ENT ESSAYS

[Document subtitle]

2019
Contents
1). Anatomy and physiology of the external ear. Non-inflammatory diseases and inflammatory
diseases. Otomycosis. ............................................................................................................................. 3
2). Anatomy and Physiology of the middle ear. Methods of investigations. Acute otitis media in
adults and infants. Otitis media with effusion, mastoiditis, facial nerve paralysis. Clinical
complications. ....................................................................................................................................... 10
3). Chronic Otitis media – types. Clinical complications. Traumatic rupture of the tympanic
membrane............................................................................................................................................. 16
4). Anatomy and physiology of the inner ear. Methods of investigation. Otosclerosis. Clinical
complications. ....................................................................................................................................... 21
5). Vestibular disorders. Examination of the Vestibular System. Meniere’s Disease, labryrinthitis.
Vestibular Neuritis ................................................................................................................................ 24
6). Otogenic complications- extracranial and intracranial. Investigation and treatment .................... 27
7). Anatomy and Physiology of the nose. Clinical examination of the nose. Nasal pyramid fracture.
Epistaxis. ............................................................................................................................................... 31
8). Anatomy and physiology of the paranasal sinuses. Clinical Examination of acute and chronic
rhinosinusitis ......................................................................................................................................... 36
9). Paediatric Rhinosinusitis. Orbital complications in diseases of the nose and paranasal sinuses. CSF
rhinorrhoea. .......................................................................................................................................... 38
10). Allergic Rhinitis. Nasal polyposis. Neoplasms of the nose and paranasal sinuses. ....................... 39
11). Basic Anatomy and physiology of the lips and oral cavity. Inflammation of the lips and oral
cavity. Oral floor abscess. Angioedema. Anatomy, physiology and immunology of the pharynx.
Methods of examining then pharynx.................................................................................................... 41
Anatomy, physiology and immunology of the pharynx. Methods of examining then pharynx. .......... 44
12). Diseases of pharynx. Diseases of Nasopharynx- adenoids, juvenile angiofibroma. Acute and
chronic tonsillitis, scarlet fever, plaut-vincent angina, diphtheria, infectious mononucleosis.
Tonsillogenic complications: peritonsillar abscess. Retropharyngeal and parapharyngeal abscess.
Disease of the hypopharynx ................................................................................................................. 46
13). Diseases of the salivary glands. Anatomy, Clinical examination, imaging studies and biopsy of the
salivary glands. Non-inflammatory and inflammatory diseases. Sjogren syndrome. Tumours of
salivary glands. ...................................................................................................................................... 52
14). Adult and paediatric obstructive sleep apnoea. Diagnosis. Physical examination and treatment
.............................................................................................................................................................. 58
15). Anatomy and physiology of the larynx. Methods of Examination. Stridor. Malformation of the
larynx. Diphtheria. Acute Subglottic Laryngitis. Acute Epiglottitis. Acute laryngitis. Angioneurotic
laryngeal Oedema. Chronic non specific laryngitis. Reinke’s oedema. Tuberculous laryngitis ............ 61
16). Tumours of the Larynx. Vocal cord polyps. Vocal cord nodules. Laryngeal papilloma. Laryngeal
squamous cell carcinoma. Spindle cell carcinoma. Neuroendocrine carcinoma. Surgical treatment
options for laryngeal carcinoma. Laryngectomy effects and voice rehab. Tracheotomy and
cricothyrotomy...................................................................................................................................... 66

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17). Laryngeal trauma. Recurrent laryngeal nerve paralysis. Basic principles of speech. Dysphonia.
Vocal cord paralysis. Stridor. Cough ..................................................................................................... 70
18. Emergencies and primary measures in the ear, nose, and throat. Foreign bodies. Anatomy,
physiology of the oesophagus. Corrosive esophagitis. Treatment. ...................................................... 73

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1). Anatomy and physiology of the external ear. Non-inflammatory
diseases and inflammatory diseases. Otomycosis.

• Anatomy
o The external ear consists of the auricle (pinna)
and external auditory canal (external auditory
canal (external acoustic meatus and ear canal)
o And ends at the tympanic membrane
o formative elements of the external ear are
composed of flexible cartilage and of bone,
which are attached to the skin by their
perichondrium and periosteum
o Auricle
▪ Paired structure found on either side
of the head
▪ Functions to capture and direct sound
towards the external acoustic meatus
▪ Most cartilaginous structure (except the
lobule)
▪ Forms the outer curvature known as the
helix
▪ The second innermost curvature runs in
parallel with the helix =antihelix
• can be subdivided into 2 cura:
inferoanterior crus and
superioposterior crus
▪ Middle of the auricle is a hallow depression
= concha
• It continues into the skull as the external acoustic meatus
• The concha acts to direct sound into the external acoustic meatus.
• Immediately anterior to the beginning of the external acoustic meatus is
an elevation of cartilaginous tissue – the tragus
• Opposite the tragus is the antitragus.
o External Acoustic Meatus
▪ Sigmoid shaped tube
• Initially it travels in a superoanterior direction.
• In then turns slightly to move superoposteriorly.
• It ends by running in an inferoanterior direction.
▪ Extends from deep part of the concha to the tympanic membrane
▪ External third = cartilage
▪ Inner 2/3 = temporal bone
o Tympanic membrane
▪ lies at the distal end of the external acoustic meatus
▪ It is a connective tissue structure
▪ covered with skin on the outside and a mucous membrane on the inside

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 ▪ The membrane is connected to the
surrounding temporal bone by a
fibrocartilaginous ring
▪ The translucency of the tympanic membrane
allows the structures within the middle ear
to be observed during otoscopy
▪ On the inner surface of the membrane, the
handle of malleus attaches to the tympanic
membrane, at a point called the umbo of tympanic membrane
▪ The handle of malleus continues superiorly, and at its highest point, a small
projection called the lateral process of the malleus can be seen
▪ The parts of the tympanic membrane moving away from the lateral process are
called the anterior and posterior malleolar folds
o The external ear is supplied by branches of the external carotid artery:
▪ Posterior auricular artery
▪ Superficial temporal artery
▪ Occipital artery
▪ Maxillary artery (deep auricular branch) – supplies the deep aspect of the
external acoustic meatus and tympanic membrane only
▪ Venous drainage is via veins following the arteries
o The sensory innervation to the skin of the auricle comes from numerous nerves:
▪ Greater auricular nerve (branch of the cervical plexus) – innervates the skin of
the auricle
▪ Lesser occipital nerve (branch of the cervical plexus) – innervates the skin of the
auricle
▪ Auriculotemporal nerve (branch of the mandibular nerve) – innervates the skin
of the auricle and external auditory meatus.
▪ Branches of the facial and vagus nerves – innervates the deeper aspect of the
auricle and external auditory meatus
o The lymphatic drainage of the external ear is to the superficial parotid, mastoid, upper
deep cervical and superficial cervical nodes
• Physiology
o Function of the external ear is to transmits sound waves to the middle ear structures
o The auricle and ear canal together form an acoustic funnel that amplifies selected
frequency bands (2-4 kHz)
▪ Amplification does not involve an increase in the amplitude of sound wave
▪ But is based on resonance, meaning that certain wavelengths vibrate better
o There are 2 acoustic pathways
▪ Direct route: Through the conchal cavity
▪ Indirect route
• Via helix and antihelix
• Slightly longer pathway creates a brief sound delay pf approx. 0.2 ms
(which plays an important role in acoustic analysis, especially for
localising a sound source in the vertical plane)
o The auricles also functions as a wind-breaker by creating air turbulence, thereby
diminishing the constant acoustic effects of moving air
• Non- inflammatory diseases

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Prominent Ears • Prominent or protruding ears are usually congenital and has no functional consequence
• Normally angle should by approximately 20-30 degrees (this can be increased due to a
deep concha or lack of development of the antihelix
• Treatment involves surgical correction by reducing the size of the concha and
reconstructing the antihelix
Hyperostoses Hyperostosis
and Exotoses of • an appositional growth of the bony ear canal, usually induced by periosteal irritation such
the Ear Canal has frequent contact with cold water
• Also known as swimmers’ ear
Exostoses
• Exotoses of the external ear canal are true osteomas that are more commonly located
near the annulus on the superomedial canal wall
• They develop from ossification centres and appear otoscopically as pale, rounded bony
prominence
• Diagnosis
The ear canal is usually narrowed in its bone portion by several
smooth, pale prominences
This may form a stenosis that covers the tympanic membrane
The narrowed site is hard and tender when probed with a small, blunt
hook
• Complications
Stenosis causing retention of squamous debris and water can lead to
recurrent otitis externa
In the absence of inflammation, only high-grade stenoses cause conductive
hearing loss
• Treatment
If complications arise, the growths should be surgically removed
Cerumen • May result from a disturbance of the normal self-cleansing mechanism or from excessive
Impaction cerumen secretion
• The cerumen plug consists mainly of secretions from the cerumen glands mixed with
sebum, exfoliative debris and contaminants
• Imprudent cleaning of the ear canal (esp with cotton swabs) can interfere with the self-
cleansing mechanism and displace the cerumen toward the tympanic membrane
• Obstruction of the ear canal by cerumen may be caused by the impaction or swelling of a
cerumen plug
• Often occurs after contact with water
• With aging, drying of the meatal skin and changes in secretions can lead to the formation
of a hard cerumen that tends to be retained in the ear, especially with a narrow canal
• Symptoms
Causes pressure sensations in the ear
Concomitant hearing loss
Vertigo or tinnitus (sometimes)
• Diagnosis
Otoscopy may show obstruction of the ear canal by a yellowish-brown to
black material
• DDX
Epithelial plug or crust can result from a cholesteatoma in the external
ear canal
Occasionally the ear canal is obstructed by a thin skin flap, or cuticle
Tumours, foreign bodies an crusted blood should also be excluded
• Complications
Otitis externa may develop but generally are rate
• Treatment
Cerumen and cerumen plug are removed with a small instrument (hook,
curette) or by a aural irrigation
Foreign bodies • Causes
in the ear canal Usually occur when small children insert small play object
• Diagnosis
Otoscopy
Check for signs of associated injury to middle or inner ear structures,
tympanic membrane perforation, otitis media, facial nerve lesions, vertigo ,
nystagmus or sensorineural hearing loss

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 • DDX
Cerumen impaction, dried blood, tumours of the ear canal,
cholesteatoma, otitis externa
• Complications
Middle and inner ear damage
Prolonged retention of a foreign body in the ear generally leads to secondary
otitis externa, often with a fetid discharge
• Treatment
Careful removal with a small extraction hook
Take care not to push deeper into the ear canal or through tympanic
membrane
Auricular • Collection of blood or serous fluid between the perichondrium and auricular cartilage
hematoma / • Seen in combative sport (e.g.: wrestling, boxing and water polo)
Seroma • Causes the sin and attached perichondrium to separate from the auricular cartilage
• If the injury remains closed, a hematoma or seroma may form between these layers
• There is very little tendency for the fluid collection to be reabsorbed
• Symptoms
Pain
• Diagnosis
Very obvious on palpation and inspection
Lateral auricular cartilage shows swelling and fluctuation
• DDX
Recurrent polychondritis can give rise to a spontaneous seroma
• Complication
Secondary infection often caused by needle aspiration of the hematoma can lead
to perichondritis
Poor reabsorption of the fluid collection can result in permanent deformity of
the cartilaginous framework with the development of an irreversible cauliflower
ear
• Treatment
Hematoma or seroma is surgically evacuated, and the perichondrium is
retracted to the cartilage
Sharp auricular • In an open auricular injury, the cartilage is exposed over the area of variable size
injury and • Can be partial; intact bridge of skin or complete; part of the auricle is completely detached
auricular • Diagnosis
avulsion Injury site is carefully cleaned, and the extent of the injury is determined
Associated injuries to temporal bone, ear canal, middle ear or TMJ should be
excluded
• Complication
Soft tissue infection and perichondritis
Necrosis of compressed structures
• Treatment
Bandage the wound
Reanastomosis if an adequate skin bridge is present
For complete avulsions, the cartilage can be implanted subcutaneously at a
retroarticular or cervical site and used 6 months later to perform a secondary
reconstruction
Burns and • Thermal injuries to the auricle are graded as:
Frostbite • Grade I : Localized erythema
Injuries • Grade II: blistering of the skin
• Grade III: deep tissue necrosis (damages entire skin-cartilage unit)
• Diagnosis
Burns are diagnosed from recent history
Frostbite may appear initially as white skin discolouration that is demarcated
from its surroundings
Patient doesn’t usually realise there is damage until the frostbitten area is
rewarmed
• DDX
Caustic chemical injuries and electric injuries
• Complication
Cartilage necrosis and permanent deformity
Cillblains, and ulceration, itching and perichondritis

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 • Treatment
Local treatment (dressing)

• Inflammatory Diseases
Eczema and • Aetiology
dermatitis of the Mechanical injury, toxicity or allergy- gives rise to an acute bacterial infection
Auricle • Symptoms
Itching, pain (acute infection), crusting, purulent discharge, obstruction can lead to
conductive hearing loss
• Diagnosis
Otoscopic examination – appear dry, cracked and scaly
Bacteriological examination is necessary for recurrent infection
• DDX
Acute otitis media or chronic suppurative otitis media, can lead to an accompanying otitis
externa (exclude using otoscopy)
If otalgia present then consider necrotizing otitis externa
• Complication
Perichondritis, cellulitis, abscess formation and necrotising otitis
• Treatment
Repeated cleansing and drying, followed by antiseptic and antibiotic drops for swelling
Perichondritis of the • Acute inflammation of the skin and perichondrium that also involves the auricular cartilage
Auricle • Usually a bacterial infection caused by Staphylococci and Pseudomonas species
• Less commonly caused by allergic or autoimmune aetiology
• Symptoms
Severe pain of rapid onset and a feeling of tension
Swelling of concha with marked tenderness
Blisters may form on the skin
• Diagnosis
TM is normal of otoscopy and hearing loss does not occur unless otitis externa is
present
CBC- leucocytosis and eleveate CRP, ESR
• DDX
Eczema, dermatitis, cellulitis, zoster oticus
• Complication
Unless treated, the inflammation will cause cartilage destruction and permanent
deformity
• Treatment
Systemic antibiotics and cleansing of the external ear with an ointment
Auricular Cellulitis • Acute streptococcal infection of the subcutaneous tissue involving the auricle and is surroundings
• Symptoms
Redness, swelling an warmth
Malaise, fever, otalgia
• Diagnosis
Inspection and cleansing of the ear canal to exclude middle ear infections
• DDX
Eczema, dermatitis, perichondritis
• Complications
Necrotising fasciitis, glomerulonephritis, rheumatic fever, rheumatic endocarditis
• Treatment
Penicillin G (IV) and NSAIDs for pain
Herpes Zoster Oticus • Reactivation of the dormant varicella zoster virus in ganglion cells
(Ramsay Hunt • Involves nerves VII and VIII (occasionally IX and X)
syndrome) • Symptoms
Pain and buring on one side (no physical findings)
Hearing loss, vestibular complaints (vertigo, disequilibrium), facial nerve palsy
• Diagnosis
Inspection: herpetiform vesicles in the meatus, concha or pinna and lymphadenitis is seen in
the high cervical lymph nodes
Clinical exam: facial neve palsy, sensorineural hearing loss, nystagmus
• DDX

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 Early stages of HZO is similar to sudden hearing loss
Bullous otitis externa
• Complications
Secondary infection with staph or pseudomonas species, a severe post zoster neuralgia may
develop as a late complication, especially in older patients
• Treatment
Acyclovir systemic therapy, corticosteroids (if facial nerve palsy is present), local antiseptic
solution
Diffuse Otitis externa • Due to mechanical injury, toxicity or allergy
and Eczema of the ear • Gives rise to an acute bacterial infection (pseudomonas auruginosa, proteus mirabilis and anaerobes)
canal • Symptoms
Itching, pain, crusting and purulent discharge, obstruction can lead to conductive hearing loss
• Diagnosis
Otoscopy: dry scaly skin (may show sites of desquamation)
• DDX
Acute otitis media or chronic suppurative otitis media, fungal infection. Tumour of the ear
canal, necrotising otitis externa (if otalgia is present)
• Complications
Cracked skin allows bacterial entry causing perichondritis, cellulitis or abscess formation
• Treatment
Repeated cleaning and drying of the ear followed by the instillation of antiseptic and
antibiotic drops that will reduce the swelling
Circumscribed Otitis • Furuncle of the cartilaginous portion of the ear canal (acute bacterial infection)
externa • Symptoms
Very painful, tender swelling (lead to mild hearing loss), otorrhea (rare)
• Diagnosis
Inspection and palpation: tragal tenderness, painful swelling in the ear canal
Otoscopy: swelling and debris in the ear canal
Simple hearing test: swollen shut leading to conductive hearing loss
• Bacteriologic examination: purulent centre of lesion opened with a hook to obtain smear
• Complications
Abscess and spread to infra-auricular and preauricular sites
• Treatment
Cleaning of the ear canal and after swelling has subsided antibiotics and NSAIDs given for
pains
Necrotizing Otitis • Seen in older patients with diabetes mellitus
Externa (Malignant • Infected by pseudomonas aeruginosa leading to ulceration and ostetitis in the ear canal and spread to
Otitis extera) middle ear
• Symptoms
Pain (increasing with progression), aural discharge
• Diagnosis
Otoscopy: ulcer on ear canal floor
Smear: indication of P. aeruginosa
CT: see extent of infection to underlying bone
• DDX
Simple otitis externa and cholesteatoma of the ex. ear canal, tumour
• Complications
Otitis media, mastoiditis, petrostitis, soft-tissue abscess, cranial nerve deficit, sepsis, venous
sinus thrombosis
• Treatment
Wound debridement and cleaning, if no bone involvement then high dose antibiotics is
sufficient, if any complications occur then the bone must be resected

o Otomycosis
▪ Cerumen often harbour fungi such as: Aspergillus, candida albicans
▪ If ear canal has been altered by use of steroids, antibiotics containing ear drops
can cause severe skin infections
▪ Commonly seen in summer months due to warm moist climate (which creates
favourable conditions for fungal growth

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▪ Symptoms
• Severe itching
• Feeling of fullness in the affected ear
▪ Diagnosis
• Otoscopy: white/yellow or black membrane lining the ear canal; which is
usually swollen or erythematous skin
• Mycelia can be identified in direct samples
• Causative agent is established by microbiological examination
▪ DDX
• Otitis externa (diffuse type)
▪ Complication
• Spread to the tympanic membrane epithelium
o And cause perforation and subsequent otitis media
• Necrosis in immunocompromised patients
▪ Treatment
• Clean ear canal and dried
• Local antimycotics
• Salicylate-containing solution to soften the upper most epithelial layer
• Systemic antimycotics only used in immune-supressed patients

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 2). Anatomy and Physiology of the middle ear. Methods of
investigations. Acute otitis media in adults and infants. Otitis media
with effusion, mastoiditis, facial nerve paralysis. Clinical
complications.

