BJA Education, 17 (4): 117–123 (2017)

doi: 10.1093/bjaed/mkw054
Advance Access Publication Date: 10 December 2016
Matrix reference
1A01, 2A05, 3C00

Management of acute upper GI bleeding

Ingi Adel Salah Elsayed MRCP FFICM1, Pavan Kumar Battu FRCA2, and
Sarah Irving MRCP FRCA FFICM3,*
1
ST7 Trainee, Intensive Care and Renal Medicine, Sheffield Teaching Hospitals NHS Foundation Trust,
Sheffield S5 7AU, UK, 2ST7 Trainee, Anaesthesia, Sheffield Teaching Hospitals NHS Foundation Trust,
Sheffield S5 7AU, UK, and 3Consultant in Critical Care Medicine and Anaesthesia, Sheffield Teaching Hospitals
NHS Foundation Trust, Northern General Hospital, Herries Road, Sheffield S5 7AU, UK
*To whom correspondence should be addressed. Tel: 0114 2434343; Fax: 0114 2269342; E-mail: Sarah.Irving@sth.nhs.uk.

The reported incidence of acute upper gastrointestinal bleeding

Key points
• Acute upper gastrointestinal bleeding has a high
mortality rate.
• Initial priorities are resuscitation, risk assessment,
and early endoscopic treatment as described in
National Institute for Health and Care Excellence
Guidance 141.
• Non-variceal re-bleeds require interventional
radiological embolization, or surgery. Repeat
oesophagogastroduodenoscopy may allow deci-
sions to be made at this point.
• Variceal bleeds not responding to endoscopic
therapy need management in a specialist centre,
benefit from balloon tamponade if unstable and
should be considered for transjugular intrahepatic
portosystemic shunt.
• Upper gastrointestinal bleeding due to stress
ulceration in the ICU will occur in up to 15% of
patients not on prophylactic treatment. Current
National Institute for Health and Care Excellence
guidance recommends either H2-receptor antago-
nists or proton pump inhibitors for primary
prophylaxis.
(UGIB) in the United Kingdom varies over the range 84–172/
100 000 year1. 1 Mortality due to upper GI bleeding was found
to be 7% among new admissions, rising to 30% in those who
bled as inpatients.2
UGIB refers to bleeding from any point proximal to the duo-
denojejunal flexure. It presents clinically with haematemesis
and/or melaena. Fresh bleeding per rectum is usually indicative
of lower GI bleeding, however massive UGIB can present with
passing of red blood clots rectally. In 90% of cases, melaena
results from any upper GI bleeding. Bleeding from parts of small
bowel distal to the ligament of Treitz and the right hemicolon
may also lead to melaena.
Causes of UGIB can be classified in two ways. The first is
based on the underlying pathophysiological mechanism (see
Table 1). The second is based on the type of bleed—i.e. variceal
or non-variceal.
In developing countries with endemic viral hepatitis, vari-
ceal bleeding is the commonest category. In Western com-
munities, peptic ulcer disease (PUD) is the commonest cause.
In the UK, the commonest causes of UGIB are PUD, oesopha-
gogastric varices with or without portal hypertensive gastro-
pathy and oesophagitis.
Management of acute UGIB
The National Institute for Health and Care Excellence (NICE)
Clinical Guideline 141 (CG 141), published in June 2012 in the
UK, outlines the management of acute upper GI bleeding. NICE
Quality Standards Document 38 was then published in July
2013.3 A subsequent Evidence Update 63 was published in

