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Management of splenic injury in the adult trauma


patient
Authors: Adrian A Maung, MD, FACS, Lewis J Kaplan, MD, FACS
Section Editor: Eileen M Bulger, MD, FACS
Deputy Editor: Kathryn A Collins, MD, PhD, FACS

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Jan 2021. | This topic last updated: Oct 01, 2019.

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 "Evaluation of splenomegaly and other splenic disorders in adults",
section on 'Trauma/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 "Evaluation of
splenomegaly and other splenic disorders in adults", section on 'Properties of the normal
spleen'.)

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.

● (See "Initial evaluation and management of blunt abdominal trauma in adults".)


● (See "Initial evaluation and management of abdominal gunshot wounds in adults".)
● (See "Initial evaluation and management of abdominal stab wounds in adults".)
● (See "Initial evaluation and management of blunt thoracic trauma in adults".)

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: Physiologic effects and
administration", section on 'Safety'.)

Associated injuries — With blunt abdominal trauma, lower rib fractures, pelvic fracture, and
spinal cord injury may also be present [9]. Hollow viscous injuries are estimated to occur in 3
percent of patients with blunt splenic injury [10]. Although the presence of rib fractures
increases the likelihood of splenic injury, there is no association between the number of ribs
fractured and splenic injury severity [11].
The injuries associated with penetrating trauma depend upon the type of implement or missile
used and its 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 uses focused


assessment with sonography in trauma (FAST exam) and computed tomography (CT). 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. The
use of 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
initial evaluation of the patient with blunt or penetrating abdominal or thoracic trauma is
discussed in detail elsewhere.

● (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".)

● (See "Initial evaluation and management of blunt thoracic trauma in adults" and "Initial
evaluation and management of penetrating thoracic trauma in adults".)

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 around the spleen, which may represent subcapsular fluid or
intraperitoneal perisplenic fluid, or fluid in Morrison's pouch (hepatorenal space).

CT findings — In noninjured 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, nonintravenous contrast CT scan has
low sensitivity for parenchymal injury and cannot establish the presence of active bleeding (ie,
contrast blush, active extravasation) [12]. However, the benefits of using IV contrast
administration to diagnose bleeding need to be weighed against the risk of complications
related to IV contrast (eg, contrast-induced nephropathy), particularly in elderly patients. A
screening noncontrast CT scan may provide some adequate information. When IV contrast is
used, the arterial phase of image acquisition improves detection of traumatic contained splenic
vascular injuries and should be considered to optimize detection of splenic injuries in trauma
with CT [13,14].
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 [15-17]. (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 with indeterminate
spleen lesions on CT scan [18], or in those who cannot undergo CT scan (eg, allergic to IV
contrast) [19]. 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 computed tomography (CT) scan or
intraoperatively ( table 1) [20,21]. 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 [22-26]. (See 'Management approach' below.)

The AAST imaging criteria for splenic injury are as follows [21]:

● Grade I – Subcapsular hematoma <10 percent surface area. Parenchymal laceration <1 cm
in depth ( picture 1). Capsular tear.

● Grade II – Subcapsular hematoma 10 to 50 percent surface area; intraparenchymal


hematoma <5 cm. Parenchymal laceration 1 to 3 cm in depth.

● Grade III – Subcapsular hematoma >50 percent of surface area; ruptured subcapsular or
intraparenchymal hematoma ≥5 cm. Parenchymal laceration >3 cm in depth.

● Grade IV – Any injury in the presence of a splenic vascular injury or active bleeding confined
within splenic capsule. Parenchymal laceration involving segmental or hilar vessels
producing >25 percent of devascularization ( picture 2).

● Grade V – Any injury in the presence of splenic vascular injury with active bleeding
extending beyond the spleen into the peritoneum. Shattered spleen.

The AAST grade identified in the operating room is not always concordant with the grade of
injury identified on imaging due to technical issues and variability of CT scan interpretation
[22,23]. A modified CT grading system has been proposed that may better identify those
patients who would benefit from initial angiographic embolization [27].

