Splenic Rupture

Etiology

Splenic rupture may be traumatic or nontraumatic. Trauma accounts for most cases, with motor vehicle collisions comprising 50% to 75% of mechanisms, followed by direct abdominal impact and falls. Rupture may occur immediately after injury or present in a delayed fashion. Deceleration forces can stretch or tear the splenic capsule, and rib fractures may directly lacerate the parenchyma. Nontraumatic rupture is rare but carries a mortality rate of approximately 12% and is frequently associated with underlying pathology. Infectious mononucleosis is a well-recognized example, leading to rupture in approximately 0.1% of cases.[2]

Nontraumatic rupture most commonly results from neoplasms or infections, each accounting for 30% of cases. Inflammatory diseases contribute to 15%, while medications or medical treatments account for 10%. Mechanical factors and idiopathic cases each represent about 7%.[3] Medications implicated in nontraumatic rupture include anticoagulants, thrombolytics, and agents used to treat hematologic malignancies. Inflammatory or infectious processes increase splenic friability, rendering the organ susceptible to rupture from mild physiologic strain such as coughing, vomiting, or defecation.

Epidemiology

Splenic rupture predominantly affects male individuals, with a 2:1 ratio, most commonly between the ages of 18 and 34. Blunt abdominal trauma, particularly from motor vehicle collisions, is the leading cause. Contact sports such as football, hockey, cycling, and equestrian activities increase the risk of splenic injury. Military training and occupational accidents have also been identified as contributing factors. Nontraumatic rupture is rare but may occur in individuals with underlying disease or following minor trauma, especially in the presence of splenomegaly.[4]

In regions where malaria and typhoid fever are endemic, chronic infection may lead to splenomegaly and elevate the risk of spontaneous rupture. Immunocompromised individuals, including those with hematologic malignancies or solid organ transplants, may be predisposed to splenic rupture either spontaneously or following minimal trauma.

Pathophysiology

The spleen is a highly vascular organ, making it particularly susceptible to hemorrhage following parenchymal or vascular disruption. Injury may result in subcapsular or intraparenchymal hematoma, laceration, or complete devascularization. The spleen plays essential hematologic and immunologic roles, including the maturation and storage of red blood cells and platelets, filtration of opsonized bacteria and abnormal cells, and contribution to both humoral and cell-mediated immunity. Loss of splenic function following rupture or splenectomy compromises the body's ability to clear encapsulated organisms and increases the risk of overwhelming postsplenectomy infection (OPSI), particularly in children and immunocompromised individuals.

In healthy adults, the spleen weighs up to 250 grams and measures approximately 13 cm in length. With advancing age, the organ typically undergoes involution and may become nonpalpable.[5][6]

History and Physical

Trauma is the most common mechanism of splenic injury, and blunt impact to the LUQ, left rib cage, or left flank should raise suspicion for splenic involvement. However, the absence of substantial trauma does not exclude this possibility, as individuals with splenomegaly require significantly less force to sustain rupture.[7]

A focused history should assess prior surgery, liver disease, recent infections, use of anticoagulants or antiplatelet agents, and known bleeding disorders. External findings such as abrasions, contusions, or a seatbelt sign increase concern for intra-abdominal trauma, although 20% of patients with intra-abdominal injury may lack visible external signs. Physical examination findings may be subtle in the early stages, and altered mental status or distracting injuries can further reduce the reliability of the clinical assessment.[8][9]

Severely ill patients may present with signs of hypovolemic shock, including tachycardia, hypotension, and pallor. Additional findings may include LUQ tenderness, guarding, peritonitis, or the Kehr sign—referred pain to the left shoulder. The Kehr sign is uncommon, but it is suggestive of diaphragmatic or peritoneal irritation from intra-abdominal bleeding.[10][11]

In adults, up to 20% of patients with left lower rib fractures have an associated splenic injury. In children, the compliance of the chest wall may conceal underlying injury in the absence of rib fractures.

Evaluation

A splenic injury may not always be clinically apparent. Spontaneous or pathological rupture can occur following minor trauma or even in the absence of any identifiable inciting event. Ultrasound, particularly the Focused Assessment with Sonography for Trauma (FAST), provides a rapid bedside evaluation and can detect free intraperitoneal fluid with approximately 90% sensitivity when volumes exceed 100 mL. However, this modality cannot reliably identify pseudoaneurysms or early parenchymal injury. Computed tomography (CT) with intravenous contrast remains the gold standard for evaluating hemodynamically stable patients, offering detailed visualization of the splenic parenchyma, vascular integrity, and associated intra-abdominal injuries.[12][13]

Splenic injuries are classified according to the American Association for the Surgery of Trauma (AAST) Organ Injury Scale, which standardizes grading based on the extent of hematoma, laceration, and vascular involvement.[14] Accurate injury grading guides appropriate decision-making for nonoperative versus operative management. 

