Ch5: HEENT Flashcards
majority of cases of acute rhinosinusitis is usually caused by…..
virus
less than ____% of viral URIs are complicated by acute bacterial rhinosinusitis
2%
and the majority will resolve without antimicrobial therapy!!!!
what is acute rhinosinusitis
inflammation of the mucosal lining of the nasal passages and paranasal sinuses lasting up to 4 weeks, caused by allergens, environmental irritants, and/or infection (viruses [majority], bacteria, or fungus)
what is acute bacterial rhinosinusitis
secondary bacterial infection of the paranasal sinuses, usually following a viral URI. relatively UNCOMMON
Less than 2% of viral URIs are complicated by bacterial infection. and the majority will resolve without antimicrobial therapy
DRSP
drug-resistant strep pneumonia
top (3) causative pathogens in ABRS
- Strep pneumoniae (gram-positive)
- H. influenzae (gram-negative)
- M. catarrhalis (gram-negative)
in treating ARBS, an antimicrobial activity against gram ______ should be chosen
positive and negative
strep pneumoniae = gram pos
H. influenzae and M. catarrhalis = gram neg
do you need a culture of sinus drainage in order to give abx for ABRS?
no, empiric therapy knowing the most common causative agents
COMPS mnemonic is for conditions caused by which (2) bacteria
- Strep pneumonia
2. H. influenzae
Conditions caused by strep pneumonia
COMPS
- conjunctivitis
- otitis media
- meningitis
- pneumonia
- sinusitis
Conditions caused by H. influenzae
COMPS
- conjunctivitis
- otitis media
- meningitis
- pneumonia
- sinusitis
1 most common causative agent for acute bacterial rhinosinusitis
strep pneumoniae
gram-positive diplococci
strep pneumoniae
gram _____
shape:
gram positive
diplococci
% of strep pneumonia in the US that is drug-resistant (DRSP)
> 25%
2 most common causative agent of ABRS
H. influenzae
gram-negative bacillus
h. influenzae
gram_______
shape:
gram negative
bacillus
% of h. influenzae that is penicillin-resistant via production of beta lactamase
> 30%
most ______ [abx class] are stable in the presence of bacteria that produce beta-lactamase
cephalosporins
bacteria that produce beta lactamase will be…..
resistant to penicillins
clauvulanate (e.g., added to amoxicillin to make Augmentin) will neutralize….
beta lactamase
making the abx work against otherwise resistant bacteria
3 causative agent of ABRS
M. catarrhalis
gram-negative coccus
% of m. catarrhalis that are resistant to penicillins
> 90%
conditions caused by m. catarrhalis (2)
- ABRS
- CAP (uncommon)
for whom is it appropriate to prescribe antibiotics with acute rhinosinusitis
URI-like symptoms and either:
- persistent symptoms that are not improving after 10 or more days
- severe symptoms for >3-4 days (fever >102, purulent nasal discharge, facial pain),
OR - worsening or “double-sickening” (initial improvement followed by worsening with fever, headache, nasal discharge, usually after 5-6 days of illness)
standard viral URI is gone within…..
7-10 days
why do you wait 10 days before initiating antibiotic therapy for acute rhinosinusitis?
most acute rhinosinusitis is caused by a VIRUS
> viral infections typically last 7-10 days
> > if it lasts longer than 10 days, consider a bacterial superinfection
Risk factors for antibiotic resistance (5)
MOST COMMON
- age <2 or >65yo, daycare attendance
- prior systemic antibiotics within the last month (oral or parenteral)
LESS COMMON
- hospitalization within previous 5 days
- comorbidities
- immunocompromised
how long should you prescribe abx for and when should they feel improvement in ABRS
complete 5-7 days of antibiotic therapy (consider 7-10 days if they have risk factors for resistance)
they should experience improvement after 3-5 days
if you prescribe abx for ABRS and they have no improvement or worsening symptoms after 3-5 days, what is your next step?
broaden coverage or switch to a different antimicrobial class
if you prescribe abx for ABRS and they have no improvement or worsening symptoms after 3-5 days. you then switch antibiotic classes and they report no improvement in another 3-5 days. What is your next step?
