Abstract
Background:
Giant chronic splenic infarction is an extremely rare condition with insidious onset and atypical imaging features, carrying a high risk of misdiagnosis as splenic neoplasm. This case highlights the atypical clinical features and important diagnostic considerations of this uncommon disorder.
Case description:
A 73-year-old female presented with recurrent epigastric pain for 2 years, with a medical history of rheumatic heart disease and hypertension. Contrast-enhanced abdominal computed tomography showed a huge splenic mass measuring approximately 18.0 × 14.2 × 19.1 cm with heterogeneous enhancement and calcification, which was highly suggestive of splenic neoplasm. The patient received splenectomy, and pathological examination confirmed extensive splenic infarction with focal fibrosis and calcification. The patient had an uneventful postoperative recovery, with no evidence of thrombosis or infectious complications during the 3-month follow-up period.
Conclusion:
Rheumatic heart disease with mitral stenosis may have contributed to splenic infarction as a possible cardioembolic source in this patient. Giant chronic splenic infarction may be misdiagnosed because of atypical clinical manifestations, tumor-mimicking imaging features, and insufficient integration of clinical, laboratory, and imaging findings. A comprehensive assessment of clinical history, laboratory results, imaging findings, and cardiac status may help reduce misdiagnosis and guide appropriate management.
Introduction
Splenic infarction occurs when branches of the splenic artery become obstructed, leading to tissue ischemia and necrosis. Typical imaging findings are well-defined, wedge-shaped peripheral lesions (, ). Giant chronic splenic infarction is rare and may gradually form a huge mass with organization, fibrosis, and calcification (). Its clinical and radiologic features can closely mimic splenic neoplasm, leading to frequent misdiagnosis. We present this case to clarify the etiology, diagnostic pitfalls, and clinical lessons for optimal clinical practice.
Case presentation
A 73-year-old female presented to The People's Hospital of Lezhi in January 2026 with recurrent epigastric pain for 2 years. The chief complaint was intermittent left upper abdominal pain, occasionally associated with nausea and minor non-bilious vomiting. There was no history of chills or fever. The patient had a history of rheumatic heart disease and hypertension, but no history of trauma or surgery. She denied regular cardiac evaluations or anticoagulant treatment.
Physical examination revealed marked distension of the left upper abdomen with a palpable mass demonstrating firm consistency and limited mobility; no superficial peripheral lymphadenopathy was detected. Contrast-enhanced abdominal computed tomography (CT) revealed a large mass in the left upper abdomen measuring approximately 18.0 × 14.2 × 19.1 cm. The mass contained patchy areas with mildly increased attenuation and calcification and capsular calcification. Portions of the lesion had indistinct borders with the spleen. After contrast administration, peripheral rim enhancement and septal enhancements were observed. The spleen, diaphragm, stomach lumen, and adjacent tissues were compressed (Figures 1A,B). Cardiac enlargement and calcification were observed in the aorta and portions of the valves. Echocardiography revealed rheumatic heart disease, calcified plaques on the mitral and aortic valves, moderate mitral stenosis with mild regurgitation, as well as mild tricuspid and mild aortic regurgitation. Complete blood count showed low hemoglobin and platelet levels, with a hemoglobin level of 107 g/L (normal range: 115–150 g/L) and a platelet count of 90 × 109/L (normal range: 125–350 × 109/L), which might be related to hypersplenism secondary to chronic splenic infarction. The coagulation profile was within the normal range, including prothrombin time of 12.80 s, activated partial thromboplastin time of 29.50 s, international normalized ratio of 1.07, and fibrinogen level of 2.50 g/L. The D-dimer level was not available. The 12-lead electrocardiogram and tumor marker levels, including AFP, CEA, CA-199, CA-125, and CA-153, were normal. A multidisciplinary team (MDT) consultation involving hepatobiliary surgeons, medical oncologists, radiologists, and pathologists was conducted to formulate the optimal therapeutic strategy. No definite evidence of malignancy was identified on imaging studies or laboratory tests; however, surgical resection was deemed necessary due to the mass effect and diagnostic uncertainty. After obtaining informed consent from the patient and her family members, splenectomy was performed. Specimens of the splenic mass and spleen were measured (Figures 1C,D). Pathological analysis of the surgical specimen indicated an extensive splenic infarction with focal fibrosis and calcification (Figure 2). The patient had an uneventful recovery and was discharged on postoperative day 10.
Figure 1
Figure 2
At the 3-month telephone follow-up after discharge, the patient reported a good mental status, with no evidence of venous thrombosis, pulmonary infection, or abdominal infection. Given that the patient's CHA₂DS₂-VASc score was 3, indicating high thromboembolic risk, long-term oral anticoagulation was indicated.
Discussion
Massive chronic splenic infarction shows a bimodal age distribution, with its etiology shifting from hematological disorders in younger patients to cardioembolic events in older adults (). It may result from cardiac thromboembolism, hematological disorders, and iatrogenic factors such as partial splenic embolization (). Notably, the misdiagnosis rate can be as high as 30%–50%, and the condition is most commonly misdiagnosed as a splenic neoplasm or abscess (). The present case is noteworthy because a giant chronic splenic infarction was initially suspected to be a splenic neoplasm, highlighting the diagnostic difficulty of this uncommon presentation.
