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Lower Gastrointestinal Bleeding
Gastrointest Endoscopy Clin N Am 17 (2007) 273–288
Lower Gastrointestinal Bleeding Brenna Casey Bounds, MD*, Peter B. Kelsey, MD Harvard Medical School, Gastrointestinal Unit, Massachusetts General Hospital, 55 Fruit Street, Blake 453D, Boston, MA 02114, USA
Lower gastrointestinal (GI) bleeding is defined as blood loss that originates from a source distal to the ligament of Treitz and that results in hemodynamic instability or symptomatic anemia. The annual incidence of lower GI bleeding is approximately 0.03% in the adult population as a whole, with a greater than 200-fold increase from the second to the eighth decade [1,2]. This rise in incidence with age may be explained by the increasing prevalence of colonic diverticulosis and colonic angiodysplasia with age. The mean age of patients with lower GI bleeding ranges from 63 to 77 years, with a reported mortality rate of 2% to 4% [2–7]. Although approximately 10% to 15% of patients presenting with acute severe hematochezia have an upper GI source of bleeding identified on upper endoscopy, the most common causes of lower GI bleeding are diverticulosis, hemorrhoids, ischemic colitis, and angiodysplasia [4,8,9]. As with upper GI bleeding, lower GI bleeding ceases spontaneously in most cases.
Initial evaluation and resuscitation The patient presenting with acute lower GI hemorrhage may complain of passing bright red blood per rectum, dark blood with clots, or less commonly melena. Pallor, fatigue, chest pain, palpitations, dyspnea, tachypnea, tachycardia, postural changes, or syncope are suggestive of hemodynamic compromise. Commencement of resuscitation efforts should take place concurrently with the initial evaluation of the patient. In patients who have hemodynamic compromise, intravenous access, with a minimum of two large-caliber peripheral catheters or a central venous line, should be secured immediately. Resuscitation is imperative to restore euvolemia and prevent complications of red blood cell loss, such as cardiac, pulmonary, * Corresponding author. E-mail address: [email protected] (B.C. Bounds). 1052-5157/07/$ - see front matter Ó 2007 Published by Elsevier Inc. doi:10.1016/j.giec.2007.03.010
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renal, or neurologic consequences. Initial laboratory testing should include a complete blood count, electrolytes, coagulation profile, and a sample for typing and crossmatching. A directed history may identify risk factors helpful in defining the source of the bleeding. For example, the use of aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) is associated strongly with lower GI bleeding, chiefly diverticular bleeding, as it is with upper GI bleeding. Lower GI bleeding preceded by hypovolemia suggests ischemic colitis, whereas a history of prior radiation therapy for prostate or pelvic cancer may indicate radiation proctitis (which may present months or even years after the radiation exposure). Severe constipation should prompt an investigation for a stercoral ulcer, while a history of recent colonoscopy with polypectomy incriminates postpolypectomy bleeding as the likely source. Physical examination should include careful cardiac, pulmonary, abdominal, and rectal examinations. A digital rectal examination is helpful for excluding anorectal pathology and confirming the patient’s description of the appearance of the stool. In addition, approximately 40% of rectal carcinomas are palpable during a digital rectal examination [10]. The presence of coagulopathy (international normalized ratio [INR] O1.5) or thrombocytopenia (!50,000/mL) should prompt correction with fresh-frozen plasma or platelet transfusions, respectively. The blood transfusion requirement is determined by the patient’s age and rate of bleeding and also is influenced by the presence of comorbid conditions such as coronary artery disease, cirrhosis, or chronic obstructive pulmonary disease. Orthostatic hypotension, a decrease in the hematocrit value of at least 6%, a transfusion requirement of more than two units of packed red blood cells, or continuous active bleeding merit admission to an ICU for close observation.
Diagnostic evaluation Colonoscopy Diagnostic endoscopic studies should be done only after the patient has been hemodynamically resuscitated. If there is any possibility of an upper GI source, upper endoscopy should be performed first. A lower endoscopic study is established as the diagnostic procedure of choice in the setting of acute lower GI hemorrhage. If selected as the initial endoscopic approach, sigmoidoscopy should be undertaken with the caveat that it should be considered diagnostic only if an actively bleeding lesion can be demonstrated. Many endoscopists prefer to perform a total colonoscopy as the initial evaluation, however. The diagnostic accuracy of colonoscopy ranges from 72% to 86% in the setting of lower GI bleeding [11,12]. Cecal intubation is achieved in greater than 95% of attempts in this setting [13]. No consensus has been reached regarding the need for colonic purge before colonoscopy in a patient with active lower GI bleeding [4,12,14,15].
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Because the risk of colonic perforation may be increased when colonoscopy is performed in an unprepared colon, however, only experienced endoscopists should attempt colonoscopy in this setting. Plain abdominal radiography should be performed before colonoscopy if perforation or obstruction is suspected. Radiographic evidence of thumbprinting is indicative of transmural injury to the colon caused by ischemic or infectious colitis. Radionuclide imaging and angiography Evaluation with either radionuclide imaging or angiography may be appropriate in patients who have massive hemorrhage that precludes colonoscopy or in whom a bleeding source is not identified on colonoscopy. Radionuclide imaging detects active bleeding at rates of 0.1 to 0.5 mL/min and is more sensitive than angiography but less specific than a positive endoscopic or angiographic study [16]. The two techniques of radionuclide scanning commonly employ either technetium sulfur colloid or 99mTc pertechnetate-labeled red blood cells. Whereas technetium sulfur colloid can detect a bleeding rate as low as 0.1 mL/min, the short half life of the colloid within the vascular system requires active bleeding at the time the radionuclide is present in the intravascular space. Conversely, imaging following injection of 99mTc pertechnetate-labeled red blood cells is performed at 30-minute intervals for up to 24 hours, allowing patients to be scanned multiple times. Radionuclide imaging is tolerated well by patients but is limited by highly variable accuracy rates for bleeding localization, ranging from 24% to 91% [17]. Angiography requires a GI bleeding rate of at least 1 mL/min for accurate detection of extravasation of contrast into the bowel lumen [18]. Unfortunately, bleeding is frequently intermittent and may occur at a much lower rate, resulting in inability to detect the causative lesion. The overall yield of angiography for detection of a GI bleeding source ranges from 40% to 78% [6,19–22]. Diverticular disease and angiodysplasia are the most common findings when angiography is positive, with 50% to 80% of sources occurring in bowel supplied by the superior mesenteric artery [23]. In some centers, angiographers request that a bleeding scan be performed before arteriography, because a patient who has a negative nuclear imaging scan is likely to have a negative angiogram. Unfortunately, bleeding may cease during the time required for performance of the bleeding scan, and the opportunity to localize a lesion by angiography therefore may be missed. Angiography has a specificity of 100% but a sensitivity of only 30% to 47% [24]. A positive angiogram is associated strongly with the need for surgical intervention [24]. Angiography does not require bowel preparation, provides accurate localization of the bleeding source (when identified), and permits therapeutic intervention in some cases. Intra-arterial infusion of vasopressin or arterial embolization may be performed by means of the
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catheter and is highly effective in controlling lower GI hemorrhage. This procedure, however, is associated with a substantial risk of serious complications, including intestinal infarction of up to 20% [25]. Other complications of arteriography occur in approximately 9% of patients and include arterial thrombosis, embolization, and renal failure [4]. Therefore, colonoscopy remains the procedure of choice in the evaluation of the patient with acute lower GI bleeding. Angiography should be reserved for the patient who has massive bleeding that precludes colonoscopy, persistent or recurrent bleeding, or a colonoscopy that has failed to identify the bleeding source. Small bowel evaluation An evaluation of the small bowel is indicated for those patients in whom an upper GI endoscopy and colonoscopy are negative. Small bowel evaluation in patients who are hemodynamically stable may be performed with push enteroscopy, which allows endoscopic evaluation of the proximal 60 cm of the jejunum. If examination of the remaining jejunum and ileum is desired, a video capsule study provides imaging of the entire small bowel and is tolerated well by patients. A video capsule study is reported to identify the bleeding source in up to 89% of examined patients with GI bleeding resulting in successfully executed definitive therapy in 87% of patients undergoing the study while actively bleeding [26]. A nuclear medicine scan for a Meckel’s diverticulum may be appropriate in young patients presenting with lower GI bleeding [27].
