NOM is the gold-standard treatment for hemodynamically stable trauma patients and is eligible for 80% of patients (5, 6). Performing a CT scan with different injection times and especially arterial allows a precise morphological assessment and guides the therapeutic strategy. CT enables searches for active bleeding or pseudoaneurysm resulting in angioembolization (5, 7–10). However, NOM can fail in multiple ways, leading to secondary splenectomy (5, 6, 11–14).
Many risk factors for NOM failure have been proposed, but none can accurately predict the failure of NOM.
Grade 3 or higher lesions are more at risk of NOM failure (according to AAST classification) (5, 6, 14, 16, 17). In AAST 4 and 5 splenic lesions, the failure rate of NOM is 54.6% (19).
Arterial blush on CT in the absence of angio-embolization is described as a risk factor of conservative treatment failure (5, 8, 18), as well as diffuse hemoperitoneum (14, 16).
A severe injury associated with a high ISS would be predictive of a higher rate of NOM failure. Different ISS values are reported in the literature as limiting to a NOM [e.g., 15 (9), 25, and others (14, 16, 17)]. Combining a splenic trauma with a brain injury can complicate the surveillance (19).
The importance of age in NOM has been debated. Age greater than 55 years would increase the risk of NOM failure, especially for high-grade lesions (5, 14, 20); age greater than 40 years could be a NOM failure factor, according to other authors (16). In our study, the median age was 39 years. We detected no statistically significant difference for age; nor did we detect a statistically significant difference according to AAST classification, ISS, or mechanism of injury.
Biological abnormalities, such as a decrease in hemoglobin, pH, or an increase in arterial lactates, might be factors for NOM failure. Alcohol consumption is common during trauma and might result in a falsely high value of lactate or prolong lactate clearance; it must, therefore, be taken into account when evaluating patients with a high blood alcohol level (21). The value of lactate and bicarbonates was identified as an important independent predictor of the polytrauma patient with acute alcohol and drug use (22, 23).
In our study, there is a difference in hemoglobin values at H0 and H6 between the groups having failed angioembolization and the successful group of angioembolization. This result, however, remains nuanced since it is, by little, not statistically significant (p = 0.064). This result can probably be explained because of the small number of patients. This result is nevertheless interesting since it is understood that biological deglobulization may be the first sign of true bleeding requiring secondary splenectomy.
In the literature, a decreased value of hemoglobin in the hours following the admission of trauma patients has never been described as NOM failure factors. On the other hand, the need for transfusion of red blood cells is a risk factor for NOM failure (16, 18).
In our study, the lack of data can represent a bias. Thus, the study of lactate levels could not be performed; this is explained by the disparity of care and evolution of patients. Indeed, lactate often dosed at H0 was not necessarily dosed in the aftercare. A study addressing the variation of lactatemia as a failure factor of NOM in splenic trauma might be interesting.
In this study, we could not demonstrate that angioembolization prevented secondary splenectomy. However, this is not comparable to the lack of benefit and is likely due to the lack of power of the study.
A multivariate analysis of the different predictors of NOM failure would also be useful. Unfortunately, we could not achieve this because of the amount of missing data. A multicenter prospective study would address these limitations and should now be conducted to confirm the role of deglobulization in the management of patients with splenic trauma.