bluuebunny/crossref_metadata_2025 huggingface dataset:
1930 Ventriculoperitoneal Shunt Migration Into the Stomach: Case Report and Review of Literature
Authors: Reddy Yala K. , Lingala Shilpa , Ahmed Nazneen
Published: October 2019

INTRODUCTION:

Complications of ventriculoperitoneal (VP) shunting includes shunt migration, meningitis, peritonitis and peritoneal pseudocyst. Bowel perforation following VP shunt placement is rare, occurring in about 0.01 to 0.03% with the colon being the most common site. We report a case of migration of a VP shunt catheter into the stomach, in a patient who presented with iron deficiency anemia.

CASE DESCRIPTION/METHODS:

A 65-year-old African-American woman was referred to gastroenterology clinic for iron deficiency anemia. She had no gastrointestinal symptoms and fecal immunochemical test was negative. Colonoscopy was unremarkable. EGD showed no evidence of peptic ulcer disease or any arteriovenous malformation up until the fourth part of duodenum. A foreign body protruding into the gastric fundus [Figure 1] was noted. On review of her PMH, she had a VP shunt procedure in 1995 after clipping of an intracranial aneurysm. CT of abdomen confirmed the presence of the VP shunt in the stomach [Figure 2]. The patient was referred to General Surgery for laparoscopy. During surgery, approximately five-six cm of the distal tip of the VP shunt was intragastric, forming a fistula between the stomach and the abdominal wall. The fistula was sealed, and the shunt was repositioned intraperitoneally. The patient was stable after the surgery.

DISCUSSION:

From a review of the literature, our patient’s presentation with iron deficiency anemia and no gastrointestinal symptoms was unusual. Only 16 cases of intragastric migration of a peritoneal catheter have been previously described. Most patients complained of abdominal discomfort prior to the intragastric perforation. This complication predominantly affects children . The mean interval between the last shunt procedure and perforation was approximately 48.3 months (1 day to 23 yrs) and is unpredictable. The possible mechanisms of bowel perforation includes catheter adherence causing a local inflammation resulting in fibrosis or the continuous pressure from the catheter tip leading to erosion of the bowel and delayed perforation. Our patient could also have had chronic gastric bleeding which may have contributed to her iron deficiency anemia. Treatment approaches include injection of fibrin glue to close the perforated stomach wall, and direct suture of the stomach wall by laparotomy. In our patient, the latter approach was taken. To our knowledge, this is the only reported case of a patient with intragastric migration of a VP shunt presenting with iron deficiency anemia.
1934 Atrioesophegeal Fistula, a Rare but Devastating Cause of Upper Gastrointentinal Bleeding
Authors: Ball Timothy , Kaila Vishal , Franklin Jay , Assar Manish , Frost Beth , Barnard Jeffrey , Jain Rajeev
Published: October 2019

INTRODUCTION:

Atrial fibrillation is the most common cardiac arrhythmia globally, with an estimated prevalence of 33.5 million persons. Over the past 20 years, catheter ablation for atrial fibrillation has grown in acceptance and is now a first-line treatment option for patients with symptomatic paroxysmal atrial fibrillation. Atrioesophegeal fistula (AEF) is a rare but often fatal complication associated with atrial fibrillation ablation.

CASE DESCRIPTION/METHODS:

A 73-year-old woman who underwent radiofrequency ablation for atrial fibrillation 7 weeks prior to presentation to the hospital presented with right-hand weakness, numbness, and ataxia. Initial laboratory evaluation was remarkable for hemoglobin 9.2 g/dL(13.0–17.0 g/dL). Initially, a head computerized tomography (CT) was unremarkable but a subsequent magnetic resonance imaging study demonstrated a right cerebellar stroke. Tissue plasminogen was not prescribed. Transthoracic echocardiogram showed normal left ventricular systolic function, with dilated atria. Later on the day of admission, she developed hematemesis. On day 2 of her admission, she underwent esophagogastroduodenoscopy (EGD) and was found to have a large esophageal defect with thrombus and active bleeding (See Figures 1 and 2). Her clinical status declined quickly and she was taken emergently to the operating room. Unfortunately, despite maximal supportive care, she died prior to surgery. Autopsy revealed an atrioesophageal fistula involving the middle 1/3 of the esophagus and the posterior wall of the left atrium adjacent to the left pulmonary veins. The defects measured 1.5 × 1.0 cm on the esophageal portion and 1 cm × 1 cm on the atrial aspect (See Figure 3). The stomach contained 910 cc of both liquid and clotted blood.

