Ears/Eyes Flashcards
Conductive hearing loss
From (physical/mechanical) problems that limit movement of the sound wave through the external and middle ear.
CAUSES:
- Obstructed external ear canal – eg. cerumen impaction, foreign body, exostosis, psoriais
- Perforated tympanic membrane – eg direct trauma, otitis media, or explosion
- Dislocated ossicle (malleus, incus, or stapes) - trauma to the ear
- Otitis media or serous otitis media
- Otitis externa - infection of the ear canal that causes it to swell
- Otosclerosis or ossicular chain fixation
- Congenital: eg external auditory canal atresia
- Cholesteatoma: growth of squamous epithelium in middle ear
Sensorineural hearing loss (SNHL)
Damage to the hair cells or nerves that sense sound waves (sensory problem in inner ear)
CAUSES and Associated Conditions:
- acoustic trauma - prolonged exposure to loud noises
- barotrauma (pressure trauma) or ear squeeze - eg divers, climbers
- head trauma - eg fracture of the temporal bone
- ototoxic drugs – (Bilateral loss) - antibiotics (aminoglycosides, erythromycin, and minocycline, tetracycline), diuretics (furosemide), salicylates (aspirin), NSAIDs, antineoplastics, antimalarial drugs, cocaine
- Aging—presbycusis: progressive bilateral hearing loss (high pitches), normal neuro exam
- Acoustic neuroma - tumor in the auditory nerve.
- Sudden SNHL (SSNHL) - unilateral hearing loss over 72 hr. Associated with microvascular event, head trauma
- Ménière disease - hearing loss, vertigo and tinnitus. Gradual onset, often progresses to deafness and severe vertigo
- vascular diseases eg sickle cell disease, diabetes, polycythemia, and excessive clotting
- Multiple sclerosis
Mixed hearing loss
combination of both conductive an sensorineural loss
Subjective tinnitus
Perception of sound (eg buzzing, ringing, roaring clicks) in absence of an acoustic stimulus may be intermittent, continuous, pulsatile; unilateral or bilateral
Audible only to pt, high frequency, due to damage of fine hair cells
Etiology: Acoustic trauma , Presbycusis, Barotrauma, CNS tumors, Eustacian tube dysfunction, Infections (OM, labryinthitis, meningitis), Meniere disease, Ear canal obstruction (wax, foreign body, tumor), Drugs (salicylates, loop diuretics, cisplatin, aminoglycosides)
Can accompany SNHL
Objective tinnitus
Rare, can be heard by listening directly over the patients ear
Etiology: A-V malformations, Monoclonus (palatal ms, tensor tympani, stapedius), Turbulent flow in carotid or jugular, Vascular middle ear tumor (esp if unilateral—R/O by ordering CT)
Other types/causes of tinnitis
hyperlipidemia, allergies, diabetes, hypertension, hypotension, syphilis, cardiovascular, endocrine, and metabolic disease, TMJ disorders, cervical injuries, stress, dietary deficiencies, and intake of stimulants (nicotine, caffeine).
Work-up for Tinnitus
History: get good description of “sound” (episodic/constant, pitch, quality)
Ask about noise exposure, head trauma, hearing problems, dizziness, loss of balance, recent dental problems/work, bruxism, stress, ototoxic drug use, smoking, caffeine, HTN, anxiety, insomnia
PE: Otoscopic exam, cranial N VIII function and hearing (whispered, tuning fork tests)
Check for: carotid artery bruits, HTN, oral exam, neck and jaw hypertonicity, TMJ dysfunction
Additional work-up: audiology, angiography
Vertigo
Nonspecific term describing a sensation of altered spatial orientation “illusory movement”
Most often caused by dysfunction of the vestibular, visual, or proprioceptive (posterior column) systems, or by diffuse impairment of blood flow to the brain
More common in aging, increased incidence of falling in those > 65 years.
