GI Bleeding



    Upper GI Bleeding

    • Most common
    • Defined as: Intraluminal blood proximal to ligament of Treitz
    • Causes 500,000 hospital admissions, mortality 5-10%, 80% stop spontaneously.
      • Continued bleed or re-bleed are at high risk of death.
    • High Risk Features:
      • Advanced age, variceal bleeding, comorbid conditions (organ failure or disseminated malignancy), shock, hematemesis
      • Increasing number of erythrocyte transfusions, active bleeding, and a visible vessel or clot in an ulcer base on endoscopy​
    • Causes:



    Cause of GIB Incidence Bleeding Comments
    Peptic Ulcer Disease 38% ACUTE  
    Esophageal Varices 16% ACUTE

    - High mortality (15-20%).

    Esophagitis 13% ACUTE


    Malignancy 7%    
    Angioectasia 6%    
    Mallory-Weiss Tear 4%    
    Dieulafoy Lesions 2%   Submucosal arteriole that intermittently protrudes through mucosa and cause hemorrhage


    (incl. GI Stromal Tumors)

    (aka GIST)

    <1%   Esophageal or gastric cancers

    Portal Hypertensive

    Gastropathy (PHG)


    - Seen with cirrhosis

    - Characteristic mosaic apperance seen in body and fundus.

    - Severe if presence of "red spots".

    Typically chronic bleeds (not acute)

    Gastric Antral

    Vascular Ectasia (GAVE)


    - "Watermelon stomach" seen in cirrhosis and connective tissue diseases.

    - Linear ectatic vessels that resemble stripes extending from pylorus.

    - Typically chronic bleeds (not acute)

    Cameron Lesions   Chronic

    Mechanical: large hiatal hernia causing erosion through gastric folds, as moves in the hernia)

    - Present in up to 5% of pts, can cause bleeding.

    - Typically chronic bleeds (not acute)

    Proximal Crohn's Disease      
    GI telangiectasias      
    Hemobilia   ACUTE

    Bleed from biliary tree post-liver biopsy, ERCP, or after TIPS.

    Triad: Biliary colic, obstructive jaundice (clotted blood), melena.

    Hereditary Hemorrhagic

    Telangectasia (HHT)

    (aka Osler-Weber-

    Rendu Dis.)


    Acute or


     Acute or chronic gastrointestinal blood loss.

    Most typically have recurrent epistaxis, mucocutaneous telangiectasia,

    other visceral involvement (lung, liver, brain), and a family history of HHT.

    Aorto-enteric fistulas


    - High mortality risk

    - Often following repair of abdominal aortic aneurism (often graft infection/inflammation)

    - Often presents as minor herald bleed, followed by MASSIVE GI bleed.

    Pancreatic Pseudocyst



    - Erodes into adjacent artery creating a pseudoaneurisms.

    - VERY brisk bleed called "hemosuccus pancreaticus"

    • History
      • Focus on history/physical to find origin of bleeding.
      • (See "overview" for basic concepts)
      • Some specific helpful historic Featurs:
      • History Type Suggested
        Hematemesis Variceal bleed?
        Coffee Ground Emesis Gastritis or PUD

        Hx of PUD, NSAID use , EtOH

        Liver Disease Variceal Bleed
        Hx of pancreatitis Pseudoaneurism Bleed
        Chronic GERD Esophagitis
        Aortic Endovascular Stent Aorto-enteric fistula
        Biliary manipulation
        Radiation Therapy Radiation-related GI Bleed


