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Gastrointestinal (GI) Bleeding
Ralph Lee, MMEd(Dist), MD, FRCPC Gastroenterologist and Assistant Professor University of Ottawa, September 18, 2015
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Objectives Define upper and lower gastrointestinal (GI) bleeding.
Outline the etiologies and clinical features of upper and lower GI bleeding Apply a systematic clinical approach to GI bleeding. Outline the investigation and management of GI bleeding Recognize clinical indicators suggesting urgent versus non‐urgent assessment.
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What is Gastrointestinal Bleeding? (1)
Bleeding from anywhere in the GI tract Esophagus to rectum Traditionally, classified into two groups, based on presumed location of bleeding: Upper Lower 3rd category, ‘Mid- GI’ bleeding, is present, but infrequently used
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What is Gastrointestinal Bleeding? (2)
Upper GI (UGI) Bleeding Traditional: Proximal to the Ligament of Treitz New: Proximal to the Ampulla of Vater Lower GI (LGI) Bleeding Traditional: Distal to Ligament of Treitz New: Distal to terminal ileum Mid GI bleeding New: Ampulla of Vater to terminal ileum
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Upper GI Bleeding
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UGI Bleeding 75 – 80% of GI bleeding
annual hospitalization rate = 160/100,000 (US) Mortality rate = 3.5 – 10% Sex – M:F – 2:1 incidence with age More likely to present with hemodynamic instability due to rich blood supply of UGI tract
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UGI Bleeding Causes (Common)
Peptic Ulcer disease ( %) Varices (5 - 20%) Mallory-Weiss tears (8 - 15%) Erosions (8 - 15%) AV Malformations (5%) Tumours (5%) Dieulafoy’s lesions (1%)
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UGI Bleeding Causes (Other)
Gastric Antral Vascular Ectasia (GAVE) AKA ‘Watermelon’ stomach Portal hypertensive gastropathy Hemobilia Hemosuccus pancreatitis Aortoenteric fistulas Cameron’s lesions/ulcers
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UGI Bleeding How Do They Present? (1)
Hematemesis Vomiting blood Bright red blood, clots, ‘coffee ground’ emesis Melena Passage of black, tarry, foul-smelling stools Digested blood Appears with ≥ 50cc of bleeding from UGI tract Things that mimick melena: Iron pills - greenish Bismuth subsalicylate (Peptol Bismol™) - non-foul smelling
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UGI Bleeding How Do They Present? (2)
Bowel movement frequency Blood is cathartic and a great laxative Rough indicator of rapidity of bleeding Hemodynamic symptoms Pre/Syncope Orthostatic dizziness/lightheadedness Chest pain, dyspnea
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UGI Bleeding How Do They Present? (3)
(Hematochezia - red blood per rectum) Usually sign of LGI Bleeding, but can occur with rapid UGI bleeding (i.e. ≥ 1000cc) patient usually hemodynamically unstable Other symptoms Dependent on cause Abdominal pain, heartburn, dysphagia, nausea, vomiting
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Lower Gi Bleeding
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LGI Bleeding 20 – 30% of gastrointestinal bleeding
Usually less hemodynamically significant, higher Hb level, less blood transfusion requirements than UGI bleeds Increased incidence with age Mean age at presentation: 63 – 77 Mortality rate among hospitalized acute lower GI bleeds – 2 - 4%
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LGI Bleeding Causes Diverticulosis (25 - 65%) Cancers/polyps (17%)
Colitis/ulcers (18%) IBD, ischemic, vasculitis, infectious, radiation-induced, NSAID-induced Unknown (16%) Angiodysplasia (3 - 15%) Other (8%) Post-polypectomy, stercoral ulcers, aorto-colonic fistulas Anorectal ( %) Fissures, hemorrhoids
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LGI Bleeding How Do They Present? (1)
Red Blood per Rectum Bright Red Blood Per Rectum (BRBPR) – left colonic? Dark/maroon – right colonic/lower small bowel? Stool frequency – blood is cathartic form – diarrhea Location of blood Surface/side of stool/dripping – perianal source? Mixed in stool – R colonic? (Melena)* Usually sign of UGI bleeding, but can occur with distal small bowel, cecum or R-sided colonic bleeding source Typically, hemodynamically stable with less rapid bleeding
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LGI Bleeding How Do They Present? (2)
Other Symptoms Dependent on cause Fecal urgency, tenesmus, incontinence Abdominal pain/cramps Fevers/chills Weight loss
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GI Bleeding
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GI Bleeding Other important historical items
