Chapter 5 - Eyes, Ears, Nose, & Throat Disorders
CHAPTER 5 - ENT (EARS. NOSE. & THROAT DISORDERS!
EYE DISORDERS
314
EAR DISORDERS
332
NEOPLASMS
340
NOSE/SINUS DISORDERS
340
NOSE/SINUS DISORDERS
343
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Chapter 5 - Eyes, Ears, Nose, & Throat Disorders
EAR
OTITIS
DISORDERS
EXTERNA
• Inflammation of the external auditory canal.
RISK FACTORS
• Water i m m e r s i o n aka "swimmer's ear" - excess moisture raises t h e pH from the normal acidic pH
of t h e ear, facilitating bacterial overgrowth.
• Local mechanical trauma (eg, use of Q-tips), age 7-12 years, aberrant ear wax (too much or too little).
ETIOLOGIES
• Pseudomonas
• Staphylococcus
aeruginosa m o s t c o m m o n (50%).
(eg, a u r e u s & epidermis), GABHS, Proteus, anaerobes; Aspergillus. Fungi.
CLINICAL MANIFESTATIONS
• Ear pain, pruritus in the ear canal (may have recent activity of swimming).
• Auricular discharge, e a r p r e s s u r e or fullness, hearing loss.
• Physical exam: p a i n o n traction of t h e e a r canal o r tragus, p u r u l e n t auricular discharge.
DIAGNOSIS
• Clinical + otoscopy: e d e m a of t h e external auditory canal with erythema, debris, or discharge.
MANAGEMENT
• Protect t h e ear against moisture (drying agents include isopropyl alcohol & acetic acid) + removal of
debris & cerumen + topical antibiotics with coverage against Pseudomonas & Staphylococcus (with
or w i t h o u t glucocorticoids for inflammation).
• Topical antibiotics:
- Ciprofloxacin-dexamethasone, Ofloxacin.
- Aminoglycoside combination: Neomycin/Polymyxin-B/Hydrocortisone otic. Not used if tympanic
perforation suspected or if TM cannot be visualized - aminoglycosides are ototoxic.
MALIGNANT (NECROTIZING) OTITIS
EXTERNA
• Invasive infection of t h e external auditory canal and skull b a s e (temporal bone, soft tissue and
cartilage). A complication of Acute otitis externa.
• Pseudomonas aeruginosa >95%.
• Risk factors: i m m u n o c o m p r o m i s e d states - elderly diabetics m o s t common, high-dose
glucocorticoid therapy, chemotherapy, advanced HIV.
CLINICAL MANIFESTATIONS
• Severe auricular pain, otorrhea. Cranial nerve p a l s i e s (eg, CN VII) if Osteomyelitis occurs.
• May radiate to temporomandibula r joint (pain with chewing).
• Physical examination: s e v e r e auricular p a i n o n traction of t h e e a r canal o r tragus.
DIAGNOSIS
• Otoscopy: edema of the external auditory canal with erythema, discharge, granulation t i s s u e at the
b o n y cartilaginous junction of the ear canal floor, frank necrosis of t h e ear canal skin.
• CT o r MRI to confirm t h e diagnosis. Biopsy is t h e m o s t accurate t e s t
MANAGEMENT
• Admissio n + IV Antipseudomonal antibiotics - IV Ciprofloxacin
• Alternatives include Piperacillin-tazobactam, Ceftazidime, Cefepime.
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first-line.
Chapter 5 - Eyes, Ears, Nose, & Throat Disorders
MASTOIDITIS
Infection of the mastoid air cells of the temporal bone. Largely a disease of childhood (esp. < 2 years).
• Etiologies: usually a complication of Acute otitis media.
• Clinical manifestations: d e e p ear pain (usually w o r s e at night), fever, lethargy, malaise.
PHYSICAL EXAMINATION
• Otalgia, fever, signs of Otitis media (bulging & erythematous tympanic membrane).
• Mastoid (postauricular) tenderness, edema, & erythema.
• Protrusion of t h e auricle. May develop cutaneous abscess (fluctuance). Narrowe d auditory canal.
DIAGNOSIS
• CT scan with contrast first-line diagnostic t e s t
MRI.
MANAGEMENT
• IV antibiotics + middle ear or mastoid drainage (myringotomy) with or without t y m p a n o s t o m y
tube placement. IV Vancomycin PLUS either Ceftazidime or Cefepime or Piperacillin-tazobactam.
• Tympanocentesis can be performed to get cultures. Refractory or complicated: m a s t o i d e c t o m y
CHRONIC
OTITIS
MEDIA
• Recurrent or persisten t infection of the middle ear & / o r mastoid cell system in the p r e s e n c e of
tympanic m e m b r a n e perforation > 6 weeks.
• Complication of Acute otitis media, trauma or cholesteatoma.
ETIOLOGIES
• Pseudomonas m o s t c o m m o n , S. aureus, gram-negative rods (eg, Proteus), anaerobes,
• Can become w o r s e after a URI or after w a t e r enters the ear.
Mycoplasma.
CLINICAL MANIFESTATIONS
• Perforated tympanic m e m b r a n e + p e r s i s t e nt o r recurrent purulen t otorrhea (often painless),
ear fullness, varying degrees of conductive hearing loss.
• May have a primary or secondary Cholesteatoma.
MANAGEMENT
• Removal of infected debris + topical antibiotic d r o ps first-line (Ofloxacin or Ciprofloxacin).
• Systemic antibiotics reserved for severe cases.
• In patients with a tympanic m e m b r a n e rupture, avoid water, moisture, & topical
aminoglycosides in the ear w h e n e v e r there is a tympanic m e m b r a n e rupture.
• Surgical: tympanic m e m b r a ne repair o r reconstruction.
mmurn
Acute otitis media: effusion + signs or symptoms of inflammation (fever, ear pain with bulging &
marked erythema of the tympanic membrane).
Chronic otitis media: perforated tympanic m e m b r a n e + persistent or recurrent purulent otorrhea,
otalgia (ear pain), ear fullness, & varying degrees of conductive hearing loss.
Serous otitis media (otitis media with effusion): asymptomatic effusion + no signs or symptoms of
inflammation (no fever, no ear pain & no marked erythema or bulging of the TM).
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Chapter 5 - Eyes, Ears, Nose, & Throat Disorders
CUTE OTITIS MEDIA
(AOM)
• Infection of middle ear, temporal bone, & mastoid air cells.
• Acute otitis media: rapid onset + signs or symptoms of inflammation.
• Risk factors: p e a k age 6 - 1 8 months (Eustachian tube in children is shorter, n a r r o w er & more
horizontal), day care, pacifier or bottle use, second-hand smoke, n o t being breastfed.
4 MOST COMMON ORGANISMS:
• Streptococcus
pneumoniae
m o s t c o m m o n , H. influenzae,
Streptococcus (same organisms seen in Acute sinusitis).
Moraxella
catarrhalis,
Group A
PATHOPHYSIOLOGY
• Most c o m m o n l y p r e c e d e d b y v i r a l URI, leading to blockage of the Eustachian tube.