- referral to specialist
- CT or MRI to investigate non-infectious causes or suppurative complications (e.g., periorbital abscess)
- sinus or meatal cultures for pathogen-specific therapy
Symptomatic treatment in ABRS
- saline nasal irrigation
- intranasal corticosteroids when they are additionally accompanied by allergic rhinitis
- abx as indicated
intranasal corticosteroids are only useful in ABRS when they have what comorbidity
allergic rhinitis
the US FDA advises that the adverse effects associated with what antibiotic class generally outweighs the benefits for patients with - acute sinusitis - acute bronchitis - uncomplicated UTI who have other treatment options
fluoroquinolones
e.g., levofloxacin, ciprofloxacin, moxifloxacin
which antibiotic class is NOT recommended in ABRS treatment due to their rising resistance rates
macrolides & TMP-SMZ (Bactrim)
e.g., azithromycin, clarithromycin, erythromycin
coverage is very poor because azithromycin was incredibly over-used and now most strep pneumo is resistant
First line antibiotic therapy for ABRS
amoxicillin-clavulanate (Augmentin) 875/125mg PO BID x5-7 days
First & second line antibiotic therapy options for ABRS
FIRST LINE
amoxicillin-clavulanate (Augmentin) 875/125mg PO BID x5-7 days
amoxicillin-clavulanate (Augmentin) 500/125mg PO TID x5-7 days
SECOND LINE
amoxicillin-clavulanate (Augmentin) 2000mg/125mg PO BID
doxycycline 100mg PO BID
doxycycline 200mg PO QD
the clavulanate aspect of Augmentin specifically causes this particular side effect
GI upset
is really hard on the stomach
how high a dose of amoxicillin-clavulanate do you need to overcome resistance in drug-resistant strep pneumo (DRSP)
3-4g (3000-4000mg) per day
can doxycycline be used in pregnancy
NO (teeth staining of the child)
beta-lactamase inhibitor drug
clavulanate
doxycycline in ABRS – is it better against the gram positive (strep pneumo) or gram negative (h. flu or m. cat) organisms?
does well against the gram NEGATIVES (h. flu and m. cat)
does ok against gram POS (strep pneumo), particularly bad if it is a drug-resistant strep pneumo (DRSP)
ABRS treatment options if they have an allergy to beta-lactams/penicillins (4)
doxycycline 100mg PO BID
doxycycline 200mg PO QD
levofloxacin 500mg PO QD x5 days
moxifloxacin 400mg PO QD x5 days
what is the only advantage the respiratory fluoroquinolones have over doxycycline in ABRS
they have better activity against drug-resistant strep pneumo (DRSP)
what are the (3) RESPIRATORY fluoroquinolones
moxifloxacin, gemifloxacin, levofloxacin
what are your antibiotic treatment options for folks with ABRS who have failed initial therapy or who are at high risk for antibiotic resistance (3)
amoxicillin-clavulanate (Augmentin) 2000/125mg PO BID (4g total daily - HIGH DOSE)
levofloxacin 500mg PO QD
moxifloxacin 400mg PO QD
only (4) antibiotics we should consider for ABRS
- amoxicillin-clavulanate (Augmentin)
- doxycycline (second line)
- levofloxacin (last resort)
- moxifloxacin (last resort)
CYP450 is an example of a ….
drug-metabolizing isoenzyme
what is a substrate
a medication or a substance that utilizes a specific enzymatic pathway (e.g., CYP450) to be metabolized and modified in some way such that it can reach the drug site of action and/or be eliminated
what % of all prescription drugs are substrates of CYP450 3A4
50%
e.g., sildenafil (Viagra), atorvastatin, simvastatin, alprazolam (Xanax), and many many other
50% of all prescription drugs are substrates of this isoenzyme….
