bluuebunny/crossref_metadata_2025_split huggingface dataset:
1945 Isolated Gastric Varices as the Sole Manifestation of Renal Cell Carcinoma
Authors: Okenye Emmanuel , Fielding Cory , Singh Kamal 
Published: October 2019

INTRODUCTION:
Isolated gastric (fundal) varices (IGV) are a consequence of left (sinistral) portal hypertension commonly caused by splenic vein thrombosis (SVT). It occurs when SVT results in a backflow into the collateral short gastric and gastroepiploic vessels. Common causes of SVT include pancreatic and splenic pathologies. Renal cell carcinoma (RCC) is an extremely rare cause, and by itself, RCC is lethal because of the vagueness of its presenting symptoms.

CASE DESCRIPTION/METHODS:
A 76 year-old male with a past medical history of chronic anemia is presenting with two day history of hematochezia. He denies any personal or family history of colon cancer. He is not on anticoagulation or NSAID regimen. On evaluation, patient was noted to have non-remarkable vital signs. Physical exam was fairly unremarkable. Initial CBC was remarkable for severe anemia with hemoglobin of 6.1. MCV was normal. After routine transfusion, he was evaluated by gastroenterology and underwent an EGD, colonoscopy and capsule endoscopy. EGD was remarkable for 2 cm diameter non bleeding fundic gastric lesion. Colonoscopy and capsule endoscopy were unremarkable except for findings of dark blood in the distal ileum and throughout the colon. Tagged RBC scan was negative. Endoscopic ultrasound was obtained that showed multiple tubal, anechoic structures in the cardia of the stomach consistent with varices. CT abdomen and pelvis then confirmed a giant mass filling the left renal fossa presumably primary renal cell neoplasm with displacement of the pancreas and splenomegaly. CT chest was obtained and confirmed pulmonary nodules likely suggesting metastatic lesions. He then underwent splenectomy and nephrectomy with adjuvant chemotherapy for the metastatic disease.

DISCUSSION:
Sinistral (left) portal hypertension (SPH) was first outlined by Greenwald and Wasch in 1939. It is a clinical syndrome in which a patient with a patent portal vein and normal hepatic (liver) function tests develops isolated gastric variceal bleeding secondary to splenic vein thrombosis. Interestingly, only two cases have documented renal cell carcinoma as a cause of SPH in the last 30 years. Patients with this condition need to be considered for a prophylactic splenectomy and removal of associated arteries and veins, as well as a total nephrectomy. In this case, with metastatic lesions to his lungs, involving hematology/oncology and general surgery and gastroenterology in the multidisciplinary decision making process would be in his best interest.
1957 CHF - Chronic Hernial Failure Presenting as Congestive Heart Failure
Authors: Pisipati Sailaja , Taha Mohamed , Hinojosa Tomas , Canaday Omar 
Published: October 2019

INTRODUCTION:
While sliding hernias (type I) constitute 90%–95% of hiatus hernias (HH), paraesophageal hernias (PEHs) (type II–IV) account for the remaining 5%–10%. PEHs have become increasingly common with age and obesity being the contributory factors. They can either be symptomatic or asymptomatic. We report a case of large PEH presenting with symptoms masquerading as new-onset heart failure.

CASE DESCRIPTION/METHODS:
A 71-year-old healthy gentleman with no known prior cardiac history was evaluated in urgent care for progressively worsening exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, bilateral lower extremity edema, weight gain and dizziness for two months. Review of systems was negative except for recent intake of NSAIDs. Past history was significant for a small HH and chronic gastritis, sigmoid diverticulosis and hemorrhoids on endoscopic evaluation ten years prior. He was hemodynamically stable. Examination revealed pitting edema of lower extremities and S3 gallop. Patient was commenced on oral furosemide; urgent lab work, chest x-ray and echo were requested. He was advised to be admitted for blood transfusion and in-patient evaluation of anemia when his hemoglobin returned at 5.5 g/dl. Evaluation by gastroenterology suggested that patient had early satiety for few months. Urgent upper endoscopy revealed several Cameron lesions possibly accounting for chronic blood loss anemia. Barium upper series demonstrated an intrathoracic gastroesophageal junction (GEJ) and a large PEH with organoaxial gastric volvulus and no signs of obstruction. CT thorax confirmed a type III PEH. There was no evidence of primary cardiopulmonary pathology on echo and thoracic CT. Laparoscopic repair of large HH and Nissen’s fundoplication were performed following which symptoms and anemia resolved.

