ENT Notes Crak

OTOLARYNGOLOGY
Dr. J. Irish and Dr. B. Pap sin Avik Bane rje e and Francis Ling, e d itors T.J. Lou, associate e d itor
PHYSICAL EXAMINATION . . . . . . . . . . . . . . . . . . . 2 Head and Neck Ear Nose Oropharynx Nasopharynx Hypopharynx and Larynx Other Areas of Examination ANATOMY OF THE EAR . . . . . . . . . . . . . . . . . . . . . 5 AUDIOLOGY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6 Pure Tone Audiometry Speech Audiometry Impedance Audiometry Auditory Brainstem Response (ABR) Tuning Fork Tests HEARING LOSS . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10 Differential Diagnosis Otitis Externa Acute Otitis Media and Otitis Media with Effusion Cholesteatoma Mastoiditis Otosclerosis Congenital Sensorineural Hearing Loss Presbycusis Sudden Sensorineural Hearing Loss Drug Ototoxicity Noise-Induced Sensorineural Hearing Loss Acoustic Neuroma Temporal Bone Fractures Aural Rehabilitation VERTIGO . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .16 Differential Diagnosis Otoneurological Examination TINNITUS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .19 OTALGIA . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20 FACIAL NERVE PARALYSIS . . . . . . . . . . . . . . . . . . 21 Bells Palsy NASAL OBSTRUCTION . . . . . . . . . . . . . . . . . . . . . . 21 Acute Rhinitis Allergic Rhinitis Vasomotor Rhinitis Adenoid Hypertrophy Nasal Polyps Septal Deviation Septal Hematoma Septal Perforation EPISTAXIS. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25 SINUSITIS. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27 Acute Suppurative Sinusitis Chronic Sinusitis PEDIATRIC OTOLARYNGOLOGY . . . . . . . . . 29 Acute Otitis Media Otitis Media with Effusion Adenoid Hypertrophy Acute Tonsillitis Tonsillectomy Airway Problems in Children Signs of Airway Obstruction Acute Laryngotracheobroncheitis - (Croup) Acute Epiglottitis Subglottic Stenosis Laryngomalacia Foreign Body Surgical Airway Management DYSPHAGIA . . . . . . . . . . . . . . . . . . . . . . . . . . . 36 Differential Diagnosis DEEP NECK SPACE INFECTIONS. . . . . . . . . 37 Peritonsillar Abscess (Quinsy) Retropharyngeal Abscess Ludwigs Angina Acute Tonsillitis and Tonsillectomy HOARSENESS. . . . . . . . . . . . . . . . . . . . . . . . . . . 39 Differential Diagnosis Acute Laryngitis Chronic Laryngitis Vocal Cord Polyps Vocal Cord Nodules Benign Laryngeal Papillomas Laryngeal Carcinoma SALIVARY GLANDS . . . . . . . . . . . . . . . . . . . . . . 41 Sialadenitis Sialolithiasis Salivary Gland Manifestations of Systemic Disease NECK MASSES. . . . . . . . . . . . . . . . . . . . . . . . . . 42 Differential Diagnosis Evaluation Congenital Neck Masses NEOPLASMS OF THE HEAD AND NECK . . 44 Introduction Etiological Factors in Head and Neck Neoplasia Principles of Management Carcinoma of the Nose and Paranasal Sinuses Carcinoma of the Nasopharynx Carcinoma of the Lip Salivary Gland Neoplasms Carcinoma of the Oral Cavity Carcinoma of the Oropharynx Carcinoma of the Hypopharynx Carcinoma of the Larynx Thyroid Neoplasms Thyroid Carcinoma
Otolaryngology 1
MCCQE 2000 Re vie w Note s and Le cture Se rie s
PHYSICAL EXAMINATION
HEAD AND NECK
Ins pe ction of He ad and Ne ck ! position of head ! symmetry of facial structure ! look for neck scars, asymmetry, masses, enlarged thyroid Palpation of He ad and Ne ck ! lymph node examination observe size, mobility, consistency, tenderness, warmth, regular/irregular border occipital, posterior auricular, superficial posterior cervical, deep cervical, preauricular, tonsillar, submandibular, submental, supraclavicular ! salivary gland examination palpate parotid and submandibular glands for tenderness, swelling, masses, or nodules Thyroid Gland ! inspection of gland symmetry and mobility ! palpation via anterior or posterior approach note size, shape, and consistency of gland identify any nodules or areas of tenderness ! if gland is enlarged, auscultate with bell listen for thyroid bruit suggestive of a toxic goiter
Note s
EARS
Exte rnal Examination of Ear ! inspect external ear structures note position of ear look for deformities, nodules, inflammation, or lesions potential findings discharge: note colour and consistency remnant of first branchial arch: small dimple in front of tragus tophi: sign of gout microtia or macrotia: congenitally small or large auricles cauliflower ear: gnarled pinna due to repeated trauma ! palpate external ear structure examine for infection of external ear pain elicited by pulling pinna up or down, or pressing on tragus apply pressure on mastoid tip tenderness may indicate infective process of the mastoid bone Auditory Acuity mask one ear and whisper into the other Rinne test Weber test Otos copic Examination ! select largest speculum that will fit into external canal ! inspect external canal look for evidence of inflammation, foreign bodies, or discharge ! inspect tympanic membrane normal membrane: intact, translucent, gray note landmarks handle of the malleus light reflex: directed anteroinferiorly may see chorda tympani nerve behind short process of malleus possible abnormal findings diseased dull, red or yellow membrane injection of blood vessels tympanosclerosis: dense white plaques fluid or pus in middle ear membrane perforation
Otolaryngology 2 MCCQE 2000 Re vie w Note s and Le cture Se rie s
. . . CONT.
Note s
! mobility of tympanic membrane only if there is a question of middle ear infection pneumatic otoscopy to demonstrate decreased movement of tympanic membrane Pars flaccida Handle of Malleus
Pars tensa
Fibrous Annulus
Light reflex
Figure 1. Normal Appe arance of Tympanic Me mbrane on Otos copy

Drawing by Monique LeBlanc
NOSE
Exte rnal Examination of Nos e ! inspect nose look for swelling, trauma, congenital anomalies, deviation test patency of each nostril if deviation is suspected ! palpate sinuses tenderness over frontal and maxillary sinuses may indicate sinusitis Inte rnal Examination of Nos e ! inspect with nasal speculum position of septum colour of nasal mucosa normally dull red and moist with a smooth clean surface size, colour and mucosa of inferior and middle turbinates possible abnormal findings septal deviation or perforation exudate, swelling, epistaxis nasal polyps Othe r Te s ts ! transillumination of the sinuses maxillary direct light downward from under the medial aspect of the eye observe transilluminated hard palate frontal direct light upward from under medial aspect of eyebrow
OROPHARYNX
Examination of Oral Cavity ! lips ! buccal mucosa pull cheek away from gums and inspect for lesions identify Stensens duct (parotid gland duct)opposite upper first or second molar ! gingivae and dentition 32 teeth in full dentition look for malocclusion ! hard and soft palates ask patient to remove dentures inspect for ulceration or masses
MCCQE 2000 Re vie w Note s and Le cture Se rie s Otolaryngology 3
. . . CONT.
Note s
! floor of mouth palpate for any masses identify Whartons duct (submandibular gland duct) on either side of the frenulum of the tongue ! tongue inspect for colour, mobility, and masses palpate tongue for any masses test cranial nerve XII Examination of Pharynx ! anterior faucial pillars, tonsils, tonsillolingual sulcus depress middle third of tongue with tongue depressor and scoop tongue forward in order to visualize tonsils note size and inspect for any exudates from tonsils ! posterior pharyngeal wall
NASOPHARYNX
Pos tnas al Mirror (Indire ct) ! ensure good position of the patient must sit erect with chin drawn forward ! with adequate tongue depression, the mirror is placed to next to uvula and almost touches the posterior pharyngeal wall ! rotate mirror to inspect the following areas choana posterior end of the vomer: should be in midline inferior, middle, and superior meatus may see pus dripping over posterior end of inferior meatus (sign of maxillary sinusitis) eustachian tubes adenoids (mostly in children) Nas opharyngos cope (Dire ct) ! detailed view of nasal cavities and nasopharynx
HYPOPHARYNX AND LARYNX

Indire ct Laryngos copy ! ensure good position of the patient ! while holding tongue with some gauze, introduce a slightly warmed laryngeal mirror into mouth and position mirror in the oropharynx ! ask patient to breathe normally through mouth while mirror is pushed upward against the uvula touching the uvula and soft palate usually does not elicit a gag reflex, unlike touching the back of the tongue the gag reflex can sometimes be suppressed if patients are told to pant in and out ! image seen in mirror will be reversed anterior structures are seen at the top while posterior structures are seen at the bottom of the mirror (see Figure 2) ! inspect the following structures circumvallate papillae and base of tongue lingual tonsils valleculae epiglottis aryepiglottic folds and pyriform fossae should be smooth, pink, and symmetrical false vocal cords should be dull pink, symmetrical and thicker than true cords abnormal if they overhang and conceal the true cords true vocal cords white and sharp-edged attached anteriorly to the thyroid cartilage (fixed) attached posteriorly to the vocal processes of the arytenoid cartilages (mobile) note any irregularity of the edges, nodules or ulcerations
. . . CONT.
Note s
note position and movement of cords quiet respiration cords are moderately separated inspiration cords abduct slightly ask patient to say eeee cords adduct to midline look for signs of paralysis or fixation
Base of tongue Epiglottis
Pyriform fossa
True vocal cord False vocal cord
Trachea
Arytenoid cartilage
Figure 2. Appe arance of Normal Larynx on Indire ct Laryngos copy

Drawing by Jason Guerrero
Dire ct Laryngos copy with Fibre optic Nas opharyngos cope ! prepare patient with topical anesthetic administered by nasal spray ! flexible scope passed via nasal cavity to view structures in the larynx as mentioned above
OTHER AREAS OF EXAMINATION

Cranial Ne rve s (see Neurology Notes) Ve s tibular Function (see Otoneurological Examination Section)
ANATOMY OF THE EAR
Figure 3a. Anatomy of the Ear For descriptive purposes the ear is divided into three parts: external, middle and inner ear
Figure 3b. Se ction through the Cochle a Hair cells in the organ of Corti transform mechanical energy (vibration) into electrical impulses
Reproduced with permission from Churchill Livingston, Dhillon, R.S, East, C.A. Ear, Nose and Throat and Head and Neck Surgery. Churchill Livingston, UK, 1994.
Otolaryngology 5
AUDIOLOGY
PURE TONE AUDIOMETRY
! threshold is the faintest intensity level at which a patient can hear the tone 50% of the time ! thresholds are obtained for each ear for frequencies 250 to 8000 Hz ! air conduction thresholds are obtained with headphones and measure outer, middle, inner ear, and auditory nerve function ! bone conduction thresholds are obtained with bone conduction oscillators which effectively bypass outer and middle ear function
Note s
Clinical Pe arl ! Air conduction thre s holds can only be e qual to or gre ate r than bone conduction thre s holds ! degree of hearing loss determined on basis of the Pure Tone Average (PTA) at 500, 1000, 2000 Hz 0-15 dB normal 16-25 dB slight 26-40 dB mild 41-55 dB moderate 56-70 dB moderate-severe 71-90 dB severe 91 + dB profound ! types of hearing loss (see Figure 4) ! conductive (something is impairing the conduction of sound to the cochlea i.e. fused or broken ossicular chain) bone thresholds in normal range air conduction thresholds increased by 15-20 dB or more above bone conduction thresholds ! sensorineural (the sensory component of the inner ear, brainstem or cortex is damaged) air and bone conduction thresholds below normal and similar (if the loss is unilateral it should be investigated further to rule out acoustic neuroma, noise-induced hearing loss, etc...) ! mixed air and bone conduction thresholds below normal, as well as an air-bone gap
Otolaryngology 6
AUDIOLOGY . . . CONT.
250 500 1 000 2 000 4 000
Note s
> X > X
8 000 -10 250 500 1 000 2 000 4 000 8 000 -10
Inte rpre tation X = AC Unmasked > = BC Unmasked [ ] = AC Masked ] = BC Masked
> X
> X
> X
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>
>
> X
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HEARING LEVEL (dB)
HEARING LEVEL (dB)
30 40 50 60 70 80 90 100 110 120
Figure A. Normal Audiogram
Figure B. Conductive He aring Los s (Otitis Me dia)
250
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8 000 -10 0 10 20 30
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50 60 70 80 90 100 110 120
> O
HEARING LEVEL (dB)
> O
30
> O
> O > O O
40 50 60 70 80 90 100 110 120
100 110 120
Figure C. Conductive He aring Los s (Otos cle ros is )
Figure D. Se ns orine ural He aring Los s (Nois e Induce d)
Figure E. Se ns orine ural He aring Los s (Pre s bycus is )
Figure 4. Type s of He aring Los s
SPEECH AUDIOMETRY
Spe e ch Re ce ption Thre s hold (SRT) ! lowest hearing level at which patient is able to repeat 50% of two syllable words ("spondees", e.g. hotdog, baseball) ! SRT and best pure tone threshold in the 500-2000 Hz range (frequency range of human speech) usually agree within 5 dB. If not, suspect a retrocochlear lesion or functional hearing loss Spe e ch Dis crimination Te s t ! percentage of words the patient correctly repeats from a list of 50 monosyllabic words (e.g. boy, aim, go) ! tested at a level 35-50 dB > SRT, so degree of hearing loss is taken into account ! classification of speech discrimination testing 90-100% excellent 40-60% poor 80-90% good < 40% very poor 60-80% fair
Otolaryngology 7
! patients with normal hearing or conductive hearing loss score > 90% ! score depends on amount of sensorineural hearing loss present ! a decrease in discrimination as sound intensity increases is typical of a retrocochlear lesion (rollover effect)
Note s
IMPEDANCE AUDIOMETRY
Tympanogram ! eustachian tube equalizes the pressure between outer and middle ear ! tympanogram is a graph of the compliance of the middle ear system over a pressure gradient ranging from +200 to 400 mm H2O ! peak of tympanogram occurs at the point of maximum compliance where the pressure in the external canal is equivalent to the pressure in the middle ear ! normal range: 100 to +50 mm H20 Type A Tympanogram
O + normal middle ear pressure peak at 0 mm H2O, note that with otosclerosis the peak is still at 0mm H2O but has a lower amplitude (called an As tympanogram) Type B Tympanogram
O + no pressure peak, and poor TM mobility indicative of middle ear effusion (e.g. otitis media with effusion) or perforated TM Type C Tympanogram
O + negative pressure peak indicative of chronic eustachian tube insufficiency (e.g. serous or secretory otitis media) Static Compliance ! volume measurement reflecting overall stiffness of the middle ear system ! normal range: 0.3 to 1.6 cc ! negative middle ear pressure and abnormal compliance indicate middle ear pathology Acous tic Stape dial Re fle xe s ! stapedius muscle contracts when ear exposed to loud sound and results in increased stiffness or impedance of middle ear system (TM and ossicles) ! stimulating either ear causes reflex to occur bilaterally and symmetrically ! reflex measured ipsilaterally by stimulating and measuring from same ear, or contralaterally by stimulating one ear and measuring impedance in the contralateral ear ! reflex pathway involving vestibulocochlear cranial nerve, cochlear nucleus, trapezoid body, superior olivary nucleus, facial nucleus, and facial nerve (i.e. a measure of central neural function) ! acoustic reflex thresholds occur at 70-100 dB above hearing threshold if hearing threshold is greater than 85 dB, the reflex is likely to be absent
! for reflex to be present, CN VII must be intact and there must be no conductive hearing loss in the monitored ear if reflex absent without conductive loss or severe sensorineural loss, suspect CN VIII lesion ! acoustic reflex decay test: tests the ability of the stapedius muscle to sustain contraction for 10 s at 10 dB stimulation ! normally, little reflex decay occurs at 500 and 1000 Hz ! with cochlear hearing loss the acoustic reflex thresholds are typically 25-60 dB ! with retrocochlear hearing loss (e.g. acoustic neuroma) may find absent acoustic reflexes or significant reflex decay (> 50%) within 5 second interval
Note s
AUDITORY BRAINSTEM RESPONSE (ABR)
! the patient is exposed to an acoustic stimulus while an electroencephalogram is recorded to assess any changes in brain activity ! delay in brainstem response is suggestive of cochlear or retrocochlear abnormalities (for the latter think tumour or MS)
TUNING FORK TESTS

