Recent Hemorrhage Research Articles

3135 A Case of Epstein-Barr Virus (EBV) Mediated Acquired Hemophagocytic Lymphohistiocytosis (HLH) Presenting With Upper GI Bleed (UGIB)

INTRODUCTION: HLH often follows a fatal disease course with inflammation due to uncontrolled proliferation of macrophages causing multi-organ failure. Acquired HLH presents in adults secondary to infection (most commonly CMV or EBV) or malignancy. Several case reports have linked gastrointestinal bleed (GIB) to acquired HLH. We present a case of acquired HLH presenting with UGIB. CASE DESCRIPTION/METHODS: A 34 year old man with a history of chronic active EBV (CAEBV) presented from clinic for treatment of acquired HLH flare. He was diagnosed with HLH secondary to CAEBV infection 1.5 years prior and has been treated with steroids, rituximab, and etoposide with plans for stem cell transplant. Exam was notable for fever 102°F and hepatosplenomegaly. Labs were notable for EBV quant >1 million IU/mL, new CMV quant 7000 IU/mL, elevated ferritin, transaminitis, lactic acidosis, pancytopenia, and labs consistent with DIC (fibrinogen 155 mg/dL, D-dimer 1,082 ng/mL, platelets 41.6 × 103/cmm). He later developed episodes of hematemesis preceded by vomiting, requiring transfer to MICU due to hemodynamic instability. Abdominal ultrasound was without cirrhosis. EGD showed a 5 mm non-bleeding Mallory-Weiss tear (MWT) with stigmata of recent bleeding and clot extending down to GEJ; no intervention was conducted. The following day, he had more episodes of hematemesis. Emergent EGD showed large burden of clots in the esophagus extending to the GEJ; the clots were aspirated until mucosal defect could be visualized, revealing ulcerations with one actively oozing (Figure 1). Three hemostatic clips were placed followed by the application of hemospray with complete cessation of bleeding (Figure 2). DISCUSSION: HLH has been associated with GIB manifesting as diffuse or isolated ulceration anywhere in the GI tract. Here we present a patient with HLH who had a GIB that manifested as hematemesis and was found to have endoscopic evidence of MWT. About 80-90% of MWT heal spontaneously. However, this patient's coagulopathy manifesting as DIC resulting from his HLH prevented spontaneous healing leading to hemorrhagic complications. His GIB required clipping and the addition Hemospray aided in achieving hemostasis and hemodynamic stability. Hemospray's efficacy has been shown in peptic ulcer bleeds and cancer related GIB, however, there is minimal data on its use in acute esophageal bleed making this a unique case. Overall, this case highlights the GI complications of HLH and the importance of endoscopic management in controlling such a bleed.

1984 Helicobacter pylori-Negative MALT Lymphoma Presenting as Massive Recurrent Gastrointestinal Hemorrhage

INTRODUCTION: Extranodal marginal zone lymphoma or low-grade B cell lymphoma of mucosa-associated lymphoid tissue (MALT), an uncommon type of non-Hodgkin lymphoma (NHL), accounts for 5–10% of NHL in the US (18.3 cases per 1 million person-years1). It usually presents as gastro-esophageal reflux, nausea, anorexia, weight loss or occult GI bleeding2. Massive GI bleeding is unusual and rare. CASE DESCRIPTION/METHODS: Here we present a 68-year-old woman who presented with weakness and syncope after large volume hematemesis. Physical exam showed tachycardia, hypotension and conjunctival pallor. Her hemoglobin and hematocrit on admission were 8.5 g/dL and 25.6 %. She was managed with IV fluids, packed RBC transfusion and Pantoprazole and Octreotide infusions. An EGD within 24 hours showed erythematous, friable, spontaneously oozing mucosa with neovascularization in gastric fundus which was treated with bipolar cautery. A biopsy was not obtained due to recent bleeding. She was discharged on oral Pantoprazole. Two days later she was readmitted due to severe recurrent hematemesis with similar findings on repeat EGD. Bleeding was controlled with APC and biopsies were obtained from the gastric fundus. Due to the recurrent bleeding, an angiogram was performed. Active bleeding could not be seen. Prophylactically, left gastric artery was embolized. Biopsies revealed low-grade B cell MALT lymphoma with negative H.pylori. She was treated with 20 fractions of radiotherapy with the intention to cure. She did not experience further episodes of bleeding and has remained in remission since. DISCUSSION: Studies show the indolent nature of GI MALT lymphoma3, but our case illustrates the life-threatening presentation of a rare low-grade B cell MALT lymphoma as massive and recurrent hematemesis with negative underlying H.pylori infection or autoimmune process45. H.pylori positive localized MALT lymphoma is treated with the eradication of infection. H pylori negative, localized and recurrent disease is treated with radiotherapy6. Chemotherapy and/or immunotherapy is given when patients fail to respond to radiotherapy or develop metastasis. Long term endoscopic and laboratory follow up is needed as gastric MALT lymphoma is associated with a significant risk of gastric adenocarcinoma8 and increased incidence of gastric cancer and residual NHL. Our case emphasizes the importance of early diagnosis and timely intensive radiotherapy of a localized but aggressive gastric MALT lymphoma which induced remission and cessation of GI bleeding.

