Lower Gastrointestinal Bleeding


Practice Essentials

Lower gastrointestinal bleeding (LGIB) is a frequent cause of hospital admission and is a factor in hospital morbidity and mortality. LGIB is distinct from upper GI bleeding in epidemiology, management, and prognosis. The image below illustrates the different types of LGIB.

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Types of lower gastrointestinal bleeding (LGIB).

Signs and symptoms

The clinical presentation of LGIB varies with the anatomical source of the bleeding, as follows:

In practice, however, patients with upper GI bleeding and right-sided colonic bleeding may also present with bright red blood per rectum if the bleeding is brisk and massive.

The presentation of LGIB can also vary depending on the etiology. A young patient with infectious or noninfectious (idiopathic) colitis may present with the following:

An older patient with diverticular bleeding or angiodysplasia may present with painless bleeding and minimal symptoms. Ischemic colitis, abdominal pain, and varying degrees of bleeding are usually observed in patients with multiple comorbidities such as congestive heart failure (CHF), atrial fibrillation, or chronic renal failure (CRF). LGIB can be mild and intermittent, as often is the case of angiodysplasia and colon carcinoma, or moderate or severe, as may be the situation in diverticula-related bleeding. Colon carcinoma rarely causes significant LGIB.

Massive lower GI bleeding usually occurs in patients aged 65 years and older who have multiple medical problems, and produces the following manifestations:

See Clinical Presentation for more detail.


Nonsurgical modalities used to diagnose LGIB include the following:

Fiberoptic flexible colonoscopy is the initial diagnostic method of choice in most patients who are hemodynamically stable. Colonoscopy should be performed following a rapid bowel preparation (“prep”) with volume cathartic agents. Rapid bowel prep colonoscopy has higher diagnostic and therapeutic yields compared to unprepped colonoscopic evaluation. In hemodynamically unstable patients and in those with brisk ongoing LGIB, angiography with or without a preceding radionuclide scan can be performed. Angiography is also performed if colonoscopy has failed to identify a bleeding site. Rarely, exploratory laparotomy and intraoperative push enteroscopy can be performed in truly hemodynamically unstable patients owing to the speed and the volume of the bleeding.

Appropriate routine blood tests include the following:

Helical CT scanning of the abdomen and pelvis can be used when a routine workup fails to determine the cause of active GI bleeding. Multiple criteria are used for establishing the bleeding site, including the following[1, 2] :

Patients who have experienced multiple episodes of LGIB without a known source or diagnosis should undergo the following:

See Workup for more detail.


The management of LGIB has 3 components, as follows:

Resuscitation and initial assessment

Initial resuscitation involves establishing large-bore IV access and administration of normal saline. The patient's blood loss and hemodynamic status should be ascertained, and in cases of severe bleeding, the patient may require invasive hemodynamic monitoring to direct therapy.


Once the bleeding site is localized, nonsurgical therapeutic options that may be considered include the following:

In patients in whom the bleeding site cannot be determined, vasoconstrictive agents such as vasopressin (Pitressin) can be used. If vasopressin is unsuccessful or contraindicated, superselective embolization is useful.


The indications for surgery include the following:

See Treatment and Medication for more detail.


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.[3] Indeed, LGIB continues to be a frequent cause of hospital admission and is a factor in hospital morbidity and mortality, particularly among elderly patients.[4] 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[4] and requires transfusion of at least 4 units (U) of blood.

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Types of lower gastrointestinal (GI) bleeding. HR = heart rate; SBP = systolic blood pressure.

Massive LGIB is defined as follows:

LGIB has a mortality rate ranging from about 10% to 20%, with patients of advanced age (>60 y) and patients with comorbid conditions (eg, multiorgan system disease, transfusion requirements in excess of 5 U, need for operation, and recent stress, such as surgery, trauma, and sepsis) at the 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.

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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.[5] 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 site.

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.[6, 7] The most feared complication of embolization of the mesenteric vessels is ischemic colitis, which has limited its use in 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 the GI tract; this modality can detect hemorrhage at rates as low as 0.1 mL/min.

Key points

The physical examination should be thorough and include the skin, oropharynx, nasopharynx, abdomen, perineum, and anorectum. Therefore, nasogastric tube insertion, digital rectal examination, and anoscopy/proctoscopy should be part of the initial physical examination in all patients.

In most patients with LGIB, colonoscopy is the initial diagnostic method of choice. Colonoscopy is successfully used to identify the site of severe LGIB in approximately 80-90% of patients.

Nuclear scintigraphy is a sensitive diagnostic tool and can detect hemorrhage at rates as low as 0.1 mL/min (0.1-0.5 mL/min), as opposed to angiography, which detects bleeding at rates of 1-1.5 mL/min.

Because of the high false-localization rate (10-60%) for the bleeding site, performing segmental resections based solely on scintigraphy results is not recommended unless an immediate blush can be identified at the start of the study.

Emergency angiography as an initial study is indicated in a highly select group of patients with massive ongoing LGIB.

Segmental bowel resection following precise localization of the bleeding point is preferred treatment because of low postoperative morbidity and mortality when compared with subtotal colectomy.

Subtotal (total abdominal) colectomy with temporary end ileostomy is the procedure of choice in patients who are actively bleeding from an unknown source.

Blind segmental resection should not be performed because of a prohibitively high rebleeding rate, morbidity, and mortality rate.

For patient education information, see Digestive Disorders Center, as well as Gastrointestinal Bleeding (GI Bleeding), Rectal Bleeding, Inflammatory Bowel Disease (IBD), Diverticulosis and Diverticulitis, and Anal Abscess.


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. 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.


Diverticulosis, angiodysplasia, colitis, carcinoma, and anorectal disease in the pathophysiology of LGIB are briefly discussed in this section.


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 the 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.[8] 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.[8] This may be because false right-sided diverticula have wider necks and domes, which expose the vasa recta to injury over a greater length. The incidence of true right-sided diverticula is uncommon (1%-2%) in the United States, unlike in Asian populations. True right-sided diverticula are usually solitary and originate in the anterior cecum adjacent to the ileocecal valve. Usually true right-sided diverticula cause right-sided diverticulitis and are misdiagnosed as appendicitis.


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.


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.

Other diseases

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.[9]

Postpolypectomy hemorrhage is reported to occur in 0.1%-3% of patients up to 1 month following colonoscopic polyp resection.

Various small intestinal conditions, such as Crohn disease, Peutz-Jeghers syndrome, hemangiomas, and small intestinal adenocarcinomas, may cause small intestinal bleeding, but these hemorrhages are usually occult in nature.


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.

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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%).[10] 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).[9] 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%.[11]

Table 1. Common Causes of Lower Gastrointestinal Bleeding in Adults

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See Table

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%).[12] 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

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See Table


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 anti-inflammatory drugs (NSAIDs) and aspirin.


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.[13]

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.[14] 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.[14]

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.


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.[15] Patients with HIV can also bleed from hemorrhoids and anal fissures, in which situations 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. Using the lowest effective dose for both short and long-term users is recommended.[16] 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.[17]

Benign small intestinal neoplasms are usually asymptomatic, but up to 10% may cause small intestinal bleeding. Small intestinal adenomatous polyps, leiomyomas, Peutz-Jeghers syndrome, and hemangiomas may cause occult or frank LGIB.

Other uncommon causes of LGIB include stercoral ulcer and Dieulafoy lesion of the small or large bowel.


LGIB that requires hospitalization represents less than 1% of all hospital admissions in the United States.[9] 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.[12] LGIB is somewhat more common in men than in women, because diverticulosis and vascular disease are more common in men.

Worldwide, acute LBIG accounts for 1-2% of hospital emergencies, with 15% of these presenting as massive bleeding and about 5% requiring operative intervention.[18] The small bowel represents 5% of all LGIB bleeding sites, but it is the most common site of obscure bleeding.[18]

The leading causes of significant LGIB are diverticulosis and angiodysplasia. Colonic diverticular disease is the most common cause of LGIB.[19]  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 is 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.[20]


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 the greatest risk.[4] 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 colonoscopy. Pharmacologic discoveries are also improving patient care and outcome. Therefore, the therapeutic armamentaria have expanded greatly in the last 50 years.


History and physical examination are essential parts of an initial evaluation of lower gastrointestinal bleeding (LGIB). These can provide valuable clues to the etiology and anatomical source of bleeding. Document whether this is a first or recurrent episode of gastrointestinal (GI) bleeding as well as significant medical history (including peptic ulcer disease, liver disease, cirrhosis, coagulopathy, inflammatory bowel disease [IBD]) and previous medication use (eg, nonsteroidal anti-inflammatory drugs (NSAIDs) and/or warfarin). In patients with cancer, the history of radiation, chemotherapy, or both should be considered.

The clinical presentation of LGIB varies with the anatomical source of the bleeding as well as with the etiology. Commonly, LGIB from the right side of the colon can manifest as maroon stools, whereas a left-sided bleeding source may be evidenced by bright red blood per rectum. In practice, however, patients with upper GI bleeding (UGIB), and right-sided colonic bleeding may also present with bright red blood per rectum if the bleeding is brisk and massive. Similarly, cecal bleeding may present with melena, which is typically seen with UGIB, suggesting no distinct method exists for determining the anatomic source of bleeding based solely on stool color.

The presentation of LGIB can also vary depending on the etiology. A young patient may present with fever, dehydration, abdominal cramps, and hematochezia caused by infectious or noninfectious (idiopathic) colitis. An older patient may present with painless bleeding and minimal symptoms caused by diverticular bleeding or angiodysplasia. LGIB can be mild and intermittent, as often is the case with angiodysplasia, or moderate or severe, as may be the situation in diverticula-related bleeding.