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 [28,29]. The management approach used may vary
from institution to institution depending upon the availability of resources [30].

● Hemodynamically unstable – Based upon Advanced Trauma Life Support (ATLS) principles,
the hemodynamically unstable trauma patient with a positive focused assessment with
sonography in trauma (FAST) scan or diagnostic peritoneal aspiration/lavage (DPA/DPL)
requires emergent abdominal exploration to determine the source of intraperitoneal
hemorrhage [31,32]. (See 'Trauma evaluation' above.)
● Hemodynamically stable – Hemodynamically stable patients with low-grade (I to III) blunt
or penetrating [33] splenic injuries without any evidence for other intra-abdominal injuries,
active contrast extravasation, or a blush on computed tomography (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 [16]. 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 [34]. 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 surgical exploration and splenectomy or
attempted splenic salvage 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 [35-38]. (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 early infectious complications and postsplenectomy
sepsis [28,39].

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 [28].

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. In a review of the National Trauma Data Bank, patients with liver cirrhosis had
higher rates of complications, failure of nonoperative management, and mortality compared
with noncirrhotic patients [40]. In a separate case control study, cirrhosis was an independent
risk factor for splenectomy following splenic injury [41]. However, after propensity score
matching, mortality after splenic injury was associated only with the admission MELD (Model
for End-stage Liver Disease) score and not the splenectomy procedure. (See "Model for End-
stage Liver Disease (MELD)".)

Other relative contraindications include higher-grade splenic injury (>grade III) [42,43], active
contrast extravasation, large-volume hemoperitoneum (though difficult to accurately quantify),
traumatic brain injury [42,44], refusal of blood transfusion in the setting of preexisting 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 [43,45,46].
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 [47]. 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, but, overall, the experience with
nonoperative management of higher-grade splenic injury in older patients is limited.
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 [36,48,49]. The largest of these
studies examined 1008 patients ≥55 years of age who sustained blunt splenic injury [36]. 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. In a 2011 review of the National Trauma Data Bank, increasing age was
associated with a slightly increased risk for failure of nonoperative management (odds ratio
1.014 per year of age) [50].

Observation — Successful observation during nonoperative management for splenic trauma


depends upon proper patient selection and the availability of adequate resources within the
institution [28,51,52]. Clinical grading based on computed tomography (CT) combined with the
abdominal abbreviated injury score (AIS) were identified as the best predictor of successful
observation [53]. 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.)

General care — 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 [54,55]. We initially place the patient on bed rest,
though no clear benefit exists for this practice. In a small retrospective study, early mobilization
of patients with nonoperative spleen injuries appeared to be safe [56]. In agreement with an
expert panel, we obtain serial hemoglobin levels every six hours in the first 24 hours [57].
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.
Small retrospective studies have suggested that early thromboprophylaxis (within 48 hours)
may be safe, but there are currently no standards for the initiation of prophylaxis in patients
who are managed nonoperatively [58-60]. Venous thromboembolism prophylaxis may be
contraindicated by other associated injuries.

Follow-up imaging — There is debate in the literature and among clinicians regarding the
utility of follow-up imaging. In a consensus study using the Delphi method, only 46 percent of
the experts surveyed recommended routine inpatient follow-up imaging [57]. In one
retrospective review that included 773 patients with blunt splenic injury, outcomes of a cohort
of patients (n = 616 patients from 2000 to 2012) who had mandatory repeat CT evaluation at 48
hours and angioembolization (if indicated) were compared with an earlier cohort for whom
repeat scanning was selective (n = 157 from 1995 to 1999) [61]. The proportion of patients
managed nonoperatively (77 versus 53) and overall rate of splenic salvage (77 versus 46
percent) were significantly higher in the later cohort of patients.

We perform a follow-up study in patients whose clinical situation indicates the need (eg, falling
hemoglobin, increasing abdominal pain, left shoulder pain, fever). 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.

Duration — 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 [54]. Another expert group observed patients for one to
three days [57]. 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 [62].

