ENT review and pearls

ENT review and pearls..........................................................................................................................................1

Ear Notes...............................................................................................................................................................5
OME-Glue ear.......................................................................................................................................................6
Cholesteatoma.......................................................................................................................................................7
Otosclerosis...........................................................................................................................................................9
Meniers Disease(MD)........................................................................................................................................13
Facial nerve.........................................................................................................................................................15
AN_Cerebello-Pontine angel Tumor...................................................................................................................20
Congenital SNHL................................................................................................................................................25
Congenital hearing loss and syndromes with hearing loss...................................................................................25
Sudden Hearing loss(SSHL)...............................................................................................................................27
Presbycusis..........................................................................................................................................................30
CT terminology and consideration......................................................................................................................30
Grommet insertion current trends........................................................................................................................33
Keratosis obturans...............................................................................................................................................33
Anatomical notes and landmarks.........................................................................................................................35
Facial recess........................................................................................................................................................36
Surgical notes-Tympanoplasty- mastoidectomy..................................................................................................37
Stepedectomy......................................................................................................................................................38
Endolymphatic sac decompression......................................................................................................................42
Tuning fork tests.................................................................................................................................................44
Myringitis granulosa...........................................................................................................................................46
Middle ear cleft, Tympanum...............................................................................................................................47
Rhynology...........................................................................................................................................................49
Epistaxis..............................................................................................................................................................49
Sinusitis and scoring system................................................................................................................................51
Nasal polyposis...................................................................................................................................................60
inverted papilloma(IP).........................................................................................................................................62
Antrochoanal polyp ACP-..................................................................................................................................64
Juvenile angiofibroma (JNA)..............................................................................................................................64
Rhinoscleroma....................................................................................................................................................66
Allergic rhinitis...................................................................................................................................................67
FESS...................................................................................................................................................................67
FESS complications............................................................................................................................................68
Agger nasi(heap):................................................................................................................................................70
Haller cell:...........................................................................................................................................................70
Onodi cells..........................................................................................................................................................71
Concha bullosa....................................................................................................................................................72
Faciomaxillary trauma.........................................................................................................................................74
FACIO-MAXILLARY INJURY......................................................................................................................74
Total Maxillary swing approach..........................................................................................................................79
Lemierre syndrome.............................................................................................................................................79
Susac syndrome ( ......................................................................................................................80
Youngs syndrome: (similar to immotile cellia) Exposure to mercury................................................................80
Nasal cholesteatoma............................................................................................................................................80
Endoscopic Frontal sinuplasty.............................................................................................................................85
Pharynx and Laryngology...................................................................................................................................86
Killian's dehiscence.............................................................................................................................................86
Phaynigeal suppuration.......................................................................................................................................87

Parapharyngeal space(PPS) Tumor.....................................................................................................................88

SLN (Superior laryngeal nerve............................................................................................................................92
Superior laryngeal nerve paralysis......................................................................................................................93
Hoarseness of voice.............................................................................................................................................95
Spasmodic dysphonia current management trends............................................................................................101
Laryngopharyngeal reflux.................................................................................................................................102
Epiglottitis.........................................................................................................................................................103
Subglottic stenosis (SGS)..................................................................................................................................104
Obstructive sleep apnea(OSA)..........................................................................................................................106
Myocardial ischemia and infarction..........................................................................................................113
Oral Manifestations of Systemic Diseases.........................................................................................................113
Hematologic Disorders.............................................................................................................................114
HIV Disease......................................................................................................................................................119
Aphthous like ulcerations.........................................................................................................................119
Cutaneous Diseases.......................................................................................................................................119
Eosinophlic oesophagitis...................................................................................................................................120
Anatomy of neck spaces....................................................................................................................................121
Types of sulcus vocalis......................................................................................................................................123
Sialosis..............................................................................................................................................................124
Audiology Highlights and notes for ENT master candidates.............................................................................134
PTA (Pure-tone audiometry...............................................................................................................................135
Types of hearing loss................................................................................................................................135
Speech audiometry............................................................................................................................................137
Otoacoustic Emission (OAE)............................................................................................................................138
Acoustic reflex..................................................................................................................................................140
ABR.................................................................................................................................................................. 142
Electrocochleography........................................................................................................................................144
Implantable Hearing Aids..................................................................................................................................146
What is a Baha?.................................................................................................................................................147
Digital hearing aids with enhanced processing and features..............................................................................148
Audiology Site of Lesion_cards........................................................................................................................149
Dysphasia......................................................................................................................................................151
Ear pearls and cases..........................................................................................................................................152
Problem solving:...............................................................................................................................................154
Pharynx pearls and cases...................................................................................................................................155
http://www.ncbi.nlm.nih.gov/pmc
http://www.ajronline.org/content/177/6/1465.full
http://www.drtbalu.co.in/index.html
http://lessons4medicos.blogspot.com/search/label/ENT
http://www.ent.com.au/Information%20For%20Students.htm
Oral Q:
Ear:Complications of CSOM- sites of otoscleroma-Stridor- SOM RxCholestatoma theory, hidden sites- improve CHL=bridging the gap by cholestatoma
Otosclerosis-MeneireBells- multiple papillomatosis- otomycosis
DD of blue-red ear drum
DD of vertigo+ discharge
Lat sinus thrombosis: Tobey Ayer test- Griesenger sign
Petrositis- Brain abscess-extradural
Nose:Epistaxis- Angiofibromy: bleeds? Lack of muscular coat-vestibulitis- oroantral fistula
Atrophic rhinitis-DD of unilat nasal obst not responding to Rx=FB

Rhinosceleroma-stages- intracell do not use penicillin- Rx: streptomycin

Laryngitis types- Reinke edema-Laryngomalecia- cong web- VC mass in 20y/o-comp of TracheostomyLudwig
Tensor muscle of pharynx-Quinzy
When do paertial/total laryngectomy
Apnea-OSA- inves
( supra-laryng obs=snoring, lower bronch= asthma, allergy
2012 -November
Cranial compl of CSOM
Nasal Mass( Unilat-Bilat) VINDICATE
Esophageal dysphagia-Obstructive sleep apnea
Topo diagnosis of Facial palsy
2007
2010
2011
2012- April
Otologic facial palsy

Cranial comp of
CSOM
Cystic nasal lesion

Unilateral nasal mass

Otologic facial palsy

SNHL

Oropharyngeal ulcer
VC paralysis

Benign lesion of nose

and paranasal sinus

Sudden
SNHL( discuss one of
them)

Stridor-CSOM(

Unilateral nasal mass

Otoclerosis

Cancer larynx
Trauma of Middle ear

Esophageal dysphagia

Unilateral VC
paralysis

Acute laryngitis
Compl of Ch sinusitis

Tonisllar abscess
Trauma of Middle ear
and temporal bone

Pharyngeal manif of
systemicDx

Obstructive sleep
apnea

Suppurative pharynx
cancer larynx
CHL with intact TM

Audiology
http://home.mans.eun.eg/FacMed/arabic/postexams/msterexam_ENT.htm
ENT master exam-Mansoura University
Verification of Hearing aid fitting
Verbotonal method of rehab
BAHA- K Amp
Evoked potential in dizzy pt
MMN-Audiometric config
Diag of Cochlear dead region
Masking of low tones by high ones ,vice versa
Find overall SPL of 2 identical sound source,
each produce 60 dB SPL
Discuss sound cues for localization
Clinical application of speech audiometry
Tone decay
Metabolic hearing loss= Otosclerosis
Recruitment
BPPV

improve signal to noise( S/N ratio) hearing aid

Values , limitations of digital tech in hearing
aids
Rehabilitation of multiple handicapped child
Inner ear prostheses
Unilateral hearing loss with normal otoscopy
(otoscelorosis- tymnaposcelorosis)
Tennitus(theories, assessment and management
Implantable devices for hearing loss
PTA Speech audiometry
Acoustic emission
Acoustic reflex
Evoked response audio
Electrochocleograph--ABR
Presbyacusis

DPOAEs
Common mode rejection
Electric microphone
Speech audiometry calibration

Speech disorders(Dysphonia- diag of voice

disorders- Aphasia
Delayed language in kids
Rhinolalia

Ear:

Nose:

Pharynx- Larynx:

Otoscelerosis, Diag, managCarhart notch DD,

Otalgia-Menieres disease
Cholesteatoma
BPP vertigoConductive hearing
Sudden SNHL
Facial Paralysis( traumatic)
Bells Palsy

Smell disordersUnilateral nasal massUnilat proptosis

Frontal sinusitis ,
complications

Hoarseness in Middle,old age

Suppuration of Pharynx
Subglottic stenosis
Parapharyngeal mass
Cancer oesophagus
Early cancer larynx
Oral manifes of systemic Ds
Stridor in childern
Cancer togue
Tongue swellings
Cystic lesion of the jaw
Jaw swellings
DD of submandibular swelling

Operative
Parotid tumors-Post op
haemorrahgic diathesisFactors affecting wound
healing
AOM-CSOM

AOM

Tubo-tymbanic

FAHM(fever,
anorexia, headache,
malaise
CHL

CHL(CHL)in large posterior

perforation( lost round window
baffle effect)and discharge for
years
Profuse
Mucopurulent
intermittent
oderless
Exam
Central perfor

-/+ discharge

Signs
TM(congested)
bulge/-/+perforation

Edematous mucus mem-+ polyp

Atticoantral=Cholesteatoma
CHL+ discharge

Scanty
Purulent
Continuous
Offensive
Attic/marginal perf
Choles. Debris-+ polyp

TB Nose
Syphilis nose(Bone)

Anterior cartilage perf

Posterior( Bone vomer) perf

Syphils Larynx

Anterior

TB larynx

Post( interarytenoid)
OME-Glue ear

Etiology:1. OME preceded by an episode of AOM. common in children who is prone for URTI. viral damages
the eustachean tube epithelium.2. Craniofacial abnormalities: cleft palate =poor eustachean tube function =
Otitis media with effusion. despite a surgical repair. Down's syndrome : prone for OME. Note: Children with
bifid uvula donot appear to have higher incidence of OME
3. Allergy: Previously nasal allergy has been postulated as an important factor in the developmentof Otitis
media with effusion. Studies have been unequivocal.
4. GERDS: common in children with OME. ,hi pepsin .
5. Parental smoking : important predisposing .
Age : bimodal distribution. @ 2years of age, @ about 5 years of age. =preschool . Seasonal association: OME
common in winter =URTI, closer contact with affected children. , seen during rainy season.
Clinical features: A high index of suspicion ,. Every child with URTI must be otoscopically examined.
Otoscopic findings: TM: may be bulging, or retracted with a distorted cone of light. drum : yellow, blue or
white. Pneumatic otoscopy will reveal : restricted mobility. Microbiology of OME: effusions is sterile. Rarely
bacteria could be cultured. The incidence of these pathogens are higher in children under the age of 2, and in
children with recurrent upper respiratory infections.
Investigations:PTA: Demonstrates mild to CHL .Tympanograms (Type B) is commonly with OME. Type A is
infrequently associated while Type C falls somewhere in between.
Tympanometry : screening test to identify patients with OME. PTA: CHL
Management:1. Amoxycillin is the drug of choice followed by cephalosporins.2. Nasal decongestants like
oxymetazoline / xylometazoline.3. Topical nasal steroids : in resistant cases.4. Autoinflation of eustachean tube
by valsalva maneuver. Balloon blowing may also help. Surgical management:1.
Adenotonsillectomy2. Myringotomy and insertion of ventilation tubes
Cholesteatoma
a cyst of keratin sq epith, avascular in the middle ear, mastoid and temporal bone
Congenital : a "small white pearl" behind an intact TM (ant/ medial to malleus) or as a CHL
due to aberrant migration of ectoderm
not associated with otitis media/eustachian tube dysfunction
Acquired (common) consequence of CSOM, or ETD( tube dysfunction
retraction pockets in the pars flaccida ,and marginal perforations (2" acquired) of the TM
chronic inflame= progressive destruction of surrounding bony structures
Bactria in CSOM: PP= Pseudomonus- Proteus
Toss classification
symptoms: history of otitis media ,ventilation tubes. ear surgery
progressive CHL , may SNHL in late stage) improve Hearing if bridging over ossciles
otalgia, aural fullness, fever= intracranial complication
signs: retraction pocket in TM, keratin debris- TM perforation, Fistula test+ if complication
granulation tissue, polyp visible on otoscopy- malodorous, unilateral otorrhea
Complication of Cholesteatoma
Local: Ossicular erosion: CHL-Inner ear erosion: SNHL, dizziness= labyrinthitis
Temporal bone infection: mastoiditis, petrositis , VII paral
Intraracranial complicatin
Meningitis-Sigmoid sinus thrombosis Intracranial (subdural, epidural, cerebellar) abscess
Modified Radical Mastoidectomy
eradicate disease of the epitympanum and mastoid , accessible cavity by removal of post,and superior EAC
walls. TM and functioning ossicles are left intact. hearing preserved.
Radical Mastoidectomy:in extensive, complicated Ds( osscilce, VII, labrynth, fistula)to eradicate (ME,
mastoid ) ME is exteriorized =cavity with EAC. TM, malleus, incus, chorda tympani, mucoperiosteal lining
are all removed.

Cortical

Modified radical

radical

Limited Ds
Land mark
Spine of Henle

Not extensive

In child, extensive

Mcewan triangle= suprameatal

triangle or mastoid fossa
Mastoid antrum 1:2 cm deep to triangle.
anterior - posterior border of EAC
superior :posterior root of the zygomatic
arch

posterior bony canal wall (PCW),

mastoid bowl is saucerized.
air cells are removed inferiorly, digastric
ridge(DR) is identified and preserved as a
pointer to VII.

tegmen(T) and the sigmoid sinus(SS)

As the tegmen is exposed superiorly, the sinodural angle(SA) is
defined and all air cells removed in this area, an important part of
mastoid surgery for cholesteatoma

Classification of Tympanoplasty by Wullstein(= Myringoplasty+TORP/

Type Damage to Middle Ear
Method of Repair
I
II
III
IV

Perforated TM+ normal ossicular

chain
Perforation of TM+ erosion of
malleus
Destruction of TM and ossicular
chain ( intact and mobile stapes)
III+( head, neck, and crura of stapes

Closure of perforation, type I same as

myringoplasty
Closure with graft against incus or remains of
malleus
Graft contacts normal stapes. Also gives sound
protection for round window.
exposed or graft attaches to mobile footplate; air

missing; footplate mobile

V

Similar to type IV plus fixed

footplate.

pocket between round window and graft provides

sound protection for round window.
Fenestra in horizontal semicircular canal; graft
seals off middle ear to give
sound protection for round window

Patch Test
When ( CHL+ central perforation, it is possible to assess damaged ossicls by patching ( Teflon)
perforation. If hearing improves= ossicular chain is intact, and that myringoplasty is likely to succeed.
Otosclerosis
AD- fissula ante fenestram (MC site) then post crura, cochlea F :M(2:1)+ Measles
female 30yr, bilat, prog HL while chewing, after pregnancy, Family hist
C/P (CHL, mixed) Tinnitus, paracusis willsi, tinnitus,+/-Vertigo,
Otoscope: 90%: normal TM or Schwartz sign, role out OME
Inve: audiometry: CHL/Mixed/ SNHL (First low tones CHL)If SNHL( high tones affected)- Carhart notch =Cookie bite
Tympanometry: As- decrease compliance
Stapedial reflex: biphasic, reduced, then lost
CT: double ring sign/halo
TX: Hearing aid(old pt) stapedectomy/ laser stapedotomy (young pt)
NaFl in :SNHL-(+schwartz)- child- pregnant women- if pt refused surg
Compl of syrgery: floating foot plate, perilymph gusher, chorda, VII n inj, SNHL
Shambaugh's 7 criteria to identify SNHL due to otosclerosis
Carahart's notch: dip around 2k Hz and recovery at 8kHz( 5dB at 500,10 at 1k, 15@2k)
Some consider carhart's notch artifact. This notch is closely related to the carhart's effect.
Carhart's effect: after stapes surgery, over closure of air bone gap. = improve in hearing at 2 KHz.
How carhart's effect is created?skull vibrates by bone conduction, sound is transferred to cochlea via( 1. direct
vibration of skull ,2.vibration of ossicles 3. via EAC (normal route)In CHL routes 2 and 3 are affected, but can
be regained following successful stapes surgery. Hence bone conduction thresholds improve around 2 KHz.
1-phases of otosclerosis: 1. otospongiosis (early: inc bone resorption and vascularity, new spongy bone - 2.
transitional phase 3. otosclerosis (late phase): dense sclerotic bone.
3.biscuit footplate: otosclerosis involving only the footplate, sparing annular ligament (high risk of postop
SNHL because of minimal fixation - footplate can become mobilized inadvertently)
4-What percentage is round window involved?: 30%
* 1% of caucasian, 2:1 female ratio
*genetic: AD - incomplete penetrance
*hearing loss type - otosclerosis: primarily CHL/mixed and SNHL
*how often is the of clinical cases, complete closure is rare
9.mechanism of SNHL in OS: toxic metabolities in inner ear, vascular compromise, extension to cochlea.
SNHL usu associated with stapedial otosclerosis.
10.obliterative otosclerosis: otosclerosis that fills oval window niche
11.What is % of OS with dizziness: 30% - OS lesions in lat SCC +veENG. called OS "inner ear syndrome"
12.physiological etiology of otosclerosis: abnormal deposition/resorption of bone
13.shambaugh's 7 criteria for otosclerosis.:
1. Schwartze sign in either ear-2. Family history of otosclerosis
3. Unilateral CHL consistent with otosclerosis and bilateral symmetric SNHL
4. audiogram with a flat / "cookie - bite" curve with excellent speech discrimination
5. Progressive pure cochlear loss beginning at the usual age of onset for otosclerosis

6. CT : Halo sign= demineralization of the cochlea

7. Stapedial reflex : biphasic "on-off effect" seen before stapedial fixation
14.what is cochlear otosclerosis: pure SNHL without CHL.
15.what is schwartz sign?: red hue behind TM - vascul promontory = active (otospongiosis). in 10%
16.what is the most common location otosclerosis?: fissula ante fenestram (anterior to oval window) =90% .
Border of round window, apical medial wall of cochlear, posterior to cochlear aqueduct, adjacent to
semicircular canals, stapes footplate itself.
17.what type of bone does otosclerosis begin in: endochondral bone - as it evolves the endosteal and periosteal
layers become involved
Surgery: * contraindication for stapedectomy: Meniere's (enlarged endolymphatic space, saccule may be
adherent to underside of stapes footplat( risk of SNHL, PSA(persistant stapedial artery)- floating foot plate
DD of OS:
1-typanoscelerosis- aseptic necrosis of malleus-paget dis-Osteogenis imperfect-Cholesteatoma3-Superior SSCCD dehiscence:CHL similar to otosclerosis,mobile ossicles and TM on pneumatic otoscopy
vertigo or nystagmus with loud noise, pneumatic, or valsalva
Oscillopsia:pressure induced vertigo- Sound induced vertigo= Tullio phenomenonAutophony( hear own heart-sound)-pulsatile tinnitus
- CT : defect of superior canal dehiscence
- CHL+ air-bone gap, normal TM, +hyperacusis to their pulse or eye movements.
BC < 0 dB NHL=supranormal, intact reflexes, and normal speech discrimination.

4-Ossicular discontinuity: avasc necrosis of incus

- conductive loss of 60 dB usually without sensorineural component
- flaccid TM on pneumatic otoscopy
- type Ad tympanogram
5-Congenital stapes fixation
No Family history, non-progressive CHL, first decade of life
- 25% incidence of other anomalies (3% for juvenile otosclerosis)
6-Malleus head fixation
- when congenital, + (aural atresia), tympanosclerosis
- pneumatic otoscopy,type As tympanogram (only in advanced otosclerosis)
7-Pagets disease(osteitis deformans)
- diffuse involvement of the bony skeleton
- elevated alkaline phosphatase
- CT - diffuse, bilateral, petrous bone , extensive de-mineralization
- More commonly crowds the ossicles in the epitympanum, partially fixing
the ossicular chain
8-Osteogenesis imperfecta
- blue sclera, multiple bone fractures
- CT more common involves the otic capsule and to a greater extent
Physical Exam:
TM : normal in 90%. (Schwartze sign)10% : red promontory and oval window = active Ds (vascularity ).

Rinne test :Early, low frequency CHL , negative Rinne ( 256-Hz only. then : 512 then 1,024.
Otosclerosis is 2ed MCC of CHL in age 10-45 (eftar cerumen impaction)
Audiometry
Tympanograms : A low peak /normal ME pressure = type As (stiff,stunted), malleus fixation:= advanced Dx
II_Acoustic reflexes : first sign (before any CHL) 1-diphasic reflex pattern (on and off). (posterior footplate
moves with stapedius contraction and relaxation). 2-As stapes fixation progresses, reflex is reduced, hi
ipsilateral, then contralateral thresholds, and finally,3- Loss of the reflexes altogether.
PTA: assess severity , frequency specific. first sign: AC in low frequency, (< 1000 Hz. The rising air line =
stiffness tilt , caused by compliance 2ry to stapes fixation. with progresses, the air line flattens=otosclerotic
focus has a mass effect on the entire system. involve the cochlea : bone conduction thresholds. ( high
frequencies are affected first , focus near basal turn of the cochlea. More isolated cochlear otosclerosis may =
mixed hearing loss with a cookie-bite pattern with both air and bone lines.
Carhart notch : hallmark bone conduction thresholds ( 5 dB at 500 Hz, 10 dB at 1000 Hz, 15 dB at 2000 Hz,
and 5 dB at 4000 Hz. It mechanical artifact , not a true cochlear reserve. (stapes fixation disrupts normal
ossicular resonance / perilymph immobility of stapes fixation. As it disappears after stapedectomy.
bone conduction improves + air conduction: results based on postoperative air-bone gaps. This prevents
overclosure, postoperative air line is compared to the preoperative, which may result in a air-bone gap closure
of more than 100%, even when a postoperative gap is present.
Majority of cases associated with conductive or mixed hearing loss.
No firm evidence to support or refute relationship of SNHL and cochlear endosteal involvement exists.
Imaging
It is controversial if needed. CT : extent of focus at oval window and , when diagnosis is in doubt
(mixed hearing loss).to determine if capsular involvement is present. An enlarged cochlear aqueduct =
potential perilymph gusher during footplate fenestration or removal.
CT :evaluating the post-stapedectomy ,who had a good result but then lost. The coronal is the best view for reobliteration of the oval window , position of the prosthesis. Necrosis of long process of incus can also be
detected. If vertigo, = piston displaced medially in to the vestibule. hyperacusis and a Tullio phenomenon or
Hennebert sign = CT evaluation for superior semicircular canal dehiscence. Foci of early or active otosclerosis
or otospongiosis are poorly calcified and may actually make the oval window appear larger than normal. As
re-ossification = oval window appears smaller or obliterated by bone. In cochlear otosclerosis, ( ring around
cochlea= double ring effect = halo sign+ve in CT= > 1mm focus density , different from normal otic
capsule, and it must appose the periosteal or endosteal surfaces of the capsule.
Management
Asymptomatic in90%. The average age is 20 years. CHL progressive / mixed. Rarely is pure
SNHL .progresses in a stepwise fashion, ( quiescence /deterioration. worsening hearing+ worsening tinnitus, a
positive Schwartzes sign, mild imbalance. foci mature by age 50 :70, ( 50 dB CHL+SNHL.
Patient selection and preoperative counseling
best treatment : results of tuning fork , audiometry, skill of the surgeon, patient wishes/individual
basis. avoid rushing, best candidate : socially unacceptable ABG, a negative Rinne test, excellent
SDS(discrimination, and the desire for surgery.

2- age, occupation, prior stapes surgery(poorer results in the high frequency range). Children with congenital
stapes fixation = lower success rate of ABG closure (44%) / juvenile otosclerosis (82%). Younger patients : reossification. (divers, pilots, airline stewardess) were counseled ( risk offistula ) with small fenestra
technique, newer pistons, , displacement of prosthesis and perilymph fistula is no more common
Most discourage :Meniere's /any vestibular symptom is a contraindication to surgery. greater risk of SNHL
after stapes surgery. injury to the saccule which is dilated and abuts the oval window. Further testing in these
patients with ENG and electrocochleography. Tympanic perforations repaired prior to stapedectomy. Active
otitis media or the presence of cholesteatoma is a contraindication to stapedectomy.
Patients with downsloping SNHL / mixed loss = poor speech discrimination, not improve after surgery
and may even worsen. In addition, these patients are considered to have a compromised cochlea with
sensorineural loss often worsening after any degree of intra-operative trauma.
Surgery: Stapedectomy: reverse stapedectomy
Variations Encountered at Surgery

Persistent stapedial artery(PSA)= stop surgery

Round window obliteration

Prominent promontory

Facial dehiscence

Narrow oval window

Gusher

Floating footplate

Depressed fragments

Obliterative otosclerosis
Complications

Altered taste in about 20% of cases but almost all resolve with time.

Infection, meticulous cleaning of the canal should reduce this risk.

Vertigo: minor , settle within few hours. If severe and persistent might suggest perilymph fistula.

Perilymph fistula: need re-exploration.

Tinnitus

Sensorineural hearing loss: 1% - severe or total sensorineural loss. Rx tapering high dose steroids.

Facial palsy, rare complication may be delayed in which case steroids should be used.

Granuloma: gradual post operative hearing loss after initial good result.

Perforation of TM, this can be repaired easily at the same sitting.

Medical: Bisphosphonates Fosamx( Alendronate)-Zolendronat(Zometa) fluoride ion replaces hydroxyl ion in
periosteal bone, = bone resorption and calcification of new bone. Improvs: tinnitus , vertigo, Schwartzes
sign becomes negative. side effects osteonecrosis, arthritis, and gastric distress. dose : 20-120mg of fluoride a
day. for children and pregnant women. After 2 years, re- evaluate: Schwartzes sign, tinnitus and
imbalance , a CT scan is repeated. If Dx is stabilized, placed on a life-long maintenance : 25mg of fluoride a
day.
use of NaFl : debated. no evidence of histologic improvement ,Shambaugh, supports demonstrated its value
in arresting progressive SNHL. Sodium fluoride :not surgical candidates, SNHL or vestibular symptoms due
to otosclerosis. , active focus = Schwartzes sign may be given fluoride treatments for 6-12 months prior to
surgery to induce focus maturation. If the focus is active during surgery, postoperative treatment can be

10

initiated. Overall, 50% : stabilization, 30% improve, and the rest continue to progress. Stopping treatment in
those patients who stabilized while on therapy may result in a reactivation of the disease in 2-3 years.
Contraindications of fluride: chronic nephritis, rheumatoid arthritis,pregnant / lactating, children, allergy
http://www.utmb.edu/otoref/grnds/Otosclerosis-061018/Otosclerosis-061018.htm
Vistibular Schwannoma/Acoustic Neuroma:
C/P: unilat tinnitus, gradual SNHL, may be sudden, vertigo(absent if compensation)
+/- VII -V palsy -( loss of corneal reflex) early
(jugular foramen synd)VII, IX,X,XI,XII choking, hoarsness, drop shoulder
Cerebellar: ataxia, imbalance-disdiadkokinesia
Late: ICT, headache, hydrocephalus, coma, death
Inves: Gadolinium-enhanced MRI ( gold standard)
audiomety(asymmetric (SNHL) at high frequencies (down-sloping).
Speech discrimination (SDS)=Word recognition SDS out of proportion of pure tone thresholds
(PTT).stapedial reflex decay then lost
Stacked ABR( delay waveV>0.2ms) sensitive and specific 90% for large tumor
ENG:Electronystagmograph: response to caloric test
TX: observe: wait and scan, small(<1cm) old age, poor health( MRI/yearly)
50% of tumors remain same size
Surgery (retrosigmoid or in good hearing or translabrynthine if bad)
Radiation: Gamma knife= Sterotactic
AAO-HNS classification ( 1995, patients falling into 4 categories (classes)
Serviceable hearing
class A (>70% SDS and < 30
ClassB (>50% SDS and < 50
Speech discrim score SDS
dB PTT loss) Pure tone
dB PTT loss)
testing
non-serviceable. Hearing
Class C (>50% SDS, > 50dB
class D (< 50% SDS)
PTT loss)
Cause of hearing loss in AN: ??. gradual or sudden (compression on VIII nerve, vascular disruption of int
auditory artery, and biochemical changes in inner ear fluids.
hearing could be normal even in larger tumors > 3 cm.
Hitzelbergers sign: =vestibular schwan, Taste in Ant 2/3 of tongue, lost sens in post wall of EAC
Meniers Disease(MD)

Mechanism( Autoimmune-idiopathic, sympathetic, viral-Syphilis- Chochlear ostosc-) build up in pressure -micro-ruptures of memb labyrinth( hydrops may not have Menier) Bilateral in 50%(Compression on scala
media to scala tympani)
C/P: Male 40 yr, attacks (Vertigo= 20 min, Tinnitus, SNHL vomiting in severe case

11

 Lermoyz SNHL improves with vertigo Revers Lermoyz

Tumarkin :drop attacks
Hennerbert sign:False +ve fistula test in 25%
Invest: Audiometry: Fluctuant SNHL( low tone early), poor SDS (matches PTA)
Glycerol test(PTA after glycerol, PTT improve by 10dB
+ve recruitment= Cochlear, ABR: normal wave V, -ve tone decay( + in Retrococh)
ECG(Electrocochleography: diagnostic(SP/AC ratio > 2fold(not sensitive nor specific)
Summation potential:Action potential
ENG Electronystagmograph: response to caloric test- Rotatory nystagmus
DD: BPPV-pure Cochlear Otosclerosis- Dix-Hallpike testTx: medical: Frosting diet (low salt)diuretics, antivertigenous ,e betahistine, steroid= placebo
Surg: Vestibular neurectomy-succus decompression- inject of Streptomycin/gentamycine(vestibulotoxic ), prednisolone- vancyclovir ,mycostatine/steroid-( daily/weeky/once) intra aural ( absorbed by
round window) Labrynthectomy
When to preserve hearing: SDS>20%, PTT>70dB
Tx of bilateral MD: streptomycine, mycostatin, pressure device(safe, effective)
9S(salt, smoking, stress, symptomatic,sedatives,steroid, streptomycine, success
decomp+ shunt) (betaserc)
Round window catheter: transtympanic: -Gentamycin
Tonotomy:cut tensor tympani( neck of malleus)
AAO-HNS calssification
Possible MD (vertigo >20 min) not documented HL, or SNHL:fluctuating or fixed, with
dysequilibrium but without definitive episodes
Probable MD :1 definitive episode of vertigo, Tinnitus or fullness, documented HL
Definite MD: 2 or more vertigo >20 min , Tinnitus or fullness, documented HL
Certain MD :Definite MD, plus histopathologic confirmation
DD of vertigo: Syphilis(periph vestibulopathy)Cogans(non Syph keratitis)- Cholesteatoma,Vest neuritis,
BPPV(Post SCC otolith),SCC dehiscence , Acoustic neuroma, CPA tumor, AOM, MS,
Migrain(MAV)disembarking, Vertebrobasilar insuff ,ETD with stapedopexy
Labrynthitis: days,+ SNHL/may be CHL if colesteatoma
Acoustic neuroma: progressive unilateral SNHL( hi frequency)
Vestibular neuritis: days, no hearing loss, history of flu, rhinitis
BPPV: seconds, disappear when position change, no hearing loss, fatiguabley
MAV: mainly headach, vertigo, is mild(no vomiting) lasts for minutes
Glomus Jugulare/Tympanicum
Slow, invasive benign vascular tumor arise from non-chromaffin paraganglion
C/p: Female 20-50 pulsatile tinnitus, CHL then later SNHL, bleeding/ear, VII pasy(early)
Hormonal(epineph) headache, flushing, tachycardia, sweating
Types( jugulare, Tympanicum, vagale, carotid body)
Browns sign (red rising sun behind TM blanch on pressure) poly(friable, bleed)
Tuning fork: CHL, then SNHL
Jug foramen syndrome(VII,IX, X,XI,XII)
Inv: CTMRI : typical salt and pepper mixture of intensities ( T1 and T2 ).
Angiography : Lyres sign (splaying of carotid bifurcation)
VMA:24 urine if hormonal function 10%, serum epinephrine level

12

Audiometry, Tympanogram: pulsatile waves

TX: preop embolization+ excision( trans tympanic, facial recess, inferior temporal)
Observ, wait and scan:, CT and/or MRI scans periodically(very slow growth)
DD of pulsatile Tinnitus: 4As
Objective: dural AVM- PSA(pers stapedial artery), Glomus, Carotid aneyrysm,SCCD
Subjective:Thyrotoxicosis, anemia
persistant stapedial artery: never ligate it, as it might be the only internal carotid artery)
Facial nerve
Sunderlands classification of nerve injury
First-degree: neuropraxia": compression or ischemia (conduction block, )recovery 2-3 weeks
Second-degree axonotmesis, wallerian degeneration; recovery at 1mm/day
Third-degree: endoneurium disruptured, ,recovery ( poor to complete.
Fourth-degree: interruption of all neural and supporting; perineurium intact; nerve is enlarged.
Fifth-degree: complete transection with loss of continuity.
House Brackmann Grading: III/VI
I: normal, II: mild, III, mod: complete eye closure, IV:incomp closure, V:asymmetry at rest, VI complete
Evaluation : Onset, course, Duration, Progression (no improve after 6 months= Tumor)
Associated s: Fever-Pain behind ear ( 1st symptom), SNHL-Aural fullness, Vertigo-vesicels=H Zoster
History of Previous VII paralysis, CSOM-Surgery-Trauma, infec( Herpes,Lyme= Bilateral)
Physical Exam: asymmetry, House Brackmann Grading
vesicles In EAC, soft palate, or concha:HZ, parotid mass- Bells palsy:@ stylomastoid
- Hitselbergers sign: Cant taste burger! taste in ant 2/3 of tongue=A.Neuroma,
- Electromyography: prognostic only
- Electroneurography (3 :12 days of injury, degeneration >90%,not useful in acute setting:
Audiogram- Nerve conduction velocity
Topognostic tests: Taste quantitive, qualitative, Schirmer(lacrim), saliv flow, stapedial reflex
Injury@geniculate or @ transverse=loss of (taste-salivation-lacrimation)- hyperacusis
blood tests: Lead, Sarcodosis(ACE, Ca), Syphylis(, Malaria, mono spot test) PCR of Blood & saliva for EBVCMV,
Rx: hypoglosso-facial anastomoses (reliable for re-innervation of facial muscles
Idiopathic (Bells palsy) common , 15-40/100,000, recurrent,40% ( family history
Probable causes:Viral (HSV,VZ,IMN), Vascular, Polyneuropathy, autoimmune
- Diagnostic criteria: Sudden
o If complete paralysis: perform electrophysiologic testing
- Treatment :Self-limiting
- Eye protection : artificial tears / day, sunglass , jelly and eye patches at night
o Steroids + antivirals ( eg. Acyclovir) = improved outcome 800mg for 5 days
o IVIG if GBS is suspected(Bilat palsy,cytoalb dissociation, ascend paralysis)
o Surgery (decompression) is controversial; mostlyimprove in 4-6 months
Infection: H.zoster- (prodromes vesiculs on EAC,palate, SNHL, tinnitus, vertigo (Ramsay Hunt
syndrome) HZ is dormant in geniculate ganglion
- Treatment: Steroids + Acyclovir 800mg/d*5days+ analgesics Worse recovery
Conginital: 2M( Milkersson Rosenthal, Mobius
Tumor: schwanoma of VII or VIII, menigioma, cholesteatoma, hamangioma

13

Systemic Ds cause facial nerve paralysis

- 4 Syndromes: Guillan Barre, Milkersson Rosenthal, Mobius, Heerfordts=SarcoidosisInfection: mononucleosis, Malaria, Menengitis 4 Ls:Leprosy, Lyme Leukemia, Lead ,HIV
- poison, Sarcoidosis
- Bilateral palsy= Mobius-Melkerson, Lyme, Lead Guillan Barre
Facial nerve anatomy: Pons to internal auditory canal (IAC) 24 mm (parasymp+motor+sensory=nervus
intermedius)
Intratemporal segment
Meatal segment 8-10 mm; porus acusticus to meatal foramen of the IAC
- Labyrinthine segment(Fallopian canal- narrowest is meatal foramen =entrapped .
- Tympanic segment (majority of intratemporal Trauma) Mastoid segment( 10-14mm from
pyramidal process to the stylomastoid foramen) Chorda is 30 degree of VII,runs between 2
layers of T membrane
Extratemporal segment
Gives off posterior auricular nerve to stylohyoid, nerve to posterior digastrics and
terminates( Pes anserinus( the branching point of the extratemporal segment in the parotid gland).
facial nerve divides the parotid ( superficial and deep lobes.
5 temporal branches (Frontal-Zygomatic-Buccal- mandibular-Cervical
Zygomatic and buccal are the most important branches (BZ)

FN=VII, BB:Bills Bar(bony) Transverse crest(bony)

SVN=Sup vest- IVN=infer vest, CN=Cochlear Nerve
"Seven-Up and Coke (Cochlear) Down"
Both anterior 7

Components
Branchial motor (Special Visceral Efferent/SVE)
- Supplies the muscles of facial expression
- lower face : bilateral innervation;
Parasympathetic (General Visceral Efferent/GVE)

14

Innervates the lacrimal, submandibular, and sublingual glands thru different connections
Sensory (General Sensory Afferent/GSA)
Sensation to the auricular concha, post auricular skin, part of the posterosuperior wall of the EAC (EAC), and
part of the TM
- Hitzelbergers sign: Cant taste burger! taste in ant 2/3 of tongue=A.Neuroma,
Evaluation
Important _ incomplete= do just follow up
- Onset of paralysis-Duration-Progression
Paralysis of 3 wks, no improvement after 6 m=. Tumor till proven otherwise
Investigation: One or more of the following tests can be performed:
a. Nerve excitability test b. Conduction latency test
c. Strength-duration studies d. Electromyography (EMG)
e. Maximal stimulation test
f. Salivary flow.
Nerve Excitability Test (NET)- wait 3 days
no use in a partial paralysis or within 3 days of total paralysis. After 3 days of total paralysis, the normal side is
first tested to obtain the threshold needed to flicker of facial muscle. The electrode on stylomastoid foramen
and main branches of VII nerve. Record and compare thresholds for the normal side, to diseased side. A > 3-4
mamp difference = denervation=decompression of VII is done. avoid stimulating the muscle directly so that a
false threshold is not obtained.
Conduction Latency Test: wait 3 days
uses a once per second square-wave pulse, 1 msec in duration. A second electrode is placed in a distal facial
muscle. impulse time to distal electrode is recorded as conduction latency. The normal conduction time is
about 4 msec. not prolonged until 72 hours after denervation, after which=increasing conduction time until no
excitability is demonstrable. A lengthening of conduction = imply partial denervation. harder to perform =not
used clinically in the office.
Strength-Duration Studies: wait 1 wk
A particular muscle is selected for this test. A square-wave pulse of varying duration and intensity is applied
until a just visible twitch is noted. As one goes from longer pulse duration to shorter pulse duration, the
threshold needed to elicit a just visible twitch is recorded. The intensities for various pulse durations are
recorded for the normal side. A denervated nerve will show higher thresholds. The strength-duration curve is
not altered in neuropraxia and is not altered till 7 days after denervation.
Rheobase: The strength of current just strong enough to depolarize (mamp).
Chronaxie: The length of duration needed to depolarize using an intensity two times the rheobase (msec).
Electromyography (EMG): wait 2 wk-OMG!- prognostic not diagnostic
determines the activity of the muscle itself. A Muscle electrode recording during rest and voluntary
contraction. (fibrillation potential, and polyphasic reinnervation potential) Degeneration of LMN is followed in
14-21 days by spontaneous activity = fibrillation potential. EMG is not of diagnostic until 2 weeks after
denervation. clinical usage of EMG is in the determination of reinnervation. Polyphasic reinnervation
potentials in 6-12 weeks before clinical return of facialfunction.
Maximum Stimulation Test
Similar to the nerve excitability test but uses maximal rather than minimal stimulation. The main trunk, major
distal branches on the normal and abnormal side are stimulated with an intensity that produces discomfort. The
results = difference in facial movement. difference is considered evidence of abnormality.
Salivary Flow Test=Shirmer test

15

Preganglionic parasympathetic nerve fibers are outer fibers of VII nerve; hence , injured before motor fibers.
nerve excitability tests : (nerve distal to injury) while the salivary flow test checks the nerve at the site of
injury. after anesthetizing the anterior floor of the mouth, first dilating the Wharton's duct. A polyethylene
cannulated into each duct. Lemon juice stimulate salivary flow ( number of drops secreted / minute is counted
for each side. A difference of 70% is significant = surgical decompression of the VII nerve.
Electroneuronography
Similar to the maximal stimulation test ( instead of visual response, there is a recording of the summation
potential ). The normal side is compared with the abnormal side and the degree of degeneration
estimated from the difference between the amplitude of the measured summation potentials
on the two sides. Fisch recommends surgical decompression if evoked summation potential is 10% or less than
the normal side = 90% degeneration. ENG done within 2 weeks of paralysis. Other felt that if the reduction
was > 25%, decompression was indicated since by the time the level reached 10%, results are poor.
Treatment of Bell's Palsy
majority of Bell's palsy patients have either partial or total paralysis without degeneration, i.e. maintaining the
neuropraxia state. unless denervation has occurred, the patient more than likely will recover spontaneously
with little synkinesis. Hence surgical treatment, if proposed, is reserved for those with total paralysis that have
shown signs of denervation. There is no conclusive evidence to date that surgical decompression is of definite
benefit. Some protocols treat Bell's palsy of all severities with steroids, others treat only cases of total facial
palsy with steroids. Some clinicians believe that if the nerve is allowed to degenerate completely, the prognosis
is poor and synkinesis is common.
Supranuclear

Nuclear
Angle

Geniculate
ganglion
General=all
Tympanomastoid
Extracranial

Good tone, intact upper face,

presence of spontaneous smile,
neurologic
deficits.
Involvement VI+VII, corticospinal
tract signs
vestibular and cochlear portions of
the eight cranial nerve; the
VII,(taste, lacrimation and salivation
altered; V and later IX,X,XI cranial
nerves may become impaired.
Facial paralysis, hyperacusis,
alteration of lacrimation, salivation,
and taste.
Facial paralysis, alteration in
salivation and taste; lacrim intact.
Facial paralysis (usually a branch is
spared), salivation and taste intact,
deviation of jaw to normal side

Cerebrovascular accident,
trauma.
Vascular or neoplastic,
poliomyelitis, MS, encephalitis
Neurinoma,
meningioma,
fracture,
cholesteatoma,
arachnoid cyst
HZ, oticus, fracture, Bell's palsy,
cholesteatoma, neurinoma,
AVM, meningioma
Bell's palsy, cholesteatoma,
fracture, infection
Trauma,
tumor,
parotid
carcinoma,
pharyngeal
carcinoma

Lateral sinus thrombophlebitis(LST)

formed by sup petrosal sinus and transverse sinus. The right transverse sinus is continuation of the sagittal
sinus, and the left transverse sinus is a continuation of straight sinus. The lateral, or sigmoid, sinus exits the
skull through the jugular foramen to become the internal jugular vein. It is called the lateral sinus because it is
encountered laterally in mastoid surgery.

16

LST is a potentially fatal , early diagnosis is difficult ( antibiotic therapy. ( vague symptoms,high index of
suspicion to make diagnosis.LST suspected in : persistent fever, otorrhea, and headache despite antibiotic
treatment.LST accounts for 6% of all intracranial complications of suppurative ear disease.
Etiology: proximity of the middle ear and mastoid air cells to the dural venous sinuses predisposes them to
thrombosis and thrombophlebitis secondary to infection and inflammation in the middle ear and mastoid.
LST develops as a complication of ASOM or CSOM by the direct dissemination of infection through the
neighboring eroded bone or through the emissary vein in the intact bone.
LST was 2ed to meningitis in the preantibiotic era as the most frequent fatal complication of otitis media and
occurred largely as a complication of AOM. More often, it is seen in the adult patient after a long history of
chronic ear disease.
Initially, a perisinus abscess , penetrates the dura , intima, a mural thrombus develops. Damage to the tunica
intima = fibrin + aggregation of blood platelets. , clot grows and necrotizes, forming an intramural abscess. A
mural thrombus then develops within the lumen of the sinus, propagates proximally and distally, and may
become infected. The lumen of the vessel is eventually occluded by the propagating thrombus, and infected
material may be embolized into the systemic circulation, causing septicemia.
C/P: headache, fever, and otorrhea. fever( preantibiotic era ) picket fence fever = periodic release of hemolytic
streptococci from thrombus. Sinus occlusion = obstruct cortical venous = headache, papilledema, and ICP.
,torcular and sagittal sinus involement= otitic hydrocephalus.
Tenderness and edema on mastoid (the Griesinger sign) : =LSTand reflex thrombosis of mastoid emissary vein.
+ extension to jugular bulb and internal jugular vein, pain in the neck on rotation. Internal jugular vein :tender
cord. IX,X and XI nerve may be paralyzed (jugular foramen syndrome).
right transverse is usually dominant, C/P occur when this sinus is involved. Recovery depends on collateral
circulation / recanalization of the sinus. anastomotic channel is important for recovery.
Investigations
Tobey Ayer test ( measure ICP when occluding jugular ven=no increase in ICP on ipsilateral side)
Culture and sensitivity of purulent material
CBC count and differential count(anamia from toxicity and B hemolytic strept)
Blood culture
usually preceded by chronic rather than acute ear infection. Beta hemolytic strept is no longer a dominant
organism. cultures : mixed flora, Bacteroides, Staphylococcus, Enterobacteriaceae, Proteus, Pseudomonas,.
Because antibiotics are commonly used : culture is often negative.
MRI is more sensitive than CT in detecting the thrombus. : flow, sinus obstruction, reversal of flow. On
gadolinium-enhanced MRI, thrombus appears as soft tissue signal associated with vascular bright appearance
of the dural wall ("delta" sign. in conjunction with CT , evaluating associated otologic and cerebral pathology.
MRI venogram (MRV) used for follow up (assess clot progression and resolution.

17

MR venogram that shows nonfilling of the lateral sinus on the left side.
http://emedicine.medscape.com/article/1048625-overview#showall
AN_Cerebello-Pontine angel Tumor
Cerebellopontine angle (CPA) tumours can be divided into
1-Extra axial tumours/ intercanalicular
A. MCC : Acoustic tumours / schwannomas ),meningiomas and cysts (epidermoid, arachnoid, etc)
Neurofibromatosis II( Bilat VS+ meningioma+cataract+glioma) AD in 50%.
B. Rare extra-axial tumours :neuromas (V, VII, IX, X, XI, XII) vascular malformations (aneurysms)
2-Axial tumours : astrocytoma, ependymoma, papilloma, haemangioblastoma.
3-Extradural tumours : glomus tumours and bone lesions.
4-Petrous apex lesions : cholesterol granulomas, epidermoid cysts, mucoceles and carotid aneurysms.
Anatomy: CPA is a triangular (temporal bone laterally, pons medially, cerebellar :anteriorly, tentorium
cerebelli superiorly and lower cranial nerves inferiorly.
Its contents ( ant inf cerebellar artery (AICA), 7th, 8th cranial nerves. ( to reach (IAM).
IAM extends from porus to the medial wall of the vestibule. The lateral wall of the meatus is divided by two
crests. The horizontal (Falciform) and vertical crest (Bills Bar) : divide meatus into 4 compartments. Larger
anterior ( VII n superiorly and Cochlear n inferiorly). posterior compart ( superior vestibular nerve superiorly
and inferior vestibular nerve inferiorly. inferior vestibular nerve supplies the saccule + separate nerve (singular
nerve) to posterior semicircular canal.
Arterial and venous relations in the CPA are variable. The AICA for example can loop into the meatus. Jugular
bulb if high can interfere with surgical access.
Acoustic Neuroma (Vestibular Schwannoma) VS
(VS) 90% of all CPA tumours (10% of all primary brain tumours. benign slow growing.
(Neurofibromatosis type2) chrom22q (AD50%- sporadic and bilateral VS.
Grossly : firm , capsule. : cysts and necrotic tumour. bleeding = sudden dangerous in the size.
The site of origin : glial neurilemmal junction.
Histologically : Antoni A and B. Both in the same tumour. Intracanalicular( inside internal auditory)
Antoni A cells :orderly arrangement into whorls Antoni B cells : disorderly + degeneration.

