This document provides an overview of upper gastrointestinal bleeding, including: - The definition, incidence, mortality, and common causes of upper GI bleeding. The most common causes are gastric and duodenal ulcers, esophagitis, and esophageal varices. - Principles of management including initial assessment, resuscitation, localization of bleeding site usually through endoscopy, and risk stratification to determine need for inpatient care or intervention. - Endoscopy is the gold standard for diagnosis and treatment. The Forrest classification guides prognosis and need for endoscopic therapy based on stigmata of recent hemorrhage seen. Proton pump inhibitors are commonly used for prevention of rebleeding.

1. UPPER GIT BLEEDING :
PRINCIPLES AND MANAGEMENT
Presenter: Dr Haruna Iddrisu
Moderator: Dr Joseph Yorke

2. OUTLINE
• Introduction
• Principles of management
• Risk stratification
• Specific therapy
• Definitive management
• Conclusion
• References

3. Introduction
• It is a potentially life threatening emergency that remains a common
cause of hospitalisation
• Definition; Refers to bleeding that arises from the GI tract proximal
to the ligament of Trietz
• Incidence is approximately 100/100000 per year in the US
• It is 4 times more common than lower GIT bleeding and constitute
80% of significant GIT bleeding
• Overall mortality 6-10%
• Many factors have influenced GIT bleeding in the past 20yrs
i.e. NSAID and Specific serotonin reuptake inhibitors ( SSRI ) usage, as
against use of Proton Pump inhibitors (PPI) and agents to eradicate H
pylori.
• Over all effect is decrease in hospitalization
Fallah MA et al. Acute gastrointestinal bleeding. Med clin North Am.2000 Sept.84(5):1183-208

4. Introduction ctd
Nonvariceal bleeding 80% Portal hypertensive
bleeding
20%
Gastric and duodenal ulcers 30% -40% Gastroesophageal varices > 90%
Gastritis or duodenitis 20% Hypertensive portal
gastropathy
<5%
Esophagitis 5% -10% Isolated gastric varices rare
Mallory Weiss ( MW ) tears 5% -10%
Arteriovenous malformations 5%
Tumours 2%
Others 5%
Courtney MT et al(1949)
Sabiston’s Textbook of
th

5. Introduction ctd
• Gastroesophageal varices 21.9%
• Gastritis 21.7%
• Peptic ulcer 30.2%
• Esophagitis 5.9%
• Gastric ca 5.8%
• Gastric erosions 3.9%
• Normal findings 20.0%
• Etiology of upper GIT bleeding following endoscopy at KBTH, 2007-2010

6. Introduction ctd’
• Gastritis and duodenitis 38.9%
• Gastric and duodenal ulcers 15.8%
• Esophageal varices 15.8%
• Gastric ca 7.3%
• Esophageal ca 3.1%
• Esophagitis 3.0%
• No cause was found for 15.8% of presentation
JAN 2019/SEPT 2020 ENDOSCOPY REPORT FOR UPPER GIT BLEEDING AT KATH

7. AETIOLOGY OF NON VARICEAL BLEEDING
PEPTIC ULCER DISEASE( PUD )
• Accounts for 40% of nonvariceal bleeding
• Approximately 15-20% bleed from PUD
• Bleeding results from acid or peptic erosion
• Most bleeding stop spontaneously and require no intervention
• 60-70 % are associated with H. pylori infection
• Eradication of H- pylori is associated with reduced rebleeding and need for long
term acid suppression (Liu, 2013)
• Significant bleeding results when duodenal or gastric ulcers erode into the
gastroduodenal and left gastric artery respectively

9. Aetiology ctd
Stress ulcers
• Stress related gastritis is characterised by multiple superficial erosions of the
entire stomach just as NSAID gastritis
• Results from injury from pepsin and acid in the setting of ischaemia from
hypoperfusion, e.g. severe sepsis, burns, trauma, respiratory and renal failure
etc.
Esophagitis
• An infrequent source of UPPER GIT bleeding
• Results from repeated exposure to acid in gastroesophageal reflux disease
• This can result in mucosal ulceration with chronic blood loss from
insignificant bleed
• Other causes are infection, Crohn’s, radiation

