Background
Lower gastrointestinal bleeding (LGIB) accounts for approximately 20-33% of episodes of gastrointestinal (GI) hemorrhage, with an annual incidence of about 20-27 cases per 100,000 population in Western countries. However, although LGIB is statistically less common than upper GI bleeding (UGIB), it has been suggested that LGIB is underreported because a higher percentage of affected patients do not seek medical attention.[1] Indeed, LGIB continues to be a frequent cause of hospital admission and is a factor in hospital morbidity and mortality LGIB is distinct from UGIB in epidemiology, management, and prognosis.
LGIB encompasses a wide spectrum of symptoms, ranging from trivial hematochezia to massive hemorrhage with shock. Acute LGIB is defined as bleeding that is of recent duration, originates beyond the ligament of Treitz, results in instability of vital signs, and is associated with signs of anemia with or without need for blood transfusion.
LGIB is classified under 3 groups according to the amount of bleeding, as shown in the image below. Massive hemorrhage is a life-threatening condition and requires transfusion of at least 5 U of blood.
Types of lower gastrointestinal (GI) bleeding. HR = heart rate; SBP = systolic blood pressure. Massive lower GI bleeding is defined as follows:
- Passage of a large volume of red or maroon blood through the rectum
- Hemodynamic instability and shock
- Initial decrease in hematocrit (Hct) level of 6 g/dL or less
- Transfusion of at least 2 U of packed red blood cells (RBCs)
- Bleeding that continues for 3 days
- Significant rebleeding in 1 week
LGIB has a mortality rate ranging from about 10-20%, with patients of advanced age (>60 y) and patients with comorbid conditions (eg, multiorgan system disease, transfusion requirements in excess of 5 units [U], need for operation, and recent stress, such as surgery, trauma, and sepsis) at greatest risk. LGIB is more likely in the elderly because of a higher incidence of diverticulosis and vascular disease in these groups. The incidence of LGIB is higher in men than in women.
Advances in diagnostic and therapeutic colonoscopy and in interventional angiography have resulted in a shift away from the need for surgical treatment (see the image below). Effective management with less invasive modalities has also reduced healthcare costs and, more importantly, patient morbidity and mortality.
Methods used to treat lower gastrointestinal bleeding (LGIB). Historical details
Understanding of the pathogenesis, diagnosis, and treatment of LGIB has drastically changed during the last 50 years. In the first half of the 20th century, large intestinal neoplasms were believed to be the most common cause of LGIB. In the 1950s, this condition was commonly attributed to diverticulosis; surgical treatment consisted of blind segmental bowel resections, with disappointing results. Patients who underwent these procedures suffered from a prohibitively high rebleeding rate (up to 75%), morbidity (up to 83%), and mortality (up to 60%).
In the last 4 decades, diagnostic methods for locating the precise bleeding point greatly improved. The flexible endoscope was developed in 1954. The full-length colonoscope was developed in 1965 in Japan. Also in 1965, Baum et al described selective mesenteric angiography, which permitted the identification of vascular abnormalities and the precise bleeding point.[2] The first anal colonoscopy was performed in 1969.
Experience with mesenteric angiography in the late 1960s and 1970s suggested that angiodysplasias and diverticulosis were the most common reasons for LGIB. Since its discovery, mesenteric angiography remains the criterion standard in precise localization of the bleeding.
Rosch et al described superselective visceral arteriography for infusion of vasoconstrictors in 1971 and superselective embolization of the mesenteric vessels as an alternative technique to treat massive LGIB in 1972.[3, 4] The most feared complication of embolization of the mesenteric vessels is ischemic colitis, which has limited its use for GI bleeding.
The initial experience with vasopressin infusion was reported in 1973-1974. Vasopressin causes vasoconstriction and arrests the bleeding in 36-100% of patients. The recurrence rate following completion of vasopressin infusion can be as high as 71%; therefore, vasopressin is used to temporize the acute event and to stabilize patients before surgery.
