Lower gastrointestinal bleeding

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 is defined as blood loss originating distal to the ligament of Treitz. It accounts for 24% to 33% of all hospital admissions for gastrointestinal bleeding and is responsible for 1% of hospital admissions in the United States. It can present with frank blood loss per rectum or may be occult in nature, presenting with anemia. Bleeding can vary in severity from passage of small amounts of blood to massive life-threatening hemorrhage. Acute LGIB is described as bleeding of recent onset, which may result in hemodynamic instability and need for blood transfusion. Most commonly originates in the colon or ano–rectum; only 5% arise in the small bowel. Etiologies vary among adult, elderly, and pediatric populations. Ninety percent of lower gastrointestinal bleeding stop spontaneously; however, the underlying etiology needs to be diagnosed and treated accordingly. Overall mortality is less than 4%, but may be higher in elderly populations and in those with comorbid disease. Even bleeding of moderate rate can have significant sequel in a group of patients with the comorbid disease. A thorough history and detailed examination are essential steps in establishing the cause and the source of bleeding. Patients with severe bleeding or hemodynamic disturbance require hospitalization and urgent investigation. It is essential to distinguish between lower gastrointestinal bleeding and brisk upper gastrointestinal bleeding as they can present with similar symptoms. Treatment depends on the cause and the severity of the bleeding.

Roman encyclopedist, Aulus Cornelius Celsus, was the first to describe band ligation treatment for hemorrhoidal bleeding. In the 1700s, Alexis Littre described the association between diverticular diseases and bleeding. In 1885, Allchin gave a detailed description of ulcerative colitis which can present with 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.

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

Superior mesenteric artery and inferior mesenteric artery are the two major blood vessels that supply lower gastrointestinal tract. Disruption of this blood vessel junction 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.

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.

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

The prevalence of lower gastrointestinal bleeding is approximately 20 per 100,000 population in the United States. Lower gastrointestinal bleed is more common in men than women.

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

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

If left untreated 90% of the time lower gastrointestinal bleeding is usually self-limited. However, 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 four percent.

Colonoscopy is the gold standard test for the diagnosis of lower gastrointestinal bleeding. However, Endoscopy is the investigation of choice in cases of lower gastrointestinal bleeding caused by ischemic colitis or colonoscopy is unequivocal.

The hallmark symptom of LGIB is bleeding per rectum or frank blood in stools. The presentation of associated symptoms depends upon the source of the bleeding and underlying etiology. Associated symptoms of lower gastrointestinal bleeding include fever, abdominal pain, bloody diarrhea, dehydration, history of constipation, and hypotension in severe cases, and weight loss. A detailed description of the nature of the blood loss can also help in pinpointing the likely source of bleeding.

The most common physical examination finding is the passage of frank blood per rectum (hematochezia).

The essential blood work in diagnosing lower gastrointestinal bleeding includes a complete blood count, renal function and liver function tests, and coagulation studies. Although not diagnostic, a blood type and crossmatch should be done in patients who present with life-threatening bleeding.

There are no specific ECG findings associated with lower gastrointestinal bleeding. However, an electrocardiogram is be performed in order to exclude arrhythmia and cardiac causes of hypotension (following acute MI).

There are no abdominal x-ray findings associated with lower gastrointestinal bleeding. However, an x-ray may be helpful in the diagnosing the complications of underlying disease.

There are no specific ultrasound findings associated with lower gastrointestinal bleeding. However, ultrasound can be useful in diagnosing various etiology or conditions responsible for lower gastrointestinal bleeding.

Helical CT scanning of the abdomen and pelvis is recommended when a routine workup fails to determine the cause of active gastrointestinal bleeding. Findings of helical CT scan in lower gastrointestinal bleeding include vascular extravasation of the contrast medium, contrast enhancement of the bowel wall, thickening of the bowel wall, hyperdensity of the peri-bowel fat, and vascular dilatations.

There are no MRI findings associated with lower gastrointestinal bleeding.

Other imaging studies include angiography and radionuclide imaging that can be helpful in diagnosing lower gastrointestinal bleeding.

