ENT Flashcards
Neck triangle containing spinal accessory nerves
Pisterior
Triangle containing hypoglossal nerve
Carotid
Ciliary ganglion
Pupillary constriction
Pterygopalatine ganglion
Parasympathetic:
Lacrimal gland
Nasal mucosa
Submandibular ganglion
Parasympathetic:
Submandibular
Sublingual
Otic ganglion
Parasympathetic:
Parotid gland
Functions if facial nerve
Stapedius muscle
Lacrimation (lacrimal gland)
Salivation (parotid gland)
Facial muscles
Sensation of anterior 2/3 of tongue (via chorda tympani)
Peripheral vs Central vertigo in terms of persistence of symptoms
Vertigo/nystagmus will never last longer than a few weeks in peripheral lesions.
But persist if central lesion
Auditory acuity tests
Whispered-voice test
Tuning fork test (512 Hz)
Interpretation of Rinne test
If AC> BC: positive Rinne test: Nl
Interpretation of Weber test
If heard centrally: negative Weber test: Nl
Others: Weber right, Weber left
Will only lateralize if difference between ears > 6 dB
More sensitive in detecting conductive hearing loss than the Rinne test
Order of neural pathway for hearing
ECOLI:
Eighth nerve Cochlear nucleus Olivary nucleus Lateral lemniscus Inferior colliculus
Minimum hearing loss for Rinne to reverse with 512 Hz
30 dB
Range of frequencies audible to human ear
20-20,000 Hz
Most sensitive: 1000-4000
Human speech: 500-2000
Conductive hearing loss in Pure tone audiometry
BC: normal range
AC: outside of normal range
Gap > 10 dB
SNHL in PTA
BC: below normal
Gap < 10 dB (no air-bone gap)
Mixed hearing loss on PTA
Both AC and BC below normal threshold
Gap > 10 dB
Occupational hearing loss frequency
SNHL
At 4000 Hz
Otosclerosis hearing loss frequency
Conductive
2000 Hz (Carhart notch)
Speech reception threshod
Lowest hearing level at which pt is able to repeat 50% of two syllable words with equal emphasis on each syllable
Used to assess reliability of PTA
If > 5 dB difference between SRT and PTA in 500-2000 Hz range:
Retrocochlear lesion
Or
Functional hearing loss
Speech discrimination test
Percentage of words pt correctly repeats from a list of 50 monosyllabic words
Tested at 40 dB above SRT
If normal hearing: Score > 90%
If conductive hearing loss: score > 90%
If difference between ears > 20%: retrocochlear lesion
If rollover effect ( decrease in discrimination as sound intensity increases) retrocochlear lesion
Best predictor of hearing aid response: poor response = significant neural degeneration = hearing aid not the best option
Normal range of tympanogram peak
-100 to +50 mmH2O
Normal middle ear pressure
Tympanogram in otosclerosis
Normal, but lower amplitude
Type A curve
Tympanogram in ossicular chain discontinuity
Normal peak pressure but higher amplitude
Type A curve
Tympanogram in perforated TM
No peak
Type B
Tympanogram in middle ear effusion
No peak
Type B
Tympanogram in eustachian tube dysfunction
Negative pressure peak
Type C
Tympanogram in early otitis media without effusion
Negative peak pressure
Type C
Normal static compliance (ear canal volume)
0.3-1.6 cc
Static compliance
What does static compliance show?
Overall stiffness of middle ear system
Type B curve + static compliance > 2cc in children and 2.5 cc in adults indicates:
TM perforation
Patent ventilation tube
Acoustic reflex threshold
70-100 dB greater than hearing threshold
Bilateral and symmetrical in either ear stimulation
Needs: intact conduction an nerve VII function
If hearing threshold > 85 dB, reflex likely absent
Acoustic reflex decay test
Ability of stapedius muscle to sustain contraction for 10 sec
Normal: little decay at 500 and 1000 Hz
Acoustic reflex threshold in cochlear hearing loss
25-60 dB
ART in retrocochlear pathology
Absent or marked decay
Auditory brainstem response
Can be used to determine the site of lesion
If delay in brain response: cochlear/retrocochlear abnormalities
Of value in children or malingering (co-operation not needed)
Otoacoustic emissions
Measures echo generated by cochlea
Absence of emission: hearimg loss or fluid in the middle ear
Newborn hearing screening test
Otoacoustic emissions
Tests used in malingering
Auditory brainstem response
Otoacoustic emission
Negative prognostic factors in aural rehabilitation
Poor speech discrimination
Narrow dynamic range (recruitment)
Unrealistic expectations
Indication for cochlear implants
Profound, bilateral SNHL, not rehabilitated with conventional hearing aids
Post-lingually deafened adults
Pre- and post- lingually deaf children
The best candidates for aural rehabilitation
Pre-lingually deaf infants
Bone anchored hearing aid indications
Conductive hearing loss
Unilateral hearing loss
Mixed hearing loss
(Who cannot wear conventional hearing aids)
Vertigo with duration of seconds
BPPV
Vertigo with minutes to hours duration
Ménière’s disease
Vertigo with duration of hours to days
Labyrinthitis/ vestibular neuronitis
Vertigo with chronic duration
Acoustic neuroma
Vertigo with bilateral hearing loss
Ménière disease (also unilateral possible)
Vertigo with unilateral hearing loss
Accoustic neuroma
Labyrinthitis
Ménière
Vertigo with tinnitus
Accoustic neuroma
Labyrinthitis
Ménière
Vertigo with whistling tinnitus
Labyrinthitis
Vertigo with aural fullness
Meniere
