Head and neck cancers are a major burden in India. Lip and oral cavity cancers have the highest incidence rates in India compared to other sites globally. Tobacco and alcohol use are significant risk factors. Premalignant lesions like leukoplakia can develop and have risks of malignant transformation. Cancers commonly arise from squamous mucosal lining and spread via lymphatic routes to cervical lymph nodes. Staging incorporates primary tumor size, lymph node involvement, and distant metastasis. The document reviews epidemiology, risk factors, sites of head and neck cancers like oral cavity, oropharynx, larynx and staging.

1. Pre-management in Head
and Neck Cancers
Presented by:
Dr. Bonnie R K Singh
Moderated by:
Dr. Punita Lal

2. Epidemiology
• As per the GLOBOCON 2020 data, among Head and Neck cancers (HNC):
Gender specific incidence of Head and Cancers:
- MC in males (16.2%)
- 4th MC in females (4.6%)
So, from the figures, it is crystal clear, the overall burden of HNC is very high in India, compared to the world and that of lip and oral cavity cancers
exceeds that of other sites by a much greater margin in India.
*2nd MC cancer after Breast Cancer
**3rd MC cause of cancer related deaths after Breast and cervical cancers
INCIDENCE DEATHS
Worldwide India Worldwide India
Lip and Oral Cavity 3,70,000 1,35,000* 1,70,000 75,000**
Larynx 1,84,000 34,000 99,000 21,000
Nasopharynx 1,33,000 5,600 80,000 4,000
Oropharynx 98,000 20,000 48,000 12,000
Hypopharynx 84,000 28,000 38,000 11,000
Salivary Gland 53,000 7,800 22,000 5,000

3. Risk Factors
• Tobacco consumption (chewing betel/ smoking)
• Most important known risk factor for the development of head and neck
cancer.
• There is some evidence for a genetic predisposition to the carcinogenic
effects of tobacco.
• In addition, tobacco and alcohol consumption appear to have a synergistic
effect.
• Alcohol drinking
• Field Cancerisation
Carcinogens like tobacco and alcohol tend to get exposed to a vast mucosal
area of the UADT. This may induce generation of multiple patches of gentically
altered mucosa, in which, the epithelium has many independent foci of
abnormal tissue. These tissue patches can inturn give rise to potentially
malignant and malignant lesions.
Development of recurrences and 2nd primary tumors in completely treated
cases of HNC (even after LVI/PNI -ve and margin free tumor resection),
corroborates the concept of field cancerisation.

4. • Human Papilloma Virus (HPV) infection:
• Typically in younger men who are non users of tobacco/ alcohol (or have remote smoking
history)
• MC HPV 16, esp. in oropharyngeal cancers arising from the base of tongue and tonsils,
presents with an early stage primary tumor and an advanced stage nodal disease (N2/N3).
• Usually, they tend to haver better OS and DFS (better prognosis). Also, tend to be more
responsive to therapy. But simultaneous use of tobacco decreases survival and treatment
response in HPV-positive HNC patients. The risk of progression/mortality and second primary
with oral squamous cell carcinoma (OSCC) increases by 1% and 1.5%, respectively.
• Methods of detection-
• PCR and ISH of HPV DNA are highly sensitive tests
• The tumor p16 status (detected via IHC) is a recommended surrogate marker for HPV.
• If we look at individual Indian studies,
• Elango et al. and Ramshankar et al. reported a prevalence of 48% and 51.2%, respectively, in oral tongue
cancers.
• Balaram et al. reported a high prevalence of 73.6% in the South
• Prevalence in the North and Northeast ranged from 7 to 29%
• D’Costa et al. reported 15% prevalence in the western region
• 33.6% prevalence in the Eastern region
• The only study from Central India by Gheit et al. reported 27.5% prevalence
• Hepatitis B Virus (HBV) infection:
• least common; primarily responsible for Nasopharyngeal Cancers

