Bleeding Esophageal Ulcers Research Articles

Novel hemostatic gel used in bleeding esophageal ulcer to promote mucosal healing

Intraprocedural bleeding during endoscopic intervention, gastrointestinal bleeding, or bleeding tumors can be treated with many different modalities such as heat therapy, endoclipping, or embolization. One alternative option that has been proven in literature to be safe and effective is PuraStat, which is a novel self-assembling peptide used for hemostasis during endoscopic procedures such as polypectomies, submucosal dissection, and mucosal resection. This matrix-forming gel can be easily and safely applied to prevent delayed bleeding, accomplish hemostasis and effectively promote mucosal healing. Our case represents a patient who presented with active upper gastrointestinal bleeding that achieved hemostasis and wound healing with the use of PuraStat.

S2306 Massively Bleeding Esophageal Ulcer Treated With an Over-the-Scope Clip

S2306 Massively Bleeding Esophageal Ulcer Treated With an Over-the-Scope Clip

2024 Novel Approach for Management of Stomal Variceal Bleed

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 As the scope was withdrawn, an osteal varix was noted and due to the manipulation of the scope, the varix started squirting blood.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.

1818 Acute Hematemesis From Kayexalate-Induced Esophageal Ulcer

INTRODUCTION: Hyperkalemia is one of the most common electrolyte abnormalities encountered in clinical practice. The treatment of hyperkalemia includes removal of the unwanted potassium from the body by cation exchange resins. e. g sodium polystyrene sulfonate (Kayexalate). The serious gastrointestinal side effects of sodium polystyrene sulfonate (SPS) have been reported with or without concomitant use of sorbitol including colonic perforation. The U.S food and drug administration (FDA) has issued a warning to avoid kayexalate administration with sorbitol. We present an individual with acute hematemesis due to bleeding esophageal ulcer immediately after treatment with kayexalate therapy. CASE DESCRIPTION/METHODS: 63-year-old Hispanic man who was recalled to ED by renal team due to elevated potassium level of 6.6mg/dl. On arrival to ED his vitals were WNL. His physical examination includes distended non- tender abdomen and 2+ pitting edema of lower extremities. Rest of physical was within normal limits. His comorbid conditions include alcohol related decompensated cirrhosis, nephrotic syndrome and small nonbleeding esophageal varices seen on endoscopy performed 3 weeks before current illness. He was treated with oral kayexalate 30mg along with intravenous (I/V) dextrose, calcium gluconate and insulin. 45 minutes after oral SPS therapy patient developed large episode of hematemesis. He was intubated for airway protection. An emergent endoscopy was performed which showed multiple round, sharply demarcated, esophageal ulcers with mucosal oozing (Figure 1A) and small non bleeding esophageal varices were again seen. The two of the esophageal ulcers were actively oozing, to achieve the hemostasis, two hemostatic clips were deployed with cessation of bleeding (Figure 1B). The esophageal ulcer biopsies were not taken due to concern of causing iatrogenic bleeding in the presence of coagulopathy. He had no evidence recurrent gastrointestinal bleeding. DISCUSSION: Kayexalate induced colonic ulcer, colonic ischemia and colonic necrosis has been repeatedly described in the literature. The kayexalate induced esophageal ulcer with significant hematemesis is rarely reported. Although the exact mechanism by which kayexalate causes esophageal ulcer to be elucidated but it is worthwhile to be vigilant about its potential adverse effects. Our case highlights the rare but certainly the life threatening complication of kayexalate therapy.

Variceal band ligation in the prevention of variceal bleeding: a multicenter trial.

Background/Aim:Variceal bleeding is a life-threatening complication of portal hypertension with a high probability of recurrence. Treatment to prevent first bleeding or rebleeding is mandatory. The study has been aimed at investigating the effectiveness of endoscopic band ligation in preventing upper gastrointestinal bleeding in patients with portal hypertension and to establish the clinical outcome of patients.Patients and Methods:We analyzed in a multicenter trial, the efficacy and side effects of endoscopic band ligation for the primary and secondary prophylaxis of esophageal variceal bleeding. We assigned 603 patients with portal hypertension who were hospitalized to receive treatment with endoscopic ligation. Sessions of ligation were repeated every two to three weeks until the varices were eradicated. The primary end point was recurrent bleeding.Results:The median follow-up period was 32 months. A total of 126 patients had recurrent bleeding. All episodes were related to portal hypertension and 79 to recurrent variceal bleeding. There were major complications in 51 patients (30 had bleeding esophageal ulcers). Seventy-eight patients died, 26 deaths were related to variceal bleeding and 1 to bleeding esophageal ulcers.Conclusions:A great improvement in the prevention of variceal bleeding has emerged over the last years. However, further therapeutic options that combine higher efficacy, better tolerance and fewer side effects are needed.

