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Management of Splenic Trauma in Adults
CHAPTER
139
Management of Splenic Trauma in Adults Sara A. Mansfield
|
Amy P. Rushing
T
he spleen, an important component of the reticuloendothelial system in normal adults, is a highly vascular solid organ that arises as a mass of differentiated mesenchymal tissue during early embryonic development. The normal adult spleen weighs between 75 and 100 g and receives an average blood flow of 300 mL/min. It functions as the primary filter of the reticuloendothelial system by sequestering and removing antigens, bacteria, and senescent or damaged cellular elements from the circulation. In addition, the spleen has an important role in humoral immunity because it produces immunoglobulin M and opsonins for the complement activation system.1 Although the spleen resides under the confines of the left lower rib cage, it is frequently subject to both blunt and penetrating trauma. Isolated splenic injury after blunt trauma is common in children, whereas the adult trauma population will often sustain associated injuries to the thorax, kidneys, extremities, and head.2 The mechanism of injury in blunt trauma stems from abrupt deceleration resulting in vascular torsion of the splenic hilum, shearing of the short gastric vessels within the gastrosplenic ligament, or capsular tearing at sites of ligamentous fixation. Clinical features that suggest splenic trauma include left upper quadrant or flank ecchymosis and abrasions, as well as left shoulder pain caused by irritation of the left hemidiaphragm by subphrenic blood (Kehr sign). In instances of penetrating trauma, a wound track traversing the left upper quadrant raises the suspicion for splenic injury. Regardless of mechanism, all trauma patients should receive the primary survey, followed by the appropriate secondary evaluation and ancillary studies. Currently, the accepted standard of care for most splenic trauma is expectant management with close observation. Operative intervention is reserved for the hemodynamically labile patient who shows signs of active hemorrhage and who does not respond appropriately to fluid resuscitation. Although these clinical scenarios seem straightforward, it is often the condition of the patient who falls in between the two ends of the spectrum that can be the most challenging to manage. In the setting of advanced imaging techniques and interventional radiology, the trauma surgeon has more diagnostic information and more treatment options for the patient with splenic trauma.
DIAGNOSIS Patients who present with evidence of ongoing intraabdominal hemorrhage should undergo immediate operative exploration. For those who present with normal hemodynamics, a thorough diagnostic evaluation should be completed. Following the primary survey, a focused abdominal examination should be performed, looking for signs of significant intraabdominal injuries. Abdominal
1622
wall ecchymosis, abrasions, flank pain, and distention should raise suspicion for an injury and prompt further diagnostic work-up. The patient who presents with left-sided rib fractures should also be evaluated for a concomitant splenic laceration. A laboratory panel should be sent to obtain an index hemoglobin and hematocrit, platelet count, and coagulation profile. While in the emergency department, the focused abdominal sonography for trauma (FAST) exam offers a rapid and noninvasive approach to detecting intraperitoneal blood. The sensitivity of FAST has been reported between 43% and 93%, whereas its specificity ranges in various reports between 90% and 98%.3,4 The primary limitations of FAST are the heavy operator dependence of the ultrasonographic exam, as well as the technical limitations caused by the patient’s body habitus or intestinal gas. Branney et al. demonstrated the technical shortcomings of the technique by infusing volumes of diagnostic peritoneal lavage fluid into the peritoneal cavity and found that only 10% of participants performing FAST could detect fluid volumes of less than 400 mL.5 In spite of these obstacles, the FAST exam is helpful in the preliminary evaluation of the patient, especially when the patient cannot undergo further imaging because of hemodynamic instability. Given the ranges in sensitivity, it is important to remember a negative FAST without a computed tomography (CT) may result in missed intraabdominal injuries. In addition, in hemodynamically labile patients, the decision of exploratory laparotomy should not be distracted by a negative FAST.6 Unlike ultrasonography, CT has dramatically changed the way we characterize splenic injuries. The CT scan is the diagnostic modality of choice for the hemodynamically stable patient in whom a splenic injury is suspected. The sensitivity and specificity of CT imaging approaches 100% and 98%, respectively.7 Current-generation multislice scanners provide a detailed survey of the splenic architecture and allow the clinician to differentiate simple subcapsular hematomas from more severe parenchymal and vascular injuries. Although exposing patients to increased radiation, the arterial phase of CT image acquisition—in addition to traditionally obtained portal venous and delayed phase images—should be considered to optimize the detection of traumatic splenic injuries.8 Several grading systems have been used for classifying splenic injuries, and these have important implications in both the operative and nonoperative management decisions. The Organ Injury Scaling Committee of the American Association for the Surgery of Trauma (OISCAAST) devised an anatomic grading system that defines the severity of splenic injuries.9 The system incorporates both CT scan findings and intraoperative assessment of the spleen and consists of five grades (Table 139.1). This grading scale provides universal definitions that all
Management of Splenic Trauma in Adults CHAPTER 139 1622.e1
ABSTRACT This chapter addresses the diagnostic evaluation and initial treatment of acute splenic trauma with a focus on nonoperative intervention. Specifically, the text reviews available diagnostic modalities, indications for operative and nonoperative management, and the application of angioembolization for splenic hemorrhage.