CLINICAL MANIFESTATIONS
• Fever, o t a l g i a (ear pain), e a r t u g g i ng in infants, stuffiness, conductive hearing loss.
• Tympanic m e m b r a n e rupture: rapid relief of pain + otorrhea (usually heals in 1-2 days).
PHYSICAL EXAMINATION
• Bulging & e r y t h e m a t o u s t y m p a n i c m e m b r a n e (TM) w i t h effusion, loss of landmarks.
• Pneumatic otoscopy: d e c r e a s e d TM m o b i l i t y f m o s t s e n s i t i v e ) .
DIAGNOSIS
• Clinical.
• Tympanocentesis for a sample of fluid for culture definitive (eg, in recurrent cases).
MANAGEMENT
• Observation can be done depending on age and severity. Children over age of 2 should receive
antibiotics if the diagnosis is certain and the infection is severe.
• Amoxicillin initia l a n t i b i o t i c of choice.
• Second-line: Amoxicillin-Clavulanic acid, Cefuroxime, Cefdinir, Cefpodoxime.
• Penicillin allergy: Azithromycin, Clarithromycin, Erythromycin-Sulfisoxazole, Trimethoprim sulfamethoxazole.
• Severe or recurrent cases: myringotomy (surgical drainage) with tympanostomy tube insertion.
• In children with recurrent otitis media, may need an Iron deficiency anemia w o r k u p & CT scan.
SEROUS
OTITIS
MEDIA WITH
EFFUSION
• Middle ear fluid + n o s i g n s o r s y m p t o m s of a c u t e i n f l a m m a t i o n (no fever, no ear pain, & no marked
erythema or bulging of the TM).
• May be seen after resolution of Acute otitis media o r in patients with Eustachian t u b e dysfunction
DIAGNOSIS
• Otoscopy: effusion w i t h t y m p a n i c m e m b r a n e t h a t i s r e t r a c t e d o r
insufflation.
flat
Hypomobility with
MANAGEMENT
• O b s e r v a t i o n in m o s t c a s e s (usually spontaneously resolves).
• Persistent or complicated: Tympanostomy tube for drainage (eg, children with hearing impairment,
developmental delays, or specific conditions).
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Chapter 5 - Eyes, Ears, Nose, & Throat Disorders
EUSTACHIAN
TUBE
DYSFUNCTION
• Eustachian tube (ET) swelling inhibits the ET ability to auto insufflate, causing negative pressure.
• Often follows v i r a l URI o r a l l e r g ic r h i n i t i s ; sinusitis, tumors.
CLINICAL MANIFESTATIONS
• Obstructive dysfunction: ear fullness or pressure, p o p p i n g of t h e e a r s , u n d e r w a t e r
disequilibrium, fluctuating conductive hearing loss, tinnitus.
feeling,
DIAGNOSIS
• Clinical. Otoscopic findings usually normal. May have fluid behind t h e TM (serous otitis media).
MANAGEMENT
• Treating the underlying cause & symptom management is the mainstay of treatment.
• Autoinsufflation (eg, swallowing, yawning, blowing against a slightly-pinched nostril).
• Intranasal corticosteroids if sinonasal inflammation present.
• D e c o n g e s t a n t s for c o n g e s t i v e s y m p t o m s : Pseudoephedrine, Phenylephrine, Oxymetazoline nasal.
BAROTRAUMA
• Damage to the tympanic m e m b r a n e can occur with sudden pressur e changes (eg, flying, diving,
decompression, hyperbaric oxygen).
CLINICAL MANIFESTATIONS
• Ear pain, fullness, & h e a r i n g loss t h a t p e r s i s t s after t h e etiologic e v e n t .
PHYSICAL EXAMINATION
• May have bloody auricular discharge if traumatic.
• Visualization of the tympanic m e m b r a n e may reveal r u p t u r e o r petechiae.
MANAGEMENT
Avoidance is the best treatment:
• Avoidance of flying with a cold.
• Autoinsufflation (eg, swallowing, yawning, chewing gum).
UDITORY EXAMINATION
Assessed with a tuning fork
FINDINGS
AC = air conduction. BC = bone conduction.
RINNE: place on mastoid by ear
Normal (Positive) AC > BC
Normal: AC > BC.
Difficulty hearing their own voice &
deciphering words.
Lateralizes to AFFECTED e a r
BC > AC (Negative)
s e n s o r i n e u r a l l a t e r a l i z e s t o N o r m a l e a r + N o r m a l R i n n e (think of the N for sensorineural).
NORMAL
WEBER: place on top head
No lateralization
Lateralizes to NORMAL ear
CONDUCTIVE HEARING LOSS:
External or middle ear disorders: defect in sound
conduction (ex. obstruction from a foreign body or
cerumen
impaction),
damage
to
ossicles
(otosclerosis, cholesteatoma), mastoiditis, otitis
media.
Cerumen impaction most common cause
.NSORINEURAL HEARING LOSS:
Unner e a r disorders: ex presbycusis, chronic loud
noise exposure, CNS lesions (eg, acoustic
neuroma), Labyrinthitis, Meniere syndrome.
Presbycusis most common cause
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Chapter 5 - Eyes, Ears, Nose, & Throat Disorders
CERUMEN
IMPACTION
• External auditory canal wax impaction.
CLINICAL MANIFESTATIONS
• May lead to conductive hearing loss & ear fullness.
PHYSICAL EXAMINATION
• Otoscopy: direct visualization of the impacted cerumen
• Conductive hearing loss pattern: lateralization to the affected ear on Weber testing.
conduction > air conduction.
Bone
MANAGEMENT
Cerumen softening:
• Hydrogen Peroxide 3%
• Carbamide peroxide
Aural toilet:
• Irrigation, curette removal of cerumen, suction.
• Irrigation (if no evidence of tympanic m e m b r a n e perforation & w a t e r m u s t be at body t e m p e r a t u re to
prevent vertigo).
TYMPANIC
MEMBRANE
PERFORATION
• Rupture of the tympanic m e m b r a n e
• May lead t o Cholesteatoma d e v e l o p m e n t
ETIOLOGIES
• Most commonly occurs d u e to penetrating or noise t r a u ma (most commonly occurs at the p a r s tensa)
or Otitis media.
CLINICAL MANIFESTATIONS
• Acute ear pain, hearing loss.
• Patients with otalgia prior to r u p t u r e may develop s u d d e n pain relief w i t h b l o o d y otorrhea.
• Tinnitus & vertigo.
DIAGNOSIS
• Otoscopic examination: perforated TM. Do n ot perform pneumatic otoscopy.
• May have conductive hearing loss (Weber: lateralization to the affected ear, Rinne: bone conduction
greater than air conduction.
MANAGEMENT
• Most perforated TMs heal spontaneously. Follow up to e n s u r e resolution.
• Topical antibiotics (eg, Ofloxacin in some).
• Avoid w a t e r & topical aminoglycosides in t h e ear w h e n e v e r t h e r e i s a TM rupture.
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Chapter 5 - Eyes, Ears, Nose, & Throat Disorders
CHOLESTEATOM
• Abnormal keratinized collection of desquamated squamous epithelium in the middle ear t h a t can lead
to bony erosion of the mastoid.
