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Literature review current through: Mar 2014. | This topic last updated: Aug 16, 2012.

INTRODUCTION — The spleen is one of the most commonly injured intra-abdominal organs. The diagnosis and prompt management of potentially life-threatening hemorrhage is the primary goal. The preservation of functional splenic tissue is secondary and in selected patients may be accomplished using nonoperative management or operative salvage techniques. Any attempt to salvage the spleen is abandoned in the face of ongoing hemorrhage or other life-threatening injuries. Emergent and urgent splenectomy remains a life-saving measure for many patients.

This topic will discuss the diagnosis and management of splenic injury. The management of spontaneous splenic rupture related to infectious or hematologic diseases as opposed to injury is discussed separately. (See "Approach to the adult patient with splenomegaly and other splenic disorders", section on 'Splenic rupture'.)

SPLENIC ANATOMY AND PHYSIOLOGY — The spleen is located posterolaterally in the left upper quadrant of the abdomen beneath the left hemidiaphragm and lateral to the greater curvature of the stomach. The gross anatomy of the spleen is described elsewhere. (See "Surgical management of splenic injury in the adult trauma patient", section on 'Anatomy of the spleen'.)

The spleen is a major lymphopoietic organ, comprising approximately 25 percent of the total lymphoid mass of the body. Normal splenic function is important for opsonization of encapsulated organisms. Splenic physiology is discussed in detail elsewhere. (See "Approach to the adult patient with splenomegaly and other splenic disorders", section on 'Normal splenic function'.)

MECHANISM OF INJURY — Splenic injury most commonly occurs following blunt trauma due to motor vehicle collisions (driver, passenger, or pedestrian). However, blunt splenic injury can also result from falls, sport-related activities, or assault [1]. Penetrating splenic trauma is less common than blunt injury and is typically due to assault, but inadvertent impalement may also occur. Assault with a knife compared with gunshot or shotgun wounds is less likely to result in penetrating injury due to the spleen's protected location.

Iatrogenic traumatic injuries to the spleen can result from surgical or endoscopic manipulation of the colon, stomach, pancreas, kidney, or with exposure and reconstruction of the proximal abdominal aorta [2-4]. Most commonly, the primary mechanism is capsular tear, laceration from retraction devices, or tension on the spleen during manipulation of the colon [5]. The risk is greatest for patients undergoing colon resection. A study from the National Inpatient Sample (NIS) database found, among nearly a million patients, a 1 percent incidence of splenic injury during colorectal surgery [6]. Transverse colectomy was the colon procedure most commonly associated with splenic injury. Other factors related to iatrogenic splenic injury include prior surgery, obesity, malignancy, diverticulitis, and peripheral artery disease [4,6].

TRAUMA EVALUATION — We perform initial resuscitation, diagnostic evaluation and management of the trauma patient with blunt or penetrating trauma based upon protocols from the Advanced Trauma Life Support (ATLS®) program, established by the American College of Surgeons Committee on Trauma. The initial resuscitation and evaluation of the patient with blunt or penetrating abdominal or thoracic trauma is discussed in detail elsewhere.

The spleen and liver are the most commonly injured intra-abdominal organs following blunt trauma. In up to 60 percent of patients, the spleen is the only organ injured [7]. Specific elements of the history, physical examination and diagnostic evaluation pertaining to splenic injury are presented below.

History and physical examination — A history of trauma to the left-upper quadrant, left rib cage, or left flank should increase the suspicion for splenic injury. However, a negative history does not reliably exclude splenic injury. A penetrating object can injure the spleen even if the entrance wound is not in proximity to the spleen.

The patient may complain of left upper abdominal, left chest wall, or left shoulder pain (ie, Kehr's sign). Kehr's sign is pain referred to the left shoulder that worsens with inspiration and is due to irritation of the phrenic nerve from blood adjacent to the left hemidiaphragm.

Abdominal tenderness and peritoneal signs are the most common findings indicative of intra-abdominal injury; however, these are not sensitive or specific for splenic injury. Physical findings associated with splenic injury include left-upper quadrant or generalized abdominal tenderness, abdominal wall contusion or hematoma (eg, seat belt sign), as well as left lower chest wall tenderness, contusion, or instability due to rib fractures. However, an unremarkable physical examination does not exclude splenic injury [8].

In the setting of injury, many patients have altered mental status (eg, neurologic injury, intoxication) or are intubated and sedated and cannot relate their symptoms or medical history. Every attempt should be made to identify any preexisting medical conditions by contacting the patient's primary care physician or family members. The presence of significant medical comorbidities and medical conditions requiring antiplatelet or anticoagulant medications needs to be determined as these may impact management decisions. A social history should be obtained to determine the feasibility of nonoperative management of splenic injury, if warranted. (See 'Contraindications to nonoperative management' below.)

A history of herbal medicine use is also important as some (eg, ginkgo biloba, saw palmetto, fish oil) have anticoagulant activity. (See "Overview of herbal medicine and dietary supplements", section on 'Surgical patients' and "Overview of herbal medicine and dietary supplements", section on 'Herb-drug interactions' and "Fish oil and marine omega-3 fatty acids", section on 'Safety'.)

Associated injuries — With blunt abdominal trauma, lower rib fractures, pelvic fracture, and spinal cord injury may also be present [9].

The injuries associated with penetrating trauma depend upon the implement or missile trajectory. Injuries to adjacent organs including the heart, esophagus, aorta, stomach, diaphragm, pancreas, bowel, or left kidney can occur in conjunction with splenic laceration. (See "Initial evaluation and management of abdominal gunshot wounds in adults" and "Initial evaluation and management of abdominal stab wounds in adults".)

