COMMON ENT DISORDERS

1. OTOLOGY
 Common symptoms
i. Otalgia
ii. Hearing loss
iii. Tinnitus
iv. vertigo
v. Ear discharge/ otorrhea – mucoid/ purulent/ mucopurulent/
watery
 Common diseases
i. ME diseases; Chronic suppurative otitis media with/out
cholesteatoma
ii. Diseases of the outer ear
iii. Inner ear diseases
 Common emergency
i. ASOM
ii. Acute mastoiditis/ mastoid abscess
iii. Acute Vertigo
iv. Sudden hearing loss
v. Ear & temporal bone trauma
 Common OT procedure
i. Myringotomy
ii. Myringoplasty
iii. Mastoidectomy (cortical/ radical/ Modified radical)

A. Outer ear diseases

a.1 congenital i.e Pre-auricular sinus, EAC microtia, canal atresia
a.2 inflammatory
a.3 Growth
a.4 FB
B. Middle ear diseases
C. Inner ear diseases

OTITIS EXTERNAL
-definition:

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 -clasification:

Otitis external

acute chronic

viral fungal bacterial

diffuse Localized (furunculosis)

Malignant type

 Swimmer’s ear
 Ear trauma/ water exposure
 Sx: otalgia, pruritus, scanty otorrhea – tender, edema
 Pseudomonas sp & staph.aureus
 Tx: local heating, toileting, Ichthamol glycerine (Ig) wick, topical &
systemic antibiotics

OTOMYCOSIS:
 Contributing factors: moisture, high temperature, hygiene, body immunity
 Sx: pruritus & otalgia --- fungal mycelia
 Organism: aspergillus sp, candida
 Tx: toileting, topical anti-fungal

EXOSTOSIS
 Benign periosteal outgrowths occur in the bony canal
 Multiple exposure to cold water
 Bilateral & multiple, near to the annulus

OSTEOMA
 Single, unilateral
 At bony-cartilaginous jx.

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DISEASES OF THE MIDDLE EAR
1) Acute suppurative otitis media (ASOM)

 Def: inflammation of the ME mucosa < 3/52

 Route of infx:
a. Via ET – esp.in infants or young adults
b. Via external ear

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 c. Blood borne
 Pre-disposing factors
d. URTI
e. Tonsillitis/ adenoiditis
f. Sinusitis
g. Nasal packing
 Bacteriology; strep pneumoniae/ HI/ Moraxella catarrhalis
 Pathophysiology: 4 stages
h. Tubal occlusion
i. Pre-suppurative
j. Suppurative
k. Resolution/ complication
 Treatment
l. Antibiotic
m. Topical nasal decongestant
n. Oral decongestant
o. Antipyrexia/ pain-reliever
p. Myringotomy

OTITIS MEDIA

ACUTE
CHRONIC
<3/52
>6/52

ACTIVE INACTIVE
OME/MEE/ serous
OM

+CHOLESTEATOMA

-CHOLESTEATOMA

2) CHRONIC OTITIS MEDIA

 Inflammation of the mucosal lining of the middle ear (ME) dt persistent/ recurrent
purulent otorrhea from the infx of the ME space/and mastoids in the presence of
the TM perforation – sequelae of persistent/ recurrent AOM
 Pathogens: mixed infx – gram –ve, gram +, anaerobs
 Sx: purulent otorrhea, inflamed ME mucosa, Hearing loss (CHL/ mixed)
 Tx: aural toilet, topical ear drop, systemic antibiotics, ear care

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Cholesteatoma

 Def: a sac of keratinizing epit.surrounded by granulation tissue. Able to expand

and destroy surrounding str.
 One of the consideration in the 1) unresolved CSOM despite optimum earcare &
treatment. 2) CSOM with granulation tissue
 Divided into congenital & acquired; 1) primary; 2) secondary; 3) tertiary
 Congenital – remnant of embryonic epithelial tissue; white mass at anterosup.ME
o Congenital cell rest
o No h/o ear disease
o Intact & normal TM Acquired:

 Primary acquired
o ET obstruction – retraction pocket at attic/ posteriorsuperior marginal
o Impaired migration
o Accumulated debris – cholesteatoma formation
o Other theory – papillary ingrowth of epit.thru its own Basement
Membrane

