Head and neck cancers are heterogenous cancers with rising incidence of treatable/curative cancers. They are treated comprehensively by multidisciplinary teams. Survivors of head and neck cancers often deal with the sequalae of therapy and with increasing survival rates, it is anticipated that the primary care physicians are going to encounter more patients in their clinics in the coming years. The clinicians should be aware of physiologic and functional changes in vital organs involving daily activities such as eating, drinking, speech and communication, and also be prepared to be a part of the cancer survivorship plans.
Key points
- •
Head neck cancers are heterogenous cancers with rising incidence of treatable/curative cancers.
- •
Human papilloma virus and tobacco use are major risk factors.
- •
They are treated comprehensively by multidisciplinary teams involving surgery, radiation, chemotherapy, and ancillary services.
- •
With rising survival in certain subsets, it is important for primary care providers to be aware of long-term surveillance and sequela.
Introduction
Head and neck cancers are cancers that arise in the mucosa and spread to the lymph nodes in the neck and can metastasize to other areas in the body such as lung, liver, and bone. They constitute 4% of all cancers in the United States of America (USA) and are the seventh leading cause of cancer worldwide. These cancers can arise in the oral cavity, oropharynx, larynx, pharynx, sinus areas, and nasopharynx. Non-mucosal cancers of the head and neck can also arise in the parotid glands and other endocrine glands such as thyroid. We will limit our discussion to the cancers that arise predominantly from the mucosal lining of the head and neck area.
The sites and subsites from which these cancers can arise dictate the management decisions. It is important to understand the anatomy and pattern of lymphatic spread of each subsite as there is a considerable variation within each subsite. The definition of each site is as follows ( Fig. 1 ):
Oral cavity: Oral cavity includes the lips, the anterior two-thirds of the tongue, the mucosa of the cheek (buccal mucosa) and lips, the floor of mouth, hard palate, and retromolar trigone.
Oropharynx: The oropharynx includes the soft palate, the tonsils and the tonsillar pillars, and the base of tongue (posterior third of the tongue). The incidence of human papillomavirus (HPV) positive tumors is highest in this subsite.
Nasopharynx : Nasopharynx is the part behind the nasal cavity and superior to the soft palate. The Eustachian tube opens on the lateral walls. It has rich lymphatics, and the incidence of lymph nodal spread is over 70% at presentation. The cancers in this subsite are related to Epstein-Barr virus (EBV) infection and common in South Asia. It is more frequently seen in the coastal areas of the USA. These cancers are mostly managed non-surgically.
Hypopharynx : Hypopharynx is the area extending from the posterior larynx to esophageal opening. It includes the pyriform sinus, posterior pharyngeal wall, and post cricoid area. Cancers in this area are uncommon and present with dysphagia and invasion into larynx or lateral neck.
Larynx: Larynx comprises the voice box with subsites including the supraglottic, glottic, and subglottic tumors. Tumors of the glottis have limited lymphatic spread in contrast to the other sites and tend to present earlier than other subsites. Subglottic tumors are uncommon in presentation.
Nasal Cavity and Paranasal sinuses : Tumors of these areas tend to invade locally with involvement of skull base and orbital invasion.
Epidemiology
It is estimated by the American Cancer Society, that there will be close to 66,920 cases of oral cavity and pharyngeal cancers diagnosed in the USA and there will be approximately 15,400 deaths from disease progression. In the USA, the incidence of HPV associated oropharyngeal cancers is increasing and there is a drop in the incidence of non-HPV related cancers. Over 75% of current oropharyngeal cancers are related to HPV infection. HPV can be detected in cancers of other sites in the head and neck, but it does not impact management decisions to the same extent. EBV virus infection is the common etiologic factor for nasopharyngeal cancers. , Radiation exposure and some genetic diseases such as Fanconi anemia are associated with higher risk of head and neck cancers. Chewing betel nut is implicated as a causative agent in buccal mucosa cancers on the Indian subcontinent.
