Introduction

The specialty of the Ear, Nose and Throat (ENT) system is relatively young compared to certain medical
practices. Even to function as a unified discipline, pioneers of the specialty had to wage a protracted
struggle to surmount considerable hindrances. Initially confined to managing ear infections alone, the
introduction of surgical intervention skills gradually led the specialty to adapt a unified approach.
Furthermore, with improved technological advances, the specialty‟s horizon for surgical intervention
broadened enabling it to handle disorders of the face, head and neck. As a result, the discipline has
become alternatively to be known as the specialty of Oto-Rhino-Laryngology - Head & Neck surgery
(ORL - HNS).

This specialty deals with a system that:

 Occupies a strategic location at the very entrance of the aero – digestive
tract.
 Performs, among other things, four main sensory functions: hearing,
balance, smell and taste,
 Is very closely related to the body‟s certain vital organs ……… the CNS,
Eyes and major blood vessels destined for the head and neck.
 Frequently encounters most common disorders (20 – 30% of all cases) –
an estimate of a typical primary practice.
The above facts obviously imply that the ENT system plays a very
significant role for the survival of the individual. Therefore, exposure to
and acquiring basic knowledge of the system, would be instrumental to the
young medical practitioners.

Aims
This short attachment course is designed to accomplish the following aims:
 To review essential ENT anatomy and physiology
 To demonstrate the use and application of basic equipments
employed in ENT practice.

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  To show and exercise methods in examining the ear, the nose, the
throat, and the head and neck region.
 To present trainees with commonly encountered ENT disorders.
 To orient trainees with practical approach in the management of
ENT disorders:-
 Planning diagnostic approaches
 Considering most relevant differential diagnoses
 Enable design and initiate appropriate therapeutic measures.
Identify and facilitate referral cases as early as possible.
 To assess how much has been absorbed by the trainees regarding
attitude, knowledge, examination skill, ability to diagnoses and manage
common ENT disorders.
 To stimulate enthusiast pursue the ENT practice.

Objectives
By the end of this brief attachment to the ENT discipline it is hoped that the trainees
will:
 Have refreshed essential ENT anatomy and physiology
 Be well-oriented to symptoms related to disorders of the ENT system and head
and neck.
 Have acquired the ability to differentiate normal from abnormal; and recognize
the nature of abnormality.
 Be able to relate symptoms and physical examination findings to specific
disorders of the ear, nose and throat.
 Be able to:
 Do appropriate investigations to confirm the diagnosis
 Do required basic procedure
 Give primary care treatment
 Design follow ups visits
 Plan referral for specialist‟s care.

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The Ear
1. Structure and Function
Structurally, the ear is considered to have three parts: the external ear, the middle ear
and the inner ear.
1.1 The external Ear
This includes the pinna, the external auditory canal (meatus) and the tympanic
membrane.
1.1.1. The Pinna (Auricle) is made up of a framework if elastic cartilage covered by
skin. It lies between the temporomandibular joint (TMJ) anteriorly and the
mastoid process posteriorly. The covering skin on its anterior surface is
adherent to the perichondrium, but is more loosely attached posteriorly.
1.1.2. The External auditory canal is about 3cm long consisting of an outer
cartilaginous (1/3) and inner bony (2/3) portions. The cartilaginous portion is
covered and lies at an angle to the bony part. The skin over the outer part or
portion contains hair follicles and cerumen (wax) secreting glands.

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1.1.3. The tympanic membrane is the window to the middle ear. It is a translucent
membrane and lies obliquely and is concave on the outside. It is divided into a
small superior flaccida and a larger inferior tensa portions by the lateral
process of the malleus. The main landmark on the tympanic membrane is the
handle of the malleus.
1.2 The middle Ear (the tympanic cavity)
This is an air - containing compartment, connected to the nasopharynx via the
Eustachian tube. The entire middle ear cleft is lined by respiratory mucosa. The
middle ear cleft comprises the eustachian tube, the middle ear cavity, and the mastoid
air cell complex. It contains two elements vital to the conduction of sound to the inner
ear, an ossicular chain and clean, moist warm air. The ossicular chain consists from
outward inward of the malleus (hammer), incus (anvil) and stapes (stirrup). The
handle of the malleus is embedded in the tympanic membrane, while its head lies in
the attic where it articulates with the incus. (Attic is the area of the middle ear cavity
above the pars flaccida). The middle ear cavity is traversed by the cranial VII nerve and
contains two small muscles:
 stapedius and tensor tympani
 Two muco-fibrous tissue recesses: the oval and round windows. Both located on
the medial wall of the tympanic cavity, the round below the oval.
The foot-plate of the stapes rests on the oval window by a mobile circumferential joint.
1.2.1 Important Relations to the middle Ear:
 Medial to the Eustachian tube lies the internal carotid artery.
 Superior to the middle ear and to mastoid is the middle cranial fossa
containing the temporal lobe of the cortex (cerebrum).
 Posterior to the mastoid is the posterior cranial fossa containing the cerebellum
separated from the mastoid by the sigmoid sinus.
 Medial to the middle ear is the inner ear/labyrinth/ separated from it by
cranial VII nerve.
1.3 The Inner Ear (Labyrinth)
The inner ear is embedded in the petrous part of the temporal bone. It is divided into
two functionally separate receptor mechanisms:
The cochlea – the acoustic (hearing) end organ and

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  The vestibule and the three semicircular canals (The vestibule
/equilibrium/) end organ
Morphologically, the labyrinth is divided into a bony and membranous part. The
openings from the tympanic cavity to the bony and membranous labyrinth are sealed off
respectively, by the stapes footplate/the oval window/ and the round window
membrane.
1.3.1 The fluid compartments of the inner ear
The membranous part contains endolymph. Another fluid perilymph, contained in the
bony compartment, encircles the endolymph contained by the membranous part. The
endolymph is a filtrate of perilymph, but has a completely different Na+ and K+
concentrations. The concentration of the Sodium and Potassium ions is believed to be
kept constant by the epithelium of the stria vascularis. The endolymph passes via the
endolymphatic duct to end up in a blind sac… saccus endolymphaticus which lies in
the epidural space on the posterior surface of the petrous pyramid, close to the
sigmoid sinus. The perilymph is the immediate substrate of the cochlea and vestibular
sensory cells. It is formed by filtration from blood and partly by diffusion of the
CSF.
1.3.2 The Mechanism of Hearing
The tympanic membrane vibration, initiated by sound waves striking its outer surface,
is relayed to the cochlear fluid, through the ossicular chain, thereby stimulating the
hair cells. The difference in surface areas between the tympanic membrane and the
stapes footplate (17:1) combined with the lever effort of the ossicles (1.3:1), provide a
transference enhancement of nearly 22.1….. (17x1.3). This ensures sound wave
traversing the cochlear fluid, thus circumventing the mismatch created by the air
to fluid media.
As a result of hair cells stimulation, a nerve impulse is produced in their
neurons. Remember that within the endolymphatic compartment is a
membrane /the basilar membrane/ which supports the hair cells. The hair
cells are connected to neurons. The neurons in turn combine to form the
auditory portion of cranial VIII nerve. Because of the tonotopic representation
of sound waves according to frequencies in the cochlea, the basal ends
respond to high frequencies while the apical ends to low frequencies. Each
frequency in the sound wave thus stimulates a different part of the basilar

