Esophageal inflammation is a relatively common malady that is often misdiagnosed. The clinical signs can be vague, and failure to diagnose it in a timely fashion can lead to severe stricture formation with a guarded prognosis.
Distinguishing Vomiting from Regurgitation
Regurgitation occurs when there is either an anatomic obstruction or a physiologic weakness in the esophagus. In either case, food is retained in the esophagus and, if it passively migrates back into the oropharynx, can be regurgitated. The problem should be diagnosed quickly in an attempt to solve it before the esophagus becomes irreversibly-dilated or the patient experiences an aspiration pneumonia.
First, be sure to try to distinguish vomiting from regurgitation. We usually start doing this by considering the history and physical examination. This can be hard to do, and the following are guidelines only - some animals that clearly appear to be vomiting are in fact regurgitating and vice-verse. In particular, it is very easy for a vomiting dog to appear to be regurgitating. However, these guidelines are still useful and usually point us in the correct direction.
Prodromal nausea is commonly found with vomiting. Since vomiting is a centrally-mediated response, other signs such as salivating, discomfort and "gurgling" stomach are often seen beforehand. Many animals that are about to vomit will pace, whine or show some sort of anxiety or discomfort. With regurgitation the animal may be sitting and suddenly "gag" up some material. In general, animals know that they are going to vomit, but they are often unaware that they are going to regurgitate until they actually start doing it. Sometimes the regurgitation is as much a surprise to them as it is to the client. These are not absolutes - animals don't always read the book.
Retching typically follows prodromal nausea and is characterized by forceful, abdominal contractions in animals that are vomiting. (You will see some abdominal contractions with regurgitation but they are not severe or forceful and they do not tend to be repetitive.) If you're not sure what retching is like, just think back to the last time you had to vomit. Don't just ask owners "Did the animal retch?" because they may consider any contractions of the abdomen to be retching. Clearly describe precisely what you mean so that they can give you an accurate answer.
The material the animal expels sometimes help us distinguish what is going on. If possible, let the client describe the material first so they're not just agreeing with you to make you happy. So-called "undigested" material can be either vomited or regurgitated. If it is digested, then this would indicate that the material came from either the stomach or intestines; however, it can be very difficult or impossible to visibly differentiate undigested material that was chewed up, mixed with mucus and saliva and has been sitting in the esophagus for a long time from digested material.
Mucus can come from either the salivary glands (i.e., the regurgitating animal) or the stomach (i.e., the vomiting animal).
Red blood can be seen with either vomiting or regurgitation, but semi-digested blood that looks like coffee grounds is only seen with vomiting. However, finding digested blood does not ensure that the bleeding originated in the stomach.
Bile indicates that the material is from the stomach or intestines. Bile is a green, yellow or dark brown color. Don't just ask if the animal is vomiting bile; many clients assume that vomitus contains bile (i.e., my animal "vomited", therefore it must have vomited bile). Clearly describe what you mean by "bile".
The amount of material ejected from the mouth varies from large to small with both vomiting and regurgitation. Likewise, the timing of the episode relative to eating can vary from immediately after eating to 1½ days after the last meal, regardless of whether the animal is vomiting or regurgitating. Don't forget that you can regurgitate mucus even though you have not eaten for days.
If you are still confused as to whether the patient if vomiting or regurgitating, the most definite method of distinguishing vomiting from regurgitation usually consists of performing plain thoracic radiographs, possibly followed by a barium contrast esophagram. There are some causes of regurgitation that will be missed by such studies, but they are far and few between.
Physical examination may also help distinguish vomiting from regurgitation. Occasionally the esophagus is so dilated and flaccid that it can be seen expanding and collapsing near the thoracic inlet as the animal breathes (much like a bellows). A particularly nice trick is to test the expelled material with a urine dipstick. If the pH of the material that the animal spit out is ≤ 5 or if bile is present, then the material has been vomited. Otherwise, it has probably been regurgitated. Do not trust the reaction for blood. It is invariable positive and does not help distinguish vomiting from regurgitation.
