Endovascular management of hemosuccus pancreaticus secondary to splenic artery pseudoaneurysm: a case report

Introduction

Hemosuccus pancreaticus (HP) is a rare, yet potentially life-threatening gastrointestinal emergency, accounting for 1 in 1,500 cases of upper gastrointestinal bleeding (1). The etiology of HP is multifactorial, with the primary causes including pancreatitis, pancreatic tumors, trauma, vascular abnormalities, and iatrogenic injuries (2). Due to the absence of specific clinical manifestations, HP is frequently misdiagnosed or remains undetected. Although rare, HP can result in severe clinical outcomes, with studies indicating that the mortality rate may be as high as 90% if left untreated (3).

Although splenic artery pseudoaneurysm (SAP) is the most common visceral pseudoaneurysm, its overall incidence remains low (4,5). The primary etiology of SAP is pancreatitis (acute or chronic) (6). SAP is a high-risk vascular lesion prone to rupture, with a reported rupture risk of 37–47%. Ruptured SAP carries a mortality rate of up to 90% (3,7). The formation of a fistulous tract between an SAP and the pancreatic duct may manifest as upper gastrointestinal bleeding.

The conventional management for SAP-induced HP involves open splenectomy combined with distal pancreatectomy. Although this approach allows for the definitive eradication of the lesion, it is associated with significant trauma and a high rate of complications (8). With advancements in endovascular techniques, transcatheter embolization has been increasingly employed in the management of HP secondary to SAP (9,10).

We present the case of a patient with HP secondary to SAP rupture, which manifested as upper gastrointestinal bleeding. Endovascular embolization achieved complete hemostasis with favorable outcomes. We present this article in accordance with the CARE reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1918/rc).

Case presentation

A 62-year-old male was admitted to a referring hospital with a 3-month history of recurrent abdominal pain and hematochezia, acutely exacerbated in the last 72 hours. Laboratory investigations revealed severe anemia, with a hemoglobin level of 5.4 g/dL. Inflammatory markers were elevated, with a C-reactive protein (CRP) level of 4.2 mg/L. Coagulation studies, including prothrombin time (PT) and activated partial thromboplastin time (APTT), were within normal limits. Contrast-enhanced abdominal computed tomography (CT) revealed a saccular SAP measuring 2.2 cm × 2.0 cm, located proximally, with partial intraluminal thrombus but no radiological evidence of active contrast extravasation or direct communication with the gastrointestinal tract. Supportive treatment was initiated with proton pump inhibitors, combined with somatostatin infusion, intravenous fluid resuscitation, and blood transfusion. Post-transfusion, the hemoglobin level increased to 7.8 g/dL. The patient denied any history of abdominal trauma, surgery, or pancreatitis.

On hospital day 2, the patient developed recurrent hematochezia. Subsequent angiographic evaluation of the celiac, superior mesenteric, and inferior mesenteric arteries revealed no evidence of contrast extravasation, but confirmed the presence of an SAP. Given the patient’s hemodynamically stable condition at that point and the lack of definitive evidence linking the SAP to the gastrointestinal bleeding, the referring hospital did not proceed with embolization of the pseudoaneurysm. On day 3, the patient developed hematemesis (approximately 250 mL), accompanied by the passage of dark red, bloody stools, and his hemoglobin level decreased to 6.2 g/dL. Emergency esophagogastroduodenoscopy (EGD) and colonoscopy revealed blood pooling in the proximal small intestine, with no identifiable source of active bleeding.

Following transfer to our emergency department, the patient exhibited marked pallor on physical examination, along with abdominal pain and distension. A repeat measurement of his hemoglobin levels demonstrated a further decline to 4.0 g/dL. Coagulation studies revealed a slightly prolonged PT of 16.9 seconds (reference range, 11.5–14.5 seconds), while the activated APTT was within normal limits at 48.5 seconds (reference range, 29.2–41.2 seconds). The CRP level remained elevated at 5.6 mg/L. Emergency contrast-enhanced abdominal CT revealed a 2.8 cm × 2.3 cm pseudoaneurysm in the proximal splenic artery, with evidence of active bleeding into the descending duodenum (Figure 1A-1C). Repeat EGD identified active bleeding from the duodenal papilla (Figure 1D). The constellation of imaging findings (a pseudoaneurysm with adjacent extravasation) and direct endoscopic visualization of bleeding from the ampulla strongly supported the diagnosis of HP secondary to the SPA, with the proposed mechanism being erosion into the pancreatic ductal system.

Figure 1 CT and endoscopic findings of hemosuccus pancreaticus secondary to splenic artery pseudoaneurysm. (A) Contrast-enhanced CT demonstrated contrast extravasation into the descending duodenum (black arrow). (B) CT revealed a 2.8 cm × 2.3 cm pseudoaneurysm in the proximal splenic artery with complete contrast opacification and intraluminal thrombus (black arrow). (C) Three-dimensional CT reconstruction visualized the splenic artery pseudoaneurysm (white arrow). (D) Esophagogastroduodenoscopy showed active bleeding from the ampulla of Vater (white arrow). CT, computed tomography.

