Lower gastrointestinal bleeding

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Muhammad Saad, M.D.[2] Aditya Ganti M.B.B.S. [3]

Lower gastrointestinal bleeding (LGIB) is bleeding originating from a colorectal source distal to the ileocecal valve, typically presenting with hematochezia or bright red blood per rectum. The older definition based on bleeding distal to the ligament of Treitz has been superseded; bleeding between the ligament of Treitz and ileocecal valve is classified as small-bowel bleeding and follows a separate diagnostic and therapeutic pathway.^[1] Stool appearance does not reliably determine anatomic source; brisk upper gastrointestinal bleeding can present with hematochezia, whereas slower LGIB may occasionally present with melena.^[2]

LGIB accounts for up to approximately 30% of gastrointestinal bleeding and causes more than 100,000 hospitalizations annually in the United States, with more than 270,000 emergency department visits and a hospitalization incidence of approximately 36 per 100,000 population, lower than that reported for upper gastrointestinal bleeding.^[1][3][4] Patients are predominantly older adults with substantial comorbidity, and antiplatelet and anticoagulant use is common.^[3] The burden has increased with population aging and expanding use of antithrombotic therapy.^[3]

Most episodes of LGIB are self-limited, and many patients do not require endoscopic, radiologic, or surgical hemostasis.^[5] In-hospital mortality is generally low but varies across populations, with reported rates of approximately 3.4–8.8%.^[1][6] Mortality is influenced substantially by comorbidity, hemodynamic instability, in-hospital onset of bleeding, and rebleeding. Patients who develop LGIB while already hospitalized have substantially higher mortality than those presenting from the community.^[1][6]

Initial assessment and hemodynamic resuscitation should proceed simultaneously, with focused history, physical examination, digital rectal examination, and laboratory assessment.^[1] The principal triage decision is based on hemodynamic stability and whether significant bleeding is ongoing.

• Hemodynamically stable patients → assess severity and risk, then perform colonoscopy after appropriate resuscitation and bowel preparation when indicated. Colonoscopy provides diagnostic evaluation and permits endoscopic therapy when a bleeding source is identified.^[1][2]
• Hemodynamically significant or severe ongoing bleeding → promptly consider an upper GI source and obtain CT angiography (CTA) to localize active bleeding; a positive CTA can guide transcatheter arterial embolization.^[1][7]
• In a hemodynamically stable patient with a high suspicion of active bleeding, CTA may also be considered as an initial diagnostic test when rapid localization of active bleeding is clinically important.^[7]
• CTA is not useful once clinically significant bleeding has subsided, because the likelihood of demonstrating active extravasation falls substantially.^[1][7]

The Oakland score may supplement clinical judgment when identifying patients with LGIB who are at sufficiently low risk for adverse outcomes to permit early discharge and outpatient evaluation. An Oakland score of ≤8 identifies a low-risk group, but the score should not replace clinical assessment or consideration of ongoing bleeding, comorbidity, social circumstances, and follow-up reliability.^[1] External validation studies support its ability to identify low-risk patients, although the evidence underlying threshold-based discharge remains limited.^[1][3]

Severe hematochezia should not automatically be attributed to a colorectal source. Clinical features favoring an upper GI source include hemodynamic instability, a history of peptic ulcer disease or decompensated liver disease, and a BUN-to-creatinine ratio >30; a BUN-to-creatinine ratio above this threshold has been associated with a substantially increased likelihood of upper GI bleeding.^[1][2] The presence of blood clots in stool argues against an upper GI source.^[1] Nasogastric aspirate has poor sensitivity for excluding an upper GI source and should not be relied upon as a definitive rule-out test.^[1]

• Resuscitation and diagnostic assessment occur concurrently rather than sequentially in patients with significant bleeding.^[1]
• The initial diagnostic pathway should be determined primarily by hemodynamic status and whether significant bleeding is ongoing.^[1][7]
• CTA has high value when significant active bleeding is suspected but limited yield after bleeding has stopped.^[1][7]
• In stable patients, colonoscopy remains an important diagnostic and therapeutic modality, but the optimal timing of colonoscopy remains unsettled.^[1]
• Risk scores, including the Oakland score, should be treated as adjuncts to clinical judgment rather than absolute disposition rules.^[1]

• Anchoring on a diagnosis of LGIB and missing a brisk upper GI source in a patient with severe hematochezia.
• Sending a hemodynamically unstable patient directly for bowel preparation and colonoscopy rather than prioritizing stabilization and appropriate localization of active bleeding.
• Obtaining CTA after clinically significant bleeding has ceased, when the likelihood of detecting active extravasation is low.
• Treating the Oakland score as a substitute for clinical judgment.
• Assuming that every patient with LGIB requires urgent endoscopic or radiologic hemostasis.
• Using nasogastric aspirate as a definitive test to exclude an upper GI source.

