This article provides an overview of the evaluation and management of lower gastrointestinal bleeding (LGIB) in children. The common etiologies at different ages are reviewed. Conditions with endoscopic importance for diagnosis or therapy include solitary rectal ulcer syndrome, polyps, vascular lesions, and colonic inflammation and ulceration. Diagnostic modalities for identifying causes of LGIB in children include endoscopy and colonoscopy, cross-sectional and nuclear medicine imaging, video capsule endoscopy, and enteroscopy. Pre-endoscopic preparation and decision-making unique to pediatrics is highlighted. The authors conclude with a summary of current and emerging therapeutic hemostatic techniques that can be used in pediatric patients.
Key points
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Common causes of significant lower gastrointestinal bleeding (LGIB) in children are often different from those seen in adults.
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Endoscopy and colonoscopy are the mainstays of initial diagnostic testing in most children with LGIB.
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In the absence of an endoscopic diagnosis, other diagnostic modalities may be used, with varying degrees of diagnostic yield depending on the clinical scenario.
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The pediatric gastroenterologist is well served in becoming familiar with available hemostatic tools for small-diameter endoscopes, as well as developing comfort in performing at least 2 modes of therapeutic technique.
Introduction
Gastrointestinal (GI) bleeding in children, although uncommon, can be life threatening. Lower GI bleeding (LGIB) in pediatric patients occurs less commonly then upper GI bleeding (UGIB). However, its presentation often demands a similar degree of urgency. Causes of LGIB can run the gamut of severity from benign conditions such as anal fissures to an exsanguinating lesion, for example a vascular anomaly, and therefore deserves a careful yet expedient approach. This article reviews definitions and important causes of LGIB in children that typically require endoscopic knowledge and skill for diagnosis. We also discuss approaches to the management of LGIB from initial evaluation through definitive endoscopic therapies.
Introduction
Gastrointestinal (GI) bleeding in children, although uncommon, can be life threatening. Lower GI bleeding (LGIB) in pediatric patients occurs less commonly then upper GI bleeding (UGIB). However, its presentation often demands a similar degree of urgency. Causes of LGIB can run the gamut of severity from benign conditions such as anal fissures to an exsanguinating lesion, for example a vascular anomaly, and therefore deserves a careful yet expedient approach. This article reviews definitions and important causes of LGIB in children that typically require endoscopic knowledge and skill for diagnosis. We also discuss approaches to the management of LGIB from initial evaluation through definitive endoscopic therapies.
Definitions
LGIB can be acute or chronic, and assumed to be originating distal to the ligament of Treitz at the duodenojejunal junction, which marks the anatomic transition between the upper and lower GI tract. Acute LGIB is loosely characterized as active bleeding of less than 3 days’ duration accompanied by anemia, hemodynamic compromise, altered consciousness, or the need for a blood transfusion. In adults, at least 10% to 20% of GI bleeding is thought to occur from colonic and rectal sources, with diverticulitis considered the most common cause of clinically significant bleeding in adults. In contrast, colonic diverticulitis is an extremely rare condition in children. The most common causes of LGIB in children include anal fissures, allergic colitis, enteric infections, and juvenile polyps.
Determining the source of either an upper or lower GI bleed is aided by accurate characterization of the appearance of stool during the bleeding event. In addition, it may be helpful to document the presence or absence of hematemesis, which is usually associated with bleeding proximal to the ligament of Treitz. Melena is stool that can be described as dark and sticky, like “tar,” and usually represents the end-product of blood after traveling from the upper or middle digestive tract. Occasionally, bleeding from the proximal colon can appear melanotic. In contrast, hematochezia describes bright red blood per rectum, which often arises from the distal colon or rectum.
However, these stool patterns must be interpreted with caution, because profuse bleeding from the upper GI tract can appear as hematochezia, especially in younger patients with shorter intestinal transit times. Even in adult populations, up to 11% of patients with hematochezia were found to have an upper intestinal bleeding source. This phenomenon is likely also because blood is a cathartic and any source of active bleeding can cause frequent loose melena or hematochezia. Furthermore, subjective variability in interpretation of stool color exists, although this can be minimized by using a standardized stool color card, which has been shown to aid in distinguishing upper (2 darker colors) from lower (2 brightest red colors) sources of GI bleed.
