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53 Cards in this Set
- Front
- Back
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Physiologic Response to Acute Blood Loss
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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) |
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Splanchnic circulation
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Supplies the alimentary tract
- Celiac artery - Superior mesenteric artery - Inferior mesenteric artery Normally receives ¼ of cardiac output at rest Increases to consume 40-50% of cardiac output after a heavy meal |
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What is important when you are examining blood loss?
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Color (bright red, maroon, black)
Amount (keeping in mind a little blood goes a long way) Timing, frequency |
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Signs of Upper GI Bleeding
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Hematemesis and Melena
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Hematemesis
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Vomiting of blood
Based on how long the blood has been in the stomach it could be: • Bright red (active hemorrhage) - Massive, hemodynamically unstable, ulcer or esophageal varices • Bright red with clots (mixture of active hemorrhage and older, clotted blood) • “coffee grounds” (older blood that has completely clotted) |
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Melena
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Black, tarry, sticky, pungent
Digested blood that has passed through the GI tract |
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Signs of Lower GI Bleeding
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Hematochezia
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Hematochezia
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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, especially in hemodynamically unstable. |
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Etiologies of Upper GI Bleeding
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Ulcerative or Erosive Disease
Portal Hypertension Arteriovenous malformations Traumatic or post procedure Tumors Hemobilia Hemosuccus pancreatitus |
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Ulcerative or Erosive Disease
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55% of Upper GI Bleeding
Peptic Ulcer Disease Esophagitis Pill induced |
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Peptic Ulcer Disease
Ulcerative or Erosive Disease |
Gastric > duodenal
• White ulcer base • Surrounding edematous, inflamed tissue (in gastric ulcers) Drug induced (aspirin, NSAIDs) Infectious (H. pylori, rarely CMV and HSV) Rare causes (stress-induced ulcers, Zollinger Ellison syndrome) |
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Esophagitis
Ulcerative or Erosive Disease |
Reflux (acid induced)
Infectious (C. albicans, rarely CMV and HSV) |
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Pill Induced
Ulcerative or Erosive Disease |
Usually esophageal bleed
Alendronate, Tetracycline, KCl, ASA, NSAIDs Often underlying stricture or esophageal dysmotility |
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Arteriovenous malformations
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Idiopathic AVMs
Dieulafoy’s lesion - Bleeding vessel with no surrounding ulcer Gastric Antral Vascular Ectasia (GAVE) - “watermelon stomach” - Linear streaks of AVM in pylorous • Cauterize them to stop GI blood loss |
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Traumatic or Post Procedure causes of Upper GI Bleeds
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Mallory-Weiss tears
- Tear of gastric and esophageal mucosa at the GEJ, usually after retching (think alcoholic or bulimic) Post-surgical anastomosis Post-polypectomy Aortoenteric fistula |
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Tumors that cause Uppen GI Bleeding
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Benign
- GI stromal tumors (GIST) • Massive hematemesis • Submucosal mass with ulceration - Polyps (adenomatous, hyperplastic, hamartomatous) Malignant (a chronic ooze) - Adenocarcinoma - Lymphoma - Metastatic implants |
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Etiologies of Lower GI Bleeding
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Diverticulosis (33%)
Neoplasms (19%) Colitis (18%) Angiodysplasia (8%) Anorectal Post polypectomy |
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Diverticulosis as a cause of Lower GI Bleeding
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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 (vasa recta) 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. |
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Neoplasms as a cause of Lower GI Bleeding
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Cancers and large polyps usually bleed from overlying ulceration and erosion.
Ulceration occurs when the mass outgrows the blood supply |
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Colitis as a cause of Lower GI Bleeding
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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. - Can be a healthy person… they are just dehydrated - Pathology • Edematous folds, ischemic ulcers • Necrosis of colonic wall: Black colored mucosa that is sloughing off >If BP is restored, then areas with heal very quickly Infectious, radiation (rare) |
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Angiodysplasia as a cause of Lower GI Bleeding
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Dilated tortuous (spiderlike) submucosal vessels (usually veins) which can rupture
More common in elderly, and those with multiple medical problems. |
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Anorectal as a cause of Lower GI Bleeding
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Hemorrhoids
- Internal and external • Internal hemorrhoids bleed more frequently Anal fissures Rectal ulcers - Idiopathic - Infectious - Prolapse |
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Post polypectomy bleeding as a cause of Lower GI Bleeding
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< 5% of all polypectomies
Can be immediate or delayed (up to 10 days); think if recent colonoscopy with polypectomy Usually occurs after cautery is used to resect polyps (presumably from sloughing of the cautery induced ulcer base) - Can stop the bleeding with metal clip insertion |
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History
In Management of Acute GI Bleed |
Aspirin and NSAID use
Anticoagulant and antiplatelet use (coumadin, clopidogrel) History of ulcers Heartburn (esophagitis) Could this be a portal hypertensive bleed? Could it be a tumor? What are you seeing? Hematemesis? Melena? Hematochezia? |
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What questions should you ask to determine if a GI bleed could be from a tumor?
