GASTROINTESTINAL

BLEEDING

MUAYAD ABASS FADHEL

ASSISTANT PROFESSOR
SURGERY DEPARTMENT
MEDICAL COLLEGE –BAGHDAD UNIVERSITY
Anatomy
• Anatomy
• Bleeding can occur anywhere along the gastrointestinal (GI) tract from
the oropharynx to the anus.
• Bleeding is the initial presentation in 1/3 of patients with
gastrointestinal pathology, and the majority of GI bleeding cases stop
spontaneously.
• Knowledge of the GI tract anatomy and blood supply is critical in
locating and treating any GI bleed.
Upper GI Tract

• Bleeding from the upper GI tract occurs anywhere between the oropharynx and ligament of Treitz which
delineates the transition between the duodenum (foregut) and the jejunum (midgut). This encompasses the
oral cavity, esophagus, stomach (fundus, cardia, body, and pyloric region) as well as the entirety of the
duodenum. The duodenum is composed of 4 portions: the superior or duodenal bulb, descending, inferior,
and ascending, termed 1-4 respectively.
• The blood supply to the upper GI tract arises from the celiac trunk and includes the left gastric artery which
supplies the cardia and lesser curve of the stomach, the splenic artery which has a tortuous course behind
the stomach and gives rise to the short gastric arteries, as well as the left gastroepiploic artery on the greater
curve of the stomach. The right gastric artery and gastroduodenal artery (GDA) both have their origin from
the common hepatic artery which arises from the celiac trunk. The GDA passes just distal to the pylorus and
posterior to the duodenum and splits into the anterior and posterior superior pancreaticoduodenal arteries
as well as the right gastroepiploic artery along the greater curvature of the stomach.
• Duodenal ulcers located on the posterior wall are more common than those found on the anterior wall.
Posterior ulcers are more likely to erode through intestinal wall into branches of the GDA, resulting in
massive bleeding. Ulcers located on the anterior side of the duodenal wall are more likely to perforate, and
therefore, present with free air and peritonitis.
Lower GI Tract

• Important blood supply to the lower GI tract comes from the superior
mesenteric artery which supplies the small bowel as well as the
cecum, ascending, and proximal transverse colon via the ileocolic,
right, and middle colic branches. The superior mesenteric vein drains
the right side of the colon, joining the splenic vein to form the portal
vein. The inferior mesenteric artery supplies blood to the distal
transverse, descending, and sigmoid colon. The inferior mesenteric
vein carries blood from the left side of the colon to the splenic vein. A
rich network of vessels from the superior, middle, and inferior
hemorrhoidal vessels supplies the rectosigmoid junction and rectum.
Definitions

• Hematemesis Is defined as vomiting of blood and suggests an upper GI

source. Bright red blood or clots indicates rapid bleeding while “coffee-
ground” emesis signifies a slower, chronic bleed.
• Melena is the passage of black, tarry stool and suggests an upper GI source.
The source is likely distal to ligament of Treitz if not accompanied by
hematemesis. The dark appearance is due to digested blood, and only 50-
60cc of blood is required to cause melanotic stools and it can persist 5-7
days after the initial bleed.
• Hematochezia is the passage of maroon blood and clots per rectum.
• Occult bleeding is not visible to the patient or physician and is identified on
stool guaiac testing for occult blood.
COFFE GROUND HEMATEMESIS
Pathophysiology

• The first step in the diagnosis and treatment of GI bleed is to

distinguish between an upper and lower source.
• Upper GI bleeds are more common than lower GI bleeds and account
for about 70% and 30%, respectively,
• patients over 60 years old represent about 60% of patients presenting
with an upper GI bleed.
• Mortality in this older age group is as high as 20-25% but is much lower
in younger patients at about 4%.
• Common etiologies and pathologies leading to both upper and lower GI
bleeds are outlined below.
 Causes of upper GIT bleeding:
Condition percentages
Ulcer 60
Esophageal 6
Gastric 21
Duodenal 33
Erosions :
Esopghageal 13
Gastric 9
Duodenal 4
Mallory -Weiss tear . 4
Esophageal varices 4
Tumor 0.5
Vascular lesion 0.5
Other : 5
UPPER GI BLEED

