The mortality rate of patients with hemodynamic instability due to severe pelvic fracture is reported to be 40–60 % despite a multidisciplinary treatment approach. Angioembolization and external fixation of the pelvis are the main procedures used to control bleeding in these patients. Several studies have shown that preperitoneal pelvic packing (PPP) is effective for hemorrhage control, despite being small and observational in nature. The purpose of this study was to describe a Korean trauma center’s early experience with PPP in unstable patients with pelvic fractures and to evaluate its effectiveness. Between January 2012 and May 2015, 30 patients with hemodynamic instability caused by pelvic fracture were enrolled in this study. PPP has been performed in 14 patients since May 2014. Data of pelvic fracture patients with hemodynamic instability were selected from Wonju Severance Christian Hospital Pelvic Trauma Database and were analyzed retrospectively. Mean age and mean ISS were 60.4 ± 18.8 years and 39.2 ± 8.1 in 30 unstable patients with pelvic fracture. Mean SBP was 89.1 ± 24.7 mmHg, and mean hemoglobin was 10.6 ± 2.3 g/dL. When the non-PPP group (16 patients) and the PPP group (14 patients) were compared, there was no significant difference in the age, gender, ISS, and occurrence of associated injury (p = 0.82, p = 0.23, p = 0.92, and p = 0.60, respectively). Mortality rate due to acute hemorrhage were 37.5 % in the non-PPP group and 14.3 % in the PPP group. In the PPP group, three patients underwent PPP in the hybrid operating room, and a laparotomy was performed in three patients. Mean systolic blood pressure increased significantly after PPP (71.6 ± 9.8 vs. 132.2 ± 36.4 mmHg, p = 0.002). In unstable patients with pelvic fractures, PPP can be used as an effective treatment, complementary to AE, to control pelvic bleeding.

Traumatic pancreatic injuries are rare and present diagnostic and therapeutic difficulties. We evaluated the usefulness of endoscopic retrograde pancreatography and transpapillary pancreatic stent in the diagnosis and treatment of pancreatic trauma patients. We reviewed medical records of 83 pancreas trauma patients who underwent endoscopic retrograde pancreatography for the suspicion of pancreas duct injury between January 1983 and December 2016. Patient notes, radiologic findings, laboratory investigations, operative records, and endoscopic retrograde pancreatography reports were reviewed. Pre-endoscopic retrograde pancreatography abdominal computed tomography was performed in 52 patients. Twenty-seven patients of them were diagnosed with a major pancreatic duct injury by subsequent endoscopic retrograde pancreatography. Eleven major pancreatic duct injuries (40.7%) were missed by the pre-endoscopic retrograde pancreatography abdominal CT. Major pancreatic duct injury was confirmed by endoscopic retrograde pancreatography in 43 patients. These 43 major pancreatic duct injury patients were classified into the Operative (n = 21), Stent (n = 15), and Conservative (n = 7) groups according to the first treatment modality which was chosen by attending surgeon. Age, initial white blood cell count, initial serum amylase, associated injury, and major pancreatic duct injury site were similar among groups, while the rate of parenchymal leakage (Dye leakage confined to pancreatic capsule) on endoscopic retrograde pancreatography findings differed. Parenchymal leakage was most common in the Conservative group. Pancreas related mortality occurred in 1 (4.76%) Operative group, 2 (13.33%) Stent group, and 0 (0%) Conservative group. Pancreas related complication occurred in 16 (76.19%) Operative group, 10 (66.67%), Stent group and 5 (71.43%) Conservative group. There were no statistically significant differences in the occurrence rate of pancreas related complications and mortalities among three groups. Endoscopic retrograde pancreatography helps clinicians choose a treatment modality for major pancreatic duct injury since it provides information about the precise condition of the major pancreatic duct injury. Endoscopic retrograde pancreatography with transpapillary pancreatic stenting also shows promise as a substitute for laparotomy or pancreatic resection in selected patients.

