Ischemic Gastritis Research Articles

S5084 Sick to my stomach: An Unusual Case of Severe Combined Celiac and Superior Mesenteric Arterial Stenosis Causing Ischemic Gastritis

S5084 Sick to my stomach: An Unusual Case of Severe Combined Celiac and Superior Mesenteric Arterial Stenosis Causing Ischemic Gastritis

S3124 Ischemic Gastritis Secondary to Aortic Dissection

S3124 Ischemic Gastritis Secondary to Aortic Dissection

S4239 Two Cases of Ischemic Gastritis Secondary to Septic Emboli

S4239 Two Cases of Ischemic Gastritis Secondary to Septic Emboli

S4296 Ischemic Gastritis Due to Mycotic Embolism in the Setting of Group B Strep Bacteremia: A Fatally Rare Case

S4296 Ischemic Gastritis Due to Mycotic Embolism in the Setting of Group B Strep Bacteremia: A Fatally Rare Case

S2675 Ischemic Gastropathy vs. Severe H. pylori Gastritis in a Patient With Extensive Vascular Disease

Introduction: Approximately half of gastric ulcers are associated with H. pylori. Conversely, gastric ulceration secondary to ischemia is rare due to the stomach’s abundant vascular supply from all three branches of the celiac artery. Here we present a case of a patient with upper gastrointestinal bleeding and concern for gastric ischemia who was diagnosed with H. pylori associated gastritis. Case Description/Methods: A 70-year-old female with severe peripheral artery disease, abdominal aortic aneurysm status post endovascular repair, hypertension, HIV, chronic kidney disease and B-cell lymphoma was admitted for pathologic right hip fracture and underwent open reduction and internal fixation. The procedure was complicated by lactic acidosis, an elevated troponin, and transaminitis in the setting of intraoperative hypotension. Six days later the patient had coffee ground emesis and melena with a lactate of 9.8 mmol/L and a hemoglobin of 6.4 g/dL, from 8.9 g/dL one day prior. 2 units of packed red blood cells were administered, anticoagulation was stopped, and a proton pump inhibitor was given. CT angiography of the abdomen and pelvis demonstrated splenic infarction, marked attenuation of multiple mesenteric vessels including the celiac artery, concern for ischemia of the stomach and cecum, and significant distention of the stomach (Figure A). Upper endoscopy demonstrated severe gastric mucosal pallor and decreased vascular pattern, diffuse linear erosions throughout the gastric fundus and body, and multiple large superficial ulcerations without active bleeding (Figure B and C). Given the appearance of the mucosa and overall clinical picture, there was concern for ischemic gastritis and biopsies were taken. Histology later revealed erosive gastritis, regenerative change and H. pylori without evidence of microthrombi or changes consistent with ischemia and the patient was started on quadruple therapy for H. pylori gastritis. She had one further episode of melena and received an additional blood transfusion before she was discharged one week later. Discussion: Our patient had extensive vascular disease and systemic hypotension with endoscopic findings highly suspicious for ischemic injury but with biopsies consistent with severe H. pylori gastritis. Although ischemic gastropathy should be considered in cases of an upper GI bleed in patients with vascular risk factors, careful histopathologic review is important for accurate diagnosis, and severe presentations of more routine diagnoses should also be considered.Figure 1.: A) CT angiography of the abdomen and pelvis demonstrating significant gastric distention. B) Esophagogastroduodenoscopy demonstrating mucosal pallor and C) large ulcerations within the gastric body.

Ischemic Gastritis in a Patient with Chronic Constipation.

Ischemic Gastritis in a Patient with Chronic Constipation.

