Embolization Therapy: Principles and Clinical Applications, 1 Ed.

Thoracoabdominal Trauma

Lawrence J. Keating • Ashley Adamovich



During the past three decades, management of traumatic abdominal organ injury has evolved from a predominantly surgical approach to a strategy of nonoperative therapy in most cases. There is now broad consensus that most patients with injuries to solid abdominal viscera who are hemodynamically stable are candidates for nonoperative management (NOM), although debate persists about the specifics including when to use angiography and which patients should proceed directly to surgery. The change in philosophy has been in large part a result of rapid advances in imaging capabilities, specifically computed tomography (CT), and the increasing capability of interventional radiology to treat vascular injuries using minimally invasive endovascular techniques. During the 1980s, diagnostic peritoneal lavage (DPL) was obviated by the development and availability of CT. With concurrent expansion in the capabilities of interventional radiology, the risks of surgery began to outweigh the risks of conservative management, defined as observation with or without angiography and embolization, in many cases.

The Organ Injury Scale (OIS)—created by a committee of the American Association for the Surgery of Trauma (AAST) in 1987 and since updated and validated for the liver, kidney, and spleen using National Trauma Data Bank (NTDB)—is the most commonly used grading system for evaluation of abdominal trauma (Table 22.1).1 The current scale was revised in 1994 for the spleen and liver, partly to reflect the increasing reliance on CT for diagnosis and grading. It provides a common nomenclature for studies and outcomes research that is used almost exclusively in the trauma literature, although it is imperfect, particularly when used to assign prognostic value, which is not its fundamental objective.1,2 It is designed primarily to allow comparison of equivalent injuries managed differently.3 In a study designed to evaluate and compare injury grading scales, Barquist et al.4 found significant interreader variability among radiologists in higher grade injuries as well as a tendency to underestimate injury grades based on CT compared to operative findings. Contrast extravasation indicating continuing hemorrhage and vascular injuries such as pseudoaneurysm or arteriovenous fistula are prognostic factors and may be indications for nonoperative interventions such as angioembolization but are not specifically described in the scale. Modifications addressing these concerns including a new CT grading system for splenic injuries and substratification of the renal OIS grade IV into IVa (high risk) and IVb (low risk) have been proposed but not yet widely adopted.5,6

The OIS enables accurate outcomes comparisons among institutions with differing protocols, but urgent decisions in the trauma setting are typically made based on clinical status combined with imaging findings. Current surgical guidelines support emergency surgery for hemodynamically unstable patients (hypotension and tachycardia unresponsive to ongoing fluid and packed red blood cell resuscitation) and a trial of NOM for stable patients in settings where monitored beds and surgical teams are readily available.610

The new standard of conservative management has been supported and improved by the increasing availability and effectiveness of angiography with embolization. By 2005, up to 85% of traumatic injuries involving liver, spleen, and kidney were managed nonsurgically.10 Shafi et al.11 studied operative intervention and mortality rates at 152 level I and level II trauma centers and demonstrated that hospitals with higher risk-adjusted mortality rates tend to also have the highest rates of surgical intervention for abdominal trauma. Various conclusions can be drawn from this, but the lowest mortality rates will occur when we have the best understanding of which patients need operative versus conservative management. Because randomized trials are impractical in this setting, collective experience in the form of retrospective studies is our principal guide.


The spleen may be the most commonly injured organ in blunt abdominal trauma.12 Aristotle considered the spleen an unnecessary organ and this was the prevailing view until recently.13 From the first splenectomy for trauma by Nicholaus Matthias in 1678 until the 1970s, removal of the injured spleen was accepted, if not standard, practice. The notion that without splenectomy most patients with splenic injury would bleed to death because the spleen cannot heal nor be easily repaired was rarely questioned.13 Interest in splenic preservation increased after the description in 1952 by King and Schumacker14 of overwhelming postsplenectomy infection (OPSI) in infants. Upadhyaya and Simpson performed the first case-control study of operative versus nonoperative management for pediatric splenic injury and demonstrated the safety of the latter approach in 1968.13 Children were found to recover from these injuries surprisingly well, and by the late 1980s, the conservative management of pediatric splenic trauma was universally accepted, a change largely predating the radiologic advances that were crucial to the broad adoption of this strategy in adults.14,15

New understanding about the spleen’s role in immunocompetence encouraged early efforts at salvage in adult trauma patients. OPSI, although rare, with a lifetime risk of less than 0.05%, carries a mortality rate of 50%.12,16Less severe infectious complications are more common, including abscess, wound infection, and pneumonia, all of which are increased after splenectomy, compared to splenic preservation after trauma.17 The reasons for this remain incompletely understood. The spleen represents one-quarter to one-half of the lymphoid tissue in the body; is a reservoir of macrophages, which remove bacteria and red blood cells infected with parasites; and produces vital immunomodulators such as opsonins, which are needed to clear encapsulated organisms. Asplenic patients are probably more susceptible to gram-negative bacteria and fungi as well.12 Splenectomized patients should be immunized against Streptococcus pneumoniae, meningococcus, and Haemophilus influenzae type B, the encapsulated organisms for which vaccines are currently available.12,16,17

The trend toward conservative management of splenic injury coincided with the development of endovascular techniques to achieve hemostasis and support organ preservation. Although balloon occlusion and gelatin foam embolization had been previously reported,18,19 in 1981, Sclafani20 described endovascular occlusion of the proximal main splenic artery with coils, and he predicted that this would improve the outcomes of NOM. In 1991, Sclafani and his colleagues21 reported a striking 97% splenic salvage rate with routine angiography and selective proximal splenic artery occlusion in patients with splenic lacerations diagnosed with CT.

