HENT: Audiology, Ear Disorders, and Peds PDF

INTRO TO HENT: AUDIOLOGY, EAR DISORDERS, AND PEDS Ryane Lester, PA-C January 21, 2025 Augsburg PA Program Clinical Medicine II OBJECTIVES ANATOMY & PHYSIOLOGY REVIEW: EXTERNAL EAR Pinna  Helps localize sound sources  Directs sound into the ear  Each individual's pinna creates a distinctive i...

INTRO TO HENT: AUDIOLOGY, EAR DISORDERS, AND PEDS Ryane Lester, PA-C January 21, 2025 Augsburg PA Program Clinical Medicine II OBJECTIVES ANATOMY & PHYSIOLOGY REVIEW: EXTERNAL EAR Pinna  Helps localize sound sources  Directs sound into the ear  Each individual's pinna creates a distinctive imprint on the acoustic wave traveling into the auditory canal External auditory canal  Average 26mm in length, 7mm diameter  Every EAC is different  Blood supply of TM- branches from external carotid artery  Nerve supply of TM- medial/inner surface (glossopharyngeal nerve CNIX), lateral outer surface anteriorly CN V trigeminal , posterior half vagus (CN X) AUDIOLOGY OVERVIEW OF HEARING  Pinna  directs sound toward opening of ear canal/acoustic meatus  Sound waves reach the TM  vibrations  movement of the bones of middle ear  In middle ear – air filled cavity with muscles and 3 bones – incus, malleus, stapes  Oval and round window on the inner wall  Stapes on oval window  vibrations to the oval window  vestibule vibrates  Inner ear = labyrinth  Bony and membranous part  Lymph in both  Vestibule separate the semicircular canals from cochlea  Vibrations of the vestibule transmit to organ of corti = hearing receptors, and send electrical impulse to brain by 8th CN  Vibrations in the ampulla of the semicircular canals have receptors  sends a signal to 8th CN to brain  In macula have balance receptors that detect changes in equilibrium  Converts sound waves to brain and perceive movement and head position – to brainstem  INNER EAR  Bony: contains perilymph that encircles membranous labyrinth. Vestibule, cochlea, semicircular canals.  Membranous- contains endolymph  Vestibule- encircles utricle and saccule in membranous labyrinth  Receptors (maculae) that are hair cells topped with small calcium carbonate crystals (otoliths). Provide sensations of gravity and linear acceleration  3 semicircular canals- sensory hair cells activated by movement of endolymph with rotation of head, then sends nerve impulses through acoustic nerve to the brain INNER EAR VIDEO OF HEARING  https://www.youtube.com/watch?v=RiVx5Lih_44 HEARING LOSS  Conductive or sensorineural hearing loss  Audiologic testing  Normal, mild, moderate, severe, or profound  Conductive hearing loss:  Mechanically there is something wrong  Lack of transmission of sound from the EAC or middle ear  transmission of sound vibrations to the inner ear are IMPAIRED  Very simple reason  cerumen impaction = obstruction  Middle ear effusion, stiffness = otosclerosis  Most common = cerumen impaction or ETD (transient)  Persistent = persistent infection, trauma, otosclerosis, perforations  Does this seem correctable or not? HEARING LOSS  Sensorineural loss:  Defects in the INNER EAR or CENTRAL auditory pathway  Deterioration of the cochlea  Common in older adults = most common form = age related hearing loss = Presbycusis  Gradual, progressive  High frequency loss  Other reasons:  Excessive noise exposure, trauma, ototoxic drugs, systemic disease  If sudden  EMERGENCY (called idiopathic sudden sensorineural hear loss), why?  