ENT Notes PDF

ENT - 2018
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ENT Notes
ENT Notes 1
Ear 1
Nose 29
Throat 43
List of practical exercises 62
A Note on Text Boxes. As these notes move into a more clinical setting the goal is to make
them more useful for a practicing junior doctor, as such, the text boxes include specific
guidelines relevant to NHS practitioners. These have been taken from sources that
specifically site NHS guidelines (rather than simply text books that may offer treatments that
aren’t necessarily wholly applicable in the NHS). If others have particular insights in specific
diseases that they wish to share, this would be greatly appreciated.
asic Otorhinolaryngology 2nd E.d.

Recommended Text: B
Ear
1. Clinical anatomy of the middle ear
The ear can be split into three parts, external, middle and inner ear. The external ear
includes the pinna (auricle) and external auditory canal which are responsible for collecting
and conducting sound waves to the tympanic membrane (eardrum), which is
considered part of the middle ear.
The middle ear has two parts, the tympanic cavity and the epitympanic recess. The
tympanic cavity lies directly medial to the tympanic membrane, and contains most of the
bones of the middle ear, while the epitympanic recess is found superiorly, near the mastoid
air cells.
navidmtomlinson@gmail.com 1/66
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The tympanic membrane is a cone shaped membrane that transmits sound from air to the
ossicles in the middle ear. The tympanic membrane has three tissue layers, (cutaneous,
fibrous and mucosal) and two parts (flaccida and tensa). It is supplied by the
auriculotemporal nerve, a branch of the mandibular nerve.
Borders of the middle ear

- Roof - Thin bone from the petrous part of temporal bone
- Floor - Known as the jugular wall, separates middle ear from internal jugular vein
- Lat wall - tympanic membrane and lateral wall of epitympanic recess
- Medial wall - lateral wall of internal ear (facial nerve travels nearby)
- Ant wall - bony plate, with openings for auditory tube and tensor tympani muscle. Int.
carotid lies the other side
- Post wall - Mastoid wall, bony partition between the tympanic cavity and mastoid air
cells. There is a hole in this wall known as the aditus to the mastoid antrum (an air
space in the petrous portion of the temporal bone).
Bones of the middle ear

- Malleus, Incus and Stapes (MIS, in order)
- Middle ear auditory ossicles that take the vibrations of the tympanic membrane and
transmit to the oval window, amplifying by mechanical movement as a result of their
angle of formation.
- Stapes inserts on Oval window, transmitting vibrations at higher order.
- Movement controlled by two muscles (tensor tympani and stapedius) that help to
protect the ear from excessive noise.
Eustachian tube
- Links nasopharynx to middle ear, approx 3.5cm long, helps to equalise pressure.
- Has bony ⅓ and cartilaginous ⅔.
Mastoid Air Cells
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- Located posterior to the epitympanic recess, a collection of air-filled spaces in

mastoid process of temporal bone.
- Mastoid air cells communicate with mastoid antrum, which in turn communicates with
middle ear via aditus.
Muscles
- Tensor tympani, inserts on handle of malleus, contracting in response to loud noise,
inhibiting the vibrations and reducing sound to inner ear
- Known as the acoustic reflex
Tympanic
membrane
A = Normal, B = OM with effusion (note reflection is dot shaped showing

membrane retraction with visible fluid levels), C = AOM (opaque bulging
TM, reflex is shattered, surface is irregular, unable to view malleus handle),
D = Chronic suppurative otitis media (view perforated TM)
Clinical relevance
- Otitis media with effusion
- (aka glue ear). Arises from persistent dysfunction of the auditory tube
- Tube unable to equalise middle ear pressure, leads to middle near negative
pressure, which draws out transudate, creating environment for pathogens.
- Eardrum appears inverted with fluid visible inside ear
- Mastoiditis
- Otitis media can spread to mastoid air cells which can then spread to mastoid
process, in turn spreading to middle cranial fossa and then meningitis.
- Observe swelling behind ear (where mastoid process is)
2. Clinical anatomy of the inner ear
The ear can be split into three parts, external, middle and inner ear. We have covered the
outer and middle ear above, here we review the inner ear. The inner ear houses the
vestibulocochlear organs. It has two main functions:
1. To convert mechanical signals of the middle ear into electrical signals
2. To maintain balance by detecting position and motion
The inner ear is located in the petrous part of the temporal bone, between the middle ear
and the internal acoustic meatus. The inner ear has two main parts:
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- The bony labyrinth, a series of bony cavities with the cochlea, vestibule and three
semicircular canals. These structures are lined with periosteum and contina a
perilymph fluid.
- Membranous labyrinth, lies within bony labyrinth, consisting of cochlear duct,
semicircular ducts, utricle and saccule. Filled with endolymph.
Cochlear
As the stapes bone inserts into the oval window the vibrations are transmitted into the
fluid filled cochlea. The cochlea is a bony tube filled with fluid, within it sits the Organ of
Corti, the sensory organ of hearing. The Organ of Corti is separated into three sections, the
Scala vestibuli, Scala media and Scala Tympani. Scala vestibuli and Tympani are filled
with Perilymph while media is filled with endolymph.
The vibrations of the oval window cause displacement of fluid in the Scala vestibuli, and in
turn cause displacement in the Scala Media. The waves of fluid displacement cause
movement of the basilar membrane of the organ of corti, which causes movement of the
stereocilia which project from the surface of hair cells.
The movement of these hair cells, modulated by the tectorial membrane, then triggers
depolarization in the nerve fibers of the cochlear nerve. These stereocilia are linked to one
another by protein ‘Top Links’ which help to control opening of ion channels. The bending of
the stereocilia prompts the depolarization of the cells, thanks to the opening of K+ channels.
As the endolymph they are bathed in has high K+ levels, rapid depolarization is achieved.
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Different parts of the organ of Corti are most sensitive to different sound frequencies, with
the hair cells closest to the apex most sensitive to low frequency waves.
The displacement of the fluid, and the energy contained within it, is then displaced by
vibrations of the Round window, which sits along Scala Tympani.
Vestibular Apparatus
Balance is achieved by the integration of Sensory information, including Visual,
Proprioceptive and Vestibular. We will look here at Vestibular.
The vestibular apparatus are located in the labyrinth of the inner ear. It contains three
semicircular canals located at right angles to one another. The three canals are located
horizontally, posteriorly and superiorly. These canals work with the Utricle and Saccule
within the vestibule which respond to changes in the position of the head.
The semicircular canals are filled with endolymph, as we rotate our heads the fluid in the
semicircular canals moves, and it, in turn, moves the hair cells that sit within these canals.
The movement of these hair cells triggers depolarization of the hair cells, and in turn triggers
an AP in the vestibulocochlear cranial nerve.
Meanwhile, within the Utricle and Saccule are Otoconia crystals. As we change speed, or
move our head position, these crystals move. The movement of these crystals then move
the underlying otolithic membrane, kinocilium and stereocilia that are attached to hair cells.
These stereocilia are responsible for the transducing the movement of the cilia into an action
potential. This ability, to detect this kind of movement, is known as Detection of Linear
Acceleration.
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3. Clinical physiology of hearing
We can divide the physiology of hearing into two main sections, the sound transmission in
the middle and inner ear, and the central neurological transmission of sound.
Sound transmission in the middle and inner ear. Organ of Corti

The middle ear is an air filled space connected to the back of the nose by the Eustachian
tube. It houses the Malleus, Incus and Stapes bones which conduct sound. As the
tympanic membrane vibrates, it causes the bones to oscillate, and transmits the signal
to the oval window.
From the oval window, the vibration is transmitted into the fluid filled cochlea. The
cochlea is a bony tube filled with fluid, within it sits the Organ of Corti, the sensory organ
of hearing. The Organ of Corti is separated into three sections, the Scala vestibuli, Scala
media and Scala Tympani. Scala vestibuli and Tympani are filled with Perilymph while
media is filled with endolymph.
The vibrations of the oval window cause displacement of fluid in the Scala vestibuli, and
in turn cause displacement in the Scala Media. The waves of fluid displacement cause
movement of the basilar membrane of the organ of corti, which causes movement of the
stereocilia which project from the surface of hair cells.
The movement of these hair cells, modulated by the tectorial membrane, then triggers
depolarization in the nerve fibers of the cochlear nerve. These stereocilia are linked to one
another by protein ‘Top Links’ which help to control opening of ion channels. The
bending of the stereocilia prompts the depolarization of the cells, thanks to the opening of
K+ channels (NOT Na+ AS WITH NERVES). As the endolymph they are bathed in has high
K+ levels, rapid depolarization is achieved.
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Different parts of the organ of Corti are most sensitive to different sound frequencies, with
the hair cells closest to the apex most sensitive to low frequency waves.
The displacement of the fluid, and the energy contained within it, is then displaced by
vibrations of the Round window, which sits along Scala Tympani.
Central sound transmission

When sound waves reach the ear, the ear transduces this mechanical stimulus into a nerve
impulse that the brain perceives as sound. This process of mechanical stimuli to nerve
impulse (transduction) is what we will look at there.
Transduction is done by the inner hair cells of the organ of Corti, of which there are
around 3,500. There are also 12,000 outer hair cells that are responsible for fine tuning
incoming sound waves. As the inner hair cells bend, they prompt the opening of K+ ion
channels in the hair cells, causing depolarization. This depolarization is transmitted to the
cochlear nerve. The intensity (loudness) of the sound is determined by how many hair
cells are stimulated, while the frequency is determined by where these hair cells are in
the organ (nearer to the middle ear = higher frequency, nearer to the apex = lower
frequency).
Once the signal has been triggered down the cochlear nerve, the signal is sent to the
cochlear nucleus. From here, the signal is sent to the olivary nuclei, fibers then project to
the ipsilateral inferior colliculus, via the lateral lemniscus and thence to the medial
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geniculate body of thalamus. From here, auditory fibers project to the primary auditory
cortex, on the upper aspect of the lateral fissure, associated with Wernicke’s area.
Our ability to detect the location of sound is based on the fact that we have two ears in
different locations. Based on the delay between when a sound reaches each ear, we can
identify where a sound has come from with remarkable accuracy.
4. Clinical physiology of vestibular system

Balance is achieved by the integration of Sensory information, including Visual,
Proprioceptive and Vestibular. We will look here at Vestibular.
The vestibular apparatus are located in the labyrinth of the inner ear. It contains three
semicircular canals located at right angles to one another. The three canals are located
horizontally, posteriorly and superiorly. These canals work with the Utricle and Saccule
within the vestibule which respond to changes in the position of the head.
The semicircular canals are filled with endolymph, as we rotate our heads the fluid in the
semicircular canals moves, and it, in turn, moves the hair cells that sit within these
canals. The movement of these hair cells triggers depolarization of the hair cells, and in
turn triggers an AP in the vestibulocochlear cranial nerve.
Meanwhile, within the Utricle and Saccule are Otoconia crystals. As we change speed, or
move our head position, these crystals move. The movement of these crystals then move
the underlying otolithic membrane, k inocilium and stereocilia that are attached to hair
cells. These stereocilia are responsible for the transducing the movement of the cilia
into an action potential. This ability, to detect this kind of movement, is known as Detection
of Linear Acceleration.
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5. Non Inflammatory diseases of the outer ear - othaematoma, wax, foreign

bodies in the meatus acustici externi
The outer ear, or auris externa, consists of the auricle and the ear canal. The primary
disorders of the outer ear involve blockage.
The external canal is 2.5 cms long, with an outer ⅓ cartilaginous and an inner ⅔ bony.
Disorders of the outer ear can be congenital, inflammatory, reactive, trauma or tumors.
Some general thoughts about examination of the outer ear, ask about discharge, pain,
hearing loss, additional noises etc and make sure to palpate the Tragus (the inner sticky out
bit of the ear!). Pain here would indicate inflammation of the cartilaginous portion of the ear
canal. Following this, Otoscopy (the looky in the ear thing) can be used to inspect the
external ear canal and tympanic membrane (to do this you should pull the auricle gently
upwards to straighten the ear canal).
Othaematoma (haematoma of the auricle)

- Accumulation of blood between the auricular cartilage and its perichondrium
- Etiology
- Blunt trauma (boxers ear/cauliflower ear)
- Spontaneous in elderly
- Haemorrhagic blood diseases
- Clinical picture presents with painful, swollen auricular, slightly cyanotic
- Can complicate to perichondritis
- Treatment with incision and evacuation under aseptic conditions
GP NOTEBOOK SAYS: Treat with drainage of the haematoma, and firm packing of
the injured area to oppose the cartilage and perichondrium. Compression bandage
should be left on for a week.
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Wax
- The ear canal produces cerumen (ear wax) which protects tympanic membrane.
- If glands overproduce cerumen it can solidify, and block the canal. This is often
compounded by at-home removal, using cotton swabs which push the wax deeper.
- Symptoms include hearing loss, tinnitus and earache
- Can complicate to infection
- Commonly problematic in young and elderly
- Treat with over-the-counter ear wax softeners and or canal irrigation.
NICE SAYS: GP surgeries or community clinics should offer to remove earwax if it

is impacting hearing. Can be removed using electronic machine that pumps water
into ear (irrigation), this is done along with wax softeners given before irrigation.
Other methods include microsuction and manual removal (only done if appropriate
training given). Ear syringing, as done in bulgaria, should not be done as is harmful.
Foreign Body (F.B.)