• Anatomy and Physiology

o The middle ear, occupies a central position in the temporal bone
o Sound transmission by the ossicles and the ventilation of the temporal air cells via the eustachian
tube
o The middle ear consists of three parts
▪ tympanic cavity bounded laterally by the tympanic membrane
▪ system of temporal bone air cells
▪ eustachian tube.
o Tympanic membrane
▪ Function
• it gathers sound like the membrane of a microphone, and
• it provides sonic shielding of the round window membrane
▪ Anatomy
• Consist of two portions called the pars tensa and pars flaccida
o pars tensa is a funnel-shaped area stretched between the malleus
handle and the bony ear canal
▪ It is composed of three layers; outer layer of the pars tensa,
called the cutaneous layer, consists of smooth, stratified
squamous epithelium
▪ Between the outer and inner layers is the lamina propria. It
consists of two layers of connective-tissue fibres: an outer
layer of radially directed fibres (radiate layer) and an inner
layer of circular fibres (circular layer).
o The pars flaccida (Shrapnell membrane) is located superior to the
malleolar folds.
o Tympanic cavity
▪ allows for unrestricted mobility of the tympanic membrane, which is
necessary for sound transmission
▪ Most of the air enters the tympanic cavity through the eustachian tube, but
some gases diffuse directly into the middle ear through blood vessels in the
mucosa
▪ 3 Levels of the tympanic cavity:
• Mesotympanum- at the level of the tympanic membrane
Anatomical relations of the tympanic cavity: o It contains the round window, the oval window with the
stapes, and the promontory
• laterally: tympanic membrane and the
bony ear canal • Epitympanum- above the level of the tympanic membrane
• Medially: the cochlea o It contains the principal mass of the auditory ossicles with their
• Inferiorly: the bulb of the jugular vein.
• Superiorly: the dura of the middle
associated ligaments and several mucosal folds
cranial fossa. o communicates with the mastoid antrum via the aditus ad antrum and
• Anteriorly: internal carotid artery also with the air cells of the mastoid process
• Posteriorly: mastoid part of the facial
nerve. o The antrum contains the bony prominence of the lateral semicircular
canal
o Roof is formed by A thin bony layer, the tegmen tympani and
separates it from the middle cranial fossa.

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 • Hypotympanum- below the level of the tympanic membrane
o It borders on the bulb of the jugular vein and contains cells (tympanic
cells) that communicate with the mastoid air cells
o Auditory ossicles
▪ Bones that are freely suspended, being nourished entirely through their periosteal
attachments
▪ attached by thin tendons to the smallest muscles in the body, the intra-aural muscles
(tensor tympani and stapedius).
o Intra-aural muscles
▪ The stapedius muscle inserts onto the head of the stapes and occupies a bony canal
parallel to the mastoid part of the facial nerve, which also innervates the muscle
▪ The tensor tympani muscle is innervated by the trigeminal nerve
o Blood supply and innervation
▪ various branches of the external carotid artery (middle meningeal artery, ascending
pharyngeal artery, maxillary artery, and stylomastoid artery)
▪ sensory innervation from the tympanic nerve, from the glossopharyngeal nerve
• Air cells of the temporal bone
o mucosa-lined air cells of the temporal bone all communicate with the tympanic cavity
o are aerated via the eustachian tube
• Eustachian tube
o connects the tympanic cavity with the nasopharynx,
o runs more horizontally in infants and small children than in adults
▪ It is considerably shorter and broader and consists of softer
cartilage
▪ accounting for the higher incidence of otitis media in children
o Function:
▪ Ventilates the tympanic cavity and air cells
▪ Equalizes pressure differences between the tympanic cavity and
the atmosphere
▪ Drains the middle ear space
▪ Creates a barrier to ascending infection
• Examination
o History
▪ Any Otalgia, aural discharge (otorrhea), a feeling of pressure, or hearing loss
• can occur with diseases of the external ear or inner ear
▪ But a history of chronic inflammatory ear diseases usually signifies otitis media
• This type of inflammation can lead to scarring and decreased ventilation of the
middle ear
▪ Before any otologic manipulations are performed, the patient should be asked
specifically about tympanic membrane perforation, previous trauma to the ear, or any
surgery of the middle ear
o Otoscopy
▪ The auricle is rotated gently backward and upward for the examination, avoiding
excessive traction
• This manoeuvre straightens the external ear canal
• The speculum is introduced into the ear canal inserting it past the vibrissae but
without touching the bony and pain-sensitive medial portion of the ear canal
• Begin with Inspection of the external ear and its surroundings, particularly the
mastoid
• The normal tympanic membrane has a greyish colour and variable transparency
• Normal tympanic membrane

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 o reflects light: A cone of light is often seen in the anterior inferior
quadrant
o it Is differentiated: Normal anatomic structures such as the
fibrocartilaginous ring and malleus handle can be distinguished
o it Is mobile: To perform its function, the tympanic membrane must be
able to vibrate. Its mobility can be tested by having the patient
perform a Valsalva manoeuvre or by using a Siegle pneumatic
otoscope.
• Function tests
o Tympanic membrane mobility can be tested actively or passively during otoscopy.
▪ Passive mobility test
• The external ear canal is sealed with the speculum, and a positive pneumatic
pressure is produced in the ear canal, causing movement of the tympanic
membrane (Siegle pneumatic otoscopy).
▪ Active mobility tests:
• A test of tympanic membrane mobility, air is forced up the eustachian tube
into the middle ear, including an outward movement of the tympanic
membrane. Usually most clearly seen in the posterosuperior quadrant
o Valsalva manoeuvre
▪ the patient is told to swallow, then pinch the nostrils and bear down to produce a
positive pressure in the pharynx.
o Politzer manoeuvre
▪ air is forced into one side of the nose by squeezing an air bag while the other nostril is
occluded and the soft palate is closed off
o Toynbee manoeuvre
▪ a negative pressure is created in the pharynx by having the patient swallow with the
nostrils pinched shut this induces an inward movement of the tympanic membrane.
o None of these manoeuvres should be used in patients with an acute inflammation of the middle
ear or nasopharynx
o Hearing tests
▪ typically middle ear disease includes conductive hearing loss in which the Weber test is
lateralized to the affected ear and the Rinne test is negative.
▪ Pure-tone audiometry shows a difference between bone conduction and air conduction
thresholds
▪ Tympanometry, which can be performed only with an intact tympanic membrane, may
show a flattening or shifting of the peak into the negative pressure region
▪ If the tympanogram is normal, the function of the ossicles can be assessed by testing the
stapedial reflex.
• Imaging studies-
o Schiiller view: projection along the ear canal to show the mastoid air cells
o Stenvers view: projection angled 45° forward to show the petrous ridge and petrous apex
o X-ray aims are routinely obtained on both sides for purposes of comparison
o CT- consists of axial and/or coronal scans
• Diagnostic Tympanotomy
o Surgical exploration of the middle ear (tympanotomy) is also available as a diagnostic option. The
tympanic cavity is opened for inspection through the ear canal under an operating microscope
o In most cases, diagnostic tympanotomy is combined with the surgical correction of any
abnormalities that were noted in preoperative studies

• Acute otitis media

o The most common pathologic process in the middle ear

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 o generally followed by several weeks of middle ear effusion like that occurring in serous or otitis
media with effusion.
o common disease in infants and small children but can occur at any age
o Aetiology
▪ caused by an infection that ascends to the middle ear through the eustachian tube
▪ main causative organisms are Streptococcus pneumoniae, Haemophilus influenzae, and
Branhamella catarrhalis.
o Factors that increase or reduce risk:
▪ A previous episode of acute otitis media or the presence of chronic serous otitis media
will increase the risk for a recurrence of acute otitis media
▪ Parental smoking is a proven risk factor
▪ However, extending the period of breastfeeding has shown to lower the risk of
o Symptoms
▪ often preceded by a viral infection of the upper respiratory tract.
▪ severe earache, which in babies may be manifested by rubbing the affected ear or by
nonspecific disease symptoms
▪ Fever is usually present during the first 24 hours
▪ In infants, nonspecific symptoms such as irritability, vomiting, or diarrhoea
▪ Perforation of the tympanic membrane is manifested by aural discharge and by an
improvement or resolution of otalgia.
o Diagnosis
▪ On physical examination, the mastoid shows no swelling but may be moderately tender
to pressure
▪ Otoscopy reveals an opaque, thickened, erythematous, and sometimes bulging tympanic
membrane
▪ The tympanic membrane is immobile by pneumatic otoscopy
▪ a Valsalva manoeuvre should not be performed.
▪ The typical features of conductive hearing loss are also present
▪ Paracentesis for a bacteriologic examination is indicated in immunocompromised
patients, treatment failures and if complications arise.
o Differential diagnosis
▪ otitis externa
▪ acute exacerbation of chronic otitis media
o Treatment
▪ NSAIDS or acetaminophen are given for pain relief
▪ Decongestant nose drops or irrigations may be necessary for relieving nasal airway
obstruction
▪ Antibiotic therapy
• If there is no response or if signs and symptoms worsen within 48 hours, a
different antibiotic should be tried
▪ If improvement is unsatisfactory, paracentesis should be performed to obtain a fluid
sample for bacteriologic examination

• Otitis Media with Effusion

o an inflammatory effusion behind an intact tympanic membrane that is not associated
with acute otologic symptoms or systemic signs.
o Classification
▪ acute (effusion lasting up to 3 weeks)
▪ subacute (up to 3 months)
▪ chronic (more than 3 months)

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 Children
• two functional disturbances: impaired
middle ear ventilation and inflammation
Etiopathogenesis
• can be caused by: adenoid hyperplasia and
chronic adenoiditis
• Symptoms of acute inflammation are usually
absent in children
• The major symptom is hearing loss, but the
Symptoms
children themselves rarely report this.
• Speech and language developmental delay
may occur in bilateral case
• otoscope : often appears opaque, thickened,
and occasionally retracted. Its colour may be
pale, reddish, yellowish, or bluish, depending
on the effusion.
Diagnosis • Pneumatic otoscopy showed decreased or
absent mobility of the tympanic membrane
• The tympanogram: a flat curve (type B) or
occasionally a negative-pressure peak (type
C) in mild and acute cases
• acute or subacute form is treated
conservatively by use of decongestant
nose drops, moisturizing and hygienic
measures, or topical steroids
Treatment • The chronic form should be treated
surgically if hearing loss is present
• Paracentesis provides access for
aspirating the effusion, which will
immediate restore normal hearing
Adult
• the same patho as in children
• Caused by eustachian tube dysfunction
• such as: sleep apnoea syndrome and tumours of
the nasopharynx
• clogged or pressure sensation in the affected ear
• Pain is rarely present.
• complain of a popping or sloshing sound
• A history of a cold often precedes the complaints.
• otoscopically. This examination reveals an
opaque tympanic membrane with very poor
mobility
• A Valsalva manoeuvre either does not force air
into the tympanic cavity or does so only with
difficulty
• The effusion in the tympanic cavity is easily
recognized when air is present (bubbles, level)
but is often difficult to appreciate with a
complete middle ear effusion
• Hearing tests show the presence of conductive
hearing loss.
• The Weber test is lateralized to the affected ear
in unilateral cases, and the Rinne test is negative
• Tympanography shows a flat curve
• Pure-tone audiometry indicates an air-bone gap,
and otoacoustic emissions are absent
• If a middle ear effusion persists for more than 3
weeks, an endoscopic examination of the nose
and nasopharynx should be performed to exclude
a tumour.
• Acute and subacute OME are treated
conservatively as in children
• perform regular Valsalva manoeuvres
• If the disease persists for more than 3
months and the tympanic membrane
becomes markedly thickened, Surgical
treatment is recommended for these cases,
and a myringotomy tube should be inserted
if conductive hearing loss is present

• Mastoiditis
o an inflammation of the air cells in the mastoid process
o Involvement of the mucous membranes of these air cells consistently occurs in acute otitis media
and is referred to as associated mastoiditis
o Mastoiditis in the strict sense is present when the inflammatory process is focused on the
mucous membranes and bony structures of the mastoid
o When the temporal bone is well pneumatized, the inflammation may also involve the cells of the
petrous bone (petrositis) or zygomatic arch (zygomaticitis)
o Etiopathogenesls
▪ originates from an infection of the middle ear
▪ most frequent complication of otitis media
▪ Inadequate antibiotic treatment can predispose to mastoiditis

14
 ▪ an infrequent cause is Wegener disease
o Symptoms
▪ fever and local pain
▪ In infants:malaise, abdominal pain, and anorexia (occult mastoiditis or antritis)
o Diagnosis:
▪ The classic clinical triad consists of:
• a prominent auricle with retroauricular swelling
• tenderness over the mastoid
• otorrhoea
▪ Mastoiditis should be suspected if acute otitis media fails to improve or worsens over a
2-3-week period.
▪ Otoscopy
• features of acute or subacute otitis media with or without tympanic membrane
perforation
• The posterior wall of the external auditory canal may be red and swollen
• CT can dx detect other complications as well
• WBC: increase in CRP and ESR
o Differential diagnosis:
▪ Otitis externa with abscess formation behind the ear (pseudomastoiditis)
▪ Inflamed retroauricular lymph nodes can also produce tenderness and swelling over the
mastoid like that seen with mastoiditis.
▪ Tumours of the temporal bone such as eosinophilic granuloma, sarcoma, metastases
(breast carcinoma, bronchial carcinoma, renal tumours), and lymphomas can mimic the
features of mastoiditis
o Treatment:
▪ mastoidectomyand IV antibiotics.
▪ Riracentesis and the placement of a myringotomy tube are frequently necessary to
decompress the middle ear
▪ Antibiotics without surgery are sufficient only in an early stage of mastoiditis
• Facial nerve paralysis
• Most common complication in of otitis media
• Caused by direct inflammation involvement of the peripheral nerve; usually the tympanic branch is
affected
• Children
o Otitis media in children needs to be treated with antibiotics (and corticosteroids if needed)
o With concomitant mastoiditis, it is usually necessary to proceed with mastoidectomy and
drainage of the middle ear spaces
• Adults
o Cholesteatoma most common cause
o Surgery required ASAP
• Aetiology: direct toxic insult, inflammatory epineural oedema and pressure, and in some cases by
osteitis
• Symptoms: Otologic symptoms are usually the dominant findings, and facial paralysis occurs as a
complication. A chronic process (cholesteatoma) may have an insidious onset.
• Diagnosis: The otoscopic findings, an audiologic examination and CT scans of the temporal bone
• Differential diagnosis: infectious diseases, especially herpes zoster oticus, tumours of the lateral skull
base, temporal bone, and parotid gland.
• Treatment: Except for facial paralysis in the setting of acute otitis media (antibiotics), treatment
consists of surgical exposure of the nerve and appropriate antibiotic therapy

15
 3). Chronic Otitis media – types. Clinical complications. Traumatic
rupture of the tympanic membrane

• Types:

Chronic Otits
media

Chronic non- Chronic

suppurative Suppurative
otits media otitis media

Secreatory Otitis Atelectactic Adhesive otitis Tubo-tympanic Attico-antral

Typanosclerosis
media middle ear media (safe type) (unsafe type)

• Chronic Non-Suppurative Otitis Media

o Secretory Otitis Media (Otitis Media with Effusion)
▪ Definition:
• Accumulation of non-suppurative effusion (serous or mucoid) in the
middle ear cleft behind an intact tympanic membrane.
• More in children and is commonly bilateral.
▪ Aetiology:
• Prolonged eustachian tube obstruction: due to adenoids,
nasopharyngeal tumour, rhinitis, sinusitis, radiotherapy or cleft palate
• Unresolved ASOM: due to inadequate antibiotics or inadequate tubal
drainage
• Otitic barotrauma
• Viral infection
• Allergy
• Hypogamma-globulinaemia
▪ Types: Effusion could be: Serous, Mucoid (glue ear) or Sero-mucinous.
▪ Symptoms:
• Deafness, tinnitus and ear discomfort.
• May be bubbling sound in the ear.
• May be asymptomatic.
▪ Signs:
• Tympanic membrane: retracted, colour is amber yellow or dull grey,
mobility is restricted, and there may be a fluid level (biconcave hairline)
and air bubbles.
• Tuning fork tests: Conductive deafness.
▪ Diagnosis
• Pure tone audiometry: CHL.
• Tympanometry: type B flat tympanogram.
• X-ray nasopharynx lateral view: for adenoids.
▪ Treatment:
• Medical: should be tried initially for 3 months.
o Treatment of predisposing factors.

16
 o Antibiotics, corticosteroids, mucolytics and nasal decongestants.
o Auto-inflation of the Eustachian tube by Valsalva’s manoeuvre.
• Surgical: After failed medical treatment myringotomy with ventilation
tube insertion
o Atelectatic middle ear:
▪ Displacement of the drum medially towards the ossicles and the promontory
▪ The drum becomes very thin due to loss of its middle fibrous layer
▪ This condition may lead to retraction pocket and cholesteatoma
▪ Complaint: Deafness & tinnitus.
▪ Examination: Severely retracted and very thin drum and conductive deafness
▪ Treatment:
• Trials of repeated inflation of E.T e.g. by Valsalva Manoeuver and
insertion of ventilation tube.
• In resistant cases cartilage tympanoplasty
o Adhesive otitis media
▪ Long standing untreated secretory otitis media may lead to adhesions of the
drum to the bony structures inside the middle ear, the patient will have
deafness, and the drum is fixed.
▪ Treatment: Hearing aid.
o Tympanosclerosis
▪ Definition: Whitish patches (chalky patches) seen on the tympanic membrane,
due to calcium carbonate deposition in the tympanic membrane
▪ Site: Commonly in the drum but may invade the ossicles.
▪ Treatment: If no symptoms no treatment. Tympanoplasty in severe conductive
deafness.
• Chronic Suppurative Otitis Media (CSOM)
o Definition: Chronic suppurative inflammation of the mucoperiosteum lining the middle
ear cleft with drum perforation and purulent discharge.
o Types
o Tubo-tympanic CSOM (safe type):
o Infection lies mainly in the E.T. and tympanic cavity
o It is safe type as it affects the mucosa only and less liable to cause complications
o Aetiology:-
▪ Incomplete resolution of ASOM with perforation due to:-
• Inadequate medical treatment of acute suppurative otitis media
• Inadequate drainage through small or high perforation
• Recurrent attacks of infection
• Highly virulent organism (exanthemata)
• Low patient's resistance
o Symptoms:
▪ Discharge: recurrent attacks of profuse, mucopurulent odourless discharge
▪ Deafness and tinnitus.
o Examination:
▪ Mucopurulent non fetid discharge in the external meatus.
▪ Perforation of membrane tensa of the ear drum is central.

