This document discusses gastrointestinal tract bleeding. It defines upper and lower GI bleeding and provides epidemiological data. Common causes of upper GI bleeding include peptic ulcers, varices, Mallory-Weiss tears, and angiodysplasia. Lower GI bleeding is commonly caused by diverticular disease, angiodysplasia, and ischemic colitis. Management involves resuscitation, endoscopy for diagnosis and treatment, and angiography for severe or obscure bleeding. The mortality of GI bleeding remains significant.

1. GASTROINTESTINAL TRACT
BLEEDING
By
Dr. Wasfi M Salayta
KHMC

2. Epidemiology
• Upper GI bleeding:
– Is defined as bleeding from a gastrointestinal source that is proximal to the
ligament of Treitz.
– It is more common than lower GI bleeding.
– Annual incidence 149-172/100,000.
– Increased in males and in older patients.
– Over 50% of upper GI bleeds are due to erosive or ulcerative disease of the
stomach or duodenum.
– The mortality associated with GI bleeding remains significant at 5% to 11%.
– The following factors increased the mortality rate in upper GI bleeding :
• Age > 60.
• Co morbid diseases especially pulmonary and hepatic diseases.
• Physical findings consistent with cardiorespiratory or hemodynamic
compromise.
• Blood transfusion requirement greater than 5 units.
• Requirement for surgery (patients requiring emergency surgery had increased
mortality compared with those undergoing more elective surgery).
• Recurrent bleeding after hospitalization.
• Those who develop GI bleeding after hospitalization for other reasons.

3. Epidemiology
• lower GI bleeding:
– Is defined as bleeding distal to the ligament of Treitz. It can range in severity
from trivial to massive.
– LGIB accounts for approximately 20% of all major GI bleeds.
– More commonly bleeding is from a colonic rather than a small bowel source.
– Annual incidence 21 cases per 100,000.
– Increased in males and in older patients (mean age at presentation of 63 to 77
years).
– 80-90% of cases will stop bleeding spontaneously.
– As many as 25% will re-bleed either during or after their hospital admission.
– While most patients have a self-limited illness, the reported mortality ranges
from 2-4%.
– Among all patients presenting with lower GI bleeding, diverticular disease is
the most common cause, followed by, vascular anomaliesor ischemic colitis.

4. Etiology- Upper GI bleeding
• Chronic Peptic ulcer disease : is the most common cause of upper
GI bleeding ,over 50% of cases
– Duodenal ulcer 29%.
– Gastric ulcer 16%.
– Stomal ulcer 5%
• Acute mucosal ulceration(Stress gastritis )
– 1-33% of the upper GI bleeding causes.
– Often multiple and not extend through muscularis mucosa.
– Diffuse and typically involve the gastric body and fundus.
– More frequently seen in the following conditions ( shock-sepsis-
surgery-trauma-burn-renal failure-respiratory failure-jaundice).
– The pathogenesis is due to an imbalance between aggressive and
protective mucosal factors.
– Both H2-blocker and Antacid are effective in prevention.

5. Etiology- Upper GI bleeding
• Mallory-Weiss tear:
– A mucosal laceration of the gastric cardia or
gastroesophageal junction.
– Account for approximately 5% to 15% of all cases of upper
GI bleeding and are relatively common in alcoholics.
– The classic presentation is that of repeated retching,
vomiting or coughing followed by hematemesis.
– Up to 50% of patients do not give a history of antecedent
retching or vomiting.
– Only 10% present with hemodynamic compromise.
– Bleeding is self-limited in 90% of cases
• Esophagitis/esophageal ulcer (seen in HIATUS HERNIA )

6. Etiology- Upper GI bleeding
• Esophageal/gastric varices.
– The incidence of bleeding is approximately 10% to 15% per year, and in
patients with large varices is 20% to 30%.
– Bleeding due to varices is typically brisk and associated with hemodynamic
compromise.
– The mortality associated with the first variceal bleed ranges from 30% to 50%.
– Treatment :
• Endoscopic sclerotherapy and band ligation of varices are the mainstay of emergent
therapy.
• medical therapy for variceal hemorrhage has been extensively studied, the benefit of
such therapy remains uncertain (vasopressin, More recently somatostatin and
the somatostatin analogue, octreotide)
• The Senkstaken-Blakemore tube remains an important therapeutic tool in patients with
brisk esophageal or gastric variceal hemorrhage that cannot be controlled on initial
endoscopy.
• Patients who continue to bleed or who have more than one rebleeding episode despite
endoscopic and medical therapy should be considered for portal decompression.

