Oral, pharyngeal and oesophageal phases of deglutition

Deglutition is divided into three stages:

Prehension

Prehension in the horse relies on the incisor teeth to grasp and section herbage and on the lips to pick up smaller pieces of ingesta as well as to contain it within the mouth and to manipulate food towards the cheek teeth.

Mastication

The molar and premolar teeth are responsible for the mechanical crushing of the fibrous diet.

The tongue and buccal musculature assist in manipulating the ingesta between the maxillary and mandibular dental arcades.

Mastication requires free opening and closure of the temporo-mandibular joints (TMJs) through the action of the masticatory muscles – the masseter, pterygoid and temporal muscles close the jaws, and gravity, assisted by the digastric muscles, opens them. The masticatory muscles receive their innervation through the mandibular branch of the trigeminal nerve (V).

The shape of the articular surfaces of the TMJs together with the presence of menisci permit lateral movements by the mandibular teeth across the wearing surfaces of the upper cheek teeth.

Lingual function

The tip of the tongue assists in prehension and moves the ingesta between the cheek teeth.

Contraction of the tongue base helps in the formation of boluses and, once collected, each bolus is driven caudally; this triggers the involuntary phases of deglutition by driving food and fluid caudally from the oro-pharynx.

The tongue is attached to the hyoid apparatus, and free movement at the tympano-hyoid articulation is required for the craniocaudal tongue motion which facilitates bolus formation in the oro-pharynx.

The glossal musculature receives its motor supply via the hypoglossal nerve (XII).

Elevation of palate

The action of the levator palatini muscles draws the soft palate dorsally to close off the naso-pharynx and prevents the nasal reflux of ingesta; this marks the onset of the involuntary stages of deglutition.

The horse has an intra-narial larynx at all times other than during the momentary disengagement for deglutition. (See 5.18 and 5.21.)

The levator palatini muscles lie parallel with the drainage ostia of the auditory tube diverticula (ATDs) so that when they contract the ostia open to allow exchanges of air for pressure equilibration across the ear drum.

Pharyngeal constriction

The constrictor action of the circular muscles of the pharyngeal walls embraces both oro-pharynx and naso-pharynx – the latter can be appreciated during endoscopic examinations of the naso-pharynx. A wave of constriction follows the contraction of the tongue base and passes from rostral to caudal efficiently to empty the oro-pharynx – the pharyngeal ‘stripping’ wave – leaving minimal quantities of ingesta at the base of the tongue.

Laryngeal protection

Aspiration of food and fluid through the rima glottidis is prevented primarily by the tight adduction of the vocal folds and arytenoid cartilages and to a lesser extent by the retroversion of the apex of the epiglottis.

Crico-pharyngeal relaxation

The upper oesophageal sphincter is formed by the thyro- and crico-pharyngeus muscles, and these are maintained in a state of contraction to prevent involuntary aerophagia, especially during forced exercise. Relaxation of the crico-pharynx simultaneous with the pharyngeal stripping wave permits the food and fluid boluses to pass caudally into the proximal oesophagus.

Primary and secondary oesophageal peristalsis

After each bolus has passed through into the proximal oesophagus, primary peristaltic waves are initiated by active closure of the cricopharynx.

Primary oesophageal peristalsis carries individual boluses to the cardia, but the process is not completely efficient and small quantities of ingesta are left at variable levels in both the cervical and thoracic oesophagus, even in normal horses. These ingesta are either picked up in the bolus of a subsequent primary wave or by locally generated secondary peristalsis.

History – signs of dysphagia

The signs of dysphagia include:

Obviously, horses that are unable to eat and swallow food are likely to lose weight rapidly, but this process is accelerated if the horse develops secondary inhalation pneumonia, which is a common sequel to dysphagia. A moist cough is typical of animals aspirating food or saliva into the rima glottidis. In addition to a clear case history, careful observation of the patient’s attempts to eat and drink should be made.

If the horse shows return of ingesta from its mouth, the site of the lesion causing the dysfunction must lie in the oral cavity or oropharynx.

