Flashcards in ENT Deck (349):
what is involved in the ENT exam?
ear - external, otoscopy, tuning forks
nose- anterior rhinoscopy
throat- oral cavity/pharygeal exam
neck - palpation, thyroid exam
this is common in wrestlers, where blood collects between mucoperipchonidrium and cartilage.
tx: drainage and bolster dressing to avoid cauliflower ear
this is a benign condition, more common in AA. Difficult to treat because comes back, and is treated by surgical removal or steroids
this comes from an alkalotic environment/trauma by the pathogen pseudomonas or staph aureau
otitis externa (swimmers ear)
how is otitis externa treated?
oto-topical drops, oral abx (quinolones to tx pseudomonas)
what are complications of otitis externa and who are they more common in?
malignant otitis externa (skull base osteomyelitis)
more common in diabetics- usually admitted for IV abx
this is a fairly commonly seen benign body overgrowth of the ear canal. typically doesn't cause any problems or pain
why does an ear drum become retracted?
eustachian tube dysfunction
common problem secondary to q-tips
ruptured tympanic membrane - wait 3 months for healing, keep dry, most heal on their own
what is the difference between otitis media and effusion?
otitis media is an inflammatory condition of the middle ear space - think eustachian tube dysfunction
effusion just means there is fluid in the middle ear space. middle ear liquid resulting from infection of inflammation (can be serous, mucoid, purulent)
different classifications of otitis media
acute ( 12 weeks)
what is acute otitis media?
fluid with infection
2nd most common disease in children (URI is #1)
what is the cause of acute otitis media?
eustachian tube dysfunction
sxs: fever, otalgia, bulging red TM
pathogens for otitis media
s pneumo, h flu, m cat
what is the first line treatment for otitis media?
amoxicillin (usually 45 mg/kg 2x a day)
beta-lactamase inhibitor is 2nd line
Tympanocentesis if not improving with abx
what is otitis media with effusion and how do you treat?
fluid without infection
cause: eustachian tube dysfunction
sxs: hearing loss, speech delay
treatment depends on chronicity, dont need antibiotics
these are used to help ventilate middle ear space and normalize pressures
ear tubes (surgery)
what are the indications for ear tubes?
recurrent acute otitis media - 3 infections in 6 months or 4 in 1 year with current effusion on exam
Chronic Otitis Media with Effusion – greater than 3 months of effusion with evidence of hearing loss
Think about the adenoids!!! – sits in posterior nasopharynx. If enlarged, can cause obstruction of orifices and can be cause
what will the tympanic membrane look like with otitis media with effusion and acute otitis media?
otitis media with effusion will have yellow or amber colored fluid behind tympanic membrane (indicated serous fluid)
acute otitis media with be Erythematous
what are some complications of otitis media/chronic ear disease?
they're uncommon now because of antibiotics but infection can spread to brain, sigmoid sinus, mastoid air cells (mastoiditis)
all need to be treated aggressively with IV antibiotics, ear tube drainage, possible mastoidectomy
#1 chronic complication of otitis media
cholesteatoma - skin debris gets trapped in middle ear space and continues to dequemate
inflammation of tympanic membrane as opposed to middle ear space in AOM. very painful, due to pathogen mycoplasma pneumonia
if associated with blisters in canal need to think about zoster infection
first test for hearing. you place the fork on the top of the head in midline. conduction losses latralize to side of lesion, sensorineural losses lateralize to opposite ear
hearing test for bone vs air conduction
AC>BC in SNHL, BC>AC in CHL
t or f: almost all cases of conductive hearing loss are correctable with surgery
true - osteosclerosis
how should you treat a sudden sensorineural HL?
should be evaluated by an ENT within 24 hours and treated with steroids
asymmetric SNHL is what until proven otherwise?
acoustic neuroma- benign tumor on vestibulocochlear nerve. patient needs MRI
perception of motion in the absence of movement. usually described as the room spinning
vertigo - this is a symptom, not a diagnosis
what body parts are involved in balance system?
this is caused by otoliths in the semicircular canal, lasts seconds to minutes, associated with head movement. patients usually say that they "“Lay in bed, turn to my right side and the room spins really badly for 2 min then goes away”
benign paroxysmal position vertigo (BPPV)
Dx: Dix-Hallpike test
Rotary nystagmus beating toward affected ear
Tx: Canolith repositioning – done in office. Lay back and hit mastoid bone repeatedly
when someone has acute onset vertigo, what should be your first thought?
what is acute onset vertigo?
sudden onset that lasts hours to days, even weeks
central: Central (neurologic cause) – NEEDS IMAGING!
Vestibular, unclear cause
Labrynthitis (associated with hearing loss) vs Vestibular Neuritis (just vertigo)
Meclizine, valium, anti-emetics
this is caused by an increase in endolymphatic pressure, and symptoms include episodic vertigo usually lasting several hours with fluctuating SNHL, aural fullness, and tinnitus.
Initial main treatment goal is to reduce pressure in inner ear
Low salt diet
most common causes of epistaxis
mucosal drying and trauma (picking your nose)
Auto Dominant disorder with defect in contractile elements of blood vessels and formation of AV malformations
Osler-Weber-Rendu Syndrome (Hereditary Hemorrhagic Telangiectasia)
what is the difference between the classifications of sinusitis?
acute: 3 months
something going on thats causing poor drainage of the mucus at sinus ostia
most common pathogen of acute sinusitis
then S. pneumo, H flu, M Cat
Fungus – Aspergillus/Mucor
Staph Aureus, anaerobes
how do you treat sinusitis?
acute: abx 10-14 days
chronic: 3-6 weeks antibiotics, needs CT if not responding
benign, jelly filled sacks formed off the mucosa. can cause some secondary sinusitis because blocking drainage
think of intranasal drug use or trauma
benign oral presentations
bony overgrowth of the palate
dark veins under tongue
lymphoid tissue that sits in continuous circle in the oro and nasopharynx to accept Ag’s for the upper AD tract.
if adenoids are enlarged (adenoid hypertrophy), what can they affect?
the eustachian tube (usually in kids)
what is the most frequent cause of otolaryngologic infection in children?
rhinovirus, influenza, parainfluenza, adenovirus, RSV
Viral pharyngitis usually more mild in presentation.
symptoms of common cold
sore throat, dysphagia, fever with tonsillar erythema
Small vesicles with erythematous base that become ulcers and spread
high fever, malaise, large swollen dirty gray exudative tonsils. Hepatosplenomegaly
Large bilateral tender posterior LAD
Petechiae at junction of hard and soft palate not pathognomonic.
most specific test for EBV
monospot - latex agglutination assay
very specific but low sensitivity so high false negative rate- (False negative rates 25% in first week down to 5% by 3rd week.)
If clinical suspicion is high despite negative Monospot, can do EBV antibody testing.
treatment for EBV
what should be avoided in patients with EBV?
ampicillin because a rash can develop
when should you hospitalize a patient with EBV?
cases of severe hypertrophy with dehydration, upper airway obstruction – treat with steroids or emergent tonsillectomy if needed in rare cases.
most common pathogen for pharyngitis
group A streptococcus - Public health importance due to its frequency and serious sequelae.
treatment for Streptococcal Tonsillitis-Pharyngitis
symptoms of Streptococcal Tonsillitis-Pharyngitis
odyophagia (pain when swallowing food) , otalgia (ear pain), fever, headache, malaise, cervical adenopathy, enlarged red exudative tonsils
in which patients is thrush most common?
patients you use inhaled corticosteroids, diabetics
tx with nystatin, clotrimazole, diflucan
Classic complication of tonsillitis that brings patients to the ER for evaluation and treatment. patient presents with tonsillitis that is not responding appropriately to ABX and is now worsening after days of treatment. UNILATERAL symptoms, OTALGIA, drooling with severe odynophagia (poor PO intake), trismus (irritation of pterygoid musculature)
peritonsillar abscess (quinsy)
on exam, uvula pushed off midline
Can occur as a sequelae from an infection of the nose, sinuses, or pharynx since the lymph nodes of this space drain these areas. They usually occur in children less than 2 years old and present with some of the same symptoms in addition to having a stiff neck and sometimes some muffled speech.
retropharyngeal space abscess
indications for tonsillectomy
chronic tonsillitis (7 infections in one year, 5 for past two years, or 3/year for the past 3 years)--> just guidelines, everyone is diff
if one tonsil is bigger than other (unilateral), then most concerning so would probs do tonsillectomy
Note size of tonsils in children with loud snoring and breathing difficulties at night noted by parents.