10. Aetiology ctd
Mallory Weiss (MW) Tears
• 1-4cm longitudinal tear in the gastric mucosa and submucosa near the gastroesophageal
junction
• Few extend into the distal oesophagus.
• Typical patient is an alcoholic ,who vomits gastric content and after prolonged vomiting
or retching has hematemesis
Dieulafoy lesion
• Vascular malformation usually along the lesser curvature within 6cm of
gastroesophageal junction
• Bleeding is from an unusually large vessel (1-3mm) in the submucosa after erosion of
gastric mucosa overlying vessel
• Mucosal defect is usually small (2-5mm) and difficult to identify
• Bleeding can be elusive and massive

11. Aetiology ctd
Malignant neoplasm of upper GIT
• Usually present as chronic anaemia or haemoccult positive blood than significant
haemorrhage
• Significant haemorrhage more likely for GIST, lymphomas and leiomyomas
• Rebleeding rates are high with endoscopic therapy
• Surgical resection is hence advised

12. Aetiology
Heamobilia
• Diagnosis difficult to make
• Usually associated with trauma, recent instrumentation of the biliary tree, liver
biopsies and intraductal neoplasms
• Suspect in haemorrhage, right upper quadrant pain and jaundice
• Triad seen in 50% of patients
• Endoscopy shows bleeding from ampulla
• Angiography is the diagnostic procedure of choice followed by angiographic
embolization

13. Aetiology
Heamosuccus pancreaticus
• Another rare cause of upper GIT bleeding
• Bleeding from pancreatic duct
• Caused by erosion of pancreatic pseudocyst into the splenic artery
• High index of suspicion in a patient with abdominal pain, blood loss and previous
history of pancreatitis
• Angiography is diagnostic and permits embolization
• In cases amenable to distal pancreatectomy, the procedure results in cure

14. Portal hypertensive bleeding/variceal bleeding
• Serious complication of portal hypertension, most often in the setting of
cirrhosis
• Bleeding is most commonly from varices
• Dilated submucosal veins that develop in the setting of Portal hypertension
(PH), serving as a collateral passage
• Most common in the distal oesophagus but may be gastric
• Develop in 30% of people with cirrhosis or PH
• 30% of people who develop gastroesophageal varices bleed
• Hematemesis is massive and associated with increased risk of rebleeding,
transfusion, prolonged hospital
Habib A, et al, acute variceal bleeding, gastrointestinal endoscopy, Clin N Am 2007,17:223

15. Principles of management
• Initial assessment and resuscitation
• History and examination
• Localisation of bleeding
• Initiation of therapy
• Prevention of recurrence

17. Initial assessment and resuscitation
• Presentation of UGIT bleeding is varied, from haemoccult positive stools on DRE
to exsanguinating haemorrhage, hence need for structured assessment
ATLS Protocol
• A B C D
• Intubate if airway cannot be maintained :GCS <_8, massive hematemesis
• Predominant concern is patients haemodynamic status
• Assess pre-existing deficit and ongoing loss
• Frequency, quantity of blood provides guidance

18. ATLS Classification of haemorrhagic shock
CLASS I II III IV
Blood loss <750MLS 15% 750MLS-1500MLS
15%-30%
1500MLS-2000MLS
30%-40%
>2000MLS
>40%
HR <100 >100 >120 >140
BP NORMAL NORMAL DECREASED DECREASED
PP NORMAL DECREASED DECREASED DECREASED
RR 14-20 20-30 30-40 >40
U.O >30 20-30 5-15 NEGLIGIBLE
CNS SLIGHTLY ANXIOUS MILDLY ANXIOUS ANXIOUS AND
CONFUSED
CONFUSED AND
LETHGARGIC

19. RESUSCITATION
• Class I and II = Crystalloids and or colloids
• Class III and IV = Blood + Crystalloids
• NB
• Patients with severe blood loss may respond with bradycardia
• Hemodynamic signs are less reliable in elderly and patients on b blockers
• Recommendation International Consensus Group is to initiate blood transfusion
 Hb <8g/dl for hemodynamically stable patients
 Hb <9g/dl for patients with increased risk of adverse outcome in setting of
significant anaemia .e.g. unstable angina, evidence of ongoing active bleeding
• Meta-analysis of 70 trials with 22392 patients found no difference in mortality for
crystalloids and colloids in fluid resuscitation.(Perel et al, 2013)