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117
Management of acute upper GI bleeding
Table 1 Classification of UGIB according to underlying pathophysiological mechanisms
Ulcerative
Gastric
Idiopathic
Drug induced e.g. NSAIDs
Infective: H. pylori
Stress ulcers
Zollinger Ellison
Oesophageal
Infective e.g. candidal, CMV
Drug induced e.g. alendronate, potassium chloride
August 2014.4 Much of this review is based on the evidence pre-
sented in these documents.
Initial assessment
Mortality associated with UGIB is high, so assessment of
severity, general supportive measures and identification of the
cause, should occur in parallel with direct, specific therapies.
Taking an adequate history is an essential part of managing
UGIB. As discussed, UGIB usually presents with haematemesis
and/or melaena. Associated symptoms at presentation such as
postural dizziness or collapse may point towards severity of
bleeding.
It is imperative to clarify if the patient has previously pre-
sented with UGIB. Sixty per cent of patients who re-bleed, do so
from the same source. A history of recent GI surgery might sug-
gest a very different origin for bleeding and necessitate early
surgical and potentially radiological input.
Drug history is equally important. For example, non-
steroidal anti-inflammatory drugs (NSAIDS) may be identified
as a precipitant for bleeding. Anticoagulant therapies such as
warfarin and new oral anticoagulants (NOACs; direct inhibitors
of thrombin or activated factor Xa) increase the likelihood of
severe bleeding and require specific treatment.
Co-morbid illness may point to a cause for bleeding, such as
chronic liver disease and variceal bleeding. It also identifies
patients at higher risk of developing complications, so requiring
tailored treatment. Examples are those with ischaemic heart
disease who require a lower threshold for blood transfusion, or
patients with heart or renal failure who may need invasive
monitoring of resuscitative fluid therapy.
Careful physical examination can further establish a poten-
tial cause for bleeding and determine severity, so aiding appro-
priate triage of patients. Signs of chronic liver disease such as
jaundice and spider naevi point to variceal bleeding. Significant
upper abdominal tenderness and rigidity may suggest a compli-
cation such as perforation.
Severity of bleeding determines the changes in vital signs,
with some caveats. Initial signs of mild blood loss would
include resting tachycardia. Fifteen per cent loss of blood vol-
ume is associated with postural hypotension indicated by a
drop in systolic blood pressure greater than 20 mm Hg or with
an increase in heart rate greater than 20 beats min1 on chang-
ing posture from recumbent to standing. A loss of 40% blood
volume leads to recumbent hypotension. However, beta-
blockade masks the development of reflex tachycardia expected
with blood loss. Potent vasodilating antihypertensive drugs will
exaggerate hypotension.
118 BJA Education | Volume 17, Number 4, 2017
Portal hypertension Tumours
Gastric varices Benign
Oesophageal varices Polyps
Hypertensive gastropathy Lieomyoma
Vascular malformations e.g. Malignant
Dieulafoy’s lesion Adenocarcinoma
Hereditary hemorragic telangiectasia Carcinoid
(Osler–Weber–Rendu syndrome)
Traumatic/surgical e.g. Lymphoma
Mallory–Weiss syndrome Metastatic carcinoma
Aortoenteric fistula
Post anastomosis or polypectomy
Initial laboratory tests should include full blood count, liver
enzymes, bilirubin, serum albumin, urea and electrolytes, coag-
ulation screen, and samples for cross matching of blood. Other
specific tests may be required as appropriate, such as screening
for viral hepatitis.
General supportive measures
Patients may require supplemental oxygen to increase oxygen
delivery, particularly with co-morbid lung or heart disease.
Early elective tracheal intubation should be considered in those
with ongoing haematemesis and altered mental or respiratory
status to minimize the risk of aspiration, whilst aiding endos-
copy. Significant co-morbidities lead to a much higher risk of
complications. For those patients and others with signs of
refractory shock (e.g. lactate > 4 mmol litre1, pH < 7.3 after
resuscitation), admission to a critical care area should be con-
sidered early. Invasive arterial monitoring allows closer moni-
toring of haemodynamic status and facilitates frequent blood
gas and laboratory samples to be taken. Central venous line
insertion, provided coagulation is not deranged, gives secure i.v.
access and allows central venous pressure measurements to be
taken. Flow guided methods of monitoring such as LidCO or
oesophageal pressure monitoring give a more accurate guide to
volume status.
In all patients, two wide-bore cannulas (16G at least) should
be established. Patients should not be given anything by mouth.
Fluid resuscitation starts with rapid infusion of isotonic crystal-
loid solution, such as Hartmann’s. In patients non-responsive
to crystalloids, resuscitation is continued using blood and fresh
frozen plasma (FFPs). In many centres, a major haemorrhage
protocol can be activated. In extreme circumstances, O negative
blood may be required initially. The authors do not advocate
the use of colloids in resuscitation, given concerns over kidney
injury, worsened coagulopathy, risk of anaphylaxis, and a lack
of benefit over crystalloids.
NICE CG 141 recommends individualizing decisions for
blood transfusion according to the full clinical picture, whilst
recognizing the risks of overtransfusion. Blood transfusion
should usually be targeted at patients with haemoglobin (Hb)
level below 70 g litre3. 4 Evidence comes from a randomized
controlled trial which compared mortality rates at 45 days
between patients randomised to either a restrictive transfusion
strategy (if Hb <70 g litre1) or liberal transfusion strategy (if Hb
<90 g litre1). The trial reported significantly less mortality in
the restrictive group (P ¼ 0.02) and fewer adverse events. The
TRIGGER (Transfusion in Gastrointestinal Bleeding) trial5 ran-
domly compared clinical outcomes including 28-day mortality

