COMMON TUMORS IN ENT BY LOVENESS ULUNJI CHAWINGA.pdf

This is a brief discussion on common tumors in ENT and common to people living on the sub Saharan Africa.

1. COMMON TUMORS IN
ENT
BY
LOVENESS ULUNJI CHAWINGA
MODERATOR: DR D. MWALE

2. OUTLINE
➢Tumors of the Ear
➢Tumors of the Nasopharynx
➢Tumors of the Oropharynx
➢Tumors of the Larynx

3. TUMORS OF THE EAR

5. HISTOLOGICAL ANATOMY
•The auricle (pinna) and the external ear canal: both have a lining
keratinized stratified squamous epithelium.
•The tympanic membrane: outside (keratinized stratified squamous
epithelium) and a mucous membrane (non-keratinized stratified
squamous epithelium) inside
•The middle ear: lining of non-keratinized stratified squamous
epithelium
•The inner ear is in the bony labyrinth of the temporal bone

6. EXTERNAL EAR
AURICLE (PINNA)
BENIGN
•Sebaceous cyst
•Keloids
•Papilloma
•Hemangioma
•Neurofibroma
•Dermoid cyst
•Pre auricular sinus cyst
•Keratoacanthoma
MALIGNANT
•Squamous cell carcinoma
•Basal cell carcinoma
•Melanoma
•Adenoid cystic carcinoma
•Ceruminous
adenocarcinoma

7. BENIGN
•Pre Auricular sinus: faulty union of hillocks of the 1
st
and 2
nd
brachial
auricle during development of the pinna
•Sebaceous Cyst : Post auricular sulcus / below and behind the ear
lobule
•Dermoid cyst: round mass over the upper part of the mastoid behind
the pinna
•Keloid : scar tissue secondary to trauma such as piercing the ear or
onarments/ surgical incision
•Papilloma : a rough slow tustedgrowth or flat grey plaque.

8. SQUAMOUS CELL CARCINOMA
•most common cause of malignancy involving the external ear canal and temporal
bone
•Oncogenic human papillomavirus (HPV) genotypes 16 and 18 have been
anecdotally reported in SCCs of the middle ear though the role of HPV in
carcinogenesis at this site is not known
•frequently accompanied by concurrent otitis externa or otitis media

9. SQUAMOUS CELL CARCINOMA
RISK FACTORS
•fair skin
•solar ultra violet light exposure
•Immunosuppression
•HIV
•Diabetes Mellitus
•Longtermsteroid use
•Smoking
CLINICAL FEATURES
•Chronic discharge
•Bleeding,
•Otalgia
•Hearing loss
•With or without facial palsy
•Non-specific symptoms; Fatigue,
weight loss, nausea, vomiting

10. SQUAMOUS CELL CARCINOMA
DIAGNOSIS
•History and physical examination
•Investigations
INVESTIGATIONS
•Biopsy for histology
•Infiltrating nests and cords or nests of polygonal cells with moderate amounts of eosinophilic
cytoplasm and intercellular bridging
•Presence of keratin, nuclear pleomorphism, mitoses and necrosis depend upon the grade of the
carcinoma.
•High resolution computed tomography (HRCT) of the petrous temporal bone
•Detect erosion of the temporal bone
•Difficult to differentiate benign and malignant tumors
•Contrast enhanced magnetic resonance imaging (MRI)
•Defines soft tissue involvement
•Distinguishes benign and malignant tumors

11. SQUAMOUS CELL CARCINOMA
OTOSCOPY HISTOPATHOLOGY

12. SQUAMOUS CELL CARCINOMA
STAGING
•No universally accepted staging system for carcinoma of the temporal
bone
•Most commonly used system for carcinoma of the EAC is the
pittsburghclassification
•The 2nd system is the one proposed by stelland mccormickwith
subsequent modifications
•Both of these systems are based on clinical and radiologic findings

14. TREATMENT
•Surgery
•Enbloc lateral temporal bone resection (LTBR)
•indicated for very extensive tumors that extend intracranially or into the infratemporal
fossae
•removal of the entire petrous temporal bone, including the petrous apex and its contents,
with or without removal of the petrous carotid
•Enbloc subtotal temporal bone resection (STBR)
•indicated for tumor extending into the middle ear space
•resection of temporal bone lateral to the petrous carotid artery
•This includes the cochlear and the vestibular structures.
•Other associated structures, such as the parotid gland and mandibular ramus
•Radiotherapy is commonly used as a post-operative adjuvant
•For advanced primary tumor stage (T3/T4), close or involved tumor margins,
perineural invasion, and lymph node metastases