An observation period of five days identifies at least 95 percent of patients who would require
some form of intervention [63,64]. 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 [45]. 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." A prospective study of 383 patients from 11 trauma centers ascertained the long-term
risk of splenectomy after an initial 24 hours of nonoperative management [65]. Twelve patients
(3.1 percent) underwent in-hospital splenectomy between 24 hours and nine days after injury.
Only one patient, among 366 patients discharged with a spleen, ruptured on postinjury day 12.
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. In one review, delayed pseudoaneurysm or
arterial extravasation was detected in 6 percent of patients and distributed among all injury
grades [61].

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.

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 packed red
blood cells (PRBCs) 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 [16,24,25,66-69].

A number of observational studies have demonstrated that nonoperative management is more


successful with the adjunctive use of angioembolization [15,70-77].
● 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 [74]. 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.

● A retrospective multicenter trial that included 1275 patients found that angioembolization
significantly increased the likelihood of splenic salvage (odds ratio [OR] 5, 95% CI 1.8-13.5)
[71].

● In a small study of 39 patients, splenic artery embolization increased the success rate for
nonsurgical management from 74 to 89 percent [73].

Retrospective reviews have found variable success rates (57 to 95 percent) for splenic salvage
that include embolization in patients with higher-grade (III, IV, V) splenic injuries
[15,38,66,68,76,78-82]. However, in a study where the trauma protocol was adapted to require
arteriography and possible embolization for all patients with grade III to V injuries, the failure
rate of nonoperative management decreased from 15 to 5 percent [76].

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 [38]. 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 [83]. However, complication rates related to splenic
embolization may be higher with distal embolization [84].

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 [38,85]. 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 4. 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 that
transfusion-related risks do not justify nonoperative management strategies for which the
volume of transfusion may be increased. 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-related acute lung injury (TRALI)" and "Leukoreduction to
prevent complications of blood transfusion", section on 'Immunosuppression' and "Transfusion-
associated circulatory overload (TACO)".)

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 [84]. 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 "Contrast-associated and contrast-induced
acute kidney injury: Clinical features, diagnosis, and management" and "Prevention of contrast-
induced acute kidney injury associated with angiography".)

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.

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 [37,45,46,86,87]. In retrospective studies, up to 40 percent of patients failing
nonoperative management were found to have inappropriate indications for a nonoperative
approach [37,88,89].

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 [45,90].

The need for subsequent splenectomy following conservative management is overall low. In a
review of the United States Healthcare Cost and Utilization Project's Nationwide Readmission
Database, adult patients with isolated splenic injury were studied [91]. The overall readmission
rates at six months was 21.1 percent, which did not differ significantly based on initial
management strategy (ie, angioembolization, splenectomy, no procedure). The rate of delayed
splenectomy was 4.5 percent among readmitted patients, and overall, the chance of
readmission for splenectomy after initial nonoperative management was 1.2 percent.

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 reinjury [54]. 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 [92].

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 concluded that there are insufficient data to determine whether routine follow-up
imaging is necessary [30]. In one survey of EAST members, 85 percent of respondents did not
routinely reimage [54]. The delayed presentation of splenic pseudoaneurysms have been
reported and may support a decision to reimage [61,66,93]. In a study of 104 patients, delayed
formation of splenic pseudoaneurysms occurred in 15.4 percent of patients and was detected
one to eight days after admission [94]. Approximately one half of the pseudoaneurysms
spontaneously thrombosed without the need for specific intervention.

Repeat CT scan or contrast-enhanced ultrasound (provided that the injury can be adequately
visualized) can be considered in select patients [95]. Reimaging may be indicated to lift an
activity restriction, or for patients whose work requirements or lifestyles place them at higher
risk for reinjury if healing is not complete [96]. Examples include professional athletes, military
service personnel, and extreme sports enthusiasts. Reimaging may also be appropriate for
those who are planning to travel to regions of the world with limited health care access to
document complete healing prior to travel. For these patients, reimaging 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 [97,98]. Information on specific vaccines and vaccine schedules are
discussed elsewhere. (See "Prevention of infection in patients with impaired splenic function",
section on 'Vaccinations'.)

