CLINICAL CLERK SEMINAR SERIES

SESSION 10:

APPROACH TO GI BLEEDS
 Approach to GI bleeding

GI bleeding is a common reason for referral from the emergency department. After
initially ensuring that your patient is stable a reasonable approach would be to then try
and determine the site of bleeding. This can be divided into:

1. Upper GI bleeding (above the ligament of Treitz)

2. Lower GI bleeding (below the ligament of Treitz)

Upper GI Bleeding

Upper GI blood loss can occur anywhere along the GI tract and the differential diagnosis
reflect this.
1. Esophagus:
• Esophageal varices
• Esophagitis
• Esophageal cancer
• Mallory Weiss tear
2. Stomach
• Gastric ulcer
• Gastritis
• Gastric cancer
3. Duodenum
• Duodenal ulcer
• Aortoenteric fistula (if previous aortic graft)
4. Coagulopathy (drugs, renal disease, liver disease)

History:
Adequate history taking may help identify the severity, duration, location and cause of
the bleeding. GI bleeding may present with a wide spectrum of symptoms…if slow and
chronic may only present with non-specific findings of anemia or fatigue. More acute
serious bleeding however can present with things like hematemesis, chest pain and
hemodynamic instability.

Questions to consider include:

1. Severity of bleeding:
• Hematemesis – frequency, volume of blood
• Melena - usually due to upper GI bleeding. Occurs when blood comes in
contact with hydrochloric acid in the gut. Only need ~50cc of blood loss
• Hematochezia – Usually a sign of a lower GI bleed and rarely seen unless the
patient is having a very large, brisk upper GI bleed
• Chest pain
• Shortness of breath
• Syncope
2. Possible etiology
• Symptoms or risks for PUD (Abdominal pain, smoking, alcohol)
• Protracted retching or vomiting (Mallory-Weiss tear)
• Drug history (aspirin, coumadin, NSAIDs, steroids)
• Prior history of GI bleeding, PUD or GI surgery
• Weight loss, night sweats, fevers (malignancy)
• History of liver disease, cirrhosis, portal hypertension

Physical Exam/Investigations:

The physical exam should confirm information found on the history. Things to look for
include:
1. Vitals:
• Tachycardia, hypotension, postural changes
2. Abdominal Exam
• Distension, tenderness, masses
• Evidence of chronic liver disease
• Rectal – masses, Melena, bright red blood
3. Skin Exam
• Jaundice, ecchymosis, telangectasia
4. Laboratory
• CBC – in rapid blood loss the initial Hct may not accurately reflect the
amount of blood loss as equilibration of the extravascular fluid may take
several hours
• PTT, PT, INR, LFTs
• BUN, Creatinine – ratio >10:1 suggestive of a UGIB. Occurs as a result of
breakdown of blood proteins by bacteria to urea and re-uptake of this from the
gut
• Very important to repeat lab values in a couple hours to follow clinical course

Management:

The initial evaluation of a patient with an upper GI bleed involves an assessment of the
hemodynamic stability and resuscitation if necessary.
1. ABC’s
• 2 large bore IVs, patient should be placed in a monitored area
• Fluid resuscitation – Ringers lactate or normal saline
• Type and cross match pRBCs
• Correct any Coagulopathy
2. Keep NPO – in case of sudden repeat bleed, may need urgent endoscopy or even
intubation
3. EKG – looking for signs of ischemia or infarct
4. PPI – Losec PO if hemodynamically stable, IV pantoprozole for hemodynamically
unstable UGIB
5. Endoscopy – attempts to identify the source of bleeding +/- therapeutic intervention
to achieve hemostasis
• Risks for rebelling include spurting or oozing, visible vessel or fibrin clot
• UGI barium studies are contraindicated in the setting of an acute UGI bleed as
it will interfere with subsequent endoscopy or surgery if needed
80% of UGIB stop spontaneously. Mortality is approximately 10%

Peptic Ulcer Disease

Peptic ulcer disease is the most common cause of an upper GI bleed. An erosion
(superficial to the muscularis mucosa) or ulcer (penetrates the mucosa) is a result of an
imbalance between protective factors of the gut and things known to damage the lining of
the gut. The two most common risk factors are H. Pylori and NSAID use. Others
include smoking (increases risk and length of time to heal), alcohol, incompetent LES,
stress, Zollinger-Ellison syndrome (gastrinomas). Reduction of these risk factors reduces
ulcer recurrence and rebelling rates.