Epidemiology
In the adult literature, UGIB is thought to occur at least 5 times as frequently as LGIB. In addition, the incidence of LGIB increases with age, reflecting its association with the onset of common conditions such as diverticulitis and angiodysplasia. There is a paucity of data in the literature concerning the epidemiology of GI bleeding in childhood. A nationwide emergency department database analysis from 2006 to 2011 identified just fewer than 450,000 pediatric emergency department visits (ages birth to 19 years, with a median age of 9 years) to be associated generally with GI bleeding, of which UGIB accounted for 20% and LGIB for 30%. Patients who were aged 15 to 19 years accounted for 40% of encounters, whereas patients aged 0 to 5 years comprised 38% of the total number of GI bleeding visits. This large dataset review also detected an increase in visits for GI bleeding during the study period from 82.18 per 100,000 children in 2006 to 93.93 per 100,000 in 2011. The greatest increase in encounters was seen in LGIB in patients 10 to 19 years old. Interestingly, 83% of children did not have other medical comorbidities. In multivariable logistic regression analysis, the investigators identified the following factors to be associated with increased risk of pediatric hospital admission for GI bleeding:
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Presence of ≥3 comorbid conditions (odds ratio [OR] 112.2)
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Presentation to a teaching hospital (OR 3.2)
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Occurrence of UGIB (OR 3.1)
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Age younger than 5 years (OR 1.3)
Mortality rates from LGIB in the adult literature are less than 5%, and some reports are as low as 0.6%. Recurrent bleeding occurs in 10% to 20% of LGIB, depending on the etiology and use of definitive therapy. The use of nonsteroidal anti-inflammatory drugs (NSAIDs) has been associated with an increased risk of rebleeding.
Clinical presentation and course
Adult patients with LGIB may present with less hemodynamic instability than with UGIB, and demonstrate spontaneous resolution in up to 80% of cases. However, this “truism” has not been replicated in studies of children. It is likely that children follow a similar course, as common causes of pediatric LGIB, such as milk protein colitis and juvenile polyps, are unlikely to cause prolonged and severe bleeding. Regardless of etiology, 3 parameters that may predict severe LGIB at time of initial presentation to an emergency department include initial hematocrit less than 35%, abnormal vital signs after the first hour, and gross blood on initial rectal examination. In pediatrics, the age of the patient is one of the most important factors in narrowing the etiology of LGIB at presentation ( Table 1 ). This article highlights some of the causes affecting the lower GI tract that are particularly amenable to endoscopy for diagnosis and therapy.
| Severity | Infant | Child | Adolescent |
|---|---|---|---|
| Often mild bleeding | Anal fissure Dietary protein allergy Vitamin K deficiency Lymphoid nodular hyperplasia | Anal fissure Infectious colitis Polyp: juvenile or syndromic IBD SRUS | Infectious colitis Anal fissure Hemorrhoids SRUS |
| Often moderate to severe bleeding | Necrotizing enterocolitis Hirschsprung enterocolitis Malrotation with volvulus Duplication cyst Vascular malformation | Meckel diverticulum Henoch-Schönlein purpura Hemolytic uremic syndrome Duplication cyst Vascular malformation Intussusception Typhlitis/neutropenic colitis Dieulafoy lesion | NSAID enteropathy IBD Vascular malformation Meckel diverticulum |
Etiology
Solitary Rectal Ulcer Syndrome
The prevalence of solitary rectal ulcer syndrome (SRUS) in children is unknown. Nevertheless, delay in diagnosis is common, indicating SRUS may be more common than currently suspected. The condition usually presents with a constellation of symptoms that include rectal bleeding, mucous discharge, constipation with prolonged straining, tenesmus, and lower abdominal and/or perianal pain. Anemia is unusual in SRUS, unless the diagnosis is delayed.
SRUS results from asynchronous contraction of the pelvic floor and external anal sphincter muscles, leading to high intrarectal voiding pressures, which induces anterior rectal wall prolapse and ischemic changes. If the process exists long enough, ulcer formation occurs. However identifying an ulcer on colonoscopy is not required for the diagnosis.
Endoscopic findings vary greatly, including nodularity, erythema, exudate, sessile or pedunculated polypoid lesions, frank ulceration, or may be normal. The visualized lesion may be single or multiple, in any shape or size. Most often, SRUS is found on the anterior rectal wall within 5 to 10 cm of the anal verge. Obtaining multiple mucosal biopsies is essential even when minimal to no macroscopic findings are found, as histology is the gold standard for diagnosis. Histology of SRUS includes a thickened mucosal layer with smooth muscle bundles extending between the crypts, crypt architectural distortion, muscularis mucosae hyperplasia, and fibromuscular obliteration.
