Vol. 19, No.

3 March 1997


Small Animal Gastroenterology

Continuing Education Article
Refereed Peer Review

Canine and Feline Megaesophagus
FOCAL POINT 5Acquired megaesophagus
can result from numerous neuromuscular, endocrine, or inflammatory disorders as well as from obstructive lesions in the esophagus. University of Tennessee

Erick A. Mears, DVM Christine C. Jenkins, DVM

s Disruption of the afferent pathway has been implicated in the pathophysiology of both congenital and adultonset idiopathic canine megaesophagus. s Definitive diagnosis of either generalized or focal myasthenia gravis requires identification of circulating antibodies against acetylcholine receptors. s The most common endocrine diseases associated with megaesophagus are hypoadrenocorticism and, possibly, hypothyroidism. s Advanced techniques, including manometry and nuclear scintigraphy, are useful in evaluating esophageal motility.


egaesophagus refers to a diffusely dilated esophagus with decreased or absent motor function. Canine megaesophagus can occur as a congenital disorder (with signs first appearing before or soon after weaning), as an acquired disorder (secondary to an underlying primary condition), or as an adult-onset idiopathic disease. Feline megaesophagus is rare and occurs as a congenital or secondary acquired disorder.1 Congenital megaesophagus is recognized at weaning and is believed to be caused by a lack of innervation of the esophagus.2,3 The mode of transmission in most breeds of cats and dogs has not been well defined.4,5 However, congenital megaesophagus is known to be inherited in wirehaired fox terriers and miniature schnauzers.6,7 It is transmitted in wirehaired fox terriers as a simple autosomal-recessive trait, whereas in miniature schnauzers, it is transmitted as a simple autosomal-dominant or a 60% penetrance autosomal-recessive trait.6–8 A predisposition may exist in other canine breeds, including Great Danes, German shepherds, Irish setters, Labrador retrievers, Newfoundlands, and Chinese shar-peis.8 Feline breeds that may have a hereditary predisposition include the Siamese and Siamese-related breeds.9 Acquired megaesophagus can result from numerous neuromuscular, endocrine, or inflammatory disorders as well as from obstructive lesions in the esophagus.4,5 Early diagnosis and elimination of predisposing diseases are essential for successful management because prolonged dysfunction can cause irreversible distention. Adult-onset idiopathic megaesophagus is associated with a poor to grave prognosis. A high percentage of patients are euthanatized because of the progression of clinical signs and recurrent aspiration pneumonia.

ANATOMY The esophagus consists of the upper esophageal sphincter proximally, the esophageal body, and the lower esophageal sphincter distally. The upper esophageal sphincter separates the pharynx from the body of the esophagus and indirectly prevents aspiration of ingesta into the respiratory tract. This sphincter is composed of striated muscle and is innervated by the somatic branches (glossopharyngeal, pharyngeal, and recurrent laryngeal) of the vagus nerve, which originates from the brain stem nucleus ambiguus.10

Small Animal

The Compendium March 1997

tone of the lower esophageal sphincter, the interdigitating esophageal and gastric rugal folds, the diaphragmatic crus (which serves as a muscular Vagus/glossopharyngeal nerves sling), the oblique angle of the distal esophagus as it enters the stomach, and the compression Nucleus solitarius exerted on the short intraabdominal esophageal segment by positive intraabdominal pressure.13 Dorsal motor nucleus Nucleus ambiguus In dogs, the lower esophageal sphincter contains fibers of both striated and smooth muscle, Vagus nerve (motor) Vagus nerve (motor) whereas in cats, it contains only fibers of smooth muscle. Esophageal contraction, or Neuromuscular junction Neuromuscular junction peristalsis, follows swallowing and the movement of food from the pharyngeal area into the Striated and smooth muscle Striated muscle esophagus. Sensory, or afferent, receptors in the pharynx and proximal esophagus are stimulatEsophageal contraction ed by the presence of food. Solid boluses are more effective than Figure 1—Neural pathway for esophageal motility. liquid in stimulating a swallowing reflex.12 The afferent recepThe esophageal body consists of two muscle layers tors stimulate the afferent nerve fibers of the vagus. The that propel food via coordinated contractions from the origin of the vagus nerve (i.e., the nucleus ambiguus for oral cavity to the stomach. The entire length of the castriated muscle and the dorsal motor nucleus for smooth nine esophageal body is composed of two oblique layers muscle) initiates an efferent response via the somatic of skeletal muscle, which contains predominantly type and parasympathetic nerve fibers of the vagus. This neuIIA fibers and is innervated by the somatic branches of ronal pathway ends at the myoneural junction with a the vagus nerve.11 The two layers of skeletal muscle of coordinated contraction of the upper esophageal sphincthe esophagus in the cat are in an oblique orientation ter.12 This peristaltic wave propagates caudally through the body of the esophagus, passes through the lower in the proximal portion of the esophagus and become esophageal sphincter, and then moves into the stomach. spiral in the distal portion, thus forming a longitudinal The initial wave that begins at the pharynx is called priand circular pattern.12 Unlike the dog, the cat has an increased quantity of smooth muscle in the distal third mary peristalsis. Any remaining intraluminal ingesta within the esophagus stimulates esophageal afferent reof the esophageal body. The striated muscle of the ceptors and initiates secondary peristalsis, which clears esophagus of the cat is also innervated by the vagus the lumen of the esophagus12 (Figure 1). nerve; however, the smooth muscle is innervated by the autonomic branches of the vagus nerve, which origiPATHOGENESIS nates from the dorsal motor nucleus. Congenital The lower esophageal sphincter is considered a physiThe neural pathway of esophageal innervation has ologic sphincter and not a true anatomic sphincter bebeen identified.12 Any lesion along this neural pathway cause of the absence of muscle mass at the sphincter could alter the normal motility of the esophagus.4,5 A site.12 This sphincter separates the esophagus and the cardia of the stomach and allows ingesta to pass into the study that evaluated the efferent pathway found that stomach while preventing reflux of most stomach condogs with congenital idiopathic megaesophagus had tents into the esophagus. Esophageal reflux is prevented normal vagal efferent innervation and decreased by various contributing factors at the site of the lower esophageal motor function, possibly secondary to alesophageal sphincter. These factors include the resting tered biomechanical or viscoelastic properties of the Presence of food in the proximal esophagus Afferent receptors (sensory)