Diagnostic evaluation — Evaluation of the abdominal trauma patient commonly utilizes focused assessment with sonography in trauma (FAST exam), and computerized tomography (CT scan). The FAST exam is more useful in hemodynamically unstable patients; however, a negative FAST examination is not adequate to exclude splenic injury, particularly intraparenchymal injury. Diagnostic peritoneal aspiration/lavage (DPA/DPL) is less common, having been largely replaced by the FAST examination in most major trauma centers. The value of these tests in the diagnostic evaluation of the trauma patient is discussed in detail elsewhere.

Specific diagnostic findings of splenic injury are described in the sections below.

FAST findings — Signs of splenic injury observed with FAST examination include a finding of hypoechoic (ie, black) rim of subcapsular fluid or intraperitoneal fluid usually found around the spleen or in Morrison’s pouch (hepatorenal space).

CT findings — In non-injured patients, CT scan is typically performed with both oral (PO) and intravenous (IV) contrast. However, most trauma centers no longer administer PO contrast because scans performed without oral contrast, particularly in children, have sufficient detail to establish and grade splenic injury. For obvious reasons, non-intravenous contrast CT scan cannot establish the presence of active bleeding (ie, contrast blush, active extravasation). However, the risk of IV contrast administration to diagnose bleeding needs to be weighed against the risk of complications related to IV contrast (eg, contrast-induced nephropathy), particularly in elderly patients. A screening non-contrast CT scan may provide some adequate information.

The differentiation between ascites and blood is made using the Hounsfield unit scale, which is a transformation of the linear attenuation coefficient of a material relative to water (at standard temperature and pressure). The Hounsfield unit of water (eg, ascites) is zero, and that of IV contrast 130. The value for blood varies depending upon whether it is clotted, and if so, the age of the clot. (See "Principles of computed tomography of the chest", section on 'General description'.)

CT scan findings that indicate splenic injury include:

  • Hemoperitoneum – Localized fluid collections around the spleen (especially those with an elevated Hounsfield unit measurement) are highly suggestive of hemoperitoneum. Briskly bleeding splenic lacerations may establish blood density fluid throughout the abdomen.
  • Hypodensity – Hypodense regions represent areas of parenchymal disruption, intraparenchymal hematoma or subcapsular hematoma.
  • Contrast blush or extravasation – Contrast blush describes hyperdense areas within the splenic parenchyma that represent traumatic disruption or pseudoaneurysm of the splenic vasculature. Active extravasation of contrast implies ongoing bleeding and the need for urgent intervention [10,11]. (See 'Management approach' below.)

Other imaging — Plain films, organ-based ultrasound imaging, and magnetic resonance imaging (MRI) are of limited value in the acute diagnosis of splenic injury.

Plain films are generally nonspecific but may demonstrate rib fracture, or medial displacement of the gastric air bubble (ie, Balance sign) raising suspicion for a splenic injury.

MRI and organ-based ultrasound examination may be time-consuming to perform, and may put the patient in a location of the hospital remote from ready access and intervention. However, MRI may be applicable in a subset of hemodynamically stable patients who cannot undergo CT scan (eg, allergic to IV contrast) [12]. Noncontrast CT remains preferable for the acute diagnosis of splenic injury due to speed and accessibility.

SPLENIC INJURY GRADING — The American Association for the Surgery of Trauma (AAST) has published a spleen injury grading scale based upon the anatomic injury identified on CT scan [13]. The grade of injury and the degree of hemoperitoneum on CT scan relate to the success of nonoperative management, but do not consistently predict the need for initial operative intervention [14-18]. (See 'Management approach' below.)

The AAST criteria for hematoma and laceration for each splenic injury grade are as follows [13]:

  • Grade I — Hematoma: subcapsular, <10 percent of surface area. Laceration: capsular tear <1 cm in depth into the parenchyma (picture 1).
  • Grade II — Hematoma: subcapsular, 10 to 50 percent of surface area. Laceration: capsular tear, 1 to 3 cm in depth, but not involving a trabecular vessel.
  • Grade III — Hematoma: subcapsular, >50 percent of surface area OR expanding, ruptured subcapsular or parenchymal hematoma OR intraparenchymal hematoma >5 cm or expanding. Laceration: >3 cm in depth or involving a trabecular vessel.
  • Grade IV — Laceration involving segmental or hilar vessels with major devascularization (ie, >25 percent of spleen) (picture 2).
  • Grade V — Hematoma: shattered spleen. Laceration: hilar vascular injury which devascularizes spleen.

The AAST CT grade is not always concordant with the grade of injury identified in the operating room due to technical issues and variability of CT scan interpretation [14,15]. A modified CT grading system has been proposed that may better identify those patients who would benefit from initial angiographic embolization [19].

MANAGEMENT APPROACH — Splenic injury can be initially managed with observation, angiographic embolization, or surgery depending upon the hemodynamic status of the patient, grade of splenic injury, and presence of other injuries and medical comorbidities. The management approach used may vary from institution to institution depending upon the availability of resources.

  • Hemodynamically unstable — Based upon ATLS principles, the hemodynamically unstable trauma patient with a positive FAST scan or DPA/DPL requires emergent abdominal exploration to determine the source of intraperitoneal hemorrhage [20,21]. (See 'Trauma evaluation' above.)
  • Hemodynamically stable — Hemodynamically stable patients with low-grade (I to III) blunt or penetrating splenic injuries without any evidence for other intra-abdominal injuries, active contrast extravasation, or a blush on CT, may be initially observed safely. In general, patients who meet the criteria for observation but who require intervention to manage extra-abdominal injuries (eg, leg fracture stabilization) can also be safely observed. (See 'Observation' below.)

