Episode Of Hematemesis Research Articles

Management of refractory rectal variceal bleed using computed tomography.

The management of refractory rectal variceal bleed using a minimally invasive percutaneous approach is described. Rectal varices are portosystemic collaterals that arise as a complication of portal hypertension. Bleeding is less common from rectal varices than from esophageal varices, but it is potentially life-threatening. Hence, it is of interest to describe a novel minimally invasive percutaneous technique to control refractory bleeding from rectal varices in a complex scenario where other proven treatments have failed. In the present study, a 28-year-old male presented to the Emergency department with one episode of hematemesis, hematochezia and severe abdominal pain. Sigmoidoscopy revealed actively bleeding rectal varices. CT abdominal angiogram revealed variceal formation in the rectum. we successfully performed CT guided percutaneous N- butyl cyanoacrylate (NBCA) glue injection of rectal varices with immediate and complete cessation of rectal bleed after failed endoscopic sclerotherapy.

Noncirrhotic Portal Hypertension – A Case Report on a Sequela of Portal Vein Cavernoma

Introduction: Increased pressures in the portal vein (portal hypertension) which occurs following portal vein thrombosis, results in cavernous transformation of the portal vein. Though portal vein thrombosis (PVT) is a frequent complication in cirrhotic patients, it may also exist as a basic vascular condition without any liver damage. Among the predisposing factors for portal vein cavernoma are deficiencies in protein C, S & antithrombin III, antiphospholipid syndrome and mutations in factor V Leiden and JAK2. Determination of the aetiology aids in the management plan to not only relieve symptoms of the patient but also to treat the underlying cause. Gastroesophageal variceal bleeding, splenomegaly, portosystemic collaterals, and ultimately hematologic abnormalities are among the prominent clinical features. Case Presentation: We present a case of a 16-year-old male with portal vein cavernoma complicated by bleeding oesophageal varices presenting with a second episode of hematemesis and melena within a 10-year period. He underwent endoscopic variceal band ligation and was put on oral warfarin and propranolol. The patient was followed up once at the outpatient clinic after discharge without the laboratory investigations we requested due to financial constraints. He has since been lost to follow up. Conclusion: Bleeding oesophageal varices from noncirrhotic causes are common and a high index of suspicion is needed to make a diagnosis. Though investigations tailored towards identifying the underlying cause presents a challenge in a resource constrained setting like ours, management of complications and symptoms to reduce morbidity and mortality cannot be over-emphasized.

A201 AORTO-ESOPHAGEAL FISTULA AS A COMPLICATION OF ESOPHAGEAL VARICEAL BANDING

Abstract Aims This is the first reported case of bleeding from an aorto-esophageal fistula as a consequence of ischemic esophageal ulceration post esophageal variceal banding. Methods A 46-year-old male presented with epigastric pain for one-week, which was not associated with fever, jaundice, or symptoms of GI bleed. He was hemodynamically stable with an unremarkable exam and basic labs. He underwent a CT scan which showed chronic portal vein thrombosis extending from the main portal vein into the superior mesenteric vein and evidence of portal hypertension, along with massive esophageal varices. Anticoagulation was not started due to risk of GI bleed. Upper endoscopy confirmed the presence of three columns of large esophageal varices in the distal and mid esophagus, the largest was 3 cm in size. There was no stigmata of recent bleeding and no gastric varices. Seven bands were applied. CT abdomen was repeated on the seventh day of admission, showing extension of portal vein thrombosis. As such, the thrombosis team started a low dose of anticoagulation. (dalteparin 7500 IU). He tolerated it well and showed no signs of bleeding prior to discharge. The day after discharge, the patient presented again with an episode of melena. Examination was remarkable for tachycardia, hypotension and melena. Hemoglobin was stable. Patient was admitted with impression of upper GI bleed most likely secondary to post banding ulcer. He was started on medical therapy. Anticoagulation was held. Next day, the patient had an episode of hematemesis with large amount of blood and clots. Emergent upper endoscopy showed active bleeding in the distal esophagus. Further examination showed a full-thickness, 7 mm defect in the lower esophagus with fresh red blood emptying from it into the esophagus (Figure 1). Thoracic surgery was consulted and suspected a perforated esophageal ulceration at the site of previous banding, with an aorto-esophageal fistula. Patient deteriorated immediately and passed away. The cause of death was cardiac arrest secondary to acute blood loss anemia. Results AEF is a recognized cause of upper GI bleeding with a high mortality rate. While rare, it can occur secondary to ischemic esophageal ulcer post EV banding. Conclusions This is the first reported case of an aorto-esophageal fistula as a consequence esophageal variceal band ligation. While extremely rare, this complication should be considered as a potentially fatal complication of variceal banding, especially in the setting of a diseased or previously repaired aorta.