Burden of disease
The incidence of these cancers has shown a 1% increase per year over the past 2 decades. This reflects the increase in the rise of the HPV-associated oropharyngeal cancers. These are more in the 40 to 50 y old population and non-smokers and are related to HPV exposure. It is increasingly recognized that these are biologically different from the non-HPV associated cancers and have a different outcome and clinical behavior. , The management of these cancers has been changing with better identification of prognostic factors and higher anticipated survival. Survivors of head and neck cancers often deal with the sequalae of therapy as they are living longer, it is anticipated that the primary care physicians are going to encounter more patients in their clinics in the coming years. ,
Pathogenesis
Most head and neck cancers arise from the mucosa of the head and neck. More than 90% of these are squamous cell cancers and other cancers such as lymphomas, sarcomas, and adenocarcinomas can arise from these areas but the management for those cancers is different and will not be discussed in this article. The known risk factors for these cancers are the use of tobacco products in any form, as well as alcohol consumption. The risk is increased 30-fold or so in people who smoke and drink heavily. Other contributory factors in non-smokers is the HPV-associated cancers transmitted through sexual contact. There is robust evidence of causation of nasopharyngeal cancers and EBV infection especially from Southeast Asia. ,
Clinical presentation
Most head and neck cancers present with symptoms from where they arise ( Table 1 ) ( Fig. 2 ).
| Oral Cavity | Nasal Cavity | Pharynx | Larynx |
|---|---|---|---|
| Non -healing ulcers in mouth | Epistaxis | Nasopharynx – cranial nerve involvement, orbital and visual changes massive LNE | Changes in voice hoarseness |
| Leucoplakia or Erythroplakia | Nasal blockage -unilateral | Oropharynx – LNE, dysphagia, odynophagia, tonsillitis, referred pain to ear | Swallowing choking spells |
| Pain at the site or referred pain to ear- late stage | Anosmia | Hypopharynx- mostly silent and present with LNE. late stage – dysphagia and weight loss | Late stage-stridor referred pain to ear |
| Lump/Lymph node enlargement (LNE) | Weight loss | ||
| Dysphagia, choking on food weight loss- late stage |
There are close to 300 to 400 lymph nodes in the head and neck area and involvement of lymph nodes is common at presentation. Based on the location of the primary site the involvement of lymph nodes may vary. The incidence of lymph nodal spread is higher amongst the tongue and floor of mouth cancers in contrast to other subsites. Base of tongue cancers tend to present with adenopathy in the neck and often asymptomatic primary tumors. The sinus and oral cavity cancers as a rule tend to have less than 5% incidence of lymph node involvement whereas lymph nodal enlargement in the neck may be a presenting sign for a cancer arising from the oropharynx or laryngeal areas.
About 2% to 5% of tumors that present with lymph node enlargement in the neck are without an obvious primary site. These are thought to arise from an unknown (occult) primary site. The cancers that behave in this fashion usually arise from the tonsil, base of tongue, nasopharynx, or the pyriform sinus areas. Bilateral nodal involvement is common in tumors arising from the nasopharynx (40%), base of tongue (40%), supraglottic laryngeal cancers (15%), and soft palate cancers (15%). It is less common (10%) with tonsillar cancers, hypopharyngeal cancers, and oral tongue. Glottic tumors rarely have lymph nodal spread unless the tumors have spread into other subsites in the larynx. Lip and subglottic tumors have low lymph nodal involvement overall.
Cancer management
Cancer management of mucosal tumors is based on tissue pathology, stage of cancer, and co-morbid factors. All cancers are staged based on information obtained from imaging modalities and clinical examinations. The staging is clinical if patients do not undergo surgery and categorized as pathologic if patients are resected and have a lymph nodal dissection performed.
Non-mucosal cancers: The other common non-mucosal cancers in the head and neck area tend to arise from the salivary glands or as lymph nodal deposits from skin of the face. They tend to be unilateral and treated with surgery and assessed for adjuvant therapy based on risk factors. The major salivary glands are the parotids (majority of cases), submandibular, and submental glands. The minor salivary glands are distributed on the hard and soft palate and other areas in the nasopharynx and oropharynx. The incidence of these cancers is extremely low, probably less than 5%. Parotids tend to be a site of metastatic disease from skin cancers. Primary squamous cell cancers of the parotid are extremely rare, and most are lymph nodes metastasize from the skin of the face ( Box 1 ). ,
- •
Detailed medical history and complete physical including head and neck examination including screening for Depression.
- •
Mirror and Fiberoptic examination if needed.
- •
Endoscopy and examination under anesthesia (EUA)as needed.
- •
Biopsy of tumor or Lymph node site – HPV testing by p16 for throat cancers and EBV (DNA) for nasopharynx- Fine needle aspiration cytology of Lymph Node or tissue biopsy-special stains for genetic analysis for immunotherapy.