Central pathway causes:  Some issue in the auditory pathway  cortex; acoustic neuroma, MS, auditory neuropathy HOW TO ASSESS HEARING LOSS  Normal spoken voice is about 60 decibels (whisper, normal, shout)  512 HZ tuning fork helps to distinguish conductive from sensorineural hearing loss  Weber test:  Tuning fork on the forehead  IF CONDUCTIVE LOSS, SOUNDS LATERALIZES TO THE AFFECTED EAR (the ear with poor hearing)  IF SENSORINEURAL LOSS, SOUND LATERALIZES TO THE UNAFFECTED EAR (the ear that hears good)  Stop  talk about this HOW TO ASSESS HEARING LOSS  Rinne test:  Tuning fork on the mastoid process  When here, it is doing bone conduction  When they don’t hear this sound anymore  place the tuning fork in front of the ear  Air conduction should be > then bone conduction  They should here sound here if there is no conductive loss  If there is conductive loss > then 25 dB, bone conduction is louder  Stop  talk about this HOW TO ASSESS HEARING LOSS  Formal audiometric studies  Soundproof room  Auditory brainstem-evoked response screening  Newborns  MRI used to find a defect  Every patient with hearing loss should be referred for audiologic evaluation HEARING AMPLIFICATION  Hearing aids  Bone conducting hearing aids for conductive loss:  Stimulate the ipsilateral cochlea directly  Bone conduction hearing aids for sensorineural loss:  Stimulate the contralateral cochlea  Cochlear implants for profound sensorineural loss  Electronic device that is implanted into the cochlea to stimulate the auditory nerve  COCHLEAR IMPLANTS  Cochlear implants: bilateral severe to profound SNHL, poor speech discrimination.  External speech processor delivers sound to the internal device. The electrode will send the signals directly to the auditory nerve. The cochlear implant enables the recipient to hear sound and it improves their speech discrimination ability to varying degrees. PREVENTION OF HEARING LOSS  CDC: An estimated 12.5% of children and adolescents aged 6–19 years (approximately 5.2 million) and 17% of adults aged 20–69 years (approximately 26 million) have suffered permanent damage to their hearing from excessive exposure to noise.  Starts at a young age:  Nose reduction headphones  Parades, fireworks, shows, movies  Headphones, how loud are they?  How loud is music  Mowing the lawn, power washer, construction, etc.  Damage over time = CAN’T BE CORRECTED  WEBER AND RINNE EXAMPLE  Tuning fork is placed on the mastoid then moved to the outside of the right and left ears.  The patient says they can hear the fork better when it is held in the air next to both ears.  What test is this and result?  The PA strikes the tuning fork and places it on the top of the patient’s head.  The patient states that they hear the tone better in the right ear.  What test is this and what result(s)?  Diagnosis? DISORDERS OF THE EAR EXTERNAL EAR CERUMEN IMPACTION  Cerumen is protective, we need it  Produced in the outer ear canal  Impactions often due to personal hygiene practices or due to failing of normal self-cleaning  S/s:  Decreased hearing, fullness, tinnitus, pain, itching  Treatment:  Cerumenolytics  Removal with ear curette/loop  Irrigation  Ensure TM is intact  Foreign body*  OTITIS EXTERNA  “Swimmer’s ear”  Tx:  Often preceded by by water exposure, or  Protection from moisture and injury mechanical trauma  Antibiotics = otic solution  Etiology:  Aminoglycoside  Gram negative rods = Pseudomonas (neomycin/polymyxin B)  Fungi = Aspergillus  Fluroquinolone (ciprofloxacin +/- corticosteroid)  S/s:  Ear wick  Otalgia, erythema, edema, and purulence of  Oral FQ if associated cellulitis skin of external auditory canal  PE:  Want to ensure that you can see  Erythema and edema of the ear canal skin, the TM if possible purulent exudate, surrounding cellulitis  Auricle motion tenderness, tragal motion tenderness  May not see TM  MALIGNANT OTITIS EXTERNA (NECROTIZING)  Patients who are immunocompromised  PE: or DIABETICS  Granulation tissue at the bony-  High mortality, older patients cartilaginous junction of the external auditory canal is considered  Persistent otitis media can evolve into pathognomonic osteomyelitis of the skull base =  CN palsies malignment otitis externa  Dx:  Originates from the EAC  CT scan = osseous erosion  OE  cellulitis  chondritis  temporal  Elevated ESR, CRP bone  