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weight loss
dysphagia change in bowel habits |
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Resuscitation
in the management of acute GI Bleeding |
Two large caliber (16 gauge or larger) peripheral or central catheters.
ICU for frequent monitoring of vital signs Initiate fluid resuscitation (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 - Especially if ongoing bleeding or Altered Mental Status |
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Diagnositc Studies
in the management of acute GI Bleeding |
CBC
Type and Cross Platelets PT, PTT (coagulopathy) Electrolytes including creatinine and BUN LFTs (cirrhosis) Nasogastric lavage |
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CBC
in the management of acute GI Bleeding |
keeping in mind that the initial hematocrit may be normal if bleeding is acute and volume has not been restored… this can give you a false sense of security
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Nasogastric lavage
in the management of acute GI Bleeding |
- 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. |
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Medical Therapy
in management of GI blood loss |
Blood Products
Proton Pump Inhibitors - and check for H. pylori If an endoscopy is to be preformed, administer a promotility agent (reglan or erythromycin) |
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Blood Products
in management of GI blood loss |
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) • If on coumadin, give FFP. |
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Proton Pump Inhibitors
in management of GI blood loss |
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 Initiate IV PPI therapy early in upper GI bleeding. Usually continued IV for 24-48 hours and then converted to per oral dosing. |
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Endoscopy
in management of GI blood loss |
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). In lower GI bleeding endoscopy plays primarily a diagnostic role, and can usually be delayed until after the colon has been prepped. Endoscopic treatment has been shown to reduce rebleeding rates and transfusion requirements. |
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Upper Endoscopy
Risk Stratification |
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) |
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Endoscopic Therapies
in GI Bleeding |
Injection Therapy
Contract Thermal Coagulation Probes Clips Combination Therapy Noncontact Thermal Therapy |
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Injection Therapy in Endoscopic Therapy
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Usually epinephrine
- After injection, tissue goes from pink to white. Effective in immediate hemostasis, but high risk of rebleeding |
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Contract Thermal Coagulation Probes in Endoscopic Therapy
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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) |
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Clips in Endoscopic Therapy
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Small metallic clips placed through the endoscope grasp and tamponade arteries.
Most effective with larger arteries. - Stay in place for a few hours to several days to provide tamponade. |
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Combination Therapy in Endoscopic Therapy
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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 |
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Contract Thermal Coagulation Probes in Endoscopic Therapy
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Thermal energy is delivered via ionized argon gas.
• Afterwards, the area is charred white. Coagulation is superficial. The probe does not touch the mucosa. Ideal for treating angiodysplasia, especially in the colon, and GAVE Superficial, mucosally based lesions. |
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Endoscopic Failure in GI Bleeding
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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 |
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Angiography with embolization in GI Bleeding
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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) |
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Surgery in GI Bleeding
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Usually reserved for endoscopic and/or angiographic failures
Can entail oversewing (ligation) of the vessel, resection, vagotomy (decrease acid secretion) |
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Etiologies of Occult Bleeding
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GI cancers (upper and lower)
Ulcers Esophagitis Angiodysplasia IBD Hemorrhoids And all other causes of GI bleeding |
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Occult Bleeding
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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
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Occult GI Bleeding Diagnostic evaluation
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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. |
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Fecal Occult Blood Test
(FOBT) How does it work? |
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 |
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Fecal Occult Blood Test
(FOBT) Is it a good 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 |
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Obscure GI bleeding
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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 |
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Etiologies of Obscure GI bleeding
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Missed lesion on EGD or colonoscopy (most common)
Angiodysplasia Small bowel tumors NSAID enteropathy Meckel’s diverticulum Cameron’s lesion Dieulafoy lesion GAVE Hereditary hemorrhagic telangiectasia Celiac Sprue Crohn’s disease |
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Diagnosis and Management of
Obscure GI Bleeding |
Repeat Endoscopy
- yield of repeat EGD>repeat colonoscopy - commonly both repeated Wireless capsule video endoscopy Enteroscopy |
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Wireless capsule video endoscopy
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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. |
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Enteroscopy
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Usually only pursued after a “positive” capsule.
• Only do after endoscopy, colonoscopy, repeat endoscopy and pill. 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). |
