MAVIR

EAR

NOSE

THROAT

ORINOARYNGOKO
HIGHLIGHTS OF THE BOOK
Topic-wise Listing of Questions & their Answers
Answered all Questions of SIA, Osmania & Falcon QBs
Suitable to read ONE-MONTH before Final Exams
All Previous years' Questions ill 2022 are covered

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 CONTENTS
DISEASES OF EAR
LQS

SQs. .. 15
3

VSQs. ... 39
 Diseases of EAR
LQS
1) How will you manage a 24-year-old lady who has bilateral equal conductive hearing loss? [16]
a. Causes of conductive hearing loss (02, 01]
Ans.
Conductive Hearing Loss (CHL): The disorders of external and middle ear interfere with the conduction of
sound and cause conductive hearing loss. Box 2: Causes of conductive hearing loss
MANAGEMENT of CHL External auditory canal: Wax, foreign bodies, otitis extema,
congenital and acquired stenosis, exostoses, osteomas,
History: Side of affected ear; mode and age of tumors, cyst
onset; duration and progression of hearing loss; Tympanic membrane: Perforations (traumatic, acute sup
associated symptoms of ear fullness, ear pain, purative otitis media, chronic suppurative otitis media).
tympanosclerosis, retraction
otorrhea, tinnitus, vertigo/dizziness; preceding
Ossicles: Fixation (otosclerosis, tympanosclerosis, congeni-
history of URI, trauma, medications & family tal); discontinuity (traumatic, inflammatory, cholesteatoma)
history. Middle ear: Eustachian tube dysfunction, otitis media with
effusion, adhesive otitis media, hemotympanum, cholestea
Physical examination: Local examination of
toma,tumors (benign and malignant)
external ear, tympanic membrane, middle ear;
TABLE 3 Diferent modalities of treatment of con-
otoscopy; tuning fork tests; complete nose, throat, ducive hearing loss and their indications
head & neck examination. Removal of external Impacted wax, foreign body, osteoma,
auditory canal exostosis, keratosis obturans, tumors
Indicationsof imaging obstructions meatal stenosis

Temporal bone fracture Myringotomy Acute otitis media

Grommet Otitis media with effusion
Cholesteatoma
Stapedectomy Otosclerosis (fixation of stapes
Tumors (glomus and acoustic neuroma) footplate)
Tympanoplasty ympanic membrane perforations and
Surgical correction (except grommet) in children ossicular disruptions
Treatment: Hearing aids When surgery is not possible, refused
or failed

2) Cholesteatoma - EtiopatholoEy, Clinical features, Dx, Management & Complications [13, 11, 07, 051
a. How will you manage a case of atticoantral type of CSOM? [13]
b. Evaluation of a case of chronic otorrhoea fdischarging ear} [14] CSOM
c. Theories of Cholesteatoma formation [06
d. How does cholesteatoma cause erosion of bone [05]
e. What is the commonest intracranial complication of otitis media? [03] MeningitisS
f.Otitis meningitis -etiology, pathology, signs, symptoms & medical treatment (Aug-73, Oct-70)
Ans.
Chronic suppurative otitis media (COM) is a long-standing infection of the middle ear cleft characterized
by ear discharge and a permanent perforation.

TYPES OF CSsOM: Chronic obts media

2 types
1.Tubotympanic type Mucosal disease Squamosal disease

2. Atticoantral type
ACIve Inactive Healed Retraction pockets (in pars Active
(ohronic suppurative (permanent (adhesive otitis tensa or pars tlaccida or (cholesteatoma
otilis media) pertoration media) also called atelectatic ear) with discharge)

Classification of chronic otitis media.

 Tubotympanic type Atticoantral type of 44
a.k.a Safe/ benign type / mucosal disease Unsafe/ dangerous type/Squamosal disease
Commonly seen in Children
1. Ascending infections from tonsils,
adenoids and infected sin uses via (Refer Cholesteatoma below)
eustachian tube.
Aetiology
Can be a sequela of ASOM
Causative Organisms:
Aerobic-Pseudomonas aeruginosa, Proteus, Escherichia coli & Staph aureus
Anaerobes Bacteroides fragilis & anaerobic Streptococci
It has a capacity for progressive and
It remains localized to the mucosa of independent growth at the expense of
the anteroinferior part of the middle underlying bone in posterosuperior of the
ear cleft; the processes of healing and middle ear cleft.
destruction go hand in hand & either Granulation Tissue surrounds the area of
of them may take advantage over the osteitis
Pathogenesisoner, on
depending the virulence of Ossicular Necrosis profound hearing loss
Pathogenesis
organism and resistance of the Occasionally, the cholesteatoma bridgés the gap
patientTympanosclerotic masses caused by the destroyed ossicles & hearing lossis
(appear as chalky white deposits) not apparent (cholesteatoma hearer)
may interfere with the mobility of When it is associated with cholesteatoma
Ossicular Chain Conductive the disease is called active squamosal type
Hearing Loss Pus may find its way internally and cause
complications
Eardischarge: scanty, purulent & foul
Ear Discharge: Profuse, mucoid, smelling (due to bone destruction).
odourless Progressive deafness
Symptoms Conductive Hearing Loss maybe Fleshy red polyp may fill the meatus
-

a/w round window shielding effect Itching and pain in the ear
BleedingIt may occur from granulations
or the polyp when cleaning the ear
or marginal perforation of Pars tensa
Central Perforation of Pars tensa Attic
Retraction Pocket (invagination of tympanic
Middle Ear Mucosa is edematous
in active cases & membrane) may collect keratin plugs and
Signs a pale polyp form cholesteatoma. It can also get
maybe seen infected.
Pearly-white flakes of cholesteatoma can be
sucked from the retraction pockets
1) Examinatlon Under Microscope -Look for presence of granulations, cholesteatoma,
in-growth of squamous epithelium from the edges of perforation, status of ossicular
chain, tympanosclerosis and adhesions.
2) Tuning Fork Tests & Audiogram-to assess the degree & type of hearing loss
GRinne negative, Weber lateralized to affected side, ABC normal
Investigations 3) Culture and Sensitivity of Ear Discharge helps to select proper antibiotic ear drops
-

4) Mastold X-rays/CT scan Temporal Bone-to look for evidence of bone destruction.
* X- ray is taken in Schuller-Law view- Cholesteatoma appear as cotton wool.
Blunting of the scutum is the earliest sign in CT scan
*Destruction of lateral attic wall (normal figure of eight pattern is lost)
5) MRI: It provides complimentary information about soft tissue masses
 5 of 44
Primary aim is to remove the disease and
secondary is to reconstruct hearing but never
at the cost of the primary aim.

Post-aural (wildes) incision pinna is retracted

forward with self-retaining mastoid retractor
through mac evan's triangle, mastoid is drilled
by using cutting burr
1. Aural Toilet Remove all
discharge and debris from the 2 types of surgeries are done to deal with
ear. cholesteatoma:
2. Antibiotic Ear drops.
a) Canal wall down procedures
3. Systemic Antibiotics used in Done if the disease ís extensive
acute exacerbation of CSOM. They leave the mastoid cavity open into
4. Treatment of Contributory causes the external auditory canal so that the
-
Infected tonsils, adenoids, diseased area is fully exteriorized.
maxillary antra and nasal allergy Examples: atticotomy, modified radical
5. Surgery -to remove Aural polyp mastoidectomy and the radical
or granulations mastoidectomy.
6. Precautions: keep the ear dry. b) Canal wall up procedures:
Hard nose blowing can also push the
infection from nasopharynx to middle
Done if the disease is limited
ear and should be avoided. Here mastoid cavity is not opened into EAC.
It gives dry ear and permits easy
reconstruction of hearing mechanism.
However, there is danger of leaving some
Treatment cholesteatoma

Conservative Treatment (same as of

tubotympanic type) can be tried in elderly
patients who are unfit for surgery
Reconstructive Surgery-Once ear is dry, myringoplasty t ossicular reconstruct can
be done to
CSOM
restore hearing

Without cholesteatoma With cholesteatoma

Wet perforation Dry perforation Surgery:

CWU or cWD procedure with or
without tympanoplasty

Aural toilet
Topical antimicrobials
Systemic antimicrobials
Precautions

Persistent discharge Dry perforation

Tympanoplasty Myringoplasty
with or without
mastoidectomy tympanoplasty
Management of chronic suppurative otitis media (CSOM).
CWu, canal wall up; cWD, canal wall down.
Cholesteatoma is defined as a white, pulpy mass in the Clasification of cholesteatoma
Cholesteatoma
middle ear, which is lined by keratinizing stratified squamous
epithelium. It is also described as skin in the wrong place.
Classification of Cholesteatoma: Congenital Acquired

Congenital Cholesteatoma: It arises from embryonic

epidermal cell rests in the middle ear cleft or temporal Primary Secondary
acquired acquired
bone. Levenson Criteria is used for its Diagnosis.
Acquired Cholesteatoma Mochanism of bony eroslon in cholestoatome

Primary acquired cholesteatoma: occurs in the ear where Cholesteatoma

there is no previous history of ear discharge from the ear

or tympanic membrane perforation. Bony
erosion
Newbone
formation
Secondary acquired cholesteatoma: always occurs in an
already diseased ear where there is a pre-existing Physical Activation of ostecclasts
pressure due to release of
tympanic membrane perforation. inflammatorymediators
Theories of Cholesteatoma formation:
Wittmaack's Retraction pocket theory (primary acquired
cholesteatoma): Eustachian tube obstruction -ve pressure in
middle ear cavity formation of a retraction pocketobstruct the
normal migration ofthe epithelium of EACaccumulation of the Retraction pocket
desquamated epithelium > cholesteatoma of the middle ear
Haberman's Theory of migration: {secondary acquired
cholesteatoma) Skin of the external auditory meatus will migrate to
the middle ear cavity through the tympanic membrane perforation
secondary acquired cholesteatoma. Basal cell hyperplasia

3. Ruedi's Basal Cell Hyperplasia theory: The basal cells of germinal

layer of skin proliferate under the influence of infection and lay down
keratinizing squamous epithelium
Sade's Metaplasia theory: Because of recurrent/ chronic infection
Epithelial Invasion through posterosuperior pertoration
normal columnar epithelium turns into squamous epithelium. Genesis of a cholesteatoma.

Implantation theory: At the time of middle ear surgery squamous

epithelium may get implanted
Clinical Features & Management refer Atticoantral column in the above table
Features Indicating Complications in csOM
1. Pain indicate extradural, perisinus or brain abscess.
Vertigo-It indicates erosion oflateral semicircular Complications of Suppurative Otitis Media
canal labyrinthitis or meningitis. INTRATEMPORAL INTRACRANIAL
3. Persistent Headache: suggest intracranial complication.
extracranial)
4. Facial Weakness- indicates erosion of facial canal.
1) Meningitis {MC)
5. Fever, Nausea and Vomiting. (Intracranial 2) Extradural abscess
1. Mastoiditis
infection). 3) Subdural abscess
2. Petrositis
6. Iritability and Neck Rigidity. (meningitis). 3. Facial 4) Brain abscess
7. Diplopia. (Gradenigo's syndrome) petrositis. paralysis 5) Lateral sinus
8. Ataxia- (Labyrinthitis or cerebellar abscess). 4. Labyrinthitis thrombophlebitis
9. Abscess Roundthe Ear: (mastoiditis). 6) Otitic hydrocephalus.
3) Describe the aetioloEY, signs, symptoms and management of Secretory otitis media [12, 10]
a. Otitis media with effusion [10]
b. Glue Ears [04]
Ans.
OTITIS MEDIA WITHEEFUSION = Serous Otitis Media, Secretory
Otitis Media, Mucoid Otitis Media, "Glue Ear"
This condition is characterized by accumulation of non-purulent, sterile effusion in the middle ear cleft.

Etiopathogenesis:
1. Malfunctioning ofEustachian Tube- The causes are:
a) Adenoid hyperplasia. d) Tumours of nasopharynx.
b) Chronic rhinitis and sinusitis. e) Palatal defects, e.g., cleft palate, palatal paralysis
c) Chronic tonsillitis.
2. Allerev to inhalants or foodstuff is common in children. This not only obstructs eustachian tube by
oedema but also lead to t secretory activity of middle ear mucosa.
3. Unresolved Otitis Media, Inadequate antibiotic therapy in ASOM may inactivate infection but fail to
resolve it completely. This acts as stimulus for mucosa to secrete more fluid.
ViralInfections of upper respiratory tract may invade middle ear mucosa and stimulate it's increased
secretory activity.

Clinical Features
1) Symptoms- The disease
commonly seen in school-going children:
is
Hearing loss -This is the
presenting and sometimes the only symptom.
Delayed and defective speech -it is because of hearing loss
Mild earaches a/w H/o URTI
-

2) Signs-Otoscopic Findings:
G Tympanic membrane is dull and opaque with loss of light reflex
G Thin leash of blood vessels may be seen along the handle of
malleus or at the periphery of tympanic membrane.
G Tympanic membrane show varying degrees of retraction &
restricted mobility
G Fluid level and air bubbles may be seen in the middle ear on
Valsalva manoeuvre.
Oits media with effusior

Investigations
1. Tuning fork tests show conductive hearing loss.
2. Audiometry reveal conductive hearing loss. Sometimes, a/w sensorineural hearing loss due to fluid
-

pressing on the round window membrane. This disappears with evacuation of fluid.
Impedance audiometry reduced compliance and flat curve with a shiftto negative side indicates
the Presence of fluid.
4. X-ray mastoids-There is clouding of air cells due to fluid.

Treatment
The aim of treatment is removal of fluid and prevention of its recurrence.
 Medical Treatment Surgical Treatment
a. Topical decongestants-to When fluid is thick and medical treatment alone does not help,
oedema of eustachian tube. fluid must be surgically removed.
b. Antihistaminics-for allergy. a) Myringotomy and Aspiration of Fluid.
b) Grommet Insertion - to provide continued aeration of
C. Antibiotics - useful in cases of
URTI or unresolved ASOM.
middle ear. It is left in place forweeks or months or tillit is
spontaneously extruded.
d. Middle Ear Aeration: c) Tympanotomy or Cortical
Patient should repeatedly
Mastoidectomy for removal
perform Valsalva manoeuvre.
of loculated thick fluid or
This helps to ventilate middle
cholesterol granuloma.
ear and promote drainage of
d) Surgical Treatment of
fluid.
Causative Factor:
Children can be given chewing
Adenoidectomy, tonsillectomy
gum to encourage repeated Grommet in the tympanic membrane
and/or wash-out of maxillary
swallowing which opens the
antra may be required.
tube.

4) Discuss aetiopathogenesis, clinical features, complications & Management of Acute Otitis media
(ASOM) in a 2-year-old child [14, 09, 02]
Ans.
Acute ottis media (AOM) faka ASOM) implies an acute pyogenic inflammation of the middle ear cleft.
Though AOM can occur in all ages, it is mainly the disease of children as the ET is shorter, wider and more
horizontal in children.
ETIOLOGY
Routes of Infection
1. Through Eustachian tube
G Infections from Adenoiditis, tonsillitis, rhinitis, sinusitis, pharyngitis.
G latrogenic: Postnasal packing and after adenoidectomy.
G Feedingbottle: In the supine position, bottle-feeding may force milk to
enter middle ear via ET.
2. Pre-existing TM perforation due to CSOM & trauma while cleaning the EAC or hard slap on the ear.
3. Fracture of temporal bone in cases of head injury

Predisposing Factors
a) Low immunity: Malnourishment, poor dietary
habits, exposure to extremes of climate etc.
b) Barotrauma: pressure changes especially during flying
and deep-water diving can affect ET.
c)Swimmingin infected water
d) Exanthematous fevers: Measles, diphtheria,
whooping cough.
e) Palatal disorders: Cleft palate and palatal palsy.
f) Nasal allergy: Inhalants and foods.

Causative Microorganisms: Generally viral nasal infection

precedes the ear bacterial infection.
Most common Bacteria: Strep pneumoniae, Haemophilus
influenzae, Branhamella catarrhalis.
Other Bacteria: Streptococcus pyogenes, Staphylococcus aureus.
Viruses causing AOM: Respiratory syncytial
virus, Rhinovirus, Coronavirus, influenza
adenovirus etc. type A,
 STAGES of ASOM Pathogenesis Clinical Features
Infection from the pharynxinfectsthe
1. Stage of tubal ET oedema & obstruction of ET Patient presents with blocked feeling of
occlusion negative pressure in the middle ear & the earand earache.
TMretraction
From the Eustachian tube, the infection Patient presents with severe pain in the
2. Stage o
now reaches the middle ear
ear and on examination the TM appears
hyperaemia or very red and congested. Since the
inflammation and hyperaemia of
stage of pre vessels on the TM run radially, this
middle ear mucosa exudation of
suppuration
fluid. hyperaemicappearance is also known
as Cart wheel appearance of TM
Exudate in the middle ear along with
pus cells forms the suppurate The patient here presents with severe
suppurated fluid> TM starts to bulge pain and fever. On examination the TM
tothe point of rupture. is red and bulging
3. Stage of If
the pressure increases further, the
TM ruptures
{MC site of rupture
is in Patient here presents with the
suppuration
the antero-inferior quadrant} pus complaint of mucopurulent (which may
comes out from the middle ear which be blood tinged also) discharge from
being in a lot of pressure gives an the ears
appearance known as "pulsatile
otorrhoea or light house sign".
4. Stage of Resolution can occur in early stages also if the antibiotics are started early. With
resolution therelease of pus, the pain and fevercome down
Stageof complication: If virulence of the organism or the immunity of the patient is low
is high
Intratemporal complications like acute mastoiditis, labyrinthitis, facial nerve palsy and petrositis
or
Intracranial complications like meningitis, extradural abscess, brain abscess & lateral sinus thrombophlebitis
can occur.
Management: Early treatment will prevent the suppuration/ rupture of TM.
1. Antibiotics against MC organism -Strep pneumoniae and H. influenzaeampicillin (50 mg/kg/day in
four divided doses) and amoxicillin (40 mg/kg/day in three divided doses) for a minimum of 10 days
2. Nasal decongestants (drops) to relieve Eustachian tube oedema
3. Analgesics, antipyretics and antihistamines.
4. Myringotomy: The indications of myringotomy in a patient of ASOM are:
a. Red bulging TM with intense pain
b. Persistent effusion (>12 weeks): Here the pain has subsided but effusion is still there causing deafness
c. ASOM with facial nerve palsy.

Prognosis of ASOM It usually resolves completely without sequelae

Allcases of ASOM should be carefully followed till tympanic membrane returns to its normal appearance
and conductive hearing loss disappears
7"****"

5) Discuss the clinical features, diagnosis and treatment of intratemporal facial nerve paralysis [03]
a. Intratemporal course of facial nerve [07]
b. Bell's palsy [04]
c. Tic-doulourexu [94]
d. Crocodile tears [93]
Ans.
Intratemporalcourse of facial nerve - From internal acoustic meatus to stylomastoid foramen
further divided into
It is TABLE 14.1 CAUSES OF FACIAL PARALYSIS

1. Meatal segment- Within internal acoustic meatus. Central

Brain abscess
2. Labyrinthine segment- From meatus to the geniculate Pontine gliomas
Poliomyelitis
ganglion where nerve takes a turn posteriorly forming a Multiple sclerosís
"genu." Thisthe narrowest segment oedema or Introcranial port (cerebellopontine angle)
Acoustic neuroma
inflammation can easily compress the nerveparalysis. Meningioma
Congenital cholesteatoma
3. Tympanic or horizontal segment: From geniculate ganglion Metastatic carcinoma
to just above the pyramidal eminence. Meningitis
Intratemporal part
lies above the oval window and below the lateral .Idiopathic
Bell palsy
semicircular canal.
-

- Melkersson syndrome
4. Mastoid or vertical segment: From the pyramid to Infections
- Acute suppurative otitis media
stylomastoid foramen. - Chronic suppurative otitis media
- Herpes zoster oticus

- Malignant otitis externa

Trauma
Bell's Palsy Surgical: Mastoidectomy and stapedectomy
Accidental: Fractures of temporal bone
defined as idiopathic, peripheral facial paralysis or Neoplasms
It is
- Malignancies of external and middle ear
paresis of acute onset - Glomus tumour
- Facial nerve neuroma
It is the MC type of facial paralysis Metastasis to temporal bone (from cancer of breast,
bronchus, prostate)
Aetiology Extracranial part
Malignancy of parotid
1. Viral Infection - herpes simplex, herpes zoster or the EBV. Surgery of parotid
2. Vascular Ischaemia of the nerve induced by cold or Accidental injury in parotid region
Neonatal facial injury (obstetrical forceps)
emotional stress. Systemic diseases
Diabetes mellitus
3. Hereditary-The canal is narrow because of hereditary Hypothyroidism
Uraemia
predisposition and this makes the nerve susceptible to early Polyarteritis nodosa
compression with the slightest oedema. 10% cases of Bell Wegener's granulomatosis
Sarcoidosis (Heerfordt's syndrome)
palsy have a positive family history. Leprosy
Leukaemia
4. Autoimmune Disorders Demyelinating disease
5. Risk of Bell palsy is more in diabetics (angiopathy) and
pregnant women (retention of fluid).
Clinical Features-Onset is sudden; Paralysis may be complete or incomplete
a. Patient is unable to close his eye.
b. On attempting to close the eye, eyeball turns up and out (Bell Loss of
wrinkles
phenomenon).
C.Saliva dribblesfrom the angle of mouth. Wide palpebral
Tissure
d. Face becomes asymmetrical.
Epiphora
e. Tears flow down from the eye (epiphora).
Absence ol
f. Pain in the ear may precede or accompany the nerve paralysis. nasolabial
fold
8. Noise intolerance (stapedial paralysis) or loss of taste (involvement
Drooping of angle
of chorda tympani) ol mouth
Facial paralysis left side.
Diagnosis is always by exclusion.
All other known causes of peripheral facial paralysis should be excluded by careful history, complete
otological and head and neck examination, X-ray studies, blood tests etc.
Nerve excitability tests are done and compared with the normal side to monitor nerve degeneration.
Localizing the site of lesion helps in establishing the aetiology
Treatment:
General measures: Medical management Surgery
1. Reassurance. Steroids: Prednisolone is the drug of choice.
2. Analgesics to relieve ear
pain.
-

»If patient reports within 1 week, the adult

Nerve
dose of prednisolone is 1 mg/kg/day divided
Care of the eye to protect
decompression
into morning and evening doses for 5 days.
relieves pressure
against exposure keratitis. Patient is seen on the fifth day.
on the nerve
Physiotherapy of the facial If paralysis is incomplete or is recovering,
fibres and thus
muscles dose is tapered during the next 5 days. improves the
Prognosis: Ifparalysis remains complete, the same dose microcirculation
is continued for another 10 days and
85 to 90% of the patients of the nerve
recover fully.
thereafter tapered in next 5 days (total of
10-15 % recover incompletely
20days)
and may be left with some stigmata of degeneration.
------- ---*

6) Discuss the term 'Vertigo' [03, 99]

a. Benign positional vertigo [06] Posterior
Semicircular
b. Benign Paroxysmal vertigo [05 Canal

C. Mention the common causes of Vertigo. Briefly

outline the treatment of each condition [71]
Ans. utrice
upula Cbarrier)
Particles
Ampulla
Causes: The most common causes of vertigo in crnciple of repositioning

descending order are: ePpv is paroxysmal episodes of vertigo occurring with change ot
position
(1) benign paroxysmal positional vertigo (BPPV),
is the most common cause o¥ ertigo.
(2) acute vestibular neuritis and Pathophysiology
(3) Ménière's disease, otoliths dislodge from utricle into the semicircular canas
Posterior semicircular canal Hori2ontal SC> Superior SC

Pathogenesis & Clinical Features Otoliths irritate the endolymph.

Otoliths (Calcium carbonate erystals) settle doun with gravty

Treatment: repositioning maneuvers.
Reliet of symptoms til the patient changes head posture again.

episodic vertigo on change of head position.

-------

7) Otosclerosis-Etiolo8Y, C/F, Investigations& Treatment [20, 16, 09]

a. Differential diagnosis of Otosclerosis [17]
b. Carhart's notch [15,06]
C.Schwartze'ssign [05]
d. Otospongiosis [88]
Ans.
Otosclerosis (aka Otospongiosis), is a primary disease of the bony labyrinth. In this, one or more foci of
irregular spongy bone replace part of normal enchondral layer of bony otic capsule.
AETIOLOGY
1) The exact cause of otosclerosis is not known;
2) Risk Factors:
a. Heredity: About 50% cases are autosomal dominant
b. Race: It is common in Indians but rare among Chinese and Japanese.
 c. Sex: Females> Males {2:1}
d. Aggravating Factors for hearing loss: pregnancy, menopause, after accident or a major operation.
e. Van der Hoeve syndrome: triad of osteogenesis imperfecta, otosclerosis and blue sclera
f. Measles Virus infection.
YPES OF OTOSCLEROSIS
1. Stapedial Otosclerosis: MC type.
Pathogenesis: Fissula ante fenestram (area in front of the oval window) contain cartilage rests which
due to certain factors are activated to form a new spongy bone(anterior focus).
Lesion may also start behind the oval window (posterior focus), around margin of the stapes footplate
(circumferential), in
the footplate but
annular ligament
being free (biscuit
type). Sometimes, it
may completely B

obliterate the oval

window niche
(obliterative type).
Clinical Features:
Conductive HL
D
Cochlear Figure 13.1. Types of stapedial otosclerosis. (A) Anterior focus. (8) Posterior focus. (C) Circumferential. (D) Biscuit type (thick plate).
Otosclerosis; It (E) Obliterative.

involves region of round window or other areas in the otic capsule sensorineural hearing loss due to
liberation of toxic materials into the inner ear fluid.
3. Histologic Otosclerosis. asymptomatic and causes neither conductive nor sensorineural hearing loss.
SYMPTOMS
a) Hearing Loss: painless and progressive with insidious onset. Often it is bilateral conductive type.
b) Paracusis Willisii: An otosclerotic patient hears better in noisy than in quiet surroundings.
c)Tinnitus: It is more commonly seen in cochlear otosclerosis and in active lesions.
d) Speech: Patient has a monotonous, soft speech.
SIGNS&Investigations:
1. Tympanic membrane
TM in Mature cases chalky white, greyish or yellow.
TM in Active cases Flamingo pink (schwartze sign). It is due to T vascularity.
2. Eustachian tube function is normal.
3. Tuning fork tests:
ve Rinne (i.e., BC> AC) ABC test: Normal in Stapedial Otosclerosis {CHL}.

Weber test: lateralized to the ear It is in cochlear otosclerosis (SNHL}.

with greater conductive loss. Schwabach's test: lengthened
Gelles test: -ve 2000O00
0
4. Pure tone audiometry features: G
gap is present
AB
Shows loss of air conduction, more for lower frequencies.
There is a dip in bone conduction curve, maximum at 2000 Hz and is
called Carhart's notch. Carhart's notch disappears after successful
stapedectomy.
5. Speech audiometry reveals normal discrimination score (except in Olosclerosis keft ear. Note dip at 2000 R n bone
onductiorn (Carnart no
cochlear otosclerosis).
6. Tympanometry: BEST investigation As sclerosis type of curve
 Stapedial reflex: absent (due to fixed stapes)
HRCT of temporal bone- shows thickening & narrowing of foot plate; lucent & hypodense area of otic
capsule in active cases

DDx: serous otitis media, adhesive otitis media, tympanosclerosis, attic fixation of head of malleus,
ossicular discontinuity or congenital stapes fixation.

TREATMENT
Medical: Sodium fluoride is used to hasten the maturity of active focus and arrest further cochlear loss.
Surgical: Stapedectomy/stapedotomy with a placement of prosthesis (Teflon piston etc.) is the treatment
of choice.
Contraindications to Stapes Surgery
a) The only hearing ear
b) Associated Ménière's disease more chances of SNHL after stapedectomy.
c)Young children: Recurrent eustachian tube dysfunction is common in children. It can displace the
prosthesis or cause acute otitis media.
d) Professional athletes, high construction workers, divers and frequent air travellers. Stapes surgery has
the risk to cause post-op vertigo and/or dizziness and thus interfere with their profession
e) Those who work in noisy surroundings: After stapedectomy, they would be more vulnerable to get
sensorineural hearing loss due to noise trauma.
Steps of Stapedectomy
1. Meatal incision and elevation of the tympanomeatal flap.
2. Exposure of stapes area & Removal of stapes suprastructure.
3. Creation of a hole in the stapes footplate (stapedotomy) or removal of a part of footplate
(stapedectomy).
4. Placement of prosthesis & repositioning the tympanomeatal flap.
Post-OP findings:
a) Carhart's notch- disappears b) Tympanogram -Ad type of curve
Complications of Stapedectomy
1. Tear of tympanomeatal flap and later perforation of tympanic membrane
2. Injury to chorda tympani taste disturbance
3. Incus dislocation & Perilymph fistula
4. Vertigo-due to intra-op trauma, serous labyrinthitis, long prosthesis, perilymph fistula etc.
5. Conductive hearing loss-It can be due to short prosthesis or Displacement of prosthesis
6. SNHLE It can be due to Intraoperative trauma, Labyrinthitis or Perilymph fistula

Hearing Aid: Patients who refuse surgery or are unfit for surgery can use hearing aid. It is an effective
alternative to surgery.

8) What is otitis Externa? Describe etiology, clinical features & Mx of Malignant Otitis externa (97]
a. Clinical features of malignant otitis externa [13]
b. Furuncle of the Ear [13]
Etiological Classification of Otitis Externa (OE)
C. Otitis externa [11] A. Infective OE

d. Malignant Otitis Externa [04] a Bacterial: Localized OE (Furunculosis), diffuse OE and

OE
malignant
Ans. b. Fungal: Otomycosis (Candida and Aspergillous)
a. Viral: Herpes zoster oticus (Ramsay Hunt syndrome) and
Otitis externa (OE) is an inflammation of the EAC. bullous OE
Causative Organisms B. Reactive OE
a. Eczematous OE
b. Seborrhelc OE
G Pseudomonas aeruginosa (MC) c. Neurodermatitis
GOthers: Staphylococcus aureus, Staphylococcus epidermidis, Actinomyces israelii etc.
Acute Otitis Externa:
Occurs due to removal of hydrophobic ceruminous coating of EAC exposes the underlying epithelium to
water, infection and other contaminants and lead to progressive erythema and edema.
Predisposing Factors
Warm humid environment: 1 sweating changes the canal pH to alkaline-favors bacterial growth.
Obstruction of EAC: Stenosis, impacted wax.
Ear trauma: Use of ear swabs, in-the-canal hearing aids, digital ear thermometers etc.
Water contamination of EAC esp. swimming.
Clinical Features
G Presenting complaints: Otalgia and otorrhea
GEarly stage: An erythematous canal with scanty discharge
G Later on: Edematous and tender canal occluded with purulent squamous debris
Chronic Otitis Externa:
Types of Chronic OE: Eczematous OE, Dermatitis, Psoriasis (seborrheic) & Granular otitis externa
Clinical Features:
No prior history of trauma or water contamination
Usually not painful
Examination may reveal fungal hyphae in the canal or keratin debris from chronic dermatitis
Acute exacerbation is usually preceded by itching.
Treatment of Otitis Externa
Debridement of EAC-clears the infected material & allows topical Abx to reach the infected site.
Acidification of EAC (Abx in acidic suspensions and solutions) kills many bacteria and fungus.
Topical antibiotics
Abx impregnated ear wicks (cotton, merocele) offer better absorption through an edematous EAC.
GOfloxacin/ciprofloxacin + dexamethasone in an acidic vehicle are the best as they have no
ototoxicity and no potential for allergic reactions
Oral antibiotics are reserved for complications of OE
Complications of Otitis Externa:
Cellulitis: It presents as an erythematous ear. There is no induration like in perichondritis. Treat with systemic Abx.
Perichondritis or Chondritis
Medial canal fibrosis: In chronic otitis externa, thick fibrous scar may obstruct EAC.
Malignant otitis externa

Malignant Otitis Externa

It necrotizing infection starting in the EAC, progresses rapidly involving the temporal bone and
is a
adjacent soft tissue
Seen in Immunócompromised patients: Elderly diabetics, HIV/ AIDs, myeloid malignancies, anti-cancer
drugs and organ transplant recipients
Causative organisms: Pseudomonas aeruginosa is most common. S. aureus and S. epidermidis are rare
Clinical Features
Severe otalgia and otorrhea.
Hallmark finding: Granulations in the floor of EAC at the bony-cartilaginous junction.
Involvement of Cranial Nerves: Facial nerve (MC), 9th, 10th &11th CN palsy.
Intracranial spreadHeadache, fever, neck stiffness and altered levels of consciousness.
Spread of infection to neighbouring structures: Such as TMJ, mastoid, middle ear and petrous bone.
Investigations
Bacterial and fungal culture
High-resolution CT scan
Single-photon emission tomography with radionuclide tracers
Scans: Gallium-67 (taken up by monocytes and RE cells) reveals soft tissue infection while Tc 99 bone
scan will show bone infection.
Treatment
Antipseudomonal Abx: Oral or parenteral (depending upon the severity) ciprofloxacin for 6-8 weeks
or longer. In ciprofloxacin resistance cases, other antibiotics such as tobramycin, ticarcilin and third
generation cephalosporins may be used along with the ear toilet.
Hyperbaric oxyaentherapy
Thetreatment ofthecause ofimmunosuppression, such as diabetes and HIV/AIDs.
Suraicaldebridement of non-viable sequestra of bone is required when bone involvement is resistant
to antibiotic therapy.

Furunculosis: This localized form of acute otitis externa (AOE) is a staphylococcal infection of the hair
follicles, which are present only in the outer cartilaginous part of EAC
Clinical Features
Severe pain which increases on movements of pinna andjaw (while speaking or chewing).
The retro-auricular groove is obliterated if the furuncle is on the posterior meatal wall
On examination ofthe EAC there is edema and we might be able to see the furuncle or if it has
ruptured then a frankly purulent (without mucus) discharge. (Mucopurulent discharge comes anly from the middle
ear because EAC is lined by stratified squamous epithelium which has no mucus glands)
Tragal sign: On pressing the tragus patient complains of pain.
Treatment:
1. Anti-staphylococcal antibiotics.
2. A 10% to oedema (due to hygroscopic action of glycerine) & pain.
ichthammol glycerine pack can be put in EAC

3. Incision and drainage is done, if the abscess has formed.

SQs
1) Impedance Audiometry [20]
a. Tympanometry curves. [12]
b. Tympanometry [06]
Ans.
Impedance Audiometry is an objective test, particularly useful in children.
It consists of: Tympanometry & Acoustic reflex

Tympanic
Tympanometry membrane

Principle: When a sound hits tympanic membrane, some of

the sound energy is absorbed while the rest is reflected. A
stiffer tympanic membrane reflects more of sound energy
than a compliant one. By charting the compliance of
tympano-ossicular system against various pressure changes,
different types of graphs called tympanograms are obtained Probe of impedance audiometer showing three channels
to know the status of healthy or diseased middle ear (1) Oscillator-producing tone: (2) Air pump for increasing and
|decreasing of air pressure; and (3) Microphone that picks up and
measures reflected sound pressure level
Equipment: It consists of a probe which snugly fits into the external auditory canal and has 3 channels
Oscillator, Air pump & Microphone TABLE 5 Different types of tympanogram
Interpretations: Characters of graph Diseases of middle ear
ype A Normal curve Nomal middle ear
The middle ear pressure with normal Eustachian tube function
Type As Normal curve with low Fixation of ossicles such
function is 0 to -150 mm H20 compliance at or near as otosclerosis, malleuss
ormal amblent air fbxation
The middle ear pressure more negative than 150 mm H20 pressure
suggests poor Eustachian tube function Type Ad High compliance at or Ossicular discontinuity
near normal ambient thin and l8x ympanic
Acoustie Reflex pressure membrane
Type B A Mlat or dome-shaped Middle ear fuid
It based on the fact that a loud sound causes bilateral
is Curve. No change
in compliance with
pressure changes
contraction of the stapedial muscles which can be detected
Type C Maximum compliance tracted tympanic
by tympanometry. peak) at negative membrane, negatve
pressure range pressure or some fluid in
Tone can be delivered to one ear and the reflex picked from -150 mm of H,o middleeBar

the same or the contralateral ear.

Uses:
1. To test the hearing in infants
and young children.
2. To find malingerers: A person
who feigns total deafness and
does not give any response on
pure tone audiometry but -200-100 0 +100 +200 -200-100 0 100 200 -200 -100 0+100 200
mo mm
shows a positive stapedial reflex A ypeA B Type B Type C
Tympanograms (Table 5). Type (A) A, normal; As, otosclerosis; Ad, ossicular disuption; Type (B) Flat or dome-shaped
is a malingerer. audiogram (middle ear fuid); Type (C) Maximum compliance at -200 mm of H,0 (Eustachian tube dysfunction)
3. To detect cochlear pathology.
Presence of stapedial reflex at lower intensities, e.g. 40
60 dB than the usual 70 dB indicates recruitment and
thus a cochlear type of hearing loss. VII N. °

4. To detect 8th nerve lesion (stapedial reflex decay).

Supenor
5. Lesions of facial nerve (Absence of stapedial reflex) olivary
complex
6. Lesion of brainstem. If ipsilateral reflex is present but the VII N.
contralateral reflex is absent, lesion is in the area of
crossed pathways in the brainstem.
Acoustic reflex.

Physical Volume of Ear Canal: Acoustic immittance can also measure the physical volume of air between
the probe tip and tympanie membrane. Normally it is up to 1.0 ml in children and 2 ml in adults. Any
increase in volume indicates perforation of the tympanic membrane.

