University of Edinburgh



Canine and feline emphysematous gastritis may be differentiated from gastric emphysema: clinical and imaging description of 5 cases F. Thierry, M.F. Ferreira, G.K. Paterson, T. Liuti, J. Del-PozoFrom the Royal (Dick) School of Veterinary Studies and Roslin Institute, The University of Edinburgh, Roslin, EH25 9RG, UK. Address all correspondence to Florence Thierry; e-mail: fthierry@exseed.ed.ac.ukKeywordsGastric pneumatosis, portal gas, pneumoperitoneum, cat, dogRunning head 1: Thierry et al. Running head 2: Canine and feline gastric pneumatosisAbstractGastric pneumatosis is an imaging finding defined as the presence of gas foci in the gastric wall. In humans, this imaging feature can result from one of two separate clinical entities: life-threatening emphysematous gastritis or clinically benign gastric emphysema. This retrospective descriptive case series describes the clinical and imaging features in five animals diagnosed with spontaneous gastric pneumatosis without gastric dilatation-volvulus. Three canine and two feline cases of spontaneous gastric pneumatosis were identified on radiographic and ultrasonographic examinations. In addition to gastric pneumatosis, one dog and two cats presented concomitant systemic signs such as lethargy, hematemesis, anemia or leukocytosis. Two dogs remained asymptomatic or presented mild gastrointestinal signs. Portal gas was described in two dogs and one cat, and pneumoperitoneum in one dog. These features were not considered clinically significant. The dog and two cats with systemic signs were euthanized due to clinical deterioration and diagnosed with emphysematous gastritis. The gastric pneumatosis of both dogs without systemic signs resolved while on medical management without antibiotic therapy. These latter cases were interpreted as consistent with gastric emphysema. Findings from the current study indicated that gastric pneumatosis can occur without gastric dilatation-volvulus in cats and dogs and that a combination of systemic abnormalities may help to differentiate between apparent life-threatening emphysematous gastritis and relatively benign gastric emphysema. More studies are needed to further understand the etiology and risk factors associated with these conditions.INTRODUCTIONGastric pneumatosis is defined as the presence of gas foci in the gastric wall.1 This entity remains an imaging finding rather than a definitive diagnosis and can be divided into two separate clinical entities: emphysematous gastritis and gastric emphysema, both with similar imaging features.1,2 In humans, emphysematous gastritis is a life-threatening disorder triggered by the presence of gas-forming organisms in the gastric wall and can lead to acute abdominal pain, hematemesis, pyrexia, leukocytosis and sepsis. It is generally caused by a local infection through a mucosal defect but hematogenous dissemination to the stomach is also possible.3 On endoscopy, erosive mucosa and wall necrosis are commonly found in half of the patients, who may require gastrectomy.2 Ischemia can be caused by vascular occlusion, gastric infarction or gastric volvulus.1Conversely, gastric emphysema is defined as air trapping within the gastric wall due to a traumatic rupture of the gastric mucosa.2 Patients do not generally present with an acute abdomen and wall necrosis is a rare finding.2,3 Importantly, it is typically asymptomatic and resolves spontaneously. Several underlying etiologies of gastric emphysema have been identified in humans such as gastric distension, gastric neoplasia or intestinal obstruction. A direct injury to the mucosa or mucosal tearing due to increased intraluminal pressure has been suggested.2The stomach remains an uncommon site of pneumatosis due to its abundant vascular supply, acidic pH and efficient mucosal barrier.2,3 Over the last 35 years of small animal veterinary literature, two feline cases and a single canine case of spontaneous gastric pneumatosis have been reported without gastric dilatation-volvulus.4-6 Other digestive sites can be affected, such as pneumatosis coli being previously described in one dog, and resolving with dietary and antibiotic therapy.7 Aims of the current study were to describe the clinical and imaging characteristics of gastric pneumatosis in a group of dogs and cats and to determine whether any of these characteristics could potentially be used to differentiate life-threatening emphysematous gastritis from benign gastric emphysema.METHODSThe study design was a retrospective descriptive case series. The database of the Hospital for