Interventional management of lower gastrointestinal bleeding

Eur Radiol (2008) 18: 857–867 DOI 10.1007/s00330-007-0844-2 Derik T. Weldon Stephen J. Burke Shiliang Sun Hidefumi Mimura Jafar Golzarian Received: ...
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Eur Radiol (2008) 18: 857–867 DOI 10.1007/s00330-007-0844-2

Derik T. Weldon Stephen J. Burke Shiliang Sun Hidefumi Mimura Jafar Golzarian

Received: 28 February 2007 Revised: 16 November 2007 Accepted: 10 December 2007 Published online: 8 January 2008 # European Society of Radiology 2007

D. T. Weldon . S. J. Burke . S. Sun . H. Mimura . J. Golzarian (*) Department of Radiology, University of Iowa Hospitals and Clinics, 200 Hawkins Drive, Iowa, IA 52242-1107, USA e-mail: [email protected] Tel.: +1-319-3564316 Fax: +1-319-3562220


Interventional management of lower gastrointestinal bleeding

Abstract Lower gastrointestinal bleeding (LGIB) arises from a number of sources and is a significant cause of hospitalization and mortality in elderly patients. Whereas most episodes of acute LGIB resolve spontaneously with conservative management, an important subset of patients requires further diagnostic workup and therapeutic intervention. Endovascular techniques such as microcatheter embolization are now recognized as safe, effective methods for controlling LGIB that is refractory to endoscopic intervention. In addition, multidetector CT has shown the ability to

Introduction Lower gastrointestinal bleeding (LGIB) is defined as bleeding that originates from a source distal to the ligament of Treitz. Multiple potential etiologies and variable clinical presentations of LGIB present diagnostic and management challenges for clinicians. The estimated annual incidence of acute LGIB in a large health maintenance organization population is 20.5 patients/100,000 with a significantly greater number of bleeds occurring in males [1]. Acute LGIB is 200× more common in the 9th decade of life versus the 3rd [1]. In four large series totaling 1,368 patients, percent mortality for LGIB ranges from 2–5% [1–4]. Patients who develop acute LGIB while already hospitalized for a comorbid condition are at significantly increased risk of death (23%) versus those who are admitted for acute LGIB (2.4%) [1]. The source of LGIB may be identified by angiography, radionuclide scintigraphy, multidetector CT (MDCT) or endoscopy with endovascular, endoscopic or surgical treatment options for bleeding not amenable to control

identify areas of active bleeding in a non-invasive fashion, enabling more focused intervention. Given the relative strengths and weaknesses of various diagnostic and treatment modalities, a close working relationship between interventional radiologists, gastroenterologists and diagnostic radiologists is necessary for the optimal management of LGIB patients. Keywords Lower gastrointestinal bleeding . Angiography . Embolization . Diverticular . Angiodysplasia

with conservative management. These diagnostic and treatment options have inherent limitations, and their utility for a given patient depends on the rate of bleeding and the patient’s hemodynamic stability. The purpose of this paper is to review the diagnosis and treatment of LGIB, focusing on the role of interventional radiology.

Etiology The etiology of LGIB in adults is diverse, both in the anatomic position of causative lesion(s) and in the propensity of these lesions to cause clinically significant bleeding. The most common causes of LGIB, comprised from a Veterans Administration database study and discharge data from a large health maintenance organization, are listed in Table 1 [1, 5]. Approximately 80% of LGIB derives from a colorectal source, 5–10% from a small bowel source and 10–15% of LGIB is blood of upper gastrointestinal origin. The source of small bowel bleeding is more apt to be obscure/occult as compared to bleeding from a colorectal source [6, 7].


Diverticula The presence of colonic diverticula is strongly associated with age, increasing from approximately 30% at age 50 to 66% in patients over 85 years. Bleeding, ranging from occult to massive, occurs in 10–25% of individuals with diverticula [8]. Diverticular bleeding is typically painless and acute in onset. Overall, bleeding stops spontaneously in 75% of patients; in patients with a transfusion requirement of less than 4 units per day, bleeding stops spontaneously in >90% [9]; 25% of patients with diverticular bleeding have a recurrence within 4 years of initial diagnosis [1]. In addition to age, use of non-steroidal anti-inflammatory drugs is a risk factor for diverticular bleeding [10]. Whereas >75% of diverticula are found in the left side of the colon, diverticular bleeding detectable by angiography has a propensity for the right colon [11]. A diverticulum forms where a colonic arteriole penetrates the mucosal wall, with the dome of the diverticulum displacing the vasa recta submucosal branch. This displacement exposes the vasa recta to trauma and potential bleeding. Diverticula in the right colon have wider domes and necks as compared to the left colon, which may expose relatively more vessel to injury [10, 12].

ulcerative colitis (UC) admissions, with diffuse colonic involvement more common in affected patients than disease restricted to the left colon [15]. Up to 10% of emergency surgery for UC is attributable to severe LGIB [16]. Ischemic enteritis is the cause of LGIB in 5.5–8.7% of cases [1, 17]. Watershed areas, including the right colon, splenic flexure and the rectosigmoid junction, are the most frequent areas of ischemia, with crampy abdominal pain and bloody diarrhea the most common clinical presentation [11]. Anorectal LGIB is attributable to anorectal sources in 7–11% of cases, with etiologies including hemorrhoids, anal fissure, rectal varices, fistula-in-ano and radiation proctitis [1, 5, 18]. The prevalence of hemorrhoids is particularly high, with 76% of outpatients evaluated for bright red blood per rectum demonstrating internal hemorrhoids by anoscopy [19]. LGIB caused by radiation proctitis can result from acute mucosal injury and chronic intramural vasculitis, with the initial bleeding episode occurring up to 41 months following radiotherapy [20].

