pneumoniae,group A (5-hemolytic Streptococcus)
fungal infection (e.g. Aspergillus,Zygomycetes,Candida)
systemic physiologic factors
allergy/allergic rhinitis,
chronic inflammatory disorder (e.g.GPA)
Allergic Fungal Rhinosinusitis
- A chronic sinusitis affecting mostly
young,immunocompetent atopic
individuals
• Treatment options include FESS
± intranasal topical steroids and
immunotherapy
Management
• identify and address contributing or predisposing factors
• obtain CT or perform endoscopy
• if polyps present:1NCS, oral steroids ± antibiotics (ifsigns of infection), refer to otolaryngologist/
H&N surgeon
• if polyps absent:INCS, antibiotics,saline irrigation, oralsteroids (severe cases)
• antibiotics for 3-6 wk
• amoxicillin-clavulanic acid,fluoroquinolone (moxifloxacin), macrolide (clarithromycin),
clindamycin, metronidazole
• surgery if medical therapy fails or fungal sinusitis:HSS, balloon sinuplasty
ESS - Endoscopic Sinus Surgety
Opening of the paranasal sinuses in
order to facilitate drainage while sparing
the sinus mucosa
Complications
• same as acute sinusitis, mucocoele
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Epistaxis
Blood Supply to the Nasal Septum {seeFigure 4, 073)
1.superior posteriorseptum
internal carotid -> ophthalmic -> anterior/posterior ethmoidal
2.posteriorseptum
external carotid -> internal maxillary -> sphenopalatine
3.lower anteriorseptum
external carotid -> facial artery -> superior labial artery -> nasal branch
• external carotid -> internal maxillary -> descending palatine -> greater palatine
• vessels anastomose to form Kiesselbach’s plexus, located in Little'
s area (anterior-inferior portion of
the cartilaginous septum)
90% of nosebleeds occur in Little'
sarea
Table 14. Etiology of Epistaxis Special Cases
• Adolescent male with unilateral
recurrent epistaxis:consider juvenile
nasopharyngeal angiofibroma (JNA):
this is the most common benign
tumour of the nasopharynx
• Thrombocytopenic patients:use
resorbable packs to avoid risk of
re-bleeding caused by pulling out (he
removable pack
Type Causes
Primary Epistaxis Idiopathic or spontaneous
Secondary Epistaxis
local Trauma (most common)
Fractures:facial, nasal
Sell-induced: digital, lorcign body
Tumours
Benign: polyps, inserting papilloma, angiofibroma
Malignant:SCC.esthesioncuroblastoma (olfactory
neuroblastoma)
Inflammation
Rhinitis: allergic, non-allergic
Infections: bacterial, viral, fungal
Iatrogenic: nasal,sinus, orbitsurgery
Nasal dryness: dry air, supplemental nasal oxygen
Structural abnormalities:septal deviation, chronic
septal perforation
Chemical:nasal cocaine, nasal sprays, etc.
Coagulopathies
Medications: anticoagulants, NSAIDs
Hemophilias, von Willobrand disease
Hematological malignancies
liver failure, uremia
Vascular: KIN.atherosclerosis, Osler-Weber-Rendu disease (hereditary hemorrhagic telangiectasia)
Others:OPA.SIE
Systemic
Investigations
• CBC, PT/PTT/INR/platelet function assay (if suspicious ofbleeding disorder)
• CT as needed
Treatment
• locate bleeding and achieve hemostasis
1. ABCs
• lean patient forward to minimize swallowing blood and avoid airway obstruction
• apply constant firm pressure for 15 to 20 min on cartilaginous part of nose (not bony pyramid) while
the head isin neutral position
• ifsignificant bleeding, assess vitals for signs of hemorrhagic shock ± IV NS, cross-match blood
2. Determine Site of Bleeding
• anterior/posterior hemorrhage defined by location in relationship to bony septum
• visualize nasal cavity with speculum
• use cotton pledget with topical lidocaine ± topical decongestant (Otrivin*) to help identify area of
bleeding (often anteriorseptum)
3. Control the Bleeding
• first-line:topical decongestant (Otrivin*)
if first-line fails and bleeding source adequately visualized, cauterize with silver nitrate
• do not cauterize both sides of the septum at one time due to risk ofseptal perforation from loss of
septal blood supply
A. Anterior hemorrhage treatment
if failure to achieve hemostasis with cauterization
place anterior pack with expandable nasal tampons (Merocel*) or fabric sponges (Rapid
Rhino Riemann)*
considerlubricated absorbable packing (e.g. Gelfoam wrapped in Surgicel*) for patients with
coagulopathy or on anticoagulation medication to prevent recurrent epistaxisfrom packing
removal
alternatively, use a half inch Vaseline*
-soaked ribbon gauze strips layered from nasal floor
toward nasal roof and extending to posterior choanae
can also apply l-
'
loseal* (hemostatic matrix consisting of topical human thrombin and crosslinked gelatin) if other methodsfail
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B. Posterior hemorrhage treatment
• if unable to visualize bleeding source,the source islikely posterior
• place posterior pack* using a Foley catheter,gauze pack, or Epistat* balloon
• subsequently, layer anterior packing bilaterally
• admit to hospital with packs in for 3 d
• watch for complications: hypoxemia (nasopulmonary reflex), toxic shock syndrome (remove
packsimmediately), pharyngeal fibrosis/stenosis, alar/septal necrosis,aspiration
C.If anterior/posterior packsfail to control epistaxis
transnasal endoscopic sphenopalatine artery ligation +/- anterior ethmoid arteryligation by
otolaryngology or embolization of culprit arterialsupply by interventional radiology
± septoplasty
'antibioticsfor any posterior packor any pack leftfor >48 hduetorid[ofIrakshock syndrome
4. Prevention
•prevent drying of nasal mucosa with humidifiers,saline spray,or topical ointments
•avoidance of irritants
•medical management of HTN and coagulopathies
Hoarseness
Definitions
• change in voice quality,ranging from voice harshnessto voice weakness
• reflects abnormalities anywhere along the vocal tract from oral cavity to the lungs
• dvsphonia:a general alteration in voice quality
• aphonia:no sound emanatesfrom vocal folds
If hoarseness is presentfor >2 wk in a
smoker,laryngoscopy must be done to
rule out malignancy
Acute Laryngitis Vocal Cord Paralysis
• Unilateral: Affected cord lies in the
paramedian position,inadequate
glottic closure during phonation
-weak, breathy voice.Usually
medializes with time,whereby
phonation and aspiration improve.
