Massive Hematemesis Research Articles

Button battery removed from the stomach resulting in a missed aortoesophageal fistula \u2013 a multidisciplinary approach to rescuing a very young patient: a case report

BackgroundWhile coins are still the most common foreign bodies swallowed by children, ingestion of batteries has become more frequent among children due to the increasing access to electronic toys and devices.Coin battery ingestion is potentially life threatening for children. Aortoesophageal fistula is the most common cause of death in children who have swallowed coin batteries, and there have not been any reported survivors.Case presentationA 3-year-old Caucasian girl presented to the emergency room of a community hospital complaining of abdominal pain. An abdominal X-ray showed a coin lithium battery located in the fundus of her stomach, and she was transferred to a referral pediatric hospital. In the following hours she developed massive hematemesis and severe hypovolemic shock. An emergency laparotomy was attempted, and the coin battery was removed. The initial surgery and multiple blood transfusions did not, however, improve the clinical situation.She was then referred to our tertiary referral center, where a multidisciplinary team decided to attempt a combined angiographic and endoscopic approach to resolve a life-threatening aortoesophageal fistula. A 3-year follow-up was uneventful.ConclusionsCoin batteries are designed for a wide variety of small appliances, such as hearing aids, watches, remote controls, and toys.Although a change in the clinical approach to battery ingestion is needed to avoid misdiagnosis or delayed treatment, primary prevention of battery ingestion would be even more effective than an improved treatment.

The Bends in the Blood Vessels: Dieulafoyʼs Vascular Malformation

Dieulafoy's lesion (DL) also known as the caliber-persistent artery of the stomach, cirsoid aneurysm and submucosal arterial malformation, is a developmental malformation in the gastrointestinal (GI) tract characterized by a large submucosal tortuous artery. Here we present a case of Dieulafoy's lesion with massive hematemesis and despite aggressive resuscitative efforts, the patient could not be revived. A 76-year-old hypertensive male presented with an episode of syncope and bright red emesis. After admission, he had two more episodes of massive hematemesis. His vital signs quickly deteriorated with HR- 98/min, BP- 71/35 mm Hg. On examination, there was blood in the mouth, no epigastric tenderness. Labs revealed Hb- decreased from 12.7 to 8.5 gm/dl. Four endoclips were placed during an emergent esophagogastroduodenoscopy (EGD) which showed a non-bleeding DL. He was managed with normal saline, pantoprazole and two units of packed red blood cells (PRBC). He was stabilized and discharged after four days. He was admitted again a week later with massive volume hematemesis. His hemoglobin was 6.0 gm/dl, and he became hypotensive and was started on normal saline and norepinephrine. An emergent EGD was done which showed a large clot and blood in the stomach, endoclips could not be visualized and a 2 mm DL in the proximal body. 600 mL of blood was suctioned, 4 ml of epinephrine was injected, and the lesion was cauterized. Massive transfusion resuscitation protocol was initiated with nine units of fresh frozen plasma (FFP), nine units of PRBC, two units of platelets. Despite all the measures, he continued having multiple episodes of hematemesis An emergent celiac arteriogram for embolization of a bleeding branch of the left gastric artery was done, during which he had a cardiac arrest, and could not be successfully resuscitated. The management of acutely bleeding DLs can be challenging needing early detection, aggressive treatment and close follow up. Clinicians should be cautious and aware of rebleeding risks due to significant mortality. There are no clear guidelines for monitoring of post-endoclip interventions for DLs.2988_A Figure 1. Initial EGD2988_B Figure 2. EGD 1 Week Later2988_C Figure 3. Emergent IR Embolization

