ENT

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ENT
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2014-04-20 10:02:18
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  1. What percentage of HEENT problems are ear related, and what percentage of family practice visits occur due to ear disease?
    • ear related disease accounts for nearly 1/2 of all HEENT problems
    • they make up about 20% of all family practice visits
  2. Label the picture!
  3. Describe the innervation of the superior, anterior, inferior, posterior aspects of the auricle along with the concha and external auditory meatus.
    • superior, anterior innervation: auriculotemporal nerve
    • posterior, inferior innvervation: greater auricular and lesser occipital nerve
    • concha, external auditory meatus: vagus nerve
  4. Describe the anatomy of the external canal (EAC).
    • approx 2.5 cm long (adult)
    • S shaped
    • holds cerumen (wax) secreted by sebaceous glands in the distal 1/3 of the EAC (provides protection)
  5. What part of the ear is air filled, and holds the ossicles (malleus, incus, stapes) and openings (oval window, round window)?
    middle ear
  6. What structures are part of the inner ear? What do they do?
    • cochlea: contains organ of corti
    • semicircular canals (superior, posterior, lateral loops): responsible for vestibular control
    • CN VIII: transmits sound and equilibrium info
  7. Structure that is part of the temporal bone, contains numerous air cells, and communicates with the middle ear space making it a potential area for infection.
    mastoid process
  8. What are the dermatological diseases of the auricle?
    • skin cancers from UV exposure (BCC/SCC/MM)
    • epidermal inclusion cyst (EIC)
    • cellulitis
  9. What is the importance of recognizing and promptly treating (draining) a traumatic auricular hematoma?
    • prevents deformity (cauliflower ear)
    • prevents EAC blockage
  10. How is perichondritis differentiated from cellulitis?
    • by deflection of the auricle
    • **cellulitis must be treated promptly to prevent perichondritis and its resultant deformity**
  11. This lesion most often occurs on the face and is characterized as a nodular lesion with a raised, pearly white border that grows slowly.
    BCC
  12. How are BCC lesions managed?
    • dermatologist may freeze or curette them
    • facial plastic surgeons usually excise them with a small margin
    • Mohs techique...takes longer, is more expensive but recurrence rate is lower (97.1%)
  13. What are some indications for using the Mohs technique to treat BCC?
    • recurrent BCC
    • near vital structures (eyelids, nose, ears)
    • morpheaform BCC (aggressive histology)
    • very large BCC (>2 cm)
  14. Surgical technique that involves complete micrographic excision of the tumor using intraoperative histopathoogy to assess the margins.
    • Mohs technique
    • **cut, then look, cut, look again, etc**
  15. Most common neoplasm of the ear canal, is more aggressive and requires excision of a larger margin than BCC to ensure removal, can mets but usually not early on and presents as a hard, nontender, red, indurated papule, nodule or plaque which may be friable and prone to bleeding.
    SCC
  16. How are SCC lesions managed?
    • evaluate neck nodes & schedule careful follow up for recurrence/mets as needed
    • use Mohs technique for recurrent lesions, >2 cm or aggressive histology
  17. How is BCC and SCC prevented?
    minimize sun exposure
  18. Unpredictable tumor that affects pts of all ages, has a high mortality rate and presents as a pigmented lesion that changes by either growth, color, or margin, ulceration, or bleeding or is deeply pigmented or raised.
    MM
  19. Where does malignant melanoma (MM) begin? What ultimately determines the patient's survival?
    • begins in the epidermis, then invades the dermis
    • depth of invasion is predictive of spread and pt survival
  20. What is the risk of mets for MM with thin and thick lesions?
    • thin: <10%
    • thick: >90%
  21. A lesion that is usually asymptomatic, is common around the ear and is characterized as a well-defined, non tender, soft, mobile mass that is slow growing.
    • epidermal inclusion cyst (EIC)
    • **can spontaneously drain, diagnosis is clinical**
  22. How is an EIC treated?
    • often resolves spontaneously
    • tx not necessary unless desired by patient
    • excision
  23. How is local anesthetic injected into the skin prior to draining/excising an EIC?
    • kenalog 3 mg/mL into surrounding inflamed dermis can resolve inflammation (may prevent need for I&D)
    • use only small amounts (enough to slightly distend cyst) since injecting larger amounts can result in scarring
  24. When is excision of an EIC best accomplished? Why?
    • when lesion is not inflamed (cyst wall is very friable)
    • complete excision is usually not possible when inflamed and recurrence is likely so wait 4-6 weeks after inflammation is resolved to excise
  25. Accumulation of blood in subperichondrial space, usually due to blunt trauma (boxing, wrestling, rugby, etc) though they may occur following wound closure.
    auricular hematoma
  26. What is the pathophysiology of an auricular hematoma?
    • cartilage lacks its own blood supply (relies on diffusion)
    • hematoma develops and blocks the diffusion
    • necrosis of cartilage ensues, predisposing to infection and further injury
  27. How is an auricular hematoma managed?
    PROMPT drainage and application of pressure dressing required!
  28. What is the clinical presentation of an auricular hematoma?
    • edematous
    • fluctuant
    • ecchymotic
    • loss of normal landmarks
  29. What are the four steps to treating an auricular hematoma?
    • 1: evacuate hematoma
    • 2: pressure dressing and splint (prevents reaccumulation...use cotton bolsters, plaster molds, silicon putty, etc)
    • 3: prophylactic antibiotic against staph and/or psuedomonas (dicloxicillin/cephalexin/cipro [pseudomonas])
    • 4: refer to ENT with hematoma >7 days old
  30. What are the complications of an auricular hematoma?
    • necrosis & infection
    • cauliflower deformity if not treated promptly (48 to 72 hours)
  31. How is an auricular hematoma evacuated?
    • 1: cleanse ear & give anesthesia
    • 2: needle aspiration of most fluctuant part for small, acute hematomas <24 hours old with an 18g needle while milking to ensure drainage
    • 3: incision of large hematomas or those >24 hours but <7 days old...incise along posterior aspect of hematoma following skin curvature and use curved hemostats to completely evac the hematoma and any clot, then irrigate gently with saline
    • 4: dressing x 1 week with recheck at 24 hours...place cotton into canal conforming material into the folds of the auricle, place posterior pack behind auricle (cutout gauze sheet), wrap around head for bulky dressing
    • 5: PO antibiotic covering pseudomonas (cipro) and/or staph (diclox/cephalexin)
  32. What are the cartilaginous subunits of the auricle and EAC?
    • helix
    • antihelix
    • concha
    • tragus
    • antitragus
  33. What are some things found in a pt's history that may negatively affect healing and increase the likelihood of a bad outcome from an ear laceration?
    • PMH of DM, cancer, keloid formation
    • use of certain medications like immunosuppressives
    • SocHx of tobacco use
  34. After using a local anesthetic to infiltrate the area of an ear laceration, what needs to be evaluated?
    • location & depth of injury
    • degree of cartilage involvement
    • extension of laceration into EAC
    • presence of tissue avulsion
    • associated middle ear trauma and basilar skull fx
  35. What are some signs of middle ear/more serious injury when evaluating an ear laceration?
    • hemotympanum
    • amber/clear middle ear effusion
    • otorrhea
    • HL with Weber/Rinne (deficit of CN VIII)
    • retroauricular hematoma or "battle sign" (typically appears 2 days after injury, may appear within 6-12 hours, may indicate basilar skull fx)
    • facial nerve dysfunction (possible dmg to CN VII) and/or parotid gland involvement
  36. What imaging study should be done to evaluate serious underlying injuries with ear lacerations?
    CT without contrast (fine axial and coronal cuts)
  37. When should a pt with an ear laceration be referred to a plastic or maxillofacial surgeon, ENT, or neurosurgeon?
    • auricular avulsion
    • laceration w/ EAC extension
    • lacceration with middle/inner ear injury (HL, vestibular sxs)
    • laceration with basilar skull fx
    • chronically split earlobe/cleft caused by heavy earrings or allergy to ring metal
  38. Why is primary closure of an ear laceration preferred?
    limits time underlying cartilage is exposed, reducing the risk of infection
  39. What constitutes a delayed closure of an ear laceration?
    if >24 hours old and/or there are signs of inflammation (redness, warmth, swelling, pus)
  40. What suture material is used for repairing ear lacerations?
    • skin: 5-0 or 6-0 nonabsorbable nylon, Novafil, or Prolene
    • children: 6-0 absorbable (avoids trauma of suture removal)
    • perichondrium: undyed 5-0 absorbable Monocryl, Vicryl, or Dexon
  41. What anesthetic is used to suture ear lacerations?
    • 10mL syringe of 1% lidocaine using a small 25g or 27g (1.5 inch) needle
    • NO EPINEPHRINE!!
  42. A local block is sufficient for most simple lacerations. How is this achieved?
    • posterior: inject 3-4 mL in posterior sulcus by inserting the needle just behind the inferior pole of the auricle and gradually aspirating/injecting toward the superior pole following the crest
    • anterior: inject 3-4 mL just superior and anterior to tragus
  43. A regional block is used for extensive lacerations and is best for avoiding tissue distrotion. How is this achieved?
    • insert needle subQ ~1cm above the superior pole of the auricle
    • direct it to a point just anterior to the tragus (skin of scalp, not cartilage)
    • redirect needle aiming at skin just behind the mid-auricle
    • repeat from below by inserting needle just inferior to the ear lobule insertion
    • use up to 5 mL of anesthetic on each pass (x4) depending on pt's weight
    • **total dose should NOT exceed 4mg/kg of 1% lidocaine**
  44. After fixing an ear laceration, what are some other management options that should be considered?
    • tetanus prophylaxis
    • prophylactic antibiotics (best for pts with bites, contamination, vascular insufficiency or immunodeficiency)
    • aftercare (daily cleansing, topical abx, pressure dressing reapplication; f/u in 24-48 hrs; remove nonabsorbable suture in 7-10 days if healed)
  45. Define cellulitis, perichondritis, and chondritis.
    • cellutitis: infection of the skin
    • perichondritis: infection of the tissue surrounding cartilage
    • chondritis: infection of the cartilage
    • **often indistinguishable, usually d/t injury from surgery, ear piercing or contact sports**
  46. What is the clinical presentation of cellulitis/perichondritis/chondritis?
    • swollen warm, tender, erythematous auricle
    • pain on deflection of auricle (pinch=pain)
    • may involve lobule (chondritis technically does NOT involve lobule)
  47. Why is chondritis difficult to treat? What is the most common microbe that causes infection?
    • poor blood supply to cartilage (remove jewelry)
    • pseudomonas aeruginosa (95% of cases)
  48. How is mild, moderate and severe cellulitis/perichondritis/chondritis of the ear treated?
    • mild: PO levofloxacin (f/u in 24 hrs max)
    • moderate to severe: requires IV abx and potentially surgical debridement
    • ENT consult is highly advisable (these infections may cause necrosis & disfigurement regardless of proper abx treatment)
  49. Name the diseases of the external auditory canal (EAC).
    • cerumen impaction & FB
    • traumatic external otitis
    • acute otitis externa (AOE)
    • pruritus
    • malignant otitis externa (MOE)
    • exostosis & osteomas
    • EAC neoplasia
    • congenital abnormalities
  50. Substance that protects the skin of the EAC by acidifying the canal to prevent overgrowth of bacteria and fungus, and is lipid rich (hydrophobic) which prevents skin penetration and maceration.