Treatment options include voice
therapy,injection laryngoplasty
(Radiesse).mediatization using
silastic block,recurrent laryngeal
nerve reinnervation (RUf
anastomosistoansa cervicalis)
• Bilateral:Cords rest in midline,
therefore voice remains unchanged
but respiratory function is
compromised and may present
asstridor. If no respiratory issues,
monitor closely and waitfor
improvement.If respiratory issues,
try CPAP or intubate if necessary.
The patient will likely require vocal
cord lateralization,arytenoidectomy.
posterior costal cartilage graft,
or tracheotomy.Selective nerve
reinnervation (Marie technique) in
the proper hands may reestablish
movement
Definition
• <2 wk inflammatory changes in laryngeal mucosa after exposure to a trigger
Etiology
• infectious(most common):viral (influenza,adenovirus, HSV), bacterial (Group A Streptococcus),
fungal
• mechanical:acute voice strain -» submucosal hemorrhage -» vocal cord edema -> hoarseness
• environmental:toxic fume inhalation
Clinical Features
• URTI symptoms, hoarseness, aphonia, cough attacks
• true vocal cords erythematous/edematous with vascular injection and normal mobility
Treatment
• usually self-limited, resolves within 1-2 wk
• voice rest
• humidification
• hydration
• avoid irritants(e.g.smoking, caffeine)
• treat with antibiotics if there is evidence of coexistent bacterial pharyngitis
• treat with proton pump inhibitors if there is evidence of reflux
Chronic Laryngitis
Definition
• >3wk inflammatory changes in laryngeal mucosa
Etiology
- repeated attacks of acute laryngitis
• infectious:chronic rhinosinusitis with postnasal drip
• mechanical:chronic voice strain
• environmental:chronic irritants(dust,smoke, chemical fumes), chronic alcohol use
• esophageal disorders:GERD, Zenker'
s diverticulum, hiatus hernia
• systemic:allergy, hypothyroidism, Addison'
sdisease
Clinical Features
• chronic dvsphonia
• cough,globussensation,frequent throat clearing 2°toGERD
• laryngoscopy:erythematous and thickened cords with ulceration/granuloma formation and normal
mobility,rule out malignancy
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OT29 Otolaryngology Toronto Notes 2023
Treatment
• remove offending irritants
• treat related disorders(e.g. antisecretory therapy for GERD)
• speech therapy with vocal rest
• ± antibiotics ± steroids to decrease inflammation
Vocal Cord Polyps
Definition
• structural manifestation of vocal cord irritation
• acutely, polyp forms 2” to capillary damage in the subepithelial space during extreme voice exertion
Etiology
• most common benign tumour of vocal cords
• voice strain (e.g. muscle tension dysphonia)
• laryngeal irritants(e.g. GERD, allergies, tobacco)
Vocal Cords: Polyps vs. Nodules
Nodules
Unilateral.
asymmetric
Acute onset
May resolve
spontaneously
BJaleral
Gradual onset
Often followa chronic
course Epidemiology
• ages 30-50 y/o
. M>E
Subepithelial capillary Acute:submucosal
hemorrhage or
edema
Clinical Features
• primary symptom is dysphonia ± dyspnea (if polyps are large)
• othersymptoms:hoarseness, aphonia, cough attacks
• pedicled orsessile polyp on free edge of vocal cord
• typically, polyp is asymmetrical,soft, and smooth
• more common on the anterior 1/3of the vocal cord
Soli,smooth,
fusiform.
pedunoiatedmass
Acute:small,discrete
nodules
Chronic:hard,while,
thickened,fibrosed
nodules
Protonpumpinhibitor Vocal rest with
whispering,
hydration,voice
therapy
Surgical enisionif Surgicalexcision as
persistent or in the lastresort
presence of risk
factors for laryngeal
cancer
Treatment
• avoid irritants
• voice therapy may improve voice
• vocal fold steroid injections (percutaneous or transoral)
• endoscopic laryngeal microsurgical removal if persistent or if high-risk of malignancy
Vocal Cord Nodules
Definition
• vocal cord callus, bilateral by definition and symmetric
• also known as “screamer’s
"
or “singer’s
"
nodules
Etiology
• early nodules occur secondary to submucosal hemorrhage
• mature nodules result from hyalinization, which occurs with long-term voice abuse
• chronic voice strain
• frequent URT1,smoking, alcohol consumption
Epidemiology
• frequently in singers, children, bartenders, and school teachers
• I >M
Clinical Features
• hoarseness worst at end of day
• on laryngoscopy
• bilateral symmetric nodules at the junction of the anterior 1/3 and posterior 2/3of the vocal cords
(point of maximal cord vibration)
• chronic nodules may become fibrotic, hard,and white
Treatment
• primary treatment is voice rest and voice therapy
• hydration
• avoid irritants
• surgery rarely indicated for refractory nodules
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OT30 Otolaryngology Toronto Notes 2023
Recurrent Respiratory Papillomatosis
Definition
• small, benign wart-like growths (papillomas) in the respiratory tract
Etiology
• most commonly HPV types 6, 11, but can be caused by types 16, 18, 31, 33
• possible hormonal influence, possibly acquired during delivery through birth canal
Epidemiology
• biphasic distribution
birth to puberty (most common laryngeal tumour)
• adult-onset (age >12 y)
Clinical Features
• progressive hoarseness,stridor, and respiratory distress; less commonly wheezing, chronic cough,
recurrent pneumonia, dyspnea, hemoptysis, dysphagia,failure to thrive, apneic events
• can seed into tracheobronchial tree
• highly resistant to complete removal, high tendency of recurrence
• some juvenile papillomas resolve spontaneously at puberty
• may undergo malignant transformation to squamous cell carcinoma
Investigations
• flexible nasolaryngoscopy shows wart-like lesions with vascular core in supraglottic larynx and
trachea
• bronchoscopy with biopsy to confirm diagnosis and rule out malignancy
• chest x-ray followed by CT chest if indicated,findings of pulmonary involvement require referral to
respirology
• for high-risk patients, rule out TB, HIV
Treatment
• prevention using quadrivalent HPV recombinant vaccine
• suspension microlaryngoscopy with laser removal and preservation of normal mucosa is gold
standard (not curative, goal is improvement in voice and/or breathing)
preferably with CO:or KTP laser
• other optionsinclude microdebridement and cold steel
• consider systemic adjuvants if requiring >4 surgeries/yr. These include quadrivalent HPV
recombinant vaccine, bevacizumab,cidofovir, interferon,indole-3-carbinol
• PP1 if concomitant GERD
Laryngeal Carcinoma
• see Neoplasms of the Haul < uni Neck,0735
Salivary Glands
Sialadenitis Bilateral enlargement of the parotid
glands may be a manifestation of a
systemic disease ,such as mumps. HIV,
Sjogren's,or an eating disorder (Le.