- Most commonly occurs in children and those with learning difficulties
- Can be inanimate (vegetative or non vegetative) or animate (e.g. flies, larvae)
- Asymptomatic if small, hearing loss if larger with occlusion of external canal. Animate
FB can cause severe irritation with additional noises
- Can complicate to injury of canal, tympanic membrane or ossicles, can in turn
become inflammatory.
- Treat by removal of FB (using hooks and/or ear wash). Insects should be killed by
alcohol or oil before.
BMJ SAYS: Patients are best managed under operating microscope in ENT
emergency clinic. Removal with Jobson Horne probe, wax hook, suction and/or
microforceps, with raking action. Avoid irrigation as organic materials will expand,
blind instrumentation may cause trauma to canal or tympanic membrane.
6. Inflammatory diseases of the outer ear - otitis externa circumscripta et diffusa,

perichondritis auriculae, eczema auris externa
Inflammation of the external ear may manifest acutely with pain, subacutely or with chronic
complaints such as itching and scaly skin.
Otitis externa
It is worth explaining otitis externa circumscripta vs diffusa:
- Otitis externa circumscripta = otitis externa where there is local involvement of the
auditory canal
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- Otitis externa diffusa = diffuse involvement of the auditor canal

It is also worth saying, these are obsolete terms, and nobody since the 1800s uses
these...not that I’m trying to be negative about the authors of this syllabus at all!!!
Otitis externa is inflammation or infection of the external auditory canal, auricle or both. Most
commonly due to acute bacterial infection of the skin in the ear canal.
- Classification
- Acute diffuse (common in swimmers)
- Acute localised (furunculosis - infection of a hair follicle)
- Chronic (as acute, but duration >6 weeks)
- Eczematous (dermatologic conditions that may infect external ear canal)
- Necrotising (malignancy - found in immunocompromised adults usually)
- Otomycosis (fungal infection)
- Etiology
- Absence of cerumen, high humidity, retained water in ear canal, trauma
- All of which give access to pathogen
- Signs and symptoms
- Itchy, otalgia, hearing loss, ear fullness, edema, tinnitus, discharge, redness
- Diagnosis
- Looking in ear we should see typical signs of inflammation and/or infection in
the ear canal
GP NOTEBOOK SAYS: Send swab to lab if discharge, prescribe suitable eardrops (e.g.
with antibiotics and anti-inflammatory, gentisone -HC ( gentamicin and hydrocortisone) and
occasionally oral antibiotics (flucloxacillin, unless pseudomonas, then ciprofloxacin). If px
over 50, test urine for sugar. If no improvement after one week, px to return and try
alternative ear drops. Referral if malignancy is suspected (if otalgia and headache more
severe than expected, or granulation tissue present in ear canal, or exposed bone), also
refer if extreme cellulitis present.
Perichondritis auriculae
Inflammation of the perichondrium of the auricle, a layer of connective tissue around the
auricular cartilage.
Generally caused by bacterial infection following trauma, most prominent pathogen is

Pseudomonas. Presents with severe pain of rapid onset, with changing of auricular shape
with swelling of conca and tenderness.
Diagnosis through history and clinical observation of the auricle. Tympanic membrane
should appear normal, with no hearing loss unless otitis externa also present.
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Differential diagnosis: ensure pain is not from eczema or dermatitis or spreading infection
(e.g. cellulitis). Complications can be cartilage destruction. Treat with Antibiotics.
GP NOTEBOOK SAYS: Treatment should focus on eradicating Pseudomonas

aeruginosa and S. aureus. Use oral ciprofloxacin or IV ticarcillin. Failure to respond
then admit to ENT, surgical intervention at earliest sign of abscess.
Eczema auris externa

This is an inflammatory condition of the auricle confined to the dermis.
Pathogenesis based on immune/allergic reaction, can be caused by jewelry, soaps, hearing

aids and others. Itching is the primary symptom, with dry and scaly skin, which may progress
to weeping, note, contours of auricle are unchanged (use this to differentiate between
perichondritis)
7. Otitis media acuta - catarrhalis and suppurativa
Otitis media is inflammation of the middle ear. It is worth noting that otitis media often comes
with Myringitis (inflammation of the tympanic membrane) which is rarely isolated.
Acute otitis media is a common disease in infants and small children. This is due to the fact
that the eustachian tube in infants is shorter and wider, and it is through the eustachian tube
that the pathogen enters the middle ear. Most common causative agents are S.
pneumoniae, H. influenzae and Branhamella catarrhalis.
The condition is often preceded by viral infection of the upper respiratory tract with
associated rhinitis. Initial symptom is a severe earache, accompanied with fever in the first
24 hours. If the tympanic membrane is perforated, discharge can occur (this is chronic
suppurative otitis media, see below).
Diagnosis:
- Mastoid normal
- Otoscopy shows opaque, thickened, erythematous, and sometimes bulging tympanic
membrane.
- Conductive hearing loss present
Otitis media acute can lead to spontaneous perforation of the tympanic membrane, beyond
this complications are rare. Treatment should be with NSAIDs and AB therapy (continued for
7-10 days).
Types
- Acute suppurative otitis media
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- May be viral or bacteria

- Causes ear pain and tenderness, it is the stereotypical ‘otitis media’.
- Otitis media with effusion (aka serous or secretory otitis media)
- Glue ear, fluid fills middle ear due to negative pressure produced by
dysfunction of eustachian tube. This then facilitates middle ear infection
- Note, the tympanic membrane stays in tact
- Symptoms are usually absent in children. Main symptom is hearing loss that
is often not reported, can lead to speech and language development delay.
- Diagnosis by observing tympanic membrane which is opaque, thickened, and
may be retracted. Often pale, reddish, yellowish or bluish.
- Treatment is conservative at first, with effort to improve nasal breathing and
eustachian tube function (e.g. decongestants). In chronic form, treat with
surgery via paracentesis (incision of tympanic membrane).
- Chronic suppurative otitis media
- Chronic inflammation of middle ear characterised by discharge through a
perforated tympanic membrane for at least 6 weeks.
- Often associate with Cholesteatoma, often the result of otitis media with
effusion.
- This is the primary cause of hearing loss in children
- Also see Q12 + 13
- Adhesive otitis media
- Thin retracted tympanic membrane becomes sucked into middle ear space
and adheres to ossicles of the middle ear
Recurrent otitis media, gets its own section in the book so we’ll look at it here, is classified as
5+ infections in a year, or 3+ in six months. It is worth noting, it is helpful to observe a normal
tympanic membrane after each bout to ensure we are seeing a new acute infection, not just
a flare up of a chronic condition. Where children have recurrent otitis media we should
consider vaccinations against pneumococcus, and potentially prophylactic antibiotics.
Adenotomy can decrease bacterial burden and improve eustachian tube function, while
placement of a ventilation tube in the tympanic cavity can also help.
GP NOTEBOOK SAYS:
AOM suppurative - 80% recover in three days without antibiotics, treatment may
benefit specific subgroups (e.g. under two years with bilateral infection, with
discharge, systemically unwell or with recurrent infections). Paracetamol and
ibuprofen are good choices.
Chronic suppurative otitis media - Quinolone antibiotic drops (e.g. ciprofloxacin)

indicated, systemic treatment no better.
Secretory otitis media - should assess hearing and be vigilant for signs of deafness
(note 50% resolve in 6 weeks). If hearing affected, and no improvement, consider
adenoidectomy or myringotomy, or hearing aids if surgery not possible.
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8. Otitis media acuta by infectional diseases
I’m considering this covered above.
9. Otitis media in young children
I’m also saying this is covered above, just know everything about otitis media, and know that
children are more susceptible due to the shorter, wider nature of their eustachian tube.
10. Paralysis n. Facilias
Before talking about paralysis in the facial nerve I’m going to talk about Cholesteatoma, as
this is an important risk factor for facial nerve paralysis, has its own chapter in the book, and
was mentioned a lot in the lecture, despite not being a question.
Cholesteatoma is keratinizing squamous epithelium that is found in bony spaces at an
abnormal location, where bone is destroyed through an inflammatory osteoclastic process.
Cholesteatoma can be acquired or congenital, with acquired the most common, occurring in
conjunction with inflammatory processes of the middle ear.
Acquired cholesteatoma has two types:

- Primary - where the cholesteatoma develops from a squamous epithelial pocked in
pars flaccida, and expands in the epitympanum, destroying the lateral wall
- Secondary - where the cholesteatoma originates from pars tensa.
Pathogenesis starts with the impairment of eustachian tube, causing negative pressure and
therefore encouraging squamous epithelial cells to migrate into the middle ear where they
cause inflammation.
Symptoms are primary functional deficits, with a common initial symptom of increased
pressure in the ear, with hearing loss and, potentially, facial nerve palsy and vestibular
dysfunction. Very common is infected cholesteatoma with a foul smelling discharge due to
the bone destruction.
GP SAYS: Often presents as recurrent Suppurative OM which shows no signs of

improvement with ABs, along with conductive hearing loss. (Hearing loss + fetid
secretion classic clinical picture).
Diagnosis is done with otoscopy, which shows white epithelial debris in retraction pocket or
in the posterosuperior quadrant of the tympanic membrane. Bone erosion can also
sometimes be observed.
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Now to the facial nerve. The facial nerve supplies motor innervation to the mimetic muscles
of the face, along with some secretory and sensory functions. The loss of these mimetic
muscles is the most common symptom we look for in diagnosis. Possible causes of
peripheral (one-sided) facial nerve paralysis are:
- Idiopathic
- Bell's palsy (most common)
- Traumatic
- Temporal bone fracture, mandibular fracture, surgical trauma, obstetric
trauma
- Infectious
- Borreliosis, Herpes zoster oticus, acute otitis media, mastoiditis,
necrotising otitis externa, AIDS, TB, Mononucleosis
- Inflammatory
- Cholesteatoma, Sarcoidosis
- Neoplastic
- Metabolic
- Diabetes mellitus
(Bold indicates ENT cause).
The key division is traumatic vs non-traumatic, if traumatic, CT and X-ray may be needed to
observe, if non-traumatic, observe audiology, with MRIs to determine full cause of palsy.
11. Mastoiditis
Mastoiditis is an inflammation of the air cells in the mastoid process, this commonly occurs in
acute otitis media and is known as associated mastoiditis.
Presents with fever and local pain of the mastoid region. Diagnosis with a clinical triad of
- Retroauricular swelling
- Tenderness over mastoid
- Otorrhea (ear discharge)
However, these three do not always appear, and it can be tricky to diagnose, a CT is the
gold standard for viewing, as we see clouding of the mastoid air cells and middle ear spaces,
along with erosion of the mastoid process. In primary care, where CT is unavailable, if there
is no improvement of otitis media after 2 weeks, mastoiditis should be considered.
Complications can be severe, including labyrinthitis, facial nerve palsy, intracranial abscess
and meningitis.
Treatment often consists of mastoidectomy, with IV antibiotics and the placement of

myringotomy tubes to decompress middle ear. ABs without surgery only possible in the early
stages of the condition.
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GP NOTEBOOK SAYS: Antibiotics, determined by sensitivity or organism, ideally

IV. Cortical mastoidectomy where AB response is poor or abscess formation.
12. Otitis media supp. Chronica-mesotympanic
Mesotympanic and epitympanic are the two types of chronic otitis media. Here we describe
mesotympanic type.
Chronica-mesotympanic only affects the mucosa of the ear, it will cause perforation of the
tympanic membrane in a central form (not affecting annulus fibrosus). There is not significant
danger to the patient in cases like this, the only thing to be seriously aware of is that patients
should not swim and they should use ear plugs when washing.
Etiology may be:

- Chronic inflammation secondary to eustachian tube dysfunction
- Trauma
- Genetic factors
Symptoms include chronic otorrhea, with discharge, through hole in tympanic membrane.
After infection clears, it is possible to live with perforated eardrum without any symptoms.
Diagnosis is from history and otoscopic findings, specifically a central perforation in the
tympanic membrane that does not involve the fibrocartilaginous ring.
Complications can include mastoiditis or abscess formation, although these are rare. In
chronic cases conductive hearing loss is the most common complication. Treat with AB in
acute cases, with ear drops, ear cleaning and drying and protection from water in cases with
chronic tympanic perforation. Once infection has been clear for 3 months, a tympanoplasty
can be performed to repair the tympanic membrane.
13. Otitis media supp. Chronica-epitympanitis
Epitympanic recess = hollow recess located on the superior aspect of the middle ear
The second form of chronic otitis media, this is an inflammation of the connective tissue in
the tympanic cavity and has a high risk of infection which can go into the brain as the
infection affects the bone, tendons and muscles in and around the middle ear. It is
distinguishable from mesotympanitis as the perforation of the tympanic membrane is
peripheral (it affects the annulus fibrosus).
It has two types, granulatus osteomyelitis, and chronic otitis media with cholesteatoma (see
above).
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Can be congenital or acquired, thought to relate to inflammatory processes. Complications

can include facial nerve paralysis, intracranial complications and others.
Treatment may require destruction of mastoid and tympanic cavity.
14. Noninfectious diseases on vestibular system (toxic, traumatic, vascular)
The vestibular labyrinth is part of the inner ear, consisting of three semicircular canals which
are sensitive to angular acceleration, and the otolithic apparatus, sensitive to linear
acceleration. The three canals are the posterior, lateral and anterior canals, each lying at
right angles to one another. Each canal has a dilation (an ampulla) at the end, which houses
the sensory cells, the so called crista and cupula which detect endolymph movement and in
turn stimulate the vestibular sensory cells.
The otolithic apparatus contain two static maculae, with calcium crystals on an otolithic
membrane. These are sensitive to linear acceleration, not perceptible to the macula.
Signals from the vestibular system go via the vestibular nerve (CN IIX), feeding to the
diencephalon, where information is integrated with nonvestibular information including visual,
spinal and cerebellar information.
Important reflexes
- Vestibulo-ocular reflex
- As the vestibular system detects head movement, it projects signals to the
eye muscles via the oculomotor nuclei, which allows the eye to fix on a
specific point.
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- Vestibulospinal reflexes
- Important for stabilising the head position and maintaining visual orientation,
vestibular information combines with proprioceptive and visual information to
control an upright gait. If two of these systems are damaged, we generally fall
over.
Standard vestibular tests

- Romberg tests
- Patient stands upright with eyes closed and feel parallel and close together.
Normal vestibular system can stand for 30 seconds without body sway
- Unterberger stepping test
- With eyes closed patient takes 50 steps, bringing knees up horizontal position
with each step. Discrepancy due to vestibular lesion will see the patient rotate
towards the side of the affected nerve. (Up to 45 degrees rotation is normal)
- Finger to nose test
- With eyes closed the arm extends and then slowly touches nose. Look for
ataxia, tremor and others difficulties
- Walking straight with eyes closed
- Should be able to walk 4 meters with eyes closed, one foot in front of another
(heal to toe).
- Walking forward and backwards
- Patient alternately takes two or three steps forwards and backwards. As with
Unterberger test, rotation observed on side of lesion.
Nystagmus
Nystagmus in the broadest sense is rhythmic eye movement, this may be physiologic or
symptomatic of abnormal condition. In the strict sense we mean it here, it refers to
coordinated eye movement about an axis, an easier way of saying this is that the eyes
‘dance’.
In normal state, while the head rotates, the semicircular canals feed information into the
solitary nucleus which in turn feeds the extraocular muscles to control eye movement and
allow for smooth pursuit tracking of the eyes. Nystagmus occurs when the canals are being
stimulated when the head is not in motion, and thus the eyes are tricked into moving along
an axis although the head is still.
There are a number of forms of nystagmus which we will review:

