Erratum to: The management of intra-abdominal infections from a global perspective: 2017 WSES guidelines for management of intra-abdominal infections.

[This corrects the article DOI: 10.1186/s13017-017-0141-6.].

Erratum to: Antimicrobials: a global alliance for optimizing their rational use in intra-abdominal infections (AGORA).

[This corrects the article DOI: 10.1186/s13017-016-0089-y.].

Erratum to: 2016 WSES guidelines on acute calculous cholecystitis.

[This corrects the article DOI: 10.1186/s13017-016-0082-5.].

2016 WSES guidelines on acute calculous cholecystitis.

Acute calculus cholecystitis is a very common disease with several area of uncertainty. The World Society of Emergency Surgery developed extensive guidelines in order to cover grey areas. The diagnostic criteria, the antimicrobial therapy, the evaluation of associated common bile duct stones, the identification of "high risk" patients, the surgical timing, the type of surgery, and the alternatives to surgery are discussed. Moreover the algorithm is proposed: as soon as diagnosis is made and after the evaluation of choledocholitiasis risk, laparoscopic cholecystectomy should be offered to all patients exception of those with high risk of morbidity or mortality. These Guidelines must be considered as an adjunctive tool for decision but they are not substitute of the clinical judgement for the individual patient.

The Glue Grant experience: characterizing the post injury genomic response.

Despite ongoing improvements in resuscitation, care, and outcomes, traumatic injury remains a significant health care and economic burden. The causes are multifactorial, but our approach to the clinical management of these patients remains limited by our current understanding of the pathobiology of the disease. A multicenter, multidisciplinary program known as the "Inflammation and the Host Response to Injury" Large Scale Collaborative Research Program was created by the National Institute of General Medical Sciences (NIGMS, U54 GM062119-10) in 2001 in a 10-year effort to address some of these issues. Its primary goal is to describe the human genomic response to severe trauma and burns, and to examine changes in gene expression in the context of different clinical outcomes. The Program has not only successfully implemented clinical care guidelines for managing the severe trauma patient based on the best available evidence to minimize iatrogenic variability, but it has also examined the genome-wide, immune-inflammatory response in total and isolated blood leukocyte populations. This review will address current milestones as well as future directions for the Program.

Prevention of immunization to D+ red blood cells with red blood cell exchange and intravenous Rh immune globulin.

BACKGROUND: Although young women who are D- occasionally receive unintentional transfusions with D+ red blood cells (RBCs), there are little data to assist with management of such an event. Two cases of D- girls transfused with D+ RBCs are reported. In an effort to prevent formation of anti-D, RBC exchange followed by administration of intravenous (IV) Rh immune globulin (RhIg) was used. CASE REPORTS: Patient 1, a 56-kg, 16-year-old D- girl, was involved in a motor vehicle crash. She received 4 units of Group O uncrossmatched D+ RBCs. Thirty-six hours after admission, she underwent RBC exchange with 10 units of D- RBCs, followed by a total of 2718 microg of IV RhIg over 32 hours. Six months later, her antibody screen was negative. Patient 2, a 39-kg, 10-year-old D- girl with aplastic anemia, received 1 unit of D+ RBCs. She underwent RBC exchange on the same day with 5 units of D- RBCs, followed by a total of 900 microg of IV RhIg over 8 hours. Six months later her antibody screen was negative. CONCLUSION: RBC exchange followed by a calculated dose of IV RhIg was successful in preventing allo-immunization to D. Several small studies suggest that both trauma and hematology patients may be less capable of becoming immunized with the transfusion of D+ blood components. Until these findings are more clearly defined, there will be times when prevention of immunization of any D- girl is desired. RBC exchange followed by RhIg appears to be one way to achieve this goal.

Stapled versus sutured gastrointestinal anastomoses in the trauma patient: a multicenter trial.

