Splenic abscess is an infectious lesion characterized by pus collection within the splenic parenchyma. It is rare but has very high mortality if untreated (40-100%). The most common routes are hematogenous spread (bacteremia, endocarditis), direct spread from adjacent infection (left subphrenic abscess, perinephric abscess), or superinfection of splenic infarction. Causative agents include bacteria (Staphylococcus aureus, Streptococcus spp., E. coli, Salmonella), fungi (Candida, Aspergillus in immunosuppressed patients), and mycobacteria. Risk factors: immunosuppression (HIV/AIDS, chemotherapy, transplantation), IV drug use, diabetes mellitus, endocarditis, sickle cell anemia, and trauma. Clinical presentation: fever, left upper quadrant pain, leukocytosis, and splenomegaly. May be solitary or multiple; fungal microabscesses may present in miliary pattern.
Age Range
20-80
Peak Age
50
Gender
Equal
Prevalence
Uncommon
Splenic abscess formation occurs through multiple mechanisms: (1) Hematogenous spread — microorganisms settle in splenic sinusoids during bacteremia; the spleen's RES function normally clears bacteria but intense bacteremia or virulent organisms overwhelm this defense; septic emboli from endocarditis are particularly high risk. (2) Superinfection — necrotic tissue in infarct or hematoma areas provides substrate for bacterial colonization. (3) Direct spread — adjacent organ infections (left subphrenic abscess, pancreatic abscess, colonic perforation) directly invade the spleen. Abscess formation: bacterial colonization → neutrophil infiltration → proteolytic enzyme release → tissue liquefaction → pus formation (necrotic debris, bacteria, neutrophil remnants). Pus contains high protein, cellular debris, and fibrin network — this viscous content forms the basis of diffusion restriction on DWI (high viscosity impedes water diffusion). Rim enhancement on CT reflects intense neovascularization of granulation tissue in the abscess wall — new capillaries take up contrast and form a bright rim. Gas formation results from fermentation metabolism of gas-forming bacteria (E. coli, Klebsiella, Clostridium).
Thick rim enhancing hypodense lesion on CT + marked diffusion restriction on DWI (low ADC) + internal gas bubbles combination is diagnostic for splenic abscess. Even without gas, rim enhancement + low ADC combination is highly specific for abscess.
In the portal venous phase, a lesion with thick, irregular enhancing wall (rim enhancement) and non-enhancing hypodense center is seen. Wall thickness varies, typically 2-5 mm. The central hypodense area corresponds to pus collection (density 10-30 HU — proteinaceous fluid). Mild density decrease in surrounding splenic parenchyma may be seen due to reaction zone (edema, hyperemia). Multiloculated abscesses may show internal septa and lobulated margins. Internal gas bubbles or air-fluid level may be seen with gas-forming bacteria — this finding is highly specific for abscess.
Report Sentence
A hypodense lesion with thick, irregular rim enhancement is seen in the spleen with internal gas bubbles; consistent with splenic abscess.
On DWI, abscess shows marked diffusion restriction — hyperintense signal at high b-value (b=800-1000) and low ADC values on ADC map (typically <0.8 × 10⁻³ mm²/s). This is the most valuable MRI finding for abscess diagnosis and critical for differentiation from simple cyst (high ADC >2.5), necrotic tumor (heterogeneous ADC), and cystic lesions. As pus viscosity increases, ADC value decreases — thick pus shows the lowest ADC values.
Report Sentence
Marked diffusion restriction is seen in the cystic lesion in the spleen on DWI with low ADC values; this finding is consistent with viscous pus content and supports abscess diagnosis.
On T2-weighted MRI, the abscess center shows hyperintense signal (pus fluid content). The abscess wall (granulation tissue + fibrous capsule) appears as a T2 hypointense rim — 'double target sign'. Perilesional edema may be seen as a hyperintense zone in surrounding splenic parenchyma. Abscess becomes more conspicuous on T2 fat-sat sequences. Fungal microabscesses appear as small (<1 cm) hyperintense nodules on T2.