Vertigo with associated ataxia, CN VII palsy
Acoustic neuroma
Vertigo with recent AOM
Labyrintitis/ vestibulitis
Imbalance in peripheral vs central vertigo
Peripheral: mod-sev
Central: mild-mod
Nausea and vomiting in peripheral vs central vertigo
P: severe
C: variable
Auditory symptoms in peripheral vs central vertigo
P»_space;> C
Neurologist symptoms in peripheral vs central vertigo
C»_space;>P
Compensation in peripheral vs central vertigo
P: rapid
C: slow
Nystagmus in peripheral vs central vertigo
P: unidirectional, horizontal or rotatory
C: bidirectional, horizontal or vertical
Nystagmus in BPPV
Tortional, geotropic (. Fast phase towards the floor)
The most common cause of episodic vertigo
BPPV
The most common semicircular Canal affected in BPPV
Posterior
BPPV in Dix-Hallpike maneuver
Latency: 20 sec
Lasting: 20 sec
Crescendo-decrescendo vertigo
Nystagmus ( must be present)
Sitting up: Reversal of nystagmus
Fatigability
Tx of BPPV
Reassurance
Resolves spontaneously
Epley maneuver
Brandt-Daroff exercises
Refractory: surgery
If N/V: antiemetic
Drugs that are not to be used in BPPV
Drugs to suppress the vestibular system delay eventual recovery and are therefore not used
Diagnostic criteria for Meniere
All 3 of:
2 spontaneous episodes of rotational vertigo 20 minutes or longer
Audiometric confirmation of SNHL
Tinnitus and/or aural fullness
Type of hearing loss in meniere
SNHL, low frequencies
Meniere time course
Attacks come in clusters
In each attack, vertigo disappears within minutes to hours bur SNHL persists
Early: fluctuating SNHL
Late: progressive SNHL, persistent tinnitus
Triggers of Meniere
High salt intake
Caffeine
Stress
Nicotine
Alcohol
Acute Mx of meniere
Bed rest
Antiemetics
Antivertiginous drugs:
Betahistine,
Meclizine,
Dimenhydrinate
Anticholinergics:
Scopolamine
Long-term Mx of Meniere
Low salt diet
Diuretics
Serc (betahistine)
Intratympanic gentamycin (results in complete SNHL), first an MRI to check for CPA tumor
Intratympanic CS (may improve symptoms)
Surgical vestibular neurectomy, endolymphatic sac decompression
Monitor opposite ear (35% bilateral)
Drop attack
Without LOC
Meniere
Nystagmus in labyrinthitis
Acute phase: Fast phase towards affected ear
Convalescence: away from affected side
Ataxia in vestibular neuritis/labyrinthitis
Pt veers towards affected side
Tx of acute vestibular neuritis
Bed rest
Antivertiginous drugs
Methylprednisolone
+/- antivirals
If bacterial:
IV AB
drainage
Mastoidectomy
Tx of convalescent phase of vestibular neuritis
Progressive ambulation
Vestibular exercise
Symptoms of acoustic neuroma
SNHL
Tinnitus
Dizziness, unsteadiness, but true vertigo is rare
Unilateral tinnitus/SNHL in elderly
Acoustic neuroma until proven otherwise
RFs of acoustic neuroma
Exposure to loud noise
Childhood low-dose radiation
Parathyroid adenoma
Gold standard for Dx of acoustic neuroma
MRI with gadolinum contrast
Vestibular test in acoustic neuroma
Caloric test: Nl or asymmetric
Objective tinnitus DDx
Vascular lesions Hypo/Hyperthyroidism Patulous eustachian tube Palatal myoclonus Stapedial muscle spasm
Drugs causing tinnitus
ASA NSAIDs Aminoglycosides Antihypertensives Heavy metals
Metabolic causes of tinnitus
Hyper/hypothyroidism
Hyperlipidemia
Vitamin A, B, Zn deficiency
General recommendations for tinnitus
Avoid loud noise
Avoid ototoxic meds
Avoid caffeine
Avoid nicotine
Tinnitus clinics
Identify situations where tinnitus is most bothersome
Mask tinnitus with soft music or white noise
Hearing aid for coexistent hearing loss
Trial of tocainamide
Contraindications for syringing of the ear canal
Active infection
Previous ear surgery
Only hearing ear
TM perforation
Tx of cerumen impaction
Water or ceruminolytics:
Bicarbonate solution Olive oil Glycerine Cerumenol Cerumenex
Disease possibly associated with swimming in cold water
Ear canal exostosis
RFs of acute otitis externa
Swimming Skin conditions Q-tips Aggressive scratching Devices occluding ear canal
Indications for ear syringing for cerumen impaction
Decreased hearing
Totally occlusive cerumen with pain
Tinnitus
External otitis etiology
90% bacterial:
Pseudomonas, S. Aureus
Tx of acute otitis externa
Clean ear: irrigation, suction, dry swabbing
C&S
If bacterial:
Ciprofloxacin otic drop (anti-pseudomonal)
+/- otic steroids
Pop wick if edematous external canal
+/- 3% acetic acid solution to acidify ear canal
If cervical LAP : systemic AB
If cellulitis: systemic AB
If fungal:
Repeated debridement
Topical antifungals (gentian violet, mycostatin powder, boric acid…)
+/- analgesics
Tx of chronic otitis externa
CS drops (diprosalic acid)
RFs for malignant otitis externa
Elderly diabetics
ImComp
Etiology of malignant otitis externa
99% pseudomonas
Complications of malignant otitis externa
CN palsy
VII > X > XI
Systemic infection
Death
Mx of malignant otitis externa
Imaging:
High resolution temporal bone CT
MRI with gadolinium
Technetium scan
Hospital admission
Debridement
IV AB
Hyperbaric O2
Gallium vs technetium scans
Gallium: shows sites of active infection. Presence of PMNs. It will not show the extent of osteomyelitis. Helps with F/U
Technetium: shows sites of osteomyelitis. Osteoblast activity. Help with diagnosis.
