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Otalgia, Temporal bone fracture, C.S.F. otorrhea, Ototoxicity Dr. Vishal Sharma Otalgia 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 • Bullous myringitis • Acute otitis media • Secretory otitis media Mastoid • Mastoiditis • Mastoid abscess • Granulomas • Neoplasm • Traumatic perforation • Hemotympanum Inner ear • Acoustic trauma • Otitic barotrauma • Meniere’s disease • Neoplasm • 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, posttonsillectomy, 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 posterosuperior 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 Incidence Trauma site Longitudinal Transverse 80% 20% 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 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 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 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 • 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 + transmastoid). 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-LanguageHearing 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. • 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 (highfrequency 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 cochleotoxic; 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