Etiology of lower gastrointestinal bleeding in adults
(uptodate.com)
Author
Rome Jutabha, MD
Section Editor
J Thomas LaMont, MD
Deputy Editor
Anne C Travis, MD, MSc, FACG
Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jan 2012. |This topic last updated: Dec 5, 2011.
INTRODUCTION — Lower gastrointestinal bleeding (LGIB) refers to blood loss of recent onset originating from a site distal to the ligament of Treitz [1]. It is usually suspected when patients complain of hematochezia (passage of maroon or bright red blood or blood clots per rectum). This is different from the clinical presentation of upper GI bleeding, which includes hematemesis (vomiting of blood or coffee-ground like material) and/or melena (black, tarry stools). Although helpful, the distinctions based upon stool color are not absolute since melena can be seen with GI bleeding from the right colon (or small intestine), and hematochezia can be seen with massive upper GI bleeding [2-4]. A nasogastric tube lavage that yields blood or coffee-ground like material confirms the diagnosis of upper GI bleeding; however, lavage may not be positive if bleeding has ceased or arises beyond a closed pylorus. (See "Approach to acute upper gastrointestinal bleeding in adults".)
This topic review will focus on the major causes of LGIB, and briefly summarize the management of some of these disorders. The diagnostic approach to such patients and to those with occult gastrointestinal bleeding are discussed separately. (See "Approach to resuscitation and diagnosis of lower gastrointestinal bleeding in the adult patient" and "Evaluation of occult gastrointestinal bleeding".)
ETIOLOGY — The causes of LGIB may be grouped into several categories (table 1):
•Anatomic (diverticulosis)
•Vascular (angiodysplasia, ischemic, radiation-induced)
•Inflammatory (infectious, idiopathic)
•Neoplastic
In most series, diverticulosis accounts for approximately 15 to 55 percent and angiodysplasia for 3 to 37 percent of LGIB [5-8]. Angiodysplasia may be the most frequent cause in patients over the age of 65 [9,10], though more recent data suggest that angiodysplasia may be a less common cause of LGIB than once thought [8]. (See "Angiodysplasia of the gastrointestinal tract".)
Hemorrhoids are the most common cause of rectal bleeding in patients under the age of 50 [11]. However, hemorrhoidal bleeding is usually minor and thereby distinguished from LGIB. Similarly, bloody diarrhea due to infectious causes can sometimes be distinguished from other causes of LGIB because of the clinical setting.
In a review of several large studies that included 1559 patients with acute LGIB, the following bleeding sources were identified [8]:
•Diverticulosis — 5 to 42 percent
•Ischemia — 6 to 18 percent
•Anorectal (hemorrhoids, anal fissures, rectal ulcers) — 6 to 16 percent
•Neoplasia (polyps and cancers) —3 to 11 percent
•Angiodysplasia — 0 to 3 percent
•Postpolypectomy — 0 to 13 percent
•Inflammatory bowel disease — 2 to 4 percent
•Radiation colitis — 1 to 3 percent
•Other colitis (infectious, antibiotic associated, colitis of unclear etiology) — 3 to 29 percent
•Small bowel/upper GI bleed — 3 to 13 percent
•Other causes — 1 to 9 percent
•Unknown cause — 6 to 23 percent
Diverticulosis — A diverticulum is a sac-like protrusion of the colonic wall. The prevalence of diverticular disease is age-dependent, increasing from less than 5 percent at age 40, to 30 percent by age 60, to 65 percent by age 85 [12,13]. (See "Epidemiology and pathophysiology of colonic diverticular disease".)
The high prevalence of the disease explains why diverticulosis is the most common cause of LGIB even though fewer than 15 percent of patients with diverticulosis develop significant diverticular bleeding. Diverticular bleeding typically occurs in the absence of diverticulitis [14], and the risk of bleeding is not further increased if diverticulitis is present [15].
As a diverticulum herniates, the penetrating vessel responsible for the wall weakness at that point becomes draped over the dome of the diverticulum, separated from the bowel lumen only by mucosa (picture 1) [14]. Over time, the vasa recta is exposed to injury along its luminal aspect, leading to eccentric intimal thickening and thinning of the media. These changes may result in segmental weakness of the artery, predisposing to rupture into the lumen. (See "Colonic diverticular bleeding".)
In western countries, 75 percent of diverticula occur on the left side of the colon and, when right-sided diverticula do occur, they are usually associated with left-sided diverticula [16]. However, the right colon is the source of diverticular bleeding in 50 to 90 percent of patients [6,14,17]. The anatomic relationship between diverticula and the vasa recta is similar in both the right and left colon, but right-sided diverticula have wider necks and domes. This could expose the vasa recta to injury over a greater length, which may explain the higher incidence of right-sided hemorrhage [14].