Nasal reflux of ingesta points to an abnormality of the pharyngeal or oesophageal phase of deglutition (Figure 1.1).

Physical examination, external and oral inspection

Evidence of systemic and/or toxic disease, including Streptococcus equi infection, botulism, grass sickness, rabies, upper motor neuron disease, lead poisoning and tick paralysis should be sought.

The external assessment should check for evidence of concurrent neuropathies such as facial palsy, Horner’s syndrome or head tilt.

Thoracic auscultation should check for signs of inhalation pneumonia.

Local lymphadenopathies and firm distension of the oesophagus to the left side of the trachea are changes which might be found during palpation of the throat area.

Useful information can be obtained by attempting to pass a nasogastric tube. This should determine whether pharyngeal swallowing reflexes are still present or whether the upper alimentary tract is physically obstructed.

Under sedation and with a Hausmann gag in place, a detailed inspection of the oral cavity with the aid of a dental mirror should look for evidence of dental malalignment, enamel pointing of the cheek teeth, fractures of the dental crowns, periodontitis, soft-tissue lesions of the buccal cleft and palate, oral foreign bodies and lesions of the tongue. The structures involved may require digital manipulation to complete the examination, and a tell-tale foul smell points to the presence of stale entrapped ingesta.

Defects of the palate cannot always be appreciated from a conscious examination of the mouth because they are often restricted to the caudal section of the soft palate.

Endoscopy per nasum

The presence of ingesta in the nasal meati, nasopharynx, larynx or trachea is never normal and confirms the broad diagnosis of pharyngeal or oesophageal phase dysphagia. Such contamination may range from clods of green grass to tiny flecks of chewed ingesta. The latter may be appreciated only on examination of tracheal aspirate samples.

Endoscopy per nasum is necessary to confirm whether pharyngeal paralysis is present (Figure 1.2). The usual findings consist of:

Where functional pharyngeal paralysis is diagnosed, many horses are afflicted with pharyngeal hemiplegia, i.e. the pharyngeal neuropathy is unilateral, for example in cases of guttural pouch mycosis (see ‘Aetiopathogenesis’ in 5.6).

True pharyngeal paralysis may be seen in cases of botulism.

Conchal necrosis may accompany prolonged dental suppuration and may be seen on endoscopy of the nasal chambers (see ‘Conchal necrosis and metaplasia’ in 5.16).

Provided that an endoscope with a diameter of 8.0 mm or less is available, the diagnosis of a palatal defect by inspection of the floor of the nasopharynx per nasum presents no difficulties, even in quite young foals (Figure 1.3).

Other abnormalities which may cause dysphagia and which can be confirmed by endoscopy of the pharynx and larynx include:

The extent of tracheal aspiration of ingesta which accompanies the dysphagia can be deduced by advancing the endoscope into the trachea to the level of the thoracic inlet. This is particularly helpful to assess compromised swallowing after ‘tie-back’ surgery.

Oesophagoscopy is often unrewarding in the investigation of equine dysphagia simply because physical or functional obstructions of the oesophagus invariably lead to a build-up of ingesta and saliva in the lumen which, in turn, inhibits a satisfactory field of view. However, when the patient has been starved prior to endoscopy, evidence of conditions such as oesophagitis, megaoesophagus, stricture, rupture, tracheo-oesophageal fistula, diverticulum, intra-mural cyst, dysautonomia and neoplasia may be found.

Radiography and fluoroscopy

Plain lateral radiographs of the pharynx, larynx and cervical oesophagus are used to investigate the relationships between normal anatomical structures and to identify intra-luminal, mural and extra-mural soft-tissue swellings. Contrast media can be helpful to outline these structures. Fluoroscopic studies – again, using contrast media – are required for the dynamic investigation of deglutition.

Lateral radiographs of the chest are a useful aid to monitor the progress of aspiration pneumonia which shows a characteristic pattern of consolidation in the dependent lung lobes.

