Imaging Diagnosis-Gastric Pneumatosis in a Cat

IMAGING DIAGNOSIS—GASTRIC PNEUMATOSIS IN A CAT LINDA G. LANG, HILLARY H. GREATTING, KATHY A. SPAULDING Gastrointestinal foreign bodies were removed surgically from a 9-year-old Siamese cat. Two days later the cat became lethargic and started regurgitating. A degenerative leukocytosis and drop in packed cell volume were present. Gastric wall thickening with intramural gastric air was detected radiographically and sonographically. Gastric ulceration with a focal necrotic area was seen endoscopically. At surgery, the stomach wall was emphysematous. Clinical signs resolved following partial gastrectomy and medical management. Intramural gastric air with declining clinical course was a significant impetus to return to surgery. r 2011 Veterinary Radiology & Ultrasound, Vol. 52, No. 6, 2011, pp 658–660. Key words: cat, emphysematous gastritis, gastric pneumatosis, ultrasonography. Signalment, History, and Clinical Findings toneal air and fluid was present, but were compatible with the celiotomy. Perforation of the stomach wall and a septic peritonitis were concerns. Pneumoperitoneum and a large volume of gas in the thickened wall of the distended stomach were confirmed radiographically (Fig. 2). The gas was fairly, evenly distributed circumferentially in the fundic wall. A 9-YEAR-old Siamese cat had vomiting and inappetence for 2 days. Two weeks earlier, the cat had been successfully treated for vomiting following possible ingestion of ibuprofen. The cat was dehydrated and had a tense, painful abdomen. A firm object was palpated in the right ventral abdomen. Radiographically, there was foreign material in the stomach, small intestine, and colon. The stomach and segments of small intestine were distended and obstruction was diagnosed. A laparotomy was performed. Carpet material, hair bands, plastic, foam, and a sponge were removed from the stomach and small intestine. The cat improved clinically but after surgery became anorexic, lethargic, and developed hypersalivation and regurgitation. A degenerative leukocytosis was present. Sepsis was suspected. The packed cell volume decreased from 30.2% to 20.2%. The central venous pressure indicated hypotension despite intravenous fluid and dopamine therapy. Surgery and Outcome Endoscopically, small, focal gastric ulcerations were present along the greater curvature with a focal area of necrosis immediately aboral to the previous gastrotomy site (Fig. 3). A laparotomy was performed. The stomach was distended with gas and fluid. The stomach wall was emphysematous along the greater curvature. There was a 2 cm region that was purple and thickened near the pylorus. Subserosal gas bubbles were noted. A rupture of the stomach with leakage of contents was not seen. The gastrotomy site was healing normally. A partial gastrectomy was performed, removing the greater curvature including the emphysematous area and the area of necrosis. Enterococcus sp., Escherichia coli, Candida albicans, and Lactobacillus minitus were isolated from the stomach. The cat recovered, and at 30 days there was resolution of the intramural gas and gastric wall thickening. Imaging Sonographically, the stomach was distended with fluid and there was no gastric motility. A large portion of the stomach wall, including the left body and the fundus, was thickened. The wall had multifocal to diffuse loss of wall layering, likely due to edema or inflammation (Fig. 1). There was a large amount of gas within and distending the wall of the fundus of the stomach. The gas extended to the serosal surface in several sites, making exact measurement of wall thickness difficult (Fig. 1). A small volume of peri- Gross and Histopathologic Findings The excised section of the greater curvature was edematous and had six, well-demarcated, irregularly shaped, dark brown ulcers ranging from 2 to 5 mm in diameter that were surrounded by hemorrhage. The gastric mucosa was replaced multifocally by necrosis, accumulations of fibrin, protein edema, and hemorrhage. There were inflammatory cells in the mucosa, submucosa, tunica muscularis, serosa, and mesentery. The submucosa was expanded by edema. Blood vessels were congested and had hypertrophied endothelium. The histopathologic diagnosis was acute From the Department of Small Animal Clinical Sciences, (Greatting), Department of Large Animal Clinical Sciences (Spaulding), Texas A & M University College of Veterinary Medicine 442 University Drive College Station, TX 77845. Address correspondence and reprint requests to Kathy A. Spaulding, at the above address. E-mail: kspaulding@cvm.tamu.edu Received February 16, 2011; accepted for publication April 21, 2011. doi: 10.1111/j.1740-8261.2011.01834.x 658 Vol. 52, No. 6 GASTRIC PNEUMATOSIS IN A CAT Fig. 1. Ultrasonographic image of the stomach wall. There is thickening of the gastric wall with loss of layering. The serosal and mucosal–luminal interface are outlined (large arrows). The intramural air is seen as both small hyperechoic bubbles (small arrows) within the wall, as well as larger hyperechoic accumulations with reverberation artifact (medium arrows). neutrophilic and lymphoplasmacytic gastritis with ulceration, hemorrhage, and edema. The changes were consistent with trauma to the mucosa and secondary gastritis. Discussion Pneumatosis is the abnormal accumulation of gas in any tissue. Gastric pneumatosis is rare.1–3 In the human Fig. 2. Ventrodorsal radiograph of the abdomen. There is gas in the lumen of the stomach and thickening of the gastric wall with intramural gas. Note the radiolucent area between the mucosal (medium arrows) and serosal (large arrows) surfaces depicting the gas within the stomach wall. There is also free abdominal air in the left cranial abdomen (small arrows). 