Severe upper gastrointestinal hemorrhage from linear gastric ulcers in large hiatal hernias: a large prospective case series of Cameron ulcers (original) (raw)
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Open Access Macedonian Journal of Medical Sciences
BACKGROUND: Cameron lesions are seen in 5.2% of patients with hiatal hernia who undergo esophagogastroduodenoscopic examinations. The prevalence of Cameron lesions seems to be dependent on the size of the hernial sac, with an increased prevalence in the larger-sized sac. In about two-thirds of the cases, multiple Cameron lesions are noted rather than a solitary erosion or ulcer. AIM: The aim of this case report is to present the patient with Cameron ulcers associated with hiatal hernia. CASE PRESENTATION: Our patient presented with postprandial retrosternal pain, especially immediately after eating, vomiting, dyspnea, weight loss, fatigue, signs, and symptoms of severe hypochromic microcytic anemia without signs of acute gastrointestinal bleeding. No history of gastroesophageal disease. Colonoscopy was done and eliminate colic cause of anemia. The endoscopy showed a large hiatal hernia and linear erosions and ulcerations at the level of gastrodiaphragmatic contact (Cameron ulcers) a...
Cameron Ulcer Causing Severe Anemia in a Patient with Diaphragmatic Hernia
American Journal of Case Reports, 2015
Rare co-existance of disease or pathology Background: Cameron lesions are linear gastric erosions on the mucosal folds at the diaphragmatic impressions found in patients with large hiatal hernias. While usually asymptomatic, hiatal hernias can result in serious sequelae, as this case report will clearly illustrate. Cameron lesions are clinically significant because of their ability to cause significant acute, chronic, or obscure gastrointestinal bleeding, often requiring blood transfusions. Case Report: In this report, we present the case of a 51-year-old white woman who originally presented to the Emergency Department with complaints of a runny nose, dry cough, generalized weakness, and muscle cramping ascribed to a viral infection. However, closer examination revealed substantial pallor with pale conjunctiva prompting further workup that revealed substantial anaemia. Upon further inquiry of her past medical history, she revealed the need for previous blood transfusions, and meticulous review of her medical record indicated a previous diagnosis of hiatal hernia with the presence of Cameron lesions based on esophagogastroduodenoscopy 2 years prior. Conclusions: This case emphasizes the need for a high index of suspicion for Cameron lesions as a causative agent of substantial blood loss in patients with hiatal hernias after other common causes of gastrointestinal bleeding have been ruled out.
Hiatal hernia and Cameron ulcer: an overlooked association in pediatric patients
Revista espanola de enfermedades digestivas : organo oficial de la Sociedad Espanola de Patologia Digestiva, 2021
Cameron lesions were first described 30 years ago (by Cameron and Higgins) as linear erosions or ulcers in hiatal hernia. They are uncommonly reported in adults evaluated for gastrointestinal bleeding, whereas in children they are only few case reports. We describe a ten-years-old boy presenting with a history of iron deficiency anemia and occasional vomiting. Esophagogastroduodenoscopy revealed a sliding hiatal hernia and a Cameron ulcer. We highlight that although a rare cause of gastrointestinal bleeding, a hiatal hernia in a child with iron deficiency anemia should raise the suspicion for Cameron lesions. In fact, the rarity of these lesions makes them a diagnostic challenge, as their identification requires knowledge and a meticulous endoscopy.
Cureus, 2020
Cameron lesion is an uncommon cause of overt upper gastrointestinal bleed (GI bleed). Though hiatal hernia is a well-known entity, Cameron lesions that may occur in them are usually missed during upper endoscopy. Patient with Cameron lesions usually presents as chronic iron deficiency anemia, rarely as acute GI bleed. Multiple other risk factors such as non-steroidal anti-inflammatory drug use, alcohol consumption, gastro-esophageal reflux disease (GERD) may be present concomitantly which makes initial differential diagnosis of Cameron lesions more difficult as seen in our case.