    cerumen
  51. What portion of children and adults are affected by cerumen impaction?
    • children: 1/10
    • adults: 1/20
  52. Describe the lateral third, isthmus and medial two thirds of the EAC.
    • lateral third: cartilagenous EAC with hair and glandular bearing skin
    • isthmus: canal narrows here
    • medial two thirds: bony EAC with thin skin attached to periosteum of temporal bone
  53. What are the four main reasons for cerumen impaction?
    • obstruction from EAC disease: exostoses, infectious/derm dz (otitis externa, eczema), systemic dz that causes excess exfoliation of canal skin and atrophy/hypertrohpy of glands (SLE, crohn's, sjogren's)
    • narrowing of EAC: nl anatomy, tumors, excess hair, collapse of cartilage (trauma)
    • failure of epithelial migration: aging (glands atrophy and produce harder/thicker cerumen), FB, ear plugs, hearing aids, inappropriate use of q-tips/cotton buds to remove cerumen (most common)
    • overproduction
  54. What is the clinical presentation of cerumen impaction and how is it treated?
    • presentation: usually asymptomatic, will most often notice it incidentally with otoscopic exam; may be symptomatic with HL, otalgia/fullness, itching
    • treatment: hygiene! have pt clean external opening with a washcloth over the index finger w/o entering canal no more than once a week
  55. What are the indications for removal/nonremoval of impacted cerumen?
    • symptomatic: REMOVE! most will have improved symptoms including an avg 10dB hearing improvement
    • if asymptomatic: LEAVE IT ALONE! removal can cause dmg, most will clear it w/o treatment
  56. What are the three recommended therapeutic options for impacted cerumen removal?
    • 1: cerumenolytic agent (primary care, first line tx)
    • 2: irrigation (if cerumenolytic fails)
    • 3: manual removal (by otolaryngologist)- provides direct visualization and limited damage to EAC skin/TM
    • **no method is superior to the other**
  57. What should the selection of method for removing impacted cerumen be based on?
    • provider experience
    • available time
    • equipment (irrigation, curettes, etc)
    • ancillary staff
  58. In which patients should the use of cerumenolytics be avoided?
    • pts w/ suspected TM damage (otorrhea, otalgia, hx of frequent ear infections)
    • **safe to use in pts with no hx of infection, perforation or otologic surgery**
  59. How long should cerumenolytics be used?
    3-5 days (should not exceed this)
  60. What are the types of cerumenolytics used to clear impacted cerumen?
    • mineral oil preps/hydrogen peroxide (OTC)
    • carbamide peroxide (debrox) 5-10 drops for 15 mins bid x 5 days (RX)
  61. What are some complications of using cerumenolytics?
    • allergic reactions
    • otitis externa
    • ear ache
    • transient HL
    • dizziness
  62. Method for treating cerumen impaction that tends to be most effective for HARD impactions.
    irrigation
  63. How is irrigation for the removal of impacted cerumen performed?
    • use a large syringe and WARM water treated with a bacteriostatic agent (dilute hydrogen peroxide 1:10)....
    • saline/tap water can be as effective and is ok for trained staff to perform
    • straighten canal as much as possible
    • do not place tip of syringe beyond the later third of the ear canal (about 8mm)
    • direct stream upwards in canal
  64. What is the management of cerumen impaction following treatment with irrigation?
    • exam with otoscopy
    • best results if followed by acidification to discourage bacterial growth on wet desquamated skin (H2O and 2% acetic acid/boric acid powder) a must in immunocomped pts
  65. What are the complications of irrigation for removal of impacted cerumen?
    • retention of water behind incompletely removed cerumen (potential infection)
    • TM perforation
    • HL, tinnitus, and/or vertigo
    • pain
  66. A manual removal of impacted cerumen should only be performed if proper equipment and trained, experienced staff are available, and the patient can remain still. What are the indications for submitting an ENT consult for cleaning under microscopic guidance?
    • TM perforation
    • recurrent impaction
    • no response to routine measures
    • h/o chronic otitis media or TM perforation
  67. What are complications of manual impacted cerumen removal?
    • ear pain (too aggressive!)
    • TM perforation (too far with curette!)
    • bleeding/laceration (too aggressive! caution w/ pts on anticoag therapy)
  68. What is a method of cerumen removal that has NOT been shown to be effective and may even have the potential to injure the ear or cause facial burns, therefore is not recommended?
    ear candling, AKA ear coning/thermal auricular therapy
  69. Most patients with conditions predisposing them to cerumen accumulation (eczema, otitis externa, etc) cannot prevent recurrent episodes and have a need for regular removal. What are three methods in which these pts can prevent further impaction?
    • 1: cotton ball dipped in mineral oil place in EAC for 10-20 mins once a week helps liquefy cerumen and aid normal elimination mechanisms
    • 2: remove hearing aids during sleep if applicable
    • 3: routine cleaning by health professional q6-12 months if needed
  70. How do pts with a FB in the EAC present?
    • pain
    • pruritus
    • conductive HL
    • +/- bleeding
    • **persistent FB may lead to infection and formation of granulation tissue**
  71. How are FB in the EAC removed?
    • minimize injury with use microscope and proper instrument (right angle pick, curet, forceps, suction)
    • minimize pt movement
    • irrigation may dislodge small objects but should NOT be performed for organic FB (beans, insects)
    • immobilize living insects w/ 2% lidocaine (kills bug, numbs EAC)
    • remove firm material with a loop/hook without displacing object medially toward TM
  72. An inflammatory and infectious process of the EAC usually caused by either staph aureus or gram neg rods like pseudomonas which flourish in environments with excessive moisture, can also be caused by other bacteria or fungal organisms.
    external otitis (AOE) aka swimmer's ear
  73. What are predisposing factors for developing external otitis (AOE)?
    • frequent/aggressive cleaning
    • exposure to water
    • scratching
    • lack of cerumen (ear is too clean!)
  74. What is the clinical presentation of a patient with external otitis (AOE)?
    • otalgia, pruritus, otorrhea, aural fullness, HL
    • erythema, swelling of canal w/ varying degrees of discharge and crusting on exam
    • pain on distraction of auricle/tragus
    • erythematous TM (should still be mobile unless perfed)
    • **culture may be helpful if infection is persistent**
  75. What is the single most important aspect of treating external otitis (AOE)?
    • CLEANING! (aural toilet)
    • **removing wax, desquamated skin, and purulent material facilitates healing and enhances penetration of ear drops (use manual removal with direct vision through otoscope/irrigation with dilute hydrogen peroxide if TM is visible and intact)**
  76. How is inflammation and infection with external otitis (AOE) treated?
    • topicals given TID
    • tilt head, pull superior aspect of auricle upward and fill ear canal with drops
    • keep drops in ear for 20 mins by lying on side or by placing cotton ball in the ear canal
    • massaging tragus helps distribute drops
    • warming solution curtails dizziness
  77. What are the topical agents used to treat mild external otitis (AOE)?
    • 2% acetic acid (VoSol), 5 gtts in canal tid-qid
    • **can be irritating to inflamed skin**
  78. At what pH do staph aureus and pseudomonas aeroginosa readily grow in?
    6.5-7.3
  79. What are the topical agents used to treat moderate external otitis (AOE)?
    • polymyxin B/hydrocortisone (cortisporin): cheap, contains neomycin which is a potent sensitizer
    • aminoglycosides (gentamycin sulfate 0.3%): more expensive, potentially ototoxic
    • quinolones (cipro/ofloxacin): expensive, highly effective (10 gtts once daily x 7 days)
  80. How should external otitis (AOE) be treated in a patient who has a NON intact TM?
    • focus should shift to middle ear with secondary infection of EAC (question dx of AOE)
    • choose ototopical with LOW acidity and LOW ototoxicity
    • ofloxacin with/without systemic oral abx is a good choice
  81. What should NOT be used to treat external otitis (AOE) in a patient with a non-intact TM?
    • alcohol
    • aminoglycosides
    • neomycin/polymyxin B/hydrocortisone
  82. When should systemic antibiotics in combination with ototopicals be used to treat external otitis (AOE)?
    • diabetes
    • immunodeficiency
    • h/o radiation to ear
    • severe otitis externa
    • significant edema inhibiting application of topical meds
  83. Which ototopicals provide adequate coverage for P aeurginosa and S aureus?
    quinolones (ofloxacin or cipro)
  84. How is the pain involved with external otitis (AOE) controlled?
    NSAIDs to opioid analgesics depending on severity
  85. How are promoting factors for external otitis (AOE) avoided?
    • protect ear from water (cotton ball w/ petroleum jelly during bathing, no water sports x 10 days)
    • educate on prevention, proper ear hygiene and keeping ear dry
  86. A common ear problem that is usually self-induced either from excoriation or by overly zealous ear cleaning, and may be associated with external otitis or derm conditions like psoriasis or seborrheic dermatitis.
    pruritus!
  87. How is EAC pruritus treated?
    • avoid causes: allow cerumen layer to regenerate
    • avoid soap/cotton swabs in canal: NO SCRATCHING!