2747 A Rare Case of Esophageal Squamous Cell Carcinoma With Intramural Gastric Metastasis

INTRODUCTION: Esophageal cancer makes up about 1% of all cancers diagnosed in the United States . Gastric metastasis from esophageal cancer is relatively rare. Four different types of metastatic mechanisms were reported: 1) via peri-gastric lymph nodes; 2) gastric intramural metastasis; 3) direct invasion of the gastric wall, and 4) intra-epithelial spread to the gastric epithelium . Here we present a case with intramural gastric metastasis in a patient with esophageal squamous cell carcinoma. CASE DESCRIPTION/METHODS: A 76-year-old Indian male with past medical history significant for idiopathic pulmonary fibrosis and coronary artery disease, recently started on aspirin and clopidogrel, presented with new onset fatigue and five days of black tarry stools. Hemoglobin (Hgb) on admission was 7.1 g/dL. Despite transfusion of one unit of packed red blood cells, repeat Hgb dropped to 6.6 g/dL. Emergent upper endoscopy was performed for suspected active gastrointestinal bleeding in the setting of blood thinner use. Endoscopy showed a 3 cm, non-bleeding, fungating and ulcerated mass in the middle third of the esophagus, as well as a 4-5 cm fungating, infiltrative and ulcerated gastric mass in the cardia with stigmata of recent bleeding (adherent clot) (see Figure 1). Removal of the clot revealed underlying oozing from the ulcer bed which was treated successfully with dilute epinephrine injection followed by hemostatic clip placement. Forceps biopsies of both the esophageal and cardia masses were obtained. Histopathology of both lesions revealed keratinized squamous cell carcinoma. CT of the chest, abdomen and pelvis showed no evidence of other metastatic disease. Oncology consultation was scheduled to discuss potential chemotherapy, radiation, and endoscopic interventions. DISCUSSION: Esophageal cancer with intramural gastric metastasis is very rare compared to other mechanisms of tumor spread. The prognosis is very poor with the mean survival time reported to be 8.6 months . Conventional chemotherapy or radiotherapy after surgery were ineffective in improving prognosis in current report, suggesting other techniques could provide a benefit when used adjunctively or in combination with more traditional approaches.

2371 Non-Cirrhotic Portal Hypertension Presenting With Variceal Bleeding in a Patient With Breast Cancer on Capecitabine

INTRODUCTION: We describe a case of variceal bleeding in a cancer patient with improving liver metastases without radiographic evidence of cirrhosis. CASE DESCRIPTION/METHODS: A 66 year-old woman with stage IV bilateral breast cancer presented to the hospital with hematemesis. Platelet count was 98,000/mcL and INR 1.2 with normal albumin and liver enzymes. Upper endoscopy showed large varices with stigmata of recent bleeding and portal hypertensive gastropathy. Varices were banded without further bleeding. CT abdomen/pelvis with contrast showed left hepatic lobe atrophy, normal spleen, normal liver contour and no portal venous thrombosis (PVT). She was diagnosed with breast cancer 26 years prior and underwent lumpectomy and radiation. Eight years ago, she had recurrence, underwent mastectomy and then was diagnosed with contralateral breast cancer followed by mastectomy. Six years ago, she had recurrence requiring axillary dissection with chemotherapy and radiation. Four years ago, imaging showed new metastases with heavy left liver tumor burden with left portal vein cut off, ascites and bony metastases. Liver lesion biopsy showed breast cancer. She started doxorubicin with resolution of ascites and marked left lobe atrophy by imaging. For two years, she was remained on doxorubicin without evidence of disease. Three months prior to admission, PET CT showed two small right hepatic lobe metastasis, and she was started on capecitabine. DISCUSSION: Non-cirrhotic portal hypertension in the setting of liver metastases occurs for various reasons. One etiology is PVT, which imaging ruled out. Pseudocirrhosis describes a radiographic appearance of cirrhosis without histopathologic cirrhosis due to capsular retraction from metastases shrinkage after therapy, nodular regenerative hyperplasia (NRH) due to chemotherapy and fibrotic changes around metastases. While this is reported with capecitabine, our patient did not appear cirrhotic on imaging. Portal hypertension due to micronodular metastases is reported, but this is unlikely with improved liver lesions on imaging. Hepatic steatosis with elevated transaminases is reported with capecitabine. Several chemotherapies cause NRH, including doxorubicin. We suspect underlying NRH from previous doxorubicin and left hepatic lobe atrophy from shrinkage of metastases combined with new capecitabine caused an increased in liver stiffness. This case demonstrates the complex effects on the liver from both metastases and cancer treatments in a patient without known liver disease.

