Although pancreatic injury is rare, it has an overall mortality of 3–70%[10]. In this study, we included a large retrospective documented cohort of patients with pancreatic trauma treated in a referral trauma center. The mortality rate was 15.8% in this severe pancreatic injury group (ISS median was 27), lower than previous reports[11, 12]. Determining the risk factors that affect the prognosis of patients undergoing surgery for pancreatic trauma is very important for preventing complications and reducing the mortality rate. Here, we conducted univariate and binary logistic regression analyses on several mortality-related parameters collected during the perioperative period. Our study first indicated preoperative hemodynamic instability, postoperative severe inflammation, renal function failure and age to be important determinants of postoperative mortality in pancreatic trauma.
This study indicated that postoperative severe infection (CRP ≥ 154 mg/L) may be an important prognostic factor for survival after surgery in pancreatic trauma. It is currently considered the most valuable acute-phase response indicator[13]. The levels of trypsin released during pancreatic trauma can cause the pancreas and its surrounding tissues to self-digest and cause the influx of a large number of inflammatory factors, such as cytokines, into the blood, which in turn triggers a series of inflammatory responses and results in a drastic increase in CRP. CRP is also a reliable predictor of in-hospital mortality in acute pancreatitis. In this study, the incidence of complications, including postoperative pancreatic fistula, intestinal fistula, and sepsis, was higher in the nonsurvival group. The CRP concentration was significantly higher in patients with postoperative infections.
Multivariate analysis indicated that preoperative hemodynamic instability was also an independent risk factor for surgery prognosis in pancreatic trauma. Traumatic bleeding is the most common cause of hemodynamic instability[14]. Approximately 80% of patients with hemorrhagic shock die in the operating room, and nearly 50% of patients with hemorrhagic shock die within the first 24 hours after injury. Accompanying large vessel injury, hemorrhagic shock associated with pancreatic trauma can cause erosion of the surrounding blood vessels due to pancreatic juice leakage. Repeated intraperitoneal hemorrhage is an important mortality risk in patients with pancreatic trauma[15]. In this study, the mortality rate was as high as 41.2% in unstable patients but only 8.5% in patients with stable hemodynamic status. Logistic regression analysis showed the risk of death in patients with hemorrhagic shock to be 0.150 times that of patients with stable hemodynamic status. For patients with traumatic hemorrhagic shock, the keys to successful damage control resuscitation (DCR) include active control of bleeding, rapid blood and fluid resuscitation, and accurate determination of the endpoint of resuscitation[16]. Despite the use of aggressive resuscitation in patients with hemorrhagic shock, patients are often stressed by repeated hemorrhagic shock, and the mortality rates remained high.
Correlation analysis of the risk factors associated with prognosis also revealed that the occurrence of acute kidney injury (creatinine ≥ 177 µmol/L) was significantly higher in the nonsurvivor group. Posttraumatic AKI is a clinical syndrome that includes sequential events such as trauma-induced renal dysfunction, oliguria or anuria, failure to excrete metabolites, rapid azotemia, fluid and electrolyte imbalance, acid-base imbalance, and a variety of functional changes[17]. Direct renal injury, ischemia-reperfusion injury, rhabdomyolysis, hypovolemic shock, celiac compartment syndrome, and sepsis may contribute to AKI in pancreatic trauma patients. Posttraumatic AKI is an independent risk factor for death after trauma, and it can be used for the early evaluation of kidney injury[18]. After AKI, renal function may recover if the primary cause has been removed, inflammation is controlled, tissue perfusion is preserved, and electrolyte and acid-base balances are well maintained. Few patients develop chronic renal deficiency after trauma.
Although this study represents the largest series of patients with pancreatic trauma, there are several limitations when interpreting these conclusions. First, some on-duty surgeons, especially during the night shift, have limited experience with pancreatic trauma in China. In fact, few surgeons ever see a severe pancreas injury during a lifetime, let alone achieve vast operative experience with these dreaded injuries. A large number of “second-hand” patients have been referred due to the lack of definitive guidelines and appropriate management strategies, which is determined by the current medical running systems. Second, these data were generated from a highly selective cohort of patients treated in a large-volume well-resourced tertiary referral academic level I trauma center. Although these results might be similar to those of other major trauma centers, they may not be applicable to lower-level hospital systems. Finally, and the most obvious, is the limitation that comes with a retrospective, observational study spanning a long time (8 years). One would think that the evolution in knowledge and practice of fluid resuscitation, acute traumatic coagulopathy, transfusion protocols and concepts of damage control surgery and, more recently, damage control resuscitation to have changed over the period. The improvement of health care facilities, clinical strategies and surgeries’ preferences may have contributed to the differences; thus, these findings might not provide an authoritative or comprehensive analysis of the current situation.