REGURGITATION

Regurgitation refers to a passive, retrograde movement of ingested material to a level proximal to the upper esophageal sphincter. Usually this occurs before ingested material reaches the stom­ach.

Regurgitation is usually a clinical sign of an esophageal disorder. In most cases it results from abnormal esophageal peristalsis or esophageal obstruction. The most common cause of regurgi­tation seen in clinical practice is megaesophagus. Megaesophagus refers to a specific syndrome characterized by a dilated, hypoperistalic esopha­gus. By definition and for use in this text, megae­sophagus is differentiated from other causes of esophageal dilation (e.g., esophageal foreign body, vascular ring anomaly, neoplasia) that may or may not be characterized by abnormal peristalsis. Megaesophagus is discussed in detail in Chapter 4.

Many patients with disorders causing regurgita­tion have owners who incorrectly but understand­ably interpret the problem as vomiting.

From Tams TR:Vomiting, regurgitation, and dysphagia.

TABLE 1-2

Vomiting or Regurgitation? A Checklist for Differentiation

Rights were not granted to include this table in electronic media. Please refer to the printed publication.

From Burrows CFrVomiting and regurgitation in the dog: a clinical perspective. In Viewpoints in veterinary medicine, ed 2, Lehigh Valley, Pa, 1993, Alpo Pet Foods.

consist entirely of thick white foam. The fre­quency of regurgitation can vary dramatically, from as few as 1 to 2 episodes per week in some patients with megaesophagus to as often as 10 to 15 times per day.

Vomiting involves active expulsion of food and/or fluid.Vomiting is accompanied by retching and active abdominal contractions. Frequently signs of nausea (salivation, restlessness, increased swallowing motions) occur prior to retching. Occurrence of any of these associated signs should be discussed with the owner as the history is reviewed. Vomited material may include bile, and food may be present in various states of digestion. Vomiting may occur seconds to minutes to many hours after eating. With regard to incidence, patients with vomiting disorders far outnumber those with disorders associated with regurgitation. It is important to note that some patients with a history more suggestive of regurgitation may actu­ally be vomiting. If it is unclear based on the his­tory or clinical impression whether or not the patient is actually regurgitating rather than vomit­ing, a survey thoracic radiograph should be made at the outset to look for evidence of esophageal dilation. A barium swallow may be necessary to rule out esophageal dilation.

In evaluation of a patient with regurgitation, important historical factors to be considered by the clinician include signalment; nature of onset of clinical signs (i.e., acute and persistent versus inter­mittent [recent or chronic]); environment (e.g., likelihood of foreign body or toxin ingestion); pertinent history (e.g., recent anesthetic event sug­gesting possible development of a reflux-related esophageal stricture); presence of any systemic signs, such as weakness (e.g., myasthenia gravis, hypoadrenocorticism, polymyositis) or vomiting (e.g., hypoadrenocorticism, toxin ingestion such as lead); and whether there are any signs of complica­tions from regurgitation (e.g., coughing or dysp­nea, suggesting that an aspiration event with subsequent development of pneumonia has occurred).

Signalment

The signalment, particularly age and breed, pro­vides important diagnostic clues. If regurgitation begins at the time of weaning onto solid food, a vascular ring anomaly (e.g., persistent right aortic arch) or congenital megaesophagus should be sus­pected. Regurgitation is persistent, and affected patients are often malnourished and weak. Dog breeds most commonly affected with vascular ring anomalies include the German shepherd, Irish set­ter, English bulldog, and Boston terrier.Vascular ring anomalies are extremely uncommon in cats.

Idiopathic megaesophagus is the most common cause of regurgitation in dogs, including puppies. Idiopathic megaesophagus is now recognized somewhat more frequently in adults than in young patients. Idiopathic megaesophagus is known to be hereditary in wirehaired fox terriers and miniature schnauzers. A breed predisposition for idiopathic megaesophagus exists for the German shepherd, Great Dane, Irish setter, and golden retriever. Although idiopathic megaesophagus can occur at any age, a later age of onset (8 to 12 years) seems to predominate. A recent study has shown that dogs with acquired megaesophagus and focal myasthenia gravis have a bimodal age of onset of clinical signs, with a younger group of dogs showing clinical signs at 2 to 4 years of age and an older group at 9 to 13 years of age. Although megaesophagus related to focal myasthenia gravis has been reported in a number of breeds, it may be more common in golden retrievers and German shepherds.

Megaesophagus may rarely occur secondary to hypoadrenocorticism. Retrospective studies have shown that hypoadrenocorticism is more common in young to middle-age female dogs (with a majority younger than 7 years of age at the time of diagnosis). Dogs with megaesophagus and hypo­adrenocorticism often present with vomiting and diarrhea, as well as regurgitation.

Nature of Clinical Signs

Regurgitation that begins acutely at a time other than weaning is most often due to an esophageal foreign body. Most esophageal foreign bodies that cause nearly complete or complete obstruc­tion are bones (e.g., steak, chicken, pork chop). If the esophageal lumen is only partially ob­structed, regurgitation may occur only after ingestion of solids. Although an acute onset of regurgitation may also occur as a developing esophageal stricture results in significant narrow­ing of the esophageal lumen, generally there is a more gradual onset over a period of 2 to 3 days, with regurgitation of solids then becoming more persistent.

If regurgitation begins acutely, the owner should be questioned carefully about the possibility of for­eign body ingestion. Frequently owners will relate that a bone was purposely fed or that they observed their pet on a foray into the garbage or saw evi­dence after the fact that the garbage had been invaded. If the patient has been free outdoors, there may be no known history of foreign body inges­tion.

