OTITIS MEDIA

Definition

 “It is an inflammation of middle ear that most often occur in infant &
young children but can occur at any age”

Incidence

 Most common in children under 15 yr of age.

Types

 Acute otitis media

 Chronic otitis media
 Other
o Serous otitis media
o Secretory otitis media
o Suppurative otitis media

Acute otitis media

Definition

 “It is an acute infection of the middle ear, usually lasting less then 6
weeks”

Etiology

 Bacteria
o eg. Streptococcus pneumoniae,
o H. Influenza
 Upper respiratory tract infection
 Infection nasopharynx
Pathophysiology

 Due to etiological factor(URTI, Bacteria)

 Exudates & edema in middle ear
 Decrease retraction of tympanic membrane
 Serous exudates in middle ear
 Pus formation
 Tympanic membrane rupture
 It occur the acute otitis media

Clinical features

 Otorrhea
 Otalgia
 Fever
 Rhinitis
 Tympanic membrane erythema, may be perforated
 Hearing loss
 Irritability

Diagnosis

 History
 Physical examination
 Otoscopic examination
 Culture
 Audiometry & Tympanometry

Medical Management

 Antibiotic
 Analgesic
  Antihistamine

Surgical management

 Myringotomy or tympanotomy (incision in the tympanic membrane)

Complication

 Chronic otitis media

 Hearing loss
 Perforation
 Poor speech develop

Chronic otitis media

Definition

 “It is a long standing infection of a part of whole of the middle year

characterised by ear discharge & permanent perforation”
OR
 “Inflammation of the middle ear that lasts for more than 6 weeks”

Incidence

 Common in the age 3-6

Etiology

 Inappropriate treatment of acute otitis media.

 URTI, Allergic rhinitis
 Breastfeeding and long time group child care
 Eustachian tube deformity
 Septal deviation, cleft palate, sinusitis

Types

 Suppurative (+ perforation)
 o atico-antral type
o Tubo-tympanic type
 Non suppurative Mucoid or serous

Atico-antral chronic otitis media

 Inflammation involves bones (e.g. mastoid, tympanic ring, ossicles )

Tubo-tympanic otitis media

 Acute otitis media

 permanent perforation
 muco-purulent discharge.

Serous Otitis media

Stages

 URTI or acute otitis media–> Fluid collection in middle ear and

obstruction of eutachian tube
 tympanic membrane retraction. Fluid become pus like
 necrosis
 Tympanic membrane perforation. Could end up with mastoiditis ( if not
stopped ).

Medical management

 careful suctioning of the ear under microscopic guidance.

 Instillation of antibiotic drops Surgical management
 tympanoplasty
 Ossiculoplasty (surgical reconstruction of the middle ear bones to restore
hearing)
 Mastoidectomy
Assessment

 Collect health history includes

o a complete description of the ear problem.
o Collect data about the duration and intensity of the problem, its
causes, and previous treatments.
o Obtain Information about other health problems and medications
 Physical assessment includes
o observation for erythema, edema, otorrhea, lesions, and
characteristics such as odor and color of discharge.

Diagnosis

 Pain R/T Infection

 Risk for infection R/T eustachian tube dysfunction.
 Altered auditory sensory perception R/T Fluid in the middle year.
 Anxiety R/T surgical procedure, potential loss of hearing
 Risk for trauma R/T balance difficulties or vertigo during the immediate
postoperative period
 Disturbed sensory perception R/T potential damage to facial nerve
(cranial nerve VII).
 knowledge deficient R/T disease, surgical procedure,and postoperative
care.

MENIERE'S DISEASE

Defiition

Meniere's disease (idiopathic endolymphatic hydrops) is a disorder of the inner

ear associated with a symptoms consisting of
  spontaneous, episodic attacks of vertigo
 sensori neural hearing loss which usually fluctuates
 tinnitus
 sensation of aural fullness.

Incidence

 Roughly 1 in 1000 individuals are affected

 Constitutes 10% of all patients attending vertigo clinic
 Female preponderance  Rare in children under the age of 10
 Commonly begins between 3th to 6th decades of life
 Bilateral Meniere’s syndrome is seen in 5% of these patients

Types of meniere's disease

 Classical Meniere’s disease

 Vestibular Meniere’s disease – vestibular symptoms and aural pressure
 Cochlear Meniere’s disease – cochlear symptoms and aural pressure
 Lermoyez syndrome – Reverse Meniere’s
 Tumarkin’s crisis – Utricular Meniere’s

Lermoyez syndrome

This is a variant of Meniere’s disease. It is characterized by sudden sensori

neural hearing loss which improves during or immediately after the attack of
vertigo.

Tumarkin’s drop attacks

 abrupt falling attacks of brief duration without loss of consciousness. due

to excess endolymphatic volume. Utricular crisis is used to indicate this
condition.
  In the later disease stages the valve of Bast remaining patent may cause
sudden drainage of endolymph from the utricle due to longitudinal flow
resulting in these drop attacks
 Several pathophysiological mechanisms are thought to be implicated in
the otolithic catastrophe of Tumarkin:
 sudden shift of the utricular macula, sudden changes in the
endolymphatic fluid pressure, and sudden electrolyte changes secondary
to the rupture of the membrane labyrinth.
 Thus, the inappropriate stimulation of the otolithic organs might generate
a failure of the vestibulospinal reflex with the loss of postural tonus and,
consequently, the falling

Etiology

 Genetic
 Autonomic
 Endocrine

Pathophysiology

Theories behind endolymphatic hydrops

 Obstruction of endolymphatic duct/sac

 Hypoplasia of endolymphatic duct/sac
 Alteration of absorption of endolymph
 Alteration in production of endolymph
 Autoimmune insult
 Vascular origin
 Viral etiology

Pathology

 Defective absorption by endolymphatic sac

  Poor vascularity of sac
 Less absorptive tubular epithelium
 increased peri saccular fibrosis
 Rupture of reissner’s membreane leading to mixing of perilymph &
endolymph- Schuknecht
 allow leakage of the potassium-rich endolymph into the perilymph,
bathing the eighth cranial nerve and lateral sides of the hair cells

Histopathological changes

 Loss of shorter stereocilia of outer hair cell first occuring in the apical
region
 Outer hair cell->inner hair cell->intercellular edema b/w marginal
cell->vacuolization- >atrophy of marginal and intermediate cells->
loss of spiral ganglion cell
 High concentrations of extracellular potassium depolarize the nerve
cells, causing their acute inactivation.
 The result is a decrease in auditory and vestibular neuronal outflow
consistent with the hearing loss and features of acute vestibular
paralysis seen in a typical Meniere's attack
 The chronic deterioration in inner ear function presumably is the
effect of repeated exposure to the effects of the potassium

Mechanism of meniere’s disease

Hearing loss

 Sensori neural in nature

 Fluctuating and progressive
 Affects low frequencies
 Mild low frequency conductive hearing loss (rare)
  Profound sensori neural hearing loss (End stage)

Tinnitus

 Roaring in nature
 subjective
 Could be continuous / intermittent
 Non pulsatile in nature
 Frequency of tinnitus corresponds to the region of cochlea which has
suffered the maximum damage

