GIB

Dr. Mohamed Alshekhani

Professor in Medicine.

MBChB-CABM-FRCP-EBGH.

2015

Download from:http://www.slideshare.net/shaikhani/gib-2015-for-4th-year

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Overview:

• Common.

• Hospitalizations decreased by 4%.

• Inpatient death decreased by 23%, from treatment of H pylori & use of PPIs.

• Mortality is dependent on:

• Age.

• Comorbid illness.

• Source of bleeding.

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Overview:

• Severe GIB:

• Orthostatic hypotension, shock, Hb decreased >2 g/dL (Hct>6%) from baseline or the need for >2 units of PRBCs.

• Hematemesis:

• Vomiting of fresh blood or coffee-ground ; most commonly from the esophagus,stomach, or duodenum

• Melena (black,tarry stool):

• Occurs when as litle as 50-100 mL of blood enters GIT; source is from eso, stomach, SI, or proximal colon.

• Hematochezia (bright red blood per rectum):

• Most commonly caused by a LGIB & if from UGI source often leads to hemodynamic instability, but distal colon or rectal bleeding rarely cause that.

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UGIB:• The most common type of GIB.

• It is proximal to the ligament of Treitz.

• Mortality 5-10%.

• 80% stop spontaneously

• Adverse prognostic indicators are:

• Advanced age Variceal bleeding

• Comorbid conditions (organ failure or disseminated malignancy),

• Shock Hematemesis

• Increasing number of erythrocyte transfusions

• Active bleeding or rebleeding

• Visible vessel or clot in an ulcer on endoscopy.

• The goal: identify patients at highest risk of mortality so that the adequate in-hospital care can be provided & early discharge low risk ones.

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UGIB: Causes• 1.NVUGIB:

• PUD(38%)

• Eso varices (16%)

• Esophagitis (13%)

• Malignancy (7%)

• Angioectasia (6%)

• Mallory-Weiss tear (4%)

• Dieulafoy (2%): submucosal arterioles intermittently protrude through the mucosa & cause hemorrhage.

• Other rare causes.

• 2.Varicceal UGIB:

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UGIB: Causes• Other important but less common lesions are:

• Cameron lesions: erosion in hiatusn hernia, 5% of HH.

• Proximal Crohn’s disease.

• UGI cancers rarely result in severe bleeding (1%) include; eso or gastric cancer or GIST.

• GAVE (or "watermelon stomach") seen in cirrhosis& connective tissue diseases; linear ectatic vessels (erythematous stripes) that arise from the pylorus.

• Bleeding from PHG, GAVE,Cameron lesions is typically chronic rather than acute.

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UGIB: Causes• PHG: commonly seen with cirrhosis

• Has a characteristic mosaic appearance at endoscopy

• Most often seen in body & fundus

• Classified as mild or severe depending on the absence or presence of red spots, respectively.

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UGIB: Causes• Hemobilia is a rare cause of acute GIB from the biliary tree.

• Occur after liver biopsy, ERCP, or TIPS

• May present with the triad of biliary colic, obstructive jaundice (from clotted blood)&melena.

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UGIB: Causes• Telangiectasias in stomach & proximal small bowel in patients with

hereditary hemorrhagic telangiectasia (HHT, Osier-Weber-Rendu).

• Results in acute or chronic GIB,most typically recurrent epistaxis, mucocutaneous telangiectasia, other visceral involvement (lung, liver, brain)& a family history of HHT.

• Lesions should not be overlooked because bleeding can be brisk & mortality high, include varices, pseudoaneurysms& aortoentericfistulas.

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UGIB: Causes• Variceal bleeding may be the first presentation of cirrhosis&

therefore a high index of suspicion is needed.

• Liver diseases is common & 1/3 with cirrhosis will have bleeding from esophageal varices with resultant 15-20% mortality.

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UGIB: Causes• Acute or chronic pancreatitis can be associated with pseudocyst

formation, erode an adjacent artery (pseudoaneurysm) &rarely, cause very brisk GIB (hemosuccus pancreaticus).

• A repaired abdominal aortic aneurysm (especially endovascular repair) lead to the rare complication of an aortoenteric fistula, often as a result of graft infection or inflammation.

• An aortoenteric fistula can present with a minor herald bleed, followed by a torrential, life-threatening GIB.