    • mineral oil: helps with dryness, repels moisture
    • topical corticosteroid (0.1% triamcinolone): beneficial for inflammation
    • oral antihistamine (diphenhydramine): MAY help
    • topical isopropyl alcohol: PROMPTLY relieves pruritus but is drying
  88. Severe bacterial infection of the EAC and skull base, is the most feared complication of AOE, and occurs most commonly in elderly diabetics and immunocompromised patients.
    necrotizing otitis externa (aka Malignant otitis externa)
  89. What is the usual bacteria that causes necrotizing/malignant otitis externa (MOE)?
    pseudomonas
  90. What is the pathophysiology of necrotizing/malignant otitis externa (MOE)?
    • starts as AOE that spreads to the temporal bone
    • further extends readily to the skull base leading to fatal complications if not treated right
  91. How to patients with necrotizing/malignant otitis externa present?
    • deep otalgia (out of proportion to exam)
    • EAC granulation
    • persistent foul otorrhea
    • **CN palsies are a poor prognostic sign**
  92. How is necrotizing/malignant otitis externa diagnosed?
    CT with bone windows to look for osseous erosion
  93. How is necrotizing/malignant otitis externa (MOE) treated?
    • prompt ENT consult
    • daily debridement of EAC
    • pseudomonal ear drops
    • systemic antipseudomonal antibiotics (quinolones)
    • continue tx for several months until gallium scan shows marked reduction of inflammation
    • surgical debridement if refractory to medical therapy
    • **cure rates 90-100% w/ early dx & tx**
  94. Bony overgrowths of the ear canal, associated with chronic cold water exposure (surfer's ear), present as skin-covered bony mounds in the medial EAC which obscure the TM to varying degrees, most are asymptomatic and found incidentally (however may lead to cerumen impaction, external otitis, HL).
    • exostosis (surfer's ear, cold water)
    • osteomas
  95. How are exostosis and osteomas treated?
    • single lesion: no tx required unless large & causing obstruction/infection
    • multiple lesions: often progress and require surgical removal
  96. Links the pharynx to the middle ear, is ~35mm long in adults, and functions to provide pressure equalization and mucus drainage from the middle ear.
    eustachian tube
  97. How does the eustachian tube provide pressure equalization, and how do ear infections occur in this structure?
    • pressure: normally it is closed but can open to let small amts of air go between middle ear and atmosphere, ear clearing methods like yawning, swallowing, chewing gum, or valsalva may open the tube
    • infection: mucus normally drains from middle ear but minor infections/allergies can cause tube to get swollen, trapping bacteria
  98. Drains the middle ear into the nasopharynx, is nearly horizontal in infancy, and becomes more vertically aligned in late childhood.
    • eustachian tube
    • **younger children get more infections d/t horizontal configuration**
  99. What conditions can eustachian tube dysfunction cause?
    • otitis media
    • otitis media with effusion (OME)
    • barotitis
    • patulous eustachian tube (remains open causing echoing of pt's heartbeat, breathing and speech aka autophony)
  100. How is TM mobility assessed?
    • valsalva (easy way to see TM integrity and ET patency)
    • otoscope with bulb
    • tympanogram
  101. If HL is on the same side as the affected ear during a Weber test, what type of HL is it?
    conductive HL
  102. If HL is on the opposite side as the affected ear during a Weber test, what type of HL is it?
    sensorineural loss
  103. If bone conduction hearing is greater than air conduction during a Rinne test, what type of HL is it?
    conductive HL (normally AC>BC)
  104. What is the best definition of eustachian tube dysfunction (ETD)?
    failure of the ET to open and/or close properly
  105. Why are children at higher risk for obstruction and reflux of nasopharyngeal secretions and pathogens?
    • shorter, more horizontal ETs
    • immature floppy elastic cartilage
    • larger adenoids
    • **tube reaches adult length by age 6**
  106. What are the three primary functions of the eustachian tubes (ET)?
    • 1: equalization of pressure (essential for optimal hearing)
    • 2: protecting middle ear from infection & reflux of nasopharyngeal secretion
    • 3: clearance of middle ear secretions
  107. What are the 3 main reasons for dilatory dysfunction of the eustachian tubes?
    • 1: any cause of inflammation
    • 2: pressure dysregulation from changes in depth or altitude
    • 3: anatomic and congenital abnormalities
  108. What can cause the inflammation that leads to dilatory dysfunction of the eustachian tubes?
    • infection: adenoids, nasopharynx, nose, sinuses
    • allergies
    • irritants: tobacco smoke, wood burning stoves, pollution
    • acid reflux: laryngopharyngeal & gastroesophogeal
    • hormone changes: pregnancy (esp 3rd tri when progesterone peaks)
    • other mucosal dz/ciliary disorders
  109. What can cause the pressure dysregulation that leads to dilatory dysfunction of the eustachian tubes?
    • scuba diving
    • air travel
  110. What anatomic and congenital abnormalities can lead to dilatory dysfunction of the eustachian tubes?
    • nasopharyngeal masses
    • trauma (cleft palate surgery, intubation, etc)
    • hypertrophied adenoids
    • Down's, Turner syndrome
  111. What can cause patulous dysfunction of the eustachian tubes?
    • weight loss: little as 6lb loss
    • scarring: procedures, inflammation, radiation
    • neuromuscular disorders leading to atrophy: CVA, MS, etc
    • allergy/chronic reflux: causes atrophy
    • hormonal factors: high estrogen of pregnancy, OCPs, tx for prostate CA
    • others: nasal decongestants/cocaine, craniofacial abnormalities, chronic gum chewing
  112. How is the clinical diagnosis made for dilatory or patulous dysfunction of the eustachian tubes?
    • dilatory: HL, TM retraction/effusion
    • patulous: autophony, TM looks normal without HL
  113. What is examed when performing a nasal endoscopy (flexible) to evaluate possible ETD?
    • nasal cavity: adenoids, inflammation, secretions, masses, etc
    • oropharynx, hypopharynx, larynx: look for evidence of reflux
    • ask pt to swallow/yawn: assess quality of ET function
  114. How is dilatory dysfunction of the eustachian tubes treated?
    • decongestants, antihistamines, nasal steroids for presumptive URI or allergic rhinitis
    • educate on second hand smoke/smoking cessation (rhinitis)
    • behavioral modification/PPI (acid reflux)
    • excision vs radiation (neoplasm)
    • leave it alone: most cases of simple ETD caused by cold/changes in altitude will self resolve
    • swallow and chew: symptoms may improves with swallowing, chewing gum, drinking or yawning
    • avoid air travel, rapid alt changes, and underwater diving during active dz
    • **tx directed at underlying etiology**
  115. How is patulous dysfunction of the eustachian tubes treated?
    • mild: reassurance and education
    • hydration + normal saline drops to nose (tubal orifice)
    • mucosal thickening: potassium iodide, 8-10 gtts PO TID if hydration/NS drops ineffective
    • severe, refractory: surgery (TM tubes, cartilage grafting, etc)
  116. Middle ear is gas-filled and separate from the outside world, when environmental pressures change it must be equalized via eustachian tube...if equalization does not occur the TM retracts severely with eventual fluid and possible blood secretion into space and TM rupture. This describes what?
    barotrauma
  117. What are some reasons for barotrauma?
    • air travel
    • diving 
    • blast injuries
  118. What are the symptoms and physical findings in a patient with barotrauma? How is it diagnosed?
    • symptoms: auralfullness, pain, HL, tinnitus, nausea, vomiting
    • PE: TM retraction, hemotympanum, perforation
    • dx: clinical
  119. How can barotrauma be prevented?
    • avoid air-travel/diving when ear won't clear from cold or allergies: TM perf is absolute CI to diving
    • use meds prior to flying: pseudoephedrine 30 mg taken 30 mins prior to flight/descent, oxymetazoline
    • swallow, yawn, valsalva frequently: chewing gum or sucking on hard candies, feed babies during ascent and descent
    • don't sleep during ascent/descent
    • descend/ascend slowly when diving
    • ventilating tubes for pt with repeated episodes
  120. How is barotrauma treated?
    • most heal with time including edematous and/or hemorrhagic TMs (however restore ET function!)
    • antibiotics only if TM perf and contamination of middle ear
    • analgesics
    • refer to ENT if severe otalgia or HL, tinnitus, vertigo, persistent >4-5 days
    • tympanoplasty or patching of round/oval window
    • ossicular disruption, perilymphatic fistula
    • bed rest w/ HOB elevated
    • myringotomy (preventive or treatment)
  121. What are the disorders of the middle ear?
    • otitis media
    • cholesteatoma
    • otosclerosis
    • trauma
    • neoplasia
  122. What are the different types of otitis media?
    • acute: presence of middle ear fluid + inflammation
    • recurrent: recurrence soon after tx of AOM
    • otitis media with effusion (OME): presence of fluid without signs of illness or inflammation
    • chronic suppurative otitis media (CSOM)
    • mastoiditis
  123. What is the pathophysiology of otitis media?
    • if ET is obstructed negative pressure develops in the middle ear leading to trasudation of serious fluid
    • when this is innoculated with bacteria from nasopharynx, an acute otitis media (AOM) develops
  124. An inflammatory response to bacteria or viruses causing malfunctioning of the ET, involves infection of the URT leading to mucosal inflammation which diminishes the diameter of the ET which in turn results in inadequate ventilation and leads to backflow of secretions from the throat up into the middle ear, causing an accumulation of microorganisms that precipitates infection.
    acute otitis media (AOM)
  125. What is the most common illness affecting children between the ages of 3-6 years?
    acute otitis media (AOM)
  126. Why is prescribing antibiotics for AOM generally not a good idea despite protests from concerned mothers (or fathers)?