 Secondary acquired
o Migration theory
o Metaplasia theory

 Tertiary acquired
 Dx – “pearly” mass in ME/ mastoid, non-resolving CSOM. Higher suspicion if;
o Scanty d/c but foul-smelly
o Marginal perforation of TM (attico-antral)
o Polyps/ granulation tissue dt low-grade osteitis
o A/w deafness

 Adjunctive Ivx – mastoid X-ray/ HRCT

 Microb.study – mainly Pseudomonas aereginosa & Proteus spp
 Tx – Radical Mastoidectomy (RM)/ Modified RM

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  Complications- ossicular chain disuption, unresolved CSOM, labyrinthine fistula,
FN paralysis, intracranial Cx.

How does cholesteatoma cause bony erosion?

 Pressure
 Proteolytic enzyme plus infx & osteoclastic activities

Complications of CSOM with/without Cholesteatoma

 Routes of spread of infx

o Thru pathological bony defect caused by mineralization/ bony erosion
o Infected thrombus within small veins
o Thru normal anatomical defect – round/ oval window
o Thru non-anatomical defect – TBF or iatrogenic
o Straight into brain tissue – periareolar spaces of Virchow-Robin

 Intracranial Cx
o X’tradural/ subdural/ brain abscess
o Lateral sinus thrombosis
o Meningitis
o Otitic hydrocephalus

 Intratemporal Cx
o FN palsy
o Labyrinthitis
o Labyrinthine fistula
o Acute mastoiditis
o Subperiosteal Abscess
o Postauricular fistula
o Petrous apicitis

Lateral sinus thrombosis (LST)

o Sx: “Picket fence”fever; raised ICP, Cavernous Sinus tthrombosis, Griesinger’s

sign
o Dx: clinical + CT (delta sign), Queckenstedt/ Tobey-Ayer test
o Tx: high dose antibiotic, anti-coagulant, surgery
o Surgery: combined neuro & ENT

Temporal lobe abscess

 General Sx: ICP raised, fever&chill, irritable, drowsy

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  Local Sx: Nominal aphasia, quandratic homonymus hemianopia, epileptic fits,
contralateral hemipheresis, oculomotor nerve invx, visual hallucination,

Posterior cranial fossa abscess

 Nystagmus, + cerebellar signs

 Dx: clinical & CT/MRI
 Tx: combined neuro+ENT

Otitic hydrocephalus

 Raised ICP a/w ME infection

 Aka benign intracranial HPT
 Sx: raised ICP, reduced visual acuity, drowsy
 CT – normal ventricular size
 Probable aetiology – sagittal sinus thrombosis following LST

Labyrinthine fistula

 Exposure of membranus labyrinth with/out leak

 Sx: episodic vertigo & HL, tinnitus & possible otalgia
 Dx: Fistula test & HRCT & intraops.findings
 Mx: Surgery - controversy

Petrous apicitis

 2 ways spread of infx: posterosup route around the semicircular canal &
anteroinf.route from hypotymp, peritubal air-cells.
 Gradenigo sign – close anatomy to V & VI nerves
 Dx: clinical & CT

Labyrinthitis

3) SEROUS OM/MEE

 Fluid in the ME
 Sequelae of Acute OM/ Eusthac.Tube Dysfx
 Sx: aural fullness, discomfort, hearing loss, tinnitus
 Dx: clinical, Tuning fork exam, toynbee’s maneuver, tympanometry
 Tx: observation, topical decongestant, nasal steroid, ventilation tube

OTOSCLEROSIS (OTOSPONGIOSIS)
 Abn resorption & deposition of bone in all three layers of the otic capsule

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  AD trait
 Most common site is at oval window (fissula ante fenestrum), 2nd most is at round
window causing fixation of the stapes to the oval window.
 Clinical presentation: hearing loss most commonly CHL, paracusis willisii,
tinnitus, vertigo, Schwartze’s sign.
 HL – unilateral/ bilateral, rapidly worsening during pregnancy.
 DX: clinical & Audiometric assessment: tuning fork exam, PTA, Cahart notch,
tympanometri,