This Overview provides a high-level clinical framework. Detailed causes and epidemiology, diagnostic testing and performance characteristics, risk-stratification tools, colonoscopy, CT angiography, embolization, transfusion strategy, antithrombotic management, medical therapy, and surgical therapy should be addressed in their respective dedicated microchapters.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Roman encyclopedist Aulus Cornelius Celsus was the first to describe band ligation treatment for hemorrhoidal bleeding. In the 1700s, Alexis Littre was the first to describe the association between diverticular diseases and bleeding. In 1885, Allchin gave a detailed description of ulcerative colitis along bleeding.Until 1967, mesenteric ischemia was a diagnostic dilemma. In 1887, Welch proposed that ischemic bowel changes occur secondary to 80% stenosis of superior mesenteric artery (SMA) resulting in bleeding as a complication.

• Roman encyclopedist Aulus Cornelius Celsus was the first to describe band ligation treatment for hemorrhoidal bleeding.
• In the 1700s, Alexis Littre was the first to describe diverticular diseases, where he reported “diverticular hernia” without explaining it.^[1]
• In 1885, Allchin gave a detailed description of ulcerative colitis for the first time.^[2]
• Until 1967, mesenteric ischemia was a diagnostic dilemma.^[3]
• In 1887, Welch proposed that ischemic bowel changes occur secondary to 80% stenosis of superior mesenteric artery (SMA).^[4]
• In 1849, Jean Cruveilheir, a French anatomist, was the first to describe in detail the diverticular herniations through the muscular wall of the colon.
• In 1913 Giovanni Battista Morgagni (1682-1771) and Scottish physician T. Kennedy Dalziel described inflammatory bowel diseases in detail for the first time.
• In 1936, Dunphy was the first one to establish an association between mesenteric artery occlusion and gut infarction.
• In 1963, Boley was the first to describe ischemic colitis as a vascular occlusion of the colon.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Lower gastrointestinal bleeding can be classified into occult, moderate and severe bleeding based on the severity of bleeding.

Lower GI bleeding can be classified into 3 groups based on the severity of bleeding:^{[1][2][3][4][5][6]}

• Occult lower GI bleeding
• Moderate lower GI bleeding
• Severe lower GI bleeding

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Superior mesenteric artery and inferior mesenteric artery are the two major blood vessels that supply lower gastrointestinal tract. Disruption of blood vessel junction, formed by these two vessels, by any of the disease process results in bleeding. Diverticulosis is the most common etiology of lower GI bleeding accounting for 30% of all cases, followed by ano-rectal disease, ischemia of bowel, inflammatory bowel disease (IBD), neoplasia, and arteriovenous (AV) malformations. The characteristic gross and microscopic findings of lower gastrointestinal tracts depends upon the underlying pathology.

• Superior mesenteric artery and inferior mesenteric artery are the two major blood vessels that supply lower gastrointestinal tract.^[1][2][3]
• The superior mesenteric artery and inferior mesenteric artery are interconnected through a branch of anastomosis between various branches which are collectively called as marginal artery of Drummond. 
• This vascular arcade runs in the mesentery close to the bowel.

The pathogenesis of lower gastrointestinal bleeding can be discussed based on the etiology. Diverticulosis is the most common etiology of lower GI bleeding accounting for 30% of all cases, followed by anorectal disease, ischemia, inflammatory bowel disease (IBD), neoplasia, and arteriovenous (AV) malformations.

• Diverticulosis
  • The colonic wall weakens with age and results in the formation of sac-like protrusions known as diverticula.^[4][5][6][7]
  • These protrusions generally occur at the junction of blood vessel penetrating through the mucosa and circular muscle fibers of the colon.
  • Hemorrhage results from rupture of the intramural branches (vasa recta) of the marginal artery at the dome of a diverticulum and can give rise to a massive, life-threatening LGIB.