• Grade I: Subcapsular hematoma involving less than 10% of surface area, or capsular laceration less than 1 cm in depth
• Grade II: Subcapsular hematoma involving 10% to 50% of surface area, intraparenchymal hematoma less than 5 cm, or laceration 1 cm to 3 cm in depth without involvement of trabecular vessels
• Grade III: Subcapsular hematoma involving more than 50% of surface area or expanding, intraparenchymal hematoma greater than 5 cm or expanding, or laceration greater than 3 cm in depth or involving trabecular vessels
• Grade IV: Laceration involving segmental or hilar vessels with devascularization of more than 25% of the spleen
• Grade V: Shattered spleen or hilar vascular injury resulting in complete splenic devascularization 

Higher-grade injuries often require surgical management, while lower grades may be managed conservatively in stable patients. Timely and accurate grading improves interprofessional coordination and enhances clinical outcomes.

Treatment / Management

Management of splenic rupture depends on the severity of injury, presence of associated trauma, and degree of hemodynamic stability. Primary goals include controlling hemorrhage, preserving immune function when feasible, and preventing complications such as infection or delayed rupture.

Nonoperative management is preferred for hemodynamically stable patients without peritonitis or ongoing transfusion requirements. This approach is particularly effective for blunt splenic injuries, with success rates ranging from 60% to 90%.[15] Success exceeds 90% in pediatric patients, who have more resilient splenic tissue and a greater tolerance for nonoperative strategies. Appropriate candidates require monitoring in a facility equipped for frequent hemodynamic assessment, serial abdominal examinations, and immediate access to imaging and intervention.

Monitoring protocols typically include serial hematocrit measurements, vital sign surveillance, and repeated abdominal examinations. Bedside ultrasound may assist in detecting increasing hemoperitoneum. Many institutions also perform follow-up CT in cases involving grade III or higher injuries, active extravasation, or new symptoms such as abdominal pain, hypotension, or tachycardia. Surgical management should be pursued in the setting of hemodynamic instability, transfusion requirements exceeding 40 mL/kg within 24 to 48 hours, or clinical signs of peritonitis.

Interventional radiology plays a critical role in preserving splenic function. Splenic artery embolization may be performed proximally to reduce perfusion pressure across the entire organ or distally to occlude specific bleeding vessels. Indications include active contrast extravasation (contrast blush) on CT, pseudoaneurysm, arteriovenous fistula, and high-grade injury with hemoperitoneum. This technique is particularly valuable in hemodynamically stable patients at increased risk for delayed bleeding or failure of nonoperative management. Proximal embolization offers shorter procedural times and reduced contrast use, whereas distal embolization allows for greater tissue preservation. Access for embolization may be obtained via the femoral or radial artery.[16](B3)

Surgical management is indicated in cases of persistent hemodynamic instability, signs of peritonitis, expanding intra-abdominal hematoma, or failure of nonoperative treatment. Exploratory laparotomy remains the standard surgical approach. When appropriate, splenic preservation techniques such as splenorrhaphy, partial splenectomy, or topical hemostatic agents may be employed. In cases involving extensive parenchymal disruption or uncontrolled hemorrhage, splenectomy is frequently required and may be life-saving.

Intraoperatively, careful dissection is required to control hilar vessels while avoiding injury to adjacent structures such as the tail of the pancreas. Patients undergoing splenectomy should receive appropriate vaccinations prior to discharge or within 14 days postoperatively to reduce the risk of OPSI. Recommended immunizations include vaccines against Streptococcus pneumoniae (PCV13 or PCV20), Haemophilus influenzae type b, and Neisseria meningitidis. Annual influenza vaccination is also advised. In pediatric patients and select high-risk adults, antibiotic prophylaxis with penicillin or amoxicillin may be continued for up to 5 years or longer, depending on immune function and clinical judgment.[17]

Pediatric management prioritizes nonoperative strategies whenever feasible, even in the context of higher-grade injuries. Lower splenectomy rates have been reported in children treated at pediatric centers compared with those managed in general trauma facilities. When splenectomy is unavoidable, long-term follow-up is essential to reinforce vaccination compliance and ensure appropriate education regarding infection risk.

Patient education and discharge planning are essential components of posttreatment care. Clear instructions should be provided regarding the need for urgent evaluation in the event of fever, abdominal pain, or rigors. Asplenic individuals should carry medical alert identification and may benefit from laminated vaccine records or reminder systems for prophylaxis adherence. Patients in regions where travel-related infections such as malaria or babesiosis are prevalent should receive counseling on preventive strategies and the heightened risks associated with asplenia.

Differential Diagnosis

Splenic rupture may mimic or overlap with various intra-abdominal and thoracic pathologies, necessitating careful diagnostic evaluation. Consideration should be given to the following:

• Genitourinary trauma: Injuries to the bladder, ureters, or kidneys may present with hematuria, flank pain, or lower abdominal tenderness. CT urogram may be necessary for evaluation.

• Hollow viscus injury: Perforation of the stomach, small intestine, or colon may present with peritonitis, free intraperitoneal air, or sepsis. CT with oral contrast can assist in diagnosis.

