Transcript Otalgia - The Medical Post | Trusting Medicine

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