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Management Protocols
Ca Oropharynx
Dr. Bikram Choudhury
Pune
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Why is OPSCC Important?
Increasing Incidence! More than any other site UADT.
RISE in OPSCC in NON-SMOKERSHPV Induced Tumors
Increased CRT Usage, Decreased Radical Sx + Post-Op RT
HPV Induced Tumours exquisitely Radiosensitive
Trans-Oral Micro-laser Resection techniques developed
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Introduction
Relatively uncommon but fastest growing incidence.
Rate of increasing incidence is also increasing.
90% - OP-SCC
8% - OP-NHL
2% - OP- Minor Salivary Gland Tumors
Distinct male preponderance in classical OPSCC
Now 50% OPSCC HPV induced -> Prevalance M:F equal
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Surgical anatomy
Oropharynx - from hard palate to hyoid level
Subsites Tonsillar fossa (Lateral walls)
Base of tongue (Anterior wall)
Posterior pharyngeal wall
Soft palate
Innervations: IX, X, XII, V
Lymphatic drainage: Level II, III and IV
Retropharyngeal Lymph Nodes from PostPharyngeal wall
Bilateral from central regions
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Surgical anatomy
Surrounded by potential fascial spaces
Retropharyngeal space
Parapharyngeal spaces
Masticator space Potential routes for cancer spread
Neurovascular relations in the neck/ skull base
Surgical margins difficult to achieve if tumor extendsto nasopharynx/base skull and encases carotid
Mandible/ maxilla may be involved
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Usual Presentations
FB feeling
Dysphagia
Pain throat with/ without Odynophagia
Referred otalgia
Neck swelling
Trismus
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OPSCC-Epidemiology
Tobacco ++, Alcohol Synergistic
HPV-16. Effect responsible for increasing incidence
OPSCC over last decade.
Increased Tonsillar Ca parallels OPSCC rise & HPV +ve
cases
Detect HPV using biomarkers using in situ hybridization
(Detect HPV genome integration into host genome) +
HPV E7 protein overexpression
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Characteristics of HPV Induced OPSCC
Younger patients
Relatively more females equalizing ratio
HPV-16 infection, orogenital sex, NO SMOKING/TOBACCO
relationship need be present
Non-poorly keratinizing Basaloid SCC
Genetically - Loss at 13q, gain at 20q ; disruptive p53
mutations
IMPROVED prognosis with CRT ; Survival approaching 90-
95% at 3 years. If Sx used, no change in prognosis.
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Patterns of Presentation
Symptoms of Primary disease with/w-out LN Metz
LN Metz with Clinically Detectable OPSCC Primary
LN Metz with Unknown Primary
With PET-CT assessment vast majority CUPS are OPSCC
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Lateral Wall Tumors
>50%
Usually Tonsillar
Inferior Pole and other Submucosal Primaries clinically
difficult to visualize
PALPATE! SPREAD
ANT-SUP RMT, Buccal Mucosa, BOT
LAT Erode to Pterygoid Muscles TRISMUS & Pain
POST-LAT Parapharyngeal Space/ Carotid Sheath
INF Lat Pharyngeal Wall PF
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BOT Tumors
40% OPSCC
Early are Submucous & evade detection
PALPATE!
Advanced lesions cross midline & pass throughGenioglossusOral Tongue/ FOM/ Vallecula/
Epiglottis & Pre-Epiglottic Space involvement
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Soft Palate Tumors
Rare, usually site for Minor Salivary Gland
Tumors
Spreads
Nasopharynx
Superior Tonsillar Pole
Palatine Nerves
Maxillary Antrum
AGGRESSIVE BILATERAl LN INVOLVEMENTwith
little Primary tumour volume
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Posterior Wall Tumors
Unusual
Contiguous submucosal spread naso & hypo-pharyngeal posterior wall
Prevertebral fascia barrier to spread
Late presentation
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T-Staging
Tx: Primary tumour cannot be assessed Tis: Carcinoma-in-situ
T1: Tumour 2 cm or less in greatest dimension
T2: Tumour more than 2 cm but not more than 4 cm in
greatest dimension T3: Tumour more than 4 cm in greatest dimension
T4a: Tumour invades larynx, deep/ extrinsic muscle of thetongue, medial pterygoid, hard palate or mandible
T4b: Tumour invades lateral pterygoid muscle, pterygoidplates, lateral nasopharynx, skull base or carotid artery
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N-staging
Nx: Regional lymph nodes cannot be assessed
N0: No regional lymph node metastasis
N1: Metastasis in a single ipsilaterallymph node, 3 cm orless in greatest dimension
N2a: Metastasis in a single ipsilaterallymph node, >3 cmbut
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M-staging
Mx: Distant metastasis cannot be assessed
M0: No distant metastasis
M1: Distant metastasis present
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Staging
CONVENTION : IV a operable, IV b inoperable, IV c - metastatic
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Factors affecting prognosis
Site of lesion
Exophytic/infiltrative
TNM Staging
Nutritional status- PEG/ nasogastric tube
Co-morbidities
Performance status
Patient preferences, ability to cope withtreatment and its functional consequences
Treatment received
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Clinical Examination
EVALUATE ENTIRE UADT
FIBREOPTIC ENDOSCOPIES
PALPATE TONGUE BASE & TONSILS
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Evaluation
FNAC
Initial workup of palpable node
USG Guidance if needed
BIOPSY
Under GA
MAPPING done
look for SYNCHRONOUS growth Deep incisional Biopsy, including from Tonsillar
growth
Tonsillectomy if CUPS
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Imaging
CT Scan Mandible invasion assessment/ THORAX for
Metz
MRI BOT assessment/ Parapharyngeal Spread
Chest radiograph
OPG assess mandible/ inf alveolar N (rarely needed
after CT)
PET-CT N0 neck, post CRT neck assessment, CUPS
UGI Endoscopy look for synchronous growth (BaSwallow if NA)
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CT showing enhanced lesion in BOT
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MRI
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MRI Showing basetongue lesion
PET scanshowing lungnodule
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PET Scan Malignancyleft tonsil
Liver metastases
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Investigations
Laboratory studies: CBP, LFT, RFT, ECG, Nutritionalassessment
EUA at Biopsy
Per-oral panendoscopy for synchronous secondprimary
Assessment of local extent- completevisualization and palpation
Submucosal Mandibular
Tumor fixation
Prevertebral fascia
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Treatment
Multidisciplinary Team approach forcomprehensive treatment
Optimal treatment for the individual patient
Aim at functional preservation/ restoration inaddition to increased disease free survival status
Cosmetic appearance
Quality of life
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Treatment modalities
Surgery
Radiotherapy
Chemotherapy
Supportive and supplementary measures
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Choice of treatment modality
Site of malignant tumor
TNM staging
General condition of the patient
Patient preferences
Availability of facilities, expertise and social support
Financial status
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Organ preserving strategies Newer and are now advocated as preferred approach
Concurrent chemotherapy with radiotherapy
Significant survival increase when concurrent carboplatin
and 5 FU was added to RT.