CT scan findings of contrast extravasation or vascular blush have higher failure rates for observational management [11]. These patients may benefit from initial splenic embolization followed by continued observation to verify the success of the intervention. Another indication for embolization is intraparenchymal pseudoaneurysm formation. Splenic embolization is controversial for higher grade (IV, V) injuries and in patients older than 55. (See 'Splenic embolization' below.)

Surgery is indicated in patients who cannot be adequately observed (due to limited resources or other injuries), are unlikely to tolerate a significant episode of hypotension, and those who fail nonsurgical management (ie, observation, embolization). (See 'Failure of nonoperative management' below and 'Operative management' below.)

Whether the management approach adopted for trauma patients can be extrapolated to guide the management of iatrogenic splenic trauma is unclear. Although splenic salvage is sometimes attempted for iatrogenic splenic trauma that occurs during surgery, more than 70 percent of patients ultimately undergo splenectomy [22]. It is unclear whether this is truly necessary or due to surgeons’ “discomfort” at watching a slowly oozing low-grade injury that would then necessitate a second surgery if nonoperative management fails.

NONOPERATIVE MANAGEMENT — Splenic trauma was nearly uniformly managed with surgery prior to the introduction of nonoperative management algorithms in the pediatric population. What seemed initially to be a radical approach was adopted over time by the adult trauma community. Nonoperative management, encompassing both observation and embolization techniques, is used to manage 50 to 70 percent of cases, typically for patients with lower grade injuries [23-26]. (See 'Splenic injury grading' above.)

The rationale for nonoperative management is based upon the assumption that salvaging functional splenic tissue avoids the surgical and anesthetic risks and complications associated with laparotomy and abrogates the risk of postsplenectomy sepsis.

However, immune competence after injury that does not require removal of the spleen (eg, embolization, partial splenectomy) depends on the immunologic functionality of the residual splenic tissue and does not appear to be grade specific. The small risk of postsplenectomy sepsis appears higher at the extremes of age, but may be influenced by concomitant immune deficiency from solid organ transplantation, malignancy, and HIV disease. (See 'Immunocompetence after splenic injury' below.)

Contraindications to nonoperative management — Nonoperative management is not appropriate in patients with hemodynamic instability, generalized peritonitis, or for patients with other intra-abdominal injuries requiring surgical exploration. Portal hypertension is a relative contraindication due to the increased venous pressures that may prevent clot formation and control of hemorrhage even after successful splenic embolization. Other relative contraindications include higher-grade splenic injury (>Grade III), active contrast extravasation, large volume hemoperitoneum (though difficult to accurately quantify), refusal of blood transfusion in the setting of pre-existing anemia, or altered neurologic status precluding adequate serial abdominal examination.

There is a higher failure rate of nonoperative management with increasing grade of injury, though all grades of splenic trauma can bleed and often in an unpredictable fashion [27,28]. The optimal management of hemodynamically stable patients with higher-grade (IV, V) injuries remains controversial, though grade V injuries are generally unsuitable for embolization due to vascular disruption. Some also consider Grade IV injuries to be a relative contraindication to splenic embolization. In one small retrospective review, 60 percent of patients with higher grade injuries were taken directly to the operating room. The remaining patients were managed nonoperatively with 55 percent of these patients ultimately requiring surgery [29]. We prefer to initially manage hemodynamically stable patients with Grade III or IV splenic injury with angiographic embolization as part of their nonoperative management, provided that they do not have large volume hemoperitoneum or other injuries that require abdominal exploration or medical comorbidities providing a contraindication.

Embolization is also relatively contraindicated in patients older than 55 due to higher failure rates in these patients. The splenic capsule thins with age (age >55 years) and may render nonoperative management of higher-grade injuries (>Grade III) in these patients less successful. However, injury severity-adjusted mortality rates do not appear significantly higher in this population compared with younger patients. Retrospective reviews suggest, however, that carefully selected individuals over 55 who are hemodynamically stable, and have no significant medical comorbidities, can also be safely managed with observation, with or without embolization [24,30,31]. The largest of these studies examined 1008 patients ≥55 years of age who sustained blunt splenic injury [24]. Of the patients who did not require immediate surgical intervention, 75 percent were successfully managed nonoperatively. Among three age groups, 55 to 64, 65 to 74, and >75 years of age, failure rates for nonoperative management increased and were 19, 27, and 28 percent, respectively, but these differences were not significant, possibly due to the small number of patients in each group. Overall, the experience with nonoperative management of higher grade splenic injury in older patients is limited.

Observation — Successful observation during non-operative management for splenic trauma depends upon proper patient selection, and the availability of adequate resources within the institution [32,33]. Patients must be closely monitored by nursing and medical staff, and sufficient flexibility should be available to allow urgent/emergent intervention should arteriography or surgery be required. (See 'Failure of nonoperative management' below.)

Wide variation exists in the clinical application of nonoperative strategies but, in general, patients are admitted to a monitored care setting, either an intensive care or step-down unit, depending upon the capabilities of the unit, grade of splenic injury, nature and severity of other injuries, and clinical status [34,35]. We initially place the patient on bed rest, though no clear benefit exists for this practice. We obtain serial hemoglobin levels every six hours in the first 24 hours. Patients are not given a diet (ie, nil per os [NPO]) for at least the first 24 hours. When the hemoglobin level is stable and operative intervention unlikely, the patient may eat.

For patients being observed, we do not routinely perform repeat CT imaging during the course of hospitalization. Follow-up study is performed for patients whose clinical situation (ie, falling hemoglobin, increasing abdominal pain, left shoulder pain, fever) indicates a need. In some patients with higher grade injuries (III to V), a repeat scan within 24 to 48 hours may be needed if the clinical situation is unclear, such as in the setting of evolving neurologic injury when the physical examination may be sequentially less reliable than upon admission.

