Table 67-3 DRUGS USED FOR TREATMENT OF GASTRIC DISEASE

Chapter 67 Diseases of the Stomach

Susan E. Johnson, Robert G. Sherding, Ronald M. Bright

VOMITING

Vomiting is a common clinical sign associated with many gastrointestinal (GI) and non-gastrointestinal (non-GI) disorders of dogs and cats. Vomiting is a central nervous system reflex that is integrated in the vomiting center of the brain stem. Afferent stimuli can originate from the cerebral cortex, chemoreceptor trigger zone, pharynx, peritoneum, or abdominal viscera. Vomiting must be differentiated from regurgitation, which is the passive expulsion of undigested food indicating a pharyngeal (swallowing) or esophageal disorder (see Chapter 65).

The metabolic consequences of vomiting vary, depending on the volume and composition of the expulsed fluid. Mild vomiting of short duration usually is not accompanied by overt fluid, electrolyte, or acid-base imbalances. Frequent or profuse vomiting can cause metabolic complications such as dehydration; electrolyte imbalances such as hypokalemia, hyponatremia, and hypochloremia; and acid-base imbalances such as metabolic acidosis or metabolic alkalosis. Metabolic alkalosis is most likely to occur in dogs and cats with vomiting secondary to pyloric obstruction. Other potential complications of vomiting include aspiration pneumonia and reflux esophagitis.

Etiology

Vomiting is a clinical sign, rather than a diagnosis, and can be associated with numerous GI and non-GI disorders (Table 67-1).

Key Point

Remember that non-GI disorders commonly cause vomiting; do not overlook these before evaluating for primary GI causes of vomiting.

Clinical Signs

• Vomiting frequently is preceded by nausea (evidenced by hypersalivation, licking of the lips, repeated swallowing), retching, and abdominal contractions.

• Vomitus consists of stomach and duodenal contents such as food, mucus, and foamy or bile-stained fluid with a neutral or acidic pH.

• The term hematemesis is used when vomitus contains blood flecks, blood clots, or brown coffee grounds–like material (digested blood).

• Vomitus may contain hair, plant material, or other ingested foreign material that can irritate the stomach.

• Vomiting of undigested or partially digested food more than 12 hours after eating suggests delayed gastric emptying (functional or mechanical).

• Projectile vomiting (the forceful ejection of vomitus from the mouth that may be expelled a considerable distance) usually indicates gastric outlet or upper small bowel obstruction.

• Other clinical signs may be present depending on the underlying cause of vomiting and the presence of complications such as dehydration or electrolyte and acid-base imbalances.

Diagnosis

The diagnostic approach to vomiting is directed toward identifying the underlying disorder (see Table 67-1) and is influenced by whether vomiting is acute or chronic and by the associated historical and physical findings.

Table 67-1 CAUSES OF VOMITING IN DOGS AND CATS

Acute Vomiting (<1wk)	Chronic Vomiting (>1–2wk)
Gastrointestinal Disorders Diet-related Sudden diet change Food intolerance or allergy Dietary indiscretion (e.g., garbage) Acute gastritis or enteritis Ingested bacterial enterotoxins Foreign bodies (e.g., bones, plants, plastic, rocks, hairballs) Ingested chemical irritants or toxins Drug-induced (e.g., aspirin and other NSAIDs, glucocorticoids, antineoplastics, erythromycin) Viral enteritis (e.g., canine parvovirus, feline panleukopenia, canine distemper) Bacterial infection (e.g., Helicobacter spp.) Parasites (e.g., Physaloptera) Gastric or intestinal obstruction Foreign bodies Intestinal volvulus Intestinal intussusception Gastric dilatation-volvulus Nongastrointestinal Disorders Acute pancreatitis Acute renal failure Acute hepatic failure Ketoacidotic diabetes mellitus Pyometra Prostatitis Peritonitis Drug-induced (e.g., cardiac glycosides, narcotics, antineoplastics) Sepsis CNS disorders (inflammation, edema) Motion sickness Vestibular disease	Gastrointestinal Disorders Diet-related Food intolerance Food allergy Chronic gastritis Lymphocytic-plasmacytic Eosinophilic Granulomatous (e.g., pythiosis) Foreign bodies (including hairballs) Parasites (Ollulanus, Physaloptera) Reflux gastritis Hypertrophic gastropathy Gastrointestinal ulceration Gastric neoplasia Gastric outflow obstruction Foreign bodies Gastric neoplasia Gastric polyps Hypertrophic gastropathy Pyloric stenosis Chronic gastritis Granuloma (pythiosis) External compression Partial gastric dilatation-volvulus Gastric motility disorder Hiatal hernia Diaphragmatic hernia Chronic colitis Obstipation Partial distal intestinal obstruction Nongastrointestinal Disorders Renal failure Hepatic disease Hypoadrenocorticism Hyperthyroidism (feline) Chronic pancreatitis (feline) Heartworm (feline) CNS disorders (e.g., inflammatory, neoplastic, visceral epilepsy) Lead toxicity Sialadenosis

