July 7, 2009 | In: TRAUMA
26 SPLENIC TRAUMA
David J. Ciesla M.D., Ernest E. Moore M.D.
1. What is the physiologic role of the spleen?
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In fetal development, the spleen serves as a major site for hematopoiesis. In early childhood the spleen produces immunoglobulin M (IgM) and tuftsin. The spleen also functions as a filter, allowing resident macrophages to remove abnormal red blood cells (RBCs), cellular debris, and encapsulated and poorly opsonized bacteria.
2. What injury patterns are associated with splenic trauma?
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Direct blunt force, deceleration, and compression to the left torso. Think spleen after a motor vehicle accident or fall: lower rib fractures, left side-only rib fractures, and high-energy transfer (big hits) increase the probability of splenic injury.
3. What are the signs and symptoms of splenic injury?
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The main sign is pain in the left upper quadrant. This is produced by stretching the splenic capsule. Peritoneal irritation (rebound tenderness) is caused by extravasated blood (blood is very irritating). Vital signs vary depending on associated blood loss and are not specific for injuries to the spleen. Unfortunately, a large number of patients with a significant splenic injury exhibit no signs or symptoms at all.
4. What studies can help in diagnosing splenic trauma?
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Ultrasound (US) can be performed in the emergency department and can rapidly identify as little as 200 mL fluid/blood. When US is not available, diagnostic peritoneal lavage (DPL) is an accurate and sensitive measure of intraabdominal bleeding.
Hemodynamically stable patients permit more thorough evaluations. Although US is extremely sensitive for detecting intraabdominal bleeding, computed tomography (CT) not only can detect and quantify intraabdominal blood but also can characterize specific intraabdominal injuries.
5. How are splenic injuries classified, and why is that important?
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Management is governed by the hemodynamic status of the patient, but therapy is also influenced by the CT grade of splenic injury. Nonoperative management is most successful in grades I-III, whereas operative intervention is often required for grade IV injuries. Grade V injuries demand prompt operative intervention. (See Table 26-1.)
6. Do splenic injuries require laparotomy?
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No. Nonoperative management is successful in approximately 95% of patients with grades I-III. Hemodynamically stable patients with evidence of ongoing bleeding (requiring transfusion) may be treated by selective arterial embolization if a bleeding site is identified on angiography.
7. What are contraindications to nonoperative management of splenic injuries?
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* Hemodynamic instability
* Persistent coagulopathy
* Additional intraabdominal injury requiring operative intervention
. GRADES OF SPLENIC INJURY
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Grade
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Description
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I
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Hematoma: nonexpanding subcapsular < 10% surface area
Laceration: nonbleeding capsular < 1 cm parenchymal depth
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II
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Hematoma: nonexpanding, subcapsular < 50% surface area
Nonexpanding intraparenchymal < 5 cm diameter
Laceration: bleeding, capsular < 3 cm parenchymal depth
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III
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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
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IV
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Hematoma: ruptured, intraparenchymal, with active bleeding
Laceration: involves segmental or hilar vessels with > 25% splenic devascularization
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V
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Laceration: shattered spleen
Vascular: hilar avulsion or complete splenic devascularization
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8. What is the failure rate of nonoperative management of splenic injury?
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Any patient with signs of hemodynamic instability, persistent bleeding, worsening pain or tenderness, or progressive injury by CT scanning has failed nonoperative management. Approximately 60% of all splenic injuries can be managed nonoperatively with a failure rate of 12%. Factors that predict nonoperative failure include multiple injuries, grade III-V spleen injuries, age > 55 years, and blood traunsfusion.
KEY POINTS: EXPECTANT MANAGEMENT OF SPLENIC INJURIES
1. Nonoperative management is successful in 95% of grades I-III injuries.
2. 60% of all splenic injuries are managed nonoperatively, with a 12% failure/conversion rate.
3. Factors that predict failure/conversion to operative treatment include injury > grade III, age > 55 years, and blood transfusion requirements.
4. Patients with evidence of ongoing bleeding (e.g., contrast “blush” on CT or ongoing transfusion requirements) may be managed with selective arterial embolization.
9. What is delayed rupture of the spleen?
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This is a rare complication that occurs in < 1% of patients with a splenic injury. Delayed splenic rupture should be distinguished from a delay in diagnosis of splenic injury and rupture of a known splenic injury. True delayed splenic rupture occurs > 48 hours in a patient with a history of abdominal trauma and no overt clinical evidence of intraabdominal injury on initial presentation.