Questions/Critical exam features to look for in hoarse patient
progression over time
associated breathing problems
signs of infection
poor secretion management
pain associated with voice changes
presents with drooling, hot potato voice, rapid progression, posturing forward, systemic toxicity/fever, inspiratory stridor
epiglottitis - now more common in adults (Group A strep, Staph aureus)
Thumbprint sign – inflamed/swollen epiglotis
treat with IV abx, rapidly secure airway if necessary
infection of the subglottic larynx causing biphasic stridor. commonly caused by parainfluenza virus but any upper repiratory infection in young child can cause it. steeple sign on xray
how do you treat croup?
cool mist humidity, steroids in severe cases with hospital admit
usually presents slowly over few months and almost always in a chronic smoker/EtOH abuse but not always.
common/benign disease of larynx
vocal cord nodules
vocal cord polyps
what are the symptoms of laryngopharyngeal (LPR) reflux?
hoareseness, globus, throat clearing, AM symptoms
diff from GERD which has heartburn, chest pain, regurgitation, and PM symptoms
how do you treat LPR (Laryngopharyngeal Reflux)?
more aggressive PPI (bid)
which salivary glands are most commonly affected in parotitis/sialoadenitis?
parotid and sublingual
common symptoms of Parotitis/Sialoadenitis?
painful swelling, often worse after eating. erythema over the area, purulent drainage from the duct
image looks like a swollen neck
common causes of parotitis/sialoadenitis?
sialolithiasis (a condition where a calcified mass or sialolith forms within a salivary gland, usually in the duct of the submandibular gland )
treatment of parotitis/sialoadenitits
conservative measures: massage, warm compresses, sialogogues
abx: augmentin, clindamycin
recurrent episodes may require excision of the gland
Most common non-cutaneous head and neck site for masses/cancer
oral cavity - vast majority is squamous cell carcinoma
risk factors: smoking/EtOH use
presentation of head and neck masses/cancer
unexplained throat pain, dysphagia, hoarseness especially in patient with above risk factors needs further workup
when evaluating a patient with a neck mass, what should be the first consideration?
age of the patient
Pediatric (0-15 years old)
Young Adult (16-40 years old)
Adult (40+ years old)
second consideration of a patient with a neck mass?
location of the mass
If it is in the anterior compartment, think either thyroid neoplasm or lymphoma
when inflammation is suspected with a neck mass, what is the longest amount of time you can have an antibiotic trial?
what is the most cost effective and most productive single diagnostic evaluation available for a patient with a neck mass?
FNA (fine needle aspiration)
an undiagnosed neck mass in an adult is what until proven otherwise?
t or f: Excisional biopsy of a mass in an adult prior to a complete head and neck evaluation is recommended
FALSE. contraindicated and could lead to a worse treatment outcome
prefix for eyelids
sebaceous glands of eye
Meibomian: inner eyelid
glands of zeis: outer eyelid
large sweat glands at the outer eyelid margin
glands of moll
eyelids are given shape and form by the tarsal plates within them
differences between chalazion and stye
chalazion is internal in the meibomian gland so treated from inside the eye
stye is outside so tx from outside
where are the lacrimal glands located?
upper outer eyelids. Tears are secreted from the glands secretory ducts --> collected at the nasal edge of the palpebral fissure and pass through the puncta into the sup &inf canaliculi --> lacrimal sac
From the lacrimal sac, they pass into the nasolacrimal duct and then into the nose in the inferior meatus (below the inferior turbinate)
blockage of tear duct/not fully matured in babies
dacrocystitis - tx with warm compress
function of tears
form smooth refractive surface on epithelium- inhibits bacterial growth
maintains moist environment for epithelium
carries oxygen to the eye
what is the term for inflammed conjuctivae?
three coats of eye
inner layer - retina
-inner nerve layer (axons and ganglia)
- outer pigmented (photoreceptive layer with rods and cones)
middle vascular layer - uveal tract (iris, ciliary body, choroid)
outer fibrous layer (sclera)
white of the eye which surrounds the entire eye except for the cornea
sclera (superficial is episcler- and deep is scler-)
this composes the anterior 1/6 of the eye and is avascular
cornea - receives nourishment from aqueous humor
where does the greatest change in refractive index occur
at the air-corneal tear film interface
where does the bulbar conjuctiva meet the cornea?
limbus (limbic margin)
round sphincter muscle that controls pupil size
Outer aspect of the iris forms an angle with the cornea (the “anterior chamber angle”) that is important in glaucoma
kayser-fleischer rings are associated with what?
wilsons disease - copper storage disease
term for pupillary dilation
midriasis - when the iris dilator muscle contracts (under SNS control), the pupil dilates
Pupils dilate under dark conditions and when focused on a distant object
term for pupillary constriction
miosis - When the iris constrictor muscle contracts (under PSNS control), the pupil constricts
Pupils constrict under light conditions and when focused on a near object
Both pupils should be equal
Pupils diameter should not vary by more than 1 mm between the eyes
Be sure to check in dim light if you see a difference in a bright room
term when there is a pupil size difference of > 1 mm
is the lens vascular or avascular?
avascular (65% water)
biconvex, colorless, transparent
when does the lens become thicker and thinner?
It is an elastic structure that becomes more spherical (thicker) when relaxed for near vision, and more flat (thinner) when stretched for far vision
what divides the eye into the aqueous cavity in front and a vitreous cavity behind?
what determines the shape of the lens?
ciliary muscle tension - lens is suspended from the suspensory ligaments that are attached to the ciliary muscle
Contraction of the ciliary muscles pulls on the choroid, thereby relaxing tension on the suspensory ligaments. This then allows the lens to assume a more spherical shape for near vision
Relaxation of the ciliary muscles results in more tension on choroid, thereby increasing tension on the suspensory ligaments. This then causes the lens to assume a more flattened shape for distance vision
the space between the cornea and iris, filled with aqueous humor
what maintains IOP and nourishes the avascular lens and cornea?
blood in the anterior chamber is called what?
pus in the anterior chamber is called what?
the space between the iris and the lens, filled with aqueous humor
large eye cavity located behind the lens
Filled with a jelly-like vitreous humor
*Acts as a “shock-absorber”
what are little dots, circles, lines, to clouds or cobwebs in the vitreous cavity?
floaters - if you have an increase, may be retinal detachment
The dark brown/black vascular coat of the eye, located between the sclera and retina
this is comprised of the iris, ciliary body and choroid
The anterior uveal tract consists of the iris & ciliary body
The posterior uveal tract consists of the choroid
yellow spot in the posterior central area of the retina, just lateral to the optic disk
this is an area in the macula lutea with densely packed cones, that is the area of most acute vision
fovea centralis - has deeper blood supply than the rest of the retina
The “fundus” refers to that part of the retina that is able to be visualized with an ophthalmoscope
Tasacks disease (sp?) – lipid disorder **cherry red spots - preserved in fovea
which area is responsible for the blind spot?
optic disk - point of transition from the retinal to the optic nerve
This area contains the optic nerve (containing over 1 million nerve axons), central retinal artery & vein
how many bones make up the walls of the orbit?
Many Friendly Zebras Enjoy Lazy Summer Picnics
a lesion here will result in bi-temporal vision loss?