5. Grossly, premalignant lesions can present as:
 Leukoplakia:
 Characterised by hyperkeratosis
 Usually a/w underlying epithelial hyperplasia
 In absence of underlying dysplasia, probability of malignant changes is <5%
 Erythroplakia:
 Characterised by red superficial patch adjacent to normal mucosa
 Commonly a/w epithelial dysplasia and CA- in situ or invasive CA in up to 40% of
cases
 Oral Lichen Planus:
 chronic, autoimmune, inflammatory disease which may affect skin, oral mucosa,
genital mucosa, scalp, and nails
 most commonly affected areas are in oral cavity are dorsum of the tongue, buccal
mucosa and gingiva.
 Malignant transformation ratio has been reported in 0% to 10% of patients
 Increased malignant transformation risk occurs greater in erosive and atrophic forms
and in cases of lesions of lateral border of the tongue
 Oral submucous fibrosis
 chronic and potentially malignant disorder characterized by juxtaepithelial fibrosis of
the oral cavity.
 eventually, stiffness of oral mucosa, trismus and an inability to eat develops
 strongest risk factor is the chewing of betel quid containing areca nut
Pathology

6. • Majority of tumors arising in Head and Neck (other than non melanoma
skin cancers) arise from the squamous mucosal lining of the UADT (Upper
Aero Digestive Tract). Hence, Squamous Cell Cancers account for 90-95% of
lesions in Head and Neck region, which can further be classified into:
• Well Differentiated
• Moderately Differentiated
• Poorly Differentiated
• Other less common histologies include:
• Verrucous Carcinoma
(a variant of Squamous Cell Carcinoma)
• Adenocarcinoma
• Adenoid cystic carcinoma
• Mucoepidermoid carcinoma

7. Sites of Head and Neck Cancers
• The major sites of HNC are a/w or tend to lie along the UADT:
• Begins: where the skin meets mucosa
of nasal vestibule and vermillion
borders of lip
• Ends: at the level of cricoid, marked by
the junction of cricoid cartilage & trachea
and hypopharynx & esophagus

8. • It includes the following major sites:
• Oral Cavity
• Oropharynx
• Nasopharynx
• Hypopharynx
• Larynx
• Nasal Cavity (along with the paranasal sinuses)
• Salivary Glands

9. WHAT’S THE STAGE..?

10. AJCC 8th edition of TNM Staging

11. Lymph Node Groups
• The head region consists of the following major
Lymph Nodes (LNs):
• Tonsillar (Jugulodiagastric) LNs
• Parotid LNs
• Preauricular LNs
• Postauricular LNs
• Occipital LNs
• The neck region has a level system to describe the location of LNs:
• Level Ia: Submental LNs
• Level Ib: Submandibular LNs
• Level II: Upper Deep cervical/jugular LNs
• Level III: Middle Deep cervical/jugular LNs
• Level IV: Lower Deep cervical/jugular LNs
• Level V: Posterior Triangle group of LNs
• Va: Spinal Accessory LNs
• Vb: Transverse Cervical and Supraclavicular LNs
• Level VI: Pre and Para tracheal
Lindbergh series
Robert Lindbergh had reported on the incidence and topographical distribution of
lymph node metastasis on admission in patients with squamous cell carcinomas of
the major anatomical sites of the upper respiratory and digestive tracts.
We will see these with the respective sites

12. Major Sites of HNC

13. Oral Cavity
• Most common site for Squamous Cell Carcinoma of UADT among HNC
• It extends:
• Anteriorly: Skin Vermillion Junction of lip
• Posteriorly:
• Superiorly: Junc. Of Hard and Soft Palate
• Laterally: Anterior Tonsillar Pillar
• Inferiorly: Line of circumvallate papillae
• The various subsites of Oral Cavity include:
• Mucosal Lips
• Alveolar ridges (Lined by gingiva)
• Hard Palate
• Buccal Mucosa
• Anterior 2/3rd of Tongue: 4 parts – Tip, Lateral Borders, Dorsum,
Under surface
• Floor of Mouth
• Retromolar Trigone (RMT)

