Pharyngeal Disorders

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EAR, NOSE, AND THROAT

PHARYNGEAL DISORDERS Anne Mattson, DVM, MS

ANATOMY OF THE PHARYNX

The pharynx is a shared funnel-shaped passage of both the respiratory and digestive systems, connecting the oral cavity with the esophagus and the nasal cavity with the larynx. The boundaries of the pharynx are the cervical flexor muscles and floor of the cranium dorsally, the root of the tongue ventrally, and the constrictor muscles of the pharynx laterally.47 The pharynx of the dog and cat is separated into the nasopharynx (jorsally and oropharynx ventrally by the soft palate. The shared cavity caudal to the end of the palate is called the laryngopharynx. The caudal-most aspect of the pharynx includes the cricopharyngeus muscle and the caudal part of the thyropharyngeus muscle. Together they form the pharyngoesophageal sphincter.

APPROACH TO PHARYNGI:AL DISORDERS Introduction

A history of inappetence, apparent pain, dysphagia, retching, gagging, dyspnea, and coughing often help to localize a disease process to the pharynx, but seldom identify the specific disorder. Careful attention to the patient's signalment, other components of the history, and the physical examination are prerequisites for identifying the problem. A thorough oropharyngeal examination should be performed. In some in-

From the SpecialCare Pet Hospital, Minneapolis, Minnesota

VETERINARY CLINICS OF NORTH AMERICA: SMALL ANIMAL PRACTICE VOLUME 24 • NUMBER 5 • SEPTEMBER 1994

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stances, a neurological examination and/ or evaluation of the patient while eating is warranted. After arriving at differential diagnoses, appropriate diagnostic procedures may include hematology, serum biochemistry or serologic evaluations, cytology, histopathology, radiology, or fluoroscopy. Because the differential diagnoses for pharyngeal disorders are diverse, specific identification of the problem is required for appropriate therapy.

Signalment and History

Signalment should be used to help narrow the list of possible diagnoses. Some disorders, such as primary tonsillitis in dogs and nasopharyngeal polyps in cats, are more likely to be found in young animals. Breed predisposition has been identified in numerous pharyngeal disorders, such as mucoceles, canine eosinophilic granulomas, soft palate disorders, and cricopharyngeal achalasia. Obtaining a careful history, inclusive of all body systems, may also provide valuable clues to a possible diagnosis. For example, a history of otorrhea in a young cat might be highly suggestive of a nasopharyngeal polyp, or a history of generalized weakness in a patient with dysphagia could lead to a search for a systemic or metabolic cause.

Physical Examination

A complete physical examination of the oropharyngeal area is essential and often requires general anesthesia. Sedatives or preanesthetic agents should be avoided in the dyspneic patient because they may impair the muscular activity for respiration. If required, premedications should have a short duration of action. Preinduction oxygenation for 5 to 10 minutes is advisable, and induction and intubation should be as rapid as possible.59 The open airway should be maintained until anesthetic recovery.

Diagnostics

Hematologic, serologic, or biochemical evaluations may be extremely important in evaluating some patients. A complete blood cell count in a cat with stomatitis-pharyngitis, for example, may identify hyperglobulinemia and hyperproteinemia as a sign of plasma cell stomatitis-pharyngitis. Fine-needle aspirates may be diagnostic for some

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problems, including sialocoeles, but for space-occupying or proliferative lesions, histopathology may be required. Microbial investigation is unlikely to give useful information because invariably a large number of bacteria are cultured from the pharynx. There is little difference between the bacterial isolates from dogs and cats with clinical pharyngitis and those who are healthy. Antibiotic administration based on culture and sensitivity may result in an apparent response regardless of the underlying etiology; the normal resident bacteria flora proliferate in areas of inflamed tissue.27 However, response is usually temporary, and clinical signs return once the antibiotics are discontinued. Radiology is often necessary to evaluate pharyngeal disease and may demonstrate a foreign body, abscess, tumor, the extent of a neoplasm, or nasopharyngeal polyp (Fig. 1). Generally, a single lateral radiograph is sufficient to view pharyngeal lesions, except when a unilateral lesion or foreign body is suspected.19 Radiographs of the bulla are recommended with nasopharyngeal polyps. In the ventrodorsal position, the hyoid apparatus, laryngeal structures, and upper airway are obscured by the overlying base of the skull and cervical vertebral column. The primary beam should be centered between the wings of the atlas and the angular processes of the mandible. Occasionally, ultrasound may provide a three-dimensional localization of a foreign body or structure, which is not possible on radiological examination.18 In some instances,

Figure 1. A lateral radiograph demonstrates the presence of a pharyngeal fishhook foreign body in a dachshund. (Courtesy of Brett M. Feder, DVM)

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such as the determination of the etiology of dysphagia of no apparent cause, a diagnosis can only be obtained via fluoroscopy and barium swallow.

PHARYNGEAL MUCOCELES

A sialocele or mucocele is an extravasation and collection of saliva, resulting from the disruption of a salivary gland or its duct; the sublingual salivary gland is the most frequently affected. Although the pharynx has been reported as the least common site for a mucocele to develop, it is clinically very important because of the likelihood of associated respiratory obstruction?· 23• 57 A dog of any age may be affected, but miniature poodles may be more frequently affected than other breeds?· 57 The presenting complaint of noisy respiration or labored breathing is a consistent finding and results from upper airway obstruction?· 28• 57 Respiratory problems may include snoring, intermittent inspiratory dyspnea, cyanosis, syncope, and coughing with excitement or exercise. Upper airway obstruction may result in respiratory arrest.57 Although traumatic etiologies, such as dog bites or pulling against a choke collar, have been suggested, most cases will not have a history of known trauma. However, because experimental evidence suggests sialocoeles can arise up to 1 year after the inciting trauma,23 owners should be asked to recall recent and past possible associations. Prompt diagnosis and treatment are essential because affected dogs frequently present in respiratory distress. A tentative diagnosis is made on identifying a soft, nonpainful, dome-shaped swelling or pedunculated mass in the caudal pharynx (Fig. 2). For visualization, rapid induction with immediate tracheal intubation is recommended (rather than heavy sedation) to assure a patent airway. 29 Emergency treatment with corticosteroids to relieve secondary edema of the pharynx and laryngeal orifice may be required. The diagnosis may be confirmed by aspiration of a thick, tenacious fluid with the characteristics of saliva. Drainage of fluid is also a palliative measure, but should not be considered the sole treatment because reformation inevitably occurs. Surgical management is described elsewhere7• 57 and frequently requires removal of the mandibular and sublingual salivary glands from the affected side to prevent recurrence.