17
 ▪ Central perforation in the drum means a perforation at any site in the
membrana tensa of the drum with any size but it is surrounded by drum
remnant all around the perforation
o Site: according to the sectors of the drum: Anterosuperior, Anteroinferior,
Posterosuperior or Posteroinferior of membrane tensa.
o Size: Small, large, or subtotal
o Shape: Round or kidney shaped.
o Middle ear mucosa: red and oedematous in active stage, pale and dry in inactive stage.
o Aural polyp: is a pale oedematous mucosa coming through the perforation.
o Tuning fork test: conductive i.e. negative Rinne's test.
o Investigations:
▪ Hearing tests: by pure tone audiometry mild to moderate conductive deafness.
▪ Culture sensitivity test for ear discharge.
o Differential Diagnosis:-
▪ Between traumatic and pathological perforations of the drum
▪ Attico-antral CSOM

o Treatment:
▪ Medical therapy to convert active stage into an inactive stage.
• Treatment of predisposing factors (adenoid and chronic sinusitis).
• Proper antibiotic (systemic and local).
• Aural toilet (repeated suction).
• Follow up to assess complete healing to get the inactive stage (dry
central perforation).
▪ Surgical treatment: For inactive CSOM i.e. dry ear for 3 months
• Tympanoplasty without or with ossiculoplasty
• Tympanoplasty with mastoidectomy for persistant discharge
• Attico-antral CSOM (Cholesteatomatous, or unsafe type)
o The infection is in the attic and antral areas of the middle ear cleft with affection of the
mucosa and bone and almost is associated with cholesteatoma.
o This area of infection is lined by flat epithelium that responds to infection by
granulations and exudation of scanty pus
o It is unsafe type as it is more liable to cause complications

• Complications of suppurative otitis media

o Cranial complications (bony skull):
▪ Mastoiditis
▪ Petrositis

18
 ▪ Otitic labyrinthitis
▪ Otitic facial paralysis
o Intra-cranial complications (inside the intra cranial cavity):
▪ Extra-dural abscess.
▪ Sub-dural empyema.
▪ Lateral sinus thrombosis or thrombo-phlebitis
▪ Meningitis.
▪ Brain abscess (Temporal lobe or Cerebellum).
▪ Otitic hydrocephalus
o Extra-cranial complications (in the soft tissues of the head and neck):
▪ Otitis externa
▪ Retropharyngeal abscess
• Rupture of the tympanic membrane
o Causes:
▪ Direct trauma:
• Foreign body or during its removal.
• Self-inflicted trauma.
• Improper ear wash or instrumentation.
• Longitudinal fracture of temporal bone.
▪ Indirect trauma: Due to rapid pressure changes:
• Hand slap on the ear (commonest)
• Otitic barotrauma.
• Blast injury (explosion).
• Sudden fluid compression in jumping in swimming pool.
o Clinical picture:
▪ Ear pain: transient at the time of rupture.
▪ Bloody ear discharge: mild and transient at the time of rupture.
▪ Hearing loss and Tinnitus.
▪ Air escapes out of the ear on blowing of the nose producing whistle.
▪ Perforation occurs commonly in pars tensa. It usually locates in the antero-
inferior quadrant (in indirect trauma as slap), irregular in shape, has hyperaemic
edges and is surrounded by blood clots. In self-inflicted cases, the perforation is
posteroinferior.
▪ Tuning fork tests: conductive hearing loss
o Differential diagnosis of traumatic perforation of TM

o Complications:
▪ Otitis media.
▪ Permenant drum perforation.
▪ Ossicular dislocation.

19
 ▪ Implantation cholesteatoma.
o Treatment:
▪ Conservative treatment:
• Prophylactic systemic antibiotic therapy, decongestant nasal drops,
avoid ear contamination, do not wash the ear, do not use eardrops and
do not blow the nose forcibly
▪ Surgical treatment: Myringoplasty when the perforation fails to heal after three
months

20
4). Anatomy and physiology of the inner ear. Methods of
investigation. Otosclerosis. Clinical complications.

• Anatomy- Located in the petrous part of the temporal bone, the inner ear consists of multiple
interconnected ducts that are collectively called the labyrinth
• Membranous labyrinth:
o contains cilia bearing sensory cells that are also known as hair cells.
o It is divided into the vestibular labyrinth and the cochlea {cochlear labyrinth
▪ The vestibular labyrinth is composed of three semicircular canals, the utricle,
and the saccule
▪ The utricle and saccule are connected by the utriculosaccular duct
▪ the endolymphatic duct (vestibular aqueduct), which extends to the
endolymphatic sac on the posterior surface of the petrous bone
▪ The membranous labyrinth of the cochlea is the cochlear duct (scala media)
• Bony labyrinth:
o The membranous labyrinth is embedded in the bony labyrinth within the petrous
bone
o separated from the membranous labyrinth by a space filled with perilymph
o can be subdivided into three parts: the semicircular canal system, the cochlea, and
the vestibule
o The perilymphatic space of the bony labyrinth communicates with the subarachnoid
cerebrospinal fluid (CSF) space via the perilymphatic duct, known also as the
cochlear aqueduct
• Blood supply
o The inner ear derives its blood supply from the labyrinthine artery (arises from the
anterior inferior cerebellar artery or the basilar artery)
o venous drainage to the superior bulb of the jugular vein and to the inferior petrosal
sinus

• Examination
o History
o Former and current noise exposure, also previous acute noise trauma, cranial
trauma, a direct contusion of the cochlea
o prior history of chronic otitis media, which may be an indirect cause of cochlear
damage, family history of hearing disorders, current or previous use of ototoxic
medications or exposure to toxic substances.
• Clinical Examination
o Inspection and otoscopy will show no abnormalities in patients with an isolated
lesion of the cochlea or auditory nerve.
o tuning fork tests will also be normal
o With a unilateral or asymmetrical disturbance, the Weber test is lateralized to the
better-hearing ear and the Rinne test is normal
o The whispered speech test usually shows significant impairment in the ability to
repeat whispered numbers
• Audiometry
o The hearing threshold in the pure-tone audiogram is increased for air and bone
conduction.
o This generally occurs first and most conspicuously in the high- frequency range
(high-tone loss)

21
 o Sound conduction is not impaired- the air and bone conduction thresholds are equal
in the pure- tone audiogram, and immittance measurements are normal
• Imaging studies
o CT scan of the temporal bone can detect changes in the bony labyrinth like those
associated with malformations, trauma, or bone diseases such as osteogenesis
imperfecta, Paget disease, or advanced otosclerosis
o MRI is a particularly good modality for examining the auditory nerve
▪ Method of choice for diagnosing a retrocochlear lesion in patients with
severe hearing loss

• Otosclerosis
o disease of the bony otic capsule in which structural changes in the bone often cause
stapes fixation resulting in conductive hearing loss
o Symptoms:
▪ Patients notice a slowly progressive hearing loss in one or both ears
▪ one ear is usually affected more than the other
▪ Tinnitus may be present
o Diagnosis:
▪ Typical signs of conductive hearing loss are accompanied by normal otoscopic
findings
▪ The Weber test is lateralized to the affected ear, the Rinne test is negative, and
pure-tone audiometry shows that the air conduction threshold is considerably
higher than the bone conduction threshold
▪ CT is not generally needed to confirm otosclerosis, however, except in the rare
cochlear form.
o Differential diagnosis:
▪ Middle ear anomalies
▪ Ossicular chain disruption due to:
• Inflammatory changes such as aseptic necrosis
• Traumatic dislocation of the ossicular chain
• Generalized disorders of bone metabolism
o Complications:
▪ When otosclerotic foci occur at other sites in the otic capsule (capsular
sclerosis), they can produce a variable degree of cochlear hearing loss ranging to
deafness
▪ Even in cases with stapes fixation, cochlear hearing loss may eventually develop
o Treatment:
▪ There is no known treatment for the structural bone changes
▪ With cochlear involvement and in other special situations, oral sodium fluoride
may halt the progression of inner ear changes
▪ The rehabilitation of conductive hearing loss may rely on surgical treatment or a
hearing aid
▪ Surgical treatment consists of replacing the fixed stapes with a prosthesis that
can transmit acoustic vibrations to the inner ear.
• Other clinical complications
o Hearing impairment with a cochlear cause usually involves a diminished hearing ability,
or hearing loss which is generally accompanied by a distortion of hearing
o Tinnitus- auditory sensation that occurs in the absence of an external acoustic or
electrical stimulus and has no subjective information content.
o Retrocochlear disorders

22
 ▪ Usually caused by tumours of the internal auditory canal and cerebellopontine
angle
• Hereditary Sensorineural Hearing Loss
o non-syndromic, hereditary hearing disorders are reasonably symmetrical
o Hereditary hearing loss of later onset may progress intermittently with recurrent attacks
of sudden hearing loss (especially in children), or there may be a gradual progression of
hearing loss over time
• Labyrinthitis
o Pathogenesis and classification: Labyrinthitis can result from an infection or other
inflammatory process affecting either the labyrinth itself or its surroundings

23
5). Vestibular disorders. Examination of the Vestibular System.
Meniere’s Disease, labryrinthitis. Vestibular Neuritis

The Vestibular System is a sensory system that

significantly contributes to spatial orientation
including movement and a sense of balance.
• Vestibule is the central part of the bony
labyrinth of the inner ear.
• The bony labyrinth is located in the petrous
part of the temporal bone and houses the
organs of hearing and balance which
include the vestibule, the semi-circular
canals and the cochlea.
• The Vestibule contains two Otoliths: the
Utricle and the Saccule. These two otoliths
work together to perceive linear acceleration (horizontal movement) and gravity (vertical
movement).
• The Semi-circular canals include three canals: Superior, Posterior & Horizontal. They detect
rotational movement on three dimensional planes.
• The semi-circular canals are located at right angles to each other and are filled with a fluid
called endolymph.
• The Cochlea is the spiral part of the inner ear which perceives sound. Knowing which
direction the sound is coming from is useful in spatial orientation.

A Vestibular Disorder is one where temporary or permanent damage to the vestibular system
results in dysfunction. This damage can be caused by:
➢ Excess fluid in the inner ear
➢ The displacement of inner ear crystals
➢ Malformation of the inner ear structure
➢ Disease or infection; toxic chemicals
➢ An immunological response
➢ Membrane tear or a tumorous growth.

Common vestibular disorders include: benign paroxysmal positional vertigo (BPPV), labyrinthitis and
vestibular neuritis, Meniere’s disease and perilymph fistula.

Symptoms:
➢ The Vestibular System together with vision, hearing and muscle feedback helps control your
sense of balance and enables movement. Together with the cochlea it forms the inner ear.
➢ If the semi-circular canals or otolith organs of the Vestibular system are damaged, a person
will have difficulty with balance, equilibrium and orientation to their surroundings.
➢ Feelings of nausea, disorientation, fullness of the ear and loss of hearing can accompany
vertigo.

Causes: The underlying causes of these symptoms are very difficult to diagnose. There may be
complications from allergies, autoimmune disorders, ageing. A definite diagnosis takes time.
Treatments: may include medication, head repositioning manoeuvres, surgery, Vestibular
Rehabilitation Therapy, dietary changes especially low salt diets, reduction of stress.

24
Examination of Vestibular system: The diagnosis of a vestibular disorder relies on a combination of
tests performed to measure hearing, eye movement, and balance.

Hearing: Because the vestibular system is closely connected to the hearing apparatus, identifying a
change in hearing can give clues about how the vestibular system is functioning.
• Auditory testing may include audiometry tests to measure a person’s ability to hear sounds
and recognize words at various frequencies and volumes,
• Tympanometry to measure eardrum function, and an acoustic-reflex test to measure muscle
reflexes in the ear with loud sounds.
• Otoacoustic emissions (OAE) test measures the responsiveness of hair cells in the cochlea
• Electrocochleography (ECoG) measures how sound signals move from the ear along the
beginning of the hearing nerve.

Eye movements: The ability of the eyes to keep objects in focus during head movement depends
upon information from the vestibular system. Eye movements occurring with various positional
changes can be recorded during electronystagmography (ENG) or videonystagmography (VNG) and
rotary-chair testing.

Balance: The vestibular organs provide sensory information about equilibrium, movement, and
acceleration. Disorders of these organs negatively affect balance, posture, and movement. These
negative effects can be measured and recorded with computerized dynamic posturography (CDP),
which uses a special moving platform.

Meniere's disease is caused by a dysfunction of the endolymphatic sac (semi-circular canals) in the
inner ear - also known as the labyrinth.
• Symptoms: Vertigo (Dizziness, Vomiting, Nausea), Tinnitus (ringing/buzzing in ear) and some
hearing loss.
• Causes: abnormality in the composition and/or amount of endolymph in the inner ear
• Diagnosis: No single test exists for a quick Meniere's disease diagnosis. Combination of
audiogram to check for hearing loss, Electronystagmography (ENG) to assesses eye
movement to evaluate balance function and Rotary-chair testing to measures inner ear
movement by assessing eye movement.
• Treatment: Medications for vertigo - Motion sickness drugs - examples include cyclizine or
diazepam. Drugs for nausea – prochlorperazine. Diuretics – to reduce the amount of fluid
the body retains the patient's fluid volume and pressure in the inner ear may improve.
Hearing aid - a patient with Meniere's disease who has suffered hearing loss from the
affected ear may benefit from a hearing aid.
• Surgery – only if severe and no response to other symptoms:
o Endolymphatic sac decompression - a small portion of bone is removed from over
the endolymphatic sac.
o Labyrinthectomy - a portion of the inner ear is surgically removed. This takes away
both the hearing and balance function of the affected ear.
o Vestibular nerve section - the vestibular nerve is cut. This nerve connects the
balance and movement sensors in the inner ear to the brain.

Labyrinthitis is a disorder that's believed to be caused by an infection that inflames the inner ear
(the labyrinth) and the nerves connecting the inner ear to the brain. Vestibular neuritis' be confined
to cases in which the vestibular nerve only is involved, with the term 'labyrinthitis' being used in
cases in which the vestibular nerve and the labyrinth are affected.

25
 • Symptoms: gradually subside over several weeks, though dizziness can become chronic.
Since the inner ear is responsible for balance, an infection may cause you to suddenly
become dizzy or feel as if the earth is spinning (vertigo).The dizziness can lead to nausea and
vomiting. Ear symptoms include ringing in the ear (tinnitus) or hearing loss in the affected
ear.
• Causes: usually caused by a virus or by bacteria. Viral infection of the inner ear, stomach, or
respiratory tract. Herpes virus infection. Bacteria, such as that which causes lyme’s disease.
• Diagnosis: No specific test, elimination of other conditions depending on symptoms
• Treatment: labyrinthitis usually goes away on its own within a few weeks, it may last for
months. Antibiotic if present bacterial infection. Antihistamines, Medicines to control
nausea and vomiting and to relieve dizziness. Steroids & antiviral drugs in severe cases
caused by viruses. Or physical therapy to challenge vestibular system.

Vestibular neuritis is an inflammation of the vestibular portion of the vestibulocochlear nerve, which
relays messages from the vestibular organs of the inner ear to the brain.
• Symptoms: mild dizziness to a violent spinning or swaying sensation (vertigo). Symptoms
can also include nausea, vomiting, difficulty with vision, and impaired concentration.
• Causes: most commonly by some of the systemic viral infections such as herpes virus,
measles, influenza, etc.
• Diagnosis:
o process of elimination to rule out other causes of dizziness.
o Check for horizontal nystagmus, or rapid eye movements, in the direction of the
unaffected ear, especially if there are no other neurologic symptoms
o Hearing tests, balance tests, and a test that measures a person's ability to focus on
objects during rapid head movements (head thrust test) can be carried out
• Treatment: Acute vestibular neuritis- medicines to suppress nausea and dizziness. Steroids,
antiviral drugs, and antibiotics (if a bacterial infection is present) may also be prescribed, and
intravenous fluids may be administered if a person has become dehydrated from vomiting.

26
6). Otogenic complications- extracranial and intracranial. Investigation
and treatment

• Extra-cranial complications:
o Otitis externa
▪ See essay 1
o Retropharyngeal abscess
▪ Retropharyngeal space: Lies between the bucco pharyngeal fascia of posterior
pharyngeal wall anteriorly and prevertebral fascia posteriorly
▪ Can be acute or chronic
▪ Acute
• Aetiology:
o It is due to suppuration of the retropharyngeal L.N., which
present on each side of the median raphe. The source of
infection is usually from adenoiditis or tonsillitis.
o Age: Classically, retropharyngeal abscess is a disease of infancy
and early childhood, because the glands of Henle usually
become atrophic at the age of five years.
• Symptoms:
o There is usually a preceding acute infection in the throat.
o The patient then complains of fever, malaise, aneroxia, pain in
the throat, painful dysphagia and difficulty in suckling,
obstructive symptoms snoring, noisy breathing, nasal
obstruction and mouth breathing
o Fever and irritability
o Swelling of the posterior pharyngeal wall limited to one side. It
is cystic swelling and pus on aspiration.
o Enlarged cervical L.N.
• Differential diagnosis:
o Carotid aneurysm (pulsating and blood on aspiration) and TB
spine (swelling is midline).
• Treatment:
o Parenteral antibiotics, analgesics and hydration.
o Trans oral incision and drainage: -
▪ Under general anaesthesia with a cuffed endotracheal
tube.
▪ From inside the pharynx.
▪ The head should be kept downward to avoid inhalation
of pus.
o Suction of the pus.
• Intra-cranial complications:
o Extra-dural abscess
▪ Collection of pus between the dura, and the eroded temporal bone.
▪ Usually seen in the tegmen tempani, sinodural angle, or over the lateral sinus
▪ Symptoms:

27
 • Usually symptomless, and is an incidental finding during surgery for
chronic suppurative otitis media.
• Low-grade fever. Persistent earache and headache with persistent
discharge
▪ Signs: Chronic suppurative otitis media with pulsating discharge
▪ Investigations: CT is diagnostic, locates the abscess & detects other
complications.
▪ Treatment: Surgical drainage, usually through radical mastoidectomy
o Sub-dural empyema
▪ It results from collection of big amounts of pus (empyema) in the capacious
subdural space, causing rapid mass effect and increase in the intracranial
tension
▪ The patient presents with a downhill course with convulsions, stupor, coma and
death
▪ Investigations: CT is urgent, and can define the size of the collection.
▪ Treatment: Is urgent, with trephine and drainage of the pus (by the
neurosurgeon) and radical mastoidectomy and antibiotics
o Lateral sinus thrombosis or thrombo-phlebitis
▪ The infection spreads through the wall of the sinus causing a mural thrombus,
which enlarges to occlude the sinus (thrombosis) and gets infected
(thrombophlebitis)
▪ Symptoms depend on area affected:
• Down spread to the internal jugular vein, with tender cord like vein,
palpated in the carotid triangle in the neck.
• Upward spread to the superior sagittal sinus interfering with drainage of
the CSF leads to increased intracranial tension (Otitic hydrocephalus)
causes severe headache, projectile vomiting (without nausea and not
related to meals) and blurred vision.
• Papilloedema (oedema of the optic disc) occurs in neglected cases (after
1-3 weeks).
• Forward spread via the superior petrosal sinus to the cavernous sinus
leads to unilateral chemosis, ptosis, proptosis, papilloedema, and
ophthalmoplegia.
• Lateral spread to the mastoid emissary vein causes tender postauricular
oedema (Griesinger's sign).
• Fever, usually hectic or intermittent with irregular intervals, between
which the patient is relatively well. Rarely the fever is continuous or
masked by the use of antibiotics.
• Rigors, due to septic emboli.
• Signs of meningism with headache, neck rigidity, and nystagmus
▪ Investigations:
• WBC: leucocytosis
• Positive culture for bacteria if samples taken during rigors
• CT: failure to visualize the contrast in the lumen of the lateral sinus is
diagnostic
▪ Differential diagnosis:
• Malaria

