Canine Giant Hypertrophic Gastritis Treated Successfully with Partial Gastrectomy

Introduction

Giant hypertrophic gastritis is a rare cause of vomiting and weight loss in the dog. Affected dogs have a marked thickening and characteristic cerebriform appearance of the gastric rugae. Those changes are confined to the gastric body and fundus and are characterized microscopically by mucosal hypertrophy.^1–4 This report outlines successful long-term treatment of this condition, which has not been previously described.

Case Report

A 4 yr old castrated male Jack Russell terrier weighing 5 kg was presented to Mississippi State University College of Veterinary Medicine with an 8 wk history of vomiting, diarrhea, anorexia, and weight loss. The patient had been hospitalized by the referring veterinarian four times in a 7 wk period, with stays of 5–7 days’ duration. Treatments during each hospital stay varied, but included IV fluids, sucralfate, famotidine, enrofloxacin, and metoclopramide. The patient’s clinical signs improved during hospitalization, but returned within 4–5 days following discharge. At the time of referral, the patient was receiving famotidine (0.5 mg/kg per os [PO] q 12 hr) and maropitant citrate (2 mg/kg PO q 24 hr).

On initial examination at Mississippi State University College of Veterinary Medicine, the patient was depressed, but alert and responsive. On physical examination, mucous membranes were tacky and the patient was estimated to be 5–7% dehydrated. The patient’s body condition score was 3 out of 9. No other abnormalities were noted on physical examination. Complete blood count and serum biochemical analysis were performed. Notable abnormalities included panhypoproteinemia consisting of low total protein (44 g/L; reference range, 55–80g/L), hypoalbuminemia (24 g/L; reference range, 25–39 g/L), and hypoglobulinemia (20 g/L; reference range, 21–43 g/L). Fecal flotation was negative for parasites. The patient was admitted to the hospital and an IV catheter was placed. Lactated Ringer’s solution was administered to correct the estimated 5% dehydration over a 12 hr period. Previously prescribed medications were continued in injectable form, including famotidine (0.5 mg IV q 12 hr) and maropitant citrate (1 mg/kg subcutaneously q 24 hr).

The following day, abdominal radiographs were obtained. Abnormalities included loss of serosal detail consistent with emaciation and increased soft-tissue opacity within the lumen of the stomach consistent with either a mass or a foreign body. Abdominal ultrasound was performed to better characterize the gastric findings. Ultrasonography revealed marked gastric wall thickening without loss of wall layering. Only a minimal amount of gastric lumen was present, as the stomach wall, specifically the mucosa, was severely thickened and projected intraluminally. A foreign body was ruled out based on those findings. Differential diagnoses for the gastric mass included pythiosis; gastric neoplasia, such as gastric carcinoma, lymphosarcoma, leiomyoma, fibrosarcoma, leiomyosarcoma, and plasmacytoma; and benign conditions, such as hypertrophic gastropathy and adenomatous polyps.

Given the diagnostic imaging findings, an exploratory celiotomy was recommended. After premedication with hydromorphone (0.1 mg IV), general anesthesia was induced with propofol (8 mg/kg IV to effect) and maintained with inhaled isoflurane. A ventral midline celiotomy was performed, revealing a palpable mass in the stomach and proximal duodenum causing moderate to severe dilatation of the gastric outflow tract. No other abnormalities were noted. A 5 cm gastrotomy was performed on the ventral aspect of the body of the stomach between the greater and lesser curvatures, and a mass was seen originating from the gastric mucosa of the dorsal aspect of the body of the stomach. At that time, the gastrotomy was extended to improve visualization of the mass. The free portion of the mass was protruding through the pylorus into the proximal duodenum. Digital traction was applied to the mass to reduce the free portion of the mass from the duodenum into the stomach. The mass was then exteriorized through the ventral gastrotomy. Mass dimensions were approximately 9 cm × 6 cm × 5 cm. In addition, another smaller mass was noted also originating from the dorsal gastric body, slightly orad to the larger mass. Both masses had similar characteristics, with billowing irregular rugal folds with a cerebriform appearance (Figure 1). The portions of the stomach not affected by the mass lesions appeared grossly normal. A full-thickness partial gastrectomy was performed to excise both masses together through the open ventral gastrotomy site, taking an approximately 1 cm margin of grossly normal tissue around the masses. The gastrectomy site was closed with a full-thickness simple continuous pattern of 3-0 polydioxanone through the gastrotomy site, with the suture knots placed within the gastric lumen. The ventral gastrotomy was closed using a full-thickness simple continuous pattern and oversewn with a continuous Cushing pattern using 3-0 polydioxanone. Abdominal wall closure was routine.