• Etiologies: most commonly due to c h r o n i c m i d d l e e a r d i s e a s e o r E u s t a c h i a n t u b e dysfunction.
CLINICAL MANIFESTATIONS
• P a i n l e s s o t o r r h e a ( b r o w n o r yello w d i s c h a r g e w i t h a s t r o n g o d o r ) .
• May develop peripheral vertigo, tinnitus, dizziness, or cranial nerve palsies.
DIAGNOSIS
• Otoscopy: g r a n u l a t i o n t i s s u e (cellular d e b r i s ) . May have perforation of the tympanic membrane.
• Conductive h e a r i n g loss - lateralization to the affected ear on Weber testing and bone conduction >
air conduction in the affected ear on Rinne.
MANAGEMENT
• Surgical excision of the debris & Cholesteatoma with reconstruction of the ossicles.
OTOSCLEROSIS
• Abnormal bony overgrowth of the footplate of the stapes bone leading to c o n d u c t i v e h e a r i n g loss.
• Autosomal dominant disorder (may have family h i s t o r y of conductive hearing loss)
CLINICAL MANIFESTATIONS
• Slowly progressive c o n d u c t i v e h e a r i n g loss, especially l o w - f r e q u e n c i e s, tinnitus.
• Vertigo uncommon.
DIAGNOSIS
• Conductive h e a r i n g loss - lateralization to the affected ear on Weber testing and bone conduction >
air conduction in the affected ear on Rinne.
• Tone audiometry (most useful)
MANAGEMENT
• Stapedectomy with prosthesis or hearing amplification (eg, hearing aid).
• Cochlear implantation if severe.
VERTIGO
• False s e n s e of m o t i o n for exaggerated sense of motion). 2 types:
PERIPHERAL VERTIGO
LOCATION
Labyrinth or Vestibular nerve (which is part of CN VIII/8).
OF PROBLEM
ETIOLOGIES
1. BENIGN POSITIONAL VERTIGO (MO eDisodic vertieo. no hearing loss
2. MENIERE: episodic vertigo + hearing loss
3. VESTIBULAR NEURITIS continuous vertieo. no hearing loss
4. LABYRINTHITIS: continuous vertigo + hearing loss
CLINICAL
5. Cholesteatoma
I • HORIZONTAL nvsraemus fusuallv heats awav from affected side!.
Fatigahle.
• Sudden onset of tinnitus & hearing loss usually associated with
peripheral compared to central causes.
CENTRAL VERTJGO
Brainstem or cerebellar
Cerebellopontine tumors
Migraine
Cerebral vascular disease
Multiple sclerosis
Vestibular Neuroma
• VERTICAL nvstapmus.
Nonfatigable (continuous)
• Gait issues more severe.
• Gradual onset
• Positive CNS signs.
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Chapter 5 - Eyes, Ears, Nose, & Throat Disorders
MANAGEMENT OF NAUSEA/VOMITING IN PATIENTS WITH VERTIGO:
Nausea & vomiting is caused by sensory conflict m e d i a t e d b y t h e n e u r o t r a n s m i t t e r s GABA,
acetylcholine, histamine, dopamine, & serotonin.
Therefore, antiemetics w o r k primarily by blocking these transmitters.
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ANTICHOLINERGICS
Meclizine
Scopolamine - anticholinergic
Dhiientrydriiiatc
Diphenhydraniine
MOA: acts on the brain's control center for nausea, vomiting & dizziness.
Ind: first-line for vertigo (nausea/vomiting), m o t i o n sickness.
S/E: anticholinergic - dry mouth, blurred vision (dilated pupils), urinary
retention, constipation, dry skin, flushing, tachycardia, fever, delirium.
Cl/Caution: a c u t e n a r r o w angle glaucoma, BPH w i t h u r i n a r y retention.
DOPAMINE BLOCKERS
Prochlorperazine
MOA: blocks CNS d o p a m i n e r e c e p t o r s (Di Dz) in the brain's vomiting center.
Ind: nausea/vomiting, motion sickness.
S/E: QT prolongation, sedation, constipation.
Extrapyramidal Sx (EPS"): rigidity, bradykinesia, tremor, akathisia (restlessness).
3 EPS syndromes include:
1. [HBSBffiM!ffiHBnTl3niB?nyiTBffiffl reversible EPS hours-days after initiation «*
intermittent, spasmodic, sustained involuntary contractions (trismus, protrusions
of tongue, forced jaw opening, difficulty speaking, facial grimacing, torticollis).
Mgmt; Diphenhydramine IV or add anticholinergic agent (eg, Benztropine).
Promethazine
Metoclopramide
2. Tardive Dyskinesia: repetitive involuntary movements mostly involving extremities
&face~ lip smacking, teeth grinding, rolling of tongue* Seen with long-term use.*
3. fSWWWBinTHffl (due to I dopamine in nigrostriatal pathways) - rigidity, tremor.
Neuroleptic Malignant Syndrome (NMS): life threatening disorder due to D2 inhibition in
basal ganglia: mental status changes, extreme muscle rigidity, tremor, fever,
autonomic instability (tachycardia, blood pressure changes, tachypnea, profuse
diaphoresis, incontinence, dyspnea). Ice to axilla/groin, ventilatory support
Dopamine Agonists: Bromocriptine, Amantadine, Levodopa/CarbidorjaJ__
BENZODIAZEPINES
Lorazepam, Diazepam used in refractory patients (potentiates GABA).
SEROTONIN ANT/
Ondansetron
Granisetron
Dolasetron
MOA: blocks s e r o t o n i n r e c e p t o r s (5-HT3) both peripherally & centrally in the
chemoreceptor trigger zone of the medulla (suppressing the vomiting center).
BENIGN
S/E: neurologic: headache, fatigue. GI sx: nausea, constipation.
Cardiac: prolonged QT interval & cardiac arrhythmias.
PAROXYSMAL
POSITIONAL
VERTIGO
• A type of peripheral vertigo most commonly due to d i s p l a c e d o t o l i t h p a r t i c l e s (calcium crystals)
within the semicircular canals of the inner ear (canalithiasis).
• Most common cause of peripheral vertigo.
CLINICAL MANIFESTATIONS
• Recurrent episodes of s u d d e n , e p i s o d i c p e r i p h e r a l v e r t i g o ( l a s t i n g 6 0 s e c o n d s o r less) &
p r o v o k e d w i t h specific h e a d m o v e m e n t s (eg, rolling over in bed, lying down, getting up from bed,
looking up).
• May be accompanied by nausea or vomiting.
• Not a s s o c i a t e d w i t h h e a r i n g loss, tinnitus, or ataxia.
DIAGNOSIS
• P i x H a l l p i k e fNvlen B a r a n y ) t e s t - produces fatigable nystagmus.
MANAGEMENT
• Canalith r e p o s i t i o n i n g t r e a t m e n t of c h o i c e - Eplev m a n e u v e r o r Semont maneuver.
• Because the episodes are so brief, medical therapy is n o t usually needed.