KEYWORDS Spleen, hemorrhage, shock, FAST, nonoperative management, interventional radiology, angioembolization, overwhelming postsplenectomy sepsis (OPSS)
Management of Splenic Trauma in Adults CHAPTER 139
TABLE 139.1 Organ Injury Scaling Committee of the American Association for the Surgery of Trauma (1994 Revision) Grade
Injury Description
I
Hematoma—subcapsular, <10% surface area Or Laceration—capsular tear, <1 cm parenchymal depth Hematoma—subcapsular, 10%–50% surface area, intraparenchymal, <5 cm in diameter Or Laceration 1–3 cm parenchymal depth which does not involve a trabecular vessel Subcapsular, >50% surface area or expanding, ruptured subcapsular or parenchymal hematoma, intraparenchymal hematoma >5 cm or expanding Or Laceration >3 cm parenchymal depth or involving trabecular vessels Laceration involving segmental or hilar vessels producing major devascularization (>25% of spleen) Completely shattered spleen Or Hilar vascular injury which devascularizes spleen
II
III
IV
V
Advance one grade for multiple injuries, up to grade III. Modified from Moore EE, Cogbill TH, Jurkovich GJ, Shackford SR, Malangoni MA, Champion HR. Organ injury scaling: spleen and liver (1994 revision). J Trauma. 1995;38:323.
clinicians can understand, and it becomes particularly useful when a patient requires transfer to a tertiary trauma center from an acute care hospital as the severity of injury is readily appreciated. Although the trauma community recognizes that the primary predictor of operative intervention is hemodynamic instability, the organ injury severity scale can also serve as a predictor of further therapeutic intervention. Haan et al. reported a splenic salvage rate of 94% over a 5-year period; however, they found that the salvage rate decreased with increased splenic injury grade.10
NONOPERATIVE MANAGEMENT The increased availability of high-resolution CT scan and advances in arterial angiography and embolization techniques have contributed to the success of nonoperative management of splenic injuries. The hemodynamically stable patient with blunt splenic trauma can be adequately managed with bed rest, serial abdominal exams, and hemoglobin and hematocrit monitoring. This approach, in combination with occasional angiography, especially for grade III and IV injuries, confers a splenic salvage rate of up to 95%.11,12 In the setting of expectant management, indications for angiography have been delineated by several studies and include the following CT scan features: contrast extravasation, the presence of a pseudoaneurysm, significant hemoperitoneum, high-grade injury, and evidence of a vascular injury.13 The goal of angiography is to localize bleeding and embolize the source with coils or a gelatin foam product. Embolization can occur either at the main splenic artery just distal to the dorsal pancreatic portion of the vessel—known as
1623
proximal embolization—or selectively at the distal branch of the injured vessel. The goal behind the former technique is to decrease the perfusion pressure to the spleen to encourage hemostasis. The disadvantage to this technique is global splenic ischemia, and many have questioned the spleen’s immunocompetence following proximal embolization. Malhotra et al. examined the effects of angioembolization on splenic function by examining serum levels of a particular T-cell line. T-cell proportions between patients who had undergone splenic embolization with asplenic patients and healthy controls were similar suggesting some degree of splenic immunocompetency was maintained.14 A Norwegian study comparing blood samples from patients who had undergone angioembolization with healthy controls demonstrated that the study samples had similar levels of pneumococcal immunoglobulins and no HowellJolly bodies, suggesting normal splenic function.15 Although these preliminary studies remain encouraging, there is no definitive evidence that splenic immunocompetency is fully maintained following angioembolization. There is no question that advancements in interventional techniques have contributed to the successful nonoperative management of splenic injuries. This has certainly changed the strategy, but it has not completely replaced operative intervention. The challenge now remains predicting those patients who will ultimately require splenectomy. Many groups have studied potential predictors of nonoperative failure. Earlier studies found that a higher injury grade, increased transfusion requirement, and hypotension on initial presentation consistently predicted failure of nonoperative management. More recent literature reflects the use of advanced imaging techniques for predicting which patients will ultimately require splenectomy. Haan looked at the overall outcomes of patients admitted with blunt splenic trauma and reported several radiographic findings that were prevalent among patients requiring splenectomy after angioembolization: contrast extravasation, pseudoaneurysm, significant hemoperitoneum, and arteriovenous fistula. Among these characteristics, an arteriovenous fistula had the highest rate of nonoperative failure at 40%.10 Nonradiographic features associated with significant risk of nonoperative failure include age greater than 40, injury severity score of 25 or greater, or presence of large-volume hemoperitoneum.16,17 Aside from radiographic findings, some groups have also examined the mechanism of injury and its association with nonoperative failure. Plurad et al. conducted a retrospective review over a 15-year period and found that patients who were victims of blunt assault were more likely to fail nonoperative management: 36% of these patients required splenectomy versus 11.5% of patients from all other mechanisms combined. These findings suggest that regardless of overall injury severity, individuals who sustain a direct transfer of injury to the left torso are more likely to require splenectomy.18