2) Tuning Fork Tests [17]

a. Absolute bone conduction test [o5]
b. Weber's Test [12, 11
C. Rinne's test [91]
Ans.
A tuning fork (TF) consists of a base (footplate), stem and two prongs. The TF of S12 Hz is most commonly
used.
 Type of TF test Principle Normal CHL SNHL

It compares patient's AC with AC> BC BC>AC AC BC

Rinne test (Rinne+)
BC (Rinne +) (Rinne-)
BC of both ears is compared Lateralized to Lateralized to
Weber Test Not lateralized
simultaneously affected ear better ear
Itcompares the duration of
Absolute Bone patient's BC with that of the Same as Same as Reduced
Conduction Test examiner. examiner's examiner's
EAC is ocluded
BC of patient is compared
with that of the normal Same as Redu
Schwabach's Test Lengthened
hearing examiner but EAC is examinerrs (Shortened)
not ocluded
Negative
It tests the effect of occlusion Positive Positive
Bing Test (No change in
of EAC on BC hearing
hearing)
It tests the effect of air Negative
Gelle's Test pressure in EAC (via Siegel's Positive (Ossicular chain is Positive
speculum) On the BC hearing |fixed)

3) Presbycusis [Feb-17, 04]

Ans.
Sensorineural hearing loss, which occurs due to the aging process, is called presbycusis.
Predisposing Factors hereditary predisposition, chronic noise exposure, ototoxicity, metabolic disorders,
arteriosclerosis and diet.
Pathogenesis: 4 types of presbyeusis have been described according to the area of degeneration.
1. Neural presbycusis -degeneration of spiral ganglion; Speech
Left ear Frequency
z
1500 3000 6000 10000

discrimination is poor 125 250 500 1000 20004000 800O

2. Sensory presbycusis-degeneration of the organ of Corti; Speech

discrimination remains good.
3. Metabolic presbycusis- atrophy of stria vascularis; Speech
discrimination remains good.
4. Cochlear conductive presbycusis- basilar membrane becomes stiff
Audiometry will show descending type (sloping type) of curve
Clinical Features 10

Audiogram of a patient with presbycusis. Patient wil

a) Deafness: 51owly progressiye, symmetric SNHL in people > 60 have bilateral symmetrical sensorineural hearing loss (SNH
years
b) Discrimination: Poor speech understanding. Typical complaint is "I can hear but cannot understand."
c)Recruitment may be positive
d) Tinnitus & Vertigo
Investigations
Weber lateralized to better ear & ABC is reduced.
TFTS: Rinne +;
Audiogram: SNHL is greatest in frequencies > 2,000 Hz with poor speech discrimination
Differential Diagnosis
1. Cochlear otosclerosis- Paracusis of Willis will be present in otosclerosis.
2. Meniere's disease: Hearing loss will be fluctuating in character. Glycerol test will be positive.
3. Acoustic trauma: The audiogram will show sudden dip at 4 kHz, History of noise trauma
 18 of 44
Treatment
1. Prophylaxis Avoidance of noise, high fat diet, cold, excessive smoking and stress.
-

2. Paychological Support: Inform and explain the disease process and its effect in the body to the patient
Hearing Aids
4. Drugs: However, B1, Bs, B12 & iron may be tried in long-term basis to prevent deterioration of hearing.
***** --*****=*--*-----*---***-*-- ------

4) Fistula test [17]

a. False positive fistula sign [15]
Ans.
Principle: The pressure changes in the external canal are transmitted to the labyrinth. In cases of
labyrinthine and perilymphatic fistula, it stimulates labyrinth and results in nystagmus and vertigo.
When pressure is increased in EAC, displacement of endolymph results in nystagmus of the same side.
If pressure is decreased in EAC, displacement of endolymph results in nystagmus of the opposite side.
Method-It can be performed in two ways:
1. Pressure on tragus: Sudden inwards pressure on the tragus air pressure in the ear canal and
stimulates the labyrinth.
2. Siegel's speculum: The T pressure in the ear canal produces vertigo and nystagmus.
Interpretation
Negative fistula test Normal persons & Dead labyrinth.
Positive fistula testLabyrinthine fistula, Perilymphatic fistula & Fenestration operation
Folse-negative fistula test: It occurs when cholesteatoma covers the site of fistula and does not allow
pressure changes to be transmitted to the labyrinth.
False-positive fistula test (Hennebert's sign): It is the positive fistula test in the absence of a fistula. It is
seen in -

Congenital syphilis: Footplate of Stapes becomes hypermobile

Ménière's disease: Movements of stapes result in stimulation of the utricular macula in about 25%
cases)

5) Otomycosis [17, 13, 12]

Ans.
Otomycosis/Fungal infection of ear: It is seen in hot & humid climate of tropical and subtropical countries.
Superficial fungal infection is the most common and limited to EAC.
Invasivetype is rare and involves temporal bone.
Fungal Sps Specific Clinical features Treatment
Aspergillus Pigmented tufts of hyphae resembling a Debridement, acidic drops (acetic acid) and
niger cotton ball dotted with black debris ("wet gentian violet painting of ear canal and TM.
newspaper), Ear should be kept dry
Candida Opportunistic fungal infection; Antifungal creams {clotrimazole, nystatin)
albicans EAC appears wet macerated and filled
& is Ear should be kept dry
with soft, curd-like debris
General Complaints of the patients:
Intense itching, discomfort, or ear pain
Discharge with musty odor and ear blockage
Sodden, red and edematous meatal skin
Complications:
Systemic invasive mycoses (Aspergillosis, Mucormycosis, Candidiasis, Cryptococcosis, Coccidioidomycosis &
Histoplasmosis) involve temporal bone in cases of defective host defences (DKA, chemotherapy,
corticosteroids, AIDS).
 Chronic fungal or bacterial middle ear infections spread to inner ear through oval or round window or
osteomyelitis of petrous bone

6) Myringotomy [16]
a. Grommet [10]
Ans.
Myringotomy refers to an incision of the tympanic membrane to drain middle ear fluid, which may be
suppurative or nonsuppurative.
Tympanostomy tube (grommet) is inserted through myringotomy incision for draining middle ear fluid as
well as for providing aeration in case of malfunctioning Eustachian tube.
Indicationsfor Myringotomy
Indications in acute otitis media (AOM):
Acute excruciating pain
Bulging eardrum
Unresponsive to antibiotics
Complications: Facial paralysis, labyrinthitis or meningitis with
bulging tympanic membrane. Myringotomy incisions Cramterendal for scu
suppuratve otitis medie (ASOM) and radial (R) fcr otuts meda
Otitis media with effusion (OME). wh ofuoion (OME)
Aero-otitis media to drain middle ear fluid and "unlock" the Eustachian tube.
Preoperative Evaluation
History and physical examination
Audiometry
Tympanometry.
Anesthesia
General anesthesia: In children and uncooperative adults; Acutely inflamed TM.
Local anesthesia: In cooperative adults.
Technique: The procedure is always done under operating microscope. Clean wax and debris from EAC.
Perform myringotomy in {preferably anteroinferior quadrant} of tympanic membrane using a sharp
myringotome. Either radial or circumferential incision is employed
Complications: EAC laceration, Otorrhea, injury to ossicles & TM (perforation, atrophy, retraction), loss of
grommet into middle ear etc.

7) Theories of hearing [15, 08]

Ans.
Helmholtz's place theory (1883): It states that the basilar membrane acts as a series of tuned
resonators similar to a piano string. Each pitch would cause resonant vibration of the basilar membrane
which is particular to its own place. High frequency waves excite the basal region and low frequency
waves excite the apical region.
Rutherford's frequency/telephone theory (1886): it states that all frequencies activate the entire length
of the basilar membrane along with the hair cells. He postulated that the frequency of the signal is
represented by the rate of firing of the auditory nerve fibers. He believed that all vibrations are
portrayed by the nerve impulses to the brain without complex vibrations in the cochlea.
Wever's volley resonance theory (1949): Combines both the place & telephone theories postulating
that:
High frequencies (5000 Hz) are perceived in the basal turn;
Low frequencies (1000 Hz) stimulate nerve action potential equal to frequency stimulation;
 Intermediate frequencies (1000-5000 Hz) are represented in the nerve by asynchronous discharges
which then combine actively to represent the frequency of stimulus.
Von Bekesy's travelling wave theory (1960): It states that travelling wave begins from the base and
moves towards the apex.
High-frequency stimuli cause a short travelling wave not beyond the basal turn.
Low frequency stimuli cause maximum displacement near the apex.
Middle frequency changes occur in between these two.
It is now known that the basilar membrane is much more sharply tuned for frequency filtering.

8) Acute Mastoiditis aetiology, signs, symptoms &

- Rx. What are indications for 'Mastoidectomy' [15]?
a. Signs of acute coalescent mastoiditis [12]
Ans.
Inflammation of mucosal lining of antrum and mastoid air cell system is k/a Mastoiditis
AETIOLOGY: Acute mastoiditis usually accompanies ASOM. Children are affected more.
GPredisposing Factors: poor nutrition or associated systemic disease such as diabetes.
G B-haemolytic streptococcus is the MC causative organism.

PATHOLOGY: it involves the following events-

1) ASOM infection spread to mastoid air cells> T amount of pus producedDrainage of this pus,
through a small perforation of tympanic membrane & eustachian tube, cannot keep pace with the
amount being produced. Clinical Features
2) Hyperaemia and
Symptoms Signs
engorgement of mucosa
causes dissolution of 1. Pain behind the1) Mastoid tenderness.
ear. 2) Ear discharge-purulent, often pulsatile (light-
calcium from the bony
2. Fever. house effect).
walls of the mastoid air
3. Ear discharge: 3) Sagging of posterosuperior meatal wall It is -

cells (hyperaemic Any persistence due to periostitis of bony party wall between the
decalcification). of discharge > antrum and the EAC.
3) Destruction and 3 weeks, in a Perforation is seen in pars tensa with congestion
coalescence of mastoid case of ASOM, of the rest of tympanic membrane.
aircellssingle points to 5) Swelling over the mastoid.
irregular cavity flled mastoiditis. 6) Conductive type of hearing loss is always
with pus (empyema of present.
mastoid) is formed. Pus may break through mastoid cortex subperiosteal abscess burst on surface
leading to a discharging fistula
Investigations
1. Blood tests show polymorphonuclear leucocytosis & 1 ESR.
2. X-Ray Mastoid & CT scan temporal bone.
3. Ear Swab for culture and sensitivity.
Treatment
1. Hospitalization of the Patient.
2. Antibiotics: In the absence of culture and sensitivity, start with amoxicillin or ampicillin. Specific
antimicrobial is started on the receipt of sensitivity report.
3. Myringotomy-to relieve pus,
4. Cortical Mastoidectomy It is indicated when there is:
a) Subperiosteal abscess.
b) Sagging of posterosuperior meatal wall.
cPositive reservoir sign, i.e., meatus immediately fills with pus after it has been mopped out.
 d) No change in condition of patient or it worsens in spite of adequate medical treatment for 48 h.
e) Mastoiditis, leading to complications, e.g., facial paralysis, labyrinthitis, intracranial complications,
etc.
Complications of Acute Mastolditis
1. Subperiosteal abscess 6. Subdural abscess
2. Labyrinthitis 7. Meningitis
3. Facial paralysis 8. Brain abscess
4. Petrositis 9. Lateral sinus thrombophlebitis
5. Extradural abscess 10. Otitic hydrocephalous.

9) Clinical presentation of lateral sinus thrombophlebitis [15]

Ans.
aka Sigmoid Sinus Thrombosis: It is an inflammation of inner wall of lateral venous sinus with formation of
an intrasinus thrombus.
Aetiology: It occurs as a complication of acute coalescent mastoiditis, masked mastoiditis or CSOM and
cholesteatoma.
Causative agents in acute infections > Haemolytic streptococcus, pneumococcus or staphylococcus.
Causative agents in chronic infectionBacillus proteus, Pseudomonas, E. coli and Staphylococci

Pathology: Formation of Perisinus Abscess Endophlebitis and Mural Thrombus formation within the
lumen of sinusObliteration of Sinus Lumen release infected emboli into the blood stream
septicaemia.
Clinical Features
1. Hectic Picket-Fence Type of Fever with Rigors This is due to septicaemia.
Clinical picture resembles malaria but lacks regularity (fever is irregular)
2. Headache
3. Progressive Anaemia and Emaciation
4. Griesinger's Sign: due to thrombosis of mastoid emissary vein > Oedema appears over the posterior
part of mastoid.
5. Papilloedema.
6. Tobey-Ayer Test-Compression of vein on the thrombosed side produces no effect while compression
of vein on healthy side produces rapid rise in CSF pressure
7. Crowe-Beck Test-Pressure on jugular vein of healthy side produces engorgement of retinal veins
(seen by ophthalmoscopy) and supraorbital veins.
8. Tenderness Along Jugular Vein-a/w enlargement & inflammation of jugular chain of lymph nodes and
torticollis.
Investigations
1. Blood Smear is done to rule out malaria.
2. Blood Culture is done to find causative organisms.
CSF Examination - cSF is normal except for rise in pressure
x-Ray Mastoids-may show clouding of air cells (acute mastoiditis) or destruction of bone (cholesteatoma).
5. Contrast-enhanced CT scan can show sinus thrombosis by typical delta sign in posterior cranial fossa
on axial cuts. "Delta sign" may also be seen on contrast-enhanced MRI.
MR venography is useful to assess progression or resolution of thrombus.
7. Culture and Sensitivity of ear swab.
Complications
1) Septicaemia and pyaemic abscesses in lung, bone, joints or subcutaneous tissue. 22 of 44
2) Meningitis and subdural abscess.
3) Cerebellar abscess.
4) Thrombosis of jugular bulb and jugular vein with involvement of 9th, 10th & 11th cranial nerves.
5) Cavernous sinus thrombosis chemosis, proptosis, fixation of eyeball and papilloedema.
6) Otitic hydrocephalus, when thrombus extends to sagittal sinus via confluence of sinuses.
Treatment
1) iv. Antibacterial Therapy -Choice of antibiotic will depend on sensitivity of organism.
2) Mastoidectomy and Exposure of Sinus to drain the perisinus abscess.
-

3) Ligation of Internal Jugular Vein -It is indicated when antibiotic and surgical treatment have failed to
control emboli and rigors, or tenderness and swelling along jugular vein is spreadin8
4) Anticoagulant Therapy.
5) Supportive Treatment - Repeated blood transfusions done to combat anaemia and improve patient's
resistance.

10) Meniere's disease C/F & management [14, 13, 08]

-

a. Endolymphatic Hydrops (98]

b. Lermoyez' s syndrome [94]
Ans.
Ménière's disease, aka ldiopathic endolymphatic hydrops, is a disorder of the inner ear where the
endolymphatic system is distended with endolymph.
Pathogenesis: Various theories have
been postulated- mbra

1. Defective Absorption by Endolymphatic

Sac distension of endolymphatic
system bulging of Reissner's membrane
scala vestibuli herniate into apical part
of scala tympani through the helicotrema A
A) Normal cochlear duct. ( ) Cochlear duct distended with endolymph pushing the Reissner's membrane into scala vestbu
rupture of Reissner's membrane is

mixing of perilymph with endolymph > vertigo

Vasomotor Disturbance: sympathetic overactivity spasm of internal auditory artery {Labyrinthine
artery) deafness and vertigo
3. Allergy: Nearly 50% cases are allergic tó foodstuff or an inhalant > inner ear acts as the "shock organ'
producing excess of endolymph.
4. Sodium & Water Retention: Excessive amounts of fluid are retained leading to endolymphatic hydrops.
5. Hypothyroidism: About 3% of cases. Such cases benefit from thyroid replacement therapy
6. Autoimmune diseases
7. Viral infections:HSV, CMV or VZV
Clinical Features
Age &Sex: 35-60 years; Males Females >

Triad: episodic Vertigo, sensorineural hearing loss (SNHL) & Tinnitus

1. Vertigo- sudden onset. Some cases show Tullio phenomenon {noise induced vertigo}
2. Hearing Loss: fluctuating in nature (improves after an attack of vertigo)
Hearing loss is Progressive due to repeated membranous rupture.
Intolerance to loud sounds occur due to recruitment phenomenon.
3. Tinnitus: It is low-pitched roaring type and is aggravated during acute attacks.
.Ear fullness: It is fluctuating and may occur with the acute attack or before that.
 Emotional stress can be the cause as well as effect of Ménière's disease.
VARIANTS OF MÉNIÈRE'S DISEASE
a) Cochlear Hydrops: Here, only the cochlear symptoms are present. Vertigo is absent.
b) Vestibular Hydrops: Patient gets episodic vertigo while cochlear functions remain normal.
c)Drop Attacks without loss of consciousness or vertigo or fluctuations in hearing loss.
d) Lermovez Syndrome: Here symptoms of Ménière's disease are seen in reverse order. First there is
progressive deterioration of hearing, followed by an attack of vertigo, at which time the hearing
recovers.
Nystagmus: It is seen only during acute attack. The quick (fast) component of nystagmus is towards the
unaffected ear
Investigations:
3Otoscopy: TM is normal
Tuning Fork Tests: Rinne's +ve; Weber's test is towards normal side; ABC test is Normal; Schwabach's
test is shortened frequency Hz
PTA: AB gap is present; Up-sloping (tent-like 250 500 1k 2k k k

audiogram)
Special Audiometry Tests- done to indicate the
O x Left air conduction
cochlear nature of disease. They are: Left bone conduction

a) Recruitment test is positive. O Rightair conduction

Right bone conduction
OBHL

b) SISI (short increment sensitivity index) score is>

70% (normal 15%).
c) Tone decay test: Normally, there is decay of <
20 dB
Speech Audiometry: Speech Discrimination is Low Frequency Sensory Deafness
much impaired during the attack
Glycerol test: is positiveGlycerol is a dehydrating agent. When given orally, it reduces endolymph
pressure and thus causes an improvement in hearing
Electronystagmography: Caloric response
Electrocochleography: SP/AP ratio> 30% (SP = Summating potential; AP Action potential of CN VIII}
Hennebert's sign: distended endolymphatic system come in contact with stapes footplateFALSE +ve
fistula test
3 Caloric test: Canal paresis on affected side and/or directional preponderance on healthy side is seen
3 Imaging:
CT scan: Hypoplasia of endolymphatic sac and duct
Gadolinium-enhanced MRI: Enhancement of endolymphatic sac reflects inflammation of sac.
TREATMENT
A. GENERAL MEASURES
1. Reassurance and psychological support to allay worry and anxiety
2. Cessation of smoking {Nicotine causes vasospasm).
3. Low salt diet.
4. Bed rest with head supported on pillows to prevent excessive movements.
5. Avoid stress and bring a change in lifestyle.
B. MEDICAL MANAGEMENT:
1) Labyrinthine sedatives to relieve vertigo Promethazine, Prochlorperazine & Cinnarizine
2) Vasodlilators to improves labyrinthine circulation Betahistine & Carbogen
3) Elimination of allergen (foodstuffs or inhalant)
4) Transtympanic steroids in inner ear by Microwick fto alter the water metabolism
 44
5) Chemical Labyrinthectomy: Aminoglycosides (Gentamycin, Streptomycin)Drug is absorbed through
the round windowVestibulotoxic Damage type 1 & type 2 hair cels.
SURGICALMANAGEMENT: is used only when medical treatment fails
1. Conservative Procedures: They are used in cases where hearing needs to be preserved. They are:
a) Decompression of endolymphatic sac.
b) Endolymphatic shunt operation: A tube is put to connect endolymphatic sac with subarachnoid
space drain excess endolymph
Sacculotomy (Fick's operation): It is puncturing the saccule with a needle through stapes footplate.
d)Section of vestibular nerve: It controls vertigo but preserves hearing.
e) Ultrasonic destruction of vestibular labyrinth: Cochlear function is preserved.
2. Destructive Procedures (Labyrinthectomy): Membranous labyrinth is completely destroyed to relieve
vertigo.
3. Intermittent Low-Pressure Pulse Therapy [Meniett Device Therapy): Pressure waves pass through the
perilymph and cause reduction in endolymph pressure by redistributing it through endolymphatic sac
or the blood vessels. Meniett device therapy has been recommended for patients who have failed
medical treatment and the surgical options are being considered

11) Anatomy of membranous labyrinth [14, 12]

Ans. Reissner s Scala vestibuli
membrane
Membranous Labyrinth consists of the following structures: Cochlear duct
(1) Cochlear Duct- aka membranous cochlea or the Scala media: It (scala media)

Strla
is a blind coiled tube. It appears triangular on cross-section and vascularis

its 3 walls are formed by:

(a) the basilar membrane, which supports the organ of Corti;
(6) the Reissner's membrane, which separates it from the scala
Usseous Basilar
vestibule; and spiral lamina membrane

(c) the stria vascularis, which contains vascular epithelium and Scala tympani

is concerned with secretion of endolymph.

Cochlear duct is connected to the saccule by ductus reuniens. Utricie
Cochlear duct
(2) Utricle and Saccule. Saccule
Crus
commune
The utricle lies in the bony vestibule. receives the openings of the
It 5
three semicircular ducts. It is also connected to the saccule through
utriculosaccular duct.
Ductus reuniens
The saccule also lies in the bony vestibule, anterior to the utricle. Endolymphatic duct Endolymphabic

The sensory epithelium the utricle and Saccule is called macula andis
of
concerned with linear acceleration and deceleration
(3) Semicircular Ducts: They are three in number and correspond exactly to the three bony canals. They
open in the utricle. The ampullated end of each duct contains a thickened ridge of neuroepithelium
called crista ampullaris.
(4) Endolymphatic Duct and Sac: Endolymphatic duct is formed by the union of two ducts, one each from
the saccule and the utricle. It passes through the vestibular aqueduct. Its terminal part is dilated to
form endolymphatic sac, which lies between the two layers of dura on the petrous bone
Endolymphatic sac is surgically exposed for drainage or shunt operation in Ménière's disease

12) Physiology of hearing (12, 07]

a. Middle ear transformer mechanism [10
Ans.
 25 of 44
MECHANISM OF HEARING It can be broadly divided into 3 Stages:

Mechanical Conduction of Sound

Sqund in the environment collected by pinna-> EAC strikes the tympanic membrane ossicles
pressure changes the labyrinthine fluids move the basilar membrane > stimulates the hair cells of
in
the organ of Corti. 1. Lever action of ossicles

Middle Ear Transformer Mechanism: The middle ear Length of long process of malleus
1.3
Length of long process of incus
acts as an impedance transformer to facilitate the
efficient flow of acoustic energy from the air into the 2-0ssicular
fluids of the inner ear. This can be divided into 3 stages: ever ac

1. Catenary lever- provided by the eardrum.

2. Ossicular lever-provided by the ossicles.
17 14 .21
3. Hydraulic lever provided by the difference in
- (56 mm
mm
surface area of the tympanic membrane and the Effective
arearatio Malleus and incus
stapes footplate. benave a
1st degree lever
1. Catenary Lever: As the bony annulus is immobile, sound 14:1
Diagrammatic representation of ossicular lever
energy applied to the tympanic membrane is amplified
at its central attachment, directing it into the ossicular chain for transmission to the perilymphatic fluid.
It provides almost 2 times (2x) gain in sound pressure at the malleus.
2. Ossicular Lever: Handle of malleus is 1.3 times longer than long process of the incus
3. Hydraulic Lever: Area of the tympanic membrane is approx. 55 mm-. The effective vibratory area of
tympanic membrane is 45 mm2, whereas foot plate area is 3.2 mm?. Hence, effective areal ratio is 14:1

The product of areal ratio into lever ratio is known as transformer ratio, i.e., 14 x 1.3 = 18:1.
Phase difference: In normal ear, sound pressure waves never reach the oval window and round window in
the same time. If air waves reach round window and the oval window at the same time it cancels the
effect of sound waves leading to stasis of perilymph. This reciprocal action at oval window and round
window is called phase difference. Loss of this phase difference (due to large perforation) lead to deafness.
Transduction of Mechanical Energy to Electrical Impulses (sensory system of cochlea)
Basilar membrane movements set up shearing force between tectorial membrane & the hair cells.
Distortion of hair cells gives rise to cochlear microphonics, which trigger the nerve impulse.
Travelling wave theory of von Bekesy.
Conduction of electrical impulses to the brain (Neural Pathways): Hair cells get innervation from the
bipolar cells of spiral ganglion axons of these cells collect to form the cochlear nerve ventral and
dorsal cochlear nucleicrossed and uncrossed fibres
travel to the superior olivary nucleus, lateral lemniscus,
inferiorcoliculus, medial geniculate body auditory Auditory cortex
(Area 4)
Auditory
cortex of the temporal lobe (Brodmann's area 41) radiations
Medial geniculate
membrane body

Reissner's Ventral and dorsal Inferior

cochlear nuclei coliculus
Stria vascularis

Tectorial membrane Spiral ligament

VIll Nerve Nucleus of
Ouler hair cells
inner h Cells of Hensen lateral lemniscus
Lateral lemniscus
Superior olivary
Cells of Claudius complex

Cochlea Trapezoid body

Bpiral ganglion OO Cor Boettchers cells Auditory pathways from the right cochlea. Note bilateral
Nerve fibres (unmyelinaleo
Codhlear nerve fibres (myelinalod) Baslar membrane
route through brainstem and bilateral cortical representation.
Stnicture of organ of Cort
ELECTRICALPOTENTIALS OF COCHLEAAND CN VIL
4 types of potentials have been recorded; 3 from the cochlea and 1. Endocochlear potential

1 from CN VIl fibres.

2. Cochlear microphonic from cochlea
3. Summating potential
Compound action potential from nerve fibres
Theyare:
4.

13) Eustachian tube [11, 08]

Ans. Elastin Greater wing
ANATOMY hinge of sphenoid
Tubal
Eustachian tube (auditory or pharyngotympanic Petrous cartilage
tube) connects nasopharynx with the tympanic temporal
bone
cavity. Mandibular
Auditory nerve
It develops from tubotympanic recess. tube Otic ganglion
Parts: 2 Fibrous. Ostmann's pad
(1) fibrocartilaginous {Anteromedial 2/3rd) band ffat
Levator Tensor palat
(2) bony (Posterolateral 1/3dy palati
The area where two parts meet is the narrowest Salpingopharyngeus
part of the tube called isthmus.
- Relations and structure of the cartilaginous
Ostmann's pad of fat: It keeps the tube closed to part of eustachian tube

protects itself
TABLE1Differences between infant and adult eustachian tube (ET)
and middle ear Infant Adult
from the reflux Length 13-18 mm at birth 31-38 mmn
of Direction More horizontal. Forms an angle of 10° Forms an angle of 45° with the horizontal
nasopharyngeal Angulation at isthmus Absent Present
Bony part Relatively longer and wider Relatively short and narrow
secretions. Flaccid Comparatively rigid and keeps ET closed
Tubal cartilage
Openings of Less dense
Density of elastin at the hinge More dense and keeps ET closedd
Eustachian Ostmann's pad of fat Less in volume Large in volume and keeps ET closed
Tube: 2 Box 1: Tests for eustachian tube function

openings 1) tympanic and 2) pharyngeal. Maneuver building positive pressure in nasopharynx

-Valsalva test
Mucosa of Eustachian Tube: pseudostratified ciliated columnar Politzer test
Catheterization
epithelium is interspersed with mucous-secreting goblet cells Maneuver building negative pressure in nasopharynx
Toynbee's test
The cilia beat in the direction of nasopharynx to drain middle Tympanometry (see Chapter 11: Hearing Evaluation)
Mucociliary drainage/clearance
ear secretions and fluid into the nasopharynx. Saccharine
The 3 muscles, which are related to the ET, are: Methyleneblue
-Antiblotic/steroid ear drops
(1) tensor veli palatini (tensor palati), Sonotubometry

(2) levator veli palatini (levator palati), and

(3) salpingopharyngeus
Nerve Supply:
(1) Mandibular branch of trigeminal (CN V3) supplies tensor veli palatini and tensor tympani
(2) Tympanic branch of CN IX carries sensory and parasympathetic secretomotor fibers to the tubal
mucosa.
(3) Cranial part of CN XI through vagus supplies the levator veli palatini and salpingopharyngeus

The tube attains adult morphology and functions by the age of 7-10 years
PHYSIOLOGY
Eustachian tube usually remains closed. It opens during swallowing, yawning and sneezing.
The 3 main functions of the ET are:
1. Ventilation and regulation of middle ear pressure;
 2. Protection of middle ear against nasopharyngeal sound
OBSTRUCTION OF EUSTACHIAN TUBE (ET)
pressure and reflux of nasopharyngeal secretions; and Etiology
3. Drainage of middle ear secretions Adenoids
Cleft Palate
Disorders of ET Down's Syndrome
After Effects of ET Obstruction
G The poor tubal functions are responsible for middle ear Clinical Features
infections. They are more common in infants and young Retraction Pockets and Atelectasis of Tympanic
Membrane
children. PATULOUS EUSTACHIAN TUBE
Posture can affect the tubal function. The tubal mucosa gets Etiology
congested in recumbent position and during sleep due to Clinical Features
Treatment
venous engorgement.

14) Tympanoplasty [11]

a. Ossiculoplasty [01]
Ans.
The TYMPANOPLASTY operation consists of both eradication of middle ear disease and reconstruction of
hearing mechanism ftympanic membrane and ossicles).
*Myringoplasty: The limited repair of tympanic membrane is called myringoplasty.
Ossiculoplasty: The limited reconstruction of ossicular chain is called ossiculoplasty

TABLE 1 Types of tympanoplasty (Wullstein)

Types Defect Graft lies on
Type (myringoplasty)
I
Tympanic membrane perforation Tympanic membrane or malleus
Type I Tympanic membrane perforation with Incus or remnant of malleus
erosion of malleus
Type ll myringostapediopexy or Malleus and incus absent Stapes superstructure
columella tympanoplasty
Type V Stapes superstructure absent Stapes footplate
Type V fenestration operation Stapes footplate fixed Fenestra in horizontal semicircular canal

Indications of Tympanoplasty: Conductive hearing loss due to the following causes:

1) Congenital middle ear defects such as fixity of malleus head and congenital cholesteatoma.
2) CSOM
3) Trauma to tympanic membrane and Incus

ossicles Malleus-
4) Tympanosclerosis
5) Deep retraction pockets
A Tympanic membrane grat

ateral
Contraindications of tympanoplasty emicircular canai

1. Acute exacerbation of CSOM

2. Residual cholesteatoma Sapos ootplate-
ROund window
3. Dehiscent tympanic part of facial
nerve over oval window D

4. Sensorineural hearing loss Types of tympanoplasty. (A) Tympanic membrane graft touches malleus (ype 1); (B) lncus or remnant of maileus
(ype 1); (C) Slapes supersinucture (type ll); (0) Mobile stapes footplate (ype V; and (E) Lateral semicircular canal (ype V) stapes
fixed
 TIT
OSSICULOPLASTY: It is 28of 44
the reconstruction of
ossicular chain.
GSeveral types of
prosthesis are
A B
available to replace
ossicles depending
on the ossicular
defects
Ossicular reconstruction. Sculptured autograft or homo
1. Incus prosthesis graft ossicles have been used. A Malleustapes ssemby
Oe
Used when incus is
incus graft connecting malleus handle with stapes head.
Mae
Eootplate.agsembly Modified malleus connecting maleus handle w
Modified incus connectng tympanic membrane
9
stapes lootplate.

ngto
missing C D (TM) stapes head. Malleus is missing QModiiedNES COnnec
TM to stapes lootplate.
Hydroxyapatite TORP and PORP. (A) Centred and (B) off
Incus-stapes set types. (C) Titanium TORP. (D) Titanium PORP.
prosthesis: Used when incus and stapes
superstructure are missing.
3. Partial ossicular replacement prosthesis (PORP)- Used when malleus and incus are absent. Stapes is
present and mobile.
4. Total ossicular replacement prosthesis (TORP)- Used when malleus, incus and stapes superstructure
are absent. Only the stapes footplate is present and is mobile.

15) Anatomy of normal tympanic membrane [11

a. Draw the Diagram of Left tympanic Membrane and name the parts [95]
Ans.
Origin: The tympanic membrane develops from all the 3 embryonic layers; therefore, it has an outer
epithelial layer in continuation with the epithelium of bony EAC, a middle fibrous layer & an inner
mucosal layer in continuation with the lining of middle ear Anterior
malleolar
Lateral- fo Pars
cavity process flaccida
Postenor
of malleus
Position: naileolar
Handle of- foid
present at an angle of S5 with horizontal malleus Umba
Cono
It is obliquely set; therefore, its postero-superior part is of lgn Pars
tensa
more lateral than antero-inferior part which medial.
is A (Right) B (Ler

Colour: pearly grey in colour and is translucent

Parts:2-Iower "pars tensa" and an upper "pars flaccida"
Pars Tensa: This is so called because it is firm and tense. This is because in its periphery the fibrous
layer coalesces to form a fibrous annulus which fits tightly into the surrounding bone.
It forms lower 2/3rd of the TM.
In the centre, the TM is attached the tip of the handle of malleus leading to central tenting "UMBO".
Since the TM is fixed at the centre as well as the annulus, therefore the paramedian portion of the
TM (on either side of malleus) is most mobile.
A cone of light extends from the umbo to the periphery of pars tensa in the antero-inferior
quadrant. This is the reflection of the handle of malleus due to the obliquity of the tympanic
membrane. This cone helps in identification of the TM drawing.
ParsFlacdda: This is so called because it is loose or flacid, as the middle fibrous layer here contains
loosely arranged collagen fibrils.
The fibro cartilaginous ring, i.e. the tympanic annulus is deficient superiorly. This deficient area is
known as the notch of Rivinus.
Pars flaccida is also known as "SHRAPNELL'S Membrane".
 of 44
The pars flaccida being flaccid, is the MC site of retraction pocket formation leading to primary
cholesteatoma formation.
Nerve supply of the tympanic membrane:
1. Auriculotemporal (Va) supply the anterior half of the lateral surface of the TM.
2. Auricular branch of Vagus (X) supplies the posterior half of the TM.
3. Glossopharyngeal (IX): Tympanic branch of Glossopharyngeal also called Jacobson's nerve supplies
the medial aspect of the TM.

16) Physiology of equilibrium [09, 08

Ans. The receptor organs are:
1. Maculae containing otolith (for sensing linear movements, gravitational & head tilft movements) within
the utricle & saccule.
2. Cristae containing cupula (for sensing angular movements) within the semicircular canals.
The receptor organs, detect the movement of the head in space. This information is converted into
electrical signals that travel along the vestibular nerve to the vestibular nuclei in the brainstem. From here,
the messages will be sent to the following:
a. To the spinal cord via the vestibulo-spinal tract for the regulation of muscle tone to facilitate postural
and righting reflexes.
b. To the eyes via the medial longitudinal fasciculus (vestibulo-ocular tract) to control the eyeball
movement via vestibulo-ocular reflex. It can be tested by caloric test and head impulse test.
C. To the cerebellum via the vestibulo-cerebellar tract to maintain coordination of the eyes, neck, body,

and limbs in relation to position and movements of the head

d. To the reticular formation in the brainstem and thereby preparing the autonomic nervous system.
e. To the cerebral cortex via the thalamus for conscious perception of position.
Push and Pull System: Balance system (vestibular, visual and somatosensory) two-sided push and pull
is a

system. In static neutral position, each side contributes equal sensory information, i.e., push and pull
system of one side is equal to that of the other side. If one side pulls more than the other, balance of the
body is disturbed. If any component of push and pull system of one side is diseased, then it results in
vertigo and ataxia.

17) Caloric Test [09, 03]

Ans. It compares the labyrinthine (lateral semicircular canal) functioning of two ears.
Procedure: The patient lies in supine positioni with head flexed at 30". Ears are alternately irrigated for 40
seconds with water that is 7"C above and below the normal body temperature, i.e., 30°C and 44°c. The
eyes are observed for nystagmus. A gap of 5-10 minutes is kept
between each ear test.
Cold water will produce nystagmus on the opposite side while warm water on
the same side [COWS], ateral
semicircular Gravity
The time is recorded from the start of irrigation to the endof
canal

nystagmus on a calorigram.
Interpretations:
1) Canal paresis: Lesser response than normal = depressed
function of labyrinth Ménière's disease. odeg
2) Dead labyrinth: No response = absence of labyrinthine
Caloric testing. In reclined position, 30 elevation of head
functionsacoustic neuroma, purulent labyrinthitis & end of table brings the lateral semicircular canal in vertical plane
(inset)
ototoxicity.
3) Directional preponderance:
Ipsilateral canal paresis and contralateral directional preponderance: It occurs in Ménière's disease.
 Ipsilateral canal paresis and ipsilateral directional preponderance: It occurs in acoustic neuroma

18) Hearing Aids [08, 07, 06, 03]

a. Mention '4' different types of hearing aids (13]
b. Bone anchored hearing aids [11]
Ans. Hearing aids:
A hearing aid machine presents amplified sounds to the ear.
Body-won
Behind-the-ear (BTE)
Indications of Hearing aid: Any patient of hearing loss, conductive or Spectacle
In-the-ear (1TE)
sensorineural who cannot be helped by medical and surgical means, is a Canal types:
In-the-canal (ITC)
candidate for hearing aid 0 Completely-in-canal (CIC)
Invisible in the canal (IC)
Types of Hearing Aids:
Partsofa Hearing Aid
1. Microphone: It picks up sounds and converts them into electrical impulses
2. Amplifier: It amplifies electrical impulses.
3. Receiver: It converts electrical impulses back to sound.
Volume control
5. Battery power source
6. Earmold: The amplified sound is carried to the ear through the earmold.
Electroacoustic Properties: The following terms are used to describe the properties of hearing aid:
1) Saturation sound pressure level: It is the max amount of sound pressure output (power), which can be
produced by an aid.
2) Acoustic gain: It is the difference between the output and input of a hearing aid.
3) Frequency response: It expresses the gain of a hearing aid across a range of frequencies.
Distortion: It is the clarity of sound produced by a hearing aid.
5) Loudness compression: To avoid uncomfortable output level when hearing input increases.
6) Acoustic feedback: It occurs when amplified sound leaks from the receiver back into the microphone. It
leads to an unpleasant high-pitched squeal.

Evaluation of Hearing Aid Candidates:

History &physical examination should note the following: Age of patient, Condition of the outer and
middle ear, Cosmetic concerns of the patient & Type of earmold
Audiogram: It determines following parameters and helps in selecting the type of hearing aids:
Type of hearing loss: Conductive or sensorineural
G Degree of hearing loss & Frequencies affected
BONE ANCHORED HEARING AID (BAHA
Indications: In patients with conductive or mixed hearing loss with good cochlear function where air
conduction hearing aid cannot be used, e.g., atresia of EAC, microtia, and following MRM with large
mastoid cavities, BAHA is a very good option for rehabilitation of hearing
The BAHA system consists of 3 parts:
1. The fixture (or implant): It is a small titanium screw, surgically implanted into the bone behind the ear,
with the upper surface exposed outside the skin.
2. The abutment: It is a socket attached by screw to the fixture
3. The sound processor
Mechanism of Action: The implant vibrates the skull bone. The bone carries vibrations that bypass the
external and middle ear and travel directly to the cochlear nerve.
Eligibility:
 »BAHA is implanted after 3 years of age because by this time the skull reaches sufficient thickness to
allow osseointegration.
The cochlea and nerve should be functional.
»The BC threshold should be better than or equal to 45 dB on PTA.