Specific causes of lower gastrointestinal bleeding Colonic diverticula Colonic diverticular hemorrhage results from asymmetric rupture of the intramural branches (vasa recta) of the marginal artery at the dome of a diverticulum or at the antimesenteric margin [28,29]. Although most patients with diverticulosis are asymptomatic, approximately 20% will develop diverticulitis, and 3% to 5% will develop acute severe hematochezia [9]. In the elderly patient who has comorbid conditions, diverticular bleeding results in morbidity and mortality rates of 10% to 20%, respectively [20,30,31]. Although greater than 75% of diverticula are found in the left colon, the right colon is the source of diverticular bleeding in 50% to 90% of patients when angiography is positive [28,29,31]. On the other hand, when diverticular bleeding is diagnosed at colonoscopy, the bleeding is from the left colon in 60% of cases [2]. Diverticular bleeding ceases spontaneously in 75% of patients; 99% of patients will require less than four units of transfused blood [9]. Bleeding recurs in 14% to 38% of cases following the primary episode and in up to 50% of cases following a second episode of bleeding [9,31].
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When managed conservatively, diverticular bleeding resolves spontaneously in most patients. Persistent hemodynamic instability despite aggressive resuscitation efforts warrants intervention. Nonsurgical therapy may be performed during either angiography or colonoscopy. Angiography permits directed intra-arterial infusion of vasopressin, which results in resolution of bleeding in 91% of cases [20]. In up to 50% percent of cases, however, bleeding recurs on cessation of the vasopressin infusion [20]. Transcatheter embolization effectively controls diverticular bleeding but is associated with a risk of intestinal infarction of up to 20% [20]. Endoscopic therapy may be performed using epinephrine injection therapy, bipolar coagulation, or both [32]. One study reported that patients with demonstrable diverticular bleeding who received endoscopic therapy with epinephrine injection, bipolar coagulation, or both, had no recurrent bleeding during the 30-month follow-up period, compared with a 53% rebleeding rate in patients who received conservative medical therapy alone [32]. Less frequently employed methods for control of diverticular bleeding include endoscopic band ligation and placement of vascular clips (Fig. 1) [33,34]. Surgical intervention is required when hemodynamic instability persists despite aggressive resuscitation. Surgical intervention is necessary in 18% to 25% of patients who require blood transfusion [9,35]. Operative mortality is 10% despite improved methods of localization of bleeding that permit segmental rather than subtotal colectomy [20,35,36]. Blind segmental resection is contraindicated and is associated with a high rebleeding rate of 42% and excessive rates of morbidity and mortality, which may be as high as 83% and 57%, respectively [37]. Management by a dedicated bleeding team may reduce mortality associated with acute diverticular hemorrhage [31].
Fig. 1. Hemostasis was achieved with application of a band to this bleeding diverticulum following injection with epinephrine. (Courtesy of Massachusetts General Hospital, Boston, MA; with permission.)
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Angiodysplasia Angiodysplasia is the most common vascular anomaly of the GI tract (Fig. 2). Composed of ectatic, dilated submucosal veins, colonic angiodysplasia are responsible for 20% to 30% of cases of acute lower GI bleeding [20]. They occur with equal frequency in men and women, and most occur in persons over the age of 60, with two-thirds occurring in persons over 70. More than one angiodysplasia is present in most patients [38–40]. In the colon, angiodysplasias are most common in the cecum and proximal ascending colon (54%), followed by the sigmoid colon (18%) and rectum (14%) [40]. Although angiodysplasia can be found throughout the small intestine, bleeding angiodysplasia in the small bowel usually presents as iron deficiency anemia with fecal occult blood and rarely as severe hematochezia. At colonoscopy, angiodysplasias are recognized by their characteristic appearance as red, flat lesions consisting of ectatic blood vessels that appear to radiate from a central feeding vessel; they may have a diameter of 2 to 10 mm. A pale mucosal halo also may be seen around the lesion. When the colon is examined completely, the sensitivity of colonoscopy for detecting angiodysplasia exceeds 80% [39,41]. A poor bowel preparation, however, may lead to incomplete evaluation of the colonic mucosa. Additionally, the use of narcotic medications for sedation and analgesia may decrease the sensitivity of colonoscopy for detecting angiodysplasia because of a transient decrease in mucosal blood flow. Administration of intravenous naloxone has been demonstrated to enhance the appearance of angiodysplasia during colonoscopy in patients who have received meperidine for sedation [42]. Unfortunately, use of naloxone may result in significant discomfort for the patient, particularly when the procedure is prolonged by the application of therapeutics. Conventional endoscopic treatment of colonic angiodysplasia is performed with contact thermal probes. To prevent brisk bleeding from
Fig. 2. A large colonic angiodysplasia. (Courtesy of Massachusetts General Hospital, Boston, MA; with permission.)
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angiodysplasia when contact electrocautery is performed, large angiodysplasia should be cauterized from the outer margin toward the center to obliterate feeder vessels. Injection therapy with sclerosing agents, such as ethanolamine, also has been described for control of bleeding from colonic angiodysplasia but is not employed widely [43]. Argon plasma coagulation is a noncontact method that is increasingly popular for the treatment of bleeding colonic angiodysplasia [44,45]. Extra care must be taken when treating lesions in the cecum to minimize the risk of perforation [44]. Angiography remains the gold standard for the diagnosis of larger angiodysplasia. Following injection of contrast, angiodysplasias are seen as ectatic slowly emptying veins, vascular tufts, or small veins with early filling. When angiography identifies a bleeding angiodysplasia, treatment with embolization therapy or directed infusion of vasopressin may be performed. Use of hormonal therapy (estrogen) for control of GI bleeding of obscure origin thought to be caused by angiodysplasia is controversial and may be ineffective [46,47]. Surgery should be considered in patients in whom a bleeding source clearly has been identified and in whom more conservative therapies have failed. Hemorrhoids The frequency of hemorrhoids in patients with lower GI bleeding is as high as 75%, but a causal relationship is established infrequently. Hemorrhoids have accounted for 2% to 9% of cases of acute severe hematochezia in studies that include anorectal sources of hemorrhage [1,2,12]. Nonsteroidal anti-inflammatory-induced lower gastrointestinal bleeding NSAIDs have been implicated in small bowel and colonic pathology and gastroduodenal ulceration. The terminal ileum and cecum are particularly susceptible to NSAID-induced injury. NSAIDs have been demonstrated to exacerbate inflammatory bowel disease, cause colitis resembling inflammatory bowel disease, and complicate diverticular disease by increasing the risk of perforation and severe hematochezia [48,49]. Elderly patients and those on long-term NSAIDs are at greatest risk of NSAID-induced complications. NSAIDs also may cause localized mucosal injury, as suggested by the finding of NSAID shells at the site of perforating ulcers. Intestinal and colonic ulcers caused by NSAIDs often have sharp demarcations with a predilection for the terminal ileum and proximal colon, where pills may be static for a longer period of time than in other segments of the bowel. The diaphragm-like stricture is a lesion pathognomonic of NSAID injury that occurs as a result of a scarring reaction secondary to ulceration. These most frequently are found in the midsection of the small intestine, but also have been reported to occur in the terminal ileum and colon [48,50–53]. Diaphragm-like strictures typically occur in multiples with normal intervening mucosa.