Symptoms are also important in identifying the source of bleeding. Young patients may present with abdominal pain, rectal bleeding, diarrhea, and mucous discharge that may be associated with IBD. However, elderly patients presenting with abdominal pain, rectal bleeding, and diarrhea may have ischemic colitis, or elderly patients with atherosclerotic heart disease may present with intermittent LGIB and syncope that may be due to angiodysplastic lesions. Stools streaked with blood, perianal pain, and blood drops on the toilet paper or in the toilet bowl may be associated with perianal pathology, such as anal fissure or hemorrhoidal bleeding.

Massive lower GI bleeding is a life-threatening condition in which patients present with a systolic blood pressure of less than 90 mm Hg and a hemoglobin (Hb) level of 6 g/dL or less. These patients are usually aged 65 years and older, have multiple medical problems, and are at risk of death from acute hemorrhage or its complications. The passage of maroon stools or bright red blood from the rectum is usually indicative of massive lower GI hemorrhage.

Diverticular bleeding

Although diverticular bleeding is painless, patients may experience mild abdominal cramping due to the intraluminal blood that triggers spasmodic contraction of the colonic wall. Bleeding is usually acute, without antecedent symptoms, and is self-limited in about 70-80% of cases. Rebleeding can occur in up to 25% of patients.[21]

If the bleeding is brisk and voluminous, patients may be hypotensive and display signs of shock. Clinical recommendations for diverticular bleeding published by the American Academy of Family Physicians (AAFP) in 2009 state that bleeding or unstable vital signs require rapid assessment and resuscitation before diagnostic testing.[22]

Chronic, intermittent, minimal blood loss per rectum is unlikely to be caused by diverticular bleeding, because diverticular bleeding is arterial in origin.


Significant angiodysplasia-related bleeding, like diverticular bleeding, presents as painless, self-limited hematochezia or melena; angiodysplasia-related bleeding is venocapillary. Unlike diverticular bleeding, angiodysplasia tends to cause slow but repeated episodes of bleeding. Therefore, patients may present with Hemoccult-positive stools, iron-deficiency anemia, and syncope. Occasionally, patients can present with bleeding of large quantities.


Ischemic colitis may or may not present with abdominal pain and associated bloody diarrhea. The bloody diarrhea is self-limited but can recur if the underlying cause is not corrected. Although the clinical presentation is indistinguishable at times from that of infectious colitis, idiopathic colitis, and radiation-induced colitis, patients with ischemic colitis are usually older with cardiovascular comorbidities. Ischemic colitis may be fulminant, presenting with acute abdominal pain, rectal bleeding, and hypotension, or this condition may be insidious, presenting with pain and rectal bleeding over several weeks.

In infectious colitis, the clinical examination findings vary depending on the volume status, amount of blood loss, extent of abdominal pain, and accompanying peritoneal signs. The clinical presentation of fever, diarrhea, dehydration, and abdominal pain can be caused by any of a number of bacterial, viral, or parasitic pathogens. The specific etiology can only be determined by isolating the organism from the stool, blood, or other tissue fluid. Patients may be quite ill and may experience intravascular volume depletion, abdominal pain, and generalized malaise, but blood loss is usually mild and a minor factor in symptomatology.

The clinical presentation of ulcerative colitis depends on whether the disease is mild, moderate, or severe. Although bleeding is minimal to none in people with mild disease, those with moderate-to-severe ulcerative colitis present with bloody diarrhea with pus, abdominal cramps, and dehydration. Symptoms of weight loss and fever occur in those with severe disease. Patients with Crohn disease usually present with fever, nonbloody diarrhea, and abdominal pain. However, patients with Crohn colitis can present with bloody diarrhea.

Colon carcinoma

The bleeding associated with colon cancer, particularly right-sided bleeding, can be insidious, with patients presenting with iron-deficiency anemia and syncope. Right-sided colon cancer may also present with maroon-colored stools or melena, whereas left-sided colonic cancers can present as bright red blood per rectum, which can sometimes be confused with hemorrhoidal bleeding.

Anorectal disease

Hemorrhoidal bleeding is most often painless, whereas bleeding secondary to fissures tends to be painful. Hemorrhoids can also present with strangulation, hematochezia, and pruritus. Typically, bright red blood coats the stool at the end of defecation or blood may stain the toilet paper. Rarely, the bleeding may be copious, distressing to the patient.

Physical Examination

The physical examination should be thorough and include the skin, oropharynx, nasopharynx, abdomen, perineum, and anorectum to evaluate for sources of bleeding.

Because brisk UGIB can present as LGIB, a nasogastric (NG) tube may be necessary and the aspirate or lavage examined for the presence of blood and bile. These aspirates usually correlate well with upper gastric hemorrhage proximal to the Treitz ligamentum; therefore, insert an NG tube to confirm the presence or absence of blood in the stomach.

If necessary, perform gastric lavage with warm isotonic fluids to obtain bilious discharge; an aspirate that is positive for bile is comprehensive in that it includes fluid even beyond the pylorus. In such a scenario, if no blood is present, a UGIB source only makes sense if the bleeding has stopped. If this possibility exists, an esophagogastroduodenoscopy (EGD) should be performed to obtain a more specific evaluation of the upper GI tract. Place a Foley catheter to monitor urine output. Careful digital rectal examination, anoscopy, and rigid proctosigmoidoscopy should exclude an anorectal source of bleeding.

Patients who have rectal varices with portal hypertension may develop painless massive LGIB; therefore, examining the anorectum early in the workup is important. If active bleeding is identified, treat it aggressively. Note that the discovery of benign anorectal disease does not exclude the possibility of more proximal bleeding from the lower GI tract.

Once the bleeding is determined to be from the lower GI tract as opposed to an upper GI source, the tempo of the bleeding and the extent of blood loss should be quickly estimated so that a precise and targeted algorithm is adopted (see an example in the image below). Patients with massive LGIB usually present with bright red blood per rectum, hypotension, and a markedly reduced hematocrit as opposed to patients with mild bleeding who may present with intermittent passage of maroon-colored stools. The emergency implementation of aggressive resuscitation, diagnostic evaluation, and early involvement of a gastroenterologist (and surgeon in the case of a rapid LGIB) is key to reducing the morbidity and mortality and to improving outcomes.

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Algorithm for massive lower gastrointestinal (GI) bleeding, surgical perspective. EGD = esophagogastroduodenoscopy; NG = nasogastric; 99mTc RBC = tech....

Approach Considerations

The 3 nonsurgical modalities used to diagnose lower gastrointestinal bleeding (LGIB) are colonoscopy, radionuclide scans, and angiography. Apart from colonoscopy, endoscopic procedures, such as esophagogastroduodenoscopy (EGD), wireless capsule endoscopy (WCE), push enteroscopy, and double-balloon enteroscopy, are used depending on the clinical circumstance. The sequence of using various modalities depends on such factors as rate of bleeding, hemodynamic status of the patient, and inability to localize bleeding with the initial modality.

Patients who have experienced multiple episodes of LGIB without a known source or diagnosis should undergo elective mesenteric angiography, upper and lower endoscopy, Meckel scanning, upper gastrointestinal (GI) series with small bowel examination, and enteroclysis. Elective evaluation of the entire GI tract may identify uncommon lesions and undiagnosed arteriovenous malformations (AVMs).

Ryan et al performed 17 elective provocative bleeding studies for occult LGIB in 16 patients.[23] Although an abnormality was identified in 50% of patients, bleeding was provoked in 6 (37.5%) patients. Most of the positively provoked patients (ie, 5 patients) had a previously positive tagged red cell scintigraphy.[23] Of the 6 patients with provoked bleeding, 3 were treated with superselective embolization at the time of provoked bleeding, 2 were treated with estrogen therapy, and 1 was treated with palliative therapy.[23] Ten patients did not bleed during the provoked study.[23]

Routine Testing

Appropriate blood tests include a complete blood cell (CBC); serum electrolytes levels (eg, sequential multiple analysis 7 [SMA7]); and a coagulation profile, including activated partial thromboplastin time (aPTT), prothrombin time (PT), manual platelet count, and bleeding time.

Computed Tomography Scanning

Macari et al assessed the ability of computed tomography (CT) scanning to differentiate between intestinal ischemia and intramural hemorrhage and found that although some of the CT features overlap, ischemia typically involves a long segment with wall thickening of less than 1 cm, whereas intramural hemorrhage typically involves a short segment with wall thickening of 1 cm or greater.[24] Diagnosis was confirmed by laboratory findings, clinical parameters, and follow-up examinations, or at surgery.

Helical CT scanning of the abdomen and pelvis can be used when a routine workup fails to determine the cause of active gastrointestinal (GI) bleeding. Multiple criteria, including vascular extravasation of the contrast medium, contrast enhancement of the bowel wall, thickening of the bowel wall, spontaneous hyperdensity of the peribowel fat, and vascular dilatations, are used to establish the bleeding site with helical CT scans.[1, 2] The presence of diverticula alone is not enough to define the bleeding site.[1]

Three-phase helical CT scanning should be performed using intravenous (IV) contrast. Water can be used as an oral contrast in the workup of patients who are actively bleeding.

A pilot study done in Sydney, Australia, to evaluate helical CT scanning as a diagnostic tool for acute LGIB suggested that this imaging modality is a safe, convenient, and an accurate diagnostic tool relative to mesenteric angiography and colonoscopy.[25] The authors proposed a new management algorithm for acute lower GI hemorrhage using helical CT scanning as the preselective mesenteric angiography screening tool.