- Pathological
- Excessive drifts of stationary retinal images that degrades vision and may
produce illusion of motor
- De to damage of vestibular system (may include vestibulocerebellum)
- Types
- Central - result of abnormality in the brain
- Gaze induced - exacerbated when changing one's gaze
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- Peripheral - result of vestibular dysfunction

- Positional - occurs in specific position (e.g. BPPV)
- Post rotational - occurs after head rotation
- Spontaneous - occurs randomly
- Alternative classification
- Vestibular spontaneous nystagmus
- Any directional nystagmus that beats towards the same side.
Can be peripheral or central vestibular lesion, generally beats
towards healthy side.
- Gaze-evoked nystagmus
- Fixed nystagmus
- Most pronounced in central position and during fixation
- Physiological
- Form of involuntary eye movement part of the vestibulo-ocular reflex (VOR)
allowing smooth pursuit in one direction and saccadic (jumpy) movement in
the other.
It can be useful to induce nystagmus. Methods of doing this are:

- Caloric stimulation
- Patient lies with head elevated 30 degrees, and irrigate ears with warm or
cold water. Will cause unilateral stimulation of the vestibular labyrinth and
induce nystagmus. In normal case, both labyrinths are stimulated equally, if
nystagmus more prevalent in one eye, we have pathology. (quick video here:
https://www.youtube.com/watch?v=IiE0_AKGlWA)
- Rotational stimulation
- Rotation about an axis stimulates the semicircular canals on each side, and
should induce nystagmus towards the same side as rotation, when rotation
ceases, the nystagmus reverses to the opposite side.
Diseases
- Acoustic neuroma (vestibular schwannoma)
- Non Malignant tumour that develops on the sheath of the vestibulocochlear
nerve
- Idiopathic age related vestibular dysfunction
- Benign paroxysmal positional vertigo (BPPV)
- Frequent cause of sudden vertigo attacks. Possible cause is head trauma,
history of neuronitis and other inner ear disorders
- Pathogenesis due to particles floating in the endolymph, therefore sending
false signals to the brain regarding head movements.
- Diagnosis with Hallpike maneuver (position change with head hanging) treat
with therapeutic exercises to break up debris in endolymph
- Treatment known as Epley maneuver. After Hallpike, turn head 90
degrees opposite to the way the head was before, then have px turn
on their side (the same side you just turned the head), then rotate
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head another 90 degrees in same direction. Now px can sit up,

keeping head in same position (head to finish with chin resting on
chest). BMJ video here:
https://www.youtube.com/watch?annotation_id=annotation_25862680
99&feature=iv&src_vid=8RYB2QlO1N4&v=jBzID5nVQjk
- Meniere’s disease
- Triad of vertigo attacks lasting several hours, tinnitus and fluctuating hearing
loss
- Idiopathic. Endolymph overproduction in cochlear, with cochlear duct
distention identified as pathogenesis.
- Bilateral vestibular loss
- Loss of balance caused by severe, bilateral hypofunction of peripheral
vestibular apparatus. Usually systemic cause, such as ototoxic drugs
(aminoglycosides) or renal failure (increased toxins).
- Patient describes ‘drunken’ feeling, complaints worse in darkness
- Central neurological tumours
- May also present with ataxia, saccades during smooth pursuit tracking,
disturbed optokinetic reflex
- Hypoperfusion of brainstem region (stroke of brain stem)
- Ischaemic areas damaging neurology associated with vestibular function.
GP SAYS: If sudden acute vestibular dysfunction, might be vestibular neuritis (see

below) or a stroke. If thought to be a stroke, send patient straight into emergency
department, if vestibular neuritis, no need to treat (possible antiemetics).
If px comes in complains of longer term dizziness, check for drug induced causes,
do full neurological workup, if all else normal, refer for scans.
15. Infectious diseases on vestibular system
Infectious diseases of the vestibular system are:

- Vestibular neuronitis
- Infection of the vestibular nerve in the inner ear. Also known as labyrinthitis
and acute unilateral vestibular loss
- Causes vertigo, along with possible hearing loss and tinnitus
- May be a series of separate attacks, or persistant up to six weeks
- Generally viral cause (but can also be bacterial, head injury, allergy or
medication induced).
- Is unilateral
- Cholesteatoma
- A result of repeated infections, these can also damage the delicate bones of
the middle ear, and progress to damaging the labyrinth
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GP NOTEBOOK SAYS: Can trat with antivertiginous medicine (e.g.

prochlorperazine) for first two days only, and twice-daily vestibular rehabilitation
exercises can fully resolve condition.
The below approach to dizziness was published in 2017 in the American journal of Family
Physicians.
Notes:
- Dix Hallpike maneuver: Sit px on couch, turn head 45 degrees and observe eyes.
Then ‘drop’ patient back, head falling off back of couch (hold head so they don’t
break neck…). +ve result shows nystagmus after they’ve been laid back. (BMJ vidoe
here: https://www.youtube.com/watch?v=8RYB2QlO1N4)
- HINTS examination: Px should try hold gaze on your nose,
then move px head gently to one side, then rapidly back to the neutral
position, should see a small corrective saccade. +ve test shows
significant lag with corrective saccades in both directions, if lag only in
one direction, suggests peripheral etiology. Image on the left shows A,
normal and B, positive finding.
-
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16. Otosclerosis
Otosclerosis is a disease of the bony otic capsule in which structural changes in the bone
cause stapes fixation resulting in conductive hearing loss.
It occurs between 20-50 years of age, twice as common in women as men. The structural
changes of the bone are idiopathic, presumed to be due to family history and possibly
female hormonal changes, infections can also cause the condition.
Symptoms show progressive hearing loss in one

or both ears (with bilateral involvement, one ear
is usually affected more than the other). Tinnitus
may be present, but vestibular dysfunction is
rare.
Diagnosis - conductive hearing loss, normal

otoscope. Weber lateralized to affected ear,
Rinne test negative. As many as 10% of people
may have otosclerotic lesions, but never showed
symptoms.
GP NOTEBOOK SAYS: Treatment is not essential, especially when hearing loss is

minor, hearing aids and lip-readers can help, with none of the risks of surgery.
Surgery involves a stapedectomy, where the tympanic membrane is lifted to expose
the middle ear, stapes is then removed na replaced with plastic prosthesis.
NOTE: ANY UNILATERAL DEAFNESS - REFER UNDER TWO WEEK RULE
17. Morbus Meniere
Meniere’s diseases ia a unilateral diseases which consists of vertigo attacks lasting hours,
tinnitus and fluctuating hearing loss. The full diseases is only diagnosed when all three
symptoms are present. This triad can also be accompanied with headaches and a sense of
fullness of the ears. Disease is idiopathic although thought to be both genetic and
environmental.
Pathogenesis:
- Relative overproduction of endolymph with cochlear duct distention and displacement
of Reissner membrane towards the scala vestibuli.
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- Often due to decreased draining of endolymph rather than actual

overproduction
- This overproduction creates unfavorable mechanical environment for the hair cells,
leading to sensorineural hearing loss and tinnitus. It is theorised that the vertigo
comes from small ruptures of the Reissner membrane, allowing the mixing of
perilymph and endolymph leading to potassium intoxication in the perilymphatic
space.
Diagnosis based on clinical picture, otoscopic findings are normal, although signs of
previous inflammation or trauma can sometimes be found.
Treatment consists of rest and anti-vertiginous (or antiemetic) medication. In severe cases,
possible destruction of the labyrinth (vestibular neurotomy) or intratympanic gentamicin (via
myringotomy tube) can be considered.
GP NOTEBOOK SAYS: Surgery reserved for patients with severe condition.

Possible procedures include endolymphatic sac decompression, division of
vestibular nerve and ultrasonic destruction of vestibular end organs. Total
labyrinthectomy may also be done, but this destroys inner ear, causing deafness,
only done where deafness already exists and px has severe unilateral Meniere’s.
18. Abscessus extradural and subdural
Intracranial complications of otitis media are:

- Extradural abscess
- Subdural abscess
- Meningitis
- Brain abscess
- Lateral sinus thrombophlebitis
- Otitic hydrocephalus
Here we consider the first two.
Also known as a epidural abscess, is a rare infection between the bones of the skull (or
spine) and the meninges. These are generally less symptomatic than other forms of
intracranial abscesses.
Meanwhile, subdural infections spread to under the dura mater, between the meningeal
layers. These lie on a continuum with meningitis and subdural empyema and are more
symptomatic.
Infection is generally bacterial in origin, although can be fungal, and is as a result of an

infection that has spread through the blood. Specifically, abscess inside the skull can be
caused by:
- Chronic ear infections
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- Chronic sinusitis
- Head injury
- Mastoiditis
Infections can spread from the middle ear into the temporal bone and intracranial space,
either through eroded bone of the tegmen tympani, of Trautmann’s triangle or via retrograde
thrombophlebitis. These abscesses are usually a complication of chronic middle ear
infections, although acute instances can occur.
Common early symptoms include headaches, with fever, and in some cases neurological
symptoms such as confusion, convulsions and altered consciousness. Patients are most
commonly middle aged (35-60).
Treatment takes the form of severe IV, pre-surgical antibiotics, along with surgery to
evacuate the abscess.
19. Meningitis otogenik
Otogenic meningitis can result from otitis media, especially with cholesteatoma. In cases
where meningitis appears from unknown focus, s. Pneumoniae from the middle ear and
lateral skull base should be considered possible sites of origin.
The spread of infections can occur through the labyrinth, bone gaps of laterobasal fractures,
or contiguous spread from infected osteitis or cholesteatoma. Symptoms include headache,
fever, clouded consciousness and confusion.
Diagnosis via CT scanning of temporal bone and lumbar puncture. Treat with Antibiotics and
corticosteroids. Otogenic meningitis can in turn lead to inner ear disorders or even deafness.
20. Sepsis otogenic - thrombophlebitis sinus sigmoidei
Thrombophlebitis is the inflammation of a vein, related to a thrombus (clot). The proximity of

the middle ear and mastoid cells to the sigmoid venous sinus lends itself to the spread of
infection through the neighbouring eroded bone.
It may develop as a complication of acute suppurative otitis media by thrombophlebitic

dissemination through the emissary vein in the intact bone. It is most often found in adult
patients after a long history of chronic ear disease.
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(sagittal section)
A perisinus abscess is initially formed, as the infection penetrates the dura and approaches
the intima, with a mural thrombus developing. Damage to the intima blood vessels, with
hypercoagulation and decreased blood flow, all contributing to the formation of thrombus
within the vessels. The thrombus that forms in the sinus gros and necrotising, forming an
intramural abscess, developing in the lumen of the snus, propagation proximally and distally
which in turn may become infected. The lumen of the vessel is eventually occlude by the
thrombus, and infected material may embolize into systemic circulation, causing sepsis!
Clinical presentation often shows as headache, fever, and otorrhea. The fever was typically
‘picket fence’ (on-off) due to the periodic release of hemolytic streptococci from the septic
sinus thrombosis.
21. Thrombophlebitis sinus cavernosus
Thrombophlebitis sinus cavernosus (or Cavernous sinus thrombosis (CST)) is the formation
of a blood clot within the cavernous sinus (at the base of the brain).
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Most common cause is spread of infection from elsewhere in the body, 50% from a nasal
furuncle, 30% from sphenoidal or ethmoidal sinuses, 10% from dental infections and less
commonly from the tonsils, soft palate, middle ear or orbit.
The most common form of infection is S. aureus. MRI and MR venogram are the gold
standard for identification. The basic pathophysiology is the same as above, bacteria cause
damage to the vein, encouraging thrombotic formation, which occludes the vein, necrotising
and becomes infected.
22. Abscessus cerebri otogenica
Chronic otitis media with cholesteatoma (and/or granulation tissue) are most commonly the
cause, specifically S. aureus as the most common bacterial pathogen. Patients commonly
present with headache and vomiting, as such, these symptoms along with cholesteatoma
are very suggestive for cerebral abscesses. Exact symptoms can vary based on the location
of the patients abscess (additional symptoms include otorrhea, facial palsy, confusion,
hemiparesis, neck stiffness).
Typically best established by CT scanning with and without contrast, located at the same
side as the diseased ear. Temporal lobe and cerebellum (see below) are the two common
locations for otogenic brain abscesses. The most common cause is direct extension of
infection through a bony defect, in the tegmen antri (cerebral) or trautmann's triangle
(cerebellar).
Successful management should involve local drainage and administration of systemic

antibiotic and cleansing of primary focus of infection. Steroid and anti-edema drugs can also
be administered.
23. Abscessus cerebelli otogenica
Look, just see all of the above stuff, just make sure you know that its through the weakness
of the trautmann’s triangle. Obviously symptoms here include issues regarding balance and
proprioception.
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24. Different types of hearing loss
There are four types of hearing loss:
- Auditory processing disorders

An term for individuals who struggle to process information arising from dysfunction in the
CNS. It presents with individuals having trouble remembering words, need sentences
repeated, talk louder than normal and in general struggle with verbal processing.
Such disorders are generally idiopathic or hereditary, with a strong genetic component.
- Conductive
Commonly presents in childhood or young adulthood, possible causes include:
- Otosclerosis
- Otitis media (with or without serous effusion)
- Ear barotrauma (eustachian tube dysfunction that prevents pressure
equalisation)
- Cerumen impaction
- External auditory canal atresia (narrowing)
Clinical features show improvement in noisy environments, volume of voice remains normal
and sounds are not usually distorted. Features of external auditory canal pathology should
be evident.
The Weber test shows lateralisation to impaired ear (remember weber, fork on head) while
Rinne test shows Rinne positive (bone conduction greater than air conduction)
- Sensorineural
Commonly presents in middle or late age, possible causes include:
- Meniere’s disease
- Acoustic neuroma
- Noise-induced hearing loss
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- Internal ear infections