Helicobacter Pylori
• Common infection (20-40%), gram negative rod
• Present in 90% of duodenal ulcers, 60% of gastric ulcers and 50% of non-ulcerative
dyspepsia
• Most commonly acquired in childhood, presumably by fecal-oral route
• The bacteria generally does not invade gastric tissue but instead disrupts the mucosal
layer making it more susceptible to acid damage
• Can be easily diagnosed either invasively on biopsy or non-invasively with a urea
breath test or serology. A positive urea breath test indicates current active infection,
however it is not useful to repeat serology after the patient has been treated as
antibodies will remain positive for a long time after treatment

Dyspepsia is the most common clinical presentation. Other things on history that suggest
PUD include epigastric burning, pain that develops 1-3 hours after meals and is relieved
by eating. Patients may also present with one of the complications of ulcers including
bleeding (10%), perforation (2%), gastric outlet obstruction (2%), penetration (2%) – this
may cause massive bleeding or pancreatitis.

Diagnosis can be made with either endoscopy or UGI series. Endoscopy is the preferred
method as it has higher accuracy (~90-95%), able to identify superficial gastritis,
esophagitis or very small ulcerations, allows for biopsy of any suspicious looking lesion
or ulcers in the stomach (“benign looking” gastric ulcers have a much higher rate of
malignancy), allows for immediate treatment of bleeding ulcers or visible vessels, can
biopsy for H.pylori.

Treatment involves:
1. Stopping the offending agents
 • NSAIDs, smoking
2. Acid neutralization
• Proton pump inhibitors - Irreversibly inhibits the parietal cell proton pump
• H2-receptor antagonists
3. H. pylori eradication
• Several treatment options – patients are treated for 1 week
• 1st line
• PPI + clarithromycin (500mg OD) + amoxicillin (1000mg BID) or
metronidazole (500mg) if patient has a penicillin allergy
nd
• 2 line
• PPI + bismuth + metronidazole + tetracycline

Mallory-Weiss Tears

These are esophagogastric mucosal tears that occur in the region of the esophagogastric
junction. They are often characterized by a history of retching or non-bloody vomiting
(causing rapid increases in gastric pressure) followed by hematemesis. Bleeding occurs
when the tear involves the underlying esophageal venous or arterial plexus. 90% of these
bleeds stop spontaneously, however if persistent may need endoscopy with
electrocaudery or surgical repair. Rebelling usually occurs in the first 24 hours, however
is rare in the absence of portal hypertension or a Coagulopathy.

Esophageal Varices

Patients typically present with massive upper GI bleeding. Varices develop as a result of
portal hypertension, the most common cause of this in the United States and Canada
being alcoholic liver disease and chronic active hepatitis. Varices are also often found in
the stomach and if found in isolation suggests obstruction of the splenic vein.

Management depends on if the varices are actively bleeding. If there is no active

bleeding then patients should be placed on a beta-blocker. Commonly used agents
include propranolol or nadolol. These agents reduce portal hypertension by decreasing
cardiac output and splachnic vasoconstriction. The addition of nitrates may also further
lower portal pressures.

If the patient has active bleeding then management must be directed at resuscitation and
stabilization of the patient. IV fluids, blood products should be given to maintain blood
pressure and any coagulation abnormalities should be corrected with FFP. Emergent
endoscopy should be preformed for rubber band ligation or injection of bleeding varices.
IV octreotide or somatostatin should also be given. Somatostatin decreases splachnic
blood flow by direct action on mesenteric smooth muscle and octreotide decreases portal
blood flow through a direct vasoconstrictive effect and indirectly by inhibition of
glucagon which normally increases portal blood flow.
Bleeding stops spontaneously in more then 50% of patients, but mortality approached
70% in those with continued bleeding. Each bleed is associated with a 30% mortality and
the risk of rebelling is high until the varices are obliterated.

TIPSS (transjugular intrahepatic portal-systemic shunt) is a procedure that may be

considered when the above measures are not effective in controlling recurrent varaceal
bleeds. It is a radiological procedure in which a stent is inserted to connect the portal and
systemic circulation, thus lowering portal pressures. It is however associated with a high
rate of hepatic encephalopathy and stent occlusions.

