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Noise-induce hearing loss

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Title: Noise-induce hearing loss Ototoxicity Author: Computer Last modified by: iLLUSiON Created Date: 1/7/2007 1:14:54 AM Document presentation format – PowerPoint PPT presentation

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Title: Noise-induce hearing loss


1
Noise-induce hearing loss Ototoxicity
  • ??? ??.??????? ??????????
  • ????????????????
  • ?.??????? ???????

2
Noise - induce hearing loss
  • Pure tone one frequency (ex. Tuning fork
    ,piano)
  • Complex tone multi frequency ( ex. Talking
    ,music)
  • Noise undesirable loud sound to harm hearing

3
Measurement of noise
  • Frequency(Hz)
  • Sound pressure level (SPL) measure by sound level
    meter (SLM) in decibel unit
  • dBA scale is weighting formula measure sound
    level minimal threshold sensitivity curve for
    human ears
  • -greater weight at 1 to 5 kHz

4
  • Pathogenesis
  • Rupture mb of outer hair cell
  • Inc.glutamate,NO,produce ROS free radical
  • Dec. Mg , inc. Ca in intracellular

5
PATHOGENESIS
  • Temporary threshold shift (TTS) exposure
    moderately intense sounds and lead to elevate
    thresholds for higher mid frequency (3000-6000
    Hz)
  • TTS can occur minute to hr day and it can
    recovery in 16 hr (24 hr)
  • If TTS is not recovery reexposed to noise , it
    change to PTS
  • Longer expose gt increase TTS but interrupt expose
    gtless TTS ( recovery within the rest interval)

6
???????????????????? Temporary threshold shift
  • ??????
  • - Temporary threshold shift ?????????????????????
    ?????? 100 ??????? ?????????? ????????????????????
    ??????????????? ??????????????????????????????????
    ??????? 40 ???????
  • - ????????????????????????????????????????????????
    ?????????????? ???????????????????????????????????
    ??????????????????????????????????????? 4000-6000
    Hz
  • - ?????????????????? TTS ???????????????? 2
    ??????? ?????????????????????????????

7
???????????????????? Temporary threshold shift
  • - ????????????????????????????????????????????????
    ??????????????????????????????????????????????????
    ???????? ?????????????????????????????????????????
    ???????????????????????????????????????????
    ??????????????????????????????????????????????????
    ?????????????????????????????????????????

8
???????????????????? Temporary threshold shift
  • - ????????????????????????????????????????????????
    ??????????? 1 ???? 2 ??????? ?????????????????????
    ?????
  • - ????????????????????????????????????????????????
    ??????????????????????????????????????????????????
    ????????
  • - ????????? Audiogram ????????????????????????????
    ??????????????????????????????????????????????????
    ??????????????

9
Permanent threshold shift (PTS)
  • Permanent threshold shift (PTS) elevated
    threshold is irreversible because cochlea is
    damaged
  • Protective against NIPTS
  • 1. expose intermittency
  • 2. acoustic reflex
  • 3. efferent innervation of OHC ( strong
    resistance to NIHL)
  • -The precise relationship between the TTS
    and PTS stages of hearing loss due to noise
    exposure is unknown
  • - Recent studies unrelated

10
Earliest changes in high freq. After 10 ys. loss
in high freq. tends to plateau
11
Pathology
  • TTS stereocillia of OHC are floppydisarray may
    recover function again
  • PTS fusion loss stereocilia , primary side
    inj. at rootlets(connection of stereocilia with
    top of hair cell)

12
  • PTS has been seperated to 2 Dz
  • Acoustic trauma
  • singer short lasting exposure to intense sound
    , painful
  • direct damage middle inner ear(organ of Corti,
    tearing Mb, rupturing cell, periendolymph to
    mix), not proceeded by TTs
  • NIHL
  • chronic exposure to less intense sound , result
    hearing loss ,damage inner ear ( gradual loss of
    stereocilia hair cell),proceeded by TTs
  • usually attributed to metabolic process