 Investigations

 Tuning forks tests : SNHL

 PTA
 Speech audiometry
 Recruitment test +ve
 SISI >70%
 Tone decay <20 dB
 Caloric testing – canal paresis
 ENG
 Head Thurst test
 ECoG – SP is larger & more negative
 SP/AP ratio increases > 30%
 Dehydration/Glycerol test
 VEMP (Vestibular evoked myogenic potentials) elevated threshold

Loudness recruitment

 This is abnormal growth in the perceived intensity of sound

 This is usually positive in patients with Meniere’s disease
  ABLB (alternate binaural loudness balance test)is the test used to look
for the presence of recruitment
 This test is really time consuming

Electro cochleography

 Increased summating potential / action potential ratio. 1:3 is normal

 Widened summating potential / action potential complex. A widening of
greater than 2 ms is significant

Vestibular tests

 Not mandatory for diagnosis of Meniere’s disease

 Caloric test is still performed
 It is low frequency stimulation (0.003 Hz) of lateral canal
 Caloric asymmetry will point to the diseased ear 5. 20% difference
between the two ears (Jongkee’s formula) is significant

Vemp

 Vestibular evoked myogenic potential

 Measures the relaxation of sternomastoid muscle in response to
ipsilateral click stimulus
 Brief high intensity ipsilateral clicks produce large short latency
inhibitory potentials (VEMP) in the toncially contracted Ipsilateral
sternomastoid muscle
 This test is due to the presence of vestibulo collic reflex
 Afferent arises from sound responsive cells in the saccule, conducted via
the inferior vestibular nerve.
 Efferent is via vestibulo spinal tract
 Normal responses are composed of biphasic (positive-negative) waves
 VEMP reveals saccular dysfunction
Dehydration tests

 Glycerol
 Frusemide
 Isosorbide

test is considered positive if

 there isa 10-dB or more improvement in pure tone thresholds at 2 or

more frequencies (250 to 2000 Hz), or
 there is a 12% or greater improvement in speech discrimination
score.

Glycerol test

 First introduced by Klockhoff and Lindblom – 1966

 Glycerol is administered in doses of 1.5 mg/kg body wt in empty
stomach
 Serum osmolality should increase at least by 10 mos/kg
 Side effects include Headache, Nausea, vomiting, drowsiness
 PTA is performed 2-3 hours after administration
 False positivity is rare
 Positivity depends on the phase of the disease

Management

 Conservative treatments include lifestyle and dietary

adjustments,diuretics, and supplemental use of vestibular suppressants.
 Invasive or destructive procedures are indicated only in the 5% to 10%
of patients with Meniere’s disease who fail conservative and medical
measures.
 Overall, vertigo control is achieved in more than 99% of patients with
Meniere’s disease.
Medical management

 Dietary management
 Physiotherapy
 Psychological support
 Pharmacological intervention

Treatment of acute exacerbation

 Intravenous fluids – dehydration

 Vestibular suppressants – May delay recovery / rehabilitation process
 Corticosteroids – May help if tinnitus and deafness are debilitating

Low salt diet

 Frustenberg diet
 2 grams / 24 hours (restricted salt intake)
 Life style modification

Role of diuretics

 Diuretics play a vital role in alleviating acute symptoms

 This has been in use since 1930’s
 Thiazide group of drugs are commonly used
 Frusemide may be used to alleviate acute symptoms
 Clear scientific evidence is lacking regarding the usefulness of diuretics

Betahistine

 Cochlear vascular insufficiency has been proposed as one of the

mechanism of Meniere's disease
 Betahistine is supposed to cause vasodilatation of cochlear blood vessels
  Betahistine has weak H1 agonistic property and considerable H3
antagonist properties
 It reduces the frequency & intensity of vertigo. Has minimal effect on
tinnitus
 Doesn’t help much with hearing loss

Other treatment modalities (ancillary)

 Stress reduction
 Patient education
 Hearing aids – can be used to suppress troublesome tinnitus
 Tinnitus retraining

Vibrator therapy

 Meniett Device
 Low pressure pulse generator
 Vibrations are transmitted via external auditory canal
 Vibrations alter inner ear fluid dynamics by their effects on the oval and
round windows
 Exact mechanism of action is not known
 It is totally non invasive
 This device is portable

Vibrator therapy steps

 Diagnosis should be confirmed

 Ventilation tube should be inserted
 Patient should be trained for self administration of the treatment
 Usually administered thrice a day about 5 mins each time
 Treatment lasts for 5 weeks
Indications for vibrator therapy

 Classic unilateral Meniere’s disease

 Intense vestibular / cochlear symptoms
 Failed medical therapy
 Over 65 years of age
 Imbalance / aural fullness / tinnitus after gentamycin treatment

Intratympanic gentamycin

 Fixed dose protocol is used

 40 mg/ml gentamycin is buffered with soda bicarb (pH6.4) final
concentration 26.7mg/ml.
 T tube grommet inserted into the postero inferior quadrant of ear drum. A
mcirocatheter is inserted through the grommet
 1ml of gentamycin solution is injected into the middle ear cavity via the
microcatheter
 Three injections are given per day in outpatient setting 6. Injections are
given for 4 days
 After injection patient should lie supine with the infiltrated ear up for 30
mins
 Vertigo usually develops between 2-4 days after cessation of treatment

Surgical management

 Sac enhancement procedure

 Sac decompression procedure
 Labyrinthine ablative procedures

Endolymphatic Sac Surgery

 Decompression: Removal of bone overlying the sac

  Shunting: Placement of synthetic shunt to drain endolymph into mastoid
 Drainage: Incision of the sac to allow drainage
 Removal of sac: Excision of the sac

Ablative procedures

 Labyrinthectomy
 Translabyrinthine vestibular neurectomy
 Retrolabyrinthine vestibular neurinectomy
 Retrosigmoid vestibular neurinectomy
 Middle cranial fossa vestibular neurinectomy

Shunt procedure

 External shunts – Drains the sac into mastoid cavity / subarachnoid space
 Internal shunts – Drains excessive endolymph into the perilymphatic
space (cochleosacculotomy / labyrinthotomy)

Cochleosacculotomy / labyrinthotomy

 Helpful in treating debilitated patients

 Involves disruption of osseous spiral lamina
 Angular pick introduced via round window towards oval window. It will
accommodate 3 mm long pick
 After perforation the pick is withdrawn and the round window is sealed
by fat

HEARING AND HEARING LOSS

Definition
  Hearing- transduction of sound to neural impulses and its interpretation
by the CNS
 Hearing loss- defect at any level from sound transduction to
interpretation

Types of hearing loss

 Conductive- sound is not conducted efficiently through the outer ear

canal to the eardrum and the tiny bones (ossicles) of the middle ear
 Sensorineural (SNHL)- damage to the inner ear (cochlea), or to the nerve
pathways from the inner ear to the brain.
 Mixed
 Central- Problem lies in the central nervous system

Known causes

Hereditary sensorineural hearing loss

 Hereditary- 1/3 of all cases of SNHL

 Syndromic- Usually present at birth usually AR
 Ex; Treacher-Collins syndrome
 Non-syndromic- based on onset
 Congenital form
 Late onset form- more common, tend to be AD, manifested after birth