1665 A Baffling Case of Gastrocolitis

INTRODUCTION: Chronic mesenteric ischemia often has a subtle presentation requiring a high index of suspicion. Average time to diagnosis is 10.7 months, often delayed due to the vague nature of complaints. We present a challenging case of severe chronic mesenteric ischemia in a young woman. CASE DESCRIPTION/METHODS: A 42-year-old female smoker presented with abdominal pain, constipation, and >70-lb weight loss. She had developed black, watery stools one week prior. Vital signs were normal, BMI was 12.6. She was cachectic, had abdominal distention and tenderness worse in the right lower quadrant. A contrasted CT scan revealed a distended colon and large stool burden. She failed conservative management. Endoscopy revealed multiple Forrest III gastric ulcers (Figure 1) and deep cecal ulcerations (Figure 2) with normal TI. Biopsies showed inflammation with granulation tissue. Work up was negative for vasculitis and infection. She failed a steroid trial for a presumptive diagnosis of Crohn’s disease. CT enterography was normal. Repeat endoscopy showed persistent gastric ulcers. Biopsies revealed ischemic gastritis with associated ulceration and submucosal blood vessels with fibrin thrombi. A CT angiogram showed severe stenosis of the celiac artery and chronic occlusion of the superior mesenteric artery (Figure 3.) Endovascular celiac and SMA stenting failed requiring surgically-placed retrograde celiac and SMA stents. Her symptoms recurred due to celiac stent thrombosis and SMA stent migration to the left iliac artery. Finally, an antegrade supraceliac to celiac and SMA bypass was performed with excellent results. DISCUSSION: A high index of suspicion is required to diagnose chronic mesenteric ischemia. Risk factors include age > 60, female gender, history of PAD, CVD, or CAD. Typical symptoms include weight loss, postprandial pain, and diarrhea though most people are asymptomatic or present with atypical symptoms including nausea, vomiting, early satiety, or bleeding which often lead to misdiagnosis or delayed diagnosis. Management is aimed at preventing further bowel infarction via endovascular or open revascularization. Patients who fail stenting or angioplasty have a much higher risk of perioperative mortality during open repair (15% vs. 2%.) Our patient’s young age, normal initial CT abdomen, gastric and cecal ulcerations with lack of vascular disease history blurred the clinical picture. A high index of suspicion is required in patients with an initial negative work up.

Upper Gastrointestinal Bleeding From Ischemic Gastropathy After TACE Therapy

Transarterial chemoembolization (TACE) therapy is used in the treatment of unresectable hepatocellular carcinomas. TACE involves the injection of a chemotherapeutic agent into the hepatic artery which results in decreased blood supply to the liver tumor and resultant tumor cell death. Rare complications of TACE therapy including hepatic artery occlusion, tumor rupture, liver abscess, and ischemic injury related to non-target embolization. GI bleeding due to ischemic gastropathy, however, is rare due to the extensive collateral blood supply of the stomach. A 63 year-old male with hepatitis C and alcoholic cirrhosis complicated by esophageal varices, hepatic encephalopathy, and hepatocellular carcinoma was admitted for his fourth TACE therapy. The patient developed abdominal discomfort and hematemesis the following day. Patient was tachycardic during episodes of hematemesis but was otherwise stable with no transfusion requirements. Upper endoscopy later that day revealed non-bleeding small esophageal varices and extensive areas of blackened mucosa from the proximal stomach to duodenum with nodularity, tissue friability, erosions, and adherent clots. Mucosal changes were most pronounced in the mid and distal stomach. Diffuse erosions were also noted in the proximal duodenum, but there was a discrete transition point to normal mucosa between the 2nd and 3rd portions of the duodenum. Hematemesis was thought to be related to severe inflammation and friability in stomach and proximal duodenum, and patient had clinical improvement with supportive care. Gastrc biopsies demonstrated fibrinoid change of lamina propria, glandular atrophy, and purulent exudate consistent with ischemic gastritis. Duodenal biopsies also demonstrated focal fibrinoid change of lamina propria and glandular atrophy also consistent with ischemia. This case was discussed with interventional radiology, and previously treated branches of the right and left hepatic artery had appeared atretic. Visualization of the hepatic lesion was therefore limited, and the decision was made to treat non-selectively via the left hepatic and middle hepatic artery which likely resulted in embolization of vasculature supplying the stomach and proximal duodenum. Most patients have resolution of symptoms with supportive care. PPI therapy has also been suggested to promote mucosal healing. Patients would benefit from monitoring after TACE therapy especially if less-selective embolization is performed.2338_A Figure 1 No Caption available.2338_B Figure 2 No Caption available.2338_C Figure 3 No Caption available.