anorexia, bulimia)
Definition
• inflammation ofsalivary glands
Etiology
• viral most common (mumps)
• bacterial causes:S. aureus, S. pneumoniae, H.influenzae
• obstructive vs. non-obstructive
• obstructive infection involves salivary stasis and retrograde bacterial flow Mumps usually presents with bilateral
parotid enlargement*
SNHlt orchitis
Predisposing Factors
. HIV
• anorexia/ bulimia
• Sjogren’ssyndrome
• Cushing’ssyndrome, hypothyroidism, DM
• hepatic/renal failure
• medications that increase stasis: diuretics, tricyclic antidepressants, (5-blockers, anticholinergics,
antibiotics
• sialolithiasis (can cause chronic sialadenitis)
Treatment
<D
of Sialadenitis(MASH)
Mnemonic
Mas sage
Analgesics/Antibiotics
Sialagogues
Heat/Hydration
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0T31 Otolaryngology Toronto Notes 2023
Clinical Features
• 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
Investigations
• U/S imaging to differentiate obstructive vs. non-obstructive sialadenitis
Treatment
• hydration, warm compresses,sialogogues, massage
• cloxacillin ± abscess drainage, if bacterial
Sialolithiasis
Definition
• ductal stone (mainly hydroxyapatite in adults,sand/sludge in children), leading to chronic sialadenitis
• 80% in submandibular gland, <20% in parotid gland, ~1% in sublingual gland
Risk Factors
• any condition causing duct stenosis or a change in salivary secretions(e.g. dehydration, diabetes,
EtOH,hypercalcemia, psychiatric medications)
Clinical Features
• pain and tenderness over involved gland
• intermittentswelling related to meals
• digital palpation reveals presence of calculus
Investigations
• U/S first, and if stone identified,CT for localization; may consider sialogram
Treatment
• may resolve spontaneously
• encourage salivation to clear calculus
• massage, bimanual expression, analgesia, antibiotics,sialogogues (e.g. lemon wedges,sour lemon
candies), warm compresses
• remove calculi endoscopically, by dilating duct or orifice, or by excision through floor of the mouth
• gland-preserving surgery has long-term symptom improvement and favourable gland retention rates
Salivary Gland Neoplasms
Etiology
• anatomic distribution
• parotid gland; 70-85%
• submandibular gland; 8-15%
• sublingual gland: 1%
minorsalivary glands: 5-8%
• malignant (see Table 16, OT36 and Table 17,OT37)
• benign
• benign mixed (pleomorphic adenoma):80%
. Warthin'
s tumour (5-10% bilateral, M>F):10%
cysts,lymph nodes, and adenomas:10%
oncocytoma:<1%
Parotid Gland Neoplasms
Clinical Features
• 80% benign (most common: pleomorphic adenoma), 20% malignant (most common:
mucoepidermoid)
• if bilateral,suggests benign process (e.g. Warthin'
s tumour, Sjogren'
s, bulimia, mumps) or possible
lymphoma
• facial nerve involvement (e.g. facial paralysis) increases risk of malignancy
A mass sitting above an imaginaiy line
drawn between the mastoid process
and angle of the mandible is a parotid
neoplasm until proven otherwise
Investigations
• FNA biopsy
• CT, U/S,or MRI to determine extent of tumour +
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OT32 Otolaryngology Toronto Notes 2023
Treatment
• treatment of choice issurgery for allsalivary gland neoplasms- benign and malignant
• pleomorphic adenomas are excised due to risk of malignant transformation (5% risk over prolonged
period of time)
• superficial tumour
superficial parotidectomy above plane of CN VII ± radiation
incisional biopsy contraindicated
• deep lesion
near-total parotidectomy sparing as much of CN V11 as possible
if CN VII involved, then it is removed and cable grafted
• complications of parotid surgery
• hematoma, infection,salivary fistula, temporary or permanent facial paresis, Frey'
ssyndrome
(gustatory sweating),sialocele, numbness of the overlying skin
• postoperative radiotherapy, if high risk of locoregional recurrence
• chemotherapy is largely reserved for palliative cases
DDx Parotid Tumour
Benign
• Pleomorphic adenoma
• Warthin's tumour|M>F)
• Benign lymphoepithelial cysts (viral
etiology,e.g. HIV)
• Oncocytoma
Malignant
• Mucoepidermoid carcinoma
• Adenoid cystic carcinoma
• Acinic cell carcinoma
Frey's syndrome is a postoperative
complication characterized by gustatory
sweating. It is thought that damaged
parasympathetic nerve fibres of the
auriculotemporal nerve regenerates
abnormally to innervate the cutaneous
sweat glands
Prognosis
• benign: excellent, <5% of pleomorphic adenomas recur
• malignant: dependent on stage and type of malignancy (see Table 17, OT37 )
Neck Masses
Approach to a Neck Mass
• ensure that the neck mass is not a normal neck structure (e.g. hyoid, transverse process of Cl vertebra,
prominent carotid bulb)
• any neck mass persisting for >2 wk should be investigated for possible neoplastic causes
Table 15. Prevalence of Acquired Causes of Neck Lumps According to Age
Age|yr) Possible Causes of Neck Lump
2.Congenllal/Develepmentii!
