Occult bleeding of small bowel endovascular embolization and literature review

OpenAlex İngilizce

Occult gastrointestinal bleeding (OGIB) is defined as bleeding of unknown origin that persists or recurs after a negative initial or primary endoscopy result. It has a wide spectrum and may be acute or chronic, intermittent or continuous. Most causes of OGIB are located in the small bowel.1 Angiodysplasia is an important cause of occult as well as overt gastrointestinal (GI) bleeding, especially in the elderly. The colon, in particular the cecum, is the most common site of involvement.2 These lesions are ectatic, dilated, thin-walled vessels that are lined by endothelium, either alone or with small amounts of smooth muscle. The thin-walled vessels can rupture readily and cause bleeding.3 Endovascular embolization as a treatment of choice is also not well established in small bowel angiodysplasia in contrast to gastric and colonic angiodysplasia.4–6 In only a limited number of case reports was an endovascular embolization reported as the sole procedure or primary treatment method.7–9 The safety of this procedure for small bowel angiodysplasia remains unknown. The goal of this report is twofold: to report on the management of GI bleeding due to huge small bowel angiodysplasia by using endovascular embolization as a primary treatment method and to review the literature. A 35-year-old woman presented with GI bleeding. She had a history of chronic iron deficiency anemia over a 10-year period and no site of blood loss having been found at two previous esophago-gastro-duodenoscopies and three colonoscopies. In the previous 10 years her hematocrit (Hct) values ranged between 15% and 23%. She described chronic to intermittent blood loss, presented with brown heme-positive stools several times and massive bleeding as melena that had occurred three times. She was managed with blood transfusions (total 25 units) whenever her Hct values were under compensation levels, especially at massive melena periods. She had an uneventful medical history and was under no current medication. Capsule endoscopy revealed a mucosal reddish swelling at the distal part of the jejunum (Fig. 1). There was no evidence of active bleeding. The small intestine, distal to the angiodysplasia, was normal. Capsule endoscopy photograph revealing scattered mucosal reddish swellings without active bleeding. According to the capsule endoscopy findings and a strong suspicion of vascular malformation, the patient was referred to our clinic for diagnostic angiography and, if needed, endovascular embolization. An abdominal aortagram revealed an abnormal blush of contrast at the distal jejunal loop, consistent with a small intestinal vascular lesion (Fig. 2). A selective superior mesenteric artery (SMA) catheterization with diagnostic catheter (Sos-Omni Selective, AngioDynamics, Queensbury, NY, USA) revealed a high-flow vascular malformation (angiodysplasia) characterized by multiple dilated dysplastic arterial feeders, an intense mucosal blush and early venous filling (Fig. 3). The size of the angiodysplasia was 7 × 6 × 5 cm and the length of the involved intestinal segment was approximately 9 cm. Abdominal aortagram showing increased vascularization (arrow) suspicious for vascular malformation at the right lower quadrant. Selective superior mesenteric artery (SMA) angiogram showing angiodysplasia at the region of distal jejunal segments supplied by a branch of the SMA. The feeding arteries were superselectively catheterized using a micro-catheter (EmboCath, BioSphere Medical, Rockland, MA, USA) and microguide-wire (Segway, BioSphere Medical, Rockland, MA, USA) combination. As an embolizing agent, 500–700-µ and 700–900-µ sized microspheres (Embogold microspheres; BioSphere Medical, Rockland, MA, USA) were injected through the micro-catheter. At post-embolization arteriograms, stagnation of arterial flow and significant reduction in the filling of angiodysplasia observed; because of the risk of intestinal ischemia, embolization procedure was discontinued (Fig. 4). After embolization, a selective superior mesenteric artery angiogram shows stagnation at the arterial feeder and approximately 80% reduction of angiodysplasia filling at (a) early arterial phase; (b) late arterial phase. The patient made an uneventful recovery after the embolization, with no clinical signs of small intestinal ischemia or infarction. She was discharged after 2 days of hospitalization. Over a 12-month follow-up period after embolization she was well with no further GI bleeding, no signs of small intestinal ischemia or infarction. The repeated Hct values at 2-months intervals were between 31% and 35%. Small bowel angiodysplasias are very rare vascular lesions. Despite of their rarity, small bowel angiodysplasias are one of the most common etiologies in OGIB. The diagnosis can be made by scintigraphy, endoscopy or angiography.10 Tc-99m-labeled red blood cell scanning can often help in the localization of active hemorrhage but has no ability to determine the type of the lesion. Scintigraphy is best suited for hemodynamically stable patients who may not be actively bleeding at the time of the study.11 Push enteroscopy is likely to detect and treat vascular lesions at the proximal small bowel. Electrocoagulation in focal lesions and hormonal treatment in diffuse angiodysplasias can be performed. However, the long-term outcome is considered to be good in only 50% of the patients.12 Capsule endoscopy (CE) can detect the lesions even at distal small bowel segments. It can be performed with less technical difficulty than other endoscopic procedures. The limitations of CE include difficulty in localizing mucosal lesions, its restricted use in patients with dysphagia, strictures or motor dysfunction, and its inability to treat the lesion.13 In a recent article it was reported that the diagnostic yield of CE for the diagnosis of OGIB ranged from 39% to 77%.14 Because of the nature