EENT Flashcards
Tx dacrocystitis
= blockage/infection of medial canthal lacrimal sac = swelling/erythema +/- purulence
Tx = Clindamycin
Crusting, scaling, & red-rimming of eyelids bilaterally = ?
Blepharitis = inflammation of the eyelids - BILATERAL
Anterior = skin & base of eyelash - more likely infectious (staph), viruses, or seborrheic
Posterior = moeibomian gland dysfunction (a/w rosacea and allergic rhinitis)
Tx anterior = eyelid hygiene = warm compresses, +/- abx
Tx posterior = eyelid higiene, massage
Stye (hordeolum) vs chelazion?
Both cause swelling/lump in eyelid
Chelazion is NOT painful & stye is SUPER painful, red, warm etc.
Chelazion is under the eyelid itself, stye is at the lid margin
Stye = sudden onset
Chelazion is larger, firmer (= RUBBERY nodule) slower growing than a stye (= abscess)
Tx for stye = warm compresses
Tx for chelazion = eye hygiene (warm compresses, washing etc)
Abx may be necessary with stye if actively draining but are usually not necessary with chelazion
Pterygium vs pinguecula
Ptyergium = triangular-shaped growing fibrovascular mass on inner corner of eye & grows laterally
A/w inc UV exposure, sand, wind dust exposure etc
Mnemonic: Pterygium is like a terrarium that grows to inner eye
Tx - needs removed if affects vision. Otherwise observe.
Pinguecla = yellow deposit of fat/protein on nasal side of sclera that does NOT grow
Pinguecula has a C in it & it’s a Cute lil deposit that just needs observed
Globe rupture - dx, signs & tx
Dx:
Hx penetrating trauma, +enopthalmos or exopthalmos,
+ seidel’s sign (fluorescein dye is parted by a stream of clear aqueous humor streaming from the anterior chamber) - DO NOT USE FLUOROSCEIN IF SUSPECT THO….
Teardrop or irregularly shaped pupil
Tx: RIGID eye shield, immediate ophtho consult, IV abx, leave impaled objects in place
DO NOT PRESSURE PATCH - EYE CUP & EMERGENT REFERRAL
If hyphema, keep at 45 deg angle to prevent RBC staining of cornea
Orbital floor blowout fx -CP, dx, tx
Fracture of orbital floor 2/2 TRAUMA - can lead to entrapment of eye structures
Diplopia w/ upward gaze = entrapment of inferior rectus muscle
Orbital emphysema = eyelid swelling after blowing nose 2/2 air from maxillary sinus
Anesthesia to anteriomedial check 2/2 stretching of infraorbital nerve
Dx: CT
Tx: Nasal decongestants, no nose blowing, steroids, antibiotics (unasyn or clinda)
Macula is responsible for what kind of vision?
Central vision
Detail
Color vision
C = central vision, color vision
Dry macular degeneration
Gradual breakdown of the maucla = gradual blurring of central vision
Dry = DRUSEN bodies = small, round, yellow-white spots on the outer retina (scattered, diffuse)
Drusen = DIFFUSE spots
Drusen = accumulation of waste products from the retinal pigment epithelium
Wet macular degeneration
Called wet b/c there’s neovascularization and exudates
New abnormal vessels grow under the central retina which leak & bleed = retinal scarring –> more rare than dry but progresses more rapidly
CP macular degeneration
B/l blurred central vision & loss of detail/color
Scotomas (blind sports, shadows)
Metamorphopsia (strait lines appear bent, can test w/ amsler grid)
Dry also = drusen bodies = DIFFUSE small round yellow-white spots on outer retina
Dx of wet macular degenration
Fluorescein angiography
Tx dry macular degeneration
Amsler grid at home to monitor stability
Zinc, and vitamins A, C, E = slows progression
Tx wet macular degeneration
Intravitreal anti-angiogenics = Bevacizumab
`= VEGF inhibitors = dec neovascularization
Patho diabetic retinopathy
Sugar attaches to collagen of blood vessels = capillary wall breakdown (glucose is toxic to our vessels!) = retinal ischemia = edema
Types of diabetic retinopathy
- Nonproliferative = microaneurysms = leak & cause… blot & dot hemorrhages, flame-shaped hemorrhages, cotton wool spots, hard exudates, retinal vein beading (tortuous & dilated veins). NOT as/w vision loss
- Proliferative = neovascularization = new abnomral blood vessel growth, vitreous hemorrhage –> Tx = same as wet macular degeneration = VEGF inhibitors & strict glucose control
- Maculopathy - macular edema and exudates = blurred central vision & central vision loss - can occur at any stage –> 2/2 microaneurysm leakage = edema and damage
Cotton woll spots a/w? What are they actually?