There are several methods of treatment depending on the severity with variable outcomes. Conservative management includes laxatives, steroid and mesalamine enemas, and defecation biofeedback therapy, the latter of particular importance in children who can cooperate with behavioral modification. Endoscopic steroid injection and excisional surgery of the lesion have been used in cases resistant to conservative treatment. Endoscopic therapy with argon plasma coagulation (APC) has been used with some promise ( Fig. 1 ). In a randomized controlled trial, 24 adult patients received biofeedback therapy, increased fiber intake, and laxatives, or the same regimen with several sessions of APC, with improved outcomes in those receiving APC therapy. Further pediatric studies are needed to better determine the utility of APC in refractory cases of SRUS in children.
Polyps and Postpolypectomy Bleeding
Bleeding from polyps is described in pediatric patients of all ages, but is most commonly associated with juvenile polyps in children younger than 5 years. Juvenile polyps are hamartomatous lesions with little malignant potential. Other polyposis syndromes can present in childhood, including juvenile polyposis syndrome, PTEN hamartoma tumor syndromes (Cowden syndrome, Bannayan-Riley-Ruvalcaba syndrome), Peutz-Jeghers syndrome, familial adenomatous polyposis syndromes, and hereditary nonpolyposis colorectal cancer. Each GI polyposis syndrome must be monitored and surveyed according to available detailed guidelines.
Colonoscopy is the most useful tool for diagnosis and treatment. A complete colonoscopy is necessary to thoroughly identify all polyps because they can be found proximal to the rectosigmoid colon in 35% of children with juvenile polyps. Most polyps in children are pedunculated ( Fig. 2 ) and amenable to polypectomy using a snare wire loop passed through the colonoscope working channel, coupled with electrocautery. A juvenile polyp is typically 1 to 3 cm or smaller, with a smooth or “chicken-skinned” red surface. Peutz-Jeghers syndrome polyps can be sessile or pedunculated with a lobulated surface. Tubular adenomas are typically pedunculated with smooth red surface, whereas villous adenomas are often sessile and broad based.
Each polyp type has distinct histologic characteristics, therefore polyp retrieval is important for pathologic analysis, especially to investigate its malignant potential. Intraprocedural bleeding after polypectomy can be controlled using hemostasis techniques, including clips, thermocoagulation, and detachable loop snares. In a study of 83 children with juvenile polyps, postpolypectomy bleeding occurred in 10%, and only 2 patients required endoscopic hemostasis for severe bleeding.
Dieulafoy Lesion
A Dieulafoy lesion is a rare but potentially life-threatening cause of LGIB that can be found in children. It is a vascular abnormality that involves a large tortuous submucosal artery that reaches the mucosa without tapering its size. The theorized pathogenesis involves an ulcer that forms at the site of the exposed artery secondary to its pulsations on the surrounding tissue, and eventually the vessel ruptures into the lumen. Clinically, a Dieulafoy lesion presents with intermittent and painless gastrointestinal bleeding, which can be hematemesis, melena, or hematochezia depending on anatomic location. Key elements to the diagnosis and management of a Dieulafoy lesion include the following:
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Most are found in the upper GI tract, with fewer than one-third of lesions found in the colon, with an absence of mucosal inflammation surrounding the artery.
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An actively spurting pulsatile arteriole from a mucosal defect with normal surrounding mucosa is characteristic. A dense clot with a narrow point of attachment to a mucosal defect may be found.
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A colonic Dieulafoy lesion may rupture due to stercoral ulceration over an abnormally dilated submucosal arterial vessel.
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Endoscopy is the first-line diagnostic and therapeutic modality, with angiography reserved for endoscopic failure to localize or treat the lesion.
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Combination therapy with epinephrine injection followed by clip or band ligation has been shown to achieve permanent hemostasis in 95% of cases.
Angiodysplasias and Other Vascular Anomalies
The term angiodysplasia refers to a vascular ectasia manifesting as a thin-walled, dilated, punctate red vascular structure in the bowel mucosa or submucosa. It is most often found in the left colon or terminal ileum. Therefore, detection necessitates a complete colonoscopy that reaches the terminal ileum, and enteroscopy should be considered for more proximal lesions. Diagnosis of angiodysplasia can be made by cross-sectional imaging modalities, such as computed tomography angiography (CTA), or directly by colonoscopy. The preferred endoscopic treatment is by thermoablation or APC. Angiodysplasia often recurs despite treatment due to incomplete treatment or a newly developed lesion.