osteomyelitis  MRI to rule out abscesses  Etiology: Pseudomonas  TX:  S/s:  Prolonged anti-pseudomonal abx  Unrelenting pain, pain at night  IV then oral  Otorrhea Eczematoid  Ofloxacin or ciprofloxacin (ciprodex) preferred. Polymyxin/neomycin (corticosporin) is cheap but OTITIS Bacterial neomycin can be ototoxic if TM perf. Often otic drops have boric or acetic acid. EXTERNA: TREATMENT Severe Bacterial add ear wick. If cellulitis of periauricular tissue and fever- add oral antibiotic Acidify with acetic acid or Domeboro astringent Debridement is Fungal and/or anti-fungal drops or cream (lotrimin or key! butenafine hcl, ketoconazole, clotrimazole, nystatin) Chronic or Debride first! Then 0.1% triamcinolone cream, recurrent- eliminate Dermatitis mometasone cream, or dermotic drops precipitating factor. Often dermatitis is underlying cause- Necrotizing Oral antibiotic (ciprofloxacin). CT temporal bone , causes acute (malignant) CBC, ESR, glucose, culture. Refer infectious flares OE Keep ears clean and dry, do not put objects in ear Prevent canal! Consider drying ear drops after swimming (1:1 isopropyl alcohol and white vinegar)  LESIONS OF EXTERNAL EAR CANAL - RECALL  Herpes zoster:  Burning severe pain, HA, malaise. Then 3-7 days later- vesicular eruption  With facial paralysis and/or dizziness- Ramsay Hunt syndrome.  Tx: high dose acyclovir and prednisone.  Neoplasia- most common is squamous cell carcinoma. If otitis externa doesn’t resolve with treatment- refer (possible underlying CA) MIDDLE EAR DISORDERS OF THE EUSTACHIAN TUBE  EUSTACHIAN TUBE DYSFUNCTION  Connects the middle ear to the nasopharynx  Normally closed, opens during swallowing or yawning  Dysfunction = air trapped in the middle ear is absorbed  negative pressure  Etiology:  Edema of the tubal linings  viral URTI, allergies  S/s:  Fullness, hearing issues, popping of the tube  PE:  Retracted TM, decreases mobility  Tx:  Intranasal decongestants; intranasal corticosteroids BAROTRAUMA  Barometric pressures are sometimes difficult to equalize in certain situations:  Air travel, rapid altitude change, underwater diving  Some have more difficulty  More common during descent  Yawn, swallow, gum, auto insufflate to enhance function  Oral decongestants before flying  If this persists on the ground – same methods as above  Myringotomy if severe  Underwater diving:  Much more intense on decent  Descend slowly and equalize often  If severe negative pressure develops  hemorrhage (hemotympanum); peri lymphatic fistula OTITIS MEDIA: SEROUS  Prolonged ET dysfunction  negative middle ear pressure  Negative pressure  fluid shift into the middle ear and stasis of the fluid  Adults:  Occurs with URTI, barotrauma, or chronic allergic rhinitis  S/s:  Maybe some conductive hearing loss  PE:  Dull and hypomobile TM, air fluid levels  Tx:  Same as ETD DISEASES OF THE MIDDLE EAR OTITIS MEDIA: ACUTE  Infection or the air spaces of the middle ear  Usually follows a viral URTI  ET obstruction  Accumulation of fluid and mucus  secondarily infected  Peak is 6-12 months old  What happens?  Normally, the middle ear is aerated by the eustachian tube  nasopharynx  Inflammation/edema/mucus  obstruction  secretions build up  AOM  Children more at risk due to orientation of ET OTITIS MEDIA  Etiology:  Streptococcus pneumoniae – Strep pneumo  Haemophilus influenzae – H flu  Streptococcus pyogenes – Strep pyogenes  Viruses: rhinovirus, enterovirus, RSV, parainfluenza  These are common in the nasopharynx and enter middle ear through ET  S/s:  Rapid onset OTALGIA, ear pressure, decreased hearing, fever  Infants/non-verbal – trouble sleeping or eating, tub or rub the ear, fever  Previous URI symptoms  DDX: for otalgia  What do we think?  