TONSILLITIS

The palatine tonsil is a long, thin lymph node that rests within the palatine fossa, in the lateral wall of the oropharynx, just caudal to the

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Figure 2. A pharyngeal sialocele in a dog. (Courtesy of John P. Hoover, DVM.)

palatoglossal arch. The larger fusiform portion of the tonsil normally protrudes somewhat from the crypt,IS particularly in young animals.5 Bacterial infection of the tonsils is usually bilateral and is uncommon in dogs and rare in cats. Primary bacterial tonsillitis generally occurs in young, small-breed dogs and is associated with anorexia, fever, coughing, retching, and lethargy.4 In puppies, recurrent tonsillitis may be a reflection of an immature immune system, and maturation of the dog usually will result in resolution of signs. 24 Both tonsillitis and pharyngitis are usually secondary to other diseases, particularly in adult animals. Tonsillar hypertrophy and inflammation results from lymphoid activity and secondary bacterial proliferation on the surface of pharyngeal and tonsillar tissues. If the surface bacteria invade tonsillar tissues, clinical signs may warrant antibiotic administration. The most common etiology for secondary tonsillitis and pharyngitis is upper respiratory tract infection, but they may also occur with periodontitis, lower respiratory tract disease, mouth breathing, regurgitation, dysphagia, gastric disorders causing vomiting, and even chronic lower gastrointestinal disease when associated with anallicking.4 • 14• 27 A foreign body may result in unilateral tonsillitis. Diagnosis can usually be based on history and physical examination alone, but careful attention should be paid to ruling out underlying etiologies. Acute tonsillitis is evidenced by bright red, friable, tonsils that may or may not be enlarged or prominent.24 The surrounding pharyngeal mucosa is often visibly inflamed (Fig. 3). Punctate hemorrhages or small,

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Figure 3. Tonsillitis and pharyngitis in a dog. (Courtesy of John P. Hoover, DVM)

white, speckled areas of surface abscessation may be present. Acutely inflamed tonsils might not protrude from the crypt, especially in the cat.24 Bacterial culture and sensitivity, generally, is not useful, except possibly in recurrent cases. The wide variety of bacterial isolates from dogs with clinical tonsillitis do not differ significantly from those of normal dogs.Z7 Choosing a broad-spectrum antibiotic is likely to be sufficient, and ampicillin, trimethoprim/ sulfa, chloramphenicol, and cephalosporins have been recommended.14· 27 The pain associated with tonsillitis may require the use of liquid oral or parenteral antibiotics. For primary tonsillitis, treatment with antibiotics and, occasionally, mild analgesics, generally results in a prompt clinical response and tonsillectomy43 is infrequently required. PHARYNGITIS

As with the case oftonsillitis, primary pharyngitis in the dog and cat is uncommon and is usually a manifestation of other oral diseases or systemic illness. Feline viral infections may cause palatial ulceration without other signs of upper respiratory tract disease, but this is unusual (Fig. 4). Localized infection may be caused by foreign bodies, and radiographs may be helpful to locate radiodense objects. Pharyngitis and glossitis may also occur secondary to ingestion of irritating or caustic substances (Fig. 5).

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Figure 4. Feline viral stomatitispharyngitis. (Courtesy of John P. Hoover, DVM)

FOREIGN BODIES AND RETROPHARYNGEAL ABSCESSATION

Clinical signs associated with oropharyngeal foreign bodies include dyspnea, retching, gulping, and dysphagia. Occasionally, airway obstruction may be severe enough to warrant an emergency tracheotomy. Long-term complications of a foreign body may include sinusitis or abscessation in peripharyngeal areas. Depending on the location in which

Figure 5. Severe pharyngitis in a dog from a caustic alkali burn. (Courtesy of John P. Hoover, DVM)

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the object migrated, retrobulbar, submandibular, or retropharyngeal abscesses may develop. Pharyngeal abscesses are common in the dog and are frequently secondary to bones, grass awns, sticks, pins, or needles. The penetration point is usually not visible, and the foreign body frequently has been expelled. Clinical signs of abscessation include anorexia,..pyrexia, pharyngeal pain, and swelling. Dtlgnosis may be aided by surgical exploration of the wound or abscess'(which may not always yield the object) and radiology or ultrasonography to localize or identify the problem. Removal of the object is recommended for treatment, as well as drainage and antibiotic therapy for concurrent abscessation.

SOFT PALATE DEFECTS

Cleft Palate The palate separates the oral and nasal cavities. Acquired defects in the hard palate, or oronasal fistulae, are described elsewhere.49 Congenital defects of the hard and soft palate may be an inherited trait with incomplete penetrance in the Shih Tzu breed, and possibly in pointers, bulldogs, and Swiss sheepdogs.B Cleft palate sometimes follows a familial pattern in the Siamese cat.35 However, the usual cause is probably an intrauterine insult during the stage when the two fetal palatine shelves fuse and results in the sporadic finding of cleft palate in a variety of breeds.32 Many teratogens, most notably the antifungal agent griseofulvin in the cat, can cause cleft palate.35 Cleft palate decreases the suckling ability of the neonate, allows fluid to enter the nasal cavity, and often results.in neonatal death by choking or lower airway aspiration. When food and fluid enter the nasal cavity, a foreign-body rhinitis results and sneezing, gagging, and retching during feeding occur. Physical examination of clefts involving the hard palate, or the hard and soft palates together (Fig. 6), usually shows a midline malformation (except when accompanied by harelip or cleft lip, an anomaly in the incisive bone or primary palate). Defects in the soft palate alone can be either midline or unilateral. Uncommonly, unilateral hypoplasia of the soft palate may occur, and, rarely, a severely shortened soft palate may result from bilateral absence of the soft palate. This defect may be overlooked on cursory pharyngeal examination because the palate defect is symmetrical and does not have a midline cleft. As is the case with all congenital defects, affected neonates should be examined for concurrent congenital defects. Prognosis without surgical correction is grave, but the patient must

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Figure 6. Midline cleft in the hard and soft palates of a cat. (Courtesy of Marilyn Kostolich, DVM)

be maintained until grown enough for surgery. Enough tissue for surgical manipulation is usually available at 2- to 4-months of age. Until then, tube feeding is generally required to prevent aspiration pneumonia. Details of surgical correction are described elsewhere.26• 34 Traumatic Injury to the Soft Palate

Clinical signs associated with trauma to the soft palate are similar to those of congenital palate defects and include sneezing, gagging, and retching during eating. All but the smallest defects should be repaired . Repair of full-thickness tears requires two suturing layers. When tissue has been lost or is badly damaged, tonsillar sinus material may be used to close the defects. Tracheotomy may be considered to maintain the airway during and after surgery, particularly in smaller patients. Tracheotomy tubes provide an advantage to endotracheal tubes in surgeries involving the soft palate because they increase access to the surgical site and improve the management of pharynge-al edema.4 Elongated Soft Palate

A relative excess of the soft palate is the most important factor in the a irw ay obstructive syndrome of brachycephalic breeds.4 Other com-

