Gastrointestinal Intervention 2018; 7(3): 100-105  https://doi.org/10.18528/gii180024
Clinical assessment and treatment algorithm for lower gastrointestinal bleeding
Soo-Kyung Park
Division of Gastroenterology, Department of Internal Medicine and Gastrointestinal Cancer, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea
*Division of Gastroenterology, Department of Internal Medicine and Gastrointestinal Cancer, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, 29 Saemunan-ro, Jongno-gu, Seoul 03181, Korea. E-mail address: sk0103.park@samsung.com (S.K. Park). ORCID: https://orcid.org/0000-0001-8822-9632
Received: July 9, 2018; Revised: August 10, 2018; Accepted: August 10, 2018; Published online: October 31, 2018.
© Society of Gastrointestinal Intervention. All rights reserved.

cc This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract

Lower gastrointestinal bleeding (LGIB) is diagnosed in 20% to 30% of all patients presenting with major gastrointestinal (GI) bleeding. Although most patients with acute LGIB stop bleeding spontaneously and have favorable outcomes, morbidity and mortality ranges from 2% to 4%, and is higher in older patients and those with comorbid medical conditions. Common etiologies of LGIB are diverticular bleeding, ischemic colitis, angioectasia bleeding and hemorrhoid. Patients presenting with acute severe hematochezia should undergo a focused evaluation simultaneous with hemodynamic resuscitation. An upper GI bleeding source must be excluded in patients with hematochezia and hemodynamic instability. Colonoscopy following a colon preparation is the initial test of choice in most patients presenting with acute hematochezia and hemodynamic stability.

Keywords: Hemorrhage, Intestines, Therapeutics
Introduction

Lower gastrointestinal bleeding (LGIB) is diagnosed in 20% to 30% of all patients presenting with major gastrointestinal (GI) bleeding.1,2 Compared with acute upper GI bleeding (UGIB) patients, patients with LGIB tend to present with a higher hemoglobin level and are less likely to develop hypotensive shock or require blood transfusions.3 Although most patients with acute LGIB stop bleeding spontaneously and have favorable outcomes, morbidity and mortality ranges from 2% to 4%,4,5 and is higher in older patients and those with comorbid medical conditions.6

Definition of LGIB

LGIB has been defined as bleeding originating distal to the ligament of Treitz. However, since the advent of capsule endoscopy and enteroscopy, small-bowel sources have been placed in the category of midgut bleeding from the small intestine (middle GI bleeding), which is distinct from colonic bleeding in terms of presentation, management, and outcomes.7 Thus, the new definition of LGIB has been proposed as bleeding from a source distal to the ileocecal valve, with hematochezia originating from either the colon or the rectum.8 Acute LGIB is defined as recent bleeding (< 3 days) that may result in hemodynamic instability, anemia, and/or the need for blood transfusion. Chronic LGIB is the passage of blood per rectum over a period of several days or longer, and usually implies intermittent or slow loss of blood.3

Etiologies of LGIB

Diverticular bleeding

Diverticular bleeding accounts for 30% to 65% of acute LGIB episodes (Table 1). Colon diverticula are present in up to 30% of patients aged ≥ 50 years, with the prevalence increasing to approximately 60% in those aged ≥ 80 years in studies from Western countries.9 In Korea, the prevalence of colonic diverticulosis has increased to 12% in conjunction with the adoption of Western dietary habits, extension of lifespan, and advances in diagnostic modalities.10 Nonsteroidal anti-inflammatory drugs (NSAIDs) increase the risk for diverticular bleeding, while hypertension and anticoagulation may also contribute to severe bleeding.11,12 The clinical presentation of diverticular bleeding is characterized by painless hematochezia. Bleeding resolves spontaneously in 75% to 80% of patients, but recurs in 25% to 40% within 4 years.4 The diagnosis of diverticular hemorrhage is presumptive in most patients, and is based on the presence of colon diverticula and the absence of another obvious source of LGIB. A definitive diagnosis is made in approximately 22% of patients who have active bleeding or high-risk stigmata of a visible vessel or clot on colonoscopy.13 After endoscopic treatment, early rebleeding is uncommon.14,15 Late rebleeding may occur from diverticula at a location different from that of the index bleed.