Lower GI Bleeding

Lower GI bleeding occurs from a site distal to the Ligament of Treitz. As with a upper
GIB the lesion can occur anywhere along the lower GI tract:

1. Small Bowel
• Neoplasm
• Mocker’s diverticulum
• Chron’s disease
• Aortoenteric fistula
• Vascular problems
2. Colon
• Diverticuli
• Angiodysplasia
• Inflammatory bowel disease
• Ischemic gut
• Neoplasm
• Infectious
3. Perianal
• Hemorrhoid
• Fissure
• Fistula
4. Coagulopathy

History

A well taken history can help determine the site of blood loss. As with the upper GI
bleed it is very important to ask question regarding the severity of the bleeding (sx of
hemodynamic instability – see above). These bleeding episodes are usually bright red as
the blood is not first degraded in the gut. Other questions should be directed at the
character of bleeding or other associated symptoms:

1. Volume:
• Occult blood loss is associated with colon cancer
 • Small amounts on the tissue or surface of stool associated with hemorrhoids or
fissures
• Hematochezia
• Massive blood loss likely due to either diverticulosis, angiodysplasia,
or occasionally aortoenteric fistula
• Must always rule out a massive UGIB! Usually site is distal to the
pylorus
2. Symptoms associated with inflammatory bowel disease or any other systemic disease
3. Constitutional symptoms or recent change in bowel habits – suggesting a malignancy
4. Food intake which may give a false impression of rectal bleeding – beets or iron
5. Infectious symptoms or recent ingestion of any poorly cooked meat

Physical Exam

See UGIB exam. The exam should evaluate signs of large volume loss, abdominal exam
with rectal, skin exam looking for other systemic problems. Laboratory tests should
include CBC, lytes, BUN, creatinine, PTT, PT, INR, LFTs.

Management

Volume resuscitation and management of ABC’s should be the first priority for these
patients. If the patient is hemodynamically stable with low volume blood loss then the
patient can be followed clinically with volume resuscitation and blood as needed. Once
the bleeding has settled, the patient can be prepped for colonoscopy and the cause of
bleeding determined.

If patients are hemodynamically unstable with rapid rates of blood loss other
investigations can be arranged.

1. Tagged red blood cell scan

• Non-invasive, but only localized bleeding to areas of the abdomen. Accuracy
ranges from 24-91%
• Can be positive with 0.1cc/min but diagnostic in less then 50%
• Once tagged can be easily rescanned
2. Angiography
• Needs blood flow of 0.5cc/min to be positive
• Identifies site in 60% of bleeds, 50-80% are a result of bleeding from the
superior mesenteric artery
• Allows for therapeutic intervention
3. Surgery
• Consider in patients with ongoing bleeding and hemodynamic instability but
with failure of other therapeutic maneuvers.
Colonoscopy is not useful in the setting of ongoing bleeding so there is no urgent
indication. Barium enemas may detect proximal lesions not detected by colonoscopy, but
interferes with subsequent angiography and colonoscopy, thus there is no indication for
urgent use.

Diverticulosis

• Most common cause of lower GI bleeds. Occurs in ~33% of LGIB although only
15% of patients with diverticulosis will develop significant bleeding
• A diverticulum is a sac-like protrusion of the colonic wall.
• Prevalence is age dependent - <5% at 40yrs, 30% at 60yrs and 65% at 85 yrs
• 75% of the diverticular occur on the left side of the colon, however 50-90% of
diverticular bleeding is from right sided diverticuli
• May be massive since they often form at sites of arterial vascular penetration
• Bleeding is usually painless
• Bleeding usually stops spontaneously, however rebelling occurs in up to 25% of
medically patients
• Risk factors for development include:
• Lack of dietary fiber, aspirin and NSAID use, advanced age and constipation

Angiodysplasia

Angiodysplasia refers to dilated tortuous submucosal vessels. The walls are composed of
endothelial cells which lack smooth muscle. Much less uncommon, accounting for 8% of
lower GI bleeds. The risk does however increase with age and the incidence of bleeding
increases with time due to degeneration of vessel walls.

Angiodysplasia occurs throughout the colon but bleeding usually originates from the
cecum or the ascending colon. As with diverticular disease this bleeding is also usually
self-limited. Blood loss is also usually painless but because this is venous blood loss, not
arterial, it is often lower volume blood loss.

On colonoscopy lesions appear as cheery red spots on the mucosa. Endoscopic caudery
or injection sclerotherapy often achieves coagulation.

Colon Cancer

Cancer is a relatively rare cause of hematochezia, it usually presents with occult blood
loss. Bleeding occurs when there is overlying erosion or ulceration. It is usually low
volume and recurrent.