2010 Gastrointestinal Hemorrhage Due to Large B-Cell Lymphoma Treated With Hemospray

INTRODUCTION: Gastrointestinal bleeding (GIB) is a common cause of hospitalization and is associated with significant morbidity and mortality The most frequent causes of non-variceal upper GIB are peptic ulcers, erosions, Mallory-Weiss tears and malignancy. Current endoscopic hemostatic methods; including injections, thermal and mechanical modalities, have a 5-10% chance of recurrent bleeding. Hemospray (Cook Medical, USA) is a recently approved modality and can be helpful in treating tumor-related gastrointestinal bleeding. CASE DESCRIPTION/METHODS: A 57-year-old male with advanced diffuse large B-Cell lymphoma of the stomach with a contained perforation presented to the hospital with hematemesis. On exam, the patient had epigastric tenderness and dull bowel sounds. Labs revealed Hgb of 7.2 g/dL. CT of abdomen/pelvis revealed a gastric mass in the greater curvature of the stomach with a 3.1 cm perforation (Figure 1). EGD revealed a large blood clot attached to a giant ulcer in the great curvature of the fundus (Figure 2a). No active bleeding was noted, intravenous pantoprazole was initiated. Two days later, the patient developed recurrent hemorrhage with hemodynamic instability. Blood transfusion was initiated and repeat EGD showed large gastric perforation with evidence of recent bleed. The overlying clot was removed using a snare and Hemospray was deployed achieving hemostasis of the entire ulcer (Figure 2b). Post EGD, no immediate complications were seen. CT abdomen was performed which revealed a decreased amount of intraperitoneal free air without evidence of new perforation and no active bleeding. At this point, the patient was cleared to start chemotherapy. On follow-up EGD 2 months later, the contained perforation was seen nearly resolved (Figure 3). DISCUSSION: Tumor-related gastrointestinal bleeding is a challenging problem as it is difficult to control with conventional endoscopic hemostatic techniques. Hemospray is a newly FDA approved modality that can be helpful in controlling upper, lower and tumor-related GIB. Hemospray is an inorganic compound that when in contact with blood, absorbs water and adhesively forms a barrier over the bleeding site. Hemospray, unlike traditional therapies is a nonthermal, nontraumatic, and noncontact modality that doesn’t require precise targeting of other endoscopic devices. Hemospray is not absorbed by the body and usually passes through the lower GI tract within 72 hours. Overall the spray is 95% effective to achieve hemostasis in cases with upper and lower GIB.

2019 Lower Gastrointestinal Bleeding Due to Sevelamer-Induced Colitis

INTRODUCTION: Acute lower gastrointestinal (GI) bleeding is uncommonly due to medication induced-colitis, reported in less than 6% of all lower GI bleeds. Identifying medications that may cause GI bleeding is particularly important in chronically ill patients at high risk for morbidity and mortality. A commonly used medication in patients with advanced renal disease is sevelamer, a phosphate binder in renal failure patients. CASE DESCRIPTION/METHODS: A 53-year-old female with end-stage renal disease presented with hematochezia for 2 days. She notes dark black stools for two weeks followed by rectal bleeding. Her past history is notable for a renal transplantation in 2008 with graft failure requiring hemodialysis. She has no history of NSAID use and her prior screening colonoscopy showed no evidence of colitis. Her medication list was extensive and included sevelamer and cinacalcet. The patient was hemodynamically stable. Initial labs showed a hemoglobin of 6.0 g/dl, baseline was 8.0-9.0 g/dl. She was resuscitated with intravenous fluids and received 2 units of blood. Next, the patient’s upper endoscopy showed gastric erythema only with no stigmata of recent bleeding. Her colonoscopy showed a macroscopically normal appearing colon however random biopsies revealed expansion of the lamina propria with significant population of increased eosinophils. Several crystals were embedded within the colonic mucosa and submucosa resembling sevelamer crystals. Based on the pathology, she was diagnosed with sevelamer-induced colitis and this medication was discontinued. Follow-up at 3 months showed the patient remained asymptomatic without further GI bleeding. DISCUSSION: Sevelamer is a common medication used in renal failure patients. It is a resin that binds and prevents absorption of phosphate within the GI tract and has been shown to cause GI issues such as nausea, vomiting and diarrhea. Rarely it can crystalize, become embedded in the GI tract and ulcerate and cause bleeding. A few case reports have described rectosigmoid ulceration and pseudotumor presentation of sevelamer induced colitis.1,2 Understanding and recognizing the potential for sevelamer-induced colitis is important with such a widely used medication.