A Fatal Case of Occult Aortoenteric Fistula

Aortoenteric fistulae (AEF) are a rare but serious cause of massive hematemesis. Due to the substantial mortality risk, it is crucial that prompt diagnosis and early management are initiated. Multiple diagnostic modalities are considered valuable in the evaluation of AEF, including endoscopy and computed tomography (CT). We present a case that highlights the limitations of these common diagnostic procedures. We describe a 58-year-old male who has a history of hypertension, dyslipidemia, and severe peripheral vascular disease (PVD). He previously underwent an aortobifemoral bypass, axillofemoral bypass, and recent hospital admission for removal of an infected aortic graft. He presented to the emergency room following massive hematemesis, and underwent urgent esophagogastroduodenoscopy (EGD). This revealed a large clot in D3 with no evidence of active bleeding. Given his significant history of PVD, a CT angiogram was obtained. The radiologist reported no evidence of aortoenteric fistula. The patient was transferred to a monitored setting, and started on a pantoprazole infusion. The next morning the patient had significant hematemesis of approximately 2L of blood, requiring CPR and urgent transfusion. He was transferred to the intensive care unit for repeat EGD. The vascular surgeon and radiologist reviewed the case and felt that despite normal imaging, the patient should be transferred emergently to the operating room. Intraoperatively, a large aortoenteric fistula was noted in D3, which was surgically managed. The patient unfortunately passed away the next day. This case highlights that even with a high index of suspicion, AEF can be difficult to identify despite gold standard diagnostic testing. The delay in diagnosis is often fatal as AEF carry high a mortality risk1. The risk is estimated to be greater than 70% in secondary AEF2,3. Endoscopy has a low sensitivity for diagnosis of AEF4. High resolution CT remains the imaging modality of choice5,6, although it carries a broad sensitivity (40-90%) and specificity (33-100%)7. In our case, the fistula likely thrombosed spontaneously resulting in a normal CT angiogram, and then subsequently exsanguinated the next day. We also want to emphasize the substantial variability of endoscopic management in the treatment of non-bleeding clots, especially in patients with a history of aortic surgery. Further research is warranted to illuminate a more reliable diagnostic and therapeutic model in these patients.1994_A Figure 1. Large clot identified in D31994_B Figure 2. CTA demonstrating no AEF (no contrast leaking into D3), as well as evidence of axillofemoral bypass

Carnitine Palmitoyltransferase 1A Deficiency: A Rare Cause of Chronic Liver Disease with Rare Presentation

Carnitine Palmitoyltransferase 1A (CPT1A) deficiency is a very rare autosomal recessive disorder of fatty acid oxidation (FAO) which presents in children during concurrent febrile or gastrointestinal illness with hepatic encephalopathy (HE), hepatomegaly and rarely acute liver failure. Chronic liver damage is not reported in CPT1A deficiency. A 27-year-old female with history of CPT1A deficiency diagnosed in early childhood and chronic liver disease (CLD) complicated by thrombocytopenia, splenomegaly with model for end stage liver disease (MELD) score of 12; presented to emergency department with massive hematemesis. Vitals signs were stable. Physical exam was unremarkable except splenomegaly. Labs were significant for hemoglobin 7 g/dL, platelets 45 uL, electrolytes and liver enzymes unremarkable, INR 1.42, prothrombin time 17.2 sec, and total bilirubin 1.6 mg/dL. Computed tomography abdomen revealed prominent para-esophageal and peri-splenic varices, marked splenomegaly and fatty infiltration of liver (Image 1). The patient was started on IV fluids, ceftriaxone and octreotide. EGD revealed four columns of Grade IV esophageal varices (EV) that required 10 variceal bands (Image 2). Hospital course was further complicated by HE, thought to be multifactorial i.e. worsening liver function, poor oral intake and underlying defect in FAO. The patient was treated with lactulose, rifaximin with minimum improvement. Liver function continued to worsen with bilirubin 5.2 mg/dL, INR of 1.8 and MELD score of 24. A diagnosis of ACLF was made as her liver function 3 months prior to this admission was with in normal limits. She was high risk for re-bleeding and not a candidate for TIPS, so emergently transferred to a liver transplant center. CPT1A deficiency is a rare disorder with 60 cases reported so far. Either CLD or presentation as ACLF has not been reported in CPT1A deficiency. Our patient did not have history alcohol use or risk factors for NAFLD and Hepatitis B and C, hemochromatosis, Wilson's disease, autoimmune hepatitis were ruled out.2293_A Figure 1 No Caption available.2293_B Figure 2 No Caption available.