Subjective: if patient has the impression they are “moving in space” (self-motion)
Objective: if objects “moving around” the patient (motion of the environment)
True Vertigo (most common)
Caused by asymmetry in the vestibular system (CN8, inner ear, cerebellum)
SSx: either surroundings are moving (objective) or patient is moving within surroundings (subjective)
Postural instability, nausea and vomiting common, sweating, worse when moving head
Nystagmus is commonly seen on eye exam (involuntary movements of the eye)
Peripheral vertigo: labyrinth or CN VIII
Central vertigo: cerebullum, vestibular cortex in temporal lobe
Non-vertigo (syncope, fainting or sensation of impending fainting)
- Lightheadedness
“graying out” of vision, pallor, and a roaring sound in the ears
Results from hypoperfusion due to: hypotension, drugs, decreased cardiac output, hypoglycemia, shock, dehydration, severe anemia, cardiac arrhythmias - Disequilibrium
occurs only while standing or walking (gait impairing), unsteady without any dizziness
pt says that “dizziness is in feet, not in head”
Source of problem may be: cerebellum, basal ganglia, cervical spondylosis, lobe tumor, stroke, motor neuron diseases - Miscellaneous
Chronic hyperventilation syndrome
Often unaware to patient
Frequent deep breaths while relaxed
New eyewear & diplopia
Phobias (agoraphobia, acrophobia)
Extra-ocular muscular palsy results in diplopia
Work-up for Vertigo
History:
Onset: sudden or gradual?
Sudden onset and vivid memory of episodes are often due to inner-ear disease
Gradual and ill-defined vertigo most common in CNS, cardiac, and systemic diseases
Duration:
Episodic true vertigo that lasts for seconds, associated with head or body position changes likely benign paroxysmal positional vertigo (BPPV)
Vertigo of sudden onset that lasts for minutes can be due to brain or vascular disease
Vertigo that lasts for hours or days probably caused by Ménière disease or vestibular neuronitis
PE:
General examination - vital signs, supine and standing BP, orthostatic BP, CVS
Otological exam: examine ears for cerumen, discharge, foreign body, TM - perforation may result in sudden vertigo
Extraocular movements (H/X in space) - check for nystagmus
Hearing tests - Gross hearing (whispered voice test), Weber (Conductive), Rinne (SNHL)
Sensory exam to assess proprioception
Vestibular imbalance:
Red flag concomitants: head or neck pain, ataxia, loss of consciousness, focal neurological deficit
Earache (otalgia)
Causes:
external ear –impacted cerumen or foreign body, local trauma, otitis externa
middle ear – eustacian tube obstruction, OM, neoplasms
referred pain from TMJ, wisdom teeth
local infections: tonsillitis, enlarged adenoids, peritonsillar abscess
atlas/axis subluxation
tumor in pharynx, tonsils, tongue, larynx; thyroiditis
neuralgia: trigeminal, sphenopalatine, glossopharyngeal, geniculate
colds, allergies, cold wind blowing in ear
Red flag concomitants: Diabetes or immunocompromised pt, redness/pain over mastoid, Severe swelling of canal meatus, chronic pain with head/neck symptoms
Ear Discharge (otorrhea)
Causes:
Acute: Acute OM with TM perforation, Post-tympanostomy tube, CSF leak from head trauma,OE (infection or allergy)
Chronic: Cancer of ear canal, Cholesteatoma, Chronic purulent OM, Foreign body, Mastoiditis
Red flag concomitants: head trauma, cranial nerve dysfunction, fever, erythema of the ear, diabetes or immune compromised
External ear Obstruction
cerumen may block & cause itching, pain, conductive hearing loss
foreign body, esp. with children- beads, erasers, insects, just about anything!
Acute Otitis Externa (AOE)
Etiology: Infection (strep, staph, E. coli, pseudomonas, aspergillus), “swimmers ear”, forceful cleaning of the ear, trauma
SSxs: itching, pain, discharge possible, loss of hearing if canal becomes swollen or filled with purulent debris
PE: pinna & tragus painful when pressed or tugged (different from OM)
external canal appears red, swollen
TM (may not be visualized) is normal pearly gray
Pseudomonas infx produces purulent green/ yellow otorrhea
Aspergillus looks like a fine white mat topped by black spheres
fever, swollen lymph nodes possible
Chronic Otitis Externa
Etiology: often follows psoriasis, seborrheic dermatitis, eczema, or can be from allergy or fungus
SSxs: pruritis, redness, discharge
PE: pinna & tragus less likely painful
external canal appears irritated, perhaps dry, flaking tissue
TM not usually affected
May get secondarily infected, increased pain and swelling
Perichondritis
Trauma, insect bites may lead dec blood supply to ear cartilage: avascular necrosis/deformity
Tumors
sebaceous cysts, osteomas (bony growths, often from cold sea water) may occlude ear canal gouty deposits (tophi on outer ear) BCC or SCC - hx of sun exposure on external ear
Acute Otitis Media (AOM)
2nd most common dz of childhood (URI # 1); ~ 20 million annual physician visits
Etiology: Organism, anatomic position of eustacian tube and immunologic factors
Common: Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis
Less common: Group A streptococcus (older kids), Staph aureus, Gram neg bacilli (newborns, immunocompromised), viruses, Mycoplasma pneumoniae
Can also be sterile effusions (no organism found)
Risk factors: daycare exposure, bottle-feeding (lying down), smoker(s) in the household
AOM in the first year of life is risk factor for recurrent acute otitis media.