The duration of observation should be individualized based upon the grade of splenic injury, nature and severity of other injuries, and the patient's clinical status. In a survey of actively practicing trauma surgeons, there was agreement that higher-grade injury generally required longer observation periods [34]. A common, but not evidence-based practice regarding the duration of observation following splenic injury is that the number of days of observation is equal to the injury grade plus one [36].

An observation period of five days identifies at least 95 percent of patients who would require some form of intervention [37,38]. One multicenter trial found that 86 percent of patients who failed nonoperative management did so within 96 hours of hospital admission, with 61 percent of failures occurring during the first 24 hours [27]. Patients with higher-grade injuries may require more prolonged periods of observation. (See 'Failure of observation' below.)

Failure of observation — Patients who fail observation require either splenic embolization, or more commonly, operative management. Patients may fail observational management either as an inpatient or, more rarely, as an outpatient presenting with "delayed splenic rupture". It is likely that "delayed rupture" more accurately describes those patients with splenic parenchymal pseudoaneurysms, the walls of which degrade during the normal process of clot dissolution with bleeding in a delayed fashion.

Indications to pursue intervention include hemodynamic instability, the development of diffuse peritoneal signs, or decreasing hemoglobin attributed to splenic hemorrhage. Hypotension may be absolute or relative, or evidenced as persistent tachycardia in spite of adequate fluid resuscitation. The clinical manifestations of hypovolemia due to blood loss are discussed in detail separately. (See "Shock in adults: Types, presentation, and diagnostic approach", section on 'Clinical presentation'.)

When observing the patient with splenic injury, there is no consensus with respect to level of hemoglobin, change in hemoglobin, or transfusion volume that prompts a need for intervention. Some surgeons intervene prior to the need for any transfusion as a means of avoiding allogeneic exposure, while others make provisions for one to two units of PRBC prior to further intervention.

The choice to pursue embolization or surgery in many institutions is governed by the availability of the appropriate resources and the patient's ability to tolerate the time needed to set up the interventional radiology suite (or operating room with dedicated arteriography), get personnel in place, and perform the embolization procedure which, depending upon the patient's anatomy, can be lengthy. (See 'Splenic embolization' below and 'Operative management' below.)

Splenic embolization — Angiographic embolization was first applied to the management of splenic injury in 1981. Splenic embolization requires specialized imaging facilities and a vascular interventionalist (ie, interventional radiology, vascular surgeon) experienced with celiac artery catheterization and embolization techniques. Success rates for embolization vary depending upon institution, embolization technique, arterial accessibility, operator skill, and the type of embolization material. Where available, embolization is potentially most useful when employed selectively in hemodynamically stable patients who have CT findings that include active contrast extravasation, splenic pseudoaneurysm, or large volume hemoperitoneum [11,16,17,39-41]. Retrospective reviews have found variable success rates (57 to 93 percent) for splenic salvage that includes embolization in patients with higher-grade (III, IV, V) splenic injuries [10,26,39,41-44].

A number of small, retrospective studies have demonstrated that nonoperative management is more successful with the adjunctive use of angio-embolization [10,45-48]. In one study of 39 patients, splenic artery embolization increased the success rate for nonsurgical management from 74 to 89 percent [46].

In a cohort analysis, 222 patients with blunt splenic injury treated between 1991 and 1998 were compared with 408 patients treated between 1998 and 2005 [47]. The frequency of nonoperative management (61 versus 85 percent, respectively), injury severity scale (21 versus 27, respectively), frequency of splenic artery embolization (3 versus 23 percent, respectively) and success of nonoperative management (77 versus 96 percent, respectively) all increased significantly between the earlier and later cohort. Hospital mortality rates (12 versus 6 percent) and mean hospital length (15 versus 9 days) decreased significantly.

The technique of splenic embolization involves first gaining percutaneous access to the abdominal aorta via the brachial or femoral artery. The celiac axis is cannulated and a celiac arteriogram is performed to confirm the CT findings and evaluate the splenic vasculature. The presence of contrast extravasation from the splenic parenchyma supplied by the short gastric vessels on celiac arteriogram should prompt operative intervention, as these injuries are less amenable to embolization due to the technical difficulties in accessing the short gastric vessels.

Embolization of the splenic artery proximally or distally can be performed [26]. Nonrandomized studies have not demonstrated the superiority of one technique over the other, though failure rates for nonoperative management may be greater when proximal embolization is applied to patients with higher-grade injuries [49]. Depending upon the nature of the injury and technical factors, embolization coils, microspheres, absorbable gelatin sponge, endogenous clot, or a vascular plug device can be used to interrupt blood flow in major or branch vessels of the spleen effecting total or partial splenic embolization [26,50]. Splenic artery embolization may not completely interrupt blood flow from short gastric vessels due to their collateral flow from the left gastric and gastroepiploic arteries. Ongoing bleeding from these vessels may not be obvious with selective splenic artery angiogram, and thus, selective celiac arteriography should be performed.

Benefits and risks of nonoperative management — Because there is no operation, surgical risks and potential complications are eliminated with successful nonoperative management. An additional benefit of successful nonoperative management is the preservation of functional splenic tissue. Disadvantages of nonoperative management include an increased risk of missed injury, particularly hollow viscus injury, a risk of delayed bleeding, transfusion-related illness, and, when used, the additional risks associated with embolization techniques.

Patients with missed hollow viscus injury present with worsened abdominal pain and the development of peritoneal signs, generally by postinjury day four. These patients require operative intervention and should undergo concomitant definitive management of their splenic injury, if indicated. (See "Traumatic gastrointestinal injury in the adult patient".)

