Coffee Ground Emesis Research Articles

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Introduction: Acute esophageal necrosis (AEN), commonly referred to as "black esophagus", is a rare disease. Its endoscopic finding shows diffuse circumferential black mucosal discoloration in the distal esophagus. The etiology of AEN is multifactorial; a combination of an ischemic insult to the esophagus, impaired mucosal barrier systems, and a chemical injury from backflow of gastric secretions. We present a case of AEN, whose etiology is thought to be an ischemia due to alcoholic ketoacidosis (AKA). Case Description: A 48-year-old male, with a history of alcohol abuse, presented to the ED complaining of coffee ground emesis. He was in shock state on admission (BP 88/62 mmHg, HR 127 beats/min) with a score of 13 on the Glasgow coma scale. Arterial blood gas showed raised anion gap metabolic acidosis with elevated ketone bodies including beta-hydroxybutyrate. From these findings, we diagnosed as a case of AKA associated with dehydration. Initial endoscopic evaluation on admission revealed a black esophagus in the distal one-third, with clear-cut margin at the gastroesophageal junction. Hemodynamic state was recovered by aggressive fluid resuscitation, and severe metabolic acidemia was also improved by continuous renal replacement therapy. Lansoprazole had also been started on admission. Secondary endoscopic examination on day 10 showed a mixture of residual black areas and ulcer formation covered with thick white exudates. Third endoscopic examination on day 25 showed the regeneration of the esophagus mucosa. The patient was discharged without any complications on day 49. Discussion: AEN is a very rare condition and its estimated prevalence is 0.01%-0.28%. The mortality of AEN is reported to be up to 30%, depending on the underlying medical condition. In this case, dehydration and AKA associated with malnutrition were the main causes of the hemodynamic instability, which led the ischemia of distal esophagus. Conclusion: AEN is potentially fatal disease despite of its low prevalence. It should be considered as the differential diagnosis of upper GI bleeding.

Gastric Mucosal Calcinosis: A Rare Cause of Bleeding

A52-year-old man with end-stage renal disease on hemodialysis presented with coffee-ground emesis and black stools. The physical examination revealed pale conjunctivae but was otherwise unremarkable. The laboratory analysis was significant for hemoglobin 4.4 g/dL, creatinine 7.8 mg/dL, and normal calcium and phosphorus (8.7 mg/dL and 2.5 mg/dL, respectively). The esophagogastroduodenoscopy revealed multiple smooth, nonbleeding nodules measuring 3–5 mm in diameter, extending radially in linear rows throughout the antrumwith an overlying clot (Figure A). Two similar lesions were noted in the second portion of the duodenum (Figure B). Biopsies showed benign gastric and small bowel mucosa with calcinosis (Figure C). The bone scan demonstrated radiotracer within the region of the stomach, also compatible with calcinosis. The computed tomography scan was significant for mitral annular calcification and scattered pancreatic parenchymal calcifications. The patient did not have any risk factors for chronic pancreatitis. A review of laboratory studies over the past year revealed a persistently elevated parathyroid hormone as well as frequent hyperphosphatemia with occasional hypercalcemia. Two sessions of argon plasma coagulation, 14 days apart, were performed on the gastric lesions. No other endoscopic therapy was undertaken. After 8 months of follow-up, the patient did not have further bleeding. Gastric mucosal calcinosis (GMC) is a rare disorder typically encountered incidentally on routine biopsy or at autopsy. Metastatic calcification is the most common cause of GMC and occurs in the setting of abnormal calcium-phosphate metabolism. Hypercalcemia and/or hyperphosphatemia cause the deposition of calcium salts

Do Stable Bed Bound Nursing Home Residents with Recurrent Coffee Ground Emesis Need Repeat Endoscopy? A Small Retrospective Study

Purpose: Upper gastrointestinal bleeding (UGIB) is a common geriatric problem. In the United States approximately 350,000 patients are hospitalized for UGIB each year and 40 are 60 years of age or older. In the elderly, esophagitis, gastritis and peptic ulcer disease account for 70-90% of hospital admissions for UGIB. In this study, we evaluated the yield of repeat EGDs in a nursing home population presenting repeatedly with coffee ground emesis. Methods: The study was performed at our urban community based teaching hospital. All EGD performed for the indication of coffee ground emesis from 2003-2012 were retrospectively reviewed. Only stable nursing home residents who were bedbound were included for analysis. Indications other than coffee ground emesis and hemodynamically unstable patients were excluded. Endoscopic findings and histopathology results were compared to previous studies performed within 1 year. Results: 17 patients met all the inclusion and exclusion criteria. African Americans represented 93.4%, females were 68.7% and mean age was 80.7 years. Gastritis and esophagitis were most common findings on previous endoscopy and on current endoscopy. There were no findings that were meaningfully different or had a clinical impact on care between the two sets of endoscopies and histopathology. Conclusion: In this small study, we conclude that stable bed bound nursing home residents presenting repeatedly with coffee ground emesis do not require repeat endoscopy. The findings on repeat endoscopy did not change clinical management in this setting.