TINNITUS
 Def: sound arising in the head/ auditory hallucination
 Most intermittent & short duration
 One of the ear sx. Character: uni/bilateral/ onset/ duration/ constant/ intermittent/
pitch etc
 Any associated symptoms.
 Problems arising from this sx
- ?underlying pathologic condition
- debilitating
 Prevalent study: 32% of adult: at sometime in their lives; 6% debilitating
 Pathogenesis: theories
- excitation of one nerve by neighboring nerve leading to synchronization
- spont.excess influx of potassium & calcium into sensory hair cells causing
a synchronization.
 classification
tinnitus

Pulsatile/vascular Non-pulsatile/vascular

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 extracranial arterial diseases muscular
intratemporal arterial anomalies cochlear disorders
arteriovenous malformations noise-induced
(AVM) TBF
Meniere’s
increased intracranial pressure Presbycusis
glomus tumor SSNHL
venous anomalies ototoxicity
hyperdynamic circulations middle ear pathology
EAC pathology

 clinical assessment & diagnosis

 audiometric & radiographic studies
 management
- medical
- surgical
- masking
- hearing aid
- psychosocial aspects

2. NOSE & PARANASAL SINUSES

 Common symptoms
i. Nasal blockage/ stuffiness
ii. Rhinorhea
iii. Post nasal dripping
iv. Sneeze
v. Itchy
vi. epistaxis
 Common clinical cases/ diseases
i. Allergic/ non-alergic rhinitis
ii. Sinusitis
iii. Nasal polyps
 Common emergency cases
i. Epistaxis
ii. Septal hematoma
iii. FB nose
iv. Nasal trauma
 Common OT procedures
i. Septoplasty
ii. Turbinate reduction ( turbinectomy/ turbinoplasty/ electrical
cautery)
iii. Polypectomy

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 iv. Functional endoscopic sinus surgery

Rhinitis

Def: Inflammation of nasal mucosa lining characterized by ……..

rhinitis

allergy Non-allergy

Intrinsic/vasomotor
Seasonal Perennial Other causes
rhinitis

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ALLERGIC RHINITIS
Definition
Predominates in younger age group esp.first 2 decades of life (15-45 y/o)
Most common form of rhinitis
Tendency for self-limiting, decreasing/cease with age
Classification
 Seasonal- intermittent/ acute/ occasional
 Perennial- persistent/ chronic/ long duration
Mechanism of AR
 Type I HSS- Ig-E mediated
o Inflammatory cell infiltration
 Primary & secondary exposure
 Preformed & newly synthesized mediators
 Early-phase & late-phase reaction
Perform mediators
 Histamine
 Chemotactic factors – ECF, NCF
Newly-synthesized
 Leukotriens
 Prostaglandins
 PAF
 Cytokines – TNF, IL
Triggers of A/R
 Indoors aero-allergens- HDM, animal dander, fungal spores
 Outdoors aero-allergens- pollens, fungal spores
 Indoor pollutant & outdoor pollutants, haze
 Aspirin & NSAID

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  latex
Symptoms & signs
Co-morbidities
 Asthma- 40-50% * rhinitis in Asthmatic is >75%
 Allergic conjunctivitis
 Sinusitis
 Eczema
 Otitis media
Diagnosing AR
 Detail personal & Family history + nasal examination
 Allergic skin test: skin prick test/ Scratch test/ Intradermal dilution test
 Measurement of specific Ig-E antibody
 Nasal provocation/ challenge test
 Imaging – not usually necessary
Management
 Avoidance and education
 pharmacotherapy
 specific immunotherapy
 surgery if indicated

NON-ALLERGIC RHINITIS

1. infectious
 viral (common cold)
 rhinovirus, coronavirus, influenza, RSV, Adenovrus
 bacterial
 pnemococcal, HI, Staph spp, Moraxilla spp
 rhinoscleroma
 rhinosporidiosis
2. intrinsic/ VMR
- disease of adult, increase in intensity with age
- non-immunological pathophysiology
- idiopathic/ diagnosis of exclusion
- autonomic imbalance: parasympathetic predominant
- vasodilation & gland hyperresponsiveness
- might sensitive to cold air, fume, perfumes, smoke,
irritants etc
3. Nonallergic rhinitis with eosinophilia syndrome (NARES)
- negative allergy history & testing
- nasal smear shows eosinophilic count >10%
4. hormonal-induced
 pregnancy/puberty