13
Acoustic trauma VS NIHL
??????????? Acoustic trauma Noise induced hearing loss
??????????????????? ?????????????????????????????????????????????????????????????????????????? ?????????????????????????????????????????????????????
??????????????? ????????????????????????????????????? ??????????????????????????? ????????????????????????????????????????????????????? ????????????????????????
???????????????????? ???????????????????????????????????????????????????????????? ??????????????????????????
?????????????????????? ?????????????????????????? ???????????????????? ??????????????????????????
14
Symp Obj finding in NIHL
  • Permanent SNHL with damage cochlear hair cell
    primarily OHCS
  • Hx long term expose to dangerous noise
    level(i.e., 90 dBA for 8 hour/day)
  • Gradual loss of hearing over 5-10 yr of exposure
  • Hearing loss that stabilizes once the noise
    exposure is terminated
  • Speech recognition score that are consistent with
    audiometric loss
  • Hearing loss involve initially higher frequency
    3-8 kHz before including lt 2kHz

15
Symp Obj finding in NIHL
  • symptom difficulty in hearing and
    understanding ordinary speech
  • Profile of noise - induced threshold hearing
    is usually symmetric for both ears.
  • Other forms of noxious sound, such as the
    gunfire associated with sport shooting cause
    an asymmetric pattern of hearing loss
  • Length of time of exposure to loud noise
    increases, hearing loss becomes greater and
    begins to affect adjacent higher and lower
    frequencies

16
Anatomic mechanisms underlying noise damage
  • Classical audiometric pattern NIHL 4 kHz notch
    explained by resonator fx of EAC
  • The other mech.
  • Severe motion basilar mb
  • Metabolic exhaustion of activated cell
  • Activity induce vv narrowing ? isch.
  • Ionic damage

17
New knowledge about cellular/Molecular
Mechanisms of Noise-Induced hearing Loss
  • Hair Cell Regeneration and Repair
  • -In human noise induced hair cell loss
    ? irreversible
  • -In animal Hair Cell Regeneration and
    Repair
  • Protection from Conditioning the Cochlear
    Efferent System
  • Both TTSPTS amount of threshold shift can be
    reduced by prior exposure toughening or
    conditioning
  • Efferent func. Of OHC related resistance to NIHL

18
New knowledge about cellular/Molecular
Mechanisms of Noise-Induced hearing Loss
  • Pharmacologic Protection from Noise Induced
    Hearing Loss
  • Hypoxia is a major pathogenic factor in
    NIHL
  • Noise-induced oxidative stress leading to
    cochlear injury was related to
  • (1) impaired mitochondrial function
  • (2) glutamate excitotoxicity
  • (3) depletion of glutathione (GSH)

19
  • pharmacologic agent
  • acetyl-L-carnitinehelp maintain mb of
    mitochondria
  • Carbamathione is glutamate antagonist
  • Allopurinol,xanthine oxidase blocker,N-L-acetylcys
    teine,GSHperoxidase,superoxide dismutate combat
    cellular oxidative stress

20
New knowledge about cellular/Molecular
Mechanisms of Noise-Induced hearing Loss
  • Susceptibility
  • Some ears are more easily damaged by noise
    than others.
  • Genetically cochlea (e.g., stiffness of the
    cochlear partition), or cochlear
    ultrastructure (e.g., density of hair cells).
  • Most exciting in current experimental
    research genetic origin.

21
Interaction
  • Age relate elevate SPL in adult (expose to
    noise) but not relate in elderly
  • HL sum of threshold shift from aging from
    noise

22
Interaction
  • Vibration relate elevate SPL in pt (expose to
    noise)
  • Drug chemical ototoxic drug
    aminoglycoside,Platinum anti tumor,Loop diuretic,
    salicylate
  • chemical (CO
    , hydrogen cyanide , toluene) relate elevate
    SPL in pt (expose to noise)
  • Individual susceptibility

23
Other Adverse Effects Caused By Noise
  • Damage to the vestibular system because
  • balance receptors are coupled with the auditory
    receptors.
  • Great similarity cochlear and vestibular hair
    cell ultrastructure.
  • Common arterial blood supply.
  • Complaints of disequilibrium.