between restrictive transfusion (Hb <80 g litre1) and liberal
transfusion (Hb <100 g litre1). Neither study included patients
with massive ongoing bleeding. To summarize, restrictive strat-
egies are generally preferred with the exception of patients with
ischaemic heart disease and possibly those with ongoing
haemorrhage.
The NICE CG 141 also recommends giving FFP to bleeding
patients with a prothrombin time (or INR) or activated partial
thromboplastin time greater than 1.5 times normal, which are
generally accepted times in other scenarios with major haemor-
rhage. Cryoprecipitate should be given for fibrinogen levels
below 1.5 g litre1 despite FFP administration. Platelet transfu-
sion should be given to patients with platelet count <50  109
litre1 and considered in those actively bleeding while estab-
lished on anti-platelet therapy such as clopidogrel. Patients
actively bleeding while taking warfarin therapy should receive
Prothrombin complex concentrate (PCC).
In bleeding, the activation of a major haemorrhage protocol
and early involvement of senior clinicians, including haematol-
ogists is vital. This is particularly important for those taking
NOAC drugs, the effects of which are not easily reversed. The
European Heart Rhythm Association produced practical guid-
ance on their use.6 Recommendations include the use of PCC
alongside general resuscitation in life threatening bleeding.
Dabigatran is the only NOAC drug which may be fully
reversed using an antidote. Idarucizumab has been shown in a
pilot trial to achieve haemostasis in serious bleeding from
dabigatran.7 This monoclonal antibody drug is currently pend-
ing approval for use in the UK.
Pharmacotherapy
Proton pump inhibitors (PPIs) increase gastric pH to above 6.0.
This optimizes platelet function, inhibits fibrinolysis and
reduces peptic activity, so increasing clot stabilization over
bleeding ulcers. PPI use prior to endoscopy in UGIB was eval-
uated in a Cochrane systematic review of RCTs comparing PPI
vs control [placebo, or H2-receptor antagonists (H2RAs) or no
treatment].8 It found that PPI significantly reduced the need for
endoscopic therapy and reduced the stigmata of recent hae-
morrhage during index endoscopy, but there was no evidence
of improved clinically important outcomes, namely mortality,
re-bleeding or need for surgery. NICE therefore advises against
the use of PPI prior to endoscopy.3 PPIs should be prescribed
postendoscopy for those with non-variceal UGIB and stigmata
of recent haemorrhage.
Terlipressin is a synthetic analogue of Vasopressin, with a
slow, sustained release allowing administration via
Table 2 Rockall score
Score 0 1
Age (yr) <60 60–79
Pulse <100 >100
Systolic blood pressure >100 >100
Comorbidities None Nil major
Diagnosis Mallory–Weiss or All other diagnosis Malignant lesion
no lesion/pathology
Stigmata of haemorrhage None, or dark spot only None, or dark
on endoscopy spot only
Score of 2 good prognosis.
Score >7 10–35% mortality, 25–50% mortality with re-bleed.
Management of acute upper GI bleeding
intermittent injections. It reduces portal blood flow, hence vari-
ceal bleeding. It is the only vasoactive drug proven to reduce
mortality.9 It should be given to patients with suspected vari-
ceal bleeding during resuscitation measures and prior to endo-
scopic confirmation. Terlipressin can be stopped once definitive
haemostasis is achieved and in any case after 5 days. Other
agents have been studied. In a recent RCT, somatostatin and its
metabolite octreotide have proven to be as effective as
terlipressin.10 In 2015 the British Society of Gastroenterology
(BSG) published guidance on managing variceal haemorrhage.11
This suggests using terlipressin or somatostatin and if unavail-
able using octreotide off license.
I.V. erythromycin as a prokinetic administered prior to
endoscopy vs no erythromycin was evaluated in a systematic
review of seven RCTs.12 Erythromycin was associated with a
greater chance of adequate visualization of the gastric mucosa,
less need for second endoscopy, less blood transfusion and
shorter hospital stay. Due to limitations in the studies (e.g. gas-
tric visualization definitions varied across the studies), an
update to NICE CG 141, did not recommend erythromycin use
as standard.
Tranexamic acid is not currently recommended by NICE for
acute UGIB. The BSG document recommends further study to
look for benefit in variceal bleeding.
Antibiotics with gram negative cover, such as third genera-
tion cephalosporins, improve mortality rates and reduce bacte-
rial infections. Cochrane meta-analysis13 also shows fewer
early re-bleeds. Antibiotic choice is dictated by local resistance
patterns and availability.
Risk stratification
The Rockall and Blatchford scores are well-validated risk strati-
fication systems used in UGIB. The full Rockall score (RS) incor-
porates preendoscopic and postendoscopic data14 to predict re-
bleeding and mortality. The Glasgow Blatchford score1 (GBS)
uses only clinical and laboratory data (see Tables 2 and 3).
Used appropriately, these scores help identify patients likely
to require Critical Care support, ensure timely interventions
and help identify those suitable for early discharge from hospi-
tal. NICE advises the use of GBS at first assessment and full RS
postendoscopy.3
Specific therapies in non-variceal UGIB
Oesophagogastroduodenoscopy (OGD) is the cornerstone in
managing acute UGIB. NICE CG 141 stipulates that haemody-
namically unstable patients with UGIB should be offered OGD
2 3
80 N/A
>100 N/A
<100 N/A
Ischaemic heart disease, cardiac failure, Renal or liver failure,
other major co-morbidity disseminated malignancy
N/A
Blood, adherent clot, visible/spurting N/A
vessel
BJA Education | Volume 17, Number 4, 2017 119
Management of acute upper GI bleeding