2.Inflammatory
3.Neoplosllc
3,Congenital
•40 1.Inllammalory
>40 1. Neoplastic
Differential Diagnosis
• congenital
• lateral (branchial cleft cyst, laryngocele, plunging ranula, lymphatic/venous/venolymphatic
malformation)
• midline (thyroglossal duct cyst, dermoid cyst, teratoma, thyroid/thymus anomaly, vascular
malformation)
• infectious/inflammatory
• reactive lymphadenopathy (2° to tonsillitis, pharyngitis)
• infectious mononucleosis
Kawasaki, Kikuchi-Fujimoto, Kimura, Cat-scratch,Castleman, Rosai-Dorfman disease
• HIV
• sialolithiasis,sialadenitis
thyroiditis
• granulomatous disease
mycobacterial infections
• sarcoidosis
• neoplastic
lymphoma
salivary gland tumours
thyroid tumours
metastatic malignancy (“unknown primary")
lipoma,fibroma, hemangioma, nerve or nerve sheath tumour
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Evaluation
Investigations
• history and physical (including nasopharynx and larynx)
• all other investigations and imaging are dependent upon clinicalsuspicion following history and
physical
congenital:CT with contrast,excisional biopsy
inflammatory/infectious:WBC (infection vs. lymphoma), trial of antibiotics, chest radiograph,
Mantoux TB test,CT with contrast, FNA
neoplasms:thyroid function tests and scans,CT with contrast, FNA (histologic examination),
panendoscopy (identification of possible primary tumour)
panendoscopy: nasopharyngoscopy,laryngoscopy, esophagoscopy, bronchoscopy with
washings,and biopsy'ofsuspiciouslesions
primary identified 95% of time -> stage and treat
primary occult identified 5% of time:excisional biopsy of node for histologic diagnosis ->
manage with radiotherapy and/or neck dissection (SCC)
Inflammatory vs. Malignant Neck
Masses
Inflammatory Neoplastic
History
Painful Y YiN
H£N infection Y H
Fever Y
Weight loss N
Ct risk factors H
Y
Y
Age Younger Older
Physical
lender Y H
Rubbery Y
Rock hard N
H
Y
Congenital Neck Masses Mobile Y r(bed
Branchial Cleft Cysts/Sinuses/Fistulae
Embryology
• at 4th wk of embryonic development, there are 4 pairs of branchial arches and 2 rudimentary arches,
which are separated internally by pouches and externally by clefts
• branchial anomalies form when pouches and clefts persist and fall into 3 types:
1.branchial fistula: persistent communication between skin and G1 tract
2.branchial sinus:blind-ended tract opening to skin
3.branchial cyst: persistent cervical sinus with no external opening
Clinical Features
• 2nd branchial cleft malformations most common
• sinuses and fistulae present in infancy as a small opening anterior to the SCM muscle
cysts present as a smooth, painless,slowly enlarging lateral neck mass, often following a URT'
I
• 1st branchial cleft malformations present as sinus/fistula or cyst in preauricular area (Type I) or on
face over angle of mandible (T ype 11)
• 3rd branchial cleft malformations present as recurrent thyroiditis or thyroid abscess and have a
tract which usually leadsto the left pyriform sinus. Air on CT scan in or near the thyroid gland is
pathognomonic for this anomaly
• there is controversy whether 4th branchial cleft anomalies exist, as they may be remnants of the
thyrothymic axis
Treatment
• surgical removal of cyst or fistula tract
• if infected:allow infection to settle before removal (antibiotics may be required)
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OT3-J Otolaryngology Toronto Notes 2023
External carotid a.
Internal carotid a.
;
Middle constrictor m.
Hyoid
Type Thyrohyoid membrane I anomaly
Thyroid cartilage
Type II anomaly
Common carotid a.
A. First Branchial Anomaly B. Second Branchial Anomaly
Thyroid cartilage
Cricoid cartilage
Internal carotid a.
External carotid a
Hyoid
^
XII Left common carotid a.
Right common carotid a.
- A
i
Thyroid cartilage
Cricoid cartilage Leftsubclavian a.
P
Brachiocephalic trunk
Arch of aorta I
£
s
C. Third Branchial Anomaly D. Fourth Branchial Anomaly
Figure 19.Branchial cleft anomalies
Thyroglossal Duct Cysts
Embryology
• vestigial remnant of tract made by thyroid gland as it travelsfrom its origin as a ventral midline
diverticulum at the base of the tongue, caudal to the junction of 3rd and 4th branchial arches
(foramen cecum), and migratesto the inferior aspect of the neck (see Figure 19)
Clinical Features
• most common congenital cervical anomaly
• usually presents in childhood or from ages 20-40 as a midline cyst that enlarges with URT1 and
elevates with swallowing and tongue protrusion
• location can he suprahyoid or infrahyoid
• may have fibrous cord, dysphagia, globus sensation
Thyroglossal duct cysts are the most
common congenital neck mass found
in children
Treatment
• preoperative antibioticsto reduce inflammation (infection before surgery is a well-described cause of
recurrence)
• small potential for neoplastic transformation,so complete excision of cyst and tissue around tract
up to foramen cecum at base of tongue, with removal of central portion of hyoid bone (Sistrunk
procedure) recommended
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OT35 Otolaryngology Toronto Notes 2023
Lymphatic, Venous, or Mixed Venolymphatic Malformations
Definition
• lymphatic malformation arising from vestigial lymph channels of neck
Clinical Features
• commonly identified in many fetuses, but regress before birth and never cause a clinical problem
• usually present by age 2
• macrocystic:soft, painless compressible mass (lymphatic dilation) with skin discolouration