- Presbycusis (old age deafness)
Clinical features show that hearing worsens in noise environments, and volume of voice
goes up. Higher frequencies lost preferentially, and there is an absence of features of
external auditory pathology.
The Weber test shows lateralisation to good ear, Rinne test shows air conduction is better
than bone conduction (as is physiologically normal).
- Mixed
This is, of course, a combination of neurosensory and conductive hearing loss.
25. Treatment of hearing loss
Treatment for conductive hearing loss

- Usually temporary
- Treat underlying cause
- Otosclerosis - hearing aid or stapedectomy (insertion of prosthetics)
- Otitis media (with or without serous effusion) - treat with ABs
- Ear barotrauma (eustachian tube dysfunction that prevents pressure
equalisation) - treat by keeping ear clean and decongestants
- Cerumen impaction - use wax softeners and warm water
- External auditory canal atresia (narrowing) - surgery to widen
- In the case these do not work, hearing aids or cochlear implants are possible
Treatment for neurosensory hearing loss

- Most widely used is that of hearing aids. The inner ear
and/or auditory nerve that is damaged in sensorineural
hearing loss cannot be medically treated once damaged,
so hearing aid is the best treatment
- Hearing aids have a microphone and a speaker, to
capture and amplify the sounds and direct them into the
auditory canal.
- Types of hearing aid include
- Completely the canal (A)
- In the ear (B)
- In the ear (C)
- Behind the ear (D)
- Receiver in canal (E)
- Open fit (F)
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Note, cochlear implants are slightly different, they are useful for individuals with very severe
hearing loss, they bypass the normal auditory pathway and directly stimulate the auditory
nerve. They do not make acoustic signals, but rather deliver the acoustic signal as an
electrical pulse!
NICE SAYS: Referral criteria for deafness in adults

- For adults who present for the first time, first exclude impacted wax or
infections, then arrange audiological assessment and refer for additional
diagnosis if required
- Sudden or rapid onset
- If sudden (>3 days) within last 30 days, 24 hour ENT referral
- If sudden not last 30 days - 2 week rule
- If hearing worse rapidly (over 4 days in last 90), urgent 2 week rule
- Hearing loss with additional signs/symptoms
- With face droop - 24 hour ENT referral
- If IC + otalgia + otorrhoea and not responded in 72 hours to AB, refer
24 hour ENT
- Those of Chinese or SE asian origin who have hearing loss and
middle ear effusion not associated with upper respiratory tract
infection - 2 week rule referral (high incidence of nasopharyngeal
carcinoma)
- Additionally, refer if any deafness/tinnitus that is not obviously
associated with upper respiratory tract infection.
NICE SAYS: Children screening

- There is a national hearing screening programme in the UK
- Infants up to 8 months assed via distraction testing
- 1-2 babies of every 1000 are born with hearing loss. All babies are
offered hearing screen 0-5 weeks of age, GPs are notified separately
- Confirmed by GP at 6 week check
- Child after 2 years performs word-object test (points to objects that examiner
names, child then points to the object when examiner whispers name of the
test objects)
Nose
26. Clinical anatomy of the nose and paranasal sinus
Anatomy of nasal cavity

Functions to warm and humidify air, removes and traps pathogens, gives sense of smell,
and drains paranasal sinuses and lacrimal ducts.
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Has three parts, vestibule (area surrounding anterior external opening), respiratory region
(lined by ciliated pseudostratified epithelium with mucus-secreting goblet cells) and olfactory
region (at apex of nasal cavity with olfactory receptors.
The walls of the nasal cavity are:

- Medial (ant = septal nasal cartilage, post = vomer)
- Floor (hard and soft palate)
- Roof (cribriform plate of ethmoid bone with nasal spine of frontal and nasal bones
anteriorly and sphenoid and vomer more posteriorly.)
- Lateral (maxilla, palatine and pterygoid plate)
Nasal Conchae
Projecting out of the lateral walls of the nasal cavity are curved shelves of bone known as
conchae (inferior, middle and superior) creating four pathways for air flow (inferior, middle,
superior meatuses and sphenoethmoidal recess), These function to increase the surface
area, disrupting air flow.
Openings into nasal cavity

- Frontal, maxillary and anterior ethmoidal sinuses open into middle meatus
- Middle ethmoidal sinus empties onto ethmoidal bulba (bulge in lateral wall formed by
middle ethmoidal sinus)
- Only the sphenoid sinus does not drain onto lateral wall, this drains into posterior roof
- Additionally, Nasolacrimal duct and eustachian tube drain into inferior meatus
Note - infection can travel between middle ear and upper respiratory tract via the
eustachian tube-nasal cavity connection. Infection in the auditory tube causes swelling of
the mucus linings, blocking of tube and reduction of hearing.
Vasculature
- Internal carotid artery
- Anterior ethmoidal a
- Posterior ethmoidal a
- External carotid branches
- Sphenopalatine a
- Greater palatine a
- Superior labial a
- Lateral nasal a
These arteries anastomose in the anterior portion of the nose, in an area known as Little’s
area. The rich blood supply can lead to Epistaxis (nosebleed). This can most commonly
occur in the anterior third of the nasal cavity, an area known as Kiesselbach area.
Innervation
Innervation is divided into special innervation (the olfactory nerve, whose branches run
through the cribriform plate to provide special sensory innervation), and general innervation
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(nasopalatine and nasociliary nerve for the septum and lateral walls, and the trigeminal
nerve for the external skin of the nerve).
Clinically, a fracture of the cribriform
plate can occur as a result of trauma,
which can in turn penetrate the
meningeal linings of the brain, causing
leakage of cerebrospinal fluid. The
olfactory bulb, that lies on the
cribriform plate, can be irreversibly
damaged by fracture, resulting in
anosmia (loss of smell).
Anatomy of paranasal sinuses

Paranasal sinuses are air-filled extensions of the
respiratory part of the nasal cavity. There are four paired
sinuses, maxillary, frontal, sphenoid and ethmoid. They
assist in humidifying the air and reduce the weight of the
skull.
Upper respiratory tract infections can spread to the

sinuses. Infections of the sinuses cause inflammation
known as sinusitis (pansinusitis if more than one sinus).
The maxillary nerve supplies both the maxillary sinus and maxillary teeth, so inflammation of
that sinus can present with toothache!
I’m also going to add some details here about the Anatomy of the Eustachian tube, as this
is something that was focused on in our classes.
The so called ‘forgotten organ’ the eustachian tube is a cartilaginous (medial ⅔) and bony
tube (lateral ⅓) that connects cavum tympani to the nasopharynx. It has three functions:
1. To equalise middle ear pressure
2. To drain fluid from the middle ear
3. To clean and prevent infections of the middle ear
The tube is approximately 4 cm long, with variable diameter, widest at the opening of the
tympanic cavity. The tube is closed by default, but opens with swallowing and yawning,
muscles tensor and levator veli palatini are responsible for its opening by contraction of
the soft palate.
As mentioned the eustachian tube opens into the nasopharynx, behind this sits the
Pharyngeal tonsil, present only in children. A common cause of eustachian tube dysfunction
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in children is inflammation or adenoma of the pharyngeal tonsil which causes blockage of

the orpheus. Additionally, surrounding the
27. Clinical physiology of the nose and paranasal sinus
Smell is the product of the conversion of a chemical signal into an electronic one.
Particles are sucked up into the nasal cavity where they dissolve into the mucosal lining
of the nasal cavity. Olfactory receptor cells are embedded into the epithelium that detect
these odor molecules and transmit this
information into the CNS. The receptor
cells function by virtue of the cilia they
have, which bind to molecules, causing
an increase in intracellular cAMP,
opening selective cation channel, leading
to depolarization of the olfactory
receptor. This electrical response then
spreads through the receptor cells to the
olfactory nerve fibers at the back of the
nasal cavity.
From the olfactory sensory neurons the

signal is passed, through the cribriform
plate, to the tufted and mitral cells. These
cells help to form the olfactory bulb. From
the olfactory bulb the signal is passed to the
Uncus of the brain which houses the
olfactory cortex. The olfactory cortex
includes the piriform cortex, amygdala, olfactory tubercle and parahippocampal gyrus.
From here the Olfactory tubercle connects with a range of different parts of the brain,
including the Thalamus, Hypothalamus, Hippocampus, Brainstem and others. This is why
odors can produce such a strong wider response, by virtue of the interconnection of the
olfactory cortex with the rest of the brain.
Physiology of paranasal sinuses

Ummm…..not much to add to the above….just say some stuff!
28. Foreign bodies in the nose. Furuncles vestibuli nasi. Epistaxis
Foreign bodies in the nose

Commonly occur in toddlers and children aged 1-8 and those with learning difficulties.
Objects can be animate or inanimate, common objects include food, tissue, paper, beads,
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toys and rocks. Button batteries are of particular concern as they can cause severe damage
in a very short period of time.
Symptoms of an NFB will be increased nasal drainage, breathing difficulty and discomfort of
the nose along with, of course, Epistaxis. They can be found in any portion of the nasal
cavity, although typically found around the floor of the nose, below the inferior concha.
Removal is most commonly via cupped forceps, nasal vasoconstrictors may be useful prior
to the attempt. If objects is round, a curved hook is preferable. No aesthetic is usually
required, although local acting may be advisable in some patients. Nasal endoscope can aid
visualisation of the NFB if the object has found its way to the posterior nasal cavity.
Additionally suction methods have been described to aid NFB removal. In the case of
animate objects (e.g. worms, flys etc) these should be killed prior to removal attempts.
In extreme cases, such as where the NFB is underneath the submucosa, rhinoplasties may
be required to remove the object.
BMJ SAYS: Nasal FBs should be removed by ENT specialist who will grasp object
firmly with crocodile forceps, or passing blunt hook beyond object and drawing it
forward. Microsuction can be used for smaller objects. Battery insertion into cavity
requires immediate action and should be removed under general. Phenylephrine
can be used to reduce mucosal edema before removal, along with lidocaine as local
anaesthetic.
Furuncles vestibuli nasi

Inflammation of the hair follicle in the nasal vestibule is known as folliculitis, where the
infection spreads to deeper tissues and forms a central core of purulent liquefaction, this is
known as a furuncle.
Symptoms include pain, tenderness and erythematous swelling about nasal tip. Changes are
generally confirmed to the outer skin and do not involve the mucosa, fever can be present.
Treatment is with high administration of antibiotics (most common causative agent is

staphylococci) such as flucloxacillin sodium, with local application of AB ointment
(chlortetracycline HCl). These are important as we must prevent potentially lethal
complication of intracranial spread. Venous drainage of the nose and upper lip drain to the
cavernous sinus, if the infection spreads from here into the cavernous sinus, we can be
faced with an intracranial infection.
GP NOTEBOOK SAYS: Systemic antibiotics should be given immediately (ideally by

injection), drainage of abscess may be required but should be deferred until px has
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had AB treatment.
Epistaxis
Nosebleeds! Possible causes:
- Local
- Change in nasal septum (e.g. perforation, traumatic, iatrogenic, inflammation)
- Mucosal or vascular injury (NFB, rhinoliths, trauma, allergy, rhinitis
- Neoplasia (benign and malignant of nose, paranasal sinuses and
nasopharynx)
- Idiopathic
- Systemic
- Hemorrhagic diseases
- High blood pressure
- Endocrinopathies
Treatment flow chart

- General measures
- Upright, ice bag on back of neck, compress nostrils, do not swallow blood (IV
if needed)
- Check BP
- High - give antihypertensive
- Normal/decreased - volume replacement
- Then decongest and anesthetize nasal mucosa
- Inspect nasal cavity to ID source of bleed
- Kiesselbach’s area - cautery/ nasal pack
- Other site on anterior nose - nasal pack
- Posterior site - posterior nasal pack
- Changes in nasal septum - surgery
- Lab tests (Hb, platelet, clotting, coagulation)
- Treat as required
It should be self evident that
knowing the arteries and the location
of bleeding is important here. If the
bleeding is Anterior (Kiesselbach’s
plexus/little's area) the bleed is from
the sup. Labial a., ant + post
ethmoidal a. Anastomosis. If the
bleed is posterior it is from the
sphenopalatine a. Learn the blood
supply of the nasal cavity and this
picture!
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GP NOTEBOOK SAYS: hospital admission can be considered for elderly, posterior

bleeding, coagulopathy or severe hypertension. Use ‘complete epistaxis tray’ which
should include nasal decongestant sprays, local anesthetics, silver nitrate cautery
sticks, bayonet forceps, nasal speculum, frazier suction tip, post double balloon
system with syringe for balloon inflation, packing materials, suction cautery. Order
of treatment:
- First aid
- Cautery
- Nasal packing
- Secondary care
GP SAYS: In reality, GPs rarely cauterise or pack noses. If bleeding does not stop
following first aid measures, patient is to be sent to A&E for nasal packing.
More common are recurrent cases of epistaxis. In cases like this, blood clotting
screen and full blood count (to ensure not anemic) should be done. If abnormal,
refer (ENT or haematology), if normal then refer ENT (who will generally cauterise
Little’s area).
29. Fracture osseum nasaleum. Haematoma and abscessus septi nasi

Fracture osseum nasaleum
Due to its exposed location the nasal pyramid is predisposed to fractures. These can be
open or closed.
Diagnostic procedure
- Look for deviation, depression or swelling (caused by hematoma) externally
- Internal inspection with anterior rhinoscopy or endoscopy to check for mucosal injury,
and septum damage
- Crepitus on palpation confirms fracture, as does X-ray.
The main risk of complication is a septal fracture, covered by intact soft tissue, which
develops into a subperichondrial hemorrhage with hematoma, which becomes infected,
causing septal abscess, causing cartilage necrosis, causing loss of nasal septum! (that
escalated fast). This can also spread infection to the cranial cavity.
Treatment indicated, open fractures require surgical care with drug prophylaxis, closed
fractures can be reduced for a week, followed by internal nasal splint to straighten and an
external plaster cast.
GP NOTEBOOK SAYS: Criteria for immediate referral is:
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- Septal haematoma (swelling of septum blocking up nose)