SSxs: throbbing pain (or maybe NO pain), fever, decreased hearing, n/v, moodiness, irritability
child may tug on ear; sleep may be disrupted due to pain
PE: bulging, red (or cloudy) TM, possible fluid line (yellow-gray if pus)
decreased mobility on pneumatic otoscopy (insufflation)
Complications:
Otitis media with effusion most common.
If bilateral, hearing loss with resultant speech delay may occur in infants.
Mastoiditis used to be a common complication, but now rare.
Perforation (rupture) of the TM is frequent, but usually not serious (unless peripheral)
IF TM perforates: discharge and sudden loss of pain
If perforation is peripheral, check regularly for cholesteatoma
May persist during Abx treatment, or relapse within 1 mo
Otitis Media with Effusion (OME, Serous OM)
Effusion (fluid) in the middle ear - incomplete resolution of acute OM or due to inflammation
Risk factors: Prior tympanostomy tube placement, Allergy (often food – dairy, oranges, apples; environmental), adenoid hypertrophy, Summer/Fall months
SSxs: Hearing impairment – child’s behavior may be described as inattentive (ADD misdiagnosis?)
Mild otalgia - intermittent ear pain tends to worsen at night
Ear fullness or popping
May also have overlapping sx of common cold (nasal d/s, sore throat)
PE: Amber or gray TM, INTACT but typically retracted or in the neutral position
Impaired mobility of the TM during pneumatic otoscopy
Bubbles or air/fluid level may be seen
Chronic cervical LA
Course: can persist: (COME) fluid behind intact TM; Risk of infection, recurrent AOM and/or perforation
Chronic Suppurative Otitis Media (CSOM)
Chronic inflammation of middle ear that persists at least 6 wks with TM perforation and otorrhea
Etiology: acute OM resulting in perforation (conductive hearing loss), trauma to ear/head
SSxs: hearing loss, chronic purulent d/c, painless
PE: Perforation of the tympanic membrane (pars flaccida in patients with atticoantral disease and pars tensa in patients with tubotympanic disease)
May see: retraction pocket in the posterosuperior quadrant, choleseatoma, granuloma, polyps
Course: May have a perforation without ever getting any symptoms, but sometimes a chronic bacterial infection develops.
May flare up after a URI or after water enters the middle ear while bathing or swimming. Usually, flare-ups result in a painless discharge of malodorous pus from the ear. Persistent flare-ups may result in the formation of polyps, from the middle ear through the perforation and into ear canal.
Persistent chronic infection can destroy parts of the ossicles leading to conductive hearing loss. In a child, this can lead to delayed intellectual development
DDX: Otitis externa, cholesteatoma (congenital or acquired), myringits, chronic mastoiditis, impacted cerumen, tympanosclerosis, Wegener granulomatosis
Myringtitis
Inflammation and/or infection of the TM. Primary or Secondary, Acute or Chronic forms
Primary causes: can accompany Mycoplasma pneumonia URI
TM trauma (foreign body, cleaning, explosion)
Acute bullous Myringitis: vesicles on TM from infx (S pneumoniae, herpes)
Acute hemorrhagic myringitis: bact or viral infx
Fungal and eczematous forms
Myringitis granulosa—unclear cause
Secondary causes: Acute otitis media, acute otitis externa, Chronic otitis media, chronic otitis externa
SSxs: Serosanguinous otorrhea, otalgia, hearing impairment
acute: sudden onset of ear pain that lasts 24 to 48 hours, fever
PE: Vesicles develop on the TM in bullous form, granulomatous tissue in granulosa form
Cholesteatoma
Growth of keratinizing squamous epithelium in middle ear and/pars tensa, can enlarge
Etiology: congenital, primary acquired, and secondary acquired. (prev perforation, retraction pocket)
SSxs: painless otorrhea, either unremitting or frequently recurrent.