Ischemic colitis

Ischemic colitis is the underlying etiology in 1% to 19% of patients with LGIB and most commonly affects elderly patients.16,17 Ischemic colitis results from a sudden, often temporary, reduction in mesenteric blood flow secondary to hypoperfusion, vasospasm, or occlusion of the mesenteric vasculature. Ischemic colitis manifests with a wide spectrum of injuries, including reversible colopathy (subepithelial hemorrhage and edema), transient colitis, chronic colitis, stricture, gangrene, and fulminant universal colitis. The typical locations affected by nonocclusive colon ischemia are the splenic flexure and rectosigmoid junction; the rectum usually is spared, because of its dual blood supply.18 Patients with ischemic colitis often have underlying cardiovascular disease and present with hypotension or hypovolemia, which results in mesenteric hypoperfusion and vasoconstriction. The clinical presentation of ischemic colitis is cramping abdominal pain over the segment of colon involved, followed by a short course of bloody diarrhea.19 Typical endoscopic findings are submucosal hemorrhage and ulcerations in the colon and a single linear ulcer that runs along the longitudinal axis of the colon on the antimesenteric border (Fig. 1A, 1B).20 Angiography should be considered in patients with severe ischemic colitis or right-side involvement, when there is suspicion for an underlying thromboembolism or concomitant mesenteric ischemia involving the small bowel.21 The majority of patients diagnosed with ischemic colitis show improvements with conservative management including intravenous hydration and correction of the underlying etiology, although some with more severe disease require antimicrobials and/or surgical intervention.21

Angioectasia

Angioectasias, also named angiodysplasias are caused by degenerative changes and chronic intermittent low-grade obstruction in the submucosal vessels.22 The prevalence of colon angioectasia is 3% to 15% in patients with LGIB.17 The presence of colonic angioectasia is associated with valvular heart disease, liver cirrhosis, and chronic renal failure, and risk factors for bleeding include advanced age, comorbidities, the presence of multiple angioectasias, and the use of anticoagulants or antiplatelet agents.23 Patients can present with occult bleeding, melena, or painless intermittent hematochezia.24 Colonoscopy has a sensitivity of 80% for the detection of angioectasias, and typical endoscopic findings are red, flat lesions, ranging in size from 2 mm to several centimeters, with ectatic blood vessels radiating from a central feeding vessel, predominantly in the cecum and the ascending colon (Fig. 1C, 1D).22

Hemorrhoids

The prevalence of hemorrhoidal bleeding has been reported as 2% to 64% in patients presenting with hematochezia.4,17 Hemorrhoids are a plexus of dilated arteriovenous vessels that arise from the superior and inferior hemorrhoidal veins; these plexuses are located in the submucosa of the distal rectum and are classified as internal or external, based on their location relative to the dentate line.25 Patients typically present with painless, intermittent, scant hematochezia characterized by bright red blood on the toilet paper, coating the stool, or dripping into the toilet bowl.

Colorectal neoplasia

Colorectal neoplasia accounts for up to 17% of all etiologies in patients with LGIB and presents more commonly with occult bleeding.4,26 In addition to LGIB, symptoms of bowel habit changes and weight loss should raise suspicion for colorectal neoplasia and prompt colonoscopy should be performed. LGIB associated with colorectal neoplasia usually results from surface ulcerations of an advanced tumor. Patients with tumors in the right side of the colon are more likely to present with occult blood loss and iron deficiency anemia, whereas those with left-side tumors more commonly present with hematochezia.25,26 Endoscopic treatment for hemostasis is rarely required because bleeding from colorectal neoplasia is slow in the majority of patients.25

