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UGI Bleeding Epidemiology of Upper GI Bleeding Bleeding from a source above the ligament of Treitz 1 case/1,000 adults/year 50% of cases are peptic ulcer.

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Presentation on theme: "UGI Bleeding Epidemiology of Upper GI Bleeding Bleeding from a source above the ligament of Treitz 1 case/1,000 adults/year 50% of cases are peptic ulcer."— Presentation transcript:


2 UGI Bleeding

3 Epidemiology of Upper GI Bleeding Bleeding from a source above the ligament of Treitz 1 case/1,000 adults/year 50% of cases are peptic ulcer disease (25% rebleed) 40-80% of cases of bleeding cease spontaneously 10% mortality rate

4 Prognostic Factors Hemodynamic instability Hematochezia from upper GI source Increasing number of units transfused Age > 60 years Concurrent illness (cardiac, respiratory, renal, neoplastic, CNS) Onset while hospitalized for other reason Coagulopathy

5 Etiology of UGI Bleeding Non GI Hemopytsis, nose bleed Esophageal Esophagitis, ulcer, varices, malignancy, MW tear Gastric Gastritis, ulcer, varices, malignancy, AVM Duodenal Duodenitis, ulcer, varices, malignacy (rare), AVM, aortoenteric fistula

6 Etiology Incidence 1.PUD 50% 2.Esophagitis 15% 3.Gastritis 10% 4.Varices 10% 5.Duodenitis 5% 6.MW tear 3% (much more common in young) 7.Esophageal ulcer 3% 8.Carcinoma 3%


8 Presentation Melena or hematochezia 70% (charting, iron pepto) Hematemesis or coffee ground emesis 30% (charting, testing) Syncope 14%, presyncope 40% Heartburn 40%, epigastric pain 20% Dysphagia 10% Wt. loss 12%

9 Important History Evidence of complications CP/SOB/presyncope Appearance, frequency and amount of vomit/BM (elderly unreliable) Duration of symptoms Use of NSAID/ASA/corticosteroids Previous history of GI bleeding Co-morbidities = cardiac, respiratory, neoplastic, CNS

10 Physical Exam ABCs Vitals Orthostatic bp (scoping) Rectal exam (what does –ve OB really mean)

11 Initial Management ABCs Npo Head down, raise legs 2 IVs CBC Urea/Cr (? upper vs lower bleeding, ? reliable) G&T LFTs Coagulation status ECG/cardiac enzymes NG?

12 Prognostic Factors: Endoscopic Laine, Peterson, N Engl J Med 1994.


14 Clot on Vessel - Gastric Ulcer

15 Overview of Management Initial management Endoscopic therapy Surgical therapy Pharmacologic therapy

16 Endoscopic Therapy Perform early (ideally within 24 h) Indications for haemostatic therapy: (1) +/-Adherent clot, (2) Nonbleeding visible vessel, (3) Active bleeding (oozing, spurting) (Laine, Peterson. 1994) Heater probe, bipolar electrocoagulation or injection therapy Decreases in rebleeding, surgery and mortality (Cook, et al. 1992, Sacks, et al. 1990)

17 Surgical Therapy Endoscopic management failure Other extenuating circumstances Patient survival improved by optimal timing Individualized by clinical context, endoscopic and surgical expertise

18 Surgical Therapy Outcomes in 92 patients with rebleeding after endoscopic therapy: endoscopic retreatment vs. surgery. Lau, et al. NEJM N/A=not applicable

19 Pharmacologic Therapy Splanchnic blood pressure modifiers vasopressin, somatostatin, octreotide Anti-fibrinolytic agents tranexamic acid Acid suppressing agents H 2 -receptor antagonists (H 2 RAs), proton pump inhibitors (PPIs)

20 Somatostatin/Octreotide Effects: Lowers splanchnic blood pressure Decreases gastric acid secretion Increases duodenal bicarbonate secretion Meta-analysis: (Imperiale, Birgisson, 1997) 14 trials (n=1,829); SOM (12 trials), OCT (2 trials) 0.53 risk of rebleeding vs. H 2 RAs RR=0.73 among investigator-blinded trials Studies did not control for confounders, i.e., endoscopic therapy

21 Acid Suppressing Agents H 2 -receptor antagonists (H 2 RAs) Cimetidine, ranitidine, famotidine, nizatidine Proton pump inhibitors (PPIs) Pantoprazole, omeprazole (oral, IV) Esomeprazole (Nexium) (oral) Lansoprazole (oral)

22 Role of Acid in Hemostasis Impairs clot formation Impairs platelet aggregation & causes disaggregation Accelerates clot lysis Predominantly acid-stimulated pepsin May impair integrity of mucus/bicarbonate barrier


24 Effect of PPI on Gastric pH Increase intragastric pH pH>6.0 for 84->99% of day Continuous infusion (CI) superior to intermittent bolus administration Clinical improvements in rebleeding and/or surgery with: Bolus 80 mg + CI 8 mg/h