Despite the use of a multidisciplinary treatment approach, the mortality rate of hemodynamic instability due to severe pelvic fracture remains 40–60%. Several recent studies have shown that preperitoneal pelvic packing (PPP) was useful for achieving hemostasis in these patients in the acute phase. However, few studies have examined postoperative complications. The purpose of the present study was to evaluate clinical outcomes and wound infections of PPP in these patients. We retrospectively reviewed the medical charts of 62 patients with hemorrhagic shock due to pelvic fracture between March 2011 and May 2017. Excluding four patients (two with other major hemorrhage sites and two who experienced cardiac arrest in the emergency room), the patients were divided into PPP (n = 30) and non-PPP (n = 28) groups according to PPP application. Clinical outcomes including early-stage mortality, transfusion amount, and surgical site infection (SSI) were compared between the two groups. The overall mortality rate was 48.3% and the mean Injury Severity Score (ISS) was 39 ± 9. The 30 patients in the PPP group had a significantly lower hemorrhage-induced mortality rate than the 28 patients in the non-PPP group (16.7% vs 50%, p = 0.019), although both groups had similar patient characteristics (age, ISS, and initial serum lactate level). Independent factors associated with hemorrhage-induced mortality were PPP and the requirement of packed red blood cells for 4 h. In the PPP group, SSI occurred in 5 of 25 (20%) patients. PPP may be considered as a hemostatic modality for hemodynamic instability due to pelvic fracture because it reduces the hemorrhage-induced mortality rate. However, wound infections after the procedure should be considered.

The pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-1β upregulate TNF-α-stimulated gene 6 (TSG-6); however, current knowledge about the optimal conditions for TSG-6 expression in mesenchymal stem cells (MSCs) is limited. Here, we investigated whether TSG-6 expression varies depending on the polarization state of macrophages co-cultured with adipose tissue-derived stem cells (ASCs) and analyzed the optimal conditions for TSG-6 expression in ASCs. TSG-6 expression increased in ASCs co-cultured with M0, M1, and M2 macrophages indirectly; among them, M1 macrophages resulted in the highest increase in TSG-6 expression in ASCs. TSG-6 expression in ASCs dramatically increased by combination (but not single) treatment of TNF-α, IL-1β, interferon-gamma (IFN-γ), and lipopolysaccharide (LPS). In addition, phosphorylation of signal transducer and activator of transcription (STAT) 1/3 was observed in response to IFN-γ and LPS treatment but not TNF-α and/or IL-1β. STAT1/3 activation synergistically increased TNF-α/IL-1β-dependent TSG-6 expression, and JAK inhibitors suppressed TSG-6 expression both in ASCs and macrophages. In LX-2 hepatic stellate cells, TSG-6 inhibited TGF-β-induced Smad3 phosphorylation, resulting in decreased α-smooth muscle actin (SMA) expression. Moreover, fibrotic activities of LX-2 cells induced by TGF-β were dramatically decreased after indirect co-culture with ASCs and M1 macrophages. These results suggest that a comprehensive inflammatory microenvironment may play an important role in determining the therapeutic properties of ASCs by increasing TSG-6 expression through STAT1/3 activation.

Mesenchymal stem cells (MSCs) regulate immune cell activity by expressing tumor necrosis factor-α (TNF-α)-stimulated gene 6 (TSG-6) in inflammatory environments; however, whether anti-inflammatory responses affect TSG-6 expression in MSCs is not well understood. Therefore, we investigated whether transforming growth factor-β (TGF-β) regulates TSG-6 expression in adipose tissue-derived stem cells (ASCs) and whether effective immunosuppression can be achieved using ASCs and TGF-β signaling inhibitor A83-01. TGF-β significantly decreased TSG-6 expression in ASCs, but A83-01 and the p38 inhibitor SB202190 significantly increased it. However, in septic C57BL/6 mice, A83-01 further reduced the survival rate of the lipopolysaccharide (LPS)-treated group and ASC transplantation did not improve the severity induced by LPS. ASC transplantation alleviated the severity of sepsis induced by LPS+A83-01. In co-culture of macrophages and ASCs, A83-01 decreased TSG-6 expression whereas A83-01 and SB202190 reduced Cox-2 and IDO-2 expression in ASCs. These results suggest that TSG-6 expression in ASCs can be regulated by high concentrations of pro-inflammatory cytokines in vitro and in vivo, and that A83-01 and SB202190 can reduce the expression of immunomodulators in ASCs. Therefore, our data suggest that co-treatment of ASCs with TGF-β or p38 inhibitors is not adequate to modulate inflammation.