Nasogastric tube lavage may be helpful in the diagnosis of lower gastrointestinal bleeding. Nasogastrictube lavage helps in differentiating lower gastrointestinal bleeding from upper gastrointestinal bleeding. Evidence of old (brown colored or ‘coffee grounds’) or fresh blood on NGT aspirate documents presence of upper gastrointestinal bleeding. Evidence of bilious material rules out bleeding distal to the pylorus.

The aims of treatment are to resuscitate the patient, identify the source of blood loss and stop any ongoing bleeding, and reduce the risk of a recurrent bleed. It is essential to identify patients who are high risk. This would include elderly patients; those with severe ongoing bleeding or recurrent bleeding; and patients with multiple comorbid conditions, in particular, those patients with cardiac, renal, respiratory, and liver disease. Treatment depends on the mode of presentation, the severity of the bleed, and the underlying pathology. Bleeding points can be treated with endoscopy, interventional radiology, or surgery. After identification of the source of bleeding using endoscopy, therapeutic options include monopolar or bipolar diathermy, argon plasma coagulation (APC), epinephrine injections, and endoloops and hemoclips, used individually or in combination. These methods can be used to treat many of the causes of LGIB, including diverticular bleeding, angiodysplasia, radiation proctitis, and post-polypectomy bleeding interventional radiology can be used to visualize a bleeding vessel and to stop the bleeding through embolization of the vessel. Surgery may be required if less invasive measures cannot be applied or are not effective. Pharmacotherapy is only used as an adjuvant therapy for all patients with LGIB. Epinephrine is used alone or in conjunction with other surgical techniques to treat a variety of causes of LGIB.

Emergency surgery may be needed to control bleeding in about 10% to 25% of patients in whom nonoperative management is unsuccessful or unavailable. The various endoscopic interventions employed in the management of lower gastrointestinal bleeding include argon plasma coagulation, bipolar or Heater probe, endoloops and hemoclips, and interventional radiology.

Effective measures for the primary prevention of lower GI bleeding include techniques to prevent the related conditions. Promoting a healthy lifestyle by eating a healthy diet, exercising lightly, and avoiding alcohol and tobacco can reduce the risk associated conditions.

Secondary primary preventive measures of lower gastrointestinal bleeding is similar to primary prevention.

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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]

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

	Severe lower GI bleeding	Moderate lower GI bleeding	Occult lower GI bleeding
Age	> 65 years	Occur at any age	Any age
Presenting symptoms	Hematochezia or bright red blood per rectum.	Hematochezia or melena	Symptoms of anemia (fatigue, tiredness)
Hemodynamics	Unstable	Stable	Stable
Lab findings	Hemoglobin equal to or less than 6 g/dl.	Microcytic anemia	Microcytic hypochromic anemia due to chronic blood loss.
Differential	Diverticulosis Angiodysplasia	Neoplastic disease Inflammatory Infectious Benign anorectal Congenital diseases	Inflammatory Neoplastic Congenital

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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.

Lower GI Tract		Arterial Supply	Venous Drainage
Midgut	Distal duodenum Jejunum Ileum Appendix Cecum Ascending colon Hepatic flexure Proximal transverse colon	Superior mesenteric artery (SMA) Ileocolic artery Right colic artery Middle colic branches	Superior mesenteric vein
Hindgut	Distal one-third of the transverse colon Splenic flexure Descending colon Sigmoid colon Rectum	Inferior mesenteric artery (IMA) Left colic artery Sigmoid artery Superior rectal branches	Portal system ɸ
ɸ -Except lower rectum, which drains into the systemic circulation.