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In patients with NSAID-induced mucosal injury and bleeding, colonoscopy reveals nonspecific ulcerations of the colon and small bowel, particularly the cecum and terminal ileum. Histology is also nonspecific, and infectious etiologies, radiation injury, and inflammatory bowel disease must be excluded [50,54]. Treatment of NSAID-induced mucosal injury is discontinuation of the offending NSAID. A repeat colonoscopy should be performed 6 to 8 weeks after cessation of the NSAID to confirm resolution of ulcerations and/or colitis. If ulceration or colitis persists, an alternative diagnosis such as inflammatory bowel disease should be entertained. Rarely, surgical intervention is required for NSAID-induced bleeding or perforation [50]. Colonic ischemia Colonic ischemia, the most common ischemic disorder of the GI tract, results from a sudden, often temporary, reduction in mesenteric blood flow. Mesenteric hemodynamics may be compromised by changes in the systemic circulation or by anatomic or functional changes in the mesenteric vasculature. Frequently, a specific precipitating event or vascular lesion on angiography cannot be identified. In patients who have undergone aortoiliac reconstructive surgery, the frequency of significant postoperative colonic ischemia is 1% to 7% [55–57]. Nonocclusive colonic ischemia most commonly involves the splenic flexure, right colon, or rectosigmoid junction, the watershed areas. Clinically, ischemic colitis presents with the sudden onset of mild left lower quadrant crampy abdominal pain. The pain may be accompanied or followed in the ensuing 24 hours by bright red blood per rectum or bloody diarrhea. Acute severe hematochezia should raise the suspicion of an alternative etiology. Ischemic colitis must be differentiated clinically from acute mesenteric ischemia. Patients who have acute mesenteric ischemia (involving the small intestine) have severe abdominal pain, often out of proportion to physical examination findings; they appear critically ill and frequently have an identifiable acute precipitating event. In patients who have ischemic colitis, sigmoidoscopy reveals ulceration of the colonic mucosa, with sparing of the rectum in most cases. Histology reveals necrosis, not acute and chronic inflammatory changes as seen in inflammatory bowel disease. Treatment is supportive, and most cases resolve spontaneously within several days to weeks. One fifth of patients develop a chronic colitis that differs from ulcerative colitis in that it is segmental and spares the rectum; colonic strictures also may develop. Chronic colitis caused by ischemia does not respond to standard medications used to treat inflammatory bowel disease, and many affected patients eventually require colectomy. Inflammatory bowel disease Although GI bleeding is a common manifestation of inflammatory bowel disease, acute severe hematochezia is infrequent. Most patients who have
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ulcerative colitis report clinically apparent bleeding, in contrast to patients with Crohn’s disease, of whom only one third report bleeding [58–61]. Acute severe hematochezia accounts for up to 6% of hospitalizations for patients with Crohn’s disease and 1.4% to 4.2% of patients with ulcerative colitis [62–69]. Although acute severe hematochezia is not a predictor of the bleeding site in patients with Crohn’s disease, most patients with ulcerative colitis who present in this manner are found to have pancolitis at colonoscopy [58,59,64,70]. Recurrence of bleeding is not uncommon following an episode of acute severe hematochezia in patients who have inflammatory bowel disease, and when it occurs, surgery is required for control of hemorrhage in 57% of cases [70]. Postpolypectomy bleeding Endoscopic polypectomy is now the primary treatment for most colonic polyps. Complications occur in less than 5% of colonoscopies performed for polypectomy [71], and of the complications, postpolypectomy bleeding is the most frequent and accounts for approximately 2% to 8% of cases of acute lower GI bleeding (Fig. 3) [4,7,12]. The frequency of delayed postpolypectomy bleeding as a cause of acute severe hematochezia is increasing, possibly because of the increasing use of a blended (rather that pure coagulation) current in the polypectomy snare. Massive bleeding that occurs at the time of polypectomy is typically arterial in nature and often can be controlled by resnaring the stalk of the polyp and applying pressure [72,73]. Delayed bleeding likely occurs because of the sloughing of the eschar at the polypectomy site [72,73]. Delayed bleeding usually is self-limited and resolves with supportive care in more than 70% of cases. For persistent or severe bleeding at a polypectomy site, several endoscopic techniques have proven safe and effective. These include loop ligation of the remaining polyp stalk, endoscopic band ligation, injection with epinephrine followed by thermal therapy, and application of endovascular clipping devices [33,74–80].
Fig. 3. A bleeding colonic polyp stalk immediately following snare polypectomy. (Courtesy of Massachusetts General Hospital, Boston, MA; with permission.)
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Less common sources of lower gastrointestinal bleeding Infectious colitis Acute severe hematochezia infrequently is caused by an infectious etiology. The most common bacterial causes resulting in lower GI bleeding are Salmonella and Escherichia coli O157:H7 infections. The patient may relate a history of crampy abdominal pain and watery diarrhea that was followed by grossly bloody diarrhea. Salmonella, Campylobacter, and Yersinia may cause mucosal edema, hyperemia, erosions, and ulceration and should be distinguished by culture results; colonoscopy rarely is indicated. Other infectious causes of lower GI bleeding include amebiasis, cytomegalovirus infection, and Mycobacterium avium complex infection, particularly in immunosuppressed persons. Radiation colitis Acute severe hematochezia is a rare complication of radiation therapy. Rectal bleeding as a result of radiation proctitis accounts for 1% to 5% of cases of acute lower GI bleeding [81]. Inflammation caused by exposure of the rectum or rectosigmoid area to radiation during therapy for prostatic or gynecologic malignancy may result in significant bleeding that may occur as early as 9 months or as late as 4 years following therapy [82–84]. Following acute mucosal injury, the patient may complain of diarrhea and tenesmus accompanied by abdominal cramping and a mucoid or bloody rectal discharge. A chronic proctocolitis may develop and may be complicated by bleeding of mild-to-moderate severity. Endoscopically, the mucosa demonstrates characteristic telangiectases. Bleeding may be controlled effectively with sucralfate enemas, instillation of formalin, or endoscopic treatment using either laser or argon plasma coagulation [85–101]. Neoplasms Bleeding, either occult or gross, is the most common presenting symptom of colonic neoplasms, but is rarely brisk. The reported frequency of acute lower GI bleeding resulting from colonic neoplasms ranges from 2% to 26% [1,7,12,36,102–104]. Stercoral ulcers Stercoral ulceration should be included in the differential diagnosis when an elderly patient presents with hematochezia and antecedent constipation. Most commonly seen as an isolated lesion in the rectosigmoid area, a stercoral ulcer occurs as a result of pressure necrosis from a fecal mass. Although colonic perforation and bleeding are the most common complications, acute severe hematochezia is rarely attributable to a stercoral ulceration [2,7].
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Other causes of lower GI bleeding include intestinal intussusception, trauma to the colonic mucosa from an endoscope or enema, solitary rectal ulcer syndrome, portal colopathy, colonic varices, endometriosis, Dieulafoy lesion, and bleeding from the appendiceal orifice or a Meckel’s diverticulum.
Outcomes Mortality rates for lower GI bleeding are less than 5% [1,2,104,105]. One bleeding outcomes study reported a mortality rate of 0.6% for lower GI bleeding and an overall mortality rate of 2% for bleeding arising from an upper GI source [105]. Although the highest mortality rates are reported for patients in whom bleeding occurs during a hospitalization for other reasons, in most series, lower GI bleeding rarely has been the cause of death [2]. A population-based study of patients enrolled in a health maintenance organization reported an in-hospital mortality rate of 3.6% for patients hospitalized with lower GI hemorrhage and 23.1% for those who developed lower GI bleeding following hospitalization [2]. For patients who had a discharge diagnosis of diverticular bleeding who did not require definitive therapy, the rate of recurrent bleeding was 9% at 1 year, 10% at 2 years, 19% at 3 years, and 25% at 4 years [2]. In the 89 patients with diverticular bleeding who survived to discharge, mortality at 4 years was not related to recurrent hemorrhage, although diverticular bleeding may portend a poor prognosis from other causes [2]. Another factor that impacts the outcome of lower GI bleeding includes the use of NSAIDs, particularly in combination with aspirin. One study reported that 75% of patients with severe diverticular hemorrhage had a combined exposure to NSAIDs and aspirin compared with none of the patients with nonsevere hemorrhage [49]. Although the presence of stigmata of recent bleeding, such as a visible vessel or adherent clot with active bleeding, is a reliable marker of severe diverticular hemorrhage, the presence of a clean-based ulcer within a diverticulum may indicate a low risk of recurrent hemorrhage and permit early discharge from the hospital [49]. Numerous studies have proposed clinical prognostic criteria to distinguish patients with a high risk and low risk of recurrent hemorrhage [7,105,106]. Early colonoscopy has been associated with both shorter hospital stays and lower overall costs per patient [7,107]. Additional studies are needed to enhance understanding of the benefit of available interventions in the treatment of lower GI hemorrhage.
