Mitchell C. Sokolosky
EPIDEMIOLOGY
Acute upper gastrointestinal (UGI) bleeding.
Lower GI bleeding has an annual incidence of 20 per 100,000.
Both upper GI bleeding and lower GI bleeding are more common in males and the elderly.
PATHOPHYSIOLOGY
UGI bleeding originates proximal to the ligament of Treitz.
Peptic ulcer disease is the commonest cause of UGI bleeding followed by erosive gastritis and esophagitis, esophageal and gastric varices, and Mallory–Weiss tear.
Predisposing factors for UGI bleeding include alcohol, salicylates, and NSAIDs.
The most common cause of lower GI bleeding is diverticular disease, followed by colitis, adenomatous polyps, and malignancies.
Lower GI bleeding may be due to an UGI source 10% to 14% of the time.
It is estimated that 80% of lower GI bleeding will resolve spontaneously.
CLINICAL FEATURES
Most patients will volunteer complaints of hematemesis (UGI source), hematochezia (bright red or maroon-colored bleeding usually from lower GI source), or melena (dark or black stools usually from UGI source).
Hypotension and tachycardia suggests severe bleeding.
Some patients will have more subtle presentations of hypotension, tachycardia, angina, syncope, weakness, and confusion.
Vomiting and retching followed by hematemesis is suggestive of a Mallory–Weiss tear.
A history of aortic graft should suggest the possibility of an aortoenteric fistula.
Spider angiomata, palmar erythema, jaundice, and gynecomastia suggest underlying liver disease.
Weight loss and changes in bowel habits are classic symptoms of malignancy.
DIAGNOSIS AND DIFFERENTIAL
The diagnosis may be obvious with the finding of hematemesis, hematochezia, or melena.
A careful ear, nose, and throat (ENT) examination can exclude swallowed blood as a source.
A rectal examination is mandatory to detect the presence of blood, its appearance (bright red, maroon, or melanotic), and the presence of masses.
Ingestion of iron or bismuth can simulate melena, and certain foods such as beets can simulate hematochezia; however, stool guaiac testing will be negative.
Nasogastric (NG) tube placement may have both diagnostic (identify occult UGI source and assess for ongoing active bleeding) and therapeutic (prepare patient for endoscopy) benefits. A negative NG aspirate does not conclusively exclude a UGI source of bleeding. Concerns that NG tube passage may provoke bleeding in patients with varices are unwarranted.
Guaiac testing of NG aspirate can yield both false-negative and false-positive results. Most reliable is gross inspection of the aspirate for bloody, maroon, or coffee-ground appearance, reserving guaiac testing to confirm that what appears to be blood actually is blood.
In patients with significant GI bleeding, the most important laboratory test is the type and crossmatch of blood.
Other important tests include a complete blood count, blood urea nitrogen (BUN), creatinine, electrolytes, glucose, coagulation studies, and liver function tests. The initial hematocrit level often will not reflect the actual amount of blood loss. UGI bleeding may elevate the BUN.
UGI endoscopy is the diagnostic study of choice in the evaluation of UGI bleeding.
Where available, angiography should be considered for the evaluation (detect site of bleeding) and management (embolization or infusion of vasoactive substances) of cases of severe lower GI bleeding.
Scintigraphy has been used to localize the site of bleeding in obscure hemorrhage.
Endoscopy is more accurate than angiography or scintigraphy, but the timing of colonoscopy is controversial for lower GI bleeding.
Multidetector CT’s role in the emergent evaluation of lower GI bleeding remains in evolution.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Emergency stabilization of the airway, breathing, and circulation takes priority.
Oxygen, large-bore IVs, and monitors should be applied. Immediately replace volume loss with IV crystalloids.
The decision to start blood should be based on clinical factors (continued active bleeding and no improvement in perfusion after infusion of 2 L of crystalloids) rather than initial hematocrit.
An NG tube should be placed in all patients with significant bleeding, regardless of presumed source. Room temperature water is the preferred irrigant for gastric lavage if performed.
Where available, early therapeutic endoscopy should be considered the treatment of choice for significant UGI bleeding. Endoscopic therapeutic interventions include injection therapy, coaptive therapy, endoscopic clips, and band ligation.
Proton pump inhibitors should be considered for the treatment of bleeding peptic ulcers. Pantoprazole and esomeprazole, 80 milligram IV bolus followed by 8 milligram/h infusion, or lansoprazol, 60 milligram IV bolus followed by 6 milligram/h infusion, may be used.
Octreotid, 25 to 50 microgram IV bolus followed by 25 to 50 microgram/h infusion, may be considered for patients with uncontrolled UGI bleeding awaiting endoscopy or when endoscopy is unsuccessful, con-traindicated, or unavailable.
Histamine-2 antagonists are not beneficial in acute GI bleeding.
Balloon tamponade with the Sengstaken-Blakemore tube or its variants can control documented variceal hemorrhage, but because of adverse reactions, it should be considered only a temporizing measure until therapeutic endoscopy.
Emergency surgical intervention may be necessary with patients who do not respond to medical or endoscopic therapy.
Patients with significant GI hemorrhage will require hospital admission and early referral to an endoscopist.
Clinical features predicting adverse outcomes include initial hematocrit <30%, initial systolic BP <100 mm Hg, red blood in the NG lavage, history of cirrhosis or ascites on examination, and a history of vomiting red blood.
For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed., see Chapter 78, “Upper Gastrointestinal Bleeding,” by David T. Overton, and Chapter 79, “Lower Gastrointestinal Bleeding,” by Bruce M. Lo.