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Evaluation:• History

• Physical exam clues to the cause of bleeding.

• Attention to hemodynamic status to quantify amount of blood loss.

• Stratification of risk for ongoing or recurrent GIB (Rockal& Balchfordscores).

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Evaluation:History

• Type of blood loss—hematemesis, coffee grounds,melena, or hematochezia—can suggest the origin.

• Slow or intermittent UGIB usually presents with IDA.

• Brisk UGIB presents with hematemesis or coffee-ground emesis.

• Fresh Hematemesis may indicate variceal bleeding.

• Coffee-ground emesis is more typical of gastritis or PUD.

• H/O PUD or NSAID use, chronic alcohol consumption or liver disease, recent history of pancreatitis, or chronic GERD symptoms can point to PUD, variceal bleeding, pseudoaneurysmal bleeding, or esophagitis, respectively.

• H/O aortic endovascular stent placement, biliary manipulation, or radiation therapy may indicate bleeding from an aortoentericfistula, hemobilia, or radiation-related, respectively.

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Evaluation: PE

• The most important components of Physical Exam are:

• Routine & orthostatic vital signs.

• Tachycardia indicates a 15-30% blood loss

• Hypotension indicates >30% blood loss.

• Orthostasis alone indicates large-volume bleeding even when routine vital signs are normal.

• Signs of chronic liver disease such as scleral icterus, spider angiomata, gynecomastia, ascites.

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Evaluation:Lab tests

• A complete blood count, INR, BUN, serum creatinine.

• The hemoglobin&hematocrit are not accurate measurements of blood loss during the acute phase of bleeding but may aid decisions on erythrocyte transfusion requirements.

• Macrocytosis & an elevated INR are clues for underlying liver disease.

• Microcytosis can indicate chronic bleeding.

• An elevated BUN to creatinine ratio suggests an UGI source.

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Evaluation: prognostic stratification

• Several prognostic scoring systems (Rokal & Blatchford) to quantitate the risk of needing endoscopic intervention, but these are not widely used in clinical practice.

• Blatchford Score can be used to predict patients with signs of UGIB who can be managed as outpatients if all of the following are present:

• BUN <18 mg/dL; normal hemoglobin; systolic blood pressure>109 mm Hg; PR<100/min;absence of melena, syncope, , hepatic &cardiac disease.

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UGIB: Management

• Prompt hemodynamic assessment.

• Risk stratification.

• Support with IVF /or blood products

• consideration of the origin of blood loss by OGD.

• The initial management is the same until upper endoscopy performed to verify the cause of bleeding, but variceal bleeding is managed differently from NVGIB.

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UGIB: Management

• The initial management:

• Airway protection.

• Placement of two large-bore IV cannulas .

• Resuscitation with IV crystalloids & packed red blood cell infusions.

• Continuous hemodynamic monitoring is more helpful than hemoglobin & hematocrit, in guiding resuscitation, but a Hb <7.0 g/dL is an absolute indication for packed red blood cell transfusion.

• For suspected NVGIB, IV PPI is often initiated before endoscopy.

• NGT is not routinely recommended.

• Erythromycin & metoclopramide (motility agents) decrease the need for repeat endoscopy by improving visibility at the initial endoscopy.

• Not routinely used ,because not shown to alter the need for erythrocyte transfusion or surgery or shorten hospital stay.

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UGIB: Management

• Patients on anticoagulation with a suprathcrapeutic INR should receive fresh frozen plasma.

• The risk of continued bleeding on warfarin must be weighed against the risk of stopping anticoagulation & endoscopy should not be delayed for anticoagulation reversal unless the INR is supratherapeutic (INR >3.0).

• If a variceal bleed is suspected, octreotide & antibiotics should be administered as soon as possible.

• Upper endoscopy should be performed after hemodynamic stabilization but within 24 hours of presentation & within 12 hours for suspected variceal bleeding.

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UGIB: Management

• Endoscopic trt of a bleeding ulcer depends on the ulcer characteristics, an important predictors of recurrent bleeding.

• Low-risk stigmata: (a clean-based ulcer [rebleeding risk with medical therapy 3-5%] or a nonprotuberant pigmented spot in an ulcer bed [rebleeding risk with medical therapy 5-10%]) can be fed within 24 hours,should receive oral PPI therapy& can undergo early hospital discharge.

