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UPPER GI BLEEDING

  1. http://www.free-powerpoint-templates-design.com Upper Gastrointestinal Bleeding BAGIAN/SMF ILMU PENYAKIT DALAM FAKULTAS KEDOKTERAN ULM RSUD ULIN BANJARMASIN Oktober, 2022 Pembimbing: dr. Fauzia Noor Liani, Sp. PD, K-EMD, FINASIM Oleh: dr. Muhammad Fazar Adhytia (1930912320063)
  2. Book Reading
  3. Harrison’s Harrison’s Principles Internal Medicine 20th Edition. Section 6 44 Gastrointestinal Bleeding (page 272) Harrison’s Principles Internal Medicine 20th Edition. References References
  4. Anatomy upper gastrointestinal are from mouth-duodenum (part of small intestine). Vascular upper gastrointestinal from superior mesenteric artery branch of aortic abdominal.
  5. Gastrointestinal Bleeding ~1.3. Ratio UGIB and LGIB <3% Fatality of patient hospitalized $4.85 Cost GIB in United States 507.000 Admissions in US Gastrointestinal bleeding (GIB) is the most common gastrointestinal condition leading to hospitalization in the United State. Patients generally die from decompensation of other underlying illnesses rather than exsanguination. Upper GIB (UGIB) incidence has decreased in recent decades, primarily due to decreases in GIB from ulcers
  6. GIB is also categorized by the site of bleeding as UGIB (esophagus, stomach, duodenum), LGIB (colonic), small intestinal, or obscure GIB. Bleeding Gastroinstinal GIB presents as either overt or occult bleeding. Overt GIB is manifested by hematemesis, vomitus of red blood or “coffee-grounds” material; melena, black, tarry stool; and/or hematochezia, passage of red or maroon blood from the rectum. Upper Gastrointestinal Bleeding In the absence of overt bleeding, occult GIB may present with symptoms of blood loss or anemia such as lightheadedness, syncope, angina, or dyspnea; or with iron-deficiency anemia or a positive fecal occult blood test on routine testing.
  7. Upper Gastrointestinal Sources of Bleeding 01 PEPTIC ULCER 02 MALLORY- WEISS TEARS 03 ESOPHAGEAL VARICES 04 EROSIVE DISEASE 05 OTHER Mallory-Weiss tears account for ~2– 10% of UGIB hospitalizations. 02 Erosions are endoscopically visualized breaks which are confined to the mucosa and do not cause major bleeding due to the absence of arteries and veins in the mucosa. 04 The proportion of UGIB hospitalizations due to varices varies widely, from ~2–40%, depending on the population. 03 Peptic ulcers are the most common cause of UGIB, accounting for ~50% of UGIB hospitalizations. 01 Less common causes of UGIB 05
  8. 1. PEPTIC ULCER Peptic Ulcer Endoscopy provide important prognostic. Approximately 20% of patients with bleeding ulcers have the highest risk benefit from endoscopic therapy with bipolar electrocoagulation, heater probe, injection therapy (e.g., absolute alcohol, 1:10,000 epinephrine), reductions in bleeding, hospital stay, mortality, and costs. Three main factors in ulcer pathogenesis, Helicobacter pylori, nonsteroidal anti- inflammatory drugs (NSAIDs), and acid. NSAIDs must be given, a cyclooxygenase (COX)-2 selective NSAID plus a PPI is recommended.
  9. 2. MALLORY- WEISS TEARS Mallory-Weiss tears Mallory-Weiss tears account for ~2–10% of UGIB hospitalizations. The classic history is vomiting, retching, or coughing preceding hematemesis, especially in an alcoholic patient. Bleeding from these tears, which are usually on the gastric side of the gastroesophageal junction, stops spontaneously in 80–90% of patients and recurs in only 0–10%. Endoscopic therapy is indicated for actively bleeding Mallory-Weiss tears.