7. Etiology- Upper GI bleeding
• Neoplasm
– Gastric cancer
– Esophageal cancer
– Stromal tumor

8. Etiology- Upper GI bleeding
• Vascular anomalies
• An unusual cause of upper GI bleeding, accounting for only 5% of cases..
• Angiodysplasia, whether sporadic or secondary, is the most common vascular anomaly seen in the GI
tract.
– Angiodysplasia/ectasia
• Are dilated, tortuous vessels in the mucosa and submucosa.
• The pathophysiology unclear, but is felt to be due to intermittent obstruction of the submucosal veins
because of the colonic wall tension, which is highest in the cecum.
• May be sporadic, usually developing in the elderly.
• May be found in association with a number of disorders including renal failure, cirrhosis, the CREST
syndrome, radiation injury, von Willebrand’s disease, and aortic stenosis.
• May occur anywhere in the GI tract, but are more commonly found in the colon(most common in the cecum
and ascending colon) , followed by the small intestine and the stomach.
• These lesions usually lead to occult blood loss, but can also cause overt GI bleeding.
• Usually apparent at endoscopy, at which time therapy with laser or thermal probes may be applied.
• Bleeding that is refractory to endoscopic or medical therapy is an indication for surgical resection
– Dieulafoy lesion
• is characterized by an aberrantly large and tortuous submucosal artery that may erode through a small
mucosal defect, resulting in massive hemorrhage
• 75% to 95% occur in the proximal stomach, usually on the lesser curvature and within 6 cm of the
gastroesophageal junction, although they have been reported to occur thoughout the GI tract
• These lesions often respond to endoscopic therapy with injection of saline or 1:10,000 epinephrine
and/or endoscopic application of thermal probes
• Patients who do not respond to endoscopic therapy require surgical intervention
• wide wedge resection of the artery and bleeding site is preferable to oversewing the artery in the area
of the mucosal defect
• Patients who are poor surgical candidates may respond to angiographic embolization
– Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu)
– Arteriovenous malformation

9. Etiology- Upper GI bleeding
• Aortoduodenal erosion or fistula
– Representing 80% of all aortoenteric fistulas.
– It is estimated that 0.4% to 4% of patients with aortic grafts
develop an aortoenteric fistula.
– Primary aortoduodenal fistulas associated with atherosclerotic
aneurysms or trauma are much less common.
– rarely is seen endoscopically
– Angiography is seldom helpful unless a pseudoaneurysm is seen
– CT visualization of an aneurysm with associated extraluminal
gas is virtually diagnostic, this finding is also uncommon.
– The diagnosis is usually made or confirmed on laparotomy.
Surgical repair is the only therapeutic option.

10. Etiology- Upper GI bleeding
• Hemobilia
– Is usually associated with intraductal neoplasm, trauma, or iatrogenic injury
such as percutaneous liver biopsy and cystic artery pseudoaneurysm.
– Suggested by jaundice, right upper quadrant pain and gastrointestinal
bleeding.
– May be confirmed at endoscopybut often requires angiography.
– Angiographic therapy is the treatment of choice, although occasionally
surgical therapy is necessary
• Hemosuccus pancreaticus (This is most commonly due to a
pseudoaneurysm of the splenic artery in patients with a pancreatic
pseudocyst or chronic pancreatitis but rarely may occur in patients with
pancreatic duct malignancy
• Non-GI source (epistaxis)
• Factitious bleeding (ingestion of animal blood or human blood after
auto-phlebotomy).

11. Etiology- lower GI bleeding
• Anorectal causes :
– Include hemorrhoids -anal fissure and rectal ulcer.
– Bleeding from hemorrhoids and fissure is uncommonly
associated with hemodynamic instability or large volume
of blood loss.
– While rectal ulcer can cause severe hemorrhage and
hemodynamic instability
– Possible causes of rectal ulcer are :
• Radiation.
• Sexual transmitted disease.
• NSAIDs.
• Liver disease.
• Trauma.

12. Etiology- lower GI bleeding
• Diverticular disease:
– Contributes 20-60% of the cases of LGIB.
– In 75% of patients bleeding will stop spontaneously.
– Rebleeding rate after first episode 25% and increase to
50% after two episodes.
– 5% will have severe hemorrhage.
– diverticular bleeding is distributed equally between the
right and left sides of the colon.
– Observation alone is generally recommended following
the first episode of diverticular hemorrhage. However,
following a second episode, the risk of subsequent
episodes appears to approximate 50%, and thus elective
resection has been recommended.