CYP450 3A4
what is a CYP450 inhibitor
blocks the activity of the isoenzyme, limiting substrate excretion»_space; allows an increase in substrate levels, and possible risk of substrate-induced toxicity
erythromycin and clarithromycin are CYP450 3A4 ______
inhibitors
clarithromycin + simvastatin = risk for……
statin-induced rhabdomyolysis
d/t clarithromycin being a CYP450 inhibitor
clarithromycin + alprazolam = risk for…..
sedation and fall risk
d/t clarithromycin being a CYP450 inhibitor
what is a CYP450 inducer
accelerates the activity of the isoenzyme so that the substrate is pushed out the exit pathway»_space; reduction of the substrate level
St. John’s wort is a CYP450 3A4 _______
inducer
CYP inducers can lead to [increased vs. reduced] target drug levels
reduced target drug levels»_space;
diminished therapeutic effect
CYP inhibitors can lead to [increased vs. reduced] target drug levels
increased target drug levels»_space; risk for toxicities
St John’s Wort + COCs = increased risk for…..
decreased COC efficacy, spotting, contraceptive failure
d/t st johns wort being a CYP450 inducer
St John’s Wort + cyclosporine = increased risk for….
decreased cyclosporine efficacy (organ transplant anti-rejection med)
never give this antibiotic to a patient whom you don’t know every med that they are on
clarithromycin (CYP450 3A4 inhibitor)
what possible condition may occur after resolution of acute otitis media? (common, not considered treatment failure)
serous otitis (otitis media with effusion)
the inner ear is filled with fluid that can last days-weeks after resolution of the otitis media infection
can caused continued sensation of ear fullness and muffled speech sounds
what type of hearing impairment occurs in serous otitis
conductive hearing loss
conductive hearing loss is usually [temporary vs. permanent]
temporary
sensorineural hearing loss is usually [temporary vs. permanent]
permanent
Cause of conductive hearing loss
sound is being blocked by something in the outer ear or middle ear (earwax, foreign object, damaged ear drum, serous otitis media, bone abnormality)
Cause of sensorineural hearing loss
inner ear disorder whereby the vestibulocochlear nerve (CN VIII) becomes damaged
caused by advancing age, ototoxic medications, immune disorders, trauma
ototoxic medications cause _____ hearing loss
sensorineural
ear infections cause _____ hearing loss
conductive
Weber hearing tests will localized to the side with…..
increased tissue density, consolidation
e.g., fluid build-up in acute otitis media
Weber test results in conductive vs. sensorineural hearing loss
CONDUCTIVE
- buzzing sound will lateralize to the AFFECTED ear, heard louder in the affected ear due to increased tissue density, e.g., fluid build-up
SENSORINEURAL
- buzzing sound lateralizes to the UNAFFECTED ear, heard better in the unaffected ear; the buzzing sound is heard less well or not at all in the affected ear
Rinne test results in conductive vs. sensorineural hearing loss
CONDUCTIVE
- Negative: bone conduction heard better than air conduction
SENSORINEURAL
- Positive or Normal: air conduction is heard better than bone conduction
Generally-speaking, treatment options for conductive hearing loss
often self-limiting post-URI, AOM resolution, or cerumen impaction removal
rarely, further pharmacological or surgical intervention is needed
Generally-speaking, treatment options for sensorineural hearing loss
hearing aids, cochlear implants, expert consultation
positive vs. negative Rinne test
POSITIVE = NORMAL (air > bone conduction)
NEGATIVE = ABNORMAL (bone > air conduction)
what is allergic rhinitis