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ponents of the "brachycephalic syndrome" include stenotic nares and everted laryngeal saccules.34 Because the maxillae is foreshortened, the caudal aspect of the soft palate extends beyond the tip of the epiglottis and interferes with laryngeal function. At rest, this creates the classical snoring noise during inspiration in affected dogs. During exercise, excitement, or other increased inspiratory efforts, the caudal border of the soft palate may become sucked into the glottis. This severely reduces airway diameter, causes trauma to the palate and larynx, and creates tissue edema. The severity of the resulting inspiratory dyspnea depends on the degree of soft palate elongation, the amount of edema, and the presence of other airway problems. Clinical signs include gagging and coughing in addition to the common inspiratory noise. Diagnosis is based on history and physical examination (Fig. 7). Treatment is aimed at shortening the soft palate. In a partial palatectomy, palate material beyond the distal one-third of the tonsils is excised with a scissors.4 A full-thickness excision is made by grasping the caudal border of the soft palate at its midpoint and removing first one half and then the other. Reverse Sneeze

Reverse sneezing is a forceful inspiratory motion initiated by dorsapharyngeal wall stimulation. The accompanying inspiratory noise is frequently described by owners as wheezing. Although many cases are idiopathic, other sources of irritation and inflammation including dorso-

Figure 7. Elongated soft palate in a dog. (Courtesy of John P. Hoover, DVM)

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pharyngeal foreign bodies, parasites, infections, excessive secretions, allergies (atopy), idiopathic follicular pharyngitis, and neoplasia must be considered differential diagnoses. Epiglottal entrapment by the soft palate, if present, is usually a secondary phenomena associated with the underlying irritative/inflammatory disorder. Episodes of idiopathic reverse sneezing usually last several seconds, and the dog returns to normal immediately after the episodes. Small dogs may be affected more frequently, and the problem may be exacerbated by exercise. Recovery may be hastened by having the owner massage the throat, compress the thorax, or avert the dog's attention by making a loud noise (e.g., clapping hands). Severe or persistent reverse sneezing warrants a thorough examination of the posterior nasopharyngeal region. Reverse sneezing related to allergies generally responds to glucocorticoids and may also respond to antihistamines. Unfortunately, some cases of severe reverse sneezing may be very debilitating, remain idiopathic, and have no therapy. OROPHARYNGEAL DYSPHAGIAS Stages and Physiology of Swallowing

Normal swallowing is a complex, coordinated process involving cranial nerves, the swallowing center in the reticular formation of the brainstem, the muscles of mastication, tongue, soft palate, pharynx, larynx, upper esophageal sphincter, esophagus, and lower esophageal sphincter.48• 50• 51• 54• 55 Swallowing has been divided into oropharyngeal, esophageal, and gastroesophageal phases.54 Dysphagia refers to trouble with swallowing and can be either functional (a motor disturbance) or mechanical (the result of a local anatomical lesion). Oropharyngeal dysphagia indicates a difficulty in moving a bolus from the oral cavity to the cervical esophagus. The oropharyngeal phase of swallowing is further subdivided into three stages-oral, pharyngeal, and pharyngoesophageal or cricopharyngeal.52• 54 An understanding of each of the stages of swallowing is important in identifying the cause and treatment of dysphagia. Oral Stage. The oral stage of swallowing requires input from cranial nerves V (trigeminal), VII (facial), and XII (hypoglossal). In this voluntary first stage, food is prehended and transported caudally to the base of the tongue and accumulated into a bolus.54 Food is organized and transported primarily by the tongue. Motor fibers to the tongue are supplied by cranial nerve XII (hypoglossal). Sensory fibers from the oral cavity and motor fibers to the masticatory muscles and the soft palate are supplied by cranial nerve V. Clinical findings in an animal with oral dysphagia vary and may range from barely perceptible to severe.48 Signs include difficulty in prehending food or lapping water, excessive salivation, dropping of food

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from the mouth, variably reduced tongue movement but no protrusion of the tongue from the mouth, and decreased or absent gag reflex.48 A differential ability to handle solids and liquids is not noted. 48 Frequently, compensatory maneuvers to bring the food bolus into the pharynx are present, such as exaggerated head movements during eating, excessive chomping, head tossing, or dipping the muzzle deeply into a water bowl.48 These maneuvers are attempts to offset reduced control of the tongue and to keep food moving caudally. Placing the food directly into the pharyngeal area or providing the food at an elevated location may improve the ability to swallow. Because pharyngeal contraction and cricopharyngeal relaxation are normal, little material is retained in the pharynx and respiratory signs (nasal discharge, coughing, aspiration pneumonia) are absent or mild.48 Pharyngeal Stage. During the pharyngeal phase of swallowing, the bolus is propelled across the pharynx by the tongue and pharyngeal constrictors.48 The epiglottis covers the glottis and the openings to the oropharynx and nasopharynx are covered by the tongue and contracted palatopharyngeal muscles. This stage of swallowing depends primarily on the activity of the swallowing center and cranial nerves IX (glossopharyngeal) and X (vagus). Clinical features of pharyngeal dysphagia include multiple, unsuccessful attempts at swallowing.48 Because the epiglottis returns to its resting position at the end of a swallow, laryngotracheal aspiration is common. Food can remain in the pharynx for hours, and regurgitation may occur with no time relation to eating. Placing food at the base of the tongue does not facilitate swallowing, and a reduced gag reflex is common. Because this stage of swallowing is involuntary, compensatory maneuvers are less successful. Pharyngoesophageal Stage. The pharyngeal phase blends into the pharyngoesophageal stage when the cricopharyngeal muscle relaxes and the upper esophageal sphincter opens, the bolus passes into the cranial esophagus, the sphincter closes, and the pharyngeal muscles relax. The cricopharyngeal muscle is innervated by the pharyngoesophageal nerve/ 5 formed by cranial nerves IX and X. Pharyngoesophageal, or cricopharyngeal, dysphagias result from asynchrony, achalasia, or chalasia of the upper esophageal sphincter.48• 55 In asynchrony, the more common form of cricopharyngeal dysphagia,54• 55 pharyngeal contraction occurs without coordinated relaxation of the upper esophageal sphincter's cricopharyngeal muscles. In achalasia, the cricopharyngeal muscles fail to open at all during pharyngeal contraction. Rarely, persistent opening (chalasia) of the cricopharyngeal muscle is noted. Some dogs may have both poor pharyngeal contractility and cricopharyngeal nonrelaxation, a mixed type of dysphagia. 55 Clinical signs of cricopharyngeal dysphagia include repeated attempts to swallow food which drops from the mouth.55 Cricopharyngeal dysphagia is the most common form of oropharyngeal dysphagia. It has

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been primarily identified in young dogs displaying persistent dysphagia from the time of weaning, but may occur in old dogs as well.55 Diagnosis of Dysphagia