28
 • Typhoid
▪ Treatment:
• Antibiotics
• Radical mastoidectomy, and exploration of the lateral sinus
• Proper heparinization and postoperative follow up
o Otogenic Meningitis
▪ an inflammation of the pia-arachinoid with infection of the CSF.
▪ Clinical manifestations:
• severe fever and toxemia (toxic earthy look, aneroxia and rapid pulse)
• Irritability, photophobia, neck rigidity, retracted head and opisotonus
position
• Kernig's sign positive: - hip flexion limits knee extension.
• Brudziniski's sign positive: - neck flexion causes flexion of the hips and
knees.
• Severe generalized headache.
• vomiting which is not related to meals, not preceded by nausea.
• Blurred vision with papilloedema, drowsiness, stupor
▪ Investigations:
• CT scan: - outlines the ear pathology and detects other
complications.
• Lumbar puncture for CSF analysis and culture
▪ Treatment: Should be urgent as the condition is fatal.
• Antibiotics, parenteral, massive, broad-spectrum, and cross the blood
brain barrier, such as 3rd generation cephalosporins, ciprofloxacins,
metronidazoles, sulfatrimethoprim
• Reduce the high intracranial pressure by i.v. Mannitol, glucose 25%,
lasix, or repeated lumbar puncture. Intra-thecal penicillin may be given if
puncture is performed
• mastoidectomy after control of the general condition.
• Rehabilitation of the sequalae of meningitis e.g. deafness treated by
hearing aid or cochlear implantation
o Brain abscess (Temporal lobe or Cerebellum)
▪ It is the result of encephalitis with collection of pus in the brain parenchyma. It
either collects in the temporal lobe or the cerebellum.
▪ 4 stages (see book if you give a shit)
▪ Temporal lobe abscess:
• Nominal aphasia: inability to name objects and persons due to affection
of speech areas, especially in the dominant hemisphere
• Homonymous hemianopia: due to affection of the optic radiation
• Uncinate fits: hallucination of smell and taste due to pressure on the
uncinate gyrus
• Contralateral hemiplegia and hemianaesthesia: according to the size of
the abscess, due to affection of pre and post-central gyri respectively
▪ Cerebellar lobe abscess:
• Ipsilateral hypotonia and muscle weakness.
• Intension tremors.
• Incordination: dysmetria on finger to nose test

29
 ▪ Investigations: CT & MRI are diagnostic for otogenic brain abscess.
▪ Treatment:
• Neurosurgeons: - drain the acute abscess or excise the chronic abscess
• ENT:- treat source of infection through the mastoidectomy few days
after the neuro-surgical procedure to avoid recollection
o Otitic hydrocephalus

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7). Anatomy and Physiology of the nose. Clinical examination of the
nose. Nasal pyramid fracture. Epistaxis.

• Anatomy
o External Nose
▪ The shape of the external nose is defined by the nasal bones, a pair of
rectangular bones in the upper nasal dorsum, and by the paired lateral cartilages
(upper nasal cartilages) and alar cartilages (major alar cartilages) in the central
and lower portions of the nose
▪ The lateral portions of the nasal alae also contain several small accessory
cartilages, called the minor alar cartilages , which are embedded in the lateral
soft tissues of the nose.
▪ The shape and stability of the alar cartilages, each of which consists of a medial
and lateral crus , chiefly determine the appearance of the nasal tip and the
shape of the nares
o Nasal Cavities
▪ begin anteriorly at the nasal vestibule, posteriorly by the internal nasal valve
(limen nasi) located between the posterior border of the alar cartilage and the
anterior border of the lateral cartilage
▪ This valve area is the narrowest portion of the upper respiratory tract and, as
such, has a major bearing on the aerodynamics of nasal air-flow
▪ The anterior bony opening of the nasal cavity, called the piriform aperture , is
▪ bounded laterally and inferiorly by the maxilla and superiorly by the nasal bone
▪ The interior of the nose behind the nasal valve is divided by the nasal septum
into two main cavities. The nasal septum is composed of an anterior
cartilaginous part and two posterior bony parts
▪ Abnormalities in the shape of the nasal septum, which may consist of a deviated
septum, tension septum, spurs or ridges, are a frequent cause of nasal airway
obstruction.
▪ The choanae are the paired posterior openings through which the nasal cavities
communicate with the nasopharynx
o Paranasal Sinuses
▪ air-filled cavities that communicate with the nasal cavities

o Vascular supply
▪ External nose = facial artery and ophthalmic artery
▪ Internal nose = sphenopalatine artery and ant+ pos ethmoid arteries
▪ Venous drainage by facial vein, retromandilbular vein and internal jugular vein

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 ▪ Regional lymphatic drainage = face and external nose is drained by
submandibular lymph nodes, while nasal cavity is drained by retropharyngeal
and deep cervical lymph nodes
o Nerve supply
▪ Sensory innervation from terminal branches of the trigeminal nerve
▪ Only the skin over the mandibular angle and the lower portions of the auricle
are supplied by the great auricular nerve
▪ Mimetic muscles = facial nerve
▪ Masticatory muscles = mandibular nerve branch from the trigeminal nerve
• Examination
o History
▪ any nonspecific symptoms such as obstructed nasal breathing and nasal
discharge present for some time or is of recent onset, possibly in connection
with trauma to the nose.
▪ unilateral, bilateral, or alternate between the sides and whether they are
seasonal or present year-round.
▪ In patients with nasal discharge, the consistency of the secretions should be
assessed: is the discharge watery, mucopurulent, or blood-tinged (which may
▪ suggest a tumour)
▪ To exclude allergic rhinitis, the patient should be questioned about sneezing
attacks, itchy eyes (conjunctival irritation), cough, and respiratory complaints
(evidence for allergic involvement of the lower respiratory tract).
• This includes the family and personal history (bronchial asthma, atopic
dermatitis, food allergies)
▪ details on the household and occupational environments, giving particular
attention to pets, indoor plants, and potential allergen exposure at the
▪ workplace (e.g., in a bakery or hair salon).
▪ Headaches may signify an accompanying paranasal sinus inflammation.
▪ Dryness of the nasal mucosa is a common finding in colds but can also result
from changes in air quality, previous nasal surgery, or the chronic use of
vasoconstricting nose drops or sprays that contain corticosteroids
▪ Olfactory dysfunction is another possible symptom of rhinologic diseases
• Clinical Examination
o Inspection
▪ Any mouth breathing may direct to nasal airway obstruction
▪ The shape of the external nose may suggest intranasal abnormalities (e.g., a
cartilaginous nasal deviation with a tension septum).
▪ If the alar cartilages are too soft, they will be indrawn even during normal,
unforced inspiration.
▪ Skin changes such as erythema or swelling can occur with orbital complications
of paranasal sinus inflammations (erythema and swelling of the upper and lower
▪ lids), in erysipelas (“butterfly”-shaped erythema of the midfacial skin), or with
nasal furuncles, which present with circumscribed redness and swelling in the
nasal vestibule.
o Palpation
▪ useful for detecting bony discontinuities.
▪ with suspected neuralgias, it is also done to check for tenderness over the
supraorbital, infraorbital, or mental foramina

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 ▪ In patients with a recent trauma history, palpation of the external nose will
disclose any mobility or crepitus suggesting a fracture of the nasal pyramid.
▪ The midfacial bones (especially the bony orbital rim) are also palpated to check
for step-offs indicating a fracture line.
o Anterior Rhinoscopy
▪ begins with anterior rhinoscopy to evaluate the nasal vestibule and the anterior
portions of the nasal cavity
▪ used not only for nasal examination but also for minor therapeutic procedures
▪ such as intranasal packing for epistaxis, foreign-body removal, and polypectomy
o Nasal Endoscopy
▪ provides only close-up views of small intranasal areas
▪ flexible endoscopes are also available for inspecting the nose and nasopharynx
and exploring all of the pharynx and larynx in one sitting
o X-ray
▪ Standard paranasal sinus radiographs in the occipitomental projection,
occipitofrontal projection are used in cases of acute inflammation and to
evaluate midfacial fractures
o Computed Tomography (CT)
▪ Besides an occasional malformation, the main indications for CT scanning of the
nose and paranasal sinuses are chronic sinusitis, trauma (especially frontobasal
fractures), and tumours.
o Magnetic Resonance Imaging (MRI)
▪ indicated in diseases that involve the paranasal sinuses in addition to the cranial
cavity or orbit (e.g., tumours and congenital malformations such as
encephaloceles)
▪ It can also supply information that is useful in differentiating soft-tissue lesions
within the paranasal sinuses (mucocele, cyst, polyp), and it can distinguish
between solid tumour tissue and inflammatory perifocal reaction
• Nasal pyramid fracture
o The fractures are classified as open or closed on the basis of concomitant soft-tissue
injuries
o Diagnostic procedure:
▪ Inspection may show obvious deviation of the external nose or a simple
depression of the lateral nasal wall
▪ Swelling of the surrounding soft tissues is also present, usually caused by a
hematoma
▪ Intranasal inspection by anterior rhinoscopy or endoscopy is done to check for
concomitant mucosal injuries and especially to evaluate the nasal septum, which
also may be fractured
▪ radiographs of the nose in the lateral projection and standard sinus projections
to exclude bony involvement of the lateral midface
o Complications:
▪ When a septal fracture is covered by an intact soft-tissue envelope, there is a
danger of subperichondrial hemorrhage with hematoma formation
▪ The hematoma may become infected, giving rise to a septal abscess which in
turn can lead to cartilage necrosis with loss of the nasal septum and dorsal
saddling

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 ▪ Alternatively, the infection may spread to the cranial cavity by the vascular
route, causing meningitis.
o Treatment:
▪ Surgical treatment is generally indicated due to the potential for permanent
nasal deformity.
▪ An open fracture requires immediate surgical care accompanied by tetanus
prophylaxis or a tetanus booster
▪ If the fracture is displaced and closed, it can be safely reduced during the initial
week after the injury
• Epistaxis
o Aetiology

o Diagnosis
▪ The diagnostic work-up begins with blood
pressure measurement. Except in very minor
cases
▪ Hb levels should also be determined, and a
coagulation disorder should be excluded by determining the platelet count,
bleeding time, thromboplastin time, partial thromboplastin time (PTT), and
thrombin time.
▪ Bleeding site: The nasal cavity is inspected by anterior rhinoscopy or endoscopy
following decongestion and local anesthesia of the mucosa
▪ In most cases the bleeding site is in Kiesselbach’s area
o Treatment
▪ The intensity of the bleeding and risk of aspiration can be reduced before the
cause and
▪ location have been established.
▪ The nostrils are compressed against the nasal septum, and the patient is told not
to swallow blood running down the pharynx.
▪ The patient is kept in an upright posture to reduce blood flow to the head and
inhibit the swallowing of blood.
▪ An ice bag can be placed on the back of the neck to induce reflex
vasoconstriction
▪ An intravenous line should be placed if bleeding is severe.
▪ Silver nitrate cautery: Mild epistaxis from Kiesselbach’s area can often be
controlled by selective local cauterization of the bleeding site with silver nitrate.

34
▪ Opposing sites on the nasal septum should not be cauterized due to the risk of
septal perforation.
▪ Nasal packing: For severe epistaxis, the anterior nasal cavity can be packed with
ointment-impregnated gauze strips
▪ Both nasal cavities should always be packed in order to produce adequate
counterpressure
▪ Vascular ligation or embolization: coagulated or clipped under endoscopic
control
▪ The ligation or angiographic embolization of a larger arterial trunk may be
considered as a last recourse
▪ Prevention of recurrent bleeding: Besides the conservative treatments noted
above, some causes of epistaxis require surgical treatment since nasal packing
alone is of only temporary, symptomatic benefit

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8). Anatomy and physiology of the paranasal sinuses. Clinical
Examination of acute and chronic rhinosinusitis

• The paranasal sinuses are air-filled cavities in the frontal, ethmoid, maxilla, and
sphenoid bones. They’re lined with a mucosal membrane and have small openings into
the nasal cavity:

Maxillary sinus:
• located in the body of the maxilla behind the cheek just above the roots of the premolar
and molar teeth
• It opens into the nasal cavity via the semilunar hiatus
• It is the largest of the group of para nasal sinuses
• The maxillary sinus has biphasic growth.
o The first phase of growth occur during the first 3 years of life while the second
phase occur between 7 - 18 years
• Arterial supply: By facial artery branch of external carotid artery (ECA). And by infra
orbital & greater palatine arteries branch of maxillary artery which is branch of ECA.
• Venous return: To anterior facial vein & pterygoid plexus.
• Nerve supply: Anterior superior alveolar nerve & middle superior alveolar nerve which
are both from infraorbital nerve and Posterior superior alveolar nerve from maxillary
nerve

Ethmoid sinuses:
• The anterior, middle, and posterior ethmoid sinuses are located in the ethmoid bone
between the nose and the eye
• Anterior sinus opens into the nasal cavity by the infundibulum, the middle sinus opens
into the ethmoidal bulla, and the posterior sinus opens into the superior meatus.
• It is made up of complex bony labyrinth of thin walled cells.
• A few ethmoid cells may be present at birth. The common infections affecting the
pediatric age group occur in these sinuses. In adults 6 - 10 ethmoid cells may be present.
• Anterior: Anterior ethmoidal nerve and vessels and submandibular lymph nodes.
• Middle: Anterior ethmoidal nerve and vessels and orbital branches of pterygopalatine
ganglion and submandibular nodes.
• Posterior: Posterior ethmoidal nerve and vessels and orbital branches of
pterygopalatine ganglion and retropharyngeal nodes.

Sphenoid sinuses:
• These sinuses are found in the sphenoid bone.
• Each opens into the sphenoethmoid recess.
• Development of sphenoid starts during the 4th year of childhood and gets completed by
the 17th year.
• They drain through the superior meatus via a small ostium.
• Arterial supply: Posterior ethmoidal and internal carotid arteries.
• Venous return: Pterygoid venous plexuses and cavernous sinus.
• Nerve supply: Posterior ethmoidal nerve and orbital branches of pterygopalatine
ganglion. Lymphatic drainage: Retropharyngeal nodes

Frontal sinuses:
• Found within the frontal bone and run above the medial end of the eyebrow and
backward to the orbit

36
 • They open into the nasal cavity via the semilunar hiatus.
• Among the para nasal sinuses this sinus shows the maximum variations.
• It is more or less shaped like a L. Frontal sinus appear very late in life and are not seen in
skull films before the age of 6.
• The sinus drains into the anterior part of the middle meatus through the fronto nasal
duct.
• Blood supply - Supra orbital artery
• Venous return - veins connecting supra orbital and superior ophthalmic veins.
• Lymphatic drainage – Submandibular nodes.
• Nerve supply - Supra orbital nerve(ophthalmic nerve)

Physiology of paranasal sinuses

• Decreasing the relative weight of the front of the skull, and especially the bones of the
face.
• Increasing resonance of the voice.
• Providing a buffer against facial trauma.
• Insulating sensitive structures like dental roots and eyes from rapid temperature
fluctuations in the nasal cavity.
• Humidifying and heating of inhaled air because of slow air turnover in this region.
• To provide extended surface for olfaction.
• Immunological defense

Rhinosinusitis is the inflammation of the membranous lining of one or more of the sinuses.
Sinusitis is also referred to as rhinosinusitis because inflammation of the nasal mucosa
generally accompanies sinusitis.
• Major symptoms: Facial pain/pressure/fullness, Nasal obstruction/blockage, Nasal or
discharge/purulence
• Minor Symptoms: Headaches, Fever (other than acute rhinosinusitis) Halitosis, Fatigue,
Dental pain, Cough

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9). Paediatric Rhinosinusitis. Orbital complications in diseases of the
nose and paranasal sinuses. CSF rhinorrhoea.

• Paediatric rhinosinusitis:
o There is some controversy as to whether this diagnosis can be made in young
children who have very poorly developed sinuses - radiographic evidence of sinuses
is only visible from about 9 years of age.
o Current consensus is that it can occur in children over the age of 1 year
o Symptoms may vary a little from those of adults and can include irritability,
lethargy, snoring, mouth breathing, feeding difficulty and hyponasal speech

• Orbital Complications: -
o The commonest complications of sinusitis and usually occur in children.
o They are common in ethmoid sinusitis.
o The extension of infection can occur either by direct extension from the ethmoid
through the medial orbital wall (lamina papyracea) or by retrograde thrombophlebitis
via valveless veins.
▪ Eyelid oedema (preseptal cellulitis)
▪ Orbital cellulitis (postseptal cellulitis) is inflammation of the orbital contents. It
is manifested by axial proptosis, chemosis and ophthalmoplegia. It may progress
to orbital abscess and blindness
▪ Subperiosteal abscess: collection of pus between periorbita (periostium of orbit)
and the bony orbital well. The clinical picture shows pain, lateral proptosis and
limitation of eye movements.
▪ Orbital abscess: collection of pus in the orbit. It has the same clinical
presentation of orbital cellulitis. CT scan with contrast on paranasal sinuses and
orbit can distinguish between orbital cellulitis, subperiosteal and orbital abscess.
▪ Cavernous sinus thrombosis: proptosis, ophthalmoplegia, chemosis, lid oedema
and visual loss with development of contralateral ocular signs if the case is
neglected
o Treatment:
▪ Medical: Extensive broad spectrum antibiotics should be given.
▪ Surgical: surgery in the form of FESS or external frontoethmoidectomy

• Cerebrospinal Fluid Rhinorrhea:

• CSF rhinorrhea is the drainage of the fluid which surrounds the brain into the
nose (CSF=cerebral spinal fluid + rhinorrhea = fluid draining from the nose).
• A breach in dura (the periosteal or nutrient membrane lining the inside of the skull) over or
adjacent to the nose, sinuses or ear can provide a pathway for CSF to drain from the
subarachnoid space into the nose. CSF rhinorrhea can be the result of trauma to head, nasal
or ear surgery or occur spontaneously.
• CSF rhinorrhea requires medical attention and any change in the individual's level of
consciousness, fever, chills or stiff neck implies meningitis.
• CSF rhinorrhea is a sign of basal skull fracture. Management includes watchful waiting - leaks
often stop spontaneously; if this does not occur then neurosurgical closure is necessary to
prevent the spread of infection to the meninges
As bacterial meningitis can be fatal and survival is dependent on rapid treatment, such inflicted
individuals must seek immediate medical care

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10). Allergic Rhinitis. Nasal polyposis. Neoplasms of the nose and
paranasal sinuses.
• Allergic rhinitis;
o Etiopathogenesis and classification- allergic inflammation of the mucosa is triggered by
an immediate, IgE-mediated reaction of the immune system to any of a number of
foreign substances, particularly pollens and animal allergens.
• Seasonal allergic rhinitis is mainly cause by pollens
• Clinical symptoms appear between February and September, depending on
the individual allergen spectrum of the patient, and disappear at the end of
the pollen season.
• Perennial allergic rhinitis is caused by year-round allergen exposure that incites a
permanent inflammation of the nasal mucosa.
• The predominant causative allergens are house dust, pet dander, and
molds. The diseases may also be caused by certain foods (E.g.
strawberries, nuts, eggs, and fish)
• A new occupational allergen, especially prevalent in health workers, is
latex, which is used to manufacture disposable gloves.
o Symptoms; blocked nose, sneezing attacks, a watery nasal discharge, itching of the nose
and eyes.
o Diagnosis; detailed allergy history.
▪ Seasonal allergic rhinitis, inspection of the nasal cavity typically reveals a bluish-
purple discoloration of the mucosa.
▪ With perennial rhinitis, the mucosa is bright red and shows inflammatory
changes. Careful allergy testing is necessary to identify the antigens involved.
o Treatment; the best treatment strategy is to avoid contact with the allergen or eliminate
allergenic irritants from the environment. Most patients with allergic rhinitis receive
antihistamines or nasal inhaled corticosteroids.

