Faculty Bibliography

HYPOTHESIS: Discrepancies exist in complications and outcomes at teaching trauma centers (TTCs) vs nonteaching TCs (NTCs). DESIGN: Retrospective review of the National Trauma Data Bank research data sets (January 1, 2007, through December 31, 2008). SETTING: Level II TCs. PATIENTS: Patients at TTCs were compared with patients at NTCs using demographic, clinical, and outcome data. Regression modeling was used to adjust for confounding factors to determine the effect of house staff presence on failure to rescue, defined as mortality after an in-house complication. MAIN OUTCOME MEASURES: The primary outcome measures were major complications, in-hospital mortality, and failure to rescue. RESULTS: In total, 162 687 patients were available for analysis, 36 713 of whom (22.6%) were admitted to NTCs. Compared with patients admitted to TTCs, patients admitted to NTCs were older (52.8 vs 50.7 years), had more severe head injuries (8.3% vs 7.8%), and were more likely to undergo immediate operation (15.0% vs 13.2%) or ICU admission (28.1% vs 22.8%) (P < .01 for all). The mean Injury Severity Scores were similar between the groups (10.1 for patients admitted to NTCs vs 10.4 for patients admitted to TTCs, P < .01). Compared with patients admitted to TTCs, patients admitted to NTCs experienced fewer complications (adjusted odds ratio [aOR], 0.63; P < .01), had a lower adjusted mortality rate (aOR, 0.87; P = .01), and were less likely to experience failure to rescue (aOR, 0.81; P = .01). CONCLUSIONS: Admission to level II TTCs is associated with an increased risk for major complications and a higher rate of failure to rescue compared with admission to level II NTCs. Further investigation of the differences in care provided by level II TTCs vs NTCs may identify areas for improvement in residency training and processes of care.

BACKGROUND: Increasing evidence suggests that the spleen harbors stem cells that act as precursors to insulin-producing pancreas cells. Additionally, small studies with short-term follow-up associate splenectomy with increased rates of diabetes mellitus. The purpose of this study was to analyze the long-term effect of trauma splenectomy on blood glucose. MATERIALS AND METHODS: Patients were included if a blood glucose level was measured more than 5 y after trauma splenectomy or laparotomy with bowel repair. Mean blood glucose level was then compared between the two groups. RESULTS: During the 10-y study period 61 patients underwent trauma splenectomy and 50 survived until discharge. In comparison, 229 patients underwent trauma laparotomy and bowel repair and 207 survived until discharge. Nine splenectomy patients compared with 12 control patients had, blood glucose measured at least 5 y after initial trauma. Mean follow-up period was not significantly different between groups (splenectomy 82.8 +/- 17.6 mo versus control 96.0 +/- 44.3 mo, P = 0.41). In the splenectomy cohort mean glucose level was significantly higher compared with the control (114 +/- 34 mg/dL versus 90 +/- 13 mg/dL, P = 0.04), as was the number of patients with recorded blood glucose level greater than 130 mg/dL (4 patient versus 0 patients P = 0.02). One new diagnosis of diabetes mellitus was noted only in the trauma splenectomy cohort. CONCLUSIONS: This small study suggests that trauma splenectomy may be associated with hyperglycemia at long-term follow-up.