Oral examination under general anaesthesia

General anaesthesia is necessary to complete the inspection of the oral cavity. The tendency for soft tissues to obscure the view, particularly towards the base of the tongue, can be overcome by the use of an endoscope passed through a polypropylene mare gynaecological speculum. Again, general anaesthesia is required for a more detailed manual or endoscopic examination of the caudal oral cavity, especially in the region of the epiglottis and ary-epiglottic folds.

Facial palsy and lip lesions

Facial paralysis inhibits the ability of a horse to prehend and retain ingesta in the oral cavity (see Chapter 11).

A laceration at the commissures of the lips can arise when a horse becomes hooked at the corner of the mouth and a major avulsion injury follows. Careful anatomical reconstruction of the lip margins is required.

Sarcoids may develop at the lip margins, especially the commissures, and the method of therapy (excision, cryosurgery or chemical cautery) which is used to ablate the lesions must also take regard of the acceptance of a bit after healing.

Temporo-mandibular joint and hyoid disorders

The temporo-mandibular joints (TMJs) lie very superficially immediately ventral to the zygomatic arch and are vulnerable to direct trauma, including penetrating wounds. However, TMJ disorders are rare in the horse but when they do occur they cause marked pain and a rapid loss of bodily condition. Disuse leads to obvious atrophy of the masticatory muscles, most obviously the masseters. Clinical examination shows resentment of attempts to open the mouth and even under general anaesthesia the range of opening may be severely reduced. A diagnosis of TMJ disease is difficult to confirm by radiography and other techniques such as ultra-sonography, scintigraphy, MRI or CT scanning, depending on availability, will provide superior images.

Ankylosis of the joint between the stylo-hyoid and petrous temporal bones is often a feature of temporo-hyoid osteoarthritis (THO) in horses and may limit a horse’s ability to move the tongue (see ‘Temporohyoid osteoarthropathy, THO’ in 5.2)

Lingual abnormalities

The well protected location of the hypoglossal nerve in horses is such that injuries to the nerve with lingual paralysis are rare.

Trauma, either in the form of lacerated wounds or tongue-strap strictures, accounts for the majority of tongue lesions of the horse. A horse with a severely injured tongue may be unable to manoeuvre ingesta around the mouth and is inclined to drop food or to collect it in the buccal cleft.

Horses which lose the rostral portion of the tongue through incisive wounds can maintain normal bodily condition, albeit showing messy feeding patterns.

Foreign bodies may become buried in the lingual tissues, and the painful suppurative response can reduce a horse’s inclination to eat.

Dental disorders

Dental disorders are discussed at length later in this chapter, but the reason why dental diseases cause dysphagia is through oral pain. There is little evidence that horses are afflicted with ‘tooth-ache’ per se, but soft-tissue pain through ulceration of the oral mucosa, particularly at the gingival margins in the form of periodontitis, is a major contributor to an inability to masticate food adequately and to reject partly masticated food to the ground – ‘quidding’.

Congenital and acquired palatal defects

The presence of a defect in the soft palate prevents an effective seal between the oral cavity and the naso-pharynx during the lingual propulsion of ingesta towards the tongue base and during pharyngeal contraction. The result is that food and fluids are refluxed via the nasal chambers to the nares.

Simple midline linear defects of the soft palate are the most common cause of the nasal reflux of milk by foals in early life (Figure 1.3). Rarely, the midline cleft extends rostrally into the hard palate.

Other forms of palatal defect include unilateral hypoplasia and pseudo-uvula formation which can escape confirmation until the patient is considerably older. They often occur in association with epiglottal entrapment.

Palatal reconstructive surgery using mandibular symphysectomy has been described, but the results are invariably disappointing.

Excessive palatal resection (staphylectomy) (see 5.21) in the treatment of dorsal displacement of the soft palate (DDSP) is irreparable.

Inadvertent splits in the palate have been reported after the relief of epiglottal entrapment by section with a hooked bistoury passed per nasum in the standing horse (see 5.22).