NSAID use

NSAID use is associated with an increased risk of LGIB, including diverticular bleeding.11 The prevalence of NSAID use is reported to be as high as 86% in patients with LGIB.27 The mechanisms involved in the induction of LGIB by NSAIDs are not well understood and may include local mucosal trauma and platelet inhibition in susceptible individuals as well as the concomitant use of warfarin and other antiplatelet agents.28 Use of NSAIDs can induce NSAID colopathy, which is characterized by colon ulcerations and diaphragm-like strictures, predominantly located in the terminal ileum and right side of the colon.28

Miscellaneous Etiologies

Post-polypectomy bleeding has been reported to account for 2% to 8% of acute LGIB.29 The initial assessment of the patient presenting with presumed acute LGIB should include a focused history including recent polypectomy (Fig. 2). Rectal ulcers have been reported in 8% of patients who present with severe hematochezia,30 and are an important cause of acute LGIB in patients with critical illness such as end-stage renal disease on hemodialysis, respiratory failure requiring mechanical ventilation, decompensated cirrhosis, or malignancy.31 Endoscopic findings range from clean-based ulcers (82%) to adherent clots (17%), non-bleeding visible vessels (33%), and active bleeding (50%).30 Early rebleeding after endoscopic treatment has been reported in 44% to 48% of patients, and a mortality rate of 33% to 48% has been reported in patients with high-risk stigmata who have multiple comorbidities.31

In radiation proctopathy, LGIB has been reported in 4% to 13% of patients. This disorder is caused by radiation-induced endarteritis obliterans, which results in neovascularization and telangiectasias in the rectum.26

Patients with inflammatory bowel disease commonly present with LGIB. Clinically significant bleeding in Crohn’s disease is more common in patients with colon involvement than in those with isolated small-bowel disease.32

Management

Evaluation

A directed history-taking, physical examination, and laboratory evaluation should be performed at the time of patient presentation with the goal of determining the severity of bleeding, its possible location, and etiology.3335 The history obtained should include the color, amount, frequency, and duration of bleeding and any associated symptoms that may suggest a specific source such as abdominal pain and diarrhea (colitis), and altered bowel habits and weight loss (malignancy). In addition, a targeted history of medications that may influence bleeding risk (NSAIDs, antiplatelet agents, and anticoagulants), prior bleeding episodes, recent polypectomy, radiation therapy for prostate or pelvic malignancies, inflammatory bowel disease, and risk factors for colorectal cancer may be useful to determine the potential source of bleeding and guide further management.34

The physical examination should include the measurement of vital signs, and a cardiopulmonary, abdominal, and digital rectal examination should also be performed. Initial laboratory studies should include a complete blood count, serum electrolytes, and coagulation studies, with blood typing and cross-matching.34,36

Hemodynamic resuscitation

Hematochezia associated with hemodynamic instability and/or suspected ongoing bleeding should receive intravenous fluid resuscitation.37,38 In addition, some patients will require blood transfusions. Large observational studies and a meta-analysis of three small trials of UGIB suggest that blood transfusion compared with no transfusion is associated with an increased risk of rebleeding and possibly death.39,40 These findings are supported by results of a large randomized trial of patients with UGIB that found that a restrictive transfusion strategy with a transfusion threshold of hemoglobin < 7 g/dL improved survival (95% vs 91%) and decreased rebleeding (10% vs 16%), when compared with a threshold of 9 g/dL.39 Patients with massive bleeding, acute coronary syndrome, symptomatic peripheral vascular disease, or a history of cerebrovascular disease were excluded, and all patients underwent upper endoscopy within 6 hours of presentation. Therefore, patients with LGIB who have significant comorbid disease, massive, ongoing bleeding, or delayed therapeutic interventions may benefit from a more lenient blood transfusion threshold (9 g/dL).