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 membrane. The auditory center (auditory cortex) receiving the nerve impulses,
decodes into the sounds we hear and comprehend.
NB: Hearing depends on the fulfillment of two conditions:
 Sound wave conduction from an air medium to a fluid medium and,
 The processing of sound waves by the sense organ, (The Organ of Corti) into the
auditory nerves, then conveyed to the auditory center in the CNS, where they
are categorically decoded!!
1.3.3 The maintenance of Balance (Equilibrium)
The vestibular system (End Organ of Balance) consists of the three semicircular
canals, the utricle and the saccule. These structures have highly specialized hair cells
embedded in a covering cap called cupola. Stimulation of the hair cells generates a
nerve impulse – which occurs when the cap is displaced by acceleration (utricle),
gravity (saccule) or rotation (semicircular canals). These nerve impulses will be
interpreted as movement in the vestibular center – in the CNS.
The most important sensory input into the balance system, besides the vestibular
system, is vision; but muscle tone and joint proprioception from both the neck and limbs
are also significant.
Regulation of eye movement in response to rotation, Nystagmus, is accomplished by
the vestibulo–ocular reflex (VOR): a complex and extensive link in the brainstem
between the vestibular and occulomotor reflex. (Nystagmus is a physiological response
to rotation). All these sensory information are coordinated by the vestibular nuclei in
the brainstem. From here, there are connections both to the cerebellum and the
cerebrum. The cerebellum coordinates the body’s responses to the changes in
sensory input. The cerebrum is thought to exert some overall control, but
mostly concerned with our awareness of changes.
1.3.4 The Nerves of Balance and Hearing ( Stato-acoustic Nerve)
The vestibular nerve and the auditory nerve constitute cranial VIII nerve. It passes to
the brainstem via the internal auditory canal (meatus), together with cranial VII nerve.
1.3.5 The Facial Nerve
The facial Nerve – cranial VII nerve follows a complex path from its origin in the
brainstem, enters the internal auditory canal (meatus) alongside cranial VIII nerve
passes over the cochlea. It then angles backwards in the middle ear towards the

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stylomastoid foramen. Through the foramen, it exists from the temporal bone to enter
the parotid salivary gland where it divides to innervate the muscles of facial expression.
During its complex course injury or any pathological disorder may lead to its
dysfunction. In such cases functional testing of its various branches may help localize
the injury sites:
 The greater superficial petrosal nerve transmits secreto-motor fibers to the
lacrimal gland.
 The chorda tympani nerve transmits secreto-motor fivers to the submandibular
salivary gland and sensory fibers from the anterior 2/3 of the tongue.
 The motor nerve fiber to the stapedius muscle, involved in stapedial reflex.
2. Examination of the Ear
Examination of the ear may sometimes be a very challenging task, more so when
examining young children and certain grown-ups under stress. So adapting a step-
wise and systematic approach with cool temper is advisable.
Step 1: Begin by obtaining brief medical history pertinent to the presenting
complaints.
Step 2:- Observation :
General examination of the head from the front: Focus on the ears. Are both ears in
normal position? Low set and anteriorly displaced ears represent congenital
abnormalities. As there may be other more significant abnormality features:
View from the sides. Focus on the ear. Are both ears normal? If no, what is the
abnormality?
Step 3:- examination of the external ear
(Normality is determined by exclusion of abnormality)
 Deformity ……. Congenital
…….. Acquired – old or recent
 Inflammatory swelling …… Mastoiditis …? abnormal middle ear
……Lymphadenitis …. Normal middle ear
 Surgical scars: …………….? Mastoidectomy, tympanoplasty
Step 4:- Examination of the Ear Canal
(Normality is determined by exclusion of abnormality)
 Look for foreign body, cerumen impaction.
 Infection …. Otitis externa …. Is it localized or generalized?

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  A defect in the posterior canal wall.
 Others: exostoses, hyperkeratosis; stenosis or adhesion
Step 5:- The tympanic membrane
(Normality is determined by exclusion of abnormality)
 Inflammation: As in acute otitis media
 Retraction: As in otitis media with effusion/OME/
 Perforation: As in post-trauma. Active chronic otitis media – (CSOM)
 Inactive chronic otitis media - (CNSOM)
 Scarred tympanic membrane – a perforation healed by scarring
 Others: uncommon conditions – uninfected cholesteatoma.
Step 6:- The Hearing… preliminary assessment
 Normal hearing: Accurate response to whispered voice test – delivered at a
distance of >150cm
 In cases of abnormal Response
 Normal speech voice – when delivered as a distance of indicates moderate
hearing impairment.
 Loud speech voice – severe hears impairment.
 Tuning fork (512 Hz): to distinguish the hearing impairment
whether conductive or sensor neural.
 Assessment of Hearing in babies should commence as early after
birth as possible:
 Few weeks of age... blinking, listening to noise
 At about six months: Turning head to localize the source of round.
 At a 9 month: babbling and making other noises.
 At 1 year: responding to familiar words
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 As 1 years: picking up or pointing to things
2
 At about 2years: ability to hear soft music
Disorders of the Ear
Ear disorders are better considered according to the anatomic classification, as this
enables thorough and systematic coverage:
The External Ear
Pinnal Deformity