24
Other Adverse Effects Caused By Noise
  • Nonauditory problems biologic stressor ?
  • prolonged activation of the autonomic nervous
    system, the pituitary-adrenal complex, resulting
    in general health impairment.
  • Circulatory problem, such as hypertension
  • Disorders involving gastrointestinal motility,
    such as peptic ulcers
  • Emotional unrest

25
Evaluate diagnosis
  • Hx PE
  • PTA
  • pure tone average asymmetriesgt 15dB ?another
    etiology or asymmetric exposure( rifles and
    shotguns)
  • NIHL is devided 2 type
  • Nonoccupational exposure
  • occupational exposure ( table diag.
    occupational NIHL)

26
table diag. occupational NIHL
27
Early detection of NIHL
  • Detecting small acoustically induced injuries
    to the organ of Corti (i.e., the beginning
    stages of NIHL)
  • OAEs is ideal for assesing cochlea fx , it well
    recognized sensitivity to detect OHC class of
    receptor cell which involved in initial stage
  • OAE 2 type
  • DPOAE
  • TEOAE

28
Treatment
  • Terminate noise at least 48 hr
  • if TTS is recovery in 16 hr
  • if HL gt 60 dB recovery 48 hr 20d
  • Anti noise elixir pharmacologic agent ,
    antioxidants and related compounds

29
Handicap compensation
  • Hearing handicap sufficient to affect the
    individuals efficiency in the activity living
    ,interfere with speech communication
  • Typical pt. can hear speech
  • without difficulty in vowel sound
  • difficulty discriminating among consonant sound
    (high frequency ,low intensity sound)

30
Hearing conservation program( HCP)
  • Essential components of HCP
  • 1. Noise measurement
  • -Assessment of noise levels
  • OSHA (occupational safety health
    administration) Regulations
  • 5dB rule
  • Allowable levels
  • 90dBA for 8 hours
  • 95dBA for 4 hours
  • 100dBA for 2 hours
  • 105dBA for 1 hour
  • 110dBA for 30 minutes
  • 115dBA for 15 minutes

31
Hearing conservation program( HCP)
  • 2. Engineering or administrative control to
    reduce exposure improve machine for dec. sound
    vibration
  • 3. Periodic audiometry f/u Serial audiograms
    , exam before start working and then exam every 6
    mo

32
4. Use of personal hearing protection
devices(HPDs)
Earplugs Earmuffs
33
  • ??????????????????????????????????????????????????
    ?????????????? ?????????????? ?????????????????

5. Education,motivation,counseling
34
Evaluation of hearing handicap in thailand
  • ??????????????????????? 12 ?? 2537
  • ??? 1 ?????????????????????????????????????????
    ???????? 18(2)????????????????????????????????
  • (5) ????????????????? ?????????????
  • (6) ??????????????? ?????????????
  • ????????????????????????????? 500 1000 2000 3000
    Hz gt25dB
  • ??????????????????????????? ??????????????????????
    ???????????????????????????1.5

35
Evaluation of hearing handicap in thailand
  • ????????????????????????????????????????
  • ????????????????????? 100 dB ??????? 100 dB
  • ???????????????????? 0 dB ??????? 0dB
  • ??????????????????????????????????????? 500 1000
    2000 3000 Hz
  • ??????????????????????
  • ???????????????????????? ???? ????????
    20??????????? 7020/10014
    ?????

36
Ototoxicity
  • Introduction
  • Ototoxicity tendency of a drug or
    chemical agent to cause inner ear
    dysfunction, producing symptoms of hearing
    loss, dizziness, or both.

