UPPER GI BLEED Presentation designed by Wendy Gerstein, MD Department of Medicine NMVAHCS

download UPPER GI BLEED Presentation designed by Wendy Gerstein, MD Department of Medicine NMVAHCS

of 49

  • date post

  • Category


  • view

  • download


Embed Size (px)

Transcript of UPPER GI BLEED Presentation designed by Wendy Gerstein, MD Department of Medicine NMVAHCS

  • Slide 1

UPPER GI BLEED Presentation designed by Wendy Gerstein, MD Department of Medicine NMVAHCS Slide 2 O BJECTIVES Recognize bleeding and level of severity. Have a differential diagnosis for the bleeding. Know how to stabilize the patient and stop the bleeding. Decrease risk of future bleeding. Slide 3 Slide 4 M R. J HPI: Pt is a 43 yo male with h/o etoh abuse who presented with 3 day h/o vomiting blood (3-4x each day), about cup each time. Pt fainted after vomiting on morning of admission, and friend brought him to the ER. No food or drink for last 2-3 days. Never happened before. Also with dark tarry stools x 2 days and sharp epigastric abdominal pain. Pmhx: Alcoholism, (6-30 beers/day x 25 years). Low back pain secondary to military accident 1980. Heart burn x 5 years uses Tums. Slide 5 Meds: methocarbamol 750 mg po tid, etodolac 400mg po bid**. No known drug allergies Shx: etoh, current tobacco, lives on Isleta Pueblo, partial disability. PE: AF, p 80-86, bp 146/92, nl o2 sat Exam remarkable for no jaundice or signs of liver disease **, nl abd exam. Labs: wbc wnl, hct 37.3 with mcv 85, rdw 16.9, platelets 74. Bun 21, creat.8, potassium 2.9, chloride 99**. Liver enzymes sgot 88, sgpt 70, Tbili 1.4 (direct.2). Inr 1.2 CXR wnl Slide 6 In ER nasogastric tube placed removed 400 cc dark red liquid, lavaged to clear with 500cc of normal saline. Slide 7 Slide 8 D IFFERENTIAL Upper GI bleed: Peptic ulcer disease (majority of cases) Esophageal varices (14%) Mallory-Weiss tear Gastric erosions Esophagitis/ulceration Neoplasm AVM malformations Slide 9 Slide 10 E PIDEMIOLOGY 100 cases of UGI bleed per 100,000 adults. Incidence increases with advancing age. 150,000 hospitalizations per year in the US. $2 billion per year in costs. Mean length of stay 5.7 days. Mortality ranges from 3.5%-7% (death usually from co-morbid conditions). Bleeding stops spontaneously in 80%. Slide 11 Slide 12 TRIAGE Slide 13 Slide 14 I NITIAL EVALUATION / MANAGEMENT Assess hemodynamic stability **. Assess for active bleeding **. 2 large bore IVs, fluid resuscitation. Tranfusion based on hct and co-morbidities. Correct coagulopathies (FFP, platelets). NGT lavage. Evaluate need for airway protection. Slide 15 Notify GI consultants, surgeons if severe and acute. Consider octreotide (somatostatin). Endoscopy. For complicated cases, can also use angiography, tagged rbc scan. Slide 16 V ERY LOW RISK Normal hemodynamics, no bleeding within last 48 hours, negative NGT aspirate (bilious w/ no blood)**, normal labs. Outpatient evaluation acceptable. Follow up within one week. Oral PPI. Slide 17 L OW RISK Hemodynamics return to normal within 1 hour of resuscitation. No evidence of active bleeding **. No active cardiopulmonary or liver disease. No co-morbid conditions requiring hospitalization. Immediate endoscopy with discharge from endoscopy suite. Slide 18 M ODERATE RISK Tachycardia continues despite resuscitation. Requires more than 2 units PRBCs. Advanced age, cardiopulmonary disease, liver disease. Admit to hospital bed. Early EGD when patient stable. Slide 19 H IGH RISK Active bleeding. Persistent hypotension. Severe co-morbidities. Needs airway protection. ICU admission. Endoscopy when stable. Slide 20 T RIAGE FOR M R. J Actively bleeding, low hct, probable liver disease, vitals normal on admission (although h/o syncope). Where would you place him? Slide 21 He was admited to MICU, 2 peripheral IVs secured, started on IV octreotide, IV pepcid, IVFs, vitals and hct monitored. GI performed EGD that afternoon: No varices, large hiatal hernia, hemorrhagic gastritis in fundus. They injected 3cc epinephrine, and then used cautery on lesions in fundus. Slide 22 Patient stared on IV protonix, switched to oral omeprazole 40 mg po bid next day. Hematocrit reached nadir of 29.5 (required no transfusions). Discharged with substance abuse follow up, and recommendations for repeat EGD in 3 months time. Slide 23 Slide 24 E NDOSCOPY Should be performed within 12 hours of admission. Reduces rebleeding rates, number of surgeries, number of units transfused. Mortality has not yet been shown to be reduced based on meta-analysis. Non-thermal and thermal methods used for hemostasis. Slide 25 Complications of endoscopy include: Aspiration Hypotension/hypoventilation (due to sedation) Perforation Slide 26 O CTREOTIDE Long-acting analog of somatostatin. Inhibits release of vasodilator hormones such as glucagon indirectly causes splanchnic vasoconstriction which decreases portal inflow. Has not yet been shown to have a clearly established benefit on mortality. Used as infusion for up to 5 days in variceal bleeds. Slide 27 A CID SUPPRESSION Essential for preventing re-bleeding in the initial 72-hour period after index bleed. HCL and pepsin in UGI tract appear to be antihemostatic. Want to maintain intragastric pH at 7 or higher (pepsin destruction occurs at 8). H2 blockers: block histamine H2 receptors on the parietal cell. Slide 28 Proton Pump Inhibitors: inhibit production of H+/K+ adenosine triphosphate (final step in acid production). In high risk lesions, certain studies have shown that omeprazole significantly decreases risk of rebleeding. Another study showed omeprazole infusion after endoscopic treatment reduced risk of re-bleed, reduced length of stay, and transfusion requirements. Slide 29 Break point: continue for specific discussions on PUD, H. pylori, varices, and Mallory-Weiss tears, if time permits. Otherwise skip to slide 45 for final slides. Slide 30 Slide 31 PUD ( PEPTIC ULCER DISEASE ) Major causes include H. pylori, NSAIDs, stress, gastric acid (and various combinations). Tobacco and alcohol can exacerbate existing lesions. Initial symptoms can be vague only 50% of patients with PUD present with typical symptoms, which include: Slide 32 - burning/gnawing pain - post-prandial pain 2-5 hours after eating. - relief with antiacids. - bloating, nausea, early satiety. If ulcer is bleeding, typically presents with epigastric abdominal pain, hematemesis/coffee ground emesis, melena. Slide 33 Complications (other than bleeding) include obstruction, penetration (pancreas, duodenum) or perforation. Slide 34 Slide 35 H. PYLORI No data to support routine testing in patients without ulcer disease. Test patients with active or documented PUD or gastric MALT (biopsy urease test: 95% sensitive, 95% specific). H. pylori infection doubles the risk of GI bleed in patients taking NSAIDs. Slide 36 One study from Hong Kong in 2002 showed that the prevalence of ulcers was significantly decreased in patients who had H. pylori eradicated (prior to starting NSAIDs). Other tests for H. pylori : Stool antigen (4 weeks post therapy). Urease breath test. H. pylori serum antibody. Slide 37 Treatment is with various combinations of a PPI and two antibiotics for 2 weeks. Test for cure. Slide 38 Slide 39 Slide 40 V ARICES ( GASTRIC AND ESOPHAGEAL ) Secondary to systemic or portal hypertension. Associated with alcoholic liver disease and chronic active hepatitis (25-40% of patients with cirrhosis will have a variceal hemorrhage). 30% mortality with each bleeding episode. Risk of rebleed 60-70% in one year. Slide 41 Risks factors predictive of bleed: Location (GE junction highest risk). Size (diameter related to Laplaces law). Appearance (red wale marks). Clinical picture (Childs classification). Variceal pressure (essentially 0% risk of bleeding over 12 months if pressure 13mmHg. 72% chance if >16mmHg). Slide 42 Slide 43 Acute therapy: band ligation and sclerotherapy. Primary prophylaxis: Propranolol (shown to reduce risk of hemorrhage at two years). Variceal ligation (for high risk patients). Secondary prophylaxis TIPS procedure. Slide 44 M ALLORY -W EISS T EARS Longitudinal intramural dissection in distal esophagus/proximal stomach (submucosal artery bleed). Usually associated with retching. Described in 1929 by Mallory and Weiss in 15 alcoholic patients. Predisposing conditions: Hiatal hernia (seen in 40-100%) Slide 45 Chronic alcohol (40%-80%). Amount of blood loss usually small and self-limited. Heal within 24-48 hours. Treat actively bleeding lesions with endoscopy. PPIs/H2 blockers promote healing. Slide 46 Slide 47 K EY POINTS Triage and resuscitate patient quickly and appropriately. Obtain quick endoscopy. Test for H. pylori if ulcers present, and treat if positive. Use PPIs to reduce risk of rebleeding. Remove medications that increase risk of bleeding. Slide 48 THE END Slide 49 R ESOURCES www.uptodate.com Lung E. Evaluation and Management of Gastrointestinal bleeding Part 1: Nonvariceal Upper GI Bleeding. Advanced Studies in Medicine. Vol 4 (4) April 2004. 186-190. Papatheodoridis GV et al. Effect of Helicobacter pylori infection on the risk of upper GI bleeding in users of NSAIDs. Am J Med. 2004 May 1: 116(9) 601-5. Exon DJ, Sydney Chung SC. Endoscopic therapy for upper GI Bleed. Best Pract Res Clin Gastroenterol. 2004 Feb; 18(1):77-98.