A 67-Year-Old Man With Hypertension Presenting With Spontaneous Rupture of a Large Splenic Artery Aneurysm Associated With Thrombus

Introduction

Splenic artery aneurysms (SAAs) account for 60% of visceral artery aneurysms (VAAs) [1]. Their reported incidence has increased 7-fold with modern imaging [2]. Giant SAAs are defined by a diameter ≥5 cm [3,4]. Their management remains controversial, owing to the relative rarity of this condition, limited follow-up of enlisted therapeutic measures, and the absence of randomized controlled prospective studies. Despite occurring in 2% to 3% of cases [5,6], the rupture of a giant SAA is a startling event, causing high mortality, at a rate of 33% [3]. Herein, we report a case of spontaneous thrombosis of a giant splenic artery aneurysm following its rupture. We emphasize the challenges encountered in management and decision-making, and explain the rationale behind our chosen approach. Although thrombosis may be regarded as a potential cure for SAA, the possibilities of recanalization and secondary rupture remain significant concerns. Therefore, definitive treatment should be considered. Through this report, we aim to shed light on the key issues involved in such complex clinical scenarios. This work has been reported in accordance with the SCARE criteria [7].

Case Report

A 67-year-old man with a medical history of hypertension (treated with angiotensin-converting enzyme inhibitors and calcium channel blockers) and a prior stroke (on prophylactic aspirin therapy) presented to our Emergency Department. He had no history of pancreatitis, peptic ulcer disease, abdominal trauma, infective endocarditis, hepatobiliary disease, prior abdominal surgery, or connective tissue disease. His family members had no known history of connective tissue disease. He presented with severe, persistent pain predominantly in the upper abdomen. On clinical examination, he was not pale. His vital signs revealed a blood pressure of 80/50 mm Hg, a regular thready pulse at 100 beats/min, and a respiratory rate of 24 breaths/min. Abdominal examination showed tenderness, guarding, and rigidity, most marked in the left upper quadrant. No masses or organomegaly were palpated.

Initial laboratory workup revealed a normal hematologic and coagulation profile (prothrombin time: 82%, platelet count: 223 000/mm3), with a hemoglobin level of 12.4 g/dL. Renal function test results showed an elevated creatinine level (144 μmol/L) and a normal urea level (5.31 mmol/L). There were no electrolyte disturbances. C-reactive protein was within the reference range (4.4 mg/dL), but the white blood cell count was elevated (17 730/mm3). The patient’s condition was hemodynamically stabilized, and he underwent an urgent contrast-enhanced computed tomography (CT) scan. The CT scan demonstrated a well-defined, oval lesion (98 mm) at the origin of the splenic artery, with marked contrast enhancement and evidence of complete intraluminal thrombosis, which was highly suggestive of a thrombosed SAA (Figure 1). Moderate hemoperitoneum and retroperitoneal hemorrhage were also present, without active extravasation. The patient was then transferred to our department for further management.

Following resuscitation, the patient’s condition improved: he became normotensive and pain-free, with a soft abdomen. The hemoglobin level dropped to 10.7 g/dL. Electrocardiogram showed ST-segment elevation in the inferior leads, and troponin levels rose from 117 to 470 ng/mL. However, in the absence of respiratory or cardiac symptoms and given the subsequent decline in troponin level to 10 ng/mL, the elevation was attributed to acute anemia. He received a blood transfusion, which raised the hemoglobin level to 12 g/dL.

In an interdisciplinary team meeting, radiological embolization was discussed, but it was not pursued, owing to complete thrombosis of the aneurysm. Moreover, given his acute kidney injury, arteriography was not ordered. Surgery was scheduled on hospitalization day 5. Through a left subcostal approach, intraoperative findings included a large 13-cm thrombosed true saccular aneurysm with a thickened wall, firmly adherent to the superior border of the corporeo-caudal pancreas. Owing to the high risk of rupture during dissection and the presence of splenic ischemia, the decision was made to ligate the splenic artery proximally and proceed with caudal splenopancreatectomy and aneurysmectomy (Figure 2).

Postoperative recovery was uneventful, and the patient was discharged on postoperative day 5. Histopathological examination confirmed a round 11-cm encapsulated vascular lesion with intraluminal blood, consisting of ulcerated intima, fibrotic media, and inflamed adventitia (Figures 3, 4). Thus, the encountered aneurysm was caused by atherosclerosis. The patient remained well at the 5-month follow-up. Prophylactic management of asplenia included daily amoxicillin and vaccination against Pneumococcus, Haemophilus influenzae type B, Meningococcus, and influenza.

In this report, we describe the clinical course of a 67-year old man with hypertension who underwent surgery for a giant true SAA complicated by spontaneous thrombosis. This report highlights the challenges in clinical decision-making: whether to opt for observation while accepting the risk of inherent complications, or to pursue additional intervention despite anticipated difficulties.

Discussion

In this report, we provide insight into a rare complication of SAA: spontaneous thrombosis following rupture. By carefully analyzing the presentation, imaging findings, and treatment options, we aimed to address the therapeutic dilemma often faced in such situations, in which the choice between conservative management, endovascular intervention, or surgery remains debated. Our report contributes valuable insights that may guide decision-making in similar cases, offering practical considerations to optimize patient outcomes.