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Congenital:-
Minor: - minor prominance (bat) ears
-Pre-auricular sinuses (pits)…. debris may accumulate and if
infected abscess may form that requires excision and drainage.
Major: - Microtia severe deformity of pinna and stenosis or atresia of the canal. These
may result in conductive hearing loss (CHL). If bilateral, urgent
intervention is required.
Acquired: - Lacerations, burns, etc .may produce defect and scarring.
- Haematoma:- beneath the perichondium – if untreated
causes cauliftower ear deformity. Haematoma should be
incised evacuated.
- Trauma involving the canal may cause fibrotic stenosis. As
this interferes with the normal epithelial migration out of the
canal, debris accumulates, acting as a focus for infection. If
repeatedly manipulated/scratched/,keratin sloughs may
accumulate which may lead to meatal obstruction, keratisis
obturans.
Neoplasm
May be benign and malignant. The most common malignant neoplasm involving the
pinna … basal cell and squamous cell carcinoma (SCC). Any persistent ulceration has
to be suspected!!
Ear canal
Impacted wax (cerumen):- Having some wax in the external part of the ear canal is
normal. Increased wax accumulation hinders ear canal out- ward epithelial migration,
the self-cleansing action. As ear wax consists of sebaceous and ceruminous gland
secretion, combined with hairs and desquamated skin, its impaction may result in
CHL. Removal maybe accomplished by careful syringing.
Otitis external: may be localized or generalized
Localized … e.g. furuncle
Generalized …with possible complications: cellulites, adenitis, perichondritis,
necrotizing otitis externa. The cause could be infection: bacterial, fungal, viral or allergy
(dermatitis). In a diabetic or immunocompromised patient, pseudomonas infection

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may rapidly spread into the surrounding temporal bone and beyond (necrotizing otitis
externa)

Symptoms & signs relate to the pathological process, its site and the extent.
Symptoms include: itching /irritation/; pain, blocked ear; discharge.
Signs: may be one or a combination of the following: tenderness on manipulating the
pinna or tragus; inflammation and swelling, localized or generalized; accumulation of
debris; purulent discharge; conductive deafness; cellulitis; tender lymph nodes; swollen,
tender and inflamed pinna, ulceration, granlulation tissue.
Treatment: directed at the cause to abort anticipated complications.
This may include:
- Cleaning ……? Syringing
- Installation of:
 Soothing preparations: glycerine/ichthmol, either as drops or
soaked into wool wick gently inserted into the ear canal.
 Antiseptic ear drop.
 Anti–inflammatory – preferably steroid – containing drops in
combination of antibiotics.
 Specific formularies: anti-fungal drops or creams.
NB – Cellulitis requires antibiotics
- Perichondntis : I.V antibiotics
- Necrotising otitis external: High dose specific I.V antibiotics and surgical
debridement.

Foreign Bodies (FBs)

A wide range of FBs (material, shape, size, etc) some how introduced into the ear
canal, encountered more often in children. Un-intelligent manipulation may result
in regrettable complications. So, before any attempt to remove:
 Know the nature of the FB – material, shape, etc.

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  Assess its positioning
 Observe any traumatic scratch from a previous removal attempt. Is the
tympanic membrane status known?
 Have the instruments you would like to use ready?
 Inform the patient what you have to do.
The Middle Ear
For a quick appreciation of the overall status of middle ear disorder, reference may be
made to the following summary:
Acute otitis media
 More commonly occurs in young children,1 – 2 years of age; no age
is immune.
 Initiated by cold or viral induced URI
 Secondary bacterial infection: H. infuenzae, Streptococcus pneumoniae,
Streptococcus pyogenes – involving the mucous membrane of the middle ear
cleft.
 Inflammation smalling obstructes the Eustachian tube; middle ear
effusion/empyema/ „bulging‟ the tympanic membrane, which may cause
perforation. Complications more likely to occur if the infection is
trapped in the mastoid air cells.

Otitis Media with effusion

Middle ear effusion develops when the Eustachian tube function is impaired, usually
following an episode of URI/acute otitis media/. Ventilation failure may be due to:
 Mechanical blockage due to tube mucosal edema
 Excess mucus secretion the middle ear mucosa
As a result, any residual air is absorbed, thus creating a negative middle ear pressure
leading to accumulation of mucus. This impairs both tympanic membrane vibration
and the ossicular chain movement, causing a conductive deafness.
In children, natural resolution may be expected, but there are two problems:
 Impairment of the child’s speech and development. Insertion of a ventilation
tube/grommet/ may be required.
 The overstretched tympanic membrane may become atrophic that may lead to
formation of a retraction pocket for cholesteatoma.

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In an adult with middle ear effusion, suspect a tumour in the nasopharynx!!
Chronic suppurative otitis media
Chronic discharging ears classified as active chronic otitis media. Causes include:
 Common causes.
- Chronic suppurative otitis media (CSOM), the usual type
- Cholesteatoma
 The less common causes, like tuberculous otitis media
Reasons of failure to resolve some cases of acute otitis media that have
progressed as far as perforation are:
1. Colonization by colliform bacteria… (Proteus, Klebsilla, Escherchia coli,
Pseudomonas).
2. Certain changes at perforation margins prevent closure of the perforation during
the healing phase: A seal margin created by the squamous epithelium forming a
junction with the mucosal layer.
Thus, the perforation remains open long after the infection is controlled. This is
inactive chronic otitis media.
Chronic middle ear infection with persistent perforation contributes to
conductive deafness. The degree of deafness will be greater when there is:
 Osteitis or erosion of the individual ossicle, or
 Fixation of the ossicular chain by fibrous deposition during the healing phase.
Treatment: - Aural toileting
- Ear drop instillation
-Supplementary antibiotics
NB: The more frequently the ear is cleaned and appropriate ear
drops instilled, the more effective the treatment likely to be.
Cholesteatoma: This is a very destructive middle ear disorder, caused by
accumulation of squamous epithelium and keratin debris in the middle ear. It may
result from a traction pocket of the tympanic membrane or in growth of squamous
epithelium from a perforation margin. It is sometimes described as a result of ‘skin in
the wrong place’. Cholesteatoma is classified as:

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 Epidermoid Cholesteatoma

Congenital Acquired

Arising from epithelial cell rests

in the temporal bone Primary Secondary

(No previous Previous otitis

otitis media) media
Concerning cholesteatoma formation, there are three main hypotheses:-
 The skin may arise from embryonic cell rests derived from surface ectoderm
in the formation of otocysts
 The skin may arise from invasion as invagination of external meatal skin.
 The skin may arise from cell metaplasia.
Whatever, the importance of cholesteatoma is the fact that it steadily increases
in size at the expense of the surrounding tissues.
When the squamous-lined choleteatomas have come in contact with bone, which may
be eroded, the outcome depending on the part involved:
 With the ossicles, conductive deafness
 The facial nerve, facial nerve palsy
 The semicircular canals, vertigo
Treatment: surgery, aimed at eradicating the cholesteatoma and reconstructing
the middle ear sound conducting mechanism.
Mastoiditis
This is a complication arising form middle ear cleft infection with a high risk of
intracranial spread. It may manifest as extra-dural abscess, sigmoid sinus
thrombosis, leayseral tube abscess, cerebellar abscess.
Mastoiditis occurs when the infection is trapped within the mastoid air cell
system/mastoid air cells/ and then spreads into the surrounding bone to cause
osteitis mastoiditis. As osteitis develops, the soft tissue over the mastoid becomes
inflamed, resulting in retro-auricular swelling. This indicates the formation of a sub-
periosteal abscess over the mastoid bone. Abscess formation may also extend
anterioly towards the zygoma, or inferiorly in retromandibular area/Bezold‟s abscess/.

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Treatment: -High dose intravenous antibiotics, preferably a
combination of amoxicillin and metronidazole…? antimeningeal
regimen!!
- urgent surgical intervention to decompress the mastoid
abscess and eradicate the osteitic bone /cortical
mastoidectomy/.

Otosclerosis
In otosclerosis, there is an overgrowth of “spongy” bone in the bony capsule of the
inner ear. When the oval window is involved, the stapes becomes fixed, resulting in
conductive deafness:
 Probably of a genetic origin, frequently seen in European origin, less common in
Asian, almost unknown in the African counter-parts
 Present usually in the 20 to 40 age group
 Occurs usually on one side
 Is occurs in women during pregnancy.
Treatment: Surgical…. stapedectomy; the stapes is resected and replaced by piston-
shaped prosthesis. In case of surgical contra-indication, wearing a hearing aid is the
alternative.

Unusual Middle ear Disease: TB to be considered when the tympanic membrane

perforation is multiple with chronic suppurative otitis media
Middle Ear Neoplasim: is rare!
Benign neoplasim /glomus tumour, a chemodectoma/ may present like pulsatile
tinnitus and an abnormal reddish tympanic membrane.
Malignant neoplasims present with persistent severe pain in an ear full of granulation
tissue.
The Inner Ear
Disorders affecting both cochlea and vestibular components
Trauma: Basal skull fracture (bleeding and CSF leakage from the internal auditory
meatus.
 May transect the temporal bone with disruption of the inner ear to
cause:

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  Permanent Deafness
 Vertigo /compensation may occur/
 Occasional cranial VII Nerve palsy – requires surgical decompression.
 Lesser degrees of head injury may cause Labyrinthine concussion.
Labyrinthitis /perilymph of the inner ear communicates with
the CSF/
 Rare, deafness as a complication may occur
 vertigo may also manifest
Treatment: - Intravenous – antibiotics
- Surgical - to eradicate middle ear disease
- wide exposure of the labyrinth to facilitate
drainage
Acoustic Neuroma /Schwannoma/ Rare

If it occurs, it involves both auditory and vestibular nerves in the intemal

auditory canal, causing sensori-neural deafness and balance disorder /non
specific/
Treatment: - stereo-tactic radiotherapy, or
- surgical excision
Disorder affecting the cochlea:
- Sensorineural deafness /SNHL/
Potential causes: congenital, birth asphyxia, neonatal jaundice,
intrauterine meningitis, ototoxic drugs.
Treatment: – Prevention
- Directed at the cause
Disorders affecting the vestibular system (vertigo)
Causes: - vestibular neuronitis, meniere’s disease, benign positional vertigo,
labrynthitis, vertebro-basilar insufficiency(VBI).
Management: requires understanding the specific nature.
Facial (cranial VII nerve) palsy
In the developed world, its prevalence is about 1:500, majority benign.
Its manifestation as upper and lower motor lesions, is well known.

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  Upper motor Neuron facial palsy occurs as part of a cerebrovascular accident
affecting the motor cortex.
Diagnosis: - “Forehead sparing”
 Lower motor neuron facial palsy
Idiopathic Bell’s palsy: A diagnosis by exclusion. Its variation:
Herpes zoster oticus/RamsayHunt Syndrome/, Shingles.
Lesions erupt in and around the external auditory canal

Treatment: - Directed at the specific cause to secure quick recovery. Delayed

management may end up in residual complications.
For Ramsay Hunt syndrome, Acyclovir is advised.

The Nose and the PN Sinuses

This is considered in three parts: the external nose, the nasal cavities and the PN
sinus, and the postnasal space.
The external Nose
The supporting structure of the nose organized in the shape of a pyramid, consists of
bone, cartilage and connective tissues.
The bony superior portion is formed by the projecting facial skeleton from both sides,
joined by the formal processes at the interior cartilaginous portion consists of the
upper lateral and alar cartilages.

The shape, position and proportion of the bony and cartilaginous components
remarkably influence both the form and cosmetics) harmony of the face as well as the
function of the nasal cavity.
Blood Vessels of the external Nose that are of practical importance:
 Facial Artery and its braches
 Dorsal Nasal Artery, a branch of the ophthalmic a. Profuse bleeding from
these vessels occurs following trauma, accidents or surgery.
The angular vein: A retrograde infection from a furuncle of the upper tip of the nose,
may spread via the ophthalmic vein to the cavernous sinus, causing cavernous sinus
thrombosis.
Nerve supply to the External Nose