Acute Vomiting (<1wk)

Chronic Vomiting (>1–2wk)

Gastrointestinal Disorders

Diet-related

Sudden diet change

Food intolerance or allergy

Dietary indiscretion (e.g., garbage)

Gastric or intestinal obstruction

Foreign bodies

Intestinal volvulus

Intestinal intussusception

Gastric dilatation-volvulus

Nongastrointestinal Disorders

Acute pancreatitis

Acute renal failure

Acute hepatic failure

Ketoacidotic diabetes mellitus

Pyometra

Prostatitis

Peritonitis

Drug-induced (e.g., cardiac glycosides, narcotics, antineoplastics)

Sepsis

CNS disorders (inflammation, edema)

Motion sickness

Vestibular disease

Gastrointestinal Disorders

Lymphocytic-plasmacytic

Eosinophilic

Granulomatous (e.g., pythiosis)

Foreign bodies (including hairballs)

Parasites (Ollulanus, Physaloptera)

Reflux gastritis

Hypertrophic gastropathy

Gastrointestinal ulceration

Gastric neoplasia

Gastric motility disorder

Partial distal intestinal obstruction

Nongastrointestinal Disorders

Renal failure

Hepatic disease

Hypoadrenocorticism

Hyperthyroidism (feline)

Chronic pancreatitis (feline)

Heartworm (feline)

CNS disorders (e.g., inflammatory, neoplastic, visceral epilepsy)

Lead toxicity

Sialadenosis

CNS, central nervous system; NSAIDs, nonsteroidal anti-inflammatory drugs.

Acute Vomiting

Acute vomiting is a common problem in dogs and cats and may be caused by benign, self-limiting disorders such as acute gastritis or serious life-threatening diseases such as acute pancreatitis, intestinal obstruction, or acute renal or hepatic failure (see Table 67-1).

• Extensive diagnostic testing is not necessarily warranted in every dog or cat with acute vomiting, because nonspecific, self-limiting acute gastritis is a common cause of acute vomiting.

• Base the decision to perform further testing in an acutely vomiting dog or cat on historical and physical findings.

• Further evaluation is usually warranted at initial presentation if abnormal physical findings are detected, such as fever, lethargy, depression, weakness, dehydration, or palpable abdominal abnormalities.

• A history of possible GI foreign body exposure may warrant abdominal radiographs even if the physical examination is normal.

• If the history and physical examination are unremarkable, further diagnostic evaluation may be postponed and symptomatic therapy may be given on an outpatient basis.

• If vomiting does not resolve in 2 to 3 days or if additional clinical signs develop, further evaluation is indicated.

Chronic Vomiting

Chronic or persistent vomiting is always an indication for further workup.

Physical Examination

Perform a complete physical examination. However, physical findings are often unremarkable in animals with gastric disorders.

• Perform a complete oropharyngeal examination to detect a sublingual string foreign body (especially in cats).

• Palpate the GI tract for masses, foreign bodies, trichobezoars, thickenings, distention, plication, or pain.

• Evaluate for evidence of non-GI causes of vomit-ing (e.g., lumpy, enlarged, or small kidneys with renal failure; cranial abdominal pain and fever with pancreatitis; icterus or hepatomegaly with liver failure; or palpable thyroid nodule with feline hyperthyroidism).

• Perform a digital rectal examination to evaluate the character of the feces (e.g., presence of melena, foreign material, blood, and mucus) and to obtain a sample for fecal evaluation.

• Evaluate for systemic effects or complications of vomiting (e.g., dehydration, weakness, and cachexia).

• Findings that suggest potentially serious underlying disease include hematemesis, weakness, severe depression, anorexia, abdominal mass, fever, abdominal pain, abdominal distention, dehydration, and shock.

Laboratory Evaluation

When further diagnostic testing is indicated, a stepwise strategy is recommended.

