Telemedicine: Is endoscopy needed when dog presents with vomiting, anorexia?

Signalment:

Canine, mixed breed, 11 years old, female spayed, 76 pounds.

Photo 1

Clinical history:

The dog presents with a recent history of vomiting and anorexia for the last two weeks. There has been a weight loss of about 5 lbs. When the dog eats for the owner, she will vomit the food soon after. At home, the dog is lethargic and quiet, but in the examination room today the dog is active and alert.

Physical examination:

The findings include rectal temperature 101.0° F, heart rate 144/min., respiratory rate 25/min., pink mucous membranes, capillary refill time less than 2 seconds, and normal heart and lung sounds. The dog is alert and responsive. The cranial abdomen is slightly tense on palpation. Several subcutaneous lipomas are palpated along the ventrum.

Table 1: Results of laboratory tests

Laboratory results:

A complete blood count, serum chemistry profile and urinalysis are performed and outlined in Table 1.

Radiographic review:

Survey thoracic and abdominal radiographs are done. The thoracic radiographs are normal for this dog's age. The abdominal radiographs show a prominent spleen. The liver shadow is of normal size for this dog's age. The upper GI contrast study shows that the contrast media moved through the GI tract quickly and no obvious masses were seen. The stomach wall looks to be of normal thickness and uniform in thickness. The duodenum and proximal jejunum appear to have the contrast media irregularly distributed. Otherwise, there are no other abnormal findings in the abdomen.

L to R: Photo 2, 3, 4, 5, &6

Ultrasound examination:

Thorough abdominal ultrasonography is performed with the dog positioned in dorsal recumbency. The ultrasonographic image provided hereafter is of the duodenum and pancreatic region.

My comments:

The liver shows uniform, slightly increased echogenicity in all liver lobes. There is some periportal infiltrate or fibrosis that makes some of the portal vessels appear slightly more prominent then normal. The gallbladder is mildly distended, and its walls are not thickened or hyperechoic. The spleen has uniform, slightly increased echogenicity - no masses noted. The left and right kidneys are similar in size, shape and echotexture. No masses or calculi were noted in either kidney. The urinary bladder is distended with urine and contains some urine sediment material - no masses or calculi noted. The stomach wall may be slightly thickened. The pancreas is seen but has uniform echogenicity. I did not visualize the walls of the duodenum and remaining intestinal loops well.

Case management:

In this case, chronic inflammatory bowel disease is the clinical diagnosis. This is the type of case in which it is always good to pass an endoscope into the stomach and duodenum for direct visualization and collection of appropriate surface biopsies, especially if supportive care does not resolve the vomiting and anorexia.

I do not believe that lymphoma or chronic pancreatitis is a concern in this case.

Follow-up report:

Two days following the initial diagnostic evaluation, the dog returned with acute cranial abdominal pain, generalized weakness to almost the point of collapse, and more vomiting. An exploratory laparotomy was performed and multiple duodenal ulcers and one perforated duodenal ulcer were found. The following is state-of-the-art information on duodenal ulceration and its clinical management in older dogs.

Review on duodenal ulceration

Duodenal erosions are superficial mucosal defects that do not penetrate the lamina muscularis mucosae. Duodenal ulcers penetrate deeper into the muscular mucosae layer.

Duodenal ulcers are less commonly observed than duodenal erosions and diagnosed more commonly in adult dogs than in adult cats.

Duodenal ulceration or erosions may result from any of the agents that cause acute or chronic gastritis and acute or chronic duodenitis. The most important causes include drugs (NSAIDs, corticosteroids), primary gastric or duodenal diseases (inflammatory bowel disease, gastric dilatation-volvulus, neoplasia, chemical toxins), stress factors (hypotension, severe illness, environmental stress), neurologic disease, metabolic disorders (renal disease, liver disease, hypoadrenocorticism), gastric hyperacidity conditions (systemic mastocytosis, neoplasia), and miscellaneous disorders (pancreatitis, shock, foreign objects).

The most common causes of duodenal ulceration in older dogs include drugs, liver disease, renal disease, pancreatic disease, neoplasia and shock. Drugs (especially NSAIDs), chronic inflammatory bowel disease and neoplasia are more commonly ulcerative, whereas other causes more commonly result in erosions.

Acute or chronic vomiting with or without hematemesis is the most common clinical sign associated with duodenal ulcer or erosion formation. "Not all dogs with duodenal ulcers vomit, and not all dogs that vomit blood have gastric and/or duodenal ulcers." Other clinical signs observed include anorexia, abdominal pain, melena, anemia, edema (from hypoproteinemia related to active alimentary hemorrhage) and/or septicemia (from existing perforation). The other signs may be more related to the underlying cause (such as liver disease, pancreatic disease, renal disease, neurologic disease). Perforation of the duodenum often results in the sudden onset of severe generalized weakness, severe abdominal pain, fever, shock, abdominal distention and death caused by peritonitis.

The diagnosis of duodenal ulcers or erosions requires either direct visualization with endoscopy or possibly indirect documentation with an upper GI contrast study.