37
Aminoglycoside Antibiotics
  • Vestibular toxicity 15 ????????????
    methylamine gr., Cochlear toxicity 20
    ???????????? free amino gr.
  • - Vestibular toxicity streptomycin,
    Gentamicin, Tobramycin, kanamycin, dmikacin,
    neomycin, netilmycin, sisomycin
  • - Cochlear toxicity neomycin, amikacin,
    kanamycin, tobramycin, Gentamycin,
    streptomycin, netilmycin, sisomycin

38
  • Pharmacokinetics
  • ????????????????????????????????????????? ???????
    perilymph ??? spiral ligament ??? stria
    vascularis ????????????????????? endolymph
    ???organ of Corti ????????
  • Histopathology
  • Cochlear and/or vestibular hair cells serve
    as primary targets for injury.
  • In the organ of Corti, OHC of basal turn
    are first damaged.
  • IHC more resistant.
  • Progressive destruction of spiral ganglion
    cells.
  • The stria vascularis become thinner.

39
  • Mechanisms of ototoxicity
  • Ototoxicity complex ? reactive oxygen
    species (ROS) react with various cell
    components, phospholipids, proteins, DNA? cell
    death.
  • Clinical Manifestations
  • High-frequency hearing loss,tinnitus
  • Continued exposure hearing loss progresses to
    lower frequencies.
  • Vestibular ototoxicity imbalance, ataxia,
    dramatically worsened by motion, with
    relative freedom from symptoms during periods
    of complete immobility.

40
  • Some clinical improvement (beginning 2 months
    after onset of symptoms) it is rarely
    complete ? irreversible HL
  • Various risk factors Bactermia, fever,
    hepatic and renal dysfunction, combinations of
    another ototoxicity drug

41
Suggested guidelines for monitoring
  • (1) In patients with normal kidney
    function, the peak level ( first day or two
    of treatment), the trough level (1 week)
    and both peak and trough levels (every week
    after )
  • (2) In patients with impaired but stable
    renal function, the peak level ( within the
    first 2 days of treatment), the trough and
    peak level within 1 week, then both peak
    and trough levels ( twice weekly thereafter)
  • (3) In the presence of impaired and
    unstable kidney function, peak and trough
    levels ( within the first 2 days), Serum
    levels may need to be measured as
    frequently as every day as long as renal
    function is unstable.
  • (4) After any changes in dosage, peak and
    trough levels are determined within the
    next 2 days.

42
  • Prevention
  • ?????????? fosfomycin, glutathione,
    poly-L-aspartic acid (PLAA) ,
  • 4-methylcatechol ?????????????????????????????
    aminoglycoside ???
  • Iron chelation (iron aminoglycosides gt free
    radicals)

43
Antineoplastic Agents Cisplatin
  • Potent antineoplastic agent.
  • Side effects include nausea and vomiting,
    neurotoxicity, ototoxicity, and
    nephrotoxicity.
  • Pharmacokinetics
  • ?adenylate cyclase ,lateral wall of stria
    vascularis??endolymph,endocochlear potential
  • ???????????????????? ?????? ca ???????????

44
  • Histopathology
  • Degeneration of outer hair cells in the
    lower turns of the cochlea, spiral ganglia,
    and cochlear nerve.
  • Fusion of stereocilia of the outer hair
    cells, with damage to the cuticular plate.
  • Stria vascularis was atrophic.

45
  • Mechanisms of Ototoxicity
  • Production of reactive oxygen species (ROS)
    superoxide anion, hydrogen peroxide ,
    reactive nitrogen species (RNS) nitric
    oxide ? cell damage.
  • OHC in the basal turn( most susceptible)
  • low stores of glutathione.
  • In vitro, evidence that cisplatin
    ototoxicity mediated by the cell death
    pathways.

