Definition/General
Introduction:
Splenic trauma refers to injury to the spleen resulting from blunt or penetrating abdominal trauma
The spleen is the most commonly injured organ in blunt abdominal trauma due to its location, vascularity, and friable nature
Splenic injuries range from minor capsular tears to complete organ disruption
Modern management emphasizes splenic preservation when possible due to the organ's immunologic importance.
Origin:
Results from direct impact to left upper quadrant or indirect forces transmitted through adjacent structures
Blunt trauma accounts for 95% of cases (motor vehicle accidents, falls, sports injuries)
Penetrating trauma includes gunshot wounds and stab injuries
Pathologic spleens (splenomegaly, malignancy) have increased susceptibility to injury.
Classification:
American Association for Surgery of Trauma (AAST) Grading: Grade I (minor capsular tear)
Grade II (capsular tear 1-3 cm)
Grade III (capsular tear >3 cm)
Grade IV (segmental devascularization)
Grade V (shattered spleen/hilar disruption)
By mechanism: Blunt trauma
Penetrating trauma
Iatrogenic injury.
Epidemiology:
Most common solid organ injury in blunt abdominal trauma (40-55% of cases)
Peak incidence: Young adults (15-40 years), male predominance
Motor vehicle accidents: Most common cause (50-60%)
Sports-related injuries: Contact sports, cycling
Associated injuries: Left rib fractures (40-60%), other abdominal organs (30-40%).
Clinical Features
Presentation:
Left upper quadrant pain (90% of patients)
Hemodynamic instability in severe cases (tachycardia, hypotension)
Kehr's sign: Left shoulder pain from diaphragmatic irritation
Abdominal distension from hemoperitoneum
Guarding and rigidity on examination.
Symptoms:
Pain characteristics: Left-sided abdominal pain, may radiate to shoulder
Worsened by movement or deep inspiration
Hemorrhage symptoms: Weakness, dizziness, syncope
Pallor and diaphoresis
Peritoneal irritation: Nausea and vomiting
Shock symptoms: In severe bleeding.
Risk Factors:
High-risk activities: Contact sports (football, hockey, martial arts)
High-speed activities (motor racing, cycling)
Anatomic factors: Splenomegaly (infectious mononucleosis, malignancy)
Left lower rib fractures
Medical conditions: Coagulopathy, anticoagulant therapy
Age factors: Elderly patients more prone to severe injury.
Screening:
Clinical assessment: FAST exam (Focused Assessment with Sonography in Trauma)
Physical examination for peritoneal signs
Imaging studies: CT scan with IV contrast (gold standard)
MRI in selected cases
Laboratory studies: Serial hemoglobin, hematocrit
Coagulation studies
Hemodynamic monitoring: Vital signs, urine output.
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Gross Description
Appearance:
Variable appearance depending on injury grade and time since trauma
Fresh injuries: Bright red blood, active bleeding
Capsular tears: Linear lacerations through splenic capsule
Parenchymal lacerations: Deep cuts extending into pulp
Subcapsular hematomas: Blood collections beneath intact capsule.
Characteristics:
Grade I-II injuries: Superficial capsular tears with minimal bleeding
Grade III injuries: Deep lacerations with moderate bleeding
Grade IV-V injuries: Extensive fragmentation, massive bleeding
Associated findings: Clot formation, tissue devitalization
Healing changes: Granulation tissue, fibrosis in chronic cases.
Size Location:
Injury distribution: Lower pole most commonly affected
Upper pole and hilar injuries more severe
Laceration depth: Ranges from superficial to trans-hilar
Hematoma size: Variable from small subcapsular to massive collections
Multiple injuries: Common in severe trauma.
Multifocality:
Multiple lacerations common in high-energy trauma
Bilateral involvement of splenic poles
Associated organ injuries: Left kidney, pancreatic tail, stomach
Hilar involvement: May affect splenic vessels and pancreatic tail
Delayed bleeding: May occur hours to days after initial injury.
Microscopic Description
Histological Features:
Acute phase (0-24 hours): Fresh hemorrhage, tissue disruption, inflammatory cell infiltration
Subacute phase (1-7 days): Organization of hematoma, granulation tissue formation
Chronic phase (>7 days): Fibroblastic proliferation, scar formation, hemosiderin deposition.
Cellular Characteristics:
Acute inflammatory cells: Neutrophilic infiltration at injury margins
Macrophages: Phagocytosis of red blood cells and debris
Fibroblasts: Proliferation for tissue repair
Endothelial cells: Angiogenesis in healing areas
Hemosiderin-laden macrophages: In areas of old hemorrhage.
