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UPPER GASTROINTESTINAL
BLEEDING
Prof. HESHAM MAGED
GENERAL SURGERY DEPARTEMENT
AIN SHAMS UNIVERSITY
Upper gastrointestinal bleeding
occurs proximal to ligament of Treitz
and can be classified into
A- Variceal (portal hypertension
esophageal varices) and nonvariceal
B- Acute or Chronic determined by
clinical presentation
Epidemiology of upper GI Bleeding
1 case/1000 adults/year
40-50% of cases are variceal hemorrhage
(Egypt),10-20%world wide
30-40% of cases are peptic ulcer disease
80% of cases of bleeding cease
spontaneously
6-7% mortality rate
Etiology of Upper GIT Bleeding
Duodenal Ulcer-25%
Gastric Ulcer-15%
Varices-10% (30-40%) in Egypt
Gastritis and duodenitis-5-10%
Esophagitis-5%
Mallory Weiss Tear-3%
GI Malignancy-1%
Dieulafoy Lesion( abnormal dilated sub mucosal arterioles)
AV Malformation-angiodysplasia
Upper Gastrointestinal Bleeding
Despite a decreased incidence of ulcer
disease and improvements in the
management of acute upper GI bleeding,
mortality remains at + 6-7 % in most series
in the literature for the past 30 years.
Clinical presentation
Upper GIT bleeding can presents in 5 ways:
1- Hematemesis: vomitus of red blood or coffee grounds
material.
2- Melena: black tarry foul smelling stool develops with
approximately 150-200cc of blood in the upper GI tract.
3- Hematochezia: passage of bright red or maroon blood
from the rectum.
4- Occult blood in stool.
5- Symptoms of chronic blood loss and anaemia.
Evaluation : History /physical examination
-previous episode of GIT bleeding
- History of CLD
-History of PUD
-Medication use
(NSAID,anticoagulant,corticosteroid)
-Bleeding disorders
-Significant comorbid diseases as HF
Physical examination
-Signs of volume loss as orthostatic hypotension
chest pain and dyspnia.
-Resting tachycardia( HR> 100/m suggest 15-30%
loss of blood volume while a blood pressure below
normal suggest more than 30% loss of blood
volume.
-Significant postural pulse change >30 beat/m
suggest hypovolumia from significant blood loss.
-Investigations:
- A CBC with blood type and cross match
-Coagulation profile
-S.electrolyte
-LFT
-BUN ,S. createnine
-Hct initially appear normal ,but following
hemodilution, it will fall
-ECG if patient >50 years, or with history of heart
disease
Medical treatment
- Proton pump inhibitors reduce gastric acid production
and enhance healing of bleeding lesions.
- Tranexamic acid (antifibrinolytic agent)reduces
fibrinolysis and may decrease blood product
requirements.
-Correction of coagulopathy: Vit.k or fresh frozen plasma
may need to be administered.
-Reduction of portal pressure'': if the bleeding is thought
to be due to esophageal varices, vasopressin
analogues and rarely octreotide may be administered.
Rarely, a Sengstaken-Blakemore tube may be inserted to
mechanically compress varices.
--- Non selective Ăź-adrenergic blockers -
proprandolol, nadolol or timolol
-They decrease portal venous inflow by two
mechanisms
- decreasing cardiac output (Ăź1 blockade)
- splanchnic vasoconstriction (Ăź2 blockade
and unopposed alpha adrenergic activity)
At intragastric pH < 7, coagulation is
deficient due to ineffective function
of clotting factors and platelets
Maintenance of a high intragastric
pH > 6 during management of upper
G I Bleeding is warranted.
IV PPI’s are able to maintain gastric
pH > 6 for 24 hours a day.