Severe hematochezia

Severe hematochezia associated with hemodynamic instability should lead to consideration of a brisk UGIB source, especially in at-risk patients such as those with a history of peptic ulcer disease or liver disease with portal hypertension and those using antiplatelet or anticoagulant medications.15,34,36 If suspicion for an UGIB source is modest, nasogastric aspirate/lavage can be used to assess possible UGIB.34,36 The nasogastric tube can be left in place to facilitate subsequent colon preparation.13 If the likelihood of UGIB is high, emergent esophagogastroduodenoscopy (EGD) is the test of choice for the evaluation and management of high-risk upper GI lesions, followed by colonoscopy after an upper GI source is ruled out.41

Radiographic interventions should be considered in patients with hemodynamically unstable and ongoing bleeding and are therefore unlikely to tolerate bowel preparation and urgent colonoscopy. Angiography localizes a LGIB source in 25% to 70% of exams.42,43 A systematic review found that super-selective angiographic embolization achieves immediate hemostasis in 40% to 100% of cases of diverticular bleeding with a rebleeding rate ranging from 0% to 50%.44 Because angiography relies on active bleeding and has the potential for serious complications, it should be reserved for patients with very brisk, ongoing bleeding.

Colonoscopy should be performed first in hemodynamically stable patients with severe hematochezia.45 The main advantage of colonoscopy is ability to perform a therapeutic intervention with diagnosis of the underlying lesion.46 The diagnostic yield of colonoscopy ranges from 45% to 100% in LGIB and is significantly higher than radiologic evaluation with a red blood cell scan and angiography.47,48 It is important to carefully inspect the colonic mucosa both on insertion and withdrawal, as culprit lesions often bleed intermittently and may be missed when not actively bleeding. The endoscopist should intubate the terminal ileum to rule out proximal blood suggestive of a small bowel lesion. An adult or pediatric colonoscope with a large working channel (at least 3.3 mm) should be used because the larger working channel facilitates suctioning of blood, clots, and residual stool, and allows for the passage of large diameter (e.g., 10 Fr) endoscopic hemostasis tools. In addition, the use of a water-jet irrigation device (foot pedal controlled by the endoscopist) is recommended to facilitate removal of adherent material and residue from the colonic mucosa.

An urgent colonoscopy is recommended in the evaluation of severe hematochezia and should be performed within 8 to 24 hours of admission.15,47 Early performance of colonoscopy increases both its diagnostic yield and the likelihood of a therapeutic intervention, and reduces the duration of hospitalization and cost of care.15,47,49 However, there is no improvement in outcomes of rebleeding or surgery after urgent colonoscopy.15,50

Colon preparation is important before colonoscopy to improve visualization, increase the diagnostic yield, and reduce the risk of perforation.34,36 Thus, once the patient is hemodynamically stable, colonoscopy should be performed after adequate colon cleansing, and unprepared colonoscopy/sigmoidoscopy is not recommended. Polyethylene glycol-based solutions can be administered orally at a rate of approximately 1 L every 30 to 45 minutes until the effluent is free of fecal material.51 A nasogastric tube can be considered to facilitate colon preparation in patients who are intolerant of oral intake and are at low risk of aspiration.33 After bowel preparation, colonoscopy should be performed within 1 to 2 hours.

Scant intermittent hematochezia

Chronic intermittent passage of small amounts of blood per rectum is the most common pattern of LGIB and usually is caused by an anorectal or distal colon source of bleeding.52,53 A digital rectal examination and flexible sigmoidoscopy may be sufficient for the evaluation of average risk patients with minimal bright red bleeding per rectum.54 The diagnostic yield of flexible sigmoidoscopy ranges up to 58% in patients with LGIB, and colonoscopy should be pursued in the absence of a definitive source of bleeding on flexible sigmoidoscopy, patients aged > 50 years, the presence of iron deficiency anemia, risk factors for colorectal neoplasia, or alarm symptoms of weight loss or bowel habit changes.36,55

Melena

In the evaluation of melena, the majority of patients have UGIB and EGD should be the initial test.41 However, melena also may result from slow bleeding emanating from the colon or small bowel. Therefore, if there are negative results on EGD, colonoscopy should be performed. Persistent melena after negative results with bidirectional endoscopy may warrant small-bowel endoscopy for evaluation of occult GI bleeding.56

Conclusion

A management approach for patients presenting with acute LGIB is outlined in Fig. 3. To summarize, patients presenting with acute severe hematochezia should undergo a focused evaluation simultaneous with hemodynamic resuscitation. A UGIB source must be excluded in patients with hematochezia and hemodynamic instability. Colonoscopy following a colon preparation is the initial test of choice in most patients presenting with acute hematochezia and hemodynamic stability.

