SOME EAR DISORDERS

DEPT OF OTOLARYNGOLOGY-SMD/CHS-KNUST
EAR
EAR DRUM
A Section of Cochlear
Symptomatology of the Ear
Otalgia
Otorrhea
Otorrhagia
Hearing loss
CSF Otorrhea
Tinnitus
Vertigo
Symptomatology of the Ear
Imbalance
Autophony
Ear Fullness/Heaviness
Hyperacusis
Itchy ear Ear tugging
Myiasis
FB in the Ear
Mass/Swelling/Something in the Ear
Symptomatology of the Ear
Constitutional Symptoms
Fever Vomiting
Chills Abdominal discomfort & Diarrhea
Headache Anorexia/Poor feeding
Malaise Decreased performance @ School/Work
Insomnia Convulsions
Irritability
CONGENITAL ANOMALIES
Microtia Macrotia
Anotia Atresia
Bat Ear
Lot Ear
Wildermuth’s Ear Collaural Fistula
Ear Tags A Ears
Preauricular Sinus
Stenosis-Meatal / Canal
 OTITIS EXTERNA ( SWIMMERS’ EARS )
Risk Factors
-PH Changes: Warm Humid Env’t. Anatomic Obs: EAC stenosis, Eostoses, Wax Impactions
-Disrupted Epithelium : Ears picking, Hearing aid or plug use
CLASSIFICATION

Infective (Dermatitis) Circumscribed

Reactive (Dermatosis) Diffused
Infective
a. Bacterial
i-Non-specific :( Furunculosis, Perichondritis, and Otitis Externa)
ii-Specific : ( Lupus vulgaris )
b. Malignant Otitis
c. Fungal Otomycosis
d. Viral ( Herpes simplex and Herpes zoster )
OTITIS EXTERNA

Reactive
a. Seborrheic / Psoriatic dermatitis
b. Neuro-dermatitis
c. Allergic dermatitis
d. Eczematous
OTITIS EXTERNA
TREATMENT
a. General
b. Local

-Pain Relief
-Warm compresses
-Aural Toileting , suctioning, Irrigation.
-Specific Treatment-Topical and/or Systemic. Based on possible c/s
-Treatment of risk factors DM, Vit. deficiency, etc.
-Surgical (Debridement, treating stenosis and Perichondritis )
 OTITIS MEDIAS (OM)
Definition: Inflammation of middle ear cleft; i.e. tympanic cavity, Eustachian tube, mastoid antrum
and mastoid air cells

Types:
Acute:3-4 wks Subacute: 3 or 4 wks – 3mo Chronic: 3mo & above
Acute OM Chronic OM
a. AOM a. Chr. Non Specific OM
b. ASOM OME
CSOM with or without Cholesteatoma
Adhesive Otitis
Atelectactic Ear
Tympanosclerosis
Cholesterol granuloma
b. Chr. Specific OM
Tuberculous OM
Acute Otitis Media
Common Precursors
Rhinitis
Sinusitis
Tonsillitis
Pharyngitis
Nasopharyngitis(Chlorinated H2O)
Others
TM perforations
Swimming/Diving
Nasal/Throat surgeries
Postnasal packing
Exxv Nose blowing
Acute Otitis Media
Risk Factors in Children
Anatomy; Eustachian tube, Cleft palate, (GERD), Adenoids hyp.