46
  • Clinical Ototoxicity
  • Hearing loss highly related to dose, age
    of the patient, and other factors, such as
    noise exposure, other ototoxicity drugs,
    depleted nutritional state, cranial
    irradiation, Children.
  • Symptoms hearing loss ( irreversible) , ear
    pain, or tinnitus( 2 to 36 , may be
    transient or permanent)
  • gt50 of patients who received cisplatin in
    dose gt400 mg/ m2 cumulative dose had
    permanent hearing loss.

47
  • Prevention
  • sodium thiosulfate ???????????? Cisplatinum
    ?????? 4 ????????????????????????????????????????
  • D- Methionine, Fosfomycin , free oxygen radical
    scavengers ???? glutathione, gingko biloba
    extract
  • Caspase inhibitors (inhibitor of cell death
    cascade)

48
  • Carboplatin
  • Newer platinum compound.
  • Less nephrotoxic, Less ototoxicity than
    cisplatin.
  • High dose carboplatin (2 g/m2 total dose) ?
    hearing loss.
  • Mechanisms of ototoxicity production of
    reactive oxygen and nitrogen species

49
Loop Diuretics
  • Pharmacokinetics Clinical findings
  • Furosemide average half life of 29.5
    minutes may be as long as 10 to 20 hours.
  • Cause temporary
    and some permanent of hearing loss
    tinnitus and vertigo.
  • Bumetanide more potent sulfonamide loop
    diuretic.
  • Smaller incidence
    of hearing loss than furosemide.
  • Piretanide no patients were found to
    have hearing loss.
  • Torsemide a new loop diuretic , No
    evidence .

50
Histopathology Mechanisms of Ototoxicity
  • Primary target stria vascularis (extensive
    edema) loss of auditory function.
  • ?The Na/2Cl/K transporter (SLG12A2)
  • Biochemical interaction b/w aminoglycosides
    loop diuretics aminogly. promotes penetration of
    loop diuretics to inner ear

51
  • Prevention
  • Ototoxicity of furosemide may be reduced by
    infusing rates of less than 15 mg./minute.
  • No combinations of another ototoxicity drug

52
Salicylates
  • Pharmacokinetics.
  • ??????????????????????? ??????????? stia
    vascularis ??? spiral ligament
  • ??????? ??????? cyclooxygenase
    prostaglandins ??????????? leukotrienes
    ???????????????????????????????????
  • Histopathology not show

53
  • Mechanisms of Ototoxicity
  • Effects on the cochlea by changes in
    blood flow , by changes in the stiffness the
    lateral membrane of the outer hair cells.
  • Clinical Ototoxicity
  • Hearing loss ( reversible) related to
    concentration in blood.
  • ?20 to 50 mg/dL can have hearing losses 30
    dB.
  • ? 11 mg/dL hearing loss was 12 dB.

54
  • Prevention
  • ????????????? chinchilla ??? dexamethasone ????
    round window membrane ????????????????????????????
    ?????????? ??????? adrenergic blockers ??? zinc
    ????????????????????????????????

55
Quinine and Related Drug
  • Pharmacokinetics
  • Block Ca K channel ? cell edema,dec.blood,abnorma
    l OHC func.
  • Clinical findings
  • Quinine toxicity syndrome (cinchonism)
    Deafness, vertigo, tinnitus, headache, visual
    loss and nausea.
  • prolonged courses of treatment 20 high
    frequency hearing loss (reversible) , 4-kHz
    notch, speech discrimination score may be
    less than 30
  • Prevention
  • effect blocked by nimodipine, a calcium
    channel blocker

56
Erythromycin and Related Macrolide Antibiotics
  • Pharmacokinetics
  • ???????????????????????????????????????????????
  • Clinical findings
  • Erythromycin ototoxicity bilateral
    sensorineural hearing loss, blowing
    tinnitus, some cases vertigo , confusion,
    fear, psychiatric disturbances.
  • Most hearing loss and tinnitus transient
    (reversible), Recovery within 1 to 2 weeks
    after stopping.