- Other facial/skull fracture (numbness of cheek, malocclusion of teeth,
trismus (spasm of V), CSF rhinorrhoea, anosia or mental status changes).
Management is with airway security, assessment of related injuries, control of
epistaxis, inspection for septal haematoma and cleaning and suturing of
lacerations. Later, assessment and correct of nasal bone fracture if there is a
deformity.
Haematoma and abscessus septi nasi

So we just touched on this above, here I want to break down the pathophysiology chain:
- Breaking of septum with soft tissue mucosa intact
- Develops subperichondrial hemorrhage with hematoma
- Becomes infected
- Develops to septal nasal abscess
- Cartilage necrosis
- Loss of nasal septum
- Risk of infection spread to cranial cavity
Caused by nasal trauma, nasal surgery, furuncle, sinusitis or rarely, infection from dental
extraction. Diagnostic gold standard is CT, treatment is surgical drainage under local.
Patients present with fluctuant, tender, nasal obstruction (bi or unilateral) as a result of nasal
septum swelling) with localised pain, swelling, fever headache, or perinasal tenderness.
External portion of nose usually swollen, erythematous and tender.
GP NOTEBOOK SAYS: Urgent drainage and firm nasal packaging to ensure

adherence of the perichondrium to the cartilage should be done by specialist. It
should be aspirated immediately or can be incised with aid of local anesthesia.
Complications if neglected include septal abscess and collapse of nasal bridge.
30. Rhinitis acuta
This is the common cold, an the most prevalent infectious disease. Rhinoviruses and
coronaviruses comprise most of the causative agents (others are influenza and
adenoviruses), traminsted by airborne droplet route, cold exposure increases susceptibility.
Incubation 3-7 days.
Symptoms:
- Dry stage - malaise (lethargy, headache, fever) and local nasal discomfort in nose
- Catarrhal stage - watery, serous nasal discharge and mucosal swelling causing nasal
obstruction (mostly thanks to the cochlear).
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The virus damages the mucociliary transport system, hampering normal secretion clearing,
this in turn causes inflammatory changes, along with the viral damage to the mucous cells.
Treat with supportive, decongestive measures, Antibiotics only in cases of bacterial

superinfection.
GP NOTEBOOK SAYS: Avoid ABs as 80% resolve in 14 days without any marginal
benefit. Use analgesia, consider 7-day delayed or immediate ABs when purulent
nasal nasal discharge. If using ABs, use amoxicillin (500mg) or doxycycline 200mg
than 100mg
31. Rhinitis chronica
Can be specific or non-specific. First we will consider nonspecific.
Can be caused by:

- Recurrent acute inflammations with progressive mucosa damage
- Due to anatomical changes (septal spur, septal deviation)
- Nasal lesions (polyps, tumors)
- Environmental factors (air pollutants)
Symptoms show chronic nasal obstruction with nasal discharge and frequent throat clearing
with occasional hoarseness.
Treat by eliminating irritants, or correcting anatomical change. Supportive measures as with

acute rhinitis.
Specific chronic rhinitis can have a range of causes:

- Tuberculosis - can involve nasal mucosa as primary infection. Look for lupus vulgaris
(painful skin lesions around face, nose and eyelids) as well
- Sarcoidosis - granulomatous systemic disease of unknown etiology, lymph nodes,
lung, joints and skin mostly affected, although nasal symptoms can present.
Characteristic skin changes to external nose (lupus pernio) resemble chilblains
- Fungal infections - more common in immunocompromised patients
- Other diseases include Rhinoscleroma, Actinomycosis, Syphilis and Malleus
It is worth mentioning here, that both chronic and acute rhinitis often come with sinusitis as
the swelling of the mucosa prevents adequate sinus drainage, therefore encouraging sinus
inflammation.
32. Ozena
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Ozena is a disease of the nose where the bony ridges and mucous membranes waste away,
also known as atrophic rhinitis.
Characterised by pronounced dryness of nasal mucosa, sever cases are marked by a fetid
nasl odor (not perceived by patient due to olfactory damage). Has a primary and secondary
form.
Etiology of primary form is unknown, while secondary form can be a result of prior tumor
resection, excessive nose drop use, drug abuse (cocaine) or radiotherapy for nasal and
sinus tumors.
Diagnosis via endoscopic examination which reveals a broad nasal cavity lined with dry
crusted mucosa. Treat with saline nasal douche and ointments, decongestants
contraindicated. If problem continues, surgical intervention may be required.
33. Sinusitis maxillaris - acuta, chronica and odontogenica
Sinusitis usually develops along with rhinitis. The book deals with frontalis and maxillaris
together, so we shall do so here, only adding specific detail for the frontal sinus below.
Note sinus drainage:

- Inferior meatus - nasolacrimal duct drains in
- Middle matus - frontal, anterior + middle ethmoidal and maxillary drain in
- Superior meatus - posterior ethmoidal
- Sphenoethmoidal recess - sphenoid sinus
Acute sinusitis
Etiopathogenesis:
- Acute sinusitis in children generally affects the ethmoid cells
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- In adults, the most frequent is maxillary, then ethmoid, frontal and sphenoid sinus.
Inflammation may be one or many.
- Generally inflammation is from the spread of intranasal inflammation. In additional to
rhinitic etiologies, H. influenza and S. pneumoniae are important causative agents.
- Note, individual anatomy, immune status and causative agent all play a role in
the likelihood of infectious spread to the sinuses
Symptoms
- Variable headache, pain more intense over sinus, which worsens when bending
over.
Diagnose with rhinoscopy or nasal endoscopy to view pus tracking along middle meatus of
nasal cavity. Sinus radiographs may also show partial opacification of affected sinuses.
Treat with conservative therapy (decongestants, antibiotics, heat therapy, inhalation of

chamomile or sage) first, and possible surgery later
For the Maxillary sinus, a sharp puncture through the inferior meatus is possible, or a blunt
puncture via the maxillary sinus ostium in the middle meatus
Chronic sinusitis
Aside from anatomical deviations (e.g. septal spurs) causative agents may be allergic,
traumatic or neoplastic. Common pathogenesis is impaired sinus ventilation due to
obstruction, hampering drainage. This is particularly a problem for the maxillary sinus and
anterior ethmoid cells.
The symptoms are the same as acute, just for a long time, with the addition of
nasopharyngeal drainage (post nasal drip). Diagnosed with CT scanning, for treatment, see
acute sinusitis.
Odontogenic sinusitis
This is an instance of dentogenic (arising from the teeth) sinus infection, where an infection
of a dental root. These may be responsible for up to 20% of maxillary sinus infections. Such
infections can then spread to the orbit, or the ethmoid sinus.
It occurs when the Schneiderian membrane is violated by conditions arising from the
dentoalveolar unit. The key distinguishing features of such sinusitis is the presence of a foul
taste and/or smell, which should encourage CT examination for evidence of dental
abscesses.
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Recommended treatment is functional endoscopic sinus surgery (FESS), a minimally

invasive surgery which uses nasal endoscopes to enlarge the nasal drainage pathways of
the sinuses to improve sinus ventilation.
34. Sinus frontalis - acute and chronic
For all details on acute and chronic sinusitis see 33.
Frontal sinus treatment can be via a Beck puncture, through the bone at the medial border of
the eyebrow. This can be high risk and is only done with great caution.
GP NOTEBOOK SAYS: For acute sinusitis

- Do not offer AB prescription
- Give advice about managing symptoms, reassess if worsening symptoms
- After 10 days, considered high-dose nasal corticosteroids for 14 days
(>12y.o.)
- Where patients present as systemically very unwell, or have signs of a
serious illness or condition, offer immediate ABs
- Refer to Hx if symptoms show intracranial or orbital complication
35. Deviatio septi nasi
A deviated septum is a congenital or traumatically acquired bending or bowing of the nasal

septum. This is common in mild forms, and non-pathological, but more pronounced
curvature can obstructed nasal breathing and cause olfactory impairment. Furthermore, can
increase risks of sinusitis and epistaxis along with rarerer symptoms including repetitive
sneezing, pain, and loss of smell.
Reminder, the nasal septum is the bone and cartilage that separates the nasal cavity into
two nostrils. The cartilage is the quadrangular cartilage and the bones are the maxillary
crest, vomer and ethmoid.
It is most commonly caused by impact trauma (such as a blow) but may be congenital.
Diagnosis is via external inspection of the nasal base, or a rhinoscopy or endoscopy, which
can verify the morphological changes of the nasal septum. In reality, nasal septum deviation
is only diagnosed where symptoms are present.
Treatment is a choice of surgical straightening (septoplasty), this involves removing the

deviated cartilaginous and bony portions of the septum, and reimplanting them as needed.
Such treatment should only be taken in patients over the age of 18, unless pressing, as such
surgery can damage the growth zones of the septum, causing long term problems.
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36. Mucocele and pyocele
Mucoceles are epithelium-lined, mucus-containing sacs that completely fill a paranasal

sinus. They are caused by the obstruction of the sinus ostium, or obstruction of a mucous
secreting gland (as such sinusitis and rhinitis are often common concomitant conditions).
They are benign, but can become infected (known as pyoceles). Histologically, they are
formed of pseudostratified columnar epithelium with a few ciliated cells, mucus and
cholesterol crystals with a fibrous thickening of the submucosa.
The read danger of mucoceles is the continued growth, due to continued mucus secretion,
which increases pressure, leads to bone devascularization and osteolysis. Presents with
facial pressure and swelling, with dental pain, nasal obstruction and ophthalmic
manifestations. Also possible neurological manifestations such as confusion, meningitis and
CSF leak.
- Ophthalmic manifestation from the Maxillary, Frontal and anterior ethmoids shows
ocular pain with decreased ocular mobility, pushing globe outwards.
- Ophthalmic manifestation from the Sphenoid and posterior ethmoid shows blurred
vision, with symptoms in line with optic nerve compression or compression of ocular
blood supply.
Complications include:
- Vision loss (may be sudden - poor prognosis as this indicates optic nerve damage, or
gradual - better prognosis as this indicates ischemia)
CT scanning best method for identifying issue, treat with surgery (may be open or
endoscopic).
37. Orbital complications by sinusitis
Complications of sinusitis include lesions affecting soft tissues and surrounding bones of the
orbit and intracranial area. Due to the thin lamina papyracea of the ethmoid bone, and the
proximity of the paranasal sinuses with the orbit, spread of infection is not uncommon.
We categorise orbital complications as follows:

- First degree - Inflammatory oedema of the orbit
- Upper eyelid swollen and hyperaemic due to venous blockage from ethmoid
sinusitis. Vision unaffected with full visual motility. Oedema most visible in the
morning.
- Second degree - Orbital cellulitis
- Third degree - Subperiosteal abscess
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- Us forms between bones of the orbit and periorbita (generally lamina

papyracea and periorbita). Limited eyeball movement, pain experienced when
superior medial border of the orbit is touched.
- Fourth degree - Orbital abscess
- Accumulation of pus in retro orbital adipose tissue. A precursor to the below
(cavernous sinus thrombosis). Pain in the affected eyeball, sensitive to touch,
risks the patient's vision.
- Fifth degree - Cavernous sinus thrombosis
- Infection follows veins into the cavernous sinus
We see higher instances of orbital complications in men and young children than in women
and adults.
CT scans are the gold standard for diagnosis, while treatment is surgical with strong
Antibiotic course.
38. Rhinitis polyposa
Rhinitis polyposa (or Polypous rhinitis) is rhinitis associated with polyps in the nasal cavity.
Please see above for rhinitis (Q30), and below for nasal polyps.
39. Polyposis nasi
Nasal polyps are edematous, hyperplastic growths that occur in the nasal cavity, often
growing from anterior ethmoid cells and maxillary sinus.
Causes include genetic and chronic irritation of mucosa (eg. chronic rhinitis, allergic rhinitis).
When the presence of nasal polyps becomes symptomatic, we know this as polyposis.
Nasal polyps are rare in children (only present in cases of cystic fibrosis).
Clinical manifestation depends on level of nasal passage occlusion. If sufficiently obstructed

we can see hyposmia or insomnia, headache, snoring, rhinophonia, loss of smell and
postnasal drainage (which can lead to laryngitis with hoarseness). Typically polyps occur in
both nostrils and can lead to rhinitis polyposa and sinusitis.
Diagnosis via rhinoscopic or endoscopic evaluation of nasal cavity, particularly the lateral
nasal wall where the polyps develop. Treatment is generally conservative (e.g. corticosteroid
nasal sprays with antihistamines), but where severely symptomatic a polypectomy may be
performed.
GP NOTEBOOK SAYS: A unilateral polyp should be assumed to be neoplastic until

proven otherwise, and should be sent to ENT. Management should be the following:
- Test for allergy
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- In children exclude CF with sweat test and meningocele with CT

- Biopsy unilateral to exclude neoplasia
- Either prescribe topical steroids or surgery (nasal polypectomy)
- Beconase (OTC) or Avamys (best in class, can use longer term)
- Systemic steroids may be prescribed by ENT
40. Malignant tumors of nose paranasal sinus
Here we list the key malignant tumors, first the external tumors:
- Basal cell carcinoma
- Peak incidence aged 60-70, most common nose malignancy
- Etiology is genetic and high sun exposure
- Local invasiveness, but does not metastasize, morphologically diverse, show
crusting and string-of-beads margin
- Diagnose with biopsy, treat with surgery
- Spindle cell carcinoma
- Second most common nasal malignancy
- Etiology uncertain, but UV radiation is important
- Unlike BCC, spindle cell carcinoma can metastasize to regional lymph nodes
- Treat with tumor removal and facial reconstruction along with radiation if
required. Neck dissection also advised to remove lymph nodes.
Now we consider the internal tumors. Most of the tumors of the nasal cavity and paranasal
sinuses are malignant, and most are epithelial. It is worth noting that symptoms can be tricky
to spot, especially in the sinus, as they’re well hidden. Suspicious symptoms include
obstructed nasal breathing, bloody rhinorrhea and fetid nasal odor, especially in patients
over 50. The main sites for carcinomas are nasal cavity and maxillary sinus, followed by
ethmoid, frontal and sphenoid sinuses.
- Squamous cell carcinoma
- The vast majority of internal malignant tumors are SCCs. They will be treated
with surgery and post operative radiation, often with extensive excavation and
reconstruction.
Throat
41. Clinical anatomy and physiology of larynx
42. Angina catarrhalis, acuta, follicularis, lacunaris

