For purposes of study, the swallow has been divided into three phases: oral, pharyngeal, and oesophageal.

Prior to the onset of the oral phase, the major portion of a food bolus is formed into a cohesive mass and is held between the anterior tongue and the hard palate. The soft palate is pulled anteriorly and rests against the back of the tongue, which is slightly elevated, closing the oral cavity. The oral phase begins when the tongue moves the bolus posteriorly and ends when the bolus passes the anterior tonsillar pillars. During this phase, the tongue elevates in an anterior to posterior direction. An anterior labial seal and a lateral buccal seal keep the bolus in proper position (Table 1) 282.

The pharyngeal phase begins when the food bolus passes the anterior tonsillar pillars and ends when the bolus passes through the upper oesophageal sphincter into the oesophagus. During this phase the palate elevates and retracts, closing the nasopharynx. The laryngeal valves close and the suprahyoid muscles elevate the larynx under the base of the tongue. The bolus is propelled through the pharynx by the backward motion of the base of tongue and contraction of the pharyngeal constrictor muscles. When the upper oesophageal sphincter opens it creates a negative pressure in the hypopharynx, facilitating passage of the bolus into the oesophagus. During the pharyngeal phase respiration is inhibited. The exact trigger for initiation of this phase of the swallow is unknown; it may be related to the position of the base of the tongue (Table 2) 283.

The oesophageal phase begins when the bolus enters the oesophagus and ends when it passes through the lower oesophageal sphincter into the stomach. A sequential peristaltic wave in the oesophagus propels the bolus. The lower oesophageal sphincter relaxes as the bolus passes into the stomach (Table 3) 284.

The upper oesophageal sphincter is a zone of high pressure between the pharynx and the oesophagus that prevents air from entering the oesophagus and helps prevent oesophageal contents from refluxing into the pharynx. The muscles which form the upper oesophageal sphincter are the cricopharyngeus and either the lower fibres of the inferior pharyngeal constrictor or the upper fibres of the cervical oesophagus.

At rest the sphincter is closed, and closure is maintained by both tonic contraction of the intrinsic sphincter muscle and passive elastic forces. Inhibition of the intrinsic musculature contraction of the sphincter and contraction of the suprahyoid muscles creates anterosuperior displacement of the cricoid cartilage, thereby opening the sphincter (Fig. 1) 882.

Dysphagia, or difficulty in swallowing, is a common complaint. For purposes of discussion, abnormalities in swallowing can be divided into dysfunction in each of the separate phases. In reality, these phases are so inter-related that the abnormalities are often in more than one phase.

In some patients the tongue holds the bolus too far forward on the palate, resulting in anterior leakage. Weakness of the labial or cheek muscles leads to malpositioning of the bolus either out of the oral cavity or into the lateral sulci. Any decreased sensation in the oral cavity makes it much more difficult to manipulate the bolus into proper position. Tongue dysfunction may be due to either tethering of the tongue or decreased tongue movement. Many patients have a inco-ordination of the normal anterior to posterior tongue motion. This inco-ordination can be a devastating problem because it leads to difficulty in initiating the pharyngeal phase of the swallow.

In the pharyngeal phase, limitation in palatal motion leads to nasal regurgitation of the bolus. A frequent abnormality is decreased propulsion of the bolus by the pharynx. This response may be secondary to poor function of the tongue, decreased pharyngeal constrictor muscle activity, or dysfunction in opening of the upper oesophageal sphincter. Decreased laryngeal elevation may compromise the opening of the upper oesophageal sphincter or may result in poor laryngeal protection due to reduced epiglottic deflection or because the larynx is not positioned properly under the base of the tongue. Failure of the vocal cords to close during the swallow will also leave the larynx unprotected. Many patients have a delay in the onset of the pharyngeal phase of the swallow.