Endoscopic control of bleeding with thermal modalities or sclerosing agents has been in use since the 1980s. One of the advantages of upper (or lower) endoscopic evaluation is that it provides a means to administer therapy in patients with GI bleeding. Nuclear scintigraphy has been used since the early 1980s as a very sensitive diagnostic tool to evaluate bleeding from GI tract; this modality can detect hemorrhage at rates as low as 0.1 mL/min
Anatomy
The average length of the large intestine is 135-150 cm. Ascending and descending segments of the colon are fixed to the retroperitoneum. However, the transverse and sigmoid colon are supported by a mesentery in the abdomen. A comprehensive understanding of small bowel and colonic vascular anatomy is essential for any physician performing a primary lower GI procedure for hemorrhage or other diseases.
The ileocolic, right colic, and middle colic branches of the superior mesenteric artery supply blood to the cecum, ascending, and proximal transverse colon, respectively. The superior mesenteric vein drains the right side of the colon, joining the splenic vein to form the portal vein. The inferior mesenteric artery supplies blood to the distal transverse, descending, and sigmoid colon. The inferior mesenteric vein carries blood from the left side of the colon to the splenic vein. A rich network of vessels from the superior, middle, and inferior hemorrhoidal vessels supplies the rectosigmoid junction and rectum.
Pathophysiology
Diverticulosis, angiodysplasia, colitis, carcinoma, and anorectal disease in the pathophysiology of LGIB are briefly discussed in this section.
Diverticulosis
Diverticulosis is a common acquired condition in Western societies; approximately 50% of adults older than 60 years have radiologic evidence of this disease. A diverticulum is a saclike protrusion of the colonic wall that develops at a small point of weakness where the penetrating vessel has perforated through the circular muscle fibers. The vessel becomes draped over the dome of the diverticulum, separated from the bowel lumen only by mucosa. Subsequent chronic trauma to the vasa recta along the luminal aspect, as well as contraction and relaxation of the surrounding muscularis propria, leads to eccentric thinning of the media. Ultimately, erosion of the vessel and bleeding can occur.
Diverticula are most commonly located in the sigmoid and descending colon, and diverticular bleeding originates from vasa rectae located in the submucosa, which can rupture at the dome or the neck of the diverticulum.[5] Up to 20% of patients with diverticular disease experience bleeding, which stops spontaneously in 80% of patients; however, in 5% of patients with diverticular disease, the bleeding from diverticular disease can be massive.
Although about 75% of the diverticula occur on the left side of the colon, right-sided diverticula are responsible for approximately 50-90% of the bleeding.[5] This may be because right-sided diverticula have wider necks and domes, which expose the vasa recta to injury over a greater length.
Angiodysplasia
Colonic angiodysplasias are arteriovenous malformations located in the cecum and ascending colon; these are acquired lesions that affect elderly persons older than 60 years. Most colonic angiodysplasias are degenerative lesions that arise from chronic, intermittent, low-grade colonic contraction that obstructs the mucosal venous drainage. Over time, mucosal capillaries dilate, become incompetent, and form an arteriovenous malformation.
Colitis
Massive hemorrhage due to inflammatory bowel disease (IBD) is rare. Ulcerative colitis causes bloody diarrhea in most cases. In up to 50% of patients with ulcerative colitis, mild to moderate LGIB occurs, and approximately 4% of patients with ulcerative colitis have massive hemorrhage.
LGIB in patients with Crohn disease is not as common as in patients with ulcerative colitis; 1-2% of patients with Crohn disease may experience massive bleeding. The frequency of bleeding in patients with Crohn disease is significantly more common with colonic involvement than with small bowel involvement alone. The mucosal pattern of injury is similar to that found in patients with infectious and ischemic colitis, with the mucosa appearing friable, erythematous, edematous, and ulcerated. In severe Crohn disease, the inflammatory process may extend into the serosa, leading to colonic perforation.
Ischemic colitis is a disease of the elderly population and is commonly observed after the sixth decade of life. This condition is the most common form of ischemic injury to the digestive system, frequently involves the watershed areas, including the splenic flexure and the rectosigmoid junction. Ischemia causes mucosal and partial-thickness colonic wall sloughing, edema, and bleeding. In most cases, the precipitating event cannot be identified. However, although abdominal pain and bloody diarrhea are the main clinical manifestations, ischemic colitis is not associated with significant blood loss or hematochezia.