The specific indications and most appropriate candidates for NOM and adjunctive angioembolization have been a topic of debate and many retrospective studies in the intervening period; the object has been to elucidate the vital factors which contribute to the success or failure of conservative management. Failure is indicated by continued or recurrent splenic bleeding, often referred to as delayed splenic rupture. Peitzman et al.22 found that the success of NOM is directly correlated with increasing hematocrit and blood pressure and inversely correlated with OIS grade and quantity of hemoperitoneum. Advanced age has been shown to be a risk factor; Renzulli et al.23 found age older than 55 years to be the only independent risk factor for failure of NOM. The direct relationship between increasing OIS grade and failure rate of conservative therapy has been demonstrated in multiple retrospective analyses.22,2427

Patient Selection

Most large trauma centers include splenic artery embolization (SAE) as a variable component of NOM. Much of the current literature supports angiography for hemodynamically stable patients with CT findings suggesting contrast extravasation and/or grade IV or V injuries. Several studies have demonstrated that in low-grade injuries (OIS I to III), angioembolization does not result in an improvement in outcomes, whereas in higher grade injuries, a marked improvement is seen.2527 For example, Requarth et al.27 showed that although failure of nonoperative management (FNOM) was less than 5% in OIS grades I and II injuries with or without SAE, it rose with each OIS grade to 83.1% in grade V observation-only patients but only to 25% in patients who underwent SAE.

Although most trauma centers include angiography and embolization as an adjunct to NOM of splenic trauma in hemodynamically stable patients, there are no randomized trials. Thus, the Eastern Association for the Surgery of Trauma (EAST) assigns a level 2 recommendation to use SAE in grades IV and V injuries or whenever contrast extravasation is noted on CT.8 Bhullar et al.28 supported this recommendation in a 2013 study, pointing out that significantly higher failure rate of NOM in grades IV and V injuries may be affected by the fact that many centers do not perform angiography in cases where extravasation is not noted on CT. Although evidence of active bleeding is more common in higher grade injuries, it may be seen in lower grade (OIS I to III) injuries as well.


If the splenic artery is clearly identified on the admission CT, a flush aortogram may not be necessary before splenic artery selection. Typically, a Cobra (Angiodynamics, Latham, New York) or reverse curve catheter such as an Sos or Mikaelsson (Angiodynamics, Latham, New York) is used to select the celiac axis. Splenic angiography should be performed with automated injection. If angiography reveals active extravasation, then selective distal coil embolization may be performed using a microcatheter with microcoils and/or gelfoam, followed by proximal main splenic artery coil embolization (Fig. 22.1). If there is no evidence of active hemorrhage, then only proximal main SAE is performed using coils, either via the main catheter or a microcatheter.

The rationale for proximal main SAE is reduction of splenic blood pressure, facilitating hemostasis without causing infarction. The abundant arterial supply to the spleen makes this possible. Perfusion is maintained by pancreatic, omental, and short gastric arteries at relatively lower pressure, which gives splenic vascular injuries an opportunity to heal; as the collateral arteries enlarge, pressure is believed to eventually return to preembolization levels, although when this happens is unknown.29,30 Requarth and colleagues30 conducted a study demonstrating significant variability in the distal splenic arterial pressure during proximal balloon occlusion of the splenic artery. They concluded that some patients, such as those with celiac stenosis, might already have well-developed splanchnic collaterals, which would negate the impact of proximal splenic artery occlusion on parenchymal pressure. Interestingly, their results suggest that it may be reasonable to perform splenic artery balloon occlusion with pressure measurements in all splenic trauma patients before deciding whether to embolize; patients who do not demonstrate a significant decrease in splenic artery pressure during balloon occlusion may be better served with either surgery or observation.

The diameter of the splenic artery should be measured and coils oversized by at least 2 mm to avoid coil migration and increased risk of splenic infarction. Appropriate sizing is difficult. Detachable coils allow the operator to retract a partially deployed coil if it appears that migration is likely. For proximal main SAE, coils should be placed distal to the dorsal pancreatic artery and proximal to the greater pancreatic artery (often called by its Latin name arteria pancreatica magna), although the ideal location is not known (Fig. 22.2). The dorsal pancreatic artery is usually the largest splenic artery branch to the pancreas and there is at least a small risk that occluding this vessel could lead to pancreatic ischemia.29 It also gives rise to distal branches that become a collateral source of splenic perfusion after occlusion of the splenic artery. However, there is variability in the anatomic origins of these pancreatic branches, and they cannot always be identified with certainty. The omental and short gastric arteries, left gastroepiploic artery, and other branches from the inferior and caudal pancreatic artery will also serve as collateral blood sources for the spleen after proximal embolization.29,30 Postembolization angiography should demonstrate occlusion of the main splenic artery with delayed splenic parenchymal perfusion via collateral flow.


In a comprehensive retrospective analysis of 33 blunt splenic injury outcomes articles from 1994 to 2009 by Requarth et al.,27 patients were stratified based on type of NOM (with or without SAE) as well as splenic injury grade. They found the overall failure rate of observational management to be 17%, with much worse rates of 44% and 83% in grades IV and V injuries, respectively.27 However, SAE significantly decreased the failure rates in grades IV and V to 17% and 25%, respectively.27 Bhullar et al.28 found a 4% failure rate in patients with high-grade splenic injuries who underwent SAE, including those with contrast blush on CT, only 9% of whom ultimately required laparotomy (splenectomy or splenorrhaphy). In one of the largest single-center studies using a protocol of selective embolization in patients with CT evidence of vascular injury or active bleeding, Sabe et al.31 reported an NOM success rate of 97%. Banerjee et al.32 compared outcomes across four level I trauma centers with varying rates of embolization and found that SAE is an independent predictor of spleen salvage; centers in which it was used more had higher NOM success rates. Haan et al.33 published another large single-center study which demonstrated 90% success overall with NOM and over 80% success in grades IV and V splenic injuries. Many of the successful cases had CT scans demonstrating pseudoaneurysm or active extravasation and were treated with SAE. However, in patients with traumatic arteriovenous fistula (AVF), failure rates were high (40%) even after SAE. They concluded that AVF requires direct embolization and that proximal SAE is insufficient in these cases.33