Colitis/enteritis Neoplasia/post-polypectomy Inflammatory bowel disease and ischemic enteritis are relatively rare causes of severe LGIB. Acute, severe gastrointestinal hemorrhage occurs in 1.3% of Crohn’s disease (CD) admissions, more commonly in patients with colonic disease as versus disease confined to the small bowel [13]. When identified, the bleeding site is most commonly a left or sigmoid colon ulceration [14]. Interestingly, only 35% of hemorrhages occur in patients who are clinically deemed to be having a CD flare at the time of the bleed. Massive hemorrhage occurs in 1.4% of

Table 1 Causes of lower gastrointestinal bleeding Source of Bleeding

Frequency (%) Vernava [5]

Frequency (%) Longstreth [1]

Diverticular Colitis (IBD, ischemic, other) Anorectal Neoplasia Coagulopathy Post-polypectomy hemorrhage AVM/angiodysplasia Other/unknown

60 13

42 17

11 9 4

7 11 4


3 16

Neoplasia, most commonly colonic adenomatous polyps and carcinoma, is responsible for 9–11% of LGIB [1, 5, 21]. Bleeding from neoplasia ranges from occult to major and often originates from surface erosion, ulceration or polyp stalk rupture [12]. Of small bowel hemorrhage, 5– 10% is tumor-related, with melena or bright red blood per rectum more typical of leiomyoma/leiomyosarcoma and occult bleeding more typical of adenocarcinoma, lymphoma and carcinoid [7]. LGIB following endoscopic polypectomy can be seen up to 15 days post-procedure; acutely, post-polypectomy bleeding is due to insufficient stalk vessel coagulation, with later bleeding thought secondary to sloughing of surface coagulum [16]. Angiodysplasia Angiodysplasia is a relatively rare source of LGIB [1, 5]. However, in patients >65 it is the identifiable source of LGIB in 20% of cases, and up to 15% of these patients will present with massive bleeding [22, 23]. Angiodysplasia is most commonly found in the cecum and right colon, but can occur anywhere in the gastrointestinal tract. Of LGIB, 70–80% originating in the small bowel is attributable to angiodysplasia [7]. If angiodysplasia is found, there is a 20% chance of at least one synchronous lesion being


present elsewhere in the gastrointestinal tract. These lesions are likely acquired rather than congenital, as occurrence in patients younger than 40 is rare. Angiodysplasia is thought to arise from submucosal venules that become dilated and ectatic secondary to degeneration, transient intraluminal pressure elevation or obstruction [24, 25]. Painless bleeding is the classic presentation, similar to diverticular bleeding, although the rate is typically less in angiodysplasia. Bleeding stops spontaneously in over 90% of cases, but recurs in approximately 80% if left untreated [25].

Clinical presentation Bright red blood per rectum or melena is the most common presentation of acute LGIB. Initial triage of patients and the subsequent choice of diagnostic and treatment modality, depend on the nature of the bleeding and resultant hemodynamic compromise. Acute blood loss may result in hemodynamic instability, symptomatic anemia and need for blood transfusion [26, 27]. For the purposes of diagnosis and initial management, patients with acute LGIB can be grouped into four categories based on severity and chronicity of bleeding [27, 28]: 1. Patients who are hemodynamically stable with minor bleeding may be managed conservatively, as spontaneous resolution of bleeding occurs in 75-90% of patients. 2. Low grade/intermittent bleeding is best evaluated with endoscopy, as masses or clot can be directly visualized and sporadic bleeding is difficult to detect via angiography. 3. Intermittent severe bleeding may be evaluated with tagged red blood cell (RBC) scintigraphy or urgent colonoscopy if the patient is adequately fluid resuscitated. 4. Severe bleeding in a hemodynamically unstable patient necessitates prompt angiography versus surgery. Based on data available to the clinician at patient presentation, a model is proposed to predict outcomes for patients with LGIB [29]. Seven risk factors are identified in this model: heart rate >100, systolic blood pressure 2 comorbid illnesses. Using this data, patients are stratified into low risk (no risk factors), moderate risk (1–3 risk factors) and high risk (>3 risk factors) groups. Significant differences are shown across the three groups in need for surgery, death, length of hospital stay and quantity of transfusion. In the low-, medium- and high-risk groups, respectively, there is a

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