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<article xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" article-type="research-article"><?properties open_access?><front><journal-meta><journal-id journal-id-type="nlm-ta">Korean J Intern Med</journal-id><journal-id journal-id-type="publisher-id">KJIM</journal-id><journal-title-group><journal-title>The Korean Journal of Internal Medicine</journal-title></journal-title-group><issn pub-type="ppub">1226-3303</issn><issn pub-type="epub">2005-6648</issn><publisher><publisher-name>The Korean Association of Internal Medicine</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">19949729</article-id><article-id pub-id-type="pmc">2784974</article-id><article-id pub-id-type="doi">10.3904/kjim.2009.24.4.318</article-id><article-categories><subj-group subj-group-type="heading"><subject>Original Article</subject></subj-group></article-categories><title-group><article-title>Endoscopic Treatment of Dieulafoy Lesions and Risk Factors for Rebleeding</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Lim</surname><given-names>Won</given-names></name><xref ref-type="aff" rid="A1-kjim-24-318"/></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Kim</surname><given-names>Tae Oh</given-names></name><xref ref-type="aff" rid="A1-kjim-24-318"/></contrib><contrib contrib-type="author"><name><surname>Park</surname><given-names>Su Bum</given-names></name><xref ref-type="aff" rid="A1-kjim-24-318"/></contrib><contrib contrib-type="author"><name><surname>Rhee</surname><given-names>Ha Rin</given-names></name><xref ref-type="aff" rid="A1-kjim-24-318"/></contrib><contrib contrib-type="author"><name><surname>Park</surname><given-names>Jin Hyun</given-names></name><xref ref-type="aff" rid="A1-kjim-24-318"/></contrib><contrib contrib-type="author"><name><surname>Bae</surname><given-names>Jung Ho</given-names></name><xref ref-type="aff" rid="A1-kjim-24-318"/></contrib><contrib contrib-type="author"><name><surname>Jung</surname><given-names>Hong Ryeul</given-names></name><xref ref-type="aff" rid="A1-kjim-24-318"/></contrib><contrib contrib-type="author"><name><surname>Kim</surname><given-names>Mi Ra</given-names></name><xref ref-type="aff" rid="A1-kjim-24-318"/></contrib><contrib contrib-type="author"><name><surname>Lee</surname><given-names>NaRiA</given-names></name><xref ref-type="aff" rid="A1-kjim-24-318"/></contrib><contrib contrib-type="author"><name><surname>Lee</surname><given-names>Sun Mi</given-names></name><xref ref-type="aff" rid="A1-kjim-24-318"/></contrib><contrib contrib-type="author"><name><surname>Kim</surname><given-names>Gwang Ha</given-names></name><xref ref-type="aff" rid="A1-kjim-24-318"/></contrib><contrib contrib-type="author"><name><surname>Heo</surname><given-names>Jeong</given-names></name><xref ref-type="aff" rid="A1-kjim-24-318"/></contrib><contrib contrib-type="author"><name><surname>Song</surname><given-names>Geun Am</given-names></name><xref ref-type="aff" rid="A1-kjim-24-318"/></contrib></contrib-group><aff id="A1-kjim-24-318">Department of Internal Medicine, Pusan National University College of Medicine, Busan, Korea.</aff><author-notes><corresp>Correspondence to Tae Oh Kim, M.D. Department of Internal Medicine, Pusan National University College of Medicine, 1-10 Ami-dong, Seo-gu, Busan 602-739, Korea. Tel: 82-51-240-7869, Fax: 82-51-244-8180, <email>kto0440@yahoo.co.kr</email></corresp></author-notes><pub-date pub-type="ppub"><month>12</month><year>2009</year></pub-date><pub-date pub-type="epub"><day>27</day><month>11</month><year>2009</year></pub-date><volume>24</volume><issue>4</issue><fpage>318</fpage><lpage>322</lpage><history><date date-type="received"><day>15</day><month>7</month><year>2008</year></date><date date-type="accepted"><day>18</day><month>4</month><year>2009</year></date></history><permissions><copyright-statement>Copyright &#xA9; 2009 The Korean Association of Internal Medicine</copyright-statement><copyright-year>2009</copyright-year></permissions><abstract><sec><title>Background/Aims</title><p>Dieulafoy lesions are an important cause of upper gastrointestinal bleeding. The purpose of this study was to assess the efficacy of endoscopic treatment for these lesions and to identify the possible predictive factors for rebleeding associated with clinical and endoscopic characteristics.