Lower Gastrointestinal Bleeding

EXECUTIVE SUMMARY

• Lower gastrointestinal bleeding (LGIB) is commonly seen in the emergency department, and most will stop spontaneously. The most common cause in an adult is diverticulosis, which usually is painless.
• Hemorrhoids can be internal or external and are a very common cause of LGIB. Nearly all cases are self-limited. Internal hemorrhoids generally are painless. Most external hemorrhoids also are painless unless thrombosed. Anal fissures are painful. All cause bleeding around the stool or on toilet wipes.
• Angiodysplasia is seen in older adults and can be the site of significant bleeding.
• Most patients who are hemodynamically stable and whose bleeding has stopped can be considered for discharge with an outpatient workup. Colonoscopy should be performed as soon as feasible.
• Patients who are unstable may require imaging in the emergency department, with computed tomography angiography or standard angiography. Surgical intervention may be necessary when bleeding is brisk and continuous.

Introduction

Lower gastrointestinal bleeding (LGIB) is a common cause of presentation to the emergency department (ED) and often is associated with substantial morbidity and mortality. It traditionally has been described as bleeding in the gastrointestinal (GI) tract that originates distal to the ligament of Treitz.¹ More recently, the term LGIB is reserved for bleeding of the colon and anorectum, whereas bleeding from small bowel or “mid-colonic bleeding” is a distinct entity.² There is a wide array of clinical presentations and causes of LGIB. In some cases, patients will require emergent resuscitation for their bleeding; however, most cases of LGIB will resolve without any immediate intervention. This article will focus mainly on acute LGIB, including small bowel bleeding, in the adult patient.

Epidemiology

GI bleeding is the most common cause of hospitalization related to GI disease in the United States.³ Using data from the Nationwide Emergency Department Sample (NEDS) database, which is a stratified sample of approximately 20% of all ED visits in the United States, Peery et al estimated that there were more than 840,000 encounters annually for GI bleeding. LGIB was the diagnosis in more than 360,000 of those encounters, with more than 160,000 patients requiring admission to the hospital.⁴ Population-based studies to determine the overall incidence of LGIB are lacking. One older single-center study from the United States estimated the incidence to be 20.5 per 100,000 patient years.⁵ While the incidence of upper gastrointestinal bleeding (UGIB) has decreased because of treatment of Helicobacter pylori and the use of proton pump inhibitors,⁶ the study by Peery et al demonstrated that the annual visit rate for LGIB has increased 25% since 2006 and admission rates have increased by 2% in approximately the same time frame.⁴ Using data from the Nationwide Inpatient Survey, Charilaou et al showed an increasing trend of admission rates for LGIB from 676 to 714 per 100,000 admissions during the period from 2005 to 2014, with decreasing rates of colonoscopy from 64.9% to 60.0%. The mean age of patients admitted for LGIB was 72.1 years. Females accounted for 53.3% of that cohort, and inpatient mortality was 1.1%.⁷

Etiology

In adults, the causes of LGIB can be broadly categorized as anatomic, vascular, inflammatory, infectious, drug-induced, neoplastic, and iatrogenic. Common causes of LGIB include diverticular disease, hemorrhoids, angiodysplasias, ischemic colitis, colorectal neoplasms, and inflammatory bowel disease. Other less common sources include post-polypectomy bleeding, isolated colorectal ulcers, radiation colitis/proctitis, and intussusception in adults.⁸ Rare sources of LGIB include Dieulafoy’s lesions, colonic varices, portal hypertensive enteropathy, Meckel’s diverticula, prostate biopsy sites, and endometriosis.⁹ (See Table 1.)