Functional; Cerebral palsy, Immunodeficiencies, Other Neurological dx.s

Cilliary dyskinesia, Cystic fibrosis, Down syndrome, Allergies

Environmental; Bottle feeding, Passive smoking, Low socioeconomy

Day Care attendance, Poor Housing & Overcrowding.
Acute Otitis Media
Antecedent Viral URTI’s---Respiratory syncytial virus
and influenza virus etc.
Initiation of infection cascade
Release of inflammatory mediators
Bacterial colonization & adherence
Host immune suppression
Acute Otitis Media
Bacteriology
Acute O/M Chronic O/M
-Strep. Pneumonia;35% -(G-ves e.g.) Pseudomonas auregnosa,
-H. Influenzae ;23% Proteus sp. , E coli
-Moraxella (Branhamella) -(Anaerobes e.g. ) Bacteroides fragilis
catarrhalis 14%
-Hemolytic streptococcus - Staphylococcus albus and aureus
Acute Otitis Media
PATHOGENESIS
Tubal (Eustachian) dysfunctioning
STAGES
Stage I- Hyperemia
Acute tubal occlusion phase.
(Ac. Eustachian salpingitis).
Otalgia, Fullness, Fever,
Injection of TM along manubrium and periphery,
Retraction of TM,
CHL, Autophony
Acute Otitis Media
Stage II – Exudation
Presuppurative phase. Between 12 and 24 hours
Infection of the tympanic cavity.
( Ac. Tympanitis commonly called “ ACUTE OTITIS MEDIA”)
In addition to above; Red, thickened, bulging TM,
Lusterless with loss of landmarks,
Bubbling sound in the ear
Otalgia at its peak.
NORMAL/ABNORMAL
Acute Otitis Media
Stage III —
Suppurative phase
Spontaneous rupture of TM,
Otorrhea (serous, bloodstained, mucopurulent or purulent)
SUDDEN DROP of Fever, Otalgia and Mastoid pain if was present.
Lighthouse sign -Pulsation of pus in the EAC

Stage IV –
Coalescence/Surgical Mastoiditis phase ( 1-2 wks. after onset)
Mucopurulent Otorrhea, Mastoid tenderness,
Sagging of posterosuperior EAC wall
Acute Otitis Media
DIAGNOSIS
History, Clinical examination, Tuning fork tests, Audiometry,
Tympanometry, Tympanocentesis & C/S , etc.
TREATMENT
General: Bed Rest, Sedation,, Warm compresses,
Medical: Antibiotics, Analgesia, Antipyrexia, Nasal drops,
Ear drops, Steroids in adults.
Surgical: Myringotomy, Grommets insertion, Adenoidectomy,
Mastoidectomy, Tympanoplasty, Ossiculoplasty.
Rehabilitations: H-Aids
Preventions: Immunization, MDG’s attainments etc.
Acute Otitis Media
COMPLICATIONS
Intratemporal Chronic O/M
CHL, SNHL, TM Perforation, Retraction Pockets, Mastoidits,Bezold’s abscess
Petrositis, Gradenigo’s syndrome, Labyrinthitis, Perilymphatic Fistula
Cholesteatoma, Tympanosclerosis, Cholesterol granulomas, Facial paralysis,
Ossicular chain fixation,
Intracranial
Meningitis, Extradural abscess, Subdural abscess,
Otitic hydrocephalus, Focal Otitic encephalitis,
Brain abscess, Lateral (Sigmoid) sinus thrombosis
 RISK FACTORS FOR CHILDHOOD SNHL HEARING LOSS

Prematurity
Birth Weight Less than 1500gm
Congenital Craniofacial Anomalies
In Utero Infections
Hyperbilirubinemia requiring Exchange Transfusion
Apgar Scores less than 5 At 1 minute and than 7 At 5 minutes
Requirement for Mechanical Ventilation for 5 Days or Longer
Head Trauma (acoustic, blunt, penetrating)
Exposure to Ototoxic Agents
Family Hx. of hereditary childhood SNHL
Otitis Medias
CONGENITAL ACQUIRED FACTORS
Prenatal
Infections (TORCH)S
Cytomegalovirus(CMV)-1% to 2% live births;
90% asymptomatic(10% H/L )
CMV inclusion dix. (CID) (50% H/L)
Rubella- (1st or 2nd trimester )
Hazy discoloration of the cornea or
Opacification of the lens
Heart issues and Hearing loss
Toxoplasmosis;
Syphilis- (Meningoneurolabyrinthitis-Profound SNHL)
Herpes Simplex Encephalitis,
Cl. Tetani (Tetanus)
 CONGENITAL ACQUIRED FACTORS
Prenatal

Teratogens
-Alcohol
-Smoking
-Thalidomide
-Radiation(esp. 1st trimester)
-Ototoxins(cross the placenta)
Aminoglycosides, Antimalarial,
Chemotherapeutic agents
Gestational DM and Hypothyroidism
 CONGENITAL ACQUIRED FACTORS
Perinatal

Severe Perinatal Dx’s

-NICU admissions
-Hypoxia/Anoxia
-Kernicterus (injury to cochlear nuclear)
-Persistent fetal circulation
 CONGENITAL ACQUIRED FACTORS
Postnatal