Small Animals of the University of Edinburgh was searched for dogs and cats that were diagnosed with gastric pneumatosis during the period of January 2017 to January 2018. Permission to use clinical and diagnostic imaging data for research was provided through informed consent from the owners at the time of admission. Criteria for inclusion in the current study were diagnostic quality ultrasonographic images, available gastric histology or resolution of the gastric pneumatosis on subsequent ultrasonographic examinations (performed by the same operator), complete patient history, and available hematology and serum biochemistry analyses. All decisions for study inclusion or exclusion were made based on a consensus of the first author (final year small animal imaging resident) and a board-certified veterinary radiologist (T.L). The diagnosis of gastric pneumatosis was based on detection of diffuse intramural gas on ultrasonography by the first author under the direct supervision of a board-certified veterinary radiologist (T.L.). At the time of ultrasonographic examination, both observers were aware of the presenting clinical signs. Diagnosis of emphysematous gastritis was based on gastric histology, or if not available, on the presence of gastric pneumatosis and systemic abnormalities such as lethargy, pyrexia, hematemesis, leukocytosis, anemia or hypoalbuminemia. The presumed diagnosis of gastric emphysema was based on the absence or mild presence of gastrointestinal signs and absence of systemic abnormalities. Age, sex, clinical signs, radiographic, ultrasonographic, histological, bacteriological results and outcome, were retrospectively recorded by the first author and this observer was aware of final diagnosis at the time of data recording. RESULTSClinical findings A total of three dogs and two cats met the inclusion criteria. Animals were 1 to 13 years old. Two of the three male and both female patients were neutered. The breed distribution included a Miniature Schnauzer, Fox Terrier and Dachshund and two Domestic Shorthaired cats.Clinical signs and systemic abnormalities are summarized in Table 1. Three cases (dog 1, cats 1 & 2) presented with systemic clinical abnormalities such as lethargy (3/3), anorexia (2/3), anemia presumptively resulting from gastrointestinal blood loss (2/3), neutrophilia indicative of an active inflammatory process (2/3), and were diagnosed with emphysematous gastritis. These animals showed gastrointestinal signs such as hematemesis (2/3) and/or diarrhea (2/3). One case had elevated feline pancreas-specific lipase, consistent with pancreatitis (cat 1). Hypoalbuminemia was documented in all three severely affected animals with emphysematous gastritis and may be explained by an acute inflammatory state, possibly combined with loss via the gastrointestinal tract.Two patients (dogs 2 & 3) presented none (1/2) to only mild gastrointestinal signs (1/2) with no evidence of systemic abnormality. Presenting complains included the presence of perianal masses in one dog and diarrhea with mild hematochezia in the other one. Physical examination was unremarkable on presentation in both animals apart from the presence of perianal masses in dog 2. Hematology and serum biochemistry were unremarkable apart from elevated hepatic enzymes and borderline results for a quantitative pancreatic lipase immunoreactivity assay in both animals. Both dogs were staged for oncological purposes. Dog 2 was diagnosed with hepatoid gland adenoma, pancreatitis, and iatrogenic Cushing’s disease secondary to corticosteroid therapy for atopic dermatitis. Dog 3 was eventually diagnosed with urothelial carcinoma on histology after cystoscopic biopsies, and was followed for chemotherapy and restaging purposes.Ultrasonographic and radiographic findingsB-mode ultrasonographic examinations (MyLab Twice Esaote, Genova, Italy) were performed on transverse and sagittal planes with electronic microconvex (SC 3123) and electronic linear array (LA 435) probes, with frequencies ranging between 8-14 MHz. Both lateral and dorsoventral abdominal radiographic examinations were performed using a digital radiography system (Apollo DRF, Villa Sistemi Medicali s.p.a., Buccinasco, Italy). Exposure parameters varied between 61 to 67kV and 3 to 5 mAs. Radiographic assessments were performed using dedicated DICOM viewer software (OsiriX 64-bit, Geneva, Switzerland).Reasons for abdominal imaging were either investigation of the gastrointestinal signs (4/5) or clinical staging due to potential neoplasia (1/5). On admission, ultrasonographic examination described