Dueling with Fire: A Case Series of Dieulafoyʼs Lesions

Dieulafoy's lesion is a rare cause of gastrointestinal (GI) bleeding that is often misdiagnosed or missed, accounting for 1-5.8% of cases of acute GI bleeding, 1.9% of all endoscopies for acute GI bleeding and 0.09% of all colonoscopies performed for lower GI bleeding. It is thought to affect already hospitalized or otherwise incapacitated patients, thus it is essential to understand the clinical presentation and approach to care. Three female patients aged 56, 64 and 75 presented with melena and symptomatic anemia with hemoglobin levels ranging from 4.7 to 8.4. Two of the patients had coffee ground emesis prior to admission. One patient had a history of taking NSAIDs, two taking daily aspirin and one patient on warfarin for a mechanical valve. All three patients underwent an EGD. All patients had a normal esophagus; the first patient had a bleeding Dieulafoy's lesion in the lesser curvature of the antrum, the second in the greater curvature of the antrum and the third with a lesion in the second portion of the duodenum. Lesions were treated by regional hemostasis with epinephrine injections and thermal hemostasis via heat probe in two of the three cases, and mechanical hemostasis was achieved with haemoclips in two of the three patients. Repeat melena occurred in two patients and was thought to be due to inadequate hemostasis or re-bleeding in the duodenum. All patients were discharged on a PPI. Dieulafoy's lesion is a rare cause of GI bleeding due to histologically normal but tortuous and dilated submucosal vessels. The most common location is in the stomach followed by the duodenum, with duodenal and jejunal lesions making up 15% and 1% of all lesions respectively. Patients present with painless and often massive periodic hematemesis, melena, or hematochezia. Risk factors include a history of NSAIDs, aspirin, or warfarin use. Diagnosis can be made most often by direct visualization via endoscopy. Treatment consists of hemostasis achieved thermally, regionally with local epinephrine injections, and sclerotherapy, or mechanically with banding or haemoclips. Literature suggests that mechanical haemostatis methods are most effective and successful. For those unresponsive to treatment, angiography with embolization has been used. If both fail, surgery is advised if no source can be defined and active bleeding continues. Prognosis has improved significantly in recent years, from 80% mortality down to 8.5%.

Massive Gastric Variceal Hemorrhage Due to Splenic Vein Thrombosis: A Rare Initial Presentation of Asymptomatic Metastatic Pancreatic Adenocarcinoma

Isolated sinistral portal hypertension (SPH) is extremely rare, representing less than 5% of all portal hypertension cases [1]. Rare cases of gastric varices can cases occur due to non-cirrhotic splenic venous thrombosis causing SPH. Here, we present massive gastric variceal bleeding from splenic vein thrombosis as the initial presentation of pancreatic adenocarcinoma. A 71-year old man presented to the emergency department with acute onset massive hematemesis and epigastric pain. He had tenderness in the epigastric and left upper quadrant without peritoneal signs. Hemoglobin was decreased at 8.3 g/d from baseline 12. Total bilirubin and liver function tests were within normal limits. Contrast enhanced CT showed splenic vein thrombosis (Figure 1A), gastric varices (Figure 1B) with active hemorrhage noted, and a 5 cm mass in the pancreatic tail (Figure 1C). No changes of cirrhosis were noted in the liver. The patient underwent successful splenic artery embolization (Figure 2). Diagnosis of metastatic pancreatic adenocarcinoma was confirmed with peritoneal biopsy. Gastric variceal bleeding as the initial presentation of pancreatic adenocarcinoma is incredibly unusual. Splenic vein thrombosis causes SPH and formation of collateral pathways to shunt blood around the occluded splenic vein, increasing pressure within the submucosal veins of the gastric fundus forming varices. Splenic vein thrombosis arising from pancreatic cancer carcinoma represents a rare occurrence. One study showed only 49% of 209 patients were correctly diagnosed with SPH after the first episode of bleeding with a median delay of 11 months[2]. Splenectomy is the standard treatment for splenic vein thrombosis, with splenic artery embolization reserved for patients who are poor surgical candidates with metastatic disease. Massive gastricvariceal hemorrhage due to non-cirrhotic portal hypertension from splenic vein thrombosis as the initial presentation of pancreatic adenocarcinoma is a rare occurrence. Recognizing rare causes of gastric varices such as SPH due to splenic vein thrombosis is important for early diagnosis of possible pancreatic adenocarcinoma.1357.tif Figure 1: Figures for Case Report