The pathophysiologic mechanism of infectious colitis may be due to either colonic tissue invasion by bacteria, such as Salmonella and Shigella, or toxin-mediated damage, as with Escherichia coli 0157:H7.
Colon carcinoma
Colorectal adenocarcinoma is the third most common cancer in the United States. Colorectal carcinoma causes occult bleeding as a result of mucosal ulceration or erosion, but the incidence of massive bleeding due to colorectal carcinoma varies from 5% to 20% in different series. Postpolypectomy hemorrhage is reported to occur in 0.1-3% of patients up to 1 month following colonoscopic resection.
Anorectal disease
Benign anorectal disease (eg, hemorrhoids, anal fissures, anorectal fistulas) can cause intermittent rectal bleeding. Massive rectal bleeding due to benign anorectal disease has also been reported. A review of the Department of Veterans Affairs (VA) database revealed that 11% of patients with LGIB had hemorrhage from anorectal disease.[6]
Etiology
Comprehensive knowledge of the etiology of LGIB is essential for patient management and, ultimately, for patient outcome. The diagram below outlines the most common causes of LGIB, including anatomic (eg, diverticular bleeding), vascular (eg, angiodysplasia, ischemic colitis, radiation-induced colitis), neoplasms, and inflammatory.
Types of lower gastrointestinal bleeding (LGIB). In a retrospective review of medical records from approximately 1100 patients with acute LGIB, all of whom were admitted to the surgical service of a single urban emergency hospital, Gayer et al determined that the most common etiologies for bleeding in these patients were diverticulosis (33.5%), hemorrhoids (22.5%), and carcinoma (12.7%).[7] The investigators also found that most patients in the study (55.5%) presented with hematochezia, with the next most frequent presentations being maroon stools (16.7%) and melena (11%).
In a review by Vernava and colleagues, patients with LGIB made up only 0.7% of all hospital admissions (17,941 patients); among the patients who underwent a diagnostic workup (4410 [24%]), the most common causes of bleeding were diverticular disease (60%), IBD (13%), and anorectal diseases (11%) (see Table 1 below).[6] These figures differ somewhat from the study by Gayer et al. Although some publications have reported arteriovenous malformations (AVMs) as a common cause of LGIB, Vernava et al reported the true incidence of these lesions at 3%.[8]
Table 1. Common Causes of Lower Gastrointestinal Bleeding in Adults (Open Table in a new window)
| Lower Gastrointestinal Bleeding in Adults | Percentage of Patients |
Diverticular disease
| 60% |
Inflammatory bowel disease
| 13% |
Benign anorectal diseases
| 11% |
Neoplasia
| 9% |
| Coagulopathy | 4% |
| Arteriovenous malformations (AVMs) | 3% |
| TOTAL | 100% |
| Source: Vernava AM, Longo WE, Virgo KS. A nationwide study of the incidence and etiology of lower gastrointestinal bleeding. Surg Res Commun. 1996;18:113-20.[6] | |
Longstreth reviewed the discharge summary and colonoscopy data from a large health maintenance organization with members in the San Diego, Calif, area; of 235 hospital admissions for 219 patients, the estimated hospital admission rate for LGIB was found to be 20 patients per 100,000 admissions, with bleeding from diverticular disease the most common reason (42%), followed by colorectal malignancies (9%) and ischemic colitis (8.7%).[9] The incidence of LGIB due to colonic angiodysplasias was 6%. These findings were consistent with those of the VA database study by Vernava et al, although that study was limited to males.
The common causes of LGIB in infants, children, and adolescents differ from those found in adults. Meckel diverticulum, intussusception, polyposis syndromes, and IBD are the common causes in this subset (see Table 2 below).
Table 2. Common Causes of Lower Gastrointestinal Bleeding in Children and Adolescents (Open Table in a new window)
| Lower Gastrointestinal Bleeding in Children and Adolescents |
| Intussusception |
Polyps and polyposis syndromes
|
Inflammatory
|
| Meckel diverticulum |
Diverticulosis
Diverticulosis is the dominant etiology of LGIB, reported as the most common reason for massive LGIB in most of the single-institution publications. Most diverticular bleeding occurs without concomitant diverticulitis, and diverticulitis does not increase the risk of bleeding. Risk factors for diverticular bleeding include lack of dietary fiber, constipation, advanced age, and use of nonsteroidal antiinflammatory drugs (NSAIDs) and aspirin.