In cases of late rebleeding after observation or SAE, it appears that many, if not most, centers favor splenectomy even though conservative management has become standard therapy for acute splenic injury. The reasons for this are unclear but likely reflect a reluctance to continue with a “failed” strategy. In a paper by Liu et al.,34 15 cases of “delayed splenic rupture” were reviewed. Twelve were treated nonoperatively with 83% success rate, and 5 of these underwent SAE with 80% success rate. These results are comparable to those of primary NOM with or without SAE and they conclude that embolization is a reasonable strategy for late rebleeding.34

The most common complication directly related to SAE is splenic infarction, of which there is a higher risk when distal embolization is performed.35,36 The clinical significance of these typically small or segmental splenic infarcts is unclear, as most ultimately resolve without further intervention.35 In a meta-analysis by Schnuringer et al.,35 no difference in the rate of major complications such as large infarct or abscess requiring splenectomy was found when comparing proximal and distal embolization techniques. Other complications are predominantly technical and rare, including arterial dissection, coil migration into the aorta, and femoral artery pseudoaneurysm.36

Protocols regarding observation, discharge, and follow-up imaging vary but typically include inpatient stay of 3 to 5 days, as recommended by Peitzman et al.22 Rebleeding, the most common cause of failure, most often occurs within 3 days of injury.37,38 Smith et al.38 demonstrated that 95% of failures would be detected within 3 days. Significantly improving this risk is unlikely because statistically, to detect 99% of failures, 30-day observation would be required.38 Most surgeons do not perform routine postdischarge imaging.9 This is supported by a study by Haan and colleagues37 examining splenic pseudoaneurysms after NOM. In their series, distal splenic embolization was only performed if free extravasation of contrast was seen at angiography. Pseudoaneurysm, AVF, and extravasation confined to the spleen were treated with proximal SAE. Patients found to have persistent or new pseudoaneurysms on follow-up CT after NOM had similar splenic salvage rates (94%) without additional therapies. Most pseudoaneurysms had resolved on follow-up imaging.37

Finally, the question of immunocompetence after splenic angioembolization has been addressed in several papers. Although our understanding of immunomodulating functions of the spleen is incomplete, authors of several studies have concluded that there is no evidence that immune function is significantly affected by SAE.17,39 Therefore, immunization is not recommended for these patients.


• When performing a proximal SAE, ideal coil deployment is between the dorsal pancreatic and great pancreatic artery (also known as arteria pancreatica magna). Given the anatomic variability and often poor visualization of these branches, a good rule of thumb is to deposit coils at the junction of the proximal and middle third of the splenic artery.

• Sizing coils for a proximal SAE can be difficult. Detachable coils or Amplatzer Vascular Plugs (St. Jude Medical, Inc., St. Paul, Minnesota) may be partially deployed and retrieved if they do not “hold,” which helps to avoid distal coil migration.

• Selective distal coil occlusion should only be performed if there is active extravasation, pseudoaneurysm, or AVF. Given the likelihood in high-grade injuries of other vascular lesions that may not be evident on angiography due to thrombus or vasospasm, this should be followed by proximal SAE.


Hepatic arterial embolization, similar to splenic embolization, is an important adjunct in the NOM of liver trauma, although technique, rationale, and complications are different. Owing to the greater inherent difficulty of controlling hemorrhage from hepatic compared to splenic injury, angiography and embolization may play a larger role during and after surgery.40 This is because high-OIS-grade liver injuries often produce arterial bleeding, which is well controlled by transarterial embolization, as well as venous bleeding, which is not.41 Juxtahepatic venous hemorrhage often requires laparotomy, sometimes with perihepatic packing and temporary closure (“damage control”) for the most critical patients.4042 In many modern operating rooms which are equipped with adequate fluoroscopy, embolization of deep, surgically inaccessible arterial bleeding can be accomplished immediately after laparotomy.

Identifying the patients with injuries to the retrohepatic inferior vena cava and hepatic veins therefore is vital. In a 2003 paper by Mohr et al.,43 patients with juxtahepatic venous injuries had the highest mortality rates among liver injuries. However, according to Hagiwara and colleagues,41 CT has low specificity and positive predictive value for venous injury. In their 2002 prospective study of liver trauma patients, the highest sensitivity, specificity, and positive predictive value of juxtahepatic venous injury was resuscitative requirement of greater than 2 L of fluids per hour.41 Although most would agree that these patients are not stable and should be brought to the operating room, in a 2009 paper by Misselbeck and colleagues,44 52% of patients who underwent laparotomy for hepatic injury demonstrated continued postoperative arterial bleeding requiring embolization. In the same study, patients with CT evidence of active extravasation were 20 times more likely to have positive angiograms compared to those with no evidence of active hemorrhage on CT.44 The 2012 EAST guidelines assign a level 2 recommendation to angiography with embolization in patients who are transient responders to resuscitation as an “adjunct to potential operative intervention.”7


Hepatic angiography should generally begin with flush aortography due to the high incidence of variable anatomy. A 5-Fr catheter is used to select the celiac axis and angiography is performed from the common hepatic artery. Even if there is no evidence of hemorrhage, selective angiography should be performed with a microcatheter targeting areas of extravasation identified on CT. In contrast to proximal splenic artery occlusion in which decreasing blood pressure to the spleen is the primary goal, the goal in hepatic injury is to embolize distally where there is evidence of hemorrhage (Fig. 22.3). The dual arterial and portal venous blood supply to the liver likely confers some protection from ischemic complications, but proximal hepatic artery occlusion is typically unnecessary and may be detrimental, particularly in patients with preexisting liver disease or compromised portal venous blood flow.