Angina catarrhalis = Acute tonsillitis with tonsil enlargement
Tonsillitis is a bacterial inflammation of the palatine tonsils, generally caused by viral

infection or group A beta-hemolytic streptococci. Common in children, presenting with pain
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on swallowing which often radiates to the ear, along with reddening and swelling of the
tonsils. Tonsillitis is a type of pharyngitis. Tonsillitis is generally taken to mean palatine tonsil
infection, as opposed to any other type of tonsillitis.
Diagnose with mirror examination, can perform a rapid immunoassay to confirm nature of
causative agent prior to starting antibiotic therapy (penicillin V for 10-14 days, macrolides or
oral cephalosporins alternatives).
Complications can include lingual tonsillitis and streptococcal gingivostomatitis. In chronic

cases, tonsillectomies can be performed to remove the tonsils. There is a predisposition to
tonsilitis in patients who have post-nasal drip.
GP NOTEBOOK SAYS: Treat with rest, paracetamol and fluids. ABs not required for
most (85% of cases resolve in one week). If required prescribe
phenoxymethylpenicillin (500mg 2-4x/day)
Follicular tonsillitis
A form of tonsillitis that specifically affects the follicles on the surface of the tonsil which
become filled with pus. Identified by white spots on the surface of the tonsils.
Lacunaris
A form of tonsillitis where there is inflammation of the mucous membrane lining the tonsillar
crypts.
43. Tonsillitis - virosa, by haematological diseases. Plaut Vincent
Virosa
Etiology
- Adenomas, rhinovirus, coronavirus, herpes simplex virus, epstein barr virus
- Any viral infection of the upper respiratory tract
- (see 42)
Hematological diseases
- Necrotic tonsillitis in leukemia patients
- Deep necrosis of mucosa of tonsils and hemorrhage causing gangrenous
angina
- Can complicate to retropharyngeal abscess, sepsis and ludwig's angina.
Plaut Vincent
An inflammatory disease caused by fusiform rods and spirochetes that presents with
unilateral dysphagia and fetid breath though little malaise. Mirror examination shows
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unilateral, fibrin coated ulcer on palatine tonsil. Causative agents can be detected on
analysis, treatment with Silver nitrate locally usually sufficient to resolve.
Note, differential diagnosis from tonsillar carcinoma.
44. Pharyngitis cronica
Chronic pharyngitis is often caused by chronic exposure to noxious agents, commonly

nicotine in cigarette smoke. Chronic mouth breathing can also increase the risks.
Symptoms include, dry throat with frequent throat clearing and viscous mucous, sometimes
with a sensation of an FB in pharynx. On examination pharyngeal mucosa is red and grainy
due to hyperplasia of lymphatic tissue on posterior pharyngeal wall, may also be shiny
(atrophic form). Additionally, check nasal airways to exclude nasal obstruction as etiology.
Treatment via exclusion of etiological factor, and herbs such as sage or chamomile along
with steam.
45. Tonsillitis chronica
Chronic tonsillitis, the result of multiple bouts of acute tonsillitis, can lead to permanent
structural changes with scaring. The palatine tonsils provide a focus that can sustain a
variety of diseases in other parts of the body (such as rheumatic fever, glomerulonephritis,
psoriasis and others).
Symptoms present with pain, along with systemic features of lethargy, poor appetite, bad
taste in mouth and fetid breath. Diagnose with mirror examination, showing small, immobile
tonsils with peritonsillar redness, occasionally peritonsillar purulents. Tonsillar lymph nodes
(at mandibular angle) may be enlarged. Treatment with tonsillectomy under general
anesthesia.
46. Abscess peritonsillar
A peritonsillar abscess (aka quinsy) is pus due to an infection behind the tonsil. Symptoms
present as fever, throat pain, trouble opening the mouth and changes to voice, pain is
usually worse on one side. Typically caused by bacteria (often following streptococcal
pharyngitis), it is generally a complication of untreated episode of acute tonsillitis which then
spreads to the peritonsillar region. Note, the important thing we’re looking for is swelling,
especially on one side.
The condition has an even age spread (unlike tonsillitis which is predominantly children), and
symptoms appear 2-8 days before abscess formation. Diagnosis based on the symptoms,
while medical imaging may be done to rule out complications.
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Treatment with pus removal, antibiotics, pain medication and possibly steroids.
GP SAYS: Send to emergency (on the day) ENT for drainage and medication.
Complications can include:

- Retropharyngeal abscess (see 47)
- Extension of abscess causing airway compromise
- Sepsis
- Glomerulonephritis and rheumatic fever
- Decreased oral intake
47. Abscess retropharyngeal
UNCLEAR - PROF SAYS ONLY OCCURS UNDER AGE OF 1, BOOK AND OTHERS SAY
CAN OCCUR OF ANY AGE - CONFIRM.
A retropharyngeal abscess is an abscess located in the tissue in the back of the throat
behind the posterior pharyngeal wall (in the retropharyngeal space). They occur deep in the
tissue and as such are hard to diagnose with physical examination, as such observation of
the clinical picture of stiff neck, malaise and difficulty swallowing is the primary early
diagnostic tool. Some form a palpable neck pain, fever, croup like cough and enlargement of
cervical lymph nodes. Following this, x-ray helps to confirm the diagnosis.
Etiology can often be as a secondary complication of parapharyngeal infection, although can

also be from infection originating in nasopharynx, tonsils, sinuses, adenoids, teeth and
middle ear. ???The condition and can occur at any age????
Treatment is a surgical intervention to drain the abscess along with high dose IV antibiotics.
Chronic retropharyngeal abscess is usually secondary to TB and the patient should be
treated for the TB.
48. Abscessus lateral pharyngeal
The lateral pharyngeal space (also known as the parapharyngeal space) is a deep area of
the neck where abscesses can form. The cause of such abscess, is the shifting of an
infection from the pharynx (including tonsils and adenoids), teeth, ear, and other spaces in
the neck.
Symptoms include fever, sore throat, odynophagia and swellings in the neck. Anterior space
abscesses can cause spasm of the jaw muscle, with a hard mass forming along the angle of
the mandible, with bulging of tonsils and lateral pharyngeal wall. Posterior space abscesses
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cause swelling in the posterior pharyngeal wall. Posterior abscesses can involve structures
within the carotid sheath, causing rigors, high fever, bacteremia, neurologic deficit,
haemorrhage and carotid artery rupture.
49. Tumors of mesopharynx

Benign tumors and precancerous lesions
- Relatively rare, generally arise from epithelial and mesenchymal tissues. Can include
fibromas, lipomas, rhabdomyomas, leiomos and chrondromas.
- Leukoplakia are the most common precancerous lesion. Exogenous irritants cause
damage, and in turn can cause cancer. Appear white.
Malignant tumors
- The vast majority are SCCs, 80% located in the palatine tonsils or tongue base (less
commonly the soft palate and posterior wall of the pharynx)
- Etiology is alcohol and nicotine
- Appear clinically silent for a long time, dysphagia and odynophagia, along with fetid
breath and blood tinged saliva are all possible causes.
- Surgical removal is most common solution.
50. Tumors of epipharynx
Benign tumors
- Juvenile Angiofibroma
- Most common of all the benign tumors, which in themselves are rare, almost
exclusively found aged 10-18.
- Symptoms include obstructed nasal breathing, recurrent epistaxis, headache,
and eustachian tube dysfunction
- Diagnose with endoscope to observe vasculated mass.
- Treat with surgical removal
Malignant tumors
Carcinomas of squamous cell origin (Nasopharyngeal carcinoma) account for the majority of
malignant nasopharyngeal tumors (50%). Much less common tumors of this region are
adenocarcinoma, adenoid cystic carcinoma, malignant melanoma, sarcoma, lymphoma and
plasmacytoma.
- Etiology commonly Epstein-Barr virus
- Symptoms include unilateral conductive hearing loss with middle ear effusion. Along
with airway obstruction, recurrent epistaxis, headaches and cranial nerve palsies
later in time.
- Note, any persistent middle ear effusion for long duration in adult without prior
symptoms should be treated suspiciously
- Cervical lymph-node metastasis, often involving nodes at mandibular angle.
- Diagnosed with endoscopy of nasopharynx along with CT to check for metastasis
- Treatment is high voltage radiotherapy, these tumors are highly radiosensitive.
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51. Tumors of hypopharyngeal
Benign tumors
- Considered a rarity, present with dysphagia, regurgitation, or retrosternal pain
- Diagnosis via incisional biopsy, taken endoscopically, under general anesthesia
Malignant tumor
- Almost all are squamous cell carcinomas, as with oral and oropharyngeal carcinomas
there is an etiologic link to chronic alcohol and nicotine abuse
- No early symptoms (so often not diagnosed early), initial companies tend to be
nonspecific including dysphagia and fetid breath odor. Hoarseness is possible, and
dyspnea signifies extension of tumor to larynx.
- Diagnosis from indirect laryngoscopy and endoscopy with biopsy.
- Treat with surgery (often have spread to larynx so laryngectomy required)
52. Clinical anatomy of larynx
So, we covered this at the beginning, but they want us to go through it again, so that's what
we’re going to do. However, I am going to write this from scratch, because I sense it is useful
to have two seperate ways of structuring this.
The skeleton of the larynx is composed of hyaline thyroid cartilage, cricoid cartilage and
arytenoid cartilage, as well as the epiglottis at the top.
The inferior horns of the thyroid cartilage articulate with the cricoid cartilage, which form the
cricothyroid joint. Each of the arytenoid cartilages have an anterior vocal process, which
attaches to a vocal cord.
The base of the arytenoid cartilage articulates with the superior border of the cricoid
cartilage, forming the cricoarytenoid joint, permitting rotation.
The stalk of the epiglottis is attached to the posterior surface of the thyroid cartilage by the
thyroepiglottic ligament. The thyrohyoid membrane extends from the hyoid bone to the
thyroid cartilage, while the cricothyroid membrane connects the cricoid to the thyroid, it is
what is divided in a cricothyrotomy.
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The paired vocal cords (vocal folds) stretch between the vocal process of the arytenoid
cartilage, and are controlled by muscles that make them more or less taught, all are
controlled by the inferior laryngeal nerve, itself a branch of the vagus (this will be
important), except for the cricothyroid, which is innervated by the external branch of the
superior laryngeal nerve (again a branch of vagus). We will consider the important muscles
here:
- Cricothyroid - stretches and tenses vocal ligaments - only one innervated by external
laryngeal nerve.
- Thyroarytenoid - relaxes vocal ligament
- Posterior cricoarytenoid - abductors of vocal cords
- Lateral cricoarytenoid - adducts vocal cords
- Transverse and oblique arytenoids - adducts arytenoid cartilage
When we consider the internal structure of the larynx, we divide the larynx based on relation
to the vocal cords. Above the vocal cords is the supraglottis, between the vocal cords is the
transglottic space, below which we have the glottis and the subglottis.
It is useful to talk about the internal structural division first, as this is how we divide the blood
supply, with the supraglottic and glottic levels being supplied by the superior laryngeal artery
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(from the external carotid) while the subglottic area is supplied by the laryngeal artery
(arising from the subclavian and thyrocervical trunk).
53. Physiology of larynx
The larynx is the organ of phonation, and also serves as an airway. The epiglottis keeps
food and liquid away from the airway when being ingested (via the reflex closure in response
to swallowing). If food does get past the glottic plane, the cough reflex is activated that
protects the lower airways.
The vocal cords are responsible for allowing us to properly phonate, thanks to
vibrations that occur with speech or singing. When we breathe, the vocal cords
are abducted, opening the airway, when we speak, the cords are adducted to
allow the vibrations to occur.
Males and females have different sized vocal cords (males are thicker, and
therefore, have a lower pitch). The vocal cords oscillate by being brought close
enough to each other, so they press against one another, these vibrations are what change
the pitch of a person's voice, and allow us to form words.
54. Laryngitis subchordal
Subchordal laryngitis (or Acute subglottic laryngitis) is a viral inflammation of the larynx in the
subglottic region, and by far the most common cause of croup. Croup is the inspiratory
stridor (high pitched breathing), associated with respiratory disorders, cough, and
hoarseness.
The condition occurs predominantly in infants (6 months - 3 years of age), peak incidence in
spring and fall. The disease develops over 1-3 days during the course of an upper
respiratory viral disease transmitted by viruses.
Voice hoarseness is due to vocal cord involvement, along with a dry, harsh, barking cough
and stridor in the evening hours. Body temperature is only moderately elevated, leukocytosis
is usually absent.
Treatment is airway humidification and fluid intake, generally no need for antibiotics or
steroids, most cases resolve in 3-5 days.
GP SAYS: usually no temperature, usually symptoms of upper respiratory tract

infection followed by hoarseness. No treatment unless persistent after 2 weeks (at
which point they become 2 week rule).
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55. Stenosis acute laryngitis
Acute laryngitis often occurs with upper respiratory tract diseases that descent to involve the
larynx, it is primarily viral, although bacterial superinfection may occur.It is the most common
of laryngeal infections and has no serious consequences. Note, we often drop the ‘stenosis’
part, but this is simply adding that the larynx is narrowed due to the inflammation.
Hoarseness (sometimes with a dry, nonproductive cough) is the most common symptoms,
along with possible dyspnea due to severe mucosal swelling. Diagnosis with laryngeal
inspection which shows redness and thickening or edema of the vocal cords.
Treatment is simply that of voice rest, inhalation therapy, mucolytics and anti-inflammatories
if required. ABs are only prescribed where bacterial infection can be confirmed.
56. Stenosis chronic laryngitis
Chronic laryngitis is defined as acute laryngitis that has lasted more than 3 weeks. It has
slightly different etiologies, commonly:
- Acid reflux
- bacterial/fungal/parasitic
- Chronic sinusitis
- Excessive coughing
- Exposure to irritants/toxins/smoking
- High alcohol intake
- Overuse of voice
Symptoms are all the same as above, although maybe add swallowing problems. Treatment
is the removal of the etiological factor (e.g. if acid reflux is the cause, antacids may be
prescribed, if it is smoking, this should be stopped etc).
57. Tracheotomia
Tracheotomia = tracheotomy. This is an incision in the trachea made to relieve an

obstruction to breathing.
The procedure includes making an incision in the anterior aspect of the neck and opening a
direct airway in the trachea which can serve as an airway, allowing the patient to breath
without the vocal cords, throat, mouth or nose.
There are two types of tracheostomy, acute and chronic forms. The acute form is indicated
for conditions such as severe facial trauma, tumors of head and neck, acute angioedema,
and inflammation of the head and neck, and immovable FBs from the upper airway. Chronic
tracheostomies are indicated in some comatose patients, as well as those who have had
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extensive head and neck surgery. Additionally, in extreme cases of obstructive sleep apnea
a tracheotomy may be required.
A tracheostomy tube consists of an outer cannula (main shaft), inner cannula and an
obturator (used when inserting the tube to guide the placement). May also have cuffs and/or
inflatable balloons at the end to secure it.
The process of the operation is fairly simple, the patient is placed with a cushion underneath
the shoulders, lifting up the neck to make it more prominent. An incision is made into the
trachea, from which the tracheostomy tube is inserted.
Complications include tracheal ring fractures, obstruction of the hole due to mucus
accumulation, and infection.
58. Paralyses laryngis
Paralysis of the vocal cord muscles supplied by the recurrent laryngeal nerves often has
iatrogenic cause (i.e. surgery) as well as idiopathic causes. Unilateral vocal cord paralysis is
commonly associated with hoarseness, while bilateral paralysis is manifested by dyspnea,
often required emergency intervention.
Recurrent laryngeal nerve paralysis - Unilateral

