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A. Symptoms and Signs navigator

  1. Hematemesis
  2. Melena
  3. Pain: usually epigastric, burning
  4. Orthostatic Hypotension
  5. Anemia (may be only sign)
    1. May be only manifestation of an upper or lower GI bleed
    2. About ~60% of adults with Iron deficiency anemia have a GI source for blood loss
    3. Peptic ulcer is most common cause or upper GI bleed in iron deficiency anemia
    4. Neoplasms on colonoscopy most common cause of lower GI bleed in iron deficiency anemia
    5. In patients with iron deficiency of unknown cause, GI evaluation should be done
  6. Positive fecal occult blood tests do occur with upper GI bleeding [18]

B. Causes of UGI Bleeding navigator

  1. Esophageal (uncommon)
    1. Reflux (GERD) - uncommon
    2. Diverticulum (Zenker's) - uncommon
    3. Carcinoma - more common
    4. Mallory-Weiss Tare - particularly with recurrent vomiting (~5%)
    5. Esophageal Varices - common (~10%) [2]
    6. Arteriovenous malformation - uncommon
  2. Stomach (common)
    1. Erosion
    2. Ulceration - most common cause (~34%)
    3. Carcinoma
    4. Juvenile capillary hemangiomas of the stomach may lead to hematemesis [22]
    5. Majority of bleeding ulcer cases are associated with NSAID use (risk >4 fold) [14]
    6. Helicobacter pylori (H. pylori) infection is also prevalent and contributory
    7. Gastric ischemia can lead to recurrent ulceration and malabsorption [9]
  3. Duodenum (common)
    1. Peptic Ulcer Disease (PUD) - very common cause (~28%)
    2. H. pylori associated PUD (particularly with concomitant aspirin use) [5]
    3. NSAID associated PUD
    4. Invasive Metastatic Carcinoma
  4. Risk Factors for NSAID-Associated Gastroduodenal Ulcers [19]
    1. Advanced age (linear increase)
    2. History of ulcer
    3. Concomitant use of glucocorticoids
    4. Higher doses of NSAIDs / use of >1 NSAID at a time
    5. Ketorolac and piroxicam have highest risk; ibuprofen low risk, naproxen modest risk [21]
    6. Concomitant administration of warfarin or other anticoagulants
    7. Serious underlying systemic disorder, especially liver disease
    8. Concomitant infection with H. pylori may be a risk factor (see above)
    9. Use of nitrovasodilator (nitrates) drugs had 40% reduced risk of GI bleeding [6]
    10. Cigarette smoking and alcohol consumption may be risk factors
  5. Post-Operative Bleeding
  6. Mesenteric Ischemia
    1. Uncommon cause of upper GI bleeding
    2. Usually older persons
    3. Coagulopathy or heart failure often present
  7. Crohn's Disease with ulceration
  8. Diverticulosis (very uncommon cause for UGI bleeding)
  9. Arteriovenous Malformations (AVM) in UGI Tract
    1. Fairly common cause of upper GI bleeding
    2. Most commonly arises spontaneously in renal failure patients
    3. Most common cause of obscure GI bleeding
    4. These small intestinal AVM's are located in proximal jejunum
    5. These are treated by electrocautery
  10. Diffuse AVM's [11]
    1. More common in patients with chronic renal failure than in general population
    2. Also occur in hereditary hemorrhagic telangiectasia (Rendu-Osler-Weber Syndrome)
    3. Estrogen therapy significantly decreases transfusion requirements
    4. Doses typical for oral contraceptives: 50µg ethinylestradiol + 1mg norethistrone daily
    5. In patients with idiopathic diffuse AVM's, hormonal therapy is not useful

