Feline eosinophilic sclerosing fibroplasia of the duodenum treated with gastrojejunostomy in a domestic shorthair cat

Abstract

Case summary

A 2-year-old female spayed domestic shorthair cat was presented for evaluation of severe thickening of the proximal duodenum identified on abdominal ultrasound after a 1-year history of vomiting. At surgery, a proximal duodenal mass encompassed the areas of the major and minor duodenal papillae. A gastrojejunostomy was performed to bypass the proximal duodenum and maintain the integrity of the major duodenal papilla. Histopathology revealed changes consistent with feline eosinophilic sclerosing fibroplasia. The cat was treated with prednisolone and survived for 2.5 years. It was euthanized for bronchopneumonia.

Relevance and novel information

This case report describes a surgical approach for cats with lesions involving the pylorus and proximal duodenum. Gastrojejunostomy provided a therapeutic option that preserved exocrine pancreatic and biliary secretion in this cat.

Introduction

Feline eosinophilic sclerosing fibroplasia (FESF), also referred to as feline gastrointestinal eosinophilic sclerosing fibroplasia (FGESF), is an idiopathic inflammatory eosinophilic condition that usually affects the gastrointestinal tract and associated lymph nodes. ¹ This lesion is most frequently described in the stomach, small intestine and regional abdominal lymph nodes, though recent reports describe histopathologically similar lesions in the mesentery, retroperitoneum and retropharyngeal lymph node.^{1 –5} Lesions are characterized histologically by branching trabeculae of collagen with reactive fibroblasts and infiltrates of eosinophils, mast cells and other white blood cells.^1,3 Historically debated, sclerosing mast cell tumor and FESF can have similar histopathologic patterns and some cases of FESF may be misidentified as sclerosing mast cell tumors.^{6 –8} The pathogenesis of FESF is currently unknown, but may represent an aberrant inflammatory response to a variety of inciting pathogens.^1,2 Bacteria, including Gram-negative and Gram-positive bacilli, and Gram-positive cocci, may be found in lesions.^1,2,5 Intracellular bacteria have been noted in 56–69% of cases, with one study noting bacteria in all ileocolic junction and colic lesions, and in some pyloric lesions.^1,2 Nematodes have been associated with histologically similar lesions in pumas, and phycomycetes were associated with FESF in one case report.^9,10 Clinical signs include inappetence, vomiting, diarrhea and lethargy.^2,11 In one recurrent case, FESF responded completely to corticosteroids alone. ¹² Most reported cases have been treated with surgical resection, antibiotics, corticosteroids and other immunomodulatory agents.^1,2 This report details the successful use of gastrojejunostomy to treat FESF at the proximal duodenum to preserve the major and minor duodenal papillae.

Case description

A 2-year-old female spayed domestic shorthair cat presented to the University of Pennsylvania Matthew J Ryan Veterinary Hospital for a 1-year history of vomiting, which initially occurred approximately 3–4 times weekly, then increased to almost daily. The cat had no history of diarrhea, and a fecal examination showed no parasites. Ultrasonography by the referring veterinarian identified a 3 × 0.6 cm area of severe thickening of the descending duodenal wall with possible involvement of the pylorus and three enlarged, hypoechoic mesenteric lymph nodes (Figure 1). The cat had been treated with three courses of prednisolone over the previous year (doses unavailable), which did not improve the vomiting. Several 3-month diet trials all decreased vomiting frequency initially; however, the vomiting resumed after each trial.

Figure 1

Proximal duodenal and pyloroduodenal junction asymmetric mass-like mural thickening (white bracket) consistent with biopsied feline eosinophilic sclerosing fibroplasia as observed on ultrasound. This image was obtained during a postoperative follow-up, but the lesion’s appearance is similar to that observed with the referring veterinarian

On physical examination, the cat was bright and alert with a normal body condition. A complete blood count revealed eosinophilia (2.145 × 10³/ml; reference interval 0.000–1.5000). There were no significant findings on a serum chemistry panel. The cat was not icteric and had a normal serum bilirubin level. Feline leukemia virus/feline immunodeficiency virus testing was negative. Three-view thoracic radiographs, which included part of the abdomen, showed a thick duodenal wall and gas distension of the small intestines.