    • Physical Exam
      • Ruotine + ORTHOSTATIC vital signs. (supine + standing or sitting pulse and BP)
        • Orthostasis: Large volume bleeding even when ruotine vitals are normal.
      • Tachycardia: 15-30% blood loss
      • Hypotension: >30% blood loss
      • Other things to look for:
        • Chronic liver disease  (Scleral icterus, spider angiomata, gynecomastia, ascites, etc..)
    • Labs:
      • CBC, INR, BUN, Serum Creat
      • Hb or Hct are NOT accurate measure of blood loss acutely, but help transfusion decisions.
      • Macrocytosis + elevated INR --> clues for liver disease.
      • Microcytosis --> chronic bleed.
      • Elevated BUN to creat ratio --> upper GI source (blood protein absorbed proximally making urea)
    • Prognostic Scoring Systems (not used)

      • Blatchford Score: Predict patients with UGIB who can be managed as outpatients if all are present:
        • BUN less than 18 mg/dL (6.4 mmol/L); normal Hb; sBP > 109 mm Hg; HR < 100/min;
        • and absence of melena, syncope, and hepatic and cardiac disease.
      • Rockall Score (pre-endoscopic and complete versions)
    • Management:
      • Distinguish Variceal vs. Non-Variceal
      • Initial Management:
        • Protect airway
        • Two large bore IV catheters
        • Resuscitation with IV crystalloids and pRBC infusions.
        • Continuous Hb and Hct monitoring (Hb <70 g/L = absolute indication for RBC transfusions)
        • If INR supratheraputic --> FFP
          • Guidelines: Weigh risk of continued anticoag with benefits.
          • Guidelines: Endoscopy SHOULD NOT be delayed for anticoagulation reversal, unless INR > 3.
        • Other Management Notes:
          • NG tubes NOT ROUTINELY recommended.
          • Promotility Agents (Erythromycin/Metaclopramide) NOT ROUTINELY recommended
            • (did not alter RBC transfusion, surgery, or hosp stay, slightly improved visiblity at endoscopy and decr. need for repeat endoscopy)
      • Non-Variceal Bleed:
        • IV PPI started before endoscopy
        • Endoscopy in 24hrs (once hemodynamically stable) - Non-Variceal Bleeds
      • Variceal Bleeding
        • Antibiotics (Prevent infection complications)
        • Octreotide (Reduces splanchnic blood flow, transiently decr. variceal pressure)
        • Endoscopy in 12hrs (once hemodynamically stable)- Variceal bleeds


    Endoscopic Features

    • Treatment depends on ulcer characteristics (predictors of recurrent bleeding)
    • Characteristics Re-Bleeding Risk
      w medical therapy
      Endoscpic Mgmt Post-Endoscopy Care
      Clean-Based Ulcer 3-5% - LOW


      - Feed within 24hrs

      - Oral PPI therapy (Duration variable)

      - Early hospital discharge

      Nonprotuberant pigmented

      spot in ulcer bed

      5-10% - LOW
      Adherent clot 25-30%

      - Irrigate to disrupt clot

      +/- Endoscopic tx


      Visible Vessel in an ulcer

      base (non-bleeding)

      40-50% - HIGH

      - Epinephrine inj. + ONE of:

         - Hemoclips

         - Thermocoagulation

         - Sclerosant

      - Bolus + maintenance of IV PPI x72hrs

        followed by oral PPI

      - Hospitalize at least 72hrs post intervention

      - Surgery/IVR embolization reserved if 

        bleeding refractory to all methods.

      Active arterial spurting 80-90% - HIGH

    • Forrest classification:
    • Type Class Lesion Risk of Rebleed



      Ia Spurtic Vessel 55-100%
      IB Oozing Vessel



      IIa Visible vessel 43%
      IIb Adherent Clot 22%
      IIc Hematin covered flat spot 10%



      III No stigmata of hemorrhage 5%


    • Routine 2nd look endoscopy is not recommended (only if initial visualization is suboptimal)
      • Also repeat endoscopy recommended for re-bleeding prior to consideration of IVR or surgery.

    Follow-up Care:

    • Treatment and confirmation of eradication of H. pylori (if present)
    • Counselling regarding cessation of NSAIDs
    • Resuming ASA (for cardiovascular protection) should be done WHILE on PPI (when benefits > risks).
    • Surveillance endoscopy for gastric ulcers should be performed in 6-8 weeks to R/O malignancy.

