Neck, Cervical Metastases, Surgery

Neck, Cervical Metastases, Surgery

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Approximately 300 lymph nodes are located in the head and neck, and they comprise 30% of the total 800 lymph nodes in the human body. In 1880, Kocher and Uber reported the detrimental effect of neck metastasis in patients with head and neck cancer. In 1906, George Washington Crile reported his experience with 132 neck dissections in JAMA: The Journal of the American Medical Association. The advent of functional neck dissections, aimed at reducing morbidity and maintaining function, was made possible with the further advancement of understanding of the lymphatic spread in the 1960s. [1]

Cervical metastasis has a tremendous impact on the prognosis in patients with carcinomas of the head and neck. The presence of neck metastasis is known to reduce survival by 50%, and the frequency of such spread is greater than 20% for most squamous cell carcinomas (SCCAs). The presence of extra capsular spread further halves the chances of cure. Predictive factors of cervical metastasis are primary site, primary tumor size, degree of differentiation of tumor, perineural invasion, perivascular invasion, inflammatory response, and tumor DNA content (ploidy).

Advantages of modified neck dissection (MND) over radical neck dissection (RND) are preservation of neck and shoulder functions, better cosmetic results, protection of the internal carotid artery (ICA), and availability of simultaneous bilateral surgeries. [2] MND offers the same survival rate and disease-free survival benefits as classic RND.

See the list below:

1906: Crile developed the en bloc cervical lymphadenectomy known as the RND. In his classic series, spinal accessory and hypoglossal nerves were preserved.

1945: Dargent and Papillon proposed the preservation of the spinal accessory nerve (SAN) in clinically node-negative necks.

1950: Martin popularized the RND without preserving the spinal accessory nerve.

1963: Suarez demonstrated, based on his necropsy studies, that a complete cervical lymphadenectomy could be accomplished while sparing the sternocleidomastoid (SCM) muscle, the internal jugular vein (IJV), and the SAN.

1967: Bocca and Pignataro popularized functional/conservative neck dissections.

1969-1981: Roy and Beahrs, Carenfelt, and Eliasson advocated the possibility of preservation of SAN in clinically node-positive necks as well. [3, 4, 5]

1972: Lindberg’s classic study of carcinomas of various upper aerodigestive tracts indicated consistent patterns of lymphatic drainage. [6]

1986-1994: Byers, Medina, and Spiro reported their satisfactory results with selective neck dissection (SLD). [7, 8]

Management of a neck mass requires understanding of anatomic, pathologic, and oncologic characteristics of the tumor. Differential diagnoses of neck masses are vast and need careful consideration in all patients who present with a neck mass. Imaging is an important tool to identify cervical metastasis; however, it may not clearly identify metastatic disease in early cancers. The management of neck masses has undergone a paradoxical shift from radical neck dissections, which were performed for N0 neck masses in the early 1900s, to the present era, in which chemoradiotherapy is advocated for advanced neck disease. This change in management has been brought about by several factors, such as morbidity of the procedure, better understanding of the tumor biology, patterns of spread, and advances in radio therapy.

To bring uniformity to the nomenclature for various neck dissections, the classification adopted today is the one adopted by the subcommittee for neck dissection terminology and classification of the American Academy of Otolaryngology Head and Neck Surgery in 2002. [9] Cervical metastases, most of which originate in the aerodigestive tract, are strong prognostic factors in head and neck cancers.

In the United States, the frequency of metastatic disease for the upper aerodigestive tract varies widely from 1-85%, depending on the site, size, and differentiation of the tumor. For example, larger tumors have a greater likelihood of cervical spread, and pharyngeal lesions metastasize more frequently than those in the larynx or oral cavity.

Ipsilateral metastatic disease occurs in approximately 50% of patients with carcinoma of the oral cavity, oropharynx, hypopharynx, or supraglottis. Bilateral and/or contralateral metastatic disease occurs in 2-35% of these patients.

Nasopharyngeal carcinoma manifests as a neck metastasis in approximately 50% of patients.

Metastatic neck disease in individuals with thyroid gland tumors occurs as follows: papillary (55%), medullary (50%), and follicular (25%).

Tumors localized in the oral cavity, oral mucosa, oropharynx, hypopharynx, and supraglottis have a higher frequency of metastasis compared to areas such as the superior gingiva, hard palate, and glottis.

Most cervical metastases are SCCAs that originate from primary sites in the aerodigestive tract. Other sources of cervical metastasis include neoplasms of the skin, salivary glands, thyroid, lung, kidney, prostate, gonads, stomach, and breast. In some individuals, no primary cancer can be detected. In this situation, the carcinoma is labeled a metastasis from unknown origin.

Within the aerodigestive tracts, various factors contribute to the risk of neck metastasis. Young patients with oral carcinoma have a higher risk of developing nodal metastasis than older patients. Risk of neck involvement by metastasis increases with an increase of tumor size. Carcinomas in anterior portions of the oral cavity are less likely to metastasize to the neck than carcinomas in posterior portions. Perineural and perivascular invasion are associated with a high risk of nodal metastasis. Poorly differentiated tumors are associated with a higher risk of neck metastasis than well-differentiated tumors. Patterns of lymphatic metastasis are as follows:

With oral, tongue, retromolar trigone, and tonsillar fossa subsites, the jugulodigastric, submandibular, and midjugular lymph node stations are involved.

With the floor of the mouth as the subsite, the submandibular and jugulodigastric lymph node stations are involved.

With the soft palate, base of the tongue, oropharynx, supraglottis, and hypopharynx subsites, the jugulodigastric, midjugular, and contralateral lymph node stations are involved.

With the nasopharynx as the subsite, lymph node stations of the widest nodal distribution are involved.

Contralateral metastasis is found in the supraglottis, the base of the tongue, and the posterior pharyngeal wall palate.

Bilateral metastasis is found in the nasopharynx, the base of the tongue, the soft palate, the floor of mouth, and the supraglottis.

The highest rate of occult cervical metastasis is found in the oral cavity, pyriform sinus, tonsil, supraglottis, and pharyngeal wall.

Multiple cervical metastases (adenocarcinoma) occur with thyroid carcinoma, breast carcinoma, and nasopharyngeal carcinoma.

Involvement of particular groups of neck nodes includes the following:

Posterior cervical nodes in nasopharyngeal and tonsillar carcinoma

Tracheoesophageal nodes in thyroid, pyriform sinus, and subglottic carcinoma

Periparotid and parotid nodes in SCCA of the skin of the temporal region and the cheek

A detailed understanding of the pathophysiology is mandatory step in the management of neck metastasis.

The intrinsic behavior of any malignant tumor in the body is to grow, invade, and metastasize. Head and neck SCCs predominantly metastasize via lymphatic channels to the lymph nodes as tumor emboli. In addition, they also spread through a venolymphatic pathway. The metastatic process largely depends on various tumor factors, such as expression of adhesion molecules like CD44 by the tumor cells or host immune factors.

Advances in molecular biology have given a better insight into the mechanisms involved in head and neck cancer.

