1. UPPER GASTROINTESTINAL BLEEDING

2. Causes of Esophago-Gastro-Duodenal Bleeding Varices Mallory Weiss Esophagitis Gastric Ulcer NSAID’s/ Aspirin Neoplasm Acute Gastritis Duodenal Ulcer Arterio-Venous Malformation

3. Upper Gastrointestinal Bleeding

4. Upper Gastrointestinal Bleeding

5. Upper Gastrointestinal Bleeding Severe UGIH is a common and serious medico-surgical problem

6. Upper Gastrointestinal Bleeding Despite a decreased incidence of ulcer disease and improvements in the management of acute upper GI bleeding, mortality remains at + 6-7 % in most series in the literature for the past 30 years.

7. Upper Gastrointestinal Bleeding Endoscopic hemostatic therapy has been demonstrated to be the mainstay of management.

8. Upper Gastrointestinal Bleeding At intragastric pH < 7, coagulation is deficient due to ineffective function of clotting factors and platelets

9. Upper Gastrointestinal Bleeding Maintenance of a high intragastric pH > 6 during management of upper G I Bleeding is warranted. IV PPI’s are able to maintain gastric pH > 6 for 24 hours a day.

10. Upper Gastrointestinal Bleeding Recent clinical trial data support the use of PPI’s to decrease the rate of re-bleeding and the need for surgery.

11. Epidemiology of upper GI Bleeding • 100 cases/100,000 adults/year • 50-60% of cases are peptic ulcer disease • 150,000 hospital admissions/y (U.S. 1985) • 80% of cases of bleeding cease spontaneously • 6-7% mortality rate

12. Upper GI bleeding Pathophysiology

13. Risk factors for ulcers and bleeding Risk factor H. pylori • 70-90% in non-bleeding duodenal ulcers • Lower in bleeding ulcers and gastric ulcers NSAIDs/ASA (dose dependent) • Increased risk of ulcers and bleeding with doses as low as 75 mg day ASA Corticosteroid + NSAIDs • Little increased risk when used alone • With NSAIDs increased risk: • Ulcer complications – 2 x • GI bleeding – 10 x Oral anti-coagulants +/- NSAIDs • Increased risk of bleeding vs. controls: • Alone – 3.3 • With NSAIDs – 12.7

14. NSAID Induced Ulcers Main Risk Factors: • Older age > 75 years • Active R.A. • Concomitant use of corticosteroids • History of peptic ulcer disease, GI bleeding or heart disease.

15. Prognostic Factors Clinical: • Haemodynamic instability • Fresh red blood in the emesis • Haematochezia • Increasing number of units transfused

16. Prognostic Factors • Age > 60 years • Concurrent illness - Cardiovascular, pulmonary and Diabetes Mellitus • Onset while hospitalised for other reasons • Recurrent bleeding

17. Prognostic Factors Urgent Endoscopy: • Patients with coffee-ground vomiting with melena • Haematemesis with or without melena

18. Prognostic factors: endoscopic Incidence of rebleeding by appearance of ulcer at endoscopy 80% 60% 40% 20% 0% 55 % of patients rebleeding 43 22 10 5 Clean base Flat spot Adherent clot Nonbleeding visible vessel Active bleeding Laine & Peterson; 1994

19. Outcome of Acute G I Bleeding

20. Influence of Diagnosis on Outcome

21. Vascular Anatomy

22. Vascular Anatomy - Relationship to Therapy

23. Role of Endoscopy

24. Forrest Classification Endoscopic Observation Rebleeding Chance %

25. Endoscopic intervention is only required in Forrest Ia, Ib, IIa and probably IIb at first to stop the active bleeding (Ia, Ib) and prevent subsequent rebleeding.

26. In Forrest IIb (probably), but surely IIc and III, the risk of rebleeding is very low and does not warrant active endoscopic hemostatic techniques.

27. Stigmata of Recent Haemorrhage - Prevalence

29. Nature of the visible vessel

30. Overview of management • Initial management • Endoscopic therapy • Surgical therapy • Pharmacological therapy

31. Initial Management • Assess haemodynamic instability • Resuscitation • Haemogram and coagulation studies • Nasogastric tube (in/out) • Monitoring of vital signs and urine output

32. Endoscopic therapy • Perform early (ideally within 24 h) • Indications for haemostatic therapy1 • 1. +/- Adherent clot • 2. Nonbleeding visible vessel • 3. Active bleeding (oozing, spurting) • Heater probe, bipolar electrocoagulation or injection therapy • Decreases in rebleeding, surgery and mortality2,3 1. Laine & Peterson; 1994 2. Cook et al; 1992 3. Sacks et al; 1990

35. Effect of Therapy on re-bleeding rates (Visible Vessel)

36. Effect of Therapy on re-bleeding rates (Active Bleeding)

37. In a comparative study (AJG 2001) between adrenaline injection alone • and adrenaline followed by hemoclips • in Forrest Type I or II patients • Control of bleeding achieved in 83,3% of patients in the injection - only group and 95,6% in the combination group (NSS)

38. In sub-group Forrest Ib patients, rebleeding was 31% in the injection - only group and 0% for the combination group (p< 0,05) • Re-bleeding rate in adrenaline - only group is 17% compared to 4,42% in the combination group - clinically meaningful but NSS.

39. Endoscopic therapy may not be possible in up to 12% of bleeding duodenal ulcers and at least 1% of bleeding gastric ulcers because of inaccessibility of the lesion or massive hemorrhage.

40. Patients who do not have active bleeding, non-bleeding visible vessels, or adherent clots are low risk for further bleeding.

41. Bleeding from a P.U. recurs after initial endoscopic hemostasis in 15-20% of patients. Endoscopic re-treatment reduces the need for surgery without increasing the risk of death and is associated with fewer complications than surgery

42. Hypotension and ulcer size of at least 2cm are independent factors predictive of the failure of endoscopic re-treatment. Patients with larger ulcers and therefore heavier bleeding, surgery may be a better choice than endoscopic re-treatment.

43. Salvage surgery for recurrent bleeding is associated with a mortality rate ranging from 15-25%.

44. Surgical therapy • Endoscopic management failure • Other extenuating circumstances • Patient survival improved by optimal timing • Individualized by clinical context, endoscopic and surgical expertise

45. Pharmacological Therapy • Vasopressin - lowers splanchnic blood pressure - induces vasoconstriction - high rate of complications

46. Pharmacological Therapy - Lower toxicity - additional effects of decreasing gastric acid secretion and increasing duodenal bicarbonate secretion - decreased risk of re-bleeding compared to H2RAs • Somatostatin and Octreotide

47. Pharmacological Therapy - appears to decrease mortality - increased risk of thrombo-embolic events • Tranexamic acid - Antifibrinolytic agent

48. Pharmacologic Therapy • Acid suppressing agents - H2 Receptor Antagonists - Proton Pump Inhibitors

49. Pharmacologic Therapy • Aggressive acid suppression with PPI’s reduce the rate of recurrent bleeding, the need for transfusions, and the need for surgery. They represent an important adjunct to endoscopic therapy.

50. Role of acid in haemostasis • Impairs clot formation • Impairs platelet aggregation and causes disaggregation • Accelerates clot lysis • Predominantly acid-stimulated pepsin • May impair integrity of mucus/bicarbonate barrier