Other oral conditions: foreign bodies, neoplasia

The most common foreign bodies in the oro-pharynx are brambles/thorned plant material which become lodged in the sub-epiglottal area or in the lateral food channels causing acute-onset dysphagia. Endoscopy per nasum will show oedema in the ary-epiglottic folds, even when the foreign body itself cannot be seen. Such an endoscopic finding is an indication for an oral examination, either by palpation or with a guarded endoscope, under general anaesthesia. Other foreign bodies such as wire fragments may become wedged between teeth.

Squamous cell carcinomas, lymphosarcoma and connective tissue tumours arise sporadically in horses, and they tend to cause dysphagia simply by virtue of space occupation.

Pharyngeal paralysis

Paralysis or paresis of the pharyngeal constrictor muscles arises when the function of glosso-pharyngeal nerve (IX) is compromised. When food and fluids are not propelled into the upper oesophagus they may be returned via the nostrils, aspirated into the laryngeal airway, or spilled out of the mouth. The most common causes of pharyngeal paralysis are:

It is always correct to investigate the possibility of ATD disease in cases of pharyngeal dysfunction. When there is marked inhalation of ingesta leading to broncho-pneumonia or evidence of dehydration, the condition of the patient demands euthanasia on humane grounds. However, some horses with partial pharyngeal dysfunction may survive without distress and simply show an occasional cough and nasal discharge without progress to aspiration pneumonia. Restoration of pharyngeal function may occur, but this takes many months.

Nasopharyngeal cicatrization inhibits the efficiency of pharyngeal constrictor function, but horses with this disorder are more likely to present for the investigation of respiratory noises and/or exercise intolerance.

Pharyngeal compression: strangles abscessation

The presence of extra-mural soft-tissue swellings adjacent to the pharynx may cause dysphagia because of external compression of the pharynx and also, in the case of an abscess because of the pain associated with the movement of food boluses past the lesions (see Chapter 19).

Pharyngeal cysts, palatal cysts

The origin of pharyngeal wall cysts is not known, but intra-palatal cysts may well develop from salivary tissue which is normally distributed widely in the palatal mucosa. Diagnosis of both conditions is by a combination of endoscopy and radiography. While cysts on the pharyngeal walls can be excised or ablated by trans-endoscopic laser application, lesions within the substance of the soft palate are not as easily treated because fistulation of the palate is a likely sequel to surgery.

Epiglottal lesions, including sub-epiglottic cysts

Peracute epiglottitis, with oedema and cellulitis may occur as a complication of upper respiratory tract viral infections and can be so severe that a potentially fatal airway obstruction occurs. Emergency tracheotomy intubation may be necessary to prevent asphyxiation.

A less severe form of epiglottitis with swelling and distortion of the epiglottis may have a similar aetiology and causes dysphagia and coughing presumably through discomfort during deglutition. Afflicted horses also produce untoward respiratory sounds at exercise. The diagnosis is established by endoscopy, but it can be difficult to differentiate this form of epiglottitis, which is likely to be responsive to vigorous antibiotic therapy, from a para-epiglottic foreign body.

The increased mass of the epiglottis arising in entrapment by the glosso-epiglottal mucosa (see 5.22) or by a sub-epiglottic cyst (Figure 1.4) (see 5.23) causes dysphagia because of space-occupation and a restriction of the freedom for epiglottal retroversion. Secondary persistent dorsal displacement of the palatal arch may occur. Persistent DDSP is an indication for oral endoscopy and lateral radiography possibly using contrast medium. Both conditions are amenable to successful excisional surgery.

Laryngeal abnormalities

Compromised glottic protection leading to the aspiration of ingesta into the lower airways may arise spontaneously in cases of arytenoid chondropathy, or through iatrogenic causes such as complications of prosthetic laryngoplasty or partial arytenoidectomy (see 5.20). The precise cause of post-laryngoplasty dysphagia is not known, but over-abduction of the arytenoid cartilage, the physical presence of the implants themselves and nerve injuries are amongst the suggestions which have been proposed. Removal of the prosthesis is often, but not always, effective in control of the dysphagia, but, of course, the respiratory obstruction for which the surgery was originally performed can be expected to return as the arytenoid cartilage reverts to its collapsed state.

