Definition/General
Introduction:
Splenic necrosis refers to death of splenic tissue due to various pathologic processes
It can be ischemic (from vascular compromise), infectious (from overwhelming sepsis), or toxic (from chemical injury)
The pattern of necrosis (coagulative vs liquefactive) depends on the underlying cause
Splenic necrosis may be focal, multifocal, or diffuse and can lead to serious complications including rupture and sepsis.
Origin:
Results from cellular energy failure due to various mechanisms
Ischemic necrosis: Vascular occlusion, hypoperfusion
Infectious necrosis: Direct cellular damage from pathogens
Toxic necrosis: Chemical or drug-induced cellular injury
Immunologic necrosis: Autoimmune destruction of splenic tissue
Neoplastic necrosis: Tumor outgrowing blood supply.
Classification:
By pattern: Coagulative necrosis (ischemic)
Liquefactive necrosis (infectious)
Caseous necrosis (granulomatous)
By extent: Focal necrosis
Multifocal necrosis
Diffuse necrosis
By etiology: Ischemic
Infectious
Toxic
Neoplastic
By complications: Uncomplicated
With secondary infection
With rupture.
Epidemiology:
Ischemic necrosis: Most common type, associated with vascular disease
Age distribution: Varies by etiology - young adults (trauma) vs elderly (vascular disease)
Gender: No specific gender predilection except for specific causes
Geographic variation: Infectious causes more common in developing countries
Associated conditions: Sickle cell disease, vasculitis, malignancies.
Clinical Features
Presentation:
Left upper quadrant pain (80-90% of symptomatic cases)
Fever in infectious or extensive necrosis
Splenomegaly may be present
Constitutional symptoms: Malaise, anorexia, weight loss
Complications: Rupture, abscess formation, sepsis.
Symptoms:
Pain characteristics: Sharp, stabbing left upper quadrant pain
May radiate to left shoulder (Kehr's sign)
Systemic symptoms: Fever, chills, night sweats
Fatigue and weakness
Gastrointestinal symptoms: Nausea, vomiting, early satiety
Acute complications: Sudden severe pain (rupture).
Risk Factors:
Vascular causes: Sickle cell disease, vasculitis, thromboembolism
Infectious causes: Immunocompromise, endocarditis, sepsis
Toxic causes: Chemotherapy, radiation, drugs
Neoplastic causes: Lymphomas, metastatic disease
Systemic diseases: Autoimmune disorders, hypercoagulable states.
Screening:
High-risk patients: Those with predisposing conditions
Imaging studies: CT or MRI showing areas of necrosis
Laboratory studies: CBC, inflammatory markers, LDH elevation
Microbiologic workup: Blood cultures, specific pathogen testing.
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Gross Description
Appearance:
Variable appearance depending on cause and age of necrosis
Acute coagulative necrosis: Pale, firm areas with preserved architecture
Liquefactive necrosis: Soft, purulent areas with tissue breakdown
Caseous necrosis: Cheese-like, yellow-white material
Hemorrhagic necrosis: Dark red to black areas.
Characteristics:
Size and distribution: From small foci to entire organ involvement
Demarcation: Well-demarcated vs poorly defined borders
Consistency: Firm (coagulative) to soft (liquefactive)
Color changes: Pale to yellow-white to black
Associated findings: Hemorrhage, inflammation, cavitation.
Size Location:
Focal necrosis: Small, scattered areas (<2 cm)
Segmental necrosis: Involving specific vascular territories
Global necrosis: Entire spleen affected
Location patterns: May follow vascular distribution
Multifocal pattern: Multiple discrete areas of necrosis.
Multifocality:
Multiple necrotic foci: Common in embolic disease (60-70% of cases)
Random distribution: Suggests hematogenous spread
Vascular distribution: Following arterial territories
Associated findings: Abscess formation, cavitation, calcification in chronic cases.
Microscopic Description
Histological Features:
Coagulative necrosis: Preservation of tissue architecture with loss of cellular detail
Liquefactive necrosis: Complete tissue breakdown with inflammatory infiltrate
Caseous necrosis: Amorphous, eosinophilic material
Fat necrosis: Foamy macrophages, giant cells
Fibrinoid necrosis: Vessel wall necrosis with fibrin deposition.
Cellular Characteristics:
Nuclear changes: Pyknosis, karyorrhexis, karyolysis
Cytoplasmic changes: Eosinophilia, loss of organelles
Inflammatory response: Variable depending on cause and age
Ghost cell outlines: In coagulative necrosis
Complete cellular dissolution: In liquefactive necrosis.