  10. 3. ESOPHAGEAL VARICES Esophageal Varices The proportion of UGIB hospitalizations, from ~2–40%. Patients with variceal hemorrhage have poorer outcomes. Urgent endoscopy within 12 h is recommended. Combination of endoscopic and medical therapy is superior. Transjugular intrahepatic portosystemic shunt (TIPS) is recommended in persistent or recurrent bleeding. Portal hypertension is also responsible for bleeding from gastric varices.
  11. 4. EROSIVE DISEASE Erosive Disease Erosions are endoscopically visualized breaks the mucosa. Mild UGIB perhaps ~10–15% that hospitalizations ~1–10%. The most important cause of gastric and duodenal erosions is NSAID use: ~50%. Stress-related gastric mucosal injury occurs only in extremely sick patients. Indicate that PPIs are more effective than H2 - receptor antagonists.
  12. 5. OTHER CAUSES Other Causes Less common causes of UGIB include neoplasms, vascular ectasias, gastric antral vascular ectasia, prolapse gastropathy, aortoenteric fistulas, and hemobilia or hemosuccus pancreaticus
  13. Patient without sources of GIB ~75% of GIB previously labeled obscure is now estimated to originate in the small intestine . ~75% of GIB previously labeled obscure is now estimated to originate in the small intestine Small-intestinal Small-intestinal vascular ectasias are treated with endoscopic therapy if possible based on observational studies suggesting initial efficacy. Octreotide, Thalidomide reported significant benefi. Estrogen/progesterone compounds are not recommended for prevention of recurrent bleeding. Sources of Bleeding Small-Intestinal
  14. Gastrointestinal Bleeding Measurement of the heart rate and blood pressure is the best way to initially assess a patient with GIB. Hemoglobin will fall immediately with acute GIB maytake up to 72 h. Transfusion is recommended when the hemoglobin drops below 7 g/dL. Hematemesis indicates an UGIB source. Melena indicates blood has been present in the GI tract for ≥14 h and as long as 3–5 days. When hematochezia is the presenting symptom of UGIB, it is associated with hemodynamic instability and dropping hemoglobin. Get a modern PowerPoint Presentation that is beautifully designed. APPROACH TO THE PATIENT
  15. Figure 44-1 Suggested algoritm for patien with acute upper gastrointestinalbleeding based on endoscopic findings. A nonbloody nasogastric aspirate may be seen in ~15% of patients with UGIB. A bilestained appearance does not exclude UGIB because reports of bile in the aspirate are incorrect in ~50% of cases.
  16. Table 44-1 Glasgow-Blatchford Score Discharge from the emergency room with outpatient management has been suggested for patients with a Glasgow-Blatchford score (possible range 0–23) of 0–1 or 0–2 among patients. 1. PPI infusion may be considered at presentation: it decreases highrisk ulcer stigmata. 2. The promotility agent erythromycin, 250 mg intravenously ~30 min before endoscopy. 3. Antibiotics decrease bacterial infections, rebleeding, and mortality, and vasoactive medications. 4. Upper endoscopy should be performed within 24 h in most patients with UGIB. 5. Patients at higher risk may urgent endoscopy within 12 h.
