Splenic infarct is ischemic necrosis resulting from interruption of arterial blood supply to the spleen. The most common causes are cardiac embolism (atrial fibrillation, valvular heart disease, endocarditis), hematologic diseases (sickle cell anemia, myeloproliferative diseases, polycythemia vera), thrombophilia states (antiphospholipid syndrome, protein C/S deficiency), and vascular pathologies (splenic artery aneurysm, atherosclerosis, vasculitis). Due to the spleen's end-arteries, peripheral regions are the most vulnerable areas, and a wedge-shaped peripheral involvement pattern is pathognomonic. In the acute phase, left upper quadrant pain, fever, and left shoulder pain due to left diaphragmatic irritation (Kehr sign) may occur. In the chronic phase, fibrosis and contraction produce calcified scar tissue.
Age Range
20-80
Peak Age
55
Gender
Equal
Prevalence
Common
Splenic infarct develops from thromboembolic or in situ thrombotic occlusion of arterial blood flow supplying the spleen. The vascular anatomy of the spleen predisposes to infarct development: splenic artery branches terminate as end-arteries in the splenic parenchyma — no significant collateral circulation exists between these arteries. Occlusion of one end-artery leads to ischemia of the entire territory it supplies. The ischemic zone is always located at the periphery of the spleen and extends to the capsule — due to the vascular territory geometry, a wedge-shaped infarct forms (broad capsular base, narrow apex pointing toward hilum). This wedge shape is pathognomonic. In the acute phase, coagulation necrosis develops and inflammatory response begins — during this period, CT shows a hypodense, non-enhancing area (absence of perfusion → iodinated contrast cannot reach → low attenuation). Within 2-4 weeks, peripheral revascularization and granulation tissue formation begin → peripheral enhancing rim develops. In the chronic phase (weeks-months), fibrotic scar and contraction form → retraction and capsular notching. Long-term dystrophic calcification may develop. In sickle cell anemia, recurrent infarcts shrink and eliminate splenic function → 'autosplenectomy'.
A wedge-shaped, non-enhancing hypodense area at the splenic periphery with broad capsular base and narrow apex pointing toward the hilum in the portal venous phase is pathognomonic for splenic infarction. This shape is the geometric reflection of the spleen's end-artery vascular territory and no other splenic pathology shows this configuration.
In the portal venous phase, a wedge-shaped, broad-based (capsule-based) non-enhancing hypodense area with narrow apex (pointing toward hilum) is seen at the splenic periphery. This wedge shape reflects the end-artery vascular territory of the spleen and is pathognomonic for splenic infarction. While normal splenic parenchyma enhances homogeneously, the infarct area does not enhance at all (absence of perfusion). Lesion edges are generally sharp and smooth. Multiple infarcts may affect several vascular territories and appear as multiple wedge-shaped areas in different splenic regions. Acute massive infarct may involve the entire spleen ('global infarct').
Report Sentence
A wedge-shaped, capsule-based, non-enhancing hypodense area is seen at the splenic periphery, consistent with acute splenic infarction; embolic source investigation is recommended.
On unenhanced CT, the acute infarct area may appear mildly hypodense relative to normal splenic parenchyma or may be imperceptible (low contrast difference). In hemorrhagic infarction, hyperdense areas (acute blood — 60-80 HU) may be seen. In chronic infarct, calcification (hyperdense) and retraction of splenic contour are visible. Unenhanced CT is insufficient for infarct diagnosis and contrast-enhanced CT is required; however, it is important for evaluating hemorrhagic complications.
Report Sentence
A focal mildly hypodense area is seen in the spleen on unenhanced CT; evaluation with contrast-enhanced CT is recommended.
In acute splenic infarction, marked diffusion restriction is seen on DWI — hyperintense signal at high b-value and low ADC values on ADC map. Diffusion restriction reflects cytotoxic edema and is the earliest MRI finding of acute infarction (detectable before T2/T1 changes). The wedge shape is also visible on DWI and has diagnostic value. In the subacute phase, diffusion restriction decreases and ADC values begin to normalize. In the chronic phase, diffusion restriction disappears.
Report Sentence
Wedge-shaped diffusion restriction is seen in the spleen on DWI with low values on ADC map; consistent with acute splenic infarction.
On T2-weighted MRI, the acute-subacute infarct area shows hyperintense signal relative to splenic parenchyma — vasogenic edema and cellular necrosis lead to increased free water. The wedge shape is also visible on T2. In hemorrhagic infarction, hemosiderin deposition may create T2 hypointense foci (susceptibility effect). In the chronic phase, fibrotic scar tissue shows low signal on T2 (fibrous tissue has short T2). The infarct area becomes more conspicuous on T2 STIR sequences.