A/w non-proliferative diabetic retinopathy (also a/w hypertensive retinopathy stage III)
A type of “soft” exudate from leaking of microaneurysms & nerve layer microinfarctions
= Fluffy white gray spots = why they’re named cotton wool spots - larger and more irregularly shaped than the small round drusen bodies at edge of retina 2/2 dry macular degeneration
Hard exudates - what are they? A/w?
Hard exudates are yellow spots with SHARP margins - well-demarcated (unlike fluffy cotton spots)
A/w nonproliferative diabetic retinopathy
Due to microaneuysm leakage - lipids leak out and form the hard exudates - seen in hpertensive retinopathy as well
Vitreous hemorrhage = what? a/w?
Vitreous hemorrhage is a/w proliferative diabetic retinopathy
It is
Flame shaped and blot hemorrhages are what? a/w what?
they are small hemorrhages in the eye 2/2 to microaneurysm rupture and vascular occlusions
Seen in diabetic retinopathy and stage III HTN retinopathy
They are a/w cotton wool spots b/c distal to the hemorrhage or ischemia the cotton wool spot is created
Is non-proliferative diabetic retinopathy a/w vision loss?
NO
What are dilated tortious retinal artery/veins a sign of?
Neo-vascularization ….
“Proliferation of the endothelial cells of retinal veins results in marked changes in the caliber of the veins with formation of tortuous loops”
Occurs in diabetic retinopathy AND hypertensive retinopathy
HTN retinopathy = ?
Damage to retinal blood vessels 2/2 long-standing HTN
Grade I HTN retinopathy
Arterial narrowing - abnl ligt reflexes on dilated tortuous arteroile shows up as colors:
Copper-wiring (moderate) Silver wiring (severe)
Grade II HTN retinopathy
AV nicking (venous compression at arterial-venous junctions 2/2 increased arterial pressure)
Grade III HTN retinopathy
Retinal hemorrhages (“flame-shaped”) and associated cotton wool spots
Note stages are alphabetical - Artrial narrowing, AV nicking, Cotton wool, flame hemorrhages, then papilledema!
Stage IV HTN retinopathy
Papilledema
Normal cup:disc ratio
<0.5
Retinal detachment - etio
Etio - 3 types:
1. Rhegmatogenous - MC type= retinal tear - RF = myopia & cataracts
- Traction - adhesions separate the retina from its base - proliferative DM retinopathy, trauma
- Exudative (serous) - fluid accumulates behind retina & = detachment - HTN, central retinal v. occ, papilledema
Flashes of light come first = retina tugging then the “curtain over eye” as it actually detaches
MCC = VITREOUS DETACHMENT/hemorrhage - vitreous separation tears hold in retina - vitreous detachment caused by neovascularization (proliferative DM retinopathy
Retinal detachment dx, tx
Dx:
Retinal tear = detached tissue”flapping” in vitreous humor
+ SHAFER’s sign = clumping of brown-colored pigment cells in the anterior vitreous humor resembling tobacco dust
Tx:
OPHTHO EMERGENCY
Keep supine, don’t use miotic drops
Laser, cryotherapy, ocular surgery
First thing to check in EVERY pt with eye complaint (besides chemical burns)
Visual acuity
If got chemical in eye then wash out first but
ALL OTHERS = get visual acuity FIRST
Common antihistamine eye drop for itching/redness in viral or allergic conjunctivitis
Olopatadine = H1 blocker eye drop = benadryl for the eyes
Viral conjunctivitis a/w what other PE finding?