2197 Successful EUS-Guided Treatment of Duodenal Varices With Coil Embolization

INTRODUCTION: Ectopic varices are unusual and can involve any site along the GI tract. Only 5% of variceal bleeding is related to ectopic varices such as duodenal varices. Ectopic variceal bleeding is usually massive, difficult to treat, and associated with high mortality rates. High clinical suspicion is warranted. No standardized treatment is recommended, and the management remains challenging with limited success in controlling recurrent bleeding. EUS-guided therapy has evolved as an effective therapeutic modality in gastric varices and this case demonstrates the role of EUS-guided coil embolization (EUS-CE) with cyanoacrylate (CYA) injection in the management of duodenal variceal bleeding. CASE DESCRIPTION/METHODS: 81-year-old female with history of Diffuse large B cell lymphoma on chemotherapy presented with intermittent massive upper gastrointestinal bleeding. CT abdomen showed cirrhotic liver and portal vein thrombosis due to lymphoma involvement. Three endoscopies performed over a period of 5 days revealed 1 cm non-bleeding duodenal ulcer at the duodenal sweep without stigmata of recent bleeding. Due to recurrent bleeding, empiric coil embolization of the gastroduodenal artery and multiple duodenal branches through angiography was done by interventional radiology. However, severe bleeding recurred after the embolization, and the fourth urgent EGD showed large subepithelial violaceous lesions next to the deep penetrating ulcer, highly suspicious for duodenal varices. EGD-EUS confirmed these lesions were duodenal varices. By the fifth day of admission, patient had required 8 units of PRBC. Therefore, the decision was made to treat with EUS-CE. Two coils of 8 and 9 mm were deployed into the larger varix through a 19G EUS-FNA needle followed by 2 ml injection of CYA. A third 6 mm coil was also deployed in the feeder vessel also followed by CYA. Both lead to embolization and cessation of blood flow as demonstrated through Doppler investigation at the end of the procedure. Bleeding stopped and patient was discharged home to complete chemotherapy. DISCUSSION: Bleeding from duodenal varices require high suspicion as vessels could be miss if collapsed soon after bleeding. High clinical suspicion can result in early angiographic evaluation and intervention. Ideal management of ectopic variceal bleeding is still unclear. Multiple endoscopic technique modalities have been reported. EUS-CE with or without CYA injection is a safe endoscopic technique with effective variceal obliteration in most cases.

2159 Endoscopic Management of Isolated Gastric Varices: Hematemesis in Pancreatitis-Induced Splenic Vein Thrombosis

INTRODUCTION: Brisk upper GI bleeding with acute blood loss anemia requires emergent endoscopic evaluation. Often, lesions are due to peptic ulcer disease or variceal hemorrhage. Here, we present a case of isolated bleeding gastric varices in a patient with splenic vein thrombosis likely due to recurrent episodes of acute pancreatitis. CASE DESCRIPTION/METHODS: A 48-year-old man with alcohol abuse, thrombocytopenia, and chronic LUQ abdominal pain presented with four days of hematemesis and melena. He intermittently takes PPI, but reported no NSAID use or history of H. pylori. Previously, two similar episodes associated with severe epigastric pain radiating to his back occurred with heavy drinking. On exam, he is hemodynamically stable with an unremarkable abdominal exam. His admission hemoglobin is 4.9 g/dl and BUN is 26 mg/dl. He is resuscitated with blood products and EGD reveals type 1 isolated gastric varices (IGV) in the fundus with stigmata of recent bleed (Figure 1). Subsequent EUS confirms presence of fundal varices. Hemostasis is achieved with coiling and cyanoacrylate (CYA) glue (Figures 2 and 3). CT A/P shows splenomegaly with chronic splenic vein thrombosis with collateral gastric varices. On discharge, he is counseled on alcohol cessation, as his bleeding gastric varices were attributable to pancreatitis-induced splenic vein thrombosis (PISVT). DISCUSSION: PISVT is a sequalae of acute and chronic pancreatitis. The pathophysiology is centered on left-sided portal hypertension with collateral blood flow developing in the splenoportal or gastroepiploic systems. Most patients with subsequent IGV are asymptomatic, but in high-risk symptomatic groups, EUS guided CYA glue injection and intravascular coil embolization is an emerging therapy that has the potential to achieve higher rates of hemostasis and lower rebleeding rates compared to sclerotherapy or balloon-occluded retrograde transvenous obliteration. A recent study demonstrated that out of 100 patients who underwent EUS-guided coil and CYA glue injection, 93 had complete obliteration (on Doppler study) of gastric fundal varices on follow-up EUS examination (Bhat, GIE 2016). Patients who do not achieve hemostasis after CYA injection and coil should be considered for splenic artery embolization or splenectomy, which is currently the gold standard for management of splenic vein thrombosis complicated by variceal hemorrhage. A large comparison trial would be most beneficial to validate this treatment modality compared to existing conventional therapies.

