Presence of Microscopic Hematuria Does Not Predict Clinically Important Intra-Abdominal Injury in Children.

OBJECTIVE: Screening for blunt intra-abdominal injury in children often includes directed laboratory evaluation that guides need for computed tomography. We sought to evaluate the use of urinalysis in identifying patients with clinically important intraabdominal injury (ci-IAI). METHODS: A retrospective chart review was performed for all patients less than 18 years who presented with blunt mechanisms at a level I trauma center between 2016 and 2019. Exclusion criteria included transfer from an outside facility, physical abuse, and death within thirty minutes of arrival. Demographics, physical exam findings, serum chemistries, urinalysis, and imaging were reviewed. Clinically important intraabdominal injury was defined as injury requiring ≥2 nights admission, blood transfusion, angiography with embolization, or therapeutic surgery. RESULTS: Two hundred forty patients were identified. One hundred sixty-five had a completed urinalysis. For all patients an abnormal chemistry panel and abnormal physical exam had a sensitivity of 88.9% and a negative predictive value of 99.3%. Nine patients had a ci-IAI. Patients with a ci-IAI were more likely to have abdominal pain, tenderness on exam, and elevated hepatic enzymes. When patients were stratified by the presence of an abnormal chemistry or physical exam with or without microscopic hematuria, urinalysis did not improve the ability to identify patients with a ci-IAI. In fact, presence of microscopic hematuria increased the rate of false positives by 12%. CONCLUSIONS: Microscopic hematuria was not a useful marker for ci-IAI and may lead to falsely assuming a more serious injury.

Derivation and Validation of a Machine Learning Algorithm for Predicting Venous Thromboembolism in Injured Children.

BACKGROUND: Venous thromboembolism (VTE) causes significant morbidity in pediatric trauma patients. We applied machine learning algorithms to the Trauma Quality Improvement Program (TQIP) database to develop and validate a risk prediction model for VTE in injured children. METHODS: Patients ≤18 years were identified from TQIP (2017-2019, n = 383,814). Those administered VTE prophylaxis ≤24 h and missing the outcome (VTE) were removed (n = 347,576). Feature selection identified 15 predictors: intubation, need for supplemental oxygen, spinal injury, pelvic fractures, multiple long bone fractures, major surgery (neurosurgery, thoracic, orthopedic, vascular), age, transfusion requirement, intracranial pressure monitor or external ventricular drain placement, and low Glasgow Coma Scale score. Data was split into training (n = 251,409) and testing (n = 118,175) subsets. Machine learning algorithms were trained, tested, and compared. RESULTS: Low-risk prediction: For the testing subset, all models outperformed the baseline rate of VTE (0.15%) with a predicted rate of 0.01-0.02% (p < 2.2e-16). 88.4-89.4% of patients were classified as low risk by the models. HIGH-RISK PREDICTION: All models outperformed baseline with a predicted rate of VTE ranging from 1.13 to 1.32% (p < 2.2e-16). The performance of the 3 models was not significantly different. CONCLUSION: We developed a predictive model that differentiates injured children for development of VTE with high discrimination and can guide prophylaxis use. LEVEL OF EVIDENCE: Prognostic, Level II. TYPE OF STUDY: Retrospective, Cross-sectional.

Low doses of celecoxib attenuate gut barrier failure during experimental peritonitis.

The intestinal barrier becomes compromised during systemic inflammation, leading to the entry of luminal bacteria into the host and gut origin sepsis. Pathogenesis and treatment of inflammatory gut barrier failure is an important problem in critical care. In this study, we examined the role of cyclooxygenase-2 (COX-2), a key enzyme in the production of inflammatory prostanoids, in gut barrier failure during experimental peritonitis in mice. I.p. injection of LPS or cecal ligation and puncture (CLP) increased the levels of COX-2 and its product prostaglandin E2 (PGE2) in the ileal mucosa, caused pathologic sloughing of the intestinal epithelium, increased passage of FITC-dextran and bacterial translocation across the barrier, and increased internalization of the tight junction (TJ)-associated proteins junction-associated molecule-A and zonula occludens-1. Luminal instillation of PGE2 in an isolated ileal loop increased transepithelial passage of FITC-dextran. Low doses (0.5-1 mg/kg), but not a higher dose (5 mg/kg) of the specific COX-2 inhibitor Celecoxib partially ameliorated the inflammatory gut barrier failure. These results demonstrate that high levels of COX-2-derived PGE2 seen in the mucosa during peritonitis contribute to gut barrier failure, presumably by compromising TJs. Low doses of specific COX-2 inhibitors may blunt this effect while preserving the homeostatic function of COX-2-derived prostanoids. Low doses of COX-2 inhibitors may find use as an adjunct barrier-protecting therapy in critically ill patients.