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  hypothytoidism
 acromegaly
 OCP/HRT
5. drug-induced
 aspirin/ NSAIDs
 Anti-Hpt
 B-blocker
 ACE inhibitor
 A-adrenoceptor antagonist
 Vasoconstrictors
 Cocaine
 CPZ

6. Atrophic Rhinitis
 Primary/ secondary
 Excessive surgical removal
 Cx of sinusitis/ irradiation
 Ch.granulomatous disease
 Patent but feel blocked, crusted, smelly
 Atrophy of the mucosa & bone with decreased glands
 Klebsiella ozaenae
7. rhinitis medicamentosa

Rhinosinusitis/ Sinusitis

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 Definition of sinusitis: inflammation of sinus mucosa/ mucus membrane
 Pathogenesis:
o Obstruction: O2 lowered, PH
o Impaired ciliary fx – stagnation of secretion
o Mucus retention – bacterial overgrowth + mediators
o Infx – change the ‘Q’ of secretion
 Causes of ostial obstruction
o Mucosal swelling: URTi, AR, NAR, smoking, swimming
o Anatomy: DNS, CB, trauma, polyps, FB, neoplasm
 Other causes:
- Dental cause; recurrent unilateral
- ciliary dysfx & cystic fibrosis

 Bacteriology
- in acute: same as URTI
- in chronic: polymicrobial but anaerobs play
significant role
- in dental: anaerobs also play a role
 Classification of sinusitis
o Acute RS
o Subacute
o Recurrent
o Chronic RS
o Acute on chronic infx
 Symptomatology
o ARS: congestion, d/c, purulence, PND -- cough, facial pressure, fullness
or pain, halitosis, sore throat, dental pain, hyposmia, fever
o Major sx of CRS
 Facial pressure/ pain
 Facial congestion/ fullness
 Obstruction/ blockage
 D/c/ purulence/ PND
 Hyposmia
 Fever
o Minor sx of CRS
 Headache
 Fever
 Halitosis
 Fatigue
 Dental pain
 Cough
 Earache/ pressure/ fullness
 May present with recurrent pneumonia
 Clinical signs: pain at specific places, pus in nasal cavity
 Nasal endoscopy & C+S

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  Imaging techniques
o PNS X-ray; opacities & A-F level; advantages & disadvantages
 Caldwell (frontooccipital): mainly frontal, ethmoid & nasal cavity
 Water’s (OM): maxillary, frontal & facial trauma & orbit
 Lateral: frontal, sphenoid & maxillary.
 When to do?
o CT PNS: advantageous
 Indications: chronic refractory dis, complications, b4 FESS
 Translumination test
 Medical treatment
 Simple office/ minor surgery – wash-out procedure
 Functional Endoscopic Sinus Surgery
 Invasive surgical procedure
o Caldwell-luc
o Ext fronto/ ethmoidectomy
o Osteoplastic surgery
 Complications
o Orbital – Chandler’s classification
o Intracranial: meningitis, x’tradural, subdural, brain abscess
o Osteitis/ osteomyelitis
o Dental Cx
o Mucocele

Nasal polyp

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 General term for mass or Swelling – sessile, pedunculated etc in nasal cavity
o Spectrum of disease – swollen mucosa to neoplasm (benign/ malignant)
 Def of mucosal polyp - benign neoplasm/ prolapsed edematous mucosa/ ‘pale bags’
of edematous tissue
 Appearance – smooth, shiny, pale, opalescent to grey/ pink with stalk, base & body
 Hallmark for Chronic Rhinosinusitis
 Male> female, age 30-60 years.
 Incidence
o < 4% in population
o 7% in asthmatic
o 2% in CRS
o 20% in Cystic Fibrosis
o 36% in Aspirin intolerance (Samter’s triad- intrinsic asthma)
o rarely: primary ciliary dysfx syndrome

 Etiology – unknown
 In descending order of most affected sinuses: ethmoids/ maxillary/ frontal/ sphenoid
 Theories
o Infx
o Allergy
o Mucopolysaccoride theory
o Bernoulli’s phenomenon
o VM imbalance
o Epithelial-rupture theory- breaks in LP with prolapsed stroma
 Symptoms

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 o Congestion
o Hyposmia
o Thick mucous/ mucopus
 HPE
o Oedematous
o Thickened BM
o Hyperplasia of goblet cells
o Pronounced presence of eosinophil & mast cells
 Treatment
- pharmacotherapy
- surgery: polypectomy, Functional endoscopic sinus surgery

*polyps in children < 10 year-old – suspect CF

*polyps in < 2 year-old – TRO intracranial in origin.