Table 3 Glasgow Blatchford score of administration in terms of clinical outcomes, remains con-
troversial. However, high dose IV PPI seems the most cost-
Admission risk marker Score component value
effective.19 Current international consensus guidelines recom-
Blood urea (mmol litre ) 1 mend high-dose i.v. PPI therapy e.g. Pantoprazole 80 mg bolus
6.5–8.0 2 followed by 8 mg h1 for 3 days.15
8.0–10.0 3 Helicobacter pylori eradication should be offered to all who test
10.0–25 4 positive for the infection. Eradication therapy was shown to be
>25 6 superior to PPI alone in preventing re-bleeding. Those with PUD, but
Haemoglobin (g litre1) for men negative for H. pylori at the time of acute UGIB, should be retested.3
120–130 1 NICE suggest offering a repeat endoscopy in the event of re-
100–120 3 bleeding with a view to further endoscopic treatment or emer-
<100 6 gency surgery. However, unstable patients who re-bleed require
Haemoglobin (g litre1) for women interventional radiology. If there is a delay in such therapy,
100–120 1 urgent referral for surgery should be made.
<100 6
Systolic blood pressure (mm Hg)
100–109 1 Specific therapy in variceal UGIB
90–99 2 The BSG guidelines on the management of variceal bleeding
<90 3 complement NICE guidance and add more detail, some of which
Other markers have been included below.11 Broad spectrum antibiotic therapy
Pulse 100 (min1) 1 should be given, as dictated by local protocol. Terlipressin
Presentation with melaena 1 should be commenced during resuscitation.
Presentation with syncope 2
Hepatic disease 2
Procedures for control of bleeding
Cardiac failure 2
Endoscopic therapy for oesophageal varices: Definitive therapy
should take place at the time of diagnostic endoscopy. The techni-
Score 0 low risk, consider outpatient management.
Score >5 high risk of needing intervention
ques involved are either endoscopic variceal ligation (EVL) or
endoscopic sclerotherapy (ES). Initial success rates of 90% are
reported. EVL was found to be as effective as ES in achieving hemo-
immediately after resuscitation and within 24 h in all other stasis, but in meta-analysis EVL was found superior in rates
patients.3,4 OGD is both a diagnostic and therapeutic tool. of re-bleeding, strictures and mortality.16 NICE CG 141, recom-
mends the use of EVL for controlling bleeding oesophageal varices.
Endoscopic therapies Gastric varices are more difficult to control. Endoscopic
These are warranted in patients with high risk lesions, meaning injection of N-butyl-2-cyanoacrylate into the lumen of bleeding
active bleeding, visible non-bleeding vessels and adherent clots. gastric varices (where it polymerises into firm clot in aqueous
They include injection therapies, mechanical therapies, and medium) is the currently established initial treatment and is
thermal interventions. recommended by NICE. It appears more effective than EVL and
Adrenaline (1:10 000 or 1:20 000) is injected in increments of better in preventing re-bleed than beta blockers.