15. EXTERNAL ACOUSTIC MEATUS
BENIGN
•Osteoma
•Exostosis
•Glomus tumors
MALIGNANT
•Squamous cell carcinoma
•Basal cell carcinoma
•Melanoma

16. OSTEOMA
•Benign round bonetumor deep portion of external auditory
meatus
•Most common inmiddle-agedindividualsbut may develop
at any age
•Tend to occur in people who frequently swim
•Multiple osteomas associated withGardner’s syndrome
•Composed of lamellar bone; outer cortical and inner
cancellous trabeculated areas with marrow spaces

17. OSTEOMA

18. CLINICAL FEATURES
•Often asymptomatic
•obstruction of the ostium, with subsequent congestion and pressure
headaches.
•Gardner syndrome: extracolonic manifestation of familial
adenomatous polyposis (FAP)
•osteomas of the skull or mandible,
•hypertrophy of the retinal pigment epithelium,
•adrenal adenomas,
•desmoid tumors, dental abnormalities, and cutaneous lesions

19. OSTEOMA
TREATMENT
•Surgical removal may be required if expansive tumor growth leads to
symptoms.

20. EXOSTOSIS
•Deeper in the ear canal
•Appositional new bone formation; thin layer of woven bone
on lamellar bone
•Differs from osteoma
•Bone formations of exostosis do not possess marrow space
•multicentric and bilateral nature
•most often observed in individuals with a history of cold-
water exposure, such as swimmers or surfers
•present in approximately 1 of every 150 patients examined
for otolaryngologic problems.

21. CLINICAL FEATURES
•Asymptomatic
•Canal occlusion
•Conductive hearing loss
•Post obstructive cerumen impaction
•Cholesteatoma
•Otitis externa.

22. EXOSTOSIS
oInvestigation:
•Biopsy for histology
•dense stratified arrangement of new bone that is remodeled over time into normal lamellar
bone.
•CT scan of the head
oTreatment
•Avoidance of water exposure (eg, watertight ear plugs)
•Avoiding and preventing secondary otitis externa
•Ototopical drops are used for infection eglidocaine, chloraphenical,
beclomethasone, clotrimoxazole
•Surgical intervention if canal obstruction and symptom e.g. canalplasty
oComplications: Approx. 1% transform into chondrosarcoma.

23. EXOSTOSIS

24. GLOMUS TYMPANICUM
•Paraganglioma of the middle ear
•Occur at the auricular branch of the vagusnerve
•highly vascular
•most common primary neoplasm of the middle ear, and the second
most common tumourof the temporal bone.
•commonly occur in women in the fifth to sixth decades of life

25. CLINICAL FEATURES
•Pulsatile tinnitus
•Conductive hearing loss
•Large glomus tumor
•Vertigo
•Facial palsy
•Sensory neural hearing loss

27. GLOMUS TYMPANICUM
INVESTIGATION
•computerisedtomography Scans (CT scans),
•magnetic resonance imaging (MRI),
•magnetic resonance angiography (MRA).
TREATMENT
•observation
•surgical excision
•radiotherapy
•Alpha-blockers and beta-blockers are also usually administered
for 2–3 weeks before embolization

28. GLOMUS TYMPANICUM

29. GLOMUS JUGULARE
•Rare, slow-growing neuroendocrine paraganglioma of the head and
neck
•Arises within the jugular foramen and is localized to the jugular fossa
in the temporal bone of the skull base
•Occur at the superior vagal ganglion
•Hypervascular
•1% to 5% are malignant
•80% are sporadic
•Female presentation is 3 to 6 times more common than men

30. GLOMUS JUGULARE
•Hearing loss,
•Pulsatile tinnitus
•Otorrhagia
•Aural polyp
•Earache
•Ear discharge
•Ear bleeding.
•present with neurological
deficits, resulting in
•facial palsy,
•dysphagia,
•hoarseness,
•shoulder weakness,
•tongue deviation.