Summary Lower GI hemorrhage is a significant cause of morbidity and mortality, particularly in elderly patients. Lower endoscopic evaluation is established as the diagnostic procedure of choice in the setting of acute lower GI
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hemorrhage. An upper source of bleeding may be found in up to 15% of patients who present with lower hemorrhage, and must be ruled out [4,8,9]. Video capsule endoscopy is reported to identify the bleeding source in up to 89% of examined patients with GI bleeding, although the optimal timing and use of this technology have yet to be defined [26]. Evaluation with either radionuclide imaging or angiography may be appropriate in patients with massive hemorrhage that precludes colonoscopy or in whom a bleeding source is not identified on endoscopy. Numerous factors, including use of NSAIDS, inpatient status at the time of hemorrhage, and endoscopic appearance with stigmata of recent bleeding, are all predictors of worse outcomes. Early colonoscopy in the setting of lower GI hemorrhage has been associated with both shorter hospital stays and lower overall costs per patient, and should be considered in the appropriate clinical setting. Emergent management of severe lower GI hemorrhage requires the concomitant initiation of medical resuscitation and the preparation for endoscopic evaluation and coordination of a multidisciplinary team including gastroenterology, interventional radiology, and surgery. References [1] Bramley PN, Masson JW, McKnight G, et al. The role of an open-access bleeding unit in the management of colonic haemorrhage. A 2-year prospective study. Scand J Gastroenterol 1996;31:764–9. [2] Longstreth GF. Epidemiology and outcome of patients hospitalized with acute lower gastrointestinal hemorrhage: a population-based study. Am J Gastroenterol 1997;92:419–24. [3] Boley SJ, DiBiase A, Brandt LJ, et al. Lower intestinal bleeding in the elderly. Am J Surg 1979;137:57–64. [4] Jensen DM, Machicado GA. Diagnosis and treatment of severe hematochezia. The role of urgent colonoscopy after purge. Gastroenterology 1988;95:1569–74. [5] Jensen DM, Machicado GA. Colonoscopy for diagnosis and treatment of severe lower gastrointestinal bleeding. Routine outcomes and cost analysis. Gastrointest Endosc Clin N Am 1997;7:477–98. [6] Leitman IM, Paull DE, Shires GT 3rd. Evaluation and management of massive lower gastrointestinal hemorrhage. Ann Surg 1989;209:175–80. [7] Richter JM, Christensen MR, Kaplan LM, et al. Effectiveness of current technology in the diagnosis and management of lower gastrointestinal hemorrhage. Gastrointest Endosc 1995;41:93–8. [8] Foutch PG. Angiodysplasia of the gastrointestinal tract. Am J Gastroenterol 1993;88: 807–18. [9] McGuire HH Jr. Bleeding colonic diverticula. A reappraisal of natural history and management. Ann Surg 1994;220:653–6. [10] Steer ML, Silen W. Diagnostic procedures in gastrointestinal hemorrhage. N Engl J Med 1983;309:646–50. [11] Jensen DM. Diagnosis and treatment of patients with severe hematochezia: a time for change. Endoscopy 1998;30:724–6. [12] Rossini FP, Ferrari A, Spandre M, et al. Emergency colonoscopy. World J Surg 1989;13: 190–2. [13] Waye JD, Bashkoff E. Total colonoscopy: is it always possible? Gastrointest Endosc 1991; 37:152–4.
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[37] Parkes BM, Obeid FN, Sorensen VJ, et al. The management of massive lower gastrointestinal bleeding. Am Surg 1993;59:676–8. [38] Clouse RE, Costigan DJ, Mills BA, et al. Angiodysplasia as a cause of upper gastrointestinal bleeding. Arch Intern Med 1985;145:458–61. [39] Moreto M, Figa M, Ojembarrena E, et al. Vascular malformations of the stomach and duodenum: an endoscopic classification. Endoscopy 1986;18:227–9. [40] Hochter W, Weingart J, Kuhner W, et al. Angiodysplasia in the colon and rectum. Endoscopic morphology, localisation and frequency. Endoscopy 1985;17:182–5. [41] Richter JM, Hedberg SE, Athanasoulis CA, et al. Clinical presentation and colonoscopic diagnosis. Dig Dis Sci 1984;29:481–5. [42] Brandt LJ, Spinnell MK. Ability of naloxone to enhance the colonoscopic appearance of normal colon vasculature and colon vascular ectasias. Gastrointest Endosc 1999;49: 79–83. [43] Bemvenuti GA, Julich MM. Ethanolamine injection for sclerotherapy of angiodysplasia of the colon. Endoscopy 1998;30:564–9. [44] Wahab PJ, Mulder CJ, den Hartog G, et al. Argon plasma coagulation in flexible gastrointestinal endoscopy: pilot experiences. Endoscopy 1997;29:176–81. [45] Johanns W, Luis W, Janssen J, et al. Argon plasma coagulation (APC) in gastroenterology: experimental and clinical experiences. Eur J Gastroenterol Hepatol 1997;9:581–7. [46] Lewis BS, Salomon P, Rivera-MacMurray S, et al. Does hormonal therapy have any benefit for bleeding angiodysplasia? J Clin Gastroenterol 1992;15:99–103. [47] Barkin JS, Ross BS. Medical therapy for chronic gastrointestinal bleeding of obscure origin. Am J Gastroenterol 1998;93:1250–4. [48] Bjarnason I, Hayllar J, MacPherson AJ, et al. Side effects of nonsteroidal anti-inflammatory drugs on the small and large intestine in humans. Gastroenterology 1993;104: 1832–47. [49] Foutch PG. Diverticular bleeding: are nonsteroidal anti-inflammatory drugs risk factors for hemorrhage, and can colonoscopy predict outcome for patients? Am J Gastroenterol 1995;90:1779–84. [50] Kaufman HL, Fischer AH, Carroll M, et al. Colonic ulceration associated with nonsteroidal anti-inflammatory drugs. Report of three cases. Dis Colon Rectum 1996;39:705–10. [51] Lang J, Price AB, Levi AJ, et al. Diaphragm disease: pathology of disease of the small intestine induced by nonsteroidal anti-inflammatory drugs. J Clin Pathol 1988;41:516–26. [52] Huber T, Ruchti C, Halter F. Nonsteroidal anti-inflammatory drug-induced colonic strictures: a case report. Gastroenterology 1991;100:1119–22. [53] Matsuhashi N, Yamada A, Hiraishi M, et al. Multiple strictures of the small intestine after long-term nonsteroidal anti-inflammatory drug therapy. Am J Gastroenterol 1992;87: 1183–6. [54] Kwo PY, Tremaine WJ. Nonsteroidal anti-inflammatory drug-induced enteropathy: case discussion and review of the literature. Mayo Clin Proc 1995;70:55–61. [55] Ernst CB, Hagihara PF, Daughtery ME, et al. Ischemic colitis incidence following abdominal aortic reconstruction: a prospective study. Surgery 1976;80:417–21. [56] Hagihara PF, Ernst CB, Griffen WO Jr. Incidence of ischemic colitis following abdominal aortic reconstruction. Surg Gynecol Obstet 1979;149:571–3. [57] Brewster DC, Franklin DP, Cambria RP, et al. Intestinal ischemia complicating abdominal aortic surgery. Surgery 1991;109:447–54. [58] Greenstein AJ, Geller SA, Dreiling DA, et al. Crohn’s disease of the colon. IV. Clinical features of Crohn’s (ileo) colitis. Am J Gastroenterol 1975;64:191–9. [59] Farmer RG, Hawk WA, Turnbull RB Jr. Regional enteritis of the colon: a clinical and pathologic comparison with ulcerative colitis. Am J Dig Dis 1968;13:501–14. [60] Homan WP, Tang CK, Thorbjarnarson B. Acute massive hemorrhage from intestinal Crohn’s disease. Report of seven cases and review of the literature. Arch Surg 1976;111: 901–5.