Multiple gene products are involved in angiogenesis, all of which are critical for regulating the angiogenic phenotype. This has raised the need for comprehensive analysis of the angiogenic phenotype using microarray analysis and global proteomic approaches. [2] A complex interplay between positive and negative regulators determines the degree of neovascularization in and around the tumor.

Various markers assessing the role of regulators have been studied.

Matrix metalloproteinases (MMP) have the ability to degrade connective tissue such as the basement membrane, which is a crucial step in the initiation of metastatic process. Thus it serves as a negative regulator of metastasis. Similarly, E-cadherin is an important molecule that promotes cell-to-cell adhesion and serves as a positive regulator of metastasis. A study by Weiss et al indicated that angiogenesis and MMP and E-cadherin (M/E) ratio were specific predictors for metastases of renal cell carcinoma, especially to the lung or lymph node. [10] Therefore, MMP and E-cadherin are considered relevant targets for novel therapeutic strategies to control or prevent the metastasis of renal cell carcinoma. These results support exploring the role of angiogenetic regulators in head and neck cancer.

Expression levels of molecules involved in tissue remodeling and cell–extra cellular matrix (ECM) adhesion, especially MMP-1 and integrin-3 , can provide an accurate biomarker system for predicting the risk of cervical lymph node metastasis in oral SCC. [11] Low expression of E-cadherin should be considered a high risk for late cervical metastasis when a wait-and-see policy for the neck is adopted. [12]

Vascular endothelial growth factor (VEGF) promotes angiogenesis in many different tumor types. VEGF is a highly potent angiogenic agent that acts to increase vessel permeability and enhance endothelial cell growth, proliferation, migration, and differentiation. [13] VEGF levels may affect tumor growth, metastatic potential, and response to radiotherapy. VEGF positivity was the most significant predictor of poor prognosis. VEGF status may prove to be an important prognostic factor in head and neck cancer. In addition, the potent role of VEGF in angiogenesis has spurred interest in using this molecule as a therapeutic target in antiangiogenetic therapy.

Most of the probable primary carcinomas can be elicited in the history taking. Probable primary carcinoma sites and symptoms are as follows:

Oral – Bleeding or painful ulcer in the mouth

Nasopharynx – Nasal fullness, epistaxis, change in voice resonance, sinusitis

Maxillary – Patch of anesthesia over cheek, toothache, epistaxis, sinusitis, change in the visual field

Larynx, hypopharynx – Change in voice, cough, dysphagia, referred otalgia, hemoptysis, airway obstruction

Tongue, base of tongue – Painful lesion, oral bleeding, odynophagia, ankyloglossia

Esophageal – Dysphagia, weight loss, hoarseness, regurgitation

Stomach – Dyspepsia, vomiting, epigastric pain

Pancreatic head – Jaundice, epigastric pain, white stools

Testicular – Painless testicular enlargement

Lung – Cough, hemoptysis

Breast – Breast lump

Thyroid – Neck swelling

Review of the medical history should include allergies to medications, hypertension, diabetes mellitus, cardiopulmonary disease, other chronic illnesses, previous surgeries, and radiation therapy. Reviewing the use of tobacco products (smoked and chewed), consumption of alcohol, and use of betel nuts is also important.

Clinical staging of cervical metastasis is accurate in 65% of cases. It understages in 28% and overstages in 8% of cases. Short neck, obesity, and prior radiotherapy reduce the physician’s ability to detect metastasis.

Clinical examination of the neck mass is the most sensitive parameter for assessing the operability of a neck node metastasis. The physical examination includes assessment and documentation of site and size of node, contralaterality and bilaterality, mobility, and skin involvement. In addition, examine the oral cavity and mucous membranes of the pharynx. Careful examination of the thyroid gland is essential to assess the presence of a primary carcinoma. Perform an indirect laryngoscopic examination of the larynx and the hypopharynx. If a lesion is noted in the aerodigestive tract, an evaluation under anesthesia further documents the location and size of the lesion, and it allows for a biopsy.

Periabdominal examination should be performed to look for primary carcinomas in the abdomen.

Perirectal/perivaginal examination should be performed in persons in whom primary carcinoma is suspected in the gastrointestinal (GI) or genitourinary tract.

Perform a breast examination in selected individuals.

Auscultate the chest to detect a possible pulmonary primary carcinoma.

Perform a testicular examination.

Indications for a radical neck dissection (RND) are N2 or N3 cervical adenopathy with or without bulky disease in the upper jugular region, presence of multiple lymph nodes, and residual or recurrent disease after radiation therapy.

Modified RND indications are N0 neck (especially if the primary tumor is in the larynx or hypopharynx) in SCCA or melanoma, N1 neck disease, and papillary and follicular carcinoma of the thyroid.

SND indications include the following:

Lateral neck dissection is indicated in a tumor of the larynx, oropharynx, and/or hypopharynx staged T2-4, N0-1, and/or T1 N1 node within level I-II.

Supraomohyoid neck dissection is indicated in SCCA of the oral cavity staged T2-4, N0/Tx N1 within level I-II.

Bilateral procedure is indicated in anterior tongue and base of tongue cancers as well as T3-T4 carcinomas of the supraglottis.

Posterolateral neck dissection is indicated in melanoma, SCCA, or another skin tumor with metastatic potential from the occipital scalp.

Anterior neck dissection is indicated for thyroid, subglottic larynx, trachea, and cervical esophagus cancers.

Mediastinal dissection is indicated in thyroid cancers, stomal recurrence, and postcricoid and esophageal invasion.

Lymph nodes of the head are located in the occipital, posterior auricular (postauricular), anterior auricular (preauricular), parotid, facial, deep facial, and lingual regions.

Lymph nodes of the neck are located in the superficial cervical, anterior cervical, submental, submaxillary, deep cervical, retropharyngeal, jugular, superior, inferior, spinal accessory, and transverse cervical node regions.

The skin of the neck derives its blood supply from the descending branches of the facial occipital arteries and from ascending branches of the transverse cervical and suprascapular arteries; therefore, the incisions most likely to safeguard the blood supply to the skin flaps are superiorly based apronlike incisions.

The following division of the neck nodes into regions as described at Memorial Sloan-Kettering is accepted universally (see the image below):

See the list below:

Level 1 contains the submental and submandibular nodes.

Level 2 is the upper third of the jugular nodes medial to the SCM, and the inferior boundary is the plane of the hyoid bone (clinical) or the bifurcation of the carotid artery (surgical).

Level 3 describes the middle jugular nodes and is bounded inferiorly by the plane of the cricoid cartilage (clinical) or the omohyoid (surgical).

Level 4 is defined superiorly by the omohyoid muscle and inferiorly by the clavicle.

Level 5 contains the posterior cervical triangle nodes.

Level 6 includes the paratracheal and pretracheal nodes.

The platysma is a wide quadrangular sheetlike muscle extending obliquely from the upper chest to the lower face. The skin flap is raised in a plane deep to the platysma. If the disease involves the platysma or is close to it, the platysma may be left attached to the specimen and the skin flap raised superficial to it.

