- The document provides an overview of gastrointestinal bleeding (GIB), including causes, evaluation, and management. - Common causes of upper GI bleeding (UGIB) include peptic ulcer disease, esophageal varices, esophagitis, and malignancy. Evaluation involves history, physical exam, and laboratory tests to assess severity and risk of rebleeding. - Initial management of UGIB includes IV fluids, blood transfusions if needed, and upper endoscopy within 24 hours to identify the source of bleeding and guide treatment. Management depends on the cause and risk of rebleeding.

1. GIB
Dr. Mohamed Alshekhani
Professor in Medicine.
MBChB-CABM-FRCP-EBGH.
2015
Download from:http://www.slideshare.net/shaikhani/gib-
2015-for-4th-year
1

2. 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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3. 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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4. 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. 4

5. 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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6. 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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7. 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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8. 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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9. 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& aortoenteric
fistulas.
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10. 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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11. 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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12. 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& Balchford
scores).
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13. 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 aortoenteric
fistula, hemobilia, or radiation-related, respectively.
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14. 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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15. 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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16. 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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17. 17

18. 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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19. 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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20. 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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21. 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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22. 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 [rebleeding
risk 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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25. 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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26. 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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27. 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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28. 28

29. 29

30. LGIB:
• Bleeding distal to the ligament of Treitz, typically from the colon or
anorectum.
• Presents with bright red blood per rectum or red/maroon-colored
stool (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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31. 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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32. LGIB: Causes
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33. 33

34. 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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35. 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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36. 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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37. 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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38. 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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39. 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 visual
impairment during colonoscopy ,surgical conslutation should be
done parralel with angiography for emobotherapy / or RBC scan to
identfy bleeding source to guide surgery if embolotherapy was not
successful or not available.
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40. 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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41. 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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42. 42

43. 43

44. 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.
44

45. 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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46. 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.
46

47. 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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48. 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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49. 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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50. 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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51. 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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52. 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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53. BO5 10:
• Testing for H Pylori during UGI bleeding is
frequently:
• A. Positive.
• B. False positive.
• C. False negative.
• D. Negative.
• E. None.
53

54. 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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55. Thanks for attention
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