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UGIB: Management• High risk stigmata:

• Ulcers with adherent clots (rebleeding risk with medical trt 25-30%) can be irrigated to disrupt the clot& endoscopic trt provided after.

• Patients with high-risk stigmata (active arterial spurting [rebleedingrisk with medical therapy 80-90%] or a nonbleeding visible vessel in an ulcer base [rebleeding risk with medical therapy 40-50%]) should be treated with epinephrine injection+ one of" the following:

• Hemoclips, thermocoagulation, or a sclerosant .

• Duration of PPI depends on the underlying cause of the ulcer &future need for NSAIDs.

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UGIB: Management

• Bolus + maintenance IV PPI for 72 hs is recommended for patients at high risk to decrease risk of rebleeding, followed by oral PPI.

• Patients at high risk require hospitalization for at least 72 hours after intervention.

• Surgery or interventional radiology (for embolization) is reserved for refractory bleeding or rebleeding despite 2 endoscopic therapies

• Routine second-look endoscopy (within 24 hs) is not recommended, but it should be performed if visualization or endoscopic treatment during the initial examination was suboptimal.

• A repeat endoscopy should be performed for rebleeding prior to considering surgery or interventional radiology.

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UGIB: Management

• Surveillance endoscopy for gastric ulcers to rule out malignancy (6-8 weeks later) is recommended when biopsies of the ulcer were not performed during the initial endoscopy, which is generally the case in the context of a bleeding event.

•

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UGIB: Management

• Further management of PUD should focus on the cause, with treatment & confirmation of eradication of Helicobacter pylori when present & counseling regarding cessation of NSAIDs when they are causative.

• For patients who require aspirin for cardiovascular prophylaxis, aspirin should be restarted while continuing PPI therapy when the benefit outweighs the risk of bleeding.

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LGIB:

• Bleeding distal to the ligament of Treitz, typically from the colon or anorectum.

• Presents with bright red blood per rectum or red/maroon-coloredstool (hematochezia) that is acute in onset, usually without significant abdominal pain.

• Patients typically have evidence of anemia but less commonly have hemodynamic instability.

• Although significant hypotension can result from LGIB, it should prompt consideration of a briskly UGI source.

• The risk increases with age; typically 7th or 8th decade of life.

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LGIB: Causes

• 75% with hematochezia have a colonic source of bleeding.

• 15-20% have bleeding from UGI

• 5% have bleeding from small bowel.

• 3% not identified.

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LGIB: Causes

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LGIB Causes: colonic diverticuli

• The most frequent cause in the west.

• Colonic diverticula occur when increased intraluminal pressure causes herniation of colonic mucosa& submucosa through the muscular layers at points of relative weakness.

• Diverticula tend to occur at site of entry of the small arteries (vasa recta)&may bleed at the base of the diverticular neck.

• Diverticulosis is most common in the left colon, but right-sided diverticula are more likely to bleed.

• 3- 5% experience diverticular bleeding at some time.

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LGIB: Int hemmorrhoids

• The second most common colonic cause of LGIB( 1st here).

• Characterized by bright red blood on the outside of the stool, on the toilet paper, or in the toilet bowl.

• Occasionally, large amount of fresh blood & some can pass clots.

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LGIB: Postpolypectomy

• 13% of LGIB.

• May occur immediately following polyp removal ,typically caused by vascular injury at the base of the polyp stalk

• bleeding may also be delayed for several days, resulting from ulceration of colon from electrocautery used for polyp removal.

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LGIB: Angioectasias

• Angiodysplasia( often incorrectly called AVM) occur less frequently than diverticular or hemorrhoidal bleeding but are an important cause & frequency increases with age.

• Can be numerous yet subtle & can be easily missed on colonoscopy if not actively bleeding.

• Associated with AS & LVAD.

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LGIB: Evaluation

• Consider whether the bleeding source could be from UGI.

• UGIB typically presents with melena; but may present with hematochezia when brisk & can be life threatening if not treated early.

• NGT (even if bile-stained aspirate) can miss 15% of actively bleeding lesions.

• NGT aspirate cannot rule out a postpyloric bleeding source&can be incorrect up to 50% of the time.

• if UGI source is suspected, OGD is the most appropriate.

• If an upper source is not a consideration or the patient has had a negative upper endoscopy, next step colonoscopy.