“asthma in the head”
recurrent, inflammatory disease of the upper-airways mediated by IgE (just like asthma) due to genetic and environmental interactions
characterized by nasal congestion, rhinorrhea (nasal drainage), sneezing, intraocular and/or nasal itching
characteristic of allergic rhinitis, not a common cold or URI
itch
first line therapy in any allergic disorder, including allergic rhinitis
allergen avoidance/environmental control
patient education to avoid the allergen whenever possible
first line MEDICATION therapy in allergic rhinitis
CONTROLLER therapy, not PRN to prevent symptoms and preventing formation of inflammatory mediators
FIRST LINE = intranasal corticosteroids
high efficacy
e. g., fluticasone propionate (Flonase), triamcinolone (Nasarcort AQ)
* * both OTC and lower-price
SECOND LINE = leukotriene modifiers
e.g., Montelukast (Singulair)
best as add-on therapy if symptoms are not adequate controlled with intranasal corticosteroids
anticipatory guidance for intranasal corticosteroids for allergic rhinitis
cannot expect results for a few days
Reliver therapies for acute symptoms of allergic rhinitis (second line to controller therapies)
block the action of histamine, which is a potent inflammatory mediator
- 2nd gen oral antihistamines (loratidine [Claritin], cetirizine [Zyrtec], levocetirizine [Xyxal - most potent]
- *avoid first-gen like diphenhydramine (Benadryl) due to sedation
- intranasal antihistamines (azelastine [Astelin, Astepro])
- ocular antihistamines for allergic conjunctivitis (olopatadine, aezlastine, bepotastine)
Most potent of the oral antihistamines for allergic rhinitis
levocetirizine (Xyxal)
examples of ocular antihistamines for allergic rhinitis
eyedrops filled with antihistamines
- olopatadine (Patanol, Pataday)
- azelastine (Optivar)
- bepotastine (Bepreve)
examples of intranasal antihistamines for allergic rhinitis
- azelastine (Astelin, Astepro)
Treatment option for patients with allergic rhinitis refractory to standard therapies
sublingual or injection immunotherapies to reduce IgE production, requires specialty consultation
can also consider acupuncuture
examples of 2nd-gen oral antihistamines for allergic rhinitis
- loratadine (Claritin)
- cetirizine (Zyrtec)
- levocetirizine (Xyxal)
examples of intranasal corticosteroids for allergic rhinitis
- fluticasone (Flonase)
- triamcinolone (Nasacort AQ)
example leukotriene modifier for allergic rhinitis
montelukast (Singulair)
WBC that is activated in allergic disorders
eosinophils
“dandruff of the eyelids”
blepharoconjunctivitis
treat with baby shampoo on a q-tip
____ lymph nodes are tender
infected
non-tender enlarged notes tend to be infected
medical term for canker sore
aphthous stomatitis
classic presentation of squamous cell carcinoma of the mouth
painless, persistent oral lesion
indurated margins
associated nontender firm lymphadenopathy
h/o cigarette smoking, h/o HPV 16
inhaled corticosteroids puts folks at risk for oral…..
thrush
95% of oral cancers are….
squamous cell carcinoma
what are the 12 cranial nerves
OOOTTAFAGVAH
I = olfactory II = optic III = oculomotor IV = trochlear V = trigeminal VI = abducens VII = facial VIII = acoustic IX = glossopharyngeal V = vagus VI = accessory, spinal VII = hypoglossal
Risk factors for squamous cell carcinoma of the mouth
STRONG
- longstanding HPV, especially HPV16
- tobacco use
- alcohol abuse
LESS POTENT
- male
- older age (>55yo)
60yo male pt with h/o tobacco use and HPV presents with a painless, ulcerating oral lesion x3 months with immobile, nontender lymphadenopathy to the ipsilateral cervical chain.
