Splenic infarction associated with persistent atrial fibrillation: A case report

Abstract

BACKGROUND

Splenic infarction is an uncommon thromboembolic condition associated with atrial fibrillation (AF) but with nonspecific abdominal manifestations, leading to diagnostic challenges.

CASE SUMMARY

A 56-year-old male with persistent AF and inadequate anticoagulation management presented with acute left upper quadrant pain without cardiac symptoms. Contrast-enhanced computed tomography was performed and revealed a characteristic wedge-shaped splenic infarction. Following therapeutic anticoagulation, the patient's symptoms rapidly resolved.

CONCLUSION

Acute left upper quadrant pain in patients with AF should raise a clinical suspicion of splenic infarction. The early initiation of therapeutic anticoagulation when cardioembolic etiology is suspected and contraindications are absent may contribute to a favorable outcome and reduce the risk of recurrent embolic events.

Key Words: Splenic infarction; Atrial fibrillation; Abdominal pain; Anticoagulants; Case report

Core Tip: In patients with persistent atrial fibrillation and inadequate anticoagulation, splenic infarction should be considered when acute left upper quadrant pain occurs. A normal initial non-contrast computed tomography (CT) does not exclude splenic infarction, and contrast-enhanced CT is essential for diagnosis. Timely therapeutic anticoagulation and long-term guideline-directed anticoagulation management may be considered.

INTRODUCTION

Splenic infarction is relatively rare and may be frequently overlooked as a cause of acute abdominal pain in clinical practice. It results from an interruption of the blood supply within the splenic artery or its branches and is generally considered a secondary manifestation of an underlying systemic disorder, such as cardiac embolism, a hypercoagulable state, infection, hematological disorder, malignant tumor, and pancreatic disease[1-3]. Atrial fibrillation (AF) is an important potential cardiac source of embolism in patients with splenic infarction, whereby thrombi originating from the atrium may detach and subsequently embolize to multiple parenchymal organs, including the spleen and kidneys[4]. However, splenic infarction associated with cardiac embolism remains frequently under-recognized in clinical practice. The main diagnostic challenge for splenic infarction is that its nonspecific abdominal manifestations may mimic common gastrointestinal acute abdominal conditions, resulting in its delayed diagnosis[5]. Herein, we report a case of a 56-year-old male with a history of persistent AF who had not yet received adequate anticoagulation therapy. The patient had developed acute left upper quadrant abdominal pain during a meal after consuming alcohol and spicy food and sought medical attention due to the symptoms persisting. Further evaluation confirmed the diagnosis of acute splenic infarction, which was presumed to be cardioembolic in origin and associated with persistent AF. This case highlights the importance of the early recognition of splenic infarction, the potential diagnostic limitations of traditional non-enhanced computed tomography (CT) during the initial evaluation, and the favorable clinical outcome achieved through the timely initiation of therapeutic anticoagulation. Previous imaging studies and case reports have also highlighted that non-enhanced CT may fail to detect splenic infarction, whereas contrast-enhanced CT can clearly identify characteristic wedge-shaped hypoattenuating lesions within the spleen that are indicative of splenic infarction[6]. This case report provides valuable clinical insights into the early diagnosis and standardized management of presumed cardioembolic splenic infarction in an emergency setting.

CASE PRESENTATION

Chief complaints

A 56-year-old male presented to the emergency department of our institute on June 9, 2026. Left upper quadrant abdominal pain for 20 minutes.

History of present illness

The pain was constant, well localized, and non-radiating, accompanied by profuse diaphoresis but without nausea or vomiting.

History of past illness

The patient’s medical history was found to be significant for persistent AF, coronary artery disease, and chronic heart failure, all diagnosed approximately 10 years previously. His CHA₂DS₂-VASc score was 2, including 1 point for heart failure and 1 point for vascular disease attributed to coronary artery disease. The patient reported regularly using aspirin (100 mg daily) but acknowledged only intermittently using warfarin for thromboprophylaxis over the preceding 2 years, without regular international normalized ratio monitoring.

Personal and family history

He also admitted a long-standing history of alcohol consumption, with intake occurring 1-3 times per week, but denied smoking. No known drug allergies were reported. The patient’s medical history was otherwise unremarkable for hypertension, diabetes mellitus, recent trauma, or surgical procedures, and there was no family history of thromboembolic disorders.