</p></sec><sec><title>Methods</title><p>Records from 44 patients admitted with Dieulafoy bleeding between January 2006 and December 2007 were reviewed. We retrospectively analyzed the clinical and endoscopic findings and then correlated the rebleeding risk factors with Dieulafoy lesions.</p></sec><sec><title>Results</title><p>Primary hemostasis was achieved by endoscopic treatment in 39 patients (88.6%). There were no significant differences between the rebleeding and non-rebleeding groups with respect to age, gender, initial hemoglobin levels, presence of shock, concurrent disease, location of bleeding, or initial hemostatic treatment methods. However, the use of non-steroidal anti-inflammatory drugs or anticoagulants (<italic>p</italic>=0.02) and active stages in the Forrest classification (<italic>p</italic>&lt;0.01) were risk factors for rebleeding after endoscopic therapy.</p></sec><sec><title>Conclusions</title><p>Endoscopic therapy is effective and safe for treating Dieulafoy lesions, and it has both short- and long-term benefits. Early identification of risk factors such as the use of non-steroidal anti-inflammatory drugs or anticoagulants and the Forrest classification of bleeding predict the outcome of Dieulafoy lesions.</p></sec></abstract><kwd-group><kwd>Dieulafoy</kwd><kwd>Gastrointestinal hemorrhage</kwd><kwd>Endoscopy</kwd><kwd>Hemostasis</kwd><kwd>Anticoagulants</kwd></kwd-group></article-meta></front><body><sec sec-type="intro"><title>INTRODUCTION</title><p>Upper gastrointestinal (GI) bleeding is a common medical emergency in clinical practice, and Dieulafoy lesions are an important cause of potentially life-threatening GI bleeding. Typically, these lesions consist of large-caliber submucosal arteries in close contact with the mucosa over a variable distance, and massive bleeding can occur with erosion of the mucosa and arterial wall [<xref ref-type="bibr" rid="B1-kjim-24-318">1</xref>]. These lesions are responsible for 0.5 to 14% of acute upper GI bleeding [<xref ref-type="bibr" rid="B2-kjim-24-318">2</xref>]. Most lesions are located in the proximal stomach, but they can also be found in other GI tract locations [<xref ref-type="bibr" rid="B3-kjim-24-318">3</xref>]. The therapy for this condition has evolved from surgery to endoscopy.</p><p>In addition to the different endoscopic techniques used for GI bleeding, such as injection with or without thermal therapy, mechanical methods such as the use of hemoclips and rubber band ligation have recently been used.</p><p>The aims of the study were to assess the efficacy of endoscopic treatment for Dieulafoy lesions and to identify possible predictive factors for rebleeding in patients with these lesions.</p></sec><sec sec-type="methods"><title>METHODS</title><sec><title>Patients</title><p>Between January 2006 and December 2007, 312 patients with nonvariceal upper GI bleeding were admitted to Pusan National University Hospital. A total of 44 patients with a Dieulafoy lesion in the upper GI tract were examined. After basic life support was provided, all patients underwent emergent endoscopy. All procedures were performed by two expert endoscopists within 12 hours of patient admission. Informed consent was obtained from every patient or from family members. All patients received only topical analgesics and an intravenous proton pump inhibitor. No systemic sedative agent was given to any patient. Follow-up endoscopy was performed within 24 hours of the initial procedure and at 7 days. Patient data were collected during hospitalization and included demographic information, medical history, initial hemodynamic status, laboratory values, endoscopic findings, endoscopic therapy, and outcome (<italic>i.e.</italic>, complications, death, rebleeding, and the need for surgery). Information on rebleeding and mortality following discharge was obtained during follow-up outpatient visits. Because this study was a retrospective review, institutional review board approval was not necessary.