Rectal Variceal Bleeding in a Cirrhotic Patient with Peptic Ulcer Disease

Purpose: Cirrhosis is a known sequelae of chronic liver disease. Complications include ascites, encephalopathy, and bleeding varices. Esophageal varices are the most commonly encountered type of bleed, with estimated mortality from first episode approaching 30-50%. Bleeding ectopic varices can be a rare form of GI bleed in cirrhotics. We present a case of a 57-year-old man with a history of hepatitis C cirrhosis who presented with melena and coffee ground emesis. Initial laboratory values were notable for hemoglobin 9.9 g/dL, platelets 158 K/UL, BUN 55 mg/dL, serum Cr 1.7 mg/dL, total bilirubin 1.8 mg/dL, AST 36 U/L, ALT 27 U/L, and INR 1.4. While in the ER he was noted to have 4-5 episodes of coffee ground emesis with a drop in hemoglobin by 2 gm. He was transfused packed red blood cells (PRBCs), started on Protonix and octreotide drips, and underwent emergent esophagogastroduodenoscopy (EGD). The EGD revealed two small columns of non-bleeding esophageal varices, esophagitis, a clean-based ulcer in the antrum, and an oozing 2-3 cm ulcer with a visible vessel in the second portion of the duodenum, treated with epinephrine injections and gold-probe cautery. Later that day, his mental status deteriorated and he developed hypotension with a drop in hemoglobin. After endotracheal intubation, initiation of pressor, and transfusions support, a second EGD was performed. The previously bleeding ulcer was again bleeding, and was treated with epinephrine injections and two endo-clips. Over the next hospital day, his hemoglobin stabilized between 8-9 g/dL and he was weaned off pressors. On the fourth day, he again became hypotensive, and developed hematochezia. A third EGD revealed the same duodenal ulcer, this time with no stigmata of bleeding. Using the same gastroscope, a flexible sigmoidoscopy was performed, revealing a large rectal varix with a fibrin clot (“nipple sign”). Banding was not attempted due to the very large nature of the varix. The patient subsequently underwent a transjugular intrahepatic portosystemic shunt procedure (TIPS). He was stable after TIPS, and only required a transfusion of one unit of PRBCs transfusion. Unfortunately, his condition deteriorated in the following days, and he succumbed to sepsis and multi-organ failure. There are important points that this case highlights. First, peptic ulcer disease is the most common etiology of upper GI bleeding. Second, the management of a brisk lower GI bleed, affecting hemodynamics, is EGD first. Third, TIPS is the appropriate management for bleeding ectopic varices.

Eosinophilic Gastritis Masquerading as Recalcitrant Giant Gastric Ulcer

Background: Eosinophilic gastroenteritis (EG) is a rare condition of unknown etiology characterized by an intense eosinophilic infiltrate throughout the GI tract, and has been reported in poorly controlled asthmatics. We present a rare case of eosinophilic gastritis in a poorly controlled asthmatic that presented as a bleeding giant gastric ulcer. Case: A 70-year-old male with HTN and poorly controlled asthma presented with bloating, coffee ground emesis and melena. He was a former heavy alcohol user, took one baby aspirin daily, no recent steroid use. The patient was stable with a Hg of 13. His WBC count was 8.8 with an elevated eosinophil count (12.9%). EGD showed a 4.2cm gastric ulcer with stigmata of recent bleeding. Biopsies showed severe eosinophilic gastritis, negative for H. pylori. In the past he also had a bleeding gastric ulcer despite use of PPIs. With each presentation there was a parallel marked peripheral eosinophilia and appeared to coincide with, or shortly precede his asthma exacerbations. Discussion: EG is a very rare disease, usually presenting as abdominal pain, vomiting and distention. A diagnosis of eosinophilic gastritis is made when >30 eosinophils are seen per high power field. About 50% of patients with EG have asthma or other atopic disorders, which may be diagnosed at the same time or years beforehand. Previously reported peripheral eosinophilia to >4000/ul have been noted. These patients may have thickened gastric mucosal folds, nodularity, or ulcerations seen on radiographs, reflecting intense eosinophilic infiltrate. Endoscopy may reveal normal or edematous mucosa with prominent gastric folds or surface erosions. Treatment with systemic corticosteroids led to bronchial and abdominal symptom resolution. Conclusion: We presented an unusual case of a patient with a history of uncontrolled asthma presenting with eosinophilic gastritis manifested as a recalcitrant giant gastric ulcer. To our knowledge this is only the second case described in the literature of eosinophilic gastritis presenting this way, and highlights the importance of considering eosinophilic disorders of the GI tract in patients with severe asthma.FigureFigure