• Perform routine hematology, biochemistries (including serum amylase and lipase in dogs; serum pancreatic lipase immunoreactivity [PLI] in dogs and cats), urinalysis, survey abdominal radiographs, and miscellaneous ancillary tests, such as serum thyroxine (T₄) in cats greater than 6 years of age, feline leukemia virus (FeLV) antigen test, and feline immunodeficiency virus (FIV) antibody test, as indicated by the history and physical examination. These evaluations are necessary to rule out non-GI disorders that cause vomiting before evaluating for primary GI disorders with contrast radiology, endoscopy, or exploratory laparotomy.

• Routine blood tests are also helpful to detect and characterize metabolic complications of vomiting such as dehydration and electrolyte imbalances.

• Perform a fecal flotation test to diagnose GI parasitism, especially if vomiting is accompanied by diarrhea.

• Evaluate cats for heartworm disease in endemic areas, since vomiting is a frequent presenting sign in cats.

• Perform a fecal occult blood test to detect occult GI bleeding when blood loss is suspected but overt melena is absent.

Radiography

Perform routine ventrodorsal and lateral abdominal radiographs to identify radiopaque foreign bodies, gastric or intestinal obstruction, and abdominal masses or abnormalities of the kidneys, liver, and pancreas.

• Perform barium contrast radiography to evaluate for GI causes of vomiting such as radiolucent foreign bodies, obstruction, and mural thickening or irregularity. Use barium administered by stomach tube as recommended in Chapter 4.

• Barium mixed with food may be better than liquid barium to detect gastric retention disorders.

• Double air-barium contrast gastrography is also useful.

• Use aqueous iodide contrast (iohexol; Omnipaque, Amersham Health) rather than barium if perforation is suspected.

• Barium-impregnated plastic spheres (BIPS) are an alternative to liquid barium for evaluating gastric emptying and GI transit times.

Ultrasonography

Perform abdominal ultrasonography to evaluate for non-GI disorders associated with vomiting that are suspected based on initial blood test results (e.g., pancreatitis and hepatic or renal disease). Ultrasonography may also be helpful to evaluate for primary GI disorders such as intussusception, GI masses, and gastric outflow obstruction.

Endoscopy

Endoscopy of the stomach and proximal duodenum is a non-invasive technique for evaluation of primary upper GI disorders associated with vomiting. Endoscopy is used to visually examine the GI lumen, obtain biopsies, remove foreign bodies, and collect intraluminal juices.

• Endoscopy requires general anesthesia and a flexible fiberoptic endoscope. Appropriate endoscopes for use in evaluating the GI tract of dogs and cats are 100 to 150 cm long with a 7.5- to 9.4-mm-diameter shaft, 2.0- to 2.8-mm biopsy channel, four-way angulation of the tip, and flush and suction capabilities.

• Routinely evaluate the esophagus, stomach, pylorus, and proximal duodenum. Perform mucosal biopsies in all cases because abnormal histologic findings may be present despite a normal gross appearance.

Exploratory Laparotomy

• Exploratory laparotomy is sometimes indicated for diagnosis or treatment of primary GI disorders, especially when endoscopy is not available.

• Obtain full-thickness gastric and intestinal biopsies (see Chapters 68 and 70).

Treatment

Treatment strategies in the vomiting animal are directed toward the following:

• Correction of the underlying cause of vomiting, whenever possible.

• Symptomatic and supportive therapy of vomiting and its metabolic complications.

• Surgery is indicated to remove large gastric foreign bodies, excise localized tumors and deep ulcers, and correct gastric outflow obstruction.

Fluid Therapy

• Give fluids parenterally because vomiting usually precludes adequate oral intake of fluid. Subcutaneous fluid administration can be used to treat mild dehydration in the absence of other systemic signs, but IV fluid therapy is preferred for animals with moderate to severe dehydration. Daily fluid therapy requirements in the vomiting dog or cat depend on the degree of dehydration, ongoing fluid losses, and maintenance needs (see Chapter 5).

• Ideally, base the choice of replacement fluid on serum electrolyte concentrations and blood gas analysis, because the electrolyte and acid-base changes that occur secondary to vomiting may vary considerably. In the absence of such information, use a balanced electrolyte solution such as lactated Ringer’s solution, Plasma-Lyte 148, or 0.9% saline. Additional potassium supplementation (see Chapter 5) usually is necessary because hypokalemia is a common complication of vomiting.

