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Otalgia, Temporal

bone fracture, C.S.F.

Dr. Vishal Sharma
Etiology of Primary Otalgia
Pinna External auditory canal
Laceration & bite Impacted wax
Hematoma Foreign body
Otitis externa Keratosis obturans
Perichondritis Otitis externa
Infected pre-auricular sinus Herpes zoster oticus
Frostbite, sunburn Exostoses
Neoplasm Neoplasm
Middle Ear Mastoid
Bullous myringitis Mastoiditis

Acute otitis media Mastoid abscess

Secretory otitis media
Traumatic perforation
Inner ear
Acoustic trauma
Otitic barotrauma Menieres disease
Neoplasm Vestibular schwannoma
Etiology of referred
A. Via trigeminal nerve
Teeth: infection, impacted 3rd molar, malocclusion
Oral cavity: infection, ulcer, malignancy, Ludwigs
angina, sialadenitis, salivary calculus
Temporo-mandibular joint: arthritis, dysfunction
Nose & PNS: impacted DNS, sinusitis, neoplasm
Nasopharynx: infection, post- adenoidectomy,
adenoiditis, tumor
Trigeminal neuralgia
B. Via glossopharyngeal nerve

Tonsil: tonsillitis, peritonsillar abscess, post-

tonsillectomy, neoplasm

Oropharynx: infection, ulcer, retropharyngeal +

parapharyngeal abscess, trauma, neoplasm

Eagles syndrome (stylalgia)

Glossopharyngeal neuralgia
C. Via facial nerve:

Herpes zoster oticus, vestibular schwannoma

D. Via vagus nerve:

Larynx + hypopharynx: neoplasm, infection,
tuberculosis, trauma,
foreign body

E. Via second & third cervical nerves:

Herpes zoster, cervical spondylosis &
Temporal bone
30% of head trauma cases result in skull fracture

Temporal bone # comprises 15-25% of all skull #

Classification of temporal bone fracture:

1. Longitudinal (80%)

2. Transverse (20%)

Recent view: > 90% are mixed or oblique fractures

especially in severe trauma

Longitudinal fracture
80% of all temporal bone fractures

Caused by lateral blows over temporal bone

Fracture line parallels long axis of petrous pyramid

Starts in pars squamosa, extends through postero-

superior bony external canal, continues across roof

of middle ear space (anterior to labyrinth), ends
antero-medially in middle cranial fossa in close
proximity to foramen lacerum & ovale
Longitudinal fracture
Clinical features
Bleeding into ear canal from skin & TM laceration

External auditory canal fracture, hemotympanum

Conductive deafness: due to ossicular disruption

Facial nerve paralysis (20%): late onset, involves

tympanic segment, usually temporary

CSF otorhinorrhea: common, usually temporary

Sensori-neural hearing loss & vertigo are rare

Transverse fracture
20% of all temporal bone fractures

Caused by frontal or occipital blows

Fracture line at 900 to long axis of petrous pyramid

Starts in middle cranial fossa (close to foramen

lacerum), crosses petrous pyramid transversely &

ends at foramen magnum. May extend through

internal auditory canal & injure nerves directly.

Transverse fracture
Clinical features
Profound sensori-neural hearing loss

Severe ablative vertigo

Third degree nystagmus present with fast

component beating away from fracture site
Facial nerve paralysis (50%): early onset, permanent

Intensity of vertigo + nystagmus es after 7-10

days, continues to decrease steadily until
compensation finally occurs after 3-6 months
Examination for temporal #
Complete neurologic + ENT examination

Otoscopy: EAC & TM lacerations, fracture lines

Siegalization: for presence of fistula

Eyes for nystagmus (direction + degree)

Tuning fork tests: type of hearing loss

Battle sign (ecchymosis of postauricular skin)

Raccoon sign (ecchymosis of periorbital area)