Aspiration is a symptom of dysphagia; it can result from dysfunction in either the oral or pharyngeal phases. Aspiration itself is divided into three components: that occurring before, during, or after the swallow. Aspiration before the swallow is caused by presentation of the bolus to the pharynx before the larynx has closed and elevated, probably because of either poor oral control, causing spillover of the bolus into the pharynx or delay in the onset of the pharyngeal phase of the swallow. Aspiration during a swallow occurs because of abnormalities in the pharyngeal phase such as poor laryngeal elevation or closure, or both. Aspiration after a swallow results from inability of the pharynx to clear the bolus during the pharyngeal phase. This leaves residue in the pharyngeal recesses that is subject to spillover into the pharynx at a time when the larynx is unprotected.

Insertion of a tracheotomy tube exacerbates dysphagia by limiting laryngeal elevation and decreasing normal vocal fold reflexes. Hyposalivation makes it difficult to initiate a swallow. Radiation therapy often causes hyposalvation and may also lead to tissue oedema and fibrosis, affecting both the oral and pharyngeal phases of the swallow. The effect of medications on swallowing function is not well known, but drug therapy may play an important role in dysphagia.

A precise history is essential when evaluating a patient with dysphagia. The distinction between dysphagia and odynophagia must be made: odynophagia is pain on swallowing, and is often associated with either neoplasia or infection. The presence of referred pain, such as otalgia, may be caused by a hyopharyngeal lesion.

When a patient complains of dysphagia, specific symptoms must be known and the consistencies of food or liquid which exacerbate the symptom must be defined. Patients may describe a bolus as being ‘stuck’ or ‘caught’. The location of this sensation and the kind of manoeuvre used by the patient to dislodge the bolus are all helpful points. Regurgitation of the bolus is common in patients with a major oesophageal obstruction.

Aspiration in a patient with normal laryngotracheal sensation causes coughing; the timing of this cough can help to indicate the timing of the aspiration. For example, patients with Zenker's diverticulum often aspirate anywhere from several minutes to some hours after the meal, when the contents of the filled diverticulum spill over into the unprotected pharynx. Nasal regurgitation and voice change may indicate problems with palatal and vocal cord function, respectively. Change in diet and weight loss can reflect the degree of severity of the swallowing abnormalities.

Because dysphagia is often associated with other systemic disorders, a thorough clinical history must be obtained. Neurological abnormalities such as change in mental status, dysarthria, and diplopia are all potentially relevant. Gastrointestinal symptoms might include dyspepsia or acid regurgitation. Rheumatological manifestations include diffuse muscle weakness or skin disorders. Psychosocial factors that may have either precipitated or exacerbated the dysphagia should be investigated.

Physical examination should include the muscles of facial expression, tongue mobility and strength, and palatal elevation and sensation. The correlation between the gag reflex and dysphagia is not known and may not be clinically important. A full examination of the nasopharynx, hypopharynx, and larynx is important to determine whether there are any structural or neurological lesions.

Videofluoroscopy is a radiological technique used for evaluating dysphagia. The patient is seated in an upright position and given small quantities of barium in liquid, paste, and solid forms. A camera is focused on the oral and pharyngeal regions throughout the swallow, recording the images on videotape. If a swallowing abnormality is seen, various manoeuvres, such as change in bolus texture, head position, and breathing, are used to attempt to correct the abnormality.

The specific events evaluated during fluoroscopic examination include oral transit time, pharyngeal transit time, the presence and degree of residue in the pharyngeal recesses, the extent of laryngeal elevation, the presence and timing of aspiration, degree of upper oesophageal sphincter relaxation, the effect of various bolus textures and position on the swallow, and the integrity of cervical oesophageal peristalsis.

Swallowing videofluoroscopy is indicated for almost all symptomatic dysphagia patients who are able to co-operate to some degree. The small quantities of barium used carry minimal risks, even for a patient with gross aspiration. There have been no reported complications from this test. The test is also particularly helpful in any patient in whom aspiration is suspected, whether or not the patient is subjectively aware of the problem. Videofluoroscopy does not accurately demonstrate structural abnormalities, and subtle oesophageal abnormalities may be missed.

The barium swallow is a cineradiographic study of the oesophagus. Following administration of a large quantity of liquid barium to the supine patient, the fluoroscopy camera follows the bolus from the upper oesophageal sphincter to the lower oesophageal sphincter. Suspected reflux can be accentuated by procedures such as the Valsalva manoeuvre.