31. GLOMUS JUGULARE
OTOSCOPY
•pulsatile red middle ear mass behind
an intact tympanic membrane.
•tympanic membrane can show
increased vascularity
•inferiorly based red ear mass (rising
sun appearance)
•tympanic portion of the tumor may
erode into the ear canal
INVESTIGATIONS
•Pure tone and speech audiometry
•Head computed tomographic scan with
fine-cuts
•Magnetic Resonance Imaging (MRI)
•“salt-and-pepper” appearance on T1 and
T2 weighted images.
•Angiography
•differentiate paragangliomas from other
pathologies
•demonstrate the tumor blush and the
feeding vessels, which can then be
embolized

32. GLOMUS JUGULARE

33. GLOMUS JUGULARE
TREATMENT
•Surgical resection
•Sub-total resection
•External beam radiotherapy (EBRT)
•bilateral glomus jugularetumors
•adjunct to limited surgical approaches
•Stereotactic radiosurgery (SRS)-new treatment

34. GLOMUS JUGULARE

35. MIDDLE AND INNER EAR
BENIGN
•Cholesteatoma
•Middle Ear Papilloma
•Vestibular Schwannoma
(Acoustic neuroma)
•Otosclerosis
MALIGNANT
•Middle Ear Neuroendocrine
Tumour(MeNET)
•Middle Ear Squamous Cell
Carcinoma
•Endolymphatic Sac Tumour
•Middle Ear Adenocarcinoma

36. ACOUSTIC NEUROMA
•Benign tumors that arise from Schwann cells
•Median age: 52 years
•Incidence: 4:100,000 people per year (♂= ♀)
•Commonly located within the internal acoustic canal and can extend
into the cerebellopontine angle (most common tumor of the
cerebellopontine angle)
•Most commonly unilateral
•Bilateral acoustic neuromas are strongly associated with
neurofibromatosis type II.

37. CLINICAL FEATURES
Early symptoms: as a result of tumor expansion into the internal
acoustic canal (internal auditory meatus), causing pressure on the
vestibulocochlear nerve (CN VIII)
oCochlear nerve involvement
oUnilateral sensorineural hearing loss (most common symptom)
oTinnitus
oVestibular nerve involvement
oDizziness
oUnsteady gait and disequilibrium

38. CLINICAL FEATURES
Late symptoms: caused by pressure of adjacent structures within the
cerebellopontine angle
oTrigeminal nerve (CN V) involvement: paresthesia (numbness), hypoesthesia
(decreased sensation), and/or unilateral facial pain
oFacial nerve (CN VII) involvement: peripheral, unilateral facial weakness that
can progress to paralysis
oCompression of structures in posterior fossa
oCerebellum: ataxia
o4th ventricle: hydrocephalus

40. INVESTIGATION
EXAMINATION
•Cochlear nerve (CN VIII):sensorineural hearing loss
•Weber test: lateralization to the normalear
•Rinne test:air conduction >bone conduction in bothears
•Brainstem-evokedaudiometry: delay in cochlear nerve conduction time on
affected side finding
•Can be used as an additional test in patients with asymmetric audiometry findings
•Morecost-effectivebut less sensitive than anMRI
•Trigeminal nerve(CN V):ipsilateraldecreasedcorneal reflex
•Facial nerve(CN VII):ipsilateralfacial twitching or weakness

41. INVESTIGATION
•Pure tone Audiometry
•Hearing losswith agreater deficit for higher frequencies
•Best initial test:> 90%of patients will have some type ofhearing loss.
•ContrastMRI(imaging modality of choice)
oRecommended in patients with abnormal audiometric testing or high clinical
suspicion of acousticneuroma(cerebellopontine angle syndrome)
•CT with and without contrast is an alternative for those who cannot
undergoMRI
oShows an enhancing lesion by the internal auditory canal, with possible
extension into thecerebellopontine angle

42. TREATMENT
•Surgeryorradiation therapy.
•large tumors or significanthearing loss
•Observation of thetumor
•can be considered in patients with small tumors or minimalhearing
loss,
•advanced age.
•MRIsurveillance every6–12 months.
•Good prognosis: Neuromas are a WHO grade I brain tumor with a low
rate of recurrence (< 5%).