Blood transfusion is associated with complications that can include intravascular volume overload (Transfusion Associated Circulatory Overload [TACO]), transfusion-related acute lung injury (TRALI), hypothermia, coagulopathy, immunologic and allergic reactions as well as immunomodulation (Transfusion Related Immune Modulation, TRIM). Some clinicians feel these risks do not justify nonoperative management strategies, given an uncertain benefit. The risks associated with blood transfusion are discussed in detail elsewhere. (See "Use of blood products in the critically ill", section on 'Complications' and "Transfusion reactions caused by chemical and physical agents", section on 'Transfusional volume overload (TACO)' and "Transfusion-related acute lung injury (TRALI)" and "Leukoreduction to prevent complications of blood transfusion", section on 'Immunosuppression'.)

Splenic embolization is associated with additional risks that include bleeding, pseudoaneurysm formation at the arterial puncture site, splenic infarction, splenic/subdiaphragmatic abscess, inadvertent embolization of other organs (eg, kidneys) or lower extremities, allergic reaction to contrast and contrast-induced nephropathy. The risk of contrast-induced nephropathy may be greater when embolization is performed following contrast CT scan, especially in patients who may already be volume depleted. Contrast-induced nephropathy and its prevention are discussed in detail elsewhere. (See "Pathogenesis, clinical features, and diagnosis of contrast-induced nephropathy" and "Prevention of contrast-induced nephropathy".)

Failure of nonoperative management — Failure of nonoperative management (observation and/or embolization) is defined as the need for operative intervention, and is generally associated with ongoing bleeding as indicated by the need for ongoing volume expansion or transfusion, or hemodynamic instability. Hypotension may be absolute or relative, or evidenced as persistent tachycardia despite adequate fluid resuscitation. The clinical manifestations of hypovolemia due to blood loss are discussed in detail separately. (See "Shock in adults: Types, presentation, and diagnostic approach", section on 'Clinical presentation'.)

Failure rates for observational management range from 6 to 20 percent and depend upon age, injury severity score, grade of splenic injury, frequency with which embolization techniques are employed, and, most importantly, the appropriateness of patient selection for nonoperative management [25,27,28,51]. In retrospective studies, up to 40 percent of patients failing nonoperative management were found to have inappropriate indications for a nonoperative approach [25,52,53].

Rebleeding and/or secondary splenic "rupture" following "successful" nonoperative management is a rare but potentially disastrous complication that cannot be reliably predicted. More than 90 percent of secondary splenic "ruptures" occur within 10 days following the initial trauma; most of the remainder occur within two weeks [27,54].

Follow-up care

Resumption of normal activities — Upon discharge, patients are typically restricted from participation in high-risk activities such as skiing, mountain biking, skydiving, wrestling, contact sports, military combat, and vigorous sexual intercourse for a period of up to three months. While there are no clinical studies to support this duration, one assumes that repeat trauma to the fragile, healing spleen could lead to re-injury [34]. In one retrospective review, healing was demonstrated radiographically within two months of injury in 80 percent of patients; however, grade V injuries were excluded in this study [55].

Imaging studies — With successful nonoperative management of splenic injury, we do not routinely perform repeat CT imaging. The Eastern Association for the Surgery of Trauma (EAST) guidelines do not support routine follow-up imaging. In one survey of EAST members, 85 percent of respondents did not routinely re-image [34]. The delayed presentation of splenic pseudoaneurysms have been reported and may support a decision to re-image [39,56].

Repeat CT scan or ultrasound (provided that the injury can be adequately visualized) can be considered in select patients [57]. Re-imaging may be indicated to lift an activity restriction, or for patients whose work requirements or lifestyles place them at higher risk for re-injury if healing is not complete. Examples include professional athletes, military service personnel, and extreme sports enthusiasts. Re-imaging may also be appropriate for those who are planning to travel to regions of the world with limited healthcare access to document complete healing prior to travel. For these patients, re-imaging is typically performed at three months following the injury.

OPERATIVE MANAGEMENT — Patients sustaining abdominal trauma who are hemodynamically unstable, those who are not candidates for nonoperative management, and those who fail nonoperative management strategies require surgical exploration and either splenic salvage or splenectomy. The choice of procedure depends upon the nature and severity of splenic injury, clinical status of the patient, and associated injuries. Surgical management of traumatic splenic injury is discussed separately. (See "Surgical management of splenic injury in the adult trauma patient".)

IMMUNOCOMPETENCE AFTER SPLENIC INJURY — Immunization is recommended for asplenic patients, since splenectomy impairs opsonization of encapsulated organisms [58,59]. Information on specific vaccines and vaccine schedules are discussed elsewhere. (See "Prevention of sepsis in the asplenic patient", section on 'Immunizations'.)

Ideally, vaccines are administered either 14 days prior to or 14 days following splenectomy for maximal immunologic benefit [60,61]. Delaying vaccinations for 14 days postoperatively increases the antibody response, but may not be feasible in all trauma patients given the historically sporadic follow-up in this patient population. Many centers will therefore vaccinate the patient at the time of discharge, regardless of the postoperative day. Asplenic patients should also receive yearly influenza vaccinations.

We recommend that asplenic patients wear medical jewelry and carry medical information cards identifying them as asplenic to alert future healthcare providers under the circumstance that the patient is unable to do so.

The need for immunization of patients following treatment for splenic injury compared with those undergoing elective splenectomy is still being defined. We vaccinate all patients who have undergone splenectomy because the extent to which a patient may (or may not) have functional residual splenic tissue (ie, splenosis) is uncertain. Patients with deliberate replantation or spontaneous splenosis (image 1) have pitted red cell counts (counts less than 15 percent are consistent with immunocompetence) that are lower than those seen in splenectomized patients who do not have splenosis, but the count is not necessarily normal [62]. (See "Approach to the adult patient with splenomegaly and other splenic disorders", section on 'Splenosis'.)

