Definition/General
Introduction:
Splenic hematoma is a localized collection of blood within or around the spleen following trauma or spontaneous bleeding
It can be subcapsular (beneath the splenic capsule), intraparenchymal (within splenic tissue), or perisplenic (around the spleen)
Hematomas may expand over time and lead to delayed rupture
Understanding hematoma evolution is crucial for clinical management decisions.
Origin:
Results from bleeding into tissue spaces following splenic injury
Subcapsular hematomas form when blood collects beneath intact capsule
Intraparenchymal hematomas occur within splenic tissue from torn vessels
Traumatic etiology most common (blunt abdominal trauma)
Spontaneous hematomas in coagulopathy or vascular malformations.
Classification:
By location: Subcapsular hematoma
Intraparenchymal hematoma
Perisplenic hematoma
By etiology: Traumatic
Spontaneous
Iatrogenic
By evolution: Acute (<48 hours)
Subacute (2-14 days)
Chronic (>14 days)
By size: Small (<5 cm)
Large (>5 cm).
Epidemiology:
Common in splenic trauma: Present in 80-90% of splenic injuries
Age distribution: Peak in young adults due to trauma exposure
Gender: Male predominance (2:1) related to trauma patterns
Spontaneous cases: More common in elderly with anticoagulation
Subcapsular type: Most clinically significant due to rupture risk.
Clinical Features
Presentation:
Left upper quadrant pain (70-80% of symptomatic cases)
Asymptomatic in small hematomas
Delayed rupture risk: Expanding subcapsular hematomas
Mass effect: Large hematomas may compress adjacent organs
Hemodynamic stability: Usually stable unless rupture occurs.
Symptoms:
Pain characteristics: Dull, aching left upper quadrant pain
May increase with hematoma expansion
Referred pain: Left shoulder pain (diaphragmatic irritation)
Gastrointestinal symptoms: Early satiety, nausea
Acute symptoms: Sudden severe pain if rupture occurs.
Risk Factors:
Trauma exposure: Motor vehicle accidents, falls, sports injuries
Anticoagulant therapy: Warfarin, novel anticoagulants
Bleeding disorders: Thrombocytopenia, coagulation factor deficiencies
Liver disease: Coagulopathy from hepatic dysfunction
Procedures: Biopsy, interventional procedures.
Screening:
Post-trauma monitoring: Serial imaging in splenic injury patients
Clinical observation: Pain assessment, vital signs monitoring
Laboratory studies: Serial hemoglobin, coagulation studies
Imaging follow-up: CT scan to assess hematoma size and stability.
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Gross Description
Appearance:
Well-defined blood collection with variable appearance based on age
Acute hematomas: Dark red, liquid blood
Organizing hematomas: Brown color with clot organization
Chronic hematomas: Fibrous capsule with hemosiderin deposits
Subcapsular location: Crescentic shape following capsular contour.
Characteristics:
Size variation: From few centimeters to massive collections
Consistency changes: Liquid to gelatinous to firm organization
Capsule formation: Fibrous capsule in chronic cases
Contents: Blood, clots, serum in different phases
Calcification: May occur in longstanding cases.
Size Location:
Subcapsular: Beneath splenic capsule, crescentic shape
Intraparenchymal: Within splenic tissue, round to oval
Size correlation: Larger hematomas more likely symptomatic
Location significance: Subcapsular more prone to rupture
Multiple hematomas: Possible in severe trauma.
Multifocality:
Multiple hematomas: Common in high-energy trauma (40-50% of cases)
Different stages: May have hematomas of different ages
Associated injuries: Other splenic lacerations, adjacent organ injury
Bilateral involvement: Both splenic poles may be affected.
Microscopic Description
Histological Features:
Acute phase (0-3 days): Fresh blood, intact red blood cells, minimal organization
Early organization (3-7 days): Fibrin mesh, early inflammatory infiltrate
Organizing phase (1-4 weeks): Granulation tissue, hemosiderin-laden macrophages
Mature organization (>4 weeks): Fibrous capsule, organized clot.
Cellular Characteristics:
Red blood cells: Variable morphology based on age
Fresh vs crenated vs hemolyzed
Inflammatory cells: Neutrophils initially, then macrophages
Hemosiderin-laden macrophages: Characteristic of organizing hematomas
Fibroblasts: Proliferation in organizing phase
Giant cells: May be present around organized clot.
