ABIM - GI Bleeding

Here are key facts for ABIM from the GI Bleeding tutorial, as well as points of interest at the end of this document that are not directly addressed in this tutorial but should help you prepare for the boards. See the tutorial notes for further details and relevant links.

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1. Hematemesis means vomiting blood ("heme" = blood; "emesis" = vomit). 2. When bloody vomit has a dark, mottled "coffee ground" appearance, this indicates that blood flow has slowed or stopped. 3. Melena refers to black, tarry stools with blood. 4. Hematochezia refers to the passage of bright red fresh blood. 5. Bleeding in the upper gastrointestinal tract produces hematemesis and/or melena; bleeding in the lower gastrointestinal tract produces melena or hematochezia. 1. The Upper Gastrointestinal tract lies proximal to the duodenal attachment of the ligament of Treitz (suspensory ligament of the duodenum) and the Lower Gastrointestinal tract lies distal to it. 1. Duodenal and gastric ulcers & erosion are most common cause of upper GI bleeding, resulting from H. pylori infection, drugs, stress, or autoimmune disorders. 2. Esophagitis leads to erosion of the esophageal lining and bleeding, associated with severe acid reflux and alcohol consumption. 3. Varices in the esophagus and proximal stomach can rupture and cause potentially life-threatening hemorrhages, associated with cirrhosis and portal hypertension. 4. Mallory-Weiss tears occur in the distal esophagus from fits of violent vomiting or coughing and are rare. 1. Infectious colitis, particularly bacterial, produces fever, tenesmus, abdominal pain, and purulent, loose bloody stools. 2. C. difficile infection following antibiotic use is an example of bacterial colitis. 3. Inflammatory bowel disease, particularly ulcerative colitis, causes bloody diarrhea when active. 4. Acute and chronic intestinal ischemia causes lower GI bleeding along with nausea, vomiting, and abdominal pain. 5. Diverticular hemorrhage is a top cause of lower GI bleeding characterized by brisk hematochezia with possibility of massive bleeding. 6. Hemorrhoids are swollen veins in rectum and perianal region that can rupture and produce hematochezia. 1. Neoplasms can occur anywhere along the GI tract and are often the presenting sign. 2. Vascular lesions including arteriovenous malformations can cause upper and lower GI bleeding.

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1. "Coffee ground" appearance indicates that blood flow has slowed or stopped. 2. Viral colitis is associated with watery diarrhea and is more common in infants and children. 3. Amoebic colitis is associated with diarrhea and mucoid discharge. 4. Ulcerative colitis is characterized by mucosal and submucosal inflammation with sunken ulcers creating a friable or crumbly appearance. 1. Diverticula are not necessarily inflamed when bleeding occurs in diverticular hemorrhage. 2. Anal fissures produce bright, fresh blood and cause pain during and after bowel movements. 3. Varices can cause potentially life-threatening hemorrhages and are associated with portal hypertension. 4. Arteriovenous malformations are atypical arrangements of blood vessels that divert blood from proper targets; the tangled vessels can rupture and cause bleeding. These are rare.

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1. Early risk stratification using validated tools (Glasgow-Blatchford, AIMS65, Rockall scores) helps determine level of care and guides management. 2. Initial assessment should focus on hemodynamic stability, with aggressive resuscitation for unstable patients. 3. Two large-bore IVs, crystalloid resuscitation, and blood product transfusion based on hemoglobin thresholds (typically <7 g/dL for most patients, <9 g/dL for those with active ischemic heart disease). 4. Pre-endoscopic PPI therapy for suspected peptic ulcer bleeding. 5. Vasoactive drugs (octreotide, terlipressin) and prophylactic antibiotics for suspected variceal bleeding. 1. Upper endoscopy within 24 hours for most upper GI bleeding; urgent (<12 hours) for severe bleeding. 2. Forrest classification for risk stratification of peptic ulcers (Ia: spurting bleeding, Ib: oozing bleeding, IIa: visible vessel, IIb: adherent clot, IIc: flat pigmented spot, III: clean base). 3. Endoscopic hemostasis options: injection therapy, thermal therapy, mechanical therapy (clips), and combination therapy. 4. Band ligation is preferred over sclerotherapy for esophageal varices. 5. Colonoscopy after adequate bowel preparation for lower GI bleeding; consider urgent colonoscopy after rapid purge for severe bleeding. 1. H. pylori testing and eradication for peptic ulcer disease, with confirmation of eradication. 2. Non-selective beta-blockers for primary and secondary prevention of variceal bleeding. 3. Considerations for resumption of anticoagulation and antiplatelet therapy based on indication and risk-benefit assessment. 4. Recurrent bleeding management including repeat endoscopy, interventional radiology (angiographic embolization), or surgery. 5. Prevention strategies: PPI co-therapy with NSAIDs in high-risk patients, alternative to NSAIDs when possible, eradication of H. pylori. 1. Approach to obscure GI bleeding: video capsule endoscopy, deep enteroscopy, CT enterography. 2. Angiodysplasia management: endoscopic therapy, medical therapy (octreotide, thalidomide, estrogen-progesterone), and association with aortic stenosis, chronic kidney disease, and von Willebrand disease. 3. GAVE (gastric antral vascular ectasia, "watermelon stomach"): association with cirrhosis, management with endoscopic ablation. 4. Small bowel bleeding: role of capsule endoscopy, deep enteroscopy, and push enteroscopy. 5. Dieulafoy's lesion: large submucosal artery that can cause massive, unexplained GI bleeding.