57
  • Audiometric flat type of sensorineural
    hearing loss. High frequency loss.
  • Auditory brain stem response absence of
    waves I to III. Normalized after cessation
    of erythromycin.
  • Related Elderly, liver or kidney disease,
    high dose erythromycin.

58
  • Prevention
  • (1) Pretretment audiograms in elderly
    patients , impaired liver or kidney function
  • (2) Caution should be used in combining
    erythromycin with other potentially ototoxic
    drugs.
  • (3) If the serum creatinine ins gt1.8 , the
    daily dose of erythromycin should not be gt
    1.5 g.

59
  • Azithromycin
  • Clinical findings hearing loss
  • -audiograms mild to moderate
    sensorineural hearing loss.
  • -Resolved within 2 to 4 weeks after
    cessation of treatment ( reversible )
  • mechanisms of ototoxicity not know.

60
  • Vancomycin
  • Vancomycin have a low probability of causing
    permanent ototoxicity if it is not given
    in combination with another ototoxic agent
    or high doses (gt200mg/kg/d), or liver or
    kidney failure.
  • Not know temporary or permanent.

61
Topical ototopic agent
  • ???????????????????????????????????????? ??????
  • ??antibiotics ???? aminoglycosides ,
    chloramphenicol , polymyxin B ???????
  • ??? antiseptics ???? acetic acid, alcohol,
    chlorhexidine , cresylate, povidone iodine,
    potassium iodide ???????
  • ???????? ???? propylene glycol,polyethylene
    glycol ???????

62
  • Ototoxicity several factors
  • 1.Status of middle ear
  • ??????????????????????????????????????????????????
    ????????? middle ear effusion ??? inflammatory
    changes ??? middle ear mucosa ????? toxic agent
    ???????????????????????????? ?????????? round
    window membrane ??????
  • 2. Size of TM defect large TM defect gt? agent
    to ME
  • 3. ET tube function ability to open affect
    duration of exposure

63
  • 4. Status of round window membrane
  • ??????????????????????????????????????????????
    ???? ??????
  • 1) round window membrane ????????? ???? false
    membrane ??????? cuboidal epithelium ????
  • 2) round window membrane ?????????????????????????
    ???
  • 3) round window membrane ??????????? densely
    structured intermediate layer
  • 5. Concentration of agent used duration of
    exposure
  • Prevention
  • Avoid prolong use esp.TM defect
  • Avoid use in healthy ear

64
Chemicals
  • Oraganic solvents Trichlorethylene, Xylene ,
    Styrene , Hexane , Carbon disulfide , Toluene
  • Gas Carbon monoxide
  • Heavy metals Arsenic ,Mercury , Tin, Lead

65
DIAGNOSIS
  • Cochleotoxicity
  • 1.Audiometry ?????????????????????????????????????
    ????????????? ?????? high frequency audiometry
    ?????????????????????????? ototoxicity
    ?????????????????
  • Limit by not perform at bedside,require
    pt.participation concentration
  • 2. Electrocochleography ?????????????????????
    ototoxicity ?????????????? ??? ???????
    ?????????????? ?????????????

66
  • 3. Otoacoustic emission
  • Adv. rapid bedside testing, Specific toward OHC
    , no pt. participation requirement
  • Disadv. cannot be used in all pt.( ME fluid)
  • 4. Auditory brainstem response ?????
    ??????????????????????????????????????????

67
  • Vestibulotoxicity 1.Electronystagmography
  • 2.Rotation test
  • 3.Dynamic posturography
  • ? impractical, often impossible to detect early
    changes

68
TREATMENT
  • 1.????????????????????????????????????????????????
    ????????????????
  • 2.??????????????????????????
  • 3.????????????????????????????????????????????????
  • 4.?????????????????
  • ??????????????? ????????????????? , Cochlear
    implant
  • ????????????????? ????????????????????
  • ??????????????????????????? ????????????????????
    ???????????????????????????????

69
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