Definition/General
Introduction:
Splenic infarction is ischemic necrosis of splenic tissue due to interruption of blood supply
It occurs when the splenic artery or its branches are occluded, leading to tissue death
Splenic infarcts can be segmental or global, depending on the level of vascular compromise
The condition ranges from asymptomatic small infarcts to life-threatening massive infarction requiring emergency intervention.
Origin:
Results from arterial occlusion due to thrombosis, embolism, or vasculitis
The spleen's end-arterial circulation makes it particularly susceptible to ischemic injury
Embolic infarcts typically arise from cardiac sources
Thrombotic infarcts occur in hypercoagulable states
Watershed infarcts develop in hypotensive episodes.
Classification:
By extent: Segmental (partial)
Global (complete)
By etiology: Embolic (cardiac, arterial sources)
Thrombotic (in situ thrombosis)
Hemodynamic (hypoperfusion)
By pattern: Wedge-shaped (typical)
Geographic (atypical)
Multiple small infarcts
By age: Acute (<24 hours)
Subacute (1-7 days)
Chronic (>7 days).
Epidemiology:
Most common cause is embolic disease (60-70% cases)
Cardiac emboli from atrial fibrillation, infective endocarditis
Peak incidence in middle-aged adults (40-60 years)
Associated with hematologic malignancies in 15-20% cases
Sickle cell disease causes recurrent infarcts
Post-procedural infarcts in 5-10% of splenic interventions.
Clinical Features
Presentation:
Left upper quadrant pain (most common symptom - 90% cases)
Acute onset severe pain with radiation to left shoulder (Kehr's sign)
Fever and leukocytosis in 70-80% of patients
Nausea and vomiting in 40-50% cases
Splenomegaly may be present in underlying conditions.
Symptoms:
Pain characteristics: Sharp, stabbing left-sided pain
Worsened by movement and deep inspiration
Constitutional symptoms: Fever (often low-grade)
Chills and malaise
Gastrointestinal symptoms: Nausea and vomiting
Early satiety
Referred pain to left shoulder due to diaphragmatic irritation.
Risk Factors:
Cardiovascular conditions: Atrial fibrillation (most common)
Infective endocarditis
Myocardial infarction
Hematologic disorders: Sickle cell disease
Polycythemia vera
Essential thrombocythemia
Hypercoagulable states: Protein C/S deficiency
Antiphospholipid syndrome
Malignancies: Pancreatic adenocarcinoma
Hematologic malignancies.
Screening:
High-risk patients: Those with atrial fibrillation and acute abdominal pain
Patients with known endocarditis
Imaging modalities: Contrast-enhanced CT scan (gold standard)
MRI with gadolinium
Laboratory studies: CBC with differential
Comprehensive metabolic panel
Coagulation studies
Cardiac evaluation in suspected embolic cases.
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Gross Description
Appearance:
Wedge-shaped areas of pallor with base toward capsule and apex toward hilum
Dark red to black discoloration in acute phase
Gray-white appearance in subacute phase (3-7 days)
Well-demarcated borders between infarcted and viable tissue
Capsular involvement may cause surface depression.
Characteristics:
Firm consistency in acute infarcts due to edema
Soft, mushy texture in liquefactive areas
Hemorrhagic borders in early phase
Fibrous scarring in chronic infarcts
Calcification may develop in old infarcts
Cystic degeneration possible in large infarcts.
Size Location:
Size variation: From small subcapsular areas to massive involvement (>50% of spleen)
Location patterns: Upper pole most commonly affected
Lower pole and central areas less frequent
Multiple small infarcts in shower emboli
Geographic distribution follows arterial territories.
Multifocality:
Multifocal infarcts suggest embolic etiology
Bilateral involvement rare due to collateral circulation
Associated findings: Splenic rupture (2-5% of cases)
Abscess formation in infected infarcts
Concurrent organ involvement: Kidney, brain, or extremities in systemic embolic disease.
Microscopic Description
Histological Features:
Coagulative necrosis with preservation of tissue architecture
Loss of nuclear staining throughout infarcted area
Hemorrhage and congestion at margins of infarct
Inflammatory infiltrate at periphery after 24-48 hours
Fibrin thrombi may be visible in vessels at border zone.
Cellular Characteristics:
Ghost cells with eosinophilic cytoplasm and pyknotic nuclei in acute phase
Nuclear fragmentation and karyolysis
Red blood cell extravasation throughout infarcted tissue
Neutrophilic infiltrate at border beginning 24-48 hours
Macrophage infiltration for debris clearance after 3-5 days.
Architectural Patterns:
Preservation of splenic architecture in early coagulative necrosis
Loss of white pulp structure with follicular dissolution
Sinusoidal congestion and hemorrhage
Zonal pattern with central necrosis and peripheral inflammation
Vascular thrombosis at feeding arteries.
