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SSAT Articles Etiology, Treatment, and Outcome of Esophageal Ulcers: a 10-Year Experience in an Urban Emergency Hospital

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SSAT Articles Etiology, Treatment, and Outcome of Esophageal Ulcers: a 10-Year Experience in an Urban Emergency Hospital SSAT Articles Etiology, Treatment, and Outcome of Esophageal Ulcers: A 10-Year Experience in an Urban Emergency Hospital Daisuke Higuchi, M.D., Choichi Sugawa, M.D., Sachin H. Shah, M.D., Satoshi Tokioka, M.D., Charles E. Lucas, M.D. Esophageal ulcers are a rare cause of upper gastrointestinal bleeding. This report describes the etiology, treatment, complications, and outcome of esophageal ulcers. An esophageal ulcer is defined as a discrete break in the esophageal mucosa with a clearly circumscribed margin; esophageal ulcers were seen in 88 patients from a total of 7564 esophagogastroduodenoscopies done by one surgeon at an urban hospital from 1991 to 2001. All hospital reports were reviewed. The etiology of esophageal ulcers included the following: gastrointestinal reflux disease (GERD) (n ϭ 58, 65.9%), drug induced (n ϭ 20, 22.7%), candidal (n ϭ 3, 3.4%), caustic injury (n ϭ 2, 2.3%), and herpes simplex virus (HSV), human immunodeficiency virus (HIV), marginal ulcer, foreign body, and unknown etiology (n ϭ 1 of each, 1.1%). The mean size of GERD-induced esophageal ulcers and drug-induced esophageal ulcers was 2.78 and 2.92 cm, respectively; 80.3% of GERD-induced esophageal ulcers and 13.8% of drug-induced esophageal ulcers were located in the lower thoracic esophagus. Morbidity (n ϭ 44, 50%) included hemorrhage (n ϭ 30, 34%), esophageal stricture (n ϭ 11, 12.5%), and esophageal perforation (n ϭ 3, 3.4%). Nonoperative therapy sufficed in 81 patients (92%). Three patients (3.4%) had a recurrence of esophageal ulcers. Fifteen patients (17.0%) required endoscopic intervention including esophageal dilatation for stricture in 11 patients and endoscopic hemostasis for esophageal bleeding in four patients. Surgery (n ϭ 7, 8.0%) was reserved for esophageal stricture and perforation. Two patients (2.3%) died from complications of esophageal ulcers: hemorrhage in one and perforation in one. Three patients died of their primary disease. GERD and drug ingestion are common causes of esophageal ulcers. Midesophageal ulcers have a greater tendency to hemorrhage compared with ulcers at the gastroesophageal junction; this may reflect the etiology. Strictures complicate GERD-induced esophageal ulcers but not drug-induced esophageal ulcers. Esophageal dilatation is an effective treatment for most stric- tures associated with esophageal ulcers. Esophageal ulcers rarely cause death. (J GASTROINTEST SURG 2003;7:836–842) Ć 2003 The Society for Surgery of the Alimentary Tract KEY WORDS: Esophageal ulcers, etiology, treatment outcome Esophageal ulcers most commonly occur as a result in demographics, diagnostic modalities, and thera- of gastroesophageal reflux disease (GERD) with a peutic interventions. Esophageal ulcers secondary to reported prevalence of 2% to 7%.1,2 Because of the nonsteroidal anti-inflammatory drugs (NSAIDs), an- rarity of these ulcers, there is little comprehensive lit- tibiotics, radiation therapy, Crohn’s disease, and der- erature regarding etiology and clinical course. Tiles- matologic diseases have also been reported.1,2 More ton,3 in 1906, identified the causes of esophageal recently esophageal ulcers due to cytomegalovirus, ulcers—namely, peptic ulcer disease, carcinoma, cor- herpes simplex virus, and human immunodeficiency rosive substances, foreign body, infectious disease, virus have become more prevalent.2,4,5 This report aneurysm, catarrhal, traction diverticula, tuberculo- defines the incidence, etiology, treatment, and sis, syphilis, esophageal varices, and thrush. Since outcome of esophageal ulcers seen in a large urban then, the etiology has changed reflecting differences medical center. Presented at the Forty-Fourth Annual Meeting of The Society for Surgery of the Alimentary Tract, Orlando, Florida, May 18–21, 2003 (poster presentation). From the Department of Surgery (D.H., C.S., S.H.S., S.T., C.E.L.), Wayne State University School of Medicine, Detroit, Michigan. Reprint requests: Choichi Sugawa, M.D., 6C UHC, 4201 St. Antoine, Detroit, MI 48201. e-mail: [email protected] Ć 2003 The Society for Surgery of the Alimentary Tract 1091-255X/03/$—see front matter 836 Published by Elsevier Inc. doi:10.1016/S1091-255X(03)00138-0 Vol. 7, No. 7 2003 Etiology and Outcome of Esophageal Ulcers 837 METHODS heavy alcohol consumption within 24 hours of admis- sion occurred in 32 patients (36.4%); 35 patients This study was performed at Detroit Receiving (39.8%) smoked cigarettes daily or used illicit street Hospital, a large urban teaching emergency trauma drugs such as cocaine or heroin mix daily (n ϭ 4, hospital. Review of 7564 consecutive esophagogastro- 4.5%). Nonsteroidal anti-inflammatory agents or cly- duodenoscopies (EGDs) performed by a single surgi- cooxygenase-2 (COX-2) inhibitors had been re- cal endoscopist from August 1991 to June 2001 cently used in 28 patients (31.8%). H blockers or identified 88 patients (1.2%) with esophageal ulcers. 