Emergency Medicine

Gastrointestinal Bleeding

Which are the most common etiologies in GI bleeding? What does the presence or absence of abdominal pain suggest when bleeding is suspected? Which bleeding patients are candidates for transfusion? These and other questions are addressed.

By Neera Khilnani, MD, and Nasir Hussain, MD

Gastrointestinal (GI) bleeding is a common problem that carries a mortality rate of 5% to 10%, depending on the site, severity, etiology, and underlying risk factors. That mortality rate has not changed over the past 50 years, despite diagnostic and therapeutic advances. In general, GI bleeding is twice as common in males, and the incidence increases with age. Evaluation of GI bleeding involves assessing hemodynamic stability, resuscitating the patient as needed, locating the source of the bleed, and treating the underlying cause.

Who is at risk for developing a GI bleed?

Several predisposing factors have been identified, including a history of a GI bleed and the use of aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, anticoagulants, alcohol, and cigarettes. Alterations of the GI mucosa, such as in esophagitis, gastric or duodenal ulcers, polyps, diverticuli, inflammatory bowel disease, colitis, and prior intestinal anastomosing surgeries, must also be considered. Additional risk factors include vascular abnormalities, such as esophageal, gastric, and intestinal varices seen in cirrhosis, and hemorrhoids, angiodysplasia, and other vascular malformations such as hereditary hemorrhagic telangiectasias. Coagulopathies, anal fissures, and GI malignancies may also predispose to GI bleeding.

What are the common etiologies of GI bleeding?

Etiologies of GI bleeding can originate in either the upper GI tract (proximal to the ligament of Treitz) or lower tract. However, upper GI bleeding is four times more common than lower GI bleeds.

Peptic ulcer disease secondary to Helicobacter pylori, NSAID use, increased gastric or duodenal acidity, or stress is a common cause of upper GI bleeding, accounting for 25% to 50% of cases. Esophageal or gastric varices that develop from sustained portal hypertension may be responsible for up to 15% of upper GI bleeds. Arteriovenous malformations, Mallory-Weiss tears, and tumors account for 5% each. DieulafoyÍs lesion, which may be congenital, is only responsible for 1% of upper GI bleeds.

Lower GI bleeds, by anatomic definition, originate distal to the ligament of Treitz. Diverticulitis and angiodysplasia, which account for 30% and 8% of lower GI bleeds, respectively, are more prevalent in patients over age 65, whereas hemorrhoidal bleeding (5% of lower GI bleeds) is more common in patients under age 50. Colitis (from ischemic, post-radiation, or infectious causes) and polyps or malignancies each account for approximately 18% of lower GI bleeds.

Intussusception and Meckel’s diverticulum are more common in the pediatric population but must still be considered when the more common etiologies of lower GI bleeding have been excluded. In approximately 15% of cases, the etiology of lower GI bleeding is never identified.

What is the clinical presentation of a GI bleed?

Initial presentation depends on the rate of bleeding. Patients may lose a significant amount of blood before GI bleeding is revealed as hematemesis, melena, or hematochezia. The patient may present with dizziness, syncope, or symptoms of shock due to hemodynamic compromise. The physical exam may reveal a change in mental status, clammy skin, tachycardia, dyspnea, or hypotension.

Upper GI bleeding usually presents with hematemesis (of frank blood or digested "coffee-ground" blood) or melena. Rarely, a massive upper GI bleed with a rapid transit time can present as hematochezia rather than melena. Hematemesis that accompanies melena, as seen in almost 50% of upper GI bleeds, implies a large, brisk bleed. In patients with underlying coronary artery disease, initial presentation may be a coronary event precipitated by severe anemia or hemodynamic compromise.

Slower upper GI bleeds may present with weakness and malaise, dyspnea on exertion, angina, and other nonspecific symptoms. Physical examination may find pallor, tachycardia, and possibly signs of heart failure. Blood work may show microcytic hypochromic anemia with a high red cell distribution width and a positive fecal occult blood test (FOBT). Fecal occult blood testing has a low sensitivity and low positive predictive value. For example, false positives may be seen if the patient has ingested red meat, turnips, or horseradish in the previous two to four days. Conversely, vitamin C ingestion may result in a falsely negative test.

Patients with lower GI bleeding may complain of hematochezia. Regardless of the FOBT result, a rectal exam is important to assess for the presence of hemorrhoids or anal fissures. Just as in upper GI bleeds, the rate of lower GI hemorrhaging determines the type and severity of symptoms on presentation.

Abdominal pain, which may be the chief complaint in patients diagnosed with any type of GI bleed, is not always a reliable sign. The presence of abdominal pain does not necessarily imply a bleed is occurring (low specificity), nor does it accurately localize the site of the bleed. Similarly, the absence of pain does not exclude the possibility of a bleed (low sensitivity). On the other hand, peritoneal signs elicited on physical examination of patients with GI bleeding warrant early surgical consultation.

