Abdominal trauma is a major cause of ACS, and using data from a large database, we show that the prevalence of ACS among patients with severe blunt abdominal trauma was low (at 1.3%) in the Japanese national trauma registry. Further, interestingly, ACS development was associated with the number of organs injured in the abdomen rather than the type of organ injured, and injury to most organs in the abdomen, except for the pancreas, was not associated with ACS. Coagulopathy, including DIC, was also associated with ACS, and it is possible that these complications represent a cause-and-effect phenomenon. Thus, focusing on the number of abdominal organs injured may help clinicians stratify patients based on risk of ACS development during the early stages of trauma care.
The prevalence of ACS associated with trauma widely varies among reports and ranges from 0 to 14%.5,7–9,14 This variation may be due to the diversity in the study populations and advances in trauma care, including damage-control surgery.5
Our analysis of a national trauma registry identified an independent association between the number of injured organs in the abdomen and development of ACS. This result is as expected because hemorrhage is the main pathology in trauma, and multiple organ injuries, as well as severity of injury, are related to greater hemorrhage.15 In addition, hemorrhaging ascites directly increase intraabdominal pressure. Thus, copious fluid resuscitation to counter massive hemorrhage induces capillary leak and intestinal edema,16 both of which are risk factors for ACS secondary to increased intraabdominal pressure.2 Therefore, clinicians should be aware of the risk of developing ACS when patients present with multiple organ injuries in the abdomen.
Anatomical features of the injured organ may be important for the development of ACS, and in our cohort, only pancreatic injury was associated with the development of ACS. The pancreas is located in the retroperitoneum and is typically present near the great vessels, i.e., the inferior vena cava, portal vein, and abdominal aorta, which not only make surgical repair of the pancreatic injury challenging 17,18 but also, thereby, delay hemorrhage control. Moreover, physiological and biochemical features of pancreatic trauma, such as leakage of pancreatic enzymes, can contribute to the development of both ACS and pancreatitis.
In our study, coagulopathy, including DIC, was associated with ACS, but a cause-and-effect relationship, i.e., whether DIC associated with trauma precedes ACS, could not be established because the JTDB does not capture data about the timing complication onset. It is rational to expect that, pathophysiologically, DIC may have preceded ACS, with subsequent trauma not only exacerbating hemorrhage but also contributing to the increased intraabdominal pressure and resulting in the development of ACS. Nevertheless, it must be noted that the reverse could also be true. Very few previous studies have discussed the association between DIC and development of ACS; specifically, a single case series showed that two patients developed ACS following DIC.19 Although trauma-induced coagulopathy might be present in the early phase after trauma,20 it is unknown whether coagulopathy in the early phase progresses to DIC.21,22
Preventing complications will undoubtedly improve mortality,11 and we confirm that ACS is one of the most severe complications of severe abdominal trauma because more than half of the patients who developed ACS died. Although primary injury of the abdominal organs or DIC induced by trauma may be unmodifiable, clinicians should pay attention when patients present with these risk factors as it can help to potentially retard or stop the development of ACS, consider open abdomen procedures, and avoid excessive positive fluid balance.5,6,23
Our study has some limitations. First, unmeasured potential confounders could have affected the results, and although the amount of fluid or blood transfused are risk factors for developing ACS,6,23 our database did not contain this data. Nonetheless, we adjusted the logistic regression models using a related variable, i.e., blood transfusion within 24 h of admission. Second, celiotomy may be a potential risk factor because a few previous studies have reported abdominal surgery to be a risk factor for ACS.5,8 However, we did not include celiotomy in the logistic regression analysis because time elapsed between celiotomy and ACS was unknown. In addition, ACS rapidly develops after injury and can present early, often within 3–6 h of admission to the emergency department;1,6,7,24 hence, presumably, ACS could have developed before primary surgery in some cases. Third, potential information bias, due to the ACS diagnosis being based on the reports of the physician in-charge, along with possible underdiagnosis, cannot be ruled out. However, as most of the institutions participating in the JTDB were nationally certified emergency centers, we believe that most of the patients received appropriate trauma care.