OPERATIVE MANAGEMENT When a patient presents with hemodynamic lability in spite of timely resuscitation, operative intervention remains the most prudent course of treatment. In this situation,
1624
SECTION III Pancreas, Biliary Tract, Liver, and Spleen
standard principles of trauma care are followed: the patient should have reliable intravenous access, appropriate volume resuscitation, preparation of type and crossmatched packed red blood cells, nasogastric decompression, and preoperative intravenous antibiotic administration. It is standard practice to use a vertical midline incision for laparotomy because this affords the quickest access to the peritoneal cavity. If this incision proves to be insufficient, it can be extended cephalad and to the left of the xiphoid process. In addition, the left triangular ligament of the liver may be incised to allow reflection of the liver away from the area of interest. Although it may seem practical, an oblique left upper quadrant incision for a presumed isolated splenic injury is more time-consuming and offers little access to the remainder of the peritoneal cavity should a concomitant injury present itself. After entering the peritoneal cavity, a standard initial survey should be performed. All four quadrants should be packed and systematically inspected for bleeding or enteric contamination. If other injuries are recognized and require more urgent attention, one can achieve adequate hemostasis of the spleen with proper packing. Multiple laparotomy packs should be placed around the splenic parenchyma in such a manner that a tamponade effect is maintained between the diaphragm, lateral abdominal wall, and retroperitoneum. When it is time to address the injury, mobilization is achieved by placing laparotomy packs posterior to the spleen and lifting it directly into the operative field. Following its inspection, the spleen’s ligamentous attachments to the diaphragm, kidney, and colon should be sharply incised. These connections are avascular and can be divided with impunity in most circumstances. The spleen can then be rotated to the midline and further elevated, thus enabling complete access to its anterior and posterior surfaces, as well as to the hilum. Once accomplished, the operator can easily achieve virtually complete hemostasis of any splenic injury by direct manual compression of the splenic parenchyma or by control of the splenic artery and vein at the hilum. At this point, a decision is made regarding splenectomy or splenorrhaphy. After the spleen has been fully mobilized, one may proceed with splenectomy by first individually ligating and dividing the short gastric vessels. These vessels should be addressed far from the greater curvature of the stomach so that the risk of gastric wall necrosis is minimized. Because the short gastric vessels are divided and the splenic hilum is skeletonized, one must pay attention to the tail of the pancreas. Careless technique can result in disruption of the pancreatic capsule and the development of a pancreatic fistula with subsequent morbidity. Following the division of the short gastric vessels, the splenic artery is then doubly ligated and divided within the splenic hilum. The splenic vein is dealt with in the same manner, and the splenectomy is completed. After removal of the spleen, the splenic bed should be thoroughly irrigated and inspected for hemostasis. These steps are essential to minimize the chances of postoperative splenic bed hematoma, which in turn predisposes to the risk of a subphrenic abscess. Although there are no conclusive data regarding the use of closed-suction drains in the surgical bed, we do not routinely drain the
splenic fossa following splenectomy. Meticulous hemostasis tends to be the best method in avoiding splenic bed complications. The term splenorrhaphy refers to a variety of “spleensparing” techniques aimed at controlling hemorrhage so that the patient may retain the immunologic benefits of the spleen. The intraoperative decision to attempt splenorrhaphy should be made only after the spleen has been fully mobilized and inspected. 19,20 As a general rule, splenorrhaphy is most appropriately considered in cases of less severe injury (e.g., grades I and II, and occasionally grade III). Splenorrhaphy should not be attempted to repair extensive or complex injuries of the spleen, nor is it well advised to undertake splenorrhaphy in the face of multiple concomitant injuries or associated hypotension. With the spleen fully mobilized and controlled in the surgeon’s hand, splenorrhaphy may consist of mere manual compression of the parenchyma to achieve hemostasis of simple lacerations. In addition, there are a variety of topical hemostatic agents that may be applied directly to the bleeding parenchymal surface. Other options include suture repair of the spleen using a monofilament suture in a mattress technique, where one can also incorporate a piece of omentum or gelatin sponge product into the repair. Alternatively, wrapping the entire spleen in absorbable mesh has been described as a means of effective tamponade and has not been associated with a significant increase in infectious complications.20 Examining splenic salvage rates over a 9-year period, Feliciano et al. found that the majority of splenorrhaphy cases were accomplished with simple techniques and less than 10% required a mesh wrap. In this series, the incidence of rebleeding was 1.3%.21
