Gastrointestinal Bleeding: A Merck Manual of Patient Symptoms podcast
GI bleeding can originate anywhere from the mouth to the anus and can be overt or occult. The manifestations depend on the location and rate of bleeding.
Hematemesis is vomiting of red blood and indicates upper GI bleeding, usually from an arterial source or varix. Coffee-ground emesis is vomiting of dark brown, granular material that resembles coffee grounds. It results from upper GI bleeding that has slowed or stopped, with conversion of red Hb to brown hematin by gastric acid.
Hematochezia is the passage of gross blood from the rectum and usually indicates lower GI bleeding but may result from vigorous upper GI bleeding with rapid transit of blood through the intestines.
Melena is black, tarry stool and typically indicates upper GI bleeding, but bleeding from a source in the small bowel or right colon may also be the cause. About 100 to 200 mL of blood in the upper GI tract is required to cause melena, which may persist for several days after bleeding has ceased. Black stool that does not contain occult blood may result from ingestion of iron, bismuth, or various foods and should not be mistaken for melena.
Chronic occult bleeding can occur from anywhere in the GI tract and is detectable by chemical testing of a stool specimen. Acute, severe bleeding also can occur from anywhere in the GI tract. Patients may present with signs of shock. Patients with underlying ischemic heart disease may develop angina or MI because of coronary hypoperfusion.
GI bleeding may precipitate portosystemic encephalopathy (see Portosystemic Encephalopathy) or hepatorenal syndrome (kidney failure secondary to liver failure—see Renal and Electrolyte Abnormalities).
There are many possible causes (see see Common Causes of GI Bleeding), which are divided into upper GI (above the ligament of Treitz), lower GI, and small bowel.
Bleeding of any cause is more likely, and potentially more severe, in patients with chronic liver disease (eg, caused by alcohol abuse or chronic hepatitis), in those with hereditary coagulation disorders, or in those taking certain drugs. Drugs associated with GI bleeding include anticoagulants (eg, heparin, warfarin), those affecting platelet function (eg, aspirin and certain other NSAIDs, clopidogrel, SSRIs), and those affecting mucosal defenses (eg, NSAIDs).
|Common Causes of GI Bleeding
Upper GI tract
Gastric or duodenal erosions (20–30%)
Mallory-Weiss tear (5–10%)
Erosive esophagitis (5–10%)
Arteriovenous malformations (< 5%)
Gastrointestinal stromal tumors
Lower GI tract (percentages vary with the age group sampled)
Angiodysplasia (vascular ectasia)
Colitis: Radiation, ischemic, infectious
Inflammatory bowel disease: Ulcerative proctitis/colitis, Crohn disease
Small-bowel lesions (rare)
Stabilization with airway management, IV fluids, or transfusions is essential before and during diagnostic evaluation.
History of present illness should attempt to ascertain quantity and frequency of blood passage. However, quantity can be difficult to assess because even small amounts (5 to 10 mL) of blood turn water in a toilet bowl an opaque red, and modest amounts of vomited blood appear huge to an anxious patient. However, most can distinguish between blood streaks, a few teaspoons, and clots.
Patients with hematemesis should be asked whether blood was passed with initial vomiting or only after an initial (or several) nonbloody emesis.
Patients with rectal bleeding should be asked whether pure blood was passed; whether it was mixed with stool, pus, or mucus; or whether blood simply coated the stool. Those with bloody diarrhea should be asked about travel or other possible exposure to GI pathogens.
Review of symptoms should include presence of abdominal discomfort, weight loss, easy bleeding or bruising, previous colonoscopy results, and symptoms of anemia (eg, weakness, easy fatigability, dizziness).
Past medical history should inquire about previous GI bleeding (diagnosed or undiagnosed); known inflammatory bowel disease, bleeding diatheses, and liver disease; and use of any drugs that increase the likelihood of bleeding or chronic liver disease (eg, alcohol).
General examination focuses on vital signs and other indicators of shock or hypovolemia (eg, tachycardia, tachypnea, pallor, diaphoresis, oliguria, confusion) and anemia (eg, pallor, diaphoresis). Patients with lesser degrees of bleeding may simply have mild tachycardia (heart rate > 100). Orthostatic changes in pulse (a change of > 10 beats/min) or BP (a drop of ≥ 10 mm Hg) often develop after acute loss of ≥ 2 units of blood. However, orthostatic measurements are unwise in patients with severe bleeding (possibly causing syncope) and generally lack sensitivity and specificity as a measure of intravascular volume, especially in elderly patients.
External stigmata of bleeding disorders (eg, petechiae, ecchymoses) are sought, as are signs of chronic liver disease (eg, spider angiomas, ascites, palmar erythema) and portal hypertension (eg, splenomegaly, dilated abdominal wall veins).