Physical examination

Upon arrival at our institute at 8:30 am, the patient underwent a physical examination and his vital signs revealed tachycardia (heart rate, 121 beats/minute; irregularly irregular rhythm) and an elevated blood pressure (140/97 mmHg), while his body temperature and respiratory rate were within normal ranges. Abdominal examination revealed a soft and non-distended abdomen with localized tenderness in the left upper quadrant, without rebound tenderness or guarding. Neither the liver nor spleen was palpable below the costal margin, and the bowel sounds were normal.

Laboratory examinations

Initial laboratory testing revealed a platelet count of 182 × 10⁹/L, white blood cell count of 7.03 × 10⁹/L, hemoglobin level of 130 g/L, and C-reactive protein level < 0.5 mg/L. Coagulation testing showed a prothrombin time of 12.2 seconds, an international normalized ratio of 1.02, and an activated partial thromboplastin time of 21.1 seconds. The D-dimer and fibrinogen levels were 0.47 μg/mL and 2.00 g/L, respectively. Blood cultures were negative. Also, the renal and hepatic function, and serum amylase, electrolytes, blood glucose, and cardiac troponin I levels were all within normal limits.

Alternative etiologies, including infective endocarditis, hematological disorders, malignancy, hypercoagulable state, and other arterial thromboembolic sources, were clinically considered. Among these, infective endocarditis was considered unlikely because the patient had no fever, the blood cultures were negative, and no valvular vegetation was identified on echocardiography. Meanwhile, there was no clinical, laboratory, or imaging evidence suggestive of an underlying hematological disorder or active malignancy, and computed tomography revealed no apparent tumor. Also, a hypercoagulable state was considered unlikely given the absence of a relevant clinical history or suggestive routine laboratory findings, while no other apparent arterial thromboembolic source was identified.

Imaging examinations

A 12-lead electrocardiogram test was performed and confirmed rapid AF (Figure 1A). Transthoracic echocardiography revealed a left atrial diameter of 42 mm, a left ventricular diameter of 42 mm, and a left ventricular ejection fraction of 57%. Mild mitral, tricuspid, and pulmonary regurgitation was noted. No intracardiac thrombus or spontaneous echo contrast was detected (Figure 1B). Transesophageal echocardiography (TEE) was not performed. These findings were compatible with a potential cardiac source of the patient’s embolism, although no definite intracardiac thrombus was directly demonstrated.

Figure 1 Electrocardiographic and echocardiographic findings in a patient with persistent atrial fibrillation. A: Electrocardiogram test; B: Echocardiography.

An initial non-contrast abdominal CT scan was performed at 9:15 am and was interpreted as showing no significant abnormalities. Considering the patient’s history of alcohol consumption and recent spicy food intake, a gastrointestinal disorder was initially suspected, and symptomatic treatment with antispasmodic agents and gastric mucosal protective therapy was initiated. However, because the patient’s abdominal pain persisted despite 7 hours of conservative management, contrast-enhanced abdominal CT was performed later at 4:30 pm on the same day, and revealed a segmental, peripheral wedge-shaped hypoattenuating area involving the posterolateral portion of the spleen, consistent with acute splenic infarction. No definite filling defect or thrombus was identified in the main splenic artery or its visible branches. In the clinical context of persistent AF, these findings were considered consistent with a presumed cardioembolic splenic infarction (Figure 2). No other intra-abdominal abnormalities were identified.

Figure 2 Imaging findings during the diagnostic evaluation ofcardioembolic splenic infarction associated with persistentatrial fibrillation. A and B: Initial non-contrast computed tomography showedno definite abnormalities despite persistent abdominal pain; C and D: Follow-up contrast-enhanced computed tomography revealed a peripheral wedge-shaped low-attenuation lesion in the spleen, confirming the diagnosis of acute splenic infarction.

FINAL DIAGNOSIS

Based on the characteristic imaging findings and the patient’s history of persistent AF without adequate anticoagulation, a diagnosis of acute splenic infarction, presumed to be cardioembolic and associated with persistent AF, was established and the patient was admitted to the hospital (Day 1). Alternative etiologies, including infective endocarditis, hematological disorder, malignancy, hypercoagulable state, and other arterial thromboembolic sources, were clinically considered. Infective endocarditis was considered unlikely because there was no fever, no valvular vegetation on echocardiography, and no other supportive evidence of infection. Meanwhile, a hematological disorder and malignancy were not supported by the complete blood count, coagulation studies, inflammatory markers, or imaging findings, which showed no significant abnormalities. Furthermore, CT revealed no obvious signs of tumor. Also, a hypercoagulable state was considered unlikely in the absence of a relevant history of such and the laboratory findings. No other arterial thromboembolic source was identified. Therefore, the splenic infarction was presumed to be cardioembolic in origin, most likely associated with persistent AF and inadequate anticoagulation.