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[61] Greenstein AJ, Kark AE, Dreiling DA. Crohn’s disease of the colon. II. Controversial aspects of hemorrhage, anemia, and rectal involvement in granulomatous disease involving the colon. Am J Gastroenterol 1975;63:40–8. [62] Robert JH, Sachar DB, Aufses AH Jr, et al. Management of severe hemorrhage in ulcerative colitis. Am J Surg 1990;159:550–5. [63] Truelove SC, Pena AS. Course and prognosis of Crohn’s disease. Gut 1976;17:192–201. [64] Farmer RG, Hawk WA, Turnbull RB Jr. Clinical patterns in Crohn’s disease: a statistical study of 615 cases. Gastroenterology 1975;68:627–35. [65] Driver CP, Anderson DN, Keenan RA. Massive intestinal bleeding in association with Crohn’s disease. J R Coll Surg Edinb 1996;41:152–4. [66] Cirocco WC, Reilly JC, Rusin LC. Life-threatening hemorrhage and exsanguination from Crohn’s disease. Report of four cases. Dis Colon Rectum 1995;38:85–95. [67] Belaiche J, Louis E. Severe lower gastrointestinal bleeding in Crohn’s disease: successful control with infliximab. Am J Gastroenterol 2002;97:3210–1. [68] Tysk C, De Keersmaecker J, Al-Been H, et al. Crohn’s disease presenting as life-threatening ileal bleeding. Saudi Med J 2000;21:971–3. [69] Robert JR, Sachar DB, Greenstein AJ. Severe gastrointestinal hemorrhage in Crohn’s disease. Ann Surg 1991;213:207–11. [70] Pardi DS, Loftus EV Jr, Tremaine WJ, et al. Acute major gastrointestinal hemorrhage in inflammatory bowel disease. Gastrointest Endosc 1999;49:153–7. [71] Waye JD, Lewis BS, Yessayan S. Colonoscopy: a prospective report of complications. J Clin Gastroenterol 1992;15:347–51. [72] Waye JD, Kahn O, Auerbach ME. Complications of colonoscopy and flexible sigmoidoscopy. Gastrointest Endosc Clin N Am 1996;6:343–77. [73] Rex DK, Lewis BS, Waye JD. Colonoscopy and endoscopic therapy for delayed postpolypectomy hemorrhage. Gastrointest Endosc 1992;38:127–9. [74] Sobrino-Faya M, Martinez S, Gomez Balado M, et al. Clips for the prevention and treatment of postpolypectomy bleeding (hemoclips in polypectomy). Rev Esp Enferm Dig 2002; 94:457–62. [75] Brooker JC, Saunders BP, Shah SG, et al. Treatment with argon plasma coagulation reduces recurrence after piecemeal resection of large sessile colonic polyps: a randomized trial and recommendations. Gastrointest Endosc 2002;55:371–5. [76] Parra-Blanco A, Kaminaga N, Kojima T, et al. Hemoclipping for postpolypectomy and postbiopsy colonic bleeding. Gastrointest Endosc 2000;51:37–41. [77] Ardengh JC, Ferrari AP, Ganc AJ, et al. Endoscopic banding ligation and postpolypectomy bleeding. Endoscopy 1999;31:S61. [78] Dumonceau JM, Deviere J. Early rebleeding after successful hemoclipping of a postpolypectomy rectal ulcer. Endoscopy 1999;31:S54–5. [79] Uno Y, Satoh K, Tuji K, et al. Endoscopic ligation by means of clip and detachable snare for management of colonic postpolypectomy hemorrhage. Gastrointest Endosc 1999;49: 113–5. [80] Waye JD. Management of complications of colonoscopic polypectomy. Gastroenterologist 1993;1:158–64. [81] Ajlouni M. Radiation-induced proctitis. Curr Treat Options Gastroenterol 1999;2:20–6. [82] Schultheiss TE, Lee WR, Hunt MA, et al. GU complications in the treatment of prostate cancer. Int J Radiat Oncol Biol Phys 1997;37:3–11. [83] Gilinsky NH, Burns DG, Barbezat GO, et al. The natural history of radiation-induced proctosigmoiditis: an analysis of 88 patients. Q J Med 1983;52:40–53. [84] Lucarotti ME, Mountford RA, Bartolo DC. Surgical management of intestinal radiation injury. Dis Colon Rectum 1991;34:865–9. [85] Kochhar R, Patel F, Dhar A, et al. Prospective, randomized, double-blind controlled trial of oral sulfasalazine plus rectal steroids versus rectal sucralfate. Dig Dis Sci 1991;36: 103–7.
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[86] Kochhar R, Sriram PV, Sharma SC, et al. Natural history of late radiation proctosigmoiditis treated with topical sucralfate suspension. Dig Dis Sci 1999;44:973–8. [87] Kochhar R, Sharma SC, Gupta BB, et al. Rectal sucralfate in radiation proctitis. Lancet 1988;2:400. [88] Sasai T, Hiraishi H, Suzuki Y, et al. Treatment of chronic postradiation proctitis with oral administration of sucralfate. Am J Gastroenterol 1998;93:1593–5. [89] Stockdale AD, Biswas A. Long-term control of radiation proctitis following treatment with sucralfate enemas. Br J Surg 1997;84:379. [90] Mathai V, Seow-Choen F. Endoluminal formalin therapy for haemorrhagic radiation proctitis. Br J Surg 1995;82:190. [91] Seow-Choen F, Goh HS, Eu KW, et al. A simple and effective treatment for hemorrhagic radiation proctitis using formalin. Dis Colon Rectum 1993;36:135–8. [92] Biswal BM, Lal P, Rath GK, et al. Intrarectal formalin application, an effective treatment for grade III haemorrhagic radiation proctitis. Radiother Oncol 1995;35:212–5. [93] Fantin AC, Binek J, Suter WR, et al. Argon beam coagulation for treatment of symptomatic radiation-induced proctitis. Gastrointest Endosc 1999;49:515–8. [94] Silva RA, Correia AJ, Dias LM, et al. Argon plasma coagulation therapy for hemorrhagic radiation proctosigmoiditis. Gastrointest Endosc 1999;50:221–4. [95] Tjandra JJ, Sengupta S. Argon plasma coagulation is an effective treatment for refractory hemorrhagic radiation proctitis. Dis Colon Rectum 2001;44:1759–65 [discussion: 1771]. [96] Taieb S, Rolachon A, Cenni JC, et al. Effective use of argon plasma coagulation in the treatment of severe radiation proctitis. Dis Colon Rectum 2001;44:1766–71. [97] Berken CA. Nd:YAG laser therapy for gastrointestinal bleeding due to radiation colitis. Am J Gastroenterol 1985;80:730–1. [98] Barbatzas C, Spencer GM, Thorpe SM, et al. Nd:YAG laser treatment for bleeding from radiation proctitis. Endoscopy 1996;28:497–500. [99] Viggiano TR, Zighelboim J, Ahlquist DA, et al. Endoscopic Nd:YAG laser coagulation of bleeding from radiation proctopathy. Gastrointest Endosc 1993;39:513–7. [100] Taylor JG, Disario JA, Bjorkman DJ. KTP laser therapy for bleeding from chronic radiation proctopathy. Gastrointest Endosc 2000;52:353–7. [101] Taylor JG, DiSario JA, Buchi KN. Argon laser therapy for hemorrhagic radiation proctitis: long-term results. Gastrointest Endosc 1993;39:641–4. [102] Farrands PA, Taylor I. Management of acute lower gastrointestinal haemorrhage in a surgical unit over a 4-year period. J R Soc Med 1987;80:79–82. [103] Makela JT, Kiviniemi H, Laitinen S, et al. Diagnosis and treatment of acute lower gastrointestinal bleeding. Scand J Gastroenterol 1993;28:1062–6. [104] Peura DA, Lanza FL, Gostout CJ, et al. The American College of Gastroenterology Bleeding Registry: preliminary findings. Am J Gastroenterol 1997;92:924–8. [105] Kollef MH, O’Brien JD, Zuckerman GR, et al. A classification tool to predict outcomes in patients with acute upper and lower gastrointestinal hemorrhage. Crit Care Med 1997;25: 1125–32. [106] Kollef MH, Canfield DA, Zuckerman GR. Triage considerations for patients with acute gastrointestinal hemorrhage admitted to a medical intensive care unit. Crit Care Med 1995;23:1048–54. [107] Machicado GA, Jensen DM. Acute and chronic management of lower gastrointestinal bleeding: cost-effective approaches. Gastroenterologist 1997;5:189–201.
Lower Gastrointestinal Bleeding Brenna Casey Bounds, MD*, Peter B. Kelsey, MD Harvard Medical School, Gastrointestinal Unit, Massachusetts General Hospital, 55 Fruit Street, Blake 453D, Boston, MA 02114, USA
Lower gastrointestinal (GI) bleeding is defined as blood loss that originates from a source distal to the ligament of Treitz and that results in hemodynamic instability or symptomatic anemia. The annual incidence of lower GI bleeding is approximately 0.03% in the adult population as a whole, with a greater than 200-fold increase from the second to the eighth decade [1,2]. This rise in incidence with age may be explained by the increasing prevalence of colonic diverticulosis and colonic angiodysplasia with age. The mean age of patients with lower GI bleeding ranges from 63 to 77 years, with a reported mortality rate of 2% to 4% [2–7]. Although approximately 10% to 15% of patients presenting with acute severe hematochezia have an upper GI source of bleeding identified on upper endoscopy, the most common causes of lower GI bleeding are diverticulosis, hemorrhoids, ischemic colitis, and angiodysplasia [4,8,9]. As with upper GI bleeding, lower GI bleeding ceases spontaneously in most cases.