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Chapter 5 - Eyes, Ears, Nose, & Throat Disorders
VESTIBULAR NEURITIS &
LABYRINTHITIS
DEFINITIONS
• Vestibular neuritis: inflammation of the vestibular portion of cranial nerve VIII.
• Labyrinthitis: inflammation of the vestibular and cochlear portion of CN VIII.
ETIOLOGIES
• Idiopathic. May be associated with viral or postviral inflammation.
CLINICAL MANIFESTATIONS
• Vestibular s y m p t o m s (both): continuous peripheral vertigo, dizziness, nausea, vomiting, & gait
disturbances. Nystagmus is usually horizontal and rotary (away from the affected side in the fast
phase).
• Cochlear s y m p t o m s (Labyrinthitis only): unilateral hearing loss, tinnitus.
DIAGNOSIS
• Primary clinical (imaging not usually needed).
• Neuroimaging (MRI preferred > CT) to rule out alternative causes if the symptoms are not fully
consistent with a peripheral lesion.
MANAGEMENT
• Glucocorticoids first-line management.
• Symptomatic relief: antihistamines (eg, Meclizine) or anticholinergics. Benzodiazepines.
• Both are self-limited - symptoms usually resolve in weeks even without treatment.
MENIERE'S DISEASE
(IDIOPATHIC ENDOLYMPHATIC
HYDROPS)
• Idiopathic distention of the endolymphatic c o m p a r t m e nt of the i n n er ear d ue to e x c e s s fluid.
• Meniere SYNDROME is due to an identifiable cause. Meniere DISEASE is idiopathic.
CLINICAL MANIFESTATIONS
• Characterized by 4 findings - episodic peripheral vertigo (lasting minutes - hours) +
sensorineural hearing loss (low-tones initially), tinnitus & ear fullness.
• Horizontal nystagmus, nausea, vomiting.
fluctuating
DIAGNOSIS
• Diagnosis of exclusion (no specific test).
• Transtympanic electrocochleography, loss of nystagmus with caloric testing seen with Meniere.
MANAGEMENT
• Initial: dietary modifications: avoidance of salt, caffeine, nicotine, chocolate, & alcohol
(because they increase endolymphatic pressure).
• Medical: if no relief with dietary modifications. Antihistamines (Meclizine, Dimenhydrinate);
Prochlorperazine or Promethazine, benzodiazepines (Diazepam), anticholinergics (Scopolamine),
& Diuretics (eg, Hydrochlorothiazide) to reduce endolymphatic pressure are all options.
• Refractory: surgical decompression (eg, tympanostomy tube), labyrinthectomy, or intraaural
Gentamicin.
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Chapter 5 - Eyes, Ears, Nose, & Throat Disorders
C O U S T I C ( V E S T I B U L A R ) CN VIII
NEUROMA
• Vestibular Schwannoma - benign t u m o r involving Schwann cells, which produce myelin sheath.
• Arises in the cerebellopontine angle & can compress structures (eg, Cranial n e r v es VIII, VII, & V).
CLINICAL MANIFESTATIONS
• Unilateral sensorineural hearing loss is an Acoustic n e u r o m a until p r o v e n otherwise.
• Tinnitus, vertigo, ataxia, headache, facial n u m b n e s s (CN V) or facial paresi s (CN VII).
DIAGNOSIS
• MRI imaging test of choice. CTscan.
• Audiometry is the laboratory test of choice: asymmetric sensorineural hearing loss most common.
MANAGEMENT
• Surgery o r focused radiation therapy (depending on age, t u m o r location, size, etc.).
NOSE/SINUS
CUTE
DISORDERS
RHINOSINUSITIS
Symptomatic inflammation of the nasal cavity and paranasal sinuses.
Acute = 1 - 4 weeks. Subacute: 4-12 weeks. Chronic >12 weeks.
ETIOLOGIES
• Viral: most cases a r e viral in etiology - rhinovirus, influenza & parainfluenza.
• Bacterial: same organisms associated with Acute otitis media - Streptococcus pneumoniae
c o m m o n ) , Haemophilus influenzae, Moraxella catarrhalis, & group A Streptococcus.
(most
RISK FACTORS
• Most c o m m o n in the setting of a viral URI, dental infections, smoking, allergies, Cystic fibrosis,
CLINICAL MANIFESTATIONS
• Facial pain or p r e s s u r e w o r s e w i t h b e n d i n g d o w n & leaning forward, headache, malaise,
p u r u l e n t nasal discharge, fever, nasal congestion.
• Often, patients develop w o r s e n i n g s y m p t o m s after a period of i m p r o v e m e n t
DIAGNOSIS
• Primarily a clinical diagnosis.
• Imaging is n o t indicated if classic presentation & uncomplicated.
• CT s c a n is t h e imaging test of choice if imaging is needed. Sinus radiographs not usually needed (if
ordered. Water's view most helpful).
• Biopsy or aspirate: definitive diagnosis. Usually not needed in most uncomplicated cases.
MANAGEMENT
• Symptomatic management: decongestants (promot e sinus drainage), analgesics, antihistamines,
mucolytics, intranasal glucocorticoids, analgesics, nasal lavage.
Antibiotics:
• Indications: s y m p t o m s should b e present for > 1 0 - 1 4 days with worsening of symptoms or earlier
if severe.
• Amoxicillin-clavulanic acid is often the antibiotic of choice.
• Second-line: Doxycycline. Respiratory fluoroquinolones (Levofloxacin, Moxifloxacin) usually
reserved t o preven t resistance.
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Chapter 5 - Eyes, Ears, Nose, & Throat Disorders
CHRONIC
SINUSITIS
• Inflammation of the nasal cavity and paranasal sinuses for a t l e a s t 12 c o n s e c u t i v e w e e k s .
ETIOLOGIES
• Bacterial: S. aureus most common bacterial cause, Pseudomonas, anaerobes.
• Wegener's granulomatosis (necrotic).
• Fungal: A s p e r g i l l u s m o s t c o m m o n fungal cause, M u c o r m y c o s i s second most common fungal
cause.
CLINICAL MANIFESTATIONS
• Same as Acute sinusitis - facial pain or pressure worse with bending down & leaning forward,
headache, malaise, purulent nasal discharge, fever, nasal congestion.
DIAGNOSIS
• B i o p s y o r h i s t o l o g y d i a g n o s t i c t e s t of c h o i c e (allows for identification of t h e organism a n d
determination of the appropriate management).
MANAGEMENT
• Depends on etiology.
• The goal of therapy is to promote sinus drainage, reduce edema, & eliminate infections. This is usually
achieved with a combination of nasal irrigation, topical or oral glucocorticoids, ENT follow-up.
• Antibiotics (if bacterial) with ENT follow up.
MUCORMYCOSIS
(ZYGOMYCOSIS
• Invasive fungal infection t h a t infiltrates the sinuses, lungs & central nervous system.
• The fungus rapidly dissects the nasal canals and eye into the brain. High mortality.
ETIOLOGIES
• Mucor, Rhizopus , Absidia, & C u n n i n g h a m e l l a fungal species.