• Peptic Ulcers
• Gastric and duodenal ulcers are the most common cause of upper GI
bleeding and occur in 50-70% of patients.
• However, bleeding is the presenting symptom in only 10% of patients with
peptic ulcers.
• Bleeding from duodenal ulcers is four times more common than from gastric
ulcers.
• As described above, posterior duodenal ulcers are the most likely to bleed
based on proximity to branches of the GDA. Significant bleeding occurs in 10-
15% of peptic ulcers while 20% of these require surgical therapy for control.
• Infection with the bacterium Helicobacter pylori (H. pylori) is the most common cause of
peptic ulcers.
• These bacteria are known to colonize >50% of the population, with ultimately 10-20% of
colonized individuals becoming symptomatic and developing ulcers.
• Chronic, slower bleeds tend to be associated with H. pylori.
• Another notable cause of peptic ulcers is chronic use of over the counter medications such as
aspirin and non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, and
naproxen.
• Medical therapy including H2 blockers and proton pump inhibitors for acid suppression has
drastically improved the treatment of peptic ulcers.
• However, these patients can experience rebound with an increase in acid secretion with
sudden cessation of medical therapy making medication adherence an important piece of
information to obtain through history questions.
Stress Ulcers

• These acute gastroduodenal lesions occur secondary to episodes of shock, sepsis,

surgery, trauma, burns, or intracranial pathology.
• Curling’s ulcers occur after burns, while Cushing’s ulcers occur after intracranial
processes.
• Risk factors for stress ulcers include multisystem trauma, hypotension, respiratory
failure, sepsis, and jaundice.
• Stress ulcers are possibly due to bile reflux causing damage to the gastric protective
barrier along with decreased blood flow secondary to splanchnic vasoconstriction.
• Sepsis, coagulopathy, and activation of cytokines may also contribute.
• Patients with the aformentioned risk factors are often given stress ulcer
chemoprophylaxis with an H2 blocker or proton-pump inhibitor, thereby, reducing the
incidence of stress ulcers.
Esophageal and Gastric Varices

• Varices are extremely dilated veins in the submucosa due to portal hypertension.
• Variceal hemorrhage is precipitated by ulceration of the varix due to reflux
esophagitis or increased pressure within the varix.
• Varices account for about 10% of upper GI bleeds in patients with liver disease.
• However, variceal hemorrhage accounts for 50-75% of upper GI bleeds in
patients with advanced disease consisting of cirrhosis and portal hypertension.
• These bleeds are often life threatening.
• Patients with liver disease have a diminished ability to synthesize clotting factors
increasing the risk of complication from bleeding.
• Knowing the status of liver disease helps direct therapy in these patients.
Erosive Gastritis

• Diffuse gastritis causes 1/3 of all upper GI bleeds.

• Erosions are typically multiple and found primarily in the fundus and
body of the stomach.
• Brisk bleeds are more likely due to NSAIDs, alcohol, or steroids which
are harmful to the gastric mucosa.
• Chronic, slower bleeds are associated with H. pylori.
Mallory Weiss Syndrome

• Mallory-Weiss syndrome is caused by prolonged or severe retching which results in a

partial thickness mucosal tear at the gastroesophageal junction.
• This is in contrast to Boerhaave syndrome in which a full thickness tear results in
mediastinitis.
• Mallory-Weiss tears account for about 5-10% of all upper GI bleeds.
• Classically, patients will present with an episode of vomiting without blood. Further
emesis leads to pain and the development of hematemesis due to a tear in the
esophagogastric mucosa.
• Bleeding due to a Mallory-Weiss tear resolves spontaneously 90% of the time with no
further intervention required.
• Endoscopic therapy with epinephrine injection or balloon tamponade may be
necessary in the other 10% that don’t resolve spontaneously.
Reflux Esophagitis

