4. Definition
• UGIB can be defined as
bleeding from any site along the
gastrointestinal tract (GIT) that
is above the ligament of treitz.
5. Epidemiology
• The annual incidence of hospital
admissions for UGIB in the United States
and Europe is approximately 0.1%, with a
mortality rate of about 5-10%.
• The mortality rate of patients under 60
years of age in the absence of malignancy
or organ failure is < 1%.
• The three independent clinical predictions
of death in patients hospitalized with UGIB
are increasing age, co morbidities and
haemodynamic compromise (tachycardia &
hypotension)
6. Aetiology
• Common causes
1) Peptic ulcers – most common
cause of UGIB – 35-62% of cases
2) Varices (oesophageal & gastric) –
5-30%
3) Mallory-Weiss syndrome – 5-15%
4) Haemorrhagic gastropathy &
erosions – 3-11%
5) Erosive oesophagitis – 2-8%
7. Aetiology (contd)
• Uncommon causes; they include Erosive
duodenitis, neoplasms, aortoenteric
fistulas, vascular lesions[ including
hereditary haemorrhagic
telengectasias(Osler- Weber-Rendu) and
gastric antral vascular ectasia (‘Water-
melon stomach’)], Dieulafoy’s lesion (in
which an aberrant vessel in the mucosa
bleeds from a pinpoint mucosal defect),
prolapse gastropathy, haemobilia and
hemosuccus pancreaticus.
8. Clinical Presentation
• This bleeding from the GIT can present in 5 ways;
a) Haematemesis:- Vomitus of red blood or ‘coffee-
grounds’ material.
b) Melaena:- Black, tarry foul smelling stool.
c) Haematochezia:- Is the passage of bright red or
maroon blood from the rectum.
d) Occult GIB:- This is identified in the absence of
overt bleeding by special examination of the stool
(e.g. Guaiac testing)
e) Symptoms of blood loss/anaemia:- Light-
headedness, syncope, angina or dyspnoea.
10. Management (contd)
• This depends on the following;
1) Age of patient
2) The amount of blood lost
3) Continuing visible blood loss
4) Signs of chronic liver disease on
examination
5) Evidence of co morbidity e.g. cardiac
failure, ischaemic heart disease and
malignant disease.
6) Presence of the classical features of
shock.
11. Quick history
• Any of the already mentioned
C/P, shock and unconscious.
• Hx of epigastric pain or a known
PUD patient
• Intake of NSAIDS e.g. Asprin
• Alcohol binge
12. • Gastric erosions (black arrows)
caused by Ibuprofen as seen on
upper endoscopy
14. Investigations
• FBC – especially Hb
• S E/U/C – access renal status
• Liver function test
• Endoscopy (diagnostic) – performed
within 24hrs in most patients.
- Bleeding site is seen in >80% of
cases. i.e. Varices, Mallory-Weiss
tear or PUD.
16. Medical
• ABC Resuscitation- for emergency cases,
when patient presents with an ongoing blood
loss, in shock or unconscious.
A- Clear airway Suctioning in cases of
haematemesis
Left lateral position to
avoid aspiration.
B- Ensure breathing Oxygen therapy for
shocked patients.
17. Medical (ABC
resuscitation contd)
C- Circulation Establish one or more
intravenous accesses with wide bore
cannulae, if bleeding is brisk and massive.
- Blood transfusion with fresh whole blood
- Colloid (dextran) or crystalloid (N/S) until
blood becomes ready.
-continue monitoring pulse and BP
-avoid circulatory overload
For continued bleeding - reendoscope
18. Medical contd
(Therapeutic Endoscopy)
• This depends on cause;
• VARICES: (i) can be injected with a sclerosing
agent that produces vessel thrombosis e.g. 5%
phenol in almond or arachis oil
(ii) Banding
Both are said to arrest bleeding in 80% of cases
• BLEEDING PUD: (i) Bipolar electrocoagulation
(ii) Heater probe
(iii) Injection therapy with
absolute alcohol, 1:10,000 epinephrine.
19. Medical contd (Drug
Therapy)
• In about 20% of cases of bleeding
PUD, following use of heater probe,
epinephrine or laser therapy they
rebleed within 72hrs.
• Such cases will require intravenous
Omeprazole 80mg bolus followed by
infusion 8mg/hr for 72hrs.
• This reduces rebleeding rates and
need for surgery.
20. Medical contd (Drug
Therapy)
• FOR VARICES: Vasoconstrictor
therapy with Terlipressin(2mg
6hrly x48hrs then 1mg 4hrly)
and Somatostatin infusion (250-
500ug/hr) is helpful.
Also Octreotide 50ug bolus and
50ug/hr intravenous infusion x2-
5/7 can control acute bleeding.
21. Mgt of Varices contd.
• Balloon tamponade: with Sengstaken
- Blakemore tube is successful in
90% of cases & very useful in first
few hrs of bleeding.
• Some drawbacks include aspiration
pneumonia, oesophageal rupture &
mucosal ulceration, which leads to a
5% mortality.
23. Additional mgt of acute
bleeding
• Prophylactic antibiotics: e.g.
oral or i.v. quinolones –
Ciprofloxacin
• Nursing – Intensive care nursing
& NPO until bleeding stops.
• Sucralfate: 1g 6hrly – this
reduces oesophageal ulceration
following endoscopic therapy.
24. • Further bleed from a varice will
require TIPS (Transjugular
intrahepatic portosystemic
shunt)- a minimal invasive
procedure – done if endoscopic
& medical therapy fail.
25. Surgery
• This is indicated when other measures fail
or if TIPS is not available.
TYPES
• a) Oesophageal transection & ligation of
the feeding vessels to the bleeding
Varices.
• b) Portosystemic shunting – but this
causes significant encephalopathy
Rebleed following treatment can be
reduced by giving a non-selective B-
blocker e.g. Propranolol
26. Mgt of Mallory – Weiss
tears
• Bleeding stops spontaneously in 80-
90% of cases & recur in only 0-5% of
patients.
• Endoscopy therapy is indicated in
actively bleeding cases.
• Angiographic therapy with intra-
arterial infusion of vasopressin or
embolization and operative therapy
with oversewing of the tear are
rarely required.
27. Prognosis
• This depends on;
1) Age: Mortality is < 0.1% for patients
< 60yrs but >20% for patients >80yrs.
2) Recurrent haemorrhage increases
mortality.
3) Co morbidities increase mortality
4) Melaena is a better prognostic
factor than haematemesis
5) Shock increases mortality.
28. Conclusion
• Upper gastrointestinal bleeding
can be life threatening seeking
immediate medical care for
aggressive resuscitation.
• Both medical and endoscopic
therapy have been shown to
significantly improve patient
outcomes.