POSTOPERATIVE CONSIDERATIONS Overwhelming postsplenectomy sepsis (OPSS), first described by Diamond in 1969, is an infrequent but potentially catastrophic complication of splenectomy resulting from an increased susceptibility to infection by encapsulated microorganisms.22 The overall standard incidence ratio for hospitalization for sepsis was 5.7, with lower incidences in trauma patients (3.4; 95% confidence interval [CI], 3.0 to 3.8), compared with 18 (95% CI, 16 to 19) for patients with hematologic malignancies.23 Early reports of OPSS indicated mortality rates of 50% to 70% in spite of the use of intravenous antibiotics and intensive therapeutic intervention. With advances in antibiotic therapy and intensive care, the mortality rate of OPSS can be expected to be approximately 10%, with more than half of all fatalities occurring within 48 hours of presentation.1,24 Given these findings, it is a widely accepted practice to immunize patients with pneumococcal vaccine shortly after undergoing emergency splenectomy prior to discharge from the hospital.25 The incidence of OPSS does not appear to have decreased during the vaccine era.23 In fact, Streptococcus pneumoniae remains the causative organism in 42% of cases.26 The efficacy and clinical importance of Neisseria meningitidis and Haemophilus influenzae type b vaccination in splenectomized individuals is unknown but should be considered in patients who are deemed more likely to encounter these organisms.25 We
Management of Splenic Trauma in Adults CHAPTER 139
typically administer all three of the vaccines to patients undergoing emergency splenectomy. Although these patients should take all necessary precautions to avoid serious infections, prophylactic antibiotics are not thought to be necessary following splenectomy in adults.27 Antibody response appears to be preserved following splenic artery embolization, especially in selective embolization, indicating vaccines may not be needed; however, larger studies are needed to confirm this.28
REFERENCES 1. Lynch AM, Kapila R. Overwhelming postsplenectomy infection. Infect Dis Clin North Am. 1996;10:693. 2. Miller PR, Croce MA, Bee TK, Malhotra AK, Fabian TC. Associated injuries in blunt solid organ trauma: implications for missed injury in nonoperative management. J Trauma. 2002;53:238. 3. Rozycki GS, Ballard RB, Feliciano DV, Schmidt JA, Pennington SD. Surgeon-performed ultrasound for the assessment of truncal injuries: lessons learned from 1540 patients. Ann Surg. 1998;228:557. 4. Natarajan B, Gupta PK, Cemaj S, Sorensen M, Hatzoudis GI, Forse RA. FAST scan: is it worth doing in hemodynamically stable blunt trauma patients? Surgery. 2010;148:695. 5. Branney SW, Wolfe RE, Moore EE, et al. Quantitative sensitivity of ultrasound in detecting free intraperitoneal fluid. J Trauma. 1995; 39:375. 6. Carter JW, Falco MH, Chopko MS, Flynn WJ Jr, Wiles Iii CE, Guo WA. Do we really rely on FAST for decision-making in the management of blunt abdominal trauma? Injury. 2015;46:817. 7. Wing VW, Federle MP, Morris JA, Jeffrey RB, Bluth R. The clinical impact of CT for blunt abdominal trauma. AJR Am J Roentgenol. 1985;145:1191. 8. Uyeda JW, LeBedis CA, Penn DR, Soto JA, Anderson SW. Active hemorrhage and vascular injuries in splenic trauma: utility of the arterial phase in multidetector CT. Radiology. 2014;270:99. 9. Moore EE, Cogbill TH, Jurkovich GJ, Shackford SR, Malangoni MA, Champion HR. Organ injury scaling: spleen and liver (1994 revision). J Trauma. 1995;38:323. 10. Haan JM, Bochicchio GV, Kramer N, Scalea TM. Nonoperative management of blunt splenic injury: a 5-year experience. J Trauma. 2005;58:492. 11. Miller PR, Chang MC, Hoth JJ, et al. Prospective trial of angiography and embolization for all grade III to V blunt splenic injuries: nonoperative management success rate is significantly improved. J Am Coll Surg. 2014;218:644.
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12. Renzulli P, Gross T, Schnurger B, et al. Management of blunt injuries to the spleen. Br J Surg. 2010;97:1696. 13. Haan JM, Biffl W, Knudson MM, et al. Splenic embolization revisited: a multicenter review. J Trauma. 2004;56:542. 14. Malhotra AK, Carter RF, Lebman DA, et al. Preservation of splenic immunocompetence after splenic artery angioembolization for blunt splenic injury. J Trauma. 2010;69:1126. 15. Skattum J, Titze TL, Dormagen JB, et al. Preserved splenic function after angioembolisation of high grade injury. Injury. 2012;43:62. 16. Olthof DC, Joosse P, van der Vlies CH, de Haan RJ, Goslings JC. Prognostic factors for failure of nonoperative management in adults with blunt splenic injury: a systematic review. J Trauma Acute Care Surg. 2013;74:546. 17. Bhangu A, Nepogodiev D, Lal N, Bowley DM. Meta-analysis of predictive factors and outcomes for failure of non-operative management of blunt splenic trauma. Injury. 2012;43:1337. 18. Plurad DS, Green DJ, Inaba K, et al. Blunt assault is associated with failure of nonoperative management of the spleen independent of organ injury grade and despite lower overall injury severity. J Trauma. 2009;66:630. 19. Berry MF, Rosato EF, Williams NN. Dexon mesh splenorrhaphy for intraoperative splenic injuries. Am Surg. 2003;69:176. 20. Pachter HL, Hofstetter SR, Spencer FC. Evolving concepts in splenic surgery: splenorrhaphy versus splenectomy and postsplenectomy drainage—experience in 105 patients. Ann Surg. 1981;194:262. 21. Feliciano DV, Spjut-Patrinely V, Burch JM, et al. Splenorrhaphy—the alternative. Ann Surg. 1990;211:569. 22. Diamond LK. Splenectomy in childhood and the hazard of overwhelming infection. Pediatrics. 1969;43:886. 23. Edgren G, Almqvist R, Hartman M, Utter GH. Splenectomy and the risk of sepsis: a population-based cohort study. Ann Surg. 2014;260: 1081. 24. Brigden ML, Pattullo AL. Prevention and management of overwhelming postsplenectomy infection—an update. Crit Care Med. 1999;27:836. 25. Shatz DV. Vaccination practices among North American trauma surgeons in splenectomy for trauma. J Trauma. 2002;53:950. 26. Theilacker C, Ludewig K, Serr A, et al. Overwhelming postsplenectomy infection: a prospective multicenter cohort study. Clin Infect Dis. 2016;62:871. 27. Working Party of the British Committee for Standards in Haematology Clinical Haematology Task Force. Guidelines for the prevention and treatment of infection in patients with an absent or dysfunctional spleen. BMJ. 1996;312:430. 28. Olthof DC, Lammers AJ, van Leeuwen EM, Hoekstra JB, ten Berge IJ, Goslings JC. Antibody response to a T-cell-independent antigen is preserved after splenic artery embolization for trauma. Clin Vaccine Immunol. 2014;21:1500.
