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UPPER%20GASTROINTESTINAL

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Incidence of rebleeding by appearance of ulcer at endoscopy. Nonbleeding visible vessel ... Role of Endoscopy. Forrest Classification. Endoscopic Observation ... – PowerPoint PPT presentation

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Title: UPPER%20GASTROINTESTINAL


1
UPPER GASTROINTESTINAL BLEEDING
2
Causes of Esophago-Gastro-Duodenal Bleeding
Varices
Mallory Weiss
Esophagitis
NSAIDs/ Aspirin
Gastric Ulcer
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 lt 7, coagulation is deficient
    due to ineffective function of clotting factors
    and platelets

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

10
Upper Gastrointestinal Bleeding
  • Recent clinical trial data support the use of
    PPIs 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 gt 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 gt 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
28
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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
33
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34
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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 (plt 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 PPIs
  • 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
A
?
0 20 40 60 80 100
pH 5.9
? ADP
pH 6.8
pH 7.4
Aggregation ()
0 1 2 3
4 5
Time (minutes)
Green et al 1978
52
Effect of PPI on gastric pH
  • Increase intragastric pH
  • pHgt6.0 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
  • pHgt6.0 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
  • 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
  • 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
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