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

2. Otalgia

4. 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

11. 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

12. 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

13. 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

14. Temporal bone
fracture

15. 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

17. 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

18. Longitudinal fracture

19. 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

20. 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.

21. Transverse fracture

22. 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

23. 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

24. 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,
delayed onset
50%, permanent,
early onset
Vertigo + nystagmus Occasional Common, severe

25. CT scan axial cut
Longitudinal Transverse

26. 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

27. C.S.F. otorrhea

28. 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

29. 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

30. • 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

31. Wide facial nerve canal

32. Patent Hyrtl fissure

33. Wide vestibular aqueduct

34. Arachnoid villi granulations

35. 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

36. 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

37. 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)

38. 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

39. 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

40. Ototoxicity

41. 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)

42. 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

43. Classification of
ototoxic agents

44. 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

45. 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

46. 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

47. 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

48. 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

49. 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

50. Macrolides
• Drugs: Erythromycin, Azithromycin, Clindamycin,
Vancomycin
• Cause reversible ototoxicity
• Onset generally within 3 days of starting treatment
• Speech frequencies affected rather than higher
frequencies

51. 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

52. 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

53. • 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

54. 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

55. 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

56. 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.

57. 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

58. Thank You