• If metabolic acidosis is present, use an alkalinizing solution such as lactated Ringer’s solution or Plasma-Lyte 148. Sodium bicarbonate administration is necessary only in the treatment of severe metabolic acidosis (pH < 7.1–7.2) (see Chapter 5).

• Hypochloremic metabolic alkalosis is most likely to occur with pyloric obstruction. Give 0.9% saline supplemented with potassium chloride.

• For a comprehensive discussion of fluid therapy, refer to Chapter 5.

Dietary Management of Acute Vomiting

• Restrict oral intake of food to minimize vomiting and further fluid loss. Withhold food for at least 12 to 24 hours.

• If vomiting resolves, offer a bland, digestible, moderately fat-restricted diet such as chicken and rice, low-fat cottage cheese and rice, or a commercially available veterinary diet that meets these requirements.

• After 2 to 3 days on the bland diet, gradually reintroduce the animal’s routine diet over a period of 2 to 3 days.

Antiemetics

Antiemetics are used for symptomatic control of acute vomiting on a short-term basis or to control profuse vomiting that results in fluid, electrolyte, or acid-base disturbances.

Phenothiazines

Phenothiazine derivatives are broad-spectrum, central-acting antiemetics that inhibit the chemoreceptor trigger zone (CRTZ) at low doses and depress the vomiting center at higher doses. Phenothiazines, especially chlorpromazine (0.5 mg/kg SC, IM, or IV q6–8h), and prochlorperazine (0.5 mg/kg SC, IM, or IV q6–8h) are the most widely used antiemetics.

• Hypotension, a potentially serious side effect, is caused by alpha-adrenergic receptor blockade. Consequently, use phenothiazines cautiously in patients with preexisting dehydration.

• Sedation may occur because of concurrent tranquilizing properties.

• Phenothiazine derivatives decrease the seizure threshold and should not be used in animals with seizure disorders.

• Phenothiazine derivatives are the most effective central-acting antiemetic in cats, regardless of the underlying cause.

Metoclopramide

Metoclopramide (Reglan, Robins) (0.2–0.4 mg/kg PO, IM, or SC q8h or 1–2 mg/kg q24h as a constant-rate IV infusion) possesses both central and peripheral antiemetic properties. Central effects are attributed to antidopaminergic activity at the CRTZ and at higher doses, antagonism of 5-hydroxytryptamine type 3 (5-HT₃) serotonergic receptors. The peripheral antiemetic effect is due to its stimulant effect on GI motility.

• Metoclopramide promotes gastric emptying by increasing the tone and amplitude of gastric contractions and relaxation of the pylorus (Fig. 67-1). Because gastric relaxation and retroperistalsis are key events preceding vomiting, their inhibition may account in part for the drug’s peripheral antiemetic effect.

• Metoclopramide is indicated for broad-spectrum antiemetic therapy. It is frequently used to prevent chemotherapy-induced nausea and vomiting.

• It is indicated for control of vomiting associated with parvoviral gastroenteritis because this disorder may be complicated by delayed gastric emptying.

• Metoclopramide may not be as useful a central-acting antiemetic in cats as in dogs because D₂ dopamine receptors are less important in mediating vomiting in cats.

• Metoclopramide should not be used in animals with seizures or those receiving phenothiazines, butyrophenones, narcotics, or anticholinergic drugs.

• Decrease the dose in renal failure.

Figure 67-1 Effects of promotility agents such as cisapride and metoclopramide on the gastrointestinal tract. Promotility drugs increase gastroesophageal sphincter (GES) tone and promote gastric emptying by coordinating increased gastric contractions with pyloric relaxation and increased intestinal peristalsis.

Serotonin Antagonists

Ondansetron (Zofran, GlaxoSmithKline) (0.1–0.2 mg/kg SC q8h, 0.5 mg/kg IV loading dose, and 0.5 mg/kg IV infusion q1h or 0.5–1.0 mg/kg PO q6–12h) and dolasetron (Anzemet, Aventis Pharmaceuticals) 0.6 mg/kg q24h (prevention of nausea and vomiting) or 1 mg/kg q24h (control of vomiting) represent a relatively new class of antiemetics known as 5-HT₃ serotonergic receptor antagonists. The site of antiemetic action is the CRTZ and vagal afferent neurons in the intestinal tract.