BACKGROUND: The purpose of this study was to evaluate how beta-adrenergic receptor inhibition after traumatic brain injury (TBI) alters changes in early cerebral glucose metabolism and motor performance, as well as cerebral cytokine and heat shock protein (HSP) expression. METHODS: Mouse cerebral glucose metabolism was measured by microPET fluorodeoxyglucose uptake and converted into standardized uptake values (SUV). Four groups of C57/Bl6 mice (wild type [WT]) were initially evaluated: sham or TBI, followed by tail vein injection of either saline or a nonselective beta-adrenergic receptor inhibitor (propranolol, 4 mg/kg). Then motor performance, cerebral cytokine, and HSP70 expression were studied at 12 hours and 24 hours after sham injury or TBI in WT mice treated with saline or propranolol and in beta1-adrenergic/beta2-adrenergic receptor knockout (BARKO) mice treated with saline. RESULTS: Cerebral glucose metabolism was significantly reduced after TBI (mean SUV TBI, 1.63 vs. sham 1.97, p < 0.01) and propranolol attenuated this reduction (mean SUV propranolol, 1.89 vs. saline 1.63, p < 0.01). Both propranolol and BARKO reduced motor deficits at 24 hours after injury, but only BARKO had an effect at 12 hours after injury. TBI WT mice treated with saline performed worse than propranolol mice at 24 hours after injury on rotarod (23 vs. 44 seconds, p < 0.01) and rearing (130 vs. 338 events, p = 0.01) results. At 24 hours after injury, sham BARKO and TBI BARKO mice were similar on rotarod (21 vs. 19 seconds, p = 0.53), ambulatory testing (2,891 vs. 2,274 events, p = 0.14), and rearing (129 vs. 64 events, p = 0.09) results. Interleukin 1beta expression was affected by BARKO and propranolol after TBI; attenuation of interleukin 6 and increased HSP70 expression were noted only with BARKO. CONCLUSION: beta-adrenergic receptor inhibition affects cerebral glucose metabolism, motor performance, as well as cerebral cytokine and HSP expression after TBI.

BACKGROUND: Conclusions from in vivo and in vitro studies suggest hypothermia may be protective in traumatic brain injury (TBI). Few studies evaluated the effect of admission temperature on outcomes. The purpose of this study is to examine the relationship between admission hypothermia and mortality in patients with isolated, blunt, moderate to severe TBI. METHODS: The Los Angeles Trauma Database was queried for all patients >/= 14 y of age with isolated, blunt, moderate to severe TBI (head abbreviated injury score (AIS) >/= 3, all other <3), admitted between 2005 and 2009. The study population was then stratified into two groups by admission temperature: hypothermic (35 degrees C). Demographic characteristics and outcomes were compared between groups. Logistic regression analysis was used to determine the relationship between admission hypothermia and mortality. RESULTS: A total of 1834 patients were analyzed and then stratified into two groups: hypothermic (n = 44) and normothermic (n = 1790). There was a significant difference noted in overall mortality (25% versus 7%), with the hypothermic group being four times more likely to succumb to their injuries. After adjusting for confounding factors, admission hypothermia was independently associated with increased mortality (AOR 2.5; 95% CI 1.1-6.3; P = 0.04). CONCLUSIONS: Although in-vivo and in-vitro studies demonstrate induced hypothermia may be protective in TBI, our study demonstrates that admission hypothermia was associated with increased mortality in isolated, blunt, moderate to severe TBI. Further prospective research is needed to elucidate the role of thermoregulation in patients sustaining TBI.

We sought to investigate the effect of trauma center designation on organ donor outcomes during a 5-year period. A retrospective study of the southern California regional Organ Procurement Organization database comparing trauma centers (n = 25) versus nontrauma centers (n = 171) and Level I (n = 7) versus Level II (n = 18) trauma centers between 2004 and 2008 was performed. A total of 16,830 referrals were evaluated and 44 per cent were from trauma centers. When compared with nontrauma centers (n = 171), trauma centers (n = 25) had a higher percentage of medically suitable eligible deaths (29 vs 16%, P < 0.001), total eligible deaths (22 vs 12%, P < 0.001), and eligible donors (14 vs 7%, P < 0.001). Trauma Centers had a significantly higher number of organs procured per donor (4.0 +/- 1.6 vs 3.5 +/- 1.6, P < 0.001), organs transplanted per donor (OTPD) (3.6 +/- 1.8 vs 2.8 +/- 1.8, P < 0.001), and higher organ yield (per cent 4 or greater OTPD [48 vs 31%, P < 0.001]). No significant differences were found between Level I and Level II trauma centers. Trauma centers demonstrate significantly better organ donor outcomes compared with nontrauma centers. Factors responsible for improved outcomes at trauma centers should be evaluated, reproduced, and disseminated to nontrauma centers to alleviate the growing organ shortage crisis.