Rinne 's Te s t ! 512 Hz tuning fork is struck and held firmly on mastoid process to test bone conduction (BC) ! when it can no longer be heard it is placed close to ear to test air conduction (AC) ! if it can then be heard then AC > BC or Rinne positive We be r's Te s t ! vibrating fork is held on vertex of head and patient states whether it is heard centrally or is lateralized to one side ! lateralization indicates ipsilateral conductive hearing loss or contralateral sensorineural hearing loss Table 1. The Inte rpre tation of Tuning Fork Te s ts
Example s Normal or Bilateral Sensorineural Hearing Loss Right Sided Conductive Hearing Loss, Normal Left Ear Right Sided Sensorineural Hearing Loss, Normal Left Ear Right Sided Severe Sensorineural Hearing Loss or Dead Right Ear, Normal Left Ear We be r Central Lateralizes to Right Lateralizes to Left Lateralizes to Left Rinne AC>BC (+) bilaterally BC>AC () right AC>BC (+) bilaterally BC>AC () right *
* a vibrating fork on the mastoid stimulates both cochlea, therefore in this case, the left cochlea is stimulated by the Rinne test on the right, i.e. a false negative test These tests are not valid if the ear canals are not free of cerumen (i.e. will create conductive loss)
Otolaryngology 9
HEARING LOSS
DIFFERENTIAL DIAGNOSIS
Conductive ! external ear canal cerumen otitis externa foreign body congenital atresia keratosis obturans tumour of canal: squamous cell carcinoma (rare) ! middle ear acute otitis media serous otitis media tympanic membrane perforation otosclerosis congenital: ossicular fixation trauma, i.e. hemotympanum tumour, i.e. cholesteatoma Se ns orine ural ! congenital ! acquired presbycusis (very common in elderly) Menire's disease noise-induced (dip at 4000 Hz on audiogram) ototoxic drug (high frequency loss) head injury sudden sensorineural hearing loss labyrinthitis (viral or bacterial) meningitis demyelinating disease (e.g. MS) trauma (e.g. temporal bone fracture) tumour (e.g. acoustic neuroma)
Note s
OTITIS EXTERNA
Clinical Pe arl ! Otitis e xte rna has two forms : a be nign painful infe ction of the oute r canal that could occur in anybody and a pote ntially le thal le s s painful (damage d s e ns ory ne rve s ) dis e as e in old, immunos uppre s s e d or diabe tic patie nts Etiology ! caused by bacteria: P. aeruginosa, P. vulgaris, E. coli, S. aureus fungi: Candida albicans, Aspergillus niger ! more common in summer ! associated with swimming ("swimmer's ear"), mechanical cleaning (Q-tips, skin dermatitides) Pre s e ntation ! acute pain aggravated by movement of auricle (traction of pinna or pressure over tragus) +/ unilateral headache, +/ low grade fever otorrhea - sticky yellow purulent discharge conductive hearing loss - due to obstruction of external canal with purulent debris post-auricular lymphadenopathy ! chronic pruritus of external ear +/ excoriation of ear canal atrophic and scaling epidermal lining +/ otorrhea, +/ hearing loss wide meatus but no pain with movement of auricle tympanic membrane appears normal Tre atme nt ! clean ear under magnification with irrigation, suction, and dry swabbing
HEARING LOSS
. . . CONT.
Note s
! bacterial etiology topical aminoglycoside antibiotics +/ corticosteroids (e.g. Garamycin, Neosporin, Corticosporin) introduction of fine gauze wick (pope wick) if external canal edematous +/ 3% acetic acid solution to acidify ear canal systemic antibiotics when cervical lymphadenopathy or cellulitis present - obtain cultures from external canal ! fungal etiology alcohol/acetic acid instillation, clotrimazole, locacortin (Vioforme) ! +/ analgesics ! chronic otitis externa pruritus without obvious infection corticosteroid alone e.g. diprosalic acid Malignant Otitis Exte rna ! due to Pseudomonas osteomyelitis of temporal bone ! associated with diabetics, elderly, perichondritis, cellulitis, parotitis, +/ chronic symptoms ! requires hospital admission, debridement, IV antibiotics and emergent CT scan
ACUTE OTITIS MEDIA AND OTITIS MEDIA WITH EFFUSION

(see Pediatric ENT Section)
CHOLESTEATOMA ( s e e
Colour Atlas I7) ! keratinized squamous epithelium in middle-ear or mastoid
Conge nital ! behind an intact tympanic membrane small white pearl", not associated with otitis media ! usually presents with conductive hearing loss Acquire d ! frequently associated with pars flaccida and marginal perforations of the tympanic membrane ! erodes mastoid bone, then ossicles ! associated with chronic otitis media with painless otorrhea Complications ! chronic otitis media ! CNS dysfunction/infection ! late complications: hearing loss, vertigo, facial palsy Tre atme nt ! excision via cortical, modified radical, or radical mastoidectomy depending on the extent of disease +/ tympanoplasty ! tympanic membrane repair and ossicle reconstruction if no sign of recurrence
MASTOIDITIS
! osteomyelitis (usually subperiosteal) of mastoid air cells, most commonly seen approximately two weeks after onset of untreated (or inadequately treated) acute suppurative otitis media ! previously common but is now rare due to rapid and effective treatment of acute otitis media with antibiotics
Pre s e ntation ! pinna displaced laterally and inferiorly ! persistent throbbing pain and tenderness over mastoid process ! development of subperiosteal abscess > post-auricular swelling ! spiking fever ! hearing loss ! otorrhea with tympanic membrane perforation (late) ! radiologic findings: opacification of mastoid air cells by fluid and interruption of normal trabeculations of cells Tre atme nt ! IV antibiotics with myringotomy and ventilating tubes ! cortical mastoidectomy debridement of infected tissue allowing aeration and drainage requires lifelong follow-up with otolaryngologist ! indications for surgery failure of medical treatment after 48 hours symptoms of intracranial complications aural discharge persisting for 4 weeks and resistant to antibiotics
HEARING LOSS
OTOSCLEROSIS
. . . CONT.
Note s
! commonest cause of conductive hearing loss between 15 and 50 years of age ! autosomal dominant, variable penetrance approximately 40% ! female > male - progresses during pregnancy (hormone responsive) ! 50% bilateral
Pre s e ntation ! progressive conductive hearing loss first noticed in teens and 20s (may progress to sensorineural hearing loss if cochlea involved) ! +/ pulsatile tinnitus ! tympanic membrane normal +/ pink blush (Schwartz's sign) associated with the neovascularization of otosclerotic bone ! characteristic dip at 2000 Hz (Carhart's Notch) on audiogram (Figure 4) Tre atme nt ! stapedectomy with prosthesis is definitive treatment ! hearing aid may be used, however usually not a good long term solution
CONGENITAL SENSORINEURAL HEARING LOSS

! genetic factors are being identified increasingly among the causes of hearing loss He re ditary De fe cts ! non-syndrome associated (70%) often idiopathic autosomal recessive ! syndrome associated (30%) Waardenburg's - white forelock, heterochromia iridis, wide nasal bridge and increased distance between medial canthi Pendred's - goiter Treacher-Collins - first and second branchial cleft anomalies Alport's - hereditary nephritis Pre natal TORCH Infe ctions ! Toxoplasmosis ! Others e.g. HIV ! Rubella ! Cytomegalovirus (CMV) ! Herpes simplex Pe rinatal ! Rh incompatibility ! anoxia ! kernicterus ! birth trauma (hemorrhage into inner ear) Pos tnatal ! meningitis ! mumps ! measles High Ris k Re gis try (For He aring Los s in Ne wborns ) ! risk factors low birth weight/prematurity perinatal anoxia (low APGARs) kernicterus - bilirubin > 25 mg/dL craniofacial abnormality family history of deafness in childhood 1st trimester illness - CMV rubella , neonatal sepsis ototoxic drugs perinatal infection, including post-natal meningitis consanguinity ! 50-75% of newborns with sensorineural hearing loss have at least one of the above risk factors, and 90% of these have spent time in the NICU ! presence of any risk factor: Auditory Brainstem Response (ABR) study done before leaving NICU and at 3 months adjusted age ! refer for hearing assessment
HEARING LOSS
. . . CONT.
Note s
! if not identified and rehabilitated within six months, intellectual deterioration in deaf children occurs ! must detect and rehabilitate hearing loss near birth in every case so that the child can reach his/her potential
PRESBYCUSIS
! hearing loss associated with aging - 5th and 6th decades ! most common cause of sensorineural hearing loss
Etiology ! hair cell degeneration ! age related degeneration of basilar membrane ! cochlear neuron damage ! ischemia of inner ear Pre s e ntation ! progressive and gradual bilateral hearing loss initially at high frequencies, then middle frequencies ! loss of discrimination of speech especially with background noise present - patients describe people as mumbling ! recruitment phenomenon: inability to tolerate loud sounds ! tinnitus ! refer to audiogram in Figure 4 Tre atme nt ! hearing aid if hearing loss > 30-35 dB ! +/ lip reading and auditory training
SUDDEN SENSORINEURAL HEARING LOSS (UNILATERAL)

! presents as a sudden onset of significant hearing loss (usually unilateral) +/ tinnitus ! unexplained etiology autoimmune microcirculation viral trauma (barotrauma) - perilymph leak ! r/o TIA and SLE ! CT to rule out tumour or CVA if associated with any other focal neurological signs (e.g. vertigo, ataxia, abnormality of CN V or VII, weakness) ! treat with low molecular weight dextran corticosteroids bedrest ! prognosis 70% resolve spontaneously within 10-14 days 20% experience partial resolution 10% experience permanent hearing loss
DRUG OTOTOXICITY
Aminoglycos ide s ! increased toxicity with oral administration ! destroys sensory hair cells ! high frequency hearing loss develops earliest ! ototoxicity occurs days to weeks post-treatment ! streptomycin (vestibulotoxic), kanamycin and tobramycin (toxic to cochlea), gentamicin (vestibulotoxic and cochlear toxic) ! must monitor levels with peak and trough levels when prescribed, especially if patient has neutropenia, history of ear or renal problems ! q24H dosing, with amount determined by creatinine clearance not serum creatinine alone Salicylate s ! hearing loss with tinnitus ! reversible if discontinued
Otolaryngology 13
HEARING LOSS
Cis platinum
. . . CONT.
Note s
Quinine and Antimalarials ! tinnitus ! reversible if discontinued but can lead to permanent loss ! treat drug ototoxicity with IV low molecular weight dextrans
NOISE-INDUCED SENSORINEURAL HEARING LOSS