BACKGROUND: Construction of gastrointestinal anastomoses utilizing stapling devices has become a familiar procedure. In elective surgery, studies have shown no significant differences in complications between stapled and sutured anastomoses. Controversy has recently arisen regarding the accurate incidence of complications associated with anastomoses in the trauma patient. The objective of this multi-institutional study was to determine whether the incidence of postoperative complications differs between stapled and sutured anastomoses following the emergent repair of traumatic bowel injuries. METHODS: Using a retrospective cohort design, all trauma registry records from five Level I trauma centers over a period of 4 years were reviewed. RESULTS: A total of 199 patients with 289 anastomoses were identified. A surgical stapling device was used to create 175 separate anastomoses, while a hand-sutured method was employed in 114 anastomoses. A complication was defined as an anastomotic leak verified at reoperation, an intra-abdominal abscess, or an enterocutaneous fistula. The mean abdominal Abbreviated Injury Scale score and Injury Severity Score were similar in the two cohort groups. Stapling and suturing techniques were evenly distributed in both small and large bowel repairs. Seven of the total 175 stapled anastomoses and none of the 114 hand-sewn anastomoses resulted in a clinically significant leak requiring reoperation (RR = undefined, 95% CI 1.08-infinity, p = 0.04). Each anastomotic leak occurred in a separate individual. Nineteen stapled anastomoses and four sutured anastomoses were associated with an intra-abdominal abscess (RR = 2.7, 95% CI 0.96-7.57, p = 0.04). Enterocutaneous fistula formation was not statistically associated with either type of anastomoses (stapled cohort = 3 of 175 and sutured cohort = 2 of 114). Overall, 22 (13%) stapled anastomoses and 6 (5%) sutured anastomoses were associated with an intra-abdominal complication (RR = 2.08, 95% CI 0.89-4.86, p = 0.076). CONCLUSION: Anastomotic leaks and intra-abdominal abscesses appear to be more likely with stapled bowel repairs compared with sutured anastomoses in the injured patient. Caution should be exercised in deciding to staple a bowel anastomosis in the trauma patient.

Antioxidants in critical illness.

Oxidative stress has been implicated in the manifestations of critical illnesses, including ischemia and reperfusion injury and systemic inflammatory states. This review describes the evidence for increased oxidative stress in critically ill patients and explores the data regarding antioxidant therapy for these conditions. Antioxidant therapies reviewed include N-acetylcysteine, selenium, vitamins E and C, superoxide dismutase, catalase, lazaroids, and allopurinol. We focus on the results of these interventions in animal models and human trials, when available.

The relationship between trauma center volume and outcome.

In spite of the limited direct evidence available, increasing data support a positive volume-outcome association in trauma care. When coupled with the extensive indirect data suggesting that regions with organized systems of trauma care are associated with lower trauma-related mortality rates than regions where the number of centers and their level of commitment are unlimited and untested, there is little doubt that experience improves outcome and that volume plays a critical role in the accrual of experience. Although regionalization of trauma care has the inevitable consequence of increased prehospital transport times, particularly in rural areas remote from large trauma centers, some states have designed inclusive systems where a large number of smaller centers have been verified and designated as lower level trauma centers (i.e., level 3-5). The process of trauma center verification holds these smaller volume centers to a standard of care such that the quality of care of the trauma patient may exceed that of other, less-regulated aspects of medical or surgical care. Several reports have suggested that trauma outcomes in smaller rural level 3 centers or centers with dedicated trauma programs with appropriate, functional triage protocols are comparable to national norms, thus reflecting the importance of commitment to outcome. These data suggest that quality of care does not only follow volume, particularly when stipulations and requirements are clear regarding the process of care and ongoing quality assurance.

Payer status: the unspoken triage criterion.

BACKGROUND: The cost of uncompensated trauma care is a significant barrier to trauma system development. Trauma center designation may burden an institution with an unprofitable mix of underinsured, severely injured patients. Concerns about inadequate reimbursement may motivate interhospital transfers on the basis of insurance status rather than medical necessity, potentially undermining the effectiveness of the system. We set out to explore whether this phenomenon exists in a mature trauma system. METHODS: Trauma patients receiving definitive care at Level III or IV trauma centers were compared with patients transferred from these centers to the only Level I regional center. Insurance status was classified as either commercial or noncommercial. Logistic regression was used to determine the independent predictors of transfer after adjusting for differences in injury severity. RESULTS: Only 12% of 2,008 patients initially evaluated at Level III/IV centers were transferred to the Level I center, an indicator of the effectiveness of prehospital triage protocols in the region. The presence of specific complex injuries, younger age, male gender, and insurance status were all associated with an increased likelihood of transfer. Insurance status was an independent predictor of transfer: patients without commercial insurance were 2.4 (95% confidence interval, 1.6-3.6) times more likely to be transferred to a Level I facility than patients with commercial insurance after adjusting for differences in injury severity. CONCLUSION: Insurance status influences the decision to transfer to higher levels of care. These findings suggest that the financial burden of a trauma system may be inequitably distributed. This inequitable distribution may be necessary for trauma system sustainability and calls for the development of disproportionate reimbursement strategies to support regional referral centers.