Emphysematous changes as red flag signs preceding rapidly progressive infectious aortic disease: two case reports

BackgroundInfectious aortic disease is a rare and fatal disease, that requires the appropriate intervention. An accurate diagnosis should be promptly established. However, this is difficult because the clinical manifestations of this disease vary and are non-specific.Case presentation(CASE 1) An 87-year-old male, presenting with generalized malaise and weight loss, was admitted for further examination. A chest computed tomography (CT) showed mediastinal emphysema. Empirical intravenous antibiotics were administered to address the non-specific infectious findings in the laboratory data. The treatment was effective, and the patient fully recovered. However, he was in shock due to aortic rupture and marked pseudo aneurysmal formation around the aortic arch day 25 of hospitalization. An emergency total aortic arch replacement was performed, and the patient was discharged. (CASE 2) An 82-year-old male who had undergone Y-graft replacement in the abdominal aorta 15 years previously was admitted due to general malaise and anorexia. Abdominal CT revealed emphysematous changes adjacent to the abdominal aorta. The patient responded favorably to empirical treatment with intravenous antibiotics and was discharged 19 days after admission. Four days after discharge, the patient went into cardiac arrest after an episode of hematemesis. Abdominal CT revealed an enlarged stomach and duodenum, filled with massive high-density contents proximal to the abdominal aorta. He died of hemorrhagic shock despite cardiopulmonary resuscitation.ConclusionsAlthough emphysematous changes are rare, they are red flag signs during the early stage of infectious aortic disease. Thus, physicians should remain vigilant for this kind of critical sign.

132 Pseudoaneurysm of the Facial Artery After Tonsillectomy Managed with Endovascular Coiling: A Case Report

Abstract Introduction We present a case of pseudoaneurysm of the facial artery after tonsillectomy managed with successful endovascular coiling. Presentation of Case 41-year-old lady presented with a history of throat pain and 3 episodes of hematemesis on the 3rd, 4th, and 7th postoperative days after tonsillectomy and styloidectomy. She had undergone the operation 20 days back. Neurological examination was normal. Contrast-enhanced computed tomography scan of the neck showed – contrast-filled dilatation of a branch of the right facial artery in the right palatine tonsillar fossa within the operative bed – likely pseudoaneurysm which was managed endovascularly. The patient recovered fully after treatment. Discussion Tonsillectomy can have various complications among which one is the pseudoaneurysm of the facial artery which can be managed with coiling in the catheterization laboratory. Conclusions Pseudoaneurysm of the facial artery is a rare complication of tonsillectomy. Endovascular treatment of a pseudo aneurysm can be done.

Ectopic Spleen with Segmental Portal Hypertension, About a Case

Ectopic spleen is a condition in which the spleen does not sit in the left hypochondrium but has an atypical, often pelvic, location. We report the case of a 35-year-old patient suffering from chronic abdominal pain for 11 years associated with an episode of hematemesis, pollakiuria and dysuria, with anemia and notion of multiple transfusions. Abdominal ultrasound found an ectopic spleen in the pelvic position, enlarged in size, with multiple collateral venous circulations and extensive partial thrombosis of the splenic vein. A total splenectomy by midline laparotomy was performed. Perioperative exploration found a bulky pelvic spleen with a long and tortuous splenic pedicle, involuted in 3 turns without splenic infarction. When the splenic artery is clamped, the colonic and gastric varicose veins lose half their diameter, so the decision is made to perform total splenectomy. Post-splenectomy antibiotic prophylaxis and vaccination was administered. The follow-up was favorable, with a follow-up of 4 years. The patient was then lost sight of.

