GIT Kurdistan Board GEH Journal club Lower GIB 2014.

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GIT Kurdistan Board GEH Journal club; Lower GIB ASGE Guidelines 2014.

Transcript of GIT Kurdistan Board GEH Journal club Lower GIB 2014.

  • 1.Dealing with LGIB:Overview LGIB Algorhythm Causes Endoscopic interventions Recommend ations

2. Lower GIB: Overview F Introduction A Aetiologies S Management algorythms T Endoscopic hemostasis 3. Introduction: LGIB is diagnosed in 20-30% of all patients presenting with major GI bleeding. The annual incidence is 0.03%. increases * 200 from 2nd- 8th decades of life. The mean age at presentation is 63 - 77 years. A full-time gastroenterologist manages >10 cases/ year. Blood loss can be trivial or massive & life-threatening, but the majority have self-limited& uncomplicated hospitalization. LGIB tend to present with a higher Hb &less likely to develop hypotensive shock or require blood transfusions. Mortality is 2- 4%, usually from comorbidities& noscom infs. Reported decreased incidence of LGIB & lower age/gender- adjusted fatality rate over the past decade. 4. Definitions: Before deep enteroscopy: Bleeding from a source distal to the ligament of Treitz Now: bleeding from a source distal to ICV. Now small-bowel sources called midgut bleeding. Acute LGIB: of recent duration (50 ys, to 60% >80 ys. Accounts for 20- 65% of acute LGIB episodes. Clinically significant bleeding occurs in 3-15% with colon diverticula, usually as a result of trauma to the vasa recta at the neck or dome of the diverticulum. NSAIDs increase the risk for diverticular bleeding. Hypertension&anticoagulation also may contribute to severe bleeding. 6. Diverticular bleeding: The clinical presentation: Painless hematochezia, resolves spontaneously in 75-80% but recurs in 25-40% within 4 years. Early rebleeding is uncommon after endoscopic treatment. Using epinephrine/or thermal coagulation early (2/3 of these lesions are seen in > 70 years. Angioectasias are caused by degenerative changes& chronic intermittent low-grade obstruction in the submucosal vessels. They are located predominantly in the cecum & the ascending colon. Multiple angioectasias may be seen on colonoscopy appear as red, flat lesions, 2 mm- several cms, with ectatic blood vessels radiating from a central feeding vessel 12. Angioectasias(angiodysplasias): Risk factors include: Advanced age, comorbidities, the presence of multiple angioectasias & the use of anticoagulants or antiplatelet agents. Patients can present with occult bleeding, melena, or painless intermittent hematochezia. Colonoscopy has a sensitivity of 80% for detection of angioectasias. Narcotics for sedation may reduce mucosal blood flow and impair the detection of these lesions at colonoscopy. Bleeding from angioectasias in AS( Heyde syndrome) explained that severe AS may result in type 2 VWD, which precipitates bleeding in patients with underlying angioectasias. There is a high rebleeding rate despite endoscopic treatment& defi nitive management may involve AV replacement. 13. Hemorrhoids: Aplexus of dilated AV vessels that arise from the superior & inferior hemorrhoidal veins,located in the submucosa of the distal rectum classified as internal or external, based on their location relative to the dentate line. Although may be present in up to 75% with LGIB, the majority are considered incidental findings. Hemorrhoidal bleeding accounts for only 2- 10- 24- 64.4% of acute LGIB or hematochezia. Patients typically present with painless, intermittent, scant hematochezia characterized by bright red blood on the toilet paper, coating the stool, or dripping into the toilet bowl. 14. CR neoplasias: Bowel habit changes&weight loss should raise suspicion for a colorectal neoplasia&prompt colonoscopy in patients with LGIB. Accounts for up to 17% of GIB & presents more commonly with occult bleeding. Acute LGIB associated with colorectal neoplasia usually results from surface ulcerations of an advanced tumor. Patients with tumors in the right side of the colon are more likely to present with occult blood loss &IDA whereas those with left-sided tumors more commonly present with hematochezia. Endoscopic hemostasis is rarely required because bleeding is slow in the majority. 15. Postpolypectomy bleeding: Account for 2- 8% of acute LGIB, 8.7/1000 procedures. 16. NSAID use : Associated with increased risk of LGIB, including DD. NSAID users had a significantly higher incidence of lower GI adverse events, including bleeding The prevalence of NSAID use is up to 86% LGIB. Mechanisms not well understood: local mucosal trauma &platelet inhibition in susceptible individuals & concomitant use of warfarin&other antiplatelets. Use of NSAIDs is associated with exacerbations of IBD. NSAIDs can induce NSAID colopathy, which may be misdiagnosed as IBD, characterized by colon ulcerations and diaphragm-like strictures, predominantly located in the terminal ileum& right side of the colon. NSAID colopathy may be associated with LGIB &perforation. 