! may be occupational, often associated with tinnitus ! 85-90 dB over months or years causes cochlear damage ! early-stage hearing loss at 4000 Hz, extending to higher and lower frequencies with time ! speech reception not altered until hearing loss > 30 dB at speech frequency, therefore considerable damage may occur before patient complains of hearing loss ! difficulty in discriminating, especially in situations with competing noise ! refer to audiogram in Figure 4
Phas e s of He aring Los s ! dependent on intensity level and duration of exposure ! temporary threshold shift when exposed to loud sound, decreased sensitivity or increased threshold for sound with removal of noise, hearing returns to normal ! permanent threshold shift hearing does not return to previous state Limits of Nois e Caus ing Damage ! continuous sound pressure of 85-90 dB and higher ! single sound impulses > 135 dB Tre atme nt ! hearing aid ! prevention ear protectors: muffs, plugs machinery which produces less noise limit exposure to noise with frequent rest periods regular audiologic follow-up
ACOUSTIC NEUROMA
! Schwannoma of the vestibular portion of CN VIII ! most common intracranial tumour causing hearing loss ! starts in the internal auditory canal and expands into CPA, compressing cerebellum and brainstem ! may be associated with Type 2 neurofibromatosis (bilateral tumours of CN VIII in internal auditory canal, cafe-au-lait lesions, multiple intracranial lesions)
Pre s e ntation ! usually presents with unilateral sensorineural hearing loss ! dizziness and unsteadiness may be present, but no true vertigo ! facial nerve palsy and trigeminal (V1) sensory deficit (corneal reflex) late complications Clinical Pe arl ! Any unilate ral s e ns orine ural he aring los s is an acous tic ne uroma until prove n othe rwis e Diagnos is ! enhanced CT/MRI ! audiogram - puretone threshold elevated ! poor speech discrimination and stapedial reflex ! absent or significant reflex decay ! Acoustic Brainstem Reflexes - increase in latency of the 5th wave ! electronystagmography (ENG) Tre atme nt ! definitive management is surgical excision from middle fossa, from posterior fossa or translabyrinthine approach ! if unresectable: gamma knife, XRT
HEARING LOSS
. . . CONT.
Note s
TEMPORAL BONE FRACTURES

Type s 1. transverse fractures extends into bony labyrinth and internal auditory meatus (20%) 2. longitudinal fractures extends into middle ear (80%)
1 2
Figure 5. Type s of Te mporal Bone Fracture s

Drawing by Teddy Cameron
Table 2. Fe ature s of Te mporal Bone Fracture s

Trans ve rs e Incidence Etiology CN pathology Hearing loss Vestibular symptoms 10-20% frontal/occiptal CN VII palsy sensorineural loss due to direct cochlear injury sudden onset vestibular symptoms due to direct semicircular canal injury (vertigo, spontaneous nystagmus) intact external auditory meatus, tympanic membrane +/ hemotympanum spontaneous nystagmus CSF leak in eustachian tube to nasopharynx +/or rhinorrhea (risk of meningitis) Longitudinal 70-90% lateral skull trauma CN VII palsy (10-20%) conductive hearing loss secondary to ossicular injury rare
Other features
torn tympanic membrane with hemotympanum bleeding from external auditory canal step formation in external auditory canal CSF otorrhea Battles sign = mastoid ecchymoses Raccoon eyes = periorbital ecchymoses
Diagnos is ! otoscopy ! do not syringe or manipulate external auditory meatus due to risk of inducing meningitis via TM perforation ! radiology Schueller's view - longitudinal Stenver's view - transverse tomograms CT ! facial nerve tests (for transverse fractures), EMG, Schirmer's test, gustometry, stapedial reflexes, ENG Tre atme nt ! hemotympanum signifies significant force sustained by the temporal bone, therefore monitor hearing until it returns to normal
HEARING LOSS
. . . CONT.
Note s
! medical - expectant, prevent otogenic meningitis IV antibiotics if suspect CSF leak (penicillin G for 7-10 days) ! surgical - explore temporal bone, indications are early meningitis (mastoidectomy) bleeding from sinus CSF otorrhea CN VII palsy gunshot wound depressed fracture of external auditory meatus Complications ! acute otitis media +/ mastoiditis ! meningitis/labyrinthitis ! epidural abscess / brain abscess ! post-traumatic cholesteatoma
AURAL REHABILITATION
! dependent on degree of hearing loss, communicative requirements and difficulties, motivation and expectations, age, and physical and mental abilities ! factors affecting prognosis with hearing aid/device poor speech discrimination narrow dynamic range (recruitment) unrealistic expectations cosmetic ! types of hearing aids behind the ear - BTE all in the ear - ITE bone conduction contralateral routing of signals (CROS) ! assistive listening devices direct/indirect audio output infrared, FM, or induction loop systems telephone, television, or alerting devices ! cochlear implant electrode is inserted into the cochlea to allow direct stimulation of the auditory nerve for profound bilateral sensorineural hearing loss not rehabilitated with conventional hearing aids established indication: post-lingually deafened adults and children
VERTIGO
! patients can present with a wide range of subjective descriptions of their symptoms: dizziness, spinning, lightheadedness, giddiness, unsteadiness ! true vertigo defined as an illusion of rotary movement of self or environment, made worse in the absence of visual stimuli ! it is important to distinguish vertigo from other disease entities that may present with similar complaints (e.g. cardiovascular, psychiatric, neurological, aging) ! diagnosis is heavily dependent upon an accurate history description of rotary movement onset and duration hearing and tinnitus effect of dark/eye closing relation to body position alcohol and drug history (antihypertensives, aminoglycosides) medical history (vascular disease, anxiety disorder)
! peripheral vestibular (labyrinthine) disorders Meniere's disease benign positional vertigo (BPV) vestibular neuronitis recurrent vestibulopathy - post traumatic or post viral tumour - acoustic neuroma trauma - skull fractures, barotrauma, surgery suppurative labyrinthitis
Otolaryngology 16
VERTIGO
. . . CONT.
Note s
! central vestibular disorders - brainstem tumour multiple sclerosis ! systemic hypoglycemia hyperventilation anemia ototoxic drugs vascular lesions - vertebrobasilar insufficiency Table 3. Diffe re ntial Diagnos is of Ve rtigo
Condition BPV Me nie re 's Dis e as e re curre nt ve s tibulopathy ve s tibular ne uronitis labyrinthitis acous tic ne uroma Duration seconds minutes-hours precedes attack minutes to hours hours-days days chronic He aring Los s none uni/bilateral none unilateral unilateral progressive Tinnitus none + none none whistling none Aural Fullne s s none pressure/warmth none none none none recent AOM ataxia CN Vll palsy Othe r Fe ature s
Clinical Pe arl ! True nys tagmus and ve rtigo will ne ve r las t longe r than a couple of we e ks if caus e d by a pe riphe ral le s ion be caus e compe ns ation occurs ; s uch is not true for a ce ntral le s ion Be nign Pos itional Ve rtigo (BPV) ! most common cause for episodic vertigo ! acute attacks of transient vertigo initiated by certain head positions lasting seconds to minutes, accompanied by nystagmus that fatigues on repeated testing ! due to migration of a small flake of bone or detached mineral crystals from utricular otolith organ (cupulolithiasis) into posterior semicircular canal > floats to rest on one of the sensitive balance organs may occur following a head injury, viral infection (URTI) degenerative disease or idiopathic results in slightly different signals being receive by the two balance organs resulting in sensation of movement ! diagnosed by history and positive Dix-Hallpike manoeuvre (see Otoneurological Examination Section) ! treat symptomatically and reassure patient that process resolves spontaneously commonly treated with exercise to continually stimulate vestibular system to allow it to compensate drugs to suppress the vestibular system delay eventual recovery and are therefore not used Me nie re 's Dis e as e (e ndolymphatic hydrops ) ! affects the young to middle-aged ! characterized by the quadrad of vertigo, hearing loss, tinnitus, and aural fullness ! early in the disease, hearing returns to normal in the attack-free states ! later stages are characterized by a unilateral, fluctuating low-tone deafness and a persistance of tinnitus ! attacks come in clusters and may be very debilitating to the patient, may be triggered by stress ! most hearing loss becomes bilateral with time ! vertigo disappears with time and patient is left only with hearing loss ! pathogenesis: abnormal buildup of K+ increase in osmotic pressure causes a rupture of Reissner's membrane which divides the endo- and perilymphatic spaces disruption allows for mixing of endo and perilymph resulting in a net rise of K+ in the intracellular space as a result afferent neurons of the acoustic and vestibular nerves are depolarized (causing symptoms)
VERTIGO
. . . CONT.
Note s
periodic resolution occurs when the membrane reseals and chemical composition of endolymph and perilymph normalizes ! treatment acute management may consist of bedrest, IV antiemetics, antivertiginous drugs, and low molecular weight dextrans longterm management may be medical low salt diet, K+ sparing diuretics (e.g. triamterene, amiloride) local application of gentamicin to destroy vestibular end-organ surgical - selective vestibular neurectomy or transtympanic labyrinthectomy may recur in opposite ear after treatment Re curre nt Ve s tibulopathy ! episodic vertigo of similar duration as Meniere's ! etiology unknown ?transient deafferentation of vestibular nerve ?post-traumatic ?post-viral ! no hearing loss, tinnitus, or focal neurological deficit ! peak age 30-50 years old, M = F ! treatment: symptomatic, most eventually go into remission Ve s tibular Ne uronitis ! unknown etiology (microvascular upset due to infection, autoimmune process, or a metabolic disorder) ! severe vertigo with nausea, vomiting, and inability to stand or walk ! symptoms can last for 3 to 4 days (risk of dehydration from vomiting) ! attacks leave patient with unsteadiness and imbalance for months ! repeated attacks can occur Labyrinthitis ! sudden onset of dizziness, nausea, vomiting, whistling noises, and deafness, with no associated fever or pain ! may occur through spread from a cholesteatomic fistula or through direct infection after a transverse fracture of the temporal bone or post-operative infection ! treat with IV antibiotics, drainage of middle ear +/ mastoidectomy ! beware of meningeal extension and labyrinth destruction
OTONEUROLOGICAL EXAMINATION
! otoscopy ! cranial nerve testing (II-XII inclusive) ! cerebellar testing
Nys tagmus ! assess nystagmus - describe quick phase, avoid examining in extremes of lateral gaze ! horizontal nystagmus that beats in the same direction = peripheral vestibular disorder the lesion is usually on side of the slow beat, with the fast phase beating away from the side of the lesion ! horizontal nystagmus that changes direction with gaze deviation = central vestibular disorder ! vertical upbeating nystagmus = brainstem disease ! vertical downbeating nystagmus, usually = medullocervical localization (e.g. Arnold-Chiari) Dix-Hallpike Pos itional Te s ting with Fre nze l's (Magnifying) Eye glas s e s ! the patient is rapidly moved from a sitting position to a supine position with the head hanging over the end of the table, turned to one side, this position is held for 20 seconds ! onset of vertigo is noted and the eyes are observed for nystagmus ! the patient sits up and the maneouvre is then repeated with the head turned to the opposite side ! rotatory nystagmus beating towards floor (geotropic), which is accompanied by vertigo, is reproducible and fatigues, is associated with benign positional vertigo (BPV)
Otolaryngology 18
VERTIGO
. . . CONT.
Note s
As s e s s Brain Pe rfus ion ! carotid bruits, subclavian stenosis ! positional blood pressure measurements Balance Te s ting ! Rombergs test: patient stands upright with feet together, eyes closed, and arms folded in front of chest sway is associated with loss of either joint proprioception or a peripheral vestibular disturbance the patient leans or tends to fall toward the side of the diseased labyrinth ! Unterbergers test: marching on the spot with the eyes closed peripheral disorders: rotation of body to the side of the labyrinthine lesion central disorders: deviation is irregular Ele ctronys tagmography (ENG) ! electrodes placed around eyes ! eye is a dipole, cornea (+), retina () ! used to measure rate, amplitude, and frequency of nystagmus elicited by different stimuli Caloric Stimulation Te s t ! with the patient supine, the neck is flexed 30 degrees to bring the horizontal semicircular canal into a vertical position. The volume of endolymph is changed by irrigating the labyrinthine capsule with water at 30C or 44C for 35 seconds ! the change in volume causes deflection of the cupula and subsequent nystagmus through the vestibuloocular reflex ! the extent of response indicates the function of the stimulated labyrinth ! cold water will result in nystagmus to the opposite side of irrigation and warm to the same (COWS - cold opposite, warm same)
TINNITUS
! an auditory perception in the absence of stimulation, often very annoying to the patient ! etiology presbycusis (most common cause in elderly) serous otitis media (most common cause in young) Meniere's Disease acoustic trauma labyrinthitis = acoustic neuronitis acoustic neuroma MS ! pulsatile (objective) tinnitus (rare) bruits due to vascular lesions (e.g. glomus jugulare, hemangiomas, carotid body tumours, AVM, internal carotid artery bruits) patulous eustachian tube ! clicking tinnitus myoclonus of muscles - stapedius, tensor tympani, levator and tensor palati tetany Tre atme nt ! mask tinnitus white noise masking devices hearing aid music earphones ! tinnitus support groups ! psychotherapy ! trial of tocainamide
Otolaryngology 19
OTALGIA
Local ! furuncle ! foreign body in external auditory canal/impacted cerumen ! otitis externa ! trauma to tympanic membrane and canal ! acute otitis media and its complications ! acute mastoiditis and its complications ! barotrauma Re fe rre d (10 T's + 2) - see Figure 6 ! pain referred to ear from sites in pharynx or oral cavity ! CN V and CN X refer to external canal and CN IX to middle ear 1) teeth - impacted 2) throat - cancer of larynx, vallecula, pyriform fossa 3) thyroiditis 4) tic (CN IX) - glossopharyngeal neuralgia 5) TMJ syndrome 6) tongue 7) tonsillitis, tonsillar cancer, post tonsillectomy 8) trachea - FB, tracheitis 9) trismus (i.e. pterygoids, quinsy) 10) eustachian tube 11) geniculate herpes and Ramsey Hunt Syndrome 12) +/ CN VII palsy
Note s
This can be due to pathology in those sites which have a dual nerve supply with the ear. All these potential penpheral areas must be examined in all cases of referred otalgia
Figure 6. Re fe rre d or Non-Otological Otalgia

Reproducedwith permission from Churchill Livingston, Dhillon, R.S, East, C.A. Ear, Nose and Throat and Head and Neck Surgery. Churchill Livingston, UK, 1994.
Otolaryngology 20
FACIAL NERVE PARALYSIS