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Sensory supply: 1 to 2 branches (divisions) of Cranial V Nerve
Motor: cranial VII nerve
The Nasal cavity
The interior of the nose is divided into two cavities by a median partition, the nasal
septum. Each cavity opens anteriorly through the vestibule at the anterior nares and
posteriorly, it communicates with the nasopharynx through the choanae.
The nasal vestibule contains hair/ vibrissae/ bearing skin. The vestibules are
separated by the columella, which forms the front end of the nose. The nasal cavities
are lined by ciliated respiratory mucosa, containing mucus secreting glands which can
produce 750ml of mucus daily. This mucus blanket has both protective and cleansing
functions and is continuously moved by the activities of cilia, the ciliary’s action
The Nasal septum has a cartilaginous skeleton anteriorly and a bony component (
) posteriorly and it is covered by adherent mucosa, with prominent blood vessels in its
anterior-inferior 1/3 portion, „Little‟s area‟, a common site for nosebleed/Epistaxis/.
This is also a site for vascular anastmosis/Kiesselbach‟s Plexus/.The septum is often
deviated to one or both sides. This may follow trauma, at birth or later in life. It may
also be developmental. Such a deformity may need correction /septoplasty/.
The lateral Nasal wall
Each lateral nasal wall of the nasal cavity consists of three bony projections, the
turbinates, arranged roughly in a staircase fashion. Going from below upwards, they
are the inferior, middle and superior turbinates. Each is covered by a thin mucous
layer, beneath which there is a rich vascular plexus which act as erectile tissues
acting under
The Autonomic Nervous System Control: sympathetic stimulation causing
vasoconstriction and parasympathetic stimulation causing vasodilatation.
The turbinates increase the surface area for the air conditioning function of
the nose: warming and humidification of the air during breathing.
The inferior turbinate is the largest of all. Beneath each turbinate, is a trough-like
opening, called a meatus/plural meati/. The most significant of all is the middle
meatus, because into it drain/ empty many of the PN sinuses. The nosolacrimal duct
opens anteriorly into the inferior meatus.
The olfactory epithelium is situated above the superior turbinates in the roof of the
nose. This serves are the primary site for olfactory perception. Remember that for

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olfaction to occur. the scent containing particles must reach the olfactory epithelium.
What is unclear is what mechanism actually stimulates the olfactory /Cranial –I/
nerve.
The Nasal cycle: For unknown reasons, the mucosa over the turbinates swells and
shrinks. In addition, the degree of patency or obstruction of normal nose varies even
from hour to hour and side to side. This is known as the nasal cycle.
The PN sinuses
The major portion of the facial selection is some what hollowed out by air containing
cavitations. These are the PN Sinuses, four pairs, one on each side of the face, along
the nasal passages. They are: the frontal, the maxillary, the ethmoidal and the
sphenoidal sinuses. The sphenoidal sinus, the most posterior of all opens into the
posterior aspect of the nasal cavity above the choanae; the others open into the middle
meatus. The anterior group/the frontal, the maxillary and the anterior ethmoids/
drain into a common trough known as the ostiomeatal complex.
Functions of the PN Sinuses
The function of PN sinuses is uncertain; suggestions however include that they
 Lighten the skull
 Resonate the voice
 Strengthen the facial skeleton and
 Act as shock absorber during violent below
The anatomic locations of the PN Sinuses, however, have important influence over the
spread of infections or malignant diseases to neighboring structures:
 Frontal sinus: orbit, anterior cranial fossa, saggital sinus
 Ethmoidal sinuses: orbit (lamina) papyracea and anterior cranial fossa
(cribriform plate) lacrimal sac, nasal cavity
 Maxillary sinus: orbit, infra orbital nerve, teeth, nasal cavity, check
 Sphenoidal sinus: internal carotid artery, optic nerve, cavernous sinus
(containing cranial III, IV and VI nerves) and the 1st and 2nd divisions of Cranial
V Nerve.
The Postnasal Space
This is the space posterior to the nasal cavity and above the soft palate also known as
the nasopharynx. The soft palate which separates it from the pharynx, relaxes to
facilitate airflow and, tightens to close off the space to avoid regurgitation into the nose

18
during swallowing. The adenoids ,when present, is situated centrally in the roof of the
space.
Examination of the Nose
Examination of the nose needs to be conducted systematically and initiated by
pertinent history retrieval. This is followed by a general assessment of the face from
the front, then progressing to the sides and finally reviewing from above, every time
focusing on the nose:-
 Does the nose look abnormal in relation to the rest of the face? If so what is
wrong about it?
 Look for its bony and cartilaginous components for asymmetry, deviation or
depression, hump.
 Check the alar cartilage for asymmetry (cleft lip or palate or deformity)
 Assessment of the interior of the nose (nasal passages) requires a good light
source and a nasal speculum
 Evaluation of the nasal passages include:
1. Symmetry: usually both nasal passages not fully symmetrical the septum is
NOT perfectly central. As long as no breathing disturbance is encountered,
minor asymmetry is acceptable.
2. Nasal mucosa should be assessed for crusts, muco-epithelial debris
3. Continue assessment sequentially including the septum, nasal floor, the lateral
wall, and the nasal roof.
4. Look for secretion or discharge: If there is, what does it look like?
 Watery: consider CSF rhinorrhea
 Clear and mucoid: Viral rhinitis? Allergic rhinitis
 Mucopurulent: Bacterial /pyogenic/ rhinosinusitis
- If unilateral in a child, suspect a FB
- If unilateral in an adult, suspect a tumour
 Blood stained: consider infection, a common cause for nosebleed or a
tumour
5. What does the septum look like?
 Straight: Normal
 Deviated to side one; may be c – shaped, s-shaped. Is there spur?
6. Any mass in the nasal cavity?

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  Nasal polyps, foreign body……
Disorders of the Nose
1. Vestibulitis and Impetigo
The opening to the nasal cavities/the nostrils, or nasal vestibules/ are lined by hair–
bearing skin. It is frequently subject to trauma, predominantly digital, as in nasal
picking. A breech of the skin surface may predispose to localized infection, furuncle in
a hair follicle. It may also ulcerate. If the organism is staphylococci, this may spread to
the surrounding skin (= impetigo). Other conditions encountered in this area include:
- herpes simplex sores
- warts
- malignancy – in adults, in case of persistent ulceration
In general, this area is considered as part of “the danger area” for infection.
Backward/retrograde/ intracranial venous blood flow, via the angular vein, may be
complicated by Cavernous Sinus Thromophlebits.
Treatment: Urgent IV antibiotics
1. Rhinitis: Inflammation of the lining mucosa of the nose with variable degree of
nasal obstruction. Most commonly encountered is viral in origin.
. The most common presenting symptom include:
- Nasal obstruction – due to inflammatory nasal mucosal swelling
- Sneezing – due to irritation to nasal mucosa
- Rhinorrhoea – due to excessive mucosal production with impaired ciliary
function
Types:
 Allergic Rhinitis
 Non- Allergic Rhinitis
 Atrophic Rhinitis
1.1. Allergic Rhinitis
This occurs in individuals exposed to or sensitized by an allergen. They undergo a type
– I hypersensitivity reaction in the nasal mucosa. The allergen bind to IGE on the
surface of the mast cells within the mucosa. This leads to mast cell degranulation and
the release of two kinds of mediators such as histamine. These cause vascular
dilatation and mucosal oedema [nasal obstruction] mucosal irritation [sneezing] and
mucus hyperscretion [rhinorrhoea]. Reflex stimulation of the parasympathetic nerves