• Esophagitis is more likely to result in chronic occult bleeding

associated with grade II-III esophagitis with friable mucosa and is an
uncommon cause of acute upper GI bleeds. Significant bleeding in this
area is more likely due to complications from paraesophageal hernias.
Dieulafoy’s Vascular Malformations
• Dieulafoy’s lesions are large, tortuous arterioles found within the
stomach in the submucosa.
• The lesions are typically located in the fundus and body of the stomach
along the lesser curvature.
• These dilated arterial lesions, up to 5mm, are uncommon accounting
for less than 5% of all upper GI bleeds.
• Bleeding from Dieulafoy’s lesions is due to a defect in the gastric
mucosa likely due to the pressure from the underlying protruding,
pulsatile arteriole.
• Aortoenteric Fistulas
• Aortoenteric fistulas are also uncommon causes of GI bleed, however, they
are life threatening.
• In patients with prior aortic reconstructions, aortoenteric fistulas result from
erosion of a prosthetic graft into nearby bowel typically in the setting of a
perigraft infection.
• If no prior intervention occurred, the bleed is more likely from compression of
an abdominal aortic aneurysm against the bowel.
• Patients typically present with a herald bleed which stops spontaneously
followed by a massive bleed resulting in rapid hemodynamic deterioration
requiring immediate intervention.
Aortoduodenal Fistula

Aorta

Duodenum

Fistula

Graft
Gastric Neoplasms

• Both malignant and benign lesions can cause upper GI bleeding.

Bleeding from neoplasms is typically mild and chronic, commonly
presenting with symptoms of anemia.
• These masses are usually diagnosed with endoscopy and biopsy.
LOWER GI BLEED
Diagnosis
• Diagnosing a GI bleed is typically straightforward based on the patient
presentation.
• In order to further identify the location and cause of the bleed within
the GI tract, it is extremely important to obtain a thorough history
and perform a complete physical examination.
HISTORY

• The history of present illness should elicit details about the characterization of stool or
emesis. This includes bright red versus dark, tarry stools or emesis and any alleviating or
exacerbating factors.
• For instance, duodenal ulcers produce pain several hours after eating which is alleviated
by further PO intake.
• Pain from gastric ulcers is typically exacerbated by eating.
• The length of symptoms and temporal sequence of events is also important, for instance,
in the case of a Mallory-Weiss tear, non-bloody retching precedes bloody emesis.
• Associated symptoms such as dizzines, dyspnea, lightheadedness, should be obtained.
• These constitutional symptoms are suggestive of anemia in slower, more chronic bleeds,
or hypovolemia in larger, more brisk GI bleeding.
• Recent weight loss could indicate food aversion due to an ulcer or malignancy.
• A review of systems should be thorough and identify any risk factors that could complicate an
invasive procedure or surgery.
• This includes, but is not limited to, signs of active infection, angina, dyspnea, and poor exercise
tolerance.
• A past medical history should inquire about peptic ulcer disease, cirrhosis, heartburn, and reflux.
• Past surgical history, including any abdominal surgeries and endoscopies, should be obtained.
• Review medications in particular NSAIDS and steroids including how much, how frequently, and
for how long the patient has been taking these medications.
• Inquire specifically about medication adherence to identify possible rebound acid secretion.
• Obtain a relevant family history including colon cancer, inflammatory bowel disease, and any GI
malignancies.
• A social history should include current and past alcohol consumption and smoking status.
Additionally, sick contacts and recent travel outside of the country should be elicited.
PHYSICAL EXAMINATION

