PURPOSE: A task force appointed by the Korean Society of Acute Care Surgery reviewed previously published guidelines on antibiotic use in patients with abdominal injuries and adapted guidelines for Korea. METHODS: Four guidelines were assessed using the Appraisal of Guidelines for Research and Evaluation II instrument. Five topics were considered: indication for antibiotics, time until first antibiotic use, antibiotic therapy duration, appropriate antibiotics, and antibiotic use in abdominal trauma patients with hemorrhagic shock. RESULTS: Patients requiring surgery need preoperative prophylactic antibiotics. Patients who do not require surgery do not need antibiotics. Antibiotics should be administered as soon as possible after injury. In the absence of hollow viscus injury, no additional antibiotic doses are needed. If hollow viscus injury is repaired within 12 hours, antibiotics should be continued for ≤ 24 hours. If hollow viscus injury is repaired after 12 hours, antibiotics should be limited to 7 days. Antibiotics can be administered for ≥7 days if hollow viscus injury is incompletely repaired or clinical signs persist. Broad-spectrum aerobic and anaerobic coverage antibiotics are preferred as the initial antibiotics. Second-generation cephalosporins are the recommended initial antibiotics. Third-generation cephalosporins are alternative choices. For hemorrhagic shock, the antibiotic dose may be increased twofold or threefold and repeated after transfusion of every 10 units of blood until there is no further blood loss. CONCLUSION: Although this guideline was drafted through adaptation of other guidelines, it may be meaningful in that it provides a consensus on the use of antibiotics in abdominal trauma patients in Korea.
Abdominal Injuries* ; Advisory Committees ; Anti-Bacterial Agents ; Antibiotic Prophylaxis ; Cephalosporins ; Consensus ; Humans ; Korea ; Shock, Hemorrhagic

Animals ; Cats ; Diagnostic Tests, Routine ; Hemorrhage ; Humans ; Injury Severity Score ; Mortality ; Odds Ratio ; Resuscitation ; ROC Curve ; Sensitivity and Specificity

PURPOSE: This study aimed to investigate the incidence and risk factors of early postoperative small bowel obstruction (EPSBO) after laparotomy for trauma patients. METHODS: From 2009 to 2016, consecutive patients who had undergone laparotomy for trauma were retrospectively evaluated. EPSBO was defined as the presence of signs and symptoms of obstruction between postoperative days 7 and 30, or obstruction occurring anytime within 30 days and lasting more 7 days. RESULTS: Among 297 patients who met the inclusion criteria, 72 (24.2%) developed EPSBO. The length of hospital stay was significantly longer in patients with EPSBO than in those without EPSBO (median [interquartile range], 34 [21–48] days 24 [14–38] days, P < 0.001). Multivariate logistic analysis identified male sex (adjusted odds ratio [AOR], 3.026; P = 0.008), intraoperative crystalloid (AOR, 1.130; P = 0.031), and Abbreviated Injury Scale (AIS) score for mesenteric injury (AOR, 1.397; P < 0.001) as independent risk factors for EPSBO. The incidence of adhesive small bowel adhesion after 30 days postoperatively did not significantly differ between the 2 groups (with EPSBO, 5.6% without EPSBO, 5.3%; P = 0.571). Most of the patients with EPSBO were recovered by conservative treatment (95.8%). CONCLUSION: After laparotomy for trauma patients, the incidence of EPSBO was 24.2% in our study. EPSBO was associated with a longer hospital stay. Male sex, use of intraoperative crystalloid, and AIS score for mesenteric injury were significant independent risk factors for EPSBO. Patients with these risk factors should be followed-up more carefully.
Abbreviated Injury Scale ; Abdominal Injuries ; Adhesives ; Humans ; Ileus ; Incidence ; Laparotomy ; Length of Stay ; Male ; Odds Ratio ; Retrospective Studies ; Risk Factors

PURPOSE: Pancreatic trauma is infrequent because of its central, deep anatomical position. This contributes to a lack of surgeon experience and many debates exist about its standard care. This study aimed to investigate the postoperative pancreatic fistula (POPF) and mortality of pancreatic trauma after operation. METHODS: We reviewed records in the trauma registry of our institution submitted from January 2006 to December 2016. The grade of pancreatic injury, surgical management, morbidity, mortality, and other clinical variables included in the analyses. RESULTS: Data from a total of 26,072 trauma patients admitted to the Emergency Department were analyzed. Pancreatic trauma was observed in 114 of these patients (0.44%). Laparotomy was performed in 81 patients (2 pan creatico duodenectomies, 2 pancreaticogastrostomies, peripancreatic drainage in 41 patients, distal pancreatectomies in 34 patients, and 9 patients who underwent surgery for damage control). The incidence of POPF was 38.3%. The overall mortality was 8.8% (7 of 81). In multivariate analysis, pancreas injury grade IV (≥4) (adjusted odds ratio [AOR], 4.071; P = 0.029) and preoperative peritonitis signs (AOR, 2.903; P = 0.039) were independent risk factors for POPF. All patients who died had also another major abdominal injury (≥grade 3). Multiorgan failure was a major cause of death (6 of 7, 85.7%). The mortality rate of isolated pancreas injury was 0%. CONCLUSION: The pancreas injury grade and preoperative peritonitis were significant risk factors of POPF. The mortality rate of isolated pancreatic trauma was very low.
Abdominal Injuries ; Cause of Death ; Drainage ; Emergency Service, Hospital ; Humans ; Incidence ; Intraoperative Complications ; Laparotomy ; Mortality* ; Multivariate Analysis ; Odds Ratio ; Pancreas ; Pancreatectomy ; Pancreatic Fistula* ; Peritonitis ; Risk Factors ; Trauma Centers*