      (Unless biopsies were taken during initial upper scope - RARE)



    Lower GI Bleeding

    • Distal to the ligament of Treitz - typically colon and anorectum.
    • Presents as bright red blood per rectum (BRBPR) or red/maroon colored stools (hematochezia).
    • Usually acute in onset without pain.
    • Clinical Features:
      • Anemia, (rarely hemodynamically unstable).
      • If hypotensive, consider brisk bleed, or brisk upper GI bleed.
    • Risk:
      • Increases in age, usually 7th-8th decade of life.
    • Causes:
      • LowerGIBleed.png
    • Figure and data adapted/reprinted from Savides TJ, Jensen DM. Gastrointestinal bleeding. In: Feldman M, Friedman LS, Brandt LJ, eds. Sleisenger and Fordtran's Gastrointestinal and Liver Disease. Volume 1. 9th ed. Philadelphia: Saunders Elsevier, 2010:285-322. AND Reprinted/adapted from Clinical Gastroenterology and Hepatology. 6(9). Strate LL, Ayanian JZ, Kotler G, Syngal S. Risk factors for mortality in lower intestinal bleeding. 1004-1010. PMID: 18558513
    • Cause of bleed Notes


      (Most Common)

      Actually pseudodiverticula (outpouching between muscle fibers).

      • Increased intraluminal pressure causes outpouching of colonic mucosa+submucosa through muscular wall  (at points of weakness in colon wall)
      • Occur at sites of entry of "vasa recta" (small arteries).
      • Can bleed at the base of diverticular neck.
      • Most common in L colon, but R-sided are more likely to bleed.
      • 5-10% of pts with diverticulosis experience bleeding at some point.

      Internal Hemorrhoids

      (2nd Most Common)

      - Bright red blood on outside of the stool, toilet paper, or toilet bowl.

      - Occasionally very large volumes and clots.


      (w/ polypetctomy)

      bleeding - 13% of lower GI bleeds!

      - Can happen immediatley after procedure or days later from colonic ulceration due to electrocautery.


      Aka Angiodysplasia

      - NOT arteriovenous malformations

      - frequency increases with age

      - Can be easily missed on colonoscopy


    • Acute management:
      • ABC's - 2 large bore IVs
      • Hospitalize if predictors of severe bleeding:
        • Orthostatic vital signs
        • Bleeding in first 4 hours of evaluation
        • Use of anticoagulants (incl. ASA)
        • Multiple comorbidities.
      • Most LGIB self-terminates within 24hrs, but can re-bleed.
    • Could it be from upper GI tract?
      • Often melena, but can be hematochezia if brisk (life threatening).
      • In the past: placed NG tube to r/o upper GI bleed (misses 15% of UGI bleeds, even if bile stained)
      • IF suspected: Upper Endoscopy is best test.
    • Colonoscopy
      • Timing unclear: the sooner, the more likely cause is found.
        • Typically performed on 2nd day to allow for resuscitation + bowel prep.
      • Sigmoidoscopy / Anoscopy are alternatives if high suspicion of hemorrhoids (anoscopy) or L-sided bleeding (sigmoidoscopy)
      • Majority require complete Colonoscopy
      • Can treat bleeding:
        • multipolar electrocoagulation, epinephrine, hemoclips.
      • If Colonoscopy negative:
        • Evaluate for "obscure GI bleeding" (see below)
    • Angiographic embolization -> if colonoscopy fails to control bleed.
      • High risk of complications (bowel ischemia, femoral artery thrombosis, contrast dye, AKI) - 3%
    • Surgery - if angiography cannot be done