• Physical exam should include up-to-date vital signs and a general

assessment of the patient.
• This will help determine how sick or critical the patient is upon
presentation. Hemodynamic instability with tachycardia (occurs first)
or hypotension (occurs second) indicates a more urgent situation.
• Keep in mind older patients on beta blockade may not be able to
mount a tachycardic response to massive GI bleeding.
• Resuscitation should begin immediately for unstable patients while
further history and exam is being completed.
• Always look for signs of anemia or dehydration including pallor,
lethargy, dry mucous membranes, skin tenting, or flat neck veins.
• A thorough abdominal exam should be performed to locate any
tenderness, rebound, guarding, or other signs of peritonitis.
• Pay attention to signs of cirrhosis including spider angiomata,
prominent abdominal veins, caput medusa, and ascites.
• A rectal exam MUST be performed in patients presenting with a GI
bleed in order to identify perianal causes of bleeding in addition to
the presence of blood in the rectal vault.
• Perform an occult blood test at time of rectal exam.
• In women, include a pelvic examination.
LABORATORY TESTS

• Laboratory investigations should include CBC, biochemical test, coagulation studies, type and cross,
occult blood test, and possibly an ABG if shock is suspected.
• The CBC will reveal derangements in hemoglobin and hematocrit as well as potential platelet
deficiency in patients with liver disease.
• A large drop in hgb/hct would not be expected immediately in an acute bleed until resuscitation is
initiated and hemodilution occurs.
• Chronic GI bleeding will result in an iron deficiency anemia.
• The biochemical test can reveal hepatic dysfunction and the renal status of the patient.
• A proportional elevation in BUN:Creatinine ratio can be a sign of prerenal azotemia.
• Isolated elevated of BUN can be the result of blood digestion and absorption of breakdown
products in the GI tract.
• A ratio greater than 36:1 likely represents bleeding from an upper GI source.
• The BUN can be elevated as high as 30-50 mg/dL.
Management

• ACUTE MANAGEMENT
• Management should begin with the ABCs (airway, breathing,
circulation).
• The airway needs to be secured if sensorium is altered or the patient
is unable to protect the airway.
• Simultaneously, two large bore IVs (16 gauge or larger) should be
placed for access.
• An arterial line can be placed in those patients with deteriorating clinical status
for dynamic blood pressure monitoring.
• Fluid resuscitation should start with a 1L bolus of crystalloids, either NS or LR. If
the patient responds well with improvement in hemodynamic parameters, a
second 1L crystalloid bolus can be administered.
• If the patient remains unstable with a suspected GI bleed, resuscitation should
be continued with packed RBCs.
• Fluid balance should be monitored with strict ins and outs and a Foley catheter
may be placed for monitoring urine output.
• An NGT should also be placed and gastric lavage performed.
• Bloody return indicates a gastric or upper GI bleed.
DIAGNOSTIC AND THERAPEUTIC INTERVENTIONS

• In order to appropriately manage GI bleeding, it is important to

identify the source of bleeding.
• Many GI bleeds can be managed with medical management, or with
the help of endoscopy and interventional radiology.
• Whenever possible, it is important to identify a source of bleeding
even if surgery is indicated.
Endoscopy

• Endoscopy is typically the next step as it is both diagnostic and therapeutic.