0.5–1.5 ml aliquots to the four quadrants around high-risk stig- Balloon tamponade is effective at achieving haemostasis in
mata. It is easy to administer and can produce a clear field acute variceal bleeding, but has high rates of re-bleeding and com-
around a bleeding vessel. plications. Balloons should be used temporarily when endoscopic
The tissue adhesives, thrombin and fibrin, create a tissue therapy has failed and until either further endoscopic treatment,
seal at the site of bleeding and also a tamponade effect. Due to transjugular intrahepatic portosystemic shunt (TIPSS) or surgery
the risk of tissue necrosis, a volume limit of 1.0 ml is used. is performed. Definitive treatment will depend on local resources
The endoscopic clip is the most commonly used mechanical and expertise. The BSG suggest the use of the Sengstaken–
device. Lesions on the gastric lesser curvature or posterior wall Blakemore tube but alternatives include a Minnesota tube. Balloon
may not be amenable to mechanical therapy. insertion is preferably preceded by tracheal intubation to avoid
Thermal therapies include electrocautery probes and the aspiration. Endoscopic insertion over a guide wire has been sug-
argon plasma coagulator (APC). Haemostasis is achieved by gested to reduce the risk of oesophageal rupture. The gastric bal-
direct tamponade of visible vessel and tissue coagulation using loon is inflated up to a volume of 500 ml with air, with the
delivered heat or electric current. APC does not use direct tissue oesophageal balloon inflated up to 45 mm Hg for ongoing bleeding.
contact and is used mainly in superficial lesions. Balloons are usually left in situ for 24–48 h, with deflation regularly
NICE CG 141 advocates the use of either a mechanical to assess for re-bleeding. Endoscopically placed oesophageal
method with or without adrenaline, thermal coagulation with stents, which remain in place for up to 2 weeks have been used as
adrenaline, or fibrin or thrombin with adrenaline. It advises an alternative in oesophageal bleeding, but no data have yet been
against the use of adrenaline as monotherapy. published to compare outcomes with balloon tamponade.
TIPSS should be considered when variceal bleeding is not
After endoscopy controlled via endoscopic therapy alone. This involves radiolog-
Acid suppression using a PPI should be used after endoscopic ically establishing a porto-caval shunt, using the transjugular
haemostasis. An updated large Cochrane meta-analysis showed intrahepatic route. Its success rate at stopping bleeding is
that compared with H2 blocker or placebo, PPI reduced re-bleed- quoted as 90–100%, especially in oesophageal varices. With gas-
ing, surgical intervention and need for repeated endoscopic tric varices, development of spontaneous splenorenal collater-
treatment. Use of PPI reduced mortality in those with active als may cause re-bleeding. With refractory bleeding and no
bleeding or non-bleeding vessels.13 The optimal dose and route other therapeutic options, salvage TIPSS may be considered but