Ideally, vaccines are administered either 14 days prior to or 14 days following splenectomy for
maximal immunologic benefit [99,100]. 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 health care 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 following traumatic rupture because the extent to which a patient may
(or may not) have functional residual splenic tissue (ie, splenosis) is uncertain. An experimental
study demonstrated the ability of autogenic splenic implants to increase the rate of bacterial
clearance and to remove colloidal substance and altered erythrocyte corpuscular inclusions,
such as Howell-Jolly, Heinz, and Pappenheimer bodies, from the bloodstream [101]. However,
whether this occurs with traumatic splenosis is unknown. 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 [102]. (See
"Evaluation of splenomegaly and other splenic disorders in adults", section on 'Splenosis'.)

Following splenic salvage surgery, splenic embolization, or nonoperative management, we feel


that immunization is not necessary, though some clinicians may disagree [103-105]. Available in
vitro studies indicate immunocompetence in these patients [106-115]. 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
[116,117]. In a systematic review of 12 observational studies, most found that splenic function
was preserved after partial splenectomy or splenic embolization [118]. The validity of the
studies that did not was questioned as splenic function was assessed only after the first week
following embolization. However, uncertainty remains since these studies used a variety of
clinical parameters to assess the immunologic and hemofiltrative function of the spleen, and
the best parameter/test to assess immunocompetence in this population has not been
determined. 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 [119].

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Blunt splenic and
hepatic injury".)
SUMMARY AND RECOMMENDATIONS

● 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 infection in
patients with impaired splenic function".)

● 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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REFERENCES
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, Moore EE, Feliciano DV, Mattox KL
(Eds), McGraw-Hill Medical, New York 2008. p.661.

10. Swaid F, Peleg K, Alfici R, et al. Concomitant hollow viscus injuries in patients with blunt
hepatic and splenic injuries: an analysis of a National Trauma Registry database. Injury
2014; 45:1409.

11. Swaid F, Peleg K, Alfici R, et al. The severity of liver injury following blunt trauma does not
correlate with the number of fractured ribs: an analysis of a national trauma registry
database. Surg Today 2015; 45:846.

12. Murken DR, Weis JJ, Hill GC, et al. Radiographic assessment of splenic injury without
contrast: is contrast truly needed? Surgery 2012; 152:676.

13. Boscak AR, Shanmuganathan K, Mirvis SE, et al. Optimizing trauma multidetector CT
protocol for blunt splenic injury: need for arterial and portal venous phase scans.
Radiology 2013; 268:79.

14. Uyeda JW, LeBedis CA, Penn DR, et al. Active hemorrhage and vascular injuries in splenic
trauma: utility of the arterial phase in multidetector CT. Radiology 2014; 270:99.

15. Haan JM, Biffl W, Knudson MM, et al. Splenic embolization revisited: a multicenter review. J
Trauma 2004; 56:542.

16. 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.
17. Fu CY, Wu SC, Chen RJ, et al. Evaluation of need for operative intervention in blunt splenic
injury: intraperitoneal contrast extravasation has an increased probability of requiring
operative intervention. World J Surg 2010; 34:2745.

18. Gordic S, Alkadhi H, Simmen HP, et al. Characterization of indeterminate spleen lesions in
primary CT after blunt abdominal trauma: potential role of MR imaging. Emerg Radiol
2014; 21:491.

19. Hedrick TL, Sawyer RG, Young JS. MRI for the diagnosis of blunt abdominal trauma: a case
report. Emerg Radiol 2005; 11:309.

20. Kozar RA, Crandall M, Shanmuganathan K, et al. Organ injury scaling 2018 update: Spleen,
liver, and kidney. J Trauma Acute Care Surg 2018; 85:1119.

21. 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.

22. 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.

23. 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.

24. 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.

25. 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.

26. Harbrecht BG. Is anything new in adult blunt splenic trauma? Am J Surg 2005; 190:273.

27. 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.