View Figure

• Download as Powerpoint
• Download Figure

Postoperatively, the patient received lactated Ringer’s solution (4 mL/kg/hr IV as a constant rate infusion [CRI]), lidocaine (10 μg/kg/min IV as a CRI), hydromorphone (0.1 mg/kg IV q 6 hr) for analgesia, and ampicillin Na/sulbactam Na (30 mg/kg IV q 8 hr) as antibiotic prophylaxis for potential peritoneal contamination during gastrectomy. Due to pre-existing nausea and anorexia and considering the extensive gastric resection performed, treatment with maropitant citrate (1 mg/kg subcutaneously q 24 hr) and famotidine (0.5 mg/kg IV q 12 hr) was continued and treatment with sucralfate (0.5 g PO q 12 hr) was added. Postoperative monitoring included periodic noninvasive blood pressure, temperature, pulse, and respiration, which were all within normal limits. Packed cell volume and total protein were evaluated immediately following surgery. Packed cell volume was 40% (reference range, 33–58%) and total protein was 50 g/L (reference range, 50–80 g/L). The day following surgery, hydromorphone was discontinued and buprenorphine (0.01 mg/kg IV q 6 hr) therapy was initiated due to anorexia and perceived nausea. Additionally, the lidocaine CRI was discontinued and the patient was placed on metoclopramide (2 mg/kg/day IV as a CRI) and omeprazole (0.5 mg/kg PO q 24 hr). The patient drank a small amount of water and ate a small meal within the subsequent 24 hr. On the third day following surgery, IV fluid therapy, the metoclopramide IV CRI, IV buprenorphine, sucralfate, famotidine, maropitant citrate, and ampicillin Na/sulbactam Na were discontinued due to continued clinical improvement and improved appetite. Oral metoclopramide (0.1 mg/kg q 6 hr) therapy was initiated, along with sublingual buprenorphine (0.01 mg/kg q 8 hr). At the time of discharge 5 days postoperatively, the patient was bright, alert, and responsive with a normal appetite. Outpatient medications included metoclopramide (0.1 mg/kg PO q 6 hr for 5 days), omeprazole (0.1 mg/kg PO q 24 hr for 7 days), and buprenorphine (0.01 mg/kg sublingually up to q 8 hr as needed for pain for 4 days). One yr postoperatively, a telephone follow-up conversation with the owner found the patient to be healthy with no recurrence of clinical signs.

On evaluation of the cut section of the mass, the narrow base of the mass was evident (Figure 2). Histopathology revealed the gastric mucosa had irregular arborizing hyperplastic folds lined by a single layer of tall columnar gastric epithelium cells (Figure 3). Foveolar hyperplasia was marked and often the gastric pits branched and small fingerlike protrusions occurred along the broader-based grossly visible prominent hypertrophic folds. Most of the gastric glands were moderately atrophic. The parietal cells were very small and more mucous cells were seen among the glands. Fibromuscular stroma was found, often between the atrophic glands. Irregular bundles of smooth muscle often followed the protruding irregular gastric folds. Prominent hypertrophic arteries were found among the smooth muscle with marked thickening of the tunica muscularis and a very narrow luminal diameter. Inflammation was found to be limited to a small number of lymphocytes and plasma cells in the superficial lamina propria. Those histologic findings were consistent with giant hypertrophic gastritis.