Noise induced hearng loss

Can cause direct mechanical trauma to cochlea

 Acute acoustic trauma- sudden intense sound event of short duration

 Exceeds 140 db and pressure rise is very short (<1.5ms)
 Ex; gunshot
 Blast injury- pressure wave from an explosive blast
  Exceeds 140db but duration of pressure rise is longer (>2ms)
 longer frequency spectrum
 Ruptured tympanic membrane

Noise induced hearng loss

 Acute noise-induced hearing loss- high levels of continuous or

intermittent noise for seconds to hours
 Often reversible or partially reversible
 muffled sensation and tinnitus
 Ex; loud power tools, rock concerts, engine noise
 Chronic noise-induced hearing loss- irreversible cochlear hearing loss
 Typical features of sensorneural hearing loss
 Tinnitus can be constant
 Safe if levels below 85db for 8hrs/day

Traumatic injury to inner ear

 Functional- labyrinthine concussion

 Structural- labyrinthine contusion
 Temporal bone fracture
 Impact to the skull- accelerating and decelerating forces
 Barotrauma
 Symptoms: nonspecific vertiginous complaints and hearing impairment

Labyrinthitis

 Infection or inflammatory process affecting the labyrinth or its

surrounding 3 routes: Tympanogenic, meningeal and hematogenous
 Tympanogenic- infection/inflammation maybe transmitted through oval
or round window
  Acute toxic (serous labyrinthitis)- labyrinth itself is not infected;
becomes inflamed by substances released in middle ear.
 Acute supporative- bacterial infection of middle ear spreads to labyrinth.
 Chronic Labyrinthitis- manifested as inner ear damage.
 Chronic otitis media as possible cause

Ototoxicity

 Toxic damage to inner ear affects both cochlear and vestibular functions
 Endogenous or exogenous
 Effects generally symmetrical
 Symptom: Tinnitus maybe initial presenting symptom

Unknown causes

Presbyacusis

 Age related (over 50 yr old), symmetrical SNHL

 Ageing process
 Endogenous genetic predisposition
 Cummulative exposure to exogenous factors
 Symptoms: Speech recognition more affected than pure tone
 Diagnosis: Pure tone audiometry- symmetrical SNHL (High tone loss)

Sudden sensorineural hearing loss

 Immediate, unilateral hearing loss with no apparent external cause.

 Symptomatic or Idiopathic
 Idiopathic- cause: Viral, vascular, autoimmune
 Symptoms: within seconds to hours. Mild loss of hearing to sudden
deafness
 Vestibular symptoms less common
Chronic, progressive, idiopathic sensorineural hearing loss

 Bilateral SNHL
 Onset before age 50
 Etiology unknown
 Symptoms: Variable- sudden hearing loss or progress gradually
 Frequently associated by tinnitus
 Vestibular symptoms generally absent

Test for auditory function

 Tuning Fork test

 Pure tone audiometry
 Speech audiometry
 Tympanometry

Tuning fork test

 Differentiate between conductive and SNHL

 Weber and Rinne test
 Weber- TF placed in midline of skull. Vibrations are transmitted by bone
conduction
 Normal- Vibrations perceived equally on L+R
 SNHL- Lateralizes to better ear
 CHL-Lateralizes to affected ear
 Rinne- compares level of air and bone conduction in the same ear.
 AC test- TF just outside the ear canal
 BC test- TF firmly against mastoid
 Normal: AC>BC
 CHL: BC>AC
 SNHL: AC>BC but both equally depreciated
Pure tone audiometry

 used to identify hearing threshold levels of an individual, enabling

determination of the degree, type and configuration of a hearing loss.
 NORMAL HEARING - both air and bone conduction will be
superimposed at each test frequency between 0 to 10 dB.
 CONDUCTIVE HEARING LOSS - air conduction is < normal bone
conduction.
 SENSORINEURAL HEARING LOSS - both air and bone conduction
below normal threshold at any frequency tested
 Mixed hearing loss

Tympanometry

 an examination used to test the condition of the middle ear and mobility
of the eardrum (tympanic membrane) and the conduction bones by
creating variations of air pressure in the ear canal.
 Permits a distinction between sensorineural and conductive hearing loss,
when evaluation is not apparent via Weber and Rinne testing.
 Can be helpful in making the diagnosis of otitis media by demonstrating
the presence of a middle ear effusion.
 A- Normal
 AD- abnormally compliant
 AS- Stiff (otosclerosis)
 B- Presence of non-compressible fluid within middle ear space(Otitis
Media)
 C-Eustachian tube dysfunction

VERTIGO
Definition

 Not a disease, But a symptom.

 A feeling in which the external world seems to revolve around the
individual or in which the individual itself seems to revolve in space.

Types

 Rotation
o Rotatory
o Non-rotatory
 Patient’s perception
o Subjective
o Objective
 Stimulus involved Spontaneous Induced

Physiological Vertigo

 Balance between 3 stabilising sensory systems is lost.

 Non-adaptation of vestibular system to unfamiliar head movements.
 Unusual head & neck positions

Peripheral & Central Vertigo

 Peripheral: Lesions of vestibular end organs ( 85% of all cases of

vertigo)
 Intermediate: Lesions in vestibular nerve
 Central: Lesions of central nervous system(vestibular nuclei) ( 15% of all
cases)

Peripheral & Central Vertigo

Central Vertigo Vascular causes:

 Hypertension, Basilar artery insufficiency

 Epilepsy: both disease & its treatment
 Road Traffic Accident: Head trauma Tumor: of brainstem, 4th ventricle
& cerebellum
 Infection: Meningitis, Encephalitis Glial diseases: Multiple sclerosis
 Others: Parkinsonism, Psychogenic

Peripheral Causes for Vertigo

 BPPV
 Vestibular Neuronitis
 Meniere’s disease
 Labrynthitis
 Vestibulotoxic Drugs
 Perilymph Fistula
 Head injuries & Surgical trauma
 Syphillis

Evaluation of Vertigo

Tests for assessment of Vestibular functions

 Clinical tests
 Laboratory tests

Clinical Tests of Vestibular Function

 Spontaneous Nystagmus
 Fistula test
 Romberg Test
 Gait
  Past-Pointing & Falling
 Dix Hallpike Maneuver
 Test of Cerebellar Dysfunction

Nystagmus

 Involuntary rhythmical oscillatory movement of the eyes.

 Triggered by inner ear stimulation.
 Slow pursuit movement initially, fast rapid resetting phase
 Nystagmus is always named after direction of the fast phase Nystagmus
Based on Direction Rotatory/ Tortional Horizontal Vertical

Laboratory Tests

 Caloric Test
 Electronystagmography
 Optokinetics
 Rotational Test
 Galvanic Test
 Posturography

Caloric test

Principle:

 To induce nystagmus by thermal stimulation of the vestibular system

Advantages

 Each labryinth can be tested separately

 Also checks for labrynthine origin of vertigo

Types

 Modified Kobrak Test: 60°, 60 s, Ice water

  Fitzgerald-Hallpike Test/Bithermal Caloric Test:
 Supine position
 Water at 30° & 44°
 Head tilt: 30° forward
 5 mins gap b/w 2 ears
 Direction of Nystagmus: COWS Cold- Same Warm- Opposite 3. Cold
air caloric test: Done in TM perforation

Electronystagmography

 Detects both Spontaneous and Induced nystagmus.