Architectural Patterns:
Disrupted architecture: Loss of normal splenic organization at injury site
Hematoma organization: Progressive replacement with granulation tissue
Scar formation: Dense fibrous tissue in chronic cases
Regenerative changes: Attempted restoration of normal architecture
Vascular changes: Thrombosis, recanalization.
Grading Criteria:
Acute injury: Fresh hemorrhage, minimal organization
Organizing injury: Granulation tissue, early fibrosis
Healed injury: Mature scar tissue, hemosiderin deposits
Complications: Secondary infection, pseudocyst formation
Regeneration: Partial restoration of splenic architecture.
Immunohistochemistry
Positive Markers:
Vascular markers: CD31, CD34 for assessing vascular integrity and angiogenesis
Macrophage markers: CD68 for tissue macrophages involved in cleanup
Proliferation markers: Ki-67 in areas of active repair
Smooth muscle markers: SMA in organizing areas.
Negative Markers:
Normal splenic markers: May be lost in areas of severe injury
Infectious markers: To exclude secondary infection
Tumor markers: To exclude underlying malignancy
Specific pathogen markers: In suspected infected cases.
Diagnostic Utility:
Assessment of healing: Proliferation markers in repair areas
Vascular assessment: Integrity of blood vessels
Inflammatory evaluation: Degree of inflammatory response
Exclusion of complications: Infection, malignancy.
Molecular Subtypes:
Acute trauma: Predominant inflammatory markers
Healing trauma: Angiogenesis and repair markers
Chronic trauma: Fibrosis and remodeling markers
Complicated trauma: Additional pathologic markers.
Molecular/Genetic
Genetic Mutations:
Wound healing genes: Variations may affect healing response
Coagulation genes: Factor V Leiden, prothrombin mutations affect bleeding risk
Inflammatory response genes: Cytokine gene polymorphisms
Angiogenesis genes: VEGF variants may influence healing.
Molecular Markers:
Inflammatory cytokines: IL-1, TNF-α, IL-6 in acute phase
Angiogenic factors: VEGF, PDGF in healing phase
Coagulation markers: D-dimer, fibrin degradation products
Tissue damage markers: LDH, troponin-like markers.
Prognostic Significance:
Injury severity: AAST grade correlates with outcomes
Patient age: Older patients have worse outcomes
Associated injuries: Multiple organ trauma increases mortality
Hemodynamic status: Shock at presentation indicates severe injury
Time to treatment: Delay increases complications.
Therapeutic Targets:
Conservative management: Observation, bed rest, serial monitoring
Interventional radiology: Splenic artery embolization
Surgical interventions: Splenorrhaphy, partial splenectomy, total splenectomy
Supportive care: Blood transfusion, fluid resuscitation.
Differential Diagnosis
Similar Entities:
Splenic infarction: Ischemic necrosis vs traumatic injury
Spontaneous splenic rupture: Pathologic vs traumatic rupture
Splenic abscess: Infected collection vs hematoma
Splenic cysts: Pre-existing vs post-traumatic
Splenic tumors: Underlying neoplasm vs trauma.
Distinguishing Features:
Trauma vs infarction: History of trauma vs vascular occlusion
Fresh blood vs coagulative necrosis
Traumatic vs spontaneous rupture: Clear trauma history vs underlying pathology
Hematoma vs abscess: Sterile blood vs infected contents
Clinical correlation essential.
Diagnostic Challenges:
Delayed presentation: May present hours to days after injury
Underlying pathology: Splenomegaly, malignancy may predispose
Multiple trauma: Other injuries may overshadow splenic trauma
Pediatric cases: Different management considerations.
Rare Variants:
Delayed splenic rupture: Rupture >48 hours after trauma
Iatrogenic injury: During surgical procedures
Birth trauma: Splenic injury during delivery
Pathologic rupture: In diseased spleen with minor trauma
Post-embolization changes: Following therapeutic intervention.
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
[Splenectomy/splenorrhaphy] specimen with history of [trauma mechanism] [time] ago
Gross Description
Splenic [laceration/hematoma] measuring [dimensions] with [characteristics] and [bleeding status]
AAST Injury Grading
Grade [I-V] splenic injury based on [laceration depth/hematoma size/vascular involvement]
Microscopic Findings
[Acute/subacute/chronic] changes with [hemorrhage/organization/healing] and [inflammatory response]
Healing Assessment
Healing phase: [acute/organizing/healed] with [granulation tissue/fibrosis/regeneration]
Diagnosis
Splenic trauma, AAST Grade [grade], [acute/subacute/chronic]
Complications
[Present/absent]: [infection/devascularization/pseudocyst formation]
Clinical Correlation
Recommend [conservative management/surgical intervention] based on injury grade and patient stability