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