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

    Cancer

    (incl. GI Stromal Tumors)

    (aka GIST)

    <1%   Esophageal or gastric cancers

    Portal Hypertensive

    Gastropathy (PHG)

      Chronic

    - 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)

      Chronic

    - "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

    Chronic

     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

      ACUTE

    - 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

    Erosion

      ACUTE

    - 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

        PUD
        Liver Disease Variceal Bleed
        Hx of pancreatitis Pseudoaneurism Bleed
        Chronic GERD Esophagitis
        Aortic Endovascular Stent Aorto-enteric fistula
        Biliary manipulation
        (ERCP/Tips/LiverBx)
        Hemobilia
        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

      NONE

      - 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

      ACUTE
       

      HEMORRHAGE

      Ia Spurtic Vessel 55-100%
      IB Oozing Vessel

      RECENT

      HEMORRHAGE

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

      NOT ACTIVE

      BLEEDING

      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

      Diverticulosis

      (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.

      Post-colonoscopy

      (w/ polypetctomy)

      bleeding - 13% of lower GI bleeds!

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

      Angioectasias

      Aka Angiodysplasia

      - NOT arteriovenous malformations

      - frequency increases with age

      - Can be easily missed on colonoscopy

    Management

    • 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

    Location

    Differential Diagnosis

    Age (Years)

    Clinical Clues

    Proximal to the ligament of Treitz

    Cameron erosion

    20-60

    Large hiatal hernia

     

    NSAID ulcerations

    >20

    Medication review

     

    Dieulafoy lesion

    >40

    Intermittent large-volume bleeding

     

    Crohn disease

    20-60

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

     

    Gastric antral vascular ectasia

    20-60

    Female, autoimmune disease

    Small bowel

    Angioectasias

    >60

    Intermittent, usually occult bleeding; may also occur in colon

     

    Peutz-Jeghers syndrome

    <20

    Perioral pigmentation, obstructive symptoms

     

    Meckel diverticulum

    20-60

    Possible abdominal pain

     

    Hemangioma

    <20

    Possible cutaneous hemangiomas

     

    Malignancy

    >50

    Weight loss, abdominal pain

     

    Hereditary hemorrhagic telangiectasia

    >50

    Facial telangiectasias

    Colon

    Diverticulosis

    >50

    Intermittent, painless bleeding

     

    Malignancy

    >50

    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

      Angiography

       

      (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

      Scan

       

      (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

      Enteroscopy

      - 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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