14. Lymphatic Drainage
• Lip:
• Level Ia and Level Ib LNs (Neck nodes a
potential site for relapse)
• Nodal involvement rare (<5%at presentation)
• Incidence higher in large, PD, mucosa invading
tumors; those at angle of the mouth, in
recurrent cases
• Remaining Oral Cavity:
• Level Ia, Ib and Level II LNs
• Ds. can SKIP directly to Level III and IV LNs
(Skip LNs)
• Midline tumors may present with B/L
nodal involvement

15. Clinical Presentation
• Tongue:
• Longstanding h/o leukoplakia or erythroplakia
• Infiltrative/ Exophytic lesion
• c/o dysarthria s/o deep ms. involvement
• Remaining subsites:
• Non healing ulcer ± Bleeding
• Mouth pain
• Loosening of teeth/ ill fitting dentures
• Dysphagia/ odynophagia
• Referred otalgia

16. TNM staging of Primary Tumor (T)
• Recent data has shown that primary tumor
depth of invasion (DOI) has a significant
impact on disease outcomes and
compliments the previous criteria used for
T-stage classification. As a result, the new
8th edition of AJJC - TNM staging system
incorporated DOI to reflect this influence on
prognosis.

17. Oropharynx
• It extends:
• Anteriorly: marked
• Superiorly by hard palate- soft palate junction
• Inferiorly by line of circumvallate papilla
• Superiorly: level of superior surface of soft palate
• Posterolaterally: Pharyngeal wall (C2-C3)
• Inferiorly: level of superior surface of hyoid bone
• The various subsites of oropharynx include:
• Soft palate
• Tonsillar Pillars
• Palatine Tonsils
• Base of Tongue
• Lat. And Post. Pharyngeal wall

18. Lymphatic drainage
• 60% cases of Oropharyngeal Carcinomas
present with LN involvement
• Cancers of Base of Tongue, Soft Palate
and posterior pharyngeal wall can
present with B/L nodal involvement as
they are midline structures
• Primarily drainage to Level II, III > IV LNs.
• Tonsillar LNs with Tonsillar Carcinomas
• Retropharyngeal LNs with Tumors of Soft
Palate and Posterior Pharyngeal Wall

19. Clinical Presentation
• Dysphagia
• Pain (Odynophagia or otalgia)
• Snoring
• Hypersalivation and Hot potato (change in) voice (esp. with BoT
tumors)
• Neck Mass
• Especially in pt.’s of HPV+ve oropharyngeal CAs.
• Often cystic in nature

20. TNM staging of Primary
Tumor
• Staging of oropharyngeal cancers now is different for HPV(+) and HPV(-)
cancers, reflecting the different biologic behaviour of these two different
disease entities.
• Mucosal extension to lingual surface of epiglottis from primary tumors of the
base of the tongue and vallecula does not constitute invasion of larynx.

21. Hypopharynx
• It extends:
• Superiorly: Level of Hyoid Bone
• Inferiorly: Level of Cricopharyngeus Muscle
(UES)
• The various subsites of hypopharynx
includes:
• Anteriorly: Post Cricoid region (MUCOSAL
IMORESSION/BULGE INTO HYPOPHARYNX)
and Pyriform Sinus (B/L GUTTERS FORMED
ON EITHER SIDES OF THE POST CRICOID
AREA)
• Posterolaterally: Hypopharyngeal Wall (C4 –
C6)

22. Lymphatic Drainage
• The hypopharynx has an extensive lymphatic
supply.
• The majority of piriform fossae cancers have
nodal involvement at presentation. There is early
spread to Level II, III >> IV LNs, but the drainage
can include all levels including the
supraclavicular nodes.
• The posterior pharyngeal wall drains to the
retropharyngeal nodes (of Ranviour) and deep
cervical lymph nodes (Level II, III, IV >> V).
• The postcricoid region drains to levels III, IV and
VI LNs.