 Depends on presence of Corneo-retinal potentials

Optokinetic Test

 Useful to diagnose a Central lesion

Rotation Test

 Barany’s Revolving chair, 30° forward head tilt

Galvanic test

 Only test which helps in differentiating end organ lesion from that of
nerve lesion. Posturography

Treatment of Vertigo

 Reassurance/Psychological Support
 Pharmacotherapy
 Adaptation exercises
 Intratympanic antibiotic injections
 Surgery
  Conservative
 Destructive

BENIGN PAROXYSMAL POSITIONAL VERTIGO

Definition

 Abnormal sensation of motion that is elicited by certain provocative

positions.
 These provocative positions usually trigger specific eye movements i.e.
Nystagmus Rotational Geotropic Latency: 1- 5 s Duration: 20-30 s
Fatiguable Associated with Vertigo Reversible

Signs & Symptom

symptoms

 Sudden Onset
 Have few asymptomatic periods in between
 Dizziness triggered by head movements
 Classic BPPV: erect to supine, 45°
 During attacks, Rolling spin
 Symptoms dissipate within 20-30 s after a violent start.

Signs

 Neurological examination: Normal

 Dix-Hallpike maneuver:
 Caloric Test: Normal or Hypofunctional

Investigations

 Electronystagmography(ENG)
 Caloric Test
  Audiometry
 Posturography

Treatment Medical

 Wait & watch

 Vestibulo-suppressant medication
 Vestibular Rehabilitation: Cawthorne exercises
 Canalith repositioning (CRP):
 Epley Maneuver
 Semont maneuver

Surgical (failure of CRP)

 Labyrinthectomy
 Posterior canal Occlusion
 Singular neurectomy
 Vestibular nerve section
 Transtympanic Aminoglycoside application

TINNITUS

Definition

 Any sound that is perceived by the listener that does not originate from an
external sound source May be perceived in one or both ears (peripheral)
and/or in the head (central)
  60% bilateral
 30% unilateral
 10% central
 From latin word, tinniere, which means “to ring”

Descriptive Labels

 Ringing
 Hissing
 Buzzing
 Roaring
 Clicking
 Ocean sound
 Cicadas
 Pulsing
 Heartbeat

Causes

 Most commonly caused by some sort of change to the auditory system

 80% of patient’s with SNHL have tinnitus Hearing loss results in
changes in the neural activity of the auditory system, which the auditory
cortex interprets as sound
 Much like phantom limb syndrome. Areas of the cochlea where there is
hair cell damage can no longer amplify sounds where damage has
occurred so a phantom sound is interpreted by the brain.

Other Causes

 Hearing loss, especially in cases of noise-induced hearing loss (NIHL)

 External or middle ear issues (wax, fluid)
 Acoustic neuroma (UNILATERAL tinnitus)
  Medications Sinus/allergy issues
 Dental issues (TMJ-temporal-mandibular joint syndrome)

Medications that cause tinnitus

 Anti-inflammatories
 Antibiotics
 Antidepressants
 Aspirin
 Quinine
 Loop diuretics
 Chemotherapy drugs

Types

 Subjective - Can only be perceived by the patient Most common type

(95%)
 Objective - Can be heard by others Rare (<5% of all tinnitus cases)
Usually pulsatile (in sync with heartbeat) Causes: vascular or muscular

Causes of Objective Tinnitus

 Vascular
 Arteriorvenous aneurysm
 Glomus jugulare tumor Muscular
 Patent eustachian tube
 Palatal myoclonus: involuntary muscle jerk of the roof of the mouth
Spasm of stapedius or tensor tympani muscles

Bothersome/Uncompensated Tinnitus
  Only about 20% of people with tinnitus are bothered by it The tinnitus
itself isn’t the problem. The person’s REACTION to it is what is
problematic.
 Tinnitus may result in irritability, fatigue/sleep disturbance, depression,
suicidal thoughts These patient’s need to be referred to a mental health
professional
 A Viscious Cycle
 Attentional Factors (patient chooses to attend to tinnitus)
 Emotional reaction
 Limbic system: negative emotional labeling of the tinnitus Autonomic
system: activation of the fight-or-flight mechanism (Can this tinnitus
harm me?) Stress
 Amplification of tinnitus signal (louder)

Treatment

 Surgery (uncommon option)

 Medication (usually xanax, valium, antidepressants)
 Dietary restrictions (caffeine, alcohol, salt, MSG)
 Masking
 Counseling
 Cognitive Behavioral Therapy Tinnitus Retraining Therapy
 Sound treatment
 Neuromonics

Masking

 Use of noise to temporarily mask or “cover up” the tinnitus so it cannot

be perceived This is often successfully accomplished when patient’s with
 hearing loss use traditional hearing aids. The amplification of
environmental noises often reduces or completely masks tinnitus.
 Our newest generation hearing aids have optional tinnitus maskers built-
in for when hearing aids aren’t enough to mask tinnitus
 There are companies that manufacture tinnitus maskers for those with
normal hearing. May be in-the-ear with a very large vent or a behind-the-
ear, open-ear device
 The use of a sound machine or external noise source (i.e. ceiling fan) can
be very helpful at night Different types of noise are utilized in masking:
white noise, pink noise, brown noise, grey noise (all have varying
complexity based on frequency components)

Tinnitus Handicap Inventory

 Patient self-survey Sample questions

 Do you feel you have no control over your tinnitus? Because of your
tinnitus do you feel tired? Because of your tinnitus do you feel depressed?
Does your tinnitus make you feel anxious? Quantifies the severity of
tinnitus
 Rates degree of handicap from slight to catastrophic

Tinnitus Retraining Therapy

 Jastreboff created TRT Combines counseling with use of noise generators

Counseling
  Reclassify tinnitus to a category of neutral signals Sound therapy: weaken
the tinnitus-related neural activity Goal: Habituation to the tinnitus (no
longer pay attention to it)

Neuromonics

 Six to eight month therapy protocol Uses spectrally modified music that
has been tailored according to each patient’s hearing and tinnitus
characteristics
 Combined with an underlying neural stimulus
 Retrains the brain to filter out tinnitus disturbance Very expensive~$5000
for treatment that lasts less than a year

Other Sound Disorders

 Hyperacusis - Everyday sounds seem “too loud” or “uncomfortable”

 About ½ of those with tinnitus, also have hyperacusis
 Affects 1 in 50,000

Causes

 Hearing loss 
 Head injury (i.e air bag deployment)
 Ototoxicity Lyme disease
 Viral infections involving the inner ear or facial nerve (Bell’S palsy) TMJ
PTSD (post-traumatic stress disorder)
 Chronic fatigue syndrome
 Epilepsy
 Depression
 Migraine headaches

IMPACTED CERUMEN
Introduction

 Ear Wax (Cerumen) is a natural protective oily substance which is

produced in the outer third of the ear canal.
 Its function is to remove small foreign particles, such as dust, from the
canal.
 This is achieved by the ciliary hairs.

Definition

 Excess collection of thick ear wax is known as impacted wax.

Symptoms

 Diminished hearing – often of sudden onset after “cleaning” the ears

 Discomfort – seldom complain of pain unless the wax is pressing on the
drum
 Tinnitus occasionally

Educational Points

 Wax is a normal physiological substance which has an important role in

protecting the ear canal The ear canal is a self-cleaning system, do not to
use cotton buds as wax is more likely to be pushed back against the
eardrum and become impacted.
 Ear wax only needs to be removed if it causes symptoms or if a proper
view of the eardrum is needed.