Meningitis
-Results in supp. labyrinthitis
-Causes 25% of profound H/L in children
-Results in progressive ossification of the labyrinth
-Bacteria: S.pneumoniae, H.influenzae,
Neisseria meningitides, E. coli (neonatal)
-Decrease incidence and severity of H/L with
concomitant administration of systemic steroids
-Viral Infections; Measles, Mumps, Varicella, etc.
TINNITUS
Definition: Perception of sound not generated from the external environment.
Sound sensation originating from the head. No external stimulus.
TYPES
1-Subjective (95%) 2-Objective (5%)-
Sound able to be heard by the practitioner
3-Nonpulsatile 4-Pulsatile
5-Aural 6- Binaural (both ears)
7-Cerebri ( Centered in the head )
8-With Hearing Loss 9-Without Hearing Loss
Tinnitus-pathology & pathophysiology
OBJECTIVE TINNITUS
-Pulsatile (Vascular)
A-V malformations; Glomus tumors; Jugular bulb anomalies

Carotid stenosis , dissections, aneurysms, atherosclerosis;

Benign Intracranial HPT (pseudotumor cerebri. Binaural)

Tinnitus
High Cardiac Output States
Anemia HPT
Pregnancy Exercise
Thyrotoxicosis
Myogenic
Palatal myoclonus
Stapedius muscle contractions
Tensor tympani contractions
Patulous Eustachian tube
Tinnitus-pathology & pathophysiology
SUBJECTIVE TINNITUS
Involves tinnitus generation tinnitus perception
Tinnitus generation: resulting from some dysfunction in the auditory tracts
May result from CENTRAL or PERIPHERAL dysfunction

With Hearing loss Without Hearing loss

Wax, FBs, Otitis Externas/Media, -Psychogenic, Epilepsy,
Eustachian tube dysfunctioning, -Hypotension, Hypoglycemia,
Hemotympanum, Meniere’s dx. -Idiopathic, Migraine
Presbycusis, Ototoxicity, noise Exposure
Other causes SNHL
Tinnitus-pathology & pathophysiology
SUBJECTIVE TINNITUS
Pathogenesis (theories)
Cochlear pathology, Neural pathology, Central pathology, Jastreboff neurophysiological model
Factors Aggravating Tinnitus Factors Relieving Tinnitus
Stress/Fatigue, Changes in body position -Regular exercise
Excessive noise Exposure -Avoidance of noise ( earplugs and earmuffs )
URTI & Allergy -Keeping oneself busy
Moving jaws/Clenching teeth -Personal relationships and socialization
Head and neck trauma
Changes in altitude
Overuse of Alcohol, Caffeine, P’mol or Ibuprofen
Tobacco and Marijuana
Tinnitus-Treatment
TREATMENT

Treatment of DIAGNOSED conditions,

comorbidities and associated symptoms
Placebo (40% Efficacy)
No Medication
Homeopathy and Herbal preps (Also effective)
Hypnotherapy
Psychological or Psychiatric interventions
Tinnitus Retraining Therapy (TRT)-Counselling
Electrical Stimulation (50% effective)
 Tinnitus-Treatment
TREATMENT
Acoustic Therapies:
White noise & Use Pleasant environmental sounds
Tinnitus maskers; Sound pillows, Pillow speakers,
Headphones and Earphones
Hearing-Aids
Medical Therapies (Conservative Management)
-Vasodilators,
-Sedatives,
-Vitamins,
-Tranquilizers
-Zinc therapy,
-Carbamazepine and
-Clonazepam
Tinnitus-Treatment

SURGICAL TREATMENT; Treatment of the etiological cause.

PROGNOSIS;
Majority (90%-95%) of patients accommodate
their tinnitus within 3-6 months of onset.
OTOTOXICITY
Definition
Damage to the cochlear and/or vestibular part of inner ear by drugs.

