Supraglottic Cancer

Updated: Aug 18, 2015
  • Author: Joshua D Hornig, MD, FRCSC; Chief Editor: Arlen D Meyers, MD, MBA  more...
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Overview

Background

Cancer of the supraglottis (supraglottic cancer) is almost exclusively squamous cell carcinoma (SCC). This article discusses the anatomy of the supraglottis, explains the staging of supraglottic lesions, and provides an overview of treatment options.

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History of the Procedure

During the past 150 years, the treatment of supraglottic tumors has progressed significantly. In 1852, Horace Green reported the first surgical resection of a laryngeal lesion, a polyp in the ventricle, removed under direct vision. By 1859, the first transcervical resection of an epiglottic neoplasm was reported. Chevalier Jackson revolutionized supraglottic surgery in 1915, when he used a laryngoscope and a punch biopsy to remove an epiglottic tumor. [1] Alonso first described conservation surgery for cancer of the supraglottic larynx in 1947, and, in 1958, Ogura formalized the procedure as the supraglottic laryngectomy. [2, 3] During the 1950s, the surgical microscope and endotracheal anesthesia were brought to bear on this disease. In the 1970s, the carbon dioxide laser began to be used for supraglottic tumors.

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Problem

SCC of the supraglottis is seen less frequently than cancer of the glottis, and is treated differently from tumors of the glottis or subglottis. Because of its location, the disease and its treatment can affect the function of the larynx, including speech, swallowing, and breathing.

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Epidemiology

Frequency

Laryngeal cancer is the second most common type of head and neck cancer worldwide. [4] In the United States, approximately 12,500 new cases are diagnosed each year. In 2002, approximately 160,000 cases of laryngeal cancer and 90,000 deaths were reported worldwide. [5]

Laryngeal cancer is the 11th most common cancer in men worldwide but is much less common in women. Men have been reported to have as much as 30 times the risk that women have for this disease. Older individuals are also at a higher risk for laryngeal cancer; the highest number of diagnoses is made in patients age 60-74 years.

The percentage of laryngeal cancers that originate in the supraglottis varies from country to country. In the United States, for example, approximately 30-40% of laryngeal cancers originate in the supraglottis, while most occur in the glottis. In Spain and Finland, however, the supraglottis is the most frequent subsite. [6]

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Etiology

Generally, the international occurrence of SCC is proportional to tobacco and alcohol use. In societies in which tobacco is chewed rather than smoked, tumor location favors the oral cavity rather than the larynx.

Numerous studies have correlated smoking of tobacco products with SCC of the larynx. In fact, some studies have show that97% of patients with laryngeal cancer smoked. When compared with men who did not smoke, men who smoked at least 1.5 packs of cigarettes per day for more than 10 years were found to have a 30-fold increased risk of developing laryngeal cancer.

The risk for supraglottic cancer has been found to be higher with the use of black (air-cured) tobaccos than with the use of blonde (flue-cured) tobaccos. This difference is not found with glottic cancers, suggesting that the etiology for supraglottic cancers and glottic cancers may differ. [7]

Studies with controls for age, race, and smoking habits also suggest that consumption of alcohol increases the risk of laryngeal cancer. Alcohol consumption has been shown to have a synergistic effect with smoking; thus, the risk of developing carcinoma of the larynx is increased 100-fold in individuals who both smoke and drink. This may be partly due to the fact that alcohol serves as a solvent for the carcinogens of tobacco.

In 1946, Slaughter developed the theory of field cancerization in tumors of the head and neck. [8] In essence, this theory posits that the entire mucosa of the aerodigestive tract, when exposed to the same toxins, risks development of carcinoma. The vulnerable epithelium undergoes progressive changes that lead to malignancy as exposure to toxins continues. Hence, multiple areas of precancerous change can give rise to synchronous lesions. Supporting this theory is the high rate (4%) of synchronous lesions found upon workup of patients with lesions of the upper aerodigestive tract.

Dietary deficiencies, radiation exposure, human papillomavirus (HPV), and gastroesophageal reflux are other factors associated with laryngeal SCC.

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Pathophysiology

The supraglottis is embryologically derived from the buccopharyngeal anlage in the region of the third and fourth branchial arches. The glottis and subglottis originate from the tracheobronchial anlage in the region of arches 5 and 6. Hence, the larynx virtually consists of 2 hemilarynges, each with different embryonal derivation and largely independent lymphatic circulation. Despite the theoretical separation of the supraglottis from the rest of the larynx, no anatomical or histological barrier has been identified. Furthermore, supraglottic tumors invading the paraglottic space have access to the glottis via the medial surface of the thyroid cartilage.

Lymphatic vascularity in the supraglottis is much denser than in the glottis and subglottis. This is important in the development of supraglottic cancer and leads to a significantly higher incidence of cervical lymph node metastases in tumors of this subsite. [9]

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Presentation

Symptoms

Minimal changes in the vibration of the vocal cord due to tumor growth often cause dysphonia or hoarseness at an early stage in glottic cancer. Subglottic carcinomas can cause airway compromise at an early stage. Supraglottic cancers are less likely than glottic and subglottic cancers to produce noticeable symptoms such as these early in the disease course and are more likely to present with the less specific symptoms of persistent dysphagia, odynophagia, or otalgia. [4] Patients with SCC of the supraglottis are not limited to these symptoms, however, and may also present with hoarseness, hemoptysis, stridor, or chronic cough. Patients with SCC of the supraglottis are more likely to present with a neck mass, partly because patients with supraglottic cancer generally present later than patients with glottic cancer, and partly because of the differences in anatomy and lymphatic drainage,

Examination

Due to the fact that supraglottic patients with SCC often present with nodal disease, palpation of the neck is important. Physical examination may reveal laryngeal or cervical findings.

Examination with a laryngeal mirror or a flexible nasopharyngoscope aids in visualization of supraglottic lesions.

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Relevant Anatomy

The supraglottic larynx is partitioned into 4 subdivisions, as follows: (1) aryepiglottic folds, (2) arytenoids, (3) false cords, and (4) epiglottis. For tumor-staging purposes, the epiglottis is further subdivided into suprahyoid and infrahyoid regions. These areas of the supraglottis are structured within the framework of the supraglottic larynx, which includes the upper half of the thyroid cartilage, the arytenoid cartilages, and the epiglottis. In the image below the vocal fold, epiglottis, aryepiglottic fold, and arytenoids are seen.

A surgical specimen after laryngectomy. The arrow A surgical specimen after laryngectomy. The arrow points to the vocal fold. Note the epiglottis, aryepiglottic fold, arytenoids, and false folds superior to the arrow.

Supraglottis subsites

See the list below:

  • Suprahyoid epiglottis (lingual and laryngeal surfaces)
  • Infrahyoid epiglottis
  • False cords
  • Arytenoid
  • Aryepiglottic folds

Supraglottic squamous cell carcinoma (SCC) follows a predictable pattern of spread. Although tumors may extend inferiorly to involve the vocal folds and subglottis, invasion more often occurs in adjacent sites outside the larynx such as the base of tongue, vallecula, pyriform sinus, and postcricoid region. As the disease progresses, tumors of the supraglottis tend to metastasize to regional lymph nodes.

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