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محاضرات عين شمس
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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 ß-adrenergic blockers - proprandolol, nadolol or timolol
-They decrease portal venous inflow by two mechanisms
- decreasing cardiac output (ß1 blockade)
- splanchnic vasoconstriction (ß2 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 therapy1. +/- Adherent clot 2. Nonbleeding visible vessel 3. Active bleeding (oozing, spurting)
Decreases in rebleeding, surgery and mortality
1. Laine & Peterson; 19942. Cook et al; 19923. 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.
AngiographyAngiography 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