Herald Bleeding: A Hidden Catastrophe

Purpose: The word “herald” means to indicate or sign that something is about to happen. Herald bleeding is defined as an episode of hemorrhage, often accompanied by abdominal pain, which may precede, by hours to weeks, a catastrophic hemorrhage. Case Report: A 57-year old male with past medical history of abdominal aortic aneurysm repair around 15 years ago and peptic ulcer disease diagnosed 10 years ago, presented to the hospital with maroon-colored stool of 2 weeks' duration, along with a few days' onset of melena, coffee ground emesis, and sharp epigastric pain. Medications included Plavix, Protonix, Tramadol, and occasional NSAIDs. Physical examination revealed normal vital signs, and epigastric tenderness without any peritoneal signs. Laboratory analysis showed hemoglobin of 7.1 mg/dL, platelets of 355,000 /μL, and INR of 1.2. A CT scan of abdomen and pelvis with IV contrast showed 1.6 x 1.6 x 1.8 cm saccular aneurysm originating from the termination of the distal abdominal aorta without adjacent acute findings, and 3.1 cm aneurysm infrarenal abdominal aorta with circumferential thrombus. Upper gastrointestinal endoscopy showed L.A. grade B esophagitis and hiatal hernia. Colonoscopy showed a scant amount of blood in colon without any obvious bleeding source. Tagged RBC scan was negative. Second look endoscopy was performed with pediatric colonoscope, revealing 3- 4 mm clean-based ulcer over the fourth portion of duodenum, and two vascular clips were placed. Vascular surgery was consulted and, based on the location of the ulcer on the lateral wall of the abdominal aorta, along with CT finding of induration and inflammation of the aortic graft right at the renal arteries, suspicion was made for aortoenteric fistula (AEF). The patient underwent emergent laparotomy and was found to have AEF. The patient then underwent repair of AEF with a successful outcome. Discussion: AEF is a direct connection between abdominal aorta and gut, most commonly duodenum. It occurs in 0.3-4% of patients who underwent open AAA repair. The most common clinical manifestations are upper or lower gastrointestinal bleeding (herald bleeding; 64%), abdominal pain (32%) and a pulsatile abdominal mass (25%). The proposed theories for the formation of primary ADF are direct wear and inflammatory destruction triggered by infection, foreign bodies or erosions. The characteristic site of formation is the third or fourth part of the duodenum. AEF should be considered in all patients with GI bleeding and a history of AAA or previous aortic revascularization with prosthetic graft. A high index of suspicion is the key. The mortality rate of untreated AEF is 100%. Surgical intervention is mandatory for survival and successful outcome.

Water-soluble Contrast for the Diagnosis of Esophageal Perforation: A Note of Caution

Purpose: Esophageal perforation requires early diagnosis and carries a high penalty for delayed treatments. Even with a rapid diagnosis, esophageal perforation holds an overall mortality of nearly 20%. When treatment is delayed over 24 hours mortality doubles. Water-soluble contrast agents, such as gastrografin, are supported as first line screening of suspected perforation due to their rapid absorption. If perforation is not initially detected and clinical suspicion remains high, a serial barium contrast esophagography is recommended to follow. We present a fatal case of esophageal perforation complicated by gross thoracic contamination of water-soluble contrast. A 57-year-old man was transferred with coffee ground emesis. Prior to transfer, he underwent an upper endoscopy showing a potential disruption of the esophagus. For further evaluation a swallow study with a non-ionic water-soluble contrast was performed. A subsequent unenhanced CT scan of the thorax demonstrated a well-defined defect along the anterior wall of the esophagus with a large accumulation of contrast in this area of the thorax. Upon transfer, emergent upper endoscopy revealed a perforation of the esophagus, 36 cm distally to 34 cm proximally with a large adjacent area of ulceration. After appreciation of gross thoracic contamination, the endoscope was advanced through the perforation into the right thorax with the intent of using a 6-mm port scope to lavage the region and remove the liquid and solid debris. The entire thorax was covered with a thick, gelatinous glue-like covering. Copious lavage and suctioning of the exudative debris and tissue was performed using an estimated 700 mL of normal saline; however, the glue-like contrast precluded meaningful results. After decompression, a 22 mm x 12 cm fully covered esophageal stent (Alimaxx, Merit Medical Co, South Jordan, UT) was successfully deployed. The family declined further procedures and opted for a palliative approach. The patient expired 1 week later. Endoscopic assessment and immediate treatment (temporary stenting) is playing an increasing role in esophageal perforation. When extraluminal contamination is identified, it has been our practice to use low-pressure washout and decompression prior to stenting or direct surgical management in cases where endoscopic treatment is likely to be insufficient. Here we describe a case of a thoracic cavity covered in contrast media that stifled efforts to provide an effective washout. This reinforces the movement towards upper endoscopy as first-line evaluation. This allows for direct visualization of the esophageal defect and potential avoidance of contrast agents given the ramifications of gross thoracic contamination.