Because a majority of esophageal strictures develop within 1 to 3 weeks of a general anesthetic event, the history should be reviewed carefully regarding any recent anesthetic procedures. In addition, strictures occasionally develop in cats within 1 to 2 weeks after significant difficulty is experienced in vomiting a large hairball and in dogs or cats as a sequela to frequent vomiting. An esophageal stricture may also develop as a sequela to caustic acid or alkali ingestion, foreign body trauma, lodgment of tablet or capsule medication in the esophagus (e.g., doxycycline tablets in cats), and thermal burns.

Most disorders other than vascular ring anomaly, congenital megaesophagus, esophageal foreign body obstruction, and esophageal stricture cause a grad­ual onset of clinical signs. The clinician should inquire about details that might suggest a systemic disorder. Although idiopathic megaesophagus is the most common cause of regurgitation, every effort is still made to identify a potentially treatable cause. Inquiries should be made about potential exposure to toxins such as lead or thallium or exposure to carrion that could cause botulism. Any clinical signs such as weakness, collapse, vomiting, and diarrhea should be discussed, looking for evidence to sup­port a likely diagnosis of such disorders as myasthe­nia gravis, hypoadrenocorticism, polymyositis, or systemic lupus erythematosus.

Physical Examination

Physical examination findings may vary consider­ably. If dysphagia, as well as regurgitation, is present, the same steps in physical examination previously outlined for evaluation of dyspha­gia should be followed (oral examination, exter­nal palpation). Excessive salivation may suggest odynophagia associated with an esophageal foreign body or esophagitis. Many megaesophagus patients are thin and in poor condition. A Heimlich type of maneuver on the thorax or anterior abdomen may produce an externally visible bulge on the left side of the neck resulting from a gas-filled flaccid cervical esophagus. Occlusion of the nostrils with compression of the thorax may also allow visuali­zation of a dilated cervical esophagus. Gurgling sounds and halitosis might result from fermenta­tion of food in a hypomotile esophagus. Thoracic auscultation may reveal pulmonary crackles sec­ondary to aspiration pneumonia. Fever, mucopu­rulent nasal discharge, coughing, and dyspnea also suggest the presence of pneumonia.

Patients with intraluminal esophageal strictures are often normal on physical examination. Other examination findings, such as weakness and/or decreased palpebral reflex (myasthenia gravis), weak­ness and bradycardia (hypoadrenocorticism), muscle pain (polymyositis), and signs that may include joint pain and shifting limb lameness (systemic lupus ery­thematosus), erosive glossitis, and others, often occur with systemic disorders. Cats that regurgitate sec­ondary to an anterior mediastinal mass often have a noncompressible anterior chest cavity. Physical find­ings in cats with Key-Gaskell syndrome, a neuro­logic disorder characterized in part by regurgitation due to megaesophagus, include persistent pupillary dilation, decreased nasal and lacrimal secretions, bradycardia, and constipation.

Diagnostic Studies

Survey radiography of the esophagus is the first and most important step in the diagnosis of a regurgitation disorder. Radiographs are evaluated for evidence of esophageal dilation, presence of a foreign body, or thoracic mass. If survey radio­graphs fail to provide a definitive diagnosis, a barium esophagram should be performed to evaluate the cervical and thoracic esophagus. Barium paste offers the best mucosal coating and should be used to evaluate suspected mucosal or mass lesions. Esophageal dilation is best detected with liquid barium suspension. Liquid barium mixed with food is best for evaluating disorders of motility and examining for esophageal stricture (strictures often allow fluid but not food to pass).

Although young patients with congenital megaesophagus are not usually evaluated with detailed diagnostic tests, patients with acquired megaesophagus should be evaluated as thoroughly as possible. Baseline tests should include a CBC, biochemical profile, serum thyroid hormone analysis, urinalysis, and fecal examination for Spirocerca lupi ova (in endemic areas). Specific tests to evaluate for systemic disorders such as hypo­adrenocorticism (adrenocorticotropic hormone [ACTH] stimulation), systemic lupus erythe­matosus (antinuclear antibody), and myasthenia gravis (acetylcholine receptor antibody titer, Tensilon test) are done if the history, physical examination, or baseline tests indicate that these primary disorders may exist. It is recommended that the acetylcholine receptor antibody titer test be run in any patient with acquired megaesopha­gus because many with focal myasthenia gravis do not show classic signs associated with generalized myasthenia gravis (weakness, collapse). Serum lead levels are indicated if lead toxicity is consid­ered a possibility.

Endoscopic examination of the esophagus (esophagoscopy) is a valuable diagnostic and thera­peutic tool. Endoscopy is most effective in diagnosis of disorders that affect the mucosa (esophagitis, mass lesions, strictures), for retrieval of foreign bodies, in management of esophageal strictures with guided bougienage or balloon dilation, and as an adjunctive step in diagnosis of hiatal hernia. Hiatal hernia is best diagnosed using a combination of contrast radiogra­phy (with fluoroscopy if available) and endoscopy (looking for anatomic and secondary inflammatory changes [esophagitis]). In most patients with mega­esophagus, endoscopic examination is not necessary for diagnosis and is rarely of benefit in determining a cause. Esophageal motility disorders in which clear radiographic evidence of marked esophageal dila­tion is lacking are best recognized by esophageal fluoroscopy and manometry studies. If this equipment is not available, esophagoscopy may be beneficial; in some cases pooling of fluid or mild esophageal dilation can be identified.