• microcystic:soft, noncompressible masses with mucosal orskin vesicles
• may have dysphagia, dyspnea, possible pain with acute infection
• infection or trauma causes a sudden increase in size
Treatment
• can regressspontaneously after bacterial infection, therefore do not plan surgical intervention until
several mo after infection
• macrocystic lesions can be treated by surgical excision or sclerotherapy (doxycydine)
• microcystic lesions are difficult to treat, but can be debulked if it will not cause loss of function of
normalstructures,or injected with sclerotherapy (bleomycin) in surrounding tissues All patients presenting with a H&N mass
should be asked if they are experiencing
the following obstructive, referred,or
local symptoms
Oropharyngeal;Odynophagia,
dysphagia, non-healing oral ulcers
Otologic Otalgia. HL
Laryngeal;Dyspnea orstridor (positional
vs.non-positional). hoarseness,
dysphonia positional vs. non-positional
Nasopharyngeal:Recurrent epistaxis,
unilateral nasal obstruction, persistent
ihinorrhea orsinusitis
Hemoptysis, hematemesis
Neoplasms of the Head and Neck
Pre-Malignant Disease
• lichen planus
lacy white lines of oral mucosa +/- erythema
exact cause unknown,thought to be immune-mediated
treatment:topical corticosteroids (first-line), topical calcineurin inhibitors(second-line)
risk of malignant transformation 5-10%,follow-up every 6-12 mo
• leukoplakia
white keratotic plaque/patch of oral mucosa that cannot be rubbed off
treatment;surgery, cryosurgery,laser ablation,retinoids
risk of malignant transformation 5-20%, follow-up every 3-12 mo
• ervthroplakia
• red mucosal plaque adjacent to normal mucosa
• commonly associated with epithelial dysplasia
associated with carcinoma in situ or invasive tumour in 40% of cases
• treatment:similar to leukoplakia
• dysplasia (a feature of pre-malignant lesions)
• histopathologic presence of mitoses and prominent nucleoli
involvement of entire mucosal thickness
= carcinoma in situ
• associated progression to invasive cancer 15-30%
Investigations
• initial metastatic screen includes chest x-ray
• scans of liver, brain, and bone only if clinically indicated
• CT scan superior to MK1 for the detection of pathologic nodal disease and bone cortex invasion
• MKI superior for discriminating tumour from mucus and detecting bone marrow invasion
. ± PET scans
• endoscopy with biopsy
Treatment
• treatment depends on:
• histologic grade of tumour,stage
physical and psychological health of patient
facilities available, expertise and experience of the medical and surgical oncology team
• in general:
1°surgery for malignant oral cavity tumours with radiotherapy reserved for salvage or poor
prognostic indicators
1° radiotherapy for nasopharynx,oropharynx,hypopharynx, and larynx malignancies with
surgery reserved for salvage, although laser endoscopic surgery for early stage larynx cancer is an
option and 1°surgery for advanced (T4) pharyngeal and laryngeal cancer is the standard of care
there is a growing interesting in studying 1°surgery (transoralsurgery (TOS)) for OPC
palliative chemotherapy for metastatic or incurable disease
concomitant chemotherapy increasessurvival in advanced disease
chemotherapy has a role asinduction therapy prior to surgery and radiation
panendoscopy (bronchoscopy, esophagoscopy, laryngoscopy and pharyngoscopy) to detect 1°
disease when lymph node metastasis is identified
anti-epidermal growth factor receptor treatment (cetuximab, panitumumab) has a role as
concurrent therapy with radiation for SCC of the H&N (for advanced local and regional disease)
Detection of cervical lymph nodes on
physical exam
False negative rate:15-30%
False positive rate; 30-40%
Pathological lymphadenopathy defined
radiographically as
A jugulodigaslric node >1.5cm in
diameter, or a retropharyngeal node >1
cm in diameter
A node of any sire which contains
central necrosis
Common
o
sites of distant metastasesfor
H&N neoplasms
(most common to least common) lungs >
(ver > bones
Risk Factorsfor H&N Cancer
• Smoking
• EtOH (synergistic with smoking)
• Radiation
• Occupational/environmental
exposures
• Oral HPV infection (independent of
smoking and EtOH exposure)
. Family history of cancer
. Previous cancer
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The smaller the salivaiy gland,the
greater the likelihood that a mass in the
gland is malignant
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OT36 Otolaryngology Toronto Notes 2013
Prognosis
• synchronous tumours occur in 0.8-18% of patients
• late development ofsecond primary is most common cause of post-treatment failure after 36 mo
Table 16. Quick Look-Up Summary of H&N Malignancies - Etiology and Epidemiology
Etiology Epidemiology Risk Factors
Oral Cavity
95% SCC
Others:sarcoma,melanoma,
minor salivary gland tumour
HPV ndSnrvival otPatients with OPC
KLItl 2010:363(1)
^
4-35
ItProds te-jsoedvearaysaof oatesiswith
stage 111 or IK o-optaryogea SCC er:ed isaKI
comja-ng acctoaSd ot standard
‘
rectoatos
radolherapy.eacS ctracedwiSCBfhato ttfraoy.
Results:;;- ar 3 ytoxeraCsumalrate- bob!
treaties aras.Pabeds HPV-josibietreour
hadSetter -ass of ore-a il ssnuaI at 3 yr (823% is.
57.1%) a-d a 51'
rad.ct xnrisk of death (Hazard
Katie0.42.55%0017-0.561after a
^
ssteg So- age.
rate,honour andnodal stage.toSacco eiposu-e.
a-rdteatseut.
Siaaarj:I-etBMrHFIfstatzsmpatertsat;
t>-orarpgaa SCC is a strj-gaod dependent
prognosticFactor for s»mal.
