM, IS, elderly).
it is caused by Pseudomonas, and often complicate to osteomyelitis of the temporal bone or facial palsy, as it is rapidly
spreading, and potentially deadly (10%).
the symptoms are similar but more severe (pain, itch, hearing loss, redness, swelling, pus).

otoscopy reveals granulation tissue at the bone-cartilage junction.

diagnosis is based on Head CT with contrast which shows erosion of the bone.
therapy: Aggressive (mostly for osteomyelitis) and stopping the infection
• Systemic ATBs (FQs, Cephalosporin, Piper-Taz) for 6w (bone penetration!)
• Surgery (drainage / debridement of bone)

Foreign body of the external auditory meatus

complete or partial mechanical obstruction that can be asymptomatic (even unknown for years) lead to some hearing
loss, harm to membrane or Otitis externa.
• usually in the cartilaginous part
• usually seen in children

obstruction can be:

• Inanimate – in children (beads, Lego, erasers, broken pieces of hearing aid, glass, seeds)
• Living (insects) – drowned in water/oil before removal – can be painful / noisy
• Cerumen Obturans – accumulation of cerumen plug due to poor cleaning technique →dries and hardens

Therapy: removal under direct visualization– depending on the properties (lodged, smooth, round) we choose the
approach:
• approaches: from behind and roll out (hooks), with alligator forceps, or suction tools.
• use illumination, magnification, and visualization tools (microscope is ideal)
• may require sedation (“operation”) in complicated cases or non-compliance (kids)

after removal – check for infection / inflammation / harm to the membrane.

2 Congenital malformations of the ear

Congenital defects effect ranges from merely cosmetic issues (with possible psychological effect if left), to hearing and
speech development problems.
some will resolve spontaneously over time (relieved pressure on the ear) and others require intervention.

Anotia – Microtia – Macrotia - Polyotia

• Anotia – complete absence of auricle/pinna, caused by genetic defect / taking isotretinoin (for acne)
• Microtia – underdeveloped external ear - can be isolated or syndromic (Treacher – Collins syndrome)
• Macrotia – enlarged ear due to an inherited genetic disorder
• Polyotia – having accessory (additional) auricles

Anotia and Microtia cause hearing impairment are treated surgically

Ear canal stenosis and Ear canal Atresia

the ear canal develops during 7th month in utero.
ECS – a congenital narrowing. Atresia – a complete or partial failure to develop the ear canal
corrected surgically as it affects hearing.

Preauricular sinuses
aka preauricular cysts or congenital auricular fistula. it is quite common, presenting as a nodule next to the external ear.
treated with antibiotics and surgical removal.
Mandibulofacial Dystosis (Treacher-Collins syndrome)
hypoplasia of the middle 1/3 of the face: hypoplastic mandible and ear, with downward slanted eyes.

Cosmetic Anomalies
• Darwin’s tubercles: a thickening at the helix made of cartilage, of no clinical significance (evolutionary remnant),
but can be removed for cosmetic reasons.
• Wildermuth ear: the helix is turned backwards, and anti-helix is large.
• Bat ear

Middle Ear anomalies

ossicular deformities: most commonly it is the Malleus that is malformed, can cause hearing loss.
Congenital Cholesteatoma: benign growth in the middle ear, can lead to hearing loss. Associated with teratogenic
anomalies of the middle ear. Keratinizing squamous epithelium proliferate in the middle ear and cause CHL by damaging
the ossicles. Erosion of temporal bone and CN VII paralysis may complicate the course. Treatment with surgical excision.

Inner Ear anomalies

Mondini Dysplasia – the cochlea in abnormal or underdeveloped. presents with hearing loss or vestibular dysfunction
(vertigo, nystagmus, dizziness) – diagnosed with CT. Anomaly of modiolus. - Treated with cochlear implants.
Intrauterine infections (CMV, rubella, syphilis) - Treated with cochlear implants.
Cochlear and vestibular agenesis - Michel’s deformity - Treated with cochlear implants.

3 Ear injuries

Auricular Hematoma
Auricular Hematomas usually occur due to Blunt force trauma (contact sports like boxing/wresting).
The trauma causes bleeding from perichondral vessels → fluid accumulates between cartilage and perichondrium,
leading to hematomas.

the auricle swells (confluent), it is tense and tender. possible ecchymoses are visible.

management depends on extent, but cannot be left untreated

• small – needle aspiration
• large (>2cm) and fresh (2-7d) – incision and drainage, and compression dressing (prevent recurrence)
• old (>7d) – plastic surgery

all of these procedures require anesthesia.

failure to treat may result in Cauliflower ear – permanent deformity – the ischemia causes fibrosis.

Auricular Laceration and Avulsion

Laceration (deep/thru cut) of the Auricle can be classified according to:
• Location
• Depth/Involvement of structure:
o Simple – no cartilage
o Complex – with cartilage
o Auditory canal / Middle ear / inner ear – symptoms vary accordingly
• Hematoma
• Infectious risk (Dirt / Animals)- prophylactic ATB or vaccine (tetanus/rabies)

Therapy depends on classification:

• suturing (skin / perichondrium, but never thru cartilage)
• reconstruction surgery

in avulsion – the “torn” part should be placed in a bag and kept in cold water (4c*) until reconstruction surgery.
Perforated Eardrum
cause can be direct or indirect:
• Direct: Trauma (fractures, swabs) / Iatrogenic (removal procedures)
• indirect: Barotrauma (Diving) [RF: blocked eustachian tube], Blast injuries (or slap), Strong suction

Clinically they present with sudden sharp pain, bleeding, hearing loss, tinnitus
• inner ear involvement → Vertigo

Diagnosis: Otoscopy (visible hole), Audiometry and fork tests, (pneumatic) Tympanometry (membrane function test)
• if superinfection – lab/culture the discharge

therapy: nothing (within weeks it will heal) or tympanoplasty

Often seen as complication of purulent otitis media or less commonly after direct traumatization with foreign objects.
Symptoms include sudden decrease of pain level in otitis media, sudden unilateral hearing loss and discharge from EAM.
Conservative treatment for smaller injuries, usually heals within 2 months, prescribe ATB. Larger defects may require
myringoplasty.

Inner ear Fractures (fractures of the pyramidal bone – can be longitudinal and causing hemorrhage into ear canal or
perforation of the membrane, or Horizontal and cause facial nerve palsy.

4 Secretory otitis media

serous/mucoid effusion in the Tympanic cavity without infection, lasting for >3m.
Pathophysiology: a dysfunctional ET causes negative pressure in the middle ear, leading to fluid
production. then obstruction of that ET leads to accumulation of the fluid. it is mostly seen in
toddlers after Acute OM, but can present in adults as well.

RFs:
• children – enlarged adenoids, cleft lip/palate
• Adults – nasal (nasopharynx) tumors, polyps, URTIs
Clinical: asymptomatic or very mild
• Painless sensation of pressure, popping sound
• conductive hearing loss
o → speech impairment

! presence of fever / pain indicates Acute OM !

Diagnosis: Pneumatic otoscopy (pneumatic – with tool to touch the membrane gently)
• it is opaque (not translucent), yellowish, possible retracted
• air fluid levels are seen (“bubbles”)
• Tympanometry – reduced compliance of membrane – Type B
• in adult: Endoscopy of nose (rule out NP Carcinoma, Polyps)
• Audiometry (Hearing loss)

Therapy: depends on age, but generally resolve spontaneously within 3 months granted the
etiology is treated (Adenoidectomy, removal of tumor).
• conservative (Tympanostomy / Myringotomy tubes)
• Adults may benefit from Valsalva maneuver (to induce drainage)
• hearing aid can help until resolution

5 Acute otitis media

infection of the tympanic cavity, usually due to Bacteria (Pneumococcus, [Link], Moraxella catarrhalis, S. aureus)
it is seen in infants (6-24m) and children, as their ET is narrower, shorter, and horizontal.

pathophysiology: obstruction of the drainage (ET) in which the stagnant secretions become superinfected.
In children – secondary to viral URTI / 2nd hand smoking / enlarged adenoids. in adults – tumors / Polyps.
Occlusion => exudation => suppuration => reparation
Clinical presentation: FEVER +
• Infants: Irritability, crying, touching the ear
• Children, adults: pain, conductive hearing loss

Diagnosis: Clinical – Otoscopy (bulge, red, no CoL, opaque/milky). if membrane is torn → pus, hearing loss
• Tuning fork tests (conductive HL) – Weber (to affected ear), Rinne test (bone conduction normal)
• Otoscopy and TF tests are comparative to good ear (hyperemia and anatomical differences are relative)
• culture the fluid if no response to therapy – by aspiring with a needle (Tympanocentesis)

important DDx: Otitis media with Effusion (asymptomatic- only bulge without the rest)

Therapy – spontaneous resolution in 80% of unilateral cases!!!

• Paracentesis +/-
• 10d Oral ATB (Amoxiclav) –infants <6m, bilateral, persistent (3d) or severe symptoms, Cochlear implant
o topical ATBs are useless, unless a tympanostomy is present
• symptomatic (pain, fever)

Complications: Due to the potential communications with temporal bone, cranial cavity, external and inner ear:
• Mastoiditis (to mastoid air cells) and Osteomyelitis and Meningitis
• Labyrinthitis (Vertigo, hearing loss, balance issues)
• TM Rupture (secondary OE)
• Brain Abscesses (thru blood / lymphatics)
• CN7 Palsy (mechanism unknown – compression, irritation)

Chronic OM can also cause Tympanosclerosis (scarring of eardrum by the constant inflammation) or Cholesteatoma
(epithelium creeps after rupture)
6 Chronic otitis media

chronic Suppurative OM refers to bacterial infection following TM perforation (usually due to recurring Acute OM,
Trauma, or iatrogenic – tube). MC in children/adolescents <15y.
Classification: secretory/suppurative. Active (w, w/o cholesteatoma)/non-active.
Etiology is infection following Perforation (either due to acute OM, trauma, Iatrogenic causes)
• agents: Pseudomonas, S. Aureus

Clinical: Painless discharge and conductive Hearing loss

Diagnosis: Clinical (otoscopy, Audiogram)

Therapy: Drainage, topical FQs, and if membrane doesn’t fix by itself – Myringoplasty (aka type 1 Tympanoplasty)

7 Surgical treatments of chronic otitis + 8 Tympanoplasty, myringoplasty

surgical approach in chronic OM can be retro-auricular and transmastoid, Endo-meatal, endaural (thru the skin of the ear)

Mastoidectomy
therapy aimed at removing the mastoid air cells and drainage from the middle ear.
it is indicated in Mastoiditis or Chronic OM (with or without cholesteatoma).
It has 2 approaches using retro-auricular access, that differ based on whether the ear canal wall is preserved:
• Canal wall UP mastoidectomy – without connecting the middle ear to the ear canal – used in limited spread
disease where increased drainage is not needed. entry thru the bone directly to middle ear.
o pros: preserved anatomy, less complications, shorter recovery
o cons: poor visualization, risk of residual cholesteatoma, may require follow-up operation

• Canal wall DOWN (radical) mastoidectomy – retro-auricular access thru the mastoid into the middle ear. after
clearing the pathology, a connection between the middle ear and the ear canal is created (NOT THRU THE
MEMBRANE), that allows drainage. not used in young
o pros: better drainage (used in more severe cases), better visuals and easy access for follow-up
o cons: altered anatomy, more complications (infection, bleeding), longer recovery

Reconstruction Surgeries
reconstructive surgery to damaged TM or ossicles, aimed at restoring hearing and middle ear function.
often times, TM heal spontaneously, and thus surgery is only the 2nd line of therapy.
Tympanoplasty refers to surgery of the Ossicular chain*, while Ossiculoplasty refers to reconstruction of ossicles.

Tympanoplasty
refers to surgeries that involve the ossicular chain (from membrane to stapes), without actual reconstruction of the
ossicles. it is aimed at restoring hearing using “what is preserved”.
it can be done immediately during the therapeutic surgery (mastoidectomy) or 9-12m after.
there are 5 types:
1. Type 1: Myringoplasty – for perforation in the pars tensa, with or without a graft
a. done under local or generalized anesthesia
b. we collect the graft (we need fascia-temporalis/ perichondrium and cartilage-tragus)
c. Underlay technique: the skin & eardrum are lifted, and a graft is placed behind the perforation.
d. cartilage is added behind the graft to support it, as well as dissolvable sponges which support the
process (a wall to work against). alternatively: tissue glue.
e. after everything is aligned and in place, more sponges are placed on top of the TM (with ATB) to
support and stabilize until the tissue heals.
f. an alternatively approach exists: Overlay technique (graft placed on outer membrane)

2. Type 2: malleus absent, membrane attached to the incus

3. Type 3: malleus and incus absent, then membrane attached to head of stapes
4. Type 4: membrane attached to footplate of stapes
5. Type 5: Fenestration operation - membrane attached to stapes footplate + fenestrations of lateral circular
canals is made.
Ossiculoplasty
using titanium or hydroxyapatite, we can introduce prosthetics instead of lost ossicles.
this may be indicated in otosclerosis (bony buildup around the bones).
Stapedectomy – removal of stapes and introducing the prosthesis
Stapedotomy – removing part of stapes (leaving foot with niche for prosthesis) + connecting to incus

9 Mastoiditis

Mastoiditis is usually a complication of acute OM, and involves inflammation/infection of the mastoid bone and mastoid
air cells. MC seen in children <2y.

Anatomy: the mastoid is part of the petrous temporal bone, situated behind the external acoustic meatus.

Pathophysiology
the infection in the middle ear spreads ([Link], Pneumo, Moraxella) to the mastoid air cells, which swell in response to
the infection. this prevents proper drainage of these cells, and as a result, exudate and pressure builds up. this can
further progress to destruction of the bone (the walls between the air cells break), filling with Pus, and complicates later
to abscess formation.

Diagnosis and Clinical presentation

Mastoiditis is a clinical diagnosis (history + symptoms) - the patient initially complains of persistent pain behind the ear
(the child touches, pulls on their ear). they exhibit fever, the mastoid appears red, swollen and tender, and the ear is
pushed out: displaced forward and laterally (rotates to the front).
• if there is concurrent OM, otoscopy may be significant.

if symptoms don’t improve within 48h of ATB → CT (either erosions in air cells, or fluid in them - Image)
• since this mostly occurs in children, MRI is actually the better modality (radiation), but is less useful in the
diagnosis
• in the image – arrow 1 shows otitis media, arrow 2 shows mastoiditis, and arrow 3 shows fluid in canal

always consider Audiometry to check for hearing loss, and a CBC, CRP, and cultures for other general markers.

Therapy
• supportive (Pain, fever)
• Empirical IV ATB (Pip-Taz / Vancomycin / Ceftriaxone)
• Severe / refractory cases –Tympanocentesis or Mastoidectomy (removal of the air cells → drainage)

Complications
depends on where the infection spreads to–the temporal bone, the brain, or outside of the cranium:
• Post-auricular abscess or Bezold abscess (to the neck – behind SCM)
• CN7 Palsy (usually transient)
• rare: Meningitis and Brain abscess
10 Otosclerosis

Otosclerosis is an idiopathic hardening of the ossicles in the middle ear, causing conductive hearing loss.
it mostly occurs in women <40y, and is usually bilateral (90%).

etiology: Idiopathic, Genetic x Env. , with 50% showing AD inheritance pattern, and incomplete penetrance.
• can be part of syndrome, with osteogenesis imperfecta, + blue sclera and pathological fractures
it mostly affects the foot of the stapes (stiffness, fixation), but other variants such as on round window exist.