Preauricular LAD
BILATERAL
Gonococcal conjunctivitis
ADMIT
IV CEFTRIAXONE and topical abx
OPHTHO EMERGENCY!
MCC bacterial conjunctivitis
staph aureus
Dx bacterial conjunctivitis
Clinical dx BUT you must still do fluorescein staining to rule out an abrasion & keratitis!!!
Allergic conjunctivitis pathognomonic finding
Cobblestone appearance to inner eyelid and upper eyelid, itching, tearing, redness, bilateral
What is pheniramine and naphazoline drops?
They are an antihistamine and decongestant eye drop used for allergic conjunctivitis
Orbital cellulitis - occur when? CP? Dx? Tx?
Occur: MC ofter sinus infection (ethmoid) - staph, s. pna, gabhs, h. flu or after dental and facial infections - MC in CHILDREN
CP: Decreased vision, pain with ocular movement, proptosis, eyelid erythema & edema
Tx: emergent referral, admission for systemic abx & orbital imaging
Preseptal (preorbital) cellulitis vs orbital?
Orbital = pain with EOM, and VISUAL changes
Pre-orbital (infection of eyelid and periocular tissue) & NO pain with EOM, NO visual changes
Si/sx keratitis (corneal ulcer)
Corneal ulcer AKA keratitis
Corneal ulceration/defect on slit lamp exam
Ciliary injection (limbic flush)
Tx: Cipro drops
DO NOT PATCH EYE
There are various types of keratitis, but most commonly it occurs after an injury to the cornea, dryness or inflammation of the ocular surface or contact lens wear.
PE bacterial keratitis
Hazy cornea, ulcer, +/- hypopyon
Tx: CIPRO DROPS - DO NOT PATCH EYE
Uveitis (iritis)
Autoimmune dz, unilateral
CP: Pain w/ direct & consensual light in BOTH eyes b/c iris will constrict (pain) & dilate (pain) along with the unaffected eye when light is shone in unaffected eye. Also inflammatory cells (WBC) & flare (protein) in aqueous humor
IF ALL OF THE FLARE IS AROUND THE IRIS
= LIMBIC FLUSH OR UVEAL FLARE = BAD
(SLCERA IS CLEARER)
Tx:
URGENT referral for topical steroids & cycloplegic drops for pain (cyclopentolate or homatropine)
Workup: HLA-B27 (a. spondylitis), ANA (SLE), RPR (syphilis), ESR (general inflammation), CCP (RA)
BFTP - SARCO-Not ME mnemonic, the A = anterior uveitis = one of CP of sarcoidosis AI dz!
Scary reasons for red eye
Red eye w/ ciliary injection = ALL SCARY:
Corneal ulcer (keratitis)
Iritis (uveitis)
Acute angle closure glaucoma
Cataract -what is it? RF, CP, d/dx, Tx
What: lens opacification
RF: Age, cigs, sun, DM, steroids, ToRCH syndrome
CP: Painless loss of vision over months to years - one or both eyes, reduced visual acuity on exam, NO RED REFLEX
PE: Absent red reflex, opaque lens
Tx: Surgical - done when dec vision affects ADLs
Ddx: Retinoblastoma - absent red reflex + white pupil
Papilledema definition, etio, CP, dx, tx
Definition: Optic disc (nerve) swelling
Etio: IIHT, space-occupying lesions, Ceregral edema, malignant HTN
CP: Headache, N/V
Dx: Fundoscopy - swollen optic disc w/ blurred margins. MRI or CT 1st to rule out mass effect then an LP (will show inc opening pressure)
Tx: Diuretics - acetazolamide (dec production of aqueous humor & CSF)
Papilledema vs optic neuritis vs glaucoma
Papilledema is 2/2 inc CSF pressure = edema of optic nerve head, BILATERAL, visual defect = enlarged blind spot. Tx = reduce ICP.
Optic neuritis = edema of the optic nerve head IN the orbit, usu UNILATERAL, Visual defect: range from central scotoma to complete loss of vision, + RAPD (marcus gun pupil) & Tx = corticosteroids. A/w MS, pain w/ EOM
Glaucoma = edema of optic nerve from increased intraocular pressure - acute = unilateral, chronic = bilateral. Visual defect = halos around lights –> blindness. Tx = reduce IOP.
