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Upper gastrointestinal bleeding

Defined as blood loss that originates proximal to the ligament of Treitz, in the esophagus, stomach, or duodenum.

Most common manifestations are melena or hematemesis.

The severity of an upper G.I. bleed is defined by the patient’s hemodynamic status and transfusion requirements.

Fatality rate about 10%.

Incidence of 48-160 cases per 1000 adults per year and a mortality rate of 5-14%.

There are approximately 350,000 hospitalizations annually for upper G.I. bleeding.

The incidence of hospitalizations for UGIB generally increases with age and is more common in men than women.

Most upper G.I. bleeding is non-variceal, accounting for 80-90%, and peptic ulcer disease is an important cause of non-variceal bleeding.

17% of patients with upper GI bleeding have gastric and esophageal varices.

Esophagitis accounts for approximately 10% of UGIB.

South of Chinese who counts for approximately 10% of UGG ID cases

The three most common causes of UGIB are peptic ulcer disease, esophagogastric varices, and erosive esophagitis.

Other causes of bleeding related to esophagitis include pill esophagitis and infectious esophagitis.

Ischemia rarely may lead to esophageal necrosis and is considered in patients with hemodynamic instability that preceded an upper G.I. bleed.

In patients with an UGI bleed secondary to esophagitis, hematemesis is more common than melena.

Risk increases with the use of antiplatelet medications, including aspirin and clopidogrel, warfarin or combinations of these medications.

Overt upper G.I. bleeding usually presents as melena or hematemesis but can also present is hematochezia in cases of brisk bleeding.

The incidence of major bleeding found to be 1%, with 325 mg/dL or less of aspirin alone, 0.85% with clopidogrel alone, 1.7% with aspirin plus clopidogrel and 2.5% with warfarin alone in a pooled analysis of published data (Usman MH et al).

Recurrence rate of UGI bleeding in patients who continue to take aspirin after an episode of peptic ulcer disease-related bleeding can reach 300 per 1000 person years and can vary with a patient’s age, gender, and use of nonsteroidal anti-inflammatory agents.

In bleeding peptic ulcer disease an infusion of a high dose of proton pump inhibitor after hemostasis has been achieved during endoscopy reduces recurrent bleeding and improved outcomes.

Endoscopy performed within six hours, rather than between 6-24 hours does not reduce mortality among patients in stable condition who were hospitalized with acute upper G.I. bleeding and who were assessed is having a high risk of further bleeding and death (Lau JY).

The initial evaluation of the patient when suspected of the G.I. bleed begins with assessment of the hemodynamic status, identification of potential risk factors, and appropriate triage of level of care.

After the resuscitation measures are in place, endoscopic evaluation can be performed to diagnose and potentially treat the source of bleeding.

Clot formation over arterial bleeding is pH dependent.

Gastric pH above 6 is critical for platelet aggregation.

When proton pump inhibitors are given at high dose and intravenously can maintain a neutral gastric pH.

Optimal acid suppression facilitates clot formation over bleeding arterial peptic ulcers.

Low dose aspirin, in patients at low risk for gastrointestinal complications, increases the risk of major non-variceal upper G.I. bleeding by 1.5-3.2 fold and an absolute rate increase of 0.12% per year (Laine L).

A meta-analysis found the rate of UGI bleeding associated with aspirin use at doses less than 100 mg daily to be 1.1%, at doses 100-325 mg per day to be 2.4%, and doses greater than 325 mg to be 2.5% (Serebruany VJ et al).

Risk of gastrointestinal bleeding with aspirin increases with prior peptic ulcer disease, age greater than 70 years, concomitant use of clopidogrel, anticoagulants, corticosteroids, and nonsteroidal anti-inflammatory drugs.

Arterial venous malformations, which are typically benign, can on enlargement result in a clinically significant upper G.I. bleed.

Other causes of upper G.I. bleed including gastric antral vascular changes, Mallory-Weiss tears, dieulafor lesions, portal hypertension, esophageal, gastric, and duodenal malignancies.

Coadministration of low dose aspirin and a PPI for prevention of cardiovascular events results in fewer lifetime upper G.I. bleeding events (3.4% vs. 7.2%) and fewer recurrent myocardial infarctions (26 fewer events per 10,000 patients), and an additional 38 days of life for patient compared with aspirin alone (Saini SD et al).

Clopidogrel use increases the odds ratio for developing an upward G.I. bleed by 1.3, which is less than that of associated with aspirin.

Among patients with a history of G.I. bleeding. Approximately 22% develop bleeding while taking clopidogrel in the following year (Cryer B , Ng FH, et al).

The risk of bleeding associated with clopidogrel is greatest in the first year.

Adjusted rate ratio for G.I. bleeding for patients receiving warfarin was 1.98 and when administered with aspirin was 6.48 (Delaney JA et al).

Among patients on oral anticoagulant treatment-apixaban, dabigatran, rivaroxaban, or warfarin with or without PPI therapy: upper gastrointestinal bleeding was the highest in patients prescribed rivaroxaban and lowest in patients prescribed apixaban, and bleeding was lower among patients receiving PPI cotherapy.

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