1. ACUTE UPPER GI BLEEDING
Prevalence
Causes
Presentation
Management – Immediate Resuscitation
Investigations
Assessing severity and risk of rebleeding
Definitive management

2. PREVALENCE
•It Is twice as common in men than in women
and increases with age.
•Mortality rate remains around 10%, highest in
the elderly and in patients with significant
comorbidity even with hospital management

3. CAUSES
• Peptic ulcer disease and esophagogastric
varices secondary to chronic liver disease are
the commonest causes of severe haemorrhage
in acute UGIB
• Other pathologies usually cause self-limiting
bleeding.
• In the developing world, hemorrhagic viral
infections can cause significant gastrointestinal
bleeding.

4. CAUSES

5. Bleeding esophageal varices

6. S PURTING U LCER

7. POINTERS TOWARDS ETIOLOGY

8. PRESENTATIONS
• Patients present with haematemesis (vomiting of either fresh blood or
‘coffee ground’) and/or melaena (passage of black, tarry stools).
• As blood has a cathartic effect, the latter tends to appear within 2–6 hours of
the acute bleed and may persist for up to 48 hours in the absence of further
haemorrhage.
• Hematochezia (passage of minimally altered blood) occurs in
approximately 30% of patients with massive UGIB but the bleeding must be
massive and is almost always accompanied by shock. Features that predict
AUGIB in cases of haematochezia include haemodynamic instability, increased
serum urea:creatinine ratio, and reduced haematocrit.
• Acute blood loss can lead to hypovolemic shock (weakness, sweating,
postural dizziness, tachycardia and hypotension).
• All patients with severe bleeding are at risk of developing acute renal
failure, whilst those with coexistent cardiovascular disease carry the
additional risk of myocardial infarction and/or stroke.

9. EXAMINATION
• Tachycardia, orthostatic blood pressure changes suggest
moderate to severe blood loss; hypotension suggests life-
threatening blood loss (hypotension may be late finding in healthy
younger adult)
• Rectal examination is performed to assess stool colour (melaena
versus hematochezia versus brown)
• Significant abdominal tenderness accompanied by signs of peritoneal
irritation (e.g. involuntary guarding) suggests perforation

10. MANAGEMENT – RESUSCITATION AS PER
ABCD PROTOCOL
• Intravenous access
The first step is to gain intravenous access using the placement of two large-bore
cannulae. (eg 14–16G). Intravenous crystalloid should be started ASAP.
• Initial clinical assessment
•Define circulatory status. Severe bleeding causes tachycardia, hypotension and
oliguria. The patient is cold and sweating, and may be agitated.
• Seek evidence of liver disease. Jaundice, cutaneous stigmata,
hepatosplenomegaly and ascites may be present in decompensated cirrhosis.
• Identify comorbidity. The presence of cardiorespiratory, cerebrovascular or renal
disease is important, both because these may be worsened by acute bleeding and
because they increase the hazards of endoscopy and surgical operations.

11. BLOOD TRANSFUSION
• Urgent blood transfusion can be lifesaving in patients with haemodynamic
instability.
• Blood transfusion is itself not without risk – it has has been shown to be associated
with a higher rebleeding rate and a trend towards higher mortality
• Therefore, transfusion should be restricted to patients with a haemoglobin 10
g/dl or below, with 10 ml (4.5 mEq) of 10% calcium gluconate given after every 3–4
units of blood transfused. ESGE recommends a restrictive transfusion strategy
(target haemoglobin between 70 –90 g/L) after haemostasis.
• Iron replacement: Patients are often discharged from hospital with anaemia after
AUGIB. Although iron supplementation is not prescribed in AUGIB guidelines this
should nonetheless be considered prior to discharge.

12. INTRAVENOUS PROTON PUMP INHIBITOR
THERAPY
• Proton pump inhibitor (PPI) therapy raises intragastric pH reducing acid-
dependent protease clot lysis.
• A landmark placebo-controlled randomised trial from Hong Kong showed that
continuous omeprazole infusion (80 mg intravenous bolus followed by 8
mg/h for 72 h – by mixing 5 vials Omeprazole with 1L NS and infusing
continuously at 10d/min) after endotherapy for peptic ulcer was superior to
placebo in reducing recurrent bleeding, transfusion requirements and hospital
stay.
• It is prudent to commence PPI therapy if endoscopy is delayed, although this
will be without significant clinical benefit in approximately 70%.