In a study from 1996, Vernava et al analyzed data over a four-year period from the Department of Veterans Affairs. The study cohort comprised 17,941 patients. Diverticular disease was the most commonly identified cause of LGIB, followed by inflammatory conditions. Arteriovenous malformations only accounted for approximately 2% of cases.¹⁰ In the more recent Charilaou study, diverticular disease accounted for 47.5%, whereas colorectal polyps were the cause in 20.4% of cases.⁷ No identifiable cause of LGIB is found in as many as 22.8% of cases.¹¹

Diverticular Hemorrhage

Diverticular bleeding is the most common source of LGIB, accounting for approximately 18% to 50% of all cases.^12,13 (See Table 2.) Diverticular disease is strongly associated with the Western diet, which is low in fiber and high in red and processed meats.¹⁴ Most diverticular disease is due to false diverticula (pseudodiverticula), which are extrusions of colonic mucosa and submucosa through the muscularis propria where the wall has been weakened by the insertion of blood vessels that run underneath the mucosal layer. True diverticula involve all layers of the colonic wall and typically are seen in right-sided diverticular disease in people of Asian descent.¹⁵ The incidence of diverticulosis increases with age. It affects less than 1% to 2% of people younger than 30 years of age, but up to 66% of those 80 years of age and older.¹⁶

Patients with diverticular bleeding typically present with sudden-onset painless hematochezia and often with significant blood loss. Although the full pathophysiology of diverticular bleeding is not completely understood, the bleeding most likely is a result of the rupture of the nutrient vasa recta vessels stretching over the dome of the diverticula.⁸ Diverticular bleeding is not associated with inflammation; therefore, diverticulitis is not a common cause of LGIB.¹⁷ Approximately 3% to 15% of patients with diverticula will develop bleeding over their lifetime, and while a small number of these patients will require urgent or emergent intervention, the majority stop bleeding spontaneously.⁸ In a 2015 systematic review by Cirocchi et al, only 16% of the 700 included patients required interventional treatment.¹⁸ Despite high rates of simultaneous resolution of diverticular bleeding, recurrence of bleeding episodes occurs frequently. In a study by Aytac et al, 47% of patients with proven diverticular bleed treated non-operatively developed a recurrent bleeding episode at a median of 8.1 months after the initial episode.¹⁹

Anorectal Disorders

Anorectal sources of LGIB include hemorrhoids, anorectal fissures, stercoral ulcers, and radiation proctitis. Hemorrhoids are the most common anorectal source of LGIB and commonly present with small amounts of bright red blood noted on toilet paper or streaked on stool. In a study by Gayer et al, hemorrhoids were the source of LGIB in 21% of patients.²⁰

Internal hemorrhoids are located above the dentate line and arise from the internal hemorrhoidal venous plexus located within three fibrovascular cushions. The anal cushions are located in the left lateral, right anterior, and right posterior positions (3, 7, and 11 o’clock positions), which correspond to the usual location of internal hemorrhoids.²¹ Internal hemorrhoids usually are painless unless they become prolapsed and strangulated. External hemorrhoids are located below the dentate line and arise from the external hemorrhoidal venous plexus, which surrounds the rectum. Anoderm composed of squamous epithelium covers external hemorrhoids and is innervated by somatic sensory nerve fibers, which transmit pain.²²

In one study of adult patients who were having a colonoscopy performed for colorectal cancer screening, hemorrhoids were found in 39% of patients. Of these, 55% reported no symptoms associated with hemorrhoids.²³ Bleeding is the most common presenting complaint for patients with hemorrhoids. It often is associated with defecation and usually is painless.²⁴ Patients also may present with pruritis, soiling, a mass-like protrusion from the anus, and pain if the hemorrhoid is thrombosed.²⁵ Hemorrhoids in general are unlikely to be a cause of large amounts of bleeding and rarely cause significant anemia.²⁶

Anal fissures (fissure-in-ano) are tears or splits in the skin of the anal canal that typically cause pain, especially during defecation.⁹ Patients with anal fissures may note bright red blood on toilet paper after defecation. Blood also may be seen on the surface of stool.²⁷ Blood that is mixed with stool or stool that is black in color suggests a more proximal source of bleeding. Anal fissures occur more than 90% of the time in the posterior anal commissure, which is the most poorly perfused portion of the anal canal. High resting anal pressure and poor blood flow likely contribute to the development of anal fissures.²⁸

