Pediatric Ingestions.

Pediatric ingestions encompass a wide range of diseases, including foreign body ingestions, caustic ingestions, and aspiration. Specific topics of interest in the pediatric age group for adult general surgeons are button batteries and magnets, which have significant morbidity and mortality and require a high index of suspicion to provide timely care. Evaluation and management of these cases should be tailored to the offending agent and managed at an appropriate pediatric center.

Utilization of Machine Learning Approaches to Predict Mortality in Pediatric Warzone Casualties.

BACKGROUND: Identification of pediatric trauma patients at the highest risk for death may promote optimization of care. This becomes increasingly important in austere settings with constrained medical capabilities. This study aimed to develop and validate predictive models using supervised machine learning (ML) techniques to identify pediatric warzone trauma patients at the highest risk for mortality. METHODS: Supervised learning approaches using logistic regression (LR), support vector machine (SVM), neural network (NN), and random forest (RF) models were generated from the Department of Defense Trauma Registry, 2008-2016. Models were tested and compared to determine the optimal algorithm for mortality. RESULTS: A total of 2,007 patients (79% male, median age range 7-12 years old, 62.5% sustaining penetrating injury) met the inclusion criteria. Severe injury (Injury Severity Score > 15) was noted in 32.4% of patients, while overall mortality was 7.13%. The RF and SVM models displayed recall values of .9507 and .9150, while LR and NN displayed values of .8912 and .8895, respectively. Random forest (RF) outperformed LR, SVM, and NN on receiver operating curve (ROC) analysis demonstrating an area under the ROC of .9752 versus .9252, .9383, and .8748, respectively. CONCLUSION: Machine learning (ML) techniques may prove useful in identifying those at the highest risk for mortality within pediatric trauma patients from combat zones. Incorporation of advanced computational algorithms should be further explored to optimize and supplement the diagnostic and therapeutic decision-making process.

Addition of neurological status to pediatric adjusted shock index to predict early mortality in trauma: A pediatric Trauma Quality Improvement Program analysis.

INTRODUCTION: Pediatric adjusted shock index (SIPA) has demonstrated the ability to prospectively identify children at the highest risk for early mortality. The addition of neurological status to shock index has shown promise as a reliable triage tool in adult trauma populations. This study sought to assess the utility of combining SIPA with Glasgow Coma Scale (GCS) for predicting early trauma-related outcomes. METHODS: Retrospective review of the 2017 Trauma Quality Improvement Program Database was performed for all severely injured patients younger than 18 years old. Pediatric adjusted shock index and reverse SIPA × GCS (rSIG) were calculated. Age-specific cutoff values were derived for reverse shock index multiplied by GCS (rSIG) and compared with their SIPA counterparts for early mortality assessment using area under the receiver operating characteristic curve analyses. RESULTS: A total of 10,389 pediatric patients with an average age of 11.4 years, 67% male, average Injury Severity Score of 24.1, and 4% sustaining a major penetrating injury were included in the analysis. The overall mortality was 9.3%. Furthermore, 32.1% of patients displayed an elevated SIPA score, while only 27.5% displayed a positive rSIG. On area under the receiver operating characteristic curve analysis, rSIG was found to be superior to SIPA as a predictor for in hospital mortality with values of 0.854 versus 0.628, respectively. CONCLUSION: Reverse shock index multiplied by GCS more readily predicted in hospital mortality for pediatric trauma patients when compared with SIPA. These findings suggest that neurological status should be an important factor during initial patient assessment. Further study to assess the applicability of rSIG for expanded trauma-related outcomes in pediatric trauma is necessary. LEVEL OF EVIDENCE: Prognostic study, level IV.

Celecoxib inhibits Ewing sarcoma cell migration via actin modulation.