Clinical:
Conductive HL (low freq.), tinnitus, Mild vertigo (25%), Paracussis willisi (hear better in noisy environment)
• since bone conduction is ok, the patient perceives their own voice as loud, and as a result they speak quietly.

Diagnosis:
• Audiometry – bone conduction normal, air conduction poor in low frequency
• Weber (lateralization to bad side if unilateral due to amplification) and Rinne (shows conductive HL)
• Tympanometry – reduced sound absorption (TM is not compliant, and thus bounces sound back)
• Otoscopy – can be normal, but may show Schwartz sign – red/blue hue seen thru TM
• Imaging (CT) – shows sclerosis

Management:
• Hearing Aids
• Surgery (good prognosis)
o Stapedectomy – removal of stapes and placing prosthesis
o Stapedotomy – removing part of stapes (leaving footplate with drill hole for prosthesis) + connecting to
incus

11 Complications of otitis media

inflammation erodes various communications:

• Mastoiditis (to mastoid air cells), Osteomyelitis and Meningitis (rare)
• Labyrinthitis (Vertigo, hearing loss, balance issues)
• Tympanic Rupture (secondary OE)
• Brain Abscesses (thru blood / lymphatics)
• CN7 Palsy (mechanism unknown – compression, irritation)

Chronic OM can also cause Tympanosclerosis (fibrosis of eardrum by constant inflammation) or Cholesteatoma:

Tympanosclerosis
• scarring of tympanic membrane due to Chronic OM or OM with effusion – due to chronic inflammation
• can lead to hearing loss otoscopy reveals calcified plaques

Cholesteatoma
a special chronic OM - growth of keratinized Sq epithelium from TM → middle ear / mastoid air cells. it can be:
• acquired (MC)
o Primary – dysfunction of ET → retraction of TM → retraction pocket
o Secondary – pearly white mass behind membrane
▪ Migration: in Chronic OM –perforated eardrum allows epithelium to migrate inwards
▪ Implantation: surgery / foreign body introduces epithelium
▪ Metaplastic: inflammation causes change in epithelium (Cuboidal → Squamous)
• Congenital (behind compact eardrum)

symptoms are those of Chronic OM: Painless foul discharge, perforated eardrum → hearing loss.

Diagnosis: Otoscopy reveals a white/pearly mass behind the membrane – resembles wax, but can’t be removed
since it can penetrate bone → XR/CT scan the hearing loss can be diagnosed by audiometry
Therapy: Surgery – remove the cholesteatoma, mastoidectomy to ventilate the discharge → dry the ear , followed by
reconstruction of harmed structures to fix the hearing loss.
• approaches – outside in (transcortical and then transmastoid) or inside out (trans meatal – also with
preauricular approach – we enter the external canal thru the skin of mastoid, not to be confused with Endaural
approach – entry thru external meatus)

Complications: the cells secrete enzymes that destroy and invade bone and nerve: Destruction of ossicles, vertigo, facial
nerve palsy, meningitis / brain abscess

12 Prosthetics and surgical therapy of deafness and hearing loss

Hearing loss and deafness can be corrected completely or compensated by various ways. include:
1. Hearing Aids – devices that amplify sound, to compensate for some degree of hearing loss
2. Cochlear implant – prosthetic devices that are surgically implanted, and function like the cochlea, conducting
signals to CN8.
3. Bone conduction hearing Aids (BAHA device)

what leads the choice of one over the other?

1. Audiometry results – after determining the type and frequency lost, we can tailor the right device. no longer
held in a quiet room, to mimic real-life situations.
2. Lifestyle of patient
3. Motivation – old people often don’t care for the change in hearing

Hearing Aids
these are electronic devices, that are either analog or digital (MC).
both types are made of the same structure:
Microphone → Amplifier → microchip* (not in analog) → Speaker into the eardrum
• in addition – a battery

the general idea is mechanical signal is converted to electrical signal, and then back to mechanical signal.

Analog aids amplify the sound as it is recorded by the microphone (with background noise), while digital aids can modify
the sound using a microchip, increasing certain frequencies more than others and lowering others, according to the
results of the audiometry.

Analog devices: cheaper, longer battery life, easy to set up \ non-adjustable, hard to use phones
digital devices: have the signal converted to digital signals, and the microchip can analyze them and control the levels of
different frequencies (lowering background noise, amplifying speech, etc.)

disadvantage of a hearing aid – require patient training, can’t produce normal hearing, material allergy.

Cochlear Implants
a cochlear implant is indicated in SN hearing loss, specifically – in harm to the cochlea (but
with CN8 preserved) or if hearing aid is not enough for the patient.
• will not be effective in HL lasting >25y, as the nerve as likely deteriorated (no stim.)

the implant consists of an external part (in the bone) and an Internal part.
 • External part: the input is received by a microphone, coded by a speech processor → transmitter → internal
receiver (the first component of the internal part)
• Internal part: Utilizing a mastoidectomy, the internal receiver extends electrode fibers that are inserted thru the
round window into and along the canals of the cochlea. The electrical signals coming from the receiver can then
stimulate CN8.
Criteria: bilateral, <25y/ deaf, words at 55dB <40%
Bone Conduction (BAHA – Bone Anchored Hearing Aid)
bone conduction is an alternative to electronic hearing aids, in patients who cannot use hearing aids
(Chronic OE or OM, allergies, atresia of ear canal). the idea is insertion of a small titanium implant and
it’s osteointegration, and the external connection of a sound processor that transmits the sound
directly to the inner ear bones.

13 Ddx of hypoacusis and classification of hearing impairment

Hypoacusis means hearing loss.
classifications: conductive x SN x mixed , Bi x Unilat, Sudden x Gradual x Congenital, Early x Late, by severity*
for the DDx it is often useful to classify according to
• Conductive hearing loss – outer or middle ear dysfunctional
• SN Hearing loss – cochlea, CN8 or the rest of the pathway dysfunctional

Conductive HL Sensorineural HL
Onset
Early age Late age
Side Can be unilateral or bilateral, and this helps the DDx
Etiologies
Congenital: Canal atresia Congenital: TORCH infection
Sudden: Cerumen impaction, OM / OE, Sudden: Meniere disease, Labyrinthitis, AGs
Barotrauma or TM rupture / Loop diuretics
Gradual: Otosclerosis, Cholesteatoma, Glomus Gradual: Acoustic neuroma, Noise-induced
HL, Presbycusis (age-related HL)
Clinical
Hearing improves in noise Hearing worse in noise
normal/quiet voice (perceives self as loud) loud voice (bad self-perception)
pain in OM/OE distortion of sound, loss of high frequencies
Otoscopy features Present Not-present
Weber (unilat)
Lateralization to bad ear (“turns up the volume”) Lateralization to good ear
Rinne (unilat)
Bone > Air Air > Bone (aka normal)
Speech Audiometry
(word comprehension)
No discrimination loss Discrimination loss (regardless of increasing
volume)
Audiogram
Bone x Air different Bone X air similar, with High freq. loss

Severity: see table – usually refers to speech range Frequencies (500-4000 Hz)

the DDx is led by History (onset? uni/bilateral? pain? tinnitus?) Tests (Weber, Rinne),
and Examinations (Otoscopy, audiograms, audiometry, Tympanometry)
14 Tinnitus

a common (most people will experience it at some point) condition in which sound is perceived without any actual
external source. it (subjective form) is believed to arise from background sound generated by the cochlea, that is not
filtered by the CNS.

it is a symptom that can arise in various diseases, usually associated with hearing loss (subjective)
it can be acute/chronic, Unilateral / Bilateral, Intermittent / constant, Primary / Secondary.
helpful analogy: In a sense, when the ears are having a tough time hearing the surrounding, they turn up the volume,
making the high-pitch sound discernable.

types:
• Non-pulsating (MC) (subjective) – false perception of sound that no one else can hear. it is usually a buzz or
ring, high-pitched tone associated with hearing loss, common etiologies:
o Noise-induced hearing loss
o Meniere’s disease
o Head injury or TMJ dysfunction
o OM and TM perforation
o drug-related damage (Aspirin, NSAIDs, Loop diuretics, AGs)

• Pulsating (Objective) – sounds created by the body, that can be perceived by others (stethoscope on ear or
neck). usually caused by CV cause. etiologies include:
o Vascular: carotid or aortic stenosis, AV malformations, ET dysfunction
▪ systemic causes: Anemia or hypo/Hyperthyroidism (causing changes in flow)
o Non-vascular: Paget’s disease (impingement), Otosclerosis, myoclonus of stapedius (clicking)

Investigation
• History
o classify it: Bi/Unilateral, Acute/Chronic, duration, Pain? alleviating / exacerbating stimuli?
▪ example: Meniere’s – unilateral, acute, lasting <1m
o Risk factors (sound exposure, chronic illness, ototoxic meds)
• Otoscopy (Infection, impaction, tumors behind membrane)
• Audiological Examination (Audiogram, Tympanometry)
• Auscultation of head/neck (check for murmurs, bruits, hums)
• Neurological and Behavioral examination (depression, and to determine if suicidal thoughts arise from it)
• Imaging (MRI, angiography, carotid Duplex) only if red-flags appear: if unilateral, pulsatile, asymmetric, with
focal neurological deficits or Vertigo – finding CV or neoplastic causes.
• Others: Blood tests (CBC, Glucose, T3/T4, Lipids), Infection panel

Therapy: usually resolve by treating underlying condition, Hearing Aids or supportive therapy (learning to adapt)
• supportive treatment includes Counseling (living with tinnitus), TRT (Tinnitus retraining therapy- Cognitive
behavioral therapy for tinnitus), Sound Therapy (Hearing aids, cochlear implants)
• usually worsens at night, and thus sleeping with headphones or white noise machine helps

prognosis of acute tinnitus is great (80%), and bad for chronic (25%)

15 Hearing examination

The diagnosis of hearing loss starts with an initial complaint of the patient or family member.

1. History:
a. complaints of hearing loss in one ear or both
b. complaints of tinnitus
c. onset (gradual x sudden)
d. pain or painless.
e. perceiving voice as quiet or loud
the doctor will then preform several initial examinations

2. Otoscopy: to examine the External ear, the membrane, and the immediate vicinity of the middle ear.
a. Canal changes (narrowing, injuries, bulging – osteoma / exostosis)
b. membrane changes (bulging, color, pulsating mass, white mass, perforation, loss of landmarks)
c. Drainage (pus, blood, serous fluid)

3. Tuning fork test: useful only in unilateral hearing loss

a. Weber test – lateralization test: in conductive HL → to bad side and in SNHL → to good side
b. Rinne test – compares bone to air conduction – bone is better if external ear is blocked, but it is
normal in SN hearing.

4. Audiometry: the threshold of hearing is tested at various frequencies. the plotted graph profile can tell us
a. which ear is bad
b. which type of HL it is – Bone conduction, Air conduction, or SN HL.
c. what is the severity – cannot tell the difference between cochlear and pre-cochlear SN hearing loss
(only a difference between left and right ears can – asymmetry tends to be post-cochlear)

normally, the plot ranges

between 0 - 20 dB. in conductive
HL – air is affected, and in SN –
high frequency affected.

Other Tests
• AEP – Auditory Evoked Potential / ABR - Auditory brainstem response – an objective method of testing
the hearing loss, by reading brain activity (EEG) in response to sound. used in newborn screening. normally
has 7 peaks, number 3 and 5 are most important for the brainstem nuclei. the waves need to have
certain amplitude and latency.

• Tympanometry – checking the compliance of the membrane/ossicles. by applying air pressure and a
sound (226Hz for adults, 1Khz for infants) we see what “bounces back” to probe, and what is absorbed to
TM. a rigid TM means less absorption. seen in Otosclerosis, OM with effusion.
o yields Tympanogram (graph) with one of 3 profiles: Type A (good middle ear – highest
compliance at ambient pressure of 0), Type B (low compliance: Effusion or perforation),
Type C (low pressure - Blockage of ET)
o To understand the graph – e.g. A – means that TM was most compliant when pressure
was 0 for a pure tone of 226Hz. C means that Compliance was greatest at low
pressures, while B means that compliance was terrible along all pressures.
o Peak compliance means most absorption (aka least reflection to the probe).

• Otoacoustic emissions – the acoustic energy produced by the cochlea (by the hair cells) is recorded in the
external auditory canal – used to screen newborns (an objective test)

• Imaging (CT/MRI)
16 ENT aspects of facial nerve injury

Facial Nerve Anatomy

the facial nerve arises from the pontomedullary junction. it has motor (facial, stapedius, posterior digastric and stylohyoid), sensory
(ear of skin, taste of tongue) and ANS (SM, SL, lacrimal glands) function.

As it arises from the pons it enters the Internal Acoustic Meatus, traveling close to the inner ear, and then out thru the Stylomastoid
foramen. some branches it gives off along its course:
• Greater petrosal (ANS glands – lacrimal and mucus)
• Nerve to stapedius
• Chorda Tympani (anterior 2/3 taste, ANS - salivary glands)

once out of the cranium it gives rise to motor fibers

• motor fibers for muscles around the ear, digastric, and stylohyoid
• Motor root (all facial muscles – Temporal, Zygomatic, Buccal, Mandibular, Cervical)

Facial Nerve Lesions

depending on the location and fibers affected, we can get various clinical presentation.
• IC lesions (potential harm to all functions) – usually Idiopathic or Ear-associated
• EC lesions (usually just motor functions)

Some etiologies are more common to specific clinical presentations. these include:
• Idiopathic (50%) – Bell’s palsy
• Trauma (temporal bone fracture, parotid or ear surgery)
• Tumors (Parotid gland, Vestibular schwannoma, Cholesteatoma)
• Infection (OM/OE, Lyme’s disease, VZV shingles – dormant from DRG, HSV – dormant from trigeminal)
• Systemic diseases (Sarcoidosis, DM, MS, GB syndrome)

alternative classification is Central (UMN) palsy vs Peripheral (LMN) palsy:

the eyelids and forehead muscles are innervated by nerves from both sides.
a peripheral palsy blocks fibers from both sides and affects same-side as lesion (droopy eyelids and forehead)
remember that central innervation is contralateral – meaning that UMN lesions of left side cause mouth drooping on
right side, while peripheral innervation is already crossed the decussation hence lesions appear ipsilateral.

as a rule of thumb:
• UMN lesion on right cortex = all is well except left lip
• LMN lesion on right nerve = entire right side is bad

Potential Clinical Signs

• pain/numbness around the ear
• taste disorders (unilateral)
• Dry mouth / eyes → ulcerations and scarring
• Hyperacusis (stapedius doesn’t tone down)

Diagnosis: History, Facial examination (smile, lift eyebrow, open eyes)

A peripheral palsy will show inability to lift eyebrow or open eyes – the patients mouth and eyelids are droopy.
• Bell’s Phenomenon: when asked to close eye, the eye moves up and out
• additionally: Audiogram (Conductive HL – Cholesteatoma, SN HL – Acoustic neuroma)

Prognosis and Therapy: Idiopathic BP usually completely resolves within 3w, while secondary palsies require etiological
therapy (Acyclovir, Steroids, decompressive surgery, tumor removal)
until resolution: Symptomatic therapy of eye drops (artificial tears) and taping eyes at night to keep them closed.
17 Peripheral vertigo, vestibular examination + 18 Meniere’s disease

Vertigo is a descriptive term, for the sensation of movement between patient and environment, or in other word – it
feels like the room is spinning / patient is spinning, often on the HORIZONTAL axis (like carousel).

other forms of “dizziness” as it exhibits several additional features:

• Presyncope – the sensation of almost passing out (palpitations, light-headed, blurry vision) – cardiac etiologies,
vasovagal response, orthostatic hypotension
• Disequilibrium- imbalance, more in walking – etiologies includes: Parkinson, cerebellar or spinal disorders
• Non-specific dizziness – due to anxiety, hypoglycemia, anti-Cholinergics

Symptoms that accompany vertigo:

• Nausea/Vomiting
• Sweating
• Feeling unwell

Pathophysiology: a mismatch between the various sensory inputs responsible for maintaining upright posture.
inputs:
• Vision
• Proprioception (GTOs, muscles, tendons)
• Vestibular Apparatus – the semicircular canals (with associated otoliths)

The Vestibular apparatus

the SC canals are 3 canals in different axes, they are the posterior & anterior (more diagonal) and lateral.
the lateral right is aligned with the lateral left, the posterior left is aligned with the anterior right, and vv.
these canals are responsible for sensing rotation on the horizontal axis (by detecting shift in fluid on the stereocilia in the
ampulla region of each canal), the vertical axis (nodding, Anterior SCC) or coronal axis (tilt ear to shoulder, Posterior
SCC). vertigo occurs here if there is a discrepancy between right and left sides*
• similar damage on both sides will NOT LEAD TO VERTIGO.