20. RESUSCITATION
• Elevate legs about 15 degrees
• Secure 2 IV access with size 16 or 18 cannula, and blood is taken for GXM, FBC,
BUE, LFT, Clotting profile
• 1.0L crystalloid is given in 45mins , the rate is adjusted depending on the CVP, ¼
hrly pulse, BP, venous filling, moistness of mucous membranes and more
importantly urine output
• Use 3 to 1 rule as a guide; 1 ml of estimated blood loss :3 ml of crystalloids
• Supplemental oxygen

21. History and examination
• Possible site and cause of bleeding
• Severity, timing, duration and volume of the bleeding
• Risk factors and co-morbidities
• Previous surgery or previous history of UGIT bleeding
• Medications

22. History
• Heamatemesis 40- 50%
• Malena 70-80%
• Hematochezia 15-20%
• Hematochezia or malena 90-98%
• Syncope 14.4%
• Dyspepsia 5%
• Heartburn 21%
• Diffuse abd pain 10%
• Dysphagia 5%
• Weight loss 12%

23. Probable source of GI bleeding with the gut
Clinical indicator Probability of upper GIT source Probability of lower GIT source
Hematemesis Almost certain rare
Melena probable possible
Hematochezia possible probable
Blood streaked stool rare Almost certain
Occult blood in stool possible possible

24. HISTORY
• Previous history of dyspepsia suggestive of PUD
• A history of liver disease or alcohol abuse may be suggestive of bleeding
oesophageal varices
• Prolonged vomiting or retching after a bout of alcohol is typical of MW tear
• If a patient has had surgery, severe trauma, burns, severe sepsis, or in renal failure
stress ulceration is suspected although bleeding may be due to reactivated chronic
peptic ulcer disease
• Massive bleeding preceded by hematemesis and /melena and abdominal or back
pain is suggestive of aorta-enteric fistula in 50% of cases in a patient with
previous aortic surgery
• Weight loss raises spectre of malignant disease
• History of ingestion of salicylates, NSAIDS, SSRI, anticoagulants particularly in
elderly

25. Examination
• Signs pointing to extent of bleeding
Pallor, sweating, cold extremities, collapsed veins, tachycardia, hypotension, restlessness
and coma
• Signs pointing to cause
Epigastric tenderness =PUDx
Hepatosplenomegally spider naevi, ascites =oesophageal varices
Epigatric mass = ca stomach
Telangiectasia of mouth and lips= hereditary telangiectasia
Pulsatile expansile mass suggestive of aorto-enteric fistula
DRE must be performed to exclude rectal ca or haemorrhoids
Oropharynx and nose should be examined

26. Localisation of bleeding
• Passage of NG tube and gastric lavage to examine aspirate and remove
particulate matter and clots to enhance endoscopy
• Increasing data shows its unreliable in localising the bleeding site
• But still important in diagnosis, prognosis, visualisation and has therapeutic effect
• May show
Coffee ground = recent bleeding
Active bleeding= red blood in aspirate that doesn’t clear
No blood/clear =active bleeding not likely, but doesn’t exclude UGIT lesion(15-
18%)
Bilious aspirate= almost definitely not UGIT bleeding

27. ENDOSCOPY
• After haemodynamic stability
• It is the diagnostic modality of choice with high sensitivity and specificity for
localising the site of ongoing bleeding
• It is used therapeutically and for biopsy
• Usually within first 24hrs
• No additional benefit doing it earlier (within 6 or 12hrs), in stable patients(Sarin
Monga et al, 2009)

28. Endoscopy ctd
• Urgent or emergent endoscopy is associated with:
 Decreased accuracy o/a poor visualisation
Increased risk of complications .e.g. aspiration, respiratory depression, GI perforation
• Urgent endoscopy (<12hrs) is however associated with good outcome in high risk
patients such as heamodynamic instability despite adequate resuscitation,
cirrhotics with esophageal varices and persistent heamatemesis (Laurson, 2017)
• For patients with cirrhosis or on warfarin endoscopy is done if INR <2.5