Multidetector row CT (MDCT) scanning is also useful in the evaluation of LGIB.[26] Frattaroli et al compared the sensitivity of MDCT scanning with endoscopy in identifying the site and etiology of acute UGIB and LGIB and reported that, in terms of identifying the anatomic location and etiology of UGIB, MDCT scanning had a sensitivity of 100% and 90.9%, respectively, whereas endoscopy had a sensitivity of 72.7% and 54.5%, respectively.[27] For LGIB, MDCT had a sensitivity for site and etiology identification of 100% and 88.2%, respectively, whereas endoscopy had a sensitivity of 52.9% for both identifications.[27]


In most patients with LGIB, colonoscopy is the initial diagnostic method of choice.[28] Colonoscopy is successfully used to identify the site of severe LGIB in approximately 74-82% of patients.[11] In addition to its diagnostic utility, colonoscopy offers the opportunity for therapeutic intervention[4] in the treatment of vascular ectasias, diverticular bleeding, neoplastic lesions, and ulcerative processes. Rapid colonic lavage with GoLYTELY (orally or by nasogastric [NG] tube) clears the intraluminal blood, clot, and stool, providing an adequate environment for visualization of the lower GI mucosa and lesions.

Fiberoptic flexible colonoscopy can be utilized in two different fashions. The historical urgent colonoscopy includes rapid bowel preparation using 1-liter volume cathartic agents such as GoLYTELY every 30 to 45 minutes. This rapid preparation is completed in 2 to 3 hours using 4 L to 6 L of GoLYTELY. Placement of an NG tube with/without 10 mg IV metoclopramide can be used in patients who cannot tolerate rapid drinking. Emergent/immediate unprepared hydroflush colonoscopy can be also performed in an emergent fashion.[29]

The 2008 SIGN guideline recommends the use of early colonoscopy to determine the cause and site of massive LGIB; the procedure can be used with CT scanning, CT angiography, or digital subtraction angiography. If colonoscopy fails to define the site of bleeding in patients with massive LGIB, angiographic transarterial embolization is recommended as an effective approach to control hemorrhage.[17]

Urgent colonoscopy has become the first choice of diagnostic modality following rapid purge with volume cathartics, such as GoLYTELY. Jensen and Machicado prospectively evaluated the role of urgent colonoscopy after purge in 80 consecutive patients with severe hematochezia and noted 74% of patients had colonic lesions, 11% had upper GI lesions, and 9% had presumed small bowel lesions; in 6%, no bleeding site was identified.[30] Although the investigators recommended that EGD be performed before urgent colonoscopy, upper and lower endoscopies can be performed simultaneously.

In another study, urgent colonoscopy yielded a diagnosis in 90% of the patients, which provided an opportunity for therapy at the same time. The patients who underwent urgent colonoscopic evaluation had a significantly shorter hospital stay. One can perform the urgent colonoscopy in the operating room or endoscopy suite in hemodynamically stable patients. If patients become unstable or colonoscopy reveals an active fulminant inflammation, the procedure should be aborted.

Urgent colonoscopy tends to result in improved patient outcomes. In patients who are hemodynamically stable with moderate to severe bleeding, diagnostic urgent colonoscopy is the test of choice, because of its higher diagnostic yield and lower complication rate as compared with angiography.[30, 31] The 2009 AAFP diverticular bleeding recommendations emphasize that urgent colonoscopy in the context of lower GI bleeding is safe.[22]

Large amounts of blood in the GI tract act as a cathartic and provide adequate cleanup from stool and other debris. Emergent unprepared hydroflush colonoscopy can be performed in patients with massive LGIB. Initially, these patients are given 1 L of tap water enema 3 or 4 times over 1 hour prior to emergent colonoscopy. This technique utilizes a hydro-jet endoscopic irrigation system with a high-powered mechanical suction system. The irrigation pump rate is set to maximum flow rate at the time of the colonoscopy.[29]

Actively bleeding lesions can be treated with colonoscopic thermoregulation, epinephrine injection, photocoagulation, clip application, and a combination of these methods.[13] Incidentally discovered lesions should be left alone.

Candidate screening criteria

Candidates for urgent colonoscopy should be properly screened and include patients who are hemodynamically stable with no ongoing brisk bleeding, because the diagnostic yield is lowered in such patient populations. Thus, the best candidates for urgent colonoscopic evaluation are patients who are bleeding slowly or who have already stopped bleeding. The bowel should be well prepared, with a rapid oral purge (or via NG tube in selected patients), because performing an urgent colonoscopy on an unprepared bowel is difficult and frequently unsuccessful.

Alternatively, emergent/immediate unprepared hydroflush colonoscopy can be performed in a patient in the intensive care unit with ongoing active severe LGIB.[29]

The bowel preparation does not reactivate or increase the rate of bleeding. In cases of suspected perforation or obstruction, plain abdominal radiography should be performed before colonoscopy to rule out these complications.

A randomized controlled trial comparing urgent versus elective colonoscopy was performed for patients with serious lower gastrointestinal bleeding. This study recommended that upper endoscopy should be performed initially to rule out an upper gastrointestinal source. This study also showed that the use of urgent colonoscopy does not improve the clinical outcome or cost of care when compared with elective colonoscopy in patients with serious hematochezia.[32]

Advantages and disadvantages of colonoscopy

The advantages of colonoscopy include the following: (1) A bleeding lesion is localized in about 50-70% of patients; (2) definitive treatment, such as thermoregulation, epinephrine injection therapy, clip application, or laser photocoagulation, is possible during the procedure; (3) massively bleeding lesions that have stopped hemorrhaging are identified more often with colonoscopy than with angiography.

The disadvantages of colonoscopy include the following: (1) urgent or emergent colonoscopy must be performed by skilled endoscopists; (2) urgent colonoscopy requires a bowel preparation that can cause a 4- to 6-hour delay; (3) emergent unprepared hydroflush colonoscopy requires several 1 L of tap water enemas and a 1-hour delay; (4) a perforation during the examination is possible, particularly in a patient who is ill; (5) colonoscopy carries the risks of sedation for patients who are acutely bleeding; and (6) technical problems can make diagnosis and treatment more difficult.

Radionuclide Scanning/Nuclear Scintigraphy

The role of radionuclide scanning, or nuclear scintigraphic imaging, in the diagnosis and treatment of patients who present with LGIB remains controversial. Radionuclide scans include the technetium-99 (99 Tc) sulfur colloid scan and the99m Tc pertechnetate–labeled autologous red blood cell scan (TRBC scan), as well as indium-111 (111 In)–labeled RBC scintigraphy.

Nuclear scintigraphy is a sensitive diagnostic tool (86%) and can detect hemorrhage at rates as low as 0.1 mL/min (0.1-0.5 mL/min), as opposed to angiography, which detects bleeding at rates of 1-1.5 mL/min. This technique is reportedly 10 times more sensitive than mesenteric angiography in detecting ongoing bleeding, but it suffers from a low specificity (50%) compared with endoscopy or angiography due to its limited resolution; this has led many investigators to recommend that scintigraphic imaging be used primarily as a screening examination to select patients for mesenteric angiography. The 2008 SIGN guideline suggests nuclear scintigraphy may be effective in determining the source of bleeding in patients with significant recent hemorrhage.[17]

Radionuclide scans frequently are performed before angiography, because the scans detect bleeding at a slower rate than what can be detected with angiography, thereby potentially eliminating the need for an invasive procedure.[33] Negative findings on radionuclide scan make subsequent angiography less likely to be of benefit. In patients who are hemodynamically unstable and in patients with brisk ongoing LGIB, an angiography with or without a preceding radionuclide scan can be performed.

Ng and colleagues retrospectively reviewed the records of 86 patients with positive TRBC scintigraphy findings and found that those with an immediate blush (within 2 min of the study) revealed a positive predictive value of 75% for angiography.[34] However, patients with a delayed blush (after 2 min of the study) had a negative predictive value of 93% for angiography. Thus, patients with delayed blush should proceed with colonoscopic evaluation instead of mesenteric angiography. Use TRBC scintigraphy as a prescreening test for selective mesenteric angiography. The 2009 AAFP recommendations state that TRBC or arteriography may be used in patients with continued bleeding when endoscopy has not aided in making a diagnosis.[22]

In a study by Ryan et al, TRBC scintigraphy identified the site of bleeding accurately in 9 patients with massive LGIB[35] ; in 6 of 9 patients, the scintigraphy finding was positive in the first 5 minutes of the study. In 3 patients, the scintigraphy finding was positive at 14-45 minutes.

Emslie et al found that TRBC scanning is effective in localizing GI bleeding when positive within the continuous phase of imaging.[33]

TRBC scans

The TRBC scan is preferred, because its half-life is longer and abdominal images can be obtained for up to 24 hours, which is advantageous in patients with intermittent bleeding. TRBC scans detect slow bleeds and have a sensitivity ranging from about 80% to 98%.[36] The bleeding site can be identified accurately when intraluminal accumulation of TRBC is observed during the dynamic phase of scanning, but the site may be less accurately identified if only the still images are reviewed.

Tc sulfur colloid scans

No preparation is required for99m Tc sulfur colloid. This agent has a very short half-life (2.5-3.5 min), because it is rapidly cleared by the reticuloendothelial system; as a result, images provided by such scans can be taken for the few minutes that the colloid is in circulation. However, these scans may not adequately demonstrate abnormalities in patients with intermittent bleeding.99m Tc sulfur colloid enhances the liver and spleen such that bleeding from both the hepatic flexures and the splenic flexures may be obscured.

In-labeled RBC scintigraphy

The use of111 In–labeled RBC scintigraphy to detect intermittent bleeding has been described in the medical literature in a handful of publications. Ferrant and colleagues initially used111 In-labeled RBC scintigraphy in patients with lower GI bleeding in 1980,[37] but this technique remains underutilized because of a prolonged half-life of 67 hours. It is also a more expensive and more labor-intensive technology than99m Tc labeling. Furthermore, the image quality and localization of bleeding can be less than desirable because of the prolonged half-life and intestinal motility.