18

Clinical presentation
early stage it is asymptomatic. unilateral tinnitus , asymmetrical progressive SNHL(sudden SNHL 10% =
vascular event). slow growth : vertigo and imbalance is rare ( compensates for the loss. few :acute vertigo
=vascular event in the labyrinth.
facial nerve often stretched by tumour, facial weakness is uncommon ( motor neurons are more resistant.
significant facial weakness , think of facial Neuroma.
If > 2cm it affects VIII n : corneal reflex initially then facial numbness or pain.
late stage :compresses cerebellum + brain stem = Ataxia , tremor , fall to the side of lesion.
At pre terminal stage : severe headaches , obstructive hydrocephalus, Obstruct 4th ventricle, foramen Lushka.
Clinical Examination: 4 items
Ear (hearing) Eye, cranial nerve exam and cerebellar function.
1-Ear exam : exclude other causes of hearing loss. ,Tuning fork : confirm side of SNHL.
2-Cranial nerves: V, VII and lower cranial nerves. ( VII motor nucleous is resistant to compression)
3-Eyes should be examined for sign of nystagmus.
4-Cerebellar exam: finger to nose test ( tremor, Rombergs and Unterbergers tests with eyes closed and finally
gait with eyes open and closed. fall to the side of the lesion.
Investigations
1- (MRI) with gadolinium (gold standard). Identify small tumors assess extension
( this will affect the surgical planning in regards to hearing preservation).
2- CT :with contrast can pick up small tumours.
3-ABR: interaural delay of wave V 0,4 ms(= retrocochlear lesion. not sensitive. good waveform needs HL >
70 dB.
4-PTA:SNHL slowping hi frequency
5-caloric test: preoperative to assess the balance loss on contralateral side.
Management
1-conservative management, 2-radiotherapy and 3-surgery.
conservative : small tumours. average growth (1-2 mm/yr).
active :if growth rate > 2mm/yr.
When to use Conservative : small, only hearing ear, advanced age, poor health and Neurofibromatosis type 2.
MRI : at 6 month then yearly. risk of rapid growth making the surgical result poorer as far as hearing
preservation and facial nerve function.
2-Gamma knife radiosurgery/Sterotactic ( for small to medium ). preservation of facial n 100% . Hearing
preserved in 60%. delayed malignant transform. treatment failure (2-7%),V neuropathy (3-8%),
hydrocephalus (Rx: shunt.
3-Microsurgical ( translabyrinthine, retrosigmoid (suboccipital) and middle fossa approaches. mortality 2%.
facial nerve palsy depending on the size of tumour, meningitis 3-8%, CSF leak 10-15% and rarely lower
cranial nerve palsies 1.

19

Translabyrinthine: MC for VS / direct , wide exposure of CPA & IAM, highest rate of facial n preservation ,
least retraction on cerebellum: loss of hearing/ balance on operated side.
Retrosigmoid (suboccipital) Approach
preserves hearing + wide exposure , cerebellar retraction, facial nerve is not identified at the fundus and there
is intradural drilling.
**Middle Fossa Approach: hearing preservation but only useful for small tumours temporal lobe retraction.
Neurofibromatosis
Neurofibromatosis type 1(von Recklinghausens disease) AD- chromosome 17q. Caf-au-lait skin lesions,
skin neurofibromas, iris hamartomas (Lisch nodules), axillary or inguinal freckling, sphenoid dysplasia and
optic glioma (two or more). no in the incidence of acoustic neuromas in these patients.
Neurofibromatosis type 2(NF2) AD- chromosome 22q. bilateral VS or a family history of NF2 +; unilateral
acoustic neuroma, meningioma, glioma, neuroma or cataract. In NF2 :neuromas at an early age = tumour
suppressor gene defect.milder type bilateral VS (Gardner) aggressive type , multiple cranial nerve and spinal
neuromas (Whishart).
Primary Cholesteatomas (Epidermoids)
Primary cholesteatomas of the CPA :from epithelial nests in the temporal bone and CPA. slow growing present
late in the third or forth decade of life.
Histology: epithelial lined sacs + keratin ,invade surrounding (least resistance ) irregular surface.
Signs/Symptoms
CPA epidermoids : similar audio-vestibular symptoms ( more facial twitching and progressive facial palsy.
Investigations
Auditory investigations can not distinguish these tumours from other CPA lesions. Standard investigations are
CT and MRI scans. On CT scan cholesteatoma is irregular, none enhancing and eccentric to the IAM.
On MRI scan they have similar signal to the acoustic neuromas but none enhancing and more irregular. In this
way they are distinguished from arachnoid cysts which have smooth surface.
Management: Microsurgical removal is standard treatment.
Facial nerve Neuroma (Schwannoma)
Schwannomas of the facial nerve can arise from any part of the facial nerve from its origin in the CPA until it
branches in the parotid gland. Facial nerve schwannomas represents only about 1% of all CPA tumours 11.
Histology: identical to vestibular schwannomas.
Signs/Symptoms
Depending on the site of the neuroma, in CPA tumours give rise to similar audio-vestibular symptoms as
acoustic neuroma but if there is preoperative facial weakness then the possibility of facial neuroma must be
considered and discussed with the patient. In tympanic part it might give rise to a conductive loss and in
peripheral cases might present with a parotid mass.
Investigations
Auditory : can not distinguish these tumours from CPA lesions. Except for impedance test which might show
an absent ipsilateral reflex.

20

Electroneurography (ENOG) : measures muscle response to max stimulation near stylomastoid foramen 13.
On the MRI scan it is almost identical to the acoustic neuroma but there might be involvement of the
labyrinthine portion or enlargement of the fallopian canal on the more distal tumours. High resolution CT scan
(1.0-1.5 mm cuts) can be used to look at the bone surrounding the labyrinthine, geniculate ganglion, tympanic
and vertical segments of the nerve12.
Management: Microsurgical removal followed by anastomosis or cable grafting. enucleation with fascicle
preservation which gives better postoperative facial function 11.
Glomus Tumours (Paragangliomas) Benign
arise from paraganglionic cells ( from neural crest cells) adrenal (pheochromocytomas) and extra-adrenal.
Extra-adrenal ( carotid body tumours Jugulotympanic , vagal paragangliomas ,extend to CPA , erode skull
base.
Benign, slow-growing ,highly vascular , cause symptoms by 1) mass effect in ear, 2) high blood flow, 3)
invasion of adjacent structures, and 4) secretion of hormones( rare.
1-glomus tympanicum." a small limited to the middle ear
2-glomus jugulare." larger tumor originates from jugular bulb and involves skull base
3-Glomus vagale from vagus nerve, (affect vocal cords and muscles of swallowing.
4-carotid body tumor from the main carotid artery in the neck,
These tumors can occur in multiple areas, including the eye socket, the larynx, or inside the chest or abdomen.
Histology: typical neoplastic chief cells (Zellballen) with eosinophilic cytoplasmic granules , round nuclei,
surrounded by sustentacular cells which do not contain granules.
Signs/Symptoms: depend on site and size: pulsatile tinnitus, CHL and lower cranial nerve palsies. Tumours
in CPA: similar symptoms as acoustic neuromas.
mass effect can block sound =CHL +high blood flow :pulsating tinnitus). With larger tumors, can be
invaded,facial paralysis, or the inner ear(SNHL)or vertigo. Rarely, Epiniphrine, (sweating, flushing, headache,
and fluttering).
Investigations: CT : destruction of bone in contrast to smooth expansion of jugular foramen in schwannomas.
MRI : typical salt and pepper mixture of intensities on T1 and T2 sequences.
Angiography might show Lyres sign (splaying of carotid bifurcation) and is useful in assessing the vascular
supply of the tumour and plan for preoperative embolization.

21

Temporary balloon occlusion of the carotid artery might be used to estimate collateral circulation.
VMA and metanephrine in 24 Urine if functioning
Management
Surgery: Small Glomus tympanicum with all borders visible removed by transcanal approach. If all the
borders are not visible and not involving the jugular bulb then a combined approach with extended facial
recess can be used.
Larger tumours involving the base of skull can be approached by infratemporal fossa approach and tumours
with intracranial extensions will need multidisciplinary approach with reconstruction.
The key to successful surgery : securing VII n and the internal carotid artery. If the lower cranial nerves have
been sacrificed then early rehabilitation is very important. This might include tracheostomy, gastrostomy, eye
care and phonosurgery.
Radiotherapy: There is a great debate about role of radiotherapy in the management of glomus tumours. It is
generally agreed that it should not be used in the younger patients because of potential for malignant
transformation.
Prelimphatic fistula PLF
(PLF) is an abnormal opening between the air filled ME & the fluid-filled inner ear due to a defect in one of
three locations:
Oval Window (most common site)Stapedectomy surgery (for otosclerosis)
Head trauma or barotrauma (pressure injury),Acoustic trauma
Round window Barotrauma -- SCUBA diving, airplane pressurization
Congenital malformations (such as Mondini dysplasia)
Otic capsule-This is a rare , bone between the ear and brain area is missing or thin, causing symptoms very similar to that of
a round or oval window fistula. Problems in the otic capsule that may cause a perilymph fistula include:
SCCD (dehiscence syndrome (anterior SCC)
Cholesteatoma
Fenestration : after a fenestration previously done for otosclerosis;
Temporal bone fracture
Micro-fissure: MCC of otic capsule fistula , just above SCC =SCCD canal dehiscence syndrome.
False positive fistula test(Hennebert sign)
Congenital syphilis
( stapes footplate is hypermobile, small pressure
changes in ear, cause excessive movement of
stapes footplate & excessive stim of utricular
macule)

False negative fistula test

In Dead ear ( inner ear is damaged), there will
be NO response even if a Perilymphatic fistula
exists.

25% cases of Meneires disease.

Also seen when cholesteatoma covers the site of
fibrous bands form connecting to utricular macule fistula & doesnt allow pressure changes to be
to stapes footplate)
transmits to labyrinth.
Cholesterol Granuloma
Cholesterol granulomas are the most common lesions of the petrous apex.
Their etiology is not clear 1- The obstruction-Vacuum hypothesis :blockage of air cells with subsequent
negative pressure will lead to hyperemia and bleeding.
2-An alternative theory ( Jackler and Cho) blood from areas of exposed marrow.

22

In either case blood products such as cholesterol, fibrin and hemosiderin will lead to foreign body
granulomatous reaction. The new blood vessels will in turn cause more bleeding and the cycle repeats itself,
which results in expansion of the lesion.
Histology consists of granulomatous reaction to the cholesterol crystals. Cholesterol clefts are surrounded by
giant cells, fibrosis and hemosiderin laden macrophages.
Signs/Symptoms
Depend on the location and size of the lesion. Retrocochlear symptoms include hearing loss, tinnitus and
dizziness. Involvement of the middle fossa dura may cause headaches as well as trigeminal and abducent nerve
palsies. Blockage of the eustatian tube can lead to serous otitis media. Small lesions might be entirely
asymptomatic.
DD: Meniers disease, Acoustic neuroma,
CT scan :punched out lesion. preoperative : relation of the lesion with the major vascular structures.
MRI scan is important to distinguish the cholesterol granulomas from other petrous apex lesions i.e.
cholesteatoma, chondroma, petrous apicitis, carotid aneurysm, meningioma, schwannoma and metastatic
tumours19. Cholesterol granulomas are typically hyperintense on T1 and T2 images and do not enhance with
contrast.
Management
Small asymptomatic : observed by serial MRI. Larger tumours : surgical drainage. (hearing preservation =
infracochlear or infralabyrinthine -unserviceable hearing = translabyrinthine approach can be used.
http://otologytextbook.com/webtext/
Congenital SNHL
Hereditary Defects
non-syndrome associated (70%): idiopathic, AR-connexin 26 (G]B2) most common
syndrome associated (30%):
Waardenburg's - white forelock, heterochromia iridis, hypertelorism (side inter canthi
Pendred's - deaf, thyroid disorders, Euthyroid-U shape audiogram-SLC26A4 gene, enlarged vestibular
aqueducts
Treacher-Collins - first and second branchial cleft anomalies
Alpert's - hereditary nephritis
Prenatal TORCH( toxoplasmosis, rubella, CMV), herpes simplex, others (e.g. HIV; syphilis)
Perinatal Rh incompatibility- anoxia- hyperbilirubinemi- birth trauma (hemorrhage into inner ear)
Postnatal=3 Ms meningitis- mumps-measles
High Risk Registry (for Hearing Loss in Newborns)
risk factors: low birth weight/prematurity- perinatal anoxia (low APGARs)
kernicterus- bilirubin >25 mgldL-craniofacial abnormality
famlly history of deafness in childhood
1st trimester illness - TORCH infections
neonatal sepsis-ototoxic drugs
perinatal infection, including post-natal meningitis- consanguinity
50-75% of newborns with SNHL have at least one of the above risk factors, 90% : spent time in the NICU

23

 presence of any risk factor: auditory brainstem response (ABR) study performed before leaving
NICU and at 3 months adjusted age
early rehabilitation improves speech and school performance
NB: Congenital SNHL is decreasing due to the availability of vaccines and improved neonatal
Congenital hearing loss and syndromes with hearing loss
"what are the two AR,
membranous
dysplasias?"
Crouzon's disease

Jervell Lange Nielsen

syndrome
Pendred syndrome
Red= goiter

Describe Treacher
Collins
TrEACherEAC
Collincoloboma

Diagnostic criteria for

NF II

Michele's aplasia

Mondini aplasia

Name 7 syndromes

"scheibe's dysplasia, alexander's dysplasia"

AD
Oto sx: atresia/stenosis of EAC, ossic deformities
Other sx: cranial synostosis, Midface
exophthalmos, parrot nose, short upper lip, small maxilla, mandible
prognathism, hypertelorism
"bilateral severe-profound SNHL, cardiac abnormliaties (10% of all
cases, prolonged QT, large T waves, syncope, sudden death). Dx:
EKG. Tx: beta blockers, amplification"
AD or AR
defect in tyrosine iodination. prelingual and profound. Temporal
bone abnormalities = dilated vestibular aqueduct (DVA) and
Mondini dysplasia. Associated with goiter (failure of iodine
organification. dx: positive perchlorate test (dec perchlorate
discharge). tx: synthroid/ suppress goiter (no effect on hearing)
AD- normal intelligence
Otologic sx: (pre)auricular deformities, EAC atresia, ossic probs,
bony replacement of TM, widened aqueduct, displaced facial
nerve ,palate defects
Other sx: maxilla/mandibular hypoplasia,
Eye: down slanting palp fissures, coloboma of lower eyelid,
Rx: BAHA, poss correction of atresia, Tracheostomy
"Bilateral vestibular schwannomas
chromosome 22q12 encoding tumor suppressor protein merlin
Family history of NF2 plus one of following:
Unilateral vestibular schwannoma by age 30
2 of meningiomas, gliomas, schwannomas or (juvenile cortical
cataract)
AD, thalidomide.
Complete failure of dev of inner ear
CT: hypoplastic petrous pyramid, absent cochlear/labyrinth
Rx: vibrotactile devices
AD
progressive/fluctuating uni or bilat HL (or no HL)
Inc risk of perilymphatic gushers/meningitis from dilated cochlear
aqueduct
CT: single turn cochlea (1.5 turns), wide/absent semicircular canals,
no interscala septum, wide vestib aqueduct)
Rx: amplify, CI
"Branchial-oto-renal syndrome, Treacher Collins, and Klippel-Feil,

24

( middle ear anomalies

and CHL(CCC-KGold)
Scheibe aplasia
Sheep graze
down=inferior

Alport syndrome?

two AD inner ear

dysplasias?
What is DFNB1?
MCC malform of
memb labyrinth causing
deafness?
what is Usher syndrome
and how is it
diagnosed?

What percent of genetic
deafness is syndromic?
What percent of
nonsyndromic SNHL is
transmitted by AR
inheritance? AD,Xlinked?
What persent of
congenital SNHL is
genetic vs. noninherited?

Crouzon syndrome, Apert syndrome, CHARGE association, and

Goldenhar syndrome."
AR
partial/complete aplasia of pars inferior (cochlea/saccule)
normal pars superior (semicirc canals, utricle)
assoc with Usher/Waardenburg syndrome-SNHL
cannot dx with CT (membranous defect, need histo)
rx: Hearing aid=amplify
X-linked. (Can be AR or AD ).
"Mutation in chains of type IV collagen, basement membrane
Progressive high frequency SNHL
Family history of hematuria=glomerular BM
eye lesions (anterior lenticonus or macular flecks)
Order UA, BUN, Creatinine-Tx: dialysis, renal transplant
"Mondini, Michel's"
AR, non-syndromic HL, mutations in connexin 26. prelingual nonprogressive bilateral hearing loss."
Scheibe's dysplasia (cochleosaccular dysplasia).
MCC of congenital deafness
congenital SNHL (degen of organ of corti), vestib probs
progressive retinitis pigmentosa (loss of night vision, tunnel
vision/blindness), cataracts-MR
Dx: electroretinography
type I most common: profound SNHL, vestib dysf, , blind by 20 yr
20%
75-85% AR.
15-20% AD.
1-2% x-linked.
50% inherited

Sudden Hearing loss(SSHL)

Abrupt , rapid progressive hearing loss. Awakening with a hearing loss, hearing loss noted over a few days,
selective low- or high-frequency loss, and distortions in speech perception have all been classified as sudden
hearing losses.
criterion (SNHL)> 30 dB over 3 contiguous PTA frequencies within 3 days.
unilateral, and the prognosis for some recovery of hearing is good.
Sudden deafness or sudden sensorineural hearing loss (SSNHL) has many possible etiologies.

25

Pathophysiology (4 theoretical pathways, as follows:

Labyrinthine (viral infection-vascular compromise
Intracochlear membrane ruptures
Immune-mediated inner ear disease.(Meniere disease)
Each theory may explain a fraction of the episodes of sudden SNHL but none account for all episodes.

Viral infection
moderate prevalence of recent viral. Temporal bone histopathologic : viral injuries. Loss of hair cells and
supporting cells, atrophy of the tectorial membrane, atrophy of the stria vascularis, and neuronal loss were
observed. similar to findings in hearing loss secondary to mumps, measles, and maternal rubella. Cannot, as
yet, be proven. In one study of ISSHL, subclinical mumps documented in 9 of 130 pts by + (IgM)
Vascular compromise
The cochlea is an end organ , no collateral , Cochle is sensitive to changes in blood supply. thrombosis,
embolus, reduced blood flow, or vasospasm seems to be a likely etiology ,abrupt SNHL. A reduction in
oxygenation of the cochlea is the likely consequence of alterations in cochlear blood flow. Alterations in
perilymph oxygen tension have been measured in response to changes in systemic blood pressure or
intravascular carbon dioxide partial pressure (pCO 2).
cochlear damage post vessels ocumented. Intracochlear hemorrhage was noted as an early development;
subsequently, fibrosis and ossification of the cochlea evolved.
In one study, a partial overlap was found between classical coronary risk factors and risk factors for sudden
hearing loss.
Intracochlear membrane rupture
Immune-mediated inner ear disease
The association of hearing loss in Cogan syndrome, systemic lupus erythematosus, and other autoimmune
rheumatologic disorders has been well documented. With better markers for inner ear autoimmunity, perhaps a
greater linkage with ISSNHL will be found. A recent prospective study on 51 patients with ISSNHL supported
the existence of multiple immune-mediated disorders in these patients. [6]
History
SSNHL is otologic emergency. Patients should also be assessed for bilateral sudden hearing loss, recurrent
episodes of sudden hearing loss, or focal neurologic findings Information about the onset, time course,
associated symptoms, and recent activities may be helpful.

o
o

Past medical history may reveal risk factors for hearing loss.
All medications, including over-the-counter products, must be described.
Aspirin can cause a reversible sensorineural hearing loss,

Physical: head and neck ,otologic and neurologic examination.

Tuning fork tests , a fistula test using pneumatic speculum must be performed

Causes
Infection 3Ms (eg, meningitis, mumps, measles, syphilis),cytomegalovirus, varicella/zoster)
Inflammation Sarcoidosis, Wegener granulomatosis, Cogan syndrome
Vascular - Hypercoagulable states (eg, Waldenstrom macroglobulinemia), emboli (eg,
postcoronary artery bypass graft [CABG] surgery), postradiation therapy
Tumor -Vestibular schwannoma, temporal bone metastases, carcinomatous meningitis
Trauma -Temporal bone fracture, acoustic trauma, penetrating temporal bone injuries
Toxins - Aminoglycoside antimicrobials, cisplatin
MCC:idiopathic. ISSHL (idiopathic sudden SNHL) endpoint with sudden hearing loss.
Differential Diagnoses

26

Inner Ear, Autoimmune Disease(cogans- Meniers)

Inner Ear, Ototoxicity
Inner Ear, Perilymphatic Fistula
Temporal Bone Fractures
Laboratory Studies
Routine, non-targeted, laboratory testing is not recommended. [8] Laboratory studies should be directed by the
history and physical examination findings.

(FTA-Abs),VDRL, for syphilis

(ANA), rheumatoid factor, and (ESR) for autoimmune diseases
(INR), activated partial thromboplastin time (aPTT), and clotting time for coagulopathy
CBC infection- (TSH) for thyroid disease
Fasting blood glucose for diabetes mellitus
Cholesterol and triglycerides for hyperlipidemia
Imaging Studies
internal auditory canal (IAC) or CPA tumors. 10% of VS present with sudden SNHL.
(MRI) with gadolinium : standard test for CPA masses, 30-40% false-negative rate exists with ABR.
(AAO-HNSF) 2012 guidelines : (CT) : not helpful , nor recommended in SSNHL. [8]However, in young
patients, ( small possibility of detecting a vest schwannoma , noncontrast temporal bone CT scan could be
obtained. Anatomic defects ( Mondini dysplasia or enlarged vestibular aqueduct might = sudden hearing loss

Other tests
PTA and speech tests and immittance (tympanometry and acoustic reflex) tests, is mandatory.
ABR -otoacoustic emissions (OAE) tests :assess cochlear, and auditory nerve function, also assist in
diagnosing a functional hearing loss.
Medical Care
if no definitive or treatable etiology is found, Rx dictated by the most likely factors involved.
Vasodilators: improve the blood supply to the cochlea, reversing hypoxia. (Papaverine, histamine, nicotinic
acid, procaine, niacin, and carbogen (5% carbon dioxide) : improve cochlear blood flow.
Carbogen inhalation : perilymph oxygen tension,without significantly affecting CO2 tension. A carbogen
combined with drugs is superior to drug therapeutics alone.

Rheologic agents: By altering blood viscosity with the use of low molecular weight dextrans,
pentoxifylline, or anticoagulants (eg, heparin, warfarin), better oxygen delivery. Dextrans cause a
hypervolemic hemodilution and affect factor VIII, with both these effects influencing blood flow.
Pentoxifylline affects platelet deformability, presumably improving blood flow. Anticoagulants interfere with
the coagulation cascade as a mechanism to avoid formation of thrombi and emboli.
Corticosteroids : reduction of cochlear and auditory nerve inflam. value of steroids in ISHL unclear. [10]
o
(AAO-HNSF) guidelines : corticosteroids as initial therapy
intratympanic dexamethasone is effective, A paucity of data on NSAID
Acyclovir and amantadine : limited use in treating ISSHL,
Diuretics: (some causes due to endolymphatic hydrops as in Mnire disease, the mechanism of action for
diuretics in sudden hearing loss is not understood.
Hyperbaric oxygen
Surgical Care
Repair of oval and round window perilymph fistulae (PLF) if positive fistula test or a history of recent trauma
or barotrauma.

Perilymph leaks could produce sudden hearing loss in accordance with the intracochlear membrane
rupture theory. Alternatively, low perilymph pressure could produce a relative state of cochlear endolymphatic
hydrops.

27

Controversy exists regarding the role of surgical repair of perilymphatic fistulae because no universal
standard exists for positive identification of a fistula. The tau transferrin test on perilymph fluid has not
proven to be useful in the diagnosis of this entity.
http://emedicine.medscape.com/article/856313-overview#showall
Presbycusis
MCC of SNHL, associated with aging (staging in 5th and 6th decades)
Etiology
hair cell degeneration
age related degeneration of basilar membrane
cochlear neuron damage- ischemia of inner ear
Clinical Features
progressive, gradual bilateral SNHL initially at high frequencies, then middle frequencies
loss of discrimination of speech especially with background noise present (people as mumbling
recruitment phenomenon: inability to tolerate loud sounds
tinnitus
Treatment: hearing aid if difficulty functioning, hearing loss >30-35 dB+ good speech discrimination
lip reading, auditory training, auditory aids (doorbell and phone lights)
CT terminology and consideration
CT axial and coronal every 4mm, but thin cuts every 2mm
Axial( hard palate till: roof of orbit
Coronal( sella or orbital apex) till: ant frontal sinus wall)
Using contrast in all cases but Fracture or accident
Soft tissue window and bone window
Rule:To see any organ or lesion best take a perpendicular cut not parallel
So soft palate lesion will show best in coronal section not in axial
Stylomandibular tunnel:
Ptregoid fossa( between lat and med ptregoid)
Retro styloid space--Palatine foramen

Fig. 7C. Pterygopalatine canal and greater palatine foramen in adult without evidence of cancer. Bone
algorithm axial CT scan shows greater palatine foramen (arrows) in posterolateral palatal region.
The parapharyngeal space may be divided into two compartments on the basis of its relationship to the
styloid process or, more precisely, to the tensor-vascular-styloid fascia (Fig. 1A,1B,1C,1D). The importance of
the parapharyngeal space also lies in its relationship with the other spaces of the neck [1]. The masticator and
parotid spaces are located laterally, the pharyngeal mucosal space is located medially, and the retropharyngeal
space is located posteromedially (Fig. 1A,1B,1C,1D). The contents of the prestyloid compartment include the
minor or ectopic salivary gland, branches of the mandibular division of the trigeminal nerve, internal maxillary

28

artery, ascending pharyngeal artery, and pharyngeal venous plexus, whereas those of the poststyloid
compartment include the internal carotid artery, internal jugular vein, cranial nerves IX-XII, cervical
sympathetic chain, and glomus bodies.

Fig. 1A. Normal anatomy of parapharyngeal space. BS = buccal space, ICA = internal carotid artery, IJV =
internal jugular vein, MS = masticator space, PMS = pharyngeal mucosal space, PPS = parapharyngeal space,
PS = parotid space, PVS = prevertebral space, RPS = retropharyngeal space, SMS = submandibular space, T =
torus tubarius. Axial unenhanced T1-weighted spin-echo MR at nasopharynx level shows fat-filled prestyloid
parapharyngeal space (asterisks) located between masticator space and pharyngeal mucosal space. Torus
tubarius represents pharyngeal mucosal space at nasopharynx level. Poststyloid parapharyngeal space
containing major neurovascular bundle of internal carotid artery and internal jugular vein is located posteriorly.

View larger version:

Fig. 1B. BS = buccal space, ICA = internal carotid artery, IJV = internal jugular vein, MS = masticator
space, PMS = pharyngeal mucosal space, PPS = parapharyngeal space, PS = parotid space, PVS = prevertebral
space, RPS = retropharyngeal space, SMS = submandibular space, T = torus tubarius. Axial unenhanced T1weighted spin-echo MR image obtained at oropharynx level shows that parotid space containing parotid gland
forms posterolateral boundary of parapharyngeal space (asterisks), and retropharyngeal space and prevertebral
space form posteromedial boundary of parapharyngeal space (asterisks).
Scutum is a small constellation (Latin for shield.)
Thin bony plate separating the upper part of the middle ear (epitympanon) from the mastoid cells; its

lower edge is the upper part of the bony ridge on which the TM is attached. The scutum is eroded at a
relatively early stage by secondary cholesteatoma.
Ice-cream cone appearance= incus and malleus= u r in the epitempanum, in
While in mesotempanum it appear as 2 dots or 2 lines
Molar tooth sign( incus and malleus)
Loss of Molar tooth sign indicates eroded incus in cholesteatoma

29

oblique sagittal view of left malleus and incus. (a, b) Orthogonal axial (a) and coronal (b) reference images
show the plane of reconstruction (white line). (c) Double-oblique sagittal image shows the molar toothlike
appearance of the incudal body (IB), incudomallear joint (IMJ), mallear manubrium (MM), and incudal long
process (ILP). (d) Double-oblique sagittal image in another patient shows a missing cusp of the molar tooth
(arrow), a finding that indicates the complete erosion of the incus by a cholesteatoma, at surgery.

Fig. 36. Acquired middle ear cholesteatoma. (A) Axial 1.25-mm CT through the left temporal bone showing
complete opacification of the middle ear and mastoid with erosion of the mastoid septa (curved arrow), long
process of incus (arrow), and stapes (arrowhead). Note location of the Prussak's space (). (B) Coronal
reformats of axial CT showing truncated scutum (double arrowhead), opacification of Prussak's space (), and
erosion of the ossicular chain, all hallmarks of acquired cholesteatoma. Erosion of the long process of incus
(arrow) and stapes extending to the round window (curved arrow) is noted, as well as erosion of the inferior
wall of the tympanic facial nerve canal (arrowhead).

Fig. 37. recurrent, acquired cholesteatoma ,intracranial localization. (A) Sagittal T1 postgadolinium
MRI showing predominantly low-signal mass lesion (arrowheads) centered above the temporal bone
(arrow) and displacing the temporal lobe, demonstrating central strands of enhancement (unusual for
cholesteatoma). (B) Diffusion-weighted MRI, signal in the lesion (arrows), suggesting diffusion
restriction characteristic of cholesteatoma.

30

Fig. 38. New bone formation in chronic mastoiditis. Axial CT at bone windows setting showing
replacement of the mastoid air cells predominantly by sclerotic bone (arrow). Low-attenuation
material in the middle ear was suspicious for a cholesteatoma (arrowhead).
http://www.sciencedirect.com/science/article/pii/S0891552007000281
Grommet insertion current trends
used to manage Otitis media catarrhalis. MC surgical procedure performed in children.
Indications: Bluestone and Klein (2004) revised indications /prevailing antibiotic spectrum.
1. chronic OME not responding to antibiotic/ persisted > 3 months if bilateral or 6 months (unilateral.
2. Recurrent AOM , antibiotic prophylaxis fails. 3/4 in previous 6 m / 4 or more attacks in previous year.
3. Recurrent episodes of OME ( duration of each episode does not meet the criteria , cumulative duration
is excessive (6 episodes in the previous year)
4. Suppurative complication is present / suspected. It can be identified if myringotomy is performed.
5. Eustachean tube dysfunction even if the patient doesnt have middle ear effusion. Symptoms are
usually fluctuating (dysequilibrium, tinnitus, vertigo, autophony and severe retraction pocket).
6. Otitis barotrauma to prevent recurrent episodes.
Problems with Grommet insertion: Common problems include:
1. Segmental atrophy of TM
2. Tympanosclerosis
3. Persistent perforation syndrome (rare)
Before treating OME the following factors should be borne in mind.
Pneumatic otoscopy :differentiate otitis media with effusion from acute otitis media.
Duration of symptoms should be carefully documented.
Children with risk for learning / speech problems should be carefully identified.
Hearing should be evaluated in all children who have persistent effusion for more than 3 months.
Grommet insertion can be performed under local anesthesia.

31

Incision is made in the antero inferior quadrant of ear drum. The incision is given along the direction of radial
fibers of the middle layer of ear drum. This causes minimal damage to the radial fibers. It also enables these
fibers to hug the grommet in position.
Keratosis obturans
accumulation of desquamated keratin in the external auditory meatus.
DD: primary auditory canal cholesteatoma = invasion of squamous tissue from the external ear canal into a
localized area of bone erosion.
Pathology: The keratin plug in lumen of expanded ear canal. keratin squames are shed from deep ear canal
forming a lamina. It appears like onion skin.

Etiology: due to abnormal reversed epithelial migration of ear canal skin.. (surface epithelium over pars
flaccida migrates downwards to the pars tensa and then moves inferiorly across the drum).
Keratosis tympanicum: Is also caused by abnormal migration of squamous epithelium lining the deep portion
of the EAC. This condition is also associated with unilateral tinnitus.
Types of keratosis obturans:
a. Inflammatory type: Viral infections commonly cause. The inflammatory temporarily alters epithelial
migration. This condition can only be cured by removal
b. Silent type: no predisposing acute infections. caused by abnormal separation keratin that persists even after
the removal, and will need repeated removals.
c. Primary auditory canal cholesteatoma: Etiology is uncertain. thought to be caused by trauma to the bone
covering the external canal. This could also be caused by surgical trauma as in stapedectomy. The piece of
exposed bone in the external canal becomes infected and sequests. The lining epithelium migrates into this area
causing the formation of cholesteatoma. This condition is characterized by ear pain which is dull and aching in
nature. It is not associated with hearing impairment.
Keratosis obturans commonly occur in young patients.
Clinical features:
1. Severe ear pain
2. Mild / moderate CHL
3. Associated bronchitis / sinusitis - common
On examination:
The ear canal appears to be widened, making the ear drum stand out. CT scan of temporal bones may reveal
canal erosion and widening.
After surgical removal the specimen evaluated to rule out malignancy.

32

Management:
1. Surgical removal under G.A.
2. Canal plasty is helpful in recurrent cases
3. Mastoidectomy should done in cases with primary cholesteatoma of external canal.
Anatomical notes and landmarks
Sup SCC is the deepest
Facial n below lat SCC, if you remove the lat canal= loss of hearing
Processus cochleariform= landmark for :horizontal VII n is posterior to it
Short process of incus(, lies in fossu incudis) point toward tympanic segment of facial
digastric ridge(DR) is identified and preserved as a pointer to the facial nerve
Subarachnoid artery runs between SCC= bleeding
Stapes ant crora: long & thin- Post crura: short and thick
Henle spine: indicates mastoid antrum
Santorini's fissures: Vertical fissures in anterior cartilage of the external acoustic meatus (ear canal).
McEwen's triangle (suprameatal), mastoid fossa, foveola suprameatica, or, ( instrument pushed to antrum.
Stapedius ms origin from pyramidal eminence

(singular nerve) supplying ampulla of PCC lies close to 2ry TM. = landmark in singular neurectomy
Pinna: fibro elastic cartilage, develop by 20wk from 1st,2ed pharyngeal pouch
Koerner septum: persistence petro-squamus suture line(between squamous and petrous bone...
Koerner septum separates superficial from the deeper Cells and antrum
Cog: transverse ridge between anter & post epitympanum , bony septum that detaches from the tegmen
tympani cranially, heading vertically toward the cochleariform process, in front of malleus head
Traumanns triangel: Bony labyrinth anteriorly. Sigmoid sinus poster. Dura +sup petrosal sinus superiorly
= weak spot for infections spread to cerebellum, drilled as approach to posterior cranial fossa lesions
ated at the petrous apex containing the abducent nerve.
Donaldson line : line drawn posteriorly from the course of horizontal SCC. The line is perpendicular to
PSCC. The endolymphatic sac is located inferior to this line.

33

Dorello's canal :osteo-fibrous canal situ,It lies below Gruber's ligament (petrosphenoidal ligament)
between the petrous apex and clivus. In majority of cases it is found at the medial most end of petrous
ridge at the confluence of inferior petrosal sinus, basal sinus and posterior end of cavernous sinus.

Abducens nerve. Axial 0.8-mm-thick SSFP MR image shows the abducens nerve where it enters the Dorello
canal (arrow) along the posterior aspect of the clivus. Vascular landmarks include the basilar artery (black
arrowhead) and the anterior inferior cerebellar artery (white arrowhead).
It is important to note that the abducens nerve runs almost the entire length of the clivus.
Facial recess
aerated extension posterior superior portion of the middle ear cavity medial to the tympanic annulus and lateral
to the fallopian canal.
Boundaries:
Medial Facial nerve
Lateral Tympanic annulus
Superior Incus buttress (near the short process of incus)
Running through the wall between these two structures with varying degrees of obliquity is the chorda tympani
nerve. Chorda tympani nerve always run medial to the TM.
Drilling in this area between the facial nerve and annulus in the angle formed by the chorda tympani nerve
leads into the middle ear cavity. This surgical approach to the middle ear = facial recess approach.
Uses of facial recess approach:
1. Used to reach hypotympanum of middle ear
2. Used to place cochlear implant electrode into the cochlea via the round window.
3. Horizontal portion of facial nerve can be accessed via this approach. used for decompression of horizontal
division of facial nerve.
Occasionally cholesteatoma of middle ear cavity can invade the mastoid antrum without involving the aditus.
It has been hypothesized that drilling this area can provide additional avenue for mastoid aeration.
Land marks used to identify this region:
1. External genu of facial nerve medially
2. Fossa incudes superiorly
3. Chorda tympani laterally

34

4.

TM anteriorly and laterally.

Mastoidectomy drilling tips

1. It is better to set Microscopic magnification : 4 - 6X = complete orientation. Higher magnification levels
are necessary to appreciate the minute details.
2. choose the largest possible burr bit for initial drilling = less damage. Using small burrs is dangerous.
3. The length of the cutting burr is adjusted according to the depth of the area to be drilled. Shorter the burr
length better is the control.
4. Majority of bone drilling should be performed by using cutting burrs.
Diamond burrs : when drilling over facial nerve area, dura, sigmoid sinus or sometimes to obtain hemostasis
over bleeding from bone.
5. The hand piece should be held like a pen.
6. Drilling should be performed in a tangential direction as the cutting surface of the burr is present in its
sides.
7. The tip of the burr not be used for drilling.
8. Only minimal pressure should be exerted over burr bits during drilling.
9. For fine drilling the head of the patient should always be supported.
10. The direction of rotation of burr should always be away when drilling over important structures.
(Reverse).
11. Liberal irrigation should be performed during the whole of the drilling process. This is more important
when drilling is performed over facial nerve area / labyrinth.
12. It will be prudent to place the suction tip between the burr bit and an important structure as it will prevent
damage to the structure even if the hand
piece slips.
13. Canalplasty should be performed whenever a bony overhang obscures complete visualization of the ear
drum.
14. while drilling care should be taken not to touch the ossicular chain.
15. Middle cranial fossa dural plate should not be drilled as this could cause CSF otorrhoea.
Surgical notes-Tympanoplasty- mastoidectomy
First canaloplassty, make it wider to better access,Use conical burr first, then diamond burr
Make 2 falps:sup- infer in EAC
Antrum is 3 mm above the level of superior EAC
Notice bone color change- Clean granulation- glue from aditus
Bone bleeding: control by bone dust/dimanond burr
Do not make posterior meatal wall paper thin in mastoidectomy- but it is done in Tympanoplasty
Notch of Rivinus: defect in sup annulus/tempomastoid suture/ in post ear canal, above sharp process of maleus,
Important: Chorda Tympani identified
there is a small cartilage named after Indian Dr
Sino-dural angel @ 3 Oclock: open it
First land mark: lateral semicicular canal- Spine of Henle
Tympanomastoid- suture line @ 5 Oclock: if very promonant
Tempano squamus looks like anterior spine of henle @ 10 Oclock, remove it by conical burr
Mastoid air sinus is very variable anatomy, be patient,

35

Hypotensive tech: raise pt head, ask anathesiologist, infiltration of epi in aud canal before
surgery( 9-6-3 Ocklock)
Stepedectomy
worst hearing ear should be approached first. local anesthesia (hearing restoration can be immediately
evaluated , can report symptoms of vertigo, useful in patients with medical conditions that preclude them from
general anesthesia.
The EAC is injected with 1% lidocaine with epinephrine in four quadrants at the bony cartilaginous junction.
Raising the tympanomeatal flap: incision (roller / round knife). The canal skin is incised at the 6 and 12
oclock , 6-8 mm lateral to the annulus(to allow enough skin to drape back over the scutum ( partially
removed). A lateral curved cut parallel to the annulus connects these incisions. If the flap is too big, = difficult
to retract it out of the way of the operating field. The flap is elevated anteriorly to the annulus. Cotton soaked
with adrenaline can be helpful in with elevation and controlling bleeding. The annulus is then removed from
its sulcus with a Rosen needle. The chorda tympani preserved if possible. Releasing its attachments to the
medial surface of the malleus can slack on the nerve and allow it to be move out of the way without
stretching it. it should be cut rather than stretched. severe prolonged dysgeusia from stretching rather than
cutting it. risk of retrograde inflammation to the facial nerve with possible delayed facial nerve paralysis.
Exposure: Removal of a portion of scutum (= adequate visualization of footplate, oval window
niche). A curette removes bone just lateral to scutum first=thins the scutum = easy removal. Attempts to
remove the edge first may result in slipping of the instrument and injury to surrounding structures. It is
important to remove enough bone posteriorly to allow for visualization of the pyramidal eminence and
superiorly = visualization of inferior facial nerve. A small amount of bone should be left over the incus
superiorly to prevent retraction of the TM onto the lateral surface of the ossicles.
Middle ear examination: 3 ossicles palpated for fixation prior & after division of the incudostapedial joint.
If malleus or incus fixation ,must be addressed = optimal hearing results. small focus of active otosclerosis is
found, @ anterior pole of the stapes footplate. Gentle palpation of the footplate will sometimes mobilize it. Pt
treated with sodium fluoride to convert the focus into the sclerotic phase. In general, re-fixation usually
occurs, making this technique less appealing. The tympanic segment of the facial nerve should be examined
and overhang into the oval window niche as well as any bony dehiscence should be noted. Dehiscence s in
50% of all ears :on the medial and inferior aspect of the nerve. The distance between the footplate and the
medial surface of the lower aspect of the long process of the incus is then measured (usually 4.5 mm). About
0.25 to 0.50mm is added to the measured distance to accommodate entrance of the prosthesis slightly in to the
vestibule. Measurement before disarticulation of the incudostapedial = accurate, since movement of the incus
is possible with joint disarticulation. Some surgeons still prefer to perform the measurement after
disarticulation.
Harvesting a graft: oval window seal grafts: vein ( hand), temporalis fascia, tragal perichondrium,
ear lobule fat, and periosteum. Gelfoam not used (granuloma , SNHL). The graft is harvested prior to
footplate fenestration or removal so that it is immediately available for use to prevent excessive perilymph
leakage. This is particularly important if a perilymph gusher is encountered for immediate patching.
Retrograde Stapedectomy/Stapedotomy: Decision (total or partial stapedectomy versus
stapedotomy depends on the extent of stapes fixation. Hough 1960 suggested performing a partial anterior
stapedectomy for small anterior foci of otosclerosis. fracturing the middle of the footplate and anterior crus
and extracting the anterior half of the stapes. without cutting the stapedius tendon. advantage in patients who
work around loud noises.

36

Total stapedectomy : for extensive fixation , for a floating footplate. The incudostapedial joint is first
divided with a round or joint knife prior to division of the stapedius tendon. Pressure is applied at the joint,
parallel and opposite that of the tendon. The tendon supports the footplate preventing inadvertent avulsion and
inner ear trauma. place a small hole with a pick/perforator(0.3/0.6/.8mm) in center /post footplate/ poster is
deeper) (if it is thin) prior to division of the joint. = place for a hook to be used to extracted the footplate if it
becomes mobile during manipulation. Use .3,then .6, then .8mm perforator to widen the finistrum(never
suction on fenestrum)
Incus and malleus mobility are then checked. The stapedius tendon is divided (microscissors / laser. A curved
pick is then used to down fracture the superstructure towards the promontory and is then extracted. The
footplate is then removed with right angle hooks. graft is placed over the oval window and an appropriate
sized piston or prosthesis is placed from the long process of the incus to the graft.
Stapedotomy or the small fenestra : originally used in obliterated or solid footplates. many began using
stapedotomy for non-obliterative cases. The advantage : less risk of trauma to the vestibule and less incidence
of migration of the prosthesis and fixation by scar tissue as is seen in stapedectomy techniques. Initially sharp
instrumentation was used to make the fenestration which required a great degree of technical proficiency. In
1978, the first laser stapedotomy was performed by Perkins and has since become a widely accepted method
for fenestrating the footplate.
3 most commonly used lasers : K titanyl phosphate (KTP/532), argon, and Co2. The KTP/532 and
argon both are visible, do not require a separate laser to act as an aiming beam, greater target accuracy
absorbed by hemoglobin making them better coagulators than the CO2 laser. The CO2 laser is an invisible
beam and must be used with a separate aiming beam, usually a red helium-neon beam which produces an illdefined fuzzy border. The CO2 laser is less expensive and requires less maintenance. The risk of using the any
laser in the oval window area is overheating of surrounding tissue including the facial nerve. Causse
recommends allowing 10 to 15 seconds between pulses for cooling. Suction must be used to evacuate the
smoke and inadvertent suctioning of perilymph may occur.
laser, or microdrill : create a fenestration in the footplate. ,use the drill after laser to complete the
fenestration. The fenestration at the center, Causse placing the fenestration more posteriorly. (vestibular fluid
wave by rocking posteriorly, )more physiologic.
Sealing the oval window and placement of the piston: Causse is a proponent of vein grafts. He
makes the argument that it is important to reconstruct the annular ligament. The function of the annular
ligament is to provide both resistance (dissipation force) to protect the inner ear from acoustic trauma and
elasticity for acoustic transfer (disrupted by otosclerosis). Because of the inherent elastic properties of vein, it
is better suited to recreate this physiologic function. Vein, fat, and perichondrial grafts require additional
incisions unlike temporalis fascia or blood.
Once the oval window has been sealed the appropriately sized prosthesis is placed into the fenestra and
around the incus. Multiple stapes prostheses developed. The sharp or beveled polyethylene strut, and the wire
prosthesis attached to gelfoam has been associated with fistula, Most stapedectomies today are repaired with a
wire prosthesis attached to a connective tissue graft that covers the oval window. Stapedotomies are usually
repaired with a piston type prosthesis of 0.6 mm or 0.8 mm diameter, rests on a connective tissue graft. The
prosthesis usually attaches to the long process of the incus, either with a wire that is crimped into place, or a
bucket handle that fits under the lenticular process of the incus. After placement of the prosthesis, the malleus
is palpated to insure appropriate movement of the repaired ossicular chain. When choosing the diameter of the
prosthesis see how wide the oval window niche is. A deep narrow niche may require a thinner prosthesis such
as a wire. If the patient is awake, hearing can be tested by whispering into the patient's ear. The
tympanomeatal flap is then redraped and the ear canal is packed with Gelfoam.

37

Complications in stapes surgery

Overhanging and dehiscent facial nerve
Occasionally the facial nerve is dehiscent in the fallopian canal and protrudes over the oval window
niche such that it obstructs the view of the stapes footplate. If the surgeon is not familiar with management of
this problem the surgery should be aborted. Facial nerve displacement can be used for conventional manual
stapedectomy or in laser stapedotomy. Perkins (2001) describes the maneuver for use with the laser. The
nerve is first displaced to allow for examination of the footplate. This is done by compressing it superiorly for
short periods of time (5 seconds) using No. 24 suction. 10 to15 seconds is allowed to lapse before performing
the maneuver again. This should be repeated until adequate assessment of the footplate is complete. Then,
while the nerve is retracted and the footplate visualized, the laser is pulsed and the usual rosette pattern is
created. A wire type prosthesis is then used. It can be bent to accommodate the facial nerve, however hearing
results will not be as good. An addition 0.50 to 0.75mm should be added to the selected length of the piston to
allow for curve around the nerve.
Floating footplate
occurs when the footplate dislodges from the surrounding oval window niche. Commonly due to iatrogenic
( palpation of the footplate with a pick or the when burring a fenestra, or during division of the incudostapedial
joint). The first issue in management of the floating footplate is prevention. Use of the laser to perform
stapedotomies may prevent this complication by reducing direct manipulation. H. House recommends drilling
a safety hole into the footplate at the beginning of the procedure to help in the removal of the footplate should
it become mobile.
If the surgeon is inexperienced, termination of the procedure and referral to someone more familiar with this
complication is not unreasonable. One way to manage this problem is to perform a total stapedectomy.
Proponents of this technique do so to prevent a sinking footplate. Attempts at removing the footplate can,
however, result in fragments of the stapes falling into the vestibule. These fragments should not be removed.
Howard House (2001) recommends drilling down the posteroinferior promontory to allow access of a right
angle cooked underneath the footplate without touching it. It is then elevated toward the facial nerve and is
removed. Other surgeons advocate performing a fenestra with the laser. In these situations hearing results are
adequate (97% ABG closure) if the footplate is thin or blue (diffuse footplate). If the footplate is very thick or
white (biscuit footplate), hearing results are much poorer (52% ABG closure) and refixation occurs in 30%.
Perkins recommends that if the laser is not available, the surgery should be postponed for 4 months followed
by laser stapedotomy.
Diffuse obliterative otosclerosis
When the footplate, annular ligament and edges of the oval window niche are all involved with
otosclerosis it is termed obliterative otosclerosis. These cases are managed by thinning the bone with a
small cutting burr. First the anteroposterior edges are thinned until they are blue. Then the opening in is
enlarge sufficiently to cover the area with a graft and to insert a prosthesis. Long-term hearing results for
obliterative disease are poorer, with re-ossification and obliteration occasionally occurring.
Perilymph gusher
This complication is associated with a patent cochlear aqueduct and results in excessive perilymph
leakage after fenestration of the footplate. It occurs more common on the left side and in patients with
congenital footplate fixation. A perilymph gusher the risk of post-operative SNHL. Another benefit of the
control hole placed initially during the surgery is that it can lead to early identification of a gusher.
Management includes roughing up the surface of the footplate followed by rapid placement of an oval window
seal. Completion of stapes reconstruction with a prosthesis can still proceed, however stapedectomy is
contraindicated. Postoperatively the patient should be treated as if they had a cerebrospinal fluid leak or
perilymph fistula with the head of the bed elevated, bed rest, stool softeners, avoidance of Valsalva maneuvers,
occasionally a lumbar drain.