139
Management of Splenic Trauma in Adults Sara A. Mansfield
|
Amy P. Rushing
T
he spleen, an important component of the reticuloendothelial system in normal adults, is a highly vascular solid organ that arises as a mass of differentiated mesenchymal tissue during early embryonic development. The normal adult spleen weighs between 75 and 100 g and receives an average blood flow of 300 mL/min. It functions as the primary filter of the reticuloendothelial system by sequestering and removing antigens, bacteria, and senescent or damaged cellular elements from the circulation. In addition, the spleen has an important role in humoral immunity because it produces immunoglobulin M and opsonins for the complement activation system.1 Although the spleen resides under the confines of the left lower rib cage, it is frequently subject to both blunt and penetrating trauma. Isolated splenic injury after blunt trauma is common in children, whereas the adult trauma population will often sustain associated injuries to the thorax, kidneys, extremities, and head.2 The mechanism of injury in blunt trauma stems from abrupt deceleration resulting in vascular torsion of the splenic hilum, shearing of the short gastric vessels within the gastrosplenic ligament, or capsular tearing at sites of ligamentous fixation. Clinical features that suggest splenic trauma include left upper quadrant or flank ecchymosis and abrasions, as well as left shoulder pain caused by irritation of the left hemidiaphragm by subphrenic blood (Kehr sign). In instances of penetrating trauma, a wound track traversing the left upper quadrant raises the suspicion for splenic injury. Regardless of mechanism, all trauma patients should receive the primary survey, followed by the appropriate secondary evaluation and ancillary studies. Currently, the accepted standard of care for most splenic trauma is expectant management with close observation. Operative intervention is reserved for the hemodynamically labile patient who shows signs of active hemorrhage and who does not respond appropriately to fluid resuscitation. Although these clinical scenarios seem straightforward, it is often the condition of the patient who falls in between the two ends of the spectrum that can be the most challenging to manage. In the setting of advanced imaging techniques and interventional radiology, the trauma surgeon has more diagnostic information and more treatment options for the patient with splenic trauma.
DIAGNOSIS Patients who present with evidence of ongoing intraabdominal hemorrhage should undergo immediate operative exploration. For those who present with normal hemodynamics, a thorough diagnostic evaluation should be completed. Following the primary survey, a focused abdominal examination should be performed, looking for signs of significant intraabdominal injuries. Abdominal
1622
wall ecchymosis, abrasions, flank pain, and distention should raise suspicion for an injury and prompt further diagnostic work-up. The patient who presents with left-sided rib fractures should also be evaluated for a concomitant splenic laceration. A laboratory panel should be sent to obtain an index hemoglobin and hematocrit, platelet count, and coagulation profile. While in the emergency department, the focused abdominal sonography for trauma (FAST) exam offers a rapid and noninvasive approach to detecting intraperitoneal blood. The sensitivity of FAST has been reported between 43% and 93%, whereas its specificity ranges in various reports between 90% and 98%.3,4 The primary limitations of FAST are the heavy operator dependence of the ultrasonographic exam, as well as the technical limitations caused by the patient’s body habitus or intestinal gas. Branney et al. demonstrated the technical shortcomings of the technique by infusing volumes of diagnostic peritoneal lavage fluid into the peritoneal cavity and found that only 10% of participants performing FAST could detect fluid volumes of less than 400 mL.5 In spite of these obstacles, the FAST exam is helpful in the preliminary evaluation of the patient, especially when the patient cannot undergo further imaging because of hemodynamic instability. Given the ranges in sensitivity, it is important to remember a negative FAST without a computed tomography (CT) may result in missed intraabdominal injuries. In addition, in hemodynamically labile patients, the decision of exploratory laparotomy should not be distracted by a negative FAST.6 Unlike ultrasonography, CT has dramatically changed the way we characterize splenic injuries. The CT scan is the diagnostic modality of choice for the hemodynamically stable patient in whom a splenic injury is suspected. The sensitivity and specificity of CT imaging approaches 100% and 98%, respectively.7 Current-generation multislice scanners provide a detailed survey of the splenic architecture and allow the clinician to differentiate simple subcapsular hematomas from more severe parenchymal and vascular injuries. Although exposing patients to increased radiation, the arterial phase of CT image acquisition—in addition to traditionally obtained portal venous and delayed phase images—should be considered to optimize the detection of traumatic splenic injuries.8 Several grading systems have been used for classifying splenic injuries, and these have important implications in both the operative and nonoperative management decisions. The Organ Injury Scaling Committee of the American Association for the Surgery of Trauma (OISCAAST) devised an anatomic grading system that defines the severity of splenic injuries.9 The system incorporates both CT scan findings and intraoperative assessment of the spleen and consists of five grades (Table 139.1). This grading scale provides universal definitions that all
Management of Splenic Trauma in Adults CHAPTER 139 1622.e1
ABSTRACT This chapter addresses the diagnostic evaluation and initial treatment of acute splenic trauma with a focus on nonoperative intervention. Specifically, the text reviews available diagnostic modalities, indications for operative and nonoperative management, and the application of angioembolization for splenic hemorrhage.