The choice of embolic material depends on the extent of the injury and how distal the microcatheter can be placed. If there is a wide area of arterial extravasation or the patient is decompensating, relatively proximal embolization with particles or gelfoam slurry may be necessary to achieve rapid hemostasis. However, it must be understood that this will increase the risk of hepatic failure or necrosis requiring operative debridement. If the hemorrhage is focal, superselective catheterization is preferable. Microcoils, particles, and gelfoam have all been used successfully. However, the presence of bile is a unique and possibly complicating feature of liver lacerations because it inhibits granulation and scar formation, thereby arresting the normal reparative process.45 Biloma formation is a known complication of hepatic trauma, occurring after 2% to 8% of cases.46 Theoretically, therefore, use of gelfoam, which causes temporary vascular occlusion, may increase the risk of pseudoaneurysm formation because in the presence of bile, there may not be sufficient time for healing of vascular injuries before recanalization occurs. Hagiwara et al.46 presented evidence supporting this theory in a small review of 11 patients with posttraumatic biloma; pseudoaneurysm formation was significantly more likely in patients initially treated with gelfoam embolization compared to those embolized with metallic coils. Although this was a small retrospective study, their conclusion that in the liver, permanent coil embolization is preferable to gelfoam when technically feasible is worth considering.46


The safety and efficacy of hepatic arterial embolization for hemodynamically stable trauma patients has been established.40,41,43,44,47 Clinical success rates of greater than 90% have been reported by several investigators.4850Complications of severe hepatic injury, such as biloma, necrosis, and abscess, have been reported to occur in up to 50% of cases and are similar to those which could be attributed to embolization. Mohr et al.43 reported the occurrence of such complications in 58% of hepatic trauma patients in her series and concluded that liver-related morbidity is not increased or decreased by angioembolization. Gallbladder ischemia and necrosis, however, can often be attributed directly to embolization; Mohr et al.43 and Misselbeck et al.44 both describe gallbladder-related complications, all of which occurred in patients who underwent selective right hepatic artery embolization. This can be avoided with judicious use of particles and superselective embolization distal to the cystic artery origin when treating injuries to branches of the right hepatic artery.

Hepatic necrosis after trauma often requires open debridement, but bilomas and abscesses can be effectively managed using interventional radiology techniques.51 In the patients who undergo hepatic artery embolization, the risk of these complications can be mitigated with more selective technique. Bile leaks complicated 23% of cases in the series by Mohr et al.43 and were managed by interventional radiologists with percutaneous drainage for a median of 1 month. Carrillo and colleagues51 brought attention to the importance of interventional radiologic techniques for management of these more common complications.


• Microcoils should be used for superselective embolization to limit necrosis.

• If there is a large territory with multifocal arterial injuries, realize that particles or gelfoam may be necessary for hemostasis but will increase the risk of liver failure and may lead to necrosis requiring operative debridement.

• When embolizing the right hepatic artery, the catheter should be positioned distal to the cystic artery to avoid gallbladder necrosis.


In comparison with hepatic and splenic injuries, renal injuries are less common, occurring in 1% to 5% of all traumas.52 Hemorrhagic renal injuries requiring intervention are more commonly iatrogenic, that is, related to percutaneous nephrostomy, biopsy, nephrostolithotomy, etc., than traumatic.53 As in all solid organ injuries, conservative management with selective angioembolization is now the standard in patients with grades I to IV injuries who are hemodynamically stable. A common theme throughout this chapter is organ preservation; patients with renal injuries who undergo laparotomy are more likely to have a nephrectomy, the implications of which may ultimately be severe, particularly in the event of future trauma, nephrolithiasis, malignancy, or other renal insult.54 In one series of patients with renal trauma, 28% of patients undergoing nephrectomy developed renal failure.55 Grades I and II injuries are managed conservatively (observation-only), with near 100% success rate.54 In grades III and IV injuries, management depends on imaging findings and clinical status.

The optimal management of grade V lesions is uncertain, and published results are variable. Many surgeons advocate nephrectomy in grade V, particularly renovascular lesions. Breyer et al.56 reported a failure rate of 100% (5/5) for angioembolization of grade V injuries. Brewer et al.57 reported 100% success rate of angioembolization for grade V injuries in unstable patients. These differences in outcomes may be due to inhomogeneity of grade V injuries, with renal pedicle avulsion, for example, likely requiring surgery.58 Hagiwara et al.59 reported on his success with angioembolization in all grade III through grade V renal injuries in which it was attempted. Eight of the patients in this series were grade IV or grade V, and each of these was successfully embolized.59 In the study by Brewer et al.,57 nine hemodynamically unstable patients with grade V parenchymal and renovascular injuries were successfully embolized with no further interventions required. Most of these patients, however, underwent main renal artery occlusion with coils. Follow-up after a mean of 2.7 years revealed no adverse effects of the embolizations.60

Complete renal embolization is an alternative to nephrectomy in patients who may be poor surgical candidates, with low complication rates and few long-term sequelae. In a 1999 paper by Hom et al.,61 eight patients underwent complete renal embolization for various reasons including recurrent bleeding from tumor or angiomyolipoma, none of which related to trauma. Most of the patients required narcotics for pain control for up to 48 hours, but in mean follow-up of 30 months, no abscess, hypertension, or renal failure developed.61 Main renal artery embolization for trauma, however, is essentially a nonoperative nephrectomy with the benefits limited to avoidance of exploratory laparotomy. Optimal management of grade V vascular renal injury remains uncertain and for now depends on individual trauma center expertise and availability of interventional radiologists.