    • 70-90% of cases resolve spontaneously
    • **regardless abx prescriptions have increased**
  127. What are some modifiable risk factors to developing acute otitis media (AOM)?
    • bottle/pacifier use: causes backflow of secretions from pharynx and nasal cavity to middle ear (breastfeeding protects against this)
    • day care attendance: exposure to pathogens
    • exposure to second hand smoke: increased infection rates
  128. What are some non-modifiable risk factors to developing acute otitis media (AOM)?
    • atopic states: IgA deficiency impairs ability to fight off AOM and leads to buildup of secretions in nasopharynx that congests the ET
    • craniofacial abnormalities: cleft palate, trisomy 21 can lead to abnl development of the palate and/or ET
  129. What is the clinical presentation of AOM in young children?
    • fever
    • irritability
    • crying
    • drainage from ears
    • altered sleeping habits
    • **ear pulling w/o other symptoms is NOT associated with infection of TM**
  130. What is the clinical presentation of AOM in older children/adults?
    • sudden onset pain in affected ear
    • TTP
    • fever
  131. How is AOM diagnosed?
    • PE findings (erythematous, bulging TM without landmarks)
    • pneumatic otoscopy
    • tympanometry (expensive, often used in clinic)
  132. What are the common pathogens associated with AOM?
    • strep pneumoniae
    • h influenzae
    • m catarrhalis
  133. What are the not so common pathogens associated with AOM?
    • RSV
    • influenza
    • parainfluenza
  134. What is the only way to definitely find out the pathogen causing AOM and is generally only reserved for pts with resistant cases for which no definitive treatment has been effective?
    tympanocentesis
  135. How should AOM be treated?
    • antipyretics/analgesics (ibuprofen, acetaminophen)
    • observation if >2 yo, healthy with nonsevere illness (mild otalgia and fever <102.2F), and able to f/u and start abx if observation is unsuccessful
    • **NO ABX!! 70-90% of cases begin to resolve on their own within 48-72 hrs**
  136. When should antibiotics be used for treating AOM?
    • no improvement after 48-72 hrs of observation
    • <2 yo
    • more severe sxs, bilateral dz, otorrhea
  137. What antibiotics should be used if needed to treat AOM?
    • children: amoxicillin (first line) 80-90 mg/kg/day x 10 days
    • adult: amox OR augmentin 875 mg bid or 500 mg tid x 10 days
    • non-type 1 allergic reaction to PCN: cefdinir 300 mg bid OR ceftriaxone 2 g IM/IV once
    • known severe allergy to PCN: azithromycin x 5 days (10 mg/kg day 1, then 5 mg/kg days 2-5)...macrolides lack activity against H flu and some pneumococcal isolates
  138. What is the SNAP approach to treating AOM?
    • Safety Net approach to Antibiotic Prescription
    • based on clinical suspicion of AOM, give Rx but urge it be filled ONLY if the child does not respond to analgesics after 2 days or if condition gets worse
  139. How is AOM treated other than using analgesics or antibiotics?
    • tympanocentesis for culture if immunocompromised or persistent/recurrent infection: 20g spinal needle bent at 90 degrees inserted through inferior portion of TM
    • myringotomy: severe otalgia/complications of AOM occur (mastoiditis, meningitis)
  140. What are some of the side effects that can occur with antibiotics for conditions that do not warrant their use?
    • nausea, vomiting, diarrhea, oral thrush, rash
    • C difficile infection
    • allergic/anaphylactic reaction
  141. Late-developing (>72 hrs after taking meds and never having taken PCN before) often itchy maculopapular or morbilliform rash that occurs in children and adults that starts on the trunk and can spread, is not a CI for future amox usage and does not warrant stopping current regimen.
    "amoxicillan rash" (occurs in 3-10% of kids taken PCN)
  142. What type of infection can an "amoxicillin rash" indicate?
    • infectious mononucleosis
    • 80-90% of pts with acute EBV infection who are treated w/ amox develop the rash
  143. What is the prognosis of AOM?
    • 50% of pts still have fluid in ears at 2 weeks
    • ~10% will have residual fluid by 10 weeks
    • cycle starts again in many children resulting in as many as 5 or 6 bouts of AOM in as many months (recurrent AOM)
    • small portion goes on to develop chronic serous otitis media d/t failure of TM to heal from perf with otorrhea
  144. What is the usual definition of recurrent AOM?
    • ≥3 distinct and well documented episodes of AOM within 6 months OR...
    • ≥4 episodes within 12 months
    • infants w/ 1st episode within 6 months of age or with siblings with recurrent AOM are at higher risk
  145. What are the available interventions for recurrent AOM and what determines which ones to choose?
    • >2 yo less aggressive interventions preferred...
    • ID & tx underlying predisposing conditions
    • parent education
    • breast feeding
    • influenza and/or pneumococcal vaccines
    • <2 yo, multiple RF or predisposing conditions, more aggressive preferred...
    • antibiotic prophylaxis
    • surgery (myringotomy and placement of tympanostomy tubes)
    • **case by case, concern for abx resistant bacteria in nasopharynx, language development, values and preferences from family**
  146. What are the immune deficiencies that can cause recurrent AOM?
    • IgG deficiency (most common), consult immunology
    • HIV
  147. What prophylactic treatment offers a modest reduction in the frequency of AOM but appears to decrease the need for placement of tympanostomy tubes in recurrent AOM?
    pneumococcal and influenza vaccines during infancy
  148. What are the indications for antibiotic prophylaxis for recurrent AOM?
    • ≥3 episodes within 6 months OR...
    • ≥4 episodes withing 12 months
    • age <2 years
    • multiple risk factors
    • predisposing conditions
    • **benefit is fewer episodes of AOM as compared to tympanostomy tube placement**
  149. What is the recommendation for antibiotic prophylaxis again recurrent AOM?
    • amoxicillin 40 mg/kg PO once daily
    • sulfisoxazole 50 mg/kg PO once daily (PCN allergy)
    • start in fall, winter, or early spring when resp infections are prevalent
    • no longer than 6 months
  150. What should be used if there is breakthrough AOM while pt is on prophylaxis against recurrent AOM? What does this breakthrough indicate?
    • amox-clavulanate (augmentin) 90 mg/kg PO daily OR...
    • ceftriaxone 50 mg/kg IM once daily as alternative
  151. When should f/u be conducted for a pt with recurrent AOM?
    • anytime symptoms return
    • at least every 2 months with presence of middle ear effusion
  152. Device that permits drainage and aeration of middle ear and return middle ear mucosa to normal.
    tympanostomy tubes
  153. What are the indications for inserting tympanostomy tubes?
    • ≥3 episodes AOM within 6 months OR...
    • ≥4 episodes within 12 months
    • breakthrough episodes of AOM while on chemoprophylaxis
    • chemoprophylaxis declined by parents
    • **kids often grow out of ETD by the time tubes fall out on their own (6-18 months)**
  154. What are the adverse effects of tympanostomy tubes?
    • otorrhea
    • persistent TM perf
    • tympanosclerosis
    • focal atrophy of TM
    • cholesteatoma formation
  155. Presence of middle ear fluid without acute signs of illness or inflammation, usually follows AOM but can result from barotraumas or allergy, typically leads to CHL and can be a precursor to retraction and perforation of TM, ETD is often a predisposing factor.
    otitis medias with effusion (OME) aka serious otitis media (SOM)
  156. What is the presentation of otitis media with effusion (OME) aka serious otitis media (SOM)?
    • CHL, aural fullness
    • h/o recurrent AOM possible
    • h/o antecedent URI, exacerbation of seasonal allergy sxs or airplane travel
    • fluid behind TM with/without retraction
    • reduced TM mobility with viscous bubbles often visible
    • tympanometry (best means to dx) type C, flat config
    • audiometry (CHL)
  157. What must be ruled out in any adult with persistent unilateral SOM?
    nasopharyngeal carcinoma with nasopharyngeal endoscopy
  158. What is the initial treatment for OME?
    • observe for 3 months if hearing impairment is mild
    • most cases resolve spontaneously without tx
    • autoinsufflation may be effective in adults (not children)
  159. If initial observation and autoinsufflation (adults) of OME fail, what is the treatment?
    • PE tubes
    • adenoidectomy (relieves nasal obstruction, improves ET function, eliminates potential reservoir for bacteria; often performed at same time as PE tube placement if pt is on 2nd set of tubes)
    • **sharp decline in OME after 7 yrs old**
  160. Why is nasopharyngeal examination with a flexible endoscope MANDATORY for any adult with persistent unilateral OME?
    • early nasopharyngeal carcinoma is know for its silent nature and usually the only sign is unilateral OME
    • in later dz the tumor mets to the cervical lymph nodes and extends to skull base causing cranial neuropathies
    • **ALWAYS BE SUSPICIOUS!**
  161. What are the nine main indications for getting tympanostomy tubes?
    • 1: severe/recurrent AOM
    • 2: HL >30 dB in pt with OME
    • 3: impending mastoiditis/intra-cranial complication d/t otitis media
    • 4: OME >3 months
    • 5: chronic retraction of TM (ETD)
    • 6: prevention or tx of barotrauma
    • 7: autophony (echoing) d/t patulous eustacian tube (PET)
    • 8: craniofacial anomalies that predispose to middle ear dysfunction
    • 9: middle ear dysfunction d/t head and neck radiation and skull base surgery
  162. What is the procedure for placing TM tubes?
    • myringotomy (slit) is made in eardrum
    • chronic ear fluid is suctioned out
    • ear tube is placed to allow air to enter and keep middle ear healthy (also allows drainage if another infection occurs)
    • performed in oupt OR for children & office for adults, is quick (<10 mins)
  163. What should a pt with TM tubes placed be educated on?
    • avoid dunking head under water, protect ears when around water
    • tube provides a direct route for contaminated water to enter the middle ear (is supposed to be sterile)
  164. What are the complications of otitis media?
    • TM perf (path of least resistance for purulence to drain)
    • chronic suppurative otitis media (CSOM)
    • mastoiditis
    • meningitis
    • tympanosclerosis
    • facial paralysis
    • labrynthitis
    • HL
    • petrositis
    • epidural, subdural, brain abscess
    • otitic hydrocephalus
    • otitic meningitis
    • sinus thrombosis
  165. How is a TM perforation d/t otitis media treated?
    • ofloxacin otic (low acidity & ototoxicity)
    • orals x 10 days (same as AOM)
    • prevent water entry into ears
    • refer to ENT for eval of CSOM if perf persists >6 weeks with/without suppurative drainage
    • f/u with audiogram  and ENT consult for persistent subjective HL after resolution of perf
  166. What are the three layers of the TM?
    • squamous epithelium on outside
    • collagen fibrous layer
    • cuboidal layer in middle ear
    • **all 3 layers proliferate in event of TM perf but if the squamous and cuboidal layers meet the fibrous layer will stop which can lead to chronic perf...tympanoplasty may be indicated at this point**
  167. Defined as chronic otorrhea (>6-12 wks) through a perforated TM with mucosal changes (degeneration & granulation tissue) and osseous changes (osteitis and sclerosis) which bacteriology that is different from AOM (P aeruginosa, proteus spp, staph aureus along with other anaerobes).
    chronic suppurative otitis media (CSOM)
  168. How do pts with CSOM present?
    • purulent discharge that is continuous/intermittent (hallmark) with increased severity during URI/following water exposure
    • pain during exacerbations
    • CHL from destroyed ossicular chain, TM or both
    • TM perforation present
  169. How is CSOM treated?
    • refer to ENT for eval and management which includes...