RISK FACTORS
• Most c o m m o n l y s e e n w i t h D i a b e t e s m e l l i t u s (especially in DKA) & other i m m u n o c o m p r o m i s e d
states (eg, post-transplant, chemotherapy, HIV).
CLINICAL MANIFESTATIONS
• R h i n o - o r b i t a l - c e r e b r a l infections: S i n u s i t is (facial pain or p r e s s u r e w o r s e w i t h bending d o w n &
leaning forward, headache, malaise, purulent nasal discharge, fever & nasal congestion) progressing
to orbit & brain involvement.
• Physical examination: may develop erythema, swelling necrosis or b l a c k e s c h a r o n t h e p a l a t e , n a s a l
m u c o s a , o r face.
DIAGNOSIS
• Biopsy and histopathologic examination of involved tissue - n o n - s e p t a t e b r o a d h y p h a e w i t h
irregular right-angle (90 degree) branching.
MANAGEMENT
• IV A m p h o t e r i c i n B first-line + s u r g i c a l d e b r i d e m e n t of necrotic areas.
• Posaconazole or Isavuconazole.
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Chapter 5 - Eyes, Ears, Nose, & Throat Disorders
RHINITIS
3 types: allergic, infectious, & vasomotor.
• Allergic: m o s t c o m m o n type overall - IgE-mediated m a s t cell histamine release due to allergens
(eg, pollen, mold, dust etc.).
• Infectious: Rhino virus m o s t c o m m o n infectious caus e (common cold). Streptococcal species less
commonly seen.
• Vasomotor: nonallergic & noninfectious dilation of the blood vessels (eg, t e m p e r a t u r e change, strong
smells, humidity etc.).
CLINICAL MANIFESTATIONS
• Sneezing, nasal congestion, itching, clear, watery rhinorrhea.
• Eyes, ears, nose & throat may be involved.
• Bluish discoloration around the eyes may be seen in allergic.
PHYSICAL EXAMINATION:
• Allergic: p a l e or v i o l a c e o u s boggy turbinates, nasal p o l y ps with c o b b l e s t o n e m u c o s a of the
conjunctiva. May develop an "allergic shiner" purple discoloration around the eyes or a nasal bridge
crease from constant rubbing.
• Viral: e r y t h e m a t o u s turbinates.
MANAGEMENT OF ALLERGIC:
• Intranasal corticosteroids first-line if allergic or nasal polyps.
• Antihistamines, m a s t cell stabilizers & short-term decongestants may also be used. Anticholinergics
can be used for rhinorrhea.
• Avoidance and environmental control, exposure reduction. Intranasal corticosteroids if allergic.
I n t r a n a s a l glucocorticoids:
Mometasone, Fluticasone.
• Indications: m o s t effective medicatio n for Allergic rhinitis (moderat e to severe or persistent)
especially w i t h nasal nolvps.
Decongestants:
• MOA: improve congestion (little effect on rhinorrhea, sneezing, pruritus).
• Intranasal: Oxymetazoline, Phenylephrine, Naphazoline. Oral: Pseudoephedrine.
• Intranasal d e c o n g e s t a n t s u s e d >3-5 days may cause rhinitis m e d i c a m e n t o s a
congestion).
NASAL
(rebound
POLYPS
• Allergic rhinitis m o s t c o m m o n cause. May be seen with Cystic Fibrosis.
CLINICAL MANIFESTATIONS
• Most are incidental findings b ut if large, they can cause obstruction or anosmia (decreased smell).
DIAGNOSIS
• Direct visualization: p a l e boggy m a s s on t h e nasal mucosa. May have findings associated Allergic
rhinitis (eg, pale or violaceous, boggy turbinates & cobblestone mucosa of the conjunctiva).
MANAGEMENT
• Intranasal glucocorticoids initial treatment of choice.
• Surgical removal may be needed in some cases that a r e large and if medical t h e r a py is unsuccessful.
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Chapter 5 - Eyes, Ears, Nose, & Throat Disorders
EPISTAXIS
ANTERIOR EPISTAXIS
• Source: Kiesselbach v e n o u s plexus mos t c o m m o n site.
• Etiologies: most commonly associated with nasal t r a u ma (eg, nose picking most common in children,
blowing nose forcefully etc.), low humidity, hot environments (dried nasal mucosa), rhinitis, alcohol,
cocaine use, antiplatelet meds, foreign body. Hypertension doesn't cause it but may prolong i t
POSTERIOR EPISTAXIS
• Source: s p h e n o p a l a t i ne artery branches & W o o d r u f f s p l e x u s m o s t c o m m o n s i t e (may cause
bleeding in both nares & the posterior pharynx).
• Risk factors: Hypertension, older patients, nasal neoplasms.
MANAGEMENT OF ANTERIOR
• Direct p r e s s u r e first-line therapy i n m o s t cases. Pressure applied a t least 5-15 minutes with t h e
patient in the seated position, leaning forward (to reduce vessel pressure). Untreated septal
hematomas can lead to septum destruction if not evacuated.
• Adjunct medications: topical vasoconstrictors may be adjunctive therapy with direct pressur e (eg,
Oxymetazoline nasal, lidocaine with epinephrine, 4 % cocaine) - cautious use in patients with
hypertension.
• Cauterization: electrocautery or silver nitrate if the above measures fail & the bleeding site can be
visualized.
• Nasal packing: if direct pressure, vasoconstrictors, & cautery are unsuccessful or in sever e
bleeding. May consider antibiotic (Cephalexin or Clindamycin) to prevent toxic shock syndrome if
packed (controversial).
• Septal h e m a t o m a s a r e associated w i t h loss of cartilage if t h e h e m a t o m a is n o t r e m o v e d .
• Post t r e a t m e n t care: avoid exercise for a few days, avoid spicy foods (they cause vasodilation).
Bacitracin, petroleum gauze & humidifiers helpful to moisten t h e nasal mucosa.
MANAGEMENT OF POSTERIOR
• Balloon catheters m o s t c o m m o n initial management.
• Foley catheter
• Cotton packing
NASAL FOREIGN
BODY
• Most commonly seen in children.
• Many a r e asymptomatic.
• Classically presents with epistaxis associated with a mucopurulent discharge, foul odor, & nasal
obstruction (mouth breathing).
DIAGNOSIS
• Direct visualization (head light & otoscope).
• Rigid or flexible fiberoptic endoscopy.
• Radiographs not usually needed (may be helpful if button batteries are suspected & not visualized).
MANAGEMENT
• Removal via positive pressur e technique or instrument.
• Positive pressur e technique: involves having the patient blow his or her nose while occluding the
nostril opposite of the foreign body.
• Oral positive pressure: p a r e n t blows into the mouth while occluding the unaffected nostril (used in
smaller children).
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Chapter 5 - Eyes, Ears, Nose, & Throat Disorders
CUTE
PHARYNGITIS/TONSILLITIS
ETIOLOGIES
• Viral m o s t c o m m o n o v e r a l l c a u s e of p h a r y n g i t i s - Adenovirus, Rhinovirus, Enterovirus, EpsteinBarr virus. Respiratory syncytial virus, Influenza A & B, Herpes zoster virus.