Etiology ! supranuclear and nuclear MS cerebral vascular lesions, pseudobulbar palsy poliomyelitis cerebral tumours ! infranuclear Bell's palsy trauma: birth, temporal bone fracture, surgical cholesteatoma CPA tumours (acoustic neuroma, glomus jugulare, meningioma, neurofibroma) suppuration: acute/chronic otitis media Ramsay Hunt syndrome (Herpes zoster infection of external auditory meatus and auricle, may affect CN VII) MS Guillain-Barr syndrome Diagnos is ! supranuclear lesions: movement of upper part of face is likely to be unaffected as the frontalis muscle receives bilateral corticobulbar innervation ! nerve conduction tests and EMG ! site of lesion testing (e.g. stapedial reflexes, Schirmer's, taste to anterior 2/3 of tongue) Tre atme nt ! treat according to etiology plus provide corneal protection with artificial tears, nocturnal lid taping, tarsorrhaphy, gold weighting of upper lid
Note s
BELL'S PALSY (s e e
Colour Atlas I1) ! a diagnosis of exclusion, therefore must rule out other causes of facial paralysis (e.g. ear infection) ! idiopathic, may be a disturbance of microcirculation +/ viral etiology ! 80% recover ! sequelae: "crocodile tears", facial asymmetry and ectropion, corneal abrasions ! treat with steroids (e.g. oral prednisone), stellate ganglion block or low molecular weight dextrans with decompression of nerve reserved for progressive denervation
NASAL OBSTRUCTION
Table 4. Diffe re ntia1 Diagnos is of Nas al Obs truction
Acquire d nas al cavity rhinitis - acute/chronic - vasomotor - allergic polyps foreign bodies trauma enlarged turbinates tumour - benign- inverting papilloma - malignant- squamous cell carcinoma esthesioneuroblastoma adenocarcinoma nas al s e ptum septal deviation septal hematoma/abscess nas opharynx adenoid hypertrophy tumour - nasopharyngeal carcinoma - benign - juvenile nasopharyngeal angiofibroma - malignant: nasopharyngeal carcinoma Conge nital nasal dermoid encephalocele glioma
dislocated septum choanal atresia
Otolaryngology 21
NASAL OBSTRUCTION
. . . CONT.
Note s
Table 5. Nas al Dis charge : Characte r and As s ociate d Conditions

Characte r watery/mucoid mucopurulent serosanguineous bloody As s ociate d Conditions allergic, viral, vasomotor, CSF leak bacterial, foreign body neoplasia trauma, neoplasia, bleeding disorder, hypertension/vascular disease
Middle meatus Inferior meatus
Middle turbinate Septum Inferior turbinate
Figure 7. Normal Appe arance of Nas al Cavity on Spe culum Exam

Drawing by Vince Mazzurco
ACUTE RHINITIS
! ! ! !
irritation of nasal mucosa due to any cause most common cause is common cold children < 5 years most susceptible spread by droplet contact from sneezing
Figure 8. Caus e s of Rhinitis

Etiology ! viral (ususally rhinovirus), may have secondary bacterial infection Pre s e ntation ! irritation/burning sensation in nasopharynx; sneezing ! serous nasal discharge, may be purulent if secondary bacterial infection ! nasal obstruction, mucosal swelling and erythema ! +/ fever and malaise ! symptoms subside in 4-5 days
NASAL OBSTRUCTION
Complications ! sinusitis ! otitis media ! bronchitis ! tonsillitis ! pneumonia
. . . CONT.
Note s
Tre atme nt ! rest, fluids, normal diet ! oral decongestants for symptomatic relief ! +/ analgesics, antihistamine, corticosteroid spray ! (e.g. triamcinolone, fluticasone, betamethasone) ! no indication for antibiotics, unless secondary bacterial infection present Clinical Pe arl ! Conge s tion re duce s nas al airflow and allows the nos e to re pair its e lf. Tre atme nt s hould focus on the initial ins ult rathe r than at this de fe ns e me chanis m
ALLERGIC RHINITIS (HAY FEVER)
! acute and seasonal or chronic and perennial ! perennial allergic rhinitis often confused with recurrent colds
Pre s e ntation ! early onset (< 20 years) ! past history or family history of allergies/atopy ! obstruction ! sneezing ! clear, recurrent rhinorrhea (containing increased eosinophils) ! itching of nose and eyes ! tearing ! frontal headache and pressure ! mucosa - swollen, pale, lavender colour, and boggy" ! seasonal (summer, spring, early autumn) pollens from trees lasts several weeks, disappears and recurs following year at same time ! perennial inhaled: house dust, wool, feather, foods, tobacco, hair, mould ingested: wheat, eggs, milk, nuts occurs intermittently for years with no pattern or may be constantly present Complications ! chronic sinusitis ! serous otitis media ! nasal polyps Diagnos is ! history ! skin/allergy testing: scratch test, intradermal injections ! nasal speculum exam Tre atme nt ! identification and avoidance of allergen ! oral decongestants ! antihistamines ! injection of long-lasting steroid if severe ! topical steroid sprays, e.g. fluticasone (Flonase) - effective for seasonal rhinitis ! desensitization by allergen immunotherapy
VASOMOTOR RHINITIS
! neurovascular disorder of nasal parasympathetic system (vidian nerve) affecting mucosal blood vessels ! nonspecific reflex hypersensitivity of nasal mucosa ! caused by temperature change alcohol, dust, smoke stress, anxiety, neurosis endocrine - hypothyroidism, pregnancy, menopause parasympathomimetic drugs beware of rhinitis medicamentosa: reactive vasodilation due to prolonged use (> 2 days) of nasal drops and sprays (Dristan, Otravin)
Otolaryngology 23
NASAL OBSTRUCTION
. . . CONT.
Note s
Pre s e ntation ! chronic intermittent nasal obstruction, varies from side to side ! rhinorrhea: thin, watery, worse with temperature changes, stress, exercise, EtOH ! nasal allergy must be ruled out ! mucosa and turbinates: swollen, pale between exposure ! symptoms are often more severe than clinical presentation suggests Tre atme nt ! elimination of irritant factors ! parasympathetic blocker (Atrovent nasal spray) ! decongestants (nose drops/oral) ! steroids (e.g. Beclomethasone) ! surgery: electrocautery, cryosurgery, laser treatment or removal of inferior or middle turbinates ! vidian neurectomy (rarely done) ! symptomatic relief with exercise (increased sympathetic tone)
ADENOID HYPERTROPHY (see Pediatric ENT Section) NASAL POLYPS

! benign pedunculated/sessile masses of hyperplastic ethmoidal mucosa caused by inflammation ! antrochoanal polyps - (uncommon) arise from maxillary sinus and extend beyond the soft palate into the nasopharynx ! may obstruct airway Etiology ! mucosal allergy (majority) ! chronic rhinitis/sinusitis (ethmoids) ! idiopathic ! note: triad of polyps, aspirin sensitivity, asthma ! cystic fibrosis/bronchiectasis (child with polyps - cystic fibrosis until proven otherwise) Pre s e ntation ! progressive nasal obstruction, hyposmia, snoring ! post-nasal drip, stringy colourless/purulent rhinorrhea ! solitary/multiple glazed, smooth, transparent mobile masses (often bilateral) Tre atme nt ! eliminate allergen ! steroids (preoperative prednisone) to shrink polyp ! polypectomy - treatment of choice, however, polyps have marked tendency to recur Complications ! sinusitis ! mucocele ! nasal widening (pseudohypertelorism)
SEPTAL DEVIATION
Etiology ! developmental - unequal growth of cartilage and/or bone of nasal septum ! traumatic - facial and nasal fracture or birth injury Pre s e ntation ! unilateral nasal obstruction (may be intermittent) ! anosmia, crusting, facial pain ! recurrent ear infections, recurrent sinus infections ! septum: S-shaped, angular deviation, spur ! compensatory middle/inferior turbinate hypertrophy on nasal space
NASAL OBSTRUCTION
. . . CONT.
Note s
Tre atme nt ! if asymptomatic - expectant management ! if symptomatic - submucous resection (SMR) or septoplasty Complications of s urge ry ! post-op hemorrhage (can be severe) ! septal hematoma, septal perforation ! external deformity (saddle-nose) ! anosmia (rare but untreatable) ! most common in children - secondary to trauma, even mild trauma may lead to infection > abscess > cavernous sinus thrombosis ! septal perforation ! ischemic necrosis of septum and saddle deformity Pre s e ntation ! nasal obstruction ! pain/tenderness ! occurs in anterior part of septum ! swollen nose Tre atme nt ! incision and drainage with nasal packing ! antibiotics
SEPTAL HEMATOMA
SEPTAL PERFORATION
Etiology ! trauma: surgery, physical, digital ! infection: syphilis, tuberculosis ! inflammatory: SLE ! neoplasia: squamous/basal cell, malignant granuloma infection ! miscellaneous: cocaine sniffing, chromic gases Pre s e ntation ! perforation seen on exam ! crusting ! recurrent epistaxis ! whistling on inspiration/expiration Tre atme nt ! refer suspected neoplasia for biopsy ! surgical closure for small perforations, occlusion with Silastic buttons, free fascial graft, mucosal flap
EPISTAXIS
anterior ethmoid posterior ethmoid frontal sinus sphenoidal sinus
Kiesselbachs plexus branch from superior labial
septal branch of sphenopalatine greater palatine
Figure 9. Nas al Se ptum and its Blood Supply

Drawing by Victoria Rowsell
Otolaryngology 25
EPISTAXIS
. . . CONT.
Note s
! blood supply to the nasal septum superior posterior septum: internal carotid > ophthalmic artery > ant and post ethmoidal posterior septum: external carotid > internal maxillary > sphenopalatine artery lower anterior septum: external carotid > facial artery > superior labial artery these arteries all anastomose to form Kiesselbachs plexus, located at Littles area (anterior portion of the cartilaginous septum), this area is responsible for approximately 90% of nosebleeds bleeding from above middle turbinate is internal carotid, from below, external carotid Table 6. Etiology of Epis taxis
Type local Caus e s idiopathic (most) injection (vestibulitis) trauma (digital, dry air) foreign body tumours benign - junvenile angiofibroma (occurs in adolescent males) - polyps maligant - squamous cell carcinoma hypertension arteriosclerosis drugs (anticoagulants, e.g. aspirin and coumadin) bleeding disorders hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease)
s ys te mic
Tre atme nt ! aim is to localize bleeding and achieve hemostasis ! first-aid patient sits upright with mouth open (to prevent swallowing) firm pressure is applied for 5 minutes superior to nasal alar cartilages (not bony pyramid!) ! assess blood loss (it can be a potentially fatal hemorrhage) pulse and BP sign of shock IV NS, cross match for 2 units packed RBCs if significant ! determine site of bleeding if suspicion, coagulation studies insert cotton pledget of 4% cocaine, visualize nasal cavity with speculum and aspirate excess blood and clots anterior/posterior hemorrhage defined by location in relationship to bony septum ! control the bleeding first line topical vasoconstrictors if first line fails and can adequately visualize bleeding source can try and cauterize with silver nitrate do not attempt to cauterize both sides of the septum because of the risk of septal perforation ! anterior hemorrhage treatment if fail to achieve hemostasis with cauterization anterior pack with half inch vaseline and bismuth-coated gauze strips or absorbable packing (i.e. Gelfoam) layered from nasal floor toward nasal roof extending to posterior choanae for 2-3 days can also attempt packing with Merocel or nasal tampons of different shapes ! posterior hemorrhage treatment if unable to visualize bleeding source, then usually posterior source insert cotton pledget with 4% cocaine different ways of placing a posterior pack with a Foley catheter, gauze pack or a Nasostat balloon bilateral anterior pack is layered into position antibiotics for any posterior pack or any pack in longer than 48 hours admit to hospital with packs in for 3 to 5 days watch for complications such as hypoxemia (naso-pulmonic reflex) and toxic shock syndrome (if present remove packs immediately) Otolaryngology 26 MCCQE 2000 Re vie w Note s and Le cture Se rie s
EPISTAXIS
. . . CONT.
Note s
! if anterior/posterior packs fail to control epistaxis selective catheterization and embolization of branches of external carotid artery vessel ligation of anterior/posterior ethmoid artery internal maxillary external carotid Pre ve ntion ! prevent drying of nasal mucosa with humidifiers, saline spray, or topical ointments ! avoidance of irritants ! medical management of hypertension
SINUSITIS
De ve lopme nt of Sinus e s ! birth - ethmoid and small maxillary buds present ! age 9 - maxillary full grown, frontal and sphenoid cell starting ! age 18 - frontal and sphenoid cell full grown Drainage of Sinus e s ! frontal, maxillary, anterior ethmoids: middle meatus ! posterior ethmoid: superior meatus ! sphenoid: sphenoid ostium (at level of superior meatus) Pathoge ne s is of Sinus itis ! inflammation of the mucosal lining of the paranasal sinuses ! anything that blocks air entry into the sinuses predisposes them to inflammation
Figure 10. The Paranas al Sinus e s