38

Round window closure

Unlike the oval window, hearing loss is not affected by closure of the round window unless it
becomes complete. Upwards of 50% of patients with otosclerosis have round window involvement, however
<1% have complete closure affecting hearing. In these patients, surgery should be avoided because they have
a higher risk of post-operative SNHL.
SNHL
Permanent sensori-neural hearing loss is the most dreaded complication of stapes surgery. The incidence of
this complication ranges between 0.6% and 3% in large series. The incidence depends on multiple factors
including extent of disease (particularly the presence of cochlear involvement), experience of the surgeon,
techniques employed, age of the patient, and history of prior surgery. Most authors report that in experienced
hands, the risk should be < 1% for non-revision cases.
SNHL after stapes surgery may be either temporary or permanent. Most patients develop some degree
of serous labyrinthitis in the first couple of postoperative days which is manifested clinically by gait
unsteadiness, vertigo with head movement, and a slight in hearing for frequencies above 2 kHz, along with
reduced speech discrimination. By definition, all symptoms including hearing loss resolve. Reparative
granuloma may cause temporary SNHL if it is addressed within the first two weeks of development.
Permanent SNHL may result when serous becomes suppurative labyrinthitis. More commonly it is
due to direct trauma during surgery particularly if extensive drilling is carried out. This is confounded in
patients with extensive cochlear otosclerosis with endosteal involvement. In these cases the cochlear is fragile
and prone to basilar membrane breaks. Other potential causes of permanent SNHL are large or sudden drops
in perilymph pressure (perilymph gusher, or extensive suctioning of perilymph), impaired cochlear blood flow
following neck torsion during surgery, and medial displacement of the prosthesis.
Facial nerve paralysis
The risk is always present which any manipulation of the middle ear structures. Despite the close
proximity of the nerve in stapes surgery, the risk of injury and paralysis is low (<1/1000 cases). it may be a
result of : direct trauma with cold instrumentation or with the laser may occur. If the laser is pulsed too
frequently, the nerve may become heated and swell. 2-stretching of the chorda tympani nerve may result in
retrograde inflammation of the facial nerve. The majority of cases of facial nerve paralysis are incomplete and
temporary. A steroid taper is usually given and resolution of the paralysis or paresis can be expected in weeks
Vestibular symptoms
The purpose of performing stapes surgery under local anesthesia besides immediate hearing evaluation
is to avoid injury to the saccule. There are multiple other sources of vestibular stimulants during these
surgeries, however. These include irrigation around the lateral semicircular canal, palpation of the stapes, and
local anesthetic. Some authors feel that these confounding factors make intra-operative monitoring of
vestibular symptoms less reliable.
Postoperative vestibular symptoms are usually short lived but may persist for several days and less
commonly up to months. Small fenestra techniques, particularly with the laser, have been shown to reduce the
frequency, severity, and duration of vestibular symptoms after stapes surgery when compared to stapedectomy
techniques.
An oval window fistula should be suspected in patients with vertigo and associated fluctuating or
progressive SNHL and tinnitus. This occurs early in the postoperative course. A history of sudden barometric
trauma should be elicited from the patient and documented and audiometry should be performed. If there is a
high index of suspicion, middle ear exploration should be performed. Findings may include a medially

39

displaced prosthesis with or without perilymph leakage. The oval window should be patched. Progression of
the hearing loss should be halted and vestibular symptoms should diminish.
Reparative Granuloma
a well known cause of SNHL after stapes surgery. commonly reported when gelfoam used as an oval window
sealant. 1% and 2% of cases. C/P :initial good hearing , develops a drop in their bone conduction thresholds
(1-2 weeks postop )+ tinnitus and vertigo, a reddish TM posteriorly. Rx: is exploration and removal of the
granuloma (surrounds prosthesis and incus. complete resolution of there original postop hearing if the problem
is addressed early.
Recurrent CHL and revision stapedectomy
The most common cause of failure of stapes surgery for otosclerosis is displacement or slippage of the
prosthesis. ABG may occur immediately secondary to technique or over months to years secondary to
gradual thinning of the incus with subsequent slippage of the prosthesis. If the prosthesis is placed to tight
around the incus compression necrosis may result. The tip of the prosthesis sometimes becomes adherent to
the edge of the niche. Other causes may include stapes re-fixation or continuation of disease progression with
re-obliteration of the oval window niche and ankylosis of the malleus or incus.
Any of these causes may be an indication for revision stapes surgery. It is important to counsel
patients extensively on the reduced success rate of revision surgery. Glasscock reported on 828 cases of stapes
surgery from 1970-1994. Air-bone gap closure to within 5 dB was achieved in 91% of primary operations
compared to 66% of revision cases. The best candidates for revision surgery are those patients who had
excellent results from there first surgery and have experienced gradual worsening of the ABG over a period of
months to years.
Non-surgical
Amplification: A hearing aide is an acceptable option for patients who do not want to undergo surgery
for otosclerosis or in those patients who are not fit for surgery. Certainly the option of amplification as an
alternative to surgery should be discussed with all patients. The benefit over surgery is the avoidance of the
risk of significant SNHL. Patients who undergo successful surgery have a higher satisfaction rate than those
wearing hearing aids. This is probably due to a couple of reasons. The first is the canal occlusion effect in
which the hearing aide gives the patient the sensation they are hearing in a barrel. The other is the fact that
amplification is not used at night.
Endolymphatic sac decompression
Donaldson line : line between lat SCC and infer SCC ,endolymphatic sac is inferior to this line.
The plane lateral to the temporalis fascia is entered.
A periosteal T-shaped incision along the linea temporalis. A perpendicular incision from the linea temporalis
incision is extended inferiorly toward the mastoid tip.
The musculoperiosteal flap is elevated forward until the posterior bony EAC is reached. The remainder of the
musculoperiosteum is elevated posteriorly ,Mastoidectomy : high-speed drill using cutting burs for aggressive
bone removal and using diamond burs : nears critical structures. The tegmen mastoideum, sigmoid sinus, and
sinodural angle are skeletonized, and the posterior bony ear canal wall is thinned. The mastoid tip air cells are
opened to the level of the digastric ridge, near level of descending facial nerve as it courses toward the
stylomastoid foramen.
Bone removal anterosuperiorly to mastoid antrum as Koerner septum is identified and opened. The prominence
of horizontal semicircular canal is identified. The zygomatic root toward the epitympanum (posterior
epitympanotomy) is opened to identify incus = landmarks for orientation within the mastoid.

40

Bone removal over the sigmoid sinus inferiorly toward the jugular bulb. The mastoid segment of the facial
nerve is skeletonized. This will assist in locating the retrofacial air cells and protecting facial nerve.
Using horizontal semicircular canal, Donaldson line is identified , sac is inferior to this line.
The endolymphatic sac usually presents as a dural duplication or dural thickening during exposure of the
posterior fossa dural plate between the sigmoid sinus posteriorly and the posterior SCC anteriorly. Removal of
the retrofacial air cells, =gain more exposure to locate the endolymphatic sac. endolymphatic sac is deep and
inferior to the posterior SCC (infralabyrinthine). sac is located, followed forward toward the endolymphatic
duct that courses just medial of the posterior semicircular canal.
Once the endolymphatic sac is identified, the sac may be incised with a sharp sickle knife, and the lumen,
characterized by its glistening and shiny appearance, is entered with an annulus elevator or blunt probe.

The right endolymphatic sac is opened. Shunt may be placed inside the
lumen of the sac.
A silicon sheet (thickness 0.010 in or 0.05 mm) is cut and positioned inside the lumen. A commercially
available shunt may also be used . There is usually no need to secure this silicone fashioned shunt.
The musculoperiosteal flaps are then re-approximated and sutured together. The postauricular tissues are
closed in layered fashion.
A mastoid pressure dressing is placed.
Tuning Fork Tests: Rinne, Weber, ABC, Schwabachs Test
http://earnosethroatclinic.blogspot.com/2010/12/tuning-fork-tests-rinne-weber-abc.html
The clinically useful tuning fork tests include:
(a) Rinne test. In this test air conduction > bone conduction. A vibrating tuning fork is placed on the patient's
mastoid and when he stops hearing, it is brought beside the meatus. If he still hears, AC is more than Be.
Alternatively, the patient is asked co compare the loudness of sound heard through
air and bone conduction. Rinne test is += AC is longer or louder than BC. in normal or SNHL.
negative Rinne (BC > AC) = conductive deafness ,minimum air-bone gap of 15-20 dB.
A Rinne test equal or negative for 256 Hz but positive for 512 Hz indicates air-bone gap of 20-30 dB.
A Rinne test negative for (256 and 512 Hz )but positive for 1024 Hz =AB gap of 30-45 dB.
A Rinne negative for all of 256, 512 and 1024 Hz, indicates air-bone gap of 45-60 dB .Remember that a
negative Rinne for 256, 512 and1024 Hz indicates a minimum AB gap of 15, 30, 45 dB respectively.

False negative Rinne. in severe unilateral SNHL. no air conduction but responds to bone conduction (from the
opposite ear / transcranial transmission of sound. correct diagnosis : masking non-test ear with Barany's noise
box during bone conduction. Weber test will further help as it gets lateralised to the better ear.

41

(b) Weber test. In this test, a Vibrating tuning fork is placed in the middle of the forehead or the vertex and the
patient is asked in which ear the sound is heard.
Normally, it is heard equally in both ears. It is lateralized to the worse ear in conducti ve deafness and to the
better ear in sensorineural deafness. In weber test, sound travels
directly to the cochlea via bone. Lateralisation of sound (512 Hz) =CHL of 15-25 dB in ipsilateral ear or a
SNHL in the contralateral ear.

(c) Absolute bone conduction (ABC) test. BC is a measure of cochlear function. In ABC test, patient's bone
conduction is compared with examiners. EAC of both occluded , to prevent noise entering through AC route.
In CHL, the patient and the examiner hear the fork for the same duration of time.
In SNHL, patient hears the fork for a shorter duration.

(d) Schwabach's test. BC is compared with normal hearing person (examiner) but meatus is not occluded. It
has the same significance as absolute bone conduction test. Schwabach is reduced in SNHL and lengthened in
conductive deafness.( show off= shwabach)
Tuning fork tests
subjectively assess a persons hearing acuity. This test can in fact be performed by using tuning forks of the
following frequencies (254 Hz, 512 Hz, and 1024 Hz). Frequencies below 254 Hz are better felt than heard
and hence are not used. Sensitivity for frequencies above 1024 Hz is rather poor and hence is not used.
Prerequisites for an ideal tuning fork:
1.
It should be made of a good alloy
2.
It should vibrate at the specified frequency
3.
It should be capable of maintaining the vibration for one full minute
4.
It should not produce any overtones
Methodology of using tuning fork:
The tuning fork must be struck against a firm surface (rubber pad / elbow of the examiner). The fork should be
struck at the junction of upper 1/3 and lower 2/3 of the fork. It is this area of the fork which is capable of
maximum vibration.
The vibrating fork should be held parallel to the acoustic axis of the ear being tested.
Advantages of tuning fork tests:
1.
Easy to perform
2.
Can even be performed at bed side
3. Will give a rough estimate of the patients hearing acuity
The following tests can be performed using a tuning fork:
1.
Rinne test
2. Weber test
3. ABC test
4.
Bing test occlude EAC
5.
Politzer test
6.
Bing Entotic test
7.
Stengers test
8.
Gelle test
9.
Chimani-Moos test

42

Rinne test:
compare AC with BC thresholds. ( normally AC > BCconduction. 512 fork is used. it is placed at the mastoid.
Pt signal when he stops hearing , fork is put close to the EAC (prongs vibrate parallel to the acoustic axis.
normal pt: hears fork as soon as it is on front of the ear. = +ve Rinne test. (AC is > BC ).
In CHL unable to hear the fork when in front of the ear (BC > AC). = negative Rinne.
In profound unilateral deafness , sound is heard by opposite ear = false positive Rinne.
Use of Rinne test in quantifying conductive deafness:
Conductive deafness of more than 25 dB is indicated by negative Rinne with 512 Hz fork, while it is positive
for 1024 Hz.
If Rinne is negative for 256, 512 and 1024 Hz then conductive deafness should be greater than 40dB.
Weber's test: done first
Is a tuning fork test ,assess hearing levels , easily detect unilateral CHL/SNHL.
MC used is 512 Hz
Fork on vertex / chin. which ear hears the sound better. In normal ear and in bilateral equally deaf ears the
sound will be heard in the mid line. This test is very sensitive in identifying unilateral deafness. It can pick out
even a 5 dB difference between the ears.
Theory:
unilateral CHL: hears loudest in the affected ear. conduction problem masks noise of the room, whilst inner ear
picks the sound by skull bones perceived as a louder sound than in the unaffected ear.
Inadequacies:
useful in individuals with hearing that is different between the two ears. It cannot confirm normal hearing
because it does not measure sound sensitivity in a quantitative manner. Hearing defects affecting both ears
equally, as in Presbycusis will produce an apparently normal test result.
Absolute Bone conduction test: identify sensorineural hearing loss. hearing of the patient is compared to that of
the examiner(assumed to be normal). In this test the vibrating fork is placed over the mastoid process of the
patient after occluding the EAC. As soon as the patient indicates that he is unable to hear the sound anymore,
the fork is transferred to the mastoid process of the examiner after occluding the external canal. In cases of
normal hearing the examiner must not be able to hear the fork, but in cases of sensori neural hearing loss the
examiner will be able to hear the sound, then the test is interpreted as ABC reduced. It is not reduced in cases
with normal hearing.
Bing test:
modification of webers test. The vibrating fork over the mastoid process and when it ceases to be heard the
examiners finger is used to occlude the EAC. In normal individuals the sound will be heard again. This is
because by occluding the EAC the examiner is preventing sound from escaping via the external canal. The
EAC acts as a resonating chamber. If the vibrating fork is not heard again after the external canal is occluded
=middle ear conduction is the cause for deafness. In patients with pronounced deafness if the vibrating fork is
heard after occlusion of EAC then deafness is due to labyrinthine causes.
Politzer test:
In this test the vibrating fork is held in front of open mouth and the patient is asked to swallow. If the
Eustachian tubes are patulous then sound will be intensified during swallowing. If only one tube is patulous

43

then sound will be accentuated only in that ear. Sometimes normal persons too may not hear the vibrating
fork.
Bing Entotic test:
Hypothetically this test is supposed to differentiate between deafness due to ankylosis of foot plate of stapes
from that of conditions interfering with mobility of other ossicles. This test is actually of historic value only.
Eustachian catheter is passed and to one of its ends is attached a speaking tube. If the patient is able to hear the
fork better via this tube than that from the EAC then middle ear ossicles other than foot plate of stapes is
supposed to be at fault.
Stengers test:
identify malingering. auditory phenomenon Stengers principle. :when 2similar sounds are presented to
both ears only louder of the two would be heard. When two tuning forks of same frequencies vibrate and held
simultaneously in the acoustic axis of both ears only the louder fork will be heard. Loudness : adjusted by
distance of the fork from EAC. ( closer to allegedly deaf ear. The patient will not acknowledge hearing in that
ear. According to Stengers principle he should be able to hear the louder fork. If the hearing loss in worse ear
is genuine, patient will respond to the signal presented to the better ear. This is known as negative Stengers
test. Feigning patient will not acknowledge hearing when louder sound is presented to the worse ear. This is
known as positive Stengers test.
Gelle test:
In this test, the air pressure in the external canal is varied using a Siegles speculum. The vibrating fork is held
in contact with the mastoid process. In normal individuals and in those with sensorineural hearing loss, d
pressure in the external meatus causes a in the loudness of the bone conducted sound. In stapes fixation no
alteration in the hearing threshold is evident.
Chimani-Moos test:
a modification of Weber test. fork is placed on the vertex, pt indicates that he hears it in the good ear and not
in the deaf ear. The meatus of the good ear is then occluded. A genuine deaf pt is able to lateralize the sound
to the good ear, where as a malingerer will deny hearing the sound at all.
Myringitis granulosa = granular/granulating
Granular myringitis (Myringitis granulosa) is a specific form of otitis externa characterized by granulation
tissue on the lateral aspect of ear drum sometimes with involvement of EAC.
Synonyms:
1. Granular myringitis
2. Granulating myringitis
3. Granulomatous otitis externa 4. Chronic myringitis
5. Acute granulomatous myringitis
Histopathology: Specimen for HPE is easy to obtain.
1. Oedematous granulation tissue with capillaries and diffuse infil of chronic inflam cells.
2. There is no lining epithelium over these granulation tissue
Etiology:
1. High ambient temperature
2. Swimming
3. Lack of personal hygiene
4. Exposure to local irritants
5. Foreign bodies
6. Bacterial and fungal infections
7. Occasionally may complicate grafted ear drum
Symptoms:
1. Foul smelling discharge from the involved ear
2. There is very little or negligible pain
3. There may be fullness / irritation in the affected ear
4. Hearing is nearly normal

44

5. Some patients may be totally asymptomatic

Signs: The ear drum is covered with purulent secretions, which on removal reveals the underlying granulation
tissue. Granulations may be localized (common) or diffuse., here small areas of the drum are affected, with
formation of one or more polyps. These granulations are common over the postero superior margin of the ear
drum. These granulations may also affect the adjacent wall.Despite all these signs the ear drum is intact.
All these patients must undergo PTA evaluation to rule out middle ear pathology.
Management: should be treated over a prolonged period to time.
Localized form: Meticulous microscopic debridement will help.
Topical administration of steroid / antibiotic ear drops will help
Application of caustic agents like formalin / trichloroacetic acid can be tried.
In refractory cases surgical removal of granulations can be attempted.

Middle ear cleft, Tympanum

The middle ear cleft includes the tympanum (cavity proper), the eustachean tube, and the mastoid air cell
system. The tympanic cavity is an air filled irregular space contained within the temporal bone. It also contains
the three auditory ossicles (malleus, incus and stapes) along with their attached muscles. For the purpose of
description the tympanic cavity may be considered as a box with four walls, a roof and a floor. The corners of
this hypothetical box is not sharp.
Lateral wall: The central portion is TM, while above and below the TM there is bone, forming the lateral walls
of the epitympanum (attic) and hypotympanum. The lateral wall of the epitympanum (attic) also includes that
part of the TM lying above the anterior and posterior malleolar folds - this portion of the ear drum is also
known as pars flaccida. ( lacks the middle fibrous layer)
The lateral attic wall (bony portion) is wedge shaped, its lower portion is also called the outer attic wall
(scutum =sheild in latin).. This bony portion is thin and its lateral surface forms the superior portion of the
deep portion of the external meatus.
Three openings in medial surface of the lateral wall of the tympanic cavity. 1-posterior canaliculus for the
chorda tympani nerve. This opening is situated at the junction between the lateral and posterior walls of the
tympanic cavity. This opening is usually present at the level of the upper end of the handle of the malleus. This
opening leads to the bony canal which descends through the posterior wall of the tympanic cavity(canal for
chorda tympani ). This canal also contains a branch from the stylomastoid artery which usually accompanies
the chorda tympani nerve.

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2- second opening : petrotympanic (Glaserian) fissure. opens anteriorly, above attachment of TM. This opening
is small slit about 2 mm long. It receives the anterior malleolar ligament. transmits tympanic branch of
maxillary artery to the tympani cavity.
3-third is the canal of Hugier. (medial to the Glaserian fissure) The chorda tympani nerve enters through this.
Roof: formed by the tegmen tympani which separates the middle ear cavity from the dura of the middle cranial
fossa. ,formed by the petrous portion and squamous portion of the temporal bone, The suture line between
these two is known as the petrosquamous suture line. This suture line is unossified in the young, and does not
close until adult life is reached. Through this suture veins from the middle ear may pass to the superior petrosal
sinus.
Floor: is narrower than the roof. lies in close relationship with the jugular bulb. The middle ear cavity is
separated from the jugular bulb by a thin piece of bone. Rarely may be deficient and the jugular bulb is
separated from the middle ear cavity only by fibrous tissue and mucous membrane. At the junction of the floor
and the medial wall of the middle ear there is a small opening which allows the entry of tympanic branch of
glossopharyngeal nerve to pass into the middle ear. This nerve takes an important part in the formation of
tympanic plexus.
Anterior wall: very narrow. because medial and lateral walls converge anteriorly. The lower portion is larger
than the upper portion. It has a thin plate of bone which separates this portion from the internal carotid artery
as it enters the skull. This plate has two openings for the carotico tympanic nerves. The upper opening
transmits the superior carotico tympanic nerve and the inferior opening transmits the inferior carotico tympanic
nerve. It is through these nerves that sympathetic nerves reach the tympanic plexus.
The upper smaller part of the anterior wall has two tunnels placed one below the other. The upper tunnel
transmits the tensor tympani muscle, and the lower tunnel transmits the bony portion of the eustachean tube.
Medial wall: separates the middle ear from the inner ear. most prominent is the promontory. projection by
basal turn of cochlea. + small grooves on its surface. These grooves contain the tympanic plexus of nerves.
Behind and above the promontory is the oval window (fenestra vestibuli). opening connecting the tympanic
cavity with the vestibule. closed by the foot plate of stapes and its surrounding annular ligament. The long axis
of the fenestra vestibuli is horizontal. Its inferior border is concave. on an average it is 3mm * 2 mm wide.
Above this fenestra vestibuli is the canal for facial nerve (horizontal portion) and below lies the promontory.
Hence the fenestra vestibuli lies at the bottom of a depression also known as fossula that can be of varying
depths depending on the position of the facial nerve and the prominence of the promontory.
The fenestra cochlea (RW_round window) lies just below and behind the oval window. closed by 2ry
TM( divided into an anterior and posterior portions by the presence of a transverse thickening). RW diameter
2mm. (3 layers; outer mucosal, middle fibrous and an inner endothelial layer). The membrane of the fenestra
cochleae does not lie at the end of the scala tympani but forms part of its floor. The ampulla of the posterior
semicircular canal is the closest vestibular structure to this membrane. The nerve supplying the ampulla of the
posterior semicirular canal (singular nerve) lies close to this secondary TM. The secondary TM forms a
landmark for the position of the singular nerve. ( useful in singular neurectomy for treatment of intractable
vertigo).
These two windows (oval & round) are separated by the posterior extension of the promontory. This is known
as the subiculum. Rarely a spicule of bone arises from the promontory above the subiculum and runs to the
pyramid on the posterior wall of the middle ear cavity. This spicule of bone is known as the ponticulus.
The round window faces inferiorly and a little posteriorly, lying under promontory and hence usually is
difficult to visualize.

46

The round window niche : trianglular : anterior, (posterosuperior and posteroinferior walls , meet posteriorly
leading to sinus tympani. : difficult area to visualise. Cholesteatoma may lurk in(/hidden site (MCC of
cholesteatoma recurrence, also sinus tympani).
Small mirrors = zinne mirror , used to visualise this area indirectly. Since sinus tympani lies under the pyramid,
removal of pyramid will bring the sinus tympani area into view .
The facial nerve canal : runs above the promontory and fenestra vestibuli in an anteroposterior direction. The
canal may occasionally be deficient leaving an exposed facial nerve (easily injured in ME surgery , ME
infections can cause VII palsy ). The anterior end of the facial nerve canal is marked by the presence of a bony
process known as processus cochleariformis. This curved projection of bone is concave anteriorly and it
houses the tendon of the tensor tympani muscle as it turns laterally to the handle of the malleus. Behind the
fenestra vestibuli, the facial nerve turns inferiorly to begin its descent in the posterior wall of the tympani
cavity.
The region above the level of the facial nerve canal forms the medial wall of the epitympanum or attic. The
dome of the lateral semicircular canal extends a little lateral to the facial canal and is the major feature of the
posterior portion of the epitympanum. In well pneumatised bones this dome of the lateral canal can be very
prominent.
Semicircular canals open into the utricle by Five orifices;
The length of eustachean tube is36mm; bony portion of eustachean tube is 12 mm
Sharpnell's membrane is Pars flaccida of ear drum;
Ampullary crest is seen in Semicircular canals;
The condyloid process of the mandible is closely related to Anterior wall of EAC canal;
Macula is found in Utricle and saccule
Supra pyramidal recess is the other name for Facial recess;
Prussak's space lies between Neck of the malleus and pars flaccida;
tensor tympani muscle arises from Cartilagenous portion of eustachean tube;
Rhynology
Epistaxis

Epistaxis is:commonly arising from the Little's area of the nose..

The Little's area contains the Kiessel bach's plexus. This plexus is formed by the following blood vessels:

Anterior ethmoidal artery

47

Superior labial artery

Sphenopalatine artery
Greater palatine artery

Woodruff's plexus : arterial plexus , anastomosis : pharyngeal, posterior nasal, sphenopalatine and posterior
septal arteries. histological : venous in origin.

Bleeding of Woodruff's plexus : slow but prolonged ooze. vessels have no muscle walls, hemostasis is
poor. Post nasal packing will have to be resorted to in rare cases to stop bleeding.

Common causes of epistaxis are as follows:

(A) Hereditary:Oslers Dis( HHT(telengietasia), lips, GIT, lack of contractile vessel walls
Bleeding disorders:Christmas disease, haemophilia and leukemia.
(B) Local causes of epistaxis:
Trauma: To the nose, paranasal sinuses +/- cerebrospinal fluid rhinorrhea.
Inflam/infec: Acute or chronic infections of the nose like.
Nasal diphtheria- Tuberculosis
Sinusits-Rhinosporidosis-Atrophic Rhinitis
Tumours:Benign: Nasopharyngeal angiofibroma, septal hemangiomas.
Malignant: Carcinoma of the maxilla, and ethmoidal sinuses.
Foreign Bodies: Maggots, Rhinolith
Aneurysms: In the extradural portion of internal carotid artery.
(C) Systemic causes:
Hypertension: MCC causes of epistaxis in the elderly. Atherosclerotic -Cirrhosis of liver
Chronic nephritis-Pyrexial illness
Bleeding disorders
(D) Miscellaneous:
Environmental: Turbinate epistaxis is common in places with low humidity.
Vicarious menstruation is a rare cause.
C/P
Bleeding from anterior prat of nose.Posterior bleeding my also present as Oral bleeding
Anxiety-Shock if severe and uncontrolled bleeding
Epistaxis digitorum: by aggressive nose picking. common in children. Bleeding from the little's area
investigations ::Monitoring of blood pressure-Bleeding Profile
Haemogram-CT Scan or Radiography
What is the treatment for epistaxis?
(1) General management of epistaxis:Ice pack over nose and head
Head high position-Pinching of the nostrils
Blood transfusion -Treatment of the medical cause if any
Coagulants like vitamin K, vitamin C if any deficiency
(2) Specific management of epistaxis:
Anterior nasal packing ( gauze or nasal tampons
Posterior nasal packing: under general anaesthesia. Ballon/ foley's
Local cautery with 50% trichloroacetic (TCA) required rarely
Endoscopy with cauterization of the bleeders.

Deviated septums
COTTLE TEST:,cheek is drawn laterally ,If the nasal airway improves on test side,the test is positive
=abnormality of vestibular component of nasal valve

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SMR(Submucus resection)
Elevating the mucoperichondrial and mucoperiosteal flaps on either side of the septal framework by a
single incision made on one side of the septum
Removing the deflected parts of bony and cartilaginous septum
Repositioning the flaps
Septal Hematoma: if small aspiration, if big, drainage, Nose is packed on both sides to prevent
reaccumulation
Ohngren's line : important prognosis of carcinoma maxillary :line drawn between what two
structures? Medial canthus and angle of the jaw
divides the maxillary sinus into (1) an anterior-inferior part, (2) a superior-posterior part. Tumours that
arise in the anterior-inferior part, i.e. below Ohngren's line, have a better prognosis
Sinusitis and scoring system

RHINOSINUSITIS
inflammation of the mucosa of the nose and paranasal sinuses
Most but not all are rhinologic in origin.
normally functioning sinuses depend on:1- normal :/patent sinus2. cilia 3. Mucous blanket
INCIDENCE

Acute viral rhinosinusitis is very high.

o Adults suffer 2-5 colds/year Children may suffer 7-10 colds/year

Only 0.5-2.0% of viral URTIs are complicated by bacterial infection. Be wise in giving them
antibiotics since most viral infections are self limiting (5-10 days)

However, it is the 5th most common diagnosis for antibiotic prescription (NAMCS). This is the reason
why there are a lot of resistant strains.
THE PREDISPOSING FACTORS

Upper Respiratory Tract infection. Viral/ Bacterial URTI- with ciliotoxins

Allergy. Cytokines causes cell death, renders mucociliary function inefficient

Laryngopharyngeal reflux (HCl and pepsin from GI tract (stomach) Can go up and irritate the
nasopharynx and eventually cause rhinosinusitis

Irritants: fumes, tobacco, cigarette, smoke. irritation to mucocilliary system. , changes mucous blanket
1-Systemic causes
quantitative and qualitative changes in mucus blanket.

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 Cystic fibrosis ciliary dyskinesia, the thicker/more viscid mucous causes stasis
Wegners granulomatosis: (necrotizing vasculitis- Respiratory- Renal) C-ANCA +ve
8S(Sinusitis-Septal perf, Saddle nose, Secretory OM, Sialadenitis, strawberry gum SNHL, Subglottic stenosis)
Ciliary dyskinesia ( Kartageners or Youngs syndrome), AR:absence of dynein arms, transposition of
microtubules
- recurrent sinusitis , nasal polyposis, Eustachian tube catarrh, otitis, bronchitis, and bronchiectasis
Immune deficiency
oPrimary IgA deficiency Secondary AIDS
2-Anatomical Causes
Causes problems in the mucociliary transport system
Deviated Septum (congenital)
Osteomeatal complex abnormalities
Choanal Atresia, Concha paradox, ConchaBullosa(air pocket forms in the middle turbinate
Abnormal Uncinate Process Adenoid Hypertrophy
3-Mechanical factors cause obstruction
Nasal polyps
Synechiae/ Stenosis post-surgery
Tumors
Deviated septum (traumatic)
Foreign Body( NG tube)
Post Surgery, Mucocoele, Pyocoeles
OSTEOMEATAL UNIT(OMU)
Very important unit, where all the problems takes place.
Parts
oHiatus semilunaris
oMiddle meatus, Maxillary sinus ostia
oUncinate process, Frontal recess
oEthmoidal-bullae ,Ethmoidal infundibulum
PATHOGENESIS
Main Problem: OMU obstruction
oImpaired ventilation
oStasis of secretions
oProliferation of microorganisms gram positive to gram negative
oMucoperiosteal thickening
If you have OMU obstruction you will have impaired ventilation, --secretions stasis). oxygen content is being
used up, organisms will shift from aerobic to anaerobic, gram (+) to gram (-). Cell death and chronic irritation
will result to mucoperiosteal thickening.
MUCOCILIARY TRANSPORT SYSTEM OF MAXILLARY SINUS
MULTIDIRECTIONAL
All secretions = normal ostia. Persistence/recurrence infection will develop biofilm. [2013 B]
All secretions go to the nomal ostium. Even if it is high,. in chronic infection, the mucociliary beatings cannot get
rid of the thick secretions, called biofilm. This is usually seen in patient with persistent infections even with
antibiotics thus requiring surgery to get rid of the secretions in the sinus.
MUCOCILIARY TRANSPORT SYSTEM OF FRONTAL SINUS
UNIDIRECTIONAl and Difficult to treat.

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 ciliary beating :renders it difficult to treat because it follows one direction. Supposedly, secretions should be
going down by gravity. Unfortunately, some of the secretions go back to the normal circulation.
TRADITIONAL PATHOGENS
Viruses (RICA) Rhinoviruses, Influenza ,Corona ,Adenoviruses
Predominant organisms recovered in bacterial sinusitis
Acute(ABRS): Strept pneumoniae, H.influenzae, Moraxella catarrhalis
CRS: Staph. aureus + ARS organisms,
Anaerobic: Fusobacterium spp. Peptostreptococcus spp
Acute (nosocomial) Pseudomonas, Staph. Aureus, Enterobacteriaceae
Anaerobic Fusobacterium
AFS& Chronic fungal: Aspergillus. Rhizopus
If you give antibiotic, S. pneumonia, H. influenzae, M. catarrhalis must be covered.
If nosomial or chronic infections, consider Pseudomonas.
Fungal infections are more common in adults.
Organism producing beta-lactamase: Staph.aureus, H.influenzae, Moraxella, Pseudomonas, Fusobacterium spp
HOW DO YOU DIAGNOSE ACUTE VIRAL/ ACUTE BACTERIAL RHINOSINUSITIS(ABRS)?
HISTORY
Acute Viral: self limiting
Acute BacteriaI: if symptoms:not resolved after 10 days,Or worsened after 5 -7 days
oBut lasts less than 30 days
Classify first if acute or chronic. Duration of the symptoms is important.
WHAT ARE THE SYMPTOMS OF RHINOSINUSITIS?
Nasal congestion,discharge, Post nasal drip
Olfactory disturbance
Cough, irritability (Common in pediatric age group)
Halitosis- offensive/metallic smell
Fever, Headache- important to locate the sinus involved
In children, ethmoid commonly affected. In adults, maxillary > ethmoid > Frontal > sphenoid sinus
Major SYMPTOMS
Headache-pain-discharge- anosmia-fever
Headache
oPersistent and recurrent, in the morning, more intense in the noon time
oExacerbated by bending and jarring motion
o Maxillary midface, temples
o Ethmoid bridge of the nose, medial canthus of the eyes
o Frontal :tenderness on forehead, radiating to the medial canthus (Probst)
o Sphenoid - nonspecific, dull pressure at the center of skull radiating to the occiput
Facial pain and pressure, fullness
Nasal congestion

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 Discharge Thick colored or purulence(nasal or postnasal)

Hyposmia, anosmia
*Fever (in ARS only)
Minor
Cough-Halitosis- Fever(in chronic) Fatigue,
Dental pain, Ear pain, pressure, or fullness
DIAGNOSIS
2 major symptoms or 1 major+ 2 minor < 4 weeks or discharge itself
Diagnostic Measures:
oRhinoscopy /endoscopy :pus on middle meatus (not seen if mucosa swollen)
- Isolated sphenoid sinusitis - pus on ostium in anterior wall or on posterior wall of the pharynx
oSinus radiographs- partial opacification = mucosal swelling; fluid level
oUltrasonography (A-or B-mode) ; for follow-up and in children and pregnant women.
Sinus Puncture Gold standard in Dx of (ARS-CBRS)Not performed because of morbidity and cost.
oDone only in: immunocompromised ,severe infection to determine culture and sensitivity
CHRONIC RHINOSINUSITIS
Persistence of sinus > 12 weeks (3 months)
Presence of nasal congestion, obstruction ,acial pain/pressure, discharge or hyposmia or anosmia
Impaired ventilation of ostiomeatal unit. It affects drainage : maxillary > ant ethmoid cells this is why these
are frequently affected); frontal and sphenoid sinuses are less commonly involved
How to diagnose Chronic Rhinosinusitis
Physical Examination
Palpation of maxillary and frontal sinus
Rhinoscopy/Endoscopy
Nasal Discharge -presence of discharge itself will tell you its rhinosinustis)
Septum deviated or presence of spur
Turbinates hyperplastic, pneumatized
Presence of mucosal swelling, polyps, tumors
Transillumination very low sensitivity is
Imaging studies
Not mandatory for diagnosis of uncomplicated ABRS
Reserved for patients with Persistent/recurrent disease, When sinus surgery is contemplated
PNS (Paranasal Sinus Xray) Caldwell and Waters View
oCaldwell specific for frontal sinus
oWaters specific for maxillary sinus
Submentovertical View specific for ethmoid sinus
Never request for an AP X-ray of the skull! You wont see anything!

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 Caldwells view, with air-fluid levels =meniscus sign, this is acute sinusitis.
2nd picture shows Waters view. The third is the submentovertical view.
Normal Cilia beat back and forth propelling mucus and trapped particles our of the sinus
Cilia can become paralyzed during acute sinusitis; sinuses are congested with mucus.
Chronic sinusitis may further damage cilia; the mucosal lining becomes thick and scarred.
Mucoperiosteal thickening. in the Lateral view/Waters view. = irritation of the turbinates and the cilia within
the sinus, scarring and fibrosis of the turbinates and maxillary sinus.
Edema, mucoperiosteal thickening consider chronic rhinosinusitis [2013B]
All the sinuses are involved.
Complete opacification of the left maxillary sinus (indicate chronic infection
CT scan Gold standard. Accurately defines key anatomic structures
It is worth it, especially for these indications:
orefractory to medical management
oBefore surgery/ repeat surgery (dont remove entire sinus but only diseased portions.
oConsidered only if chronic sinusitis is suspected [2013 B]
odont do CT scan to diagnose rhinosinusitis but to evaluate if candidate for surgery!

Polysinusitis
Pansinusitis
CT Scan can capture
oIsolated frontal sinus disease
oIsolated ethmoid sinus disease
oPolysinusitis majority of the sinuses are involved
oPansinusitis all of the sinuses are involved
MRI
Not recommended
May be done if entertaining fungal or neoplastic disease
SINUSITIS IN DESCENDING FREQUENCY (MEFS)
Maxillary> Ethmoid >Frontal> Sphenoid

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TREATMENT
The primary Treatment of ABRS is Antibiotics
NO RECENT ANTIMICROBIAL USE IN THE PAST 4 6 WEEKS
First line
Amoxicillin 15 mg/kg/d
Amoxicillin/Clavulanate-Cefpodoxime-Cefuroxime
Alternatives if allergic to Beta Lactams
Trimethoprim-Sulfamethoxazole (TMP/SMX)-Doxycycline
Macrolides (Azithromycin for five days, Clarithromycin for 1 week, Erythromycin for 1 week)
WITH RECENT ANTIMICROBIALS USE IN THE PAST 4 6 WEEKS
First line
High dose amoxicillin (double the dose)
Amoxicillin/Clavulanate
Ceftriaxone
Levoflaxcin (Quinolones; not given under 18 yr old because they affect the growth centers)
Alternatives if allergic to Beta Lactams
Gatifloxacin, Levofloxacin or Moxifloxacin (if not yet given)
Clindamycin
oadded anaerobic coverage;
oimportant if considering dental complications [2013B]
Erythromycin
oPoor coverage for Gram (-) bacteria
oMay not cover for H. Influenza and M. catarrhalis if used empirically
Decongestants [2013B]
Both oral and topical, are useful for symptomatic relief of nasal congestion
Topical (Drixine and Oxymetazoline) instantaneous effects, be able to decongest in a few seconds. This is
only good for examination purposes not for maintenance since patient may develop rhinitis medicamentosa
Excessive use may lead to side effects
Adrenergic agonist may bring up BP, ICP, sphincteric tone (caution for hypertensives, glaucoma, BPH)
Not given with sympathomimetics, MAO inhibitors and TCA side effects hypertensive crisis
Mucolytics
MOA: Break down the disulfide bond which is responsible for making the phlegm viscid
Improves mucus clearance
May be used as supportive treatment, however, its use is not recommended for all cases
May serve as a lubricant, make the crust easier to move
Helps the mucocililary transport system [2013B]
Antihistamines
With some anti-inflammatory effects

54

 Not recommended in the treatment of ABRS except in cases with concomitant allergic rhinitis (very strong
history of allergy)
1st generation more side effects; cholinergic effects viscosity of mucus
2nd generation antihistamines more selective (Citirizine) (2013B)
Nasal saline spray, nasal irrigation and mist humidification
Are safe to use and may provide some symptomatic relief. Serves as a lubricant and helps in removal of crust,
used post op for 1 month for flushing the crust, no side effect and no overdosage.[2013 B]
Intranasal steroids may be used as adjuncts in the treatment of ABRS if again there is a strong history of allergy
ACUTE SINUSITIS: TREATMENT (Probst)
Conservative Therapy
oDecongestant nose drops; nasal spray; by inserting cotton pack soaked with nose drops into middle meatus
oAntibiotics (amoxicillin) if with fever and significant malaise
Surgical Therapy (if unresponsive and with persistent sinus empyema)
oMaxillary sinusitis
- Sharp puncture through inferior meatus and below inferior turbinate; high risk of complications due to
air embolism
- Blunt puncture - via maxillary sinus ostium
- Watch out for (a) perforation of the lateral sinus wall buccal abscess; (b) perforation of the sinus roof
infection of orbital contents
oFrontal sinus empyema- surgically drained through Beck puncture; risk of meningoencephalitis or frontal
brain abscess
Conservative treatment options should be exhausted before considering surgery
CHRONIC SINUSITIS:TREATMENT
Primary: Augmentin (Amoxicillin/Clavulanate)
Alternatives
oClindamycin
oCefuroxime + Metronidazole
oQuinolones (Gatifloxacin or moxifloxacin or gamifloxacin
Polyps with pseudomonas: Ciprofloxacin (Quinolone) + Metronidazole
Case of patient who had tooth extraction and primary complaint is halitosis. As discussed earlier, not all sinusitis
are rhinologic in origin. This patient suffers from oroantral fistula. Treatment for this patient was a palatal
transposition flap.

Remove the granulation tissue surrounding the fistula put suction inside design a rotation flap from the
palate and close the fistula suture, therefore avoiding sinusitis
Surgical Therapy

55

oEndoscopic Sinus Surgery

- Minimally invasive procedure
- Definitive treatment for chronic sinusitis
oCaldwell- Luc Surgery (modified)
- lift skin of the face for access (drilling the anterior maxillary wall, remove the disease mucosa and
secretions inside
- true: open up sinus & strip off the lining nonfunctional sinus
- modified: open up and get rid only the infected musosa
oAll conservative therapies are of symptomatic benefit only cannot eliminate the cause of chronic sinusitis.
Surgery is the only definitive treatment for chronic sinusitis. (Probst)

Nosocomial sinusitis- prone to this are patients with NGT, immunocompromisedpatiens

oPrimary: Ticarcillin/Clavulanate
oAlternatives: Ceftazidime and Aminoglycosides
COMPLICATIONS
Orbital complications
More commonly arise from the ethmoid cells and frontal sinus
Orbital edema, Periosteitis
o treat with high dose IV antibiotics
Subperiosteal abscess, Orbital cellulitis, Orbital apex syndrome CN 2-6, ophthalmic vein and artery
o treat with high dose antibiotics and immediate surgical decompression
Acute Orbital Cellulitis
Microbiology:S. pneumonia, S. pyogenes (beta hemolytic strep), or Hemophilus influenzae
Drug Choices:cross blood-brain barrier and effective against pneumococcal and hemophilus strains
oCeftriaxone (Rocephin) IVCefotaxime (Claforan) IV
oTrovafloxacin
with or without Vancomycin IV
Orbital Edema from acute sinusitis- managed by antibiotics

Frontal sinusitis with abscess causing orbital protrusion/ frozen orbit (left). At the right is the CT scan, empyema
in the frontal sinus and the abscess in the periosteum.
Endoscopic Sinus Surgery
BONE AND SOFT TISSUE INFLAMMATIONS
Osteomyelitis
oMainly from Frontal sinus
- Tender, doughy erythematous swelling over the forehead

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oDanger: infection may spread to the entire calvaria

oDiagnosis is by CT scan
oTreatment: High dose antibiotics and generous resection of the affected bone
INTRACRANIAL COMPLICATIONS
Epidural, Subdural and Intracerebral abscess signs of d ICP with nausea, headache, vomiting and occasional
papilledema, somnolence or seizures (2013B)
oMostly from the frontal sinus: in children ethmoids and sphenoids are common nidus due to lack of
aeration
oClinical manifestations: nonspecific
oDiagnosis: CT scan or MRI
oTreatment: High dose of antibiotics and surgical drainage
MENINGITIS
Headache, stiff neck, fever, nausea, photophobia, increasing somnolence, seizure
Diagnosis done by CSF sampling
in sugar (glucose) because the organisms are using them up, in protein in CSF sample because of the
presence of organism proliferation
Treatment: high dose antibiotic and surgical drainage of the affected sinus
Classification of nasal polyposis is important in order to decide the magnitude and the optimal management
modality. Various methods have been attempted. The fact that numerous scoring system indicates that none of them
are fool proof.
These methods can be classified into:
1-Questionnaire based categorization
2-CT based grading system(Lund-Makay)
3-Nasal endoscopic scoring system(Lund Kennedy)
4- Clinical and Nasal functional scoring system(Hadley's clinical scoring)
Questionnaire based categorization (SNOT-20/22 score)
Disease based questionnaires are more sensitive than general quality of life questionnaires. (contain the following
parameters:
a. Assessment of facial pain
b. Nasal blockage
c. Olfactiond. Nasal discharge e. Post nasal drip
Used to assess the patient's response to a treatment. Most bothersome complaint is nasal blockage and impaired
olfaction. None of the questionaires designed so far are specific for nasal polyposis.
Rhinosinusitis outcome measure - ( 31 questions spread over six domains (subheadings). The patient score each
item according to its severity and importance to the patient.
SNOT-20 (Sino-Nasal Outcome) is a modification of Rhinosinusitis outcome-31. easier to complete. Ironically
does not include questions on nasal blockage or sense of smell.
Rhinosinusitis disability index This index includes 30 questions relating to nose and sinus symptoms. These
symptoms pertain to limitations on daily functioning of the individual.
Chronic sinusitis survey index This includes duration based 6 questions. The questions include symptoms like
pain, congestion, drainage and medication usage.

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Rhinitis utility symptom index This is a 10 question (focus on severity of nasal obstruction, rhinorrhoea,
sneezing, itching and watery eyes).
RhinoQol questionnaire / symptom frequency, used to evaluate both acute and chronic rhinosinusitis
Visual analogue scale This is used for assessing discrete symptoms. The patients can mark on a line the severity
of symptoms. A scale of 5 has been known to affect the quality of life of the patient.
Sinonasal questionnaire This is a 5 item questionnaire with a scale of 0-3. Higher scores indicates more frequent
symptoms.
Lund & Mackay scoring :widely used). a scale of 0-2 (0= absence, 1=partial or 2=complete opacification of sinus
and osteomeatal complex. on CT scan ( maximum score of 12 per side(2*6).
Maxillary, Ant. ethmoid Post.ethmoid, Sphenoid, Frontal (0,1,2) Osteomeatal complex (0 or 2)
Zinreich modification of Lund Mackay score(more discrimination in grading sinusitis.
Scores each sinus ( scale of 0-5, and osteomeatal complex involvement ( 1 and 2).
Score 0 0% opacity of sinuses,
Score 1 25% opacification
Score 2 26-50% opacification
Score 3 51-75% opacification
Score 4 76 99% opacification
Score 5 100% opacification
Lund & Kennedy scoring system (meticulous endoscopy study of of nose and paranasal sinuses. used to study post
operative results following FESS( poly- edema-discharge). on each side
Presence of polyp (0,1,2,3)
Edema (0,1,2)
Discharge (0,1,2)
Post operative scoring system of Lund Kennedy:
Scarring, left (0,1,2)
Scarring right (0,1,2)
Crusting left (0,1,2)
Crusting right (0,1,2)
Hadley's clinical scoring system of nasal polyposis include ( polypi in sizes. divided into 4 stages.
Stage 0 No visible nasal polyp
Stage 1 Small amount of polypoidal tissue confined to the middle meatus
Stage 2 Multiple polypi occupying the middle meatus
Stage 3 Polypi extending beyond the middle meatus
Stage 4 Polyp completely obstructing the nasal cavity
Stage 5(modification : polyp touching the floor of the nasal cavity.
https://sites.google.com/site/drtbalusotolaryngology/rhinology/classification-of-nasal-polyposis
Nasal polyposis
inflammatory condition of unknown etiology, and the most common tumors of the nasal cavity. Approximately
30% of patients with nasal polyps test positive for environmental allergies. The prevalence of nasal polyps is d in
children with cystic fibrosis and persons with known aspirin hypersensitivity. Nasal polyposis can impair a
person's quality of life more than perennial allergic rhinitis. Olfaction and nasal obstruction are the most important
considerations in terms of symptoms.
Pathophysiology
chronic inflame= reactive hyperplasia of mucosa(mm), = polyps.
In 1990, Tos reported 10 pathogenic theories of nasal polyp formation:[1]

58

Adenoma and fibroma theories

Necrosing ethmoiditis theory
Mucosal exudate theory-Blockade theory
Cystic dilatation of the excretory duct and vessel obstruction theory
Periphlebitis and perilymphangitis theory
Glandular cyst theory
Glandular hyperplasia theory-Gland new formation theory
Ion transport theory
chemical mediators: eosinophils. Cysteinyl leukotriene receptors and interleukin-5 (IL-5) : most well studied.
Epidemiology
Nasal polyps : 5% of nonallergic people and only 1.5% of people with allergic rhinitis. No racial or sexual
predilection. The prevalence is in patients with cystic fibrosis and aspirin-hypersensitivity triad.
Mortality/Morbidity
Morbidity from polyps is directly related to their location and size.

