Jejunal diverticula bleeding: A challenging diagnosis entity

Abstract

Jejunal diverticula (JD) bleeding is an uncommon but clinically significant cause of lower gastrointestinal bleeding (LGIB), representing a diagnostic and therapeutic challenge due to its rarity, nonspecific symptoms, and frequent overlap with colonic diverticular disease. While diverticulosis predominantly affects the colon, JD—often asymptomatic—carry a higher risk of severe complications, including massive hemorrhage. This review synthesizes current evidence on the epidemiology, risk factors, pathogenesis, clinical presentation, diagnostic approach, and management of JD bleeding. Jejunal diverticulosis occurs most commonly in older patients and frequently coexists with diverticula in other segments of the gastrointestinal tract. Risk factors include age, male sex, obesity, smoking, alcohol consumption, connective tissue abnormalities, and alterations in intestinal neuromuscular performance. Bleeding results from erosion or rupture of the vasa recta running over the diverticular dome. Clinically, patients may present with painless hematochezia, anemia, or hemodynamic instability. Diagnosis is often delayed, requiring a combination of colonoscopy, computed tomography angiography, capsule endoscopy, and, in selected cases, angiography. Although most diverticular bleeding episodes resolve spontaneously, endoscopic hemostasis remains the first-line treatment when feasible, while angiographic embolization and surgery are reserved for refractory or severe cases. Early recognition and precise localization of the bleeding source are essential to reduce morbidity and mortality. This review underscores the importance of considering JD as a potential source of bleeding in patients with obscure or recurrent LGIB and highlights the need for individualized, multidisciplinary management strategies.

Key Words: Diverticula; Diverticulitis; Jejunum; Gastrointestinal bleeding; Inflammation; Pathophysiology

Core Tip: Jejunal diverticula (JD) predominantly affects older patients, with higher prevalence observed in Western populations. Most cases are discovered incidentally during imaging studies or autopsy, as clinical manifestations ranging from abdominal pain to melena are often nonspecific and may mimic other gastrointestinal conditions. The pathogenesis of JD is multifactorial, involving increased intraluminal pressure, bowel wall weakness, gut dysbiosis, low fiber intake, and possible genetic predispositions. Jejunal diverticulosis is frequently misdiagnosed due to vague presentation and diagnostic limitations. Therefore, early recognition and appropriate management are essential to reduce morbidity and prevent life-threatening outcomes.

INTRODUCTION

Gastrointestinal bleeding (GIB) is a potentially life-threatening condition that can develop anywhere in the digestive tract. It is a common cause of hospital admission, especially in older people. Thus, it demands both an accurate diagnosis and multidisciplinary management. This disorder is usually categorized as upper GIB (UGIB) or lower GIB (LGIB), depending on its location relative to the ligament of Treitz. That is, this anatomic landmark between the foregut and midgut helps distinguish between upper and LGIB. Bleeding arising from the small intestine is considered a specific anatomical hemorrhage[1]. UGIB develops proximal to the ligament of Treitz, and common clinical presentations are hematemesis or melena. In contrast, rectal maroon or red blood (hematochezia) appears in LGIB. However, clinical presentations may overlap. Accordingly, hematochezia may develop in hemodynamically unstable patients with UGIB, and bleeding arising in the right colon may appear as melena. Studies of patients with apparent LGIB have reported that in 15% of cases, the true hemorrhagic source was the upper gastrointestinal (GI) tract[2,3]. LGIB has been studied for more than 50 years. It has represented a significant diagnostic challenge for clinicians, since its earliest descriptions. This diagnostic entity (LGIB) was initially described as obscure GIB, a term that reflected the difficulty in identifying its source. It was first tailored by Jones et al[4] in 1959 and then properly studied by Thompson et al[5] in 1987.