A barium swallow should be performed in any patient with odynophagia. If the laryngoscopic examination is normal, the barium study reveals the source of the odynophagia. If the laryngoscopy reveals any infection, such as candidiasis, or a tumour, the extent of oesophageal disease needs to be assessed. Any patient with dysphagia for solid foods should also undergo a barium swallow since a structural lesion may not be visualized on videofluoroscopy. A standard barium swallow is often used as one method for detecting gastro-oesophageal reflux. Patients whose symptoms localize to the lower neck or sternum are likely to have oesophageal disease and they should also undergo a barium swallow. Any unexplained dysphagia in a patient in whom a swallowing videofluoroscopy is normal should be further studied with a standard barium swallow.

Endoscopic examination performed under anaesthesia might include direct laryngoscopy, nasopharyngoscopy, oropharyngoscopy, oesophagoscopy, and bronchoscopy. In patients with head and neck cancer it is important to delineate the exact site of the lesion and also to rule out any other synchronous primary lesions. Flexible fibreoptic oesophageal endoscopy is indicated for patients with suspected oesophageal disease. Endoscopy may be combined with a dilatation in patients with a known stricture.

Techniques such as scintigraphy, sonography, and electromyography are being developed and refined so that they may have more applicability in the clinical sphere.

Many disorders can cause dysphagia (Table 4) 285. Neurological deficits may be associated with cerebral vascular accidents, head trauma or cranial nerve neuropathies and often result in gross swallowing inco-ordination. Muscular disorders such as polymyositis can affect the laryngopharyngeal musculature, resulting in severely reduced ability to propel a bolus. Oculopharyngeal muscular dystrophy is a rare genetic disorder which affects people of French Canadian descent. The two symptoms, bilateral ptosis and dysphagia, usually present after age 50. There is progressively poor bolus propulsion and aspiration.

Zenker's diverticulum is an outpouching of the pharynx, usually between the upper border of the cricopharyngeus muscle and the lower border of the inferior constrictor muscle (Fig. 2) 883. Dysfunction of the upper oesophageal sphincter, such as delayed or decreased relaxation, may contribute to its aetiology. In this condition, the food bolus collects in the diverticulum, and spills over into the unprotected larynx, causing aspiration. Cricopharyngeal achalasia is a rare entity defined as isolated incomplete relaxation of the cricopharyngeus muscle without dysfunction of the other pharyngeal constrictor muscles (Fig. 3) 884. Structural lesions, such as oesophageal webs, rings, or strictures, often cause solid food dysphagia.

Dysphagia is sometimes relieved by treating the underlying disorder with specific drugs. For example, Parkinson's disease may respond to Sinemet and polymyositis may respond to oral steroids. Oesophageal lesions such as strictures or webs are treated by dilatation.

The indications for upper oesophageal sphincterotomy (often called a cricopharyngeal myotomy) are unclear. Isolated cricopharyngeal achalasia and oculopharyngeal muscular dystrophy respond well to a sphincterotomy; for achalasia occurring in conjunction with diffuse pharyngeal dysfunction, however, the benefit of a myotomy is questionable. Of the several surgical approaches to Zenker's diverticulum, the most frequently performed is diverticulectomy through a left lateral cervical incision. A myotomy should always be performed concurrently or the diverticulum is likely to occur.

Patients with disorders that do not respond to medication or surgery may benefit by ‘swallowing therapy’. After the swallowing abnormalities are identified on videofluoroscopy various manoeuvres are tried to see which facilitates the most nearly normal swallow; for example, patients with a supraglottic laryngectomy, who often aspirate postoperatively, must be taught a ‘supraglottic swallow’, which involves flexing the neck, holding the breath on inspiration, swallowing, coughing, and then exhaling.

If none of the above treatment options results in the ability to swallow without aspiration and to maintain nutritional status, the patient requires a non-oral feeding route, such as a gastrostomy tube or a jejunostomy tube.

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