The Compendium March 1997

Small Animal

esophagus.14,15 Two other studies confirmed a normal efferent limb and implicated a disruption of the afferent limb of the neural pathway as the cause of congenital canine megaesophagus.16,17

Disorders that Cause Megaesophagus
Central Nervous System s Distemper7,20 s Cervical vertebral instability with leukomalacia20 s Brain stem lesions20 s Neoplasia20 s Trauma20 Peripheral Neuropathies s Polyradiculoneuritis20 s Dysautonomiaa,21,22 s Ganglioradiculitis23 s Giant cell axonal neuropathy24 s Spinal muscular atrophy25 s Polyneuritis26 s Thallium toxicity27 s Lead toxicitya,28 s Acrylamide toxicity29 s Mediastinitis30 s Bronchoesophageal fistula30 s Bilateral vagal damage Neuromuscular Junction s Myasthenia gravisa,20,31–33 s Botulism34,35 s Tetanus5 s Anticholinesterase toxicity36 Esophageal Musculature s Systemic lupus erythematosus20,37 s Glycogen storage disease38 s Polymyositis20,39 s Dermatomyositis40 s Cachexia26 s Trypanosomiasis41 s Hypoadrenocorticism20 s Hypothyroidism (?) Obstructive Lesions s Neoplasia s Granulomas s Vascular ring anomalies s Strictures s Foreign body Miscellaneous s Pyloric stenosisa,42 s Gastric dilatation volvulus s Gastric heterotopiaa,43 s Pituitary dwarfism s Thymomaa s Familial reflex clonus s Dystrophin deficiencya,44

Adult-Onset Idiopathic In an evaluation of the afferent nerve pathway in adult dogs with acquired idiopathic megaesophagus, pressure measurements were taken from the upper esophageal sphincter, the esophageal body, and the lower esophageal sphincter after both swallowing and intraluminal distention.18 Pressure measurements of the lower esophageal sphincter after swallowing were normal and indicated appropriate relaxation of the sphincter,18,19 thus suggesting a normal efferent pathway. However, measurements taken after intraluminal distention of the esophagus revealed failure of the lower esophageal sphincter to relax.18 Therefore, a defect probably exists in the afferent pathway of dogs with both congenital and adultonset idiopathic megaesophagus. Similar studies have not been done in cats. Secondary Acquired Megaesophagus can be caused by any disease that inhibits esophageal body peristalsis by disrupting central, efferent, or afferent neural pathways or esophageal musculature.8 The various causes and their proposed mechanisms will be discussed in the following section.

CAUSES Congenital a The neurologic dysfunction that results in Diagnosed in cats. diffuse megaesophagus is unclear. It has been cal obstruction and possibly generalized esophageal dishypothesized that the innervation of the esophagus is tention. incomplete in congenital megaesophagus and that innervation may improve with maturity.2,3 Myasthenia Gravis Myasthenia gravis is a common cause of secondary Secondary Acquired megaesophagus in dogs and, although rare in cats, has The list of specific diseases that cause megaesophagus been reported to cause proximal esophageal dilatation.45 is extensive. Broad disease categories include central Myasthenia gravis can be either congenital or acquired, and peripheral neuropathies, diseases of the neuromusand both can result in megaesophagus.31 Because concular junction, myopathies, and obstructive lesions of genital myasthenia gravis is less common, it will not be the esophagus (see Disorders that Cause Megaesophaaddressed in this article. gus20–44). The following discussion focuses on several of Acquired myasthenia gravis is a disorder of neurothe most common specific diseases—myasthenia gravis, muscular transmission in which autoantibodies against a disorder of the neuromuscular junction; hypoadrenonicotinic acetylcholine receptors at the neuromuscular corticism (and possibly hypothyroidism), which alter junction result in a reduction of acetylcholine receptors the function of the esophageal musculature; and all and subsequent muscle weakness.46 Two forms of actypes of obstructive lesions, which cause focal mechaniAFFERENT PATHWAY DEFECT s SECONDARY DISORDERS s MYASTHENIA GRAVIS