Angiodysplasia
Angiodysplasia is by far the most common vascular anomaly found in the GI tract. The lesions can occur anywhere in the GI tract; however, they occur most often in the proximal colon. Because bleeding from angiodysplasia is venocapillary in origin, it is generally less vigorous than diverticular bleeding. However, as opposed to diverticular bleeding, about 80% of patients with resolved but untreated angiodysplasia bleeding experience rebleeding.[10]
Saperas et al found that earlier bleeding with a high bleeding rate, overanticoagulation, and multiple angiodysplastic lesions predict an increased risk of recurrent bleeding due to angiodysplasia.[11] The investigators also noted that although there was a better trend for management and prevention of such recurrent bleeding with endoscopic argon plasma coagulation, this therapy was not predictive of a lower rate of hemorrhage recurrence.[11]
Angiodysplasia is associated with a number of medical conditions, including aortic stenosis, von Willebrand disease, and chronic renal failure. The incidence of angiodysplasia increases with age because of degeneration of the vascular walls. Angiodysplasia was previously believed to be associated with the presence of aortic stenosis, but data supporting this relationship are lacking.
Ischemic and radiation-induced colitis and other vascular causes
Ischemic colitis is rarely a cause of significant blood loss; thus, large-volume or brisk bleeding should prompt a search for an alternate etiology. Tissue injury is typically caused by hypotension and vasoconstriction, which leads to mucosal friability and endoscopic findings often resembling changes of IBD. Ischemic colitis usually involves the left side of the colon with rectal sparing. Elderly patients with comorbidities, such as heart failure and arrhythmia, are more susceptible.
Radiation therapy can cause inflammatory changes in the bowel resulting in mucosal telangiectasias that bleed. When this treatment is used for abdominal and pelvic cancers, bleeding due to mucosal damage in the colon can lead to complications of acute colitis or ulceration. Complications can occur early or late, with a median time of occurrence from 9 to 15 months. Risk factors for radiation LGIB include arteriosclerosis and concomitant chemotherapy.
Other vasculitic entities, such as polyarteritis nodosa and Wegener granulomatosis, can also cause LGIB because of the underlying necrotic process that causes sloughing of the mucosa. Bleeding may also occur secondary to immunosuppressive therapy, which can cause thrombocytopenia. Aortocolonic fistulas, which rarely develop after aortic-graft surgery, can cause LGIB as much as 10-20 years after surgery.
Infectious colitis
The most common infectious causes of colitis worldwide are Salmonella, Shigella, Campylobacter jejuni, E coli 0157:H7, and Entamoeba histolytica. In the United States, Salmonella, Shigella, and Campylobacter are the most common causative agents; such microbial agents cause an inflammatory diarrhea characterized by fever, bloody diarrhea, lower quadrant cramps, and tenesmus.
Noninfectious (idiopathic) colitis
Even though IBD due to Crohn disease or ulcerative colitis causes LGIB, it is rarely massive hemorrhage. Ulcerative colitis can cause mild to moderate bloody diarrhea in about 50% of patients, with an estimated 4% of patients experiencing massive bleeding. In Crohn disease, massive bleeding is less common, occurring in about 2% of patients with Crohn colitis.
Neoplasm
Neoplastic bleeding can be from a polyp or carcinoma. Colon cancer is the predominant cause of neoplastic bleeding and is responsible for around 10% of rectal bleeding in patients older than 50 years. The bleeding is usually low-grade and recurrent, occurring as a result of mucosal ulceration or erosion. Though neoplastic bleeding can present as bright red blood per rectum, it is unusual for it to cause massive colonic bleeding.
Postpolypectomy bleeding occurs in approximately 0.1-3% of patients, is more often arterial, and can produce significant bleeding. Bleeding can occur at the time of polypectomy but can also manifest several hours to a few weeks after the procedure.
Anorectal disease
Anorectal diseases, such as hemorrhoids, fistulas, and fissures, typically cause intermittent rectal bleeding.