Gastric Ulcer and Perforation Due to Mucormycosis in an Immunocompetent Patient

Mucormycosis is a rare fungal disease with high mortality and morbidity in immunocompromised patients that typically involves the nasal sinuses, orbit and brain. In recent years increased gastrointestinal involvement of mucormycosis has been reported. Here we present a case of gastric ulcer and perforation due to gastrointestinal mucormycosis (GIM) in an immunocompetent individual. A 48-year-old healthy male was brought to the emergency department after a transpelvic gunshot wound. Patient was in hypotensive shock upon arrival and was immediately taken to the operative room (OR) for further evaluation. He sustained rectal and small bowel injury for which he underwent multiple bowel resections but his hospital course was complicated by multiple anastomotic perforations. Hepatic and mesenteric biopsies showed mucormycosis and he was started on liposomal amphotericin B. Subsequently, he developed coffee ground emesis and an EGD showed a large gastric ulcer in the proximal stomach. Biopsies taken from the ulcer showed fungal organism consistent with mucormycosis. Two days later, he developed massive hematemesis and frank blood was seen in his wound vacuum assisted closure and multiple surgical drains. He became hemodynamically unstable and was taken back to the OR for emergent laparotomy where he was noted to have a 8 x 4 cm area of perforated ulcer in the lesser curvature of the stomach. He succumbed to his injuries in the OR. GIM accounts for only 7% of all mucormycosis cases but is associated with a high mortality rate of 85%. Traditional risk factors include immunodeficiency states such as poorly controlled diabetes mellitus, bone marrow or solid organ transplantation, neutropenia, glucocorticoid use and HIV. The stomach is the most common site of GIM followed by the colon and ileum. The fungus has a tendency to invade blood vessels causing disseminated infection. Per our literature search, in the past 5 years, there appears to be an increase in reported cases of GIM after penetrating traumas such as gunshot wound and car accidents regardless the immunocompetent states of the patients. Polyene antifungal drugs such as liposomal amphotericin B is the recommended first-line therapy. Early diagnosis, timely initiation of antifungal treatment and surgical debridement of infected tissues are the keys to improve a patient's survival against this highly fatal opportunistic infection.1970_A Figure 1. EGD demonstrated a large ulcer in the proximal stomach with biopsy showing mucormycosis.1970_B Figure 2. Gastric ulcer, H+E stain, low-magnification, showing necrotic exudate containing fungal aseptate hyphae morphologically consistent with mucormycosis.1970_C Figure 3. Gastric ulcer, H+E stain, high-magnification, showing mucormycosis.

PS01.037: APPLYING THORACIC ENDOVASCULAR AORTIC REPAIR (TEVAR) AND SURGICAL RESECTION WITH RECONSTRUCTION OF ESOPHAGUS IN MANAGING OF AORTA-ESOPHAGEAL FISTULA

Abstract Background Aorta-esophageal fistula (AEF) is very dangerous with high mortality. Treatment is difficult because of hemorrhagic shock in acute stage and infection in sub-acute stage. We develop a method to manage both perforations from aorta and esophagus successfully. Methods A 56 male patient had fish bone incarcerated in thoracic esophagus. Two months after this accident, intermittent massive hematemesis occurred. The esophagoscopy displayed active bleeding and AEF was diagnosed by computed tomography angiography (CTA). TEVAR is applied immediately and stopped bleeding successfully. Fever with sepsis and mediastinitis was happened after oral intake. The perforated esophagus was removed by wire-stripper through neck and abdomen incisions and reconstructed with gastric tube via retro-sternal route. Results After subtotal esophagectomy with gastric tube reconstruction, the ventilator is weaned and endotracheal tube was removed. No leakage from anastomosis between cervical esophagus and gastric tube. Patient could swallow regular diet smoothly. No further post-operative complication was happened after follow up two years. Conclusion TEVAR is the first step in managing AEF in acute stage to prevent hemorrhagic shock. Although esophageal perforation could be managed with esophageal stent, the marginal ulcer with pain and bleeding may cause other side effects. Esophageal stent is also another contra-indication applied in benign disease. Subtotal esophagectomy with wire-stripper and reconstruction with gastric tube could provide definite treatment for this esophageal perforation. Disclosure All authors have declared no conflicts of interest.

When the Diagnosis is a Victim of the Circumstances.

IntroductionHaemoptysis is a common symptom which can sometimes mimic gastrointestinal bleeding.Case descriptionWe describe the case of a 31-year-old man who presented to the emergency department after an episode of sudden nausea and presumed massive haematemesis. The situation was interpreted as gastrointestinal bleeding but clinical evolution and greater attention to the anamnesis resulted in a diagnosis of pulmonary tuberculosis and the provision of appropriate care.DiscussionThis report emphasizes the difficulty of differentiating between haemoptysis and haematemesis and the importance of a careful anamnesis and attention to all clinical circumstances for an accurate diagnosis.LEARNING POINTSHaematemesis and haemoptysis are not always distinguished from each other when a patient’s history is being collected.Despite being a rare manifestation of tuberculosis, in the correct epidemiological context, haemoptysis should raise the suspicion of pulmonary tuberculosis.The clinical setting and the need for immediate care should not limit clinical investigation or the differential diagnosis.