• Mesenteric injury: Often subtle initially, these injuries may lead to delayed bleeding, bowel ischemia, or mesenteric hematoma. CT imaging may show mesenteric stranding or active extravasation.

• Gastric or duodenal ulcer perforation: May present with acute abdominal pain, free fluid, or subdiaphragmatic free air. History of nonsteroidal anti-inflammatory drug use or known peptic ulcer disease provides diagnostic context.

• Acute coronary syndrome: In older adults, this condition may mimic intra-abdominal pathology, presenting with epigastric discomfort, hypotension, or referred shoulder pain.

• Musculoskeletal injury: Rib fractures, abdominal wall hematomas, and costochondritis can produce localized pain that resembles splenic injury, particularly after trauma.

• Retroperitoneal hemorrhage: Often due to vascular injury or anticoagulation, this condition may present with flank ecchymosis (Grey Turner sign), hypotension, and abdominal distension.

• Diaphragmatic rupture: Typically results from blunt trauma and may lead to bowel herniation into the thoracic cavity. Chest radiography or CT may show an elevated hemidiaphragm or intrathoracic bowel loops.

• Pancreatic injury: Often related to high-velocity trauma, this injury may present with midabdominal pain, elevated pancreatic enzymes, or retroperitoneal fluid.

• Splenic infarction: Usually presents with LUQ pain in patients with sickle cell disease, hypercoagulable states, or embolic conditions. CT typically reveals wedge-shaped hypodense regions.

Accurate distinction among potential mimics of splenic injury is critical for initiating condition-specific management. Imaging, clinical context, and hemodynamic status guide diagnostic clarity.

Prognosis

Prognosis following splenic rupture depends on several factors, including injury severity, hemodynamic status at presentation, presence of associated injuries, and availability of advanced trauma care. Hemodynamically stable patients with low-grade injuries (AAST grades I-II) managed nonoperatively typically experience excellent outcomes, with high rates of splenic preservation and minimal long-term complications. Favorable outcomes can also be achieved in select patients with high-grade injuries (AAST grades III-V) when treated at centers equipped with interventional radiology and intensive monitoring.

Timely diagnosis and appropriate triage are essential to reduce morbidity and mortality. Delays in recognizing splenic rupture or failure to stabilize unstable patients increase the risk of poor outcomes. Mortality is most strongly associated with exsanguination from uncontrolled hemorrhage and the presence of concomitant injuries, particularly traumatic brain injury or polytrauma. The overall mortality rate for isolated splenic injury remains low when modern trauma protocols are applied.

Patients who undergo splenectomy face an increased long-term risk of infection from encapsulated organisms and may require lifelong preventive measures. Adherence to vaccination protocols and education regarding infection risk reduces this vulnerability. Some studies have also reported elevated risks of thromboembolism and certain malignancies after splenectomy, although the causal relationship remains uncertain. Splenic artery embolization offers partial preservation of immune function and is associated with fewer infectious complications compared to splenectomy.

Prognosis for splenic rupture has improved substantially due to advancements in imaging, resuscitation, and interprofessional trauma care. Optimal outcomes are achieved when management is individualized based on clinical presentation, imaging findings, and institutional resources.

Complications

Splenic rupture carries the risk of both immediate and delayed complications, particularly when diagnosis or intervention is delayed. Hemorrhagic shock from uncontrolled intra-abdominal bleeding is the most serious acute complication. Delayed rupture and rebleeding may occur even in initially stable patients, most often within 7 to 10 days following injury. This risk increases with higher-grade injuries and highlights the importance of close monitoring throughout the observation period.

In patients managed nonoperatively, potential complications include expanding hematomas, persistent abdominal pain, and formation of vascular lesions such as pseudoaneurysms or arteriovenous fistulae. Pseudoaneurysms may develop several days after the initial injury and pose a risk for delayed rupture. Repeat imaging may be indicated if clinical status changes or initial imaging demonstrates high-grade injury or active contrast extravasation.

Patients who undergo splenic artery embolization may experience complications such as splenic infarction, abscess formation, coil migration, and rebleeding. Distal embolization, or the combination of proximal and distal techniques, increases the risk of infarction. Most infarcts are clinically silent. However, extensive devascularization may lead to secondary infection or necessitate surgical intervention.

Postsplenectomy complications include early postoperative infections, wound-related issues, and long-term susceptibility to OPSI, particularly from encapsulated organisms. An increased incidence of thromboembolic events, including deep vein thrombosis and pulmonary embolism, has also been documented. In pediatric patients and immunocompromised individuals, lifelong infection prophylaxis may be appropriate based on clinical judgment.

Additional complications of splenic rupture include left-sided pleural effusion, subphrenic abscess, pancreatitis due to adjacent inflammation or ischemia, and iatrogenic injury during diagnostic or therapeutic interventions. Optimal outcomes depend on close coordination among trauma surgeons, radiologists, critical care specialists, and primary care providers to minimize preventable complications and ensure appropriate long-term follow-up.