Galactoria and bitemporal visual field loss – PITUITARY ADENOMA
a lesion here will result in homonymous (same side) defects
optic tracts and radiations
a lesion here will result in loss of vision of only this one eye
90% of eye's blood supply is through what?
choroid layer blood supply - Supplied by 10-20 short posterior ciliary arteries that enter near the optic nerve
normal cup: disk ratio
hemorrhages with central clearing
roth spots - endocarditis
Blot hemorrhages occur deep in the retina
Flame hemorrhages are superficial hemorrhages that follow the nerve layer pattern
these represent focal retinal ischemia
soft (cotton wool) exudates
Must be distinguished from myelination of the optic nerve
Represent leakage of proteins and lipids from blood vessels
represent small white hyaline (a substance from cell degeneration) deposits that develop beneath the retinal pigment epithelium. Occur most frequently in persons older than 60 y/o (a consequence of aging)
May be a precursor of age-related macular degeneration
Must be distinguished from hard exudates
difference in vision loss between glaucoma and macula
macula is central vision loss
glaucoma is peripheral vision loss
drusen is deposited right over where you would see optic nerve
patients describe this as a curtain being drawn over vision
Sometimes gravity will help so just have them lay supine
cherry red spots are pathomneumonic for what?
no refractive error
hyperopia (shorter than normal eye)
Require a bi-convex lens to converge the light rays more
myopia (longer than normal eye)
Light rays focus in front of the eye
Require a bi-concave lens to diverge the light rays more
A distortion of vision caused by a difference in refractive power along different meridians of any of the main refractive surfaces (cornea, anterior lens, or posterior lens surfaces)
a pinhole corrector will overcome most refraction errors and is helpful in determining in refraction is the cause of visual loss or not
outward displacement of the eyeball with a widening of the palpebral fissure
May be bilateral or unilateral
More serious (pathological) causes:
Thyroid orbitopathy (e.g., Graves Disease)
Intraorbital inflammation and edema (cellulitis)
Intraorbital trauma (to bones or EOMs resulting in hemorrhage)
lack of parallelism (misalignment) of the visual axes of the eyes such that the optic axes cannot be directed to the same object (eyes don't focus and move together properly)
May be convergent strabismus (“Esotropia”) resulting in crossed-eyes,
or divergent strabismus (“Exotropia”)
May be unilateral, bilateral, alternating
May be permanent or intermittent
at what age should you be concerned about strabisumus?
after age 6, when binocular vision should be well established
Leads to vision loss if not corrected early-on (by age 5 or 6 at the latest)
Eye patching in kids may cause an iatrogenic strabismus!
this refers to poor or complete loss of vision in one eye that cannot be corrected with a lens. It usually is the end result of when the images of the two eyes cannot be properly fused into one, leading the occipital cortex of the brain to ignore one of the images. Complication or sequela of strabismus
can be caused by :
Strabismus (misalignment of the eyes)
Anisometropia (a large diffference in refraction between the eyes)
Opacity anywhere along the visual axis (corneal opacity, congential cataract, etc.)
how do you treat amblyopia
Correct the underlying cause as soon as possible
Congenital cataracts should be corrected in the first few months of life
If underlying cause of the amblyopia is not corrected by age 5 or 6, the brain will permanently ignore the bad eye’s image
Patch the good eye to force the brain to use the image from the bad eye
diplopia. usually from an imbalance in EOMs.
May result from many different causes, such as orbital blowout fracture, myasthenia gravis, head injury, intracranial tumors, et al.
You must distinguish between binocular diplopia and monocular diplopia. You must distinguish between horizontal diplopia and vertical diplopia
painful aversion to light
Corneal inflammation (abrasions, ulcerations, etc.)
Inflammation of the iris
Inflammation of the sclera
During acute glaucoma
what are potential causes of eye pain?
Inflammation of the EOMs
Inflammation of the uveal tract (iris, ciliary body, choroid)
Corneal abrasion or ulceration
Acute closed angle glaucoma (markedly elevated IOP)
Referred pain from extra-orbital problems (e.g., sinusitis)
spots that are occasionally seen floating across the visual field
and are usually due to vitreous opacities and are of no consequence
sudden onset of floaters or a marked increase in the number of floaters, especially if associated with other signs or symptoms of eye disease, may be associated with what?
Posterior uveitis (inflammatory cells in the vitreous humor cause floaters)
Retinal tears or detachments (floaters + photopsia ( flashes of light))
how are most ophthalmic meds administered?
topically. ointments have greater therapeutic effectiveness than solutions but drops are preferred to ointments because they do not retain discharge or interfere with vision
Should be administered systemically for intraocular infections, orbital cellulitis, GC keratitis, severe conjunctivitis
most common ophthalmic antibiotic
Sulfacetamide sodium (Sulamyd) 10% opthalmic soln. or ointment TID X 2-3 days
(unless sulfa allergy)
Idoxuridine (Stoxil), an antimetabolite is used for Herpes simplex keratitis
Several antiviral agents are now available (Viroptic), et al.
Want to treat herpetic infections, so treat systemically(gancyclovirs) and antiviral drops
what should you always remember with topical anesthetics
Never send a patient home with topical ophthalmic anesthetics!
Don’t want to send some with number because won’t realize that its hurting and will touch it and cause more harm (think if dog cones)
Adrenergic (SNS) Agent for pupil dilation
Phenylephrine Hydrochloride (Neo-Synephrine)
Exhibit little cycloplegic effect
Effects last 2-3 hours
Anti-Cholinergic (anti-PSNS) Agents
Both mydriatic & cycloplegic agents
Paralyze the ciliary muscles AND dilate the pupil. By paralyzing the ciliary muscles, there is less pull on the choroid leading to more tension on the suspensory ligaments. This causes the lens to flatten more, helps increase the distance between the lens and adjacent iris
May help prevent synechiae formation in anterior uveitis
Reduce the pain associated with ciliary muscle spasm in certain conditions
Shorter acting, lasting only 15-20 min.
Cyclopentolate Hydrochloride (Cyclogyl)
Ophcon-A or Naphcon-A
Systemic Medications That Affect The Eye
Anticholinergics (e.g. atropine, scopolamine): dilate the pupil
Steroids: may cause cataracts, increase IOP, reactivate Herpes simplex, increase risk of infection
Morphine: causes pupillary constriction
Streptomycin: may cause optic neuritis
Tetracycline: pseudotumor cerebri
Quinine (chloroquine): may lead to acute blindness
Ethambutal: may cause optic neuritis & loss of color vision
technique for examining the circulation of the retina using the dye tracing method.Sensitive way of demonstrating changes of diabetic retinopathy, Retinal vein thrombosis, macular degeneration
when should you refer to an audiologist in an adult?
Reports change in hearing
Hearing Loss – Sudden, Gradual, or fluctuating.
Reports of being able to hear but not being able to understand conversations
Dizziness or Vertigo
Ear Infections/Otitis Media
TV/Radio volume loud.
Tympanic membrane perforation
History of ear surgery
when should you refer to an audiologist in pediatric patients?
DNP newborn hearing screening.
Recurrent/Chronic Otitis media.
Speech development slower than peers.
Child decreases amount of talking.
Child less responsive to name and other familiar sounds.
Says “huh” or “what” frequently.
Has learning difficulties.
Hyperactive or overly inattentive.
Family history of childhood hearing loss.
Syndrome associated with hearing loss.
Trauma to head/ear
Ear anomalies – microtia or atresia, ear pits/tags
pulsatile (rhythm with heart beat) tinnitus suggests what
what is in the middle ear?
what are behavioral hearing tests?
Behavioral Observation Audiometry
Visual Reinforcement Audiometry
Conditioned Play Audiometry
this auditory test records acoustic energy created by active mechanism of outer hair cells (cochlea)
otoacoustic emisisons (OAE)
not a test of hearing, this is pre-neural
when is otoacoustic emissions (OAE) usually done?
newborn hearing screening
differential diagnosis of site of lesion (sensory vs. neural)
monitoring effects of ototoxicity or noise exposure
this auditory test measures electrical activity of the nerve up to brainstem
auditory brainstem response (ABR)
The other screening tool used for infants at high-risk for hearing loss is auditory brainstem response. Electrodes are placed on the babies head, and sound presented to the ear. A brainwave is recorded in response to the sound.
measures beyond cochlea
when is ABR test used?
newborn hearing screening
assesses the auditory pathway;
look at latencies of the waveform;
generally used in the adult population
Identify presence or absence auditory neuropathy
Hearing threshold estimation
Intensity is reduced and Wave V threshold is tracked to estimate hearing.