Obstruction of ostia , acute or chronic sinusitis. bony destruction(nasal bones or orbital bones.
Nasal obstruction = hyposmia or even anosmia.
not premalignant. ,DD: inverting papillomas,
polyps can arise from inflame by malignant or premalignant nasal lesions. These polyps can obstruct
visualization of the more concerning lesions and sometimes cause delay in diagnosis.
History
nasal congestion, hyposmia to anosmia, changes in sense of taste, and persistent postnasal drainage. Headaches and
facial pain in the periorbital and maxillary regions. symptoms of obstructive sleep apnea.OSA
solitary polyps = nasal obstruction, change with position. (supine, swing poster, opening nasal cavity. In an
upright : more obstructive effect.
acute, recurrent, or chronic rhinosinusitis if the polyps obstruct the sinus ostia.

examination : fleshy translucent mass or masses in the superior nasal vault. Polyps originating in ethmoid ,
from maxillary ostium (antral choanal polyps), the turbinates, or the septum. Obstructing polyps may make
thorough intranasal

.
Nasal polyposis, right nasal passage. Nasal polyposis, right nasal passage.
Mucopurulent discharge from the ethmoid or the superior nasal vault, suggesting an underlying
rhinosinusitis. Septal deformities may make the examination more difficult.

Causes: Allergy-Chronic sinusitis-Chronic inflam of indeterminate etiology

Differential Diagnoses
Allergic Rhinitis- cystic fobrosis
Juvenile Nasopharyngeal Angiofibroma
Malignant Tumors of the Nasal Cavity
Turbinate Dysfunction
Laboratory Studies

59

Allergy testing : if history of allergies or family history of allergies.

Children should be tested for cystic fibrosis ( sweat chloride >60 mEq).
Imaging Studies
Coronal sinus CT (of choice) underlying pathology, the extent , possible bony destruction.
Nonenhanced CT : location and origin, anatomy of the paranasal sinuses
MRI is not an appropriate unless intracranial extension. Bony details are poorly visualized on MRI.
X-Ray: Waters views may show opacification of the sinuses.
Nasal endoscopy :
Biopsy if Lack of classic appearance of bilateral polyps or not respond to conservative Rx with careful biopsy
edematous tissue , few glands to an in glandulas. Eosinophils =allergic component.
Epithelial damage : by allergens, pollutats, infectious = inflame & repair. The epithelium : goblet hyperplasia and
mucous = nasal obstruction and rhinorrhea.
goblet cell hyperplasia :control of epidermal growth factors (EGF). Inhibitors may block mucous production and
goblet cell hyperplasia. Free radicals are highly reactive molecules with an unpaired electron in the outer orbit and
may also play a role in polyp formation. The body produces endogenous oxidants as a result of the leakage of
electrons from electron transport chains, phagocytic cells and endogenous enzyme systems (MAO, P450, etc).
Exogenous factors include radiation, air pollutants, tobacco smoke, sun exposure, ozone, and others. A certain
physiologic level of reactive oxygen species is necessary for proper regulation of cell functions. Exposure to
oxidants can initiate free radical-mediated reactions and lead to oxidative stress. Free radicals can result in cellular
damage or death and subsequent tissue damage.
Several inflammatory factors ,vascular cell adhesion molecule (VCAM)-1, nitric oxide synthase, granulocytemacrophage colonystimulating factor (GM-CSF), eosinophil survival enhancing activity (ESEA), cysleukotrienes (Cys-LT) and many other cytokines
Medical Care
etiology in most cases is inflammatory, medical management is aimed at nonspecific treatment of this
inflammatory disorder.
Oral corticosteroids are the most effective The nonspecific anti-inflammatory agent quickly and substantially
reduces the size of inflammatory polyps and improves symptoms. Patients whose polyps respond to oral
corticosteroids may be re-treated safely 3-4 times a year, especially if they are not candidates for surgery. The
mechanism of action of corticosteroids is unclear. One study showed that corticosteroids induce apoptosis in
inflammatory cells in human nasal polyps in vitro.
Intranasal steroid sprays :reduce or retard the growth of small nasal polyps, most effective in the
postoperative .ineffective in massive nasal polyposis.
( improvements may be due to Rx of rhinitis, )
Intrapolyp steroid injections have been shown to reduce polyp growth and nasal symptom scores compared with
intranasal medical therapy and appear to be a safe alternative to surgery in select patients. More studies are
necessary.[7]
Leukotrienes ( Benefits more patients with concomitant allergic rhinitis and eosinophilic infiltration of the nasal
polyps on histology.
Antifungal agents have no role in the management of nasal polyposis, useful in cases of allergic fungal sinusitis
with polyposis.
Other agents with a possible role in management of nasal polyposis are macrolides antibiotics, topical diuretic
therapy, and intranasal lysineacetylsalicylic acid.

60

http://emedicine.medscape.com/article/861353-overview
inverted papilloma(IP)
Synonyms: Schneiderian papilloma, Benign papilloma of mucosal lining of nose , sinuses : Schneiderian
membrane,Papillomas growing inwardly = inverted papilloma
mucosa of is unique : from the ectoderm, (Vs epithelium of laryngobronchial : from endoderm.
behave like neoplasms, thickening of the epithelium assumes an inverting, fungiform or combination growth
pattern. metaplasia varying :cylinderical. Rarely the papilloma may be composed entirely of cylinderical cells,
and hence the term cylinderical cell papilloma is used to describe this subtype.
classified / site : lateral wall and septal papillomas. septal papillomas remain confined to the nasal septum and may
very rarely involve the roof and floor of the nasal cavity. Carcinomatous transformation is rare in septal
papillomas.
Papilloma of lateral wall : floor, roof of nasal cavity, para nasal sinuses and naso lacrimal duct.
Carcinomatous transformation is common in this variety.
Clinical classification of inverted papilloma was proposed by Krouse. He used his classification and staging
protocol to decide on the optimal treatment modality of these patients.
Krouse classification:
T1 - The disease is limited to the nasal cavity alone
T2 - Disease is limited to ethmoid sinuses and medial and superior portions of maxillary sinuses
T3 - Disease involves the lateral or inferior maxillary /or extension into frontal or sphenoid sinuses
T4 - spread outside the confines of nose and sinuses. This stage also includes malignancy
Incidence: common occurring in 2% of patients with nasal polypi. Men > women. mean age : 50.
Etiology: HPV : causative ,mutation , Herpes simplex may interact with HPV to cause inverted papilloma.
CT scan :determining the optimal surgical approach , differentiating other mass Classically inverted papillomas in
middle meatus and lateral nasal wall , areas of higher density = bony sclerosis. If contrast CT : enhancement .
MRI: Is very useful when the tumor has extrasinosal involvment or show malignant transformation. It also helps in
the differentiation of tumor tissue from inflammatory mucosa.
Gross apprearance: 2 patterns: 1. Papillary and exophytic in the nasal septum
2. Inverted : invaginating epithelial to stroma. in the lateral wall of the nose and sinuses.
Microscopy: fungiform papilloma , thin core of connective tissue. Inversion of epithelial masses is usually not
present. In the case of inverted papilloma the predominant growth is directed inwards into the underlying stroma.
The stroma is not breached in these patients. When they undergo malignant transformation the stroma is found to
be breached. The predominant cell type in these papillomas is epidermoid in nature. Intercellular bridges can be
clearly demonstrated. Microscopic mucous cysts can also be identified in both these types. Keratinisation is very
minimal. Excessive keratinisation is very rare, and should prompt the pathologist to other diagnosis like malignant
transformation
C/P: unilateral nasal mass, fleshy , behind a sentinel nasal polyp. erodes the medial wall of maxilla and may
present inside the maxillay sinus.
Symptoms: :compression of adjacent structures like orbit, pterygopalatine fossa, base of skull or soft tissues.
1. Unilateral nasal obstruction
2. Nasal bleeding

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3. Nasal discharge
4. Proptosis if lamina papyracea is breached
Surgury. Recurrence :20%. huge mass: lateral rhinotomy for complete removal( Weber Furgson incision)
Complications:
1. Haemorrhage
2. Malignant transformation
http://www.drtbalu.co.in/inver_papi.html
Oral questions on :Inverting papilloma(IP) & JNA( Jeuvinile Nasal angiofibroma)
1. types of sinonasal papillomas: fungiform (nasal septum), inverted (lateral nasal wall), cylindrical (lateral nasal
wall)
2.biopsy a JNA?: Never. Very VASCULAR. If biopsy needed - do it in the OR.
3.Cancer most commonly associate with inverting papilloma?: Sq CC

4.CT findings for JNA:

mass in post nasal cavity with widening of pterygopalatine canal (arrow)
5.Etiology of IP: HPV 6, 11,16, and 18. No definite correlation with subtype and dysplasia which is the case out
side the sinonasal tract.
6.feeding vessels of JNA: most commonly ECA (internal maxillary/ascending pharyngeal), poss ICA if
intracranial/intraorbital extension.
7.frequency/recurrence/malign rates for inverted vs fungiform vs cylindrical papilloma:
Inverted papilloma
fungiform
Cylindrical papilloma
Site
Lateral wall
septum
Lateral wall
frequency
47%
50%
3%
Recurrence rate
50%
20-50%
25-35%
malignancy
13
3%
15%
8.Is radiation an option?: Generally no.
9.JNA Physical exam: FOL: reddish smooth polypoid mass. May have cranial nerve dysfunction
10.JNA treatment: surgery. poss XRT/chemo if poor surgical candidate or massiave intracranial extension.
11.Management of IP: Medial maxillectomy : lateral rhinotomy Weber-Ferguson incision is the gold standard excellent exposure. The success is related to the en bloc resection of the lateral nasal wall, ethmoid labyrinth, and
medial portion of the maxilla. Now often done endoscopically.
12.patient population for sinonasal papillomas?: white males during 5th - 7th decade
13.patient populations for juvenila nasal angiofibroma: adolescent males

62

14.presentation of JNA: unilateral epistaxis/nasal obstruction/middle ear effusion, proptosis, cheek swelling, in
adolescent males,
15.rate of persistent disease? rate of recurrence?: 7% persistence, 10% recurrence rate
16.Recurrence rate with medial maxillectomy/mid face degloving.: 0-14%. Recurrence directly related to
thoroughness of resection.
17.risks of embolization with JNA: poss to embolize ophthalmic artery, risk of cerebral embolization ( anastomoses
between ICA and ECA.
18.site of origin of JNA: superior to sphenopalatine foramen at junction of sphenod process of palatine bone and
pterygoid process of sphenoid bone
19.What are other open approaches to IP: Mid face degloving
20.What are some complications of medial maxillectomy?: Epiphora ( most common). , transient diplopia,
mucocele, CSF leakage, epistaxis, and scar formation.
21. complications of mid face degloving?: (1) potential vestibular stenosis, and (2) Difficulty with superior ethmoid
exposure in large tumors. The vestibular stenosis can be avoided with proper incision design. oroantral fistula,
epistaxis, and nasal crusting which are present with the medial maxillectomy as well as the midfacial degloving.
The advantage is avoidance of a facial scar and allows bilateral exposure.
22.What are some risk factors in recurrence of inverting papilloma?: Incomplete removal of the tumor is the most
important factor in recurrence. Involvement of the paranasal sinuses, nasofrontal duct, lacrimal fossa and the
infraorbital recess of the maxillary sinus are sites associated with high recurrences. It is rare the recurrence will
occur 2 years after surgery
23.What does a papilloma look like microscopically?: Thickened epithelial covering with extensive invasion into
the underlying stroma. Invaginates into bone but does not invade unless malignant. This invasive behavior leads to
the belief that the origin of inverting papillomas is from the schneiderian Membrane.
24.What is the malignancy conversion rate of inverting papilloma?: 5-15%
25.What is MC presentation of inverting papilloma?: Unilateral nasal polyp / lateral nasal wall. Firm more pink/red
than polyp (vascular) with granular mulberry appearance
26.What is the schneiderian membrane? is of ectodermal origin from the nasal placode, there may be some
difference in the underlying stroma which permits inversion of the papilloma
27.What percent of nasal polyps are papillomas?: 4%
28.Why is inverting papilloma dangerous?: Had malignant potential. Can invade and destroy local structures such as
orbit and Cns even when benign.
29.workup for JNA: CT sinus WITH contrast, poss MRI if intracranial/intraorbital extension, angiogram for
surgical planning (will need embolization prior to surgery - operate within 24 hours optimally)
Antrochoanal polyp ACPprolapsed, pedunculated, painless, pearly white oedematous nasal mucosa of maxillary sinuses.
ACP: common in children, Males > females
causes of ACP?:Infection- Bernoullis phenomenon : -ve pressure in Highmoro antrum: Pressure drop next to a
constriction causes a suction effect pulling thesinus mucosa into the nose
Polysaccharide changes of ground substance-Vasomotor imbalance, growth of the polyp is due to impediment to
the venous return from the polyp, cilia of the ciliated columnar epithelial cells lining the nasal cavity always beats
anteroposteriorly pushing the polyp behind

63

Histology:Shows respiratory epithelium over normal basement membrane. The interstitial layer is grossly
oedematous, with no eosinophils. The interstial layer contains other inflammatory cells.
pathology : extend into the nasopharynx and oro pharynx. It has an antral part, a choanal part and a nasal part. The
choanal part in the largest.( forced to herniation through the accessory ostium
C/P: unilateral Nasal obstruction, not relieved by nasal decongestant ,discharge: mucupurulent ,blood tinged.
Post nasal drip: It is present and mucopurulent in nature.chronic cold ,
signs :Rhinolalia clausa: Present due to nasal obstruction. Broadening of nasal bridge, OSA, Dysphagia:if
the polyp extends into the oropharynx
insensitive to touch
Anterior rhinoscopy may show the polyp as glistening polypoidal structures. insensitive to touch. this feature helps
to differentiate it from a hypertrophied nasal turbinate. Postnasal examination will show the polyp if extending
posteriorly at the level of choana. If it fillsup the nasopharynx it will be visible there.
investigations :?
X-ray of Paranasal Sinuses: extent - soft tissue shadow in maxillary , convexity upwards hazy mazillary antrum.
CT :of choice, extent, orbital involvement, vascularity , altered anatomy , polyp filling the maxillary antrum
andexiting out through the accessory ostium into the nasal cavity.The antrochoanal polyp is dumb bell shaped with
three components i.e. antral, nasal andnasopharyngeal
Rx of Antrochoanal nasal polyp? Antibiotics, decongestants, analgesics +
surgical treatment. (FESS). of choice , along with microdebridor.
Caldwell Luc Surgery: Rarely done now a days. Performed only for recurrent antro-choanal polyposis.
FESS: completely remove the polypoid tissue. Uncinectomy must be done excised. complete surgical excision
with negligible recurrance rates.
Juvenile angiofibroma (JNA)
nasopharyngeal benign tumor that bleeds and occurs in the of prepubertal and adolescent males.
The image below depicts a coronal CT scan.

Coronal CT ( filling the left nasal cavity and ethmoid sinuses, blocking the
maxillary sinus and deviating the nasal septum to the right side.
Epidemiology
(JNA) 0.05% of all head and neck tumors. A frequency of 1:5,000-1:50,000 in otolaryngology patients has been
reported.
Sex: exclusively in males. Females + (JNA) should undergo genetic testing.
Age: 7-19 years. (JNA) is rare in patients older than 25 years.
Etiology
close proximity to the posterior attachment of middle turbinate, near the superior border of the sphenopalatine
foramen.
Theories: hormonal theory (adolescent males.desmoplastic response of the nasopharyngeal periosteum or the
embryonic fibrocartilage between the basiocciput and the basisphenoid.

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nonchromaffin paraganglionic cells of maxillary artery. deletions of chrom 17, + tumor suppressor gene p53 , Her2/neu oncogene.
Pathophysiology
The tumor starts adjacent to the sphenopalatine foramen. Large bilobed or dumbbell-shaped, ,1 portion filling the
nasopharynx and the other portion extending to the pterygopalatine fossa.
Anterior growth :under mucous membrane, displacing it anteriorly and inferiorly toward the postnasal space. nasal
cavity is filled on one side, and the septum deviates to the other side. Superior growth toward the sphenoid sinus, =
eroded. The cavernous sinus may become invaded if the tumor advances further.
Lateral spread : toward the pterygopalatine fossa, bowing the posterior wall of the maxillary sinus. Later, the
infratemporal fossa is invaded. greater wing of the sphenoid may be eroded, exposing the middle fossa dura.
Proptosis and optic nerve atrophy result if orbital fissures are encroached upon by the tumor. Extranasopharyngeal
angiofibroma : rare.in older patients, predominately in females, tumor is less vascular and less aggressive than
juvenile nasopharyngeal angiofibroma (JNA).
C/P:

Nasal obstruction (80-90%) - Epistaxis (50%) - unilateral and recurrent; severe; angiofibroma in
adolescent males to be ruled out
Headache (25%) - paranasal sinuses are blocked-Facial swelling (10-18%)
Unilateral rhinorrhea, anosmia, hyposmia, rhinolalia, deafness, otalgia, swelling of the palate, deformity of
the cheek
Signs
Nasal mass (80%) Orbital mass (15%) Proptosis (10-15%)
Other signs include serous otitis due to eustachian tube blockage, zygomatic swelling, and trismus that
denote spread of the tumor to the infratemporal fossa, decreasing vision due to optic nerve tenting (rare)
Differentials
Other causes of nasal obstruction, (eg, nasal polyps, antrochoanal polyp,teratoma, encephalocele,
dermoids, inverting papilloma, rhabdomyosarcoma,squamous cell carcinoma)
Imaging Studies
Plain radiography : nasopharyngeal polyp. Bowing of the posterior max wall, opacification (JNA).
CT scan : extent. Extension to the sphenoid, erosion of the greater sphenoidal wing, or invasion of the
pterygomaxillary and infratemporal fossae is usually visualized, as in the images below.

Coronal CT:lesion filling the left nasal cavity ethmoid sinuses, blocking the maxillary sinus and deviating the nasal
septum to the right side. Axial CT scan of lesion involving the right nasal cavity and paranasal sinuses. Courtesy of
J Otolaryngol 1999;28:145
(MRI) : extent of the tumor, intracranial involvement. Coronal MRI : extension of the lesion to the cavernous sinus
: image below.

65

Angiography :external carotid , primary feeders (94%). from internal maxillary artery, but ascending pharyngeal
or vidian arteries may contribute. internal carotid artery contribute. Bilateral vascular supply , angiography of
bilateral carotid preoperatively.[1] An angiofibroma before and after embolization can be seen in the images below.

Angiogram depicting angiofibroma before embolization. Courtesy of J Otolaryngol 1999;28:145.

http://emedicine.medscape.com/article/872580-workup
Adjunctive treatment:Hormonal therapy: Since JNA : endocrine tumor testosterone receptor blocking drugs /
estrogens have been tried to reduce the mass. These hormones cause disaggreable side effects such as increased
breast size. Hormones could even act as carcinogens.Embolisation: Was first attempted by Robertson in 1972. This
was notphonation meant to be therapeutic measure. After embolisation bleeding is minimised during surgery. It is
ideally carriedout a few days before surgery. Hence it is a valuable preliminary to surgery. The feeding
vessels tothe tumor is identified. It is then deliberatly occluded by means of materials injected through aselectively
placed catheter. Materials used:Autologous substances like fat, blood clot, or chopped muscle fragments.Artifical
materials: Gelfoam, Oxidised cellulose, Tantalum powder, glass beads, polyvinyl alcoholetc.Embolisation should
always be preceded by angiography. Subtraction films may be helpful in areascontaining complex bony
structures.Immediate complications of embolisation are pain, embolisation of normal
vessels,hypersensitivity. Delayed complications include fever, pain and infections.Cryosurgery and Lasers can also
be used during surgery to minimise bleeding.III.
Rhinoscleroma
chronic granulomatous condition of nose and upper airway. By Klebsiella rhinoscleromatis. =Firsch
bacilli).Pathophysiology: direct inhalation of droplets / contaminatedmaterial. This infection usually prefers
transitional epithelial zones (like vestibule of nose where thesquamous epithelium changes in to ciliated columnar
epithelium and supraglottic area of larynx).
Clinical features:1. Nasal obstruction2. Rhinorrhoea3. Epistaxis4. Nasal deformity5. Anesthesia of palate6.
AnosmiaClassically this condition passes through three stages:
Catarrhal stage: This initial stage begins with non specific rhinitis progressing on to formation of foul smelling thick
discharge and crusting of the nasal mucosa.Granulomatous stage: This stage is also known as hyperplastic stage.
Nasal mucosa shows rubberynodules / polypoidal lesion. Epistaxis may be present. The nasal cavity appears
enlarged withdestruction of nasal cartilages. Involvement of maxillary antrum is common in this stage and mayform
the reservoir.The soft palate appears to be thickened at its junction with that of hard palate. If the lesion presentslike
a tumor with evidence of tissue destruction it is known as pseudotumerous rhinoscleroma.
Sclerotic stage: sclerosis and fibrosis. , nodules of nasal mucosa gets replaced by fibrous tissue.
Management: Tetracycline = drug of choice. Ciprofloxacillin and rifampicin have also found to be effective.
Steroids :prevent e scarring of tissues.
Surgery: in extensive scarring of the nose.
Allergic rhinitis:
inflammation of nasal mucous membrane caused by abnormal reaction to exposure to allergens.
C/P: Sneezing Nasal congestion, Itching of nose and eyes ,allergic salute.= horizontal line on dorsum of the nose
Darriers line. Since the mucous membrane lining the nasal cavity also lines the nasopharynx and the middle
ear cavity.

66

2 types of allergic rhinitis: Seasonal : during pollen seasons. Starts at 6 years of age.
Perennial rhinitis: throughout the year and is commonly seen in younger children. The symptoms begin minutes
after exposure to the offending antigen. It causes nasal congestion by impeding venous return from the nasal
mucosa. There is also increased vascular permeability andincreased secretion of nasal mucous-glands.
Management:1. Avoiding exposure to allergen2. Antihistamines3. Topical steroids4. Nasal decongestants during
acute phase5. Immunotherapy 5. Meniere's disease:Endolymphatic hydrops is also known as Meniere's disease. This
condition is due to swelling up of the endolymphatic sac. This causes fluctuating low tone sensori neural hearing
loss, tinnitus andepisodic vertigo.Features of classic Meniere's disease:Periodic episodes of rotatory
vertigoFluctuating sensorineural hearing loss involving lower frequenciesRoaring tinnitusSensation of aural
fullnessCauses:1. Idiopathic (Most common)2. Viral infections
FESS
Functional Endoscopic Sinus Surgery. aims at restoring the normal function of paranasal sinuses.Indications for
FESS:1. Chronic sinusitis resistant to medical management2. Repeated acute exacerbations of chronic sinusitis3. In
order to remove resistant focal infections from the paranasal sinuses4. In the management of fungal sinusitis in an
effort aimed at ventilation of paranasal sinuses Aim of FESS -Aim of FESS is to remove paranasal sinus drainage
block there by facilitating faster recovery of the mucociliary mechanism of nose and paranasal sinuses. Experiments
have shown thatdrainage of sinuses always occur through their natural ostium because cilia always beat
towardstheir natural ostium. Procedure: under local / general anesthesia. The nasal cavity is packed with 4%
xylocaine mixed with 1 in 100,000 units of adrenaline. (reduces bleeding during surgery.
0 degree nasal endoscope is used to perform the surgery.Steps of surgery:1. Medialization of the
middle turbinate. This is done gently using a freer's elevator. Infiltratingthe root of middle turbinate with cc of 2%
xylocaine mixed with 1 in 100,000 units adrenalinewill ensure anesthesia of the middle meatus which is the area of
surgery.Uncinectomy:Uncinate process is identified and medialized using a probe. It is completely removed
using asickle knife / back biting forceps. It is important that the uncinate process is removed completelyincluding its
inferior horizontal portion. Natural ostium of maxillary sinus can be seen when thehorizontal portion of inferior part
of uncinate is removed. The natural ostium can be widenedusing a back biting forceps.
Clearance of frontal recess area comes next. The frontal recess widened after bullaethmoidalis is deroofed. The
horizontal portion of middle turbinate separates the anterior ethmoidal cells from the posterior group. If the
posterior group of ethmoidal cells are found to be involved then they can be accessedafter breaching the basal
lamella. The idea is to remove the diseased mucosa, widening thedrainage channels of paranasal sinuses
thereby allowing them to be ventilated normally. Thisensures faster regeneration of the ciliated columnar epithelium
and restoration of normal ciliarymotility.
Complications of FESS:1. Bleeding 2. CSF leak3. Injury to orbit and its contents 4. Synechiae formation
FESS complications
Orbit is separated from the nasal cavity by a paper thin bone known as lamina papyracea which can be easily
breached during endoscopic sinus surgery.
Various orbital complications of FESS include:
a.
b.
c.
d.
e.
f.

Orbital hematoma( arteria, venous)

Blindness(temporary, permenant)
Diplopia
Nasolacrimal duct injury
Subcutaneous emphysema
CSF leak, meningitis

67

Orbital hematoma: due to inadvertent breach to lamina papyracea. can occur irrespective of the status of
Periorbita. It should be borne in mind that the risk of orbital hematoma quadruples with penetration of Periorbita.
Ecchymosis can occur due to breach involving the lamina papyracea. This occurs irrespective of breach of
Periorbita.
Orbital hematoma is commonly due to post septal injury. (The septum is defined as the fibrous membrane that
divides the eyelid into anterior and posterior chambers). Orbital hemorrhage is commonly caused due to injury to
orbital veins lining the lamina papyracea and rarely due to injuries involving anterior and posterior ethmoidal
arteries.
Clinically these two types of injuries can be differentiated by the speed at which the signs and symptoms
develop. In cases of injury to ethmoidal arteries the symptoms are fairly rapid. In patients with injury to orbital
veins the symptoms are rather slow to develop.
Differences between ecchymosis and orbital hematoma:
Ecchymosis is preseptal accumulation of blood. It is commonly caused due to injuries to angular vessels which
commonly occur during infiltration. It is darker than orbital hematoma and is more diffuse. It also produces more
lid oedema.
Orbital hematoma is actually post septal hematoma. Orbital / post septal hematoma is characterized by
conjunctival chemosis, pupillary changes, mydriasis and proptosis. Proptosis signals d orbital pressure and
eventually it could cause damage to optic nerve.
Orbital hematoma is of two types:
1. Fast hematoma arterial in nature (due to damage to ethmoidal arteries).
2. Slow hematoma Venous in nature (due to damage to orbital veins).
Blindness: a surgery grossly gone wrong. Blindness could be temporary or permanent.
Temporary blindness: Is caused by increasing orbital pressure due to orbital hematoma. This d orbital pressure
compromises the vascular supply to the optic nerve which is highly sensitive to ischemia. Studies have shown that
d intraocular pressure gradually returns to normal within a couple of hours. Light perception may not return to
normal for several more hours. Pupillary reflexes may take up to 2 days to recover.
Permanent blindness: by retrobulbar and retro orbital hematoma, the retina can tolerate extreme ocular pressures
only for a couple of hours. Intervention immediately. (2hrs for venous hematoma, 30 min for arterial bleed). Any
damage to the retina and optic nerve becomes irreversible after this window elapses; hence this light window
should always be borne in mind before embarking on surgical decompression procedures.
During surgery : leave the eyes of the patient uncovered / proptosis can be appreciated on the table. The tissues
removed should always be deposited in a container containing water. If the tissue floats then it should be
considered that it is orbital fat unless proved otherwise.
A right handed surgeon is more prone to cause damage to left orbit because of the anatomical illusion on the left
side. The left ethmoidal sinuses are actually more medial than appreciated by the right handed surgeon.
Bulb press test:
if performed will avoid damage to orbit. Nurse press the eye while viewing endoscopically the lateral nasal
wall. Any transmitted movement seen in the area indicates breach to lamina papyracea.
Management:
In arterial hematoma intervention should be immediate. Intravenous mannitol : reduce intraocular pressure. 1-2
g /kg in a 20% infusion. Orbital massage , Steroids i.e. Dexamethazone 1 mg /kg in divided doses in a day. If

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not successful then endoscopic decompression of orbit / ligation of bleeding vessels / lateral canthotomy may be
resorted to.
In cases of venous bleed, the management regimen is pretty same but surgical urgency is not necessary.
Diplopia by injury to ocular muscles closely related to the paranasal sinuses. medial rectus and the superior
oblique. The medial rectus lies lateral to lamina papyracea. commonly involved during FESS.
Unintentional injection of local anesthetics in to the orbit via lamina papyracea may cause transient diplopia due to
paralysis of medial rectus.
Nasolacrimal duct injury: lacrimal sac and duct lie close to ethmoidal in 90% of patients. The agger nasi cells lie
adjacent to the sac. The ethmoidal sinus and natural ostium of maxillary sinus lie close to the duct. To avoid
damage to the sac and duct, the ethmoidal sinus / natural antrostomy should not be opened anterior to the anterior
end of the middle turbinate. Patients with naso lacrimal sac / duct injury suffer from epiphora. Commonly it
resolves on its own. If spontaneous resolution fails to occur then DCR should be resorted to.
http://www.drtbalu.co.in/orbital_comp.html
FESS review/ vaiation in OMC(osteameatal complex)
Agger nasi(heap):Most Anterior ethmoidal cells (anterolateral and inferior to frontoethmoidal recess and anterior
and above attachment of middle turbinate. within lacrimal bone , have as lateral relations the orbit, the lacrimal
sac and the nasolacrimal duct.
Haller cell: pneumatized ethmoid air cells, along medial roof of maxillary sinus and inferior to LP(lamina
papyracea. lies below the ethmoid bulla and lateral to the uncinate process.( down the Hall= Haller is infer to LP,
hall bet Max& eth)
known as infraorbital ethmoidal cells /Infra orbital recess cells or maxilloethmoidal cells. They are extramural
ethmoidal air cells extend into inferomedial orbital floor /at roof of maxillary ( in 30% of patients,.
mostly from anterior ethmoid , related to infundibulum. (Rarely from posterior ethmoidal cells , not compromise
infundibulum.
Mostly asymptomatic, clinically significant in a number of situations:

become infected, with the potential for extension into the orbit
may narrow osteomeatal complex (OMC) if large and may cause maxillary antrum obstruction
(
compromise and narrow the infundibulum causing obstruction to the drainage of maxillary sinus ostium.
suggested as a factor in recurrent maxillary sinusitis.
may lead to inadvertent entry into the orbit if unrecognized at endoscopic surgery

As it is closely related to ethmoidal infundibulum enlarged Haller cells may contribute to narrowing of the
ethmoidal infundibulum and recurrent sinus disease

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http://uwmsk.org/sinusanatomy2/FrontalAbnormal.html

Sagitttal image ( anterior and posterior ostiomeatal sinus

disease. mucosal thickening of FSDP, AE and sphenoid
sinus ostium and sphenoethmoidal recess. (FS: frontal sinus,
FSDP: frontal sinus drainage pathway, U: uncinate, HS:
hiatus semilunaris, AE: anterior ethmoid, MT: middle
turbinate, SpS: sphenoid sinus, double arrowheads:
sphenoid sinus ostium and sphenoethmoidal recess)

Etymology:Named after Albrecht von Haller, a Swiss anatomist.

Onodi cells
An Onodi cell (or sphenoethmoidal air cell) is ethmoidal air cell that lies posteriorly, sometimes, superiorly to the
sphenoidal sinus. its location the optic nerve, and internal carotid artery, are closely related with as little a 0.03mm
(median 0.08mm) of bone seperating them. The incidence is variable between 8 and 13%.
Potential damage to the optic nerve and ICA occurs when attempts to enter the sphenoid sinus endoscopically by
passing through what is thought to be the posterior most ethmoidal air cells is instead an Onodi cell.
Additionally, isolated mucocoeles of Onodi cells, squamous cell carcinoma and sinusitis have all been reported,
leading to early optic nerve involvement.
Onodi cell(sphenoethomoid cell):
lateral and posterior pneumatization of the most posterior ethmoid cells over the sphenoid sinus.

70

It is posterior ethmoid cells positioned superolateral to the sphenoid sinus ,optic nerve & carotid artery
course through the lateral aspect of onodi cell instead of sphenoid sinus proper.
Kainz and Stammberger defined an Onodi cell as a posterior ethmoid cell with an endoscopically visible
bulge of the optic canal.
The vulnerability of the optic nerve with or without Onodi cell is further compounded by the thin lamina
papyracea in the posterior ethmoid area .
found in 8-14%
Onodi cells optic nerve and/or carotid artery would be exposed (or nearly exposed) in the pneumatized
cell.
The optic nerve, and more rarely, the internal carotid artery, may be exposed within or lie immediately
adjacent to such an air cell.
During endoscopic sinus surgery attempts to localise the sphenoidal sinus via instrumentation through the
posterior most ethmoidal air cells can lead to optic nerve, and even, internal carotid artery, injury.

Wigand's approach
Posterior Wigand approach endoscopic sinus surgery:
Posterior approach endoscopic sinus surgery was popularized by Wigand. This is actually a posterior to anterior
approach. This approach is very useful in patients who have undergone previous nasal surgeries with very few intra
nasal landmarks or distorted landmarks. In these patients a more consistent landmark needs to be identified before
proceeding with the surgery.
similar to the traditional ESS technique with a minor difference.
1- intranasal ethmoidectomy and sphenoidectomy is performed after identifying the anterior face of
the sphenoid sinus. The sphenoid ostium is identified and the sinus entered. The choana is also
identified.
2- The skull base is followed anteriorly along the fovea ethmoidalis into the posterior and anterior
ethmoidal sinuses. Working laterally the lamina papyracea is identified, and now the natural
ostium of the maxillary sinus is also identified.
It is always better to start the dissection from a known region to other less easily recognized zones.
Concha bullosa
A concha bullosa (middle turbinate pneumatisation by frontal recess) : common , with DS, of little clinical
importance.
Concha bullosa is a normal variant :MC variations of sinonasal anatomy, in 30-50% of patients
Clinical presentation
Mostly asymptomatic. sinus disease? The air space within the turbinate is susceptible to the same pathologies as
other sinuses, and may thus become infected, obstructed (mucocoele), or be the site of malignancy.
Concha bulloae are associated with deviation of the nasal septum = incidence of sinus disease.

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Radiographic features
Although in most instances concha bullosa refers specifically to pneumatisation of the middle concha, similar
appearances may be occasionally seen of either the superior or inferior conchae.
Concha bullosa of the middle turbinate can be divided into one of three types:

lamellar : pneumatisation of the vertical lamella of the concha (many authors do not regard this as a concha
bullosa) 1
bulbous : pneumatisation of the bulbous segment
extensive (total) : pneumatisation of both lemellar and bulbous parts

They are associated with deviation of the nasal septum away from the concha bullosa, with preserved surrounding
air spaces (suggesting developmental asymmetry rather than mass effect)
It is worth noting that a concha bullosa and a deviated septum may interfere with transnasal surgery and is thus a
relevant finding on imaging of the region for other reasons 6.
Treatment and prognosis
As most are asymptomatic and the relationship between a concha bullosa and sinusitis is controversial, in general
no treatment is required.
If infected or large and associated with ipsilateral maxillary sinus obstruction resection may be undertaken, in
which case the lateral wall of the concha is resected, leaving the medial wall intact to maintain the middle turbinate
6
.
http://radiopaedia.org/articles/concha_bullosa
MCQ
http://1aim.net/fourm/showthread.php?22356-MCQ-Facial-trauma
Buttress system of mid-face
formed by strong frontal, maxillary, zygomatic and sphenoid bones and their
attachments to one another. The central mid-face contains many fragile bones that could easily crumble when
subjected to strong forces. These fragile bones are surrounded by thicker bones of the facial buttress system
lending it some strength and stability.
Components of Buttress system:
For better understanding the components of the facial buttress system have been divided into:
1. Vertical buttresses
2. Horizontal buttresses
Vertical buttress: These buttresses are very well developed.
They include:
1. Nasomaxillary
2. Zygomaticomaxillay
3. Pterygomaxillay
4. Vertical mandible
Majority of the forces absorbed by mid-face are masticatory in nature. Hence the vertical buttresses are
well developed in humans.

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Horizontal buttresses:
These buttresses interconnect and provide support for the vertical buttresses. They include:
1. Frontal bar
2. Infraorbital rim & nasal bones
3. Hard palate & maxillary alveolus

Myospherulosis of nose and sinuses

This condition was first described in 1969 in 6 Africans who presented with nodular swellings inside the nasal
cavity. These swellings were painful and develop in relation to skeletal muscle. Possibly ? iatrogenic.
Histology: fibrous and inflammatory granulomatous tissue in which there are cyst like spaces lined by flattened
foam cells presumed to behistiocytes. Some of these spaces contain clusters of rounded bodies slightly larger than
red blood cells and are surrounded by a thin refractile membrane. Neither the cyst like spaces or their contents
stain with usual fungal stains.
Pathophysiology: Almost all patients had history of previous operative procedures prior to the first histological
identification of the lesion.
A common feature identified in these patients was the use of gauze packing with petrolactum based antibiotics.
Thus it could be considered to be due to reaction to the ointment. The conclusion was that the spherules were red
cells modified
by the petrolactum based antibiotics.
This lesion should be differentiated from fungal lesions
FESS complications
Functional endoscopic sinus surgery is known to cause various complications involving the orbit due to its
proximity to ethmoidal sinus. Orbit is separated from the nasal cavity by a paper thin bone known as lamina
papyracea which can be easily breached during endoscopic sinus surgery.
Faciomaxillary trauma
FACIO-MAXILLARY INJURY
The facio-maxillary injury is usually obvious clinically. Haemorrhage and upper airway obstruction are the most
important aspects of facio-maxillary injuries.
1-Airway
Take out dentures. Loose teeth should be re-implanted ASAP
Head down position.
Airway : proper suction if intubated. Keep the tube patent.

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2-Bleeding: suction, nasal packing, ligation, embolization 3-Facial N injurey

mandibular fracture:common

4-Eye (blow out trauma)

5-

Examination Equipment Requested

Oral/nasopharyngeal airway.
Tongue suture Yankeur sucker
Oxygen
Good lighting and an assistant for the examining Doctor.
ENT tray for packing.( in case of hemorrhage)
Intra oral examination requires a good light and two pairs of hands.
Check for chest injures.
Check clinical state - if shocked, then there are other injuries.
Facio-maxillary injuries obscure other injures.
Eye: exam, edema, black eye, blow out fracture, look for contact lenses.
Mandible: Most common fracture site is the subcondylar region. It is a ring of bone somewhat like the Pelvis, so if
you see one fracture look for others elsewhere. Isolated fractures of the subcondylar region are common and
treated conservatively.
Other common sites

Body of the Mandible - numb lower lip if nerve affected.

Guardsmans Fracture - fracture of the chin and both condyles.
Coronoid Fracture
o Usually associated with fracture of the Zygomatic arch.
o It is important, because if it is missed, can lead to a rigid trismus of the mouth some months later.
This is an anaesthetic hazard for corrective surgery.
Fractures of edentureless mandible - bucket handle fracture are plated early because of difficulty with
eating. Can be repaired under local anaesthetic.

X-RAYS in two planes:

Lateral oblique- AP mandible including Odontoid Process

OPG - Orthopantomogram - view of the whole mandible on one film.

PLATING Internal fixation: Patients resume eating easily and can resume work in two weeks.
INFECTION CONCERN - any fractures of the tooth bearing region should be admitted. Avoid abscess formation,
Osteomyelitis of the jaw. proper antibiotic regime and oral hygiene is given.
Malar
lateral middle third Zygomatic bone, i.e. cheek bone eminence.

black eye (tense tissues)

bleeding into white of eye.

74

surgical emphysema around eyelids.

numb upper lip, nose and teeth.
diplopia (not always).
eye is dropped down and back if the orbital floor is blown out
the malar prominence is flat.
limited opening/closing of mouth if malar pushed back onto mandible.
looked at from above the patient, it is flat.

X-RAYS

occipito mentals x 2.
Lateral view shows opaque antrum, and a step is sometimes seen.
X-rays are not essential for diagnosis.

Blow Out Fracture

treated 10 days to two weeks later when swelling has subsided.
get Ophthalmologist opinion also.
Middle Third Fracture
Pushes face back and down the incline plane "Dish Face".
Jacks the patients mouth open as far as it will go which can cause respiratory problems.
Finger in the mouth, hooked behind the soft palate. Lift the middle face up and out and then a nasopharyngeal tube usually passed.
The nasopharyngeal haematoma of the pre-vertebral fascia be careful and wary of this when passing the
tube.
X-RAYS

Facial views Panorex(OPG if available.

R & L lateral oblique.
AP of the jaws.
Towns view for the Occiput (shows condyle very well).
OM and lateral face views (same as for malar).

CT SCAN: More useful than x-rays, take instead of x rays if high clinical suspicion.

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Le Fort Fractures: Tested by putting hand under the occiput, fingers on the R & L molar teeth and NOT on the
palate.
Le Fort 1:moves across the nasal base.
Le Fort 2
moves through the cribiform plate (base of the brain) i.e. across the nasal bridge.
Leaks C.S.F. rhinorrhoea (indicates a need for antibiotic cover).
The C.S.F. leak dries up once the facial bones are repositioned.
Le Fort 3
moves across the floor of the orbit and out the Zygomatic frontal suture, lateral aspect of the face.
Signs: Marked swelling - dished in appearance.
Check: surgical emphysema-sensory deficit( numbness

facial lacerations
eyes
edema-the patients bite
rhinorrhoea, otorrhoea
bony tissues - orbits, zygomatic arches, nose, temporo-mandibular joints, mandible.

Aims

Restore functional oral anatomy - talking, eating, swallowing

Functional dental occlusion
Normal jaw movement
Normal facial contour restored
Minimise and alleviate pain
Minimise the need for secondary procedures.

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Adapted from Box Hill Emergency Manual SLJ 4/10/2000

http://emedsa.org.au/EDHandbook/trauma/faciomaxillary_fractures.htm
Acute Management
focus on airway patency, haemorrhage, treat hypovolaemia, and evaluate for associated life-threatening injuries.
When these are satisfied, management is directed towards the facial, neck and other injuries.2
Never Nasotracheal intubation in midfacial injuries are present, or basal skull fractures are suspected.
Blind intubation techniques are contraindicated in the acute phase of injury. Formal tracheostomy is best ,airway
patency
Soft tissue injuried and facial lacerations may mitigate against the use of an air-tight face mask for oxygen therapy
or general anaesthesia. The presence of an associated cervical spine injury should be confirmed
topical vasoconstrictors, nasopharyngeal packs, or a Foley balloon catheter inflated in the
nasopharynx, may control or reduce blood loss. If bleeding persists, coagulation studies should be performed and
appropriate replacement therapy given.
instability and movement of facial fragments, motor and sensory function, visual disturbances
(ie, diplopia, limitation of eye movement, and loss of vision) and presence of cerebrospinal
fluid (CSF) rhinorrhoea.
3. Fractures of Zygoma and Orbit.
The malar region absorbs lateral and oblique blows to the mid-face. The zygoma is uncommonly fractures, but its
attachments to the maxilla, frontal, and temporal bones are vulnerable and may be disrupted. When the zygoma is
displaced, disruption of the lateral wall and floor of the orbit may ensue. The eye and its function must be carefully
examined when fractures involving the orbit are suspected. Isolated zygomatic arch fractures are often stable after
operative reduction, and may require no other active management other than "protective" measures to ensure the
area is not accidently bumped. Unstable and comminuted fractures require internal or external fixation. "Tripod"
fracture of the zygoma require open reduction. Herniation of orbital contents and entrapment of ocular muscles
must be relieved by distraction of the fractures which, in turn, are stabilized by wiring. Autogenous bone grafts and
use of alloplastic materials may be required to reconstruct the orbital floor, if the fractures are severely
comminuted and if there is bone loss. Orbital blowout fractures are managed in the same manner.
4. Nasal Fractures.
These are the most common fractures of the facial skeleton. Bleeding may be copious, particularly in patients with
underlying hypertension or bleeding tendency. Vasoconstrictor agents, such as adrenaline, may be useful in
controlling bleeding; in most cases the bleeding will settle. In some cases, nasal packing or inflation and traction of
a Foley catheter balloon into the nasopharynx may be required. Closed reduction and external splinting is required
to manage nasal fractures and must be performed within 10 days of injury.
Soft Tissue Injuries
The region is complex, and contains many important structures, and extensive wound debridement should be
avoided. The rich vascular supply, protects against devitalization. Minimal debridement and delayed wound
closure provides the best approach to management of the heavily contaminated wound. Where there is extensive
tissue loss, once the wound is clean, myocutaneous or osteocutaneous grafts may be performed by microsurgery.
Penetrating neck injuries, ( knife and gunshot wounds), may produce life-threatening exsanguination injuries and
require careful evaluation and early surgical exploration.
1. Facial Nerve Injuries.
nerve stimulator before wound closure is performed.
Recovery of function, even in the best circumstances, is less than 50%.
Dyskinesis is a frequent. Lacerations of marginal mandibular branch have poor recovery after repair. There are a
number of procedures, including cross-facial nerve grafts and vascularized
muscle transplants, which have been used with mixed results to improve outcome in long established facial palsy.
2. Parotid Injuries.
3. Laryngeal Trauma.
Outcome

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Management of the airway and other life-threatening injuries are priorities in the care of the traumatized patient.
Mortality will be influenced by the care in the acute phase.
However, appropriate and prompt definitive care of facial and neck injuries may significantly affect morbidity. In
most cases, definitive treatment while the patient is receiving life support, may avoid complications which will
significantly affect the patient's quality of life after recovery.
http://hannaziegler.tripod.com/general/icu/oh/ohc068.pdf
Total Maxillary swing approach
Introduction: Total maxillary swing approach is utilized to approach nasopharynx in order to remove benign
tumors of nasopharynx like nasopharyngeal angiofibroma.
This procedure involves disarticulation of maxilla, and swinging it away laterally with its attached facial skin
exposing the nasopharynx.
Anesthesia General
Position Rose position (tonsillectomy position)
Incision Weber Ferguson incision without gingivolabial component
Bilateral tarsorraphy should be performed
Inverted U shaped incision is marked out on the hard palate
After deepening the facial incision the lacrimal sac should be skeletonized and sectioned at its lower end.
Infra orbital nerve should be sectioned as it comes out of infraorbital foramen.
Periosteum of the inferior orbital wall should be elevated. Appropriate sized miniplates should be used to drill out
holes in the area for future anchorage of the maxilla.
Osteotomies should be performed on the frontal process of maxilla and at the maxillo zygomatic suture.
The maxillo ethmoidal junction should be separated using a straight osteotome.
The mucoperiosteum over the hard palate should be elevated based on the contralateral greater palatine vessels.
The ipsilateral greater palatine vessels were cauterized and sectioned.
A straight osteotome should be placed between the arms of a v shaped notch located on the anterior nasal spine
and hammered in order to separate the maxilla down the middle.
A curved osteotome is used to disarticulate the maxilla from the pterygoid process.
Now the whole maxilla with its attached cheek tissue can be swung like a door laterally exposing the whole of
nasopharynx.
Mass in the naso pharynx can now be removed under direct vision.
Maxilla can be repositioned after surgery and secured in position by using miniplate and screws.
Occlusal wafer and palatal splints can be used to secure the mucoperiosteal lining of the palate in place.
Complications:
1. Palatal necrosis
2. Floating palate
3. Rhinolalia aperta
4. Nasal regurgitation of fluids
5. Palatal fistula could be temporary
Lemierre syndrome
suppurative thrombophlebitis of internal jugular vein.
Etiology: extension of infection into the carotid space by deep neck space infections.