Diverticular bleeding may be massive and life-threatening since diverticula often form at the site of arterial vascular penetration. The bleeding is usually painless except for mild crampy abdominal discomfort due to colonic spasm from intraluminal blood. Diverticular bleeding is self-limited in over 70 to 80 percent of cases. However, the rebleeding rate approaches 25 percent after the initial bleeding episode in those who do not undergo surgery [18].
Risk factors for diverticular bleeding include a lack of dietary fiber, aspirin and nonsteroidal antiinflammatory drug (NSAID) use, advanced age, and constipation [19-22]. Aspirin and NSAIDs may increase the risk of LGIB by a variety of mechanisms, including local erosive topical damage and platelet dysfunction [23].
The management of diverticular bleeding is discussed separately. (See "Colonic diverticular bleeding".)
Angiodysplasia — Angiodysplasia refers to dilated tortuous submucosal vessels. The walls of these blood vessels are composed of endothelial cells that lack smooth muscle (picture 2 and picture 3). Angiodysplasia appears endoscopically as peripherally expanding dilated capillaries with a central origin measuring between 0.1 to 1.0 cm in diameter (picture 4). They are not visualized by barium enema or at autopsy (since blood volume is removed). (See "Angiodysplasia of the gastrointestinal tract".)
Lower gastrointestinal angiodysplasia is uncommon in the general population. A study of 964 asymptomatic patients undergoing screening colonoscopy found that less than 1 percent had angiodysplasia [24]. No cases of bleeding were identified during three years of follow-up, suggesting that treatment of asymptomatic lesions is not necessary. Nevertheless, similar to diverticulosis, the incidence of angiodysplasia increases with age and the risk of bleeding increases with time due to degeneration of the vascular walls. In addition, several conditions have been associated with angiodysplasia [25], including aortic stenosis and chronic renal failure. (See "Angiodysplasia of the gastrointestinal tract", section on 'Conditions associated with angiodysplasia'.)
Angiodysplasia may occur throughout the colon, although bleeding most often originates from the cecum or ascending colon. Similar to diverticular disease, bleeding from angiodysplasia tends to be episodic and self-limited. The blood loss usually is overt, presenting with painless hematochezia or melena. However, chronic bleeding manifested by Hemoccult positive stools and iron deficiency anemia can occur. (See "Evaluation of occult gastrointestinal bleeding" and "Evaluation of obscure gastrointestinal bleeding".)
Bleeding from angiodysplasia is venous in origin (in contrast to arterial bleeding with diverticula) and therefore tends to be less massive than diverticular bleeding. Rebleeding occurs in approximately 80 percent of patients with untreated angiodysplasia [26].
Endoscopic coagulation (with bipolar probe or heater probes), injection sclerotherapy, and argon laser coagulation can all achieve definitive hemostasis in patients with angiodysplasia [25]. Recurrent bleeding after local therapy occurs in up to 30 percent of patients. Identification of upper gastrointestinal or small bowel angiodysplasia should prompt the investigation of additional lesions in the lower gastrointestinal tract. (See "Angiodysplasia of the gastrointestinal tract".)
Colitis — Infectious and ischemic colitis and inflammatory bowel disease can all present initially with hematochezia. Mucosal inflammation (colitis) is the common response to acute injury, resulting in activation of the immune system and inflammatory cascade.
The clinical presentation and endoscopic appearance of the various types of colitis can be indistinguishable. Patients can present with abdominal pain, hematochezia (with or without diarrhea), fever, and dehydration. Endoscopically, colitis appears as edema, friability, erythema, and ulceration (picture 5). Histologically, there is evidence of nonspecific acute and chronic inflammation, fibrin exudates, crypt abscesses, and ulceration.
Establishing a specific diagnosis is paramount in the treatment of acute colitis since therapy depends upon the underlying disease process. The diagnosis requires an interpretation of the histologic and gross findings within its clinical context.
Infectious colitis — There are many infectious causes of colitis. A routine stool culture will identify Salmonella, Campylobacter, and Shigella, the three most common causes of bacterial diarrhea in the United States. As noted above, bleeding due to infectious causes can sometimes be distinguished from other causes of LGIB because of the clinical setting. (See "Approach to the adult with acute diarrhea in developed countries".)
Ischemic colitis — Elderly patients are most likely to experience ischemia-related colitis because of relative hypotension, heart failure, or arrhythmia. Patients classically have associated abdominal pain, although its absence does not preclude the diagnosis. Ischemic colitis tends to be continuous, left-sided (figure 1), and associated with mucosal friability, findings that resemble ulcerative colitis (picture 6). The rectum is spared. Bleeding is self-limited and recurrence is related to the ability to correct the underlying cause. Therapy must be directed at correcting the underlying cause and volume repletion. (See "Colonic ischemia".)