The etiology of UGIB encompasses a wide variety of pathologies. Peptic acid disease is the leading cause, followed by esophagogastric varices and esophagitis. Other etiologies include vascular lesions, Mallory-Weiss syndrome, esophageal, gastric, and duodenal malignancies, and aortoenteric fistulas[6]. Diverticulosis, hemorrhoids, angiodysplasia, and neoplasms are the most common causes of LGIB in adults, while intussusception and infectious diarrhea are more common in children[7]. Although uncommon, GI tuberculosis (GTB) should be considered as a clinical diagnosis when studying patients with LGIB. Most recent evidence shows that GTB represents 1%-3% of all tuberculosis cases worldwide[8]. The terminal ileum and ileocecal valve are the most affected GI areas. Clinical presentation may mimic other intra-abdominal pathologies, requiring a high index of suspicion. Accordingly, some cases may present with GIB. LGIB accounts for approximately 20%-30% of all major GI hemorrhages. Incidence increases with age and overall mortality ranging from 2% to 4%[1,9,10]. Furthermore, most cases of LGIB develop in the colon and rectum. However, the small intestine is the bleeding source in a small number of cases (5%-10%), which are frequently underdiagnosed (Table 1)[11].

Table 1 Bowel diverticular disease: Clinical overview.

Study variable		Duodenum diverticula	Jejunum diverticula	Ileum diverticula	Colon diverticula
Epidemiology[14,19]	Prevalence	15%-42% (second most common in small bowel)	0.3%-2.3% (higher in Asia)	< 5% (usually jejunoileal)	30%-75% (most common worldwide)
	Age presentation	60-80 years old	Elderly patients	> 50 years old	> 60 years old
	Incidence	5%-10% (Western countries)	0.4%-4.6% (necropsy findings)	< 1%	10%-50%
Clinical presentation[29,37]		Upper GI bleeding; melena	Most commonly asymptomatic; bleeding, nausea, vomiting, diarrhea, vague abdominal pain	Hematochezia or melena	Hematochezia (90%); usually painless
Bleeding characteristics[30]		Usually mild to moderate	Often massive	Variable often self-limited	Most cases stop spontaneously
Diagnostic challenges[3]		Periampullary development	“Silent entity” if uncomplicated; Inaccessible through standard endoscopy	Site development	Intermittent bleeding
Endoscopic treatment[3,39]		60%-80% success rate	Enteroscopy useful in bleeding cases: If diagnosis is suspected	Limited data	Successful in 85%-95%
Re-bleeding rates[2]		20%-35% within 1 year	20% after initial endoscopic management	Limited data	10%-25% within 1 year

The epidemiology, clinical presentations, bleeding patterns, diagnostic challenges, and endoscopic management of diverticula throughout the gastrointestinal tract are described. Although jejunal diverticula are of low prevalence, they are of substantial clinical relevance due to their propensity for severe gastrointestinal bleeding and the diagnostic challenges related to their limited accessibility with conventional endoscopy. GI: Gastrointestinal.

Given the complex anatomy of the GI tract, the ligament of Treitz spreads from the right crus of the diaphragm to the duodenojejunal flexure. Therefore, the jejunum could be considered the origin of LGIB. However, diverticular disease of the colon is the most common cause of LGIB[12]. Thus, clinicians consider the sigmoid colon as the primary hemorrhagic source. Accordingly, study protocols almost never contemplate jejunal diverticula (JD) as the bleeding place of origin. Therefore, recurrent bleeding with ongoing transfusion requirements, upper and lower negative endoscopies and hemodynamic instability should make clinicians consider JD bleeding. Currently, the mechanisms underlying the development of JD are poorly understood but are likely to involve mechanical pressure, the microbiota, reduced fiber intake, and genetic predisposition[3,12]. Diverticula are pouches of mucosal membrane that are classified as either true or false, depending on whether the herniation involves the muscular layer[13]. False diverticula represent herniation of the mucosa and submucosa through defects in the muscularis propria at the vascular penetration site of the vasa recta[14]. Diverticula occur more frequently in the sigmoid colon of individuals in Western countries (90%), whereas the ascending colon is the most common site in individuals of Asian descent (70%)[15,16].

Diverticular disease is classified based on clinical severity. It is diagnosed as either symptomatic uncomplicated or complicated diverticular disease. Complicated cases involve acute diverticulitis and diverticular hemorrhage[17]. Diverticular inflammation is usually triggered by the obstruction of the diverticulum sac by a fecalith. This leads to mucosal injury, bacterial overgrowth, and local inflammation. This process may eventually progress to complicated diverticulitis, characterized by abscesses, fistulas, obstruction, and/or perforation[18]. However, when studying LGIB, clinicians hardly ever consider JD. In this minireview, we aim to elucidate the approach to LGIB in diverticular disease, with particular emphasis on JD. The main goal is to achieve accurate, timely management of this challenging diagnostic entity[3].