    Obscure GI Bleeding

    • Defined as: Recurrent bleeding without defined source following standard upper endoscopy and colonoscopy.
      • "Overt Bleeding" -->  If blood/melena present:
      • "Occult Bleeding" --> Clinically suspected without overt blood lost (anemia of FOBT)
    • 5% of GI bleeds.
    • Causes of Obscure/Overt Bleeding:
      • Angioectasias
      • Cameron erosions (if large hiatal hernia)
      • NSAID-induced ulcers
      • Malignancy
    • Causes of Obscure/Occult Bleeding:
      • Angioectasias
      • Dieulafoy Lesions
      • Colonic Diverticula
      • Meckel Diverticula


    Causes of Obscure Gastrointestinal Bleeding


    Differential Diagnosis

    Age (Years)

    Clinical Clues

    Proximal to the ligament of Treitz

    Cameron erosion


    Large hiatal hernia


    NSAID ulcerations


    Medication review


    Dieulafoy lesion


    Intermittent large-volume bleeding


    Crohn disease


    Family history, extraintestinal manifestations; may also occur in small bowel and colon


    Gastric antral vascular ectasia


    Female, autoimmune disease

    Small bowel



    Intermittent, usually occult bleeding; may also occur in colon


    Peutz-Jeghers syndrome


    Perioral pigmentation, obstructive symptoms


    Meckel diverticulum


    Possible abdominal pain




    Possible cutaneous hemangiomas




    Weight loss, abdominal pain


    Hereditary hemorrhagic telangiectasia


    Facial telangiectasias




    Intermittent, painless bleeding




    Weight loss, family history

    • Source: MKSAP16




    • Evalutation:
      • Should undergo repeat upper or lower scope (depending on suspected site)
        • 30-50% of lesions detected on repeat endoscopy.
        • If site of bleeding not known... then do secondary tests (below):
      • Capsule Endoscopy is the first-line test for repeated negative endoscopy


    • Technique Notes



      (For Active Bleeding)

      - Only in ACTIVE OVERT bleeding (requires a bleeding rate >1mL/min)

      - Esp works if hemodynamically unstable.

      - Allows for embolization immediately

      - 40% sensitivity, operator dependent.

      - Complications: AKI, organ necrosis, vascular dissection/aneurism.

      Technetium-Labeled Nuclear



      (For Active Bleeding)

      - Best sensitivity for ACTIVE bleeding (requiers bleed 01-0.5mL/min)

        (more sensitive than angiography, often first test performed)

      - Uses Tc99m-labeled RBCs

      - Non-specific (often do not show specific site or intervention)

      Two types of scans

        1. Tc99m pertechnetate RBC

        2. Tc99m surfur colloid

        - RBC scanning positive in 45% of pts with active bleed, 78% accurate for localizing bleed.

      Wireless Capsule

      Endoscopy (NEW!)


      (Active Bleed Not Required)

      - NEW: Excellent visualization of small bowel.

      - Effective even if absence of active bleeding (50-75% find bleed)

      - Complication: Capsules can get stuck at small bowel tumors or stenosis.

      - Generally replaced push enteroscopy as test of choice in occult bleeding

      Push Enteroscopy


      (For therapy/diagnosis)

      - Performed with dedicated enteroscope or pediatric colonoscope.

           - See distal jejunum/duodenum....

           - Allows visualization up to 80cm beyond ligament of Treitz

      - Now less often (use wireless capsule endoscopy)

      - Allows for intervention (i.e. coagulation of angiodysplasias)

      Compilcations: RARE, perforation, mucosal evulsion, bleeding.

      Spiral Enteroscopy (NEW!)

      - NEW technique for deep bowel scoping

      - Spiral-shaped overtube that fits over a standard colono/enteroscope.

         Using "corkscrew" motion allow deep visualization into jejunum and ilium.

      - Can deliver intervention (also useful for ERCP post Roux-en-Y)

      - No comparison data with capsule/push endoscopy.

      Complications: perforation (increased torque on bowel)

      Single and Double-Balloon


      - Simliar to spinal endoscopy to see small bowel.