    • regular removal of debris
    • use of earplugs for water protection
    • topical abx drops during exacerbation
    • surgery (definitive tx): TM repair (90% success), mastoidectomy
  170. Mastoid effusion often seen on CT scan in pts with AOM (not usually significant), if symptomatic it can be serious d/t proximity of the mastoid to other important structures like the post cranial foss, lateral sinuses, CN VII, and semicircular canals.
    mastoiditis (rare complication of acute & chronic otitis media)
  171. How do patients with mastoiditis present?
    • fever
    • posterior ear pain and/or local erythema over the mastoid
    • edema of pinna or posterior/downward displaced auricle
    • protruding auricle & loss of postauricular crease
    • ALWAYS perform CT (axial) if mastoiditis is suspected since it can cause loss of trabecular bone!
  172. What is the treatment for mastoiditis?
    • immediate ENT referal: tx with myringotomy, admission and IV abx
    • from AOM: tx for streptococcus pneumoniae and H influenzae
    • from chronic otitis media: tx for staph aureus, pseudomonas, enteric gram-neg rods
    • if no response from above within 24 hrs: mastoidectomy for debridement of necrotic bone
  173. Firm submucosal scarring that can appear as milky white patches on the TM, is a disease limited to the middle ear with formation of hyaline deposits and calcification in the TM, can be caused by injiries to the eardrum and chronic disease in the middle ear, deposits can cause CHL d/t decreased mobility of the TM and immobilization of the ossicular chain.
    tympanosclerosis
  174. Develops from chronic negative middle ear pressure, MC cause is prolonged ETD with resultant negative middle ear pressure that draws the upper flaccid portion of the TM inward (pars flaccida), creating a squamous epithelium-lined sac which may fill with desquamated keratin and become chronically infected. Typically erodes bone with early penetration of the mastoid and destruction of the ossicular chain, and with time may erode the inner ear, involve CN VII and even invade and spread intracranially.
    cholesteatoma
  175. How do patients with cholesteatoma present?
    PE reveals TM retraction pocket, perforation that exudes keratin debris or granulation tissue
  176. What is the imaging modality of choice for cholesteatomas?
    • CT, d/t it's ability to deomonstrate the bony anatomy of the temporal bone
    • **MRI can't delineate bony anatomy, instead in can potentially distinguish non-specific opacification from cholesteatoma, useful post-op**
  177. What is the treatment for cholesteatoma?
    • surgical excision to remove cholesteatoma (recurrence common d/t difficulty of removing mass completely)
    • however excision does not fix the ETD! (PE tube will prevent chronic negative pressure)
  178. Abnormal bony growth in the middle ear that results in CHL from impedance of sound through the ossicular chain.
    otosclerosis
  179. How do pts with otosclerosis present?
    • slow progressive unilateral or bilateral CHL
    • onset in early life (3rd-4th decade)
  180. How are other causes of CHL besides otosclerosis ruled out?
    • CT/MRI
    • Rinne/Weber
    • tympanometry
  181. What is the treatment for otosclerosis?
    • observation: unilateral dz & mild CHL
    • nonsurgical: sodium flouride/bisphosphonates to prevent progression
    • amplification: those with normal cochlear function & speech discrimination
    • surgery: stapes prosthesis (stapedectomy)
  182. Trauma to middle ear that can be caused by diving/flying, overpressure from explosion or blow to ear, infection, or myringotomy.
    TM perforation
  183. How is a TM perforation treated?
    • spontaneous healing occurs in most cases
    • large perfs may require tympanoplasty
    • persistent perf may result from secondary infection by exposure to water (protect from water)
  184. Trauma to middle ear that may follow blunt trauma or extreme barotrauma, usually resolves spontaneously over several weeks.
    hemotympanum
  185. Trauma to middle ear that should be considered if CHL is >30 dB, and persists for >3 months following trauma.
    disruption of ossicular chain
  186. How is disruption of the ossicular chain treated?
    • middle ear exploration with reconstructin of ossicular chain
    • TM repair (usually restores hearing)
  187. Arises because of asymmetry in the vestibular system d/t damage to or dysfunction of the labyrinth, vestibular nerve, and central vestibular structures in the brainstem.
    vertigo
  188. Lightheadedness, feeling like one might faint (presyncope), also vertigo or a feeling like the room is spinning or moving, most causes are not serious and quickly get better on their own or are easily treated.
    dizziness
  189. Can happen when there is not enough blood getting to the brain ie if there is a sudden drop in BP or if person is dehydrated from vomiting, diarrhea, fever, or other causes. May happen d/t a vagal response, and many people especially the elderly, experience it if they get up too quickly from a lying or seated position.
    lightheadedness
  190. Type of dizziness felt as a shift in a person's relationship to the normal environment involving a feeling that the room is spinning or a sense of moving (falling) through space, person may vomit or experience tinnitus or nystagmus.
    vertigo (more of a movement hallucination)
  191. What is true vertigo primarily associated with?
    balance organs of the inner ear
  192. What should be addressed when taking history for possible vertigo?
    • duration: seconds, minutes, hours, days?
    • symptoms: tinnitus, HL, etc
    • triggers: diet (salt in meniere dz), stress, fatigue, bright lights (migraine associated)
  193. What should be included in the physical exam when trying to diagnose vertigo?
    • ears
    • eye motion in response to head turning/nystagmus
    • CN
    • romberg
    • special tests (dix-hallpike for BPPV)
  194. What type of vertigo is caused by problems with the labyrinth or vestibular nerve?
    peripheral (aka otologic or vestibular)
  195. What are the causes of peripheral vertigo?
    • positional (most common)
    • meniere's dz
    • labrynthitis (vestibular neuritis)
    • acoustic neuroma
    • perilymphatic fistula
    • chemical insults like ototoxic drugs
    • labrynthine concussion
    • otitis media
  196. What type of vertigo arises from the balance centers of the brain, and is usually milder and more discrete and may have accompanying neurologic deficits such as slurred speech, diplopia, or pathologic nystagmus?
    • central
    • **high suspicion often warranted for dx, brain pathology can cause sensation of disequilibrium**
  197. What are the causes of central vertigo?
    • migrainous vertigo
    • MS
    • vertebrobasilar insufficiency
    • brainstem ischemia
    • cerebellar infarction/hemorrhage
    • chiari malformation
  198. What type of vertigo has a sudden onset, is so severe that pt is unable to stand or walk, is frequently accompanied by N/V, excessive perspiration, nystagmus, and may have associated tinnitus and HL (otologic)?
    peripheral
  199. What type of nystagmus is associated with peripheral vertigo?
    • fatigable
    • horizontal with torsional component
    • latency
    • suppressed by visual fixation
  200. What type of vertigo has a gradual onset, becomes progressively more severe and debilitating, is associated with CNS deficits, spares auditory function, and has sxs of nystagmus, diplopia, dysarthria, HA, AMS or cerebellar, motor, or sensory abnormalities?
    central
  201. What type of nystagmus is associated with central vertigo?
    • nonfatigable
    • VERTICAL
    • without latency
    • unsuppressed with visual fixation (often is worse)
  202. Type of vertigo cause by otoconia (calcium carbonate crystals) or other sediment that have become free floating and enter one of the balance canals so when pt turns their head quickly or to a certain position (rolling over in bed) the material moves the balance canal fluid (endolymph) and stimulates the vestibular nerve, creating an intense feeling of vertigo that lasts <30 secs but not >1 min until material settles in place.
    • benign paroxysmal position vertigo (BPPV)
    • **pts can usually describe the precise motion that precipitates this intense brief episode of vertigo, sxs occur in clusters that persist over several days**
  203. What solidifies the dx of BPPV in pts with a typical hx of vertigo?
    • observation of nystagmus with dix-hallpike maneuver
    • **dx uncertain if no nystagmus is seen...nystagmus & vertigo usually appear with a latency of a few seconds and lasts <30 secs**
  204. When will dix-hallpike maneuver usually provoke paroxysmal vertigo and nystagmus?
    if posterior canal dysfunction is present
  205. When doing the DHM when does nystagmus usually appear and how?
    • appears after latency of a few seconds and lasts <30 seconds
    • beats are horizontal-torsional with upper poles beating down to the ground
    • after sitting up nystagmus will occur in the opposite direction
    • intensity decreases with repetition (fatigability) as does the therapeutic benefit of the repositioning maneuver
  206. Single safe, and effective treatment maneuver for vertigo that encourages debris to migrate toward the common crus of the anterior and posterior canals and exit into the utricular cavity, can be repeated if no response or relapse after first attempt.
