History

A 14.5-year-old 6.3-kg (13.9-lb) spayed female West Highland White Terrier was examined because of a long-term history of vomiting that had progressed over the last 4 months from 3 to 5 episodes/wk to 3 episodes/d. These episodes were reported to occur approximately 15 minutes after water intake. The dog was current on core vaccinations and was receiving a monthly preventative against fleas, ticks, and heartworm.

On physical examination, the dog was bright, alert, and responsive and had a rectal temperature of 38.5°C (101.3°F; reference range, 37.8°C to 39.2°C [100°F to 102.6°F]), pulse rate of 110 beats/min (reference range, 80 to 160 beats/min), and respiratory rate of 36 breaths/min (reference range, 10 to 30 breaths/min). Abdominal palpation revealed a large, firm, rounded mass that extended caudal to the ribs on the dog's right side, and the dog showed signs of mild discomfort when the mass was palpated. Results of a CBC indicated a stress leukogram (relative neutrophilia [89%; reference range, 60% to 77%], lymphopenia [802 lymphocytes/μL; reference range, 1,200 to 6,500 lymphocytes/μL], and monocytopenia [2%; reference range, 3% to 10%]) combined with polychromasia, mild anisocytosis, and mild hypochromasia. Serum biochemical analyses revealed moderately high concentrations of SUN (44 mg/dl; reference range, 8 to 24 mg/dL) and creatinine (2.85 mg/dL; reference range, 0.50 to 1.40 mg/dL), and urinalysis revealed a urine specific gravity of 1.026 combined with proteinuria involving albumin and nonalbumin proteins. Orthogonal abdominal radiographic images were obtained (Figure 1)

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Ventrodorsal (A) and right lateral (B) radiographic images of a 14.5-year-old 6.3-kg (13.9-lb) spayed female West Highland White Terrier with a long-term history of vomiting that had progressed over the last 4 months from 3 to 5 episodes/wk to 3 episodes/d.

Citation: Journal of the American Veterinary Medical Association 258, 6; 10.2460/javma.258.6.575

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Diagnostic Imaging Findings and Interpretation

Abdominal radiography revealed severe gastric distention with homogeneous fluid or soft tissue opaque material and a moderate amount of granular, variably sized and shaped, smoothly marginated, mineral opaque material (Figure 2) The numerous, mineral opaque structures in the stomach were likely desiccated feed material (consistent with a gravel sign) or foreign material. Gravel sign (accumulation of fine, mineral opaque material) in a greatly distended stomach is a classic finding in patients with partial outflow obstruction. The pylorus was filled with gas on the left lateral projection and was considered radiographically normal. The distended stomach caused caudal displacement of the small and large intestines. Thoracic radiography (not shown) revealed no evidence of pulmonary metastatic neoplasia or any esophageal abnormality. Differential diagnoses for the described gastric distention and gravel sign combined with the long-standing history of vomiting included gastritis, enteritis, metabolic disorders, and chronic pyloric outflow obstruction (partial or intermittent), with differential diagnoses including pyloric hypertrophy, neoplasia (eg, adenocarcinoma or lymphoma), or infection (eg, pythiosis).

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The same images as in Figure 1. The stomach is severely distended with homogeneous fluid and soft tissue opaque material (white arrows) and a moderate amount of granular, variably sized and shaped, smoothly marginated, mineral opaque material (black arrows). The small and large intestines are displaced caudally.

Citation: Journal of the American Veterinary Medical Association 258, 6; 10.2460/javma.258.6.575

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Abdominal ultrasonography was performed. The pyloric wall had an ultrasonographically normal pattern of wall layering; however, all layers were thickened. For instance, the muscularis layer was up to 5.3 mm thick (reference range,¹ 0.3 to 0.75 mm). The lumen of the pylorus was severely narrow, and there was a hyperechoic nodule (approx 1.14 × 0.88 × 0.60 cm) confluent with the mucosal layer at the pyloric antrum (Figure 3) During peristaltic contractions, this nodule intermittently entered into the orad portion of the gastric lumen, impeding the outflow of fluid from the stomach to the duodenum. Regional and distant abdominal lymph nodes were ultrasonographically normal. Our primary differential diagnosis for this nodule was a gastric inflammatory polyp; however, neoplasia or granuloma formation had not been ruled out. The primary differential diagnosis for the other changes to the pyloric wall was pyloric hypertrophy, with neoplastic and infectious causes considered less likely because of the preserved pattern of layering in the wall.

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Sagittal (A) and transverse (B) ultrasonographic images of the pyloric region of the stomach of the dog described in Figure 1. A—The stomach (star) contains a small amount of hyperechoic material. A heterogeneously echoic nodule (solid arrow) is at the antrum of the pylorus. Aborad to the nodule, the pyloric lumen is severely narrowed and serpentine (outlined arrow). The mucosal layer (brackets) is thickened and undulating. The dog is in dorsal recumbency, with its head toward the right of the image. The scale toward the right of the image is in centimeters. B—The muscularis layer (between the dashed outlines) and the pyloric wall (distance between the calipers) are abnormally thick (approx 0.54 and 0.93 cm, respectively).

Citation: Journal of the American Veterinary Medical Association 258, 6; 10.2460/javma.258.6.575

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Treatment and Outcome

Endoscopy of the upper gastrointestinal tract was performed and revealed inflamed gastric mucosa and a lobulated mass (approx 3 × 3 × 3 cm) at the pylorus that obstructed the pyloric outflow tract. On the basis of endoscopic findings, we considered the polyp to have contributed to the obstruction already caused by the stenotic pylorus but to have been secondary to the underlying disease process that caused inflammation of gastric mucosa. During endoscopy, several pinch biopsy samples were collected from the nodule and other regions of the pylorus.