Black Esophagus and Recurrence of Duodenal Ulcers: Two Signs of the Same Pathogenic Pathway? A Case Report

Black esophagus or acute esophageal necrosis is characterized by circumferential black discoloration of the distal esophageal mucosa. It is a rare condition with a multifactorial pathogenesis, and its most common clinical presentation is acute upper gastrointestinal bleeding. It usually affects elderly patients with multiple comorbidities and is associated with a high mortality rate. This is a case report of a 90-year-old man with multiple comorbidities, including diabetes mellitus, atrial fibrillation with complete atrioventricular block, and a history of ischemic stroke, who presented to the emergency department for a syncopal episode followed by coffee ground emesis. Thoraco-abdominal computer tomography showed thickening of the distal esophagus and ruled out major complications such as perforation. The following esophagogastroduodenoscopy showed black circumferential necrosis of the mid and distal esophagus. Multiple irregular ulcers with black necrotic areas were also present in the bulb and second duodenal portion. During the hospitalization, the patient was treated with PPI, NPO nutrition, and broad-spectrum antibiotics with benefits. Two months later, the patient returned to the emergency department due to a new episode of hematemesis with endoscopic evidence of esophageal stricture without necrosis and recurrence of duodenal ulcers. After a few days, the patient died due to worsening of the underlying comorbidities. A black esophagus is associated with duodenal ulcers, which may recur and are possibly due to a common ischemic origin. In this case report, we explore the potential link between black esophagus and duodenal ulcers, discussing the underlying mechanisms and relevant literature supporting this association.

Congenital absence of splenic artery: a rare cause of upper gastrointestinal bleed

A 21-year-old woman presented as an emergency with upper abdominal discomfort and one episode of haematemesis. Physical examination, blood results and oesophagogastroduodenoscopy (OGD) were unremarkable. The patient collapsed following a large haematemesis 24 hours later and was intubated, ventilated and resuscitated. Repeat OGD demonstrated multiple areas of gastric angiodysplasia with active bleeding. Attempted haemostasis was unsuccessful. computed tomography angiography (CTA) demonstrated an absent splenic artery and multiple abnormal collaterals supplying the stomach, pancreas and spleen originating from a hypertrophied left gastric artery and gastro-epiploic arteries. Angiography demonstrated active bleeding from these abnormal collaterals, which were successfully embolised and haemostasis attained. On follow-up CTA, no evidence of further bleeding or infarction was noted. Congenital absence of the splenic artery is rare, with only four reported cases, and is an extremely rare cause of upper gastrointestinal bleeding.

S2282 Black Esophagus Manifesting as Upper Gastrointestinal Bleeding in Diabetic Ketoacidosis: A Case Report

Introduction: Acute esophageal necrosis, or black esophagus, is a rare clinical entity manifesting as upper gastrointestinal bleeding and complicating various conditions. However, black esophagus in the setting of diabetic ketoacidosis (DKA) has been rarely reported. We present a case of a 36-year-old male with black esophagus presenting as hematemesis complicating an episode of DKA. Case Description/Methods: A 36-year-old male with uncontrolled type 1 diabetes mellitus complicated by end-stage renal disease and hypertension presented to the emergency department with abdominal pain, nausea, and vomiting. Patient reported worsening abdominal pain and associated blood-tinged emesis. On presentation, patient was hemodynamically stable. Physical exam included an abdomen that was diffusely tender to palpation without peritoneal signs. Initial labs remarkable for serum glucose 1491, anion gap 41, bicarbonate 9, and hemoglobin 7.5. Patient was admitted to Critical Care for insulin drip and intravenous fluid resuscitation for DKA. Later, patient had an episode of hematemesis resulting in tachycardia, hypotension, and drop in hemoglobin to 5.6. Patient was further resuscitated with blood transfusions with improvement in hemodynamics and hemoglobin to 8.9. Continuous pantoprazole infusion was initiated. Upper endoscopy demonstrated severe, ulcerative necrotizing circumferential esophagitis in the middle and lower third esophagus and a medium size blood clot without evidence of active bleeding. No biopsies were taken due to concern for possible false lumen; CT chest with contrast demonstrated no signs of esophageal perforation. Following EGD, patient had several small self-limiting episodes of hematemesis and melena, while maintaining hemodynamics. He was continued on pantoprazole infusion and placed on strict nothing by mouth (NPO) precautions for 3 days with gradual advancement of diet. He received 6 days of empiric antimicrobial therapy with ampicillin-sulbactam and fluconazole. Patient reported no further episodes of hematemesis. Hemoglobin stabilized around 8.0 (Figure). Discussion: DKA is a rare but life-threatening cause of acute esophageal necrosis which may develop due to a combination of tissue hypoperfusion, impaired mucosal defenses, and gastric reflux. Upper gastrointestinal bleeding in the setting of DKA should raise suspicion for black esophagus which is a potential cause of mortality. Early diagnosis and treatment of underlying etiology are the key factors in management.Figure 1.: Severe, ulcerative necrotizing circumferential esophagitis in the middle and lower third esophagus and a medium size blood clot without evidence of active bleeding.