EPIDEMIOLOGY

As previously indicated, when studying patients with LGIB, diverticula are the primary etiology to consider, especially in patients over 50. Colonoscopy and sigmoidoscopy series have reported a prevalence over 70% in patients in their 80s[17,19]. JD represents a diagnostic challenge for healthcare professionals owing to infrequency and nonspecific clinical presentation. When JD develop, approximately 75%, 20%, and 15% of the cases involve the proximal jejunum, the distal jejunum, and the distal ileum, respectively. Diverticula appear simultaneously in the jejunum and ileum in 5% of cases[13-16]. These incidence rates have been reported in radiologic and autopsy series. The issue is that data on incidence and prevalence are very limited. The most recent evidence reveals incidence rates (autopsy findings and imaging series) ranging from 0.06% to 2.3%. These results raise concerns about delayed diagnosis and appropriate treatment. Autopsy series have reported an estimated general prevalence of jejunum diverticula of approximately 0.1%, with JD accounting for about 1% of all GI diverticula (Figure 1)[20,21]. Interestingly, simultaneous jejunum and colon diverticula are diagnosed in 50% of cases. Most patients remain asymptomatic, but approximately 10%-20% may develop complications such as perforation, hemorrhage, or bowel obstruction. Jejunal bleeding accounts for roughly 30% of these complications. These prevalences have been reported in upper GI roentgenologic evaluation, mesenteric arteriography, exploratory laparotomy, and incidental intraoperative findings[22]. JD disease primarily develops in older patients, with an incidence of between 0.5% and 2.3%. The prevalence is higher in Western countries, and most cases are diagnosed following incidental findings on imaging studies[23]. Age appears to be a key element, with only 1%-2% of JD occurring in patients under 30 years old. In contrast, over 63% of cases occur in patients aged 60 years or older, with a higher prevalence in females than in males. When considering colon and small bowel diverticula, the small bowel accounts for 0.3%-1.3% of cases, and 2.3% of all cases are found at autopsy. Radiologic series reveal that 80% of small bowel diverticula occur in the jejunum, 15% in the ileum, and 5% involve both segments[19,23].

Figure 1 Anatomic distribution of diverticula and site-specific bleeding incidence. Black arrows show gastrointestinal (GI) diverticula incidence. Incidence of diverticula bleeding is highlighted with a orange arrow. Jejunal diverticula accounts for a disproportionately higher bleeding rate (10%-30%). This distribution highlights the clinical relevance of jejunal diverticular disease in the assessment of unspecific GI bleeding. D: Duodenal; J: Jejunal; E: Esophageal; G: Gastric; C: Colon.

PATHOGENESIS

The pathophysiology of diverticulosis is characterized by structural alterations in the intestinal wall and neuromuscular dysfunction. Structurally, defects in collagen and elastin are observed, with excess cross-linking of collagen fibers resulting in a more rigid wall with reduced tensile strength. Additionally, elastosis in the longitudinal muscular layer contributes to wall thickening. Functionally, there is dysregulation of the nervous and motility systems due to reduced numbers of myenteric plexus neurons and key cells (myenteric glial and Cajal cells), leading to denervation hypersensitivity. These myenteric plexus and/or smooth muscle disorders play a key role in acquired pulsion diverticula on the mesenteric border. Therefore, neuromuscular dysfunction displays as uncoordinated contractions, increased bowel pressure, and muscular atrophy, being the direct cause of symptoms such as abdominal pain and cramps associated with diverticular disease. Consistently, patients often exhibit visceral hypersensitivity, and motility is affected by a significant decrease in mucosal serotonin transporter levels[15]. Diverticula develop at weak points in the bowel wall, precisely where the blood vessels that typically run outside the circular muscular layer penetrate obliquely to lie beneath the mucosa. As the diverticulum develops, the vessel is often displaced over the fundus (or dome) of the diverticulum and lies near the mucosa. Bleeding occurs due to the erosion or rupture of the straight vessels (vasa recta; Figure 2). The bleeding, unlike diverticulitis, is generally not associated with inflammation and is therefore not a characteristic sign of diverticulitis[11,16,24]. That is, diverticular bleeding may develop in the absence of inflammation.