• They are especially effective for control of chemotherapy-induced vomiting in dogs and cats but are also useful to control vomiting associated with parvoviral enteritis and acute pancreatitis.

• Because they are expensive, ondansetron or dolasetron are not used as first-choice general antiemetics.

• Side effects in dogs include sedation, lip licking, and head shaking.

Anticholinergic Drugs

Avoid the use of anticholinergic drugs such as isopropamide, atropine, and aminopentamide (Centrine, Fort Dodge) for routine symptomatic control of vomiting.

• Although anticholinergics may decrease peripheral afferent stimulation of the vomiting center by relieving GI smooth muscle spasms or inhibiting intestinal secretions, their side effects include xerostomia, mydriasis, tachycardia, urinary retention, ileus, and gastric retention.

• Because delayed gastric emptying caused by anticholinergics can in itself cause vomiting, these drugs should not be used any longer than 3 days in a vomiting patient.

ACUTE GASTRITIS

Acute gastritis is a common disease in dogs and cats. It is usually a mild, self-limiting condition that rarely warrants biopsy confirmation. Clinical diagnosis of acute gastritis often is made when acute vomiting occurs without apparent cause and resolves on its own in 24 to 48 hours.

Etiology

There are numerous potential etiologies of acute gastritis (see Table 67-1), but the cause often is not determined. Possible causes include the following:

• Dietary indiscretion is frequently associated with acute gastritis and vomiting. Gastritis is most likely due to ingestion of rancid or spoiled foods that contain fermentation byproducts, bacterial enterotoxins, or mycotoxins.

• Foreign body ingestion (e.g., rocks, aluminum foil, small toys, food wrappings, or plastic) can cause mechanical irritation of the gastric mucosa.

• Ingested plant material including grass and house plants is a common cause of acute gastritis.

• Chemical irritants or toxins (e.g., fertilizers, herbicides, cleaning agents, and heavy metals such as lead) can cause gastric irritation.

• Drugs (e.g., aspirin, nonsteroidal anti-inflammatory drugs, and glucocorticoids) can cause acute gastritis, which is frequently accompanied by erosions and ulceration. Antibiotics and chemotherapeutic drugs can also cause acute gastritis, anorexia, and vomiting.

• Viral infections such as canine parvovirus, feline panleukopenia, or canine distemper can cause lesions of gastritis in addition to more diffuse intestinal and systemic involvement.

• Bacterial infections causing gastritis are uncommon. Gastric spiral bacteria (Helicobacter spp.) may play a role in gastritis in some dogs and cats, but these bacteria are also present in many clinically healthy animals.

• Parasitic infections of the stomach are uncommon. Physaloptera spp. infect dogs and cats but the infection is not consistently associated with clinical signs. Ollulanus tricuspis is a cause of chronic gastritis in cats.

• Systemic disorders such as uremia, liver disease, neurologic disease, shock, stress, and sepsis may cause secondary gastritis by altering the gastric mucosal barrier, mucosal blood flow, or gastric acidity.

Clinical Signs

• Acute onset of nausea and vomiting

• Acute anorexia, lethargy, and diarrhea (from concurrent enteritis)

Diagnosis

Because acute gastritis is usually self-limiting, diagnostic evaluations are not usually warranted unless specific historical or physical findings suggest a more serious problem. Response to supportive therapy in 1 to 3 days indirectly supports the diagnosis of uncomplicated acute gastritis as the cause of vomiting.

GASTRIC FOREIGN BODIES

Gastric foreign bodies are most common in dogs owing to their dietary habits and indiscriminant chewing behavior.

Etiology

Gastric foreign bodies cause clinical signs because of mechanical irritation (e.g., acute or chronic gastritis) or gastric outflow obstruction.

• Gastric foreign bodies frequently seen in dogs include needles, coins, stones, sticks, peach pits, plastic, aluminum foil, cloth, rubber balls, and small toys.

• String and other linear foreign bodies are more likely in cats.

Treatment

When a gastric foreign body is identified radiographically, consider whether immediate removal is necessary.

• Remove the object promptly if it is large, sharp, or potentially toxic (e.g., pennies, nuts and bolts, and lead objects) or if the animal is persistently vomiting, anorexic, or dehydrated.

• Small, non-toxic foreign bodies may pass through the GI tract uneventfully and thus can be managed conservatively if the animal is not symptomatic. Allow a period of 7 to 10 days while periodically repeating radiographs to monitor progress. If clinical signs develop, immediate removal is recommended.