23. Clinical Presentation
• Due to the large volume available to grow, tumours of
hypopharynx tend to present symptomatically at
advanced stages (though nodal staging may be seen at
presentation):
• Difficulty with swallowing
• Difficulty with speech
• Sore Throat

24. TNM staging of Primary Tumor

25. Larynx
• It is lined entirely by squamous epithelium, except for the
ventricles and subglottis (lined by respiratory
pseudostratified ciliated columnar epithelium).
• Extends b/w C3 to C6 cervical vertebrae:
• Speriorly: Oropharynx
• Posterolaterally: Hypopharynx
• Inferiorly: Trachea
• The larynx has 3 major subsites:
• Supraglottis
• Glottis
• Subglottis

26. Supraglottis
It contains the following structures:
• Epiglottis
• Aryepiglottic folds
• False Vocal Cords (VC)
• Arytenoid cartilages
Pre-epiglottic Space:
• Lies sup-ant. to the epiglottis
• Has a rich network of lymphatic drainage -
early and (USUALLY) b/l nodal spread to Level
II, III and IV >> VI LNs.

27. Glottis
• It extends upto 1 cm below the True VC
• It is marked by the following structures:
• Anterior Commisure
• True Vocal cords
• Posterior Commisure
• Ventricle (space b/w the VC)
• Routes of Spread:
• No definite lymphatic drainage – regional LN
involvement is less common
• Paraglottic Space
• Allows (Transglottic) spread of tumors from glottis to
supra/subglottis and vice versa

28. Subglottis
• Extends from 1cm below the True VC to level of inferior aspect of
cricoid cartilage
• Lymphatic Drainage
• Level III, IV and VI LNs
• Tumors are rare; usually present with transglottic spread of
supraglottic tumors

29. Clinical Presentation:
• The first symptom in more than 90% of patients with true glottic
cancer is hoarseness. Loss of laryngeal crepitus.
• Advanced tumours of the vocal cords may narrow the airway,
especially if a vocal cord is paralysed, leading to stridor.
• Hoarseness is less common as a symptom for early supraglottic
cancer - complain initially of either a sore throat or a foreignbody-like
sensation
• Hoarseness only develops when the tumour reaches the vocal cord.
More advanced tumours may have pain referred to the ear (BY VAGUS
NERVE AND IT’S AURICULAR BRANCH (N. OF ARNOLD)) and patients
may occasionally cough up blood (haemoptysis).

30. TNM staging of Primary Tumor

31. Nasopharynx
• Extends:
• Anteriorly: Posterior choana of the nasal cavity
• Superiorly: Base of Skull formed by the Sphenoid
bone (above which, lies the sphenoid sinus)
• Posteriorly: Tissue of the prevertebral fascia
adjacent to C1 and C2 cervical vertebrae in
continuation with the posterior pharyngeal wall
• Laterally: Pharyngobasilar fascia – contains 2
important structures –
• Opening of Eustachian Tube
• Fossa of Rossenmuller
• Inferiorly: Level of superior surface of soft palate

32. Routes of Spread:
• Rich lymphatic supply – therefore, commonly spread and,
indeed, present with neck nodes (70% to 90% of cases have
nodes at some point).
• Levels Ia and Ib are rarely involved
• Levels II to V can be considered the first echelon nodes for this
tumour site.
• Can spread to Retropharyngeal LNs too.
• Nasopharyngeal cancers have a high propensity for distal
haematogenous spread and, as a consequence, distal failure.
Clinical Presentation:
• The first presenting symptom is often painless node
enlargement confirmed on examination typically involving the
posterior cervical chain (Level V LNs).
• Other common symptoms:
• nasal obstruction and epistaxis through expansion into the nasal
cavity; Sore Throat
• auditory disturbances, especially unilateral deafness and recurrent
otitis media (d/t blockage of Eustachian tube).

33. TNM staging of Primary
Tumor & Regional LNs and
Group Staging

34. Nasal Cavity (and paranasal sinuses)
Nasal Cavity
• The normal lining of nasal cavity is
pseudostratified ciliated columnar epithelium
except for the vestibule lined by squamous
epithelium (containing sweat and sebaceous
glands)
• It extends:
• Superiorly: Cribriform plate of the ethmoidal bone
with olfactory apparatus
• Inferiorly: Hard palate
• Anteriorly: Nasal bones and cartilage
• Posteriorly: Posterior choana
• Laterally: marked by 3 bony turbinates
• Superiorly: medial wall of ethmoid sinus
• Inferiorly: medial wall of maxillary sinus
• Medially: Nasal Septum