Conflicts of Interest

No potential conflict of interest relevant to this article was reported.

Figures
Fig. 1. Ischemic colitis at sigmoid colon (A, B). Angioectasias at ascending colon (C, D)
Fig. 2. Post-polypectomy bleeding. (A) Polyp at ascending colon, (B) post-polypectomy ulcer, (C) post-polypectomy bleeding at next day, (D) bleeding control with clips.
Fig. 3. Treatment algorithm for lower gastrointestinal (GI) bleeding. IV, intravenous; NG, nasogastric; UGI, upper gastrointestinal; EGD, esophagogastroduodenoscopy; PEG, polyethylene glycol.
Tables

Table 1

Causes of Acute Lower Gastrointestinal Bleeding

CauseCases (%)
Diverticulosis30–65
Ischemic colitis4–20
Hemorrhoids4–20
Angioectasias4–15
Colitis, other3–15
Colorectal polyps or neoplasms2–15
Postpolypectomy bleeding2–7
Inflammatory bowel disease3–5
Rectal ulcer0–8

Data from the article of Gralnek et al (N Engl J Med. 2017;376:1054–63).35

References
  1. Gostout, CJ, Wang, KK, Ahlquist, DA, Clain, JE, Hughes, RW, and Larson, MV (1992). Acute gastrointestinal bleeding. Experience of a specialized management team. J Clin Gastroenterol. 14, 260-7.
    Pubmed CrossRef
  2. Peura, DA, Lanza, FL, Gostout, CJ, and Foutch, PG (1997). The American College of Gastroenterology bleeding registry: preliminary findings. Am J Gastroenterol. 92, 924-8.
    Pubmed
  3. Zuckerman, GR, and Prakash, C (1998). Acute lower intestinal bleeding: part I: clinical presentation and diagnosis. Gastrointest Endosc. 48, 606-17.
    Pubmed CrossRef
  4. Longstreth, GF (1997). Epidemiology and outcome of patients hospitalized with acute lower gastrointestinal hemorrhage: a population-based study. Am J Gastroenterol. 92, 419-24.
    Pubmed
  5. Richter, JM, Christensen, MR, Kaplan, LM, and Nishioka, NS (1995). Effectiveness of current technology in the diagnosis and management of lower gastrointestinal hemorrhage. Gastrointest Endosc. 41, 93-8.
    Pubmed CrossRef
  6. Strate, LL, Ayanian, JZ, Kotler, G, and Syngal, S (2008). Risk factors for mortality in lower intestinal bleeding. Clin Gastroenterol Hepatol. 6, 1004-10.
    Pubmed KoreaMed CrossRef
  7. Prakash, C, and Zuckerman, GR (2003). Acute small bowel bleeding: a distinct entity with significantly different economic implications compared with GI bleeding from other locations. Gastrointest Endosc. 58, 330-5.
    Pubmed
  8. Raju, GS, Gerson, L, Das, A, and Lewis, B (2007). American Gastroenterological Association (AGA) institute technical review on obscure gastrointestinal bleeding. Gastroenterology. 133, 1697-717.
    Pubmed CrossRef
  9. Niikura, R, Nagata, N, Shimbo, T, Aoki, T, Yamada, A, and Hirata, Y (2015). Natural history of bleeding risk in colonic diverticulosis patients: a long-term colonoscopy-based cohort study. Aliment Pharmacol Ther. 41, 888-94.
    Pubmed CrossRef
  10. Song, JH, Kim, YS, Lee, JH, Ok, KS, Ryu, SH, and Lee, JH (2010). Clinical characteristics of colonic diverticulosis in Korea: a prospective study. Korean J Intern Med. 25, 140-6.
    Pubmed KoreaMed CrossRef
  11. Laine, L, Connors, LG, Reicin, A, Hawkey, CJ, Burgos-Vargas, R, and Schnitzer, TJ (2003). Serious lower gastrointestinal clinical events with nonselective NSAID or coxib use. Gastroenterology. 124, 288-92.
