Splenic Infarct: Causes, Risks, Signs, and Treatment Approaches

A splenic infarct occurs when the blood supply to the spleen is disrupted, leading to tissue damage. Though uncommon, it can indicate underlying medical conditions requiring prompt attention. Symptoms range from mild discomfort to severe pain, often making diagnosis challenging.

Recognizing and addressing the causes of splenic infarction early can help prevent complications. Understanding its risks, symptoms, and treatment options is essential for effective management.

Mechanisms Leading To Splenic Infarction

Splenic infarction occurs when blood flow to the spleen is interrupted, typically involving the splenic artery or its branches. As a highly vascular organ, any disruption in perfusion can quickly lead to ischemic injury. The splenic artery, a branch of the celiac trunk, supplies oxygenated blood to the spleen. Its occlusion—whether by embolism, thrombosis, or vascular compromise—can cause infarction. The severity of tissue damage depends on the size and location of the affected vessel, with larger blockages leading to more extensive necrosis.

Embolic events are a frequent cause, often originating from cardiac or aortic sources. Atrial fibrillation increases the risk of thrombus formation in the left atrium, which can dislodge and travel to the splenic artery. Similarly, infective endocarditis can lead to septic emboli obstructing splenic blood flow. Atherosclerosis may also contribute, as plaque rupture in major arteries can release cholesterol emboli, further narrowing vessels.

Localized thrombosis within splenic vasculature is another cause, particularly in individuals with hypercoagulable states such as antiphospholipid syndrome, polycythemia vera, or malignancy-associated thrombophilia. Splenic vein thrombosis, often secondary to pancreatitis or abdominal malignancies, can impair venous outflow, leading to congestion and arterial insufficiency.

Vascular integrity plays a crucial role in maintaining splenic perfusion. Conditions like polyarteritis nodosa or giant cell arteritis can inflame and narrow the splenic artery, reducing blood flow. Trauma, whether from blunt injury or surgical manipulation, can also disrupt arterial supply, leading to ischemia. In rare cases, congenital vascular anomalies such as splenic artery aneurysms or arteriovenous malformations may alter normal blood flow, contributing to infarction.

Clinical Presentation

Symptoms vary depending on the extent of ischemic injury and underlying conditions. Many individuals experience acute pain in the left upper quadrant, often radiating to the left shoulder due to diaphragmatic irritation (Kehr’s sign). This discomfort can range from a dull ache to a sharp, stabbing sensation, particularly if inflammation affects the peritoneal lining. Some report a gradual worsening of pain, while others experience a sudden, severe onset resembling other acute abdominal emergencies.

Systemic symptoms frequently accompany localized pain. Fever is common, reflecting tissue necrosis or an underlying infection. Nausea and vomiting may occur due to autonomic stimulation or peritoneal irritation. Large infarcts can cause splenomegaly, leading to a palpable mass and a sensation of fullness or early satiety if the spleen compresses the stomach.

Laboratory findings can provide diagnostic clues but are not always specific. Leukocytosis is frequently observed, particularly if inflammation or infection is present. Elevated lactate dehydrogenase (LDH) levels indicate cellular breakdown due to ischemic injury. Mild anemia may result from red blood cell sequestration or hemolysis in cases linked to hematological disorders. Inflammatory markers such as C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR) may be elevated, reflecting an immune response to tissue necrosis.

Some cases present with only vague discomfort or fatigue, especially if the infarct is small or collateral circulation preserves blood flow. This variability can delay diagnosis, particularly in patients with preexisting conditions that mask or mimic typical symptoms. In individuals with cardiovascular disease or hematologic abnormalities, even mild symptoms warrant further investigation.

Common Diagnostic Approaches

Diagnosing a splenic infarct requires clinical evaluation and imaging, as symptoms often overlap with other abdominal conditions. Physicians begin with a thorough history, focusing on risk factors such as arrhythmias, hypercoagulable disorders, and recent infections. A physical exam may reveal left upper quadrant tenderness or splenomegaly, though these findings are not always present. Laboratory tests assess inflammation, hemolysis, and organ dysfunction, but imaging is essential for confirmation.

Computed tomography (CT) with intravenous contrast is the preferred imaging modality due to its high sensitivity. Contrast-enhanced CT scans reveal wedge-shaped areas of hypoattenuation, indicating ischemic necrosis. These findings distinguish infarction from other splenic conditions, such as abscesses or malignancies. If contrast is contraindicated, non-contrast CT or magnetic resonance imaging (MRI) with diffusion-weighted imaging (DWI) can serve as alternatives.