During history taking, differentiating the passive process of regurgitation, which occurs in dysphagia, from vomiting is initially very important. The physical examination should include close examination of the pharynx and larynx and the area under the tongue structural abnormalities or foreign bodies. The patient should be observed eating and drinking to help localize the region of involvement. A neurological examination with a focus on evaluation of cranial nerves is indicated. Particular attention should be paid to the gag reflex and tongue movements. As described, clinical features vary depending upon the stage of the swallowing process affected45• 48• 53• 55 and some generalizations may be noted. Difficulty in prehending food is noted only in oral dysphagia. If the animal can swallow normally once a bolus is placed at the base of the tongue, oral dysphagia is likely. If the animal cannot pass food from the pharynx to the esophagus, either a pharyngeal or cricopharyngeal dysphagia could exist. A reduced or absent gag reflex, present in oral and pharyngeal dysphagias, is not present in pharyngoesophageal dysphagias. Respiratory involvement and a differential ability to handle liquids and solids may occur with pharyngeal and pharyngoesophageal dysfunction, but usually not in oral dysphagia. Clinical features common to all three stage dysfunctions include regurgitation and drooling. Causes of dysphagias include space-occupying masses (abscesses, inflammatory lesions, tumors), foreign bodies, congenital abnormalities (cleft palate), strictures and trauma-induced lesions, as well as neuromuscular disorders.45 Probably most functional pharyngeal dysphagias are caused by idiopathic neuropathies and myopathies.48 Reported causes of cricopharyngeal dysphagias are inflammation, fibrosis, atrophy and hypertrophy of the cricopharyngeal muscles or are associated with motor abnormalities of the cranial esophageal sphincter.53 Neuromuscular disorders may include disorders of the central nervous system, peripheral neuropathies, diseases of the neuromuscular junction (myasthenia gravis), skeletal myopathies (polymyositis, muscular dystrophy, hyperthyroidism and hypothyroidism) and lesions from surgical resections of the pharynx.53 A possible increased incidence of cricopharyngeal dysphagia in cocker spaniels, and its diagnosis in two cocker spaniellittermates, suggests a genetic component to the disorder. 55• 56 A primary muscular dystrophy, a hereditary disease, has been proposed as the cause of dysphagia in Bouviers.38 In the report of 24 Bouviers with dysphagia, 7 dogs had cricopharyngeal achalasia, 5 had ineffective pharyngeal contractions, 1 dog each had chalasia or dramatically decreased tongue movements, and the remaining 12 dogs had esophageal dysfunction.38

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Diagnostic evaluations should include survey radiographs of the cervical region to identify any morphologic abnormalities, such as radiodense foreign bodies, signs of trauma, and masses. Thoracic radiographs are warranted to rule out secondary aspiration pnewnonia that may be present in pharyngeal and pharyngoesophageal dysphagias. Static contrast radiographs will show retained contrast mediwn in a dilated pharynx with both pharyngeal and cricopharyngeal dysphagias.52 Because swallowing is an active process, motility can only be assessed with fluoroscopy or cinefluoroscopy. Plain radiographs of a barium swallow can not distinguish between pharyngeal, pharyngoesophageal, and mixed dysphagias. In oral dysphagia, fluoroscopic examination of a barium swallow may show decreased tongue motion and resultant difficulty in accumulating a bolus at the base of the tongue. Often over-sized boluses are accumulated before the swallowing reflex is induced. No abnormalities are noted in pharyngeal muscle contraction and cricopharyngeal muscle relaxation.48 An animal with a pharyngeal dysphagia will show weak or absent pharyngeal contractions on barium swallow.55 Fluoroscopic examination of an asynchronous upper esophageal sphincter shows a cricopharyngeal muscle that contracts too early or too late in relation to the contraction of pharyngeal muscles, and contrast media is misdirected into the nasopharynx rostrally. In cricopharyngeal achalasia, good pharyngeal contractions are present that force the passage of a small stream of contrast through a closed, distorted cricopharyngeal area or into the caudal pharyngeal wall.55 Clinical pathological studies may be warranted to identify systemic abnormalities and potential metabolic or endocrine disorders.52 When autoimmune disease may be a cause of neuromuscular disease, an antinuclear antibody test (ANA) may be appropriate. Muscle biopsy and creatine phosphokinase levels may be evaluated for suspected myopathies. Electromyography can also be used to differentiate between neuropathies and myopathies.

Therapy

Appropriate treatment requires accurately identifying the disorder; in particular, a pharyngeal disorder must be differentiated from a separate or concurrent cricopharyngeal disorder. Cricopharyngeal myotomy in patients with achalasia or asynchrony leads to immediate improvement.20·55·56 However, this procedure is not helpful in oral dysphagia and may lead to fatal aspiration pneumonia in patients with decreased pharyngeal contractility.1· 48• 55 Cricopharyngeal myotomy involves resecting the dorsal part of the cricopharyngeus muscle.1· 20· 21· 42 A ventral midline incision is made from the cranial larynx to the distal one-third of the

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trachea. The trachea and larynx are exposed by separating the sternothyroid muscle on the midline. The left sternothyroid muscle is retracted and dissection is continued to the left of the trachea and larynx, allowing the larynx to be rotated clockwise. The rotation exposes the cricopharyngeal muscle, which is distinguished from the proximal esophagus by its transverse muscle fibers converging on the dorsal median raphe. The cricopharyngeal muscle is dissected free and transected, perpendicular to its fibers, down to the level of esophageal mucosa. Closure is routine and drain placement should not be necessary. Patients may be fed the day after surgery. Any identified underlying diseases should be treated. For example, myasthenia gravis may be responsive to anticholinesterase therapy. An intravenous test dose of 0.1 to 0.2 mg/kg44 of edrophonium chloride may be given during fluoroscopy. 44• 45 If an improvement is noted in swallowing, the patient may benefit from oral medication. When the dysphagia cannot be resolved, adjustments in feeding should be tried. Some animals may do better when fed liquids or gruels or with elevated feedings. A pharyngotomy tube1 or gastrostomy tube may also be used to improve nutritional status while an underlying disease is treated or before surgery.2• 10• 58 When generalized neuromuscular disorders are present, a more generalized, mixed dysphagia is more likely to exist. Clinical signs, including poor nutritional status and aspiration pneumonia, are more severe and the overall prognosis for survival decreases.