Initial evaluation and resuscitation The patient presenting with acute lower GI hemorrhage may complain of passing bright red blood per rectum, dark blood with clots, or less commonly melena. Pallor, fatigue, chest pain, palpitations, dyspnea, tachypnea, tachycardia, postural changes, or syncope are suggestive of hemodynamic compromise. Commencement of resuscitation efforts should take place concurrently with the initial evaluation of the patient. In patients who have hemodynamic compromise, intravenous access, with a minimum of two large-caliber peripheral catheters or a central venous line, should be secured immediately. Resuscitation is imperative to restore euvolemia and prevent complications of red blood cell loss, such as cardiac, pulmonary, * Corresponding author. E-mail address: [email protected] (B.C. Bounds). 1052-5157/07/$ - see front matter Ó 2007 Published by Elsevier Inc. doi:10.1016/j.giec.2007.03.010
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renal, or neurologic consequences. Initial laboratory testing should include a complete blood count, electrolytes, coagulation profile, and a sample for typing and crossmatching. A directed history may identify risk factors helpful in defining the source of the bleeding. For example, the use of aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) is associated strongly with lower GI bleeding, chiefly diverticular bleeding, as it is with upper GI bleeding. Lower GI bleeding preceded by hypovolemia suggests ischemic colitis, whereas a history of prior radiation therapy for prostate or pelvic cancer may indicate radiation proctitis (which may present months or even years after the radiation exposure). Severe constipation should prompt an investigation for a stercoral ulcer, while a history of recent colonoscopy with polypectomy incriminates postpolypectomy bleeding as the likely source. Physical examination should include careful cardiac, pulmonary, abdominal, and rectal examinations. A digital rectal examination is helpful for excluding anorectal pathology and confirming the patient’s description of the appearance of the stool. In addition, approximately 40% of rectal carcinomas are palpable during a digital rectal examination [10]. The presence of coagulopathy (international normalized ratio [INR] O1.5) or thrombocytopenia (!50,000/mL) should prompt correction with fresh-frozen plasma or platelet transfusions, respectively. The blood transfusion requirement is determined by the patient’s age and rate of bleeding and also is influenced by the presence of comorbid conditions such as coronary artery disease, cirrhosis, or chronic obstructive pulmonary disease. Orthostatic hypotension, a decrease in the hematocrit value of at least 6%, a transfusion requirement of more than two units of packed red blood cells, or continuous active bleeding merit admission to an ICU for close observation.
Diagnostic evaluation Colonoscopy Diagnostic endoscopic studies should be done only after the patient has been hemodynamically resuscitated. If there is any possibility of an upper GI source, upper endoscopy should be performed first. A lower endoscopic study is established as the diagnostic procedure of choice in the setting of acute lower GI hemorrhage. If selected as the initial endoscopic approach, sigmoidoscopy should be undertaken with the caveat that it should be considered diagnostic only if an actively bleeding lesion can be demonstrated. Many endoscopists prefer to perform a total colonoscopy as the initial evaluation, however. The diagnostic accuracy of colonoscopy ranges from 72% to 86% in the setting of lower GI bleeding [11,12]. Cecal intubation is achieved in greater than 95% of attempts in this setting [13]. No consensus has been reached regarding the need for colonic purge before colonoscopy in a patient with active lower GI bleeding [4,12,14,15].
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Because the risk of colonic perforation may be increased when colonoscopy is performed in an unprepared colon, however, only experienced endoscopists should attempt colonoscopy in this setting. Plain abdominal radiography should be performed before colonoscopy if perforation or obstruction is suspected. Radiographic evidence of thumbprinting is indicative of transmural injury to the colon caused by ischemic or infectious colitis. Radionuclide imaging and angiography Evaluation with either radionuclide imaging or angiography may be appropriate in patients who have massive hemorrhage that precludes colonoscopy or in whom a bleeding source is not identified on colonoscopy. Radionuclide imaging detects active bleeding at rates of 0.1 to 0.5 mL/min and is more sensitive than angiography but less specific than a positive endoscopic or angiographic study [16]. The two techniques of radionuclide scanning commonly employ either technetium sulfur colloid or 99mTc pertechnetate-labeled red blood cells. Whereas technetium sulfur colloid can detect a bleeding rate as low as 0.1 mL/min, the short half life of the colloid within the vascular system requires active bleeding at the time the radionuclide is present in the intravascular space. Conversely, imaging following injection of 99mTc pertechnetate-labeled red blood cells is performed at 30-minute intervals for up to 24 hours, allowing patients to be scanned multiple times. Radionuclide imaging is tolerated well by patients but is limited by highly variable accuracy rates for bleeding localization, ranging from 24% to 91% [17]. Angiography requires a GI bleeding rate of at least 1 mL/min for accurate detection of extravasation of contrast into the bowel lumen [18]. Unfortunately, bleeding is frequently intermittent and may occur at a much lower rate, resulting in inability to detect the causative lesion. The overall yield of angiography for detection of a GI bleeding source ranges from 40% to 78% [6,19–22]. Diverticular disease and angiodysplasia are the most common findings when angiography is positive, with 50% to 80% of sources occurring in bowel supplied by the superior mesenteric artery [23]. In some centers, angiographers request that a bleeding scan be performed before arteriography, because a patient who has a negative nuclear imaging scan is likely to have a negative angiogram. Unfortunately, bleeding may cease during the time required for performance of the bleeding scan, and the opportunity to localize a lesion by angiography therefore may be missed. Angiography has a specificity of 100% but a sensitivity of only 30% to 47% [24]. A positive angiogram is associated strongly with the need for surgical intervention [24]. Angiography does not require bowel preparation, provides accurate localization of the bleeding source (when identified), and permits therapeutic intervention in some cases. Intra-arterial infusion of vasopressin or arterial embolization may be performed by means of the
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catheter and is highly effective in controlling lower GI hemorrhage. This procedure, however, is associated with a substantial risk of serious complications, including intestinal infarction of up to 20% [25]. Other complications of arteriography occur in approximately 9% of patients and include arterial thrombosis, embolization, and renal failure [4]. Therefore, colonoscopy remains the procedure of choice in the evaluation of the patient with acute lower GI bleeding. Angiography should be reserved for the patient who has massive bleeding that precludes colonoscopy, persistent or recurrent bleeding, or a colonoscopy that has failed to identify the bleeding source. Small bowel evaluation An evaluation of the small bowel is indicated for those patients in whom an upper GI endoscopy and colonoscopy are negative. Small bowel evaluation in patients who are hemodynamically stable may be performed with push enteroscopy, which allows endoscopic evaluation of the proximal 60 cm of the jejunum. If examination of the remaining jejunum and ileum is desired, a video capsule study provides imaging of the entire small bowel and is tolerated well by patients. A video capsule study is reported to identify the bleeding source in up to 89% of examined patients with GI bleeding resulting in successfully executed definitive therapy in 87% of patients undergoing the study while actively bleeding [26]. A nuclear medicine scan for a Meckel’s diverticulum may be appropriate in young patients presenting with lower GI bleeding [27].
Specific causes of lower gastrointestinal bleeding Colonic diverticula Colonic diverticular hemorrhage results from asymmetric rupture of the intramural branches (vasa recta) of the marginal artery at the dome of a diverticulum or at the antimesenteric margin [28,29]. Although most patients with diverticulosis are asymptomatic, approximately 20% will develop diverticulitis, and 3% to 5% will develop acute severe hematochezia [9]. In the elderly patient who has comorbid conditions, diverticular bleeding results in morbidity and mortality rates of 10% to 20%, respectively [20,30,31]. Although greater than 75% of diverticula are found in the left colon, the right colon is the source of diverticular bleeding in 50% to 90% of patients when angiography is positive [28,29,31]. On the other hand, when diverticular bleeding is diagnosed at colonoscopy, the bleeding is from the left colon in 60% of cases [2]. Diverticular bleeding ceases spontaneously in 75% of patients; 99% of patients will require less than four units of transfused blood [9]. Bleeding recurs in 14% to 38% of cases following the primary episode and in up to 50% of cases following a second episode of bleeding [9,31].
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When managed conservatively, diverticular bleeding resolves spontaneously in most patients. Persistent hemodynamic instability despite aggressive resuscitation efforts warrants intervention. Nonsurgical therapy may be performed during either angiography or colonoscopy. Angiography permits directed intra-arterial infusion of vasopressin, which results in resolution of bleeding in 91% of cases [20]. In up to 50% percent of cases, however, bleeding recurs on cessation of the vasopressin infusion [20]. Transcatheter embolization effectively controls diverticular bleeding but is associated with a risk of intestinal infarction of up to 20% [20]. Endoscopic therapy may be performed using epinephrine injection therapy, bipolar coagulation, or both [32]. One study reported that patients with demonstrable diverticular bleeding who received endoscopic therapy with epinephrine injection, bipolar coagulation, or both, had no recurrent bleeding during the 30-month follow-up period, compared with a 53% rebleeding rate in patients who received conservative medical therapy alone [32]. Less frequently employed methods for control of diverticular bleeding include endoscopic band ligation and placement of vascular clips (Fig. 1) [33,34]. Surgical intervention is required when hemodynamic instability persists despite aggressive resuscitation. Surgical intervention is necessary in 18% to 25% of patients who require blood transfusion [9,35]. Operative mortality is 10% despite improved methods of localization of bleeding that permit segmental rather than subtotal colectomy [20,35,36]. Blind segmental resection is contraindicated and is associated with a high rebleeding rate of 42% and excessive rates of morbidity and mortality, which may be as high as 83% and 57%, respectively [37]. Management by a dedicated bleeding team may reduce mortality associated with acute diverticular hemorrhage [31].
