GI Bleed Presentation PDF

GI Bleed Dave Dvorak, MD  Definitions ◼ Hematemesis ◼ Coffee ground emesis ◼ Hematochezia ◼ Melena ◼ Occult blood testing  Acute GI Bleed ◼ Presentation may be subtle or dramatic ◼ Life-threatening until proven otherwise ◼ Mortality: 6-...

GI Bleed Dave Dvorak, MD  Definitions ◼ Hematemesis ◼ Coffee ground emesis ◼ Hematochezia ◼ Melena ◼ Occult blood testing  Acute GI Bleed ◼ Presentation may be subtle or dramatic ◼ Life-threatening until proven otherwise ◼ Mortality: 6-14% ◼ Distinguish upper vs. lower ◼ Upper: esophagus, stomach, duodenum ◼ Lower: jejunum, ileum, colon, rectum  Risk Factors ◼ NSAIDs, aspirin ◼ Coumadin, Plavix, Pradaxa, Heparin, Thrombolytics ◼ Steroids ◼ Alcohol ◼ Cirrh osis ◼ Impaired synthesis of clotting factors ◼ Esophageal varices ◼ Blood disorders (thrombocytopenia, leukemia, hemophilia, etc. ) ◼ Prior GI bleed  Sources of GI Bleed ◼ Upper: above ligament of Treitz ◼ Lower: below ligament of Treitz  Upper GI Bleed Sources ◼ Ulcer (gastric or duodenal) ◼ Most common source: 50% of upper GI bleeds ◼ Esophageal varices ◼ Most likely to rebleed (40-70%) ◼ Mallory-Weiss tears ◼ Esophagitis/Gastritis Gastric ulcer with recent bleed  Gastric ulcer with eroded vessel Duodenal ulcers Endoscopy: esophageal varices Bleeding esophageal varices Gastritis  Lower GI Bleed Sources ◼ Upper GI bleed: apparent lower GI bleed ◼ Diverticulosis ◼ Most common cause of lower GI bleed ◼ Carcinoma (e. g. colon cancer) ◼ AVM’s ◼ Infectious diarrhea ◼ Inflammatory bowel disease (Crohn ’s, u lcerative colitis) ◼ Hemorrhoids/anal fissure Diverticulosis Sigmoid diverticulosis Colon Cancer Stages of colon cancer AVM of Colon Hemorrhoids Hemorrhoids  History ◼ Hematemesis, coffee-ground emesis ◼ Upper GI bleed ◼ Melena ◼ Suggests upper GI bleed (90%) ◼ Hematochezia ◼ Suggests lower GI bleed ◼ GI bleed mimics ◼ Iron and bismuth can simulate melena ◼ Beets can simulate hematochezia ◼ Hemoccult will differentia te  History (cont’d) ◼ Duration, quantity of bleed, history of previous bleed ◼ Weight loss, change in bowel habits (suggests malignancy) ◼ Vomiting/retching followed by hematemesis suggests Mallory-Weiss tear  Physical Exam ◼ Vital signs ◼ Resting tachycardia ◼ Hypotension ◼ Tachypnea ◼ VS may be normal: check orthostatics ◼ Skin ◼ Cool, clammy: shock ◼ Jaundice: liver disease ◼ Petechia/purpura: underlying coagulopathy  Ph ysical Exam (continued) ◼ ENT ◼ Look for oral/nasal source of swallowed blood ◼ Abdomen ◼ Tenderness, mass, ascites, organomegaly ◼ Rectal ◼ Stool: bright red, maroon, melena, occult blood positive ◼ Check for masses  Lab ◼ Type and crossmatch immediately if bleed is significant ◼ CBC (don’t be reassured by normal Hgb) ◼ INR/PTT ◼ LFT’s if appropriate ◼ EKG if elderly or underlying coronary artery disease  Radiographic Studies ◼ Abdominal X-rays ◼ Of very limited value, generally not indicated ◼ Lower GI contrast study ◼ Detects colorectal pathology ◼ May miss mucosal lesions, may obscure later endoscopic visualization ◼ Not used acutely ◼ Technecium-labeled RBC scan ◼ Can localize bleeding site, very sensitive ◼ Angiography ◼ Less sensitive ◼ Allows embolization or vasoconstrictor infusion Lower GI Angiography Management : Acute GI Bleed ◼ High flow oxygen ◼ Possible intubation for airway control if profuse UGI bleed ◼ Cardiac monitor ◼ Volume replacement, large bore IV lines ◼ Begin with crystalloid (normal saline or LR) ◼ Blood transfusion  Transfusion ◼ PRBC’s ◼ Hgb < 7 ◼ Failure to improve after 2 liters of crystalloid ◼ Severe ongoing bleeding ◼ Coagulation factors ◼ FFP, platelets as needed  NG tube ◼ Controversial ◼ Possible benefits ◼ Establish source: upper vs lower ◼ Monitor whether bleeding is ongoing ◼ Remove fresh blood and clots to facilitate endoscopy  Meds ◼ Proton pump inhibitors (e. g. , pantoprazole) ◼ Decreases rate of rebleed ◼ Octreotide, vasopressin ◼ Vasocontrictors ◼ If endoscopy not immediately available ◼ Most effective for esophageal varices ◼ Side effects: hypertension, myocardial ischemia  Endoscopy ◼ Upper endoscopy ◼ Diagnostic: identifies source of UGI bleed ◼ Therapeutic: can achieve hemostasis ◼ Sclerotherapy, electrocoagulation, laser, variceal banding ◼ Colonoscopy ◼ For LGI bleed source, requires prep time ◼ Sigmoidoscopy ◼ Proctoscopy/Anoscopy ◼ Anorectal source (e.g., hemorrhoids)  Other measures ◼ Sengstaken-Blakemore tube ◼ Balloon tamponade ◼ Useful for controlling significant UGI hemorrhage ◼ Gastric and esophageal balloons inflated to tamponade source of bleed ◼ Possible complications: mucosal ulceration, esophageal/gastric rupture, tracheal compression, aspiration ◼ Surgery ◼ Indicated if medical and endoscopic interventions fail Sengstaken-Blakemore tube  Some final caveats ◼ Food or medication may be mistaken for blood in vomit or stool ◼ Brisk upper GI bleed may present as hematochezia ◼ Don’t be reassured by normal BP: HR and orthostatic VS more sensitive ◼ Don’t be reassured by normal initial Hgb ◼ Unstable patients should undergo prompt fluid resuscitation while H&P are being performed Questions?