4Mr. JHPI: 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 ½ 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.
5Meds: methocarbamol 750 mg po tid, etodolac 400mg po bid Meds: methocarbamol 750 mg po tid, etodolac 400mg po bid**. No known drug allergiesShx: etoh, current tobacco, lives on Isleta Pueblo, partial disability.PE: AF, p 80-86, bp 146/92, nl o2 satExam 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 1.2CXR wnl
6In ER – nasogastric tube placed – removed 400 cc dark red liquid, lavaged to clear with 500cc of normal saline.
10Epidemiology 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%.
14Initial evaluation/management Assess hemodynamic stability **.Assess for active bleeding **.2 large bore IV’s, fluid resuscitation.Tranfusion based on hct and co-morbidities.Correct coagulopathies (FFP, platelets).NGT lavage.Evaluate need for airway protection.
15Notify GI consultants, surgeons if severe and acute. Consider octreotide (somatostatin).Endoscopy.For complicated cases, can also use angiography, tagged rbc scan.
16Very low riskNormal 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.
17Low 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.
18Moderate risk Tachycardia continues despite resuscitation. Requires more than 2 units PRBC’s.Advanced age, cardiopulmonary disease, liver disease.Admit to hospital bed.Early EGD when patient stable.
19High risk Active bleeding. Persistent hypotension. Severe co-morbidities.Needs airway protection.ICU admission.Endoscopy when stable.
20Where would you place him? Triage for Mr. J…Actively bleeding, low hct, probable liver disease, vitals normal on admission (although h/o syncope).Where would you place him?
21GI performed EGD that afternoon: He was admited to MICU, 2 peripheral IV’s secured, started on IV octreotide, IV pepcid, IVF’s, 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.
22Patient 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.
24Endoscopy 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.
25Complications of endoscopy include: AspirationHypotension/hypoventilation (due to sedation)Perforation
26Octreotide 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.
27Acid suppressionEssential 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.
28Proton 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.
29Otherwise skip to slide 45 for final slides. 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.
31PUD (peptic ulcer disease) Major causes include H. pylori, NSAID’s, 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:
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.
33Complications (other than bleeding) include obstruction, penetration (pancreas, duodenum) or perforation.
35H. pyloriNo 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 NSAID’s.
36Other tests for H. pylori: 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 NSAID’s).Other tests for H. pylori:Stool antigen (4 weeks post therapy).Urease breath test.H. pylori serum antibody.
37Treatment is with various combinations of a PPI and two antibiotics for 2 weeks. Test for cure.
40Varices (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.
41Risks factors predictive of bleed: Location (GE junction highest risk).Size (diameter – related to Laplace’s 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).
43Acute 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.
44Mallory-Weiss TearsLongitudinal 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 %)
45Amount of blood loss usually small and self-limited. Chronic alcohol (40%-80%).Amount of blood loss usually small and self-limited.Heal within hours.Treat actively bleeding lesions with endoscopy.PPI’s/H2 blockers promote healing.
47Key points Triage and resuscitate patient quickly and appropriately. Obtain quick endoscopy.Test for H. pylori if ulcers present, and treat if positive.Use PPI’s to reduce risk of rebleeding.Remove medications that increase risk of bleeding.
49Resources www.uptodate.com Lung E. “Evaluation and Management of Gastrointestinal bleeding Part 1: Nonvariceal Upper GI Bleeding.” Advanced Studies in Medicine. Vol 4 (4) AprilPapatheodoridis GV et al. “Effect of Helicobacter pylori infection on the risk of upper GI bleeding in users of NSAID’s.” Am J Med May 1: 116(9)Exon DJ, Sydney Chung SC. “Endoscopic therapy for upper GI Bleed.” Best Pract Res Clin Gastroenterol Feb; 18(1):77-98.