The SAN exits the jugular foramen (medial to the digastric and styloid muscles) and lies lateral and immediately posterior to the IJV. The nerve can also be medial to the IJV in 30% of the cases. It runs obliquely inferiorly and posteriorly to reach the SCM near the junction of its upper and middle thirds or within 1 cm of the Erb point (where the greater auricular nerve curves around the posterior border of the SCM).

The digastric muscle originates from the digastric ridge in the mastoid process. The marginal mandibular nerve (a branch of the facial nerve) is the only structure superficial to the posterior belly of the digastric muscle that must be identified and preserved. It lies superficial to the 11th nerve, IJV, ICA, hypoglossal nerve, and the branches of the external carotid artery (ECA). When raising the upper skin flap or while incising the deep cervical fascia, care must be taken to identify the marginal mandibular nerve. It is located 1 cm in front of or below the angle of the mandible, deep to the superficial layer of the deep cervical fascia that envelops the submandibular gland.

The omohyoid muscle has 2 bellies and is the anatomic landmark separating levels III and IV. The posterior belly lies superficial to the brachial plexus, phrenic nerve, and transverse cervical artery and vein. The anterior belly lies immediately superficial to the IJV.

The posterior boundary of neck dissection is the anterior border of the trapezius muscle. The levator scapula is commonly mistaken for the trapezius, placing the 11th nerve and the nerve to the levator at risk. Dissection must be kept superficial to the fascia of the levator muscle to preserve the cervical nerves.

The brachial plexus exits between the anterior and middle scalene muscles. It extends inferiorly deep to the clavicle, under the posterior belly of the omohyoid muscle. The transverse cervical artery and vein lie superficial to it.

The phrenic nerve lies superficial to the anterior scalene muscle and derives its cervical supply from C3-5. Cervical rootlets must be transected only anteriorly to their contribution to the phrenic nerve.

The thoracic duct is located in the lowermost part of the left neck and arises immediately posterior to the lower end of the jugular vein and anterior to the phrenic nerve and transverse cervical artery. Care must be taken to handle it gently during ligation to avoid avulsion or tearing of walls.

The hypoglossal nerve exits via the hypoglossal canal, passes over the ICA and ECA, under the IJV, and loops deep to the posterior belly of digastric, where it is enveloped by a ranine venous plexus. It then travels under the fascia of the submandibular triangle before entering the tongue.

The neck is divided into the anterior and the posterior triangle, each of which is divided into smaller triangles. The anterior triangle is divided into the submental triangle, submandibular triangle, superior carotid triangle, and inferior carotid triangle. The posterior triangle is subdivided into the occipital triangle and subclavian triangle.

The submental node is located in the submental triangle and receives afferent flow from superficial lymphatics from the cheek, lower lip, and chin.

The submandibular node is located between the anterior and posterior bellies of digastric muscle and receives afferent flow from the lower lip, sublingual area, ipsilateral oral cavity, eyelid, cheek, and nasal mucosa.

The facial node is located superficial to the facial muscle and along the facial vein and receives afferent flow from facial skin, palate, and buccal mucosa.

The parotid node is located in the intraglandular or extraglandular part of the parotid, and it receives afferent flow from the scalp, auricle, external auditory canal (EAC), eardrum, and the eustachian tube (E-tube).

The retropharyngeal node is located posterior to the pharyngeal wall, between the prevertebral fascia and the pharyngeal wall, and it receives afferent flow from the posterior nasal cavity, palate, nasopharynx, and eustachian tube.

The anterior cervical node is located in the superficial anterior jugular chain, and pretracheal, prelaryngeal, and paratracheal regions, and it receives afferent flow from the larynx, upper trachea, and esophagus.

The spinal accessory node is located along the SAN and receives afferent flow from the occipital, mastoid, and maxillary sinus.

The supraclavicular node is located at the jugulosubclavian junction and receives afferent flow from the spinal accessory, lower neck, upper chest, lung, and GI tract.

The internal jugular node is located along the internal jugular chain and receives afferent flow from the superior nodal group, mucosal site in the head and neck, and thoracic and axillary nodes.

General contraindications to surgery include too great a surgical risk because of cardiopulmonary disease and cases in which the patient cannot be optimized preoperatively.

RND contraindications include the inability to control the primary tumor or distant metastasis, a fixed neck mass through the deep cervical fascia, a mass in the supraclavicular triangle, and the inability of the surgeon to completely remove all gross disease from the neck, including the skull base, vertebral fascia, carotid artery, deep muscle, phrenic nerve, and brachial plexus.

Contraindications for SND are N2 and N3 disease, recurrence or previous treatment with radiation therapy, involvement of spinal accessory chain, and melanoma of clinically positive nodes.

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Pankaj Chaturvedi, MBBS, MS, FACS Professor of Head and Neck Surgery, Department of Head and Neck Surgery, Tata Memorial Hospital, India

Pankaj Chaturvedi, MBBS, MS, FACS is a member of the following medical societies: American Association for the Advancement of Science, American Head and Neck Society, Association of Surgeons of India

Disclosure: Nothing to disclose.

Apurva Garg, MBBS, MSurg Senior Research Fellow in Head and Neck Oncosurgery, Department of Head and Neck Surgery, Tata Memorial Hospital, India

Apurva Garg, MBBS, MSurg is a member of the following medical societies: Foundation for Head and Neck Oncology

Disclosure: Nothing to disclose.

Uma Chaturvedi, MD, MBBS, DPB Lecturer, Department of Pathology, KJ Somaiya Hospital and Research Center, India

Disclosure: Nothing to disclose.

Thabet Abbarah, MD, FACS Consulting Staff, Department of Otolaryngology, North Oakland Medical Centers

Thabet Abbarah, MD, FACS is a member of the following medical societies: American College of Surgeons

Disclosure: Nothing to disclose.

Nafisa K Kuwajerwala, MD Staff Surgeon, Breast Care Center, William Beaumont Hospital

Nafisa K Kuwajerwala, MD is a member of the following medical societies: American College of Surgeons, American Society of Breast Surgeons, American Society of Breast Disease

Disclosure: Nothing to disclose.

Vishal U S Rao, MBBS, MS Assistant Professor, Visiting Consultant-Head and Neck Surgeon, Raja Rajeshwari Medical College and Hospital; Consultant Oncologist-Head and Neck Surgeon, Fortis Hospital; Visiting Consultant Oncologist-Head and Neck Surgeon, Apollo Hospital and Bangalore Institute of Oncology, India

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Nader Sadeghi, MD, FRCSC Professor and Chairman, Department of Otolaryngology-Head and Neck Surgery, McGill University Faculty of Medicine; Chief Otolaryngologist, MUHC; Director, McGill Head and Neck Cancer Program, Royal Victoria Hospital, Canada

Nader Sadeghi, MD, FRCSC is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Head and Neck Society, American Thyroid Association, Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Arlen D Meyers, MD, MBA Professor of Otolaryngology, Dentistry, and Engineering, University of Colorado School of Medicine

Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, American Head and Neck Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cerescan;RxRevu;Cliexa;Preacute Population Health Management;The Physicians Edge<br/>Received income in an amount equal to or greater than $250 from: The Physicians Edge, Cliexa<br/> Received stock from RxRevu; Received ownership interest from Cerescan for consulting; for: Rxblockchain;Bridge Health.

