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

Colonization with Escherichia coli EC 25 protects neonatal rats from necrotizing enterocolitis

Necrotizing enterocolitis (NEC) is a significant cause of morbidity and mortality in premature infants; yet its pathogenesis remains poorly understood. To evaluate the role of intestinal bacteria in protection against NEC, we assessed the ability of naturally occurring intestinal colonizer E. coli EC25 to influence composition of intestinal microbiota and NEC pathology in the neonatal rat model. Experimental NEC was induced in neonatal rats by formula feeding/hypoxia, and graded histologically. Bacterial populations were characterized by plating on blood agar, scoring colony classes, and identifying each class by sequencing 16S rDNA. Binding of bacteria to, and induction of apoptosis in IEC-6 enterocytes were examined by plating on blood agar and fluorescent staining for fragmented DNA. E. coli EC 25, which was originally isolated from healthy rats, efficiently colonized the intestine and protected from NEC following introduction to newborn rats with formula at 106 or 108 cfu. Protection did not depend significantly on EC25 inoculum size or load in the intestine, but positively correlated with the fraction of EC25 in the microbiome. Introduction of EC25 did not prevent colonization with other bacteria and did not significantly alter bacterial diversity. EC25 neither induced cultured enterocyte apoptosis, nor protected from apoptosis induced by an enteropathogenic strain of Cronobacter muytjensii. Our results show that E. coli EC25 is a commensal strain that efficiently colonizes the neonatal intestine and protects from NEC

Low doses of Celecoxib attenuate gut barrier failure during experimental peritonitis

The intestinal barrier becomes compromised during systemic inflammation, leading to 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 E(2) (PGE(2)) 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-associated proteins JAM-A and ZO-1. Luminal instillation of PGE(2) 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 PGE(2) seen in the mucosa during peritonitis contribute to gut barrier failure, presumably by compromising tight junctions. 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