! associated with common cold swimming/diving diseased tooth roots ! organisms S. pneumonia H. influenza S. aureus - diabetic Klebsiella, Pseudomonas, anaerobes in immunocompromised patients beware of fungal sinusitis > mucormycoses 50% fatal Pre s e ntation ! stuffy nose, purulent rhinorrhea ! malaise, fever, headache exacerbated by bleeding ! pressure/pain over involved sinus maxillary - over cheek and upper teeth ethmoids - medial and deep to eye frontal - forehead sphenoid - vertex ! mucosa hyperemic and edematous with enlarged turbinates ! x-ray - involved sinus opaque +/ fluid level (s e e Colour Atlas I9)
ACUTE SUPPURATIVE SINUSITIS
SINUSITIS
. . . CONT.
Note s
Tre atme nt ! analgesics and decongestants - systemic and nose drops ! hot compresses ! antibiotics - oral with maxillary, and IV with frontal or ethmoid sinus involvement or orbital complications ! first line: amoxicillin, if failure can go to amoxicillin + clavulanic acid (Clavulin) or cefaclor ! surgery maxillary - antral puncture and lavage frontal/ethmoid - trephine of superior medial orbital canthus, irrigate, and drain sphenoid - drain via posterior ethmoids
CHRONIC SINUSITIS
! irreversible changes in lining membrane of one or more sinuses due to neglect of acute and subacute phase recurrent attacks or obstruction of osteomeatal complex (by polyp, deviated septum, FB, allergic rhinitis, or anatomic narrowing)
Pre s e ntation ! chronic nasal obstruction ! pain over sinus or headache ! halitosis ! yellow-brown post-nasal discharge Tre atme nt ! dependent upon involved sinus, as confirmed by coronal CT of head ! decongestants, antibiotics, steroids; if fails, then surgery Surgical Tre atme nt ! removal of all diseased soft tissue and bone, post-op drainage and obliteration of pre-existing sinus cavity ! Functional Endoscopic Sinus Surgery (FESS) ! open surgical approach for extensive disease ! Ethmoid intranasal ethmoidectomy via endoscopy - fenestration made into the maxillary sinus which usually restores mucociliary clearance complications of unresolved ethmoid sinusitis first signs - proptosis, diplopia, chemosis, ophthalmoplegia, poor acuity periorbital or orbital edema, cellulitis, abscess periostitis phlegmon ! Frontal trephination frontoethmoidectomy - removal of mucosa and floor of sinus together with an ethmoidectomy complications of frontal sinusitis (see Figure 11) mucocele Pott's puffy tumour (osteomyelitis of frontal bone often with fistula formation)
Osteomyelitis Subdural Abscess
Figure 11. Complications of Frontal Sinus itis

Otolaryngology 28
SINUSITIS
. . . CONT.
Note s
! Maxillary antrostomy by either enlarging the natural ostium or removing a segment of the sinus floor Caldwell-Luc operation - a sublabial approach to removal of diseased lining of the sinus complications mucocele oroantral fistula facial cellulitis tooth-loosening osteomyelitis of skull vault bones or upper jaw
PEDIATRIC OTOLARYNGOLOGY
ACUTE OTITIS MEDIA
! inflammation of middle ear associated with pain, fever, irritability, anorexia, or vomiting ! 60-70% of children have at least 1 episode of AOM before 3 years of age ! 18 months to 6 years most common age group ! peak incidence January to April ! one third of children have had 3 or more episodes by age 3
Etiology ! S. pneumoniae - 35% of cases ! H. influenzae - 25% of cases ! M. catarrhalis ! S. aureus and S. pyogenes (all -lactamase producing) ! anaerobes (newborns) ! viral Pre dis pos ing Factors ! eustachian tube dysfunction/obstruction swelling of tubal mucosa URTI allergies/allergic rhinitis chronic sinusitis obstruction/infiltration of eustachian tube ostium tumour - nasopharyngeal CA (adults) adenoid hypertrophy barotrauma (sudden changes in air pressure) inadequate tensor palati function - cleft palate abnormal spatial orientation of eustachian tube Down's Syndrome (horizontal position of eustachian tube), Crouzon's, and Alport's syndrome ! disruption of action of cilia of eustachian tube - ?Kartagener's syndrome mucus secreting cells capillary network that provides humoral factors, PMNs, phagocytic cells ! immunosupression due to chemotherapy steroids diabetes mellitus hypogammaglobulinemia cystic fibrosis Ris k Factors ! bottle feeding ! passive smoke ! day care/group child care facilities Pathoge ne s is ! obstruction of eustachian tube > air absorbed in middle ear > negative pressure (an irritant to middle ear mucosa) > edema of mucosa with exudate > infection of exudate
Otolaryngology 29
PEDIATRIC OTOLARYNGOLOGY . . . CONT.

Pre s e ntation ! triad of otalgia, fever, and conductive hearing loss ! fullness of ear ! otorrhea if tympanic membrane perforated (s e e Colour Atlas I8) ! pain over mastoid ! infants/toddlers ear-tugging irritable, poor sleeping vomiting and diarrhea anorexia ! otoscopy of tympanic membrane (s e e Colour Atlas I5) hyperemia bulging contour of handle of malleus and short process disappear Tre atme nt ! antibiotic treatment hastens resolution - 10 day course amoxicillin - 1st line trimethoprim-sulphamethoxazole (Bactrim) - if penicillin-allergic AOM deemed unresponsive if clinical signs and symptoms and otoscopic findings persist beyond 48 hours of antibiotic treatment change to broad spectrum: cefaclor (Ceclor), erythromycin + sulfisoxizole (Pediazole), cefixime (Suprax) clarithromycin (Biaxin) for recurrent AOM ! antipyretics (e.g. acetaminophen) ! no role for decongestants in AOM ! myringotomy with tubes - indications complications of AOM suspected recurrent AOM (> 5 in a year) immunologically compromised child failure of 3 different antibiotics - fever and bulging of drum Complications of AOM ! extracranial (see Figure 12) acute mastoiditis, chronic suppurative otitis media facial nerve paralysis febrile seizures nystagmus - bacterial labyrinthitis TM perforation ! intracranial meningitis extradural, subdural, cerebral abscess petrositis lateral sinus thrombosis
Note s
OTITIS MEDIA WITH EFFUSION
! not exclusively a pediatric disease ! chronic middle ear effusions (may or may not be associated with initial episode of pain and fever) ! follows AOM frequently in children ! can be mucoid - follows AOM resolving mucoid serous barotrauma in adults
Figure 12. Extracranial Complications of Middle Ear Infe ction

Otolaryngology 30

Pre s e ntation ! fullness - blocked ear ! hearing loss +/ tinnitus confirm with audiogram (see Figure 4) and tympanogram (flat) ! minimal pain, possibly low grade fever, no discharge ! otoscopy of tympanic membrane (s e e Colour Atlas I6) discolouration - amber or dull grey with glue" ear meniscus fluid level air bubbles retraction pockets/TM atelectasis foreshortening of malleus prominent short process tenting of tympanic membrane over short process and promontory of malleus most reliable finding with pneumotoscopy is immobility Tre atme nt ! expectant - 90% resolve by 3 months ! antibiotics thought to decrease viscosity of effusion by killing residual organisms ! no statistical proof that antihistamines, decongestants, antibiotics clear faster than no treatment ! surgery: myringotomy +/ ventilating tubes +/ adenoidectomy (if enlarged) (s e e Colour Atlas I10) ! ventilating tubes indications persisting effusion > 3 months hearing loss > 30 dB speech delay atelectasis of tympanic membrane function equalization of middle ear pressure aeration and drainage of middle ear restoration of hearing and balance duration - 9 to 18 months complications tympanosclerosis persistent TM perforation persistent otorrhea Complications of Otitis Me dia with Effus ion ! chronic inflammation ! hearing loss, speech delay, learning problems in young children ! can lead to chronic suppurative otitis media ! chronic mastoiditis ! ossicular erosion ! cholesteatoma especially when retraction pockets involve pars flaccida or postero-superior TM ! retraction of tympanic membrane, atelectasis, ossicular fixation
Note s
ADENOID HYPERTROPHY
! size peaks at age 6 and resolves by 12 to 18 years of age ! increase in size with repeated URTI and allergies
Pre s e ntation ! nasal obstruction adenoid facies (open mouth, dull facial expression) hypernasal voice history of snoring long term mouth breather; minimal air escape through nose ! choanal obstruction chronic sinusitis/rhinitis obstructive sleep apnea ! chronic inflammation nasal discharge, post-nasal drip and cough cervical lymphadenopathy Diagnos is ! enlarged adenoids on mirror nasopharyngeal exam ! enlarged adenoid shadow on lateral soft tissue x-ray ! lateral view of the nasopharynx may show a large pad of adenoidal tissue

Complications ! eustachian tube obstruction leading to serous otitis media ! interference with nasal breathing, necessitating mouth-breathing ! malocclusion ! sleep apnea/respiratory disturbance Indications for Ade noide ctomy ! chronic upper airway obstruction with sleep disturbance/apnea +/ cor pulmonale ! chronic nasopharyngitis resistant to medical treatment ! chronic serous otitis media and chronic suppurative otitis media ! recurrent acute otitis media resistant to antibiotics ! suspicion of nasopharyngeal malignancy ! chronic sinusitis Contraindications for Ade noide ctomy ! bleeding disorders ! recent pharyngeal infection ! short or abnormal palate
Note s
ACUTE TONSILLITIS
Etiology ! Group A -hemolytic Strep and Group G Strep ! Pneumococci ! S. aureus ! H. influenza ! EBV Pre s e ntation ! symptoms sore throat dysphagia, odynophagia malaise, fever otalgia (referred) ! signs cervical lymphadenopathy especially submandibular, jugulodigastric tonsil enlarged, inflamed +/ spots (s e e Colour Atlas I2) strawberry tongue, scarlatiniform rash (scarlet fever) palatal petechia (infectious mononucleosis) Inve s tigations ! CBC ! swab for C&S ! latex agglutination tests ! Monospot - less reliable children < 2 years old Tre atme nt ! bedrest, soft diet, ample fluid intake ! gargle with warm saline solution ! analgesics and antipyretics ! antibiotics only after appropriate swab for C&S start with penicillin (erythromycin if allergic to penicillin) x 10 days rheumatic fever risk emerges approximately 9 days after the onset of symptoms: antibiotics are utilized mainly to avoid this serious sequela and to provide earlier symptomatic relief no evidence for the role of antibiotics in the avoidance of post-streptococcal glomerulonephritis Complications (see Pediatrics Notes) ! uncommon since the use of antibiotics rheumatic heart disease nephritis arthritis scarlet fever ! deep neck space infection

! abscess: peritonsillar (quinsy), intratonsillar ! sepsis
Note s
TONSILLECTOMY
Abs olute Indications ! acute airway obstruction +/ cor pulmonale ! excisional biopsy for suspected malignancy (lymphoma/squamous cell carcinoma) Re lative Indications ! age 1-4 years: tonsillar hypertrophy leading to sleep apnea > cor pulmonale mouth breathing > malocclusion difficulty swallowing > FTT ! school age: chronic recurrent tonsillitis if > 5 episodes ! any complication of tonsillitis quinsy > parapharyngeal abscess > retropharyngeal abscess Strep bacteremia: rheumatic heart disease, nephritis, arthritis Strep carrier: infective or has halitosis
AIRWAY PROBLEMS IN CHILDREN

DIFFERENTIAL DIAGNOSIS Ne onate s ! extralaryngeal choanal atresia nasopharyngeal dermoid, glioma, encephalocele glossoptosis - Pierre Robin, Down's, lymphangioma, hemangioma ! laryngeal laryngomalacia - most common laryngocele vocal cord palsy (Arnold-Chiari) glottic web subglottic stenosis laryngeal cleft ! tracheal tracheoesophageal fistula tracheomalacia 2-3 Months ! congenital laryngomalacia vascular: innominate artery compression, double aortic arch, subglottic hemangioma laryngeal papilloma ! acquired subglottic stenosis - post intubation tracheal granulation - post intubation tracheomalacia - post tracheotomy and TEF repair Infants - Sudde n Ons e t ! foreign body aspiration ! croup ! caustic ingestion ! epiglottitis Childre n and Adults ! congenital lingual thyroid/tonsil ! infection Ludwig's angina peritonsillar-parapharyngeal abscess retropharyngeal abscess ! neoplastic squamous cell carcinoma (adults): larynx, hypopharynx retropharyngeal: lymphoma, neuroblastoma nasopharyngeal: rhabdomyosarcoma

! allergic angioneurotic edema polyps (suspect cystic fibrosis in children) ! trauma laryngeal fracture, facial fracture burns and lacerations post-intubation caustic ingestion
Note s
SIGNS OF AIRWAY OBSTRUCTION
! symptoms and signs of airway obstruction require a full assessment to diagnose potentially serious causes
Stridor ! note quality, timing ! body position important lying prone: subglottic hemangioma, double aortic arch lying supine: laryngomalacia, inominate artery compression, glossoptosis ! site of stenosis larynx or above: inspiratory stridor trachea: biphasic stridor bronchi/bronchioles: expiratory stridor Re s piratory Dis tre s s ! nasal flaring ! supraclavicular and intercostal indrawing ! sternal retractions ! tachypnea ! cyanosis Fe e ding Difficulty and As piration ! supraglottic lesion ! laryngomalacia ! vocal cord paralysis ! post laryngeal cleft > aspiration pneumonia ! tracheoesophageal fistula
ACUTE LARYNGOTRACHEOBRONCHITIS (CROUP)

! inflammation of tissues in subglottic space +/ tracheobronchial tree ! swelling of mucosal lining and associated with thick viscous, mucopurulent exudate which compromises upper airway (subglottic space narrowest portion of upper airway) ! normal function of ciliated mucous membrane impaired
Etiology ! viral: parainfluenzae I (most common), II, III, influenza A and B, RSV Pre s e ntation ! age 4 months - 5 years ! preceded by URTI symptoms ! generally occurs at night ! biphasic stridor and croupy cough (loud, sea-lion bark) ! appear less toxic than with epiglottitis ! supraglottic area normal ! rule out foreign body and subglottic stenosis ! "steeple-sign" on AP of neck ! if recurrent croup, think subglottic stenosis Tre atme nt ! humidified O2 ! racemic epinephrine via nebulizer q1-2h prn ! systemic corticosteroids (e.g. dexamethasone, prednisone) ! adequate hydration ! close observation for 3-4 hours ! intubation if severe ! hospitalize if poor response to steroids after 4 hours and persistent stridor at rest ! consider alternate diagnosis if poor response to therapy (e.g. bacterial tracheitis)
ACUTE EPIGLOTTITIS
Otolaryngology 34
! acute inflammation causing swelling of supraglottic structures of the larynx without involvement of vocal cords