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Clinical features:
1. Swelling and redness over the angle of the jaw and along the sternocleidomastoid muscle
2. Spiking fevers 3. Chills
4. Evidence of pulmonary embolism.
Investigations:
1. High resolution ultrasonography
2. CT scan (contrast enhanced computerized tomography) 3. MRI / MRA
Treatment:
antimicrobial therapy. ( culture / sensitivity results.
Anticoagulants are recommended for 3 months ( evidence of thrombus or septic emboli.
Fibrinolytics : within 4 days of onset.
Surgical ligation / resection of internal jugular vein is reserved for patients with evidence of septic pulmonary
emboli not resolving to medical management.
Endovascular stenting / superior vena cava filters can also be considered.
Dangers of Lemierre syndrome:
Carotid aneurysmSeptic pulmonary emboli
Susac syndrome (
rapidly progressing encephalopathy, blindness and hearing loss.
immune mediated endotheliopathy affecting precapillary arterioles. causes infarction
Women > men. age group is between 20 40.
Severe headache-Rapid dementiaMicro infarcts in corpus callosum demonstrable in MRI scans
Photopsia and black spots due to retinal artery occlusion-Scintillating scotoma
Rapidly progressive SNHL on both sidesVertigo-Nystagmus
Management: steroid + IV immunoglobulin.Cyclophosphamide administration.
Rituximab ( monclonal Ab against CD20 of B lymphocytes.
Youngs syndrome: (similar to immotile cellia) Exposure to mercury
1.
Obstructive azoospermia
2.
Bronchiectasis
3.
Sinus disease
History: In 1970 a Liverpool Urologist David Young observed a group of patients with infertility (obstructive
azoospermia) and lung disease. He coined the term Berry Perkins Youngs syndrome. In 1978 Hendry shortened
the name to Youngs syndrome. He also classically described this syndrome as a complex of Obstructive
azoospermia, sinusitis and bronchiectasis. It should also be pointed out that this term Youngs syndrome was
already used in 1953 to describe women with prolonged fetal growth, high fetal / neonatal mortality, large babies,
hyperlactation, obesity and diabetes.
Nasal cholesteatoma
This is another name for Rhinitis caseosa. which was coined by Duplay in 1868. Eggston and Wolff after a detailed
study in 1947 concluded that this condition could occur secondarily following pent up secretions in the sinus
cavities. Their studies revealed that this condition is more common in patients with extensive bilateral ethmoidal
polyposis. caused obstruction , led to accumulation of secretions. Whitish to yellow cheesy material were found

79

within the nasal cavities of these patients behind the nasal polypi. This cheesy material also caused expansion of
sinus cavities, erosion of bone and extension into orbit.
Eggston used the term pseudocholesteatoma to describe this condition which resembled cholesteatoma only
morphologically. Histologically squamous elements could not be identified in them.
Histologically this tissue comprises of inflammatory tissue, granulation mixed with mucoid debris.
Presently allergic fungal sinusitis also resembles this condition and hence included under this category.
Clinical features:
1. Nasal obstruction
2. Presence of nasal polypi
3. Telecanthus
4. Swelling over medial canthal region
5. Proptosis with the eye being pushed downwards and laterally
6. These patients may present with loss of vision due to involvement of optic nerve
7. Intracranial extension due to erosion of anterior cranial fossa skull base is also seen
This disease could be considered to be end stage manifestation of sinus inflammation. Hence the use of the term
Rhinitis caseosa syndrome makes lot of sense.
Pinus theory of nasal cholesteatoma: majority of patients suffering from nasal cholesteatoma also suffered from
dental cysts which obliterated the entire maxillary sinus cavity.
Management: Rhinitis caseosa can be managed by debridement followed by regular douching using normal saline
vidian nerve :formed by post synaptic parasympathetic + presynaptic sympathetic fibers. = Nerve of pterygoid
canal.
Nerves that gets involved in the formation of vidian nerve:
1. Greater petrosal nerve (preganglionic parasympathetic fibers)
2. Deep petrosal nerve (post ganglionic sympathetic fibers)
3. Ascending sphenoidal branch from otic ganglion
Vidian nerve is formed at the junction of greater petrosal and deep petrosal nerves. This area is located in the
cartilagenous substance which fills the foramen lacerum. From this area it passes forward through the pterygoid
canal accompanied by artery of pterygoid canal. It is here the ascending branch from the otic ganglion joins this
nerve.
The vidian nerve exits its bony canal in the pterygopalatine fossa where it joins the pterygopalatine ganglion.

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Vidian canal:
vidian nerve passes in it. short bony tunnel seen close to the floor of sphenoid sinus. transmits the vidian nerve and
vidian vessels from the foramen lacerum to the pterygopalatine fossa.
According to CT scan findings the vidian canal is classified into:
Type I: The vidian canal lies completely within the floor of sphenoid sinus
Type II: In this type the vidian canal partially protrudes into the floor of sphenoid sinus
Type III: Here the vidian canal is competely embedded in the body of sphenoid bone

Figure showing the formation of vidian nerve

Study of these anatomical differences of vidian canal in relation to the floor of sphenoid sinus helps in deciding the
surgical approach to the nerve.

CT
images showing the anatomical types of vidian canal and their relationship to the floor of sphenoid sinus
TESPAL by drtbalu
Tespal: (Trans nasal endoscopic sphenopalatine artery ligation)
History: This procedure was first reported by Budrovich and Saetti in 1992.

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This procedure can safely be performed under GA. / L.A.

Indication: Epistaxis not responding. Posterior epistaxis
Procedure: The nose should first be adequately decongested topically using 4% xylocaine mixed with 1 in 50,000
units adrenaline.
A 4mm 0 degree nasal endoscope is introduced into the nasal cavity. The posterior portion of the middle turbinate
is visualized. 2% xylocaine with 1 in 1lakh units adrenaline is injected in to this area to further reduce bleeding.
Incision: An incision ranging between 10 - 20 mm is made vertically about 5 mm anterior to the attachment of
middle turbinate. The mucosal flap is gently retracted posteriorly till the crista ethmoidalis is visualized. The
crista ethmoidalis is a reliable land mark for the sphenopalatine artery. The artery enters the nose just posterior to
the crista. The crista can be removed using a Kerrison's punch for better visualization of the artery.
The sphenopalatine artery is clipped using liga clip or cauterized as it enters the nasal cavity. This is done as close
to the lateral nasal wall as possible, this would ensure that the posterior branches may also be reliable included.
Following successful ligation / cauterization, the area is explored posteriorly for 2 - 3 mm to ensure that no more
vessels remain uncauterized.
Nasal packing is not needed.
Complications of TESPAL:
1. Palatal numbness 2. Sinusitis3. d lacrimation 4. Septal perforation
5. Inferior turbinate necrosis
This procedure in combination with transnasal anterior ethmoidal artery ligation control t epistaxis .

Image showing cauterized sphenopalatine artery area

Pott's puffy tumor
Definition: osteomyelitis of frontal bone. first described by Pott in 1775.
It is subperiosteal abscess of frontal bone which appears as a localized swelling of the frontal region associated
with frontal osteomyelitis.
Etiology:
It can be caused by acute / chronic frontal sinusitis. This entity is getting uncommon these days due to the advent
of powerful excellent antibiotics.
This condition is also associated with epidural purulent collection, subdural empyema and intracerebral abscess.

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Applied anatomy:
The mucosal lining of frontal sinus, marrow cavity and frontal bone share common venous drainage through
valveless diploeic veins.
This venous drainage permits spread of infection from frontal sinuses into the frontal bone. Local suppuration of
frontal bone propagates to the Haversian system of inner and outer tables of skull causing local demineralisation
and necrosis. This leads to perforation of the anterior table of frontal sinus, resulting in subperiosteal collection of
pus and granulation tissue formation causing Pott's puffy tumor.
Microbiology: staph aureus, streptococci, and oral anaerobes. In cases of intracranial complications anaerobes like
Fusobacterium, Bacteroids have been implicated. It has been postulated that relatively low oxygen concentration
in frontal sinuses could
predispose to this problem.
Diagnosis:
1. Headache
2. Photophobia
3. Swelling / deformity of forehead - Fluctuant tender erythematous swelling of scalp at the mid forehead region is
pathognomonic
4. Fever
5. Purulent rhinorrhoea
6. Signs of raised intracranial tension in complicated cases due to intracranial abscess
Investigation:
CT scan is diagnostic. MRI should be considered as gold standard for diagnosis of intracranial complication.
In CT scan picture taken with contrast hypodense collection of fluid external to the frontal bone with an enhancing
rim suggests Pott's puffy tumor.
Treatment:
1. Intravenous administration of broad spectrum antibiotics
2. Surgery - Endoscopic frontal sinusotomy / Frontal sinus trephining
Frontal trephination is a simple and effective procedure, and still remains the main stay of treatment of complicated
frontal sinusitis.

Picture showing a patient with Pott's puffy tumor

Accessory sinuses of frontal region and their classification:
Frontal sinus drainage region is the most variable portion of the whole of the nasal cavity. These variations
can lead to obstruction to the frontal sinus outflow tract causing frontal sinusitis.
Attempts have been made to classify the variations of these cells abutting this vital area. Going by their drainage

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channels these cells are generally believed to be ethmoidal in origin.

Synonyms: Air cells abutting the frontal sinus have been given various names. They include: Frontal cells, frontal
bullae, Supernumerary frontal sinuses, supraorbital sinuses and supraorbital cells.
Why these cells are important ?
These cells can impinge on the frontal sinus and frontal recess area causing obstruction. These cells can also be
mistaken for frontal sinus itself during endoscopic surgery. Failure to address these cells could lead to persistence
of frontal sinus disease.
Accessory cells in the frontal region can be classified under three categories:
1. Frontal cells
2. Supraorbital cells
3. Intersinus septal cells
Frontal cells: are ethmoidal cells that have pneumatized into the frontal bone.
Van Alyea classified these cells into two groups:
1. Cells that occupy the area of frontal recess
2. Cells that have managed to invade the frontal sinus cavity. These cells have been described in three different
locations: 1. the floor of the frontal sinus, 2. Medial wall of frontal sinus, 3. posterior wall of frontal sinus.
According to Van Alyea supra orbital and intersinus septal cells are invading cells.
Bent's classification of accessory frontal cells: 4 different types based on their location.
Type I: represents a single frontal cell just above the agger nasi cell
Type II: two or more air cells superior to the agger nasi cell.
Type III: single frontal cell / massive and it pneumatizes superiorly into the frontal sinus
Type IV: These cells within the frontal sinus, cell inside a cell appearance.
Among these types types III and IV are considered to be invasive types.

Fig showing type II frontal cell

Supraorbital cells: These cell pneumatize the orbital plate of the frontal bone posterior to the frontal recess and
lateral to the frontal sinus. These cells appear to extend over the orbit, appearing as the lateral cell in a coronal CT
scan. Endoscopically these cells appear as separate ostia present along the anterolateral aspect of the roof of the
ethmoid. These cells lie postero lateral to the frontal sinus ostia and anterior to the anterior ethmoidal artery.
Intersinus septal cell: is a midline cell that pneumatizes the frontal bone between the two frontal sinuses.

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Endoscopic Frontal sinuplasty

introduced at the American Academy of Otolaryngologists in September 2005. This is the least invasive of all
frontal sinus surgical procedures. involves introduction of a Balloon catheter into the frontal sinus outflow tract
and dilatation. When inflated this balloon widens the frontal sinus outflow tract in a least traumatic way. This
dilatation does not affect the mucociliary clearance mechanism of the sinus outflow tract mucosa. Dilatation of the
balloon pushes the medial wall of agger nasi cell laterally and the Bulla ethmoidalis posteriorly. The inflating
balloon does not crush the agger nasi cell completely thereby reducing the incidence of post operative obstruction
to frontal sinus drainage pathway.
Indications:
1.
2.
3.
4.

Management of isolated frontal sinus disease not responding to medical management

Can be used in conjunction with sinuplasty of maxillary and sphenoid sinuses
Can be used in combination with endoscopic ethmoidectomy as a hybrid procedure
It can be used to effectively identify frontal sinus ostium

Procedure:
Instruments needed:
1.
tract
2.
3.
4.

Angled endoscopes 30 and 70. These scopes will enable visualization of frontal sinus drainage
Balloon catheter and guide wire
Curved ball probe
Image intensifier

After anesthetizing and decongesting the nasal mucosa the guide wire is introduced into the frontal recess area. If
there is resistance then its position can be verified using an image intensifier. If the passage is smooth the balloon
catheter can be rail roaded over the guide wire. After removing the guide wire, the balloon is inflated by pushing
in air after checking its position using image intensifier. On inflation the ends of the balloon fills first because the
natural ostium creates a pinching effect in the middle. On increasing pressure the bone around the ostium fractures
causing expansion of the bulb. This causes a dilatation of the ostium. Usually 4-6 atmospheres of pressure may be
reached on inflating the balloon.

Balloon catheter in position

Pharynx and Laryngology
Killian's dehiscence

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Killian's dehiscence: Killian's dehiscence:Is the junction between thyropharyngeus and cricopharyngeus muscles.
This isa potentially weak area not supported by other constrictor muscles. The cricopharyngeus muscle isthicker and
bulkier than the thyropharyneal component of inferior constrictor. The pressuregenerated by the constriction of
cricopharyngeus muscle is sufficient to cause prolapse of mucosallining through this potentially weak area.Posterior
pharyngeal diverticula is commonly seen in this area. Among the various types of posterior pharyngeal diverticula,
the posterior pulsion diverticulum (Zenker's diverticulm) is morecommonly encountered.Diagram showing Killian's
dehiscence

Phaynigeal suppuration
Chronic retropharyneal abscess:Retropharyngeal abscess is a collection of pus between the posterior pharyngeal
wall and the fasciaand muscles covering the cervical vertebrae. It occurs in two forms - 1. The acute
primaryretropharyngeal abscess which is common in infants, and 2. Chronic retropharyngeal abscess whichis
common in adults. These two types of abscesses differ in their etiology and management.Chronic retropharyngeal
abscess commonly known to occur in adults. This is usually caused bytuberculosis. The tuberculous foci occur in
the bodies of the cervical vertebrae( Pott's disease)which later spread into the retropharyngeal space. 1ry syphilis of
pharynx mayalso cause retrophrayngeal abscess. abscess usually is present in midline and is free to spreadto either
side also. Rarely infections can spread from tonsils to involve this space.Symptoms: These patients have
excruciating pain while swallowing (odynophagia). Young infantswith retrophryngeal abscess will refuse feed, may
have extensive drooling. In adults the head maybe held straight. Torticollis is also common in these patients. These
patients may have difficulty inbreathing (stridor), in which case tracheostomy must be considered to secure the
airway in the firstplace. Constitutional symptoms like fever / toxicity is very common in acute
retropharyngealabscess.Investigations:Complete blood count show leucocytosis. Blood cultures can also be
performed to ascertain theappropriate antibiotics to be used.C reactive proteins are also found to increased in these
patients
Xray soft tissue neck - A.P. and lateral views.These pictures show prevertebral soft tissue widening. This can be
ascertained by estimating thesize of the prevertebral soft tissue which is normally half the size of the body of the
correspondingvertebra. If the widening is more than half the body size of the corresponding vertebra
thenretropharyngeal abscess must be considered. The cervical spine are straightend with loss of thenormal lordosis
(Ram Rod spine). Above the prevertebral shadow air shadow is seen in almost allcases of retropharyngeal
abscesses. This gas shadow is caused by entrapped air which occur duringbreathing. Some bacteria esp. Clostridium
: gases which may be entrapped in prevertebral space. If tuberculosis is considered to be the cause of chronic
retropharyngeal abscess then surgery is contraindicated. Anti tuberculous therapy is initiated.Patients with non
tuberculous chronic retropharyngeal abscess need to undergo incision anddrainage under local anesthesia. Local
anesthesia is preferred in order to prevent aspiration.
The commonest cause of retropharyngeal abscess in children is suppuration of retropharyngeal LN (Henle's node
Pathology: lymphadenitis of the retropharyngeal nodes of Henle, situated on either side of midline between the
posterior pharyngeal wall and theaponeurosis over the bodies of the second and third cervical vertebrae. These
glands receivethe lymphatics of the post nasal space, pharynx, nose, Eustachian tube and middle ear. Thesenodes
atrophy between the 3rd and 5th year of life hence acute retropharyngeal abscess isuncommon in children above the
age of 4.The Henle's node when infected from the lymphatics, there is first adenitis, and thenperiadenitis and
abscess formation occur. The suppuration is usually one sided, and mostprominent in the oro pharynx. If not
evacuated in time or when it does not rupture, pus mayspread along the oesophagus or burst in different directions
- towards the larynx, the angle tothe jaw or even in to the external auditory canal. The pus is generally foul smelling
yellow orwhitish in color. It usually contains streptococci, and more rarely staphylococci andpneumococci.Chronic

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retropharyngeal abscess: Is commonly known to occur in adults. This is usuallycaused by tuberculosis. The
tuberculous foci occur in the bodies of the cervical vertebrae(Pott's disease) which later spread into the
retropharyngeal space. Primary syphilis of themouth and pharynx may also cause retrophrayngeal abscess. This
abscess usually is presentin midline and is free to spread to either side also.Symptoms: These patients have
excruciating pain while swallowing (odynophagia). Younginfants with retrophrayngeal abscess will refuse feed,
may have extensive drooling. In adultsthe head may be held straight. Torticollis is also common in these patients.
These patientsmay have difficulty in breathing (stridor), in which case tracheostomy must be considered tosecure
the airway in the first place. Constitutional symptoms like fever / toxicity is verycommon in acute retropharyngeal
abscess.Investigations:Complete blood count shows leucocytosis. Blood cultures can also be performed
to ascertainthe appropriate antibiotics to be used.C reactive proteins are also found to be increased in these
patientsX-ray soft tissue neck - A.P. and lateral views.These pictures show prevertebral soft tissue widening. This
can be ascertained by estimatingthe size of the prevertebral soft tissue which is normally half the size of the body of
thecorresponding vertebra. If the widening is more than half the body size of the correspondingvertebra then
retropharyngeal abscess must be considered. The cervical spine is straightenedwith loss of the normal lordosis (Ram
Rod spine). Above the prevertebral shadow air shadowis seen in almost all cases of retropharyngeal abscesses. This
gas shadow is caused byentrapped air which occurs during breathing. Some bacteria esp. Clostridium is known
toform gases which may be entrapped in the prevertebral space.C.T. scan neck or MRI study of neck will also help
in clinching the diagnosis. This mustideally be performed using intravenous contrast agents. It appears as a hypo
dense lesion inthe retropharyngeal space with ring enhancement. Other effects that could be seen are softtissue
swelling, and obliteration of normal fat planes.
C.T. scan is really helpful in differentiating cellulitis from abscess.Axial CT Image showing retropharyngeal
abscessComplications:
1. Mediastinitis
2. Airway obstruction
3. Atlanto occipital dislocation
4. Jugular vein thrombosis
5. Cranial nerve deficits especially the lower three ones
6. Haemorrhage secondary to involvement of the carotid artery
http://www.drtbalu.co.in/ret_abs.html

Lymphoma pyriform fossa

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65 years old male patient presented with c/o1. Sticky sensation in the throat - 6 months2. Difficulty in swallowing 2 months3. Change in voice - 1 month4. Breathlessness - 15 daysSticky sensation was present on the right side of
the throat. It was more for solids.This sticky sensation gradually progressed to difficulty in swallowingChange in
voice started suddenly 1 month back.Breathlessness started 15 days back. Initially it was more on exertion. Now it
is so badthat even simple tasks make the patient feel breathless. It is always associated withnoisy wheeze.Patient
was treated for pulmonary tuberculosis 15 years back.Patient gave h/o fever which lasted for 10 days 8 months
back.Laryngoscopic examination showed: A proliferative mass seen occupying the whole of right pyriform fossa. It
was also found involving the epiglottis, arytenoid andaryepiglottic fold on the right side. Right vocal cord was
found to be fixed.Figure showing mass in the pyriform fossa
Peritonisllar abscess: post tonsilitis
Paratonisillar Abscess: acute, Chronic TB
Retrotonisillar( LN of Henle) age:2-5y
Ludwig: diabetic, dental caries, trismus, drooling, stridor, Hospitalization: Ax- tracheostomy, U incision
Parapharyngeal space(PPS) Tumor
(PPS) is a potential space lateral to the upper pharynx.
Tumors of the parapharyngeal space (PPS) are uncommon, comprising less than 1% of all head and neck
neoplasms. Both benign and malignant tumors may arise from any of the structures contained within the
parapharyngeal space (PPS). Of parapharyngeal space (PPS) tumors, 70-80% are benign, and 20-30% are
malignant. Most parapharyngeal space (PPS) tumors are of salivary or neurogenic origin, although metastatic
lesions; lymphoreticular lesions; and a variety of uncommon, miscellaneous lesions may arise in this location. [1]
Salivary gland neoplasms
50% of parapharyngeal space (PPS) lesions. Salivary neoplasms may arise from the deep lobe of the parotid gland,
ectopic salivary rests, or minor salivary glands of the lateral pharyngeal wall. The prevalence of neoplasms that
arise within the deep lobe of the parotid gland is identical to that of those that arise in the superficial lobe. The
most common prestyloid parapharyngeal space (PPS) lesion is pleomorphic adenoma, which represents 80-90% of
salivary neoplasms in the parapharyngeal space (PPS).
Other benign salivary lesions, including Warthin tumors and oncocytomas, develop in the prestyloid
parapharyngeal space (PPS), as do malignant salivary lesions. Carcinoma ex pleomorphic adenoma and adenoid
cystic carcinoma are the most frequently reported salivary malignancies of the parapharyngeal space (PPS).
Approximately 20% of all salivary lesions in the parapharyngeal space (PPS) are malignant.
Common benign neoplasms include pleomorphic adenomas, monomorphic adenomas, and oncocytomas.
Malignant neoplasms include adenoid cystic carcinomas, mucoepidermoid carcinomas, adenocarcinomas, and
acinic cell carcinomas.
Neurogenic lesions
Neurilemomas, or schwannomas, are the most common neurogenic tumors and arise from any nerve surrounded by
Schwann cells. In the parapharyngeal space (PPS), the most common sites of origin are the vagus nerve and the
sympathetic chain. Neurilemomas are slow growing and rarely cause palsy of the nerve of origin. They are
encapsulated and histologically distinct from the nerve itself. Treatment is by enucleation, and preservation of the

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nerve of origin is usually possible; however, every patient should be cautioned about the possibility of
postoperative paralysis.
Neurofibromas, in contrast, are unencapsulated and intimately involved with the nerve of origin. Neurofibromas
are often multiple. They may occur as a manifestation of the neurofibromatosis-1 (NF-1) syndrome, and, in these
patients, the incidence of malignant transformation is d. The nerve of origin usually has to be sacrificed during
excision to ensure complete removal of the neoplasm.
Paragangliomas are benign vascular neoplasms that arise from the paraganglia or extra-adrenal neural crest tissue.
Paraganglia function as chemoreceptors and are associated with the carotid body, the jugular bulb, and the vagus
nerve in the poststyloid parapharyngeal space (PPS). Carotid body tumors, glomus jugulare, and glomus vagale are
slow-growing paragangliomas that may not produce symptoms but do cause cranial nerve (CN) deficits, bone
erosion, or intracranial extension as they in size.
Approximately 2% of head and neck paragangliomas secrete catecholamines and may cause paroxysmal symptoms
of catecholamine excess. Ten percent of paragangliomas are multiple and associated with paraganglioma at other
locations. Ten percent of paragangliomas are hereditary, associated with a familial paraganglioma syndrome. In
patients with hereditary paraganglioma, the prevalence of multicentricity is 35%.
Hypertension and flushing are suggestive of either a secreting paraganglioma or an associated pheochromocytoma.
If these symptoms are present, obtain urinary catecholamine levels. If the level of catecholamines is elevated, rule
out a concomitant pheochromocytoma. Malignant transformation occurs in fewer than 10% of patients and is
associated with rapid growth and development of metastatic disease.
Lymphoreticular lesions
Lymphoma is the most common malignant lymphoid process, but metastases from thyroid cancer, osteogenic
sarcoma, squamous cell carcinoma, renal cell carcinoma, hypernephroma, and meningioma may also appear as
parapharyngeal space (PPS) masses. The most common lymphoreticular lesions are lymphomas and metastases.
Miscellaneous lesions
hemangiomas, arteriovenous malformations, and internal carotid artery aneurysms, may occur in the
parapharyngeal space (PPS) is important. Imaging studies of this region must be performed before attempting to
obtain a biopsy or to excise the lesion.
Presentation
Neck mass-Oropharyngeal mass
Unilateral eustachian tube dysfunction
Dysphagia-Dyspnea
Obstructive sleep apnea
CN deficits
Horner syndrome
Pain-Trismus
Symptoms of catecholamine excess
tumors of the parapharyngeal space (PPS) :asymptomatic neck or oropharyngeal mass ,only the inferior and medial
boundaries of the parapharyngeal space (PPS) are distensible as seen in the images below.

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PPS tumor manifesting as oropharyngeal mass.

PPS tumor manifesting as a neck mass.

Tumors must be at least 2 cm in size before the bulge or abnormality is palpable. Often, a parapharyngeal space
(PPS) lesion is discovered incidentally on routine physical examination. Unilateral eustachian tube dysfunction
may result from significant medial extension, causing soft palate and nasopharyngeal swelling. Oropharyngeal
bulging from an underlying parapharyngeal space (PPS) mass may cause significant displacement of the ipsilateral
tonsil and may create the appearance of a primary tonsillar lesion. An ill-fitting denture may be the first symptom
of a benign prestyloid lesion.
Symptoms of dysphagia, dyspnea, and obstructive sleep apnea may result from distortion of the lateral pharyngeal
wall by a massive parapharyngeal space (PPS) lesion. In such cases, tracheostomy has been recommended for
relief of airway obstruction.
Cranial neuropathies may result from enlargement of parapharyngeal space (PPS) lesions with compression of CN
IX, X, XI, or XII, hoarseness, dysarthria, and dysphagia. Horner syndrome . With the exception of glomus vagale
tumors, vagal paresis, most benign lesions of the parapharyngeal space (PPS) do not result in cranial nerve
dysfunction. Pain is unusual with benign lesions and may be due to compression or hemorrhage into the lesion;
however, pain and neurologic dysfunction are more often indicative of malignancy with infiltration of the skull
base. Under these circumstances, CN VII may be involved. Trismus results from malignant invasion of the
pterygoid musculature or involvement of the coronoid process of the mandible.
Physical examination : painless oropharyngeal or neck mass. ( oropharynx, tonsillar area, pharynx, and neck.
Lesions arising from the deep lobe of the parotid ( bimanual palpation) full cranial nerve evaluation, laryngoscopy,
to test the motor and sensory innervation of the larynx. The vagus nerve MC involved cranial nerve, vagal palsy is
suggestive : paraganglioma or a malignancy.
A neck mass that is pulsatile , thrill to auscultation = vascular tumor. Paragangliomas are typically mobile in an
anteroposterior direction but not in a vertical direction. Any patient with aural symptoms should undergo thorough
audiologic evaluation as well as careful examination of the nasopharynx.
Indications
surgical excision is diagnostic and therapeutic ,choice of surgical approach : size , location, its relationship to the
great vessels, and the suspicion of malignancy (see Surgical therapy). However, when surgery is contraindicated,
alternatives to surgical therapy consist of observation or radiation therapy.
Relevant Anatomy
The parapharyngeal space (PPS) is a potential space lateral to the upper pharynx. shaped like an inverted pyramid,
extending from the skull base superiorly to the greater cornu of the hyoid bone inferiorly.

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The superior border of (PPS) : temporal and sphenoid bones, including the carotid canal, jugular foramen, and
hypoglossal foramen. The parapharyngeal space (PPS) is limited anteriorly by the pterygomandibular raphe and
pterygoid fascia and posteriorly by the cervical vertebrae and prevertebral muscles. The medial border of the
parapharyngeal space (PPS) is the pharynx, and the lateral border is comprised of the ramus of the mandible, the
medial pterygoid muscle, and the deep lobe of the parotid gland. Below the level of the mandible, the lateral
boundary consists of the fascia overlying the posterior belly of the digastric muscle.
The fascia from the styloid process to the tensor veli palatini divides the parapharyngeal space (PPS) into an
anteromedial compartment (ie, prestyloid) and a posterolateral (ie, poststyloid) compartment. The prestyloid
compartment contains the retromandibular portion of the deep lobe of the parotid gland, adipose tissue, and lymph
nodes associated with the parotid gland. The poststyloid compartment contains the internal carotid artery, the
internal jugular vein, CNs IX- XII, the sympathetic chain, and lymph nodes.
These lymphatics receive afferent drainage from the oral cavity, oropharynx, paranasal sinuses, and thyroid. The
distinction between the prestyloid and poststyloid space is more than just semantic because imaging studies can
delineate between the 2 compartments and can assist in reaching the correct diagnosis preoperatively.
Contraindications
nonoperative management of parapharyngeal space (PPS) : poor surgical candidates ( elderly; balloon occlusion
fails; those who have unresectable lesions; and those who have benign, slow-growing tumors that would carry a
significant risk of sacrifice of multiple cranial nerves if resected. The risks and benefits of surgery must be weighed
in every case.
Complete surgical excision is the mainstay of treatment ,FNAB may be a useful adjunct when the mass is readily
accessible, either transcervically or transorally, and may provide useful information if a diagnosis of malignancy is
suspected. However, if imaging studies suggest a vascular lesion, FNAB provides little if any useable information
and is not indicated.
o Incisional biopsy should be considered only if the patient is not an operative candidate and FNAB
findings are inconclusive and if a diagnosis of malignancy or lymphoma is strongly suspected.
o Transoral open biopsy has been described but carries a significant risk of hemorrhage and of
contamination of the pharyngeal mucosa by tumor, which requires excision of that site during
subsequent definitive resection. Most surgeons, including the authors, denounce this practice.

http://emedicine.medscape.com/article/849385-overview#showall
Wagner and Grossman theory
This is the most popular and widely accepted theory.
1-RLN (in paralysis of recurrent laryngeal nerve the cord lies in the paramedian position because the intact
cricothyroid muscle adducts the cord. (as SLN is intact).
2-If SLN + RLN are paralysed the cord will assume an intermediate(cadaveric position) because of the loss of
adductive force. This theory has been confirmed by electro myological studies.
According to this theory, chest lesions should cause recurrent laryngeal nerve paralysis alone, but in many patients
with lung cancer the cord assumes intermediate position. ( retrograde atrophy of the vagus nerve up to the level of
nucleus ambiguus.
Paralysed vocal cords may demonstrate some movement due to the action of interarytenoid muscle which gets
bilaterally innervated.

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Semon's law
the abductor fibres in the recurrent laryngeal nerves are more susceptible to pressure than the adductor fibers.
lesion involving the recurrent laryngeal nerve three stages can be observed.
1-only the abductor fibers are damaged, the vocal folds approximate in the midline and adduction is still possible.
2-In the second stage the additional contracture of adductors occur so that the vocal folds are immobilized in the
median position. 3-In the third stage the adductors become paralyzed and the vocal folds assume a cadaveric
position". Lateral position)
This theory is fraught with clinical and experimental inconsistencies. It was assumed that the nerve fibers
supplying the abductors of the vocal folds lie in the periphery of the recurrent laryngeal nerve and any progressive
lesion involves these fibers first before involving the deeper fibers that supply the adductors. It was even
suggested that adductors are more resistant to insults than the newer abductors. According to this theory in all
progressive lesions involving the recurrent laryngeal nerve the abductors paralyze first followed by the adductors.
When recovery takes place the first muscle group to recover will be the adductors before the abductors could
recover.
SLN (Superior laryngeal nerve
This branch from the vagus supplies the main sensory innervation of larynx in the glottic and supraglottic regions
with some minimum contribution to posterior subglottic area. It branches out of the vagus nerve just below the
nodose ganglion. It is branched from the medial aspect of the vagus nerve. It lies superficial to the superior
cervical ganglion form which it receives sympathetic supply. This nerve also supplies the carotid body. Its motor
innervation supplies the cricothyroid muscle. Traditional belief is that paralysis of superior laryngeal nerve causes
bowing and flaccidity of true vocal cords with d vocal range and laryngeal rotation. According to Sulica this
premise is not entirely accurate. In human larynx the superior laryngeal nerve has complex functional inter
relationship with the recurrent laryngeal nerve. Hence the degree of compensation of these two nerves following
injury is not entirely straight forward.

The average length of superior laryngeal nerve is about 2 cm in males and 1.5 cms in females. It divides into an
internal and external laryngeal branches.
Internal laryngeal nerve branch: is predominantly sensory in nature. This nerve runs parallel and medial to the
superior laryngeal artery. At the level of greater cornu of hyoid bone it turns medially, passing deep to thyrohyoid
muscle. This nerve enters the larynx through the thryohyoid membrane just above the superior border of inferior
pharyngeal constrictor muscle. After entering into the larynx this nerve divides into three branches i.e. superior,
middle and inferior. The superior division divides into two / three branches supplying sensations to the lingual
surface of epiglottis, lateral aspect of glosso epiglottic fold. The middle division innervates the aryepiglottic fold,

92

vocal folds, vestibular folds and the posterior aspect of arytenoid. The inferior division is the largest of the
branches of superior laryngeal nerve. It lies along the medial aspect of pyriform fossa. It is this nerve which is
blocked when pyriform fossa block is given for endolaryngeal surgical procedures. This branch supplies the
interarytenoid muscle. This nerve gives out a branch to communicates with RLN= (Galen's loop).
External branch of superior laryngeal nerve is smaller in caliber when compared to the internal branch. It supplies
motor fibers to the cricothyroid muscle. It may provide occasional supply to the thyroarytenoid muscle. Rarely it
may also provide sensation to the glottis. This nerve arises from the superior laryngeal nerve at the level of greater
cornu of hyoid bone. At this level it lies just posterior to the superior thyroid artery.
Kierner classified the superior laryngeal nerve into 4 types depending on the relationship of its external branch to
the superior pole of thyroid gland.
Type I nerve: In this type the external branch of superior laryngeal nerve cross the superior thyroid artery about
1cm above the superior pole of thyroid gland.
Type II nerve: In this type the external branch of superior laryngeal nerve crosses the superior thyroid artery within
1 cm of the superior pole of thyroid gland.
Type III nerve: In this type the external branch of superior laryngeal nerve crosses the superior thyroid artery under
cover of the superior pole of thyroid gland.
Type IV nerve: In this type the external branch of superior laryngeal nerve descends dorsal to the superior thyroid
artery and crosses its branches just superior to the upper pole of thyroid gland.
Awareness of these anatomical variations will help the surgeon in preserving this branch during head and neck
surgeries.
The external branch of the superior laryngeal nerve divides into two branches and supplies the oblique and rectus
bellies of cricothyroid muscle. It should be borne in mind that this nerve pierces the inferior constrictor of pharynx
before supplying the cricothyroid muscle.
Features of superior laryngeal nerve injury:
Unilateral superior laryngeal nerve injury:
These patients have very slight voice change. Patients may even complain of hoarseness of voice. Singers find it
difficult to maintain the pitch. Diplophonia is common in these patients (defect in the production of double vocal
sounds). The pitch range is d in these patients. This is due to the fact that cricothryoid muscle is very important
in maintenance of vocal cord tension and this muscle is supplied by the superior laryngeal nerve.
On indirect laryngoscopy examination the vocal folds appear normal during quiet respiration. There could be seen
a deviation of the posterior commissure to the paralysed side. The posterior commissure points towards the side of
the paralysis. At rest the paralysed vocal fold is slightly shortened and bowed and may lie at a lower level than the
opposite cord.
There is also associated loss of sensation in the supraglottic area causing subtle symptoms like frequent throat
clearing, paroxysmal coughing, voice fatigue and foreign body sensation in the throat.
Bilateral superior laryngeal nerve injury: Fortunately this condition is very rare. It could result in fatal aspiration
and pneumonia. This condition is in fact difficult to diagnose as there is no asymmetry between the vocal folds.
Superior laryngeal nerve paralysis
SLN is one of the branches of vagus nerve. Paralysis is frequently overlooked because of complex clinical
picture. Functionally speaking the superior laryngeal nerve function can be divided into sensory and motor
components. The sensori function: provides a variety of afferent signals from supraglottic larynx.
Motor function involves motor supply to ipsilateral cricothyroid muscle.

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Role of cricothyroid muscle in phonation:

Contraction of cricothyroid muscle tilts the cricoid lamina backward at the cricothyorid joint causing lengthening,
tensing and adduction of vocal folds , in the pitch of the voice.
Causes of superior laryngeal nerve paralysis:
1. Thyroid surgery 2. Skull base tumors
3. Oesophageal tumors- 4. Trauma
Diagnosis of superior laryngeal nerve paralysis is based largely on symptomatology and clinical suspicion.
Symptoms:
1. Raspy voice 2. Voice fatigue
3. Volume deficit 4. Loss of singing volume
Investigations:
Laryngeal electromyographic examination:
Potentials generated by the contracting cricothryoid muscle can be recorded by placing electrodes in appropriate
sites. A paralysed muscle usually generates injury potentials / no potential.
Patient should assume supine position, with head slightly extended by keeping a shoulder roll.
Laryngeal electromyography is performed using a 37mm monopolar electrode.
Reference electrode - is placed over sternum.
Ground disk electrode - is placed over clavicle.
Identity of strap muscles is confirmed by slight head elevation without phonation. The brisk signal is seen during
this maneuver is from
the strap muscles.
The cricothyroid muscle is located by inserting the needle 5 - 10 mm off midline a the cricothyroid membrane
level and angling it laterally
towards the cricoid cartilage. Recordings from both sides are made.
Kymograph:: vibrations of the vocal folds studied. Movements : recorded using strobe light.
Kymogram of normal human phonation displays a characteristic rhomboid shape with symmetry. The glottic
excursions on both sides begin in the midline,
travel equal distances at equal rates and return back to the midline.
Management::Speech therapy will go a long way in restoring a near normal voice.
Pathophysiology of vocal cord paralysis: In recurrent laryngeal nerve paralysis the vocal folds may assume a any
of Six positions: median, paramedian, cadaveric (intermediate), gentle abduction and full abduction.
Semon's law: abductor fibres : more susceptible to pressure than the adductor fibers. After a number of
amendments this law is stated as " In gradually progressing 3 stages observed, stage I only the abductor fibers are
damaged, the vocal folds approximate in the midline and adduction is still possible. stage the additional
contracture of adductors occur so that the vocal folds are immobilized in the median position. In the third stage the
adductors become paralysed and the vocal folds assume a cadaveric position".
This theory is fraught with clinical and experimental inconsistencies. It was assumed that the nerve fibers

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supplying the abductors of the vocal folds lie in the periphery of the recurrent laryngeal nerve and any progressive
lesion involves these fibers first before involving the deeper fibers that supply the adductors. It was even
suggested that adductors being phylogentically older are more resistant to insults than the newer abductors.
According to this theory in all progressive lesions involving the recurrent laryngeal nerve the abductors paralyze
first followed by the adductors. When recovery takes place the first muscle group to recover will be the adductors
before the abductors could recover.
Differential innervation theory: This theory was based on the anatomic fact that the recurrent laryngeal nerve often
branched outside the larynx. Injury to individual branches could cause paralysis of specific groups of muscles
accounting for the varying positions assumed by the paralysed cord.
Changes in the cricoarytenoid joint and paralysed muscles: These changes have been proposed to explain the
position of the cord in vocal fold paralysis. This theory of progressive fibrosis of muscles has no anatomical proof.
Interarytenoid muscle contraction: In this theory the paramedian position of a paralysed vocal cord is attributed to
contraction of interarytenoid muscle which is supposed to receive bilateral innervation. In reality this is not true as
the interarytenoid muscle just helps to close the posterior glottic chink.
Disturbance of autonomic supply: This theory has no experimental evidence. It suggests that the vocal cord
position is determined by the laryngeal muscle tone due to autonomic innervation.
Wagner and Grossman theory: most popular / accepted : account for the varying positions by a paralysed vocal
cord. in complete paralysis of RLN : VC lies in the paramedian position because the intact cricothyroid muscle
adducts the cord. (Because the superior laryngeal nerve is intact). If the superior laryngeal nerve is also paralysed
the cord will assume an intermediate position because of the loss of adductive force. This theory has been
confirmed by electro myological studies.
According to this theory, chest lesions should cause recurrent laryngeal nerve paralysis alone, but in many patients
with lung cancer the cord assumes a intermediate position. This has been attributed to the phenomenon of
retrograde atrophy of the vagus nerve up to the level of nucleus ambiguus.
Paralysed vocal cords may demonstrate some movement due to the action of interarytenoid muscle which gets
bilaterally innervated.
Functional aphonia: This condition is due to under adduction or non adduction of vocal volds while attempt is
being made to speak. The voice in these patients are rather weak. This condition is seen in patients who are
depressed / under emotional stress, shock etc.
Hoarseness of voice
any change in the quality of human voice (lay terms)=nonspecific one. This term could imply breathiness,
roughness, voice breaks or unnatural pitch changes.
Dysphonia is the corresponding term used by otolaryngologists to describe this condition.
Causes of hoarseness of voice:

Inflammatory causes including acute injuries

Mucosal disorders of vocal folds
Benign tumors of vocal folds
Malignant tumors of vocal folds
Laryngeal foreign bodies

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Neurogenic causes affecting larynx

Mnemonic of causes of hoarseness of voice:((VINDICATE/ Vit E and D

V - Vascular (thoracic aneurysm)
I Inflammation(laryngitis-acute, chronic, specific and non)
N Neoplasm( papilloma, cancer)
D - Degenerative (Amyotrophic lateral sclerosis)
I - Intoxication (smoking / alcohol)
C Congenital(cyst, hemangioma,)
A - Allergies (angioneurotic oedema)
T - Trauma / Thyroid surgery- VC paraysis
E - Endocrinology (Reidel's struma)
Inflammatory: commonest causes of hoarseness of voice. either acute / chronic.
Acute inflam: laryngitis, epiglottis, laryngotracheal bronchitis, diphtheria etc.
Chronic inflammatory: non specific laryngitis (GERD, vocal abuse etc).
Chronic specific laryngitis (TB / syphilitic laryngitis).
Acute vocal cord injuries = tears / hematoma causing hoarseness of voice(resolves with complete voice rest).
Mucosal fold disorders:
Laryngeal oedema, Reinke's oedema.
Vocal nodule-Vocal cord polyp-Vocal cord cysts
Benign tumors:( Papilloma-Fibroma-Adenoma-Chondroma
Precancerous lesions:Hyperkeratosis-Pachydermia-Leukoplakia
Malignant tumors of larynx:
Carcinoma vocal cords
Congenital conditions:
Congenital vocal cord webs
Foreign bodies
Vocal cord paralysis

Acute vocal fold tear

Hematoma of vocal cord

Reinke's oedema

Possible clinical presentations in patients with hoarseness of voice:

1.
2.
3.
4.
5.
6.

Change in voice
Cough
Fever
Vocal fatigue
Irritation / soreness of throat
Weight loss

7. Painful vocalization
8. Breathy voice( gap, unilateral VC paralysis)
9. Neck swelling
10. Dysphagia, odynophagia
11. Heart burn / vomiting
12. Haemoptysis

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13. Stridor(bilateral VC paralysis)

Diagnosis:
Evaluation of hoarseness of voice should include:
Assessment of Anatomy-Physiology-Behavioral factors
A complete history : surgery, voice abuse, smoking, GERD.
Laryngeal visualization : Indirect laryngoscopy / Direct laryngoscopy
Objective voice assessment: simplest method would be a tape recording of the voice in question. This method
should be considered to be subjective.
Acoustic analysis: In this test voice is examined as electrical signals. The term fundamental frequency is used to
measure the number of vocal fold vibrations per second. A normal adult male vocal cord vibrates between 100 130 Hz, where as in females it vibrates at the rate of 200 - 230 Hz. Abnormally high fundamental frequencies
corrected for age and sex changes would indicate hyper contraction of
cricothyroid muscle representing a functional pathology or compensatory dysphonia.
Aerodynamic analysis:
The quality of voice is dependent on breath support. Even subtle respiratory problems can lead to changes in
voice. Aerodynamic measurements play a role in quantifying airflow during respiration and phonation.
Pulmonary function tests may play a role in identifying subtle respiratory problems.
Maximum phonation time: This is a measurement of the amount of time a patient can sustain a vowel sound in
one breath. Normal values range between 15 - 25 seconds. d values indicate incomplete glottic closure or
insufficient lung support.
Glottal air flow: This sensitive test captures the amount of air flowing through the glottis during phonation.
This is measured in cc/second by dividing the total volume of air flowing through the glottis by the amount of
time in seconds. This gives information about the lung capacity and the efficiency of vocal folds. d glottal flow
is associated with incomplete closure of glottis.
The voice in patients with d glottal flow is usually breathy / whispering in nature.
d glottal air flow is seen in patients with spasmodic dysphonia due to hyperadduction of vocal folds.
Management:
1.
2.
3.
4.
5.
6.
7.

Absolute voice rest - very useful in acute conditions

Speech therapy - useful in chronic disorders
Antibiotics
Anti inflammatory drugs
Treatment of GERDS
Surgical intervention
Laryngeal causes of stridor

Stridors in Kids

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8. Inflammatory causes:These includeAcute laryngitis very rarely they cause stridor Diptheria Membrane
dislodges and obstructs laryngeal inletAngioneurotic oedema Steroids will help in these patientsAcute
laryngotracheal bronchitis common in childrenForeign bodies:Aspiration of foreign bodies are rare causes
of stridor. More common in children.Neurological:Vocal cord paralysis Bilateral abductor paralysis will
cause stridor. This can be caused due toinvolvement of recurrent laryngeal nerve on both sides due to
thyroid malignancy / or due toinjury following total thyroidectomy. Hypocalcemic tetany can also lead to
stridor in rare cases.Trauma This includes birth trauma, burns and scalds etc.
9. Figure showing extralaryngeal causes of stridor

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10. Extralaryngeal causes of stridor: Congenital: PIERRE ROBIN SYNDROME: small mandible
(Micrognathia), posterior displacement of tongue (glossoptosis)= airway obstruction.
11. Tracheo oesophageal fistula (congenital / acquired) = surgical emergency.
12. Inflammatory causes: Ludwig's angina Submental oedema causing tongue to fall back obstructing the
airway. Retropharyngeal abscess = Surgical emergency
13. A big foreign body at the level of cricopharynx = airway obstruction by oedema.
14. Neoplasm:Enlarged thymus.Cystic hygroma ,prelaryngeal / cervical lymphnodes causing airway
compression.Management:Priority should be given to securing the airway as early as possible.
15. stridor management : Depending on cause. oxygenate : immediate ,O2 / face mask. Nasal prongs are better
tolerated. Intubation- :may not work if stridor is caused due to tumors / oedema of larynx. Attempting to
intubation would do more harm .Contraindications for intubation:1. hoarseness + stridor =coexistant
malignancy. Larynx:indirect laryngeal examination / video laryngoscopic examination. 2. Absence of
laryngeal crepitus =+ve Moure sign= indicates either the presence of foreign body at the level of
cricopharynx or growth at the level of cricopharynx. Intubation should not be attempted in these patients.3.
Extralaryngeal causes of stridor is a contraindication for intubation.

16. Tracheostomy should be performed as a life-saving procedure in these patients if intubation failsor if it is
contraindicated.Before taking up the patient for tracheostomy the following investigations are a must:Xray
soft tissue neck lateral view to assess the adequacy of subglottic air column. For aa successful tracheostomy
a patient must have an adequate subglottic air column. This x raywill also show any foreign body at the
level of cricopharynx, retropharyngeal abscess etc.Surgically securing the airway can be performed by any
of these following methods: Percutaneous tracheostomy Criothyroidotomy Tracheostomy The aim of all
these procedures is to secure the airway by surgically bypassing the obstructing airway lesion.2. Mention
the differential diagnosis of white patch in tonsilCauses of white patch seen over the tonsil can be classified

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according to their etiology. Infections: Could be viral, bacterial and fungal. Viral infections: Viral infections
causing a white patch in the tonsil include:Infectious mononucleosis This infection is caused by
EB virus. This infection commonly causeunilateral enlargement of tonsil. The involved tonsil is covered
with membrane (pseudomembrane).These patients also have cervical adenitis and
hepatosplenomegaly. Paul Bunnel test is positive. HSV infections involving the tonsil will be seen as
ulcerative lesions which are covered with membranous slough. Initially these lesions appear as
multiple shallow small ulcers. Theseulcers coalesce to form a large ulcer covered with membranous
slough.HIV infection Membranous tonsillitis in these patients occur due to secondary infections.Bacterial
infections:Can be further subclassified into:Acute non specific type Acute specific type Chronic non
specific type Chronic specific typeAcute non specific type This type is caused by a variety
of bacteria. Acute follicular tonsillitis belong to this category. Organism involved include streptococci,
H influenza, pneumococci etc. The dirty white membrane which is formed over the crypts of the tonsil can
easily be peeled off the tonsil without any bleeding. In this condition membrane is seen only over the tonsil
and not over any other portion of the oral cavity. Staphylococcal pseudomembranous tonsillitis is another
condition in which a membrane is seen over the tonsil. Membrane formed is pseudomembrane type and can
easily be peeled off without bleeding. These patients commonly manifest with cutaneous lesions
characteristic of staphylococcal
Spasmodic dysphonia current management trends
commonly of adductor type is a focal form of adult onset laryngeal dystoniaby excessive adduction , adductor
spasm of vocal folds.
C/P: huskyVoice , strained and , tremors and involuntary pitch breaks. deteriorates during stressful speaking.
social isolation.
caused by a chronic neurologic disorder of central motor processing, causing action induced muscle spasms of
larynx.
Management: highly resistant to voice therapy.
Rx: recurrent laryngeal nerve section and Type II thyroplasty have high failure rates. d incidence of
complications.
Botox (Botulinum toxin) injections into the thyroarytenoid muscle provides variable relief with no side effects.
Voice improvement lasts only for a limited period of time lasting for weeks - months. Botox causes chemical
denervation of thyroarytenoid muscle by interfering with release of acetyl choline at motor end plates.
Laser thyroarytenoid myoneurectomy:
This surgery is performed under general anesthesia.
Co2 laser with 10 watts intensity is used in continuous mode, slightly defocused.
Ventricular bands are partially resected on both sides exposing the vocal cords completely.