19) Causes of Otalgia [05]

a. Differential diagnosis of acute otalgia [12]
Ans.
Pain in the ear can be due to causes occurring locally in the ear or referred to it from remote areas.
Clinical diagnoses of causes of otalgia

Otalgia

Ear signs &

Symptoms
No ear signs &ear)
symptoms
(nomal
Nasal discharge - Rhinosinusitis
Swelling with pain
Tympanic membrane Sore throat with fever- Tonsillitis, pharyngitis
ofpinna Sore throat with dysphagia
-malignancy oropharynx & laryngopharynx
Perichondritis or
chondritis Neck swelling- Parotiditis
Thyroiditis
Neck pain cervical spine disease
Visible Nonvisible Painful chewing TMJ dysfunction
(Abnomal EAC) Dental disease
Congested &
bulging-AOM Neurological findings-Referred to neurologist
Impacted ear
Perforation wax f ear pain after physical exertion
Ereferred to cardiologist
ASOM & cSOM body
oreign
Otomycosis No other findings
AOM Otitis externma Neuralgia- Tngeminal
ASOM Acute
otitis media
Acute suppurative oMLMalignancy
CSOM- Chronic SOM
- Glossopharyngeal
Geniculate
EAC External auditory Atypical facial pain
canal Referred to psychiatrist

20) Petrositis [04]

a. Gradenigo's Syndrome [16]
Ans.
Spread of infection from middle ear and mastoid to the petrous part of temporal bone is called petrositis.
Etiopathogenesiss
Predisposing Factors: Acute coalescent mastoiditis, Latent mastoiditis or Chronic middle ear infections.
From Middle ear & mastoid, Infective process runs along the cell tracts and reaches the petrous apex
epidural abscess at the petrous apex involving trigeminal ganglion & cranial nerve VI.
Clinical Features-Gradenigo's syndrome is the classical presentation, and consists of a triad of:
External rectus palsy (6th nerve palsy)
Deep-seated ear or retro-orbital pain (5th nerve involvement) and
(ii) Persistent ear discharge.
Fever, headache, vomiting and sometimes neck rigidity may also be associated.
Diagnosis
CTscan of temporal bone will show bony details of the petrous apex and the air cells
MRI helps to differentiate diploic marrow-containing apex from the fluid or pus.

Treatment-Cortical, modified radical or radical mastoidectomy.

The fistulous tract should be found out, which is then curetted and enlarged to provide free drainage.
 Suitable i.v. antibacterial therapy should precede and follow surgical intervention.

21) Otogenic Brain Abscess [98]

Ans.
Etiology
adults, this usually follows CSOM with cholesteatoma, while in children, it is usually the resultof
In
acute otitis media.
Route of Infection: As a direct extension of middle earinfection through the tegmen or Trautmann's
triangle or by retrograde thrombophlebitis.
Causative organisms: Both aerobic and anaerobic organisms are seen.
Aerobic pyogenic staphylococi, Streptococcus pneumoniae, Streptococcus haemolyticus, Proteus
mirabilis, Escherichia coli and Pseudomonas aeruginosa.
Anaerobic-Peptostreptococcus, Bacteroides fragilis & Haemophilus influenzae.
Pathology Brain abscess develops through 4 stages.
1) Stage of Invasion (Initial Encephalitis): Patient may have headache, low-grade fever, malaise and
drowsiness.
2) Stage of Localization (Latent Abscess): There are no symptoms during this stage. Body tries to localize
the pus.
3) Stage of Enlargement (Manifest Abscess): Abscess begins to enlarge. A zone of oedema appears round
the abscess> aggravation of symptoms.
4) Stage of Termination (Rupture of Abscess): An expanding abscess ruptures into the ventricle or
subarachnoid space meningitis.
Clinical Features
a. Headache worse in the morning
1)1 Those b. Nausea and projectile vomiting
due to C. Level of consciousness: Lethargy drowsiness, confusion, stupor & finally coma
TICP d. Papilloedema
e. Slow pulse and subnormal temperature
1. Nominal aphasia-if abscess involves dominant hemisphere patient fails
to tell the names of common objects such as key, pen, etc. but can demonstrate their use
2. Homonymous hemianopia due to pressure on the optic radiations
-

Temporal 3. Contralateral motor paralysis

lobe 4. Seizures, hallucinations of taste, and smell and involuntary smacking
2) Those
abscess movements of lips and tongue
due to
area of 5. Pupillary changes & oculomotor palsy-indicates transtentorial
brain herniation
affected Headache involves suboccipital region
Spontaneous nystagmus to the side of lesion
Cerebellar
lpsilateral hypotonia, ataxia and weakness
abscess & intention tremor (can be elicited by finger nose test)
Past-pointing
Dysdiadochokinesia.
Investigations
a) Skull X-Rays: are useful to see midline shift, if pineal gland is calcified, & also reveals gas in the abscess
cavity.
b) CT Scan: helps to find the site and size of an abscess.
c) Xray Mastoids or CT scan of the temporal bone for evaluation of associated ear disease.
d) Lumbar Puncture: CSF will show some rise in pressure, increase in protein content but normal glucose
level. White cell count of CSF is raised but is much less than seen in cases of meningitis.
 Treatment
Medical Neurosurgical Otologic
High doses of antibiotics are Associated ear disease which
given parenterally. The choice of surgical caused the brain abscess should
Culture of discharge from the procedure is left to the be treated.
ear may be helpful in the judgement of the Acute otitis media might
choice of antibiotic neurosurgeon. have resoved with the
Chloramphenicol and 3rd gen Options include: antibiotics given for the
cephalosporins are usually a) Repeated aspiration abscess.
effective. through a burr hole, G Chronic otitis media would
Aminoglycosides, e.g, b) Excision of abscess and require radical
gentamicin, may be required if c) Open incision of the mastoidectomy to remove
infection suspected is abscess and evacuation of the irreversible disease.
pseudomonas or proteus. pus.
ICP can be lowered by Surgery of the ear is undertaken
mannitol. Pus recovered from the only after the abscess has been
Discharge from the ear should abscess should be cultured for controlled by antibiotics and
be treated by suction clearance sensitivity. neurosurgical treatment.
and use of topical ear drops
------

22) Otitic Hydrocephalous [93]

Ans.
It is characterized by TICP with normal CSF findings.
Etiology: It is seen in children and adolescents Clinical Features
with acute or chronic middle ear infections. Symptoms Signs
Pathology: Middle ear infection Lateral sinus 1. Severe headache, may S Papilloedema.
thrombosis extends to superior sagittal sinus
be accompanied by G Nystagmus.
nausea and vomiting8 G Lumbar puncture-
impede the function of arachnoid villi to
2. Diplopia due to CSF pressure exceeds
absorb CSF-TICP. paralysis of 6th cranial 300 mm H20 (normal
Treatment nerve. 70-120 mm H20). CSF is
The aim is to reduce pressure to prevent
CSF 3. Blurring of vision due bacteriologically
optic atrophy and blindness. to papilloedema or sterile.
*Medical: acetazolamide and corticosteroids optic-atrophy
and repeated LP or placement of a lumbar drain.
Sometimes, draining CSF into the peritoneal cavity is necessary.
Middle ear infection may require Abx therapy and mastoid exploration to deal with sinus thrombosis.

23) Attic perforation [91]

a. Types of perforation of tympanic membrane [Feb-13, 06]
b. Traumatic perforation of tympanic membrane [10]
Ans.
A defect in the TM can be produced by direct trauma from a foreign body inserted into the EAC or
indirectly from a relative change in pressure between the external and middle ear, e.8, from a slap to the
ear or a blast injury.
Clinical Features: Patients complain of otalgia, hearing loss (characteristically conductive), and may have
blood-stained otorrhoea.
 Investigations:
Pure tone audiometry (PTA) is obtained
to document the degree of hearing loss
An air-bone gap of more than 30 dB
should raise the suspicion of ossicular
damage. Central perforation Central perforation Subtotal perforation
(medium sized)
Management (anterior)

In the majority of cases, a traumatic

perforation will heal spontaneously
within 10 weeks of the injury, thus
conservative management is
advocated. Patients should be
advised to keep the affected ear
dry. Total perforation with Attic perforation Posterosuperior margina
If the TM perforation shows no sign destruction of even
the fibrous annulus
perforation

of healing after 3 to 6 months,

Types of perforations seen in the tympanic membrane in CSOM.
surgical repair should be
considered.
Persistent conductive hearing loss (CHL) after the TM has healed is suggestive of ossicular damage

24) Dangerous area of the face [89]

Ans.
The facial vein and its communications are devoid of valves in their lumens.
Since facial vein rests directly on the muscles of facial expression, the
movements of these muscles may facilitate the spread of septic emboli
from infected area of the lower part of the nose, upper lip, and adjoining
part of the cheek in retrograde direction through deep facial vein,
pterygoid venous plexus, and emissary vein into the cavernous sinus
Dangerous
leading to meningitis and cavernous sinus thrombosis. rea of
face

OFor this reason, this portion of the face is called dangerous area of the
face

25) Audiometry [80]

a. Pure tone audiometry features of noise induced hearing loss [15]
b. Puretone Audiometry [Sept 03]
Ans.
Pure Tone Audiometry
*An audiometer is an electronic device which produces pure tones, the intensity of which can be T or
steps.
in 5 dB
Audiometer is so calibrated that the hearing of a normal person, both for air and bone conduction, is at
o dB and there is no A-B gap, while tuning fork tests normally show AC> BC
*The amount of intensity that has to be raised above the normal level is a measure of the degree of
hearing impairment at that frequency.
It is charted in the form of a graph called audiogram.
The threshold of bone conduction is a measure of cochlear function.
The difference in the thresholds of air and bone conduction (A-B gap) is a measure of the degree of
conductive deafness.
Uses of Pure Tone Audiogram
1) It is a measure of threshold of hearing by AC & BC and thus the degree and type of hearing los.
2) A record can be kept for future reference.
3) Audiogram is essential for prescription of hearing aid.
4) Helps to find degree of handicap for medicolegal purposes. AUDIOGRAM
MQUENCYNMETZ
s00 1000 2000
5) Helps to predict speech reception threshold.
Pure Tone Audiometry features of Noise-nduced HL(NIHL G
When NIHL occurs the graph shape will be like a hillside the
steeper the hill the worse the loss
On an audiogram, NIHL Will be seen first as a 'notch' in 4 kHz region.
Theorder of involvement: Higher frequencies> middle frequencies.
In the most severe cases, even the lower frequencies may eventually 10

become involved.

26) Perceptive deafness [79]

Ans.
Aka Sensorineural hearing loss (SNHL}
SNHL results from lesions of the cochlea, 8th nerve or central auditory pathways.
It may be present at birth (congenital) or start later in life (acquired).
AETIOLOGY
Congenital: It is because of damage to the hearing apparatus by prenatal or perinatal factors.
Acquired
Itappears later in life.
Characteristics of Sensorineural Hearing Loss
The cause may be genetic or
1. +ve Rinne test, i.e., AC > BC
nongenetic.
2. Weber lateralized to better ear
Common causes of acquired
3. Bone conduction reduced on Schwabach's and ABC tests.
SNHL include:
4. More often involving high frequencies.
1. Infections of labyrinth No gap between air and bone conduction curve on audiometry.
5.
viral, bacterial or 6. Loss may exceed 60 dB.
spirochaetal 7. Speech discrimination is poor.
2. Trauma to labyrinth or 8th 8. There is difficulty in hearing in the presence of noise.
nerve, e.g. fractures of
temporal bone or the ear surgery
3. Noise-induced hearing loss
4. Ototoxic drugs 8. Sudden hearing loss
5. Presbycusis 9. Familial progressive SNHL
6. Ménière's disease 10. Systemic disorders, e.g., DM, hypothyroidism,
7. Acoustic neuroma kidney disease, autoimmune disorders, MS, etc.
DIAGNOSIS
1) History-to know whether disease is congenital or acquired, stationary or progressive, associated with
other syndromes or not, involvement of other members of the family & possible aetiologic factors.
2) Severity of Deafness by audiometry
3) Site of Lesion- cochlear, retrocochlear or central.
4) Laboratory Tests: based on the aetiology suspected like-
X-rays or CT scan of temporal bone for evidence of bone destruction (congenital cholesteatoma,
glomus tumour, middle ear malignancy or acoustic neuroma),
 blood counts (leukaemia),
34 of 44
thyroid functions (hypothyroidism),
blood sugar (diabetes), kidney function tests, etc.
serology for syphilis,
MANAGEMENT
a) Syphilis of the inner ear is treatable with high doses of penicillin
b) Hearing loss of hypothyroidism can be reversed with replacement therapy.
c)Serous labyrinthitis can be reversed by attention to middle ear infection.
d) Early management of Ménière's disease can prevent further episodes of vertigo and hearing loss.
e) SNHL due to perilymph fistula can be corrected surgically by sealing the fistula.
Ototoxic drugs should be used with care and discontinued if causing hearing loss,
8)Noise-induced hearing loss can be prevented if the person is removed from the noisy surroundings.

27) Ramsay Hunter's syndrome [75]

Ans.
Herpes Zoster Oticus (Ramsay-Hunt Syndrome): facial paralysis + vesicular rash in the EAC and pinna.
There may also be anaesthesia of face, giddiness and hearing impairment due to involvement of 5th and 8th
nerves.
Medical management Surgery
Treatment: (same as for Bell palsy). Steroids: Prednisolone is the drug of choice.
General:
1. Reassurance.
»If patient reports within 1 week, the adult Nerve
dose of prednisolone is 1 mg/kg/day divided
2. Relief of ear pain by decompression
into morning and evening doses for 5 days.
analgesics. relieves pressure
Patient is seen on the fifth day.
on the nerve
3. Care of the eye to protect If paralysis is incomplete or is recovering,
fibres and thus
against exposure keratitis. dose is tapered during the next 5 days.
improves the
4. Physiotherapy of the facial »If paralysis remains complete, the same dose microcirculation
muscles is continued for another 10 days and
of the nerve
thereafter tapered in next 5 days (total of
20 days).

28) Perichondritis of the ear [74] N

Ans.
Etiology: Pseudomonas and mixed flora are the common pathogens & can produce-
»Infection secondary to lacerations, haematoma or surgical incisions.
»Extension of infection from diffuse otitis externa or a furuncle of the meatus.
Clinical Features: Initial symptoms are red, hot and painful pinna which feels stiff. Later abscess may form
between the cartilage and perichondrium with necrosis of cartilage
Treatment in early stages consists of systemic antibiotics and local application of 4% aluminium acetate
compresses. When abscess has formed, it must be drained promptly and culture and sensitivity of the pus
obtained. Incision is made in the natural fold and devitalized cartilage removed.

29) Bullous myringitis [73]

Ans. It is a painful condition characterized by formation of haemorrhagic blebs on the tympanic membrane
and deep meatus. It is probably caused by a virus or Mycoplasma pneumoniae.

30) Briefly describe the 'Anatomy of Middle Ear' [67]

a. Intratympanic muscles [03]
Ans.
 37 of 44
The middle ear can be assumed to be like a cuboid and therefore has 6 walls.
1. Lateral wall: is formed
Fossa incudis Aditus Lateral semicircular canal bulge
largely by the tympanic Chorda tympani enty Horlzontal part of fnciaf nerve

Processus cochlearibrmis
membrane and to a lesser
extent by the bony outer
Canal for
attic wall called scutum. ensor lympan
Anterlor
2. Medial wall: This is the
anaf of Huguer
common wall between ympani)
chorda
O

Faciel
middle ear and inner ear
CA
verlical Medial wall
part
The important structures on
Pyramid CHUAN
this medial wall are: Jugular bub
Sympathetic
a) Promontory: This is a Posterior wall
TUBE
piexus

bulge in the centre of the FRFacialrecess (suprapyramidal recess)

Internal carotld

STSinus ympani (infrapyramidal recess) acobson's nerve

medial wall, produced by P: Promontory
OW:Oval window
the basal turn of cochlea. Rw:Round window

b) Processus Cochleariformis: This is a hook like structure present antero-superiorly on the medial wall.
The 1st genu of facial nerve lies above the processus cochleariformis.
Bulge of lateral semicircular canal & Oval window: lie postero-superiorly on the medial wall
d) Round window ffenestrà cochleae; covered by the secondary tympanic membrane: separate the
middle ear from the scala tympani.
e) Canal for facial nerve - present above the oval window
3. Posterior wall: This is the common wall between middle ear and mastoid. The 7 important structures
on this posterior wall are:
1) Aditus: opening on the upper border of posterior wall which connects the attic to mastoid antrum.
2) Pyramid: It is a projection on the posterior wall from which originates the stapedius muscle.
3) Facial nerve: At the junction of medial and posterior wall, the tympanic (or horizontal segment) of
facial nerve takes a turn onto the posterior wall known as the 2nd genu.
4) Sinus tympani/Infra pyramidal recess: It is the area medial to the bulge of mastoid (or vertical) part
of facial nerve It is the most common site for residual cholesteatoma.
5) Chorda tympani nenve entry
6) Fossa incudis: It is a fossa on the posterior wall on which rests the short process of incus.
7) Facial recess/Supra pyramidal recess/ posterior sinus: is a depression in the posterior wall lateral to
the pyramid. Here, opening is made on the posterior wall to access the middle ear cavity, e.g. in
"INTACT CANAL WALL" surgeries of the ear. Also, the electrodes of cochlear implant are introduced
into the middle ear from the mastoid through the facial recess.
4. Anterior wall: It separate the middle ear from internal carotid artery. It has 2 openings; the lower one
for the eustachian tube and the upper one for the canal of tensor tympani muscle.
GThe canal of Huguier: this is the exit site for chorda tympani from middle ear
GPetro-tympanic fissure (Glaserian fissure): is the site for entry of anterior tympanic artery
5. Roof: The roof of the middle ear is known as "TEGMEN TYMPAN". It contributes to the anterior slant
of the petrous part of the temporal bone and separates the middle ear from the middle cranial fossa
(temporal lobe).
6. Floor: It separates the middle ear from the jugular bulb along with the 9th and 10th cranial nerves. The
tympanic segment of glossopharyngeal nerve (also known as "JACOBSON'S NERVE") enters the middle
ear through floor and along with sympathetic plexus (coming into the middle ear from around the
internal carotid artery) forms tympanic plexus on the promontory.
 Scutum (the bone above Tegmen tympani
MIDDLE EAR CAVITY: It is divided into 3 parts by lines drawn from pars fncdnorming
wall of attic)
lateral

the upper and lower borders of pars tensa. These are: rUssakS Space
(he most common site of
1 Epitympanum or Attie primary choles teatoma)

Uppermost part & the widest part of the middle ear cavity. Pars flaccida4

lies medial to pars flaccida below and scutum above.

The space of the epitympanum, lying in between pars Parstensa Meso
ympanumn
flaccida and the neck of malleus is known as "PRUSSAK'S
SPACE". When a retraction pocket on Pars flaccida grows
Hypotympanum
medially, it goes into this Prussak's space
2) Mesotympanum: It is the middle part & the narrowest part of
middle ear due to the constrictions caused by umbo laterally and promontory medially.
Mesotympanum contains the handle of malleus, the long process Malleus Incus

of incus which articulates with the stapes.

Booy

Head-

3) Hypotympanum: This is the lower compartment of middle ear NecK -

Snor
orocess

cavity. It is the smallest part of middle ear cavity. Long

process orocess

osSICLES OFTHE MIDDLE EAR: Lateral

process
-

Stapes
malleus, incus and stapes
Handle-
3 the Head
They conduct sound energy from the tympanic membrane to the oval Anterior-
Crus

window and then to the inner ear fluid. Foctplate

Figure 1.16 Ear ossicles ae

INTRATYMPANIC Attachment Functions Nerve Supply

MUSCLES
neck of malleus tenses the tympanic branch of mandibular
Tensor tympani nerve (Va)
membrane
7th
neck of stapes dampen very loud Nerve
Stapedius
sounds

TYMPANIC PLEXUS: It lies on the promontory & supplies innervation to the medial surface of the tympanic

membrane, tympanic cavity, mastoid air cells and the bony eustachian Aditus
Antrum
tube. It also carries secretomotor fibres for the parotid gland.
EUstachian ube

MIDDLE EAR CLEFT: The middle ear together with the eustachian tube,
aditus, antrum and mastoid air cells is called middle ear cleft.
Eustachian tube is lined by ciliated epithelium, which is ear
Middle

pseudostratified columnar in the cartilaginous part, columnar in the

bony part. Mastoid air cels
Miode ear ce
Tympanic cavity is lined by ciliated columnar epithelium in its
anterior and inferior part which changes to cuboidal type in the posterior part.
Epitympanum and mastoid air cells are lined by flat, non-ciliated epithelium.

BLOOD SUPPLY OF MIDDLE EAR Middle ear is supplied by six arteries

1) Anterior tympanic branch of maxillary artery which supplies tympanic membrane.
2) Stylomastoid branch of posterior auricular artery which supplies middle ear and mastoid air cells
 3) Petrosal branch of middle meningeal artery (runs along greater petrosal nerve).
4) Superior tympanic branch of middle meningeal artery traversing along the canal for tensor tympani
muscle.
5) Branch of artery of pterygoid canal (runs along eustachian tube).
6) Tympanic branch of internal caratid.
Veins drain into pterygoid venous plexus and superior petrosal sinus.
LYMPHATIC DRAINAGE OF Middle ear and eustachian tube: Retropharyngeal nodes upper jugular chain

VSQs
1) Mention 4 Ototoxic drugs [16]
Ans.
A. Aminoglycoside antibiotics E. Analgesics
Streptomycin Salicylates
Dihydrostreptomycin Indomethacin
Gentamicin Phenylbutazone
Tobramycin Ibuprofen
Neomycin F. Chemicals
Kanamycin Alcohol
Amikacin Tobacco
Netilmycin Marijuana
Sisomycin Carbon monoxide
B. Diuretia poisoning
Furosemide G. Miscellaneous
Ethacrynic acid Erythromycin
Bumetanide Ampicillin
.Antimalarials Propranolol
Quinine Propylthiouracil
Chloroquine Deferoxamine
Hydroxychloroquine
D. Cytotoxc drugs
Nitrogen mustard
(Mechlorethamine)
Cisplatin
Carboplatin

2) Haematoma auris [Feb 16]

Ans.
Haematoma of The Auricle: It is collection of blood between the auricular cartilage and its perichondrium.
GCause: Result of blunt trauma seen in boxers, wrestlers and rugby players.
G Extravasated blood may clot and then organize, resulting in a typical deformity called Cauliflower
/F:
ear (pugilistic or boxer's ear).
GTreatment is aspiration of the haematoma under strict aseptic precautions and a pressure dressing,
carefully packing all concavities of the auricle to prevent re-accumulation. When aspiration fails,
incision and drainage should be done. All cases should receive prophylactic antibiotics
G Complications: If haematoma gets infected, severe perichondritis may set in.

3) Keratosis obturans [14, 11]

Ans. Collection of a pearly white mass of desquamated epithelial cells in the deep meatus is called
keratosis obturans. This, by its pressure effect, causes absorption of bone leading to widening of the
meatus so much so that facial nerve may be exposed and paralyzed.
Aetiology: It is commonly seen between 5 and 20 years and may affect one or both ears. It may
sometimes be associated with bronchiectasis and chronic sinusitis.
 Pathogenesis: Normally, epithelium from surface of tympanic membrane migrates onto the posterior
meatal wall. Failure of this migration or obstruction to migration caused by wax may lead to
açcumulation of the epithelial plugin the deep meatus.
Clinical features. Pain in the ear, hearing loss, tinnitus and sometimes ear discharge.
On examination, ear canal may be full of pearly white mass of keratin material. Removal of this mass
may show widening of bony meatus with ulceration and even granuloma formation.
Treatment: Keratotic mass is removed either by syringing or instrumentation. Secondary otitis externa
may be present and should be treated. Recurrence can be prevented by the use of keratolytic agent
such as 29% salicylic acid in alcohol.

4) Management of a live insect in the ear [14]

a. Foreign body in the ear [97]
Ans.
Foreign Bodies of Ear They can be Living or Non-living things

1. Non-living:
»In Children a piece of paper
or sponge, grain seeds (rice, Methods of removinga Indications
wheat, maize), slate pencil, foreign body from Ear
piece of chalk or metallic ball Soft and irregular foreign bodies like a
bearings. piece of paper, swab or a piece of
a. Forceps removal sponge can be removed with fine
-
»In Adults broken end of crocodile forceps
matchstick used for scratching
Most of the seed grains and smooth
the ear or an overlooked b. Syringing
objects
cotton swab.
C. Suction Earwax removal
Vegetable foreign bodies tend
to swell up with time and get d. Microscopic removal In all impacted foreign bodies, it is
preferable to use general anaesthetic
with special
tightly impacted in the ear
instruments and an operatingmicroscope
canal or may even suppurate.
foreign bodies impacted in deep
2. Living:
meatus, medial to the isthmus or those
Insects like mosquitoes, beetles, e. Post-aural approach
which have been pushed into the
cockroach or an ant may enter middle ear
the ear canal and cause intense
irritation and pain. No attempt should be made to catch them alive. First, the insect should be killed by
instiling oil fa household remedy), spirit or chloroform water. Once killed, the insect can be removed
by any of the methods described in the table.
Maggots in the ear:
Flies may be attracted to the foul-smelling ear discharge and lay eggs which hatch out into larvae
called maggots in the ear canal severe pain with sweling round the ear and blood-stained watery
discharge.
Treatment consists of instilling chloroform water to kill the maggots, which can later be removed by
forceps.

5) Hearing evaluation for deaf mutism [14)

Ans.
Suspicion of hearing loss. Hearing loss is suspected if
the child sleeps through loud noises unperturbed or fails to startle to loud sounds,
 fails to develop speech at 1-2 years.
FINDING THE CAUSE

1. Scheibe dysplasia- affects cochlea and saccule

Infant 2. Alexander dysplasia - affects only the basal turn of membranous cochlea
Factors 3. Bing-Siebenmann dysplasia complete absence of membranous labyrinth
PRENATAL
CAUSES
4. Michelaplasia -complete absence of bony & membranous labyrinth
1) Infections during pregnancy TORCH
Maternal 2) Use of ototoxic drugs during pregnancy
Factors 3) Radiation to mother in the first trimester
4) Others-DM, Nutritional deficiency, Thyroid deficiency, Alcohol etc.
a. Anoxia: Placenta praevia, prolonged labour, cord round the neck and
prolapsed cordFetal Anoxia damages the cochlear nuclei.
b. Prematurity And Low Birth Weight (<1.5 kg)
PERINATAL CAUSES C. Birth Injuries. e.g. forceps delivery may cause intracranial haemorrhage
with extravasation of blood into the inner ear.
d. Neonatal Jaundice, Meningitis, Sepsis etc.
e. Ototoxic Drugs -used for neonatal meningitis orsepticaemia.
1. Genetic-Deafness may occur alone as in familial progressive sensorineural
deafness or in association with certain syndromes, e.g. Alport, Klippel-Feil,
Hurler, etc.
Nongenetic:
Viral infections (measles, mumps, varicella, influenza), meningitis
POSTNATAL CAUSES
Secretory otitis media.
Ototoxic drugs
Trauma, e.g., fractures of temporal bone, middle ear surgery or perilymph
leak.
.Noise-induced deafness.
TABLE 19.2 METHODs OF HEARING ASSESSMENT
IN INFANTS AND CHILDREN

Neonatal screening procedures

ABR/OAEs
Arousal test
Auditory response cradle
Behaviour observation audiometry
Moro's reflex
Cochleopalpebral reflex
Cessation reflex
Distraction techniques (6-18 months)
Conditioning techniques (7 months - 2 years)
Visual reinforcement audiometry
Play audiometry (2-5 years)
Objective tests
ABR
Otoacoustic emissions
Impedance audiometry

6) Electronystagmography [14]
Ans.
It is amethod of detecting and recording of nystagmus, which is spontaneous or induced by caloric,
positional, rotational or optokinetic stimulus.
The test depends on the presence of corneoretinal potentials which are recorded by placing electrodes
at suitable places round the eyes.
The test is also useful to detect nystagmus, which is not seen with the naked eye. It also permits to
keep a permanent record of nystagmus
7) Labyrinthine nystagmus [12]
Ans.
defined as involuntary, rhythmical, oscillatory movement of eyes.
It is
It may be horizontal, vertical or rotatory
----------------=-------*-**** ****-*--**--*******

8) Tinnitus j09]
Ans.
Tinnitus is ringing sound or noise in the ear.
c/E: Patient describe this as roaring, hissing, swishing, rustling or clicking type of noise. Tinnitus is more
annoying in quiet surroundings, particularly at night, when the masking effect of ambient noise from the
environment is lost.
Two types of tinnitus are described:
a. Subjective, which can only be heard by the patient.
b. Objective, which can even be heard by the examiner with the use of a stethoscope
TABLE 22.1 CAUSES OF TINNITUS
Subjective Tinnitus Objective Tinnitus
TREATMENT OF TINNITUS Otologic Vascular
Tinnitus symptom and not a disease.
is a Impacted wax AV shunts
Fluid in middle ear -Congenital AV
Where possible, its cause should be discovered and Acute otitis media maltomations
Glomus tumour of
Chronic otitis media
treated. Ménière's disease
Presbycusis
middle e ar
Arterial bruit
When no cause is found, management of tinnitus includes: Noise-induced hearing - Carotid aneurysm

oss Carotid stenosis

Reassurance and psychotherapy Idiopathic sudden SNHL Vascular loop pressing9
AcoustiC neuroma on Villth nerve in
Techniques of relaxation and biofeedback. Metabolic internal auditory canal
Hypothyroidism High-riding carotid
Sedation and tranquillizers. Hyperthyroidism artery
Obesity Persistent stapedial
4. Masking of tinnitus. Hyperlipidaemia artery
Vitamin deficiency Venous hum
Tinnitus is more annoying at bedtime when the (e.g. B12) Dehiscent jugular bulb
Neurologic Patulous eustachian tube
surroundings are quiet. Head injury (labyrinthine Palatal myoclonus
Idiopathic stapedial or tensor
G Use of a fan, loudly clicking clock or a similar device may Concussion)
Temporal bone tractures tympani myoclonus
mask the tinnitus and help the patient to go to sleep Whiplash injury
Multiple sclerosis
.DDenta
Cicking of TM joint
G Use of tinnitus masker for a short time may provide, in Postmeningitic
Brain haemorrhage
some individuals, a symptom-free period for several Brain infarct
Cardiovascular
hours due to the phenomenon of residual inhibition. Hypertension
Hypotension
naemia
Cardiac arrhythmias
Arteriosclerosis
Pharmacologic
Certain drugs used by the
patient
All ototoxic drugs
Psychogenic
Anxiety
Depression

9) Universal neonatal hearing screening [08]

Ans.
 43 of 44
UNIVERSAL NEONATAL HEARING SCREENING FOR NEWBORNS
WITHOUT RISK FACTORS
Otoocoustic emisslone (TEOAE) before dlschange, 24 hou Pass
af ter birth day)

Refer
Level II fecilities (ond lev ITI}: Otoeoceustic eminion (EOAE)* Befere diechorge", **

outomatic ABR Refer

T level foc: Oteacoustic emissions (TEOAE) eene diecherge", ***
Pass
fAefer send to lev, IT (and lev. IIT ) facilities to execute automatie ABR tha
JRefer *
CMV DNA reering by PCR in urine
hefore dischage within 2 weeks of ife
if fir
Clinic ABR (ABR) impedence audiometry within the 3r month Pass
Rer sho unilhterlly fail
ofeecoustic emissions (clinie test)
oflife
newborns nr at 11EOAE (no
Refer
In
submimed AABK betore dischaQ
Diagnosis and hearing aid fiting speech training
to

s1EOAE
eommended the repetition of
within 7-15 days of
in lev. LII focilities, within the h (grd.4) month
test lufe f life
--**----

10) Otoacoustic emission [07]

Ans.
OAEs are generated at outer hair cells and can be picked up from the external ear as the energy
produced by them travels in reverse direction from outer hair cells0ssicles tympanic membrane
ear canal where it is picked up.
OAEs are absent if outer hair cells in the cochlea are non-functional or there is middle ear effusion or
canal debris due to meconium which may persist for 3-4 days.
They are normal even when 8th nerve is non-functional. Thus, can be used in the diagnosis of
neuropathy of 8th nerve

11) Cochlear implants [o5]

Ans.
A cochlear implant is an electronic device that can provide useful hearing and improved communication
abilities for persons who have severe to profound sensorineural hearing loss and who cannot benefit from
hearing aids.
Components of Cochlear Implant:
1) External component It consists of an external speech processor and a transmitter. The speech
processor may be body worn or behind the ear type.
2) Internal component - It is surgically implanted and comprises the receiver/stimulator package with an
electrode array

peech processor
and transmiter Receiver/sumulalor
Extenal speech processor captures sound
o
Andconvers iga gnas
gas 20.3 COMPLICATIONS OF cOCHLEAR
To brain
tointemaimlan TABLE

Intemal implant tuns signals IMPLANT SURGERY

into electncal enorgy, s0no Early complications Late complications
lo an arrayslimulale
. Electrodes
inside the cochiea
hearing Facial paralysis Exposure of device and
nerve, Dypassing ddmaged na Wound infection extrusion
colls, and the brain percoives
sgnais; you near sound
Wound dehiscence Pain at the site of implant
Flap necrosis Migrationdisplacement or
Array of elecirodes
Electrode migration
Device failure Ice
Late device failure
CSF leak Oitis medid
Meningitis
Postoperative dizziness/
Principle of cochlear implant vertigo

12) Vestibular neuronitis [05]

Ans. 44 of 44
It is a peripheral vestibular disorder, characterized by severe vertigo of sudden onset with no cochlear
symptoms. Attacks may last from a few days to 2 or 3 weeks.
Cause: It is thought to occur due to a virus that attacks vestibular ganglion.
Management of acute attack is similar to that in Ménière's disease. The disease is usually self-imiting.

13) Bezold's Abscess [04]

Ans.
It can occur following acute coalescent mastoiditis when pus breaks through medial side of the tip of the
mastoid and presents as a swelling in the upper part of neck.
The abscess may:
a lie deep to sternocleidomastoid, pushing the muscle outwards,
b) follow the posterior belly of digastric and present as a swelling between the tip of mastoid and
angle of jaw,
c) be present in upper part of posterior triangle,
d) reach the parapharyngeal space or
e) track down along the carotid vessels.
Clinical features. Onset is sudden. There is pain, fever, a tender swelling in the neck and torticollis. Patient
gives history of purulent otorrhoea.
Diagnosis: CT scan of the mastoid and swelling of the neck may establish the diagnosis
Treatment
1. Cortical mastoidectomy for coalescent mastoiditis with careful exploration of the tip for a fistulous
opening into the soft tissues of the neck.
2. Drainage of the neck abscess through a separate incision and putting a drain in the dependent part.
3. Administration of intravenous antibiotics guided by the culture and sensitivity report of the pus taken
at the time of surgery.

14) Aditus-ad-antrum [03] Mastoid antrum

Ans. Mastoid oir zells Acdinus
ympanicC cavity
Aditus ad antrum is a short canal connecting the Epitympanic recess
epitympanum with the mastoid antrum. The short process of
incus lies on its floor. The facial nerve runs in its canal in the
floor, while the lateral semicircular canal lies in the medial
wall.
Auditory tube

Tegmen tympani

***** -****
**=****-****==********=****-******* ***=*************************
 CONTENTS
DISEASES OFORAL CAVITY. 3
SQs .. 3
VSQs

DISEASES OF NOSE& PNS.e.6

LQS 6
SQs. 15
VSQs.... 28
 Diseases of Oral Cavity & Salivary Glands
SQs
1. Non healing ulcer of tongue [11]
Ans. It indicates Carcinoma of Tongue.
Are&Sex: men in the age group of 50-70 years.
Majority are squamous cell type.
Site: lateral border or the ventral aspect (MC), the tip or the dorsum of the tongue
Spread: Localy, it may infiltrate the lingual musculature causing ankyloglossia or may spread to the
floor of mouth & mandible. Lymph node metastases go to the submandibular and upper jugular nodes
(from the lateral border of tongue) and to the submental and jugulo-omohyoid group (from the tip).
Clinical Features
Signs Symptoms
Cancer of the tongue may present as 1) A lump in the mouth
a) An exophytic lesion like a papilloma 2) Early lesions are painless (hence asymptomatic for a long time).
b) A non-healing ulcer with rolled 3) Pain in the tongue occurs at the site of ulcer.
edges, greyish white shaggy base 4) Pain in the ipsilateral ear, it is due to common nerve supply of the

and induration tongue (lingual nerve) and ear (auriculo-temporal) from Va.
5) Enlarged lymph node mass in the neck.
c)A submucous nodule with
6) Dysphagia, difficulty to protrude the tongue, slurred
induration of the surrounding
speech and bleeding from the mouth are late features.
tissue.
Staging- TNM classification is used.
Treatment
Small tumours give equal results if treated with radiotherapy or surgery.
Stage ll or IV tumours require combined treatment with surgery and
postoperative radiotherapy.
Depending on the size &extent of the primary lesion of the tongue, surgery
may consist of hemiglossectomy including a portion of the floor of mouth,
hemimandibulectomy and block dissection of neck nodes-the so-called "commando operation"

2. Oral Submucosal fibrosis [05] Areca nut chewing

Ans.
Oral submucous fibrosis (OSF) Is a chronic insidious process Collection of activated T-ymphocytes
and macrophages in subepithelial
characterized by juxtaepithelial deposition of fibrous tissue in layers of oral mucosa

the oral cavity and pharynx.

RISK FACTORS
Activated t-lymphocytes Macrophag
1) Tobacco chewing & Alcohol
2) Areca nuts-they are chewed alone, with tobacco or in
the form of pan (Betel quid) Reduced production o Increased production ot.
antifibrotic cytokines fibrinogenic cytokines
3) Poor Socioeconomic status Act on
4) Deficiency of vitamins (Vit-A) & micronutrients (Zn).
Less collagenase Mesenchymal cells
5) Age: 20-40 years
PATHOGENESIS:
Proliferation of fibroblasts
*OSF is considered a cell-mediated immune reaction to
arecoline in areca nuts
Increased production of collagen
 OSF occurs due to production of collagen & its degradation in subepithelial layers of oral mucosa
*It is a premalignant condition and malignant transformation has been seen in 3-7.6% of cases.
CLINICAL FEATURES OF ORAL SUBMUCOSAL FIBROSIS

Symptoms Signs
a) Intolerance to chillies & In initial stages, there is patchy redness of mucous membrane
spicy food. with formation of vesicles > rupture to form superficial ulcers.
b) Difficulty to protrude the
Inlaterstages, when fibrosis develops in the submucosal layers,
tongue & open the mouth there is blanching of mucosa.
fully
Fibrosis and scarring also extend to the underlying muscle >
c)Soreness of mouth with
further restrictive mobility of soft palate, tongue and jaw.
constant burning sensation;
Trismus is progressive, so much so that patient may not be able
d) Repeated vesicular eruption
to put his finger in the mouth or brush his teeth.
on the palate and pillars.
Orodental hygiene is affected badly & teeth become carious

TREATMENT

Medical
Surgery is indicated in advanced cases to relieve
trismus.Various surgical techniques used are:
1. Topical injection of steroids into the affected 1. Simple release of fibrosis and skin grafting.
area Dexamethasone 4 mg ml) combined2. Bilateral tongue flaps.
(1
with hylase, 1500 ml is injected into
IU in 1 Nasolabial flaps.
3.
the affected area biweekly for 8-10 weeks. Island palatal mucoperiosteal flap.
4.
2. Avoid irritant factors, e.g., areca nuts, pan, 5. Bilateral radial forearm free flap.
tobacco, pungent foods, etc. 6. Superficialtemporal fascia flap and split-skin
3. Treat existent anaemia or vitamin graft.
deficiencies 7. Coronoidectomy and temporal muscle
4. Encourage jaw opening exercises. myotomy
----===- -***** **====-====--- -----------=------------------------

3. Leucoplakia [04]
Ans.
WHO defined leukoplakia as a clinical white patch that cannot be characterized clinically or pathologically
as any other disease.
Risk factors:
Smoking, tob o chewing, alcohol abuse.
Chronic trauma due to ill-fitting dentures or cheek bites.
It may also be a/w submucous fibrosis, hyperplastic candidiasis or Plummer-Vinson syndrome
Age and sex-mostly occur in 4th decade, Males> Females.
Sites involved- Buccal mucosa and oral commissures are the
most common sites, It can also involve floor of mouth, tongue, LEUKOPLAKIA
gingivobuccal sulcus and the mucosal surface of lip.
Clinical types FLAT, WHITE LESIONS THAT CANNOT
BE B2USHED FROM THE ORAL MCOSA
1) Homogenous variety presents as a white patch. It is less often
a/w malignancy.
2) Nodular (speckled) variety presents as nodules on erythematous
MALIGNANTr POTENTIAL
base. WARRANTS BIOPaT

3) Erosive (erythroleukoplakia) variety- here leukoplakia is

interspersed with erythroplakia and has erosions and fissures.
 Histology&Mallgnant Potentilalt About 25% of leukoplakias may show some form of epithelial
dysplasia. Higher the grade of dysplasia more are the chances of its going into malignant change. On an
average about 5% become malignant
Management
1) Many of the lesions will disappear spontaneously if causative agent is removed.
2) In lesions with higher potential for malignant change, a biopsy is taken to rule out malignancy.
3) In suspicious small lesions, surgical excision or ablation with laser or cryotherapy can be done.

