Haematemesis necessitates a slightly different approach than we take with other vomiting cases because some rule-outs become more likely while others become much less likely. We will be including upper gastrointestinal bleeding of any cause in this discussion. For starters, we will not be discussing vomiting that produces “flecks” of blood because this can be seen in any dog (and perhaps cat) with vigorous vomiting in which the gastric mucosa is traumatized by the physical act of vomiting. It is easy to identify fresh blood in the vomited material as long as the patient is not eating something that is red or that produces a pink color to the vomited material simply secondary to pigment leaching out of the food material. Most of the time, haematemesis is denoted by a “coffee-grounds”-like material that most clients (and some veterinarians) do not recognize as blood. A common mistake is being concerned over “dark stools.” Noting that a patient has dark stools is generally useless. Lots of dogs have dark stools and no problems or GI blood loss at all. The color of the stool is not an issue until the stool is pitch-tar-coal-asphalt black. Then it may be melaena (if it is not due to Bismuth or a lot of green bile giving it a near-black appearance). If in doubt, just place some fresh faeces on absorbent white paper and see if a reddish color diffuses out from the faeces, confirming that there is blood present. Melaena is only seen if there is acute loss of a lot of blood into the upper GI tract. Most dogs losing blood in the upper GI tract do not have any important changes in the colour of the faeces. Rather, you might see anaemia and hypoalbuminaemia. Also remember, you may or may not see hypoglobulinaemia; it all depends upon what the serum globulin concentration was before you started losing blood. Sometimes the BUN is higher than expected based upon the serum creatinine, but again this is only expected if there is a lot of blood being lost in a short period of time. Faecal occult blood tests are seldom that helpful or necessary, but can occasionally be informative in confusing cases. However, you need to use a test for which the laboratory has substantial experience in dogs so that the results can be meaningfully interpreted. Some faecal blood tests will routinely give a positive reaction when used on canine faeces.

When there is a substantial amount of blood being ejected from the mouth, there tend to be 3 major reasons: coagulopathy, swallowing blood from elsewhere, and gastrointestinal ulceration/erosion (GUE).

Ulcers and Erosions

Drugs are still a very important cause of GUE in the dog, despite all the newer, “safe” NSAIDs. High doses of dexamethasone also have substantial potential for significant GUE. Prednisolone by itself is generally not ulcerogenic unless it is used in very high doses (e.g., >2–3 mg/lb/day) or is administered to a patient with other “ulcerogenic” risk factors (e.g., hypoxia, poor perfusion), and even then, it is not particularly bad. Combining steroids and non-steroidal drugs can be devastating. You can use ultra-low dose aspirin (0.5 mg/kg once daily) when treating IMHA dogs with steroids.

There continues to be a substantial problem with the use of nonsteroidal anti-inflammatory drugs (NSAIDs) 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, naproxen, flunixin). Ibuprofen is also particularly ulcerogenic in the dog because it undergoes an enterohepatic circulation. Flunixin is a particularly dangerous drug from the standpoint of causing GUE. It is extremely potent and can be devastating if combined with steroids like dexamethasone. While able to cause significant ulceration and bleeding all by themselves, the ulcerogenic potential of NSAIDs is particularly augmented by other factors, especially concurrent administration of another NSAID or a corticosteroid, and hypoperfusion of the alimentary tract. Even though many dogs seemingly tolerate such combination therapy, you need to realize that you are “walking on thin ice” (see comments above on use of ultra-low dose aspirin). Many to most of the dogs treated with NSAIDs have endoscopically visible erosions, haemorrhages and/or ulcers, depending upon the drug used and the dose administered. It is important to note that most dogs with GUE due to NSAIDs may be completely asymptomatic. Finally, there is tremendous between-dog variation regarding the alimentary tract response to NSAIDs; some dogs may almost bleed to death because of a small dose of aspirin while most dogs would tolerate a much larger dose with relative impunity.

While the newer Cox-2 NSAIDs (e.g., carprofen, EtoGesic, deracoxib, meloxicam, etc.) have much less potential for causing GUE than the older NSAIDs, you can still see GUE (and even perforation) due to these drugs. Part of the problem is that these “safe” drugs are being used so extensively and casually. The problem often revolves around using inappropriately high doses (after all, the drug is so safe that...), using the drug at the wrong time (e.g., when the patient is experiencing shock or has poor perfusion to the alimentary tract), and possibly using the drug too soon after stopping some other NSAID. The concept of a “washout” period when changing from one NSAID to another is extremely controversial. There is published literature to the contrary, but the fact is that nobody really knows at this time.