  17. • Angiography as the initial test, with CT angiography or 99mTc-labeled red cell scan suggest to massive bleeding suspected from the small intestine. • CT enterography may be used initially, and may follow a negative video capsule for suspected small-intestinal GIB, given its higher sensitivity for small-intestinal masses. • “Deep” enteroscopy (double-balloon, single-balloon, or spiral enteroscopy) is commonly the next test undertaken for clinically important GIB. Fecal occult blood testing is recommended only for colorectal cancer screening, beginning at age 50 in average-risk adults. A positive test necessitates colonoscopy. If evaluation of the colon is negative, further workup is not recommended unless iron- deficiency anemia or GI symptoms are present. EVALUATION AND MANAGEMENT OF SMALL- INTESTINAL OR OBSCURE GIB
  18. Daftar Pustaka 1. De Franchis R: Expanding consensus in portal hypertension. J Hepatol 63:743, 2015. 2. Garcia-Tsao G et al: Portal hypertensive bleeding in cirrhosis: Risk stratification, diagnosis, and management: 2016 practice guidance by the American Association for the Study of Liver Diseases. Hepatology 65:310, 2017. 3. Gerson LB et al: ACG clinical guideline: Diagnosis and management of small bowel bleeding. Am J Gastroenterol 110:1265, 2015. 4. Gralnek IM et al: Diagnosis and management of upper gastrointestinal hemorrhage: European Society of Gastrointestinal Endoscopy (ESGE) guideline. Endoscopy 47:1, 2015. 5. Laine L: Upper gastrointestinal bleeding due to a peptic ulcer. N Engl J Med 374:2367, 2016. 6. Laine L, Jensen DM: ACG Practice Guidelines: Management of patients with ulcer bleeding. Am J Gastroenterol 107:345, 2012. 7. Strate LL, Gralnek KM: ACG clinical guideline: Management of patients with acute lower gastrointestinal bleeding. Am J Gastroenterol 111:459, 2016. 8. Sung JJ et al: Continuation of low-dose aspirin therapy in peptic ulcer bleeding: A randomized trial. Ann Intern Med 152:1, 2010. 9. Villaneuva C et al: Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med 368:11, 2013. Get a modern PowerPoint Presentation that is beautifully designed.
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Hinweis der Redaktion

  1. Gastrointestinal bleeding (GIB) is the most common gastrointestinal condition leading to hospitalization in the United States, accounting for over 507,000 admissions and $4.85 billion in direct costs annually. Upper GIB (UGIB) incidence has decreased in recent decades, primarily due to decreases in GIB from ulcers. The ratio of UGIB to lower GIB (LGIB) among GIB admissions from U.S. emergency rooms is ~1.3. The case fatality of patients hospitalized with GIB has also decreased and is in the United States. Patients generally die from decompensation of other underlying illnesses rather than exsanguination. GIB presents as either overt or occult bleeding. Overt GIB is manifested by hematemesis, vomitus of red blood or “coffee-grounds” material; melena, black, tarry stool; and/or hematochezia, passage of red or maroon blood from the rectum. In the absence of overt bleeding, occult GIB may present with symptoms of blood loss or anemia such as lightheadedness, syncope, angina, or dyspnea; or with iron-deficiency anemia or a positive fecal occult blood test on routine testing. GIB is also categorized by the site of bleeding as UGIB (esophagus, stomach, duodenum), LGIB (colonic), small intestinal, or obscure GIB (if the source is unclear).
  2. Recent meta-analysis of randomized trials documents that high-dose intermittent PPIs are non-inferior to constant-infusion PPI therapy and thus may be substituted in this population. Patients with lower-risk findings (flat pigmented spot or clean base) do not require endoscopic therapy and receive standard doses of oral PPI. Approximately 10–50% of patients with bleeding ulcers will rebleed within the next year if no preventive strategies are employed. Prevention of recurrent bleeding focuses on the three main factors in ulcer pathogenesis, Helicobacter pylori, nonsteroidal anti-inflammatory drugs (NSAIDs), and acid. Eradication of H. pylori in patients with bleeding ulcers decreases rebleeding rates to <5%.
  3. Recent meta-analysis of randomized trials documents that high-dose intermittent PPIs are non-inferior to constant-infusion PPI therapy and thus may be substituted in this population. Patients with lower-risk findings (flat pigmented spot or clean base) do not require endoscopic therapy and receive standard doses of oral PPI. Approximately 10–50% of patients with bleeding ulcers will rebleed within the next year if no preventive strategies are employed. Prevention of recurrent bleeding focuses on the three main factors in ulcer pathogenesis, Helicobacter pylori, nonsteroidal anti-inflammatory drugs (NSAIDs), and acid. Eradication of H. pylori in patients with bleeding ulcers decreases rebleeding rates to <5%.
