Otalgia, Temporal bone fracture, C.S.F. otorrhea, Ototoxicity Dr. Vishal Sharma

Otalgia, Temporal bone fracture, C.S.F.

otorrhea, Ototoxicity

Dr. Vishal Sharma

Otalgia

Etiology of Primary Otalgia Pinna

• Laceration & bite

• Hematoma

• Otitis externa

• Perichondritis

• Infected pre-auricular sinus

• Frostbite, sunburn

• Neoplasm

External auditory canal

• Impacted wax

• Foreign body

• Keratosis obturans

• Otitis externa

• Herpes zoster oticus

• Exostoses

• Neoplasm

Middle Ear

• Bullous myringitis

• Acute otitis media

• Secretory otitis media

• Traumatic perforation

• Hemotympanum

• Otitic barotrauma

• Neoplasm

Mastoid

• Mastoiditis

• Mastoid abscess

• Granulomas

• Neoplasm

Inner ear

• Acoustic trauma

• Meniere’s disease

• Vestibular schwannoma

Etiology of referred otalgia

A. Via trigeminal nerve

• Teeth: infection, impacted 3rd molar, malocclusion

• Oral cavity: infection, ulcer, malignancy, Ludwig’s

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

• Eagle’s 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 &

arthritis

Temporal bone fracture

Introduction

• 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)

• Kernig’s & Brudzinski’s test: for meningitis

Features Longitudinal TransverseIncidence 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, delayed onset

50%, permanent, early onset

Vertigo + nystagmus Occasional Common, severe

CT scan axial cutLongitudinal Transverse

Treatment of facial nerve palsyA. 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

exploration

C.S.F. otorrhea

Introduction

Abnormal communication between subarachnoid

space & tympano-mastoid space leading to

discharge of cerebrospinal fluid through external

auditory canal or via Eustachian tube into

nasopharynx

EtiologyA. 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 Hyrtl’s fissure (congenital fusion plane

found b/w otic capsule & jugular bulb)

– wide vestibular aqueduct (Mondini’s 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

Investigations• 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

Ototoxicity

Definition

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 definitionPure 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.

• Tinnitus

• 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

Aminoglycosides

• 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

Macrolides

• Drugs: Erythromycin, Azithromycin, Clindamycin,

Vancomycin

• Cause reversible ototoxicity

• Onset generally within 3 days of starting treatment

• Speech frequencies affected rather than higher

frequencies

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 &

reversible

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

• Quinine

• 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: • Rare

• Only possible if mastoid cavity is open or

tympanic membrane perforated

Brock’s 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

Management• 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

• α-tocopherol (vitamin E derivative)

• D-methionine (amino acid)

• Desferrioxamine (iron chelator)

• N-acetyl-cysteine (antioxidant)

• Caspase & Calpain inhibitors (prevent apoptosis)

• Gene therapy

Thank You