Fissures located off the midline suggests an underlying pathology, such as inflammatory bowel disease, infection, or neoplastic disease, and require further evaluation.²⁹ Acute hemorrhagic rectal ulcers (AHRUs) and stercoral ulcers can present with massive rectal bleeding. Stercoral ulcers are associated with chronic constipation, whereas AHRUs are not. In both types, the pathophysiology likely is caused by ischemic insult to the rectal tissue. Stercoral ulcers are the result of pressure necrosis that occurs as a result of impacted stool pushing against the bowel wall.³⁰ Most patients are elderly and bedridden, and have significant comorbidities.³¹ These ulcerations can present with massive bleeding and often have high mortality rates, reported as high as 33% to 47%.^31,32

Vascular Malformations

Gastrointestinal angiodysplasia (GIA), also called angioectasia, is a vascular malformation that can be located throughout the GI tract but is most commonly found in the ascending colon and cecum.^33,34 GIAs originate in the GI mucosa and submucosa. They are slightly elevated, bright red, and have irregular contours. There is no gender predominance for GIAs, and the incidence increases with age older than 60 years. GIAs can be associated with various comorbid conditions, such as Von Willebrand disease, heart failure requiring left ventricular assist device, and chronic renal failure. Angiodysplasia in the setting of aortic stenosis is known as Heyde’s syndrome.³⁴ In a study of 1,964 men and women (median age 62 years) undergoing screening colonoscopy, Foutch et al found angiodysplasia in eight (0.83%) patients.³⁵ In the Charilaou study of patients admitted for LGIB, angiodysplasia was the source of the bleeding in 8%.⁷ GIAs can cause both chronic occult as well as acute large volume bleeding. Overt bleeding from GIAs typically is brisk, painless, and recurrent.⁹

Another vascular cause of LGIB is colonic ischemia, a result of episodes of hypoperfusion and reperfusion injury to the colon in addition to poor collateral circulation, relative low blood flow during periods of exertion, and the impact of autonomic stimulation.^36,37 One study reported that 1.9% of LGIB admissions were due to colonic ischemia.⁷ Previous studies reported that colonic ischemia was the cause of 9% to 24% of LGIBs.^5,38,39 Patients with comorbid conditions, such as hypertension, diabetes, coronary artery disease, congestive heart failure, atrial fibrillation, chronic obstructive pulmonary disease, and chronic kidney disease, are at greater risk of developing colonic ischemia.⁴⁰ Patients may present with acute crampy abdominal pain, an urge to defecate, and, within 24 hours of the onset of symptoms, passage of bloody diarrhea or frank blood from the rectum.⁴⁰ In a study of 401 patients, the most common symptoms associated with colonic ischemia were abdominal pain (87%), rectal bleeding (84%), diarrhea (56%), and nausea (30%).⁴¹ In another study, patients with isolated right colon ischemia (IRCI) presented with rectal bleeding much less frequently than patients with non-IRCI (36.4% vs. 83.9%).⁴²

Post-Polypectomy Bleeding

Post-polypectomy bleeding is seen in about 0.4% to 6% of patients undergoing polypectomy.^43,44,45 Most cases of post-polypectomy bleeding occur during the first week, but delayed bleeding can be seen up to three or four weeks later. Risks include age 65 years or older, comorbid diseases, anticoagulant use, large polyp size (> 1 cm), thick polyp stalk, and location of the polyp in the right colon.^46,47 Aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) may increase the risk of minor self-limited bleeding and delayed bleeding.⁴⁸

Infectious Colitis

Infectious causes of LGIB in the developed world often include E. coli 0157:h7, Salmonella, Shigella, Clostridioides difficile, Campylobacter, Yersinia, and cytomegalovirus.¹⁷ Inflammatory bacterial diarrhea typically is bloody and mucopurulent. Other symptoms include fever, tenesmus, and crampy abdominal pain.⁴⁹ Most causes of infectious diarrhea will be self-limited and do not require treatment. Transmission is through the fecal-oral route and results from ingestion of food or water that is contaminated with the culprit organisms.