28. Stassen NA, Bhullar I, Cheng JD, et al. Nonoperative management of blunt hepatic injury:
an Eastern Association for the Surgery of Trauma practice management guideline. J
Trauma Acute Care Surg 2012; 73:S288.

29. Hildebrand DR, Ben-Sassi A, Ross NP, et al. Modern management of splenic trauma. BMJ
2014; 348:g1864.
30. Stassen NA, Bhullar I, Cheng JD, et al. Selective nonoperative management of blunt splenic
injury: an Eastern Association for the Surgery of Trauma practice management guideline. J
Trauma Acute Care Surg 2012; 73:S294.

31. Lo A, Matheson AM, Adams D. Impact of concomitant trauma in the management of blunt
splenic injuries. N Z Med J 2004; 117:U1052.

32. Wahl WL, Ahrns KS, Chen S, et al. Blunt splenic injury: operation versus angiographic
embolization. Surgery 2004; 136:891.

33. Berg RJ, Inaba K, Okoye O, et al. The contemporary management of penetrating splenic
injury. Injury 2014; 45:1394.

34. Holubar SD, Wang JK, Wolff BG, et al. Splenic salvage after intraoperative splenic injury
during colectomy. Arch Surg 2009; 144:1040.

35. Stein DM, Scalea TM. Nonoperative management of spleen and liver injuries. J Intensive
Care Med 2006; 21:296.

36. 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.

37. McIntyre LK, Schiff M, Jurkovich GJ. Failure of nonoperative management of splenic
injuries: causes and consequences. Arch Surg 2005; 140:563.

38. 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.

39. Demetriades D, Scalea TM, Degiannis E, et al. Blunt splenic trauma: splenectomy increases
early infectious complications: a prospective multicenter study. J Trauma Acute Care Surg
2012; 72:229.

40. Bugaev N, Breeze JL, Daoud V, et al. Management and outcome of patients with blunt
splenic injury and preexisting liver cirrhosis. J Trauma Acute Care Surg 2014; 76:1354.

41. Cook MR, Fair KA, Burg J, et al. Cirrhosis increases mortality and splenectomy rates
following splenic injury. Am J Surg 2015; 209:841.

42. Velmahos GC, Zacharias N, Emhoff TA, et al. Management of the most severely injured
spleen: a multicenter study of the Research Consortium of New England Centers for
Trauma (ReCONECT). Arch Surg 2010; 145:456.

43. Olthof DC, Joosse P, van der Vlies CH, et al. Prognostic factors for failure of nonoperative
management in adults with blunt splenic injury: a systematic review. J Trauma Acute Care
Surg 2013; 74:546.

44. Teixeira PG, Karamanos E, Okoye OT, et al. Splenectomy in patients with traumatic brain
injury: protective or harmful? A National Trauma Data Bank analysis. J Trauma Acute Care
Surg 2013; 75:596.

45. 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.

46. 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.

47. Watson GA, Rosengart MR, Zenati MS, et al. Nonoperative management of severe blunt
splenic injury: are we getting better? J Trauma 2006; 61:1113.

48. 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.

49. 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.

50. Ong AW, Eilertson KE, Reilly EF, et al. Nonoperative management of splenic injuries:
significance of age. J Surg Res 2016; 201:134.

51. Demetriades D, Hadjizacharia P, Constantinou C, et al. Selective nonoperative


management of penetrating abdominal solid organ injuries. Ann Surg 2006; 244:620.

52. 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.

53. Saksobhavivat N, Shanmuganathan K, Chen HH, et al. Blunt splenic injury: use of a
multidetector CT-based splenic injury grading system and clinical parameters for triage of
patients at admission. Radiology 2015; 274:702.

54. 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.
55. Gomez D, Haas B, Al-Ali K, et al. Controversies in the management of splenic trauma.
Injury 2012; 43:55.

56. Teichman A, Scantling D, McCracken B, Eakins J. Early mobilization of patients with non-
operative liver and spleen injuries is safe and cost effective. Eur J Trauma Emerg Surg
2018; 44:883.