DISCUSSION:
Large PEH can be an incidental finding on endoscopic or radiological evaluation for unrelated reasons. Despite this, most patients have had symptoms attributed to other causes. Common symptoms include heartburn, regurgitation, dysphagia, early satiety, chest pain, dyspnea. Microcytic anemia was reported in 17%–47% of cases; this was attributed to chronic blood loss from Cameron lesions which are gastric mucosal erosions from crural pressure at the neck of HH. Our patient likely had high-output cardiac failure due to profound anemia in the setting of Cameron’s lesions from a large PEH. Other common causes of chest symptoms and anemia should be excluded before attributing these symptoms to a large PEH.
1962 Rectal Amyloidosis: An Unusual Cause of Rectal Bleeding
Authors: Chen Vida , Newman Gary 
Published: October 2019

INTRODUCTION:
Rectal amyloidosis is a rare cause of gastrointestinal bleeding and should be on the differential in patients with amyloid involvement of other organs. We present a case of rectal amyloidosis as the source of rectal bleeding.

CASE DESCRIPTION/METHODS:
A 76-year-old female with recently diagnosed multiple myeloma resulting in renal amyloidosis requiring hemodialysis, LV outflow obstruction from cardiac amyloidosis (on CyBORD regimen – cyclophosphamide, bortezomib, dexamethasone) presented with a 1-week history of hematochezia without associated abdominal pain, constipation, diarrhea, melena, nausea, or vomiting. Rectal examination revealed a large, firm anterior rectal mass. Laboratory findings were significant for profound anemia with Hgb 5.6 g/dL (compared to Hgb 7.2 g/dL one week prior). CT abdomen and pelvis showed a lumen-obliterating rectal mass measuring up to 9.3 cm and multiple perirectal calcific masses that were suspicious for metastases. She underwent flexible sigmoidoscopy and was noted to have a granular, non-obstructing, non-circumferential large mass in the rectum with active bleeding. Biopsies were consistent with amyloidosis. She was initiated on pelvic radiation therapy. A few weeks later, she passed away after cardiac arrest. Autopsy revealed cardiac and renal amyloidosis as well as rectal amyloidosis with pelvic lymph node involvement. There was no other gastrointestinal involvement of amyloid on autopsy.

DISCUSSION:
The overall prevalence of AL amyloidosis is between 6–10 cases per million person-years, correlating to approximately 2,200 annual cases in the US. In a retrospective review of 2,334 patients with amyloidosis, only 3% had biopsy proven amyloidosis of the gastrointestinal tract. Hepatic amyloid is the most common location of gastrointestinal amyloidosis and has been reported in up to 90% of patients with AL amyloid on autopsy. The clinical symptoms are based on the location of gastrointestinal amyloidosis and are usually nonspecific. This is a rare case of rectal amyloidosis without any other gastrointestinal amyloid involvement presenting with rectal bleeding. Gastrointestinal amyloidosis is treated with autologous stem-cell transplant or systemic chemotherapy. Our patient was treated with CyBORD chemotherapy and pelvic radiation for symptomatic rectal bleeding. Rectal amyloidosis should be included in the differential diagnosis of a rectal mass causing rectal bleeding in patients with history of AL amyloidosis.
1981 A Case of Jejunal Diverticulum Causing Life-Threatening Hemorrhage
Authors: De La Ossa Juan , Kachechian Talar , Panicker Linoj , Sobrado Javier , Mohan Karthik 
Published: October 2019

INTRODUCTION:
Diverticulosis seldom causes life threatening hemorrhage and is frequently found in the large bowel. Rare cases of small bowel diverticula are most notably known to appear in the duodenum. Even rarer are severe small bowel diverticulum bleeds in the jejunum with one study noting approximately 50 cases reported in the literature. Due to the difficult location, many have gone unidentified and ultimately resulted in small bowel resections. We present a 58-year-old man with a life threatening jejunal diverticular bleed that was diagnosed and treated conservatively.

CASE DESCRIPTION/METHODS:
A 58-year-old Hispanic male with past medical history significant for upper GI bleed requiring multiple transfusions, chronic pancreatitis, and SMA thrombosis presented to the ED for recurrent melena. He was previously admitted for suspected GI bleed with no identifiable source on colonoscopy, EGD, and outpatient capsule endoscopy. On this admission, vitals were hemodynamically stable but labs revealed a hemoglobin of 3.3. After appropriate resuscitation, push endoscopy revealed a bleeding proximal jejunal diverticulum which was tattooed, coagulated with epinephrine and clipped. CTA of abdomen showed a stable dissecting aneurysm in between the origin of the inferior pancreaticoduodenal arcade and jejunal branches. He was stabilized and discharged with follow up.