Neoplasms

Neoplasms are more commonly associated with chronic bleeding.⁹ Colon cancer was the source of LGIB in only 1.5% of admitted patients in one study.⁷ Bleeding often occurs due to ulceration of the malignant lesion.⁵⁰ Colon cancer is an important source of chronic LGIB, and patients may present with weight loss, anemia, and have positive fecal occult blood tests of their stool, or they may be asymptomatic until the cancer has progressed to an advanced stage.⁵¹

Inflammatory Bowel Disease

Inflammatory bowel disease is an autoimmune disease categorized as either Crohn’s disease or ulcerative colitis, based on histologic findings and clinical features of the disease.⁵² Rectal bleeding is more commonly associated with ulcerative colitis than Crohn’s disease. Inflammatory bowel disease, like neoplastic diseases, is unlikely to result in acute massive GI bleeding but is a very common cause of chronic LGIB.⁵³

Clinical Presentations of Lower GI Bleeding

Patients may present to the ED anywhere on the spectrum from stable with non-life-threatening bleeding to unstable with active, life-threatening bleeding that requires immediate resuscitation and intervention. Classically, LGIB presents with bright red or maroon-colored blood per rectum, although in some cases of right-sided colonic bleeding, black tarry stools may be seen. Many episodes of LGIB will resolve spontaneously without the need for any immediate intervention.⁵⁴

Initial ED Evaluation

Consistent with the evaluation of any ED patient, the initial evaluation of a patient with a suspected LGIB should begin with assessing the stability of the patient.⁵⁵ A comprehensive history of present illness and physical examination will help to narrow the differential diagnosis for the cause of bleeding. The time of onset of bleeding, duration, quality, and quantity should be ascertained.^1,8 Any prior history of GI bleeding should be noted, as well as any symptoms associated with the bleeding, like abdominal pain or diarrhea. Recent travel and diet history should be included for evaluation of potential exposures to pathogens that cause infectious diarrhea. The patient’s past medical history and medication history may reveal risk factors for certain etiologies of LGIB and the presence of comorbidities (i.e., cardiopulmonary, hepatic, and renal) that would predispose the patient to poor outcomes.

A family history of GI disease, such as inflammatory bowel disease or colon cancer, may suggest increased risk of the same disease. It should be determined if the patient is currently taking medications such as anticoagulants, aspirin, NSAIDs, or other antiplatelet agents, since these agents can contribute to more severe or prolonged bleeding. For the physical examination, there should be an evaluation for pallor or poor capillary refill time as well as visual and digital anorectal examination. Rectal examination is essential to identify anorectal sources and to assess the color of the patient’s stool and the presence of any gross blood.^1,8,56 The remainder of the physical examination can be tailored to the individual patient presentation.

Initial ED Management

Patients who are tachycardic, hypotensive, have active bleeding, or are otherwise regarded by the emergency physician as unstable should be monitored with two large-bore intravenous catheters placed promptly.^1,8,56 Resuscitation of the patient should occur simultaneously with the medical workup. Laboratory tests should include a complete blood count, electrolytes, renal function, liver function tests, coagulation studies, and a type and screen. If there is a reasonable chance that the patient will need transfusion of blood products, then a type and crossmatch should be ordered. Additional laboratory tests may be needed based on the individual patient presentation.

Fluid Management and Blood Transfusions

The American College of Gastroenterology (ACG) clinical guidelines on LGIB from 2016 recommend that hemodynamically unstable patients and patients with ongoing or suspected ongoing bleeding should receive intravenous fluids with a goal to normalize blood pressure and heart rate prior to urgent colonoscopy.¹ No clinical trials provide evidence for an exact resuscitative strategy for patients with LGIB, but a small, underpowered study evaluating 72 patients with UGIB suggested that early intensive resuscitation vs. standard of care was associated with a decrease in mortality.^57,58

Infusion of large volumes of crystalloid fluids can lead to hemodilution.^59,60 Large volumes of normal saline are associated with the development of hyperchloremic acidosis, which can affect coagulation.⁶¹ Currently, there is no evidence-based consensus on timing, amount, or type of fluids to be used during the resuscitation of a patient with LGIB.⁶²