VSQs
1. Ranula [15]
Ans.
It is a cystic translucent lesion seen in the floor of mouth on one side of the frenulum and pushing the
tongue up.
arises from the sublingual salivary gland due to obstruction of its ducts.
It

Treatment is complete surgical excision if small, or marsupialization, if large.

------------------------- -
 Diseases of NOSE & PNS
LQS
Rhinitis'- etiopath, C/F & Mx [17, 16, 08]
1. 'Atrophic
a. Treatment of Primary Atrophic Rhinitis {20
b. Ozaena-surgical management [2000]
Ans.
ATROPHIC RHINITIS (OZAENA): It is a chronic inflammation of nose characterized by atrophy of nasal
mucosa and turbinate bones. The nasal cavities are roomy and full of foul-smelling crusts.
Types of Atrophic rhinitis; 2 types-primary and secondary.
Primary Atrophic Rhinitis
Aetioloay (Mnemonic HERNIA)
1. Hereditary- runs in the family.
Endocrinal factors: female gender; menstruation; pregnancy; tends to cease after menopause
3. Racial factors: White & yellow races are more susceptible
4. Nutritional deficiency: Deficiency of vitamin A, D or iron etc.
5. Infections (2°): Klebsiella ozaenae, Diphtheroids, Proteus vulgaris, E. coli, staphylococci & streptococci
(responsible for foul smell)
6. Autoimmune process: The body reacts to the antigens released from the nasal mucosa.
Pathology:
Ciliated columnar epithelium of nose is lost and is replaced by stratified squamous type.
There atrophy of seromucinous glands, venous blood sinusoids and nerve elements.
is
Arteries in the mucosa, periosteum and bone show obliterative endarteritis.
The bone of turbinates undergoes resorptionwidening of nasal chambers.
Paranasal sinuses are small due to their arrested development.
Clinical Features
Symptoms Signs
1) Commonly seen in females and starts around puberty 1. Presence of fetor (offensive smell)
2) Offensive smell (ozaenae) perceived by others near the Roomy nasal cavity due to atrophy of
patient,than the patient himself known as merciful the turbinates
anosmia (due to atrophy of the olfactory receptors) 3. Greenish yellow crust formation due
3) Nasal obstruction due to large crusts filling the nose to drying of the stagnant secretions
4) Epistaxis may ocur when the crusts are removed. because of loss of ciliary motility
5) Hearing impairment may be seen because of 4. Dryness and atrophy of nasal mucosa
obstruction to eustachian tube and middle ear effusion. 5. Atrophy of all the turbinates
6) Nose may show a saddle deformity 6. Paranasal sinuses are usually small
with thick walls
Investigations:
Complete blood picture, serum proteins and iron
X-ray PNS/CT scan
Chest X-ray: To rule out tuberculosis
Nasal swab: To rule out infective granulomatous conditions caused by acid-fast bacilli.
Serological test for syphilis and other granulomatous conditions
Nasal biopsy.
Treatment: It may be medical or surgical.
 Medical Treatment Surgical Treatment
29% alkaline nasal irigation-It 1) Young's operatlon: Both the nostrils are closed mucosa
loosens the crusts. may revert to normal and
b. 25% glucose in glycerine: inhibits crusting reduced.
Bacterial growth. 2) Modifled Young's Young's
operation
Modifed

c. Local antibiotics {Kemicetin operatlon: partially close

antiozaena) the nostrils.
d. Systemic use of streptomycin is 3) Narrowing the nasal
effective against Klebsiella cavitles: It helps to 31.4: Surgical procedure for atrophic thinits
Pig.

e. Oestradiol spray: to increase crusting. Techniques are:

vascularity of nasal mucosa and a. Submucosal injection of teflon paste.
regeneration of seromucinous b. Insertion of fat, cartilage, bone or teflon strips under the
glands mucoperiosteum of nose & the mucoperichondrium of
f. Potassium iodide-liquefy nasal the septum.
secretion. c. Section & medial displacement of lateral wall of nose.
Secondary Atrophic Rhinitis: 2° to infections like syphilis, lupus, leprosy and rhinoscleroma.
Atrophic rhinitis can also result from excessive surgical removal of turbinates
*****
2. Epistaxis etiopath, sites, classify & C/F. Discuss the Mx of acute profuse epistaxis in a 50-year-old
male smoker [14, 12, 11, 09, 07]
a. List the causes of Epistaxis & Treatment [20]
b. Posterior nasal packing [15
Ans.
Bleeding from inside the nose is called epistaxis.
CAUSES OF EPISTAXIS
IDIOPATHIC: Most Common
1. Trauma: Finger nail, intranasal surgery, fractures of face and base of skull, hard-
blowing of nose, violent sneeze.
2. Anfections
Acute: Viral rhinitis, nasal diphtheria, acute sinusitis.
Chronic: All crust-forming diseases, eg., atrophic rhinitis, rhinitis sicca, TB,
syphilis, septal perforation, Rhinosporidiosis.
LOCAL
NOSE Foreign bodies
CAUSES i. Non-living: Any neglected foreign body, rhinolith.
.
Living: Maggots, leeches.
4. Neoplasms of nose and paranasal sinuses.
i. Benign: Haemangioma, papilloma.
ii. Malignant: Carcinoma or sarcoma.
5, Atmospheric changes. High altitudes, sudden decompression (Caisson disease).
6. Deviated nasal septum.
NASOPHARYNX: Adenoiditis, Juvenile angiofibroma & Malignant tumours.
1) CVS: Hypertension, arteriosclerosis, mitral stenosis
2) Disorders of blood & blood vessels: Aplastic anaemia, leukaemia, thrombocytopenic

SYSTEMIC 3)
purpura, haemophilia, scurvy, vitamin K deficiency etc.
,
Liver disease: Hepatic cirrhosis (deficiency of factor VI, IX and X).
CAUSES 4) Kidney disease: Chronic nephritis.
5) Drugs: Salicylates, anticoagulant therapy (for heart disease).
6) Tumours of mediastinum (T venous pressure in the nose).
7) Vicarious menstruation (epistaxis occurring at the time of menstruation).
SITES OF EPISTAXIS Anterlor epistaxls Posterlor epistaxis
1. Little's area: In 90% cases Incidence More common Lesscommon
Site Mostly from Little's Mostly from posterosuperior
2. Above the level of middle turbinate: from ethmoidal area or anterior part part of nasal cavity; often
of lateral wal difflicult to localize the
vessels bleeding point
Mosty occurs in After 40 years of age
Below the level of middle turbinate: from the branches Age
children or young
of sphenopalatine artery. adults
Cause Mostly trauma Spontaneous; often due
4. Posterior part of nasal cavity to hypertension or
arteriosclerosis
5. Diffuse - Both from septum & lateral nasal wall: seen in Bleeding Usually mild, can be Bleeding is severe, requires
general systemic disorders and blood dyscrasias. easily controlled by
local pressure or
hospitalization; postnasal
pack often required
anterior pack
CLASSIFICATION OF EPISTAXIS
Pinch the nose and rake the patient sit bending
foruard
Anterior Epistaxis: When blood flows out from the Hippocrotc/ Trotter's rethod).
front of nose with the patient in sitting position. Also get ivV access

Posterior Epistaxis:; the blood flows back into the

Local cautery Agno,)
throat. Patient may swallow it and later have a
"coffee-coloured" vomitus. This may erroneously be Anterior nasal packing Gauge/ merocel pack)
diagnosed as haematemesis.
air)
Posterior nasal pacK Foley's catheter inated wth

MANAGEMENT: Ligotion
1) FIRST AID: pinch the nose for about 5 min (to Sphenopalatine artery at sphenopalatine ¥oramen
compress the vessels of the little's area).
Anterior ethmoidal artery
2) CAUTERIZE the bleeding point with a bead of silver
nitrate or electrocautery. maxillary artery - Calduell luc approach
3) ANTERIOR NASAL PACKING: If bleeding profuse, is
external carotid artery
use a ribbon gauge soaked liquid paraffin to
in

pack the nasal cavity. Pack can be removed after Never ligate internal carotid artery
Nouadays ligation o sphenopalatine artery gives ioo% resut becouse
24 h, if bleeding has stopped.
POSTERIOR NASAL PACKING: For posterior of endoscopu_
epistaxis, either use a Foley's catheter
inflated with air or nasal balloons.
5) ELEVATION OF MUcOPERICHONDRIAL FLAP
AND SMR OPERATION: In case of persistent
or recurrent bleeds from the septum, just
elevation of mucoperichondrial flap and then
repositioning it back helps to cause fibrosis Packing in horizontal layers
Methodi.ol NIecoL DASALpaSNDg, (A) Packing in wertical layers. (6)
and constrict blood vessels. SMR operation
can be done to achieve the same result or remove any
septal spur which is sometimes the cause of epistaxis.
6) LIGATION OF VESSELS: may be required only in refractory
cases where bleeding fails to stop after packing.
External carotid > Maxillary artery (Approach is via Caldwell-Luc operation)
Ethmoidal arteries. Nowadays TESPAL (Transnasal Endoscopic
Sphenopalatine Artery Ligation) gives 100% success rate
7) Embolization: It is done through femoral artery
catheterization. Internal maxillary artery is localized and the Epistaxis balloon for posterior epistaxis. Posterior
bal-

embolization is performed. Embolization may have risks like loon (A) is inflated with 10 ml and anterior balloon
(8) with 30 mL
Catheter provides nasai aiway,
cerebral thromboembolism, haematoma at local site.
3. Allergic rhinitis (or) nasal allergy-C/F & Mx [13, 09, 67]
a. Medical management of allergic rhinitis [13]
b. Tests to screen nasal allergy [13]
C. Newer Anti-histaminics (03]

d. Nasal decongestants [02]

Ans.
It is anIgE-mediated immunologic response of nasal mucosa to airborne allergens.
2 clinical types have been recognized:
a) Seasonal: Symptoms appear in a particular season when the pollens of a particular plant, to which the patient is sensitive, are present in the air.
b) Perennial. Symptoms are present throughout the year.
CLINIGAL FEATURES
Symptoms Signs
Seasonal type Perennialtype Nasal signs: transverse nasal crease (allergic salute), pale and
Paroxysmal oedematous nasal mucosa which may appear bluish.
the symptoms are
sneezing, 10- Turbinates are swollen. Thin, watery or mucoid discharge is
less severe; may
20 sneezes at a usually present.
present as
time. Ocular signs: oedema of lids, congestion and cobble-stone
Nasal recurrent 'cold' or
appearance of the conjunctiva, and dark circles under the eyes
obstruction, stuffy nose with
shiners).
Watery nasal Sneezing, postnasalalergic
drip, watery
.Otologic signs: retracted tympanic membrane or serous
discharge & otitis media due to eustachian tube blockage.
Itching in the rhinorrhoea &
Pharyngeal signs: granular pharyngitis due to hyperplasia of
nose, eyes, hearing impairment
due to eustachian submucosal lymphoid tissue.
palate or Laryngeal signs: hoarseness and oedema of the vocal cords
tube blockage
pharynx
DIAGNOSIS: Allergic Rhinitis and Its Impact on Asthma (ARIA) TABLE 30.1 CLASSIFICATION OF ALLERGIC
RHINITIS (ARIA)

Classification: Duration of disease

Intermittent: Symptoms are present
INVESTIGATIONS - Less than 4 days a week or
Oress than 4 weeks
1. Total and differential count: eosinophilia. Persistent: 5ymptoms are present
-More than 4 days a week or
2. Nasal smear: shows Teosinophils. - For more than 4 weeks
Severity of disease
Skin tests (prick, scratch & intradermal tests): help to identify the Mild: None of the folowing symptoms are present
Sleep disturbance
allergen. Impairment of daily activities, leisure and sport
Impairment of school or work
4. Specific JgE measurements: to find the specific allergen. Troublesomesymptoms
an
Moderate to severe: One or more of the above symptoms
5. Radioallergosorbent test (RAST), It is an in vitro test and present

measures specific lgE antibody concentration in the patient's serum.

6. Nasal provocation test: A crude method is to challenge the nasal mucosa with a small amount of
allergen placed at the end of a toothpick and asking the patient to sniff into each nostril and to observe
if allergic symptoms are reproduced.

cOMPLICATIONS: Nasal allergy may cause:

1) Recurrent sinusitis because of obstruction to the sinus ostia.
2) Formation of nasal polyps.
3) Serous otitis media.
4) Orthodontic problems and other ill-effects of prolonged mouth breathing
5) Bronchial asthma (Patients of nasal allergy have 4x more risk of developing bronchial asthma).
TREATMENT OPTIONSs
1. Avoidance of Allergen: Removal of a pet from the house, food allergen allergic can be eliminated from
the diet, change of place of work etc.
2. Treatment with Drugs
a) Antihistaminics: to control rhinorrhoea, sneezing and nasal itch
b) Alpha-adrenergic drugs constrict blood vessels and reduce nasal congestion and oedema.
c)Torticosteroids
d) Sodium cromoglycate: prevents degranulation of mast cells.
e) Anticholinergics: Ipratropium bromide - control rhinorrhoea.
f) Leukotriene receptor Flowchart 34.1: Management protocol for allerglc hinitis
antagonists Management of allergic rhinitis
Montelukast,
Pranlukast and Treatment options
Zafirlukast.
3. Immunotherapy: or Environmental control Pharmacotherapy Immunotherapy
Avoidance of allergen Sublingual
hyposensitization is used and irritants subcutaneous
SystemicC Local
when drug treatment Non-sedative H1 blocker Intranasal steroid
Nasalloral decongestant Sodium
fails to control Montelukast chromoglycate
symptoms. Allergen is
given in gradually
increasing doses till the Mild Mild Moderate/severe Moderate/severe
intermittent persistent intermittent persistent
maintenance dose is
reached. Pharmacotherapy Pharmacotherapy Pharmacotherapy Pharmacotherapy
-Systemic Local Local Local
Immunotherapy H1 blocker -
Systemic - Systemic Systemic
Decongestant Environmental Environmental 'Environmental
suppresses the Environmental control control control
control Immunotherapy Immunotherapy
formation of IgE.

4. Chronic frontal & maxillary sinusitis - aetiopathogenesis, clinical features & management [10]
a. Chronic sinusitis-C/F, Mx & complications [17, 16]
b. Caldwell-Luc operation [14]
c. Signs of Rhinosinusitis [07]
d. What are the signs, symptoms, DDx and Rx of chronic frontal sinusitis? (68]
Ans.
DEFINITION of Chronic Sinusitis: It is a chronic inflammatory disease of nasal & paranasal sinus mucosa

where symptoms has continued beyond 12 weeks. It is aka CRS (Chronic Rhinosinusitis
a
ETIOPATHOGENESIS: CRS is multifactorial disease. The causative factors form a vicious cycle which runs in

both dlockwise & anticlockwise directions

Pollution
Viral infections
Chemicals
Ostial obstruction Cillary dyskinesia

Negative pressure in sinus LOSs of cila

Anatomical abnormalities
Polypi Alergy
Hypoxia and acidic pH.
Adenoid Mucosal VMR
Alergic tungal sinusitis
Alergy
ABpirnin triad
Deranged mucocliary clearance Tumours

Thick mucus

Stasis of mucus in sinus eci

Inadequale therapy ol acute

Bacterial infection infection
Dental inlections
Bacterial resiatance
Persistent sinus infection Environmental fung
Sequence of events following sinus ostial obstructlon
leading to chronic rhinosinusitis. Causative factors and pathophysiology of chronic sinusitis.
For clinical purposes, CRS is divided into 2 categories: CRS without polyps &CRS with polyps
CRSWithout Polyps CRSwith Polyps
Bacteria S. aureus, P. aeruginosa, K. pneumoniae,
Aetiology
E.coli,Anaerobic organismsetc. Polyp formation in the nose and
1. Structural deformities: DNS, concha bullosa etc.
sinuses can be due to infections or
ostial obstruction. systemic disorders such as
2. Loss of ciliary function: due to infection & toxins
Primary ciliary dyskinesia,
(pollution and smoking). Cystic fibrosis,
3. Cystic fibrosis and vOung syndrome: Mucus is
Samter's triad (aspirin
Predisposing too thick to be moved by cilia. sensitivity, nasal polypi and
4. Osteitis/osteomyelitis (seen after nasal surgery) asthma),
Factors
5. Dental infections spread into maxillary sinus. Asthma,
6. Asthma: seen in 50% of CRS cases. Churg-Strauss syndrome and
7. Allergy: It causes oedema of the nasal mucosa and Allergic fungal sinusitis.
obstructs the sinus ostia.
8. Biofilm formed by the microbes is impervious to
antibiotics bacterial resistance & chronicity
Nasal obstruction, Purulent discharge, Facial pain Symptoms are similar to that seen
Symptoms
and Disturbance of smell (hyposmia or anosmia). in CRS without polyps but nose
Endoscopic examination of nose reveal: shows multiple nasal polyps.
Signs
Edemaof nasal mucosa & Purulent discharge
made based on history, physical examination and imaging studies.
is
Diagnosis CT scan of sinuses reveals the extent of disease, predisposing structural abnormalities
andany extension to orbit and cranial cavity. MRI with contrast may be required
1. Broad-spectrum antibiotics should be chosen based on the culture and sensitivity of
discharge from the middle meatus. Macrolides are bacteriostatic & also have an anti-inflammatory
effect hence can be used.
2. Saline irrigations: They help to wash out bacteria, allergen & disrupt biofilms.
Medical 3. Topical decongestants: They provide the symptomatic relief from nasal obstruction
Treatment and open the sinus ostia.
4. Steroid sprays: are anti-inflammatory in nature and relieve oedema.
5. Systemic steroids- used in pre-op to size of polyps & in post-op to prevent recurrence
6. Anti-allergy treatment: antihistamines& LT receptor antagonists (Ex: montelukast).
7. Treatment of asthma-(since Asthma is a predisposing factor)
Treatment of choice for CRS with or without polypi is FESS (tunctional endoscopic sinus surgery).
Surgical
Structural variants which obstruct sinus drainage are corrected to provide drainage and
Treatment
ventilation to sinuses. Medical treatment should be continued after surgery for long-term relief
OLDER Surgical Techniques for CHRONIC SINUSITIS
CHRONIC MAXILLARY SINUSITIS 1 Antral puncture and irrigation
2. Intranasal antrostomy: A window is created in the inferior meatus.
3. Caldwell-Luc operation: In this, antrum is entered through its anterior wall by a
sublabial incision. All irreversible diseases are removed and a window is created
between the antrum and inferior meatus
CHRONIC FRONTAL SINUSITIS 1. Intranasal drainage operations
2. Trephination of frontal sinus.
3. External frontoethmoidectomy (Howarth's or Lynch operation):
4. Osteoplastic flap operation
CHRONIC ETHMOID SINUSITIS Intranasal ethmoidectomy or External ethmoidectomy.
CHRONIC SPHENOIDITIS Sphenoidotomy
*******
*****

Describe the anatomy of Nasal Septum. What are the signs, symptoms & treatment of DNS? (08, 06]
 a. Management of deviated Nasal Septum [13]
b. Nasal septum [10]
Nasal spine of
Ans. frontal bone
NASALSEPTUM consists of 3 parts: Crest of nas Perp. plate of
Done ethmoid
1. Columellar Septum: It is formed of columella containing
Membranous
the medial crura of alar cartilages united together by septum Septal cart Vomer Rostrum of
sphenoid
fibrous tissue & covered on either side by skin. Columellar
septum
2. Membranous Septum: /t consists of double layer of skin
Ant. nasal spine
with no bony or cartilaginous support. It lies between the of maxilla Crest of maxilla
columella and the caudal border of septal cartilage. Both Crest of palatine bone
columellar & membranous parts are freely movable. Anatomy of nasal septum,

3. Septum Proper:
It consists of osseocartilaginous framework, covered with nasal mucous membrane. Its principal
constituents are: Olfactory nerves

a) the perpendicular plate of ethmoid,

b) the vomer and
c) a large septal (quadrilateral) cartilage Ant. ethmoidal
nerve
wedged between the above two bones
anteriorly.
Other bones which make minor contributions at the
periphery are crest of nasal bones, nasal spine of
frontal bone, rostrum of sphenoid, crest of palatine
bones & the crest maxilla, and the anterior nasal spine
of maxilla. Nasopalatine
nerve
Blood Supply of Nasal Septum (Refer 11th sa). Infraorbital

Nerve Supply of Nasal Septum:

Greater palatine
nerve

DEVIATED NASAL SEPTUMDNS

MCC: Birth Trauma

CLINICAL FEATURES

Symptoms Signs
1. Elevate the tip of the nose to look for caudal
1) Nasal obstruction: May be unilateral in C dislocation and the vestibule of the nose.
shaped deviation or bilateral in S-shaped
2. Anterior rhinoscopy: site & type of deviation, presence
deviation
of compensatory hypertrophy, status of nasal mucosa,
2) Headache: Usually occurs due to
discharge from the meatus, crusting, etc.
associated sinusitis. (Sludgers Neuralgia) Local application of decongestant like cocaine/
3) External deformity of Nose: subluxation
xylocaine with adrenaline helps in better assessment
and caudal dislocation of the cartilage of the deeper areas in the nasal cavity.
loss of support to the tip and columella 4. Cottle's test- pulling the cheek outwards at the
Disturbance in sense of Smell: nasofacial crease improves the nasal patency at the
Hyposmia/Anosmia
valve area
5) Epistaxis: It is due to spur or crusting of
5. Cold Spatula Test-to identify the U/L or B/L nasal
nasal mucosa
obstruction
INVESTIGATIONS
1) X-ray PNS (Water's iew and Caldwell view): To look for haziness of the various sinuses. The alignment
of the septum and the size of the turbinates may also be assessed.
2) CT scan of the paranasal sinuses: to identify any sinus pathology.
3) Diagnostic nasal endoscopy (DNE)
4) Bleeding and clotting profile: BT, CT, PT and APTT

TREATMENT
1) Minor septal deviation with no symptoms are commonly seen & require no treatment.
2) Séptal surgery is usually done after the age of 17 so as not to interfere with the growth of nasal
skeleton.
a. Submucous Resection (SMR) Operation Complication: Saddle Nose Deformity
b. Septoplasty: It is a conservative approach. In this operation, much of the septal framework is
retained. Septoplasty has now almost replaced SMR operation.
**********

6. Nasal polyp- Define, types, etiopath, C/F & Dx. Briefly outline their Mx [04]
a. Antrochoanal Polyp-pathology, C/F, DDx & Mx [14, 03, 90]
b. Discuss C/F and Mx of ethmoidal polyposis [12]
C. Mxof sinonasal polyposis [11]

d. Ethmoidal polyp [03, 01]

Ans.
Nasal polypi are non-neoplastic masses of oedematous nasal or sinus mucosa.
They are divided into 2 main varieties: 1 Antrochoanal polyp. &2. Blateral ethmoldal polyp
ANTROCHOANAL POLYP (syn-killant BILATERALETHMOIDAL POLYPI
polyp)
or multifactorial
Infection AAllergy
Predisposing Factors:
AETIOLOGY 1) CRS of both allergic & non-allergic origin
2) Samter's triad: nasal polypi, asthma and aspirin intolerance
3) Cystic fibrosis
4) Kartagener syndrome; Young syndrome; Churg-Strausssyndrome etc.
PATHOGENESIS Nasal mucosa becomes oedematous due to collection of ECF causing
infection/ Alergy polypoidal change
Edema in middle meatal area Origin: Maxillary sinus near the Origin: Multiple nasal polypi
ostium. always arise from the lateral wall
Nasal narrouing
Laterality: Unilateral of nose.
velocity Growth: Backwards into the choana|Laterality: ilateral
& nasal cavity. It has 3 parts. Common sites are uncinate
Negative pressure 1. Antral, which is a thin stalk. process, bulla Ethmoidalis, ostia of
2. Choanal, which is round globular. sinuses, medial surface of middle
&
Puling of muscosa into pothuuay of ai
3. Nasal, which isflatfrom sideto side turbinate
1) Multiple polypi -grape-like
masses; mostly seen in adults.
U/L nasal obstruction is the 2) Nasal stuffinesstotal nasal
obstruction.
presenting symptom.
3) Disturbance in sense of smel.
Voice may become thick and dull
SYMPTOMSs 4) Headache due to associated sinusitis
due to hyponasality. 5) Sneezing & watery nasal
Nasal discharge (mucoid) may be
discharge due to associated
seen.
allergy
6) Mass protruding from the
nostril.
 14 of 29
On anterior rhinoscopy, or
endoscopic examination, polypi
1) Polvp may bemissedon anterior rhinoscopy as the appear as smooth, glistening,
bulk of the mass lies in the posterior part of the
grape-like masses often pale in
nasal cavity and in the nasopharynx. Probe cannot
colour.
be passed around the mass as it arises in the lateral
wall
They may be sessile or
pedunculated, insensitive to
SIGNS
|2) Posterior rhinoscopy will reveal a large polyp,
probing and do not bleed on
which is pale white and translucent. Sometimes it
comes out into the oropharynx, pushing the soft touch.
palate downwards Longstanding cases present
with broadening of nose and
3) Examination of the nose with an endoscope will increased intercanthal distance.
reveal the polyp hidden posteriorly in the nasal
A polyp may protrude from the
cavity
nostril and appear pink and
vascularsimulating neoplasm.
|1) blob of mucus often looks like a polypus but it would disappear on
A
blowing nose.
DIFFERENTIAL 2) Hypertrophied middle turbinate
DIAGNOSIs 3) Angiofibroma & Other neoplasms (fleshy pink appearance & tendency
to bleed).
4) Rhinosporidosis, rhinoscleroma etc.
Diagnostic nasal endoscopy
Nasal swab for fungal culture
Biopsy if neoplasm or granulomatous condition is suspected
Allergy tests including prick test/ intradermal skin test/ RAST.
INVESTIGATIONS Radiological:
X-rays of paranasal sinuses will show opacity of the maxillary antrum
(in Antrochoanal polyp)
X-ray (lateral view) reveals a globular swelling in postnasal space.
Non-contrast CT scans show the extent of the polyp & helps to plan
surgery
Medical Treatment
1. Anti-histaminics for early polypoidal changes
2. A short course of steroids for people who cannot tolerate
antihistaminics or in those with asthma & polypoidal nasal mucosa.
Endoscopic sinus surgery (FESS)
Caldwell-Luc operation: in recurrent cases of Antrochoanal polyp
Surgical Treatment Prior to the advent of FESS, following operations were done for
Ethmoidal polyp:
Polypectomy
Ethmoidectomy (Intranasal/ Extranasal/Transantral)

7. Maxillary sinusitis- etiopath, C/F, Dx & Rx [80, 78, 70]

Ans
ACUTE MAXILLARY SINUSITIS
AETIOLOGY
1. Viral rhinitis (MC).
2. Diving and swimming in contaminated water.
3. Dental infections.
 15 of 29
4. External trauma to the sinus, e.g., fractures, penetrating injuries or gunshot wounds may be followed
by sinusitis.
CLINICAL FEATURES

Symptoms Signs
1. Constitutional symptoms: fever, general Tenderness over the canine fossa.
malaise and body ache. Edema of the cheek may be seen in children
2. Headache On anterior rhinoscopic examination, the nasal
3. Pain: Typically, over the upper jaw, but may be mucosa will be swollen especially in the region
referred to the gums or teeth; Pain by chewing. of the middle meatus a/w mucopurulent
4. Redness & oedema of cheek: The lower eyelid discharge.
may become puffy. Associated dental infection has to be ruled out.
5. Nasal discharge. Factors like DNS etc. contributing to the
6. Postnasal discharge. infection should be looked for.
DIAGNOSISs

Transillumination test: Affected sinus will be found opaque

Xrays: Waters' view will show either an opacity or a fluid level in the involved sinus.
Computed tomography (CT) scan is the preferred imaging modality to investigate the sinuses.
TREATMENT
Medical Surgical
Antral lavage: It
Antimicrobial drugs: Ampicillin/amoxicillin/Erythromycin or doxyeycline or
1.
is done only
cotrimoxazole.
2. Nasal decongestants: 1% ephedrine or 0.1% xylo- or oxymetazoline to decongest when medical
sinus ostium & encourage drainage. treatment has
3. Steam inhalation: Steam alone or medicated with menthol provides symptomatic
relief and encourages sinus drainage.
ied
too
and tnat
only under
4. Analgesics: Paracetamol. cover of
antibiotics.
cOMPLICATIONS
1) Acute maxillary sinusitis may change to subacute or chronic sinusitis.
2) Frontal sinusitis: Due to obstruction of frontal sinus drainage pathway because of oedema.
3) Osteitis or osteomyelitis of the maxilla.
4) Orbital cellulitis or abscess: Infection spreads to the orbit because of oedema either directly from the
roof of maxillary sinus or indirectly, after involvement of ethmoid sinuses.
CHRONICMAXILLARY SINUSITIS REFER 4TH LQ

SQs
1. Rhinosporidiosis [16, 10, 04] Trophocyte
a. Signs of nasal Rhinosporidiosis [14] Endospore
b. Nasal Rhinosporidiosis [96]
Ans.
It is a chronic granulomatous disease caused by
Intemediate
Rhinosporidium seeberi. sporangia

Life Cycle: G Liberated

endospore
3 stages: trophic stage, development of sporangia and
production of endospores.
Sporangium
Lfe cycle of Rhinosporidium seeber
Clinical Features 16 of 29
Mode of Transmission: contaminated water of ponds.
*Nose: leafy, polypoidal mass, pink to purple in colour; attached to nasal septum or lateral wall.
Sqmetimes, it extends into the nasopharynx and may hang behind the soft palate.
The mass is very vascular & bleeds easily on touch. Its surface is studded with white dots representing
the sporangia.
*In early stages, the patient may complain of nasal discharge which is often blood tinged and nasal
stuffiness.
Diagnosis: This is made on biopsy. t shows several sporangia, filled with spores.
Treatment: Complete excision of the mass with diathermy knife and cauterization of its base. Recurrence
may occur after surgical excision.

2. Maggots in Nose [16]

a. Nasal Myiasis [04]
Ans.
Nasal Myiasis (Maggots in Nose)
Maggots are larval forms of flies. They infest nose, nasopharynx & PNS causing extensive destruction.
Flies, particularly of the genus Chrysomyia, are attracted by the foul-smelling discharge from cases of
atrophic rhinitis, syphilis, leprosy or infected wounds and lay eggs, which within 24h hatch into larvae.
In India, they are mostly seen from the month of August to October.
CLINICAL FEATURES
1. In the first 3- or 4-days maggots produce intense irritation, sneezing, lacrimation and headache.
2. Thin blood-stained discharge oozes from the nostrils. The eyelids and lips become puffy. Till this time
patient is not aware of maggots. He may present simply as a case of epistaxis.
3. It is only on the 3'd or 4th day that the maggots may crawl out of the nose.
4. Maggots cause extensive destruction Fistulae may form in the palate or around the nose.
5. Death may occur from meningitis.
TREATMENT
All visible maggots should be picked up with forceps. Many of them try to retreat into darker cavities
when light falls on them. Instillation of chloroform water and oil kills them.
Nasal douche with warm saline is used to remove slough, crusts and dead maggots.
A patient with maggots should be isolated with a mosquito net to avoid contact with flies which can

perpetuate this cycle.

All patients should receive instruction for nasal hygiene before leaving the hospital.

3. Anatomy of lateral wall of the nasal cavity [15, 13, 071

Ans.
3 and occasionally 4 turbinates or conchae mark the
lateral wall of nose. Sup. turoinale and meatus

Conchae or turbinates are scroll-like bony projections

Aggernasi
covered by mucous membrane. The spaces below the
Atrum-
turbinates are called meatuses. Middle turbinat
and mealus
InferlorTurblnates It is a separate bone and below it,
into the inferior meatus, opens the nasolacrimal duct
guarded by a mucosal valve called Hasner's valve. Vestibule nt. turbinate
and mealus

Middle Turbinate: It is a part of ethmoid bone. It is

Structures on lateral wall of nose
attached to the lateral wall in an S-shaped manner
 17of 29
Middle Meatus; It is a space below the middle turbinate. Structures seen here are:
1) Uncinate process is a hook-like structure.
2) Bulla Ethmoldals: It is an ethmoidal cell situated behind the uncinate proces.
3) Hiatus semilunaris: The gap between the Uncinate process & Bulla Ethmoidalis.
4) Atrium of the Middle Meatus: It is a Hlatus semilnaris
Sphenoethmoid recess with
opening of sphenoid sinus
shallow depression lying in front of middle Uncinate process
Bulla
othmolidals
turbinate. Opening ofl frontal sinu

5) Agger Nasi: It is an elevation just anterior Opening of post. ethmold

Opening ol max. sinus

to the attachment of middle turbinate.
pening of middle
6) Haller cells are air cells situated in the roof ethmoida Sinuses

of maxillary sinus.
Pneumatization of middle turbinate leads to pening of
nasolacrimal ouct

an enlarged ballooned out middle turbinate Accessory opening

ofmax. sinus
called concha bullosa Latecal,walotnose with turbinates cemovsd.shwng.openings.lvarious nue

nbriform plate

Superlor Turblnates It is also a part of ethmoid bone.

Bulla ethmoidalis
Superior Meatus. It is a space below the superior turbinate
Lamina papyracea
Posterior ethmoid cells open into it.
Midde turbinate
Onodi cell is a posterior ethmoidal cell which is surgically Septum - Uncinate process
important as the optic nerve is related to its lateral wall.
Sphenoethmoidal Recess: It is situated above the
Interior -
superior turbinate. Sphenoid sinus opens into it. turbinate
Max. sinus

Supreme Turbinates It is sometimes present above the

superior turbinate and has a narrow meatus beneath it.

4. Physiology of olfaction [15, 14]

Ans. Olfaction is important for pleasure and for enjoying the taste of food.
Olfactory Pathways Olfactory patthway

Complex interaction among smel, taste,

Disorders of Smell: feedingbehavior and reproduction
Olfactory ract

Sense of smell can be tested by

Olfactory epithelium
asking the patient to smell Mitralcell
Oltfactory bulb
common odours such as lemon, Glomerular lfactory bulb
-Olfactory glomerulus

peppermint, rose, garlic or Olfactory tract Cribriform plate of

ethmoid bone
cloves from each side of the
Olfactory trgone
nose separately, with eyes
Oifactory receptor
closed Medial striae Latera
Shae
Anosmia is total loss of sense of
Hypothalamus Sustentacular cell
smell while hyposmia is partial
Ofactory rod
loss. Central connections-amygdala
Mucus membrane
and hippocampus
Parosmia is perversion of smell;
the person interprets the odours incorrectly. It is seen in the recovery phase of post-infuenzal anosmia

5. Acute frontal sinusitis etiology, C/F & Sx [14]

Ans.
AETIOLOGY
1. Viralinfections of upper respiratory tract followed by 2 bacterial invasion.
2. Diving and swimming in contaminated water.
3. External trauma to the sinus, e.g., fractures.
4. Oedema of middle meatus, 2° to maxillary or ethmoid sinus infection.
CLINICAL FEATURES

Symptoms Signs
1) Frontal headache: It shows characteristic periodicity, i.e., comes up 1) Swollen nasal mucosa.
on waking8, gradually increases and reaches its peak by about mid- 2) Presence of pus in the
day and then starts subsiding. It is also called "office headache". middle meatus
2) Swelling of the upper eyelid. Tenderness: over the
3) Nasal discharge is absent initially. It may later present as purulent frontal sinus (just above
and may be blood stained on forceful blowing of the nose. the medial canthus).
4) Anosmia or hyposmia is usually present due to mucosal edema 4) Edema of the upper eyelid.
INVESTIGATIONS:
X-rays {Waters' and lateral views}: Opacity of the frontal sinus can be seen.
the preferred modality.
CT scan is
TREATMENT
Medical Surgical
|
Mainstay of treatment is medical. Trephination of frontal sinus: It is indicated if the pain is
a) Antimicrobials. severe and persistent in spite of antibiotic treatment.
b) Antihistaminic + oral nasal Procedure: horizontal incision below the eyebrowDrill
decongestant (phenylephrine a holePus istaken for culture and
hydrochloride) is useful. sensitivity Irigate the Sinus with
c)Placing a pledget of cotton soaked in normal saline until frontonasal duct
a vasoconstrictor in the middle becomes patent.
meatus, once or twice daily, helps to Endoscopic sinus surgerv (FESS)
relieve ostial oedema. limited to frontal sinus may be done
d) Analgesics like aceclofenac can be as an alternative procedure
pnaon inus of nght lhonta

given
COMPLICATIONS
1. Orbital cellulitis.
2. Osteomyelitis of frontal bone and fistula formation.
3. Meningitis, extradural abscess or frontal lobe abscess.
Chronic frontal sinusitis, if the acute infection is neglected or improperly treated.