A Rare Case of Emphysematous Gastritis - Sarcina Ventriculi

Emphysematous gastritis (EG) is a type of gastritis with characteristic features of gas along the gastric wall. The common organisms associated with EG are Klebsiella pneumoniae, Escherichia coli, Pseudomonas aeruginosa. It is considered to be a severe variant of Phlegmonous gastritis. A 65-year-old male with multiple comorbidities presented to the emergency room with abdominal pain, nausea, vomiting and cough for three days. Denied any history of corrosive ingestion, non-steroidal anti-inflammatory drugs, melena, hematochezia and trauma. On admission, he was afebrile, tachycardic (130), tachypneic (22), blood pressure 126/88 mmHg. Physical examination was positive for confusion, abdominal distension and epigastric tenderness. Laboratory examination revealed a white count 21.4 cells/dl, Hemoglobin 14.0 g/dl, platelets 350 cells/dl, INR 1.21, sodium 140 meq/l, potassium 4.2 meq/l, chloride 101 meq/l, bicarbonate 22 meq/l, blood urea nitrogen 30 mg/dl, creatinine 1.4 mg/dl, procalcitonin of 0.84 ng/dl. KUB X-ray was significant for gastric emphysema, Computer tomography (CT) abdomen demonstrated marked distention of the stomach with pneumatosis, consistent with EG and hepatic portal venous gas. He was empirically treated with broad-spectrum antibiotics. Esophagogastroscopy demonstrated few clean based ulcers at gastroesophageal[GE] junctions and bluish discoloration just distal to GE juntion suggestive of ischemic gastritis. Histopathology demonstrated reactive gastric epithelium due to Sarcina Ventriculi gastritis. Given his co-morbidities family opted for the hospice. Sarcina ventriculi is a gram positive anaerobic, sugar fermenting and spore forming organism.It is very difficult to culture in laboratory. The characteristic morphological features are basophilic staining, cuboid shape arranged in tetrad packets near the mucosal surface. The mechanism of injury is uncertain. It is considered delayed gastric emptying and carbohydrate stasis in association with acidic content of gastric juices provides an ideal culture medium. The by-products of the fermentation could induce the stomach and duodenal injuries. EG with S.ventriculi is most invariably fatal. CT abdomen is the most useful initial investigation followed by gastric biopsy as a confirmatory test. Regardless of the biopsy report it is prudent to start treating with broad-spectrum antibiotics and supportive therapy when EG is suspected, as early and aggressive treatment is the key to the prognosis.1919_A Figure 1. CT Abdomen- pneumatosis and portal venous air.1919_B Figure 2. Gastric mucosa with basophilc stained sarcina ventriculi arranged in tetrads.1919_C Figure 3. EGD demonstrating retained food material with bluish discoloration distal to the GE Junction

Thickened Gastric Folds in Ischemic Gastritis: A Rare Presentation of an Uncommon Condition