• Bacterial: G r o u p A Streptococcus
[S. pyogenes) m o s t c o m m o n b a c t e r i a l c a u s e .
CLINICAL MANIFESTATIONS
• Sore throat, pain or swallowing or with phonation. Other s y m p t o m s based on the etiology.
• Viral often associated with cough, hoarseness, coryza, conjunctivitis, diarrhea.
DIAGNOSIS
• Usually clinical.
• Rapid strep or throat culture may be performed to rule out bacterial cause if suspected.
MANAGEMENT
• S y m p t o m a t i c m a i n s t a y of t r e a t m e n t - fluids, w a r m saline gargles, topical anesthetics, lozenges,
NSAIDs.
STREPTOCOCCAL
PHARYNGITIS
("STREPTHROAT)
• Group A Streptococcus [Streptococcus
pyogenes).
• Rare in children < 3 years of age.
• Highest incidence of Rheumatic fever if u n t r e a t e d in children 5-15 years of age.
CLINICAL MANIFESTATIONS
• Dysphagia (pain on swallowing), fever.
• Not usually associated with symptoms of viral infections (eg, cough, hoarseness, coryza, conjunctivitis,
diarrhea).
PHYSICAL EXAMINATION
• Pharyngeal e d e m a or exudate, tonsillar exudate a n d / o r petechiae
• Anterior cervical lymphadenopathy .
DIAGNOSIS
• R a p i d a n t i g e n d e t e c t i o n t e s t : b e s t initial t e s t 95% specific b ut only 55-90% sensitive (most useful
jf positive, b u t if n e g a t i v e , t h r o a t c u l t u r e s s h o u l d b e o b t a i n e d especially in c h i l d r e n 5-15y).
• T h r o a t c u l t u r e : definitive d i a g n o s i s (gold standard).
MANAGEMENT
• Penicillin first-line t r e a t m e n t (eg, PCN G or VK, Amoxicillin).
• Penicillin allergy: Macrolides , Clindamycin, Cephalosporins.
COMPLICATIONS
• R h e u m a t i c fever ( p r e v e n t a b l e w i t h a n t i b i o t i c s )
• Acute glomerulonephritis (not preventable with antibiotics)
• Peritonsillar abscess
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Chapter 5 - Eyes, Ears, Nose, & Throat Disorders
LARYNGITIS
• Acute inflammation of the mucosa of t h e larynx.
ETIOLOGIES
• Viral u p p e r respiratory tract infection m o s t c o m m o n - Adenovirus, Rhinovirus, Influenza,
Respiratory Syncytial virus (RSV), Parainfluenza.
• Bacterial causes include M. catarrhalis & Mycoplasma
pneumoniae.
• Vocal strain (eg, screaming or singing), irritants (eg, acid - GERD), polyps, & laryngeal cancer.
CLINICAL MANIFESTATIONS
• Hoarseness hallmark, aphonia. Dry or scratchy throat.
• May have viral (URI) symptoms (eg, rhinorrhea, cough, sore throat).
DIAGNOSIS: usually a clinical diagnosis.
MANAGEMENT
• Supportive care mainstay - hydration, humidification, vocal rest, w a r m saline gargles, anesthetics,
lozenges, and reassurance t h a t it is usually self-limited.
ENT follow-up if workup needed.
PERITONSILLAR ABSCESS
(QUINSY)
• Abscess betwee n the palatine tonsil & the pharyngeal muscles resulting from a complication of
tonsillitis or pharyngitis. Most common in adolescents & young adults 15-30y.
ETIOLOGIES
• Often polymicrobial - the predominant species include Group A Streptococcus
Staphylococcus aureus, and respiratory anaerobes.
(S.
pyogenes),
CLINICAL MANIFESTATIONS
• Dysphagia, severe unilateral pharyngitis, high fever.
• Muffled "hot potato" voice, difficulty handling oral secretion s (drooling), trismus (lockjaw).
PHYSICAL EXAMINATION
• Swollen or fluctuant tonsil causing uvula deviation to the contralateral side, bulging of the
posterior soft palate, anterior cervical lymphadenopathy.
DIAGNOSIS
• Primarily a clinical diagnosis without the need for imaging or labs if classic. Ultrasound.
• CT scan imaging test of choice if imaging is n e e d e d to differentiate Cellulitis vs. Abscess.
MANAGEMENT
Drainage (aspiration or I & D) + antibiotics.
• Drainage: n e e d l e aspiration (preferred) or incision & drainage.
• Antibiotics: oral (Amoxicillin-clavulanic acid, Clindamycin);
Parenteral (Ampicillin-sulbactam,
Clindamycin).
• Tonsillectomy: usually reserved for patients who fail to respond to drainage, PTA with complications,
prior episodes of PTA, or recurrent severe pharyngitis.
PREVENTION
• Prompt treatment of Streptococcal infections.
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Chapter 5 - Eyes, Ears, Nose, & Throat Disorders
RETROPHARYNGEAL
ABSCESS
• Deep neck space infection located behind the posterior pharyngeal wall.
• Most common in children 2 - 4 years. In adults, it is often a result of penetrating trauma (eg, chicken
or fish bones, instrumentation, dental procedures).
ETIOLOGIES
• Similar to Peritonsillar abscess - often polymicrobial (eg, Group A Streptococcus,
aureus & respiratory anaerobes).
Staphylococcus
CLINICAL MANIFESTATIONS
• Neck: torticollis (unwilling to move the neck secondary to pain and spasms), n e c k stiffness
especially w i t h n e c k extension.
• Fever, drooling, dysphagia, odynophagia, chest pain, muffled "hot potato" voice, trismus.
PHYSICAL EXAMINATION
• Midline o r unilateral p o s t e r i o r pharyngeal wall e d e m a ( m o s t c o m m o n ) .
• Anterior cervical lymphadenopathv, lateral neck mass or swelling.
DIAGNOSIS
• Lateral neck radiograph: increased prevertebral space > 5 0 % of t h e w i d t h of adjacent vertebral
body (may be performed if low suspicion).
• CT s c an of neck w i t h contrast preferred if suspicion is high.
• In smaller children with respiratory distress, evaluation often done in the operating room.
MANAGEMENT
• Surgical incision & drainage with antibiotics for large & m a t u r e abscesses in the OR.
• Abscess <2.5cm 2 may be observed for 24-48 hours with antibiotic therapy.
• Antibiotics: IV Ampicillin-Sulbactam or Clindamycin (similar to Peritonsillar abscess).
COMPLICATIONS
• Airway obstruction, Mediastinitis (due to spread of the infection), sepsis, atlantoaxial dislocation.
ORAL
LICHEN
PLANUS
• Idiopathic cell-mediated autoimmune response affecting the skin & mucous membranes.
• Most common in middle-age range. Increased incidence w i t h hepatitis C infection.
CLINICAL MANIFESTATIONS
• Reticular: lacy reticular leukoplakia of the oral mucosa most common (Wickham striae). Usually
painless. Most c o m m o n type.
• Erythematous: red patches (may accompany the reticular lesions). May be painful.