Inflammatory bowel disease — Inflammatory bowel disease refers to both Crohn's disease and ulcerative colitis. Hematochezia is a more common initial presentation with the latter and tends to occur in the setting of active inflammation. (See "Clinical manifestations, diagnosis and prognosis of Crohn's disease in adults" and "Clinical manifestations, diagnosis, and prognosis of ulcerative colitis in adults".) Differentiating Crohn's disease from ulcerative colitis during an episode of acute LGIB is not imperative since the acute management is similar for both conditions. (See "Overview of the medical management of mild to moderate Crohn's disease in adults" and "Medical management of ulcerative colitis".) However, it is important not to misdiagnosis inflammatory bowel disease as ischemic or infectious colitis since the therapy is different [27]. In elderly patients in particular, it can be difficult to differentiate ischemic colitis from inflammatory bowel disease [28].
Neoplasm — Colon cancer is a relatively less common but serious cause of hematochezia. Neoplasm is responsible for approximately 10 percent of cases of rectal bleeding in patients over age 50 but is rare in younger individuals [29]. Bleeding occurs as the result of overlying erosion or ulceration. The bleeding tends to be low grade and recurrent. Bright red blood suggests left-sided lesions; right-sided lesions can present with maroon blood or melena. (See "Clinical manifestations, diagnosis, and staging of colorectal cancer".)
Endoscopic therapy of colon cancer presenting with rectal bleeding is limited. There is a significant risk of inducing more bleeding or causing a perforation with endoscopic therapy due to the friability and size of the lesions. The endoscopist should biopsy suspicious masses, look for synchronous lesions, and exclude additional causes of bleeding.
Miscellaneous anorectal disorders — Hemorrhoids are dilated submucosal veins in the anus that are located above (internal) or below (external) the dentate line. They are usually asymptomatic but can present with hematochezia, thrombosis, strangulation, or pruritus. Hematochezia results from rupture of internal hemorrhoids which are supplied by the superior and middle hemorrhoidal arteries. Hemorrhoidal bleeding is almost always painless. Bright red blood typically coats the stool at the end of defecation. Blood may also drip into the toilet or stain toilet paper. Occasionally, bleeding can be copious and distressing for the patient. However, serious lower GI bleeding (as defined above) from hemorrhoids is uncommon. The risk of serious bleeding is increased in patients with a coagulopathy such as those with advanced cirrhosis. Hemorrhoids should be suspected particularly in young patients with hematochezia [11]. (See "Overview of hemorrhoids".)
A variety of other lesions in the anorectum may be associated with bleeding. These include solitary rectal ulcers, anal fissures, and Dieulafoy's lesions. (See appropriate topic reviews).
Radiation telangiectasia or proctitis — Radiation therapy of abdominal and pelvic cancers (such as cervical or prostate carcinoma) can lead to lower gastrointestinal bleeding as either an early or late complication of radiation damage. Risk factors for radiation-induced damage include immobilization of the bowel in the rectosigmoid area, arteriosclerosis, and concomitant chemotherapy.
The timing of rectal bleeding relative to the administration of radiation therapy can narrow the differential diagnosis. Acute radiation injury occurs within six weeks of therapy. Symptoms include diarrhea and rectal urgency or tenesmus, and, uncommonly, bleeding. Chronic radiation proctosigmoiditis has a more delayed onset. The first signs often occur at about 9 to 14 months following radiation exposure, but may develop after more than two years in some patients and rarely up to 30 years after exposure. (See "Clinical features, diagnosis, and treatment of radiation proctitis".)
Ulceration or cancer recurrence can also be seen as late complications following radiation therapy. These entities must be excluded in patients with rectal bleeding.
Following biopsy or polypectomy — Bleeding following endoscopic biopsy or polypectomy is usually self-limited, although active arterial bleeding can occur acutely [30]. Acute bleeding is due to involvement of an underlying artery or inadequate coagulation of the polyp stalk. Delayed bleeding can occur as late as seven days following endoscopic polypectomy, presumably due to sloughing of the coagulated eschar. (See "Bleeding after colonic polypectomy".)
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Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
•Basics topics (see "Patient information: Ulcerative colitis (The Basics)" and "Patient information: Crohn's disease (The Basics)")
•Beyond the Basics topics (see "Patient information: Ulcerative colitis (Beyond the Basics)" and "Patient information: Crohn's disease (Beyond the Basics)")
SUMMARY
•Lower gastrointestinal bleeding (LGIB) refers to blood loss of recent onset originating from a site distal to the ligament of Treitz, which results in hemodynamic instability, anemia, or the need for blood transfusion.
•The causes of LGIB may be grouped into several categories: anatomic (diverticulosis); vascular (angiodysplasia, ischemic, radiation-induced); inflammatory (infectious, idiopathic); and neoplastic (table 1).
•In most series, diverticulosis accounts for approximately 15 to 55 percent of LGIB. (See 'Diverticulosis' above.)