Liver Transplantation for Children: Red Cross Children's Hospital Experience

Background The liver transplant program for infants and children at the Red Cross Children's Memorial Hospital is the only established pediatric service in sub-Saharan Africa. Since 1985, 250 infants and children have been assessed and 155 accepted for transplantation. Methods Since 1987, 76 children (range 6 months to 14 years) have had 79 liver transplants, with biliary atresia being the most frequent diagnosis. The indications for transplantation include biliary atresia (n = 44), metabolic (n = 7), fulminant hepatic failure (n = 10), redo transplants (n = 3), and other (n = 15). Three combined liver/kidney transplants have been performed. Forty-nine were reduced-size transplants with donor: recipient weight ratios ranging from 2:1 to 11:1, and 29 children weighed < 10 kg. Results Fifty-six (74%) patients survived 3 months to 12 years posttransplant. Cumulative 1- and 5-year patient survival data are 79% and 70%, respectively. However, with the introduction of prophylactic intravenous gancyclovir and the exclusion of hepatitis B virus (HBV) IgG core Ab-positive donors, the projected 5-year pediatric survival has been >80%. Early (<1 month) post–liver-transplant mortality was low, but included: primary malfunction (n = 1); inferior vena cava thrombosis (n = 1); bleeding esophageal ulcer (n = 1); and sepsis (n = 1). Late morbidity and mortality was mainly due to infections: de novo hepatitis B (5 patients, 2 deaths); Epstein–Barr virus (EBV)-related posttransplantation lymphoproliferative disease (12 patients, 7 deaths); and cytomegalovirus disease (10 patients, 5 deaths). Tuberculosis (TB) treatment in three patients was complicated by chronic rejection (n = 1) and TB drug-induced subfulminant liver failure (n = 1). Conclusions Despite limited resources, a successful pediatric program has been established with good patient and graft survival figures and excellent quality of life. Shortage of donors due to HBV and human immunodeficiency virus (HIV) leads to significant waiting list mortality and infrequent transplantation.

肝細胞癌の縦隔リンパ節転移巣が食道内に穿破した1例

肝細胞癌の縦隔リンパ節転移巣が食道内に穿破した1例

Bleeding esophageal ulcers caused by NSAIDs

Bleeding esophageal ulcers caused by NSAIDs

Nsaid-induced bleeding esophageal ulcer: Report of six cases

Nsaid-induced bleeding esophageal ulcer: Report of six cases

Does Prophylactic Endoscopic Sclerotherapy Prevent Variceal Bleeding Or Not? A Question of Experimental Design

From January 1985 through July 1987, adult patients accepted for liver transplantation with large esophageal varices were enrolled in a study evaluating the use of prophylactic vs emergency sclerotherapy. Six hundred forty-eight subjects received prophylactic scleratherapy, and 172 received emergent sclerotherapy. Esophageal stricture formation was increased 12.9-fold (P ＜ 0.001), esophageal perforation 6.4-fold (P ＜ 0.005), and postsclerotherapy bleeding esophageal ulcers 3.7-fold (P ＜ 0.001) in those receiving emergency sclerotherapy as opposed to prophylactic sclerotherapy. These differences were even greater if the number of sclerotherapy sessions rather than the number of patients was used as the denominator for the comparisons. In total, 19.6% of emergency sclerotherapy cases were associated with an untoward outcome of sclerotherapy; only 1.9% of cases receiving prophylactic sclerotherapy experienced an untoward outcome (P ＜ 0.001). These data demonstrate that leinergency sclerotherapy is associated with a greater prevalence of complications and support earlier studies that show that sclerotherapy prevents variceai bleeding over the short term. The data also suggest that when applied to patients with large varices awaiting orthotopic liver transplantation, it enhances the chance of a patient surviving to be transplanted by preventing a variceal bleed and the spiral of liver failure and death that frequently follows an episode of acute variceal bleeding.