Fig. 1. Hemostasis was achieved with application of a band to this bleeding diverticulum following injection with epinephrine. (Courtesy of Massachusetts General Hospital, Boston, MA; with permission.)
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Angiodysplasia Angiodysplasia is the most common vascular anomaly of the GI tract (Fig. 2). Composed of ectatic, dilated submucosal veins, colonic angiodysplasia are responsible for 20% to 30% of cases of acute lower GI bleeding [20]. They occur with equal frequency in men and women, and most occur in persons over the age of 60, with two-thirds occurring in persons over 70. More than one angiodysplasia is present in most patients [38–40]. In the colon, angiodysplasias are most common in the cecum and proximal ascending colon (54%), followed by the sigmoid colon (18%) and rectum (14%) [40]. Although angiodysplasia can be found throughout the small intestine, bleeding angiodysplasia in the small bowel usually presents as iron deficiency anemia with fecal occult blood and rarely as severe hematochezia. At colonoscopy, angiodysplasias are recognized by their characteristic appearance as red, flat lesions consisting of ectatic blood vessels that appear to radiate from a central feeding vessel; they may have a diameter of 2 to 10 mm. A pale mucosal halo also may be seen around the lesion. When the colon is examined completely, the sensitivity of colonoscopy for detecting angiodysplasia exceeds 80% [39,41]. A poor bowel preparation, however, may lead to incomplete evaluation of the colonic mucosa. Additionally, the use of narcotic medications for sedation and analgesia may decrease the sensitivity of colonoscopy for detecting angiodysplasia because of a transient decrease in mucosal blood flow. Administration of intravenous naloxone has been demonstrated to enhance the appearance of angiodysplasia during colonoscopy in patients who have received meperidine for sedation [42]. Unfortunately, use of naloxone may result in significant discomfort for the patient, particularly when the procedure is prolonged by the application of therapeutics. Conventional endoscopic treatment of colonic angiodysplasia is performed with contact thermal probes. To prevent brisk bleeding from
Fig. 2. A large colonic angiodysplasia. (Courtesy of Massachusetts General Hospital, Boston, MA; with permission.)
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angiodysplasia when contact electrocautery is performed, large angiodysplasia should be cauterized from the outer margin toward the center to obliterate feeder vessels. Injection therapy with sclerosing agents, such as ethanolamine, also has been described for control of bleeding from colonic angiodysplasia but is not employed widely [43]. Argon plasma coagulation is a noncontact method that is increasingly popular for the treatment of bleeding colonic angiodysplasia [44,45]. Extra care must be taken when treating lesions in the cecum to minimize the risk of perforation [44]. Angiography remains the gold standard for the diagnosis of larger angiodysplasia. Following injection of contrast, angiodysplasias are seen as ectatic slowly emptying veins, vascular tufts, or small veins with early filling. When angiography identifies a bleeding angiodysplasia, treatment with embolization therapy or directed infusion of vasopressin may be performed. Use of hormonal therapy (estrogen) for control of GI bleeding of obscure origin thought to be caused by angiodysplasia is controversial and may be ineffective [46,47]. Surgery should be considered in patients in whom a bleeding source clearly has been identified and in whom more conservative therapies have failed. Hemorrhoids The frequency of hemorrhoids in patients with lower GI bleeding is as high as 75%, but a causal relationship is established infrequently. Hemorrhoids have accounted for 2% to 9% of cases of acute severe hematochezia in studies that include anorectal sources of hemorrhage [1,2,12]. Nonsteroidal anti-inflammatory-induced lower gastrointestinal bleeding NSAIDs have been implicated in small bowel and colonic pathology and gastroduodenal ulceration. The terminal ileum and cecum are particularly susceptible to NSAID-induced injury. NSAIDs have been demonstrated to exacerbate inflammatory bowel disease, cause colitis resembling inflammatory bowel disease, and complicate diverticular disease by increasing the risk of perforation and severe hematochezia [48,49]. Elderly patients and those on long-term NSAIDs are at greatest risk of NSAID-induced complications. NSAIDs also may cause localized mucosal injury, as suggested by the finding of NSAID shells at the site of perforating ulcers. Intestinal and colonic ulcers caused by NSAIDs often have sharp demarcations with a predilection for the terminal ileum and proximal colon, where pills may be static for a longer period of time than in other segments of the bowel. The diaphragm-like stricture is a lesion pathognomonic of NSAID injury that occurs as a result of a scarring reaction secondary to ulceration. These most frequently are found in the midsection of the small intestine, but also have been reported to occur in the terminal ileum and colon [48,50–53]. Diaphragm-like strictures typically occur in multiples with normal intervening mucosa.
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In patients with NSAID-induced mucosal injury and bleeding, colonoscopy reveals nonspecific ulcerations of the colon and small bowel, particularly the cecum and terminal ileum. Histology is also nonspecific, and infectious etiologies, radiation injury, and inflammatory bowel disease must be excluded [50,54]. Treatment of NSAID-induced mucosal injury is discontinuation of the offending NSAID. A repeat colonoscopy should be performed 6 to 8 weeks after cessation of the NSAID to confirm resolution of ulcerations and/or colitis. If ulceration or colitis persists, an alternative diagnosis such as inflammatory bowel disease should be entertained. Rarely, surgical intervention is required for NSAID-induced bleeding or perforation [50]. Colonic ischemia Colonic ischemia, the most common ischemic disorder of the GI tract, results from a sudden, often temporary, reduction in mesenteric blood flow. Mesenteric hemodynamics may be compromised by changes in the systemic circulation or by anatomic or functional changes in the mesenteric vasculature. Frequently, a specific precipitating event or vascular lesion on angiography cannot be identified. In patients who have undergone aortoiliac reconstructive surgery, the frequency of significant postoperative colonic ischemia is 1% to 7% [55–57]. Nonocclusive colonic ischemia most commonly involves the splenic flexure, right colon, or rectosigmoid junction, the watershed areas. Clinically, ischemic colitis presents with the sudden onset of mild left lower quadrant crampy abdominal pain. The pain may be accompanied or followed in the ensuing 24 hours by bright red blood per rectum or bloody diarrhea. Acute severe hematochezia should raise the suspicion of an alternative etiology. Ischemic colitis must be differentiated clinically from acute mesenteric ischemia. Patients who have acute mesenteric ischemia (involving the small intestine) have severe abdominal pain, often out of proportion to physical examination findings; they appear critically ill and frequently have an identifiable acute precipitating event. In patients who have ischemic colitis, sigmoidoscopy reveals ulceration of the colonic mucosa, with sparing of the rectum in most cases. Histology reveals necrosis, not acute and chronic inflammatory changes as seen in inflammatory bowel disease. Treatment is supportive, and most cases resolve spontaneously within several days to weeks. One fifth of patients develop a chronic colitis that differs from ulcerative colitis in that it is segmental and spares the rectum; colonic strictures also may develop. Chronic colitis caused by ischemia does not respond to standard medications used to treat inflammatory bowel disease, and many affected patients eventually require colectomy. Inflammatory bowel disease Although GI bleeding is a common manifestation of inflammatory bowel disease, acute severe hematochezia is infrequent. Most patients who have
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ulcerative colitis report clinically apparent bleeding, in contrast to patients with Crohn’s disease, of whom only one third report bleeding [58–61]. Acute severe hematochezia accounts for up to 6% of hospitalizations for patients with Crohn’s disease and 1.4% to 4.2% of patients with ulcerative colitis [62–69]. Although acute severe hematochezia is not a predictor of the bleeding site in patients with Crohn’s disease, most patients with ulcerative colitis who present in this manner are found to have pancolitis at colonoscopy [58,59,64,70]. Recurrence of bleeding is not uncommon following an episode of acute severe hematochezia in patients who have inflammatory bowel disease, and when it occurs, surgery is required for control of hemorrhage in 57% of cases [70]. Postpolypectomy bleeding Endoscopic polypectomy is now the primary treatment for most colonic polyps. Complications occur in less than 5% of colonoscopies performed for polypectomy [71], and of the complications, postpolypectomy bleeding is the most frequent and accounts for approximately 2% to 8% of cases of acute lower GI bleeding (Fig. 3) [4,7,12]. The frequency of delayed postpolypectomy bleeding as a cause of acute severe hematochezia is increasing, possibly because of the increasing use of a blended (rather that pure coagulation) current in the polypectomy snare. Massive bleeding that occurs at the time of polypectomy is typically arterial in nature and often can be controlled by resnaring the stalk of the polyp and applying pressure [72,73]. Delayed bleeding likely occurs because of the sloughing of the eschar at the polypectomy site [72,73]. Delayed bleeding usually is self-limited and resolves with supportive care in more than 70% of cases. For persistent or severe bleeding at a polypectomy site, several endoscopic techniques have proven safe and effective. These include loop ligation of the remaining polyp stalk, endoscopic band ligation, injection with epinephrine followed by thermal therapy, and application of endovascular clipping devices [33,74–80].