Externa, FB, impacted cerumen, AOM = most common OTITIS MEDIA: ACUTE  PE:  Erythema and decreased mobility of the TM (JUST can’t be red)  Bullae on the TM  Bulging TM  rupture  Complications:  Mastoiditis  TM perforation  DX: clinical – more to come next slide  Tympanocentesis is the gold standard  TX:  Antibiotic:  First line: Amoxicillin  Alternatives: amoxicillin-clavulanate, cefuroxime, cefpodoxime  Pain control  OTITIS MEDIA: ACUTE  Treatment:  Initial antibiotics:  Initial observation:  All infants less than 6 months  6-23 months with unilateral AOM without  All children with severe signs or severe signs or symptoms symptoms  Mild ear pain less than 48 hours  Moderate or severe ear pain or ear  Temperature less then 102.2 pain ≥ 48 hours  Temperature more than 102.2  Children ≥ 24 months with unilateral or bilateral AOM without severe signs or  < 24 months with bilateral AOM symptoms  Mild ear pain less than 48 hours  Temperature less then 102.2 Patient education: Even with abx, expect fever and pain for 1-2 days If symptoms don’t improve  return If not started with abx, f/u in 2-3 days, start abx only if symptoms worsen/no improvement Wait and see abx  OTITIS MEDIA: CHRONIC  Consequence of recurrent acute otitis media  Etiology:  P. aeruginosa, Proteus, Staph aureus and mixed anaerobic  S/s:  Purulent discharge is the hallmark  Chronic otorrhea +/- otalgia  Hearing loss  PE:  Perforation or retraction of the TM  Conductive hearing loss  Tx:  Topical abx drops; ofloxacin or ciprofloxacin with dexamethasone for exacerbations  Oral cipro  Surgery COMPLICATIONS OF OTITIS MEDIA  Cholesteatoma  Mastoiditis  Petrous apicitis  Facial paralysis  Sigmoid sinus thrombosis  CNS infection OTOSCLEROSIS  Progressive disease that affects the bony otic capsule  Familial tendency  Lesions will impair the passage of sound  conduction hearing loss  Tx: hearing aid or surgery TYMPANIC MEMBRANE PERFORATION/MIDDLE EAR TRAUMA  Perforation from:  Impact trauma or noise  Usually spontaneous healing  Exposure to water can bring a secondary infection  Wear ear plugs while healing  If conductive hearing loss persists  eval for disruption of the ossicular chain CHOLESTEATOMA  Variety of chronic otitis media  Most commonly due to chronic ETD  Causes inward migration of the upper flaccid part of the TM  makes a sac  Abnormal collection of keratinized squamous cells in the middle ear  Discharge from the ear, unilateral conductive hearing loss  more symptoms  Otoscopy: collection of debris in the upper TM  CT can dx/MRI  Tx: surgical removal INNER EAR TINNITUS  Phantom noise or sound = sensation of sound in the absence of a sound source  Can accompany any form of hearing loss  > 20% of aging population experience some type of tinnitus  Persistent tinnitus often indicates the presence of hearing loss  S/s:  Variable – some is so severe it affects sleep and concentration  Pulsatile: hearing ones own heartbeat  Tonal: continuous sound (ringing, buzzing, whistling)  Staccato “clicking”: middle ear muscle spasm, popping sounds, fluttering feeling TINNITUS  PE:  Complete head and neck exam, CN evaluation, otoscopy  Dx:  Audiometry should be ordered to r/o associated hearing loss  Unilateral  MRI  Pulsatile  CT/MRA to exclude vascular cause  Tx:  S/s of stroke  ER; suspected vascular  eval with neuro/ENT  Should refer to audiometry/ENT for eval  Avoidance of excessive noise, ototoxic agents  Mask with music or amplification of normal sounds (hearing aid)  Tinnitus retraining therapy, and CBT  Antidepressants and antipsychotic meds  help with coping ACOUSTIC NEUROMA  Vestibular schwannoma, 8th CN schwannoma  Most commonly arising from vestibular portion  Lesions of 8th CN  hearing loss and dizziness, vestibular dysfunction, facial nerve dysfunction  Common, unilateral, benign  5% associated with NF type 2 = bilateral, associated with other tumors  Etiology:  Arise in the internal auditory canal and gradually grow (can ultimately grow into the pons and cause hydrocephalus)  S/s:  Unilateral hearing loss, deterioration