V156- Hematemesis and GI Bleeding

80th Western Veterinary Conference
V156
Hematemesis and GI Bleeding
Michael Willard
Texas A&M University
College Station, TX, USA
OBJECTIVES OF THE PRESENTATION

The attendee will know the main causes of hematemesis as well as GI blood loss.

The attendee will know the major diagnostic steps and the common mistakes in patients with GI
blood loss.

The attendee will know things that look like GI blood loss that are not GI at all.
GENERAL KEY POINTS

It is common to miss hematemesis if the blood is semi-digested.

Many animals with upper GI blood loss do not have hematemesis.

Melena is rare, even when there is GI blood loss.

Respiratory hemorrhage can look just like GI blood loss.

Hypoadrenocorticism can cause major GI blood loss.

Dogs can have major GI hemorrhage and no clinical signs at all.
KEY CLINICAL DIAGNOSTIC POINTS

Gastroduodenoscopy is a key diagnostic tool; it is much more sensitive than surgery in finding the
source of gastric bleeding.

Don’t give carafate before doing endoscopy.

If gastroduodenoscopy shows nothing, it may be very valuable to look in the trachea and in the
choana to see if bleeding is originating there.

It is reasonable to do endoscopy if surgery did not find anything.
KEY ETIOLOGIC AND PATHOPHYSIOLOGIC POINTS

The new COX-2 NSAIDs are “safer”, but that is not the same word as “safe”—they can cause severe
GI hemorrhage.

Dexamethasone is an important cause of GI hemorrhage, but prednisolone is a very rare cause
unless there are additional “stressors”.

Liver disease can cause significant gastric bleeding.

Severe stress causes GI erosions and ulcers.
KEY THERAPEUTIC POINTS

It is hard to treat ulcers medically if you do not get rid of the cause.

H-2 receptor antagonists and proton pump inhibitors are good at treating ulcers, but are not nearly
as effective at preventing ulcers, especially from NSAIDs and dexamethasone.

Misoprostol is not as effective in dogs and cats for the prevention of NSAID-induced ulcers as it
appears to be in people.

Misoprostol will cause cramps and diarrhea and abortion.

If medical management does not show some evidence of benefit within 5–6 days, you need to
seriously consider resecting the ulcers, but do endoscopy first so you know how many there are and
where they are.
KEY PROGNOSTIC POINTS

If you get rid of the cause, the prognosis with medical management is excellent. If you cannot get
rid of the cause, the prognosis is very guarded.

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OVERVIEW OF THE ISSUE
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 simple secondary
to pigment leaching out of the food material. Most of the time, hematemesis is denoted by a “coffee-
grounds”-like material that most clients (and some veterinarians) do not recognize as blood. In like
manner, we will not discuss hematochezia; rather, we will discuss melena and occult GI bleeding. 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 melena (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 feces on
absorbent white paper and see if a reddish color diffuses out from the feces, confirming that there is
blood present. Melena is only seen if there is acute loss of a lot of blood. Most dogs losing blood in the
upper GI tract do not have any important changes in the color of the feces. Rather, you will see anemia
and hypoalbuminemia. Also remember, you may or may not see hypoglobulinemia; it all depends upon
what the serum globulin concentration was before you started losing blood. Fecal 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 fecal blood tests will routinely give a positive reaction when used on
canine feces.
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).
Coagulopathies: Most coagulopathies cause concomitant bleeding from the nose or accumulation of
blood in body cavities or petechia. However, there are many cases in which the only sign of a systemic
coagulopathies is GI bleeding. Therefore, it is always appropriate to check the platelet count and some
measure of clotting factor adequacy in animals with hematemesis or GI blood loss. While coagulopathies
are a relatively uncommon cause of GI bleeding compared to ulceration/erosion, they can have
devastating consequences if not diagnosed promptly. In particular, remember that some cats with
intestinal disease will malabsorb vitamin K to the point of having vitamin K-responsive coagulopathies.
Also remember that just because the patient did well during a surgical procedure a few days before the
current bleeding episodes does not mean that a coagulopathy is impossible; sometimes the prior surgical
procedure apparently depletes the limited amounts of coagulation factors in patients with subclinical
coagulation defects, causing them to become clinical after the procedure.
Ulcers and erosions: Gastritis due to any number of causes typically has some degree of GUE
present. We will not discuss this cause too much since most of these cases quickly and spontaneously
resolve. Helicobacter is an extremely important cause of GUE in people, but to date has not been shown to
have a cause-and-effect relationship with GUE in dogs and cats. There are often incredible numbers of
Helicobacter found in ulcer craters; however, Helicobacter can be found in ulcers caused by almost
anything. Therefore, it seems likely that the Helicobacter are there because a) they are found in most dogs
and cats and b) the ulcer crater is an opportune place for them to grow. Renal disease is often named as a
cause of gastric ulceration, but this is quite rare.
The most common causes of chronic, unresolving GUE that are also the easiest to check for are mast
cell tumor, drug administration and “stress”.
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 (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, but this only works because
the NSAID is being used at such a low dose.