17. Rectal ulcers : 8% of severe hematochezia&32% LGIB after ICU admissions for other critical illnesses. Patients often have major medical comorbidities: ESRD on HD Respiratory failure requiring mechanical ventilation, Decompensated cirrhosis Malignancy. Endoscopic findings:clean-based ulcers (82%),adherent clots (17%),nonbleeding visible vessels (33%),active bleeding (50%). Early rebleeding after endoscopic treatment is 44% -48% &mortality rate of 33-48% in high-risk stigmata who have multiple comorbidities. 18. Radiation proctopathy: LGIB occurs in 4-13% with rad colitis. This disorder is caused by radiation-induced endarteritis obliterans, which results in neovascularization& telangioectasias in the rectum. 19. IBD: Commonly present with LGIB. Acute LGIB requiring hospitalization is uncommon & reported to account for only 1.2-6% of all admissions in patients with Crohn s disease &0.1- 4.2% in patients with ulcerative colitis. Clinically significant bleeding in Crohn s disease is more common in patients with colon involvement than in those with isolated small-bowel disease. Bleeding resolves spontaneously in up to 50% of patients, but there is a recurrence rate of up to 35%. Medical management with biologics can be effective in the management. 20. HIV: LGIB occurs in 2.6% of patients with HIV, usually in the setting of AIDS-related thrombocytopenia&associated with an inpatient mortality rate of 28%. The most common etiologies of LGIB in these patients are opportunistic infections, including cytomegalovirus, herpes simplex virus, Kaposi s sarcoma& idiopathic proctocolitis. 21. U& SI source of LGIB : UGI source may be present in 11- 15% of patients with suspected LGIB Small-bowel sources constitute 2-15% of cases. 22. Management: Resuscitation/ evaluation Initial assessment: whether or not an urgent intervention is necessary. The majority, manifesting as occult fecal blood or scant hematochezia, can be managed electively in OP. Patients presenting with acute LGIB with melena or hematochezia usually require inpatient management, because the majority are elderly with significant comorbidities. Should undergo stabilization&resuscitation with crystalloids or blood products. Coagulation factors &platelets may be necessary in patients who are on antithrombotics or with underlying bleeding disorders. 23. Management: Resuscitation/ evaluation ICU admission: Clinical evidence of ongoing or severe bleeding. Transfusion > 2 units of packed RBCs Significant comorbidities. NGT lavage to exclude an upper GI bleeding source should be considered in patients presenting with hematochezia & hemodynamic instability. An actively bleeding upper GI source is unlikely if bile is seen in NG Lavage, but it cannot be ruled out with clear aspirate. A targeted history: NSAID use, prior bleeding episodes, recent polypectomy, radiation therapy for prostate or pelvic malignancies, IBD, CRC risk. 24. Management: Resuscitation/ evaluation Risk stratification: High risk of severe bleeding 80%: > 3 the following RFs. Moderate risk (45%) with 1-3 RFs. Low risk No Rfs (< 10%):. HR 100/minute, systolic blood pressure % 115 mm Hg, syncope, nontender abdominal exam, rectal bleeding during the first 4 hours of evaluation, aspirin use, multiple comorbid illnesses. 25. Management: Resuscitation/ evaluation Another model: independent predictors of severe LGIB. Initial hematocrit! 35%, presence of abnormal vital signs (SBP 100/minute) 1 hour after initial medical evaluation& gross blood on initial rectal exam. Kollef et al100 developed and validated another BLEED model; Outcome prediction tool for UGIB&LGIB: predict resource utilization& inpatient adverse events, including mortality. Ongoing bleeding, low SBP, elevated PT, erratic mental status, &unstable comorbid illness. 26. Occult GI bleeding Colonoscopy for evaluation of underlying CR neoplasia. CT colonography may be an alternative if high risk for colonoscopy-related adverse events& for the detection of proximal lesions in those who have had an incomplete colonoscopy. An EGD should be considered if a bleeding source is not identifi ed in the colon, especially in those patients with upper GI symptoms, IDA, or NSAID use( overall yield 13- 41%, with PUD &esophagitis) Small-bowel evaluation if fecal occult blood&persistent anemia, after negative EGD &colonoscopy. 27. Melena: EGD is the initial test in the evaluation of melena Melena also may result from slow bleeding emanating from the colon or small-bowel. Colonoscopy should, be pursued after negative EGD. Persistent melena after negative results with bidirectional endoscopy warrant small-bowel endoscopy. 28. Intermitent scant hematochesia: Is the most common pattern of LGIB. Usually is caused by an anorectal or distal colon source A digital rectal exam&flexible sigmoidoscopy ( yield of 9-58%), with or without anoscopy, may be suffici