Conway: Upper And Lower Gi Bleeding

Front 1

GI cardiac output

Back 1

At rest ~25%
After meals ~40-50%%

Front 2

Physiologic response to acute blood loss

Back 2

Peripheral vasoconstriction (cold, clammy skin)
Diminished cardiac output (compensatory tachycardia and hypotension)
Oliguria
Orthostatic Hypotension (> 25-30% blood loss)
Signs of shock (> 50% blood loss)

Front 3

Hematemesis

Back 3

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 4

Melena

Back 4

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

Front 5

Hematochezia

Back 5

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 6

Upper GI bleeding etiology: Ulcerative or erosive disease

Back 6

~55% of upper GI bleeds

Peptic ulcer disease
-Gastric or 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 (usually esophageal)
-Alendronate, Tetracycline, KCl, ASA, NSAIDs
-Often underlying stricture or esophageal dysmotility

Front 7

Upper GI bleeding etiology: Portal hypertension and arteriovenous malformation

Back 7

Portal hypertension (14%)
-Covered in another lecture

Arteriovenous malformations (7%)
-Idiopathic AVMs
-Dieulafoy’s lesion
--Bleeding vessel with no surrounding ulcer
-Gastric Antral Vascular Ectasia (GAVE)
--“watermelon stomach”

Front 8

Upper GI bleeding etiology: Traumatic or post procedure, tumors, miscellaneous

Back 8

Traumatic or post procedure (6%)
-Mallory-Weiss tears
--Tear of gastric and esophageal mucosa at the GEJ, usually after retching
-Post-surgical anastomosis
-Post-polypectomy
-Aortoenteric fistula

Tumors (4%)
-Benign
--GI stromal tumors (GIST)
--Polyps (adenomatous, hyperplastic, hamartomatous)
-Malignant
--Adenocarcinoma
--Lymphoma
--Metastatic implants

Miscellaneous (really rare)
-Hemobilia (bleeding from the biliary tree)
-Hemosuccus pancreaticus

Front 9

Lower GI bleeding etiology: Diverticulosis

Back 9

33% of lower GI bleeding
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 10

Lower GI bleeding etiology: neoplasm, colitis

Back 10

Neoplasm (19%)
-Cancers and large polyps usually bleed from overlying ulceration and erosion.

Colitis (18%)
-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

Lower GI bleeding etiology: angiodysplasia, anorectal, postpolypectomy

Back 11

Angiodysplasia (8%)
-Dilated tortuous submucosal vessels (usually veins) which can rupture
-More common in elderly, and those with multiple medical problems.

Anorectal (4%)
-Hemorrhoids
--Internal and external
-Anal fissures
-Rectal ulcers
--Idiopathic
--Infectous
--Prolapse

Post polypectomy bleeding
-< 5% of all polypectomies
-Can be immediate or delayed (up to 10 days)
-Usually occurs after cautery is used to resect polyps (presumably from sloughing of the cautery induced ulcer base)

Front 12

Acute GI bleeding: history

Back 12

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

Hematemesis and/or melena are usually signs of an upper GI bleed.
Hematochezia is usually a sign of lower GI bleeding. (But brisk upper GI bleeding can present as hematochezia)

Front 13

Management of acute GI bleeding: resucitation

Back 13

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 14

Management of acute GI bleeding: labs

Back 14

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)

Front 15

Management of acute GI bleeding: nasogastric lavage

Back 15

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 16

Mangement of acute GI bleeding: blood products

Back 16

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)

Front 17

Mangement of acute GI bleeding: PPI

Back 17

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.

Front 18

Management of acute GI bleeding: help gastroenterologist see, H.pylori

Back 18

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).

Check serum IgG for H.pylori and treat for patients with PUD

Front 19

Management of acute GI bleeding: endoscopy

Back 19

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 20

Upper endoscopy risk stratification

Back 20

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 21

Endoscopic therapy for acute GI bleeding

Back 21

Injection therapy
-Usually epinephrine (vasoconstriction)
-Effective in immediate hemostasis, but high risk of rebleeding

Contact Thermal coagulation probes
-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)

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

Combination therapy
-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

Noncontact thermal therapy
-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 22

Definition of endoscopic failure

Back 22

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 23

Management of acute GI bleeding: angiography with embolization, surgery

Back 23

When other methods and endoscopy fails

Angiography with embolization
-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)

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

Front 24

Definition of occult GI bleeding

Back 24

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 25

Occult GI bleeding etiologies

Back 25

GI cancers (upper and lower)
Ulcers
Esophagitis
Angiodysplasia
IBD
Hemorrhoids

Front 26

Fecal occult blood test: method, problems

Back 26

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

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 27

Occult GI bleeding colonoscopy and upper endoscopy

Back 27

Diagnostic evaluation

Colonoscopy
-Due to the relatively high prevalence of colon pathology (especially neoplasia) colonoscopy should be the initial test.

Upper Endoscopy
-In 5-17% of patients with occult GI bleeding an upper GI source is found.
-Can be done at the same time as colonoscopy.

Front 28

Obscure GI bleeding definition

Back 28

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 29

Obscure GI bleeding etiologies

Back 29

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 30

Obscure GI bleeding diagnosis and management

Back 30

Repeat endoscopy
-Yield of repeat EGD > repeat colonoscopy.
-Commonly, both are repeated.

Wireless capsule video endoscopy.
-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.
-Can deliver therapy or biopsy lesions.
-Usually can’t visualize the whole small bowel.
-Long (several hours) procedure with significant potential complications (perforation).

Front 31

List the common causes of upper and lower GI bleeding.
Understand the terms used to describe GI blood loss.
Describe the basic initial evaluation and medical management of patients with acute GI bleeding.

Back 31

List the common causes of upper and lower GI bleeding.
Understand the terms used to describe GI blood loss.
Describe the basic initial evaluation and medical management of patients with acute GI bleeding.