25 Role of PPI For UGI Bleeding: Summary of Clinical Trials 10 RCTs PPI (n=1,150); controls (n= 1,142) Minimal benefit with intermittent bolus Clinical benefits with bolus plus continuous infusion (CI) Decreased need for surgery and/or rebleeding Dose: Bolus 80 mg + CI 8 mg/h x 3 d

26 Role of PPI For Upper GI Bleeding: Summary H 2 RAs Unlikely to provide necessary pH increases Tolerance a problem Minimal benefit in clinical trials PPIs can provide profound acid suppression pH>6.0 over 24-hours Suggested benefits on rebleeding and/or need for surgery Mortality benefits not yet demonstrated

27 Role of PPI For Upper GI Bleeding: Summary Reasonable to consider initiating as soon as possible following presentation to hospital Administer as bolus + continuous infusion (CI) IV bolus 80 mg + CI 8 mg/h x 3 d Continue therapy, probably with an oral PPI Likely most beneficial for patients with high risk, non- actively bleeding lesions Further trials needed to determine optimal patient group for acute IV PPI therapy


29 Peptic Ulcer Disease Causes: Infectious: H.P., Herpes, CMV Drugs: NSAIDS, corticosteroids Neoplastic ICU Stress Types: DU = pain between meals GU = pain with meals, epigastric

30 Risk Factors for Ulcers and Bleeding

31 Peptic Ulcer Disease – Helicobacter Pylori Most common chronic bacterial infection in man 15% of infected go on to PUD Dx via C 13 /C 14 breath testing, histology, serology, urease testing (5-15% false negative) –false negative if ABO or acid suppression within the last week (except serology) Serology $30 (not for eradication) Breath Testing 13 C non-radioactive urea metabolized to CO 2 exhaled and quantified

32 Peptic Ulcer Disease – When to Test for H.P. GU = test for H.P. as other causes of GU are common, especially NSAID induced ulcers, maliganancy (repeat endoscopy) DU = if not on NSAID may treat empirically for H.P.

33 Helicobacter Pylori Eradication Proven to decrease ulcer recurrence/bleeding Tx if any history of upper GI bleeding and H.P. positive Treatment Options: PCA= PPI + Clarithomycin 500mg bid + Amoxil 1g bid for 7 days PCM = PPI + Clarithoromycin 500mg bid + Metronidazole 500 mg bid X 7 days (resistance)

34 H.P. Eradication Antibiotics are very effective Test for eradication only in complicated ulcer disease eg. bleeding, pyloric outlet obstruction, recurrent ulceration or persistent symptoms Most cost effective method = breath testing –1/12 after antibiotics are complete – 7/7 after stopping acid suppression

35 NSAID And Upper GI Ulceration 2-4% annual risk of PUD related complication on NSAID (bleeding, outlet obstruction, symptomatic ulcer) Lowest possible dose of NSAID/ASA (2-4X risk even if <325 mg ASA daily) Prophylaxis if: –Previous PUD or GI bleed –NSAID + corticosteroids –>65 (75 in Ontario guidelines) –serious comorbidity

36 NSAIDS & UGI Bleeding Classic NSAID inhibit COX-1 and COX-2 Inhibition of COX 1 results in decreased gastric PG and hence poor protective barrier in the GI tract COX-2 expressed predominantly in actively inflammed tissues, therefore less damage to normal GI tract COX-2 ulcer risk approx to that of classic NSAID + PPI

37 COX-2 Inhibitors & UGI Ulceration 1149 pt. with R.A. endoscopy pre and post 12 weeks therapy for GI ulceration Compared celecoxib (2x max. dose) vs. naproxen (max. dose) vs. placebo No difference ulceration between placebo and celecoxib vs. p<0.001 difference between celecoxib and naproxen Near identical study with Vioxx (rofecoxib)

38 NSAIDS and UGI Bleeding Prophylaxis Options: Misoprostol 200mg qid + standard NSAID –Side effects diarrhea, cramps –$38/month, 4% S/E PPI + standard NSAID –More effective than Misoprostol –$53/month (Pantoprazole) Cox –2 inhibitor ($40-75/month) –? Add PPI

39 NSAIDS, H.P. And UGIB Prophylaxis In high risk patients (previous PUD or ongoing dyspepsia), test and treat for H.P. prior to NSAID initiation decreases risk UGI to that of PPI or celebrex How to test Time consideration of breath testing Most bleeds in first month Previous studies show no benefit for primary prophylaxis with H.P. eradication if already on an NSAID



42 Esophageal Variceal Bleeding BE SUPICIOUS, if patient is cirrhotic/heavy drinker think varices first 30-50% mortality without early intervention Causes of death are classically aspiration, sepsis, renal failure or encephalopathy Treatment options: -Medical- endoscopic -Tamponade- TIPS - Surgical

43 Esophageal Variceal Bleeding Medical = octreotide (72 hours) or somatostatin forget vasopressin Endoscopic = ligation (banding), sclerotherapy


45 Esophageal Varices Tamponade = Blakemore tube

46 Esophageal Varices TIPS = transjugular intrahepatic portosystemic shunts or Surgical Shunts = desperate measures





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