Can be done in natural sleep or performed under sedation.
Not a test of hearing – makes estimate
this test measures admittance of sound energy into middle ear. used in diagnosis of OME and eustachian tube dysfunction
tympanometry - Not a measure of hearing, but rather a measure of middle ear status.
gold standard of diagnostic hearing test
This is a subjective measure that tells us the quietest level at which the patient is responding to sound. The patient can “tell” us they hear the sound in any number of ways. (Button press
Raising hand, Clapping, Toy in bucket, Head turn)
VRA (visual reinforcement)– testing method used in children 6 months to 3 years old and children with developmental delays. Speech and tonal sounds are presented through speakers or headphones and the child’s head turn response is reinforced with lights and/or animated toys.
this is a visual depiction of hearing loss
x-axis is frequency (pitch)
y-axis is intensity (loudness)
Test through air conduction (AC) and through bone conduction (BC).
Occurs when there is damage or obstruction in the outer and/or middle ear, but the inner ear is intact.
conductive hearing loss
causes of conductive hearing loss
otitis externa or otitis media - acute or chronic
-otitis media is the number one cause of conductive hearing loss in children. Fortunately, it is usually transient.
foreign object in ear canal
Rupture or perforation of the tympanic membrane
Otosclerosis – calcification of the middle ear bones, particularly the stapes.
Cholesteatoma – skin cyst, can erode ossicles causing hearing loss
hearing loss caused by damage to the cochlea or auditory nerve
sensorineural hearing loss - can be congenital or acquired
causes of sensorineural hearing loss
Ototoxicity (gentamicin, cisplatin, carboplatin…)
Labyrinthitis – inflammation of the labyrinth
Auto immune inner ear disease
Acoustic neuroma/Vestibular Schwannoma
what is mixed hearing loss?
Air conduction thresholds and bone conduction thresholds are outside the normal range and there must be a significant air bone gap.
Example: Combination of presbyacusis and tympanic membrane perforation.
what gene is strongly associated with congenital non-syndromic hearing loss?
GJB2 or connexin-26 gene.
treatments for conductive hearing loss
Effusive otitis media
treatment for sensorineural and permanent conductive hearing loss
how do cochlear implants work?
Stimulate cochlear bundle of auditory nerve
Appropriate for severe to profound sensory hearing loss
Not appropriate for retrocochlear loss (e.g., neurofibromatosis)
what are the CDC guidelines for managing hearing loss?
tested by one month of age
confirmed diagnosis by 3 months of age
intervention by 6 months of age
difference between dizziness and vertigo
Dizziness – Sensation of lightheadedness, faintness, or unsteadiness. Does not involve a rotational component.
Vertigo – Perception of movement or spinning, either of self or surrounding.
Intense short duration of vertigo that occurs with changes in head/body position.
Caused by displaced otoconia that move from saccule into one of the semi-circular canals
benign paroxysmal positional vertigo
inflammation caused by viral infection that affects hearing and balance. pt experiences a sudden onset of hearing loss, tinnitus, and aural fullness. Vertigo lasts for several days until central compensation occurs.
May have residual lightheadedness after compensation.
Vestibular Neuritis is also caused by viral infection. Damage to vestibular function only.
No auditory component.
Vertigo/dizziness symptoms last for several days.
Benign slow growing tumor on the 8th nerve
Occurs in area of IAC / CPA
Can affect hearing, balance, and/or facial nerve function
Always concerned when asymmetric hearing is noted on audiogram
acoustic neuroma/vestibular schwannoma
Cause is unknown but thought to be a result of excessive endolymph fluid in inner ear.
Can affect both ears, but usually is unilateral.
Results in fluctuating hearing, tinnitus, aural fullness, vertigo.
Vertigo generally lasts for several hours and is often accompanied by nausea and vomiting.
Meniere's disease - no cure
Manage symptoms with medications and diet – reducing sodium/diuretic.
Occurs when the defense capabilities of a mal-functioning immune system harm the cells of the body that affect the ear.
Some examples are Cogan’s syndrome, Wegener’s granulomatosis, systemic lupus, Sjogren’s syndrome.
autoimmune inner ear disease
tests for assessing vestibular/balance function
Electronystagmography/Videonystagmography (ENG/VNG) – most common; assessing peripheral vestibular function and central control of eye movements
Rotary chair testing – if ENG is normal and pt is still dizzy; peds; not ear specific
Vestibular Evoked Myogenic Potential (VEMP) – concern for SSCD and/or vestibular migraine.
Dynamic Posturography – functional balance measurement; predominantly used by physical therapists
Usually described as ringing or buzzing in the ears.
Is a symptom that reflects some region of unhealthiness in the auditory system.
Results from spontaneous nerve activity that the brain interprets as sound.
what are some tinnitus aggravators?
Loud noise exposure w/o use of adequate hearing protection.
High blood pressure
Caffeine, Alcohol, Nicotine
is there a cure for tinnitus?
no, but various treatment options available.
Use sound to take attention away from tinnitus.
Use sound to improve sleep, concentration, and relaxation.
Use Background Noise to make tinnitus less noticeable. Ex: fan noise, white noise, nature sounds, water sounds, etc
Use attention-getting sounds to distract you from tinnitus. Ex: Lectures, book on tape, talk shows, etc
Opening/Dehiscence in the bone overlying the uppermost semicircular canal within the inner ear.
Patients present with:
Autophony (increased resonance of own voice)
vertigo and oscipllopsia with loud noise or changes in middle ear or intra cranial pressure (coughing, sneezing, or straining)
Hypersensitivity to bone conducted sounds
Conductive hearing loss in low frequencies on audiometry with no other findings to support conductive hearing loss.
Superior Semicircular Canal Dehiscence
what is the most common eye disease?
most cases are infectious (non-STD)
Allergic Conjunctivitis (would have sneezing, etc)
Infectious (STD-Associated Conjunctivitis):
viral conjunctivitis presentation
Erythematous palpebral & bulbar conjunctivae
Copious watery discharge
Hallmark: lymph follicles are prominent in the lower conjunctival fornix
Look for palpable pre-auricular adenopathy
treatment for viral conjunctivitis
warm compress, usually clears in 2 weeks
Local topical ophthalmic antimicrobial agents to prevent secondary bacterial infection
presentation of bacterial conjunctivitis
More of a tendency to be unilateral (unlike viral conjunctivitis)
No blurring of vision after blinking (unlike allergic conjunctivitis)
Contagious, but less contagious than viral conjunctivitis
Self-limiting in 10-14 days (if untreated), but it should be treated
treatment for bacterial conjunctivitis
Polymyxin B/Bacitracin (Polysporin) ophthalmic drops or ointment
Sulfacetamide sodium (Sulamyd) 10% opthalmic solution or ointment
Gentamycin sulfate (Garamycin) ophthalmic drops or ointment
Erythromycin (Ilotycin) ophthalmic drops or ointment
Vigamox is most expensive and unecessary
Itching, tearing, redness
Stringy discharge that causing blurriness when blinking
Often follows a seasonal occurrence (esp. in Spring, Summer, or Fall), but may be perennial
allergic conjunctivitis -
tx : Topical ophthalmic mast cell stabilizers (cromolyn sodium), or topical antihistamines
Topical vasoconstrictors or vasoconstrictor-antihistamine combinations
Avoid allergens, if possible
Copious purulent eye discharge
A markedly inflamed eye with swollen lids
Gonococcal Conjunctivitis - Opthalmologic Emergency!
