Gastric ulcers happen when the surface layer that lines the stomach (often referred to as the mucosal barrier), becomes disrupted. A variety of disease states and toxins can lead to these focal lesions, which are characterized by the painful disintegration and death of these superficial tissues.
The stomach's mucosal barrier provides a complex mechanism of defense against a) all the potential harm that can befall the body after eating all kinds of foodstuffs and b) the highly acidic environment required to help break these foodstuffs down.
Rough, corrosive, even infectious material is rebuffed by this complex mechanism. Its ability to secrete mucus helps protect it from damage. Meanwhile, tightly knit cells keep harmful elements out and a high rate of blood flow throughout helps it repair itself rapidly when it's compromised.
It's a formidable obstacle, indeed. Which probably explains why gastric ulceration isn't very commonly observed in dogs and cats. Yet should this barrier be breached by injury, disease or drugs, what results is nothing short of a catastrophe: a self-perpetuating cycle of continuous damage fueled by the caustic gastric environment and the body's own inflammatory mechanisms. In fact, complete perforation of the stomach wall with a life threatening loss of blood is not an uncommon sequel to severe ulceration.
In dogs, certain drugs (NSAIDs and corticosteroids, in particular), cancer, and liver disease are the most common causes in dogs. Other conditions correlated with GI ulceration in dogs include kidney disease, Addison's disease, anxiety disorders, primary gastrointestinal diseases (such as inflammatory bowel disease and gastric dilatation volvulus), shock and sepsis. Extreme exercise has also been associated with gastric ulceration, particularly among sled dogs.
Gastric ulceration is even less commonly seen in cats. Cancers like lymphoma and adenocarcinoma are most commonly associated with gastric ulceration in felines.
It's important to note that while Helicobacter organisms (the primary cause of gastric ulceration among humans) have been identified in the gastrointestinal tracts of dogs and cats, their role in gastric ulceration has not yet been determined.
Symptoms and Identification
In dogs, the most common clinical signs observed in gastric ulceration patients include:
Dark, tarry stools
Vomiting, with or without signs of bleeding (bright red blood or partially digested blood that appears as "coffee grounds")
Poor appetite or no appetite
Unlike dogs, cats with gastric ulceration rarely show specific signs like these. They may, however, show signs of life-threatening internal bleeding in the end stages of this disease process.
In the case of severe ulceration, especially if gastric perforation occurs, may present with signs of pain, weakness, pallor, and shock. Sadly, some dogs and cats with GI ulceration never not show any clinical signs at all.
Diagnosis of gastric ulceration is often presumed from clinical signs and laboratory corroboration of blood in the stool or vomitus but can be diagnosed definitively via direct observation with an endoscope or surgical exploration (with or without biopsy and full histopathological examination of the retrieved tissues).
A complete blood count (CBS), biochemistry profile (serum chemistry analysis), and urinalysis are typically employed to help differentiate primary gastrointestinal disease from other causes and can identify secondary problems. Additional testing, including liver function testing or testing for specific diseases, may be helpful as well. X-rays, unfortunately, are not often helpful. Ultrasound can be useful but can't definitively confirm the presence of ulceration.
There is no known breed predisposition for gastric ulceration. Some potentially causative conditions, however, have been associated with a breed predisposition in dogs. Gastric dilatation volvulus, Addison's disease, and inflammatory bowel disease are among these.
Treatment of gastric ulceration may be undertaken via drug therapy. A class of medications referred to as gastroprotectants are commonly employed to help reduce gastric acid production, alleviate inflammation, reduce pain, and generally help the body heal itself.
Emergency surgery may be indicated in cases of suspected or confirmed perforation (or imminent perforation). It's worth noting that the prognosis for gastric perforation patients tends to be poor.
Treatment of the underlying cause, if identifiable, is always crucial to the long-term success of gastric ulcer therapy.
Because definitive diagnosis requires an expensive imaging technique and/or a surgical procedure, the cost of diagnosis can be prohibitive for many pet owners. Typical costs for an endoscopic examination range anywhere from $750 to $1,500.
Surgical exploration alone typically involves costs that are nearly identical to that for endoscopy. However, it's important to note that both diagnostic approaches may prove far more expensive should the need for biopsy and/or definitive treatment arise. Upwards of $5,000 is not unusual for the surgical management of gastric perforation, for example.
The cost of treatment depends greatly on the severity of the disease. If medical management is considered sufficient and hospitalization isn't required, expenses are likely to remain under $500 to $1,000 for an acute episode. However, the reality is that because many of these patients aren't identified until they're very, very sick, few patients fall under this category.
Treatment of causative diseases can prove very expensive as well. Their expenses may be considered separately under articles describing these disease entities, their treatments, and their costs.
Prevention isn't generally considered a feature of this particular disease's overall landscape. Except for cases in which pets are accidentally exposed to gastric ulcer-causing medication, in which careful safekeeping of drugs can prevent the effects of overdose, prevention isn't possible.
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Lascelles BD, Blikslager AT, Fox SM, et al. Gastrointestinal tract perforation in dogs treated with a selective cyclooxygenase-2 inhibitor: 29 cases (2002-2003). J Am Vet Med Assoc 2005;227(7):1112-1117.
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