DISCUSSION:

AEF typically occur 20 ± 12 days post-ablation, ranging from 2 to 60 days. AEF has been reported in surgical RFA, percutaneous RFA, and cryoballoon ablation for atrial fibrillation. CT of the chest with intravenous contrast can show pneumomediastinum, pericardial effusion, and communication between the atrium and esophagus. EGD and transesophageal echocardiogram are not recommended if AEF is suspected, as air insufflation during either procedure may lead to massive air embolization and worsening bleeding. Following the diagnosis of AEF, early surgical intervention is critical as the mortality rate without intervention is 100%. AEF is a rare but often fatal complication of catheter ablation for atrial fibrillation. Untreated, the mortality rate of AEF is 100%.
1939 A Malignant Case of Gastrointestinal Bleed
Authors: Asif Samia , Saeed Lyla
Published: October 2019

INTRODUCTION:

Richter’s Syndrome (RS) is an infrequent complication of chronic lymphocytic leukemia (CLL) involving transformation of CLL into aggressive large-cell lymphoma. Gastrointestinal (GI) involvement with RS is rare, previously described in only 9 case reports in literature. Here we present a unique case of RS manifesting as GI bleed.

CASE DESCRIPTION/METHODS:

A 70-year old male presented with one day history of painless hematochezia. He was diagnosed with CLL four years prior and was currently in remission following chemotherapy. Vitals revealed a blood pressure of 88/35 mmHg and pulse rate of 114/minute. Abdominal exam was unremarkable. Rectal exam showed blood in the vault. Work-up showed a hemoglobin of 4.8 g/dl and white cell count of 5300/microliter. Coagulation profile was normal. After initial resuscitation, an esophagogastroduodenoscopy (EGD) was performed showing an excavated lesion with minimal oozing in second part of duodenum; biopsy was obtained and endoclip was applied. Colonoscopy showed blood in terminal ileum and throughout the colon. Capsule study revealed scattered erosions and ulcers with hemorrhage in the jejunum and active bleeding from the distal ileum. Urgent tagged red-cell scan was obtained followed by coil embolization of a focus of brisk active extravasation arising from a terminal ileal branch of ileocolic artery by Intervention Radiology (IR). Duodenal biopsy demonstrated lymphocytic infiltrate consistent with his history of CLL with a background of larger lymphocytes concerning for Richter’s transformation to diffuse large B-cell lymphoma (DLBCL). Computed Tomography (CT) abdomen/pelvis showed splenomegaly and diffuse abdominal and pelvic lymphadenopathy. Pathology report of an excisional biopsy of left axillary lymph node confirmed Richter’s transformation to DLBCL. Systemic chemotherapy and immunotherapy was initiated. GI bleed resolved few days into chemotherapy.

DISCUSSION:

Patients with prior history of hematological malignancies presenting with GI symptoms such as nausea/vomiting, intestinal obstruction, acute perforation or GI bleed should be evaluated for recurrence. In addition to imaging, a low threshold for invasive work-up such as EGD or colonoscopy with biopsy of any lesions seen may be necessary for timely initiation of therapy. This case demonstrates that evaluation for etiology in each case of GI bleed has to be individualized. Identifying the correct diagnosis is the key to successful patient treatment.
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.
2011 Jejunal Varices: A Diagnostic and Therapeutic Nightmare!
Authors: Adoor Dayyan M. , Buffie Charlie
Published: October 2019

INTRODUCTION:

Gastrointestinal hemorrhage is a common complication among cirrhotic patients with portal hypertension, due to the development of bleeding varices. While esophagus and stomach are the most common location for development of varices, it can also rarely occur in ectopic locations, such as the jejunum, ileum, rectum and duodenum. Here, we report a case of a patient with severe gastrointestinal hemorrhage due to a bleeding jejunal varix.

CASE DESCRIPTION/METHODS:

A 55-year-old male with a history of hypertension, splenectomy, and alcoholic cirrhosis had presented initially to an outside ED with complaints of bright red blood per rectum. At admission, he required multiple infusions of pRBCs, and several upper endoscopies due to refractory bleeding with unclear source. Initial endoscopies showed non-bleeding esophageal varices, for which he underwent ligation banding. However, he continued to deteriorate, developing recurrent melena, hypotension, and syncope. On admission to our hospital, he had a repeat upper endoscopy, lower endoscopy, CT angiography and tagged red blood cell study; but we were unable to localize the source of the bleeding. He continued to deteriorate, and also developed a PEA arrest in the setting of a profuse bright red blood per rectum, requiring massive transfusion protocol. After successful resuscitation, he underwent a small bowel enteroscopy, which finally revealed a bleeding jejunal varix. However, the varix was not amenable to any endoscopic intervention. Subsequently, he underwent a successful balloon-occluded retrograde transvenous obliteration (BRTO) of varix. Patient’s condition stabilized and after adequate recovery, he was extubated.