Benoit J Gosselin, MD, FRCSC Associate Professor of Surgery, Dartmouth Medical School; Director, Comprehensive Head and Neck Oncology Program, Norris Cotton Cancer Center; Staff Otolaryngologist, Division of Otolaryngology-Head and Neck Surgery, Dartmouth-Hitchcock Medical Center

Benoit J Gosselin, MD, FRCSC is a member of the following medical societies: American Head and Neck Society, American Academy of Facial Plastic and Reconstructive Surgery, North American Skull Base Society, American Academy of Otolaryngology-Head and Neck Surgery, American Medical Association, American Rhinologic Society, Canadian Medical Association, Canadian Society of Otolaryngology-Head & Neck Surgery, College of Physicians and Surgeons of Ontario, New Hampshire Medical Society, Ontario Medical Association

Disclosure: Nothing to disclose.

Neck, Cervical Metastases, Surgery

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Neck, Cervical Metastases, Detection

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Cervical metastasis by a tumor is firm statement of its aggressive malignant nature. Nothing is more controversial than the management of cervical metastatic disease. This is not surprising considering the lack of knowledge of carcinogenesis, pathophysiology of metastases, and implications of tumor spread. Fortunately, great strides have been made in the understanding of the intricate processes related to metastatic disease. Proper understanding of anatomy and the detection of cervical metastatic disease is crucial to this process. Forthcoming techniques will also facilitate the detection of primary and metastatic disease.

For excellent patient education resources, visit eMedicineHealth’s Cancer Center. Also, see eMedicineHealth’s patient education article Cancer of the Mouth and Throat.

The lymphatic system has 3 components: the capillaries, vessels, and nodes.

Larger than arteriovenous capillaries, lymphatic capillaries are thin-walled, with a single layer of endothelial cells. Lymphatic capillaries are found in all tissues; however, they are more abundant in the upper respiratory and GI tracts. Pooled capillaries drain lymphatic fluid into lymphatic vessels, which have 3 layers.

As in the capillaries, the vessels have a single layer of endothelial cells surrounded by an inner, longitudinal elastic layer. This first muscle layer is surrounded by a circular smooth muscle layer, which, in turn, is enveloped by an outer connective tissue layer. Lymphatic vessels contain many more valves than the venous system, with the lymph circulation entirely dependent on compression by surrounding muscles. Lymphatic vessels drain into lymph nodes.

These nodules of tissue are of variable size. Typically, as many as 75 nodes are located on each side of the neck. Nodes contain a subcapsular sinus below a prominent capsule, into which lymphatic fluid drains. This capsule is often the first site of metastatic growth. The fluid permeates the substance of the node (composed of a cortex and a medulla) and exits through the hilum to enter more lymphatic vessels. These nodes are located between the superficial cervical and prevertebral fascia and, thus, are very amenable to surgical removal. The lymphatic fluid eventually enters the venous system at the junction of the internal jugular and subclavian veins. Many nodal descriptions exist today; Rouvière’s is the classic model. The following describes the main cervical node groups:

The occipital nodes are in the superficial group, which includes 3-5 nodes. This group of nodes is localized between the sternocleidomastoid (SCM) and trapezius muscles, at the apex of the posterior triangle. These nodes are superficial to the splenius capitis.

The deep posterior cervical group includes 1-3 nodes. This group of nodes is located deep to the splenius capitis and follows the course of the occipital artery. These nodes drain the scalp, the posterior portion of the neck, and it’s the deep muscular layers of the neck.

The postauricular nodes vary in number from 2 to 4; they are located in the fibrous portion of the superior attachment of the SCM muscle to the mastoid process. Postauricular nodes drain the posterior parietal scalp and the skin of the mastoid region.

The parotid nodes can be divided into intraglandular and extraglandular groups. The extraglandular parotid nodes are located outside but adjacent to the parotid gland, where they drain the frontolateral scalp and face, the anterior aspects of the auricle, the external auditory canal, and the buccal mucosa. Embryologically, the lymphatic system develops before the parotid gland, which surrounds the intraglandular nodes as it develops. This explains why the parotid gland contains lymphoid tissue. The intraglandular nodes drain the same regions as the extraglandular nodes, to which they interconnect and then drain into the upper jugular group of lymph nodes. As many as 20 parotid nodes may be found.

The submandibular nodes are divided into 5 groups: preglandular, postglandular, prevascular, postvascular, and intracapsular. The preglandular and prevascular groups are located anterior to the submandibular gland and facial artery, respectively. The postglandular and postvascular groups are posterior to these structures. Differing from the parotid gland in embryological development, there is no true intraglandular node; however, occasionally, a node has been identified inside the capsule of the gland. The submandibular nodes drain the ipsilateral upper and lower lip, cheek, nose, nasal mucosa, medical canthus, anterior gingiva, anterior tonsillar pillar, soft palate, anterior two thirds of the tongue, and submandibular gland. The efferent vessels drain into the internal jugular nodes.

For the submental nodes, 2-8 nodes are located in the soft tissues of the submental triangle between the platysma and mylohyoid muscles. These nodes drain the mentum, the middle portion of the lower lip, the anterior gingiva, and the anterior third of the tongue. The efferent vessels drain into both the ipsilateral and contralateral submandibular nodes or into the internal jugular group.

The sublingual nodes are located along the collecting trunk of the tongue and sublingual gland and drain the anterior floor of the mouth and ventral surface of the tongue. These nodes subsequently drain into the submandibular or jugular group of nodes.

The retropharyngeal nodes are divided into a medial and lateral group, located between the pharynx and the prevertebral fascia. The lateral group, located at the level of the atlas near the internal carotid artery, consists of 1-3 nodes, which may extend to the skull base. The medial group extends inferiorly to the postcricoid level. This group drains the posterior region of the nasal cavity, sphenoid and ethmoid sinuses, hard and soft palates, nasopharynx, and posterior pharynx down to the postcricoid area. Management of these nodes must be considered if any malignancy arises from the mentioned drainage areas.

The anterior cervical nodes are divided into the anterior jugular chain and the juxtavisceral chain of nodes. The anterior jugular chain nodes follow the anterior jugular vein, located superficial to the strap muscles. These nodes drain the skin and muscles of the anterior portion of the neck, and the efferent vessels empty into the lower internal jugular nodes.

The juxtavisceral nodes are separated into the prelaryngeal, prethyroid, pretracheal, and paratracheal nodes. Prelaryngeal nodes are located from the thyrohyoid membrane to the cricothyroid membrane and drain the larynx and the thyroid lobes. A single delphian node is often found overlying the thyroid cartilage.