Ototoxic drugs include:

Aminoglycosides
Cochleotoxicity greater than Vestibulotoxicity
Amikacin, Kanamycin, Dihydrostreptomycin
Vestibulotoxicity greater than Cochleotoxicity
Gentamycin, Streptomycin
Vestibulotoxicity equals Cochleotoxicity
Tobramycin
Neomycin has the highest incidence of ototoxicity
Netilmycin is the least ototoxic of all above
OTOTOXICITY
Pathology
AGs result in hair cell death.
1-Degeneration of stria vascularis
2-Degeneration of sensory epithelia (in organ of Corti and vestibular labyrinth)
In the cochlear, injury to;
-OHC greater than IHC
-Base greater than Apex

Symptoms
Cochleotoxicity----------------- Tinnitus and high freq. Hearing loss
Vestibulotoxicity--------------- Imbalance, ataxia and Oscillopsia (in bil. Vestibular loss)
OTOTOXICITY
Other Ototoxic drugs include:
1-Vancomycin—Potentiate effects of other ototoxic drugs
2-Loop Diuretics—Also potentiate ototoxicity of AGs
Esp. in children where it is IRREVERSIBLE
Eg. Furosemide, bumetanide and Ethacrynic acid
3- Cytotoxics---Cisplastin, Carboplatin and Nitrogen mustard
4-Analgesics----NSAIDS; Salicylates, Indomethacin,Phenylbutazone and Ibuprofen
(REVERSIBLE OTOTOXICITY)
5-Antimalarials---Quinine and Chloroquin. These cause REVERSIBLE OTOTOXICITY
6-Chemical-----Alcohol, Tobacco, Marijuana, Carbon monoxide poisoning
Topical applications—Chlorhexidine
7-Miscellaneous---Erythromycin(REVERSIBLE OTOTOXICITY),Ampicillin, Propranolol,
Propylthiouracil, Deferoxamine
OTOTOXICITY
FACTORS AFFECTING OTOTOXICITY
Age extremes
Prolonged use
Individual Dosage of drug
Cumulative dosage of drug
Route of administration
Coadministration of other ototoxins
Febrile state
Renal failure
Liver failure
Dehydration
OTOTOXICITY
TREATMENT

Preventive

1-Avoid or Discontinue ototoxic drugs. Use others

2-Monitor (Blood titers) Treatment
3-Monitor Hearing and Balance during treatment
 MENIERRE’S DISEASE

Definition
Idiopathic inner ear disorder X’sed by a triad of;

SNHL (Progressive)

Vertigo (Recurrent and Episodic, usually preceded aural fullness)

Tinnitus (Fluctuating)
MENIERRE’S DISEASE
Epidemiology

Males=Females
Peak incidence: Fifth decade

Pathology
Endolymphatic Hydrops
MENIERRE’S DISEASE PATHOGENESIS
 MENIERRE’S DISEASE Clinical Features
Clinical Features

SNHL (@ the Low frequencies Progressive)

Vertigo (Recurrent and Episodic lasting for hours, usually preceded aural fullness)

Tinnitus (Fluctuating)

Investigation: Audiometry-----------------------SNHL
Vestibular function test--------Support for diagnosis of Peripheral vestibular dx.
MENIERRE’S DISEASE TREATMENT
MEDICAL
-Salt Restriction Diets
-Diuretics
-Antivertiginous / Vestibular Suppressant Drugs

SURGICAL
-Endolymphatic sac (SHUNT) surgeries
-Vestibular/cochlear nerve divisions
-Labyrinthectomy
-Gentamycin Inner Ear Perfusion
LABYRINTHITIS
DEFINITION
Inflammation of the inner ear.
Acute onset of single episode of vertigo and hearing loss.

Classification:
-Toxic L.
-Viral L.
-Circumscribed L.
-Syphilitic L.
-Suppurative L. (Acute, Chronic, Healed)
LABYRINTHITIS
Patho(genesis)logy
Inflammatory infiltrate within the labyrinth.

--Viral infection within the inner ear

--Meningitis may result in bacteria spreading to the

inner ear via the IAC or Cochlear aqueduct.

--Otitis media may allow spread of bacteria to the

inner ear via the round or oval window
LABYRINTHITIS
Clinical Picture
Three Stages; (Acute, Chronic, Healed)

--Acute Stage- Nausea, Vomiting, Intense vertigo, Tinnitus, H/L and Nystagmus

--Chronic Stage-Total deafness in the affected ear and absence caloric reaction.

--Healed Stage-(Labyrinthitis Ossificans). After 6 months.

Relief from vestibular symptoms because
other ear is compensating
LABYRINTHITIS
TREATMENT

-Acute / Chronic Stages

…….Bed rest. IV Antibiotics. IV steroids. Anti vertiginous drugs.

Treatment of the cause (O/M, Meningitis) with Myringotomy
with or without Grommet insertion.