Figure 2 Development and bleeding of gastrointestinal diverticula. Chronic intraluminal pressure at weak areas along with structural and functional alterations are key elements in gastrointestinal diverticula formation. Weak points are the areas where penetrating vessels traverse the circular muscle layer obliquely to stream within the submucosal plane. Structural alterations include abnormalities in collagen and elastin architecture, characterized by excessive collagen cross-linking, which leads to increased wall stiffness and diminished tensile integrity. Additionally, elastosis in the longitudinal muscular layer contributes to wall thickening. Bleeding occurs due to the erosion or rupture of the straight vessels (vasa recta).

Collagen in the digestive tract builds cross-links to support its structure. But excessive cross-linking can lead to stiffness and loss of tensile strength. In Caucasian men, diverticulosis has been strongly associated with single-nucleotide polymorphisms in COL3A1; which encodes vascular collagen and is linked to inflammation[25]. Furthermore, missense variants were identified in the COLQ gene in Icelandic and Danish populations. Mutations in COLQ gene can cause muscle weakness by decreasing the amount of AChE available at the neuromuscular junction, as COLQ encodes a collagen-like subunit that anchors AChE. In this context, an association between diverticulosis and mutations in the ELN gene was found. Neuromuscular performance is intrinsically linked to signaling pathways and the downstream effects of the extracellular matrix. In diverticulosis, histological staining shows an increase in collagen fibers between smooth muscle bundles, associated with decreased expression of the TACR1 and TACR2 genes, which encode the NK2 receptor. Additionally, patients with diverticular disease exhibit thicker circular and longitudinal muscle layers, an increased connective tissue index, and alterations in smooth muscle. This has been linked to a deficiency in the GDNF system, which reduces mRNA expression of SNAP-25 and GDNF. This leads to decreased immunoreactive signaling in the enteric ganglia and reduced expression of GFRα1 and rearranged in transfection (RET) tyrosine kinase receptors. Key candidate genes associated with altered neuromuscular function include ANO1, PPP1R14A, COLQ6, COL6A1, CALCB, and CALCA. Out of these, ANO1 is relevant because it modulates calcium-activated chloride channels in the interstitial cells of Cajal; thereby affecting muscle contraction (Figure 3)[15,19,24,25].

Figure 3 Biomolecular pathways involved in diverticular development. Genes associated with connective tissue laxity including BMPR1B, EFEMP1 and ELN predispose to arterial shearing at the level of the diverticulum (blue circle). Genes involved in neuromuscular dysfunction such as ANO1, PPP1R14A, COLQ6, COL6A1, CALCA and CALCB (yellow circle) regulate calcium-activated chloride channels in the interstitial cells of Cajal, thereby affecting muscle contraction. Genes linked with vascular damage and structural integrity are CALCB, COL3A1, COLQ, SLC35F3, CACNB2 and WNT4. These genes contribute to vascular smooth muscle cell proliferation, increase collagen fibers between smooth muscle bundles and reduce AChE available at the neuromuscular junction leading to muscle weakness (red circle).

The ELN, BMPR1B, and EFEMP1 genes are associated with connective tissue laxity, a factor that could predispose to the shearing of the responsible artery in diverticular bleeding. The ABO (blood group) gene, linked to the blood group system, encodes carbohydrates on the tissue surface that increase the risk of thrombosis and GI hemorrhage. Other genes associated with vascular disease, such as CALCB, SLC35F3, and CACNB2, support the hypothesis that vascular disease plays a key role in diverticulitis. Additionally, the WNT4 gene is associated with vascular smooth muscle cell proliferation, supporting the link between smooth muscle hypertrophy and atherogenesis in diverticulosis. Finally, WNT family proteins also differentiate intestinal neural and glial cells and play an anti-inflammatory role, suggesting a fundamental role for WNT genes in the development of diverticulosis and the risk of diverticular bleeding (Figure 3)[17,19]. It is important to highlight that nonsteroidal anti-inflammatory drugs (NSAIDs) can damage the GI tract via COX-dependent and COX-independent processes. NSAIDs disrupt phospholipid integrity and inhibit phosphorylation essential to maintain intestinal barrier integrity. The consequence is an increase in intestinal permeability, which promotes intestinal inflammation[26].

