Mx Protocols Oropharyngeal Malignancy Compat

7/30/2019 Mx Protocols Oropharyngeal Malignancy Compat

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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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Mx Protocols Oropharyngeal Malignancy Compat

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