Dysphagia i.e. difficulty in swallowing has three main causes i.e. disorders of the oral cavity (uncommon), disorders of the pharynx and disorders of the oesophagus. Horses with ileus may have nasal reflux of stomach/small intestinal contents which must be differentiated from dysphagia but the associated presence of colic pain will indicate that an abdominal disorder is present. 

The prehension and mastication of food are distinct from the initial, i.e. oral phase of swallowing. Dropping partially masticated food (quidding) is usually caused by pain during mastication (e.g. with cheek teeth diastemata - see dental lecture notes) and is a dysmastication rather than an inability to swallow or to pain during the oral phase of swallowing. Less commonly fractures, in particular mandibular and premaxillary fractures (e.g. due to kicks), can cause oral dysphagia. Fractures of one hemi-mandible in the horse usually do not need to be surgically supported as the normal hemi-mandible will effectively act as a splint. 

Disorders of the tongue can be due to paralysis of the 12th cranial nerve, rarely by inappropriately restraining a horse by the tongue, but most commonly as part of general neurological disorders such as botulism. Occasionally, acute onset oral dysphagia can be caused by sharp wooden or metallic foreign bodies lodging in the tongue or oropharynx. Such cases present with anorexia and excessive salivation. Careful examination of the oral cavity, and of the oropharynx in larger horses, using a mouth gag will commonly reveal these foreign bodies which can be manually removed. Tumours of the oral cavity such as squamous cell carcinoma are another rare cause of oral dysphagia. 

In contrast to the signs of oral dysphagia, the main clinical signs in horses with pharyngeal dysphagia (and oesophageal dysphagia) are the presence of masticated food flowing down both nasal cavities after eating and frequently, the presence of coughing due to aspiration of food material and saliva. 

1. 1)  Congenital neonatal neuromuscular pharyngeal dysfunction

2. 2)  Cleft palate

3. 3)  Guttural pouch mycosis

4. 4)  Strangles infection

5. 5)  Botulism

6. 6)  Heavy metal poisoning (eg lead)

7. 7)  Naso-pharyngeal foreign bodies

8. 8)  Naso-pharyngeal tumours (Lymphosarcoma and melanosis of Guttural pouch)

   9) Guttoral pouch disease  

Dysphagia in neonates (1 &2) cause food (milk) to come down the foal’s nose and coughing soon after suckling. Some cases develop inhalation pneumonia. Endoscopy is required to differentiate cleft palate from neuromuscular dysfunction. The prognosis is very with a severe cleft palate, surgery being very difficult and invariably unsuccessful in restoring normal function, as horses are obligate nasal breathers and the soft palate-epiglottis relationship is crucial during exercise. Many cases of neuromuscular dysphagia in foals (especially premature or dysmature foals) can improve over a week or so and such cases need feeding by NG tube during this period . (see medicine lectures) 

With swallowing, the guttural pouch ostia transiently open. GP endoscopy can be aided by using a guide wire or biopsy forceps inserted through its biopsy channel. 

Aspergillus fumigatus is an opportunist pathogen present in the URT (including the GPs) of many indoor horses in temperate climates. For unknown reasons it can invade the roof of the guttural pouch causing very destructive changes and secondary bacterial infection Endoscopically, blood or mucopurulent material may be seen flowing from the diseased ostium. Within the guttural pouch, grey, black or white fungal and possibly fibrinous plaques can be visualised on the mucosa overlying vital nerves and blood vessels. The clinical signs of GPM largely depend on which of the many vital underlying nerves or blood vessels are damaged. 

If haemorrhage has occurred, the affected artery should have a balloon or embolising coil inserted up the internal carotid to beyond the sigmoid flexure to prevent back-bleeding, and then surgically ligated at its origin. Local antimycotic treatment with natamycin or enilconazole, sprayed onto the roof of the pouch using self-retaining or transendoscopic catheters should be repeated daily 2-3 times. Prognosis depends on the presence, and if so the degree and severity of nerve damage. Cases with pharyngeal dysphagia have the poorest prognosis. 

Guttural pouch empyema/chrondroids 

This is a sequel to strangles, with abscessation and drainage of the retropharyngeal lymph nodes into the guttural pouches, which have poor natural drainage. Extensive swellings of the guttural pouch(es) can interfere with upper airway or swallowing, occasionally leading to stridor(tracheostomy may be required) or dysphagia. With more chronic cases, chronically draining lymph nodes, empyema or chondroid formation can occur. The signs may just be a chronic low grade purulent nasal discharge, which is usually unilateral. These cases are significant, long term carriers of strangles. 

Endoscopically, collapse of the nasopharyngeal roof may be seen, along with a purulent exudate draining from the affected pouch(es). Guttural pouch endoscopy will show abscessed lymph nodes on the floor of the median compartment of the GP, pus or chondroids. Feeding horses from the ground. Lavage of affected pouches with lukewarm, very dilute antiseptics using a self-retaining catheter can be used in more refractory cases. When inspissation of pus, i.e. chondroid formation occurs, transendoscopic removal (if just a few) or surgical drainage of the affected pouch is indicated, preferably using a ventral (modified Whitehouse) approach in the standing horse. 