International Journal of Research in Medical Sciences
A giant paraesophageal hernia is defined when at least 30% of the stomach has moved to the thorax or the presence of another intra-abdominal organ. We describe the presentation of a clinical case of a giant hiatal hernia with perforated gastric ulcer in a 52-year-old man who presented to the emergency department with pain in the inguinal region developing obstructive shock. Presentation of hiatal hernias is usually asymptomatic and in some cases with atypical signs and symptoms involving cardiovascular and respiratory disorders. In patients with a history of gastroesophageal reflux disease/ with atypical thoracic symptoms, hiatal hernia and its complications should be ruled out.
An Unusual Cause of a Solitary Giant Gastric Ulcer
Gastroenterology, 2019
Question: An 83-year old woman with congestive heart failure, chronic obstructive pulmonary disease, and peptic ulcer disease was readmitted to our institution with recurrence of upper gastrointestinal bleeding 1 week after her initial episode. The patient's initial presentation was characterized by hematemesis that occurred after she stopped her proton pump inhibitor and in the setting of steroid use for possible polymyalgia rheumatica. An upper endoscopy at that time showed a large, 4-cm, cratered gastric ulcer with a necrotic base within the patient's 8 cm-hiatal hernia sac. There were visible cardiac pulsations noted at the ulcer base. The appearance of the ulcer was concerning for malignancy, so the margins of the ulcer were biopsied; the results were unremarkable. An endoscopic ultrasound examination was performed to better characterize this ulcer and it revealed diffuse gastric wall thickness with no evidence of intramural or extramural mass at the site of the ulcer base. The left ventricle was seen contracting adjacent to the gastric wall at the site of the giant ulcer. The patient was restarted on twice daily PPI therapy and was discharged home in stable condition. One week later, she represented with melena and an episode of hematemesis. On admission, her blood pressure was 120/60 mm Hg and pulse rate 81 bpm. The remainder of her physical examination was unremarkable. Her hemoglobin was 7.8 g/dL (down from 8.7 g/dL 4 days earlier). The patient was transfused 1 unit of packed red blood cells and underwent an upper endoscopy. Unfortunately, the patient became hypoxic after receiving propofol, so the upper endoscopy was rescheduled for the next day. The patient remained hemodynamically stable and so was her hemoglobin. She had no signs of ongoing gastrointestinal bleeding. The following day, upper endoscopy showed the large 4-cm ulcer with a protuberance in the midst of it, suspicious for a nonbleeding visible vessel (Figure A, blue arrow). The rest of the stomach was grossly unremarkable with the exception of the large hiatal hernia. There was no old or fresh blood noted throughout the examination. How would you treat this visible vessel knowing the ulcer size and its proximity to the left ventricle? What do you think the etiology of this giant gastric ulcer is? See the Gastroenterology web site (www.gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and Images in GI.
World journal of emergency surgery : WJES, 2008
With an incidence of less than 5%, type II paraesophageal hernias are one of the less common types of hiatal hernias. We report a case of a perforated prepyloric gastric ulcer which, due to a type II hiatus hernia, drained into the mediastinum. A 61-year old Caucasian man presented with acute abdominal pain. On a conventional x-ray of the chest a large mediastinal air-fluid collection and free intra-abdominal air was seen. Additional computed tomography revealed a large intra-thoracic air-fluid collection with a type II paraesophageal hernia. An emergency upper midline laparotomy was performed and a perforated pre-pyloric gastric ulcer was treated with an omental patch repair. The patient fully recovered after 10 days and continues to do well. Type II paraesophageal hernia is an uncommon diagnosis. The main risk is gastric volvulus and possible gastric torsion. Intrathoracic perforation of gastric ulcers due to a type II hiatus hernia is extremely rare and can be a diagnostic and tr...