Nasal polyposis;
• Pathogenesis and morphology-
o develops in response to a variety of noxious stimuli, appearing morphologically as
oedematous, polypoid hyperplasia of the sinus mucosa and projecting into the nasal
cavity in the form of polyps.
• Aetiology;
o besides genetic causes, chronic irritation of the mucosa, form in response to allergic
rhinitis and acetylsalicylic acid intolerance. Nasal polyps are rarely observed in
children.
• Symptoms;
o blocked nose, hyposmia or anosmia (loss of smell), headache (due to impaired
ventilation and drainage in the paranasal sinuses), snoring, and frequent throat
clearing due to associated postnasal drainage.
• Diagnosis;
o rhinoscopic or endoscopic evaluation of the nasal cavity, giving particular attention
to the lateral nasal wall. Further diagnostic measures; allergy tests, olfactory testing
and CT scan.
• Treatment;
o the use of corticosteroids containing nasal sprays and systemic antihistamines.
Systemic steroids may also be tried. Many cases will require surgical treatment; an

39
 important current option is intranasal sinus surgery using endoscopic or
microsurgical technique to carry out polypectomy

• Neoplasms of the nose and paranasal sinuses;

o It is a very rare condition (about 3%)
o Delay in diagnosis due to similar to benign conditions
o Nasal cavity – half is benign (papilloma and osteoma) and other half is malignant
(mainly squamous cell and adenocarcinoma).
o Paranasal sinus is mostly affected by malignant type.
o Epidemiology;
▪ Predominately of older males
▪ Exposure; wood, nickel-refining process, industrial fumes, and leather
tanning
▪ Cigarette and alcohol consumption
o Location;
▪ Maxillary sinus- 70%
▪ Ethmoid sinus- 20%
▪ Sphenoid- 3%
▪ Frontal- 1%
o Presentation;
▪ Oral symptoms- pain, trismus, alveolar ridge fullness, erosion
▪ Nasal findings- obstruction, epistaxis, rhinorrhoea
▪ Ocular findings- epiphora, diplopia
▪ Facial signs- paresthesias, asymmetry
o Radiography;
▪ CT- bony erosion and limitations with periorbital involvement
▪ MRI- 95% correlation with surgical findings, inflammation- low T1 and high
T2 and Hypercellular malignancy
o Treatment
▪ Surgical resection with postoperative radiation

40
11). Basic Anatomy and physiology of the lips and oral cavity.
Inflammation of the lips and oral cavity. Oral floor abscess.
Angioedema. Anatomy, physiology and immunology of the pharynx.
Methods of examining then pharynx.

• Anatomy
o Oral Vestibule
▪ The oral vestibule is bounded externally by the lips and cheeks and internally
by the alveolar processes and teeth
▪ The oral cavity opens into the pharynx at the facial isthmus
o Lips and Cheeks
▪ the morphologic framework of which is formed largely by the mimetic
muscles, are lined on their mucosal side by nonkeratinized squamous
epithelium
▪ The lips are separated from the cheek by the nasolabial fold, an oblique
sulcus that runs laterally and inferiorly from the nasal alae
▪ The orbicularis oris muscle forms the muscular foundation of the lips
▪ The lips receive their blood supply from the superior and inferior labial
arteries, which arise from the facial artery. The lips are drained primarily by
the facial vein, which also communicates with the orbital veins via the
angular vein above the upper lip.
▪ The submandibular and submental lymph nodes receive the lymphatic
drainage from the lips.
▪ The upper lip receives its sensory innervation from the infraorbital nerve,
the lower lip from the mental nerve.
▪ The cheeks, which form the lateral boundaries of the oral vestibule, also
contain small salivary glands in their mucosa. The buccinator forms the
muscular framework of the cheek. Like the orbicularis oculi, the buccinator
is a mimetic muscle and receives its motor innervation from branches of the
facial nerve.
o Masticatory Muscles
▪ The masseter muscle, located in the posterior part of the cheek, covers the
vertical ramus of the mandible and the mandibular angle from the outside.
It is one of the masticatory muscles, along with the temporalis muscle and
the medial and lateral pterygoid muscles
▪ These muscles form both a functional and phylogenetic unit and accordingly
are all supplied by the mandibular nerve (third division of the trigeminal
nerve).
o Teeth
▪ The human dentition consists of
• Two incisors
• One canine
• Two premolars
• Three molars

41
 ▪ Each tooth consists of a crown and a root, which terminates at the apex. The
area between the crown and root is the neck (cervix), which protrudes
fromsockets (dental alveoli) in the alveolar processes of the maxilla and
mandible.
o Oral Cavity
▪ The oral cavity is bounded anteriorly and laterally by the alveolar ridge and
teeth, superiorly by the hard and soft palate and posteriorly by the facial
isthmus.
▪ oral cavity is sealed posteriorly by the soft palate with its penduline process,
the uvula
• Inflammation Of Lips And Oral Cavity
o Herpes Simplex Virus
▪ are most often caused by HSV type 1
▪ Symptoms:
• Primary infection with HSV is usually acquired in early childhood
and predominantly affects the oral mucosa as herpetic
gingivostomatitis (aphthousstomatitis)
• The appearance of local lesions (bullae) on the oral mucosa is
preceded by fever and lethargy consistent with a flu like infection.
• This is often accompanied by regional lymphadenitis
• In rare cases, the nasal mucosa is also involved (herpetic rhinitis).
▪ Diagnosis:
• based on the history and clinical examination
• A simple method is to demonstrate classic giant cells by the
cytologic
• examination of a Tzanck smear
▪ Complications:
• A feared complication is secondary bacterial superinfection by
Staphylococcus aureus or streptococci (aka: herpes impetiginatus)
• Sometimes, postherpetic exudative erythema multiforme,
characterized by skin lesions as well as typical ulcers around mouth,
lips and genitals
▪ Treatment:
• The treatment of herpes simplex labialis should include the use of
topical antiseptics to prevent superinfection
• Acyclovir, administered as a topical ointment or systemically, is
available for severe forms of the disease. Therapy is generally
continued for 5–7 days, but some cases (especially
immunosuppressed patients) may require a more prolonged course
of treatment
o Varicella-Zoster Virus
▪ Chickenpox occurs predominantly in children and results from primary
infection
▪ with the varicella-zoster virus.
▪ After the cutaneous lesions have healed, the virus persists in the ganglion
▪ cells of sensory nerves.
▪ Symptoms:

42
 • Chickenpox presents with a characteristic skin rash consisting of
erythematous papules and thin-walled vesicles with watery
contents, covering the body but especially pronounced on the head
and trunk
• Aphtha-like vesicles also consistently appear on the oral mucosa and
especially on the hard palate, buccal mucosa, and gingiva.
• signs such as lethargy, fatigue, and occasional neuralgiform pain in
the distribution of the affected nerve
▪ Treatment:
• with a 5–7-day course of acyclovir or famciclovir
• Analgesics and anti-inflammatory drugs (especially carbamazepine)
• Antibiotics may be indicated in elderly or immuno-compromised
patients to prevent superinfection
• Herpangina
o Caused usually by group A cosackievirus and affect children more than adults
o Symptoms:
▪ fever, malaise, headache, and muscle pain, bullous eruptions surrounded by
a red halo appear on the oral mucosa, particularly affecting the anterior
faucial pillars, uvula, and palatine tonsils
▪ As a rule, the vesicles rupture in a few days, leaving behind shallow
ulcerations
o Differential diagnosis:
▪ The gingivostomatitis caused by HSV is considerably more painful and runs a
longer course.
o Treatment:
▪ symptomatic treatment—anti-inflammatory agents or mouth rinses with
chamomile.
▪ The disease generally resolves in 14 days without complications
• Oral floor abscess
o Aka: Ludwigs angina
o Commonly the inflammation originates from the lower molars
o leading to abscess formation in the tongue muscles or connective-tissue spaces of
the oral floor
o seen in diabetic or immunosuppressed patients (especially children).
o Symptoms and diagnosis:
▪ An oral floor abscess is manifested clinically by edematous expansion with a
firm, erythematous swelling in the submental to submandibular areas
▪ Patients complain of difficulty swallowing and speaking (“muffled speech”)
▪ High fever is also present.
▪ can lead to dyspnea with acute respiratory distress, and descending
infection can incite mediastinitis
▪ The principal options are ultrasonography and computed tomography
o Treatment:
▪ The treatment of choice is incision and drainage of the abscess via the
intraoral and transcervical route
▪ Concomitant antibiotic therapy should be appropriate for a mixed spectrum
of aerobic and anaerobic organisms

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 • Angioedema
o Angioedema denotes a transient, frequently pronounced vascular reaction which, in
the head and neck region, can lead to swelling of the face, lips, tongue, and larynx.
o Clinical manifestations:
▪ massive facial swelling that is most pronounced in the periorbital region but
also affects the lips, tongue, tongue base, and laryngeal area
▪ Massive tongue swelling in particular can cause acute obstruction of the
upper airways
▪ The hereditary form is additionally characterized by swelling of the
extremities and episodes of abdominal pain
o Treatment:
▪ The cause of the angioedema is a key factor in selecting the appropriate
treatment.
▪ The treatment of choice in cases not induced by C1-INH deficiency is
symptomatic treatment with corticosteroids or epinephrine (especially in
the form of the disease induced by ACE inhibitors)
▪ In the form that is induced by a C1-INH deficiency, direct replacement with a
C1-inhibitor concentrate should be provided in acutely life-threatening cases
with swelling of the tongue and larynx

Anatomy, physiology and immunology of the pharynx. Methods of

examining then pharynx.

• The pharynx is a tubular, fibromuscular space extending from the skull base to the inlet of
the oesophagus (upper oesophageal sphincter)
• Anatomically and clinically, the pharynx consists of a nasal part (nasopharynx), an oral part
(oropharynx), and a laryngeal part (hypopharynx)
• The entire pharynx is bounded externally by several muscles, which perform diverse
functions and are continuous distally with the muscles of the oesophageal wall.
• The primary function of the pharynx and oesophagus is to coordinate the act of swallowing,
which is regulated by a complex interaction of various cranial nerves and peripheral
muscular and connective-tissue structures located in the oral cavity, pharynx, and
oesophagus.
• The pharynx also contains the tonsillar ring, a series of lymphoepithelial organs that are
important in the immune response to infection
• Finally, portions of the pharynx function as a variable resonance chamber for modulating
vocal sounds
• Neurovascular Supply
o The pharynx receives its blood supply from the territory of the external carotid
artery (branches of the facial artery, maxillary artery, ascending pharyngeal artery,
o lingual artery, and superior thyroid artery)
o The veins of the pharynx drain into the internal jugular vein.
o The lymphatic drainage of the upper portions of the pharynx is through the
retropharyngeal lymph nodes, while the lower portions drain to the parapharyngeal
or deep cervical nodes

44
 o Nerve supply: The muscles and mucosa of the pharynx receive their motor and
sensory innervation from the pharyngeal plexus
• Examination of Pharynx
o Nasopharynx
▪ Endoscopy
• Nasopharyngeal endoscopy may be performed using a transoral or
transnasal technique. The latter technique is described fully in 2.1
and permits the nasopharynx to be examined from the front
• It can also provide detailed views of the eustachiantube region, the
pharyngeal recess
• Transoral endoscope is basically a postrhinoscopic technique that
provides the examiner with an excellent overview of the
nasopharynx.
o Oropharynx
▪ Most structures of the oropharynx can also be evaluated during the
examination of the oral cavity.
▪ The palatine tonsils are evaluated for their symmetry, mobility, and for the
presence of any coatings or ulcerations
▪ A laryngeal mirror or telescopic laryngoscope should be used to examine the
tongue base and the lateral walls of the oropharynx
o Hypopharynx
▪ Clinical examination of the hypopharynx (mirror examination, endoscopy) is
performed concurrently with the examination of the larynx
• Imaging Methods
o Oral contrast radiography
▪ For diagnosing hypopharyngeal and oesophageal diverticula, tumours,
stenoses, and disorders of oesophageal motility
▪ Various contrast media can be used (e.g., barium, Gastrografin, Ultravist,
Isovist), depending on the nature of the investigation and any pre-existing
disorders.
▪ If there is a risk or suspicion of a perforation, barium should not be used.
o In patients with equivocal swallowing disorder a high-speed cineradiography. This
technique can be used to evaluate the different phases of swallowing
o CT and MRI
▪ Used in diagnosis of pharyngeal tumour masses as well as certain
inflammatory processes in this region.
▪ MRI has proven particularly effective for the soft-tissue discrimination
▪ of tumours in relation to surrounding structures, while CT is the method of
choice for excluding osseous involvement

45
12). Diseases of pharynx. Diseases of Nasopharynx- adenoids, juvenile
angiofibroma. Acute and chronic tonsillitis, scarlet fever, plaut-vincent
angina, diphtheria, infectious mononucleosis. Tonsillogenic
complications: peritonsillar abscess. Retropharyngeal and
parapharyngeal abscess. Disease of the hypopharynx.

• Adenoids
o Enlargement of the nasopharyngeal tonsil (adenoids) sufficient to produce
symptoms
o Physiological enlargement occurs at the age of 3 to 7 years
o Pathological enlargement is due to simple inflammation during recurrent attacks of
upper respiratory tract infection
o Clinical picture:
▪ Nasal obstruction: this leads to mouth breathing, snoring, difficulty in
feeding specially in infants, hyponasal voice and obstructive sleep apnea
syndrome (OSAS)
▪ Nasal discharge:-
• Mucoid or mucopurulent (egg-white plug of mucus seen behind the
uvula on gagging), the post-nasal discharge leads to recurrent
nocturnal cough and excoriation of the nasal vestibule.
▪ Eustachian tube obstruction
• predisposes to secretory otitis media, recurrent acute suppurative
otitis media and later on chronic otitis media may occur
▪ Adenoid facies:
• May develop with pinched nostrils, prominent incisors, open mouth
leading to spongy gums and dental caries, high arched palate and
flat or pigeon chest
• Mental dullness and apathetic looking due to hearing loss, chronic
hypoxia and look of adenoid face
• Nocturnal enuresis
o Diagnosis:
▪ Posterior rhinoscopy: can show the adenoids but difficult.
▪ Digital palpation: to feel the adenoids but should be avoided.
▪ Endoscopic examination is the best method if possible.
▪ Lateral X-ray nasopharynx for soft tissue is good.
o Complications:
▪ Descending infection: secretory otitis media, suppurative otitis media,
sinusitis, rhinitis, laryngitis and bronchitis.
▪ Obstructive sleep apnea syndrome (OSAS).
▪ Impaired concentration and excessive day time sleepiness.
o Treatment:
▪ Adenoidectomy.
• Juvenile Angiofibroma
o The commonest benign tumour of the nasopharynx.

46
 o Age: 10-20 years.
o Sex: Onlymales.
o Site of origin: Periosteum of the roof of nasopharynx or margin of the
sphenopalatine foramen in the posterior part of lateral nasal wall
o Histopathology: Large sinusoidal vascular spaces with no muscular coat, separated
by fibrous tissue stroma.
o Although histologically benign, but it is clinically aggressive in behaviour because of
its extension by pressure necrosis and displacement of surrounding structures, into
nasal cavity, orbit, pterygopalatine fossa, infratemporal fossa, cheek and intracranial
cavity
o Spontaneous regression: may occur at the age of 25 years.
o Symptoms:
▪ Nasal obstruction with recurrent severe attacks of epistaxis and
hyponasality of speech.
▪ Aural: Hearing loss due to Eustachian tube obstruction leads to secretory
otitis media.
▪ Proptosis and Swelling of cheek due to extension.
o Signs:
▪ by endoscopic examination as following: unilateral nasal pinkish mass, which
bleeds on touch with nasopharynx geal: smooth pinkish lobulated mass
covered by intact mucosa
▪ Secretory otitis media and conductive deafness may present
o Signs of extension of the tumour:
▪ Widening of the nasal bones and broadening of the nose (frog face
deformity), unilateral swelling of the cheek, unilateral proptosis and
manifestations of intracranial extension
o Investigations:
▪ CT scan and MRI: To confirm diagnosis and to assess tumour extension.
▪ Carotid angiography: To identify the feeding vessels.
▪ Biopsy: usually not necessary to avoid severe bleeding. When indicated,
should be done in the operating room with facilities to control bleeding.
o Differential diagnosis:
▪ Nasopharyngeal carcinoma: CT scan is diagnostic.
▪ Antro-choanal polyp: never bleeds and CT scan is diagnostic.
o Treatment:
▪ Better preoperative embolization of the feeding vessels to minimize
intraoperative bleeding.
▪ Surgical excision: Transnasal endoscopic excision, transpalatal, lateral
▪ rhinotomy or mid-facial degloving approach.
• Acute and Chronic tonsillitis
o Acute Tonsillitis
▪ Acute non-specific inflammation of the palatine tonsils.
▪ Aetiology:
• Causative organism: Group A β-haemolytic Strept. (the commonest),
Strept. pneumoniae, Staph. aureus and Haemophilus influenzae.
▪ Symptoms:
• Sore throat, dysphagia and foetor oris associated with ear ache
• High fever, malaise and arthralgia.