Risk identification by OGD
Low risk finding:
Clean base ulcer
Clean Mallory weir tear
Gastritis Duodenitis
Portal hypertensive gastropathy
Management : Discharge patient if stable
Medium risk finding
-AVMs
-Ulcer with stigma of recent hemorrhage
-Varices with recent hemorrhage
-Mallory weir tear stigma of recent hemorrhage
-Cancer
Management: admission in medical or intermediate care
unit with haemostatic measures
High risk finding
-Active variceal bleeding
-Active ulcer bleeding
-Active bleeding from Dieulafoy’s lesion
- Management :admission in I.C.U. with haemostatic
measures
Endoscopic therapy
-Indications for haemostatic therapy
1. +/- Adherent clot
2. Nonbleeding visible vessel
3. Active bleeding (oozing, spurting)
Decreases in rebleeding, surgery and mortality
1. Laine & Peterson; 1994
2. Cook et al; 1992
3. Sacks et al; 1990
Endoscopic therapeutic options
- Injection: epinepherin 1:10,000
- ethanol
- thrombin
- sodium tetradecyl sulfat
- ethanolamin oleate
- Thermal: heat probe
- bipolar probe
- Nd:YAG laser
- argon plasma coagulation
- Mechanical: hemoclip
- banding
Effect of Therapy on re-bleeding rates
(Visible Vessel)
Effect of Therapy on re-bleeding rates
(Active Bleeding)
Endoscopic therapy may not be
possible in up to 12% of bleeding
duodenal ulcers and at least 1% of
bleeding gastric ulcers because of
inaccessibility of the lesion or massive
hemorrhage.
Hypotension and ulcer size of at least 2cm
are independent factors predictive of the
failure of endoscopic re-treatment.
Patients with larger ulcers and therefore
heavier bleeding, surgery may be a better
choice than endoscopic re-treatment.
Angiography
Angiography is often the next step if medical management
or endoscopy fails to control upper gastrointestinal
bleeding (UGIB). Angiography is minimally invasive; it
often allows precise localization of bleeding; and it
enables the use of therapeutic options, which include
embolization or vasopressin infusion. A hemorrhage
rate of 0.5-1.0 mL/min is required before it can be
visualized with angiography
-Success rate 50-90%.
-Can replace surgery in high risk patients.
-Complications: uncommon as bowel ischemia, hepatic
, splenic infarction.
Indications for surgery in patients with bleeding
peptic ulcers include the following:
-Severe, life-threatening hemorrhage not responsive to
resuscitative efforts (pesistant shock inspite of more than 6 units
of blood.
-Failure of medical therapy and endoscopic hemostasis with
persistent or recurrent bleeding
-A coexisting reason for surgery (eg, perforation, obstruction,
malignancy)
-Prolonged bleeding >2-3 days, with loss of 50% or more of the
patient's blood volume
-A second hospitalization for peptic ulcer hemorrhage
Surgery for bleeding P.U
-The appropriate surgical procedure depends on the
location and nature of the ulcer.
-simple oversewing of the ulcer with treatment of the
underlying H pylori infection or cessation of NSAIDs
for bleeding PUD.
- Additional surgical options for refractory or complicated
PUD include vagotomy and pyloroplasty, vagotomy
and antrectomy with gastroduodenal reconstruction
(Billroth I) or gastrojejunal reconstruction (Billroth II),
or a highly selective vagotomy.
Surgery for bleeding esophageal varices
-Surgical management of BEV remains both frustrating
and challenging.
-Associated with increased incidence of mortality,
rebleeding and hepatic encephalopathy especially in
Child B,C
- Hassab’s operation and Warren’s shunt
- (distal spleno-renal shunt)
- Esophageal transection
-The distal splenorenal shunt was designed to decompress
esophageal varices while maintaining portal perfusion
pressure and associated with a low incidence of
complications.
-The operative mortality rates for elective distal
splenorenal shunt averaged 13 percent. In the urgent
setting, has a 38 percent mortality rate.
-Hassab's decongestion operation esophagogastric
devascularization and splenectomy has high incidence of
mortality about 44% especially if combined with
esophageal transaction
Transjugular Intrahepatic Portosystemic
Shunt (TIPS)
-TIPS reroutes blood flow in the liver and reduces
abnormally high blood pressure in the veins of the
stomach, esophagus
-Studies have shown that this procedure is successful in
reducing variceal bleeding in more than 90 percent of
patients
-complications:
stent obstruction
liver lacertion, bleeding
encephalopathy
infection
Thank you

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Ugi bleeding

  • 1. UPPER GASTROINTESTINAL BLEEDING Prof. HESHAM MAGED GENERAL SURGERY DEPARTEMENT AIN SHAMS UNIVERSITY
  • 2. Upper gastrointestinal bleeding occurs proximal to ligament of Treitz and can be classified into A- Variceal (portal hypertension esophageal varices) and nonvariceal B- Acute or Chronic determined by clinical presentation
  • 3.