Architectural Patterns:
Central organization: Clot organization from periphery inward
Capsule formation: Fibrous tissue surrounding hematoma
Vascular ingrowth: Granulation tissue with new vessel formation
Hemosiderin deposition: Brown pigment in chronic cases
Calcification: Dystrophic calcification in old hematomas.
Grading Criteria:
Acute hematoma: Fresh blood, minimal cellular response
Subacute hematoma: Early organization, mixed inflammatory cells
Chronic hematoma: Organized clot, fibrous capsule, hemosiderin
Complicated hematoma: Secondary infection, cystic degeneration.
Immunohistochemistry
Positive Markers:
Hemoglobin: Positive in red blood cells and breakdown products
Iron stains: Prussian blue positive for hemosiderin
CD68: Positive in macrophages involved in cleanup
Factor VIII: Positive in organizing vessels
Trichrome: Highlights fibrous organization.
Negative Markers:
Epithelial markers: Negative (excludes cystic lesions)
Tumor markers: Negative (excludes neoplasms)
Infectious markers: Negative unless secondarily infected
Vascular markers: Variable in organized areas.
Diagnostic Utility:
Age determination: Hemosiderin staining indicates chronicity
Organization assessment: Degree of fibrosis and granulation tissue
Exclusion of other lesions: Differentiate from cysts, tumors
Infection detection: Special stains for organisms.
Molecular Subtypes:
Acute traumatic: Minimal organization markers
Organizing hematoma: Repair and angiogenesis markers
Chronic hematoma: Fibrosis markers predominant
Infected hematoma: Additional inflammatory markers.
Molecular/Genetic
Genetic Mutations:
Coagulation disorders: Factor V Leiden, prothrombin mutations
Bleeding disorders: von Willebrand disease, hemophilia genes
Vascular disorders: Hereditary hemorrhagic telangiectasia
Connective tissue disorders: Affecting vessel wall integrity.
Molecular Markers:
Coagulation cascade markers: D-dimer, fibrin degradation products
Inflammatory mediators: Cytokines in organizing phase
Angiogenesis factors: VEGF in granulation tissue
Hemoglobin breakdown products: Bilirubin, iron.
Prognostic Significance:
Hematoma size: Larger hematomas higher risk of complications
Location: Subcapsular location higher rupture risk
Patient factors: Age, coagulopathy affect outcomes
Time course: Acute expansion indicates active bleeding
Associated injuries: Multiple trauma worse prognosis.
Therapeutic Targets:
Conservative management: Observation with serial imaging
Interventional procedures: Drainage for large symptomatic hematomas
Surgical intervention: If rupture or expansion occurs
Coagulopathy correction: Reversal of anticoagulation.
Differential Diagnosis
Similar Entities:
Splenic cysts: Clear fluid vs bloody contents
Splenic abscesses: Infected vs sterile blood collection
Splenic tumors: Solid masses vs fluid collection
Perisplenic fluid: Ascites, lymphocele
Splenic infarction: Tissue necrosis vs blood collection.
Distinguishing Features:
Hematoma vs cyst: Bloody vs clear contents, different imaging characteristics
Hematoma vs abscess: Sterile vs infected, different clinical presentation
Hematoma vs tumor: Fluid vs solid on imaging
Clinical correlation: Trauma history, anticoagulation.
Diagnostic Challenges:
Evolution over time: Changing appearance may be confusing
Secondary infection: May convert sterile hematoma to abscess
Cystic degeneration: Chronic hematomas may appear cystic
Multiple lesions: May represent different stages of injury.
Rare Variants:
Spontaneous hematoma: Without significant trauma in coagulopathic patients
Iatrogenic hematoma: Following biopsy or intervention
Expanding hematoma: Progressive enlargement with active bleeding
Infected hematoma: Secondary bacterial contamination
Calcified hematoma: Chronic cases with dystrophic calcification.
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
[Drainage/splenectomy] specimen with clinical history of [trauma/bleeding] [timeframe] ago
Gross Description
[Subcapsular/intraparenchymal] hematoma measuring [dimensions] with [appearance] and [organization characteristics]
Location and Classification
[Type] hematoma, [size category], [age assessment based on appearance]
Microscopic Findings
[Organization phase] hematoma with [cellular response] and [hemosiderin deposition]
Organization Assessment
Hematoma shows [acute/subacute/chronic] organization with [granulation tissue/fibrosis]
Diagnosis
Splenic hematoma, [location], [age], measuring [size]
Complications
[Present/absent]: [secondary infection/expansion/rupture/calcification]
Clinical Correlation
Findings support [conservative management/intervention] based on size and organization phase