Past medical history: GI Previous PUD/H. Pylori infection? GI Malignancy? Previous endoscopies Previous polypectomy Diverticulosis IBD Cirrhosis? Varices? Cardiac CAD, angina, MI, CHF Previous aortic aneurysms/grafts/vascular surgery? Previous radiation therapy? Bleeding episodes Medications Anti-platelet agents (i.e. ASA, Plavix), anticoagulants (i.e. warfarin, pradaxa) NSAIDs Habits – EtOH Family history: PUD, gastric cancer Colonic polyps, cancer IBD
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GI Bleeding Physical Exam (1)
Look for: Hemodynamic instability Intravascular depletion Potential etiologies of bleeding General: Altered mentation, jaundice Vitals Hypotension Tachycardia Orthostatic changes in BP and/or HR with position change from supine to standing Suggests intravascular volume depletion of ≥ 2L Head and Neck: Conjunctival pallor Scleral icterus Dry mucous membranes, furrowed tongue, ↓ JVP Chest: ↓skin turgor at sternal angle Axilla: dry or moist Abdomen: Tenderness, masses, hepatosplenomegaly, stigmata of chronic liver disease Digital rectal exam: Red blood? Melena? Hemorrhoids, fissures Masses
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GI Bleeding Shock SHOCK Class I Class II Class III Class IV
Blood Loss (mL) Up to 750 >2000 Blood Loss (%) Up to 15 15-30 30-40 >40 HR (bpm) <100 >100 >120 >140 BP (mmHg) Normal ↓ RR (breaths/min) 14-20 20-30 >35 Urine Output (cc/h) >30 5-15 Insig. CNS Slightly anxious Mild anxious Anxious, confused Confused/ lethargic
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GI Bleeding Management (Overview)
ABC’s Resuscitation Focused History and Physical Exam Upper vs. lower GI bleed Investigations Treatment
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GI Bleeding Initial Management
ABC’s Resuscitation Intravenous (IV) access Monitoring Need for monitored area ? (i.e. ICU) Cardiac, respiratory (i.e pulse oximetry) Volume re-expansion IV fluids Keep patient NPO (nil per os) Focused history and physical exam Upper vs. lower GI Bleed
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GI Bleeding Investigations (1)
Bloodwork Type and crossmatch - PRBC’s, blood products Complete Blood Cell Count Hemoglobin MCV – mean corpuscular volume MCV Fe deficiency chronic blood loss? Platelets Clotting ability Electrolytes
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GI Bleeding Investigations (2)
Blood Urea Nitrogen (BUN), Creatinine Intravascular dehydration renal perfusion BUN, Cr UGI bleed blood digestion in stomach/duodenum protein absorption urea nitrogen [BUN x 10]: Cr > 1.5:1 May suggest UGI bleed Liver enzymes and liver function tests INR - Coagulation status (i.e. INR) Liver disease (i.e. cirrhosis) Albumin INR AST > ALT Platelets, MCV (Nasogastric aspirate)
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GI Bleeding Initial Treatment (1)
Fluid Management IV crystalloids (i.e. normal saline); colloids (i.e. volume expanders) Transfusion - Packed red blood cells Reverse anti-coagulation INR - Vitamin K, fresh frozen plasma, prothrombin complex concentrate (i.e. Octaplex) Platelets – Platelets transfusion
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GI Bleeding Initial Treatment (2)
Pharmacotherapy UGI Bleeds: IV Proton Pump Inhibitor Mechanism: ↑ pH > 6 Promotes clot stability ↓ acid/pepsin on lesion ↑ platelet aggregation + fibrin formation Empirically started to treat possible PUD until EGD performed IV PPI before endoscopy: Lau et al. (2007): ↓ need for endoscopic therapy + accelerated healing of ulcers Cochrane Meta-analysis (Sreedharan et al., 2010): DOESN’T: mortality, rebleeding or progression to surgery DOES: high risk stigmata, need for endoscopic therapy IV PPI after endoscopic therapy: rebleeding, mortality Dose: Pantoprazole 80mg IV bolus, then 8mg/h x 72 hours
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GI Bleeding Initial Treatment (3)
IV Somatostatin (i.e. octreotide) For possible variceal bleeds (i.e. patients with cirrhosis) – started empirically Mechanism: splanchnic vasoconstriction portal hypertension bleeding Prokinetics (20 – 120 minutes before) i.e. metoclopramide (Maxeran) or IV erythromycin To clear UGI tract of blood for better visualization Meta-analysis (Barkun et al., 2010): need for repeat endoscopy LGI Bleeds: No specific medications
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Urgent vs. Non-urgent Management
Hematemesis Serious co-morbid illness Malignancy, cirrhosis Hemodynamic instability Shock SBP < 100mmHg HR > 100bpm (Orthostatic hypotension) Hb < 80 Transfusion requirement > 2u PRBC’s Severe, ongoing bleeding Young, healthy, minimal bleeding
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GI Bleeding Endoscopy UGI Bleed – EGD LGI Bleed – Colonoscopy