Small Animal

The Compendium March 1997

quired myasthenia gravis (generalized and focal) have been identified. Generalized myasthenia gravis causes muscle weakness that worsens after exercise and improves with rest. Most dogs with generalized myasthenia gravis and muscle weakness have concurrent megaesophagus. One report showed that two of four cats with generalized myasthenia gravis had a dilated proximal esophagus, possibly the result of the proximal distribution of skeletal muscle.45 Focal myasthenia gravis in dogs has been recognized to cause weakness involving the esophageal, pharyngeal, and/or facial muscles.33 One study found that 40 of 152 (26%) dogs with a diagnosis of “idiopathic” megaesophagus had focal myasthenia gravis. Fortyeight percent of these dogs showed clinical improvement or remission of clinical signs, which was associated in all cases with decreased titers of antibody to acetylcholine receptors. Another more recent study revealed that 36% of dogs diagnosed with acquired myasthenia gravis had focal disease with megaesophagus but without evidence of general muscle weakness.32

have underlying or concurrent diseases that may interfere with the evaluation of the hypothalamic-pituitary-thyroid axis. Some hypothyroid dogs with megaesophagus have improved with thyroxine supplementation.49,50 However, spontaneous improvement of megaesophagus has been previously documented.52 In addition, a recent retrospective megaesophagus risk factor analysis showed that hypothyroidism is not a significant risk factor.a Until a correlation between hypothyroidism and megaesophagus is established, “hypothyroid” dogs with megaesophagus should be monitored closely while under treatment.

Hypoadrenocorticism and Hypothyroidism The most common endocrine diseases associated with megaesophagus are hypoadrenocorticism47,48 and, possibly, hypothyroidism.49 With hypoadrenocorticism, it is suspected that megaesophagus results from impairment of muscle carbohydrate metabolism due to glucocorticoid insufficiency. In addition, depleted muscle glycogen stores and decreased catecholamine activity may play a role.32 In one case report, atypical Addison’s disease was diagnosed and subsequent therapy with prednisone resolved the megaesophagus.48 The cause-and-effect relationship between hypothyroidism and megaesophagus is controversial. Hypothyroidism has been implicated in the pathogenesis of various myopathies and neuropathies.33,49,50 The results of treating hypothyroid dogs with megaesophagus have been equivocal.49,50 In a retrospective study of 29 dogs with hypothyroidism, 4 had megaesophagus. After appropriate thyroxine supplementation, the clinical signs improved in only one dog; however, all four continued to have radiographic evidence of a dilated esophagus.49 Another study identified five dogs with neurologic abnormalities; all five had myasthenia gravis and signs consistent with hypothyroidism.50 These dogs showed clinical signs and radiographic evidence of megaesophagus. Clinical signs resolved in two of the five dogs after administration of thyroid hormone. The tenuous association between hypothyroidism and megaesophagus is often complicated by the current lack of both sensitive and specific diagnostic tests for hypothyroidism.51 In addition, many patients with megaesophagus

Obstructive Lesions Lesions that cause focal mechanical obstruction (e.g., vascular ring anomalies, tumors, granulomas, strictures, and foreign bodies) can progress to generalized esophageal distention. Constricting vascular ring anomalies are the most common cause of segmental obstructive megaesophagus in young animals. These include persistent right aortic arch, double aortic arch, left aortic arch and right ligamentum arteriosum, persistent left or right subclavian arteries, ductus arteriosus with normal aortic arch, persistent right dorsal aorta, and aberrant intercostal arteries.5 Persistent right aortic arch is the most common vascular ring anomaly in both dogs and cats.53,54 The right, instead of the left, fourth aortic arch becomes functional. As a result, the trachea and esophagus are encircled by the base of the heart ventrally, the aortic arch to the right, the dorsal aorta dorsally, and the ligamentum arteriosum and pulmonary artery to the left.55 Clinical signs associated with secondary megaesophagus usually become evident at the time of weaning to solid food. They are apparent in 90% of animals by 6 months of age.56 Diagnosis is confirmed by barium contrast radiography, which demonstrates an esophageal dilatation cranial to the base of the heart. Esophagoscopy may help rule out primary esophageal stricture or a foreign body but is often unnecessary. The treatment of choice is early surgical ligation of the aberrant vessels or ligamentum arteriosum to release the esophageal stricture.57 Although the primary defect is corrected, many animals continue to have abnormal esophageal motility and some continue to have clinical signs.58 In one study, postsurgical fluoroscopy showed that all surgically corrected patients had abnormal motility; 58% occasionally exhibited clinical signs.59 Although esophageal cancer in dogs and cats is rare, squamous cell carcinoma, leiomyosarcoma, fibrosarcoma, and osteosarcoma have been reported.60 Benign tuaGaynor

A, Shofer F, Washabau RJ: Personal communication, School of Veterinary Medicine, University of Pennsylvania, 1996.


