Expectoration

Expectoration is the coughing up of material from the lungs or major airways. The material typically is frothy mucus or red blood; bile and food are absent. The characteristic sequence of coughing followed by oral expulsion must be determined from the history or observation. Regurgitation and vomiting typically occur without simultaneous coughing, although regurgitation is often accompanied by tracheitis and aspiration pneumonia. However, a patient that is expectorating may “gag” so hard because of pharyngeal/laryngeal irritation that it eventually vomits.

Regurgitation

Regurgitation is due to oral, pharyngeal, or esophageal dysfunction and is typically characterized as a relatively passive expulsion of esophageal contents. Gagging is the expulsion of oral or pharyngeal material and may be associated with disorders causing dysphagia (i.e., difficult swallowing) or regurgitation. The relatively minor abdominal contractions associated with gagging are typically different than the vigorous abdominal contractions that classically occur with vomiting. Regurgitation may follow seconds to hours after eating or drinking. Patients may regurgitate white foam (i.e., salivary secretions that have been swallowed) and/or food. Regurgitated food material is undigested and sometimes has a tubular form conforming to the shape of the esophageal lumen. Most clients cannot reliably distinguish undigested from digested food. Regurgitated material that has remained in the esophagus for long time periods can appear “partially digested” because it is macerated, odoriferous, and mixed with saliva. If blood is present, it is usually undigested (i.e., bright red), whereas blood originating from the stomach is usually partially digested by gastric acid and has a “coffee grounds” appearance readily distinguishing it from the undigested form (unless the patient vomits before the blood can be partially digested).

It is sometimes difficult to differentiate vomiting from regurgitation via history, and in some patients the processes are concurrent. Vomiting may cause secondary esophagitis and subsequent regurgitation, or a patient with long-standing esophageal disease may develop another concurrent disorder causing vomiting. It is therefore important to clarify the chronologic order of specific signs. Finally, some patients with signs “classic” for regurgitation are vomiting instead. To aid in differentiation, one may attempt to observe the act of expulsion by feeding the patient, although this is very unreliable (“watched” regurgitating patients often do not regurgitate). Watching the patient eat occasionally helps if there is obvious pharyngeal dysphagia that suggests oropharyngeal disease. Some patients with pharyngeal dysphagia also have concurrent esophageal dysfunction. Contrast radiographs and/or fluoroscopy of the pharynx and esophagus can usually differentiate vomiting from regurgitation.

Regurgitation is usually best evaluated by history, physical examination, plain and contrast radiographs, and/or esophagoscopy (Figure 9-1). Contrast radiographs should use barium instead of iodide contrast agents unless esophageal rupture is suspected (e.g., finding air or fluid in the mediastinum on plain radiographs). The main purpose of a contrast esophagram is to distinguish esophageal motility abnormalities from anatomic lesions (e.g., obstruction, mass, inflammation, fistula). Some drugs (e.g., xylazine, ketamine) can cause esophageal hypomotility, making the radiographs potentially misleading. Esophagoscopy is insensitive for diagnosing esophageal muscular weakness but sensitive for finding anatomic lesions, differentiating intramural from extramural obstruction, identifying esophagitis, and removing foreign objects. Patients with acquired esophageal weakness should be evaluated for myopathies, neuropathies, and myasthenia gravis (generalized or localized to the esophagus). Occasionally, hypoadrenocorticism, hyperkalemia, lead poisoning, Spirocerca lupi, and selected central nervous system (CNS) disorders (e.g., distemper, hydrocephalus) may be responsible. Generalized or localized myopathies and neuropathies have several causes (e.g., trauma, dermatomyositis, thymoma, botulism, tick paralysis, systemic lupus erythematosus, nutritional factors, toxoplasmosis, trypanosomiasis). Dysautonomia occurs in dogs and cats, causing generalized dysfunction of the autonomic nervous system producing esophageal hypomotility. It is important to detect underlying disorders so that one may treat the cause rather than just the symptoms. It is also wise to evaluate patients with unexpected esophageal foreign objects (e.g., a relatively small bolus of food) for partial obstructions (e.g., subclinical vascular ring anomaly, stricture).

FIGURE 9-1 Diagnostic approach to chronic regurgitation in dogs and cats. ACTH, Adrenocorticotropic hormone; CBC, complete blood count; CNS, central nervous system; EMG, electromyogram.