! 2-5% of laryngeal inflammatory disease ! occurs in northern USA, Europe, and Canada ! highest in December Etiology ! H. influenza type B ! relatively uncommon condition due to Hib vaccine Pre s e ntation ! any age, most commonly 1-4 years ! rapid onset ! toxic-looking, fever, anorexia, restless ! cyanotic/pale, inspiratory stridor, slow breathing, lungs clear with decreased air entry ! prefers sitting up, open mouth, drooling, tongue protruding, sore throat, dysphagia ! rule out severe tonsillitis, peritonsillar abscess, retropharyngeal abscess Inve s tigations and Manage me nt ! investigations and physical examination may lead to complete obstruction, thus preparations for intubation or tracheotomy must be made prior to any manipulation ! ENT/Anesthesia emergency consult(s) ! lateral neck radiograph - cherry-shaped epiglottic swelling ! bag-mask ventilation with Ambu bag prior to endoscopy ! intubate prior to any other treatment ! endoscopy in operating room suite ! WBC (elevated), blood and pharyngeal cultures after intubation Tre atme nt ! IV access with hydration ! antibiotics - IV cefuroxime, cefotaxime, or ceftriaxone ! moist air ! extubate when leak around tube occurs and afebrile ! watch for meningitis
Note s
SUBGLOTTIC STENOSIS
Conge nital ! diameter of subglottis < 4 mm in neonate (due to thickening of soft tissue of subglottic space or maldevelopment of cricoid cartilage) Acquire d ! following nasotracheal intubation due to long duration trauma of intubation large tube size infection Pre s e ntation ! biphasic stridor ! respiratory distress ! recurrent/prolonged croup Diagnos is ! laryngoscopy ! CT Tre atme nt ! if soft tissue - laser and steroids ! if cartilage - wait, do tracheostomy, and laryngotracheoplasty when older
LARYNGOMALACIA
! most common laryngeal anomaly ! elongated omega-shaped epiglottis, short aryepiglottic fold, pendulous mucosa
Pre s e ntation ! high-pitched crowing inspiratory stridor at 6 weeks being constant or intermittent and more pronounced supine

! associated with feeding difficulties ! symptoms gradually subside at 18-24 months as larynx grows and thus requires no treatment
Note s
FOREIGN BODY
Inge s te d ! usually stuck at cricopharyngeus ! coins, toys ! presents with drooling, dysphagia, stridor if very big As pirate d ! usually stuck at right mainstem bronchus ! peanuts, carrot, apple core, popcorn, balloons ! presentation stridor if in trachea unilateral "asthma" if bronchial, and therefore is often misdiagnosed as asthma if impacts to totally occlude airway: cough, lobar pneumonia, atelectasis, mediastinal shift, pneumothorax Diagnos is and Tre atme nt ! bronchoscopy and esophagoscopy with removal
SURGICAL AIRWAY MANAGEMENT
! surgical creation of secondary airway ! laryngotomy also known as cricothyroidotomy 14 gauge needle or IV cannula inserted through cricothyroid membrane ! tracheostomy incision made at the level of 2nd tracheal ring division of strap muscles division +/ ligation of thyroid isthmus removal of circular window of cartilage placement of double lumen tracheostomy tube ! indications to bypass obstruction bronchial toilet long-term ventilation > 1-2 weeks, to prevent endotracheal tube-induced glottic/subglottic stenosis ! complications hemorrhage: innominate artery midline scar subglottic stenosis
DYSPHAGIA
(see Gastroenterology Notes)
Oral Cavity ! viral ulcers (gingivitis): Coxsackie, aphthous, Herpes ! trauma (including caustic ingestion) ! tumour ! Ludwig's angina Oropharynx ! tonsillar carcinoma/tonsillitis/tonsillar hypertrophy/pharyngitis ! retropharyngeal abscess, pharyngeal/palatal paralysis/VPI Hypopharynx/Larynx ! tumour: intrinsic or extrinsic (thyroid mass and other neck masses) ! trauma (including caustic ingestion) ! foreign body ! neuromuscular disturbance pharyngeal/laryngeal paralysis cricopharyngeal spasm ! Plummer-Vinson syndrome ! inflammatory
DYSPHAGIA
. . . CONT.
Note s
Es ophagus ! obstructive (sudden onset with progression) intrinsic hiatus hernia tumour corrosive esophagitis and stricture esophageal web foreign body esophageal diverticulum (Zenkers) extrinsic mediastinal abnormalities vascular compression ! motility (gradual onset) achalasia diffuse esophageal spasm scleroderma diabetic neuropathy ! trauma/perforation His tory ! chronology of the symptoms: acute vs. chronic, static vs. progressive ! liquids, solids or both ! associated symptoms that may give insight to the etiology of the dysphagia such as cough, odynophagia, hoarseness, reflux Phys ical ! assess labial competence for control of oral secretions, foods and fluids ! assess the tongue: sensory and motor functions ! gag reflex ! examine the oro- and hypopharynx, pooling of secretions in the vallecula, pyriform sinuses or oral cavity often indicate swallowing dysfunction, with the amount of pooled secretions signifying the severity of the problem ! examine the larynx and neck Inve s tigations ! soft tissue x-rays of the neck looking for swelling, displacement of airway, presence of foreign body ! chest x-ray: displacement of airway, esophageal air-fluid levels ! dynamic imaging studies: barium pharyngoesophagogram ! assessment of reflux: pH probe manometer, endoscopy ! CT/MRI or U/S Tre atme nt (see Gastroenterology Notes)
DEEP NECK SPACE INFECTIONS

! ! ! ! ! most deep neck space infections (DNSI) contain mixed flora most common cause is odontogenic which will have anaerobes salivary gland infections in adults pharyngeal and tonsillar infections in children note: infections of the retropharyngeal space can spread to the superior mediastinum
Pre s e ntation ! fever, pain, swelling ! +/ trismus, fluctuance, dysphagia, and dental abnormalities ! r/o mediastinitis if associated with dyspnea, chest pain and fever Diagnos is ! CT or MRI ! ultrasound ! chest x-ray may show mediastinal widening if mediastinitis present ! soft tissue lateral x-rays of the neck can be diagnostic for retropharyngeal abscess

Tre atme nt ! with all DNSI assess and secure airway ! identify and drain space, either by incision and drainage or by needle aspiration +/ U/S guidance ! IV antibiotics
. . . CONT.
Note s
PERITONSILLAR ABSCESS (QUINSY)
! cellulitis of space behind tonsillar capsule extending onto soft palate leading to abscess ! can develop from acute tonsillitis ! unilateral, most common in 10-30 year old age group
Etiology ! bacterial: Group A Strep, S. pyogenes, S. aureus, H. influenzae and anaerobes Pre s e ntation ! dysphagia and sore throat ! hot potato voice ! increased salivation and trismus ! referred otalgia ! cervical adenopathy and fever ! extensive peritonsillar swelling but tonsil may appear normal ! uvula deviated across midline ! edema of soft palate Tre atme nt ! surgical drainage (incision or needle aspiration) - do C&S ! tonsillectomy at presentation or 6 weeks later ! IV antibiotics (clindamycin) ! warm saline irrigation
RETROPHARYNGEAL ABSCESS
! in adults secondary to spread from parapharyngeal space due to an abscess or trauma of posterior pharyngeal wall ! infants/children < 2 years old ! in children due to accumulation of pus between posterior pharyngeal wall and prevertebral fascia pus is from breakdown of lymph node in retropharyngeal tissue often secondary to posterior pharyngeal trauma (e.g. ETT or suction in neonate, popsicle stick abrasion in child)
Pre s e ntation ! child infant/child with unexplained fever post URTI with loss of appetite, speech change, or difficulty swallowing stridor ! adult dysphagia odynophagia symptoms of airway obstruction pain and swelling in neck Diagnos is ! lateral soft tissue radiograph showing increased soft tissue between pharyngeal airway and cervical vertebral bodies +/ trapped air ! barium swallow Tre atme nt ! IV antibiotics ! surgery: incision and drainage with airway secured
LUDWIG'S ANGINA
! cellulitis/inflammation of superior compartment of suprahyoid space between geniohyoid and mylohyoid muscles ! causes firmness of floor of mouth, tongue protrudes upward and back causing airway obstruction
Otolaryngology 38

Etiology ! dental infection (anaerobic bacilli + Vincents spirochete) ! suppurative lymph node in submaxillary space
. . . CONT.
Note s
Tre atme nt ! incision through midline and prepare for possible tracheostomy because of the difficulty in intubation ! IV penicillin + metronidazole
ACUTE TONSILLITIS and TONSILLECTOMY

(see Pediatric ENT Section)
HOARSENESS
Clinical Pe arl ! If hoars e ne s s pre s e nt for > 2 we e ks in a s moke r, laryngos copy mus t be done to rule out cance r ! Acute < than 2 we e ks , chronic > 2 we e ks
Infe ctious ! acute viral laryngitis ! bacterial tracheitis/laryngitis ! laryngotracheobronchitis (croup) Inflammatory ! from gastro-esophageal reflux, smoke irritation, or chronic cough vocal cord polyps Reinkes edema contact ulcers or granulomas vocal cord nodules Trauma ! external laryngeal trauma ! endoscopy and endotracheal tube Ne oplas ia ! benign tumours vocal cord polyps papillomas chondromas, lipomas, hemangiomas ! malignant tumours squamous cell carcinoma Kaposis sarcoma Cys ts ! retention cysts ! laryngoceles Sys te mic ! endocrine hypothyroidism virilization ! connective tissue disease rheumatoid arthritis, SLE ! angioneurotic edema Ne urologic (vocal cord paralys is ) ! central lesions CVA head injury MS Arnold-Chiari neural tumours
HOARSENESS
. . . CONT.
Note s
! peripheral lesions tumours: glomus jugulare, thyroid, bronchogenic, esophageal, neural surgery: thyroid surgery, cardiovascular or thoracic/esophageal surgery cardiac: left atrial enlargement, aneurysm of aortic arch ! neuromuscular myasthenia gravis presbylaryngeus spastic dysphonia Functional ! psychogenic aphonia (hysterical aphonia) ! habitual aphonia ! ventricular dysphonias
ACUTE LARYNGITIS
Etiology ! viral +/ URTI - influenza, adenovirus, GAS ! voice abuse ! toxic fume inhalation Pre s e ntation ! URTI symptoms and hoarseness, aphonia, cough attacks, +/ dyspnea ! indirect laryngoscopy shows true vocal cords erythematous and edematous with vascular injection and normal cord mobility Tre atme nt ! self-limited ! voice rest with humidification to prevent further irritation of inflamed cords ! removal of irritants (e.g. smoking) ! if bacterial - treat with antibiotics
CHRONIC LARYNGITIS
! long standing inflammatory changes in laryngeal mucosa
Etiology ! repeated attacks of acute laryngitis ! exposure to irritating dust/smoke ! voice abuse ! esophageal disorders: Zenker's diverticulum/hiatus hernia/GERD ! systemic: allergy, hypothyroidism, Addison's Pre s e ntation ! longstanding hoarseness and vocal weakness - rule out malignancy ! indirect laryngoscopy - cords erythematous, thickened with normal mobility Tre atme nt ! remove offending cause ! treat related disorders ! speech therapy with voice rest ! +/ antibiotics, +/ steroids to decrease inflammation
VOCAL CORD POLYPS
! commonest benign tumour of vocal cords usually in men between 30 and 50 years of age
Etiology ! vocal abuse ! agents causing laryngeal inflammation Pre s e ntation ! hoarseness, aphonia, cough attacks +/ dyspnea ! laryngoscopy shows polyp on free edge of vocal cord on a pedicle or sessile Tre atme nt ! remove with endoscopic laryngeal microsurgery
Otolaryngology 40
HOARSENESS
. . . CONT.
Note s
VOCAL CORD NODULES

Etiology ! chronic voice abuse ! URTI, smoke, alcohol
! called screamers or singers nodules ! more frequently occur in females, singers and children
Pre s e ntation ! laryngoscopy shows red, soft looking nodules, often bilateral at the junction of the anterior and middle 1/3 of vocal cords ! chronic nodules may become fibrotic, hard and white Tre atme nt ! voice rest ! speech therapy ! avoidance of aggravating factors ! surgery is rarely indicated
BENIGN LARYNGEAL PAPILLOMAS

Etiology ! human papilloma virus types 6, 11 ! ?hormonal influence
! biphasic distribution - birth to puberty (most common laryngeal tumour) and adulthood
Pre s e ntation ! hoarseness and airway obstruction ! can seed into tracheobronchial tree ! recurs after treatment ! some juvenile papillomas resolve spontaneously at puberty ! papillomas in adults may undergo malignant degeneration ! laryngoscopy shows wart-like lesions in supraglottic larynx and trachea Tre atme nt ! CO2 laser and microsurgery ! +/ interferon if pulmonary involvement
LARYNGEAL CARCINOMA (see Neoplasms of the Head and Neck Section)
SALIVARY GLANDS
SIALOADENITIS
Etiology ! obstructive vs. non-obstructive ! bacterial: (commonly S. aureus) patient prone to bacterial infection when salivary flow is decreased or obstructed ! viral: most common infectious cause Pre s e ntation ! acute onset of pain and edema of parotid or submandibular gland that may lead to marked swelling ! +/ fever ! +/ leukocytosis ! +/ suppurative drainage from punctum of the gland ! mumps usually presents with bilateral parotid enlargement, +/ sensorineural hearing loss, +/ orchitis Diagnos is ! imaging with U/S employed to differentiate obstructive vs. non-obstructive sialadenitis
SALIVARY GLANDS
. . . CONT.
Note s
Tre atme nt ! bacterial: treat with cloxacillin +/ abscess drainage ! viral: no treatment
SIALOLITHIASIS
! ductal stone with chronic sialadenitis ! predisposing factors are any conditions causing duct stenosis or a change in salivary secretions (e.g. dehydration, diabetes, EtOH, hypercalcemia)
Pre s e ntation ! pain and tenderness over involved gland ! intermittent swelling related to meals Diagnos is ! by digital palpation of calculi ! sialogram Tre atme nt ! remove calculi by dilating duct and orifice or excision through floor of mouth ! if calculus is within the gland parenchyma then the whole gland must be excised
SALIVARY GLAND MANIFESTATIONS OF SYSTEMIC DISEASE
! Sjgrens syndrome: diffuse non-tender, asymptomatic enlargement of the parotid glands and occasionally other salivary glands ! bulimia nervosa: bilateral swelling of parotid glands, approximately 30% of patients will have resolution with control of bulimia
NECK MASSES
The stemocleidomastoid divides the neck into two triangles, the boundaries of which are shown. The anterior triangle contains lymph nodes, submandibular gland, tail of the parotid, and the carotid bifurcation. The posterior tnangle contains lymph nodes and the spinal accessory nerve.
Figure 13. Anatomical Triangle s and Lymphatic Drainage of the Ne ck