of angiodysplasias, to examine the entire small bowel segments, double-balloon endoscopy (DBE) and intra-operative enteroscopy are the two novel approaches that are useful for both diagnostic and therapeutic purposes.15 The most common indication of DBE is the OGIB. Severe complications like small bowel perforation and aspiration pneumonia have been reported in a few patients.16,17 Intra-operative enteroscopy is an ultimate diagnostic procedure for small bowel investigation. It enables the diagnosis and treatment of pathological findings by endoscopic or surgical means in the same session. By visualizing the mucosa, it can provide information that enables more precise surgery, thereby limiting resection. Serious GI bleeding and aorto-enteral fistula leading to death have been reported as major complications.18 Angiography has transformed the management of lower gastrointestinal bleeding. It remains the gold standard for the preoperative diagnosis and localization of the lesion. The sensitivity of angiography for the diagnosis of angiodysplasia ranges from 58% to 86% and depends on whether there is active bleeding at the time of the procedure. Extravasation of the contrast medium representing active bleeding can be demonstrated in between 6% to 20% of patients only.19 The three other angiographic signs, listed from the most common (90%) to the least (60%), and also from the early stage to the late one are as follows: first; densely opacified, dilated, tortuous and slowly emptying intramural veins; next, a vascular tuft representing dilated mucosal venules and capillaries in the arterial phase and at the latest stage, arteriovenous communication due to precapillary sphincter loss.9 Angiography also has the potential to become a therapy as well as a diagnostic tool in the treatment of vascular lesions by endovascular embolization. In the literature, data are extremely limited on the effectiveness and safety of endovascular embolization in the treatment of small bowel angiodysplasias. About 21 cases of endovascular embolization of angiodysplasias have been reported to date, most of which were performed in colonic segments. Microcoils, microspheres, polyvinyl alcohol (PVA) particles and gelfoam were used as embolic agents in the treatment.4–9 The physical and biological properties of embolic agents affect their level of occlusion, which constitutes the heart of the matter in the endovascular embolization of angiodysplasias. It is generally accepted that the recommended level of embolization is the radiological end artery just beyond the intestinal arcades of the vasa recta, while avoiding the intramural branches of the vasa recta. This allows occlusion with patency distally via collateral flow, thus avoiding distal transmural infarction. Agents or particles smaller than 100 µm, such as Gelfoam Powder (Pharmacia & Upjohn, Kalamazdo, MI, USA) PVA particles, alcohol and Ethibloc (Ethnor Laboratories/Ethicon, Norderstedt, Germany) can reach the capillary level and are thus more likely to cause significant infarction and even death.5 In contrast, it was reported that no large bowel infarction and only two cases of asymptomatic mucosal ischemia were observed in 10 patients treated with larger (100–590 µm) PVA particles for lower GI bleeding.6 To the best of our knowledge, only three cases of endovascular embolization as the sole procedure or primary treatment method in the management of GI bleeding due to small bowel angiodysplasia have been reported.7–9 Ikuta et al.8 described a case with massive bleeding from a small bowel angiodysplasia after aortic valve replacement. Emergency endovascular embolization using gelfoam was performed, and the bleeding ceased immediately. However, signs of peritonitis appeared the next morning and an emergency resection of the necrotic ileum was done. We propose that the reason for intestinal necrosis is the occlusion of intramural branches of the vasa recta because of the type and the size of the embolic agent, as discussed above. Kawamura et al.7 reported an 80-year old man with angiodysplasia in the small bowel in whom an emergency angiography revealed extravasation from a peripheral branch of the jejunal artery, in addition to tortuous and dilated ileal arteries. An embolization was performed with a micro-catheter inserted superselectively into the nearest arcade of the segmental branch of the vasa recta. After the embolization, no complications occurred. The patient was discharged and is being followed up as an outpatient. But in this article the embolic agent was not defined. Nguyen et al.9 presented an endovascular embolization of jejunal angiodysplasia with 300–500-µm sized microspheres. In this report the patient made an uneventful recovery after an embolization, with no clinical signs of small intestinal ischemia or infarction. At follow up 12 months after the embolization, he was well, with no further GI bleeding and no recurrence of anemia. In our study we attempted to embolize the huge small intestinal angiodysplasia subtotally to avoid intestinal ischemia. We preferred microspheres sized 500–700 µm and 700–900 µm to embolize the end artery just beyond the intestinal arcades of the vasa recta to avoid intestinal necrosis. Microspheres are non-resorbable embolic agent with non-aggregating property that provides complete and durable mechanical occlusion.20 Microcoils were not preferred in our case as embolic agent to avoid the occlusion of arterial access to vascular lesion for possible future endovascular interventions in the case of recurrence. In conclusion, an endovascular embolization is an effective way to control GI bleeding due to small bowel angiodysplasia. In patients with long segment involvement and younger in age, an endovascular embolization must be considered as a first-line treatment modality. It also must be kept in mind that while surgery may preclude subsequent endovascular embolization, endovascular embolization does not preclude surgery.