View Figure

• Download as Powerpoint
• Download Figure

View Figure

• Download as Powerpoint
• Download Figure

Discussion

Giant hypertrophic gastritis is a rarely diagnosed condition in the dog. All cases share certain characteristics, most notably hypertrophy of the gastric mucosa, causing a ceribriform appearance of rugal folds.^1–6 The fundus and body of the stomach are affected, and the pyloric antrum is spared. The gastric changes are associated, in most cases, with clinical signs including vomiting, weight loss and decreased appetite. Hypoalbuminemia is also a common finding, thought to be due to a protein-losing gastropathy.⁶ The variant of the disease occurring in basenjis includes the above findings along with small intestinal lymphoplasmacytic enteritis.⁴ Hypertrophic gastritis has also been described in the Drentse Patrijshond breed as part of a condition termed familial stomatocytosis-hypertrophic gastritis. In addition to the hypertrophic gastritis, affected dogs may be afflicted with numerous other conditions including stomatocytosis, progressive liver disease, cystic kidney disease, and polyneuropathy.⁵ In some texts, a variant of pyloric stenosis is grouped with hypertrophic gastritis cases as well.⁶ In those cases, older small breed dogs are affected with mucosal hypertrophy in the pylorus, causing gastric outflow obstruction.⁶ Those dogs likely have a distinctly different disease process, as only the pylorus is affected, compared with the body and fundus being affected in cases of giant hypertrophic gastritis.

Considering only cases of giant hypertrophic gastritis of similar presentation to the current case, only three clinical case reports were located in the literature.^1–3 The dog in the current report was 4 yr old at presentation, younger than the other three cases, which were 6 yr ,7 yr, and 11 yr. The four cases included three males and one female. All cases had similar descriptions of a mass originating from the gastric body and/or fundus. All dogs’ masses had a similar cerebriform appearance of the mucosa grossly, with similar microscopic findings of mucosal hypertrophy and hyperplasia. Diagnostic imaging modalities used in the various cases included abdominal radiography, contrast gastrography, and abdominal ultrasound.^1–3 Marked gastric wall thickening was noted on abdominal ultrasound in the current case, similar to a previous report.¹ In addition, gastroscopy was used for visualization of the lesions and to acquire biopsy samples in two cases.^1,3 Hypoalbuminemia was present in all three cases in which serum biochemical findings were reported.^1,3 In the two most recent cases (including the current case), panhypoproteinemia was present.¹ Additionally, anemia was reported in two cases.^1,3

In one of the previous cases, treatment was not described, only pathologic findings.³ In another case, partial gastrectomy was performed to excise the affected tissue, but the patient died acutely 24 hr after surgery, associated with hematemesis and vascular collapse.² In the most recent case report, the patient was treated medically with prednisone, cimetidine, and hyoscine butylbromide, which resulted in a remission of clinical signs and decrease in severity of the gastric lesions, as measured by ultrasonography. After a 129 day remission, that dog died suddenly from an unknown etiology.¹

In the current case, treatment consisted of resection of abnormal tissue and a 1 cm margin of grossly normal tissue via partial gastrectomy. The approach used to perform partial gastrectomy was unorthodox in this case. A ventral gastrotomy was performed initially to evaluate the pyloric antrum for the pyloric outflow obstruction evident on initial abdominal exploratory. When it was determined that the obstruction was caused by a projection of a gastric body mass that was extending through the pylorus, the ventral gastrotomy was extended to facilitate manipulation of the free portion of the mass back into the gastric lumen and determine the gross margins of the base of the mass. At that point, submucosal resection of the mass was considered, but the normal separation between the muscularis and submucosal layers was not evident. Full-thickness resection was elected, and was accomplished in this case from the luminal surface via the existing large ventral gastrotomy. That approach made delineating the gross margins of the abnormal tissue easier, but did require closure of two large gastrotomy sites following completion of the mass resection. Closure of the gastrectomy site was intraluminal because of easier access in this case. Access to the serosal surface of the dorsal gastric wall in that location would have been possible, but more difficult in the authors’ opinion.