Prophylactic versus emergency sclerotherapy of large esophageal varices prior to liver transplantation

From January 1985 through July 1987, adult patients accepted for liver transplantation with large esophageal varices were enrolled in a study evaluating the use of prophylactic vs emergency sclerotherapy. Six hundred forty-eight subjects received prophylactic sclerotherapy, and 172 received emergent sclerotherapy. Esophageal stricture formation was increased 12.9-fold (P < 0.001), esophageal perforation 6.4-fold (P < 0.005), and postsclerotherapy bleeding esophageal ulcers 3.7-fold (P < 0.001) in those receiving emergency sclerotherapy as opposed to prophylactic sclerotherapy. These differences were even greater if the number of sclerotherapy sessions rather than the number of patients was used as the denominator for the comparisons. In total, 19.6% of emergency sclerotherapy cases were associated with an untoward outcome of sclerotherapy; only 1.9% of cases receiving prophylactic sclerotherapy experienced an untoward outcome (P < 0.001). These data demonstrate that emergency sclerotherapy is associated with a greater prevalence of complications and support earlier studies that show that sclerotherapy prevents variceal bleeding over the short term. The data also suggest that when applied to patients with large varices awaiting orthotopic liver transplantation, it enhances the chance of a patient surviving to be transplanted by preventing a variceal bleed and the spiral of liver failure and death that frequently follows an episode of acute variceal bleeding.

Etiology and course of acute bleeding esophageal ulcers.

Twenty (2%) of 1,140 patients with acute gastrointestinal bleeding had esophageal ulcers. Patients with esophageal ulcers most commonly had either melena (40%) or melena and hematemesis (40%). Fifty percent had orthostatic hypotension, and 80% required transfusions. Ulcers were associated with nonsteroidal anti-inflammatory drugs (NSAIDs) use in 50%, hiatal hernia in 60%, and esophagitis in 40%. Endoscopic stigmata of recent hemorrhage consisted of oozing blood (35%) and adherent clot (25%). Six patients had multiple ulcers. The majority of ulcers (90%) were in the distal esophagus. Nine patients were endoscopically treated without complications except for rebleeding in 1 patient. Endoscopic therapy was associated with decreased duration of hospitalization. Overall mortality was 45% in these patients, but no deaths were related to bleeding. Although uncommon, esophageal ulcers are a cause of significant acute gastrointestinal bleeding that appears to respond to endoscopic treatment.

Efficacy of sucralfate in refractory reflux esophagitis. Results of a pilot study.

Patients with severe reflux esophagitis unresponsive to standard medical therapy constitute a vexing clinical problem. We evaluated 8 patients with long-standing gastroesophageal reflux disease complicated by peptic stricture (n = 6), Barrett's esophagus (n = 5), bleeding esophageal ulcer (n = 2), and/or failure or prior antireflux surgery (n = 4), and 4 patients with rapidly advancing esophagitis following surgical resection of the cardia. After an 8-week course of full-dose H2-receptor antagonists, domperidone and antacids, marginal clinical improvement and unchanged or worsened endoscopic appearance of esophagitis was observed in all patients. Thereafter, in an attempt to enhance esophageal mucosal resistance, sucralfate alone (4.0 g/d) was given for 8 weeks. Both symptoms and endoscopic appearance improved in all patients after sucralfate, and the need for dilatation of strictures was lessened. On follow-up, complete healing of esophagitis was demonstrated by endoscopy in 6 patients after 4 to 6 months of uninterrupted sucralfate therapy. The results of this pilot study indicate that (cyto)protection with sucralfate has an important therapeutic potential in reflux esophagitis. They also suggest that impaired esophageal epithelial resistance is an important pathophysiological factor in persistence of esophageal inflammation in esophagitis refractory to conventional treatment.

Serological Confirmation of Group C Streptococcal Pneumonia

Lancefield group C streptococci are a common cause of infections in animals but less frequently cause disease in humans. Studies by Duma [1] and Mohr [2] showed that only O^o-OJ^o of streptococci isolated from cultures of human blood were identified as group C. Pneumonia due to group C Streptococcus has been reported in eight individuals [2-7]: five patients were previously healthy, one was a chronic smoker, one had a hiatus hernia and a bleeding esophageal ulcer, and one had underlying Hodgkin's disease. We describe a patient with pneumonia due to group C Streptococcus, peritonitis with underlying congenital heart disease, and chronic renal failure who was receiving continuous ambulatory peritoneal dialysis. The etiologic role of the group C Streptococcus in the illness of this patient was confirmed by isolating the organism from the blood and peritoneal fluid and by demonstrating a significant rise in antibody titer to group C streptococcal carbohydrate antigen in convalescent sera.