Bright red blood is associated with left sided colon lesions. Right sided malignancies
present with maroon stools or Melena
Colitis

Colitis is mucosal inflammation of the bowel wall from any number of acute processes.
All result in activation of the immune system and inflammatory cascade. It’s important
to differentiate between them as therapy is very different. Patients present with
abdominal pain, hematochezia +/- diarrhea, fever and dehydration. On colonoscopy the
bowel appears edematous, friable, erythematous and ulcerated. The differential includes:

1. Infectious
• Clostridium difficile should be considered in patients with a history of
antibiotic use or recently hospitalized
• Others include E.coli 0157:H7, Campylobacter jejuni or Entamoeba
histolytica
2. Ischemic
• Seen with patients with hypoperfusion and vasoconstriction, usually elderly
patients.
• Lactate levels would be elevated
• Therapy should be aimed at correcting the underlying cause and volume
repletion
3. Inflammatory bowel disease

Inflammatory Bowel Disease

Chron’s disease:
• Transmural inflammation with skip lesions. Linear ulcers lead to typical
“cobble-stone” pattern on colonoscopy
• Bimodal distribution – before 30 years or after 60 years
• May affect any part of the GI tract from mouth to anus – 35% small bowel
only, 45% large and small bowel, 20% large bowel only
• Usually presents with recurrent episodes of diarrhea, abdominal pain and
fever

Ulcerative colitis
• Diffuse inflammation confined to the mucosa
• Always involves the rectum, lesions are continuous
• 2/3 of cases before the age of 30
• Hematochezia is more commonly seen with ulcerative colitis then chron’s
• Presents with diarrhea, rectal bleeding, abdominal pain and tenesmus
• Systemic features of fever, weight loss & fatigue also common

Complications/Other Manifestations
• General: Growth retardation, severe wasting due to malabsorption
• Head & neck: Uveitis, chorioretinitis, iridocyclitis
• Renal: Urinary calculi
 • GI: Cirrhosis, sclerosing cholangitis, fatty liver, cholelithiasis, vitamin
deficiencies, iron deficiency, obstruction, perforation, toxic megacolon,
strictures, fistulas, perianal abscesses, cancer
• MSK: Erythema nodosum, erythema multiforme, pyoderma gangrenosum,
arthritis, ankylosing spondylitis, migratory thrombophlebitis
• Iatrogenic – steroids, blood transfusions, surgery
• Patients with UC have more liver problems (esp. sclerosing cholangitis) and
an increased risk of colorectal cancer. Suggest yearly screening and bx in
patients with pancoloitis for >10 years

Diagnosis
• Sigmoidoscopy without prep for diagnosis
• Colonoscopy and barium enema to determine the length of bowel involved –
both contra-indicated in acute severe flares
• Stool cultures to exclude infection

Management
• 5-ASA – used to treat mild-moderate disease and maintains remissions
• Steroids – used to remit acute flares – not maintenance, may mask intra-
abdominal sepsis
• Immunosuppressive agents
• Metronidazole/Cipro – decreases disease activity and improves perianal
disease in Chron’s patients
• Surgical – indicated for toxic megacolon, pre-malignant changes, obstruction,
abscess, perforation and bleeding. Cure is only possible in UC patients.
 Bleeding Problems

1. A 35 year old developmentally delayed patient is brought in by his health care worker
because of a 3 day history of diarrhea and 1 day history of vomiting dark colored
liquid. She is concerned about Norwalk virus. Past medical history includes a
seizure disorder and daily headaches. BP is 120/80, P 80 with no postural changes.
Initial Hg was 130. While in the emergency department he has a dark, tarry bowel
movement.

What is your differential diagnosis?

What else would you like to know on history?
How are you going to manage this patient?

2. A 83 year old female presents with a one day history of bright red blood per rectum.
She has had 4-5 episodes of painless bleeding. She feels lightheaded when walking
but denies any syncope, chest pain or SOB. Her past medical history includes HTN,
chronic atrial fibrillation and colon polyps. Her blood pressure is 130/80, P 80 lying
and 110/50, P110 standing. Abdominal exam is diffusely tender but no rebound or
guarding. Rectal shows bright red blood with clots.

What else do you want to know on history?

What investigations will you order?
What is your differential diagnosis?
How will you manage the patient?

3. A 56 year old male presents to the emergency department complaining of vomiting

blood. He has a past history of alcohol abuse and IV drug use. The emergency
department is very busy and so asks you help in managing the patient soon after
arrival. His blood pressure is 90/60, pulse is 120, afebrile, sats 96% on room air.

How are you going to initially manage the patient?

What else are you looking for on history?
What are you looking for on physical exam?
What investigations will you order?
What is the differential diagnosis?
What will be your admission orders?