Gastrointestinal Bleeding

Question 1

Where does the Upper GI bleed occur?

Answer 1

esophagus, stomach and proximal small bowel

Question 2

where does a lower GI bleed occur?

Answer 2

distal small bowel, colon

Question 3

patient is not aware they are bleeding, but they have iron deficiency anemia or guaiac + stools

Answer 3

occult GI bleed

Question 4

bleeding is obvious to the patient and clinician but we have been unable to identify the source

Answer 4

obscure GI bleed

Question 5

Evidence of GI bleeding can range from?

Answer 5

• hematemesis (bright red vs ground coffee)
• melena (black stool oxidized Hgb from acid, bile, bacteria)
• hematochezia (red blood per rectum)
• hemoccult positive (brown stool)

Question 6

first step in assesing a suspected bleed?

Answer 6

• blood pressure, heart rate, orthostatics, oxygenation

Question 7

what to know to identify the source of bleed?

Answer 7

hematemesis and/or melena:

• upper GI source (rarely melena can mean a slow bleed of of right colon)

Hematochezia

• lower GI source (rarely it can mean a brisk GI bleed

Frequency of stools

• increased frequency (more active bleeding)

Question 8

labratory data to be obtained for GI bleed

Answer 8

• important labs: hemoglobin, platelets, INR, BUN, iron studies, haptoglobin
• hemoglobin (if checked to soon may be inaccurate)
• iron deficiency anemia
• elevated BUN:Cr ratio: upper GI source (BUN rises due to the breakdown of blood proteins to urea by intestinal bacteria)

Question 9

• classic presentation is a history of retching prior to the development of hematemesis
• most occur on the gastic side 10-20% involve the esophagus
• bleeding usually stops spontaneously
• treatment- usually not needed vs hemoclips, injection of epinephrine

Answer 9

Mallory-Weiss tear

Question 10

• causes include reflux, radiation, infections (candida, CMV, HSV) or direct erosive effects (pill, corrosive agents)
• tx: acid suppression, treat infections

Answer 10

esophagitis

Question 11

• primary tumors (adenoCA, squamous cell CA, lymphomas)
• metastatic tumors (melanoma, breast)
• tx: often surgical, but can slow bleeding with epi/clips +/- radiation (hemospray: temporizing measure

Answer 11

esophageal cancers

Question 12

• distended veins beneath the esophageal mucosa that result from increased portal pressure due to cirrhosis or portal vein thrombosis
• can be life threatening bleed and should be treated accordingly
• active bleed-band ligation, abx, sclerotherapy, PPI, octreotide
• primary prophylaxis- beta blockrs vs banding to obliterate the varices
• secondary prophylaxis- beta blockers with repeated banding or TIPS

Answer 12

Esophageal varices

Question 13

• vascular congestion of the stomach lining from increased portal pressure
• bleeding can be chronic as well as acute
• treat with beta-blockers, iron supplementation- consider TIPS if refractory

Answer 13

Portal gastropathy

Question 14

Clues to a source of a GI bleed

Answer 14

• NSAID use: peptic ulcer disease
• Unstable vitals: Upper GI bleed
• large drop in baseline hemoglobin: Upper GI bleed
• Liver disease: Upper GI bleed (varices of PHG)
• unexplained weight loss: consider malignancy
• known hemorrhoids or diverticulosis: Lower GI bleed

Question 15

when to perform an endoscopy for an acute GI bleed?

Answer 15

Within 24 hours

Question 16

why antibiotics in GI bleeding

Answer 16

• decreased % of any infection, bacteremia and spontaneous bacterial peritonitis
• improvement in short-term survival

Question 17

• Increased portal pressure due to cirrhosis or splenic vein thrombosis
• this can be a life threatening bleed
• tx active bleed- ocreotide, glue injection, TIPS, abx
• primary prophylaxis- beta blockers
• secondary prophylaxis: Beta blockers, glue injection, TIPS

Answer 17

Gastric Varices

Question 18

• Abnormally large submucosal artery surrounded by a very small ulcer
• moderate to severe bleed
• majority occur in the stomach
• treatment- hemoclips, epi injection, surgery, or angioembolization

Answer 18

Dieulafoy’s vessels

Question 19

NSAIDs, H.pylori- usually more of a chronic bleed than an acute bleed
Tx: treat H.pylori, stop NSAIDs

Answer 19

Duodenitis

Question 20

• Communication between the aorta and the GI tract
• can develop from a native aortic anuerysm with inflammation but most patients will have a history of graft repair
• 50% will have a “herald bleed” that stops spontaneously hours to days before the massive bleed
• endoscopy in the OR
• treatment- surgery

Answer 20

Aortoenteric fistula

Question 21

• can occur anywhere in the GI tract but most commonly in the small bowel
• association with chronic renal failure, aortic stenosis, and radiation therapy
• can cause both acute and chronic bleeding
• tx: argon plasma coagulation

Answer 21

Angioectasias (AVMs)

Question 22

• small pouches in the colon the bulge outward at weak points in the colon wall
• diverticular bleeding is distinct from diverticulitis and these two entities rarely overlap
• multiple episodes of painless maroon-colored stools or BRBPR
• accounts for 30-50% of all cases of lower GI bleeding
• Bleeding stops spontaneously, rebleeding is common
• tx: Endoscopically we can use epi/clips but it is often difficult to find source, angiography with embolization, surgery- hemicolectomy

Answer 22

Diverticulosis

Question 23

• Occult GI bleeding or hematochezia when they ulcerate
• iron deficiency anemia, abdominal pain/mass, weight loss, obstruction, constipation, change in caliber of stool
• less likely in someone who had a scope in the last 2-3 years but still possible
• treatment- surgery

Answer 23

Neoplasia