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    Gastrointestinal Bleeding

    Janak N. Shah, MD

    Assistant Clinical Professor of Medicine

    University of California, San Francisco

    Director of Endoscopy

    San Francisco VA Hospital

    October 2007

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    GI Bleeding : Definitions

    IDA : iron deficiency anemia

    FOBT: fecal occult blood test

    From Zuckerman, Lewis, et al. (AGA Clin Practice Committee). Gastroenterol 2000; 118: 201

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    Acute GI Bleeding : epidemiology

    UGI ~ 100 hospitalizations /

    100,000 persons per year

    M > F Increases with age

    Rockall, BMJ 1995, 311: 222

    Mortality 7-14%Rockall, BMJ 1995; 311: 222

    Longstreth, AJG 1995; 90: 206

    Yavorski, AJG 1995; 90: 568.

    LGI ~ 21 hospitalizations /

    100,000 persons per year

    M > F Increases with age

    Mortality 4%

    Longstreth, AJG 1997; 92: 419

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    Manifestations of Overt GI BleedingHemetemesis

    Red blood or coffee-ground emesis

    Melena

    Black, tarry, foul-smelling Blood in GI tract > 14 hours

    Hematochezia Bright red / maroon stool, bloody diarrhea, clots

    Usually LGI source : UGI source in 10%

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    How much blood does it take to

    produce

    Melena?

    Hematochezia from UGI source?

    FOBT + ?

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    How much blood does it take toproduce

    Melena? 50-100cc

    Hematochezia from UGI source? 500-1000cc

    FOBT + ?

    From UGI source: 10-20 cc

    From LGI source: 0.5 cc

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    Acute UGI Bleeding : Etiology

    What are common causes of UGIhemorrhage?

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    Acute UGI Bleeding : Etiology

    Etiology N = 4137

    Peptic ulcer disease 1448 (35%)

    Erosive mucosal disease 873 (21%)

    Mallory-Weiss syndrome 214 (5%)

    Varices 180 (4%)

    Malignancy 155 (4%)

    Other diagnoses 253 (6%)

    No diagnosis made 1014 (25%)

    Rockall, BMJ 1995, 311: 222

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    Acute UGI Bleeding : Less Common Etiologies

    Hemobilia

    Hemosuccus pancreaticus

    Aorto-enteric fistulas

    GAVE (watermelonstomach)

    AV malformation /

    vascular ectasias

    Dieulafoys lesion

    Portal HTN gastropathy

    Hereditary hemorrhagic

    telangiectasia (Osler-

    Weber-Rendu)

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    Acute LGI Bleeding : Etiology

    What are common causes of LGIhemorrhage?

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    Acute LGI Bleeding : Etiology

    From Elta, GIE 2004; 59: 402

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    Case 1:

    65-year old male presents to the ED with a 1-dayhistory of melena and coffee-ground emesis. Pt

    reports feeling weak and light-headed. You are

    called by the ED to evaluate this patient

    What are important history, physical, and laboratory featuresto assess in this patient ?

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    Overt GI Bleeding : Clinical Assessment

    History and Physical

    ASA / NSAIDs / anti-coags

    Alcohol intake

    Vitals/postural changes (vol

    depletion of 15%)

    Hx/ Signs of liver disease

    Rectal exam- stool color N/G lavage (dx / pre-egd) : 16%

    of UGI bleeds: negative N/G

    Lab studies

    CBC / coagulation studies

    type and crossmatch

    Liver tests

    Chem 7

    Clinical prognostic factors

    Hemodynamic instability

    on presentation Red blood emesis +

    hematochezia

    Failure of N/G clearing Advanced age (>60)

    Medical co-morbidities

    Laine and Peterson, Bleeding pepticulcer, NEJM 1995; 331: 717

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    Case 1: Clinical assessment performed

    History + NSAIDs QD x 1 month for back pain

    EtOH: 1-2 glasses wine, 2-3 x week

    Physical exam VS: supine 120/70, 105-sitting 105/65, 120

    No PE signs of liver disease Abd: soft, NT, rectal- black, tarry stool

    N/G lavage: large vol clots, does not clear

    after 2L lavage

    Labs CBC: wbc 9, hct 44, plts 180

    Coags: nl

    Liver tests: nl

    What should be done now?

    A) Emergent EGD in ERB) Admit to ward, EGD

    tomorrow

    C) Start PPI (IV), no needfor EGD

    D) Fluid resuscitation,

    admit to ICU, urgent

    EGD after stabilization

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    Case 1:

    There is a shortage of ICU beds. The ED team asks

    if a general ward admission would be appropriate.