47
 ▪ Signs:
• High fever with tachycardia proportionate to the rise of
temperature.
• Local: manifestations are according to the types of tonsillitis, if
acute catarrhal tonsillitis: shows congested tonsils.
• If acute follicular tonsillitis: shows congested tonsils with yellowish
spots on the surface, spots may coalesce to form yellowish
membrane which can be easily removed. If acute parenchymatous
tonsillitis shows markedly swollen congested oedematous tonsils
and enlarged tender cervical lymph nodes.
o Complications::
▪ Chronic tonsillitis.
▪ Peritonsillar abscess.
▪ Parapharyngeal and retropharyngeal abscess.
▪ Acute glomerulo-nephritis.
▪ Acute rheumatic fever, often after a latent period of about 6 weeks.
o Differential diagnosis:
▪ Scarlet fever
▪ Diphtheria.
▪ Vincent's angina.
▪ A granulocytosis.
▪ Glandular fever (Infectious mononucleosis).
o Treatment:
▪ Rest, fluids, soft diet, analgesics, antipyretics and mouth wash.
▪ Systemic antibiotics: penicillin or amoxicillin for 10 days.
• Chronic Tonsillitis
o Chronic inflammation of the palatine tonsils due to recurrent acute tonsillitis with
inadequate antibiotic treatment.
o Pathological types: Follicular, hypertrophic or atrophic tonsillitis.
o Symptoms:
▪ Local:
• Recurrent acute tonsillitis and persistant sore throat with frequent
hawking and hemming, bad mouth odour due to accumulation of
purulent material in the crypts, or obstructive sleep apnea in
hypertrophic tonsillitis.
▪ General:
• Symptoms of septic focus: General ill health, fatigue, anorexia, low-
grade fever, headache and arthralgia.
o Signs: -
▪ Irregularity of the size and shape of tonsils may be unequal, hypertrophic or
atrophic.
▪ Congestion of the anterior pillars of tonsils in absence of acute infection.
▪ The crypts ooze pus on pressure.
▪ Persistent enlargement of jugulodigastric lymph nodes.
o Complications:
▪ Rheumatic fever and acute glomerulonephritis.
o Treatment: Tonsillectomy.

48
• Scarlet fever
o The tonsillitis in scarlet fever is also caused by infection with group A β-hemolytic
streptococci
o These are highly virulent bacterial strains that produce the scarlet fever exotoxin.
o Clinically, patients present with a rash that begins on the trunk. The area around the
mouth is spared (“perioral pallor”).
o A bright red tongue with a glistening surface and hyperplastic papillae (“raspberry
tongue,”) is seen
o The tonsils are greatly swollen with a deep red colour
o Occasionally there is an enanthema of the soft palate with hemorrhagic areas
o The diagnosis is established by the overall clinical picture combined with a positive
rapid streptococcal test
o Medical therapy relies on penicillin, as in acute tonsillitis.
o Additionally, the oral cavity should be rinsed with mild antiseptic solutions, and
analgesics should begiven for pain.
• Plaut- Vincent angina
o Aetiology:
▪ The disease is usually associated with two organisms: a fusiform bacillus and
spirochate (borrelia vincenti).
o Symptoms:
▪ severe sore throat, mild fever, dysphagia, foetor oris and malaise.
o Signs:
▪ Unilateral greyish yellow membrane of the tonsil, which rarely extend to the
pillars and soft palate, and ulcer with deep and irregular edge
▪ Enlarged tender cervical lymph nodes.
o Differential diagnosis: Acute follicular tonsillitis
o Investigations: Throat swab is cultured and examined for the organisms.
o Treatment:
▪ Hydrogen peroxide mouthwash and gurgle.
▪ Penicillin and Metronidazole (Flagyl)
• Diphtheria
o Acute specific infectious disease caused by Corynebacterium diphtheria.
o It is a serious condition; fortunately now it is very rare disease due to obligatory
immunization
o Age: Children 2-5 years.
o Aetiology:
▪ Causative organism: Gram positive bacilli Corynebacterium diphtheria.
▪ Transmission: Droplet infection from patient or carrier with incubation
period: 2-5 days.
o Symptoms:
▪ Insidious onset of low grade fever, sore throat, severe toxemia and malaise.
o Signs:
▪ Moderate fever (38-39°C) with rapid weak pulse not synchronous with the
temperature.
▪ False membrane (pseudomembrane) is formed on the tonsils, pharynx and
may extend to the larynx. The membrane is greyish- yellow in colour and
usually unilateral. It is adherent to the tissues and reoccurs rapidly when
removed

49
 ▪ Bilateral enlarged cervical glands (bull's neck).
o Investigations:
▪ Throat swab from the membrane is examined for diphtheria bacilli by direct
smear stained with gram stain and culture on Loffler's serum or blood agar.
o Differential diagnosis:
▪ From other causes of membrane on the tonsil and pharynx: Acute follicular
tonsillitis, Vincent's angina, Moniliasis or Blood diseases (Agranulocytosis,
acute leukaemia, infectious mononucleosis)
o Complications:
▪ Diphtheria exotoxins have a special affinity to nervous, cardiac and renal
tissue.
▪ Paralysis may occur after 2-3 weeks.
• Head and neck:
o Paralysis of the soft palate leads to nasal regurge, nasal
tone, and uvula deviation to the normal side.
o Paralysis of the eye muscles cause lack of accomodation,
diplopia and squint.
o Paralysis of the pharynx causes dysphagia.
o Paralysis of the larynx leads to stridor.
• Chest muscles:
o Including the diaphragm and intercostal muscles cause
respiratory failure
• Heart failure may occur early due to toxic myocarditis or late due to
vagal neuritis.
• Respiratory obstruction by the membrane of diphtheria.
• Acute nephritis (Albuminuria).
o Treatment:
▪ Antitoxic serum: 40000 - 100000 units according to the severity and
extension of the diphtheric membrane and the weight of the child is given
▪ immediately if diphtheria is suspected (S.C., I.M., or I.V.).
▪ Antibiotics: penicillin acts against the organism.
▪ Rest in bed.
▪ Isolation in a fever hospital until 3 successive swabs are -ve.
▪ Treatment of complications e.g tracheostomy for laryngeal obstruction.
o Prophylaxis:
▪ Passive immunization: 3000-10000 I.U. of antitoxic serum given for contacts.
▪ Active immunization is usually given in the triple vaccine D.P.T.
▪ Tonsillectomy in diphtheric carrier.
• Infectious mononucleosis
o A.k.a.: glandular fever
o A viral infection (Epstein Barr virus) which leads to marked increase in the
mononuclear cells (lymphocytes and monocytes).
o There are three types of the disease:
▪ Glandular type: Pyrexia and malaise for few days followed by generalized
lymphadenopathy. The tonsils may be red but there is no sore throat

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 ▪ Anginose type: Sore throat and dysphagia for 2 to 3 weeks, followed by a
membranous affection of the throat resembling Vincent's angina followed
by generalized lymphadenopathy
▪ Febrile type: Pyrexia, headache and general malaise, a week later a maculo-
papular rash appears, and after other two weeks followed by generalized
lymphadenopathy.
o Investigations:
▪ Blood picture: Leucocytosis with relative monocytosis and lymphocytosis.
▪ Serological tests: Positive monospot test and positive Paul-Bunnell test.
o Treatment:
▪ Rest, fluids, analgesics, antipyretics, broad spectrum antibiotics and avoid
ampicillin because it may cause skin rashes.
• Tonsillogenic complications
o Peritonsillar abscess:
▪ Peritonsillar abscess is a unilateral inflammatory process that involves not
only the tonsillar parenchyma but also the peritonsillar tissue— i.e., the
abscess spreads past the tonsil to involve the connective tissue between the
parenchyma and pharyngeal musculature
▪ The clinical features are pronounced unilateral redness and swelling of the
soft palate, muffled speech, and possible trismus.
▪ This is frequently accompanied by uvular oedema, but the swelling may also
spread to the tongue base and lateral pharyngeal wall, causing respiratory
complications.
▪ The treatment of choice is removal or incision of the affected tonsil under
antibiotic coverage
o Tonsillogenic sepsis
▪ rare in the antibiotic era
▪ It most commonly affects patients with weakened host resistance.
▪ In these cases, bacteria enter the bloodstream by the hematogenous or
lymphogenous route, and the bacteremia can lead to full-blown sepsis.
o Retropharyngeal and parapharyngeal abscess
▪ An inflammation or abscess may arise from the prevertebral or
parapharyngeal lymph nodes or by hematogenous spread as the result of a
minor foreign-body injury or upper respiratory inflammation.
▪ The clinical hallmarks are severe pain on swallowing with progressive
dysphagia, muffled speech, and possible trismus and dyspnea.
▪ Diagnosis:
• The mirror examination shows pronounced swelling in the
oropharynx or hypopharynx, usually at a prevertebral or
parapharyngeal location. The swelling may also spread to the larynx.
• The blood count indicates leucocytosis and ESR and CRP values.
• An postcontrast axial CT scan of a right parapharyngeal abscess) to
define the extent of the abscess and exclude any spread of infection
▪ Treatment: consists of surgical incision and drainage of the abscess under
general anesthesia and antibiotics. Cortisone should also be administered in
patients with significant dyspnea

51
13). Diseases of the salivary glands. Anatomy, Clinical examination,
imaging studies and biopsy of the salivary glands. Non-inflammatory
and inflammatory diseases. Sjogren syndrome. Tumours of salivary
glands.

Anatomy

• Parotid gland
o Largest gland and produces mucoserous secretions
o It lies within a deep hollow, known as the parotid region. The parotid region is
bounded as follows:
▪ Superiorly – Zygomatic arch.
▪ Inferiorly – Inferior border of the mandible.
▪ Anteriorly – Masseter muscle.
▪ Posteriorly – External ear and sternocleidomastoid.
o The secretions of the parotid gland are transported to the oral cavity by the Stensen
duct.
o Blood is supplied by the posterior auricular and superficial temporal arteries.
o Venous drainage is achieved via the retromandibular vein
o The autonomic innervation controls the rate of saliva production
o Sensory innervation is supplied by the auriculotemporal nerve (gland) and the great
auricular nerve (fascia)
• Submandibular gland
o heir mixed serous and mucous secretions are important for the lubrication of food
during mastication to enable effective swallowing and aid digestion.
o The submandibular gland is located within the anterior part of the submandibular
triangle. The boundaries of this triangle are:
▪ Superiorly: Inferior body of the mandible.
▪ Anteriorly: Anterior belly of the digastric muscle.
▪ Posteriorly: Posterior belly of the digastric muscle.
o Blood supply is via the submental arteries
o Venous drainage is through the submental veins
o The submandibular glands receive autonomic innervation through parasympathetic
and sympathetic fibres, which directly and indirectly regulate salivary secretions
respectively
• Sublingual gland
o producing mixed secretions which are predominately mucous in nature.
o lie on the floor of the oral cavity proper. They are situated under the tongue,
bordered laterally by the mandible and medially by genioglossus muscle
o Blood supply is via the sublingual and submental arteries
o Venous drainage is through the sublingual and submental veins
o Their innervation is the same as that of the submandibular glands

Examination

• History
o Remember to ask about metabolic diseases (diabetes mellitus)

52
 o Medications: antihypertensives, psychotherapeutic drugs
o Prior illnesses, surgical procedures or therapies involving the glands and oral cavity
o Hypersalivation, hyposalivation, sialorrhea or sicca syndrome
• Inspection
o External inspection of the periauricular and submandibular region along side oral
cavity and tonsillar region
o Facial nerve motor function should always be tested
o Masseter hyperplasia can mimic parotid gland enlargement – ask to squeeze jaw
together for easy differentiation
o Orifice of the excretory duct are evaluated for redness and swelling
o Parapharyngeal or tonsillar region may appear prominent sue to selling of the deep
portions of the parotid gland
• Palpation
o Parotid is normally not palpable
o Submandibular, swelling in sublingual gland are palpable bimanually
o Intraglandular, periglandular and cervical lymph nodes should also be examined
• Imaging
o US : can differentiate between normal glandular parenchyma, inflammatory
processes, tumours, lymph nodes and calculi
o X-ray: only in patients with a suspected salivary stone in the Wharton duct
o Sialography: contrast examination of the excretory ducts after catheterization and
gives most detailed view of parotid and submandibular glands. However rarely
performed due to infectious reasons
o CT and MRI: used in cases of tumours or difficult diagnoses
• Biopsy
o Fine needle aspiration biopsy
▪ Used preoperative in investigating salivary gland swelling
▪ Used for bacterial analysis
▪ Used with US to aspirate deep lesions
▪ Main complication is secondary infection at puncture site
o Incisional biopsy and intraoperative frozen section
▪ Used in chronic inflammatory cases, ulcerative lesions and facial nerve palsy
▪ Contraindicated in benign salivary gland tumours

Non-inflammatory diseases

• Sialolithiasis (salivary stone disease)

o Stone formation in te excreatory duct system of a salivary gland
o Usually located in the main duct
o Symptoms:
▪ Eating and gustatory stimuli incite a swelling of the affected gland
▪ Severe pain
o Diagnosis
▪ Stone usually palpable in the submandibular gland
▪ US shows a dilation of the duct system
o DDX: External obstruction of the excretory duct, as by a denature or tumour
o Complication: infection and abscess
o Treatment

53
 ▪ Surgery
• Distal stones: incise the excretory duct
• Intraglandular stones: submandibular gland stones and chronically
damaged gland should be excised
• Sialadenosis
o Non-inflammatory symmetrical swelling of the major salivary glands caused by a
systemic frequently unknown cause
o Parotid usually affected
o Assocaiated with:
▪ Chronic alcoholism, vitamin deficiencies, DM, protein deficiency, anorexia
nervosa and other eating disorders
o Symptoms:
▪ Painless, symmetrical swelling unrelated to eating
o Diagnosis:
▪ Bilateral, symmetrical painless swelling of the salivary glands
▪ Histological confirmation required via glandular biopsy
o DDX
▪ Chronic sialadenitis, masseter hyperplasia and obesity with fatty
hypertrophy of the glands
o Treatment
▪ Treat underlying cause

Inflammatory diseases

• Sialadenitis
o Types

o Aetiology
▪ Sialadenitis usually occurs after hyposecretion or duct obstruction but may
develop without an obvious cause
▪ most common in the parotid gland and typically occurs in patients in their
50s and 60s
▪ Chronically ill patients with xerostomia

54
 ▪ Patients with Sjögren syndrome
▪ Adolescents and young adults with anorexia
▪ The most common causative organism is Staphylococcus aureus; others
include streptococci, coliforms, and various anaerobic bacteria.
▪ Inflammation of the parotid gland can also develop in patients who have
had radiation therapy to the oral cavity or radioactive iodine therapy for
thyroid cancer
o Symptoms and Signs
▪ Fever, chills, and unilateral pain and swelling
▪ The gland is firm and diffusely tender, with erythema and oedema of the
overlying skin
▪ Pus can often be expressed from the duct by compressing the affected
gland and should be cultured.
o Diagnosis
▪ CT, ultrasonography, and MRI can confirm sialadenitis or abscess that is not
obvious clinically,
▪ If pus can be expressed from the duct of the affected gland, it is sent for
Gram stain and culture
o Treatment
▪ Antistaphylococcal antibiotics
▪ Hydration, sialagogues (eg, lemon juice, hard candy, or some other
substance that triggers saliva flow), warm compresses, gland massage, and
good oral hygiene are also important.
▪ Abscesses require drainage.
▪ Occasionally, a superficial parotidectomy or submandibular gland excision is
indicated for patients with chronic or relapsing sialadenitis.

Sjogren Syndrome

• Sjogren syndrome is a systemic auto-immune disorder characterised by the presence of dry

eyes (keratoconjunctivitis sicca) and dry mouth (xerostomia) as a consequence of
lymphocytic infiltration into the lacrimal and salivary glands
• Glandular symptoms
o Inflammation of the salivary glands: decreased production of saliva → xerostomia
(dry mouth)
▪ Dysphagia
▪ Increased formation of dental caries and tendency to oral infections
▪ Parotitis
o Inflammation of the lacrimal glands (chronic dacryoadenitis): decreased secretion of
tears → xerophthalmia (dry eyes) → keratoconjunctivitis sicca
▪ Redness, itching, burning of eyes
▪ Sensation of sand or foreign body in the eyes
▪ Blurred vision
o Sicca syndrome: combination of dry mouth and dry eyes
▪ Nasal dryness → chronic rhinitis, nosebleeds
▪ Pharyngeal, tracheal, and bronchial dryness → persistent, dry cough
▪ Vaginal dryness → dyspareunia (painful intercourse) and increased risk of
infections
• Extraglandular symptoms

55
 o General symptoms: fatigue and arthralgias (∼ 70% of cases)
o Skin manifestations: xerosis ; Raynaud's phenomenon (∼ 15–30% of cases)
o Vasculitis (∼ 10% of cases)
▪ Palpable purpura of the legs
▪ Recurrent urticaria, skin ulcerations
▪ Glomerulonephritis
o Neurological and psychiatric manifestations
▪ Depression
▪ Variety of focal and/or diffuse findings (e.g., impaired gross motor control,
paresis, seizures, peripheral neuropathy)
o Gastrointestinal manifestations: e.g., dyspepsia, reflux esophagitis
• Diagnosis
o Blood tests
▪ Nonspecific findings: ↑ ESR, normocytic anemia, leukopenia, eosinophilia,
hypergammaglobulinemia
▪ Immunological findings - Anti-Ro/SSA antibody and anti-La/SSB antibody
o Biopsy
▪ Taken from the salivary gland or the inner mucosa of the lip
▪ Shows destruction of minor salivary glands (fibrosis, parenchymal atrophy)
▪ Sialadenitis with dense lymphocytic infiltrations
• Treatment
o Treat the underlying disease in secondary Sjögren syndrome.
o For dry mouth
▪ Regular dental care
▪ Adequate hydration and foods that stimulate salivary flow (e.g., dried fruit
slices)
▪ In moderate/severe disease: artificial saliva, muscarinic agonists, and
immunosuppression (e.g., hydroxychloroquine)
o For dry eyes
▪ Avoid dry environments (e.g., shield eyes from wind, keep air humid)
▪ Artificial tears
▪ In moderate disease: topical immunosuppression (e.g., cyclosporine),
lubricants
o Treatment of extraglandular disease depends on the specific manifestation:
arthralgia may be managed with NSAIDs or hydroxychloroquine,
o neurological manifestations require aggressive immunosuppression.