Vascular malformations can present as nonisolated syndromic conditions at any age in childhood; each syndrome has a different endoscopic appearance in the bowel.
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Osler-Weber-Rendu syndrome: widespread or multiple capillary malformations similar to angiodysplasias (also called hereditary hemorrhagic telangiectasias [HHT]).
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Klippel-Trénaunay syndrome: confluent bluish vascular discoloration from anus extending proximally.
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Blue rubber bleb nevus syndrome (BRBNS) ( Fig. 3 ): small, multifocal, well-circumscribed and demarcated venous malformations throughout the bowel. This lesion is pathognomonic for BRBNS.
Fig. 3
Blue rubber bleb nevus syndrome.
Management of vascular malformations includes therapeutic hemostasis to temporize significant acute or chronic bleeding, as well as surgical therapy. Medical therapy with sirolimus is now a promising treatment option for children with BRBNS, in addition to endoscopic and surgical approaches. In adults with HHT, successful medical therapy has been reported with bevacizumab, a vascular endothelial growth factor inhibitor, which may represent a future treatment option for children with this syndrome.
Ileocolonic Ulceration
Infectious colitis
Infections with parasites, such as Entamoeba histolytica , and bacteria, such as Clostridium difficile, Shigella, Salmonella, Escherichia coli , and Campylobacter , can infect immune competent hosts, with varying degrees of colitis and ulceration detected macroscopically and microscopically. Treatment is typically supportive care or antimicrobial agents depending on pathogen and host comorbid conditions. In the immune-compromised patient, particular pathogens such as Cryptosporidium and Cytomegalovirus (CMV) should be considered; CMV is of particular importance in children with inflammatory bowel disease (IBD).
Endoscopic appearance of CMV infection can include diffuse colitis, only discrete ulcerations, or both ( Fig. 4 ). CMV ulcers are often larger than 1 cm; can be round, oval, or irregular in shape; and with or without circumscribed boarders. The diagnosis of CMV colitis can be made by endoscopic mucosal biopsy with routine hematoxylin and eosin staining, tissue CMV polymerase chain reaction, or viral culture. Treatment is with antiviral medications such as ganciclovir or foscarnet.
Inflammatory bowel disease
IBD often presents with LGIB and has a distinct mucosal pattern. Colonoscopic appearance in Crohn disease is characterized by variable degree of aphthous ulceration and sometimes luminal narrowing, whereas ulcerative colitis is characterized by diffuse erythema, loss of vascular markings, friability, erosions, ulcers, and spontaneous bleeding. In the setting of acute severe ulcerative colitis, complete colonoscopy may incur increased risk of excess bleeding, as well as perforation. At the least, flexible sigmoidoscopy in the setting of acute severe colitis can contribute to diagnostic clarification and to evaluate for infection, such as CMV. Endoscopic hemostasis is rarely necessary for bleeding secondary to IBD colitis; rather, anti-inflammatory therapy to heal the mucosa is critical to resolution of ongoing bleeding.
Anastomotic ulceration
Postoperative anastomotic ulcers (AUs) are a complication after bowel resection and reanastomosis, and occur more in children than adults. Bleeding from these ulcers can be occult or life threatening, and should be suspected in any patient with history of previous bowel surgery. In a multicenter study of 11 children over 22 years, congenital bowel malformations and necrotizing enterocolitis were the most common initial underlying reason for bowel resection, and there was a median delay of nearly 4 years from onset of symptoms to diagnosis of AU.
Endoscopic features of AU include round 1-cm to 3-cm ulcers surrounded by normal mucosa at the proximal or distal side of the anastomosis. If therapeutic endoscopy is performed, rebleeding risk within 30 days may be less with hemoclips compared with injection and thermocoagulation. Some patients will require surgical resection of the AU.
Graft-versus-host disease
Gastrointestinal graft-versus-host disease (GVHD) can develop 3 or more weeks after hematopoietic stem cell transplantation. When present, rectal bleeding can be life threatening, and is often accompanied by diarrhea, abdominal pain, nausea, and vomiting. Sometimes a fleshy material can be excreted from the rectum in severe cases, recognized as a “colon cast.” In children with significant diarrhea with or without LGIB, sigmoidoscopy with biopsy alone (avoiding upper endoscopy) is usually sufficient for diagnosis. Endoscopic appearance can be normal, or have nonspecific findings of erythema, edema, erosions, and ulceration.
