Upper And Lower Gi Bleeding

Front 1

at rest the splanchinic circulation receives about how much of the CO

Back 1

1/4--> up to 50% after heavy meal

Front 2

Hematemesis

Back 2

Vomiting of blood
Based on how long the blood has been in the stomach it could be:
Bright red (active hemorrhage)
Bright red with clots (mixture of active hemorrhage and older, clotted blood)
“coffee grounds” (older blood that has completely clotted)

Front 3

Melena

Back 3

Black, tarry, sticky, pungent
Digested blood that has passed through the GI tract

Front 4

Hematochezia

Back 4

Passing of bloody stools
Usually a mixture of bright red (or maroon) blood and clots
Keep in mind that massive upper GI bleeding can result in hematochezia!

Front 5

Upper GI bleeding Etiologies

Back 5

Ulcerative and erosive disease
Portal HTN, and AVMs, traumatic or post procedure, tumors, and miscellaneous

Front 6

Ulcerative or erosive disease

Back 6

PUD:Gastric > duodenal
Drug induced (aspirin, NSAIDs)
Infectious (H. pylori, rarely CMV and HSV)
Rare causes (stress-induced ulcers, Zollinger Ellison syndrome)
Esophagitis:Reflux (acid induced)
Infectious (C. albicans, rarely CMV and HSV)
Pill Induced:Alendronate, Tetracycline, KCl, ASA, NSAIDs
Often underlying stricture or esophageal dysmotility

Front 7

Lower GI bleding Etiologies

Back 7

Diverticulosis, neoplasm, Colitis, angiodysplasia, anorectal, post polypectomy

Front 8

Diverticulosis

Back 8

A sac-like herniation of the colonic mucosa and submucosa through the muscularis propria, usually at the site of a penetrating vessel.
Weakening of the vessel can lead to rupture and bleeding over time.
Prevalence increases with age, 30% at age 60, 65% at age 85.
Left>>right, though right sided disease accounts for the majority of bleeding.

Front 9

Neoplasm

Back 9

Cancers and large polyps usually bleed from overlying ulceration and erosion.

Front 10

Colitis

Back 10

IBD
Crohn’s. ulcerative colitis
Ischemic colitis
Hypotension (any cause) leads to mucosal (and rarely transmural) ischemia in watershed areas of blood supply in the colon.
Infectious, radiation (rare)

Front 11

Management of acute GI bleeding: Important Hx

Back 11

Aspirin and NSAID use
Anticoagulant and antiplatelet use (coumadin, clopidogrel)
History of ulcers
Heartburn
Could this be a portal hypertensive bleed?
History of/stigmata of liver disease
Discussed in another lecture.
Could it be a tumor?
Weight loss
Dysphagia
Change in bowel habits
What are you seeing?
Hematemesis and/or melena are usually signs of an upper GI bleed.
Hematochezia is usually a signs of lower GI bleeding.
But don’t be fooled …
Brisk upper GI bleeding can present as hematochezia.

Front 12

Mangaement of GI bleeding: resucitation

Back 12

Two large caliber (16 gauge or larger) peripheral or central catheters.
ICU for frequent monitoring of vital signs
Initiate fluid resucitation (keeping in mind patient tolerance of large fluid bolus, e.g. congestive heart failure, lung disease, kidney disease)
Consider endotracheal intubation if massive hematemesis for airway protection

Front 13

Management of GI bleeding: Diagnostic Studies

Back 13

Draw labs
CBC
keeping in mind that the initial hematocrit may be normal if bleeding is acute and volume has not been restored
Type and cross, obtain consent for transfusion
Platelets
PT, international normalized ratio (INR), PTT
look for and correct coagulopathy!
Electrolytes including creatinine and BUN
BUN may be elevated in upper GI bleeds
LFT’s (cirrhosis)
Nasogastric (NG) lavage
Place a tube through the nose into the stomach.
Most helpful if there is no hematemesis and an upper GI bleed needs to be ruled out.
Can help you decide if this is an upper GI bleed and if it is active.
Aspiration of bright red blood = active bleeding
Aspiration of clots and coffee grounds = bleeding may have stopped
Aspiration of bile = may not be an upper GI bleed
Can help remove clot and food debris prior to endoscopy.
Note that duodenal bleeding may have a false negative NG lavage (if no blood refluxes into the stomach).
Do not check gastroccult. It will almost always be positive due to the trauma of the NG tube being placed. Go with what you see in the aspirate.