All look like blurred disc cup on fundoscopy. Optic neuritis = ONLY one with marcus gun pupil. And only one that’s unilateral besides acute angle closure.
Optic neuritis- MCC, CP, TX
ON= acute inflammatory demyelination fo the optic nerve - mc in young pt 20-40 YO
Etio: MCC = MS
CP: UNILATERAL, loss of color vision, visual field defects (central scotoma or blind spot), loss of vision over a few days (papilledema 2/2 inc ICP = BILATERAL and macular degeneration w/ loss of color vision is also BILATERAL!!!)
PE: RAPD (marcus gunn), fundoscopy = optic disc swelling and blurring 2/2 papillitis
Tx: IV methylprednisolone & oral corticosteroids
Note: Retrobulbar neuritis is very similar to optic neuritis except the inflammation is in the optic nerve BEHIND the eye - everything’s the same as above except the pt can have a NORMAL fundoscopy exam b/c swelling is behind eye w/ all of same other features
MCC RAPD
Optic neuritis
Also seen in severe retinal dz –> CRVO, CRAO, significant retinal datachment
Describe argyll robertson pupil, MCC?
Argyll robertson pupil menomic: ARP =
——————>
Accomodation reflex present
Pupilary Reflex Absent
Visual pathway defects:
Total blindness of ipsilateral eye caused by…
Lesion AFTER the optic chiasm
Optic nerve or retinal issue
Visual pathway defects:
Ipsilateral nasal hemianopsia caused by….
Ipsilateral = same side Hemi = half of vision lost Nasal = side of vision lost is closest to nose
Caused by lesion lateral to the optic chiasm
nasaL = Lateral
Visual pathway defects:
Bitemporal heteronymous hemianopsia
Bitemporal = both sides by temples
Hemianopsia = loss of half of visual field
Heteronymous = opposite sides of vision lost
Caused by lesion at hte midline of the optic chiasm AKA PITUITARY ADENOMA
Visual pathway defects:
Contralateral homonymous hemianopsia
Half of vision lost, homonymous = same half lost in both eyes- left side or right side - side lost = contra (opposite) the side of hte lesion
Lesion at the optic tract or occipital lobe stroke
RF for acute angle closure glaucoma
Elderly
Hyperopia (far-sighted)
Asians
W/ anything that causes mydriasis (makes angle smaller) being a precipitating factor (dim lights, anti-cholinergics)
Eye appearance in acute angle closure glaucoma
Naked eye
During fundoscopic exam
MId-dilated fixed nonreactive pupil
Eye feels hard to palpation
Conjunctival erythema (in ciliary pattern)
“Steamy” cornea - corneal epithelial edema or cloudiness, shallow chamber
Fundoscopic exam; Disc “cupping,” blurred disc-cup
Remember blurred disc-cup occurs in papiledema (any cause), optic neuritis, and glaucoma
Tx acute angle closure glaucoma
- IV Acetazolamide (dec aq humor producttion)
- Topical bb - timilol (reduces IOP)
- Miotics/cholinergics - Pilocarpine, carbachol
Peripheral iridotomy is defnitive treatment - avoid anticholinergics & sympathomimetics
CP Acute angle closure glaucoma
TUNNEL VISION = MC
A for acute - you lose vision AROUND the edges
Can also have HALOS around lights = PATHOGNOMONIC
Chronic open angle glaucoma - RF, si/sx
RF: > 60, AA, severe near-signtedness, family hx
Si/sx: Painless, vision only affected LATE in course so you need proper SCREENING!!! AKA GET EYE PUFF TEST or tonopen at optometrist yearly & examine optic nerve for cupping or blurring
Tx: 1st line: Prostaglandin agonist (Latanoprost, travatan) 2nd line: Beta-blockers (timolol)
Pressure checks q3-6 mo, formal visual field exams yearly
Eye disorders a/w diabetes
Dry eye (keratits sica) Cataract Glaucoma Retinopathy Retinal vein occlusion Cranial nerve abnl
What is the leading cause of blindness in US under age 65?