The pretracheal group consists of nodes between the isthmus of the thyroid gland down to the level of the innominate vein. Varying from 2-12 in number, these nodes drain the region of the thyroid gland and the trachea and receive afferent flow from the prelaryngeal group. The pretracheal efferents empty in the internal jugular group and the anterior superior mediastinal nodes.

The paratracheal nodes lie near the recurrent laryngeal nerve and drain the thyroid lobes, parathyroid glands, subglottic larynx, trachea, and upper esophagus. The efferent vessels travel to the lower jugular group or directly toward the junction of the internal jugular vein and the subclavian vein. The anterior nodes drain bilaterally because the midline of the neck has no division. Treatment must be planned accordingly when a tumor is located in subjacent draining areas.

The lateral cervical nodes are divided into superficial and deep groups. The superficial group follows the external jugular vein and drains into either the internal jugular or transverse cervical nodes of the deep group.

The deep group forms a triangle bordered by the internal jugular nodes, the spinal accessory nodes, and the transverse cervical nodes. The transverse cervical nodes, forming the base of the triangle, follow the transverse cervical vessels and may contain as many as 12 nodes. These nodes receive drainage from the spinal accessory group and from collecting trunks of the skin of the neck and upper chest. The spinal accessory chain follows the nerve of the same name and may account for as many as 20 nodes. This chain receives lymph from the occipital, postauricular, and suprascapular nodes and from the posterior aspect of the scalp, nape of the neck, lateral aspect of the neck, and the shoulder.

The internal jugular chain consists of a large system covering the anterior and lateral aspects of the internal jugular vein, extending broadly from the digastric muscle superiorly to the subclavian vein inferiorly. As many as 30 of these nodes may exist, and they have been arbitrarily divided into upper, middle, and lower groups. The efferents of these nodes eventually pass into the venous system via the thoracic duct on the left and multiple lymphatic channels on the right. These nodes drain all the other groups mentioned. Direct efferents may be present from the nasal fossa, pharynx, tonsils, external and middle ear, eustachian tube, tongue, palate, laryngopharynx, major salivary glands, thyroid, and parathyroid glands.

Although fairly consistent, these drainage patterns are subject to alteration with malignant involvement or after radiotherapy. In such cases, rerouting is possible, with metastases arising in unusual sites. Metastases have also been shown to skip first-echelon nodes and manifest in the lower internal jugular group.

Spread patterns of cancer from various primary sites in the head and neck to the cervical nodes have been documented in retrospective analyses of large groups of patients undergoing neck dissections. Since the first descriptions of nodal groups, various classification systems have been described.

To address surgical management of early-stage neck metastases via neck dissection, various authors have proposed a number of classification schemes. This lack of uniformity and standardization results in redundancy, misinterpretation, and confusion among clinicians. The most widely accepted terminology was originally described by a group of head and neck surgeons at Memorial Sloan-Kettering Hospital. This classification uses neck levels or zones and divides each side of the neck into 6 separate regions. This system is still used today.

Level I is bordered by the body of the mandible, anterior belly of the contralateral digastric muscle, and anterior and posterior bellies of the ipsilateral digastric muscle. Two nodal subgroups are found. The submental group (Ia) is found in the submental triangle (anterior belly of the digastric muscles and the hyoid bone), and the submandibular group (Ib) is found within the submandibular triangle (anterior and posterior bellies of the digastric muscle and the body of the mandible).

The nodes found in level II are located around the upper third of the internal jugular vein, extending from the level of the carotid bifurcation inferiorly to the skull base superiorly. The lateral boundary is formed by the posterior border of the SCM muscle; the medial boundary is formed by the stylohyoid muscle. Two subzones are also described; nodes located anterior to the spinal accessory nerve are part of level IIa, and those nodes posterior to the nerve are located in level IIb.

The middle jugular lymph node group defines level III. Nodes are limited by the carotid bifurcation superiorly and the cricothyroid membrane inferiorly. The lateral border is formed by the posterior border of the SCM muscle; the medial margin is formed by the lateral border of the sternohyoid muscle.

Level lV contains the lower jugular group and extends superiorly from the omohyoid muscle to the clavicle inferiorly. The lateral border is formed by the posterior border of the SCM muscle; the medial margin is formed by the lateral border of the sternohyoid muscle.

The lymph nodes found in level V are contained in the posterior neck triangle, bordered anteriorly by the posterior border of the SCM muscle, posteriorly by the anterior border of the trapezius, and inferiorly by the clavicle. Level V includes the spinal accessory, transverse cervical, and supraclavicular nodal groups.

Level VI lymph nodes are located in the anterior compartment. These nodes surround the middle visceral structures of the neck from the level of the hyoid superiorly to the suprasternal notch inferiorly.

A complete understanding of these anatomic relationships allows various practitioners to exchange information in an unbiased fashion and is critical in the decision-making processes involved in management of nodal metastases.

The current hypotheses on the development of malignancies relate to alterations in the normal mechanisms of cellular proliferation and differentiation and a failure of cell death (apoptosis). This loss of growth control is the result of genetic mutations, including the activation of proto-oncogenes and/or inactivation of tumor suppressor genes. The resulting phenotypic changes provide cancer cells a growth advantage, including loss of response to normal growth controls, defects in response signals for programmed cell death, resistance to cytotoxicity, and defects in terminal differentiation.

Proposed by Fidler, the concept of tumor heterogeneity suggests that tumors are composed of heterogeneous subpopulations of cells differing in immunogenicity, invasiveness, cellular growth kinetics, sensitivity to cytotoxic drugs, and ability to metastasize. The local tumor environment may favor the development of more aggressive clones in the formation of metastases. Although the size of individual clones with metastasizing potential in a given tumor is significant, only a very small percentage of circulating cells lead to the development of metastatic colonies.

The events surrounding the initiation of local tumor invasion by epithelial tumors include a loss of cellular adhesion to surrounding tumor cells and basement membrane, invasion by malignant cells of the subjacent connective tissues by the production of cellular enzymes and growth mediators, cellular attachment to extracellular membrane molecules, neovascularization, and entry or exit from the circulation through the attachment to endothelial cell ligands. A repeat of these events occurs at metastatic sites.

In the case of head and neck squamous cell carcinomas, malignant cells may progress from carcinoma in situ, to microinvasive carcinoma, to a deeply invasive tumor with lymphatic metastases. Interestingly, a head and neck squamous cell carcinoma has the ability to manifest at both extremes of histopathological development in the same anatomic location. The critical step in the transition from carcinoma in situ to microinvasive and invasive carcinoma is the destruction of the basement membrane. This destruction is accomplished by the production of specific proteolytic molecules by tumor cells, including matrix metalloproteinases, collagenases, and plasminogen activators.

Angiogenesis is the growth of new capillaries by sprouting from established vessels. In normal tissues, self-limiting angiogenesis is part of reproduction and organogenesis in addition to wound repair and healing. Conversely, pathological angiogenesis is not autoregulated, but results from alterations in growth-control mechanisms of disease processes (eg, malignant transformation). Various tumor-derived factors (eg, prostaglandin E2, platelet-derived growth factor, transforming growth factor-beta, transforming growth factor-alpha, beta-fibroblast growth factor) are still being investigated for their propensity to facilitate endothelial cell proliferation.

