Download Upper Gastrointestinal Bleeding

UPPER GASTROINTESTINAL
BLEEDING
Causes of Esophago-GastroDuodenal Bleeding
Varices
Mallory Weiss
Esophagitis
Gastric Ulcer
NSAID’s/
Aspirin
Neoplasm
Duodenal
Ulcer
Arterio-Venous
Malformation
Acute
Gastritis
Upper Gastrointestinal Bleeding
Upper Gastrointestinal Bleeding
Upper Gastrointestinal Bleeding
Severe UGIH is a common
and
serious medico-surgical problem
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.
Upper Gastrointestinal Bleeding
Endoscopic hemostatic therapy
has been demonstrated to be the
mainstay of management.
Upper Gastrointestinal Bleeding
At intragastric pH < 7, coagulation is
deficient due to ineffective function
of clotting factors and platelets
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.
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.
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
Upper GI bleeding
Pathophysiology
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 anticoagulants
+/- NSAIDs
• Increased risk of bleeding vs. controls:
• Alone – 3.3
• With NSAIDs – 12.7
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.
Prognostic Factors
Clinical:
 Haemodynamic instability
 Fresh red blood in the emesis
 Haematochezia
 Increasing number of units transfused
Prognostic Factors
 Age > 60 years
 Concurrent illness - Cardiovascular,
pulmonary and Diabetes Mellitus
 Onset while hospitalised for other
reasons
 Recurrent bleeding
Prognostic Factors
Urgent Endoscopy:
 Patients with coffee-ground vomiting
with melena
 Haematemesis with or without melena
Prognostic factors: endoscopic
% of patients rebleeding
Incidence of rebleeding by appearance
of ulcer at endoscopy
80%
60%
55
40%
43
20%
22
0%
5
10
Clean base
Flat spot
Adherent Nonbleeding
Active
clot
visible vessel bleeding
Laine & Peterson; 1994
Outcome of Acute G I Bleeding
Influence of Diagnosis on Outcome
Vascular Anatomy
Vascular Anatomy Relationship to Therapy
Role of Endoscopy
Forrest Classification
Endoscopic Observation
Rebleeding Chance %
Ia
Spurting Arterial bleed
80-90
Ib
Oozing bleed
10-30
IIa
Non-bleeding visible vessel
50-60
IIb
Adherent clot
20-35
IIc
Black hematin ulcer base
0-8
III
Clean ulcer base
0-12
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.
In Forrest IIb (probably), but surely IIc
and III, the risk of rebleeding is very low
and does not warrant active endoscopic
hemostatic techniques.
Stigmata of Recent Haemorrhage Prevalence
Nature of the visible vessel
Overview of management
 Initial
management
 Endoscopic therapy
 Surgical therapy
 Pharmacological therapy
Initial Management
 Assess
haemodynamic instability
 Resuscitation
 Haemogram and coagulation studies
 Nasogastric tube (in/out)
 Monitoring of vital signs and urine
output
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
Effect of Therapy on re-bleeding rates
(Visible Vessel)
Effect of Therapy on re-bleeding rates
(Active Bleeding)
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)
 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.
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.
Patients who do not have active
bleeding, non-bleeding visible vessels,
or adherent clots are low risk for further
bleeding.
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
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.
Salvage surgery for recurrent bleeding
is associated with a mortality rate
ranging from 15-25%.
Surgical therapy
Endoscopic management failure
Other extenuating circumstances
Patient survival improved by optimal
timing
Individualized by clinical context,
endoscopic and surgical expertise
Pharmacological Therapy
Vasopressin
- lowers splanchnic blood pressure
- induces vasoconstriction
- high rate of complications
Pharmacological Therapy
 Somatostatin and Octreotide
- Lower toxicity
- additional effects of decreasing
gastric acid secretion and increasing
duodenal bicarbonate secretion
- decreased risk of re-bleeding
compared to H2RAs
Pharmacological Therapy
 Tranexamic acid - Antifibrinolytic agent
- appears to decrease mortality
- increased risk of thrombo-embolic
events
Pharmacologic Therapy
 Acid suppressing agents
- H2 Receptor Antagonists
- Proton Pump Inhibitors
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.
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
Effect of plasma pH on platelet aggregation
A
Aggregation (%)
0

pH = 5.9

ADP
20
pH = 6.8
pH = 7.4
40
60
80
100
0
1
2
3
4
5
Time (minutes)
Green et al; 1978
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
Role of Omeprazole in the
treatment of Upper G I Bleeding
Omeprazole in the Upper GI Bleeding Patients
with Stigmata of recent haemorrhage
Omeprazole therapy in the treatment of
upper GI bleeding from specific lesions
Prevention of Recurrent Upper
GI Bleeding
Eradication of H pylori Effect on
Re-bleeding (D.U.)
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
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
Stress Bleeding prophylaxis - Indications
Stress Prophylaxis - Treatment
Role of Angiography
Goal
Stop the bleeding
Requirements
Failure of endoscopic therapy
favourable anatomical location
Method
Transcatheter embolization - gel foam or
pharmacotherapy - vasopressin
Variceal Haemorrhage
 Oesophageal varices cause + 10% of
cases of acute upper GI bleeding
admitted to hospitals
 Mortality rate 30-50%
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
Treatment of Acute Variceal
Hemorrhage
 Control of hemorrhage (24 hour
bleeding free period within first
48 hours after therapy)
 Prevention of early recurrence
Pharmacotherapy
 Vasoactive therapy - Vasopressin
High rate of major complications
Conflicting results with Terlipressin and
Nitroglycerin
Pharmacotherapy
 Native Somatostatin
Reduces splanchnic blood flow and
azygos blood flow
Use is restricted due to its short half life
(1-2 min)
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
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)
Pharmacotherapy
 Antibiotic prophilaxis is mandatory
- Reduces rate of bacterial infections
- Increases survival
 Blood replacement to target Hematocrit of
25-30%
 Avoid intravascular over expansion
 Octreotide as adjunct to endoscopic
therapy appears to be the most
promising approach in the treatment of
acute variceal hemorrhage
Endoscopic View of Oesophageal Varices
Oesophageal Varices - Sclerotherapy
Oesophageal Varices - Banding
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
Shunt Surgery
 prevents rebleeding
 increases risk of portosystemic
encephalopathy
 no effect on survival
TIPS
 reduces rebleeding
 encephalopathy
 no effect on survival
 shunt dysfunction