…….Labyrinthectomy
OTOSCLEROSIS/OTOSPONGIOSIS
Definitions
-Bony dysplasia of the temporal bone characterized by an initial
resorptive phase (spongiosis) followed by a deposition phase (sclerosis)
-Localized bony disorder ( osteodystrophy ) that
involves the labyrinth (Otic) capsule and
Results into bilateral gradually progressive hearing loss.
Incidence
More in whites
Twice in females
Over 90% bilateral
Onset Btn Puberty and 40yrs
OTOSCLEROSIS/OTOSPONGIOSIS

Etiology
Genetic / Hereditary; 60%
Viral (Measles)
Hormonal
Metabolic
OTOSCLEROSIS/OTOSPONGIOSIS
Locations
-Anterior to the oval window (fissula ante-fenestrum) 80%-90%
-Border of round window (30%-40%)
-Anterior to promontory
Clinical Features
CHL, Mixed HL, SNHL
Vestibular complaints(20%)
On Otoscopy: Schwartz's sign- Red blush on promontory
seen thru’ the TM in early dx.
Audiometry: Carhart’s notch- A dip of SNHL at 2000Hz on the audiogram
Acoustic reflex--Absent
OTOSCLEROSIS/OTOSPONGIOSIS

TREATMENT
Observation
Hearing amplification
Sodium Fluoride
Surgery-Stapedectomy / Stapedotomy
The Facial Nerve : Main Branches
•At geniculate ganglion -Greater petrosal n. –To Pterygopalatine ganglion

-Branch to Lesser petrosal n.

•In facial canal – -Stapedius n. - Chorda tympani n.
•At exit from stylomastoid (branches to the ff. )
foramen : -Post. Auricular n.
-Digastric m. (post. Belly)
- Stylohyoid m.

•On the face - Temporal -Zygomatic -Buccal

-Mandibular -Cervical
Facial paralysis - Etiology
INFECTIONS
◦Bell’s palsy(Herpes Simplex Mononeuritis)
◦Ramsay-Hunt syndrome
◦Herpes Zoster Oticus
◦ASOM
◦OME
◦CSOM, Cholesteatoma
◦Malignant Otitis Externa
(skull base osteomyelitis)
Facial paralysis – Etiology (cont’d)
Trauma
◦ Temporal Bone Fractures, RTA
◦ Penetrating Wounds Of Temporal Bone, Face
◦ Iatrogenic –Surgical Injury Esp. Mastoid/Temporal Bone
and Parotid Surgery
•Tumors
-Carcinoma -Ear, Parotid, etc.
-Glomus Jugulare or Tympanicum
-Cerebellopontine Angle Tumors
-Acoustic Neuroma/ Schwannoma
-Leukemia
-Sarcomas
Facial paralysis – Etiology (cont’d)
Metabolic Conditions /Miscellaneous
◦ Sarcoidosis
◦ Autoimmune disorders
◦ Guillain-Barre syndrome
◦ Melkerson-Rosenthal syndrome (Rec. Uni. / Bil. facial palsy in child/
adolescent with swelling lip /
tongue and fissured tongue.
Autosomal dominant, cause unknown).

*Generally over half of cases seen are Bell’s palsy,

Trauma about 20%, then
Ear infections, etc.
Clinical evaluation: History

+Good, careful hx. of onset and evolution of facial weakness -

may give idea of etiology and narrows scope of diff. diagnosis.

◦ Sudden onset or delayed/gradual

◦ Complete or incomplete
Clinical evaluation: History
+ Most causes can have sudden onset, but delayed appearance
often with many traumatic or infective pathologies.

• Palsies commonly evolve over first 2-3 weeks –

> complete degeneration or incomplete deg.
with evidence of recovery.
• Progression beyond 3 weeks ? possible neoplasm.
Facial paralysis - Symptoms
Common complaints –

-Facial weakness, difficulty with shutting eye or chewing food on

the affected side, facial asymmetry noticed;
face pulled to the normal side,
loss of nasolabial on the fold affected side.

-Associated symptoms may give diagnostic clue.