Gastric ischemia is an uncommon condition due to the rich blood supply and collateral circulation to the stomach. Typical endoscopic features include pale mucosa, erythema, erosions and ulcerations. The patient presented with these features, along with thickened gastric folds. While thickened gastric folds are often associated with other gastric conditions, histological pathology did not reveal evidence for any of these conditions. In this report, we describe a rare presentation of an uncommon condition. A 53-year-old female with past medical history of COPD, hypertension, and irritable bowel syndrome was admitted with generalized abdominal pain and renal insufficiency. The patient noted symptoms of weakness, fatigue, 70 lb weight loss over the past 9 months, and heartburn. Additionally, the patient used meloxicam for back pain and has a 40-pack-year history of smoking. Physical examination was significant for abdominal tenderness accentuated in the left upper quadrant. Lab workup was significant for a WBC of 15.6x109/L, hemoglobin of 16.7 g/dL, BUN 32mg/dL, and creatinine of 1.6mg/dL. Contrast CT scan of the abdomen and pelvis revealed thickening of the gastric mucosa in the fundus and body. EGD revealed a clean-based ulcer in the proximal gastric body surrounded by thickened gastric folds that persisted after insufflation (Figure 1). Biopsies of the stomach body showed features of ischemic gastritis as opposed to typical mucosal gastritis and were negative for Helicobacter pylori (Figure 2). CT angiography further supported the diagnosis of gastric ischemia by revealing an occluded celiac artery (Figure 3). Management included omeprazole BID, vascular surgery consult, smoking cessation, avoidance of any NSAID medications, and follow up EGD to confirm ulcer healing. We suggest that chronic gastric ischemia led to the ulcer in the proximal gastric body. Local inflammation from exposure to gastric acid, bile and peptic enzymes without an overlying mucus-bicarbonate barrier led to the surrounding edema. This caused the thickened gastric folds that were found primarily in the proximity of the ulcer. CT scan and biopsy did not reveal underlying neoplasm or Ménétrier's disease, which could have explained the thickened gastric folds. Although our case has the confounding factor of NSAID use, the histopathological examination of the thickened folds supported the inflammatory features to be ischemic in nature as opposed to mucosal gastritis.Figure: (A) Clean based ulcer in proximal gastric body surrounded by thickened folds. (B) Retroflex view showing fundus of stomach and thickened gastric folds.Figure: Stomach body biopsy revealing ghosts of pits and glands along with fibrinous exudate and interstitial hemorrhage, suggestive of ischemic gastropathy.Figure: CT-Angiography revealing occlusion of the celiac artery at its origin.

Feasibility of pancreatectomy following high-dose proton therapy for unresectable pancreatic cancer.

AIMTo review surgical outcomes for patients undergoing pancreatectomy after proton therapy with concomitant capecitabine for initially unresectable pancreatic adenocarcinoma.METHODSFrom April 2010 to September 2013, 15 patients with initially unresectable pancreatic cancer were treated with proton therapy with concomitant capecitabine at 1000 mg orally twice daily. All patients received 59.40 Gy (RBE) to the gross disease and 1 patient received 50.40 Gy (RBE) to high-risk nodal targets. There were no treatment interruptions and no chemotherapy dose reductions. Six patients achieved a radiographic response sufficient to justify surgical exploration, of whom 1 was identified as having intraperitoneal dissemination at the time of surgery and the planned pancreatectomy was aborted. Five patients underwent resection. Procedures included: Laparoscopic standard pancreaticoduodenectomy (n = 3), open pyloris-sparing pancreaticoduodenectomy (n = 1), and open distal pancreatectomy with irreversible electroporation (IRE) of a pancreatic head mass (n = 1).RESULTSThe median patient age was 60 years (range, 51-67). The median duration of surgery was 419 min (range, 290-484), with a median estimated blood loss of 850 cm3 (range, 300-2000), median ICU stay of 1 d (range, 0-2), and median hospital stay of 10 d (range, 5-14). Three patients were re-admitted to a hospital within 30 d after discharge for wound infection (n = 1), delayed gastric emptying (n = 1), and ischemic gastritis (n = 1). Two patients underwent R0 resections and demonstrated minimal residual disease in the final pathology specimen. One patient, after negative pancreatic head biopsies, underwent IRE followed by distal pancreatectomy with no tumor seen in the specimen. Two patients underwent R2 resections. Only 1 patient demonstrated ultimate local progression at the primary site. Median survival for the 5 resected patients was 24 mo (range, 10-30).CONCLUSIONPancreatic resection for patients with initially unresectable cancers is feasible after high-dose [59.4 Gy (RBE)] proton radiotherapy with a high rate of local control, acceptable surgical morbidity, and a median survival of 24 mo.