KEYWORDS Spleen, hemorrhage, shock, FAST, nonoperative management, interventional radiology, angioembolization, overwhelming postsplenectomy sepsis (OPSS)
Management of Splenic Trauma in Adults CHAPTER 139
TABLE 139.1 Organ Injury Scaling Committee of the American Association for the Surgery of Trauma (1994 Revision) Grade
Injury Description
I
Hematoma—subcapsular, <10% surface area Or Laceration—capsular tear, <1 cm parenchymal depth Hematoma—subcapsular, 10%–50% surface area, intraparenchymal, <5 cm in diameter Or Laceration 1–3 cm parenchymal depth which does not involve a trabecular vessel Subcapsular, >50% surface area or expanding, ruptured subcapsular or parenchymal hematoma, intraparenchymal hematoma >5 cm or expanding Or Laceration >3 cm parenchymal depth or involving trabecular vessels Laceration involving segmental or hilar vessels producing major devascularization (>25% of spleen) Completely shattered spleen Or Hilar vascular injury which devascularizes spleen
II
III
IV
V
Advance one grade for multiple injuries, up to grade III. Modified from Moore EE, Cogbill TH, Jurkovich GJ, Shackford SR, Malangoni MA, Champion HR. Organ injury scaling: spleen and liver (1994 revision). J Trauma. 1995;38:323.
clinicians can understand, and it becomes particularly useful when a patient requires transfer to a tertiary trauma center from an acute care hospital as the severity of injury is readily appreciated. Although the trauma community recognizes that the primary predictor of operative intervention is hemodynamic instability, the organ injury severity scale can also serve as a predictor of further therapeutic intervention. Haan et al. reported a splenic salvage rate of 94% over a 5-year period; however, they found that the salvage rate decreased with increased splenic injury grade.10
NONOPERATIVE MANAGEMENT The increased availability of high-resolution CT scan and advances in arterial angiography and embolization techniques have contributed to the success of nonoperative management of splenic injuries. The hemodynamically stable patient with blunt splenic trauma can be adequately managed with bed rest, serial abdominal exams, and hemoglobin and hematocrit monitoring. This approach, in combination with occasional angiography, especially for grade III and IV injuries, confers a splenic salvage rate of up to 95%.11,12 In the setting of expectant management, indications for angiography have been delineated by several studies and include the following CT scan features: contrast extravasation, the presence of a pseudoaneurysm, significant hemoperitoneum, high-grade injury, and evidence of a vascular injury.13 The goal of angiography is to localize bleeding and embolize the source with coils or a gelatin foam product. Embolization can occur either at the main splenic artery just distal to the dorsal pancreatic portion of the vessel—known as
1623
proximal embolization—or selectively at the distal branch of the injured vessel. The goal behind the former technique is to decrease the perfusion pressure to the spleen to encourage hemostasis. The disadvantage to this technique is global splenic ischemia, and many have questioned the spleen’s immunocompetence following proximal embolization. Malhotra et al. examined the effects of angioembolization on splenic function by examining serum levels of a particular T-cell line. T-cell proportions between patients who had undergone splenic embolization with asplenic patients and healthy controls were similar suggesting some degree of splenic immunocompetency was maintained.14 A Norwegian study comparing blood samples from patients who had undergone angioembolization with healthy controls demonstrated that the study samples had similar levels of pneumococcal immunoglobulins and no HowellJolly bodies, suggesting normal splenic function.15 Although these preliminary studies remain encouraging, there is no definitive evidence that splenic immunocompetency is fully maintained following angioembolization. There is no question that advancements in interventional techniques have contributed to the successful nonoperative management of splenic injuries. This has certainly changed the strategy, but it has not completely replaced operative intervention. The challenge now remains predicting those patients who will ultimately require splenectomy. Many groups have studied potential predictors of nonoperative failure. Earlier studies found that a higher injury grade, increased transfusion requirement, and hypotension on initial presentation consistently predicted failure of nonoperative management. More recent literature reflects the use of advanced imaging techniques for predicting which patients will ultimately require splenectomy. Haan looked at the overall outcomes of patients admitted with blunt splenic trauma and reported several radiographic findings that were prevalent among patients requiring splenectomy after angioembolization: contrast extravasation, pseudoaneurysm, significant hemoperitoneum, and arteriovenous fistula. Among these characteristics, an arteriovenous fistula had the highest rate of nonoperative failure at 40%.10 Nonradiographic features associated with significant risk of nonoperative failure include age greater than 40, injury severity score of 25 or greater, or presence of large-volume hemoperitoneum.16,17 Aside from radiographic findings, some groups have also examined the mechanism of injury and its association with nonoperative failure. Plurad et al. conducted a retrospective review over a 15-year period and found that patients who were victims of blunt assault were more likely to fail nonoperative management: 36% of these patients required splenectomy versus 11.5% of patients from all other mechanisms combined. These findings suggest that regardless of overall injury severity, individuals who sustain a direct transfer of injury to the left torso are more likely to require splenectomy.18