Kernigs & Brudzinskis test: for meningitis

Features Longitudinal Transverse
Incidence 80% 20%
Trauma site Temporal or parietal Frontal / occipital
CSF leak Otorrhea Oto-rhinorrhea
Hemotympanum Occasional Common
EAC lacerations Common Occasional
TM perforation Common Occasional
Otorrhagia Common Occasional
Hearing loss Conductive Sensori-neural
Facial palsy 20%, temporary, 50%, permanent,
delayed onset early onset
Vertigo + nystagmus Occasional Common, severe
CT scan axial cut
Longitudinal Transverse
Treatment of facial nerve palsy
A. Delayed onset & incomplete facial paralysis:
oral Prednisolone for 2 weeks + observation

B. Immediate onset or complete paralysis Nerve

stimulation done b/w days 3 to 7 of trauma:
no loss of stimulability occurs: observation

loss of stimulability within 1 week or >90%

degeneration on ENOG within 2 wks: surgical
C.S.F. otorrhea
Abnormal communication between subarachnoid

space & tympano-mastoid space leading to

discharge of cerebrospinal fluid through external

auditory canal or via Eustachian tube into

A. Acquired (more common)
Operative trauma: mastoidectomy, stapedectomy,
vestibular schwannoma excision, skull base surgery
Accidental trauma

Non-traumatic: infection, neoplasm

B. Spontaneous
Bony defect theory

Arachnoid villi granulation theory

Congenital defect theory: SNHL present
enlarged petrosal facial nerve canal
patent Hyrtls fissure (congenital fusion plane
found b/w otic capsule & jugular bulb)
wide vestibular aqueduct (Mondinis dysplasia)
annular ring of stapes footplate
Dehiscent tegmen plate
Arachnoid villi granulation theory: SNHL absent
Enlargement of arachnoid villi due to congenital
entrapments / large pressure variations
Wide facial nerve canal
Patent Hyrtl fissure
Wide vestibular aqueduct
Arachnoid villi granulations
Clinical features
H/o surgery / accidental trauma
Clear watery discharge from ear or nose:
appears during straining or leaning forward (Dandy
maneuver); salty taste
Unilateral hearing loss:
Sensori-neural: abnormality of inner ear
Conductive: leak elsewhere in temporal bone
Unexplained episode of meningitis
Confirmatory test for CSF: glucose level > 30
mg/dL; presence of beta 2 transferrin
High-resolution CT scan with contrast
Abnormality of otic capsule: Mondini deformity
Wide vestibular & cochlear aqueducts
Tegmen plate defect
Localization of leak with intrathecal Iohexol
Presence & location of pneumocephalus
Medical treatment
1. Compressive dressing + bed rest (head elevation)

2. Prophylactic antibiotics indicated in:

post-traumatic CSF leakage

immuno-suppressed patient

obvious soilage of central nervous system

postoperative & spontaneous leaks (controversial)

3. Medications to decrease production of CSF
a. Diuretics ( Frusemide, hydrochlorothiazide)
b. Carbonic anhydrase inhibitors (Acetazolamide)

4. Steroids (to reduce inflammation)

Hydrocortisone, dexamethasone
5. Continuous lumbar CSF drainage
Allows natural healing
Surgical treatment
Primary closure with multi-layer technique using

cartilage + muscle + fascia + fat + bone wax

Approaches: Trans-canal, Trans-mastoid, Middle

cranial fossa, Combined (middle fossa + trans-

mastoid). Combined approach for large defect (>2cm),
multiple defects, or defects that extend anteriorly.

Refractory cases: obliteration + closure of EAC

Tendency of certain therapeutic agents & other

chemical substances to cause functional

impairment + cellular degeneration of tissues of

inner ear (especially end organs) & neurons of

cochlear + vestibular division of the eighth

cranial nerve (Hawkins, 1976)

American Speech-Language-
Hearing Association definition
Pure tone audiometry:
20db or greater decrease in pure-tone threshold at
one frequency
10db or greater decrease at 2 adjacent frequencies

Otoacoustic Emissions or BERA:

loss of response at 3 consecutive test frequencies
where responses were previously obtained
Classification of
ototoxic agents
1. Acetyl salicylic acid (Aspirin)

2. Anti-malarial: quinine, chloroquine

3. Loop diuretic: ethacrynic acid, furosemide, bumetanide

4. Antibiotic: aminoglycoside, macrolide

5. Anti-neoplastic: cisplatin, bleomycin, 5-fluorouracil

6. Beta blocker: propranolol, atenolol, metoprolol

7. Anti-convulsant: phenytoin, carbamazepine

8. Topical: betadine, alcohol, chloramphenicol, ciprofloxacin

9. Miscellaneous: desferrioxamine, bromocriptine, imipramine

Clinical features
Hearing loss: B/L, symmetrical, high frequency,

sensori-neural; temporary / permanent; may

not manifest until several weeks or months

after completion of ototoxic agent therapy.