- Typically caused by iatrogenic injury (thyroid surgery), tumor, trauma, nerve
compression, toxic neuritis, viral nerve infection, neuritis, diabetic neuropathy or
idiopathic causes
- Chief complaint is hoarseness - This is because the recurrent laryngeal nerve is
responsible for abducting the muscles of the glottis. When these muscles fail, the
vocal cord partially adduct, but they are not close enough to successfully vibrate
together (=hoarseness).
- Diagnosis via telescopic laryngoscopy and imaging
- Treatment depends on cause, if tumor, remove, if trauma, repair, if toxic, remove
toxin etc…
Recurrent laryngeal nerve paralysis - bilateral
- Typical causes include pre existing unilateral recurrent laryngeal nerve paralysis and
both nerves affected by one of the unilateral causes specifically common is iatrogenic
nerve injury (especially thyroid surgery)
- Chief complaint is dyspnea, due to the fact that both vocal cords adduct and
therefore largely close the airway.
- Diagnosis via telescopic laryngoscopy, which shows fixed centrally positioned
- Treatment is often surgical, as we must open the airway to allow for breathing
ENT - 2018
Superior laryngeal nerve paralysis

- Generally less frequent than recurrent laryngeal nerve paralysis, motor symptoms are
limited. The only muscle it controls is cricothyroid muscle, its loss will be noticed only
by those who sing/speak a lot (looking at you Suzy!). It will cause the vocal cord on
that side to appear flaccid.
- A more serious concern is the lack of sensory innervation to the supraglottic region,
which can cause dysphagia with aspiration.
Vagus nerve paralysis
- Vagus nerve lesion are much less common that laryngeal nerve paralysis, possible
causes can be intramedullary or extramedullary. Intramedullary include congenital
causes, inflammatory causes (e.g. poliomyelitis), central vascular (e.g. stroke),
brainstem tumors and disseminated encephalomyelitis. Extramedullary include
tumors in jugular foramen, basal skull fracture, vagus neuromas and trauma
- Symptoms are basically superior laryngeal nerve paralysis + recurrent laryngeal
nerve paralysis, as these are both branches of the vagus nerve. So, dysphagia,
dysphonia, risk of aspiration, hoarseness all risks (depending if unilateral or bilateral).
- Diagnose with telescopic laryngoscopy
- Treatment depends on etiology
59. Benign tumors in the larynx

- Vocal cord polyps
- Affects adults in speaking professions, mainly males
- Commonly caused by over use of voice, examination shows mucosal
hyperplasia with inflammation, mostly unilaterally on the free edge of the
anterior two-thirds of vocal cords
- Symptoms show as hoarseness
- Diagnose with telescopic laryngoscopy and treat with removal
- Cysts and Mucoceles
- Common in older patients, originate in mucosal glands of the laryngeal
mucosa. These are retention mucoceles or extravasation mucoceles
(remember mucocele = swelling like a sac). These swellings are lined by
respiratory epithelium
ENT - 2018
- Manifestation depends on size and location of lesion, may be hoarseness and

globus sensation.
- Diagnose with telescopic laryngoscopy and treat with removal
- Papillomas and laryngeal papillomatosis
- Papillomas are the most common benign laryngeal tumor for children (age 2-4
most common). In children characterised by multiple lesions that also spread
to trachea and bronchial system
- Histologically, these are neoplasia, causative agents are the human
papillomavirus (6 +11 most common).
- Initial symptoms are hoarseness and inspiratory stridor (high pitched noise on
inspiration), aggressive growth may cause dyspnea.
- Diagnose with telescopic laryngoscopy and treat with CO2 laser surgery.
- Vocal nodules
- Often occur due to overuse of voice, and as such common in singers and
speakers.
- Nodes form bilaterally, at opposing sites at the junction of the anterior and
middle third of the cords. Histology shows fibrosis with epithelial thickening.
- Symptoms include hoarseness, diplophonia and sensation of an FB
- Treat with voice therapy, and surgical indication if required.
ENT - 2018
60. Carcinoma laryngis
OK, buckle up, this is a long one! So, laryngeal carcinoma is the most common head and
neck malignancy, accounting for 40% of them, and 1-2% of the whole lot! The primary
etiological factor is smoking, but alcohol abuse, industrial agents (notably asbestos) and
chronic infections can all increase the risk. (It is worth here reminding ourselves of the
carcinogenic steps first hyperplasia, and hyperkeratosis, dysplasia, carcinoma in situ and
finally, invasive carcinoma).
ENT - 2018
There are a number of premalignant lesions to be aware of, these are:

- Leukoplakia (white patches on mucosa)
- Erythroplakia (red patches on mucosa)
- Pachydermia (thickened epithelium with keratin scales)
60% of laryngeal carcinomas occur in the glottic plane, 40% are supraglottic and less than
1% subglottic. Glottic malignancies have a much better prognosis, partly due to their earlier
diagnosis, and partly due to limited lymphatic drainage. Distant metastasis on all cancerous
types is however unusual.
Symptoms include FB sensation, habitual throat clearing, dysphagia, respiratory distress and
hemoptysis (spitting up blood). Where the cancer is glottic, the cardinal symptom is
hoarseness that persists longer than 2-3 weeks, and all cases should be investigated by
laryngoscopy.
Diagnosis is first via telescopic laryngoscopy, with further ultrasonography of the cervical soft
tissues to detect regional metastasis, CT can also be used for this function.
The primary treatment options are surgery and radiotherapy. We have listed the surgical
options below:
- Voice sparing procedures
- Vocal cord stripping
- Removal of vocal cord epithelium via microlaryngoscopy
- Indicated where cancer is limited to vocal fold epithelium
- Partial or completed cordectomy
- Removal of tumor involved portion of vocal cord
- Indicated in a tumor limited to one vocal cord (T1a)
- More extensive partial laryngectomies
- Tissue resection for bilateral and advanced glottic malignancies
ENT - 2018
- External approach via thyroidectomy incision or microlaryngoscopy

- Indicated in more advanced glottic carcinomas
- Non-voice sparing procedures
- Total laryngectomy
- Complete removal of the larynx with separation of airway and foodway
and construction of permanent tracheostomy
- External approach, indicated where tumor is extensive and cannot be
removed in any other way
Permanent voice change is a common side effect to partial, voice sparing, laryngectomies,
as is difficulty swallowing. In cases where there is a total laryngectomy, there is total loss of
voice, and patients must either learn to use esophageal speech (where the patient swallows
air and forces it out), or use a tracheophone.
61. Clinical anatomy and physiology on the esophagus
The esophagus (oesophagus) is a fibromuscular tube, 25cm, that transports food from the
pharynx to the stomach, starting at the border of the cricoid cartilage (C6) going to T11. The
esophagus contains an internal circular and external longitudinal layer of muscle, the
superior third if voluntary, middle mixed, and lower third smooth muscle only. Food is
propelled through the esophagus via peristalsis (dysruption of this can cause dysphagia).
There are two notable sphincters, the upper esophageal sphincter, of striated muscle,
between the pharynx and the esophagus. It is produced b the cricopharyngeus muscle, it is
constricted to prevent the entrance of air into the esophagus. The lower esophageal
sphincter is at the gastroesophageal junction (T11), and is a physiological sphincter (no
muscle).
Vasculation from the thoracic aorta and inferior thyroid artery in the thoracic region of the
aorta, and the left gastric artery (branch of the coeliac trunk) in the abdominal region.
Venous drainage is into the systemic and portal system (drains to left gastric vein and
azygous vein), making it an important porto-systemic anastomosis connection. Innervation
by the esophageal plexus, a combination of parasympathetic vagal trunks and sympathetic
fibers form cervical and thoracic trunks.
Some clinical relevance to the above:

- Barrett’s esophagus - metaplasia due to chronic gastric reflux as a result of a
malfunctioning lower esophageal sphincter
- Esophageal carcinoma - 2% of all malignancies, causes dysphagia and weight loss,
commonly SCC and adenocarcinoma
- Esophageal varices - portal hypertension causes esophageal varices,
I also want to talk about the physiology of swallowing, there is a voluntary oral phase and an
involuntary pharyngeal and esophageal phase, controlled by reflex mechanisms
ENT - 2018
- Oral phase sees food broken down to a bolus, moved to the oropharynx
- Pharyngeal phase begins when bolus comes in to contact with receptors in throat
(innervated by glossopharyngeal and vagus along with other cranial nerves). At this
point the velum is elevated to close of the nasopharynx, and the larynx is sealed off
by the epiglottis
- The esophageal phase of swallowing beings with a primary peristaltic wave, which is
initiated in response to movement of bolus through the pharynx
GP SAYS: Any patients who present with dysphagia should be referred for upper GI
under the 2 week rule, to rule out cancers. Ask - Any difficulties swallowing? Is food
sticking?
62. Foreign bodies in trachea and bronchioles
FB aspiration happens in children and adults. Adults have a faster epiglottic reflex than
children, as such aspirated objects are more likely to stay in the upper airway, while children
are more susceptible to lower airway foreign bodies.
Oropharyngeal swallowing abnormalities predispose FB aspiration, and are most commonly

found in the right lung than let. Food items are commonly aspirated, with peanuts most
common in children, and tablets in adults.
Symptoms depend on nature of FB and patient. Usually there is immediate coughing fit (with
or without cyanosis, dyspnea, stridor and pain). Larger FBs may impact in the larynx and
cause asphyxiation, whereas smaller objects can get lodged in the larynx and simply cause
hoarseness and phonation.
FBs in the trachea are more dangerous than in the bronchus, and symptoms range from
slight cough to asphyxia and death. If the FB moves with breathing in the trachea, it
produces a tell-tale, palpable impact with an audible click.
Diagnosis should be with inspection, auscultation and radiographs. Chest radiographs at

end-inspiration and end-expiration help ID radiolucent objects. Endoscopies are also
indicated.
Where FB fully obstructed trachea, the Heimlich maneuver can be performed, where only
partial obstruction, endoscopic extraction is recommended.
63. Foreign bodies in oesophagus
Foreign bodies typically lodge in the hypopharynx or upper constriction of the esophagus.
Most patients are small children who swallow things such as coins, but it can also be older
ENT - 2018
patients who have decreased hard palate sensitivity. Symptoms include pressure or pain
sensation in hypopharynx/retrosternal area. Dysphagia may also present.
Inspection and palpation will help with diagnosis, as will mirror examination of the
hypopharynx. If these are inconclusive, imaging can be performed. Treatment should be via
a rigid esophagoscopy without delay to retrieve the FB, in rare cases an external approach
may be required.
The major risk and complication is of esophageal rupture.
The esophagus is the most common site of ingested foreign body impaction!
64. Combustio oesophagus
This question is asking about acid and alkali burning of the oesophagus. Alkaline materials
account for most caustic ingestions in western countries, while acids are more common in
developing countries due to availability.
Acids cause coagulative necrosis, with eschar formation (formation of dead tissue cast of
from surface) that may limit substance penetration and injury depth.
Conversely, alkalis combine with tissue proteins and cause liquefactive necrosis and
saponification, and penetrate into deeper tissues, helped by higher viscosity and longer
contact time in the esophagus. Alkalis are also absorbed and lead to thrombosis in the blood
vessels, impeding blood flow.
With both strong acids and alkalis, there may be higher incidence of systemic complications
such as renal failure, liver dysfunction and DIC with hemolysis.
Injury can being in minutes and may persist for hours. Injury is initially marked with necrosis,
swelling and hemorrhagic congestion. As time goes by, ulceration occurs, which may cause
perforation if the ulcer transcends the muscular plane. Following this, we have scar
formation, which can impact esophageal motility.
Acute management is usually conservative with hemodynamic and airway stabilisation. Milk
and activated charcoal are contraindicated, and weak acids or bases are not recommended
due to risk of exothermic reaction. Generally, ICU and nutritional support are the main early
treatments.
Patients with perforation obviously require surgery, as may areas of significant necrosis.
Steroids and ABs may be indicated in the long term, as may esophageal stents, which
prevent the scarring from constricting the oesophagus.
ENT - 2018
65. Specific diseases in ORL
Apparently, this is asking about Tuberculosis!
Like pulmonary TB, ENT localizations are increased due to immigration, poverty,
immunodeficiency and drug addiction. They are clinically primitive forms and affect young
people with a slight prevalence among females. Lymph gland localizations are the most
common.
Extra pulmonary TB represents 25% of overall morbidity, there are three clinical types of
extrapulmonary TB:
- Clinically primitive (first clinical expression, lacking any previous morbid outbreak in
pulmonary area)
- Clinically secondary (extrapulmonary morbid conditions following overt pulmonary
process)
- Late phenomena of earlier TB process
Localisations in the cervico-cephalic region are among the most frequent, with approximately
90% affecting the latero-cervical lymph glands, and others affecting the larynx, Tonsils, oral
cavity, middle ear and nose.
Presents generally as lymphadenitis (where lymph nodes affected) but can also appear as
unresponsive ulceration of mucosa (in nose, mouth or gums).
Treatment should be combined therapy of isoniazid, rifampicin and ethambutol.
66. HIV/AIDS in otorhinolaryngology
HIV (human immunodeficiency virus) infections can produce no clinical symptoms for a long
while, however, after time, symptoms develop.
Most otolaryngological manifestations of HIV are due to a range of etiologies, neoplasms or