    Pubmed CrossRef
  12. Niikura, R, Nagata, N, Aoki, T, Shimbo, T, Tanaka, S, and Sekine, K (2015). Predictors for identification of stigmata of recent hemorrhage on colonic diverticula in lower gastrointestinal bleeding. J Clin Gastroenterol. 49, e24-30.
    CrossRef
  13. Jensen, DM, Machicado, GA, Jutabha, R, and Kovacs, TO (2000). Urgent colonoscopy for the diagnosis and treatment of severe diverticular hemorrhage. N Engl J Med. 342, 78-82.
    Pubmed CrossRef
  14. Bloomfeld, RS, Rockey, DC, and Shetzline, MA (2001). Endoscopic therapy of acute diverticular hemorrhage. Am J Gastroenterol. 96, 2367-72.
    Pubmed CrossRef
  15. Green, BT, Rockey, DC, Portwood, G, Tarnasky, PR, Guarisco, S, and Branch, MS (2005). Urgent colonoscopy for evaluation and management of acute lower gastrointestinal hemorrhage: a randomized controlled trial. Am J Gastroenterol. 100, 2395-402.
    Pubmed CrossRef
  16. Newman, JR, and Cooper, MA (2002). Lower gastrointestinal bleeding and ischemic colitis. Can J Gastroenterol. 16, 597-600.
    Pubmed CrossRef
  17. Zuckerman, GR, and Prakash, C (1999). Acute lower intestinal bleeding. Part II: etiology, therapy, and outcomes. Gastrointest Endosc. 49, 228-38.
    Pubmed CrossRef
  18. Brandt, LJ, Feuerstadt, P, and Blaszka, MC (2010). Anatomic patterns, patient characteristics, and clinical outcomes in ischemic colitis: a study of 313 cases supported by histology. Am J Gastroenterol. 105, 2245-52.
    Pubmed CrossRef
  19. Theodoropoulou, A, and Koutroubakis, IE (2008). Ischemic colitis: clinical practice in diagnosis and treatment. World J Gastroenterol. 14, 7302-8.
    Pubmed KoreaMed CrossRef
  20. Zuckerman, GR, Prakash, C, Merriman, RB, Sawhney, MS, DeSchryver-Kecskemeti, K, and Clouse, RE (2003). The colon single-stripe sign and its relationship to ischemic colitis. Am J Gastroenterol. 98, 2018-22.
    Pubmed CrossRef
  21. Feuerstadt, P, and Brandt, LJ (2015). Update on colon ischemia: recent insights and advances. Curr Gastroenterol Rep. 17, 45.
    Pubmed CrossRef
  22. Höchter, W, Weingart, J, Kühner, W, Frimberger, E, and Ottenjann, R (1985). Angiodysplasia in the colon and rectum. Endoscopic morphology, localisation and frequency. Endoscopy. 17, 182-5.
    Pubmed CrossRef
  23. Sekino, Y, Endo, H, Yamada, E, Sakai, E, Ohkubo, H, and Higurashi, T (2012). Clinical associations and risk factors for bleeding from colonic angiectasia: a case-controlled study. Colorectal Dis. 14, e740-6.
    Pubmed CrossRef
  24. Richter, JM, Hedberg, SE, Athanasoulis, CA, and Schapiro, RH (1984). Angiodysplasia. Clinical presentation and colonoscopic diagnosis. Dig Dis Sci. 29, 481-5.
    Pubmed CrossRef
  25. Appalaneni, V, Fanelli, RD, Sharaf, RN, Anderson, MA, Banerjee, S, and Ben-Menachem, T (2010). The role of endoscopy in patients with anorectal disorders. Gastrointest Endosc. 72, 1117-23.
    Pubmed CrossRef
  26. Barnert, J, and Messmann, H (2009). Diagnosis and management of lower gastrointestinal bleeding. Nat Rev Gastroenterol Hepatol. 6, 637-46.
    Pubmed CrossRef