The patient underwent emergency embolization of the SAP using a right common femoral artery approach, where a 6-French vascular sheath was placed. Angiographic findings revealed saccular dilation of the proximal splenic artery, accompanied by an irregular contrast-filled protrusion (Figure 2A). The pseudoaneurysm was proximally and distally occluded using the “sandwich” technique to prevent antegrade and retrograde filling. Specifically, Amplatzer vascular plugs (AVPs) (AVPs II, Abbott Cardiovascular, Plymouth, MN, USA) were sized approximately 30–50% larger than the diameter of the adjacent native artery. Using a coaxial technique, a 6-French MPD guiding catheter (Medos International Sarl, Le Locle, Switzerland) was advanced over a 5-French MPA1 catheter (Cordis Corporation, Miami Lakes, FL, USA) to a position distal to the pseudoaneurysm to establish stable access. Through a 6-French guiding catheter, a 10-mm AVP was initially deployed distal to the pseudoaneurysm in the parent artery. Subsequently, a microcatheter was introduced, and three detachable coils (Interlock-18, Boston Scientific, Natick, MA, USA) were placed into the aneurysm sac for embolization. Finally, a 12-mm AVP was released in the proximal segment of the splenic artery to complete the flow interruption (Figure 2B). Post-procedural angiography confirmed the patency of the hepatic and left gastric arteries, complete occlusion of the pseudoaneurysm, and maintenance of splenic perfusion via short gastric artery collaterals (Figure 2C).

Figure 2 Angiographic, procedural, and follow-up findings after endovascular treatment of splenic artery pseudoaneurysm. (A) Celiac trunk angiography demonstrated a pseudoaneurysm (white arrow) in the proximal splenic artery. (B) Radiograph confirmed the embolization device placement: AVP-II at the proximal/distal pseudoaneurysm segments, and coils within the aneurysmal lumen (white arrow). (C) Post-embolization angiography demonstrated complete pseudoaneurysm exclusion, with distal splenic artery perfusion via collaterals (black arrow), and no contrast extravasation. (D) 9-month follow-up CT revealed patent distal splenic artery enhancement (black arrow) and preserved splenic parenchyma without infarction. AVP, Amplatzer vascular plug; CT, computed tomography.

The postoperative management protocol included a 48-hour continuous intravenous infusion of a proton pump inhibitor combined with a somatostatin analogue, after which oral proton pump inhibitor therapy was initiated. Prophylactic antibiotic coverage with levofloxacin was provided for 48 hours. No antiplatelet agents were administered. Vital signs were monitored closely, and daily laboratory assessments were performed, including serial measurements of hemoglobin and CRP. The patient had no further episodes of gastrointestinal bleeding. Upon discharge on postoperative day 5, laboratory values showed a hemoglobin level of 7.1 g/dL and a CRP level of 8.9 mg/L.

During the follow-up period, the patient underwent scheduled clinical assessments. At the 1-month follow-up visit, laboratory tests showed a mild increase in hemoglobin compared to the preoperative baseline, while platelet levels were slightly elevated relative to those at discharge but remained within the normal range. The patient remained asymptomatic throughout the structured 9-month follow-up (with visits at 1, 3, 6, and 9 months), reporting no recurrence of abdominal pain or hematochezia. A follow-up contrast-enhanced CT scan performed at 9 months post-procedure confirmed complete occlusion of the pseudoaneurysm, stable positioning of the embolic devices, and viable splenic parenchyma with no radiological evidence of infarction (Figure 2D).

All the procedures in this case were performed in accordance with the ethical standards of the institutional and/or national research committee(s), and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and the accompanying images. A copy of the written consent form is available for review by the editorial office of this journal.

Discussion

We reported the case of a patient presenting with a 3-month history of recurrent abdominal pain accompanied by hematochezia, who underwent comprehensive diagnostic evaluations at a referring hospital, including EGD, colonoscopy, contrast-enhanced abdominal CT scan, and digital subtraction angiography (DSA). Notably, although both contrast-enhanced CT and angiography identified the presence of an SAP, EGD failed to detect any active bleeding site. This resulted in a failure to recognize the pathological association between the SAP and gastrointestinal bleeding, ultimately delaying appropriate treatment.

It should be noted that HP secondary to SAP is extremely rare in clinical practice. Compounded by the intermittent nature of the bleeding, this condition presents significant diagnostic challenges. At our institution, a repeat EGD revealed active bleeding at the duodenal papilla. This pivotal finding confirmed the diagnosis of HP and provided definitive clinical evidence of a causal relationship between the SAP and HP through this distinctive pathological mechanism.