1693 Jejunal Lymphangioma: An Unusual Etiology for Iron Deficiency Anemia

INTRODUCTION: Lymphangiomas are benign tumors characterized by cystic dilation of lymphatic vessels, and can arise from any location throughout the lymphatic system. Small bowel lymphangiomas are rare, and are primarily described in children. When found in adults, these lesions are typically an incidental finding. Pathologic small bowel lymphangiomas are particularly unusual, and have been reported as a rare etiology of massive gastrointestinal bleeding and chronic anemia. CASE DESCRIPTION/METHODS: A 65yo African American man with a history of prostate cancer, coronary artery disease, hypertension, hyperlipidemia, and peripheral artery disease was hospitalized for a 6 month history of symptomatic anemia, without signs of overt gastrointestinal blood loss. Vital signs were stable upon presentation, and initial labs were significant for a hemoglobin 8.7, mean corpuscular volume 94, ferritin 28, and iron saturation of 3%. An esophagogastroduodenoscopy was performed which was significant for mild gastropathy, and a colonoscopy that showed mild diverticulosis, a 3 mm polyp and small internal hemorrhoids, without stigmata of recent bleeding. Iron therapy was initiated, and the patient was referred to the outpatient gastroenterology clinic for further workup. The patient next underwent capsule endoscopy which showed a friable small bowel mass, with evidence of active bleeding. A single balloon enteroscopy was then performed, which revealed a 4 cm circumferential, friable, granular mass in the mid-jejunum which was biopsied and tattooed with India Ink. Biopsies of the mass revealed benign small intestinal mucosa with prominent lymphangiectasia. The patient was then referred to surgical oncology and underwent a laparoscopic assisted enteroscopy which again demonstrated the previously seen lesion occupying 75% of the small bowel lumen. The lesion was further evaluated with endomicroscopy which revealed multiple dilated blood vessels and lymphatic channels, in a background of inflammation. The cells appeared organized and without atypical features. A small bowel resection was performed, and the surgical pathology revealed a benign lymphatic malformation involving the mucosa and submucosa consistent with a lymphangioma. No invasive features or malignant cells were identified. DISCUSSION: Small bowel lymphangiomas are a rare finding, and primarily found within the duodenum. We report an unusual case of a large jejunal lymphangioma presenting as iron deficiency anemia, which completely resolved after resection of the mass. Watch the video: http://bit.ly/2LvNhpc.

1923 Bleeding Varices in a Non-Cirrhotic

INTRODUCTION: Extra-hepatic portal vein obstruction (EHPVO) presents with manifestations of portal hypertension, including variceal bleed. Cirrhosis is the leading cause of portal hypertension (90%), and EHPVO can mask as cirrhosis, especially in a patient with risk factors such as alcohol abuse and incarceration. CASE DESCRIPTION/METHODS: 37 y/o male with h/o DVT and alcohol abuse presented to our ER for abdominal pain and hematemesis. He was a chronic alcoholic but quit drinking 6 months prior. On admission, he was afebrile, mildly tachycardic but not hypotensive. Examination showed non-specific diffuse abdominal tenderness and jaundice. Labs showed Hb 5.8 g/dL, platelets 66/mcL, INR 2.13. Liver enzymes were normal, except T Bili of 5.1 mg/dL, and albumin 3.8 g/dL. Entire cirrhotic work-up was negative. CT abdomen showed nodular liver, splenomegaly, mild ascites, and gastroesophageal varices. Doppler US showed hepatopedal flow within the main portal vein. Triple-phase CT showed portal vein thrombosis (PVT) with cavernous transformation. EGD revealed large esophageal varices with red wale sign, which were banded. No gastric or duodenal varices. Colonoscopy revealed diffuse melena up to the terminal ileum, but no varices. Liver biopsy was negative for cirrhosis. The patient was found to have a heterozygous Factor V Leiden (FVL) gene mutation. Anticoagulation was not initiated due to recent bleed. He was re-admitted, unconscious after massive GI bleeding at home. Repeat banding was performed. SMA angiography and portography showed complete occlusion of the main SMA, splenic vein, and PV. DISCUSSION: For patients with portal hypertension secondary to portal vein thrombosis, the Bevano VI guidelines on portal hypertension recommend primary prophylaxis with non-selective beta-blockers and endoscopic variceal ligation. Failure of primary prophylaxis requires secondary prophylaxis with TIPS. However, surgical devascularization, such as the modified Sugiura procedure, is a great option with lower rates of re-bleeding and higher rates of survival compared to surgical shunts. Decompressive portal therapy is an important treatment aspect for our patient due to his need for lifelong anticoagulation in the setting of inherited thrombophilia.