      - Latex balloons on overtube to deliver enteroscope into small bowel by

         inflating/deflating balloons

      - Can be given orally and rectally for diagnosis and therapy.

      Complications: perforation and bleeding via bowel avulsion.

      Contraindications: radiation enteritis, severe ulceration, recent bowel surgery

      Small-Bowel Radiography

      (Rarely Done)

      - Small bowel barium studies and enteroclysis (small bowel barium enema) 

        not first line

      - Can see luminal masses, diverticula, but cannot asses other (angioectasias etc.)

      Intraoperative Endoscopy

      - Last Resort for life threatening bleeding

      - Laparotomy or laparoscopy + colonoscopy.

      - Rarely done, yield is low (25%)

    • Treatment:
      • Depends on source and site of pathology.
      • Surgery for:
        • luminal tumors
        • Focal lesions (Meckel's Diverticulum)
      • Endoscopic Treatment (electrocautery and/or argon plasma coagulation)
        • Angioectasias (localized)
        • Dieulafoy Lesions
        • GAVE lesions
      • Angiography + embolization
        • For brisk bleeds that cannot be done endoscopically
      • NOTE:
        • Angioectasias associated with Aortic Stenosis (Heyde Syndrome) --> replace valve.
        • Von Willebrand Disease: Desmopressin or replacement of factor.
        • Diffuse Ectasias not amenable to therapy: Estrogens, Octreotide or thalidomide had some success.


    Managment of Anticoagulation

    • In patients with CAD and on ASA:
      • Restart ASA 3-5 days after bleed.
      • ASA shown to reduce all-cause mortality (cardiovascular, cerebrovascular and GI complications) 10-fold over 30 days while increasing bleeding rates only 2-fold. 
      • Long-term daily PPI should be used for H.pylori-negative patients who are on NSAIDs, anticoagulants, glucocorticoids, or antiplatlet agents.
    • Source: International Consensus Recommendations on the Management of Patients With Nonvariceal Upper Gastrointestinal Bleeding (2010) Anals of Int. Med.


    Guideline Summaries

    • International Consensus Recommendations on the Management of Patients With Nonvariceal Upper Gastrointestinal Bleeding (2010)
      • Blood transfusions to a patient with Hb < 70 g/L
      • In patients receiving anticoagulants --> correct coagulopathy, but should not delay endoscopy!
      • Do not use pro-motility agents (used prev. to increase diagnostic yield)
      • Early endoscopy < 24hrs recommended for most pts with acute upper GI bleed.
      • Endoscopy:
        • Endoscopic hemostatic therapy not indicated if low-risk stigmata (clean base, non-protuberant dot)
        • If find a clot in ulcer base --> attempt to irrigate to dislodge and treat underlying ulcer.
        • If find clot --> role of therapy controversial (endoscopic tx vs. PPI)
        • If high risk stigmata --> endoscopic therapy
        • Epinephrine injection is suboptimal, must combine with other methods.
        • NO routine second-look endoscopy.  Only re-scope if rebleeds.
        • Surgery if endoscopy fails (percutaneous embolization also preferred if available)
    • Prevent Re-Bleeding
      • IV PPI (bolus + infusion) should be used (decreases re-bleeding and mortality) if high-risk stigmata found and got successful endoscopy therapy.
      • If bleeding ulcers --> test FOR H.pylori +/- treat  + confirm eradication. 
      • Negative H.pylori tests done acutely should be repeated
    • Other:
      • If low risk --> can feed patients within 24hrs.
    • Hospitalization
      • Low risk endoscopy --> Discharge (use scoring systems)
      • High risk endoscopy --> Hospitalize for at least 72hrs.
    • Discharge
      • If bleeding ulcer + require NSAIDs
        • Combination of PPI + COX-2 inhibitor recommended.
      • If require ASA
        • Restart in 3-5 days (if low risk) with ASA + PPI.
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