The Throat

Published on 11/04/2015 by admin

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The Throat

Anatomy and physiology

This section will discuss the non-neoplastic diseases of the throat. The regions included in the broad term ‘throat’ are:

Larynx

The primary function of the larynx is to protect the tracheobronchial tree. Through evolution it has developed the secondary function of voice production. It has a rigid skeleton consisting of several cartilaginous structures (Fig. 3.4). The most prominent of these is the thyroid cartilage, which inferiorly articulates with the cricoid cartilage. The flap-like epiglottis is attached to the thyroid cartilage and occludes the laryngeal inlet on contraction of the aryepiglottic muscles. The cricothyroid membrane provides a suitable site through which the airway can be maintained in an emergency (see p. 68).

For descriptive purposes the larynx is subdivided into three parts (Fig. 3.5):

The glottis is the space between the vocal cords. The posterior third of the vocal cord is the cartilaginous arytenoids and the anterior two-thirds is membranous (vocal fold). The supraglottis extends from the apex of the laryngeal ventricle to the hyoid. The subglottis stretches from 1 cm below the glottis to the lower border of the cricoid. Food and saliva are prevented from entering the lower respiratory tract by the sphincteric action of the true and false cords. In addition, during swallowing, the larynx is elevated pari passu with the hyoid bone so as to rest under the tongue. Food then passes into the lateral recesses (piriform sinuses) rather than in the midline. The epiglottis falls back as a part of this protective mechanism.

Symptoms, signs and examination

The importance of a full and accurate history as an aid to diagnosis cannot be overemphasized. Direct questioning related to specific areas in the throat is essential, and smoking habits and alcohol intake must be assessed.

Symptoms and signs

Oral cavity

The major signs and symptoms of oral disease include:

Examination

With experience it is possible to view the oral cavity and all parts of the pharynx and larynx using good illumination, tongue depressors and mirrors. These techniques are best learnt under supervision. Increasingly, laryngopharyngeal examination is carried out using a fibreoptic nasal endoscope (Fig. 3.9). Palpation plays a vital role in a full evaluation. Often, a lesion may be more easily felt than visualized, and its limits readily defined. Neck palpation is essential in all cases of head and neck neoplasia.

Dysphonia I

Voice changes are often loosely described as hoarseness, but it is preferable to use the terms aphonia and dysphonia. Aphonia should be reserved for cases with no voice or a mere whisper. Dysphonia describes an alteration in the quality of the voice. Laryngeal disorders can present as dysphonia which may progress to stridor (p. 64). Organic causes of dysphonia may be broadly classified as in Table 3.3 and are discussed below. Other causes of dysphonia are considered on pages 62–63.

Table 3.3 Organic causes of dysphonia

Type Cause
Inflammatory Acute laryngitis (infective), chronic laryngitis
Neoplasia Carcinoma larynx, respiratory papillomata
Neurological Myasthenia gravis, carcinoma of lung/breast, post-thyroidectomy, spasmodic dysphonia
Systemic Hypothyroidism, rheumatoid arthritis

Inflammatory laryngeal lesions

Polyps

Unilateral inflammatory polyps are not uncommon (Fig. 3.11). The history is similar to acute laryngitis, but resolution of hoarseness cannot occur until the polyp is removed under microlaryngoscopic control. Inhalation of fumes, whether from tobacco, smoke or chemicals, may result in acute dysphonia. All inflammatory lesions, either infection or traumatic, may produce a sufficient degree of oedema to cause respiratory embarrassment.

Neurological lesions

Neurological lesions may be of central or peripheral origin. Central pathologies include pseudobulbar palsy, cerebral palsy and multiple sclerosis. Peripheral pathologies include myasthenia gravis, motor neurone disease, and lesions affecting the vagus and recurrent laryngeal nerves. With most peripheral causes, there will be dysarthrophonia secondary to a vocal cord paralysis.

Once a vocal cord palsy has been diagnosed and any local laryngeal pathology excluded, a systematic approach is required to determine the aetiology. This is most easily done by considering the course of the vagus and recurrent laryngeal nerves. Because of its longer route, the left recurrent laryngeal nerve is more frequently involved in pathology (Fig. 3.13). On the left this will be from the cranium via the skull base, neck and thorax back to the larynx; on the right it terminates in the neck. One of the most common causes of vocal cord palsy is malignant disease in the chest or neck, causing recurrent nerve deficits. Inspection of the neck may reveal the scar of previous surgery, e.g. carotid endarterectomy or thyroid surgery (Fig. 3.14). Unilateral vocal cord palsy, where history and examination do not reveal a cause, should therefore have CT imaging from brainstem to chest.