Chronic otitis media definition
TM perforation in the setting of chronic/recurrent ear infection
Chronic otitis types
Benign: dry, no active infection
Serous: continuous serous drainage
Suppurative: persistent purulent drainage
Presentation of congenital cholesteatoma
Small white pearl, behind intact TM
Conductive hearing loss
Not associated with otitis media/Eustachian tube dysfunction
Types of acquired cholesteatoma
Primary:
Retraction pocket in pars flaccida.
Secondary:
Pearly mass behind TM, associated with marginal perforation
Progressive destruction of surrounding bony structures due to associated chronic inflammation
Type of hearing loss in cholesteatoma
Conductive
SNHL in later stages
Positive Hx in cholesteatoma:
Otitis media
Ventilation tubes
Ear surgery
Granulation tissue in the ear
Malignant otitis media
Cholesteatoma
Inv an Tx for cholesteatoma
Inv: audiogram, CT
Tx: surgery, tympanoplasty, ossicular reconstruction
Etiology of mastoiditis
2 weeks after untreated or inadequately treated AOM
S. Pneumoniae, H. Influenza, M. Catarrhalis, S. Pyogen, S. Aureus, P. Aeruginosa
Dx of mastoiditis
CT: opacification of mastoid cells, interruption of normal trabeculation of cells
Triad of mastoiditis
Otorrhea
Tenderness over the mastoid
Retroauricular swelling with protruding ear
Tx of mastoiditis
IV AB + ventilation tube
+/-Cortical mastectomy
Indications for surgery:
failure of medical Tx after 48 h
Symptoms if intracranial complications
Aural discharge prsisting for 4 wk, resistent to AB
Otosclerosis definition
Fusion of stapes to oval window
F>M
AD
Progressive course
Otosclerosis during pregnancy
Progression
Age of onset in otosclerosis
Teens, 20s
Type of hearing loss in otosclerosis
Conductive
SNHL in later stages
TM in otosclerosis
Normal +/- pink bluish (Schwartz sign) due to neovascularization of otosclerotic bone
Audiogram of otosclerotic
Dip at 2000 Hz (Carhart notch)
Tx of otosclerosis
Monitor with serial audiogram
Hearing aid
Definitive Tx: stapedectomy/stapedotomy with laser/drill with prosthesis
The most common cause of conductive hearing loss in 15-50 yr old
1st: cerumen impaction
2nd: otosclerosis
Most common cause of non-syndromic congenital hearing loss
Connexin 26 defect
AR
RFs for hearing loss in newborn
Low birth weight Prematurity Kernicterus (Bil>25) Craniofacial abn FHx of deafness in childhood 1st trimester illness (TORCH) Neonatal sepsis Ototoxic drugs Perinatal infection (meningitis, mumps, measles) Consanguinity
Type of hearing loss in presbycusis
SNHL
Initially high frequencies, then middle frequencies
Low speech discrimination (especially with background noise)
Recruitment phenomenon (inability to tolerate loud noises)
Tinnitus
Tx of presbycusis
Hearing aid indications:
If: difficulty functioning
Hearing loss > 30-35 dB
Good speech discrimination
Lip reading
Auditory training
Auditory aids (doorbell, phone lights)
The most common cause of SNHL
Presbycusis
Inv in sudden SNHL
CBC, ESR, RF, ANA to R/O AI diseases
If other focal neurological signs:
MRI: R/O tumor
CT: R/O stroke
Tx of sudden SNHL
CS within 3 d:
Intratympanic
Or
Oral x 10-14 d
Prognosis of sudden SNHL
70% resolve within 10-14 d
20% partial resolution
10% permanent
Clinic of sudden SNHL
Usually unilateral
+/- tinnitus, aural fullness
Usually idiopathic
Clinic of AI inner ear disease
20-50 yr
Rapidly progressive or fluctuating
Bilateral
SNHL
+/- tinnitus, aural fullness, vestibular symptoms
SLE, RA, GPA, PAN, allergy
Tx of AI inner ear disease
High dose CS: early, at least 30 d
If no response: cytotoxic meds
Aminoglycosides ototoxicity
Toxic by any route
Days to weeks after treatment
Toxic to hair cells
Otoacoustic emission lost first
High frequency lost first
Mx of aminoglycosides
Monitor with peak and trough levels
(Esp if neutropenia, ear/renal problem)
q 24 h dosing
CrCl determines dosage
Immediately stop if ototoxicity develops
The most important predictor of ototoxicity in treatment with AG
Duration of treatment
Salicylate ototoxicity
Hearing loss
Tinnitus
Reversible if DC
Ototoxicity with antimalarials
Hearing loss
Tinnitus
Reversible with DC or permanent
Noise-induced SNHL pathogenesis
85-90 dB over months or years
Or
Single > 135 dB
Cochlear damage
Hearing loss type in Noise-induced hearing loss
SNHL
Most prominent at 4000 Hz (boilermaker’s notch)
Extends to lower and higher frequencies over time
Speech reception not altered first, until > 30 dB loss at speech frequency
Phases of Noise-induced SNHL
Temporary threshold shift (returns to normal with removal of noise)
Permanent threshold shift (does not return)
Tx of Noise-induced SNHL
Hearing aid
Prevention of Noise-induced SNHL
Ear protection
Limit exposure (frequent rest periods)
Regular audiologic F/U
Transverse temporal bone fx
