upper gastrointestinal bleeding

Acute Upper Gastrointestinal Bleeding

Acute Upper Gastrointestinal Bleeding

The most common presentation of upper gastrointesti­nal bleeding is hematemesis or melena. Hematemesis may be either bright red blood or brown “coffee grounds” mate­rial. Melena develops after as little as 50–100 mL of blood loss in the upper gastrointestinal tract, whereas hemato­chezia requires a loss of more than 1000 mL. Although hematochezia generally suggests a lower bleeding source (eg, colonic), severe upper gastrointestinal bleeding may present with hematochezia in 10% of cases.

Upper gastrointestinal bleeding is self-limited in 80% of patients; urgent medical therapy and endoscopic evalua­tion are obligatory in the rest. Patients with bleeding more than 48 hours prior to presentation have a low risk of recurrent bleeding.

Causes

Acute upper gastrointestinal bleeding may originate from a number of sources. These are listed in order of their fre­quency and discussed in detail below.

Peptic Ulcer Disease: Peptic ulcers account for 40% of major upper gastrointesti­nal bleeding with an overall mortality rate of less than 5%. In North America, the incidence of bleeding from ulcers is declining due to eradication of H pylori and prophylaxis with proton pump inhibitors in high-risk patients.

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Portal Hypertension: Portal hypertension accounts for 10–20% of upper gastro­intestinal bleeding. Bleeding usually arises from esopha­geal varices and less commonly gastric or duodenal varices or portal hypertensive gastropathy. Approximately 25% of patients with cirrhosis have medium to large esophageal varices, of whom 30% experience acute variceal bleeding within a 2-year period. Due to improved care, the hospital mortality rate has declined over the past 20 years from 40% to 15%. Nevertheless, a mortality rate of 60–80% is expected at 1–4 years due to recurrent bleeding or other complica­tions of chronic liver disease.

Mallory-Weiss Tears: Lacerations of the gastroesophageal junction cause 5–10% of cases of upper gastrointestinal bleeding. Many patients report a history of heavy alcohol use or retching. Less than 10% have continued or recurrent bleeding.

Vascular Anomalies: Vascular anomalies are found throughout the gastrointesti­nal tract and may be the source of chronic or acute gastro­intestinal bleeding. They account for 7% of cases of acute upper tract bleeding. The most common are angioectasias (angiodysplasias) which are 1–10 mm distorted, aberrant submucosal vessels caused by chronic, intermittent obstruction of submucosal veins. They have a bright red stellate appearance and occur throughout the gastrointestinal tract but most commonly in the right colon. Telangiectasias are small, cherry red lesions caused by dilation of venules that may be part of systemic conditions (hereditary hemor­rhagic telangiectasia, CREST syndrome) or occur sporadi­cally. The Dieulafoy lesion is an aberrant, large-caliber submucosal artery, most commonly in the proximal stom­ach that causes recurrent, intermittent bleeding.

Gastric Neoplasms: Gastric neoplasms result in 1% of upper gastrointestinal hemorrhages.

Erosive Gastritis: Because this process is superficial, it is a relatively unusual cause of severe gastrointestinal bleeding (less than 5% of cases) and more commonly results in chronic blood loss. Gastric mucosal erosions are due to NSAIDs, alcohol, or severe medi­cal or surgical illness (stress-related mucosal disease).

Erosive Esophagitis: Severe erosive esophagitis due to chronic gastroesophageal reflux may rarely cause significant upper gastrointestinal bleeding, especially in patients who are bed bound long-term.

Others: An aortoenteric fistula complicates 2% of abdominal aortic grafts or, rarely, can occur as the initial presentation of a previously untreated aneurysm. Unusual causes of upper gastrointestinal bleeding include hemobilia (from hepatic tumor, angioma, penetrating trauma), pancreatic malig­nancy, and pseudoaneurysm (hemosuccus pancreaticus).

Examination

It is critical to assess the patient’s haemodynamic status by measuring heart rate, blood pressure and postural changes. In haemodynamically compromised patients a fall in blood pressure may follow only a minor change in posture, for example from lying flat to sitting at a 450 incline. Variceal haemorrhage is more likely if stigmata of chronic liver disease are present, particularly if there is evidence of portal hypertension, for example ascites and splenomegaly. An ulcer may cause epigastric tenderness. Digital rectal examination is important to confirm the presence of true melaena.

Investigations

Haemoglobin needs to be measured in all patients but may initially underestimate true blood loss, due to delayed haemodilution of the vascular space. Blood should be sent urgently to transfusion services for cross-matching. Other important tests include platelet count, urea:creatinine ratio, coagulation indices and liver function tests including albumin. Patients with end stage liver disease may have normal liver enzymes, yet have impaired synthetic liver function as evidenced by low albumin, or reduced clotting factors.

Treatment

Early upper endoscopy (within 24 hours of presentation) is recommended in most patients with upper gastrointestinal bleeding because it confirms the diagnosis and allows for targeted endoscopic treatment, resulting in reduced morbidity, hospital stays, risk of recurrent bleeding, and need for surgery.

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Although prokinetic agents to evacuate the stomach are not recommended, gastric lavage is commonly performed to clear the stomach of blood, increasing the success of endoscopic localization of the source of bleeding. Endoscopic therapies include epinephrine injection, thermocoagulation, application of clips, and banding.

Patients with low-risk peptic ulcer bleeding (e.g., clean ulcer base) based on clinical and endoscopic criteria can be safely discharged on the same day as endoscopy. Most patients with high-risk peptic ulcer bleeding and stigmata of recent hemorrhage (e.g., active arterial bleeding, visible vessel, adherent clot) who have undergone endoscopic hemostasis should receive intravenous proton pump inhibitor (PPI) therapy and remain hospitalized for at least 72 hours because most rebleeding occurs in this time.

Use of H2 receptor antagonists is not recommended for patients with upper gastrointestinal bleeding.

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