35. Lymphatic drainage:
• Lymphatic drainage of the nasal cavity can be
divided into 2 pathways:
• Primarily, it drains via the nasopharynx to
retropharyngeal and Level II LNs
• Lower anterior portion (nasal vestibule) drains to
Level Ib, Level II and preauricular (parotid) LNs
• Paranasal sinuses has either no or very sparse
capillary lymphatics
Clinical Presentation:
• Epistaxis
• Nasal obstruction
• Mass protruding from nostril
• Facial and/or head pain may be seen in later
stages, due to pressure or tumor infiltration
into nerves or periosteum

36. Paranasal Sinuses
• They are lined by pseudostratified
ciliated columnar epithelium
• 4 in number: Maxillary Sinus,
Ethmoidal sinus (anterior, middle and
posterior group), Frontal sinus,
Sphenoid sinus
Lymphatic drainage:
• Overall, the sinuses have sparse
lymphatic drainage (typically towards
retropharyngeal and Level II LNs). As a
result, these tumors can become
quite large without LN involvement.

37. TNM staging of Primary Tumor

38. Salivary Glands
• These include:
• Major Salivary Glands:
• Parotid gland
• Submandibular gland
• Sublingual gland
• Minor Salivary Glands
• Histologically, the most common type
of benign salivary gland tumor is
pleomorphic adenoma, which
comprises approximately half of all
salivary tumors. Other rarer benign
salivary gland tumors include Warthin
tumor, basal cell adenoma, and
canalicular adenoma.
• The most common malignant salivary
gland tumors are mucoepidermoid
carcinoma and adenoid cystic
carcinoma, which together comprise
approximately one-half of all malignant
salivary gland tumors.

39. • Lymphatic Drainage:
• Parotid glands – Parotid LNs >> Level I, II and III LNs
• Submandibular glands – Level Ib LNs and perivascular LNs >> Level II and III
LNs
• Sublingual glands – Level Ia and Ib LNs
• Minor salivary glands (in the oropharynx) – Retropharyngeal LNs
• Clinical presentation
• Major salivary glands: Painless mass/swelling ± sign/symptoms of adjacent
nerve involvement
• Minor salivary glands: Depends upon the location –
• Oral cavity: Painless submucosal mass or mucosal ulceration
• Nasal Cavity/ Paranasal sinuses: Nasal obstruction/ congestion, vision changes
• Nasopharynx: Invasion of skull base, intracranial extension, CN involvement

40. TNM Staging of Primary Tumor

41. Nodal staging for HNC under the 8th edition of
AJCC TNM Staging System
• There are 3 variations:
• Specific for HPV +ve Oropharyngeal CA
• Specific for Nasopharyngeal CA
• Common for CA of rest of the sites (Oral Cavity, Nasal Cavity,
Hypopharynx and Larynx) & HPV –ve Oropharyngeal Cancers
• There is a clinical staging system (pre-operative staging or for patients
undergoing non-surgical therapy) and a pathologic post op staging system (for
individuals undergoing neck dissection as part of their management).

44. GROUP STAGING

45. Diagnosis and Staging Evaluation
• All pts. of suspected HNC should be assessed via a thorough history and
physical examination-
• History:
• Disease and pt. related information
• Detailed h/o habits and addictions
• Medical and family history, including any prior malignancy
• Co-morbidities
• Clinical Examination:
• Performance and nutritional status
• Physical Examination
• Inspection
• Palpation

46. Investigations:
• Baseline Investigations:
• Blood Investigations:
• CBC: Gives a baseline idea about the marrow functioning
• LFT: If deranged, can give an idea about any liver metastasis
• KFT: Check renal status of the pt., especially for chemotherapy purposes
• Blood Sugar: To get an idea about the glycaemic status of the pt.
• CXR:
• Done as part of the initial metastatic work up to exclude any pulmonary metastasis or
synchronous lung primary (seen in 2-5% cases of HNC, as they too are tobacco related)
• To see for aspirational changes the pt. might have as a result of their symptomatic
burden
• Radio-imaging of primary tumor site:
• CE-CT/MRI Face and Neck