Vestibular toxicity: positional nystagmus,

oscillopsia & dysequilibrium

Mechanisms of ototoxicity
Direct hair cell damage: outer hair cells affected

first. Begins at basal turn of cochlea (high-

frequency sloping SNHL) & proceeds toward apex
(involvement of lower frequencies too)

Direct vestibular injury

Direct damage to stria vascularis

Metabolic (non-morphologic) damage

Acetyl salicylic acid
Tinnitus: main symptom

Hearing loss: sensori-neural, reversible (within 72

hours of withdrawal), flat curve on audiogram

Etiology: multi-factorial due to metabolic rather

than morphological damage to cochlea

Ototoxicity first with Streptomycin (1944)

Streptomycin, Gentamicin, Netilmicin: primarily

vestibulotoxic; destroy type 1 hair cells of crista ampullaris

Kanamycin, Amikacin, Neomycin: primarily cochleo-

toxic; damage outer hair cells at basal turn of cochlea

Tobramycin: vestibulotoxic + cochleo-toxic

Aminoglycoside clearance
Aminoglycosides cleared more slowly from inner

ear fluids than from serum latency exists to

ototoxic affects of aminoglycoside progression

of hearing loss or onset of hearing loss after

cessation of aminoglycoside treatment + prolonged

susceptibility to noise-induced hearing loss

Drugs: Erythromycin, Azithromycin, Clindamycin,


Cause reversible ototoxicity

Onset generally within 3 days of starting treatment

Speech frequencies affected rather than higher

Loop diuretics
Drugs: ethacrynic acid, furosemide, bumetanide

Mechanism: changes in ionic gradients between

perilymph & endolymph causing edema + damage

of stria vascularis

Ototoxicity dose dependent, self limited &

Anti-neoplastic agents
Drugs: cisplatin, carboplatin, bleomycin, 5-fluorouracil

Mechanism: Multi-factorial, partially mediated by

free-radical production. Damage stria vascularis +

outer hair cells at basal turn of cochlea.

Hearing loss bilateral, sensori-neural, progressive

& irreversible
Toxicity produces tinnitus, hearing loss, vertigo,
headache, nausea & vision loss
Hearing loss usually sensori-neural & reversible

Characteristic notch often present at 4000 Hz

Oto-topical agent:
Only possible if mastoid cavity is open or
tympanic membrane perforated
Brocks grading of ototoxicity
Grade 0: threshold < 40 dB HL at all frequencies

Grade 1: threshold > 40 dB at 8000 Hz

Grade 2: threshold > 40 dB at 4000 - 8000 Hz

Grade 3: threshold > 40 dB at 2000 - 8000 Hz

Grade 4: threshold > at 40 dB at 1000 - 8000 Hz

High Risk Patients
Larger doses of ototoxic agent
Higher blood levels of ototoxic agent
Longer duration of therapy with ototoxic agent
Receiving other ototoxic or nephrotoxic agent
Elderly patients
Renal insufficiency
Preexisting hearing problems
Family history of ototoxicity
No therapy available to reverse ototoxic damage.
Awareness of ototoxic agents & drug monitoring
during treatment. Prompt reporting of tinnitus, hearing
loss, oscillopsia & vertigo.
Alternative therapy for high-risk patients.
Avoid noisy environments for 6 months after treatment
completion. Avoid co-prescription of ototoxic agents.
Amplification with hearing aid or cochlear implant.
Ototoxicity prevention drugs
-tocopherol (vitamin E derivative)

D-methionine (amino acid)

Desferrioxamine (iron chelator)

N-acetyl-cysteine (antioxidant)

Caspase & Calpain inhibitors (prevent apoptosis)

Gene therapy
Thank You