Timing: Within 24 hours of presentation To: Diagnose cause of bleeding (high sensitivity/specificity) Stratify risk of rebleeding/adverse events Potentially treat underlying pathology LGI Bleed – Colonoscopy Timing: Controversial Severe bleeds: Within 8 – 24 hours Generally, LGI bleeds less severe than UGI bleeds Often, more difficult to identify source; therefore, mostly diagnostic rather than therapeutic Unclear: EGD Colonoscopy
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Upper vs. Lower Endoscopy Presumed Upper GI Bleed
Hematemesis EGD
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Upper vs. Lower Endoscopy Presumed Lower GI Bleed
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Upper vs. Lower Endoscopy Massive Rectal Bleeding
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Upper vs. Lower Endoscopy Occult Bleeding
Stool testing positive for occult blood Unexplained Fe deficiency anemia
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GI Bleeding Endoscopic Hemostasis (1)
Injection i.e. Vasoconstrictors (i.e. epinephrine), saline, sclerosants, tissue adhesives Creates submucosal cushion of fluid which tamponades site +/- vasoconstriction Thermal therapy i.e. Mono/bipolar electrocoagulation, Argon Plasma Coagulation (APC), Laser Photocoagulation Cauterizes vessel closed
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GI Bleeding Endoscopic Hemostasis (2)
Mechanical therapy i.e. Hemoclips, rubber bands Closes and tamponades vessel Animation Hemospray New therapy Nano particle spray
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UGI Bleeding Peptic Ulcer Disease (1)
Most commonly due to NSAIDS, H. Pylori 75 – 80% stop spontaneously Ulcer appearance indicates risk of rebleeding and determines whether therapy required Forrest Classification
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UGI Bleeding Peptic Ulcer Disease (2)
Endoscopic intervention: Risk of rebleeding Need for surgery Mortality
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UGI Bleeding Varices Often unstable UGI bleeds Esophageal – Options:
Ligated with rubber bands (band ligation) Injection with sclerosants Gastric – Options: Injected with ‘glue’ (cyanoacrylate) Band Ligation If endoscopy unsuccessful: Transjugular intrahepatic portosystemic shunt (TIPS) Liver transplant
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LGI Bleeding Diverticular Bleeding
Complicates 3 – 15% with colonic diverticulae Pathophysiology: Trauma of vasa recta at neck or dome of diverticulum Presentation: Painless hematochezia Treatment: % resolve spontaneously Recurrence within 4 years 25 – 40% Endoscopic hemostasis If site can be identified < 30d rebleeding: Uncommon Angiography (85% effective) < 30d rebleeding: 22% Surgical resection
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LGI Bleeding Angiodysplasia
Increases with age Pathophysiology Degenerative changes Chronic, intermittent obstruction of submucosal vessels Presentation Usually asymptomatic Overt or occult bleeding Usually in right colon Treatment Iron replacement Cauterization if bleeding or Fe deficiency anemia (Estrogen/progesterone)
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GI Bleeding Other Options (1)
If endoscopy fails to identify source or fails to stop the bleeding Mesenteric angiography Performed by interventional radiology Catheter introduced through femoral artery, passed to celiac trunk, SMA, IMA + branches to: Diagnose bleeding site Requires blood loss of ≥ 0.5-1mL/min Low sensitivity (47%) but high specificity (100%) Perform therapy Feeding arteries can be embolized with microscopic gel foam, microcoils or EtOH particles Success rate: 52 – 94% Complications (17%): Nephrotoxicity, bowel infarction, hematomas
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GI Bleeding Other Options (2)
RBC scan Patient infused with technetium tagged RBC’s to locate site of bleeding Disadvantages: Not therapeutic Only localizes bleeding to generalized area of abdomen Requires blood loss ≥ 0.1mL/min Higher sensitivity; lower specificity Surgery Intraoperative enteroscopy Oversew, resection
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Summary (1) Upper GI Bleed Lower GI Bleed Hematemesis Melena
Hemodynamic instability Elevated BUN x 10: Cr Dark/bright red blood per rectum (hematochezia) Longer course Tend to be more hemodynamically stable
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Summary (2) PUD is most common cause of UGIB bleeding
Diverticular disease is the most common cause of significant LGIB Approach includes ABC’s Resuscitation History and Physical Exam Initial Investigations Initial Treatment Endoscopy Radiology Surgery IV PPI’s are started empirically if UGIB is suspected Endoscopy is the primary diagnostic and therapeutic tool for GI bleeds
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