DISCUSSION:

Early diagnosis of ectopic varices is difficult to achieve due to low likelihood of presentation and low sensitivity to various diagnostic tests. Due to its low prevalence, there are no protocols for its management. As in our patient, endoscopic intervention such as sclerotherapy and band ligation can be difficult due to the narrow lumen of the small bowel. Alternatively, BRTO and TIPS are also considered effective therapeutic options. However, due to his poor liver function, BRTO was a better alternative. In conclusion, through this case report, we want to emphasize the importance of early recognition and appropriate management of ectopic varices due to its potential for massive, even fatal hemorrhage.
2015 Dieulafoy Lesion on the Other Side of the Tract
Authors: Khan Sarosh , Pinto Jonathan , Genao Alvaro , Culpepper-Morgan Joan
Published: October 2019

INTRODUCTION:

Dieulafoy lesions involve a large-caliber, tortuous artery in the muscularis mucosa that protrudes due to a submucosal defect with fibrinoid necrosis at the base. The submucosal artery is found to have atypical branching and as a result has a diameter of 1-3 mm, which is 10 times that of a normal mucosal capillary. These lesions can be found throughout the gastrointestinal tract, though they are most frequently found in the stomach, ranging between 61 to 82%. However 10% of all gastrointestinal tract Dieulafoy lesions are found in the colon with 42% of these lesions found in the rectum.

CASE DESCRIPTION/METHODS:

A 79-year-old male with past medical history significant for prostate cancer, hypertension, gout, degenerative joint disease and alcohol abuse disorder presented with bilateral leg weakness and was admitted to the medical service for alcohol dependency and acute kidney injury. On day 12 of hospitalization, he developed melena with a drop in hemoglobin from 12.0 g/dL at the time of admission to 7.7 g/dL. He was then transferred to the critical care unit and underwent esophagogastroduodenoscopy that revealed angioectatic lesions that bled and were treated with argon photocoagulation. On day 15, he developed hematochezia, which further decreased his hemoglobin to 6.9 g/dL. He became hemodynamically unstable, requiring rapid fluid and blood resuscitation. Emergent CT angiography was concerning for vascular malformation in the rectal wall. Colonoscopy was performed and a stream of pulsatile bleeding without an ulcer or varix, consistent with a Dieulafoy lesion, was seen in the rectum. Epinephrine was applied, the lesion was clipped, and hemostasis was achieved. No repeat episodes of gastrointestinal bleeding were reported afterwards.

DISCUSSION:

Bleeding from Dieulafoy lesions can cause hemodynamic compromise as noted in this patient. Therefore prompt identification and treatment is warranted. Endoscopy serves as a gold standard for identification. Hemostasis has been achieved with many techniques in case reports including: BICAP cauterization; combined sclerotherapy and electrocoagulation; heater-probe coagulation; and epinephrine injection combined with electrocoagulation. Rebleeding rate ranges from 6 to 28%. Systemic reviews and retrospective analysis suggest that mechanical ligation to achieve hemostasis, especially the use of hemoclips, may be superior to other techniques employed.
2016 Hemorrhagic Shock Secondary to Ruptured Splenic Artery Pseudoaneurysm: A Rare Fatal Condition
Authors: Kobeszko Matthew , Sullivan Halley , Elkhatib Imad
Published: October 2019

INTRODUCTION:

Splenic artery pseudoaneurysm (SAPA) is a potentially fatal but rare complication of acute or chronic pancreatitis. We present a case of 37-year-old male with history of pancreatitis and a 7.9 cm pseudocyst complicated by hematemesis requiring coiling embolization and massive reperfusion.

CASE DESCRIPTION/METHODS:

A 37-year-old male with history of chronic pancreatitis complicated by pancreatic pseudocyst measuring 7.9 cm presented with acute left upper quadrant abdominal pain and new hematemesis. He appeared diaphoretic, pulse 125 bpm, blood pressure 141/72 mmHg; with no palpable abdominal mass or bruits. Initial labs revealed hemoglobin of 12.8 gm/dL, lipase 74,238 units/L and lactic acid 4.9 mmol/L. Patient underwent CT abdomen/pelvis that revealed acute hemorrhage into the stomach with multiple wedge-shaped splenic hypodensities suggestive of infarcts. Patient continued to rapidly decompensate progressing into hemorrhagic shock requiring massive blood transfusion and vasopressors. Emergent EGD showed plethora of blood with clots in the gastric body with no visible source of bleeding. Due to limitations of endoscopy, patient was taken emergently for mesenteric angiography. A large SAPA with active extravasation into the stomach was visualized and successfully embolized using coiling technique. Total of 30 units of RBCs, 9 units platelets, 15 units plasma and 8 units cryoprecipitate were transfused. Patient recovered well post-op requiring no further transfusions and discharged home in stable condition.

