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UPPERGITBLEEDING: PRINCIPLESAND
MANAGEMENT
Presenter: Dr abdirisaq jacda IMR1
Moderator: Dr abdulaziz MD
OUTLINE
• Introduction
• Principles of
management
• Risk stratification
• Specific therapy
• Definitive management
• Conclusion
• References
Introduction
• Definition; Refers to bleeding that
arises from the GI tract proximal to the ligament of Trietz
• Incidence 100/100000 per year in the US much higher in middle
east and Africa
• It is 4 times more common than LGIB
• 80% of significant GIT bleeding
• Overall mortality 6-10%
• Many factors have influenced GIT bleeding in the past 20yrs
i.e. H2 blockers ( SSRI ) (PPI) and AND agents to eradicate h
pylori.
• Over all effect is decrease in hospitalization
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%
Introduction ctd
• Gastroesophageal varices
21.9
%
• Gastritis
• Peptic ulcer
• Esophagitis
• Gastric ca
• Gastric
erosions
21.7
%
30.2
%
5.9%
5.8%
3.9%
• Normal
findings
20.0
%
• Etiology of upper GIT bleeding following endoscopy at KBTH,
Introduction ctd’
• Gastritis and duodenitis
• Gastric and duodenal
ulcers
• Esophageal varices
• Gastric ca
• Esophageal ca
• Esophagitis
38.9
%
15.8
%
15.8
%
7.3%
3.1
%
3.0
%
• No cause was found for 15.8% of presentation
Key terms
AETIOLOGYOFNONV
ARICEALBLEEDING
PEPTIC ULCER DISEASE( PUD )
• Accounts for 40% of nonvariceal bleeding
• 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
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
• Usually secondary to GERD
• This can result in mucosal ulceration with chronic blood loss from
insignificant bleed
Aetiology ctd
Mallory Weiss1-4cm longitudinal tear
in the gastric mucosa and submucosa near the GEJ
• 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
Aetiology ctd
Malignant neoplasm of upper GIT
• Usually present as chronic anaemia or haemoccult positive blood
• Significant haemorrhage more likely for GIST, lymphomas and leiomyomas
• Rebleeding rates are high with endoscopic therapy
• Surgical resection is hence advised
• Typical case 55yrs old male with chronic anemia with constitutional sx
• Coomon add on sx early satiety epigastric pain
• Recently emerging incidence of young adults with…….
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 dx and tx of choice
Aetiology
Heamosuccus pancreaticus
• Very 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
Portal hypertensive bleeding/varicealbleeding
• Complications of decompensated liver cirrhosis
• Bleeding is most commonly from reptured varices
• 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
Principles of management
• Initial assessment and
resuscitation
• History and examination
• Localisation of bleeding
• Initiation of therapy
• Prevention of recurrence
Initial assessmentandresuscitation
• 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
A
TLSClassification of haemorrhagicshock
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
RESUSCIT
A
TION
• Class I and II = Crystalloids and or colloids
• Class III and IV = Blood + Crystalloids
• Elderly and patients on beta blockers
• Recommendation International Consensus Group is to initiate blood transfusion
 Hb <7g/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, ongoing active bleeding
RESUSCIT
A
TION
• 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
History andexamination
• 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
Probable source of GIbleeding with thegut
Clinical indicator Probability of upper GIT source Probability of lower GIT
source
Hematemes
is
Almost
certain
rar
e
Melen
a
probabl
e
possibl
e
Hematochezi
a
possibl
e
probabl
e
Blood streaked
stool
rar
e
Almost
certain
Occult blood in
stool
possibl
e
possibl
e
history
• history of dyspepsia suggestive of PUD
• 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
• 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
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
Localisation of bleeding
• NG tube and gastric lavage to examine aspirate and remove
particulate matter and clots to enhance endoscopy
• 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
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
Endoscopyctd
• Urgent or emergent endoscopy is associated with:
 Decreased accuracy o/a poor visualisation
Increased risk of complications .e.g. aspiration, respiratory depression, GI
perforation
• For patients with cirrhosis or on warfarin endoscopy is done if INR <2.5
Other diagnostictest
• 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
• Angiography excellent in localization of bleeding site and estimation
• Can detect
 Angiography generally is diagnostic of extravasation into
the intestinal lumen only when the arterial bleeding rate is
at least 0.5 mL/min.
 The sensitivity of mesenteric angiography is 30% to 50%
(with higher sensitivity rates for active GI bleeding than for
recurrent acute or chronic occult bleeding), and the
specificity is 100%
Riskstratification
• 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
Riskstratification
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
Riskscores
• Glasgow Blatchford Score or modified GBS
• Rockall score( RS )
• Aims 65
• GBS;doesn’t take endoscopic data unlikeR
S
• GBS Out performed RS and AIMS in predicting need for clinical
intervention, rebleeding and mortality. (Stanley,2017)
Specific management
• Initially conservative for all
• Stress ulcers
Treatment of underlying condition
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
Specific managementctd’
• 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
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
Peptic ulcerdisease
surgical options
• 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
 Prophylactic antibiotic therapy should be
offered at presentation to all patients with
suspected or confirmed variceal bleeding.
 Balloon tamponade should be considered as a
temporary salvage treatment for uncontrolled variceal
haemorrhage
Management of Variceal bleeding
Complications could be:
-gastric and oesophageal ulceration.
-pneumonia.
-oesophageal perforation.
