BACKGROUND:Trauma centers use injury mechanism, physiology, and anatomic criteria to determine the extent of trauma team activation (TTA). We examined whether physiologic variables in our three-tier TTA system stratified patients appropriately by injury severity and mortality. METHODS:The trauma registry at our Level I trauma center was retrospectively reviewed for full (level 1 or L1), partial (level 2 or L2), and limited (level 3) adult TTA. Data were collected on age, injury severity score (ISS), hospital length of stay, systolic blood pressure (SBP), heart rate, respiratory rate (RR), Glasgow coma score (GCS), and intubation status. Penetrating injuries, traumatic arrests, and interfacility transfers were excluded. Data are median (25%75%). Statistical analysis included hazard ratios (HzR), Kruskal-Wallis, chi, and survival analyses. The p value overall was <0.05, and pair wise was <0.05 versus L1. RESULTS:There were 494 adult TTAs for blunt injury from the scene out of 1,969 admissions. Variables associated with mortality (HzR; 95% confidence interval) by univariate analysis include SBP <90 (9.4; 4.2, 21.2), RR >29 or <10 (17.8; 4.8, 66.0), intubation status (4.5; 2.3, 8.9), and GCS <8 (9.7; 4.8, 19.9). When combined in a multivariate model to evaluate multiple predictors simultaneously, SBP <90 and GCS <8 appear to be the strongest predictors of mortality (RR and intubation were not significant in the presence of SBP and GCS). The three-tier system identified patients with increased ISS and early (< or =4 weeks) mortality risk. There was a statistically significant difference in survival between L1 and L2 at 38 days, but not for >38 days (p = 0.739). CONCLUSIONS:TTA criteria selected patients with greater ISS and early mortality, but impact on long-term survival may not be appreciated. Full TTA criteria for blunt injury may be limited to GCS <8, SBP <90, RR >29 or <10, and intubation status.

Objective: During sepsis, a two- to four-fold increase in circulating growth hormone (GH) is seen with 40-50% reductions in plasma insulin-like growth factor (IGF)-I. The suppressors of cytokine signaling (SOCS), inhibitors of cytokine, and growth factor signaling via the janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway have been implicated in the development of hepatic GH resistance. In this study we examine the effects of sepsis on GH-induced IGF-I expression and potential mechanisms for GH resistance.Design: Prospective experimental study.Setting: University research laboratory.Subjects: Male Sprague-Dawley rats.Interventions. Rats were randomized to laparotomy alone (control) or implantation of fecal agar pellets inoculated with Escherichia coli and Bacteroides fragilis (sepsis). GH was injected intravenously to assess hepatic IGF-I synthesis and GH signaling.Measurements and Main Results: Plasma IGF-I was measured in both groups at baseline (4 hrs postoperatively) and then again at 12 hrs and 24 hrs after GH administration. Basal IGF-I levels were similar in both groups, but controls had a 35% increase in IGF-I at 12 hrs, whereas septic rats demonstrated reductions in circulating IGF-I at 12 and 24 hrs after GH. Hepatic expression of SOCS-1, -2, -3, and cytokine-inducible SH2-containing protein (CIS) were determined at 1, 4, 8, and 24 hrs in septic and control rats by Northern blot SOCS-1, SOCS-3, and CIS messenger RNA in liver were increased from 4 to 8 hrs after the induction of sepsis (p < .05 for SOCS-1 and -3). Total GH receptor (GHR), JAK2, and STAT5 signaling proteins and the time course of STAT5 activation were also measured in liver after recombinant human GH administration by immunoblot and electrophoretic mobility shift analysis. Levels of total GHR, JAK2, and STAT5 were unaltered in liver from septic rats. However, phosphorylated STAT5 and STAT5 DNA binding were significantly reduced 30 mins after GH administration in liver from septic rats.Conclusions: Sepsis diminished STAT5 phosphorylation and activity in liver as well as plasma IGF-I following GH administration. Hepatic messenger RNA expression of SOCS-1, SOCS-3, and CIS was transiently increased during abdominal sepsis and temporally associated with the development of hepatic GH resistance.

BACKGROUND:Both the systemic release of inflammatory mediators and activation of the neuroendocrine axis by sensory afferent nerves (SANs) have been implicated as initiators of the metabolic response to infection. In this study, we investigate the role of SANs as mediators of protein catabolism and the insulin-like growth factor (IGF) axis during abdominal sepsis using capsaicin (Cap) to selectively destroy nociceptive sensory axons.METHODS:Four groups of male Sprague-Dawley rats were studied: Control, Control+Cap, Sepsis, and Sepsis+Cap. Rats were injected with Cap (75 mg/kg) on day 1 and (50 mg/kg) on day 2 to destroy SANs. Time-matched control and septic rats were pair-fed and injected with vehicle on the same schedule. Controls underwent sham laparotomy, while septic rats had a fecal-agar pellet inoculated with Escherichia coli and Bacteroides fragilis implanted in the peritoneal cavity. Blood and tissues were harvested 5 days after the induction of sepsis. Plasma IGF-I, IGFBP-1, and -3 were measured by radioimmunoassay and Western blot analysis. IGF-I, acid-labile subunit (ALS), IGFBP-1 and -3 mRNA levels were determined by Northern blot analysis.RESULTS:Mortality was 40% in septic rats vs 0% in the sepsis+Cap group. Capsaicin had no effect on muscle mass, protein content, or the IGF system in control rats. However, sepsis-induced reductions in gastrocnemius mass (25%) and protein content (35%) were ameliorated by capsaicin. The sepsis-induced decrease in hepatic IGF-I mRNA and circulating IGF-I (26%), as well as the 4-fold increase in plasma IGFBP-1 and hepatic IGFBP-1 mRNA were prevented by capsaicin.CONCLUSIONS:Capsaicin-sensitive nerves mediate mortality, the catabolism of skeletal muscle, and selected elements of the IGF system during abdominal sepsis. The results suggest an important role for nociceptive SANs and the neuroendocrine system in mediating the host response to abdominal infection.

BACKGROUND Clinical pathways are believed to improve patient care and reduce costs. Our hypothesis was that a gastric bypass pathway would decrease hospital resource utilization and cost of care without adversely affecting patient care. METHODS The prepathway (Pre) group consisted of 16 gastric bypasses (6/98 to 3/99). The postpathway (Post) group includes 12 gastric bypass procedures performed after institution of the clinical pathway (4/99 to 12/99). The impact of the clinical pathway on hospital length of stay (LOS) and resource utilization was investigated. A comparison of costs was performed using cost/charge ratios. Hospital readmissions and postoperative complications were also examined. RESULTS Despite increased obesity/medical acuity of the Post group, hospital LOS decreased by 3 days (P < 0.0001). Total hospital costs decreased by over $1600/case (>15%). Postpathway savings were greatest for room and board (34%), supplies (41%), and lab/radiology costs (50%). An increase in OR costs (22%) was observed in the Post group. This was due to an increase in anesthesia time (epidural catheter placement) and equipment costs (ultrasonic shears). Despite reductions in hospital LOS and resource utilization, the complication rate (Pre 12%, Post 16%) was similar and two patients in each group required brief readmission. CONCLUSIONS A pathway for gastric bypass decreased hospital LOS and resource utilization. OR-related expenses account for 34-50% of total costs and must be monitored closely for surgical patients. The reduction in costs observed with this clinical pathway was not associated with an increase in postoperative complications or hospital readmission.

Bryant, D. Patrick MD; Cooney, Robert N. MD; Smith, J. Stanley MD; Haluck, and Randy S. MD Author Information