</p></sec><sec><title>Definitions</title><p>The endoscopic diagnosis of a Dieulafoy lesion was based on the following established criteria [<xref ref-type="bibr" rid="B3-kjim-24-318">3</xref>]: 1) active arterial spurting or micropulsatile streaming from minute (&lt;3 mm) mucosal defects, 2) visualization of a protruding vessel with or without active bleeding within a minute mucosal defect with normal surrounding mucosa, or 3) a densely adherent clot with a narrow attachment point to a minute mucosal defect or normal-appearing mucosa. Initial hemostatic failure was defined as sustained active bleeding despite initial endoscopic management or any evidence of active bleeding, such as hematemesis, hematochezia, or hemodynamic instability (systolic blood pressure &lt;100 mm Hg, pulse rate &gt;100 beats/minutes, or an orthostatic change in systolic blood pressure &gt;20 mm Hg or a pulse rate &gt;20 beats/minutes) within 12 hours of the initial hemostasis. Rebleeding was suspected in patients with additional episodes of hematemesis or in those with melena, hemodynamic instability, or a decrease in hemoglobin concentration of at least 2 g/dL in 24 hours and diagnosed when the endoscopy showed bleeding from a previously treated lesion.</p></sec><sec><title>Statistical analysis</title><p>The Mann-Whitney test was used to compare the mean values of continuous variables, and Fisher's exact test was used to compare non-ratio variables. The analysis was conducted with SPSS version 13.0 (SPSS Inc., Chicago, IL, USA). A <italic>p</italic> value of less than 0.05 was accepted as statistically significant.</p></sec></sec><sec sec-type="results"><title>RESULTS</title><p>During the study period, 44 Dieulafoy lesions were identified among 312 endoscopies performed for nonvariceal upper GI bleeding (<xref ref-type="table" rid="T1-kjim-24-318">Table 1</xref>). The locations of the bleeding lesions were as follows: proximal stomach, 28; mid-stomach, 6; and distal stomach, 10. In all, 24 patients (54.5%) were bleeding at the time of diagnosis: 4 had spurting, and 20 had an oozing hemorrhage. The remaining 20 patients had a nonbleeding visible vessel or an adherent clot. The following hemostatic methods were used as therapeutic procedures: band ligation (4 patients), hypertonic saline-epinephrine injection (2 patients), hemoclipping (15 patients), and hypertonic saline-epinephrine injection with hemoclipping (23 patients). In the treatment group, primary hemostasis was achieved in 39 patients (88.6%). Five patients with initial failure of hemostasis required emergent transarterial embolization because of continuous bleeding at sites difficult to approach. In three, permanent hemostasis was achieved by transarterial embolization. In addition, two patients received surgery. Seven patients (17.9%) had recurrent bleeding 1-3 days after the initial endoscopic procedure, and another endoscopic hemoclipping or angiography with embolization resulted in permanent hemostasis. There were no significant differences between the rebleeding and non-rebleeding groups with respect to age, gender, initial hemoglobin levels, presence of shock, concurrent disease, bleeding location, or initial hemostatic methods. However, there was a statistically significant difference in the use of non-steroidal anti-inflammatory drugs (NSAIDs) or anticoagulants and in the Forrest classification of bleeding (<italic>p</italic>=0.02 and <italic>p</italic>&lt;0.01, <xref ref-type="table" rid="T2-kjim-24-318">Table 2</xref>). A summary of the management and treatment outcomes is provided in <xref ref-type="fig" rid="F1-kjim-24-318">Fig. 1</xref>. Among the 44 patients discharged from the hospital, 6 were lost to follow-up and 38 were available for assessment. The mean follow-up was 15 months (range, 5 to 29). During the outpatient follow-up, there was no recurrence of bleeding, and there were no procedure-related complications.</p></sec><sec sec-type="discussion"><title>DISCUSSION</title><p>Although Dieulafoy lesions are an uncommon cause of GI bleeding [<xref ref-type="bibr" rid="B4-kjim-24-318">4</xref>], the results of our study show them to be a relatively frequent cause, accounting for 14.1% of nonvariceal upper GI bleeding. As in previous reports, many patients had significant comorbidities, and the ingestion of aspirin, NSAIDs, or warfarin was common. The clinical features of the patients with Dieulafoy lesions were similar to those of patients reported previously [<xref ref-type="bibr" rid="B2-kjim-24-318">2</xref>,<xref ref-type="bibr" rid="B5-kjim-24-318">5</xref>-<xref ref-type="bibr" rid="B8-kjim-24-318">8</xref>].