An exploratory laparotomy was performed 3 weeks later. The cat was anesthetized, placed in dorsal recumbency, clipped and prepared for aseptic surgery. Cefoxitin (30 mg/kg IV) was administered perioperatively. A ventral midline laparotomy was performed and the abdomen was explored. A circumferential mass with a diameter of 2.5 cm was visualized in the proximal duodenum starting at the pyloroduodenal junction and encompassing the areas of the major and minor duodenal papillae (Figure 2). The gallbladder was mildly distended but expressible; the liver and all other organs were grossly normal. The findings suggested that the mass was not obstructing the common bile duct and, by extension, the common opening of the pancreatic duct shared with the common bile duct. Resection of the mass would have required ligation of the common bile duct, cholecystojejunostomy, ligation of the pancreatic ducts and possibly subsequent exocrine pancreatic insufficiency. A gastrojejunostomy was performed to allow for passage of ingesta from the stomach to the small intestine.

Figure 2

A circumferential mass (black asterisk) with a length and diameter of approximately 3.5 cm and 2.5 cm, respectively, in the proximal duodenum (white arrow), and adjacent to the pancreas (white asterisk), starting at the pyloroduodenal junction and encompassing the major and minor duodenal papillae. This figure shows the mass encompassing the presumed ampulla at the major duodenal papilla and the entrance of the common bile duct (black rectangle)

Two stay sutures were placed at the pyloric antrum and gastric fundus. Two more stay sutures were placed at the ascending duodenum and proximal jejunum to achieve appropriate apposition of the stomach and jejunum. The dorsal aspects of the greater curvature of the stomach and proximal jejunum were directly apposed using 4-0 polydioxanone suture (PDS) in a simple continuous pattern in the serosa and muscularis layers. Doyen forceps were applied orad and aborad to the desired jejunostomy site. Two incisions measuring 3.5 cm were made in the greater curvature of the stomach and the antimesenteric portion of the jejunum, parallel to the gastric incision. The dorsal portion of the gastric and jejunal incisions were apposed using 4-0 PDS in a simple continuous pattern, taking care to include the submucosa. The ventral mucosal and submucosal layers of the stomach and jejunum were closed in the same fashion. A simple continuous suture pattern was used to close the serosa and muscularis layer on the ventral aspects of the incisions, creating a 360°, two-layer closure around the gastrojejunostomy site (Figure 3). A full-thickness wedge biopsy of the duodenal lesion was performed and submitted for histopathology. The duodenotomy was closed using 4-0 PDS in a simple interrupted pattern. The omentum was placed over both surgery sites, the peritoneal cavity lavaged with warm saline and the abdominal incision closed routinely.

Figure 3

The gastrojejunostomy site where 3.5 cm of the greater curvature of the stomach (black arrow) and 3.5 cm of the antimesenteric portion of the jejunum (black arrowhead) were apposed with a 360° two-layer closure

The mass was diagnosed as a feline eosinophilic sclerosing fibroplasia. The mucosa was focally replaced by dense collagen trabeculae that were dissected by bands of plump fibroblasts, eosinophils, mast cells and fewer lymphocytes, plasma cells and neutrophils (Figure 4). There was a focal ulcer with numerous neutrophils surrounding mineralized concretions. The remaining mucosal epithelium was surrounded by dense eosinophilic and lymphoplasmacytic inflammation, which extended to the subjacent Brunner’s glands and submucosa. The inflammation did not extend to the muscularis layers in the section evaluated, although increased numbers of eosinophils were seen within blood vessels of the muscularis. Gram and Grocott’s methenamine silver stains were performed for bacteria and fungi, respectively, and were negative. Mast cells identified on a toluidine blue stain for metachromatic granules did not exhibit signs of atypia suggestive of neoplasia and were interpreted as inflammatory.

Figure 4

Pyloroduodenal junction biopsy, feline eosinophilic sclerosing fibroplasia. Expanding the mucosa and extending through the submucosa (the portion of Brunner’s gland is highlighted by an asterisk) in the wedge biopsy sample are trabecular bands of sclerotic collagen with associated fibroblasts (arrow) surrounded by eosinophils, scattered lymphocytes, mast cells and fewer plasma cells and neutrophils. × 20 magnification

The cat was maintained on lactated Ringer’s solution at 2.86 ml/kg/h and received buprenorphine (0.01–0.02 mg/kg IV q6–8h), pantoprazole (1 mg/kg IV q24h) and maropitant (1 mg/kg IV q24h). The cat was discharged the day after surgery on omeprazole PO 1 mg/kg/day. After 2 weeks, the cat returned for suture removal and the owner reported that it was doing well with occasional episodes of diarrhea and vomiting. The cat was placed on an oral prednisolone taper (initial dose of 0.7 mg/kg/day decreased to 0.35 mg/kg/every other day after 15 days). The cat was initially lost to follow-up but was presented to the emergency service 4 months later for acute vomiting and diarrhea. This was attributed to its suspected chronic enteropathy based on ultrasonographic findings of small and large intestinal submucosa and muscularis thickening; however, this was not confirmed with further diagnostics. The peripheral eosinophilia had resolved by this time. On ultrasound, the gastrojejunostomy site was unremarkable and the duodenal mass-like mural thickening was consistent with the previously biopsied FESF. The patient’s prednisolone dose was reportedly increased, though its weight had also increased significantly (initial dose of 0.4 mg/kg/day decreased to 0.2 mg/kg/every other day after 6 days).