-The utricle and saccule are the organs responsible for sensing vertical acceleration (elevator, jumping).

input then goes to Vestibular nerve → Vestibular nuclei → cerebellum, Oculomotor nerves, SC, and thalamus.
• this allows coordination of movement of eye and the rest of the body.

Etiologies
Vertigo is Peripheral (dysfunction of vestibular apparatus) or Central (dysfunction of brainstem/cerebellum). MCC:
• Peripheral: BPPV – Benign Paroxysmal Positional Vertigo (MC), Meniere’s disease, Vestibular Neuronitis
o are often positional (movement triggers the vestibular dysfunction) or not
• Central: Posterior stroke, Tumors, MS
o are non-positional (regardless of changes in the vestibular apparatus) and sustained
o include cerebellar symptoms (ataxia, dysmetria)

Meniere’s disease
Meniere’s disease, is a chronic disease of the inner ear, occurring due to increased endolymph (Endolymphatic hydrops)
in the labyrinth of the ear, disrupting proper function.

The exact cause of increased production is unknown but may be associated with viral infection or AI disease.

It is seen in adults (40-50), and is characterized by a triad of Unilateral Vertigo, SN Hearing loss (low-freq.), and tinnitus,
as well as a pressure sensation in the ear and Nystagmus.

episodes come in clusters that occur over several weeks, with each episode lasting minutes to hours, followed by
prolonged periods (month’s to years) of no symptoms.

The diagnosis is Clinical – Unilateral Triad of:

• Vertigo: not positional, and often leading to imbalance and falls.
o Unidirectional spontaneous nystagmus often seen during an attack
 • Hearing Loss –fluctuating SN hearing loss, with Audiogram showing loss at lower frequencies (unlike regular
SNHL).
o episodes starts in concurrence with the vertigo attacks, and then becoming more persistent.
o Weber (to bad ear), Rinne Normal
• Subjective Tinnitus –starts in concurrence with the vertigo attacks, and then becoming more persistent.

10-25% of patients transit to Bilateral disease.

Management
• Acute attacks: Prochlorperazine (low-potency typical antipsychotic),1st gen Anti-histamines (suppress vestibular system) or Benzos
• Prophylaxis: avoid triggers and stressors (caffeine, alcohol, nicotine)
o Betahistine (anti-vertigo)
o Low sodium Diet (reduces fluid retention) and Diuretics
• Interventional (only in extreme cases): Intratympanic Gentamicin (ototoxic, reducing vertigo attacks)

BPPV – Benign paroxysmal positional vertigo

displacement of the otoconia (crystals) into the canals (usually posterior SCC) due to viral infection, trauma or aging, but
most commonly - idiopathic (MC), leading to positional* vertigo.
• Positional: paroxysms start upon movement (standing still will stop the attack) and last for several seconds,
symptoms last for weeks, and can re-occur years later.
• if it lasts for >1m, or there is associated hearing loss or neurological symptoms – consider other causes.
Diagnosis using the Dix-Hallpike Maneuver (see later) in which the patient moves from sitting to supine with head shifted
laterally and backwards. the doctor then checks for nystagmus to make the diagnosis.
the type of nystagmus (rotatory, vertical, horizontal) tells which canal is faulty and allows to use the right repositioning
maneuvers. for Anterior/posterior SCC – Epley Maneuver.
if the maneuver is not enough – vestibular suppressants (1st gen. anti-histamines, anti-depressants) – but never for
chronic use.

Acute Vestibular Neuritis / Labyrinthitis

another common cause of vertigo, caused by inflammation of the vestibular nerve leading to mismatch in signals
(idiopathic often following URTI/HSV infection). It causes a sudden vertigo that lasts for several weeks (constantly!)
if Hearing loss is present – it is termed Labyrinthitis (the inflammation spreads to nerve)

Other Causes of Peripheral vertigo:

• Tumors (Vestibular Schwannoma)
• Trauma to CN8
• Otosclerosis
• Ramsay-Hunt syndrome (Shingles) – CN7 Palsy, Vesicles, Vertigo

Nystagmus and Vertigo

central and peripheral causes of vertigo have associated nystagmus.
• Peripheral: Torsional/ horizontal (never vertical), direction of nystagmus doesn’t change with gaze
• Central: any type, direction of nystagmus changes with gaze change
*Gaze fixation makes central vertigo worse, while improving peripheral vertigo

Vestibular Examination
Examination of the vestibular apparatus include several steps:
• History (what symptoms, when and for how long, accompanying symptoms, recent
infection, ototoxic meds)
o Central – 4Ds – Diplopia, Dysphagia, Dysarthria, Dysmetria
o Peripheral – hearing loss, tinnitus, pressure in ear
• Otoscopy (infection, Tumor / pulsation)
• Full Neurological Examination
• Audiometry (Meniere’s disease)
• Dix-Hallpike maneuver – the results are slightly different between peripheral and central (difference in lag time
from maneuver to nystagmus onset), and different types of nystagmus.
19 Tonsilitis – Classification, symptoms, treatment

Acute Tonsillopharyngitis
inflammation of palatine tonsils / pharynx often occur together. classification is usually etiological.
70% occur due to viral infections (adults), but bacterial infection with GAS are common in children.
• Viruses: Respiratory viruses (Adeno, Influenza, Corona, rhinovirus), Mono, Herpes, Coxsackie A
• bacteria: GAS (as Scarlet fever or not), diphtheria, Vincent Angina (rare), Syphilis
• Fungal: Candida (thrush)

while there is slight variation between viral and bacterial, they commonly present with dysphagia and sore throat, LAD,
and observable edema/hyperemia.

Clinical presentation slightly varies depending on etiology:

• Viral: signs of a cold and conjunctivitis, NO FEVER but cough
o physical examination reveals edema (possible lymphoid nodules) and redness (visible vessels!) of
throat. tonsils are usually not enlarged.
o Mononucleosis – the only viral TP that shows exudation
o Herpangina / Herpetic TP – vesicles and ulcerations on the oropharynx (dew drops on rose petal)
▪ Herpangina can be part of HFM disease or standalone

• Bacterial: FEVER but no cough, sore throat, dysphagia, LAD

o physical examination reveals edema (tonsils are enlarged), redness (possible petechia), and exudate
(mostly in crypts, never grows beyond tonsil – except diphtheria)
o Diphtheria (PM angina) – a grey PM that if removed bleeds, can grow beyond tonsils
o Vincent’s Angina – ulcerative, necrotizing (foul breath, pain) – assoc. with periodontal disease
o Pharyngeal Syphilis – indurated painless Chancre

• Fungal: Candida (Oral thrush – white scrapable PM)

Diagnosis: usually clinical, but if bacterial agent is suspected start with rapid antigen test (GAS), and if negative go for
culture. if you suspect diphtheria* –start therapy until confirmed/ruled out
• suspicion of diphtheria can arise if: no history of vaccine, grey psuedomembrane, exudate but GAS-negative,
bleeds when you try to clear

treatment is supportive for viral, while bacterial infections require ATB

• GAS/ Diphtheria: Penicillin / Macrolides
o Diphtheria also requires antitoxin (to prevent cardiotoxicity)and airway support
o failure to treat GAS can lead to RF or PSGN, or other complications (peritonsillar or parapharyngeal
abscess)
• Tonsillectomy – if the tonsils are extremely large (“kissing”) to an extent they may obstruct the airway during
sleep, recurrent infection, or if there is a peritonsillar abscess
o Post-tonsillectomy Hemorrhage arises 1w after the surgery, and is deadly and not uncommon.

20 Chronic Tonsilitis and Adenoid vegetation

Chronic tonsilitis is usually a mixed-bacterial infection, that is recurrent or lasts for >3m.
it is antibiotic-resistant, and presents with focal inflammation of the tonsil parenchyma and stroma.
presentation: tonsillar scarring and LAD therapy: Tonsillectomy

Adenoid Vegetation
the adenoids are the apex of Waldeyer’s ring (Nasopharynx). Adenoid vegetation refers to the enlargement of adenoids
(hyperplasia). It is often seen in the setting of chronic/recurring tonsilitis in children (or other URTIs).
if it leads to obstruction of the choana → Symptoms:
Mouth breathing and snoring (possible sleep apnea), Hyponasal speech (nasal voice), and
adenoid facies (constant mouth breathing actually changes the face -elongated face, short
upper lip and maxilla and large lower lip, small nose, prominent upper teeth).

the potential obstruction of the ET can cause Otitis media and hearing loss.
diagnosed using Endoscopy visualization, and treated with Surgical removal of adenoids (if
symptomatic).

21 Complications of Chronic Tonsilitis

Suppurative
• Peritonsillar abscess or Parapharyngeal Abscess – high risk of airway blockage.
• Otitis media and Mastoiditis – viral infections that obstruct the ET → superinfection
• Sinusitis – viral infections that obstruct the sinus drainage → superinfection
• Lemierre’s syndrome - infection of the carotid sheath → IJV Thrombosis

Peritonsillar Abscess
MC deep-neck infection, MCC by GAS.
the infection spreads to the space between the pharynx and the tonsils.
symptoms: Tonsillitis (dysphagia, fever, sore throat, muffled voice, exudate), Lock jaw (trismus),
displaced uvula (away).
can progress to parapharyngeal abscess (spreading to the PP space)

diagnosis: clinical, and can be confirmed with purulent aspirate (can go for US or CT)
Therapy: ATB (Clindamycin, Ampicillin) and Drainage

Parapharyngeal Abscess
MC occurs following dental infections / Tonsillitis or PT abscess that invade the PP space (deep to the pharynx muscles)
Causes trismus, and a prominent swelling/bulging of the pharynx → respiratory distress
It can form posterior (displacing the lateral pharynx and tonsil) or anterior (pushing against mandible angle).
Diagnosis requires Imaging, and it is treated with ATB and drainage.
it can spread to the RP space and carotid sheath, increasing risk of mediastinitis or sepsis/Lemierre’s respectively.

Non-suppurative
these are complications of GAS infection, that are relatively rare.
• RF or PSGN
o Therapy with penicillin of GAS tonsilitis will reduce risk of RF, but not of PSGN
o RF – JONES criteria (Arthritis, Pancarditis, Nodules on extensors, Erythema marginatum, Sydenham’s
chorea), arises 2 weeks after pharyngitis.
o PSGN – a nephritic syndrome (Hematuria – cola colored urine, and facial edema), arising several weeks
after the infection.

• Scarlet fever: Fever, Pharyngitis and LAD, Rash (Cheeks are flushed but clear perioral, Sandpaper rash that starts
on neck and moves down)
o can progress to RF/PSGN

22 Ddx of Swallowing Disorders

Swallowing is divided into 3 phases: Oral → Pharyngeal → Esophageal.

It starts voluntarily at the mouth (oral phase), followed by reflex propulsion thru pharynx into the esophagus (pharyngeal
phase – sealing of nose and larynx) and propulsion towards LES in the Esophagus (Esophageal phase).

In the esophagus, 2-3 contraction waves occur:

• Primary contraction (triggered by swallowing centers, should propel full length)
 • Secondary contraction (stimulate by distention, should clean the esophagus)
• Tertiary contraction (pathological, occurring at 2 spots – non-peristaltic or propulsive)

Dysphagia can be oropharyngeal (oral phase and pharyngeal phase) and esophageal.
Dysphagia can be classified otherwise by mechanism: Structural defect or Motility disruption.
Complications / Risks: Aspiration pneumonia, Malnutrition

Classification
-Extraluminal (pressure on pharynx/esophagus): Neck mass/goiter, TAA, lung/mediastinal mass (Lymphoma)

-Intraluminal: Foreign object (impaction), Cancer, Candidal esophagitis, Varices (Po-HTN or Plummer-Vinson syndrome)

-Intramural (wall of esophagus/pharynx):

• Structural: Zenker’s diverticulum, cancer, stricture/web/stenosis/rings, Esophageal perforation
• Mucosal irritation: Esophagitis or pharyngitis (chemical/infectious)
• Motility disorders: Achalasia, GERD, Neurological (Stroke / ND disease, dystrophies, MG)
o Achalasia – LES can’t relax as neurons are degenerated
o Diffuse Esophageal spasm – several segments contract independent of each other (angina sensation)
o GERD – Burning sensation, strictures and Nutcracker esophagus (extremely strong contractions)

Diagnosis/DDx
• Patient History
o establish level of dysphagia
o solids / liquids / saliva?
o other symptoms (Halitosis, Pain, Bloody vomit, Regurgitation)
o cancer risk factors (smoking, alcohol)
• Physical: check the neck, thyroid region, and oral cavity for any clear masses or changes
• Investigations:
o CBC – iron deficiency anemia (chronic GI bleeding)
o CXR/CT – masses in lung-mediastinum-neck, vascular abnormalities (TAA)
o Endoscopy – both laryngoscopy and esophagoscopy (search for masses / fibrosis /
ring/webs/strictures/stenosis / impaction)
o Esophageal manometry (testing contractions)
o Barium swallow + Fluoroscopy (real-time imaging shows structural and motility disorders

DDx process
- which phase is affected?
- fluid or solids or both?
- Intermittent (episodic) or progressive (worsens over time)

from there, we proceed with imaging

23 ENT aspects of oesophageal diseases and injuries

Esophageal diseases and disorders can be classified according to location (upper / lower), or according to defective
structure /mechanism.

