A Comparison of Outcomes for Spinal Trauma Patients at Level I and Level II Centers.

STUDY DESIGN: Retrospective analysis of a national database. OBJECTIVE: To characterize the spine trauma population, describe trauma center (TC) resources, and compare rates of outcomes between the American College of Surgeons (ACS) level I and level II centers. SUMMARY OF BACKGROUND DATA: Each year, thousands of patients are treated for spinal trauma in the United States. Although prior analyses have explored postsurgical outcomes for patients with trauma, no study has evaluated these metrics for spinal trauma at level I and level II TCs. MATERIALS AND METHODS: The ACS Trauma Quality Improvement Program was queried for all spinal trauma cases between 2013 and 2015, excluding polytrauma cases, patients discharged within 24 hours, data from TCs without a designated level, and patients transferred for treatment. RESULTS: Although there were similar rates of severe spine traumas (Abbreviated Injury Scale≥3) at ACS level I and level II centers (P=0.7), a greater proportion of level I patients required mechanical ventilation upon emergency department arrival (P=0.0002). Patients at level I centers suffered from higher rates of infectious complications, including severe sepsis (0.58% vs. 0.31%, P=0.02) and urinary tract infections (3.26% vs. 2.34%, P=0.0009). Intensive care unit time (1.90 vs. 1.65 days, P=0.005) and overall length of stay (8.37 days vs. 7.44 days, P<0.0001) was higher at level I TCs. Multivariate regression revealed higher adjusted overall complication rates at level II centers (odds ratio, 1.15, 95% confidence interval, 1.06-1.24; P<0.001), but no difference in mortality (odds ratio, 1.18; 95% confidence interval, 0.92-1.52; P>0.10). CONCLUSIONS: ACS level I TCs possess larger surgical staff and are more likely to be academic centers. Patients treated at level I centers experience fewer overall complications but have a greater incidence of infectious complications. Mortality rates are not statistically different.

Defining the Mechanism of Subarachnoid Hemorrhage-Induced Pyrexia.

Fever can affect the majority of patients with subarachnoid hemorrhage (SAH) and many times no identifiable source is found for the fever whether infectious or sterile, like deep vein thrombosis. We hypothesized that fever in SAH is mediated by a NON-cyclo-oxygenase-dependent mechanism, which we neologized as subarachnoid hemorrhage-induced pyrexia (SAHiP). This hypothesis was investigated using genetically modified mice, pharmacological manipulation, cerebrospinal fluid from SAH patients, and a large cohort of SAH patients. Mice with deletions of neuronal prostaglandin EP3 receptor, global toll-like receptor 4 (TLR4), myeloid TLR4, and microglial TLR4 were subjected to SAH after being implanted with thermometers. Pathways necessary for SAHiP were identified. In SAH patients, cerebrospinal fluid was examined by flow cytometry and correlated with SAHiP. From a large cohort of SAH patients, independent associations with SAHiP were determined using logistic regression analysis. In our mouse model of SAH, microglial TLR4 is necessary for SAHiP, but independent of the neuronal prostaglandin EP3 receptor, cyclo-oxygenase, and prostaglandins. Macrophages from the cerebrospinal fluid of SAH patients with SAHiP expressed more TLR4-co-receptor than SAH patients without SAHiP. In a large cohort of SAH patients, SAHiP was found to be independently, yet inversely, associated with acetaminophen administration. SAHiP is independent of the neuronal prostaglandin EP3 receptor, cyclo-oxygenase, and prostaglandins, but dependent on microglial/macrophage TLR4 with evidence from both SAH mouse models and SAH patients.