No abstract available.
Hemorrhage* ; Leg* ; Perineum* ; Wounds and Injuries*

PURPOSE: Splenic injury management has shifted to non-surgical treatment to preserve the spleen because of the postoperative risks of overwhelming post-splenectomy infection. In this study, we analyzed risk factors of therapeutic options for splenic injury, using medical records of Chonnam National University Hospital. METHODS: We reviewed the medical records of 110 consecutive patients with traumatic splenic injuries admitted from January 2009 to December 2013. Demographic characteristics and therapeutic options such as conservative treatment, angiographic embolization and emergency operation and clinical parameters were analyzed in this study. RESULTS: Thirty-four patients were treated surgically and seventy-six were managed with nonsurgical treatment. Multivariate logistic regression identified age (odds ratio [OR], 1.04; 95% confidence interval [CI], 1.009~1.072; p=0.01), hematocrit (OR, 0.878; 95% CI, 0.806~0.957; p=0.003), contrast extravasation (OR, 7.644; 95% CI, 2.248~25.986; p=0.001), spleen grade (OR, 2.08; 95% CI, 1.128~ 3.836; p=0.019) as significant risk factors of emergent splenectomy. CONCLUSION: Age, hematocrit, contrast extravasation, spleen grade were significant risk factors for emergent splenectomy.
Emergencies ; Hematocrit ; Humans ; Jeollanam-do ; Logistic Models ; Medical Records ; Risk Factors ; Spleen ; Splenectomy ; Splenic Rupture

Hemorrhage is a major cause of death in trauma patients. The medical definition of hemorrhagic shock is tissue hypoperfusion resulting from a reduction of blood volume. Decreased blood pressure resulting from acute blood loss induces cardiac stimulation, systemic vasoconstriction, and volume redistribution. These effects are due to the baroreceptor reflex, the humoral compensatory mechanisms including the renin angiotensin system, and the release of catecholamine and vasopressin. Hemorrhagic shock causes acidosis, hypothermia, and coagulopathy, known as ‘the lethal triad.’ Tissue hypoxia induces metabolic acidosis by producing lactic acid. The three components of the lethal triad amplify each other and form a vicious cycle, eventually causing the death of the patient. To reduce the risk of mortality in severely bleeding patients, we need to understand the pathophysiology of hemorrhagic shock and the related complications.
Acidosis ; Anoxia ; Baroreflex ; Blood Pressure ; Blood Volume ; Cause of Death ; Disseminated Intravascular Coagulation ; Hemorrhage ; Humans ; Hypothermia ; Lactic Acid ; Mortality ; Renin-Angiotensin System ; Shock, Hemorrhagic* ; Vasoconstriction ; Vasopressins

No abstract available.
Wounds and Injuries*

No abstract available.
Humans ; Psoas Muscles*

Excessive microglial activation and subsequent neuroinflammation lead to synaptic loss and dysfunction as well as neuronal cell death, which are involved in the pathogenesis and progression of several neurodegenerative diseases. Thus, the regulation of microglial activation has been evaluated as effective therapeutic strategies. Although dieckol (DEK), one of the phlorotannins isolated from marine brown alga Ecklonia cava, has been previously reported to inhibit microglial activation, the molecular mechanism is still unclear. Therefore, we investigated here molecular mechanism of DEK via extracellular signal-regulated kinase (ERK), Akt and nicotinamide adenine dinuclelotide phosphate (NADPH) oxidase-mediated pathways. In addition, the neuroprotective mechanism of DEK was investigated in microglia-mediated neurotoxicity models such as neuron-microglia co-culture and microglial conditioned media system. Our results demonstrated that treatment of anti-oxidant DEK potently suppressed phosphorylation of ERK in lipopolysaccharide (LPS, 1 microg/ml)-stimulated BV-2 microglia. In addition, DEK markedly attenuated Akt phosphorylation and increased expression of gp91(phox), which is the catalytic component of NADPH oxidase complex responsible for microglial reactive oxygen species (ROS) generation. Finally, DEK significantly attenuated neuronal cell death that is induced by treatment of microglial conditioned media containing neurotoxic secretary molecules. These neuroprotective effects of DEK were also confirmed in a neuron-microglia co-culture system using enhanced green fluorescent protein (EGFP)-transfected B35 neuroblastoma cell line. Taken together, these results suggest that DEK suppresses excessive microglial activation and microglia-mediated neuronal cell death via downregulation of ERK, Akt and NADPH oxidase-mediated pathways.
Adenine ; Cell Death* ; Cell Line ; Coculture Techniques ; Culture Media, Conditioned ; Down-Regulation ; Microglia ; NADP* ; NADPH Oxidase ; Neuroblastoma ; Neurodegenerative Diseases ; Neurons* ; Neuroprotective Agents ; Niacinamide ; Phosphorylation ; Phosphotransferases ; Reactive Oxygen Species