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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 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, hemorrhages 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 NSAID’s; 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 due to these drugs. Part of the
problem is that these “safe” drugs are being used so extensively and casually that it is hard to imagine
side effects not occurring. In particular, it appears that 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 possible using
the drug too soon after stopping some other NSAID. While controversial, it appears that it might be
necessary to have a washout period between stopping one NSAID and starting one of the newer Cox-2
NSAIDs. There is published literature to the contrary, but this is an area that bears additional work.
Stress, when mentioned as a cause of ulcers, specifically refers to substantial decrease in visceral
perfusion (e.g., hypovolemic shock, neurogenic shock, Systemic Inflammatory Response Syndrome) that
is typically obvious from history and/or physical examination; or, it can refer to extreme exertion (e.g.,
sled dogs running in subzero weather for 100 miles).
Mast cell tumors may look like any skin lesion. In particular, they can perfectly mimic the
appearance and feel of lipomas, such that the only way to distinguish them from lipomas is by aspirate
cytology. When these tumors degranulate, they release histamine which if of sufficient magnitude can
cause gastric acid hypersecretion. This can result in severe ulceration, especially just inside or just beyond
the pylorus.
Hepatic failure seems to be another important cause of GUE in the dog. Anytime a dog with
hepatic disease suddenly becomes clinically worse (especially if it becomes obviously encephalopathic),
you should consider the possibility of GUE. Bleeding into the intestine counts as a high protein meal and
predisposes to hepatic encephalopathy in these patients. In ill patients that cannot be scoped, aggressive
therapy with famotidine and/or carafate is reasonable. Hepatic disease may cause disseminated
intravascular coagulopathy which can cloud the picture when trying to determine the cause of
hematemesis.
Gastric tumors may cause bleeding. The leiomyoma and leiomyosarcoma in particular may cause
especially dramatic bleeding due to their propensity to ulcerate. This is especially important because this
tumor is often curable with surgery, as opposed to lymphomas and carcinomas that are more common,
have less dramatic signs, seldom cause GI blood loss and yet have a much worse prognosis.
Unfortunately, it can be hard to adequately image the stomach with ultrasound, and these masses can be
missed if there is blood, ingesta and/or air in the stomach.
Surgery can be responsible for GI bleeding. If the closure is done improperly and the mucosa does
not cover the defect, then bleeding can easily result.
Hypoadrenocorticism may be responsible for severe hematemesis that can produce life-threatening
shock. Such severe hematemesis appears to be a rare complication of hypoadrenocorticism, but should be
considered in cases with appropriate history, CBC and/or serum biochemistry changes, as well as
patients that do are not readily diagnosed with other causes.