Other causes of LGIB
Infection with human immunodeficiency virus (HIV) is an infrequent cause of LGIB. Most of the LGIB is caused by HIV-related opportunistic infections and associated etiologies, including cytomegalovirus (CMV) colitis, idiopathic colon ulcers, Kaposi sarcoma, and lymphoma.[12] Patients with HIV can also bleed from hemorrhoids and anal fissures, in which the bleeding likelihood is increased due to concomitant coagulopathy.
Drug-induced bleeding is caused mainly by NSAID and aspirin use, and it is more common in the elderly. Although the risk of bleeding increases at higher doses of these agents, even low-dose aspirin given for cardiovascular prophylaxis can produce bleeding. Aspirin or anticoagulants can potentiate or aggravate hemorrhage from preexisting lesions. The 2008 Scottish Intercollegiate Guidelines Network (SIGN) guideline on the management of acute upper and lower gastrointestinal bleeding warns that oral anticoagulants or corticosteroids should be used with caution in patients at risk of GIB, especially in those who take NSAIDs or aspirin.[13]
Uncommon causes of LGIB include stercoral ulcer and Dieulafoy lesion of the small or large bowel.
Epidemiology
LGIB that requires hospitalization represents less than 1% of all hospital admissions in the United States.[6] In one study, the estimated annual incidence rate was 20.5 patients per 100,000 (24.2 in males vs 17.2 in females); however, in individuals in the third to the ninth decades, the incidence rate of LGIB increased more than 200-fold.[9] LGIB is somewhat more common in men than in women, because diverticulosis and vascular disease are more common in men.
The leading causes of significant LGIB are diverticulosis and angiodysplasia. Diverticulosis accounts for around 30-50% of the cases of hemodynamically significant LGIB, whereas angiodysplasia accounts for about 20-30% of cases. LGIB is more common in the elderly than in younger people, because diverticulosis and vascular disease are more common in these groups. Some experts believe that angiodysplasia is the most frequent cause of LGIB in patients older than 65 years.
Hemorrhoids are the most common cause of LGIB in patients younger than 50 years, but the bleeding is usually minor, and they are rarely the cause of significant LGIB. According to a review of 7 series of patients with LGIB, the most common cause of LGIB was diverticulosis, accounting for approximately 33% of cases, followed by cancer and polyps, which accounted for about 19% of cases.[14]
Prognosis
LGIB ranges from trivial hematochezia to massive hemorrhage with shock and accounts for up to 24% of all cases of GI bleeding. This condition is associated with significant morbidity and mortality (10-20%). Patients of advanced age and patients with comorbid conditions are at greatest risk. Identification of the bleeding point is the most important initial step in treatment; once the bleeding point is localized, the treatment options are straightforward and curative.
The evolution of more sophisticated diagnostic imaging (eg, angiography, bleeding scan, flexible fiberoptic colonoscope) offers the promise of precise localization of the bleeding site. These advances also provide nonoperative and less invasive control of bleeding using angiographic techniques or colonoscope. Pharmacologic discoveries are also improving patient care and outcome. Therefore, the therapeutic armamentaria have expanded greatly in the last 50 years.
Patient Education
For patient education information, see eMedicine's Esophagus, Stomach, and Intestine Center, as well as Gastrointestinal Bleeding, Rectal Bleeding, Inflammatory Bowel Disease, Diverticulosis and Diverticulitis, and Anal Abscess.
Talley NJ, Jones M. Self-reported rectal bleeding in a United States community: prevalence, risk factors, and health care seeking. Am J Gastroenterol. Nov 1998;93(11):2179-83. [Medline].
Baum S, Nusbaum M, Blakemore WS, Finkelstein AK. The preoperative radiographic demonstration of intra-abdominal bleeding from undetermined sites by percutaneous selective celiac and superior mesenteric arteriography. Surgery. Nov 1965;58(5):797-805. [Medline].
Rosch J, Gray RK, Grollman JH Jr, et al. Selective arterial drug infusions in the treatment of acute gastrointestinal bleeding. A preliminary report. Gastroenterology. 1971;59(3):341-9.
Rösch J, Dotter CT, Brown MJ. Selective arterial embolization. A new method for control of acute gastrointestinal bleeding. Radiology. Feb 1972;102(2):303-6. [Medline].