Mean age:50-60 yr Smoking.'EtOH
Poor oralhygiene
leukoplakia,erythroplakia
Lichen planus,chronic inflammation
Sun eiposure -lip
HPV infection
Plummer-Vinson syndrome
GeneticfEtlmic
M> f
Most common site of HtH cancers
50%on anterior 213 of tongue
Nose and Paranasal Sinus
75-80% SCC
Adenocarcinoma (2nd most common) and
mucoepidermoid
99% in maxillary/ethmoid sinus
10% of nose and paranasal sinus tumours arise
from minor salivary glands
Mean age:50-70 yr
Rare tumours
*
incidence in last 5-10 yr
Woodi'shoe/teitile industry
Hardwood dust (nasal'ethmoid sinus)
Nickel,chromium(maxillary sinus)
Air pollution
Chronic rhinosinusitis
Carcinoma of the Pharynx -Subtypes (Nasopharynx.Oropharynx.Hypopharynx.and Larynx)
Nasopharynx
90% SCC
~10% lymphoma
Mean age:50-59 yr
M:F-2.4:1
Incidence 0.8 per100000
100x increased incidence inSouthernChinese Poor oralhygiene
Genetic -Southern Chinese
EBV
Salted fish
Nickel eiposure
Oropharynx
95% SCC - poorly differentiated
Up to 70% of OPC attributable to HPV
Mean age:50-70 yr
HPV-patients with OPC are approximately10
yryounger
Prevalence of HPV
- OPC has increased by 225%
from1988 to 2004
M:F-4:1
Smoking EtOH
HPV 16 infection Summary of Treatment for Head and
Neck Masses
SageIN:single modality
Stage UL1V:dual modality
Hypopharynx
95% SCC
3 sites
1.pyriform sinus (60%)
2.postcricoid (30%)
3.posterior pharyngeal wall (10%)
Mean age:50-70 yr Smoking.'EtOH
M>F
8-10% of all HAN cancer
Larynx
SCC most common
3 sites
1.supraglotlic (30-35%)
2.glottic (60-65%)
3.subglottic (1%)
Mean age:45-75 yr
M:F-10:1
45% of all HAN cancer
Smoking ElOH
Salivary Gland
40% mucoepidermoid
30% adenoidcystic
5% acinic cell
5% malignant mixed
5% lymphoma
Mean age:55-65 yr Radiation eiposure
M-F
3-6% of all HAN cancer
Percentage of malignant tumours ineach
gland:
Parotid15-25%
Submandibular 37-43%
Minor salivary >80%
Thyroid (90% benign -10% malignant)
>80% papillary
5-15% follicular
5% medullary
<5% anaplastic
1-5% Hurthle cell
1-2% metastatic
Children
Adults <30 or >60 yr
Nodules more common in females
Malignancy more common in males
Radiation eiposure
Family history - papillary CA or multiple
endocrine neoplasia (MEN II)
Older age
Male
Papillary - Gardner'
s syndrome.Cowden
syndrome,FAP
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OT37 Otolaryngology Toronto Notes 2023
Table 17. Quick Look-Up Summary of H&N Malignancies - Diagnosis and Treatment
Clinical Features Investigations Treatment Prognosis
Oral Cavity
Asymptomatic neck mass(30%)
Non-healing ulcer « bleeding
Oysphagia,sialorrhea,dysphonia
Oral fetor,otalgia,leukoplakia,or
crythroplakia (pre malignant
changes or clinically isolated syndrome)
Biopsy 1“
surgery
local resection
*
neck dissection
treconstruction
2"
radiation
Syr overall survival
11/12:75%
13/14:30-35%
Poor prognostic indicators
Depth ol invasion,close surgicalmargins
location (longue worse thanHoot ol moulh)
Cervical nodes
Cl
Nose and ParanasalSinus
Early Symptoms
Unilateral nasal obstruction
Epistaxis,rhinorrhea
Late Symptoms
V lo invasion ol nose,orbit,
nerves,oral cavity,skin,skull
base,cribriform plate
Cl/MIII
Biopsy
Surgery and radiation
Chcmoradiolherapy
5 yr survival:30-60%
Poor prognosis 2olo lale presentation
Nasopharynx
Cervical nodes (60-90%)
Hasal obstruction,epistaxis
Unilateral otitis media t HL
CN III to VI.IX toXII(25%)
Proptosis,voice change,dysphagia
1°radiationt chemoradiation
Surgery for limitedor recurrent disease
5 yr survival
11:79%
12:72%
13:50-60%
14:36-42%
Hasopharyngoscopy
Biopsy
CT/MRI
Oropharynx
Odynophagia,otalgia
Ulcerated/enlarged tonsil
Fixed tongueflrismus/dysarthria
Oral fetor,bloody sputum
HP1
/- OPC predominantly arises at base of
tongue or tonsillar region
Cervical lymphadenopathy (60%)
Distant mets:lung/bone/liver|7%)
Biopsy
Determine HPV status via RT-PCR:positive if
presence of HPV DNA and p16 over expression
1”
radiation,consider therapyde-intensification 5 yr overall survival
for HPV*
patients
2"
surgery
local resection
tneck dissection
reconstruction
1“
surgery
emerging roleof Iransoral Robotic Surgery
Stratified byTNM stage (I.II.Ill,IV)
HPV negative OPC (70%.58%.50%.30%)
HPV positive OPC (92%.87%,74%.40%)
HPV positive OPC further stratified by stage,
age.and smoking pack years|PY)
groupI(I1-3N0-H2c,s20 PY|:89%
groupII(T1-3N0-N2c.>20 PY):64%
group III (14 or N3.age s70): 57%
group IVA(14 or N3,age >70):40%
Cl
Hypopharynx
Dysphagia,odynophagia
Otalgia,hoarseness
Cervical lymphadenopathy
Pharyngoscopy
Biopsy
1“
radiation
2"
surgery
5 yrsuivtval
11:53%
12/13:36-39%
14:24%
Cl
larynx
Oysphagia. odynophagia,globus
Otalgia,hoarseness
Oyspnea/slridor
Cough/hemoptysis
Cervical nodes (rare with glottic CA|
Early stage:single modality (radiation or
surgery)
lale singe:rnultimodalily (surgery,
radiotherapy, chemotherapy)
5 yr survival
14: >40% (surgery with radiation)
Controlrale early lesions:>90% (radiation)
10 to12% of smalllesions failradiotherapy
laryngoscopy
Biopsy
Ct/MRI
Salivary Gland
Painless mass (occ.pain is possible)
CN VII palsy
Cervical lymphadenopathy
Rapid growth
Invasion of skin
Constitutional signs/symptoms
1°
surgery *
neck dissection
Postoperative radiotherapy
Chemotherapy if unresectable
FNA Parotid
10 yr survival:85.69. 43.and14% for stages
111014
Submandibular
2 yr survival:82%.5 yr:69%
Minor salivary gland
10 yr survival:83.52.25.23% for stages
11to14
MRI/CI/U/S
Thyroid
Thyroid mass,cervical nodes
Vocal cord paralysis,hoarseness
Hyper/hypothyroidism
Dysphagia
FNA Recurrences occur within Syr
Need long-term follow-up:clinical exam,
thyroglobulin
1”
surgery
I
'
trfor intermediate and high-risk welldifferentiated thyroid cancer
U/S
Parathyroid
Symptoms of hypercalcemia
Neck mass
Bone disease,renal disease
Pancreatitis
Sestamibi Wide surgical excision
Postoperative monitoring of serum Ca2’
Recurrence rates
1yr: 27%
5 yr:82%
10 yr:91%
Mean survival:6-7 yr
rt
CT imaging(or Head and Neck Malignancies are done with contrast for theneck and chest. CT head is not routinely order.