6. Paranasal sinuses [13] Chibrilorm

a. Mucociliary transport mechanism of Nose [09 Roof of ethmoid-
plate

b. Mucociliary clearance mechanism of nose [08]

Orbil-
c. Maxillary sinus (98] itactory
SuCus

d. Briefly describe the anatomy of Frontal sinus [68] Uncinate

process
Middle
turbinate
Ans. Inferior

They are air filled spaces in the skull bones and are lined by mucosa. Madillary
sinus
turbinate

They are 4 on each side. F0Or o maxilary

Clinically, paranasal sinuses have been divided into 2 groups:

1. Anterior group- maxillary, frontal and anterior ethmoidal. They oronal section showing relationship of maxillary and
ethmoidal sinuses to orbit and the nasal cavity. Floor ol maxillay sinus
all open in the middle meatus. is about 1 cm below the floor of nose.
2. Posterlor Rroup -posterior ethmoidal sinuses (open in the superior meatus) and the sphenoid sinus
(opens in sphenoethmoidal recess).
Maxillary Sinus (Antrum of Highmore)l It is the largest of paranasal sinuses and occupies the body of
maxilla. It is pyramidal in shape.
Frontal Sinus: It is situated between the inner and outer tables of frontal bone. The 2 frontal sinuses are
often asymmetric.
Drainage of the frontal sinus is through its ostium into the frontal recess. Frontal recess is situated in the
anterior part of middle meatus.
Ethmoldal Sinuses (Ethmoid Air Cells: They are present in the lateral masses of ethmoid bone. Clinically,
ethmoidal cells are divided by the basal lamina into an anterior & posterior ethmoid group.
Anterior Group Posterior Group.
They include:
1. Agger nasi cells -present in the agger nasi ridge. They are 1-7 in number and open into superior
2. Ethmoid bulla. meatus or in the supreme meatus, when present.
|

3. Supraorbital cells. One important cell of this group is

Frontoethmoid cells. sphenoethmoid cell, also called the Onodi cell
5. Haller cells-situated in the floor of the orbit.
Sphenoid Sinus: It occupies the body of sphenoid. Ostium
of the sphenoid sinus opens into the sphenoethmoidal Pituitary V
nt carotid
recess, medial to the superior or supreme turbinate.
Cavernous
Sinus
MUCOCILIARY CLEARANCE OF SINUSES: PNS are lined by
ciliated columnar epithelium
Maxilary Sinus: Sphenoid sinus
Relations of sphenoid sinus.
Mucus from all the walls of the maxillary sinus is
transported by the cilia to the natural ostium and then into the middle Infundibulum

meatus.
It is observed that inferior meatal antrostomy made in Caldwell- Luc operation provides Natural
osbum
ventilation to the sinuses, but it does not help in mucociliary clearance which still takes
place through the natural ostium.
Intranasal
Frontal Sinus: antrostomy

Mucus travels up along the interfrontal septum, along the roof of the
lateral wall, along the floor and then exits through the natural ostium.
Circulation is anticlockwise in the right and clockwise in the left
frontal sinus
SphenoidSinus: Mucociliary clearance is towards its ostium into the
sphenoethmoidal recess.
Ethmoid Sinus Mucoclary clearance of trontal sinus

Mucus from anterior group of ethmoids joins that from the frontal and maxillary sinuses travels
towards eustachian tube into the nasopharynx.
Mucus from posterior ethmoids drains into superior meatus and then joins the mucus from the
sphenoid sinus in the sphenoethmoidal recess & then into the nasopharynx.
FUNCTIONS OF PARANASAL SINUSES
1) Warming and moistening of the inspired air by providing large surface area.
2) Lighten the skull bones
3) Provide resonance to voice.
4) Act as Temperature buffer to protect delicate structures in the orbit and the cranium from variations
 5) Ethmoid sinuses provide extended surface for olfaction.
6) Provide local immunologic defence against microbes.
7) Mucociliary clearance
*****************************************

7. Rhinolith [20, 09]

Ans.
It is stone formation in
the nasal cavity by deposition of calcium and magnesium salts on an untreated
foreign body or thick mucous in the nasal cavity
AETIOLOGY: Chronic foreign body in the nose or thick mucus can act as a nidus over which deposition of
calcium and magnesium salts occur over a long period. It occupies the space available inside nasal cavity
and acquires variable size and shape.
CLINICAL FEATURES: Rhinoliths are more common in adults.
>Unilateral nasal obstruction
Headache due to neuralgia
Blood-stained rhinorrhoea & Epistaxis
Anterior rhinoscopy shows brown-black mass with stony hard feel between the septum and
turbinates. It is often brittle and a portion of it may break off while manipulating.
INVESTIGATIONS
X-ray PNS shows radiopaque shadow in the nasal cavity.
Diagnostic nasal endoscopy confirms the location and extent of the rhinolith
TREATMENT
Most of the Rhinolith can be removed through anterior nares. Large ones need to be broken into pieces
before removal.
Some hard and irregular Rhinoliths require lateral rhinotomy.
COMPLICATIONS: Oroantral fistula
---------
8. Blood supply of Nose [09] NASAL SEPTUM
a. Mxof Little's area bleeding [12] InternalCarotid System
b. Little's Area [06, 98, 91] Anterior ethrnoidal arteTyBranchs of ophthalmic
2. Iosterior ethinonal artery ) atey
C. Blood supply of nasal septum [02]
External Carotid Sytem
Ans. . Sphenopulatine artery tbranch of maxillary artery) gives

Nose is richly supplied by both the external & internal carotid anneDtan a
*p h ot
phetht tmeulal naul branche
&Teater pulatine artery (branch ot

r
maxillary artery)
systems, both on the septum and the lateral walls Septalbranh of
artery.
superior labial artery (branch of tacial

Retrocolumellar Vein: This vein runs vertically downwards just behind the LATERAL WALU
columella, crosses the floor of nose and joins venous plexus on the lateral nasal Internal Carotid System
wall. This is a common site of venous bleeding in young people. .

woODRUFF'S PLEXUS:
. Anterku ethma,
usterioe ethawdal
Branchs of ophthalinic arter
It is a plexus of veins situated inferior to posterior end of
inferior turbinate. It is a site of posterior epistaxis in adults External Carotid System
LITTLE'S AREA .usterior lateral naul rom hetoguiatin
artery
rom nallary artery
situated the anterior inferior part of nasal septum, just
It is in . oarcn ou
.Grcater palatine artery
om infaoiital banch
Nal antetiy

u dental of mavillary artery

above the vestibule. .Branc hes of facial artery
to naul vestibule
4 arteries- anterior ethmoidal, septal branch of superior labial,
septal branch of sphenopalatine & the greater palatine, anastomose here to form a vascular plexus
called "Kiesselbach's plexus,"
This area is exposed to the drying effect of inspiratory current and to finger nail trauma, and is the MC
site for epistaxis
This is also the site for origin of the "bleeding polypus" (haemangioma) of nasal septum
 Internal carotld artery Internal carotid artery

Ophthelmic nrtery Ophthaimle artery

Anterior Posterior
Postenior
ethmoidal artery hmoidal artery
ethmoidal artery ethmoidal artery

Littie s area

Branches of
sphenopalatine
arntery
Septal branch Branches of
Branchesof Tacial artery
sphenopalatine
artery Sphenopalatine
artery
Superior labial Greater palatine
artery artery
Greater Lesser palatine
palatine artery
arery
Facial artery Maxillary artery Facial artery Maxillary artery
External carotid External carotid
artery atery
Suppiy o the nasal septum. Blood suppy of the lateral wall of the nose

9. Inverted nasal papilloma [05]

Ans.
Inverted Papilloma transitionalCel Papilloma or Ringertz Tumour or Schneiderian Papillomal Itis abenign tumour
of the non-olfactory mucosa of nose (Schneiderian membrane) and paranasal sinuses.
It is so named because hyperplastic papillomatous tissue grows into the stroma rather than in exophytic
manner.
Sites of origin: lateral wall of nose {MC}; less commonly maxillary, frontal or sphenoid sinus.
Etiology: HPV infection.
Clinical Features:
Symptoms Signs
It is always unilateral Pale polypoidal mass seen in
Presents with nasal obstruction, nasal discharge & epistaxis. the region ofthe middle
meatus in the lateral wall of
Invasion of Sinuses Hyponasal speech, Facial swelling, Pressure & pain
the nose.
Orbital invasion proptosis, diplopia & lacrimation It may bleed on touch.
Investigations: CT & MRI show the location and extent of the lesion. Biopsy is essential for diagnosis.
Treatment: Medial maxillectomy is the treatment of choice. It can be performed by lateral rhinotomy/
sublabial/ endoscopic approach. Recurrence can accur.
- *****-*************************

10. Cavernous sinus thrombosis [05] 38.2 SoURCE AND ROUTE OF INFECTION
TABLE

IN CAVERNOUS SINUS THROMBoSIs

Ans. Source Disease Route
Nose and danger Furuncle and Pharyngeal plexus
Aetiology area of face septal abScess
Ethmoid sinuses Orbital cellulites or Ophthalmic veins
Infection of paranasal sinuses and orbital complications from Sphenoid Sinus
abscess
Sinusitis Direct
these sinus infections can cause thrombophlebitis of the Frontal sinus Sinusitis and
osteomyelitis of
Supraorbital and
ophthalmic veins
frontal bone
cavernous sinus(es). Orbit Cellulitis and Ophthalmic veins
The valveless nature of the veins connecting the cavernous Upper lic
abscess
Abscess Angular vein and
ophthalmic veins
sinus causes easy spread of infection Pharynx Acute tonsillitis Pharyngeal plexus
or peritonsillar
Other sources of infection are abscess
Petrositis Petrosal venous
Ear
Sinuses
Clinical Features
Onset is abrupt with chills and rigors.
Patient is acutely ill; Eyelids get swollen with chemosis and proptosis of eyeball.
Cranial nerves 1, IV and VI which are related to the sinus get involved individually and sequentialy
causingtotal ophthalmoplegia.
Pupil becomes dilated and fixed, optic disc shows congestion and oedema with diminution of vision.
Sensation in the distribution of Vi (ophthalmic division of CN V) is diminished.
CSF is usually normal.
Treatment
iv. to the focus of infection, drainage of infected paranasal sinuses. Blood culture
Abx & attention
should be taken before starting antibiotic therapy.
The indication of anticoagulant is debatable.

11. Rhinophyma [04]

Ans.
Synonym: potato tumour; Elephantiasis of nose, cystadenofibroma of nose
Definitilon: It is a benign nodular enlargement of the tip of the nose due to hypertrophy of the sebaceous
glands as a complication of acne rosacea leading to potato nose deformity
Pathological Features
Nodular enlargement of the skin with dilated blood vessels and tissues
Last stage of acne rosacea.
Slow growing over a period of 10 to 15 years.
Clinical Features:
Swelling in the lower half of the nose, especially the nasal tip and the nostril;
Mostly affects men past middle age.
Treatment:
Cut the bulk of tumour with sharp knife or Co, laser and the area is allowed to re-epithelialize.
Sometimes, tumour is completely excised and the raw area is skin grafted (if nasal cartilage is exposed).
*******
12. Septal Abscess [2000, 74, 72]\
a. Mention two causes of nasal septal abscess [14]
Ans.
It is an abscess formed on the nasal septum
AETIOLOGY

2 infection of septal haematoma (MC).

Furuncle of the nose or upper lip.
It may also follow acute infection such as typhoid or measles.
CLINICAL FEATURES

B/L nasal obstruction with pain & tenderness over the bridge of nose.
Patient also complain of fever with chills and frontal headache (points towards infection)
Skin over the nose may be red and swollen.

4. Examination of nose reveals smooth bilateral swelling of the nasal septum.

TREATMENT: Abscess should be drained as early as possible.
Incision is made in the most dependent part of the abscess. Pus &necrosed pieces of cartilage are
removed by suction.
 Systemic Abx are started as soon as diagnosis has been made
cOMPLICATIONS:
a) Necrosis of septal cartilage > depression of the cartilaginous nose- may require rhinoplasty.
b) Necrosis of septal flaps septal perforation.
c)Meningitis & cavernous sinus thrombosis

13. Rhinoscleroma [04, 01]

Ans.
It is a chronic granulomatous disease caused by Gram negative bacillus called Klebsiella rhinoscleromatis
or Frisch bacillus
Pathology: The disease starts in the nose and extends to nasopharynx, oropharynx, larynx, trachea and
bronchi. Mode of infection unknown. Both sexes of any age may be affected.
is

Clinical Features! The disease runs through the following stages:

a) Atrophic stage: It resembles atrophic rhinitis foul-smelling purulent nasal discharge and crusting.
b) Granulomatous stage: Granulomatous nodules form in nasal mucosa giving a "woody" feel Nodules.
are painless and non-ulcerative.
c)Cicatricial stage: This causes stenosis of nares, distortion of upper lip, adhesions in the nose,
nasopharynx and oropharynx. There may be subglottic stenosis with respiratory distress.
Diagnosis
Biopsy shows infiltration of submucosa with plasma cells, lymphocytes, eosinophils, Mikulicz cells and
Russell bodies
Mikulicz cells are large foam cells with a central nucleus & vacuolated.cytoplasm.containing the bacilli.
*Russell bodies are eosinophilic inclusion bodies (containing gs) found in the plasma cells.
Treatment
a) Both streptomycin (1 g/day) and tetracycline (2 g/day) are given together for a minimum period of 4 -

6 weeks and repeated, if necessary, after 1 month.

b) Steroids can be added to reduce fibrosis.
Surgical treatment may be needed to establish the airway and correct nasal deformity.

14. Oroantral Fistula f02]

Ans.
It is a communication between the antrum and oral cavity. The fistulous opening may be situated on the
alveolus or gingivolabial sulcus
Aetiology
1. Tooth extraction is the most important cause. Roots of 2nd premolar and upper molars are closely related to the
antral cavity and their extraction may lead to fistula formation.
2. Failure of sublabjal incision to heal after Caldwell-Luc operation.
3. Erosion of antrúm by carcinoma.
4. Fractures or penetrating injuries of maxilla.
5. Infections: Osteitis of maxilla, syphilis or malignant granuloma.
Clinical Features
1) Regurgitation of Food: Food or fluids pass from oral cavity into the antrum and then into the nose.
2) Discharge: Foul-smelling discharge fill the nose or exude from the fistulous opening into the mouth.
3) Inability to build positive or negative pressure in the mouth: Patient will have difficulty to blow the
wind or drink through a straw.
Diagnosis: A probe can be passed from the fistulous opening in the oral cavity into the antrum.
Treatment
a) For Recent Fistula - When fistula is discovered immediately after tooth extraction
Ex: suture gum
margins+course of antibiotics.
b) For Chronic Fistula or a Large Fistula: It requires surgical repair by a palatal or a buccal flap.
Maxillary sinusitis is first treated by repeated irrigations and antibiotics
Caldwell-Luc operation may be required to remove a retained tooth root or a foreign body & to
clear the antrum of diseased mucosa
********

15. Frontal Mucocele [01]

Ans.
Mucocele of the frontal sinus usually presents in the superomedial quadrant of the orbit (90%) and
displaces the eyeball forward, downward and laterally.
Sometimes, it presents as a cystic swelling in the forehead (10%).
Etiopathogenesis: The contents of mucocele are sterile. There are two views in the genesis of a mucocele:
1 Chronic obstruction to sinus ostium accumulation of secretions which slowly expand the sinus.
2) Cystic dilatation of mucous gland of the sinus mucosa due to obstruction of its duct.
Clinical Features
Patient's complaints of headache, diplopia & proptosis.
The swelling is cystic and nontender; egg-shell crackling may be elicited
Inv.Imaging of the frontal sinus reveals clouding of the sinus with loss of scalloped outline.
Treatmentt frontoethmoidectomy with free drainage of frontal sinus into the middle meatus.

16. Nasal bone fracture [99, 89]

a. How would you manage a case of nasal bone fracture following a cricket ball injury [76]?
Ans.
Fractures of nasal bones are the most common because of the projection of nose on the face.
Tvpes of Nasal Fractures
1. Depressed: They are due to frontal blow. A severe
frontal blow will cause "open-book fracture" in which
nasal septum is collapsed and nasal bones splayed out.
2. Angulated: A lateral blow cause unilateral depression of A

nasal bone on the same side or fracture both the nasal

bones and the septum with deviation of nasal bridge.
Clinical Features
1) Swelling of nose: Appears within few hours and may
obscure details of examination. D

2) Nasal obstruction due to septal haematoma

3) Periorbital ecchymosis & Tenderness
4) Nasal deformity: Nose may be depressed from the front or
side, or the whole of the nasal pyramid deviated to one side,
5) Crepitus and mobility of fractured fragments.
6) Epistaxis.
Diagnosis is made on History & Physical examination. LYReLQLIEActures, (A) Normal. (5) Frontal blow causing
depressed Iracture or open-book fracture. () Lateral blow causing
X-rays may or may not show fracture. deviation of the nasal bridge or depression of one nasal bone.
X-rays should include Waters' view, right and left lateral views and occlusal view. 25 of 29
Treatment
Simple fractures without displacement need no treatment; others may require closed or open reduction.
1)Closed Reductlon done after 1 week/after edema subsides using Walsham forceps (for bone wall) or
Asch's forceps (for nasal septum).
2) Open Reduction: This is indicated when closed methods fail.
3) Healed nasal deformities can be corrected by rhinoplasty.
***************************************************

17. Rhinitis Caseosa [94]

Ans. Aka Nasal Cholesteatoma
*It uncommon condition where Nose is filled with offensive purulent discharge and cheesy material
is an
Usually unilateral and mostly affecting males.
A/w chronic sinusitis Sinus mucosa becomes granulomatous. Bony walls of sinus gets destroyed.
Treatment: remove of debris & granulation tissue free drainage of the affected sinus.
Prognosis is good.

18. C.S.F. rhinorhoea (93, 79]

Ans.
DEFINITION: Leakage of CSF into the nose is caled CSF rhinorrhoea.
AETIOLOGY

Irauma: can be accidental or surgical. Surgical trauma includes FESS, trans-sphenoidal

It

hypophysectomy, nasal polypectomy or skull base surgery.

Inflammations: Mucoceles, fungal infection of sinuses sinonasal polyposis, etc. can all erode the bone & dura.
Neoplasms: Tumours can invade the skull base.
Congenital lesions: Meningocele, meningoencephaloceles and gliomas
Idiopathic
sITES OF LEAKAGE:
1. CSF from anterior cranial fossa reaches the nose via (i) cribriform plate, (i) roof of ethmoid air cells or
(ii) frontal sinus
2. CSF from middle cranial fossa follows injuries to sphenoid sinus.
In fractures of temporal bone, CSF reaches the middle ear and then escapes through the eustachian
tube into the nose (CSF otorhinorrhoea)
DIAGNOSIS:

a. Clinical Examination
H/o clear watery discharge from the nose on bending the head or straining
Double Target Sign: CSF rhinorrhoea after head traumais mixed with blood and shows double
target sign when collected on a piece of filter paper. It shows central red spot (blood) and
peripheral lighter halo
Sniff Test Handkerchief Test
&

Reservoir sign- gush of fluid from Nose

b. Biochemical Examination
Beta-2 transferrin is a protein seen in CSF and not in the nasal discharge.
Beta-2 trace protein
Radiological Examination:
1. High-resolution CT scan
2. MRI:T2-weighted image
 3. Intrathecal fluorescein study- It is an invasive procedure.
4. CT cisternography- for active leak.
TREATMENT
Brain
Conservative measures: bed rest, stool softeners, and avoidance Pia mater
Arachnoid
of nose blowing, sneezing and straining.
Prophylactic antibiotics-to prevent meningitis. Graft- Dura

Surgical repair can be done by the following Bone

1. Neurosurgical intracranial approach. Mucosa

2. Extradural approaches: external ethmoidectomy for Surgicel

cribriform plate and ethmoid area, trans-septal sphenoidal Gelfoam

approach for sphenoid and osteoplastic flap approach for Pack

frontal sinus leak. Bepairof CSEhinogthoea
3. Transnasal endoscopic approach this is in use currently.

19. Mention the functions of the nose [92]

Ans.
Functions of the nose are classified as:
1. Respiration: The nose permits breathing and eating to go on simultaneously.
2. Air-conditioning of inspired air: Nose filters and purifies the inspired air and adjusts its temperature
and humidity before the air passes to the lungs.
3. Protection of lower airway
a) Mucociliary mechanism: Nasal mucosa is rich in goblet cells & secretory glands. Their secretion forms
a continuous sheet called mucous blanket spread over the
normal mucosa. Mucous blanket floats on the top of cilia Mucus
ayer
which are constantly beating to carry it like a "conveyer belt
erous
towards the nasopharynx. The inspired bacteria, viruses and ayer

dust particles are entrapped on the viscous mucous blanket

and then carried to the nasopharynx to be swallowed. Conveyor belt mechanism of mucus blanket to en
rap and cary organisms and dust particles
b) Enzymes and immunoglobulins: Muramidase (lysozyme) kill
bacteria&viruses. IgA and lgE, and interferon are present in nasal secretions to provide immunity
against upper respiratory tract infections
c) Sneezing: It is a protective reflex to expel foreign particles which irritate nasal mucosa
4. Vocal resonance: Nose forms a resonating chamber for certain- consonants in speech. When nose (or
nasopharynx) is blocked, speech becomes denasal, ie., M/N/NG are uttered as B/D/6, respectively.
Nasal reflexes:
a. Smell of a palatable food cause reflex secretion of saliva and gastric juice.
b. Irritation of nasal mucosa causes sneezing
C. Nasal function is closely related to pulmonary functions through nasopulmonary reflexes.
Pulmonary hypertension or cor pulmonale can develop in children with long-standing nasal
obstruction due to tonsil and adenoid hypertrophy.
6. OLFACTION refer 4th sQ

20. Foreign body in the nose [87, 81]

a. Animate foreign bodies in the nose [10]
Ans.
AETIOLOGY: mostly seen in children> Pieces of paper, chalk, button, pebbles & seeds are the common
objects.
CLINICAL FEATURES

Patient may present immediately if the history of foreign body is known.

If overlooked, the child presents with unilateral, foul smelling nasal discharge

INVESTIGATIONS: Radiograph of nose is done to confirm and localize a foreign body if it is radio-opaque.

TREATMENT

1 Pieces of paper or cotton swabs can be removed with forceps.

2) Rounded foreign bodies can be removed by passing a blunt hook past the foreign body and gently
dragging it forward along the floor.
3) In babies and uncooperative children, general anaesthesia is used. A nasal endoscope is useful to
locate the foreign body and carefully remove it.
cOMPLICATIONS: A foreign body left in the nose may result in:
1. Nasal infection and sinusitis.
Rhinolith formation.
Inhalation into the tracheobronchial tree.

21. Vasomotor rhinitis [86]

Ans.
nonallergic rhinitis but clinically simulating nasal allerey. The condition usually persists throughout the
It is
year and all the tests of nasal allergy are negative.
PATHOGENESIS: Nasal mucosa has rich blood supply
Parasympathetic stimulation > vasodilation and engorgement of mucosa
Overactivity of parasympathetic system > excessive secretion from the nasal glands.
ANS is under the control of hypothalamus & therefore emotions play a great role in vasomotor rhinitis
CLINICAL FEATURES

SYMPTOMS EIEE siGNS

1) Paroxysmal sneezing: Bouts of sneezing start just after getting out of the bed in morning.
Nasal mucosa over the
2) Excessive rhinorrhoea.
3) Nasal obstruction- alternates from side to side. Usually more at night.
turbinates is congested
and hypertrophic.
4) Postnasal drip.
COMPLICATIONS: Long-standing cases or VMR develop nasal polypi, hypertrophic rhinitis and sinusitis.
TREATMENT
Medical Surgical
1) Avoidance of Allergens: e.g., sudden change in 1. Reductlon in the size of the turbinates
temperature, humidity, blasts of air or dust. by partial turbinectomy, cryotherapy,
2) Antihistaminics and oral nasal decongestants-to bipolar cauterization, laser turbinoplasty
relieve nasal obstruction, sneezing and rhinorrhoea. etc.
3) Topical steroids (e.g., beclomethasone dipropionate, Other associated causes of nasal
budesonide or fluticasone), are useful to control obstruction, e.g., polyp, DNS, should
symptoms. also be corrected.
4) Systemic steroids can be given for a short time in very 3. Excessive rhinorrhoea, can be relieved
severe cases. by sectioning the parasympathetic
5) Psychological therapy: Tranquillizers may be needed in secretomotor fibres to nose (vidian
some patients. neurectomy)

*****-*===**------
VSQs
1. Septal haematoma [17]
Ans. Bood

Aetiology: It is collection of blood under the perichondrium or periosteum

of the nasal septum. It often results from nasal trauma or septal surgery.
Clinical Features
Septal haematoma
B/L nasal obstruction (MC).
a/w frontal headache and a sense of pressure over the nasal bridge.
Examination reveals smooth rounded swelling of the septum.
Palpation may show the mass to be soft and fluctuant.
Treatment
Small haematomas can be aspirated with a wide bore sterile needle.
Larger haematomas are incised and drained by a small anteroposterior incision parallel to the nasal
floor. Following drainage, nose is packed on both sides to prevent re-accumulation.
Systemic antibiotics should be given to prevent septal abscess.
Complications
Septal haematoma, if not drained, may organize into fibrous tissue leading to a permanently thickened
septum.
If2 infectionSeptal abscess with necrosis of cartilage& depression of nasal dorsum.

2. C/F of Fungal Rhinosinusitis [16]

Ans.
Causative Agents: Aspergillus, Alternaria, Mucor or Rhizopus
4 different varieties of fungal infection of sinuses are seen:
Clinical Features Treatment
1. Fungal ball: It is due to implantation of fungus into
healthy sinus. Maxillary sinus is the MC involved Surgical removal of the fungal bal and
followed by sphenoid, ethmoid and the frontal in adequate drainage of the sinus
that order
2. Allergic fungal sinusitis: a/w sinonasal polyposis, Surgical clearance of the sinuses with provision
eosinophils, Charcot-Leyden crystals and fungal of drainage and ventilation.
hyphae This is combined with systemic steroids
3. Chronic invasive sinusitis: There is bone erosion by fungus. Patient presents with chronic rhinosinusitis
Fulminant fungal sinusitis: seen in immunocompromised or diabetic individuals. Caused by Mucor or
Aspergillus. Unlike Mucor infection, there is no black eschar in Aspergillus infection
Treatment: surgical debridement of necrotic tissue and i.v. amphotericin B.

3. Rhinitis medicamentosa- cause & Rx [14, 04]

Ans.
Cause: Excess use of topical nasal decongestant can cause rebound phenomenon (rhinit
Treatment: Withdrawal of nasal drops, short course of systemic steroid therapy and in some cases, surgical
reduction of turbinates, if they have become hypertrophied.
*************************************************************************** *********
4. Enumerate the DDx of unilateral nasal mass [12]
Ans.
 TABLE32.2cOMMON CAUSES OF BILATERAL
TABLE 32.1 cOMMON CAUSES OF UNILATERAL
NASAL OBSTRUCTION NASAL OBSTRUCTION
Vestlbule
Vestibule Bilateral vestibulitis
Furuncle Collapsing nasal alae
Vestibulitis Stenosis of nares
Stenosis of nares Congenital atresia of nares
Atfesia Nasal cavity
Nasoalveolar cyst Acute rhinitis (viral and bacterial)
Chronic rhinitis and sinusitis
Papiloma
Rhinitis medicamentosa
Squamous cell carcinoma Allergic rhinitis
Nasal cavity Hypertrophic turbinates
Foreign body DNS
Deviated nasal septum (DNS) Nasal polypl
Hypertrophic turbinates Atrophic rhinitis
Concha bullosa Rhinitis sicca
Antrochoanal polyp Septal haematoma
Synecnia Septal abscess
Bilateral choanal atresia
Rhinolith
Nasopharynx
Bleeding polypus of septum Adenoid hyperplasia
Benign and malignant tumours of nose and paranasal sinuses Large choanal polyp
Sinusitis, unilateral Thornwaldt's cyst
Nasopharynx Adhesions between soft palate and posterior pharyngeal wa
Unilateral choanal atresia Large benign and malignant tumours

5. Nasal cycle [04]

Ans.
Nasal mucosa undergoes rhythmic cyclical congestion and decongestion, thus controlling the airflow
through nasal chambers
When one nasal chamber is working, total nasal respiration, equal to that of both nasal chambers, is
carried out by it.
Nasal cycle varies every 2-4h and may be characteristic of an individual.

6. Dangerous area of nose [05]

Ans.
helilum

Dangerous area of nose is olfactory area Since infection here can lead to
meningitis. This area is also connected to Superior Sagittal sinus & cavernous
sinus by venous channels

7. Ostiomeatal complex [05, 03]

Ans.
This is defined as a micro-architectural drainage pathway for anterior group of paranasal sinuses and
consists of a narrow cleft of ethmoidal infundibulum, between the uncinate process and bulla ethmoidalis.
This cleft comprises the ostium of the maxillary sinus and the frontal recess.
* Anatomical and pathological abnormalities in this region lead to persistent infection and disease within
the major sinuses.

8. Mucormycosis of nose and paranasal sinuses [05]

Ans.
It fatal fungal infection (Rhizopus, mucor etc.) of nose & PNS seen in uncontrolled diabetics or in
is a
those taking immunosuppressive drugs.
Affinity of the fungus to invade the arteries rapid destruction> infection can spread to orbit,
cribriform plate, meninges and brain
Clinical Features: Black necrotic mass fill the nasal cavity; eroding the septum and hard palate.
Special stains help to identify the fungus in tissue sections.
Treatment: amphotericin B +surgical debridement of the affected tissues and control of underlying
predisposing cause.
 CONTENTS
DISEASES OF PHARYNX..
LQS. ...3
SQs
VSQS .. ... 16
 Diseasesof PHARYNX
LOS
1. Nasopharyngeal tonsils (adenoids)-anatomy, etiology, clinical features, Dx & treatment [15)
a. 'Adenoid Facies - C/F, complications & Management [07, 05] Adenoid mess

Adenoid hypertrophy [07] Tubal orifice

Choana

c. How does Adenoids differ from a lymph node? [04] ossa of

Rossenmüler
Ans.
ANATOMY:
The nasopharyngeal tonsil, commonly called "adenoids", is situated
at the junction of the roof and posterior wall of the nasopharynx.
Soft palate
Unlike palatine tonsils, adenoids have no crypts and no capsule.
Adenoid almost completely disappears by the age of 20. Nasal seprum

Uula
Blood supply: Adenoids receive their blood supply from: Postenlor hinoscopic view showing the stuctues o
he nascpharynx
1.Ascending palatine branch of facial.
2. Ascending pharyngeal branch of external carotid.
3. Pharyngeal branch of the 3rd part of maxillary artery.
4. Ascending cervical branch of inferior thyroid artery of thyrocervical trunk.
Lymphatics: from the adenoid drain into upper jugular nodes directly or indirectly via retropharyngeal
and parapharyngeal nodes.
Nerve supply: is through CN IX &X. They carry sensation. Referred pain to ear in adenoiditis is also
mediated through them.
AETIOLOGY: Adenoids are subject to physiological enlargement in childhood.
Certain children have a tendency to generalized lymphoid hyperplasia in which adenoids also take part.
Recurrent attacks of rhinitis, sinusitis or chronic tonsillitis may cause chronic adenoid infection and
hyperplasia.
Allergy of the upper respiratory tract may also contribute to the enlargement of adenoids.
CLINICAL FEATURES

Enlarged and infected adenoids may cause nasal, aural or general symptoms.
Nasal Symptoms Aural Symptoms General Symptoms
1) Nasal obstruction mouth 1. Tubal obstruction: a) Adenoid facies: The child has an
breathing. Adenoid mass blocks the elongated face with dull
2) Nasal discharge-It is partly eustachian tube expression, open mouth,
due to choanal obstruction, as retracted tympanic prominent & crowded upper
the normal nasal secretions membrane and CHL. teeth and hitched up upper lip.
cannot drain into nasopharynx 2. Recurrent attacks of »Nose gives a pinched-in
and partly due to associated acute otitis media may appearance due to disuse
chronic rhinitis. ocur due to spread of atrophy of alae nasi.
3) Sinusitis Chronic maxillary
-
infection via the Hard palate is highly arched as
sinusitis commonly
is eustachian tube. the moulding action of the
associated with adenoids. 3. CSOM may fail to resolve tongue on palate is lost.
4) Epistaxis. in the presence of
b) Pulmonary hypertension & cor
5) Voice change Voice loses infected adenoids.
-
pulmonale- in Long-standing
nasal quality due to nasal 4. Otitis media with nasal obstruction.
obstruction effusion c)Aprosexia, i.e., lack of
concentration.
DIAGNOSIs
Posterior Rhinoscopy reveals an adenoid mass.
or a flexible nasopharyngoscope is useful to examine nasopharynx in a cooperative child.
A rigid
Soft tissue lateral radiograph of nasopharynx will reveal the size of adenoids and also the extent to
which nasopharyngeal air space has been compromised.
Detailed nasal examination should always be conducted to exclude other causes of nasal obstruction.
TREATMENT
For Mild Symptoms breathing exercises, decongestant nasal drops and antihistaminics
For severe symptoms, adenoidectomy is done (refer operative surgery)

2. Nasopharyngeal Fibroma {Angio fibroma Nasopharynx} etiopath, C/F, Dx & Rx [16, 12, 09]
Ans.
Nasopharyngeal fibroma (juvenile nasopharyngeal angiofibroma): It is the commonest of all benign
tumours of nasopharynx.
Etiopathogenesis:
The exact cause is unknown.
Tumour is predominantly seen in adolescent males in the 2nd decade of life.
Such patients have a hamartomatous nidus of vascular tissue in the nasopharynx and this is activated
to form angiofibroma when male sex hormone appears.
Site ofOrigin: posterior part of nasal cavity.
Angiofibroma is made up of vascular and fibrous tissues: Mostly, the vessels are just endothelium-
lined spaces with no elastic or muscle coat severe bleeding; also, the bleeding cannot be controlled
by application of adrenaline.
Though benign, angiofibromas do not have a capsule.
Extensions of Nasopharyngeal Fibroma: It is a benign tumour but locally invasive. It may extend into:
1) Nasal cavity nasal obstruction, epistaxis and nasal discharge.
2) Paranasal sinuses.
3) Pterygomaxillary fossa, infratemporal fossa and cheek.
4) Orbitsproptosis and "frog-face deformity"
5) Cranial cavity It can extend into Anterior & Middle cranial fossae

Clinical Features
1. Age and sex; almost exclusively males in the age group of 10-20 years.
2. Profuse. recurrent & spontaneous epistaxis MC presentation
-
severe anaemia due to repeated blood loss.
Progressive nasal obstruction
4. Conductive hearing loss and otitis media with effusion- occur due to obstruction of eustachian tube.
5. GMassin theisnasopharynx:
Tumour sessile, lobulated or smooth and obstructs one or both choanae.
G Itis pink or purplish in colour. Consistency is firm but digital palpation should never be done until at
the time of operation.
6. Other features: broadening of nasal bridge, proptosis, swelling of cheek, infratemporal fossa or
involvement of 2nd, 3rd, 4th & 6th cranial nerves will depend on the extent of tumour
Diagnosis
GIt is mostly based on clinical picture.
GBiopsy of the tumour is a/w profuse bleeding and is, therefore, avoided.
Investigations
1) CT scan of the head with contrast enhancement is now the investigation of choice.
G.Antral sign or Holman-Miller sign: Anterior bowing of the posterior wall of maxillary sinus, is
pathognomic of angiofibroma.
2) MRI is complementary to CT scans and shows any soft tissue extensions
Carotid angiography shows the extent of tumours, its vascularity and feeding vessels which mostly
come from the external carotid system. Embolization of vessels can be done at this time to decrease
bleeding at operation.
4) Arrangement for blood transfusion: 2-3 units of blood should be available and kept in reserve after
grouping and crossmatching.

Treatment Surgical excision is the treatment of choice.

Surgical approaches
Tumour Location Surgical Approach
Recurrence of juvenile A. Nose and nasopharynx Transpalatal or endoscopic
angiofibroma is Lateral rhinotomy with medial maxillectomy
common B. As in A+maxillary (or)
Management of antrum and Endoscopic
recurrenttumour pterygopalatine fossa (or)
1. Observation. The Transmaxillary Le Fort
tumour may Extended lateral rhinotomy
C. As in B + Infratemporal
(or)
spontaneously fossa
regress. Infratemporal fossa approach
D. As in C+Cheek
2. Revision surgery Extended lateral rhinotomy
extension
and removal
3. Radiotherapy: E. As in
Combined intracranial and extracranial approach
(or)
4. Chemotherapy- B+C+ Intracranial
Radiation if intracranial part is inaccessible
Doxorubicin+
vincristine+ dacarbazine have been used for very aggressive recurrent tumours

3. Acute tonsilitis etiopath, C/F & complications [13]

a. White patch on tonsil (10]
b. Membrane over the tonsils- etiopath, C/F & Management [91]
C. Acute follicular tonsilitis-Etiology, C/F, DDx & Rx [86]

d. Mention the ulcers and membranes in pharynx and their treatment [67]
Ans.
Primarily, the tonsil consists of
(0)Surface epithelium () Crypts (tube-like invaginations from the surface epithelum) & Acute follicular tonsilitis

(i) The lymphoid tissue

Acute infections of tonsil may involve these components and are thus classified as:
1) Acute catarrhal or superficial tonsillitis: Here tonsillitis is a part of generalized pharyngitis and is mostly
seen in viral infections.
2) Acute follicular tonsillitis: Infection spreads into the crypts which become filled with purulent material,
presenting at the openings of crypts as yellowish spots.
3) Acute membranous tonsillitis: It is a stage ahead of acute follicular tonsillitis when exudation from the
crypts coalesces to form a membrane on the surface of tonsil
4) Acute parenchymatous tonsillitis. Here tonsil substance is affected. Tonsil is uniformly enlarged & red.
AETIOLOGY-Bacteria may primarily infect the tonsil or may be secondary to a viral infection.
GHaemolytic streptococcus is the most commonly infecting organism.
GOthers: staphylococci, pneumococci or H. influenzae.
SYMPTOMS SIGNS
a) The breath is foetid & tongue is coasted.
1) Sore throat. b) Hyperaemia of pillars, soft palate & uvula.
2) Difficulty in swallowing: The child may refuse
c) Tonsils are red and swollen with yellowish spots
to eat anything due to local pain.
3) Fever - may be a/w chills and rigors.
of purulent material presenting at the opening
4) Earache: It is either referred pain from the
of crypts (acute follicular tonsillitis) or there
may be a whitish membrane on the tonsil which
tonsil or the result of acute otitis media which
can be easily wiped away with a swab (acute
may occur as a complication.
5) Constitutional symptoms- headache, general
membranous tonsillitis).
d) Enlarged tonsils -almost meet in the midline along
body aches, malaise and constipation.
with some oedema of the uvula (acute
There may be abdominal pain due to mesenteric parenchymatous tonsillitis).
ymphadenitis simulating a clinical picture of acute
e) Jugulodigastric lymph nodes are enlarged &
appendicitis.
tender.
TREATMENT
Patient is encouraged to take plenty of fluids.
Analgesics (aspirin or paracetamol) are given to relieve local pain and bring down the fever.
Antimicrobial therapy Most of the infections are due to Streptococcus and penicillin is the DOC.
Patients allergic to penicillin can be treated with erythromycin.
cOMPLICATIONS
1) Chronic tonsillitis with recurrent acute attacks - This is due to incomplete resolution of acute infection.
Peritonsillar abscess Parapharyngeal abscess.
&
Cervical abscess due to suppuration of jugulodigastric lymph nodes.
Acute otitis media.
5) Rheumatic fever-if tonsillitis is due to Group A beta-haemolytic Streptococci infection.
6) Acute glomerulonephritis.
7) Subacute bacterial endocarditis-if tonsillitis is due to Streptococcus viridans infection.
DIFFERENTIAL DIAGNOSIs OF MEMBRANE OVER THE TONSIL

1. Acute Membranous tonsillitis

Diphtheria The membrane in diphtheria extends beyond the tonsils, on to the soft palate and.is grey in colour. It is
adherent and its removal leaves a bleeding surface.
Vincent angina-Here removal of Membrane reveals an ulcer on the tonsil. Throat swab will show fusiform bacilli &
spirochaetes.
Infectious mononucleosis -
This often affects young adults, Both tonsils are very much enlarged covered with membrane. Lymph
nodes are enlarged in the posterior triangle of neck along with splenomegaly. Paul-Bunnell test (mono test) will show high titre of
heterophil antibody
5. Agranulocytosis- presents with ulcerative necrotic lesions not only on tonsils but also in the oropharynx. TLC <2000/

mm.
6. Leukaemia -TLC >100,000/cu mm. Blasts cells are seen on examination of the bone marrow.
7. Aphthous ulcers
8. Malignancy of tonsil
9. Traumatic ulcer-Trauma to the tonsil area may occur accidently when hit with a toothbrush, a pencil held in mouth or

fingering in the throat. Any injury to oropharynx heals by formation of a membrane

10. Candidal infection of tonsil
 Diagnosis of ulceromembranous lesion of throat thus requires: History, Physical examination, DLC (for
agranulocytosis, leukaemia, neutropenia, infectious mononucleosis), Blood smear (for atypical cells), Throat swab and
culture (for pyogenic bacteria, Vincent angina, diphtheria and Candida infection) & Other tests (Pau-Bunnell or mono spot
test and biopsy of the lesion).