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

Disease	Gross Pathology	Microscopic Pathology
Diverticulosis[37]	Numerous visible flask like protrusions along the intestinal wall. Thick and corrugated circular muscle fibers with mucosal folds.	Numerous cells of inflammation Intramucosal ganglion cells Lymphoid infiltrate Mild cryptitis Paneth cell metaplasia Ulcers
Angiodysplasia[38]	Tortuous dilatation of multiple small submucosal and mucosal blood vessels.	Clusters of numerous dilated and thin-walled vessels in mucosa and submucosa. Erosion of surrounding mucosa
Hemorrhoids[8]	Tortuous superficial dilatations of multiple blood vessels.	Dilated, thick-walled, congested submucosal vessels Papillary endothelial hyperplasia Superficial ulcerations Pagetoid dyskeratosis
Mesenteric ischemia [39]	Hemorrhagic infarctions Ulcerations Strictures	Hemorrhage in lamina propria Necrosis of superficial epithelial cells Deep crypts Fibrosis
Ischemic colitis[39]	Discrete or serpiginous ulcerations Pseudopolyps Hemorrhagic infarctions Frank blood or dark mucus in lumen Strictures	Necrotizing phlebitis Multiple thrombi Ulcerations Granulation tissue extending into surrounding submucosa and smooth muscle fibers.
Crohn’s disease[40][41]	Creeping fat Thick/rubbery intestinal wall Strictures (string sign on barium enema) Skip areas Aphthous mucosal ulcers	Superficial or deep ulcerations Granulation tissue extending into surrounding submucosa and smooth muscle fibers. Transmural inflammation with lymphoid aggregates Goblet cells Focal neutrophils in epithelium Lymphoid aggregates Plasmacytosis Edematous mucosa and submucosa
Ulcerative colitis[42]	Deep fissuring ulcerations Hemorrhagic mucosa Pseudopolyps	Mononuclear inflammatory infiltrate in lamina propria Crypt abscesses Granulation tissue extending into surrounding submucosa and smooth muscle fibers. Submucosal fibrosis Schwann cell proliferation

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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.

Disease	Symptoms							Other features	Diagnosis
	Abdominal pain	Rectal pain	Weightloss	Fever	Type of GI bleeding	Diarrhea	Constipation		Laboratory findings	Radio-Imaging findings
Diverticulosis	–	–	–	–	Red or maroon-colored blood	–	+	Self limiting Seen in elderly	Normal	Globular outpouchings on CT scan
Angiodysplasia	–	–	–	–	Frank blood	–	–	Painless bleeding Iron deficiency anemia	Normal	Normal
Hemorrhoids	–	+	–	–	Blood on tissues	–	+	Pain during defecation Anemia	–	Tortuous dilated vessels on anoscopy
Anal fissures	–	+	–	–	Blood on tissues	–	+	Pain during defecation Pain recurs with every bowel movement	Normal except mild leucocytosis	Anoscopy
Mesenteric Ischemia	+	–	+	+	Frank blood	+	–	Pain alters with eating habits Associated with other comorbid conditions	Leukocytosis Increased hematocrit High anion gap metabolic acidosis Lactic acidosis High phosphate levels	Mesenteric edema Bowel dilatation Bowel wall thickening Intramural gas Mesenteric stranding
Ischemic colitis	+	–	–	+	Frank blood	+	–	3 phases Hyperactive phase Paralytic phase (absent bowel sounds) Shock phase	Elevated white blood cell count more than 15,000/mm3 in 20 patients (27%) The serum bicarbonate level was less than 24 mmol/L in 26 patients (36%)	Mild moderate diffuse bowel wall thickening Marked hyperenhancement of the mucosa
Crohn’s disease	+	–	+	+	Blood mixed with stools	+	+	Extra intestinal manifestations Uveitis Sacroiliitis Anemia Peripheral neuropathy	Anemia Leukocytosis Thrombocytosis Anti-Saccharomyces cerevisiae antibodies	Skip lesions Bowel wall thickening Surrounding inflammation, abscess, and fistulae
Ulcerative colitis	+	+	+	+	Blood mixed with stools	+	+	Joint swelling Joint pain Inflammation of the eye Skin involvement Fatty liver Thromboembolism Parenchymal lung disease	Anemia Thrombocytosis A high platelet count	Loss of the vascular appearance of the colon Erythema (or redness of the mucosa) and friability of the mucosa Superficial ulceration, which may be confluent Pseudopolyps
Colon carcinoma	+	-†	+	+	Occult bleeding	+	+†		+ FOBT (fecal occult blood test) ↑ CEA( and CA 19-9 Hypercalcemia	Biopsy