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Thyroid Carcinoma
Table 18. Bethesda Classification of Thyroid Cytology
Diagnostic Category Risk of Malignancy
Non-diagnostic or unsatisfactory 1- 4%
Benign
follicular lesion of undetermined significance or atypia ofundetermined
significance
Follicular neoplasm or suspiciousfora follicular neoplasm
Suspicious for malignancy
Malignant
0-3%
5-15%
15-30%
60-75%
97-99%
The Bethesda System lot ftopoiting ThyioldCytopathology fTBSRTCIisa repotting system lot thyroid FNA.
Table 19. Thyroid Carcinoma
Papillary Follicular Medullary Anaplastic Lymphoma
Incidence|% of all 90-92%
thyroid cancers)
4-6% 1-2% <1% «1%
Most common is diffuse
Large B Cell Lymphoma
(DLBCL)
Route of Spread
Histology
Hematogenous
Orphan Annie nuclei Capsular/vascular
Psammoma bodies invasion influences
Papillary architecture prognosis
Lymphatic N /A
Amyloid
May secrete
calcitonin,
prostaglandins, ACIH,
serotonin, kallikrein,
or bradykinin
Giant cells
Spindle cells
Other Ps Papillary cancer Fs Follicular cancer Ms Medullary
Far away mcls
Female (3:1)
More common in
elderly
70% in women
20-30% have Hx of
Usually non- Hodgkin's
lymphoma
Rapidly enlarging
thyroid mass
dillerentiatcd thyroid Hi ol Hashimoto's
CA (mostly papillary) thyroiditis
or nodular goitre Increases risk 60i
4:1female
predominance
Dysphagia,dyspnea.
Rule outlymphoma stridor,hoarseness.
neck pain,facial edema,
accompanied by “B"
symptoms'
5 yr survival
Stage IE:55%-80%
Stage HE:20%-50%
Stage IIE7IV: 15% 35%
Non surgical
Combined radiation
thyroidectomy Chemotherapy (CHOP")
Radiotherapy
Chemotherapy and
targeted therapy
Palliative Care
Popular (most
common)
Palpable lymph nodes NOT FKA (cannot be
Positive PA’
uptake
Positive prognosis
Postoperative
Pt
'
scan to guide
treatments
cancer
Multiple endocrine
neoplasia (MEN lla
diagnosed by FNA) or lib)
Favourable prognosis aMyloid
Median node
dissection mass
Rapidly enlarging
neck
Prognosis 98% at 10 yr 92% at10 yr
Early stage: total
or near total
thyroidectomy (
- 4 cm. thyroidectomy
no high risk features) late stage: total
or total thyroidectomy thyroidectomy
t neck disseebon •
postoperative l
,
J1
treatment
Early stage:total
or near total
Total thyroidectomy Tracheostomy
Median and /or lateral local tumour: total
compartment node
neck dissection
(based on serum
calcitonin)
Modified neck
dissection
Postoperative
thyroiine.
radiotherapy
Tracheostomy
Screen relatives
Targeted therapy for
metastatic palliative
cases
Treatment
Mem)
late stage:total
thyroidectomy
meek dissection *
postoperative 1131
treatment
'B symptoms *
lever,night sweats, chills,weight loss >10% in 6mo
"CHOP 8 cyclophosphamide,adrlamycin,vincristine,prednisone
Approach to Thyroid Nodule
• all patients with thyroid nodules require evaluation of scrum TSH and ultrasound of the thyroid
gland, central and lateral neck
• when performing repeat FNA on initially non-diagnostic nodules, U/S-guided FNA should be
employed
• nuclear scanning has minimal value in the investigation of the thyroid nodule
• molecular testing is increasingly used to identify gene mutations associated with thyroid cancers to
determine “high-risk” from “low-risk" thyroid nodules
• Thyroid Imaging, Reporting and Data System (T l-RADS) provides recommendation for FNA or U/S
follow-up
TR1 (0 points): no FNA
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OT39 Otolaryngology Toronto Notes 2023
TR2 (2 points): not suspicious, no FNA
• TR3 (3 points):mildly suspicious, FNA if > 2.5cm, follow-up if >1.5 cm
• TR4 (4-6 points): moderately suspicious, l
'
NA if >1.5 cm,follow-up if >1 cm
• TR5 (>7 points): highly suspicious, l
'
NA if 1 cm, follow-up if 0.5 cm
Indications for Postoperative
Radioactive Iodine Ablation - 1
"
1
• Adjuvant therapy: decrease recurrent
disease
• Radioactive Iodine (RAI) therapy:
treat persistent cancer
Table 20. American College of Radiology Thyroid-Imaging, Reporting and Data System (TI-RADS)
Composition (Choose Echogenicity (Choose Shape (Choose 1) Margin (Choose 1) Echogenic Foci
(Choose all that
apply)
D D
Cystic or almost completely Anechoic (0 points)
cystic (0 points)
Spongiform (0 points)
Mired cystic and solid
(1 point)
Solid or iilinosl completely
solid (2 points)
Wider-than-tall (0 points) Smooth (0 points)
Hyperechoic or isoechoic Taller-thanwide (3 points) Ill-defined (0 points)
lobulaled or irregular (2
points)
fxlralhyroidal extension
(3 points)
None or large comet-tail
artifacts(0 points)
Microcalcificalions (1
point)
Peripheral calcifications
(2 points)
Punctate echogenic foci
(3 points)
|1 point)
Hypocchoic (2 points)
Very hypoechoic (3 points)
Table 21. Management of the Thyroid Nodule
Treatment Indications
Radioiodine therapy Treatment of hyperthyroidism
Alter surgery as adjuvant treatment of intermediate- high -risk papillary or follicular carcinoma
Chemotherapy and targeted therapy (tyrosine Recurrcnl/tesidual medullary CA, anaplastic CA, or thyroid lymphoma
kinase inhibitors)
Surgical excision Nodule that issuspicious on FNA cytology
Malignancy other than anaplastic CA. or thyroid lymphoma