• Bones are rapidly decalcified and softened, and they do not require removal from the stomach.

Endoscopic Removal

Attempt endoscopic removal of gastric foreign bodies before gastrotomy, because most foreign bodies can be removed in this manner.

Preparation

• Fast the animal 8 to 12 hours before anesthesia to be sure that the stomach is empty, because food can obscure the endoscopic view. Correct fluid, electrolyte, and acid-base imbalances before general anesthesia.

• Repeat abdominal radiographs immediately before induction of anesthesia to confirm that the object remains in the stomach. This avoids an unnecessary procedure if the object has already entered the intestinal tract and is beyond the reach of the endoscope.

Procedure

The key to removing foreign bodies endoscopically is to get a firm grip on the object, using a grasping forceps or a basket retrieval instrument.

• Use forceps for retrieval of needles, coins, and small, soft objects. To remove the foreign body, grasp the object, pull it up near the end of the endoscope, and remove the endoscope, instrument, and foreign body as one unit.

• Use the basket for retrieval of small, round objects such as marbles or stones that cannot be grasped with the forceps. Large smooth objects are also removed with a basket, but they can be especially difficult to maneuver back through the gastroesophageal sphincter (or upper esophageal sphincter).

• Use an overtube (a plastic tube that fits over the shaft of the endoscope and can be advanced over the end of the endoscope) to protect the esophageal mucosa when sharp or pointed objects are withdrawn. An overtube is also useful to assist removal of objects through the gastroesophageal sphincter by maintaining sphincter dilatation.

• After removing the foreign body, perform a thorough examination of the stomach to look for other objects or mucosal lesions. This should be done even if only one object is seen radiographically, because radiolucent objects may not have been detected or multiple objects may have previously adhered to each other, appearing as one. If food obscures the endoscopic view, reposition the animal in the alternate lateral position or in the ventral dorsal position.

Gastrotomy

If endoscopic equipment is unavailable or the object cannot be retrieved endoscopically, gastrotomy is indicated (see Chapter 68).

Postoperative Care and Complications

• Food and water can be given orally 12 to 24 hours after foreign body removal.

• If mucosal injury is severe, treat as for gastric ulcer (see the next section).

GASTRODUODENAL ULCERATION

For the purposes of this discussion, gastroduodenal ulceration is defined as mucosal defects associated with bleeding, which includes petechiae, erosions, and ulcers. Clinical recognition of gastroduodenal ulceration as a complicating factor in many disorders is becoming more common, most likely due to the increased use of endoscopy.

Many disorders have been associated with gastroduodenal ulceration (Table 67-2). Ulceration is more likely when two or more risk factors are present. General mechanisms of gastroduodenal ulceration include direct damage to the gastric mucosal barrier, increased gastric acid secretion, delayed gastric epithelial renewal, and decreased gastric mucosal blood flow.

Table 67-2 RISK FACTORS FOR GASTRODUODENAL ULCERATION

Infiltrative Disease

Gastric neoplasia

Lymphoma

Adenocarcinoma

Leiomyoma; leiomyosarcoma

Eosinophilic gastroenteritis

Lymphocytic plasmacytic gastroenteritis

Gastric pythiosis

^* COX-2 selective NSAIDs are less likely to cause gastrointestinal hemorrhage and ulceration.

Nonsteroidal Anti-Inflammatory Drugs

Nonsteroidal anti-inflammatory drugs (NSAIDs) (see Table 67-2) are frequent causes of gastric ulceration. These drugs inhibit prostaglandin synthesis, which decreases mucosal blood flow and alters gastric mucus production, thus predisposing to ulceration. Dogs are more susceptible to the ulcerogenic effects of NSAIDs than are humans.

• Both gastric hemorrhage and large perforating ulcers may occur. A predilection for ulceration of the pyloroantral region has been recognized.

• Ulceration is most likely to occur when NSAIDs are given to animals with other risk factors (see Table 67-2).

• Newer NSAIDs that preferentially inhibit cyclooxygenase-2 (COX-2) rather than COX-1 enzymes such as carprofen (Rimadyl, Pfizer), etodolac (EtoGesic, Fort Dodge), deracoxib (Deramaxx, Novartis), meloxicam (Metacam, Merial), and tepoxalin (Zubrin, Schering-Plough) are much less likely to cause GI bleeding. However, they should not be used in the presence of ulcers or inflammatory GI disease or concurrently with glucocorticoids.