Primary Care Treatment

 In more severe cases use of a ceruminolytic ear drop for 4 to 5 days prior
to syringing is advisable
 Removal with wax hook is also an option
 Formby cerumen hook and scoop
  Self Care Ear drops to soften ear wax (ceruminolytics) may be used as the
only treatment in mild cases.
 There are many different preparations on the market, none with any clear
clinical advantage compared to the others.
 Sodium bicarbonate may be effective at disintegrating ear wax.
 A simple home remedy is olive oil, warmed by pouring onto a warm
spoon.
 Preparations containing organic solvents are particularly likely to cause
irritation and inflammation of the external ear canal and should be
avoided
 Ear Irrigation - Ear irrigation to improve hearing in those with impacted
wax The lowest pressure possible should be used.
 It is best avoided if
o the eardrum is known or suspected to be perforated
o there is a history of mastoid surgery or chronic middle ear disease
o If patient has unilateral deafness
o A history of recurrent otitis externa or tinnitus

PERICHONDRITIS

Definition

 It refers to inflammation involving the perichondrium of the external ear,

auricle, &external auditory canal.
 However, it is commonly used to describe continuum of conditions of
the external ear from erysipelas(infection of overlying skin) through
cellulitis(infection of the soft tissue)& true perichondritis to
chondritis( infection involving the cartilage itself).
 Classification

 A practical classification might be:

o Erysipelas of external ear
o Cellulitis of external ear

Etiology

 Perichondritis usually happens secondary to trauma. Such trauma may

include
 laceration,
 surgery
 frost bite
 burns,chemical injury
 infection of a haematoma of the pinna, high piercing of the
cartilaginous portion of the auricle for the insertion of earring.
 The most common organism pseudomonas aeruginosa, &
staphalococcus aureus.

Diagnosis

 The diagnosis of perichondritis is clinical & a background of underlying

trauma to external ear should be sought. The lobule contains no cartilage,
is spared. Dull pain & sign of inflammation involving the cartilaginous
pinna is enough to diagnosis.

Outcomes

 If untreated , a subperichondrial abscess may develop , leading to

avascular necrosis of the underlying cartilage, marked deformity of the
pinna. Management options; Prevention; acute perichondritis should be
prevented by careful placement of ear piercing away from the
 cartilaginous pinna. Haematoma of the auricle should be drained
promptly.

Management

 The meticulous management of the burn injuries to the ears should

include the use of prophylactic antibiotic against Gram-negative bacteria
& diligent local care including daily dressing &removal of eschars &
crust. First line management The mildest forms are treated with oral &
topical antibiotic.
 If there is any discharge or abscess needs draining, a pus swab should be
sent for C/S.
 Prompt treatment with broad –spectrum antibiotic possibly I/V.
Subperichondrial abscesses require incision & drainage but only when
definite fluctuation is present, as premature incision may result in further
spread of the infection.
 Resistant cases Nonresponse to the above treatment ,accompanied by
persistent pain , suppuration need further intervation. Dowling ; Advocate
aggressive excision of necrosed cartilage including overlying
subcutaneous tissues & skin.
 However, it is difficult to decide how much cartilage to excise. Repeated
debridement may be needed.
 Stevenson advocates a system of continuous drainage & irrigation with
antibiotic & steroid solution as an alternative to preservation of the
structure, fenetrated polyethylene tubes are placedin the subperiosteal
tunnels on either side of the cartilage& aminoglycoside /steroid solution
to irrigate these twice daily.
 Best clinical practice Considerd broad-spectum antibiotic ( including anti-
pseudomonas) prophylaxis in severely traumatized or burnt pinna. Early
 use of local & systemic antibiotic including antipseudomonas if
perichondritis is suspected.
 In resistant cases, add effective local antibiotic delivered by irrigation.
Conservative surgery for drainage of abscesses, creation of irrigation &
excision of necrotic cartilage with preservation of the perichondrium
wherever possible.

LABYRINTHITIS

Definition

 Labyrinthitis Inflammation of the labyrinth of the inner ear.

Etiology

 Viral or bacterial infections

 Cholesteatoma
 Drug toxicity
 Head injury
 Tumour
 Vasculitis

Clinical manifestations

 Vestibular manifestations (vertigo)

 Cochlear manifestations (hearing loss)
 Nausea and vomiting

Pathology

 Infection usually occurs by one of three routes:

 From the meninges
 From the middle ear space
  Hematogenous spread
 Meningogenic: through the IAC, cochlear aqueduct, both (bilateral)
 Tympanogenic: extension of infection from the middle ear, mastoid cells
or petrous apex-most common through the round or oval window
(unilateral)
 Hematogenous: through blood, least common 6

Bacterial Infections Two types of labyrinthitis associated with bacterial

infections:

 Toxic Labyrinthitis
 Suppurative Labyrinthitis

Toxic Labyrinthitis

 Toxic Labyrinthitis: results from a sterile inflammation of the inner ear

following an acute or chronic otitis media or early bacteria meningitis.
 Toxins penetrate the round window, IAC, or cochlear aqueduct and cause
an inflammatory reaction in the perilymph space.
 Bacterial Infection Toxic Labyrinthitis produces mild high frequency
hearing loss or mild vestibular dysfunction Treatment: Antibiotics for
precipitating otitis, possible myringotomy.

Suppurative Labyrinthitis

 Suppurative Labyrinthitis: direct invasion of the inner ear by bacteria.

 From otitis or meningitis

Suppurative Labyrinthitis: 4 stages

 Serous or irritative: production of Ig rich exudates in the perilymph

 Acute or purulent: bacterial and leukocyte invasion of the perilymphatic
scala-end organ necrosis
  Fibrous or latent: proliferation of fibroblasts and granulation tissue in the
perilymph
 Osseous or sclerotic: new bone deposition throughout the involved
labyrinth

Diagnosis

 History
o severe vertigo from any movement of the head.
o Nausea and vomiting
o U/L or B/L hearing loss
o Recent URTI
o Loss of balance and falling in the direction of the affected ear.
 Physical findings
o Spontaneous nystagmus
o Jerking movements of eyes toward unaffected ear
o Purulent discharge
 Lab
o Culture and sensitivity test
 Audiometry
 A flat tympanogram
 Electronystagmography

Management

 Meclizine to relieve vertigo

 Antiemetics
 Antibiotics
 Oral fluids
 IV fluids for severe dehydration
Surgery

 Surgical excision of cholesteatoma

 Incision and drainage
 Labyrinthectomy

Complications

 Meningitis
 Permanent balance disability
 Permanent hearing loss

FURUNCULOSIS

Definition

 Furunculosis is a localized form of otitis externa resulting from infection

of a single hair follicle

Etiology & Risk factors

 Staphylococcus aureus
 Heat, Humidity, Trauma, Maceration
 Colonization of the external nares and, less commonly, the perineum with
the pathogenic strain of S. aureus is also a contributing factor in many
cases of generalized recurrent furunculosis.
 Associated conditions causing it are hypogammaglobulinaemia, diabetes
mellitus and dysphagocytosis.