Front 14

Mangaement of acut GI bleeding: Therapy-Medical

Back 14

Blood products
Transfuse blood based on hemodynamic status, not hematocrit initially.
After equilibration keep hematocrit > 30 in patients with vascular disease, >20 for others
Correct coagulapathy (fresh frozen plasma to keep INR < 1.5)) and thrombocytopenia (platelets if needed to >50,000)
Proton pump inhibitors (PPI)
In acute upper GI bleeding, high dose IV PPI therapy (esomeprazole, lansoprazole, pantoprazole) have been shown to:
Decrease rebleeding rate
Decrease hospital stay
Decrease transfusion requirements
How do they work?
Block gastric proton pumps (H-K-ATPase) in parietal cells and quickly (in high dose IV form) increase gastric pH.
Allow more effective clotting in a more neutral pH
Improved mucosal healing in a more neutral pH
Initiate IV PPI therapy early in upper GI bleeding.
Usually continued IV for 24-48 hours and then converted to per oral dosing.
Help your gastroenterologist see …
We can’t see through blood and clots, and the suction port on the scope is very small.
Use promotility agents (erythromycin IV) to increase gastric motility and improve visualization during upper endoscopy.
If it is a lower GI bleed, begin colon preparation with a orally administered polyethylene glycol (PEG) based saline lavage (e.g. Golytely).
Don’t forget to check and treat H. pylori in patients with PUD.
Usually done with serum IgG.

Front 15

Management of acute GI bleeding: Therapy-endoscopy

Back 15

A diagnostic and therapeutic modality.
In upper GI bleeding emergent or urgent endoscopy can risk stratify patients with high risk ulcers and other lesions (those which may rebleed and need continued intensive monitoring or need further therapy, e.g surgery, angiography).
Endoscopic treatment has been shown to reduce rebleeding rates and transfusion requirements.
In lower GI bleeding endoscopy plays primarily a diagnostic role, and can usually be delayed until after the colon has been prepped.

Front 16

Upper Endoscopy Risks

Back 16

High risk lesions
Ulcers
Actively bleeding
Non-bleeding visible vessels
Adherent clots
Oozing without visible vessel
Variceal hemorrhage
Low risk lesions
Ulcers
Pigmented spot
Clean based
Most other etiologies of upper GI bleeding are at low risk for rebleeding, assuming they are appropriately treated (e.g. Dieulafoy’s lesion, Mallory Weiss tears)

Front 17

Endoscopic therapies:

Back 17

injection, contact thermal coagulation, clips, combination

Front 18

Injection Therapy

Back 18

Usually epinephrine
Effective in immediate hemostasis, but high risk of rebleeding

Front 19

Contact thermal Coagulation probes

Back 19

Direct coaptive coagulation of the underlying artery using multipolar electrocautery or heat.
Effective in sealing smaller arteries
Can lead to perforation if used in thin walled organs (right colon)

Front 20

Clips

Back 20

Small metallic clips placed through the endoscope grasp and tamponade arteries.
Most effective with larger arteries.

Front 21

combination therapy

Back 21

Multiple randomized controlled trials have shown that combination therapy (injection + contact thermal probes or injection + clips) is superior to either method alone in:
Decreasing rebleeding rates
Decreasing transfusion requirements

Front 22

non contact thermal therapy

Back 22

Argon Plasma Coagulation (APC)
Thermal energy is delivered via ionized argon gas.
Coagulation is superficial.
The probe does not touch the mucosa.
Ideal for treating angiodysplasia, especially in the colon, and GAVE .