CLINICAL PRESENTATION

While diverticular disease is often considered asymptomatic, a significant number of patients (approximately 25%) experience persistent, non-specific symptoms such as vague abdominal discomfort, nausea, vomiting, diarrhea, flatulence, and malabsorption. More seriously, clinical complications develop in approximately 12% of cases, including perforation, bleeding (hemorrhage), obstruction, abscess, or fistula formation (Table 1)[27,28]. Although most LGIB cases originate in the colon (80%-85%), the small bowel is the cause of hemorrhage on a smaller number of cases (0.7%-9%). Although less common, JD are more prone to bleeding than colon diverticula (Figure 1)[29-36]. Diverticulosis is more common in the left side of the colon, but diverticular bleeding tends to develop more frequently in the right colon. This discrepancy is crucial for management, especially if surgery is being considered, as the precise bleeding site becomes a priority. Identifying the bleeding area appears to depend on the study protocol. Colonoscopy identifies the majority (60%) of bleeding in the left side, whereas positive angiography discovers between 50% and 90% in the right colon. A possible explanation for the higher tendency for bleeding in the right side is that diverticula in that area have wider necks and domes, which expose a greater portion of the underlying straight blood vessels to potential injury, thereby facilitating hemorrhage[7]. Diverticular bleeding is arterial, typically appears as painless hematochezia, and usually occurs from either the neck or dome of the diverticulum[3].

JD are typically a silent condition, often emerging without clear symptoms. However, they can cause chronic, non-complicated issues, including nausea, vomiting, vague abdominal pain, altered bowel habits, occasional bleeding, and diarrhea. When present, abdominal pain usually occurs in the periumbilical or epigastric region. It is often accompanied by bloating and is typically triggered by food intake. Crucially, these mild symptoms can progress to severe complications, such as bowel obstruction, severe hemorrhage, diverticulitis, perforation, and peritonitis. In fact, JD are often only diagnosed once these complications arise, with hemorrhage being the most frequently reported complication (Table 1)[37,38].

DIAGNOSIS

The diagnosis of LGIB can be made using various imaging modalities. However, studies suggest a better diagnostic and therapeutic yield with colonoscopy as compared to radiographic methods. This is based on the fact that colonoscopy can be both diagnostic and therapeutic in real-time, even when there is no active bleeding at the time of the exam. However, profuse and continuous hematochezia is a limiting factor for adequate hemodynamic resuscitation and bowel preparation before the study. Following initial resuscitation, the diagnosis and subsequent treatment of LGIB continues to be a difficult task for clinicians. Accurately “pinpointing” the bleeding source is a clinical priority, and this process is often more challenging than identifying the origin of UGIB. The primary diagnostic procedures used are flexible sigmoidoscopy and colonoscopy, which also provide a route for endoscopic treatment (Figure 4)[2]. These primary procedures for general LGIB are supported on epidemiological clinical presentations. In cases where the source of diverticular bleeding is associated with JD, some authors recommend alternative diagnostic procedures. These involve barium contrast study of the small intestine, capsule endoscopy and, less frequently, intravenous and oral contrast computed tomography (CT) scans[14]. The video capsule endoscopy is a novel non-invasive diagnostic alternative that allows the entire small intestine to be explored in 79%-90% of patients. Its benefits have been described in patients with obvious, dark bleeding who have had negative results from upper and lower GI endoscopy, with a sensitivity of 87%-91.9%. Disadvantages include the fact that this endoscopic technique is only diagnostic, and capsule retention has been reported in 2% of patients undergoing study for small bowel bleeding[2]. When upper and lower endoscopies are negative, capsule endoscopy has a central role in the study of LGIB (Table 2).