13. Etiology- lower GI bleeding
• Angiodysplasia:
– Only about 15% of patients with vascular ectasia will
develop gastrointestinal hemorrhage.
– The incidence in most recent studies is only 3%
compared to 15-27% previously as cause of LGIB.
• Colorectal neoplasm
– Although colorectal cancer is most commonly
associated with occult blood loss rather than overt
bleeding, patients with rectosigmoid lesions may
present with hematochezia.
– CR-cancers are source of LGIB in 9-13% of patients.

14. Etiology- lower GI bleeding
• Ischemic colitis
– Occurs in 9-18% of patients.
– Results from a sudden and often temporary reduction in mesenteric blood flow,
typically caused by hypoperfusion, vasospasm, or occlusion.
– The usual areas affected are the “watershed” areas of the colon: the splenic flexure and
the rectosigmoid junction.
– Patients tend to be elderly, often with significant atherosclerosis or cardiac disease.
• Other colonic etiologies:
– Inflammatory bowel disease:
• Acute hemorrhage occurs 0.9-6% in CD and 1.4-4% in UC.
• Bleeding occurred in both young and old patients and not related to disease duration.
• Malignant lesion must be considered in patient with long standing history of IBD and LGIB.
– Infectious colitis or enteritis :
– Radiation colitis/proctitis.
– Trauma, hematologic disorders and NSAIDs.
– Post polypectomy (occurs in 0.3% to 6.1% of polypectomies).
– Bleeding from CR-anastomosis (o.5-1.8%).

15. Etiology- lower GI bleeding
• Small bowel sources account for 3-5% of all
cases of LGIB:
– Angiodysplasia is most common cause of small
bowel hemorrhage (70-80%).
– small bowel diverticula,
– Meckel’s diverticula,
– neoplasia,
– Crohn’s disease,
– aorto-enteric fistulas.

16. Obscure Gastrointestinal Bleeding
• Defined as recurrent acute or chronic GI bleeding for which
no source has been found despite evaluation with EGD and
colonoscopy with or without routine small bowel follow-
through.
• It accounts 1.19-9% of LGIB.
• The most frequent causes are :
– Small bowel tumors.
– Angiodysplasia.
– Ulcererosion.
• The diagnosis needs more procedures than patients with
upper GI and colonic bleeding include:
– Capsule endoscopy.
– Double balloon enteroscopy.

17. MANAGEMENT OF GI BLEEDING
• Initial assessment, resuscitation and triage:
– GI bleeding may have different clinical presentations
• hematemesis or hematochezia with hemodynamic instability.
• melena or rectal bleeding without hemodynamic compromise.
• patients may have chronic GI bleeding with asymptomatic iron-deficiency
anemia, or hemoccult-positive stool on screening for colorectal cancer.
– Patients presenting to the emergency room with hemodynamic
instability require rapid clinical assessment.
• Intravenous access with at least two large-bore lines.
• nasogastric tube placement,
• determination of hematocrit and coagulation studies, and type and cross for
blood products.
• Patients with altered mental status should undergo endotracheal intubation
for airway protection
• . Emergent evaluation by a gastroenterologist should be requested.
• The patient should be stabilized before proceeding to endoscopy.

18. MANAGEMENT OF GI BLEEDING
– it is important to determine whether the bleeding is from an upper or lower
GI source ( usually relatively straightforward)
• approximately 5%-10% of patients who present with hematochezia are bleeding from an
upper GI source.
• If there is uncertainty about the presence of an upper GI bleeding source, such as when
the gastric aspirate is not bile-stained, patients with hematochezia and hemodynamic
compromise should undergo upper endoscopy before evaluation of the lower GI tract.
– Admission to the hospital is required for most patients presenting with GI
bleeding
• Those who present with frank hypotension or who have evidence for ongoing bleeding
require monitoring in an intensive care unit and urgent endoscopic evaluation
• Those who present with mild or no orthostasis, have no evidence for continued
bleeding, but have had a significant drop in hematocrit are generally hospitalized on a
medical/surgical floor.
– young patients with self-limited GI bleeding who present without orthostasis
or hemodynamic instability and who have no significant comorbid conditions
may be managed as outpatients.