  • 4. Epidemiology of upper GI Bleeding 1 case/1000 adults/year 40-50% of cases are variceal hemorrhage (Egypt),10-20%world wide 30-40% of cases are peptic ulcer disease 80% of cases of bleeding cease spontaneously 6-7% mortality rate
  • 5. Etiology of Upper GIT Bleeding Duodenal Ulcer-25% Gastric Ulcer-15% Varices-10% (30-40%) in Egypt Gastritis and duodenitis-5-10% Esophagitis-5% Mallory Weiss Tear-3% GI Malignancy-1% Dieulafoy Lesion( abnormal dilated sub mucosal arterioles) AV Malformation-angiodysplasia
  • 6. Upper Gastrointestinal Bleeding Despite a decreased incidence of ulcer disease and improvements in the management of acute upper GI bleeding, mortality remains at + 6-7 % in most series in the literature for the past 30 years.
  • 7. Clinical presentation Upper GIT bleeding can presents in 5 ways: 1- Hematemesis: vomitus of red blood or coffee grounds material. 2- Melena: black tarry foul smelling stool develops with approximately 150-200cc of blood in the upper GI tract. 3- Hematochezia: passage of bright red or maroon blood from the rectum. 4- Occult blood in stool. 5- Symptoms of chronic blood loss and anaemia.
  • 8. Evaluation : History /physical examination -previous episode of GIT bleeding - History of CLD -History of PUD -Medication use (NSAID,anticoagulant,corticosteroid) -Bleeding disorders -Significant comorbid diseases as HF
  • 9. Physical examination -Signs of volume loss as orthostatic hypotension chest pain and dyspnia. -Resting tachycardia( HR> 100/m suggest 15-30% loss of blood volume while a blood pressure below normal suggest more than 30% loss of blood volume. -Significant postural pulse change >30 beat/m suggest hypovolumia from significant blood loss.
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  • 12. -Investigations: - A CBC with blood type and cross match -Coagulation profile -S.electrolyte -LFT -BUN ,S. createnine -Hct initially appear normal ,but following hemodilution, it will fall -ECG if patient >50 years, or with history of heart disease
  • 13.
  • 14. Medical treatment - Proton pump inhibitors reduce gastric acid production and enhance healing of bleeding lesions. - Tranexamic acid (antifibrinolytic agent)reduces fibrinolysis and may decrease blood product requirements. -Correction of coagulopathy: Vit.k or fresh frozen plasma may need to be administered. -Reduction of portal pressure'': if the bleeding is thought to be due to esophageal varices, vasopressin analogues and rarely octreotide may be administered. Rarely, a Sengstaken-Blakemore tube may be inserted to mechanically compress varices.
  • 15.
  • 16.
  • 17. --- Non selective Ăź-adrenergic blockers - proprandolol, nadolol or timolol -They decrease portal venous inflow by two mechanisms - decreasing cardiac output (Ăź1 blockade) - splanchnic vasoconstriction (Ăź2 blockade and unopposed alpha adrenergic activity)
  • 18.
  • 19.
  • 20. At intragastric pH < 7, coagulation is deficient due to ineffective function of clotting factors and platelets
  • 21. Maintenance of a high intragastric pH > 6 during management of upper G I Bleeding is warranted. IV PPI’s are able to maintain gastric pH > 6 for 24 hours a day.
  • 22.