The Compendium March 1997

Small Animal

requires the identification of a dilated esophagus on survey thoracic radiographs (Figure Minimum Data Base 2) or a barium esophagogram. s Complete blood count Radiographs may show an s Chemistry panel esophagus filled with air, flus Electrolytes id, or ingested material. Thos Urinalysis racic radiographs are also indicated to evaluate for evidence s Thoracic radiographs and/or barium CLINICAL SIGNS of aspiration pneumonia. If esophagogram The most common clinical megaesophagus is diagnosed s Acetylcholine antibody test sign associated with megaon survey radiographs, an s Adrenocorticotropic hormone (ACTH) stimulation esophagus is regurgitation, esophagogram is generally uns Thyroxine (T4) level which is defined as the pasnecessary and may pose a s Thyroid-stimulating hormone (TSH) assay sive evacuation of undigested greater risk for aspiration. food from the esophagus. A minimum data base that Additional Tests The regurgitated material includes a complete blood s Lead level may contain mucus as well as count, serum chemistries, s Botulinum test undigested food but is generand a urinalysis is necessary s Antinuclear antibody (ANA) test ally not bile stained. In conto identify any underlying s Muscle biopsy trast to vomiting, there is no metabolic abnormalities. In s Creatinine phosphokinase (CPK) prodromal phase; regurgitacases of esophageal hypos Endoscopy tion may occur soon after motility without significant eating or have a lag phase of esophageal dilatation, barium s Manometry many hours. Frequency of contrast, alone or with food, s Scintigraphy regurgitation varies, and animay be necessary to identify mals may regurgitate food and/or liquids. Other clinimild esophageal dilatation or to outline an obstructive lecal signs observed with megaesophagus include vomitsion (Figure 3). The response of the esophagus is based ing, ptyalism, halitosis, gurgling noises from the on the consistency of the diet.12 Fluoroscopy is available in referral institutions and esophagus, and respiratory signs associated with aspiramay be used to visualize esophageal motility. Esophation pneumonia. An absent respiratory reflex has been goscopy can aid in the diagnosis of reflux esophagitis, identified in dogs with idiopathic megaesophagus and which may cause abnormal motility and distention of may increase the risk of aspiration.63 the esophagus.8 PHYSICAL In humans, esophageal EXAMINATION motility is evaluated with Physical examination fluoroscopy and esophageal findings may include apparmanometry. In veterinary ent ventral neck swelling medicine, the use of esophdue to esophageal distenageal manometry is limited tion. Patients with megato teaching institutions and esophagus may also be cachecresearch facilities. 19,64,65 Esophageal motility manotic from poor nutritional metric studies are best done intake. If aspiration pneuon awake animals because of monia is present, fever, the effects of anesthetics on harsh rales, and/or mucopunormal esophageal motirulent nasal discharge may lity. 65 Manometry utilizes be observed. a catheter passed into Figure 2—Right lateral thoracic radiograph of a 10-year-old the esophageal lumen for DIAGNOSIS Definitive diagnosis of dog with idiopathic megaesophagus. The air-filled, diffuse- dynamic measurement of megaesophagus (see Diagnos- ly dilated esophagus has resulted in ventral displacement of esophageal pressure, transit the trachea. tic Tests for Megaesophagus) rate, and lower esophageal

mors, including leiomyoma and plasmacytoma, can occur.60–62 Early identification and/or resolution of the obstruction via surgical or endoscopic intervention is warranted to prevent further damage.

Diagnostic Tests for Megaesophagus


Small Animal

The Compendium March 1997

pressures following swallowing. Manometry is used to evaluate subtle motility abnormalities that may not be evident on fluoroscopy.66 Baseline manometric measurements of the esophagus for both dogs and cats have been evaluated.67,68 Esophageal scintigraphy is a newer technique that is used in humans to quantitatively evaluate esophageal motility. This technique involves the use of a gamma camera to monitor radiolabeled food as it moves through the esophagus. Transit time of the food bolus through various regions of interest along the length of the esophagus is determined (Figure 4). Time activity curves are then plotted to evaluate the movement of the food bolus through the esophagus (Figures 5 and 6). Esophageal scintigraphy may be a more accurate measure of motility because it evaluates the response of the esophagus to a food bolus without the influence of foreign material, such as barium or an esophageal catheter.69 Recently, scintigraphy was used to evaluate the effect of metoclopramide and cisapride on esophageal motility in normal beagles.68 In most cases of megaesophagus, manometric and scintigraphic studies are not necessary for a diagnosis. These tests can be used to identify those animals with subtle esophageal motility abnormalities and consistent clinical signs but with no identifiable abnormality on routine radiographic imaging. Both manometry and scintigraphy also provide a quantitative measure of esophageal motility parameters. Once megaesophagus has been identified, additional testing is necessary to identify an underly-

Figure 3A

ing cause. Endocrine testing (thyroxine [T4] level, thyroidstimulating hormone [TSH] assay, adrenocorticotropic hormone [ACTH] stimulation); neuromuscular evaluation (acetylcholine antibody, antinuclear antibodies [ANA], muscle biopsy, creatinine phosphokinase [CPK]); and toxin screening (lead, botulinum) are done to identify the more common secondary causes. The diagnosis, however, is often idiopathic megaesophagus.5 Definitive diagnosis of either generalized or focal myasthenia gravis requires the identification of circulating antibodies against acetylcholine receptors. The immunoprecipitation radioimmunoassay is very specific and sensitive for demonstrating circulating antibodies. This test does not give false-positive results. However, false-negative results (less than 5% of cases tested 32) may occur and indicate either the presence of autoantibodies against other components of the motor end-plate or the presence of high-affinity antibodies. Other diagnostic tests that are available to support a diagnosis of myasthenia gravis include the edrophonium chloride challenge and repetitive nerve stimulation.