57. Olthof DC, van der Vlies CH, Joosse P, et al. Consensus strategies for the nonoperative
management of patients with blunt splenic injury: a Delphi study. J Trauma Acute Care
Surg 2013; 74:1567.

58. Kwok AM, Davis JW, Dirks RC, et al. Time is now: venous thromboembolism prophylaxis in
blunt splenic injury. Am J Surg 2016; 212:1231.

59. Rostas JW, Manley J, Gonzalez RP, et al. The safety of low molecular-weight heparin after
blunt liver and spleen injuries. Am J Surg 2015; 210:31.

60. Murphy PB, Sothilingam N, Charyk Stewart T, et al. Very early initiation of chemical venous
thromboembolism prophylaxis after blunt solid organ injury is safe. Can J Surg 2016;
59:118.

61. Leeper WR, Leeper TJ, Ouellette D, et al. Delayed hemorrhagic complications in the
nonoperative management of blunt splenic trauma: early screening leads to a decrease in
failure rate. J Trauma Acute Care Surg 2014; 76:1349.

62. 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.

63. 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.

64. Smith J, Armen S, Cook CH, Martin LC. Blunt splenic injuries: have we watched long
enough? J Trauma 2008; 64:656.

65. Zarzaur BL, Kozar R, Myers JG, et al. The splenic injury outcomes trial: An American
Association for the Surgery of Trauma multi-institutional study. J Trauma Acute Care Surg
2015; 79:335.

66. 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.
67. Sclafani SJ. The role of angiographic hemostasis in salvage of the injured spleen. Radiology
1981; 141:645.

68. 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.

69. Bhullar IS, Frykberg ER, Tepas JJ 3rd, et al. At first blush: absence of computed tomography
contrast extravasation in Grade IV or V adult blunt splenic trauma should not preclude
angioembolization. J Trauma Acute Care Surg 2013; 74:105.

70. Konev SV, Katibnikov MA, Bandarin VA, et al. [Luminescence study of the effect of
temperature on the conformational state of fibrinogen]. Biofizika 1975; 20:586.

71. Banerjee A, Duane TM, Wilson SP, et al. Trauma center variation in splenic artery
embolization and spleen salvage: a multicenter analysis. J Trauma Acute Care Surg 2013;
75:69.

72. 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.

73. 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.

74. Rajani RR, Claridge JA, Yowler CJ, et al. Improved outcome of adult blunt splenic injury: a
cohort analysis. Surgery 2006; 140:625.

75. 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.

76. 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.

77. Capecci LM, Jeremitsky E, Smith RS, Philp F. Trauma centers with higher rates of
angiography have a lesser incidence of splenectomy in the management of blunt splenic
injury. Surgery 2015; 158:1020.
78. Requarth JA, D'Agostino RB Jr, Miller PR. Nonoperative management of adult blunt splenic
injury with and without splenic artery embolotherapy: a meta-analysis. J Trauma 2011;
71:898.

79. Gaarder C, Dormagen JB, Eken T, et al. Nonoperative management of splenic injuries:
improved results with angioembolization. J Trauma 2006; 61:192.

80. 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.

81. Smith HE, Biffl WL, Majercik SD, et al. Splenic artery embolization: Have we gone too far? J
Trauma 2006; 61:541.

82. Skattum J, Naess PA, Eken T, Gaarder C. Refining the role of splenic angiographic
embolization in high-grade splenic injuries. J Trauma Acute Care Surg 2013; 74:100.

83. 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.

84. Ekeh AP, Khalaf S, Ilyas S, et al. Complications arising from splenic artery embolization:
a review of an 11-year experience. Am J Surg 2013; 205:250.

85. 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.

86. Bala M, Edden Y, Mintz Y, et al. Blunt splenic trauma: predictors for successful non-
operative management. Isr Med Assoc J 2007; 9:857.

87. Scarborough JE, Ingraham AM, Liepert AE, et al. Nonoperative Management Is as Effective
as Immediate Splenectomy for Adult Patients with High-Grade Blunt Splenic Injury. J Am
Coll Surg 2016; 223:249.