Pathology

 Bacterial invasion of a single hair follicle results initially in a well-

circumscribed deep skin infection.
  As the infection progresses a pustule forms and this progresses to local
abscess formation, often with considerable associated Cellulitis and
oedema. (Deep skin infection Pustule Abscess Cellulitis and oedema)
 Bacteria attach initially to the cells of the stratum corneum and
proliferate around the ostium of the hair follicle. There is deeper invasion
of the hair follicle between the inner and outer root sheath.

Diagnosis

 Histology is the reference standard for diagnosis (but not done is routine
clinical practice)
 The affected ear is extremely painful, feels blocked and exudes a scanty
serosanguinous discharge.
 The pinna and tragus are tender on palpation.
 Otoscopic examination usually establishes the diagnosis
 If the oedema and secondary Cellulitis spreads to the post auricular
crease, the condition may be mistaken for acute mastoiditis

Outcomes

 If untreated, the infection usually progresses to a localized abscess which

then discharges into the external ear canal. Providing there is adequate
drainage the infection will resolve spontaneously
 The infection can also spread towards the deeper tissues, where it may
cause a diffuse soft tissue infection spreading to the pinna, post-auricular
skin and parotid gland.
 Repeated infection can cause permanent scarring and fibrosis of the
external canal with subsequent meatal stenosis.
Management options

Treatment choices include:

 Oral or systemic antistaphylococcal antibiotics (penicillinase-resistant

penicillin, macrolide, cephalosporin, clindamycin or quinolone)
 Topical treatment (antibiotics, astringents, hygroscopic, dehydrating
agents);
 Incision and drainage.
 Glycerol and ichthammol solution has a specific antistaphylococcal
action and is hygroscopic
 For patients suffering generalized recurrent furunculosis who are carriers
of pathogenic strains of S. aureus : include:
o Eradication therapy with Nasal Mupirocin
o Eradication therapy with Oral Flucloxacillin for 14 days.
o Bacterial interference therapy: deliberately implanting a
nonpathogenic strain of S. Aureus (strain 502A is the most
popular) to recolonize the nares and skin.
o It has been reported that correction of specific biochemical
abnormalities (e.g. hypoferraemia, low serum zinc) may lead to a
marked reduction in the frequency of infections.

COMMON COLD

Definition

 A cold is a common infection of upper respiratory tract. that can be

caused by over 200 different viruses
 The common cold is one of the most common illnesses.
  cold is a mild viral infection of the nose, throat, sinuses and upper
airways.
 It can cause a blocked nose followed by a runny nose, sneezing, a sore
throat and a cough.

Epidemiology

 There are no major gender or ethnicity differences in incidence.

 Most infections occur in the winter period.
 A 2000 US study found that 23.6% of adults had experienced a cold in 4
weeks.
 Children get 6 to 8 colds per year. Adults get 4 to 6 colds per year.

Sourecs of common cold

 The list of types of Common cold mentioned in various sources includes:

o Rhinovirus-related colds - 30-35% of colds
o Coronavirus-related colds
o Adenovirus-related colds
o Echovirus-related colds
o Paramyxovirus-related colds –
o including several parainfluenza viruses
o Enterovirus-related colds

How does a cold spread

 A cold can be spread through:

o Direct contact – sneeze or cough, tiny droplets of fluid containing
the cold virus are launched into the air and can be breathed in by
others.
 o Indirect contact – sneeze onto a door handle and someone else
touches the handle a few minutes later, they may catch the cold
virus if they can touch their mouth or nose.

Pathophysiology

 The mechanism of this immune response is virus specific.

 For example, the rhinovirus is typically acquired by direct contact it
binds to human ICAM-1 receptors(Inter-Cellular Adhesion Molecule 2)
 This receptors present on respiratory epithelial cells.
 As the virus replicates and spreads, infected cells release distress signals
known as chemokines and cytokines(which in turn activate inflammatory
mediators).
 These inflammatory mediators then produce the symptoms.

Signs and symptoms

 Dry or sore throat.

 Runny nose
 Sneezing
 Headache
 Earaches, also brought on by the congestion (especially in children).
 Slight fever and chills
 Coughing
 Feeling tired.

Complications

Colds may aggravate the symptoms of other conditions, such as

 asthma and chronic obstructive pulmonary disease (COPD)

 Cold can also lead to
 o acute bacterial bronchitis.
o strep throat.
o pneumonia.
o ear infections.

Diagnosis

 Symptoms and a physical examination are all the doctor needs to

diagnose the common cold.
 Usually, no blood tests or X-ray are necessary.
 During the physical examination, the doctor will pay careful attention to
the head, neck, and chest.
 Examine the eyes, ears, throat, and chest to help determine if a bacterial
source is causing the illness.

Treatment

 Over-the-counter cold and cough medicines may help ease symptoms in

adults and older children.
 Nasal decongestents
o Oxymetazoline
o Phenylephrin
o Analgesics
o Acetaminophen
o Ibuprofen
o Take plenty of fluids

RHINITIS

Definition
  Rhinitis is defined as inflammation of nasal mucosal lining characterized
by one Or more of the following symptoms:
o Nasal congestion
o Rhinorrhoea
o Sneezing
o Itching

Rhinosinusitis

 It anatomically the lining mucosa is contiguous With that of paranasal

sinuses.
 It goes without Saying that if one is involved the other is also Involved.
Hence instead of using the term Rhinitis it would be apt to use the term “
Rhinosinusitis”.

Symptom complex of rhinosinusitis include

 Nasal congestion
 Rhinorrhoea
 Sneezing
 Itching
 Hyposmia
 Anosmia
 Facial pain
 Head ache

Classification

Allergic rhinitis

 Very common
 Incidence seems to be increasing
  Frequently accompanied by asthma
 Other co existing conditions include
o conjunctivitis Sinusitis and otitis media.

Symptoms

 Repeated attacks of sneezing

 Itiching in the nose
 Rhinorrhoea
 Itching of eyes
 Headache due to congestion of paranasal sinuses
 These symptoms tend to reduce with age

Allergic rhinitis classification

 Intermittent (Seasonal)
 Persistent (Perennial)
 Mild
 Moderate - severe

Seasonal rhinitis

 Also known as intermittent rhinitis

 It usually lasts less than 4 days a week
 The whole disorder lasts for about a month
 Usually caused due to exposure to seasonal Allergens like pollen
 Common during spring when flowers bloom

Perennial rhinitis

 Also known as persistent rhinitis

 Symptoms last for more than 4 days a week
 Whole disorder lasts for more than a month
  This is due to continuous exposure to allergen eg. House dust mite

Mild allergic rhinitis

 Allergic rhinitis is considered to be mild if the symptoms does'nt cause:

o Sleep disturbance
o Impairment of daily activity
o Impairment of work
o Troublesome symptoms

Moderate allergic rhinitis

 This includes one or more of the following:

o Sleep disturbance
o Impairment of daily activity
o Impairment of work
o Troublesome symptoms

Allergic rhinitis pathophysiology

 The reaction occurs in 4 phases

o Sensitization
o Subsequent reaction to allergen – early phase
o Late phase reaction
o Systemic activation

Sensitization
  Grass pollen / House dust mite / cat dander Harmless in non atopics In
atopics gets attached to antigen presenting cells Present in the nasal
mucosa
 These activated APC's stimulate hypersensitivity Mast cells are
responsible for sensitization