Mechanism: frontal/ occipital trauma
Prevalence: less common than longitudinal
CN: CN VII palsy 50% (transection)
Extension: bony labyrinth, internal auditory canal
Hearing loss: SNHL
Vestibular symptoms: present
CSF leak: via eustachian tube into pharynx, rhinorrhea
External ear, TM: intact, hemotympaneum
Longitudinal temporal bone fx
Extention: into middle ear
Incidence: more common than transverse
Mechanism: lateral skull trauma
CN: CN VII palsy: 10-20% (stretch, impingement)
Hearing loss: conductive
Vestibular symptoms: rare
TM: torn, hemotympaneum, otorrhagia
CSF leak: otorrhea
Battle sign, raccoon eyes
Dx of temporal bone fx
Otoscopy
CT head
Audiology, facial nerve test, schimmer test, stapedial reflex
If suspect CSF leak:
Halo sign, B-2 transferrin/ B trace protein in fluid
Mx of temporal bone fx
ABC
Expectant: prevent otogenic meningitis (Do not syringe or manipulateexternal auditory meatus)
Surgical if: CN VII palsy Gunshot wounds Depressed fx of external auditory meatus Early meningitis Intracranial bleeding from sinus CSF otorrhea
Bell’s palsy etiology
Idiopathic/HSV infection of VII nerve
RFs for Bell’s palsy
DM
Pregnancy
Viral prodrome
Clinic of Bell’s palsy
Acute onset
Numbness of ear
Schimer test
Hyperacusis
One side facial paralysis/paresis
Inv for Bell’s palsy
Stapedial reflex: absent
Audiology: normal
EMG: best measure for prognosis
MRI with gadolinum: enhancement of CN VII
High resolution CT
Topognostic testing
Tx of Bell’s palsy
Prevent exposure keratitis
Systemic steroids
Antivirals
F/U of Bell’s palsy
Spontaneous remission begins within 3 wk
If delayed recovery (3-6mo): some function loss
Px of Bell’s palsy
ENoG between 3-14 d of onset:
<90% degeneration: high likelihood of recovery
> 90% + no voluntary EMG potentials = surgical decompression
Poorer if: Hyperacusis >60y DM HTN Severe pain
Ramsay Hunt syndrome etiology
VZV infection of CN VII, CN VIII
RFs for Ramsay Hunt
>60 yr Impaired immunity Cancer RT Chemo
Ramsay Hunt clinic
Hyperacusis
Facial nerve paresis/paralysis
SNHL
Severe pain of pinna, mouth, face
Vesicles on pinna, external ear canal, mouth, 3-7 d after onset of pain
+/- vestibular, cochlear symptoms
Associated herpes zoster ophthalmicus (uveitis, keratoconjuctivitis, optic neuritis, glaucoma)
Inv for Ramsay Hunt
Stapedial reflex: absent
Audiology:
SNHL
Viral ELISA studies: confirm Dx
MRI with gadolinium: CN VII, CN VIII enhancement
Rx of Ramsay Hunt
Avoid touching lesions
Systemic steroids: relieve pain, vertigo, prevent PHN
Acyclovir: lessen pain, aid healing of vesicles
Px of Ramsay Hunt
Poorer than Bell’s
22% recover completely
66% incomplete paralysis
10% complete paralysis
If iatrogenic skull fx and facial nerve palsy:
Wait for lidocaine effect to wear off
If any movement present: Do nothing
If no movement: exploration
Types of atrophic rhinitis
Primary: Klebsiella ozena esp in elderly
Acquired: post-surgery (too much mucosa or turbinate resection)
Causes of non-inflammatory rhinitis
Pregnancy
Medicamentosa
Estrogen
Hypothyroidism
Allergic rhinitis types
Acute: seasonal: pollen from trees
Chronic: perennial:
Inhaled: house dust, wool, feather, foods, tobacco, hair, mould
Ingested: wheat, egg, milk, nuts
Concentration of allergens correlates with symptoms
IgE mediated
Onset <20 y
Mucosa and rhinorrhea in allergic rhinitis
Mucosa: swollen, pale, boggy
Rhinorrhea: clear, increased eosinophils
Complications of rhinitis
Chronic sinusitis
Polyps
Serous otitis media
Congestion in allergic rhinitis
Reduces nasal airflow and allows the nose to repair itself
Tx should focus on the initial insult rather than target this defense mechanism
Mx of allergic rhinitis
Identification and avoidance of allergens
Nasal irrigation with Saline
Antihistamines
Oral decongestants
Topical decongestants (up to 5-7 days) Dristan, Otrivin
Topical steroids
If severe:
Oral steroids
Desensitization by immunotherapy
Vasomotor rhinitis etiology
Disorder of nasal parasympathetic system (vidian nerve, going to sphenopalatine ganglion)
Non-specific reflex hypersensitivity of nasal mucosa
Triggers in vasomotor rhinitis
Temperature change Smoke Dust Alcohol Stress Anxiety Neurosis Hypothyroidism Pregnancy Menopause Parasympathomimetics
Tx of vasomotor rhynitis
Elimination of irritants
Parasympathetic blockers: Atrovent nasal spray
Steroids
Surgery: electrocautery/cryo/laser treatment. Removal of inferior/middle turbinates. Vidian neurectomy
Exercise: symptomatic relief
Clinical Dx of bacterial rhinosinositis
Dx if any of:
Symptoms > 7 d
Worsening after 5-7 d
High fever with purulent discharge 3-4 d
Plus 2 of:
Pain/ Pressure/ Fullness
Obstruction
Discharge (purulent, discolored)
Smell (hyposmia, anosmia)
Atleast 1 of O or D
Etiology of bacterial rhinosinositis