Administration of fluid volumes greater than 1.5 L is associated with a higher mortality. This risk was even greater for patients who received 3 L or more.⁶³

In a study by Villanueva et al, a restrictive transfusion protocol using a threshold hemoglobin of 7 g/dL was compared to a liberal transfusion protocol using a threshold hemoglobin of 9 g/dL for patients with UGIB. Patients in the restrictive protocol had improved survival at six weeks, decreased rates of rebleeding, and fewer overall adverse events.⁶⁴

The Transfusion in Gastrointestinal Bleeding (TRIGGER) study of UGIB compared a restrictive threshold of 8 g/dL to a liberal threshold of 10 g/dL. There were no statistical differences between the two study groups for the clinical outcomes measured.⁶⁵ The ACG recommendation is that packed red blood cells should be transfused when the hemoglobin is < 7 g/dL. Patients with a threshold of 9 g/dL for transfusion should be considered if the patient has massive bleeding, significant comorbidities such as cardiac disease, or if there will be a delay in intervention.¹

The ACG recommends that patients with LGIB should be transfused to maintain a platelet count above 50 × 10⁹/L in cases of severe bleeding or if endoscopic hemostasis is required. This threshold also is recommended for patients receiving massive blood transfusion.¹

Tranexamic Acid

Tranexamic acid (TXA) is a synthetic analog of the amino acid lysine that competitively binds to receptor sites on plasminogen, resulting in clot preservation.⁶⁶ The U.S. Food and Drug Administration (FDA) has approved TXA for two clinical indications: the reduction or prevention of hemorrhage following tooth extraction in patients with hemophilia and treatment of heavy menstrual bleeding.⁶⁷ However, TXA has been used off-label for multiple indications.^68,69 TXA may be useful in UGIB for the reduction of continued bleeding, need for urgent endoscopic intervention, and mortality. The effects of TXA in LGIB remain unclear.⁷⁰

The Hemorrhage Alleviation with Tranexamic Acid–Intestinal System Trial (HALT-IT) study was published in 2020. This was a randomized, double-blind, placebo-controlled clinical trial that assessed the effect of a high-dose 24-hour infusion of TXA on death and thromboembolic events in adult patients with significant acute GI bleeding. The study enrolled more than 12,000 subjects, with approximately 90% having UGIB. There was no difference in the primary outcome of death due to bleeding at five days (3.7% of the TXA group and 3.8% of the placebo group). The original primary outcome also did not show a difference between the groups for all-cause mortality at 28 days (9.5% with TXA vs. 9.2% with placebo). There was a two-fold increase in the rate of thromboembolism with the use of TXA (0.8% in the TXA group vs. 0.4% in the placebo group).⁷¹

Patients Taking Antiplatelet Agents and Anticoagulants

Use of anticoagulant medications is common. In one study of 2,528 patients with LGIB, 29.4% were taking an antiplatelet medication and 15.9% were on an anticoagulant.¹¹ In a study that included both patients with UGIB and LGIB, the routine administration of platelets to patients taking antiplatelet medications but without thrombocytopenia (platelet counts > 100 × 10⁹/L) was associated with increased mortality but not reduced episodes of rebleeding.⁷² For patients with UGIB, published guidelines do not recommend routine transfusion of platelets to patients based only on the use of antiplatelet medications.^1,55 Direct oral anticoagulants (DOACs), such as dabigatran, rivaroxaban, and apixaban, have been associated with a higher risk of GI bleeding.⁷³ A retrospective analysis from the United Kingdom of 2,528 patients with LGIB revealed a higher rate of in-hospital rebleeding in patients on antiplatelet agents but not for those taking warfarin or DOACs as compared to unexposed patients. Withholding antiplatelet medications for at least five days during the admission did not lead to a reduction in rebleeding.¹¹

In a study of patients with LGIB who were on anticoagulants, endoscopic intervention was required more often in the DOAC group as compared to the warfarin group, but mortality, recurrence of bleeding, and transfusion requirements were not different between the two groups. The DOAC group did have a shorter length of stay.⁷⁴