HP typically results from the erosion of an adjacent pseudoaneurysm into the pancreatic duct. Clinically, HP may originate from the rupture of pseudoaneurysms involving the splenic, hepatic, gastroduodenal, or pancreaticoduodenal arteries, with SAPs accounting for the highest proportion, at approximately 40% (9). SAP formation is associated with multiple etiological factors, including pancreatitis, abdominal trauma, iatrogenic manipulation, postoperative complications, and peptic ulcer disease. In the differential diagnosis, other causes of upper gastrointestinal bleeding, such as peptic ulcer disease and pancreatic tumors, were considered but were ruled out by endoscopic and imaging evaluations. In relation to the formation of the pseudoaneurysm, alternative etiologies, including arterio-enteric fistula and mycotic pseudoaneurysm, were also considered. However, the absence of imaging evidence supporting an enteric communication, coupled with the lack of clinical and laboratory signs of systemic or localized infection, made these possibilities less likely. In relation to hemorrhage sites, SAPs may rupture into the pancreatic duct, gastric lumen, abdominal cavity, or colon, with HP being the most common clinical presentation (4,8).

A distinctive feature of the present case is the absence of a documented history of pancreatitis or definitive abdominal trauma, rendering the precise etiology underlying the formation of the SAP uncertain. The pathological sequence of hemorrhage in this patient can be delineated as follows: the SAP initially ruptured into the pancreatic parenchyma, after which the contents of the hematoma drained through the pancreatic duct, ultimately entering the duodenal lumen. This mechanism comprehensively accounts for the clinical manifestations and diagnostic findings observed in the patient.

From a diagnostic perspective, endoscopy serves as the primary investigative tool; however, its diagnostic yield remains limited, with direct visualization of active bleeding at the duodenal papilla observed in only approximately 30% of cases (2). The principal diagnostic utility of endoscopy lies in its dual ability to exclude alternative potential sources of gastrointestinal hemorrhage and to raise clinical suspicion for HP when findings such as oozing from the ampulla of Vater or unexplained blood in the descending duodenum are observed. Contrast-enhanced CT enables detailed anatomical delineation of pseudoaneurysms, facilitates the detection of active contrast extravasation, and may aid in the identification of underlying etiologies. Angiography represents the diagnostic gold standard for the evaluation of pseudoaneurysms, as it enables the precise localization, dimensional assessment, and characterization of anatomical relationships, while simultaneously offering therapeutic potential (11). However, angiographic evaluation has inherent limitations in SAP-induced HP due to the intermittent bleeding pattern and obscuration by intraductal clots, which frequently preclude visualization of the pathognomonic finding of blood traversing the pancreatic duct into the duodenal lumen.

Currently, there is no consensus as to whether open surgery or endovascular therapy is superior in the treatment of HP secondary to SAP (12). Treatment selection should be individualized based on anatomical characteristics and clinical stability (12,13). Endovascular therapy is the preferred first-line treatment for hemodynamically stable patients (2,14,15). According to reports, the initial success rate of endovascular therapy for HP due to SAP ranges from 78% to 100% (5,10,16). Nevertheless, open surgical management remains a critical option in specific scenarios, including hemodynamic instability, failure of endovascular therapy, suspected infection of the pseudoaneurysm, unfavorable anatomy for embolization, or the presence of associated pancreatic pathology requiring surgical intervention (2). Relevant surgical procedures may include splenic artery ligation, splenectomy, distal pancreatectomy, and, rarely, arterial reconstruction or bypasss (8). When endovascular therapy fails or the patient presents with refractory hemodynamic instability, surgical intervention remains an effective salvage therapy (12,17).

The splenic artery, a medium-sized visceral artery, is anatomically ideal for vascular plug embolization (18). Vascular plugs can be rapidly deployed for embolization, and provide superior radial force compared to coils, reducing the risk of device migration (19,20). In this case, successful endovascular embolization was achieved using a technique involving the precise deployment of vascular plugs both proximal and distal to the pseudoaneurysm to occlude the main arterial flow, combined with coil embolization in the aneurysmal sac to promote thrombosis. At the 9-month follow-up, imaging confirmed the stable position of the embolic material with no evidence of splenic infarction.

This study had several limitations. First, as a single-case report, the generalizability of the findings is limited. Second, the exact etiology of the SAP remains uncertain in the absence of a clear history of pancreatitis or abdominal trauma. Finally, direct pathological proof of a fistulous tract between the pseudoaneurysm and the pancreatic duct, although strongly suggested by imaging and endoscopy, was not obtained.

Conclusions

HP secondary to SAP is a rare but potentially life-threatening cause of gastrointestinal hemorrhage, which presents significant diagnostic challenges due to its nonspecific clinical manifestations. A comprehensive diagnostic approach should include contrast-enhanced CT, gastrointestinal endoscopy, and DSA. Endovascular embolization offers a minimally invasive, safe, and highly effective therapeutic option, with treatment selection guided by multidisciplinary discussion to ensure individualized care.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1918/rc

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1918/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this case were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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