a normal gastric wall in dog 1, and both cats. Clinical deterioration of these animals during the hospitalization period motivated a second ultrasonographic examination. In dogs 2 and 3, gastric wall changes were detected on ultrasonography performed on admission.On ultrasonography, there was marked diffuse gastric wall thickening up to 10mm, with total (2/5) to partial loss (3/5) of the wall layering (Figures 1B, 2B, 3A, 4A). A marked (4/5) to moderate (1/5) amount of gas artefacts was diffusely noted within most of the gastric wall (Figures 1B, 2B, 3A, 4A). Gastric distension was reported in four animals. The extrahepatic (Figure 1C) and intrahepatic (Figure 2C) portal vasculature contained intraluminal gas in 3/5 patients (dogs 1 & 3, cat 1). Pneumoperitoneum was described in dog 2 (Fig. 4A). A hypoechoic right pancreatic limb surrounded by hyperechoic fat was noted in 1/5 patients, consistent with acute pancreatitis (dog 2).On abdominal radiography performed in three patients, there was moderate gastric distension by fluid and gas associated with gastric wall thickening (Figures 1A, 2A). Intramural gastric gas lucencies were described on radiography in 2/3 animals, with a cystic appearance in dog 1 (Figure 1A) and a streaky appearance in cat 1 (Figure 2A).Treatment and outcomeAll animals diagnosed with emphysematous gastritis were euthanized due to clinical deterioration. A single animal transiently improved on antibiotherapy (cat 1). Clinical and ultrasonographic improvement of gastric pneumatosis was achieved in 48 hours in this animal (Figures 2D & 2E). Intensive medical management was continued over a 3-month period but euthanasia was performed at the referring veterinarian due to relapse of clinical signs. Three patients had been treated with corticosteroids prior to diagnosis (dog 1 & 2, cat 1).Animals presumptively diagnosed with gastric emphysema were treated with standard doses of antacids, antiemetic and gastroduodenal mucosal protectants, without antibiotherapy. Complete resolution of the gastric pneumatosis was confirmed on follow-up ultrasonography, one week (dog 3, Figure 4B) and one month later (dog 2, Figure 3B), with no relapse of the presenting clinical signs, respectively, 6 and 7 months after diagnosis. Both dogs were followed at the small animal referral hospital during this period for reasons unrelated to the gastric pneumatosis.Post-mortem histology and bacteriologyPost-mortem examinations were performed in dog 1 and cat 2. Grossly, the gastric mucosa had a bubbly appearance. In dog 1, the portal vein contained bubbling dark red fluid surrounding gelatinous clots suspected to be aerated blood. Histology of the stomach revealed an edematous and hemorrhagic submucosa expanded by very large numbers of large clear spaces in dog 1, consistent with air pockets separating the connective tissue (Figure 5A, 5D). This feature was seen to a lesser extent in cat 2. Also in the submucosa, there were small to moderate numbers of scattered macrophages, extravascular erythrocytes, rare vessels with fibrinoid necrosis, and rare, small areas of submucosal necrosis around the air pockets (Figure 5B, 5C). Within the mucosa, a small number of short rod-shaped bacteria were visualized in dog 1. These findings were consistent with emphysematous gastritis. In cat 2, culture of the gastric wall, sampled immediately after euthanasia, isolated Staphylococcus felis as identified by partial 16S, rpoB and tuf gene sequencing and Enterococcus faecalis. The histological presentation of this cat was consistent with mild emphysematous gastritis, which was confirmed by a positive gastric wall culture. However, there was no evidence of mucosal necrosis in these two confirmed cases.DISCUSSIONTo the authors’ knowledge, this is the first case series describing spontaneous canine and feline gastric pneumatosis without gastric dilatation-volvulus. All animals diagnosed with emphysematous gastritis in the current study had severe clinical signs, systemic clinical abnormalities and a poor outcome. The dogs presumably diagnosed with gastric emphysema, on the other hand, presented none to only mild gastrointestinal signs and had no evidence of systemic abnormalities. The observed gastric pneumatosis in these two cases resolved quickly on medical management without antibiotic therapy. Their clinical presentation and outcome could not have been explained by a severe condition such as emphysematous gastritis. Gastric pneumatosis might be more prevalent than what is currently reported in the veterinary literature. The five cases of gastric