Structural and mucosal Diseases

• Eosinophilic esophagitis – infiltration of mucosa caused by food allergens/atopy or GERD
o diagnosed with Endoscopy: esophageal rings and furrows, confirmed with biopsy
o Therapy: PPIs or topical steroids, but avoiding allergen is definitive

• Perforation – iatrogenic (MC – endoscopy) / FB / trauma / malignancy / Mallory-Weiss tears (longitudinal tears)
→ Boerhaave syndrome (perforation)
o diagnosed with CXR (shows mediastinal widening) → Barium Swallow or CT (Uncooperative)
o medical emergency – ATB and surgery
 • Strictures / Webs / Stenosis (Congenital) – a result of inflammation (Caustic agents, GERD, infection) or
radiotherapy, mostly affect solid food ingestion

• Varices –due to dilated SM veins usually due to Po-HTN or Plummer-Vinson syndrome

o PV Syndrome (DICE Plums) – Dysphagia, Iron deficiency anemia, Cancer (SCC), Esophageal webs
▪ seen as a result of Iron deficiency
o asymptomatic, but rupture is deadly
o should be ligated, along with B-blockers (lower pressure). if they bleed → Octreotide (VC) + ATB

• Esophagitis – infectious (Candida / HSV / CMV) or chemical (caustic agents / GERD / Medications)
o Acids – Coagulative necrosis Bases – Liquefactive necrosis and saponification of fat
o caustic agents should be treated with water / milk, and no vomiting (not to spread)

• Scleroderma – as part of CREST – Esophageal Dysmotility (fibrosis and death of smooth muscle) → Reflux
• Diverticulum: true/false esophageal protrusion thru the pharynx wall, causing dysphagia, obstruction, and
halitosis. diagnosed by Barium swallow and treated surgically. risk of aspiration or SCC.
o Zenker’s (Upper Pharynx, above UES) – b/w cricopharyngeous and inferior constrictor (pseudo-)
o Tx: external or laser-assisted diverticul(ect)omy (time, scar, complications-n. lar. Rec., m-itis, fistula)
o other types: Epiphrenic (Pulsion) or Parabronchial (from traction – fibrosis)
Motility
• GERD – Reflux harms the mucosa, presenting with heart burn, regurgitation, dysphagia, cough, hoarseness.
treated with PPIs or 2nd – gen Anti-histamines.
o Schatzki rings (rings at GEJ from chronic reflux)
o Barrett’s esophagus can progress to Adenocarcinoma

• Diffuse esophageal spasm – spontaneous uncoordinated segment contractions.

o presents with angina and dysphagia
o Diagnosis: Barium swallow – corkscrew esophagus, followed by Manometry
o Therapy: Nitrates / CCBs

• Achalasia – the myenteric plexus is harmed, leading to inability to relax the LES, and defects in peristalsis
o can be idiopathic or due to Chagas / Adenocarcinoma / Amyloidosis
o diagnosed with manometry/Barium swallow and treated by Pneumatic dilation or Myotomy
• Various Neurological disease: Stroke, MG, Neurodegenerative diseases

Neoplasms
Benign
• Leiomyoma – from the circular muscle layer of the lower esophagus, appears as a mass that bulges
into the lumen. removed surgically if symptomatic or progressive.

Malignant
seen MC in men due to the risk factors: Smoking, Obesity, GERD, alcohol, Cured meats, low veg/fruit.

Adenocarcinoma SCC
Location Lower Upper
RF GERD, smoking, obesity Alcohol, smoking, Diet
Follows Barrett’s esophagus
Which countries Developed (Adeno-America) Developing (SCC – South Asia)
Clinical Dysphagia (stenosis, strictures)
Hematemesis
Weight loss
Diagnosis 1st line: Endoscopy: Shows flat or nodular masses, can bleed or ulcerate
2nd line: Barium Swallow (showing Apple core lesion – proximal dilation)

Biopsy → confirmation
 CT and transesophageal US for staging
Prognosis Poor Prognosis (advanced on diagnosis)
Therapy Chemo → Surgery (partial or total)
Most patients are diagnosed at advanced stage, and thus a stent is used to
maintain passage

24 Non tumorous diseases of salivary glands

Anatomy
SL – smallest, on top of mylohyoid. SM – horseshoe shaped, in SM triangle (+facial a/v, lingual n., CN7, CN12)
Diagnosis: history and physical (external and intraoral – salivation, ducts, oral base)→ US → FNAB (no risk of
dissemination, high sensitivity, and specificity, but not 100%) → MRI Sialography rarely used

Symptom: Xerostomia
dry mouth – can be seen in the setting of various diseases, in which production is reduced, or glands are destroyed. examples:
Sjogren’s, Radiotherapy, Medications (Anti-cholinergic: Anti-histamine, anti-psychotics, Anti-depressants).
it causes dysarthria and dysphagia, tongue fissures and papilla atrophy, and shows high risk of dental infections.
while etiological therapy is best if possible (stop meds), artificial saliva can be used to compensate.

Sialoadenosis
Non-inflammatory bilateral painless swelling of glands (usually parotid), seen in DM, alcohol abuse/Malnutrition.

Sialoadenitis
Acute inflammation of the salivary glands (usually parotid), it presents with redness and swelling (unilateral/bilateral) pain
(unilateral/bilateral), and possible fever. can be seen in the setting of:

• Non-specific infection – Sialolithiasis (rare, usually SM Gland) that causes purulent sialadenitis
o formation of stones in the gland/ducts is often idiopathic, or seen due to dehydration, trauma, or smoking. unlike
other diseases – it causes unilateral symptoms (redness, swelling, pain), that are worse around times of meals
(increased pressure from increased production).
o Therapy: Supportive (NSAIDs) and trying to cause passing of the stone: stimulation of flow, massaging of gland,
warm compress (dilate)
Purulent sialadenitis: the stagnation of flow allows bacteria (S. Aureus, GAS) to ascend the ducts and colonize, and
eventually cause infection. it is followed by pus drainage from the opening.
o the infection can progress to form an abscess, or a deep-neck infection.
o treated with IV Antibiotics (Anti-staph and Metronidazole or just Clindamycin)
o if 48 hours of ATB don’t work – surgery.

• Specific Infection – Mumps (other manifestations: Orchitis, Meningitis, Pancreatitis)

o diagnosed with IgM / PCR, treated supportively (pain, fever), prevented with MMR vaccine
o Unilateral or bilateral

• AI disease – Sjogren’s syndrome (see below)

o AI (women, 40-50) disease in which T-cell (HSR4) attack the salivary and lacrimal gland, causing dry mouth and
eyes (Sicca syndrome – where the disease doesn’t spread systemically). Xerostomia may cause dental caries and
tongue fissures, and Xeropthalmia may cause blurry vision and itch → corneal ulcers.
o 50% of cases show systemic symptoms: Arthralgia (MC), Raynaud’s, Dysphagia
o can be primary idiopathic, or secondary to another AI disease (SLE, RA)
o Diagnosis: SSA-Ab and SSB-Ab, RF or ANA, and definitive: Biopsy from labial salivary gland
o Therapy: muscarinic (if some gland function retained), artificial saliva or tears, if systemic – steroids/NSAIDs
Ranula
a rare retention cyst arising in the sublingual gland, that appears as a blue swelling below the tongue.
it can disturb speech and swallowing and must be removed surgically. high recurrence requires marsupialization.

DDx of salivary gland diseases

25 Laryngeal injuries and innervation disorders

Laryngeal Injuries
Laryngeal injuries are rare, but potentially fatal (mechanical obstruction). they can arise due to:
• Blunt force trauma (violence, car accidents)
• Inhalation injury or swallowing corrosives
• Iatrogenic
o Long-term intubation (ischemia and fibrosis by compression of mucosa)
o Surgical injury to R. laryngeal nerve (unilateral – hoarseness, Bilateral – no voice, respiratory
compromise)
Clinical
• Dyspnea, stridor
• Paralysis of vocal cords → hoarseness, airway obstruction
• Neck tenderness
• Dysphagia / Odynophagia

Diagnosis: If life-threatening go straight for Tracheostomy

• always rule out C-spine injury (CXR)
• CXR to rule out other causes of dyspnea (PTX, pneumomediastinum)
• if airway is stable – laryngoscopy

Treatment: Hospitalization with airway observation, vocal cord rest, steroids, speech therapy

Laryngeal Innervation disorders

the Recurrent laryngeal innervates the intrinsic vocal cord muscles*
• except cricothyroid – Superior laryngeal n. – innervates the tension of the vocal cords (no control of tone)
Course: Right – around SC artery Left – around AoA
this course thru the thorax (left) means more “length” to be harmed in, and that we need to do a CXR to rule out thoracic
pathologies

Etiology:
• MC: Trauma or Iatrogenic (Thyroid surgery, intubation)
• External pressure (tumors, goiter)
• Laryngeal: Vocal cord nodules, papilloma, cyst, cancer
Tx: Unilateral – medialization, Bilateral – cordectomy, laser arytenoidectomy, tracheotomy
Clinical: Unilateral – Hoarseness, Aspiration Bilateral – inability to speak, respiratory compromise

26 Acute laryngitis

non-specific Subglottic Laryngitis

Laryngitis is inflammation of the larynx (vocal cord mucosa and larynx).
Can be acute (Respiratory viruses or bacterial → epiglottitis) or chronic (GERD, smoking, nodules).
In children, specific types of Laryngitis can be classified as:
• Supraglottic (aka Epiglottitis)
• subglottic (either Laryngotracheitis aka Croup or Diphtheria)

MC Etiology: viral infections (Rhino, Adeno, Flu, Corona, RSV), or a bacterial superinfection (Respiratory bacteria)
Clinical: (3Ds, Dysphonia, Dysphagia, Dyspnea)- hoarseness and pain in speech/swallowing, dry cough, dyspnea
Diagnosis: Laryngitis is clinical + history, but may require Laryngoscopy (showing swollen red cords)
Therapy: Fluids, NSAIDs, vocal rest, ATB (if bacterial)

Specific Subglottic laryngitis: Croup

Croup (Parainfluenza virus) - infection seen in children, characterized by narrowed Subglottis, resulting in inspiratory
stridor and Seal-bark cough.
o Diagnosis is clinical by can be seen on X-ray as the Steeple sign
o Treatment: Cold air, Steroids
Acute Epiglottitis (aka Supraglottic Laryngitis)
inflammation of epiglottis mucosa classically due to H. Flu.
Following the implementation of the Hib vaccine it is in decline, and now new cases involve GAS or S. Pneumo.

it is a medical emergency (often requiring intubation), affecting mostly young children.

Clinical: patient often in tripod position (helps breath), classically – the 3Ds (Dysphagia, Drooling, Distress)
• high fever, Restlessness
• Sore throat, Dysphagia, Drooling
• Severe cases: Inspiratory Stridor (high pitch whistle) or respiratory distress (Retractions, Cyanosis), muffled
voice (hinting at obstruction)

Diagnosis: Clinical – any manipulation that may agitate the patient can lead to complete obstruction
• XR will show Thumbprint sign (large epiglottis and narrow supraglottis)
• may require direct laryngoscopy of the Cherry-red epiglottis if unsure
• if possible, swab epiglottis for culture (along with blood culture)

Management: Secure airway (intubate) in seated patient, IV Antibiotics (Amoxiclav / Ceftriaxone)

• if stridor, respiratory distress or altered mental status are present → INTUBATE

27 Suffocation – causes, symptoms, treatment, tracheotomy and coniotomy

Suffocation
a partial or complete inability to breath normally, eventually leading to generalized hypoxia → anoxia.
• may often be attributed to the act of asphyxiation (blocking airway)

causes
• Foreign body
• Laryngitis/ Epiglottitis/ Oropharynx / Hypopharynx pathology (inflammation, edema)
• Tumors of airway or external to airway (Thyroid, Neck)
• Paresis of laryngeal muscles (or laryngospasm)
• Accidents / Homicide / Suicide (rolling over baby, Hanging, asphyxiation)

Symptoms: Respiratory distress, cyanosis, stridor (upper), anxiety, black out, Sympathetic activation (tachycardia,
prolonged inspiration, pallor, sweating), Dyspnea*

Dyspnea
SoB, often associated with activation of sympathetic system (tachycardia, prolonged inspiration, pallor, sweating).
causes can be
• pulmonary (Pneumonia, Asthma, PTX, PE, ARDS)
• Cardiac (Coronary, tamponade, HF, mitral regurgitation, arrythmias)
• Toxic (CO / CN)
• CNS/PNS (Tumor on respiratory centers, stroke, Dystrophy)

Inspiratory dyspnea: connected with URT obstruction (Pharynx / Larynx), and stridor. the auxiliary muscles are employed.
handled by ENT.

Expiratory Dyspnea: connected with LRT obstruction (trachea / bronchi). not the business of ENT.

Complications – Hypoxia lasting 5-6 minutes causes brain death

Management
Critical Management if needed: ABCDE
Diagnosis:
• History
• ENT Examinations (laryngoscopy, bronchoscopy)
• internal examination (Auscultation of heart and airways, ECG)
• Neurological
• Laboratory test (Blood gas, CBC for anemia, Asthma)
• Imaging (CT/XR)

Therapy
• Resuscitation
• Upper airway clearance (Jaw thrust – lifts tongue and epiglottis, Heimlich)
• Intubation
• Direct laryngoscopy (allows clearance)
• Bronchoscopy (for deeper obstructions)
• if needed - Surgical: Coniotomy, Tracheostomy

Surgical Airway
Opening of an alternative path to the lower respiratory tract using surgical incisions below the glottis (opening between
vocal folds). Indicated in Acute (Trauma / Foreign Object) or Chronic (Cancer / CF) obstruction.

Tracheostomy
Hospital setting intubation of trachea below glottis. requires some time so not used emergently unless skilled surgeon
available.
How to do it + Anatomy: Cut the Skin (2cm above sternal notch) → SC Tissue → Platysma and SF Fascia → infrahyoid
muscles → Thyroid Isthmus (C7) – may be bloody = reveal the membrane between the 2nd and 3rd annular rings of the
trachea.

Insert cannula and inflate cuff to secure and seal

Cricothyrotomy
Emergency setting intubation of trachea below glottis.
Good for about 1h – CO2 builds up (oxygen is good, CO2 is not evacuated)
Start with vertical cut (skin, fascia) followed by horizontal puncture with scalpel. Then stretch the membrane and
introduce tube. alternatively – needles are used in QuickTrach sets.

complications:
• The anatomy of the Cricothyrotomy is covered in BVs (Superior Thyroid aa.)
• T-E Fistula (going too deep)

Anatomy:
Immediately below the Laryngeal Prominence (C4), cutting thru the Median Cricothyroid ligament and then Cricothyroid
membrane

Needle Cricothyrotomy – can be done in children

28 Foreign bodies of URT and upper GI

Foreign Body Aspiration

an emergency that usually occurs in children (1-3). the object can become lodged in the URT or LRT and cause partial or
complete obstruction. URT complete obstructions (usually Right Bronchus) are life-threatening, causing severe
respiratory distress, cyanosis and suffocation.

FBs: nuts, raisins, coins (show up on XR), toys

in adults, RFs include underlying neurological illnesses, intoxication, or altered mental status.
the air distal to the obstruction is resorbed (atelectasis) and the lung collapses. alternatively – it can act as a ball valve (1-
way valve), causing hyperinflation of the affected side, and a CXR will show mediastinal shift.