C. Risk Factors for Serious Upper GI Bleeding [17]navigator

  1. Cardiac Disease - arrhythmias, acute MI, angina, congestive heart failure
  2. Hepatic Disease - acute alcoholic hepatitis, cirrhosis
  3. Pulmonary - acute respiratory failure, pneumonia, COPD/asthma
  4. Renal Disease - serum creatinine >4mg/dL or dialysis
  5. Neurologic Disease - delirium, dementia, stroke within 6 months
  6. Malignancy - known solid tumor
  7. Other - sepsis, major surgery within 30 days, age >60, abnormal hemostatic parameters
  8. Endoscopically documented serious bleeding
  9. Patients can be risk stratified based on number of risk factors for serious bleeding
  10. Patients with 3 or more risk factors shouldbe observed for several days in hospital

D. Diagnosis of UGI Bleeding navigator

  1. Emergent endoscopy is critical test to determine cause [20]
  2. Hematocrit, coagulation parameters (PT, PTT, platelet count) are done
  3. Type and cross match >3 units of blood
  4. Nasogastric tube is usually placed (unless coagulopathy present)
  5. Orthostatic vital signs should be assessed if resting blood pressure is normal
  6. Stool Fecal Occult Blood (FOB) [2,18]
    1. Critical for evaluation of ANY patient with potential GI bleeding
    2. Several types of tests for FOB are available
    3. Guaiac-based, heme-porphyrin, and immunochemical tests
    4. The older guaiac tests have false positive results with non-human hemoglobin, dietary peroxidases, and rehydration therapy
    5. False negative stool guaiac tests from hemoglobin degradation, vitamin C, storage
    6. Newer tests have reduced false positives and negatives
    7. About 60% of positive fecal occult blood tests are due to upper GI bleeds
    8. Esophagitis, gastric ulcer, gastritis and duodenal ulcer all found with positive screens
  7. Risk Score for Aggressive Treatment of UGI Bleed [27]
    1. Combination of admission: hemoglobin, blood urea nitrogen, systolic blood pressure
    2. Presence with syncope or melana
    3. Evidence of hepatic disease or cardiac failure
    4. All of these are combined to provide a score with ROC curve area of 0.92 (best is 1.00)
    5. Strongly consider this stratification scheme in new patients with UGI bleeding
  8. H. pylori [20]
    1. H. pylori testing should be done on all patients with upper GI bleeding
    2. Eradication of H. pylori infection in any postivie patient
  9. Patient receives nothing by mouth (NPO)

E. Treatment of UGI Bleeding [20]navigator

  1. Assessment of risk score (see above) will aid in triage [27]
  2. Early Endoscopy is usually standard of care
    1. Endoscopy is best modality for diagnosis
    2. Also useful in most instances for treatment
    3. Endoscopic hemostasis for aptients with high-risk endoscopic lesions
    4. In high risk patients, combination of injection and thermal coagulation
    5. Endoscopic clips also appear promising for hemostasis
    6. Routine second look endoscopy is not recommended
  3. Rapid, Multidisciplinary Initiation of Therapy
    1. Fluids should be given intravenously (IV)
    2. Normal saline and/or Ringers' Lactate (if acidosis present) may be used
    3. Red blood cell transfusion should be considered, especially in older persons
    4. Hematocrit (HCT) will drop with IV fluid resuscitation (rather than with transfusion)
    5. For younger people, generally maintain HCT >15-18% (for acute drops) [16]
    6. For older people, especially with atherosclerosis, generally maintain HCT >25-28%
    7. Patients receive nothing by mouth
  4. Proton (Acid) Pump Inhibitor (PPI) Therapy
    1. High dose PPI strongly recommended following successful endoscopic repair [20]
    2. PPI are preferred over cimetidine and other H2 antagonists [15]
    3. High dose PPI (omeprazole 80mg IV bolus then 8mg/hour infusion) accelerated resolution of ulcer bleeding and reduced need for endoscopic therapy in PUD [4]
    4. These agents promote healing and reduce risk of rebleeding
    5. These agents do not acutely stop bleeding but high doses can accelerate healing [4]
    6. Peptic ulcer rebleedling after endoscopic repair occurs in ~20% of patients
    7. Omeprazole infusion after endoscopic repair reduced rebleed rate from 22.5 to 6.7% [25]
  5. Peptic Ulcer Bleeding
    1. Endoscopic evaluation and treatment is mainstay
    2. Somatostatin or octreotide reduce risk of continued bleeding [13]
    3. High dose PPI should be given acutely to accelerate healing, prevent rebleeding [4,15,25]
    4. PPI improve healing rates and high doses may have acute benefits [4]
    5. Nonsteroidal anti-inflammatory drugs (NSAIDS) should be discontinued
  6. Esophageal Variceal Bleeding
    1. Early endoscopic ligation or sclerotherapy is mainstay of treatment
    2. Octreotide (Sandostatin®) appears to reduce rebleeding when used for first 48 hours
    3. Octreotide reduces rebleeding events ~90% when used with variceal ligation
  7. Patients can be stratified by risk for recurrent bleeding
    1. Low risk patients can be discharged early with near-zero risk
    2. High risks, particularly malignancy, renal or liver failure, should be kept in hospital
  8. Test all upper GI bleeding patients H. pylori infection regardless of NSAID use (see above)