- •
CT with contrast and/or MRI with and without contrast of primary tumor and neck-include skull bases and thoracic inlet.
- •
CT chest with or without contrast.
- •
Imaging for distant metastasis – FDG-PET/CT.
- •
Dental Examination with Panorex.
- •
Nutrition, speech, and swallow evaluation.
- •
Hearing test.
- •
Eye and endocrine evaluation for nasopharyngeal cancer.
- •
Smoking cessation counseling.
- •
Screening for Hepatitis B.
Initial assessment of the primary site and lymph nodes can be made based on a contrast computed tomography (CT) scan of the head and neck including the skull bases and the thoracic inlet. For hypopharyngeal tumors, the scan should include the carina if a concomitant CT chest is not being performed. Imaging of the chest can be with or without contrast, but most patients have CT scans of the neck and chest performed simultaneously. An alternate imaging modality to characterize the primary site is an MRI with contrast. CT scans can be useful in situations where MRI is deficient including cortical bone, periosteal or cartilage involvement, or destruction. MRI is recommended when patients have dental fillings that impede and artifact CT images, suspect marrow invasion, cranial nerve involvement and perineural spread, orbital and skull base spread through the foramina, and for differentiating mucus plugs from tumor, especially in the sinuses. Ultrasound of the neck is useful in establishing tissue diagnosis and in follow-up. Panoramic X-rays are recommended for dental evaluation and extractions. PET scan is done for establishing the metabolic activity at the initiation of therapy and for assessing response 3 months post completion of all therapy. It has prognostic value and a negative PET scan at 3 months is a positive predictor of complete response and favorable outcome. , Most patients will not need additional metabolic imaging after a negative PET scan and can be followed with CT/MRI/ultrasound sonography test as indicated. CT/MRI/PET scans are useful in surgical and radiation planning with use of these modalities for fusion studies and dose prescription ( Table 2 ).
| Tumor | Oral Cancer | Oropharyngeal HPV+ | Nasopharynx (NP) | Oropharyngeal HPV-Hypopharynx | Larynx |
|---|---|---|---|---|---|
| T1 | <2 cm <5 mm DOI | <2 cm | Confined to NP, Nasal cavity | <2 cm | 1 subsite, Vocal cord |
| T2 | <2 to <4 cm DOI >5 mm to ≤ 10 mm | 2–4 cm | Parapharyngeal extension | 2–4 cm | >2 subsites |
| T3 | >4 cm | >4 cm | Invasion into Skull base, PNS | >4 cm | Limited to larynx with fixation of vocal cords, paraglottic spread or erosion of thyroid cartilage |
| T4a | Invades cortical bone, skin, nerves, extrinsic muscles of tongue muscle | Invades laryngeal surface of epiglottis | Intracranial extension, involvement of cranial nerves, orbit, hypopharynx, infratemporal space/masticator space | Invades Larynx, extrinsic tongue muscles, medial pterygoids, hard palate or mandible | Invades beyond larynx into trachea, soft tissue neck, strap muscles, extrinsic tongue muscles, thyroid, esophagus or through Thyroid cartilage |
| T4b | Invasion into masticator space, Pterygoid plates, skull base or Internal carotid artery | Invasion into Larynx, extrinsic tongue muscles, hard palate, mandible, medial Pterygoid | Invasion into Lateral Pterygoid, pterygoid plates skull base, lateral nasopharynx or encases carotid artery | Prevertebral space, Encases carotid artery, mediastinal structures |
| Node | Oral Cancer | Oropharyngeal | Nasopharynx | Oropharyngeal HPV-Hypopharynx | Larynx |
|---|---|---|---|---|---|
| N0 | No LN | No LN | No LN | No LN | No LN |
| N1 | Single LN <3 cm, ENE neg | Single <6 cm | Unilateral 6 cm above cricoid cartilage, Uni or Bil retropharyngeal LN <6 cm | <3 cm No ENE | <3 cm No ENE |
| N2a | >3 cm to <6 cm ENE Neg | Bilateral or Contralateral <6 cm | Bilateral <6 cm above cricoid | Same as OC | Same as OC |
| N2b | >2 nodes none >6 cm size | NA | NA | Same as OC | Same as OC |
| N2c | Bilateral <6 cm size | NA | NA | Same as OC | |
| N3a | >6 cm ENE Neg | >6 cm in size | >6 cm below cricoid | ||
| N3b | >6 cm ENE (+) |
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
