Causes of Splenic Abscess
Primary Etiologic Mechanisms
Splenic abscesses develop through three main pathways: hematogenous spread from distant infection sites (most common), contiguous spread from adjacent infections, and secondary infection of splenic infarcts. 1, 2, 3
Hematogenous Seeding (Most Common Route)
Infective endocarditis is the most important source, occurring in 40% of left-sided endocarditis cases, with 5% progressing to splenic abscess 2, 3
Bacteremia from other primary infection sites leads to splenic seeding, with positive blood cultures found in 24-80% of cases 4, 5
Splenic Infarction with Secondary Infection
Ischemic infarcts that become secondarily infected represent a critical pathway, as persistent fever, recurrent bacteremia, or enlargement of splenic defects on imaging indicate progression from bland infarction to abscess 1, 3
Splenic infarction can result from embolic phenomena (especially from endocarditis), hematologic malignancies, or vascular thrombosis 1, 3
Trauma and Direct Inoculation
Splenic trauma with subsequent infection can lead to abscess formation 6, 4
Intravenous drug use provides direct bacterial inoculation into the bloodstream 4
Contiguous Spread
Adjacent intra-abdominal infections can spread directly to the spleen 6
Infected hydatid cysts of the spleen can become abscessed 4
Major Risk Factors and Predisposing Conditions
Immunocompromised States (Most Important)
Immunosuppression is present in 72% of splenic abscess cases 7
Hematologic malignancies, particularly leukemia, represent the most common associated condition 7
Other immunocompromised states include HIV/AIDS, chemotherapy, chronic corticosteroid use, and organ transplantation 7, 6
Infectious Causes
Tuberculosis can cause splenic abscess even in immunocompetent patients 8
Salmonella infection has been documented as a causative organism 8
Plasmodium vivax malaria represents a rare but documented cause 8
Clinical Recognition Patterns
Fever (present in 90% of cases), left upper quadrant abdominal pain (31%), and chills (41%) are the classic triad, though not always complete 7, 4
Leukocytosis occurs in only 38% of cases, making it an unreliable marker 7
Clinical splenomegaly is present in only 30% of cases and should not be relied upon for diagnosis 1, 3
Critical Diagnostic Pitfall
The key distinction is differentiating bland splenic infarction from abscess formation: ongoing sepsis, recurrent positive blood cultures, and persistence or enlargement of splenic defects on serial imaging indicate abscess rather than uncomplicated infarction 1, 3. On CT imaging, bland infarcts appear as peripheral wedge-shaped low-density areas, while abscesses show single or multiple contrast-enhancing cystic lesions 1, 2, 3.