19. MANAGEMENT OF GI BLEEDING
• Diagnosis:
– History and physical:
• During the initial stabilization and evaluation, a complete history and physical should be
performed.
• History:
– Patients with upper GI bleeding should be questioned about:
» Peptic ulcer disease
» liver disease,
» malignancy,
» abdominal surgery
» bleeding disorder,
» weight loss,
» alcohol,
» aspirin or non-steroidal antiinflammatory drug (NSAID) use.
» A history of antecedent retching suggests a Mallory-Weiss tear
– Patients with suspected lower GI bleeding should also be asked about:
» hemorrhoids,
» associated diarrhea,
» change in bowel habits,
» personal or family history of inflammatory bowel disease,
» A history of radiation therapy.
» A family history of GI disorders, malignancy or bleeding disorders should also be obtained.

20. MANAGEMENT OF GI BLEEDING
• Physical examination
– Orthostatic blood pressure and pulse even if the patient
appears stable.
– cutaneous stigmata of liver disease
– splenomegaly or ascites, abdominal tenderness, an abdominal
mass or lymphadenopathy
– cutaneous or mucocutaneous manifestations of systemic
disorders associated with GI bleeding
– ENT EXAMINATION,RECTAL EXAMINATION.

21. MANAGEMENT OF GI BLEEDING
– Diagnostic studies:
• Upper GI endoscopy:
– the preferred diagnostic modality in patients with upper GI
bleeding
– advantages of endoscopy include:
» the ability to obtain biopsies for an accurate histologic
diagnosis,
» Determine the risk of rebleeding .
» Provide endoscopic therapy.
– Patients with severe upper GI bleeding should have an upper
endoscopy, or esophagogastroduodenoscopy (EGD), performed
as soon as they are stable.
– Patients in whom endoscopy cannot be performed due to
torrential bleeding should be considered for laparotomy, with or
without prior mesenteric angiography

22. MANAGEMENT OF GI BLEEDING
• Sigmoidoscopy and colonoscopy
– Patients with bright red hematochezia and minimal blood loss can
undergo initial evaluation with anoscopy and flexible sigmoidoscopy,
unless the patient is age 50 or older(a full colonoscopy is generally
recommended to rule out a colonic neoplasm)
– Those with dark hematochezia or bright red blood per rectum and
evidence for significant blood loss should undergo full colonoscopy
– Active, brisk bleeding and continued hemodynamic instability despite
ongoing resuscitation is an indication for emergency angiography rather
than colonoscopy.
» Since lower GI bleeding can originate anywhere in the small bowel
or colon, angiography is also preferable to laparotomy in the
setting of such bleeding.
» Surgery is generally reserved for patients whose bleeding site is
identified by angiography but who are inappropriate for, or fail,
angiographic therapy

23. MANAGEMENT OF GI BLEEDING
• Angiography:
– bleeding rate of 0.5 mL/min is necessary in order for
angiography to be positive
– helpful in the patient with massive GI bleeding from either an
upper or lower source
– reveals a bleeding site in up to 75% of patients with massive
upper GI bleeding
– success rate in LGIB 60-90% rebleeding rate 0-33% and
significant ischemia 7%

24. MANAGEMENT OF GI BLEEDING
• Radionuclide scanning :
– Red blood cells obtained by venipuncture are labeled with technetium 99m
(99m
Tc) and reinjected into the patient.
– red blood cell scans detect lower rates of bleeding (0.1cc/min)
– Since prolonged or repeated scanning is possible, bleeding can be detected
even if it is intermittent or too slow to be detected on angiography.
– If the red blood cell scan is negative, the angiogram is very unlikely to
demonstrate active bleeding
– Helpful in some patients with recurrent lower GI bleeding in whom all other
diagnostic studies are negative.
– is particularly helpful in the setting of bleeding from a Meckel’s diverticulum
• Multidetector row CT:
– Blood flow can be detected at the rate of 0.3 mlmin
– Considered positive when vascular contrast material is extravasated into
bowel lumen.
• Capsule endoscopy +double balloon enteroscopy for
obscure GI bleeding.

25. Surgery - Indications in upper GI
bleeding
• Age >60 years.
• Massive bleeding.
• Continued bleeding more than4 units of blood
transfused.
• Endoscopic stigmata.
– Vessel in base of ulcer.
– Arterial spurter.
– Adherent clot.
• Rebleeding within hours or days.
• Unique and shortage of blood.

26. Surgery - Indications in lower GI
bleeding
•  The majority of patients with LGIB will stop
spontaneously and never require surgery
•  approximately 10-25% of patients will require
operative intervention
•  The indications for surgery include:
• 1. Continued or recurrent hemorrhage despite
nonoperative attempts.
• 2. Transfusion requirement >6 units within 24 hours.
• 3. hemodynamic instability patients who have
massive ongoing bleeding and are unresponsive to
initial resuscitation.