CT adds small benefit on survival when added to
locoregional treatment:
Concurrent CTRT gives similar survival rates compared
to Surg + RT
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Preferred modalitiesT1 or T2
Surgery or radiation T2: Combine elective neck dissection or radiation in view of
high incidence of occult metastasis even in N0 neck
Salvage RT/ surgery for residual lesion, if any
Post-Op RT or CTRT or brachy+RT if lesion is Deeply infiltrative
Extending beyond anterior pillars
Base tongue is involved
RT given after surgery if
Positive margins Tumour exhibits aggressive behavior
Perineural or vascular invasion of primary/ node
Two or more histologically positive node
Extracapsular nodal spread
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Preferred modalities
T3 or T4 RT or CTRT
Organ preservation strategy: Concurrent CTRT or
hyperfractionated radiotherapy is now preferred as functionaloutcome is better
Salvage surgery for residual lesion, if any
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Surgical treatment
Good exposure
Wide margins of 1-2 cm from palpable extent, including its
depth
Frozen section control preferable
Attempt to spare mandible whenever possible
Functional and cosmetic outcome should be good
QOL good
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Surgical approaches
Transoral Oral Cold Steel Excision
Laser assisted Microscopic Excision
Transpharyngeal Lateral Pharyngotomy
Midline Vallecula approach
Transmandibular Paramedian Mandibulotomy
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Choice of surgical approach depends on
Size and location of tumor
Exposure required
Concomitant neck dissection is planned or not
Method of reconstruction
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Reconstruction options- Soft tissue
Primary closure/ secondary intention
Split thickness skin grafts
Local flaps
Tongue/ palatal/ pharyngeal/ cheek flaps
Regional flaps PMMC, Lat dorsi, trapezius, platysma, stenocleidomastoid, temporal,
temporalis, masseter, pericranial, DP flap, etc.
Free microvascular flaps
Faciocutneous flaps like forearm, lateral thigh, lateral arm, scapular, etc
Latissimus dorsi
Rectus abdominis
Prosthesis
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Reconstruction options-
Mandible
None
Plate
Pedicled osseous flaps
Rib, scapula, clavicle, calvarium
Free osteocutaneous flaps
Fibula, illiac crest, scapula, radial forearm, clavicle,
etc
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ComplicationsRadiotherapy
Mucositis Xerostomia
Taste dysfunction
Dysphagia
Fibrosis
Ulceration and tissue necrosis
Osteoradionecrosis of the mandible Hypoglossal palsy
Laryngeal odema and stridor
Oral/ oropharyngeal candidiasis
Surgery
Approach related
Damage to teeth Damage to nerves
Cerebral embolism
Carotid artery thrombosis
Resection and reconstructionrelated
Hemorrhage Wound dehiscence and infection
Positive resection margin
Pharyngocutaneous fistula
Aspiration
Dysphagia
Velopharyngeal incompetence
Non-union/ osteomyelitis of themandible
Malocclusion and TMJ dysfunction
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Palliative care
Pain
Swallowing
Airway
Socio-economic
Nursing
Spiritual well being
SUMMARY MX OPTIONS
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SUMMARY MX OPTIONS
PRIMARY NECK Comments
RT RT Less Toxic HPV + Better Add EGFR
inhibitor
Add
Monoclonal
Ab
RT/CRT ND followed
by RT
T1-2 N+
OPSCC
Function
sparing ND
93.5%
@33
months
CRT CRT followedby PET-CT +/-
ND
PET-CT ifve spares pt ND
CRT CRT foll by
planned NDOnly if PET NA
Trans-Oral
Surgery +/-
RT/CRT
ND +/-
RT/CRT
Unusual to NOT give CRT or Post OP RT in patients
managed Surgically
Open Surgery
+/- RT/CRT
ND +/-
RT/CRT
More Morbid. Better Histological Clearance Data.
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Conclusions
OPSCC commonest type of malignancy Incidence Increased in last decade
Due to HPV 16 induced Ca
Distinct from smoking induced Ca
Many present late
Rich lymphatic drainage and thus nodalmetastasis common (>80%)
HPV induced Ca has better prognosis
Many different treatment options &combinations challenge to multi-disciplinaryteams
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