Black Esophagus

Purpose: Acute esophageal necrosis (AEN) is rare, with prevalence reported to range from 0.001 to 0.2%. It is often seen in critically ill patients. We present a 68-year-old male with a history of diabetes mellitus and chronic kidney disease stage IV, who presented with acute onset of coffee ground emesis during his hospital admission. He was initially admitted for acute mental status change secondary to sepsis with pneumonia and urinary tract infection. At the time of his admission, he was septic with a blood pressure reading of 98/62 mmHg. He was stabilized on a medical floor with intravenous fluids and antibiotics. On day nine of his hospital course, he presented with multiple episodes of coffee ground emesis. He had no melana or abdominal pain. He had no other recorded instances of hypotension. During the episodes of coffee ground emesis, he was hemodynamically stable with HR 77 and BP 130/63. BUN was 44 mg/dL, and creatinine was 2.8 mg/dL, which was his baseline. INR was 1.2, hemoglobin was remarkably stable at 11.6 g/dL. Endoscopy showed diffuse circumferential necrosis in the middle and lower third of the esophagus. The gastro-esophageal junction was clean. The pathogenesis of AEN is not very well known, but it is unlikely to be the result of a single event. Risk factors for AEN are often multifactorial and include low flow states, vasculopathy, or direct corrosive injury to the esophagus. AEN tends to occur in older males and presents as an upper GI bleed. AEN develops at least 18 hours after the ischemic insult. In this case, however, we report the development of AEN days after the initial insult of a hypovolemic state. The diagnosis of AEN is established with endoscopy, characteristically showing black pigmentation, often in the distal part of the esophagus with a sharp demarcation of normal pink mucosa at the gastro-esophageal junction. Mortality of AEN is higher than other upper GI bleeds because it tends to occur in very sick patients. In many reported cases, death from AEN is often attributed to the underlying critical illness. By itself, however, AEN is self-limiting. In healthy patients, the mucosa heals rapidly and should acquire its normal endoscopic appearance by week two or three post ischemic injury.Figure

A Rare Cause of Upper GI Bleed Where EGD Could Have Been Fatal

Purpose: We are reporting a case of upper GI bleed in a patient with atrioesophageal fistula where EGD could have been fatal. This case also underlines the importance of complete procedural history in patients with GI bleed. A 57-year-old male with hypertension, dyslipidemia, and atrial fibrillation on rivaroxaban presented with chest pain, dyspnea on exertion, and one episode of coffee ground emesis. He was hemodynamically stable on admission with a normal CBC and BMP. Hemoglobin was 13.5 g/dL. He suddenly experienced an episode of severe chest pain and went into PEA arrest. He was resuscitated, intubated, and placed on a mechanical ventilator. NG was placed and 300 mL red blood was aspirated. Patient went into coma, but vital signs and remaining exam was normal. CT head revealed pneumocephalus and multiple cerebral infarcts. Repeat hemoglobin was 12.2 g/dL. EGD was not performed. Blood culture grew S. aureus and Strep. viridians. Later on it was found that he had catheter ablation for atrial fibrillation 18 days ago. Left atrialesophageal fistula was suspected. CTA thorax showed a 5-mm posterior left atrial diverticulum raising a suspicion of pseudoaneurysm. A fistula between the esophagus and left atrium was found intra-operatively and it was repaired. Patient showed no neurological improvement and remained in coma, so life support was withdrawn after 11 days and patient died. Atrioesophageal fistula (AEF) is a rare complication of A Fib catheter ablation procedures, incidence rate 0.2%. It is associated with high mortality rate (70%). It can present 1-6 weeks after the ablation. Presentation is nonspecific: fever, neurological deficits, and chest pain. None of the previously reported cases described GI bleeding symptoms. EGD can cause fatal air-embolism so it should be avoided. CT chest can help to establish diagnosis. Surgery can be lifesaving. AEF should always be on the differential diagnoses of UGI bleeding in appropriate setting: unexplained fever and neurological deficit after recent ablation procedure.Figure: Atrial diverticulum in the circle.