    • epley particle repositioning maneuver (repeated until no nystagmus can be elicited)
    • **premedication with vestibular suppressant can be used prior to maneuver**
  207. Rapid onset of persistent and severe vertigo, and N/V with gait instability, is idiopathic but thought to be from inflammation of the vestibular nerve and/or labyrinth, and is frequently associated with or follows a viral infection (URI)...pt with awaken with room spinning vertigo that will continue but gradually become less intense over 24-48 hrs.
    vestibular neuritis aka labyrinthitis or vestibular neuronitis
  208. Will pts with vestibular neuritis generally experience hearing changes? What sxs will they have and for how long?
    • no, hearing is generally unchanged
    • may have associated HL (labyrinthitis), tinnitus, or N/V
    • pts generally suffer severe sxs for 1-2 days, followed by gradual diminution and return of equilibrium
    • **auditory function is preserved with pure vestibular neuritis whereas unilateral HL is called labyrinthitis**
  209. What is the treatment for labyrinthitis?
    • acute period (corticosteroids): prednisone 10 day course 60 mg/day 1-5, 40 mg day 6, 30 mg day 7, 20 mg day 8, 10 mg day 9, 5 mg day day; methylprednisolone, 22 day taper
    • vestibular suppressants: discontinue after 48 hurs to avoid long term disequilibrium from inadeduate compensation
    • rehab exercises: most efficacious of pt is referring for vestibular physical therapy for individually designed program, should begin after acute sxs subside (hastens long term recover esp balance)
  210. What are the vestibular suppressants used to treat labyrinthitis?
    • antihistamines (DOC): dimenhydrinate, diphenhydramine, meclizine (DOC in pregnancy)
    • benzos: alprazolam, clonazepam, diazepam, lorazepam (sedating, use with CI to anticholinergics)
    • antiemetics: metoclopramide, ondansetron, prochlorperazine (more sedating, reserve for severe vomiting)
    • treatment room/ED use: diphenhydramine, metoclopramide, ondansetron, prochlorperazine, promethazine
  211. Idiopathic condition thought to be secondary to distention of the endolymphatic space within the balance organs of the inner ear, and is classically diagnosed by hx because pts have a particular symptom complex.
    meniere's dz aka endolymphatic hydrops (considered chronic condition)
  212. What is the particular symptom complex pts with meniere's dz typically have?
    • intense episodic vertigo: lasts from 20 mins to 2-4 hrs, sometimes up to 24 hrs (BPPV lasts <1 min)
    • SNHL: fluctuating and usually lower frequencies
    • tinnitus: low pitch (seashell/machinery)
    • sensation: aural fullness
    • pallor, sweating, N/V, falling: severe attacks
  213. How is meniere's dz diagnosed clinically?
    • 2 spontaneous episodes of vertigo lasting >20 mins
    • audiometric confirmation of SNHL
    • tinnitus and/or perception of aural fullness
    • perform audiometry on all suspected of meniere's dz (pattern shows low freq/combo low/high freq sensory loss with normal mid freq)
  214. What are the goals of treatment for meniere's dz?
    • reduce frequency/severity of attacks
    • reduce/eliminate HL and tinnitus
    • alleviate chronic sxs (tinnitus/imbalance)
    • minimize disability
    • prevent progression of HL and imbalance
    • educate pt on what dz is, expectations for response and tx options
    • up to 90% are able to maintain ADL with medical management
  215. What are the lifestyle avoidance adjustments that pts with meniere's dz can make to alleviate or ameliorate sxs?
    • high salt diet/MSG (limit Na to <2-3 grams/day, no large boluses during meals)
    • caffeine and nicotine, limit to only one beverage daily (vasoconstriction reduces flow to labyrinthine system)
    • alcohol (causes fluid/lyte shifts which stresses the labyrinthine system) limit to only 1 daily drink
    • stress
    • allergies
  216. What is the acute medical management of meniere's dz?
    • vestibular suppressants/antiemetics (start with low doses)
    • rest
  217. What are the drug treatments for meniere's disease?
    • diuretics when diet alone does not control it
    • glucocorticoids (no definitive study)
    • immunosuppresives (no definitive study)
    • vitamins, herbals, vasodilators (no provide efficacy)
  218. What is the rehabilitation that can be given to treat pts with meniere's dz?
    vestibular rehab with exercise to maximize balance and CNS compenstion for disequilibrium
  219. What are the interventional treatments for the 10% of pts who have intractable or progressive, unremitting sxs that significantly impair QOL?
    • destructive procedure for pts who failed meds and have unilateral sxs: intratympanic gentamicin injection penetrates round window and destroys hair cells in semicircular canals; surgical labyrinthectomy which relieves vertigo but causes permanent HL
    • nondestructive procedures: surgical endolymphatic sac shunts; intratympanic glucocorticoids (may work, still needs more trials)
  220. What are the causes of traumatic vertigo?
    • labyrinthine concussion (MC cause of vertigo s/p head injury): sxs generally diminish within several days but may linger for a month or more
    • basilar skull fx loss of hearing: severe vertigo lasting several days to a week with deafness in the involved ear
    • oval or round window rupture
  221. Leakage of perilymphatic fluid into middle ear through the round or oval window causing vertigo that is worse with straining and SHL.
    perilymphatic fistula
  222. What are the causes of a perilymphatic fistula?
    • physical injury (blunt head trauma, hand slap to ear)
    • extreme barotrauma during airflight or scuba diving
    • vigorous valsalva maneuvers (weightlifting)
    • post surgical complication (stapedectomy)
  223. What is the treatment for perilymphatic fistula?
    • bed rest
    • middle ear exploration and window sealing with a tissue graft
  224. A normal response to a situation in which sensory conflict about body motion exists among visual receptors, vestibular receptors, and body proprioceptors causing N/V, diaphoresis, pallor, hypersalivation, yawning, anxiety, dizziness, etc.
    motion sickness
  225. What is the treatment for motion sickness?
    • premedicate: scopolamine patch applied at least 4 hrs before travel (good for 6-12 hrs prior); PO meds 30 min-1 hr prior to travel
    • avoid alcohol
    • decrease oral intake/freq small feedings
    • avoid reading while actively traveling
  226. What is the most common cause of central vertigo?
    DRUGS!!
  227. What are the drugs that cause central vertigo?
    • aminoglycosides
    • antihypertensives, diuretics, dopaminergic agents
    • vasodilators
    • phenothiazines
    • tranquilizers, antidepressants
    • anticonvulsants
    • hypnotics
    • analgesics
    • alcohol
    • caffeine
    • tobacco products
  228. The most direct way of making the distinction between peripheral and central vertigo is to inquire and then evaluate brainstem symptoms. What are the brainstem symptoms that are being evaluated for?
    • diplopia
    • facial numbness
    • weakness
    • hemiplegia
    • dysphasia
  229. What are some reminders of how to look for central vertigo to distinguish it from peripheral vertigo?
    • evidence of brainstem involvement rules out peripheral lesion
    • absence of brainstem sxs DOES NOT rule out a central lesion
    • pattern of recurrent long standing episodes followed by remissions suggests MS
  230. Vertigo caused by an 8th CN schwannoma which is one of the most common intracranial tumors (often found incidentally), 95% are unilateral, it is a benign lesion that arises in the auditory canal and gradually grows to involve the cerebropontine angle eventually compressing the pons.
    acoustic neuroma aka vestibular schwannoma
  231. How does a pt with an acoustic neuroma present?
    • unilateral/asymmetric slowly progressive, sometimes fluctuant SNHL
    • vague and continuous disequilibrium
    • occasional tinnitus
  232. What is found during the physical exam in a pt with an acoustic neuroma (vestibular schannoma)?
    • contrast CT will detect it if >2 cm
    • MRI with gadolinium (gold standard)
  233. How is an acoustic neuroma (vestibular schwannoma) treated?
    • asymptomatic: observation with annual MRI for slow growing
    • symptomatic: excision, radiotherapy (annual MRI)
  234. What are the early signs of an acoustic neuroma (vestibular schwannoma) extending outside the internal auditory meatus?
    • slowly progressive asymmetric HL/decline of speech discrimination
    • facial numbness/weakness
    • corneal reflex decreased/absent
    • **GET MRI!!**
  235. Condition that can present with symptoms identical to meniere disease, is an inflammatory and degenerative disorder involving the CNS and presents from 20-40 yrs old (F>M) and has a strong genetic component.
    multiple sclerosis (MS)
  236. What are the symptoms of vertigo d/t multiple sclerosis?
    • episodic vertigo and chronic imbalance (in 30-50% of pts with MS)
    • SHL (MC unilateral and rapid onset)
    • subtle accompanying sxs (slight facial numbness or huskiness of voice, blurred or double vision)
    • commonly associated with symptoms reflecting dysfunction of adjacent CNs such as hyper/hypoacusis, facial numbness, and diplopia
  237. Condition typically seen in elderly with arteriosclerosis causing a reduced flow in the vertebrobasilar system which usually produces vertigo in conjunction with diplopia, sensory loss, dysarthria, dysphasia, hemiparesis and other brain stem deficits...may begin as only transient vertigo while later episodes almost always include other brainstem symptoms.
    vertebrobasilar insufficiency
  238. What is the treatment for vertigo caused by vertebrobasilar insufficiency?
    empiric treatment with vasodilators and aspirin
  239. Vertigo in pts with a h/o of migraine HA, occurs in young pts with new onset of episodic vertigo, is a more common incidence than meniere disease and it characterized by a HA occuring either during or after vertigo with photophobia/phonophobia.
    migraine-associated vertigo
  240. How is migraine-associated vertigo treated?
    • triptans
    • migraine prophylaxis (decreases freq which supports dx)
  241. What are the antihistamines (drugs of choice) used to alleviate acute episodes of vertigo that last at least a few hours to days?
    • meclizine (preg cat B)
    • dimenhydrinate (preg cat B)
    • diphenhydramine
  242. What are the anticholinergics used to alleviate acute episodes of vertigo that last at least a few hours to days?
    • scopolamine (best for prevention of sxs)
    • 1.5 mg transdermal patch applied behind ear >4 hrs prior to travel (replace q 3 days prn)
  243. What are the antiemetics used to alleviate acute episodes of vertigo that last at least a few hours to days?
    • prochlorperazine (compazine)
    • promethazine (phenergan)
    • metoclopramide (reglan)
    • ondansetron (zofran)
    • **more sedating and should be used only for severe vomiting**
  244. What are the benzodiazepines used to alleviate acute episodes of vertigo that last at least a few hours to days?
    • diazepam (valium)
    • lorazepam (ativan)
    • alprazolam (xanax)
    • **sedating and given if CI to other meds**
  245. What treatment forces pts with vertigo to perform challenging balance exercises with several benefits, and targets multisensory compensation?
    vestibular rehabilitation
  246. What is vestibular rehabilitation targeting when the pt focuses on an object with a blank background and moves their head slowly up/down and right/left, slowly increasing the speed to not exacerbate N/V and is performed 2-3 times daily for several minutes?
    acute peripheral vertigo
  247. What is vestibular rehabilitation targeting when it is much more aggressive than that used for acute disorders, and requires the pt to perform eye and head movements while standing, walking forward and backward, and while standing or walking on compliant/uneven surfaces?