Gastric Dieulafoy lesion: a rare cause of massive haematemesis in an elderly woman

A 78-year-old woman presented to her local accident and emergency department by ambulance, having collapsed following several episodes of voluminous fresh haematemesis with melaena. The patient had extensive medical comorbidities,...

Eight cases of Percutaneous Endoscopic Gastrostomy (PEG) in patients taking oral anticoagulants

Patients who undergo percutaneous endoscopic gastrostomy (PEG) placement are often on antiplatelet therapy. There is a potential risk of infarction if these medications are discontinued.The guidelines of the Japan Gastroenterological Endoscopy Society, classify PEG as an operation associated with a high risk of bleeding; however, it is known that surgery can be performed without interruption when patients are treated with low-dose aspirin alone. Nevertheless, we experienced the case of severe bleeding at the incision site, which was accompanied by massive hematemesis and hemorrhagic shock the night after PEG using the modified introducer method in an 87-year-old male patient. The patient was being treated with Bayer aspirin (100 mg/day, oral). The patient's platelet count, PT, and APTT were within the normal levels. Thus, we decided to investigate the pull method as the effective method for pressure hemostasis comparing with the modified introducer method, to reduce the risks associated with bleeding after surgery when patients are being treated with antiplatelet drugs.PEG was performed by the pull method on eight patients who were being treated with oral antiplatelet drugs (including four patients receiving dual antiplatelet therapy [DAPT]). All patients had previously suffered strokes, and they all presented with normal platelet counts, PT, and APTT values.Only slight bleeding was observed in one out of eight patients (bleeding had stopped by the following day using an alginate patch on the abdominal wall at the incision site, along with direct pressure using a stationary plate). None of the patients showed infection at the incision site.Although the study population was small, the present study showed that PEG using the pull method is safe while patients are being treated with oral antiplatelet drugs.

Post traumatic pseudo-aneurysm of carotid artery presenting as massive oropharyngeal bleed with shock and hemiparesis

Background : Aneurysm in the extracranial segment of internal carotid artery is extremely rare in the pediatric age group. They can assume large size and have catastrophic complications of thromboembolism and hemorrhage. We present a 12 year old child with recurrent oropharyngeal hemorrhage leading to massive hematemesis and shock. A distal embolism causing malignant ipsilateral cerebral infarct further complicated the management options. He was treated with an emergency placement of stent within the artery to exclude the flow in the pseudo aneurysm. A right decompressive craniectomy was performed to control the raised intra-cranial pressure secondary to malignant cerebral infarction. The tentorial herniation was relieved in the follow up CT scan of the brain and the child made progressive recovery with residual paralysis of the left side. Aim of our case report is to increase awareness and inclusion of this rare pathology in the differential diagnosis of oropharyngeal hemorrhage which would facilitate the early diagnosis and prevent devastating complications.

Esophageal submucosal hematoma developed after endovascular surgery for unruptured cerebral aneurysm under general anesthesia: a case report

BackgroundEsophageal submucosal hematoma is a rare complication after endovascular surgery. We report a case of an esophageal submucosal hematoma which may have been caused by rigorous cough during extubation.Case presentationA 75-year-old woman underwent endovascular treatment for unruptured cerebral aneurysm under general anesthesia. The patient received aspirin and clopidogrel before surgery and heparin during surgery. Activated clotting time was 316 s at the end of surgery. Protamine was not administered and continuous infusion of argatroban was started after surgery. She had a rigorous cough during removal of the tracheal tube and reported retrosternal discomfort postoperatively. She developed hemorrhagic shock after massive hematemesis. A diagnosis of esophageal submucosal hematoma was made by endoscopic examination and computed tomography. Hemostasis was achieved by compression with a Sengstaken-Blakemore tube and endoscopic cauterization. Blood pressure was recovered by blood transfusion. Endoscopic examination performed 7 days after surgery showed that esophageal submucosal hematoma had almost disappeared and slough had adhered to the mucosal laceration. The patient showed good recovery and was discharged 21 days after surgery.ConclusionsCareful extubation and postoperative observation are required in patients receiving antiplatelet and anticoagulant therapy.