OPERATIVE MANAGEMENT When a patient presents with hemodynamic lability in spite of timely resuscitation, operative intervention remains the most prudent course of treatment. In this situation,
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SECTION III Pancreas, Biliary Tract, Liver, and Spleen
standard principles of trauma care are followed: the patient should have reliable intravenous access, appropriate volume resuscitation, preparation of type and crossmatched packed red blood cells, nasogastric decompression, and preoperative intravenous antibiotic administration. It is standard practice to use a vertical midline incision for laparotomy because this affords the quickest access to the peritoneal cavity. If this incision proves to be insufficient, it can be extended cephalad and to the left of the xiphoid process. In addition, the left triangular ligament of the liver may be incised to allow reflection of the liver away from the area of interest. Although it may seem practical, an oblique left upper quadrant incision for a presumed isolated splenic injury is more time-consuming and offers little access to the remainder of the peritoneal cavity should a concomitant injury present itself. After entering the peritoneal cavity, a standard initial survey should be performed. All four quadrants should be packed and systematically inspected for bleeding or enteric contamination. If other injuries are recognized and require more urgent attention, one can achieve adequate hemostasis of the spleen with proper packing. Multiple laparotomy packs should be placed around the splenic parenchyma in such a manner that a tamponade effect is maintained between the diaphragm, lateral abdominal wall, and retroperitoneum. When it is time to address the injury, mobilization is achieved by placing laparotomy packs posterior to the spleen and lifting it directly into the operative field. Following its inspection, the spleen’s ligamentous attachments to the diaphragm, kidney, and colon should be sharply incised. These connections are avascular and can be divided with impunity in most circumstances. The spleen can then be rotated to the midline and further elevated, thus enabling complete access to its anterior and posterior surfaces, as well as to the hilum. Once accomplished, the operator can easily achieve virtually complete hemostasis of any splenic injury by direct manual compression of the splenic parenchyma or by control of the splenic artery and vein at the hilum. At this point, a decision is made regarding splenectomy or splenorrhaphy. After the spleen has been fully mobilized, one may proceed with splenectomy by first individually ligating and dividing the short gastric vessels. These vessels should be addressed far from the greater curvature of the stomach so that the risk of gastric wall necrosis is minimized. Because the short gastric vessels are divided and the splenic hilum is skeletonized, one must pay attention to the tail of the pancreas. Careless technique can result in disruption of the pancreatic capsule and the development of a pancreatic fistula with subsequent morbidity. Following the division of the short gastric vessels, the splenic artery is then doubly ligated and divided within the splenic hilum. The splenic vein is dealt with in the same manner, and the splenectomy is completed. After removal of the spleen, the splenic bed should be thoroughly irrigated and inspected for hemostasis. These steps are essential to minimize the chances of postoperative splenic bed hematoma, which in turn predisposes to the risk of a subphrenic abscess. Although there are no conclusive data regarding the use of closed-suction drains in the surgical bed, we do not routinely drain the
splenic fossa following splenectomy. Meticulous hemostasis tends to be the best method in avoiding splenic bed complications. The term splenorrhaphy refers to a variety of “spleensparing” techniques aimed at controlling hemorrhage so that the patient may retain the immunologic benefits of the spleen. The intraoperative decision to attempt splenorrhaphy should be made only after the spleen has been fully mobilized and inspected. 19,20 As a general rule, splenorrhaphy is most appropriately considered in cases of less severe injury (e.g., grades I and II, and occasionally grade III). Splenorrhaphy should not be attempted to repair extensive or complex injuries of the spleen, nor is it well advised to undertake splenorrhaphy in the face of multiple concomitant injuries or associated hypotension. With the spleen fully mobilized and controlled in the surgeon’s hand, splenorrhaphy may consist of mere manual compression of the parenchyma to achieve hemostasis of simple lacerations. In addition, there are a variety of topical hemostatic agents that may be applied directly to the bleeding parenchymal surface. Other options include suture repair of the spleen using a monofilament suture in a mattress technique, where one can also incorporate a piece of omentum or gelatin sponge product into the repair. Alternatively, wrapping the entire spleen in absorbable mesh has been described as a means of effective tamponade and has not been associated with a significant increase in infectious complications.20 Examining splenic salvage rates over a 9-year period, Feliciano et al. found that the majority of splenorrhaphy cases were accomplished with simple techniques and less than 10% required a mesh wrap. In this series, the incidence of rebleeding was 1.3%.21