4. Chronic tonsillitis -C/F & Rx [68, 67]

a. Signs of chronic tonsillitis [07]1
Ans.
AETIOLOGY
1) It may be a complication of acute tonsillitis.
2) Subclinical infections of tonsils without an acute attack.
3) Mostly affects children and young adults. Rarely occurs after 50 years.
4) Chronic infection in sinuses or teeth may be a predisposing factor.
TYPES
1. Chronic Follicular Tonsillitis: tonsillar crypts are full of infected cheesy material (yellowish spots).
2. Chronic Parenchymatous Tonsillitis: There is hyperplasia of lymphoid tissue. Tonsils are very much
enlarged and may interfere with speech, deglutition and respirátion. Attacks of sleep apnoea may
occur. Long-standing cases develop features of cor pulmonale.
Chronic Fibroid Tonsillitis: Tonsils are small but infected, with history of repeated sore throats
CLINICAL FEATURES
a) Recurrent attacks of sore throat or acute tonsillitis.
b) Chronic irritation in throat with cough.
c)Bad taste in mouth and foul breath (halitosis) due to pus in crypts.
d) Thick speech, difficulty in swallowing and choking spells at night (since tonsils are large & obstructive).
EXAMINATION-4 Cardinal Signs
1. Enlarged Tonsils
2. Persistent congestion of the anterior pillars
3. Positive tonsillar squeeze (Ervin-Moore sign).
4. Jugulodigastric lymph nodes on either side are enlarged but non-tender
TREATMENT
1) Conservative treatment consists of attention to general health, diet, treatment of coexistent infection
of teeth, nose and sinuses.
2) Tonsillectomy is indicated when tonsils interfere with speech, deglutition and respiration or cause
recurrent attacks
cOMPLICATIONS
1.Peritonsillar abscess & Parapharyngeal abscess.
Intratonsillar abscess.
3. Tonsilloliths.
4. Tonsillar cyst.
5. Focus of infection in rheumatic fever, acute glomerulonephritis, eye and skin disorders.

SQs
1. Tonsillolith [17, 10] Soft palate
Tonsil
Ans.
Tonsil
stone
Tonsilloliths:
Tongue
It is seen in chronic tonsillitis when its crypt is blocked with retention of
debris.
 Inorganic salts of calcium and magnesium are then deposited leading to formation of a stone.
It may gradually enlarge and then ulcerate through the tonsil.
ClinicalFeatures:Tonsilloiths are seen in adults & give rise to local discomfort or foreign body sensation.
Dx: by palpation or gritty feeling on probing
Treatment: Simple Removal of the stone or tonsillectomy,if that be indicated for associated sepsis or
for the deeply set stone which cannot be removed.

2. Acute pharyngitis-Causes, clinical features and treatment [16|

Ans. CAUSES OF ACUTE PHARYNGITIS
AET oLOGY
Rhinoviruses
»Causative Organisms Influenza
»Viral causes are more common. Parainfluenza
Viral infections are generally mild while the bacterial Viral Measles & chickenpox
ones are severe Coxsackie virus
CLINICAL FEATURES
Herpes simplex
Infectious mononucleosis
Symptoms Signs
Discomfort in the Pharynx shows
CMV
Mild Streptococcus (Group A,
infectionsthroat,malaise & congestion but no beta-haemolyticus)
low-grade fever Iymphadenopathy Bacterial Diphtheria
Pharynx shows .Gonococcus
erythema, exudate Candida albicans
pain in throat, Fungal
Moderate & enlargement of Chlamydia trachomatis
malaise, dysphagia,
&severe tonsils and Parasitic | Toxoplasmosis (rare)
headache & high
infectionsfever lymphoid follicles on DIAGNOSIS
the posterior
pharyngeal wall.
G Culture of throat swab
Failure to get any bacterial growth suggests
Very severe cases show oedema of soft palate & uvula
a viral aetiology.
with enlargement of cervical nodes

TREATMENT
1) General Measures: Bed rest, plenty of fluids, warm saline gargles & analgesics. Discomfort in throat in
severe cases can be relieved by lignocaine viscous before meals to facilitate swallowing.
2) Specific Treatment.
Streptococcal pharyngitis (Group A, beta-haemolyticus) is treated with peniclin G
In penicillin-sensitive individuals, Use erythromycin.
Diphtheria is treated by diphtheria antitoxin and administration of penicillin or erythromycin

Gonococcal pharyngitis responds to conventional doses of penicilin or tetracycline.

3. Quinsy (or) Peritonsillar abscess - etiology, C/F &Rx [16, 15, 14, 13, 11, 08]
Ans.
It is a collection of pus in the peritonsillar space which lies between the capsule of tonsil and the superior
constrictor muscle.
AETIOLOGY
It followsacute tonsillitis in adults & rarely in children
Causative organisms: Streptococcus pyogenes, S. aureus or anaerobic organisms
First, one of the tonsillar crypts gets infected forms an intra-tonsillar abscess bursts through the
tonsillar capsule to set up peritonsillitis and then an abscess.
CLINICAL FEATURES

1) General: They are due to septicaemia and resemble any acute infection High fever, chills & rigors,
malaise, body aches, headache, nausea & constipation.
Horizontal ine-
2) Local through base
a. Severe pain in throat - Usually unilateral. of uula

b. Odynophagia -
so marked that the patient cannot even Line along9-
swallow his own saliva which dribbles from the angle of his mouth. anterior pillar

c. Muffled and thick speech "hot potato voice."

d. Foul breath due to poor dental hygiene.
e. Ipsilateral earache This is referred pain via CN IX which
supplies both the tonsil and the ear. Peritonsillar abscess. Site of drainage is just lateral to
f. Trismus due to spasm of pterygoid muscles which are in close he junction of vertical line through anterior pillar and horizontal line
through base of uvula.
proximity to the superior constrictor.

EXAMINATION
1) The tonsil, pillars & soft palate on the involved side are congested and swollen.
2) Uvula is pushed to the opposite side.
3) Mucopus may be seen covering the tonsillar region.
4) Jugulodigastric lymphadenopathy.
5) Torticollis: Patient keeps the neck tilted to the side of abscess.
INVESTIGATION

G Contrast-enhanced CT or MRI shows the abscess and its extent.

G Culture of pus from the abscess reveal the causative agent & it's sensitivity to Abx
TREATMENT
Medical Measures Surgical Measures
Used when a frank abscess has been formed.
1. Hospitalization.
The techniques are:
2. V fluids to combat dehydration.
3. Suitable Antibiotics.
Incision and drainage of abscess.
Interval tonsillectomy: Tonsils are removed 4-
4. Analgesics- paracetamol for relief of pain and to
6 weeks after an attack of quinsy.
lower the temperature. Aspirin is avoided because of the
danger of bleeding. Abscess or hot tonsillectomy- has the risk of
rupture of the abscess during anaesthesia and
5. Oral hygiene -
by saline mouth washes.
excessive bleeding at the time of operation
COMPLICATIONS

a. Parapharyngeal abscess (a peritonsillar abscess is a potential parapharyngeal abscess).

b. Oedema of larynx-Tracheostomy may be required.
c. Septicaemia, endocarditis, nephritis, brain abscess may ocCur
d. Pneumonitis or lung abscess If
spontaneous rupture of abscess has taken place.
e. Jugular vein thrombosis.
f. Spontaneous haemorrhage from carotid artery or jugular vein.

4. Nasopharyngeal cancer- Aetiology, clinical features and investigations (14]

a. Trotter's Triad [05] Present WHO terminology
Type (256) I
Keratinizing carcinoma
Ans. ype (12%6) Nonkeratinizing differentiated
Classification: WHO classified nasopharyngeal carcinoma on carcinoma

histopathological basis into 3 types. They correlate with the titres of EB Type ll (63%) Nonkeratinizingundifferentiated
virus and also in their response to radiotherapy. carcinoma
AetiologyThe exact aetiology is not known. The factors responsible are:
1. Genetic: Chinese have a higher genetic susceptibility.
2. Viral: Epstein-Barr (EB) virus is associated with nasopharyngeal cancer.
3. Sex: Males > females (3:1)
4. Environmental: Air pollution, opium, smoking of tobacco, nitrosamines from dry salted fish, smoke
from burning of incense and wood have all been incriminated.
Clinical Features Ophthalmic symptoms
and faclal pain (CN II, M,V, VI)
Presenting symptoms and signs in
order of frequency are:
Foramen lacerum and
Cervical lymphadenopathy
renar nerve palsles
(most common) tUSL Ube- Serous OM
Horner
yndrome)
Hearing loss Parapharyngea
Space

Nasal obstruction Plerygoid Nose and orbit Nasal obstruction

muscles Proptosis
Epistaxis (trismus)
Retropharyngoal
Secondaries
Cranial nerve palsies Neck p nodes Distant metastases
lung. Iiver,
stiffne
bone
Headache Cervical nodes

Earache
Neck pain Upper-jugular and
Weight loss poslerior triangle nodes enlargement

Nasopharyngeal cancer can cause Routes of spread (green area) and clinical features (blue area) of nasopharyngeal cancer.

conductive deafness (eustachian tube blockage), ipsilateral temporopárietal neuralgia (involvement of

CN V) and palatal paralysis (CN X)-collectively called Trotter's triad
Diagnosis
1. Endoscopic evaluation of posterior wall of nasopharynx &it's Biopsy can be done under local
anaesthesia using rigid or flexible endoscopes.
2. Imaging studies
a) HRCT of neck and nasopharynx is the study of choice. It reveals primary growth, erosion of skull base and
clivus, extensions to parapharyngeal, retropharyngeal and intracranial regions.
b) MRI is better for soft-tissue extension.
c)X-ray/CT chest for secondaries to lung.
d) CT/ultrasound abdomen for secondaries to liver.
e) PET scan: to detect metastases anywhere in the body.
3. Audiogram: for diagnosis of serous otitis media.
4. Routine investigations
Treatment
1. Radiotherapy-It is the treatment of choice for Stage 1& Il nasopharyngeal cancer.
2. Chemotherapy (Cisplatin +5-FU)-for stage ll and V cancers. Chemotherapy can be given
concomitantly radiotherapy.
3. Radical neck dissection (removal of SCM, CN XI JV)for Positive nodes in the neck
& Int.

4. Recurrent or residual (persistent) disease can be treated by

a) Second course of external radiation.
b) Brachytherapy with Gold 98
c) Nasopharyngectomy.

5. Retropharyngeal abscess [13, 05, 04)

a. Space of Gilette [02]
 b. Torticollis (96]
Ans.
Prevertebral space .
Retropharyngeal space lies behind the pharynx Prevertebral
Tescia
CN IX, X, XI-
Alar fascia
between the buccopharyngeal fascia and the Parotid gland Danger space

prevertebral fascia. Buccopharyngeal

fascia
It extends from the base of skull to the Parapharyngeal space-
Retropharymgeal space
Anterior compartment
bifurcation of trachea. Posterior compartment
Peritonsilar space
This space is divided into two lateral Medial pterygold muscle

compartments (spaces of Gillette) bya

fibrous raphe.
Each lateral space conta ins retropharyngeal nodes which usually disappear at 3-4 years of age.
Chronic retropharyngeal
Acute retropharyngeal abscess
abscess(prevertebral abscess)
the nasopharynx, nose
In children: Infection in
or PNScan pass to retropharyngeal lymph
nodes.
In adults: it may result from penetrating injury Tuberculous infection of
AETIOLOGSY
of posterior pharyngeal wall or oesophagus. retropharyngeal lymph nodes
Rarely, pus from acute mastoiditis tracks along the
undersurface of petrous bone to present as
retropharyngeal abscess
Discomfort in throat
Bulge in posterior pharyngeal wall
Mild Dysphagia
2. Dysphagia and difficulty in breathing (abscess
CLINICAL Posterior pharyngeal wall
obstructs the air and food passages).
FEATUREs shows a fluctuant swelling
3. Stridor and croupy cough.
Neck may show tuberculous
+. Torticollis.
lymph nodes.
»Radiograph of soft tissue, lateral view of the
neck shows widening of prevertebral shadow
and the presence of gas.
Diagnosis findings are seen in X-rays
»Contrast-enhanced CT shows the extent of the TB

abscess and also if it extends below the hyoid

bone.
1) Incision & Drainage of Abscess 1) Incision & Drainage of Abscess
2) Systemic Abx- Suitable ones are given.
TREATMENT 2) Full course of antitubercular
3) Tracheostomy done if large abscess
therapy.
compresses the airway.

6. Ludwig's Angina [13, 08]

Ans.
Ludwig's angina is infection of submandibular space (it lies between mucous Tongu

membrane of the floor of mouth and tongue on one side and superficial layer of deep cervical fascia Sublingual
pace
extending between the hyoid bone and mandible on the other). Mylohyoid
Sub
AETIOLOGY nd muscie
naxillary
Anlerior bel

1. Causative organisms: a-haemolytic Streptococci, Staphylococci and matomy of submandibular space

bacteroides are common. Rarely Haemophilus influenzae, E. coli &Pseudomonas

2. Dental Infections-esp. premolar & molar teeth.
3. Submandibular Sialadenitis, Injuries of Oral Mucosa and Fractures of the Mandible.
 12 of 16
CLINICALFEATURES

»Odynophagia with varying degrees of trismus.

When infection is localized to the sublingual space: structures in the floor of mouth are swollen and
tongue seems to be pushed up and back.
»When infection spreads to submaxillary space: submental & submandibular regions become swollen
and tender, and impart woody-hard feel.
»Tongue is progressively pushed upwards & backwards threatening the airway.
TREATMENT
1) Systemic antibiotics.
2) Incision and drainage of abscess.
a. Intraoral approach-if infection is localized to sublingual space.
b. External approach if infection involves submaxillary space.
3) Tracheostomy, if airway is endangered.
COMPLICATIONS
parapharyngeal & retropharyngeal spaces and thence to the mediastinum.
1. Spread of infection to
2. Airway obstruction due to laryngeal oedema, or swelling and pushing back of the tongue.
3. Septicaemia.
4. Aspiration pneumonia.

7. Palatine tonsil-Anatomy & it's functions [12, 92]

Secondary cyps
Ans.
Each tonsil is an ovoid mass of lymphoid tissue. Crypta magna

Palatine tonsils are 2 in number. Primary Crypt

Site: lateral wall of oropharynx between the anterior & posterior pillars.

Parts:
2 Surfaces-a medial lateral, and 2 poles-an upper and a lower.
& a Primary and secondary crypts of tonsils.

Medial surface is covered by nonkeratinizing stratified 10

squamous epithelium which dips into the substance of
tonsil in the form of crypts.
One of the crypts is very large and deep and is called
crypta magna or intratonsillar cleft. It represents the
ventral part of 2nd pharyngeal pouch.
Lateral surface has a well-defined fibrous capsule.
Upper pole of the tonsil extends into soft palate. 9

Lower pole of the tonsil attached

is to the tongue. The Relations of tonsil. Tonsilis related laterally to its capsule
(1), loose areolar tissue containing paratonsillar vein (2), superior con
tonsil is separated from the tongue by a sulcus called strictor muscle (3), styloglossus (4), glossopharyngeal nerve (5). facial
artery (6), medial pterygoid muscle (7), angle of mandible (8) and
tonsillolingual sulcus which may be the seat of carcinoma. submandibular salivary gland (9), pharyngobasjlar fascia (10), buc-
copharyngeal fascia (11).
Bed of the tonsil: It is formed by the superior constrictor
Madlary ater
and styloglossus muscles. Descending
paiane anery
BloodSupply: The tonsil is supplied by 5 arteries Tonallar branches

1. Tonsillar branch of facial artery-This the main artery.

is Ascending
pharymge aney

2. Ascending pharyngeal artery from external carotid. pharynoe

nery Ascending
palantne &aniey

3. Ascending palatine, a branch of facial artery. Facial arfen

Tonsllar artey

4. Dorsal linguae branches of lingual artery. ungual arley-

Dorsal ingu

Extemal caroid
5. Descending palatine branch of maxillary artery.
Arienal suppy of tonsil
Venous Drainage: into paratonsillar vein which joins the common facial vein & pharyngeal venous plexus.
Lymphatic Drainages Lymphatics from the tonsil pierce the superior constrictor and drain into
jugulodigastric node situated below the angle of mandible.
Nerve Supplys Lesser palatine branches of sphenopalatine ganglion (CN v) & CN IX provide sensory nerve
supply.
Functions Of Tonsils: They act as sentinels to guard against intruders like viruses, bacteria & other antigens
coming into contact through inhalation and ingestion. There are two mechanisms:
1. Providing local immunity.
2. Providing a surveillance mechanism so that entire body is prepared for defence.
Both these mechanisms are operated through humoral and cellular immunity.
*

8. Waldeyer's ring. [10, 08] Adenoids

Lateral
Ans. pharyngeal band
Tubal tonsil

Scattered throughout the pharynx in its subepithelial layer

is the lymphoid tissue which is aggregated at places to form
masses, collectively called Waldeyer's ring.
The masses are:
1. Nasopharyngeal tonsil (adenoids)
Palatine tonsils or simply the tonsils
3. Lingual tonsil
Nodules on posterior Palatine tons
4. Tubal tonsils (in fossa of Rosenmüller) pharyngeal wall
5. Lateral pharyngeal bands Lingual tonsil
Waldeyer's ring.
6. Nodules (in posterior pharyngeal wall)

9. Glandular fever [10]

Ans.
Infectious Mononucleosis aka Glandular Fever is an Acute, benign, self-limiting lymphoproliferative disorder
caused by Epstein-Barr virus. Intimate contact
Pharyngitis Genetic susceptibility
Mode of transmission: Oropharyngeal Viral infection oen
NASOPHARYNGEAL
CARCINOMA
EBV in host cell genome

secretions (kissing); aka kissing disease. EBV shedding

Pathogenesis: EBV infects B lymphocytes

Virus remains dormant inside the B-cells B- EBV-infected
B cells
Monoclonal prolilerobon
BCELL NHL
Nmmunodeficiency
cells are immortalized" and are capable of Polyclonal activation 8:14
proliferation indefinitely BURKITTS
LYMPHOMA

C/F Classical triad of Fever, Pharyngitis&

Acivation of CD8 CLINICAL FEATURES
cell proliferation
Lymphadenopathy. B
cels (CT) Lymphadenopathy
Hepatitis
Lab Dx: 1 TLC with Absolute lymphocytosis Splenomegaly, splenitis
Encephalitis
Atypical lymphocytosis: EBV infects B-cells but Secretion of anibodies Meningia

the peripheral blood shows t CD8+ T-cells.

Pneumonitis
Sin rash

Serological tests: TPOLYCLONAL

MMUNOGLO8ULINS:
ATYPICAL
TLYMPHOCYTES
INFECTIOUS
MONONUCLEOSIS

Demonstration of heterophile antibodies role of EBV in the pathogenesis of infectious mononúcleosis, nasopharyngeal carcinoma and Burkitt's lymphoma

{Paul Bunnell test}

Demonstration specific antibodies against EBV antigens via ELISA

10. Parapharyngeal abscess [07, 05]

 Ans.
Parapharyngeal space is pyramidal in shape
with its base at the base of skull and its apex Prevertebral space-
o Prevertebral
fascla
at the hyoid bone. (Syn. Abscess of CN IX, X,
XI- Alar fascla
pharyngomaxillary or lateral pharyngeal space) Parotid gland Danger space

AETIOLOGY- Infection of parapharyngeal Buccopharyngeal

fascia
Parapharyngeal space
space can occur from: -Retropharyngeal space
Anterior compartment
1. Pharynx-infections of tonsil and adenoid, Posterior compartment Peritonsilar space
bursting of peritonsillar abscess. Medial pterygold muscle

2. Dental infection -esp. lower molar tooth.

3. Ear-Bezold's abscess and petrositis.
Infectionof other spaces - Ex: retropharyngeal and submaxillary spaces.
5. External trauma - Penetrating injuries of neck, injection of local anaesthetic for tonsillectomy etc.
CLINICAL FEATURES depend on the compartment involved.
Anterior compartment infections produce a triad of symptoms:
(i) Prolapse of tonsil and tonsillar fossa,

(i) Trismus and

(due to spasm of medial pterygoid muscle)
(iil) External swelling behind the angle of jaw.
Posterior compartment infection produces
a) Bulge of pharynx behind the posterior pillar,
b) Paralysis of CN IX, X, XI, and Xll and sympathetic chain, and
c)Swelling of parotid region. There is minimal trismus or tonsillar prolapse.
Fever, odynophagia, sore throat, torticollis (due to spasm of prevertebral muscles) and signs of toxaemia
are common to both compartments.
cOMPLICATIONS
1) Oedema of larynx > respiratory obstruction.
2) Thrombophlebitis of jugular vein with septicaemia.
3) Spread of infection to retropharyngeal space & mediastinum.
4) Mycotic aneurysm of carotid artery from weakening of its wall by purulent material.
5) Carotid blow out with massive haemorrhage
DIAGNOSIS: Contrast-enhanced CT scan neck will reveal the extent of a lesion.
Magnetic resonance arteriographyIf thrombosis of the lUV or aneurysm of the lCA is suspected.
TREATMENT
1. Systemic antibiotics: Based on the sensitivity -Ex: .V. amoxiillin-cavulanic acid, imipenem+ cdlindamycin etc.
2. Drainage of abscess-This js usually done under general anaesthesia.

11. Pharyngeal pouch [06]

a. Killian's Dehiscence [04]
-Thyropharyngeus
b. Pharyngeal Diverticulum [03]
Ans. -Killian's
dehiscence
PHARYNGEAL POUCH-aka hypopharyngeal diverticulum or
Cricopharyngeus
Zenker's diverticulum, it is a pulsion diverticulum where
Zenker's Circular and
pharyngeal mucosa herniates through the Killian's dehiscence diverticulum longitudina
fibres of
a weak area between two parts of the inferior constrictor. oesophagus

Killian's dehiscence is also called "gateway of tears" as

perforation can occur at this site during oesophagoscopPy Hypopharyngeal (Zenkers) diverticulum.
AETIOLOGY

»It formed due to spasm of cricopharyngeal sphincter or its uncoordinated contractions during the act
is
of deglutition.
»Usually seen after 60 years of age.
PATHOLOGY: Herniation of pouch starts in the midline. It is at first behind the oesophagus and then comes
to lie on its left. Mouth of the sac is wider than the opening of oesophagus and food preferentially enters
the sac.
CLINICAL FEATURES
1) Dysphagia appears after a few swallows when the pouch gets filled with food & presses on oesophagus.
-

2) Gurgling sound is produced on swallowing.

3) Undigested food may regurgitate at night, when patient is recumbent, causing cough and aspiration
pneumonia.
4) Patient is often malnourished due to dysphagia.
5) May be a/w hiatus hernia.
COMPLICATIONS: Carcinoma can develop in long-standing cases of pharyngeal pouch
DIAGNOSIS: Barium swallow will show the sac and its size.
TREATMENTT
1) Excision of pouch and cricopharyngeal myotomy: This is done via cervical approach.
2) Dohlman's procedure The partition wall between the oesophagus and the pouch is divided by diathermy
-
through an endoscope.
3) Endoscopic laser treatment-by CO2 laser.

12. Faucial diphtheria- etiology, C/F & Mx [03, 96]

Ans.
Aetiology
Causative organism: C. diphtheriae (Gram-positive bacillus).
It is an acute infection & spreads by droplet
Incubation period is 2-6 days.
Some persons are "carriers" of this disease
Clinical Features
»In the oropharynx, a greyish white membrane forms over the tonsils and spreads to the soft palate and
posterior pharyngeal wall. It is tenacious and causes bleeding when removed.
»Cervical lymph nodes become enlarged and tender "bull-neck" appearance.
Complications
1 In the larynx, diphtheritic membrane may cause airway obstruction.
2. Exotoxin produced by C. diphtheriae is toxic to the heart and nerves.
3. Neurological complications include paralysis of soft palate, diaphragm and ocular muscles.
Treatment
G Treatment of diphtheria is started on clinical suspicion without waiting for the culture report.
GAntitoxin is given by i.v. infusion in saline in about 60 min
GDose of antitoxin:
20,000-40,000 units for diphtheria when the membrane is confined to the tonsils only;
80,000-120,000 units, if the membrane is more extensive.
GAntibiotics used are benzyl penicillin co0 mg 6 hourly for 7 days. Erythromycin is used in penicillin-sensitive
individuals

13. Lingual Tonsillar Abscess [96]

Ans.
It can follow acute lingual tonsillitis & is a rare condition
»Symptoms: severe unilateral dysphagia, pain in the tongue, excessive salivation & some degree of
trismus. Protrusion of the tongue is painful. Jugulodigastric nodes will be enlarged and tender.
Complications: laryngeal oedema airway obstruction
» Treatment: Lingual tonsillectomy

VSQs Vincenis Angina

1. Vincent's Angina [14] Ulcer

Ans.
Causative Organisms: fusiform bacilli and spirochaetes
>It is insidious in onset with fever and discomfort in throat.
C/F: Membraneforms over one tonsil, can be easily removed revealing an
irregular ulcer on the tonsil.
Investigations: Throat swab will reveal fusiform bacilli and spirochaetes.
Treatment: Penicillin is the DOC+ Irrigation & removal of necrotíc areas
--*--=---*-------***
2. Causes of Trismus (Lock Jaw) [12]
Ans.
Dental abscess, parapharyngeal abscess, peritonsillar abscess, Ludwig's angina, trauma to mandible or
maxilla, OSF & malignant lesions of tongue, buccal mucosa, tonsils and retromolar trigone.
It can also be a late complication of radiotherapy (fibrosis of TMI)

3. Fossa of Rosenmuller [08, 03] Adenoid mass

Ans. -Co na
Tubal orifice
Fossa of
Rossenmuler

GThis isa deep recess in the region of the base of skull.

Importance: It is the commonest site of origin for
nasopharyngeal cancer Soft palate

Nasal seplum

Uvuia
Postorior thinoscopic view showing the shuctures of
the nasophoynx

4. Styalgia [05]
a. Elongated styloid process [09]
Ans.
Stvalgia lEagle Svndrome)
»Itis due to elongated styloid process or calcification of stylohyoid ligament.
»A normal styloid process is 25 mm, if > 30 mm, it is considered to be elongated.
»C'E: Pain in tonsillarfossa which radiates to the ipsilateral ear. Pain T on swallowing
Diagnosis: transoral palpation of the styloid process in the tonsillar fossa; Radiographs (such as AP view
with open mouth or lateral view of skul); CT scans.
Treatment: Many persons may have elongated styloid process but remain asymptomatic and do not
need treatment. Symptomatic styloid process can be excised by transoral or cervical approach
------m-.
 CONTENTS
DISEASES OF LARYNX& TRACHEA..3
LOS 3

SQs ** *** 9
VSQs 16
 Diseases of LARYNX & TRACHEA
LQs
1. Carcinoma of larynx-etiopath, C/F, DDx, Staging & Mx [17, 88]
a. C/F &Treatment of Carcinoma Glottis [20] Sit Subsite
Supraglottis Suprahyold epiglottis (both lingual and
b. Surgical management of carcinoma larynx [13] geal surfaces)
Infrahyoid epiglottis
C. Oesophageal voice/Speech [04] Aryepiglottic folds (laryngeal aspect only)
Arytenoids
Ans. Ventricular bands (or false cords)
Glottis True vocal cords including anterior and posterior
EtiopathologEy of Laryngeal Cancer: Subglottis
commissure
Subglottis up to lower border of cricoid cartilage

Risk factors
»Alcohol and smoking
»Previous radiation to neck.
»Genetic factors. Pyrilom fossa-
» Occupational exposure to asbestos, mustard gas etc. False cord
Supragio0s

Ventricle-
Glotis 1.0 am
TNM classification & staging True cord-
bgiotis
Larynx has been divided into 3 sites. Tumours arising from these
sites are further classified by TNM system where:
T-indicates tumour, e.g., T1, T2, T3, etc.
N-indicates regional lymph node enlargement e.g, No, N, Na, etc.
M- indicates distant metastasis. Absence of metastasis is Mo while presence of metastasis is Mi
Depending on TNM, tumour is further grouped into various stages.
Tumor stagng Nlode staging
TIone subsite involved. NO no neck node involvement.
Tlaonly one vocal cord involved
Tlbinvolvement of both vocal cords. TSingle node involvement; si2e /=3 em.
Taspread to adjacent substes; Naasingle node invclvement ; size 3cms to 6 cm.
slight inpairment in mobility of vocal cord Nabmutiple nodes involvement ; jpsilateral ; s2e 46 em.
T3 involement of pre-epigjottie space/para-epiglotHie spaceNacmutiple nodes involvement ; contralateral/ bilateral i
post cricoid space/inner cortex of thyroid Hxed vocal cord size < 6 cm.
T40local invasion N3asingle node invovementj size a cm.
T4bdistant invasion N3bextra nocal extension.
Histopathology:
90-95% of laryngeal malignancies are squamous cell carcinoma.
The rest 5-10% of lesions inclúde verrucous carcinoma, spindle cell carcinoma, sarcomas etc.
Symptoms Spread
Throat pain, dysphagia & referred
pain in the ear Local spread to > vallecula, base of tongue and
Supraglottic 2) Mass of lymph nodes in Neck Pyriform fossa.
Cancer 3) Hoarseness is a late symptom
Nodal metastases occur early.
4) Weight loss, resp, obstruction &&

halitosis are late features,

Local spread
Hoarseness is an early sign. Hence Anteriorly to anterior commissure & then to the
Glottic glottic cancer is detected early opposite cord;
Cancer (MC) T in tumour size will cause stridor and Posteriorly to vocal process & arytenoid region;
laryngeal obstruction Upward to ventricle and false cord; and
Downwards to subglottic region.
 Local spread
around the anterior wall to the opposite side or
Stridor or laryngeal obstruction downwards to the trachea.
Subglottic Hoarseness is a late symptom & it Upward spread to the vocal cords is late.
Cancer indicates spread of disease to the Subglottic growths can invade cricothyroid
undersurface of vocal cords. membrane, thyroid gland and muscles of neck.
Lymphatic metastases go to prelaryngeal, pretracheal,
paratracheal and lower jugular nodes.
Diagnosis of Laryngeal Cancer
1. History: Hoarseness for 2 3 weeks.
2. Indirect Laryngoscopy
a) Appearance of lesion will vary with the site of origin. B
GLesions of suprahyoid epiglottis are exophytic
while those of infrahyoid epiglottis are
ulcerative.
GLesions of vocal cord may appear as raised
nodule, ulcer or thickening. Cancer of the larynx. (A) Supraglottic, (B) glottic and
GLesions of anterior commissure may appear as (C) subglottic.

granulation tissue.
GLesions of subglottic region appear as a raised submucosal nodule
b) Vocal cord mobility: Fixation of vocal cord indicates spread of disease to thýroarytenoid muscle or
invasion of recurrent laryngeal nerve & is a bad prognostic sign.
c)Spread of disease to vallecula, base of tongue and pyriform fossa should be noticed.
Flexible Fibreoptic or Rigid Laryngoscopy or Video Laryngoscopy
4. Direct Larvngoscomy It is done to see (i) the hidden areas of larynx finfrahyoid epiglottis, anterior
commissure, subglottis and ventricle) and (i) extent of disease.
MicrolarvngOSCODy is done for small lesions of vocal cords to better visualise & take more accurate
biopsy specimens without damaging the cord.
Supravital Staining is useful in selection of the site of biopsy in leukoplakic lesion. Toluidine blue is
applied to the laryngeal lesion and then washed with saline and examined under the operating
microscope. Carcinoma in situ and superficial carcinomas take up the dye while leukoplakia does not.
7. Examination of Neck-to find (i) Extra-laryngeal spread of disease and (i) Nodal metastasis
8. Radiography
chestto rule out coexistent lung disease (e.g., TB), pulmonary mets or mediastinal nodes.
X-ray
scan
CT & MRI are useful to find the extent of tumour & cervical lymph node involvement.
TREATMENTOFLARYNGEAL CANCER
1. Radiotherapy: It is curative for early (Ti, Ta) lesions which neither impair cord mobility nor invade cartilage

2. Surgery
a) Conservation laryngeal surgery- It can preserve voice. The methods are:
Excision of vocal cord after splitting management based on tumour staging
the larynx (cordectomy via TTa radiotherapy TLm transoral laser microsurgery
laryngofissure). T 1a mid-cord lesion) Tumio radiotherapy
Excision of vocal cord and anterior T3coneurrent chemo-radiation
commissure region (partial fronto- TAatotal laryngectomy
lateral laryngectomy). TAbpalliative management.
Excision of supraglottis, false cords and ventricle (partial horizontal laryngectomy).
 b) Total laryngectomy cancer

GThe entire larynx, the hyoid bone, pre-epiglottic space, Cord mobile Cord mobility impaired

strap muscles and one or more rings of trachea are Radiotherapy to the Involvement of anterior
commissure or arytenold
removed. radiation to upper
neck node
GIndications: Fallure
1)
Ta&Ta lesions
2) Failure after radiotherapy or conservation surgery Conservation Conservation
larygectomy laryngectomy
GItis contraindicated in patients with distant metastasis Falure Failure
GVocal Rehabilitation After Total Laryngectomy
Total laryngectomy Total laryngectomy
1. Written language (pen & paper) neck disesection neck dissection

2. Aphonic lip speech (combined with sign language)

3. Oesophageal Speech: patient is taught to swallow air and hold it in the upper oesophagus and
then slowly eject it from the oesophagus into the pharynx. Patient can speak 6 to 10 words
before re-swallowing air. Voice is rough but loud and understandable.
4. Artificial Larynx It is used in those who fail to learn oesophageal speech. Ex: (a) Electrolarynx.
(b) Transoral pneumatic device.
Neck node management
5. Tracheo-Oesophageal Speech: NO managed in supraglottic carcinoma; selectve neck disection.
Drawback: food may enter into the trachea Only lateral and deiphian lymph node groups are removed

Radical neck dissection

Combined Therapy: Surgical ablation + pre- or post-op
Vgroup o lymph nodes removed,
radiation to incidence of recurrence. along ith non-lymphoatic structures
rerve, vein, muscle).
Concurrent chemoradiation:
modiled radical neck dissection
It showed better control of disease than
1-vgroup umph nodes removed and
laryngectomy with postoperative radiotherapy. non-yphatic structures are preserved.
Advantages: can preserve laryngeal function yPepirnal accessory nerve
preserve
Drawbacks: chemoradiation causes more toxicity. Type spinal accessory nerve
5. Endoscopic Resection with Co Laser temal jugular vein preserved
Typo w unetional nec dissectior)
Indications: T lesions spinal accessory nerve internmal jugular veinscm
muscle preserved
Advantages: low cost & less duration of treatment

2. Tracheostomy indications, procedure, Complications & TABLE 64.1 INDICATIONS FOR TRACHEOSTOMY

Post-Op care [16, 14, 11, 10, 06] 1. Respiratory obstruction

(a) Infections
a. 4 late complications of tracheostomy [15] (0 Acute laryngo-tracheo-bronchitis, acute epiglottitis,
diphtheria
b. Non-obstructive indications for tracheostomy [12] ) Ludwig's angina, peritonsillar, retropharyngeal or
parapharyngeal abscess, tongue abscess
Ans. TRACHEOSTOMY is making an opening in the anterior wall (6) Trauma
External injury of larynx and trachea
of trachea and converting it into a stoma on the skin surface. rauma due to endoscopies, especialy in infants and
(9
children
Gi) Fractures of mandible or maxillofacial injuries
(C) Neoplasms

() Foreign body larynx

(Oedema larynx due to steam, irritant fumes or gases,
allergy (angioneurotic or drug sensitivity), radiation
() Bilateral abductor paralysis
(9) Congenital anomalies
-Laryngeal web, cysts, tracheo-oesophageal fistula
Bilateral choanal atresia
Retained secretions
(a) Inability to cough
0 Coma of any cause, e.g. head injuries,
cerebrovascular accidents, narcotic overdose
( Paralysis of respiratory muscles, eg9. spinal injuries,
polio, Guillain-8arre syndrome, myasthenia gravis
(U) Spasm of respiratory muscles, tetanus, eclampsia,
strychnine poisoning
(b) Paintul cough
Skin incisions in tracheostomy. (A) Vertical midline (C) Aspiration of pharyngeal secretions
incision. (B) Transverse incision. Respiratory Insufficiency
Chronic lung conditions, viz. emphysema, chronic bronchitis,
bronchiectasis, atelectasis
PROCEDURE
Position. Patient lies supine with a pillow under the shoulders so that neck is extended to bring the
trachea forward.
Anaesthesia: No anaesthesia is required in unconscious patients or when it is an emergency procedure.
In conscious patients, 1-2% lignocaine with epinephrine is infiltrated in the line of incision and the area
of dissection.
Steps
1. A vertical, mid-line incision is made in the neck, extending from cricoid cartilage to just above the
sternal notch. rapid access
It gives with minimum bleeding and tissue dissection. A transverse incision,
5 cm long, made two fingers' breadth above the sternal notch can be used in elective procedures. It
has the advantage ofa cosmetically better scar.
2. After incision, tissues are dissected in the midline. Veins are either displaced or ligated.
3. Strap muscles are separated in the midline and retracted laterally.
4. Thyroid isthmus is displaced upwards and suture ligated.
5. A few drops of 4% lignocaine are injected into the trachea to suppress cough when trachea is incised.
6. Trachea is opened with a vertical incision in the region of or 2nd & 3rd 3rd & 4th
rings. The first tracheal
ring is never divided as perichondritis of cricoid cartilage with stenosis can result
7. Tracheostomy tube of appropriate size is inserted and secured by tapes
8. Skin incision should not be sutured or packed tightly as it may lead to development of subcutaneous
emphysema.
9. Gauze dressing is placed between the skin and flange of the tube around the stoma.
POSTOPERATIVE CARE

Constant supervision of the patient for bleeding, displacement of tube and removal of secretions.
Patient is given a bell ora paper pad and a pencil to communicate.
Suction Depending on the amount of secretion, suction may be required every half an hour or so;
3. Prevention of crusting and tracheitis by
a. Proper humidification, by use of humidifier or keeping a boiling kettle in the room.
b. If crusting occurs, a few drops of normal saline or Ringer's lactate are instilled into the trachea every
2-3 h to loosen crusts. Amucolytic agent (Ex: acetylcysteine) can also be used to loosen the crusts.
4. Care of tracheostomy tube:
Outer tube, should not be removed for 3-4 days to allow a track to be formed.
Tracheostomy tube should not be kept longer than necessary. Prolonged use of tube leads to tracheobronchial
infections, troacheal ulceration, granulations, stenosis and unsightly scars
GDecannulation: To decannulate a patient, tracheostomy tube plugged and the patient closely
is

observed. If the patient can tolerate it for 24 h, tube can be safely removed
GAfter tube removal, healing of the wound takes place within a few days or a week.
cOMPLICATIONSof Tracheostomy
Immedlate Intermediate Late
(atthetimeofoperation) (During first few hours or days) (useoftubefor weeks and months)
1. Haemorrhage, due to erosion of
1) Haemorrhage.
2) Apnoea: if patient had prolonged
a) Bleeding, reactionary or major vessel.
respiratory obstruction. This is due to sudden secondary. 2 Larvngeal stenosis, due to
washing out of CO2 which was acting as a
respiratory stimulus. Treatment is to
Displacement of tube. perichondritis of cricoid cartilage.
administer 5% CO2 in oxygen or assisted c)Blocking tube.
of 3. Tracheal stenosis, due to tracheal
ventilation. d) Subcutaneous ulceration and infection.
3) Pneumothorax due to injury to apical emphysema. 4. Tracheo-oesophageal fistula, due
pleura.
toprolonged use of cuffed tube or
|

4) Injury to recurrent laryngeal e) Tracheitis & erosion of trachea by the tip of

nerves. tracheobronchitis with tracheostomy tube.
5) Aspiration of blood. crusting in trachea. 5. Keloid or unsightly tracheostomy
6) Ihjury to oesophagus> Atelectasis & lun8 Scar.
tracheooesophageal fistula. abscess. 6. Corrosion of tracheostomy tube
8)Local wound infection and aspiration of its fragments
and granulations. intothe tracheobronchial tree.