• Anorectal disease

• Hemorrhoids are defined as swelling and inflammation of veins in the rectal and anal region
• Hemorrhoids can be either internal or external based on their relation to dentate line.
• The first step in the pathogenesis of either type of hemorrhoids is weakening of the surrounding connective tissue and vein wall.^[8][9][8]
• Weakening of blood vessels can result in bleeding under pressure.
• An anal fissure can be defined as disruption or tear in the mucosal surface of the skin.
• During defecation, due to increased pressure which can exaggerate the tears may present as bright red rectal bleeding with severe periodic pain.^[10]

• Mesenteric Ischemia

• Mesenteric ischemia results when there is inadequate blood supply at the level of the small intestine.^{[11][12][13][14]}
• 2 or more vessels (celiac, SMA, or IMA) must be involved for bleeding to occur.
• Decreased blood supply can occur due to obstruction of blood vessel either by emobolus or due to vasoconstriction effect of drugs.
• Decreased blood supply initiates necrosis of mucosal surface of intestine.
• unopposed blood deprivation leads to trans-mural necrosis and ultimately sloughing of the tissues with associated bleeding.

• Ischemic Colitis

• Ischemic colitis is a condition in which injury of the large intestine results from decreased blood supply.^[15][16][17]
• The colon is most commonly involved due the presence of water shed areas ( splenic flexure and hepatic flexure).
• Similar to mesentric ischemia bleeding occurs due to necrosis and sloughing of mucosal membrane.

• Inflammatory Bowel Disease^[18][19]
  • Crohn’s disease
    • In Crohn’s disease, T cell activation stimulates interleukin (IL)-12 and tumor necrosis factor (TNF)-α, resulting in chronic inflammation and tissue injury.^{[20][21][22][23][24][25]}
    • TNF-alpha induces expression of adhesion factors that allow for inflammatory cells to infiltrate and activates macrophages resulting in granuloma formations
    • The inflammatory response invades through the entire thickness of the bowel wall weakening the surrounding blood vessels resulting in bleeding.

• Ulcerative colitis
  • In ulcerative colitis, T cells, cytotoxic to the colonic epithelium, accumulate in the lamina propria, accompanied by B cells that secrete immunoglobulin G (IgG) and IgE.^{[23][26][27][28]}
  • This results in inflammation of the crypts of Lieberkuhn, with abscesses and pseudopolyps along with
  • rupturing of minute blood vessels in mucosa resulting in bleeding.

• Neoplasia
  • Colon cancer arises mostly due to sporadic mutations that originates from the epithelial cells of colon or rectum.
  • Genetic instability/mutation results in epigenetic alteration, chronic inflammation, oxidative stress, and intestinal microbiota.^[29][30][31]
  • As tumor tends to grow slowly it invades the surrounding tissue disrupting the normal blood vessels along with it.
  • This is responsible for slow occult bleeding that is found positive on FOBT.

• AV Malformation/Angiodysplasia

• In AV malformation abnormal connections occur between arteries and veins.^{[32][33][34][35][36]}
• This connections results in blood flow from high pressure arteries to low pressure veins without buffering effects of capillaries.
• The lack of capillary buffers makes the vessels weak due to increased blood flow and ultimately bleeding.
• In Angiodysplasia, with age the connective tissue of the blood vessels become weak.
• With mild increase in pressure leads to disrupture of vessels leading to painless bleeding.

Other diseases that are commonly associated with lower gastrointestinal bleeding include:

• Aortoenteric fistula
• Abdominal aortic aneurysms
• Peutz-Jeghers syndrome
• Klippel-Trenaunay-Weber syndrome
• Hereditary hemorrhagic telangiectasia
• Neurofibromatosis 
• Blue rubber bleb syndrome

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Common causes of lower gastrointestinal tract bleeding include diverticulosis, angiodysplasia, ischemic colitis, colorectal cancer, anorectal diseases, infectious colitis and inflammatory bowel disease. Less common causes of lower gastrointestinal tract include colonic polyps, radiation proctitis, and rectal varices.