Nonetheless, the longer half-life of111 In-labeled RBC scintigraphy can be useful in locating intermittent bleeding points, particularly when conventional methods have failed. Schmidt et al published a report on 6 patients in whom99m Tc scanning was initially unrewarding.[38] Subsequent scintigraphy with111 In-labeled RBCs located the site of bleeding in all patients. In another study, Mole et al detected synchronous, small and large intestinal adenocarcinomas with111 In-labeled RBC scintigraphy in a 70-year-old patient with intermittent GI bleeding and profound blood loss anemia.[39]

Advantages and disadvantages of radionuclide scanning

Advantages for radionuclide scans include their noninvasiveness and their high sensitivity. The disadvantages of radionuclide scans include the fact that the scans have a high false localization rate, ranging from approximately 3% to 59%.[40] In 24 publications, the bleeding point was accurately localized in 52-90% of positive cases, with an average of 86% and incorrect localization of 14%. Because of the high false localization rate (10-60%) for the bleeding site, performing segmental resections based solely on scintigraphy results is not recommended. Another disadvantage of radionuclide scans is that the scans must be performed during active bleeding.

The difficulty of localization was demonstrated in a study by Hunter et al in which the results of TRBC scanning were incorrect in about 25% of patients[41] ; 8 patients underwent unwarranted surgical procedures based upon the findings of more definitive tests. Poor localization of the source of the bleed in radionuclide scans often is due to the overlapping segments of bowel and the migration of tagged RBCs in the large bowel.

Recurrent lower GI bleeding occurs after negative TRBC scintigraphy. Hammond et al reported the overall rebleeding rate to be 27% and concluded that age, sex, bleeding source, use of anticoagulant/antiplatelet agents, length of hospital stay, admission hematocrit (Hct), Hct nadir, and transfusion requirements are not predictive of patients who will rebleed.


In 1965, Baum et al described selective mesenteric angiography in the diagnosis of gastrointestinal (GI) bleeding.[5] Since then, the value of mesenteric angiography in the diagnosis and management of LGIB has been well established.

Angiography is performed in the presence of active bleeding that precludes colonoscopy and after colonoscopy has failed to identify a bleeding site. Selective mesenteric angiography can detect bleeding at a rate of more than 0.5 mL/min.

In a patient with active GI bleeding, the radiologist first cannulates the superior mesenteric artery, because most of the hemodynamically significant bleeding originates in the right colon. The extravasation of contrast material indicates a positive study finding. If the findings from the study are negative, the inferior mesenteric artery is cannulated, followed by the celiac artery. In some cases, aberrant vascular anatomy can contribute to colonic or small bowel circulation; in other cases, patients with upper GI bleeding (UGIB) may present in an uncommon clinical fashion.

Diverticula, angiodysplasia, and intestinal varices can be visualized by angiography. The characteristic angiographic findings of colonic angiodysplasias are clusters of small arteries during the arterial phase of the study, accumulation of contrast media in vascular tufts, early opacification, and persistent opacification due to the late emptying of the draining veins. If mesenteric angiography is performed at the time of active bleeding, extravasation of contrast media is visualized.

Once the bleeding point is identified, angiography offers potential treatment options, such as selective vasopressin drip and embolization. Thirteen publications reported experiences with selective mesenteric angiography. When 657 patients underwent mesenteric angiography, the percentage of positive study findings fluctuated between 27% and 86%, with an average of 45%. Because of the intermittent nature of LGIB, the number of positive study findings is significantly less with this invasive diagnostic modality.

Emergency angiography

Emergency angiography as an initial study is indicated in a highly selected group of patients with massive ongoing LGIB. Browder et al used 2 criteria to triage patients for emergency angiography[42] : at least 4 units of blood transfusion in the first 2 hours following hospital admission and systolic blood pressure of less than 100 mm Hg with aggressive resuscitation. Fifty patients underwent emergency angiography, and bleeding was localized in 72% of patients. Vasopressin infusion was successful in 91%; however, 50% experienced bleeding following cessation of the vasopressin infusion.[42] Thus, in patients with ongoing hemorrhage, emergency angiography, and vasopressin infusion have improved operative morbidity, mortality, and outcome.

Widlus and Salis suggested that the use of Reteplase, a fibrinolytic agent, is safe and effective as a provocative agent in angiography. By stimulating bleeding to allow localization, in patients with occult, recurrent, massive LGIB.[43] An initial diagnostic visceral arteriogram was performed and failed to identify the source of bleeding in each patient. When Reteplase was administered and provocative arteriography was repeated, bleeding was identified in 8 of 9 (89%) patients, and these patients were treated with microembolization, segmental resection, or conservatively.[43]

Advantages and disadvantages of angiography

The advantages of angiography include: (1) This modality provides accurate localization of the bleeding; (2) it has a therapeutic utility that includes the use of vasopressin infusion or embolization; and (3) it does not require preparation of the bowel.

The disadvantages of angiography include: (1) It has a sensitivity of approximately 30-47%; (2) it can only be performed during active bleeding; and (3) it has a complication rate of about 9%. Such complications include thrombosis, embolization, and renal failure.[30]

Also see Radiologic Approach to Lower Gastrointestinal Bleeding.

Barium Enema

Double-contrast barium enema examinations can be justified only for elective evaluation of previous unexplained LGIB. Do not use barium enema examination in the acute hemorrhage phase, because it makes subsequent diagnostic evaluations, including angiography and colonoscopy, impossible.

Contrast Radiography

Elective contrast radiography of the small bowel and/or enteroclysis is often valuable in investigation of long-term, unexplained LGIB (see Small Bowel Visualization ).


An esophagogastroduodenoscopy (EGD) is performed if a nasogastric (NG) tube aspirate is positive for blood, because about 10% of patients presenting with LGIB have bleeding originating from the upper GI tract. Small bowel endoscopic procedures are usually performed after EGD, colonoscopy, radionuclide scans, and angiography have been used and the bleeding site not localized. If the nasogastric tube (NG) tube aspirate reveals bile, upper GI bleeding is practically excluded. There may be a role for EGD in a small group of patients who has both hemoglobin- and bile-negative NG tube aspirates.

Small Bowel Visualization

Small bowel visualization includes the following modalities: (1) wireless capsule endoscopy (WCE), (2) push enteroscopy, (3) enteroclysis, and (4) double-balloon enteroscopy. Although no consensus exists on which modality to use initially, WCE is increasingly being employed as the test of choice for small bowel bleeding.

Endoscopy has diagnostic and therapeutic importance in children for conditions including solitary rectal ulcer syndrome, polyps, vascular lesions, and colonic inflammation and ulceration.[44]

Advantages and disadvantages of WCE

The advantages of WCE include: (1) it is noninvasive; (2) as opposed to push enteroscopy, WCE permits visualization of most or all of the small bowel; and (3) WCE identifies bleeding more often than push enteroscopy.[45] Disadvantages of WCE include possible retention of the capsule in patients with severe motility disorders, Crohn disease with strictures, and no therapeutic capability is possible.

WCE is not a relevant study for hemodynamically significant bleeding. Contraindications to WCE include the following: (1) dementia (eg, patients not being able to cooperate with the swallowing of the capsule), (2) esophageal strictures, and (3) partial small bowel obstruction.

Push enteroscopy

Although WCE is used as the initial test for small bowel visualization, some experts recommend push enteroscopy as the initial test because of its therapeutic capability. Push enteroscopy is performed with a pediatric colonoscope or a dedicated enteroscope, and once the bleeding site is visualized, it can be treated or tattooed. The main disadvantage of push enteroscopy is that it generally reaches only the proximal 60 cm of the jejunum; bleeding sites beyond that cannot be detected.


Enteroclysis is a double-contrast study performed by passing a tube into the proximal small bowel and then injecting barium. Therefore, this evaluation is avoided in acute bleeding, because enteroclysis may compromise subsequent attempts at endoscopy and angiography. For the same reason, barium studies, such as air contrast barium enemas, are best avoided in acute LGIB.

Histologic Findings

Most colonic diverticula are false pulsion diverticula and are composed only of mucosa and submucosa herniated through the colonic wall musculature. Hemorrhage associated with diverticula comes from perforated vasa rectae located at the neck or the apex of the diverticula.

Colonic angiodysplasias are vascular ectasias commonly located on the right side of the colon. Microscopically, vascular ectasia consists of dilated thin-walled venules and capillaries localized in the submucosa of the colonic wall.

Approach Considerations

The management of LGIB has 3 components, as follows:

With advances in diagnostic and therapeutic endoscopy and angiography, the ability to localize and subsequently treat lower gastrointestinal bleeding (LGIB) has resulted in improved patient outcomes and reduced healthcare costs.[19] The need for surgery also has been significantly reduced.

The sequence of using these modalities depends on the patient's clinical status, the rate of bleeding, and local expertise in specific surgical and nonsurgical procedures. Using any one modality should not preclude the subsequent use of another modality if required. In case of surgery, preoperative localization of bleeding is essential, because segmental colectomies performed after bleeding is localized are associated with the lowest morbidity and mortality.

According to the 2008 SIGN guideline, early endoscopy should be used within 24 hours of initial presentation of acute LGIB, where possible.[17]

Massive LGIB is a life-threatening condition; although this condition manifests as maroon stools or bright red blood from the rectum, patients with massive upper gastrointestinal bleeding (UGIB) may also present with similar findings. Regardless of the level of the bleeding, one of the most important elements in the management of patients with massive UGIB or LGIB is the initial resuscitation. These patients should receive 2 large-bore intravenous (IV) catheters and isotonic crystalloid infusions. Meanwhile, rapid assessment of vital signs, including heart rate, systolic blood pressure, pulse pressure, and urine output, should be performed. Orthostatic hypotension (ie, a blood pressure fall of >10 mm Hg) is usually indicative of blood loss of more than 1000 mL.

Resuscitation and Initial Assessment

Initial resuscitation involves establishing large-bore IV access and administration of normal saline. Besides ordering routine laboratory studies (eg, complete blood cell (CBC) count, electrolyte levels, and coagulation studies), blood should be typed and cross-matched. The patient's blood loss and hemodynamic status should be ascertained, and in cases of severe bleeding, the patient may require invasive hemodynamic monitoring to direct therapy.

