Upper GI Bleed - Symposium

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    UPPERGASTROINTESTINAL

    BLEEDING

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    ANATOMY OF

    UPPER GASTROINTESTINALTRACT

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    The gastrointestinal tract extends from mouth

    to anus

    On embryologic grounds, the GI tract should

    be divided into

    upper (mouth to major papilla in the duodenum),

    middle (papilla to mid-transverse colon), and

    lower (mid-transverse colon to anus)

    Derivation of these 3 areas from the foregut,

    midgut, and hindgut, respectively.

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    From the point of view of GI bleeding,

    however, the demarcation between the upperand lower GI tract is the duodenojejunal (DJ)

    junction/ligamentum treitz

    Bleeding above the DJ junction is called upper

    GI bleeding, and that below the DJ junction is

    called lower GI bleeding.

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    Consist ofskeletal muscle from the diaphragm

    and a fibromuscular band of smooth muscle

    which inserts into the 3rd and 4th part ofduodenum and frequently the DJ junction

    Contraction widens the angle of theduodenojejunal flexure, allowing movement

    of the intestinal contents.

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    Causes and pathophysiology of

    Upper GI Bleeding

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    Causes

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    Peptic Ulcer

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    gastric erosion

    refers to endoscopically visualized

    subepithelial hemorrhages and erosions

    due to NSAID,stress and alcohol.

    not much bleeding.

    causes ulceration.

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    Due to longitudinal mucosal lacerations (known asMallory-Weiss tears) at the gastroesophagealjunction or gastric cardia.

    The original description by Mallory and Weiss in1929 involved patients with persistent retching andvomiting following an alcoholic binge.

    However, Mallory-Weiss syndrome may occur afterany event that provokes a sudden rise in intragastricpressure or gastric prolapse into the esophagus.

    May also occur in epileptic convulsions.

    Mallory-Weiss Tear

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    Bleeding esophageal varices are enlarged veins inthe walls of the lower part of the esophagus.

    Scarring ( cirrhosis) of the liver is the most commoncause of esophageal varices. This scarring reducesblood flowing through the liver. As a result, moreblood is shunted to the veins of the esophagus.

    This extra blood flow causes the veins in theesophagus to balloon outward. If these veins breakopen, they can bleed severely.

    Any type of chronic liver disease can causeesophageal varices.

    Varices can also occur in the upper part of thestomach.

    Varices

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    Clinical Features of upper

    gastrointestinal bleeding

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    Patients with upper GI hemorrhage often

    present with:

    A. hematemesis (vomiting of blood),

    B. coffee ground vomiting,

    C. melena (dark tarry stools),

    D. hematochezia (blood in the feces) if thehemorrhage is severe.

    E. dyspepsia (especially nocturnal symptoms)

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    Patients may also present with complications

    of anemia, including:

    a. chest pain,

    b. syncope (loss of consciousness resulting from

    insufficient blood flow to the brain),

    c. fatigue

    d. shortness of breath.

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    The finding of subcutaneous emphysema with

    a history of vomiting is suggestive of

    Boerhaave syndrome (esophageal perforation)

    The presence of postural hypotension

    indicates more rapid and severe blood loss.

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    Probable Source of GI Bleeding Within

    the Gut

    Clinical IndicatorProbability of Upper GI

    Source

    Probability of Lower GI

    Source

    Hematemesis Almost certain Rare

    Melena Probable Possible

    Hematochezia Possible Probable

    Blood-streaked stool Rare Almost certain

    Occult blood in stool Possible Possible

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    Investigations of uppergastrointestinal bleeding

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    Investigations in Upper GI Bleeding

    1. Urgent endoscopy (

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    1. Plain radiographs of abdomen - free air under the

    diaphragm is seen in cases of perforated viscous,

    and this may be accompanied by UGIB. Other

    etiologies, such as upper GI masses (which usually

    result in chronic, not acute, UGIB), aneurysms

    with calcifications, and ascites suggestive of

    portal hypertension, may be seen on radiographs.2. Blood alcohol concentration

    3. Blood glucose concentration

    4. CVP monitoring, blood replacement and bladdercatheterisation (for those with severe bleeding)

    5. Coagulation screen

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    Thyroid chemistries, cortisol, and calcium levels

    are obtained to exclude endocrinologic causes of

    GI symptoms. Pregnancy testing is considered for

    young women with unexplained nausea.

    Serologies tests are available to screen for celiac

    disease, IBD, and rheumatologic diseases such as

    lupus or scleroderma.

    Hormone levels are obtained for suspected

    endocrine neoplasia.

    Intraabdominal malignancies produce tumormarkers including the carcinoembryonic antigen

    CA 19-9 and -fetoprotein

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    MANAGEMENT

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    Resuscitation and initial management Shocked patients should receive prompt volume replacement. It has been

    demonstrated that early and aggressive resuscitation reduces mortality in UGIB.

    Correct fluid losses. Either colloid or crystalloid solutions may be used to achievevolume restoration prior to administering blood products; red cell transfusion

    should be considered after loss of 30% of the circulating volume.

    Transfuse patients with massive bleeding with blood, platelets and clottingfactors in line with local protocols for managing massive bleeding.

    Platelet transfusions should not be offered to patients who are not activelybleeding and are haemodynamically stable.

    Platelet transfusions should be offered to patients who are actively bleeding andhave a platelet count of less than 50 x 109/litre.

    Fresh frozen plasma should be used for patients who have either a fibrinogenlevel of less than 1 g/litre, or a prothrombin time (INR) or activated partialthromboplastin time greater than 1.5 times normal.

    Prothrombin complex concentrate should be used for patients who are takingwarfarin and actively bleeding.

    Proton pump inhibitors (PPIs) should not be used prior to diagnosis by endoscopyin patients presenting with acute UGIB.

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    Management of non-variceal bleeding

    Endoscopy is now the method of choice for controlling active peptic-ulcer related UGIB.

    Endoscopic therapy should only be delivered to actively bleeding lesions, non-bleeding visible

    vessels and, when technically possible, to ulcers with an adherent blood clot. Clean ulcer

    base with oozing do not merit endoscopic intervention since these lesions have an excellent

    prognosis without intervention.

    Adrenaline (epinephrine) should not be used as monotherapy for the endoscopic treatment

    of non-variceal UGIB. For the endoscopic treatment of non-variceal UGIB, one of thefollowing should be used:

    A mechanical method (eg clips) with or without adrenaline (epinephrine).

    Thermal coagulation with adrenaline (epinephrine).

    Fibrin or thrombin with adrenaline (epinephrine).

    Interventional radiology should be offered to unstable patients who re-bleed after

    endoscopic treatment. Refer urgently for surgery if interventional radiology is not

    immediately available.

    Acid-suppression drugs (PPIs or H2-receptor antagonists) should not be offered before

    endoscopy to patients with suspected non-variceal UGIB. PPIs should be offered to patients

    with non-variceal UGIB and stigmata of recent haemorrhage shown at endoscopy.

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    Treatment after first or failed endoscopic treatment

    Repeat endoscopy, with treatment a