43. TUMORS OF THE NASOPHARYNX

44. HISTOLOGICAL ANATOMY
•Vestibule of Nasal cavity:
•Epidermis : Keratinized stratified squamous epithelium
•Dermis
•Respiratory epithelium
•Pseudo-stratified ciliated columnar epithelium with goblet cells
•Paranasal sinus
•Pseudo-stratified ciliated columnar epithelium with goblet cells
•Nasopharynx:
•Pseudo-stratified ciliated columnar epithelium with goblet cells

46. COMMON TUMORS OF NASOPHARYNX
BENIGN
•Nasal papilloma
•Juvenile nasopharyngeal
angiofibroma
MALIGNANT
•Cutaneous squamous cell
•Nasopharyngeal carcinoma
•Carcinoma, adenocarcinoma,
•Neuroendocrine tumors,
•Mucosal melanoma

47. JUVENILE NASOPHARYNGEAL ANGIO
FIBROMA
•benign neoplasm of the nasopharynx
•Adolescents and young adults between 14 and 25 years
•male predominance
•high androgen receptor (AR) expression suggesting that JNA is
androgen dependent.
•locally aggressive tumor and invades the surrounding tissues
•attributed to a rich vasculature and lack of encapsulation.
•It impinges on adjacent structures and causes pressure erosion of
bone

48. PATHOPHYSIOLOGY
•JNAs originate from a hamartomatousnidus in the roof of
thenasopharynx
•JNAs grow rapidly, extending into and distorting adjacent
structures (e.g.,nasopharynxand nasal cavity, paranasal
sinuses,orbit,cranialcavity)
•Thetumorexpressesandrogenreceptors(testosteronedependent),
•JNAs are seen exclusively in males, especially aroundpuberty,
whentestosteronelevels begin to peak.
•JNAs have vascular and fibrous components
•The vessels are devoid of a muscular layer→ severeepistaxis

49. CLINICAL FEATURES
•Painless
•Progressive unilateral nasal obstruction
•Epistaxis
•Rhinorrhea
•Other symptoms
•Impaired Eustachian tube function,
•facial deformity,
•proptosis and
•changes in visual acuity
•cranial nerve palsy

50. FISCHCLASSIFICATION
Type I: the tumor is restricted to the nasal cavity and the
nasopharynx without bone destruction
Type II : the tumor invades the pterygomaxillary fossa and
maxillary, sphenoidal and ethmoid sinuses with bone
destruction
Type III : the tumor invades the infratemporal fossa, the orbit,
and the parasellarregion but remains lateral to the cavernous
sinus
Type IV: the tumor invades the cavernous sinus, the optic
chiasma and the pituitary fossa.

51. DIAGNOSIS
•History, clinical examination,
•Nasal endoscopy;
•Specialized imaging techniques
•Arteriography,
•CT,
•Magnetic resonance imaging (MRI)

52. TREATMENT
•preoperative embolization and surgical resection
•Surgical excision of thetumor
•Surgical approach depends on size and extent of thetumor(e.g., transmaxillary, transnasal)
•Preoperative embolisationof feeding vessels necessary to reduceintra-operativeblood loss
•Stereotactic radiatiotherapy(e.g.,gamma knife)
•Reducestumorvascularization and size
•Indicated in recurrent cases or evidence of intracranial extension
•Risk of damage to adjacent structures (e.g.,eye, brain, spinal cord) is minimisedcompared
toexternal beam radiotherapy.
•Hormonetherapy withflutamide
•Androgenreceptorblocker for presurgicaltumorreduction
•Adverse reactions(e.g.,gynecomastia, loss of libido)
•Completetumoreradication not possible

53. JNA

54. NASOPHARYNGEAL CARCINOMA
•Tumors arising in the nasal cavity
•Peakincidence:Bimodal
•≥ 50 yearsof age
•early 15-25 years
•Prevalence:< 3%of tumors in the respiratory tract
•Sex:♂>♀
•Common in people of Asian Descent
•Genetic
•Foods with nitrosamine
•Associated withEBV infection
•inhalation exposure to tobacco, wood dust, glues, and adhesives

55. CLINICAL FEATURES
•Most common sites: nasal cavity, followed by themaxillary sinus
•Unilateral nasal obstruction
•Epistaxis
•Chronic sinusitis
•Hyposmia/anosmia
•Advanced disease: a triad of facial asymmetry, palpable or
visibletumorin theoral cavity, and visible intranasaltumor

56. WORK UP
DIAGNOSIS
•Nasal endoscopy
•Biopsy and histopathological examination
•Imaging: CT and MRI
TREATMENT
•Radiation therapy combined with chemotherapy
•Mainstay treatment
•Surgery is last treatment option

57. NASOPHARYNGEAL CARCINOMA
COMPLICATIONS
•Involvement of adjacent structures (e.g., eye orbits, sinuses, palate)
causing neuralgias, facial pain, impaired vision, ocular symptoms
(e.g., exophthalmos, diplopia), and/or dentalgia
PROGNOSIS
•The five-year relative survival rate for nasal cavity and paranasal sinus
carcinomas is ∼80%.
•A patient with unilateral difficulty breathing through the nose may
have a malignant tumor.