S2371 Ripped by Chips: A Case Report of Esophageal Perforation After Consumption of Chips

Introduction: Eosinophilic esophagitis (EoE) is an uncommon condition defined as a chronic, immune-mediated, esophageal disease characterized clinically by symptoms related to esophageal dysfunction and histologically by eosinophil-predominant inflammation.1 Patients typically present with esophageal dysphagia and food impaction. We present a unique and rare case presentation of a young male patient who presents with pneumomediastinum in the setting of undiagnosed EoE. Case Description/Methods: A 31-year-old male with no significant past medical history presents to the emergency department with lower neck pain. He reports sudden onset of pain after consuming a sandwich containing potato chips. This was followed by 2 immediate episodes of hematemesis. Vital signs were within normal limits. Physical exam was significant for bilateral crepitus on exam. CT Chest with contrast was significant for extensive pneumomediastinum around the esophagus suggestive of an esophageal perforation. CT neck was significant for extensive emphysema in the neck and pneumomediastinum with esophageal wall emphysema suggestive of esophageal rupture (Figure). An esophagram revealed no evidence of gross esophageal leak suggesting a contained micro perforation, so he was managed conservatively with IV pain medications, initial period of nil by mouth followed by slow escalation to a liquid diet. His diet was slowly escalated, and he was discharged home in stable condition. Two months later at an outpatient gastroenterology follow up, an esophagogastroduodenoscopy was significant for ringed esophagus, longitudinal furrows, white plaques and white specks throughout the entire esophagus. Biopsies were consistent with eosinophilic esophagitis with increase eosinophil count in the proximal esophagus. He was started on a daily proton pump inhibitor with ongoing follow up. Discussion: The incidence of EoE appears to be increasing, in part due to rising recognition of the disorder. It is important for physicians to identify its features early to prevent further complications. Esophageal perforation is a rare but serious complication of eosinophilic esophagitis, occurring in ∼2% of cases.2 Ongoing inflammation from longstanding untreated EoE has previously been reported to have led to esophageal perforation but rarely in such a dramatic fashion.3Figure 1.: 1. Significant emphysema in the neck and pneumomediastinum with thinning of the posterolateral aspect of esophagus concerning for esophageal rupture.

S2352 No Soup for You: The Case of an Intramucosal Hematoma Found During Endoscopy for an Esophageal Food Impaction

Introduction: Esophageal food impaction (EFI) is third most common gastrointestinal emergency, which is commonly associated with obstructive lesions such as peptic strictures and Schatzki rings, eosinophilic esophagitis and rarely motility disorders. Endoscopic therapy is the mainstay option for the management of EFI if medical therapy fails. The most commonly impacted foods include beef, chicken, pork, and undercooked vegetables with liquids rarely causing an impaction. Complications from a prolonged EFI can result in mucosal disruption to an esophageal perforation. We present an unusual case of an esophageal intramucosal hematoma found in a during endoscopic retrieval of an esophageal impaction. Case Description/Methods: An 80-year-old male presented with a 2-hour history of foreign body sensation in his throat that began while eating hamburger meat and soup with potatoes. He began coughing up a large amount of mucus at symptom onset and was unable to finish his meal. He has been unable to swallow solids or liquids. History was significant for esophageal peptic strictures in the past requiring dilations. After 2 doses of glucagon failed to help pass the bolus, the patient underwent endoscopic removal of the esophageal food impaction. During the procedure, food was found in the middle and lower thirds of the esophagus and was subsequently removed with suction cap and rat toothed forceps. The esophagus was tortious and was noted to have decreased and abnormal movement throughout with a moderate stenosis found at the gastroesophageal junction. The middle and lower third of the esophagus had localized severe erythema, suspicious for the presence of intramucosal hemorrhage (Figure). The patient tolerated a diet after endoscopy and discharged home. Discussion: Esophageal food impactions are uncommon and are commonly associated with stricture and rings. Complications from a prolonged food impaction include mucosal disruption however findings of an intramucosal hematoma are rare. Intramucosal hematoma present with chest pain, dysphagia, and hematemesis. This patient presented with dysphagia however had no other pain or episodes of hematemesis. In this patient it is unclear whether his presentation was due to an acute EFI causing an intramucosal hematoma or whether the ingestion of soup caused an intramucosal hematoma resulting in an EFI. Nevertheless, one should take caution during endoscopic evaluation for patients who presented with an EFI.Figure 1.: Localized severe erythema suspicious for intramucosal hemorrhage. (1a., 1b., 1c.), Lower third of the esophagus. (1d.)- Gastroesophageal junction.