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Inflammatory bowel disease has been reported to be associated with GUE, especially in the dog.
Right now, the definition of IBD is under scrutiny, but at any rate it appears IBD is not commonly
associated with GUE. However, when idiopathic GUE is found during endoscopy, the stomach and
duodenum should be biopsied.
Heavy metal intoxication causes hematemesis, but this is fortunately uncommon at this time.
Gastrinomas are typically small pancreatic tumors which produce large quantities of gastrin, a
hormone which causes gastric acid secretion. Multifocal duodenal ulceration/erosion is very suggestive
of this tumor, as is a large ulcer just past the pylorus (as for mast cell tumors). Gastric erosions are
sometimes seen, but gastric ulcers appear to be rare in this disorder. GI bleeding is not particularly
common in these patients although it is possible. Since the gastric mucosa is stimulated to grow,
ulceration typically occurs in the duodenum instead of the stomach. Esophageal ulceration may also
occur if there is gastroesophageal reflux of the highly acidic gastric contents. Measurement of serum
gastrin concentrations may be diagnostic. However, anything which causes gastric distention or renal
failure can produce increased fasting serum gastrin concentrations. Treatment with H-2 receptor
antagonists has been rewarding, although unexpectedly large doses or the more potent proton-pump
inhibitors (e.g., omeprazole) may be necessary.
Foreign objects get a lot of press as causes of GUE, but in fact they are relatively uncommon causes.
However, they are particularly important in patients that have GUE because even the most innocuous of
GI foreign objects (e.g., paper, small piece of soft cloth) can sometimes prevent a pre-existing ulcer from
healing. They typically need to be removed in patients with GUE.
Ingesting blood: This is a possibility that is typically forgotten. However, it is surprisingly easy to
have bleeding pulmonary lesions in which the blood is coughed up, swallowed, and later vomited. In
most of these cases, the client does not report coughing (perhaps because the hematemesis “wipes” all
else from their mind). In like manner, we have seen cases in which blood was trickling from the choana
into the pharynx and being swallowed, and yet the patient had no history of sneezing or coughing or
nasal discharge.
Cats are rare diagnosed with gastric ulceration/erosion. When a cat is found to have gastric
ulceration/erosion, it is usually caused by lymphoma. However, we many times never determine the
cause in cats.
Clinical Approach to the Patient with Hematemesis 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
hematemesis 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.
Diagnostic Approach
First, as stated above, it is wise to first eliminate coagulopathy with a platelet count and some measure of
clotting factor adequacy. I typically request PT and PTT, but a mucosal bleeding time is a very useful
screening test in these patients. Sometimes there is both a mucosal defect and a coagulopathy. In
particular, if ehrlichiosis is possible, one must consider the possibility that the patient has what would
normally be an insignificant mucosal defect but which is bleeding because of the effects of Ehrlichia spp.
upon platelet numbers and their function. After coagulopathy has been eliminated, then imaging should
be done if it has not already occurred, and ultrasound is especially important as it may reveal masses that
can be aspirated percutaneously, thus avoiding the need for endoscopy/surgery.
If these tests have not revealed the diagnosis, then gastroduodenoscopy is generally performed
next. The specific reasons to do gastroduodenoscopy in a patient with GI bleeding are to:
1.
Determine if this is a case in which surgery can remove a defined number of ulcers (this is for cases
that are bleeding and have not responded to medical management or cases that are bleeding so
badly that one cannot wait on medical management). In these cases, it is important to be sure that

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bleeding is not due to widespread erosions that cannot be cured surgically. There is no relationship
between the size of the mucosal defect and the amount of bleeding; patients with lots of small
erosions often bleed as bad or worse than patients with ulcers. It is also important to determine the
number and location of such ulcers as they may be hard to find during a gastrotomy.
2.
Determine if there is a gastric tumor or some other infiltrate in a patient with GUE that is non-
responsive to appropriate therapy.
3.
Determine the cause in a patient with GUE and no apparent cause on the history, physical
examination, or routine blood work.
4.
Look for a cause of bleeding in a patient with GI blood loss of unknown cause.
It is important to note that endoscopy will not generally allow one to determine if an ulcer will or
will not respond to medical management. Only treating and observing the patient will accomplish that.
It is important to not give carafate within 24–36 hr before endoscopy because it will cover the
lesions and make evaluation more difficult. It is best if food has been withheld for at least 24 hours. Avoid
prokinetics (e.g., metoclopramide). Endoscopy of these patients may be difficult is there is substantial
blood present in the stomach. Patience is necessary to flush in water and then aspirate it and the blood
over and over again. It is important to be able to view as much of the gastric mucosa as possible. In some
cases, there are lots of huge blood clots that cannot be removed endoscopically, in which case surgery
might be necessary. It can be especially easy to miss ulcers that are in the pylorus. The pylorus is typically
infiltrated and inflamed, making it more difficult to pass the tip of the scope through that area. Therefore,
the endoscopist often does not obtain a good view of this area. One may have to go in and out of the
pylorus multiple times to be sure that there is or is not a lesion present. If a cause of upper GI bleeding
cannot be found in the stomach or duodenum, strong consideration should be given to examining the
trachea, bronchi, and choana while the patient is anesthetized. Patients with hematochezia may benefit
from colonoileoscopy, but patients with hematemesis or melena rarely benefit from lower endoscopy.
If there is substantial upper GI blood loss and these tests do not allow diagnosis, then exploratory
surgery is the next step. However, it is very easy to not be able to find the cause of the bleeding in these
patients, so warn the owner before doing the procedure.
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. 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 commonly used. Cimetidine, ranitidine, and famotidine are good
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. However,
famotidine (0.5 mg/kg) only needs to be given once or twice daily. In most patients, cimetidine is more
than adequate to allow healing of gastric ulcers. However, the over the counter (OTC) preparations are all
oral and some patients are vomiting so vigorously that they must receive parenteral medication.
Ranitidine (2.2 mg/kg) is usually effective if 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 diarrhea, drug eruption,