Diabetic retinopathy
Prevention of diabetic retinopathy
Maintain tight control of blood sugar (A1c < 7)
Control BP
STOP smoking
Reinforce need for annual dilated eye exams - can do laser surgery to prevent progression (panretinal photo-coagulation to reduce neovascularization and dec risk vitreous hemorrhage & retinal detachment)
Etiology retinal vein occlusion, CP
Etio: HTN retinopathy 2/2 AV nicking, DM, hypercoagulable states
CP: sudden painless vision loss
PE: DARK HUSKY RETINAL BACKGROUND - b/c blood is coming in (via artery) but not going out, retinal hemorrhages, cotton-wool etc
Prognosis depends on visual acuity - urgent referral - may lead to severe neovascular glaucoma
Tx: no effective tx - urgent referral. +/- antiinflam, steroids, laser photocoagulation
Retinal artery occlusion - etio, CP, PE, Tx
CP: sudden painless unilateral vision loss, usually permanent
Patho: MC in 50 - 80YO 2/2 atherosclerotic disease or an emboli
PE: PALLOR across entire retina (think of arterial occlusion in leg), cherry red spot (Macula will stay red b/c gets blood supply from a different artery
See it now because everything else gets white - white & pale just like arterial occlusion ) - OFTEN PRECEDED BY AMAUROSIS FUGAX
Tx: Place supine, ocular massage to dislodge emboli - vision loss permanent after 90 min of occlusion, decrease IOP to prevent anterior chamber involvement (acetazolamide)
URGENT REFERRAL
Exclude temporal arteritis (jaw claudication, headache) as the cause of the CRAO
Ddx sudden painless vision loss
CRAO
CRVO
Retinal detachment
Vitreous hemorrhage
Ddx sudden PAINFUL vision loss
Acute angle closure glaucoma
Vitreous hemorrhage - etio, sx, tx
Caused by bleeding from neovascularization (proliferative DM retinopathy, wet macular degeneration etc)
May lead to scarring and tractional retinal detachment 2/2 adhesions
Sx: New floaters, cobwebs, sudden loss of vision
Tx: Vitrectomy if hemorrhage doesn’t clear
Causes of tunnel vision
Acute angle closure glaucoma (sudden, unilateral, painful)
Chronic (open angle) glaucoma (slow, progressive, painless, bilateral)
Acute = AROUND the eye vision loss
Causes of central vision loss
MaCular degeneration (central vision blurry & color loss, bilateral)
Optic neuritis = “Central scotoma”, unilateral
Papilledema = “enlarged blind spot” if severe which may progress to bigger visual field defects & central vision loss, bilateral
Amaurosis fugax definition, causes
Temporary monocular vision loss (lasting minutes) with COMPLETE recovery - due to retinal emboli or ischemia - can be seen w/ TIA, giant cell arteritis, CRAO, SLE & other vasculitic d/o
Ocular trauma can cause….?
What to do first?
Blowout fracture
Ruptured globe
Foreign body
Hyphema
VISUAL ACUITY = FIRST THING
Why can hyphemas be dangerous?
B/c blood sitting in anterior chamber can clot and cause acute angle closure glaucoma
Has to stay sitting AT ALL TIMES until it clears
Needs urgent referral to ophtho
Which form of cipro is safe in otitis externa w/ perforated TM?
Can use ofloxacin (floxin otic) or ciproDEX otic
CiproHC otic is NOT sterile & contraindicated in TM Perf
NO HC IN TM perf
Which drops MUST be avoided if there is a TM perf?
Aminoglycoside drops = OTOTOXIC!!!
Chronic otitis media definiton
Chronic otitis media — COM is defined as an ear with a tympanic membrane perforation in the setting of recurrent or chronic ear infections
The most common symptom of CSOM is the presence of recurrent or persistent purulent ear drainage. CSOM is most often painless, and patients usually present without fever or other systemic signs of infection. The drainage may be foul smelling.
Pseudomonas aeruginosa and Staphylococcus aureus are the most commonly isolated aerobic bacteria in several large case series
NO AMG DROPS, NO CIPRO HC DROPS!!!