Figure 3B Figure 3—(A) Ventral dorsal and (B) right lateral thoracic radiographs taken after administration of a barium meal. The entire thoracic portion of the esophagus in this dog is distended, and the esophagus has displaced the trachea ventrally. A right mediastinal shift has displaced the heart. An alveolar infiltrate is present within the right middle and left cranial lung lobes.

MANAGEMENT Management of idiopathic megaesophagus, unresolved megaesophagus, or of esophageal hypomotility involves feeding small amounts of food to an animal in an upright position. The ability of patients with megaesophagus to swallow foods of differing consistencies varies. A barium


The Compendium March 1997

Small Animal

contrast study may help in the decision as to whether to use liquid, canned, or dry food. If the patient is difficult to feed, gastrostomy tubes can be placed to facilitate feeding. Surgical, percutaneous endoscopic, and blind (nonendoscopic) percutaneous techniques for gastrostomy tube placement have been described elsewhere.b,70–72 Aspiration pneumonia should be treated with broad-spectrum antibiotics while culture and sensitivity results from a transtracheal wash are pending. Identified causes of secondary megaesophagus should be treated promptly and appropriately to optimize resolution of esophageal dysfunction. If the diagnosis of myasthenia gravis is confirmed, treatment should include the administration of longacting anticholinesterase drugs. Both pyridostigmine bromide (0.5 to 1.0 mg/kg orally every 8 to 12 hours) and neostigmine (0.04 mg/kg intramuscularly every 6 hours) are effective. Because myasthenia gravis is an immunemediated disease, corticos teroids may be useful; however, their use is controversial, and a complete evaluation of the respiratory tract for aspiration pneumonia is recommended before using corticosteroids.73 Treatment is considered successful if clinical signs improve and the acetylcholine receptor antibody level decreases. This level should be checked

Figure 4—Esophageal scintigraphic images were obtained 20

minutes after intravenous injection of pertechnetate, a radioactive substance. A bolus of food labeled with 99mtechnetium was administered orally, and a series of images were obtained during esophageal transit of the radiolabeled food. The image shown here is a summation of the dynamic images; the course through the entire esophagus is shown. Pertechnetate localizes in the stomach and thyroid gland, allowing for visualization of esophageal landmarks. Note the residual pertechnetate at the injection site on the forelimb. The open circles represent regions of interest (see Figure 5) over different areas of the esophagus.

Figure 5—An esophageal scintigraphic study of a 10-weekold schnauzer. The images above the graph are portions of the dynamic acquisition and were obtained after swallowing of a radiolabeled food bolus. Note that the food bolus remains in the proximal esophagus. The numbers above each image represent time in seconds. The graph is a time activity curve that represents changes in esophageal activity at specified regions of interest (ROI) over time. Normally, the time activity curve should show a peak as the radioactive bolus passes through the ROI. Note the relatively flat appearance of the proximal esophageal time activity curve, which is the result of the lack of movement of the bolus from the proximal esophagus (Prox Esop = proximal esophbSee the article in this issue by agus, Thx Inlet = thoracic inlet, Dist Esop = distal esophaDr. Kathryn Michel on guide- gus).

lines for gastrostomy tubes.

every 4 to 6 weeks and therapy adjusted accordingly. If clinical remission occurs, all medications may be discontinued; however, the disease may recur.73 Esophageal dilatation has been shown to resolve in both dogs and cats after appropriate therapy.45,73 Various drug therapies have been used in an attempt to improve esophageal motility in dogs with megaesophagus. Calciumchannel blockers, such as nifedipine, have been used in dogs with suspected achalasia or asynchrony of the lower esophageal sphincter function and esophageal peristalsis. 74 Response to nifedipine in dogs, if any, is transient. Metoclopramide is a prokinetic drug that has been used without success in dogs with megaesophagus.19 Metoclopramide may be indicated in dogs with esophageal hypomotility caused by reflux esophagitis because it increases lower esophageal sphincter tone. Cisapride is another prokinetic drug that increases motility of the gastrointestinal tract by promoting the release of acetylcholine. Experimentally, cisapride has been shown to alter esophageal peristalsis in cats. 75 Anecdotal reports indicate possible clinical improvement in some dogs with megaesophagus.76 Other reports have questioned the beneficial effects of cisapride or metoclopramide in dogs with megaesophagus.75 In normal dogs, cisapride decreased or slowed the transit rate of a food bolus through the


Small Animal

The Compendium March 1997


The authors thank Dr. Greg Daniel, of the College of Veterinary Medicine, University of Tennessee, for providing Figures 2 through 6.