Symptoms depend on severity of obstruction:

• Complete: Unresponsive, can’t speak, cry, or cough, agitated until LoC, cyanotic
• Partial: choking, coughing, dyspnea, hoarseness, stridor, cyanosis, altered mental state, diminished breath
sounds on affected side or wheezing (inspiratory = upper block, Expiration = bronchial)
death is usually due to Asystole or Hypoxic brain damage.

partial can become complete over time (moving up/down, swelling with water) – so either way – therapy is guided by
weather the patient is responsive or not.

Management
partial/complete & URT/LRT is distinguished by to the clinical symptoms and imaging (Laryngoscopy/ Endoscopy/
XR/CT), in the URT:
• Responsive x partial obstruction: Encourage coughing, planned removal (Laryngoscopy / Nasal endoscopy)
o laryngoscopy risks partial becoming complete!
• Responsive x complete obstruction: Back blows → Chest thrusts (baby)/ Abdominal Thrusts
• Unresponsive: CPR, while attempting removal (every 2 minutes check airway for FB) → laryngoscopy guided
retrieval (if unsuccessful – place an endotracheal tube – might displace the FB distally, allowing ventilation of
atleast one lung), if not – Surgical airway (Cricothyrotomy or Tracheotomy)

LRT is cleared using Bronchoscopy (both for therapy and diagnosis)

Foreign body Ingestion

also – potentially life-threatening, occurring mostly in children 1-3y.
some FBs can pass thru the GI without harm (marbles), others may have Obstructive/ traumatic / Corrosive properties
that can harm the GI tract, and lead to severe complications – the worst of which – mediastinitis (by perforation of the
esophagus) – presenting with chest pain.
• other symptoms – mostly arise from transition thru the esophagus: odynophagia, nausea, vomiting

diagnosis:
• History (Parent, patient says what happened – “ingested 6 magnets of this size, 4 hours ago”)
• confirmed with XR/CT (with barium) – CHECKs for perforation

Management
• 80-90% - Expectant management
• 10-20% - IF: failure to pass (for 4w), high-risk items (Batteries, Sharp objects or bones, more than 1 magnet), or
respiratory symptoms/drooling –flexible endoscopy to remove them.
• several magnets and signs of bowel ischemia / perforation - surgery

29 Voice and speech disorders, laryngectomy rehabilitation

Voice Disorders
Muscle Tension Dysphonia (Spasmodic dysphonia)
intermittent spasms of the laryngeal muscles that causes production of abnormal voice.
mostly affects adult women. etiology is not clear – but is associated with a chronic cough.

Pathogenesis: tensing up of the vocal cords causes imbalance that alters vibrations

Clinical: Hoarseness, weak voice and pitch/vibrato changes, difficulty talking/singing, “lump”

Types (type means at what type of tension is it stuck)

• adductor type (MC): difficulty at the start of word formation, strained and full of effort
• Abductor type: sudden interruptions of sounds and escape of air during connected speech
Diagnosis – clinical: perceptual evaluation of voice, vocal cord visualization (laryngoscopy)
Therapy: Voice therapy, repeated Botulinum injection to muscles (adductor type)

Vocal Cord paralysis

caused by harm to the recurrent laryngeal nerves.
unilaterally – it presents with Hoarseness, and Laryngoscopy shows a cord close to midline.
• Left is more commonly harmed as it has a longer course (AoA)

Bilaterally – both cords close to midline (almost sealed airway) – stridor, noisy breathing, poor coughing
• Risk of aspiration (severe pneumonia, suffocation)
• difficulty and weak speech

Diagnosis: by Laryngoscopy and electromyography (nerve activity)

Treatment: Voice therapy, Surgical injections of collagen-like substance, surgical implants –
Tx: Unilateral – medialization, Bilateral – cordectomy, laser arytenoidectomy, tracheotomy

Polyps and Nodules

Laryngeal polyps – develops in response to vocal fold irritation (singing, smoking, GERD)
Compared to nodules – they are larger, unilateral and more vascularized
Remember: Polyps, Pulpy, Primary (1), Problematic (surgery), Prominent

Nodules – usually bilateral and small, develops in response to irritation

remember: Nodular, Nothing to worry, Never-ending (many)

both present with hoarseness and breathy voice.

diagnosed with laryngoscopy / biopsy (to exclude cancer)
therapy – nodules: rest for vocal cords (allow healing) Polyps: Surgical removal

Speech Disorders
Aphasia: inability/difficulty to comprehend or formulate language.
these often occur due to stroke in relevant regions of the language dominant hemisphere (left):
• Wernicke’s regions (Sensory, comprehension)
• Broca’s region (Motor, production of word and it’s execution)

the presentation is highly variable, but often we can distinguish a Wernicke aphasia from Broca aphasia
• Wernicke – the patient is fluent, speaks normally, but uses random words (“word salad”) – they are unaware of
their lacking speech and thus it is not very frustrating. often accompanied by visual field losses (right sided).

• Broca – the patient is non-fluent – they may know exactly the word they want to say, but are unable to vocalize
them properly. often also can’t write them (Agraphia) or read them out loud
Broca aphasia is very frustrating, as the patients have the word “at the tip of their tongue” but can’t express it.

they are managed by speech rehabilitation.

Laryngectomy Rehabilitation
Old method – Esophageal speech: the patient swallows air and expels it back, while using tongue and mouth
to modify speech. difficult to master.
Best method – Voice prosthesis: a connection between trachea and esophagus is made + opening to outside.
once you block the air from the outside, the air from the lungs is shunt to the one-way valve thru the
esophagus – allowing for sound to be produced in the same manner as esophageal speech.

Electro-larynx – can be used while waiting for the voice prosthesis or as an alternative. it is a battery-operated
device held against the tissue below the mandible. it produces the vibrations needed for speech, and you
shape the words using the mouth, tongue, and lip.
30 Acute and chronic rhinosinusitis + 31 Complications of rhinosinusitis

Acute Rhinosinusitis
simultaneous inflammation of the lining of PN sinuses and nose, seen in the cold season.
Sinusitis is often a progression of viral Rhinitis, and once sinusitis hits and rhinitis is still ongoing = Rhinosinusitis.
• can be acute (<4w) or chronic (>12w), often have different etiologies, complications, and presentation

Etiology:
Respiratory Viral (MC): Rhinovirus, Adenovirus, Coronavirus
• this is true for both rhinitis part and sinusitis part, which is why this is often self-limiting
• Bacterial superinfection (Pneumococcus, H. flu, Moraxella - indicated by Purulent discharge) requires ATB

chronic causes (of reduced drainage): Polyps, CF, ciliary dyskinesia

Pathophysiology: mucosal swelling = obstruction of drainage –infection of the sinus mucosa.

an alternative to sinusitis: Otitis Media (by obstruction of ET).

Presentation:
• Rhinitis - sneezing, congestion (edema), and runny nose, Hyposmia or Anosmia
• Sinusitis – similar, + facial pain (usually Maxillary, but Frontal sinus too), possibly fever (50%)
o Bacterial infection will present with purulent drainage

Chronic Rhinosinusitis
A chronic inflammatory state similar to asthma (airway inflammation). it is rhinosinusitis lasting >12w, usually due to
untreated /recurring /complicated acute RS or chronic obstruction of drainage due to ciliary dyskinesia/CF, or
anatomical abnormality such as a septal deviation / tumor / polyp

it can present as acute exacerbation (similar to acute), or a low-grade disease with persisting symptoms.
Symptoms are similar, but may also show polyps.

Diagnosis (both types)

ARS is generally a clinical diagnosis, but more complex or recurring cases require imaging (Endoscopy/ XR/ CT).
• CT with/without contrast – show air-fluid levels, swollen tissue and mucosal thickening
• blood tests show Leukocytosis, culture/PCR can identify the agent

Therapy (both types)

• Acute: Self-limiting (NSAIDs, nasal spray – don’t abuse, Saline wash) or ATB if superinfected (Amoxiclav)
• Chronic – depends on etiology:
o CF – irrigation, mucolytics
o Polyps – steroids
o Surgery (FESS – Functional Endoscopic Sinus surgery)

complications of Rhinitis: Otitis Media, Polyps

• Polyps: edematous protrusion of the nasal mucosa, due to chronic inflammation (chronic rhinitis, CF, or
Asthma). presents with post-nasal drip, nasal obstruction, hyposmia
o Risk: airway obstruction
o diagnosis: Endoscopy or CT
o Therapy: Steroids or surgery (recur if not treated etiologically)

complications of sinusitis
if the infections spreads beyond the bony wall of the sinus. relatively rare in developed countries, but lethal.
the presentation is headaches, fever, and vision / neurological signs.

• osteomyelitis – especially of frontal bone – local pain and edema – requires ATB and surgery
 • orbital abscess or orbital cellulitis –infection of the orbital contents (fat, muscles) and periorbital tissue (skin,
eyelids)
o pain (especially in movement of eyes), edema, redness, diplopia, chemosis, bulging eye
o can lead to loss of color vision → blindness and further progress into the cranium to cause a brain
abscess or cavernous sinus thrombosis
o treat with ATB

• cavernous sinus thrombosis – very rare. starts as a headache and palsy in a V1/2/3/CN3/CN4 distribution, and
characterized by eye swelling, chemosis, and vision loss

• meningitis – Fever, Headache, nuchal rigidity, nausea, photophobia

32 Epistaxis

Etiologies: (!) signifies severe bleeds – to an extent that may cause shock.
the vessels in both Ant. & Post. bleeds are in regions of anastomosis of internal & External (F/Max – PP fossa) carotid
branches
• Local
o Nasal irritation (MCC): Nose picking (MCC), foreign body, dry nose or CPAP therapy
o Vascular malformation: Telangiectasia (Osler-Weber syndrome - AD) or hemangioma
o Inflammation: Rhinitis
o Trauma (!) (blunt trauma or fractures)
o Tumors (especially Juvenile Nasopharyngeal angiofibroma)
• Systemic (MC)
o Bleeding Disorder (!): VW disease, diseases leading to TCPenia, Hepatic/Renal diseases
o Vessels: Scurvy, HTN (!)

Anterior Epistaxis (90%)

Bleeding out of the nostrils, that is mostly seen in children.
the origin of the bleed is from Kesselbach’s plexus /the “LEGS”: Labial, Ethmoidal, Greater palatine and Sphenopalatine –
these are vessels that anastomose on the anterior-inferior part of the nasal septum

Posterior Epistaxis (10%)

bleeding from the posterior nose into the throat with potential hemoptysis or hematemesis or melena (if swallowed). the
origin is from Woodruff plexus: vessels that anastomose on the posterior-inferior part of the lateral nasal wall, and
include Sphenopalatine and posterior ethmoidal.
it is difficult to diagnose as the bleed is not as apparent - it can be differentiated if the patient keeps bleeding regardless
of having nasal packing. diagnosis can be achieved by checking the posterior wall of the pharynx (even with swab) as it
appears bloody.

Usually not an emergency, but severe bleeds are more common in Posterior epistaxis, HTN, bleeding disorders or
following trauma.

Diagnosis: the full algorithm is possible in recurrent cases, where we want to investigate the cause.
• Vitals (check for signs of shock – Hypotension, Tachycardia)
• History (if possible, not emergency) and Labs (CNC, Coagulation)
• Endoscopy / rhinoscopy

Management
Anterior is easier to control
First Aid maneuver: lift head, tilt forward, and press bilaterally for 15-20m.
if uncontrolled:
• VC agents (Phenylephrine / Sanorin or by sucking ice), Cauterization
• If site cannot be found: Inflatable tampons, Nasal packing (rarely used) and transfer to ENT
o ENT will consider embolization / endoscopic cauterization/ligation (Ethmoidal / Sphenopalatine artery)
WARNING: Toxic-Shock Syndrome can arise should packing be left for too long, give prophylactic ATB regardless.
33 Nasal obstruction – ddx

Nasal obstruction causes the sensation of insufficient flow thru the nose.
It is often a symptom of other pathological processes or chronic diseases.

Infants and obstruction: in newborns obstruction can be harmful as they mostly use
* The nasal cycle –
nose to breath (the tongue is big compared to oral cavity - until 5m) – they can present
physiological shifting
with cyanosis, feeding difficulty, choking, pauses for breathing during breastfeeding.
in swelling of concha
improves with crying as they use mouth to breath when they cry.
on both sides
• MCC in infants – infectious Rhinitis

RFs: Atopy, recurring rhinosinusitis, nasal surgery, having pets or poor air quality, history of nasal polyps

according to its etiology and extent, it can manifest with mouth breathing, anosmia/hyposmia, nasal facies, discharge
(various) or stuffiness.

Etiology / Classification
Can be classified according to LOCATION
• Nasal Cavity: Rhinitis, Polyps, Foreign body, Enlarged turbinate’s, Tumors
• Nasal septum: Deviation, Hematoma
• Nasopharynx: Adenoid hypertrophy, Tumors (0041ngiofibroma, NP Carcinoma)

other classification can be MUCOSAL or STRUCTURAL

• Mucosal: sinusitis, polyps, Rhinitis (allergic / non-allergic), iatrogenic (adhesions), nasal spray dependency
• Structural: bone or cartilage defects (deviated septum), tumors, and enlarged adenoids, Various vasculitis
(affecting URT)

-trauma can fall under both categories, as it can cause fractures that harm structure, as well as inflammation or bleeding
that can harm the mucosa.
-Drugs and medications: nasal spray abuse can lead to dependence, chronic cocaine usage can cause perforation and
atrophy of the septum

Diagnosis
• History (Trauma? which side? known allergies and recent exposure? drainage? recurrent URTIs? subsiding of
symptoms or persistent? nasal spray use?)
o drainage can be watery – inflammation/allergy, purulent - infection, bloody – trauma / tumor
• Examination (Direct / Endoscopic): visualize polyps, foreign object, tumors, deviation of septum, inflamed
mucosa
• Blood tests / Swab: general inflammatory markers and microbiology, allergy panel
• Imaging (XR / CT) – tumors, polyps, sinusitis, foreign objects, septal deviation

34 Nose, paranasal sinus, and facial skeleton injuries

facial fractures can be classified as occurring in the lower 1/3 (mandible), middle 1/3 (midface), or upper 1/3
the MC facial fracture – Nasal fracture.

Nasal Fractures
the MC facial fracture, caused by trauma to the upper 1/3 of the face, usually only involving the nasal bone
symptom: pain/deformity, epistaxis, rarely – obstruction of airway
diagnosis: XR/CT and physical examination (open x closed fractures)
Therapy:
• Closed reduction with external fixation (often plaster)
• supportively: NSAIDs, ice packs, control of epistaxis (usually with packing)
nasal septum fractures and Septal hematoma
trauma to the face can harm vessels in the septum, leading to the development of a balloon-like bloody protrusion (the
mucosa is intact). it requires surgical drainage, and fracture reduced and fixated.
it is almost exclusively associated with nasal bone fractures.