Following splenic salvage surgery, splenic embolization, or nonoperative management, we feel that immunization is not necessary, though some clinicians may disagree [63-66]. Available in vitro studies indicate immunocompetence in these patients [65,67-70]. As an example, one controlled trial evaluating red blood cell pit counts found no differences for patients following successful nonoperatively managed high-grade injury (0.6 percent), and controls (0.7 percent); counts following splenectomy were 20.7 percent [71]. Furthermore, in clinical studies of patients undergoing partial splenectomy for reasons other than trauma, humoral immunity was depressed only transiently following partial splenectomy and compared with total splenectomy, partial splenectomy was associated with less risk for postsplenectomy infection [72,73].


  • Splenic injury can result from either blunt or penetrating chest or abdominal trauma; blunt mechanisms are more common. Splenic injury can also be due to iatrogenic injury during the course of another procedure involving the colon, stomach, pancreas, kidney, or with exposure and reconstruction of the proximal abdominal aorta; the risk is greatest for patients undergoing colon resection. (See 'Mechanism of injury' above.)
  • We perform initial resuscitation, diagnostic evaluation, and management of the trauma patient based upon protocols from the Advanced Trauma Life Support (ATLS®) program developed by the American College of Surgeons Committee on Trauma. (See "Initial evaluation and management of blunt abdominal trauma in adults" and "Initial evaluation and management of abdominal gunshot wounds in adults" and "Initial evaluation and management of abdominal stab wounds in adults" and "Initial evaluation and management of blunt thoracic trauma in adults".)
  • A suspicion for splenic injury is increased with left upper quadrant and/or left chest trauma; however, clinical history and physical examination are not sufficiently sensitive or specific for the presence of splenic injury. (See 'Trauma evaluation' above.)
  • Findings indicative of splenic injury on focused assessment with sonography for trauma (FAST) examination include findings of perisplenic or free intraperitoneal fluid. (See 'Diagnostic evaluation' above.)
  • Computed tomography (CT scan) findings consistent with splenic injury include splenic hypodensity, intraparenchymal or subcapsular hematoma, intravenous contrast blush, active intravenous contrast extravasation or hemoperitoneum. (See 'Diagnostic evaluation' above.)
  • Splenic injury is graded (I through V) depending upon the extent and depth of splenic hematoma and/or laceration identified on CT scan or intraoperatively. Splenic injury grading is one factor used to stratify patient management. Other factors include associated injuries and medical comorbidities. (See 'Splenic injury grading' above.)
  • Per ATLS protocol, hemodynamically unstable patients with a positive FAST exam or diagnostic peritoneal lavage or aspirate (DPL/DPA) require operative surgical exploration to determine the source of life-threatening hemorrhage that may be due to splenic injury. (See 'Management approach' above.)
  • For hemodynamically stable patients with low grade (I to III) injuries, we suggest nonoperative management over definitive surgical intervention (Grade 2C). Observation involves monitored care, serial abdominal examination, and serial hemoglobin assessment, and may involve splenic embolization depending upon resources. Failure of nonoperative management indicates a need for angiographic embolization, if not initially used, or surgical exploration. (See 'Observation' above.)
  • For hemodynamically stable patients with active contrast extravasation or contrast blush on CT scan, we suggest initial splenic embolization over observation (Grade 2C). Splenic embolization requires specialized imaging facilities and a suitably experienced interventionalist. Failure of embolization indicates the need for surgery. (See 'Splenic embolization' above.)
  • For patients who develop hemodynamic instability during the course of nonoperative management, we suggest surgical exploration over splenic embolization (Grade 2C). (See 'Failure of nonoperative management' above.)
  • Asplenic patients are regarded as having impaired immunity to encapsulated organisms and should be immunized against encapsulated organisms. (See "Prevention of sepsis in the asplenic patient".)
  • For patients who have not undergone splenectomy, either because of successful nonoperative management (ie, observation with or without embolization) or operative splenic salvage, we suggest no immunization (Grade 2C). (See 'Immunocompetence after splenic injury' above.)