PHARYNGEAL TUMORS Principles of Diagnosis, Therapy, and Prognosis

Oropharyngeal tumors are the fourth most common cancer in dogs. 61 From most to least common they include malignant melanoma, squamous cell carcinoma, fibrosarcoma, and dental tumors. In cats, squamous cell carcinomas make up 70% of oral tumors, and fibrosarcomas make up approximately 20%_61 Malignant melci.nomas are rare in cats. In most types of oropharyngeal tumors, a cause has not been identified. Presenting complaints may include a mass visualized by the owner, apparent pain, increased salivation or bloody oral discharge, halitosis, dysphagia, facial deformity, weight loss, or cervical lymphadenopathy. Loose teeth, particularly in cats, may be a sign of neoplastic osteolysis. A thorough oropharyngeal examination and critical palpation of mandibular and retropharyngeal lymph nodes for evidence of regional metastasis is indicated. Diagnostic evaluations should include a minimum data base of a complete blood cell count, serum chemistry panel,

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and urinalysis, thoracic radiographs when the cancer may be malignant, regional radiographs taken under general anesthesia of cancers adherent to bone (other than simple epulides), large incisional biopsy of mass lesions, and fine needle aspirates of enlarged or asymmetrical lymph nodes. Melanoma and squamous cell carcinoma of the caudal oral and pharyngeal area are most likely to invade regional nodes and to have visible chest metastasis at the time of diagnosis. Normal radiographs do not rule out the possibility of tumor infiltration; radiographic lysis is observed only when ;:::40% of cortical bone is destroyed.61 Large biopsy samples are required because oral cancers are frequently necrotic, infected, or inflamed. Cytological examination may only reflect these secondary changes. Samples should include healthy tissue at the center and edge of the lesion. When the tumor is small, as may be the case with epulides or papillomas, excisional biopsy may be appropriate. However, when the disease is extensive, the biopsy should be incisional and used to plan further treatment. Margins of the biopsy site should be considered to be contaminated with tumor cells and will need to be incorporated in a possible resection later. Thus, biopsy samples should be obtained through the oropharyngeal mucosa, and not through the skin, when possible. This will increase the probability of normal surgical closure and decrease the amount of tissue that must be included in the resection. Therapy for oropharyngeal neoplasia usually includes surgery, cryo' surgery and/ or irradiation. Chemotherapy has not been consistently effective for oropharyngeal tumors. 61 When possible, surgical excision is the treatment of choice. Wide surgical margins of at least 2 em are indicated for malignant cancers. Mandibulectomy and partial maxillectomy are indicated for extensive bony lesions that are not radiation responsive.36• 40• 41 Other advantages to mandibular resection include it's ease and decreased expense compared with radiation therapy. For relatively localized tumors smaller than 2.5 cin in diameter, cryosurgery may be used. Surgically freezing larger, extensive bony lesions may result in fracture of the mandible or fistulization of the maxilla. Radiation therapy may be applied to radiation-responsive tumors, any inoperable tumors, or appbed postsurgically to the site. Tumor location is a significant prognostic factor, with caudal oropharyngeal tumors having a poor prognosis.40• 41 This may be caused by late detection, more aggressive biological activity, tumor type, and difficulty of surgical excision because of location and degree of soft tissue involvement in more caudal tumors. Epulides (a benign periodontal tumor) and squamous cell carcinomas are more likely to occur in the rostral area of the mandible, while other oropharyngeal neoplasms are more likely to occur caudal to premolar i.40 Because squamous cell carcinomas may be associated with a better prognosis in dogs compared

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with other malignant tumors, location of tumor may reflect biological activity. The probability of tumor recurrence is also increased by the histological finding of neoplastic cells at the margins of the surgical excision.40 Thus, all samples submitted for histopathology should have surgical margins evaluated.

Malignant Melanoma

Malignant melanoma usually presents as a pigmented, ulcerated lesion (Fig. 8). It occurs most commonly on the gingiva, but also is found on the mucosa, hard or soft palate, and tongue.60 In dogs, dark pigmentation increases the risk of malignant melanoma and an increased incidence has been reported in males.40 One third of canine oropharyngeal malignant melanomas will not be pigmented and are occasionally misinterpreted histologically as an undifferentiated sarcoma. Presence or absence of pigment and histologic criteria do not seem prognostic.60 Melanoma has a strong predilection to metastasize to regional lymph nodes and/ or the lung. Metastasis to other sites is not uncommon and bone involvement is variable.61 The treatment of choice is early, aggressive, wide surgical excision.40 The 1-year survival rate for dogs with oral malignant melanoma is 25%, with tumor size and ability to successfully control the tumor with sur-

Figure 8. Pigmented sublingual malignant melanoma in a dog. (Courtesy of John P. Hoover, DVM)

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gery, being prognostic variables.61 When the tumor exceeded 2 em in diameter or spread to the lymph nodes, median survival has been reported as 164 days, versus 511 days in dogs with tumors less than 2 em in diameter.61

Squamous Cell Carcinoma

Biological Behavior. Squamous cell carcinoma usually appears as a red, cauliflower, raised, friable, ulcerated lesion (Fig. 9). Bone involvement is variable in dogs, but commonly severe and extensive in the cat, even with minimally visible oral disease. Squamous cell carcinoma has been reported as being more common in large-breed dogs.40 Metastasis in the dog is site dependent. The rostral oral cavity has a low metastatic rate, and the caudal tongue and tonsil have high metastatic potential to the lymph nodes and lung. In cats, the severity of the local disease usually results in euthanasia before metastasis is identified. Thus, the propensity for squamous cell carcinomas to metastasize in cats has not been well characterized.61 Accordingly, prognosis varies depending on tumor location and species. With squamous cells carcinoma of the canine pharynx (tonsil or base of the tongue), a poorer prognosis must be given than for more rostral tumors because of their metastatic nature and tendency to recur after excision. 16 Any feline squamous cell card-

Figure 9. Oropharyngeal squamous cell carcinoma in a cat. (Courtesy of John P. Hoover, DVM)

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noma carries a grave prognosis, regardless of treatment modality, with 1-year survival rates rarely exceeding 10%. The treatment of choice for all canine oral squamous cell carcinomas is wide surgical excision.36 Squamous cell carcinomas are responsive to radiation, with control being noted with radiation for 1 year or more,60 but the presence of bone involvement decreases response.36 Tonsillar Squamous Cell Carcinoma. Most primary tonsillar tumors are squamous cell carcinomas, although lymphomas and malignant melanomas may metastasize to the tonsillar area. Tonsillar tumors are rare in the cat. Dogs living in urban areas with a high level of pollution are at a greater risk for the development of tonsillar squamous cell carcinomas than are rural dogs.61 The neoplastic tonsil may be very painful, firm, or softer and friable, and enlarged. The diseased tonsil may also be of normal size and appearance.24 Cervical lymphadenopathy and thoracic metastasis are common, even with very small tumors. Retropharyngeal metastasis may result in pain and dysphagia and even displace the pharynx and larynx. An absence of visible metastasis does not rule out this possibility; more than 90% of the time metastasis will exist at the time of diagnosis. 61 The prognosis is poor. Because the disease tends to be bilateral, bilateral tonsillectomt3 should be performed. When tonsillectomy is combined with irradiation of the pharynx and cervical lymph nodes, initial control of the carcinoma is usually possible.60 However, the 1-year survival rate is 10% because of early problems in controlling localized infiltration and later effects of systemic metastasis. 61 Squamous Cell Carcinoma of the Tongue. Most tongue tumors in dogs are squamous cell carcinomas, but granular cell myoblastoma, melanoma, mast cell, fibrosarcoma and other tumor types may also occur here. The large majority of feline tongue tumors are squamous cell carcinomas, as well. More than 75% of animals with squamous cell carcinoma of the tongue will die from the disease within 1 year, with rostral tongue tumors showing a better prognosis than caudal tumors. Metastasis is common. Papillary Squamous Cell Carcinomas. Papillary squamous cell carcinomas present as proliferative, osteolytic masses of the maxilla or mandible. Dogs younger than 6 months of age are affected, and radiation therapy with debulking surgery seems to be curative.