! duration if 7 days: inflammatory if 7 months: neoplastic if 7 years: congenital Conge nital ! midline thyroglossal duct cyst thyroid tumour/goitre pyramidal lobe of thyroid gland midline dermoid cyst thymus cyst Otolaryngology 42
NECK MASSES
! lateral branchial cleft cyst cystic hygroma Acquire d
. . . CONT.
Note s
Table 7. Acquire d Caus e s of Ne ck Lumps

Age (ye ars ) < 20 20-40 Pos s ible Caus e s of Ne ck Lump inflammatory neck nodes (e.g. tonsillitis, infectious mononucleosis) lymphoma salivary gland pathology (e.g calculi, infection, tumour) thyroid pathology (e.g. goitre, infection, tumour) granulomatous disease (e.g. TB, sarcoidosis), HIV 1 or 2 malignant disease
> 40
EVALUATION
Inve s tigation ! history and physical ! indirect tests - supply information about physical characteristics of mass WBC - infection vs. lymphoma Mantoux TB test thyroid function tests and scan neck U/S CT scan angiography - vascularity and blood supply to mass ! direct test - for histologic examination fine needle aspiration - less invasive needle biopsy open biopsy-for lymphoma search for the primary tumour full otolaryngologic exam - including nasopharynx and larynx radiologic exam of stomach, bowel and sinuses panendoscopy nasopharyngoscopy laryngoscopy bronchoscopy with brushings esophagoscopy biopsy of normal tissue of nasopharynx, tonsils, base of tongue and hypopharynx ! if primary still occult (5%) - excisional biopsy of node for diagnosis, manage with radiotherapy or neck dissection (squamous cell carcinoma) ! if primary found, stage and treat
CONGENITAL NECK MASSES

Branchial Cle ft Cys ts /Fis tulae (s e e Colour Atlas I4) ! at 6th week of development, the second branchial arch grows over the third and fourth arches and fuses with the neighbouring caudal pre-cardial swelling forming the cervical sinus ! branchial fistula formed by persistence of external opening of sinus while persistent parts of the cervical sinus without an external opening cause branchial cysts ! 2nd branchial cleft cysts most common ! fistulas with an internal or external communication usually manifest during infancy as a small opening anterior to the sternocleidomastoid muscle ! branchial cysts that do not have an external or internal opening present in teens and twenties as a smooth painless slowly enlarging lateral neck mass, often following an acute URTI infection ! surgical removal of cyst or fistula tract ! if infected - allow infection to settle before removal Thyroglos s al Duct Cys ts (s e e Colour Atlas I3) ! thyroid originates as ventral midline diverticulum of floor of pharynx caudal to junction of 1st and 2nd branchial arches (foramen cecum) ! thyroid migrates caudally along a tract ventral to hyoid then curves underneath and down to cricoid with thyroglossal duct cysts being vestigial remnants of tract
NECK MASSES
. . . CONT.
Note s
! usually presents in the second to fourth decades as a midline cyst that elevates with swallowing and tongue protrusion ! treatment consists of pre-operative antibiotics to reduce inflammation followed by complete excision of cyst and tract up to foramen cecum at base of tongue with removal of central portion of thyroid (Sistrunk procedure) Cys tic Hygroma ! lymphangioma arising from vestigial lymph channels of neck ! usually presents by age 2 as thin-walled cyst in tissues from floor of mouth down to mediastinum, usually in posterior triangle or supraclavicular area ! infection causes a sudden increase in size ! surgical excision if it fails to regress - difficult dissection due to numerous cyst extensions
NEOPLASMS OF THE HEAD AND NECK

Table 8. Summary of He ad and Ne ck Ne oplas ia
Location Nos e /Paranas al Sinus Nas opharynx Pre s e ntation depends on where tumour has invaded through bone nasal obstruction neck mass epistaxis unilat. SOM white patch on lip lip Ulcer painless mass Ris k/Etiological Factors hardwood dust nickel chromium EBV salted fish nickel exposure poor hygiene UV light poor hygiene smoking/EtOH radiation nickel exposure smoking/EtOH smoking/EtOH poor hygiene Diagnos is clinical suspicion on CT biopsy flexible scope biopsy CT/MRI biopsy Tre atme nt surgery + radiation
1 radiation surgery 2nd line
Lip
1 surgery radiation 2nd line surgery
Salivary Gland
fine needle biopsy CT biopsy
Oral Cavity
neck mass ulcer +/ bleeding dysphagia/sialorrhea dysphonia odynophagia otalgia enlarged tonsil fixed tongue with trismus pain and dysphagia otalgia cervical node hoarseness dysphagia, otalgia odynophagia hoarseness foreign body feeling dyspnea/stridor cough/hemoptysis thyroid mass vocal cord paralysis cervical nodes hyper/hypo thyroid
1 surgery radiation 2nd line
Oropharynx
smoking and EtOH
biopsy
Hypopharynx
smoking and EtOH
rigid scope CXR CT indirect and direct laryngoscopy CT
Larynx
smoking and EtOH
Thyroid
radiation exposure family hx
see figure 16
1 surgery I131 for metastatic deposits
! 6-8% of all malignancies in the body ! historically M>F however increased incidence in female population in last 10-15 years due to increased prevalence of smoking in females
Otolaryngology 44
NEOPLASMS OF THE HEAD AND NECK . . . CONT.

PRINCIPLES OF MANAGEMENT
! initial metastatic screen includes chest x-ray and LFTs; ! scans of liver, brain and bone only if clinically indicated ! TNM classification widely used for staging in order to: guide treatment planning indicate prognosis assist in evaluating results of treatment facilitate accurate exchange of information ! treatment depends on histologic grade of tumour stage physical and emotional situation of patient facilities available skill and experience of the oncologist and team ! in general no role for chemotherapy in tumours of the head and neck primary surgery for malignant tumours of the oral cavity with radiotherapy reserved for salvage or for poor prognostic indicators primary radiotherapy for malignancies of the nasopharynx, oropharynx, hypopharynx, and larynx with surgery reserved for salvage ! rare tumours with decreased incidence over the last 5-10 years ! increased incidence in Africans, Japanese, and Arabs ! risk factors - dust from hard woods (ethmoid sinus and nose), nickel (maxillary sinus cancer), chromium ! 99% occur in maxillary and ethmoid sinuses ! 75-80% squamous cell carcinoma ! 10% arise from minor salivary glands (i.e. adenoid cystic + mucoepidermoid) ! 10% sarcomas
Note s
CARCINOMA OF THE NOSE AND PARANASAL SINUSES
Pre s e ntation ! symptoms begin to occur after tumour has invaded through the bony confines of the sinus ! depends where the erosion through bone has occurred nose - nasal obstruction, epistaxis, pain orbit - proptosis, diplopia, ophthalmoplegia, pain, epiphora due to nasolacrimal duct obstruction nerves - numbness, palatal palsy, CN VII palsy, facial pain dental - tooth/oral pain, loosening of teeth skin - occurs late intracranial or skull base extension - headache Diagnos is ! based on clinical suspicion ! confirmed with CT or MRI (CT used routinely) ! biopsy for histopathology Tre atme nt ! almost all sinus cancers are treated with a combined approach involving surgery and post-operative radiotherapy Prognos is ! overall 5-year survival = 25% (poor due to late presentation) 55% if inferior antral involvement only
CARCINOMA OF THE NASOPHARYNX
! the nasopharynx is the cuboidal space bounded anteriorly by the posterior choanae of the nose, posteriorly by the clivus, C1 and C2 vertebrae, superiorly by the body of the sphenoid and inferiorly by the soft palate ! the eustachian tubes open onto the lateral walls of the NP which are comprised of pharyngeal fascia ! incidence 0.8/100 000; markedly increased among those of South Chinese origin ! 50-59 year old age group, M:F = 2.4:1
Otolaryngology 45

! etiological factors include EBV salted fish consumption, nickel , exposure, poor hygiene ! squamous cell carcinoma most common (approximately 90%) ! lymphoma (approximately 10%) Pre s e ntation ! neck mass at presentation in 60-90% (note: deep posterior cervical node at mastoid tip) ! nasal obstruction/discharge, epistaxis ! voice change, mandibular neuralgia, decrease in soft palate mobility, dysphagia ! unilateral serous otitis media and/or hearing loss ! proptosis (secondary to tumour extension into orbit) ! cranial nerve involvement in approximately 25% (CN III-VI can be involved by cavernous sinus extension; CN IX-XII can be involved by retropharyngeal space encroachment or lymphadenopathy) Diagnos is ! clinical findings (include digital palpation) ! flexible nasopharyngoscopy for direct visualization ! biopsy with topical anesthetic ! CT/MRI for assessment of extent of tumour invasion and involvement of adjacent structures Tre atme nt ! primary radiotherapy of nasopharynx and adjacent parapharyngeal and cervical lymphatics is the treatment of choice ! +/ radical neck dissection for salvage and recurrence ! use of chemotherapy controversial Prognos is ! excellent local control possible for T1 lesions (90-95% control rates reported) ! 5 year survival rates vary according to stage: I: 78%; II: 72%; III: 50-60%; IV: 36-42%
Note s
CARCINOMA OF THE LIP

! ! ! ! 50-70 year age group whites > blacks M:F = 30:1 95% squamous cell carcinoma
Etiology ! UV light - to lower lip ! poor oral hygiene ! smoking and alcohol contribute but are less significant than in other head and neck SCC Pre s e ntation ! 85% lower lip ! dyskeratosis manifests as white patch on lip (actinic chelitis) ! ulcer formation may indicate carcinoma Diagnos is ! biopsy Tre atme nt ! primary surgery including wedge excision with primary closure and careful approximation of vermilion border ! local flap may be required to repair an extensive surgical defect ! radiotherapy second line - for salvage or extensive disease Prognos is ! 85% 5-year survival following surgery ! 80% 5-year survival following radiation therapy
Otolaryngology 46

SALIVARY GLAND NEOPLASMS
! ! ! ! M=F 80% of salivary gland tumours are parotid submandibular tumours uncommon (10%), sublingual rare (1%) only 20% of parotid swellings are malignant, whereas 75% of submandibular gland swellings are malignant, generally the smaller the gland the greater chance of malignancy
Note s
Pathology ! malignant mucoepidermoid (low vs. high grade) 40% adenoid cystic 30% acinic cell 5% malignant mixed 5% lymphomas 5% adenocarcinoma ! benign benign mixed (pleomorphic adenoma) 80% Warthin's tumour (5-10% bilateral M>F) 10% cysts, lymph nodes and adenomas 10% Parotid Gland ! painless slow-growing mass ! if bilateral, suggests benign process (Warthin's tumour, Sjgren's, mumps) or possible lymphoma ! signs suggestive of malignancy pain or CN VII involvement rapid growth involvement or invasion of overlying skin facial nerve dysfunction cervical lymphadenopathy Diagnos is ! fine needle biopsy ! CT scan to determine depth of tumour Tre atme nt ! surgery is the treatment of choice for salivary gland neoplasms ! benign tumours are also excised due to small but potential risk of malignant transformation of pleomorphic adenoma ! superficial lesion superficial parotidectomy above plane of CN VII, +/ radiation incisional biopsy contraindicated ! deep lesion near-total parotidectomy sparing as much of CN VII as possible if CN VII involved then it is removed and cable grafted with sural nerve, or hypoglossal attached to remaining stump Prognos is ! benign: excellent, although pleomorphic adenomas may recur ! mucoepidermoid: good if low grade - 80% 5-year survival ! others: fair, but tend to recur - 40% 5-year survival ! if neck nodes involved: 20% 5-year survival
CARCINOMA OF THE ORAL CAVITY
! oral cavity consists of the anterior/oral tongue, the floor of mouth, the alveolus, the retromolar trigone, and the hard palate above ! 1.5-3% of all cancers occurring in North America ! 50% of oral cavity cancer occurs on the anterior 2/3 of the tongue ! historically, far more prevalent among males, but recent increase in female smokers has changed this ! 50 to 60 year old age group (younger trend in recent years) ! 95% squamous cell (others include salivary gland: mucoepidermoid, adenoid cystic, acinic cell, also sarcoma and melanoma)
Otolaryngology 47