88. 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.

89. 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.

90. 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.
91. Rosenberg GM, Knowlton L, Rajasingh C, et al. National Readmission Patterns of Isolated
Splenic Injuries Based on Initial Management Strategy. JAMA Surg 2017; 152:1119.

92. Savage SA, Zarzaur BL, Magnotti LJ, et al. The evolution of blunt splenic injury: resolution
and progression. J Trauma 2008; 64:1085.

93. Norotsky MC, Rogers FB, Shackford SR. Delayed presentation of splenic artery
pseudoaneurysms following blunt abdominal trauma: case reports. J Trauma 1995; 38:444.

94. Muroya T, Ogura H, Shimizu K, et al. Delayed formation of splenic pseudoaneurysm


following nonoperative management in blunt splenic injury: multi-institutional study in
Osaka, Japan. J Trauma Acute Care Surg 2013; 75:417.

95. Poletti PA, Becker CD, Arditi D, et al. Blunt splenic trauma: can contrast enhanced
sonography be used for the screening of delayed pseudoaneurysms? Eur J Radiol 2013;
82:1846.

96. 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.

97. Schwartz PE, Sterioff S, Mucha P, et al. Postsplenectomy sepsis and mortality in adults.
JAMA 1982; 248:2279.

98. Styrt B. Infection associated with asplenia: risks, mechanisms, and prevention. Am J Med
1990; 88:33N.

99. 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.

100. 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.

101. Marques RG, Lucena SB, Caetano CE, et al. Blood clearance of Howell-Jolly bodies in an
experimental autogenic splenic implant model. Br J Surg 2014; 101:820.

102. 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.
103. Shatz DV. Vaccination practices among North American trauma surgeons in splenectomy
for trauma. J Trauma 2002; 53:950.

104. Di Sabatino A, Carsetti R, Corazza GR. Post-splenectomy and hyposplenic states. Lancet
2011; 378:86.

105. Skattum J, Naess PA, Gaarder C. Non-operative management and immune function after
splenic injury. Br J Surg 2012; 99 Suppl 1:59.

106. 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.

107. Resende V, Petroianu A. Functions of the splenic remnant after subtotal splenectomy for
treatment of severe splenic injuries. Am J Surg 2003; 185:311.

108. 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.

109. Tominaga GT, Simon FJ Jr, Dandan IS, et al. Immunologic function after splenic
embolization, is there a difference? J Trauma 2009; 67:289.

110. Skattum J, Titze TL, Dormagen JB, et al. Preserved splenic function after angioembolisation
of high grade injury. Injury 2012; 43:62.

111. 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.

112. Walusimbi MS, Dominguez KM, Sands JM, et al. Circulating cellular and humoral elements
of immune function following splenic arterial embolisation or splenectomy in trauma
patients. Injury 2012; 43:180.

113. Shih HC, Wang CY, Wen YS, et al. Spleen artery embolization aggravates endotoxin
hyporesponse of peripheral blood mononuclear cells in patients with spleen injury. J
Trauma 2010; 68:532.

114. Olthof DC, Lammers AJ, van Leeuwen EM, et al. Antibody response to a T-cell-independent
antigen is preserved after splenic artery embolization for trauma. Clin Vaccine Immunol
2014; 21:1500.
115. Foley PT, Kavnoudias H, Cameron PU, et al. Proximal Versus Distal Splenic Artery
Embolisation for Blunt Splenic Trauma: What is the Impact on Splenic Immune Function?
Cardiovasc Intervent Radiol 2015; 38:1143.

116. 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.

117. 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.

118. Schimmer JA, van der Steeg AF, Zuidema WP. Splenic function after angioembolization for
splenic trauma in children and adults: A systematic review. Injury 2016; 47:525.

119. 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.