DISCUSSION:

Due to diagnostic challenges and varied initial presentations, splenic artery pseudoaneurysm (SAPA) is a rare disorder predominantly associated with acute/chronic pancreatitis, pancreatic pseudocyst, or trauma. Mostly commonly, the splenic artery is affected in true visceral aneurysms versus the hepatic artery in visceral pseudoaneurysms. SAPAs have a high risk of rupture with a three-fold higher incidence in men, and a mortality rate of up to 90% if untreated. While computed tomography is often the first diagnostic test, mesenteric angiography is the gold standard. Treatment options vary from endoscopic ultrasound guided coiling, percutaneous coiling/stent, or surgical repair. This case emphasizes the need of early recognition, massive reperfusion, and definitive treatment before rapid decline from hemorrhagic shock. Sudden epigastric pain with hematemesis in patients with chronic pancreatitis or pancreatic pseudocysts, may be clues in the development of this rare complication.
2020 Well Differentiated Neuroendocrine Tumor Arising From the Gastric Cardia Presenting With Hematemesis
Authors: Aponte-Pieras Jose
Published: October 2019

INTRODUCTION:

Neuroendocrine tumors (NETs) of the Gastrointestinal (GI) tract are rare and arise from neuroendocrine cells of the pancreas and tubular GI tract. The annual incidence of NETs has increased from 1.09 per 100,000 in 1973 to 6.9 per 100,000 in 2012, reflecting the increased use of endoscopy. Gastric NETs (G-NETs) are divided into three subgroups, type I account for 80%. They are often incidental in workup of non-specific upper GI symptoms, GERD and epigastric pain. Endoscopically they appear as multiple polypoid lesions or ulcers arising in the fundus/body on a background of atrophic gastritis. We report an unusual case of a solitary pedunculated type I G-NET found in the gastric cardia, presenting with hematemesis.

CASE DESCRIPTION/METHODS:

An 82-year-old male with atrial fibrillation on Warfarin presented with melena and hematemesis causing hemorrhagic shock. He denied NSAID or alcohol use, but was on a steroid taper for a COPD exacerbation. Initial blood work was notable for hemoglobin 11.7, platelet count 191, INR 3.4, BUN 79 and creatinine 0.95. A CT Angiogram showed active extravasation in the distal esophagus. He was treated with K-centra, phytonadione, pantoprazole, and intubated prior to Esophagogastroduodenoscopy (EGD). A 20 mm pedunculated polyp with central ulceration and adherent clot was noted in the cardia, adjacent to the GE junction, prolapsing into the esophagus; no active bleeding. Endoloop ligation of the polyp was performed prior to ICU admission. On repeat EGD, polyp was removed with hot snare and retrieved; endoloop was left for hemostasis.

DISCUSSION:

Pathology was consistent with a well-differentiated type 1 G-NET; stains positive for synaptophysin, chromogranin, CD56, and keratin, with lack of proliferative activity. Management and surveillance of type 1 G-NETs is based on consensus guidelines. Due to their indolent nature, lesions < 6 in number and < 2 cm in size can be resected or surveilled with EGD every 3 years. In our case, a large pedunculated polyp was fully resected. A CT or MRI is not recommended as this tumor rarely metastasizes. Our patient underwent CTA to evaluate bleeding, which could have been deferred in favour of EGD given witnessed hematemesis with hemodynamic instability. For type 1 G-NETs >2 cm an endoscopic ultrasound is recommended to assess depth of mucosal invasion. An analysis showed worse survival associated with tumors of the gastric cardia and esophagus, highlighting the importance of better understanding the natural history of these tumors.
2021 Ischemic Duodenal Ulceration After Thoracic Endovascular Aortic Repair (TEVAR)
Authors: Bierle Lindsey A. , Moon Sol , Sweet Jon M.
Published: October 2019

INTRODUCTION:

Ischemia is a rare cause of duodenal ulcers due to the redundant blood supply in the duodenum. Aortic surgery is a known, but rare, risk factor for mesenteric ischemia. Endovascular aortic repair is an increasingly common alternative to open surgery for select patients with aortic aneurysms, however post-procedural complications including endoleaks and graft migration can occur. Less commonly reported complications include bowel ischemia, with only a handful of reports detailing duodenal ulceration in the current literature. Here we present a case of ischemic duodenal ulceration following thoracic endovascular aortic repair (TEVAR).