◦ Numbness in the face, Otalgia and Hyperacusis and
◦ taste alteration common in Bell’s palsy and Ramsay-Hunt Synd.
Facial paralysis - Symptoms
Common complaints –

Intense Otalgia and vesicular eruption

typical of Herpes Zoster infection (RH)
SNHL and vertigo may accompany RH but not Bell’s
•Trauma – evidence usually obvious –
Hx. of head or facial injury,
Surgical operations etc.
•Recurrent palsy may be due to tumor
But more common with Bell’s or
Melkerson –Rosenthal syndrome.
Facial paralysis – Examination & Signs
Examination & Signs
Full head and neck evaluation.
Thorough exam. of the ear and Upper Aerodigestive tract.
Focus on motor function of CN.7th nerve.
-In LMN (Peripheral) palsy all facial muscles
the on affected side are involved.
-In UMN (Central) lesion the upper face / forehead is spared.
Patient is requested to frown, close eyelids tightly,
smile or pucker the lips.
Facial paralysis – Examination & Signs
Examination & Signs

Paresis refers to incomplete paralysis.

Complete paralysis- No movement in facial musculature.
In true paresis- prognosis for recovery generally good.
Treatment is less urgent
Complete paralysis however requires rapid assessment ,
including electrophysiological tests,
so that management to prevent
further neural deterioration can be instituted.
BELL’S PALSY
DEFINITION
Facial paralysis of acute onset and limited duration –
Often rapid onset, minimal associated symptoms and spontaneous recovery.
The most common diagnosis in patients seen with acute facial paralysis.
Some cases appear to follow mild viral fever, or even prolonged cold draught.
ETIOLOGY
Long considered idiopathic, mainly by exclusion.
More recently, viral etiology postulated – herpes simplex virus (HSV).
Polymerase chain reaction techniques have helped in identification of HSV
in geniculate ganglion and nerve in patients.
BELL’S PALSY
PATHOLOGY

-Swelling of nerve - usually in vertical mastoid segment

edema sequel to ischemia
-Due to the usual level of the pathology, lacrimation is normal,
and if (commonly) below chorda tympani taste is usually present.
-Up to 75% have complete recovery within 1 month
since nerve lesion is neuropraxia-reversible

◦ Another 10 (-15) % have partial recovery, sometimes up to 3 months after

◦ Remaining 10-15% -no recovery due to complete degeneration
BELL’S PALSY-Treatment

-Effect of either medical or surgical intervention on the

course of recovery is diificult to prove and contrversial,
since majority (up to 85%) will attain recovery eventually anyway.
-Steroids most widely used – though no irrefutable proof of efficacy.
-However believed to prevent denervation and
progression of paralysis , and to speed recovery.
-Effect is best if started in first 3 days.
-Prednisolone 20-30 mg daily for 3-4 days the tapered off next 10 days.
-Additional antiviral, Acyclovir now recommended by some – 1G daily for 7 days.
 BELL’S PALSY-Treatment
•Physiotherapy – massage, heat and galvanic stimulation
to maintain muscle tone
•Eye patch- to protect cornea + eye drops
•Tarsorhaphy- in prolonged cases
•Nerve decompression -Early immediate decompression
where nerve excitability is lost
and other tests point to nerve degeneration.
Facial paralysis - Otitis Media
Treatment
Facial palsy from ASOM implies inflammation of the nerve within the bony facial canal
Or due to dehiscence. Treatment as usual for ASOM, but with parenteral antibiotics.
Myringotomy or even cortical Mastoidectomy may be done in some cases.
Nerve exploration is not usually required.
Unless nerve excitability is lost (with EP tests)
CSOM with Cholesteatoma –
Dev’t of palsy is an indication for immediate Mastoidectomy;
Cholesteatoma being an irreversible disease process
with erosion /destruction of the nerve.
Treatment Options - Surgical
PROCEDURES
-Hypoglossal crossover; hypoglossal-facial anastomosis
-Masticatory muscle/masseter transfer
-Facial nerve grafting
-Facial sling procedures esp.
where facial muscles are degenerated
-Tarsorrhaphy to protect cornea
Improvement, never complete,
requires good motivation,
physiotherapy support and
diligent practice of facial movements.
 FURTHER READINGS
• SCOTT BROWN’S OTORHINOLARYNGOLOGY,HEAD & NECK
• BRYON BAILEY
• SYNOPSIS OF ENT
• CUMMINGS ORL,HEAD & NECK
• BALLENGER’S ORL ,HEAD & NECK
• BLACKWELL.OPERATIVE.OTORHINOLARYNGOLOGY