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.
10.
11.
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
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.
34.
35.
36.
37.
38.
39.
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