S2663 The Eroding Ulcer

Introduction: Massive upper gastrointestinal (GI) bleeds can be life threatening. Common causes are peptic ulcer disease and esophagogastric varices. These, when presented, often can be managed endoscopically. Ulcers in the GI tract can, rarely, erode into major arteries including the splenic artery and cause bleeding that may need embolization or surgery to control. Here we report a case of a massive upper GI bleed. Case Description/Methods: Patient is a 65 year old male with PMH of alcohol abuse, drug use, bed bound who presented with reported hematemesis. Initially patient reported he drank red liquid prior and refused an endoscopy. A day into hospitalization he had another episode of hematemesis and hypotension and was transferred to the ICU. There he transfused and stabilized. He underwent an endoscopy discovering a gastric ulcer in the fundus. Epinephrine was injected with good effect and cautery was initiated with bipolar probe starting at the periphery of the visible vessel and on the edges of the ulcer. While performing cautery, the vessel in the ulcer started to hemorrhage causing red out and inability to visualize. He was intubated and started massive transfusion protocol. Interventional radiology (IR) and surgery was consulted. He had three cardiac arrests with rapid return of pulse. When he made it to the IR suite, underwent angiography which showing significant bleeding from mid splenic artery which was coiled (d). With the location the ulcer had eroded into the splenic artery causing a fistula. He recovered well and was later discharged from the hospital. He underwent a repeat endoscopy a few days later (a) and another a few weeks after discharge (b,c). Discussion: Often with vascular fistulas there is an initial small bleed followed by a more significant bleed as seen in this case. When encountering massive GI bleeding, one must keep enteric vascular fistulas in the differential and have interventional radiology and surgery engaged early. Presenting with a splenic artery aneurysm with bleeding is rare, 0.01 to 10.4% depending on literature. Hemorrhage is one of the most common presentation for splenic artery pseudoaneurysms with 47% of cases and mortality approaches 90% if not properly managed. This case reminds us to keep a broad differential and to involve IR and surgery early in a massive GI bleed.Figure 1.: A.Endoscopy post coiling with coil emerging from ulcer. B. Endoscopy after discharge. C. Endoscopy after discharge, coils still present from ulcer. D. Angiogram showing active bleeding.

S3302 Acute Esophageal Obstruction: An Uncommon Complication of Variceal Ligation Treated With Band Removal and Stenting