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figure showing incision lines to excise the

ventricular bands

Figure showing thryroarytenoid muscles excised

The middle and posterior third of thryoarytenoid muscles are excised / vaporized (if laser is used).Care should be
taken to prevent damage to vocalis muscles.
Laryngopharyngeal reflux
Laryngopharyngeal reflux is caused due to retrograde flow of gastric contents into laryngopharynx.
This condition is related to GERD. In fact it is a common extra oesophageal manifestation of GERD.
Clinical manifestations:

Voice change
Excessive throat clearing
Copious amount of mucous
Feeling of lump in the throat(globus sign)
Difficulty in swallowing
Heart burn
Chronic cough
Vague discomfort in the throat

To help in the diagnosis of laryngopharyngeal reflux two score charts have been devised:
1. Reflux symptom index
2. Reflux finding score.
Reflux symptom index: Suspected patients are given a questionnaire to answer. It contains about 9 questions.
Patient is supposed to award scores according to their symptoms.
Reflux symptom index chart:
Within last month how did the following problems affect you ?
1. Hoarseness of voice / voice problems : scores 0 - 5. 0 = No problem 5 = severe problem
2. Clearing your throat: Scores 0 - 5
3. Excess throat mucous / post nasal drip: scores 0 - 5
4. Difficulty in swallowing food / liquids / pills: scores 0-5
5. Cough after eating / lying down: scores 0-5
6. Breathing difficulty / choking: scores 0-5
7. Annoying cough: Scores 0-5
8. Sticky sensation in throat / lump in throat: Scores 0-5
9. Heart burn / chest pain: scores 0-5
Reflux symptom index score of more than 13 indicates laryngopharyngeal reflux.
Reflux finding score: prepared by the surgeon after performing a laryngeal examination.
1. Subglottic oedema: 0 - absent, 2 - present.
2. Ventricular obliteration: 2 - partial, 4 - complete
3. Erythema / Hyperemia: 2 - arytenoids involved, 4 - diffuse
4. Vocal fold oedema: 1 - mild, 2 - moderate, 3 - severe, 4 - polypoidal
5. Diffuse laryngeal oedema: 1 - mild, 2 - moderate, 3 - severe, 4 - obstruction
6. Posterior commissure hypertrophy: 1 - mild, 2 - moderate, 3 - severe and 4 - obstruction.
7. Granuloma / Granulation: 0 - absent, 2 - present
8. Thick mucous: 0 - absent, 2 - present.

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A score of 7 indicates possible presence of laryngopharyngeal reflux.

Pepsin Immunoassay:
Detection of pepsin in the throat sputum = laryngopharyngeal reflux.It is 100% sensitive, and 90% specific.
Management:
1. Cessation of smoking
2. d fat intake
3. Avoiding going to bed within three hours after eating
4. Elevation of head during sleep

Epiglottitis

Sore throat (95%)-Odynophagia/dysphagia (95%)-Muffled voice (54%) - "Hot potato voice," as if the
patient is struggling with a mouthful of hot food
Adults may have preceding upper respiratory tract infection (URTI) symptoms.
C/P: Drooling -Stridor: A late finding indicating advanced airway obstruction
Muffled voice -Cervical adenopathy- Mild cough-Irritability
Fever-Hypoxia- Respiratory distress
Severe pain on gentle palpation over the larynx or hyoid bone [11]

Avoid agitating the patient ,Let the patient take a position in which he or she feels comfortable.
Orotracheal intubation may be required with little warning. Equipment for intubation, cricothyroidotomy, or
needle-jet ventilation should be made available at the bedside.
Avoid therapy such as sedation, inhalers, or racemic epinephrine.
Administer supplemental humidified oxygen if possible, but do not force the patient, as the resultant agitation
could worsen the condition.
Clinical pitfalls include the following:

Underestimating the potential for sudden deterioration (most common error)

Inadequate monitoring in which deterioration goes unnoticed (second most common error)
Rushing intubation without proper support (ensure the availability of an anesthesiologist or other
individual experienced in difficult intubation)
Performing unnecessary medical procedures that result in agitation and respiratory collapse
Subglottic stenosis (SGS)

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congenital or acquired.(Iatrogenic is MCC). Often, insidious onset, and early mistaken for (eg, asthma, bronchitis).
Anatomy:
subglottic : bound by cricoid cartilage. adult trachea is 10-13 cm long and 20 mm in diameter ( from inferior
cricoid cartilage to carinal spur.
The first tracheal cartilage is partly inset in the lower border of the cricoid and, on occasion, may be fused with it.
All of the tracheal rings are incomplete posteriorly.
arterial supply: The superior thyroid artery sends a superior laryngeal in thyrohyoid membrane. inferior thyroid
artery sends an inferior laryngeal branch with the recurrent laryngeal nerve to enter the larynx near the cricothyroid
joint.
The tracheal blood supply is segmental. inferior thyroid artery to upper trachea.
bronchial arteries, +subclavian, supreme intercostal, internal thoracic, and innominate to lower trachea. The
branches arrive to the trachea via lateral pedicles.
Sensory innervation :subglottic mucosa is by the recurrent laryngeal nerve.
Etiology: Congenital laryngeal webs is 5% of (larynx anomalies ), with 75% : glottic ,25%: subglottic or
supraglottic level.
Acquired:Trauma is :MCC of stenosis in = 90% of all acquired SGS from endotracheal intubation(injury at the
level of the glottis due to pressure between the arytenoid cartilages. Intubation causes injury in the subglottis due to
the complete cartilaginous ring or can cause injury distally in the trachea. Pressure and/or motion of the tube
against the cartilage framework may cause ischemia and necrosis.
Duration of intubation is the most important factor :
Size of the tube:be no larger than 7-8 mm in diameter / adult males, Max of 6-7 mm / females. size of the
endotracheal tube needed correlates best with the patient's height.
Systemic factors may the risk of injury and include the following:

GERD-Chronic illness,Immunocompromised patient

Anemia Poor perfusion-Radiation therapy, Neutropenia
External trauma, high tracheotomy or cricothyroidotomy
Percutaneous tracheotomy (This has an emerging role as a cause.)
Radiation Chondroradionecrosis ( up to 20 years laterChronic infection

Chronic inflammatory diseases include the following:

Wegener granulomatosis-Sarcoidosis-Relapsing polychondritis

Chronic inflammation secondary to GERD
Neoplasm

Pathophysiology: Congenital stenosis has two main types, membranous and cartilaginous.<4mm in full term

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In membranous stenosis, fibrous soft tissue ( by CT or hyperplastic mucus glands with absence of inflammation.
Membranous stenosis is usually circumferential and may extend upward to include the true vocal folds.
In cartilaginous stenosis, :deformity of the cricoid MCC= shelf-like plate of cartilage and leaving a small posterior
opening. Cartilaginous stenosis is less common than membranous stenosis.
Acquired subglottic stenosis : endotracheal intubation or high tracheostomy tube (edema, congestion, ulceration
and granulation maybe with chondritis , loss of framework support. healing with fibroblast proliferation, scar ,
contracture=stenosis
Clinical presentation
Adults with mild congenital stenosis are usually asymptomatic:diagnosed after a difficult intubation or endoscopy.
Acquired stenosis : few days to 10 years after injury. mostly within a year. Symptoms include the following:
Dyspnea (on exertion or with rest, depending on severity)
Stridor Cyanosis
Hoarseness-Brassy cough-Recurrent pneumonitis
Many patients diagnosed with asthma and recurrent bronchitis prior to discovery of stenosis. A high index of
suspicion : when respiratory symptoms following intubation, regardless.
Contraindications to long-term tracheostomy are debatable and include the following:
Circumferential scarring with cicatricial contracture
A scar greater than 1 cm in vertical height
Loss of cartilage
History of severe bacterial infection associated with tracheostomy
Posterior glottic stenosis with arytenoid fixation
Prior radiotherapy (relative contraindication)
Contraindications for open repair: Need for tracheotomy, Significant GERD
Invest

history of prior trauma, evaluate for inflammatory or infectious causes, including the following:
o Wegener granulomatosis(8 S) CANCA
o Relapsing polychondritis
o Syphilis(PRP-VDRL-TPA-AB) ,Sarcoidosis(ACE-Ca) Scleroma(biopsy)
o Tuberculosis- Leprosy-Diphtheria
Radiography
o chest X ray: ( information regarding the tracheal air column.
o A-P and lateral soft tissue views of the neck ( glottic/subglottic air column.
MRI evaluate length and width of the stenotic region ( coronal and sagittal views.
CT scan :helpful as MRI because its views only in the axial plane.
o Thin cuts (1 mm) with sagittal and/or coronal reconstructions may be helpful, however. This is the
preferred initial imaging study of the author.
o New software allows virtual bronchoscopy, assess airway and surgical plan.
Videostrobolaryngoscopy evaluate glottic and supraglottic (possible concom injury).
Fiberoptic or rigid telescopic Laryngoscopy (90 or 70-degree) in the clinic is crucial to the evaluation of
airway lesions.

Medical therapy

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Any underlying cause must be addressed (TB,Syph, Sceleroma, inflam, Wegener).

Antireflux management
o Systemic steroids in early stenosis (option but has not thoroughly investigated.
o In active inflammation, as granulation tissue,(inhaled steroids are of potential benefit (eg, Flovent
220, 2 puffs twice a day for 2 weeks; this is an off-label use based on the author's own experience).

Surgical therapy
Long-term tracheostomy / intraluminal stent- Anterior and/or posterior cricoid split
(ACS/PCS)with stenting
o Anterior laryngofissure with anterior lumen augmentation
o Trachelopexy with muscle-fascia repair
Endoscopic repair
o Not indicated following blunt or penetrating neck trauma
o Advocated as a preferred initial approach in chronic subglottic stenosis
o May require several procedures to obtain desired result
o CO2 laser 4 incision, avoid circular incision=restenosis( least absorbtion=least tissue damage) +
Dilation(rigid/Ballon)+ Triamcinolone injected or mitomycin ( reduce fibroblast growth )
o Dilation of the stenotic area (effective).
Traditional rigid dilators ("Olive" or Jackson dilators) effective, but often shear the
mucosa( potential for cicatricial contraction.
o

http://emedicine.medscape.com/article/865437-overview#showall
Obstructive sleep apnea(OSA)
(OSA) /apnea/hypopnea (OSAH: sleep disorder : cessation or in airflow + breathing effort.
MCC of sleep-disordered breathing (SDB) , recurrent episodes of upper airway (UA) collapse during sleep,
hypoxia+ arousals from sleep.
OSA = daytime sleepiness= -hypopnea syndrome (OSAHS). is underrecognized (80% of Americans with OSAS
are not diagnosed.[2]

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Apnea Hypopnea Index=AHI

Apnea 10:100/ nightly,+ wide swings in heart rate, a precipitous O2aturation, brief c (EEG) arousals with
stertorous breathing sounds as a bolus of air is exhaled when the airway reopens.
symptoms = "3 S s": S noring, S leepiness, and S ignificant-other report OSA. sleepers are unaware ,regard
themselves as "good sleepers" sleep anytime, anywhere. Sleepiness : potentially most morbid = accidents ,
hypertension, cardiovascular Ds, insulin-resistance diabetes, depression, and, sleepiness-related accidents.
breathing events include the following:

Apnea (cessation of airflow for at least 10 seconds. [3] Apnea may last for 30 seconds or even longer).
Hypopnea(recognizable transient reduction of breathing for 10 seconds, a of > 50% in the amplitude
Respiratory effortrelated arousal (RERA)( effort = ,> 10 seconds or longer leading to an arousal from
sleep but one that does not fulfill the criteria for a hypopnea or apnea. standard to measure RERAs is esophageal
manometry, or nasal cannula and pressure transducer,

respiratory disturbance index (RDI) is greater than 5 and the normal RDI cutoff is greater than 15.
Obstructive apneas and hypopneas are typically distinguished from central events.
Obstructive events are characterized by continued thoracoabdominal effort in the setting of partial or complete
airflow cessation, central events by lack of thoracoabdominal effort in this setting. Mixed events have both
obstructive and central features. They generally begin without thoracoabdominal effort and end with several
thoracoabdominal efforts in breathing; they are tabulated in the obstructive apnea index.
Sleep-related breathing disorder (SRBD) continuum
The SRBD continuum suggests that snoring is the initial presenting symptom, and it s in severity over time and it
s in association with medical disorders that may serve to exacerbate the disorder, such as obesity. Snoring has a
constellation of pathophysiological effects. [6]
As the disease progresses, SRBD patients develop d UA resistance that cause hallmark symptom: sleepiness.
Sleepiness is caused by d arousals from sleep. [7] This syndrome has been described as the UA resistance syndrome
(UARS). UARS patients are not hypoxic, and hypoxia does not explain why they are sleepy, nor can sleep stage
percentages or other polysomnography (PSG) variables. The SRBD continuum predicts that over time, a UARS
patient develops OSA, if untreated (see the image below).

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Sleep-related disordered breathing continuum ranging from simple snoring to

obstructive sleep apnea (OSA). Upper airway resistance syndrome (UARS) occupies an intermediate position
between these extremes. Note areas of overlap among the conditions.
OSA has as its hallmark symptoms snoring, sleepiness, spouse apnea report, and hypoxia. The SRBD continuum
suggests that over time, untreated OSA may hasten death through heart disease, hypertension, stroke, myocardial
infarction, heart failure, cardiac arrhythmia, diabetes, metabolic syndrome, or vehicular or other accident due to
sleepiness or other behavioral effects noted.
Pathophysiology
Conceptually, the UA is a compliant tube and, therefore, is subject to collapse. [8]OSA is caused by soft tissue
collapse in the pharynx.
Transmural pressure s, the cross-sectional area of the pharynx s. If this pressure passes a critical point,
pharyngeal closing pressure is reached. Exceeding pharyngeal critical pressure (Pcrit) causes a juggernaut of
tissues collapsing inward. The airway is obstructed. Until forces change transmural pressure to a net tissue force
that is less than Pcrit, the airway remains obstructed. OSA duration is equal to the time that Pcrit is exceeded.
Most patients with OSA demonstrate upper airway obstruction at either the level of the soft palate (ie,
nasopharynx) or the level of the tongue (ie, oropharynx).
Anatomic factors (eg, enlarged tonsils; volume of the tongue, soft tissue, or lateral pharyngeal walls); length of the
soft palate; abnormal positioning of the maxilla and mandible) may each contribute to a in the cross-sectional
area of the upper airway and/or the pressure surrounding the airway, both of which predispose the airway to
collapse.[9, 10] Note that in adults, it is very rare for enlarged tonsils and adenoids to be a cause of OSA. Removing
the enlarged adenoids and tonsils alone rarely is an effective surgical remedy; in children, about 80% who have
have OSA are cured with the removal of enlarged adenoids and tonsils. There is often a misconception that
enlarged adenoids and tonsils may be a singular cause of OSA in both children and adults, but this is not true.
Neuromuscular activity in the UA, including reflex activity, s with sleep, and this may be more pronounced in
patients with OSA.[11, 12, 13]Reduced ventilatory motor output to upper airway muscles is believed to be the critical
initiating event leading to UA obstruction; this effect is most pronounced in patients with a UA predisposed to
collapse for anatomical reasons.
Central breathing instability is a well-established factor contributing to the development of central sleep apnea
(CSA), particularly in patients with severe congestive heart failure (CHF). [14, 15, 16] Evidence also indicates that
central breathing instability contributes to the development of OSAS.
UA obstruction in the absence of ventilatory motor output (central sleep apnea) has been observed.[17] Second,
reduction in pharyngeal dilator activity has been associated with periodic breathing[18, 19, 20] and hypocapnia in
subjects with evidence of inspiratory flow limitation. [21] Third, men have been shown to be more susceptible to the
development of CSA and less responsive to carbon dioxide than women are, [22] a result consistent with the greater
prevalence of OSAS in men than in women.
Static and dynamic pathophysiologic factors
Static factors include surface adhesive forces, neck and jaw posture, tracheal tug, and gravity. Any anatomic
feature that s the size of the pharynx (eg, retrognathia) s the likelihood of OSA. Gravitational forces are felt
simply by tilting ones head back to where the retroposition of the tongue and soft palate reduce the pharyngeal
space. For most patients, OSA worsens in the supine sleeping position.

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An important static factor that has been found is the reduced diameter of the pharyngeal airway in wakefulness in
OSA patients compared with non-OSA patients. In the absence of craniofacial abnormalities, the soft palate,
tongue, parapharyngeal fat pads, and lateral pharyngeal walls are enlarged in OSA patients versus non-OSA
patients.
Dynamic factors : nasal and pharyngeal airway resistance, the Bernoulli effect, and dynamic adherence.
Bernoulli effect: airflow velocity at the site of stricture. As airway velocity s, pressure on lateral wall . If the
transmural closing pressure is reached, the airway collapses. Bernoulli effect is exaggerated in most compliant
airway. Loads on the pharyngeal walls adherence and, hence, the likelihood of collapse.
Apnea clusters and oxygen desaturation
OSA often occurs in clusters. An oxygen desaturation occurs with each apnea. The end of the apnea sequence
typically ends with a brief (>3 sec) EEG arousal. In patients with severe OSA, the cluster of apneas occurs
throughout sleep. The desaturation from the first apnea event is typically
Oxidative stress, inflammation, and cardiovascular disease
An excellent review article by Gozal and Kheirandish-Gozal provides a model that attempts to integrate how
oxidative stress and inflammatory processes link OSA and cardiovascular disease. [24]
Genetic studies have revealed that the gene that encodes for oxidative stress uniquely contributes toward OSA.
[25]
This suggests that the development of OSA may be related to inflammation and is not necessarily related to a
trigger for oxidative stress, as was previously thought. The gene may play a pivotal role by operating in a positive
feedback loop, causing the OSA to begin with and then triggering an inflammatory response that further narrows
the UA, exacerbating the OSA.
Etiology
The etiology of OSA involves both structural and nonstructural factors, including genetic factors.
Structural factors
craniofacial bony anatomy that predispose patients with OSA to pharyngeal collapse during sleep:

Innate anatomic variations (facial elongation, posterior facial compression)

Retrognathia and micrognathia-Mandibular hypoplasia
Brachycephalic head form - Associated with an AHI in whites but not in African Americans.[26]
Inferior displacement of the hyoid
Adenotonsillar hypertrophy, particularly in children and young adults
Pierre Robin -Down -Marfan syndrome-Prader-Willi syndrome
High, arched palate (particularly in women)
Nasal factors: obstruction that leads to pharyngeal collapse : polyps, septal deviation, tumors, trauma, and stenosis.
retropalatal obstruction include (1) an elongated, posteriorly placed palate and uvula and (2) tonsil and adenoid
hypertrophy (particularly in children). Structural factors related to retroglossal obstruction include macroglossia
and tumor.
Craniofacial abnormalities
Nonstructural risk factors
Nonstructural risk factors for OSA include the following:

Obesity-Neck cirxumference more than 17 inch

Central fat distribution
MM Male sex -Menopausal state
AA -Age- Alcohol use
SSSS- Smoking- Sedative use- Supine sleep position- snoring with daytime somnolence
Rapid eye movement (REM) sleep

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Families with a high incidence of OSA are reported. Relatives of patients with SDB have a 2- to 4-fold d risk of
SDB compared with control subjects.
Other conditions associated with the development of OSA are as follows:

Hypothyroidism (macroglossia and soft tissue mass in the pharynx, myopathy cause UA dysfunction
Neurologic syndromes (postpolio syndrome, muscular dystrophies, autonomic failure syndromes such as
Shy-Drager syndrome.

Stroke

Acromegaly
Environmental exposures smoke, irritants or allergens, and alcohol and hypnotic-sedative medications.
patients with OSA should not be routinely screened for hypothyroidism, except possibly elderly women.
Neurologic syndromes associated with OSA include
Genetic factors
: C-reactive protein (CRP) with the AHI ,CRP appears to mediate inflammation;
The role of 5HT2A includes effects on sleep-wake cycles, importantly influencing rapid eye movement (REM)
sleep stage percentage. Medications such as selective serotonin reuptake inhibitors (SSRIs) that occupy 5HT2A
receptors reduce or eliminate REM sleep percent time. Other mentioned roles include regulation of upper airway
dilator muscle through an excitatory influence on hypoglossal motor output. 5HT2a is involved in appetite
regulation, thus playing a role in obesity, a well-known risk factor for obstructive sleep apnea.
Epidimology
OSA is increasingly prevalent, 4% for women and 9% for men.
OSA in Australian men is estimated to be 3%.
Premenopausal women with OSAHS tend to be more obese than men with the same severity of disease. Thin
women with symptoms of OSAHS appear to have an d frequency of craniofacial abnormalities.
Evidence indicates that women underreport the symptoms of loud snoring and witnessed apneas, leading to
underreferral to sleep centers. This may explain the marked male predominance (male-to-female ratio of
approximately 8:1) in sleep centerbased studies. Additionally, women have lower AHIs than men, even after
correcting for other demographic factors such as BMI and neck circumference. [42, 43, 44]
Cardiovascular mortality and morbidity
severe untreated OSA (AHI >30) is associated with an d risk of cardiovascular mortality, defined by fatal
myocardial infarction (MI) or stroke.[45] Patients with mild OSA or those undergoing treatment with CPAP did not
have a significantly d odds ratio compared with a group of subjects without OSA. significant risk factor for the
development of cardiovascular morbidity, which included nonfatal MI and stroke.
A 2012 study found that OSA was associated with all-cause mortality in patients younger than 50 years of age.
Campos-Rodriguez et al reported that severe OSA is associated with cardiovascular death in women, and adequate
CPAP treatment may reduce this risk.
CPAP mitigates the d mortality observed in OSA. patients who used CPAP > 6 hours per night had an d survival
rate (96.4%)
OSA is not an independent risk factor for the development of pulmonary hypertension
d risk of motor vehicle accidents
Patient education
All patients should receive education about sleep and proper sleep hygiene, OSA, and the risks of driving while
sleepy. They also should receive education regarding the role of nasal CPAP and the importance of daily use, as

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well as training in the use of CPAP, from a physician, trained technician, or nurse for at least the first month of
therapy. This training promotes long-term adherence with treatment.
Clinical picture:
Obstructive sleep apnea (OSA) symptoms generally begin insidiously and are often present for years before the
patient is referred for evaluation.
Nocturnal symptoms may include the following:

Snoring, usually loud, habitual, and bothersome to others

Witnessed apneas, which often interrupt the snoring and end with a snort
Gasping and choking sensations that arouse the patient from sleep, though in a very low proportion relative
to the number of apneas they experience

Nocturia
Insomnia

Restless sleep, with frequent arousals and tossing or turning during the night
Daytime symptoms may include the following:

Nonrestorative sleep (ie, waking up as tired as when they went to bed)

Morning headache, dry or sore throat
Excessive daytime sleepiness (EDS)
Daytime fatigue/tiredness
Cognitive deficits; memory and intellectual impairment (short-term memory, concentration)
Hypertension
EDS is one of the most common and difficult symptoms clinicians treat in patients with OSA. It is one of the most
debilitating symptoms because it reduces quality of life, impairs daytime performance, and causes neurocognitive
deficits (eg, memory deficits).
EDS is most frequently assessed by Epworth Sleepiness Scale (ESS). questionnaire ,determine how frequently pt
fall asleep in 8 situations.ESS > 10 = sleepy. However, a 2003 study :ESS of 12 = propensity to fall asleep =better
cutoff.[74]
(CPAP) treatment quickly reverses EDS in most patients, not all patients use the CPAP device. Moreover, some
patients remain sleepy despite effective CPAP treatment.
fatigued,

Physical exam: Mallampati score= difficult intubation

Obesity (BMI) > 30 kg/m2, enlarged neck circumf>17 inch, and hypertension,upper airway examination,
Large neck circumference >43 cm (17 in) in men and 37 cm (15 in) in women
Neck circumference may correlate with OSA better than BMI. In one study
Enlarged (ie, "kissing") tonsils (3+ to 4+) (see the image below)
Retrognathia or micrognathia, High-arched hard palate
Systemic arterial hypertension, present in approximately 50% of patients with OSA
Congestive heart failure (CHF)
Pulmonary hypertension, Stroke
Metabolic syndrome (Type 2 diabetes.
30% of patients with a BMI > 30 , 50% of those with a BMI > 40 have OSA. 20% of population are obese
Patients with obesity , OSA may have evidence of pulmonary hypertension and right-side heart failure.
The Mallampati Classification is illustrated. The airway class is based on this visual heuristic.

In this polysomnogram summary graph, obstructive sleep apnea (OSA) severity

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and the degree of oxygen desaturation (SpO2%) worsen in rapid eye movement (REM) sleep (the black underlined
sections) compared with non-REM sleep. This is often the case in OSA patients, especially in OSA patients with
comorbid lung disease.
Predictive value of history and physical exam
The predictive value of initial clinical evaluation for OSA can be based on the following:

Disruptive snoring: A history of disruptive snoring has 71% sensitivity in predicting sleep-disordered
breathing (SDB).

Disruptive snoring and witnessed apneas: These factors taken together have 94% specificity for SDB.
Questioning patients and others is necessary, as follows:

Others: Obtaining a history from someone who has observed the patients sleep behavior is important.
Patients are usually unaware of snoring and/or sleepiness or may minimize these symptoms. Sleepiness may
develop insidiously. Patients may be unaware that they are sleepy; that is, they may forget how normal alertness
feels.

Patients: Question the patient about drowsiness in boring or monotonous situations and about sleepiness
while driving.
Sex-related differences include the following:
The mnemonic STOP (Snore-Tired-Observed stop breathing- Pressure=hi BP):
If the patient answers yes to > 2 questions, AHI
The mnemonic BANG is also useful, as follows:

B: BMI > 35
A: Age > 50 years,N: Neck circumference > 43 cm (>17 in)
G: Gender, male
If the criteria from both the STOP and BANG are met, the sensitivity of the patient having an AHI of greater than 5
is 93% and an AHI of greater than 15 is 83%.[83]
Research has shown that the STOP-Bang questionnaire is both simple to use for busy clinicians and predictive of
OSA. A 2012 study supports existing research indicating that screening in presurgical patients using the STOPBang score has a high probability of OSA detection. [84] Not all patient populations can be identified to the same
degree of accuracy with the same tool, therefore research continues to find the best predictors for various patient
populations.
Cardiovascula in OSA
OSA-related pathophysiological factors may affect sympathetic activation, metabolic dysregulation, left atrial
enlargement, endothelial dysfunction, systemic inflammation, and hypercoagulability. These mechanisms can lead
to hypertension (both systemic and pulmonary), heart failure, cardiac arrhythmias, renal disease, stroke and
myocardial infarction, and sudden death in sleep.
Hypertension (ACE) inhibitor use may worsen OSA because of the adverse effects of cough and rhinopharyngeal
inflammation, 2 effects that cease with discontinuation of the drug.
Atherosclerosis
Congestive heart failure
OSA has not been established as a cause of heart failure, and whether it hastens death in patients with heart failure
is uncertain. However, a 2007 study examining untreated OSA in patients with heart failure reported that those
with an AHI higher than 15 had d mortality compared with those with an AHI below 15.
Cardiac arrhythmias
Patients with severe SDB have a 2- to 4-fold d risk of experiencing nocturnal complex arrhythmia.
Bradyarrhythmia is more common in OSA patients (occurring in approximately 10% of OSA patients), especially
during REM sleep state and when a greater than 4% drop in oxygen saturation occurs. Additionally,
atrioventricular block and asystole may occur in the absence of conduction disease.

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Premature ventricular contractions (PVCs), A-Fib :common

Myocardial ischemia and infarction
OSA patients have double the prevalence of coronary artery disease (CAD),
Stroke
OSA had a stronger relationship with stroke than with any other cardiovascular disease.
Time-to-event analyses have shown that patients with OSA (who were undergoing weight loss, CPAP treatment, or
surgery) have an d hazard ratio for stroke or death of 1.97. The risk of stroke or death was most severe in the
quartile of patients with the most severe AHI. The hazard ratio d to 3.30 when the AHI was greater than 36. This
study was not powered sufficiently to determine if obstructive sleep apnea treatment affects survival.
Metabolic syndrome
d fasting glucose levels, d blood pressure, lipid abnormalities, and obesity. OSA may contribute to the metabolic
derangements that characterize the metabolic syndrome (see the image below).
http://emedicine.medscape.com/article/295807-overview#a0104
Oral Manifestations of Systemic Diseases
Crohn disease
idiopathic disorder that can involve the entire GIT with transmural inflammation, noncaseating granulomas, and
fissures.
Symptoms :intermittent attacks of diarrhea, constipation, abdominal pain, and fever. Patients may develop
malabsorption and malnutrition. Fissures or fistulas may occur. systemically as arthritis, clubbing of the fingers,
sacroiliitis, and erythema nodosum.
Histology:Acute and chronic inflammation, with lymphocytic and giant cell perivascular infiltrates, and lymphoid
follicles in oral and GI Crohn disease. Noncaseating granulomas
Intraoral involvement in 8-29% may precede intestinal involvement. Oral manifestations can prove crucial in
diagnosis and usually parallel the intestinal disease course. The severity of oral lesions may coincide with the
severity of the systemic disease, and it may be used as a marker for intestinal impairment.
Orofacial symptoms of Crohn disease include (1) diffuse labial, gingival, or mucosal swelling; (2) cobblestoning of
the buccal mucosa and gingiva;
(3) aphthous ulcers; (4) mucosal tags; and (5) angular cheilitis.
Noncaseating granulomas are characteristic of orofacial Crohn disease. Oral granulomas may occur without
characteristic alimentary involvement (orofacial granulomatoses).
The term orofacial granulomatoses encompasses :sarcoidosis, Melkersson-Rosenthal syndrome, and, rarely,
tuberculosis.
Labial swelling is cosmetic complaint, but it can be a painful
Gingival and mucosal involvement may cause difficulty while eating. The pattern of swelling, inflammation,
ulcers, and fissures is similar to that of the lesions occurring in the intestinal tract.
dental caries and nutritional deficiencies may be related to d saliva production and malabsorption in the
intestinal tract.

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Ulcerative colitis
inflammatory condition with some similarities to Crohn disease. but restricted to the colon and is limited to the
mucosa and submucosa, sparing the muscularis. Lesions in the colon consist of areas of hemorrhage and
ulcerations along with abscesses. UC is characterized by periods of exacerbation and remission, and, generally,
oral lesions coincide with exacerbations of the colonic disease. Similar ulcerations may arise on the buttocks,
abdomen, thighs, and face.
Aphthous ulcers or angular stomatitis occurs in as many as 5-10% of patients.
Gastroesophageal reflux
(GERD) is a common condition in the United States. Regurgitation of gastric contents (pH 1-2) reduces the pH of
the oral cavity below 5.5; this acidic pH begins to dissolve enamel. It is most commonly seen on the palatal
surfaces of the maxillary dentition. Erosion of the enamel exposes the underlying dentin, which is a softer, more
yellow, material. The extent of erosion depends on the frequency and the quantity of exposure along with the
duration of disease. Newly exposed dentin is smooth and shiny, while dentin from previous exposures may be
stained. Exposed dentin is often sensitive to temperature changes and, secondary to its lower mineral content,
develops caries much more quickly.
The prevalence of caries is not d in persons with GERD, possibly because the acidic environment interferes with
the formation of the dental biofilm.
Chronic liver disease
impacts many systems ( coagulation pathway )impaired hemostasis can be manifested in the mouth as petechiae or
excessive gingival bleeding with minor trauma.
The only manifestation of advanced liver disease visible in the oral mucosa is jaundice, which is the yellow
pigmentation that results from the deposition of bilirubin in the submucosa. Jaundice manifests at serum levels
greater than 2.5-3 mg/dL or 2-3 times baseline. Because they are thinner, the mucosae on the soft palate and in the
sublingual region are often first to reveal a yellow hue. With time, the yellow changes can be visible at any
mucosal site.
The association between hepatitis C and oral lichen planus is controversial. This association is greater in Europe
and Asia than it is in the United States,
Hematologic Disorders
Anemias
The potential causes for reduction in oxygen-carrying capacity are legion. Fatigue and d resistance to infection
are common systemic symptoms. The nail beds and oral mucosa exhibit pallor. This pallor is a common and easily
recognizable feature of anemia.
Mucosal conditions, such as glossitis, recurrent aphthae, candidal infections, and angular stomatitis. Glossitis may
be the first sign of folate or vitamin B-12 deficiency[15] .
The tongue :reddened, and the smooth atrophic papillae ("bald") appearance.

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Angular stomatitis is commonly caused by a candidal infection, and it has been linked to iron deficiency. If the
anemia persists, resistance to infection may be d.
Langerhans cell histiocytosis (histiocytosis X)
( unknown etiology) abnormal proliferation of histiocytes and eosinophils. Langerhans cell histiocytosis may
manifest with either localized or more systemic involvement.
One form, ( Letterer-Siwe disease, is most common in infants and is characterized by widespread involvement of
the viscera, potentially leading to death. Skin lesions are common and include papules, plaques, vesicles, and
hemorrhagic nodules, all of which may manifest in a pattern similar to that of seborrheic dermatitis.
Oral symptoms: large ulcerations, ecchymoses, gingivitis, periodontitis, and subsequent tooth loss.
2- Hand-Schller-Christian disease, ( childhood disease)
triad of diabetes insipidus, lytic bone lesions, and proptosis.
Oral manifestations include irregular ulcerations of the hard palate, ( primary manifestation of the disease).
Gingival inflammation and ulcerated nodules, difficulty in chewing, and foul-smelling breath also occur.
3- Eosinophilic granuloma (most common form of Histiocytosis affects young adults). Radiolucent bone lesions
occur anywhere (commonly in flat bones, such as the posterior jaw. Radiologic findings demonstrate rapid
progressive alveolar bone loss with dental extrusion, producing the characteristic appearance of "floating teeth."
These lesions result in fractures and displaced teeth.
Oral swellings or ulcerations resulting from mandibular or maxillary bone involvement [17] are common. Oral
ulcerations may develop on the gingiva, palate, and floor of the mouth, along with a necrotizing gingivitis. Oral
lesions may occur without underlying bone destruction. In these rare cases, ulceration of the palate or gingiva may
be the primary oral sign. Solitary oral lesions may be part of a multisystem disease, and oral/periodontal disease
may also be an early sign of disease reactivation.
A biopsy specimen reveals the pale Langerhans cells with bilobed nuclei, which resemble coffee beans. Clusters of
eosinophils also may be present. Biopsy is necessary and should be used for diagnosis because the ulcerations are
nonspecific.
Sjgren syndrome SS
SS is the second most common autoimmune disease(after thyroid), affecting as many as 3% of women aged 50
years or older. The sex predilection is profound: approximately 90% of patients are female. Sjgren syndrome is
characterized by sicca syndrome, keratoconjunctivitis sicca, and xerostomia. A secondary form is associated with
rheumatoid arthritis.
Oral changes :difficulty in swallowing and eating, disturbances in taste and speech, d dental caries, and a
predisposition to infection, all due to a in saliva. These are nonspecific occur in any condition with diminished
saliva.
Saliva can be thick, ropey, and mucinous, or it may be altogether absent. The mucosal changes typical of
xerostomia include dry, red, and wrinkled mucosa.

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Tongue: cobblestone like appearance due to atrophy of the papillae.

Candidiasis is common in persons with Sjgren syndrome. An d incidence of dental caries is common because the
amount of saliva is insufficient to rinse away or dilute dietary sugar and the buffering capacity is greatly reduced.
Histologic examination of minor salivary or lacrimal glands : lymphocytic infiltrates surround the salivary gland
and lacrimal gland ducts. The inflammation and resultant epithelial hyperplasia render the ducts blocked and
useless. This leads to atrophy of the acini, fibrosi s, and hyalinization of the gland. These changes are irreversible,
although certain medications can help to maximize saliva production from the remaining functional glandular
tissue. Taken together, these facts reinforce the philosophy that good oral hygiene and frequent dental visits are
essential in minimize the deleterious effects of compromised salivary flow.
Kawasaki disease
is a vasculitis (+ cutaneous lymph node syndrome.. Children < 5 years : C/P:edema, erythema of the hands and
feet, fever, oral erythema, and rash. The associated temperature must exceed 38.5C (101.3F) for 5 days to meet
diagnostic criteria.
For diagnosis, 4 of the 5 criteria must also be met: (1) peripheral extremity edema, erythema, or desquamation; (2)
polymorphous exanthem; (3) bilateral conjunctival injection; (4) erythema and strawberry tongue in the oral cavity;
and (5) acute cervical adenopathy. Cardiac sequelae to the vasculitis may result in aneurysm and myocardial
infarction. Myocarditis commonly occurs within a week after the fever. Within 2-3 weeks, the previously
edematous palms and soles peel and slough.
Oral findings :swelling of papillae of the tongue (strawberry tongue) and intense erythema of the mucosal surfaces.
Ulceration in the oral cavity is a common presenting sign in a majority of patients. [22] The labia are cracked, cherry
red, swollen, and hemorrhagic. The last of these may be due to the long-standing high-grade fevers.
Wegener granulomatosis
is a necrotizing vasculitis of small-to-medium vessels associated with necrotizing granulomas of the upper and
lower airways and necrotizing glomerulonephritis. In limited Wegener (only involves the respiratory tract). Early
diagnosis of this disease is essential in order to prevent the irreversible glomerular damage that can lead to death.
8 Ss(Sinusitis- Septal perforation-Saddle nose-Sialadentis-Strawberry gingivitis- Subglotic stenosis, SNHL, Serous
Otits media)
Oral involvement is common: ulcerations and gingival enlargement. Ulcer of buccal mucosa or palate, most
common but least specific oral lesions.
Gingival pathognomonic termed "strawberry gingivitis swollen, reddened, and granular appearance. Initially,
bright red-to-purple friable diffuse papules originate on the labial interdental papillae. Involvement may eventually
include the lingual and palatal mucosa.
Tooth and alveolar bone loss are common. Oral may correlate with disease progression, thereby providing
prognostic value.

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Histologically, biopsy findings of the gingivae : necrotizing inflammation of vessels with accompanying
granulomatous inflammation. The pseudoepitheliomatous hyperplasia, microabscess formation, and multinucleate
giant cells found in this condition are seen in few other gingival conditions.
Pathological findings with a positive C-ANCA). The discovery of oral lesions during the physical examination can
direct the appropriate confirmatory tests to ensure prompt treatment and to prevent further damage to the lungs and
kidneys.
Sarcoidosis
idiopathic systemic disease characterized by bilateral hilar lymphadenopathy and noncaseating granulomas in the
lungs. Ocular and cutaneous manifestations are common.
Sarcoidosis may involve nearly any organ system; organs involved include the liver, heart, spleen, eyes, kidneys,
and lymph system. Pulmonary manifestations are the most common and include dyspnea with exertion,
nonproductive cough, chest pain, wheezing and nasal congestion, and hemoptysis.
Sarcoidosis may manifest cutaneously in 5-20% of patients and is more common in African Americans. Examples
of skin manifestations include alopecia, erythroderma, subcutaneous nodules, erythema nodosum, macules, papules
and plaques, and lupus pernio. Papules are small with a waxy consistency, and they may appear on the trunk and
around the nose and eyes. Lupus pernio is characterized by indurated purplish nodules that occur on the face of
women with chronic sarcoidosis.[28] Systemic annular plaques with pale centers and violaceous edges may also
appear on the extremities, back, buttocks, and face.
Oral manifestations : multiple, nodular, painless ulcerations of the gingiva, buccal mucosa, labial mucosae, and
palate.
Indistinct ulcerations or swellings do not aid in diagnosing sarcoidosis, but biopsy reveals noncaseating
granulomas surrounded by multinucleate giant cells along with lymphocytic infiltrate.
Salivary gland involvement (less common ) tumor like swellings.
Heerfordt syndrome : parotid gland swelling, xerostomia, uveitis, and facial nerve palsy. Rarely, sarcoidosis may
involve the tongue:swelling, enlargement, and ulcerations. in rare cases may be the presenting sign of the disease.
Oral involvement in sarcoidosis usually manifests after systemic symptoms develop. This form is commonly a
diagnosis of exclusion.
Biopsy samples are used to identify noncaseating granulomas, a nonspecific finding. Other granulomatous diseases
must be excluded, such as Wegener granulomatosis, Crohn disease, syphilis, or tuberculosis. [28, 30] Treatment with
systemic corticosteroids may be useful, but symptoms may resolve spontaneously or progress despite treatment.
Multiple organ and progressive pulmonary involvement indicate a poor prognosis. The overall mortality rate is
approximately 5%.[28]
Amyloidosis
deposition of amyloid proteins in body tissues leading to tissue damage. macroglossia, Submandibular swelling
occurs subsequent to tongue enlargement and can lead to respiratory obstruction. Rarlely, oral ulceration may
present .

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Drug-Induced Conditions
Aphthous stomatitis canker sores
Drugs are MCC of recurrent aphthous lesions, Common culprits : (NSAIDs), nicorandil, and ACE inhibitors, but
any drug can potentially produce an aphthous like reaction.
These ulcerations are round, crateriform, yellowish depressions surrounded by an area of erythema. The size varies
from 1-3 mm (minor, in 80%) to larger than 1 cm (aphthous major, in 15% of cases). Patients may have outbreaks
of multiple ulcerations at one time. These are usually quite painful but typically are self-limiting and resolve in 710 days for aphthous minor and 14-21 days for aphthous major lesions.
Dry mouth /xerostomia /hyposalivation
Is common adverse effect of many medications. The reasons for this vary from medication to medication but can
range from dehydration (eg, with diuretics) to anticholinergic activity (eg, with some antidepressants).
Consequences: altered taste, increased risk of fungal infection, d caries risk, and d prevalence of traumatic
ulceration due to lack of lubrication. Patients with severely impaired salivary flow also have difficulty with eating,
swallowing, and speech. The former can result in d food intake and poor nutrition.
Numerous management options are available for d salivation, which are beyond the scope of this chapter. These
range from the simple, such as d hydration, to the complex, such as systemic procholinergic agents to salivary
production.
Lichen planus[39]
Many medications can produce mucosal reactions that are indistinguishable both clinically and microscopically
from lichen planus. Although this is often the classic reticular form, it may also appear ulcerative or erosive.
Biopsy is warranted to verify diagnosis. The association with medication is made primarily by history and
temporal association between the lesions and starting the offending medication. In rare circumstances, the lichen
planus can become extensive or painful enough to warrant changing the culprit medication.
Common drugs that cause lichenoid reactions include ACE inhibitors, beta-blockers, NSAIDs, diuretics,
hydroxychloroquine, and others such as zidovudine.[40]
Inhaled steroids candidiasis
Gingival enlargement (hyperplasia) [42]
50% of patients taking phenytoin. 38% of patients taking nifedipine,
13-85% of patients taking cyclosporine.
HIV Disease
Candidiasis Erythematous candidiasis . Herpes simplex[53] intravenous foscarnet.
Hairy leukoplakia[54, 55] Kaposi sarcoma[56]

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Cytomegalovirus
(,60% of people being seropositive ,cause of subacute encephalitis, resulting in headaches and personality changes
in patients with AIDS. ganciclovir or cidofovir.
Human papillomavirus
Aphthous like ulcerations
Aphthous lesions manifest as yellowish-gray areas of ulceration ranging in size from a few millimeters to larger
than a centimeter. The ulcerations are surrounded with a halo of erythema and are usually very painful. Major
aphthae are larger than 1 cm in diameter and heal in 14-21 days. Major aphthae differ from the other forms of the
condition in that they can heal with scarring.
Aphthouslike ulcerations can be treated with a wide array of immune-modulating agents that can be delivered via
topical, intralesional, or systemic means. Practitioners should be careful with topical immunosuppressants in this
patient population because of the risk of candidal overgrowth that can accompany these agents. Patients who
cannot tolerate the adverse effects or additional immunocompromise from the immunosuppressive agents can
sometimes be treated with thalidomide. [59]
Because so many conditions in HIV-affected individuals can manifest with ulceration of the oral cavity and
because the presentations are often atypical, biopsy is indicated for definitive diagnosis of all HIV-related
ulcerations.
Cutaneous Diseases
http://emedicine.medscape.com/article/1081029-overview#showall
Congenital Epulis= Neumanns tumor
Epulis is a Greek = Gums., denote variety of gum lesions regardless of their pathology.
rare congenital growth affecting the gingival mucosa of neonates.
It is also known as Neumanns tumor. It is truly a benign condition affecting
predominantly female infants. It may even be multiple. This tumor was first
described in 1871 by Neumann and hence the name.present at birth arising from the gingival mucosa
of maxilla / mandible. C/P: feeding and breathing
difficulties because of the mass effect. Ultrasound studies have shown that this
tumor can arise as early as 26th week of gestation.
Clinical features:
1.Affects commonly female neonates.
2.Commonly arises over the incision canine region of maxilla
3.It can also involve the gingiva over the mandible. Involvement of
gingiva of maxilla / mandible is 3:1.
4.These lesions when large can interfere in breathing and feeding of the
neonate
Histology: congenital Epulis resembles granular cell tumors. differentiating features from
granular cell tumors include:
1.Plexiform arrangement of capillaries

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2.Lack of pesudoepitheliomatous hyperplasia

3.Immunohistochemistry shows no reactivity to S-100 protein and laminin.
It should also be borne in mind that granular cell tumors involve almost all age
groups and they rarely affect gingiva. Granular cell tumors arise from Schwann
cells and hence positive for S-100 protein.
Theories of origin of congenital Epulis:
1.Myoblastic theory
2.Neurogenic theory
3.Odontogenic theory
4.Fibroblastic theory
5.Histiocytic theory
6.Lake theory Is the most accepted theory. He attributed development
of Epulis in neonates to reactive hyperplasia due to oestrogen changes. This
explains the female preponderance of the lesion.
Management:If the lesion is small and asymptomatic it can be left alone. Spontaneous
regression has been documented. If the mass is large and symptomatic surgical
excision can be resorted to. After resection it is not known to recur.
Eosinophlic oesophagitis
relatively new disease entity. chronic / intermittent dysphagia, reflux like symptoms and intermittent oesophageal
food impaction. no evidence of anatomic obstruction. + eosinophilic infiltrates in the oesophagus. Attwood hence
applied the criteria :> 20 eosinophils / HPF =histological criteria for diagnosing.
Male : female ratio is 3:1. Age of presentation may vary between 2 nd 4th decades.
Conditions associated with oesophageal eosinophilia:6
1. Eosinophlic oesophagitis
2. GERD
3. Collagen vascular disorders
4. Parasitic infections
5. Eosinophlic gastroenteritis
Oesophageal dilatation is reserve for patients with extreme dysphagia
Anatomy of neck spaces
These spaces are present in the neck between the layers of cervical fascia. These spaces are important from the
point of view of clinician because of the propensity of infections to involve this space and to spread along these
spaces to involve other areas like the mediastinum. Many of these spaces could as well be inconsequential.
There are two types of fascial spaces in the neck.

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I.
II.

Those associated with muscles

Those associated with viscera and vessels

Fascial spaces associated with muscles are limited by the insertion of muscles to bones. These muscular insertions
serve as a limiting factor to spread of infections from these spaces. Spaces associated with viscera and blood
vessels are not limited by insertion of muscles and hence infections cross and travel long distances if these spaces
are involved.
Visceral spaces:
Lateral pharyngeal space: (Para pharyngeal space)
This space is situated lateral to the fascia covering the constrictor muscles of the pharynx (buccopharyngeal fascia).
Lateral to this space lie the pterygoid muscle, mandible and carotid sheath.
Superiorly it extends up to the skull base while inferiorly it ends at the level of hyoid bone because of the
attachment of the submandibular gland sheath to the sheaths of the stylohyoid muscle and the posterior belly of
digastric muscle.
The carotid sheath lies close to the posterolateral wall of this space.
Postero medially this space communicates with the retropharyngeal space.
Anteriorly and inferiorly this space communicates with the spaces associated with the floor of the mouth.
This space is most commonly involved in neck space infections. Infections from this space can easily spread to the
carotid and retropharyngeal spaces.
Common routes of infections of parapharyngeal space:
1. Lingual infections
2. Submandibular gland infections
3. Infections involving the parotid space
4. Spread from peritonsillar abscess

Figure showing parapharyngeal space

Diagram showing carotid space

Submandibular space:
This is actually a combination of two spaces partially separated by the mylohyoid muscle. The space below the
mylohyoid muscle is known as the submaxillary space while the space above the muscle is known as sublingual
space.
Boundaries:
Superior Oral mucosa and tongue
Medial oral mucosa and tongue
Lateral Superficial layer of deep cervical fascia with its tight attachment to the mandible and hyoid bone laterally

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Inferior Hyoid bone

The mylohyoid cleft separates the submaxillary from sublingual space. Structures passing through mylohyoid cleft
include:
1. Whartons duct
2. Lingual nerve
3. Hypoglossal nerve
4. Branch of facial artery
5. Lymphatics
There is free communication across midline between these spaces. Ludwigs angina is the characteristic example
of infections of this space.