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

Disease Clinical manifestations Diagnosis Comments Symptoms Signs Abdominal Pain Fever Rigors and chills Nausea or vomiting Jaundice Constipation Diarrhea Weight loss GI bleeding Hypo- tension Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging Acute diverticulitis LLQ + ± + − + ± − + Positive in perforated diverticulitis + + Hypoactive Leukocytosis CT scan Ultrasound History of constipation Inflammatory bowel disease Diffuse ± − − ± − + + + − − − Normal or hyperactive Anti-neutrophil cytoplasmic antibody (P-ANCA) in Ulcerative colitis Anti saccharomyces cerevisiae antibodies (ASCA) in Crohn’s disease String sign on abdominal x-ray in Crohn’s disease Extra intestinal findings: Uveitis Arthritis Infective colitis Diffuse + − ± − − + − + Positive in fulminant colitis ± ± Hyperactive Stool culture and studies Shiga toxin in bloody diarrhea PCR CT scan Bowel wall thickening Edema Colon carcinoma Diffuse/localized − − − − ± ± + + ± − − Normal or hyperactive if obstruction present CBC Carcinoembryonic antigen (CEA) Colonoscopy Flexible sigmoidoscopy Barium enema CT colonography  PILLCAM 2: A colon capsule for CRC screening may be used in patients with an incomplete colonoscopy who lacks obstruction Hemochromatosis RUQ − − − − − − − Positive in cirrhotic patients − − − N >60% TS >240 μg/L SF Raised LFT Hyperglycemia Ultrasound shows evidence of cirrhosis Extra intestinal findings: Hyperpigmentation Diabetes mellitus Arthralgia Impotence in males Cardiomyopathy Atherosclerosis Hypopituitarism Hypothyroidism Extrahepatic cancer Prone to specific infections Mesenteric ischemia Periumbilical Positive if bowel becomes gangrenous − + − − + + + Positive if bowel becomes gangrenous Positive if bowel becomes gangrenous − Hyperactive to absent Leukocytosis and lactic acidosis Amylase levels D-dimer CT angiography SMA or SMV thrombosis Also known as abdominal angina that worsens with eating Acute ischemic colitis Diffuse + ± + − − + + + + + + Hyperactive then absent Leukocytosis Abdominal x-ray Distension and pneumatosis CT scan Double halo appearance, thumbprinting Thickening of bowel May lead to shock Ruptured abdominal aortic aneurysm Diffuse ± − + − − − + + + − − N Fibrinogen D-dimer Focused Assessment with Sonography in Trauma (FAST)  Unstable hemodynamics Intra-abdominal or retroperitoneal hemorrhage Diffuse ± − ± − − − − + + − − N ↓ Hb ↓ Hct CT scan History of trauma

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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]

The prevalence of lower gastrointestinal bleeding is approximately 20 per 100,000 population in the United States. Lower gastrointestinal bleed is more common in men than women.

• The prevalence of lower gastrointestinal bleeding is approximately 20 per 100,000 population in the United States.^[1][2]

• The estimated annual incidence of lower GI bleeding is approximately 0.03% in the adult population as a whole.
• The overall incidence of lower GI bleeding is approximately 27 per 100,000 population in the United States.

• Lower gastrointestinal bleed (LGIB) is more common in men than women.^[1]

• There is no racial predilection to lower gastrointestinal bleeding.

• LGIB is rare in children.
• The incidence of lower GI bleeding increases with age with a 200-fold increase from the second to eighth decades of life.

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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 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

Risk factor	Pathophysiology of bleeding
Chronic constipation	Results in colonic diverticula and predispose patients to anal fissures and hemorrhoid formation
Hematologic disorders	Deficiencies in clotting factors, such as factor VII and factor VIII, predispose to LGIB
Anticoagulants	Patients taking warfarin, heparin, aspirin, and platelet inhibitors are at increased risk of bleeding in general
Nonsteroidal anti-inflammatory drugs	NSAIDs cause ulceration in the terminal ileum and proximal colon, and can exacerbate IBD
Human immunodeficiency virus	In patients with HIV, bleeding is caused by opportunistic infections, cytomegalovirus colitis, Kaposi sarcoma, or lymphoma

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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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