The approach to management of anticoagulation in a patient with LGIB should be individualized to the patient, taking into consideration the risk of ongoing bleeding vs. the risk of thromboembolic events. The ACG recommends that management of anticoagulation, and considerations for reversal, in patients with LGIB should be done in conjunction with a multidisciplinary team.¹

The use of aspirin and NSAIDs has been associated with an increased risk of LGIB in patients with diverticular disease.⁷⁵ One study demonstrated that discontinuing the use of NSAIDs after a diverticular bleed reduced the incidence of rebleed during the subsequent 12 months from 77% to 9.4%.⁷⁶ The ACG recommends that patients with a history of LGIB, especially those with diverticulosis and angiodysplasias, should avoid NSAIDs as a method of preventing future bleeding episodes.¹

Colonoscopy and Upper Endoscopy

According to the current ACG guidelines, colonoscopy is the initial imaging modality of choice in patients presenting with LGIB. The diagnostic yield of colonoscopy for determining the source of LGIB is 20% to 100%. The yield is increased in patients without active bleeding.⁷⁷ An older review published in 1997 found an overall complication rate of 1.3%.⁷⁸ More recently, a 2010 review found an overall complication rate of 0.3%.⁷⁹

The diagnostic yield of colonoscopy in LGIB has been reported to be up to 90%.^80,81 There have been mixed results in prospective studies evaluating the timing of colonoscopy. An early study showed that earlier colonoscopy for LGIB was associated with shorter hospital lengths of stay (LOS).⁸² Another study demonstrated that although early colonoscopy led to a more definitive diagnosis, it was not associated with a statistical difference in early or late rebleeding, total hospital or intensive care unit LOS, total blood requirement, or need for surgery.⁸³

Additional studies have shown no benefit to early urgent colonoscopy.^84,85,86 In a study in 2019, patients with LGIB received early colonoscopy (within 24 hours of presentation) or a standard colonoscopy (within 24 to 72 hours). Mortality was 0% for both cohorts. The hospital LOS was shorter in the early colonoscopy group, as was the rate of rebleeding and readmissions.⁸⁷ The ACG recommends that patients with high-risk clinical features or ongoing bleeding should have a rapid bowel purge performed along with hemodynamic resuscitation and colonoscopy performed within 24 hours of presentation. For patients without high-risk features, serious comorbid disease, or ongoing bleeding, the ACG recommends that colonoscopy should be performed after the following bowel purge at the next available time.¹

Hematochezia with significant hemodynamic instability suggests the possibility of a brisk UGIB source, especially in at-risk patients (patients with known peptic ulcer disease or portal hypertension, and patients on antiplatelet medications or anticoagulants).^1,88 The ACG guidelines recommend that patients with hematochezia who are unstable undergo upper endoscopy prior to colonoscopy.¹ An elevated blood urea nitrogen (BUN) to creatinine ratio also is highly suggestive of a UGIB source. A ratio > 30:1 has a positive likelihood ratio for the diagnosis of UGIB of 7.5, a sensitivity of 51%, and specificity of 93%.⁸⁹ If there is moderate clinical concern that a patient presenting with hematochezia may have a UGIB, nasogastric lavage can be performed, although poor sensitivity and specificity limit the utility of this evaluation.^90,91,92,93

Other Imaging Modalities

For the emergency physician caring for a patient with an LGIB, other imaging modalities may be beneficial while the patient is being resuscitated and prepped for eventual colonoscopy. These modalities include computed tomographic (CT) angiography, tagged red blood cell scintigraphy, and angiography. CT angiography is the imaging modality of choice for acute LGIB in the unstable patient.^1,55 It can be obtained quickly, does not require bowel preparations, and is preferred in patients who cannot undergo colonoscopy.⁵⁵ (See Figure 1.)