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perpetuates the nasal congestion. Late mediators promote migration of eosinophils
into the mucosa. These release substances such as – leukotrienes – responsible for
persistent nasal congestions. The following may serve as a summary:

Allergen Sneezing

Mast cells Histamine Itching

Late Mediators Early Mediator

Histamine Rhinorrhoea
Chemataxis

Eosinophils

Types of Allergic Rhinitis – Two broad types of allergicObstruction

Leukotrienes Rhinitis.
- Seasonal Allergic Rhinitis – predominantly due to pollen dust exposure
- Perennial Allergic Rhinitis – commonly due exposure to house dust mites
and animal dander. Proper history retrieving may assist to distinguish the two.
Further investigations.
 skin prick testing
 Allergy assay
Treatment include:
 Avoidance
 Anti-histamine – for acute reaction
 Mast cell stabilizing agent . . . Na cromoglycate for seasonal rhinitis
 Topical steroid nasal sprays.
 Systemic steroids to ameliorate symptoms
Non-Allergic Rhinitis – This occurs in individuals exposed to irritants like dust,
fumes, vapor pollutants reacting adversely – and with similar symptoms to those of
allergic rhinitis, but with different complaints: dry nasal obstruction. This is known

21
as vasomotor rhinitis, assumed to be due to parasympathetic over-activity. No IGE
elevation, nor could specific allergies be identified
Treatment: is often difficult!!
Rhinitis Medicamentosa
Individuals with persistent nasal congestion tend to abuse the use of nasal
decongestant spray, developing “Rhinitis medicamentosa. In such cases, a reactive
vasodilatation occurs as the effect of vasoconstriction wears off. The tendency to reuse
the spray continues. On further repetitive application, tachyphylaxis results, thus the
chronic mucosal swelling causing continual obstruction.
Atrophic Rhinitis
The cause of atrophic rhinitis – is usually obscure. It is characterized by atrophy of the
nasal mucosa, with crusting. Infection and ulceration of the mucosa beneath the
crusts further damages the mucosa. A foul nasal odor (ozaena) develops.
Treatment:-
 Decrusting and cleansing by irrigating lukewarm saline
 Moistening by use of glycerin/ alcohol solution
 Surgical procedure to reduce the nasal potency
 Selective use of antibiotics.
Sinusitis
Literally, it means inflammation of the lining mucosa of the PN sinuses. It is usually
initiated by a viral rhinitis, seen more frequently in children. The potential do develop
sinusitis is when the drainage channels for the sinuses (the ostiomeatal complex) get
obstructed or when there is impaired ciliary function.
Treatment – includes antibiotics, topical nasal decongestant.
Complications:
Complications related to sinusitis usually due to either to delayed or in- effective
treatment. The main complications include:-
 Orbital cellulitis – mainly from frontal and ethmoidal sinusitis
 Cavernous Sinus Thrombosis – involvement of venous channels,
 Chronic sinusitis – protracted symptoms of nasal obstruction, nasal stuffiness,
mucopurulent nasal discharge or postnasal drip. This is mainly due to
ineffective treatment of acute sinusitis.
Nasal Polyposis

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The etiology of nasal polyp formation is unknown. (Polyp:– a protruding growth from a
mucus membrane). Nasal Polyp more commonly arises from the ethmiod sinuses.
When an edematous reaction in the sinus mucosa causes it to fill the sinus and then
protrude through the sinus opening (ostium), thus expanding within the nasal cavity.
Polyp formation is associated:
- more frequently with nasal allergy, and
- rarely with ASA sensitivity
Polyps most often are bilateral and may have choanal extensions . . . [antro-chianal
polyp].

Nasal polyps commonly cause nasal obstruction and, sometimes, loss of sense of smell
(anosmia), if they obstruct air flow to the olfactory area.

Treatment:
- Systemic steroid augmented by topical steroid nasal spray
- Surgical removal, plus topical steroid nasal spray – [if response to conservative
treatment is poor].
- Sinus surgery – in persistent and/or/recurrent cases
Nasal Septal Deviation
Deviation /deflection) of the nasal septum to either side, is a common finding.
Cause: trauma or developmental
Symptoms: - Nasal obstruction
- Recurrent nosebleed
- Crust formation
Treatment – surgical . . . septoplasty
Nasal Trauma
Trauma to the nose is common problem. It may be blunt and only confined to the
nasal framework or may be part of injury of facial skeleton.
Proper management requires proper assessment of the severity nasal bone injury.
Look for:
- nasal bone fracture: local tenderness, swelling
- skeletal displacement

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In addition obtain a PA and Lateral radiology view of the nasal skeleton. This is for
proper assessment of the displacement. Additional views may better be taken which
will service for future references, training or legal purposes.
Treatment: Depends one the severity, the nature of the deformity.
- Manipulation to re-align the fractured pieces. (close reduction) better done a
week or ten days after the date of the injury----- after swelling has subsided,
before fibrin deposition occurs.
- Rhinoplasty (Open Reduction)
- Nasal packing: – (48 – 72hrs) – to keep reduced parts in place.
- Antibiotics – week/10days.
Choanal Atresia
This is a condition in which the posterior nasal cavity openings fail to develop.
In neonates, if it is bilateral, it is an emergency and requires urgent surgical intervention,
since, neonates are obligatory nasal breathers.
Diagnosis: - Direct endoscopy
- contrast radiogram
Treatment:- surgical – to create the choanal opening
- A stent tube introduced and held in positions for 2 – 3 weeks, to
prevent stenosis.

The Throat, Head and Neck

Functional Anatomy and Physiology

The head & neck is one of the most complex regions. For primary ENT care, it will be
appropriate to limit the discussion to those clinically significant structures within the
upper aero-digestive tract.

The oral cavity – extends from the vermilion border of the lip to the circumvallate
papillae - inferiorly, and the junction of the hard and soft palates, superiorly.
Posteriorly, it is continuous with the oropharynx through the anterior facial arch.

The vestibule of the mouth – lies between the lip and the cheek, and the teeth and
the alveolar process.

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Three significant structures within the oral cavity:

1. The dentition /teeth/: (20 deciduous; 32 permanent)

2. The openings of the salivary glands:

2.1. The Stensen’s duct – for the parotid – on the inner surface of the cheek,
adjacent to the 2nd upper molar.

2.2. Wharton’s dust – for the submandibular gland – in the floor of the mouth
on each side of the frenulum of the tongue.