Front 23

definition of endoscopic failure

Back 23

Recurrent hemorrhage after initial stabilization (with up to two attempts at obtaining endoscopic hemostasis)
Hemodynamic instability despite vigorous resuscitation (more than a three unit transfusion)
Shock associated with recurrent hemorrhage
Continued slow bleeding with a transfusion requirement exceeding three units per day

Front 24

Angiography with embolization

Back 24

Particularly effective in lower GI bleeding when the source cannot be identified endoscopically.
Carries risk of infection, bleeding, damage to vessels, mucosal ischemia and necrosis (if not selective)

Front 25

Mgmt of GI bleeding with Surgery

Back 25

Usually reserved for endoscopic and/or angiographic failures
Can entail oversewing (ligation) of the vessel, resection, vagotomy (decrease acid secretion)

Front 26

Occult GI bleeding

Back 26

Occult bleeding refers to the initial presentation of a positive fecal occult blood test (FOBT) result and/or iron-deficiency anemia (IDA), when there is no evidence of visible blood loss to the patient or physician.

Front 27

Etiologies of occult GI bleeding

Back 27

GI cancers (upper and lower)
Ulcers
Esophagitis
Angiodysplasia
IBD
Hemorrhoids
And all other causes of GI bleeding

Front 28

Fecal Occult Blood test

Back 28

Fecal Occult Blood Test (FOBT)
How it works…
Guiac (a natural compound found in certain trees) contains phenol which turns to a blue quinone mediated by a peroxidase (found in heme) in the presence of hydrogen peroxide.
Stool placed on one side of the card, the card is turned over and hydrogen peroxide is placed over the stool.
Blue = positive test
No color change = negative test

Front 29

Problems with FOBT

Back 29

So many problems …
High false positive rate
Must avoid NSAIDs and other irritant drugs
Avoid red meat, turnips, and horseradish (all have peroxidase activity)
Stool obtained from digital exams can be heme positive from trauma.
Low sensitivity
Many lesions bleed intermittently and may be missed (though the test can detect as little at 10-20 cc of blood loss/day)
Vitamin C can lead to a false negative test
Poor public acceptance rate

Front 30

Obscure GI bleeding

Back 30

Bleeding from the GI tract that persists or recurs without an obvious etiology after upper endoscopy, colonoscopy, and radiologic evaluation of the small bowel (such as by small bowel follow-through or enteroclysis).
2 subcategories
Obscure-overt – clinically evident GI bleeding (e.g. hematemesis, melena, hematochezia)
Obscure-occult – clinically absent GI bleeding

Front 31

Etiologies of obscure GI bleeding

Back 31

Missed lesion on EGD or colonoscopy
Angiodysplasia
Small bowel tumors
NSAID enteropathy
Meckel’s diverticulum
Cameron’s lesion
Dieulafoy lesion
GAVE
Hereditary hemorrhagic telangiectasia
Celiac Sprue
Crohn’s disease

Front 32

Dx and Mgmt of obscure GI bleeding

Back 32

Repeat endoscopy
Yield of repeat EGD > repeat colonoscopy.
Commonly, both are repeated.
Wireless capsule video endoscopy
How it works…
Capsule activated and patient swallows.
Images (2 frames/second) sent to receiver on belt.
Sensors taped to the abdomen track progress of capsule.
Battery lasts 8 hours.
Images downloaded to a workstation and images viewed as a movie.
Most sensitive way to diagnose small bowel blood loss.
Limited by lack of therapeutic ability.
Enteroscopy
Usually only pursued after a “positive” capsule.
Uses a long endoscope (per oral or per anal approach) to view the small bowel.
Usually balloon and overtube assisted.
Can deliver therapy or biopsy lesions.
Usually can’t visualize the whole small bowel.
Long (several hours) procedure with significant potential complications (perforation).