Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
32 Cards in this Set
- Front
- Back
at rest the splanchinic circulation receives about how much of the CO
|
1/4--> up to 50% after heavy meal
|
|
Hematemesis
|
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) |
|
Melena
|
Black, tarry, sticky, pungent
Digested blood that has passed through the GI tract |
|
Hematochezia
|
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! |
|
Upper GI bleeding Etiologies
|
Ulcerative and erosive disease
Portal HTN, and AVMs, traumatic or post procedure, tumors, and miscellaneous |
|
Ulcerative or erosive disease
|
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 |
|
Lower GI bleding Etiologies
|
Diverticulosis, neoplasm, Colitis, angiodysplasia, anorectal, post polypectomy
|
|
Diverticulosis
|
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. |
|
Neoplasm
|
Cancers and large polyps usually bleed from overlying ulceration and erosion.
|
|
Colitis
|
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) |
|
Management of acute GI bleeding: Important Hx
|
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. |
|
Mangaement of GI bleeding: resucitation
|
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 |
|
Management of GI bleeding: Diagnostic Studies
|
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. |
|
Mangaement of acut GI bleeding: Therapy-Medical
|
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. |
|
Management of acute GI bleeding: Therapy-endoscopy
|
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. |
|
Upper Endoscopy Risks
|
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) |
|
Endoscopic therapies:
|
injection, contact thermal coagulation, clips, combination
|
|
Injection Therapy
|
Usually epinephrine
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 |
|
non contact 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 . |
|
definition of endoscopic failure
|
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 |
|
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) |
|
Mgmt of GI bleeding with Surgery
|
Usually reserved for endoscopic and/or angiographic failures
Can entail oversewing (ligation) of the vessel, resection, vagotomy (decrease acid secretion) |
|
Occult GI bleeding
|
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.
|
|
Etiologies of occult GI bleeding
|
GI cancers (upper and lower)
Ulcers Esophagitis Angiodysplasia IBD Hemorrhoids And all other causes of GI bleeding |
|
Fecal Occult Blood test
|
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 |
|
Problems with FOBT
|
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 |
|
Obscure GI bleeding
|
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 |
|
Etiologies of obscure GI bleeding
|
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 |
|
Dx and Mgmt of obscure GI bleeding
|
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). |