DISCUSSION:
Small bowel diverticulosis is usually found incidentally in asymptomatic patients. Because jejunal diverticuli are novelty differentials, often forgotten, diagnosis becomes delayed even with the use of standard endoscopy, resulting in significant morbidity and mortality. Several noninvasive studies can be done initially to assess for bleeding. With advances in technology such as small bowel enteroscopy, specifically push enteroscopy, jejunal diverticulum can be diagnosed earlier and treated with clipping as opposed to surgical resection which has been the mainstay treatment for refractory bleeding. This case brings to light a rare manifestation of small bowel diverticuli where future research could be dedicated. There has been another case with similar presentation in which the patient also had history of a SMA clot. This poses the question of whether there is a correlation and if it could be explained by the compromised integrity of the small bowel wall due to the lack of blood flow making it easier for diverticuli to arise there. It also raises the question as to why certain patients are more predisposed to developing these outpouchings.
1989 A Rare Case of Renal Call Carcinoma With Metastasis to the Rectum and Gastric Body
Authors: Bernshteyn Michelle , Manocha Divey , Masood Umair , Smith-Hannah Alexandria 
Published: October 2019

INTRODUCTION:
Renal Cell Carcinoma (RCC) frequently metastasizes to the lungs, lymph nodes, bones, and liver via lymphatic, hematogenous, or direct invasion. Gastrointestinal metastasis is rare. We present a case of metastatic RCC to the gastric body and rectum presenting as melena and shortness of breath.

CASE DESCRIPTION/METHODS:
Patient is a 68-year-old male with a history of stage IV RCC to the skin and lung status post right total nephrectomy and right upper lobe wedge resection, who presented to the hospital with a one-month history of shortness of breath and 10–15 episodes of melena per day. On presentation, his heart rate was 121 bpm and blood pressure quickly dropped from 131/81 mmHg to 110/61 mmHg. Physical exam demonstrated abdominal tenderness and cachexia. Labs demonstrated hemoglobin 6.7 g/dL, which was 4 points lower than baseline and hyponatremia of 128 mmol/L. Other labs including hepatic panel and coagulation parameters were within normal limits. Hemoccult testing was positive. The patient was started on intravenous fluids, pantoprazole infusion, and blood transfusion (2 units). CT scan of the abdomen demonstrated a metastatic lesion in the sigmoid colon suggestive of an invasive metastatic lesion. Endoscopy revealed a nodule in the duodenum and mass was visualized on the greater curvature of the gastric body. Colonoscopy revealed a single polyp in the rectum, 10 mm in size. These lesions were biopsied and treated with bipolar cauterization. Pathological reports demonstrated metastatic carcinoma consistent with a renal primary source.

DISCUSSION:
RCC involves malignant cell proliferation in the proximal convoluted tubules of the kidney. Post-nephrectomy, there is still an approximate 20–40% chance of distal metastasis or locally recurrent disease. Thus, strict follow up is vital. While primary colorectal cancer is common, metastasis to this site is rare. There have been approximately 10 cases reported of metastasis of RCC to the rectum. Only 0.2–0.7% of RCC cases have been found to have metastasized to the stomach. This is the first case reported of synchronous metastasis of RCC to the rectum and gastric body presenting as melena as opposed to hematochezia. Although rare, clinicians should be mindful of this scenario and this case provides a clinical reminder.
1991 The Link Between Aortic Stenosis and Recurrent Gastrointestinal Bleeding: Heyde’s Syndrome
Authors: Alam Loba , Bhurwal Abhishek 
Published: October 2019

INTRODUCTION:
The association between aortic stenosis (AS), acquired von Willebrand disease (aVWD) type IIA, and intestinal arteriovenous malformations (AVMs) is termed Heyde’s Syndrome. We report two patients with severe AS and recurrent GI bleeding from AVMs. The aim of this case series is to recognize this syndrome and take a multidisciplinary approach in the management of these patients.