What is the initial management of an acute GI bleed?

Regardless of the source, the first and most important initial step in managing a GI bleed is assessing hemodynamic stability. Patients should be immediately evaluated for signs and symptoms of shock, and those without overt tachycardia or hypotension must be examined for orthostatic hemodynamic changes. Hemodynamic instability or evidence of significant ongoing blood loss (active hematemesis, melena, or moderate hematochezia) are indications for admission to a critical care unit for more intensive monitoring.

Resuscitation in patients with GI bleeding includes placement of two large-bore (16- or 18-gauge) intravenous (IV) lines or a central venous line. Patients with hemodynamic compromise may require immediate volume expansion with blood transfusions and IV fluids. Vasopressors may be indicated in some patients if volume expansion alone does not stabilize their blood pressure. Pulse oximetry and an ECG may be indicated in patients with a history of pulmonary disease or coronary artery disease.

While unstable patients may require an early blood transfusion, all patients with GI bleeds should be typed and cross-matched in case they need a transfusion. Initial laboratory tests include hemoglobin and hematocrit, platelets, clotting times, and electrolytes. Initial hemoglobin and hematocrit levels may not reflect the severity of GI bleeding; frequent monitoring may be necessary.

After hemodynamic resuscitation, the physician must identify the source of the GI bleed. A complete history is very important here because it will help identify risk factors and possibly the source of the bleeding. For example, a patient taking NSAIDs may have upper GI bleeding due to erosive gastritis or an ulcer.

Urgent consultation with a gastroenterologist and surgeon is necessary, not only to identify the source of the bleeding but also, if necessary, to intervene to stop the bleeding.

What is the role of blood transfusions in GI bleeding?

In patients with hemodynamically significant bleeding, a blood transfusion is required for both volume expansion and adequate tissue perfusion and to increase the hematocrit level. In patients without hemodynamic compromise, the need for a transfusion will depend on the presence of symptoms of anemia and their severity, as well as comorbid conditions. Young patients who are at low risk for recurrent bleeding and do not have any significant comorbidities may tolerate even a severe degree of anemia; they may just need an iron supplement and frequent monitoring.

Patients with coronary artery disease or chronic lung disease may need a transfusion if their hematocrit level falls below 30%. However, patients with symptoms of anemia, such as lightheadedness, dyspnea, angina, or evidence of ischemia on an ECG, may need a transfusion even if their hematocrit is at the lower limit of normal, and should be managed accordingly. In patients who are at risk for recurrent bleeding, a transfusion may be necessary to keep the hematocrit level in an acceptable range in the event of any future bleeding. During an acute bleeding episode, patients with cirrhosis and a coagulopathy may require a transfusion of fresh frozen plasma in addition to packed red blood cells (RBCs). Likewise, patients with active GI bleeding and thrombocytopenia (platelet level below 50,000/µL) may require a transfusion of platelets as well as packed RBCs.

Each unit of packed RBCs contains a volume of 300 ml and should raise the patient’s hematocrit level by approximately three percentage points. Therefore, after a transfusion of one or more units of packed RBCs, the absence of an appropriate increase or any decrease in the hematocrit should immediately raise concern for ongoing hemorrhage. It should be recognized, however, that frequent blood draws for monitoring may also cause a drop in hematocrit.

Patients receiving massive blood transfusions (more than 50% of their blood volume over a 24-hour period) are at risk for dilution of their coagulation factors and platelets. Adults receiving more than eight units of packed RBCs are consequently predisposed to develop this dilutional coagulopathy; they should have their clotting times monitored and should be transfused accordingly with fresh frozen plasma. Similarly, thrombocytopenia should be corrected in patients receiving more than 10 units of packed RBCs. Patients receiving massive transfusions for GI bleeding are also at risk for hypocalcemia and hyperkalemia, which must be corrected.

Patients with slow GI bleeding may have chronic anemia and develop congestive heart failure over time as a consequence. Transfusions in such patients may result in volume overload, so small doses of a diuretic may be used in such cases.

Finally, a blood warmer should be used in any patient receiving more than three consecutive units of packed RBCs to avoid hypothermia.

Is there a benefit to nasogastric lavage for upper GI bleeding?

Nasogastric (or orogastric) lavage should be performed in patients with upper GI bleeding. Nasogastric lavage may be useful as a diagnostic technique. A bloody lavage may be helpful in predicting a high-risk lesion, particularly in hemodynamically stable patients without hematemesis; a clear lavage may be helpful in predicting low-risk lesions. Nasogastric lavage can also facilitate endoscopic visualization by clearing blood and other gastric contents. A negative lavage, however, does not exclude upper GI bleeding; the procedure carries a false negative rate of 10%. The bleeding in such cases may be intermittent or located in the duodenum. Aspiration of bilious, nonbloody material strongly indicates that no active duodenal bleeding is occurring.