Young Male Presenting With Massive Hematemesis … Getting to the GIST of It

A 36-year old white male with no prior medical history presented with massive hematemesis and melena for one day. He endorsed lightheadedness and fatigue. Emergent esophagogastroduodenoscopy revealed a large 3 cm subepithelial, ulcerated bleeding mass in the second portion of the duodenum, distal to the major papilla (Image 1, 2). Hemostatic clipping was unsuccessful, causing more bleeding. Despite subsequent epinephrine injection, the mass continued to ooze at the end of procedure (Image 3). Interventional radiology performed a visceral arteriogram which showed no evidence of contrast extravasation; embolization was not attempted. Due to ongoing bleeding, urgent surgery with duodenotomy and excision of the mass was performed. Pathology revealed gastrointestinal stromal tumor (GIST) with zero mitoses, and reactive DOG1 and CD117 stains. He was discharged on post-operative day 5 with plans for outpatient oncology follow up. GISTs represent a rare cause of upper GI bleeds. The yearly incidence of GIST is 0.78/100,000, with only 7.5% occurring in the duodenum. GISTs are male predominate, more common in black patients, and have an average age of discovery of 63. Duodenal GISTs typically present with GI bleeding, abdominal pain, or discomfort, and are most frequently found in the second portion of duodenum. Treatment of localized duodenal GISTs without prior analysis of tissue (thus excluding from imatinib pre-treatment) is complete surgical resection. In low risk patients such as ours (no mitotic cells), post-operative imatinib is not required, and the patients only require post-treatment surveillance. Current National Comprehensive Cancer Network recommendations are a CT scan every 3-6 months for 3-5 years, and then annually. Studies have shown only a high mitotic rate as a predictive factor for mortality, as opposed to tumor size or grade. The rate of recurrence free survival is reported as 95% at one year, and 86.7% by 3 years. Even with its low malignant potential, patients with duodenal GISTs should maintain long-term follow up to avoid late relapse.Figure: Duodenal GIST.Figure: Bleeding Duodenal GIST.Figure: Continuous Bleeding of Duodenal GIST.

A Rare Case of Refractory Hematemesis Caused by a Gastric Lipoma

Lipomas in the stomach are a rare finding representing less than 1% of all stomach tumors. These are usually asymptomatic and rarely cause significant bleeding or obstructive symptoms. We report an unusual case of a gastric lipoma presenting as massive refractory hematemesis. A 76 year old female taking NSAIDs for a recent hip fracture repair presented with multiple episodes of large volume hematemesis leading to weakness and fatigue. She was initially unstable with hypotension and tachycardia. Her abdominal examination was benign. The patient was intubated for airway protection and resuscitated with blood and intravenous fluids. She had no prior history of gastrointestinal bleeding. The patient underwent an EGD which showed a 3 cm polypoid mass in the posterior gastric body that was actively bleeding. This was cauterized and injected with epinephrine but the patient became hypotensive requiring the case to be stopped. Another EGD was attempted after the patient was transferred to the ICU for stabilization. Endoscopy again showed active bleeding at the mass site and several endoclips were applied and ethanolamine injected for hemostasis. However, bleeding continued with a drop in her hemoglobin and hematocrit to a nadir of 5.9/16.9. Interventional radiology was consulted for embolization. Angiography indicated the bleeding was localized to a branch of the left gastric artery but the vessel could not be accessed due to its tortuosity. The patient was subsequently taken to the operating room given her continued hematemesis. She underwent an open partial gastrectomy removing the stomach body and antrum with retrocolic gastrojejunostomy. Post-surgery, the patient was stable with cessation of bleeding. Anatomical specimens collected from the partial gastrectomy showed a submucosal lipoma measuring 4.5 cm in its greatest dimension with fat necrosis extending into the submucosa and muscularis propria layers. Gastric lipomas are benign tumors of adipose tissue arising from the submucosal layer and rarely present with bleeding or obstructive symptoms. In cases with bleeding the blood loss is usually slow and chronic. Only a few cases of massive bleeding have previously been reported. Endoscopic techniques such as submucosal dissection or unroofing have been employed successfully for treatment of smaller lipomas or those with relatively mild symptoms. However, in the case of larger tumors and those with large volume bleeding surgical resection is usually required.Figure: Initial EGD showing an approximately 3 cm polypoid mass in the posterior gastric body.Figure: The mass seen with EGD shows evidence of active bleeding and an ulcerated tip.Figure: Endoscopic measures failed to achieve hemostasis at the lipoma site.

