The primary clinical sign of gastritis is generally considered to be vomiting, but a substantial number of patients evidence anorexia. If the patient is throwing up, you must first attempt to distinguish vomiting from regurgitation based upon history and physical examination. Prodromal nausea is commonly found with vomiting. 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. Retching follows prodromal nausea and is characterized by forceful, abdominal contractions. The material the animal expels sometimes help us distinguish what is going on. So called "undigested" material can be either vomited or regurgitated. Mucus can come from either the salivary glands or the stomach. Red blood can be seen with either, but semi-digested blood that looks like coffee grounds is only seen with vomiting. By the way, this 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. The amount of material ejected from the mouth varies, as does the timing of the episode relative to eating.
Gastric foreign objects are a common cause of vomiting, and they occasionally cause gastritis. However, the mere presence of a foreign object in the stomach does not guarantee that it is causing clinical signs, much less gastritis. Dogs can have foreign objects in their stomachs for months without any clinical signs. If you remove a foreign object with endoscopy, be sure to radiograph the patient immediately before the procedure because some objects will sit in the stomach (or for that matter, in the small intestines) for days and "decide" to move the night before you do the endoscopy.
You cannot rely on CBC's or imaging to detect gastric inflammation; you need biopsies in order to make this diagnosis. There are numerous causes, and many cases or idiopathic. One "fashionable" cause is Helicobacter. Gastric spirochetes were first discovered in the gastric mucosa of animals and people before the turn of the century. Helicobacter pylori is responsible for most of the peptic ulcers diagnosed in people, as well as non-ulcer dyspepsia and cancer. Helicobacter pylori has been shown to cause an infiltrate in people that is so severe that is has been misdiagnosed as gastric lymphosarcoma. Histopathology is more than adequate for diagnosis. Cytology is a bit more sensitive than biopsy. Treatment has involved a variety of combinations of drugs. The classic triple therapy (metronidazole, bismuth subsalicylate, and tetracycline for 2 weeks) used in people does not appear to be necessary for dogs and cats because dogs and cats are infected with Helicobacter species other than H. pylori. Therefore a much less aggressive therapy is usually satisfactory in dogs and cats. Famotidine (0.5 mg/kg bid), amoxicillin (10 mg/lb bid), and metronidazole (10-15 mg/kg bid) for 12-14 days is likely to be effective; however, re-infection or recrudescence seems to be very common. Because of our inability to look at a gastric biopsy and determine if the bacteria are responsible for the clinical signs, our current approach is to first determine if there are any other potential causes for the vomiting in the patient. If there is another potential cause that looks as or more likely to be causing the vomiting, we often treat it first. If this treatment does not work or if there is no other identifiable cause of vomiting, then one may treat for gastric Helicobacter and see if the patient responds. I believe it is also reasonable to treat vomiting dogs and cats for Helicobacter gastritis before proceeding with more aggressive diagnostics such as endoscopy. However, if the animal is particularly ill or is losing a lot of weight, I recommend the diagnostics first.
Focal gastritis is an uncommon condition in which failure to do a complete and thorough gastroscopic evaluation will result in your missing the lesion. We have seen cats that have obviously abnormal gastric mucosa just inside the lower esophageal sphincter. The rest of the gastric mucosa is grossly and histologically normal. You can also find very focal lesions of gastritis in other parts of the stomach.
Hematemesis generally means that gastrointestinal ulceration/erosion (GUE) is present, although coagulopathies are rarely the cause. Ulceration/erosion is a hallmark of gastritis. The most common causes of GUE appear to be mast cell tumor, drug administration (especially NSAIDs), "stress" (i.e., gastric ischemia/hypoxia), and inflammatory or neoplastic infiltrates.
Drugs are a very important cause of GUE in the dog. While there is some controversy whether all corticosteroids are ulcerogenic, most clinicians agree that high doses of dexamethasone have the potential for significant gastric erosion. Prednisolone by itself is not generally ulcerogenic unless it is used in very high doses (e.g., > 2-3 mg/lb/day) or is administered to an anemic animal with hypoxic tissues. However, there is no doubt about the danger of nonsteroidal anti-inflammatory drugs in dogs. All NSAIDs have the potential to cause devastating GUE, and some of these non-steroidal drugs are renowned for their toxic effects (i.e., indomethacin and naproxen). Ibuprofen is particularly ulcerogenic in the dog because it undergoes an enterohepatic circulation. While the newer Cox-2 NSAIDs (e.g., carprofen, etogesic, deracoxib [i.e., Deramaxx]) seem to have much less potential for causing GUE than the older NSAIDs, you can still see GUE due to these drugs if you used excessive amounts or use the drug at the wrong time (e.g., when the patient is experiencing shock or has poor perfusion to the alimentary tract). Deracoxib in particular seems to have a higher than anticipated incidence of gastric ulceration/erosion associated with its use. There is tremendous between-dog variation regarding the alimentary tract response to NSAID's.
Hepatic failure seems to be another important cause of ulceration/erosion in the dog. Anytime I have a dog with hepatic disease that suddenly becomes clinically worse (especially if it becomes encephalopathic), I look for GUE. Bleeding into the intestine counts as a high protein meal and predisposes to hepatic encephalopathy in these patients. Hepatic disease may cause disseminated intravascular coagulopathy which can cloud the picture when trying to determine the cause of hematemesis.
If the patient is not exsanguinating and has not had 5-7 days of appropriate medical therapy, then medical therapy is typically indicated. Adequate fluid therapy is important in the dehydrated or poorly perfused patient because mucosa probably cannot heal well if it is not well perfused. If there is significant gastroduodenal reflux of bile, metoclopramide or cisapride may be helpful in preventing bile from entering and/or staying in the stomach and augmenting the ulcerogenic process.
Cimetidine, ranitidine, and famotidine are good medications for decreasing the gastric hydrogen ion concentration. Ranitidine and nizatidine also have prokinetic activity, which may help some patients. Omeprazole and lanosprazole are the most effective inhibitors of gastric acid secretion we have available. Omeprazole is available as Prilosec®. It is from a class of drugs called proton pump inhibitors (PPI). The dose of omeprazole is 0.7-1.5 mg/kg sid, although I have often used it at up to 2 mg/kg bid in patients with severe reflux esophagitis or gastrinomas. Very rarely, an H-2 receptor antagonist will work better than omeprazole.
Sucralfate seems to be extremely effective in protecting those areas which are already ulcerated; the only common side-effect is constipation. There is minimal absorption from the intestines, but it does have the capacity for adsorbing other drugs (e.g., enrofloxacin, cimetidine). While Carafate is effective in treating ulcers, it is not always effective in preventing ulceration. In patients with severe hematemesis and anemia, we sometimes us a large "loading" dose (e.g., 3-6 grams) initially and then decreasing the dose to 1 gram tid to qid.
There is no evidence that using an H-2 receptor antagonist and Carafate simultaneously will improve results, but it is a common practice. Be sure to stop administering Carafate 1-2 days before performing endoscopy, or it may be very hard to adequately examine the gastric mucosa and find erosions and ulcers.
If the patient does not clearly show improvement after 6-8 days of excellent therapy with H-2 receptor antagonists and Carafate, then you need to determine whether a) the underlying cause is still present or b) the ulcer is so severe that it must be cut out. If surgery is being considered, it is preferable to scope the animal first. Even if you know you will cut the ulcer out (e.g., the animal is exsanguinating despite your medical therapy), it helps immensely to know exactly where the ulcer is. I have had to do endoscopy during surgery to show some excellent surgeons where some very large ulcers were--it can be that hard to find an ulcer from the serosal surface.
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