Introduction: Esophageal varices (EV) are a complication of portal hypertension. Over time, EV enlarge and may spontaneously rupture, leading to bleeding and possibly death with a high mortality rate of up to 20%. Esophageal variceal ligation (EVL) is used for prophylaxis, as well as treatment of acute variceal bleeding with the goal of eradicating varices. EVL is an effective therapy with rare but serious complications including bleeding, ulcers, strictures, and rarely acute obstruction. Amongst the few reported cases of esophageal obstruction, treatment has varied but mostly involved conservative management or band removal. We present a case of post EVL acute esophageal obstruction that was uniquely treated with band removal and esophageal stenting. Case Description/Methods: A 79yo female with nonalcoholic steatohepatitis cirrhosis and a MELD-Na of 12, complicated by portal hypertension and EV status post previous banding one year prior came to the emergency room two days after esophagogastroduodenoscopy (EGD) for routine EV surveillance with placement of two bands resulting in complete eradication. She presented with one episode of hematemesis and dysphagia to liquids, and regurgitation; denied odynophagia and chest pain. Hematologic parameters were at baseline. EGD revealed near-complete occlusion of the esophagus from banding at 40cm from the incisors (fig1). One band was dislodged with the gastroscope, which permitted the obstructed area to be traversed after downsizing the gastroscope. No active bleeding was evident. To prevent recurrent bleeding given hematemesis at presentation, the area of obstruction was stented with a 16mm x 100mm fully covered stent (fig2), proximal and distal margins at 30cm and 40cm respectively. She was discharged home after 24 hours able to tolerate soft foods. The stent was kept for seven days. At follow-up EGD for stent removal, there was slight luminal narrowing treated with graded balloon dilation from 18mm to 20mm. She continued to do well and nine months later had EGD surveillance with banding of grade II varices only. Discussion: Acute esophageal obstruction, though rare, is a complication of variceal banding that should be considered in patients with dysphagia after banding. This is a case that required innovative thinking and priority to treatment options that provide hemostasis while relieving obstruction in a cirrhotic patient with a high risk of bleeding.Figure 1.: 1. Near complete occlusion of esophagus Fig 2. After placement of esophageal stent.

S3216 When to Start Anticoagulation? A Case of Portal Vein Thrombosis in a Post-Partum Cirrhosis Patient With Variceal Bleeding

Introduction: While portal vein thrombosis (PVT) is a relatively rare disease in the general population, the prevalence of PVT in cirrhosis increases in parallel with the severity of cirrhosis. The pathogenesis of PVT in cirrhosis is thought to be multifactorial resulting mainly from alterations in the different components of Virchow’s triad. Case Description/Methods: Here we report a case of a 36-year-old woman with history of alcoholic cirrhosis who presented 2 weeks status post c-section complaining of acute onset abdominal pain, bloating, and nausea with two episodes of hematemesis. Her initial vital signs were unremarkable and hemoglobin was 7.4 gm/dL. Her model for end-stage liver disease (MELD) score was 16. She underwent upper endoscopy (EGD) with successful banding of 3 columns of large varices which showed stigmata of recent bleeding. Patient also underwent diagnostic and therapeutic paracentesis which did not show signs of spontaneous bacterial peritonitis (SBP). However, she did have history of wound dehiscence of her cesarean incision with persistent leakage of serous fluid despite prior negative pressure wound therapy. Therefore, CT abdomen/pelvis was obtained which demonstrated nonocclusive thrombus in the main portal vein extending into both the right and left branches. Due to finding of PVT, MRI was also obtained which showed no evidence of malignancy. As her hemoglobin remained stable ( >7 gm/dL) during hospitalization, she was started on therapeutic low molecular weight heparin (LMWH). Unfortunately, patient was re-admitted five days later for hematemesis and drop in her hemoglobin to 5.6 gm/dL. She received blood products, and repeat EGD showed cratered and superficial esophageal ulcers at the site of prior variceal treatment. Ultimately LMWH was held and resumed after hemoglobin stabilized. Discussion: This case demonstrates the conundrum of if/when to treat PVT in patients with cirrhosis. Current guidelines recommend anticoagulation as the mainstay of PVT treatment. However, this is can be complicated by other sequelae of decompensated cirrhosis such as variceal bleeding. Consequences of non-treatment include further increase in resistance to portal blood thus worsening portal hypertension. In this case, patient’s post-partum status also favors anticoagulation as other society guidelines have recommended anticoagulation with LMWH for postpartum patients with vascular disease of the liver. Therefore, individualized treatment algorithms should be developed and used to guide management.

Combined Transhepatic-Transsplenic Direct Intrahepatic Portocaval Shunt in a Child with Budd-Chiari Syndrome

A 6-year–old girl presented emergently with 3 episodes of hematemesis over 3 days and abdominal distension for 10 days. Physical examination revealed distended superficial abdominal veins. Ultrasonography (US) showed thrombosed hepatic veins and infrahepatic inferior vena cava (IVC) with ascites, which is diagnostic of chronic Budd-Chiari syndrome with portal hypertension. Direct intrahepatic portocaval shunt creation was planned under general anesthesia. Bilateral jugular and brachiocephalic veins were chronically occluded (Fig 1a), and femoral venography showed chronic occlusion of the IVC (Fig 1b).