Fibrosarcoma

Fibrosarcoma appears as a firm nodule with a site predilection for the gingiva in the cat and as a flat, firm, ulcerated lesion with a site predilection for the palate in the dog. A higher incidence of fibrosarcoma

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may exist in large-breed, male dogs.40 The disease is often advanced at the time of diagnosis because of its locally invasive nature.61 Bone involvement is common. Regional lymph node involvement is rare, but distant metastasis, usually to the lungs, is occasional (<20%).61 The histological appearance of the tumor often appears benign or consistent with a low-grade malignancy in spite of a clinically aggressive course. In these cases in which the tumor is invading bone, recurrent, or rapidly growing, treatment for a malignant cancer is appropriate, regardless of histologic grade. The treatment of choice is wide surgical excision with a poor to fair response. Frequently, subtotal maxillectomy is indicated.60 The usual cause of death is from local disease. Prognosis tends to be fair to good in cats for surgical resection. One year survival is limited to 25% to 40% because of the invasiveness of the tumor and lack of radiation sensitivity.61

NONMALIGNANT PROLIFERATIVE DISEASES Epulis

Fibrous and ossifying epulides are benign gingival proliferations of tissue, similar in appearance to gingival hyperplasia. They are usually confined to one or two sites at the gum margin, 1 to 4 em in diameter, slow-growing, firm, and usually nonulcerated and occasionally pedunculated. They are primarily canine tumors, may be more common in females, and have a site predilection for the rostral mandible. Fibromatous epulides are the most common epulis, are usually noninvasive and histologically contain periodontal ligament stroma. Ossifying epulides are similar to fibromatous epulides but also contain large amounts of osteoid matrix. Acanthomatous epulides, or adamantinomas, are a third subclass of epulides. They are very locally invasive and almost always invade bone. Fibrous and ossifying epulides are usually cured by surgical excision40 because they rarely invade bone or recur. In those cases of rare recurrence, electrocautery or cryosurgery may be used to more aggressively destroy the base of the tumor. Prognosis for acanthomatous epulis/adamantinoma is excellent with wide surgical excision or irradiation, with recurrence rates of less than 5% with aggressive resection and control rates of 90% with radiation therapy. Viral Papillomatosis

Viral papillomatosis usually presents as multiple wart-like growths in the oropharynx, lips, or tongue of young dogs (Fig. 10). Examination

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Figure 10. Canine viral papillomatosis. (Courtesy of John P. Hoover, DVM)

is usually diagnostic. The causative agent is the canine oral papillomavirus.12 Most affected dogs have a spontaneous regression within 4 to 8 weeks and permanent immunity prevents recurrence.60 Treatment is usually not necessary, although occasionally surgical debulking may be needed to facilitate swallowing.

Canine Oral Eosinophilic Granuloma

Canine oral eosinophilic granulomas usually occur on the palate as ulcerative plaques or on the ventral and lateral aspects of the tongue as firm, raised, proliferative masses or plaques (Fig. 11). Visually it easily may resemble, and be mistaken for, a more malignant process. A dog of any signalment may be presented, but young Siberian Huskies are most commonly affected.33• 39 Blood eosinophilia is occasionally present. Diagnosis requires biopsy. Histopathological findings of eosinophilic and histiocytic inflammation with collagen degeneration is similar to what is seen with eosinophilic granulomas in cats.39 Treatment with corticosteroids alone is usually curative, but recurrences occasionally occur.39 Treatment with prednisolone or prednisone orally at a dose of 0.5 to 2.2 mg/kg/ d has resulted in regression of the lesion within 10 to 20 days (Fig. 12).33• 39

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Figure 11. Sublingual eosinophilic granuloma in a Siberian Husky prior to treatment.

Feline Plasma Cell Stomatitis-Pharyngitis

Plasma cell stomatitis-pharyngitis is a disease of unknown etiology characterized by a non-neoplastic, dense infiltrate of plasma cells and frequently, lymphocytes into the mucosa and submucosa of the oral and

Figure 12. Siberian Husky from Figure 11 after treatment with prednisone for canine oral eosinophilic granuloma.

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pharyngeal cavities of the cat. Affected cats may be of any age or breed and no sex predisposition has been noted. Clinical signs are consistent with stomatitis in general and include anorexia, difficulty eating, halitosis and ptyalism.59 The gingival and glossopalatine arches are the most commonly affected areas, but examination may reveal the erythematous, ulcerative and proliferative lesions on the tongue, pharyngeal walls, hard palate and/ or lips as well.59 Differential diagnoses for the gingivitis and stomatitis include feline calicivirus infection, eosinophilic ulcers and eosinophilic granulomas, injuries, foreign bodies, ingestion of irritants, autoimmune diseases, and ulcers due to uremia. Definitive diagnosis requires documenting the characteristic plasmacytic and lymphocytic, or predominantly plasmacytic, infiltrates on histological examination. Satisfactory biopsies may be easily obtained using a 2.0 mm skin punch biopsy instrument. Hyperproteinemia with associated hyperglobulinemia is a frequent finding in affected cats/0• 59 which suggests evaluation of total protein may aid in initial diagnosis. A polyclonal increase in gamma globulins is identified on electrophoresis of serum proteins. Because hyperproteinemia, hyperglobulinemia, and polyclonal gammopathy are frequently associated with this disorder, and because treatment with immunosuppressive therapy alone usually results in clinical improvement, immunologic dysfunction has been cited as a primary etiology for plasma cell stomatitis-pharyngitis.30, 59 The role of dental tartar and infections with spirochetes, feline calicivirus, feline leukemia virus and feline immunodeficiency virus as contributing factors is still uncertain.25' 49• 59 In choosing a treatment option, consideration should be given to effectiveness, side effects, and ease of administration of medication, especially since long-term treatment is frequently required. Because of the discomfort associated with this disease, owner and patient compliance may be better with parenteral versus oral routes of administration and with liquid medications versus tablets. Corticosteroids or aurothioglucose are recommended for treatment and control, but complete cure is unlikely. Most cats will have some persistent lesions, particularly gingival erythema, even with continued treatment. Prednisone (1 to 2 mg/kg of body weight every 12 hours) and methylprednisolone acetate (2 mg/ kg, IM, every 7 to 30 days) resulted in improvement in 73% and 86% of cats, respectively, in a recent report. 59 Triamcinolone (4 mg, PO, every 24 to 48 hours) resulted in clinical improvement in 50% of cats.59 Effectiveness of the corticosteroids may diminish over a period of months, however. Although the efficacy of prednisone is probably due to its antiinflammatory effects, the mechanism of Aurothioglucose, an injectable gold, has not been well delineated. Aurothioglucose (Solganol, Schering Corp, Kenilworth, NJ) resulted in improvement in 82% of cats, when