About the Authors
Drs. Mears and Jenkins are affiliated with the Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, Tennessee. They are Diplomates of the American College of Veterinary Internal Medicine.

1. Hoenig M, Mahaffey MB, Parnell PG, Styles ME: Megaesophagus in two cats. JAVMA 196(5):763, 1990. 2. Diamant N, Szczepanski M: Idiopathic megaesophagus in the dog: Reasons for spontaneous improvement and a possible method of medical therapy. Can Vet J 15:66–71, 1974. 3. Diamant N, Szczepanski M, Nui H: Manometrtic characteristics of idiopathic megaesophagus in the dog: An unsuitable animal model for achalasia in man. Gastroenterology 65:216– 223, 1973. 4. Strombeck DR, Guilford WG: Diseases of swallowing, in Guilford WG, Center SA, Strombeck DR, et al (eds): Strombeck’s Small Animal Gastroenterology, ed 3. Philadelphia, WB Saunders Co, 1990, pp 216–238. 5. Twedt DC: Diseases of the esophagus, in Ettinger SJ, Feldman EC (eds): Textbook of Veterinary Internal Medicine, ed 4. Philadelphia, WB Saunders Co, 1995, pp 1124–1142. 6. Cox VS, Wallace LJ, Anderson VE, Rushmer RA: Hereditary esophageal dysfunction in the miniature schnauzer dog. Am J Vet Res 41(3):326, 1980. 7. Osborne CA, Clifford DH, Jessen C: Hereditary esophageal achalasia in dogs. JAVMA 151:572–581, 1967. 8. Guilford WG: Megaesophagus in the dog and cat. Semin Vet Med Surg Small Anim 5(1):37, 1990. 9. Clifford DH, Soifer FK, Wilson CF, et al: Congenital achalasia of the esophagus in four cats of common ancestry. JAVMA 158(9):1554, 1971. 10. Washabau RJ: Pathogenesis of canine megaesophagus: Neuropathy Proc 14th ACVIM Forum:583–584, 1996. 11. Hudson LC: Histochemical identification of the striated muscle of the canine esophagus. Anat Histol Embryol 22(2): 101–104, 1993. 12. Strombeck DR, Guilford WG: Pharynx and esophagus: Normal structure and function, in Guilford WG, Center SA, Strombeck DR, et al (eds): Strombeck’s Small Animal Gastroenterology, ed 3. Philadelphia, WB Saunders Co, 1990, pp 202–210. 13. Watrous BJ, Suter PF: Normal swallowing in the dog: A cineradiographic study. Vet Radiol 20:99–109, 1979. 14. Holland CT, Satchell PM, Farrow BRH: Oesophageal compliance in naturally occurring canine megaoesophagus. Aust Vet J 70(11):414–420, 1993. 15. Holland CT, Satchell PM, Farrow BRH: Vagal esophagomotor nerve function and esophageal motor performance in dogs with congenital idiopathic megaesophagus. Am J Vet Res 57(6):906, 1996. 16. Tan BJ, Diamant NE: Assessment of the neural defect in a dog with idiopathic megaesophagus. Dig Dis Sci 32:76, 1987.

Figure 6—A follow-up (16 weeks) esophageal scintigraphic study of the dog shown in Figure 5. The images above the graph are portions of the dynamic acquisition. Note the movement of the radioactive bolus through the esophagus (unlike the lack of movement in Figure 5). The time activity curve is more normal in appearance, with well-defined peaks as the bolus traverses the esophageal regions of interest (ROI). The residual activity in the distal esophagus may represent mild esophageal dysfunction. The improvement in esophageal function is probably related to the resolution of congenital megaesophagus (Prox Esop = proximal esophagus, Thx Inlet = thoracic inlet, Dist Esop = distal esophagus).

esophagus.68 Therefore, cisapride and other current prokinetic drugs cannot be recommended to improve esophageal motility in a patient with primary megaesophagus. Because it increases the pressure of the lower esophageal sphincter, however, cisapride (like metoclopramide) may help decrease reflux esophagitis. The result is fewer episodes of regurgitation and subsequent esophagitis, both of which may exacerbate megaesophagus.8

SUMMARY Megaesophagus can be congenital, secondary to numerous disorders, or idiopathic. Diagnosis of megaesophagus is based on consistent historical and physical examination findings in conjunction with the results of imaging techniques. Motility disorders that cannot be identified with traditional radiographic techniques may require manometric and scintigraphic evaluation. Secondary megaesophagus has the best prognosis if the underlying cause can be determined and effectively treated. Treatment of congenital or idiopathic megaesophagus is at best supportive.