of speech discrimination  Anyone with unilateral hearing loss  eval for mass  Dx:  MRI  Tx: observe  surgery VERTIGO  A cardinal symptom of vestibular disease  A sensation of movement with there is none, or an exaggerated sense of motion in response to movement  Key to this is HISTORY – onset, duration, triggers – more to come  S/s:  “spinning”, tumbling or falling  Peripheral vestibular disease:  Sudden and severe, associated with tinnitus or hearing loss  Central disease  Gradual, progressive  severe, debilitating  VERTIGO HISTORY  Onset of symptoms: spontaneous, head or visual motion provoked  Timing: Is dizziness intermittent or continuous? Does it last seconds, minutes, hours, days or weeks?  Type of dizziness: objects in room spinning, feeling of spinning in the head, imbalance, light headedness, disorientation, falls, unsteadiness, fogginess  Does the patient have signs of a central disorder (e.g. double vision, dysarthria, disturbances of sensation)?  How does the patient walk? Can they walk? Is their gait normal? Do they feel like they can walk steadily?  Other symptoms: nausea, vomiting, headaches, motion sickness, intolerance of light, heart palpitations, feeling of panic, drop attacks  Hearing: aural fullness, tinnitus (constant or pulsatile), progressive loss of hearing, fluctuating hearing loss, sensitive to noise, intolerance of sound  Past medical history: head trauma, back surgery, ototoxic drugs (e.g. gentamicin), diabetes, perilymphatic fistula, diabetes, hypertension, cardiovascular disease VERTIGO  PE:  Peripheral:  Eval HEENT, CN exam, Romberg  Nystagmus in response to head turning – horizontal nystagmus  Benign paroxysmal positioning vertigo (BPPV)  Dix- Hallpike test  Positive Dix-Hallpike  BPPV  Central  If there is nystagmus = non fatigable, vertical, unsuppressed by fixation  DX:  Audiologic evaluation, audio or visual nystagmography, MRI  Often initial presentation gets imaging PERIPHERAL VERTIGO CAUSES  Acute labyrinthitis  Acute vestibular neuritis  BPPV  Cholesteatoma  Herpes zoster  Meniere’s disease  Otosclerosis  Perilymphatic fistula  BENIGN PAROXYSMAL POSITIONING VERTIGO –  BPPV (PERIPHERAL) Posterior semicircular canal (80-90%) more  Dx: clinical common than horizontal  Tx:  Average age- 40s  Repetition of positional change leads to  Calcium carbonate crystals habituation  Spells of vertigo associated with  PT: Epley maneuver, Brandt-Daroff changes in head position exercises  Rolling over in bed, bending over quick  Recurrent cases require imaging  Provoked by the change in head position MRI/MRA  S/s:  Benign paroxysmal positioning vertigo  Vertigo symptoms with provoked onset, (BPPV)  Dix-Hallpike test sudden  Positive Dix-Hallpike  BPPV  Clusters that persist for several days  Acute vertigo lasts 10-60 seconds, but remain imbalanced for hours  Nystagmus, fatigable DIX HALLPIKE DIX HALLPIKE OTOLITH REPOSITIONING (EPLEY) LABYRINTHITIS  Etiology: unknown (peripheral issue)  S/s:  Acute onset of continuous, severe vertigo lasting DAYS  Accompanied with hearing loss and tinnitus  Recovery period lasts several weeks, during that time the vertigo improves  Hearing loss may be permanent or return  Tx:  Antibiotics if febrile or symptoms of infection  Corticosteroids  Supportive care  Vestibular suppressants = diazepam (acute symptoms only) VESTIBULAR NEURONITIS  Etiology:  PE:  Unknown, presumed viral  In acute phase, nystagmus present  Peripheral issues  Absent response to caloric stimuli  S/s:  Tx:  Paroxysmal, single attack of vertigo  Supportive care  NO impairment of auditory function  Vestibular suppressants =  Persists for days before gradually diazepam (acute phase only) improving  Oral corticosteroids  Antiemetics  Vestibular therapy OTHER ABNORMALITIES MENIERE DISEASE  Etiology: unknown  Peripheral issues  S/s:  Episodic vertigo, spells lasting 20 minutes to hours  Associated with sensorineural hearing loss, tinnitus, and unilateral aural pressure  Dx:  Clinical  CT/MRI  TX:  Decreasing dizzy episodes  Low salt diet, daily diuretics  Acute episodes = diazepam, lorazepam  Antiemetics  Refractory  surgical and procedural options  TMJ DYSFUNCTION  Disorder affecting the temporomandibular joint  Glenoid fossa of temporal bone and the mandibular condyle of the mandible  Muscles of mastication affect TMJ function  Patients can often present with ear symptoms:  Pain, tinnitus, vertigo, aural fullness, subjective hearing impairment – Why?  