29. Pre endoscopic medical therapy
• Proton pump inhibitors (PPI); intravenous PPI is been found to decrease the
stigmata of rebleeding and need for surgery. (Barkun et al, 2010)
• Prokinetics: use of Erythromycin infusion 250mg, 30-120mins before endoscopy
improves gastric motility and visualisation at endoscopy and reduced need for
reendoscopy (Rahman et al, 2016)
• Meta-analysis by Barkun et al ,did not show any benefit of preendoscopic use of
metoclopramide

30. Endoscopy ct
• Endoscopic appearance for upper GIT bleeds is described by
FORREST CLASSIFICATION
• Risk of rebleeding
• Need for endoscopic therapy
• Consist of three grades

31. FORREST CLASSIFICATION

32. stigmata of recent bleeding
• Forrest Ia /Ib, high risk
• 80% risk of rebleeding
• Iv PPI for 72hrs to reduce risk of rebleed after endoscopic therapy

33. Stigmata of recent haemorrhage
• Forrest IIa, high risk
• Visible vessel
• 50% risk of rebleeding
• Iv PPI for 72hrs, reduces risk of rebleeding after
endoscopic therapy
• Forrest IIb, intermediate risk
• Adherent clot
• 30% risk of rebleeding
• Iv PPI for 72hrs and endoscopic therapy or medical
management alone

34. Stigmata of recent haemorrhage-PUD
• Forrest IIc
• Black spot at ulcer base
• 7- 10% risk of rebleeding (low risk)
• No need for endoscopic therapy
• Iv PPI not necessary. Orals PPIs can be used
• Forrest III
• Clear ulcer base
• 3-5% risk of rebleeding (low risk)
• No need for endoscopic therapy
• Iv PPIs not necessary. Orals can be used

35. Endoscopy ctd’
• Reendoscopy is done after 24hrs, rebleeding is treated similarly
• Second rebleed is seriously considered for surgery
• In stable patients or patient with co-morbidities, arterial embolization is
recommended(Acosta, 2015)
• Mortality, transfusion requirement and duration of hospital admission is similar in
angiographic embolization and surgery
• If endoscopy fails to reveal source of bleeding, angiography is performed
• If no active bleeding is identified by angiography in a patient with recurrent
bleeding, prophylactic embolization of left gastric artery or gastroduodenal artery
can be performed
• Patients who receive endoscopic treatment should be monitored for 72hrs

36. Other diagnostic test
• RBC Scintigrapy: highly sensitive and detects bleeding rates of 0.05-0.1ml/min.
But has prolonged imaging time and therefore not ideal for unstable patients. It
has a poor spatial resolution and cannot precisely localise active bleeding
• Video capsule endoscopy: currently not considered a substitute for endoscopy
but beneficial in evaluation of obscure gastrointestinal bleeding.
• Barium meal : currently contraindicated

37. Risk stratification
• Not all patients require in patient management
• Several risk assessment models permit identification of persons with low risk of
recurrent or life threatening haemorrhage
• Such patients with low risk are suitable for early discharge or OPD care
• Stratifying results in decreased resource utilisation
• Scoring systems are used to predict the need for ICU care or emergent
endoscopic evaluation

38. Risk stratification
The most important predictors of rebleeding are:
• Age > 60yrs
• Hb < 8g/dl
• Endoscopic stigmata of significant hemorrhage (SSH)
• Co-morbidities
• Ulcer size >2cm
* These are combined in the risk stratification score

39. Risk scores
• Glasgow Blatchford Score or modified GBS
• Rockall score( RS )
• Aims 65
• GBS; doesn’t take endoscopic data unlike RS
• GBS Out performed RS and AIMS in predicting need for clinical intervention,
rebleeding and mortality. (Stanley,2017)