In three previously described cases, the mass originated near the greater curvature in two cases and was only described as originating from the body and fundus in the other.^1–3 The particular location in this case complicated ease of resection, but it was unclear how typical that presentation was, considering the paucity of cases in the literature. Ultrasound was helpful in the current case, but only identified gastric mucosal thickening and the origin within the stomach was unclear. It was only obvious after the ventral gastrotomy that the changes were focal and originating from the dorsal aspect of the gastric body. It is possible that advanced imaging such as computed tomography or MRI may have helped better characterize the gastric pathology in the current case prior to surgery.

Postoperative medical treatment in the case described herein included various gastroprotectants, a promotility agent, a short course of antibiotics, and analgesic therapy. The antibiotics were administered due to concerns about potential peritoneal contamination during the extensive gastric surgery. Hydromorphone was initially used as an analgesic, but the patient was subsequently prescribed buprenorphine due to nausea suspected to be associated with hydromorphone administration. When IV medications were discontinued 3 days postoperatively, sublingual buprenorphine was used for analgesia for the remainder of hospitalization and as a rescue analgesic for the owners to administer at home. Clinically, sublingual buprenorphine seemed to provide adequate analgesia from the time it was initiated 3 days postoperatively. Although it may have been effective in this case, the authors do not recommend using low-dose sublingual buprenorphine as a first-line analgesic for moderate to severe postoperative pain in dogs, considering its relatively low bioavailability when given by this route.^7,8

The histopathologic findings in the current case were similar to previous reports of giant hypertrophic gastritis. The lack of lymphocytic-plasmacytic infiltrates in the thickened stomach wall supports the previous suggestions by Rallis et al. (2007) that this clinical condition may be a noninflammatory gastropathy. It is also a possibility that a subclassification of canine giant hypertrophic gastritis may be necessary, dividing the cases into those which possess local lymphocytic-plasmacytic infiltrates and those which are noninflammatory in nature. That distinction may be significant in determining prognosis.

Ménétrier’s disease is a rare condition in humans characterized by the presence of marked rugal hypertrophy within the fundic glandular mucosa, hypoalbuminemia, and unique histologic findings, similar to those found in dogs with giant hypertrophic gastritis. Symptoms include abdominal pain, nausea, vomiting, anemia, hypochlorhydria, and edema in peripheral tissues secondary to hypoproteinemia.⁹ Sufferers of Ménétrier’s disease are also predisposed to thromboemboli. Histologically, the affected mucosa exhibits foveolar hyperplasia. The lamina propria can exhibit inflammation and an accumulation of eosinophils. The muscularis mucosae is thickened and disorganized, with strands of smooth muscle extending into the lamina propria.⁹ Recently, Ménétrier’s disease was found to be associated with enhanced epidermal growth factor signaling in the gastric mucosa due to local overproduction of transforming growth factor-α. Ménétrier’s disease has been treated with anticholinergic therapy, octreotide, acid suppression, prednisone, and eradication of Helicobacter pylori without consistent benefit.⁹ More recently, treatment with cetuximab, a monoclonal antibody that blocks epidermal growth factor receptor signaling, has produced clinical improvement in initial clinical trials.¹⁰ The treatment of choice in cases refractory to medical therapy is either partial or total gastrectomy.⁹

Conclusion

A 4 yr old Jack Russell terrier with clinical signs consistent with chronic gastric outflow obstruction was diagnosed with giant hypertrophic gastritis. Limited information is present in the literature regarding treatment options for this disease and successful surgical management has not been previously reported. Treatment in the case described herein included excision of the abnormal tissue and a 1 cm margin of grossly normal tissue via partial gastrectomy, which resulted in a favorable long-term outcome.