UPPER GASTROINTESTINAL
BLEEDING
UMAR BIN AZLAN
FATIN AMANINA BT SHAHRIMAN
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
UPPER GIT (Mouth to Duodenum)
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
Sign and symptoms
Symptoms
Vomiting and seeing significant amounts
of blood in your vomit
Black, tarry or bloody stools
Lightheadedness
Loss of consciousness (in severe case)
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
The Japanese Classification for the staging
of the oesophageal varices
Grade 1: small, straight varices not
disappearing on insufflation
Grade 2: medium varices occupying less
than one 3rd of the lumen
Grade 3: large varices occupying more
than one 3rd of the lumen
ENDOSCOPY
Endoscopic Variceal Ligation (EVL)
Endoscopic Sclerotherapy
Intravariceal or Paravariceal injection of
Sclerosant (i.e. Sodium tetradecyl
sulphate & ethanolamine oleate
TREATMENT AND MANAGEMENT
Exploratory Laparotomy to Secure Haemostasis
This is the most classical way before the era of
Endoscopy and Interventional Radiology
Procedures:
Underrunning of the bleeding ulcer
Antrectomy
Partial or Total Gastrectomy
Antisecretory procedure (Vagotomy)
Peptic ulcer disease
Peptic ulcer disease
An ulcer is defined as a breach in the
mucosa , which extends through the
muscularis layer or deeper.
Peptic Ulcer Disease
PEPTIC ULCERS
Peptic ulcers are chronic, most
oftensolitary, lesions that occur in any
portion of the UGIT
due to exposed to the aggressive action of
the acid-peptic juices.
Peptic ulcers are located in the following
sites :
1. Duodenum, first portion (98%).
2. Stomach, usually antrum.
3. At gastroesophageal junction, in the
setting
of gastroesophageal reflux.
4. Within the margins of a
gastrojejunostomy.
5. In the duodenum, stomach or jejunum
of
patient with Zollinger-Ellison syndrome.
6. Within or adjacent to a Meckel
diverticulum
that contains ectopic gastric mucosa.
Epidemiology
In USA, approximately 4million people
have peptic ulcers and 350,000 new cases
are diagnosed each year.
Peptic ulcers are most often diagnosed in
the middle-aged to older adults, but may
occur in young adults.
Male: Female ratio- For duodenal ulcer is
3:1 and for gastric ulcer is 1.5 - 2.1:1.
Sign and symptoms
A gnawing or burning pain in the middle or upper
stomach between meals or at night
Bloating
Heartburn
Nausea or vomiting
In severe cases, symptoms can include:
Dark or black stool (due to bleeding)
Vomiting blood (that can look like "coffee-grounds")
Weight loss
Severe pain in the mid to upper abdomen
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
1. Surface mucus secretion.
2. Bicarbonate secretion in to mucins.
3. Mucosal blood flow.
4. Apical cell transport system.
5. Epithelial cells regenerative capacity.
6. Uncertain role of prostaglandins.
Damaging influences are:
1. H pylori infection- It is a major factor in the
pathogenesis of peptic ulcer.
It is present in virtually all patients with duodenal
ulcers and about 70% of gastric ulcers.
2. Chronic use of NSAIDs- They suppresses the
mucosal prostaglandin synthesis.
3. Alcohol.
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.
6. Duodenal ulcer is more frequent in patient
with alcoholic cirrhosis,COPD, chronic renal
failure and
hyperparathyroidism.
7. Genetic influences appear to play no role.
8. Personality and psychological stress.
9. Impaired defense occurs in ischaemia, shock,
delayed gastric emptying and duodenal-gastric
reflux.
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
Endoscopy: What can be done?
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.
Management of upper GI bleed
1 unit PRBC increases Hgb by 1mg/dL
and increase Hct by 3%
FFP for INR greater than 1.5
Platelets for platelet count less than 50K
PATIENT EDUCATION
STOP smoking
avoid taking NSAIDs
Avoid excessive alcohol intake
Stress reduction theraphy
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