BACKGROUND: Several retrospective clinical studies and recent prospective animal models demonstrate improved outcomes with beta-blocker administration after isolated blunt head injury. However, no investigations to date have examined the influence of race on the potential therapeutic effectiveness of these medications. Our hypothesis was that mortality benefits associated with beta-blocker exposure after isolated blunt head injury varies based on ethnicity. METHODS: The trauma registry and the surgical intensive care unit (ICU) databases of an academic Level I trauma center were used to identify all patients sustaining blunt head injury requiring ICU admission from July 1998 to December 2009. Patients sustaining major associated extracranial injuries (Abbreviated Injury Scale [AIS] score >/= 3 in any body region) were excluded. Patient demographics, injury profile, Injury Severity Score, and beta-blocker exposure were abstracted. The primary outcome evaluated was in-hospital mortality stratified by ethnicity. RESULTS: During the 11-year study period, 3,750 patients were admitted to the Los Angeles County + University of Southern California Medical Center trauma ICU because of blunt trauma. Of these, 65% (n = 2,446) had an "isolated" head injury. When stratified by race, most patients were Hispanics (60%), followed by Whites (21%), Asians (11%), and African Americans (8%). After adjusting for confounding variables with multivariate regression, only those of Asian and Hispanic descent demonstrated significantly improved outcomes associated with beta-blocker administration. CONCLUSIONS: Our results indicate that beta-blockade after traumatic brain injury may not benefit all races equally. Further prospective research is necessary to assess this discrepancy in treatment benefit and explore other possible therapeutic interventions.

BACKGROUND: The association between admission heart rate (AHR) and mortality after trauma can assist initial emergency department triage and resuscitation. In addition, increased AHR is often associated with sympathetic hyperactivity which may require targeted treatment. We determined whether AHR was a predictor for mortality in trauma patients. METHODS: The Los Angeles County Trauma System Database was queried for all injured patients admitted between 1998 and 2005 (n = 147,788). Traumatic brain injury (TBI) patients (head Abbreviated Injury Scale score >/= 3) were excluded. Demographics were compared at various AHR subgroups (<50, 50-59, 60-69, 70-79, 80-89, 90-99, 100-109, and >/= 110). Mortality was compared at various AHR ranges, and logistic regression was performed to determine significance. RESULTS: After exclusions, 103,799 trauma patients requiring admission were identified; overall mortality was 1.4%. AHR 80 to 89 demonstrated a statistically significant lower mortality (0.5%) compared with all other AHR ranges, except AHR 70 to 79 (0.6%). In trauma patients who required admission, AHR 70 to 79 and 80 to 89 were predictors of lower mortality. Mortality for 22,232 moderate to severely injured patients was 5.5% and AHR 80 to 89 demonstrated a statistically lower mortality (2.0%) than all other AHR ranges, except AHR 70 to 79 (1.9%). After moderate to severe trauma, AHR <60 and >/= 100 were associated with significantly higher mortality. CONCLUSION: Mortality after trauma increases outside the AHR range of 70 to 89 beats per minute. AHR ranges previously considered "normal" were associated with significantly increased mortality. Prospective research is required to evaluate if resuscitation goals should target heart rate at the 70 to 89 range.

BACKGROUND: Recent evidence supports the beneficial effect of alcohol on patients with traumatic brain injury (TBI). Pneumonia is a known complication following TBI; thus, the purpose of this study was to evaluate the effects of alcohol on pneumonia rates following moderate to severe TBI. METHODS: From 2005 to 2009, the Los Angeles County Trauma Database was queried for all patients >/= 14 y of age with isolated moderate to severe TBI and admission serum alcohol levels. The incidence of pneumonia was compared between TBI patients with and without a positive blood alcohol concentration (BAC) level. The study population was then stratified into four BAC levels: None (0 mg/dL), low (0-100 mg/dL), moderate (100-230 mg/dL), and high (>/= 230 mg/dL). Pneumonia rates were compared across these levels. RESULTS: A total of 3547 patients with isolated, moderate to severe TBI were evaluated. Nearly 66% tested positive for alcohol. The pneumonia rate was significantly lower in the TBI patients who tested positive for alcohol (2.5%) compared with those who tested negative (4.0%, P = 0.017). The pneumonia rate also decreased across increasing BAC levels (linear trend P = 0.03). After logistic regression analysis, a positive ethanol (ETOH) level was associated with a reduced incidence of pneumonia (AOR = 0.62; 95%CI: 0.41-0.93; P = 0.020). CONCLUSION: A positive serum alcohol level was associated with a significantly lower pneumonia rate in isolated, moderate to severe TBI patients. This may explain the observed mortality reduction in TBI patients who test positive for alcohol. Additional research is warranted to investigate the potential therapeutic implications of this association.