13. OTHER DRUGS
• Tranexamic acid: The role of tranexamic acid in AUGIB is unclear and has not
been recommended in guidelines. A meta-analysis that included eight
randomized trials of tranexamic acid in patients with upper GI bleeding found a
benefit with regard to mortality but not with regard to bleeding, surgery, or
transfusion requirements. Dose: 1-2 amp TDS
• Vitamin K 10 mg IV slowly(1mg/min) single dose to correct coagulopathy,
FFP might be needed for rapid correction
• Prokinetics: A meta-analysis of eight studies on the use of erythromycin
infusion prior to endoscopy in AUGIB found significant improvements in
adequate mucosal visualisation, reductions in the need for second-look
endoscopy and length of stay.
• ESGE recommends a 250 mg erythromycin infusion 30–120 min pre-endoscopy
in patients with clinically severe/ongoing AUGIB. There is no evidence to support
the use of metoclopramide.

14. STOPPING DRUGS
• Non-steroidal anti-inflammatory drugs (NSAIDs)- These should be stopped at the time of
presentation. If considered essential, this medication can be re-introduced, with maintenance PPI
cover, once any mucosal ulceration has healed (usually 4–6 weeks).
• Aspirin. The data concerning the use of antiplatelet medication in patients with acute UGIB are not
clear. Low-dose aspirin, prescribed for secondary prevention of vascular events, should be
continued. Stopping this medication is associated with increased mortality due to vascular events,
with no benefit on the rate of rebleeding.
• ESGE recommends immediate resumption of aspirin following index endoscopy if the risk of
rebleeding is low. In patients with high risk peptic ulcer, ESGE recommends early reintroduction
of aspirin by day 3 after endotherapy.
• Clopidogrel. There are no data to advise whether clopidogrel should be discontinued (ie the
risk of rebleeding vs the risk of coronary stent occlusion). A decision should be made on an individual
patient basis after discussion with the cardiology team, taking into consideration the rebleeding risk

15. DRUGS FOR VARICEAL BLEEDING- TERLIPRESSIN
• Terlipressin, a vasopressin analogue, increases systemic vascular
resistance, reduces cardiac output, and reduces portal pressures by
approximately 20% in variceal bleeding.
• All patients with suspected variceal bleeding should be started on
terlipressin (2 mg qds) at presentation, continued for 3–5 days or
until definitive endoscopic haemostasis has been established.
• Physicians should be aware of contraindications to terlipressin which
include arterial disease, hyponatraemia, myocardial ischaemia, severe
cardiac failure and prolonged QTc interval. Somatostatin or octreotide
may be considered for patients with contraindications.(Stilamin 2
amp mixed with 1L NS – 40 ml bolus then rest at 10d/min until

16. • After the first variceal haemorrhage, the risk of rebleeding is 15–30% within the
subsequent 6 weeks. Currently, the mainstay of pharmacological secondary
prophylaxis is with non-selective beta-blockers, such as propranolol or
carvedilol.
• Propranolol reduces portal pressures through splanchnic vasoconstriction and
reduced cardiac output.
• Carvedilol, which has vasodilator properties due to α1-receptor blockade, has
been shown in haemodynamic studies to reduce portal pressures more
effectively than propranolol.
• As such, recent BSG guidelines recommend use of propranolol or nadolol for
secondary prevention of variceal bleeding, with carvedilol as an alternative.
NON-SELECTIVE BETA BLOCKERS

17. ANTIBIOTIC PROPHYLAXIS
• Twenty percent of patients have infections within 48 h,
increasing to 36% after 7 days. Infection is associated with
significantly increased rebleeding risk by >4 times and
mortality by 2.5 times.
• Acute variceal bleeding is associated with a risk of Gram-
negative bacteraemia and/or spontaneous bacterial peritonitis.
• All patients with possible variceal bleeding should be
treated with a prophylactic broad-spectrum antibiotic at
presentation for 5–7 days.

18. BASIC INVESTIGATIONS
• Full blood count. Chronic or subacute bleeding leads to anaemia but the
haemoglobin concentration may be normal after sudden, major bleeding until
haemodilution occurs. Thrombocytopenia may be a clue to the presence of
hypersplenism in chronic liver disease.
• Urea and electrolytes. This test may show evidence of renal failure. The blood urea
rises as the absorbed products of luminal blood are metabolised by the liver; an
elevated blood urea with normal creatinine concentration implies severe bleeding.
• Liver function tests. These may show evidence of chronic liver disease.
• Prothrombin time. Check when there is a clinical suggestion of liver disease or
patients are anticoagulated.
• Cross-matching. At least 2 units of blood should be cross-matched if a significant
bleed is suspected.