Etiology ! heavy smoking (note smokeless tobacco) ! alcohol (synergistic with tobacco) ! association with poor oral hygiene, chronic dental irritation, oral lichen planus, mucosal atrophy ! leukoplakia or erythroplakia may signify pre-malignant lesion or carcinoma in situ Pre s e ntation ! 30% present as an asymptomatic mass in the neck ! ulcer with raised edges +/ bleeding ! pain with radiation to ear and neck ! dysphagia or dysphonia may occur ! oral fetor ! sialorrhea ! 10-15% of oral cavity tumours have cervical metastases at time of presentation ! lymph node mets in tumours of tongue and anterior floor of mouth tend to involve the submental and upper deep jugular chains ! purplish brown lesions on palate or buccal mucosa suggest Kaposi's sarcoma in HIV patients Diagnos is ! adequate visualization is key ! small local biopsy of lesion ! imaging studies generally not required unless mandibular involvement is suspected or planning extensive resection Tre atme nt ! carcinoma of the oral cavity is primarily a surgical problem with post-operative radiotherapy reserved for patients with poor prognostic indicators (see below) ! primary radiotherapy occasionally employed in older or infirm patients ! surgery consists of: partial/total glossectomy +/ mandibular resection neck dissection if > 2 cm lesion or palpable nodes reconstruction: none (if small defect), skin grafts, fascio/ osseocutaneous vascularized free flaps, dental plates Prognos is ! poor prognostic indicators include: site of tumour (tongue worse than floor of mouth) and deep invasion multiple positive cervical nodes extra-capsular spread peri-neural or peri-vascular involvement close (< 5 mm) surgical margins ! early stage (T1 and T2) 75% disease free survival at 5 years ! late stage (T3 and T4) 30-35% disease free survival at 5 years ! no change in mortality in last 15-20 years but significant decrease in morbidity due to new reconstructive and rehabilitative techniques
Note s
CARCINOMA OF THE OROPHARYNX
! oropharynx consists of the tongue base (area behind the circumvallate papillae) to the back of the pharynx including the tonsillar fossae and pillars, and the soft palate down to the superior aspect of the supraglottis ! M:F = 4:1 ! 50 to 70 year old age group ! etiologic agents include alcohol abuse and smoking ! 90% squamous cell carcinoma - poorly differentiated
Pre s e ntation ! tend to present late (especially tongue base) ! odynophagia ! otalgia ! indistinct speech - hot potato voice ! ulcerated/enlarged tonsil ! oral fetor ! bleeding with blood-stained sputum

! tongue fixed with trismus ! induration of tonsil or tongue base ! 60% have nodal metastases at presentation (15% bilateral) - including small lesions ! parapharyngeal and retropharyngeal nodes at risk ! 7% distant metastases to lung, bone and liver Diagnos is ! clinical suspicion ! confirmatory biopsy Tre atme nt ! radiotherapy is primary modality with surgery reserved for salvage ! surgery depends on extent of disease and may employ composite resection, +/ neck dissection and flap reconstruction ! radiotherapy preferred modality due to high morbidity associated with surgery and inaccessibility of at-risk nodal groups Prognos is ! site dependant ! base of tongue: control rates for T1 lesions reported at >90%, however poor control rates (13-52%) reported for T4 lesions ! tonsils: cure rates of 90-100% reported for T1 and T2 lesions using external beam radiation; control rates for advanced lesions are very poor - 15-33% reported for T4 lesions
Note s
CARCINOMA OF THE HYPOPHARYNX
! continuous with the oropharynx above and extending inferiorly to the esophagus, the hypopharynx includes the area from the tip of the epiglottis to the lower surface of the cricoid cartilage ! 3 areas: 1) posterior pharyngeal wall (10% of tumours); 2) piriform sinus (60%); 3) post-cricoid space (30%) ! 8-10% of all head and neck malignancies ! 95% squamous cell carcinoma ! 50-60 year old age group; M>F ! etiological factors include alcohol, tobacco ! associated with Plummer-Vinson syndrome (post-cricoid region)
Pre s e ntation ! often presents late ! pain ! dysphagia ! otalgia ! cervical node ! +/ hoarseness Diagnos is ! clinical suspicion - definitive diagnosis often by rigid endoscopy ! chest x-ray to rule out pulmonary mets ! CT to evaluate deep extension Tre atme nt ! radiation employed as primary modality ! rigid endoscopy to determine 8-10 week post-treatment response ! favorable response to radiotherapy can be followed for 5-10 years ! if radiation fails: surgical resection of larynx and hypopharynx +neck dissection ! reconstructive options include closure of the pharynx, pedicle flap reconstruction (e.g. pectoralis major) free jejunal interposition, and gastric pull-up Prognos is ! generally poor: 60% cure rates have been reported for T2-T3, 25-40% five year survival with T4 lesions ! post-operative morbidity with fistula formation in 20-25% of previously irradiated patients ! gastric pull-up associated with 14% peri-operative mortality
Otolaryngology 49

CARCINOMA OF THE LARYNX
Note s
The commone st symp tom for e ach re gion of the larynx is illustrate d . Enlarge me nt will re sult in ad d itional symp toms d ue to sp re ad to ad jace nt or me tastatic d ise ase . (NG. ne op lastic growth)
Figure 14. Symptoms of Larynge al Ne oplas ia

! ! ! ! !
squamous cell most common 45% of head and neck carcinoma common between 45-75 years of age M:F = 10:1 etiologic agents include heavy smoking and heavy alcohol consumption
Clas s ification ! classified according to site within larynx: supraglottic (30-35%) rich in lymphatics early nodal spread with 30-40% having occult or palpable neck disease at presentation primary tumour enlarges substantially before causing symptoms glottic (60-65%) few lymphatic channels nodal metastasis rare tumour remains local for a long period produces hoarseness early giving a better prognosis subglottic (1%) abundant lymphatics, lateral neck and paratracheal nodes are involved at presentation in 20% symptoms occur late may be difficult to distinguish if primary tumour arises in subglottis or in trachea Pre s e ntation ! dysphagia, odynophagia or referred otalgia (suggest supraglottic lesion) ! hoarseness (suggests glottic involvement) ! clearing throat/foreign body feeling ! dyspnea/stridor ! cough/hemoptysis ! regional lymphadenopathy Diagnos is ! direct and indirect laryngoscopy to assess site and extent of tumour and cord mobility ! bilateral nodal metastasis more common if carcinoma crosses midline ! CT/MRI imaging: to assess depth of spread and involvement of underlying cartilage Tre atme nt ! organ preservation is goal of therapy ! primary radiotherapy for all laryngeal carcinomas except for bulky T4 lesions with radiographic evidence of cartilaginous involvement ! surgery reserved for salvage or for late stage lesions microsurgical decortication of vocal cords cordectomy partial to total laryngectomy with tracheostomy +/ neck dissection

! voice and speech rehabilitation options tracheo-esophageal puncture to allow phonation esophageal voice electrolaryngeal devices Prognos is ! 10-12% of small lesions will fail radiotherapy and can be treated with partial laryngectomy and muscle flap rehabilitation ! glottic lesions:> 90% of early lesions (mobile cords) controlled with primary radiation; this drops to 30-60% with cord fixation ! 70% of T3 supraglottic lesions controlled by radiation alone ! 5 year survival of > 40% has been reported for T4 lesions following laryngectomy and post-operative radiation
Note s
THYROID NEOPLASMS
Diffe re ntial Diagnos is ! benign colloid nodule multinodular goitre (hyperplastic or regenerative nodule) thyroid cyst follicular adenoma thyroiditis ! malignant (16% of thyroid nodules) papillary carcinoma 60-70% follicular carcinoma 15-20% medullary carcinoma 2-5% anaplastic 1-5% Hrthle cell 1-5% lymphoma 3% metastatic 1-2% His tory ! F > M for nodules but in males a nodule is more likely to be malignant ! history of head and neck irradiation ! occupational/environmental radiation exposure associated with papillary carcinoma ! local compressive neck symptoms - hoarseness, dysphagia, dyspnea, and aspiration ! family history of MEN II (medullary ca.) ! nodule in patient with a history of Hashimotos - at risk for lymphoma ! rapid increase in size of nodule - may indicate malignancy Phys ical Findings ! palpation of thyroid - solitary, hard, irregular nodule is suggestive of malignancy, multinodular suggestive of benign indirect laryngoscopy vocal cord paralysis increases suspicion of malignancy ! cervical lymphadenopathy - deep cervical chain suggestive of metastatic disease ! signs of hypo/hyperthyroidism
THYROID CARCINOMA
Papillary Ade nocarcinoma ! accounts for 60-70% of thyroid cancers ! can be multifocal ! lymphatic spread ! presents in early adulthood as a solitary nodule with 20% having palpable lymph nodes ! late metastases to lungs or bone ! rate of growth may be stimulated by TSH ! microscopically - papillary projections of columnar epithelium with nuclear notching, cytoplasmic inclusions, and 60% having Psammoma bodies (a mixed papillary-follicular or follicular variant also found) ! 84% 10 year survival
Otolaryngology 51

Follicular Ade nocarcinoma ! 10% of thyroid malignancies ! presents in later adulthood as an elastic/rubbery nodule ! pathological diagnosis can only be made by permanent section ! regional lymph node spread ! hematogenous spread to lung, bone and liver (can be ablated with radioactive iodine after total thyroidectomy) ! prognosis dependent on invasion, not on size ! 57% 10 year survival Me dullary Carcinoma ! 2-5% of thyroid malignancies, 10% familial, 90% sporadic ! contains amyloid and is solid, hard and nodular with poor radioiodine uptake ! derived from cells of ultimobranchial bodies which also secrete calcitonin ! familial occurrence associated with type IIa multiple endocrine neoplasia with bilateral pheochromocytoma and hyperparathyroidism ! screen family members with serum calcitonin and pentagastrin stimulation, and now ret oncogene mutation detections ! 40% 10 year survival Anaplas tic Carcinoma ! 5% of thyroid malignancies, principally elderly ! rapidly enlarging, solid, hard, irregular tumour often with cystic components which invades surrounding neck structures and may cause pain and obstructive symptoms ! cervical lymph node metastasis with lung metastases common ! usually recurs following surgery with radiation and chemotherapy being palliative and radioiodine ineffective ! average survival - 10 months Tre atme nt of Thyroid Carcinoma ! total thyroidectomy for papillary (> 1.5 cm), medullary and follicular tumours - risks include damage of recurrent and superior laryngeal nerves, hemorrhage, and permanent hypoparathyroidism ! neck dissection with preservation of sternocleidomastoid if lymph nodes clinically involved and radical neck dissection if extensive infiltrating tumour ! metastatic deposits of follicular and papillary tumours treated with I131 following thyroid ablation ! maintain patients on suppressive doses of thyroxine ! follow-up with serum thyroglobulin - increased if residual tumour present
Thyroid Nodule Hx, Px, TSH, T4, thyroglobulin antithyroid antibody U/S* FNA (if do U/S still must do a FNA) benign inflammatory cells or indeterminant repeat papillary (false postive < 1%) OR cystic T4 suppression follicular or indeteminant (high false negative) U/S solid thyroid scan cold short term T4 suppression functioning (warm) longer term T4 suppression
Note s
T4 suppression
Figure 16. Inve s tigation and Manage me nt of the Thyroid Nodule

* U/S findings: cystic: risk of malignancy < 1%, solid: risk of malignancy approx. 10%, solid with cystic components: risk of malignancy same as if solid
Otolaryngology 52

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OTOLARYNGOLOGY

MCCQE 2000 Re vie w Note s and Le cture Se rie s

Figure 1. Normal Appe arance of Tympanic Me mbrane on Otos copy

HYPOPHARYNX AND LARYNX

Base of tongue Epiglottis

True vocal cord False vocal cord

Figure 2. Appe arance of Normal Larynx on Indire ct Laryngos copy

OTHER AREAS OF EXAMINATION

ANATOMY OF THE EAR

MCCQE 2000 Re vie w Note s and Le cture Se rie s

MCCQE 2000 Re vie w Note s and Le cture Se rie s

Inte rpre tation X = AC Unmasked > = BC Unmasked [ ] = AC Masked ] = BC Masked

0 10 20 30 40 50 60 70 80 90 100 110 120

HEARING LEVEL (dB)

HEARING LEVEL (dB)

30 40 50 60 70 80 90 100 110 120

Figure A. Normal Audiogram

Figure B. Conductive He aring Los s (Otitis Me dia)

X> X> > X

HEARING LEVEL (dB)

40 50 60 70 80 90 100 110 120

100 110 120

Figure C. Conductive He aring Los s (Otos cle ros is )

Figure D. Se ns orine ural He aring Los s (Nois e Induce d)

Figure E. Se ns orine ural He aring Los s (Pre s bycus is )

Figure 4. Type s of He aring Los s

MCCQE 2000 Re vie w Note s and Le cture Se rie s

AUDITORY BRAINSTEM RESPONSE (ABR)

TUNING FORK TESTS

MCCQE 2000 Re vie w Note s and Le cture Se rie s

ACUTE OTITIS MEDIA AND OTITIS MEDIA WITH EFFUSION

Colour Atlas I7) ! keratinized squamous epithelium in middle-ear or mastoid

CONGENITAL SENSORINEURAL HEARING LOSS

SUDDEN SENSORINEURAL HEARING LOSS (UNILATERAL)

MCCQE 2000 Re vie w Note s and Le cture Se rie s

NOISE-INDUCED SENSORINEURAL HEARING LOSS

TEMPORAL BONE FRACTURES

Figure 5. Type s of Te mporal Bone Fracture s

Table 2. Fe ature s of Te mporal Bone Fracture s

MCCQE 2000 Re vie w Note s and Le cture Se rie s

MCCQE 2000 Re vie w Note s and Le cture Se rie s

Figure 6. Re fe rre d or Non-Otological Otalgia

MCCQE 2000 Re vie w Note s and Le cture Se rie s

FACIAL NERVE PARALYSIS

dislocated septum choanal atresia

MCCQE 2000 Re vie w Note s and Le cture Se rie s

Table 5. Nas al Dis charge : Characte r and As s ociate d Conditions

Middle meatus Inferior meatus

Middle turbinate Septum Inferior turbinate

Figure 7. Normal Appe arance of Nas al Cavity on Spe culum Exam

Figure 8. Caus e s of Rhinitis

ALLERGIC RHINITIS (HAY FEVER)

MCCQE 2000 Re vie w Note s and Le cture Se rie s

ADENOID HYPERTROPHY (see Pediatric ENT Section) NASAL POLYPS

Kiesselbachs plexus branch from superior labial

septal branch of sphenopalatine greater palatine

Figure 9. Nas al Se ptum and its Blood Supply

MCCQE 2000 Re vie w Note s and Le cture Se rie s

Figure 10. The Paranas al Sinus e s