Architectural Patterns:
Preserved architecture: In early coagulative necrosis
Complete architectural loss: In liquefactive necrosis
Zonal pattern: Central necrosis with peripheral inflammation
Hemorrhagic pattern: Red blood cell extravasation
Granulomatous pattern: In infectious or autoimmune causes.
Grading Criteria:
Early necrosis: Cellular changes without architectural loss
Established necrosis: Complete loss of cellular viability
Organizing necrosis: Inflammatory infiltrate and granulation tissue
Complicated necrosis: Secondary infection, cavitation, calcification.
Immunohistochemistry
Positive Markers:
Inflammatory markers: CD68 in macrophages responding to necrosis
Endothelial markers: CD31, CD34 in viable vessels at margins
Proliferation markers: Ki-67 in reactive areas
Specific pathogen markers: In infectious causes.
Negative Markers:
Normal cellular markers: Lost in areas of necrosis
Viability markers: Absent in necrotic tissue
Organ-specific markers: Splenic markers lost in necrotic areas
Metabolic markers: Enzymes absent due to cellular death.
Diagnostic Utility:
Confirmation of necrosis: Loss of normal cellular markers
Assessment of viability: Preserved markers in border zones
Pathogen identification: Specific stains for organisms
Inflammatory assessment: Type and extent of inflammatory response.
Molecular Subtypes:
Ischemic necrosis: Loss of metabolic markers, preserved architecture initially
Infectious necrosis: Pathogen-specific markers, inflammatory response
Toxic necrosis: May have specific drug-related markers
Neoplastic necrosis: Tumor markers may persist in viable areas.
Molecular/Genetic
Genetic Mutations:
Sickle cell disease: HbS mutation causing vaso-occlusive crises
Thrombophilia genes: Factor V Leiden, prothrombin mutations
Immunodeficiency genes: Predisposing to infections
Metabolic disease genes: Gaucher disease, other storage disorders.
Molecular Markers:
Cell death markers: TUNEL positive cells, caspase activation
Hypoxia markers: HIF-1α in ischemic areas
Inflammatory cytokines: IL-1, TNF-α, IL-6
Tissue damage markers: Elevated LDH, cellular enzymes.
Prognostic Significance:
Extent of necrosis: Larger areas have worse prognosis
Underlying cause: Treatable causes have better outcomes
Complications: Secondary infection, rupture worsen prognosis
Patient factors: Age, comorbidities affect recovery
Time to treatment: Early intervention improves outcomes.
Therapeutic Targets:
Treat underlying cause: Specific therapy based on etiology
Supportive care: Pain management, fluid support
Prevent complications: Monitor for rupture, infection
Surgical intervention: Splenectomy in severe cases
Antimicrobial therapy: In infectious causes.
Differential Diagnosis
Similar Entities:
Splenic infarction: Vascular occlusion vs other causes of necrosis
Splenic abscess: Infected necrosis vs sterile necrosis
Splenic tumor necrosis: Neoplasm with central necrosis
Splenic trauma: Traumatic tissue death
Splenic cysts: Fluid-filled lesions vs solid necrosis.
Distinguishing Features:
Necrosis vs infarction: Broader causes vs specific vascular occlusion
Sterile vs infected necrosis: Absence vs presence of organisms
Primary vs secondary necrosis: Direct tissue death vs tumor necrosis
Clinical correlation: History, risk factors, laboratory findings.
Diagnostic Challenges:
Determining etiology: Multiple potential causes require investigation
Extent assessment: Imaging may underestimate necrosis extent
Infection detection: Secondary infection may complicate picture
Sampling issues: Adequate tissue needed for diagnosis.
Rare Variants:
Massive splenic necrosis: Entire organ involvement
Recurrent necrosis: In systemic diseases like sickle cell disease
Drug-induced necrosis: Chemotherapy-related
Autoimmune necrosis: In systemic lupus erythematosus
Radiation necrosis: Following radiation therapy.
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
[Biopsy/splenectomy] specimen with clinical history of [risk factors] and [presentation]
Gross Description
[Extent] splenic necrosis with [appearance] and [distribution pattern]
Necrosis Pattern
[Type] necrosis involving [percentage] of splenic tissue in [focal/multifocal/diffuse] pattern
Microscopic Findings
[Coagulative/liquefactive/caseous] necrosis with [inflammatory response] and [architectural preservation/loss]
Special Stains
[Organism stains]: [positive/negative]. [Other special stains]: [results]
Diagnosis
Splenic necrosis, [type], [extent], likely [etiology]
Probable Etiology
[Ischemic/infectious/toxic/neoplastic] based on [clinical correlation and morphologic features]
Recommendations
Recommend [treatment of underlying cause] and [monitoring for complications]