Early phase of allergic rhinitis

 Histamine is responsible
 Rhinitis Sneezing Prurutis Mast cell degranulation plays a role
Prostaglandin D2 / cytokines may play a role

Late phase response

 This phase is inflammatory in nature Ingress of eosinophils / basophils /

mast cells / T lymphocytes / neutrophils / macrophages Eosinophils
mature and reside in the nasal mucosa For more than a week Symptoms –
Nasal block / hyper reactivity

Occupational rhinitis

 Can also be considered as one form of allergic Rhinitis

 Allergy could be due to exposure to mice / guinea Pig hair in lab
 Exposure to platinum salts could sensitize a patient

Occupational rhinitis Risk factors

 Smoking
 Intensity / duration of exposure
 Atopy

Investigations

 Skin prick tests

 Radiology
  Nasal swab
 Nasal challenge
 Nasal biopsy for assessing mucociliary function
 Rhinomanometry
 Tests for olfaction

Management

 Antibiotics
 Antihistamine
 Avoid the exposure to dust

EPISTAXIS

Definition

 Bleeding from inside the nose is called epistaxis.

 Seen in all age groups.
 Presents as an emergency.
 Epistaxis is a sign and not a disease

Blood supply of nose

 Nose is richly supplied by both the external and internal carotid systems,
both on the septum and the lateral walls.
 Nasal septum :Internal carotid system
o Anterior ethmoidal artery Branches of ophthalmic
o Posterior ethmoidal artery

Causes of epistaxis

Divided into :
 A) Local, in the nose or nasopharynx.

B) General

C) Idiopathic

Local causes in nose

 Trauma
 InfectionsAcute : viral rhinitis, nasal diphtheria, acute sinusitis.Chronic :
All crust-forming disease, e.g. atrophic rhinitis, rhinitissicca.
 Foreign bodies.
 Non-living: Any neglected foreign body, rhinolith.Living: Maggots
leeches.
 Neoplasms of nose and paranasal sinuses.Benign: Haemangioma,
papilloma.Malignant: Carcinoma or sarcoma
 Atmospheric changes. High altitudes, sudden decompression.
 Deviated nasal septum.

Nasopharynx

 Adenoiditis
 Juvenile angiofibroma
 Malignant tumours

General causes

 Cardiovascular system. Hypertension, arteriosclerosis.

 Disorders of blood and blood vessels.
 Liver disease, Hepatic cirrhosis
 Kidney disease. Chronic nephritis.
 Drugs. Excessive use of salicylates and other analgesics anticoagulant
therapy
  Mediastinal compression. Tumours of mediastinum (raised venous
pressure in the nose).
 Acute general infection.
 Vicarious menstruation (epistaxis occurring at the time of menstruation)

Idiopathic

 Many times the cause of epistaxis is not clear.

Sites of epistaxis

 Little’s area. In 90% cases.

 Above the level of middle turbinate.
 Below the level of middle turbinate.
 Posterior part of nasal cavity.
 Diffuse. Both from septum and lateral nasal wall
 Nasopharynx.

Classification of epistaxis

 Anterior epistaxis
 Posterior epistaxis .

Incidence

 Mostly occurs in children

 After 40 years of age or young adultsCause
 Mostly trauma Spontaneous; often due to hypertension or anteriosclerosis
 Bleeding Usually mild, can be easily Bleeding is severe controlled by
local pressure requires hospitalisation; or anterior pack postnasal pack
often required

Management
  In any case of epistaxis, it is important to know
o Mode of onset
o Duration and frequency of bleeding
o Amount of blood loss.
o Side of nose from where bleeding is occuring.
o Whether bleeding is of anterior or posterior type.
o Any known bleeding tendency in the patient or family.
o History of known medical ailment (hypertension, leukaemias,
mitral valve disease, cirrhosis, nephritis).8) History of drug intake
(analgesics, anticoagulant, etc.)

First aid

 Pinching the nose with thumb and index finger for about 5 minutes.
 This compresses the vessels of the Little’s area.
 In Trotter’s method patient is made to sit, leaning a little forward over a
basin to spit any blood, and breathe quietly from the mouth.
 Cold compresses to the nose to cause reflex

vasoconstriction.Cauterisation

 In anterior epistaxis when bleeding point has been located.

 The area is first anaesthetised and the bleeding point cauterised with a
bead of silver nitrate or coagulated with electrocautery.

Anterior nasal packing

 If bleeding is profuse and/or the site of bleeding is difficult to localise,

anterior packing should be done.
 Ribbon gauze soaked with liquid paraffin
 About 1 metre gauze (2.5 cm wide in adults and 12 mm in children) is
required for each nasal cavity.
  First, few centimetres of gauze are folded upon itself and inserted along
the floor, and then the whole nasal cavity is packed tightly by layering the
gauze from floor to the root and layering the gauze from floor to the roof
and from before backwards
 One or both cavities may need to be packed
 Can be removed after 24 hours if bleeding has stopped
 If it has to be kept for 2 to 3 days; systemic antibiotics should be given to
prevent sinus infection and toxic shock syndrome.

Posterior nasal packing

 For patients bleeding posteriorly into the throat.

 A postnasal pack is prepared by tying three silk ties to a piece of gauze
rolled into the shape of a cone.
 Patients requiring postnasal pack should always be hospitalised.
 Folley’s catheter can also be used.
 Nasal balloons are also available.Endoscopic cautery
 For posterior bleeding point after locating with endoxcope.
 Elevation of mucoperichondrial flap and SMR operation
 In case of persistent or recurrent bleeds from the septum, elevation of
mucoperichondrial flap and then repositioning it helps to cause fibrosis
and constrict blood vessels.
 SMR operation remove any septal spur.

Ligation of vessels

 External carotid
o Ligation of external carotid artery above the origin of superior
thyroid artery
o Embolisation or lgation of more peripheral branches.
  Maxillary artery
o Ligation in uncontrollable posterior epistaxis.
o Endoscopic ligation of the maxillary artery can also be done
through nose.
 Ethmoidal arteries
o In anterosuperior bleeding above the middle turbinate.
o The vessels are exposed in the medial wall of the orbit by an
external ethmoid incision.

Sphenopalatine artery ligation

General Measures in Epistaxis

 Make the patient up with a back rest and record any blood loss through
spitting or vomiting.
 Reassure the patient. Mild sedation.
 Keep check on pulse, BP and respiration.
 Maintain haemodynamics: Blood transfusion.
 Antibiotics to prevent sinusitis, if pack is be kept beyond 24 hours.
 Intermittent oxygen patients with bilateral packs.
 Investigate and treat the patient for any underlying local or general cause.

PHARYNGITIS

Definition

Inflammation of the pharynx is called pharyngitis.

Types

 Acute pharyngitis
 Chronic pharyngitis
Acute pharyngitis

 very common condition encountered in medicine

 One of the poorly understood condition
 Many have no scientific basis
 Several questions remain unanswered
 Do viral infections predispose to bacterialinfection
 Do viral infections involve pharyngeal lymphoidtissue without involving
tonsils?