41. Risk scores
• Blatchford score of <_ 1, is the optimum low risk threshold for therapeutic
intervention i.e. transfusion, endoscopy or surgery with 99% sensitivity and 35-
40% specificity ( Stanley et al, 2017)
• Useful tool in determining risk of serious bleeding on initial presentation
• Patients with gbs 0-1, can be treated on OPD basis, provided they have stable
vitals, normal Hb, no comorbidities, and do not live too far from hospital
• Rockall score uses clinical and endoscopic findings to predict risk of rebleeding
and in hospital mortality
• Its more helpful in determining the need for surgical intervention after
resuscitation

42. AIMS 65
• Albumin <3.0g/dl
• INR >1.5
• Altered Mental status
• Systolic BP <_90mmhg
• Age >65yrs
Reliably predict mortality

43. Specific management
• Initially conservative for all
• Stress ulcers
Treatment of underlying condition
 gastric lavage with chilled water
Antacids and iv PPIs
Bleeding usually resolves after 24-48hrs
MW syndrome ; 90% will resolve spontaneously by 72hrs
Supportive therapy
In rare cases of severe ongoing bleeding ,local endoscopic therapy with injection and
electrocoagulation is effective
Angiographic embolization with absorbable material like gelatin sponge have been
successfully employed in cases of failed endoscopic management

44. Specific management ctd’
• Peptic ulcer disease
Iv PPI started whiles preparing for endoscopy.
increase in PH above 6.0 enhances blood coagulability, inactivates pepsin which
promotes platelet aggregation and inhibit fibrinolysis
PPIs decreases the stigmata of re-bleeding and need for surgery, (Barkun et al
,2010)
Current( ICG )guideline: iv PPI 80mg bolus, followed by a continuous infusion of
8mg/hr for 72hrs, reduces rebleeding and mortality
This is followed by twice daily oral PPI for 14 days, and then once daily PPI
therapy
Intermittent use of iv or oral reduces rebleeding but not mortality(leine ,2009)

45. Peptic ulcer disease
• Endoscopic therapy indicated for FORREST I-IIa
Injection of 10-16mls of 1:10000 adrenalin +ethanol
Thermal treatment :bipolar diathermy, laser photocoagulation, heat probes
Fibrin glue or thrombin injection
 heamoclips
70% would not bleeding at re endoscopy
NEW TRENDS
Heamostatic sprays
Doppler endoscopic Probes
Over the scope clips

46. Algorithm for diagnosis and management of non variceal
bleeding

47. Variceal bleeding
MEDICAL MX after resuscitation with vasoactive therapy is started
• Allows temporal control of bleeding
• Allows time for resuscitation and diagnostic and /therapeutic interventions
vasopressin + nitroglycerin or isopretenalol
20units in 250mls of 5%dextrose in 30mins 4hrly
controls bleeding in 50% of cases and causes purgation, hence reduces risk of
hepatic encephalopathy
 Terlipressin + GTN, 2mg iv 4HRLY is longer acting alternative with positive
impact on survival
Somatostatin and its analogue octreotide can also be used
Vasoactive agents are usually given for 5 days

48. Variceal bleeding
Broad spectrum antibiotic (iv ceftriaxone or oral ciprofloxacin) is started and
continued for 7 days lowers bleeding risk (Herrera, 2014)
PPIs should not be used concurrently in those receiving somatostatin (analoge)
as the they inhibit gastric acid secretion comparable to PPIs (Avgerino, 2005)
ENDOSCOPIC MX
Early endoscopy within 12hrs can affect survival
More than ½ of bleeding is nonvariceal
• Band ligation: therapy of choice and has less complication rate

49. Variceal bleeding ctd
 Sclerotherapy: started at initial endoscopy with 3-5mls ethanolamine or Na Morrhaute
If bleeding is controlled injection is repeated weekly, then 3wkly then 3monthly until
full obliteration
Endoscopic therapy is effective in 90% of cases of esophageal varices
Less effective for gastric varices or portal hypertensive gastropathy
Injection of tissue adhesives (N-butyl cyanoacrylate) is recommended for all types of
gastric varices (American association for study of Liver Disease, 2017 guideline)
Thrombin injection for gastric varices have been described but no RCT, comparing it
with others
• if pharmacologic and endoscopic management fails
BALOON TAMPONADE using SENSTAKEN BLAKEMORE TUBE(SBT) is applied awaiting
intervention and should not be retained beyond 12hrs
This is now replaced by REMOVABLE SELF EXPANDING METAL STENTS (RSEMS)