Topic 7957 Version 28.0


GRAPHICS

AAST spleen injury scale

AAST Imaging criteria (CT


Operative criteria Pathologic criteria
grade findings)

I Subcapsular hematoma <10% Subcapsular hematoma <10% Subcapsular hematoma <10%


surface area surface area surface area
Parenchymal laceration <1 cm Parenchymal laceration <1 cm Parenchymal laceration <1 cm
depth depth depth
Capsular tear Capsular tear Capsular tear

II Subcapsular hematoma 10 to Subcapsular hematoma 10 to Subcapsular hematoma 10 to


50% surface area; 50% surface area; 50% surface area;
intraparenchymal hematoma <5 intraparenchymal hematoma <5 intraparenchymal hematoma <5
cm cm cm
Parenchymal laceration 1 to 3 cm Parenchymal laceration 1 to 3 cm Parenchymal laceration 1 to 3 cm

III Subcapsular hematoma >50% Subcapsular hematoma >50% Subcapsular hematoma >50%
surface area; ruptured surface area or expanding; surface area; ruptured
subcapsular or intraparenchymal ruptured subcapsular or subcapsular or intraparenchymal
hematoma ≥5 cm intraparenchymal hematoma ≥5 hematoma ≥5 cm
Parenchymal laceration >3 cm cm Parenchymal laceration >3 cm
depth Parenchymal laceration >3 cm depth
depth

IV Any injury in the presence of a Parenchymal laceration involving Parenchymal laceration involving
splenic vascular injury or active segmental or hilar vessels segmental or hilar vessels
bleeding confined within splenic producing >25% producing >25%
capsule devascularization devascularization
Parenchymal laceration involving
segmental or hilar vessels
producing >25%
devascularization

V Any injury in the presence of Hilar vascular injury that Hilar vascular injury that
splenic vascular injury with active devascularizes the spleen devascularizes the spleen
bleeding extending beyond the Shattered spleen Shattered spleen
spleen into the peritoneum
Shattered spleen

Vascular injury is defined as a pseudoaneurysm or arteriovenous fistula and appears as a focal collection of vascular contrast
that decreases in attenuation with delayed imaging. Active bleeding from a vascular injury presents as vascular contrast, focal
or diffuse, that increases in size or attenuation in delayed phase. Vascular thrombosis can lead to organ infarction.
Grade based on highest grade assessment made on imaging, at operation or on pathologic specimen.
More than one grade of splenic injury may be present and should be classified by the higher grade of injury.
Advance one grade for multiple injuries up to a grade III.

AAST: American Association for the Surgery of Trauma; CT: computed tomography.

Reproduced with permission from: Kozar RA, Crandall M, Shanmuganathan K, et al. Organ injury scaling 2018 update: Spleen, liver, and kidney. J
Trauma Acute Care Surg 2018; 85:1119. Copyright © 2018 American Association for the Surgery of Trauma. Available at:
https://www.aast.org/resources-detail/injury-scoring-scale#spleen (Accessed on December 10, 2019).

Graphic 67884 Version 6.0


Low grade splenic laceration

Courtesy of Lewis J Kaplan, MD

Graphic 71599 Version 3.0


High grade spleen laceration

Courtesy of Lewis J Kaplan, MD

Graphic 65830 Version 3.0


Splenosis on CT scan

This 55 year-old woman had a total splenectomy for traumatic splenic rupture. A CT scan taken a number of
years later for unrelated purposes showed two foci of splenosis (arrows) and a surgical clip (arrowhead).

CT: computed tomography.

Graphic 89598 Version 2.0


Contributor Disclosures
Adrian A Maung, MD, FACS Nothing to disclose Lewis J Kaplan, MD, FACS Nothing to disclose Eileen M
Bulger, MD, FACS Equity Ownership/Stock Options: Opticyte [Shock]. Grant/Research/Clinical Trial
Support: Atox Bio [Necrotizing soft tissue infections]; Potrero Medical [Critical care]. Consultant/Advisory
Boards: Opticyte [Shock], Atox Bio. Kathryn A Collins, MD, PhD, FACS Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must
conform to UpToDate standards of evidence.

Conflict of interest policy

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