    • chronic peripheral vertigo
    • **focused on performing increasingly difficult postural tasks with more eye and head movements while keeping sxs managable**
  248. What is vestibular rehabilitation targeting when there is complete bilateral loss of vestibular function that eliminates the possibility of adaptation (pts often do not improve), uses exercises to promote strategic substitutions that may help, and requires education on fall prevention (critical) since darkness and uneven surfaces are particularly challenging.
    bilateral vestibular injury
  249. What is vestibular rehabilitation targeting when gait and balance exercises along with head/eye movements are performed 2-3 times per week, and typically takes longer for improvement than those with peripheral dysfunction?
    central vertigo
  250. What are otologic manifestations of AIDs on the external ear?
    • kaposi's sarcoma
    • persistent fungal infections (aspergillus fumigatus)
  251. What are the otologic manifestations of AIDS in the middle ear?
    • SOM (most common): ETD to adenoidal hypertrophy
    • progressive HL and HIV: eval for cryptococcal meningitis and syphilis
    • ramsay hunt syndrome: acute facial paralysis d/t HZ (common)
    • PE tubes don't help
    • AOM pathogens seen (pneumocystis jiroveci has been reported)
  252. What is the prevalence of HL in the US by age?
    • 21-34 yrs: 3%
    • 35-44 yrs: 6%
    • 44-54 yrs: 11%
    • 55-64 yrs: 25%
    • 65-84 yrs: 43%
  253. What are external ear causes of CHL?
    • congenital: microtia (absence/malformation of auricle), atresia (stenosis of EAC)
    • infection
    • trauma
    • tumor: SCC is most common, exostosis (bony growths w/ repeated exposure to water near TM/middle of EAC), osteoma (solitary bony growth near meatus)
    • systemic dz (DM, immunocompromised predisposing to MOE)
    • dermatologic: psoriasis (scaling and/or edema of EAC and meatus), cerumen buildup
  254. What are the middle ear causes of CHL?
    • congenital: atresia (malformed ossicular chain), missing/misaligned stapes (most common)
    • ETD
    • infection: 80-90% of kids have at least one episode of OM 
    • tumor: cholesteatoma
    • otosclerosis: bony overgrowth involving footplate of stapes
    • TM perf
    • barotrauma
    • vascular
  255. What are the inner ear causes of SNHL?
    • congenital/hereditary
    • presbycusis: hallmark is progressive, symmetric high freq loss over many years (can't understand speech in noisy environment)
    • infection: viral cochleitis, meningitis
    • meniere disease: episodic HL, recovers withing 12-24 hrs, spells may recur daily, weekly, monthly, almost always low freq and can become permanent
    • noise exposure: compounded over time, excessive exposure can affect degree of presbycusis that develops
    • barotrauma: middle ear barotrauma with sxs of tinnitus, vertigo, and HL
    • trauma: temporal bone fx
    • tumors: usually benign, acoustic neuroma is most common
    • endocrine/systemic/metabolic: DM has two fold increase in prevalence of low to mid freq HL
    • autoimmune: asymmetric and progressive with overall systemic signs of disease (ESR, ANA, RF)
    • iatrogenic: surgical (stapedectomy, tympanomastoidectomy, radiation therapy), medication
    • ototoxic substance: begins at high freq usually from abx or chemotherapeutic agents
    • neurogenic: CVA/TIA, MS
  256. What is the purpose of the hearing conservation program?
    • prevent occupational HL
    • essential for "combat readiness"
    • helps maintain fitness for duty
    • retain job/specialty
    • reduce HL compensation costs
    • promote healthy hearing & good quality of life
  257. What are the elements of the hearing conservation program?
    • noise hazard ID
    • engineering controls
    • audiometric monitoring
    • hearing protective devices
    • hearing conservation education
  258. When should hearing protection be worn?
    • continuous noise >84 dB
    • impact noise >140 dB
    • single protection if >84/140 dB
    • double protection if >104 dB (continuous noise)
  259. What are the possible presentations of patient with hearing loss?
    • may c/o difficulty understanding
    • may c/o inability to hear well
    • may be brought in by family member because RV is always too loud
  260. What are the three attributes to look at when describing hearing loss?
    • 1: type of HL
    • 2: degree of HL
    • 3: configuration of HL
  261. What is the Army's hearing conservation regulation?
    DA PAM 40-501
  262. What does each of the services hearing loss conservation programs discuss?
    • overview of HCP and its elements
    • responsibilities of those involved in implementing it
    • fitness for duty issues
    • forms and processes involved in hearing conservation
    • eval of statistics of effectiveness of HCPs
  263. Perception of abnormal ear/head noises, common in elderly (ringing, buzzing, crickets, etc), is usually a manifestation of HL but may have other causes.
    • tinnitus
    • persistent indicates presence of SNHL
    • intermittent mild, high pitched tinnitus lasting seconds to minutes are common in normal hearing people
    • may interfere with sleep and ability to concentrate
  264. What are treatment options for tinnitus?
    • avoid exposure to excessive noise, ototoxic agents, other factors that cause cochlear damage
    • habituation techiques like trating therapy and masking techniques (music/amplification with hearing aid)
    • antidepressant nortriptyline 50mg PO qHS
  265. Why should a "heartbeat" or pulsatile tinnitus not be shrugged off?
    • may be d/t conductive HL
    • may be more serious cause (glomus tumor, venous sinus stenosis, carotid vaso-occlusive dz, AVM, or aneurysm)
    • get an MRI
  266. Rapid series of popping noises lasting seconds to minutes and accompanied by a flutterin feeling in the ear, "clicking", d/t middle ear muscle spasm.
    staccato tinnitus
  267. Excessive sensitivity to sound that may occur in normal-hearing folks either for psychological reasons, in association with ear disease, or following noise trauma.
    hyperacusis (earplugs in noisy places help)
  268. What should be determined when evaluating HL?
    • nature of impairment (type, degree, config)
    • anatomy (external, middle, inner, central auditory pathway)
    • etiology (what is the cause? dx?)
  269. Type of hearing loss in which sound is not conducted efficiently through the EAC to the TM and ossicle, often is medically or surgically correctable.
    CHL
  270. What are the most common etiologies for CHL?
    • swelling of EAC, FB, tumors
    • impacted cerumen
    • perforated TM/fluid in middle ear
    • ossicular chain abnormalities
  271. CHL present on audiogram and not readily apparent on the physical exam (Weber/Rinne) suggests problems with what?
    ossicular chain (otosclerosis?)
  272. Hereditary disease process involving bony proliferation within the temporal bone, bony changes commonly occur at the region of the stapes and causes gradual fixation of the ossicular chain which in turn decreases the mobility of the stapes footplate and creates CHL.
    otosclerosis (affects ossicular chain)
  273. How is otosclerosis treated?
    • surgery
    • involves removing fixed stapes ossicle and placing a prosthesis between the incus and vestibule of the inner ear, re-establishing continuity of the ossicular chain
  274. Hearing loss d/t damage to the inner ear (cochlea) or nerve pathway from the inner ear (retrocochlear) to the brain, cannot be medically or surgically corrected and is permanent.
    SNHL
  275. What are the most common etiologies for  SNHL?
    • persistent noise exposure
    • age related changes (presbycusis) is most frequent cause
    • family/genetic factors
    • infectious/postinflammatory processes
    • fracture of temporal bone
    • tumor growth along the course of CN VIII
  276. What are the ototoxic substances that can cause SNHL?
    • abx: aminoglycosides (gentamicin, tobramycin, neomycin), erythromycin, tetracycline (more pronounced with renal failure)
    • chemotherapeutics: cisplatin, 5-fluorouracil, bleomycin
    • salycilates/aspirin: high dose aspirin (6-8 g/day) reversible if discontinued
    • sildenafil, tadalafil, vardenafil
    • antimalarial (quinine, chloroquine) reversible
    • loop diuretics
    • cocaine
    • heavy metals (lead, mercury, cadmium, arsenic)
  277. MC form of HL, presbycusis being the most frequent cause d/t aging outer hair cells withing the cochlea gradually deteriorating which causes a SYMMETRICAL pattern of HL that begins in high frequencies, often causes pts to have difficulty with speech discrimination abilities and tinnitus.
    SNHL
  278. HL closely regulated by OSHA, typically pts have a "noise notch" pattern on audiometry at approximately 4000 Hz, prevention is vital, counseling should be part of routine health maintenance, pts should have regularly scheduled audiometric f/u (HCP).
    acoustic trauma (noise exposure)
  279. What is the treatment for noise exposure?
    • hearing education
    • noise avoidance
    • appropriate hearing protection with ear plugs and/or muffs depending of noise level exposure
  280. Patients with asymmetric SNHL require a more thorough eval to r/o out what etiology?
    acoustic neuroma (CN VIII tumor)
  281. How can pts with acoustic neuroma present?
    • SNHL (asymmetric)
    • poor speech discrimination
    • tinnitus in affected ear
    • disequilibrium complaints
  282. What is the gold standard diagnostic test of choice for acoustic neuroma?
    MRI!
  283. Test frequently used to assess hearing levels or measure severity of HL, requires that pt is able to cooperate (not for young kids), and uses a graph that depicts threshold as a function of frequency (Hz) with threshold being the softest intensity level that pure tone can be detected 50% of the time.
    pure tone audiometry ("hearing test")/audiogram
  284. Name the thresholds for the audiogram.
    • 0-20 dB: normal hearing-->soft whisper
    • 20-40 dB: mild HL-->soft voice
    • 40-60 dB: mod HL-->normal voice
    • 60-80 dB: sev HL-->loud voice
    • >80 dB: profound HL-->shout
  285. During pure tone testing (audiogram), the higher the threshold is the _____ the patient's hearing.
    • poorer
    • **sound levels increase in stepwise fashion**
  286. Audiogram thresholds of what are considered abnormal?
    >20 dB
  287. During audiogram, independent thresholds are determined for each ear for both ______ and ______.
    • air conduction (conductive hearing)
    • and bone conduction (SN hearing)
  288. What does AC on the audiogram measure?
    • ability of external and middle ear to transmit sound to cochlea
    • any blockage here will create an air-bone gap between thresholds on the audiogram
  289. If the AC and BC on an audiogram are equal but higher than 20 dB what type of hearing loss is it?
    SNHL
  290. What is meant by configuration of HL?
    extent of HL at each freq (Hz) and overall picture of hearing that is created (ie high-freq vs low freq HL vs flat, bilateral vs unilateral HL, symmetric vs asymmetric HL, progressive vs sudden HL, fluctuating vs stable HL)
  291. What are the pure tone audiogram thresholds that are essential for understanding speech? What is the entire human range? Where do the main human speech frequencies occur?