Clozapine induced oesophagitis: A case report

IntroductionThere are several case reports describing clozapine side effects such as agranulocytosis, constipation,tachycardia but rarely cases describing oesophagitis caused by clozapine were reported.ObjectivesTo report the first case in our country about clozapine induced oesophagitis.MethodsWe describe a case in which a patient who has no gastrointestinal past history,has developed an oesophagitis stage 2 of Savary and Miller Classification without any gastroesophageal reflux disease, few weeks after introducing clozapine at therapeutic dose.ResultsA 25 years old male patient with resistant schizophrenia managed with clozapine,was admitted to reinitiate his treatment after weeks of stopping his medication.During hospitalization, our patient developed a sudden haematemesis in 10 days after commencement of clozapine. The patient had no history of gastrointestinal symptoms or disease. The clinical examination and blood tests did not find any signs of bleeding severity.A gastroscopy was performed, revealing esophagitis stage 2 of Savary and Miller classification and a cardiac polyp removed with biopsy forceps that showed no malignant lesions .The patient was treated with acid suppressant therapy.There was no further episode of haematemesis and our patient healed uneventfully within a week.As for clozapine, it wasn’t interrupted and we continued increasing doses very carefully with no further incident.ConclusionsAlthough it is a rare side effect, oesophagitis may appear at therapeutic doses of clozapine, and this possibility should be taken into account when treating patients with resistant psychiatric disorders.DisclosureNo significant relationships.

Use of Variceal Banding in Gastric Polyps Bleed-A Prototype Technique in Children

An 8-year-old girl with a known history of Peutz-Jeghers syndrome presents a history of hematemesis to the emergency room following an episode of reaching in the early hours of the morning. Her initial evaluation showed a hemodynamically stable child but had multiple episodes of retching which were managed conservatively. She has had a past history of acute pancreatitis for which she was in pancreatic supplements and she also had a magnetic resonance imaging of the brain which was normal. She presented with a history of ileo-ileal intussusception for which she was operated 5 years ago with an end-to-end anastomosis and she has been asymptomatic since. Her annual endoscopic surveillance showed polyposis of the colon which was resected and she was under constant follow-up. She had an episode of hematemesis was an acute episode which needed evaluation with an upper gastrointestinal (GI) endoscopy which showed the presence of polyps in the gastric antrum and pylorus with Grade 2 esophageal varices. She underwent prophylactic variceal banding for her esophageal varices. Further upper GI endoscopy evaluation showed the presence of polyps in the gastric antrum, body, and pylorus. We decided to use the variceal bands to ligate the gastric polyps as an unorthodox conventional technique, as the risk of bleeding and perforation are high in polypectomy. We Find banding of gastric polyps a very safe and effective method to remove gastric polyps in the stomach.

Haemosuccus pancreaticus: a diagnostic challenge and its management through interventional radiology

BackgroundHaemosuccus pancreaticus (HP), also known as pseudohaemobilia, is defined as upper gastrointestinal tract hemorrhage originating from the pancreatic duct into the duodenum via the ampulla of Vater or major pancreatic papilla. Pseudoaneurysm formation from the splenic artery is a common complication of pancreatitis; however, upper gastrointestinal bleed resulting from rupture of splenic artery pseudoaneurysm into the pancreatic duct is unusual and challenging to diagnose.Case presentationA 26-year-old patient presented with multiple episodes of hematemesis, melena, and intermittent abdominal pain. A contrast-enhanced computed tomography (CECT) scan was performed that demonstrated chronic calcific pancreatitis with a pseudoaneurysm in the splenic artery in close relation to the main pancreatic duct. The patient was immediately shifted for endovascular management, and the pseudoaneurysm was successfully embolized. Post embolization, the patient developed splenic abscess, which was managed by percutaneous catheter drainage.ConclusionDue to its rarity and being challenging to diagnose, the mortality rate of HP is high. A high level of expertise is required to diagnose HP, and it should be considered in all upper gastrointestinal bleed patients associated with acute or chronic pancreatitis. Rapid initial CECT and angiography should be performed to confirm the diagnosis, followed by embolization of the bleeding pseudoaneurysm to eliminate the need for surgery. This case report highlights the challenges in the diagnosis and management of HP.