Efficacy and Safety of Early vs Elective Colonoscopy for Acute Lower Gastrointestinal Bleeding

We performed a large, multicenter, randomized controlled trial to determine the efficacy and safety of early colonoscopy on outcomes of patients with acute lower gastrointestinal bleeding (ALGIB). We performed an open-label study at 15 hospitals in Japan of 170 patients with ALGIB randomly assigned (1:1) to groups that underwent early colonoscopy (within 24 hours of initial visit to the hospital) or elective colonoscopy (24-96 hours after hospital admission). The primary outcome was identification of stigmata of recent hemorrhage (SRH). Secondary outcomes were rebleeding within 30 days, endoscopic treatment success, need for transfusion, length of stay, thrombotic events within 30 days, death within 30 days, and adverse events. SRH were identified in 17 of 79 patients (21.5%) in the early colonoscopy group vs 17 of 80 patients (21.3%) in the elective colonoscopy group (difference, 0.3; 95% confidence interval, -12.5 to 13.0; P= .967). Rebleeding within 30 days of hospital admission occurred in 15.3% of patients in the early colonoscopy group and 6.7% of patients in the elective colonoscopy group (difference, 8.6; 95% confidence interval, -1.4 to 18.7); there were no significant differences between groups in successful endoscopic treatment rate, transfusion rate, length of stay, thrombotic events, or death within 30 days. The adverse event of hemorrhagic shock occurred during bowel preparation in no patient in the early group vs 2 patients (2.5%) in the elective colonoscopy group. In a randomized controlled study, we found that colonoscopy within 24 hours after hospital admission did not increase SRH or reduce rebleeding compared with colonoscopy at 24-96 hours in patients with ALGIB. ClinicalTrials.gov, Numbers: UMIN000021129 and NCT03098173.

Thrombolytic therapy in older acute ischemic stroke patients with gastrointestinal malignancy or recent bleeding.

There are limited data on the safety of intravenous recombinant tissue plasminogen activator (rtPA) for treating acute ischemic stroke in patients with gastrointestinal malignancy or recent gastrointestinal bleeding within 21 days of their index stroke. To evaluate clinical outcomes in patients treated with rtPA for acute ischemic stroke who had gastrointestinal malignancy or recent gastrointestinal bleeding. We identified patients who were treated with rtPA for acute ischemic stroke between 2/2009 and 12/2015 from the Get With The Guidelines-Stroke linked to Medicare claims data. Gastrointestinal malignancy and recent gastrointestinal bleeding were defined as any gastrointestinal malignancy hospitalisation within one year prior to acute ischemic stroke and gastrointestinal bleeding hospitalisation within 21 days prior to acute ischemic stroke, respectively. Outcomes of interest included in-hospital mortality and bleeding complications. Among 40,396 patients aged 65 years or older treated with rtPA for acute ischemic stroke from 1522 sites (mean age [SD] 81.0 [8.1] years; 41.9% women), 136 (0.3%) had gastrointestinal malignancy (n = 96) or recent gastrointestinal bleeding (n = 43). Patients with gastrointestinal malignancy or bleeding had more severe stroke than those without (median NIHSS [interquartile range]: 14.0 [8.0-19.0] vs. 11.0 [6.0-18.0]). The rates of in-hospital mortality and life-threatening systemic haemorrhage were not significantly different between those with and without gastrointestinal malignancy or bleeding (mortality: 10.3% vs. 9.0%, adjusted odds ratio [aOR] 1.01, 95%CI 0.58-1.75; bleeding: 2.3% vs. 1.2%, aOR 1.72, 95%CI 0.58-5.11). In this observational cohort, we did not find increased risk of in-hospital mortality and bleeding in rtPA-treated patients with gastrointestinal malignancy or recent gastrointestinal bleeding.

Short-Term Proton Pump Inhibitor Use and Hepatic Encephalopathy Risk in Patients with Decompensated Cirrhosis.