Following an uncomplicated recovery from the endoscopic procedure, the dog was discharged with prescriptions of omeprazole^a (1 mg/kg [0.45 mg/lb], PO, q 12 h) and maropitant citrate^b (1 mg/kg, PO, q 24 h) to be used as a gastroprotectant and antiemetic, respectively, while awaiting histologic results for the biopsy samples. A food trial with a therapeutic diet^c formulated for dogs with impaired kidney function was initiated, and a follow-up recheck examination with evaluation of kidney function (eg, urinalysis and serum biochemical analyses) was recommended.

Histologic examination of the biopsy samples obtained of the dog's pyloric region revealed high numbers of lymphocytes and plasma cells with multifocal areas of hemorrhage, and results for the biopsy samples of the pyloric nodule indicated severe lymphocytic inflammation of the superficial lamina propria, with an abundant population of mixed inflammatory cells including neutrophils, lymphocytes, and plasma cells. There was no evidence of neoplastic changes involving the cells of the examined sections. Given the clinical signs, imaging findings, and histologic results, we considered acquired antral pyloric hypertrophy (AAPH) the most likely diagnosis. Surgery to excise the affected tissues was recommended; however, the owners declined and elected to continue medical management. No improvement in the dog's clinical signs was reported by the owner.

Comments

First classified as chronic hypertrophic pyloric gastropathy to reflect the hypertrophic disease process, anatomic location, and long-term benign nature, AAPH is defined as a constriction of the pyloric lumen caused by hypertrophy of either the pyloric mucosa or the circular smooth muscle, with both resulting in disorders of the passage of ingesta.^2,3 Acquired antral pyloric hypertrophy occurs most commonly in small, purebred (eg, Lhasa Apso, Shih Tzu, and Miniature Poodle), middle-aged or older dogs, with males twice as likely to be affected.^2,3,4 Chronic, intermittent vomiting that typically occurs a few hours after eating is the most common clinical sign associated with AAPH.^2,3,4 Although the exact underlying cause of AAPH has not yet been determined, genetics, hormones, environmental factors, and immunemediated mechanisms are thought to be contributing factors.^2,3

Abdominal radiography may be useful in determining a reason for vomiting, with differential diagnoses including pyloric outflow obstruction (characterized by fluid-filled gastric distention), mechanical obstruction (characterized by various degrees of intestinal dilation orad to the site of obstruction), gastritis, enteritis, dietary indiscretion, metabolic disturbances, infiltrative processes (as with neoplastic or infectious causes), or torsion (as with gastric volvulus characterized by gas and fluid distention of the stomach).⁴ Given that the dog of the present report had a long-term history of vomiting and that radiography revealed gastric distention with homogeneous fluid or soft tissue opaque material, we considered gastritis, enteritis, metabolic disorders, and chronic pyloric outflow obstruction more likely differential diagnoses but could not yet rule out neoplasia.

Abdominal ultrasonography may help rule out or prioritize differential diagnoses for causes of chronic vomiting and gastric distention as seen in the dog of the present report. For instance, abdominal ultrasonography revealed that the dog of the present report had a normal pattern of layers in its pyloric wall but that the layers were thickened. Our finding that the muscularis layer was 5.3 mm thick was consistent with previous findings⁴ of the muscularis layer being > 4 mm in affected dogs. Pseudolayering, or the presence of irregular layering of the gastric wall with an uneven and poorly echogenic pattern, and lymphadenomegaly are suggestive of gastric carcinomas.⁵ However, in the dog of the present report, the pattern of wall layering appeared ultrasonographically normal.

A presumptive diagnosis of AAPH can be made when physical, hematologic, biomechanical, and imaging findings exclude all other causes of a protracted history of vomiting.^2,4 A definitive diagnosis of AAPH is obtained with histologic results for a full-thickness biopsy sample of the stomach.² In the dog of the present report, AAPH could not be definitely diagnosed because only pinch biopsy samples obtained during endoscopy were evaluated. No full-thickness biopsy samples were obtained, and the owners elected to pursue medical management rather than surgical treatment. Unfortunately, medical management of AAPH typically does not help alleviate the abnormal clinical signs, and surgery to excise the hypertrophied epithelium is necessary to resolve the abnormal signs.² Treatment for AAPH includes excision of abnormal tissues and restoration of adequate gastric outflow. The depth of tissue excision and selection of the reconstructive process depend on the type and severity of the lesion.²

The clinical signs in the dog of the present report were likely worsened owing to the presence of a gastric polyp at the pyloric antrum identified on ultrasonography. The ultrasonographic appearance of gastric polyps is that of a sessile or pedunculated, homogeneous, echogenic nodule or mass that may potentially project into the lumen.⁶ Benign gastric polyps are uncommon in dogs but are typically found in the pyloric antrum and cause gastric outflow obstruction,⁶ as did the polyp in the dog of the present report when the nodule was ultrasonographically observed to intermittently enter into the orad portion of the gastric lumen and impede the outflow of fluid from the stomach to the duodenum during peristaltic contractions.

Although a definitive diagnosis was not reached for the lesions seen in the dog of the present report, given the clinical signs and diagnostic findings, AAPH with gastric polyp formation was considered most likely. The use of abdominal radiography coupled with ultrasonography was critical in localizing the lesion and narrowing the list of differential diagnoses for the dog of the present report.