Because the diagnosis of GVHD relies on obtaining biopsies, attention must be paid to correcting coagulopathy and thrombocytopenia before the procedure as needed. Medical therapy of the underlying GVHD is preferred when possible, although at times a focal bleeding lesion requires endoscopic therapy. A therapeutic procedure in the setting of GVHD should be performed by an experienced endoscopist and used with caution given potentially higher risks of bleeding or perforation.
Heterotopic gastric mucosa
Heterotopic gastric mucosa (HGM) in the rectum is a rare etiology of LGIB, due to hydrochloric acid secretion leading to ulceration of surrounding rectal mucosa. Unlike Meckel diverticulum, the rectal bleeding from heterotopic rectal gastric mucosa can be painful. Scintigraphy should identify HGM in the rectum and elsewhere if present. Surgical excision is often required, but endoscopic treatment has been attempted.
Stercoral ulcer
Stercoral ulcer is thought to develop secondary to impacted feces causing pressure necrosis of the bowel wall with a significant risk of perforation. Although it usually occurs in elderly patients with a history of chronic constipation, it also has been described on rare occasion in children, especially when vascular perfusion is compromised. Clinical presentation involves significant lower abdominal pain with hematochezia. The rectosigmoid colon with relatively poor blood supply and harder stool consistency is the typical location. Endoscopically, an irregular ulcer that conforms to the contours of the impacted stool can be found. Endoscopic hemostasis using thermocoagulation and injection therapy has been successful, with surgery reserved for uncontrollable bleeding.
Severe Upper Gastrointestinal Bleeding
Extensive bleeding proximal to the ligament of Treitz can cause melena or hematochezia without hematemesis. Life-threatening etiologies of UGIB that may present with LGIB that should be considered in every child include esophageal variceal bleeding and aortoesophageal fistula secondary to button battery ingestion. A more detailed description of the differential diagnosis and management of UGIB can be found elsewhere (discussed by Lirio (Management of Upper Gastrointestinal Bleeding in Children: Variceal and Nonvariceal) elsewhere in this issue).
Evaluation and resuscitation
The initial evaluation and resuscitation of a child with LGIB occurs simultaneously at presentation. A targeted history and physical examination ( Box 1 ) attempt to identify the cause of bleeding and location within the GI tract, whereas evaluation of hemodynamic status and initial laboratory tests further guide the clinician to the severity of the bleed. Clinically based scoring systems to evaluate the severity of bleed and need for endoscopic intervention in LGIB have not been developed as rigorously as in UGIB.
Targeted history
Hematochezia versus melena
Fatigue, dyspnea, orthostatic changes, syncope
Previous gastrointestinal bleeding, recent polypectomy, or other procedures
Comorbidities: liver disease, inflammatory bowel disease, bleeding diathesis, previous intestinal surgery
Medications: antithrombotics, nonsteroidal anti-inflammatory drugs, aspirin
Foreign body ingestion
Vital signs
Tachycardia
Hypotension
Physical Examination
Head, ears, eyes, nose, and throat: sclera icterus, lip pigmentation, petechiae, trauma
Cardiovascular: murmur, capillary refill, extremity perfusion
Abdominal: tenderness, distension, ascites, hepatosplenomegaly
Rectal: gross blood, fissures, fistulae
Skin: vascular malformations/hemangiomas, jaundice, pallor
Laboratory evaluation
Complete blood count
Prothrombin time/international normalized ratio, partial thromboplastin time
Complete metabolic panel
Blood type and cross match
Resuscitation measures
Crystalloid
Blood products
Vasoactive medications
As a first time bleeding episode in childhood may herald the presentation of a congenital or genetic condition, family history of IBD, polyposis syndromes, liver diseases, and bleeding diatheses should be inquired. For toddler and adolescent-age patients, accidental or intentional ingestions of foreign bodies or medications belonging to family members living in the same household may be useful information to investigate. Commonly ingested substances that may color the stool red (fruit punch, beets, candies) or black (licorice, blueberries, spinach, iron) and lead to false report of LGIB may be inquired in the very well-appearing child with no identifiable abnormality.