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used at a dose of 1 mg/kg, IM, every 7 days until improvement was noted, then every 14 to 35 days. 59 Aurothioglucose should, therefore, be considered as a treatment option, particularly for those cats who may lack or lose responsiveness to corticosteroids. Potential side effects of gold are thrombocytopenia secondary to bone marrow suppression, and renal disease leading to proteinuria. Thus, all cats receiving gold should be monitored with a complete blood count, platelet count, and urinalysis. Antibiotics, particularly amoxicillin, clindamycin and metronidazole22· 25· 59 may be used in conjunction with other therapy to decrease discomfort; however, rapid recurrence is generally expected once the antibiotic is discontinued.30• 59 Culture and antibiotic sensitivity testing of the oral flora does not generate useful information in this disease. Metronidazole's efficacy may be attributed to its immunosuppressive effects and its activity against oral anaerobic bacteria. Dental cleanings and extractions may also improve patient comfort, but alone do not control the process.59

Nasopharyngeal Polyp

Feline nasopharyngeal polyps are benign, smooth, pedunculated growths of fibrous connective tissue that are usually unilateral and located dorsally to the soft palate. Their site of origin is controversial because the mucosal lining of the nasopharynx, auditory canal, and tympanic cavity is continuous and histologically indistinguishable.3• 6• 9• 11• 31• 46 However, in a recent report of 31 cases, surgical evaluation showed the most likely site of origin was within the tympanic cavity or within the auditory (Eustachian) tube at a point close to the opening of the tympanic cavity.31 From the site of origin, the polyp enlarges into the pharynx or, less commonly, the external auditory canal.3· 4 • 6• 11• 46 Clinical signs are the result of obstruction and development of secondary bacterial infection in the nasal cavity and of mechanical obstruction in the oropharynx and auditory tube. Nasopharyngeal polyps occur in young cats11 and have been seen in sibling kittens,46 suggesting a congenital origin. No breed or sex predisposition has been identified. Nasopharyngeal polyps should be included in the differential diagnosis list for chronic upper respiratory tract disease in any young cat. The history variably includes progressive stertorous respiration, labored breathing, nasal discharge that may be mildly responsive to antibiotics, sneezing, coughing and retching, voice change, dysphagia and/or Homer's syndrome.3• 9· 31• 37 Signs of otitis media may be present.6• 46 Head shaking and otic exudate without inflammation of the aural canal are consistent with external ear canal involvement. Finding the polyp on otoscopic examination seems to be unlikely, howeverY

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Differential diagnoses for nasopharyngeal polyps include feline calicivirus and feline rhinotracheitis virus, nasal foreign bodies, and nasopharyngeal masses such as cryptococcal granuloma and neoplasms. Definitive diagnosis requires observation of the nasopharyngeal mass under anesthesia (Fig. 13), skull radiographs, and histopathology. To expose the nasopharyngeal polyp the soft palate must be gently retracted rostrally. A tissue forceps or atraumatic hook may be used. A lateral radiographic projection of the skull will reveal the soft tissue mass in the nasopharynx. Because the majority of affected cats will have radiographic signs of otitis media, a radiographic examination of the osseous and tympanic bulla and petrous-temporal bones is recommended in all cases.31 Middle ear involvement may be manifested radiographically by thickening of the osseous bulla and petrous-temporal bone and increased density within the tympanic cavity. Histologic examination of the excised polyp shows fibrous connective tissue with a ciliated columnar epithelial lining and often a lymphocytic, plasmacytic inflammatory component in the submucosa.9 • 31 Surgical correction involves removing the polyp from its attachment. An oral approach with retraction of the soft palate and steady, gentle traction is recommended (Figs. 14 and 15). Soft palate division is usually not required.4• 9 A bulla osteotomy on the affected side(s) is recommended when radiographs reveal involvement of the tympanic cavity or

Figure 13. Oral traction and exposure of a nasopharyngeal polyp in a cat. (Courtesy of Amy S, Kapatkin, DVM)

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Figure 14. A feline nasopharyngeal polyp is being removed with slow, gentle traction using a tissue forceps. An ovariohysterectomy hook is used for retraction of the soft palate. (Courtesy of Amy S. Kapatkin, DVM)

bulla. It is desirable to perform the ventral bulla osteotomy before the polyp is removed; performing the osteotomy first frees the attachment of the polyp stalk from the tympanic cavity and tympanic opening of the auditory canal. A ventral approach is described as providing good ex-

Figure 15. Nasopharyngeal polyp with attached stalk. (Courtesy of Amy S. Kapatkin, DVM)

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posure with minimal disturbance to otic ossicles.9 The tympanic cavity must be completely drained and lavaged, with special attention paid to the opening of the auditory canal because it may be difficult to expose. Incomplete removal of inflammatory tissue may allow the polyp to recur. Thus, it is also important to open the septum that separates the feline bulla into dorsomedial and ventrolateral compartments,9' 31 but curettage of the dorsomedial aspect should be avoided31 to prevent damage to the auditory ossicles, semicircular canals and cochlea. A small rubber drain should be placed in the bulla and exit from a separate site adjacent to the primary incision. Microbiological testing of the purulent exudate in the bulla is recommended and usually does not reveal bacterial isolates. Homer's syndrome occurs in the majority of the feline patients after a bulla osteotomy because of damage to the postganglionic sympathetic nerve fibers that course through the middle ear to the eye and eyelids. The characteristic miosis, ptosis, and prolapse of the third eyelid develop immediately after surgery and, although may be permanent, usually resolve within 1 month.31 Some cats with normal skull radiographs and who receive treatment with polyp removal alone can be expected to have a recurrence. When surgical removal is combined with bulla osteotomy, recurrence is uncommonY This has led some investigators to propose that a bulla osteotomy be performed in all cases, even in those patients who do not have concurrent radiographic evidence of otitis media. 31 Recently, a case of a nasopharyngeal polyp in a dog was reportedY The 7-month-old Chinese shar pei exhibited progressive clinical features similar to those in cats, including labored breathing, coughing, nasal discharge that was not responsive to antibiotic therapy, and aspiration pneumonia. Excision was performed via a modified transpalatal approach and clinical signs had not returned during the 18-month followup period. SUMMARY

Pharyngeal disorders are diverse and can include developmental, traumatic, immune-mediated, infectious, metabolic, endocrine, neurologic, neoplastic, and inflammatory etiologies. Although the clinical history and signalment frequently can localize a disease process to the pharynx, only a careful examination, usually in conjunction with diagnostic tests, can identify the problem. Pharyngeal disorders are of important diagnostic significance. If left untreated, life-threatening respiratory impairment or debilitation and malnutrition may result. For effective treatment, therapy must be aimed at the primary disease process. ACKNOWLEDGMENT The author thanks Mr. Michael Fisk for his research and computer support in the preparation of the manuscript.