The Compendium March 1997

Small Animal

17. Holland CT, Satchell PM, Farrow BRH: Vagal afferent dysfunction in naturally occurring canine esophageal motility disorder. Dig Dis Sci 39(10):2090–2098, 1994. 18. Washabau RJ: Pathogenesis and therapy of canine megaesophagus. Proc 10th ACVIM Forum:671–674, 1992. 19. Magne ML: Esophageal motility disorders in the dog. Proc 4th ACVIM Forum 12(9):9–13, 1986. 20. Boudrieau RJ, Rogers WA: Megaesophagus in the dog: A review of 50 cases. JAAHA 21:33, 1985. 21. Schrauwen E, Van Ham L, Maenhout T, Desmidt M: Canine dysautonomia: A case report. Vet Rec 128:524, 1991. 22. Canton DD, Sharp NJH, Aguirre GD: Dysautonomia in a cat. JAAHA 192(9):1293, 1988. 23. Cummings JF, DeLahunta A, Mitchell WJ: Ganglioradiculitis in the dog. Acta Neuropathol 60:29–39, 1983. 24. Duncan ID, Griffith IR: Canine giant axonal neuropathy; Some aspects of its clinical, pathological and comparative features. J Small Anim Pract 22:491–501, 1981. 25. Shell LG, Jortner BS, Leib MS: Spinal muscular atrophy in two Rottweiler littermates. JAVMA 190:878–880, 1987. 26. Watrous BJ: Esophageal disease, in Ettinger SJ (ed): Textbook of Veterinary Internal Medicine. Philadelphia, WB Saunders Co, 1983, pp 1191–1233. 27. Zook BD, Gilmore CE: Thallium poisoning in dogs. JAVMA 151:206–217, 1967. 28. Zook BC: The pathologic anatomy of lead poisoning in dogs. Vet Pathol 9:310–327, 1972. 29. Satchell PM: The neuropathic oesophagus. A radiographic and manometric study on the evolution of megaoesophagus in dogs with developing axonal neuropathy. Res Vet Sci 48:249, 1990. 30. Van Ee RT, Dodd VM, Pope ER, Henry GA: Bronchoesophageal fistula and transient megaesophagus in a dog. JAVMA 188(8):874, 1986. 31. Shelton GD: Canine myasthenia gravis, in Kirk RW, Bonagura JD (eds): Current Veterinary Therapy. XI. Philadelphia, WB Saunders Co, 1992, pp 1039–1042. 32. Shelton GD: Pathogenesis of canine megaesophagus: Neuromuscular disorders. Proc 14th ACVIM Forum:581–582, 1996. 33. Shelton GD, Willard MD, Cardinet GH, Lindstrom J: Acquired myasthenia gravis: Selective involvement of esophageal, pharyngeal, and facial muscles. J Vet Intern Med 4(6):281, 1990. 34. Darke PGG, Roberts TA, Smart JL, et al: Suspected botulism in foxhounds. Vet Rec 99:98–100, 1976. 35. Van Ness JJ: Electrophysiological evidence of peripheral nerve dysfunction in six dogs with botulism type C. Res Vet Sci 40:372–376, 1986. 36. Harris LD, Ashworth WD, Ingelfinger FJ: Esophageal aperistalsis and achalasia produced in dogs by prolonged cholinesterase inhibition. J Clin Invest 39:1744–1751, 1960. 37. Krum SH, Cardinet GH, Anderson BC, et al: Polymyositis and polyarthritis associated with systemic lupus erythematosus in a dog. JAVMA 170:61–64, 1977. 38. Walvort HC, VanNess JJ, Stokhof AA, et al: Canine glycogen storage disease type II: A clinical study of four affected Lapland dogs. JAAHA 20:279–286, 1984. 39. Kornegay JN, Gorgacz EJ, Dawe DL, et al: Polymyositis in dogs. JAVMA 176:431–438, 1980. 40. Haupt KH, Prieur DJ, Moore MP, et al: Familial canine dermatomyositis: Clinical, electrodiagnostic, and genetic studies. Am J Vet Res 46:1861–1869, 1985. 41. Marsden PD, Hagstrom JWC: Experimental Trypanosoma cruzi infection in beagle puppies. Trans R Soc Trop Med Hyg 62(Abstract):816, 1968.