pneumatosis described in this report were diagnosed in the same hospital over a 10-month period. An improved awareness of the imaging features could be helpful for improving diagnosis in future patients. Because this was a criterion for inclusion in the study, all 5 cases had ultrasonographic evidence of gas in the gastric wall. It was notable that gas was present in more than half of the entire gastric wall area in all cases. In the authors’ experience, this feature could be helpful for differentiating gastric pneumatosis from focal gastric ulceration. While focal gastric ulceration can also present with intraparietal gas, wall thickening and loss of layering8, these changes would be less likely to appear as diffuse as those seen in the current cases with gastric pneumatosis. Gastric distension was detected in four of our cases, which could possibly have caused mucosal damage. The presence of intramural gastric gas is commonly seen in cases with gastric dilatation-volvulus but is not considered to be a good predictor of wall necrosis on surgery.9 Gastric pneumatosis in cases with gastric dilatation-volvulus may more likely represent gastric emphysema due to increased luminal pressure and mucosal tearing rather than wall necrosis and bacterial colonization.9Most of the recent publications in human medicine agree on the similar radiographic appearance of emphysematous gastritis and gastric emphysema.2,10 The streaky or cystic appearance did not appear to differentiate both disorders in the dogs and cats sampled in the present study. There was a smaller amount of intramural gas detected in the patients diagnosed last (dog 3 & cat 2), likely resulting from an earlier diagnosis due to an increased suspicion index triggered by the first three cases. This was confirmed on histology for cat 2. On ultrasonography, total loss of the gastric wall layering was noted in two cases, while altered layering was described in the other three. The ultrasonographic gastric wall measurements performed in dog 1 and cat 1 were likely underestimated due to difficulty in distinguishing the interface between the gastric wall and gastric lumen because of gas artefact.Three of the cases reported here had concurrent extrahepatic and intrahepatic portal gas, which has also been recently reported in a dog due to colonic ulceration.11 In human literature, portal gas is not considered a poor prognostic factor for gastric pneumatosis, which also appears to be the case in the present study.1 Intramural gastric gas can diffuse into the gastric vascular supply before being drained by the portal vascular bed, which was not clinically significant in dog 3. Evidence of pneumoperitoneum was described in dog 2 and likely resulted from gas diffusion from the gastric wall to the peritoneum. There was no evidence that the pneumoperitoneum was clinically significant. Pneumoperitoneum has also been reported in human patients with gastric emphysema and is not considered to be a characteristic warranting surgery.1,12In human medicine, non-steroidal and steroidal anti-inflammatory drugs have been identified as risk factors for emphysematous gastritis.2,13 Two animals (dog 2 and cat 1) described in this report were on a long course of prednisolone, and one of these had a final diagnosis of emphysematous gastritis. In addition, two cases received short courses of either steroidal (dog 1) or non-steroidal (cat 2) anti-inflammatories, both having a final confirmed diagnosis of emphysematous gastritis. Previous abdominal surgery has been identified as a risk factor for emphysematous gastritis in humans, which may have predisposed cat 2.2,14 Pancreatitis has also been described as a risk factor for emphysematous gastritis, which could have been a predisposing factor for cat 1.3 Medical management with antibiotics has successfully been reported in some human patients.14Diagnosis of emphysematous gastritis and treatment in the acute phase is essential due to the associated severity and high mortality rate.2 Early recognition of the disease may therefore provide the best chance of survival. Among the three cases of emphysematous gastritis described in this study, a single patient improved with immediate medical management. In the authors’ opinion, surgery should be recommended if there is evidence of gastric wall necrosis on endoscopy, usually characterized by areas of white, yellow or brown tissue, as well as presence of green-black exudate.15 In a previously described feline case report, partial gastrectomy was performed due to evidence of necrosis during surgery.5 In human