• Erosive: erosions or ulcers. Usually painful.
DIAGNOSIS
• Mainly clinical. Biopsy often performed in the erythematous & erosive types to rule out malignancy.
MANAGEMENT
• Local glucocorticoids initial m a n a g e m e n t of choice (eg, Clobetasol, Betamethasone)
• Second-line: topical (Tacrolimus, Pimecrolimus, Cyclosporine), intralesional corticosteroid injections.
• Systemic glucocorticoids if no response to topical therapy.
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Chapter 5 - Eyes, Ears, Nose, & Throat Disorders
LUDWIG'S
ANGIN,
• Rapidly spreading cellulitis of t h e floor of t h e m o u t h (bilateral infection of submandibular space).
• Risk factors: most commonly due to spread of oral flora s e c o n d a r y t o d e n t a l i n f e c t i o n s (second or
third mandibular molars). Increased incidence in Diabetes & HIV.
• Polymicrobial (oral flora).
CLINICAL MANIFESTATIONS
• Fever, chills, malaise, stiff neck, dysphagia, drooling, muffled voice.
• Respiratory difficulty if severe (eg, stridor).
PHYSICAL EXAMINATION
• T e n d e r , s y m m e t r i c swelling, "woody" i n d u r a t i o n & e r y t h e m a of t h e u p p e r n e c k & c h i n (may
have palpable crepitus). Pus on the floor of the mouth.
• Swelling of the tongue can lead to airway compromise. No lymphadenopathy or abscess formation.
DIAGNOSIS
• CT s c a n initial t e s t of choice. MRI.
MANAGEMENT IF IMMUNOCOMPETENT
• IV antibiotics: A m p i c i l l i n - s u l b a c t a m OR Ceftriaxone plus Metronidazole OR Clindamycin plus
Levofloxacin.
• Add Vancomycin if MRSA suspected.
MANAGEMENT IF IMMUNOCOMPROMISED
• IV antibiotics: Cefepime plus Metronidazole OR Imipenem OR Meropenem OR Piperacillintazobactam. Add Vancomycin if MRSA suspected.
OROPHARYNGEAL CANDIDIASIS
(THRUSH
• Candida albicans is p a r t of the normal flora but can become pathogenic due to local or systemic
immunosuppressed states.
• Risk factors: i m m u n o c o m p r o m i s e d s t a t e s (HIV, chemotherapy, diabetics), use of i n h a l e d
C o r t i c o s t e r o i d s w i t h o u t a s p a c e r , antibiotic use, xerostomia, or denture use.
CLINICAL MANIFESTATIONS
• Asymptomatic. Loss of taste or cotton-like feel in the mouth, loss of taste, throat o r mouth pain with
eating or swallowing.
PHYSICAL EXAMINATION
• W h i t e c u r d - l i k e p l a q u e s on the buccal mucosa, tongue, palate & / o r the oropharynx that are easily
scraped off ( m a y l e a v e b e h i n d e r y t h e m a & friable m u c o s a if s c r a p e d ) .
• The dentur e form may be associated with erythema only.
DIAGNOSIS
• Clinical.
• P o t a s s i u m H y d r o x i d e : b u d d i n g yeast, & p s e u d o h y p h a e . Smear performed on scrapings.
• Fungal culture (rarely done).
MANAGEMENT
• Topical t h e r a p y : first-line t h e r a p y - Nystatin liquid swish and swallow, C l o t r i m a z o le t r o c h e s or
Miconazole mucoadhesive buccal tablets.
• Oral Fluconazole usually reserved for refractory cases or patients with both oropharyngeal +
esophageal Candidiasis.
347
Chapter 5 - Eyes, Ears, Nose, & Throat Disorders
P H T H O U S ULCERS
(CANKER SORE,
ULCERATIVE
STOMATITIS
• Unknown cause b u t may be associated with h u m a n herpes virus 6.
• Recurrent disease seen in patients with Inflammatory bowel disease, HIV, Celiac disease, SLE,
Methotrexate, & neutropenia.
CLINICAL MANIFESTATIONS
• Small, painful, s h a l l o w r o u n d o r oval s h a l l o w u l c e r (yellow, w h i t e o r g r e y c e n t r a l e x u d a t e ) w i t h
e r y t h e m a t o u s h a l o . Most common on the buccal or labial mucosa (nonkeratinized mucosa).
MANAGEMENT
• Topical oral glucocorticoids
first-line
m a n a g e m e n t (eg, Clobetasol gel or ointment,
Dexamethasone elixir swish and spit, Triamcinolone in orabase).
• Topical analgesics: 2 % v i s c o u s lidocaine, Diphenhydramine liquid; aluminum hydroxide +
magnesium hydroxide + simethicone
ORAL
LEUKOPLAKIA
• Oral potentially malignant disorder characterized by hyperkeratosis due to chronic irritation.
• Up to 6 % a r e dysplastic or S q u a m o u s cell c a r c i n o m a .
• Risk factors: chronic irritation due to tobacco, cigarette smoking, alcohol, dentures, HPV infections.
CLINICAL MANIFESTATIONS
• Most a r e asymptomatic.
• P a i n l e s s w h i t e p a t c h y l e s i o n s t h a t c a n n o t b e s c r a p e d off (in comparison to Candida which is
painful & can be scraped off).
DIAGNOSIS
• Biopsy to rule out Squamous cell carcinoma.
MANAGEMENT
• Cessation of irritants (eg alcohol, smoking).
• Cryotherapy, laser ablation and surgical excision are options if increased risk for malignancy or
malignant.
ERYTHROPLAKI
• Uncommon oral lesion with a high risk of malignant transformation.
• 9 0 % of E r y t h r o p l a k i a is e i t h e r d y s p l a s t i c o r s h o w s e v i d e n t of S q u a m o u s cell c a r c i n o m a .
• Risk factors: chronic irritation due to tobacco, cigarette smoking, age > 65 years.
CLINICAL MANIFESTATIONS
• Most a r e asymptomatic.
• P a i n l e s s e r y t h e m a t o u s , soft, velvety, p a t c h in the oral cavity, most commonly on the mouth floor,
soft palate, and ventral aspect of the tongue.
DIAGNOSIS: biopsy to rule out Squamous cell carcinoma.
MANAGEMENT
• Complete excision may be needed depending on the biopsy results.
348
Chapter 5 - Eyes, Ears, Nose, & Throat Disorders
SIALOLITHIASIS
(SALIVARY GLAND
STONES)
• Stones within the salivary glands or ducts (no inflammation).
• Most c o m m o n i n Wharton's duct (submandibular gland duct); Stensen's duct (parotid gland
duct).
RISK FACTORS
• Decreased salivation (eg, dehydration, anticholinergic mediations, diuretics).
CLINICAL MANIFESTATIONS
• Sudden o n s e t of salivary gland p a in & swelling w i t h eating or in anticipation of eating.
PHYSICAL EXAMINATION
• Stone may be palpated in the salivary gland.
• If the gland is compressed and no saliva flows, the stone can be obstructive.
DIAGNOSIS
• Usually clinical.