CP Eustachian tube dysfunction
Tx
Occurs after URI or allergic rhinitis - the blockage means tube can’t equilibrate pressure like normal = negative pressure
CP: feeling of fullness, underwater feeling, intermittent ear pain
Dx: Otoscope normal. +/- fluid behind TM
Tx: Decongestants (pseudoephedrine, phenylephrine, oxymeatzoline nasal spray)
Auto-insufflation (swallowing yawning, blowing against pinched nostril
Intranasal corticosteroids
Complications - may develop acute serous otitis media or infectious otitis media if blockage is prolonged
Causes of conductive hearing loss
Think of all the things involved with conduction of sound -
Otosclerosis (Fusion of stapes to round window - young women, familial - resect stapes) = CHL
Cholesteoma = CHL
OME= CHL
Chronic OM = CHL
Cerumen impaction = CHL
Point of the weber test?
Weber = whether or not your nerves are working
We are trying to vibrate acoustic nerve on side person says they can’t hear (bypass the conduction system to test the sensorineural system)
Pt will feel vibration more in ear without SNHL b/c the nerves are more intact - so lateralizes to the GOOD ear in SNHL
Mnemonic: SensoriNeural lateralizes to Normal ear & NORMAL rinne - focus on the “N”
What is a positive Rinne?
A positive Rinne = normal meaning that air conduction lasts longer than bone conduction
Remember SensoriNeural has NORMAL rinne & lateralizes to normal ear in SNHL
Conductive hearing loss - ear can’t conduct sound like its supposed to anymore - has lost conduction ability - and conduction straight thru the bone (mastoid) is better
Causes of SNHL
Anything that damages the nerves
AGEING = MC = PREBYACUSIS (acusis sounds like acoustic), chronic loud noise exposure, labyrinthitis, CNS lesions(acoustic neuroma_ meniere syndrome etc, MEDICATIONS (AMG TOBRAMYCIN, ASA, loop)
Signs of an acoustic neuroma
Sudden SNHL w/ poor speech discrimination w/o vertigo
MRI dx
Surgical removal tx
**Most common intracranial tumor, benign
Vertigo - central vs peripheral
Central - gradual in onset, insidious, scary, NO significant hearing loss, milder sx of vertigo, VERTICAL/ROTARY nystagmus that DOES NOT FATIGUE
+/- abnormal gait –> (more gait abnl than peripheral!) abnormal rhomberg, other CNS FOCAL DEFICITS
***Note: If pance Q give you an abnormal neuro exam then do NOT choose something benign like BPPV or labrynthitis - an issue w/ the labrytnth of the ear will not cause a focal neurological deficit….duh
Peripheral - abrupt onset, intense nausea & vomiting, HORIZONTAL nystagmus that FATIGUES EASILY, a/w hearing loss and tinnitus
Why epley maneuver is a tx for peripheral b/c it fatigues easily!
Causes of central vertigo vs peripheral
Central:
CNVIII tumor(acoustic neuroma) Cerebellar hemorrhage/ischemia Cerebellar tumor Infection MS
Peripheral:
BPPV
Acute labrynthitis
Meniere’s disease
Classic Meniere’s disease syndrome
Two known causes
Tx
Etio: 2/2 distension of the endolymphatic compartment of the inner ear = AKA endolymphatic hydrops
Classic syndrome: WAXES & WANES Episodic vertigo Low-frequency SNHL Tinnitus Sensation of ear pressure
Two known causes: Syphilis, head trauma
Tx: Refere to ENT, dec Na+ diet, meclizine
Acute labrynthitis
Acute onset of CONTINUOUS SEVERE VERGITO (meniere’s = episodic)
+ hearing loss & tinnitus
frequently follows a URI
Try meclizine
Two causes of peripheral vertigo that cause episodic vertigo
BPPV - NO SNHL
Meniere’s + SNHL & TINNITUS
Bowel Movements (BM = BPPV, meniere) are EPISODIC
LV are continuous vertigo
Two causes of peripheral vertigo that cause continuous vertigo
Vestibular neuritis - no hearing loss
Labyrinthitis + hearing loss (labyrinth is part of cochlea so inflam = hearing loss)
In a vestibule you can hear people talking = no hearing loss
If you’re in a labyrinth (maze) then you cannot hear anything (+ hearing loss)
First line treatment vertigo, next line
First line = meclizine (anticholinergic)
2nd line = dopamine blockers - metoclopramide, prochlorperazine (compazine), IV promethazine (phenergan)
Often given together or the D2 blockers are given with benadryl so that the anticholinergic doesn’t cause a dystonic reaction
BPPV
Etio - displaced otoliths = vertigo sx = one of causes of PERIPHERAL vergtigo
Remember BM - so episodic
Sudden onset, episodic, severe vertigo lasting 10-60 seconds, provoked with changes of head positioning
Dx: Dix-halpike - elicit delayed fatigable horizontal nystagmus = positive dx - if nystagmus vertical or non-fatiguable then check for central causes
Tx: Epley maneuver - canalith repositioning - meds usu not needed
First line tx vestibular neuritis & acute labyrinthitis
Corticosteroids
If sx - meclizine
What should you be thinking of if someone just had a URI and now have sx of vertigo?
