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Otalgia, Temporal bone fracture, C.S.F. otorrhea, Ototoxicity
Dr. Vishal Sharma
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Otalgia
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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
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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
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Etiology of referred otalgia
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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
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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
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C. Via facial nerve: Herpes zoster oticus, vestibular schwannoma D
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
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Temporal bone fracture
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Introduction 30% of head trauma cases result in skull fracture
Temporal bone # comprises 15-25% of all skull # Classification of temporal bone fracture: Longitudinal (80%) Transverse (20%) Recent view: > 90% are mixed or oblique fractures especially in severe trauma
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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
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Longitudinal fracture
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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
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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.
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Transverse fracture
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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
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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
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20%, temporary, delayed onset 50%, permanent, early onset
Features Longitudinal Transverse Incidence 80% 20% Trauma site Temporal or parietal Frontal / occipital CSF leak Otorrhea Oto-rhinorrhea Hemotympanum Occasional Common EAC lacerations TM perforation Otorrhagia Hearing loss Conductive Sensori-neural Facial palsy 20%, temporary, delayed onset 50%, permanent, early onset Vertigo + nystagmus Common, severe
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CT scan axial cut Transverse Longitudinal
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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 exploration
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C.S.F. otorrhea
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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
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Etiology 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
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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
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Wide facial nerve canal
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Patent Hyrtl fissure
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Wide vestibular aqueduct
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Arachnoid villi granulations
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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
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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
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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)
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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
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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
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Ototoxicity
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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)
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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
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Classification of ototoxic agents
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1. Acetyl salicylic acid (Aspirin) 2
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
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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
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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
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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
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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
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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
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Macrolides Drugs: Erythromycin, Azithromycin, Clindamycin, Vancomycin
Cause reversible ototoxicity Onset generally within 3 days of starting treatment Speech frequencies affected rather than higher frequencies
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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
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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
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Quinine Oto-topical agent:
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
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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 Hz Grade 3: threshold > 40 dB at Hz Grade 4: threshold > at 40 dB at Hz
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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
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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.
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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
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Thank You
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