659 Fig. 3. Photograph of the mucosal surface of the stomach. Note the extensive ulceration of the mucosal surface. No leakage to the peritoneal cavity was found. medical literature, gastric pneumatosis is classified as either gastric emphysema or emphysematous gastritis; an attempt is made to distinguish between the two entities as the treatment and prognosis differ significantly.1 Gastric emphysema is gas in the stomach wall without infection by gas-forming organisms.1 This can result from increased intraluminal pressure as might occur with gastroscopy, vomiting, or gastric outflow obstruction, with or without mucosal disruption.1–3 Patients are usually asymptomatic or have mild abdominal discomfort, distention, and vomiting.4 Gastric emphysema appears radiographically as well-defined linear radiolucent streaks parallel to the border of the stomach wall, separated from the lumen by soft tissue.1,2 However, gas may be cystic as opposed to linear.5 Gastric emphysema usually resolves spontaneously.5,6 Emphysematous gastritis is characterized by gastric wall inflammation, intramural air, and systemic toxicity7 and classically involves production of intramural gas by bacteria.1,2,7 However, entrance of air from the lumen via mucosal necrosis has also been reported.8 Emphysematous gastritis involves a more fulminating course. Patients usually have acute fever, abdominal pain, hematemesis, evidence of systemic toxicity, and sometimes septic shock.7 With human emphysematous gastritis, there is usually a predisposing factor that allows invasion of bacterial organisms into the gastric wall. These include ingestion of corrosive substances, alcohol abuse, gastroenteritis, recent gastrointestinal surgery, diabetes mellitus, and immunosuppression.7,9 Organisms associated with emphysematous gastritis include Streptococci, E. coli, Enterobacter species, Clostridium welchii, Clostridium perfringens, Staphylococcus aureus, Pseudomonas aeruginosa, and Klebsiella species.7,9 Radiographically, emphysematous gastritis is usually represented by mottled, cystic radiolucencies in the wall of the stomach, as opposed to the linear pattern of gastric emphysema.6,7,10 However, linear radiolucent patterns 660 LANG, GREATTING, AND SPAULDING have been described with emphysematous gastritis.4,8 The greatest concentration of these radiolucencies is often in the greater curvature.2,7 Because the appearance can vary radiographically, the clinical picture can help distinguish emphysematous gastritis from gastric emphysema.5,8,10 Ultrasonographically, emphysematous gastritis is characterized by gastric wall thickening with concurrent hyperechoic areas with reverberation artifacts within and following the internal layers of the gastric wall.11 With computed tomography there may be intramural gas collection, portal venous gas, gastric wall thickening, and pneumoperitoneum.6,9,12 Endoscopy and endoscopic ultrasound can be helpful in diagnosis and identifying the underlying cause of emphysematous gastritis.12 Few instances of intramural air in the gastrointestinal tract have been documented in animals. Emphysematous gastritis has been described in two horses13,14; both had nonresponsive colic and enterotoxemia. Clostridial organisms were isolated from gastric fluid or gastric wall. Emphysematous gastritis has been described in a dog15; intramural air was noted radiographically after bone ingestion and was thought to be caused by either trauma or production from gas-producing bacteria. Gastric pneumatosis associated with gastric dilatation-volvulus can indicate vascular compromise, gastric necrosis, and a poor prognosis, but lack of visualization of air in the wall does not rule out gastric necrosis.16,17 Pneumatosis coli has been reported in dogs.18–22 In these dogs, the diagnosis was made by radiography and ultrasonography. Clinical signs resolved with conservative treatment. 2011 The finding of intramural gastric air should be distinguished from intraluminal air, free abdominal air, and intramural fat. Intramural air can be identified both radiographically and ultrasonographically. Once intramural air is confirmed, emphasis should be placed on identifying the cause or underlying disease process. Anything that compromises gastric wall integrity can lead to intramural air. Gastric wall necrosis, vascular compromise, neoplasia, penetrating foreign bodies, or gastric ulceration may allow the entrance of air and bacteria into the wall of the stomach. In our cat, intramural gastric air was visible radiographically and sonographically. The mechanism of air entry into the gastric wall was not determined. Both mechanical and bacterial mechanisms are possibilities, or it can be a combination of both. Emphysematous gastritis is suspected based on the clinical suspicion of sepsis, isolation of bacteria from the stomach wall, and widespread gastric wall thickening. The histopathologic findings in this cat were not conclusive of the cause. This may be due to the fact that the necrotic area was submitted for bacterial isolation, and the surrounding eroded gastric tissue was submitted for histopathologic evaluation. We suspect the necrosis and ulceration in the stomach allowed bacteria to enter the stomach wall and become a source of the septicemia. In conclusion, gastric pneumatosis is a rare finding that may indicate loss of integrity of the gastric wall. Findings on radiography and ultrasonography in conjunction with the clinical course can help substantiate the presence of gastric wall air and identify the underlying cause. REFERENCES 1. Kussin SZ, Henry C, Navarro C, Stenson W, Clain DJ. Gas within the wall of the stomach report of a case and review of the literature. Dig Dis Sci 1982;27:949–954. 2. Nelson SW. Extraluminal gas collections due to diseases of the gastrointestinal tract. Am J Roentgenol Radium Ther Nucl Med 1972;115: 225–248. 3. D’Cruz R, Emil S. Gastroduodenal emphysema. 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