Gastrointestinal Bleeding

Gastrointestinal (GI) bleeding can occur from many sources and can present acutely as a medical emergency or insidiously with evidence of anemia and iron deficiency. GI bleeding is a common condition encountered in both inpatient and outpatient settings and is the most common GI diagnosis associated with a hospital admission in the United States. In this section, we cover upper and lower sources of GI bleeding, including Helicobacter pylori infection and peptic ulcer disease.

Upper Gastrointestinal Bleeding

Upper gastrointestinal (GI) bleeding refers to bleeding from a GI source above the ligament of Treitz (i.e., the esophagus, stomach, or duodenum).

Presentation

• usual presentation: melena, hematemesis, and symptoms of anemia

• rapid blood loss: hematochezia (representing the rapid transit of blood in severe cases)

• extreme blood loss: features of hemorrhagic shock (e.g., syncope and tachycardia)

Causes

• peptic ulcer disease (PUD)

  • the most common cause of upper GI bleeding (30%-65% of cases)

  • often associated with H. pylori infection or use of nonsteroidal anti-inflammatory drugs (NSAIDs)

• gastritis, esophagitis, duodenitis

  • associated with gastroesophageal reflux disease (GERD), pill-induced esophagitis, aspirin/ NSAID use, alcohol use, infections

• varices (see Liver Cirrhosis for further detail)

• Mallory-Weiss tear

  • bleeding from a laceration in the mucosa at the gastroesophageal junction, usually preceded by vomiting or retching

• tumor

• aortoenteric fistula

• arteriovenous malformation

• Dieulafoy lesion (an aberrantly dilated and tortuous submucosal arteriole, usually found in the gastric mucosa although can affect any part of the GI tract)

• gastric antral vascular ectasia (GAVE)

  • also known as watermelon stomach, with columns of red, tortuous, ectatic vessels along longitudinal folds of the gastric antrum; associated with hepatic, renal, and cardiac diseases

• procedures

  • bleeding following endoscopic procedures (e.g., polypectomy)

Evaluation

When a patient presents to an emergency department with an upper GI bleed, scores such as the Glasgow-Blatchford score can be used for risk stratification of patients. A Glasgow-Blatchford score of 0 or 1 suggests low risk of complications (<1% risk of transfusion, hemostatic intervention, or death) and identifies patients who can be considered for discharge with outpatient management. The score comprises eight variables, described in the following table, that give an indication of hemodynamic stability, severity of blood loss, and comorbidities.

(Source: Upper Gastrointestinal Bleeding Due to a Peptic Ulcer. N Engl J Med 2016.)

Management

Major or significant nonvariceal upper GI bleeding is a medical emergency that requires evaluation in an emergency department or urgent care setting. For information on variceal upper GI bleeding, please see complications of cirrhosis.

Initial management: Key initial steps for management of upper GI bleeding include:

• assessing hemodynamic stability

• securing the airway if the patient is comatose, combative, or has massive hematemesis

• establishing intravenous (IV) access with two large-bore intravenous needles (≥18 gauge) to ensure adequate volume resuscitation

• performing basic laboratory investigations, including complete blood count, metabolic panel, coagulation profile, and type and crossmatch blood sample

• correcting coagulopathy as needed

• resuscitation with packed red blood cells (RBCs) if hemoglobin (Hg) <7 g/dL, patient is hemodynamically unstable, or both

  • Randomized trials indicate that a restrictive transfusion threshold (Hg 7 g/dL) is superior to a liberal threshold (9 g/dL) in patients with upper GI bleed; the restrictive threshold was associated with lower mortality and rebleeding rates than the liberal threshold. (Read the NEJM Journal Watch Summary.)

    • Red Blood Cell Transfusion guidelines from the Association for the Advancement of Blood and Biotherapies (AABB; updated in 2023) support a restrictive transfusion threshold.

    • Hemoglobin levels can take several hours to equilibrate after an episode of bleeding. If a patient is hemodynamically unstable, continuing to have large-volume bleeding, or both, transfusion should be directed to these clinical parameters and not to a specific hemoglobin threshold.

  • A threshold of 8 g/dL can be considered in patients with preexisting cardiovascular disease, based on limited evidence.

• Pre-endoscopic proton pump inhibitor (PPI) therapy is commonly administered in clinical practice. However, high-quality evidence is lacking that PPIs improve outcomes (e.g., rebleeding or mortality). Pre-endoscopic PPI therapy may reduce the need for endoscopic intervention during endoscopy.

• Post-endoscopy, high-dose PPI therapy is recommended in patients with ulcers to reduce further bleeding in both those with high-risk stigmata of bleeding treated with endoscopic therapy and those with adherent clots that could not be treated with endoscopic therapy.

  • In patients with endoscopically treated high-risk ulcers, outcomes (e.g., rebleeding and mortality) associated with post-endoscopy intermittent high-dose PPI therapy are comparable to outcomes of a bolus plus continuous PPI infusion.

Endoscopy and treatment: Patients who are hospitalized with significant upper GI bleeding should undergo endoscopy within 24 hours of adequate resuscitation and transfusion. Consider intravenous administration of a prokinetic agent (e.g., erythromycin) 20-90 minutes prior to endoscopy to empty the stomach of blood and improve visualization. The goal of the procedure is to use endoscopic measures to control bleeding. Endoscopic treatment differs based on endoscopic findings and includes the following:

• injection of the bleeding site with epinephrine in conjunction with another hemostatic modality

• injection of the bleeding site with absolute ethanol (sclerosant)

• thermal device application (cautery in form of bipolar electrocoagulation, heater probe) to the lesion

• argon plasma coagulation

• clips (through-the-scope and over-the-scope)

• hemostatic powder spray

Transcatheter arterial embolization is the next treatment option in patients who do not respond to endoscopic therapy.