19. ASSESSMENT OF SEVERITY
Two validated scoring systems have been developed, both of
which can also be used to quantify the risk of rebleeding:
1. The Blatchford score predicts the need for endoscopy.
2. The Rockall score, calculated postendoscopy, defines the
mortality risk after both acute variceal and non-variceal
haemorrhage.

21. ENDOSCOPY IS BOTH THE MAIN
INVESTIGATION AND MANAGEMENT
• Gastroscopy is the primary intervention in patients with acute UGIB. It
establishes a cause in over 80% of cases and provides information that
defines management and prognosis
• Timing
• Patients with evidence of a large haemorrhage should undergo urgent
gastroscopy as soon as they have been stabilized.
• Because of the inherent risk of rebleeding, ideally all other patients should
undergo gastroscopy within 24 hours of admission.
• Young patients at low risk of rebleeding (Blatchford score 0) can be
discharged with provision for outpatient gastroscopy within the following 2–3
days.

22. ENDOTHERAPY - VARICEAL BAND
LIGATION (VBL)
• Patients should be scheduled for elective repeat
endoscopy 2–4 weeks after variceal haemorrhage
until eradication of varices.
• After successful eradication of varices, patients
should be booked for endoscopy at 3 months, then
6-monthly thereafter.
• Recurrent varices should be treated with VBL until
eradication.

23. A: Esophageal varices before banding; B: Esophageal varix post
banding.

24. TRANS JUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT (TIPSS) FOR
REBLEEDING – WHEN?
• Patients who rebleed should be
considered for urgent repeat endoscopy
and VBL or Sengstaken tube to balloon-
tamponade the varices for temporary
haemostasis, whilst considering the patient’s
suitability for a ‘rescue’ transjugular
intrahepatic portosystemic shunt.
• The aim of TIPSS is to rapidly reduce portal
pressures by creating a portosystemic shunt
across the liver parenchyma has been shown
to be superior to VBL for preventing
rebleeding, but with increased rate of

25. TIPSS PROCEDURE

26. ENDOTHERAPY FOR PEPTIC ULCER
DISEASE
• A peptic ulcer may present with high risk stigmata. These are: (i) active
bleeding, (ii) a non-bleeding visible vessel, (iii) adherent clot.
• Endoscopic therapies for NVUGIB comprise injection therapy, thermal
treatments, mechanical adjuncts and spray therapy.
• Endoscopic therapy involves dual therapy with one of the following
combinations:
• injection of adrenaline and placement of metal clips
• injection of adrenaline and thermal coagulation
• injection of adrenaline and fibrin/thrombin injection.
• All these techniques are equally effective in reducing rebleeding rates.

27. A BLEEDING ULCER BEFORE AND AFTER USE OF ADRENALINE

28. REFER FOR SURGERY- WHEN?
• Surgery is indicated when endoscopic haemostasis
fails to stop active bleeding and if rebleeding occurs
on one occasion in an elderly or frail patient, or twice
in a younger, fitter patient.
• If available, for variceal bleeding angiographic
embolisation is an effective alternative to surgery in
frail patients.
• The choice of operation for bleeding PUD depends on the
site and diagnosis of the bleeding lesion –
underrunning/local excision/partial gastrectomy all are

29. POST-ENDOSCOPY DISCHARGE
For Non-variceal PUD
• All patients with erosive mucosal
disease should be prescribed high-
dose PPI therapy (eg omeprazole
40 mg od or 20 mg bd) for 6–8
weeks to effect mucosal healing.
• Patients with Helicobacter pylori-
related peptic ulcer disease should
be prescribed eradication therapy.
• All patients with a gastric ulcer
require a repeat gastroscopy in 6–8
weeks to confirm complete healing,
excluding underlying carcinoma.
For Variceal Bleeding
• High-dose PPI therapy should be prescribed
for 6–8 weeks because EVL induces erosions
of UGIT.
• Patients should be started on low-dose
propranolol (20–40 mg tds) to reduce portal
pressure unless hypotensive in order to
decrease the risk of repeat bleeding, titrating
the dose until the heart rate is 25% less but
not <60 bpm.
• Repeat endoscopy with band ligation is
required at 1–2 weekly intervals until the
varices have been obliterated.

30. H. PYLORI ERADICATION
• Sensitivity of diagnostic tests for H. pylori is diminished during
AUGIB, with false negative rates estimated to be between 25 and 50%.
• AUGIB guidelines have called for H. pylori assessment (ideally during
endoscopy with biopsy methods, urea breath testing or monoclonal stool
antigen testing).
• If positive, H. pylori eradication should be commenced at reintroduction
of oral feeding. PPI treatment should continue for a total of 4 weeks, and
discontinued for at least 2 weeks before H. pylori reassessment.

31. QUESTIONS?