Definition/General
Introduction:
Splenic abscess is a localized collection of pus within the splenic parenchyma caused by bacterial, fungal, or parasitic infections
It is a rare condition with incidence of 0.14-0.7% in autopsy series
Pyogenic abscesses are most common, followed by fungal abscesses in immunocompromised patients
Early recognition and treatment are crucial due to high mortality rates of 15-47% if untreated.
Origin:
Develops through hematogenous spread from distant infection sites (60-70% cases)
Direct extension from adjacent infected organs (stomach, pancreas, colon)
Penetrating trauma with secondary infection
Immunosuppression increases susceptibility to opportunistic pathogens
Splenic infarcts may become secondarily infected.
Classification:
By etiology: Pyogenic (bacterial)
Fungal
Parasitic
Mixed infections
By number: Solitary (60%)
Multiple (40%)
By source: Hematogenous spread
Direct extension
Post-traumatic
Iatrogenic
By patient status: Immunocompetent
Immunocompromised.
Epidemiology:
Peak incidence in 4th-6th decades
Male predominance (1.5:1 ratio)
More common in immunocompromised patients
Tropical regions show higher rates due to parasitic infections
Diabetic patients at increased risk
IV drug users prone to hematogenous seeding.
Clinical Features
Presentation:
Left upper quadrant pain (90-95% of patients)
Fever and chills (80-90% cases)
Splenomegaly (60-70% cases)
Leukocytosis with left shift
Pleuritic chest pain with referred pain to left shoulder
Constitutional symptoms: malaise, anorexia, weight loss.
Symptoms:
Classic triad: Fever, left upper quadrant pain, splenomegaly (present in 50% cases)
Gastrointestinal symptoms: Nausea, vomiting, early satiety
Respiratory symptoms: Left-sided pleuritic pain, dyspnea
Systemic symptoms: Night sweats, fatigue, weight loss
Sepsis may develop in severe cases.
Risk Factors:
Immunosuppression: HIV/AIDS, chemotherapy, corticosteroids
Diabetes mellitus (present in 20-30% cases)
Hematologic malignancies: Leukemia, lymphoma
Infective endocarditis with septic emboli
Intravenous drug use
Recent invasive procedures
Penetrating abdominal trauma.
Screening:
High-risk patients with persistent fever and abdominal pain
Imaging studies: CT scan with contrast (diagnostic method of choice)
Ultrasound as initial screening
Laboratory studies: Blood cultures, CBC with differential
Microbiologic workup: Culture of abscess fluid when accessible.
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Gross Description
Appearance:
Well-circumscribed cavity containing thick, purulent material
Creamy yellow-green pus in bacterial infections
Thick, fibrous capsule surrounding the abscess cavity
Hemorrhagic areas may be present in surrounding tissue
Multiple smaller abscesses may coalesce into larger collections.
Characteristics:
Variable size: From few millimeters to >15 cm in diameter
Unilocular or multilocular appearance
Thick, indurated walls in chronic cases
Necrotic debris and inflammatory exudate
Fungal abscesses may show gray-white appearance with less purulent material.
Size Location:
Size range: 2-15 cm (average 6-8 cm)
Location distribution: Any part of spleen, no specific predilection
Solitary abscesses typically larger than multiple abscesses
Deep-seated location common in hematogenous spread
Subcapsular location in direct extension.
Multifocality:
Multiple abscesses in 40% of cases, suggest hematogenous spread
Microabscesses may be scattered throughout parenchyma
Associated findings: Reactive lymphadenopathy
Adjacent organ involvement
Complications: Rupture into peritoneal cavity
Formation of splenic-gastric fistula.
Microscopic Description
Histological Features:
Central suppurative necrosis with neutrophilic infiltrate
Thick fibrous capsule with chronic inflammatory cells
Granulation tissue at periphery with capillary proliferation
Surrounding reactive fibrosis and inflammation
Bacterial colonies may be visible within necrotic areas.
Cellular Characteristics:
Acute inflammatory infiltrate: Predominantly neutrophils in center
Chronic inflammation: Lymphocytes, plasma cells, macrophages in capsule
Giant cells may be present, especially in fungal infections
Necrotic debris with nuclear fragmentation
Fibroblasts and endothelial proliferation in healing areas.
Architectural Patterns:
Zoned architecture: Central necrosis, surrounding inflammation, peripheral fibrosis
Complete destruction of normal splenic architecture in affected areas
Preservation of normal spleen in unaffected areas
Vascular thrombosis may be present
Microabscesses show similar but smaller pattern.
Grading Criteria:
Acute abscess: Predominant neutrophilic infiltrate, minimal fibrosis
Subacute abscess: Mixed inflammatory infiltrate, early fibrosis
Chronic abscess: Thick fibrous wall, predominant chronic inflammation
Organized abscess: Extensive fibrosis with residual inflammatory foci.