Acute labyrinthitis or vestibular neuritis
Acute sinusitis - etio, CP, Dx, Tx
Etio - same as AOM = S. pneumo, H. flu, M, catarrhalis, GABHS
Often occurs w/ concurrent rhinits or follows viral URI b/c URI = edema = blocks drainage of sinuses = fluid build up = bacterial colonization
CP: Sinus pain/pressure worse bending over (maxillary MC), headache, malaise, purulent nasal discharge
Dx TOC = CT scan
Tx -Supportive/sx therapy
If sx > 10-14 days, fever etc then augmentin x 10-14 d = now the ABX of choice (used to be amoxicillin)
Note: If someone has had two appropriate courses of abx & the infection is not going away…it’s probably not being treated right - THINK FUNGAL!!!- get imaging!
Etio chronic sinusitis
S. aureus = MC bacterial cause
Aspergillus MC fungal cause
2nd MC fungal cause = MUCORMYCOSIS
Note: Chronic = > 12 weeks time
Mucormycosis
Causes chronic sinus infection
May enter CNS
Seen in immunocompromised pt (DM, HIV, chemo etc)
CP: Acute sinusitis sx and BLACK ESCHAR ON PALATE OR FACE
Tx: IV amphotericin B = 1st line
Allergic rhinitis - 2 unique clinical features
Worse in morning
A/w nasal polyps
Allergic rhinitis PE, Tx
PALE turbinates
Nasal polyps
Cobblestone mucosa of the conjunctiva
Tx = Intranasal corticosteroids = most effective tx!
Also avoidance and environmental control, exposure reduction
Oral anti-histamines for itching, sneezing, pruritis etc
Viral sinusitis PE
ERYTHEMATOUS turbinates (allergic = pale turbinates)
Think of viral strep throat = beefy red
MCC rhinovirus (common cold)
Etio, TOC nasal polyps
Nasal polyps MCC = allergic rhinitis - look for signs of that an look fro nasal polyps on inspection
**Note: Can also be caused by cystic fibrosis –> ESPECIALLY IF POLYPS ARE IN KIDS - think CF!
Tx = Refer to ENT (don’t biopsy), intranasal corticosteroids
MCC anterior nose bleed vs posterior nose bleed
Anterior = nose picking, dry environment
Posterior = hypertension and atherosclerosis –> note: they present w/ hematemesis not epistaxis
Tx = direct pressure, vasoconstrictors (phenylephrine, oxymetazoline, cocaine –> if medications fail do a packing & give antibiotics! (prevent TSS)
**Note: Septal hematomas are a/w loss of cartilage if the hematoma is not removed!!!
Nasal foreign body - MC in? CP? Tx?