Midline Fractures (LeFort, Blow Out)

Most midline fractures involve the orbit in some way
Midface fractures are complex – comprising of different bones fracturing together.
Diagnosis: Trauma History, Examination (ORBIT!), Symptoms (Pain, CSF + GCS), XR and CT scan
Treatment: ALS (consciousness and bleeding), immobilize →Surgical (ORIF / IMF / Wires / Ext. fixation)

LeFort fractures – 3 typical planes of weakness (tend to break in this pattern) – the face is edematous.
All involve pterygoid plates (floating face), mostly with other injuries to soft tissue.
• 1 – transmaxillary – the line of the alveolar sockets (horizontal) – maxilla moves (floating palate)
• 2 – subzygomatic / pyramidal – maxilla → floor of orbit → nasal bone –
maxilla and nose move – often CSF leakage (thru cribriform plate)
• 3 – craniofacial fracture – face and cranium detach – zygoma x frontal
bone detach + nasal x frontal bones detach – CSF leakage common

ENTs handle Lefort 2 and 3.

Blow-out fractures – upper 1/3 – blow to the eye → fracture of weak orbit floor into sinus
• Symptoms: enophthalmos (sinking of eye), diplopia, Subconjunctival bleed
• Diagnosis: CT
o Hanging drop sign- CT shows soft tissue in sinus
o Trapdoor sign- CT shows bone fragments in sinus
• Complications: Pneumoorbita (From sinus – DO NOT BLOW NOSE), Bleeding, Muscle laceration
• Treatment: conservatively (reposition under sedation if no entrapment) + ATB
o surgically if high risk of loss of eye or function

35 Concept of FES

FES is a minimally invasive surgical procedure, that utilizes nasal endoscopes with various “connectors”, used
to remove / debride tissue to allow proper drainage or airflow.
in general – endoscopy can be diagnostic or therapeutic

various options: Upper GI (Esophagoscopy, Pharyngoscopy), Ear (Otoscopy), Sinus (sinusoscopy), Airways
(Rhinoscopy, Laryngoscopy, Bronchoscopy), Glands (Sialoendoscopy)

the endoscope can be rigid or flexible, or special (Laryngoscopy, Capsule)

light can be white, Autofluorescent (green- normal tissue, black- dysplastic on blue fluorescent light) or NBI
(narrow band) – to discern vessels (brown dots) from mucosa (good for tumors)

Indications:
• Chronic Rhinosinusitis that doesn’t resolve pharmacologically
• Ear / Orbital complications of rhinosinusitis (OM, Sinusitis, polyps, Adenoid)
• Tumors, Polyps or Mucoceles
• Creating access to skull base surgery
• Esophageal Surgeries (Strictures, endoscopic Diverticulotomy, foreign object removal)

Pre-Op
• Imaging (CT/MRI)
• Consent, informing of complications:
o bleeding and infection
o Ductal injuries (to sinuses)
 o Nerve damage (for teeth) and Anosmia
o Orbital injury (rare) – duroplasty necessary
o Meningitis and CSF leak (rare)

Technique
• the patient is placed under general anesthesia and local anesthesia (Moffett’s solution – Lidocaine,
Epi, cocaine)
• the endoscope and tools are inserted, and surgery starts
• special type – Laser assisted Laryngoscopy

Post-Op
• Patient needs to use long-term nasal spray
• Avoid bouts of HTN (heavy lifting, defecation) to prevent bleeds
• Saline douching, steroid drops

Medialize middle turbinate, remove uncinate process => access to middle nasal meatus => maxillary
sinus + ethmoidal bulla (ant/middle)

Medial to middle turbinate and superiorly to it, and then medially to the superior turbinate => superior
nasal meatus (when l. papyracea laterally and sup. turbinate medially) => sphenoethmoidal recess (post)
=> can reach posterior skull base this way

Through agger nasi => frontal sinus

36 Sleep apnoea syndrome

A common sleep-related breathing disorder associated with obesity (large neck, high BMI), that occurs as the soft palate
and pharyngeal muscles collapse on the airway.
the typical patient is a snoring young (20-40) man or adult following stroke (loss of tone)

snorers usually have higher Friedman score (anatomy of the mouth: ratio of tongue compared to all oral cavity).
Pathophysiology: collapse of pharyngeal muscles during sleep → apnea → rise in CO2 / drop in O2
Symptoms: restless sleep→ daytime sleepiness, loud snoring and apneic episodes

• Response: SNS activation → Secondary HTN (MC)

• Response: VC of lung vessels → P-HTN → Cor pulmonale → Arrhythmias and MI
• Compensation: Metabolic alkalosis in response to the respiratory acidosis
• other complications: Strokes, sudden deafness, depression (from exhaustion)

diagnosis:
• History (self and partner) + Questionnaire (STOP-BANG)
o STOP-BANG: Snoring, Tired, Observed apnea, Pressure, BMI, Age, Neck >40cm, Gender (male)
• Sleep Lab
o Endoscopy during sleeping
o Polysomnography (check signs in sleep – saturation, Cardiac and respiratory vitals, snoring, position
and movement, EEG) → yields AHI (Apnea-Hypopnea index) / RDI (respiratory distress index) → from
10 to more than 40 (mild-mod-severe)
• CBC - Polycythemia (Hypoxia → EPO secretion)

Treatment:
• Conservative (behavior): weight loss, Not sleeping on your back, sleep with a dental device (Mandibular
advancement), PAP mask, avoid alcohol/sedatives (muscle relaxants)/smoking
• Surgical (60% success):
o #1 - UPPP (Uvulo-Palato-Pharyngo-Plasty) – removing uvula, arches, and some of the soft palate.
▪ Complications: reflux of fluid to nose (improves), Bleeding
o LAUP (Laser assisted Uvuloplasty) – for snoring only! (not OSAS)
o RFITT (RF induced thermotherapy) – radiation particle causes necrosis → stiffening and retraction at
base of tongue (smaller tongue = less risk of obstruction) – effect is not permanent
o Maxillomandibular advancement – Maxillofacial surgery pulling mandible out

Central Sleep Apnea

repetitive cessation/decrease in respiration during sleep, due to impaired function of respiratory centers
Etiology is idiopathic or due to underlying disorder (Ischemia – HF/ Stroke, tumor, Opiates) – reduced stimulation of the
breathing centers.
Clinical presentation is similar, diagnosis is similar (may show Cheyne-Stokes breathing patterns).
managed with CPAP in sleep until resolving etiology.
37 Tumors of URT and digestive tract – classification, risk factors, general principles of dx, tx.

Classifications
Head and neck cancer are the 5th MC cancer (5% of all). it includes:
• URT and GI - SCC (90%) – often arise due to “field exposure” to carcinogen (RFs) – Alcohol, smoke, HPV
• Thyroid tumors (Papillary, follicular) – good prognosis
• Salivary gland (Pleomorphic, Warthin’s, Carcinoma) – mostly benign, with good prognosis
• Nose and paranasal sinus tumors (NP carcinoma, Angiofibroma, osteomas)
• Others: Melanoma, lymphoma, osteoma, Neuroblastoma etc.

They can arise in:

• Oral cavity and oropharynx (Tongue, oral mucosa, base of tongue, palate, tonsils)
• Nose and nasopharynx
• Larynx (sub-glottic-supra)
• Upper esophagus (SCC) or lower esophagus (Adenocarcinoma)

Spread is lymphatic, and usually to Neck LNs (Dissection zones), and then to further sites such as lungs, liver and bone.
Neck metastasis is present in 40% of diagnosis @ time of diagnosis.

RFs
Alcohol, Smoking, Malnutrition (think nitrosamines), Viruses (EBV, HPV, HSV), poor hygiene
• these RFs make H&N cancers more common in males

Symptoms: mostly by mass effect:

• Airway obstruction (Stridor, dyspnea, compression)
• Hoarseness
• Dysphagia / Odynophagia
• Lumps / Masses

Principles of diagnosis
• History (RFs, duration, personal and family history, substance abuse) and symptoms
• Physical examination – Neck, oral cavity, nose
• Endoscopic evaluation – rhinoscopy, laryngoscopy
• Imaging (US – salivary, XR / CT / MRI / PET) – for diagnosis and staging
• Biopsy (FNA, Excision) → Histology → TNM staging (PET/MRI)

many tumors are diagnosed at late stage as they can often go asymptomatic for a while

Therapy is mostly guided by stage

• Low grade: Radiotherapy and partial resection (laser) – good prognosis (90% 5ys)
• High grade: Mixed chemo-radio + complete resection
• functional Reconstruction, Speech rehabilitation, cosmetic/plastic surgery

38 Tumors of epipharynx (nasopharynx)

Benign
Juvenile angiofibroma – (next page) – the MC benign tumor of the nasopharynx

Malignant (MC)
NP Carcinoma
Undifferentiated SCC that is MC seen in the pharyngeal recess / posterolateral pharynx
highly associated with EBV infection, Smoking, smoked fish (nitrosamines), genetics
• seen in Chinese adults (RFs, 3rd MC cancer) or African boys
MC histology: Undifferentiated
clinical:
• painless cervical LAD (70% present on diagnosis –early metastasis to LN, late to Bone (MC)
• epistaxis/bloody mucus/saliva
• obstruction (of airway or ET → chronic OM and tinnitus or hearing loss)
• In advanced cases – it can compress various CN (3, 5, 6) → facial pain, diplopia, ptosis.

Diagnosis: Endoscopy → Biopsy, Neck palpation, PET-CT and MRI.

Therapy: Radio/Chemoradiotherapy (very sensitive to it!) + Neck dissections

IMPORTANT: not the same as Nasal/Sinus cancer (also mostly SCC), resected, with low metastasis to neck.

Primary Nasopharyngeal-NHL
2nd MC HN cancer, usually as an extra-nodal site - Waldeyer’s ring. mostly Large-B-cell or follicular.
Can cause jaw swelling, nasal block, recurring ear infections.

diagnosis: FNA
Therapy: Chemoradiotherapy

NUT carcinoma
an aggressive SCC, arising in the midline (anywhere along the midline, 35% in head/neck), characterized by chromosomal
rearrangement (NUT-BRD fusion).

39 Tumors of oropharynx and oral cavity + 40 Tx

Benign
Papilloma
MC benign oral tumor, appears as a Cauliflower/finger-like projections. associated with HPV infection (6/11)

Fibroma
A benign proliferation of fibroblasts in the submucosa, forming nodular masses on the buccal mucosa on the bite line.
they occur in response to chronic irritation (cheek or lip biting / dentures)

Pleomorphic Adenoma
MC Salivary gland tumor (protrudes to mouth) - Benign mixed tumor, mostly parotid gland.
Pleomorphic/mixed: Cartilage + myoepithelium + Gland tissue (epithelium)
tends to recur, so resect with large margin

Benign tumors of tongue: Hemangioma/Lymphangioma (can cause macroglossia)

Pre-malignant: Leukoplakia and Erythroplakia

plaques in the oral cavity that cannot be scraped off (unlike candidiasis), associated with smoking and alcohol.
Often dysplastic, thus can undergo malignant transformation and progress to SCC (Erythroplakia > Leukoplakia).

Either Leukoplakia (DDx EBV hairy leukoplakia) or Erythroplakia (50% chance of malignancy). removed surgically or with
cryotherapy.

Malignant
Kaposi’s Sarcoma
HHV8 infection in immunocompromised (HIV usually) often in eastern European males. causes a mutation to VEGF,
leading to angiogenesis. it presents with skin/mucosal (face, oral cavity –palate or gingiva, Colon) purple/red plaques,
that rapidly grow. therapy: HAART
Oral Cavity Cancer
95% of cases are SCC, the other 5% are adenocarcinomas of salivary glands
Location: floor of the mouth/Base of tongue – MC
RFs / Etiology: Smoking, Alcohol and High-risk HPV (16/18)
• can be preceded by Leukoplakia or Erythroplakia (we take biopsy to check for dysplasia)
• HPV is now more associated with Oral cancer than with Cervical cancer as screening of the tonsillar crypts (HPV
cancer often there) is difficult

Clinical: Dysphagia, persistent ulcer/indurated lump, plaques, hemorrhage

• invasion of surrounding nerves and muscles can cause Trismus, Tongue paresis, and neck metastasis

Prognosis: poor- diagnosis occurs in advanced stages

Diagnosis: Biopsy. which lesions? RULE
• Red/white plaque, Ulcer (non-healing) Lump, Especially if indurated

Therapy: Surgery (ALWAYS) + Radiotherapy, neck dissections (if needed) → Reconstruction

• Approach: similar options like OP cancer (Trans-mandibular, Transoral – for tongue, or lateral/median
pharyngectomy)
• additional option: “Pull-Thru” – detaching tongue/base of mouth from bones (segmental mandibulectomy), and
pulling thru the neck.

Oropharyngeal Tumors
tumors of the base of the tongue, soft palate and tonsils.
they mostly affect males due to RFs: smoking, alcohol, HPV infections
they are often classified as HPV positive (young, good prognosis) or HPV negative (bad prognosis).

Clinical: swelling in mouth/base of tongue/Neck (mtx), dysphagia and odynophagia, lock-jaw, and Dysarthria

Diagnosis: Head, neck and oral cavity exam → biopsy (including LNs) → CT/MRI for staging
• Dissection group: 2-4 + para and retropharyngeal

Tumors – mostly tonsil / base of tongue

• MC: SCC – mostly affecting tonsils of older males
o Lymphoepithelioma – variant – rich in lymphocytes (often in tongue/tonsils)
• B-cell NHL – the MC extra-nodal NHL – usually affecting tonsils (lump)

• adenoid cystic carcinoma (minor salivary glands) – rare – mostly on the tonsil.
o aggressive and metastatic to lung

Treatment of oropharyngeal and oral cancers

T1/T2
• Radiotherapy
• Surgical (Transoral or External)

T3/T4
• Chemoradiotherapy
• Surgical (external- Lateral/median pharyngectomy, trans-mandibular

Surgical Approaches
Trans-oral – in low-grade tumors with clear margins (tonsils, soft palate, posterior wall). can be robotical.
• Glossotomy (splitting the tongue) is optional for small tongue tumors

External
o Non-splitting mandible (Lateral / Median pharyngectomy)
 ▪ Lateral pharyngectomy (MC) – small select tumors with no significant spread to tonsils/tongue
• less post-op complications, can be converted to TH pharyngectomy, but also has
limited access and visualization (thru neck), and risk of cutting into the tumor

▪ Trans-hyoid pharyngectomy – small select tumors of base of tongue / posterior pharynx

• similar - limited access, and risk of cutting into the tumor
• access is by separating the hyoid bone from the suprahyoid muscles

o Splitting Mandible (Trans-mandibular)

▪ Mandibular swing – for advanced tumors that have not infiltrated the mandible
• we cut the lip thru to the mandible – remove tumor – ORIF of mandible
• often accompanied by neck dissection, and is followed by adjuvant radiotherapy
• good exposure but more post-op complications. may require reconstruction

▪ Segmental mandibulectomy – for advanced tumors that have infiltrated the mandible
• the tumor is removed with a segment of the mandible
• requires reconstruction of cheek, uvula, soft palate and tongue, leaving some
deformity and often malocclusion (with speech and mastication difficulty)
• Segmental vs Marginal = see image

-Reconstruction utilizes muscular flaps (from pectoral muscles), Bone (Fibular bone) and vessels (cephalic vein and radial
artery)

41 Hypopharyngeal Tumors

the hypopharynx refers to the part of the pharynx from the Hyoid bone to the cricoid cartilage.
tumors of this region account for 10% of HN SCC (5%), and occur mostly in the elderly.

like all other SCC of the region, heavy lymphatic drainage means LN metastasis: 2-5, retropharyngeal
• 75% of tumors @ time of diagnosis show metastasis

RFs: Smoking, Alcohol, radiation (often thyroid therapy using radioactive iodine)

Hypopharyngeal tumors may cause signs of respiratory obstruction and Hoarseness/voice change, and signs of upper GI
obstruction (Dysphagia, Odynophagia)

Regions:
• Pyriform sinus
• Retrocricoid
• Posterior wall of pharynx

these do not refer to tumors of the larynx, but often removal of the larynx is part of therapy.