Common causes of lower gastrointestinal bleeding inclue:^{[1][2][3][4][5][6][7][8][9][2][10]}

• Colonic diverticulosis
• Vascular ectasias (angiodysplasias/angioectasias)
• Iatrogenic
• Ischemic colitis
• Colorectal malignancy
• Anorectal abnormalities
• Inflammatory bowel disease (IBD)
• Infectious colitis

Less common causes of lower gastrointestinal bleeding include:

• Colonic polyps
• Radiation proctitis
• Rectal varices
• Meckel diverticulum
• Intussusception
• Henoch-Schönlein purpura (HSP)

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Several diseases present with lower gastrointestinal bleeding and must be differented from each other. The common diseases responsible for lower GI bleeding inlcude diverticulosis, angiodysplasia, hemorrhoids, anal fissures, mesenteric Ischemia, ischemic colitis, inflammatory bowel disease, and colorectal carcinoma.

Several diseases present with lower gastrointestinal bleeding and must be differented from each other. The common diseases responsible for lower GI bleeding inlcude diverticulosis, angiodysplasia, hemorrhoids, anal fissures, mesenteric Ischemia, ischemic colitis, inflammatory bowel disease, and colorectal carcinoma.

The following table differentiates all the diseases presenting with abdominal pain and lower gastrointestinal bleeding.

Abbreviations: RUQ= Right upper quadrant of the abdomen, LUQ= Left upper quadrant, LLQ= Left lower quadrant, RLQ= Right lower quadrant, LFT= Liver function test, SIRS= Systemic inflammatory response syndrome, ERCP= Endoscopic retrograde cholangiopancreatography, IV= Intravenous, N= Normal, AMA= Anti mitochondrial antibodies, LDH= Lactate dehydrogenase, GI= Gastrointestinal, CXR= Chest X ray, IgA= Immunoglobulin A, IgG= Immunoglobulin G, IgM= Immunoglobulin M, CT= Computed tomography, PMN= Polymorphonuclear cells, ESR= Erythrocyte sedimentation rate, CRP= C-reactive protein, TS= Transferrin saturation, SF= Serum Ferritin, SMA= Superior mesenteric artery, SMV= Superior mesenteric vein, ECG= Electrocardiogram

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Muhammad Saad, M.D.[2] Aditya Ganti M.B.B.S. [3]

• The estimated population incidence of acute lower gastrointestinal bleeding (LGIB) is approximately **33–87 per 100,000 population**, although epidemiologic studies are heterogeneous and high-quality population-based data remain limited.^[1][2]
• US hospitalization incidence is approximately **36 per 100,000 population per year**.^[3]
• LGIB incidence has increased relative to upper gastrointestinal bleeding (UGIB) in several population-based cohorts. In a Finnish cohort, LGIB occurred at 1.26 versus 0.94 per 1,000 person-years for UGIB; in a Hong Kong cohort, LGIB also surpassed UGIB over time, with the steepest increase among adults older than 80 years.^[1]
• Proposed contributors to the increasing burden of LGIB include an aging population and greater exposure to antithrombotic medications.^[1][2]

• In the United States in 2018, LGIB accounted for approximately **271,575 emergency department visits** and **113,020 hospital admissions** as a primary diagnosis.^[1][2]
• LGIB accounts for up to approximately **30% of major gastrointestinal bleeding episodes**.^[3]
• Contemporary LGIB admissions involve an increasingly older and more comorbid population, with greater overall healthcare complexity than in earlier eras.^[1]

• In US emergency department data from 2006–2019, age- and sex-adjusted LGIB incidence increased from **146.0 per 100,000 in 2006** to a peak of **161.0 per 100,000 in 2015**, then declined to **150.2 per 100,000 in 2019**.^[4]
• During the same period, the proportion of patients with at least 1 comorbidity increased from **27.4% to 35.9%**.^[4]
• Compared with 2006, patients presenting in 2019 had more ED discharges and fewer RBC transfusions, endoscopic procedures, deaths, and shorter hospital stays.^[4]
• The etiologic composition also changed. Diverticular bleeding declined overall by **17.2%**, from 37.6 to 31.2 per 100,000, although it increased by 8.8% between 2016 and 2019. Other non-diverticular bleeding increased by **18.0%** over the study period.^[4]
• International trends are not uniform. Spanish data reported an increase in LGIB hospitalization incidence from approximately **20 to 33 per 100,000** between 1996 and 2005, whereas US emergency department data show a decline after 2015.^[2][4]