MC in children
CP: Mucopurulent nasal discharge, foul odor, epistaxis
Tx: FB removal via positive pressure technique or instrumental removal
Strep Throat - 4 points in modified CENTOR criteria & how to use it
C –Cough absent / Can't Cough E –Exudate. N –Nodes. T –Temperature (fever) OR –young OR old modifier
0-1 - no abx or throat x
2-3 - throat cx
4-5 - give abx (56% chance)
**The OR age modifier: < 15 YO add one point, > 44 YO minus one point
**Note: If 5-15 YO, throat cultures should be sent in all cases
Tx: Pen G or VK is 1st line. PCN allergy - give Macrolide
Complications of strep throat
Rheumatic fever (preventable w/ abx)
PSGN (not preventable w/ abx)
Peritonsillar abscess (PTA)
Patho peritonsillar abscess, CP, Dx, Tx
Patho: tonsillitus –> cellulitis –> abscess formation
CP: Dysphagia, pharyngitis, muffled “hot potato” voice, difficulty handling oral secretions, trismus, uvula deviation to the CONTRALATERAL side, tonsillitis anterior cervical LAD
Dx: CT scan first line (differentiates cellulitis vs abscess)
Tx: Abx (unasyn, clinda, Pen G plus metro) & aspiration I&D
Layringitis - MCC, CP, Tx
MCC = virus (adeno, rhino etc)
CP: Hoarseness = HALLMARK, also aphonia
Tx: Supportive - voice rest, warm saline gargles, fluids, etc
TOC oral thrush
Nystatin liquid = x of choice
Candida part of normal flora but can become pathogenic 2/2 local or systemic immunosuppression (HIV, chemo, steroid inhalers w/o spacer, diabetics etc)
Oral leukoplakia = ? CP? Tx?
= precancerous hyperkeratosis 2/2 chronic irritation
CP: Painless white patchy lesion that CANNOT be scraped off (PLATED ON, plakia…oral candida = PAINFUL & CAN be scraped off)
Tx: Cryptherapy, laser ablation, bx to assess for cancer risk
Erythroplakia
precancerous lesions similar to leukplakia but with erythematous appearance
> 90% are dysplastic or cancerous (Sq cell carcinoma)
Oral hairy leukoplakia
Etio = epstein barr virus (HHV4)
Painless, white plaque along LATERAL tongue borders or buccal mucosa +/- irregular, “Hairy” or “feathery” lesions with prominent folds or projections - cannot be scraped off
No tx required - often resolve spontaneously
Acute bacterial siladenitis - Etio, CP, Dx, Tx
Acute bacterial siladenitis aka suppurative sialadenitis
Etio = staph aureus or mixed aerobic/anaerobic infection
CP = tenderness, swelling, erythema near the gland, especially w/ meals, + pus if duct is massaged, fever& chills if severe
Dx = CT scan - assesses for associated abscess and the extent of tissue involvement
Tx = sialogogues (tart hard candies = inc salivary flow) + antibiotics (Dicloxacillin) OR if severe infection cover for anaerobes (clind, metro) too
Ludwig’s angina = what? occus after? etio? CP? Dx? Tx?
Ludwig’s = cellulitis of the sublingual and submaxillary spaces of the neck = MC neck space infection - lots of pockets for stuff to grow!!!
MC 2/2 dental infections (anaerobic infections)
CP = Swelling & erythema of the upper neck & chin with pus on the floor of the mouth
Dx = CT scan
Tx = Hospitalize, IV abx (Unasyn or PCN plus Metro or clinda), monitor airway
Dangerous b/c the swelling = airway compromise
Why are we super quick to give antibiotics in a suspected dental infection?
Because it can quickly turn into ludwig’s angina = BAD!!
Always cover w/ abx if toot pain, sensitive to percussion/temperature etc
Tx = Pen VK or clinda ($$$)
Chronic hoarseness workup
Indirect laryngoscopy –> have pt say “ah” –> do cords move??
IF YES –> then hoarseness could be 2/2 vocal cord nodules (overuse, singers etc) or squamous cell carcinoma of larynx so REFER TO ENT
IF NO –> then it’s vocal cord paralysis 2/2 recurrent laryngeal nerve abnormalities 2/2 something wrong in the thorax (mediastinal/apical mass (lung CA), thoracic aneurysm, marked LAD etc –> GET IMAGING OF THORAX
Salivary gland tumors
80% are parotid- mostly BENIGN
SMALLEST glands = HIGHEST risk of malignancy –> 50% of submandibular tumors are malignant & EVEN MORE of SUBMENTAL
If pt says they can “feel something” In their salivary gland, sent them to ENT b/c they can look into the gland