Objective: A window period of approximately 3–6 months is usually adopted in studies that evaluate hepatic encephalopathy (HE) risk in proton pump inhibitor (PPI) users. However, HE risk after short-term PPI exposure remains unclear. We explored the effect of short-term PPI exposure using a case-crossover study design. Design: Records of patients with decompensated cirrhosis who had received an HE diagnosis were retrieved from the National Health Insurance Research Database. PPI use rates were compared for case and control with window periods of 7, 14, and 28 days. The adjusted self-matched odds ratio (OR) and 95% confidence interval (CI) from a conditional logistic regression model were used to determine the association between PPI use and HE risk. Results: Overall, 13 195 patients were analyzed. The adjusted OR for HE risk after PPI exposure was 3.13 (95% CI = 2.33–4.20) for the 7-day window, 4.77 (95% CI = 3.81–5.98) for the 14-day window, and 5.60 (95% CI = 4.63–6.78) for the 28-day window. All PPI categories, except omeprazole and pantoprazole, were associated with an increased HE risk. Irrespective of other precipitating factors, such as recent gastrointestinal bleeding or infection, PPI significantly increased HE risk. Conclusion: Short-term PPI use is significantly associated with HE in patients with decompensated cirrhosis. Physicians should use PPI in these patients for appropriate indications, and carefully monitor signs of HE even after short-term exposure. Owing to the limitations of retrospective design in the current study, further study is warranted to confirm our findings.

Gastrointestinal: A rare cause of upper gastrointestinal bleeding: Epiphrenic esophageal diverticula

An 87-year-old man presented to the Emergency Department after a syncopal event at home associated with a 3-day history of melena. This was on a background of ischemic heart disease with previous coronary artery bypass graft and recent transesophageal echocardiogram cardioversion for atrial fibrillation 10-days prior. He was commenced on apixaban during this admission and re-commenced on aspirin by his general practitioner on review post discharge. On assessment, he was hemodynamically stable, with melena noted on digital rectal examination. His laboratory results revealed a hemoglobin of 68-g/L, urea of 22.8-mmol/L, and INR of 1.7. He was commenced on intravenous pantoprazole (proton pump inhibitor), transfused with two units of packed red blood cells, and underwent a gastroduodenoscopy the following day. Upper endoscopy revealed a 2–2.5-cm diameter esophageal diverticulum (Fig.-1) just above the gastroesophageal junction (GOJ) in the right posterior-lateral wall. There was no active bleeding, but there was evidence of recent bleeding with altered blood and mild mucosal erythema in the surrounding tissue. The remainder of the endoscopy also identified two further diverticula: one in the gastric fundus within a large hiatus hernia with evidence of some altered blood and a 3rd diverticulum noted in the second portion of the duodenum with no evidence of a recent bleed. No endoscopic therapy was required at the time for hemostatic control due to the absence of active bleeding or visible high-risk stigmata. We proceeded with a computed tomography of the chest and upper abdomen (Fig.-2) as well as a barium swallow that confirmed numerous diverticula involving the GOJ (22-×-6-mm), stomach, and duodenum. Upon further history, the patient did describe having intermittent dysphagia over many years. The patient's melena resolved, and he was discharged home off aspirin with continuation of an oral proton pump inhibitor. Esophageal diverticula have a reported annual incidence of 1:500-000 per year and epiphrenic esophageal diverticula (EED) that occur within 10-cm proximal to the GOJ account for about 15% of these. EED is a very rare cause of upper gastrointestinal bleeding. As far as we are aware, there have been only a handful of these cases published to date. Although EED are largely noted incidentally, some common symptoms of presentation include dysphagia, vomiting, chest pain, and heartburn. Assessment may also involve barium swallow and computed tomography of the chest, especially for pre-operative evaluation. There are no clear guidelines or consensus as to the best course of treatment. Therapeutic interventions that have been described in previous case reports include administration of adrenaline, heater probe thermocoagulation, and hemostasis clips. If endoscopic intervention is not successful, surgical options may include diverticulectomy, myotomy, and fundoplication. Although rare, this case demonstrates that EED could potentially cause significant upper gastrointestinal bleeding and should be considered as a differential in clinical practice.

Paramedian contralateral supracerebellar infratentorial approach to thalamic cavernous malformation.

Cavernous malformations (CVMs) located in the thalamus are uncommon. However, they pose difficulties for resection because of their close proximity to eloquent areas of the brain and vascular structures, and all surgical corridors to access them are narrow. In this video, we report the case of a 19-year-old woman who presented with a long-standing history of right hemiparesis with recent deterioration. MRI revealed a large CVM located in the left thalamus, with signs of recent hemorrhage extending to the left cerebral peduncle. Resection was achieved with a paramedian contralateral supracerebellar infratentorial approach in a semisitting position, with an uneventful postoperative course.The video can be found here: https://youtu.be/Arvu52FkHOE.

Unusual cardiac mass presenting as humeral artery embolisation

A 73-year-old man presents acute ischaemia of the left humeral artery in the upper limb. He had a recent cerebral haemorrhage in combination with multiple cerebral ischaemic lesions. A transthoracic...

Plasma expanders for people with cirrhosis and large ascites treated with abdominal paracentesis.

Plasma expanders for people with cirrhosis and large ascites treated with abdominal paracentesis.