• Anoscopy or sigmoidoscopy could be considered as alternatives if there is a high suspicion of hemorrhoids or left-sided bleeding, respectively, but majority will require a complete colonoscopy.

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LGIB: Evaluation

• Colonoscopy identifies presumed or definite cause of LGIB 2/3 of the time.

• The sooner the colonoscopy is performed, the more likely it is to identify a source; but typically performed on the second day of hospitalization to allow for resuscitation &proper bowel prep.

• If OGD/colonoscopy do not identify site of bleeding &there is ongoing bleeding, the next step is to evaluate for obscure GIB.

• If the patient is in shock or severe bleeding causing visualimpairment during colonoscopy ,surgical conslutation should bedone parralel with angiography for emobotherapy / or RBC scan toidentfy bleeding source to guide surgery if embolotherapy was notsuccessful or not available.

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LGIB: management

• Patients should be medically resuscitated.

• Two large-bore IV lines should be operational at all times.

• Patients should be hospitalized if they have predictors of severe bleeding (orthostatic vital signs, bleeding in the first 4 hours of evaluation, use of anticoagulants including aspirin, or multiple comorbidities).

• Most LGIB stops without direct intervention within 24 hours, but early rebleeding is common

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LGIB: management

• Major complications (such as bowel ischemia, femoral artery thrombosis, contrast dye reactions& acute kidney failure) occur in 3% of angiographic interventions.

• For patients at significant risk with angiography or who have persistent bleeding despite radiographic intervention, surgery may be required to identify & treat the bleeding site.

• Mortality rate is low (<5%), but highest in hospitalized for another indication.

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BO5 1:

• The minimum amount of GIT Blood loss sufficient to cause melena is:

• A. 10 mls.

• B. 20 mls.

• C. 50 mls.

• D. 40 mls.

• E. 30 mls.

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BO5 2:

• The followings should be routine during UGIB except:

• A. Pre-endoscopy PPI.

• B. Post-endoscopy PPI in high risk patients.

• C. Two IV cannulas.

• D. IV erythromycin.

• E. Hemodynamic assessment.

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BO5 3:

• The followings are high risk endoscopic lesions during UGI Bleeding except:

• A. Spurting vessel.

• B. Ozzing.

• C. Adherent clot.

• D. Ulcer with pigmentary changes.

• E. None of the above.

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BO5 4:

• The best endoscopic hemostatic intervention for high risk lesions is:

• A. Dual therapy.

• B. Single therapy.

• C. Adrenaline injection alone.

• D. APC alone.

• E. Sclerotherapy.

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BO5 5:

• Therapeutic interventional radiology can be used when endoscopic hemostasis fails in:

• A. UGI Bleeding.

• B. lower GI bleeding.

• C. Both.

• D. Neither.

• E. Only for UGI Bleeding.

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BO5 6:

• The best indication for NGI in GI Bleeding is in:

• A. UGI Bleeding routinely.

• B. lower GI bleeding routinely.

• C. In severe lower GI bleeding with shock.

• D. It can surely exclude upper GI source of bleeding .

• E. None of the above.

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BO5 7:

• IV erythromycin in UGI bleeding can:

• A. Improve survival.

• B. Can improve visualization during endoscopy & reduce the need for re-endoscopy.

• C. Reduce the need for blood transfusions.

• D. Reduces the need for surgery.

• E. Reduce hospital stay.

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BO5 8:

• Angioectasias as a cause of lower GIB is associated with:

• A. Aortic stenosis.

• B. Vasculitis.

• C. Hemophilias.

• D. Female gender.

• E. None of the above.

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BO5 9:

• Endoscopy for significant upper compared with lower GI Bleeding is usually performed:

• A. Earlier.

• B. Later.

• C. At the same time from the onset.

• D. The second day from the onset.

• E. The 3rd day from the onset.

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BO5 10:

• Testing for H Pylori during UGI bleeding is frequently:

• A. Positive.

• B. False positive.

• C. False negative.

• D. Negative.

• E. None.

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BO5 11:

• Patients with high risk endoscopic upper GI bleeding lesions should be monitored in the hospital for:

• A. 12 hours.

• B. 24 hours.

• C. 36 hourd.

• D. 72 hours.

• E. 96 hours.

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Thanks for attention

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