Headache, facial pain  TMJ pain  When will these patients have ear pain  PE:  Mandibular movement, ROM, palpation, loading, evaluate dentition, posture, head/neck/face muscles  R/o all other factors MASTOIDITIS  Etiology:  Evolves following several weeks of inadequately treated AOM  Middle ear is continuous with the mastoid air spaces  S. pneumoniae, H. flu, S. pyogenes  S/s:  Pain, postauricular cellulitis  Fever  PE:  Fever  Postauricular swelling, mastoid tenderness, lymphadenopathy, cellulitis  Dx:  CT scan  coalescence of the mastoid air cells due to destruction of the bony septa  Tx:  IV abx: cefazolin  Myringotomy for culture, surgical drainage  mastoidectomy THE GREAT IMITATORS… NON-OTOLOGIC EAR PAIN  Numerous causes- innervation of ear from trigeminal, facial, glossopharyngeal, vagus and upper cervical nerves  Cervical spine disc disease  periodontal disease  temporal arteritis  tendonitis of SCM,  parotid gland tumors  Tonsillitis  Sinusitis  GERD  Oropharyngeal CA. PEDIATRICS CROUP  Laryngotracheobronchitis – upper airway  Subglottic inflammation and narrowing  Can lead to full obstruction  INSPRIATORY STRIDOR  High-pitched respiratory sound due to turbulent airflow  Can be expiratory also  VERY common  Etiology:  Parainfluenza virus  Most common 6 mo. To 3 years, peak in fall and winter  Usually follows a common cold  Once older  laryngitis  CROUP  S/s:  Labs dx:  Harsh, barky/seal like cough  Can do neck XR: steeple sign (subglottic  Hoarseness narrowing)  Inspiratory stridor  Can so viral PCR  Respiratory distress  What would be signs of this?  Tx:  Oral or IM dexamethasone  PE:  Racemic epinephrine  Respiratory distress, tachycardia,  Humidified O2 tachypnea, fever  Cool air  Inspiratory or both inspiratory and expiratory stridor  Hospitalize  cyanosis, stridor at rest  Watch for fatigue  ?  DDX:  Clinical  Complications = viral PNA, bacterial  r/o epiglottis, FB, laryngomalacia tracheitis, bacterial PNA CROUP  Mild:  Barky cough, stridor when only agitated, no retractions or tachypnea  Meds and symptomatic care  Moderate:  Frequent barky cough, stridor at rest, some mild to moderate retractions  Meds – add racemic epi, monitor longer, if rebound  admit  Severe:  Frequent barky cough, agitated, severe retractions, stridor at rest is worse, poor air entry  Meds – IV maybe, repeat racemic, symptomatic  admit  DECREASED LOC, CYANOSIS, FATIGUE CROUP SOUNDS  https://www.youtube.com/watch?v=FMvELslY0pM  EPIGLOTTITIS  A MEDICAL EMERGENCY  PE:  Sniffing position: sitting, head forward, mouth open, and  High risk of sudden airway obstruction jaw thrust forward  Distressed, toxic, anxious  Not common due to vaccination  Respiratory distress, tachycardia, tachypnea, fever  Inspiratory or both inspiratory and expiratory stridor  Etiology:  Inflamed and swollen supraglottic structures (cherry red  Streptococcus or Staph. Aureus epiglottis)  Haemophilus influenzae type b in  DX: unimmunized  Lateral neck xray: thumb sign  Budling epiglottis and swelling of the aryepiglottic folds  S/s:  TX:  Difficulty breathing  Intubation  Fever – rapid onset  IV antibiotics: cephalosporin and staph aureaus coverage  Drooling  Blood cultures  Absence of cough, EPIGLOTTITIS (SUPRAGLOTTITIS) THANKS – QUESTIONS?  References:  Stat pearls  NIH  CDC  Osmosis  CMDT  Nelson’s  Tintinalli’s