Gastrointestinal bleeding

Incidence rises with age and among older patients may occur at a rate of nearly 1% per year.

Incidence of upper gastrointestinal complications of perforation or bleeding in the general population is approximately 1 case per 1000 person-years, with a case fatality rate of 5-10%.

The risk of major gastrointestinal bleeding nearly doubles with each decade of age, even without the use of aspirin.

In approximately 5% of all patients with gastrointestinal bleeding and anemia, standard evaluation with esophagogastroduodenoscopy and colonoscopy will not reveal a specific bleeding site. The source of bleeding in these patients is most often the small intestine.

The site of gastrointestinal bleeding between the second portion of the duodenum and the ileocecal valve is only 3-5% of patients with gastrointestinal bleeding.

Men have an approximately 50% higher risk of hospitalization for gastrointestinal bleeding than women.

Angiodysplasia is the most common cause of bleeding in the small intestine, accounting for 70-80% of cases.

Small intestinal angiodysplasia is a vascular abnormality, characterized by focal accumulation of ectatic vessels in the mucusa and submucosa,  and is a recognized cause of repeat obscure G.I. bleeding and iron deficiency anemia.

It is the most common cause of bleeding in the small intestine, especially among patients older than 50 years of age.

Small bowel angiodysplasia bleeding strategies for treatment include angiographic embolization, local ablation with the use of endoscopic techniques or surgical resection,  it recurrent bleeding is common and may result in complications, including death.

The use of thalidomide results in the reduction of bleeding in patients with the recurrent bleeding due to small intestinal angiodysplasia.iu

Optimal acid suppression improves clot formation over bleeding arteries in peptic ulcer disease, and endoscopy in bleeding peptic ulcer patients reveals fewer active bleeding cases among those receiving omeprazole than among those receiving placebo.

Early use of high dose omeprazole decreases the need for endoscopic therapy in upper gastrointestinal bleeding.

Use of omeprazole accelerates the resolution of bleeding signs and is associated with peptic ulcerations with cleaner bases than placebo treated patients.

In a placebo controlled trial by Khuroo recurrent bleeding less frequent in patients with nonbleeding visible vessels and clots given oral omperazole than those given placebo, suggesting acid suppression confers clot stability among patients with ulcers.

With upper gastrointestinal bleeding early endoscopy, within 24 hours, is the standard of care in most hospitals.

Early endoscopy involving therapy in upper gastrointestinal bleeding in selected high risk patients stops bleeding and potentially saves lives.

Early upper gastrointestinal endoscopy permits low risk patients to be discharged early from the hospital.

Patients with G.I. bleeding may benefit by the use of fewer blood transfusions, because this results in lower portal blood pressure and less recurrent bleeding: perhaps due to a thrombus plug that is not disrupted by higher blood pressures.

For upper gastrointestinal hemorrhage high dose intravenous omperazole is recommended preemptively for patients awaiting endoscopy.

Lower G.I. bleeding common cause of hospitalization occurring with an annual incidence of 20-30 cases per hundred thousand people.

In hospital mortality associated with lower G.I. bleeding is approximately 4%.

Mortality from lower G.I. bleeding is primarily related to advanced age, ischemia, and the presence of multiple comorbidities.

Retrospective studies of colon bleeding suggest the rates of recurrent bleeding and mortality within one year fis 19 and 4 .2%, respectively.

Anticoagulation, and active malignancy are risk factors for 30 day readmission’s in patients hospitalized with lower gastrointestinal bleeding.

G.I. bleeding affects an estimated 4.5% of patients treated with warfarin annually, and is associated with a significant increase in the risk of death.

Not resuming warfarin therapy in the 90 days following a G.I. bleed associated with an increased risk of thrombosis and death (Witt DM et al).

In a study of 442 patients resumption of warfarin after a G.I. bleed was associated with lower adjusted risk for thrombosis, and death, without significantly increasing the risk for recurrent GI bleeding: Suggesting that for many patients who have experienced G.I. bleeding in the presence of warfarin the benefits of resuming such therapy outweigh the risks. (Witt DM et,al).

Interruption of warfarin therapy associated with increased risk of thrombosis and death with atrial fibrillation (Raunso J et al).

Occurs in 4-8% of patients treated with warfarin annually.

In the setting of gastrointestinal bleeding with supratherapeutic INR levels, and concomitant antiplatelet therapy, upper G.I. endoscopy within 12 hours of presentation predicted identification of bleeding source.

In the above sitting however the likelihood of finding a significant lesions falls to less than 20% when INR was greater than 7.5.


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