Response to medical therapy is also a rational way to diagnose duodenal ulcers or erosions. If the case history strongly suggests ulceration caused by NSAIDs, stress and/or mast cell tumor, it may be reasonable to treat the dog and resort to endoscopy only if the dog does not respond as expected.

Upper GI contrast studies using barium sulfate and multiple positions are usually needed to identify advanced lesions. Ulcers vary in size from several millimeters to 4 cm in diameter.

Barium sulfate may adhere to a mucosal defect or penetrate into an ulcerative crater. A barium contrast study is relatively insensitive, however, and small ulcers or larger defects filled with blood or debris may not be seen. Barium sulfate produces a better contrast study than iodine contrast agents. If a duodenal perforation with peritonitis is likely, there is seldom a need for contrast radiography.

Ultrasonographic features of duodenal ulcers include thickening of the duodenal wall, possible loss of the multi-layer wall structure, the presence of a wall defect or crater, fluid accumulation in the stomach and/or duodenum, and diminished gastric motility.

Endoscopy is still the most sensitive method for diagnosing duodenal ulcers or erosions. Ulcers can be observed along the duodenal wall; however, they may be covered by a poorly distended duodenum, covered by mucous/blood, or the illumination of the endoscope may be diminished by large amounts of ingesta or blood whose dark color may absorb light.

If duodenal erosions are present instead of ulcers, there may be a small spot of fresh or digested blood on the mucosal surface.

If one wipes the blood away with the biopsy forceps, there is renewed bleeding from an erosion. Biopsy samples should be collected from the edge of the duodenal ulcer to rule out neoplasia.

Multiple biopsies of the same location should be taken because superficial inflammation often accompanies neoplasia. Non-lesioned areas should also have surface biopsies taken to identify diffuse disease. No biopsy of the center of the ulcer bed should be obtained. It is often very friable and can be easily perforated by the biopsy forceps. If perforation is known to exist, endoscopy is usually contraindicated because pressurization of the duodenum with infused air during the examination increases contamination of the abdominal cavity with duodenal contents.

Surgery should be performed if a duodenal perforation is suspected or if severe bleeding is discovered. Serial evaluations of the hematocrit and cardiovascular assessment are necessary to determine whether blood loss is sufficient to warrant surgery. Surgery is also indicated if the dog has not responded to appropriate medical therapy that has been administered for at least five to seven days. Duodenal and/or gastric lesions are resected during exploratory laparotomy. Sometimes it is difficult to locate mucosal lesions when examining the serosal surface. A thickening duodenal/gastric wall may be detected, resulting from inflammatory infiltrates in the region of the lesion. Intraoperative endoscopy is helpful in detecting gastric/duodenal lesions, so that if multiple ulcers are present they can all be located.

The goals of medical therapy are to remove the underlying cause if possible, maintain mucosal perfusion, decrease gastric acidity, and protect the ulcer. Fluid therapy is important in dehydrated dogs with duodenal ulcers or erosions to maintain mucosal perfusion. Dogs who are vomiting should be given antiemetics as is recommended for treatment of vomiting in acute gastritis/duodenitis. In addition, food should be withheld at least initially, to avoid stimulation of gastric acid and pepsin secretion. Subsequent dietary management is similar to that recommended for acute gastritis/duodenitis. Drugs commonly used to accomplish these goals include receptor antagonists that block the interaction of the secretagogues with their receptors (H2 receptor antagonists) and sucralfate for protecting ulcerated tissue. Antiulcer therapy should be continued for at least four to six weeks.

Medical management

Here are tips for general medical management of duodenal ulceration/perforation.

• Fluid therapy supplemented with potassium chloride to maintain adequate mucosal perfusion. If added cardiovascular support is needed, consider administering intravenous hetastarch at 10-20 ml/kg over a one- to two-hour time period at a single time. One may need to repeat the hetastarch infusions several times over the next several weeks.

• Administer antiemetics such as metoclopramide if vomiting exists.

• Withhold food initially and after vomiting resolves feed a diet formulated for inflammatory bowel disease.

• Administer H2 receptor antagonists such as famotidine at 0.25-0.5 mg/lb twice a day.

• Administer sucralfate at 0.5-1 gram total dose given two to four times a day. In dogs with severe blood loss, an initial loading dose of 3 to 6 grams, followed by the lower recommended dose.

Note: When treating gastric or duodenal ulcers with H2 receptor antagonist and sucralfate, one should administer the H2 receptor antagonist first and then the sucralfate 30 to 60 minutes later.

• Administer antibiotics if perforation and/or inflammatory bowel disease is suspected, such as metronidazole twice a day.

• Administer, at least initially, daily pain medication as needed (analgesic drugs other than the NSAIDs).

• Concurrently manage the underlying cause if possible.

• If inadequate response to medical therapy after five to seven days occurs, then perform an exploratory laparotomy.

• Remember: Intestinal absorption of drugs and appropriate nourishment may not be occurring well initially - injectable drugs are preferred in the beginning of therapy.

Prognosis:

The long-term prognosis in older dogs with duodenal ulceration is guarded to poor. The condition may be controlled, but not actually cured.