LOWER GI BLEEDING

A. Symptoms and Signsnavigator
  1. Melena
  2. Hematochezia - bright red blood per rectum (BRBPR)
  3. Diarrhea - blood in colon stimulates propulsion
  4. Anemia - may be only sign of chronic lower GI bleed
  5. Positive fecal occult blood may be only clue to lower GI bleed
  6. May occur in setting of thrombocytopenia without other clear cause [3]

B. Causes of LGI Bleedingnavigator

  1. Common Conditions
    1. Hemorrhoids: most common cause of BRBPR, usually in older persons
    2. Arteriovenous Malformation (AVM): very common in older persons
    3. AVMs also occur in younger persons and are a common cause of "benign" bleeding [11]
    4. Diverticulosis
    5. Celiac sprue - usually presents as chronic iron deficiency anemia []
  2. Diverticulosis [12]
    1. Outpouchings of intestine, usually found in the sigmoid region
    2. Very common in older persons
    3. Meckel's diverticulum is a remnant of vitelline duct located in distal ileum
    4. Emergent evaluation and treatment with colonoscopy (epinephrine and cauterization) appears to be more effective and considerably safer than surgery [23]
  3. Colon Polyps and Carcinoma
    1. Right sided cancers usually present with bleeding (Left sided with obstruction)
    2. Adenoma / Polyps: common cause of bleeding
    3. May present as intussusception [28]
  4. Inflammatory Bowel Disease (IBD)
    1. Ulcerative Colitis: watery, bloody diarrhea with crampy abdominal pain
    2. Crohn's Disease: watery and/or bloody diarrhea; may involve upper GI tract also
  5. Foreign Body Perforation [26]
  6. Intussusception [24,28]
    1. Uncommon cause of LGI bleeding in adults
    2. Usually due to mass outside bowel in adults
    3. Meckel's diverticulum (distal ileum) may provide nidus for intussusception [30]
  7. Ten-Year Followup of Rectal Bleeding [10]
    1. Patients gave history of visible rectal bleeding
    2. Over 10 years, 24% had serious disease: 13% polyps, 4.5% IBD, 6.5% colon carcinoma
    3. Only sigmoidoscopy with double contrast enema (or colonoscopy) detected >95% of these
    4. Clinical symptoms cannot be used to predict pathology of rectal bleeding symptoms

C. Diagnosisnavigator

  1. Any symptoms which include rectal bleeding MUST be evaluated carefully [10,29]
  2. Colonoscopy is generally recommended, even in patients 25-45 years old [29]
  3. Alternatively, or for unstable patients, sigmoidoscopy with barium enema used
  4. Wireless Video Capsule Endoscopy (Given Imaging) [7,8]
    1. Direct visualization of small bowel
    2. Patient swallows capsule 20mm long and 10mm wide
    3. This transmits 50,000 digital images over 8 hours of GI transit
    4. Images are computer reviewed and specific images selected for human assessment
    5. Diagnosis rate >60% in most series
  5. For rapid continuous lower GI bleeding:
    1. Tagged Red blood cell scan: detects bleeding rates >0.2-0.5mL/min
    2. Angiography: detects bleeding rates >1mL/min