Enumerate the causes of stridor in a child. Discuss the evaluation and management of stridor of
3
3.
[15]
days duration in a 50-year-old male who also has been having hoarseness since last 3 months
a. How will you manage a 7-year-old boy presenting with stridor? [14, 07]
b. Aetiology of stridor in children [11] Pharynx &
Supraglottis Inspiratory stridor
Signs of respiratory distress [08, 07]
Mention the types of Stridor. How do you clinically recognize
them? Briefly mention the causes of stridor [03, 80] Glottis, subglottis & cervical
trachea
Biphasic

Ans.
Stridor is noisy respiration produced by turbulent airflow through Expiratory stridor
Thoracic trachea
the narrowed air passages. It may be heard during inspiration, & bronchi

expiration or both.
Inspiratory stridor is produced in obstructive lesions of
supraglottis or pharynx, e.g., laryngomalacia or retropharyngeal Types of stridor and their site of oriqin.
abscess.
Expiratory stridor is produced in lesions of thoracic trachea & bronchi, e.g., tracheal stenosis &
bronchial foreign body.
Biphasic stridor is seen in lesions of glottis, subglotis and cervical trachea, eg, laryngeal papillomas,
vocal cord paralysis and subglottis stenosis.

AETIOLOGY
1. Nose: Choanal atresia in newborn.
2. Tongue: Macroglossia due to cretinism, haemangioma, dermoid at base of tongue, lingual thyroid.
3. Mandible: Micrognathia, Pierre-Robin syndrome. Here, stridor is due to flling back of tongue.
4. Pharynx: Congenital dermoid, adenotonsilarhypertrophy,retropharyngeal7. abscess tumours.
Lesions outside
&

5. Larynx. 6. Trachea & bronchi

respiratory tract
Vascular rings, oesophageal
Laryngeal web,
Atresia, stenosis, atresia, tracheo-oesophageal
1) Congenital laryngomalacia, cysts, fistula, congenital goitre,
tracheomalacia
subglottic stenosis cystic hygroma
Epiglottitis,
Retropharyngeal and retro-
2) Inflammatory laryngotracheitis, Tracheobronchitis
oesophageal abscess
diphtheria, tuberculosis
Haemangioma, juvenile
3) Neoplastic multiple papillomas & Tumours of trachea Masses in neck
carcinoma in adults
Injuries of larynx, foreign
Foreign body, stenosis
bodies, oedema following FB oesophagus (secondary
4) Traumatic trachea (e.g, following tracheal compression)
endoscopy, or prolonged
prolonged intubation).
intubation
5 NeurOgenic Laryngeal paralysis
 8 of 18
MANAGEMENT OF STRIDOR
Clinical Evaluation:
>History: Stridor is a physical sign & not a disease. Attempt should always be made to discover the cause.
Time of onset To find whether cause is congenital or acquired.
2. Mode of onset- Sudden onset (foreign body, oedema), gradual and progressive (laryngomalacia,
subglottic haemangioma, juvenile papillomas).
Duration-Short (foreign body, oedema), long (laryngomalacia, laryngeal stenosis, subglottic
haemangioma, anomalies of tongue and jaw).
4. Relation to feeding-Aspiration in laryngeal paralysis, oesophageal atresia, laryngeal cleft, vascular
ring, foreign body oesophagus.
5. Cvanotic spells - Indicate need for airway maintenance.
Aspiration or ingestion of a foreign body.
6.
7. Laryngeal trauma -Blunt injuries to larynx, intubation, endoscopy.
Physical Examination-Stridor is always associated with respiratory distress
1) Recession in suprasternal notch, intercostal spaces & epigastrium during inspiratory eforts
2) Note if stridor is inspiratory, expiratory or biphasic Indicates the probable site of obstruction.
3) Note associated characteristics of stridor:
a. Snoring or snorting sound nasal or nasopharyngeal cause.
b. Gurgling sound and muffled voice pharyngeal cause.
C. Hoarse cry or voice laryngeal cause
4) A/w fever indicates infective condition, e.g., acute laryngitis, epiglottitis, diphtheria etc.
5) Stridor of laryngomalacia, micrognathia & macroglossia disappears when baby lies in prone pasition.
6) Sequential auscultation with stethoscope over the nose, open mouth, neck and the chest help to
localize the probable site of origin of stridor
7) In adults, indirect laryngóscopy can be done easily while infants and children require flexible
fibreoptic laryngoscopy.
Investigations-History and clinical examination will dictate the type of tests required
Xray lateral and PA view of neck & chest help in diagnosing the foreign bodies of the airway.
CTScan with contrast -to rule out congenital vascular anomalies compressing the trachea or bronchi, e.g, anomalous
innominate artery, double aortic arch etc.
Oesophagogram with contrast-to rule out tracheobronch ial fistula, oesophageal atresia et.
4. Direct laryngoscopy &bronchoscopy:
Done in OT under general anaesthesia with ful preparation tp deal with respiratory distress.
After a quick direct laryngoscopy, bronchoscope is inserted to examine the air passage from the
subglottis to bronchi for any obstruction.
Secretions can be collected for culture and sensitivity.
Crusts and foreign body, if any, can be removed.
Treatment: Once the diagnosis has been made, treatment of exact cause can be planned.

4. Papilloma of the larynx {Laryngeal Papilloma)- etiopath & C/F [10, 74]
a. Multiple papilloma of larynx [02]
Ans. Laryngeal Papillomas can be divided into () juvenile and () adult-onset types.
1. Juvenile papillomatosis: It is the MC benign neoplasm of the larynx in children.
EtiologEY
GIt is caused by HPV- type 6 and 11
GAffected children get the disease at birth from their mothers who had vaginal HPV disease.
Clinical Features: child, presents with hoarseness or aphonia with respiratory difficulty or stridor.
 Diagnosis ismade by flexible fibreoptic laryngoscopy and biopsy. 9 of 18
Treatment- Microlaryngoscopy & CO, laser excision
In the absence of laser, tumour can be removed under microscope with cup forceps or a debrider.
Aim of therapy is to maintain a good airway, preserve voice and avoid recurrence.
Papillomas are known for recurrence but rarely undergo malignant change.
Besides surgery, various medical therapies like IFN U2a& 13-cis-retinoic acid are being used but has
several side effects.
Adult-onset papilloma: Usually, it is single, smaller in size, less aggressive & does not recur after
surgical removal.
It is common in males in the age group of 30-50 years
Site of origin: Anterior half of the vocal cord or anterior commissure.
Treatment: same as for juvenile type

5. A40 y/o man has presented in OPD with hoarseness of voice. Describe the DDx and Mx [05, 99]
a. Mention 4 causes of hoarseness [14]
TABLE 63.1 CAUSES OF HOARSENESS
Ans.
Inflammation
Hoarseness is defined as roughness of voice resulting from Acute Acute viral laryngitis, diphtheria,
whooping cough, noxious gasess
variations of periodicity and/or intensity of consecutive sound Chronic Chronic laryngitis (smoking, occupational
waves gastro-oesophageal reflux, steroid
inhalations for asthma), tuberculosis,
syphilis, leprosy, fungal infections
AETIOLOGY: Hoarseness is a symptom and not a disease per 2. Neoplasms
Benign Papillomas (solitary or multiple),
se. The causes of hoarseness are haemangioma, chondroma,
schwannoma, granular cell myoblastoma
EVALUATION OF HOARSENESS Premalignant Leukoplakia
Malignant Cancer, sarcoma
1. History: Mode of onset and duration of illness, patient's 3. Non-neoplastic Vocal nodules, vocal polyp, contact ulcer,
esions cyst, laryngocoele, amyloid deposit
occupation, habits etc. . Trauma Forceful shouting (submucosal vocal
cord haemorrhage), blunt and sharp
Any hoarseness persisting for >2 weeks deserves examination laryngeal trauma, foreign body,
of larynx. 5. Paralysis
intubation
Paralysis of recurrent, superior laryngeal
2. Direct &Indirect laryngoscopy: to rule out local laryngeal or both the nerves
6. Fixation of cords Arthritis or traumatic fixation of
causes. cricoarytenoid joints
7. Congenita Laryngeal web, cyst laryngocoele,
3. Bronchoscopy and oesophagoscopy-required in cases of paralysis, vocal sulcus
8. Systemic disorders Hypothyroidism, sarcoidosis, Wegener's
paralytic lesions of the cord to exclude malignancy granulomatosis, amyloidosis,
Examination of neck, chest, cardiovascular and myasthenia gravis

neurological system would help to find cause for laryngeal paralysis.

5. Laboratory investigations and radiological examination

sQs
1. Vocal Nodules [16, 09, 08
a. Singer's nodules [03]
Ans.
Vocal Nodules (aka Singer's or Screamer's nodes) appear
symmetrically on the free edge of vocal cord, at the
junction of anterior one-third, with the posterior two-
thirds, as this is the area of maximum vibration of the cord Vocal nodules. Typically, they form at the junction of
anterior one-third with posterior two-thirds of vocal cord.
and thus subject to maximum trauma
*Size: varies from that of pin-head to half a pea.
Etiopathogenesis: vocal trauma (vocal abuse) > oedema and haemorrhage in the submucosal space
hyalinization and fibrosis. The overlying epithelium also undergoes hyperplasia forming a nodule
Seen in - teachers, actors, vendors, pop singers, school going children who are very talkative.
 *Clinical Features: Patients complain of hoarseness, Vocal fatigue & pain in neck on prolonged phonation
*Treatment:
Conservative Rx- educate the patient in proper use of voice. With this, many nodules disappear
Surgery is required for large nodules or nodules of long standing in adults. They are excised with
precision under operating microscope either with cold instruments or laser.

2. Foreign bodies in air passages C/F & Mx [16, 09]

-

a. Radiological findings in bronchial foreign body [12]

b. Foreign body in the bronchus [11]
c. Foreign body Larynx [10]
d. Foreign body throat [08]
Ans.
A foreign body aspirated into air passage can lodge in the larynx, trachea or bronchi depending on the size,
shape and nature of the foreign body.
AETIOLOGY
Children are more often affected; Accidents occur with peanut, almond seed, watermelon seed, pieces
of carrot or apple, plastic toys, safety pins, coins etc.
In adults, foreign bodies are aspirated during coma, deep sleep or alcoholic intoxication. Loose teeth
may be aspirated during anaesthesia.
CLINICAL FEATURES

Site of foreign bodies Symptoms and signs

a) Complete obstructionDeath
Larynx
b) Partial obstruction Pain in the throat, hoarseness, croupy cough, stridor
Cough and haemoptysis
A loose foreign body like seed may move up and down"audible slap" and
Trachea
"palpatory thud".
Asthmatoid wheeze may also be present.
Most foreign bodies enter the right bronchus because it is wider and more
in line with the tracheal lumen
Cough, wheeze and diminished air entry to lung forms a "triad"
A foreign body may totally obstruct atelectasis
Bronchi
or it may produce a check valve obstruction, allowing only ingress of air but,
not the egress, thus leading to obstructive emphysema
A retained foreign body in the lung may later give rise to pneumonitis,
bronchiectasis or lung abscess.
DIAGNOSIS
It can be made by detailed history of the foreign body "ingestion",
physical examination of the neck and chest.
RadioloEY is very helpful.
1. X-ray Soft tissue PA & lateral view of the neck: A coin or a flat foreign
body in trachea lies edge on in PA view and flat on lateral view
2. Xaray chest in PA & ateral views:Jt can show
a) Radio-opaque foreign body-its size, shape & location.
ypes of bronchial obstrcton by a loregn body
b) Atelectasis (complete obstruction by foreign body). arial obstruction, Ar can pass in and oul Caing only wheee

c)Unilateral hyperinflation of lobe or entire lung.

aNna cmphysema of lungs. (C) Total obstruction, Air can neither 90
in nor out causing olbstrucive atelec tasis. (0) one way oOsiruu
everse o B, Ar can only go ou, causing atelectasia. Dark pink shows
d) Pneumothorax. normal sice of hung while lghter pink indicates effect of obstnucton.

3. Fluoroscopy
4. CT chest
MANAGEMENT
Laryngeal foreign body
May make the patient totally aphonic, unable to cry for help.
Heimlich manoeuvre: Stand behind the person and place your arms around
his lower chest and give 4 abdominal thrusts. The residual air in the lungs
may dislodge the foreign body.
Other measures: pound on the back or turn the patient upside down
Cricothyrotomy or emergency tracheostomy should be done if Heimlich
manoeuvre fails.
Once acute respiratory emergency is over, foreign body can be removed by direct laryngoscopy, if impacted.
Tracheal & bronchial foreign bodies can be removed by bronchoscopy with full preparation and under
general anaesthesia. Methods to remove tracheobronchial foreign body
1. Conventional rigid bronchoscopy.
2. Rigid bronchoscopy with telescopic aid.
3. Bronchoscopy with C-arm fluoroscopy.
4. Use of Dormia basket or Fogarty's balloon for rounded objects.
5. Tracheostomy first and then bronchoscopy through the tracheostome.
6. Thoracotomy and bronchotomy for peripheral foreign bodies.

3. Chronic Laryngitis- Etiology, C/F & Rx [16]

Ans.
CHRONIC LARYNGITIS
Without Hyperplasia
Chronic Hvperplastic Laryneitis
Chronic Hvperaemic Larvngitis)
It may follow incompletely resolved acute laryngitis,
Risk Factors are:
1) Chronic infection in PNS, teeth, tonsils, chest etc.
Aetiology 2) Occupational factors, e.g, exposure to dust and fumes such as in miners etc.
3) Smoking and alcohol.
4) Persistent trauma of cough as in chronic lung diseases.
5 Vocal abuse.
|1. Hoarseness Voice becomes easily tired & patient becomes aphonic by the end of the day.
-

Symptoms 2. Constant hawking There is dryness and intermittent tickling in the throat
3. Discomfort in the throat.
|4. Cough- It is dry and irritating.
Laryngeal mucosa is thick.
Hyperaemía of larynxX. Vocal cords appear red and swollen.
Signs
Vocal cords appear dull red & swollen. Their edges appear rounded. In late
Flecks of viscid mucus are seen on the stages, cords appear nodular.
vocal cords and interarytenoid region 3. Mobility of cords gets impaired due to
oedema and infiltration.
1. Conservative.
1) Eliminate Risk Factors.
2) Voice rest and speech therapy.
Treatment 3) Steam inhalation-it helps to loosen secretions and give relief.
4) Expectorant - They help to loosen viscid secretions and give relief from hawking.
2. Surgical: Stripping of vocal cords, removing the hyperplastic and oedematous
mucosa, may be done in selected cases. One cord is operated at a time.
**-*-*------*

4. Acute Laryngitis- Etiology, C/F & Rx [15]

Ans. 12 of 18
AETIOLOGY

The infectious tvpe is more common and usually follows upper respiratory infection. To begin with, it is
viral in origin but soon bacterial invasion takes place with Strep. pneumoniae, H. influenzae and
haemolytic Streptococci or Staph. aureus.
The Non-infectious type is due to vocal abuse, allergy, thermal or chemical burns to larynx due to
inhalation or ingestion of various substances, or laryngeal trauma such as endotracheal intubation.
CLINICAL FEATURES

Symptoms Signs
Hoarseness may lead to complete loss of O early stages, there is erythema and oedema of
In
voice. larynx, but the vocal cords appear white and near
Discomfort or pain in throat, particularly normal.
after talking. Later, hyperaemia and swelling increase. Vocal
Dry, irritating cough which is usually worse cords also become red and swollen. Subglottic
at night. region also gets involved. Sticky secretions are
General symptoms of cold, dryness of seen between the cords and interarytenoid
throat, malaise and fever if laryngitis has region.
followed viral infection of upper respiratory In case of vocal abuse, submucosal haemorrhages
tract. may be seen in the vocal cords.
TREATMENT

1Vocal rest -
Use of voice during acute laryngitis may lead to incomplete or delayed recovery.
2) Avoid smoking and alcohol.
3) Steam inhalations-it helps to loosen secretions and give relief
4) Cough sedative To suppress troublesome irritating cough.
-

5) Antibiotics-if there is secondary infection with fever or purulent expectoration.

6) Analgesics-To relieve local pain and discomfort.
7) Steroids Useful in laryngitis following thermal or chemical burns.

5. Vocal cord polyp [11

Ans.
Vocal polyp is unilateral arising from the same position as vocal nodule. It is soft, smooth & pedunculated.
It may flop up and down the glottis during respiration or phonation.
Etiology: It is also the result of vocal abuse or misuse.
Other contributing factors are allergy and smoking.
Pathology: sudden shouting > haemorrhage in the vocal cord submucosal oedema > Vocal Cord Polyp.
Clinical Features
Mostly, it affects men in the age group of 30-50 years.
Hoarseness is a common symptom.
Large polyp may cause dyspnoea, stridor or intermittent choking.
Some patients complain of diplophonia (double voice) due to different vibratory frequencies of the two
vocal cords.
Treatment is surgical excision under operating microscope followed by speech therapy

6. Physiology of speech [11]

Ans.
Voice is produced by the following mechanism NOSe

(Aerodynamic Myoelastic Theory of Voice Production): Nasal

CaMly
13 of 18
1) Vocal cords are kept adducted.
Contraction of thoracic & abdominal muscles exhale air velum

from the lungs Generate Infraglottic air pressure Pharynges

Caty
3) The air force opens the cords and is released as small puffs Vocal
Tongue
Humo MOuh
cords
which vibrate the vocal cords and produce sound which is QuDut

amplified by mouth, pharynx, nose and chest.

wngs
This sound is converted into speech by the modulatory action of
lips, tongue, palate, pharynx and teeth.
Intensity of sound depends on the air pressure produced by
the lungs while pitch depends on the frequency with which the
MUsdle
vocal cords vibrate. FORCe

----------== ---==--w--------
7. Laryngotracheal stenosis [OS]
Ventricile Thyrod

Ans.
Etiology: It occurs due to Laryngotracheal trauma as seen in-
Road traffic accidents Supragiots

latrogenic: Prolonged intubation, High tracheostomy

Cricothyroidotomy
Corrosive poisoning SuDgiottis

Chronic granulomatous conditions

.Post-RT for laryngeal malignancy Cricoid cartilage

Clinical Features: Depends on the site and extent of stenosis- True cora

Hoarseness, Difficulty in clearing secretions, Dysphonia, Stridor & Difficult decannulation

»Indirect laryngoscopy (LS: Narrowing, glottic web (adhesions), etc. may be seen.
Investigations: They are done to assess the site, length and severity of the stenosis
Xray neck-AP /lateral view
Laryngeal tomograms
Laryngogram
CT scan/MRI
Endoscopy-flexible/ rigid
Treatment options
1) Tracheostomy
2) Dilatation and stenting
3) Laser excision of web/ stenosis
4) Laryngotracheoplasty t stenting/keel insertion
5) Segmental resection of stenotic trachea and end-to-end anastomosis (<4 cm) may be done.
6) 'Laryngeal drop': The larynx is detached from the suprahyoid attachments enabling segmental
resection of trachea and end-to-end anastomosis.
Prevention
Prevent laryngotracheal trauma
Avoid prolonged intubation: If>3 to S days intubation is necessary, change over to a tracheostomy
First tracheal ring spared in tracheostomy
-**-*---**--*-=-=-*-=--*---------------------------.
 8. Laryngocele [03] 14 of 18
Ans. Dilatation of laryngeal saccule
It extends between thyroid cartilage and the ventricle.
Treatment is endoscopic or external excision.
-* --------------------------------------------------
9. Nerve supply of larynx [02]
Ans.
Sensory Motor
Above the vocal cords, larynx is supplied All the muscles which move the vocal cord (abductors,
by internal laryngeal nerve (br. of
adductors or tensors) are supplied by the recurrent
laryngeal nerve except the cricothyroid muscle.
superior laryngeal nerve) and below the Cricothyroid receives its innervation from external
Vocal cords by recurrent laryngeal nerve
laryngeal nerve (br. of superior laryngeal nerve).
-------==*==-***

10. Acute Laryngotracheobronchitis [02]|

Ans.
inflammatory condition of the larynx, trachea and bronchi
It is an
AETIOLOGY: To begin with, it is viral in origin (parainfluenza type l and l) but soon bacterial (G+ve)
invasion takes place. Male children are more often affected
PATHOLOGY: The loose areolar tissue in the subglottic region swells up and causes respiratory obstruction
and stridor. This, coupled with thick tenacious secretions and crusts, may completely occlude the airway.
CLINICAL FEATURES
Disease starts as upper respiratory infection with hoarseness and croupy cough + mild fever.
o This may be followed by difficulty in breathing and inspiratory type of stridor.
TREATMENT
1) Hospitalisation -
Administer inhalation anaesthesia (sevoflurane) and oxygen to the patient, secure i.v. line and
then perform laryngoscopy to make the diagnosis. Take laryngeal swabs for culture and sensitivity tests and
intubate the patient.
2) Antibiotics like ampicillin are effective against secondary bacterial infections.
3) Humidification helps to soften crusts and tenacious secretions which block tracheobronchial tree.
4) Parenteral fluids to combat dehydration
5) Steroids, e.g., hydrocortisone 100 mg iv. may be useful to relieve oedema.
6) Racemic adrenaline administered via a respirator is a bronchodilator and may relieve dyspnoea
7) Tracheostomy is done if intubation is required beyond 72 h.

11. Acute epiglottitis [02]

Ans.
akaSupraglottic Laryngitis: It is an acute inflammatory condition confined to supraglottic structures, i.e.,
epiglottis, aryepiglottic folds and arytenoids.
AETIOLOGYt It is a serious condition which can cause respiratory obstruction mostly in children.
H. influenzae B is the MC organism responsible for this condition in children.
CLINICAL FEATURES

Symptoms Signs
Onset is abrupt with rapid progression. 1) Depressing the tongue with a tongue depressor will
Sore throat and dysphagia are the show red and swollen epiglottis.
common presenting symptoms in
adults.
 3. Dyspnoea and stridor are the common | 2) Indirect laryngoscopy will show oedema and congestion
presenting symptoms in children. of supraglottic structure, This examination is avoided
4. Fever may go up to 40 "C. It is due to for fear of precipitating complete obstruction.
septicaemia. Lateral soft tissue X-ray of neck may show swollen
epiglottis (thumb sign),.
TREATMENT
a) Hospitalisation because there is danger of respiratory obstruction.
-

b) Antibiotics Ampicillin or 3rd generation cephalosporin are effective against H. influenzae and are given
by parenteral route (i.m. or iv.) without waiting for results of throat swab and blood culture.
c)Steroids- Hydrocortisone or dexamethasone to relieve oedema
d) Adequate hydration via parenteral fluids.
e) Humidification and oxygen via mist tent or a croupette.
)Intubation or tracheostomy-if respiratory obstruction doesn't subside
********
12. Vocal Cord Paralysis [01]
Ans.
Situation in
Position of the cord Location of the cord from midline Health Disease
Median Midline Phonation RLN paralysis
Paramedian .5mm Strong whisper RLN paralysis
Intermediate (cadaveric) 3.5 mm. This is neutral position of cricoarytenoid Paralysis of both recurrent and
joint. Abduction and adduction take place from superior laryngeal nerves
this position
Gentle abduction mm Quiet respiration Paralysis of adductors
Full abduction .5 mm Deep inspiration

Congenital Vocal Cord Paralysis:

Unilateral paralysis is more common.
Cause: birth trauma or congenital anomaly of a great vessel or heart.
Bilateral paralysis may be due to hydrocephalus or Arnold-Chiari malformation, intracerebral
haemorrhage during birth, meningocele, or cerebral or nucleus ambiguus agenesis.
*The patient of bilateral paralysis presents with features of bilateral abductor paralysis and respirator
obstruction necessitating tracheostomy.
*****=****-
--**---**-------------------------
13. Right Main Bronchus (01]
Ans.
Right main bronchus is wider, short and more vertical than the left and hence foreign body bronchus
frequently gets lodged here
The right main bronchus divides into lobar bronchi which in turn divide into segmental bronchi as follows:
1) Right upper lobe bronchus: a. Apical 6. Posterior Anterior
2) Right middle lobe bronchus: a. Medial branch b. Lateral branch
3) Right lower lobe bronchus: a. Apical b. Medial basal C, Subapical d. 3 basal bronchi
(Posterior, lateral & anterior).
********************* *** ***-*****-m==-**--***--m-***---*----------mmmmmo---

14. Carina [93]

Primary
rachea
Ans. bronchi Carina
G Carina keel-like spur produced by the lowest ring of trachea at the point of
is a
separation into two main bronchi
GThe trachea bifurcates at the upper border of 5th thoracic vertebra at about 25 cm
from the incisor teeth in adults
****** ***---**----**--------------.
 15. Bilateral abductor palsy (92]
Ans.
Aetiology: Neuritis or surgical trauma (thyroidectomy)
Position of Cords the intrinsic muscles of larynx are paralyzed, the vocal cords lie
As all in median or
paramedian position due to unopposed action of cricothyroid muscles
ClinicalFeatures
As both the cords lie in median or paramedian position, the airway is inadequate causing dyspnoea and
stridor but the voice is good.
Dyspnoea and stridor become worse on exertion or during an attack of acute laryngitis.
Treatment
Tracheostomy
Widening the respiratory airway without tracheostomy: This can be achieved by
1. Transverse cordotomy (Kashima operation)
2. Partial arytenoidectomy- Medial part of arytenoid is excised with Laser
3. Reinnervation procedures- used to innervate paralyzed posterior cricoarytenoid muscle by
implanting a nerve-muscle pedicle of sternohyoid or omohyoid muscle with its nerve supply from
ansa hypoglossi.
4 Thyroplasty type lI - It creates lateral expansion of larynx and is similar to vocal cord lateralization.
Quality of voice may not be good.

VSQs
1. Laryngomalacia [16]
Ans. Larvngomalacia (Congenital LarvngealStridor: It is the MC congenital abnormality of the larynx. It is
characterized by excessive flaccidity of supraglottic Epiglottis Omega shaped
epiglattiss-
larynx which is sucked in during inspiration producing Alrway-
Airway
stridor and sometimes cyanosis.
G Stridor is t on crying but subsides on placing the
child in prone position; cry is normal.
GThe condition manifests at birth or soon after, and
usually disappears by 2 years of age.
Direct laryngoscopy shows elongated epiglottis,
curled upon itself (omega-shaped ), floppy Normal Larynx
(Axlal view)
Laryngomalacia
(Axdal view)

aryepiglottic folds and prominent arytenoids.

GFlexible laryngoscope is very useful to make the diagnosis.
GTreatment:
In most cases, this is a harmless condition that goes away on its own without treatment
Tracheostomy is required in cases of severe respiratory obstruction.
Supraglottoplasty is required in cases of severe laryngomalacia.
-*-----pmommmm-==wmmmmmwmmwoouw=--

2. Semon's law [16]

Ans. Semon's law states that, in all the progressive organic lesions, abductor fibres of the nerve, which are
phylogenetically newer, are more susceptible and thus the first to be paralyzed compared to adductor
fibres.
It explains the median or paramedian position of the vocal cords in U/L injury to recurrent laryngeal nerve.

----|
Hypernasality (Rhinolalia Aperta): It is seen when certain words which have little nasal resonance are 18 of 18
resonated through nose.
= The defect is in failure of the nasopharynx to cut off from oropharynx or abnormal communication
between the oral and nasal cavities.
The causes are:
a) Congenitally short soft palate e) Postadenoidectomy
b) Cleft of soft palate 1) Oronasal fistula
c)Paralysis of soft palate 6) Familial speech pattern
d) Large nasopharynx h) Habitual speech patter
*****************************************************************
Ciliated columnar
7. Reinke's Oedema [04] Stratihed epithelium
squamous
Ans. epithelium

bilateral symmetrical swelling of the whole of membranous part of the

It is Reinke's space.
(Lamina propria)
vocal cords, most often seen in middle-aged people. This is due to oedema Vocal ligament-
of the subepithelial space (Reinke's space) of the vocal cords.
Vocalis muscle.
ETIOLOGY: Chronic irritation of vocal cords due to misuse of voice, heavy (hyroarytenoid)

smoking, chronic sinusitis and laryngopharyngeal reflex. It can also ccur in

myxoedema.
CLINICAL FEATURES

Hoarseness is the common symptom.

Patient uses false cords for voice production and this gives him a low-pitched and rough voice.
On indirect laryngoscopy, vocal cords appear as fusjform swellings with pale translucent look.
Ventricular bands may appear hyperaemic and hypertrophic and may hide the view of the true cords.
TREATMENT
1) Decortication of the vocal cords, i.e., removal of strip of epithelium, is done first on one side and 3
4 weeks later on the other.
2) Voice rest.
3) Speech therapy for proper voice production.
---------- ----=--=--*-*- -****=***

8. Arytenoid [03] Arytenoid cartilage

Ans. Arytenoid cartilages: They are paired hyaline cartilages.

/
Posterior surtace

Each arytenoid cartilage is pyramidal in shape.

It has a base which articulates with cricoid cartilage; a muscular process Inner surface

directed laterally to give attachment to intrinsic laryngeal muscles; a vocal

process directed anteriprly, giving attachment to vocal cord; and an apex which
supports the corniculate cártilage.
***

9. Mention 'Neoplastic benign tumors of larynx [94)

Ans.
TABLE 61.1 BENIGN TUMOURS OF LARYNX
Non-neoplastic Neoplastic
Solid Squamous papilloma
Vocal nodules Juvenie Ype
Vocal poyp Adull-onset type
Reinkes Oedema Chondroma
Contact ulcer/granuloma aemangionma
Intubation granuloma Granular cell tumours
Leukoplakia Glandular tumours, e.g.
Amyloid tumours Pleomorphic adenoma
Cystic Oncocytoma
Ductal cysts Neurilemmoma
Saccular cysts Rhabdomyoma
Laryngocele Lipoma
FIDroma
*******
----------------------------=--=--=-*------------m-****
 CONTENTS
OPERATIVE SURGERY eeeeeesoeo
LOS 3
SQs. 4
VSQs. 9

RECENTADVANCES. "o10
SQs. 10
VSQs ... 12
 Operative Surgery
LQS
1. Tonsillectomy indications, contraindications & complications [20, 15, 11, 07, 06, 05]
a. Reactionary haemorrhage & it's Mx [11, 10, 03]
b. Secondary haemorrhage [10]
Tonsillectomy bleeding (97]
Ans.
INDICATIONS
AS A PART OF ANOTHER
ABSOLUTE Indications RELATIVE Indications
OPERATION
1. Recurrent infections of throat:
1) Diphtheria carriers, who 1. Palatopharyngoplasty
a. 7 or more episodes in 1 year, or
do not respond to which is done for
b. 5 episodes per year for 2 years, or
3 episodes per year for 3 years, or antibiotics. sleep apnoea
2) Streptococcal carriers, syndrome.
d. 2 weeks or more of lost school or
3) Chronic tonsillitis with 2. Glossopharyngeal
work in 1 year.
2. Peritonsillar abscess. bad taste or halitosis neurectomy: Tonsil is
3. Tonsillitis a/w febrile seizures. which is unresponsive removed first and
Hypertrophy of tonsils causing to medical treatment then IX nerve is
4) Recurrent streptococcal severed in the bed of
Airway obstruction (sleep apnoea),
tonsillitis in a patient tonsil.
Difficulty in deglutition and
with valvular heart Removal of styloid
Interference with speech. disease. process
5. Suspicion of malignancy
cONTRAINDICATIONS
a) A-Anemia: Hb level less than 10 g%.
b) B-Bleeding Disorders eg. leukaemia, purpura, aplastic anaemia, haemophilia or sickle cell; Von Willebrand disease
c) C-Cleft palate; Children<3 years of age-to avoid surgical risks.
d) D-Disease Presence of acute infection in upper respiratory tract- since bleeding will be more.
e) E-At the time of Epidemic of polio
Uncontrolled systemic disease, e.g., diabetes, cardiac disease, hypertension or asthma.
8)Tonsillectomy avoided during the period of menses.
is
ANAESTHESIA Usually done under general anaesthesia with endotracheal intubation.
POSITION: Rose's position, ie, patient lies supine with head extended by placing a pillow under the
TABLE94.1TECHNIQUES OF TONSILLECTOMY/
shoulders. Arubber ring is placed under the head to stabilize it. TONSILLOTOMY
Cold methods
Steps of Operation (pissectton & Snare Method Dissection and snare (most common)
Guilloine method
1. Boyle-Davis mouth gag is introduced and opened. It is held in place by Draffin's Intracapsular (capsule preserving) tonsilectomy with
bipods. diebricer
Harmonik scalpel (ultrasound)
2. Tonsil is grasped with tonsil-holding forceps & pulled medially. Plasma-mediated ablation or dissection technique (coblation)
reflects tonsil to ouocal technque
Incision is made in the mucous membrane where it from the Hot
ev
anterior pillar. It may be extended along the upper pole to mucous membrane Laser tonsillectomy or tonsillotomy (CO2 or Kl
Radiofrequency
between the tonsil and posterior pillar.
A blunt curved scissor is used to dissect the tonsil from peritonsillar tissue and separate its upper pole
5. Now the tonsil is held at its upper pole and traction applied downwards and medialy. Dissection is continued with tonsillar
dissector or scissors until lower pole is reached.
Wire loop of tonsillar snare is threaded over tonsil on to its pedicle, tightened & the pedicle cut and the tonsil removed.
7. A gauze sponge is placed in the fossa and pressure applied for a few minutes
8. Bleeding points are tied with silk. Procedure is repeated on the other side.
 4 of 12
COMPLICATIONS
IMMEDIATE Complications DELAYED Complications
1. Secondary haemorrhage: occurs
1. Primary haemorrhage. Occurs at the time of operation.It between 5th to 10th post-op day. It is
can be controlled by pressure, ligation or the result of sepsis and premature
electrocoagulation of the bleeding vessels. separation of the membrane.
2. Reactionary haemorrhage 2. Infection of tonsillar fossa may lead
Occurs within 24 h and can be controlled by simple to parapharyngeal abscess or otitis
measures such as removal of the clot, application of media.
pressure or vasoconstrictor. 3. Lung complications- Aspiration of
If above measures fail, ligation or electrocoagulation of blood, mucus or tissue fragments may
the bleeding vessels can be done under general cause atelectasis or lung abscess.
anaesthesia. 4. Scarring in soft palate and pillars.
3. Injury to tonsillar pillars, uvula, soft palate, tongue or 5. Tonsillar remnants due to inadequate
superior constrictor muscle due to bad surgical surgery, may get repeatedly infected.
technique. 6. Hypertrophy of lingual tonsil This is
4. Injury to teeth. a compensatory to loss of palatine
5. Aspiration of blood. tonsils.
6. Facial oedema. 7. Sometimes, lymphoid tissue is left in
7. Surgical emphysema- Rarely ocCurs due to injury to the plica triangularis near the lower
superior constrictor muscle. pole of tonsil, which later gets
hypertrophied.