Ischemic Gastritis Improved by Supportive Care

Ischemic Gastritis Improved by Supportive Care

Ischemic Gastritis

To report a case series of ischemic gastritis and discuss its etiology, management, and associated mortality according to our results and the published English literature. Ischemic gastritis is rare, given the rich blood supply of the stomach. It has been reported in isolated case reports and small case series. Most cases are vascular in origin and associated with a high mortality. Pathology databases from 3 hospitals affiliated with the University of Minnesota Medical School were searched for cases of ischemic gastritis in the last 10 years. Patients' demographics, clinical course, and 1-month and 1-year mortalities were collected from electronic medical records. A total of 12 patients were identified (age range, 32.1 to 83.2), the largest series reported to date. The presenting symptom was gastrointestinal bleeding (8), abdominal pain (2), nausea (1), and symptomatic anemia (1). The etiology included postinterventional radiology embolization (2), hemodynamic changes in the setting of celiac axis stenosis (2), vasculitis (1), systemic hypotension (1), and unknown (6). Treatment included steroid therapy, revascularization by interventional radiology, surgery, or supportive treatment. Thirty-day and 1-year mortalities were 33% and 41%, respectively. Ischemic gastritis is rare, but associated with a high mortality. Evaluation for treatable etiologies should be sought and corrected if present.

Eosinophilic Gastroenteritis Presenting as Gastric Pneumatosis

Introduction: Eosinophilic gastroenteritis is a rare condition that causes eosinophilic infiltration of the gastrointestinal tract. Gastric pneumatosis is an unusual presentation of eosinophilic gastroenteritis. Case report: A 76 year old male with history of colectomy for intestinal pneumatosis 4 months previously presented to the hospital with acute worsening of abdominal pain, nausea and vomiting of a few days duration. He was noted to have diffuse abdominal tenderness on exam. A CT (computed tomography) scan of the abdomen demonstrated new gastric pneumatosis along with portal venous gas shadow that was not seen on a CT scan done nine days earlier. Conservative management was pursued and EGD (esophagoduodenoscopy) performed 3 days later was suggestive of ischemic gastritis of gastric fundus and body. Biopsies were obtained from the stomach and duodenum. It was initially thought that chronic mesenteric ischemia was the likely cause of these findings and the patient was treated conservatively. Pathology results showed increased eosinophils in the lamina propria. Staining for H. Pylori was negative. Stool studies for ova and parasites were negative. Upon chart review it was noted that the colectomy pathology report showed increased eosinophils within the submucosa, muscularis propria, and serosa consistent with eosinophilic colitis. Peripheral eosinophilia of serum at 6.8% was also noted. The patient was treated with intravenous steroid that was later transitioned to oral prednisone after he was able to tolerate regular diet. He continued to improve and was discharged to the extended care geriatrics unit. Discussion: Eosinophilic gastroenteritis is an eosinophilic inflammation of the gastrointestinal tract and can have a varied presentation, depending on the location and depth of the eosinophilic infiltration. Most patients present with a combination of abdominal pain, vomiting or diarrhea. We present a case of eosinophilic gastroenteritis complicated by intestinal wall pneumatosis and later gastric pneumatosis. It is thought that underlying eosinophilic gastroenteritis propagated the majority of this patient's clinical course. Pneumatosis has been described previously in one child with eosinophilic colitis. Gastric pneumatosis was found in four black and white lemurs in association with eosinophilic gastroenteritis. We believe this is a rare case of eosinophilic gastroenteritis presenting as intestinal and gastric pneumatosis.Figure 1

Histopathological Characterization of a Cameron Lesion

Cameron lesions are linear erosions located at the neck of a hiatal hernia (HH) in patients with a large HH. The prevalence has been seen in up to 5% of patients with HH who undergo esophagogastroduodenoscopy, and they can be associated with overt gastrointestinal bleeding or anemia. These lesions occur due to vascular compression by the diaphragm in a large sliding HH. Histopathologic changes seen in the biopsy tissue of a Cameron lesion are due to ischemia, but this ischemia is reversible with treatment of HH. The existence of this entity and the histopathologic picture of a Cameron lesion is not well known to pathologists, and therefore, a microscopic picture of a Cameron lesion can be easily confused with ischemic gastritis. Ischemic gastritis is the result of atherosclerosis, usually seen in older people, unrelated to HH, and is not easily reversible. The authors received a gastric biopsy of a hiatal hernia without any associated clinical diagnosis of a Cameron lesion conveyed to the pathologist. This biopsy tissue showed ischemic changes in the gastric mucosa on microscopic examination. Diagnosis of ischemic gastritis was considered but ruled out after the case was discussed with the gastroenterologist. The correct diagnosis was made once the clinical diagnosis of HH with Cameron lesion (ie, a vertical red erosion) was made known to the pathologist. By reporting this case, the authors aim to increase awareness of Cameron lesion among pathologists so that they ask about the presence of a Cameron lesion before making the diagnosis of ischemic gastritis.