47. Other Investigations:
• USG W/A:
• Done as part of metastatic work up to r/o any abdominal metastasis (especially for liver
secondaries)
• GFR:
• Tells about the renal status of the pt. in terms of clearance
• PTA:
• To check for the baseline status of hearing of the pt. for chemotherapeutic clearance
• Cardiological assessment

48. Dental Examination:
• RT for HNC often have treatment volume involve the mandible and salivary
glands.
• Throughout and after RT, pt. develop xerostomia (despite parotid sparing
approaches) - Increased risk for tooth decay and other dental problems
• Hence the need for full dental assessment and clearance before RT (a
minimum of 2 weeks prior) to get any dental problems removed
• Dental extraction
• Ensure dentures are well fitting
• Risk of dental problems post RT, especially osteoradionecrosis of mandible
are increased when RT is given after dental procedures

49. Dietary Consultation:
• HNC pts. are at increased risk of malnourishment before their diagnosis
• Excessive alcohol intake
• Impaired swallowing, mouth opening, oral discomfort
• Success of any radical treatment will be compromised by inadequate
nutrition – increased morbidity.
• Hence the need for dietary assessment
• Increase calorie intake
• Need for enteral feeding
• Before treatment
• Following reconstructive surgery
• Overcome s/e of oral mucositis, glossitis or dysphagia during acute phase of radical RT
• Need for regular dietary assessment
• Throughout the course of RT – ongoing wt. loss a negative prognostic factor
• During f/u period until parenteral nutrition no longer required and patients have
returned to sufficient oral intake and proven maintained weight.

50. Laryngoscopy (Indirect/ Direct/ Flexible):
• Allows direct visualisation of lesions beyond the oral cavity
• Examine for
• Mucosal irregularities in pharynx and larynx
• Vocal cord mobility (MI), anatomical asymmetries
• Pooling of secretions, bleeding
• Histological diagnosis:
• FNAC:
• For initial tissue diagnosis of HNC from cervical lymphadenopathy,
especially in pts. of unknown primary tumours (Diagnostic accuracy of 89-98%)
• If initial FNA is –ve, repeat FNA before an excisional biopsy from a suspicious
neck node
• US guided FNAC – overall accuracy comparable to neck CT – better detect
malignancy in radiologically –ve but clinically suspicious LNs
• Biopsy:
• For definitive histopathological confirmation, which may be direct or USG/CT
guided

51. Imaging studies (CT, MRI, PET/CT):
• Important for assessing:
• Degree of local infiltration/ extent
of primary lesion
• Involvement of regional lymph nodes Tumour staging
• Presence of distant metastases
or second primary tumours
• Assessment of operability
• Radiotherapy treatment planning
• Imaging is done with contrast, unless contraindicated.
• To achieve complete evaluation of the primary and any nodal disease, CT or
MRI of the neck should image the anatomy from the skull base to the
thoracic inlet (nape of neck).

52. CT
• Compared to MRI
• Better spatial resolution
• Better at evaluating bone (cortical) invasion
• Faster to perform
• Upstaging of HNC that have deeper local
invasion/infiltration into adjacent structures
• Dual energy/ multispectral CT have increased
specificity at evaluation of cartilage invasion (70% to
96%) with no compromise in sensitivity (86% vs 86%)
• Both CT and MRI are complementary to clinical
examination for staging of neck LNs, based on
• Size criteria (>10mm)
• Appearance (presence of central necrosis)

53. MRI:
• Provides superior soft tissue definition over CT Scan and tends to be better
at detecting bone marrow and cartilage invasion
• MRI is preferred over CT for the following conditions:
• Oral cavity cancer, like CA Tongue or if there is a need to evaluate the extent of bone
marrow invasion or in patients with extensive dental amalgam that may obscure the
anatomy on CT
• Nasopharyngeal cancer, to assess skull base invasion and cranial nerve involvement
• Sinonasal cancer, to evaluate skull base or intracranial or orbital invasion, and to
differentiate tumor from obstructed sinuses
• Any head and neck cancer with cranial nerve symptoms or if radiographic perineural
tumor spread is a possibility
• But, overall, in most studies, CT outperforms MRI in detection of nodal
metastasis with a sensitivity of MRI as low as 57-67% (as well as in terms of
logistic issues of long waiting and and cost too)