SQs
1. Adenoidectomy- Indications & Complications [15, 11]
Ans.
INDICATIONS
1. Adenoid hypertrophy causing snoring, mouth breathing, sleep apnoea syndrome or speech
abnormalities, i.e. (rhinolalia clausa).
2. Recurrent rhinosinusitis.
3. Chronic otitis media with effusion associated with adenoid hyperplasia.
4. Recurrent ear discharge in benign CSOM associated with adenoiditis/adenoid hyperplasia.
cOMPLICATIONS

1) Haemorrhage -seen during the immediate postoperative period. Nose and mouth may be full of blood.
Treatment: Postnasal pack under general anaesthesia is required.
2Injury to eustachian tube opening
Injury to pharyngeal musculature and vertebrae-occurs due to hyperextension of neck and undue pressure of curette.
Grisel syndrome Patient complains of neck pain and develops torticollis. Occurs due to spasm of
paraspinal muscles or atlantoaxial dislocation. Treatment: cervical collar & even traction.
5) Velopharyngeal insuficiency
Nasopharyngeal stenosis- It occurs due to scarring
7) Recurrence it is due to regrowth of adenoid tissue left behind

2. Diagnostic nasal endoscopy [15]

Ans.
The brighter illumination, magnification & angled view of endoscopes (sinuscopes) facilitate examination
of all the clefts and crevices of nose and nasopharynx.
Indications
1) To Diagnose any disease of nose, paranasal sinuses (PNS) and nasopharynx
2) To Locate the site of nose bleed
3) Biopsy from nose, PNS and nasoph rynx le: ons
4) Assess the response to treatment of nose, PNS and nasopharynx diseases.
Instruments
G 4 mm 0° and 30° sinuscopes
G 2.7 mm 0" and 30° sinuscopes incases of children and narrow nasal cavity
Freer's elevator; Suction cannula; Biopsy forceps
Antifog solution/savlon to avoid foBeing.
Techniques
Anesthesia: Mix 4% xylocaine in equal quantity of oxymetazoline hydrochloride. Instil these drops into
the nose and then pack nasal cavity.
Position of patient: either sitting or supine position.
Method: For thorough and complete examination, the scope is passed through the standard three
passes. The examination is conducted while inserting and withdrawing the scope.
First pass (0" sinuscope): It examines the nasal vestibule, nasal cavity in general, septum, inferior
meatus, nasal floor, nasolacrimal duct and nasopharynx.
Second pass (0" sinuscope): It examines the middle meatus, posterior part of middle turbinate,
sphenoethmoidal recess, superior meatus, superior turbinate and openings of the sphenoid sinus and
posterior ethmoid sinuses (m the superior meatus)
Third pass (30 sinuscope): It examines the osteomeatal complex in the middle meatus such as
uncinate process, bulla ethmoidalis, hiatus semilunaris, sinus of turbinate (space lateral to middle
turbinate), basal lamina, and the frontal recess.
Complication: Bleeding can occur due to improper manipulation of instruments and is usually controlled by
the application of vasoconstrictor pledgets.

Endoscopic nasal surgery [11, 06]

Ans. Endoscopic surgery is minimally invasive surgery and does not require skin incisions or removal of
intervening bone to access the disease
Indications: Besides sinusitis, Endoscopic nasal surgery is done in the following cases:
1) Removal of benign tumours, e.g., inverted papillomas or angiofibromas.
2) Orbital abscess or cellulitis management.
3) Dacryocystorhinostomy.
4) Repair of CSF leak.
5) Pituitary surgery
6) Optic nerve decompression.
7) Orbital decompression for Graves' disease.
8) Control of posterior epistaxis (endoscopic clipping of sphenopalatine artery).
9) Choanal atresia.

4. Functional Endoscopic Sinus Surgery (FESs) [09]

Ans.
It is a minimally invasive surgery and does not require skin incisions or removal of intervening bone to
access the disease
Here ventilation and drainage of the sinuses is established preserving the nasal and sinus mucosa and
its function of mucociliary clearance.
 INDICATIONS CONTRAINDICATIONS

1. Chronic bacterial sinusitis unresponsive to adequate 1. Inexperience and lack of proper

medical treatment. instrumentation.
2. Recurrent acute bacterial sinusitis. 2. Disease inaccessible by endoscopic
3. Polypoid rhinosinusitis (diffuse nasal polyposis. procedures, e.g., lateral frontal
4. Fungal sinusitis with fungal ball or nasal polypi. sinus disease and stenosis of
Antrochoanal polyp. internal opening of frontal sinus.
6. Mucocele of frontoeth moid or sphenoid sinus. 3. Osteomyelitis
7. Control of epistaxis by endoscopic cautery. 4. Intracranial or intraorbital
8. Removal of foreign body from the nose or sinus. complication
9. Endoscopicseptoplasty
ANAESTHESIA
General anaesthesia is preferred by most of the surgeons. Local anaesthesia with iv. sedation can be
used in adults when limited work is to be done.
POSITION: Patient lies flat in supine position with head resting on head rest. Some also prefer to raise it by
15 TABLE 90.1 MAJOR AND MINOR COMPLICATIONS
OF ENDOScOPIC SINUS SURGERY
TECHNIQUES 2 surgical techniques are followed: Major Minor
1. Orbital haemorrhage
1)Anterior to posterior (Stammberger's technique): In this 2. Loss of vision/blindness
1. Periorbital ecchymosis
2. Periorbital emphysema
technique surgery proceeds from uncinate process 3. Diplopia 3. Postoperative epistaxis
4. CSF leak 4. Postoperative infection:
backward to sphenoid sinus. 5. Meningitis rhinitis or sinusitis
6. Brain abscess 5. Adhesions
2) Posterior to anterior (Wigand's technique): Sureery 7. Massive haemorrhage 6. Stenosis of maxillary or
requiring blood transfusion frontal sinus opening
starts at the sphenoid sinus and proceeds anteriorly. This 8. Intracrania haemorrhage 7. Exacerbation of asthma
is mostly done in extensive polyposis or in revisional sinus and direct brain trauma 8. Hyposmia
9. Anosmia 9. Dental pain
surgery. 10. Injury to internal carotid
artery in sphenoid sinus
FIRST STEP of FESS is Uncinectomy 11. Injury to nasolacrimal duct
and epiphora
cOMPLICATIONS: 12. Death

5. Myringoplasty [06, 02, 99]

Ans. Closure of perforation of pars tensa of the tympanic membrane is called myringoplasty.
Graft materials used are temporalis fascia (MC), tragal perichondrium, -Meatal skin
Malleus
cartilage, periosteum, vein and cadaver tympanic membrane. Graft-
Anterior
Techniques: The following 3 techniques underlay (inlay), overlay (onlay) and nnulus
mid-lay. 3
1) Underlay (inlay) technique: graft is placed medial to the tympanic Gelfoam
Myringoplasty, Underlay technique
annulus.
2) Overlay (on-lay) technique: graft is placed lateral to fibrous layer of the
Meatal skin-
tympanic membrane
Malleus-
3) Mid-lay technique: Graft is placed in between the fibrous and mucosal
Anterior. Grat
layers of tympanic membrane annulus
cONTRAINDICATIONS

1 Active discharge from the middle ear. Myringoplasty. Overlay technique

Nasal allergy.
Otitis externa.
Ingrowth of squamous epithelium into the middle ear.

. When the other ear is dead or not suitable for hearing aid rehabilitation.
Children 3 years.
 COMPLICATIONS
UNDERLAY TECHNIQUE OVERLAY TECHNIQUE
1. Middle ear becomes narrow. 1. Blunting of the anterior sulcus.
2. Graft may get adherent to the 2. Epithelial pearls: They are epidermal cysts, when
promontory. squamous epithelium is buried under the graft.
3. Anteriorly, graft may lose contact from 3. Lateralization of graft: Graft loses contact from the
the remnant of tympanic membrane malleus handle resulting in conductive loss. It is
leadingto anterior perforation. prevented by tucking the graft under the handle

6. Antral lavage [01]

Ans. This procedure involves puncturing the medial wall of maxillary sinus in the region of inferior meatus
and irrigating the sinus.
CONTRAINDI
INDICATIONS
CATIONS
Middle turbinate
Chronic and subacute maxillary
Opening of
sinusitis with dual purpose of: max. sinus in
Acute
i) confirming the diagnosis & middle meatus
maxillary Interior meatus
(i) washing out the pus.
sinusitis for
To collect the specimen of the antral Cannula
fear of
contents for culture and sensitivity, or
osteomyelitis
cytological examination to exclude Antral puncture.

early malignancy
ANAESTHESIA:
G adults, local anaesthesia is preferred. A pack of 4% lignocaine with adrenaline is kept in inferior
In
meatus for 10-15 min.
In children, general anaesthesia is required.
POSITION: Sitting position is preferred in all adults, when using local anaesthesia.
When using general anaesthesia, patient is placed in tonsillectomy position
cOMPLICATIONS
1. Swelling of cheek-This is due to faulty technique cannula fails to pierce the nasoantral wall.
2. Orbital injury and cellulites If trocar and cannula pierces the roof of antrum.
Puncture of the posterior antral wall
Bleeding occurs due to injury to nasal mucosa.
5. Air embolism.

7. Uses of computerized axial tomography of SCAN in ENT [98]

Ans.
1) Images taken in one plane can be reconstructed into other planes. Thus, CT scan taken in axial view can be
reconstructed in coronal and sagittal plane.
2) 3D reconstructions can be made-useful in facial bone fractures and head & neck tumours.
3) Slices can be made thin with reduction in interslice space called high-resolution CT (HRCT). They are useful in CT
of temporal bones and show finer structures like ossicles, facial nerve, labyrinth and internal auditory canal.
4) Spiral CT helps to perform virtual endoscopy of larynx & tracheobronchoscopy & is thus a non-invasive technique.
5) By using contrast, lymph nodes of the neck in conjunction with malignant tumour can be delineated.
6) More precise aspiration cytology of deep tumours can be taken under CT guidance.
8. Bronchoscopic examination (98]
a. Bronchoscopy [95, 85]
Ans.
Bronchoscopyis of 2 types: Rigid & Flexible fibreoptic.
Rigid bronchoscopy Flexible bronchoscopy
Anaesthesia used General Topical
Route Oral only Nasal or through endotracheal tube
Bedside exam | Not possible Possible
Biopsy | Larger piece can be taken Only small piece can be taken
Control of Better control; Difficult
haemorrhage Useful in massive haemoptysis
Cost of procedureMore | Less
RIGID BRONCHOSCOPY
INDICATIONS of Rigid Bronchoscopy
Diagnostic 9 Therapeutic
1. To find out the cause for wheezing, haemoptysis or unexplained
cough. 1) Removal of foreign bodies.
2. When X-ray chest shows: 2) Removal of retained
a. Atelectasis of segment, lobe or entire lung.
a secretions or mucus plug in
b. Opacity localized to a segment or lobe of lung. cases of head injuries, chest
C. Obstructive emphysema-to exclude foreign body. trauma, thoracic or
d. Hilar or mediastinal shadows. abdominal surgery, or
3. Vocal cord palsy. comatose patients
4. Collection of bronchial secretions for culture and sensitivity tests.
ANAESTHESIA: General anaesthesia with no endotracheal tube or with only a small-bore catheter is often
preferred. It can also be done under topical surface anaesthesia.
POSITION: Same as for direct laryngoscopy
TECHNIQUE: There are 2 methods to introduce bronchoscope:
1) Direct method: Here bronchoscope is introduced directly through the glottis.
2) Through larvngoscope: Here glottis is first exposed with the help of a laryngoscope and then the
bronchoscope is introduced through the laryngoscope into the trachea. Laryngoscope is then withdrawn.
This method is useful in infants & young children, and in adults who have short neck and thick tongue.
cOMPLICATIONS
1. Injury to teeth and lips.
2. Haemorrhage from the biopsy site.
3. Hypoxia and cardiac arrest.
4. Laryngeal oedema.
FLEXIBLE FIBREOPTIC BRONCHOSCOPY
* It is easy to use in patients with neck or jaw abnormalities and injuries where rigid bronchoscopy may
almost be impossible technically.
*This can be performed under topical anaesthesia and is very useful for bedside examination of the
critically ill patients.
Flexible bronchoscope can also be easily passed through endotracheal tube or the tracheostomy
opening. However, it has limited utility in children because of the problems of ventilation.
VSQs
1. Modified Radical mastoidectomy (13]
Ans.
It is amodification of radical mastoidectomy where as much of the hearing mechanism as possible is

preserved.
INDICATIONS
1) Cholesteatoma confined to the attic and antrum.
2) Localized chronic otitis media.
ANAESTHESIA: General anaesthesia.
POSITION: Patient lies supine with face turned to one side and the ear to be operated uppermost.
cOMPLICATIONS
1. Injury to facial nerve.
2. Dislocation of incus.
3. Injury to horizontal semicircular canal.
4. Injury to sigmoid sinus with profuse bleeding
5. Injury to dura of middle cranial fossa.
6. Postoperative wound infection and wound breakdown.
 10 of 12
RECENT Advances

SQs
1. Symptomatology of ear disease [08]
Ans.
A patient with ear disease presents with one or more of the following complaints:
1. Hearing loss. 5. Earache.
2. Tinnitus. 6. Itching in the ear.
3. Dizziness or vertigo. 7. Deformity of the pinna.
4. Ear discharge. 8. Swelling around the ear.

2. Postnasal examination & Structures seen [06, 02]

a. Structures seen on posterior rhinoscopy [13]
Ans.
Posterior Rhinoscopy:
Patient sits facing the examiner, opens his mouth > examiner depresses
the tongue with a tongue depressor & introduces posterior rhinoscopic
Techniqueof posterior thinoscogy
mirror, which has been warmed and tested on the back of hand. The mirror
is held like a pen and carried behind the soft palate. Adenoidss

Light from head mirror is focussed on rhinoscopic mirror. Posterior ends-

of turbinates
Posterior border

Structures seen on posterior rhinoscopy are: of nasal septum

Fossa of
Look for the following Opening of- Rosenmüller
eustachian tuoe Torus tubarius
1) Choanal polyp or atresia.
2) Hypertrophy of posterior ends of inferior turbinates. Upper surtace
af soft palate
3) Discharge in the middle meatus. Structures seen on posterior rhinoscopy.

3. Indirect LaryngoscopyExamination & draw its diagram [03]

Ans.
Indirect Laryngoscopy
O Patient sits facing the examiner, protrude his tongue which is wrapped in
gauze and held by the examiner between the thumb and middle finger.
Index finger is used to keep the upper lip or moustache out of the way. direct laryngoscopy

O Laryngeal mirror (size 4-6) which has been warmed and tested on the back of hand is introduced into
the mouth and held firmly against the soft palate. Light is Base of tongue

focussed on the laryngeal mirror and patient is asked to breathe Ventricul

fold
quietly. Vallecuka

O To see movements of the cords, patient is asked to take deep VOcal Epiglotis
cora Ventricular space

inspiration (abduction of cords), say "Aa" (adduction of cords) uneiform

cartilage
and "Eee" (for adduction and tension). Movements of both the Corniculate
orn
cords are compared. nlerarylenoidarea
artlage

Structures seen on indirect laryngoscopy: Structures seen upon lindirect laryngoscopy

G Larynx: Epiglottis, aryepiglottic folds, arytenoids, cuneiform & corniculate cartilages, ventricular bands,
ventricles, true cords, anterior & posterior commissure, subglottis and rings of trachea.
GLaryngopharynx: Both pyriform fossae, postcricoid region, posterior wall of laryngopharynx.
G Oropharynx: Base of tongue, lingual tonsils, valleculae, medial and lateral glossoepiglottic folds.
******************
4. Branchial cyst [16, 09] 11 of 12
a. Branchial sinus in the neck [98]
Ans.
Branchial Cyst or Fistula
Definition: It occurs as a result of an abnormal development of primitive ectodermal pharyngeal
pouches and/ or the endoderm of the embryonic cervical sinus.
Site: Above or Below the hyoid bone
Second Branchial Arch Anomalies are most common. They can present as cyst, sinus, or fistula
Pathology: The cyst is lined
Symptoms Signs
by stratified squamous
epithelium & contains Painless G Swelling is smooth, round, fluctuant, non-
Cholesterol Crystals swelling in tender & non-transilluminant
upper lateral
& G Swelling can't be reduced or compressed.
Clinical Features:
part of neck. G Fluctuation test- positive
Investigations: A painful in present deep to the upper third of anterior
Contrast X-ray size at the time border of SCM
(fistulogram) of upper GBranchial sinus. If present, may exude
FNAC- cholesterol respiratory mucoid discharge.
crystals (+) infection can GWhen both internal and external openings
Complications: Recurrent ocCur are present, it is called a branchial fistula
infections & acquired
branchial fistula
Treatment; Complete excision of the cyst or fistula from the neck to the pharynx is the treatment of
choice. It can be accomplished by step-ladder incisions
Differential Diagnosis: Submandibular salivary gland swelling, Plunging ranula, Cervical dermoid, Cystic
hygroma & Cervical Ilymph node

5. Thyroglossal cyst [96, 93]

Ans.
Cystic swelling developed in the remnant of thyroglossal tract is called
thyroglossal cyst. It is the commonest retention cyst below the level of
the hyoid and is the MC congenital neck mass. Sublingual

Sites:
Suprahyoid
Features
Clinical
Symptoms Signs
Infrahyoia
OCyst can occur anywhere from
3Midline swelling seen foramen cecum to the isthmus of
Substernal
in the anterior aspect thyroid gland
of the neck O Swelling moves with deglutition &
Painless if not infected protrusion of the tongue Various sites of thyroglossal cyst

Infected cyst may 'Hood sign: The skin above the

rupture & form fistulous opening is pulled upwards
discharging by the thyroglossal tract and this
thyroglossal fistula gives rise to puckering of the skin
resemblinga hood of a snake
Investigations:
Thyroid scan to rule out an ectopic thyroid
Fistulogram is done if it is associated with fistula, which helps in identifying the extent of the tract
Treatment js complete surgical excision Sistrunk's operation.
 GSimple excision of cyst without removal of its tract leads to recurrence.
Prognosis: The patient should be followed up as papillary carcinoma as well as Hiirthle cell adenoma
has been reported to be arising from thyroglossal duct cyst
Differential Diagnosis: Dermoid cyst, Pyramidal lobe hyperplasia, Thymic cyst & Subhyoid bursitis

VSQs
1. Symptomatology of nasal disease [13]
Ans.
A patientwith disease of the nose and paranasal sinuses presents with one or more of the following
complaints:
1. Nasal obstruction. 6. Headache or facial pain
2. Nasal discharge. 7. Swelling or deformity,
3. Postnasal drip. 8. Disturbances of smell.
4. Sneezing. 9 Snoring.
5. Epistaxis. 10. Change in voice (hyper- or hyponasality)

2. Symptomatology of Laryngeal disease [12, 07]

Ans.
A patient with disease of the larynx presents with one or more of the following complaints:
1. Disorders of voice: hoarseness aphonia, puber-phonia or easy fatiguability of voice.
2. Respiratory obstruction.
3. Cough and expectoration
4. Repeated clearing of throat (chronic laryngitis, benign or malignant tumours of larynx).
5. Pain in throat. (ulcerative lesions of larynx, perichondritis of laryngeal cartilages, arthritis of laryngeal
joints
6. Dvsphagia (epiglottitis, aspiration of secretions due to laryngeal paralysis).
7. Mass in the neck (cervical nodes, direct extension of growth, laryngocele).

3. E.N.T. manifestations of AIDS [03]

Ans.
Ear Nose & paranasal sinuses Oral cavity and oropharynx
Kaposi sarcoma Herpetic lesions of nose Candidiasis
Seborrhoeic dermatitis of EAC Recurrent sinusitis Herpetic lesions of palate, buccal
.Malignant otitis externa Chronic sinus infection mucosa, lips or gums.
Serous otitis media Fungal sinusitis Giant aphthous ulcers
Acute otitis media Kaposi sarcoma Adenotonsillar hypertrophy.
Pseudomonas & candida infection Lymphomas-B cell type Generalized lymphadenopathy
Mycobacterial infections Burkitt lymphoma Kaposi sarcoma of palate
SNHL Non-Hodgkin lymphoma of tonsil or
Herpes zoster (Ramsay-Hunt synd.) tongue
Facial paralysis Hairy leukoplakia
.Gingivitis
Larynx Salivary Glands Neck
Laryngitis-fungal, viral (herpes simplex, Parotitis Lymphadenopathy. It could be only a
cytomegalovirus) or tubercular Xerostomia follicular hyperplasia or due to a
Kaposi sarcoma Diffuse parotid disease such as tuberculosis,
Non-Hodgkin lymphoma enlargement histoplasmosis, toxoplasmosis or non
Kaposi sarcoma Hodgkin or Hodgkin lymphoma.
Non-Hodgkin lymphoma
 CONTENTS

DISEASES OF ESOPHAGUS. ww.S

LQS
3
SQs.. 5
VSQs 9
 Diseases of ESOPHAGUS
LQS
1. Discuss differential diagnosis and management of a 50-year-old male, smoker with dysphagia [08, 06]
a. 4 oesophageal causes of dysphagia [15]
b. Investigation for dysphagia [11, 07]
C. Symptoms, signs, etiological factors, Mx and the prognosis of DYSPHAGIA in ENT speciality (96]
Ans
Dysphagia
PRE-OESOPHAGEAL CAUSES OESOPHAGEAL CAUSES
Disturbance in Oral Phase of Deglutitlon like-
The lesions may lie in the lumen, in the wall
MasticationTrismus, fractures of mandible,
or outside the wall of oesophagus.
tumours of the jaw & disorders of TMJ.
1) Lumen: Obstructions occur due to
Lubrication>Xerostomia following radiotherapy
atresia, foreign body, strictures&
Mikulicz's disease, Sjogren's disease
tumours.
Mobility of tongue Paralysis of tongue, painful 2) Wall. It can be acute or chronic
ulcers, tumours of tongue, lingual abscess, total oesophagitis, or motility disorders.
glossectomy Hypomotility disorders, e.g., achalasia,
Defects of palate Cleft palate, oronasal fistula. scleroderma, amyotrophic lateral
Lesions of buccal cavity: Stomatitis, ulcerative sclerosis.
lesions, Ludwig's angina. Hypermotility disorders, e.g.
Pharyngeal Phase cricopharyngeal spasm, diffuse
Obstructive lesions of pharynx, e.g., tumours of oesophageal spasm.
tonsil, soft palate, pharynix, base of tongue, 3) Outside the wall- Lesions cause
supraglottic larynx, or even obstructive obstruction by pressing on the
hypertrophic tonsils oesophagus from outside:
OInflammatory conditions, e.g, acute tonsillitis, a. Hypopharyngeal diverticulum
peritonsillar abscess, retro or parapharyngeal b. Hiatus hernia.
abscess, acute epiglottitis, oedema larynx C. Cervical osteophytes.
O Spasmodic conditions, e.g., tetanus, rabies d. Thyroid lesions.
OParalytic conditions: e. Tumours of mediastinum, lymph
G Paralysis of soft palate due to diphtheria, bulbar
node enlargement, aortic aneurysm,
palsy, cerebrovascular accidents cardiac enlargement.
S Paralysis of vagus and bilateral superior laryngeal f. Vascular rings (dysphagia lusoria).
nerves cause aspiration of food into the larynx
Investigations
1. History Ascertain, if dysphagia is of:
Sudden onset Foreign body or impaction of food on a pre-existing stricture.
G Progressive Malignancy.
Intermittent > Spasms or spasmodic episodes over an organic lesion.
More to liquids Paralytic lesions.
More to solids and progressing even to liquids > Malignancy or stricture.
GIntolerance to acid food or fruit juices > Ulcerative lesions.
GLoss of weight/appetite: Malignancy/ tuberculosis
2. Clinical Examination of oral cavity, oropharynx, larynx and hypopharynx can exclude
most of the pre-
oesophageal causes of dysphagia.
3. CBP-to rule out Plummer-Vinson syndrome & to know the nutritional status of the patient.
4. Radiography
aX-ray chest & Lateral view neck Widening of the prevertebral space shadow
b.Barium swallow- It is useful in the diagnosis of malignancy, cardiac achalasia, strictures,
diverticula, hiatus hernia or oesophageal spasms.
Manometric and pH Studies-to rule out motility disorders, GERD and to find whether oesophageal
spasms are spontaneous or acid induced.
Oesophagoscopy It gives direct examination of oesophageal mucosa and permits biopsy specimens.
Flexible fibreoptic or rigid scopes can be used.
Other Investigations: Bronchoscopy (for bronchial carcinoma), cardiac catheterization (for vascular
anomalies), thyroid scan (for malignant thyroid) may be required, depending on the case
Treatment
Supportive Treatment
Parenteral: IV fluids
Enteral feeding through Ryle's tube or through feeding gastrostomy or jejunostomy.
Treatment of the Cause
Medical: Treat the Anemia, inflammation, trauma, aspiration pneumonia, etc.
Surgical: Correct the Dilatation, conduits (bypass), resection, fracture reduction, and fixation

2. Corrosive stricture oesophagus C/F & Mx [85]4

Ans.
Causes: Ingestion of Acids, alkalies or other chemicals by accidents (in children) or for the purpose of suicide (in
adults).
PATHOLOGY: Severity of oesophageal burns depends on the nature of corrosive substance, its quantity and

concentration and the duration of its contact with the oesophageal wall.
Alkalies are more destructive and penetrate deep into the layers of the oesophagus.
Oesophageal burns run through 3 stages:
1 Stages of acute necrosis
2. Stage of granulations: Slough separates leaving granulating ulcer.
3. Stage of stricture: Stricture formation begins at 2 weeks and continues for 2 months or longer.
EVALUATIONOF PATIENTS
* Determine the chemical ingested, signs & symptoms of shock, upper airway obstruction, mediastinitis,
peritonitis, acid-base imbalance, and associated burns of face, lips and oral cavity.
Take X-ray of the chest and soft tissue lateral view of neck.
MANAGEMENT
1. Hospitalize the patient
Treat shock and acid-base imbalance by iv. fluids and electrolytes. Monitor urine output for renal failure.
Relieve pain & airway obstruction.
Neutralize the corrosive by appropriate weak acid or alkali, iven by mouth. But it is effective only if done within first 6 h.
Parenteral Abx should be started immediately.
Pass a nasogastric tube to feed the patient and to maintain oesophageal lumen.
-

Oesophagoscopy- to know the degree and extent of the burns so as to plan further treatment.
Steroids should be started within 48-96 h to prevent stricture.
Follow the patient with oesophagogram and oesophagoscopy every 2 weeks, till healing is complete, for the
development of any stricture.
10. If stricture develops it can be treated by:
 (a) Oesophagoscopy and prograde dilatations, if permeable.
(b) Gastrostomy and retrograde dilatation, if impermeable
(c) Oesophageal reconstruction or by-pass, if dilatations are impossible.
11. Patients of corrosive injuries of oesophagus may require life-long follow-up.
m--------m----m-=an---------

sQs
1. Management of 'ingested fish bone' [15]
Ans.
Etiology
Age: Children and adults
Accidental
Reduced protective reflexes - Dentures, drugs, alcohol, etc.
Carelessness: Poor mastication
Psychiatric
Esophageal strictures.
Common sites of lodgement of Fish Bones: Tonsillar crypts, Base of the tongue, Pyriform fossa &
Cricopharynx.
Clinical Features
Symptoms Signs
G History of foreign body ingestion.
Throat/retrosternal pain is the predominant symptom Fish bone may be visible in
GDiscomfort/FB sensation. oropharynx
Dysphagia/ odynophagia may be present. Tenderness in the lower part of neck
Drooling of saliva, excessive salivation Indirect Laryngoscopy: Pooling of
Dyspnea. saliva/FB in pyriform fossa
Hoarseness/ stridor in case of laryngeal edema/large FB|
Investigations
Plain X-ray lateral/ AP view soft tissue neck
GRadiopaque FB: Coronal position in prevertebral region
GRadiolucent FB Prevertebral widening & anteriorly displaced airway
Fluoroscopy with barium swallow: Radiolucent FB get coated with barium
Chest X-ray: PA view and lateral
Treatment
For Fish bone look for it in the oropharynx and it may be removed as an outpatient procedure.
impacted for 24 hours: IV abx, analgesics and fluids should be given
If FB is >
Removal of FB is done under general anesthesia using rigid hypopharyngoscope/ esophagoscope& FB
forceps.
*If the impacted FB cannot be removed endoscopically, then an external approach Ex: lateral
pharyngotomy/ thoracotomy may be required.
Complications: electrolyte imbalance, Esophagitis, Retropharyngeal/parapharyngeal abscess, Esophageal
perforation, Mediastinitis, Pneumothorax, Tracheoesophageal fistula 8&
Esophageal stenosis.
-----====-* --------------------
2. Complications of rigid esophagoscopy [15]
a. Contraindication of rigid endoscopies [07, 02
b. Oesophagoscopy- Indications and complications [04, 97]
Ans. Oesophagoscopy is of 3 types: 6 of 9
1. Rigid oesophagoscopy performed through the oral route
2. Flexible fibreoptic oesophagoscopy performed through the oral route
3. Transnasal oesophagoscopy-performed through nose
RIGID OESOPHAGOSCOPY
POSITION of the Patient: (Same as for direct laryngoscopy) Patient lies supine, head is elevated by 10-15 cm, neck flexed on chest
and head extended at atlanto-occipital joint. The purpose of this position is to attain the axes of mouth, pharynx and
oesophagus in a straight line to pass the rigid tube easily
cONTRAINDICATIONS
1. Trismus makes the procedure technicaly difficult.
2. Disease of cervical spine, e.g., cervical trauma, spondylosis, TB spine, osteophytes and kyphosis.
Receding mandible.
INDICATIONS of Rigid Oesophagoscopy
Aneurysm of aorta for
fear of rupture and fatal Diagnostic Therapeutic
haemorrhage 1. To findcause for 1) Removal of a foreign body.
Advanced heart, liver or dysphagia. 2) Dilatation in case of oesophageal
kidney disease may be a 2. To find cause for strictures or cardiac achalasia.
relative retrosternal burning. 3) Endoscopic removal of benign lesions,
contraindication. 3. To find cause for eg, fibroma, papilloma, cysts, etc.
COMPLICATONS haematemesis. 4) Insertion of Souttars or Mousseau-
4. Secondaries neck with Barbin tube in palliative treatment of
1 Injury to lips and teeth.
unknown primary (asa oesophageal carcinoma.
Injury to arytenoids. part of panendoscopy). 5) Injection of oesophageal varices
Injury to pharyngeal
mucosa.
Perforation of oesophagus -Most often it occurs at the site of Killian's dehiscence (near cricopharyngeal
sphincter) when undue force has been used to pass the oesophagoscope. Surgical emphysema develops
within an hour or so and the patient complains of pain in the interscapular region.
Compression of trachea Oesophagoscope may press on posterior tracheal wall, especially in children,
causing obstruction to respiration and cyanosis.Treatment is immediate withdrawal of oesophagoscope.
ELEXIBLE FIBREOPTIC OESOPHAGOSCOPY

»POSITION of the Patlent: The patient lies in left lateral position

Advantages over the rigid oesophagoscopy:
It is an outdoor procedure, does not require general anaesthesia and can be used in patients with
abnormalities of spine or jaw where rigid endoscopy is technically difficult.
The oesophagus, stomach and duodenum can all be examined in one sitting.
Good illumination and magnification provided by the fiberscope helps in the accurate diagnosis of the
disease and permits taking of precision biopsies, removal of small foreign bodies or benign tumours,
dilatation of webs or strictures and even injection of bleeding varices with sclerosing agents.
The procedure is performed under local anaesthesia.
TRANSNASALOESOPHAGOSCOPY-Oesophagus can be examined up to gastric fundus. It is being used:
1. to evaluate dysphagia & remove foreign bodies from the oesophagus
2. as a part of panendoscopy in the work-up of a cancer patient to look for a second primary and take a biopsy.
3. to perform tracheoesophageal puncture for oesophageal speech in laryngectomized patient.
4. to take a laryngeal biopsy.
 7 of 9
3. Mechanism of Deglutition [13, 09]
a. Stages of deglutition [03]
Ans.
The act of swallowing (Deglutition) is divided into 3 phases:
or
1. Oral Buccal Phase: Food is placed in the mouth chewed, lubricated with saliva > converted into a
boluspropelled into the pharynx by elevation of the tongue against the palate
2. Pharyngeal Phase: It is initiated when the bolus of food comes into contact with pharyngeal mucosa.A
series of reflex actions take place carrying the food past Oro- and laryngopharynx into the oesophagus:
a) Closure of nasopharynx. Soft palate contracts against the Passavant's ridge on the posterior
pharyngeal wall and completely cuts off the nasopharynx from the oropharynx.
b) Closure of oropharyngeal isthmus. The entry of food back into oral cavity is prevented by
contraction of tongue against the palate and sphincteric action of palatoglossal muscles.
)Closure of larynx. Aspiration into the larynx is prevented by temporary cessation of respiration,
closure of laryngeal inlet by contraction of aryepiglottic folds, closure of false and true cords, and
rising of larynx under the base of tongue. The role of epiglottis in providing protection to larynx is
not clear but it is seen to deflect backwards when food passes into the pyriform fossae.
d Contraction of pharyngeal muscles and relaxation of cricopharyngeus. Relaxation of
cricopharyngeus muscles is so timed and synchronous that food passes from pharynx into the
oesophagus during contraction of pharyngeal muscles
3. Oesophageal Phase: After food enters the oesophagus, the cricopharyngeal sphincter closes and the
peristaltic movements of oesophagus take the bolus down the stomach. Gastro-oesophageal sphincter
at the lower end of oesophagus relaxes well before peristaltic wave reaches and permits fluids to pass.
Bolus of food is passed by contraction of peristaltic waves and then the sphincter closes.
Regurgitation of food back from stomach into oesophagus is prevented by:
1) Tone of gastro-oesophageal sphincter,
2) Negative intrathoracic pressure,
3) Pinch-cock effect of diaphragm,
4) Mucosal folds,
5) Esophagogastric angle and
6) Slightly positive intra-abdominal pressure.

4. Oesophageal sphincters [09]

Ans.

Manometric studies have shown 2 high pressure zones in oesophagus & they UPPER
ESOAuEAL
form the physiological sphincters.
The upper oesophageal sphincter starts at the upper border of
oesophagus and is about 3-5 cm in length and functions during the act of AL

swallowing
SPHULNCTE

The lower oesophageal sphincter situated at lower portion of

is
oesophagus. It is also 3-5 cm in length and functions to prevent
oesophageal reflux.
Middle portion of oesophagus shows active peristalsis. The waves are weaker in the upper part, becoming
gradually stronger towards the lower portion.
-==
5. Achalasia cardia [04, 02]
Ans.
It is characterized by the absence of peristalsis in the body of oesophagus and high resting pressure in
lower oesophageal sphincter; the latter also does not relax during swallowing.
 Symptoms of cardiac achalasia include dysphagia, which is more to liquids than solids (reverse of that
seen in malignancy or strictures) and regurgitation of swallowed food particularly at night.
Diagnosis is made by
G Radiography- barium swallow shows dilated with narrowed rat tail lower end), sometimes also
called bird-beak appearance of oesophagus;
G Manometric studies - low pressure in the body of oesophagus & high pressure at lower sphincter and failure of LES to relax;
Endoscopy to exclude benign stricture or any development of carcinoma which is a common complication of this disorder
Treatment of choice is the modified Heller's operation (myotomy of the narrowed lower portion of the
oesophagus).

6. Dysphagia Lusoria [03, 2000]

Ans.
It is a type of dysphagia which occurs due to compression of oesophagus by subclavian artery.
seen when right subclavian artery arises from thoracic aorta & passes in front of or behind the
oesophagus.

7. Strictures of Oesophagus [01]

Ans. The strictures (narrowing of esophageal lumen) occur when muscular coat of oesophagus is damaged
AETIOLOGY: The common causes are:
1. Burns due to corrosive substances or hot fluids.
Trauma to oesophageal wall due to impacted foreign bodies or instrumentation or external injuries.
3. Ulcerations due to reflux oesophagitis.
4. Ulcerations due to diphtheria or typhoid.
5. Sites of surgical anastomosis.
6. Congenital, usually in the lower third.
CUNICAL FEATURES DIAGNOSIS
Dysphagia, first to solids and then to liquids, is the common complaint.
When obstruction is complete, regurgitation & cough may occur.
Patient is malnourished.
Barium swallow establishes the diagnosis. Oesophagoscopy is required to exclude malignancy.
TREATMENI
1. Prograde Dilatation with Bougies: It should be done under direct vision through oesophagoscope.
2. Gastrostomy: It helps to feed the patients and give rest to the inflamed area above the strictures. After
a few days, when inflammation subsides, lumen become visible & prograde dilatation can be restored.
3. Surgical Excision of strictured segment & reconstruction of food passage

8. Reflux esophagitis [96]

Ans.
It occurs mainly due to function of LES causing regurgitation of gastric contents into oesophagus.
Other causes of GERD are pregnancy, hiatus hernia, scleroderma, excessive use of tobacco and alcohol,
& drugs that relax the smooth muscle (anticholinergic, beta-adrenergic drugs and calcium-channel
blockers).
Symptoms: substernal pain, heartburn and regurgitation.
Treatment
1. Elevation of the head of bed at night.
2. Avoiding food at least 3 h before bedtime.
 of 9
3. Antacids
4. Drugs that tone of LES, e.g., metoclopramide.
5. H2 Blockers, e.g., cimetidine and ranitidine.
6. Avoiding smoking, alcohol, caffeine, chocolates, mints and carbonated drinks.
7. Antireflux surgery, e,g. Nissen's fundoplication.
Complications of Gastro-oesophageal Reflux
1. Oesophagus
Oesophagitis, oesophageal mucosal erosion and haemorrhage.
Benign oesophageal stricture.
Barrett's oesophagus (normal squamous epithelium of oesophagus is replaced by columnar
epithelium as a result of continuous inflammation). It is a precancerous condition.
2. Lungs: Aspiration pneumonia, Chronic cough, Asthma & Bronchiectasis.
3. Larynx
GPosterior laryngitis pain in throat, hoarseness and repeated throat clearing.
G Contact ulcers and granulomas.
GPosterior glottic stenosis.
GParoxysmal laryngospasm.
G Carcinoma larynx.
4. Ear-Otitis media with effusion.
5. Miscellaneous Globus hystericus.

Distance from incisor teeth

VSQs Sites of Constrictions

af Oesophagus
1) 3 constrictions of oesophagus [13] Pharyneoesophageal junction
Ans. inches

They are:
Arch of eort
a) At pharyngo-oesophageal junction (C6)15 cm from upper incisors Inches
Left principal junction
11 inches
b) At crossing of arch of aorta and left main bronchus (TA)-25 cm
from upper incisors. Right crus of diaphragm

cm
Where it piercesthe diaphragm (T10)-40 from upper incisors. 15 inche

Foreign bodies in the oesophagus can be held up at these constrictions.

2) Plummer-Vinson Syndrome [10, 07, 97, 91]

Ans.
PlummerVinson (Patterson-Brown-Kellv) Syndrome:
There is atrophy of the mucous membrane of the alimentary tract
>Classical features of this syndrome include dysphagia, iron-deficiency anaemia, glossitis, angular
stomatitis, koilonychia (spooning of nails) and achlorhydria.
Predominantly, jt affects females past 40 years.

Barium swallow shows a web in the postcricoid region and the same can be seen on oesophagoscopy.
It is due to subepithelial fibrosis in this region.
It predisposes to the development of carcinoma in the tongue, buccal mucosa, pharynx, oesophagus
and the stomach.
Treatment
be corrected.
1. To correct anaemia by oral/parenteral iron: Associated B12 and Bs deficiency should also
2. Dilatation of the webbed area by oesophageal bougies.