3. The tongue: Its body separated from its base by a V – shaped terminal sulcus, at
its center being the foramen caecum - a remnant of the thyrglossal duct.

The Pharynx

This is a fibro-muscular tubular organ in continuity with the oral cavity. It is divided
into the oropharynx, the nasopharynx and hypopharynx.

The Nasopharynx This is the space above the soft palate, limited above by the skull
base. It is also known us the postnasal space. The nasopharyx contains the
adenoids and the openings for the eustachian tubes .

The oropharynx: this ill – defined area lies between the nasopharynx above and the
hypopharynx below.

It contains the posterior pharyngeal wall – composed of the prevertebral fascia and the
bodies of the 1st and 2nd cervical vertebrae.

The hypo-pharynx: This portion of the pharynx extends from the upper border of the
epiglottis to the inferior edge of the cricoid cartilage. It opens to the larynx anteriorly.
On each side of the larynx lie the funnel – shaped pyriform sinuses. It is the area of
parting of the air and food passages.

The Ring of Lymphoid Tissues

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A collection of lymphoid tissues encircles the upper aero-digestive tract. This includes
the faucial tonsils, the adenoids the valecullae (lingual tonsils). This ring of lymphoid
tissues is described as the Waldeyer’s ring and is thought to contribute to the
immunologic competence in the early days of life.

The Larynx

The laryngeal skeleton (the hyoid, the thyroid, the cricoid, and the arytenoids)
may be felt in the neck. The laryngeal cavity is divided into – the supraglottis, the glottis
and the subglottis. The leaf-shaped epiglottis projects upwards and is anchored to the
inner surface of the thyoid cartilage where the vocal cords meet anteriorly.

Embryologically, the larynx develops from a two – part anlage.

- The supraglottis – from a buccopharyngeal bud.

- The glottis and subglottis from the tracheo- bronchial bud.

The glootis is formed by the free edge of the true vocal cords /vocal folds/. The vocal
cords include: The vocal ligament, the vocalis /thyroarytenoid) muscle, and the
mucosal covering.

Musculature of the larynx

Two groups of muscle – internal /3-paired/ and a single external muscle act both
synergistically and antagonistically to control the function of the larynx. They open
and close the glottis to put the vocal cords under tension.

Innervations of the larynx.

The nerve supply of the larynx arise from cranial X nerve – the vagus:

1. Superior laryngeal – dividing into:

- sensory /internal/ branch – supplies the interior of the larynx down into the
vagus nerve, and
- motor/external/ branch – to the external crico-arytenoid muscle.

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 2. Recurrent laryngeal nerve.

- provides motor supply to the rest of the ipsilateral intermal laryngeal

muscles and to the contralateral inter-arytenoid muscle.

- Sensory innervations to the laryngeal mucosa distal to the glottic cleft.

NB: -The Left Recurrent Laryngeal nerve (RLN) loops around the aortic

arch to reach the larynx in the groove between the trachea and

esophagus.

- The Right RLN passes around the Subclavian Artery and then runs upward
between the trachea and esophagus

Phonation

Speech production has three phases: pulmonary, laryngeal and oral.

- The pulmonary phase :- creates the energy flow with inflation and
expulsion of air. This provides the larynx with a column of air.

- The laryngeal phase

The column of air provided by the pulmonary phase sets the vocal cords into
vibrations of certain frequencies to create sound.

- The oral /supraglottic/ phase: Modifies the sound so created in the

laryngeal phase. This modified sound represents the unique individual voice.
Words are, thus, formed by the action of the pharynx, tongue, lips and
teeth.

The Swallowing Action

The act of swallowing occurs in two phases: an oral and pharyngo – esophageal
phases.

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The oral phase: Deals with displacing the food bolus backward by the pressure of the
tongue. This is an active /voluntary/ phase.

The pharyngeal and esophageal phase: this is an involuntary /inactive/ phase, and
involves several steps, the most important of which is laryngeal elevation as this
protects the airway against food entry.

To sum up, the laryngeal functions include:

- Conduit for respiratory exchange
- Sphincter to avoid aspiration
- A reflex protective mechanism
- Voice production
- Thoracic fixation for effort

The sense of taste

The basic taste sensations are sweet, salty, sour and bitter. All other tastes are
mixed sensations in which smell sensation is also integrated.

The sensory organs for taste are the taste buds found mainly in the lingual papillae
(vallate, foliate, fungiform) and the remaining scattered in the hard palate, posterior
pharyngeal wall, the buccal mucosa, etc.

These fine gustatory hair cells must bath in saliva or other fluid to allow the sense of
taste to be evoked .

The sensory innervations for the perception of taste is provided by:

- The chorda tympani, arising from Crania N VII.

- The lingual nerve, from Cranial Nerves V and IX. (Trigeminal &
Glossophayngeal).

The salivary Glands

There are 3-paired major and numerous minor salivary glands.

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The major paired salivary glands are:
- The parotid
- The submandibular and
- The sublingual

The minor salivary glands – estimated to number >100 – 1000. They are scattered in
the mucosal layers of the aero-digestive tract.

About 100 – 1500ml saliva are secreted daily, 90% being water. Physical, chemical
and mental states influence salivary production.

Embryologically, the major salivary glands arise from solid ectoderm cell accumulation
of the foregut, between the 4th – 8th weeks of gestation. The ducts become patent in the
22nd week of intrauterine life.

The following table demonstrates certain features of the individual major salivary
gland:

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Characteristic Features of The Major Salivary Glands:

Srl. Distinguishing The Parotid The The Sublingual

No. features gland Submandibular gland
Gland

1. Anatomic On the side of In the floor of the Oral floor

Location the face at mouth mucosa
angle of jaw

2 Duct, orifice Stensen‟s duct Wharton‟s duct, Into

Adjacent 2nd floor of mouth Submandibular
upper molar Gland duct

3 Type of saliva Serous 30% Serous and Mucus 5%

secretion, mucus: 55-65%

4 Size The largest 2nd large The smallest

5 Calculus Less frequent Most frequent Least, if at all

formation

Functions of Saliva:
1) Protective action – on the mouth, upper respiratory tract
2) Assists digestion: lubrication; starch splitting by amylase
3) Helps in the excretion of antigens and foreign material

4) Dental protection: formation and maintenance of dental enamel

5) Medication taste sensation.