50. Variceal bleeding
• Compaired with balloon
tamponade using SBT tube,
RSEMS is associated with
decreased complication rate
and improved bleeding
control (Escorsell, 2015)
• Percutaneous transjugular
intrahepatic portosystemic
shunting (TIPS) is the
procedure of choice when
endoscopic management
fails

51. Variceal bleeding
PREVENTION
• without any preventive measure 70% will rebleed in 2 months
• Risk increased within first few hrs to days
• Preventive therapy is combined with endoscopic management until all varices are
eradicated
Propranolol ,nadolol( longer acting )
cause splanchnic vasoconstriction by a2 inhibition and decrease cardiac output by
B1 blockage ,thus lowering portal pressure
It is given in a sufficient dose to reduce resting PR by 25%
Daily administration after bleeding has stopped reduces rebleeding by 80%

52. Variceal bleeding
SBK TUBE FOR TEMPORAL CONTROL
OF VARICEAL BLEEDIND
TIPSS FOR REFRACTORY VARICEAL
BLEEDING

53. Specific management ctd
Dieulafoy’s lesion
• its treated endoscopically by placement of heamoclips, electrocoagulation and
photocoagulation
• Effective in 80 -100 %of cases.
• In failure of the above angiographic coil embolization can be done

54. Definitive procedures
AIM
• Stop bleeding and prevent recurrence
• Possibly cure underlying cause
Indications
• massive bleeding/ blood transfusion requirement in excess of 6 units
• Severe bleeding continues or bleeding recurring after 2nd endoscopy
• Perforation
• Blood not readily available

55. Indications ctd’
• Shock associated with recurrent bleeding
• Continuous slow bleeding with transfusion requirement exceeding 3units/day
Possible need for surgery
• Increased risk of further bleeding in PUD
• Age > 60yrs
• Hb < 8g/dl
• Shock on admission . Mortality is 50%
• visible or spurting vessel or fresh or altered blood in an ulcer at endoscopy
• Giant ulcer >2cm

56. Indications ctd
• Ulcer (>1cm) at the high posterior lesser curvature or posterior inferior wall of
the duodenal bulb
• Episode of bleeding on admission

57. Definitive procedures
• Stress ulcers
few erosions: oversewn
numerous erosions: vagotomy +partial gastrectomy
• Duodenal ulcers
Quickest and safest operation is to underrun the vessels i.e. gastroduodenal artery
with non absorbable suture, preferably 4o prolene through a transpyloric
gastroduodenostomy.
To prevent rebleeding, the gastroduodenal, superior panceaticoduodenal and right
gastroepiploic vessel must be sutured continuously to cover the entire course of
the gastroduodenal artery within the ulcer base.
Definitive ulcer surgery may follow depending on patient and surgeon
Badoe EA etal (1986).BAJAS Principles and practice of surgery ,5th Edition pg 665, Ghana printing press

58. Definitive procedure
Gastric ulcer
• Stomach is opened anteriorly
• Bleeding vessel under-run
• Biopsy /excision of edge to exclude malignancy
• Followed by H2 receptor antagonist or triple therapy to prevent recurrence
• Gastrectomy for bleeding is associated with perioperative mortality

59. Definitive procedure ctd
• Aorto enteric fistula
under antibiotic cover the fistula is disconnected and closed and the aorta grafted
with antibiotic primed graft and covered with omentum
Oesophageal varices:
Stappling transection of oesophagus at gastroesophageal junction is done with
paraesophageal devascularisation and ligation of left gastric vessel .