Biomarkers of cavernous angioma with symptomatic hemorrhage.

BACKGROUNDCerebral cavernous angiomas (CAs) with a symptomatic hemorrhage (CASH) have a high risk of recurrent hemorrhage and serious morbidity.METHODSEighteen plasma molecules with mechanistic roles in CA pathobiology were investigated in 114 patients and 12 healthy subjects. The diagnostic biomarker of a CASH in the prior year was derived as that minimizing the Akaike information criterion and validated using machine learning, and was compared with the prognostic CASH biomarker predicting bleeding in the subsequent year. Biomarkers were longitudinally followed in a subset of cases. The biomarkers were queried in the lesional neurovascular unit (NVU) transcriptome and in plasma miRNAs from CASH and non-CASH patients.RESULTSThe diagnostic CASH biomarker included a weighted combination of soluble CD14 (sCD14), VEGF, C-reactive protein (CRP), and IL-10 distinguishing CASH patients with 76% sensitivity and 80% specificity (P = 0.0003). The prognostic CASH biomarker (sCD14, VEGF, IL-1β, and sROBO-4) was confirmed to predict a bleed in the subsequent year with 83% sensitivity and 93% specificity (P = 0.001). Genes associated with diagnostic and prognostic CASH biomarkers were differentially expressed in CASH lesional NVUs. Thirteen plasma miRNAs were differentially expressed between CASH and non-CASH patients.CONCLUSIONShared and unique biomarkers of recent symptomatic hemorrhage and of future bleeding in CA are mechanistically linked to lesional transcriptome and miRNA. The biomarkers may be applied for risk stratification in clinical trials and developed as a tool in clinical practice.FUNDINGNIH, William and Judith Davis Fund in Neurovascular Surgery Research, Be Brave for Life Foundation, Safadi Translational Fellowship, Pritzker School of Medicine, and Sigrid Jusélius Foundation.

Testing of Helicobacter pylori by Endoscopic Biopsy: The Clinical Dilemma of Suppressive Conditions

Background and Aims: Testing for Helicobacter pylori is frequently conducted during esophagogastroduodenoscopy (EGD). Suppressive conditions such as the intake of proton-pump inhibitors (PPIs), preceded antibiotic treatment or recent upper gastrointestinal bleeding impair H. pylori test quality. The aim of our study was to evaluate the frequency and pattern of H. pylori suppressive conditions in a large patient collective undergoing elective EGD in a German university hospital. Methods: The trial was performed as a single-center study. Only elective EGD from inpatients and outpatients were included. Prior to endoscopy, H. pylori suppressive conditions were collected using a standardized questionnaire. If H. pylori testing was indicated according to the guidelines, always both histology and helicobacter urease test were performed in analogy to the Sydney classification. Results: One thousand six hundred and thirty-one patients were included (median 61 years, 36.0% outpatients, 64.0% inpatients). Overall, 76.5% of patients were under H. pylori suppressive conditions. The main suppressive condition was the intake of PPIs (70.7%). In 819 (50.2%) of all included cases, H. pylori testing was performed. The following were the results: 17.3% (142) had a positive H. pylori testing and 82.7% (677) were negative. Of those with negative result, 70.0% were tested under suppressive conditions. Conclusion: Guidelines recommend H. pylori testing under non-suppressive conditions. However, this does not always meet the clinical practice. Our data show that de facto, many patients undergoing elective EGD are tested for H. pylori under suppressive conditions coming along with a higher risk of potentially false negative results. Particularly, concerning this issue, further research is needed to improve and clarify everyday clinical practice.

Primary gastric choriocarcinoma: a case report

Primary gastric choriocarcinoma (PGC) is an uncommon tumor. Due to its rarity, its pathogenesis is still unclear. The diagnosis is based on immunohistopathology, which is positive for human chorionic gonadotropin (hCG). It is a highly invasive and rapidly-disseminated hematogenous neoplasm, which leads to a poor prognosis. We present the case ofa 57-year-old woman with upper gastrointestinal bleeding associated with weight loss. The gastroscopy showed, on the cardia and paracardial region, a 5x4-cm ulcerated polypoid lesion with circumscribed edges and without adjacent wall infiltration, with stigmas of recent bleeding and a pathological anatomy that demonstrates ulcerated pleomorphicmalignancy with positive immunohistochemistry for pankeratin. Given the suspicion of poorly differentiated carcinoma and without evidence of metastasis, the patient underwent a total gastrectomy and the pathology was compatible with choriocarcinoma. Therefore, after the surgery, a serum hCG test was performed with a result of 714 mIU/ml, whichfurther confirmed the diagnosis. Treatment with adjuvant chemotherapy was decided, and a tomographic and serological hCG follow-up was conducted, without the presence of active disease.