Definition/General
Introduction:
Splenic rupture refers to disruption of splenic integrity with bleeding into the peritoneal cavity
It can be traumatic (following blunt or penetrating injury) or spontaneous (without significant trauma)
Splenic rupture is a life-threatening emergency requiring immediate intervention
The spleen's rich vascularity and friable nature make it particularly susceptible to rupture with relatively minor trauma.
Origin:
Traumatic rupture: Results from direct impact or sudden deceleration causing capsular tear and parenchymal disruption
Spontaneous rupture: Occurs in pathologic spleens due to increased fragility (infections, malignancies, infiltrative diseases)
Delayed rupture: May occur hours to weeks after initial injury due to expanding subcapsular hematoma.
Classification:
By etiology: Traumatic rupture (95%)
Spontaneous rupture (5%)
By timing: Immediate rupture
Delayed rupture (>48 hours)
By mechanism: Blunt trauma
Penetrating trauma
Iatrogenic
By pathology: Normal spleen
Pathologic spleen (splenomegaly, infiltration).
Epidemiology:
Incidence: 0.1-0.5% of all emergency department visits
Age distribution: Peak in young adults (20-40 years)
Gender: Male predominance (2:1) due to higher trauma exposure
Mortality: 5-15% overall, higher in delayed cases
Associated trauma: 70% have other injuries.
Clinical Features
Presentation:
Hemodynamic instability: Hypotension, tachycardia (classic triad with abdominal pain)
Abdominal pain: Left upper quadrant, may radiate to shoulder
Peritoneal signs: Rigidity, guarding, rebound tenderness
Kehr's sign: Left shoulder pain from diaphragmatic irritation
Hypovolemic shock: In severe cases.
Symptoms:
Pain characteristics: Severe left upper quadrant pain, may be diffuse
Worsened by movement or deep breathing
Hemorrhagic symptoms: Weakness, dizziness, syncope
Pallor and cold skin
Gastrointestinal symptoms: Nausea, vomiting, decreased bowel sounds
Referred pain: Left shoulder (Kehr's sign).
Risk Factors:
Splenomegaly: Infectious mononucleosis, malaria, lymphoma
Infiltrative diseases: Gaucher disease, amyloidosis
Infections: Malaria, typhoid, endocarditis
Hematologic malignancies: Leukemia, lymphoma
Coagulopathy: Anticoagulant therapy, liver disease
Activities: Contact sports, high-energy trauma.
Screening:
Emergency assessment: FAST exam, hemodynamic monitoring
Laboratory studies: Serial hemoglobin, hematocrit, coagulation studies
Imaging: CT scan with contrast (if stable)
Clinical monitoring: Vital signs, abdominal examination
Blood type and crossmatch: For potential transfusion.
Master Splenic Rupture Pathology with RxDx
Access 100+ pathology videos and expert guidance with the RxDx app
Gross Description
Appearance:
Capsular disruption: Tear in splenic capsule with active bleeding
Parenchymal laceration: Deep cuts extending into splenic pulp
Hemoperitoneum: Blood in peritoneal cavity
Clot formation: Organized clots at rupture site
Variable extent: From small tears to complete fragmentation.
Characteristics:
Active bleeding: Bright red blood from arterial sources
Tissue disruption: Irregular tear patterns, devitalized tissue
Associated hematoma: Subcapsular or intraparenchymal collections
Normal vs pathologic spleen: Underlying disease affects fragility
Healing attempts: Fibrin deposition, clot organization.
Size Location:
Rupture location: Commonly at splenic hilum or poles
Extent of injury: Single tear to multiple lacerations
Associated injuries: Other abdominal organs (liver, kidney)
Hemoperitoneum volume: Variable from minimal to massive (>2 liters)
Subcapsular hematoma: May precede frank rupture.
Multifocality:
Multiple tears: Common in high-energy trauma
Progressive rupture: Initial small tear may extend
Associated organ injuries: Left kidney, pancreas, stomach
Bilateral involvement: Both splenic poles affected
Delayed rupture: Secondary rupture from expanding hematoma.
Microscopic Description
Histological Features:
Acute rupture: Fresh hemorrhage, tissue disruption, minimal organization
Capsular tear: Disrupted connective tissue capsule
Parenchymal disruption: Loss of normal splenic architecture
Vascular injury: Torn arteries and veins with thrombosis
Inflammatory response: Acute inflammatory cell infiltration.
Cellular Characteristics:
Hemorrhage: Massive extravasation of red blood cells
Tissue necrosis: Ischemic changes in devascularized areas
Inflammatory infiltrate: Neutrophils at margins of injury
Clot formation: Fibrin and platelet aggregation
Cellular debris: Fragmented cells and tissue.