Successful Treatment of Duodenal Perforation with Over-The-Scope Clip after Failed Surgical Repair

Purpose: Over-The-Scope Clips (OTSC®) have been reported to be useful in primary repair of iatrogenic endoscopic perforations. We report the successful use of the OTSC® in an elderly patient who failed surgical repair for an iatrogenic duodenal perforation. Methods: A 94-year-old man presented with a history of chronic duodenal strictures due to a duodenal ulcer. He was limited to a liquid diet and had undergone two prior balloon dilations without fluoroscopy. The third dilation, with fluoroscopic guidance, identified the stricture at the apex of the duodenal bulb. As the balloon was dilated to 12 mm, a small amount of blood was seen coming from the stricture. The patient felt well and was discharged. The following day, the patient presented with dyspnea and an episode of coffee-ground emesis. On exam, the patient was tachypneic with a grossly distended, hypertympanic, tender abdomen. Abdominal and pelvic CT revealed a peri-duodenal fluid collection in the anterior perirenal space consistent with a duodenal perforation. The patient was taken to the OR for exploration, where a fist-sized abscess containing coffee ground material as well as a 1.5-cm posterior perforation of the duodenum was found. The duodenum was closed with an omental patch; a gastrojejunostomy was formed and a feeding jejunostomy created. He recovered well until post-operative day six when he experienced bilious emesis and a leukocytosis of 21.1 x 109/L. A CT of the abdomen with oral contrast showed a persistent duodenal perforation. The patient was made NPO and kept on IV antibiotics. Two weeks after the initial repair, endoscopy was performed which identified an abnormal area which had a white non-mucosal base and sutures, representing the area of the failed repair. An OTSC was deployed and the opening could no longer be visualized. Results: The following day, an UGI study revealed no evidence of an extraluminal leak. Five days after clip placement, abdominal CT showed persistent right pararenal fluid collections without evidence of fluid extravasation. The collections were drained by radiology. The patient was discharged on a pureed diet to a skilled nursing facility a week later without further complications. Conclusion: Over-The-ScopeClips may be an intervention to avoid surgery or re-surgery for iatrogenic endoscopic perforations. Given this patient's advanced age, OTSC was attempted and was successful. To our knowledge, this is the first case report of its use after failure of surgical repair. Our unusual case suggests that OTSC should be considered an option in repair of iatrogenic perforation even after failed surgical repair.

Hematemesis in a Patient With Diabetic Ketoacidosis and Chronic HCV Infection

292 Question: A 55-year-old man with past medical history of poorly controlled diabetes mellitus, recurrent infective endocarditis (last episode 2 months ago), and chronic hepatitis C presented to the emergency department with 2 episodes of coffee ground emesis. He also complained of fatigue, polyuria and lightheadedness for 2 days before admission. He denied any abdominal pain, prior retching,melena, or hematochezia. He denied using any nonsteroidal anti-inflammatory drugs, smoking, and recent alcohol or illicit drug use. On admission he was afebrile, tachycardic at 116 bpm, with a blood pressure of 121/92 mmHg, was breathing 24 times a minute and saturating well on room air. On physical examination, his skin and oral mucosa were dry. He was alert and oriented, with lungs clear to auscultation, heart sounds normal, and abdomen soft, nondistended, and nontender. He had no stigmata of chronic liver disease. Laboratory examination revealed blood sugar of 331 g/dL, sodium of 127 mEq/L, potassium of 6.4 mEq/L, bicarbonate of 7 mEq/L, anion gap of 29, and pH of 7.023. His blood urea was 69 mg/dL and creatinine 2.6 mg/dL. His hemoglobin was 16.7 g/dL; white blood cell count and platelets were normal. He was treated for diabetic ketoacidosis with an insulin drip and his electrolytes were corrected as needed. Nasogastric lavage was done and was clear. He was started on pantoprazole drip and an upper gastrointestinal endoscopy was performed which revealed diffuse blackish discoloration of the mid and distal esophagus (Figure A), which abruptly ended at the gastroesophageal junction. There was also evidence of erosive gastritis and erosive duodenitis (Figure B) in the bulb and second portion of duodenum. What is the diagnosis? What is the appropriate management? Look on page 491 for the answer and see the GASTROENTEROLOGY web site (www.gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and Images in GI.

PTH-140 Risk Stratification of upper Gastrointestinal Bleeding with the Glasglow-Blatchford Score: Experience of a District General Hospital in East London, United Kingdom

IntroductionThe Glasglow-Blatchford Score (GBS) is a risk stratification tool to assess the need for clinical intervention to prevent death in patients with suspected upper gastrointestinal (UGI) bleeding1. In the UK...