Diagnosis: usually late (after MTx), and using Endoscopy and biopsy + MRI/CT for staging

Therapy
according to stage and localization
• T1 – Radiotherapy or Surgery (Partial pharyngectomy / laryngectomy)
• T2 – Partial Pharyngectomy + Total laryngectomy
• T3 – Total + Total + Adjuvant radiotherapy
o requires reconstruction using Jejunal free flap
• T4 – Chemoradiotherapy

Prognosis depends on stage: stage 1-75% stage 4-15%

42 Nose and paranasal sinus tumors

Malignant
they are more common than benign tumor, and mostly from epithelial origin (70% SCC, 20% Adenocarcinoma)
they are often asymptomatic until advanced (neck mass, airway obstruction, bleeding, nerve involvement).

diagnosis (Endoscopy, Neck palpation) must be further supplemented with CT/MRI to determine spread.
most tumors are Surgery (maxilla, anterior skull base) + Adjuvant radiotherapy
• surgical approach can be endoscopic (small, increasingly common, less complications) or external (lateral
rhinotomy is MC approach or total maxillectomy for advanced tumors)
• Consider reconstruction or prosthesis if needed
• Spread to cranium = unresectable

Location is usually Maxillary sinus (80%) which also has better prognosis (earlier symptoms, far from sensitive structures),
followed by Nasal cavity (15%), which has poor prognosis.

symptoms: Like NP carcinoma but without spread to neck - rhinorrhea, obstruction, anosmia, epistaxis, diplopia, hard
palate deformation
• in the sinus –potential spread to bone / cheeks / orbit

IMPORTANT: This is not the same as NP Carcinoma – which is associated with early LN metastasis and is usually treated
with Chemoradiotherapy and neck dissections.

Other Nasal Tumors (malignant)

Lymphoma
melanoma – aggressive spread, poor prognosis
Olfactory Neuroblastoma – derived from NET olfactory cells, giving rise to anosmia, nose bleeds and obstruction.
microscopy reveals a blue-cell tumor (a neuroblastoma).

Benign

Nasal papilloma
a benign tumor of the mucosa, arising following HPV6/11 infection, seen mostly in young men.
it appears as a soft gray mass, that usually grows inwards.

Osteoma
a benign, round tumor in the PN sinuses (frontal / ethmoidal). it is usually asymptomatic, or can obstruct the drainage,
leading to congestion and sinusitis. Diagnosed with XR / CT, and treated surgically.

+ Juvenile NP angiofibroma
next page

43 Laryngeal tumors

Pseudotumors - Polyps and Nodules

Laryngeal polyps – develops in response to vocal fold irritation (singing, smoking, GERD)
Compared to nodules – they are larger, unilateral, and more vascularized
remember: Polyps = Pulpy, Primary (1), Prominent, Problematic (surgery)

Nodules – usually bilateral and small, develops in response to irritation/overuse

remember: Nodules, Never-ending, nothing to do

both present with hoarseness and breathy voice.

diagnosed with laryngoscopy / biopsy (to exclude cancer)
therapy – nodules: rest for vocal cords (allow healing) Polyps: Surgical removal
Benign – Laryngeal papilloma
Raspberry-like white clusters on the vocal cords, that arise due to HPV6/11 infection.
it causes hoarseness and in severe cases – Obstruction (stridor)
Diagnosis: Laryngoscopy + Biopsy shows Koilocytes (Perinuclear halo)
Therapy: Surgical / Laser removal
• risk for Carcinoma

Malignant - Laryngeal Carcinoma (SCC)

SCC carcinoma of the larynx, arising from the vocal cord epithelium.
RF: Smoking and Alcohol (Chronic Laryngitis), Laryngeal papilloma/HPV infection, Chronic Inflammation
Course: Smoking x alcohol x HPV = Hyperplasia → Dys → CIS → Invasive cancer
Morphological Classification: can be MC: Verrucous (Good), Endophytic or mixed.

Symptoms: Starts with hoarseness, and later causes obstruction (stridor).

• Supraglottic tumor can cause odynophagia. the tumor can bleed and cause suffocation

Metastasis differs based on relation to cartilage protection, and goes to different Dissection groups

a more important Classification - by location:

• Glottic (MC – 50%) – good prognosis – affects true vocal cords– metastasis is rare – to groups 2 and 3
• Supra-glottic (40%) – poor prognosis – metastasis is common (60% @ Dx) – to groups 2 and 3
• Sub-glottic (1%) – poorest prognosis - late diagnosis – metastasis is common - to groups 6 and 7 (central and
upper mediastinal)

Diagnostics of Tumors:
• Laryngoscopy (Direct or Indirect) + Biopsy
• Once confirmed – CT/MRI for staging

44 Treatment of laryngeal tumors

Like all cancers – it relies heavily on the staging.

T1-T2 (early)
• laser resection (endoscopic)
• or Partial laryngectomy – an external approach that is either Horizontal or Vertical
o Horizontal (above vocal cords) or vertical (midline) incision thru the thyroid cartilage and
removing all supraglottic structures or left/right sides of the cartilage.
• or Radiotherapy

T3-T4 (advanced)
therapy usually involves removal of the larynx, and some form of systemic therapy. in all cases – neck
dissections are involved.
• Total laryngectomy + Adjuvant radiotherapy
o Total laryngectomy requires a U-shaped skin incision, removal of the larynx, and placement
of a permanent tracheostomy
o the removal means we need to connect the hypopharynx solely to the esophagus, which
requires also the detach the esophagus from the trachea
o a total laryngectomy means the patient cannot ventilate thru the mouth
o perform tracheoesophageal puncture – for voice prosthesis
• Chemoradiotherapy +/- total laryngectomy
45 Chronic laryngitis and premalignant lesions

Chronic laryngitis
Laryngitis is inflammation of the larynx mucosa (including epiglottis) and vocal cords. most often symmetrical and diffuse.
it is mostly seen in men (smoking) in their 50s-60s. it can be
• acute (usually infectious – viral, chemical)
• Chronic (GERD, smoking/fumes/inhaled of occupational particles, vocal abuse/shouting/singing, allergies,
chronic cough, recurring Acute bouts, Alcohol, bulimia)

Chronic Laryngitis is MCC by GERD / reflux– in which stomach acid regularly irritates the mucosa.

Clinical: chronic Hoarseness, rapid vocal fatigue, throat “itch” and clearing, dry cough, low pitch

the constant irritation will lead to hypertrophy and leukoplakia, which may resemble cancer – hence biopsy is always
indicated. once Cancer is excluded – therapy is aimed at avoiding triggering causes.

Diagnosis:
• Laryngoscopy: initially - hyperemic mucosa, smooth surface. the constant irritation causes thickening and
possible keratosis (leukoplakia), edema, infiltration, and hypertrophy of glands (unlike atrophic laryngitis).
• Biopsy to rule out cancer

Therapy:
• Eliminate infection (ATB)
• Avoid irritating factors (vocal abuse, smoking, alcohol, polluted environment)
• Voice rest, speech therapy
• Steam inhalation and expectorants – to loosen up secretion
• Surgical – not common - remove the bad mucosa, stripping the vocal cords

Premalignant Lesions (in H&N)

SCC of the head and neck, and specifically laryngeal carcinoma are often preceded by changes to epithelium. the
appearance is highly variable, and in order to assess the degree of dysplasia – biopsy.

these include:
• Leukoplakia – white patch that cannot be scraped off
• Erythroplakia – red, epithelial lesion (high-risk of transformation, often already there)
• Pachyderma – epithelial thickening, keratin scales
• Erosive lichen planus – symmetrical lesions (resembling leukoplakia) seen on buccal mucosa, tongue, floor of the
mouth
• Laryngeal Papilloma- raspberry-like clusters on cords caused by HPV6/11 or smoking.
• CIS – all signs of malignancy (cellular, dysplasia, architecture) but still hasn’t invaded the BM.

46 Regional metastasis of head and neck cancer

regional metastasis in the scope of HN cancer, refers to spread to the neck.

• distant metastasis tends to go to lungs, liver, or bone.

many cancers (~40%) of HN have already spread to HN region @ the time of diagnosis, and often signify poor prognosis.
it is the greatest prognostic factor.

in the scope of TNM staging – N refers to this – metastasis to LNs.

It is a scale ranging from N0 (non) to N3 (metastasis creating LN >6cm). in between these – the scale takes several sub-
levels, referring to sides (ipsilateral / contralateral / bilateral), and size (<3cm, 3-6, >6cm).
other factors (not part of staging, but give us prognostic info): level, Extranodal spread, consistency, tenderness
Clinical Staging (not TNM) – diagnosis:
• Physical examination (including entire mucosal surfaces, cavities, and neck)
• Imaging and sampling (US + FNAB – salivary, CT/MRI, PET-CT)

some red-flags: size >1.5cm, central necrosis (FNAB/US), grouping of LN

remember: not all large LNs are cancer (infection), and even small nodes can be positive.

Treatment of regional metastasis – Neck dissections

• -Selective: removal of some Cervical LNs – so preserving the unaffected regions
• -Modified: removal of all LNs of zones 1-5, and some of the additional structures (partial preservation)
• -Radical (Comparative standard): removal of all LNs of zones 1-5 + SCM + IJV + CN11, high mortality
• -extended: Radical + additional structures

complications: nerve damage (shoulder, neck), bleeding/infection, air leak, IJV Thrombosis

Drainage pattern:
- higher ones + SM/SL/Pretracheal → Upper cervical → middle cervical → lower cervical
- -posterior triangle + abdominal → Supra-clavicular

Complications:
1) Shoulder syndrome (pain, weakness, shoulder drop)
2) Bleeding
3) Infection
4) Skin flap necrosis
5) Air leaks
6) Chylus fistula
7) Carotid blow out
8) IJV blow out
9) IJV thrombosis
10) Apnea
47 Ddx neck mass

A neck mass can have various etiologies, but is normally classified as Infectious or non-infectious:

Etiologies
Infectious
• Unilateral cervical LAD – seen in skin infection of neck, GAS pharyngitis/tonsilitis, TB
• Bilateral - Viral: Mumps (parotitis), Rubella, Mono, HIV (Mono-like)
• Bilateral - Toxoplasma: mono-like

infectious etiologies produce soft, warm, tender LAD, that are moveable.
• viral is usually bilateral, while Bacterial is usually unilateral

Non-infectious
Congenital
• Brachial cyst (remnant, doesn’t move when swallowing)
• Cystic Hygroma – associate with Turner’s, a cyst like space full of lymph in posterior neck. can compress the
esophagus/airway
• Thyroglossal duct cyst (embryonic remnant from thyroid gland development. moves when swallowing)

Cancer (primary HL, or Metastasis)

• Primary – Extranodal Lymphomas or Hodgkin’s lymphoma
• LN Metastasis – from H&N cancers

AI – Kawasaki’s disease: A of CRASH and BURN (unilateral, cervical)

Goiter: Hashimoto’s, Grave’s, TMG

• they differ in consistency and diffuse / multinodular

Investigation
Full History – smoking? alcohol? irradiation history?
presenting complaint
• questions: what made you notice the lump? how long? size changes? comes and goes?
• Previous lumps? previous treatment?
• Other symptoms
o Thyroid symptoms (hair loss, palpitations, weight changes)
o CRASH and BURN
o Fever? abdominal pain? throat pain?
o Voice change? ear change? cough? bloody sputum/ mucus?

Physical examination: PALPATION – tenderness, size, mobility, consistency (rubbery / hard)

Blood testing: CBC (lymphoma?), Thyroid panel, Inflammation markers (Viral / Bacterial)
Imaging: Endoscopies (Laryngoscopy, Rhinoscopy), FNA, US, CT/PET-CT, MRI
Specific tests (infections, AI)

RED FLAGS – Urgent referral to ENT: Lump with size change in 3-6w, lasting hoarseness, dyspnea, persistent parotid
swelling / sore throat, Non-healing ulcers / Plaques in mouth
48 Thyroid tumors

The worry behind a “mass” in the thyroid, is 99% unjustified – either a goitrous nodule, or a follicular adenoma.
The 10% that are malignant, usually have an indolent course, with great prognosis.
Most Tumors arise in women.
Clues that it’s Malignant tumor (rather than an adenoma goitrous nodule):
• History of irradiation (increases chance of cancer)
• Solitary is more likely to be neoplastic (compared to Multinodular goiter)
• Nodules in the young are more likely to be neoplastic
Symptoms:
• mass effect – dyspnea, dysphagia, hoarseness
• hormones (+/-)

Diagnosis
quite often, the initial complaint is a mass in the neck (LN mtx).
A physical examination may reveal a thyroid nodule that requires further investigation:
• Labs (Thyroid, TG, Calcitonin) – 90% are adenomas usually cold or MNG which are hot (low TSH)
• Scintigraphy (Hot/Cold)
• US – shows Hypoechoic lesions >1cm, irregular margins
• FNAB → Cytology and microscopy (Calcifications)

REMEMBER: Complete resection requires Thyroid HRT (PT gland often preserved or re-implanted)

Cold vs Hot
Cold means that upon injection of iodine, there is less intake of iodine to the tumor compared to the regular
parenchyma. in comparison, Hot nodules take up iodine more avidly than regular parenchyma, meaning they are
productive. this is done using Scintigraphy - Radionucleotide scan
• Hot nodules are rare: Non-neoplastic > Benign > Malignant

Benign
Follicular Adenoma
The MC benign thyroid tumor. Derived of follicle epithelium.
Morphology: slow-growing encapsulated solitary nodule
• DDx – solitary (DDx MNG), intact capsule (DDx Follicular Carcinoma)
Labs: mostly cold adenoma (normal thyroid values), 1% are hot - produce hormones (Toxic adenomas).
Subtypes:
• 1% Toxic “hot” Adenomas – a mutation of TSH receptor activates it – hormonally functional
o These are controlled with Thyroid-lowering medication (B-blockers, PTU/Methimazole)
Therapy: surgery - Excellent prognosis (no invasion, no recurrence if resected)
• Usually a lobectomy or hemithyroidectomy

Malignant
Mostly (except medullary) derived of follicular epithelium, and are usually well-differentiated (except Anaplastic)
They are usually “Cold nodules” – no hormone production.
RF: Irradiation early in life, family history, Women
General Pathogenesis: involves various mutations that downstream reach RAS pathway.