Rapidly leads to ulcerations and perforation of the cornea, and destruction of the eye if not treated within 1-2 days
diagnosed by gram stain and C&S
what are seen in conjunctival scrapings with Chlamydial Conjunctivitis or trachoma?
intracellular "inclusion bodies"
Acute erythema of conjunctivae
Eye discharge & irritation
Suspect this condition especially if conjunctivitis is associated with urethritis & urethral discharge
Conjunctivitis of the eyelids often lead to entropion and trichiasis with secondary central corneal scarring.
tx: Oral tetracycline, doxycycline, or erthromycin
Doxy is usually the drug of choice – 100 BID x 7 days -photosensitivity and yellow teeth **standard tx for clymidia
is a subconjunctival hemorrhage benign?
yes - 21st bday, vomiting, childbirth
A large area of the conjunctiva appears “blood-red”
No treatment is necessary
Reassurance +/- artificial tears
Usually resolves without sequella in about 2 weeks (like a bruise does)
A triangular fold of abnormal conjunctival tissue that may grow and extends from the inner canthus (nasal side only) over the cornea, towards the pupil
The apex of the triangle points TOWARD the pupil.
Occurs most frequently in persons exposed to dust or wind (farmers, etc.)
A yellowish, triangular thickening or nodule of the bulbar conjunctiva, nasal or temporal to the cornea
The apex of the triangle points AWAY from the pupil.
No treatment is needed since these do not grow over the cornea and obstruct vision.
inflammation of the cornea
exposure: Due to desiccation of the cornea from eyelid closure abnormalities or problems with tear secretions
Keratitis secondary to corneal abrasions
Keratitis secondary to ulcerating viral or bacterial infections
diagnostic test for hypofunctional tear glands
management for corneal abrasion
Record visual acuity PRIOR TO manipulation or treatment of the eye
Exception: when eye must be flushed immediately due to alkali or acid injury
Instill a topical ophthalmic anesthetic (after visual acuity is recorded!)
Perform a thorough eye exam (including lid eversion with a cotton-tipped applicator)
Remove the offending foreign body, if possible, with a moistened cotton-tipped applicator or needle
Apply fluorescein dye to check for corneal abrasion or ulceration
Damaged corneal epithelium stains a deeper green than the surrounding area
Apply a preventive ophthalmic antibiotic ointment (usually polymyxin-bacitracin)
When the corneal epithelium is disrupted, the cornea is very vulnerable to infection
Eye patching is no longer recommended
who has the highest risk of bacterial corneal ulcers?
extended-wear soft contact lens users
Patient will have eye pain, photophobia, tearing, and decreased vision
common etiologies of corneal ulcerations
Infectious: bacterial, viral (usually Herpes simplex or zoster), fungal, amoebic
Non-Infectious: Exposure keratitis, severe dry eyes, et al.
clinical findings of Viral (Herpetic) Keratitis/Ulceration
Characteristic “dendritic” (branching) ulcer is best seen after flourescein staining
tx for Viral (Herpetic) Keratitis/Ulceration
Immediate Ophthalmologic referral
The treatment regimen depends on whether the infection is limited to the corneal epithelium or if it is deeper into the stroma. Treatment may involve:
Topical antiviral agents
Oral antiviral agents
Topical corticosteroids, only under strict ophthalmologic supervision
Corneal grafting, if severe scarring results
which types of burns cause more damage, acid or alkali?
alkali - Alkali burn penetrate tissues, are not easily removed, and act for an hour or more
Acid burns are non-progressive
Penetration of acid is limited by the buffering action of the tissues
Damage is immediately visible
Must perform copious eye irrigation IMMEDIATELY with normal saline or plain water
Irrigate the eye away from the uninvolved eye
alkali: Continuous irrigation for at least 30 min. for alkali burns (use IV setup). A red eye is good because a white eye means that all blood vessels are dead!
inward turning of the eyelids
Eyelid margins turn inward
Surgery is indicated if the lashes rub against the eye and irritate the cornea and conjunctiva (“trichiasis”)
ectropion: eyelid margins turn outward. Potential causes:
May be age related (“senile ectroption”). This is commonly seen!
what are potential causes of ptosis?
Paresis of a branch of CN III
Weakness of the levator muscle
Tumors or infections of the eyelids
an external hordeolum is also known as what?
stye- Infection of glands of Moll or Zeis
Smaller abscesses located on external lid margin, points away from the conjunctival surface
Treat with warm compress (15 min, 3-4 times a day) + Antibiotic ophthalmic ointment (usually polymyxin-bacitracin or erythromycin)
May need I&D if no resolution within 48 hours
A hard, nontender swelling of upper or lower lid
May have some associated localized conjunctival inflammation. A common granulomatous inflammation (granuloma) of a Meibomian gland that may follow an internal hordeolum
A common, chronic (usually bilateral) inflammation of the lid margins
Classifed as Anterior, Posterior, or Mixed blepharitis
Lid hygiene (baby shampoo applied with a damp cotton applicator)
Refers to an acute or chronic (usually unilateral) inflammation of the lacrimal sac that is caused by a partial obstruction of the nasolacrimal duct. Characterized by a red, painful swelling near the inner canthus of the eye
Treated with immediate, vigorous, systemic antibiotics to prevent fistula formation to the skin or extension into the orbit or other intracranial structures
Dacrocystitis most commonly occurs in infants (Due to delayed opening in the lower portion of the nasolacrimal duct or at the orifice to the inferior meatus) and in adults over age 40 y/o
tx infant with massages with warm compress to ty to open up the duct
Red Eye due to Inflammation Of The Uveal Tract
Inflammation of the “uveal tract” involves what?
the iris, ciliary body, choroid
Iritis refers to inflammation of the iris
Cyclitis refers to inflammation of the ciliary body
Choroiditis refers to inflammation of the choroid
anterior vs posterior uveitis
“Anterior” uveal tract inflammation involves the iris and ciliary body, producing iritis or iridocyclitis
“Posterior” uveal tract inflammation involves the choroid (and often also involves the retina), producing choroiditis or chorioretinitis
clinical findings of uveitis
Unilateral “ciliary flush” or “ciliary injection” (a ring of injection at junction of cornea & sclera)
Eye pain (due to ciliary spasm)
Photophobia (due to an inflamed iris)
Decreased visual acuity (blurred vision from ciliary inflammation & problems with accommodation)
Pupil small, irregular, & poorly reactive
May present acutely, with unilateral pain, redness, photophobia, or visual loss
May present less acutely, with blurred vision and mildly inflamed eye
diagnosis for uveitis is confirmed with what?
by presence of free lymphocyte & plasma cells (“inflammatory cells”) in the aqueous humor noted by slit lamp exam
tx: Antimicrobial therapy if infectious
Refer to Ophthalmology (EMERGENCY):
Topical corticosteroids +/- systemic steroids
Topical mydriatics to dilate the pupil and prevent posterior synechias
Clinical Presentation & Findings of posterior uveitis
Gradual visual loss, may be bilateral
Inflammatory cells in the vitreous humor are seen on slit lamp exam
Fundoscopic findings: pigmented scars, patchy yellow or white areas, hemorrhages along eye vessels, opacities on retina
Always refer to ophthalmologist (EMERGENCY)
what is CMV retinitis in AIDS patients?
posterior uveitis (“tomato sauce on a white tablecloth,” or “pizza pie” fundus, or “crumpled cheese and catsup”)
CMV retinitis is the most common ocular opportunistic infection in AIDS patients
Syphilis produces a characteristic “salt and pepper” fundus
Mydriatics & cycloplegics are NOT needed in posterior uveitis because the iris and ciliary body are not involved
inflammation of both the anterior and posterior uveal tract
panuveitis (uveitis universalis)
superficial inflammation of the sclera. Redness, pain, photophobia, tearing. Characterized by a unilateral and localized inflammation of the sclera
Resembles conjunctivitis, but: Episcleritis is a more localized and deeper inflammation
Dilated vessels do blanch with topical vasoconstrictor (phenylephrine) as they do in conjunctivitis. Scleritis will NOT.