Recent research looking specifically at the production of cytokines regulating immune, inflammatory, and angiogenetic responses in patients with laryngeal squamous cell cancer has revealed higher serum concentrations of the cytokines interleukin-6, interleukin-8, and vascular endothelial growth factor. These agents may be important in proinflammatory and proangiogenetic responses of tumor cells.

The ability of a tumor to stimulate an angiogenic response should directly determine the capability of a tumor to metastasize and ultimately kill the host. A clear correlation between tumor angiogenesis and nodal metastasis has been demonstrated in early and invasive breast carcinoma, ovarian and endometrial carcinoma, non–small-cell carcinomas, prostatic carcinoma, adenocarcinoma of the colon, and squamous cell carcinoma of the esophagus.

The literature notes conflicting reports regarding microvessel density and nodal metastasis in head and neck squamous cell carcinomas. Tumor sites of varying origins with different vascularization patterns at their primary sites may behave differently. Malignancies of the head and neck, especially head and neck squamous cell carcinomas, are the result of a series of genetic misadventures of squamous epithelial cells leading to malignant transformation. Variable genetic susceptibility, prolonged tobacco and alcohol exposure, viruses, and immune suppression all can facilitate these genetic derangements.

Tumors invade local connective tissues by the production of proteinases and the expression of surface markers that facilitate attachment to extracellular matrix components. Tumor growth and size being limited by available nutrients from the surrounding milieu, recruitment of host capillaries leads to the formation of an intratumoral blood supply. Capillary and lymphatic invasion by tumor cells allow malignant cell dissemination and the establishment of histologically identical tumors at distant sites.

Most recently, the expression of vascular endothelial factor-D in a mouse tumor model was found to lead to the lymphatic spread of tumor cells, tumor angiogenesis, and tumor growth. Further research in this area will likely provide more details in the multiple steps involved in the lymphatic spread of squamous cell cancer.

The dissemination of tumor cells beyond the primary site unfortunately remains the most significant factor in prognosis and needs further study.

Evaluating neck metastases based on physical examination findings has been the classic method for patients with new tumors in the head and neck. The single most important factor in determining prognosis is whether nodal metastasis is present. Survival rates decrease by 50% when nodal metastases are present. Furthermore, the presence of cervical adenopathy has been correlated with an increase in the rate of distant metastasis.

During the clinical evaluation, careful palpation of the neck, with specific attention to location, size, firmness, and mobility of each node, is noted. Attention is particularly directed to nodes that appear fixed to underlying neurovascular structures, visceral organs, or nodes that demonstrate skin infiltration. The description of each node becomes an important part of the medical record, which can be used to assess the response to treatment or the progression of the disease.

Unfortunately, clinical palpation of the neck demonstrates a large variation of findings among various examiners. Although both inexpensive to perform and repeat, palpation findings are generally accepted as inaccurate. Both the sensitivity and specificity are in the range of 60-70%, depending on the tumor studied. Because of the known low sensitivity and specificity of palpation, a neck side without palpable metastases is still at risk of harboring occult metastasis, with the risk determined by the characteristics of the primary tumor. The incidence of false-negative (occult) nodes based on physical examination findings varies in the literature from 16-60%. Before the introduction of diagnostic imaging, particularly CT scan, clinical palpation was shown to be inadequate for detecting cervical metastasis. Soko et al reported that only 28% of occult cervical metastases were found by clinical palpation. Martis reported a 38% prevalence of occult metastasis based on clinical examination findings.

Debate persists over the relative merits of imaging in the evaluation of the neck for metastatic disease. [1] Studies that correlate radiologic and histopathologic findings show that early microscopic metastases can be present in nodes smaller than 10 mm that demonstrate no stigmata of neoplasia (ie, central necrosis, extracapsular spread). Evidence of early metastatic disease in clinically occult nodes is minimal and may evade the efforts of the pathologist and radiologist.

Ultrasound is reported superior to clinical palpation for detecting lymph nodes and metastases. The advantages of ultrasound over other imaging modalities are price, low patient burden, and possibilities for follow-up.

Sonographs of metastatic lymph node disease characteristically find enlargement with a spherical shape. Commonly, nodes are hypoechoic, with a loss of hilar definition. In cases of extranodal spread with infiltrative growth, the borders are poorly defined. Common findings of metastases from squamous cell carcinoma are extranodal spread and central necrosis together with liquid areas in the lymph nodes. Lymph node metastases from malignant melanoma and papillary thyroid carcinoma have a nonechoic appearance that mimics a cystic lesion. Sonography may also be useful for assessing invasion of the carotid artery and jugular vein.

Because lymph nodes of borderline size cannot be reliably diagnosed using ultrasound alone, ultrasound-guided fine-needle aspiration and cytologic examination of the nodes in question can be easily performed. The result of the aspirate examination depends on the skill of the ultrasonographer and the quality of the specimen (ie, harboring an adequate number of representative cells). Using this technique, most studies report that a sensitivity of up to 70% can be obtained for the N0 neck.

Since its debut in the 1970s, CT scans have been an invaluable tool in all fields of medicine, including the evaluation of head and neck cancer. Since the advent of high-resolution systems and specific contrast media, fine-cut CT scanning has allowed the detection of pathological cervical nodes of smaller size that may be missed by clinical examination. CT scanning is now used routinely for the preoperative evaluation of the neck because, presumably, it helps decrease the incidence of occult cervical lymphadenopathy. [2]

Introduced in 1998, multiple-spiral CT scanning promises further improvement of temporal and spatial resolution (in the longitudinal axis). This technique permits rapid scanning of large volumes of tissue during quiet breathing. The volumetric helical data permit optical multiplanar and 3-dimensional reconstructions. Improvement of the assessment of tumor spread and lymph node metastases in arbitrary oblique planes is another advantage of the spiral technique.

Criteria for the identification of questionable nodes are also evolving as technology advances. Central necrosis remains the most specific finding suggestive of nodal involvement, but its absence does not exclude metastasis. Unfortunately, metastasis is usually quite rare or not visible in small lymph nodes, where detection would be crucial. Because of the higher imaging resolution, various studies have reduced the traditional values of 10-15 mm for a node to be suggestive. Many authors have proposed a minimal axial diameter of 11 mm for the submandibular triangle and 10 mm for the rest of the neck. Other criteria include the presence of groups of 3 or more borderline nodes and the loss of tissue planes.

An imaging-based classification has also been proposed by Som et al, [3] and due to its specificity, has also been endorsed by clinicians managing head and neck cancer. The boundaries of the nodal levels were easily discerned by radiologists and yielded consistent nodal classifications.