TREATMENT

Anticoagulation was initiated within 2 hours after the diagnosis of splenic infarction (at 6:15 pm on Day 1) with enoxaparin (4000 U subcutaneously twice daily). The patient weighed 52 kg and had a normal renal function. Although therapeutic-dose anticoagulation, such as enoxaparin 1 mg/kg, was previously suggested for splenic infarction in a multicenter retrospective study[4], the present patient’s long-term aspirin use and associated bleeding risk, together with the resource limitations of our primary-care hospital in China, led us to choose enoxaparin 4000 U twice daily as an individualized dose-adjusted regimen and to discontinue aspirin.

OUTCOME AND FOLLOW-UP

The patient’s abdominal pain gradually resolved over the following 4 days, and he was discharged in a hemodynamically stable state on Day 5 (June 13, 2026). At discharge, rivaroxaban was initiated at the standard dose of 20 mg once daily for long-term oral anticoagulation. Outpatient follow-up was scheduled 1 month later to monitor the patient’s complete blood count, renal function, and coagulation parameters.

At the 1-month follow-up visit, the patient reported a complete resolution of his previous abdominal pain and no other specific discomfort. He reported good adherence to rivaroxaban therapy, with no treatment interruption. No bleeding complications, including gingival bleeding, subcutaneous ecchymosis, or petechiae, were reported. Furthermore, no clinically apparent recurrent thromboembolic events occurred. However, laboratory testing and repeat imaging were not performed because of the patient’s financial limitations. Moreover, the patient remained clinically stable.

The 1-month follow-up was based on clinical self-report. Planned laboratory tests and repeat imaging were not performed. Therefore, objective assessment of splenic infarction resolution and thrombus resolution, and detection of occult bleeding, was not possible. More standardized prospective follow-up is needed in the future (Figure 3).

Figure 3 Timeline of clinical presentation, diagnosis, treatment, and follow-up of cardioembolic splenic infarction associated with persistent atrial fibrillation. CT: Computed tomography; INR: International normalized ratio.

DISCUSSION

A previous multicenter emergency study demonstrated that patients with splenic infarction have a risk of in-hospital mortality, suggesting that although this condition is relatively uncommon, its clinical significance should not be underestimated, particularly with regard to risk assessment based on underlying diseases[1]. Splenic infarction commonly presents with a nonspecific left upper quadrant abdominal pain, which may contribute to its missed or delayed diagnosis[5,7]. Herein, we report a case of splenic infarction associated with persistent AF in the absence of adequate anticoagulation therapy. This case highlights the importance of considering splenic infarction in patients with cardiovascular comorbidities presenting with left upper quadrant abdominal pain and emphasizes the need for guideline-directed anticoagulation management.

The patient in this case report was a middle-aged man with a > 10-year history of persistent AF, complicated by previous heart failure and coronary artery disease. His CHA₂DS₂-VASc score was 2 (1 point for congestive heart failure and 1 point for vascular disease due to coronary artery disease). According to the 2023 American College of Cardiology/American Heart Association/American College of Clinical Pharmacy/Heart Rhythm Society guidelines[7], the 2024 European Society of Cardiology (ESC) guidelines[8], and the 2018 American College of Chest Physicians guidelines[9], male patients with AF at this risk level have an indication for oral anticoagulation. The 2024 ESC guidelines further introduced the CHA₂DS₂-VA score for risk stratification and similarly recommend oral anticoagulation for eligible patients[8]. Considering the present patient’s persistent AF, comorbid cardiovascular conditions, and the absence of guideline-directed long-term anticoagulation, inadequate anticoagulation management may have contributed to the development of presumed cardioembolic splenic infarction. Current guidelines clearly state that aspirin should not be used as a substitute for oral anticoagulation in the prevention of stroke and systemic thromboembolism in patients with AF[8,9]. Previous randomized controlled trials have further demonstrated that oral anticoagulation provides superior protection against stroke and systemic embolism compared with antiplatelet therapy[10]. This case highlights the importance of appropriate risk assessment and long-term guideline-directed anticoagulation management in patients with AF, particularly those with established indications for anticoagulation.