  27. Lanas, A, Sekar, MC, and Hirschowitz, BI (1992). Objective evidence of aspirin use in both ulcer and nonulcer upper and lower gastrointestinal bleeding. Gastroenterology. 103, 862-9.
    Pubmed CrossRef
  28. Bjarnason, I, Hayllar, J, MacPherson, AJ, and Russell, AS (1993). Side effects of nonsteroidal anti-inflammatory drugs on the small and large intestine in humans. Gastroenterology. 104, 1832-47.
    Pubmed CrossRef
  29. Bounds, BC, and Kelsey, PB (2007). Lower gastrointestinal bleeding. Gastrointest Endosc Clin N Am. 17, Array-88.
    Pubmed CrossRef
  30. Kanwal, F, Dulai, G, Jensen, DM, Gralnek, IM, Kovacs, TO, and Machicado, GA (2003). Major stigmata of recent hemorrhage on rectal ulcers in patients with severe hematochezia: endoscopic diagnosis, treatment, and outcomes. Gastrointest Endosc. 57, 462-8.
    Pubmed CrossRef
  31. Lin, CK, Liang, CC, Chang, HT, Hung, FM, and Lee, TH (2011). Acute hemorrhagic rectal ulcer: an important cause of lower gastrointestinal bleeding in the critically ill patients. Dig Dis Sci. 56, 3631-7.
    Pubmed CrossRef
  32. Belaiche, J, Louis, E, D’Haens, G, Cabooter, M, Naegels, S, and De Vos, M (1999). Acute lower gastrointestinal bleeding in Crohn’s disease: characteristics of a unique series of 34 patients. Belgian IBD Research Group. Am J Gastroenterol. 94, 2177-81.
    Pubmed CrossRef
  33. Wong Kee Song, LM, and Baron, TH (2008). Endoscopic management of acute lower gastrointestinal bleeding. Am J Gastroenterol. 103, 1881-7.
    Pubmed CrossRef
  34. Strate, LL, and Gralnek, IM (2016). ACG clinical guideline: management of patients with acute lower gastrointestinal bleeding. Am J Gastroenterol. 111, 459-74.
    Pubmed KoreaMed CrossRef
  35. Gralnek, IM, Neeman, Z, and Strate, LL (2017). Acute lower gastrointestinal bleeding. N Engl J Med. 376, 1054-63.
    Pubmed CrossRef
  36. Pasha, SF, Shergill, A, Acosta, RD, Chandrasekhara, V, Chathadi, KV, and ASGE Standards of Practice Committee (2014). The role of endoscopy in the patient with lower GI bleeding. Gastrointest Endosc. 79, 875-85.
    Pubmed CrossRef
  37. Gralnek, IM, Barkun, AN, and Bardou, M (2008). Management of acute bleeding from a peptic ulcer. N Engl J Med. 359, 928-37.
    Pubmed CrossRef
  38. Baradarian, R, Ramdhaney, S, Chapalamadugu, R, Skoczylas, L, Wang, K, and Rivilis, S (2004). Early intensive resuscitation of patients with upper gastrointestinal bleeding decreases mortality. Am J Gastroenterol. 99, 619-22.
    Pubmed CrossRef
  39. Villanueva, C, Colomo, A, and Bosch, A (2013). Transfusion for acute upper gastrointestinal bleeding. N Engl J Med. 368, 1362-3.
    Pubmed CrossRef
  40. Restellini, S, Kherad, O, Jairath, V, Martel, M, and Barkun, AN (2013). Red blood cell transfusion is associated with increased rebleeding in patients with nonvariceal upper gastrointestinal bleeding. Aliment Pharmacol Ther. 37, 316-22.
    CrossRef
  41. Hwang, JH, Fisher, DA, Ben-Menachem, T, Chandrasekhara, V, Chathadi, K, and Decker, GA (2012). The role of endoscopy in the management of acute non-variceal upper GI bleeding. Gastrointest Endosc. 75, 1132-8.
    Pubmed CrossRef
  42. Ali, M, Ul Haq, T, Salam, B, Beg, M, Sayani, R, and Azeemuddin, M (2013). Treatment of nonvariceal gastrointestinal hemorrhage by transcatheter embolization. Radiol Res Pract. 2013.