A Rare Cause of Caustic Gastric Injury in a Young Man

MAHOMEDY MC, 1975, ANAESTHESIA, V30, P190, DOI 10.1111-j.1365-2044.1975.tb00832.x; MIDDLETON SJ, 1990, POSTGRAD MED J, V66, P657; Young RJ, 1996, HUM EXP TOXICOL, V15, P259

Factors influencing clinical outcomes of Histoacryl®glue injection-treated gastric variceal hemorrhage

To determine the factors associated with clinical outcomes and complications of Histoacryl® glue injection for acute gastric variceal hemorrhage. Patients who presented to the Siriraj Gastrointestinal Endoscopy Center with active gastric variceal bleeding and were admitted for treatment between April 2008 and October 2011 were selected retrospectively for study inclusion. All bleeding varices were treated by injection of Histoacryl® tissue glue (B. Braun Melsungen AG, Germany) through a 21G or 23G catheter primed with lipiodol to prevent premature glue solidification. Data recorded for each patient included demographic and clinical characteristics, endoscopic findings, clinical outcomes in terms of early and late re-bleeding, mortality, and procedure-related complications. Data from admission (baseline) and post-treatment were comparatively analyzed using stepwise logistic regression analysis to determine the correlation between factors and clinical outcomes. A total of 90 patients underwent Histoacryl® injection to treat bleeding gastric varices. The mean age was 55.9 ± 13.9 (range: 15-88) years old, and 74.4% of the patients were male. The most common presentations were hematemesis (71.1%), melena (12.2%), and coffee ground emesis (8.9%). Initial hemostasis was experienced in 97.8% of patients, while re-bleeding within 120 h occurred in 10.0%. The presence of ascites was the only factor associated with early and late re-bleeding [odds ratio (OR) = 10.67, 95%CI: 1.27-89.52, P = 0.03 and OR = 4.15, 95%CI: 1.34-12.86, P = 0.01, respectively]. Early procedure-related complications developed in 14.4% of patients, and were primarily infections and non-fatal systemic embolization. Late re-bleeding was significantly correlated with early procedure-related complications by univariate analysis (OR = 4.01, 95%CI: 1.25-12.87, P = 0.04), but no factors were significantly correlated by multivariate analysis. The overall mortality rate was 21.1%, the majority of which were related to infections. The factors showing strong association with higher mortality risk were elevated total bilirubin (OR = 16.71, 95%CI: 3.28-85.09, P < 0.01), a large amount of transfused fresh frozen plasma (OR = 1.001, 95%CI: 1.000-1.002, P = 0.03), and late re-bleeding (OR = 10.99, 95%CI: 2.15-56.35, P = 0.02). Histoacryl® injection is a safe and effective hemostatic method for treating gastric variceal hemorrhage. Patients with compromised liver, including ascites, have a higher risk of re-bleeding.

Portal Hypertension, Nodular Regenerative Hyperplasia of the Liver, and Obstructive Portal Venopathy due to Metastatic Breast Cancer

Nodular regenerative hyperplasia (NRH) of the liver is associated with noncirrhotic portal hypertension, rheumatologic and hematologic disorders, administration of certain drugs, and other underlying conditions. This report describes a 64-year-old man with clinically presumed cirrhosis who presented to our institution with coffee-ground emesis, esophageal varices, ascites, and encephalopathy. Eleven years earlier he had been treated for breast cancer with mastectomy and chemo-radiotherapy. He died suddenly, and the autopsy showed no evidence of cirrhosis but instead demonstrated NRH with extensive emboli of recurrent breast carcinoma within the portal vein and its intrahepatic branches. Neoplastic occlusion of the portal vein as a cause of presinusoidal noncirrhotic portal hypertension has not previously been reported for metastatic breast carcinoma. This case highlights the importance of obstructive portal venopathy in the pathogenesis of NRH as well as the diagnostic difficulties that may be encountered in determining the cause of portal hypertension.