S. Pneumoniae H. Influenza M. Catarrhalis S. Aureus Dental aerobes
If immunocompromised: mucormycosis
The most common sinus affected in bacterial sinusitis
Maxillary
Factors predisposing to acute bacterial RS
URTI
allergy
Dental disease
Anatomical defects
Mx of acute bacterial RS
Depends on severity
Mild-mod: INCS
If no response after 72 h, add AB
Severe: INCS + AB
AB:
1st line: amoxicillin 10 d
If allergy to penicillin, TMP-SMX or macrolides
If no response within 72 h:
2nd line: switch to Q or amoxicillin-clavulanate
Adjunct therapies:
Saline/ HOCL irrigation
Analgesics
Oral/topical decongestants
Indications of CT in ABRS
If complications develop:
Preseptal, postseptal cellulitis Subperiosteal abscess Orbital abscess Cavernous sinus thrombosis Meningitis Intracranial abscess Sub-periostal frontal bone abscess Osteomyelitis Superior orbital fissure syndrome Orbital apex syndrome
Pott’s puffy tumor
Subperiosteal abscess of frontal bone
Superior orbital fissure sundrome
Immobile globe:CN III/IV/VI palsy
Dilated pupils
Ptosis
V1 hypoesthesia
Orbital apex syndrome
Immobile globe Dilated pupil Ptosis V1 hyposthesia \+ Optic neuritis, papilledema, decreased visual aquity
RS Timing
Acute: < 4wk
Subacute: 4-8 wk
Chronic > 8-12 wk
Dx of chronic rhinosinositis
2 of: Congestion and fullness P O D S
Mx of chronic RS
Identify and address contributing factors
CT or endoscopy
If polyps: INCS, oral CS, AB (if signs of infection), referral
If no polyps: INCS, AB, oral CS (if severe), saline irrigation
AB: 3-6 wk
amoxi-clav, Q, clarithro, clinda, metro
Surgery: if medical fails, or if fungal
Factors contributing to chronic RS
Inadequately treated ABRS
Allergy
Anatomical defects
Ciliary disorders: CF, kartagener
Chronic inflammatory disorders: GPA
Untreated dental disease
Fungal
Bacterial biofilm/colonization
Allergic fungal rhinosinositis
Young
Chronic
Atopic
Tx: functional endoscopic sinus surgery + INCS + antifungal + immunotherapy
Internal vs external carotid epistaxis
Internal: above middle turbinate
External carotid: below middle turbinate
Recurrent unilateral epistaxis in adolescent male
Juvenile nasopharyngeal angiofibroma
Epistaxis inv
CBC
PT/PTT
Xray, CT as needed
Tx of epistaxis
ABC: Lean forward Constant firm pressure for 20 min V/S \+/- IV NS, cross match blood
Determine site
Control bleeding:
1st line: topical vasoconstrictor: Otrivin
If failed: cauterize with silver nitrate
If failed:
Anterior: anterior pack 2-3 d
Posterior: admission. Posterior pack, then bilateral layer anterior pack for 3-5 d.
If packing failed: embolization +/- septoplasty
Complications of posterior packing
Hypoxemia TSS Aspiratin Pharyngeal fibrosis/stenosis Alar/septal necrosis
AB in packing
For:
All posterior packings
Anterior packing > 48h
Prevention of epistaxis
Prevent drying:
Humidifiers
Saline spray
Topical ointment
Avoidance of irritants
Mx of HTN and coagulopathies
Indication of laryngoscopy in smoker with hoarseness
> 2 wk persistence
laryngitis timing
Acute < 2 wk
Chronic > 2 wk
Tx of acute laryngitis
Self-limited
Voice rest
Humidification
Hydration
Avoid irritants
If co-existent bacterial pharyngitis: AB
If ulceration/granuloma formation on vocal cord
Chronic laryngitis
Tx of chronic laryngitis
Remove irritants:
Dust
Smoke
Chemical fumes
Treat underlying disorders: PND GERD EtOH Zenker Hiatus hernia Hypothyroidism Allergy Addison
Speech therapy with voice rest
+/- AB, CS
Laryngoscopy to R/O malignancy
Most common benign tumor of vocal cords
Polyps
M>F
30-50 yr
Etiology of polyps
Manifestation of vocal cord irritation
Voice strain
Irritants: GERD, allergy, tobacco
Most common site of polyp
Anterior 1/3 of vocal cords
Asymetrical
Tx of polyp
Avoid irritants, PPI
If persistent or high risk of malignancy:
Microsurgical removal
Vocal cord nodules etiology
Submucosal hemorrhage, hyalinization
Chronic voice strain
Frequent URTI, smoke, EtOH
Epidemiology of vocal cord nodule
F>M
Singers
School teachers
Children
Bartenders
Nodule clinic
Bilateral
Hoarseness Worse at the end of the day
Junction of anterior 1/3 and posterior 2/3
Tx of vocal cord nodule
Voice rest
Hydration
Speech therapy
Avoid irritants
Surgery for refractory nodules
Unilateral vocal cord paralysis symptoms
Early: paramedian position: weak, breathy voice
With time: medialization: improved phonation and aspiration
Tx of unilateral vocal cord paralysis
Voice therapy
Injection laryngoplasty
Medialization
Symptoms of bilateral cord paralysis
Cords in midline
Voice: good
Respiration: compromised, stridor
Tx of bilateral cord paralysis
If no respiratory issue: monitor
If respiratory issues: intubate, cord lateralization
Onset of polyp vs nodule
Polyp: acute
Nodule: gradual
Tx of laryngeal papillomatosis
Microdebridement
CO2 laser