Vomiting

Vomiting is a reflex act originating in the CNS that can be stimulated by various conditions. One must consider primary GI disease and non-GI disorders (e.g., metabolic, inflammatory, and toxic conditions) as causes of vomiting. Many vomiting patients have non-GI problems.

Vomiting is classically characterized by prodromal nausea (i.e., salivation, licking of lips) followed by retching or forceful abdominal contractions. Vomiting may occur any time after eating or drinking (seconds to hours). A patient may vomit food, water, fresh blood, or mucus that is indistinguishable from regurgitated material. Bile, partially digested blood (i.e., “coffee grounds”), or expelled material with a pH of 5 or less strongly suggests vomiting as opposed to regurgitation. Vomited duodenal contents may have a pH greater than or equal to 7 and are usually positive for bile. A urine dipstick with a pH indicator is useful in making pH determinations. A patient that has “dry heaves” is typically vomiting as opposed to regurgitating.

Vomiting patients are best divided into those with acute (<2 weeks) versus those with chronic (>2 weeks) vomiting. The most common categories of causes for each are listed in Boxes 9-1 and 9-2. Patients with acute vomiting often spontaneously resolve if they are supported by fluid therapy. A thorough history and physical examination are indicated first. Laboratory evaluation and/or imaging should be considered if the disease is severe or a serious disease (e.g., obstruction) is suspected. If vomiting persists, is progressive, or is attended by other clinical signs (e.g., polyuria-polydipsia [pu-pd], weight loss, icterus, painful abdomen, ascites, weakness, hematemesis), additional testing is indicated (Figure 9-2).

FIGURE 9-2 Diagnostic approach to chronic vomiting in a dog or cat that has been unresponsive to dietary change and anthelmintic therapy. ACTH, Adrenocorticotropic hormone; CBC, complete blood count.

Large Intestinal Disease

Large intestinal disease has different parasites (i.e., Trichuris vulpis, Tritrichomonas fetus), dietary problems (i.e., fiber-responsive diarrhea), and bacterial problems (i.e., so-called clostridial colitis that responds best to tylosin or amoxicillin) than small bowel disease. Once parasitic, dietary, and “clostridial colitis” are eliminated by diagnostics and therapeutic trials, additional diagnostic steps, such as rectal mucosal scrapings (not swabs) with cytologic examination (Figure 9-3) might be appropriate. Persistent large intestinal disease that fails to respond to these therapeutic trials or that is associated with hypoalbuminemia or obvious weight loss is usually an indication for abdominal ultrasound followed by fine-needle aspiration and/or colonoscopy-ileoscopy plus biopsy. Rigid colonoscopy of the descending colon is adequate for diagnosis in most cases. Flexible endoscopy allows access to the descending, transverse, and ascending colon; ileocolic valve; cecum; and ileum. If flexible endoscopy is unavailable, abdominal ultrasonography may reveal lesions in areas not accessible with rigid endoscopy.

FIGURE 9-3 A, A canine rectal scraping showing a macrophage with numerous engulfed yeasts. These are Histoplasma capsulatum. B, A canine rectal scraping that shows inflammatory cells and spherical organisms with a clear halo. The organisms are Prototheca.

(Courtesy of Dr. Rick Cowell.)

Small Intestinal Disease

Small intestinal disease has different parasites (e.g., Giardia), dietary problems (e.g., lymphangiectasia), and bacterial problems (i.e., so-called antibiotic-responsive enteropathy [ARE] or dysbiosis that may respond to a variety of antibacterials) than large bowel disease. Chronic and severe small intestinal diarrhea necessitates differentiation of maldigestion, protein-losing enteropathy (PLE), and malabsorptive disease without protein loss (Figure 9-4). Weight loss and diarrhea are usually present, but some patients only have weight loss.

FIGURE 9-4 Diagnostic approach to chronic diarrhea in dogs and cats in which multiple fecal examination results are negative and empirical anthelmintic, antiprotozoal, and dietary therapy do not resolve the diarrhea. CBC, Complete blood count; ELISA, enzyme-linked immunosorbent assay; EPI, exocrine pancreatic insufficiency; PCR, polymerase chain reaction; TLI, trypsin-like immunoreactivity.