Fourth branchial arch defects (4-BAD)

Approximately two thoroughbreds per thousand born are afflicted with defects of the structures which derive from the fourth branchial arch, specifically the wings of the thyroid cartilage, the crico-thyroid articulation, the crico-thyroideus muscle and the crico- and thyro-pharyngeus muscles (see 5.25). The fourth branchial arch defect (4-BAD) syndrome may arise unilaterally or bilaterally, and any or all of the structures may show partial or complete aplasia. When the 4-BAD syndrome includes aplasia or hypoplasia of the crico- and thyro-pharyngeal muscles the proximal oesophageal sphincter remains permanently open. Horses afflicted with 4-BAD usually present with abnormal respiratory noises at exercise, and it is most unusual for them to show dysphagia unless they are badly afflicted or there is another concurrent defect. Horses with 4-BAD may show bizarre eructation-like noises at rest and may be confused with wind-suckers.

Megaoesophagus

Megaoesophagus has been reported sporadically in the horse, sometimes as a primary congenital disorder and sometimes secondary to other conditions causing restriction of oesophageal function such as vascular ring strictures. Coughing, nasal reflux of ingesta and distension of the cervical oesophagus may all be features. Confirmation of the diagnosis is easily achieved by contrast radiography.

Oesophageal obstruction (‘choke’)

Obstruction of the oesophagus is discussed in greater detail at the end of this chapter (see 1.7). Impaction of dry fibrous material to occlude the lumen of the oesophagus, typically in the cervical segment, is the commonest cause of acute dysphagia in the horse. Older horses seem to be more susceptible but this may relate to the diets offered to horses which are not being fed for competitive exercise. In contrast, foals which are beginning to take herbage occasionally plug the oesophagus with a bolus of dry grass.

Oesophageal strictures/stenosis

Oesophageal strictures are thought to be the sequel of episodes of acute obstruction, and horses with this condition are presented with recurring ‘choke’. Confirmation of the diagnosis is best achieved by contrast radiography. The most common site for stricture development is at the thoracic inlet. Resection of the stenosed segment of oesophagus may be attempted, but a guarded prognosis is indicated because recurrence of the stricture at the site of anastomosis is a frequent complication.

Intra-mural oesophageal cysts

Congenital intra-mural cysts may be encountered in young horses and cause dysphagia through restricting peristalsis and obstruction to the passage of oesophageal boluses. The lesions may be seen as swellings in the oesophageal wall at endoscopy or by ultrasonography or contrast radiography.

Oesophageal rupture

Ruptures of the oesophagus may arise through external trauma by kicks or stake wounds or by misuse of a nasogastric tube. Regardless of the cause, the condition carries a poor prognosis unless affected horses are presented for treatment soon after the injury has occurred because of the rapid advance of contamination and cellulitis into the surrounding tissues.

Neoplasia

Tumours of the oesophagus are very rare in the horse, but squamous cell carcinoma at this site has been reported.

‘Wind-sucking’

Horses performing this stereotypy do not swallow air, and deglutition is not part of the sequence of events. The muscles of the upper neck contract to create a pressure gradient across the soft tissues of the throat so that the walls of the pharynx and upper oesophagus are pulled apart. The sudden in-rush of air through the open crico-pharynx coincides with the gulping sound which is typically heard during attacks of wind-sucking, but the air is returned from the oesophagus to the pharynx immediately.

Grass sickness (See Chapter 3)

‘Grass sickness’ produces dysphagia in its acute form but colic in the sub-acute and chronic forms. The condition is seen in horses of all ages throughout the United Kingdom and northern Europe. Afflicted horses are generally severely depressed with patchy sweating, elevated pulse and ileus. The dysphagia arises as a part of total gastro-intestinal stasis, and nasal reflux of ingesta adds to the pitiful appearance of the patients. There is currently no reliable in vitro diagnostic test, but the radiographic demonstration of oesophageal stasis and the endoscopic identification of ulceration of the oesophageal mucosa are helpful pointers to the likely diagnosis.