Benign & self-limited, with no permanent eye damage
tx: topical corticosteroids
deep inflammation of the sclera
scleritis- More likely to accompany systemic disease (rheumatoid arthritis, lupus, gout, psoriasis, sarcoidosis, TB, syphilis)
more severe pain than with episcleritis and more risk of permanent eye damage.
tx is difficult, refer to opthalmologist. Systemic steroids or systemic anti-rheumatic drugs to treat underlying cause. NSAIDS
what is glaucoma?
family of diseases with normal or increased IOP ultimately leading to interruption of the vascular blood supply to the nerve bundles --> death of ganglion cells --> visual field deficits, cupping of disc and other abnormalities of vision
Lens gets stiffer (less pliable) as you age and gets deposits. Doesn’t move with the angle as much
Asians and eskimos have much higher risk for complete glaucoma (closed angle)
where does aquous humor go in the eye?
90% reabsorbed by trabecular meshwork, 10% goes into bloodstream through schlemms canal
what is the most common type of glaucoma?
open angle- leading cause of blindness in the US
Primary Open-Angle glaucoma (low tension glaucoma)
Secondary Open-Angle glaucoma
Trabecular meshwork is clogged with debris from uveitis, or other ocular or systemic abnormality
what type of glaucoma is an emergency?
acute closure glaucoma
what causes Secondary Angle-Closure glaucoma
The angle is closed from a lens-iris adhesion (anterior uveitis), subluxed lens, neovascularization of the iris or anterior chamber angle from diabetes or CRVO, tumor, or other ocular abnormality
when is congenital glaucoma seen?
within first 3- months
other developmental glaucoma:
Juvenile Open Angle Glaucoma
what are risk factors for glaucoma?
-increased cup:disk ratio of >0.5, or an asymmetry of >0.2 between the two eyes
(Stereoscopic, magnified instrumentation is a better way of measuring cup:disc ratio than direct ophthalmoscopy)
Hyperopes and those with smaller eyes are at greater risk for angle-closure glaucoma
Myopes are at greater risk for open-angle glaucoma
-race (AA females have higher incidence of open angle glaucoma, whites & Asians have a higher incidence of angle-closure glaucoma)
-family history (The stronger the family history, the earlier the glaucoma is seen (familial effect)
what is normal IOP?
16+/- 5 mm. Hg (11-21 mm. Hg), representing 2.5 standard deviations on population distribution curve)
Up to 10% of all persons with ocular hypertension will go on to develop glaucoma
Glaucoma can occur in the absence of ocular hypertension (normotensive glaucoma)
30-50% of glaucoma is normotensive glaucoma!
is IOP symmetrical and when is it highest?
yes (within 2 mm Hg), highest in AM but IOP tends to be lowest in the EARLY morning.
Increases with age
Higher in women (probably due to smaller eye)
Reduced by exercise, alcohol, marijuana (transient)
Increased by steroids, fever
how is IOP measured?
tonometry - goldman applanation tonometry is the "gold standard"
should you have pain associated with glaucoma?
NO, no eye pain of VA changes (asymptomatic)
Eye pain if the problem develops acutely (acute angle-closure glaucoma)
how do you evaluate the depth of the anterior chamber?
corneal light reflux
The chamber will be nml in open-angle glaucoma and narrow in angle closure glaucoma
what will be seen on the fundoscopic exam for glaucoma?
Asymmetry of the Cup:Disc Ratio between the two eyes >0.2
A deterioration in the width (area) or health of the neural retinal rim (look at the disc donut, not the hole) occurs as the cup enlarges
signs and symptoms of open angle glaucoma?
Elevation of IOP is bilateral, chronic, and relatively slight. It may occur over years before it is detected. This is why primary open-angle glaucoma is known as “low-tension glaucoma.”
Visual fields gradually constrict (producing “tunnel vision”), but central vision remains good until late in the disease
how often should people be screened for glaucoma?
every 2-5 years if over age 40, more frequently if there is a family history of glaucoma
Over months or years, this condition, if untreated, leads to optic atrophy (and potential blindness)
medical treatments to lower IOP
prostaglandin agonist - Work to lower IOP (by 35-37%) by increasing uveal-scleral outflow
Topical Ophthalmic Beta Blockers (Timolol maleate (Timoptic, Betimol)
Topical Cholinergic (Parasympathomimetic) Agents (Miotics)
-These constrict the pupil and affect ciliary muscle tone with the end result of putting traction on the trabecular meshwork to open it up and improve drainage
Carbonic Anhydrase Inhibitors- decrease aqueous production and lower IOP
Topical Ophthalmic Adrenergic Agonist (Sympathomimetic, Epinephrine-like agents):
Although these agents cause pupillary dilation, they predominately increase outflow of aqueous humor
Neuroprotective Agents- treatment directed more at level of optic nerve head and preservation of ganglion cell axons
Exercise Therapy- Recent studies have shown that exercise may be as good or better than beta blockers
what are surgical options to create new outflow channel to lower IOP?
iridotomy (narrow angle or closed angle)
what is the prognosis for glaucoma?
1/2 to 3/4 of cases of open-angle glaucoma progress despite appropriate treatment (the bad news!)
Untreated chronic glaucoma will cause blindness within about 20 years
this occurs from closure of a pre-existing narrow anterior chamber
acute angle closure glaucoma
-precipitated by pupil dilation or lens enlargement with age
this presents with extreme eye pain, photophobia, red and stony hard eye, hazy "steamy" cornea, nausea, vomiting, prostration
acute closed angle glaucoma
emergency management of acute closed angle glaucoma
Administration of IV carbonic anhydrase inhibitor diuretics, such as acetazolamide (Diamox)
Administration of hypertonic solutions (oral glycerol, or IV mannitol or urea) to lower IOP
Administration of vasoconstricting eye drops, such as Pilocarpine, to pull the peripheral iris away from the trabecular meshwork
what is the definitive surgical treatment for acute closed angle glaucoma
peripheral iridotomy- A pie-shaped hole is made in the iris to create an opening between the posterior and anterior chambers so that fluid from the posterior chamber can drain into the anterior chamber
prognosis of acute angle-closure glaucoma
Untreated acute angle-closure glaucoma results in severe and permanent visual loss within 2 to 5 days after the onset of symptoms
Under 40 yrs old: Every 2 years (w/risk factors)
Every 4 years (no risk factors)
4o years and older: Every year (w/risk factors)
Every 2 years (no risk factors)
hereditary disorder, disease of the rods, may be mild or total blindness. Findings: bone spicules, waxy pallor, retinal vessel attenuation
tx: vita A for night blindness
this presents with blurred vision in one eye, becoming progressively worse. “A curtain (or shadow) came down over my eye”Sensation of light flashes or “floaters”
Central vision remains intact until the macula becomes detached
tx: Maintain patient in a position that allows the detached portion of retina to fall back in place with the assistance of gravity
presents with sudden visual loss (minor to near complete). sudden onset of "floaters) . Examiner is unable to see the fundus clearly, despite a clear lens, due to a “Red-out”
occurs due to : Retinal tears, with or without detachment. Diabetic proliferative retinopathy. Central retinal vein occlusions. Trauma, Other Causes
most common malignant tumor of the orbit in the 1st 10 years of life. presents with ptosis, proptosis, rapid progression with mets to brain and lung
most common intraocular malignancies in adults
metastatic intraocular tumors
highly malignant primary tumor of the retina. present from birth and the most common intraocular tumor of childhood
-Someone notices a white pupil (“Leucocoria”), or the absence of red reflex on photographs, etc.