D. Treatmentnavigator

  1. Supportive care with IV Fluids and/or blood products
  2. Reverse anti-coagulation
  3. Bleeding in Unstable Patients
    1. Invasive radiological proceedure
    2. Surgical intervention
  4. Treat underlying cause
    1. IBD - high dose intravenous glucocorticoids and/or cyclosporine
    2. Resection of tumors
    3. Resection or embolization of AVM, hemorrhoids
  5. Colonoscopic treatment for acute diverticular hemorrhage [23]

References navigator

  1. Rockey DC. 1999. NEJM. 341(1):38 abstract
  2. Sharara AI and Rockey DC. 2001. NEJM. 345(9):669 abstract
  3. Sawalha AH, Bronze MS, Saint S, et al. 2003. NEJM. 349(23):2253 (Case Discussion) abstract
  4. Lau JY, Leung WK, Wu JC, et al. 2007. NEJM. 356(16):1631 abstract
  5. Chan FKL, Chung SCS, Suen BY, et al. 2001. NEJM. 344(13):967 abstract
  6. Lanas A, Bajador E, Serrano P, et al. 2000. NEJM. 343(12):834 abstract
  7. Pennazio M, Santucci R, Rondonotti E, et al. 2004. Gastroenterology. 126:643 abstract
  8. Keroack MD, Peralta R, Abramson SD, Misdraji J. 2004. NEJM. 351(5):488 abstract
  9. Haberer J, Trivedi NN, Kohlwes J, Tierney L Jr. 2003. NEJM. 349(1):73 (Case Discussion) abstract
  10. Helfand M, Marton KI, Zimmer-Gembeck JM, Sox HC Jr. 1997. JAMA. 277(1):44 abstract
  11. Colletti RB and Compton CC. 1997. NEJM. 336(9):641 (Case Report)
  12. Jacobs DO. 2007. NEJM. 357(20):2057 abstract
  13. Imperiale TF and Birgisson S. 1997. Ann Intern Med. 127(12):1062 abstract
  14. Rodriguez LAG, Cattaruzzi C, Troncon MG, Agostinis L. 1998. Arch Intern Med. 158(1):33 abstract
  15. Lin HJ, Lo WC, Lee FY, et al. 1998. Arch Intern Med. 158(1):54 abstract
  16. Weiskopf RB, Viele MK, Feiner J, et al. 1998. JAMA. 279(3):217 abstract
  17. Terdiman JP and Ostroff JW. 1998. Am J Med. 104(4):349 abstract
  18. Rockey DC, Koch J, Cello JP, et al. 1998. NEJM. 339(3):153
  19. Wolfe MM, Lichtenstein DR, Singh G. 1999. NEJM. 340(24):1888 abstract
  20. Barkun A, Bardou M, Marshall JK. 2003. Ann Intern Med. 139(10):843 abstract
  21. Garcia Rodriguez LA, Cattaruzzi C, Troncon MG, et al. 1998. Arch Intern Med. 158(1):33 abstract
  22. Hardy S and Keel SB. 1999. NEJM. 341(21):1597 (Case Record)
  23. Jensen DM, Machicado GA, Juthaba R, et al. 2000. NEJM. 342(2):78 abstract
  24. Berger DL and Mohammadkhani MS. 2000. NEJM. 342(17):1272 (Case Record)
  25. Lau JYW, Sung JJY, Lee KKC, et al. 2000. NEJM. 343(5):310
  26. Mohanty AK, Flannery MT, Johnston BL, Brady PG. 2006. NEJM. 355(5):500 (Case Discussion) abstract
  27. Blatchford O, Murray WR, Blatchford M. 2000. Lancet. 356(9238):1318
  28. Berger DL and Mohammadkhani M. 2002. NEJM. 347(8):601 (Case Record)
  29. Lewis JD, Brown A, Localio AR, Schwartz JS. 2002. Ann Intern Med. 136(2):99 abstract
  30. Hoffman RJ, Dhaliwal G, Gilden DJ, Saint S. 2004. NEJM. 351(19):1997 (Case Discussion) abstract