The 2008 SIGN guideline states that patients in shock should receive fluid volume replacement without delay. Colloid or crystalloid solutions may be used to achieve volume restoration before administering blood products. Red cell transfusion should be considered after loss of 30% of the circulating volume.[17]

Signs of hemodynamic compromise include postural changes with dyspnea, tachypnea, and tachycardia. An orthostatic drop in systolic blood pressure of more than 10 mm Hg or an increase in heart rate of more than 10 beats per minute is indicative of at least 15% of blood volume loss. The 2009 AAFP recommendations state that severe postural dizziness with a postural pulse increase of at least 30 beats per minute is a sensitive and specific indicator of acute blood loss of more than 630 mL.[22]

A hematocrit level of less than 18% or a decrease of about 6% is indicative of significant blood loss that requires blood transfusions; the goal is to achieve a target hematocrit level of approximately 20-25% in young patients and a target hematocrit level of around 30% in high-risk, older patients. A coagulopathy, such as an international normalized ratio (INR) of greater than 1.5, may require correction with fresh frozen plasma; thrombocytopenia can be corrected with platelet transfusions.

Transfer to ICU

Patients who require admission to the intensive care unit and early involvement of both a gastroenterologist and a surgeon include the following:

Localization of the Bleeding Site

In about 10% of patients presenting with LGIB, the source of bleeding is from the upper gastrointestinal (GI) tract. Some patients with LGIB should have a nasogastric (NG) tube placed, and if the aspirate or lavage does not show any blood or coffee ground–appearing material but does show bile, bleeding originating from the upper GI tract is unlikely. In case of high suspicion, obtain an esophagogastroduodenoscopy (EGD) evaluation (see Esophagogastroduodenoscopy).

Initial Approach to Hemostasis

In patients who are hemodynamically stable with mild to moderate bleeding or in patients who have had a massive bleed that has stabilized, colonoscopy should be performed initially.[28] Once the bleeding site is localized, therapeutic options include coagulation and injection with vasoconstrictors or sclerosing agents.

In cases of diverticular bleeding, bipolar probe coagulation, epinephrine injection, and metallic clips may be used. If recurrent bleeding is present, the affected bowel segment can be resected. In cases of angiodysplasia, thermal therapy, such as electrocoagulation or argon plasma coagulation, is generally successful. Angiodysplastic lesions may be missed at colonoscopy if the lesions are small or covered with blood clots.

The 2008 SIGN guideline states that colonoscopic hemostasis is an effective way to control hemorrhage from active diverticular or post-polypectomy bleeding in patients with massive LGIB.[17]

Therapeutic Colonoscopy

Colonoscopy is useful in radiation therapy–induced gastrointestinal (GI) bleeding and in the treatment of colonic polyp lesions. Endoscopic treatment of radiation-induced bleeding includes topical application of formalin, Nd:YAG laser therapy, and argon plasma coagulation. Neoplastic bleeding due to polyps requires polypectomy. Patients diagnosed with colonic tumors may require surgical resection.

Vasoconstrictive Therapy

In patients in whom the bleeding site cannot be determined based on colonoscopy and in patients with active, brisk LGIB, angiography with or without a preceding radionuclide scan should be performed to locate the bleeding site as well as to intervene therapeutically.

Initially, vasoconstrictive agents, such as vasopressin (Pitressin), can be used. An experimental study of treatment of LGIB by selective arterial infusion of vasoconstrictors, such as epinephrine with propranolol and vasopressin, was reported. Although epinephrine and propranolol drastically reduced mesenteric blood flow, they also caused a rebound increase in blood flow and recurrent bleeding.

Vasopressin is a pituitary hormone that causes severe vasoconstriction in the splanchnic bed. Vasoconstriction reduces the blood flow and facilitates hemostatic plug formation in the bleeding vessel. Vasopressin infusions are more effective in diverticular bleeding, which is arterial, as opposed to angiodysplastic bleeding, which is of the venocapillary type. The results are less than satisfactory in patients with severe atherosclerosis and coagulopathy.

Intra-arterial vasopressin infusions begin at a rate of 0.2 U/min, with repeat angiography performed after 20 minutes. The bleeding stops in about 91% of patients receiving intra-arterial vasopressin but recurs in up to 50% of patients when the infusion is stopped.[42] If bleeding persists, the rate of the infusion is increased to 0.4-0.6 U/min. Once the bleeding is controlled, the infusion is continued in an intensive care setting for 12-48 hours and then tapered over the next 24 hours. In patients with rebleeding, surgery should be considered.


During vasopressin infusion, monitor patients for recurrent hemorrhage, myocardial ischemia, arrhythmias, hypertension, and volume overload with hyponatremia. Nitroglycerine paste or drip can be used to overcome cardiac complications. Selective mesenteric infusion induces bowel wall contraction and spasms, which should not be confused with bowel wall ischemia. Do not administer vasopressin into the systemic circulation intravenously, because this causes coronary vasoconstriction, diminished cardiac output, and tachyphylaxis. Vasopressin infusions are contraindicated in patients with severe coronary artery disease and peripheral artery disease.

Superselective Embolization

An alternative to vasopressin infusion is embolization with agents such as gelatin sponge, coil springs, polyvinyl alcohol, and oxidized cellulose. Embolization involves superselective catheterization of the bleeding vessel to minimize necrosis, the most feared complication of ischemic colitis. This therapeutic modality is useful in patients in whom vasopressin is unsuccessful or contraindicated.

Initial experience with embolization suggested that complications of intestinal infarction were as high as 20%. With the advent of superselective catheterization and embolization of the vasa recta, successful embolization has been performed without intestinal infarction.[46, 47] Embolization is performed using a 3 French (F) microcatheter placed coaxially through the diagnostic 5F catheter. The therapeutic catheter is advanced as far as the vasa recta over a 0.018-inch guidewire so as to decrease the risk of infarction.

Once the bleeding vessel is identified, microcoils are used to occlude the bleeding vessel and to achieve hemostasis. Although microcoils are most commonly used, polyvinyl alcohol and Gelfoam are also used alone or in conjunction with microcoils.[6, 48, 49] However, if terminal mural branches of the bleeding vessel cannot be catheterized, abort the procedure and immediately perform surgery.

Kuo et al concluded superselective microcoil embolization for the treatment of LGIB is safe and effective.[50] They reported complete clinical success in 86% of patients with a rebleeding rate of 14%. Minor ischemic complication rates were noted as 4.5%, and major ischemic complication rates were reported as 0%. The investigators also reviewed the data from 122 cases of lower GI superselective microcoil embolization in the literature, with meta-analysis performed in 144 patients. The combined analysis revealed a minor ischemic complication rate of 9% and a major ischemic complication rate of 0%.[50]

Rossetti at al reviewed 11 years of experience in transarterial embolization of acute colonic bleeding in Switzerland.[51] Twenty-four patients underwent colonic embolization for diverticular, postpolypectomy, bleeding, as well as bleeding from cancer, angiodysplasia, and hemorrhoids. All the different types of bleeding stopped except hemorrhoidal bleeding, requiring hemorrhoidal ligature. The risk of bowel ischemia was 21%. In another study, 44 patients underwent microcoil embolizations for arterial gastrointestinal bleeding.[52] The technical success rate was 88%, with a clinical success rate of 57%. Intestinal ischemia occurred in 5% of patients. The mortality rate was 18%. It was concluded that microcoil embolization had a high success rate and the number of preprocedural and postprocedural transfusions did not affect the technical success.[52]

In another study by Yap et al, 95 patients underwent embolization for acute GI hemorrhage[53] ; 80% of the patients had upper GI hemorrhage and the rest had lower GI hemorrhage. Vessels embolized included gastroduodenal (39%), pancreatoduodenal (20%), gastric (19%), superior mesenteric (11%), inferior mesenteric (11%), and splenic artery (4%). Immediate hemostasis was obtained in 98% of patients. Complications included bowel ischemia in 4% and coil migration in 3% of patients. The overall 30-day mortality rate was 18%.

In Japan, therapeutic upper (n=16) and lower GI (n=23) embolization was performed on 39 occasions in 37 patients.[54]  N -butyl-2-cyanoacrylate was used in 1:1 and in 1:5 mixtures. Recurrent bleeding occurred in 2 patients, hepatic abscess in 2 cases, and lower limb ischemia in 1 patient. No intestinal necrosis occurred. It was concluded that transcatheter arterial embolizations using N -butyl-2-cyanoacrylate was safe and effective with a high rate of complete hemostasis.


Rosenkrantz et al reported 3 cases of colonic infarction.[55] One patient died following segmental colectomy, and the other patients revealed full-thickness bowel wall injury in the resected specimen. Intestinal ischemia and infarction have also been reported. To prevent this complication, perform embolization beyond the marginal artery as close as possible to the bleeding point in the terminal mural arteries. At least 139 cases have been collected from the medical literature since 1972.

The relevance of surgery after embolization of gastrointestinal and abdominal surgery was also examined.[56] In a retrospective study, a total of 54 patients with 55 bleeding events were identified; only 25 patients (45%) had LGIB. Of those, 9 patients had bleeding in the small intestine, 14 in the colon, and 2 in the rectum. The rebleeding rate was 24% (n=6), and 50% of those with recurrent LGIB required surgery.[56]

The study revealed a primary clinical embolization success rate of 82%, the rate of early recurrent bleeding (< 30 d) was 18%, and the rate of delayed bleeding (>30 days) was 3.6%.[56] Surgery after embolization was required in 20% of patients (n=11). The investigators concluded that surgery has an important role after successful embolization.[56]

Endoscopic Therapies

One of the advantages of upper or lower endoscopic evaluation is that it provides access to therapy in patients with gastrointestinal (GI) bleeding. Endoscopic control of bleeding can be achieved using thermal modalities or sclerosing agents. Absolute alcohol, morrhuate sodium, and sodium tetradecyl sulfate can be used for sclerotherapy of upper and lower GI lesions.