It is a rare, but life-threatening tumor with a 20% mortality rate
The most common primary intraocular tumor of adulthood
malignant melanoma- Arises from the pigmented cells of the choroid
tumor of the optic nerve itself
glioma- Dx in children with decreased VA, proptosis, papilledema, optic atrophy and strabismus
what is the leading cause of worldwide blindness?
cataracts, followed by macular degeneration , then glaucoma
what is a cataract?
an opacity of the lens cortex, lens nucleus, or lens capsule
Normally the lens is clear
“Opalescence” refers to lens opacification
“Brunescence” refers to a yellowing or browning of the lens
“Sclerosis” refers to lens hardening
whats happens to the lens with age?
larger and less elastic
As the cataract matures, the fundus becomes less and less visible
what accelerates occurance of cataracts and macular degeneration
what are signs and symptoms of cataracts?
glaring and scanting of bright lights, especially at night
red reflex decreased or absent
May develop “phakomorphic” angle-closure glaucoma
3 types of cataracts
stages of cataracts
immature: : Not all of the lens has opacified
mature: All of the lens is opaque
hypermature: The cataract is so advanced that some of the cortical proteins have begun to liquefy
what is the most common cause of cataracts?
age --> "senile" cataract
52-64 y/o: 5%
65-74 y/o: 18%
75-85 y/o: 46% (approx. 50% of persons over age 75)
how do you get a congenital cataract?
intrauterine infection such as rubella
Rubella cataracts need to be removed by 6 weeks of age, otherwise amblyopia abnosia develops (visual cortex of brain won’t develop properly)
what is drug induced cataract result from?
secondary to systemic corticosteroid treatment (prednisone)
Phenothiazine antipsychotics, Amiodarone, certain poisons, certain lab chemicals, et al.
what are some metabolic causes of cataracts?
diabetes, thyroid disease, parathyroid disease or tumor, Wilson'd disease
Low anti-oxidant status (especially of lutein, glutathione, and ascorbic acid)
other causes of cataracts
exposure to UV light (solar radiation) --2-3X risk of cataracts @ southern latitudes- preventative to wear sunglasses/ decrease exposure to solar radiation
Smoking- Smoking decreases antioxidants and accelerates atherosclerosis
what is the treatment for cataracts?
extracapsular cataract extraction (ECCE) surgery - 99% effective and only takes 15-45 minutes- no longer done in the US
dietary changes that can prevent cataracts
increase anti-oxidants - neutralize free radicals that contribute to cell degeneration in aging and disease
vitamin C (ascorbic acid) - oranges, cartenoids (spinach, kale, carrots)
Spinach is the #1 best foot to prevent cataract & macular degeneration
5 portions of fruits and veggies
what is more common macular degeneration or glaucoma?
Macular degeneration - in next 10 years, the # of persons with it will double
**central vision loss
what is the most common form of macular degeneration?
dry ('atrophic') form -Formation of small, discrete “hard” drusen
and rarely causes blindness
what is the most severe form of macular degeneration?
wet ('exudative') form-Less common for (10% of cases), but more severe with a more rapid onset!
Formation of larger, less distinct, confluent “soft” drusen
Caused by abnormal growth of leaky blood vessels behind the retina
signs/symptoms of macular degeneration
-painless and can develop so slowly that it is hardly noticed
-may progress quickly, leading to impaired vision in one or both eyes
-Atrophy of the foveal (center) vision, with peripheral vision remaining intact
-seeing straight lines as crooked ones
what are detection tests used for macular degeneration?
low light resolution testing
recovery after glare testing
**standard eye charts are NOT satisfactory for screening for macular degeneration
how can you prevent macular degeneration?
proper nutrition (lutein and vitamin E are most important)
what is the treatment for macular degeneration?
nutritional therapy --> high lutein diet
what is the treatment for the dry form of macular degeneration?
none, only prevention
what is the treatment for the wet form of macular degeneration?
Photo Dynamic Therapy involves destruction of blood vessels using a low power (non-heat producing) infrared laser, along with a photosensitive dye ($8-10,000 per treatment x 3-4 treatments required)
unequal pupil size >1.0 mm
is the sympathetic afferent or efferent?
efferent only -midriasis
is the parasympathetic pathway afferent or efferent?
both - miosis
what occurs with the afferent path in the parasympathetic pathway?
light stimulates the retina, Travels optic nerve, chiasm, lateral geniculate nucleus to superior colliculus where fibers synapse
Fibers travel to Edinger-Westphal nucleus
what occurs with the efferent path in the parasympathetic pathway?
Fibers travel w/oculomotor nerve (III) through Cavernous Sinus
Follows inferior split of CN III
Synapses at ciliary ganglion
Short Post. Ciliary Nerve innervates the sphincter of the iris and ciliary body muscle
Outcome is miosis and accomodation
what is the sympathetic effect on the pupil?
what is the parasympathetic effect on the pupil?
constriction and accommodation
when should you check for accommodation?
only when direct and/or consensual response is abnormal
Have patient look at distant target and then near target at 40 cm
Response-convergence stimulates miosis
what does PERRLA stand for?
pupils equal round reaction light
difference between afferent and efferent pupillary defects
Afferent- Failure of response d/t blockage of transmission from eye to brainstem
Efferent- Failure of response d/t blockage of circuit from brainstem to eye
what is a unilateral afferent pupillary defect due to damage to optic nerve or retina. Consensual response induced by good eye is GREATER than the direct response produced by diseased eye
Diseased pupil appears to dilate with direct light stimulus
marcus gunn pupil / APD
what is the most common etiology of afferent pupilary defect?
optic nerve damage (Atrophy/Neuritis/neuropathy, Tumor, Glaucoma)
this is a pupil which constantly contracts and dilates. normal occurrence
what is the different between physiologic and pathalogical anisocoria?
physiologic - same size difference in light and dark, less noticeable in light
pathological - Pupil size asymmetry changes under different illuminations
Size asymmetry increase in dim illumination=abnormality of dilation
Size asymmetry increase in bright light=abnormality of constriction
No anisocoria evident in normal light
No direct light response, therefore the eyes appear to dilate
Intact consensual light response depending on the condition. (exception—CN III palsy)
Can only be a unilateral finding
Blockage of the Afferent pathway (PSNS)
afferent pupillary defect
a dilated pupil usually represents a deficit in which pathway?
CN III Palsy
Adie’s tonic pupil
Acute glaucoma attack
Fixed dilated pupil “Blown”
Dorsal Midbrain Syndrome
this presents with ptosis, motility disturbances (eye deviated out and down), no VA changes.
oculomotor (III) palsy- neurosurgical emergency and intracranial mass should be ruled out
what is the triad for cranial nerve III palsy?
total lid ptosis
eye positioned down and out
reduced direct response to light
-etiology is based on age
if someone is having a painful CN III palsy, what should you suspect?
-incomplete palsy (partial limitation of ocular movements) is a sign of intracranial aneurysm
what is the workup for CN III palsy?
MRI/MRA, although arteriogram is gold standard
*Myasthenia Gravis may mimic CN III palsy
Pt. c/o Horizontal diplopia (Abduction deficit)
May turn head toward palsied muscle
Sudden onset=ischemia (especially in those w/known vascular dz)
CN VI palsy (LR)
Depression, abducting and intorsion
Head tilt in opposite direction
Etiologies-Trauma and as above
CN IV palsy (SO)
this is an anatomic defect with enlarged pupil w/no direct light response, no consensual response, and no near object response
fixed dilated pupil "blown"
unilateral phenomenon that may occur when a rapidly expanding intracranial mass, including blood from a hemorrhage, is compressing cranial nerve III.
this occurs in females more than males, 20-40 year olds. large pupils which react slowly to light. in 70% of patients there is also absence of tendon reflexes
adie's tonic pupil
May follow infection (HSV, Trauma)
.8% or 1.0% Pilocarpine will induce miosis in Adie’s pupil **Even lesser amount due to hypersensitivity
what is the management for adie's tonic pupil?
chronic cholinergic therapy, reading glasses due to unequal accommodation and reassurance that this is usually BENIGN
What causes iatrogenic dilation of the pupils?
dilating drops (tx for Iritis)
this is a functional problem of an enlarged pupil causing total blindness and no direct response/"no light perception" +consensual response intact. therefore known as "blind eye" due to retina or optic nerve problem
amaurotic pupil (afferent problem)
this is due to a compression in midbrain and causes bilateral mydriasis, Lid retraction
, and inability to look upward. no reaction to light, but (+) accomodation
dorsal midbrain syndrome --most common cause is a mass in pineal region
horners syndrome involved damage to which system?
what is part of the horners triad?
facial anhydrosis (absence of sweat)
Increase in accommodation of affected eye
if a patient presents with horner's triad + pain ipsilateral face/neck, recent injury or accident, or pulsatile noise ipsilateral (tinnitus), what should you think of?
carotid artery dissection- EMERGENCY
Pharmacological Testing for Horner’s
Cocaine 4-10% ophthalmic solution
Hydroxyamphetamine 1% ophthalmic soln.
horners triad + heterochromia (different colored eyes)
congenital horner's-Always refer if not previously documented
inflammation of the iris
Signature of neurosyphilis/ Tertiary Syphilis
small, irregular pupils
bilateral and asymmetric
react briskly to near but not to light stimulus
argyll robertson pupil (parasympathetic problem)
J. Lawton Smith’s 9 Commandments for argyll robertson
Decreased light response
Preserved near response
Must have SOME vision
Other signs of syphilis
management of argyll robertson
is vision preserved with acute papilledema?