A digital rectal examination is necessary to search for stool color, masses, and fissures. Anoscopy is done to diagnose hemorrhoids. Chemical testing of a stool specimen for occult blood completes the examination if gross blood is not present.
Several findings suggest hypovolemia or hemorrhagic shock:
Interpretation of findings:
The history and physical examination suggest a diagnosis in about 50% of patients, but findings are rarely diagnostic and confirmatory testing is required.
Epigastric abdominal discomfort relieved by food or antacids suggests peptic ulcer disease. However, many patients with bleeding ulcers have no history of pain. Weight loss and anorexia, with or without a change in stool, suggest a GI cancer. A history of cirrhosis or chronic hepatitis suggests esophageal varices. Dysphagia suggests esophageal cancer or stricture. Vomiting and retching before the onset of bleeding suggests a Mallory-Weiss tear of the esophagus, although about 50% of patients with Mallory-Weiss tears do not have this history.
A history of bleeding (eg, purpura, ecchymosis, hematuria) may indicate a bleeding diathesis (eg, hemophilia, hepatic failure). Bloody diarrhea, fever, and abdominal pain suggest ischemic colitis, inflammatory bowel disease (eg, ulcerative colitis, Crohn disease), or an infectious colitis (eg, Shigella, Salmonella, Campylobacter, amebiasis). Hematochezia suggests diverticulosis or angiodysplasia. Fresh blood only on toilet paper or the surface of formed stools suggests internal hemorrhoids or fissures, whereas blood mixed with the stool indicates a more proximal source. Occult blood in the stool may be the first sign of colon cancer or a polyp, particularly in patients > 45 yr.
Blood in the nose or trickling down the pharynx suggests the nasopharynx as the source. Spider angiomas, hepatosplenomegaly, or ascites is consistent with chronic liver disease and hence possible esophageal varices. Arteriovenous malformations, especially of the mucous membranes, suggest hereditary hemorrhagic telangiectasia (Rendu-Osler-Weber syndrome). Cutaneous nail bed and GI telangiectasia may indicate systemic sclerosis or mixed connective tissue disease.
Several tests are done to help confirm the suspected diagnosis.
CBC should be obtained in patients with large-volume or occult blood loss. Patients with more significant bleeding also require coagulation studies (eg, platelet count, PT, PTT) and liver function tests (eg, bilirubin, alkaline phosphatase, albumin, AST, ALT). Type and cross-match are done if bleeding is ongoing. Hb and Hct may be repeated up to every 6 h in patients with severe bleeding. Additionally, one or more diagnostic procedures are typically required.
Nasogastric aspiration and lavage should be done in all patients with suspected upper GI bleeding (eg, hematemesis, coffee-ground emesis, melena, massive rectal bleeding). Bloody nasogastric aspirate indicates active upper GI bleeding, but about 10% of patients with upper GI bleeding have no blood in the nasogastric aspirate. Coffee-ground material indicates bleeding that is slow or stopped. If there is no sign of bleeding, and bile is returned, the NGT is removed; otherwise, it is left in place to monitor continuing or recurrent bleeding. Nonbloody, nonbilious return is considered a nondiagnostic aspirate.
Upper endoscopy (examination of the esophagus, stomach, and duodenum) should be done for upper GI bleeding. Because endoscopy may be therapeutic as well as diagnostic, it should be done rapidly for significant bleeding but may be deferred for 24 h if bleeding stops or is minimal. Upper GI barium x-rays have no role in acute bleeding, and the contrast used may obscure subsequent attempts at angiography. Angiography is useful in the diagnosis of upper GI bleeding and permits certain therapeutic maneuvers (eg, embolization, vasoconstrictor infusion).
Flexible sigmoidoscopy and anoscopy may be all that is required acutely for patients with symptoms typical of hemorrhoidal bleeding. All other patients with hematochezia should have colonoscopy, which can be done electively after routine preparation unless there is significant ongoing bleeding. In such patients, a rapid prep (5 to 10 L of polyethylene glycol solution delivered via NGT or by mouth over 3 to 4 h) often allows adequate visualization. If colonoscopy cannot visualize the source and ongoing bleeding is sufficiently rapid (> 0.5 to 1 mL/min), angiography may localize the source. Some angiographers first take a radionuclide scan to focus the examination, because angiography is less sensitive than the radionuclide scan.
Diagnosis of occult bleeding can be difficult, because heme-positive stools may result from bleeding anywhere in the GI tract. Endoscopy is the preferred method, with symptoms determining whether the upper or lower GI tract is examined first. Double-contrast barium enema and sigmoidoscopy can be used for the lower tract when colonoscopy is unavailable or the patient refuses it. If the results of upper endoscopy and colonoscopy are negative and occult blood persists in the stool, an upper GI series with small-bowel follow-through, small-bowel endoscopy (enteroscopy), capsule endoscopy (which uses a small pill-like camera that is swallowed), technetium-labeled colloid or RBC scan, and angiography should be considered. Capsule endoscopy is of limited value in an actively bleeding patient.