HPV vaccine may prevent or decrease the incidence
The most common cause of sialadenitis
Viral (mumps)
The most common bacterial causes of sialadenitis
S. Aureus
S. Pneumoniae
H. Influenza
Predisposing factors to sialadenitis
HIV
anorexia/bulimia
Sjögren
Cushing, hypothyroidism, DM
Hepatic/renal failure
Meds that increase stasis: diuretics, TCA, BB, anticholinergics, AB
Sialolithiasis
Inv for sialadenitis
U/S: to differentiate obstructive vs. non obstructive
Tx of sialadenitis
Viral: nothing
Bacterial:
cloxacillin
+/- abscess drainage
Sialogogues
The most common location if sialolithiasis
Submandibular gland > parotid
RFs for sialolithiasis
Duct stenosis
Change in salivary secretion: Dehydration Diabetes EtOH Hypercalcemia Psychiatric medicine
Inv for sialolithiasis
U/S +/- sialogram
Tx of sialolithiasis
May resolve spontaneously
Encourage salivation
Massage
Analgesia
AB
Sialogogues (lemon wedges, sour lemon candies)
Warm compress
Calculi removal (endoscopy, surgery)
The most common salivary gland developing neollasm
Parotid > submandibular
The most common benign salivary gland tumor
Mixed (pleomorphic adenoma): 5% risk of malignant transfusion
Proportion of parotid gland tumors that are benign
80 %
Most common malignant tumor of parotid gland
Mucoepidermoid
Inv in parotid gland tumor
FNA Bx (incisional Bx: contra)
CT
U/S
MRI
Tx of salivary gland neoplasm
Choice: surgery (malignant or benign)
When to investigate a neck mass?
If persisting > 2wk
Most common causes of neck mass in different age groups
<20 yr: congenital
20-40: inflammatory
>40: neoplastic
Inv for neck mass
Depends on findings
CBC PPD TFT, Thyroid scan U/S CT Angio FNA needle Bx Open Bx Panendoscopy (lryngo, esophago, bronchoscopy with washing and Bx)
Findings in favor of inflammatory neck mass (vs. neoplastic)
Painful Presence of H&N infection Fever Tender Rubbery Mobile Younger
No: wt loss, no CA risk factor
The most common branchial malformation
2nd branchial cleft
Sites of branchial cleft malformations
2nd: anterior to SCM
1st: preauricular area, angle of mandible
3rd: recurrent thyroiditis or thyroid abscesses. Usually have a tract leading to the left pyriform sinus.
Air on CT in or near the thyroid gland is pathognomonic
Tx of branchial malformations
If infected: AB
Tx: surgical resection
Thyroglossal duct cyst presentation
Childhood
20-40 yr
Enlarges with URTI
Small potential for malignancy
Tx of thyroglossal cyst
Pre-operative AB to reduce inflammation
Complete excision of cyst and tissue around tract up to foramen cecum and central portion of hyoid bone
Lymphatic malformation in fetus
Common
Regresses before birth
Presentation of lymphatic malformation
By age 2
Macrocystic: below level of myohyoid
Microcystic: above level of myohyoid muscle
Sudden increase in size by infection or trauma
Tx of lymphatic malformations
Do Not Plan surgical intervention until several month after infection (might regress)
Macrocystic: sclerotherapy, surgical excision
Microcystic: debulk if it dies not cause loss of function of normal structures or injected with sclerotherapy
Risk of malignant transformation in leukoplakia
5-20%
Erythroplakia is associated with in situ/invasive carcinoma in what percent of lesions?
40%
Histologic features of dysplastic epithelium
Mitoses, prominent nucleoli
Progression of dysplasia to invasive cancer
15-30%
Inv in pre-malignant oral lesions
Bx
CXR (for mets w/u)
Liver/brain/bone scans if clinically indicated
CT ( to find pathologic nodal disease, bone invasion)
MRI (to discriminate tumor from mucus and to detect bone marrow invasion)
+/- PET scan
General Tx for ENT malignancies
Oral cavity:
Surgery
RT reserved for salvage or poor prognosis
Nasopharynx, oropharynx, hypopharynx, larynx:
Primary: RT
Surgery reserved for salvage
If mets/incurable:
Palliative chemo
Chemo prior to RT, Surgery
Advanced local/regional disease:
Anti-EGFR + RT
Synchronous, late developed 2nd primary tumor rate
Synchronus: 9-15%
Late development of 2nd primary: the most common cause of post treatment failure after 36 mo
Radiographic definition of pathologic LN
Jugulodigasteric > 1.5 cm
Retropharyngeal > 1 cm
Any size with central necrosis
Most common site of distant mets for H&N tumors
Lung > liver > bone
Most common site of H&N cancer
Oral cavity
95% SCC
M> F
RF for oral SCC
Smoking/ EtOH
Poor oral hygiene
Leukoplakia/ erythroplakia
LP
Chronic inflammation
Sun exposure
HPV
RFs for nose, paranasal sinus SCC
Wood/ Shoe/Textile industry
Hardwood dust
Nickle, chromium
Air pollution
Chronic rhinosinusitis
Carcinoma of nasopharynx
EBV
Salted fish
Nickle
Poor oral hygiene
Genetic
RFs for carcinoma of oropharynx
Smoking
Alcohol
HPV 16
RFs for carcinoma of hypopharnx
Smoking
EtOH
RFs for carcinoma of Larynx
Smoking
EtOH