POSTOPERATIVE CONSIDERATIONS Overwhelming postsplenectomy sepsis (OPSS), first described by Diamond in 1969, is an infrequent but potentially catastrophic complication of splenectomy resulting from an increased susceptibility to infection by encapsulated microorganisms.22 The overall standard incidence ratio for hospitalization for sepsis was 5.7, with lower incidences in trauma patients (3.4; 95% confidence interval [CI], 3.0 to 3.8), compared with 18 (95% CI, 16 to 19) for patients with hematologic malignancies.23 Early reports of OPSS indicated mortality rates of 50% to 70% in spite of the use of intravenous antibiotics and intensive therapeutic intervention. With advances in antibiotic therapy and intensive care, the mortality rate of OPSS can be expected to be approximately 10%, with more than half of all fatalities occurring within 48 hours of presentation.1,24 Given these findings, it is a widely accepted practice to immunize patients with pneumococcal vaccine shortly after undergoing emergency splenectomy prior to discharge from the hospital.25 The incidence of OPSS does not appear to have decreased during the vaccine era.23 In fact, Streptococcus pneumoniae remains the causative organism in 42% of cases.26 The efficacy and clinical importance of Neisseria meningitidis and Haemophilus influenzae type b vaccination in splenectomized individuals is unknown but should be considered in patients who are deemed more likely to encounter these organisms.25 We
Management of Splenic Trauma in Adults CHAPTER 139
typically administer all three of the vaccines to patients undergoing emergency splenectomy. Although these patients should take all necessary precautions to avoid serious infections, prophylactic antibiotics are not thought to be necessary following splenectomy in adults.27 Antibody response appears to be preserved following splenic artery embolization, especially in selective embolization, indicating vaccines may not be needed; however, larger studies are needed to confirm this.28
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12. Renzulli P, Gross T, Schnurger B, et al. Management of blunt injuries to the spleen. Br J Surg. 2010;97:1696. 13. Haan JM, Biffl W, Knudson MM, et al. Splenic embolization revisited: a multicenter review. J Trauma. 2004;56:542. 14. Malhotra AK, Carter RF, Lebman DA, et al. Preservation of splenic immunocompetence after splenic artery angioembolization for blunt splenic injury. J Trauma. 2010;69:1126. 15. Skattum J, Titze TL, Dormagen JB, et al. Preserved splenic function after angioembolisation of high grade injury. Injury. 2012;43:62. 16. Olthof DC, Joosse P, van der Vlies CH, de Haan RJ, Goslings JC. Prognostic factors for failure of nonoperative management in adults with blunt splenic injury: a systematic review. J Trauma Acute Care Surg. 2013;74:546. 17. Bhangu A, Nepogodiev D, Lal N, Bowley DM. Meta-analysis of predictive factors and outcomes for failure of non-operative management of blunt splenic trauma. Injury. 2012;43:1337. 18. Plurad DS, Green DJ, Inaba K, et al. Blunt assault is associated with failure of nonoperative management of the spleen independent of organ injury grade and despite lower overall injury severity. J Trauma. 2009;66:630. 19. Berry MF, Rosato EF, Williams NN. Dexon mesh splenorrhaphy for intraoperative splenic injuries. Am Surg. 2003;69:176. 20. Pachter HL, Hofstetter SR, Spencer FC. Evolving concepts in splenic surgery: splenorrhaphy versus splenectomy and postsplenectomy drainage—experience in 105 patients. Ann Surg. 1981;194:262. 21. Feliciano DV, Spjut-Patrinely V, Burch JM, et al. Splenorrhaphy—the alternative. Ann Surg. 1990;211:569. 22. Diamond LK. Splenectomy in childhood and the hazard of overwhelming infection. Pediatrics. 1969;43:886. 23. Edgren G, Almqvist R, Hartman M, Utter GH. Splenectomy and the risk of sepsis: a population-based cohort study. Ann Surg. 2014;260: 1081. 24. Brigden ML, Pattullo AL. Prevention and management of overwhelming postsplenectomy infection—an update. Crit Care Med. 1999;27:836. 25. Shatz DV. Vaccination practices among North American trauma surgeons in splenectomy for trauma. J Trauma. 2002;53:950. 26. Theilacker C, Ludewig K, Serr A, et al. Overwhelming postsplenectomy infection: a prospective multicenter cohort study. Clin Infect Dis. 2016;62:871. 27. Working Party of the British Committee for Standards in Haematology Clinical Haematology Task Force. Guidelines for the prevention and treatment of infection in patients with an absent or dysfunctional spleen. BMJ. 1996;312:430. 28. Olthof DC, Lammers AJ, van Leeuwen EM, Hoekstra JB, ten Berge IJ, Goslings JC. Antibody response to a T-cell-independent antigen is preserved after splenic artery embolization for trauma. Clin Vaccine Immunol. 2014;21:1500.