Over 2 years after the gastrojejunostomy, the patient presented to the hospital in respiratory distress. The patient had received oral prednisolone until 1 month prior. A CT scan of the thorax showed a multilobar mixed lung pattern most consistent with bronchopneumonia, although an underlying component of bronchitis could not be ruled out. The patient was humanely euthanized due to the need for mechanical ventilation, and a post-mortem examination was not performed.

Discussion

This case describes the use of gastrojejunostomy to bypass a proximal duodenal obstruction caused by FESF. FESF commonly localizes to the cranial gastrointestinal tract at the pylorus, making resection challenging due to the proximity of the major and minor duodenal papillae.^1,2 Similar lesions have responded to corticosteroid therapy, and prednisolone has been reported to increase survival time.^1,2,12 The cat in this report exhibited persistent clinical signs consistent with mechanical obstruction despite prednisolone treatment, necessitating surgical intervention.

The prognosis for FESF is highly variable and largely dependent on the extent and location of the lesion. In one series of four cats, the cat with a non-resectable proximal duodenal mass had the shortest survival time. ¹³ The lesion in the present case involved the proximal duodenum, including the areas of the major and minor duodenal papillae. In cats, the common bile duct and pancreatic duct empty into the major duodenal papilla; only 20% of cats have an accessory pancreatic duct that empties into the minor duodenal papilla. ¹⁴ The use of gastrojejunostomy is proposed as a novel therapy for non-resectable FESF lesions that include the pylorus and/or descending duodenum.

Gastrojejunostomy has primarily been used in dogs and cats when gastrectomy involves removal of the pylorus and tension does not allow a gastroduodenostomy. ¹⁵ It has also been used in cases where gastrointestinal perforation necessitated partial duodenectomy and pylorectomy, leading to gastrojejunostomy (Billroth II). ¹⁶ Billroth II is infrequently indicated in dogs and cats because the body of the stomach can usually be anastomosed to the duodenum. ¹⁵ In the present case, the mass-like lesion contained the majority of the descending duodenum. Gastrojejunostomy was considered a reasonable option as the cat had no clinical or biochemical evidence of biliary or pancreatic duct obstruction. One potential disadvantage of gastrojejunostomy is ‘dumping syndrome’, in which substantial amounts of osmotically active solids, liquids and gastric acid enter the small intestine. ¹⁷ Afferent loop obstruction is another possible result of gastrojejunostomy and may be responsible for the recurrent clinical signs in this patient. ¹⁸ This occurs due to partial obstruction of the afferent loop of the intestine, relief of the obstruction, and sudden dumping of pancreatic and biliary secretions into the stomach, leading to bilious vomiting. ¹⁸ The present patient was managed in the hospital on intravenous pantoprazole, buprenorphine and maropitant, and discharged on oral omeprazole to minimize the effects of gastric acid on the small intestine. After a 2-week period, the patient resumed prednisolone therapy. This patient did not receive antimicrobial therapy, though many lesions have been associated with bacteria.^1,2,5 The cat presented 2.5 years after surgery in respiratory distress, with no gastrointestinal signs reported. Given the recurrent gastrointestinal signs observed after surgery, however, aspiration pneumonia secondary to vomiting due to the FESF lesion, gastrojejunostomy or chronic enteropathy is possible.

We did not identify an underlying cause of the lesion, potentially due to the limitations of a wedge biopsy and lack of necropsy. In addition, a necropsy may have enabled us to determine whether the cause of decline was related to the FESF lesion or surgery.

The present case suggests that gastrojejunostomy may be a viable option to bypass a pyloric or proximal duodenal obstruction in cases where the biliary and pancreatic ducts are not clinically obstructed.

Conclusions

We describe a gastrojejunostomy used to bypass a partial mechanical obstruction caused by an FESF mass lesion at the pyloroduodenal junction. We propose the use of the gastrojejunostomy procedure for patients with non-resectable lesions of the pylorus and proximal duodenum without clinical evidence of pancreatic or bile duct obstruction.