Endoscopic epinephrine injection is used commonly because of its low cost, easy accessibility, and low risk of complications. In a recent study, 175 patients underwent endoscopic epinephrine injection. Univariate analysis of 31 patients with rebleeding indicated that factors predictive of a high rebleeding rate included older age (≥60 y), American Society of Anesthesiology category III, IV, and V; severe anemia of greater than 8 g/dL; shock; epinephrine injection dose greater than or equal to 12 mL; and severe bleeding signs (hematemesis or hematochezia).[57] An additional hemostatic method such as clips or thermoregulation is needed to prevent subsequent bleeding.[57]

Endoscopic thermal modalities (eg, laser photocoagulation, electrocoagulation, heater probe) can also be used to arrest hemorrhage. Endoscopic control of hemorrhage is suitable for GI polyps and cancers, arteriovenous malformations, mucosal lesions, postpolypectomy hemorrhage, endometriosis, and colonic and rectal varices. Postpolypectomy hemorrhage can be managed by electrocoagulation of the polypectomy site bleeding with either snare or hot biopsy forceps or by epinephrine injection.

The medical literature has also been reviewed for endoscopic treatment of significant lower GI bleeding (total of 286 patients in 8 publications). Hemorrhage was successfully arrested in 70% of patients, with a rebleeding rate of 15%. Endoscopic therapy for LGIB is a minimally invasive and viable option in carefully selected patients.[58]

Hunter et al evaluated 222 GI endoscopic laser procedures in 122 patients and reported hemorrhage was arrested in 84% of the patients with GI bleeding.[59] No perforations were reported in this series, but 1 death occurred and was attributed to laser therapy in a patient with duodenal ulcer and gastroduodenal artery bleeding.

Forty patients with GI arteriovenous malformations (AVMs) underwent 72 photocoagulation sessions with mostly argon laser; 15 of the 40 patients had significant hemorrhage from colonic AVMs; of those 15, there were no deaths following ablation.

Although the treatment options for angiodysplasias are numerous, including segmental bowel resection and selective mesenteric embolization, endoscopic coagulation of angiodysplasias is becoming a treatment of choice using either heated probe or lasers, such as Nd:YAG and argon. Argon laser treatment is recommended for mucosal or superficial lesions, because the energy penetrates only 1 mm. Nd:YAG lasers are more useful for deeper lesions, because they penetrate 3-4 mm.

Emergent Surgery

Emergency surgery is required in about 10-25% of patients with lower gastrointestinal bleeding (LGIB) in whom nonoperative management was unsuccessful or unavailable.[15]  Failure of embolization warrants surgical intervention.[28]

Surgical indications

The indications for surgery include the following[21, 11] :

In addition, factors such as comorbid disease and individual surgical practices play a role in deciding which patient requires surgery. No contraindications exist with regard to surgery in hemodynamically unstable patients with active bleeding. In fact, if the patient is hemodynamically unstable because of ongoing hemorrhage, perform an emergency operation before any diagnostic study.

Segmental bowel resection and subtotal colectomy

Segmental bowel resection following precise localization of the bleeding point is a well-accepted surgical practice in hemodynamically stable patients. Subtotal colectomy is the procedure of choice in patients who are actively bleeding from an unknown source. According to the 2008 SIGN guideline, subtotal colectomy is recommended for the management of colonic hemorrhage that is uncontrolled by other procedures.[17]

Intraoperative esophagogastroduodenoscopy (EGD), surgeon-guided enteroscopy, and colonoscopy may be helpful in diagnosing undiagnosed massive GI bleeding. Depending on the availability of local resources and the patient's condition, it may sometimes be better to perform subtotal colectomy with distal ileal inspection than to try to jperform these tests, particularly if the surgeon is not privileged or comfortable with endoscopy.

Patients who are hemodynamically stable should have preoperative localization of the bleeding site; patients who are hemodynamically unstable with active bleeding may undergo emergency exploratory laparotomy with intraoperative endoscopy. In patients who are hemodynamically stable, once the bleeding site is preoperatively localized, intra-arterial vasopressin is used as a temporizing measure to reduce the bleeding before patients undergo segmental colectomy. Using this approach the operative morbidity rate is approximately 8.6%, the mortality rate is around 10%, and the rate of rebleed ranges from 0-14%.[42]

In patients undergoing emergency laparotomy, every attempt should be made to localize the bleeding intraoperatively, because segmental colectomy is the preferred procedure. If the bleeding site is not localized, a subtotal colectomy is performed with an inherent morbidity rate of around 37% and a mortality rate of about 11%-33%. In unstable patients, a two-stage procedure is preferred: temporary end ileostomy and delayed ileoproctostomy. In a small group of hemodynamically stable patients with minimal medical morbidity, this procedure can be performed as a one-stage procedure with ileoproctostomy. In addition, postoperative diarrhea can be a significant problem in elderly patients who undergo subtotal colectomy and ileoproctostomy.

In a subset of patients, surgery is still required, but with the use of nonsurgical diagnosis and intervention, the morbidity rate has been substantially reduced from around 37% to 8.6% in patients undergoing segmental colectomy. With advances in endoscopy and angiography, the rate of preoperative bleeding localization has steadily improved, impacting surgical outcomes in a positive way.

Contraindicated: Blind segmental resection

Practitioners must understand that blind segmental resection should not be performed because of a prohibitively high rebleeding rate of up to 75%, a morbidity rate up to 83%, and a mortality rate up to 60%. Once the bleeding point is identified, a limited segmental resection should be performed.

Preoperative Details

Acute LGIB is a common clinical entity and is associated with significant morbidity and mortality (10-20%). The high-risk factors are the patient's age (>60 y), the presence of multiorgan system disease, transfusion requirements (>4 units), need for operation, and recent stress (eg, surgery, trauma, sepsis).

As discussed earlier, 3 major aspects are involved in managing LGIB. The initial priority is to treat the shock. Second, localization of the source of bleeding is required to perform the third task—formulating an interventional plan.

Insert a nasogastric (NG) tube in all patients. A clear bile-stained aspirate generally excludes bleeding proximal to the Treitz ligamentum. After initial resuscitation, undertake a search for the cause of the bleeding to precisely locate the bleeding point.

Following accurate localization by an angiogram, bleeding can be temporarily controlled with either angiographic embolization or vasopressin infusion to stabilize the patient in anticipation of semiurgent segmental bowel resection. Segmental bowel resection is performed in the next 24-48 hours following correction of the patient's physiologic parameters, which include hypotension, hypothermia, acute hemorrhagic anemia, and deficient coagulation factors.

Use selective mesenteric embolization in high-risk patients for whom the operative management is associated with prohibitive risk of morbidity and mortality. If mesenteric embolization is used, these patients must be carefully monitored for bowel ischemia and perforation. Any evidence of ongoing bowel ischemia and/or unexplained sepsis following mesenteric embolization requires exploratory laparotomy to resect the affected bowel segment. Perform subtotal colectomy with ileoproctostomy in patients with nonlocalized LGIB or bilateral sources of colonic hemorrhage.

Intraoperative Details

Surgical intervention is required in only a small percentage of patients with LGIB. The surgical option depends on whether the bleeding source has been accurately identified preoperatively; if so, it is then possible to perform segmental intestinal resection.

If the bleeding source is unknown, an upper gastrointestinal endoscopy should be performed before any surgical exploration. At celiotomy, identifying the bleeding point is often impossible, as blood refluxes into the proximal and distal bowel.

The abdominal cavity is explored through a midline vertical incision. The assistance of a gastroenterologist or another surgical endoscopist or surgeon is required for intraoperative endoscopic evaluation. The colonoscope is introduced, and the surgeon assists its passage. On-table colonic lavage and colonoscopy may identify the colonic source of bleeding. Surgeon-guided intraoperative small bowel enteroscopy is also performed when no colonic source of bleeding is identified. Again, the colonoscope can be used for this procedure.

Unlike colonoscopy, enteroscopy is performed during the advancement of the scope. Colonoscopic manipulation of the small bowel may cause iatrogenic mucosal tears and hematomas, which may be mistakenly identified as a source of bleeding. Another intraoperative strategy is to clamp segments of the bowel with noncrushing intestinal clamps to identify the segment that fills with blood. If the bleeding point cannot be diagnosed through intraoperative pan-intestinal endoscopy and examination, and if evidence points to a colonic bleeding, perform a subtotal colectomy with end ileostomy.

Postoperative Details

Hypotension and shock are the eventual consequences of blood loss, but this depends on the rate of bleeding and the patient's response. Clinical development of shock may precipitate myocardial infarction, cerebrovascular accident, and renal or hepatic failure. Azotemia occurs in patients with gastrointestinal blood loss.

Complications of LGIB

Complications of blood transfusions can be summarized as acute and delayed hemolytic reactions, nonhemolytic reactions, and infectious diseases transmission. Complications related to massive blood transfusions are hypothermia, hypocalcemia, hyperkalemia, dilutional thrombocytopenia, and coagulation factor deficiencies.

Patients who have had surgery of the lower gastrointestinal (GI) tract are prone to the development of complications. The most common early postoperative complications are intra-abdominal or anastomotic bleeding, ileus, mechanical small bowel obstruction (SBO), intra-abdominal sepsis, localized or generalized peritonitis, wound infection and/or dehiscence, Clostridium difficile colitis, pneumonia, urinary retention, urinary tract infection (UTI), deep venous thrombosis (DVT), and pulmonary embolus (PE).

Intra-abdominal sepsis following colorectal surgery is a life-threatening complication and requires aggressive resuscitation. Systemic conditions (eg, severe blood loss and shock, poor bowel preparation, irradiation, diabetes, malnutrition, hypoalbuminemia) may adversely affect anastomotic healing. Changes in the anatomy and physiology of the large bowel, high bacterial content, improper operative technique, tension at the anastomosis, and ischemia can cause anastomotic leak associated with abscess and intra-abdominal sepsis. This condition requires either laparotomy (if the sepsis is generalized) or percutaneous drainage (if the sepsis is localized).