58. TUMORS OF THE OROPHARYNX

59. HISTOLOGICAL ANATOMY
Oropharynx:
•non-keratinizingstratified
squamous epithelium

60. COMMON TUMORS OF THE OROPHARYNX
BENIGN
•Pailloma
•Haemangioma
•Pleomorphic adenoma
•Mucous cyst
•Lipoma
•Fibroma
MALIGNANT
•Oropharyngeal Squamous cell
carcinoma
•Lymphoma

61. OROPHARYNGEAL SQUAMOUS CELL
CARCINOMA
•Commonly known as throat cancer or tonsil cancer
•Thesixth most common cancer worldwide
•Refers to the cancer of the base and posterior one-third of the tongue,
the tonsils, soft palate, and posterior and lateral pharyngeal walls.
•Categorized into HPV-associated and non-HPV-associated carcinomas.
•HPV16 is the most common type found in oropharyngeal cancers
•Prevalence is higher in males than females
•Peak age is at 50, may occur at 30-40
•Spread through blood and lymphatics

62. OROPHARYNGEAL SQUAMOUS CELL
CARCINOMA
CLINICAL FEATURES
•Dysphagia
•Odynophagia
•Sore throat
•Foreign body sensation
•Muffled voice
•Severe ear pain
•Dysarthria,
•Presence of a lump in the neck
•Otalgia.
•Unexplained weight loss
•Hematemesis.
RISK FACTORS
•Oral sex
•Open-mouthed kissing
•Smoking tobacco
•Alcohol consumption
•Diet low in vegetables and fruits,
•Betel quid chewing,
•Poor nutrition,
•Marijuana smoking,
•Asbestos exposure,

63. INVESTIGATIONS
•Magnetic Resonance Imaging (MRI)
•Excellent visualization of the tumor
infiltrating the soft tissue
•Optimal for the staging of the primary
tumor
•Computed Tomography (CT)
•utilized toestimate the size of the tumor
•assist indeciding on surgical removal of
the tumor
•spread to the lymph nodes in the neck or
lower mandible.
•Positron Emission Tomography (PET)
•cross-sectional imaging fails to identify
primary tumors
•assessment and detection of the
recurrence of the primary tumors
•Endoscopy and Laryngoscopy
•to visualize and examine the suspicious
sites in detail and take the biopsy sample.
•Ultrasonography
•excellent accuracy of staging the nodal
disease
•Biopsy
•Definitive diagnosis.
•Fine-needle aspiration biopsy

64. STAGING

65. STAGING

66. TREATMENT
•Radiotherapy-mainstay treatment
•Patients with HPV
•Young patients
•Good prognosis
•Surgery
•Transoral robotic surgery,
•Transoral video laryngoscopicsurgery,
•Transoral ultrasound surgery, and
•Endoscopic laryngopharyngeal surgery

67. OROPHARYNGEAL CARCINOMA

68. TUMORS OF THE LARYNX

70. HISTOLOGICAL ANATOMY
•Mucosa:
•Pseudo-stratified ciliated columnar epithelium with goblet cells
•Vocal folds and surface of the egiglottis:
•Non-keratinized stratified squamous epithelium
•Lamina propria

71. COMMON TUMORS OF LARYNX
BENIGN
•Laryngeal papilloma
•Vocal fold polyp
•Vocal fold cyst
•Vocal fold granuloma
MALIGNANT
•Laryngeal carcinoma

72. LARYNGEAL PAPILLOMA
•Laryngeal papillomatosis (LP), also known as recurrent respiratory
papillomatosis (RRP)
•Benign tumorof the laryngealepitheliumcaused byhuman
papillomavirus(HPV) infectionof the throat
•Most common benign mesenchymal neoplasm of the larynx in
children
•Most difficult benign histologic conditions to treat due to its high
tendency to recur and spread to the adjacent respiratory tract.

