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In fetal development, the spleen serves as a major site of hematopoiesis. Later in life the spleen produces immunoglobulin M (IgM), properdin, and tuftsin, important factors in immunologic function. The spleen also acts as a filter, allowing resident macrophages to remove abnormal red blood cells, cellular debris, and encapsulated and poorly opsonized bacteria.
Mechanisms associated with splenic injury include direct blunt force, deceleration, and compression to the left torso. Splenic injuries should be considered after any significant motor vehicle accident or fall—lower rib fractures, left-side-only rib fractures, and high-energy transfer increase the probability of splenic injury.
The most common sign is pain in the left upper quadrant produced by stretching of the splenic capsule. Peritoneal irritation (rebound tenderness) is caused by extravasated blood. Vital signs vary depending on the associated blood loss and are not specific for injuries to the spleen. On the other hand, patients with a significant splenic injury may exhibit no signs or symptoms at all.
Kehr’s sign is pain from blood irritation of the left diaphragm that is referred to the posterior left shoulder. A common scenario is to have a shoulder radiograph performed after a fall when the pain is actually from a ruptured spleen.
Focused assessment with sonography for trauma (FAST) is routinely performed in the emergency department and can rapidly identify as little as 200 mL of fluid or blood, although this finding is nonspecific for splenic injury. When FAST is equivocal, diagnostic peritoneal lavage is an accurate and sensitive measure of intraabdominal bleeding but is also nonspecific. Computed tomography (CT) scanning is the gold standard diagnostic test because of its ability to identify splenic injuries with a high sensitivity, define the magnitude of injury, and identify concomitant injuries.
Splenic injuries are classified based on the American Association for the Surgery of Trauma splenic injury scale ( Table 27.1 ). Operative versus nonoperative management (NOM) is governed by the hemodynamic status of the patient and concomitant injures. NOM is influenced by the CT grade of splenic injury. NOM is usually successful in grades I–III, whereas further intervention including splenic angioembolization (SAE) is often recommended for grade IV–V injuries because of their high rate of failure of nonoperative management (FNOM).
Grade | Description |
---|---|
I | Hematoma: Nonexpanding subcapsular <10% surface area Laceration: Nonbleeding capsular <1 cm parenchymal depth |
II | Hematoma: Nonexpanding, subcapsular <50% surface area, Nonexpanding intraparenchymal <5 cm diameter Laceration: Bleeding, capsular <3 cm parenchymal depth |
III | Hematoma: Subcapsular >50% surface area, expanding, ruptured with active bleeding, Intraparenchymal >5 cm diameter or expanding Laceration: Capsular >3 cm parenchymal depth, involving trabecular vessel |
IV | Hematoma: Ruptured, intraparenchymal, with active bleeding Laceration: Involves segmental or hilar vessels with >25% splenic devascularization |
V | Laceration: Shattered spleen Vascular: Hilar avulsion or complete splenic devascularization |
Hemodynamically unstable patients should undergo operative management of splenic injuries. However, in hemodynamically stable patients, NOM should be considered in approximately 75%–85% of all blunt splenic injuries in adults, with an overall success rate >90%. The overall NOM success in children <6 years old is >95%. SAE has increased the rate of successful NOM and should be considered in high-risk patients, including grade IV–V injuries as well as all splenic injuries with contrast extravasation on CT scan.
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