(See also the American College of Gastroenterology's practice guidelines on management of the adult patient with acute lower GI bleeding.) Hematemesis, hematochezia, or melena should be considered an emergency. Admission to an ICU, with consultation by both a gastroenterologist and a surgeon, is recommended for all patients with severe GI bleeding. General treatment is directed at maintenance of the airway and restoration of circulating volume. Hemostasis and other treatment depend on the cause of the bleeding.
A major cause of morbidity and mortality in patients with active upper GI bleeding is aspiration of blood with subsequent respiratory compromise. To prevent these problems, endotracheal intubation should be considered in patients who have inadequate gag reflexes or are obtunded or unconscious—particularly if they will be undergoing upper endoscopy.
IV fluids are initiated as for any patient with hypovolemia or hemorrhagic shock (see Intravenous Fluid Resuscitation): healthy adults are given normal saline IV in 500- to 1000-mL aliquots until signs of hypovolemia remit—up to a maximum of 2 L (for children, 20 mL/kg, that may be repeated once). Patients requiring further resuscitation should receive transfusion with packed RBCs. Transfusions continue until intravascular volume is restored and then are given as needed to replace ongoing blood loss. Transfusions in older patients or those with coronary artery disease may be stopped when Hct is stable at 30 unless the patient is symptomatic. Younger patients or those with chronic bleeding are usually not transfused unless Hct is < 23 or they have symptoms such as dyspnea or coronary ischemia.
Platelet count should be monitored closely; platelet transfusion may be required with severe bleeding. Patients who are taking antiplatelet drugs (eg, clopidogrel, aspirin) have platelet dysfunction, often resulting in increased bleeding. Platelet transfusion should be considered when patients taking these drugs have severe ongoing bleeding, although a residual circulating drug (particularly clopidogrel) may inactivate transfused platelets. Fresh frozen plasma should be transfused after every 4 units of packed RBCs.
GI bleeding stops spontaneously in about 80% of patients. The remaining patients require some type of intervention. Specific therapy depends on the bleeding site. Early intervention to control bleeding is important to minimize mortality, particularly in elderly patients.
For peptic ulcer, ongoing bleeding or rebleeding is treated with endoscopic coagulation (with bipolar electrocoagulation, injection sclerotherapy, heater probes, clips, or laser). Nonbleeding vessels that are visible within an ulcer crater are also treated. If endoscopy does not stop the bleeding, angiographic embolization of the bleeding vessel may be attempted, or surgery is required to oversew the bleeding site. If the patient has been treated medically for peptic ulcer disease but has recurrent bleeding, surgeons do acid-reduction surgery (see Surgery) at the same time.
Active variceal bleeding can be treated with endoscopic banding, injection sclerotherapy, or a transjugular intrahepatic portosystemic shunting (TIPS) procedure.
Severe, ongoing lower GI bleeding caused by diverticula or angiomas can sometimes be controlled colonoscopically by electrocautery, coagulation with a heater probe, or injection with dilute epinephrine. Polyps can be removed by snare or cautery. If these methods are ineffective or unfeasible, angiography with embolization or vasopressin infusion may be successful. However, because collateral blood flow to the bowel is limited, angiographic techniques have a significant risk of bowel ischemia or infarction unless super-selective catheterization techniques are used. In most series, the rate of ischemic complications is < 5%. Vasopressin infusion has about an 80% success rate for stopping bleeding, but bleeding recurs in about 50% of patients. Also, there is a risk of hypertension and coronary ischemia. Furthermore, angiography can be used to localize the source of bleeding more accurately. Surgery may be done in patients with continued bleeding (requiring > 6 units transfusion), but localization of the bleeding site is very important. Blind hemicolectomy (with no preoperative identification of the bleeding site) carries a much higher mortality risk than does directed segmental resection and may not remove the bleeding site; the rebleeding rate is 10%. However, assessment must be expeditious so that surgery is not unnecessarily delayed. In patients who have received > 10 units of packed RBCs, the mortality rate is about 30%.
Acute or chronic bleeding of internal hemorrhoids stops spontaneously in most cases. Patients with refractory bleeding are treated via anoscopy with rubber band ligation, injection, coagulation, or surgery.
In the elderly, hemorrhoids and colorectal cancer are the most common causes of minor bleeding. Peptic ulcer, diverticular disease, and angiodysplasia are the most common causes of major bleeding. Variceal bleeding is less common than in younger patients.
Massive GI bleeding is tolerated poorly by elderly patients. Diagnosis must be made quickly, and treatment must be started sooner than in younger patients, who can better tolerate repeated episodes of bleeding.
Last full review/revision September 2012 by Parswa Ansari, MD
Content last modified October 2013