73. LARYNGEAL PAPILLOMA
ETIOLOGY
•Human Papilloma Virus (HPV)
•HPV6 & HPV 11
RISK FACTORS
•Immunosuppression
•Prima-gravid women
•Firstborn child
•Recently acquired genital warts
•Oral sex

74. CLASSIFICATION
•Juvenile onset recurrent respiratory papillomatosis(JORRP)
•< 20 yearsof age
•Peak onset< 5 yearsof age
•usually due tovertical transmissionduringbirth
•Cause not well known
•Adult onset recurrent respiratory papillomatosis(AORRP)
•Cause not well known
•Suggested theories
•potentially viasexual activity
•reactivation of the dormantvirus

75. CLINICAL FEATURES
•Hoarseness,dysphonia/aphonia
•Stridor,chronic cough,dyspneadue toairwayobstruction
•Dysphagiain advanced disease

76. INVESTIGATIONS
•Laryngoscopy
•Multipleraspberry-likeswellings
•Usually located onvocal cords
•Can be unilateral or bilateral
•Histopathology
•Multiple proliferations of hyperplastic stratified squamous epithelium with a
central fibrovascular core.
•Basal and parabasal cell hyperplasia in a perpendicular orientation with
koilocytosisatypia

77. LARYNGOSCOPIC VIEW

78. MANAGEMENT
•No definitive cure, goal is to limit disease spread
•Surgical removalof symptomatic lesions
•Cold steel excision
•Coblation-controlled ablation
•Adjuvant treatmentwith
•Chemotherapy
•Avastin (bevacizumab)
•humanized monoclonal antibody against vascular endothelial growth factor A (VEGF-A)
•Antiangiogenic

79. COMPLICATIONS
•Malignant transformation intosquamous cell carcinomain up to 4%
of cases
•Airwayobstruction andlife-threateningrespiratory distress
Prognosis
•Frequently recurring
•Often regresses spontaneously inpuberty
•Papillomasthat remain till adulthood are potential precancerous
lesions.

80. LARYNGEAL CARCINOMA
•One-third of head and neck cancers
•Early-stage disease is highly curable with either surgical or radiation
monotherapy
•Sex:♂>♀
•Age of onset:40–70 years

81. RISK FACTORS
•Smoking
•Alcoholuse
•Advanced age
•Exposure topaint, asbestos, gasoline fumes and radiation
•Infection withhuman papillomavirus(HPV 16 and18)
•Betel nut chewing
•Diets rich insalt-preservedmeats (nitrosamines) and dietary fats
•Precancerous lesions:leukoplakiaorlaryngeal papillomatosisin adults

82. CLASSIFICATION
•Classified according to their location in relation to theglottis
•Glotticcarcinoma/vocal cordcarcinoma
•most common form
•approximately 60% of cases
•Supraglotticcarcinoma
•approximately 40% of cases
•Lymphatic involvement is a pathologic hallmark of supraglottic cancers
•subdivided into suprahyoid epiglottis, infrahyoid epiglottis, false vocal cords,
aryepiglottic folds, and the arytenoids.
•Subglotticcarcinoma
•approximately 1% of cases

83. CLINICAL FEATURES
•Hoarseness/change in voice
•Foreign body sensation
•Dyspnea
•Dysphagia
•Stridor
•Aspirationwhile eating or drinking

84. INVESTIGATION
•Direct laryngoscopy
•Reveals irregular, nodular, or ulcerative lesions
•Micro laryngoscopicexamination and tissuebiopsy:
•Visualize very small tumors
•Differentiate laryngeal cancer frombenign laryngeal lesions
•Stroboscopic examination: assessesvocal cordmobility
duringphonation
•Imaging: CT,MRI, and/orultrasoundof the neck to assesstumorsize
and spread to surrounding tissue

87. TREATMENT
•Early stages:
•radiotherapy or transoral endoscopic laser resection
•Advanced stages(withlymph nodeand/or distant organmetastasis)
•laryngectomy
•Voicerehabilitationafter laryngectomy: The patient can be trained to produce
speech
•Esophageal speech
•Voice prosthesis
•Electronic speaking aid

88. COMPLICATION
•Mucositis
•Xerostomia
•Dysphagia
•Esophageal stricture
•Esophagitis
•Pneumonia
•Sepsis
•Venous/pulmonary TE

89. REFERENCES
1.Abdul Ansari; Muhammad Ali Tariq; NaziaM. Sadiq. Histology,
Ear, 2023.
2.C G Jackson,M E Glasscock 3rd,P F Harris, Glomus Tumors.
Diagnosis, classification, and management of large lesions,
PMID:6284098,DOI:10.1001/archotol.1982.00790550005002
3.Zohaib Jamal; Fatima Anjum, Oropharyngeal Squamous Cell
Carcinoma, 2023