Intervention
Failure of conservative treatment involves grade III, IV, or V injuries more often than grade I and II injuries. In many studies, SA embolization (SAE) has been described by using many different approaches. One primary point of discussion concerns the differences between main SAE, selective or superselective SAE, and embolization in a combination of sites. To the authors' knowledge, no studies have been performed to compare outcomes or complication rates based on the various levels of SAE. Theoretically, the infarction rate is expected to increase as embolization becomes more selective. Conversely, therapeutic failure is expected to increase with more proximal SAE. This presumption is based on collateral blood flow differences inherent with the particular level of embolization.
Sclafani et al33 and Hagiwara et al34 have described SAE techniques dependent on angiographic findings. The visualization of extrasplenic extravasation was treated with selective Gelfoam embolization or superselective gelatin sponge particle injection, respectively, followed by main SAE by means of coil occlusion. Main SAE alone was performed if intraparenchymal contrast-material extravasation was the only finding. Hagiwara et al34 also selected an additional group of patients whose angiograms demonstrated vascular disruption without extravasation. This group also was treated by using main SAE alone. SAE was not performed if the angiogram showed only avascular areas or evidence of subcapsular hematoma without extravasation. The overall success rate in the 2 studies was greater than 90%.
The authors contend that main SAE is effective because the decreased splenic blood pressure promotes hemostasis at the injury site. This effect is accomplished with low risk of infarction, because postembolization celiac angiograms demonstrated reconstitution of the SA distal to the coil occlusion via collateral flow in all patients. In fact, Sclafani et al33 reported continued contrast-agent extravasation in most patients after SAE. The persistence of extravasation immediately after SAE was not a poor prognostic indicator in the study, which differs from the data from the study of Hagiwara et al in which the single patient reported to have extravasation on the post-SAE angiogram was 1 of 2 patients in whom therapy failed and who eventually required splenectomy. The reason for this discrepancy is not clear.
The treatment of posttraumatic arteriovenous fistulas and pseudoaneurysms appears to require a different approach. Arteriovenous fistulas probably remain patent after main SAE, and they have been reported by Hagiwara et al.34 Many investigators have reported the use of superselective coil embolization without main SAE to be successful in these patients.19,35,18 Davis et al reported successful nonoperative treatment in 20 of 20 patients in whom pseudoaneurysms were embolized. All of the 6 patients in whom pseudoaneurysms could not be coiled for various reasons eventually required splenectomy.19 Data attest to the need for definitive treatment if a pseudoaneurysm is documented angiographically.
Another interesting point elicited by Davis et al was the fact that 4 patients whose CT scans demonstrated contrast blush indicative of a pseudoaneurysm had negative findings on SA angiograms.19 All 4 patients were treated successfully without surgery. The pseudoaneurysms may have thrombosed spontaneously, or the CT findings may have related to small areas of contained extravasation that caused tamponade. In either situation, data support a scenario in which positive CT findings should lead to angiographic evaluation. Negative angiographic findings are highly correlated with a good outcome in patients undergoing conservative treatment. Positive angiographic findings necessitate some form of intervention, be it angiographic or surgical.
The complication rate of SAE appears to be sufficiently low that it is not a significant concern compared with that of splenectomy. Data by Mozes et al showed a 2.4% (3 of 126) mortality within the first 6 months, compared with an 8% (2 of 25) mortality associated with splenectomy.36 Both deaths related to splenectomy were associated with postoperative pancreatitis. Of the 126 patients who underwent SAE, 3 (2.4%) developed pancreatitis after embolization, but they did not die. Pancreatitis likely was a result of embolization of important collateral pancreatic vessels from the SA. Splenic abscess formation occurred in 4 (3%) of 126 patients. The most common cause of morbidity after SAE was the formation of pleural effusion in 9.5% of patients (12 of 126).
The morbidity of SAE is correlated with the percentage of splenic tissue embolized. Statistics reported by Mozes et al were based on the embolization of no more than 60-70% of splenic tissue.36 Others have confirmed the unacceptably high morbidity and mortality rates involved with excessive tissue embolization or attempted nonsurgical splenectomy. Morbidity rates as high as 79%37 and mortality rates ranging from 12%38 to 43%37 have been reported in the literature.
The angiographer must be aware of these reports. SAE should probably not be offered as an option if the procedure is likely to result in excessive splenic tissue loss, because splenectomy is associated with lower relative risk. A patient who has significant or total splenic volume infarction after SAE requires close observation for the development of complications. When the data are considered, continuing with splenectomy when the patient is stabilized may be prudent if complete splenic infarction occurs after SAE.
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Further Reading
Keywords
spleen trauma, splenic injury, spleen injury, blunt injury to the spleen, splenic trauma
Follow-up: Spleen, Trauma