Esophageal Polyp Arising from a Gastric Inlet Patch Causing Dysphagia

Purpose: Heterotopic gastric mucosa is usually an aymptomatic finding. We present a 58-year-old male who was admitted for nausea, vomiting and coffee ground emesis. He also noted intermittent solid food dysphagia, heartburn and epigastric pain. His history was positive for diabetes, end stage renal disease (ESRD) on hemodialysis, hypertension and chronic alcohol use. Physical exam was positive for epigastric tenderness, mild dehydration and hypotension which stabilized with medical resuscitation. Endoscopy revealed two salmon colored patches of columnar appearing epithelium in the proximal esophagus suggestive of gastric inlet patches. There was a large, 1 cm, semipedunculated esophageal polyp arising from one of these patches. In addition, there was extensive erosive esophagitis seen in the distal and middle esophagus. The gastric mucosa appeared erythematous. Biopsies from the polyp confirmed it to consist of gastric cardia type mucosa with hyperplastic foveolar epithelium and inflammatory cells with no evidence of squamous epithelium. The salmon colored mucosal patches were positive for gastric cardia type of epithelium with evidence of ulcerative esophagitis. The inflamed esophageal mucosa showed changes of reflux esophagitis. Gastric mucosal biopsy was suggestive of non specific reactive gastropathy. The patient was started on high dose proton pump inhibitor therapy and other resuscitative measures were instituted. Plan was to repeat endoscopy and an EUS after 6 weeks of treatment with PPI. However, after resolution of his symptoms, the patient deferred further invasive work-up. Esophageal polyps are a rare occurrence and may be of diverse histopathologic types. The class of hyperplastic esophageal polyps is usually found in relation to GERD, at the GE junction and is histologically characterized by proliferation of hyperplastic gastric-type foveolar epithelium, hyperplastic squamous epithelium, or an admixture of the two linings with variable inflammatory infiltrate. This case illustrates a very rare occurrence of an esophageal polyp arising from gastric inlet patch and causing symptomatic dysphagia.

Apple Green Gastritis: A Case of Gastric Amyloidosis

Case: A 55-year-old African American male with a past medical history of DM II presented to clinic for evaluation of GERD. Patient reports that symptoms started several years ago. He noted intermittent episodes of nausea, vomiting, mid-sternal chest discomfort, and increased bloating. He also reports having coffee ground emesis and black stool two and a half months ago.Initial results from the CMP, CBC, amylase and lipase were normal.CT abdominal/pelvis were unremarkable. An EGD performed for this evaluation was positive for chronic active gastritis. Biopsy results were positive for amyloidosis. The patient was was diagnosed with AL-type gastric amyloidosis and plasma cell dyscrasia. Discussion: Amyloidosis is a rare disorder characterized by the extracellular deposition of an abnormal fibrillar protein. Amyloidosis can be acquired or hereditary and systemic or localized to a single organ, such as the gastrointestinal tract.Amyloidosis is divided into six types with primary (AL) amyloidosis being the most common form. AL amyloidosis is associated with plasma cell dyscrasis and has the maximum gastrointestinal involvement. Gastric involvement occurs in 8% of patients by biopsy and 12% by autopsy, with only 1% being symptomatic. GI symptoms are usually nonspecific and they often include dysphagia, abdominal pain, hemorrhage, constipation, diarrhea and malabsorption. Histopathological patterns of amyloid deposition are associated with clinical and endoscopic features. The most common endoscopic findings include a fine granular appearance, polyps, erosions, ulcerations, and mucosal friability. There is no specific treatment for gastric amyloidosis but recently high-dose chemotherapy with hematopoietic stem cell transplantation has been used for AL amyloidosis with a 5-year survival rate of 60%.Figure: No Caption available.Figure: No Caption available.

Black Duodenum and Black Esophagus

Purpose: Acute esophageal necrosis (AEN) or ‘black esophagus' is characteristically described as diffuse, circumferential, black appearance of the esophagus that stops abruptly at the gastroesophageal junction (GEJ). AEN commonly presents with symptoms of hematemesis, melena or coffee-ground emesis in about 90% of the cases. We describe the first case in the literature of AEN associated with duodenal necrosis (black duodenum) in a patient who presented with a pulmonary embolism without these classic characteristic symptoms. An 80-year-old male ex-smoker with a past medical history of hypertension was admitted to our hospital with symptoms of worsening shortness of breath, left sided back pain, nausea and non-bloody, non-bilious vomiting. He denied abdominal pain, chest pain, fever, chills, dysphagia, odynophagia, or history of caustic ingestion. The patient was tachycardiac, mildly hypoxic on room air and had normal abdominal and rectal examination. Pertinent laboratory results included a white blood cell count of 17.8/μl with 82% neutrophils and hemoglobin of 14.4 g/dl. Computed Tomography angiogram revealed bilateral pulmonary emboli, diffuse esophageal and proximal duodenal thickening. Esophagogastroduodenoscopy (EGD) revealed black discoloration with underlying friable hemorrhagic tissue from the mid-esophagus up to the distal esophagus and a normal appearing GEJ and stomach. The duodenal bulb and the proximal aspect of the second portion of duodenum had a black discoloration similar in appearance to the involved segment of the esophagus. Biopsies of the black mucosa from the esophagus and the duodenum revealed necrosis. The patient was discharged home on warfarin and proton pump inhibitor (PPI). A follow-up EGD one week later revealed a normal esophagus and a normal duodenum. Conclusion: This is the only case of AEN described in the literature associated with a pulmonary embolism (PE) and duodenal necrosis. AEN and duodenal necrosis may have been secondary to hypoxia from the PE, explaining the complete rapid improvement with anticoagulation therapy. Given our case, we suggest that a lower threshold for a diagnosis of pulmonary embolism should be considered in a patient with AEN in an appropriate clinical setting.Figure: [1331] Figure 1. Black esophagus and black duodenum.