Nasogastric lavage should be performed manually. Continuous suction may cause gastric mucosal injuries that can precipitate further bleeding and confound endoscopic determination of the etiology of an upper GI bleed.

Patients with active upper GI bleeding should be placed in the left lateral decubitus and Trendelenburg position, and a larger nasogastric tube (34 French) should be used for tap water irrigation to remove large blood clots. (There is no proven advantage to using either sterile water or normal saline over tap water.) Irrigation should always be performed after radiographic confirmation that no free air is present in the abdomen from a gastric or duodenal perforation and that the nasogastric tube is in the correct position.

Which medications are used to stabilize an acute GI bleed?

Proton pump inhibitors have become a mainstay in the pharmacologic treatment of upper GI bleeds due to peptic ulcer disease and should be given intravenously during acute bleeding. These drugs may be more efficacious than histamine-2 receptor blockers. Octreotide, a long-acting synthetic analog of somatostatin, reduces portal pressures and thus is helpful in the treatment of variceal bleeding in patients with cirrhosis. Vitamin K is also useful in these patients, whose risk of variceal bleeding is exacerbated by their underlying coagulopathy. Propranolol is helpful in reducing splanchnic and portal pressures and in preventing recurrent variceal bleeding in patients with elevated portal pressures. However, it should only be administered in patients who are hemodynamically stable. Approximately 20% of patients with upper GI bleeding have recurrent episodes. Recurrent bleeding is associated with increased mortality, greater need for surgery, and increased health care cost. Endoscopic findings indicating a higher risk for recurrent bleeding include arterial "spurting" hemorrhage, oozing hemorrhage, visible vessels, high number of ulcers, and large ulcer size. Patients with iron-deficiency anemia secondary to GI bleeding should receive iron supplementation when they are discharged from the hospital.

Which diagnostic and therapeutic procedures are useful in the management of GI bleeding?

Most causes of upper GI bleeding, such as Mallory-Weiss tears, gastric and duodenal ulcers, esophageal varices, and malignancies of the upper GI tract, can be identified by esophagogastroduodenoscopy (EGD). Colonoscopy is recommended for patients with lower GI bleeding and is often used in combination with EGD for patients with upper GI bleeding. Endoscopy has both diagnostic and therapeutic benefits. When bleeding vessels are identified, for example, endoscopic-mediated banding or injection with dilute epinephrine and other sclerosing agents can reduce bleeding.

Laser photocoagulation, bipolar electrocoagulation, and heater probe coagulation are often used in conjunction with injection therapy to maximize hemostasis. Capsule endoscopy may be utilized in the evaluation of obscure gastrointestinal bleeding, especially when the source is the small bowel.

Angiography can help visualize GI bleeding but requires active blood loss at a rate of 1 ml/min in order to be effective. Hence, angiography is highly specific but variably sensitive. Like endoscopy, angiography has both diagnostic and therapeutic advantages; patients can undergo simultaneous identification and embolization of bleeding vessels.

Radionucleotide scanning can detect slower bleeds (0.5 ml/min) and is less invasive and more sensitive than angiography. However, it is less specific than a positive endoscopic or angiographic finding. In general, for patients without contraindications to endoscopy, EGD or colonoscopy, or both, are preferred as first-line procedures over angiography and radionucleotide scanning. Patients who cannot be stabilized by these procedures should undergo surgery to localize and control bleeding.

Which patients with GI bleeding can be managed as outpatients?

Patients who present with mild hematemesis without clinical evidence of active bleeding and have a negative nasogastric lavage may be observed for six hours and discharged, but only if they are asymptomatic and hemodynamically stable, report no melena, have a hematocrit above 30%, have no history of varices or aortic surgery, and are under 60 years of age and otherwise healthy. However, they must agree to comply with early follow-up with an EGD. These patients should be discharged on proton-pump inhibitors or histamine-2 blockers and should abstain from alcohol and NSAIDs, at least until their follow-up appointment.

Patients with scant hematochezia whose etiology can be confirmed to be anal fissures or mild hemorrhoidal bleeding can also be considered for outpatient follow-up after observation, as long as the above criteria are satisfied.

What type of counseling and follow-up recommendations should a patient who has had a GI bleed receive?

Once a patient with a GI bleed is stabilized and the etiology has been identified and managed, it is important to educate the patient on his or her condition. Most patients who have been admitted to the hospital for GI bleeding should be reassessed as outpatients within a week after discharge. Pathology reports and other pending results should be followed up on at this time, and the patient’s hematocrit should be rechecked to confirm that no further bleeding is present. Reevaluation of medications should also be done at the follow-up visit. Finally, patients should be instructed to return to their physician or emergency department immediately if they suspect symptoms of GI bleeding are recurring.