Once an endoscopic evaluation is determined likely, nasogastric tube (NGT) placement to obtain a gastric aspirate should be considered, particularly in those with hemodynamic instability who may have severe UGIB presenting with blood per rectum. This practice is a debated one without clear evidence to standardize its use. Cuellar and colleagues evaluated 62 adult patients accounting for 73 GI bleeding episodes and found an NGT aspirate appearance had a sensitivity and specificity of 79% and 55%, respectively, for determination of active UGIB, leading the investigators to conclude this practice is not supported. There are no studies evaluating the relationship between the volume of saline infused into the stomach to clear an initial bloody aspirate, and the likelihood of needing endoscopic intervention. Ultimately, a case-by-case approach for using NGT aspirate to guide therapy is needed that also accounts for the age and developmental status of the patient, as some children will become intensely agitated with this maneuver, making resuscitation more difficult.
Diagnostic assessment
Following the initial evaluation and resuscitation, one must determine if an endoscopic procedure or imaging study will be performed to further localize the bleeding source. Various algorithms for adult patients have been previously published. In children, there are multiple suitable approaches as well. In the pediatric patient with moderate to severe bleeding suspected to be from a lower intestinal source (eg, no hematemesis, stigmata of portal hypertension), the authors’ approach is often to consider the presence or absence of pain in the decision process ( Fig. 5 ).
Additionally, as blood and stool pass per rectum, it is often prudent to collect samples for infectious testing, particularly in the setting of fever or overt diarrhea. Results of tests for Clostridium difficile and a culture for pathogenic bacteria will have delay of hours to days and directly affect treatment.
Endoscopy
The initial diagnostic tests for identification of the bleeding source is typically esophagogastroduodenoscopy (EGD) and colonoscopy given the therapeutic potential; the decision of which to perform first will depend on the degree of suspicion for an upper GI source based on history and/or positive aspirate for blood from NGT lavage.
Colonoscopy has a diagnostic yield between 48% and 90% in the setting of LGIB. Performing only sigmoidoscopy may obviate the need for complete bowel preparation, but has a much lower diagnostic yield of 9%, making this a less-appealing initial approach if a complete colonoscopy is feasible. If an EGD and colonoscopy (after bowel preparation) fail to identify the bleeding source, a small bowel source of bleeding should be sought. The utility of a repeat colonoscopy to evaluate for a missed lesion is likely very low.
Technetium-99 Pertechnetate Disodium Scintigraphy (Meckel Scan)
Hemorrhage from a Meckel diverticulum with HGM should be considered early in the course of diagnostic evaluation of children. Depending on the timing between initial presentation and feasibility to complete a bowel preparation, a Meckel scan could be considered before colonoscopy, particularly in young children with painless bleeding. The test can identify HGM throughout the bowel, such as in a duplication cyst. An important limitation of scintigraphy is the sensitivity of 60% and negative predictive value of 76%, although the sensitivity may increase to 87% with use of ranitidine before the scan. Even with premedication, a negative Meckel scan does not rule out the possibility of HGM.
Technetium-99–Labeled Red Blood Cell Scan (Nuclear Bleeding Scan)
A nuclear bleeding scan may noninvasively identify the bleeding location within the GI tract. It requires a brisk bleeding rate greater than 0.1 mL/min, and therefore is not appropriate for occult obscure GI bleeding. Images are obtained frequently in the first few hours (dynamic phase) and again every few hours up to 24 hours after injection of the tagged red blood cells (delayed phase). The bleeding scan may become positive only in up to 73% of patients in the delayed phases, highlighting the utility to complete both phases. However, in a study of 23 scans performed in children, the bleeding scan had an overall sensitivity of 39% and only the scans positive in the first 2 hours highly correlated with correctly identifying the location of the lesion. A bleeding scan is often used as a second-line test if other methods of investigation fail to localize the bleeding site.
Angiography: Mesenteric and Radiologic
Direct mesenteric angiography also requires a brisk bleeding rate of 0.5 mL/min or more. The specificity is 100%; however, the sensitivity is variable depending on multiple factors, including the skill of the interventional radiologist. A sensitivity of 30% to 47% was found in one study that included 44 adults with acute bleeding. The therapeutic potential is only for arterial sources of bleeding, which can be directly accessed for embolization. Additional therapeutic benefits include preoperative coil placement in or near the bleeding location for easier identification at time of surgery ( Fig. 6 ). There are major potential risks of mesenteric angiography, including femoral artery thrombosis and bowel ischemia, which limit its use as a first-line diagnostic modality.