Conductive hearing loss initially, then can grow into inner ear causing SNHL
Dizziness is relatively uncommon
PE: canal filled with muco-pus and granulation tissue
TM perforation is present in >90% of cases.
May require surgical removal
Acute Mastoiditis
Suppurative infection in the mastoid air cells
Etiology: Complication of severe AOM
Streptococcus pneumoniae (most common), Streptococcus pyogenes, Staphylococcus spp, Haemophilus influenza, Pseudomonas aeruginosa
SSxs: redness, swelling, tenderness behind ear, fever, hearing loss, profuse creamy ear d/c, throbbing pain
PE: Bulging erythematous TM
Tenderness (redness, swelling) over the mastoid area
Postauricular fluctuance
Protrusion of the auricle, downward displacement of auricle
Complications: subperiosteal abscess, CN 7 palsy, hearing loss, osteomyelitis, meningitis, venous sinus thrombosis
Refer! - MRI or CT. Treatment with drainage and antibiotics
Otosclerosis
Genetic (autosomal dominant) metabolic bone disease affecting otic capsule and ossicles, leads to overgrowth of footplate in stapes/dysfunction
F>M 2:1; much more common in whites, most commonly appears 15-35 yrs.
SSxs: Progressive bilateral (conductive) hearing loss and tinnitus (occasionally, vertigo)
Tympanosclerosis
Sclerosis of TM: from chronic OM, post T-tube
Leads to stiffening of the tympanic membrane and impaired conductive hearing
SSxs: early asymptomatic, but hearing loss progresses
PE: Whitish plaques on TM (areas of hyalinization with deposition of calcium and phosphate crystals)
Viral labyrinthitis
Peripheral vestibular disorder - Sudden unilateral hearing loss and severe vertigo, frequently assoc nausea and vomiting
Patient is often bedridden while the symptoms gradually subside.
Vertigo eventually resolves after several days to wks; however, unsteadiness and positional vertigo and hearing loss may persist
URI precedes the onset of symptoms in up to 50% of cases
Can result from reactivation of a latent varicella-zoster virus infection, yrs after the primary infection (Herpes Zoster Oticus – Ramsay-Hunt syndrome)
Adults aged 30-60 years, rarely observed in children.
PE: spontaneous nystagmus towards the normal side with diminished or absent caloric responses in the affected ear.
hearing loss: mild to moderate, often higher frequencies (>2000 Hz)
SSxs: initial deep, burning, auricular pain followed a few days later by the eruption of a vesicular rash in the external auditory canal and concha. Vertigo, hearing loss, and facial weakness may follow
Bacterial labyrinthitis
Peripheral vestibular disorder caused by either direct bacterial invasion (suppurative labyrinthitis) or through the passage of bacterial toxins into the inner ear (serous labyrinthitis).
- meningitis typically affects both ears. Bacteria spread from the cerebrospinal fluid to the membranous labyrinth by way of the internal auditory canal or cochlear aqueduct.
- infections of the middle ear or mastoid most commonly spread to the labyrinth through a dehiscent horizontal semicircular canal. Usually, the dehiscence is the result of erosion by a cholesteatoma.
SSxs: profound hearing loss, severe vertigo, ataxia, and nausea and vomiting
Now rare in the post-antibiotic era
Vestibular neuritis
Peripheral vestibular disorder - benign and temporary disorder of the vestibular nerve resulting in vertigo NOT assoc with hearing loss
more common in the fourth and fifth decades of life . M=F
URI often precedes. More common in the spring and early summer, commonly viral
SSxs: sudden acute vertigo without hearing loss in an otherwise healthy patient.
PE: horizontal nystagmus may be present, some gait instability, NO hearing loss
Benign Paroxysmal Positional Vertigo (BPPV)
Peripheral vestibular disorder - sudden vertigo elicited by provocative positions, triggering nystagmus. The character and direction of the nystagmus are specific to the part of the inner ear affected and the pathophysiology
Subclassified by location in semicircular canal (ie, horizontal, posterior, or superior) and pathophysiology (canalithiasis and cupulolithiasis)
- canalithiasis (literally, “canal rocks”) particles residing in the canal portion of the SCCs. These densities are free floating and mobile, causing vertigo by exerting a force.