Esophagogastro- duodenoscopy (EGD) evaluates the esophagus, stomach, and duodenum.
• Several different interventions can be performed during EGD to control the bleeding.
These include direct pressure, injection with vasoconstrictive properties (epinephrine,
vasopressin), sclerotherapy, electrocautery, ligation, and clipping.
• Of note, ligation has been found to be as effective as sclerotherapy but with fewer
complications and is practiced more commonly in the acute setting.
• Failed therapy and re-bleeding occurs in 55% of patients found to have active pulsatile
bleeding or oozing at the time of endoscopy.
• A nonbleeding, visible vessel has 43% risk of re-bleeding.
• Adherent clot carries a 22% risk of re-bleed, and a clean based ulcer has 0-5% chance of
re-bleeding. (forrest clasification)
• Endoscopic intervention in patients with known cirrhosis and liver failure
needs to be well planned given the inability to synthesize clotting factors.
• For acute bleeding, initial therapy should include ligation and vasopressin.
The use of a Sengstaken-Blakemore tube which provides balloon tamponade
can help temporize bleeds in unstable patients or those in whom EGD has
not been successful.
• For lower GI bleeds, colonoscopy evaluates the rectum, colon, and distal
ileum. The same interventions mentioned above are available during
colonoscopic intervention.
• Anoscopy and proctoscopy can be done at the bedside or in the operating
room accompanied by an exam under anesthesia (EUA).
Tagged red blood cell scan
•
• If a source of bleeding cannot be identified by endoscopy, the next test is
often a tagged RBC scan.
• This test is 91% sensitive and 100% specific for diagnosing a lower GI bleed. It
can identify a bleed as slow as 0.005-0.1 mL/min compared to angiography at
0.5-1.0 mL/min.
• However, there must be active bleeding at the time of the scan in order to
identify a bleed, and it is only about 50% active in identifying the precise
location of the bleeding.
• However, it does provide very useful information for the interventional
radiologist to target angiographic embolization.
Angiographic embolization

• Angiography can be diagnostic and therapeutic.

• It can help localize a GI bleed where extravasation of contrast is seen,
and can be used for coil embolization of the bleeding vessel.
• The risk of bowel necrosis is low with super selective embolization.
However, the risk of renal failure related to dye load should be kept in
mind, particularly in those patients who may be dehydrated or
suffering from pre-existing renal compromise.
Bleeding AVM
Transjugular intrahepatic portosystemic shunt (TIPS)

• TIPS is used for bleeding secondary to portal hypertension that is not

amenable to endoscopic intervention.
• It off-loads the pressure within the portal venous system.
• However, blood then bypasses the liver potentially leading to worsening of
hepatic encephalopathy.
• In-hospital mortality of patients requiring an emergent TIPS procedure is high
at about 35-55%.
• Stenosis or occlusion of the shunt occurs up to 50% of the time at one year.
Therefore, patients may need a surgical portosystemic shunt, if their native
liver function is reasonably good, or a liver transplant, if the functional reserve
of the liver is critically low.
TIPS
IVC Coronary Vein

Splenic Vein

Portal Vein
SURGICAL MANAGEMENT

• Upper
• Elective surgeries for gastric and duodenal ulcers have significantly decreased in frequency due
to improved medical therapy with H2 blockers and proton pump inhibitors.
• However, the number of urgent or emergent surgeries for bleeding duodenal ulcers has
remained somewhat stable.
• Indications for surgical intervention include uncontrolled bleeding in a patient with a known
ulcer after failure of endoscopic treatment of the bleed.
• Pre-operative preparation includes adequate fluid resuscitation with either crystalloid or blood
pending the status of the patient.
• The operative approach for an upper GI bleed is via an exploratory laparotomy through an
upper midline incision.
• For a duodenal ulcer, dissection is carried out to expose the pylorus and first part of the
duodenum. An anterior longitudinal duodenotomy is made extending
• through the pyloric channel to the distal stomach. Bleeding from the GDA complex is
controlled with a three-vessel ligation technique. This consists of a superior suture, inferior
suture, and a horizontal mattress suture creating a “U” stitch for the transverse pancreatic
artery. A Heineke- Mikulicz closure of the duodenotomy is then performed by closing the
horizontal incision in a vertical fashion.
• Bleeding gastric ulcers are best treated with surgical excision of the ulcer and repair of the
remaining gastric defect. Given that 4-5% of benign appearing ulcers contain a malignancy, it
is of utmost importance to send all gastric ulcers specimens for pathologic evaluation.
• A truncal vagotomy can be added to the operation for long-term ulcer control. However, this
is not appropriate in an unstable or under resuscitated patient. Additionally, this should only
be performed if the patient was on adequate medical therapy prior to surgery. If a truncal
vagotomy is performed, a 1 cm portion of each vagus nerve (anterior and posterior) is
resected. It is necessary to send both of the vagal trunk specimens to pathology to document
the vagotomy was performed successfully.
• Unlike bleeding ulcers, operative therapy is first line treatment for an ulcer with an
associated perforation.
• The operation of choice for a duodenal perforation is the Graham patch repair. In
this maneuver, a portion of the omentum is placed over the perforation and is
secured in place with interrupted silk sutures. The sutures should be placed quite
wide of the ulceration to prevent tearing through the friable tissue.
• Perforated gastric ulcers can also be treated with a Graham patch or excision with
repair of the defect as done for a bleeding duodenal ulcer. Again, the specimen of
the gastric ulcer should be sent for pathology to rule out a malignancy.
• Postoperatively, patients should be treated with acid suppression therapy and for
H. Pylori infection, if positive. They should also be counseled on peptic ulcer
disease.
Lower BLEED