2 proton pump inhibitors had been used recently in 20 The records of all of these patients were reviewed. patients (22.7%). All 88 of these patients were part of a subgroup of Most patients (79, 89.8%) were initially seen in 3520 patients who had endoscopically diagnosed the emergency room for evaluation. Esophageal ulcers esophagitis. Esophageal ulcer was defined as a discrete were found in 79 patients during the initial EGD. break in the esophageal mucosa with a clearly identi- The esophageal ulcers in the remaining nine patients fiable margin. The term erosion refers to a superficial developed in the hospital while these patients were lesion that remains confined to the lamina propria being treated for another condition. The duration of and muscularis mucosae. In contrast, necrosis, hem- symptoms was less than 3 days in 43 patients, and more orrhage, and inflammation associated with ulcers than 10 days in 20 patients. These signs and symp- extend deeper into the underlying submucosa or toms included the following: hematemesis (n ϭ 36, muscularis propria. Erosions or ulcers may appear 40.9%), nausea and vomiting with regurgitation isolated or confluent, and they commonly coexist with (n ϭ 35, 39.8%), epigastric (with or without subster- one another.6 The etiology of esophageal ulcers was nal) pain (n ϭ 27, 30.7%), melena (n ϭ 22, 25%), ascertained from clinical, endoscopic, and pathologic dysphagia to solids (n ϭ 16, 18.2%), “coffee ground” findings. Data recorded included: history of caustic gastric aspirate (n ϭ 15, 17.0%), and chest pain that ingestion, location of the ulcer, morphology of the was substernal with extension to the back (n ϭ 10, ulcer, previous EGD findings and pictures, concur- 11.4%). The chest pain was thought to be a manifesta- rent EGD findings and pictures, and comorbid condi- tion of heartburn due to regurgitation. Esophageal tions. Biopsy specimens were obtained from both the ulcerswere foundon thefirst endoscopic assessmentin center and the margin of the ulcer. EGD examina- 79 patients, whereas esophageal ulcers were first tions were performed with Olympus flexible video seen on a follow-up endoscopy in nine patients. endoscopes. Esophageal ulcers after sclerotherapy Most patients (n ϭ 74, 84.1%) required in-hospital and those associated with esophageal malignancy treatment at the time of the initial diagnostic EGD. were excluded from this analysis. Eight patients (9.1%) required repeat EGD evalua- tion for esophageal ulcers or their complications after discharge. RESULTS Etiology of Esophageal Ulcers Patient Profile The etiology of esophageal ulcers (Table 1)was Of the 88 patients with esophageal ulcers, 56 were most commonly associated with GERD (n ϭ 58). All men (63.6%), and 32 were women (36.4%) with a patients with esophageal ulcers caused by GERD had a mean age of 56.4 years (Ϯ16 years standard deviation [SD]). Comorbid conditions included: hypertension Table 1. Etiology of esophageal ulcers (n ϭ 33, 37.5%), diabetes mellitus (n ϭ 18, 20.5%), central nervous system disorders such as cerebrovas- Etiology No. of patients % cular accident and head trauma (n ϭ 16, 18.2%), GERD 58 65.9 peptic ulcer disease including four patients with gas- Drug-induced 20 22.7 tric ulcers, three patients with duodenal ulcers, and Candida 3 3.4 one patient with both gastric and duodenal ulcers Caustic injury 2 2.3 (n ϭ 8, 9.1%), congestive heart failure (n ϭ 8, 9.1%), AIDS 1 1.1 cirrhosis (n ϭ 6, 6.8%), pneumonia (n ϭ 5, 5.7%), Herpes simplex virus 1 1.1 asthma (n ϭ 5, 5.7%), recurrent episodes of acute Marginal 1 1.1 pancreatitis (n ϭ 5, 5.7%), and renal failure (n ϭ 4, Foreign body 1 1.1 4.5%). Eight patients (9.1%) were bedridden. A his- Unknown 1 1.1 tory of chronic, moderate, daily drinking or heavy Total 88 100 (more than 8 ounces of alcohol per day) alcohol con- GERD ϭ gastrointestinal reflux disease; AIDS ϭ acquired immune sumption was given in 40 patients (45.5%), and recent deficiency syndrome. Journal of 838 Higuchi et al. Gastrointestinal Surgery definite hiatal hernia. Hiatal hernia was diagnosed Table 3. Endoscopic morphology of esophageal ulcers endoscopically when the squamocolumnar junction GERD Drug was more than 3 cm above the diaphragmatic impres- 7 sion. In moderate-sized or large hiatal hernias, the Location gastric mucosal folds can be seen running proximally Upper third 2 (3.4%) 9 (4.9%) over the hiatal margin into the bulbous cavity of the Middle third 11 (19.0%) 16 (80.0%) distended hernia pouch. A hiatal hernia is also con- Lower third 53 (91.4%) 4 (20.0%) firmed based on a retroflexed endoscopic view of the Total 66 29 hernia pouch and the squamocolumnar junction from Size below.7 All 58 patients with ulcer associated with Minimum 0.6 cm 0.6 cm hiatal hernia had moderate-sized or large hiatal Maximum 10.0 cm 6.0 cm Mean Ϯ SD 2.78 cm Ϯ 2.13 2.92 cm Ϯ 1.98 hernias.
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