You suspect…
oral squamous cell carcinoma
Function of CN I
olfactory = smell
Function of CN II
optic = vision
Function of CN III
oculomotor = eyelid and eyeball movement
eye movements upward, medial, and downward
Function of CN IV
trochlear = innervates the superior oblique, turns eye downwards and laterally
eye movements inward and downward
Function of CN V
trigeminal = chewing, face and mouth sensation, touch and pain
touch the forehead & cheek
clench teeth
Function of CN VI
abducens = turns eye laterally
ability to look to each side
Function of CN VII
facial = controls most facial expressions, secretion of tears and saliva, taste
smiling, taste for the anterior 2/3 of the tongue
Function of CN VIII
acoustic = hearing, equilibrium, sensation
Function of CN IX
glossopharyngeal = taste, senses carotid blood pressure
taste for posterior 1/3 of the tongue
Function of CN X
vagus - senses aortic blood pressure, slows the HR, stimulates digestive organs, defecation, taste
Function of CN XI
spinal accessory = controls trapezius and sternocleidomastoid muscles, controls swallowing movements
shoulder shrug
Function of CN XII
hypoglossal = controls movement of the tongue
Tongue movements tests Cranial Nerve….
12 (CN XII) - hypoglossal
Shoulder shrug tests Cranial Nerve ….
11 (CN XI) - spinal accessory
Facial expresses tests Cranial Nerve….
7 (CN VII) - facial
Eye movements in all directions tests Cranial Nerves ….
3 (CN III) - oculomotor
4 (CN IV) - trochlear
6 (CN VI) - abducens
Perceiving light sensation to the face tests Cranial Nerve….
5 (V) - trigeminal
Sense of smell tests Cranial Nerve….
1 (I) - olfactory
Vision tests cranial nerve….
2 (II) - optic
Hearing tests Cranial Nerve….
8 (VIII) - acoustic
“puff out your cheeks” tests which cranial nerve
CN VII (facial)
“shrug your shoulders” tests which cranial nerve
CN XI (spinal accessory)
“raise your eyebrows” tests which cranial nerve
CN VII (facial)
“do you recognize this scent” tests which cranial nerve
CN I (olfactory)
paralysis of cranial nerve VII is called….
bell’s palsy
does bell’s palsy require special imaging or labs for diagnosis
no, clinical diagnosis
most appropriate initial therapy for bell’s palsy
initiating a short-course of oral corticosteroids – the sooner initiated, the better the clinical response
the longer they have these symptoms without treatment, the poorer the outcome
Pt presents with sudden onset of inability to raise his eyebrow or smile on the right side of his face. Additionally reports decreased lacrimation in the right eye and difficulty closing the right eyelid. The rest of the exam is otherwise unremarkable. You suspect….
Bell’s palsy (paralysis of cranial nerve VII, aka idiopathic facial paralysis)
anticipatory guidance for bell’s palsy
short course of oral corticosteroids is first line
most folks recover completely over the course of 3 months
vital sign of the eye
visual acuity
pathology of bell’s palsy
acute paralysis of CN VII in the absence of brain dysfunction. cause is largely unknown – might involve inflammation of the cranial nerve d/t viral infection
classic presentation of bell’s palsy
sudden onset unilateral facial paralysis including inability to raise the eyebrow or smile on the affected side, decreased lacrimation on the affected side with inability to close the eyelid may be present
how do you diagnose bell’s palsy
clinical diagnosis based on HPI and physical exam whereby the only abnormality is facial nerve paralysis
tests to exclude other conditions may be considered on a case-by-case basis including lyme disease serology, electromyography, neuro imaging only if symptoms do not resolve over time
treatment overview for bell’s palsy
prompt initiation of systemic oral corticosteroids (PO prednisone) for new-onset. appropriate eye care due to impaired eyelid closure and reduced lacrimation
little evidence to support antiviral therapy
most patients recover completely in 3 months
facial physical therapy is possibly needed if incomplete recovery
surgical intervention can be considered to prevent ocular desiccation when facial nerve appears permanently damaged
who needs a visual acuity exam and how is it done?
with all comprehensive annual physical examinations of adults or children
typically done in the office with a Snellen eye chart
Refer to eye care specialist for additional evaluation if they fail the test
They should be using their typical visual aid (e.g., glasses) if that is what they normally use
with any eye complaint, always do this test…..
