"Inadequate source control and inappropriate antibiotics are key determinants of mortality in patients with intra-abdominal sepsis and associated bacteremia." Surgical Infections. 16,6. 785-793. (2015 Background: Patients with intra-abdominal sepsis and associated bacteremia have a high mortality rate. However, outcomes studies in this population are limited, in part because of the small numbers of such patients. The objective of this study was to describe characteristics of critically ill patients with secondary blood stream infection (BSI) of intra-abdominal origin and identify predictors of mortality.Methods: This retrospective, single-center study evaluated patients admitted between January 2005 and January 2011 with bacteremia because of an intra-abdominal source. Patients were included if they met criteria for severe sepsis based on International Classification of Diseases, 9th Revision (ICD 9) codes for acute organ dysfunction, had a positive blood culture, had at least one ICD 9 code indicative of an intra-abdominal process, and had a confirmed or clinically suspected intra-abdominal infection (IAI) within 72 h of the blood culture. Chart review was performed to confirm the presence of these criteria and also the absence of any other potential source of bacteremia. Data were collected on patient demographics, BSI source, source control procedure details, microorganisms isolated, and antibiotics administered. Multivariable logistic regression analysis was performed to identify independent predictors of mortality. Results: Three hundred six patients with BSI were identified, of which 108 episodes were deemed to be of intraabdominal origin. Gram-negative organisms comprised 43% of blood isolates, followed by gram-positives (33%), anaerobes (14%), and yeast (9%). Appropriate antimicrobial therapy was administered in 71% of patients. The overall mortality rate was 27.8%. As compared with survivors, non-survivors were older, more likely to have underlying COPD or asthma, and have renal or metabolic failure (p < 0.05 for all). Among non-survivors, adequate source control was obtained less frequently (64% vs. 91%, p = 0.002) and median time to appropriate antibiotics was longer (23 h vs. 4 h, p = 0.004). Logistic regression analysis revealed inadequate source control (p = 0.002) and inappropriate antibiotics (p = 0.016) to be independently associated with mortality. Conclusions: Critically ill patients with a BSI of abdominal origin are at high risk for mortality. Failure to achieve adequate source control and administration of inappropriate antibiotics were independent predictors of mortality. Thus, these represent potential opportunities to impact outcomes in patients with complicated IAI.

Background.There are limited data on risk factors for surgical site infection (SSI) after open or laparoscopic cholecystectomy.Methods.A retrospective cohort of commercially insured persons aged 18–64 years was assembled using International Classification of Diseases, 9th Revision, Clinical Modification (ICD-9-CM) procedure or Current Procedural Terminology, 4th edition codes for cholecystectomy from December 31, 2004 to December 31, 2010. Complex procedures and patients (eg, cancer, end-stage renal disease) and procedures with pre-existing infection were excluded. Surgical site infections within 90 days after cholecystectomy were identified by ICD-9-CM diagnosis codes. A Cox proportional hazards model was used to identify independent risk factors for SSI.Results.Surgical site infections were identified after 472 of 66566 (0.71%) cholecystectomies; incidence was higher after open (n = 51, 4.93%) versus laparoscopic procedures (n = 421, 0.64%; P < .001). Independent risk factors for SSI included male gender, preoperative chronic anemia, diabetes, drug abuse, malnutrition/weight loss, obesity, smoking-related diseases, previous Staphylococcus aureus infection, laparoscopic approach with acute cholecystitis/obstruction (hazards ratio [HR], 1.58; 95% confidence interval [CI], 1.27–1.96), open approach with (HR, 4.29; 95% CI, 2.45–7.52) or without acute cholecystitis/obstruction (HR, 4.04; 95% CI, 1.96–8.34), conversion to open approach with (HR, 4.71; 95% CI, 2.74–8.10) or without acute cholecystitis/obstruction (HR, 7.11; 95% CI, 3.87–13.08), bile duct exploration, postoperative chronic anemia, and postoperative pneumonia or urinary tract infection.Conclusions.Acute cholecystitis or obstruction was associated with significantly increased risk of SSI with laparoscopic but not open cholecystectomy. The risk of SSI was similar for planned open and converted procedures. These findings suggest that stratification by operative factors is important when comparing SSI rates between facilities.

Our results show that synthetic meshes are not inferior to biologic meshes in contaminated AWR. This is important in view of the tremendous cost disparity between these two products and the questionable ability of biologic mesh to offer a durable hernia repair.

Loss of functional small bowel surface area following surgical resection for disorders such as Crohn's disease, intestinal ischemic injury, radiation enteritis, and in children, necrotizing enterocolitis, atresia and gastroschisis, may result in short bowel syndrome, with attendant high morbidity, mortality and health care costs in the U.S. Following resection, the remaining small bowel epithelium mounts an adaptive response resulting in increased crypt cell proliferation, increased villus height, crypt depth and enhanced nutrient and electrolyte absorption. Although these morphologic and functional changes are well-described in animal models, the adaptive response in humans is less well understood, and clinically the response is unpredictable and often inadequate. Here we address the hypotheses that human intestinal stem cell populations are expanded and the stem cell niche is regulated following massive gut resection in short bowel syndrome. We use intestinal enteroid cultures from SBS patients to show that the magnitude and phenotype of the adaptive stem cell response is regulated by stromal niche cells including intestinal subepithelial myofibroblasts, which are activated by intestinal resection to enhance epithelial stem and proliferative cell responses. Our data suggest that myofibroblast regulation of bone morphogenetic protein signaling pathways plays a role in the gut adaptive response post resection.

After the World War II, fecal diversion became the standard of care for colon injuries, although medical, logistic, and technical advancements have challenged this approach. Damage control surgery serves to temporize immediately life-threatening conditions, and definitive management of destructive colon injuries is delayed until after appropriate resuscitation. The bowel can be left in discontinuity for up to 3 days before edema ensues, but the optimal repair window remains within 12 to 48 hours. Delayed anastomosis performed at the take-back operation or stoma formation has been reported with variable results. Studies have revealed good outcomes in those undergoing anastomosis after damage control surgery; however, they point to a subgroup of trauma patients considered to be "high risk" that may benefit from fecal diversion. Risk factors influencing morbidity and mortality rates include hypotension, massive transfusion, the degree of intra-abdominal contamination, associated organ injuries, shock, left-sided colon injury, and multiple comorbid conditions. Patients who are not suitable for anastomosis by 36 hours after damage control may be best managed with a diverting stoma. Failures are more likely related to ongoing instability, and the management strategy of colorectal injury should be based mainly on the patient's overall condition.