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32. Kirk RW: A catalogue of congenital and hereditary disorders of dogs (by breed). In Kirk RW (ed): Current Veterinary Therapy IX, Small Animal Practice. Philadelphia, WB Saunders, 1986, pp 1281-1285 33. Muller GH, Kirk RW, Scott DW: Miscellaneous diseases. In Small Animal Dermatology, ed 3. Philadelphia, WB Saunders, 1983, pp. 667-716 34. Nelson AW, Wykes PM: Upper respiratory system. In Slatter DH (ed): Textbook of Small Animal Surgery. Philadelphia, WB Saunders, 1985, pp 950-990 35. Noden DM: Normal development and congenital birth defects in the cat. In Kirk RW (ed): Current Veterinary Therapy IX, Small Animal Practice. Philadelphia, WB Saunders, 1986, pp. 1248-1257 36. Oakes MG, Lewis DD, Hedlund CS, et al: Canine oral neoplasia. Compend Contin Educ 15:1, 1993 37. Parker NR, Binnington AG: Nasopharyngeal polyps in cats: three case reports and a review of the literature. JAm Anim Hosp Assoc 21:4, 1985 38. Peeters ME, Venker-van Haagen AJ, Goedegebuure SA, et al: Dysphagia in Bouviers associated with muscular dystrophy; evaluation of 24 cases. Vet Q 13:2, 1991 39. Potter KA, Tucker RD, Carpenter JL: Oral eosinophilic granuloma of Siberian Huskies. JAm Anim Hosp Assoc 16:4, 1980 40. Schwarz PD, Withrow SJ, Curtis CR, et al: Mandibular resection as a treatment for oral cancer in 61 dogs. JAm Anim Hosp Assoc 27:6, 1991 41. Schwarz PD, Withrow SJ, Curtis, CR, et al: Partial maxillary resection as a treatment for oral cancer in 61 dogs. JAm Anim Hosp Assoc 27:6, 1991 42. Seim HB III: Cricopharyngeal achalasia. In Binnington AG, Cockshutt JR (eds): Decision Making in Small Animal Soft Tissue Surgery. Toronto, Canada, BC Decker, 1988, pp. 12-13 43. Seim HB III: Tonsillar abnormality. In Binnington AG, Cockshutt JR (ed): Decision Making in Small Animal Soft Tissue Surgery. Toronto, Canada, BC Decker, 1988, pp. 6-7 44. Shelton GD: Megaesophagus secondary to acquired myasthenia gravis. In Kirk RW, Bonagura JD (eds): Current Veterinary Therapy XI, Small Animal Practice. Philadelphia, WB Saunders, 1992, pp 580-583 45. Shelton GD: Swallowing disorders in the dog. Compend Cantin Educ 4:7, 1982 46. Stanton ME, Wheaton LG, Render JA, et al: Pharyngeal polyps in two feline siblings. J Am Vet Med Assoc 186:12, 1985 47. Strombeck DR, Guilford WG: Pharynx and esophagus-Normal structure and function. In Small Animal Gastroenterology, ed 2. Davis, CA, Stonegate Publishing, 1990, pp. 128-139 48. Suter PF, Watrous BJ: Oropharyngeal dysphagias in the dog: A cinefluorographic analysis of experimentally induced and spontaneously occurring swallowing disorders. I. Oral stage and pharyngeal stage dysphagias. Vet Radiol21:1, 1980 49. Thompson RR, Wilcox GE, Clark WT, et al: Association of calicivirus infection with chronic gingivitis and pharyngitis in cats. J Small Anim Pract 25:4, 1984 50. Venker-van Haagen AJ, Hartman W, van den Brom WE, et al: Continuous electromyographic recordings of pharyngeal muscle activity in normal and previously denervated muscles in dogs. Am J Vet Res 50:10, 1989 51. Venker-van Haagen AJ, Hartman W, Wolvekamp WTC: Contributions of the glossopharyngeal nerve and the pharyngeal branch of the vagus nerve to the swallowing process in dogs. Am J Vet Res 47:6, 1986 52. Watrous BJ: Clinical presentation and diagnosis of dysphagia. Vet Clin North Am Small Anim Pract 13:3, 1983 53. Watrous BJ: Dysphagia and regurgitation. In Ford RB (ed): Clinical Signs and Diagnosis in Small Animal Practice. New York, Churchill Livingstone, 1988, pp. 389-423 54. Watrous BJ, Suter PF: Normal swallowing in the dog: A cineradiographic study. Vet Radiol20:3, 1979 55. Watrous BJ, Suter PF: Oropharyngeal dysphagias in the dog: A cinefluorographic analysis of experimentally induced and spontaneously occurring swallowing disorders. II. Cricopharyngeal stage and mixed oropharyngeal dysphagias. Vet Radiol24:1, 1983 56. Weaver AD: Cricopharyngeal achalasia in cocker spaniels. J Small Animal Pract 24:4, 1983 57. Weber WJ, Hobson HP, Wilson, SR: Pharyngeal mucoceles in dogs. Vet Surg 15:1, 1986

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58. Wheeler SL, McGuire BH: Enteral nutritional support. In Kirk RW (ed): Current Veterinary Therapy X, Small Animal Practice. Philadelphia, WB Saunders, 1989, pp. 30-37 59. White SD, Rosychuk RAW, Janik TA, et al: Plasma cell stomatitis-pharyngitis in cats: 40 cases (1973-1991). JAm Vet Med Assoc 200:9, 1992 60. Withrow SJ: Principles and specifics of oncology, Part IV A. Oral and pharyngeal tumors. In Scientific Proceedings of the 51st Annual Meeting of the American Animal Hospital Association, San Francisco, CA, 1984, pp. 283-285 61. Withrow SJ: Tumors of the gastrointestinal system. In Withrow SJ, MacEwen EG (eds): Clinical Veterinary Oncology. Philadelphia, JB Lippincott, 1989, pp. 177-189

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