Mass that is benign on FNA but increasing in sice on serial imaging and/or >3- 4 cm in sice
Hyperthyroidism not amenable to medical therapy
Paediatric Otolaryngology
Acute Otitis Media
Definition
• both presence of MEE/M FI and acute onset of MEE/MEl symptoms
Epidemiology
• most frequent diagnosis in sick children visiting clinicians’offices and most common reason for
antibiotic administration
• peak incidence between 6-15 mo:
-85% of children have >1 episode by 3 yr old
• seasonal variability: peaks in winter
Etiology
• primary defect causing AOM: Eustachian tube dysfunction/obstruction > stasis/colonization by
pathogens
• bacterial: S. pneumoniae, non-typeable H. influenzae, M.catarrhalis,group A Streptococcus, S. aureus
• viral:RSV, influenza, parainfluenza, adenovirus
• commonly due to bacterial/viral co-infection
Predisposing Factors
• Eustachian tube dysfunction/obstruction
• swelling of tubal mucosa
. URTT
allergic rhinitis
chronic rhinosinusitis
obstruction/infiltration of Eustachian tube ostium
tumour: nasopharyngeal carcinoma (adults)
adenoid hypertrophy (by maintaining a source of infection rather than obstruction)
barotrauma (sudden changes in air pressure)
• inadequate tensor palati function: cleft palate (even after repair)
• abnormal Eustachian tube
Down syndrome (horizontal position of Eustachian tube), Crouzon syndrome, cleft palate,
and Apert syndrome
• aberrant function of:
cilia of Eustachian tube: Kartagener’ssyndrome
mucus secreting cells
• capillary network that provides humoral factors, PM Ns, phagocytic cells
• immunosuppression /deficiency due to chemotherapy,steroids, DM, hypogammaglobulinemia, cystic
fibrosis
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Risk Factors
• non-modifiable:young age,family history of OM, prematurity, orofacial abnormalities,
immunodeficiencies, Down syndrome, race, and ethnicity
• modifiable:lack of breastfeeding, daycare attendance, household crowding, exposure to cigarette
smoke or air pollution, pacifier use
Clinical Assessment of SOM in Paediatrics
JAMA 2010:304:2161 69
In assessment ot AOM in pedulrks, tar pain is Die
most useful symptom with an It between 3.0-7.3.
Useful otoscopic signs include erythematous(It 8.4.
95% Cl Ml),ttoudy (It 34.95% Cl 28-42).bulging (It
51,95% Cl 38-73).and immobile tympanic membrane
ltd 31, 95% Q 26-37) on pneumatic otoscopy.
Protective Factors
• breastfeeding
• xylitol
Pathogenesis
• obstruction of Eustachian tube -> air absorbed in middle ear -> negative pressure (an irritant to middle
ear mucosa) -> edema of mucosa with exudate/clTusion -> infection of exudate from nasopharyngeal
secretions Antibiotics lot AON la Children
Cochrane D6 Systtev 2013:1X0000219
Study:Meta -analysis ol Kardonired Controlled trials
(dCIs) on children (1-15 mo)with acuteotitis media
comparing any antibiotic regime to placebo and
expectant obseruatioo.
Data Sources:CochraneCentral Register ol
Controled trials(2012 issue10).MEDLINE (1966 to
October 20)2). 010ME0UNE (1958 to1965|. EMBASE
(January 1990 to November 2012).Cu nentContents
11966 to November 2012).CINAHl (2000 lo November
20121and UlACS (2008 to November 2012) without
language restrictions.
Main Outcomes:t) Pam at 24 h,2-3d, and 4-7 d;2|
Abnormal tympanometry Endings:3|1M perforation;
4) Contralateral otitis;5|AOM recurrences;6)Serious
com plicationsfrom AOM;7)Adverse eltectsfrom
antibiotics.
Results: treatment with antibiotics had no significant
Impact on pain at 24 h. However, pa n at 2-3il and 4 -7
d was lower in the antibiotic groups with a HHI of 20.
Antibiotics had no significant effect on tympanometry
Endings, number of AOM recurrences, or severity ol
complications.Antibiotic treatment led toa significant
reduction in IM perforations(NHI 33) and halved
contralateral AOM (NNT tl).Adverse events(vomiting,
diarrhea,or rash)occotred moreolte n in children
taking antibiotics.
Conclusion: Hit role of antibiotics is largely
restricted lo pain control at 2-7 d. but mast (82%)
settle without antibiotics.Ihts can also be achieved
by analgesics. However,antibiotic treatment can
reduce nsk of IM perforation and contralateral AOM
episodes.These benefits must be weighed against
risks of adverse eventsfrom antibiotics.
Clinical Features
• triad of otalgia,fever (especially in younger children), and CHL
• rarely tinnitus, vertigo, and/or facial nerve paralysis
• otorrhea if TM perforated
• infants/toddlers
ear-tugging (this alone is not a good indicator of pathology)
HL, balance disturbances(rare)
• irritable, poor sleeping
vomiting and diarrhea
anorexia
• otoscopy of TM
hyperemia
bulging, pus may be seen behind TM
loss of landmarks: handle and long process of malleus not visible
Diagnosis
• history
acute onset of otalgia or ear tugging in a preverbal child,otorrhea,decreased hearing
unexplained irritability,fever, upper respiratory symptoms, poor sleeping, anorexia, N/V, and
diarrhea
• physical
febrile
MEE on otoscopy: immobile TM,acute otorrhea, loss of bony landmarks, opacification of TM,
air-fluid level behind I
'
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