</p><p>Endoscopic therapy, which has emerged as the mainstay for managing Dieulafoy lesions, is safe and highly successful in terms of achieving initial hemostasis [<xref ref-type="bibr" rid="B2-kjim-24-318">2</xref>,<xref ref-type="bibr" rid="B9-kjim-24-318">9</xref>]. There are many reports of successful hemostasis using a variety of endoscopic modalities, including injection of sclerosants [<xref ref-type="bibr" rid="B2-kjim-24-318">2</xref>,<xref ref-type="bibr" rid="B10-kjim-24-318">10</xref>,<xref ref-type="bibr" rid="B11-kjim-24-318">11</xref>], thermal coagulation [<xref ref-type="bibr" rid="B5-kjim-24-318">5</xref>,<xref ref-type="bibr" rid="B10-kjim-24-318">10</xref>], and mechanical methods such as band ligation [<xref ref-type="bibr" rid="B12-kjim-24-318">12</xref>] or hemoclip application [<xref ref-type="bibr" rid="B13-kjim-24-318">13</xref>]. The success rate of various forms of endoscopic therapy range from 75 to 98% [<xref ref-type="bibr" rid="B10-kjim-24-318">10</xref>,<xref ref-type="bibr" rid="B14-kjim-24-318">14</xref>-<xref ref-type="bibr" rid="B16-kjim-24-318">16</xref>]. In the present study, primary hemostasis was achieved in 39 patients (88.6%). If endoscopic therapy fails, management with other options such as transarterial embolization or surgery is indicated. Five patients with initial failure of hemostasis required emergent transarterial embolization and surgery, and all had permanent hemo-stasis. Seven patients (17.9%) had rebleeding 1-3 days after the initial endoscopic procedure, and endoscopic retreatment and transarterial embolization resulted in permanent hemostasis.</p><p>There was a significant difference in the intake of NSAIDs and anticoagulants as well as in the type of bleeding between the rebleeding group and the non-rebleeding group.</p><p>Long-term results for patients treated by endoscopic methods are excellent [<xref ref-type="bibr" rid="B12-kjim-24-318">12</xref>,<xref ref-type="bibr" rid="B17-kjim-24-318">17</xref>,<xref ref-type="bibr" rid="B18-kjim-24-318">18</xref>], and mortality is generally low with prompt diagnosis and treatment. In our study, the mean follow-up was 15 months. During the outpatient follow-up, there was no recurrence of bleeding, and there were no procedure-related complications.</p><p>This study has several limitations. The first limitation is the small sample size and the retrospective design. Medical records that are not designed for research purposes may not include all of the variables of interest or may contain inaccurate descriptions. In addition, there was limited power to show statistical differences because of the small sample size. The second limitation is that this series of patients was enrolled from a single institution and reflected a number of factors associated with this institution; therefore, the post-discharge outcome data may be incomplete. However, we believe that most patients discharged from our hospital would return to the same institution if upper GI bleeding recurred. The third limitation is the impact of treatment. Although we limited the drug options for acute bleeding, the drugs chosen reflect the preferences of the clinical physicians; however, we believe these drug options did not influence the results of the study.</p><p>Despite these limitations, this study remains important for demonstrating the efficacy of endoscopic treatment for Dieulafoy lesions and the factors associated with rebleeding in the context of these patients and the diagnostic and treatment algorithm.</p></sec></body><back><ack><title>Acknowledgements</title><p>This work was supported by clinical research grant from <funding-source>Pusan National University Hospital</funding-source> 2008.</p></ack><ref-list><ref id="B1-kjim-24-318"><label>1</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Veldhuyzen van 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pub-id-type="pmid">15844024</pub-id></element-citation></ref></ref-list></back><floats-group><fig id="F1-kjim-24-318" position="float"><label>Figure 1</label><caption><p>Summary of the management pathways and treatment outcomes.</p><p>HSE, hypertonic saline-epinephrine.</p></caption><graphic xlink:href="kjim-24-318-g001"/></fig><table-wrap id="T1-kjim-24-318" position="float"><label>Table 1</label><caption><p>Endoscopic findings and hemostatic methods</p></caption><graphic xlink:href="kjim-24-318-i001"/><table-wrap-foot><fn><p>HSE, hypertonic saline epinephrine.</p></fn></table-wrap-foot></table-wrap><table-wrap id="T2-kjim-24-318" position="float"><label>Table 2</label><caption><p>Clinical characteristics of the rebleeding and non-rebleeding groups</p></caption><graphic xlink:href="kjim-24-318-i002"/><table-wrap-foot><fn><p>Values are number (%).</p><p>NSAIDs, non-steroidal anti-inflammatory drugs; HSE, hypertonic saline epinephrine; NS, not significant.</p></fn></table-wrap-foot></table-wrap></floats-group></article>
