Predictors of Mortality in Trauma patients Receiving massive Transfusion Protocol.

INTRODUCTION: Massive transfusion protocol (MTP) is often defined as the transfusion of ≥10 units of packed red blood cells (PRBCs) in 24 hours. The purpose of this study is to determine which factors most significantly contribute to mortality in patients receiving MTP after trauma. METHODS: An initial database search followed by retrospective chart review was performed on patients treated at four trauma centers in Southern California. Data were collected on all patients who received MTP, defined as at least 10 units PRBCs within the first 24 hours of admission, between January 2015 and December 2019. Patients with isolated head injuries were excluded. Univariate and multivariate analyses were used to determine which factors most significantly influenced mortality. RESULTS: Of 1278 patients who met our inclusion criteria in the database, 596 (46.6%) survived and 682 (53.4%) died. On univariate analysis initial vitals and labs, except for initial hemoglobin and initial platelet count were significant predictors of mortality. A multivariate regression model showed the strongest predictors of mortality were pRBC transfusions at 4 hours (OR 1.073, CI 1.020-1.128, P = .006) and 24 hours (OR 1.045, CI 1.003-1.088, P = .036), and FFP transfusion at 24 hours (OR 1.049, CI 1.016-1.084, P = .003). CONCLUSION: Our data indicates that several factors may contribute to mortality in patients receiving MTP. In particular age, mechanism, initial GCS, and PRBC transfusions at 4 and 24 hours provided the strongest correlation. Further multicenter trials are indicated to provide further guidance in deciding when to discontinue massive transfusion.

Thoracoscopic versus open repair of tracheoesophageal fistula and esophageal atresia.

BACKGROUND/OBJECTIVE: Recent studies show the minimally invasive approach to the repair of esophageal atresia (EA) and tracheoesophageal fistula (TEF) is feasible. This study aimed to evaluate the efficacy and safety of the thoracoscopic versus open techniques. METHODS: We performed a retrospective review of EA/TEF cases from June 2000 to July 2006. Patient characteristics, operative time, blood loss, duration of narcotic usage, time to extubation, time to first oral feeding, length of stay, complications, and follow-up were analyzed. RESULTS: Thirty-five type-C EA/TEF patients were evaluated. Two patients with excessively long gaps who required esophageal "bougienage" stretching were excluded. Twenty-five patients underwent traditional repair through thoracotomy. There were 8 thoracoscopic attempts, 7 of which were successfully completed without a conversion. The mean operative time was 130 minutes (range, 75-240) for the thoracoscopic approach, compared to 123 (range, 82-205) for the thoracotomy; mean duration of narcotic use was 5 days (range, 1-12), as compared to 23 (range, 2-190); the mean time to extubation was 4.6 days (range, 1-12), compared to 19 (range, 3-150); the mean days to per os feeding were 9.8 days (range, 7-17) versus 37 (range, 7-360); and the mean length of stay was 21.8 days (range, 11-38), compared to 66 (range, 8-280). There were no intraoperative complications or deaths in either group. The anastomotic leak rate was 14 versus 20%, whereas the stricture rate was 14 versus 50% for the closed and open techniques, respectively. Of the thoracoscopic group, 87.5% had at least one major associated anomaly, compared with 70% of patients undergoing thoracotomy. Follow-up for the thoracoscopic and open groups were 18 and 28 months, respectively. CONCLUSION: Our results suggest that the outcomes of the thoracoscopic technique are comparable to that of the open technique. However, the number is small, and more data are needed to further evaluate the procedure.

Molecular signaling in necrotizing enterocolitis: regulation of intestinal COX-2 expression.

Necrotizing enterocolitis (NEC) is the most common surgical emergency in premature infants. The underlying etiology of NEC remains unknown, although bacterial colonization of the gut, formula feeding, and perinatal stress have been implicated as putative risk factors. The disease is characterized by exuberant gut inflammation leading to ischemia and coagulation necrosis of the intestinal epithelium. The molecular and cellular mechanisms responsible for these pathologic changes are poorly understood. It has been shown that various exogenous and endogenous mediators such as lipopolysaccharide, inflammatory cytokines, platelet activating factor, and nitric oxide may play a role in the pathogenesis of NEC. Recent studies in our laboratory and others have established a link between NEC and activation of cyclooxygenase-2, the enzyme that catalyzes the rate-limiting step in the biosynthesis of prostanoids. The challenge is in defining the molecular signaling pathways leading to accumulation of these mediators early in the disease progression, before the onset of tissue necrosis and systemic sepsis. Identification and characterization of these pathways could lead to the development of novel treatment strategies to alleviate the morbidity and mortality associated with NEC.

Mathematical modeling in necrotizing enterocolitis--a new look at an ongoing problem.

Necrotizing enterocolitis (NEC) is the most common and lethal disease that affects the gastrointestinal (GI) tract of the premature infant. The etiology of NEC remains undefined. The only consistent epidemiological precursors for NEC are prematurity and enteral alimentation. Various inflammatory mediators, including tumor necrosis factor (TNF)-a, interleukin (IL)-1, IL-6, IL-8, IL-10, IL-18, platelet-activating factor (PAF), and nitric oxide (NO) have been implicated in the pathogenesis of NEC, but the kinetics and role of these agents are ill-defined. Currently, there are no biomarker predictors of NEC risk and severity. Sera or tissue from early time points in the development of the disease may help delineate early inflammatory events that predispose an individual to NEC, thus providing an interventional opportunity. We suggest that the lack of diagnostic and therapeutic modalities for NEC are due to the absence of a systems view of the disease, which in turn is hindered by a lack of sensitive physiological measurements that predict perturbations in the intestinal tissue compartment and an inability to reliably test serial samples for the presence of inflammatory mediators in small volumes and in a high-throughput manner. Computational modeling is a useful tool in the study of complex systems such as the inflammatory process. Computation models provide an "existence proof" for a given mechanism, uncover subtle inconsistencies between the underlying hypotheses and quantitative data, and force one to ask how much is known. We suggest that a properly validated and calibrated mathematical model of inflammation and its pathologic consequences in NEC will be useful for predicting the physiologic and biologic response in infants suffering from the disease.

Bladder prolapse through a patent urachus: fetal and neonatal features.

We report a term male neonate who was born with a large, red, tubular, mucosa-lined umbilical mass containing a patent lumen. Prenatal ultrasonographic screening at 20 to 28 weeks of gestation revealed a large cyst at the umbilicus, communicating with the urinary bladder. The cyst resolved at 32 weeks, and a small solid mass was newly seen on the fetal abdominal wall, inferior to the umbilical cord insertion. At operation, the mass was discovered to be the prolapsed, open, everted dome of the urinary bladder. The dome was resected, and the bladder was repaired in 2 layers after identification of the ureteral orifices. Bladder prolapse through a patent urachus can be predicted by prenatal ultrasound and has a distinct neonatal appearance.

Fatal variceal rupture after sildenafil use: report of a case.

Sildenafil may increase the risk of variceal bleeding in portal hyptertension by increasing splanchnic blood flow. We report herein the second case of variceal rupture after sildenafil use.