Epithelial cyclooxygenase-2 expression: a model for pathogenesis of colon cancer.

BACKGROUND: Recent studies indicate a close relationship between cyclooxygense-2 (COX-2) expression and the pathogenesis of colorectal cancer, yet little information exists regarding the stimuli and pathways involved in COX-2 expression by the colonic epithelium. We studied the induction of COX-2 in response to such environmental stress as hyperosmolarity and lipopolysaccharide (LPS) in a human colon cell line. We further investigated the transduction cascades mediating COX-2 expression, focusing upon the mitogen-activated protein kinase pathways p38 and extracellular signal-regulated kinase (ERK). MATERIALS AND METHODS: Human colon cancer cells (Caco-2) were stimulated with increasing concentrations of sodium chloride (NaCl) or LPS. Total protein was extracted at different time points and subjected to Western blot analysis with antibodies to human COX-2, COX-1, or phospho-specific antibodies to ERK and p38. RESULTS: LPS failed to induce COX-2 or COX-1 expression. Hyperosmolarity induced COX-2 expression by 2 h, with peak levels occurring at 6-8 h. NaCl at 40 and 100 mM induced a 2-fold and more than 50-fold increase in COX-2 expression, respectively; COX-1 expression was not affected. Hyperosmolarity induced both p38 and ERK activation within 30 min; however, only p38 inhibition attenuated osmotic-induced COX-2 expression; inhibition of ERK activation had no effect. CONCLUSIONS: Increase in osmolarity activates p38 and induces COX-2 expression in the colonic epithelium. The lack of response to LPS is teleologically expected of the colonic epithelium that is in constant contact with the fecal bacteria. This model also predicts that an increase in luminal osmolarity in the colon may induce COX-2 and thereby promote a neoplastic phenotype.

Relationship between trauma center volume and outcomes.

CONTEXT: The premise underlying regionalization of trauma care is that larger volumes of trauma patients cared for in fewer institutions will lead to improved outcomes. However, whether a relationship exists between institutional volume and trauma outcomes remains unknown. OBJECTIVE: To evaluate the association between trauma center volume and outcomes of trauma patients. DESIGN: Retrospective cohort study. SETTING: Thirty-one academic level I or level II trauma centers across the United States participating in the University Healthsystem Consortium Trauma Benchmarking Study. PATIENTS: Consecutive patients with penetrating abdominal injury (PAI; n = 478) discharged between November 1, 1997, and July 31, 1998, or with multisystem blunt trauma (minimum of head injury and lower-extremity long-bone fractures; n = 541) discharged between June 1 and December 31, 1998. MAIN OUTCOME MEASURES: Inpatient mortality and hospital length of stay (LOS), comparing high-volume (>650 trauma admissions/y) and low-volume (

Ethanol abuse and the trauma patient.

BACKGROUND: Alcohol intoxication has long been associated with an increased risk of injury from a number of mechanisms and with trauma recidivism. It is less certain whether alcohol abuse is associated with worse outcomes for a given degree of injury. METHODS: Review of the pertinent English-language literature. RESULTS: The vasodilator effects of alcohol may hamper fluid resuscitation, especially in head-injured patients. Acute and chronic alcohol intoxication both have substantial effects on the cellular and molecular responses necessary to fight infection. High alcohol concentrations exert an immunosuppressive effect on production of proinflammatory cytokines such as tumor necrosis factor and interleukin-1. However, the clinical effects of the immunosuppression are variable and difficult to discern in heterogeneous trauma patient populations with variable degrees of intoxication. CONCLUSION: Alcohol has a profound impact on the epidemiology of injury, but the physiology and biochemical effects in an individual patient may be difficult to predict. Identification of intoxicated persons is essential, despite economic disincentives to do so, because even brief targeted intervention programs can decrease substantially the patient's risk of subsequent injury.