10. What are the general principles of operative management of the injured spleen?
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The first priority is to control bleeding. This can usually be accomplished by packing and manual compression of the spleen. If successful, the abdomen is then thoroughly explored for other injuries. Complete mobilization of the spleen by division of the splenocolic, splenorenal, phrenosplenic, and gastrosplenic ligaments is required for complete assessment of the spleen. The short gastric vessels can be ligated with division of the gastrosplenic ligament. Repair of the spleen can be accomplished by application of hemostatic agents, direct pledgeted suture repair of the splenic parenchyma, partial splenectomy, and construction of a “splenic wrap” using absorbable mesh. If splenectomy is required, the splenic artery and vein should be ligated individually prior to removing the spleen.
11. What early complications arise after splenectomy?
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Bleeding, acute gastric dilatation, gastric perforation, pancreatitis (the splenic artery courses along the top of the pancreas), and subphrenic abscess.
12. What is splenic autotransplantation?
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Autotransplantation is accomplished by implanting splenic tissue parenchymal slices into pouches created in the gastrocolic omentum.
13. Does splenic autotransplantation preserve splenic function?
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Autotransplantion after splenectomy is controversial. At least 30% of the original splenic mass is needed to provide normal function. After autotransplantation, IgG and IgM levels are increased in response to pneumococcal vaccine compared with patients after splenectomy alone.
14. Does postsplenectomy leukocytosis predict infection?
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Elevations in white blood cell (WBC) count and platelet count (PC) after splenectomy are a common physiologic event. After the fourth postoperative day, however, a WBC > 15 x 103 and a PC/WBC < 20 are highly associated with sepsis and should not be confused with the physiologic response to splenectomy.
15. Should a follow-up CT scan be performed after nonoperative management of splenic injuries before patient discharge?
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No. Most patients who fail nonoperative management do so within 5 days and will exhibit hemodynamic evidence of ongoing hemorrhage. However, follow-up CT should be performed for grade III and IV injuries at 4-6 weeks before getting back to vigorous physical activity.
16. What is OPSS, and how is it prevented?
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Overwhelming post splenectomy sepsis (OPSS) is a devastating bacteremia (typically encapsulated bacteria) that occurs in 2% of patients after splenectomy. The risk of OPSS is greatest when splenectomy is performed during infancy. The most common organisms are pneumococcus (50%), meningococcus, Escherichia coli, Haemophilus influenzae, staphylococcus, and streptococcus. Although rare, OPSS carries a mortality rate of 75% and has spurred interest in splenic preservation. OPSS is primarily prevented by postoperative vaccination. Pneumococcal, meningococcal, and Haemophilus flu vaccines should be given 2 weeks after splenectomy and are recommended every 5 years. Sepsis can occur despite vaccination; consequently, long-term prophylaxis with oral penicillin is recommended for children.
References
WEB SITES
1. http://www.east.org/tpg/bluntabd.pdf
2. http://www.acssurgery.com/abstracts/acs/acs0506.htm
BIBLIOGRAPHY
1. Cocanour CS, Moore FA, Ware DN, et al: Delayed complications of nonoperative management of blunt adult splenic trauma. Arch Surg 133:619-624, 1998. Medline Similar articles Full article
2. Leemans R, Manson W, Snijder JA, et al: Immune response capacity after human splenic autotransplantation: Restoration of response to individual pneumococcal vaccine subtypes. Ann Surg 229:279-285, 1999. Medline Similar articles Full article
3. Moore EE, Cogbill TH, Jurkovich GJ, et al: Organ injury scaling: Spleen and liver (1994 revision). J Trauma 38:323-324, 1995.
4. Shatz DV: Vaccination practices among North American trauma surgeons in splenectomy for trauma. J Trauma 53:950-956, 2002. Medline Similar articles Full article
5. Toutouzas KG, Velmahos GC, Kaminski A, et al: Leukocytosis after posttraumatic splenectomy: A physiologic event or sign of sepsis? Arch Surg 137:924-928, 2002. Full article
6. Uecker J, Pickett C, Dunn E: The role of follow-up radiographic studies in nonoperative management of spleen trauma. Am Surg 67:22-25, 2001. Medline Similar articles