- cupulolithiasis (literally, “cupula rocks”) refers to densities adhered to the cupula of the crista ampullaris. Cupulolith particles reside in the ampulla of the SCCs and are not free floating.
BPPV is due to posterior semicircular canal canalithiasis ~ 90% of the time.
Etiology: risk factors–inactivity, alcohol, caffeine, major surgery, and CNS disease.
Idiopathic, head/ear trauma, otitis media, vestibular neuritis, Ménière disease, otosclerosis, SSNHL, acoustic neuroma, vertebral basilar insufficiency
SSxs:
Sudden onset: vertigo while trying to suddenly sit up, lying down, rolling over in bed, looking up.
Symptoms start very violently and usually dissipate within 20 or 30 seconds
Severe dizziness occurs as “attacks” some cases, even the slightest head movement causes N&V.
Between episodes, patients usually have few or no symptoms. However, some patients complain of a continual sensation of a “foggy or cloudy” sensorium.
In many, the symptoms periodically resolve and then recure
PE: Generally unremarkable.
Dix-Hallpike maneuver - standard clinical test for BPPV - rapidly move the patient from a sitting position to the supine position with the head turned 45° to the right. After waiting approximately 20-30 seconds, the patient is returned to the sitting position. If no nystagmus is observed, the procedure is then repeated on the left side. Vertigo and nystagmus seen in posterior canal dysfunction
Positive test: classic rotatory nystagmus with delay and limited duration is considered pathognomonic.
Acoustic Neuroma (Vestibular Schwannoma)
Peripheral vestibular disorder
Benign, slow growing tumor derived from Schwann cells of CN VIII
SSxs: unilateral, progressive SNHL, Vertigo, tinnitus, disequilibrium can be concomitant
Headaches are present in 50-60% of patients
Facial numbness occurs in about 25% of patients
A large tumor can compress the brainstem and affect other cranial nerves, inc intercranial pressure
Consider any unilateral sensorineural hearing loss an acoustic neuroma until proven otherwise.
Ménière disease (lesion called “endolymphatic hydrops”)
Peripheral vestibular disorder
Increase in volume and pressure of the endolymph in the endolypmhatic spaces of inner ear.
Typically occurs in early- to mid-adulthood; M=F
Etiology: exact cause is unknown. Up to 50% of patients have a positive FHx
SSxs: Triad - waxing and waning SN hearing loss, tinnitus, vertigo
a. Prodrome: fullness or blocked sensation in one ear (like listening to shell)
b. Tinnitus followed by a decrease in hearing (esp low pitches), nausea, vomiting, diarrhea, pallor, and sweating common with an acute attack
c. Vertigo is experienced concurrently with or follows shortly after the hearing symptoms; typically lasts min to hrs but may last several days.
d. headache and gait unsteadiness may persist for several days
Course: following an acute episode, hearing may return to normal. Recurrence is common but unpredictable; hearing usually is decreased over time
Tumarkin crises - patients may experience such severe vertigo that they will collapse to the ground.
PE: complete neurological examination is necessary to R/O other conditions, esp. cranial nerve examination
Vestibular maneuvers (Nylen-Bárány, Dix Hallpike) may be helpful in diagnosing this syndrome.
DX:
i. isolated attacks of whirling, vertigo usu with n/v for at least 20 min, up to several hrs
ii. tinnitus - multipitched, multisounds, roaring, whistling: severe, unilateral, constant or fluctuating
iii. sensory hearing loss (progressive) [10-15% are bilateral]
DDX: migraine headache, hypothyroidism, labyrinthitis, multiple sclerosis, OM, ischemic stroke subarachnoid hemorrhage , TIA, vestibular neuritis, acoustic neuroma, salicylate toxicity
Toxic vestibulopathy
Central vestibular disorder from ingestion of various agents:
Aminoglycoside antibiotics - creates bilateral vestibular damage, may have blurred vision while moving the head (eg streptomycin, gentamicin most vestibulotoxic; neomycin, kanamycin, tobramycin most auditory toxicity)
Aspirin can produce dose-related reversible tinnitus, hearing loss, dizziness
Alcohol produces reversible positional nystagmus