Clinical Approach to the Patient with Haematemesis or GI Bleeding

There is often something in the history that is suggestive of the cause of the bleeding (e.g., use of NSAIDs, shock, etc.). If that is the case, then it is often reasonable to begin appropriate therapy after requesting basic laboratory testing (e.g., CBC, serum chemistry panel) to determine the severity of the bleeding and if there are other diseases (e.g., hepatic disease, renal disease) present. Imaging (especially ultrasound) is typically appropriate but not necessarily imperative at this time. If the cause of the GI bleeding or haematemesis is not obvious, if the patient has not responded to 5–7 days of appropriate therapy, or if the bleeding is severe, then additional diagnostics are important and should be performed promptly.

Medical Management

If the patient is not exsanguinating, the cause is known or strongly suspected, and the patient has not had 5–7 days of appropriate medical therapy, then medical therapy is often reasonable as opposed to doing a major diagnostic work up. In distinction, if the patient is exsanguinating or if the patient has not shown any appreciable response to 5–7 days of appropriate medical therapy for the ulceration, then it is usually reasonable to surgically resect the ulcerated area. Note - when I say “response,” I am not referring to the patient being cured; I am referring to clear evidence of improvement. If surgery will be considered, it is usually very wise to perform gastroduodenoscopy before the surgery to be sure that you find all of the sites of ulceration. It is very easy to fail to detect an ulcer at surgery, and endoscopy usually allows one to easily find all areas of ulceration. Sometimes intraoperative endoscopy is necessary to help the surgeon find the ulcer(s).

If medical management is elected, first be sure to remove the cause of the GUE. If the cause is not removed, medical management tends to be far less successful. Next, be sure that the patient is well hydrated; healing of the gut requires or is at least benefitted by adequate perfusion. 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.

H-2 receptor antagonists are, unfortunately, commonly used. Cimetidine, ranitidine, and famotidine are very poor medications for decreasing the gastric hydrogen ion concentration. Cimetidine (5–10 mg/kg) needs to be given 3–4 times per day if you are really serious about decreasing gastric acid secretion. Famotidine (0.5 mg/kg) only needs to be given once or twice daily. Ranitidine (2.2 mg/kg) is given twice daily, but may cause vomiting if given as an IV bolus. Side-effects of the H-2 receptor antagonists are rare but may include diarrhoea, drug eruption, hyperpyrexia, thrombocytopenia, granulocytopenia, and CNS problems including seizures. I think (?) I have seen a couple of dogs in which ranitidine was responsible for large bowel diarrhoea or seizures.

Proton pump inhibitors are the most effective antacid drugs we have. Omeprazole, lansoprazole, and pantoprazole are the most effective inhibitors of gastric acid secretion we currently have available. In the USA, omeprazole is available OTC as Prilosec®. The dose of omeprazole is 1–2 mg/kg bid. The dose of lansoprazole (Prevacid®), pantoprazole (Protonix®), and esomeprazole (Nexium®) is 1 mg/kg IV (not approved for use in dogs). It generally takes 2–5 days for a PPI to have maximal efficacy; but, the immediate effect on gastric acid secretion is often still better than that obtained by high dose H-2 receptor blockade.

Misoprostol (Cytotec®) is a prostaglandin E analog which was primarily designed to be a prophylactic drug used to prevent GUE due to NSAIDs. It is also useful in treating existing ulcers, but its higher cost and more plentiful side effects usually make it undesirable as a first line therapy for GUE. It is typically used at a dose of 2–5 ug/kg, 3–4 times daily. It can cause abdominal cramping and diarrhoea, but the drug seems relatively safe in dogs. The main disadvantage is that it must be given orally, which is not possible in some vomiting animals. Because it is a prostaglandin analog, it should not be used in pregnant females for fear of causing abortion or miscarriage. It is the best drug available that can be used to prevent NSAID-induced ulceration, but it is not uniformly effective in dogs. The main indications to use it appear to be a) the patient that must have NSAIDs to function, but which evidences side-effects from them (e.g., anorexia, vomiting) and b) the patient that seemingly needs to receive NSAIDs that have substantial potential for such side-effects (e.g., piroxicam).

Sucralfate seems to be extremely effective in protecting those areas which are already ulcerated and helping them heal. 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). While Carafate® is effective in treating ulcers, it is not always effective in preventing ulceration. My major problem with this drug is that it must be given orally, which does not always work in vomiting dogs. The suspension form is probably more effective than the tablet form.