OIS grade and clinical status are important but imperfect indicators for the need for intervention, particularly with regard to OIS grades III and IV injuries. Several retrospective studies have helped to clarify this issue by identifying specific CT findings indicative of the need for intervention, either angiographic or surgical.6,62,63 Contrast extravasation and perirenal hematoma rim distance (PRD) were found to be significant predictors of intervention in the studies by Dugi et al.6 and Nuss et al.62 In the study by Dugi et al.,6 medial as opposed to lateral laceration site was also found to be a significant predictor of the need for intervention. Most recently, Lin et al.63 found that the combination of contrast extravasation and extent of hematoma “remarkably increased the predictive value of the need for intervention.” Dugi et al.6 recommended substratifying the OIS grade IV into grades IVa (low risk) and IVb (high risk: PRD >3.5 cm, contrast extravasation, and medial renal laceration), with IVb indicating the need for angioembolization or surgery. These CT findings could also be used to upgrade grade III injuries with two or more risk factors to IVb injuries.6


Arterial lacerations and pseudoaneurysms in the kidney, like those in the liver or spleen, are preferably treated with coil embolization of the artery as close as possible to the site of injury (Fig. 22.4). Given the variability in arterial supply to the kidney, flush aortography is typically necessary. A Cobra or reverse curve (Sos or Mikaelsson, for example) catheter is most commonly used to select the renal artery. If extravasation, pseudoaneurysm, or AVF is present, the injured artery is selected using a microcatheter, and embolization with microcoils is performed as close to the injury as possible. In cases of extravasation from the main renal artery, a covered stent may be deployed. If this is suspected based on CT findings or clinical status, starting with a longer 6-Fr or 7-Fr sheath or shaped guiding catheter, which can be advanced to the renal artery ostium for stent delivery, will save time. As described earlier, main renal artery embolization may be required in renal hilar injuries; close communication between the interventional radiologist and trauma surgeon is particularly important in these cases to determine the optimal course of action.


Reported outcomes of transarterial embolization for renal vascular injury are excellent and demonstrate the effectiveness of this therapy in fulfilling the dual goals of hemostasis and preservation of renal function. In a series of five patients with nontraumatic arterial injury and pseudoaneurysm who underwent transarterial coil embolization, Poulakis et al.53 demonstrated 100% success rate in cessation of bleeding and return to preinjury creatinine values. Average estimated area of renal infarct in follow-up CT was 5%.53 Segmental renal arteries are considered end arteries, so infarcts typically occur after renal angioembolization, but they tend to be subclinical and are reported to decrease in size over time.64,65 This process may represent collateral blood flow restoring perfusion to initially ischemic parenchyma (i.e., these may not actually be true end arteries) or contraction of scar tissue.65 There is a significant association between OIS grade based on initial CT and decrease in renal function in patients managed expectantly with or without embolization, with overall poor functional outcome in grade V as well as certain grade IV injuries.66,67 One may therefore conclude that embolization in grade V injuries is unlikely to significantly affect the degree of renal function preservation. Several studies have demonstrated that superselective angioembolization of renal arterial injuries does not result in a clinically significant long-term decrease in renal function.53,64,65

Huber et al.68 analyzed 26 studies of renal embolization for traumatic and nontraumatic hemorrhage and found 89% primary success rate and 82% success rate in repeat angioembolization for those who failed the initial therapy. In patients who failed angioembolization and did not undergo repeat attempt, 100% underwent nephrectomy. Based on this data, they concluded that patients who fail angioembolization should undergo a repeat session instead of laparotomy.68 In the largest such study of renal trauma patients to date, Hotaling et al.69 analyzed NTDB data of renal injuries from 2002 to 2007 and also found high success rates for repeat angioembolization.

Finally, the type of renal vascular injury, penetrating versus blunt, may play a role in outcomes of expectant management and influence the decision to intervene. Specifically, penetrating renal trauma may require a more aggressive approach due to the higher likelihood of arterial laceration. This was the conclusion of Muir et al.70 who reported a 20% failure of observation in penetrating renal trauma and support the use of early angiography in this setting. In a study by Bjurlin et al.71 reviewing 98 penetrating renal injuries, selective NOM resulted in lower mortality rate, shorter mean intensive care unit and hospital stays, and fewer blood transfusions compared with nephrectomy; angioembolization was not a part of the protocol at their institution. Most of the cited studies of renal trauma did not substratify patients based on mechanism of injury.


• Microcatheters should be used for superselective coil occlusion to preserve renal function.



Blunt and penetrating thoracic trauma often results in persistent intrathoracic hemorrhage and hemothorax, for which exploratory thoracotomy has historically been the “gold standard” treatment.72 However, many patients are poor candidates for surgery due to associated injuries or comorbidities. In patients with slow or intermittent arterial bleeding, thoracotomy may fail to identify and control the source.72,73Excluding injuries to the aorta and great vessels, which are also often treated endovascularly with stent grafts, a common cause of hemothorax is intercostal arterial injury, which is well suited to transcatheter embolization. Compared with the literature regarding solid organ injury, embolization for thoracic trauma has received little attention. Several case reports and small retrospective series have demonstrated its safety and effectiveness.7275

Up to 85% of patients who survive blunt or penetrating thoracic trauma require only conservative measures, including tube thoracostomy, adequate volume resuscitation, and serial chest radiographs.72 Chest tube output of between 500 and 1,000 mL over a defined period is considered a threshold for thoracotomy.74 In keeping with the theme of this chapter, transarterial embolization is an effective alternative in the hemodynamically stable patient and can obviate the need for thoracotomy.