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  1. Brady RR, Bandari M, Kerssens JJ, et al. Splenic trauma in Scotland: demographics and outcomes. World J Surg 2007; 31:2111.
  2. Tan K, Lewis GR, Chahal R, et al. Iatrogenic splenectomy during left nephrectomy: a single-institution experience of eight years. Urol Int 2011; 87:59.
  3. Kamath AS, Iqbal CW, Sarr MG, et al. Colonoscopic splenic injuries: incidence and management. J Gastrointest Surg 2009; 13:2136.
  4. Cassar K, Munro A. Iatrogenic splenic injury. J R Coll Surg Edinb 2002; 47:731.
  5. Merchea A, Dozois EJ, Wang JK, Larson DW. Anatomic mechanisms for splenic injury during colorectal surgery. Clin Anat 2012; 25:212.
  6. Masoomi H, Carmichael JC, Mills S, et al. Predictive factors of splenic injury in colorectal surgery: data from the Nationwide Inpatient Sample, 2006-2008. Arch Surg 2012; 147:324.
  7. Davis JJ, Cohn I Jr, Nance FC. Diagnosis and management of blunt abdominal trauma. Ann Surg 1976; 183:672.
  8. Salim A, Sangthong B, Martin M, et al. Whole body imaging in blunt multisystem trauma patients without obvious signs of injury: results of a prospective study. Arch Surg 2006; 141:468.
  9. Jacoby, R, Wisner, D. Injury to the Spleen. In: Trauma, 6th ed, Feliciano, D, Mattox, K, Moore, E (Eds), McGraw-Hill Professional, New York, 2008. p.661.
  10. Haan JM, Biffl W, Knudson MM, et al. Splenic embolization revisited: a multicenter review. J Trauma 2004; 56:542.
  11. Schurr MJ, Fabian TC, Gavant M, et al. Management of blunt splenic trauma: computed tomographic contrast blush predicts failure of nonoperative management. J Trauma 1995; 39:507.
  12. Hedrick TL, Sawyer RG, Young JS. MRI for the diagnosis of blunt abdominal trauma: a case report. Emerg Radiol 2005; 11:309.
  13. Tinkoff G, Esposito TJ, Reed J, et al. American Association for the Surgery of Trauma Organ Injury Scale I: spleen, liver, and kidney, validation based on the National Trauma Data Bank. J Am Coll Surg 2008; 207:646.
  14. Cohn SM, Arango JI, Myers JG, et al. Computed tomography grading systems poorly predict the need for intervention after spleen and liver injuries. Am Surg 2009; 75:133.
  15. Sutyak JP, Chiu WC, D'Amelio LF, et al. Computed tomography is inaccurate in estimating the severity of adult splenic injury. J Trauma 1995; 39:514.
  16. Becker CD, Spring P, Glättli A, Schweizer W. Blunt splenic trauma in adults: can CT findings be used to determine the need for surgery? AJR Am J Roentgenol 1994; 162:343.
  17. Kohn JS, Clark DE, Isler RJ, Pope CF. Is computed tomographic grading of splenic injury useful in the nonsurgical management of blunt trauma? J Trauma 1994; 36:385.
  18. Harbrecht BG. Is anything new in adult blunt splenic trauma? Am J Surg 2005; 190:273.
  19. Marmery H, Shanmuganathan K, Alexander MT, Mirvis SE. Optimization of selection for nonoperative management of blunt splenic injury: comparison of MDCT grading systems. AJR Am J Roentgenol 2007; 189:1421.
  20. Lo A, Matheson AM, Adams D. Impact of concomitant trauma in the management of blunt splenic injuries. N Z Med J 2004; 117:U1052.
  21. Wahl WL, Ahrns KS, Chen S, et al. Blunt splenic injury: operation versus angiographic embolization. Surgery 2004; 136:891.
  22. Holubar SD, Wang JK, Wolff BG, et al. Splenic salvage after intraoperative splenic injury during colectomy. Arch Surg 2009; 144:1040.
  23. Stein DM, Scalea TM. Nonoperative management of spleen and liver injuries. J Intensive Care Med 2006; 21:296.
  24. Siriratsivawong K, Zenati M, Watson GA, Harbrecht BG. Nonoperative management of blunt splenic trauma in the elderly: does age play a role? Am Surg 2007; 73:585.
  25. McIntyre LK, Schiff M, Jurkovich GJ. Failure of nonoperative management of splenic injuries: causes and consequences. Arch Surg 2005; 140:563.
  26. Bhullar IS, Frykberg ER, Siragusa D, et al. Selective angiographic embolization of blunt splenic traumatic injuries in adults decreases failure rate of nonoperative management. J Trauma Acute Care Surg 2012; 72:1127.
  27. Peitzman AB, Heil B, Rivera L, et al. Blunt splenic injury in adults: Multi-institutional Study of the Eastern Association for the Surgery of Trauma. J Trauma 2000; 49:177.
  28. 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.
  29. Watson GA, Rosengart MR, Zenati MS, et al. Nonoperative management of severe blunt splenic injury: are we getting better? J Trauma 2006; 61:1113.
  30. Godley CD, Warren RL, Sheridan RL, McCabe CJ. Nonoperative management of blunt splenic injury in adults: age over 55 years as a powerful indicator for failure. J Am Coll Surg 1996; 183:133.
  31. Krause KR, Howells GA, Bair HA, et al. Nonoperative management of blunt splenic injury in adults 55 years and older: a twenty-year experience. Am Surg 2000; 66:636.
  32. Demetriades D, Hadjizacharia P, Constantinou C, et al. Selective nonoperative management of penetrating abdominal solid organ injuries. Ann Surg 2006; 244:620.
  33. Harbrecht BG, Zenati MS, Ochoa JB, et al. Management of adult blunt splenic injuries: comparison between level I and level II trauma centers. J Am Coll Surg 2004; 198:232.
  34. Fata P, Robinson L, Fakhry SM. A survey of EAST member practices in blunt splenic injury: a description of current trends and opportunities for improvement. J Trauma 2005; 59:836.
  35. Gomez D, Haas B, Al-Ali K, et al. Controversies in the management of splenic trauma. Injury 2012; 43:55.
  36. St Peter SD, Keckler SJ, Spilde TL, et al. Justification for an abbreviated protocol in the management of blunt spleen and liver injury in children. J Pediatr Surg 2008; 43:191.
  37. McCray VW, Davis JW, Lemaster D, Parks SN. Observation for nonoperative management of the spleen: how long is long enough? J Trauma 2008; 65:1354.
  38. Smith J, Armen S, Cook CH, Martin LC. Blunt splenic injuries: have we watched long enough? J Trauma 2008; 64:656.