BACKGROUND: Ewing sarcoma (ES) is an aggressive childhood solid tumor in which 30% of cases are metastatic at presentation, and subsequently carry a poor prognosis. We have previously shown that treatment with celecoxib significantly reduces invasion and metastasis of ES cells in a cyclooxygenase-2-independent fashion. Celecoxib is known to downregulate ß-catenin independently of cyclooxygenase-2. Additionally, the actin cytoskeleton is known to play an important role in tumor micrometastasis. We hypothesized that celecoxib's antimetastatic effect in ES acts via modulation of one of these two targets. METHODS: ES cells were treated with celecoxib, and the levels of ß-catenin and total actin were examined by Western blot and quantitative polymerase chain reaction. Cells were transfected with small interfering RNA targeting ß-catenin, and invasion assays were performed. Immunofluorescence staining for ß-catenin and F-actin was performed on treated and untreated cells. Additionally, cells were subjected to a wound healing assay to assess migration. RESULTS: Celecoxib had no effect on the messenger RNA or protein levels of ß-catenin but did significantly decrease the amount of total actin within ES cells. Reduction of ß-catenin by small interfering RNA had no effect on invasion, and celecoxib treatment of the ß-catenin depleted cells continued to inhibit invasion. Immunofluorescence staining demonstrated no change in ß-catenin with treatment but did show a significant reduction in the amount of F-actin, as well as morphologic changes of the cells. Wound healing assays demonstrated that celecoxib significantly inhibited migration. CONCLUSIONS: Celecoxib does not exert its antimetastatic effects in ES through alteration of ß-catenin but does significantly modulate the actin cytoskeleton.

An analysis of pancreas transplantation outcomes based on age groupings--an update of the UNOS database.

INTRODUCTION: Previously, increasing age has been a part of the exclusion criteria used when determining eligibility for a pancreas transplant. However, the analysis of pancreas transplantation outcomes based on age groupings has largely been based on single-center reports. METHODS: A UNOS database review of all adult pancreas and kidney-pancreas transplants between 1996 and 2012 was performed. Patients were divided into groups based on age categories: 18-29 (n = 1823), 30-39 (n = 7624), 40-49 (n = 7967), 50-59 (n = 3160), and ≥60 (n = 280). We compared survival outcomes and demographic variables between each age grouping. RESULTS: Of the 20 854 pancreas transplants, 3440 of the recipients were 50 yr of age or above. Graft survival was consistently the greatest in adults 40-49 yr of age. Graft survival was least in adults age 18-29 at one-, three-, and five-yr intervals. At 10- and 15-yr intervals, graft survival was the poorest in adults >60 yr old. Patient survival and age were found to be inversely proportional; as the patient population's age increased, survival decreased. CONCLUSION: Pancreas transplants performed in patients of increasing age demonstrate decreased patient and graft survival when compared to pancreas transplants in patients <50 yr of age.

Celecoxib inhibits invasion and metastasis via a cyclooxygenase 2-independent mechanism in an in vitro model of Ewing sarcoma.

BACKGROUND/INTRODUCTION: Previously, we reported that celecoxib, a cyclooxygenase-2 (COX-2) inhibitor, prevented lung metastases but did not affect tumor growth in a model of Ewing sarcoma. Cyclooxygenase-2 inhibition has been proposed as an antimetastatic strategy. The mechanism of action remains unclear. METHODS: Ewing sarcoma cells were suspended in a soluble basement membrane extract (Cultrex; Trevigen, Inc, Gaithersburg, MD) and supplemented with celecoxib or with rofecoxib, a second COX-2 inhibitor, above a filter. Controls received solvent. After 48 hours, the cells that invaded through the basement membrane and filter were stained and counted. The assay was repeated with the addition of 500-nM prostaglandin E2 (PGE(2)). RESULTS: Invasion was significantly decreased in the celecoxib groups compared with the control. The addition of PGE(2) did not overcome celecoxib inhibition. Rofecoxib did not significantly affect invasion compared with control either with or without PGE(2). CONCLUSIONS: Celecoxib significantly inhibits invasion of Ewing sarcoma cells in vitro. Prostaglandin E2, a downstream product of COX-2, did not reverse in vitro inhibition, suggesting that celecoxib acts through a COX-2-independent mechanism. This is further supported by the failure of rofecoxib to inhibit invasion despite more selectively inhibiting COX-2.