In this congenital condition, a neuromuscular defect or rarely an abnormal tissue fold at the nasopharyngeal ostium act as a one-way valve, allowing air into but not freely out of one or both guttural pouches. Radiography will show an enlarged, air-filled pouch and a ventral fluid line is common. In cases of unilateral GP tympany, a Foley catheter can be placed into the GP for a few weeks and may distort the ostium into an open position. Alternatively a window is created in the thin midline septum between the two pouches with a transendoscpic laser, allowing air to exit via the normal ostium- good prognosis. With bilateral cases, surgical enlargement of one of the ostia and GP septal perforation can be attempted or a fistula created between the roof of the nasopharynx and GP. 

Guttural pouch melanosis 

Melanosis of the lateral GP wall is very common in older grey horses – often an extension of melanomas from the parotid region- rarely the tumours can cause dysphagia and stridor 

This upper respiratory tract infection often involves groups of horses (see respiratory notes). It can cause retropharyngeal abscessation or accumulation of pus in the guttural pouches which compresses the nasopharynx and causes dysphagia. Other associated signs include purulent bilateral nasal discharge and abscessed submandibular lymph nodes. Treatment involves isolation of cases and drainage of guttural pouches by feeding off ground, lavage or rarely GP surgery. 

and heavy metal poisoning will cause weakness of all skeletal muscles, however pharyngeal dysphagia can be an initial presenting sign. Endoscopy will confirm the presence of pharyngeal dysphagia without any detectable underlying lesion (eg GP mycosis). Closer examination of such cases may also reveal weakness of the hindlimbs and a flaccid tail (see medicine lectures). 

Choke is a very common condition due to obstruction of the lumen of the oesophagus with impacted food resulting in sudden onset of distress, salivation and dysphagia – thus causing a nasal discharge containing food. If uncorrected, dehydration and hypochloraemia will occur after a day or so. In the UK, the obstruction is most commonly due to sugar beet pulp or pelleted food which for unclear reasons (oesophageal spasm?), blocks the oesophagus and obstructs a variable distance of its lumen. Diagnosis is by a history of sudden access to e.g. large amounts of sugar beet pulp or to dry (unsoaked) sugar beet pulp when previously fed wet pulp and an inability to fully pass a nasogastric tube (should be peformed with care to avoid iatrogenic damage). A diagnosis may also be confirmed endoscopically and by ultrasound. Palpation of the cervical oesophagus may reveal a swelling in fine skinned horses with rostral oesophageal obstruction. 

ases should immediately be starved and also taken off all bedding or muzzled. Most cases will get better spontaneously or respond to medical treatment with spasmolytics and sedatives e.g. (Acepromazine or romifidine and Buscopan) and such conservative treatment is safe for up to 24 hours. If the choke has not cleared by that stage, i/v correction of hydration should be performed and gentle lavage of the oesophagus (by stomach tube and stomach pump) in the heavily sedated horse, with the head lowered. Care should be taken to avoid aspiration of food during attempted lavage and antibiotics (penicillin and/or metronidazole) should be administered to help prevent aspiration pneumonia – as some degree of aspiration is inevitable. Non-response to standing lavage (rare) might indicate a long, firm impaction (eg up to 1.5 meters of oesophagus) and may require clearance by lavage under general anaesthesia, or else severe oesophageal ulceration may occur. This is best performed with the horse on a sloping table (head down), using a cuffed endotracheal tube and gently lavaging the obstruction to soften and gradually break it down. 

This is the result of scarring following circumferential ulceration of the mucosa resulting in circumferential fibrosis and decreased luminal diameter, resulting in recurrent obstruction. It is most common following choke that has not been cleared by 36-48 hours. Diffuse but non- circumferential focal ulcers and scarring can usually be managed by feeding of soft soaked food, however circumferential strictures are extremely difficult to manage and although resection or bouginage (balloon dilation) can be attempted, new strictures may reform at the surgical site and euthanasia may be eventually required in some horses. 

Oesophageal diverticulum 

Developmental defects or rupture of the muscular layers results in an outpouching or diverticulum of the mucosa (pulsion diverticulum), or scarring and adhesion of the layers of the lumen together (traction diverticulum). Traction diverticula carry a better prognosis and may heal by second intention. Surgical treatment of pulsion diverticula by inversion of the lumen and overlying with a (eg mersilene) mesh may be attempted. There is a risk of recurrent laryngeal nerve damage with this surgery. 

This is very rare in horses (cf dogs) may result from trauma such as a kick to the ventral aspect of the neck with the oesophagus compressed between the hoof and the ventral aspect of a vertebral body. It may also be caused by an oesophageal foreign body or occasionally iatrogenic damage with a sharp nasogastric tube. It may be difficult to identify, and is potentially very serious leading to widespread emepysema, cellulitis and mediastinitis. Oesopagoscopy and contrast (fluoroscopy) enable a diagnosis