MANAGEMENT
• Conservative m a n a g e m e n t : first-line therapy - sialagogues to increase salivary flow (eg, tart,
hard candies, l e m o n drops, Xylitol-containing gum or candy), increase fluid intake, gland massage,
moist heat to affected area. Avoid anticholinergic drugs if possible (anticholinergics decrease
salivation).
• Minimally invasive therapy: includes sialoendoscopy, laser lithotripsy, extracorporeal lithotripsy.
• Surgery (eg, sialoadenectomy) reserved for recurrent stone or failure of less invasive techniques.
CUTE BACTERIAL SIALADENITIS (SUPPURATIVE
SIALADENITIS)
• Bacterial infection of the parotid or submandibular salivary glands.
• Etiologies: S. aureus m o s t c o m m o n , S. pneumoniae, S. viridans, H. influenzae,
Bacteroides.
• Risk factors: salivary gland obstruction from a stone, dehydration, chronic illness.
CLINICAL MANIFESTATIONS
• Sudden onset of very firm and t e n d e r gland swelling w i t h purulent discharge (may be able to
express p u s if t h e duct is massaged), dysphagia, trismus (reduced opening of the jaw due to
spasms of the muscles of mastication).
• Fever & chills if severe.
DIAGNOSIS
• CT Scan to assess for associated abscess or extent of tissue involvement.
MANAGEMENT
• Anti-staphylococcal antibiotics + sialagogues to increase salivary flow (eg, tart or hard candies).
• Dicloxacillin or Nafcillin. Metronidazole can be added for anaerobic coverage.
• Clindamycin,
349
Chapter 5 - Eyes, Ears, Nose, & Throat Disorders
CUTE
HERPETIC
GINGIVOSTOMATITIS
• Inflammation of t h e gums and the oral mucosa.
• P r i m a r y m a n i f e s t a t i o n of HSV-1 i n c h i l d r e n .
• Most commonly occurs between 6 months - 5 years.
CLINICAL MANIFESTATIONS
• Prodrome: sudden onset of fever, anorexia, malaise and refusal to eat a n d / o r drink followed by oral
lesions.
• Gingivostomatitis: u l c e r a t i v e l e s i o n s of t h e gingiva ( g u m s w e l l i n g w i t h friability & bleeding ) &
v e s i c l e s on the mucous m e m b r a n e s of the mouth, often with p e r i o r a l v e s i c u l a r l e s i o n s clustered
o n a n e r y t h e m a t o u s b a s e (dew drops on a rose petal).
• After rupture, t h e vesicles become u l c e r a t e d , yellow, and a r e s u r r o u n d e d by a n erythematous halo.
They may coalesce to form painful ulcers.
• Regional lymphadenopathv.
DIAGNOSIS: clinical
MANAGEMENT
• S u p p o r t i v e c a r e m a i n s t a y - hydration, oral hygiene, b a r r i er cream (eg, petroleum jelly) to the lips.
Lesions usually heal within 1 week.
• O r a l Acyclovir if within 72-96 hours of disease onset if they are unable to drink, have significant pain.
• IV Acyclovir if immunocompromised.
CUTE
HERPETIC
PHARYNGOTONSILLITIS
• P r i m a r y m a n i f e s t a t i o n of h e r p e s s i m p l e x v i r u s - 1 in a d u l t s .
CLINICAL MANIFESTATIONS: fever, malaise, headache, sore t h r o a t
PHYSICAL EXAMINATION: vesicles that rupture, leaving u l c e r a t i v e l e s i o n s w i t h g r a y i s h e x u d a t e s in
t h e posterior pharyngeal mucosa.
MANAGEMENT: oral hygiene - lesions usually resolve within 7-14 days.
ORAL HAIRY
LEUKOPLAKIA
• Mucocutaneous manifestation of E p s t e i n - B a r r v i r u s (Human herpesvirus-4).
RISK FACTORS
• A l m o s t exclusively s e e n w i t h HIV infection.
• Other immunocompromise d states - post-transplant, chronic steroid, chemotherapy.
CLINICAL MANIFESTATIONS
• P a i n l e s s , w h i t e s m o o t h o r c o r r u g a t e d "hairy" p l a q u e along t h e l a t e r a l t o n g u e b o r d e r s or buccal
mucosa t h a t c a n n o t b e s c r a p e d off.
MANAGEMENT
• No specific t r e a t m e n t required (may spontaneously resolve & not considered a premalignant lesion).
• Antiretroviral t r e a t m e n t in patients with HIV.
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Chapter 5 - Eyes, Ears, Nose, & Throat Disorders
OTOTOXIC
•
•
•
•
•
MEDICATIONS
Loop diuretics: Furosemide, Bumetanide, Ethacrynic acid (most ototoxic)
Antibiotics: Vancomycin, Aminoglycosides (Gentamicin), Macrolides (Erythromycin), Tetracyclines.
Anti-inflammatories: Aspirin. NSAIDs
Anti-neoplasties: Cisplatin, Carboplatin, Cytarabine
Anti-malarials: Chloroquine, Hydroxychloroquine, Quinine
PHOTO CREDITS
Pinguecula
By Red eye2008 (Own work) [CC-BY-SA-3.0 (http://creativecommons.orgaicenses/by-sa/3.0) or GFDL
(http://www.gnu.org/copyleft/fdl.html)], via Wikimedia Commons
Pterygium
By Jmvaras Jose" Miguel Varas, MD (Own work) [GFDL (http://www.gnu.org/copyleft/fdl.html) or CC-BY-3.0
(http://creativecommons.Org/licenses/by/3.0)], via Wikimedia Commons
Hypertensive retinopathy
By Frank Wood ([1]) [CC-BY-3.0 (http^/creativecommons.org/Iicenses/by/3.0)], via Wikimedia Commons
Papilledema
By Jonathan Trobe, M.D. - University of Michigan Kellogg Eye Center (The Eyes Have It) [CC-BY-3.0
(http://creativecomraons.Org/licenses/by/3.0)], via Wikimedia Commons
Eye changes
By National Eye Institute, National Institutes of Health [Public domain], via Wikimedia Commons
Normal Funduscopic Exam
By Mikael Haggstrom (Own work) [CCO], via Wikimedia Commons
Glaucoma
By James Hcilman, MD (Own work) [CC-BY-SA-3.0 (http://creativecommons.Org/licenses/by-sa/3.0) or GFDL
(http://www.gnu.org/copylefffdl.html)], via Wikimedia Commons
HordeoIumBy Andre Riemann [Own work) [Public domain], via Wikimedia Commons
Chalazion
By Poupig (Own work) [CC-BY-SA-3.0 [http://creativecommons.0rg/licenses/by-sa/3.O)], via Wikimedia Commons
Orbital Fracture
By James Heilman, MD (Own work) [CC BY-SA 4.0 (http://creativccommons.0rg/licenses/by-sa/4.O)], via Wikimedia Commons
Macular degeneration By Crdit to: National Eye Institute, National Institutes of Health http://www.nei.nih.gov/health/maculardegen/webAMD.pdfpage 14, Public Domain,
https://commons.wikimedia.org/w/index.php?curid=862686
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