General BILATERAL Optic Disc Swelling
what can you automatically diagnose with papilledema?
HTN (grade IV)
due to ICP, infection, vascular problems
what is cushings triad?
HA, papilledema, vomiting
what is the treatment for papilledema?
Elevate head of bed (HOB)
Osmotherapy (Mannitol/Hypertonic saline)
Corticosteroids—only in inflammatory causes
Young-middle age, fertile, obese women presents with papilledema
Often idiopathic (as its name states) but a cause is sometimes identified:
inflammation or demyelinating disease of the optic nerve
what is the most common ocular manifestation of MS?
*20-25% initial presenting sign
50% will develop MS within 15 yrs
cardinal symptoms of optic neuritis
UNILATERAL loss of vision
Pain in eye, especially with EOMs (it’s an inflammatory disorder) *This is a hallmark sign
tx: systemic steroids
An older person with a sudden painless loss of vision (usually IRREVERSIBLE), often only the superior or inferior visual fields affected
HA, jaw claudication w/chewing, malaise, fever and scalp tenderness
*Elevated ESR in arteritic form
Significant risk to other eye within 1-3 months (upwards of 75%)—specifically, 40% in arteriosclerotic type and 70% of arteritic cases
etiology of psudopapilledema
Drusen Bodies (deposits of hyaline material) in optic nerve create the illusion that the disc is swollen, especially in young people. Often confused with true papilledema because it mimics it
Autosomal dominant condition causes accumulation of calcium in the substance of the optic nerve. Appear as multiple glistening mounds and the optic discs appear "swollen"
Death of nerve fibers (ganglion cell) in retina and optic nerve, following injury anywhere along its course produces a very pale or white optic disc
Mean age = 60 yo
Sudden, nearly complete, painless, unilateral (permanent) visual loss (may only be able to count fingers or worse)
Symptoms can occur 15min-hours after occlusion
central retinal artery occlusion (CRAO)
Results from loss of blood supply to the inner layer of the ophthalmic artery
"cherry red macular" -> temporal arteritis
how do you treat central retinal artery occlusion?
This condition is an ophthalmologic emergency (permanent vision loss within 1-2 hrs.)
Urgent ESR (giant cell arteritis)
Fibrinogen, antiphospholipid ab, pt/ptt (coagulopathies)
Glucose (DM, atherosclerosis)
Echo (valvular dz)
Blood cultures (bacterial endocarditis)
Branch Retinal Artery Occlusion (BRAO)
Only a branch of a retinal artery is occluded by an emboli
Same etiologies as with CRAO
Less severe VF loss
a transient, but complete blindness in one eye
Predominantly >50 yo
Visual impairment from mild to severe
*Key finding is retinal hemorrhages in ALL four quandrants
central Retinal Vein Occlusion (CRVO)
2 forms (fluorescein can differentiate)
70% will have a partial occlusion
Moderate reduction in VA
No relative afferent pupil defect (RAPD)
Mild disc swelling, mild cotton wool spots
30% of cases
VA severely reduced
Many cotton wool spots, retinal heme
when will you see "blood and thunder" fundus?
central Retinal Vein Occlusion (CRVO)
Dilated, tortuous veins (venous engorgement)
Diffuse retinal flame & blot hemorrhages, esp. along the course of the veins
Cotton wool spots may occur (secondary to occlusion of small arterioles from the retinal edema)
Second most common retinal vasc dz after diabetic retinopathy
Chief complaint is blurred vision (or sudden segmental loss of vision if the macula is involved)
May be an incidental finding on funduscopic exam and present asymptomatically
Commonly in the supertemporal quadrant
branch retinal vein occlusion
Fundoscopic findings for branch retinal vein occlusion
Hemorrhages & cotton wool spots in wedge-shaped area (area drained by the occluded vein)
Occlusion may be seen at the site of the AV crossing
when are retinal changes usually seen with HTN?
Retinal changes usually not visible until diastolic >110mm Hg
The effects of BP on the retinal & choroidal vessels depends upon the degree of BP elevation, the rapidity of its rise, and its duration
what should normal retinal vessels look like?
Should be normally transparent but are visualized because of the blood contained within them
In long standing HTN, a compensatory thickening and hyalinization occurs. They develop a “copper-wire reflex” and then a “silver-wire reflex”.
At the jxns, the arteries and veins share a common sheath, therefore thickening of the arteriole may cause indentation of the venule (aka “AV nicking”). This can lead to retinal vein occlusion
normal A:V ratio
what keith-wagener classifications are considered medical emergencies and referred to as malignant hypertension
III and IV
Generalized severe arteriolar narrowing with A:V ratio about 1:4
Focal arteriolar spasm (1:3 ratio of spasmotic area to proximal arteriole)
Dot hemorrhages are deeper in the retina and probably represent microaneurysms
Blot hemorrhages are deeper
Flame hemorrhages are more superficial
Linear hemorrhages may also be seen
Soft exudates (cotton wool spots) represent focal retinal ischemia
Hard exudates represent leaking blood vessels (mainly proteins & lipids)
grade III retinopathy
Arteriolar narrowing resembles fine fibrous cords
Focal arteriolar spasm with total obliteration of distal flow
Papilledema (“malignant” HTN)
grade IV retinopathy
what is the most common type of vascular retinopathy?
what are the two types of retinopathy and which is most common?
proliferative and non-proliferative
what is non-proliferative/background
This is a clinical reflection of the hyperpermeability and incompetence of involved vessels.
The capillaries develop tiny dot-like outpouchings called microaneurysms and the retinal veins become dilated and tortuous. Multiple hemorrhages may appear.
Macular edema is the cause of visual loss in these patients. This is caused by a breakdown of the inner blood-retinal barrier at the level of the retinal capillary endothelium allowing leakage of fluid and plasma products into the surrounding retina.
what is background retinopathy characterized by?
by microaneurysms, venous dilation, hemorrhages, exudates, and retinal edema
what is the key finding for Pre-Proliferative Background Retinopathy?
Multiple cotton wool spots (ischemia)
this presents with Chronic and progressive retinal ischemia stimulates the formation of delicate new vessels that leak serum and proteins in large amounts. Neovascularization (the growth of new vessels) freq grow on the surface of the disk and become elevated and can pull on the vitreous resulting in massive heme or detachment.
-Poor visual prognosis
Vitreous hemorrhages (“red-out”) are a common sequela
this type of retinopathy leads to more new cases of blindness, and is common in Type-2 diabetics
Diagnosis of Retinopathy:
Type I diabetics should be referred for ophthalmologic exam within 3 years after diagnosis and then re-examined annually
Type II diabetics should be referred at the time of diagnosis and then re-examined annually
Pregnancy: Retinopathy can be particularly aggressive so they should be screened in the first trimester and every 3 months thereafter.
IV flourescein angiography (by an ophthalmologist)—new vessels leak the dye at a fast rate
basic physiology of diabetic retinopathy
Atherosclerosis and progressive degeneration of capillary walls leads to:
Blockage of small arterioles
Leakage (hemorrhages & exudates)
Vessel wall damage with diffuse & focal expansion (microaneurysms)
Macular edema (main cause of blurry va)
Ischemia of the retina which stimulates neovascularization & fibrous growth