Acute Cholecystitis Induced Esophageal Necrosis

Purpose: Acute esophageal necrosis (AEN), colloquially referred to as “black esophagus,” is extremely rare. Retrospective case series over 45 years document only 95 patients with AEN. The hallmark presentation on EGD is diffuse circumferential black mucosa found in the distal third of the esophagus. Here we describe the first case of AEN caused by cholecystitis. A 65 y/o male with hepatitis C decompensated cirrhosis presents with coffee-ground emesis and severe abdominal pain. He recently had an uncomplicated sphincterotomy and stent placement for choledocholithiasis. Labs show WBC 36.9 K/μL, Hgb 9.2 g/dL (baseline 13), platelets 97 K/μL, INR 2.5, Cl 81mmol/L, and lactic acid 18.7 mmol/L. Serum lipase, amylase, CPK, and transaminases were normal. CT reveals an intact biliary stent with pneumobilia, markedly distended gallbladder, abundant ascites, and a thick-walled esophagus. EGD demonstrates circumferential necrotic appearing mucosa from mid to distal esophagus. Ascites grew Citrobacter, Klebsiella; blood grew Klebsiella, Staph. Antibiotics, albumin, TPN were started. Repeat paracentesis reveal WBC 8660, 89% PMNs with growth of Klebsiella, Pseudomonas, and Vancomycin resistant Enterococcus. Patient was intubated for hypoxia. A hydropic gallbladder with thickened edematous wall, pericholecystic fluid, and sludge seen on ultrasound. Peritoneal fluid amylase and bilirubin were normal. During percutaneous choleycstostomy tube placement, cholangiogram confirmed no filling of the cystic duct consistent with cholecystitis; cultures revealed identical organisms as in peritoneal fluid. His overall septic course decompensated and palliative care was pursued. The patient passed. AEN is caused by significant hypoperfusion resulting in profound ischemia. Upper gastrointestinal bleeding is the most common presenting symptom. AEN is diagnosed clinically and treatments are conservative in nature: optimize perfusion, nutrition, and treat infection if present. Our case is unique as AEN was due to bacterial peritonitis from cholecystitis, leading to a massive ischemic event.Figure: No Caption available.

Ischemic Injury Following EUS Guided Celiac Plexus Neurolysis

Case Presentation: A 51 yo M with metastatic pancreatic adenocarcinoma with vascular invasion presents with abdominal pain. The patient had an ERCP with CBD stent exchange and EUS with celiac plexus neurolysis (CPN). During the EUS CPN, a total of 10 cc of .25% bupivicaine and 10 cc of dehydrated Etoh were injected. One day following the procedure he had melena and subsequent coffee ground emesis with a 4 gram drop in hemoglobin from admission. An EGD showed extensive ulceration and inflammation along the lesser curvature, which was suggestive of ischemic injury. Discussion: Treatment of pain in pancreatic cancer is an important objective in palliative care. Approximately 80-85% of patients have pain associated with advanced pancreatic cancer. Options for pain control include pharmacotherapy as well as CPN, which can be performed percutaneously, surgically or under the guidance of EUS. EUS CPN has been shown to be effective in achieving pain control. In one meta-analysis of 119 patients, pain was alleviated in 73% of patients. CPN is overall felt to be safe but practitioners should be aware of the possible complications. Side effects include local pain, unopposed parasympathetic activity, which can result in diarrhea (44%) and hypotension (38%). Serious complications include retroperitoneal hemorrhage and peripancreatic abscess. In a series of 189 EUS guided celiac plexus blocks and 31 CPNs, the following 4 complications were reported: hypotension, retroperitoneal abscess, and 2 with post-procedural pain. One case report notes ischemic complications following CPN, including gastric ischemia/necrosis, splenic infarction, and pancreatic necrosis in the distribution of the celiac artery. Similarly, our patient likely developed ischemic injury following CPN. Ethanol can cause vasospasm and severe cases of vasoconstriction can lead to vascular and smooth muscle cell death. Conclusion: CPN is an effective modality for treatment of pain in advanced pancreatic cancer. However, physicians should also be aware of the complications. Patients who develop signs of GI bleeding after CPN should be evaluated for ischemic injury.Figure: No Caption available.