Immunohistochemistry
Positive Markers:
Inflammatory markers: CD68 for macrophages
Myeloperoxidase for neutrophils
Vascular markers: CD31, CD34 for angiogenesis assessment
Fibroblast markers: Vimentin in capsule formation
Proliferation markers: Ki-67 in granulation tissue.
Negative Markers:
Lymphoid markers: CD20, CD3 (destroyed in affected areas)
Normal splenic markers: Loss of normal architecture markers
Epithelial markers: Cytokeratins typically negative (unless metastatic infection)
Specific pathogen markers may be negative depending on organism.
Diagnostic Utility:
Confirmation of inflammatory nature: Abundant inflammatory markers
Assessment of chronicity: Fibrosis markers in chronic cases
Differential diagnosis: Distinguishing from neoplasms
Pathogen identification: Special stains may be more useful than IHC.
Molecular Subtypes:
Bacterial abscesses: Neutrophil-predominant inflammation
Fungal abscesses: Mixed inflammation with giant cells
Mycobacterial: Epithelioid granulomas
Parasitic: Eosinophil-rich inflammation
Mixed infections: Variable inflammatory patterns.
Molecular/Genetic
Genetic Mutations:
Host susceptibility genes: Immunodeficiency-related mutations
Complement deficiency genes
Pathogen-specific markers: Bacterial resistance genes
Fungal virulence factors
Inflammatory response genes: Cytokine production variants
Healing response genes: Fibrosis-related genetic factors.
Molecular Markers:
Inflammatory cytokines: IL-1β, TNF-α, IL-6 elevation
Acute phase reactants: CRP, ESR elevation
Complement activation: C3, C4 consumption
Pathogen-specific markers: Bacterial DNA/RNA, fungal antigens
Tissue damage markers: LDH, cellular enzymes.
Prognostic Significance:
Organism virulence affects treatment response and prognosis
Host immune status determines infection severity
Abscess size and location influence complications
Time to diagnosis affects outcomes
Antibiotic resistance patterns impact treatment success.
Therapeutic Targets:
Antimicrobial therapy: Organism-specific antibiotics or antifungals
Immunomodulation: In severe sepsis cases
Drainage procedures: Percutaneous or surgical
Supportive care: Fluid management, nutritional support
Treatment of underlying conditions: Diabetes, immunosuppression.
Differential Diagnosis
Similar Entities:
Splenic infarction: May become secondarily infected
Splenic hematoma: History of trauma, different imaging
Splenic cysts: Usually sterile, different wall characteristics
Metastatic disease: May have central necrosis mimicking abscess
Primary splenic tumors: Angiosarcoma may have similar appearance.
Distinguishing Features:
Abscess vs infarct: Rim enhancement vs wedge-shaped
Purulent contents vs coagulative necrosis
Abscess vs cyst: Thick enhancing wall vs thin wall
Inflammatory contents vs clear fluid
Abscess vs tumor: Clinical presentation, imaging characteristics
Microbiologic confirmation through culture.
Diagnostic Challenges:
Sterile abscesses: Culture-negative cases, may require molecular testing
Multiple small abscesses: May mimic other pathologies
Fungal abscesses: Often require special stains for organism identification
Chronic abscesses: May appear similar to tumors
Immunocompromised patients: Atypical presentations.
Rare Variants:
Mycobacterial abscesses: Granulomatous inflammation, acid-fast organisms
Amoebic abscesses: Associated with liver involvement
Candidal abscesses: In severely immunocompromised patients
Actinomycotic abscesses: Sulfur granules, chronic draining sinuses
Hydatid cysts: Parasitic, may become secondarily infected.
Sample Pathology Report
Template Format
Sample Pathology Report
Complete Report: This is an example of how the final pathology report should be structured for this condition.
Specimen Information
Spleen, [procedure type], with clinical history of [symptoms] and risk factors [immunocompromise/diabetes]
Gross Description
The spleen contains [number] abscess(es) measuring [size], with [contents description] and [capsule characteristics]
Microscopic Findings
Sections show [central necrosis] with [inflammatory infiltrate] and [capsule formation]
Special Stains
Gram stain: [result]. GMS stain: [result]. PAS stain: [result]. AFB stain: [result]
Microbiologic Studies
Culture results: [organism identified] with antibiotic sensitivities: [sensitivity pattern]
Diagnosis
Splenic abscess, [acute/chronic], [probable organism if identified]
Complications
[Present/absent] complications: [rupture/fistula formation/sepsis]
Recommendations
Recommend [appropriate antimicrobial therapy] based on culture results and clinical correlation