Ultrasound with Doppler imaging is sometimes used, particularly in initial evaluations or when CT and MRI are unavailable. While grayscale ultrasound can detect splenic abnormalities, Doppler studies assess blood flow, confirming infarction when perfusion is absent. For suspected embolic sources, transesophageal echocardiography (TEE) helps identify cardiac thrombi or valvular abnormalities contributing to arterial occlusion.

Medical Conditions Commonly Linked To Splenic Infarction

Several conditions predispose individuals to splenic infarction by disrupting normal blood flow. Identifying these associations is crucial for diagnosis and prevention.

Cardiac-Related Causes

Cardiac conditions that promote embolism formation are among the most common contributors. Atrial fibrillation increases the risk of thrombus formation in the left atrium, which can embolize to the splenic artery. A study in Circulation (2021) found that patients with atrial fibrillation have a significantly higher incidence of splenic infarction, particularly those with inadequate anticoagulation.

Valvular heart disease, especially infective endocarditis, can lead to splenic infarction through septic embolization. Vegetations on infected heart valves may break off and travel to the spleen, causing localized ischemia. Prosthetic heart valves and intracardiac devices, such as pacemakers, also increase embolic risk. Myocardial infarction and left ventricular thrombus formation further contribute, particularly in patients with reduced ejection fraction.

Hematological Disorders

Disorders affecting blood composition and clotting mechanisms can predispose individuals to splenic infarction. Sickle cell disease is a well-documented cause, as sickled erythrocytes obstruct small vessels, leading to repeated microinfarctions and, in some cases, complete splenic atrophy. A review in Blood Advances (2022) highlighted that splenic infarction is a common early complication in sickle cell patients, particularly during vaso-occlusive crises.

Other conditions, such as polycythemia vera and essential thrombocythemia, increase blood viscosity and platelet aggregation, raising the risk of arterial thrombosis. Antiphospholipid syndrome frequently involves the splenic artery, leading to infarction. Malignancy-associated hypercoagulability, particularly in hematologic cancers, further elevates risk. In these cases, anticoagulation or cytoreductive therapy is often necessary to reduce complications.

Infectious Etiologies

Certain infections contribute to splenic infarction through vascular inflammation, septic embolization, or hypercoagulability. Infective endocarditis is a well-recognized source of embolic infarcts, including those affecting the spleen. A study in Clinical Infectious Diseases (2023) found that up to 44% of patients with infective endocarditis had evidence of splenic infarction on imaging.

Other systemic infections, such as cytomegalovirus (CMV) and Epstein-Barr virus (EBV), have been linked to splenic infarction, particularly in immunocompromised individuals. COVID-19 has also been associated with thrombotic complications, including splenic infarction, due to its prothrombotic effects. Case reports in The Lancet Infectious Diseases (2022) have documented splenic infarcts in patients with severe COVID-19, often alongside other thrombotic events.

Potential Consequences

While small infarcts may resolve without long-term effects, larger infarcts or those in individuals with underlying conditions can lead to significant complications. Persistent ischemia can result in liquefactive necrosis, increasing the risk of secondary infection and abscess formation. Splenic abscesses, although rare, may require drainage or splenectomy if antibiotic therapy is insufficient.

Splenic rupture, though uncommon, is a life-threatening complication, often presenting with internal hemorrhage. Patients with repeated infarctions, such as those with sickle cell disease, may develop functional asplenia, increasing susceptibility to infections. Over time, chronic infarction can lead to fibrosis and atrophy, compromising immune function and necessitating prophylactic vaccinations.

General Treatment And Management Strategies

Treatment focuses on symptom control and addressing the underlying cause. For most patients, conservative management with pain relief and hydration is sufficient. NSAIDs or acetaminophen help manage discomfort. If infection is suspected, broad-spectrum antibiotics may be initiated. Serial imaging monitors infarct resolution and detects complications.

For embolic or thrombotic causes, anticoagulation therapy is often necessary. Patients with atrial fibrillation or prosthetic heart valves may require long-term anticoagulation with warfarin or direct oral anticoagulants (DOACs). Those with hypercoagulable disorders may need tailored antithrombotic regimens. In rare cases, extensive infarction leading to persistent pain, recurrent infections, or rupture may require splenectomy, necessitating lifelong vaccinations to prevent infections.