  39. Davis KA, Fabian TC, Croce MA, et al. Improved success in nonoperative management of blunt splenic injuries: embolization of splenic artery pseudoaneurysms. J Trauma 1998; 44:1008.
  40. Sclafani SJ. The role of angiographic hemostasis in salvage of the injured spleen. Radiology 1981; 141:645.
  41. Raikhlin A, Baerlocher MO, Asch MR, Myers A. Imaging and transcatheter arterial embolization for traumatic splenic injuries: review of the literature. Can J Surg 2008; 51:464.
  42. Gaarder C, Dormagen JB, Eken T, et al. Nonoperative management of splenic injuries: improved results with angioembolization. J Trauma 2006; 61:192.
  43. Harbrecht BG, Ko SH, Watson GA, et al. Angiography for blunt splenic trauma does not improve the success rate of nonoperative management. J Trauma 2007; 63:44.
  44. Smith HE, Biffl WL, Majercik SD, et al. Splenic artery embolization: Have we gone too far? J Trauma 2006; 61:541.
  45. Haan J, Ilahi ON, Kramer M, et al. Protocol-driven nonoperative management in patients with blunt splenic trauma and minimal associated injury decreases length of stay. J Trauma 2003; 55:317.
  46. Liu PP, Lee WC, Cheng YF, et al. Use of splenic artery embolization as an adjunct to nonsurgical management of blunt splenic injury. J Trauma 2004; 56:768.
  47. Rajani RR, Claridge JA, Yowler CJ, et al. Improved outcome of adult blunt splenic injury: a cohort analysis. Surgery 2006; 140:625.
  48. Sabe AA, Claridge JA, Rosenblum DI, et al. The effects of splenic artery embolization on nonoperative management of blunt splenic injury: a 16-year experience. J Trauma 2009; 67:565.
  49. Duchesne JC, Simmons JD, Schmieg RE Jr, et al. Proximal splenic angioembolization does not improve outcomes in treating blunt splenic injuries compared with splenectomy: a cohort analysis. J Trauma 2008; 65:1346.
  50. Ng EH, Comin J, David E, et al. AMPLATZER Vascular Plug 4 for proximal splenic artery embolization in blunt trauma. J Vasc Interv Radiol 2012; 23:976.
  51. Bala M, Edden Y, Mintz Y, et al. Blunt splenic trauma: predictors for successful non-operative management. Isr Med Assoc J 2007; 9:857.
  52. Peitzman AB, Harbrecht BG, Rivera L, et al. Failure of observation of blunt splenic injury in adults: variability in practice and adverse consequences. J Am Coll Surg 2005; 201:179.
  53. Liu PP, Liu HT, Hsieh TM, et al. Nonsurgical management of delayed splenic rupture after blunt trauma. J Trauma Acute Care Surg 2012; 72:1019.
  54. Gauer JM, Gerber-Paulet S, Seiler C, Schweizer WP. Twenty years of splenic preservation in trauma: lower early infection rate than in splenectomy. World J Surg 2008; 32:2730.
  55. Savage SA, Zarzaur BL, Magnotti LJ, et al. The evolution of blunt splenic injury: resolution and progression. J Trauma 2008; 64:1085.
  56. Norotsky MC, Rogers FB, Shackford SR. Delayed presentation of splenic artery pseudoaneurysms following blunt abdominal trauma: case reports. J Trauma 1995; 38:444.
  57. Terrell TR, Lundquist B. Management of splenic rupture and return-to-play decisions in a college football player. Clin J Sport Med 2002; 12:400.
  58. Schwartz PE, Sterioff S, Mucha P, et al. Postsplenectomy sepsis and mortality in adults. JAMA 1982; 248:2279.
  59. Styrt B. Infection associated with asplenia: risks, mechanisms, and prevention. Am J Med 1990; 88:33N.
  60. Howdieshell TR, Heffernan D, Dipiro JT, Therapeutic Agents Committee of the Surgical Infection Society. Surgical infection society guidelines for vaccination after traumatic injury. Surg Infect (Larchmt) 2006; 7:275.
  61. Centers for Disease Control and Prevention (CDC). Updated recommendation from the Advisory Committee on Immunization Practices (ACIP) for revaccination of persons at prolonged increased risk for meningococcal disease. MMWR Morb Mortal Wkly Rep 2009; 58:1042.
  62. Traub A, Giebink GS, Smith C, et al. Splenic reticuloendothelial function after splenectomy, spleen repair, and spleen autotransplantation. N Engl J Med 1987; 317:1559.
  63. Shatz DV. Vaccination practices among North American trauma surgeons in splenectomy for trauma. J Trauma 2002; 53:950.
  64. Di Sabatino A, Carsetti R, Corazza GR. Post-splenectomy and hyposplenic states. Lancet 2011; 378:86.
  65. Pirasteh A, Snyder LL, Lin R, et al. Temporal assessment of splenic function in patients who have undergone percutaneous image-guided splenic artery embolization in the setting of trauma. J Vasc Interv Radiol 2012; 23:80.
  66. Skattum J, Naess PA, Gaarder C. Non-operative management and immune function after splenic injury. Br J Surg 2012; 99 Suppl 1:59.
  67. Resende V, Petroianu A. Functions of the splenic remnant after subtotal splenectomy for treatment of severe splenic injuries. Am J Surg 2003; 185:311.
  68. Nakae H, Shimazu T, Miyauchi H, et al. Does splenic preservation treatment (embolization, splenorrhaphy, and partial splenectomy) improve immunologic function and long-term prognosis after splenic injury? J Trauma 2009; 67:557.
  69. Tominaga GT, Simon FJ Jr, Dandan IS, et al. Immunologic function after splenic embolization, is there a difference? J Trauma 2009; 67:289.
  70. Skattum J, Titze TL, Dormagen JB, et al. Preserved splenic function after angioembolisation of high grade injury. Injury 2012; 43:62.
  71. Falimirski M, Syed A, Prybilla D. Immunocompetence of the severely injured spleen verified by differential interference contrast microscopy: the red blood cell pit test. J Trauma 2007; 63:1087.
  72. Bader-Meunier B, Gauthier F, Archambaud F, et al. Long-term evaluation of the beneficial effect of subtotal splenectomy for management of hereditary spherocytosis. Blood 2001; 97:399.
  73. Sheikha AK, Salih ZT, Kasnazan KH, et al. Prevention of overwhelming postsplenectomy infection in thalassemia patients by partial rather than total splenectomy. Can J Surg 2007; 50:382.
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