CASE DESCRIPTION/METHODS:

An 82-year-old male on dual-antiplatelet therapy presented with complaints of lightheadedness, dyspnea, and melena. He had been discharged to skilled nursing three days earlier following thoracic endovascular aortic repair (TEVAR) for DeBakey type III aortic dissection distal to the left subclavian artery. His recovery was complicated by endovascular leak at the left subclavian artery, left renal artery dissection, and thrombosis of the superior mesenteric artery (SMA), which were treated with coiling and stenting of the left renal artery and SMA. Hemoglobin upon hospital return was 6.7 g/dL compared to 8.3 g/dL on initial discharge. Esophagogastroduodenoscopy revealed a large, near-circumferential Forrest IIc ulcer in the duodenum with concern for underlying ischemic etiology. Computed tomography angiography (CTA) of the chest and abdomen revealed a duodenal ulcer with associated mural thickening and fat stranding. CTA reconfiguration identified stenosis at the bifurcation of the common hepatic artery and stenosis of the celiac artery compared to post-TEVAR CTA images. These findings were confirmed with celiac angiography and repaired using drug coated balloon catheter percutaneous transluminal angioplasty to the common hepatic artery and balloon expandable stenting to the celiac artery. The patient’s hemoglobin stabilized post-operatively and he had complete symptom resolution.

DISCUSSION:

Upper intestinal ischemia is a rare but important cause of duodenal ulceration and hemorrhage following TEVAR, as demonstrated in this case. Bowel ischemia from TEVAR is more commonly seen when the distal aspect of the graft has celiac artery involvement. Early recognition of ischemic duodenal ulceration after TEVAR is of significant clinical importance, as treatment differs from other etiologies of duodenitis and early intervention lowers morbidity.
2024 Novel Approach for Management of Stomal Variceal Bleed
Authors: Olson Kristin , Uhlenhopp Dustin , Sunkara Tagore , Gaduputi Vinaya , Chadrasekaran Bharanidhar
Published: October 2019

INTRODUCTION:

Patients with cirrhosis are prone to developing bleeding from varices. Patients with cirrhosis and ileostomy can develop ileostomy varices. Only 5% of variceal bleeds are reported to be from an ileostomy varix.

CASE DESCRIPTION/METHODS:

A 51-year-old female with heart failure, hepatitis C cirrhosis, esophageal varices with recent banding, colectomy with ileostomy presented with ostomy bleeding. Examination of the ostomy revealed oozing from the ostomy site. The ostomy site was cauterized with silver nitrate which initially stopped the bleeding. Esophagoduodenoscopy demonstrated three columns of non bleeding varices, no red whale/nipple sign and two non bleeding esophageal ulcers. Later, ostomy bleeding recurred which led to an ileoscopy. A non-bleeding ulcer was noted in the ileum. As the scope was withdrawn, an osteal varix was noted and due to the manipulation of the scope, the varix started squirting blood. Manual pressure was applied and a foley was inflated in the ostomy tract for tamponade. After 15 minutes of tamponade, the scope was re-inserted which did not demonstrate active bleeding. Banding couldn't be performed as there was no room to manipulate the scope. A CTA demonstrated two varices originating from the superior mesenteric vein within the ostomy track (Figure 1). TIPS was contraindicated due to heart failure. 2cc of Sotradecol was injected into each varix for obliteration via ultrasound guidance. After the injection, ultrasound showed successful obliteration of the varices (Figure 2). There was no further bleeding during her hospital stay.

DISCUSSION:

Ileostomy variceal bleeding is uncommon. Bleeding from an ileostomy varix can occur as early as a year after ileostomy placement in patients with cirrhosis. Diagnosis is often missed. It is key to inspect the stoma for bleeding after removal of the appliance. Doppler ultrasound or CT/MRI can aid in the diagnosis. There are multiple strategies to treat a variceal ostomy bleed including local control (ligation, sclerotherapy, intravascular coil or glue emboliziation) and portal vein decompression (TIPS). In majority of cases, local therapy is used as first line treatment as demonstrated in our patient who was successfully treated with sclerotherapy. We'd like to highlight the possibility of ultrasound guided sclerotherapy of osteal varices if endoscopic sclerotherapy is not feasible. More research is needed to assess which treatment strategy provides the best outcome for patients coming in with ileostomy variceal bleeding.