Masticator space:
This space is formed by the splitting of the superficial layer of deep cervical fascia as it encloses the mandible and
the primary muscles of mastication.
Contents of this space include:
1. Masseter muscle
2. Medial & lateral pterygoid muscles
3. Ramus & posterior portion of the body of mandible
4. Insertion of the temporalis muscle
Supero medially this space communicates with the temporal space medial to the zygomatic arch. Infections
involving this space involve the temporal space also. The most common cause of infection within this space is
from abscessed third molar tooth.

Figure showing masticator space

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Retropharyngeal space:
This space lies between the deep layer of the deep cervical fascia (prevertebral fascia) and the buccopharyngeal
fascia superiorly and the fascia covering the oesophagus inferiorly. An ancillary portion of deep cervical fascia
referred to as the alar layer extends from the base of skull to approximately the second thoracic vertebra at which
point it fuses with that of the fascial covering of the oesophagus. The prevertebral fascia lies over the vertebra and
the paraspinal muscles running from the base of the skull to the diaphragm. Thus there are two potential spaces in
the retropharyngeal space. The first one lies between the fascia covering the pharynx and oesophagus and the alar
layer of deep cervical fascia. This space is commonly referred to as the retropharyngeal / retrovisceral space. This
space ends at the level of T2 vertebra. Lying posterior to the alar fascia but anterior to the prevertebral fascia is the
danger space known as the prevertebral or Grodinsky space. This space allows wider spread of infections into the
mediastinum. This space is commonly involved by rupture of retropharyngeal space abscesses.

Figure showing retropharyngeal space

Parotid space:
This space lies between the superficial and deep capsules of parotid gland. This is actually formed by splitting of
the superficial layer of deep cervical fascia. The superficial capsule is very thick and strong and is closely adherent
to the underlying parotid gland. Multiple septa could be seen running from the superficial capsule into the gland
forming numerous intraglandular compartments. Infections of parotid gland cannot pierce the tough lateral
capsule, instead they present medially with easy access to the lateral pharyngeal space. From the lateral
pharyngeal space infections may progress to the retropharyngeal space. This is one of the most feared
complication of parotid space infections.
Types of sulcus vocalis
Sulcus vocalis can be classified into 3 types as described by Ford etal.
Type I: = physiologic sulcus. subtle depressions along the vocal fold medial edge. It is defined
as a longitudinal depression that extends within the superficial lamina propria without actually involving the vocal
ligament perse.
It also demonstrates no histopathological abnormalities.
Video stroboscopy shows mild abnormality in the mucosal wave.

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Type II: Vergeture - is defined as more extensive longitudinal invagination that extends into the vocal ligament
involving loss of superficial lamina propria.
Video stroboscopy shows moderate changes in the mucosal wave pattern.

Figure showing Type II sulcus

Type III: Classic sulcus vocalis. focal pit that extends beyond the vocal ligament into the thyroarytenoid muscle.
This type is characterized by tissue loss in the lamina propria.Video stroboscopy shows gross changes in the
mucosal wave pattern.

Sialosis
is uncommon non neoplastic and non inflammatory disorder causing bilateral non painful enlargement of the major
salivary glands.
Age of occurrence: : middle age. Its peak incidence occurs during the 5th and 6th decades.
Females tend to predominate.
Among the major salivary glands the parotid gland undergoes the maximum enlargement. The enlargement
develops
rather slowly with some in the salivary flow.

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Etiology:
Precise etiology not known. The underlying pathogenesis points towards a neuropathy.
Sialosis is commonly associated with:
1. Diabetes mellitus2. Hypothyroidism,3. Malnutrition, cirrhosis, Menopause
7. Anti hypertensive medications
Histopathology:
It is characterized by acinar cell hypertrophy, atrophy of striated ducts associated with oedema of CT
In end stage disease there is widespread replacement of acini with fatty tissue.
Management: difficult. Should always be directed at the underlying systemic disorder.
In patients with huge enlargement of parotid salivary glands, surgical reduction could be a possibility.
Use of pilocarpine has shown varying results.
Lines of Dolan and the elephants of Rogers
What are the lines of Dolan?
They are three anatomic contours best seen on the Waters view (occipitomental view )of the face, and they
were first popularized by Dolan et al.
As you can see, the 3 lines of Dolan lead the eye along some facially important structures.
Lee Rogers pointed out that the 2nd and 3rd lines together form the profile of an elephant.

1. Bezold's triad
1. Diminished perception of the deeper tones,
2. retarded bone conduction, and

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2.
3.
4.
5.

3. negative Rinne's test,

pointing, in the absence of objective signs, to otosclerosis
Bezold's abscess
abscess deep in the neck parapharyngeal space( with suppur in the mastoid cells
Bezold's sign / symptom
Inflammatory edema at the tip of the mastoid process in mastoiditis
Bezold's ganglion
An aggregation of nerve cells in the interatrial septum
Bezold's mastoiditis
Mastoiditis with perforation medially into the digastric groove and forming a deep neck abscess

fordyce spots:normal sebaceous glands that appear as small yellowish spots in the buccal mucosa or on the lips
torus palatinus:midline bony growth in the hard palate that is fairly common in adults; harmless
tori mandibulares:rounded bony growths on the inner surfaces of the mandible; typically bilateral, asymptomatic,
and harmless
acute necrotizing ulcerative gingivitis
uncommon form of gingivitis that is accompanied by fever, malaise, and enlarged lymph nodes; process spreads
along gym margins, where gray membrane develops; occurs suddenly in adolescents and young adults
gingival hyperplasia
gums enlarge due to dilantin therapy, puberty, pregnancy, and leukemia
pregnancy tumor:ginvgival enlargement , localized and forms a tumor-like mass , red, soft, bleeds easily; usually
originates in an interdental papilla
attrition: yellow-brown dentin of the teeth is exposed; usually in older people
hairy tongue: can either follow antibiotic therapy or occurs spontaneously
floor of the mouth: is a common location for carcinoma of the mouth?
Benign and Malignant Parotid Tumor
The most common benign tumor in children is the hemangioma. Of the benign epithelial tumors, the mixed tumor
(pleomorphic adenoma) is the most common.
Anatomy: parotid gland is the largest of the major salivary glands. The glands are roughly pyramidal in shape,
with the main body overlying the masseter muscle.
The glands extend to the zygomatic process and mastoid tip of the temporal bone and curve around the angle of the
mandible to extend to the retromandibular and parapharyngeal spaces. The parotid duct exits the gland medially,
crosses the superficial border of the masseter, pierces the buccinator, and enters the oral cavity through the buccal
mucosa opposite the second maxillary molar.
The gland is divided into a superficial and deep portion by the facial nerve, which passes through the gland. While
not truly anatomically discrete, these "lobes" are important surgically, as neoplasms involving the deep lobe require
sometimes significant manipulation of the facial nerve to allow excision. The superficial lobe is the larger of the
two and thereby the location of the majority of parotid tumors.
Numerous lymph nodes also are present within the parotid gland itself, subsequently draining to preauricular, infraauricular, and deep upper jugular nodes.
Parotid neoplasms account for 80% of salivary neoplasms. Of parotid masses, 75% are neoplastic; the remaining
25% are nonneoplastic cysts and inflammation.

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Of parotid neoplasms, 70-80% are benign. Except for Warthin tumors, benign tumors of the parotid gland are more
likely to occur in women than in men. The median age fifth decade of life. Parotid tumors occur most commonly in
Caucasians. The etiology of these tumors is unknown, but the possibility of an adenoma gene.
The most common benign parotid tumor in children is the mixed tumor.
Clinical Picture:
The major goal in the evaluation is to determine or exclude the malignancy.
History distinguishing inflammatory from neoplastic masses.
Characteristics of inflammatory ( sudden onset, pain, and systemic infection. The most common presentation is
that of an asymptomatic mass (81%) noted incidentally while washing or shaving the face. [1] Pain (12%) or facial
nerve paralysis (7%) is less frequent. Facial nerve paralysis is more commonly due to malignancy in the presence
of a parotid mass, but most facial nerve paralysis is due to Bell palsy.
Parotid masses occur most commonly in the lower pole, or tail, and in the superficial lobe.
Physical examination : mobile non-tender mass , firm and solitary. Evaluate the possibility of a deep tumor by
intraoral examination, with attention directed to the tonsillar fossa and soft palate. Inspect the Stensen duct :
salivary flow (clarity, consistency, purulence) and notation of redness, bulging, and irritation of the ductal orifice as
part of the physical examination. Evaluate the skin, oral cavity, oropharynx, and neck for possible primary lesions
or nodal disease.
Diagnosis:
Radiologic studies are involved minimally in the workup of an asymptomatic mass.

Plain radiography : exclude calculi.

Sialography is rarely used. : delineate disorders of ductal function or anatomy.
CT scan is almost 100% sensitive in detecting a salivary gland mass, but it cannot help the clinician
differentiate between a benign and a malignant mass. It is most helpful in specifying the size and anatomic
extent of a tumor.
MRI is superior in demonstrating benign tumors of the parotid gland because of its greater contrast than
CT scan.
Positron emission tomography (PET) : assessing malignant tumors, with attention to metastatic adenopathy
and distant metastases.

Biopsy
FNA(Fine-needle aspiration :valuable Its accuracy >96%, sensitivity and specific for benign tumors(85%) and
malignant tumors ( 50-90%,). Frozen sections are 93% accurate when performed at surgery, but their use is
controversial, since diagnosis depends on the experience of the pathologist with regard to salivary gland tumors.
The standard biopsy approach is a superficial parotidectomy For 80-90% of parotid neoplasms, this procedure is
both diagnostic and therapeutic. For this reason, preoperative fine-needle aspiration biopsy is recommended, since
it can change the clinical approach in up to 35% of patients. [2] Lymph nodes can be enucleated, as can Warthin
tumors, and sialadenitis does not require surgical intervention.

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Table 1. Classification of Benign Primary Epithelial Salivary Gland Tumors

1. Mixed tumor (pleomorphic adenoma)
2. Warthin tumor (papillary cystadenoma lymphomatosum) Male, bilat
3. Oncocytoma( multiple)
4. Monomorphic tumors
5. Sebaceous tumors
6. Benign lymphoepithelial lesion
7. Papillary ductal adenoma (papilloma)
8. Unclassified
Benign pleomorphic adenoma or benign mixed tumor
Most common parotid neoplasm (80%)[4]
Proliferation of epithelial and myoepithelial cells of the ducts and an in stromal components
Slow growing, lobular, and not well encapsulated
Recurrence rate of 1-5% with appropriate excision (parotidectomy)
Recurrence possibly secondary to capsular disruption during surgery
Malignant degeneration occurring in 2-10% of adenomas observed for long periods, with adenocarcinoma
Warthin tumor (papillary cystadenoma lymphomatosum or adenolymphoma)
Second most common benign parotid tumor (5%)
Most common bilateral benign neoplasm of the parotid
Marked male as compared to female predominance
Occurs later in life (sixth and seventh decades)
Presents as a lymphocytic infiltrate and cystic epithelial proliferation
May represent heterotopic salivary gland epithelial tissue trapped within intraparotid lymph nodes
Incidence of bilaterality and multicentricity of 10%
Malignant transformation rare (almost unheard of)
Oncocytoma
Accounts for 1% of salivary gland tumors
Composed of large oxyphilic cells (oncocytes)
May be multiple
Monomorphic tumors
Rare, usually epithelial in origin
Treatment & Management
Superficial parotidectomy is the treatment of choice for most benign tumors in the superficial lobe. Make every
effort to preserve the facial nerve. In order to preserve the facial nerve, it is important to try to determine the
proximity of the nerve to the capsule of the tumor prior to surgery. Results of a retrospective review showed that
malignant tumors were likely to have a positive facial nerve margin. [5]
Avoid enucleation (except for Warthin tumors and lymph nodes), since it greatly s the likelihood of recurrence (up
to 80%) and nerve damage. Deep lobe tumors demand total parotidectomy with preservation of the facial nerve.
For recurrences, postoperative radiotherapy may be administered, with local control rates exceeding 95%.
Surgical incision

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Parotidectomy incision should allow for adequate exposure and the most aesthetic result. The incision begins
anterior to the superior root of the helix and descends anterior to the tragus. It then is directed behind the lobule of
the pinna and can be carried down anteriorly onto the neck as dictated by the need for exposure.
If a large soft tissue defect is created by the excision of the parotid tumor, numerous autologous or allograft tissues
(ie, dermal grafts, fascial grafts, fat grafts, AlloDerm) or synthetic substances may be used for filling these defects.
Try to preserve a layer of tissue (the parotid fascia or SMAS layer) if it does not compromise the capsule of the
tumor. This preservation is important so that a layer of tissue interposes between the cut salivary tissue and the
skin. This has been shown to reduce the incidence of Frey syndrome (gustatory sweating).
Complications
Most serious complications : facial nerve paralysis (temporary or permanent). Injury to the greater auricular nerve
results in hyposthesia of the ear. A slight loss of fullness and an d prominence of the angle of the mandible may
occur after superficial parotidectomy. Uncommon sequelae include salivary fistula, seroma, hematoma, and
infection.
Frey (auriculotemporal) syndrome results from aberrant regeneration of auriculotemporal nerve fibers to sweat
glands in the skin. The result is sweating during mastication. Its incidence may be d by interposing a layer of
tissue (either preserving the SMAS layer and replacing it on the surface of the parotid gland before closing the
incision or placing a layer of allograft in a similar position).
http://emedicine.medscape.com/article/1289560-overview#showall
Malignant Parotid tumor
The parotid glands are the largest salivary glands in humans and are frequently involved in disease processes.
Approximately 25% of parotid masses are nonneoplastic; the remaining 75% are neoplastic.
Non-neoplastic causes of parotid enlargement include cysts, parotitis, lymphoepithelial lesions associated with
AIDS, collagen vascular diseases, and benign hypertrophy. Benign hypertrophy is encountered in patients with
bulimia, sarcoidosis, sialosis, actinomycosis infections, and mycobacterial infections. The vast majority
(approximately 80%) of parotid neoplasms are benign.
Clinical Picture:
History of prior cutaneous lesion or parotid lesion excision. Slow-growing masses tend to be benign. A history of
prior SQ cell carcinoma, or malignant melanoma, = metastasis or metastasis to parotid lymph nodes. Prior parotid
tumor most likely indicates a recurrence because of inadequate initial resection. painless, asymptomatic mass;
>80% of patients.
Pain (20%) indicates perineural invasion, and malignancy.
7-20% present with facial paralysis, ( poor prognosis, have nodal metastasis 80% at the time of diagnosis. These
patients have an average survival of 2.7 years and a 10-year survival of 14-26%.
Trismus often indicates advanced disease with extension into the masticatory muscles or, less commonly, invasion
of the temporomandibular joint. Dysphagia or a sensation of a foreign body in the oropharynx indicates a tumor of
the deep lobe of the gland. A report of ear pain may indicate extension of the tumor into the auditory canal. The

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presence of numbness in the distribution of the second or third divisions of the trigeminal nerve often indicates
neural invasion.
Head and neck exam: cutaneous lesions, which may the primary tumor.

Palpation : benign tumors are firm, but a rock-hard mass denotes malignancy.
Skin fixation, skin ulceration, : indicates malignancy. The EAC must be visualized for tumor extension.
All regional nodes must be carefully palpated to detect nodal metastasis.
Oral Exam: evidence of metastasis or malignant nature of the lesion.
Blood or pus from the Stenson duct is a sign of malignancy , bulging of the lateral pharyngeal wall or soft
palate, indicating tumor in the deep lobe of the gland.
Bimanual palpation:one finger against lateral pharyngeal wall and the other against external neck may
confirm extent into the tonsillar fossa and soft palate.

Fine needle aspiration(FNA)

FNA of the mass or an enlarged LN: Most surgeons recommend excision of a parotid mass whether it is
benign or malignant unless a patient's comorbidity precludes safe surgery. So, many surgeons do not
routinely perform cytology before surgery.
The sensitivity > 95%. but; negative results indicate the need for further attempts or repeat fine needle
aspiration. The results of FNA provide a diagnosis and assist in preoperative planning and patient
counseling. It may not distinguish benign from malignant epithelial lesions because malignancy of parotid
epithelial cells is related to the behavior of the tumor cells in relation to tissue planes and surrounding
structures rather than cellular architecture, which may be rather normal even in malignancy. Therefore,
nonepithelial lesions may be diagnosed with accuracy, but epithelial lesions may require further
investigation.
If FNA is unsuccessful, an incisional biopsy should not be performed. This ( high rate of local recurrence
and places the facial nerve at risk).
large core needle biopsies, ( less popular ,potential facial nerve injury and the possibility of seeding the
needle tract with tumor cells.
When all attempts at obtaining a histologic diagnosis have failed, operative exploration should proceed
after appropriate imaging studies have been obtained.
Intraoperatively, a frozen section of the specimen should be submitted for diagnosis. The use of frozen
sections has demonstrated greater than 93% accuracy in the diagnosis of parotid malignancy.
Imaging studies
Sialography : historic.
Sonography : Benign lesions are of lower density and have smaller caliber blood vessels. Cystic
component is misleading, ( cystic degeneration may occur as a result of necrosis at the avascular center of
a malignancy).
CT scan and MRI: CT provides better detail of the surrounding tissues, whereas MRI demonstrates the
mass in greater contrast than a CT scan.
Both identify regional lymph node involvement or extension of the tumor into the deep lobe or
parapharyngeal space. CT scan criteria for lymph node metastasis include any lymph node larger than 11.5 cm in greatest diameter, multiple enlarged nodes, and nodes displaying central necrosis.
Lymph nodes harboring metastasis also may appear round rather than the normal kidney bean shape, and
evidence of extracapsular extension may be identified.
Mucoepidermoid carcinoma:
most common malignant tumor of the parotid gland, ( 30% of parotid Malig)

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Three cell types are found: mucous, intermediate, and epidermoid cells.
High-grade behave like SCC carcinoma; 5-year survival of only 5%.
low-grade tumors ( behave similar to a benign. nodal5-year survival is 75-95%
Limited local invasiveness and low metastatic, If metastaticregional
Overall 10-year survival is 50%.
DD: chronic sialoadenitis, necrotizing sialometaplasia, and other carcinomas.
An association between mucoepidermoid carcinoma and myasthenia gravis.

Adenoid cystic carcinoma

unpredictable behavior and propensity to spread along nerves. It has highly invasive quality but may
remain quiescent for a long time may present for >10 years with little change and suddenly infiltrate the
adjacent tissues extensively.
The tumor has an affinity for perineural with skip lesions along involved nerves. Clear margins do not
necessarily mean that the tumor has been eradicated.
Metastasis is more common to distant sites than to regional nodes; lung metastases are most frequent.
incidence of distant metastasis, ( 30-50% ).
Three histologic types have been identified: cribrose, tubular, and solid. The solid form has the worst
prognosis; the cribrose pattern possesses the most benign behavior and best prognosis. This tumor requires
aggressive initial resection. Overall 5-year survival is 35%, and 10-year survival is approximately 20%.
Malignant mixed tumors(ex pleomorphic adenoma).
arise within a preexisting benign pleomorphic adenoma
These tumors also may develop de novo (carcinosarcoma). The longer pleomorphic adenoma has been
present, the greater the chance of carcinomatous degeneration.
Carcinosarcomas, true malignant mixed tumors, are rare. Overall 5-year survival is 56%, and 10-year
survival is 31%.
Acinic cell carcinoma
Acinic cell carcinoma is an intermediate-grade malignancy with low malignant potential. This tumor may
be bilateral or multicentric and is usually solid, rarely cystic.
Although this tumor rarely metastasizes, occasional late distant metastases have been observed. This tumor
also may spread along perineural planes. Overall 5-year survival is 82%, and 10-year survival is 68%.
Adenocarcinoma
Adenocarcinoma of the parotid develops from the secretory element of the gland. This is an aggressive
lesion with potential for both local lymphatic and distant metastases.
Approximately 33% of patients have nodal or distant metastasis present at the time of initial diagnosis.
Overall 5-year survival is 19-75%, as it is highly variable and related to grade and stage at presentation.
Primary squamous cell carcinoma
Primary squamous cell carcinoma of the parotid is rare, and metastasis from other sites must be excluded.
Overall 5-year survival is 21-55%, and 10-year survival is 10-15%.
Sebaceous carcinoma
Sebaceous carcinoma is a rare parotid malignancy that often presents as a painful mass.
It commonly involves the overlying skin.
Salivary duct carcinoma
Salivary duct carcinoma is a rare and highly aggressive tumor.

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Small cell carcinoma exists as 2 types. The ductal cell origin type is mostly benign and rarely metastasizes.
The neuroendocrine origin type is often aggressive and has higher metastatic potential.

Lymphoma
most commonly in elderly males. in 5-10% of patients with Warthin tumor .
The entire parotid is enlarged with a rubbery on palpation.
Often, regional nodes also are enlarged.
Biopsy of enlarged regional nodes avoids unnecessary parotid surgery,
definitive treatment consists of chemotherapy or radiation therapy.
Malignant fibrohistiocytoma
very rare. slow growing and painless mass.
FNA and imaging could confuse them with other kinds of parotid tumors; therefore, diagnosis :
immunohistochemical analysis of the resected tumor.
The tumor should be completely resected. [13]
Parotid metastasis from other sites
The parotid also may be the site of metastasis from cutaneous, renal, lung, breast, prostate, or GI tract
malignancies.
Operative Management
complete surgical resection followed, when indicated, by radiation therapy. [14] Conservative excisions are plagued
by a high rate of local recurrence. The extent of resection is based on tumor histology, tumor size and location,
invasion of local structures, and the status of regional nodal basins.
Most tumors of the parotid (90%) originate in the superficial lobe. Superficial parotid lobectomy is the minimum
operation performed in this situation. This procedure is appropriate for malignancies confined to the superficial
lobe, those that are low grade, those less than 4 cm in greatest diameter, tumors without local invasion, and those
without evidence of regional node involvement.
Surgical resection procedure
The most important initial step is identification of the facial nerve and its course through the substance of the
parotid gland. determine the proximity of the nerve to the capsule of the tumor prior to surgery. Results of a
retrospective review showed that malignant tumors were likely to have a positive facial nerve margin. [15] many
surgeons use a nerve stimulator. Increasingly, surgeons are using intraoperative continuous facial nerve monitoring
any time a parotidectomy is performed..

Ideally, the dissection of the facial nerve without disturbing or violating the tumor. The facial nerve may be
found exiting the stylomastoid foramen by reflecting the parotid gland anteriorly and the
sternocleidomastoid muscle posteriorly. Landmarks include the digastric ridge and the tympanomastoid
suture.
The cartilaginous EAC lies approximately 5 mm superior to the facial nerve in this region. The facial nerve
is also anterior to the posterior belly of the digastric muscle and external to the styloid process.
Identify a distal branch of the nerve and to dissect retrograde toward the trunk., the buccal branch may be
found just superior to the parotid duct, or the marginal mandibular branch may be found crossing over
(superficial to) the facial vessels. These may then be traced back to the origins of the main facial nerve
trunks.

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A final way to drill the mastoid and to locate the nerve within the temporal bone. followed through the
stylomastoid foramen antegrade towards the parotid.
Once these have been identified, superficial lobe may be removed en bloc.
If intraoperative pathologic exam reveals : high-grade or >4 cm, or lymph node metastasis is identified
within the specimen, a complete total parotidectomy should be performed.
If the facial nerve or its branches are adherent to or involved by the tumor, they must be sacrificed.
However, a pathologic diagnosis of malignancy must be confirmed intraoperatively prior to sacrificing
facial nerve branches.
All involved structures resected in continuity with tumor. skin, masseter, mandible, temporalis, zygomatic
arch, or temporal bone.
Tumors of the deep lobe are treated by total parotidectomy. Identification of the facial nerves and branches
is the first and most crucial step.
Total parotidectomy is then performed en bloc, and the fate of the facial nerve and surrounding local
structures must be decided similar to superficial lobe tumors. The specimen should be sent to the pathology
for immediate examination.
Neck dissection should be performed when malignancy is detected in the lymph nodes pre- or
intraoperatively.
Other indications for functional neck dissection include tumors >4 cm, high-grade, or invaded local
structures, recurrent tumors when no neck dissection was performed initially, and deep lobe tumors.

Reconstruction
Great auricular nerve graft, or hypoglossal nerve. (anastomosis end-to-side to avoid interfering with
normal hypoglossal nerve function.
If facial nerve recovery is not achieved, certain measures are taken to improve function.

Following parotidectomy, : gustatory sweating or Frey syndrome. an aberrant connection of regenerating

parasympathetic salivary fibers to the sweat glands in the overlying skin flap. Treatment : irradiation,
atropinelike creams, division of the auriculotemporal nerve (sensory), division of the glossopharyngeal
nerve (parasympathetic), insertion of synthetic materials (AlloDerm), fascial grafts, or vascularized tissue
flaps between the parotid bed and overlying skin flap. Intracutaneous injections of botulinum toxin A is
also an attractive option.

Adjunctive Therapy
Because of the many histologic subtypes of parotid malignancies, a general statement regarding the usefulness of
adjunctive therapy cannot be made.
If resectable, surgery is the primary modality of treatment for most malignant tumors of the parotid gland. General
indications for postsurgical radiation therapy include tumors >4 cm in greatest diameter, tumors of high grade,
tumor invasion of local structures, lymphatic invasion, neural invasion, vascular invasion, tumor present very close
to a nerve that was spared, tumors originating in or extending to the deep lobe, recurrent tumors following reresection, positive margins on final pathology, and regional lymph node involvement. Postoperative radiation is,
thus, usually indicated for all parotid malignancies with the exception of small low-grade tumors with no evidence
of local invasion or nodal/distant spread. Radiation therapy is considered the cornerstone of adjunctive therapy.
No chemotherapy has been proven effective as single modality therapy. For certain histologic subtypes, some
clinicians recommend combined chemotherapy and radiation. Presently, immunotherapy is in the clinical trial
phase.

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epidermal growth factor receptor (EGFR) is expressed strongly in the cell membranes of parotid
mucoepidermoid carcinomas and of the lymph node metastases. EGFR-targeting agents have
potential to be used for therapy.
Prognosis
The major determinants of survival :high grade, neural involvement, locally advanced disease,
advanced age, associated pain, regional lymph node metastases, distant metastasis, and
accumulation of p53 or c-erbB2 oncoproteins.
20% of all patients will develop distant metastases. [23] The presence of distant metastases heralds a poor prognosis,
with a median survival of 4.3-7.3 months.
Overall 5-year survival for all stages and histologic types is approximately 62%. The overall 5-year survival for
recurrent disease is approximately 37%. Because of the risk of recurrence, all patients who have had a
histologically proven malignant salivary gland tumor should have lifelong follow-up.
http://emedicine.medscape.com/article/1289616-overview#showall
Audiology Highlights and notes for ENT master candidates
staggered spondaic word test:test of central auditory pathway integrity in which spondaic words are presented
dichotically.
SSW correlates most with measures of cognitive ability, expressive language, and those relating to
auditory memory. As children with attention-deficit hyperactivity disorder (ADHD) have been found to
demonstrate impaired performance on the SSW, the likelihood that children with ADHD would
demonstrate impairment bilaterally as opposed to a single-ear effect was also investigated.
SPAR(sensitivity prediction from Acoustic reflex
PTA (Pure-tone audiometry
PTA is behavioral test used to measure hearing sensitivity ( peripheral and central auditory systems.
Pure-tone thresholds (PTTs) = softest sound audible to an individual at least 50% of the time. Hearing sensitivity is
plotted on an audiogram, displaying intensity as a function of frequency.
Degrees of hearing loss(HL)
Normal hearing (0-20 dB): At this level, hearing is within normal limits.
Mild hearing loss (21-40 dB): inattention, difficulty in background noise, difficulty hearing soft speech.
Moderate HL (41-55 dB): affect language , syntax , interaction, and self-esteem.trouble hearing some conversational
speech.
Moderate-severe HL (56-70 dB): difficulty with speech and speech intelligibility. Cant hear conversational-level
speech.
Severe HL (71-90 dB): may affect voice quality.
Profound hearing loss (>90 dB): (deafness), speech and language deteriorate.
PTA: This is a measurement of air conduction thresholds of audibility.
Pure tone air conduction threshold is tested using head phones:
method: note:when establishing threshold ,2 choices are ascending & descending way to change intensity.
Ascending (Hughson - Westlake ascending technique)- begins with stimuli that are below patient's threshold &
intensity is increased until patient responds.

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descending- stimuli presented first are above patient's threshold & intensity is decreased until the patient no
longer responds.
but both have drawbacks=
in descending technique the patient might continue to respond to stimuli ,when he no longer perceives (false +
response)
in ascending technique the patient may fail to respond even when stimuli are audible.(false - response)
Modified Hughson - Westlake technique : uses an ascending technique to determine threshold .but each
threshold search is preceeded by a descending familiarization trial.
ex:"Up 5-down 10" method of threshold estimation
The better ear is tested first in order to determine the need for masking.
Start with a 1000 Hz tone at a level above the threshold to allow easy identification of the tone. This tone is
selected because it is an important speech frequency, and the patient is less apt to mistake the
frequency. To ensure the subject is familiar with the task, present a tone of 1000 Hz that is clearly
audible (e.g. at 40 dB HL for a normally hearing subject or approximately 30 dB above the estimated threshold for
a subject with a hearing impairment,)
If the patient is suspected to be having a profound hearing loss then the testing should be started with 250Hz
frequency. This is because of the fact that the individuals with profound hearing loss often have testable hearing
only in the low frequency range.
Next, test 2000, 4000, 8000, 500 and 250 Hz in that order
As the threshold levels are being reached, a check should be made for the existance of abnormal tone decay. This is
done by sustaining the tone for several seconds longer than usual. If the index finger drops before the tone is
discontinued, abnormal tone decay should be suspected.
"Up 5-down 10" method =The starting intensity of the test tone is reduced in 10 dB steps following each positive
response, until a hearing threshold level is reached at which the subject fails to respond. Then, the tone is raised by
5 dB, if the subject hears this increment, the tone is reduced by 10 dB; if the tone is not heard then ti is raised by
another 5 dB increment. This 5 dB increment is always used if the preceding tone is not heard, and a 10 dB
decrement is always used when the sound is heard. The threshold is defined as the faintest tone that can be heard
50% or more of the time, and is established after several threshold crossining

Testing of the second ear should begin with the last frequency used to test the first ear. There is no need to start
again with a 1000 Hz tone because if one side of the heard has learned the listening task, the other side knows it as
well. The test is terminated after all desired frequencies have been examined.
Types of hearing loss
Conductive
o normal bone-conduction thresholds, but poorer AC ( by at least 10 dB.
o CHL is secondary to an outer ear or middle ear : AOM,CSOM,OME, perforation : reduces the
effective intensity of AC signal reaching the cochlea, but it does not affect BC signal that does not
pass through the outer or middle ear.
o mild rising CHL. Note air-bone gaps.

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CHL

SNHL

Mixed

Sensorineural
o bone- and air-conduction thresholds within 10 dB of each other, and thresholds > 25 dB HL.
o high-frequency sloping SNHL
o SNHL is secondary to cochlear , auditory nerve or auditory pathways abnormality.
o Causes: presbycusis, noise-induced hearing loss, Mnire disease, and vestibular schwannoma.

Mixed ( CHL=SNHL components.

o Pure-tone AC thresholds are poorer than BC thresholds by >10 dB, and BC thresholds < 25 dB

mixed sloping hearing loss.

Tympanometry
A Normal, peak @0, flexible TM
As- Otosclerosis or ossicular fixation
AD- Ossicular discontinuity
C- Eustachian tube dysfunction= -ve=retracted
B- Middle ear atelectasis ( TM is rigid, fixed to the
middle ear) or otitis media with effusion (glue ear)
In TM perforation , it is impossible to obtain a "seal"
of the middle ear or a tympanogram.

Audiogram
o a chart of hearing sensitivity with frequency charted on the abscissa and intensity on the ordinate
Intensity is the level of sound power measured in decibels; loudness is the perceptual correlate of
intensity.
o For threshold testing intensity, decibels are measured in hearing level (HL), based on the
standardized average of individuals with normal hearing sensitivity. HL is not equivalent to sound
pressure level (SPL), but the American National Standards Institute (ANSI) has defined a
relationship between SPL and HL for each audiometric frequency from 250-8000 Hz.
Frequency (Pitch)
o Frequency is cycles per second( hertz, = cycles per second.
o 250-8000 Hz used in testing (= most of speech spectrum) human ear can detect(20-20k Hz..

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Pure-tone average (PTA)

o (PTA) is average of hearing sensitivity at 500, 1000, and 2000. This average should approximate
speech reception threshold (SRT), within 5 dB, and speech detection threshold (SDT), within 6-8
dB.
o If the SRT is significantly better than the PTA, pseudohypoacusis
o If PTA is significantly better than SRT, central involvement
Speech reception threshold
o SRT ( softest intensity spondee words can be repeat at least 50% of time.
o Spondees are bisyllabic words equally emphasizing. (poor word recognition), a limited set of
words may be used.
Speech detection threshold
o (SDT), also speech awareness threshold (SAT), is the lowest intensity speech stimulus that an
individual can detect at least 50% of the time.
Word recognition (formerly , speech discrimination)
o ability to repeat correctly an open set of monosyllabic words (30-40 dB above SRT)at
suprathreshold intensity= Most comfortable level.

Word lists are phonetically balanced (PB)(25 words, each word = 4%). Normal 88-100%
o

score represents percent of words correct for most word recognition tests.
Speech audiometry

behavioral test used to measure hearing sensitivity. The recognition of speech is therefore of great interest to all of
us in the fields of speech and hearing.
Purposes of Speech Threshold Testing
1- used as a means to cross-check the validity of pure tone thresholds.
2-to determine the level for suprathreshold speech recognition testing.
3-evaluation of pediatric and difficult to test patients.
The accepted measures for speech thresholds : 1-Speech Recognition Threshold (SRT) and 2-Speech Detection
Threshold (SDT). they specify the stimulus, and the task required to do( recognition in SRT or detection of
presence or absence of stimulus in SDT).
The criterion: threshold or generally 50%. The SDT is most commonly performed on those individuals who have
been unable to complete an SRT, such as very young children. Because recognition is not required in the speech
detection task, it is expected that the SDT will be about 5 to 10 dB better than the SRT, which requires recognition
of the material.
Materials for Speech Threshold Testing
1- spondees: familiar two-syllable words that have a fairly steep psychometric function.
2-Cold running speech or connected discourse is an alternative for speech detection testing since recognition is not
required in that task.It (specifiy which protocols was used).
Methods and technique
1-MLV=Monitored live voice and recorded speech can both be used in SRT testing. However, recorded
presentation is recommended = standardize the test procedure. it is less important in speech threshold testing than
it is in suprathreshold speech testing.

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2-familiarization of the patient with the test words should be included as part of every test.
3-Bracketing procedure. The typical down 10 dB, up 5 dB is often used (2-4 words presented at each level, and the
threshold = lowest level at which at least 50% of the words are correctly repeated.
sentence tests in noise have become increasingly popular in hearing aid applications. Testing speech in noise is one
way to look at amplification pre and post fitting. The Hearing in Noise Test and QuickSin, have gained popularity
in those applications. The HINT was developed by Nilsson and colleagues in 1994 and later modified. It is scored
as the dB to noise ratio that is necessary to get a 50% correct performance
PIPB(performance intensity function for phonetacally balanced: use suprathreshold intensity like ( word
discrimination) but chart % of WD against different sound intensity
Roll over= PIPB max-min/PIPB max
Normal hearing: sigmoid curve ( reach 100%
In CHL ( shift to right, reach 100% but high intensity is required
Cochlear HL: never reach 100%, shift right
Retrocochlear: never reach 100%, score with intensity( Bell shaped)
Scoring. Scoring is another issue in suprathreshold speech recognition testing. It is generally done on a whole
word basis. However phoneme scoring is another option.

Excellent or within normal limits = 88 - 100% on whole word scoring

Good or slight difficulty = 78 - 88%
Fair to moderate difficulty = 66 - 76%
Poor or great difficulty = 54 - 64 %
Very poor is < 52%
Most Comfortable Listening Level(MCL)
Test for hearing aids candidates is the level at which a listener finds listening most comfortable. The listener is
asked to rate the level at which listening is found to be most comfortable. (typically a range, not a specific level.
MCL is useful in determining ANL or acceptable noise level.
Uncomfortable Listening Level (UCL)
(UCL) is also conducted with cold running speech. The instructions for this test can certainly influence the
outcome since uncomfortable loud for some individuals may not really be their UCL, but rather a preference for
listening at a softer level. It is important to define for the patient what you mean by uncomfortably loud. The utility
of the UCL is in providing an estimate for the dynamic range for speech which is the difference between the UCL
and the SRT. In normal, this range is usually 100 dB or more, but it is reduced in ears with sensorineural hearing
loss often dramatically. By doing the UCL, you can get an estimate of the individual's dynamic range for speech.
Acceptable Noise Level (ANL)
(ANL) is the amount of background noise that a listener is willing to accept while listening to speech. It is a test of
noise tolerance and it has been shown to be related to the successful use of hearing aids and to potential benefit
with hearing aids. It uses the MCL and a measure known as BNL or background noise level. To conduct the test, a
recorded speech passage is presented to the listener in the sound field for the MCL. The noise is then introduced to
the listener to a level that will be the highest level that that person is able to accept or "put up with" while they are
listening to and following the story in the speech passage. The ANL then becomes the difference between the MCL
and the BNL. Individuals that have very low scores on the ANL are considered good candidates for hearing aids.
Those that have very high scores are considered poor hearing aid candidates.

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1-test hearing aid performance. Speech test: more realistically assess hearing aid performance in "real world"
environments. use of the HINT or the QuickSin would be the most useful on a behavioral test.
Otoacoustic Emission (OAE)
Low intensity sound produced by outer hair cell of normal cochlea detedcted by a very sensitive microphone
placed in Ext ear canal.
Sounds are played and a response is measured. If a baby hears normally, an echo is reflected back into EAC and
picked up by microphone when a baby has a hearing loss, no echo can be detected. information can be obtained
from patients who are sleeping or even comatose because no behavioral response is required(produced by the
cochlear outer hair cells as they expand and contract).
USES of (OAE) tests is to determine (hair cell function. : (1) screen hearing (in infants, or individuals with
developmental disabilities), (2) diagnosis of retrochochlear lesion( Acoustic neuroma, (3) differentiate between the
sensory and neural components of SNHL, and (4) test for functional (feigned) hearing loss.
5-Early detection/ monitor and follow up of noise exposure and ototoxic effect
Limitations:
1- Absent in 50% of the individuals(good positive, but not negative test)
2- Absent in middle ear disorders
3- affected by background noise
4- Time consuming
5- Expensive
6- Experience Need
The 4 types of otoacoustic emissions: Spnotaneous, and 3 evoked
Spontaneous otoacoustic emissions (SOAEs) - emitted without stimulus
Transient evoked otoacoustic emissions (TEOAEs) - Sounds emitted in response to very short stimuli;
clicks / tone-bursts at 80 dB
Distortion product otoacoustic emissions (DPOAEs) - Sounds emitted in response to 2 simul tones of
different frequencies
Sustained-frequency otoacoustic emissions (SFOAEs): Sounds emitted in response to continuous tone
PTA Pure-tone audiometry

OAES

measures all( outer ear, middle ear, cochlea, cranial

nerve (CN) VIII, and central auditory system.

measure only the peripheral auditory system(outer ear,

middle ear, and cochlea.

OAE testing often is used as a screening tool to determine the presence or absence of cochlear function, although
analysis can be performed for individual cochlear frequency regions. OAEs cannot be used to fully describe an

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individual's auditory thresholds, but they can help question or validate other threshold measures (eg, in suspected
functional [feigned] hearing loss), or they can provide information about the site of the lesion.
Using current technology, most researchers and clinicians find a correlation between frequency-specific analysis of
TOAEs/DPOAEs and cochlear hearing loss. However, at this juncture, the correlation cannot fully describe
auditory threshold. Naturally, a correlation would not be expected for noncochlear hearing loss
Stapedial reflex: occurs under normal conditions when a loud acoustic stimulusis presented to the auditory
system. This muscle contraction causes a stiffening of thebossicular chain and decreases the compliance of the
middle ear system. This change in thebmiddle ear compliance an be recorded by tympanometry. This reflex is
binaural and simultaneouslyoccurs in both the ears. This reflex is activated in normal adults when the sound
pressure levelsrange between 70-105 dBHL.Stapedial muscle contraction in response to intense sound signal occurs
bilaterally because thereflex pathway has both ipsilateral and contralateral projections. Acoustic reflex thresholds
areusually estimated in response to stimuli of 500, 1000, 2000, and 4000 Hz. For screeningpurposes it is sufficient if
recording is made at 1000 Hz.Reflex pathway:Any reflex pathway by definition should include:1. Sensory limb Input2. Central integration3. Motor limb OutputThis stapedial reflex is designed to be protective in nature that
limits the damage caused by highintensity sound. The sensory signals travel to the cochlear nuclei via the auditory
componentof the 8Th cranial nerve. From the cochlear nucleus signals travel to the superior olivary
complexbilaterally, and from there to the lower motor neurons in the facial nucleus which innervatesthe stapedius
muscle.Indications:1. Objective assessment of hearing Range of acoustic reflex in persons with normal
hearingaverages between 70-100dB sound pressure level. In conductive hearing losses, greater the lossgreater
becomes the acoustic threshold reflex. Where as in sensorineural hearing loss theacoustic reflex threshold may be
within normal range, this is true in patients with mild tomoderate levels of sensorineural hearing losses with
recruitment.2. Can be used as a topognostic test in patients with facial nerve paralysis3. Can be used in identifying
deafness in infants4. Acoustic neuroma dianosisContraindications:1. In infants under the age of 7 months due to
extreme pliability of external canal2. In the presence of wax as the results may not be reliable
Acoustic reflex
is the contraction of the stapedius muscle elicited by loud sound( stapedius muscles on both sides contract. causing
tilts in the anterior stapes away from the oval window and stiffens the ossicular chain. This results in d impedance
which is measured as a small in compliance by an ear canal probe.
The stapedius muscle is innervated by facial (CNVII), therefore, is lost in CNVII paralysis.
Why perform reflexometry?
They can provide/confirm type (conductive, sensory, neural) and degree of hearing loss.
Under what conditions will you measure an acoustic reflex?
An acoustic reflex will most likely be elicited if all of the following conditions are met:
1. Normal middle ear function
2. Loud enough stimulus to elicit the response
3. No abnormal adaptation to stimulus
However, about 5% of the adult population have absent acoustic reflexes.
The pure tone intensity to elicit an acoustic reflex is 85 dBHL.
Ipsilateral ARTs is usually 7080dB above PTT(pure tone thresholds, and about 5dB greater for their
contralateral threshold (if PTT at 10dBHL, ipsi ARTs is 80 90dBHL, contralateral ARTs 8595dBHL).
A few contraindicators to reflex testing
Tinnitus
Outer ear infection
Severe recruitment
Hyperacusis
Ipsilateral Pathway

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The loud sound travels through the outer, middle and inner (cochlea) ear, then along the vestibulocochlear nerve
(CNVIII) to the brainstem arriving at the cochlear nucleus,to the superior olivary complex and to the CNVII
nuclei, down the CNVII causing contraction of the stapedius muscle.
Right ear --- Cochlea-- CNVIII BrainstemCNVII--Stapes
Procedure for obtaining acoustic reflex thresholds
1. Alert the client that they will hear loud sounds. Ask them to sit still and quiet.
2. Place immittance probe (for tympanometry) into tested ear, and the other ear.
3. Do tympanometry first. Acoustic reflexes measured with ear canal pressure set for maximum compliance
4. Do not go above 105dBHL unless you suspect a conductive loss.
5. Present tones at @ 0.5, 1, 2, 4 kHz &/or BBN starting from 7080dBHL up to 105dBHL in 5dB steps until an
acoustic reflex threshold is obtained. Tones should be presented for 12 seconds in duration.
6. If the tone is loud enough = stapedius contraction, immittance probe will record that an acoustic reflex is
present.
7. Confirm the test to rule out artefacts. (done by repeating test at same level or testing for a reflex 5dB above the
ART obtained.
8. Record the results. For no response = X, NR or 105 indicating no response up to 105dBHL.
Acoustic reflex test can cause hearing damage and tinnitus , not recommended higher than 105 110dBHL.
What characteristics am I looking for in my results?
present or absent stapedial reflex
an acoustic reflex threshold
acoustic reflex decay or adaptation (if tested)
Example 1: Normal hearing/middle ear function
Freq
.5kHz
1kHz
2kHz
4kHz
Probe
R

Stim R
(ispi)

85

85

85

85

90

90

90

90

Probe
L

Stim L
(contra)
Stim L
(ispi)

80

80

80

80

Stim R
(contra)

85

85

85

85

CHL
Acoustic reflexes is absent (middle ear disorders prevent the probe from measuring a change in compliance when
the stapedius muscle contracts. Reflexes will be absent even in mild CHL.
In Type C tympanogram, depending on pressure reflexes : present or absent.
If acoustic reflexes are present in the probe ear, it is unlikely that a CHL exists, except in the rare case of Superior
Semicircular Canal Dehiscence (SSCD).
Example 2: Normal hearing in the right ear & a mild conductive loss in the left ear
Freq
500 Hz
1kHz
2kHz
4kHz
Probe
R

Probe L
Mild CHL

Stim R
(ispi)

85

85

85

85

Stim
L(contra)
Stim L(ispi)
Stim R
(contra)

100

100

100

105

X
X

X
X

X
X

X
X

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In this example, the raised left contralateral reflex thresholds (probe right, stimulus left) are due to the additional
SPL needed to overcome the mild loss in the L ear. The mild middle ear pathology may affect signals travelling
through the left ear or being measured in the left ear. They will either be absent or raised.
Example 3: Normal hearing in the right ear & a moderate conductive loss in the left ear
In this example, because of the moderate loss in the left ear, stimulus (at max levels) was not loud enough to elicit
the stapedius reflex in the left contralateral recording (probe right, stimulus left).
Freq
.5kHz
1kHz
2kHz
4kHz
Right
Probe
L Probe
Mod CHL

Stim R(ispi)

85

85

85

85

Stim L(contra)
Stim L(ispi)
Stim R(contra)

X
X
X

X
X
X

X
X
X

X
X
X

Cochlear Hearing Loss

In ears with a cochlear hearing loss, it is possible for the acoustic reflex to be elicited at sensation levels (SL)of less
than 60dB. The SL is the difference between the ART and the hearing threshold. (if hearing threshold at 1kHz is
50dBHL and the ART is 90dBHL, the sensation level is 40dBSL).
When the SL is less than 60dB, a positive Metz test is indicated. This indicates a cochlear site of
lesion(sensorineural loss) due to the loudness recruitment phenomenon.
Example 4: A mild to moderate cochlear loss in both left & right ears
note that the ARTs occur at about normal levels. This is because the acoustic reflex threshold in an ear with a
cochlear loss may resemble the results of a normal ear when the air conduction thresholds are below about
50dBHL. As the hearing threshold s above this level, the chance of recording a raised or absent acoustic reflex s.
Freq
.5kHz
1kHz
2kHz
4kHz
Right
Probe
L Probe

Stim R(ispi)

85

80

80

100

Stim L(contra)
Stim L(ispi)
Stim R(contra)

85
85
90

90
90
80

90
85
85

X
100
X

Example 5: Severe to profound cochlear loss in left ear, normal hearing in the right ear
the stimulus (even at max levels) was not loud enough to elicit a stapedius reflex due to the severe/profound loss in
the left ear. Therefore whenever a stimulus is presented to the affected ear, reflexes will be absent/raised in both
ipsilateral and contralateral recordings as shown above.
Freq
.5kHz
1kHz
2kHz
4kHz
Right
Probe
L Probe

Stim R(ispi)

85

80

80

95

Stim L(contra)
Stim L(ispi)
Stim R(contra)

X
X
90

X
X
90

X
X
90

X
X
95

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ABR
Is evoked potential generated by a brief click or tone pip recorded from auditory pathway in first 10 miliseconds.
The elicited waveform response is measured by surface electrodes on vertex of the scalp and ear lobes
Technique:
Averaged signal amplitude (microvoltage) is charted against the time (millisecond), like an EEG. The waveform
peaks are labeled I-VII. occur within a 10-millisecond time period after a click stimulus presented at high
intensities (70-90 dB normal hearing level [nHL]).
Indications :
1-Screening in infants
2-Determine threshold of hearing in infants , mentaly retarded, uncoperative, malinger
3- Dx of retrocholear(A/ neuroma, diagnose Brain stem (M.S, Tumor)
4-Monitoring of VIII n intraoperative(A/N) to preserve its function.
Generators : 7 waves ( E-I- COLI)
Wave I: Extern pathway of VIII n,

wave II, internal pathway of VIIIN

Wave III: Cochlear nucleus

Wave IV: sup Olivary Nucleus

Wave V lateral Leminiscus

Wave VI, VII: inferior Colliculus

I, III, V: are the most stable and prominent( used for measurement) (all odd numbers, 1,3,5= stable)
I, II are single generator from ipsilateral ear
III,IV, V, VI: are multiple generators from both ears due to interconnection( in brain stem)
Factors affecting ABR ( stimulus, recording, subject or biological factors)
A-Stimulus factors( types, time, duration, numbers, repeatition rate, intensity)
1.Type: broad band, or click
2.Number:1000 stimulus
Summation of 1000 stimulus, amplitude of AP and cancel background of EEG
number of stimuls :save time, but if d( better response)
3-Intensity: d intensity leads to amplitude, and latency and early wave I, II disappear
Absolute latency: from beg of stimulus to peak of wave = 1.5 milisec for wave I, and 1 m/s for
each wave
Inter peak latency:I-II:
III-V: 2 m/s
I-V: 4 m/s
4- Repeatitions (20 click in 1 second)
If poor response( lower the rate to 10 clicks/second)
To save time, rates to 30 click /second
B-Biological factors (subject)
Age: infants( only wave I,III, V present, latency normally prolonged, I>V 1:5
Females: large amplitude, short latency
Hearing level: type and degree
Cooperation
C-Recording factors:
1-Base time: 10 miliseonds
2-Electrodes site: at least 3( active, reference, ground)

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Ipsilateral ear: good wave I(IV and V are complex)

Contralateral ear( unclear wave I, (IV, and V are separate)
3- filter
Diagnostic and clinical value of ABR:
Identifiable and Repeatable:
2- Latency: absolute, interpeak, interaural
3- Amplitude: absolute: less important
I:V ratio: is the most important 5:1( but in MS and infant 1:5)
Limitation of ABR:
Pt should be calm( give chloral to myogenic activity, but contraindicated in chest infect( resp center)
Represent brain stem not cortex
Measure hearing sensitivity in hi frequency(2-4KHz), doesnot represent low fr

Normal adult auditory brainstem response (ABR) audiometry waveform response.