Delayed complications usually occur more than 1 week after surgery, the most common of which are anastomotic stricture, incisional hernia, and incontinence.

Transfusion-Free Management of LGIB

The management of lower GI bleeding (LGIB) can be challenging in patients who refuse transfusions of blood or blood products. However, transfusion-free management of GI bleeding is possiblewith an acceptable mortality rate.[60]

In a retrospective review of 96 patients with LGIB who did not accept transfusions of blood and blood products, 30 of 37 patients (81%) with hemoglobin levels less than 6 g/dL, and 4 of 7 patients (57%) with hemoglobin levels lower than 3 g/dL survived.[60] The inclusion criteria were frank LGIB, presenting hemoglobin levels lower than 12 g/dL or a decrease in hemoglobin of more than1.5 g/dL. Forty-one patients had upper GI bleeding and the remaining 48 had LGIB.[60]

The mean hemoglobin level was 8.8 g/dl. Surviving patients were treated with epoetin alfa (Procrit) once daily for 5 days, IV iron dextran infusion once daily for 10 days, IV folic acid daily, vitamin C twice daily, as well as IM vitamin B12 injection once. These patients also received beta-blockers (to reduce the cardiac workload) and supplemental oxygen (100%) with intubation (to improve the oxygen delivery as much as possible without blood transfusions). The overall mortality rate was 10%.


Patients who are hemodynamically unstable with active bleeding should be admitted to the medical intensive care unit (MICU). Early consultation with both a gastroenterologist and a surgeon is recommended.

Long Term Monitoring

Postoperative office visits every 2 weeks are essential to ensure proper wound healing. Upon discharge, a general diet abundant in fruits and vegetables is recommended. Patients are instructed to drink 6-8 glasses of fluid per day. Psyllium seed preparations should also be started. The AAFP recommends 32 g of fiber supplementation per day.[22]

Increased levels of physical activity may prevent the progression of diverticular disease, according to the AAFP 2009 recommendations. The AAFP also notes that aspirin and NSAID use is associated with increased risk of diverticular bleeding.[22]

The need for a follow-up colonoscopy is determined by a recurrence of symptoms. Angiodysplasia is more likely to rebleed if untreated and may require follow-up intervention to localize and treat recurrent bleeding. Colonoscopic electrocoagulation is generally successful in such situations.

Medication Summary

Vasoconstrictive agents reduce the blood flow and facilitate hemostatic plug formation in the bleeding vessel. However, the results are less than satisfactory in patients with severe atherosclerosis and coagulopathy.

Vasopressin (Pitressin Injection)

Clinical Context:  Vasopressin is a pituitary hormone that causes severe vasoconstriction in the splanchnic bed. This agent has vasopressor and ADH activity: Vasopressin increases water resorption at the distal renal tubular epithelium (ADH effect) and promotes smooth muscle contraction throughout the vascular bed of the renal tubular epithelium (vasopressor effects). However, vasoconstriction also increases in the splanchnic, portal, coronary, cerebral, peripheral, pulmonary, and intrahepatic vessels.

Vasopressin decreases the portal pressure in portal hypertension. A notable undesirable effect is coronary artery constriction that may dispose patients with coronary artery disease to cardiac ischemia. This can be prevented with concurrent use of nitrates.

Class Summary

Agents with vasopressor and antidiuretic hormone (ADH) activity may reduce lower gastrointestinal bleeding (LGIB).


Clinical Context:  Epinephrine has alpha-agonist effects that include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Beta2-agonist effects include bronchodilatation, chronotropic cardiac activity, and positive inotropic effects. Epinephrine solution (1/10,000 ) can be injected into bleeding site at the time of the endoscopic evaluation.

Class Summary

Epinephrine can be used in lower gastrointestinal bleeding, causing vasoconstriction and physical compression of the vessel. Epinephrine may be used in cases of diverticular bleeding or postpolypectomy hemorrhage.


Burt Cagir, MD, FACS, Clinical Professor of Surgery, The Commonwealth Medical College; Attending Surgeon, Assistant Program Director, Robert Packer Hospital; Attending Surgeon, Corning Hospital

Disclosure: Nothing to disclose.


Elizabeth Cirincione, MD, Director of Colon and Rectal Surgery, Department of Surgery, Nassau University Medical Center

Disclosure: Nothing to disclose.

Gavin F Chico, MD, Consulting Staff, CHRISTUS Coushatta Rural Health Clinic

Disclosure: Nothing to disclose.

Kenneth J Manas, MD, Assistant Professor, Department of Medicine, Section of Gastroenterology and Hepatology, Louisiana State University Health Sciences Center

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Marc D Basson, MD, PhD, MBA, FACS, Associate Dean for Medicine, Professor of Surgery and Basic Science, University of North Dakota School of Medicine and Health Sciences

Disclosure: Nothing to disclose.

Chief Editor

BS Anand, MD, Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

Disclosure: Nothing to disclose.

Additional Contributors

David Greenwald, MD, Professor of Clinical Medicine, Fellowship Program Director, Department of Medicine, Division of Gastroenterology, Montefiore Medical Center, Albert Einstein College of Medicine

Disclosure: Nothing to disclose.


Michael A Grosso, MD Consulting Staff, Department of Cardiothoracic Surgery, St Francis Hospital

Michael A Grosso, MD is a member of the following medical societies: American College of Surgeons, Society of Thoracic Surgeons, and Society of University Surgeons

Disclosure: Nothing to disclose.