For an evaluation of the diagnostic abilities of Ga-SPECT, see Kotani et al. [4]

The value of MRI is its excellent soft tissue resolution. MRI has surpassed CT scanning as the preferred study in the evaluation of cancer at primary sites such as the base of the tongue and the salivary glands. The sensitivity of MRI exceeds that of clinical palpation in detecting occult cervical lymphadenopathy. Size, the presence of multiple nodes, and necrosis are criteria shared by CT scanning and MRI imaging protocols. [5, 6]

Many reports indicate that CT scanning still has an edge over MRI for detecting cervical nodal involvement. Advances in MRI technology (eg, fast spin-echo imaging, fat suppression) have not yet surpassed the capacity of CT scanning to identify lymph nodes and to define nodal architecture. Central necrosis, as evaluated by unenhanced T1- and T2-weighted images, has been shown to provide an overall accuracy rate of 86-87% compared with CT scanning, which has an accuracy rate of 91-96%. [7] The use of newer contrast media, especially supramagnetic contrast media agents, hopefully will improve the sensitivity of MRI.

This new imaging modality has been increasingly studied in the staging of head and neck cancer. [8, 9] The technique relies on the uptake of 2-fluoro-2-deoxy-D-glucose (FDG) in metabolically-active lesions. The study may also be fused to a corresponding CT scan to facilitate the localization of the lesion of concern.

In comparing their usefulness in the detection of cervical metastasis, PET/CT fusion images have been found to be superior and more accurate for the detection of cervical metastasis, compared with PET alone or with conventional imaging modalities. In addition, PET can contribute to the detection of residual or early recurrent tumors, leading to the institution of earlier salvage therapy. [2]

A study by Tan et al indicated that FDG-PET/CT scanning is more sensitive than contrast-enhanced multislice helical CT (MSCT) imaging in detecting paraesophageal lymph node metastases in patients with esophageal cancer. The study involved 115 patients with esophageal cancer, in whom a total of 946 lymph node groups were resected; metastases were confirmed histopathologically in 221 of these groups. Although no significant differences were found between FDG-PET/CT scanning and enhanced 64-slice helical CT imaging with regard to specificity and accuracy in detecting lymph node metastases, the sensitivity of FDG-PET/CT scanning was 74.7%, compared with 64.7% for enhanced MSCT scanning. The sensitivity difference was even greater for paraesophageal lymph node metastases, being 72% and 57.7%, respectively. [10]

The investigators’ findings also indicated, however, that enhanced MSCT imaging can effectively distinguish false-negative lymph node metastases visualized on FDG-PET/CT scans. Tan and colleagues concluded that combining FDG-PET/CT scanning with MSCT imaging should increase accuracy in staging lymph node metastases in esophageal cancer. [10]

A study by Jung et al suggested that in papillary thyroid carcinoma, a primary tumor with a high avidity for FDG and a high maximum standardized uptake value (SUVmax) is predictive for cervical lymph node metastasis. The study included 193 patients with papillary thyroid carcinoma who underwent FDG-PET/CT scanning prior to treatment, with the FDG-avid tumors being larger than the nonavid tumors (0.93 cm vs 0.59 cm, respectively) and the incidence of cervical lymph node metastasis being greater in the avid tumors than in the nonavid ones (49.2% vs 33.3%, respectively). Moreover, among the avid tumors, the SUVmax was higher in the ones that metastasized than in those that did not. [11]

None of the currently available imaging techniques can help depict small tumor deposits inside lymph nodes. Characteristics of metastatic lymph nodes that can be depicted are the size and presence of noncontrast-enhancing parts inside metastatic lymph nodes caused by tumor necrosis, tumor keratinization, or cystic areas inside the tumor. Only rarely does tumoral tissue enhance more than reactive lymph node tissue; in these rare cases, the tumor can be visualized within a reactive lymph node.

Patients who need an evaluation for a possible nodal malignancy require a comprehensive multidisciplinary evaluation of all potential sites of drainage to that node to identify its primary source. This includes a thorough evaluation of potential primary sites using endoscopic techniques. When appropriate, include laryngoscopy, esophagoscopy, bronchoscopy, and examination of the nasopharynx. If no primary source is identified, taking blind mucosal biopsy samples of the most likely head and neck subsites is essential. [12]

PET/CT techniques have a promising role; however, greater clinical experience is needed prior to making this modality the standard for the detection of metastasis in head and neck cancer.

Complete documentation of nodal characteristics by clinical examination and palpation guide the examiner in using adjunctive radiological tools to exclude occult nodal metastasis.

Yoon DY, Hwang HS, Chang SK, Rho YS, Ahn HY, Kim JH, et al. CT, MR, US,18F-FDG PET/CT, and their combined use for the assessment of cervical lymph node metastases in squamous cell carcinoma of the head and neck. Eur Radiol. 2009 Mar. 19(3):634-42. [Medline].

Kurien G, Hu J, Harris J, Seikaly H. Cost-effectiveness of positron emission tomography/computed tomography in the management of advanced head and neck cancer. J Otolaryngol Head Neck Surg. 2011 Dec. 40(6):468-72. [Medline].

Som PM, Curtin HD, Mancuso AA. An imaging-based classification for the cervical nodes designed as an adjunct to recent clinically based nodal classifications. Arch Otolaryngol Head Neck Surg. 1999 Apr. 125(4):388-96. [Medline].

Kotani J, Kawabe J, Higashiyama S, Kawamura E, Oe A, Hayashi T, et al. Evaluation of diagnostic abilities of Ga-SPECT for head and neck lesions. Ann Nucl Med. 2008 May. 22(4):297-300. [Medline].

van den Brekel MW. Lymph node metastases: CT and MRI. Eur J Radiol. 2000 Mar. 33(3):230-8. [Medline].

de Bondt BJ, Stokroos R, Casselman JW, van Engelshoven JM, Beets-Tan RG, Kessels FG. Clinical impact of short tau inversion recovery MRI on staging and management in patients with cervical lymph node metastases of head and neck squamous cell carcinomas. Head Neck. 2009 Jul. 31(7):928-37. [Medline].

Verhappen MH, Pouwels PJ, Ljumanovic R, van der Putten L, Knol DL, De Bree R, et al. Diffusion-Weighted MR Imaging in Head and Neck Cancer: Comparison between Half-Fourier Acquired Single-Shot Turbo Spin-Echo and EPI Techniques. AJNR Am J Neuroradiol. 2012 Feb 9. [Medline].

Chen ZW, Zhu LJ, Hou QY, Wang QP, Jiang S, Feng H. [Clinical application of positron-emission tomography for the identification of cervical nodal metastases of head and neck cancer compared with CT or MRI and clinical palpation]. Zhonghua Kou Qiang Yi Xue Za Zhi. 2008 Dec. 43(12):705-8. [Medline].

Liao CT, Fan KH, Lin CY, Wang HM, Huang SF, Chen IH, et al. Impact of a second FDG PET scan before adjuvant therapy for the early detection of residual/relapsing tumours in high-risk patients with oral cavity cancer and pathological extracapsular spread. Eur J Nucl Med Mol Imaging. 2012 Mar 21. [Medline].