Although the ABR provides information regarding auditory function and hearing sensitivity, it is not a substitute
for a formal hearing evaluation, and results should be used in conjunction with behavioral audiometry whenever
possible.
(ABR) audiometry is 90% sensitive in the diagnosis of acoustic neuromas.
Electrocochleography
records the electrical potentials of the cochlea. however, ECochG : measurement of stimulus-related (ECochG)
cochlear potentials (as opposed to the resting potentials), measurement of whole nerve or compound (AP) of the
.auditory nerve
Technique
1- transtympanic" (TT) Invasive, painful, electrode through the TM to rest on the cochlear
promontory. this "" (TT) approach to ECochG is still used widely in Europe, very favorable signalto-noise ratio
2- Extratympanic" (ET)non-invasively, sites ( ear canal or, preferably, from the lateral surface of the TM.
Applications: most popular applications for ECochG at the present time, include:
1-diagnosis/assess/monitoring of Meniere's disease(MD)/(ELH)endolymphatic hydrops
2-Monitoring of cochlear and auditory nerve function during surgery , avoid trauma to the nerve and preserve
hearing,
3-Diagnosis of auditory neuropathy.

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4-ECochG :hi SP/AP ratios =Dx of MD/ELH(endolymph Hydrop), perilymphatic fistulae.

5-enhancement of wave I of the ABR in the presence of hearing loss or less than optimal recording conditions;
Enhancement of Wave I
In Deaf with acoustic tumors, wave I of the ABR may be reduced, distorted or absent , but identifiable wave V.
This reduces the diagnostic utility of the ABR since the I-V and III-V interwave intervals (IWIs) are
immeasurable. simultaneous recording of the AP-N1 via ECochG and the ABR has been applied , combined
ECochG-ABR approach. Wave I is absent in the presence of wave V in the conventionally recorded ABR for
this patient (top tracings). However, when the ABR is recorded using a vertex (+)-to-TM (-) electrode array
(bottom tracings), N1 is identifiable, permitting the measurement of the N1-V IWI.
Stimulus Considerations
1-The broadband click : popular stimulus for short-latency AEPs to produce well-defined components.
Likewise, 100 microseconds is a popular pulse duration that produces the click
2- tonal stimuli : provide for a higher degree of response frequency specificity than clicks, and the use of
extended-duration stimuli such as tonebursts allows for better visualization of the SP and CM
Masking of the contralateral ear is not a concern ,since the magnitude of response from the non-test ear is very
small. In addition, ECochG components are generated prior to crossover of auditory pathway.
CM

alternating current (AC) voltage that mirrors the waveform of the acoustic stimulus at low-moderate levels
of stimulation. It can be either positive or negative
It has 2 types,( oxygen dependant and none( active 6 hours after death)
Generated predominantly by the outer hair cells of the organ of Corti.
Reflects predominantly basal-end cochlear activity when recorded from the round window and more
remote sites.
Phase and duration are stimulus dependent.
Often difficult to separate from stimulus artifact in non-invasive recordings.
Is inhibited in response to stimuli presented in alternating polarity.
Effectiveness in the differential diagnosis of inner ear/auditory nerve disorders has yet to be established,
but has received recent attention in the diagnosis of auditory neuropathy.

SP (summation potential)
A Direct Current reflects the time-displacement pattern of cochlear partition in response to the stimulus.
Generated by the outer hair cells of the organ of Corti
Seen as a DC (unidirectional) shift in the CM baseline. The direction of shift (+/-) is dependent on a
complex interaction between stimulus parameters and the location of the recording electrodes.

SP duration is dependent on the duration of the acoustic stimulus.

Independent of stimulus phase, but tends to be obscured by the CM or stimulus artifact when recorded in
response to stimuli presented in condensation or rarefaction polarity.

AP (action potential)

represents the summed response of the synchronous firing of several thousand auditory nerve fibers.

Dominated by high-frequency nerve fibers when generated in response to transient stimuli with rapid
onsets ( clicks)

Occurs at the onset of the stimulus, even for tonebursts.

Characterized by a series of brief, predominantly negative peaks. N1 and N2 (1 st& second -ve peaks of AP)
are virtually the same components as waves I and II of the ABR.

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Independent of stimulus phase and duration.

Normal electrocochleogram from the TM to clicks presented in alternating polarity at 80 dB HL. The amplitudes of
the Summating Potential (SP) and Action Potential (AP) can be measured from peak-to-trough (left panel), or with
reference to a baseline value (right panel). Amplitude/time scale is 1.25 microvolts/1 millisecond per gradation.
Insert phone delay is 0.90 milliseconds.

Basic Hearing Aid Options

1-Digital programmable : have all features of analog programmable aids but use digitized sound processing (DSP)
to convert sound waves into digital signals. A computer chip analyzes the signals to determine sound is noise or
speech. It then makes modifications to provide a clear, amplified, distortion-free signal.
Digital hearing aids are usually self-adjusting. flexibility in programming. the sound it transmits matches your
specific pattern of hearing loss.
Advantages: management of loudness discomfort-control of acoustic feedback (whistling sounds) noise reductioncan store several programs. chang settings in different environment. more expensive. longer life span , better
hearing for you in different listening situations.
2-Conventional analog : designed with a particular frequency response based on audiogram. audiologist determine
settings to install. amplifies all sounds (speech and noise). least expensive, appropriate for different types of
hearing loss.
2-Analog programmable : microchip that allows the audiologist to program the aid for different environments.
depend on your individual hearing loss profile, speech understanding, and range of tolerance for louder sounds.
Implantable Hearing Aids
1-Temporal bone stimulators: bone anchored hearing aids(BAHA):metallic implant directly in the temporal bone.
alternative to the classical bone conduction hearing aids which have a temporal bone stimulator worn in a head
band. These devices are useful not for SNHL but in patients with chronically draining ears or with congenital ear
malformations.
2- Middle ear implants: connected to the TM, ossicular chain, or round window. for people with moderate to severe
SNHL ) One such device called the Vibrant Soundbridge uses an electromagnetic transducer held onto the long
process of the incus connected to a magnet surrounded by a receiver coil, a demodulator package, and a conductor
link, which are implanted in the skull above the mastoid. In a phase III clinical trial patients who wore this device
showed improvements in satisfaction, performance, and preference over wearing their conventional hearing aids.

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3- Cochlear implant. :for adults with bilateral profound SNHL with poor benefit from a conventional hearing aid ,
postlingually deaf benefit most. Some prelingually deaf adults have been implanted but with poorer results.
It consists of a microphone, a speech processor worn on the body connected to an external coil attached
magnetically to an internal coil implanted on the skull, which sends the signal to an electrode, or series of
electrodes implanted in the scala tympani of the cochlea. Most modern cochlear implants have multiple electrodes
to try to reproduce some of the tonotopic reception of the cochlea.
Advanced Hearing Aid Technology
A major problem for deaf is the difficulty of hearing in noise. A simple hearing aid can amplify all the noise, not
simply speech sounds, and the result is that the noise can drown out the speech that the hard of hearing person
wants to understand. Compared to people with normal hearing, deaf need an d "signal-to-noise" ratio (the desired
speech "signal" needs to be louder than the surrounding "noise" in order for the deaf to understand speech).
several strategies used within hearing aids shown to be effective in improving the S/N ratio: hearing aids with a
single microphone which is directional, multi-microphone technology within the hearing aid itself, and hearing
aids with boots to receive FM transmission.* (It is also possible to use assistive listening devices to improve
comprehension of speech in noise.)
*Some programmable hearing aids have the ability to activate a "noise" programs which act by suppressing certain
frequencies. These may be particularly helpful in situations where there is mechanical noise, but in parties or
restaurants where much of the noise is at the speech frequencies, there may be less benefit experienced. The best
way to hear in noise is to bring one's "receiver" as close as possible to the source of the desired sound---the
receiver can be the ear itself, the hearing aid, or the microphone of an assistive listening system (such as the
microphone for an FM system, a hand-held amplifier, or a DAI microphone).
http://dana_mulvany.tripod.com/HearingAids.htm
What is a Baha?
The Baha is a surgically implantable system for treatment of hearing loss by direct bone
conduction.
Applications: treatment for CHL, mixed , and unilateral SNHL.help people with chronic
ear infections, congenital EAC atresia and single sided deafness who cannot benefit from
conventional hearing aids. The system is surgically implanted and allows sound to be
conducted through the bone rather than via the middle ear - a process known as direct bone
conduction.
How does a Baha work?
3 parts: a titanium implant, an external abutment, and a sound processor. enhancing bone conduction to the inner
ear, bypassing the EAC and middle ear. The titanium implant , naturally integrates with the skull bone. sound
processor transmits sound vibrations through the external abutment to the titanium implant. The vibrating implant
sets up vibrations within the skull and inner ear that finally stimulate the nerve fibers of the inner ear, allowing
hearing.
Who is a Candidate for the Baha System?

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1-CHL (absent or narrow EAC, congenital ear malformation, infection, or surgery

2-mixed HL., 4- SNHL single sided hearing loss as a result of surgery for a vestibular schwannoma
Congenital Hearing Loss
malformation of the middle or external ear , incomplete ear canal (EAC atresia) , managed with a Baha.
Traditionally people with this type of hearing loss have been offered an old-fashioned bone conducting hearing aid.
These are either held on the head using a steel spring headband or included in the frame of a pair of glasses.
Traditional bone conductors have several disadvantages. The sound quality is poor as the skin acts as a barrier for
the sound to travel to the inner ear. They are uncomfortable - patients complain of pain and headaches due to the
constant pressure of the headband. They are also cumbersome, obtrusive and insecure.
The Baha sound processor is directly integrated to the skull bone. Because of this direct interface, the Baha offers
significantly better sound quality than that of a traditional bone conductor. The Baha sound processor works
without pressure on the skin avoiding the headaches and soreness associated with the conventional bone conductor.
Baha offers excellent wearing comfort and a better aesthetic result.
Baha for Unilateral Deafness( Bone anchored hearing aid)
severe hearing loss on one side, but normal hearing in the other ear have difficulty understanding speech in
background noise and determining which direction sound comes from. Unilateral deafness can result from viral,
trauma, acoustic neuromas ,ear surgery.
best approach has been the CROS (contralateral routing of offside signal) hearing aid. hearing aid microphones
worn in both ears and routed sound from the deaf ear to the hearing ear. most patients were unsatisfied. The Baha
effectively transmits sounds from the bad side to the normal ear and ultimately results in a sensation of hearing
from a deaf ear. Stereo hearing results in improved understanding of speech, especially in background noise and
aids in the localization of sound.
The Baha advantages to traditional CROS : placed behind the ear leaving the canal open. worn under the hair (not
visible). held in place by a clip , no need for a head band and pressure against the skin of the head. patients prefer
the sound and speech clarity achieved with the Baha versus the CROS and versus the unaided condition.
http://www.umm.edu/otolaryngology/baha.htm#ixzz29abP9HSI
Digital hearing aids with enhanced processing and features.
Digital signal processors (DSP)
attempt to achieve 2goals. managing the comfort level of noise. by sound isolation, compression, and output
limiting based on a predetermined algorithm , there are features and advanced signal processing schemes
available in digital hearing aids that do have significant advantages over those found in analog:
1-Gain Processing. the potential for audibility of sounds of interest without discomfort of high intensity sounds.
While this is benefit of compression rather than digital processing per se, the greatly d flexibility and control of
compression processing provided by DSP--such as input signal-specific band dependence, greater numbers of
channels, and knee-points with lower compression thresholds--can lead to improved audibility with less clinician
effort. Expansion, the opposite of compression, has also been introduced in digital hearing aids. This processing
can lead to greater listener satisfaction by reducing the intensity of low-level environmental sounds and
microphone noise that otherwise may have been annoying to the user.

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2-Digital Feedback Reduction (DFR). The most advanced feedback reduction schemes monitor for feedback while
the listener is wearing the hearing aid. Moderate feedback is then reduced or eliminated by cancellation system or
notch filtering. DFR : benefit users who experience occasional feedback, with jaw movement and close proximity
to objects.
3-Digital Noise Reduction (DNR). reduce gain, in the low frequencies or in specific bands, when steady-state
signals (noise) are detected. findings supporting the efficacy of DNR systems are mixed, DNR can work to reduce
annoyance and improve speech recognition in noise. DNR is complementary processing to directional
microphones(reduce background noise from behind or to the sides of the user.
Digital Speech Enhancement (DSE). intensity of some segments of speech based on temporal, or spectral
content. DSE in hearing aids is still relatively new, and its effectiveness is largely unknown.
Directional Microphones and DSP. improve signal-to-noise ratio. combining DSP with directional microphones .
DSP calibrates microphones, control directional pattern, automatically switch between directional and
omnidirectional modes, and through expansion, reduce circuit noise generated by directional microphones.
Digital Hearing Aids as Signal Generators. have a DSP, they are able to generate/ process--sound. Current digital
hearing aids use this capability to perform loudness growth and threshold testing in order to obtain fitting
information specific to an individual patient's ears in combination with a specific hearing aid. Sound levels also
can be verified through the hearing aid once it is fit. This technology has the potential both to accuracy of hearing
aid fittings and potentially streamline the fitting process by reducing the need for some external equipment.
digital hearing aids will replace analog counterparts altogether., present this technology to patients in educational
manner. Like many other high-tech devices, high expectations often accompany digital hearing aids. Counseling
patients about appropriate expectations will continue to be more--not less--important as technology continues to
advance.
Audiology Site of Lesion_cards
Question

Answer

What are site-of-lesion tests used for? Used to differentiate and/or evaluate the site-of-lesion.
What are the two types of site-oflesion tests?
What does it mean if a test is
subjective?

Psychoacoustic (subjective) and physiological (objective).

It requires a behavioral response.

What are five examples of

Loudness balance procedures, Short Increment Sensitivity Index (SISI),
psychoacoustic site-of-lesion tests (all Threshold Tone Decay Testing (TTDT), Bekesy Audiometry, and PI-PB
barely used)?
function.
What are loudness balance
procedures?

Tests of recruitment; measure the growth of loudness.

What does the Short Increment

Sensitivity Index test? (SISI)

The ability to detect 1 dB increments near hearing threshold.

What does Threshold Tone Decay

Testing measure (TTDT)?

Measures tone decay over time (abnormal adaptation). If you can't

maintain audibility of a continuous tone over time, so( CNVIII
pathology).

What type of instrument does Bekesy

Uses an automatic audiometer.
Audiometry use?

148

What does Bekesy Audiometry

compare? Why?

Compares threshold information obtained using a pulsed and continuous

tone; if you have abnormal adaptation, threshold info for a pulsed tone
would be better than for a continuous tone.

What is a PI-PB function? What does

it test for?

It's a performance-intensity function for PB words; tests for roll-over.

What is roll-over and what does it

signal?

A curved PBMax line; once you meet PBMax, an in intensity results in

a in performance. Consistent with SNHL due to disorder of CNVIII.
(retrocochlear)

What are the three physiological siteof-lesion tests?

Acoustic Immittance Measurements, ABR, and Otoacoustic

Measurements (OAE)

Which are better: physiological or

psychoacoustic site-of-lesion tests?

Physiological; they're objective and not dependent on behavioral

responses.

What are Acoustic Immittance

Measurements used for?

Used to evaluate the functioning of the ME system; specifically, the

mechanical properties or impedance matching characteristics.

Acoustic immittance measurements

used to _

Identify, differentiate between _.Middle ear pathology.

Acoustic immittance measurements

used to
Acoustic immittance measurements e
used to evaluate
What is acoustic immittance?
What is impedance?

Sensorineural functioning.
A generic term used to refer to measuring the acoustic impedance,
acoustic admittance, or acoustic compliance of the ME at the plane of the
TM
Opposition to the flow of energy through a system.

What is impedance related to?

The mass, stiffness, and friction of the system--impedance= the vector

sum of mass, stiffness, and friction.

How can impedance be represented in

a simple mechanical model?

A box on the floor being pushed by a spring and pulled by an invisible

force.

What is the effort required to pull the

box related to?

Effort= impedance; related to the mass of the box, stiffness of the spring,
and friction.

What is acoustic impedance?

What is acoustic impedance measured
in?
What are the two components of
Acoustic Impedance?
What is Acoustic Reactance?

Opposition to flow of acoustic energy through a system.

Acoustic Milliohms (mohms), a unit of impedance.
Acoustic Reactance and Acoustic Resistance.
The interaction of mass and stiffness; mass= positive reactance, stiffness=
negative reactance.

What determines Acoustic

Resistance?
What is Acoustic Admittance?

The friction of the system.

ease at which acoustic energy flows through a system.

149

Acoustic Admittance is the reciprocal

of?

Impedance.

What is Acoustic Admittance

measured in?
What are the two components of
acoustic admittance?

Acoustic Millimhos (mmhos)

Acoustic Susceptance and Acoustic Conductance.

What is Acoustic Susceptance? What

is its reciprocal?

Interaction of mass and stiffness; reciprocal of acoustic reactance.

What is Acoustic Conductance

determined by? What is its reciprocal?

Determined by the friction of the system; reciprocal of resistance.

What is Acoustic Compliance?

A dimension of an enclosed volume of air; refers to the "mobility" of the

ME system based on a dimension of an enclosed volume of air.

What is Acoustic Compliance usually

measured/expressed in?

cc or mL

Dysphagia:
Any change in subjects voice tember or quality
Organic causes--- functional- functional leadint to organic
2- Organic:
Congen(cyct-hemangioma- stenosis
Trauma(inhalation, intubation, Irritation fumes, FB
Inflammatory: acute sp: Diph Non sp: Upper resp T infec. Tracheolaryngiobronchitis
Chronic sp: TB, S, Sceleroma
Chronic non sp= Functional leading to organic
Tumor: Bening: fibroma, hemangioma,leukoplakia
Malignant: SCC
Neurological: bulbar, suprabulbar-Peripheral N injury(sup and recurrent N injury)
3- Functional
Habitual:hyper, hypo, diplophonia,phonasthesia
Psychogenic: primary, secondary
4- Functional leading to organic( nodule, polyp, cyst, Reinkes edema
Diag: History, onest , course
Laryngoscopic:
Invest: D/L-CT-MRI, EMG, Electroglottography( Storboscopy)
Pulmonary function, Maximum phonation Time
TX: Antibiotic, anti-inflamm-steroid
Surgery:
Dysphasia
Impairment in speech and failure to arrange words in an understandable way; caused by an acquired lesion of the
brain.
Aphasia is an acquired disorder of language due to brain damage
Partial or complete loss of language after complete language development
Caused by lesion in Left side of the brain

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Aphasia does not include (1) developmental disorders of language, often called dysphasia (2) purely motor speech
disorders, limited to articulation of speech via the oral-motor apparatus, referred to as stuttering, dysarthria, and
apraxia of speech; or (3) disorders of language that are secondary to primary thought disorders, such as
schizophrenia.
Aphasia syndromes
Broca, Wernicke, conduction, and global aphasias. The nonperisylvian aphasias include anomic,
transcortical motor, transcortical sensory, and mixed transcortical, sometimes called the isolation of the speech
area syndrome. Other more specific language syndromes include aphemia, alexia with and without agraphia, and
pure word deafness. Subcortical aphasia syndromes are defined more by the anatomy of the lesion than by the
language characteristics.
o
The syndromes provide a terminology to permit clinicians to communicate with one another regarding the
patient. The presentations of the types of aphasia vary and overlap considerably, but recent studies of both stroke
patients and of normal subjects undergoing functional brain imaging have supported the general classification of
aphasia syndromes and the localizations of specific language functions.
o
MCC is cortical aphasias, (Broca, Wernicke, conduction, and global aphasias.
o
Specific information : reading and writing ability, symptom onset, any word-finding difficulty, and
underlying problems (eg, previous stroke, chronic difficulty with memory).
o

Rhinolalia: altered speech caused by abnormal air flow through the nose during phonation
1- Aperta: nasal resonance ( valeopharyngeal dysfunction by flow between oral and nasal
cavity(cleft palate, )
2- Clause: nasal resonance:caused by obstruction of the nose or oropharynx
3 layers in TM:-Outter skin layer.middle fibrous layer.inner mucosal layer.
- 3 cranial nerves innervate the TM:-V (trigeminal).
C.N. IX(glossopharyngeal).C.N. X (Vagus).
-3 Parts of middle ear:-Tympanic cavity.Eustachian tube.Mastoid air cells.
- 3 parts of the tympanic cavity:-epi-tympanum.meso-tympanum.hypo-tympanum.
3 parts of the malleus:-Head.-lateral process.-handle.
- 3 parts of labyrinth:-Bony cochlea. 3 semicircular canals. Vestibule.
- 3 semicircular canals :Posterior.lateral.superior.
- 3 compartments of cavity of bony cochlea :scala vestibuli: Upper compartment.
scala media (cochlear duct):middle compartment.
scala tympani: lower compartment.
- 3 membranes in cochlear duct:- vestibular.Tectorial. Basilar .
- 3 labyrnthine sensory end organs:-cochlea..called organ of corti.
of s c c....called crista. of utricle and saccule..called macula.
Ear pearls and cases
Ear Notes
Facial n: behind short process of incus, if you remove incus, you can injur VII

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VII n :ant inferior to LSCCAbove Cochlear n in IAC- anter to sup vestibular,( 7 UP)
Facial n in parotid( retro mand vein-VIIn- Facail artery=deepest)
Trigger point:1.5 cm below tragus= VII trunk
Temporal Bone Fracture: Battle sign-Racoon sign Long 80%- Transverse 20%- but oblique : most common
Eustachian tube=36 mm
Utricle - activated by linear acceleration
Acoustic Neuroma (Schwannoma) - Originates from superior vestibular nerve, CNVII displaced anteriorly at IAC.
Accounts for 80% of CP-angle tumors.
Benign Positional Vertigo - rotatory, fatiguable nystagmus, +Dix-Hallpike, Rx: Epley, Singular neurectomy
Labyrinthine Nystagmus - fast AND slow component. Central Nystagmus is usually pendular (without fast/slow
component).
Ampullo- or Utriculopedal flow is stimulatory in Lateral SCC, but Ampullofugal flow is stimulatory in posterior
and superior SCC.
Meniere's Disease (Crisis of Tumarkin - loss of extensor strength, falling with Vertigo
Lermoyez - Improved hearing after vertigo
Temporal Fracture- Longit - 80%-CHL 2' to perfed TM or ossicular chain dysruption
20% injure CN VII, usually at labyrinthine segment
Transverse - 20%:( hi VII 50% injur CN VII, usually at geniculate ganglion-2' to occipital force
Middle Ear CSF Leaks - Oval window or round window leaks most commonly
Hyrtl's Fissure - (usually infants) opening just anterior/infer to round window leading to subarachnoid space near
CN IX ganglion.
Acellular mastoid: low dura+forward sinus
Arnold N off Vagus to post EAC, stimul in ear wash=vasovagal, to avoid that wash direction : ant/superior
Grommet: ant inferior, close to eustichian tube
Incisora terminalis: cartilage is defect superior, used to get extra cartilage access
Middle ear contents:air-3 ossicles-2 muscles- 1 nerve
Mastoid tip developed by age of 2
Normal range of hearing: 16-20k
Tensor palatine: only ms that opens Eustachian tube
Tensor tempani insert in neck of malleus
Caloric test @ +/-7c of body temp(37) 30C and @ 44C= COWS( cold opposite- warm same)
Bilateral VII palsy: Lyme- Milkerson( fissured tongue)
Weber lateralization= minimum of 5 dB difference
When difference in hearing is > =40dB, we have to use masking
Loud recruitment =cochlear deaf=rapid growth of loudness with increase in sound intensity=loss of outer hair cell(
Cocking is loud)-retro fades away
Recruitment tested by short increment sensitivity test(SISI) or By ABLB Binaural loudness balance
Tone decay=retrocochlear lesion= abnormal adaptation, continuous tone perceived as fading intensity
Scala tempani separated from scala media by Reissner membrane
Caloric test(Cold/hot stimulation= Hallpike and Fitzgerald
Acoustic neuroma=symptoms if >= 2.5cm
Notch of Rivinus: defect in sup annulus
Short pr of incus lies in fossa incudis
Post & Sup SCC open in a common open=crus commune
Apex of cochlea=scala vest&scala Tempani meets= Helicotrem
Fistula sign: giddiness and nystagmus when the tragus is pressed and released alternatingly or during siegalization
of the ear. seen in erosion of the bony labyrinth , lateral semicircular canal 1-The main characteristics of diptheria pseudomembrane extends outside tonsillar surface
2- vertigo = dizziness
3- angle of T.M = 55 degree

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4- Traumatic T.M. rupture doesnt cause 7th paralysis .

5- cong. Meatal atresia 1st 2nd pharyngeal arch
6-Acute necrotizing otitis media pneumococi.
7- Continuous draining air after AOM mastoiditis " reservoir sign ".
8- hearing loss is greater with : post. Perforation exposing the round window
9-Mastiodectomy complications : CHL , SNHL , VII n. paralysis .
12- acoustic neuroma Dx : MRI with gadolinium.
13- Modinis dysplasia of inner ear is : hypoplasia
20 - Perinasal allergy Chronic hypertrophic Rhinitis
21- Color of mucosa indicate severity of allergy and prognosis of therapy
22- Nasal polyp pedunculated swelling of nose
24- Fleshy mass Antrochoanal polyp
25-Chronic maxillary sinusitis + purulent discharge radical antorostony
26- Post. Nasal discharge = chronic sinusitis
27- Dx temporal abscessuncinate pits.
28- Side of LST( lateral sinus thrombosis) by Lillie crews fundus examination.
29- LST(lateral sinus) Dx Picket fever, otorrhea,Anemia + Griesinger sign Tenderness and mastoid edema
30- Acute O.E Cream -Chronic O.E ointment
31- Adhesive O.M Tympanosclerosis.
32- 5h 1st pharyngeal arch ms
33- 7th 2nd pharyngeal arch ms
34- Mastoid abscess in 6 years no swelling
35- Turbid CSF cellular content.
36- Myningo plasty in central 1ry perforation.
37 Acoustic trauma acute ----- reversible, chronic --- irreversible
38- Poorly diff. max. s. cc Tx : radiotherapy.
39- Tuning Fork Test in mixed H.L ABC
40- Glomus jugulare Tinnitus : voice change & palatal paralysis.
39- M.C epistaxis in child 8 yearsnose picking
40- septal abscess 1st line of Tx : drainage.
41 History of epistaxis for 3 years haemophilia + swollen gum + bleeding joint.
42- Typhoid epistaxis due to toxic capillaritis
43- Lt frontal lobe abscess:- left : visual acuity - Rt :( papilloedema )=Foster kendy syndrome
44- Intrathecal dye metrezimide.
45- Ch. Max. Sinusitis + purulent discharge Radial antrostomy
46- Frontal swelling of 10 years duration : + diplopia mucocele.
- + pain + fever pyocele.
47- Thom Waldats disease: ( central retention adenoid cyst + morning post nasal bone Discharge )
48- Bilat. Laryngeal paralysis - Partial ( RLN ) - complete ( RLN SLN )
49 Bleeding 14 day after tracheostomy from innominate v.
50 - Bleeding 6 hours after tracheostomy from inf. Thyroid v.
51- Stridor After 10 days. of fever epiglotitis.
52- Stridor After 3 Y. of fever LTB.
53- Juvenile vocal nodule : male (5- 15) > females
54- Aspiration of retropharyngeal abscess is only for avoiding ICA aneurysm
Ear cases

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3) male pt, 16 yr, with offensive right ear discharge for 2 yr, a month ago, swelling appeared behind the right ear,
red hot, fluctuant, with fever of 39 C, swelling was incised and drained, temp dropped to 37, but pus continued to
drain from the site of incision, did not heal
What is the diag? cholesteatoma complicated by fistula
What are invest? CT, audiometry, Cx and sensitivity
What is the Tx? Tympanoplasty+ mastoidectomy
4) male pt, 25 yrs, bilateral hearing impairment started 6 yr on the right, chronic mucupurulent discharge follow
attacks of common cold, stops with med Tx, history of chronic left ear discharge, continous, scanty, purulent,
offensive, does not respond to Tx
5 weeks ago, developed vertigo on pressing on left tragus
Exam: rt central kidney shaped perf, Left perfor, +ve fistula sign on Left
Weber: lateralization to right, bilateral negative Rinne test= CHL
What is the diag? Rt tubo-tympanic, Left Cholesteatoma compl by diffuse labrynthitis
What is the type of Hearing loss? CHL more on right
What is the Tx? Left( tympanoplasty+ mastoidectomy)
5) 10 yr old child with history of right continuous otorrhea for 4 yr, a week ago become dizzy, nausea, vomiting ,
severe hearing loss in right ear, Exam: nystagmus on rt eye
Rinne ve on right, Weber lateralize to left
3 days later, developed fever 40 C, irritable and crying of headache, neck retraction and nystagmus on the left side
What is the diag? Rt tubotymbainc CSOM, comp by serous labtinthitis
What is the type of hearing loss? Right SNHL, left normal
What are the invest? L/P, CSF exam, CT to exclude intracranial complication, audiometry
What is the Tx? Antibiotic (cross BBB)
What is the proper surgery for right ear? Radical mastoidectomy(dead ear)
6) 35 yr old male pr presented by deep seated pain behind left eye, diplopia(left conver paralytic squint) PMH: left
ear discharge for 10 yr, Exam: attic perforation, foul discharge
What is the daig? Petrositis( Gradingo triad( retro orbital pain_VI paralysis+ discharge)
What are the invest? CT: confirm diag
Pt with history of right continuous otorrhea for 4 yr, a week ago developed proptosis, ptosis, ophthalmplegia? (7
Lateral Sinus complic by Cavernus sinus
!! TM Hearing Loss yrs 30 : .
Otosclrosis
otoscelrosis 3
lip reading ---- 17
stapectomy ---- 35
hearing aid ---- 60
wax more wet w warm deep )deep part superficial fungus
lyzosymes fungus
vincent angina moniliias !! sore throat :
ulcers fever
deep punched out
meningitis complications cholesteatoma
kernig brudiziniski meningeal irritaion neck rigidity..
.. neck rigidity photophobia vomiting..
fever neck rigidty
hoarsness of 50
cancer larynx cancer larynx

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larynx cancer : acute larynigitis .

bronchogenic carcinoma inflitration cancer
hoarseness infilrtation left reccurent larryngeal nerve
Problem solving:
Ear
Otomycosis (dec of hearing and tinnitus, and itching on exam, large black- white
Comp OME-AOM( mastoiditis- brain abscess- petrositis
*5 yr old, running nose fever, cry at night and rubbing rt ear- 2 days later post auricular swelling) AOMmastoiditis DD: fruncle
*55yr male, hist of rt ear discharge, deaf, tinnitus+swelling , eye dev to left, pain in rt face, petrositis, (CSOM
mastoiditis, porosities)
Lat sinus thrombophlebitis) (CSOM ,ffensive , deafness, 2 days ago : hi fever, = lat sinuscerebellar abscess :20yr rt ch ear offensive , deafness, fever, ataxia, incardination
Headache and persistent fever= Brain abscess (neck rigiditymeningitis)
Otoscelerosis( femal, bil hearing loss, family history, d after pregnancy)
Traumatic rupture of TM:35yr woman, bilateral ear wax, during wash, pain in rt ear, bl discharge, water discharge
from nose, then d hearing in rt, then discharge, whistle sound most probable, traumatic rupture of TM (Tx sys
antibiotic, avoid wet ear, )
30 yr male, flu, then fly, with facial pain, headache, nasal obstruction, then developed hearing
Otitic barotraumas, rhino-sinusitis
10yr boy, car accident, bleeding rt ear, hospitalized, then developed, rt facial palsy,
(Longitudinal F base-Delayed incomplete VII palsy, (side trauma, TM tear, dislocation of ossicle, to foramen
lacerum)CHL, TM rup, VII usually preserve or delayed due to edema.
Transverse: normal TM, immediate complete VII palsy, loss of conscience ( trauma on the back of head, do to IAC,
with VIII, and SNHL )
VII palsy ,After mastoidectomy?immediate remove the pack, confirm total palsy, then re exploration of VII,
reanastomosis, hypoglossal
vestibular neuritis :35 y male, flu, then vertigo, nausea, vomiting, no hearing loss
-2 yr/ body with running nose, fever, cry at night, rubbing both ear, Bil OM
OME+ adenoid hyperplasia: Snoring at night, deteriorate school, hearing,
OME: 5yr body, recurrent earache, and snoring, retracted TM
6yr boy, hearing, 2m ago, attack of fever 39c, severe bil earache, and running nose,
Diag: AOM comp-bil OME( secretor) inadequate treatment
Plummer Vinson: 40 female, anemia, pallor, stomatitis, spleneomegaly dysphagia :, precancerous, follow-up
hypopharyngeal /esophageal carcinoma: dysphagia, for 4 month, is, loss of weight,
AFT( acute follicular Tonsillitis), enlarged, repeated 4 times: medical then 2 wk surgical.
Fungal esophagitis: Dysphagia, no fever, after prolonged antibiotic, white coated tongue
Infection mononucleaosis: 15yr boy, fever, dysphagia, sore throat, conges mucosa, LM enlargement,
lymphocitosis, abdominal pain, splenomegaly,

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Quinzy: 20 yr male, fever, dysphagia, throbbing pain, 3 days later, drooling, localized in left, neck swelling, DD:
parapharyngeal abscess: push tonsil medially
Ludwig angina: airway obst due to tongue or laryngeal edema
Pharynx pearls and cases
Teenager with recurrent epistaxis -- nasopharyngeal angiofibroma
The best diagnostic investigation for this patient is -angiography
MCC of bilateral OME in 3 yr boy is AdenoidMain blood supply of the tonsil comes from -facial artery
Acute tonsillitis cause all the following except:
(Quinzy acute retropharyngeal abscess
parapharyngeal abscess -- chronic retropharyngeal abscess)
Vincent's angina :(fusiform bacilli & spirochete punched out ulcers penicillin No general symptoms)
dysphagia due to neuromusc disturbance includes all the following except:
(pharyngeal pouch Achalasia Myashenia gravis Aortic aneurysm)
primary haemorrhage in adenoidectomy is caused by the following except:
(incomplete removal Over removal Bleeding tendency infection)
anaethesia of the face is caused by
( Facial paralysis occulomotor paralysis trigeminal neuralgia
Polysomnography is used in cases of -Sleep apnea syndromeAdenoidectomy avoided in cleft palate for fear of: --rhinolalia apertanon tender, firm, progressively upper neck swelling is:Search for occult 1ry in silent areas
Essential surgical management of a pharyngeal pouch is:--cricomyotomyLoss of laryngeal click is occurs in -postcricoid carcinoma
most accurate inves confirm esophageal carcinoma : esophagoscopy & biopsy

Phrynx cases
Male pt 59yr. with bil neck swelling of 2 months,( progressive,) history of hearing in both ears, nasal obstruction
On exam: nasal intonation( rhinolalia averta)
Bilateral multiple hard swellings deep to Sternomastoid
Right palatal and vocal cord paralysis
Ear: drum intact, retracted- -ve rinne test in both ears- Weber: central
What is the Diag? Nasopharyngeal carcinoma+ LN metastasis(IX and X paralysis, Jugolar foramen)
What are the Invest(confirm diag, and assess ext)?
o Biopsy 2-CT 3-Tympanometry type :B, or C
o Type of hearing loss: CHL due to E.Tube obst or palatal paralysis
What are the Types of nasal intonation and causes?
Aperta( letter K) caused by palatal paralysis
Clausa( letter M&N) by nasal obstruction
What is the treatment? Radiotherapy no surgery( inoperable)
Put T tube tympanostomy, as radiation cause mucosal fibrosis
Tx of complication (Hoarsness VC paralysis)conserv6-12 month, then medialization of VC
2-52 yr male, progressive hearing in Rt ear.altered sensation of right face, lump in neck below right jaw
Exam: move of rt palate, sens of rt side of face( IX,X, V )

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Ear: OME( otitis media + effusion)

What is the diag? Nasopharyngeal carcinoma(old, male,LN, cr nerve, what is 1st nerve affected? V( sensory)
What are the inv? CT-MRI- Biopsy
What is Trotter triads? unil Fixed palate- Facial pain+ OME, trismus = nasopharyngeal carcinoma
3-5 yr child with sore throat, enlarged left LN upper deep cervical, 2 days later developed respiratory distress, and
weakness, Fever 38, pulse 150/m, Exam: cyanotic, retraction of suprasternal, intercostal
Oral: grayish membrane on left tonsil
1- diag? Diphteria( unilateral, membrane, when removed, ulcer, bleed disproportionate pulse to fever =
myocarditis+ motor neuritis diplopia, VII)
Cyanosis due to? Laryngeal obstruction by membrane or laryngitis by bacteria
First line of Tx? Tracheostomy
What is the cause of stridor? Laryngeal obstruction or cyanosis late sign)
What is the cause of absent stridor( pneumonia, Hear failure, reparatory muscle paralysis
What is DD?
1-AFT( acute follicular tonsillitis) Fever, no ulcer, scarlet fever
2-Vincet AngincaSore throat+ odynophagia+LN no fever+ membrane +single ulcer, Culture: anerobic+ spirochetes
Tx metronidazole + penicillin
3-Moniliasis( diabetic+ post antibiotics)( white mem no fever Culture: candida
4- Mononuclosis ( fever+ membrane + multiple ulcers+ multiple LN+ spleen) Blood: leukocytosis(20000,
monocytosis= atypical lymphocyte) Tx: conservative
5- Agranulosystosis (Radiotherapy methotrexate- multiple ulcer , no red margin, no neutrophiles, WBC:2000
6- Leukemia:lymphadenopathy, hepatosplenomegaly, bleeding, anemia, WBC:100000,
What is management? Antitoxins+ antibiotic , Tx of complication, myocarditis
4- Female pt, 40 yr with dysphagia for 3 yr, more to solid, for last 2 month progressive to fluid with voice
change, and swelling in right side of neck.
5- 60 yr old female pt with left earache of 3 month, one month later, swelling on left side on neck, progressive,
change of voice 2 days ago, with dysphagia, laryngoscope showed froth in left pyriform fossa
What is daig? Pyriform fossa Carcinoma
What is inv? Hypopharyngoscopy& biopsy (confirm) CT
What is the cause of earpain? Vagus nerve
What is the DD? Achalazia, Plummer Vinson syndrome
Pharyngeal pouch( regurge, undigested food) cystic swelling
6- 4o yr female , repeated chest infection, not improved by Tx, choking after meals, intermittent dysphagia to fluid
for 4 yr
What is the diag? Achalazia( intermittent- fluid-aspiration- no loss of weight- pneumonia)
What is the inv? Barium swallow, manometry( wide upper, contract lower)
What is Tx? Cardio myotomy( haller- Botox, Ca blocker)
7-65 yr male,absolute dysphagia, barium swallow: arrest at midesophagus
Esophagoscopy:FB( meat), one month later, hemoptysis, change of voice(left vocal cord paralysis)
What is diag? Esophag Carcinoma
What is inv? Esophagoscopy(FB- perforation) lipidol swallow( Barium can irritate and cause mediastinitisCT
When to use Lipidol? 1-In children, 2-if suspecting perforation, fistula

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 What should you do? 2ed look to see the cause or complication( perforation: retrosternal pain,
mediastinitis, dyspnea, fever)
8- 4 yr old child, adenotonsillectomy, discharged, 3 hours later blood pressure drop 90/60, pulse, 140/m
9- 22 yr male with sore throat, fever 39 for 2 days, 3 days later dysphagia, pain localized on left side, otalgia,
feotor oris, throbbing pain, drooling, left earache, trismus, tender firm swelling below angel of mouth
What is the diag? AFT complicated by Quinzy
What are the signs? Tonsils pushed down & medial, uvlea pushed opposite side by pus
Why there is trismus? Spasm of medial ptrygoid muscle,
Why otalgia? Referred pain along IX
What is Tx? 1-Incision inside upper pole of tonsil, 2-antibiotic,
3- tonsillectomy: 2 month later:
What is DD?
Parapharyngeal abcess: trismus, internal swelling latral wall of pharynx, and external swelling along ant
border of sternomastoid
What are Picks triad?( int, and exter swelling+ trismus) Tx inscin, ant border of sternomastoid
Retropharyngeal abscess: between buccopharyngeal and prevertebral fascia
10- 40 yr smoker male, ch cough and expectroration for 2 yr, yellow sputum, profuse, night fever, sweating, loss of
weight. Neck: flexed and dysphagia, swelling of posterior pharyngeal wall crossing midline
What is the diag? TB Ch retropharyngeal abscess (Potts)
What is the manage? Incision form outside, ant border of sternomastoid
Swelling in neck during straining?

4. Four causes of referred otalgia: phonationa. Tonsillitis b. TMJ Dx, Post tonsillectomyd. Dental pain
6. Tonsillolith:Tonsillolith is a rare dystrophic calcification occuring in the tonsil as a result of
chronicinflammation. Most commonly tonsilloliths are intratonsillar and are asymptomatic. They have been
identified incidentally. Commonly patients with tonsillolith complain of foul breath and throatpain. Throat pain
is usually very intense during acts of swallowing. Also known as tonsilconcretions or tonsillar stones.
9. 2 features in fungal sinusitis:Clinical features of fungal sinusitis:HeadacheNasal block
10. Two common sites of CSF leak in nose: Cribriform plate Roof of frontal sinus11. Bleeding polypus septum:This
is angioma involving nasal septum. This is common in the antero inferior portion of the nasalseptum. Nose picking
in these patients can lead to troublesome epistaxis.12. Functions of nose:Conditioning of the inspired
air Olfaction13. Laryngeal papillomatous:This is caused by infections with human papilloma virus. It is of
two varieties. Adult andpaediatric types. Adult papillomas are solitary while papillomas involving the children are
oftenmultiple. This commonly occurs at the junction where the transition between squamous epitheliumand
columnar epithelium occurs. These patients present with voice disturbances and breathingdifficulties.14.
Phonation:Phonation takes place at the level of larynx due to vibration of vocal folds which occur due to air flowing
from the lungs through them. There are two theories currently accepted to explain theprocess of
phonation: Myoelastic theory and aerodynamic theory.15. Aphthous ulcer:These are painful ulcers involving the
mucosa of the oral cavity.
Aphthous ulcers are classifiedaccording to the diameter of the lesion.Minor ulcersMajor ulcersHerpetiform
lesionsThese ulcers are commonly caused by herpetic infections of the oral cavitphonationy mucosa.It is also
common in individuals who are excessively stressed.Trauma to the oral mucosa can also cause this type of
ulceration.
*BATTLE SIGN- Bruising at mastoid region, due to petrous temporal bone# (middle fossa #).

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*BOCCA'S SIGN - Absence of post cricoid crackle(Muir's crackle) in Carcinoma post. cricoid.
*BROWN SIGN - blanching of redness on increasing pressure > sys BP in glomus jugulare.
*BOYCE SIGN - Laryngocoele-Gurgling on compress of ext laryngocoele + reduction of swelling.
*DODDS SIGN/CRESCENT SIGN - X-ray (Crescent of air bet mass and post phar wall. positive in AC
ployp. Negative in Angiofibroma
*FURSTENBERGERS SIGN-This is seen when nasopharyngeal cyst is communicating
intracranially,there is enlargement of the cyst on crying and upon compression of jugular vein.
*HITSELBERGER'S SIGN - In Acoustic neuroma-loss of sensation in the postero-superior part of external
auditory meatus supplied by Arnolds nerve( branch of Vagus) loss of taste in ant 1/3 of tongue, and lost sens in
ear canal of Arnold's nerve( of Vagus)
*HOLMAN MILLER SIGN, ANTRAL SIGN- in angiofibroma, pushes post wall of maxillary
*HONDOUSA SIGN--X-ray finding in Angiofibroma, indicating infratemporal fossa involvement
characterised by widening of gap between ramus of mandible and maxillary body.
*HENNEBERT SIGN- false fistula sign( cong.syphilis, Meniere's,)
*IRWIN MOORES SIGN-------- positive squeeze test in chronic tonsillitis
*LIGHT HOUSE SIGN--- seeping out of secretions in acute OTITIS media
*LYRE'S SIGN - splaying of carotid vessels in carotid body tumor
*MILIANS EAR SIGN- Erysipelas can spread to pinna(cuticular affection), but cellulitis cannot.
*PHELP'S SIGN - loss of crust of bone bet carotid canal and jugular canal in glomus jugulare
*RACOON SIGN-Indicate subgaleal hemorrhage,and not necessarly base of skull #
*STEEPLE SIGN- X-ray finding in Acute Laryngo tracheo bronchitis
*STANKIEWICK'S SIGN - indicate orbital injury during FESS. fat protrudes into nasal cavity on
compression of eye ball from ouside
*THUMB SIGN --X-ray finding A/c epiglottitis
*TRAGUS SIGN- EXTERNAL OTITIS , Pain on pressing Tragus
*TEA POT SIGN is seen in CSF rhinorrhoea..
*WOODS SIGN----- palpable jugulodigastric lymphnodes.
TEAR DROP SIGN
Seen in Orbital floor fracture. tear drop shaped opacification seen hanging from the roof of the maxillary sinus on water's view.
= blow-out fractures is the presence of a polypoid mass (the tear-drop) protruding from the floor of the orbit into the maxillary
antrum The tear-drop represents the herniated orbital contents, periorbital fat and inferior rectus muscle.

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Ear Sheet
- - - - - - :
DD of CHL: unilateral/Bilateral, MCC:wax- perforation, tympanosclerosis, otosclerosis, Tumor:Glomus,
cholesteatoma
Do not forget to examine Nose in Ear or laynx case
Weber test 1st: air, then bone, air, ( flick fork between index and thumb) lat to Dx ear= CHL
Renne Test:
How to calculate Air-Bone Gap: @ 500,+1000,+2000/divide by 3
Is it benificial for pt to do Myringoplasty/ tympanoplasty: TM+ osscile(TORP/
Complication of Cholesteatoma: intracranial: headach, fistula, pulsatild discharge, do CT
Complication of Mastoidectomy
VII palsy: landmark anterior-inferior to Lateral SCC, behind short process of incus
What is Fistula tes
False -ve: if cholesteatoma covered the fistula
False +ve: in Meniere, and syphilis
DD of pulsatile ear discharge: glomus- SCC Dehience,
Nose Sheet Cases

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 - - -
Exam: ant rhinoscopyDescribe polyp: firm, gray, mobile( by probe) smooth/fungiform,from middle meatus/septum
Perforated septum: anter= cartilage= TB, post perfor= Syphilis
Polyp: DD of unilateral, by age, 2 m: menigoenchephalocele, cystif fibrosis, angiofibroma, Antrochoalnal poly,
Tumore: Inverted pappiloma, Sq CC, mycetoma( Bropwn discharge

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