Etiology

 Viral (42%)
o Adenovirus (most common 31%)
o Epstein –Barr virus(6%)
o Influenza virus(5%)
 Bacterial –Mixed infection common(48%)
o beta-hemolytic streptococci(38%)
o H. influenza -staphylococcus aureus
o diphtheria -gonococcus -anaerobes remain uncertain.
 Fungal –Candida albicans.

clinical features

 Mild infection - discomfort ,malaise ,low grade fever ,congested ,no

lymphadenopathy
 Moderate - pain, dysphagia, headache, high fever. -congested,
oedematous, exudates, enlarged tonsils, lymphoid follicles of posterior
pharyngeal wall, lymph nodes palpable and tender.
 viral infection mild-associated with rhinorrhoea.
 Voice change-severe bacterial infection.
  Gonococcal pharyngitis-mild or even symptomless.

Diagnosis

 History & physical examination

 culture & sensitivity-may be helpful.

Treatment

general measures

 Bed rest
 Fluids
 Warm saline gargle
 Analgesics
 Specific-penicillin g-oral or injection.
 If sensitive- macrolides.

Chronic Pharyngitis

 Characterized by hypertrophy of mucosal seromucinous glands, sub

epithelial lymphoid tissue, even muscular coat.

Types

 Catarrhal (mucosal)
 Hypertrophic

Etiology

 Persistent infections
 chronic rhinosinusitis with post nasal drip
 chronic tonsillitis, dental sepsis
 Mouth breathing-nasal polyp,
  DNS with Hits, allergic/vasomotor rhinitis, nasopharyngeal adenoids,
tumours. -with mouth breathing air is not filtered, humidified and
temperature conditioned
 Chronic irritants-smoking, tobacco chewing, alcohol, highly spicy food
 Environmental-smoke, dust, chemicals, occupational fumes.
 Faulty voice production- misuse/over use

Symptoms

 Discomfort
 pain-more during morning
 Foreign body sensation-constant desire to swallow or clear throat.
 Voice tiredness
 cough

signs

 Catarrhal- congestion
 Vascular engogement, increased secretions
 Hypertrophic-pharyngeal wall thick, edematous, congested mucosa and
dilated vessels
 Posterior pharyngeal wall studded with reddish nodules-(granular
pharyngitis) due to sub epithelial lymphoid follicle hypertrophy
 Uvula congested and elongated.

Treatment

 Etiological factor sought and eradicated

o Voice rest
o speech therapy
o Warm saline gargle
o Severe granular type-chemical or diathermy cautery done.
 TONSILLITIS

Definition

 Inflammation or infection of the tonsils is medically termed as Tonsillitis

 Tonsils are protective (lymph) glands that are situated on both sides in the
throat.
 The tonsils constitute an important part of the body's immune system and
are vital defense organs.
 They protect the body from bacteria and viruses by fighting these as soon
as they enter the body (via the oral / nasal cavity).

Pathology

 When the tonsils get inflamed, they become red, swollen and may
develop pus pockets that start exuding a discharge.
 In cases with recurrent infections, the tonsils may become so swollen
over a period of time so as to almost touch each other
 Tonsillitis is very common amongst children
 No particular gender predilection is seen in cases of tonsillitis.

Causes

 Bacterial and viral infections can cause tonsillitis through droplet

infection
 A common cause is Streptococcus bacteria
 Other common causes include
o Adenoviruses
o Influenza virus
 o Epstein-Barr virus
o Parainfluenza viruses
o Enteroviruses
o Herpes simplex virus

Triggering factors

 Foods with artificial colors and preservatives

 Peanuts.
 Cold foods, cold drinks, Ice creams.
 Changes of weather
 Extremely cold climate
 Damp weather
 Exposure to a lot of pollution.
 Sour fruits, lemon, pineapple, grapes, oranges.

Signs

 Red and swollen tonsils

 White spots (specks or patches) on the tonsils
 Enlarged lymph nodes in neck region
 Bad and foul breath
 Cough
 Running Nose

Symptoms

 Soreness of throat
 Difficulty in swallowing or painful swallowing of food and drinks
 Pain / discomfort while swallowing saliva
 Change of voice
  Pain in the ears (due to common nerve supply of the back of the throat
and ears)
 Headache
 Malaise, tiredness
 Difficulty in taking feeds in babies - this may be the sole indicator in
some cases of tonsillitis in infants

Catarrhal tonsillitis

 When tonsils are inflamed as part of the generalised infection of the

oropharyngeal mucosa it is called catarrhal tonsillitis.

Membranous tonsillitis

 Some times exudation from crypts may coalesce to form a membrane

over the surface of tonsil, giving rise to clinical picture of membranous
tonsillitis.

Parenchymatous tonsillitis

 When the whole tonsil is uniformly congested and swollen it is called

acute parenchymatous tonsillitis

Diagnosis

 Examination of the throat in tonsillitis

o Redness and swelling of the tonsils
o Pus pockets on the tonsils
o Discharge from the tonsils
o In case of peritonsillar abscess, there may be a shift of the involved
tonsil towards the center of the throat. The uvula may be shifted
towards the opposite side (away from the affected tonsil).
  Throat swab - This is used to get a sample of the secretion from the back
of the throat.
 Monospot test - A blood test can detect certain antibodies, which can
help confirm that a person’s symptoms are due to mononucleosis.
 Epstein-Barr virus antibodies - If a monospot test is negative, antibodies
in the blood against EBV might help diagnose mononucleosis.
 Blood tests - This primarily includes a complete blood count (CBC)
which is done to confirm the presence of infection.

Complications

 Local: Severe swelling with spread of infection and inflammation to the

hypopharynx and larynx may occasionally produce increasing respiratory
obstruction, although it is very rare in uncomplicated acute tonsillitis.
 Peritonsillar abscess is one of the complications of acute tonsillitis and its
development means that infection has spread outside tonsillar capsule.
 Spread of infection from tonsil or more usually from a peritonsillar
abscess through the superior constrictor muscle of the pharynx first
results in cellulitis of the neck and later in parapharyngeal space abscess.

Allopathic treatment

 Acetaminophen & Ibuprufen are given for relieving the symptoms.

 Antibiotics are prescribed once bacterial infection is confirmed.
 Tonsillectomy
 For those children's who do not repond to antibiotics
 Quinsy - It is usually treated by draining the abscess and antibiotics.
Sometimes removing the tonsils is needed to treat quinsy.

Prevention

 Avoid close contact with others who are sick.

  Keep children away from kids who are known to have tonsillitis or a sore
throat.
 Remind kids about the importance of proper hand-washing, especially
when around people who appear to be sick.
 Wash and disinfect surfaces and toys.
 Teaching kids to cover their mouths when coughing or sneezing,
preferably using a tissue so that germs do not get on their hands. And
show them how to use tissues to wipe their noses.
 Carry disposable wipes and a hand sanitizer to clean hands

PERITONSILLAR ABCESS

Definition

 Peritonsillar abscess (PTA), also known as a quinsy, is pus due to

an infection behind the tonsil.

Symptoms

 Fever
 Throat pain
 trouble opening the mouth
 Change to the voice.
 Pain is usually worse on one side

Treatment

 Removing the pus

 antibiotics
 Sufficient fluids
 pain medication
 Steroids may also be useful
 Admission to hospital is generally not needed
  Tonsillectomy

Complication

 Airway obstruction
 Aspiration