Tumours of the salivary glands

• see page 148-150 if you wanna learn all the detailed bs :)

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57
14). Adult and paediatric obstructive sleep apnoea. Diagnosis.
Physical examination and treatment

• Obstructive sleep apnea (OSA): breathing-related sleep disorder in which airflow significantly
decreases or ceases because of upper airway obstruction (typically the oropharynx)
• Aetiology
o Obesity, especially around the neck (short, wide “bull neck”)
o Structural abnormalities that impair respiratory flow: tonsillar hyperplasia, nasal
septum deviation, enlarged uvula, tongue, or soft palate; nasal polyps; overbite with
a small chin; hypertrophied pharyngeal muscles
o Alcohol consumption before sleep
o Intake of sedatives and/or beta-blockers before sleep
o Smoking
o Family history
o Hypothyroidism
• Clinical features
o Restless sleep with waking, gasping, or choking
o Loud, irregular snoring with apneic episodes (third-party reports)
o Excessive daytime sleepiness (e.g., patient falls asleep, microsleep during meetings
or while watching TV)
o Impaired cognitive function (e.g., impaired concentration, memory loss)
o Depression, decreased libido
• Diagnostics
o Initial assessment: standardized questionnaires and third-party reports (interview
sleeping partner regarding snoring and respiratory interruptions)
o Laboratory tests are not usually considered useful in the diagnosis of OSA, but may
help identify underlying conditions or physiological consequences of OSA.
▪ Polycythemia
• This occurs because hypoxia induces erythropoietin secretion by the
kidneys, which stimulate the blood marrow, leading to increased
RBC production
▪ TSH (thyroid-stimulating hormone) may be considered in patients with
possible hypothyroidism.
o Sleep studies
▪ Polysomnography: first-line method
• Apnea and hypopnea events
• Oxygen desaturation
• Arousal events on EEG
• Bradycardia
• Fragmentation of sleep with pathological reduction of REM-sleep
phases and slow-wave sleep
o Home sleep apnea testing (less sensitive): Ambulatory screening method based on
the use of a device for monitoring cardiorespiratory parameters during the night.
• DDX: central sleep apnoea and Obesity hypoventilation syndrome (Pickwickian syndrome)
• Treatment
o Mild to moderate OSA (mild symptoms and < 20 apneic episodes)

58
 ▪ Weight loss
▪ Reduce and/or avoid risk factors: alcohol, nicotine, sedatives (e.g.,
benzodiazepines)
▪ Sleep hygiene: regular and sufficient sleep
▪ Lateral as opposed to supine sleeping position
▪ Blood pressure control
▪ Oral appliances
o Severe OSA (> 20 apneic episodes and alterations in arterial oxygen saturation)
▪ Surgery (uvulopalatopharyngoplasty)
• Resection of the uvula and redundant retrolingual, soft palate, and
tonsillar tissue
• This procedure should only be considered as a supplementary
treatment.
▪ Bilevel positive airway pressure (BPAP)
▪ Continuous positive airway pressure (CPAP)
• Complications
o Hypertension
o Hypoxia-induced cardiac arrhythmia
o Pulmonary hypertension and cor pulmonale
o Global respiratory insufficiency
o Cardiac infarction, stroke, and sudden cardiac death
o Risk of accidents (e.g., car crashes, occupational accidents) due to microsleep
o Increased risk of developing vascular dementia
o Poor sleep leads to increased appetite and obesity

• Pediatric obstructive sleep apnea is a sleep disorder in which your child's breathing is
partially or completely blocked repeatedly during sleep
• due to narrowing or blockage of the upper airway during sleep.
• There are differences between pediatric obstructive sleep apnea and adult sleep apnea.
While adults usually have daytime sleepiness, children are more likely to have behavioral
problems
• The underlying cause in adults is often obesity, while in children the most common
underlying condition is enlargement of the adenoids and tonsils.
• Other symptoms special to children are bed wetting and sleep terrors
• Infants and young children with obstructive sleep apnea don't always snore; they might just
have disturbed sleep
• During the day, children with sleep apnea might:
o Perform poorly in school
o Have difficulty paying attention
o Have learning problems
o Have behavioural problems
o Have poor weight gain
o Be hyperactive
• Risk factors in children include:

59
 o Down syndrome, Abnormalities in the skull or face, Cerebral palsy, Sickle cell
disease, Neuromuscular disease, History of low birth weight, Family history of
obstructive sleep apnoea
• Treatment
o Medications.
▪ Topical nasal steroids for mild obstructive sleep apnea
o Removal of the tonsils and adenoids
o Positive airway pressure therapy
▪ Proper fitting of the mask and refitting as the child grows can help the child
tolerate the mask over the face.
o Oral appliances.
▪ such as dental devices or mouthpieces, move child's bottom jaw and tongue
forward to keep your child's upper airway open.

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15). Anatomy and physiology of the larynx. Methods of Examination.
Stridor. Malformation of the larynx. Diphtheria. Acute Subglottic
Laryngitis. Acute Epiglottitis. Acute laryngitis. Angioneurotic laryngeal
Oedema. Chronic non specific laryngitis. Reinke’s oedema.
Tuberculous laryngitis

Anatomy and physiology of the larynx.

o The larynx projects forwards in the median part of the front of the neck.
o It extends from the root of the tongue to the trachea, lying opposite the third, fourth, fifth
and sixth cervical vertebrae. Its upper end opens into the laryngopharynx by the laryngeal
inlet, while its lower part is continuous withthe trachea at the level of the sixth cervical
vertebra
o It consists of a framework of cartilages, connected by ligaments and membranes, lined by
mucous membrane and moved by intrinsic and extrinsic muscles.
o Nerve supply: Branches of the vagus nerve:
o Superior laryngeal nerve: Motor to the cricothyroid muscle and sensory to the
mucosa above the vocal cords.
o Recurrent laryngeal nerve:
▪ Motor to all muscles of the larynx except the cricothyroid muscle and
sensory to the mucosa below the vocal cords.
▪ The left recurrent nerve turns around the arch of aorta in the chest, while
the right one turns around the subclavian artery in the neck.
o Blood supply:
o Superior laryngeal artery: from the superior thyroid artery.
o Inferior laryngeal artery: from the inferior thyroid artery.

Methods of Examination.

o Inspection: for position i.e. shifted to one side, movement with deglutition, dilated veins or
skin scar.
o Palpation: for tenderness and laryngeal click which is normally elicited due to moving of the
cricoid cartilage on the vertebral column from side to side (Moure's sign).
o Palpation of the neck: Cervical lymph nodes, thyroid gland and trachea.
o Indirect laryngoscopy: This examination is conducted by a warm laryngeal mirror
o Direct laryngoscopy:
o Rigid telescope or flexible fiberoptic naso pharyngoscope, under local anaesthesia
for difficult cases i.e. overhanging epiglottis or inability of the patient to tolerate
indirect laryngoscopy
o Rigid Laryngoscopy: Under general anaesthesia for examination by microscope for
magnification

Stridor

o Difficult noisy breathing due to partial laryngeal obstruction.

o Types of stridor:
o Inspiratory: due to laryngeal obstruction.

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 oExpiratory: due to lower respiratory obstruction e.g asthma.
oBi-phasic stridor (during inspiration and expiration) due to subglottic or tracheal
obstruction.
o Causes of stridor (laryngeal obstruction) leading to inspiratory stridor:
o Congenital:
▪ Congenital laryngomalacia, laryngeal web, subglottic stenosis and bilateral
vocal cord paralysis.
o Traumatic :
▪ Inhaled foreign body.
▪ Accidental trauma:
• External trauma e.g cut throat or strangulation
• Internal trauma:
o Chemical e.g corrosives.
o Physical e.g hot water or burns.
▪ Surgical trauma (Iatrogenic):
o Inflammatory:
▪ Acute non specific: in children.
▪ Acute specific: diphtheria.
▪ Chronic specific: scleroma, syphilis, T.B.
o Allergic oedema: e.g angioneurotic oedema of larynx or drug sensitivity.
o Neoplastic:
▪ Benign: multiple papillomata in children.
▪ Malignant: carcinoma.
o Neurogenic:
▪ Bilateral abductor paralysis: most commonly after thyroidectomy.
o Functional: Laryngismus stridulus

Malformation of the larynx (Laryngomalacia)

o Most frequent cause of congenital stridor

o Symptoms:
o low-pitched inspiratory stridor is audible at birth (may be constant or intermittent)
▪ louder in supine than in prone
o feeding difficulties may be seen
o Diagnosis
o Laryngoscopy: aryepiglottic folds are shortened and arytenoid cartilages are bowed
anteriorly and epiglottis is pale and lateral edges are curled inwards
o DDX
o Cleft anomalies, congenital cysts, laryngoceles
o Treatment
o Stridor resolved without treatment in 2 years
o Rarely temporary tracheotomy is required

Diphtheria

o It is very rare nowadays because of the mandatory DPT vaccination.

o Aetiology: secondary to faucial diphtheria (caused by corynbacterium diphtheria)
o Symptoms:

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 o Manifestations of diphtheritic toxemia (low grade fever, malaise, disproportionate
tachycardia).
o Stridor, due to laryngeal obstruction by the diphtheritic membrane.
o Hoarseness of voice and cough.
o Signs:
o The laryngeal mucosa is covered with a grayish yellow pseudomembrane.
o Treatment: As faucial diphtheria.
o Rest, isolation, antitoxic serum and penicillin.
o Tracheotomy, if needed

Acute Subglottic Laryngitis.

o Aka: laryngotracheobronchitis
o Viral disease aka as pseudocroup
o Droplet borne infection caused by parainfluenza, influenza and respiratory syncytial virus
o Symptoms
o Hoarse voice
o Dry, barking cough and stridor during the evenings
o Diagnosis
o Mild fever (if that)
o Laryngoscopy: inflammatory swelling below the vocal cords and in the upper part of
the cervical trachea
o Treatment
o No antibiotics needed (usually resolved within 3-5 days)
o In cases of pronounced stridor and dyspnoea, inhalation therapy with adrenaline is
given
o

Acute Epiglottitis.

o Aetiology:
• The most common pathogen is Haemophilus influenza type B.
• Age: infants and children are more common than adults.
o Symptoms:
• Rapidly progressive fever, anorexia and malaise.
• Inspiratory stridor, rapidly progressive, and potentially fatal.
• Painful swallowing with drooling and hot potato muffled voice.
o Signs:
• Examination by tongue depressor may induce laryngeal spasm, which may be fatal
• Lateral view X-ray neck shows marked thickened epiglottis.
o Treatment:
• It is an emergency condition as it is life threatening.
▪ Great care of the airway is mandatory. So endotracheal intubation is usually
needed and rarely tracheostomy.
▪ Medical treatment as acute non specific laryngitis in children

Acute laryngitis.

o Aetiology:
o Usually viral infection followed by secondary bacterial infection.

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 o Predisposing factors: Rhinitis, sinusitis, pharyngitis, smoking.
o Symptoms:
o Hoarseness of voice is the main symptom.
o Dry cough and feeling of discomfort in the throat especially on talking.
o Signs:
o Congestion and oedema of the laryngeal mucosa mainly the vocal folds.
o Treatment:
o Local treatment:
▪ Voice rest, avoid laryngeal irritants as smoking and steam inhalation
o General treatment:
▪ Antibiotics, cough suppressants

Angioneurotic laryngeal Oedema.

o Rarely paroxysmal disease predominantly affects adolescents and adults

o Congenital deficiency of C1 esterase inhibitor, leading to a rise in esterase levels, often
triggered by infections leading to laryngeal oedema
o Symptoms
o Rapid oedematous selling of the larynx
o Inspiratory stridor
o Oedema in lip, tongue, palate, uvula, throat and facial skin
o Diagnosis
o Indirect laryngoscopy reveals oedematous changes
o Serological testing: C1 esterase inhibitor deficiency
o DDX
o Allergic reaction and angioedema induced by ACE inhibitor
o Treatment
o Parenteral corticosteroids and antihistamines
o Subcutaneous or local administration of adrenaline
o Replacement therapy for C1 esterase inhibitor

Chronic non-specific laryngitis.

o Aetiology:
o Repeated attacks of acute laryngitis, repeated attacks of upper respiratory
infections as sinusitis and pharyngitis, voice abuse, prolonged exposure to laryngeal
irritants as tobacco and dust and gastro-oesophageal reflux.
o Symptoms:
o Hoarseness of voice with dry irritating cough with frequent hawking, hemming and
sore throat.
o Signs:
o Bilateral symmetrical thickening of both vocal folds, which appear whitish, reddish
or pale and oedematous.
o Treatment:
o Speech therapy.
o Avoid and /or treat the aetiologies.
o Micro-laryngeal stripping of the mucosa of the vocal cords is rarely needed.

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Reinke’s oedema.

o A subepithelial fluid collection forms in between the glottic epithelium and the vocal
ligament (Reinke’s space)
o Aetiology
o Nicotine abuse
o Vocal abuse
o Symptoms
o Hoarseness, frequent throat clearing, rapid vocal fatigue
o Diagnosis
o Laryngoscopy: glassy, oedematous swelling at the level of the vocal cords
o Treatment
o Microsurgical removal od the oedema while preserving the vocal ligament with
resection of the mucosa

Tuberculous laryngitis

o Always secondary to pulmonary tuberculosis and its site is the posterior part of larynx.
o Symptoms:
o T.B. toxemia: night fever, night sweating and loss of weight.
o Hoarseness of voice: the voice is weak and soft.
o Pain in the throat on speech and swallowing, may be referred to the ear.
o Cough and hemoptysis.
o Stridor and dyspnea (late).
o Signs:
o Pale granulations, ulcers, perichondritis and fibrosis. It affects mainly the posterior
part of the larynx in the inter-arytenoid region and posterior parts of the vocal folds.
o Complications:
o Perichondritis.
o Healing by dense fibrous tissue leading to laryngeal stenosis.
o Investigations:
o X-ray chest.
o Sputum examination for TB bacillus.
o Tuberculin test.
o Direct laryngoscopy and biopsy.
o Treatment:
o Medical treatment: Anti-tuberculous therapy.
o Surgical treatment:
▪ Tracheostomy when necessary.
▪ Treatment of laryngeal stenosis

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16). Tumours of the Larynx. Vocal cord polyps. Vocal cord nodules.
Laryngeal papilloma. Laryngeal squamous cell carcinoma. Spindle cell
carcinoma. Neuroendocrine carcinoma. Surgical treatment options
for laryngeal carcinoma. Laryngectomy effects and voice rehab.
Tracheotomy and cricothyrotomy

Tumour of the larynx

o Any hoarseness>2weeks should be investigated by laryngoscopy, specially in high risk

patients (e.g. smokers).
o Persistent hoarseness is a cardinal symptom of all neoplasms of the larynx whether benign/
malignant.
o Benign neoplasms of the larynx- constitute the MAJORITY of laryngeal neoplasms in both
children and adults.
o Clinically seen as mechanical obstruction of the upper airways with coughing, hoarseness,
wheezing and dyspnea.

Vocal cord polyps

o Epidemiology: Adults in speaking professions usually affected, preponderance of males.

o Etiopathogensis:
• Mechanical alteration of vocal cords caused by vocal cord overuse(phonotrauma)
• Chronic inflammation
• Histological examination reveals polypoid mucosal hyperplasia with inflammatory
component.
• Most vocal polyps are unilateral(90%) located on the free-edge of anterior 2/3 of
vocal cord.
o Symptoms: cardinal- hoarseness. Additionally- diplophonia (due to floating polyps
o Diagnosis: Telescopic laryngoscopy demonstrates a grayish-red sessile/ pedunculated mass
on the vocal cord.
o Treatment: microsurgical removal , may be followed by voice therapy.

Vocal cord nodules

o Epidemiology: in children(screamer’s nodules), singers(singer’s nodules), and professional

speaking patients, specially younger women.
o Etiopathogenesis:
• vocal abuse causing bilateral nodules to form at opposing sites at the junction of the
anterior and middle 1/3 of the vocal cords.
• Histological examination reveals fibrosis with epithelial thickening and submucosal
connective-tissue proliferation.
o Symptoms:
• Hoarseness, diplophonia, habitual throat clearing, foreign body sensation.
o Treatment:
• voice therapy
• Surgical removal in patients with exceptionally large nodules.

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 • Vocal nodules in puberty spontaneously regress due to longitudinal growth of the
vocal cords.

Laryngeal papilloma

• Epidemiology: most common benign laryngeal tumours in children - juvenile

papilloma(2-4yr olds) , solitary papilloma ( in 20-40 yr olds)
• juvenile laryngeal papillomatosis is characterised by multiple lesions that spread to the
trachea and bronchial system.
• multiple lesions may be found in adults too
• Etiopathogenesis: HPVs ( in particular HPV 6 and HPV 11), histologically the papilloma
are NEOPLASMS and NOT reaction to chronic inflammatory stimulus. Malignant
transformation is common in adult forms, not children
• Symptoms:
▪ Hoarseness,
▪ inspiratory stidor(developing with increasing obstruction),
▪ laryngeal/tracheal luminal obstruction(due occasional aggressive growth)
• Diagnosis
▪ Endoscopically: multiple soft, reddish-pink, villous, raspberry-like lesions
covering a large area of glottis and supraglottis. Lesions first appear on the vocal
cord
• Treatment
▪ CO2 laser surgery
▪ Complication
▪ Glottis webbing, virostatics, photodynamics
• Prognosis
▪ Spontaneously resolve/ recur after an asymptomatic interval.

Malignant Laryngeal Tumours

Laryngeal squamous cell carcinoma.

• Most squamous cell cancers of the larynx and hypopharynx start as a pre-cancer called dysplasia.
Most of the time, dysplasia doesn’t turn into cancer. It often goes away without any treatment,
especially if the underlying cause (like smoking) is stopped.
• Aetiology of laryngeal cancer:
▪ Tobacco / alcohol
▪ Infection with human papillomavirus
▪ Metal/plastic workers
▪ Exposure to paint/diesel/ radiation
▪ Laryngopharyngeal reflux
• Clinical presentation:
▪ Dysphonia/aphonia/ hoarseness in the voice
▪ Dysphagia ( difficulty or pain when swallowing)
▪ Dyspnea, aspiration, blood-tinged sputum
▪ Fatigue and weakness
▪ A sore throat or cough that does not go away.
▪ Ear pain
▪ A lump in the neck or throat
• Diagnosis: Physical exam of throat and neck, biopsy, larygnoscopy, CT

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• Treatment: Treatment includes: surgery, radiation therapy, chemotherapy. In advanced
metastatic tumours, treatment may be only palliative.

Spindle cell carcinoma

• Spindle cell carcinoma (AKA sarcomatoid carcinoma) is a highly malignant variant of squamous
cell carcinoma. Most spindle cell tumours are polypoid and pedunculated; they are often
detected at an early stage.
• Symptoms: hoarseness of his voice, dysphagia, odynophagia
• Diagnosis: laryngoscopy
• Treatment: Removed by polypectomy during diagnosis, radiation therapy.

Neuroendocrine carcinoma

• Neuroendocrine carcinomas of the larynx are rare tumours in comparison the common
squamous cell carcinoma of the larynx. They are classified as:
o Carcinoid tumour (Typical carcinoid)
o Atypical carcinoid tumour
o Small cell carcinoma (Small cell neuroendocrine carcinoma)
o Paraganglioma
• Aetiology: smoking
• Diagnosis: laryngoscopy, biopsy, CT
• Treatment: Partial or total laryngectomy depending on size and stage of tumour, radiotherapy

Surgical treatment options for laryngeal carcinoma.