CASE DESCRIPTION/METHODS:
Case 1: 67-year-old white male with a history of hypertension and severe aortic stenosis who presented to the hospital for melanotic stools, dyspnea on exertion, and worsening fatigue. Labs revealed acute blood loss anemia with hemoglobin of 6.3g/dL. Balloon enteroscopy demonstrated small-bowel AVMs, duodenitis, and bleeding from proximal jejunum (Figure 1). The lesions were treated with argon laser and patient was ultimately discharged. Patient was readmitted within a week for symptomatic anemia. Endoscopy revealed two small erosions in the duodenum which were clipped. As repeat echocardiogram showed severe aortic stenosis with valve area of 0.63 cm2 and peak gradient of 76 mmHg, patient was accepted for TAVR given the significant association of AVMs and AS. Case 2: 70-year-old male with history of coronary artery disease s/p stent, severe aortic stenosis, and multiple GI bleeds who presented with melanotic stools and hemoglobin of 6.5 g/dL. Capsule endoscopy showed multiple AVMs in the small intestine. Balloon enteroscopy confirmed 5 AVMs in the stomach, 1 duodenal AVM, and 2 AVMs in the jejunum- all of which were treated with argon laser (Figure 1). Patient was subsequently discharged home.

DISCUSSION:
In 1958, E. C. Heyde reported an association between AVMs of the GI tract with AS. The bleeding risk seems to correlate with the severity of AS causing increased wall shear forces. Such an environment predisposes to bleeding in patients due to a) decreased blood flow causing GI mucosal ischemia, and b) acquired VWF dysfunction due to breakdown of VWF multimers in high shear force environment causing coagulopathy. This case series impacts clinician decision making by highlighting 1) Heyde’s syndrome should be considered in the differential in patients with concurrent GI bleeding and severe AS, 2) electrophoresis of vWF multimers should be obtained, and 3) TAVR should be considered in hopes of cessation of coagulopathy and AVMs.
1995 Small Bowel Variceal Bleeding Successfully Treated With Percutaneous Coil Embolization
Authors: Malik Anam , Vaze Reema , Buckshaw Ricky , Kloska Michal , Nellis Eric , Wong She Yan 
Published: October 2019

INTRODUCTION:
The small intestine is the most common cause of obscure gastrointestinal (GI) bleeding. Approximately 5% of GI bleeding occurs from the small bowel, defined as the region between the ligament of Treitz and the ileocecal valve. Controlling the bleed in this area is challenging because of its intra-peritoneal location and long length. Patient with small bowel bleeding typically undergo multiple diagnostic evaluations because of the inability to visualize the small bowel properly. However, wireless capsule endoscopy, double balloon enteroscopy, and computed tomography enterography (CTE) have improved the ability to investigate these bleeds. We report a case of small bowel varices successfully treat by percutaneous coil embolization via the superior mesenteric vein (SMV).

CASE DESCRIPTION/METHODS:
A 60-year-old female with non-alcoholic steatohepatitis (NASH) cirrhosis was admitted due to dark stools and acute encephalopathy. Prior to this, the patient was worked-up extensively at another facility for the same complaints with EGD, colonoscopy, CTE, and push enteroscopy which was minimally revealing. Initial laboratory values showed a hemoglobin (Hgb) of 9.8 g/dl with a drop to 7.0 g/dl which required transfusion of three units packed red blood cells. She underwent wireless capsule endoscopy that revealed a large, active bleed in the mid small bowel due to varices. Immediately following, the patient underwent successful direct percutaneous access of the small bowel venous varix, supplied by a prominent SMV branch, by coiling a portion of the varix and the venous inflow. After the procedure, there was clinical resolution of the gastrointestinal bleeding and her hemoglobin returned to baseline.

DISCUSSION:
Even though small bowel variceal bleeding is rare, it can be life threatening without treatment. Early recognition and prompt management is useful in reducing unnecessary diagnostic tests for the patient. The treatment of small bowel varices includes surgery, transjugular intrahepatic portosystemic shunt (TIPS), dilatation of a stenosed portal vein, enteroscopic sclerotherapy, and percutaneous embolization. Intervention angiography was selected for this patient rather than TIPS due to the presence of hepatic encephalopathy. Though further studies are needed to confirm the use of embolization as first line therapy for small bowel variceal bleeding, it should be considered when evaluating small bowel bleeds as it can offer successful outcomes.
1998 Hemostatic Spray for Secondary Hemostasis Following Endoscopic Variceal Band Ligation
Authors: Stibbe Jason R. , Blanton Christie , Rhodes John B. , Hudson Catherine T. , Raines Daniel 
Published: October 2019

INTRODUCTION:
Endoscopic application of hemostatic powder for the treatment of GI bleeding has now been well-described in the literature and utilized for multiple years in clinical practice. Its use as primary and salvage therapy in upper GI bleeding has been established following its approval for non-variceal GI bleeding. Successful use has even been reported in post-variceal banding ulcers, however in very small patient numbers with comparatively less data in acute, ulcerated, post- banding bleeding occurring with simultaneous gastric and esophageal varices.