Hematemesis Secondary to Isolated Gastric Metastasis from Ovarian Carcinoma

A 49 year old female presented with two episodes of hematemesis. Six years ago she had undergone a total hysterectomy with bilateral salpingo-oophorectomy, omentectomy and pelvic lymph node dissection for a serous papillary carcinoma of the ovary (FIGO stage IIA), followed by adjuvant chemotherapy. On regular follow up she remained disease free, until presentation. Her hemoglobin was 9.1g/dl and CA-125 level was elevated-128u/ml. Gastroscopy revealed an ulcerated submucosal tumor in the antrum measuring 5x4cms with no e/o active bleeding & minimal altered blood in stomach. Biopsy showed scanty metastatic tumor deposits from ovarian cancer. CT scan of chest, abdomen & pelvis showed a large, well-defined heterogeneously enhancing serosal mass lesion in the antrum of the stomach with soft calcification within, with no ascites. Few paraortic lymph nodes were enlarged. No other organ involvement was observed. She received chemotherapy and is currently on close follow up. Isolated gastric metastasis from an ovarian cancer is extremely rare and most often occur in advanced stage with synchronous lesions in the peritoneum. Histologically serous carcinoma is the most common variety. Clinicians should consider that in patients with submucosal tumor and history of ovarian carcinoma, the gastric lesion may be metastatic and not a primary gastric carcinoma.

A117 MANAGEMENT OF VARICEAL BLEEDING WITH ENDOSCOPIC INJECTION OF N-BUTYL-2-CYANOACRYLATE IN PREGNANCY

BackgroundAlthough variceal bleeding is rare in pregnancy, pregnant woman with non-cirrhotic portal hypertension are at greater risk of variceal hemorrhage due to increased splanchnic blood flow. Variceal hemorrhage is associated with increased risk of maternal and fetal mortality. Most documented cases of variceal bleeding in pregnancy report the use of elastic ligation for hemostatic management. Histoacryl glue has become increasingly utilized in the acute management and secondary prophylaxis of gastric and ectopic varices in the general population.AimsEvidence surrounding the use of Histoacryl glue in pregnancy is limited. We report two cases of variceal bleeding during pregnancy managed successfully with glue.MethodsVarices were confirmed endoscopically. Images were obtained and reviewed. Aliquots of injected glue were recorded. Maternal and fetal outcomes were monitored during pregnancy and post-partum.Results Case 1: A 39-year-old G4P3L0, presented at 20 weeks gestation following several episodes of hematemesis. Urgent esophagogastroduodenoscopy (EGD) revealed hyperemia and portal hypertensive gastropathy in the fundus. A gastric varix with high-risk stigmata was injected with a total of 9mL of 50/50 Histoacryl/Lipodol and bleeding stopped. The patient returned to the hospital two weeks following discharge with melena. Repeat EGD showed mild portal hypertensive gastropathy with a clot at the site of the previous bleeding. No further intervention was required, and the patient delivered at 37 weeks via elective caesarian-section. Case 2: A 41-year-old G2P0L1 presented at 26 weeks gestation with severe anemia refractory to five units of blood transfusion. Urgent EGD showed a large gastric varix with recent stigmata of hemorrhage, but no active bleed. A total of 13 mL of 75/50 Histoacryl/Lipidol was injected into the varix with no further bleeding. She delivered by elective caesarian-section at 37 weeks gestation. Repeat EGD performed following delivery showed a larger varix with fresh clot at the inferior portion of the fundus. Due to concern for re-bleeding, a total of 4 mL of 50/50 Histoacryl/Lipidol was injected at the site. CT scan post-partum showed prominent gastric varices with glue visualized within the peripheral branches of the portal vein (Figure 1).ConclusionsOur cases highlight the successful management of gastric varices using Histoacryl glue in pregnancy. Risks associated with Histoacryl glue include glue embolization, local venous thrombosis, as well as extrusion of glue and ulceration. The general complication rate is quoted between 0.5%-5%. One of the two cases was associated with a maternal complication, with evidence of new portal vein thrombosis following injection. The safety of sclerotherapy in pregnancy with cyanoacrylate remains unclear, and further evaluation of the management of gastric varices in this unique population are required. Funding AgenciesNone