Case Report of Acute Liver Failure Secondary to Hemophagocytic Lymphohistiocytosis

Hemophagocytic lymphohistiocytosis (HLH), an aggressive and life threatening syndrome of excessive immune activation, most commonly affects infants Symbol < 18 months old, but can occur in older children and adults. An extremely rare case is reported of HLH presenting as acute liver failure in an adult. A 47-year-old Caucasian man with a past medical history of diabetes type II was treated with a 10 day course of trimethoprim-sulfamethoxazole for an upper respiratory infection three weeks prior to admission, and developed a pruritic rash several days later. He then presented with fatigue, pyrexia, and profound jaundice. Physical examination on admission revealed temperature=103.1 0C, blood pressure=89/48 mmHg, profound jaundice, and no hepatomegaly or stigmata of chronic liver disease. Laboratory examination revealed severe neutropenia (absolute neutrophil count=100 cells/mm3), leukocyte count=700 cells/mm3, and hemoglobin=8.6 mg/dl. The sodium=116 mmol/L and creatinine=1.67 mg/dl. Total bilirubin=45.1 mg/dl, direct bilirubin=26.4 mg/dl, alkaline phosphatase=490 U/L, AST=70 U/L, ALT=167 U/L, GGT=730 U/L, albumin=2.4 g/dl, INR=1.9, and ferritin=3100 ng/ml. The acetaminophen level was normal and an acute viral hepatitis panel was negative. Abdominal ultrasound and CT scan revealed normal hepatobiliary findings. MRCP revealed a normal biliary tree, multiple small pancreatic cysts up to 11 mm in diameter, and mild diffuse iron deposition in liver and spleen. The patient was treated empirically with doxycycline for possible leptospirosis because he works as a sewer inspector. He was treated with IV aztreonam and vancomycin after Pseudomonas and group A streptococcus were isolated from blood cultures. Serum IgG level was normal. Anti-smooth muscle antibody, and antimitochondrial antibody were absent in serum. Leptospiral antibodies were negative. Genotyping was negative for C282Y, and was heterozygous for H63D mutation for hemochromatosis. Pathologic examination of a bone marrow biopsy revealed HLH. CD25 and IL-2 receptor levels were elevated, consistent with HLH. Patient was treated with prednisone 100 mg daily. He was not a candidate for etoposide (VP16) because of his profoundly elevated bilirubin and transaminase levels. He underwent transjugular liver biopsy which revealed centrilobular hepatocellular necrosis. He developed massive hematemesis, EGD revealed deep elongated lower esophageal ulcers and esophagitis, typical for CMV/viral esophagitis. He became hypotensive, was intubated, and developed disseminated intravascular coagulopathy with intra-abdominal bleeding and perihepatic hematoma. He was transfused multiple blood products and underwent two arteriograms with embolizations of two major hepatic arteries that successfully controlled the hemorrhage. He was treated with micafungin for candidemia, and ganciclovir for possible CMV esophagitis. Repeat viral cultures and serologies were negative for CMV, VZV, EBV, HSV, and HIV. Hence ganciclovir was discontinued. During the ensuing 10 days his ferritin became >33000 ng/ml, but the bilirubin and transaminase levels significantly declined. He became more clinically stable. A case of acute liver failure is reported secondary to HLH, a rare syndrome in adults. Although DILI from Bactrim was a confounding factor, the prompt diagnosis and initiation of treatment with corticosteroids was crucial. He was unable to receive chemotherapy with etoposide or cyclosporine because he had elevated bilirubin and transaminase levels. HLH can occur as a familial or sporadic disorder, which can be triggered by various events that disrupt immune homeostasis, such as infection. Given the rarity of this syndrome, prompt diagnosis and treatment is crucial for patient survival.SymbolFigure: Medium power photomicrograph of Diff-Quik stain of bone marrow smear showing foamy macrophages engulfing mature and precursor erythrocytes (arrow).Figure: High power photomicrograph of Diff-Quik stain of bone marrow smear showing a foamy macrophage engulfing precursor erythrocytes (arrow).Figure: Medium power photomicrograph of liver showing centrilobular hepatocellular necrosis with cholestasis (asterisk).

Clinical Vignettes/Case Reports - Biliary/Pancreas.