According to Hagiwara et al.,74 common causes of hemothorax after thoracic trauma are intercostal arterial lacerations and pulmonary lacerations. Differentiating between the two is important in the patient with significant chest tube output (>200 mL per hour) because embolization would not be helpful if the bleeding is secondary to pulmonary laceration. In their study of 154 patients who underwent contrast-enhanced CT, contrast extravasation and large displacement of a fractured rib were associated with intercostal arterial injury, and 5 out of 5 of these patients were successfully embolized.74 Their findings support CT in patients with chest tube output of greater than 200 mL per hour and embolization if there is contrast extravasation on CT.74 Other authors rely on chest tube output or hemoglobin and less on CT findings.72,73


Intercostal arteries as well as bronchial arteries are not typically well seen with aortography given their small size. Reverse curve catheters such as Mikaelsson are often used. The intercostal arteries are small, and at times, 5-Fr may be too large to actually select the artery; in these cases, a microwire and microcatheter may be advanced coaxially into the artery. If extravasation or pseudoaneurysm is identified, superselective catheterization with microcoil embolization and/or particles is performed. Achieving hemostasis may be difficult because of collateral flow via internal mammary, musculophrenic, inferior phrenic, and adjacent intercostal arteries that can cause rebleeding.73 Thus, if there is injury to the intercostal artery with extravasation or pseudoaneurysm, coils should be placed distal (Fig. 22.5) and proximal to the injury and consideration should be given to occluding the adjacent intercostal artery as well.73 If the source of bleeding is ventral, then the internal mammary artery should be interrogated; this will also allow imaging of the musculophrenic artery, which is a branch of the internal mammary. The inferior phrenic artery may also anastomose with lower anterior intercostal arteries. The use of particles should be reserved for cases in which superselective catheterization is unsuccessful. This also requires particular caution because anterior segmental medullary arteries arise from various posterior intercostal arteries and supply portions of the anterior spinal cord. If these arteries are occluded, paralysis will likely result, the extent of which depends on the level of the spinal cord affected. The largest, or major, anterior segmental medullary artery (artery of Adamkiewicz) is typically present at the level of T10 on the left, but it may arise anywhere from T8 to T12, and embolization of this artery will cause anterior spinal cord ischemia and bilateral lower extremity paralysis.76

Catheterization of the internal mammary artery and other small branches of the subclavian artery such as the pectoral or lateral thoracic arteries may be difficult, often requiring placement of a 90-cm sheath or ipsilateral access via the radial or brachial artery. If access is via the femoral artery, an arch aortogram may be useful, particularly in older patients who may have difficult arch anatomy.


There is a paucity of series examining arterial embolization after thoracic trauma. Retrospective studies by Carrillo et al.72 and Chemelli et al.,73 cited earlier, demonstrate feasibility and efficacy of embolization in blunt and penetrating chest injuries, predominantly involving intercostal and internal mammary arterial injuries. Injuries to other anterior thoracic arteries originating from the subclavian artery, such as pectoral and lateral thoracic arteries, may be considered in the same category. The larger study by Chemelli et al.73 demonstrated 87.5% primary technical success rate of arterial embolization in a combination of traumatic and iatrogenic thoracic injuries. Other literature is largely limited to case reports involving, for example, pulmonary artery pseudoaneurysms77 (which most commonly result from iatrogenic injury), esophageal hematoma,78 and a report by Hagiwara and Iwamoto75 of successful embolization of bleeding from thoracic vertebral fractures via intercostal arteries.

These cases, relatively rare compared to solid organ injuries of the abdomen, do not lend themselves well to large retrospective studies. However, the basic principles and techniques of embolization are the same. The most significant variables in thoracic cases are the location of injury and presence of collateral vessels, which may cause rebleeding. When superselective catheterization is possible, every attempt should be made to exclude the injury by deploying coils across (distal and proximal to) the injury.



• For bronchial or intercostal artery embolization, look for branches with the “hairpin turn” of the anterior segmental medullary arteries; embolization proximal to these arteries must be avoided as it may cause anterior spinal cord ischemia, which can lead to paralysis.


• When embolizing traumatic pseudoaneurysms, the injured artery should be embolized from a point just distal to the pseudoaneurysm to a point just proximal to the pseudoaneurysm to completely exclude the area of injury.


 1. 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;207:646–655.

 2. Esposito TJ, Tinkoff G, Reed J, et al. American Association for the Surgery of Trauma Organ Injury Scale (OIS): past, present, and future. J Trauma Acute Care Surg. 2013;74:1163–1174.

 3. Moore EE, Cogbill TH, Jurkovich GJ, et al. Organ injury scale: spleen and liver (1994 revision). J Trauma. 1995;38:323–324.

 4. Barquist ES, Pizano LR, Feuer W, et al. Inter- and intra-rater reliability in computed axial tomographic grading of splenic injury: why so many grading scales? J Trauma. 2004;56:334–338.

 5. Marmery H, Shanmuganathan K, Alexander MT, et al. Optimization of selection for nonoperative management of blunt splenic injury: comparison of MDCT grading systems. AJR Am J Roentgenol. 2007;189:1421–1427.

 6. Dugi DD, Morey AF, Gupta A, et al. American Association for the Surgery of Trauma grade 4 renal injury substratification into grades 4a (low risk) and 4b (high risk). J Urol. 2010;183:592–597.

 7. Stassen NA, Bhullar I, Cheng JD, et al. Selective 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–S293.

 8. Stassen NA, Bhullar I, Cheng J, 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–S300.

 9. 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;74:1567–1574.

10. Moore FA, Davis JW, Moore EE, et al. Western Trauma Association (WTA) critical decisions in trauma: management of adult blunt splenic trauma. J Trauma. 2008;65:1007–1011.

11. Shafi S, Parks J, Ahn C, et al. More operations more deaths? Relationship between operative intervention rates and risk- adjusted mortality at trauma centers. J Trauma. 2010;69:70–77.