Papillary Carcinoma (MC- 85%)

The MC Thyroid malignancy.
Slow growing, well-differentiated cancer of the follicle epithelium.
Gross: Solitary / multifocal, grey/white with papillary projections (visible “fingers”)
• early metastasis to LN (often found before primary tumor) – but OK
• Prognosis and treatment: great prognosis even with the early metastasis to
LN (Neck dissections)
Follicular Carcinoma (10%)
Well-differentiated solitary nodule invading thru capsule (DDx follicular adenoma) and into vessels
Metastasis (unlike others - thru blood!): to Bone and lungs
Prognosis: good (50% live 10y)

Medullary Carcinoma (5%)

NET- Malignant proliferation of parafollicular (C) cells, that produce Calcitonin.
most cases are sporadic (old – 50-60), 25% are in MEN2 syndrome (young)
• Often contain amyloid (calcification)
• blood tests show higher calcitonin levels

Anaplastic (undifferentiated) carcinoma (<5%)

UNDIFFERENTIATED and Aggressive. Seen in elderly (the oldest tumor - >60y)
Macro: large, invasive mass (mass effect) micro: giant cells (osteoclast-like), undifferentiated
Prognosis: 100% fatal

Others
B-cell lymphoma – associated with Hashimoto thyroiditis
Secondary tumors – rare (albeit being very vascular). from lung, breast, or nearby sites (head and neck).

49 Tx of thyroid tumors

Thyroid gland pathologies are often treated surgically, when pharmacotherapy is insufficient to control the hormonal
levels, or if mass effect is symptomatic.

Several approaches are available and depend on the underlying disease.

a common approach is total thyroidectomy – as it is quite easy to manage HRT.
it is indicated for: high-risk (poorly differentiated) thyroid cancers, some forms of Graves /TMG (with Ophthalmopathy),
large goiter with symptomatic mass effect.

other approaches:
• Near total (leaving <1g) or Subtotal (leaving >1g) thyroidectomy – for benign lesions affecting the entire gland
(MNG, Graves, Goiter) – the aim is to reduce hormone production volume.

• Lobectomy (removing the bad lobe) and Hemithyroidectomy (removing the bad lobe and isthmus) – for
adenomas, cysts or low-risk well-differentiated thyroid cancers– to remove only affected tissue.

in addition – spread to neck requires neck dissections, often regions 6/7

locally advanced tumors or inoperable tumors require Chemoradiotherapy
Post-op: radioiodine therapy for 4-6w – kill the rest of the gland left over

Complication
• Bleeding – toxic glands (Graves / TMG) have extremely increased vascularity
• nerve damage- Recurrent laryngeal nerve courses behind the gland
o unilateral – hoarseness (Tx: medialization)
o Bilateral – mute, airway obstruction (Tx: cordectomy)
o the Superior laryngeal nerve can also be harmed, in which the cricothyroid muscle is denervated,
leading to poor control of tone (tension of the Vocal cords)
• Harm/removal of PTH gland – causing Hypocalcemia / Hyperphosphatemia
50 Salivary gland tumors

Salivary gland tumors are quite rare (<1% of all tumors), and are predominantly benign and predominantly parotid.
in SM (80%) or SL (45%) have higher rates of malignancy. minor salivary gland tumors are mostly malignant.
Tumors are usually slow-growing, painless and Unilateral swellings (may involve mass effect on facial nerve / duct,
causing peripheral CN7 Palsy and Xerostomia, respectively).

The diagnostic modality for Salivary gland tumors is the US (#1), MRI-T2 (#2,
Also for staging), and confirmation is achieved with pathology (FNAB)

Pleomorphic adenoma
the MC Benign tumor (85%), usually of the parotid gland (85%), of unknown etiology (possibly: Irradiation or exposure to
certain chemicals)
Pathology shows a mixed tumor: epithelial (ductal), myoepithelial + Cartilage
Clinical: a movable mass, that grows slowly and without symptoms (CN7 palsy only if malignant)
Treatment, prognosis, progression: resection
• 5% recur (if poorly resected or if “spills” during surgery) so operate with a large margin
o alternatively – radiotherapy (which is strange for benign tumor)
• 5% can become malignant - invasion is marked by CN7 palsy

Other tumors usually are called monomorphic adenomas as they originate from epithelium only.

Warthin Tumor (Papillary Cystadenoma Lymphomatosum)

A slow growing monomorphic adenoma, that usually affects the parotid gland. usually unilateral and unilocular.
Etiology: Smoking (MC in men)

Pathology: it is a Papillary (finger-like) Lymphadenoma: a double layer of ductal epithelium (finger) that extends into a
dilated duct (full of fluid), resting on stroma rich in WBCs (germinal centers).

Name explained:
-Cystadenoma = the ducts dilate due to fluid accumulation
-Papillary = the ductal epithelium folds inwards to form finger like projections.
-Lymphomatosum = germinal centers form in the stroma/BM of the papillae.

Diagnosis: US shows a cystic structure therapy: surgery

no risk of malignancy or recurrence

Carcinoma
rates of malignancy by gland: SM (90%), Minor salivary glands (80%), SL (45%), Parotid (20%).
• However, SM/SL/MSG are much rarer, and thus malignancy is more common in parotid
these tumors appear as painless swellings or mucosal ulcerations (MSGs), and signs of invasion (CN7 palsy).
MC: Mucoepidermoid Carcinoma: a mixed tumor made of mucus, IM and epidermoid (epithelium) cells. the ratio
between these cells determines the grade of the tumor (high grade or low grade)
Other subtype: adenoid cystic – slow growth, very aggressive, perineural spread, and spread to blood → lungs (late)

Diagnosis: US shows cystic structure

Therapy: Surgical: Removal of the gland, with possible additional neck dissection (LNs)
• Either SF or deep parotidectomy (preserving CN7)
• Radiotherapy can be used as adjuvant, or as primary if inoperable

Complications (of therapy):

• CN7 Palsy
• Gustatory sweating (Frey syndrome) and Gustatory hyperlacrimation (Crocodile tears) – the regenerating PS
fibers left after parotidectomy attach to blood vessels and Lacrimal glands, yielding their dilation/activation
upon gustatory stimulation (when seeing food)

prognosis is good (worse if in SM/SL glands)- depends on grade 1-100% 4 – 25%

Other Tumors (Non-epithelial)
MC in children
• Hemangiomas and Lymphangiomas
• Lipomas: Morbus-Madelung – lipomatosis of neck area – compression of trachea possible – therapy is complex
• Malignant Lymphomas: mostly MALT lymphoma (Extranodal), associated with AI sialadenitis –
radio/chemo/biological (rituximab)

51 Ear tumors

Skin Conditions: Basalioma, SCC, Keloid scar

• Keloid scar is excessive growth of scar beyond borders of injury, seen on ears and face. steroids or surgery for
therapy, but recurrence is high.
• Basalioma: low-grade malignant proliferation of basal cells due to UVB exposure. has several presentations, MC
a pearly nodule with telangiectasia, possible ulceration and a central depression. requires biopsy to confirm, and
is removed surgically / cryotherapy / laser / Topical chemo.
• SCC: proliferation of the spinous layer of the epidermis due to UVB radiation, HPV, Arsenic, or chronic
inflammation. it presents as a painless red/bloody ulcer and a possible keratotic horn. diagnosed with biopsy
and treated surgically.

Ceruminous Adenoma
a rare (still MC Benign external ear tumor) benign tumor arising from cerumen glands. slow-growing and not invasive,
and may cause hearing loss and pain, merely by compression of other structures and canal obstruction.
diagnosed by biopsy, treated surgically with low recurrence.

Exostoses and Osteomas

Exostoses: is also called Surfer’s ear (occur due to exposure to cold-water/wind), as it is a reactive localized bone growth
from the external ear canal.
they are usually multiple and bilateral, and asymptomatic until blocking the ear canal → Hearing loss and infections.
prevented with proper protection (helmets / hoods), and treated with surgery.

Osteoma: slow-growing benign bony growth in the ear canal, usually unilateral.

Cholesteatoma
an acquired / congenital special form of chronic OM, in which keratinized Sq epithelium from the TM grows into the OM.
presents with painless foul discharge and hearing loss (if perforated).
• Primary – dysfunction of ET → retraction of TM → retraction pocket
• Secondary – Otoscopy reveals - pearly white mass behind membrane
o Migration: in Chronic OM –perforated eardrum allows epithelium to migrate inwards
o Implantation: surgery / foreign body introduces epithelium
o Metaplastic: inflammation causes change in epithelium (Cuboidal → Squamous)
• Other possible diagnostics – Audiometry (HL) and XR/CT (can invade bone)
• Treated by surgery (removal) and drying the ear → reconstruction of TM/bones if needed

Glomus Tympanicum (Glomus Tympanicum Paraganglioma)

the MC tumor of the middle ear, seen mostly in adult women.
It is benign, slow-growing, highly vascular, and invasive-to-bone tumor that arises from paraganglionic cells. it arises in
the middle ear from the promontory, and appears like a polyp. it may harm CN7.
It may cause hearing loss and the vascularity can cause objective tinnitus.
diagnosis:
• Otoscopy can show a red mass that pulsates behind the membrane
• CT/MRI + Angiography
Therapy is surgical, and often preceded by radiation (to reduce vascularity). high recurrence.
52 Vestibular schwannomas

a rare benign tumor arising from the Schwann cells of CN8, seen in adults (~50s)
They usually occur in the internal acoustic meatus (compressing CN8), and arise from the
Cerebellopontine angle (compressing CN7 or other structures).
They are usually Unilateral, while Bilateral VS usually means Neurofibromatosis type 2.

Presentation – Unilateral SNHL, Tinnitus, and dizziness, pressure sensation in ear

• quite resembling a Meniere’s disease, but symptoms are not paroxysmal.
• Further growth (late symptoms) will lead to CN5 Palsy (Paresthesia, Hypoesthesia, or pain), CN7 Palsy
(peripheral), Cerebellar symptoms (Ataxia) or Hydrocephalus (4th ventricle compression)

Diagnosis:
• Weber test, Rinne test, and Audiogram - SNHL
• MRI (enhancing lesion in the internal auditory canal)
o classified on a scale I-IV(a/b), according to MRI findings (1 in meatus, 4 compressing pons/CB)
• testing the Trigeminal (corneal reflex) and the Facial (smile, wink, eyebrows)
• Pathology (Biopsy post-resection): Antoni A regions (tightly packed with cells) with Verocay body (fibrous cell
processes) and Antoni B cells (sparse cellular regions)

Therapy
• conservative (if the tumor is small, minimal hearing loss, old age) + regular MRIs (every 6-12m)
• Surgery (partial / total): 3 possible approaches
o Trans-labyrinthic (obsolete, harms hearing)
o Subtemporal (poor visualization but spares hearing)
o Retrosigmoidal (MC used)
o Gamma knife can be used for small tumors (<2cm)
• Radiotherapy (Adjuvant)

Complications and prognosis

• good prognosis, with only 5% chance of recurrence
• surgery can cause permanent Injury to CN8 or CN7

53 ENT and skull base surgery

Skull base surgery is multidisciplinary, depending on where we are trying to go, and thru where (approach).
it often requires the cooperation of MFS, ENTs, NS, Ophthalmologists, and Spinal surgeons.
it involves the use of high-speed drills and probes, to decisively enter the relevant structures.

Generally, SBS are done for various reasons (trauma, tumors, inflammation, congenital, vascular anomalies). in the scope of
ENT: Vestibular Schwannoma (becoming common), nose and sinus tumors, paragangliomas (glomus), cholesteatoma.

Approaches can be classified as:

• Extracranial (craniotomies and degloving) x Intracranial
• Extradural x intradural (requires reconstruction using synthetics or temporal fascia)
• Classic surgery (TTE) x Microsurgery (VS) x Endoscopic surgery (FESS)
• Stereoradiosurgery (Gamma knife / LINAC)

Intraoperative Neuromonitoring
the sensitive access to the brain requires that we regularly monitor function of the tissue that is being handled. often the
patients are conscious, and are asked to perform certain tasks to test function.
• Somatosensory EP (Evoked potential) – generating an ascending AP by touching the leg/arm
• Brainstem auditory EP – objective testing of hearing
• Cranial nerve EP (or spontaneous) – using electrodes on CNs roots
o Sensory - Visual EP (for CN2, 3, 4, 6)
o Motor - Tongue (CN12), Facial muscles (CN7), CN5
SRS (Stereotactic radiosurgery) in the scope of Vestibular Schwannoma (VS)
SRS is commonly used in VS, and chances of success are great ((if it is the initial therapy).
they are slightly worse if it is attempted after resection. if primary use of SRS fails, resection becomes significantly harder. other
things that might cause SRS failure: Large VS (grade 3/4), part of NF2.

specific Approaches according to the part of the SB

• Anterior approaches: trans-oral, trans-sinuses (all of them), le-fort osteotomy, trans-cranial,
• lateral approaches: trans-labyrinthine, pre-sigmoid, sub-temporal or Infra-temporal
• Posterior approaches: retro-sigmoid, sub-occipital

microsurgery in Vestibular Schwannoma

most VS surgeries utilize a retro-sigmoid approach. in most cases it is a radical removal.
CN7 usually preserved (less in HG-VSs), hearing is often lost (high grade – 100% due to radical removal, low grade 30%).

difficulties in procedure:
• scar tissue and adhesions of arachnoid mater
• Vascularization
• previous SRS or resection is very difficult to manage, and preservation of CN7 is almost impossible

Complications
• Cross anastomosis of CN7 fascicles, causes aberrant activation (synkinetic movement, blinking)
o essentially fibers mix during surgery, and activation becomes strange
• Anatomical preservation of CN7, but severe dysfunction

Conclusion
good radical removal of VS is possible even in high-grade tumors. difficulties arise mostly in recurrent surgery following poorly
executed SRS or resection. proper removal (with capsule) of VS is needed for 0 recurrence.
in NF2 (bilateral VS) – auditory brainstem implant is needed.

54 Juvenile angiofibroma

A rare benign tumor seen exclusively in adolescent males.

• still the MC benign tumor of the nasopharynx
It is locally aggressive, being highly vascular (Angio) and rapidly growing (fibroma).

Mechanism / Pathophysiology
• Localization and invasion: The tumor arises in the roof of the nasal cavity / choana, and rapidly extends into
surrounding regions (Nasopharynx, orbits, cranium) → the pressure causes necrosis
• Males: they express Androgen receptors
• Defective vessels: lacks muscular layer, hence no VC upon damage → severe bleeding

Symptoms: Nasal obstruction (unilateral), Septum deviation, Severe epistaxis

• other symptoms: Rhinorrhea, mouth breathing and nasal voice, anosmia, facial swelling (exophthalmos)
• Complications: OM (Blocking ET), Sinusitis (Blocking drainage)

Diagnostics: NO BIOPSY (risk of bleed)

• History → obstruction, deviation, bleeding
• Endoscopy: A hard pink mass that bleeds easily
• Contrast CT: to assess invasion and size. opt for MRI if suspected cranial invasion
o a carotid angiogram can be supplemented before the surgery if embolization is considered

Therapy: Surgery (transmaxillary or transnasal) with pre-surgical embolization of feeding vessels

• Gamma knife can be used in recurrence
• Androgen blockers (neoadjuvant to surgery in order to reduce size – but has serious side effects)

High recurrence rate – so follow-up is needed