Given their size, surgical management of such aneurysms often involves multivisceral resection.

VAAs are classified into 2 types based on their origin. Pseudoaneurysms consist of an encapsulated hematoma that communicates with the arterial lumen. This type carries a high risk of imminent rupture, regardless of its size [8]. Pseudoaneurysms can arise secondary to trauma, infection, or inflammatory diseases, or following interventional procedures. True aneurysms are a focal dilatation of the artery, involving all its layers. They are the consequence of atherosclerosis, fibrodysplasia, or connective tissue disorders. VAAs require treatment in symptomatic patients, pregnant women, and liver transplant recipients, in cases of pancreatoduodenal, gastroduodenal, or intrahepatic localization, and when aneurysms exceed 2 to 2.5 cm in size [9].

An SAA is defined as a localized dilatation of the splenic artery measuring at least 50% more than the vessel’s normal diameter [10]. SAAs account for 60% to 70% of reported cases of VAAs [10] and are the most common VAAs [11,12]. Despite being mostly discovered before rupture [11], such a dreadful complication demands prompt, appropriate management to avoid a fatal outcome, since the mortality rate due to rupture ranges from 25 to 70% [3]. This is particularly true in symptomatic forms, which have a tendency to rupture [12]. They are mostly true aneurysms, their main etiology is degenerative atherosclerosis [11], and they frequently develop at the distal segment [13]. Splenic aneurysms reach larger maximal diameters [11], which may explain their higher likelihood to present with symptoms [14]. Different presentations of SAA have been reported. Varnavas et al published a case of a giant SAA causing melena [15], suggesting the invasive nature of this disease in eroding adjacent vessels.

Chaer et al reported that symptomatic SAAs larger than 30 mm and in pregnant women or women of childbearing age should be treated [16]. Management often depends on the location and technical feasibility of the procedure.

The challenge in our case was to justify the operative intervention in the face of a ruptured and spontaneously thrombosed splenic SAA in a patient presenting with hypertension. Our patient, who remained in stable condition, was labeled as a high-risk patient whose homeostasis could be compromised by surgical stress. The literature addressing this scenario is sparse. To avoid a premature surgical indication, we focused on 2 key questions: (1) whether spontaneous thrombosis effectively prevents hemorrhagic recurrence, based on outcomes from endovascular treatments that induce arterial thrombosis, and (2) what is the natural course of arterial aneurysm thrombosis, as observed in other vascular sites.

First, aneurysm thrombosis can result in the release of micro-emboli to connected viscera [17,18] or in thrombus extension [19]. In our case, where the aneurysm was located proximally with a well-developed collateral network, such events could lead to ischemia of the pancreatic tail, proximal stomach [20,21], or spleen. End-organ ischemia may subsequently cause complications such as pancreatitis, gastric infarction with a risk of perforation, or splenic infarction with the potential for secondary rupture or abscess formation. Second, cases of spontaneous rupture following thrombosed arterial aneurysms have been reported [22,23], as well as thrombosis induced by radiological treatment [13]. In our case, such an event could manifest as abdominal apoplexy, potentially resulting in a catastrophic outcome, given our facility’s limited resources. Furthermore, the tortuosity of the splenic artery can render endovascular treatment technically challenging or even a failure. Third, it has been documented that the aneurysms of those with intraluminal thrombi were larger at initial presentation and grew by 2 mm per year, twice as fast as the growth rate of 1 mm per year in those without intraluminal thrombi [24]. Finally, interventional treatment carries risks, including recanalization after embolization, which occurs in 12.5% of cases [25]. The risk rises to 33% in large aneurysms [26]. In a decade-long German study, 16.7% of radiologically treated ruptured VAAs experienced rebleeding [11]. Considering the abovementioned reasons, definitive treatment is mandatory. This is particularly true given that our patient is at increased risk of secondary rupture in the event of a hypertensive crisis.

This case report has several strengths. First, it addresses an exceptional and scarcely reported situation of spontaneous thrombosis of a ruptured SAA, thus contributing valuable information to the existing literature. The discussion is enriched by a comprehensive review of available evidence on VAAs, their natural history, and potential complications, which provides an educational perspective for clinicians, particularly in under-resourced settings. Furthermore, the case highlights an important clinical dilemma between conservative and interventional management in a high-risk patient, thereby raising awareness of the potential pitfalls of relying on spontaneous thrombosis as a protective event. However, this report has limitations inherent to its single-case nature, as the findings cannot be generalized. Finally, while the rationale for management was discussed, the decision-making process could be further clarified in the context of resource availability, which may limit the applicability of these conclusions to other clinical environments.

Conclusions

Despite the existence of guidelines for SAA management based on initial presentation and aneurysm characteristics, the optimal approach to treating a thrombosed aneurysm following rupture remains uncertain. Our comprehensive review indicated that definitive treatment was necessary, providing a safe and conclusive option for our patient. Spontaneous thrombosis of a ruptured SAA should not be considered a definitive or protective event. Despite initial hemodynamic stability, the risks of recurrence, secondary rupture, or ischemic complications remain significant. Therefore, definitive treatment is warranted whenever feasible, with management decisions carefully tailored to patient comorbidities and available resources.