Rebleeding: Recurrent bleeding should be treated with repeat endoscopic therapy.

• Other, less favored options include transcatheter arterial embolization or surgery.

• High-dose PPI therapy (defined as ≥80 mg/day) for ≥72 hours after endoscopic treatment of lesions that have high-risk characteristics (i.e., active bleeding, visible vessel, adherent clot) has been reported to reduce the risk of recurrent bleeding.

Long-term management varies based on the underlying etiology. The following diagram outlines suggested strategies:

(Source: Upper Gastrointestinal Bleeding Due to a Peptic Ulcer. N Engl J Med 2016.)

H. Pylori Infection and Peptic Ulcer Disease

• H. pylori is a common cause of peptic ulcer disease (PUD) worldwide; treatment to eradicate H. pylori can reduce the risk of developing PUD and dyspepsia.

• H. pylori infection is also associated with other complications, including gastric cancer and lymphoma, iron-deficiency anemia (unrelated to PUD), and immune thrombocytopenia.

• In patients with an indication for endoscopy, direct histologic testing of gastric antral biopsies with special stains for H. pylori should be performed.

• The American College of Gastroenterology (ACG) recommends noninvasive testing with either a stool antigen or urea breath test in patients with conditions associated with H. pylori but no indication for endoscopy. Testing should be performed with patients off PPI therapy for a minimum of two weeks because acid suppression may lead to false negative results. The ACG does not recommend serologic testing for H. pylori antibodies.

• Treatment of H. pylori typically involves a combination of two or three antibiotics and a PPI. Common regimens are outlined in the following table:

(Source: Helicobacter pylori Infection. N Engl J Med 2019.)

Lower Gastrointestinal Bleeding

Approximately 30%-40% of GI bleeds occur in the lower GI tract, which was historically defined as anywhere distal to the ligament of Treitz but now generally refers to bleeding from the colon (small-bowel bleeding is considered a different entity). Patients with acute lower GI bleeding usually present with hematochezia (bright-red blood through the rectum), although melena is a less common presentation if the bleeding is slow or intermittent. Hemodynamic instability associated with hematochezia may indicate a brisk upper GI bleed.

Causes

• Common causes of lower GI bleeding include diverticulosis, ischemic colitis, hemorrhoids, colorectal polyps and neoplasms, and colonic angioectasias.

• Rarer causes include colitis (inflammatory, infectious, radiation-related), post-polypectomy bleeding, rectal or stercoral ulcers, Dieulafoy lesions, colorectal varices, and NSAID-induced colopathy.

Management

Initial management: Initial management of lower GI bleeding is similar to initial management of upper GI bleeding as discussed above and involves clinical assessment and initiation of treatment to stabilize hemodynamic status. Risk stratification can be performed using the Oakland Score to identify patients who may be appropriate for early discharge and outpatient diagnostic evaluation.

Diagnosis and treatment:

• Nonemergent colonoscopy is recommended during hospitalization. Previously, colonoscopy was recommended within 24 hours of presentation, but this has not been shown to improve clinical outcomes. However, colonoscopy during the same admission may not be necessary if bleeding resolves and a high-quality colonoscopy with adequate bowel prep has been performed within the past 12 months showing diverticulosis with no colorectal neoplasia.

• Upper endoscopy should be considered in patients with hematochezia and hemodynamic instability, as brisk upper GI bleeding can present as hematochezia.

• Noninvasive imaging techniques (e.g., computed tomographic angiography [CTA] and radionuclide technetium-99m-labeled red-cell scintigraphy) can be used to identify the potential bleeding source, but they are only diagnostic if active bleeding is present at the time of the test. CTA should be considered as the initial diagnostic test in patients with ongoing hemodynamically significant hematochezia. If active extravasation is encountered, then prompt interventional radiology consultation is recommended for consideration of arteriography and possible embolization.

  

  (Source: Acute Lower Gastrointestinal Bleeding. N Engl J Med 2017.)

• Angiography and endovascular therapy can be used to identify the bleeding source and provide therapeutic interventions in patients in whom endoscopy is not successful or practical. These therapies should be considered in patients with persistent bleeding or hemodynamic instability despite resuscitative efforts.

  

  (Source: Acute Lower Gastrointestinal Bleeding. N Engl J Med 2017.)

• Other treatment options: If no source of bleeding is identified with the techniques described above, other options include:

  • push enteroscopy/balloon enteroscopy to evaluate the small bowel

  • capsule endoscopy

  • surgery, in the rare instance when a patient is exsanguinating, and an urgent subtotal colectomy is required

• Management of patients on anticoagulation and antiplatelets:

  • A reversal agent (e.g., vitamin K, prothrombin complex concentrate, or fresh frozen plasma) should be given to unstable patients on warfarin; otherwise, warfarin should be withheld.

    • Reversal of direct oral anticoagulants (e.g., dabigatran, rivaroxaban) is rarely needed but should be considered in a life-threatening bleed that does not respond to cessation of anticoagulant and resuscitation.

  • NSAIDs should be stopped after hospitalization for diverticular hemorrhage.

  • Discontinuation of low-dose aspirin for primary prevention of cardiovascular events should be considered. Patients who are on aspirin for secondary prevention of cardiovascular events should continue on aspirin.

  • Multidisciplinary consensus should be sought for continuation of nonaspirin antiplatelet agents such as clopidogrel.

  • Anticoagulation should be resumed after cessation of lower GI bleeding, as it has been shown to decrease the risk of post-bleeding thromboembolism and mortality.