Report Sentence
The splenic lesion shows hyperintense center with hypointense rim creating 'double target sign' on T2-weighted MRI; consistent with abscess.
On B-mode US, a complex cystic lesion with hypoechoic or mixed echogenicity, irregular wall, and internal debris or septations is seen relative to splenic parenchyma. Internal echoes (pus debris) indicate the lesion is not completely anechoic — different from simple cyst. Thick, irregular wall may appear as a hyperechoic rim. 'Dirty shadowing' (acoustic shadowing) may be seen with gas. Hypervascularity in the abscess wall may be detected on Doppler US (inflammatory hyperemia).
Report Sentence
A thick-walled complex cystic lesion with internal debris and septations is seen in the spleen on US; consistent with abscess.
On unenhanced CT, a hypodense lesion is seen relative to splenic parenchyma. Internal gas bubbles appearing at very low density (-1000 HU) are highly specific for abscess diagnosis. In the absence of gas, unenhanced CT alone is insufficient and contrast-enhanced CT should evaluate rim enhancement.
Report Sentence
A hypodense lesion is seen in the spleen on unenhanced CT with internal gas bubbles; consistent with abscess.
On T1-weighted MRI, the abscess center shows hypointense signal (pus fluid). Proteinaceous pus may show mild T1 signal increase. On post-contrast T1 series, thick, irregular rim enhancement is seen in the abscess wall — gadolinium accumulates in neovascular capillaries of granulation tissue. Central pus does not enhance.
Report Sentence
Hypointense center with thick rim enhancement on post-contrast series is seen in the splenic lesion on T1-weighted MRI; consistent with abscess.
Criteria
Most common type. Staphylococcus, Streptococcus, E. coli. Solitary or multiple.
Distinct Features
Large solitary abscess or few large lesions. Rim enhancement and gas formation common. Antibiotic therapy + percutaneous drainage.
Criteria
Candida or Aspergillus. In neutropenic patient. Multiple small (<1 cm) lesions.
Distinct Features
Miliary pattern — numerous small hypodense nodules. Liver and spleen may be simultaneously involved (hepatosplenic candidiasis). 'Bulls-eye' or 'wheel-within-a-wheel' pattern.
Criteria
Mycobacterium tuberculosis. Miliary TB or focal TB. In immunosuppressed and endemic areas.
Distinct Features
Rim enhancement due to caseous necrosis. Calcification common in subacute-chronic phase. Post-treatment granuloma + calcification develops.
Distinguishing Feature
Infarct is wedge-shaped and non-enhancing (acute phase); abscess shows round rim enhancement. Subacute infarct may develop rim enhancement but thin and regular (thick and irregular in abscess).
Distinguishing Feature
Simple cyst shows no diffusion restriction on DWI (high ADC >2.5); abscess shows marked restriction (low ADC <0.8). Thin smooth wall in simple cyst, thick irregular wall in abscess.
Distinguishing Feature
Lymphoma shows homogeneous minimal enhancement without rim enhancement or gas; abscess shows rim enhancement and internal gas. Fever may occur in lymphoma but leukocytosis is not prominent.
Distinguishing Feature
Metastasis shows heterogeneous solid enhancement, may have rim enhancement but heterogeneous ADC on DWI (low in solid, high in necrotic); abscess has homogeneous low ADC.
Urgency
emergentManagement
interventionalBiopsy
Not NeededFollow-up
specialist-referralSplenic abscess requires emergency treatment — untreated mortality is 40-100%. Treatment: (1) IV broad-spectrum antibiotics (empirically started, adjusted by culture results), (2) Percutaneous drainage (US or CT-guided — preferred approach), (3) Splenectomy (for abscesses not responding to percutaneous drainage, multiloculated, or ruptured). Blood cultures should be obtained. Endocarditis investigation required (echocardiography). Fungal etiology should be considered in immunosuppressed patients. Percutaneous drainage success rate is 75-90%. Complications: rupture (peritonitis), septic shock, fistula formation.
Splenic abscess has high mortality if untreated. Percutaneous drainage or splenectomy are treatment options. Underlying immunosuppression and source of infection should be investigated.