120 BJA Education | Volume 17, Number 4, 2017

 Management of acute upper GI bleeding

Resuscitation

Risk Stratification

Haemodynamically Haemodynamically
Unstable Stable

Endoscopy within 2 h of Endoscopy within 24 h

optimal resuscitation Diagnosis

Variceal
Non-Variceal Bleeding
Bleeding
-Antibiotic treatment
-Terlipressin

-Combination or Oesophageal Gastric Varices

mechanical Varices
endoscopic method Endoscopic injection
-PPI if active bleed Endoscopic Variceal with N-butyl-2-
or stigmata of recent ligation cyanoacrylate
bleed

Controlled
Bleeding?
Continued
Bleed/re-bleed Y
-Consider repeat
N
O E
endoscopy S
-Interventional
radiology or surgery
Secondary
Consider Prophylaxis
balloon
tamponade EVL+NSBB

-Referral for TIPSS if

portal vein patent
-Surgical
/radiological options

Fig 1 Acute UGIB management summary.

may be associated with high risk of hepatic encephalopathy.
NICE recommends consideration for TIPSS in any uncontrolled
variceal bleed without contraindications such as portal vein
thrombosis, severe systemic infection, or severe pulmonary
hypertension. Some studies suggest a reduction in mortality
when TIPSS is used early rather than salvage therapy.
The Child-Pugh classification is used to assess the prognosis
of chronic liver disease, mainly cirrhosis and to predict mortal-
ity during surgery. BSG guidance is that TIPSS should be consid-
ered within 72 h of control of bleeding in Child-Pugh class B
cirrhosis or Child-Pugh class C cirrhosis with score below 14.
More research is required in this area.
Surgical techniques include decompression of the portal circu-
lation (emergency surgical shunt operations) and oesophageal
transection. Both can achieve long term haemostasis, but require
specialist surgical expertise and have associated mortality rates of
50% and higher in Child-Pugh class C cirrhosis. The BSG document
recommends that these are considered in bleeding patients with
Child’s B cirrhosis, when TIPSS is unavailable, or not possible due
to portal vein thrombosis.
TIPSS has a well-established role in variceal bleeding, as dis-
cussed. Other interventional radiological procedures have been
used. Balloon-occluded retrograde transvenous obliteration tech-
niques and percutaneous transhepatic variceal embolization with

BJA Education | Volume 17, Number 4, 2017 121

Management of acute upper GI bleeding
cyanoacrylate have been described in gastric varices, but are not
common practice.11
Prevention of further variceal bleeding
Recommendations for secondary prophylaxis are long term
beta blockade combined with regular EVL at 2–4 weekly inter-
vals until eradication, evaluation for liver transplantation and
consideration of elective shunt operations. TIPSS was found to
decrease re-bleeding rates, but with no survival advantage and
higher morbidity rates. Hence this is currently indicated for sec-
ondary prophylaxis only in the context of re-bleeding or when
combination therapy is not possible. In Child’s A and B cirrho-
sis, shunt surgery is an alternative option.
Resumption of antiplatelet therapy after UGIB
Patients who need secondary prevention of vascular events,
should restart low-dose aspirin in combination with a PPI, once
haemostasis has been secured. All NSAIDs, including COX-2 inhibi-
tors, should be withheld during the acute phase of UGIB and
should only be restarted in required cases, with PPI cover and after
risk assessment.3 Evidence for when to start clopidogrel or NOAC
drugs is lacking. A multidisciplinary discussion between specialists
should weigh the risks and benefits of restarting such medication.
Prophylaxis of UGIB due to stress ulceration in the
critically ill
The incidence of clinically important GI bleeding due to stress
ulcers in ICU patients is between 1.5 and 8.5% overall and up to
15% without ulcer prophylaxis.17 It is associated with increased
mortality. Major risk factors are mechanical ventilation and co-
agulopathy. Other risk factors include severe burns, traumatic
brain or spinal cord injury and GI ulceration. NICE CG 141 recom-
mends either H2RAs or PPIs for primary prevention of UGIB. Oral
preparations are preferred. A meta-analysis of 20 RCTs showed
that prophylaxis using either H2RAs or PPIs reduced GI bleeding,
without effect on mortality or rates of ventilator-associated pneu-
monia (VAP).18 A further systematic review19 comparing PPIs with
H2RAs, found less UGIB, without effect on mortality, pneumonia
or ICU length of stay with a PPI. A study in the US found that PPIs
were more cost-effective than H2RAs among ICU patients, in pre-
venting stress ulceration and reducing serious UGIB without
increasing VAP.20 However, NICE Guidance Evidence Update 63
did not change the recommendations in CG 141.
Summary
Mortality due to acute UGIB remains high. Successful manage-
ment relies on simultaneous resuscitation and identification of
the cause to allow timely, definitive treatment. Involvement of
specialist services early is important. Figure 1 provides a quick
summary of the management. Primary prophylaxis against
stress ulceration on the ICU reduces rates of UGIB, but without
overall effect on mortality.
Declaration of interest
None declared.
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122 BJA Education | Volume 17, Number 4, 2017
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