Fig. 3. A bleeding colonic polyp stalk immediately following snare polypectomy. (Courtesy of Massachusetts General Hospital, Boston, MA; with permission.)
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Less common sources of lower gastrointestinal bleeding Infectious colitis Acute severe hematochezia infrequently is caused by an infectious etiology. The most common bacterial causes resulting in lower GI bleeding are Salmonella and Escherichia coli O157:H7 infections. The patient may relate a history of crampy abdominal pain and watery diarrhea that was followed by grossly bloody diarrhea. Salmonella, Campylobacter, and Yersinia may cause mucosal edema, hyperemia, erosions, and ulceration and should be distinguished by culture results; colonoscopy rarely is indicated. Other infectious causes of lower GI bleeding include amebiasis, cytomegalovirus infection, and Mycobacterium avium complex infection, particularly in immunosuppressed persons. Radiation colitis Acute severe hematochezia is a rare complication of radiation therapy. Rectal bleeding as a result of radiation proctitis accounts for 1% to 5% of cases of acute lower GI bleeding [81]. Inflammation caused by exposure of the rectum or rectosigmoid area to radiation during therapy for prostatic or gynecologic malignancy may result in significant bleeding that may occur as early as 9 months or as late as 4 years following therapy [82–84]. Following acute mucosal injury, the patient may complain of diarrhea and tenesmus accompanied by abdominal cramping and a mucoid or bloody rectal discharge. A chronic proctocolitis may develop and may be complicated by bleeding of mild-to-moderate severity. Endoscopically, the mucosa demonstrates characteristic telangiectases. Bleeding may be controlled effectively with sucralfate enemas, instillation of formalin, or endoscopic treatment using either laser or argon plasma coagulation [85–101]. Neoplasms Bleeding, either occult or gross, is the most common presenting symptom of colonic neoplasms, but is rarely brisk. The reported frequency of acute lower GI bleeding resulting from colonic neoplasms ranges from 2% to 26% [1,7,12,36,102–104]. Stercoral ulcers Stercoral ulceration should be included in the differential diagnosis when an elderly patient presents with hematochezia and antecedent constipation. Most commonly seen as an isolated lesion in the rectosigmoid area, a stercoral ulcer occurs as a result of pressure necrosis from a fecal mass. Although colonic perforation and bleeding are the most common complications, acute severe hematochezia is rarely attributable to a stercoral ulceration [2,7].
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Other causes of lower GI bleeding include intestinal intussusception, trauma to the colonic mucosa from an endoscope or enema, solitary rectal ulcer syndrome, portal colopathy, colonic varices, endometriosis, Dieulafoy lesion, and bleeding from the appendiceal orifice or a Meckel’s diverticulum.
Outcomes Mortality rates for lower GI bleeding are less than 5% [1,2,104,105]. One bleeding outcomes study reported a mortality rate of 0.6% for lower GI bleeding and an overall mortality rate of 2% for bleeding arising from an upper GI source [105]. Although the highest mortality rates are reported for patients in whom bleeding occurs during a hospitalization for other reasons, in most series, lower GI bleeding rarely has been the cause of death [2]. A population-based study of patients enrolled in a health maintenance organization reported an in-hospital mortality rate of 3.6% for patients hospitalized with lower GI hemorrhage and 23.1% for those who developed lower GI bleeding following hospitalization [2]. For patients who had a discharge diagnosis of diverticular bleeding who did not require definitive therapy, the rate of recurrent bleeding was 9% at 1 year, 10% at 2 years, 19% at 3 years, and 25% at 4 years [2]. In the 89 patients with diverticular bleeding who survived to discharge, mortality at 4 years was not related to recurrent hemorrhage, although diverticular bleeding may portend a poor prognosis from other causes [2]. Another factor that impacts the outcome of lower GI bleeding includes the use of NSAIDs, particularly in combination with aspirin. One study reported that 75% of patients with severe diverticular hemorrhage had a combined exposure to NSAIDs and aspirin compared with none of the patients with nonsevere hemorrhage [49]. Although the presence of stigmata of recent bleeding, such as a visible vessel or adherent clot with active bleeding, is a reliable marker of severe diverticular hemorrhage, the presence of a clean-based ulcer within a diverticulum may indicate a low risk of recurrent hemorrhage and permit early discharge from the hospital [49]. Numerous studies have proposed clinical prognostic criteria to distinguish patients with a high risk and low risk of recurrent hemorrhage [7,105,106]. Early colonoscopy has been associated with both shorter hospital stays and lower overall costs per patient [7,107]. Additional studies are needed to enhance understanding of the benefit of available interventions in the treatment of lower GI hemorrhage.
Summary Lower GI hemorrhage is a significant cause of morbidity and mortality, particularly in elderly patients. Lower endoscopic evaluation is established as the diagnostic procedure of choice in the setting of acute lower GI
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hemorrhage. An upper source of bleeding may be found in up to 15% of patients who present with lower hemorrhage, and must be ruled out [4,8,9]. Video capsule endoscopy is reported to identify the bleeding source in up to 89% of examined patients with GI bleeding, although the optimal timing and use of this technology have yet to be defined [26]. Evaluation with either radionuclide imaging or angiography may be appropriate in patients with massive hemorrhage that precludes colonoscopy or in whom a bleeding source is not identified on endoscopy. Numerous factors, including use of NSAIDS, inpatient status at the time of hemorrhage, and endoscopic appearance with stigmata of recent bleeding, are all predictors of worse outcomes. Early colonoscopy in the setting of lower GI hemorrhage has been associated with both shorter hospital stays and lower overall costs per patient, and should be considered in the appropriate clinical setting. Emergent management of severe lower GI hemorrhage requires the concomitant initiation of medical resuscitation and the preparation for endoscopic evaluation and coordination of a multidisciplinary team including gastroenterology, interventional radiology, and surgery. References [1] Bramley PN, Masson JW, McKnight G, et al. The role of an open-access bleeding unit in the management of colonic haemorrhage. A 2-year prospective study. Scand J Gastroenterol 1996;31:764–9. [2] Longstreth GF. Epidemiology and outcome of patients hospitalized with acute lower gastrointestinal hemorrhage: a population-based study. Am J Gastroenterol 1997;92:419–24. [3] Boley SJ, DiBiase A, Brandt LJ, et al. Lower intestinal bleeding in the elderly. Am J Surg 1979;137:57–64. [4] Jensen DM, Machicado GA. Diagnosis and treatment of severe hematochezia. The role of urgent colonoscopy after purge. Gastroenterology 1988;95:1569–74. [5] Jensen DM, Machicado GA. Colonoscopy for diagnosis and treatment of severe lower gastrointestinal bleeding. Routine outcomes and cost analysis. Gastrointest Endosc Clin N Am 1997;7:477–98. [6] Leitman IM, Paull DE, Shires GT 3rd. Evaluation and management of massive lower gastrointestinal hemorrhage. Ann Surg 1989;209:175–80. [7] Richter JM, Christensen MR, Kaplan LM, et al. Effectiveness of current technology in the diagnosis and management of lower gastrointestinal hemorrhage. Gastrointest Endosc 1995;41:93–8. [8] Foutch PG. Angiodysplasia of the gastrointestinal tract. Am J Gastroenterol 1993;88: 807–18. [9] McGuire HH Jr. Bleeding colonic diverticula. A reappraisal of natural history and management. Ann Surg 1994;220:653–6. [10] Steer ML, Silen W. Diagnostic procedures in gastrointestinal hemorrhage. N Engl J Med 1983;309:646–50. [11] Jensen DM. Diagnosis and treatment of patients with severe hematochezia: a time for change. Endoscopy 1998;30:724–6. [12] Rossini FP, Ferrari A, Spandre M, et al. Emergency colonoscopy. World J Surg 1989;13: 190–2. [13] Waye JD, Bashkoff E. Total colonoscopy: is it always possible? Gastrointest Endosc 1991; 37:152–4.
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