    Pubmed KoreaMed
  43. Yi, WS, Garg, G, and Sava, JA (2013). Localization and definitive control of lower gastrointestinal bleeding with angiography and embolization. Am Surg. 79, 375-80.
    Pubmed
  44. Khanna, A, Ognibene, SJ, and Koniaris, LG (2005). Embolization as first-line therapy for diverticulosis-related massive lower gastrointestinal bleeding: evidence from a meta-analysis. J Gastrointest Surg. 9, 343-52.
    Pubmed CrossRef
  45. Eisen, GM, Dominitz, JA, Faigel, DO, Goldstein, JL, Kalloo, AN, and Petersen, BT (2001). An annotated algorithmic approach to acute lower gastrointestinal bleeding. Gastrointest Endosc. 53, 859-63.
    Pubmed CrossRef
  46. Strate, LL, and Naumann, CR (2010). The role of colonoscopy and radiological procedures in the management of acute lower intestinal bleeding. Clin Gastroenterol Hepatol. 8, 333-43.
    CrossRef
  47. Angtuaco, TL, Reddy, SK, Drapkin, S, Harrell, LE, and Howden, CW (2001). The utility of urgent colonoscopy in the evaluation of acute lower gastrointestinal tract bleeding: a 2-year experience from a single center. Am J Gastroenterol. 96, 1782-5.
    Pubmed CrossRef
  48. Strate, LL, and Syngal, S (2005). Predictors of utilization of early colonoscopy vs. radiography for severe lower intestinal bleeding. Gastrointest Endosc. 61, 46-52.
    Pubmed CrossRef
  49. Schmulewitz, N, Fisher, DA, and Rockey, DC (2003). Early colonoscopy for acute lower GI bleeding predicts shorter hospital stay: a retrospective study of experience in a single center. Gastrointest Endosc. 58, 841-6.
    Pubmed CrossRef
  50. Laine, L, and Shah, A (2010). Randomized trial of urgent vs. elective colonoscopy in patients hospitalized with lower GI bleeding. Am J Gastroenterol. 105, 2636-41.
    Pubmed CrossRef
  51. Elta, GH (2004). Urgent colonoscopy for acute lower-GI bleeding. Gastrointest Endosc. 59, 402-8.
    Pubmed CrossRef
  52. Talley, NJ, and Jones, M (1998). Self-reported rectal bleeding in a United States community: prevalence, risk factors, and health care seeking. Am J Gastroenterol. 93, 2179-83.
    Pubmed CrossRef
  53. Nikpour, S, and Ali Asgari, A (2008). Colonoscopic evaluation of minimal rectal bleeding in average-risk patients for colorectal cancer. World J Gastroenterol. 14, 6536-40.
    Pubmed KoreaMed CrossRef
  54. Eckardt, VF, Schmitt, T, Kanzler, G, Eckardt, AJ, and Bernhard, G (2002). Does scant hematochezia necessitate the performance of total colonoscopy?. Endoscopy. 34, 599-603.
    Pubmed CrossRef
  55. Peytremann-Bridevaux, I, Arditi, C, Froehlich, F, O’Malley, J, Fairclough, P, and Le Moine, O (2009). Appropriateness of colonoscopy in Europe (EPAGE II). Iron-deficiency anemia and hematochezia. Endoscopy. 41, 227-33.
    Pubmed CrossRef
  56. Fisher, L, Lee Krinsky, M, Anderson, MA, Appalaneni, V, Banerjee, S, and ASGE Standards of Practice Committee (2010). The role of endoscopy in the management of obscure GI bleeding. Gastrointest Endosc. 72, 471-9.
    Pubmed CrossRef


This Article


Cited By Articles
  • CrossRef (0)

Services
Social Network Service

e-submission

Archives