HPV16
Percentage of malignant tumors in salivary glands
Minors: >80%
Submandibular 40%
Parotid 20%
Thyroid gland carcinoma RFs
Radiation FHx: papillary carcinoma, MEN II Older age Male Gardner: papillary Cowden: papillary FAP: papillary
Survival of HPV + vs HPV - H&N tumors
Better survival in HPV +
Chemo agent with highest effect for H&N SCC
Cisplatin +/- 5-FU
Concomitant chemo better than neo-adjuvant
Poor Px factors in oral cavity carcinoma
Depth of invasion
Close surgical margins
Location: tongue is worse
Cervical nodes
Extra-capsular spread
F/U of thyroid and parathyroid cancers
Thyroid: clinical exam, Tg
Parathyroid: Ca
Histology of papillary thyroid carcinoma
Orphan annie
Psammoma bodies
Lymphatic spread
Tx of papillary thyroid carcinoma
Total/near-total thyroidectomy
+/- neck dissection
+/- post-operative I131 treatment
No RT
Follicular thyroid carcinoma Tx
Thyroidectomy/lobectomy/isthmectomy
Radioiodine therapy
Chemo
RT
Hematogenous spread
MTC pathology
Amyloid
Secrets: calcitonin, PG, ACTH, serotonin, kallikrein, bradykinin
Lymphatic/hematogenous spread
Tx of MTC
Total thyroidectomy
Node dissection
Post-operative thyroxine, RT, tracheostomy
Screen relatives
Anaplastic thyroid carcinoma pathology
Giant cells
Spindle cells
Elderly women
Hx of differentiated thyroid carcinoma/ nodular goitre mass
Rapidly enlarging
Tx of anaplastic thyroid carcinoma
Subtotal/total thyroidectomy
RT
Chemo
Palliative care
Thyroid lymphoma
NHL Rapidly enlarging Hx of hashimoto Female B symptoms
Tx: RT, chemo
If thyroid nodule, next step?
TSH
U/S
Indication of FNA for thyroid nodule
If intermediate-high suspicion: >1cm
If low suspicion: >1.5 cm
If < 1cm + clinical symptoms/LAP: further evaluation
If non-diagnostic FNA?
Repeat FNA with U/S guide
Mx of thyroid nodule with hyperthyroidism
Radioiodine
Thyroid mass, benign on FNA, but increasing in size or >3-4 cm, next step
Surgical excision
Thyroid nodule with suspicious FNA
Surgical resection
Definition of AOM
All of:
Middle ear effusion
Middle ear inflammation
Acute onset
Peak: winter
Peak: 6-15 mo
Most common bacteria in AOM
S. Pneumoniae Non-typable H. Influenza M. Catarrhalis GAS S.aureus
Primary defect causing AOM
Eustachian tube dysfunction/obstruction
The most common viruses causing AOM
RSV
Influenza
Parainfluenza
Adenovirus
Mechanism of AOM by adenoid hypertrophy
Maintaining a source of infection
RFs for AOM and OME
Young age FHx Prematurity Orofacial abnormalities ImDef Down Race Ethnicity
Lack of breastfeeding Day care Household crowding Cigarette smoke exposure Air polution Pacifier
Triad of AOM
Fever
Otalgia
Conductive hearing loss
The most useful symptom in AOM
Ear pain
Useful otoscopic signs in AOM
Erythemato
Bulging
Cloudy
Immobile TM
General Mx of AOM
Hydration
Analgesics
Antipyretic
+/- AB
Indications for AB therapy in AOM
<6 mo
Moderate-severe illness: Irritable Difficulty sleeping Poor antipyretic response Severe otalgia Fever 39 and higher Duration > 48 h Perforated TM with purulent drainage
If mildly ill child + MEE + bulging TM
Analgesic
F/U for 24-48 h
Referral of AOM if
Recurrent AOM
AB therapy for AOM
1st line: amoxicillin
2nd line: cefprozil, cefuroxime, ceftriaxone, azithro, clarithro
If failure after 2-3 d:
Amoxi-clav
If failure:
Ceftriaxone
Duration of AB therapy for AOM
If 6-24 mo: 10 d
If > 24 mo: 5 d
If TM perforation: 10 d
If recurrent: 10 d
Advantages of AB therapy in AOM
Pain control in day 2-7
Reduce risk of TM perforation
Reduce risk of contralateral AOM
Most common cause of pediatric hearing loss
Otitis media with effusion
Mx of otitis media with effusion
Observe for 3 mo
Audiogram and tympanogram
Myringotomy +/- ventilation tube
+/- adenoidectomy if:
> 4 yr
(<4 yr only if nasal obstruction, chronic adenitis)
Most reliable finding in OME
Immobile TM with pneumatic otoscopy
Complications of OME
Hearing loss Speech delay Learning problems Chronic mastoiditis Ossicular erosion Cholesteatoma Retraction of TM Atelectasis Ossicular fixation
Indications for myringotomy, tympanostomy tube
Chronic Bilateral OME and documented hearing difficulties > 3mo
Unilateral / Bilateral OME > 3 mo and: Balance problems Poor school performance Ear discomfort Other symptoms attributable to OME
Unilateral/ Bilateral OME > 3 mo and: Permanent hearing loss Speech/language delay Autism spectrum Syndromes/ craniofacial disorders Blindness Cleft palate Developmental delay
Recurrent AOM ( >3 in 6 mo or > 4 in 12 mo) with Unilateral/ Bilateral OME
Age of adenoid size peak and resolution in children
5 yr -12 yr
Dx of enlarged adenoid
Flexible nasopharyngoscope: enlarged
Lateral soft tissue x-ray
Complications of adenoid hypertrophy
Eustachian tube obstruction (leading to serous otitis media)
Problem with nasal breathing
Malocclusion