    • 250-8000 Hz
    • 20-20,000 Hz
    • 500-3000 Hz
  292. Sudden onset of unilateral HL with or without tinnitus may represent what? These pts often c/o poor sound localizationand difficulty hearing clearly with background noise.
    inner ear viral infection or vascular accident
  293. What are the possible causes for gradual hearing loss?
    • common with...
    • otosclerosis
    • noise-induced
    • vestibular schwannoma (asymmetric HL, tinnitus, imbalance, cranial neuropathy when large esp CN V or VIII)
    • meniere dz (episodic vertigo, tinnitus, aural fullness)
  294. What is part of the physical exam when evaluating hearing loss?
    • check auricle, EAC, TM with insufflation
    • HEENT (unilat serious effusion in adult prompts fiberoptic exam of nasopharynx for neoplasms; CN V and VII for dysfunction/tumors involving cerebropontine angle)
    • Weber & Rinne
    • audiologic assessment (pure tone AC and BC threshold, speech reception threshold, discrimination score, tympanometry, acoustic reflexes, acoustic reflex decay)
    • imaging (CT vs MRI)
  295. What area on the audiogram is the target hearing area for children with hearing loss?
    • "speech banana"
    • if they can hear sounds there with a hearing aid there is better chance they will understand that sound and be able to reproduce it with speech
  296. An average shift of greater than or equal to 10 dB at 2000, 3000 and 4000 Hz in either ear.
    • STS
    • **shift in hearing of 15 dB or more at 100, 2000, 3000 or 4000 Hz is no longer an STS but is consdered an early warning for couseling purposes**
  297. How is a pt with a negative STS (improved hearing) on annual/periodic test managed?
    • repeat test immediately
    • if shift confirmed, revise reference with no additional actions required
    • if negative STS resolved, return to annual testing
  298. How is a pt with a positive STS (worsened hearing) on annual/periodic test managed?
    • explain results then...
    • otoscopic exam and tympanometry to r/o canal occlusion or middle ear problem (medical referral if needed
    • if no conductive problem is evident schedule f/u #1 on another day (14 hrs noise free)
    • counsel, re-fit HPDs
    • if f/u #1 shows resolved STS, cousel/explain temporary threshold shift suggests inadequate personal protection and return to annual testing
    • if STS persists on f/u #1, perform f/u #2 immediately
    • if STS resolves on f/u #2, counsel pt, again recheck HPDs, return to annual testing
    • persisting STS now considered permanent threshold shift (PTS), action depends on SOP
    • audiologist/technician will update reference audiogram
  299. Test used to evaluate the TM and middle ear status, assesses the mobility of the TM and its response to pressure changes in the EAC, can help in the detection of middle ear fluid when the physical exam is unclear.
    tympanometry
  300. Test introduces a pure tone into EAC through a 3 function probe tip that pumps varied air pressure again TM (controls mobility), introduces 220 Hz probe tone, and measure loudness in the ear canal.
    tympanometry
  301. A graphic picture of the middle ear function that results as the pressure is varied against the TM, may be divided into 3 basic types and 2 sub-types according to shape of the graph that is obtained.
    tympanogram
  302. Type of tympanogram in which the peak of the pressure curve falls between +50 and -150 mm of pressure, peak compliance falls between 0.2 and 1.8 mm, and results indicate the absence of middle ear pathology.
    • Type A: normal tympanogram
    • intact & mobile TM with normal ET function
    • if there is hearing loss, is likely to be SNHL
  303. Type of tympanogram in which the pressure curve falls between +50 and -150 mm of pressure (WNL) but the compliance is very low (<0.2 mm), is often associated with ossicular fixation or TM scarring (NOT middle ear effusion), may result in a fairly FLAT non-fluctuating HL, ET function is normal.
    • Type As (shallow): abnormal tympanogram
  304. Type of tympanogram in which the peak of the pressure curves falls between +50 and -150 mm of pressure (WNL), peak aural immittance is >2.0 ml, peak compliance is very high or off the chart, may result in a fairly FLAT non-fluctuating HL, ET function is normal.
    • Type Ad (disarticulation): abnormal typanogram
    • indicates ossicular disarticulation
    • associated with ossicular disarticulation
  305. Type of tympanogram in which the peak is absent/poorly defined and at markedly negative middle ear pressure (> -200 mm), max compliance is below normal range, indicates fluid in the middle ear or a TM perforation.
    • Type B (flat): retracted, poorly mobile
  306. Type of tympanogram in which there is a clearly defined peak but it falls on the negative side of the chart, indicating negative middle ear pressure, peak pressure is seen at > -150 mm (moved to the left), peak compliance may be normal, may cause very mild conductive loss, or hearing can be WNL.
    • Type C: eustachian tube dysfunction
  307. What are the general diseases of the nose & paranasal sinuses?
    • nonallergic rhinitis
    • acute bacterial rhino sinusitis
    • nasal vestibulitis
    • invasive fungal sinusitis
    • allergic rhinitis
    • olfactory dysfunction
  308. What are the urgent care issues involving the nose & paranasal sinuses?
    • epistaxis
    • nasal trauma
  309. What are the classifications of tumors & granulomatous disease of the nose & paranasal sinuses?
    • benign
    • malignant
    • inflammatory dz
  310. Symptoms include nasal congestion, hyposmia, watery rhinorrhea, and cough accompanied by general malaise, throat discomfort and HA with a fever >100F, PE reveals erythematous, edematous nasal mucosa with watery discharge.
    viral rhinitis (common cold)
  311. What are complications of viral rhinitis (common cold)?
    • worsening symptoms leading to otitis media, rhinosinusitis, bronchitis or pneumonia
    • sxs generally last 3-7 days (25% up to 14 days)
  312. What structures of the respiratory tract are typically involved with illnesses categorized as URIs caused by an acute infection?
    • nose
    • sinuses
    • pharynx (pharyngitis)
    • larynx (laryngitis)
    • tonsils (tonsillitis)
    • ear (otitis media)
    • common cold
  313. How is viral rhinitis treated?
    • symptomatic relief (no effective antiviral therapy exists)
    • spontaneously resolves in 7-10 days
    • abx are NOT helpful, do not prescribe a Z-pak EVER!!
  314. What medications are ok to prescribe for symptomatic relief of viral rhinitis?
    • decongestants: PO preferred d/t longer duration of action, no risk of rebound congestion, but for children <12, pts with HTN/CAD...sudafed 30-60 mg q4-6 hrs or 120 mg bid; nasal spray like oxymetazoline & phenylephrine should not be used more than 3 days
    • anticholinergics: controls rhinorrhea, does not relieve congestion
    • antihistamines: safe, mildly effective for sneezing and rhinorrhea (dries secretions, promotes rest)
    • cough suppressant: for nasopharyngeal cough that interferes with sleep
    • expectorants: commonly prescribed, efficacy not proven
    • aromatic oils (menthol, camphor, eucalyptus): topical or lozenge form produces sensation of increased airflow
  315. What are the more serious conditions that have been associated with viral rhinitis?
    • acute rhinosinusitis
    • AOM
    • bronchitis
    • asthma
  316. Sneezing, rhinorrhea, nasal congestion, PND caused by many triggers often not known by pt but can include tobacco smoke, traffic fumes, strong odors and perfumes, NOT pollen or furred animals.
    non allergic rhinitis
  317. What are the different types of non allergic rhinitis?
    • gustatory rhinitis
    • rhinitis medicamentosa
    • occupational rhinitis
    • vasomotor rhinitis
  318. Non allergic rhinitis caused by a chronic inflammatory condition d/t prolonged use of topical decongestants (afrin) which leads to addictive need to prevent rebound nasal congestion from withdrawal of the drug (cocaine abuse also causes this problem), pt will c/o nasal obstruction.
    rhinitis medicamentosa
  319. What is the tx for rhinitis medicamentosa?
    • cessation of sprays (pt will be frustrated!)
    • topical corticosteroid (flunisolide nasal spray, 2 per nostril bid) OR...
    • intranasal anticholinergic (ipratropium 0.06% spray, 2-3 q8 hrs prn) OR...
    • short course of PO prednisone OR...
    • NSAID
    • above meds may help with process of withdrawal
  320. Non allergic rhinitis characterized by nonspecific nasal hyper-reactivity, symptoms are similar to viral rhinitis but are associated with changes in temperature, eating, exposure to odors or chemicals or alcohol abuse.
    vasomotor rhinitis
  321. Non allergic rhinitis triggered by a number of different indoor and outdoor pollutants that can affect the nose including dust, ozone, sulfur dioxide, cigarette smoke, garden sprays, ammonia, etc...can cause nasal dryness, reduce airflow, rhinorrhea, and sneezing.
    occupational rhinitis
  322. How is occupational rhinitis managed?
    • environment control is critical!
    • avoidance
    • removing agents
    • improving ventilation
    • use pf protectant particle respirator masks
  323. What is the overall treatment for non allergic rhinitis?
    • irritant avoidance: reduce exposure to tobacco smoke, wood burning stoves & fireplaces, cleaning agents & household sprays, strong perfumes & scented products
    • nasal irrigation: 1-2 times per day with bottle spray, neti pots, bulb syringe
    • nasal antihistamine: azelastine, 2 sprays/nostril bid (bad taste in mouth after use)
    • nasal glucocorticoids: fluticasone 1 squirt/nostril bid (max effect delayed days to weeks)
    • nasal ipratropium: profuse rhinorrhea, gustatory rhinitis
    • decongestants: elevate BP, can exacerbate BPH issues
  324. Condition characterized by symptomatic inflammation of the nasal cavity and paranasal sinuses lasting less than 4 weeks, most commonly d/t viral infection associated with the common cold, viral rhinosinusitis is complicated by acute bacterial infection in only 0.5 to 2.0% of episodes.
    • acute rhinosinusitis (ARS)
    • AVRS typically resolves in 7-10 days
    • ABRS is more commonly a self-limiting disease (40-60% resolve without abx)
  325. What are the classifications of acute rhinosinusitis (ARS)?
    • acute: <4 weeks
    • subacute: 4-12 weeks
    • chronic: >12 weeks
    • recurrent: ≥4 episodes in a year (with interim symptom resolution)
  326. What is the epidemiology of acute rhinosinusitis (ARS)?
    • 30 million adults in US annually
    • 1 in 7 will have sinusitis in a year
    • incidence F>M, 45-74 yo

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