Balloon tamponade
Band ligation
Stent insertion
Specificmanagementctd
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
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
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
•Thanks for your
attention

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UPPER GIT BLEEDING.pptx

  • 1. UPPERGITBLEEDING: PRINCIPLESAND MANAGEMENT Presenter: Dr abdirisaq jacda IMR1 Moderator: Dr abdulaziz MD
  • 2. OUTLINE • Introduction • Principles of management • Risk stratification • Specific therapy • Definitive management • Conclusion • References
  • 3. Introduction • Definition; Refers to bleeding that arises from the GI tract proximal to the ligament of Trietz • Incidence 100/100000 per year in the US much higher in middle east and Africa • It is 4 times more common than LGIB • 80% of significant GIT bleeding • Overall mortality 6-10% • Many factors have influenced GIT bleeding in the past 20yrs i.e. H2 blockers ( SSRI ) (PPI) and AND agents to eradicate h pylori. • Over all effect is decrease in hospitalization
  • 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%
  • 5. Introduction ctd • Gastroesophageal varices 21.9 % • Gastritis • Peptic ulcer • Esophagitis • Gastric ca • Gastric erosions 21.7 % 30.2 % 5.9% 5.8% 3.9% • Normal findings 20.0 % • Etiology of upper GIT bleeding following endoscopy at KBTH,
  • 6. Introduction ctd’ • Gastritis and duodenitis • Gastric and duodenal ulcers • Esophageal varices • Gastric ca • Esophageal ca • Esophagitis 38.9 % 15.8 % 15.8 % 7.3% 3.1 % 3.0 % • No cause was found for 15.8% of presentation
  • 8. AETIOLOGYOFNONV ARICEALBLEEDING PEPTIC ULCER DISEASE( PUD ) • Accounts for 40% of nonvariceal bleeding • 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.
  • 10. 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 • Usually secondary to GERD • This can result in mucosal ulceration with chronic blood loss from insignificant bleed
  • 11. Aetiology ctd Mallory Weiss1-4cm longitudinal tear in the gastric mucosa and submucosa near the GEJ • 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
  • 12. Aetiology ctd Malignant neoplasm of upper GIT • Usually present as chronic anaemia or haemoccult positive blood • Significant haemorrhage more likely for GIST, lymphomas and leiomyomas • Rebleeding rates are high with endoscopic therapy • Surgical resection is hence advised • Typical case 55yrs old male with chronic anemia with constitutional sx • Coomon add on sx early satiety epigastric pain • Recently emerging incidence of young adults with…….
  • 13. 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 dx and tx of choice
  • 14. Aetiology Heamosuccus pancreaticus • Very 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
  • 15. Portal hypertensive bleeding/varicealbleeding • Complications of decompensated liver cirrhosis • Bleeding is most commonly from reptured varices • 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
  • 16. Principles of management • Initial assessment and resuscitation • History and examination • Localisation of bleeding • Initiation of therapy • Prevention of recurrence
  • 17.
  • 18. Initial assessmentandresuscitation • 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
  • 19. A TLSClassification of haemorrhagicshock 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
  • 20. RESUSCIT A TION • Class I and II = Crystalloids and or colloids • Class III and IV = Blood + Crystalloids • Elderly and patients on beta blockers • Recommendation International Consensus Group is to initiate blood transfusion  Hb <7g/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, ongoing active bleeding
  • 21. RESUSCIT A TION • 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
  • 22. History andexamination • 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
  • 23. Probable source of GIbleeding with thegut Clinical indicator Probability of upper GIT source Probability of lower GIT source Hematemes is Almost certain rar e Melen a probabl e possibl e Hematochezi a possibl e probabl e Blood streaked stool rar e Almost certain Occult blood in stool possibl e possibl e
  • 24. history • history of dyspepsia suggestive of PUD • 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 • 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 • NG tube and gastric lavage to examine aspirate and remove particulate matter and clots to enhance endoscopy • 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
  • 28. Endoscopyctd • Urgent or emergent endoscopy is associated with:  Decreased accuracy o/a poor visualisation Increased risk of complications .e.g. aspiration, respiratory depression, GI perforation • For patients with cirrhosis or on warfarin endoscopy is done if INR <2.5
  • 29. Other diagnostictest • 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 • Angiography excellent in localization of bleeding site and estimation • Can detect
  • 30.  Angiography generally is diagnostic of extravasation into the intestinal lumen only when the arterial bleeding rate is at least 0.5 mL/min.  The sensitivity of mesenteric angiography is 30% to 50% (with higher sensitivity rates for active GI bleeding than for recurrent acute or chronic occult bleeding), and the specificity is 100%
  • 31. Riskstratification • 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
  • 32. Riskstratification 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
  • 33. Riskscores • Glasgow Blatchford Score or modified GBS • Rockall score( RS ) • Aims 65 • GBS;doesn’t take endoscopic data unlikeR S • GBS Out performed RS and AIMS in predicting need for clinical intervention, rebleeding and mortality. (Stanley,2017)
  • 34.
  • 35. Specific management • Initially conservative for all • Stress ulcers Treatment of underlying condition 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
  • 36. Specific managementctd’ • 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 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
  • 37. Peptic ulcerdisease surgical options • 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
  • 38.
  • 39.  Prophylactic antibiotic therapy should be offered at presentation to all patients with suspected or confirmed variceal bleeding.  Balloon tamponade should be considered as a temporary salvage treatment for uncontrolled variceal haemorrhage Management of Variceal bleeding
  • 40. Complications could be: -gastric and oesophageal ulceration. -pneumonia. -oesophageal perforation. Balloon tamponade
  • 43. Specificmanagementctd 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
  • 44. 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
  • 45. 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