Report Sentence
A wedge-shaped hyperintense area is seen in the spleen on T2-weighted MRI, consistent with acute-subacute splenic infarction.
On B-mode US, the acute infarct area appears as a hypoechoic, wedge-shaped peripheral area relative to the splenic parenchyma. However, infarct diagnosis on US is not as reliable as CT — the spleen's position, size, and intestinal gas artifact complicate evaluation. Doppler US can demonstrate absence of blood flow in the infarct area. In the chronic phase, the infarct area may appear as hyperechoic scar tissue with capsular notching. Power Doppler can show hyperemia at the infarct periphery (in subacute phase).
Report Sentence
A peripherally located wedge-shaped hypoechoic area is seen in the spleen on US with absence of vascularity in this area on Doppler; consistent with splenic infarction.
In the subacute phase (1-4 weeks), rim enhancement is seen at the periphery of the infarct area — reflecting granulation tissue formation and peripheral revascularization. The central area still does not enhance (necrotic tissue). This rim pattern must be distinguished from abscess rim enhancement — in infarction, the rim is regular and thin, while in abscess it may be thick and irregular. Over time, rim enhancement decreases and completely disappears in the chronic phase, replaced by fibrotic scar.
Report Sentence
Thin, regular rim enhancement is seen at the periphery of the wedge-shaped area in the spleen, reflecting granulation tissue revascularization consistent with subacute splenic infarction.
Criteria
0-7 days. Wedge-shaped non-enhancing area. Sharp margins. Diffusion restriction on DWI.
Distinct Features
Left upper quadrant pain, fever, Kehr sign. Leukocytosis and elevated LDH. Embolic source investigation urgent.
Criteria
1-4 weeks. Peripheral rim enhancement. Central necrotic area persists. Margins slightly blurring.
Distinct Features
Granulation tissue revascularization → rim enhancement. May mimic abscess → clinical correlation important.
Criteria
Months-years. Fibrotic scar, retraction, capsular notching. Calcification may be present. Spleen size may decrease.
Distinct Features
No enhancement. Calcified scar — hyperdense focal area on CT. Progressive splenic shrinkage in recurrent infarction (autosplenectomy — in sickle cell).
Criteria
Hemorrhage within infarct area. Hyperdense areas on unenhanced CT (acute blood). Under anticoagulant therapy or in venous drainage disruption.
Distinct Features
T1 hyperintense areas on MRI (methemoglobin). High density within infarct area on unenhanced CT. Increased risk of splenic rupture.
Distinguishing Feature
Abscess shows round rim enhancement with internal fluid/gas level; infarct is wedge-shaped and non-enhancing (acute phase). High fever, leukocytosis, and septicemia expected in abscess patients.
Distinguishing Feature
Lymphoma shows round/oval homogeneous hypodense lesions without wedge shape; infarct is wedge-shaped and capsule-based. Splenomegaly and multiple lesions are typical in lymphoma.
Distinguishing Feature
Metastasis shows round, heterogeneously enhancing solid lesions; infarct is wedge-shaped and non-enhancing. Known primary tumor history expected in metastasis.
Distinguishing Feature
Simple cyst is round, water-density (0-20 HU), thin-walled, and non-enhancing; infarct is wedge-shaped and at soft-tissue density (20-40 HU). Cyst maintains same density in all phases.
Urgency
urgentManagement
medicalBiopsy
Not NeededFollow-up
specialist-referralThe most important step in splenic infarct diagnosis is identifying the underlying etiology. Embolic source investigation should be performed urgently: echocardiography (atrial fibrillation, valvular vegetation, cardiac thrombus), blood culture (endocarditis), thrombophilia panel, and hemoglobin electrophoresis (sickle cell). Treatment is etiology-directed — anticoagulation (thromboembolic), antibiotic therapy (infective endocarditis), hydration and pain control (sickle cell crisis). Complications: abscess formation (superinfection of infarct), splenic rupture (hemorrhagic infarct), pseudocyst formation. Splenectomy is rarely needed in large infarcts. In sickle cell patients, recurrent infarcts lead to autosplenectomy, and vaccination (pneumococcal, meningococcal, Hib) is mandatory.
Splenic infarct typically presents with left upper quadrant pain. Investigation of the underlying embolic source is important. Complications include abscess formation and splenic rupture.