• Every effort should be made to locate the source of bleeding within

the lower GI tract.
• If a source is identified in the colon and other less invasive modalities
have failed, a partial colectomy can be performed.
• If colonic bleeding persists and cannot be located with less invasive
techniques, a total abdominal colectomy is the indicated operation.
This is a morbid operation and associated with an ileostomy.
PREVENTION
•
• Medication
• NSAIDs should be avoided by patients with peptic ulcer disease.
Additionally, the importance of aspirin and clopidogrel in patients
with cardiovascular disease and bleeding from peptic ulcer disease
should be discussed with the cardiologist to weigh the risks of
bleeding versus the risk of a cardiac event.
• Alcohol and Caffeine
• Both alcohol and caffeine impair the ability to heal an already present
peptic ulcer.
• Smoking cessation and moderation of alcohol should be
recommended.
• Adequate resources should to be offered to help patients with these
addictive behaviors.
H. pylori treatment

• Eradication of H. pylori is essential to improve ulcer healing and

reduce the risk of re-bleeding.
• H. pylori is treated with triple therapy including clarithromycin, a PPI,
and amoxicillin or metronidazole or quadruple therapy consisting of
bismuth, metronidazole, tetracycline, and a PPI.
• Effective treatment can be confirmed with a biopsy urease test, urea
breath test, or a stool antigen test.
• Repeat EGD should also be performed in 8-12 weeks after an upper GI
bleed to evaluate healing and perform biopsies to exclude
malignancy.
Risk stratification

is essentially accomplished by answering the following questions:

• A. What is the magnitude and the severity of the hemorrhage?
• Hypotension, tachycardia, oliguria, low hematocrit, pallor, altered
mentation, and/or hematemesis suggest a large blood loss that has
occurred over a short period of time.
• B. Does the patient have significant chronic disease, particularly lung,
liver, kidney, and/or heart disease, which compromises physiologic
reserve? If yes, this is a high-risk situation.
• C, Is the patient anticoagulated, or immunosuppressed? If yes,this is a
high-risk situation.
• D. On endoscopy, is the patient bleeding from varices, or is there
active bleeding, or is there a visible vessel, or is there a deep ulcer
overlying a large vessel (e.g., posterior duodenal ulcer overlying the
gastroduodenal artery)?
• Could the patient be bleeding from an Arterio enteric fistula? If yes,
this is a high-risk situation.
• If judged to be low risk, most patients will stop bleeding with
supportive treatment and IV PPI.
• Selected patients may be discharged from the emergency room and
managed on an outpatient basis.
• If the patient is judged to be high risk based on one or more of the
questions previously listed, then the following should be done
immediately:
• 1. Type and cross-match for transfusion of blood products.
• 2. Admit to ICU or monitored bed in specialized unit.
• 3. Consult surgeon.
• 4. Consult gastroenterologist.
• 5. Start continuous infusion of PPI.
• 6. Perform upper endoscopy within 12 hours, after resuscitation and
correction of coagulopathy. Endoscopic hemostasis should be
considered in most high-risk patients with acute upper GI bleeding.
Diverticular Bleeding
Diverticulosis