Tan R, Yao SZ, Huang ZQ, et al. Combination of FDG PET/CT and Contrast-Enhanced MSCT in Detecting Lymph Node Metastasis of Esophageal Cancer. Asian Pac J Cancer Prev. 2014. 15(18):7719-24. [Medline].

Jung JH, Kim CY, Son SH, et al. Preoperative Prediction of Cervical Lymph Node Metastasis Using Primary Tumor SUVmax on 18F-FDG PET/CT in Patients with Papillary Thyroid Carcinoma. PLoS One. 2015. 10 (12):e0144152. [Medline]. [Full Text].

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Curtin HD, Ishwaran H, Mancuso AA, et al. Comparison of CT and MR imaging in staging of neck metastases. Radiology. 1998 Apr. 207(1):123-30. [Medline].

Hao SP, Ng SH. Magnetic resonance imaging versus clinical palpation in evaluating cervical metastasis from head and neck cancer. Otolaryngol Head Neck Surg. 2000 Sep. 123(3):324-7. [Medline].

Kresnik E, Mikosch P, Gallowitsch HJ. Evaluation of head and neck cancer with 18F-FDG PET: a comparison with conventional methods. Eur J Nucl Med. 2001 Jul. 28(7):816-21. [Medline].

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Safa AA, Tran LM, Rege S, et al. The role of positron emission tomography in occult primary head and neck cancers. Cancer J Sci Am. 1999 Jul-Aug. 5(4):214-8. [Medline].

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Benoit J Gosselin, MD, FRCSC Associate Professor of Surgery, Dartmouth Medical School; Director, Comprehensive Head and Neck Oncology Program, Norris Cotton Cancer Center; Staff Otolaryngologist, Division of Otolaryngology-Head and Neck Surgery, Dartmouth-Hitchcock Medical Center

Benoit J Gosselin, MD, FRCSC is a member of the following medical societies: American Head and Neck Society, American Academy of Facial Plastic and Reconstructive Surgery, North American Skull Base Society, American Academy of Otolaryngology-Head and Neck Surgery, American Medical Association, American Rhinologic Society, Canadian Medical Association, Canadian Society of Otolaryngology-Head & Neck Surgery, College of Physicians and Surgeons of Ontario, New Hampshire Medical Society, Ontario Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Nader Sadeghi, MD, FRCSC Professor and Chairman, Department of Otolaryngology-Head and Neck Surgery, McGill University Faculty of Medicine; Chief Otolaryngologist, MUHC; Director, McGill Head and Neck Cancer Program, Royal Victoria Hospital, Canada

Nader Sadeghi, MD, FRCSC is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Head and Neck Society, American Thyroid Association, Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Arlen D Meyers, MD, MBA Professor of Otolaryngology, Dentistry, and Engineering, University of Colorado School of Medicine

Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, American Head and Neck Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cerescan;RxRevu;Cliexa;Preacute Population Health Management;The Physicians Edge<br/>Received income in an amount equal to or greater than $250 from: The Physicians Edge, Cliexa<br/> Received stock from RxRevu; Received ownership interest from Cerescan for consulting; for: Rxblockchain;Bridge Health.

William M Lydiatt, MD, FACS Head and Neck Surgical Oncologist, Methodist Estabrook Cancer Center; Chair-Elect, Department of Surgery, Nebraska Methodist Hospital; Clinical Professor, Department of Surgery, Creighton University School of Medicine; Lecturer, Department of Biology, University of Nebraska-Omaha

William M Lydiatt, MD, FACS is a member of the following medical societies: Alpha Omega Alpha, American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Head and Neck Society

Disclosure: Nothing to disclose.

Neck, Cervical Metastases, Detection

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What Is Thyroid Cancer?

What Is Thyroid Cancer?

Your thyroid is shaped like a small butterfly, and is usually found inside the lower front of your neck. It’s a gland that controls your metabolism. It also releases hormones that direct many functions in your body, including how you use energy, how you produce heat, and how you consume oxygen.

Thyroid cancer develops when cells change or mutate. The abnormal cells begin multiplying in your thyroid and, once there are enough of them, they form a tumor.

If it’s caught early, thyroid cancer is one of the most treatable forms of cancer.

 

Researchers have identified four main types:

Papillary thyroid cancer. If you have thyroid cancer, you probably have this type. It’s found in up to 80% of all thyroid cancer cases. It tends to grow slowly, but often spreads to the nymph nodes in your neck. Even so, you have a good chance for a full recovery.

Follicular thyroid cancer makes up between 10% and 15% of all thyroid cancers in the United States. It can spread into your lymph nodes and is also more likely to spread into your blood vessels.

Medullary cancer is found in about 4% of all thyroid cancer cases. It’s more likely to be found at an early stage because it produces a hormone called calcitonin, which doctors keep an eye out for in blood test results.

Anaplastic thyroid cancer can be the most severe type, because it’s aggressive in spreading to other parts of the body. It’s rare, and it is the hardest to treat. 

If you have thyroid cancer, you probably didn’t notice any signs of it in the early stages. That’s because there are very few symptoms in the beginning.

But as it grows, you could notice any of the following problems:

There is no clear reason why most people get thyroid cancer. There are certain things, though, that can raise your odds of getting it.

Inherited genetic syndromes. Some conditions, including cancer, come from the DNA you get from your parents. In 2 out of 10 cases of medullary thyroid cancer, for example, the cancer is a result of an abnormal gene you’ve inherited.

Iodine deficiency. If you don’t get much of this chemical element in your diet, you could be at more risk for certain types of thyroid cancer. This is rare in the United States because iodine is added to salt and other foods.

Radiation exposure. If your head or neck was exposed to radiation treatment as a child.

Thyroid cancer is more common in women than men. Women tend to get thyroid cancer in their 40s and 50s, while men who get it are usually in their 60s or 70s.

Follicular thyroid cancer happens more often in whites than blacks and in more women than men.

You can still get thyroid cancer if you’re younger. Papillary thyroid cancer, for example, happens most often in people between ages 30 and 50.

Thyroid cancer is usually very treatable, even if you have a more advanced stage of it. That’s because there are effective treatments that give you a great chance for a full recovery. And surgery, when it’s needed, can sometimes cure it.

SOURCES:

American Thyroid Association: “Thyroid Cancer.”

MD Anderson Cancer Center: “Thyroid Cancer Facts.”

Davies, L., Morris, L.G., Haymart, M., Chen, A.Y, Goldenberg, D., Morris, J., Ogilvie, J.B., Terris, D.J., Netterville, J., Wong, R.J., Randolph, G., Endocrine Practice, published online June 2015.

Home Health Network: “Thyroid.”

Mayo Clinic: “Thyroid cancer.”

The American Association of Endocrine Surgeons: “Thyroid cancer: Papillary Thyroid Cancer (PTC).”

American Cancer Society: “Thyroid cancer risk factors.”

Columbia University Department of Surgery: “What Causes Thyroid Cancer?”

National Cancer Institute: “Thyroid Cancer-Patient Version.”

Medscape: “Follicular Thyroid Carcinoma.”

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What Is Thyroid Cancer?

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