12. Skattum J, Naess PA, Gaarder C. Nonoperative management and immune function after splenic injury. Br J Surg. 2012;99:59–65.

13. Upadhyaya P. Conservative management of splenic trauma: history and current trends. Pediatr Surg Int. 2003;19:617–627.

14. King H, Shumacker HB Jr. Splenic Studies 1. Susceptibility to infection after splenectomy performed in infancy. Ann Surg. 1952;136:239–242.

15. Pearl RH, Wesson DE, Spence LJ, et al. Splenic injury: a 5-year update with improved results and changing criteria for conservative management. J Pediatr Surg. 1989;24:121–125.

16. Malhotra AK, Carter RF, Lebman DA, et al. Preservation of splenic immunocompetence after splenic artery angioembolization for blunt splenic injury. J Trauma. 2010;69:1126–1131.

17. Demetriades D, Scalea TM, Degiannis E, et al. Blunt splenic trauma: splenectomy increases early infectious complications: a prospective multicenter study. J Trauma. 2012;72:229–234.

18. Wholey MH. The technology of balloon catheters in interventional angiography. Radiology. 1977;125:671–676.

19. Katzen BT, Rossi P, Passariello R, et al. Transcatheter therapeutic arterial embolization. Radiology. 1976;120:523–531.

20. Sclafani SJA. The role of angiographic hemostasis in salvage of the injured spleen. Radiology. 1981;141:645–650.

21. Sclafani SJA, Weisberg A, Scalea TM, et al. Blunt splenic injuries: nonsurgical treatment with CT, arteriography, and transcatheter arterial embolization of the splenic artery. Radiology. 1991;181:189–196.

22. 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;49:177–189.

23. Renzulli P, Gross T, Schnuringer B, et al. Management of blunt injuries to the spleen. Br J Surg. 2010;97:1696–1703.

24. Olthof DC, Joose 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;74:546–557.

25. Jeremitsky E, Kao A, Carlton C, et al. Does splenic embolization and grade of splenic injury impact nonoperative management in patients sustaining blunt splenic trauma? Am Surg. 2011;77:215–220.

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. 2012;72:1127–1134.

27. Requarth JA, D’Agostino RB, Miller PR. Nonoperative management of adult blunt splenic injury with and without splenic artery embolotherapy: a meta-analysis. J Trauma. 2011:71:898–903.

28. Bhullar IS, Frykberg ER, Tepas III JJ, 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;74:105–112.

29. Hamers RL, Van DenBerg FG, Groeneveld ABJ. Acute necrotizing pancreatitis following inadvertent extensive splenic artery embolization for trauma. Br J Radiol. 2009;82:e11–e14.

30. Requarth JA. Distal splenic artery hemodynamic changes during transient proximal splenic artery occlusion in blunt splenic injury patients: a mechanism of delayed splenic hemorrhage. J Trauma. 2010;69:1423–1426.

31. Sabe AA, Cloridge 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;67:565–572.

32. 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;75:69–75.

33. Haan JM, Bochicchio GV, Kramer N, et al. Nonoperative management of blunt splenic injury: a five-year experience. J Trauma. 2005;58:492–498.

34. Liu P, Liu H, Hsieu T, et al. Nonsurgical management of delayed splenic rupture after blunt trauma. J Trauma. 2012;72:1019–1023.

35. Schnuringer B, Inaba K, Konstantinidis A, et al. Outcomes of proximal versus distal splenic artery embolization after trauma: a systematic review and meta-analysis. J Trauma. 2011;70:252–260.

36. 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;205:250–254.

37. Haan JM, Marmery H, Shanmuganathan K, et al. Experience with splenic main coil embolization and significance of new or persistent pseudoaneurysm: reembolize, operate, or observe. J Trauma. 2007;63:615–619.

38. Smith J, Armen S, Cook C, et al. Blunt splenic injuries: have we watched long enough? J Trauma. 2008;64:656–665.

39. Tominaga GT, Simon FJ, Dandan IS, et al. Immunologic function after splenic embolization, is there a difference? J Trauma. 2009;67:289–293.

40. Johnson JW, Graciac VH, Gupta R, et al. Hepatic angiography in patients undergoing damage control laparotomy. J Trauma. 2002;52:1102–1106.

41. Hagiwara A, Murata A, Matsuda T, et al. The efficacy and limitations of transarterial embolization for severe hepatic injury. J Trauma. 2002;52:1091–1096.

42. Higa G, Friese R, O’Keefe T, et al. Damage control laparotomy: a vital tool once overused. J Trauma. 2010;69:53–59.

43. Mohr AM, Lavery RF, Barone A, et al. Angiographic embolization for liver injuries: low mortality, high morbidity. J Trauma. 2003;55:1077–1082.

44. Misselbeck TS, Teicher EJ, Cipolle MD, et al. Hepatic angioembolization in trauma patients: indications and complications. J Trauma. 2009;67:769–773.

45. Sandblum P, Mirkovitch V, Gardiol D. The healing of liver wounds. Ann Surg. 1976;183:679–684.

46. Hagiwara A, Tarui T, Murata A, et al. Relationship between pseudoaneurysm formation and biloma after successful transarterial embolization for severe hepatic injury: permanent embolization using stainless steel coils prevents pseudoaneurysm formation. J Trauma. 2005;59:49–55.

47. Ciraulo DL, Luk S, Palter M, et al. Selective hepatic arterial embolization of grade IV and V blunt hepatic injuries: an extension of resuscitation in the nonoperative management of traumatic hepatic injuries. J Trauma. 1998;45:353–359.

48. Malhotra AK, Fabian TC, Croce MA, et al. Blunt hepatic injury: a paradigm shift from operative to nonoperative management in the 1990s. Ann Surg. 2000;231:804–813.