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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 diarrhea or seizures. The
primary value of the H-2 receptor antagonists is in treating existing ulcers and erosions. They can be
helpful in preventing some types of ulcers, but this is not true with all types of ulcers (e.g., they are not
effective in preventing ulcers due to NSAIDs or due to steroids).
Proton pump inhibitors are the most effective antacid drugs we have. Omeprazole and
lansoprazole are the most effective inhibitors of gastric acid secretion we have available. Omeprazole is
available as Prilosec®. The H-2 receptor antagonists seem quite adequate for GUE except in some animals
with gastrinomas and those with esophagitis due to gastroesophageal reflux: these seem to be the main
reason for using the PPI’s. The dose of omeprazole is 0.7–1.5 mg/kg qd, although I have often used it at
up to 2 mg/kg bid in patients with severe reflux esophagitis or gastrinomas. It takes 2–5 days for a PPI to
have maximal efficacy after oral administration; therefore, you will sometimes start with an H-2 receptor
antagonist while waiting for the PPI to attain maximal efficacy. Very rarely, an H-2 receptor antagonist
will work better than omeprazole; be prepared to experiment in your difficult cases. Lansoprazole and
pantoprazole may be given IV at 1 mg/kg. They are not approved for use in dogs; this is anecdotal
information.
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 diarrhea, 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 NSAID’s to function, but which evidences side-effects from
them (e.g., anorexia, vomiting) and b) the patient that seemingly needs to receive NSAID’s 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. 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. My major problem with this drug is that it must be given orally,
which does not always work in vomiting dogs. Sometimes you may dissolve the table in water or buy the
suspension and have less problem with that being vomited.
KEY DRUGS, DOSAGES AND INDICATIONS
Key Drug
Drug Class
Dose Range Frequency Route
Indications
Famotidine
H-2 receptor
0.5 mg/kg
1–2X per day
IV, SQ,
Treatment of erosions
antagonist
PO
and ulcers
Omeprazole
Proton pump
0.7–1.5 mg/kd
Once daily
PO
Treatment of erosions
inhibitor
and ulcers
Lansoprazole Proton pump
1 mg/kg
Once daily
IV
Treatment of erosions
inhibitor
(anecdotal)
and ulcers
Carafate
Coating agent
0.5–1
1–3 times per
PO Treatment
of
erosions
gram/animal
day
and ulcers

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SUMMARY

GI blood loss is a common problem in dogs, but many dogs do not show signs until it gets to be
very severe.

Endoscopy is the most important and valuable diagnostic tool, but you should do ultrasound first.

Remember that the respiratory tract can be the cause of what appears to be GI hemorrhage.
REFERENCES
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safety of short-term concurrent administration of meloxicam and dexamethasone in healthy dogs: Am J Vet Res
2003; 64: 1369–1375.
3. Davis MS, Willard MD, Nelson SL, et al. Efficacy of omeprazole for the prevention of exercise-induced gastritis in
racing alaskan sled dogs: J Vet Int Med 2003; 17: 163–166.
4. Hinton LE, McLoughlin MA, Johnson SE, et al. Spontaneous gastroduodenal perforation in 16 dogs and seven
cats (1982–1999): J Am Anim Hosp Assoc 2002; 38: 176–187.
5. Neiger R, Gaschen F, Jaggy A. Gastric mucosal lesions in dogs with acute intervertebral disc disease:
characterization and effects of omeprazole or misoprostol: J Vet Int Med 2000; 14: 33–36.
6. Rohrer CR, Hill RC, Fischer A, et al. Gastric hemorrhage in dogs given high doses of methylprednisolone sodium
succinate: Am J Vet Res 1999; 60: 977–981.
7. Rohrer CR, Hill RC, Fischer A, et al. Efficacy of misoprostol in prevention of gastric hemorrhage in dogs treated
with methylprednisolone sodium succinate: Am J Vet Res 1999; 60: 982–985.
8. Hanson SM, Bostwick DR, Twedt DC, et al. Clinical evaluation of cimetidine, sucralfate and misoprostol for
prevention of gastrointestinal tract bleeding in dogs undergoing spinal surgery: Am J Vet Res 1997; 58(11): 1320–
1323.

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