Suboptimal anticoagulation management may be influenced by multiple factors, including guideline implementation gaps, the monitoring burden of warfarin therapy, and concerns regarding the bleeding risk[7,8,11]. Moreover, the CHA₂DS₂-VASc and CHA₂DS₂-VA scores are designed to estimate the overall thromboembolic risk in AF rather than to predict specific embolic sites. Thus, non-cerebral systemic embolic events, including splenic embolism, may still occur despite the absence of an extremely high score. Comprehensive clinical assessment incorporating a consideration of a patient’s comorbidities, AF characteristics, and additional risk factors remains essential[8].

Before symptom onset, the present patient had consumed alcohol and irritating, i.e., spicy, food. Combined with the presentation of upper abdominal pain, the initial clinical assessment was thus more likely to focus on a common gastrointestinal emergency, such as acute gastric mucosal injury, acute pancreatitis, and peptic ulcer disease, potentially contributing to the delayed recognition of splenic infarction[1,2]. In the present case, the initial non-contrast abdominal CT showed no significant abnormalities. However, because the patient’s abdominal pain persisted and as he had persistent AF as an important risk factor for a cardioembolic event, contrast-enhanced CT was subsequently performed, ultimately leading to the diagnosis of acute splenic infarction. This case therefore illustrates an important diagnostic pitfall: A normal initial non-contrast CT does not exclude splenic infarction, and contrast-enhanced CT should be performed when the clinical suspicion of splenic infarction persists. Therefore, in patients with AF or other thromboembolic risk factors, abdominal pain occurring after an apparent gastrointestinal trigger should not be solely attributed to a digestive disorder, and a cardioembolic cause should be considered in the differential diagnosis. In this regard, contrast-enhanced CT can play an important role in confirming the diagnosis of splenic infarction. However, it should be emphasized that there is currently no direct evidence indicating that alcohol consumption or irritating food intake promotes the formation of a left atrial thrombus or thrombus embolization. In this case, the temporal association between the dietary factors and symptom onset should be interpreted as a potential source of diagnostic bias rather than a proven pathogenic mechanism. Although the 2024 ESC guidelines incorporate alcohol reduction in comprehensive risk factor management for AF, this case does not establish a causal relationship between alcohol consumption and splenic embolism[8]. Following diagnosis, therapeutic anticoagulation was initiated in the present patient, resulting in a rapid relief of his left upper quadrant pain. This clinical course highlights the importance of early recognition, appropriate imaging evaluation, and timely intervention in patients at risk of thromboembolic events.

To compare with previous cases, we conducted a brief literature review using the PubMed and Google Scholar databases with the search terms “splenic infarction”, “atrial fibrillation”, and “cardioembolic embolism”. Previously published cases of AF-associated splenic infarction have similarly reported nonspecific left upper quadrant pain, a reliance on contrast-enhanced CT for diagnosis, and favorable outcomes with anticoagulation in hemodynamically stable patients[3,4,12,13]. Compared with those reports, our case further emphasizes the diagnostic pitfall of relying on an initially unrevealing non-contrast CT and the importance of guideline-directed anticoagulation in patients with AF and inadequate anticoagulation.

Treatment strategies for splenic infarction should be individualized according to the clinical condition. In the present case, the patient was hemodynamically stable without evidence of complications; therefore, conservative management with therapeutic anticoagulation, analgesia, and supportive care was adopted. Previous studies have suggested that conservative treatment may achieve favorable outcomes in patients without complications. However, interventional or surgical management should be considered in patients with persistent symptoms, infection, splenic rupture, or hemodynamic instability[4,12,13].

Several limitations of this case should be acknowledged. First, the cardioembolic source is plausible but not proven. TEE was not performed, and neither intracardiac thrombus was demonstrated on transthoracic echocardiography or contrast-enhanced CT. Second, although alternative etiologies such as infective endocarditis, hematological disorders, malignancy, and hypercoagulable states were clinically considered and deemed unlikely based on the available history, laboratory findings, and imaging, alternative etiologies were not comprehensively excluded. Third, the 1-month follow-up was based on clinical self-report. Planned laboratory tests and repeat imaging were not performed. Therefore, objective assessment of splenic infarction resolution and thrombus resolution, and detection of occult bleeding, was not possible. More standardized prospective follow-up is needed in the future.

CONCLUSION

This case highlights the importance of considering splenic infarction in the differential diagnosis of patients with AF presenting with acute left upper quadrant pain in an emergency setting. In patients with suspected cardioembolic events and no contraindications to anticoagulation, the timely initiation of therapeutic anticoagulation and long-term guideline-directed anticoagulation management may be associated with an improved clinical outcome and a reduced risk of recurrent thromboembolic events.