Meyers MA, Alonso DR, Gray GF, Baer JW. Pathogenesis of bleeding colonic diverticulosis. Gastroenterology. Oct 1976;71(4):577-83. [Medline].
Vernava AM, Longo WE, Virgo KS. A nationwide study of the incidence and etiology of lower gastrointestinal bleeding. Surg Res Commun. 1996;18:113-20.
Gayer C, Chino A, Lucas C, Tokioka S, Yamasaki T, Edelman DA, et al. Acute lower gastrointestinal bleeding in 1,112 patients admitted to an urban emergency medical center. Surgery. Oct 2009;146(4):600-6; discussion 606-7. [Medline].
Vernava AM 3rd, Moore BA, Longo WE, Johnson FE. Lower gastrointestinal bleeding. Dis Colon Rectum. Jul 1997;40(7):846-58. [Medline].
Longstreth GF. Epidemiology and outcome of patients hospitalized with acute lower gastrointestinal hemorrhage: a population-based study. Am J Gastroenterol. Mar 1997;92(3):419-24. [Medline].
Gupta N, Longo WE, Vernava AM 3rd. Angiodysplasia of the lower gastrointestinal tract: an entity readily diagnosed by colonoscopy and primarily managed nonoperatively. Dis Colon Rectum. Sep 1995;38(9):979-82. [Medline].
Saperas E, Videla S, Dot J, Bayarri C, Lobo B, Abu-Suboh M, et al. Risk factors for recurrence of acute gastrointestinal bleeding from angiodysplasia. Eur J Gastroenterol Hepatol. Dec 2009;21(12):1333-9. [Medline].
Chalasani N, Wilcox CM. Etiology and outcome of lower gastrointestinal bleeding in patients with AIDS. Am J Gastroenterol. Feb 1998;93(2):175-8. [Medline].
Scottish Intercollegiate Guidelines Network (SIGN). Management of acute upper and lower gastrointestinal bleeding. A national clinical guideline. SIGN publication; no. 105. Edinburgh (Scotland): Scottish Intercollegiate Guidelines Network (SIGN); Sep. 2008:[Full Text].
Zuckerman GR, Prakash C. Acute lower intestinal bleeding. Part II: etiology, therapy, and outcomes. Gastrointest Endosc. Feb 1999;49(2):228-38. [Medline].
McGuire HH Jr. Bleeding colonic diverticula. A reappraisal of natural history and management. Ann Surg. Nov 1994;220(5):653-6. [Medline]. [Full Text].
[Guideline] Wilkins T, Baird C, Pearson AN, Schade RR. Diverticular bleeding. Am Fam Physician. Nov 1 2009;80(9):977-83. [Medline].
Ryan MJ, Key SM, Dumbleton SA, MD, et al. Nonlocalized Lower Gastrointestinal Bleeding: Provocative Bleeding Studies with Intraarterial tPA, Heparin, and Tolazoline. J Vasc Interv Radiol. 2001;12:1273-77.
Macari M, Chandarana H, Balthazar E, Babb J. Intestinal ischemia versus intramural hemorrhage: CT evaluation. AJR Am J Roentgenol. Jan 2003;180(1):177-84. [Medline].
Miller FH, Hwang CM. An initial experience: using helical CT imaging to detect obscure gastrointestinal bleeding. Clin Imaging. Jul-Aug 2004;28(4):245-51. [Medline].
Ernst O, Bulois P, Saint-Drenant S, Leroy C, Paris JC, Sergent G. Helical CT in acute lower gastrointestinal bleeding. Eur Radiol. Jan 2003;13(1):114-7. [Medline].
Yamaguchi T, Yoshikawa K. Enhanced CT for initial localization of active lower gastrointestinal bleeding. Abdom Imaging. Sep-Oct 2003;28(5):634-6. [Medline].
Sabharwal R, Vladica P, Chou R, Law WP. Helical CT in the diagnosis of acute lower gastrointestinal haemorrhage. Eur J Radiol. May 2006;58(2):273-9. [Medline].