Figure 4 Diagnostic pathways for patients with suspected jejunal diverticular bleeding. For patients without an emergent clinical presentation, in-hospital observation may be adequate. However, in cases of hemodynamic instability or ongoing hemorrhage, expeditious diagnostic assessment based on clinical urgency is imperative. When upper and lower endoscopies are negative, capsule endoscopy has a central role in the study of lower gastrointestinal bleeding. Once the diagnosis is established, endoscopic management should be pursued as the first-line therapeutic approach. U & L: Upper and lower; GI: Gastrointestinal; CT: Computed tomography.

Table 2 Diagnostic modalities in lower gastrointestinal bleeding.

Diagnostic modality	Advantages	Disadvantages	Cost-effectiveness
Colonoscopy[2]	Diagnostic and therapeutic tool	Requires bowel preparation Limited in massive active bleeding	High cost-effectiveness due to therapeutic capability
Flexible sigmoidoscopy[3]	Rapid bedside evaluation; minimal preparation	Limited to distal colon	Only in selected cases with suspected distal anorectal pathology
CTA[3]	More widely available and better accuracy in identifying the bleeding site with almost 100% accuracy; high sensitivity (79%-95%) and specificity (95%-100%)	Requires contrast; risk of nephropathy; contrast dye allergic reaction; non-therapeutic	High as initial imaging before angiography or surgery
Catheter angiography[2,3]	Diagnostic[18] and therapeutic; identifies the bleeding source in 25%-70% of the cases	Invasive; risk of bowel ischemia (30%)	Moderate
Technetium-99m-tagged red blood[1] cell scintigraphy[2,3]	Reveals intermittent bleeding Non-invasive	Low spatial resolution; may not precisely locate accurate bleeding site	Moderate
Video capsule endoscopy[2]	Non-invasive diagnostic alternative that allows the entire small bowel to be explored in 79%-90%	Only diagnostic; risk of capsule retention in 2% of patients undergoing study for small bowel bleeding	Low
Barium small bowel study[2]	Identifies structural abnormalities	Low sensitivity in active bleeding	Low

CTA: Computed tomography angiography.

In patients with an acute clinical presentation, angiography is recommended to establish the diagnosis and guide treatment. It is estimated that this study identifies the bleeding source in 25%-70% of the cases. Super-selective angiographic embolization has been reported to achieve hemostasis in 40%-100% of diverticular bleeding cases. However, intestinal ischemia has been reported as a serious complication in one third of patients undergoing this study. Therefore, this diagnostic modality should be preferred in patients with profuse, continuous active bleeding, where it provides greater benefit, with consideration of potential complications. Diverticular bleeding accounts for a significant number of severe cases of LGIB, with up to 60% being classified as severe. Notably, it is the most common indication for mesenteric embolization in LGIB. Following diverticular bleeding, the next most common diagnoses are benign anorectal conditions, which include issues such as hemorrhoids, anal fissures, and rectal ulcers[2,3].

Other radiographic modalities for acute GIB include Technetium-99m-tagged red blood cell scintigraphy and CT angiography (CTA). Tagged red blood cell scintigraphy is considered to increase the diagnostic yield of angiography by allowing targeted contrast injection at the bleeding site. However, the ability to detect the bleeding site is considered suboptimal, as it only reaches a sensitivity of 65%-80% and must be confirmed with certainty prior to surgical resection. Among the advantages of this imaging modality is the ability to repeat the study by performing multiple scans to identify the bleeding site after red blood cell tagging. This protocol can be used for intermittent or non-profuse bleeding or for cases demanding early treatment. CTA or multi-detector CT scan is more widely available and has better accuracy in identifying the bleeding site with almost 100% accuracy. Sensitivity and specificity that have been reported fluctuate between 79%-95% and 95%-100%, respectively. Therefore, CTA is a reasonable first-line screening test if needed prior to angiography or emergency surgery, as it is faster and more accurate than tagged red blood cell scintigraphy (Figure 4). Standard precautions should be considered to avoid contrast-induced nephropathy, especially since patients may undergo subsequent angiography with arterial contrast administration[2,3].