60. Definitive procedures
• This reduces pressure in the varices without affecting liver dynamics
Distal splenorenal shunt with partial devascularisation left and right gastric
arteries also decompresses varices
Effect on liver hemodynamics and function isn’t severe as Porto systemic shunt
Badoe EA etal (1986).BAJAS Principles and practice of surgery ,5th Edition pg 665, Ghana printing press

61. Prognosis
• Overall mortality of UGIT bleeding is 10-15%
• Mortality increases with age ,>33% in patients over 70
• With conservative treatment alone 20% rebleed in 5-10yrs
• Only 4.5% rebleed after surgical treatment
• Predictors of mortality are age ,shock ,co morbidity, delay in diagnosis and
rebleeding

62. conclusion
• Upper GIT bleeding is a common clinical problem with diverse presentation
• Management is multidisciplinary
• The surgeons role in management cannot be overemphasised
• Determination of site of bleeding is relevant to direct intervention without delay
but this should not override appropriate resuscitative measure
• Risk assessment helps in resource utilization
• Distinction between variceal and nonvariceal causes guides initial and definitive
management

63. •Thanks for your attention

64. References
• Aoik T, Nagata N,YamadaA etal. Next endoscopic approach for acute lower with or without identified causeon colonoscopy:
upper or capsule endoscopy?. Endosc Int Open .2019Mar.7(3):E337-E346.
• Barkun AN, Herba K, Adam V, Kenedy W et al, high dose IV PPI inhibition following endoscopic therapy in acute management
of patients with bleeding peptic ulcers in USA and Canada: a cost effective analysis. Aliment Pharmacol ther .2004 March 1.
19(5):591-600
• Carson JL, Guyatt G, Heddle NM, et al. Clinical practice guidelines from the AABB: red blood cell transfusion thresholds and
storage. JAMA 2016;316:2025-35. 10.1001/jama.2016.9185 pmid:27732721.
• Perel P, Roberts I, Ker K. Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database Syst Rev
2013;28:CD000567 .pmid:23450531.
• Stanley AJ, Laine L, Dalton HR, et al. International Gastrointestinal Bleeding Consortium. Comparison of risk scoring systems for
patients presenting with upper gastrointestinal bleeding: international multicentre prospective study. BMJ 2017;356:i6432.
10.1136/bmj. i6432 pmid:2805
• Sreedharan A, Martin J, Leontiadis GI, et al. Proton pump inhibitor treatment initiated prior to endoscopic diagnosis in upper
gastrointestinal bleeding. Cochrane Database Syst Rev 2010;7:CD005415.pm
• Rahman R, Nguyen DL, Sohail U, et al. Pre-endoscopic erythromycin administration in upper gastrointestinal bleeding: an
updated meta-analysis and systematic review. Ann Gastroenterol 2016;29:312- 7.pmid:27366031.

65. References
• Escorsell À, Pavel O, Cárdenas A, et al. Variceal Bleeding Study Group. Esophageal balloon tamponade versus
esophageal stent in controlling acute refractory variceal bleeding: A multicenter randomized, controlled trial.
Hepatology 2016;63:1957-67. 10.1002/ hep.28360 pmid:26600191.
• Laursen SB, Leontiadis GI, Stanley AJ, Møller MH, Hansen JM, Schaffalitzky de Muckadell OB. Relationship
between timing of endoscopy and mortality in patients with peptic ulcer bleeding: a nationwide cohort study.
Gastrointest Endosc 2017;85:936-944.e3. 10.1016/j. gie.2016.08.049 pmid:27623102.
• Avgerinos A, Sgouros S, Viazis N, et al. Somatostatin inhibits gastric acid secretion more effectively than
pantoprazole in patients with peptic ulcer bleeding: a prospective, randomized, placebo-controlled trial. Scand J
Gastroenterol 2005;40:515-22. 10.1080/00365520510015458 pmid:16036503.
• Laine L, McQuaid KR. Endoscopic therapy for bleeding ulcers: an evidence-based approach based on meta-
analyses of randomized controlled trials. Clin Gastroenterol Hepatol 2009;7:33-47, quiz 1-2.
10.1016/j.cgh.2008.08.016 pmid:18986845.
• Acosta RD, Abraham NS, Chandrasekhara V, et al. ASGE Standards of Practice Committee. The management of
antithrombotic agents for patients undergoing GI endoscopy. Gastrointest Endosc 2016;83:3-16.
10.1016/j.gie.2015.09.035 pmid:26621548.