Systemic causes

A number of systemic conditions can produce dysphonia. These include the following:

Management

The direction of investigation will be determined by the clinical history and physical signs. Treatment policies are then directed at abolishing or reducing the aetiological factors.

In many cases of unilateral cord palsy, no obvious aetiology is uncovered, despite extensive investigations. Such cases are eventually labelled idiopathic. Some recover spontaneously (which may take up to 6 months) or become asymptomatic as the contralateral mobile vocal cord compensates. If compensation in unilateral cord palsy is inadequate, then a medialization procedure may be beneficial. This involves techniques to medialize the palsied cord so that the mobile cord is more easily able to effect approximation (Fig. 3.15).

Patients with terminal disease, e.g. carcinoma of the lung and breast, should have a medialization procedure immediately to ameliorate the distressing symptoms of dysphonia and frequently associated aspiration.

Dysphonia II

Dysphonia from non-organic causes may have a psychogenic or habitual aetiology. Specific laryngeal pathology may develop secondary to misuse or abuse of the voice. Table 3.4 classifies non-organic voice disorders. All age groups may be affected.

Table 3.4 Non-organic causes of dysphonias

Type Cause
Habitual dysphonias Vocal abuse
  – acute laryngitis
  – vocal nodules
  – vocal oedema
  – chronic laryngitis
  – contact ulcer
Psychogenic dysphonias Musculoskeletal tension disorders
  Conversion voice disorders
  – muteness
  – aphonia
  – dysphonia
  Mutational falsetto

Habitual dysphonias

In patients with habitual, or ‘hyperkinetic’, dysphonia the voice quality is frequently related to the level of stress. Most cases reveal long-term poor voice quality of gradual onset, which is generally worse after a period of talking. These features do not occur in psychogenic voice disorders. The habitual dysphonic uses incorrect patterns in voice production. However, prolonged habitual misuse and abuse of the vocal folds can lead to secondary organic changes. These changes may be reversible by suitable re-education, but in some instances will require surgical intervention.

Vocal abuse produces hyperadduction of the vocal cords and can lead to varying degrees of secondary pathology, e.g. acute inflammation, vocal cord oedema, vocal cord nodules, chronic inflammation and contact ulcers.

Psychogenic dysphonia

Psychogenic dysphonias are voice disorders in the absence of laryngeal disease. The majority have an underlying anxiety or depression, personality disorders or psychoneuroses.

Stridor

Stridor is noisy breathing resulting from narrowing of the airway at or below the larynx. Narrowing of the supraglottis may produce inspiratory stridor, whereas narrowing at the glottis or cervical trachea tends to produce biphasic stridor. In contrast, bronchial narrowing will produce expiratory stridor.

Stertor refers to noisy breathing due to narrowing of the airway above the larynx. An example of this is adenotonsillar hypertrophy.

Causes

Stridor results from a wide range of conditions which are summarized in Table 3.5 and discussed below.

Table 3.5 Age-specific causes of stridor

Age group Cause
Neonatal* Congenital tumours, cysts
  Webs
  Laryngomalacia
  Subglottic stenosis
  Vocal cord paralysis
Children* Laryngotracheobronchitis
  Supraglottitis (epiglottitis)
  Acute laryngitis
  Foreign body
  Retropharyngeal abscess
  Respiratory papillomata
Adults Laryngeal cancer
  Laryngeal trauma
  Acute laryngitis
  Supraglottitis (epiglottitis)

*Children are at greater risk than adults from upper airway obstruction because their airways are narrower and have softer cartilage, which collapses more easily.

General symptoms and signs of respiratory failure due to airway obstruction are given in Table 3.6.

Table 3.6 Signs of severe respiratory failure due to airway obstruction

Retropharyngeal abscess

A now rare condition, retropharyngeal abscesses occur mostly in young infants and children. Inflammation and swelling in the retropharyngeal space, secondary to oropharyngeal infection, can cause respiratory embarrassment and severe dysphagia (Fig. 3.26). The child assists breathing by hyperextension of the neck, which is held rigid. Urgent parenteral antibiotics are administered and surgical drainage is performed to avoid spontaneous rupture with risk of inhalation of pus.