If Unilateral nasal polyps. Bear in mind of these possibility;

 AC polyp
 Inverted papilloma
 Fungal
 Malignant neoplasm i.e Eathasioneuroblastoma

AC polyp/ Killian polyp

 > in men less than 40 years
 unilateral nasal blockage, worst on expiration
 unilateral opaque sinus
 not associated with allergy or sinusitis
 theory – faulty development of the maxillary ostium
 Tx – surgery, CWL contraindicated in children

INVERTED PAPILLOMA
 Intermediate tumor/ neoplasm – locally invasive
 Polyp-like str, a bit fleshy BUT pt usually 45-70 yrs & present with epistaxis
 Arises from lateral nasal wall
 a/w HPV types 6 & 11
 look for warts elsewhere
 potentially malignant transformation 10 – 15%
 Dx: biopsy HPE
 Tx: wide excision – medial maxillectomy

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EPISTAXIS
Bleeding from nose
Blood supply of the nose
 septum
o external carotid system
 sphenopalatine
 greater palatine artery (septal Br)
 superior labial artery
o internal carotid system
 anterior ethmoidal
 posterior ethmoidal
 lateral nasal wall
o external carotid system
 sphenopalatine
 greater palatine
 Br from facial arteryt
o internal carotid
 anterior & posterior ethmoidal
Little area (Kiesselbach’s plexus)
Causes of epistaxis
 local
o trauma
o infx- influenzae, viral, typhoid, measles, whooping cough, scarlet
o FB
o Rhinolith
o Neoplasm
o Iatrogenic (surgery)
o Severe DNS
 general
o d/o of blood or vessels: Hemophilia/ vWD/ Osler WR synd./ leukaemia/
MM
o CVS diseases
o Liver disease: vit K def
o Kidney disease
o Drugs: aspirin/ warfarin/ NSAIDS
o Arteriosclerotic disease a/w HPT
 idiopathic

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Site of epistaxis
Classification
 anterior epistaxis
o in almost all children and young adult
o mostly from Kiesselbach’s plexus
 posterior epistaxis
o most in adult
o trauma is nor important cause
o usually due to sclerotic vessel – esp.Hpt, DM
Management

1) To stop bleeding and general well-being

 general
o reassuring the patient
o safeguard ABC – in acute & profuse
o positioning of pt
o vital signs – in acute & profuse
o I/V line ready – in acute & profuse
o FBC & GXM – in acute & profuse
o Estimate blood loss
 Local
o Local pressure ant nose
o Cauterization: chemical (TCA, Silver nitrat) / electrical
o Nasal packing
 Anterior: BIPP/ Vaseline coated gauze/ expandable sponge
 posterior
o Arterial ligation
 IMA ligation
 AEA ligation
 ECA ligation
2) Need through nasal examination to rule out important cause in cases below
 Recurrent epistaxis
 In adult

 Interventional Radiology: in JNA case, pseudoaneurysm

 Complication from packing

JUVENILE NASOPHARYNGEAL ANGIOFIBROMA



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 3. LARYNGOLOGY
 Common symptoms
i. Dysphonia/ hoarseness
ii. Noisy breathing/ stridor
iii. Associated symptoms- dysphagia/ odynophagia/ aspiration/
heartburn, drooling
 Common diseases
i. Inflammatory diseases
ii. Congenital diseases of the larynx
iii. Cancer of the larynx
iv. Benign diseases of the Vocal cord
 Common emergency
i. Stridor
 Common OT procedure
i. Tracheostomy
ii. Endolaryngeal microsurgery (ELMS)
iii. Laryngectomy

1. STRIDOR

 Classification
 Type of stridor
 Common causes in adult
 Common causes in children esp.pyrexial

4. Others
 Common diseases of the pharynx
 Obstructive sleep apnoea (OSA)
 Deep neck space abscesses
 Head & Neck masses in pediatrics & adults including cancers

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