  1. Ernst O, Bulois P, Saint-Drenant S, Leroy C, Paris JC, Sergent G. Helical CT in acute lower gastrointestinal bleeding. Eur Radiol. 2003 Jan. 13(1):114-7. [View Abstract]
  2. Yamaguchi T, Yoshikawa K. Enhanced CT for initial localization of active lower gastrointestinal bleeding. Abdom Imaging. 2003 Sep-Oct. 28(5):634-6. [View Abstract]
  3. Talley NJ, Jones M. Self-reported rectal bleeding in a United States community: prevalence, risk factors, and health care seeking. Am J Gastroenterol. 1998 Nov. 93(11):2179-83. [View Abstract]
  4. Qayed E, Dagar G, Nanchal RS. Lower gastrointestinal hemorrhage. Crit Care Clin. 2016 Apr. 32 (2):241-54. [View Abstract]
  5. 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. 1965 Nov. 58(5):797-805. [View Abstract]
  6. 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.
  7. Rösch J, Dotter CT, Brown MJ. Selective arterial embolization. A new method for control of acute gastrointestinal bleeding. Radiology. 1972 Feb. 102(2):303-6. [View Abstract]
  8. Meyers MA, Alonso DR, Gray GF, Baer JW. Pathogenesis of bleeding colonic diverticulosis. Gastroenterology. 1976 Oct. 71(4):577-83. [View Abstract]
  9. 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.
  10. 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. 2009 Oct. 146(4):600-6; discussion 606-7. [View Abstract]
  11. Vernava AM 3rd, Moore BA, Longo WE, Johnson FE. Lower gastrointestinal bleeding. Dis Colon Rectum. 1997 Jul. 40(7):846-58. [View Abstract]
  12. Longstreth GF. Epidemiology and outcome of patients hospitalized with acute lower gastrointestinal hemorrhage: a population-based study. Am J Gastroenterol. 1997 Mar. 92(3):419-24. [View Abstract]
  13. 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. 1995 Sep. 38(9):979-82. [View Abstract]
  14. 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. 2009 Dec. 21(12):1333-9. [View Abstract]
  15. Chalasani N, Wilcox CM. Etiology and outcome of lower gastrointestinal bleeding in patients with AIDS. Am J Gastroenterol. 1998 Feb. 93(2):175-8. [View Abstract]
  16. Huang ES, Strate LL, Ho WW, Lee SS, Chan AT. Long-term use of aspirin and the risk of gastrointestinal bleeding. Am J Med. 2011 May. 124(5):426-33. [View Abstract]
  17. [Guideline] Scottish Intercollegiate Guidelines Network (SIGN). Management of acute upper and lower gastrointestinal bleeding. A national clinical guideline. Edinburgh (Scotland): Scottish Intercollegiate Guidelines Network (SIGN); 2008 Sep. SIGN publication; no. 105:
  18. Andrei GN, Popa B, Gulie L, et al. Highlighted steps of the management algorithm in acute lower gastrointestinal bleeding - case reports and literature review. Chirurgia (Bucur). 2016 Jan-Feb. 111 (1):74-9. [View Abstract]
  19. Cirocchi R, Grassi V, Cavaliere D, et al. New trends in acute management of colonic diverticular bleeding: a systematic review. Medicine (Baltimore). 2015 Nov. 94 (44):e1710. [View Abstract]
  20. Zuckerman GR, Prakash C. Acute lower intestinal bleeding. Part II: etiology, therapy, and outcomes. Gastrointest Endosc. 1999 Feb. 49(2):228-38. [View Abstract]
  21. McGuire HH Jr. Bleeding colonic diverticula. A reappraisal of natural history and management. Ann Surg. 1994 Nov. 220(5):653-6. [View Abstract]
  22. [Guideline] Wilkins T, Baird C, Pearson AN, Schade RR. Diverticular bleeding. Am Fam Physician. 2009 Nov 1. 80(9):977-83. [View Abstract]
  23. 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.
  24. Macari M, Chandarana H, Balthazar E, Babb J. Intestinal ischemia versus intramural hemorrhage: CT evaluation. AJR Am J Roentgenol. 2003 Jan. 180(1):177-84. [View Abstract]
  25. Sabharwal R, Vladica P, Chou R, Law WP. Helical CT in the diagnosis of acute lower gastrointestinal haemorrhage. Eur J Radiol. 2006 May. 58(2):273-9. [View Abstract]
  26. Lee S, Welman CJ, Ramsay D. Investigation of acute lower gastrointestinal bleeding with 16- and 64-slice multidetector CT. J Med Imaging Radiat Oncol. 2009 Feb. 53(1):56-63. [View Abstract]
  27. 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. 2009 Oct. 33(10):2209-17. [View Abstract]
  28. Moss AJ, Tuffaha H, Malik A. Lower GI bleeding: a review of current management, controversies and advances. Int J Colorectal Dis. 2015 Oct 10. [View Abstract]
  29. Wong RC. Immediate unprepared hydroflush colonoscopy for management of severe lower gastrointestinal bleeding. Gastroenterol Hepatol (N Y). 2013 Jan. 9(1):31-4. [View Abstract]
  30. Jensen DM, Machicado GA. Diagnosis and treatment of severe hematochezia. The role of urgent colonoscopy after purge. Gastroenterology. 1988 Dec. 95(6):1569-74. [View Abstract]
  31. 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. 1998 Jan. 133(1):50-5. [View Abstract]
  32. Laine L, Shah A. Randomized trial of urgent vs. elective colonoscopy in patients hospitalized with lower GI bleeding. Am J Gastroenterol. 2010 Dec. 105(12):2636-41; quiz 2642. [View Abstract]
  33. 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. 1996 Jul. 39(7):750-4. [View Abstract]
  34. 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. 1997 Apr. 40(4):471-7. [View Abstract]
  35. Ryan P, Styles CB, Chmiel R. Identification of the site of severe colon bleeding by technetium-labeled red-cell scan. Dis Colon Rectum. 1992 Mar. 35(3):219-22. [View Abstract]
  36. Kester RR, Welch JP, Sziklas JP. The 99mTc-labeled RBC scan. A diagnostic method for lower gastrointestinal bleeding. Dis Colon Rectum. 1984 Jan. 27(1):47-52. [View Abstract]
  37. Ferrant A, Dehasque N, Leners N, Meunier H. Scintigraphy with In-111-labeled red cells in intermittent gastrointestinal bleeding. J Nucl Med. 1980 Sep. 21(9):844-5. [View Abstract]
  38. 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. 1986 May. 21(4):407-14. [View Abstract]
  39. 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. 2004 Aug. 16(8):795-9. [View Abstract]
  40. Bentley DE, Richardson JD. The role of tagged red blood cell imaging in the localization of gastrointestinal bleeding. Arch Surg. 1991 Jul. 126(7):821-4. [View Abstract]
  41. Hunter JM, Pezim ME. Limited value of technetium 99m-labeled red cell scintigraphy in localization of lower gastrointestinal bleeding. Am J Surg. 1990 May. 159(5):504-6. [View Abstract]
  42. Browder W, Cerise EJ, Litwin MS. Impact of emergency angiography in massive lower gastrointestinal bleeding. Ann Surg. 1986 Nov. 204(5):530-6. [View Abstract]
  43. Widlus DM, Salis AI. Reteplase provocative visceral arteriography. J Clin Gastroenterol. 2007 Oct. 41(9):830-3. [View Abstract]
  44. Sahn B, Bitton S. Lower gastrointestinal bleeding in children. Gastrointest Endosc Clin N Am. 2016 Jan. 26 (1):75-98. [View Abstract]
  45. 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. 2002 Sep. 34(9):685-9. [View Abstract]
  46. 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. 1998 Sep-Oct. 9(5):753-60. [View Abstract]
  47. 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. 1997 Jul. 174(1):24-8. [View Abstract]
  48. Frodsham A, Berkmen T, Ananian C, Fung A. Initial experience using N-butyl cyanoacrylate for embolization of lower gastrointestinal hemorrhage. J Vasc Interv Radiol. 2009 Oct. 20(10):1312-9. [View Abstract]
  49. 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. 1992 Sep. 159(3):521-6. [View Abstract]
  50. 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. 2003 Dec. 14(12):1503-9. [View Abstract]
  51. Rossetti A, Buchs NC, Breguet R, Bucher P, Terraz S, Morel P. Transarterial embolization in acute colonic bleeding: review of 11 years of experience and long-term results. Int J Colorectal Dis. 2012 Dec 4. [View Abstract]
  52. Mensel B, Kühn JP, Kraft M, et al. Selective microcoil embolization of arterial gastrointestinal bleeding in the acute situation: outcome, complications, and factors affecting treatment success. Eur J Gastroenterol Hepatol. 2012 Feb. 24(2):155-63. [View Abstract]
  53. Yap FY, Omene BO, Patel MN, et al. Transcatheter Embolotherapy for Gastrointestinal Bleeding: A Single Center Review of Safety, Efficacy, and Clinical Outcomes. Dig Dis Sci. 2013 Jan 30. [View Abstract]
  54. Yata S, Ihaya T, Kaminou T, et al. Transcatheter arterial embolization of acute arterial bleeding in the upper and lower gastrointestinal tract with N-butyl-2-cyanoacrylate. J Vasc Interv Radiol. 2013 Mar. 24(3):422-31. [View Abstract]
  55. Rosenkrantz H, Bookstein JJ, Rosen RJ, Goff WB 2nd, Healy JF. Postembolic colonic infarction. Radiology. 1982 Jan. 142(1):47-51. [View Abstract]
  56. Köhler G, Koch OO, Antoniou SA, et al. Relevance of surgery after embolization of gastrointestinal and abdominal hemorrhage. World J Surg. 2014 Sep. 38(9):2258-66. [View Abstract]
  57. Hu ML, Wu KL, Chiu KW, et al. Predictors of rebleeding after initial hemostasis with epinephrine injection in high-risk ulcers. World J Gastroenterol. 2010 Nov 21. 16(43):5490-5. [View Abstract]
  58. 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. 2009 Nov. 41(11):997-1000. [View Abstract]
  59. Hunter JG, Bowers JH, Burt RW, Sullivan JJ, Stevens SL, Dixon JA. Lasers in endoscopic gastrointestinal surgery. Am J Surg. 1984 Dec. 148(6):736-41. [View Abstract]
  60. Sharma P, Barajas FJ, Krishnamoorthy P, Campo LM, Blumenthal E, Spinnell M. Transfusion-free Management of Gastrointestinal Bleeding: The Experience of a Bloodless Institute. J Clin Gastroenterol. 2014 Aug 20. [View Abstract]
  61. Barnert J, Messmann H. Management of lower gastrointestinal tract bleeding. Best Pract Res Clin Gastroenterol. 2008. 22(2):295-312. [View Abstract]
  62. Cryer B, Li C, Simon LS, Singh G, Stillman MJ, Berger MF. GI-REASONS: a novel 6-month, prospective, randomized, open-label, blinded endpoint (PROBE) trial. Am J Gastroenterol. 2013 Mar. 108(3):392-400. [View Abstract]
  63. 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. 2007 Mar. 193(3):404-7; discussion 407-8. [View Abstract]
  64. Miller FH, Hwang CM. An initial experience: using helical CT imaging to detect obscure gastrointestinal bleeding. Clin Imaging. 2004 Jul-Aug. 28(4):245-51. [View Abstract]
  65. 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. 2009 Sep. 30(18):2226-32. [View Abstract]
  66. 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. 2009 Aug. 41(8):715-7. [View Abstract]
  67. Wong Kee Song LM, Baron TH. Endoscopic management of acute lower gastrointestinal bleeding. Am J Gastroenterol. 2008 Aug. 103(8):1881-7. [View Abstract]
  68. Zuccaro G. Epidemiology of lower gastrointestinal bleeding. Best Pract Res Clin Gastroenterol. 2008. 22(2):225-32. [View Abstract]
  69. Thomson M, Belsha D. Endoscopic management of acute gastrointestinal bleeding in children: Time for a radical rethink. J Pediatr Surg. 2015 Dec 1. [View Abstract]
  70. Nagata N, Niikura R, Yamada A, et al. Acute middle gastrointestinal bleeding risk associated with NSAIDs, antithrombotic drugs, and PPIs: a multicenter case-control study. PLoS One. 2016. 11 (3):e0151332. [View Abstract]

Types of lower gastrointestinal bleeding (LGIB).

Types of lower gastrointestinal (GI) bleeding. HR = heart rate; SBP = systolic blood pressure.

Methods used to treat lower gastrointestinal bleeding (LGIB).

Types of lower gastrointestinal bleeding (LGIB).

Algorithm for massive lower gastrointestinal (GI) bleeding, surgical perspective. EGD = esophagogastroduodenoscopy; NG = nasogastric; 99mTc RBC = technetium-99m pertechnetate–labeled autologous RBC.

Types of lower gastrointestinal bleeding (LGIB).

Methods used to treat lower gastrointestinal bleeding (LGIB).

Types of lower gastrointestinal (GI) bleeding. HR = heart rate; SBP = systolic blood pressure.

Algorithm for massive lower gastrointestinal (GI) bleeding, surgical perspective. EGD = esophagogastroduodenoscopy; NG = nasogastric; 99mTc RBC = technetium-99m pertechnetate–labeled autologous RBC.

Lower Gastrointestinal Bleeding in Adults Percentage of Patients
Diverticular disease
  • Diverticulosis/diverticulitis of small intestine
  • Diverticulosis/diverticulitis of colon
Inflammatory bowel disease
  • Crohn disease of small bowel, colon, or both
  • Ulcerative colitis
  • Noninfectious gastroenteritis and colitis
Benign anorectal diseases
  • Hemorrhoids
  • Anal fissure
  • Fistula-in-ano
  • Malignant neoplasia of small intestine
  • Malignant neoplasia of colon, rectum, and anus
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.[9]
Lower Gastrointestinal Bleeding in Children and Adolescents
Polyps and polyposis syndromes
  • Juvenile polyps and polyposis
  • Peutz-Jeghers syndrome
  • Familial adenomatous polyposis (FAP)
  • Crohn disease
  • Ulcerative colitis
  • Indeterminate colitis
Meckel diverticulum