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 % 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
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%
% of patients rebleeding 55 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. Relationship to Therapy
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 Resuscitation Haemogram and coagulation studies
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,
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

51. Effect of plasma pH on platelet aggregation 20 40 60 80
100
pH = 5.9 
ADP
pH = 6.8
pH = 7.4
Aggregation (%)
Time (minutes)
Green et al; 1978

52. Effect of PPI on gastric pH
Increase intragastric pH
pH>6.0 for 84-99% of day
No reported tolerance
Continuous infusion (CI) superior to intermittent bolus
administration
Clinical improvements in rebleeding and/or surgery with:
Bolus 80mg + CI 8mg/h

53. Role of Omeprazole in the treatment of Upper G I Bleeding

54. Omeprazole in the Upper GI Bleeding Patients with Stigmata of recent haemorrhage

55. Omeprazole therapy in the treatment of
upper GI bleeding from specific lesions

56. Prevention of Recurrent Upper
GI Bleeding

57. Eradication of H pylori Effect on
Re-bleeding (D.U.)

58. Role of PPI for upper GI bleeding: summary (1)
H2RAs
Unlikely to provide necessary pH increase
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

59. Role of PPI for upper GI bleeding: summary (2)
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 PPI therapy

60. Stress Bleeding prophylaxis - Indications

61. Stress Prophylaxis - Treatment

62. Role of Angiography Goal Requirements Failure of endoscopic therapy
Stop the bleeding
Requirements
Failure of endoscopic therapy
favourable anatomical location
Method
Transcatheter embolization - gel foam or pharmacotherapy - vasopressin

63. Variceal Haemorrhage Oesophageal varices cause + 10% of
cases of acute upper GI bleeding
admitted to hospitals
Mortality rate 30-50%

64. Variceal Haemorrhage Gastro-oesophageal varices are present
in + 50% of cirrhotic patients. Their
presence correlates with severity of liver
disease
Bleeding from oesophageal varices
ceases spontaneously in up to 40% of
patients

65. Treatment of Acute Variceal Hemorrhage
Control of hemorrhage (24 hour
bleeding free period within first
48 hours after therapy)
Prevention of early recurrence

66. Pharmacotherapy Vasoactive therapy - Vasopressin
High rate of major complications
Conflicting results with Terlipressin and
Nitroglycerin

67. Pharmacotherapy Native Somatostatin Reduces splanchnic blood flow and
azygos blood flow
Use is restricted due to its short half life
(1-2 min)

68. Pharmacotherapy Is as effective as endoscopic sclerotherapy
Synthetic somatostatin analogue - Octreotide
Half life 1-2 hours
More effective than placebo, vasopressin
and balloon tamponade
Is as effective as endoscopic sclerotherapy
and is a safe treatment for acute variceal
bleeding

69. Pharmacotherapy Non selective ß-adrenergic blockers -
proprandolol, nadolol or timolol
They decrease portal venous inflow by two
mechanisms
- decreasing cardiac output (ß1 blockade)
- splanchnic vasoconstriction (ß2 blockade
and unopposed alpha adrenergic activity)

70. Pharmacotherapy Antibiotic prophilaxis is mandatory
- Reduces rate of bacterial infections
- Increases survival
Blood replacement to target Hematocrit of
25-30%
Avoid intravascular over expansion

71. Octreotide as adjunct to endoscopic
therapy appears to be the most
promising approach in the treatment of
acute variceal hemorrhage

72. Endoscopic View of Oesophageal Varices

73. Oesophageal Varices - Sclerotherapy

74. Oesophageal Varices - Banding

75. Shunt Therapy Shunt surgery (distal spleno-renal)
in well compensated liver disease
(Child A) or TIPS are of proven
clinical efficacy as salvage therapy
for patients not responding to
endoscopic or pharmacologic therapy

76. Shunt Surgery prevents rebleeding increases risk of portosystemic
encephalopathy
no effect on survival

77. T I P S reduces rebleeding encephalopathy no effect on survival
shunt dysfunction