• The larynx includes the supraglottis, glottis (vocal cords), and subglottis.
• The cancer may spread to nearby tissues or to the thyroid, trachea, or oesophagus.
• It may also spread to the lymph nodes in the neck, the carotid artery, the upper part of the
spinal column, the chest, and to other parts of the body.

Stanadard treatment:

• Radiation therapy
• Chemotherapy
• Surgery: Cordectomy, supraglottic laryngectomy, hemilaryngectomy, partial laryngectomy, total
laryngectomy (during this operation, a hole is made in the front of the neck to allow the patient
to breathe, called a tracheostomy), thyroidectomy, laser surgery.

Effects and voice rehabilitation

• Total laryngectomy significantly alters speech production

• Successful voice restoration following total laryngectomy requires identification of an
alternative sound source with a viable power source
• The 3 basic options are:
o artificial larynx speech
o oesophageal speech
o tracheoesophageal speech.

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Tracheotomy and Cricothyrotomy.

• Tracheostomy, is a surgical procedure which consists of making an incision on the anterior

aspect of the neck and opening a direct airway through an incision in the trachea (windpipe).
• The resulting stoma (hole), can serve independently as an airway or as a site for a
tracheostomy tube to be inserted
• this tube allows a person to breathe without the use of the nose or mouth.

• Cricothyrotomy is an emergency procedure that involves placing a tube through an incision

in the cricothyroid membrane to establish an airway for oxygenation and ventilation, during
certain life-threatening situations

• Cricothyrotomy is easier and quicker to perform than tracheotomy, does not require
manipulation of the cervical spine and has fewer complications.

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17). Laryngeal trauma. Recurrent laryngeal nerve paralysis. Basic
principles of speech. Dysphonia. Vocal cord paralysis. Stridor. Cough

Laryngeal trauma

• External trauma:
▪ Closed injuries: Motor car accidents, blows and strangulation.
▪ Open injuries: Stabs, cut throat and gunshots.
• Internal trauma:
▪ Inhalation: of steam, irritant fumes or gases.
▪ Swallowing of corrosives.
▪ Surgical:
• Rough laryngoscopy
• High tracheostomy.
▪ Intubation during anaethesia: Due to rough intubation, prolonged intubation or large
tube.
▪ Radiotherapy of head and neck: laryngeal oedema and perichondritis.
• Inhaled foreign bodies:
• Voice trauma:
▪ Leads to: - submucosal haemorrhages on vocal cords or vocal cord nodules (Singer's
nodule)

Recurrent laryngeal nerve paralysis.

Unilateral recurrent laryngeal nerve paralysis

• most frequently caused by a lesion sustained in thyroid surgery although has many
cause (see book page 380)
• symptoms: hoarseness
• diagnosis: laryngoscopy to find lesion
▪ if idiopathic then further testing is conducted: US, CT and MRI
• treatment: treat the cause, if post-surgery, check is nerve was transected

Bilateral recurrent laryngeal nerve paralysis

• chief complaint is dyspnoea (due to the reduced glottic gap)

• additional mucosal swelling also seen
• diagnosis: laryngoscope shows vocal cords fixed in a paramedian position and
only display passive motions
• treatment: tracheotomy and see if both nerves regenerate, surgical procedure
to widen the glottis is considered 6 months post onset

Basic principles of speech.

• The primary voice signal is produced in the larynx by the vibrations of the vocal cords
and is sustained by a dynamic equilibrium between expiratory air pressure and the
muscular tone of the vocal cords

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Dysphonia.

Dysphonia is the impaired ability to produce voice sounds. This is distinct from dysarthria, which is
the impaired movement of muscles to produce speech, including the lips, tongue, vocal cords, and
diaphragm

• Functional dysphonia is diagnosed when no anatomical or organic cause can explain

voice dysfunction. Functional dysphonia may be classified as one of the following:
▪ Psychogenic dysphonia: Impaired voice due to a psychogenic rather than a
physical origin. It is generally associated with anxiety. Psychogenic dysphonia
may be a result of excessive laryngeal muscle tension to provide glottis closure.
▪ Vocal cord misuse: This is caused by vocal overuse.
▪ Idiopathic vocal cord dysfunction: A paradoxical adduction of the vocal folds
during inspiration, causing dyspnoea.
▪ Treatment: Depending on aetiology, treatment involves a combination of speech
therapy, psychotherapy therapy, behavioural therapy, and hypnosis.
• Organic dysphonia includes several organic and anatomic pathologies. Given the vast
differential diagnosis, organic dysphonia can be organized by system:
• Vascular: Hemangiomas, arteriovenous malformation, lymphatic
malformation.
• Infectious: Laryngitis (viral, bacterial, and fungal).
• Trauma/Toxin: Arytenoid dislocation, neck trauma, caustic inhalation
injury, laryngopharyngeal reflux.
• Autoimmune: Connective tissue disorder (rheumatoid arthritis, systemic
lupus erythematosus).
• Malignancy: Laryngeal carcinoma (squamous cell carcinoma).
• Iatrogenic: Postintubation neuropraxia; thyroid surgery; anterior
cervical disc surgery; cardiothoracic, vascular, and neurologic
procedures.
• Neoplasm: Recurrent respiratory papillomatosis; benign laryngeal
lesions (nodules, cysts, polyps); neoplasms of the skull base,
mediastinum, oesophagus, lung, and thyroid.
• Neurologic: Stroke, myasthenia gravis, Parkinson disease.
• Endocrine: Hypothyroidism (laryngeal myxedema).
• Congenital: Congenital webs.
▪ Diagnosis: based on nasolaryngoscopy for visualization or videostroboscopy for
revealing mucosal wave abnormalities.
• Ancillary Tests
o Acoustic analysis, speech aerodynamic study, laryngeal
electromyography, computed tomography (CT)/magnetic
resonance imaging (MRI).
▪ Treatment
• Treat the underlying cause when discovered. Medical treatment rarely
leads to resolution of symptoms; surgical treatment and voice therapy
are generally more appropriate.

Vocal cord paralysis.

• Aetiology:

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 ▪ Congenital:
• Birth trauma, meningocele and congenital mediastinal masses.
▪ Acquired:
• Idiopathic (25%): may be viral neuritis.
• Supra-nuclear lesions: Rare bilateral extensive cortical lesions.
• Nuclear (Bulbar) lesions:
o Brain stem tumours.
o Brain stem vascular accidents hemorrhage or thrombosis.
o Encephalitis, poliomyelitis and diphtheria.
• Vagus nerve.
o Skull base at jugular foramen:
▪ Fracture base.
▪ Basal meningitis.
▪ Nasopharyngeal carcinoma and glomus jugular tumour.
• Recurrent laryngeal nerve lesions:
o In the neck:
▪ Thyroidectomy and radical neck dissection.
▪ Malignant tumours of thyroid, lymph nodes, hypopharynx, and
oesophagus
o In the thorax: (left recurrent laryngeal nerve).
▪ Surgery of lung, heart and oesophagus.
▪ Malignant tumours of mediastinal lymph nodes, oesophagus
and bronchi.
▪ Aortic aneurysm and dilated left atrium.
• Peripheral neuritis: Influenza, diphtheria and diabetes.
• Left vocal cord paralysis is more common than right vocal cord paralysis because the left
recurrent laryngeal nerve has longer course to the chest.
▪ Unilateral paralysis is more common than bilateral paralysis.
▪ Abductor paralysis is more common than adductor paralysis

Stridor – see essay 15

Cough

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18. Emergencies and primary measures in the ear, nose, and throat.
Foreign bodies. Anatomy, physiology of the oesophagus. Corrosive
esophagitis. Treatment.

• Emergency situations are common in the head and neck region due to the complex
anatomical relationships and the broad spectrum of possible diseases.
• They may present as life-threatening conditions associated with one or more of the
following symptoms: haemorrhage, respiratory distress (dyspnea, stridor), acute dysphagia,
and signs of local or systemic inflammation.
• Acute hearing loss, acute tinnitus, acute vertigo, and facial nerve paralysis are not life-
threatening but still represent an acute situation

Otologic Emergencies

• Life-threatening haemorrhages are extremely rare, but any bleeding from the ear canal
should be investigated in order to determine its cause and confirm the integrity of the
tympanic membrane, ossicular chain, and inner ear.
• Injuries to the tympanic membrane and ossicular chain require immediate evaluation by a
specialist, one reason being to exclude a lesion of the inner ear (damage to the auditory
and/or vestibular apparatus)
• Inflammations of the ear are mainly considered emergencies when the process transcends
the boundaries of the ear (mastoiditis, brain abscess, meningitis, sepsis), there is evidence of
facial nerve paralysis, and/or there are definite signs of inner ear involvement (labyrinthitis,
hearing loss, vertigo).
o This not only applies to acute inflammations but also to cholesteatoma, which is
likely to produce complications.
o Auricular inflammations and trauma carry a risk of cartilage damage.
• Acute vestibulocochlear dysfunction that presents with hearing loss, tinnitus, and/or vertigo
generally requires immediate diagnostic and therapeutic intervention.
• The same applies to paralysis of the facial muscles, which requires immediate investigation
and treatment regardless of whether the facial nerve damage has an idiopathic,
inflammatory (otitis media, cholesteatoma), neoplastic (parotid malignancy, vestibular
schwannoma), or traumatic cause (temporal bone fracture).

Sinonasal Emergencies

• Nosebleed (epistaxis) is the most common emergency, although life-threatening bleeding is

relatively rare.
• Acute sinusitis becomes an emergency when the inflammation spreads to involve the orbit
or eye and/or the meninges or frontal lobes of the brain, and immediate action is required.
• Inflammations of the external nose can lead to cartilage liquefaction and requires
appropriate treatment due to the risk of angular vein thrombosis and cerebral venous
thrombosis.

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 • Septal hematomas and abscesses can occur after nasal trauma and generally require
immediate intervention.
• Emergencies in the broad sense include fractures of the nasal bone, zygoma, or orbital floor
and intranasal foreign bodies.

Oropharyngeal Emergencies

• Besides the inflammatory complications of tonsillitis (peritonsillar and parapharyngeal

abscess), postoperative bleeding after tonsillectomy is a typical emergency situation.
• The erosion of blood vessels by malignant tumours can also provoke massive bleeding.
Impalement injuries may create a nidus for abscess formation.
• Bilateral choanal atresia in new-borns generally requires immediate intubation because
new-borns are obligate nose breathers, especially while feeding.

Laryngotracheal Emergencies

• Obstruction of the airways by swelling, a tumour, a foreign body, and/or blood and
secretions necessitates emergency airway intervention (intubation, cricothy- rotomy,
tracheotomy).

Foreign bodies

• Oropharyngeal swallowing abnormalities predispose to foreign-body aspiration.

• For anatomical reasons, aspirated foreign bodies are found four times more often in the
right main bronchus than in the left main bronchus
• They are rarely found in the larynx and trachea.
• Food items are aspirated with particular frequency, especially peanuts caution: may swell
within the airway) and watermelon seeds.
• Tablets are common (laryngeal) foreign bodies in adults.
• Symptoms:
o The initial symptoms of foreign-body aspiration depend on the size, shape, and
composition of the foreign body, its location, and the age of the patient.
o Usually the object provokes an immediate coughing fit with or without cyanosis,
accompanied by dyspnea, stridor, and pain.
o Larger foreign bodies impacted in the larynx may cause death from asphyxiation,
whereas smaller objects lead to hoarseness and cough.
o The clinical picture of a complete obstruction is:
▪ cyanotic, aphonic patient
▪ spasmodic breathing movements that do not ventilate the lungs.
▪ Bolus death refers to acute cardiac arrest caused by a vasovagal reflex evoked by
obstruction of the upper airways
o Foreign bodies in the trachea cause far greater complaints than objects in a bronchus,
ranging from a slight cough to fatal asphyxia.
o If a foreign body in the trachea moves with respirations, it produces the signs of a small
palpable impact, an audible click, and movement of the trachea.
• Diagnosis and treatment:
o Besides the clinical examination with inspection and auscultation, radiographs are of key
importance in determining the location of an aspirated foreign body.

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 o Chest radiographs at end-inspiration and end-expiration and lateral soft-tissue views of
the neck are also helpful in locating non-radiopaque foreign bodies.

Oesophagus

Anatomy

• The oesophagus begins at the upper oesophageal sphincter,

located at the level of the C6 and C7 vertebrae (inferior border of
the cricoid cartilage)
• The oesophagus terminates at the gastric cardia at T10 vertebra.

The three physiologic constrictions of the oesophagus are clinically

important due to the tendency for ingested foreign bodies to become
lodged at those levels:

• Upper constriction: in the area of the oesophageal inlet between

the cricoid cartilage and the cricopharyngeal part of the
constrictor pharyngis inferior muscle.
• Middle constriction: where the aortic arch crosses over the tracheal bifurcation
• Lower constriction: where the oesophagus pierces the diaphragm
The wall structure of the oesophagus adheres to the pattern of the gastrointestinal tract as a whole,
consisting of several layers:

• mucosa, composed of stratified, non-keratinized squamous epithelium.

• submucosa
• muscularis, consisting of inner circular and outer longitudinal muscle fibres: upper fourth of
the oesophagus: striated fibres, second fourth: mixed striated and smooth fibres, lower half:
smooth fibres
• adventitia
• Blood supply:
o The cervical part of the oesophagus receives most of its blood supply from the
inferior thyroid artery (and a lesser amount from branches of the subclavian and
vertebral arteries)
o The thoracic oesophagus is supplied by the aorta and intercostal arteries
o the abdominal oesophagus by the left gastric artery and left inferior phrenic artery.
o Venous blood in the neck is drained by the inferior thyroid vein. Thoracic and
abdominal drainage is to the azygos and hemiazygos veins and oesophageal veins.
• Lymphatic drainage is to the lymph nodes of the posterior mediastinum and pulmonary hilum.
• Nerve supply:
o The upper, cervical part of the oesophagus is supplied with branches from the
recurrent nerve
o the lower part with unnamed branches from the vagus nerve
o Below the tracheal bifurcation is the oesophageal plexus, formed by the two vagus
nerves
• Physiology-
o voluntarily initiated oral phase of swallowing is distinguished from an involuntary
pharyngeal phase and oesophageal phase, which are controlled through reflex
mechanisms

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 o The oesophageal phase of swallowing begins with a primary peristaltic wave, which
is reflexly initiated in response to movement of the bolus through the pharynx
(cranial nerves IX, X)
o Secondary peristalsis is additionally triggered in the oesophagus by the pressure of
the bolus against the oesophageal wall
o Through the coordinated action of these mechanisms, the bolus is transported into
the stomach within 7–10 seconds.

Foreign Bodies

• Etiology and pathogenesis:

o Foreign bodies typically become lodged in the hypopharynx or in the upper
constriction of the oesophagus.
o Most patients are small children who have swallowed coins, nuts, or toy parts, but in
many cases, they are older patients who have decreased sensation in the hard
palate (due to a maxillary denture)
o Objects typically swallowed by adults are fish bones or larger bone fragments, pieces
of meat, and denture parts.
• Symptoms:
o Typical symptoms are a feeling of pressure, a pricking sensation, or pain in the
hypopharynx or retrosternal area
o Dysphagia may also be present, depending on the size and location of the foreign
body.
• Diagnosis:
o Inspection and palpation will disclose any cutaneous emphysema caused by
perforation of the hypopharynx or oesophagus (sharp object!)
o This is followed by indirect mirror examination of the hypopharynx.
o If this fails to locate the foreign body, diagnostic imaging should also be performed.
o The imaging procedure of choice depends on the nature of the foreign body
suggested by the patient’s history.
▪ If a radiopaque foreign body is believed to be lodged in the hypopharynx or
upper oesophageal constriction, the soft tissues of the neck should be
imaged with a lateral radiograph.
▪ Otherwise, an oral contrast examination (with a water-soluble medium)
should be performed.
▪ An abdominal plain film can also show evidence of a foreign body in some
cases.
▪ Since there is always a danger of perforation, barium should never be used
in oral contrast examinations
• Treatment:
o Whenever an ingested foreign body is suspected, rigid esophagoscopy should be
performed without delay to retrieve the foreign object
o With a foreign body that has skewered and cannot be removed endoscopically, this
may require a transcervical incision or thoracotomy

Corrosive oesophagitis

• usually occurs from accidental or suicidal ingestion of caustic substances (e.g. lye,
household cleaners, bleaches, washing soda), and is harmful to the oesophagus due to their
alkali medium

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• The stomach is not affected as the gastric acid can neutralize these substances, however, in
cases of acidic corrosives, the oesophagus can be spared while the stomach is severely
injured.
• The oesophageal damage depends on the concentration of the harmful material and the
time of contact between it and the oesophagus. It usually affects the middle and lower third
of the oesophagus.
• Pathology
o acute stage: in the first 10 days from ingestion; acute necrosis with mucosal blurring
and dilated atonic oesophagus
o subacute stage: 10-20 days after ingestion and characterised by oesophageal
ulceration
o chronic stage: occurs after 21 days with oesophageal inflammation healed by
fibrosis resulting in structure
• Degrees of burn
o 1st degree: [Mucosal] Mucosal hyperaemia and oedema
o 2nd degree: [Mucosal & Submucosal] Small bleeding, exudates, ulcers,
pseudomembrane
o 3rd degree: [Transmural] Mucosal slough, deep ulcers, massive bleed, complete
obstruction, charring, perforation
• Clinical features- Oropharyngeal, retrosternal or epigastric pain, dysphagia/odynophagia,
hypersalivation, vomiting and hematemesis
• Treatment
o Asymptomatic patient who gives a reliable history of a low volume, accidental
ingestion of low concentration; endoscopy may not be necessary
o Hemodynamic stability, PPIs, Adequate analgesia. Assess signs of perforation,
mediastinitis or peritonitis– need emergency surgery
o Assessment need for ET intubation or tracheostomy, use of emetics, neutralizing
agents, or nasogastric intubation to remove remaining corrosive material is
contraindicated
o In most patients, gastrointestinal endoscopy should be performed during the first
24 hours-
o contraindication: hemodynamic instability, evidence of perforation, severe
respiratory distress, or severe oropharyngeal or glottic edema and necrosis.
o Oesophageal resection in corrosive strictures is technically difficult and hazardous.
o Oesophageal bypass is better and easier, and following later by regular endoscopic
surveillance for malignant transformation.
o In 1st degree burns:
▪ 48 hours observation
▪ oral feeds are started once patient swallows’ saliva painlessly
▪ Regular follow-up endoscopy at 1st, 2nd and 8th months
▪ Structure if formed can be identified by this time
o 2nd and 3rd degree burns:
▪ they are treated with fluid therapy, antibiotics, nutrition, PPIs, aerosolised
steroids
▪ Fibreoptic guided airway intubation if needed tracheostomy
▪ Endoscopic oesophageal stenting, feeding jejunostomy, laparoscopy for
evaluation

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