visual acuity (Snellen chart)
if there is any new onset of visual acuity change, needs referral to specialist
triad of symptoms to ALWAYS refer promptly to ophthalmology (invariably something serious)
- red eye
- painful eye
- new onset visual acuity change
e.g., acute glaucoma, iritis
on fundoscopic eye exam, the arteries should NEVER be _____ than the veins
wider
arteries should be smaller, more narrow than the veins
normal for the [arteries vs. veins] to be wider and darker on fundoscopic eye exam
veins = wider, darker
normal for the [arteries vs. veins] to be narrower, brighter on fundoscopic eye exam
arteries = narrow, brighter
the optic disc margins on a normal fundoscopic eye exam should be….
sharp, saucer-shaped
optic disc should be towards the nasal portion of the ocular field
papilledema findings on fundoscopic exam
caused by increased intracranial pressure
pt reports new blind spot in the visual field
bulging optic disc (too much intracranial pressure)
arteriovenous (AV) nicking findings on fundoscopic exam
stiffened, thickened arterioles (artery laying over a vein, and the vein is causing some pressure now)
seen in chronic, poorly-controlled HTN
usually without visual changes
hemorrhagic lesion findings on fundoscopic exam
caused by high grade HTN or proliferative diabetic retinopathy or trauma
pt complains of new-onset floaters in the visual fields because they are trying to look through blood floating in the vitreous humor in the eye
deeply-cupped optic disc findings on fundoscopic exam
usually as a result of acute angle-closure glaucoma, typically with new onset of unilateral eye pain, redness, and blurred vision
what is the course of vision loss in untreated open-angle glaucoma (chronic glaucoma)
gradual PERIPHERAL vision loss, usually noted in older adult, preventable with treatment
they develop tunnel vision
what is the course of vision loss in presbyopia
gradual onset of blurring of NEAR vision, most often noted by mid-late 40s
caused by stiffening of the lens of the eye
can use reading glasses
what is the course of vision loss in macular degeneration
CENTRAL vision loss, usually in adult of advanced age
macular degeneration causes [central vs. peripheral] vision loss
central
chronic open-angle glaucoma causes [central vs. peripheral] vision loss
peripheral
presbyopia causes [near vs. far] vision loss
near
most common cause of new onset blindness in the older adult
macular degeneration
appropriate ophthalmologic test for evaluation of the anterior eye structures including the cornea, conjunctiva, sclera and iris
slit lamp examination
appropriate ophthalmologic test for early detection of macular degeneration
Amsler grid
appropriate ophthalmologic test for measurement of intraocular pressure, e.g., for glaucoma screening
tonometry
tonometry tests for….
intraocular pressure (glaucoma screening)
amsler grid tests for….
macular degeneration screening
most common cause of acquired hearing loss in older adult
presbycusis
how does presbycusis present
difficulty appreciating the content of conversation in a noisy background environment
mishear words
they can hear ok in a quiet environment
what is presbycusis
hearing loss with age
describe presbyopia
hardening of the lens which results in near-vision problems. nearly all >45yos need reading glasses or other similar correction, very common with age
describe senile cataracts
clouding of the lens, which causes progressive vision dimming, problems with distance-vision. near-vision is usually retained. risk factors include tobacco use, poor nutrition, sun exposure, and corticosteroids. potentially correctable with surgery or a lens implant
describe open-angle glaucoma
painless, gradual onset of increased intraocular pressure leading to optic atrophy. presents as loss of peripheral vision if left untreated. avoidable with appropriate and ongoing intervention.