The differential diagnosis for patients presenting with concurrent cholecystitis and hematemesis is limited and includes cystic artery pseudoaneurysm and fistula between the cystic or hepatic arteries and gallbladder. Additionally, duodenal ulcer disease has been reported to cause both gastrointestinal bleeding and bilioenteric fistulas, though few cases have been reported of cholecystoduodenal fistula presenting with concurrent hematemesis, jaundice, and cholecystitis. An 84-year-old woman with diabetes, hyperlipidemia, and back pain on chronic NSAID therapy presented with hematemesis after a two-day history of post-prandial epigastric pain, vomiting, and fevers. Exam revealed jaundice and tenderness with guarding in the right upper quadrant of the abdomen. Shortly after presenting, she developed massive hematemesis and was intubated. Initial labs revealed a leukocytosis of 18, hemoglobin 6.9, AST 89, ALT 54, total bilirubin 5.8 (direct 4.9), and alkaline phosphatase 211. A CT scan revealed cholecystitis as well as gas in the gallbladder, cholelithiasis, and mild intrahepatic biliary dilatation. Subsequent angiography was negative for active extravasation, pseudoaneurysm, and arterial abnormalities. Upper endoscopy revealed a 15mm ulcer in the duodenal bulb with overlying clot. Removal of this clot revealed a defect, and injection of contrast under fluoroscopy demonstrated that the ulcer base extended into the gallbladder, confirming a cholecystoduodenal fistula. ERCP was performed revealing filling defects in the lower third of the common bile duct, and a biliary stent was placed. She improved clinically, with plans for future cholecystectomy and fistula repair. Amongst bilioenteric fistulas, cholecystoduodenal fistulas are most common, with choledochoduodenal fistulas comprising only one-fourth of cases. Up to 90% of bilioenteric fistulas result from cholelithiasis, while only 5% result from duodenal ulcer disease. The most common presentation is with cholangitis, though it occurs in less than 10% of patients; presentation with obstructive jaundice or gastrointestinal bleeding is exceedingly rare. Pneumobilia on imaging is a hint as to the diagnosis and is seen in 14-22% of cases. It is vital for clinicians to consider this diagnosis when such clinical signs are present, as complications from delay in diagnosis can be serious, and management differs from other etiologies of upper gastrointestinal bleeding and gallbladder disease.Figure: CT scan of the abdomen demonstrating gas in the gallbladder.Figure: Endoscopic appearance of the cholecystoduodenal fistula tract.Figure: ERCP revealing filling defects in the common bile duct.

Management of aorto-esophageal fistula secondary after thoracic endovascular aortic repair: a review of literature

Aorto-esophageal fistula (AEF) is a rare and lethal entity, and the difficulty of making diagnosis of AEF is well-known. As promising results in the short-term effectiveness of thoracic endovascular aortic repair (TEVAR) promote its usage, the occurrence of AEF after TEVAR (post-TEVAR AEF) increases as one of the major complications. Therefore, we provide a review concerning the management strategy of post-TEVAR AEF. Although its representative symptom was reported as the triad of mid-thoracic pain and sentinel hematemesis followed by massive hematemesis, the symptom-free interval between sentinel hemorrhage and massive exsanguination is unpredictable. However, the physiological condition represents a surgical contraindication. Accordingly, early diagnosis is important, but either CT or esophago-gastro-duodenoscopy rarely depicts a typical image. The formation of post-TEVAR AEF might be associated with the infection of micro-organisms, which is uncontrollable with anti-biotic administration. The current first-line strategy is combination therapy as follows, (1) to control bleeding by TEVAR in the urgent phase, and (2) radical debridement and aortic/esophageal re-construction in the semi-urgent phase. In view of the high mortality and morbidity rate, it is proposed that the choice in treatment strategies might be affected by patient`s condition, size of the wall defects and the etiology of AEF. Practically, we should keep in mind the importance of making an early diagnosis and, once a suspicious symptom has occurred in a patient with a history of TEVAR, the existence of post-TEVAR AEF should be suspected. A prospective registry together with more developed technologies will be needed to establish a future strategy.

An unusual cause of massive hematemesis after treatment with terlipressin

An unusual cause of massive hematemesis after treatment with terlipressin

Management of Percutaneous Endoscopic Gastrostomy Site Gastric Ulcer in a Patient with an Esophageal Stricture and Hiatus Hernia

Percutaneous endoscopic gastrostomy (PEG) is commonly performed for feeding difficulties, in patients suffering from complications of nasopharyngeal carcinoma and its treatment, namely radiotherapy and surgery. This case report describes the challenges in hemostasis and subsequent re-establishment of enteral access for feeding, in an elderly patient with a history of NPC, treated surgically, followed by radiotherapy, who presented with massive hematemesis following reinsertion of her PEG shortly after an accidental dislodgement. Her previous nasopharyngectomy, wide field radiation therapy, and radical neck dissection precluded nasogastric tube feeding, and the presence of a large hiatus hernia made reinsertion of a new PEG technically challenging. This case highlights the methods used to overcome the above challenges.