Adherence regulates macrophage signal transduction and primes tumor necrosis factor production.

While monocyte/macrophage (Mphi) adherence to a matrix is necessary for differentiation and prolonged survival, the effect of adherence on the signaling mechanisms responsible for Mphi activation is unknown. Lipopolysaccharide (LPS) activates Mphi by signaling through members of the mitogen activated protein kinase (MAPK) family thereby inducing transcription of proinflammatory cytokines, such as TNF-alpha. Since adherence has been shown to affect different activities of various myeloid phagocytes, we investigated whether adherence affects intracellular signaling and modulates activation of the Mphi proinflammatory phenotype. We assessed the effect of adherence on activation of rabbit alveolar Mphi by measuring LPS-induced TNF-alpha mRNA and TNF-alpha secreted product in adherent versus nonadherent cells, in vitro. The effect of adherence on LPS-induced activation of MAPK was assessed by western analysis using a dual phosphospecific antibody against p38MAPK, p42,44ERK, and p54SAPK. LPS is known to induce activation of NF-kappaB and AP-1. Modulation of these two transcription factors by LPS under adherent versus nonadherent conditions was evaluated by gel-shift analyses. The results were that adherent cells treated with LPS, 10 ng/mL or 1 microg/ml, elicited a 26- and 132-fold increase, respectively, in TNF-alpha production. Nonadherent cells did not elicit significant TNF-alpha in response to LPS. Adherence alone induced significant ERK and AP-1 activation, but did not stimulate a significant TNF-alpha response and no further activation of ERK and AP-1 was observed with LPS stimulation. Adherence alone did not activate p38MAPK or NF-kappaB, but primed Mphi for an augmented response to LPS in activation of p38, NF-kappaB and in production of TNF-alpha. We conclude that adherence primes Mphi for activation and regulates MAPK signal transduction pathways.

Effect of an older sibling and birth interval on the risk of childhood injury.

OBJECTIVE: Certain family structures have been identified as putting children at high risk for injury. To further define children at highest risk, we set out to explore the effect of an older sibling and birth interval on the risk of injury related hospital admission or death. METHODS: Data were analyzed using a case-control design. Cases and controls were identified by linking longitudinal birth data from Washington state (1989-96) to death certificate records and hospital discharge data obtained from the Washington State Comprehensive Hospital Abstract Reporting System and frequency matched in a 1:2 ratio on year of birth. Cases consisted of singleton children 6 years of age or younger who were hospitalized or died as a result of injury during the years 1989-96. Multivariate logistic regression was used to identify and adjust for confounding variables. RESULTS: There were 3145 cases and 8371 controls. The adjusted odds ratio for injury in children with an older sibling was 1.50 (95% confidence interval 1.37 to 1.65). The effect was greatest in children under 2 years of age, and in those with a birth interval of less than two years. As the number of older siblings increased, so did the risk of injury, with the highest risk in children with three or more older siblings. CONCLUSION: These data suggest that the presence of an older sibling is associated with an increased risk of injury. The risk is highest in those with very short birth intervals. Potential mechanisms for this increased risk may relate to inadequate parental supervision. Pediatricians and other care providers need to be alert to these identifiable risk factors and then direct preventive strategies, such as home visits and educational programs, toward these families.

Harborview assessment for risk of mortality: an improved measure of injury severity on the basis of ICD-9-CM.