Lee S, Welman CJ, Ramsay D. Investigation of acute lower gastrointestinal bleeding with 16- and 64-slice multidetector CT. J Med Imaging Radiat Oncol. Feb 2009;53(1):56-63. [Medline].
Frattaroli FM, Casciani E, Spoletini D, Polettini E, Nunziale A, Bertini L, et al. Prospective study comparing multi-detector row CT and endoscopy in acute gastrointestinal bleeding. World J Surg. Oct 2009;33(10):2209-17. [Medline].
Jensen DM, Machicado GA. Diagnosis and treatment of severe hematochezia. The role of urgent colonoscopy after purge. Gastroenterology. Dec 1988;95(6):1569-74. [Medline].
Cohn SM, Moller BA, Zieg PM, Milner KA, Angood PB. Angiography for preoperative evaluation in patients with lower gastrointestinal bleeding: are the benefits worth the risks?. Arch Surg. Jan 1998;133(1):50-5. [Medline].
Laine L, Shah A. Randomized trial of urgent vs. elective colonoscopy in patients hospitalized with lower GI bleeding. Am J Gastroenterol. Dec 2010;105(12):2636-41; quiz 2642. [Medline].
Emslie JT, Zarnegar K, Siegel ME, Beart RW Jr. Technetium-99m-labeled red blood cell scans in the investigation of gastrointestinal bleeding. Dis Colon Rectum. Jul 1996;39(7):750-4. [Medline].
Ng DA, Opelka FG, Beck DE, Milburn JM, Witherspoon LR, Hicks TC, et al. Predictive value of technetium Tc 99m-labeled red blood cell scintigraphy for positive angiogram in massive lower gastrointestinal hemorrhage. Dis Colon Rectum. Apr 1997;40(4):471-7. [Medline].
Ryan P, Styles CB, Chmiel R. Identification of the site of severe colon bleeding by technetium-labeled red-cell scan. Dis Colon Rectum. Mar 1992;35(3):219-22. [Medline].
Kester RR, Welch JP, Sziklas JP. The 99mTc-labeled RBC scan. A diagnostic method for lower gastrointestinal bleeding. Dis Colon Rectum. Jan 1984;27(1):47-52. [Medline].
Ferrant A, Dehasque N, Leners N, Meunier H. Scintigraphy with In-111-labeled red cells in intermittent gastrointestinal bleeding. J Nucl Med. Sep 1980;21(9):844-5. [Medline].
Schmidt KG, Rasmussen JW, Grove O, Andersen D. The use of indium-111-labelled platelets for scintigraphic localization of gastrointestinal bleeding, with special reference to occult bleeding. Scand J Gastroenterol. May 1986;21(4):407-14. [Medline].
Mole DJ, Hughes SJ, Khosraviani K. 111Indium-labelled red-cell scintigraphy to detect intermittent gastrointestinal bleeding from synchronous small- and large-bowel adenocarcinomas. Eur J Gastroenterol Hepatol. Aug 2004;16(8):795-9. [Medline].
Bentley DE, Richardson JD. The role of tagged red blood cell imaging in the localization of gastrointestinal bleeding. Arch Surg. Jul 1991;126(7):821-4. [Medline].
Hunter JM, Pezim ME. Limited value of technetium 99m-labeled red cell scintigraphy in localization of lower gastrointestinal bleeding. Am J Surg. May 1990;159(5):504-6. [Medline].
Browder W, Cerise EJ, Litwin MS. Impact of emergency angiography in massive lower gastrointestinal bleeding. Ann Surg. Nov 1986;204(5):530-6. [Medline]. [Full Text].
Widlus DM, Salis AI. Reteplase provocative visceral arteriography. J Clin Gastroenterol. Oct 2007;41(9):830-3. [Medline].
Ell C, Remke S, May A, Helou L, Henrich R, Mayer G. The first prospective controlled trial comparing wireless capsule endoscopy with push enteroscopy in chronic gastrointestinal bleeding. Endoscopy. Sep 2002;34(9):685-9. [Medline].
Ledermann HP, Schoch E, Jost R, Decurtins M, Zollikofer CL. Superselective coil embolization in acute gastrointestinal hemorrhage: personal experience in 10 patients and review of the literature. J Vasc Interv Radiol. Sep-Oct 1998;9(5):753-60. [Medline].