Esophagitis causes muscular weakness by interrupting the reflex arcs within the esophagus and/or between the esophagus and the brain. Severe esophagitis may be caused by anesthetic procedures in which animals are placed in dorsal recumbency and then have gastric acid pool in their esophagus for relatively long periods of time. However, gastroesophageal reflux from any cause can be responsible. Hiatal hernias occasionally are responsible for such reflux. Rare animals ingest caustic substances (e.g., lye), and some cats will like caustic disinfectants off their fur. However, a surprisingly large number of animals are administered caustic substances by veterinarians - specifically tetracyclines, NSAIDs, ciprofloxacin, and clindamycin. Pills and capsules are notorious for lodging in the esophagus of cats, and it is therefore not surprising that doxycycline is a recognized cause of esophageal stricture in cats. Esophagitis may also be secondary to any cause of protracted vomiting. In particular, parvovirus enteritis may cause such intense vomiting that esophagitis results. If a vomiting animal has the character of its vomitus change, which seems to suggest regurgitation, consider the possibility that esophagitis has occurred secondary to the persistent vomiting. Gastrinoma (a tumor which secretes gastrin and results in massive gastric acid secretion) also causes esophagitis because of the vast and unending amounts of acid the esophagus is exposed to as the dog continually vomits. Gastroesophageal reflux may be potentiated by or even caused by esophagitis (which may be caused by reflux in the first place). Thus, there may be a positive feedback loop which can be hard to break (i.e., esophagitis causes more reflux which causes more esophagitis which causes more reflux which causes ...). Barium esophagrams do not always reflect the severity of the esophagitis while esophagoscopy typically shows an edematous, reddened, bleeding esophageal mucosa, ± structure formation. Esophagoscopy is the diagnostic method of choice to find esophagitis.
You should seek to prevent further gastroesophageal reflux by keeping the stomach as empty as possible by using prokinetics such as metoclopramide or, preferably, cisapride. Studies in people show that cisapride is clearly more effective than metoclopramide. The only real advantage of metoclopramide is that it can be given by injection; a useful fact in animals that are regurgitating profusely. In addition, gastric acid secretion should be minimized and preferably abolished. H-2 receptor antagonists (e.g., cimetidine, ranitidine, famotidine) suppress gastric acid secretion, but they do not eliminate it. This is because they are competitive inhibitors. That means that there is constantly some degree of competition between the H-2 receptor antagonists and the stimuli for acid secretion. Omeprazole, lansoprazole and pantoprazole are non-competitive inhibitors of gastric acid secretion. Therefore, these drugs can be noticeably more effective and can cause near gastric anacidity. You can try to achieve greater efficacy with the H-2 receptor antagonists by doubling or tripling their dose.
A combination of omeprazole and cisapride seems to be the most effective medical treatment regime. Antibiotics are used to treat secondary infections, but nobody really knows if they do anything in this regard. Glucocorticoids have been thought to help retard fibrous connective tissue proliferation and cicatrix, but their effectiveness is uncertain (and they might predispose to infection). Placing a PEG tube seems to have some real advantages in patients with very severe disease. First, we will then know that the cisapride and omeprazole tablets will reach the stomach. Second, we will also know that the animal will receive its caloric and protein needs, and hopefully with less irritation to the esophagus than would have occurred otherwise.
If there is severe esophagitis, cicatrix may form and obstruction develop subsequently. Diagnosis of stricture is best accomplished by esophagoscopy IF the operator is familiar with such obstructions. It is surprisingly easy to pass a slender endoscope through a stricture and never recognize the stricture. It is also surprisingly easy to miss a partial obstruction due to a stricture with a barium esophagram. If you suspect a stricture and must use a barium esophagram to make the diagnosis, use barium mixed with solid food. Balloon-dilatation or bouginage is recommended if a stricture has occurred. Many animals need to have 2–6 dilatation procedures (all the while being treated for esophagitis), although some only need one procedure and some need more than 15. Do not try to resect the stricture unless you have had prior dilatation procedures fail.
1. Bissett SA, Davis J, Subler K, et al. Risk factors and outcome of bougienage for treatment of benign esophageal structures in dogs and cats: 28 cases (1995–2004). J Am Vet Med Assoc 2009;235:844–850.
2. Gualtieri M, Olivero D. Reflux esophagitis in three cats associated with metaplastic columnar esophageal epithelium. J Am Anim Hosp Assoc 2006;42:65–70.
3. Panti A, Bennett RC, Corletto F, et al. The effect of omeprazole on oesophageal pH in dogs during anaesthesia. J Small Anim Pract 2009;50:540–544.
4. Sellon RK, Willard MD. Esophagitis and esophageal strictures. Vet Clin N Am 2003;33:945–967.
5. Wilson DV, Walshaw R. Postanesthetic esophageal dysfunction in 13 dogs. J Am Anim Hosp Assoc 2004;40:455–460.