medicine, the intraluminal gastric pressure is relieved via nasogastric decompression.2,3 Perhaps, this procedure could have been beneficial if employed in the patients of the present study where gastric distension was documented, allowing preservation of the gastric mucosa from further damage.In humans, bacterial culture of the gastric mucosa has isolated Gram-positive and Gram-negative organisms such as Klebsiella pneumoniae, streptococci, Escherichia coli, Enterobacter sp., Staphylococcus aureus or Pseudomonas aeruginosa.2,14 Two cases of equine emphysematous gastritis due to Clostridium spp. infection have been described on post-mortem examination.16,17 A feline case report has described the isolation of Enterococcus sp., E. coli, Candida albicans and Lactobacillus minitus from the stomach.5 In another feline case report, Clostridium perfringens type A was isolated and associated with wall necrosis on histology.6 In the current study, culture of the gastric wall in cat 2 yielded S. felis and E. faecalis. S. felis is a coagulase-negative bacterium, part of the normal commensal flora of the feline skin and saliva and to the best of the authors’ knowledge, has never been isolated previously from the stomach. It has however been associated as a pathogen in lower urinary tract disease, otitis and dermatitis.18,19 It is therefore possible that S. felis and E. faecalis were responsible pathogens for the development of the emphysematous gastritis in this patient, although contamination cannot be excluded and more cases would be required to evaluate this. In any case, this highlights the potential usefulness of gastric culture in cases of gastric pneumatosis.The current study was limited in that a definitive diagnosis was only available for two of the patients. Invasive procedures, such as gastric biopsy or culture, were considered not to be justifiable in the remaining three patients, given the asymptomatic presentation in dog 2 & 3, and the clinical improvement with supportive treatment in cat 1. The study was also limited in that the small number of cases for each group did not permit statistical comparisons.In conclusion, findings from the current study indicates that gastric pneumatosis can occur without gastric dilatation-volvulus in cats and dogs and that a combination of systemic abnormalities such as lethargy, pyrexia, hematemesis, leukocytosis or hypoalbuminemia may help to differentiate emphysematous gastritis from gastric emphysema that presents with none to mild gastrointestinal signs and no evidence of systemic abnormalities. More studies are needed to further understand the etiology and risk factors associated with these conditions, since differentiating between the apparent life-threatening emphysematous gastritis from the relatively benign gastric emphysema would be considered essential in providing the best care and chance of survival for affected patients.List of author contributionsCategory 1(a) Conception and DesignFlorence Thierry, marisa F. Ferreira, Gavin K. Paterson, Tiziana Liuti, Jorge Del-Pozob) Acquisition of DataFlorence Thierry, marisa F. Ferreira, Gavin K. Paterson, Tiziana Liuti, Jorge Del-Pozo (c) Analysis and Interpretation of DataFlorence Thierry, marisa F. Ferreira, Gavin K. Paterson, Jorge Del-PozoCategory 2(a) Drafting the ArticleFlorence thierry (b) Revising Article for Intellectual ContentFlorence Thierry, marisa F. Ferreira, Gavin K. Paterson, Tiziana Liuti, Jorge Del-PozoCategory 3(a) Final Approval of the Completed ArticleFlorence Thierry, marisa F. Ferreira, Gavin K. Paterson, Tiziana Liuti, Jorge Del-PozoreferencesSpektor M, Chernyak V, McCann TE, et al. Gastric pneumatosis: Laboratory and imaging findings associated with mortality in adults. Clin Radiol. 2014;69:e445–449Matsushima K, Won EJ, Tangel MR, et al. Emphysematous gastritis and gastric emphysema: similar radiographic findings, distinct clinical entities. World J Surg. 2015;39:1008–1017Paul M, John S, Menon MC, et al. Successful medical management of emphysematous gastritis with concomitant portal venous air: a case report. J Med Case Report. 2010;4:140–144Burt JK. What is your diagnosis? Emphysematous gastritis. J Am Vet Med Assoc. 1982;181:295–296Lang LG, Greatting HH, Spaulding KA. Imaging diagnosis-gastric pneumatosis in a cat. Vet Radiol Ultrasound. 2011;52:658–660Burn J, Rousset N, Henderson DW, et al. Emphysematous gastritis associated with Clostridium perfringens type A in a cat. Vet Rec Case Rep. 2017. doi:10.1136/vetreccr-2017-000540Russell NJ, Tyrrell D, Irwin PJ, et al. Pneumatosis coli in a dog. J Am Anim Hosp Assoc. 