Bleeding Gastric Ulcer: A Prospective Evaluation of Rebleeding and Mortality
ANZ Journal of Surgery, 1989
Clinical laboratory and endoscopic data were collected prospectively in 268 patients with bleeding gastric ulcer who were admitted between September 1985 and November 1987. There were 22 deaths, giving a hospital mortality rate of 8.2%. Surgery was undertaken in 68 patients (25.4%) with a mollality rate of 17.6% (I I .8'K at 30 days). There was one fatality in 104 (1.0%) patients C 60 years compared with 21 deaths (12.8%) in patients > 60 years (P < 0.001). Cirrhosis (P < 0.01). malignant disease (P < 0.03). chronic obstructive airways disease (P < 0.02). congestive cardiac failure (P < 0.02) and ischaemic heart disease (P < 0.08) were each associated with an increased risk of mortality. Outcome in patients > 60 years was related to systolic blood pressure at admission (P < 0.03), haemoglobin (P < 0.02). serum bilirubin (P < 0.02), and total transfusion requirements (P < 0.001). For ulcers 4 I cm, I-< 2cm, > 2cm in size, mortality rates were 1.9%. 11.4% and 18.0%. respectively. Initial endoscopy findings of a visible vessel, fresh blood, or active spurtingloozing haemorrhage were associated with rebleeding rates necessitating emergency surgery of 30.0%. 36.4% and 40.0%. respectively. There was no evidence of rebleeding in 187 patients (79.9%) managed conservatively and only five patients (2.7%) in this group succumbed, whereas rebleeding did occur in 47 patients (20. I%) with 13 subsequent deaths (27.7%; P < 0.001). In patients > 60 years the presence of endoscopic stigmata of recent haemorrhage should lead to early consideration of therapeutic endoscopy and/or early surgery, particularly for ulcers > I cm in size.
Giant Gastric Ulcers: An Unusual Culprit
Digestive Diseases and Sciences
Mycophenolate Mofetil (MMF) is routinely used immunosuppressant in solid organ transplantation is commonly associated with several gastrointestinal (GI) side effects. Here we present a case of giant gastric ulcer of 5 cm from MMF use post cardiac transplant. Case Description A 56-year-old male with history of severe ischemic cardiomyopathy post heart transplant was on immunosuppression with MMF, tacrolimus and prednisone for 5 months. He presented with severe epigastric pain and intermittent episodes of melena for 1 month. His pain radiated to back that is worsened with eating. Associated with loss of appetite, vomiting and 16-pound weight loss in 3 months. He never smoked, drank alcohol or used over the counter pain medications. He was profoundly anemic requiring blood transfusions. EGD performed demonstrated very large clean-based ulcer of 5 cm diameter in the body, smaller ulcer of 8 mm diameter in pre-pyloric region and 5-10 small aphthous ulcers in the gastric body and fundus. Gastric biopsies taken from the ulcer were negative for Helicobacter pylori, cytomegalovirus and malignancy. Flexible sigmoidoscopy revealed non-bleeding inflamed internal hemorrhoids. Consequently, MMF was discontinued and switched to azathioprine. He was treated with twice daily proton pump inhibitor therapy with resolution of abdominal pain, improved appetite and weight gain. Discussion MMF is well known for common GI side-effects such as nausea, diarrhea, vomiting, ulcers, abdominal pain and rarely gastrointestinal bleeding. Few studies reported 3 to 8% incidence of ulcer perforation and GI bleeding within 6 months. Risk of gastroduodenal erosions is nearly 1.83 times for MMF, with the highest lesions associated with MMFtacrolimus-corticosteroid combination treatment as seen in our patient. Hypothesis is that GI tract is vulnerable because of dependence of enterocytes on de novo synthesis of purines, which is disrupted by MMF. Typically, upper GI mucosal injuries of mucosal irritation leading to esophagitis, gastritis and/or ulcers are seen. Endoscopy is both diagnostic and therapeutic if bleeding gastric ulcers are noted. Minor complications improve with reduction of drug dose or use of enteric coated preparation if feasible. Discontinuation of the drug is main stay in the management of MMF related ulcer disease. Simple medical treatment with either H2-receptor antagonists, proton-pump inhibitors, coating agents, prostaglandins or combination has proven effective in most cases. Considering excellent results with medical management of ulcer, role of surgery is limited.