Rheumatic heart disease with mitral stenosis may have contributed to the development of splenic infarction in this patient as a possible cardioembolic source. The patient had a history of rheumatic heart disease, and echocardiography confirmed rheumatic valvular disease complicated by moderate mitral stenosis. This valvular lesion can impair left atrial blood flow and promote hemodynamic stasis, thereby increasing the risk of thromboembolic events (). If thrombi form and detach, they may embolize the splenic artery or its branches, resulting in splenic ischemia and necrosis (). However, no direct evidence of intracardiac thrombus, embolic material, or definite splenic arterial embolism was identified in this case. Therefore, the exact etiology of the splenic infarction could not be definitively established. Over the 2-year disease course, the infarcted splenic tissue may have gradually undergone organization, fibrosis, and calcification, eventually developing into a giant space-occupying lesion. This pathological process was consistent with the patient's chronic abdominal pain and giant splenic mass.
Approximately 20% of reported cases of splenic infarction are asymptomatic and may be detected incidentally, contributing to delayed diagnosis (). The patient did not present with typical manifestations of acute splenic infarction, including sudden left upper abdominal pain, tenderness, nausea, or vomiting (). The acute phase of splenic infarction was insidious and unrecognized; instead, the patient only presented with recurrent chronic upper abdominal pain that persisted for 2 years. This clinical presentation was highly consistent with chronic abdominal pain secondary to the mass effect of a splenic lesion, leading clinicians to initially favor neoplastic lesions in the differential diagnosis.
On contrast-enhanced CT, the lesion appeared as a giant space-occupying mass with heterogeneous enhancement, internal calcification, and marked compression of adjacent organs, rather than the typical wedge-shaped hypodense pattern of acute splenic infarction. The main differential diagnoses included primary splenic neoplasm, hemangioma, abscess, and chronic hematoma. Because calcification may also be observed in certain splenic tumors or vascular lesions (), the radiological appearance favored a neoplastic or hemangiomatous lesion before surgery. A similar diagnostic pitfall has been reported in chronic splenic infarction misdiagnosed as splenic neoplasm ().
Preoperatively, percutaneous splenic biopsy was not performed to confirm the pathological nature of the lesion. Although image-guided splenic biopsy can provide diagnostic information in selected cases, previous studies have reported potential bleeding-related complications (, ); therefore, its use should be carefully individualized according to lesion characteristics and procedural risk. In the present case, the lesion was extremely large, compressed adjacent organs, and malignancy could not be completely excluded before surgery. After multidisciplinary discussion and informed consent, splenectomy was performed because of the marked mass effect and the need for definitive diagnosis and treatment. This case illustrates a common diagnostic pitfall. When a splenic lesion is extremely large and shows heterogeneous enhancement with calcification, clinicians may initially favor a neoplastic process. However, negative tumor markers, long-standing abdominal symptoms, and potential thromboembolic risk factors should prompt consideration of chronic splenic infarction. A comprehensive assessment combining clinical history, laboratory results, imaging findings, and cardiac evaluation may help reduce diagnostic bias and avoid overreliance on radiological appearance alone.
Conclusion
Giant chronic splenic infarction should be included in the differential diagnosis of massive splenic space-occupying lesions, particularly in patients with potential thromboembolic risk factors such as rheumatic mitral stenosis. Although the exact etiology may not always be definitively established, a comprehensive assessment integrating clinical history, cardiac evaluation, imaging features, and laboratory findings is essential to avoid misdiagnosis and guide appropriate management.
Statements
Data availability statement
The original contributions presented in the study are included in the article/Supplementary Material, further inquiries can be directed to the corresponding author.
Ethics statement
The studies involving humans were approved by Ethics Committee of The People's Hospital of Lezhi. The studies were conducted in accordance with the local legislation and institutional requirements. The participants provided their written informed consent to participate in this study. Written informed consent was obtained from the individual(s) for the publication of any potentially identifiable images or data included in this article.
Author contributions
WT: Conceptualization, Writing – review & editing, Writing – original draft, Formal analysis, Methodology, Resources, Data curation. XD: Methodology, Writing – review & editing. CY: Writing – review & editing, Methodology. JT: Formal analysis, Writing – review & editing. ZZ: Writing – review & editing, Formal analysis. RH: Writing – review & editing, Formal analysis. WP: Writing – original draft, Formal analysis, Methodology, Writing – review & editing.
Funding
The author(s) declared that financial support was not received for this work and/or its publication.
Conflict of interest
The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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The author(s) declared that generative AI was not used in the creation of this manuscript.
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Supplementary material
The Supplementary Material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fcvm.2026.1850185/full#supplementary-material
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Summary
Keywords
misdiagnosis, rheumatic heart disease, splenectomy, splenic infarction, splenic neoplasm
Citation
Tian W, Deng X, Yang C, Tian J, Zhu Z, Huang R and Pan W (2026) Giant chronic splenic infarction mimicking splenic neoplasm in a patient with rheumatic heart disease: a case report. Front. Cardiovasc. Med. 13:1850185. doi: 10.3389/fcvm.2026.1850185
Received
09 April 2026
Revised
30 June 2026
Accepted
13 July 2026
Published
21 July 2026
Volume
13 - 2026
Edited by
Luca Spiezia, University of Padua, Italy
Updates
Copyright
© 2026 Tian, Deng, Yang, Tian, Zhu, Huang and Pan.
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*Correspondence: Wei Pan 13558814608@163.com
Disclaimer
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.