Sleep apnea/respiratory disturbance
Orofacial developmental abnormality
Indications for adenoidectomy
Sleep disturbance/apnea +/- cor pulmonale
Chronic nasopharyngitis, resistant to medical therapy
Chronic serous otitis media, chronic suppurative otitis media (with 2nd set of tubes)
Recurrent AOM resistant to AB
Suspicion of nasopharyngeal malignancy
Persistent rhinorrhea secondary to nasal obstruction
Contraindications to adenoidectomy
Uncontrollable coagulopathy
Recent pharyngeal infection
Conditions predisposing to velopharyngeal insufficiency (cleft palate, impaired palatal function, enlarged pharynx)
Complications of adenoidectomy
Bleeding
Infection
Velopharyngeal insufficiency (hypernasal voice, nasal regurgitation)
Scarring of eustachian tube orifice
Inv for sleep-disordered breathing
Flexible nasopharyngoscopy
Polysomnography
Tx of OSA in children
Wt loss Sleep hygiene CPAP BiPAP Topical nasal CS/ LT-rec antagonist Surgery
Bacteria in Quinsy abscess
(Peritonsillar abscess)
GAS S. Pyogenes S. Aureus H. Influenza Anaerobes
Tiad of Quinsy
Trismus
Uvular deviation
Dysphonia (hot potato voice)
15-30 yr
The most reliable indicator of Quinsy
Trismus
Tx of quinsy
Secure aurway
Surgical drainage (incision, needle aspiration), with C&S
Warm saline irrigation
IV penicillin G (if positive for GAS)
+ PO/IV metro or clinda x 10 d (if positive bacteroids)
Tonsillectomy: after second episode
Tonsillectomy absolute indications
Sleep disordered breathing (most common)
Recurrent throat infection (2nd most common)
Hypertrophy causing upper airway obstruction, obstructive sleep apnea, severe dysphagia, cardiopulmonary complications
Suspicion of malignancy
Orofacial/dental deformity
Hemorrhagic tonsillitis
Tonsillectomy relative indications
Recurrent throat infection \+ At least one of: T > 38.3 Cervical adenopathy Tonsillar exudate Positive test for GAS
Chronic tonsilitis with halitosis/ soar throat/tonsilloliths
Complications of tonsillitis: quinsy, parapharyngeal abscess, retropharyngeal abscess
FTT
Relative contraindications of tonsillectomy
Velopharyngeal insufficiency
Coagulopathy
Anemia
Active local infection (unless urgent obstructive symptoms)
Etiology of sleep disordered breathing
Adenotonsillar hypertrophy
Craniofacial abnormality
Neuromuscular hypotonia
Obesity
Complications of tonsillectomy
Hemorrhage Infection Odynophagia Otalgia Atlantoaxial subluxation
Most common cause of stridor in children
Laryngomalacia
Nasal polyps in children
Suspect CF
Stridor if lying prone
Double aortic arch
Stridor if lying supine
Laryngomalacia
Glossoptosis
Inspiratory stridor, site?
Vocal cords or above
Expiratory stridor
Distal tracheobronchial tree
Biphasic stridor
Subglottis and extrathoracic trachea
Inflamed tissues in croup
Subglottic space and tracheobronchial tree
If recurrent/prolonged croup, suspect:
Subglottic stenosis
Perform:
High kV croup series Xray (AP, Lat) when well
Consider bronchoscopy for definite Dx
Tx of croup
Systemic steroid Hydration If respiratory distress, racemic epinephrine via MDI q 1-2 h Close observation 3-4 h If severe, intubation
Hospitalize if: poor response to steroids after 4 h and persistent stridor at rest
Consider alternate Dx if poor response
Tx of epiglottitis
Intubation IV and hydratio IV cefuroxim, cefotaxime, ceftriaxone Moist air Extubate when: leak around tube and afebrile Watch for meningitis
Subglottic stenosis definition
<4 mm in neonate
The most common acquired cause of subglottic stenosis
Intubation
Dx and Tx of subglottic stenosis
Dx: rigid laryngoscope, bronchoscopy
Tx:
If soft: divide with knife or laser, balloon +/- steroid
If firm: laryngotracheoplasty
Laryngomalacia symptoms
High-pitched inspiratory stridor at 1-2 wk
Constant or intermittent
More pronounced in supine position or after URTI
Usually mild
Sometimes cyanosis, FTT, feeding difficulty
Spontaneously subsides by 12-18 mo
Yx of laryngomalacia
Observation + PPI
If severe: division of aryepiglotic fold
Foreign body is usually stuck at
Cricopharyngeal muscle
If aspirated: Rt main bronchus
Tx of foreign body ingestion/aspiration
NPO
older pts: Inspiratory/expiratory CXR (if stable)
Younger pts: Rt and Lt decubitus CHR. If lack of lung deflation while resting on dependent side: foreign body blocking bronchus
Bronchoscopy, esophagoscopy for removal
The most common cause of accidental death in children
Foreign body inhalation
Battery on Xray
Halo sign around the rim
Step sign on lateral Xray
Deep neck space bacteria
Often mixed
Dx of deep neck abscess
Lateral cervical Xray
CT
MRI
Surgeon should consider accompanying pt for imaging
Tx of deep neck abscess
Secure airway
Sugical drainage
Maximum dose of IV systemic AB
Ludwig angina
Infection of submandibular, sublingual spaces