    They argue that the HCT is normal, and thus this

    patient is not having substantial hemorrhage.

    What is your response ?

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    Hematocrit to Assess Blood Loss

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    Issues to consider prior to EGD for

    UGI bleeding Adequate hemodynamic resuscitation

    Good IV access Hemoglobin >8 g/dl (higher with cardiopulmonary dz)

    Carson, Lancet 1988; 1:727 , Carson, Lancet 1996; 348:1055

    Need for intubation Consider intubation for persistent hemetemesis or

    bloody N/G output

    Conscious sedation vs. deep sedation (anesthesia)

    Clotting parameters Platelets > 50,000

    INR 1.5-2.5 Choudari, Gut 1994; 35: 464.

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    Case 1: Upper Endoscopy Performed

    Visible vessel in duodenal bulbar ulcer (3cm). Active bleeding

    started during EGD prior to endoscopic therapy.

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    Endoscopic Prognostic Factors in

    Ulcer Hemorrhage

    What are the endoscopic factors associatedwith a worse prognosis (rebleeding, death)

    in this patient?

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    Endoscopic Prognostic Factors

    What are the endoscopic factors associatedwith a worse prognosis (rebleeding, death)

    in this patient?

    Actively bleeding ulcerLaine, NEJM 1995; 331: 717.

    Large ulcer size (>1cm)

    24% vs 12% rebleed, 13% vs 1.6% mortalityBranicki, World J Surg 1990; 14: 262.

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    Prevalence and Outcome of Bleeding Ulcer by

    Endoscopic Appearance

    From Laine, NEJM 1995; 331: 717.

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    Endoscopic Stigmata in PUD

    Flat spot Clot

    Clean base

    From Laine, NEJM 1995; 331: 717.

    Visible vessel Active bleeding

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    Endoscopic Treatments for PUD with High-risk

    Stigmata (active bleeding / visible vessels)

    Epinephrine injection (1:10000)

    Contact thermocoagulation(BPEC, heater probes)

    Non-contact thermal (laser,

    APC)

    Endoclips

    Sclerosant injection

    (polidocanol, absolute alcohol)

    Fibrin glue, thrombin injection Saline injection (tamponade)

    Combo tx superior to mono tx (epi alone) for high risk lesions

    10% vs 18% rebleeding (Meta-analysis) Calvet, Gastroenterol 2004; 126: 441.

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    Endoscopic Techniques : Coaptive Thermocoagulation

    Large caliber probe (10F)

    Firm tamponade

    Bipolar (multipolar electrocautery) : 15-25 Watt setting

    Heater probe : 30 joule setting

    hemostasis: > 90% Complications: induce bleeding 0.3%; perforation 0.5%

    From Laine, NEJM 1995; 331: 717.

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    Endoscopic Techniques : Endoclips

    hemostasis: > 90%

    From Raju, GIE 2004; 59: 267.

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    Case 1 : Endoscopic Therapy

    successful hemostasis with contact thermocoagulation and hemoclips

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    Case 1: Post-treatment recommendations:

    Endoscopic treatment is successful in achieving

    hemostasis. The ICU nurse manager asks you

    Can the patient be transferred to the medical ward?

    Should any other medications be started?

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    Algorithm for the Management of

    Bleeding Ulcers

    ICU for 1 day;

    Ward for 2 days

    Endoscopic Therapy

    Active Bleeding

    or

    Visible Vessel

    Ward for 3 days

    No Endoscopic Therapy

    Clot or

    Flat Spot

    Discharge within 1 day

    No Endoscopic Therapy

    Clean Base

    ULCER

    Adapted from Laine, NEJM 1995; 331: 717.

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    PPI for Bleeding Ulcers

    Low intragastric pH (

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    Case 1: continued

    The patient is hemodynamically stable over the next

    22 hours. Just prior to transfer to the medical

    floor, the patient develops hemetemesis, withhypotension and tachycardia.

    What is the recommended management :

    A) Repeat endoscopyB) Endoscopic therapy has failed call IR for angio

    C) Continue PPI (IV), no need for EGD

    D) Endoscopic therapy has failed call surgery

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    Recurrent Bleeding after Endoscopic Therapy

    ~ 20% rebleed after endoscopic txLower with PPI therapy Lau, NEJM 2000; 343: 310

    Permanent hemostasis with repeat endo tx in 50%

    of re-bleeders

    ~ 10% with high-risk stigmata require surgery

    Laine, NEJM 1994; 331: 717

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    Non-endoscopic Therapy for Bleeding Ulcers