Grading Criteria:
Acute phase (0-3 days): Coagulative necrosis with preserved architecture
Minimal inflammation
Subacute phase (3-14 days): Inflammatory infiltrate
Early granulation tissue formation
Chronic phase (>14 days): Fibroblastic proliferation
Scar formation
Complications: Secondary infection
Cyst formation.
Immunohistochemistry
Positive Markers:
Vessel markers: CD31 and CD34 for vascular architecture assessment
Smooth muscle markers: SMA for arterial wall evaluation
Inflammatory markers: CD68 for macrophages in healing phase
Proliferation markers: Ki-67 for granulation tissue activity.
Negative Markers:
Viable tissue markers: Normal cellular markers absent in infarcted areas
Endothelial markers: Loss of CD31/CD34 in necrotic vessels
Lymphoid markers: CD20/CD3 absent in necrotic white pulp
Specific exclusions: Tumor markers to exclude malignancy.
Diagnostic Utility:
Confirmation of infarction: Loss of normal cellular markers
Assessment of viability: Preserved markers in border zones
Evaluation of healing: Granulation tissue markers
Exclusion of malignancy: Tumor-specific markers negative
Vascular assessment: Thrombosis confirmation.
Molecular Subtypes:
Thrombotic infarcts: Associated with hypercoagulable markers
Embolic infarcts: May show foreign material or septic emboli features
Vasculitic infarcts: Associated with vessel wall inflammation
Hemodynamic infarcts: Border zone pattern with preserved architecture.
Molecular/Genetic
Genetic Mutations:
Thrombophilia genes: Factor V Leiden mutation
Prothrombin G20210A mutation
MTHFR mutations
Sickle cell disease: HbS mutation causing vaso-occlusive crises
Protein deficiencies: Protein C, Protein S, Antithrombin III deficiency genes
JAK2 mutations in myeloproliferative disorders.
Molecular Markers:
Coagulation pathway markers: D-dimer elevation
Fibrin degradation products
Inflammatory markers: IL-6, TNF-alpha elevation
Tissue necrosis markers: LDH elevation
Troponin-like markers for splenic injury
Hypoxia markers: HIF-1alpha expression in border zones.
Prognostic Significance:
Extent of infarction correlates with complications and recovery
Underlying etiology determines recurrence risk
Age of infarct affects treatment approach
Associated conditions: Sickle cell disease predicts recurrent episodes
Cardiac sources require anticoagulation.
Therapeutic Targets:
Anticoagulation therapy: Warfarin, direct oral anticoagulants
Antiplatelet therapy: Aspirin, clopidogrel for arterial sources
Thrombolytic therapy: In acute massive infarction (controversial)
Treatment of underlying conditions: Heart failure, arrhythmias
Pain management and supportive care.
Differential Diagnosis
Similar Entities:
Splenic abscess: May have similar pain and fever but with different imaging characteristics
Splenic hematoma: History of trauma, different CT appearance
Splenic tumor: Mass effect, different enhancement pattern
Pancreatitis: May cause similar left upper quadrant pain.
Distinguishing Features:
Infarct vs abscess: Wedge shape vs rounded mass
No rim enhancement vs rim enhancement
Infarct vs tumor: Geographic distribution vs mass effect
Acute onset vs gradual growth
Infarct vs trauma: No history of trauma
Different CT characteristics
Clinical context crucial for differentiation.
Diagnostic Challenges:
Small infarcts may be difficult to detect on imaging
Multiple small infarcts may mimic other pathologies
Chronic infarcts appear as scars and may be confused with tumors
Infected infarcts may mimic primary abscesses
Hemorrhagic infarcts may suggest trauma.
Rare Variants:
Septic infarcts: From infected emboli, associated with endocarditis
Hemorrhagic infarcts: Associated with bleeding disorders
Global splenic infarction: Rare, may require splenectomy
Recurrent infarcts: In sickle cell disease, antiphospholipid syndrome
Iatrogenic infarcts: Following interventional procedures.
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], weighing [X] g, with clinical history of [symptoms and duration]
Gross Description
The spleen shows [location and extent] of infarction with [color and consistency] and [border characteristics]
Microscopic Findings
Sections show [type of necrosis] with [inflammatory response] and [vascular changes]
Age of Infarct
Histologic features consistent with [acute/subacute/chronic] infarction, approximately [time duration]
Vascular Assessment
Vascular examination shows [thrombosis/embolism/vasculitis] with [specific findings]
Diagnosis
Splenic infarction, [extent], [age], likely due to [etiology if known]
Complications
[Present/absent] complications including [rupture/infection/abscess formation]
Clinical Correlation
Recommend clinical correlation with [cardiac evaluation/coagulation studies/hematologic workup]