BACKGROUND: There have been several attempts to develop a scoring system that can accurately reflect the severity of a trauma patient's injuries, particularly with respect to the effect of the injury on survival. Current methodologies require unreliable physiologic data for the assignment of a survival probability and fail to account for the potential synergism of different injury combinations. The purpose of this study was to develop a scoring system to better estimate probability of mortality on the basis of information that is readily available from the hospital discharge sheet and does not rely on physiologic data. METHODS: Records from the trauma registry from an urban Level I trauma center were analyzed using logistic regression. Included in the regression were Internation Classification of Diseases-9th Rev (ICD-9CM) codes for anatomic injury, mechanism, intent, and preexisting medical conditions, as well as age. Two-way interaction terms for several combinations of injuries were also included in the regression model. The resulting Harborview Assessment for Risk of Mortality (HARM) score was then applied to an independent test data set and compared with Trauma and Injury Severity Score (TRISS) probability of survival and ICD-9-CM Injury Severity Score (ICISS) for ability to predict mortality using the area under the receiver operator characteristic curve. RESULTS: The HARM score was based on analysis of 16,042 records (design set). When applied to an independent validation set of 15,957 records, the area under the receiver operator characteristic curve (AUC) for HARM was 0.9592. This represented significantly better discrimination than both TRISS probability of survival (AUC = 0.9473, p = 0.005) and ICISS (AUC = 0.9402, p = 0.001). HARM also had a better calibration (Hosmer-Lemeshow statistic [HL] = 19.74) than TRISS (HL = 55.71) and ICISS (HL = 709.19). Physiologic data were incomplete for 6,124 records (38%) of the validation set; TRISS could not be calculated at all for these records. CONCLUSION: The HARM score is an effective tool for predicting probability of in-hospital mortality for trauma patients. It outperforms both the TRISS and ICD9-CM Injury Severity Score (ICISS) methodologies with respect to both discrimination and calibration, using information that is readily available from hospital discharge coding, and without requiring emergency department physiologic data.

Sympathectomy for causalgia: experience with military injuries.

BACKGROUND: Causalgia is a rare disease in civilian practice, and most reports regarding causalgia in the literature are from major extended wars. To increase awareness of this syndrome, our wartime experience with this disease is presented. METHODS: The charts of patients with causalgia referred to two university hospitals for treatment from 1985 to 1989 were retrospectively studied. Characteristics of the cause, clinical manifestations, and the response to therapy were evaluated. RESULTS: Among 1,564 patients with peripheral nerve injuries, there were 54 cases (3.4%) of causalgia. All of the patients, except five, were injured in battle by high-velocity bullets or missiles. Upper extremities were involved in 28 patients (52 %) and lower extremities in 26 patients (48%). The most common presenting symptoms were as follows: burning pain, 100%; wet extremity, 100%; cold extremity, 93%; sensitivity to cold, 89%; paresthesia, 78%; and color changes in the extremities, 55%. In 48 patients (89%), pain was relieved by sympathetic block (3 patients had permanent cure). Six patients had no response to the blocks (11%). Of 45 patients who had temporary relief, all underwent sympathectomy. All of these patients had complete relief of symptoms in the immediate postoperative period and for follow-up from 1 to 6 years. CONCLUSION: Causalgia is essentially a war casualty disease. The condition is associated with burning pain, hyperesthesia, and symptoms of sympathetic overactivity. Sympathectomy is effective and the treatment of choice, particularly for patients who respond temporarily to sympathetic blocks.

Hypertonic saline solution induces prostacyclin production by increasing cyclooxygenase-2 expression.

BACKGROUND: Previously, we demonstrated that hypertonic saline solution (HTS) and endotoxin (lipopolysaccharide [LPS]) induce prostacyclin (PGI(2)) production in human endothelial cells. Here, we hypothesized that HTS and LPS may induce PGI(2) production by increasing cyclooxygenase (COX) expression. We further examined the activation of p38 and extracellular signal-regulated kinases (ERK) and questioned whether these transduction cascades might mediate COX expression. METHODS: Human umbilical vein endothelial cells were stimulated with varying concentrations of NaCl or LPS. RESULTS: HTS and LPS induced prompt activation of both p38 and ERKs that peaked at 30 minutes. HTS and LPS also induced a dose-related increase in COX-2 with maximal expression within 4 to 6 hours; there was no change in COX-1. This correlated with an increase in supernatant PGI(2) levels, which became statistically significant for NaCl of more than 40 mmol/L and for all LPS doses. The inhibition of p38 with SB202190 abrogated the osmotic and LPS-induced COX-2 expression and PGI(2) production. Inhibition of ERK activation had no effect on COX-2 expression. CONCLUSIONS: Hyperosmolarity and LPS induce, in chronologic order, p38 and ERK activation, COX-2 expression, and PGI(2) production. Because COX is the rate-limiting enzyme in prostaglandin synthesis, it is likely that the increase in PGI(2) production is due to, at least in part, the increased COX-2 expression. The data also suggest that p38 mitogen-activated protein kinase is involved in the signaling cascade for COX-2 expression.