CASE DESCRIPTION/METHODS:
We present a case of a 57-year-old male with medical history including hepatitis C, cirrhosis, tobacco use, chronic kidney disease, duodenal ulcer, gastritis, ascites, esophageal varices, and diffuse/infiltrative hepatocellular carcinoma associated with tumor thrombus of the portal and hepatic veins who presented to the emergency department for new melenic stools. Hemoglobin was 12.4 g/dL on presentation, decreased to 10.2 g/dL by consultation at which time the melena progressed to hematochezia with an episode of hematemesis. The calculated MELD-sodium score was 19. Physical examination was pertinent for soft, distended abdomen without tenderness and no asterixis. IV ceftriaxone, pantoprazole, and octreotide were initiated. The patient received a single unit of packed red blood cells during hospitalization. EGD demonstrated large distal esophageal varices and an actively-spurting Type 1 (GOV1) gastroesophageal varix. Two bands were placed on esophageal varices and the gastric varix was banded to eradication with cessation of bleeding. Hematemesis recurred the following day and repeat EGD was performed for salvage therapy noting that prior evaluation deemed the patient non-candidate for liver transplant or TIPS procedure. Ulcerated varices were encountered at the prior banding sites with a large pool of coagulated blood in the stomach and hemostatic spray was successfully applied to each site. Hemoglobin remained stable after repeat hemostatic therapy without subsequent need for transfusion.

DISCUSSION:
Ordinarily, persistent bleeding following variceal banding in decompensated cirrhosis warrants TIPS consideration if a candidate and needed for rescue therapy. However, this case lends credence to the use of hemostatic spray in non-TIPS candidates for treatment of post-banding ulcerated variceal bleeding in both esophageal and gastric etiologies.
2004 Gastric Kaposi's Sarcoma in a Patient With Aplastic Anemia
Authors: Ahmed Monjur , Denicola Richard 
Published: October 2019

INTRODUCTION:
Gastric Kaposi’s sarcoma (KS) is rare and mostly seen in patients with acquired immunodeficiency syndrome (AIDS). We present here a case of gastric KS presenting as upper gastrointestinal bleeding in a human immunodeficiency virus (HIV) negative patient with aplastic anemia.

CASE DESCRIPTION/METHODS:
A 70-year-old African American male was admitted with the history of hematemesis. He had sudden onset of nausea and vomiting of blood. He denied any abdominal pain or melena. He was not taking any non-steroidal anti-inflammatory drug. He was known to have aplastic anemia, diabetes mellitus, hypertension gastroesophageal reflux disease and renal insufficiency. He was undergoing treatment with cyclosporine, prednisone and anti-thymocyte globulin for his aplastic anemia. His other medications included insulin glargine, duluglutide, amlodipine, hydrochlorothiazide famotidine, prochlorperazine, valacyclovir and eltrombopag. On admission, his pulse was 125/minute and blood pressure 85/60 mm Hg which returned to normal range with infusion of 1 liter of normal saline. He looked anxious. Abdominal examination was significant for mild epigastric tenderness to palpation. Rectal examination showed heme positive stool. Remainder of the examination was normal, including no new rashes or skin lesions. Laboratory values were significant for hemoglobin of 7.8 g/dl (baseline 8.0-9.0 g/dl), white count of 4,300/cmm and platelets of 89,000/cmm in keeping with known aplastic anemia. Patient had upper endoscopy which revealed 4 cratered sub-centimeter non-bleeding ulcers with rolled edges in the gastric body (Figures 1 and 2). The edges of the ulcers appeared to have increased vascularity. Biopsies were taken from the ulcer edges. Biopsies showed atypical mucosal spindle cell proliferation (Figure 3) with positive staining for D2-40 (endothelial cell) and human herpesvirus 8 (HHV–8) confirming the diagnosis of gastric KS.

DISCUSSION:
KS is a low-grade angiolymphoproliferative tumor arising from the endothelial cells lining the blood vessels or lymphatic vessels. It can develop in patients with significant immunosuppression irrespective of HIV status. Physicians should consider gastric KS in the differential diagnoses when patients with aplastic anemia on immunosuppressive medications present with upper gastrointestinal bleed and endoscopy shows gastric ulcers. Biopsy of the gastric ulcers in this situation is essential to establish the diagnosis.