2008;44:3235Fitzgerald E, Barfield D, Lee KC, et al. Clinical findings and results of diagnostic imaging in 82 dogs with gastrointestinal ulceration. J Small Anim Pract. 2017;58:211–218Fischetti AJ, Saunders HM, Drobatz KJ. Pneumatosis in canine gastric dilatation-volvulus syndrome. Vet Radiol Ultrasound. 2004;45:205–209Johnson PT, Horton KM, Edil BH, et al. Gastric pneumatosis: the role of CT in diagnosis and patient management. Emerg Radiol. 2011;1:65–73Cartwright JA, Breheny C, Major AC, et al. Imaging diagnosis-a case of spontaneous hepatic portal vein gas in an 11-month-old West Highland White Terrier. Vet Radiol Ultrasound. 2016;57:E54–57Muthukumarasamy G, Damodharan K, Chudy M, Ablett M. Gastric emphysema and pneumoperitoneum. ANZ J Surg. 2010;80:945-6Szuchmacher M, Bedford T, Sukharamwala P, et al. Is surgical intervention avoidable in cases of emphysematous gastritis? A case presentation and literature review. Int J Surg Case Rep. 2013;4:456–459Al-Jundi W, Shebl A. Emphysematous gastritis: case report and literature review. Int J Surg. 2008;6:e63–66Tang SJ, Daram SR, Wu R, Bhaijee F. Pathogenesis, diagnosis, and management of gastric ischemia. Clin Gastroenterol Hepatol. 2014;12:246-52Weldon AD, Rowland PH, Rebhun WC. Emphysematous gastritis in a horse. Cornell Vet. 1991;81:51–58Delesalle C, Deprez P, Vanbrantegem L et al. Emphysematous gastritis associated with Clostridium septicum in a horse. J Vet Intern Med. 2003;17:115–118Igimi S, Kawamura S, Takahashi E, et al. Staphylococcus felis, a new species from clinical specimens from cats. Int J System Bacteriol. 1989;39:373–377Litster A, Moss SM, Honnery M, et al. Prevalence of bacterial species in cats with clinical signs of lower urinary tract disease: recognition of Staphylococcus felis as a possible feline urinary tract pathogen. Vet Microbiol. 2007;121:182–188Table 1. Prevalence of clinical findings, abnormal blood results and outcome, in five animals with gastric pneumatosis.Prevalence with emphysematous gastritis (n=3)Prevalence with gastric emphysema (n=2)Clinical signsAnorexia2/30Vomiting2/31/2Hematemesis2/30Diarrhea2/31/2Lethargy3/30Weight loss1/30Erythema1/30Asymptomatic01/2Hematological abnormalitiesLeukocytosis2/30Anemia2/30Biochemistry abnormalitiesIncreased ALT1/31/2Increased APIncreased cPLI/fPLI1/31/32/22/2Increased lactate1/30Decreased ALBDecreased FOL/COBDecreased K+3/31/31/3000Hospitalization duration from diagnosis6 hours ≤ Hospitalization ≤12 hours2/31/212 hours < Hospitalization ≤60 hours1/31/2OutcomeEuthanasiaComplete resolution3/3002/2WBC, white blood cell count; RBC, red blood cell count; cPLI, canine pancreas-specific lipase; fPLI, feline pancreas-specific lipase; COB, cobalamin; FOL, folate.FIGURESFigure 1. Dog 1 - Abdominal radiograph (A) with diffuse gas pattern in the entire gastric wall (arrow). Ultrasonographic images with marked thickening of the gastric wall (B, arrow) containing gas artefact. Note the loss of gastric wall layering and hyperechoic gas foci in the lumen of the extrahepatic portal vein (C).Figure 2. Cat 1 - Abdominal radiograph (A) demonstrating a linear gas pattern in the gastric wall (arrow). Ultrasonographic images showing a thickened 6.8mm gastric wall (B, arrow) containing gas artefact associated with total loss of layering and intrahepatic portal gas (C, arrow). Two days later, there was a reduction of the amount of gas pattern in the 5.1mm gastric wall delineated by calipers (D) and resolution of the intrahepatic portal gas (E). Figure 3. Dog 3 - Abdominal ultrasonographic images showing gas artefact (arrow) in the 10mm thickened gastric wall between calipers (A), and complete resolution 1 week later (B).Figure 4. Dog 2 - Abdominal ultrasonographic images highlighting gas artefact in the 9.1mm thickened gastric wall delineated by calipers (A), pneumoperitoneum (arrow) and complete resolution 1 month later (B), with normal thickness (3.5mm between calipers) and gastric wall layering.Figure 5. Dog 1 - Stomach. A: Subgross (x20) view of the gastric submucosa with multifocal emphysema (examples indicated by arrowheads. s=serosa, m=mucosa). B: High power (x200) of an area of submucosal necrosis (arrowheads) adjacent to an emphysematous space (center of picture). C: x200 image of a vein (lined by endothelium, arrow), with perivascular infiltration by macrophages, and fibrinous necrosis (arrowheads). D: x100 image illustrating submucosal hemorrhage (*). All slides are stained with Hematoxylin and Eosin. Bar = 1000 ?m (A) or 100 ?m (B to D). ................
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