49. Velmahos GC, Toutouzas K, Radin R, et al. High success with nonoperative management of blunt hepatic trauma. Arch Surg. 2003;138:475–481.

50. Van der Wilden GM, Velmahos GC, Emhoff T, et al. Successful nonoperative management of the most severe blunt liver injuries. Arch Surg. 2012;147:423–428.

51. Carrillo EH, Spain DA, Wohltmann CD, et al. Interventional techniques are useful adjuncts in nonoperative management of hepatic injuries. J Trauma. 1999;46:619–624.

52. Shoobridge JJ, Corcoran NM, Martin KA, et al. Contemporary management of renal trauma. Rev Urol. 2011;13(2):65–72.

53. Poulakis V, Ferakis N, Becht E, et al. Treatment of renal-vascular injury by transcatheter embolization: immediate and long-term effects on renal function. J Endourol. 2006;20(6):405–409.

54. Santucci RA, Fisher MB. The literature increasingly supports expectant (conservative) management of renal trauma—a systematic review. J Trauma. 2005;59:491–501.

55. Narrod JA, Moore EE, Posner M, et al. Nephrectomy following trauma—impact on patient outcome. J Trauma. 1985;25:842–844.

56. Breyer BN, McAninch JW, Elliott SP, et al. Minimally invasive endovascular techniques to treat acute renal hemorrhage. J Urol. 2008;179:2248–2252.

57. Brewer ME Jr, Strnad BT, Daley BJ, et al. Percutaneous embolization for management of grade 5 renal trauma in hemodynamically unstable patients: initial experience. J Urol. 2009;181:1737–1741.

58. Altman AL, Haas C, Dinchman KH, et al. Selective nonoperative management of blunt grade 5 renal injury. J Urol. 2000;164:27–31.

59. Hagiwara A, Sakaki S, Goto G, et al. The role of interventional radiology in the management of blunt renal injury: a practical protocol. J Trauma. 2001;51:526–531.

60. Stewart AF, Brewer ME Jr, Daley BJ, et al. Intermediate-term follow-up of patients treated with percutaneous embolization for grade 5 blunt renal trauma. J Trauma. 2010;69:468–470.

61. Hom D, Eiley D, Lumerman JH, et al. Complete renal embolization as an alternative to nephrectomy. J Urol. 1999;161:24–27.

62. Nuss GR, Morey AF, Jenkins AC, et al. Radiographic predictors of the need for angiographic embolization after traumatic renal injury. J Trauma. 2009;67:578–582.

63. Lin WC, Lin CH, Chen JH, et al. Computed tomographic imaging in determining the need of embolization for high-grade blunt renal injury. J Trauma Acute Care Surg. 2012;74:230–235.

64. Sofocleous CT, Hinrics C, Hubbi B, et al. Angiographic findings and embolotherapy in renal arterial trauma. Cardiovasc Intervent Radiol. 2005;28:39–47.

65. Chatziliannou A, Brountzos E, Primetis E, et al. Effects of superselective embolization for renal vascular injuries on renal parenchyma and function. Eur J Vasc Endovasc Surg. 2004;28:201–206.

66. Fiard G, Rambeaud JJ, Descotes JL, et al. Long-term renal function assessment with dimercapto-succinic acid scintigraphy after conservative treatment of major renal trauma. J Urol. 2012;187:1306–1309.

67. Tasian GE, Aaronson DS, McAninch JW. Evaluation of renal function after major renal injury: correlation with the American Association for the Surgery of Trauma injury scale. J Urol. 2010;183:196.

68. Huber J, Paternik S, Hallscheidt P, et al. Selective transarterial embolization for post traumatic renal hemorrhage: a second try is worthwhile. J Urol. 2011;185:1751–1755.

69. Hotaling JM, Sorensen MD, Smith TG, et al. Analysis of diagnostic angiography and angioembolization in acute management of renal trauma using a national data set. J Urol. 2011;185:1316–1320.

70. Muir MT, Inaba K, Ong A, et al. The need for early angiography in patients with penetrating renal injuries. Eur J Trauma Emerg Surg. 2012;38:275–280.

71. Bjurlin MA, Jeng EI, Goble SM, et al. Comparison of nonoperative management with renorrhaphy and nephrectomy in penetrating renal injuries. J Trauma. 2011;71:554–558.

72. Carrillo E, Heniford T, Senler S, et al. Embolization therapy as an alternative to thoracotomy in vascular injuries of the chest wall. Am Surg. 1998;64:1142–1148.

73. Chemelli AP, Thaurer M, Wiedermann F, et al. Transcatheter arterial embolization for the management of iatrogenic and blunt traumatic injuries. J Vasc Surg. 2009;49:1505–1513.

74. Hagiwara A, Yanagawa Y, Kaneko N, et al. Indications for transcatheter arterial embolization in persistent hemothorax caused by blunt trauma. J Trauma. 2008;65:589–594.

75. Hagiwara A, Iwamoto S. Usefulness of transcatheter arterial embolization for intercostal arterial bleeding in a patient with burst fractures of the thoracic vertebrae. Emerg Radiol. 2009;16:489–491.

76. Ozoilo K, Stein M. Paraplegia complicating embolization for bleeding intercostal artery in penetrating trauma. Inj Ex. 2013;44:70–73.

77. Block M, Lefkowitz T, Ravenel J, et al. Endovascular coil embolization for acute management of traumatic pulmonary artery pseudoaneurysm. J Thorac Cardiovasc Surg. 2004;128:784–785.

78. Shim J, Jang JY, Hwangbo Y, et al. Recurrent massive bleeding due to dissecting intramural hematoma of the esophagus: treatment with therapeutic angiography. World J Gastroenterol. 2009;15:5232–5235.