  • 23. Risk identification by OGD Low risk finding: Clean base ulcer Clean Mallory weir tear Gastritis Duodenitis Portal hypertensive gastropathy Management : Discharge patient if stable
  • 24. Medium risk finding -AVMs -Ulcer with stigma of recent hemorrhage -Varices with recent hemorrhage -Mallory weir tear stigma of recent hemorrhage -Cancer Management: admission in medical or intermediate care unit with haemostatic measures
  • 25. High risk finding -Active variceal bleeding -Active ulcer bleeding -Active bleeding from Dieulafoy’s lesion - Management :admission in I.C.U. with haemostatic measures
  • 26. Endoscopic therapy -Indications for haemostatic therapy 1. +/- Adherent clot 2. Nonbleeding visible vessel 3. Active bleeding (oozing, spurting) Decreases in rebleeding, surgery and mortality 1. Laine & Peterson; 1994 2. Cook et al; 1992 3. Sacks et al; 1990
  • 27. Endoscopic therapeutic options - Injection: epinepherin 1:10,000 - ethanol - thrombin - sodium tetradecyl sulfat - ethanolamin oleate - Thermal: heat probe - bipolar probe - Nd:YAG laser - argon plasma coagulation - Mechanical: hemoclip - banding
  • 28. Effect of Therapy on re-bleeding rates (Visible Vessel)
  • 29. Effect of Therapy on re-bleeding rates (Active Bleeding)
  • 30. Endoscopic therapy may not be possible in up to 12% of bleeding duodenal ulcers and at least 1% of bleeding gastric ulcers because of inaccessibility of the lesion or massive hemorrhage.
  • 31. Hypotension and ulcer size of at least 2cm are independent factors predictive of the failure of endoscopic re-treatment. Patients with larger ulcers and therefore heavier bleeding, surgery may be a better choice than endoscopic re-treatment.
  • 32.
  • 33.
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  • 40.
  • 41. Angiography Angiography is often the next step if medical management or endoscopy fails to control upper gastrointestinal bleeding (UGIB). Angiography is minimally invasive; it often allows precise localization of bleeding; and it enables the use of therapeutic options, which include embolization or vasopressin infusion. A hemorrhage rate of 0.5-1.0 mL/min is required before it can be visualized with angiography -Success rate 50-90%. -Can replace surgery in high risk patients. -Complications: uncommon as bowel ischemia, hepatic , splenic infarction.
  • 42. Indications for surgery in patients with bleeding peptic ulcers include the following: -Severe, life-threatening hemorrhage not responsive to resuscitative efforts (pesistant shock inspite of more than 6 units of blood. -Failure of medical therapy and endoscopic hemostasis with persistent or recurrent bleeding -A coexisting reason for surgery (eg, perforation, obstruction, malignancy) -Prolonged bleeding >2-3 days, with loss of 50% or more of the patient's blood volume -A second hospitalization for peptic ulcer hemorrhage
  • 43. Surgery for bleeding P.U -The appropriate surgical procedure depends on the location and nature of the ulcer. -simple oversewing of the ulcer with treatment of the underlying H pylori infection or cessation of NSAIDs for bleeding PUD. - Additional surgical options for refractory or complicated PUD include vagotomy and pyloroplasty, vagotomy and antrectomy with gastroduodenal reconstruction (Billroth I) or gastrojejunal reconstruction (Billroth II), or a highly selective vagotomy.
  • 44. Surgery for bleeding esophageal varices -Surgical management of BEV remains both frustrating and challenging. -Associated with increased incidence of mortality, rebleeding and hepatic encephalopathy especially in Child B,C - Hassab’s operation and Warren’s shunt - (distal spleno-renal shunt) - Esophageal transection
  • 45. -The distal splenorenal shunt was designed to decompress esophageal varices while maintaining portal perfusion pressure and associated with a low incidence of complications. -The operative mortality rates for elective distal splenorenal shunt averaged 13 percent. In the urgent setting, has a 38 percent mortality rate. -Hassab's decongestion operation esophagogastric devascularization and splenectomy has high incidence of mortality about 44% especially if combined with esophageal transaction
  • 46. Transjugular Intrahepatic Portosystemic Shunt (TIPS) -TIPS reroutes blood flow in the liver and reduces abnormally high blood pressure in the veins of the stomach, esophagus -Studies have shown that this procedure is successful in reducing variceal bleeding in more than 90 percent of patients -complications: stent obstruction liver lacertion, bleeding encephalopathy infection

Editor's Notes

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