MANAGEMENT

It has been reported that between 75% and 90% of cases with diverticular bleeding are self-limiting. That is, they solve spontaneously. Therefore, surgical resection is not recommended for asymptomatic diverticular disease, including ileal and JD[7,14]. Endoscopic treatment alternatives for diverticular bleeding that reduce recurrence and its complications include colonoscopy, injection therapy with epinephrine, endoscopic clipping (through-the-scope and over-the-scope), thermal therapies such as bipolar coagulation or argon plasma coagulation, and endoscopic band ligation, endoloops, or hemostatic powders (Figure 5). According to studies by the Center for Ulcer Research and Education Hemostasis Group, urgent colonoscopy is recognized as the gold standard for diagnosing diverticular hemorrhage (Figure 4)[2]. The diagnosis relies on finding some stigma of recent hemorrhage in a single diverticulum. The role of standard colonoscopy during initial workup of LGIB is mainly to exclude colonic bleeding sources. However, device-assisted enteroscopy (single of double-balloon) or intraoperative enteroscopy are fundamental for direct therapy[2,3,39].

Figure 5 Endoscopic management algorithm for diverticular bleeding. When the bleeding source is identified, appropriate endoscopic hemostatic modalities should be promptly implemented in accordance to the bleeding characteristics. In cases in which the bleeding site cannot be identified or endoscopic hemostasis fails, treatment escalation should not be delayed, and angiographic or surgical management must be considered based on clinical severity.

Due to the risk of delayed perforation induced by diathermy in a thin-walled colon, non-thermal strategies such as clipping, ligation, or hemostatic sprays, often combined with adrenaline injection, are preferred. If adherent clots are observed during endoscopic exploration, a 1:20000 epinephrine injection (1-1.5 cc) should be administered on or around the bleeding spot. This approach has been shown to provide short-term control of arterial hemorrhage while reducing rebleeding rates. Subsequently, a hemoclip or multipolar electrocoagulation can be used to achieve definitive hemostasis. For routine management of diverticular bleeding via colonoscopy, it is advised to use multipolar electrocoagulation (coaptive coagulation), if the lesion is located at the neck of the diverticulum. While hemoclips should be used if the bleeding site is located at the base of diverticulum to achieve mechanical closure of the artery. In these cases, Doppler probe endoscopy is useful because it allows confirmation of underlying arterial flow occlusion, thereby improving the likelihood of achieving thorough hemostasis. Bleeding reappearing within 30 days has been associated with several risk factors. Some of these are: Applying endoscopic therapy away from the actual bleeding site (e.g., at the neck instead of the base), the persistence of arterial blood flow after visually guided hemostasis, using only drug therapy without endoscopic intervention, and restoring anticoagulant and/or antiplatelet drug therapies early in the process. To ensure a successful and definitive endoscopic diagnosis and treatment of diverticular hemorrhage, it is crucial to achieve all: An excellent bowel preparation, organize specialized hemostatic equipment, and master the stigmata and diverticular arterial vasculature (Figure 5)[3,39,40].

High technical success rates have been reported (93%-100%) with the use of angiography. This procedure can demonstrate active extravasation and embolization can be performed. However, embolization carries the most frequent serious risk of bowel ischemia (7%-24%) and a variable short-term rebleeding rate (10%-50%). Unfortunately, no studies have compared angiography and endoscopic management. This means that the final choice relies on patient factors, local medical experience, and available resources. Lastly, emergency laparotomy and subtotal colectomy are reserved for cases of acute GI hemorrhage that have failed interventional treatments, or in rare situations where surgery is directly justified. However, a high morbidity and mortality have been reported in cases whose bleeding source has not been identified[2]. Therefore, surgery should be avoided (if possible) in these cases.

CONCLUSION

Accurate anatomical localization of diverticula throughout the GI tract is of paramount importance to achieve a precise and timely clinical diagnosis. Diverticula outside the colon (i.e., extracolonic diverticulosis) frequently pose a significant diagnostic and therapeutic challenge, demanding a highly individualized management protocol for each patient. Consequently, healthcare practitioners must develop a comprehensive understanding of the diverse phenotypic manifestations of this condition. This knowledge is crucial for optimizing patient care delivery and achieving favorable clinical outcomes. Prompt identification and expeditious therapeutic intervention are directly correlated with improved patient prognosis, leading to a consequential reduction in morbidity and mortality.