GASTROENTEROLOGY

APPROACH TO UPPER GASTROINTESTINAL

BLEEDING

Presents clinically as: 3. Cause of bleeding

 Overt bleeding:
 Melena - black, tarry, foul-smelling stool  Therapeutic approach will depend on the cause of bleeding
- at least 50mL of blood
 Hematemesis - vomitus of red blood or coffee- Causes:
ground material 1. Peptic Ulcers (Gastric/Duodenal) - most common
 Hematochezia - reddish blood from rectum 2. Varices (esophageal, gastric, duodenal)*
 Occult bleeding: 3. Mallory-Weiss Tear
- Identified in the absence of overt bleeding by fecal 4. Gastroduodenal erosions
occult blood or presence of iron deficiency anemia 5. Erosive esophagitis
6. Neoplasm
7. Vascular abnormalities (ectasia, Dieulafoy’s)
Signs and symptoms of upper GI bleeding 8. Portal hypertensive gastropathy*
9. Unidentified source
* Variceal source which are associated with liver cirrhosis + portal
hypertension
1. Assess the hemodynamic stability/severity of bleeding
 Upper endoscopy is the test of choice (diagnostic and
Assessment of severity of bleeding in relation to hemodynamic status therapeutic capability)
 Timing is important
Patient’s Hemodynamic Blood Loss (% of
For patients with massive GI bleeding: → perform
Severity of
Status Intravascular Volume)
Bleed endoscopy when resuscitation is optimum and back-up with
blood reserve
Shock (resting For patients with milder bleeding and hemodynamically
20-25 Massive
hypotension) stable: → early endoscopy can be performed

Postural (orthostatic 10-20

hypotension and
tachycardia)
Moderate Variceal Bleeding (Liver Cirrhosis)

Normal <10 Minor

Esophageal varices
Relationship of Hemoglobin to GI bleeding
Gastric varices
• Hemoglobin does not fall immediately with acute GIB, due
to proportionate loss of plasma and red cell volumes. Duodenal Varices
• Hemoglobin falls as extravascular fluid enters the vascular
space to restore volume, but this may take 72 hours
• Patients with chronic GI bleeding may have very low
hemoglobin values with normal BP and HR. Elevated portal pressure → Varices
Portal system carries capillary blood from the esophagus, stomach, SI,
LI, pancreas, GB, spleen to the liver

2. Resuscitate
ESOPHAGEAL VARICES
Resuscitation in hemodynamically unstable GI bleeder Esophageal varices

Large bore IV catheter; may insert

1.Vascular access
2 IV lines Normal Esophagus

2.Volume replacement PNSS/LR; Plasma expander

CBCP, typing and crossmatching,

3.Blood test
PT, PTT

4.Correct coagulopathy Vitamin K

5.Blood transfusion FWB, PRBC, Platelet, FFP

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 ESOPHAGEAL VARICES GASTRIC VARICES
Variceal bleeding Pharmacotherapy
(Somatostatin, Terlipressin)

Pharmacotherapy eg. Somatostatin,

Terlipressin (Vasopressin)

Balloon tamponade
Variceal ligation/Injection sclerotherapy

Hemostasis achieved Continued bleeding

Endoscopic therapy (super glue/Cyanoacrylate injection)
Repeat at 3-4 week interval Repeat ligation/sclerotherapy Hemostasis achieved Continued bleeding
Secondary prophylaxis
eg. Propanolol, Nitrates Continued bleeding Secondary prophylaxis Surgical intervention/TIPS

Surgery/TIPS

DUODENAL VARICES
ESOPHAGEAL VARICES
Duodenal varices (rare)
Esophageal varices and rubber band ligation
Pharmacotherapy (Somatostatin,
Terlipressin)

Variceal ligation

Hemostasis achieved Uncontrolled bleeding

Secondary prophylaxis Surgical intervention/TIPS

GASTRIC VARICES PORTAL HYPERTENSIVE GASTROPATHY

• Bleeding is usually slow/ chronic

• Somatostatin, Terlipressin - acute bleeding
• Non-selective B-adrenergic blocker
• TIPS - if bleeding uncontrolled

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 Non-surgical therapy for variceal bleeding DUODENAL ULCER
Pharmacotherapy of Portal Hypertension

Drugs that decrease portal blood flow

Non-selective beta-adrenergic blocking agents (Propanolol)

Normal duodenum Adherent clot
Vasopressin

Somatostatin

Drugs that decrease intrahepatic resistance

Nitrates
Clean base ulcer Bleeding visible vessel
ά-Adrenergic blocking agents (Prazosin)

Angiotensin receptor antagonist

ULCER BLEEDING
Non-surgical therapy for variceal bleeding PPI - proton pump inhibitor
IV PPI
Transjugular Intrahepatic Portosystemic Shunt (TIPS) Endoscopy
Reduces elevated portal pressure by creating a communication or Flat spot, Adherent Active bleeding,
shunt between the hepatic vein and an intrahepatic branch of
clean base clot visible vessel
portal vein via transjugular approach

IV PPI Endoscopic therapy +

No endoscopic therapy intravenous PPI

No rebleed Rebleed

PPI therapy Repeat endoscopic

therapy or surgery

Factors that predispose to ulcer bleeding:

1. Gastric acid *
GASTRIC ULCER (based on Forrest Classification ) 2. NSAID used *
3. H. pylori infection *
4. Cardiovascular, cerebrovascular disease
A. Spurting 5. Chronic pulmonary disease
B. Oozing
* most prominent factors
Type I
Non-selective NSAID in order of most harmful GI effect:
Ketoprofen
Type II Piroxicam
Indomethacin
Naproxen
Sulindac
A. Visible vessel B. Adherent clot C. Flat pigmented spot Diclofenac
ASA
Fenoprofen
Type III Ibuprofren
Established risk factors
• advanced age
Clean base • history of ulcer
• concomitant use of glucocorticoids high-dose + NSAIDs
• multiple NSAIDs
• concomitant use of anticoagulants
• serious or multisystem disease

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Possible risk factors
• concomitant infection with H. pylori
• cigarette smoking
• alcohol consumption ULCER BLEED
Adrenaline injection Argon plasma coagulation
ULCER BLEED

Pharmacotherapy:
• Used alone for low-risk endoscopic stigmata (clean based
ulcer, flat spot)
• Proton-pump inhibitor (PPI)
– Omeprazole, Esomeprazole, Pantoprazole,
Rabeprazole, Lansoprazole
– Decrease gastric acid secretion through inhibition
of H+K+ -ATPase, the proton pump of the parietal
cell
– Stabilized blood clot at pH > 6
– More effective than antacids, H2 receptor
blockers, mucosa protective agents
– Initially given as IV bolus and drip (80mg then
8mg/hr for 72 hours)
– Given for 6-8 weeks for gastric ulcer and 4 weeks Heater probe
Hemoclip
for duodenal ulcer to achieve complete ulcer
healing
• Eradicate H. pylori infection
– PPI BID + Amoxicillin 1 gm BID +
Clarithromycin 500mg BID for 10-14 days ULCER BLEEDING
• Discontinue NSAID
• Combination of COX2 inhibitor and PPI if NSAID Outcomes of endoscopic therapy for recurrence of
cannot be discontinued bleeding peptic ulcers according to the endoscopic
appearance
Most common endoscopic therapeutic methods to stop ulcer bleed Rebleeding rate (%)
include: Appearance
No ET vs ET
1. Diluted adrenaline injection
Active bleeding 55 20
2. Thermal application (contact heater probe and non-contact
argon plasma coagulation) Non-bleeding visible vessel 43 15
3. Mechanical methods (metal clips, band ligation)
Adherent clot 22 5

Flat pigmented spot 10 <1

Clean base <5 NA

ET - endoscopic therapy; NA- not assessed

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 illness, major neurologic trauma or intracranial
disease)
ULCER BLEEDING • bleeding is usually not massive hence endoscopic therapy
is generally not useful
Outcome of endoscopic therapy for bleeding peptic • PPI therapy
ulcers according to the endoscopic appearance
(need to perform surgery)
Surgery rate (%)
MALLORY-WEISS TEAR
Appearance
No ET vs ET
Active bleeding 35 7

Non-bleeding visible vessel 34 6

Adherent clot 10 2

Flat pigmented spot 6 <1

• Tear at the GE junction that occur typically at the
Clean base 0.5 NA
gastric mucosa side
ET - endoscopic therapy; NA- not assessed • Cause by forceful retching
• Bleeding stops spontaneously in 80-90%
• Supportive therapy only if bleeding stops
ULCER BLEEDING • Endoscopic therapy if with bleeding

Outcomes of endoscopic therapy for bleeding peptic

ulcers according to the endoscopic appearance
(mortality) ESOPHAGEAL BLEEDING
Mortality rate (%)
Appearance
No ET vs ET
Esophageal Erosion and Ulcer
Active bleeding 11 <5

Non-bleeding visible vessel 11 <5

Adherent clot 7 <3

Flat pigmented spot 3 <1

Clean base 2 NA

ET - endoscopic therapy; NA- not assessed

Ulcer Normal Erosion

GASTRODUODENAL EROSIONS
erosion ulcer
ESOPHAGEAL EROSION AND ULCER

• High dose PPI for reflux esophagitis

• Endoscopic treatment is usually not required since bleeding
usually is not massive
• Endoscopic treatment for ulcers with visible vessel and
severe bleeding
Erosion involves the
muscularis mucosa level
(subepithelial) while ulcer
involves the submucosa
level and beyond

GASTRODUODENAL EROSIONS

• most common cause is NSAID used

• other causes are ethanol ingestion, stress related (extensive
trauma, severe burns, major surgery, serious medical

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 NEOPLASM Dieulafoy Lesion

Esophageal/Gastric/Duodenal Malignancy

• bleeding is massive
• 6% of cases of and recurrent
upper GI bleeding
• difficult to identify
• Abnormally large arteriole that retains the large caliber of
its feeding vessel as it approach the mucosa
Gastric Gastrointestinal
Esophageal Ca • The large arteriole compress the mucosa and eventually
adenocarcinoma stromal tumor
causes a small erosion and rupture of vessel in the lu
Usually presents as occult bleeding
Palliative: Endoscopic therapy
Definite: Surgical resection of tumor

Dieulafoy Lesion

VASCULAR ABNORMALITY
Vascular Ectasia

Endoscopic therapy: Hemoclip application, band ligation,

injection sclerotherapy
: Prevents bleeding 95% of the time
• Dilatation of blood vessels
• Endoscopic treatment: Argon plasma coagulation

Gastric Antral Vascular Ectasia (GAVE) UPPER GASTROINTESTINAL

BLEEDING
Role of gastric lavage?

• To clear the blood that obscures the

endoscopic view in patients with massive
bleeding
• Endoscopic treatment: Argon plasma coagulation • No therapeutic role
• If bleeding is uncontrolled: Antrectomy
• May aggravate the bleeding (dislodged
adherent clot)

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