Using a porcine model and multi-detector-row CT angiography, Dobritz et al demonstrated a sensitivity of 97% and a specificity of 100% for detection and localization of the source of LGIB.⁹⁴ In clinical practice, the high sensitivity and specificity are maintained with reported sensitivity of 79% to 98% and specificity of 95%.^95,96 There is some evidence that CT angiography is most effective in patients who are unstable.⁹⁷

The ability to identify a source of bleeding in an unstable patient is key in planning for intervention, and CT angiography has been shown to be accurate at not only detection but also localization of bleeding sources.^97,98,99 There are little data comparing CT angiography to colonoscopy directly.¹⁰⁰ Angiography, unlike CT angiography, allows for diagnosis as well as intervention. Rates of bleeding of at least 0.5 mL/min to 1 mL/min are required to detect contrast extravasation to determine the site of bleeding.¹⁰¹ Digital subtraction angiography is a more sensitive technique than the conventional technique for the detection of LGIB.¹⁰² Embolization can be performed using a variety of materials, such as gelatin sponges, coils, and glue.¹⁰³ Nuclear medicine imaging can detect bleeding rates as low as 0.2 mL/min.⁷⁷ These studies take time and require specialized equipment and staff. Because of improvements in imaging with CT angiography, tagged red blood cell scintigraphy has a diminished role in the evaluation of patients with LGIB.⁷⁷

Consultations

Consultation with a gastroenterologist should be obtained in patients with active bleeding who are being admitted. Patients who are unstable with active bleeding will benefit from consultation with interventional radiology.

Consultation to surgery should be considered in high-risk patients with ongoing bleeding, and surgical intervention should be considered when there is ongoing brisk bleeding.¹ Overall mortality is generally high in these patients and has been reported at 6% to 27% in patients undergoing emergent total colectomy for massive GIB.^104,105,106 In a study by Farner et al, of patients undergoing surgical control for LGIB, the overall mortality was related to the amount of blood required to be transfused. Patients who received fewer than 10 units of packed red blood cells had a mortality of 7%, whereas those who received more than 10 units had a 45% mortality.¹⁰⁷ All efforts should be made to localize a source of bleeding prior to proceeding for laparotomy in a patient with LGIB.⁵⁵

Inpatient Admission vs. Outpatient Follow-Up

Most cases of LGIB are small volume and resolve spontaneously (up to 85% of cases).²⁰ In these cases, discharge with outpatient follow-up and colonoscopy is appropriate. Stable patients who have high-risk features for malignancy can be discharged but should have close outpatient follow-up for colorectal cancer screening based on their age and risks.^108,109

Patients who require inpatient admission and further evaluation are those with unstable vitals, continued bleeding, or at high risk for bleeding. Patients with continued vital sign abnormalities, those with high risk for rebleeding, or those with ongoing bleeding may require intensive care.⁸

Assessment of Patient Risk and the Severity of Bleeding

In 1997 by Kollef et al published the BLEED outcome prediction criteria for patients with either UGIB or LGIB who were admitted from the ED to the hospital or intensive care unit. The final criteria consisted of: B, ongoing bleeding; L, low systolic blood pressure; E, elevated prothrombin time; E, erratic mental status; and D, unstable comorbid disease. The presence of any of these criteria categorized the patient as high-risk. The initial study, which was externally validated, reported a significant difference between low-risk and high-risk patients regarding adverse events, including rebleeding, need for surgical intervention, hospital mortality, end organ dysfunction, and need for transfusion.¹¹⁰

Strate et al followed 252 consecutive patients admitted for LGIB. They assessed 24 potential variables based on clinical experience and a review of the literature. Independent correlates of severe bleeding were heart rate ≥ 100 beats/min, systolic blood pressure ≤ 115 mmHg, syncope, nontender abdominal examination, rectal bleeding during the first four hours, aspirin use, and more than two active comorbid conditions.¹¹¹

In 2015, Sengupta et al performed a single-center, prospective observational study of 277 patients admitted for LGIB. The risk factors for 30-day readmissions were having LGIB while in the hospital, anticoagulant use, and active malignancy. The risk factors for death at 30 days were in-hospital LGIB, Charlson Comorbidity Index scores, and active malignancy.¹¹²

