Upper Gastrointestinal Bleeding
Upper Gastrointestinal Bleeding
Upper Gastrointestinal Bleeding
BLEEDING
DEFINITION UGIB
Bleeding proximal to ligamentum terez
50% present with hematemesis
NGT with positive blood on aspirate
11% of brisk bleeds have hematochezia
Melena (black tarry stools)this develops with
apporximately 150-200cc of blood in the upper GI tract.
Stool turns black after 8 hours of sitting within the g
UGIB
Persistent bleed patient requires
8u(>60yrs) or 12u(<60yrs) or over a 48hrs
period to maintain Hb 10g/dl.
In Msia 72:100000, mortality 10%, 4050yrs old.
Clinical features
Melaena
Haematemesis
Coffee-ground vomiting
Haemochezia
Causes
Duodenal Ulcer
Gastric Ulcer
Varices
Gastritis and duodenitis
Esophagitis
Mallory Weiss Tear
Aorto-enteric fistulae
Esophagitis
Dudodenal ulcer
Esophageal varices
Esophageal varices
Abnormal enlarged veins in the lower part
of the esophagus
Occurs more often in people with serious
liver diseases
Develop when normal blood flow to the
liver is obstructed by scar tissue in liver or
clot
Causing blockage
Esophageal varices
Oesophageal submucosal veins connect
portal and systemic venous systems
Normal low pressure gradient between
two venous systems (~5mmHg)
Cotn.
If portal venous pressure increases (portal
hypertension), gradient increases
(>10mmHg)
Increased flow in submucosal veins in
oesophagus: Can bleed massively
Esophageal varices
Cotn.
signs of liver disease, including:
Yellow coloration of your skin and eyes
(jaundice)
Easy bleeding or bruising
Fluid buildup in your abdomen (ascites)
Esophageal varices
RISK FACTORS
high portal vein pressure
large varices
red marks on the varices
severe cirrhosis of liver failure
alcohol
Esophageal varices
COMPLICATIONS
-blood loss that can lead to shock, death
Esophageal Varices
INVESTIGATION
-full blood count
-coagulation profile
-renal function test
-CXR
-group and crossmatch
ENDOSCOPE
ENDOSCOPY
Endoscopic Variceal Ligation (EVL)
Endoscopic Sclerotherapy
Intravariceal or Paravariceal injection of
Sclerosant (i.e. Sodium tetradecyl
sulphate & ethanolamine oleate
Epidemiology
Pathogenesis:
Peptic ulcers appear to be produced by
an imbalance between
gastroduodenal defense
mechanism and damaging forces.
Gastric acid and pepsin are prerequisite
for all peptic ulcerations.
Mucosal defense
Cont.
4. Corticosteroid in high dose.
5. Gastric hyperacidity- Hyperacidity may
arise from increased parietal cell mass,
sensitivity to secretory stimuli, increased
acid secretory drive or impaired inhibition
of stimulatory mechanism such as gastrin
release.
Complication
Complication:
1. Anaemia.
2. Bleeding- Occurs 15-20% of patient. It
may be life threading.
3. Perforation- Occurs in 5% of patients.
Accounts for 2/3rd of ulcer deaths.
4. Gastric outlet obstruction.
5. Malignant transformation- Rare.
Investigation
-full blood count
-coagulation profile
-renal function test
endoscope
endoscopy
Injection
Adrenaline
Sclerosants
Fibrin glue
Coagulation
Argon Plasma Coagulation
Laser Therapy
Mechanical Closure
Endoclips
Combination Therapy
Treatment
Proton pump inhibitors (PPI). Proton pump medications reduce
acid levels and allow the ulcer to heal. omeprazole (Prilosec),
pantoprazole (Protonix), rabeprazole(Aciphex)
Antibiotics . If you have H. pylori infection, then antibiotics are
also used. There are multiple combinations of antibiotics that are
taken for one to two weeks along with a PPI.
Upper endoscopy . Some bleeding ulcers can be treated through
an endoscope.
Surgery. Sometimes an operation is needed if the ulcer has
created a hole in the wall of the stomach, or if there is serious
bleeding that can't be controlled with an endoscope.
Management of GI bleed
Oxygen
IV Access-central line or two large bore
peripheral IV sites
Isotonic saline for volume resuscitation
Start transfusing blood products if the
patient remains unstable despite fluid
boluses.
Altered Mental Status and increased risk
of aspiration with massive upper GI bleed.
PATIENT EDUCATION
STOP smoking
avoid taking NSAIDs
Avoid excessive alcohol intake
Stress reduction theraphy
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