• In US emergency department data, inflation-adjusted inpatient cost per GI-bleeding encounter decreased from 2012 to 2019 (relative ratio 0.92; 95% CI 0.91–0.93).^[4]
• Aggregate healthcare costs for LGIB may exceed those for UGIB, with inpatient hospitalization accounting for most of the expenditure.^[2]

• Age: LGIB predominantly affects older adults. In the first UK nationwide LGIB audit of 2,528 patients, the median age was **74 years (IQR 57–83)**, compared with 68 years in the parallel UK UGIB audit.^[5]
• LGIB incidence increases substantially with age, with particularly rapid growth among adults older than 80 years.^[1][2]
• Age-related increases in conditions associated with LGIB, including diverticulosis and ischemic colonic disease, contribute to the burden among older adults.^[1][6]
• Sex: Current high-level evidence does not establish a robust sex difference in LGIB incidence. Male sex has been associated with higher mortality and is better regarded as a demographic prognostic marker than as a definitive incidence difference.^[2]
• Antithrombotic exposure: In the UK nationwide audit, **29.4%** of patients were taking antiplatelet agents and **15.9%** were taking anticoagulants, illustrating the substantial prevalence of antithrombotic exposure among patients presenting with LGIB.^[5]
• Comorbidity: Patients with LGIB commonly have substantial comorbidity. Advanced age, higher comorbidity burden, long-term anticoagulation, and hypovolemia are associated with increased mortality.^[2]
• Pediatrics: Pediatric lower gastrointestinal bleeding has a distinct epidemiologic and etiologic spectrum and should not be extrapolated from adult LGIB data.

• Current epidemiologic estimates are definition-dependent. Modern LGIB definitions distinguish colorectal-source bleeding from small-bowel (mid-GI) bleeding, which should not be combined when comparing incidence or population burden.^[1][2]
• High-quality population-based epidemiologic studies remain limited, accounting for the wide estimated incidence range of **33–87 per 100,000**.^[1]
• Whether LGIB incidence is uniformly increasing globally remains uncertain because temporal trends differ across countries and study periods.^[2][4]
• Current high-level sources do not provide sufficiently robust evidence to establish a clinically reliable racial or ethnic incidence differential; therefore, no definitive race/ethnicity association is stated.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Common risk factors in the development of lower GI bleeding include advancing age, previous history of gastrointestinal bleeding, chronic constipation, hematologic disorders, medications such as anticoagulants, non-steroidal anti-inflammatory drugs, and human immunodeficiency virus infection.

Common risk factors in the development of lower GI bleeding include:^[1][2][3][4]

• Advancing age
• Previous history of gastrointestinal bleed
• Chronic constipation
• Hematologic disorders
• Anticoagulants
• Non-steroidal anti-inflammatory drugs
• Human immunodeficiency virus infection

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

There is insufficient evidence to recommend routine screening for lower gastrointestinal bleeding.

There is insufficient evidence to recommend routine screening for lower gastrointestinal bleeding.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

If left untreated, lower gastrointestinal bleeding is usually self-limited (90% of the time bleeding stops on its own). Massive blood loss can result in a severe drop in blood pressure resulting in decreased blood supply to organ systems leading to death. Hypovolemic shock and symptomatic anemia are the most common direct complications of LGIB. Prognosis is generally good, and the 1-year mortality rate of patients with lower gastrointestinal bleeding is less than 3%.

If left untreated, lower gastrointestinal bleeding is usually self-limited (90% of the time bleeding stops on its own). Massive blood loss can result in a severe drop in blood pressure resulting in decreased blood supply to organ systems leading to death. Chronic blood loss if left untreated results in anemia.^[1]

Common complications of LGIB include:^[2][3]

• Hypovolemic shock and symptomatic anemia are the most common direct complications of LGIB.
• Rebleeding following treatment is not uncommon.
• All treatment modalities have potential adverse affects:
  • Endoscopy carries a risk of bowel perforation.
  • Angiography and superselective embolization can result in bowel ischemia.
  • Surgery is associated with the highest complication rates and should only be considered in patients who have ongoing bleeding that cannot be controlled by other methods.

• Prognosis is generally good, and the 1 year mortality rate of patients with lower gastrointestinal bleeding is approximately <3%.^[4][5]
• With definitive intervention to treat or remove the source of blood loss, rebleeding rates are low.
• Without definitive treatment, rebleeding rates can be appreciable, as high as 38%.

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