54. PET/CT:
• As sensitive & specific as CT and MRI in detecting primary tumours of HNC
but superior to both in detecting regional nodal metastasis, distant
metastasis and 2nd primary tumours, thereby improving TNM staging of
primary tumors (and subsequent management)
• Especially useful in pts. presenting with cervical LAD with unknown primary
(sensitivity of 97%). Actually, if imaging fails to reveal an obvious primary,
PET/CT should be ordered before EUA, biopsies, and tonsillectomy, to help
identify potential primary sites before any intervention occurs.
• Sensitivity is lower for pts. with clinically negative neck nodes, due to
inability to detect nodal metastasis <5mm in size.
• Beneficial for restaging of HNC after chemoradiation. –ve findings may
accurately determine early disease response, making further surgical
intervention unnecessary.

55. NCCN FOLLOW-UP RECOMMENDATIONS for HNC 2021
(based on risk of relapse, second primaries, treatment sequelae, and toxicities)
- H&P exam (including a complete head and neck exam; and mirror and fiberoptic
examination):
• Year 1, every 1–3 mo
• Year 2, every 2–6 mo
• Years 3–5, every 4–8 mo
• >5 years, every 12 mo
- Thyroid-stimulating hormone (TSH) every 6–12 mths if neck irradiated.
- Dental evaluation for oral cavity and sites exposed to significant intraoral radiation
treatment.
- Consider EBV DNA monitoring for nasopharyngeal cancer
- Supportive care and rehabilitation:
• Speech/hearing and swallowing evaluation and rehabilitation as clinically indicated.
• Nutritional evaluation and rehabilitation as clinically indicated until nutritional status is
stabilized.
• Smoking cessation and alcohol counselling as clinically indicated.

56. - Imaging (baseline):
- Short term (<6mths f/u)
- Obtain CT and/or MRI within 3–4 months after definitive treatment for patients with locoregionally
advanced disease or with altered anatomy causing challenging physical exam assessment, in order to
establish a new baseline for future comparisons.
- The optimal timing of PET scans after radiation treatment appears to be at the 3- to 6-month
window. A negative PET at this time point predicts improved overall survival at 2 years. Early FDG
PET/CT scans before 12 weeks are associated with significant false-positive rates and should be
avoided in the absence of signs of recurrence or progression.
- In a study involving patients receiving definitive RT-based treatment with N2–N3 nodal disease, FDG
PET/CT surveillance approach led to fewer neck dissections and considerable cost savings compared
to a routine approach of planned post-treatment neck dissection.
- Long term (≥6mths to 5yrs f/u)
- CT, MRI, and PET/CT all have unique advantages and disadvantages when used as surveillance
imaging. There is evidence that FDG PET/CT may be the most sensitive of these modalities. A 12-
month PET has been shown to reveal recurrent or second primary cancers in approximately 10% of
treated patients; a 24-month FDG PET/CT imaging revealed these findings in approximately 5% of
treated cases. Most cases of asymptomatic FDG PET/CT lesion localization occur at distant sites.
Whether earlier detection leads to improved disease-specific survival is not established.
- If an FDG PET/CT at 3 months post-treatment is negative, there are no data to support substantial
benefit for further routine imaging in an asymptomatic patient with negative exam.

57. Prognostic Discussion
• Age and tumour staging are considered the most important prognostic
factors for overall survival.
• Recurrence and second primary tumours are influenced negatively by
high alcohol consumption and cigarette smoking.
• Clinical characteristics remain the best known prognostic factors in
HNC.
• A major effort in HNC prevention and modification of patients'
behaviour could lead to early diagnosis and reduction of recurrence
and second primary tumours.
• This topic will be further explored in the next class on HNC.

58. THE END