Gordon RL, Ahl KL, Kerlan RK, Wilson MW, LaBerge JM, Sandhu JS, et al. Selective arterial embolization for the control of lower gastrointestinal bleeding. Am J Surg. Jul 1997;174(1):24-8. [Medline].
Frodsham A, Berkmen T, Ananian C, Fung A. Initial experience using N-butyl cyanoacrylate for embolization of lower gastrointestinal hemorrhage. J Vasc Interv Radiol. Oct 2009;20(10):1312-9. [Medline].
Guy GE, Shetty PC, Sharma RP, Burke MW, Burke TH. Acute lower gastrointestinal hemorrhage: treatment by superselective embolization with polyvinyl alcohol particles. AJR Am J Roentgenol. Sep 1992;159(3):521-6. [Medline].
Kuo WT, Lee DE, Saad WE, Patel N, Sahler LG, Waldman DL. Superselective microcoil embolization for the treatment of lower gastrointestinal hemorrhage. J Vasc Interv Radiol. Dec 2003;14(12):1503-9. [Medline].
Rosenkrantz H, Bookstein JJ, Rosen RJ, Goff WB 2nd, Healy JF. Postembolic colonic infarction. Radiology. Jan 1982;142(1):47-51. [Medline].
Hu ML, Wu KL, Chiu KW, et al. Predictors of rebleeding after initial hemostasis with epinephrine injection in high-risk ulcers. World J Gastroenterol. Nov 21 2010;16(43):5490-5. [Medline]. [Full Text].
Fusaroli P, Grillo A, Zanarini S, Caletti G. Usefulness of a second endoscopic arm to improve therapeutic endoscopy in the lower gastrointestinal tract. Preliminary experience - a case series. Endoscopy. Nov 2009;41(11):997-1000. [Medline].
Hunter JG, Bowers JH, Burt RW, Sullivan JJ, Stevens SL, Dixon JA. Lasers in endoscopic gastrointestinal surgery. Am J Surg. Dec 1984;148(6):736-41. [Medline].
Barnert J, Messmann H. Management of lower gastrointestinal tract bleeding. Best Pract Res Clin Gastroenterol. 2008;22(2):295-312. [Medline].
Hammond KL, Beck DE, Hicks TC, Timmcke AE, Whitlow CW, Margolin DA. Implications of negative technetium 99m-labeled red blood cell scintigraphy in patients presenting with lower gastrointestinal bleeding. Am J Surg. Mar 2007;193(3):404-7; discussion 407-8. [Medline].
Moukarbel GV, Signorovitch JE, Pfeffer MA, McMurray JJ, White HD, Maggioni AP, et al. Gastrointestinal bleeding in high risk survivors of myocardial infarction: the VALIANT Trial. Eur Heart J. Sep 2009;30(18):2226-32. [Medline].
Mönkemüller K, Neumann H, Meyer F, Kuhn R, Malfertheiner P, Fry LC. A retrospective analysis of emergency double-balloon enteroscopy for small-bowel bleeding. Endoscopy. Aug 2009;41(8):715-7. [Medline].
Wong Kee Song LM, Baron TH. Endoscopic management of acute lower gastrointestinal bleeding. Am J Gastroenterol. Aug 2008;103(8):1881-7. [Medline].
Zuccaro G. Epidemiology of lower gastrointestinal bleeding. Best Pract Res Clin Gastroenterol. 2008;22(2):225-32. [Medline].
| Lower Gastrointestinal Bleeding in Adults | Percentage of Patients |
Diverticular disease
| 60% |
Inflammatory bowel disease
| 13% |
Benign anorectal diseases
| 11% |
Neoplasia
| 9% |
| Coagulopathy | 4% |
| Arteriovenous malformations (AVMs) | 3% |
| TOTAL | 100% |
| Source: Vernava AM, Longo WE, Virgo KS. A nationwide study of the incidence and etiology of lower gastrointestinal bleeding. Surg Res Commun. 1996;18:113-20.[6] | |
| Lower Gastrointestinal Bleeding in Children and Adolescents |
| Intussusception |
Polyps and polyposis syndromes
|
Inflammatory
|
| Meckel diverticulum |