42. Pearson H, Gaskell CJ, Gibbs C, Waterman A: Pyloric and oesophageal dysfunction in the cat. J Small Anim Pract 15:487, 1974. 43. Bishop LM, Kelly DF, Gibbs C, et al: Megaloesophagus and associated gastric heterotopia in the cat. Vet Pathol 16:444– 449, 1979. 44. Gaschen FP, Hoffman EP, Gorospe JR, et al: Dystrophin deficiency causes a lethal muscle hypertrophy in cats. J Neurol Sci 110(1–2):149–159, 1992. 45. Joseph RJ, Carrillo JM, Lennon VA: Myasthenia gravis in the cat. J Vet Intern Med 2(2):75, 1988. 46. Lindstrom J, Shelton D, Fujii Y: Myasthenia gravis. Adv Immunol 42:233–284, 1987. 47. Feldman EC, Nelson RW: Hypoadrenocorticism, in Feldman EC, Nelson RW (eds): Canine and Feline Endocrinology and Reproduction. Philadelphia, WB Saunders Co, 1996, pp 266–306. 48. Bartges JW, Nielson DL: Reversible megaesophagus associated with atypical primary hypoadrenocorticism in a dog. JAVMA 201(6):889, 1992. 49. Jaggy A, Oliver JE, Ferguson DC, et al: Neurological manifestations of hypothyroidism: A retrospective study of 29 dogs. J Vet Intern Med 8(5):328, 1994. 50. Dewey CW, Shelton GD, Bailey CS, et al: Neuromuscular dysfunction in five dogs with acquired myasthenia gravis and presumptive hypothyroidism. Prog Vet Neurol 6(4):117, 1995. 51. Greene R: Thyroid testing: The full circle. Int Symp Canine Hypothyroid:4–5, August 1996. 52. Hendricks JC, Maggio-Price L, Dougherty JF: Transient esophageal dysfunction mimicking megaesophagus in three dogs. JAVMA 185(1):90, 1984. 53. Buchanon JW: Symposium: Thoracic surgery on the dog and cat. III. Patent ductus arteriosus and persistent right aortic arch surgery in dogs. J Small Anim Pract 9:409–428, 1968. 54. Wheaton LG, Blevine WE, Weirich WE: Persistent right aortic arch associated with other vascular anomalies in two cats. JAVMA 184(7):848–851, 1984. 55. Eyster GE, Probst M: Basic cardiac procedures, in Slatter DH (ed): Textbook of Small Animal Surgery. Philadelphia, WB Saunders Co, 1985, pp 1107–1131. 56. Patterson DF: Canine congenital heart disease: Epidemiology and etiological hypothesis. J Small Anim Pract 12:263– 287, 1971. 57. Van Gundy T: Vascular ring anomalies. Compend Contin Educ Pract Vet 11(1):36–48, 1989. 58. Shire PK, Liu W: Persistent right aortic arch in dogs: A longterm follow-up after surgical correction. JAAHA 17: 773–776, 1981. 59. Komtebedde J, Koblik P, Mattoon J, Moore A: Preoperative and postoperative fluoroscopy in dogs with persistent right aortic arch. Vet Surg 20:340, 1991. 60. Withrow SJ: Esophageal cancer, in Withrow SJ, MacEwen EG (eds): Small Animal Clinical Oncology, ed 2. Philadelphia, WB Saunders Co, 1996, pp 241–243. 61. Culbertson R, Branam JE, Rosenblatt LS: Esophageal/gastric leiomyoma in the laboratory beagle. JAVMA 183:1168– 1171, 1983. 62. Hamilton TA, Carpenter JL: Esophageal plasmacytoma in a dog. JAVMA 204:1210–1211, 1994. 63. Strombeck DR, Troya L: Evaluation of lower motor neuron function in two dogs with megaesophagus. JAVMA 169(4): 411, 1976. 64. Rogers WA, Fenner WR, Sherding RG: Electromyographic

Small Animal

The Compendium March 1997

65. 66. 67. 68. 69.

and esophagomanometric findings in clinically normal dogs and in dogs with idiopathic megaesophagus. JAVMA 174(2): 181, 1979. Strombeck DR, Harrold D: Effects of acepromazine, meperidine, and xylazine on gastroesophageal sphincter pressure in the dog. Am J Vet Res 46(4):963–965, 1985. Maurer AH, Fisher RS: Scintigraphy. Atlas of Gastrointestinal Motility in Health and Disease. Baltimore, Williams & Wilkins, 1993, pp 85–104. Correnti FS, Little AG, Calleja IJ, et al: Manometric evaluation of the feline esophagus. J Surg Res 41(3):312–318, 1986. Mears EA, Jenkins C, Daniel G, et al: The effect of cisapride and metoclopramide on esophageal motility in normal beagles. Proc 14th ACVIM Forum:738(Abstract), 1996. Taillefer R, Jadliwalla M, Pellerin E, et al: Radionuclide esophageal transit in detection of esophageal motor dysfunction: Comparison with motility studies (manometry). J Nucl Med 31(12):1921–1926, 1990.

70. Van Sluijs FJ, Happe RP: Surgical disease: The stomach, in Slatter DH (ed): Textbook of Small Animal Surgery. Philadelphia, WB Saunders Co, 1985, pp 684–717. 71. Bright RM, Burrows CF: Percutaneous endoscopic tube gastrostomy in dogs. Am J Vet Res 49:629, 1988. 72. Mauterer JV, Abbod SK, Buffington CA, et al: New technique and management guidelines for percutaneous nonendoscopic tube gastrostomy. JAVMA 205:574–579, 1994. 73. Shelton GD: Megaesophagus secondary to acquired myasthenia gravis, in Kirk RW, Bonagura JD (eds): Current Veterinary Therapy. XI. Philadelphia, WB Saunders Co, 1992, pp 580–583. 74. Chandra NC, McLeod CG, Hess JL: Nifedipine: A temporizing therapeutic option for the treatment of megaesophagus in adult dogs. JAAHA 25:175, 1989. 75. Washabau RJ, Hall JA: Cisapride. JAVMA 207(10):1285– 1288, 1995. 76. Tams TR: Cisapride: Clinical experience with the newest GI prokinetic drug. Proc 12th ACVIM Forum:100–102, 1994.

Sign up to vote on this title
UsefulNot useful