Architectural Patterns:
Complete architectural disruption: Loss of normal splenic organization
Hemorrhagic pattern: Diffuse bleeding throughout tissue
Ischemic pattern: Areas of tissue death from vascular injury
Organization pattern: Early healing response in viable areas
Thrombotic pattern: Vascular occlusion from injury.
Grading Criteria:
Acute rupture: Fresh bleeding, minimal organization
Organizing rupture: Granulation tissue formation, clot organization
Complicated rupture: Secondary infection, continued bleeding
Healing rupture: Scar formation, tissue repair (if conservative management).
Immunohistochemistry
Positive Markers:
Vascular markers: CD31, CD34 for assessing vascular injury and repair
Smooth muscle markers: SMA in vessel walls and organizing areas
Macrophage markers: CD68 in areas of tissue cleanup
Proliferation markers: Ki-67 in areas of active repair.
Negative Markers:
Normal tissue markers: Lost in areas of rupture and necrosis
Infectious markers: To exclude secondary infection
Tumor markers: To exclude underlying malignancy
Specific pathogen markers: In cases of suspected infectious rupture.
Diagnostic Utility:
Vascular assessment: Extent of vascular injury and thrombosis
Repair evaluation: Degree of healing response
Inflammatory assessment: Secondary inflammatory response
Exclusion of underlying pathology: Malignancy, infection.
Molecular Subtypes:
Traumatic rupture: Acute inflammatory markers predominant
Spontaneous rupture: May have underlying disease markers
Healing rupture: Repair and angiogenesis markers
Complicated rupture: Additional pathologic markers.
Molecular/Genetic
Genetic Mutations:
Bleeding disorders: Factor deficiencies, von Willebrand disease
Connective tissue disorders: Ehlers-Danlos syndrome, Marfan syndrome
Metabolic diseases: Gaucher disease causing splenomegaly
Coagulation genes: Variants affecting clotting function.
Molecular Markers:
Coagulation markers: Elevated D-dimer, fibrin degradation products
Inflammatory markers: Cytokines (IL-1, TNF-α, IL-6)
Tissue damage markers: Elevated LDH, hepatic enzymes
Angiogenesis factors: VEGF in repair areas.
Prognostic Significance:
Hemodynamic status: Shock at presentation indicates severe bleeding
Time to intervention: Delay increases mortality
Underlying pathology: Pathologic spleen has worse prognosis
Associated injuries: Multiple trauma increases complications
Patient age: Elderly have higher mortality.
Therapeutic Targets:
Emergency surgery: Splenectomy vs splenorrhaphy
Conservative management: Observation in stable patients
Interventional radiology: Splenic artery embolization
Blood products: Transfusion support
Supportive care: Hemodynamic stabilization.
Differential Diagnosis
Similar Entities:
Other causes of hemoperitoneum: Hepatic trauma, mesenteric tear, aortic aneurysm rupture
Splenic pathology: Infarction, abscess, tumor rupture
Other abdominal emergencies: Appendicitis, bowel perforation, ectopic pregnancy
Retroperitoneal bleeding: Renal trauma, psoas hematoma.
Distinguishing Features:
Rupture vs other bleeding: Location-specific findings, imaging characteristics
Traumatic vs spontaneous: History of trauma vs underlying pathology
Splenic vs hepatic: Location of bleeding, associated injuries
Clinical correlation: Mechanism of injury, patient history.
Diagnostic Challenges:
Delayed presentation: May present hours to days after injury
Minimal trauma: Spontaneous rupture with minor precipitants
Associated injuries: Other trauma may overshadow splenic injury
Stable patients: May have occult bleeding without immediate symptoms.
Rare Variants:
Delayed splenic rupture: >48 hours after initial injury
Spontaneous rupture: Without significant trauma in pathologic spleen
Iatrogenic rupture: During medical procedures
Pathologic rupture: Due to underlying disease (malaria, lymphoma)
Recurrent rupture: After previous injury or surgery.
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 specimen with clinical history of [trauma/spontaneous] rupture and [hemoperitoneum volume]
Gross Description
Splenic rupture with [capsular tear/parenchymal laceration] and [active bleeding/clot formation]
Rupture Classification
[Traumatic/spontaneous] rupture with [extent description] and [associated injuries]
Microscopic Findings
[Acute/organizing] tissue disruption with [hemorrhage pattern] and [inflammatory response]
Underlying Pathology
[Present/absent]: [splenomegaly/infiltrative disease/normal spleen]
Diagnosis
Splenic rupture, [traumatic/spontaneous], [acute/organizing]
Complications
[Present/absent]: [ongoing bleeding/secondary infection/associated organ injury]
Clinical Correlation
Findings consistent with [mechanism] and support [surgical intervention/conservative management]