more than >80% of glaucoma is open-angle. should be detected on periodic screening with tonometry and assessment of visual fields
treatment includes miotics, beta blockers, and possible surgery
describe closed-angle glaucoma
sudden increase in intraoccular pressure, usually unilateral. presents with an acutely red, painful eye with vision changes including halos around lights. eyeball is firm compared to the unaffected eye. requires immediate referral to ophthalmology for rapid pressure reduction via medication or possible surgery
Pt presents with sudden onset of unilateral eye pain, redness, and visual changes including halos around lights. You suspect….
acute closed-angle glaucoma - emergency! refer for emergent pressure-reduction with ophthalmology
describe age-related maculopathy (macular degeneration)
thickening, sclerotic changes to the retinal basement membrane complex leads to painless vision changes including distortion of central vision. On fundoscopic exam, may see drusen (soft yellow deposits in the macular region). Aside from aging, risk factors include tobacco use, sun exposure, and family history.
Treatment depends on type (wet or dry)
Dry macular degeneration – develops slowly over decades. no treatment options, so prevention is the focus.
wet macular degeneration – develops quickly over a few months. tx includes laser treatment for photocoagulation to obliterate the neovascular membrane, intravitreal injection of antivascular growth factors
describe anosmia/hyposmia
neural degeneration leads to diminished sense of smell with the resulting decline in fine taste discrimination. this is accelerated by tobacco use
describe presbycusis
loss of 8th cranial nerve (CN VIII - acoustic) sensitivity. leads to difficulty with conversation in a noisy environment. can hear but cannot understand well what was said. accelerated by excessive noise exposure. hearing aids can be useful
is presbycusis sensorineural or conductive hearing loss
sensorineural
most common pathogens for suppurative conjunctivitis (3)
- staph aureus
- strep pneumonia
- h. influenzae
most common pathogens for otitis externa (3)
- pseudomonas
- s. epidermidis
- staph aureus
most common pathogen for malignant otitis externa in someone with DM, HIV/AIDs, or on chemotherapy
pseudomonas in >95%
most common pathogens for exudative pharyngitis (5)
- group A streptococcus (strep pyogenes)
- group C or G streptococcus
- viral causes (including HHV-6, human herpes virus 6)
- n. gonorrhoeae
- f. necrophorum
viral conjunctivitis is usually caused by….
adenovirus
recommended antibiotic tx for suppurative conjunctivitis
- ophthalmic treatment with fluoroquinolone ocular solution (e.g., ciprofloxacin, levofloxacin, moxifloxacin)
- alternatively, ophthalmic treatment with polymyxin B with trimethoprim solution
recommended antibiotic tx for otitis externa
- mild disease can be treated with acetic acid with propylene glycol and hydrocortisone drops (VoSoL)
- moderate to severe disease can use otic drops with ciprofloxacin with hydrocortisone
- decrease risk of reinfection by proper ear canal cleansing with 1:2 mixture of white vinegar and rubbing alcohol drops after swimming
- do not use drops if punctured tympanic membrane is suspected
describe malignant otitis externa
complication of otitis externa that can occur in folks who are immunocompromised. >95% of cases are caused by pseudomonas. Priority risks include osteomyelitis of the skull or TMJ. Consider MRI or CT imaging to rule out osteomyelitis. Consider referral for ENT consult with surgical debridement. Obtain cultures of the ear drainage or results of the surgical debridement to further guide treatment. Parenteral antibiotics are often warranted for severe disease.
recommended antibiotic tx for malignant otitis externa
- oral ciprofloxacin for early disease if suitable for outpatient therapy
- other options are available in inpatient setting for severe disease
recommended antibiotic therapy for exudative pharyngitis
- first line is penicillin V PO x10 days OR benzathine penicillin IM x1 dose (if adherence is a concern)
- alternatively, 2nd generation cephalosporin x4-6 days, azithromycin x5 days, or clarithromycin x10 days (all PO)
Priority complication of untreated strep pharyngitis
prevent rheumatic fever/ rheumatic heart disease
% of adult pharyngitis that is due to group A strep (strep pyogenes; GAS)
10%
most adult pharyngitis is caused by….
virus