In 2017, Sengupta et al published a study in which a clinical prediction tool was derived using a study population of 4,044 patients from a single academic center. The eight variables that were most associated with 30-day mortality were age, dementia, metastatic cancer, chronic kidney disease, chronic pulmonary disease, anticoagulant use, admission hematocrit, and albumin. The 30-day mortality risk for the lowest quartile was 3.6% in the derivation cohort and 4.4% in the validation cohort.¹¹³

NOBLADS is another recent risk score developed in Japan specifically for patients with LGIB. This eight-factor score includes NSAID use, no diarrhea, no abdominal tenderness, systolic blood pressure ≤ 100 mmHg, antiplatelet drug use, albumin < 3.0 g/dL, Charlson Comorbidity Index of 2 or greater, and syncope. In the validation cohort, the rates of severe bleeding with 0, 1, 2, 3, 4, and 5 or more predictors were 0%, 20%, 25%, 40%, 50%, and 92.9%, respectively.¹¹⁴

The Oakland score was derived to predict safe discharge in patients with LGIB. Safe discharge was defined as the absence of the following events: rebleeding, transfusion, therapeutic intervention to control bleeding, in-hospital death, and readmission with further LGIB within 28 days. The predictive score was based on seven clinical variables, which included age, sex, history of LGIB, digital rectal examination findings, heart rate, blood pressure, and hemoglobin level. A score of 8 or less predicts a 95% probability of safe discharge.¹¹⁵

The Glasgow-Blatchford Bleeding Score was originally developed to determine which patients with UGIB were low risk and appropriate for outpatient management. This score comprises nine features, including hemoglobin, BUN, initial systolic pressure, sex, heart rate, presence of melena, syncope, hepatic disease, or heart failure.¹¹⁶ The use of this scoring system has been evaluated and shown to predict the need for admission in patients with LGIB.¹¹⁷ In an external validation of the Oakland score and the Glasgow-Blatchford score in a Vietnamese population, the Oakland score outperformed the Glasgow-Blatchford score in predicting severe bleeding.¹¹⁸

Pediatric Populations

LGIB in the pediatric population is commonly encountered in medical practice and comprises a multitude of causes and presentations that differ according to age. As with the adult population, there is a lack of recent epidemiologic data pertaining to this topic. Patient information from the NEDS database gathered from 2006-2011 identified 132,102 visits of patients ages birth to 19 years presenting with complaints related to a complaint of LGIB. This sample also indicated an increase in pediatric patient visits for LGIB, with the greatest in patients ages 10-19 years, with 80% of patients undergoing routine discharge.¹¹⁹ Common causes of LGIB in the pediatric population can be identified according to age. For infants, the possible etiologies of LGIB include necrotizing enterocolitis, volvulus, milk-protein allergy, Hirschsprung’s disease, anal fissures, and intussusception. Intussusception also can be a cause of LGIB in older children.

Other potential causes include infectious colitis, anal fissures, hemolytic uremic syndrome, Meckel’s diverticulum, and vasculitis-related bleeding as seen in Henoch-Schonlein purpura. As a patient reaches adolescence, common causes of LGIB still may include infectious sources and anal fissures, but also may include hemorrhoids and inflammatory bowel disease.¹²⁰ LGIB in the pediatric population also may be the first presentation of a congenital or genetic condition. Unfortunately, there is little evidence or research specific to the ideal workup in pediatric patients presenting with LGIB.

Conclusion

LGIB is a common presentation in the ED and there are a vast number of associated causes and presentations. Initial management should be directed at attempts to elucidate the cause of bleeding, while simultaneously initiating laboratory evaluation, timely and appropriate consultation, as well as adequate goal-directed resuscitation of the patient. The majority of cases of LGIB will stop spontaneously without intervention, but a proportion of the patients will require continued resuscitation and urgent or emergent intervention. Unfortunately, there is a limited amount of data specific to the management of LGIB, and many of the accepted clinical recommendations are made on strong consensus but low quality of evidence. Continued research is required to help improve outcomes in patients with LGIB and further delineate appropriate LGIB-specific treatment recommendations.

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