primary neurologic disorders. Here we will list some of the most important ORL conditions
associated with HIV.
Oropharyngeal candidiasis
- Candida are a normal part of the human oral cavity, but as the immune system
weakens, candidiasis, where the candida fungi grow uncontrollably, can occur.
- It appears as whiteness on the tongue, the classic form is pseudomembranous
candidiasis. The white patches that appear can be wiped away to reveal reddened
mucosa.
- Can often be associated with angular cheilitis
- Presentation in patients is a strong indicator of immunocompromise
ENT - 2018
Kaposi’s Sarcoma
- Most common malignancy associated with HIV, often the first manifestation of HIV. It
is a pink/purple, non tender, raised lesion that can appear on the oral or nasal
mucosa.
Non-Hodgkin's lymphoma
- Second most common malignancy associated with HIV. Lymphomas may occur as
multiple ulceration or edema lesions in the oral cavity. Onset is sudden and cause no
pain and grow quickly.
Herpes simplex virus type 1
- Recurrent intraoral HSV outbreaks can occur, with outbreaks of vesicles that rupture,
producing small, painful ulcerations that may coalesce.
Herpes zoster
- Reactivation of varicella zoster virus can occur on trigeminal nerve, triggering intra or
extra oral presentation along branches of the nerve
Epstein-Barr
- May cause thickening of epithelial cells of tongue, causing hairy leukoplakia lesions.
- Presents as white lesion on lateral border of tongue that cannot be wiped away.
Chronic sinusitis
- Frequent in patients with immune deficiency caused by HIV
- Has a much wider range of causative agents than normal sinusitis.
Otitis media and externa
- Both occur with much greater regularity than in the overall population
--------------------------------------------------------------------------------------
List of practical exercises

1. Hearing tests
a. Whisper test
b. Tuning fork tests
c. Audiometry (know how to read)
2. Eustachian tube tests
3. Otoscopy
4. Anterior rhinoscopy
5. Posterior rhinoscopy/hypopharyngoscopy
6. Nasopharyngoscopy
7. Indirect laryngoscopy/hypopharyngoscopy
8. Vestibular tests
a. Test for Nystagmus
b. Statokinetic tests
ENT - 2018
Hearing tests
Can be accumetric (using natural voice) or audiometric (artificial nose). We judge loss of
hearing as follows:
- Less than 30 dB loss - normal
- 30-60 dB loss - mild loss
- 60 - 90 dB loss - severe loss
- More than 90 dB loss - deafness (indicated for cochlear implant)
First, some subjective hearing tests.
Whisper test
- Examiner stands at arms length to side of patient and whisper (at end of exhalation)
numbers.
- Walk further away until patient is no longer able to repeat the numbers
- Repeat sequence on other side of patient
- Start with ‘best’ ear
Tuning fork tests

- Weber test
- Place activated tuning fork on forehead of patient
- Webber then lateralises or equal
- If lateralises, conductive hearing loss in that ear, if equal then either equal
loss of hearing in both ears or normal hearing
- Renner test
- Place active tuning fork on mastoid behind ear
- When patient can no longer hear, move fork in front of ear, they should then
be able to hear the fork again.
- In they cannot, conductive hearing loss.
- Schwabach test
- Test bone conduction of patient in comparison to patient.
- Place tuning fork behind ear, when patient no longer hears, place behind ear
of doctor, if doctor cannot hear, normal, if doctor can hear, abnormal.
- Jelly test
- Test for otosclerosis
- Place Tuning fork behind ear, then place balloon in external ear canal and
increase pressure.
- In normal patient, increased pressure should decrease sound heard, in
otosclerosis patient, no change of sound.
Audiometry
Two lines, bone and air conduction, air conduction usually better by 40 dB, but should be
compensated for by the machine, as such we expect the two lines to run parallel (as above).
ENT - 2018
- Where both lines lower, mixed hearing loss

- Where air lower - conductive hearing loss
- Where bone lower - sensorineural loss
Objective hearing tests

- Evoked response test
- EEG of the brain, to detect if sound triggers
neurological signals (Auditory brainstem
response test - ASR).
- Otoacoustic emission testing
- Detects faint sounds made by hair cells in
response to sound
- Electrocochleography
- Checks cochlea for signs of electrical activity in
response to sound
- Tympanometry
- Detects normal movement of ear canal
- Children detecting unusual noises and move head towards stimulus
Eustachian tube tests
Subjective
- Valsalva test
- Close nose and blow - if eustachian tube is functioning there will be ‘pop’ in
middle ears
- Toynbee test
- Close nose and swallow - if eustachian tube is functioning there will be ‘pop’
in middle ear
- Polytsa test
- Blow balloon in one nostril, with other closed, patient makes ‘ooo’ sound at
the same time, should detect change in middle ear pressure.
Objective
- Tympanometry (to create tympanogram)
- Device plays noise into ear, mic detects rebound noise.
- Energy peak should be where the middle ear pressure is, this should be at 0
atms (equal with outside atmospheric pressure). Higher or lower indicates
eustachian tube dysfunction, if a flat line, indicates fluid in middle ear or
otosclerosis. (below shows normal tympanogram)
- Note, y axis can be energy or compliance!
ENT - 2018
Otoscopy
Done
Anterior rhinoscopy
Using nasal speculum, this is to observe nasal polyps and any inflammation of the mucosa
as well as tumors. Insert closed, parallel to the line of the mouth, then open and tilt head
back. Use opposite hand to nostril (when examination left nostril, hold speculum in right
hand etc).
Mesopharyngoscopy
Basically, looking at the back of the throat! This is to look at the palatine tonsils, the soft
palate and Waldeyer’s ring. Use the tongue depressor (holding like a pen) and have the
patient breathing through the mouth, and then observe the back of the throat with mirror
light.
Posterior rhinoscopy/epipharyngoscopy/Nasopharyngoscopy
Test to observe epipharynx. Depress tongue with tongue depressor (ensure patient is
breathing through mouth), then insert small mirror behind and underneath soft palate and the
uvula. From here you can observe the epipharynx in the mirror. Before you place the mirror
in the mouth you should warm it over a flame, as this prevents humidifying of the mirror.
Indirect laryngoscopy/hypopharyngoscopy
This test looks at the larynx. The larynx is the organ of phonation, connecting the
hypopharynx with the trachea. It is covered by the epiglottis, below which are the vocal folds
(vocal cords). We observe for inflammation, tumors, nodules, paralysis etc.
ENT - 2018
Indirect laryngoscopy uses a middle sized mirror, directed downwards (unlike posterior
rhinoscopy). The tongue should be grasped between middle finger and thumb, with top lip
lifted up. Then insert the mirror as far as the uvula, from where you should be able to
observe the larynx. Have the patient breathe through their mouth first, and then make an
‘oooo’ noise. This allows you to test the mobility of the vocal cords.
Note above regarding mirror (should be warmed, and held like ball point pen).
Vestibular tests
Tests for nystagmus

- Naked eye test
- Fix px head and ask to follow pen, left, right, up and down (no more than 40
degrees) and observe any nystagmus
- Frencal glasses
- Glasses which enlarge eyes with light, remove possibility of fixation which
compensates for nystagmus
- Can perform Dix Hallpike maneuver simultaneously.
- Videonystagmography
- Attach glasses which video eyes to observe any nystagmus
- Caloric tests
- Inject hot/cold (7 degrees different from body temperature) air/water into ear,
which causes current of endolymph and triggers nystagmus
When observing nystagmus observe the following:

- Direction of nystagmus (which direction is fast phase is the direction of nystagmus)
- Frequency
- Amplitude
- Synchronicity (well synced between eyes indicates peripheral vertigo)
Statokinetic tests
These tests, used with nystagmus tests, help identify if px has central or peripheral vertigo.
Where nystagmus is the same side as the patient falling/rotating, it is generally a central
condition, if opposite side, it is peripheral.
- Romberg test
- Eyes closed, feet together, hands up, observe if they fall
- Can make it harder by standing on one leg
- Finger to finger test
- Doctor has both hands out, one finger facing up, px has to touch doctors
fingers with their own, bringing their hands back above their head after each
occasion. First few attempts should be done with eyes open, followed by eyes
closed
- Finger to nose
- Eyes closed, px touches their nose, then doctors finger and so on.
ENT - 2018
- If intentional tremor, central

- If misses nose (dysmetria) peripheral
- Starwalk
- Walk forward 4 steps, then back 4 steps, eyes closed all the while.
- 30 degree rotation is ok, more than this suggests pathology (remember, rotate
in direction of nystagmus suggestive of central, opposite side suggestive of
peripheral)
- If px does ‘sailor walk’ (as if they had massive balls) this suggests bilateral
dysfunction
- Fukuda tests
- Eyes closed, arms up, walk on spot with knees up.
- Px should remain on spot with no more than 30 degree rotation.
- HINTs test
- Patient should gently move head 30 degrees while fixating on doctors
nose/forehead before head is rapidly jerked back central. Should see a small
corrective saccade. +ve test shows significant lag with corrective saccades in
both directions, if lag only in one direction, suggests peripheral etiology.
Additional ‘Should Know’ things
- Retropharyngeal abscesses only occur in children under the age of 1. This is

because the lymphoid tissue that sits in this space is reabsorbed by the body after
this age
- How many tonsils are there? 7 (8 if under 1)
- 2 tubercular tonsils
- 2 palatine tonsils
- 2 laryngeal tonsils
- 1 lingual tonsil
- 1 pharyngeal tonsil (under 1)
- Dosage of corticosteroids
- 2-5 mg/kg weight of methyl prednisolone to be prescribed for laryngeal edema
- Dosage of ABs
- Most common antibiotic is Amoxicillin
- 100 mg/kg weight in children
- 2-3g/day in adults

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ENT - 2018

​ asic Otorhinolaryngology 2nd E.d​.

Borders of the middle ear

Bones of the middle ear

Mastoid Air Cells

- Located posterior to the epitympanic recess, a collection of air-filled spaces in

A = Normal, B = OM with effusion (note reflection is dot shaped showing

2. Clinical anatomy of the inner ear

3. Clinical physiology of hearing

Sound transmission in the middle and inner ear. Organ of Corti

Central sound transmission

4. Clinical physiology of vestibular system

5. Non Inflammatory diseases of the outer ear - othaematoma, wax, foreign

Othaematoma (haematoma of the auricle)

NICE SAYS: GP surgeries or community clinics should offer to remove earwax if it

Foreign Body (F.B.)

6. Inflammatory diseases of the outer ear - otitis externa circumscripta et diffusa,

- Otitis externa diffusa = diffuse involvement of the auditor canal

Generally caused by bacterial infection following trauma, most prominent pathogen is

GP NOTEBOOK SAYS: Treatment should focus on eradicating Pseudomonas

Eczema auris externa

Pathogenesis based on immune/allergic reaction, can be caused by jewelry, soaps, hearing

7. Otitis media acuta - catarrhalis and suppurativa

- May be viral or bacteria

Chronic suppurative otitis media - Quinolone antibiotic drops (e.g. ciprofloxacin)

8. Otitis media acuta by infectional diseases

I’m considering this covered above.

9. Otitis media in young children

10. Paralysis n. Facilias

Acquired cholesteatoma has two types:

GP SAYS: Often presents as recurrent Suppurative OM which shows no signs of

Treatment often consists of mastoidectomy, with IV antibiotics and the placement of

GP NOTEBOOK SAYS: Antibiotics, determined by sensitivity or organism, ideally

12. Otitis media supp. Chronica-mesotympanic

Etiology may be:

13. Otitis media supp. Chronica-epitympanitis

Can be congenital or acquired, thought to relate to inflammatory processes. Complications

Treatment may require destruction of mastoid and tympanic cavity.

14. Noninfectious diseases on vestibular system (toxic, traumatic, vascular)

Standard vestibular tests

There are a number of forms of nystagmus which we will review:

- Peripheral - result of vestibular dysfunction

It can be useful to induce nystagmus. Methods of doing this are:

head another 90 degrees in same direction. Now px can sit up,

GP SAYS: If sudden acute vestibular dysfunction, might be vestibular neuritis (see

15. Infectious diseases on vestibular system

Infectious diseases of the vestibular system are:

GP NOTEBOOK SAYS: Can trat with antivertiginous medicine (e.g.

Symptoms show progressive hearing loss in one

Diagnosis - conductive hearing loss, normal

GP NOTEBOOK SAYS: Treatment is not essential, especially when hearing loss is

NOTE: ANY UNILATERAL DEAFNESS - REFER UNDER TWO WEEK RULE

17. Morbus Meniere

- Often due to decreased draining of endolymph rather than actual

GP NOTEBOOK SAYS: Surgery reserved for patients with severe condition.

18. Abscessus extradural and subdural

Intracranial complications of otitis media are:

Infection is generally bacterial in origin, although can be fungal, and is as a result of an

19. Meningitis otogenik

20. Sepsis otogenic - thrombophlebitis sinus sigmoidei

Thrombophlebitis is the inflammation of a vein, related to a thrombus (clot). The proximity of

It may develop as a complication of acute suppurative otitis media by thrombophlebitic

asic Otorhinolaryngology 2nd E.d.