  4. Patients with variceal hemorrhage have poorer outcomes than patients with other sources of UGIB. Urgent endoscopy within 12 h is recommended in cirrhotics with UGIB, and if esophageal varices are present, endoscopic ligation is performed and an IV vasoactive medication (octreotide, somatostatin, vapreotide, terlipressin) is given for 2–5 days. Transjugular intrahepatic portosystemic shunt (TIPS) is recommended in patients who have persistent or recurrent bleeding despite endoscopic and medical therapy. TIPS should also be considered in the first 1–2 days of hospitalization for acute variceal bleeding in patients with advanced liver disease (e.g., Child-Pugh class C with Child-Pugh score 10–13), because randomized trials show significant decreases in rebleeding and mortality compared with standard endoscopic and medical therapy. Portal hypertension is also responsible for bleeding from gastric varices, varices in the small and large intestine, and portal hypertensive gastropathy and enterocolopathy. Bleeding gastric varices due to cirrhosis are treated with endoscopic injection of tissue adhesive (e.g., n-butyl cyanoacrylate), if available; if not, TIPS is performed.
  5. Erosions are endoscopically visualized breaks which are confined to the mucosa and do not cause major bleeding due to the absence of arteries and veins in the mucosa. Erosions in the esophagus, stomach, or duodenum commonly cause mild UGIB, with erosive gastritis and duodenitis accounting for perhaps ~10–15% and erosive esophagitis (primarily due to gastroesophageal reflux disease) ~1–10% of UGIB hospitalizations. The most important cause of gastric and duodenal erosions is NSAID use: ~50% of patients who chronically ingest NSAIDs may have gastric erosions. Other potential causes of gastric erosions include alcohol intake, H. pylori infection, and stressrelated mucosal injury. Stress-related gastric mucosal injury occurs only in extremely sick patients, such as those who have experienced serious trauma, major surgery, burns covering more than one-third of the body surface area, major intracranial disease, or severe medical illness (i.e., ventilator dependence, coagulopathy). Severe bleeding should not develop unless ulceration occurs. The mortality rate in these patients is high because of their serious underlying illnesses. The incidence of bleeding from stress-related gastric mucosal injury has decreased dramatically in recent years, most likely due to better care of critically ill patients. Pharmacologic prophylaxis for bleeding may be considered in the high-risk patients mentioned above. Meta-analyses of randomized trials indicate that PPIs are more effective than H2 -receptor antagonists in reduction of overt and clinically important UGIB without differences in mortality or nosocomial pneumonia
  6. Less common causes of UGIB include neoplasms, vascular ectasias (including hereditary hemorrhagic telangiectasias [Osler-Weber-Rendu] and gastric antral vascular ectasia [“watermelon stomach”]), Dieulafoy’s lesion (in which an aberrant vessel in the mucosa bleeds from a pinpoint mucosal defect), prolapse gastropathy (prolapse of proximal stomach into esophagus with retching, especially in alcoholics), aortoenteric fistulas, and hemobilia or hemosuccus pancreaticus (bleeding from the bile duct or pancreatic duct).
  7. Patients without a source of GIB identified on upper endoscopy and colonoscopy were previously labeled as having obscure GIB. With the advent of improved diagnostic modalities, ~75% of GIB previously labeled obscure is now estimated to originate in the small intestine beyond the extent of a standard upper endoscopic exam. Small-intestinal GIB may account for up to ~5–10% of GIB cases. The most common causes in adults >40 years are vascular ectasias, neoplasm (e.g., GI stromal tumor, carcinoid, adenocarcinoma, lymphoma, metastases), and NSAID-induced erosions and ulcers. Meckel’s diverticulum is the most common cause of significant small-intestinal GIB in children, decreasing in frequency as a cause of bleeding with age.
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