Causa poco frecuente de úlcera gástrica

Drug-induced gastrointestinal tract lesions are becoming more frequent but are generally little known. Although a large number of drugs have gastrointestinal adverse effects, there are few characteristic patterns. Acute ischemic gastritis is an uncommon entity that is rarely distinguished from other forms of intestinal ischemia. We report the case of a 69-year-old woman who was diagnosed with an unusual gastric lesion in the context of an acute exacerbation of her anemia.

Severe Erosive Ischemic Gastritis Healed After Surgical Revascularization

Severe Erosive Ischemic Gastritis Healed After Surgical Revascularization

Severe Erosive Ischemic Gastritis Healed After Surgical Revascularization

Gastritis secondary to splanchnic arterial insufficiency is rare. The diagnosis should be suspected in case of gastritis associated with occlusion of celiac axis and superior mesenteric artery. We report a patient with severe ischemic gastritis who completely healed after surgical reno-hepatic bypass. This retrograde revascularization avoids aortic clamping and was well tolerated. Ischemic gastritis belongs to the celiac-territory ischemic syndrome and cholecystectomy should be added to the revascularization to prevent post-operative acute ischemic cholecystitis.

Ischemic Gastritis; an Unusual Cause of Abdominal Pain and Gastric Ulcers

Ischemic Gastritis; an Unusual Cause of Abdominal Pain and Gastric Ulcers

Ischemic Gastritis

The abundant vascular supply of oxygenated blood to the stomach via major arteries and smaller collateral vessels provides resistance to mucosal ischemia. However, mucosal changes can occur in the acute vaso-occulsive setting after a major operative procedure, or with chronic mesenteric insufficiency. We present a patient who developed diffuse gastric ischemia one day after coronary bypass surgery during a one month hospitalization for a global ischemic event. A 67 year-old female developed bright red blood output from her oral-gastric tube one day after coronary bypass surgery using a saffenous vein graft. Her bowel movements were loose and without hematochezia. She had no prior history of GI bleeding. She was initially hospitalized one month prior to the surgery for non-ST elevation myocardial infarction and cardiogenic shock with associated elevation of liver transaminases and acute renal failure. She was treated with aspirin, prophylactic esomeprazole, and vasopressors during her hospital course. She had a history of atherosclerotic disease and smoked tobacco regularly. She was intubated and sedated, with mean arterial blood pressure 81 mmHg and central venous pressure 9 cmH2O. Examination demonstrated hypo-active bowel sounds and a soft abdomen. Hemoglobin was 10.6 g/dL, pH 7.46, lactic acid 1.8 mmol/L, and stool was hemoccult negative. EGD revealed severe ulceration and friability throughout the entire gastric mucosa, with a normal esophagus and duodenum. Gastric biopsies demonstrated diffuse mucosal necrosis with preservation of only 1/3 of the mucosa, consistent with ischemia. Colonoscopy was normal. Conservative medical management was provided with an intravenous proton pump inhibitor and TPN. Five days later, she was extubated and began a liquid diet without complication. She was discharged from the hospital one week later. Mesenteric ischemia of the small and large bowel are more commonly investigated than the stomach. Gastric ischemia can be quite severe and in the presence of necrosis causes significant morbidity. A common diagnostic and treatment modality is surgery. Prior reports demonstrate either an acute or chronic etiology. We present a rare patient with ischemic gastritis and mucosal necrosis secondary to both acute and chronic injury, successfully treated with medical therapy. We conclude that certain circumstances are amenable to a conservative treatment approach.