Examination of the throat, head and neck

A stepwise approach is advisable:
1. general inspection
1.1. The head and neck – asymmetry; deformity
1.2. The face bony structures; soft tissue – asymmetry, deformity
1.3. The lips – abnormality in appearance, movement

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 1.4. Assessment of the mouth opening
1.5. Tongue: Appearance; movement
1.6. Assessment of the oral cavity: Look for any visible abnormality of buccal
sulcus, dental arches.
2. Palpation: any palpable mass. If so, describe the mass in terms of site, size,
consistency degree of tenderness
3. Mirror laryngoscopy.
Disorders of the throat, head and neck
The Mouth
The mouth may present with certain lesions that may turn out to be sources of
discomfort. As most of them are commonly encountered, proper evaluation is advised.

1. Ulcer

 Aphthous /herpetic/ – Hydrcortisone emulent; Acyclovir may at times

help!!/

 Traumatic

 Allergic /Auto-immune

 Infective: Stevens Johnson syndrome

 Neoplastic
2. Swelling:

 Polyps – cheek mucosa – repeatedly trained

 Retention cysts: – ranula

 Other cystic lesions

 Neoplasm
The tongue

 Micro-, macro- glossia

 Fissured tongue

 Black hairy tongue

 Median Rhomboids

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  Glossitis

 Smooth tongue
The teeth
Any gross abnormality
Pharynx:
Pharyngitis

Infective: - Viral, bacterial

- Fungal – candidacies

Non-infective – due to
- Inhalation
- Post-Radiotherapy
Tonsillitis: - Exudative
- Chronic and recurrent – /fever, general malaise,
reduced appetite/.
Treatment: - Medical: Antibiotic analgesics
- Surgical: Tonsillectomy
Indications: - Recurrent infections
PersistentObstructivesleep apnea/OSA/:
Adeno-tonsillar hypertrophy in
children – if untreated, complications
like core pulmonale
-Followingperitonsillarabscess/ quinsy/.
-Asymmetric unilateral tonsil enlargement
in an adult

Quinsy:- A collection of pus /abscess/ in the tonsillar bed, outside the

tonsillar capsule. It is associated with: intense pain, dysphagia and muscle spasm
leading to trismus
Treatment: - Incision and drainage /Risk of aspiration in neglected
cases, if spontaneous rupture at night occurs/.

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 - I.V antibiotics
- May require admission to hospital
- Frequent saline throat wash with luke-warm saline

Para-pharyngeal abscess:
Treatment: Incision and drainage
- I.V antibiotics, with anaerobe coverage.
Retro-pharyngeal abscess: May be due to retropharyngeal adenoids being infected,
progressing to abscess formation. Lateral neck x-ray view reveals retropharyngeal soft
tissue shadow.
Treatment: - An emergency, requiring urgent incision and drainage, UA,
assisted by suctioning, head kept reclined
- I.V antibiotics anaerobic coverage
/ In some adults, suspect TB!!/
Infectious Mononucleosis /glandular fever/
Cause: Epstein – Barr Virus

 Usually as severe membranous tonsillitis

 Inflamed and enlarged tonsils

 Marked cervical lymphadenopathy

 ? Hepatosplenomegally. Atypical lymphocytosis /Paul– Bunnel titers rising

rapidly/
Treatment: symptomatic
(Skin rash following ampicillin administration is a characteristic response!!/.
Pharyngeal Pouch: In middle age male. /M : F = 4 – 1/
Corrosive ingestion

 Accidental – more in children

Treatment: NG tube feeding

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The Larynx
Inflammatory:

 Laryngitis

 Acute laryngotracheobronchitis (ALTB) . . . Croup

 Common in winter, specially in children under 2 yrs

 Follows an acute viral URTIs

 Grossly swollen and edematous laryngeal and tracheobronchial mucosa

Treatment: - Steroid: Dexamethasone, 0.6mg/Kg po, iv, or subcut
- Nebulised epinephrine 2ml of 1:1000in 2ml N saline, or
- Nebulised ventolin 1ml of 1: 1000 in 3ml N saline
- Humidification/steamy environment/ soothes the harsh
cough
- ? Tracheotomy
Epiglottitis:- Acute epiglottitis is a localized infection of the upper part
of the larynx. The epiglottis becomes severely swollen,
thus obstructing the laryngeal inlet.

- Etiology: Haemophilus influena type B/HIB/

- rapid onset of „quack-like‟ cough, with impending airway
Obstruction
- Strider develops rapidly
- The child tends to sit up, leaning forward to relieve the
airway
Treatment: - Minimize the attempt to examine the throat, as this may
induce spasm

- Emergency admission to hospital

- Resume i.v antibiotics/Amoxicillin/
- Endotracheal intubation/tracheostomy/, for airway

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 restoration
Vocal Abuse

 Acute abuse: shouting, screaming  finger‟s nodule. Localized thickening

 A generalized oedema – of Reinke‟s space along both vocal cords

Neoplasm: The larynx is the most common site of neoplasm, both benign
and malignant
Causes: - polyp
- Recurrent laryngeal papilloma

Symptoms: hoarseness of voice, strider

Treatment: Larvngoscopic extirpation

Malignant: Most commonly encountered is squamous cell carcinoma.

General principles of management
Diagnosis: suspicision, examination, biopsy; assess staging
Treatment: - surgery and/or/; Radiotherapy
- Total Laryngectomy
- Voice Rehabilitation: Esoph,; TEF with speech value

Laryngeal Dysfunction

Impairment of either sensory nerve supply to the mucosa or motor supply to the
laryngeal muscles. Sensory loss may lead to chocking or aspiration on swallowing.
Motor loss (RLN palsy) results in the affected vocal cord assumes a median position.
Other laryngeal disorders may arise in relation to certain disorders:

 Hypothyroidism

 Angioneurotic edema

 Rheumatoid arthritis

 Foreign bodies
The head and Neck
Neck lumps may arise from:
1. Skin and subcutaneous tissue:

35
  sebaceous cysts, lipomas
2. Congenital Remnants

 Dermoid cysts

 Thyroglossal duct cysts

 Branchial cysts

 Cystic Hypgroma
3. Thyroid gland
4. The salivary glands
5. Inflammatory

 Mumps

 Calculus  submandibular

6. Neoplasm

 Squamous cell carcinoma

 Adenocystic carcinoma
7. Traumas

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