Trauma centers are designated by the American College of Surgeons (ACS) into four different levels based on resources, volume, and scientific and educational commitment. The purpose of this study was to evaluate the relationship between ACS center designation and outcomes after early thoracotomy for trauma. The National Trauma Databank (v. 7.0) was used to identify all patients who required early thoracotomy. Demographics, clinical data, and outcomes were extracted. Patients were categorized according to ACS trauma center designation. Multivariate logistic regression was used to evaluate the impact of ACS trauma center designation on mortality. From 2002 to 2006, 1834 (77.4%) patients were admitted to a Level I ACS verified trauma center, 474 (20.0%) to a Level II, and 59 (3.6%) to a Level III/IV facility. After adjusting for differences between the groups, there were no significant differences in mortality (overall: 53.3% for Level I, 63.1% for Level II, and 52.5% for Level III/IV, adjusted P = 0.417; or for patients arriving in cardiac arrest: 74.9% vs 87.1% vs 85.0%, P = 0.261). Subgroup analysis did not show any significant difference in survival irrespective of mechanism of injury. Glasgow Coma Scale score 16, no admission systolic blood pressure, time from admission to thoracotomy, and nonteaching hospitals were found to be independent predictors of death. For trauma patients who have sustained injuries requiring early thoracotomy, ACS trauma center designation did not significantly impact mortality. Nonteaching institutions however, were independently associated with poorer outcomes after early thoracotomy. These findings may have important implications in educational commitment of institutions. Further prospective evaluation of these findings is warranted.

BACKGROUND: Although avoiding hypotension is a primary focus after trauma, elevated systolic blood pressure (SBP) is frequently disregarded. The purpose of this study was to determine the association between elevated admission SBP and delayed outcomes after trauma. METHODS: The Los Angeles County Trauma System Database was queried for all patients between 2003 and 2008 with blunt injuries who survived for at least 2 days after admission. Demographics and outcomes (pneumonia and mortality) were compared at various admission SBP subgroups (>/=160 mm Hg, >/=170 mm Hg, >/=180 mm Hg, >/=190 mm Hg, >/=200 mm Hg, >/=210 mm Hg, and >/=220 mm Hg). Patients with moderate-to-severe traumatic brain injury (TBI), defined as head Abbreviated Injury Score >/=3, were then identified and compared with those without using multivariable logistic regression. RESULTS: Data accessed from 14,382 blunt trauma admissions identified 2,601 patients with moderate-to-severe TBI (TBI group) and 11,781 without moderate-to-severe TBI (non-TBI group) who were hospitalized >/=2 days. Overall mortality was 2.9%, 7.1% for TBI patients, and 1.9% for non-TBI patients. Overall pneumonia was 4.6%, 9.5% for TBI patients, and 3.6% for non-TBI patients. Regression modeling determined SBP >/=160 mm Hg was a significant predictor of mortality in TBI patients (adjusted odds ratio [AOR], 1.59; confidence interval [CI], 1.10-2.29; p = 0.03) and non-TBI patients (AOR, 1.47; CI, 1.14-1.90; p = 0.003). Similarly, SBP >/=160 mm Hg was a significant predictor for increased pneumonia in TBI patients (AOR, 1.79; CI, 1.30-2.46; p = 0.0004), compared with non-TBI patients (AOR, 1.28; CI, 0.97-1.69; p = 0.08). CONCLUSIONS: In blunt trauma patients with or without TBI, elevated admission SBP was associated with worse delayed outcomes. Prospective research is necessary to determine whether algorithms that manage elevated blood pressure after trauma, especially after TBI, affect mortality or pneumonia.