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Stewart C Wang

Publications and source records attributed to Stewart C Wang.

At least 19 recordsLinked to original sources
PubMed2006

Attenuating burn wound inflammatory signaling reduces systemic inflammation and acute lung injury.

The relationship between local inflammation and the subsequent systemic inflammatory response is poorly described. In a burn injury model, the dermal inflammatory response may act as an ongoing trigger for the systemic inflammatory response syndrome (SIRS) and subsequent systemic complications. We hypothesized that topical attenuation of burn wound inflammatory signaling will control the dermal inflammatory source, attenuate SIRS, and reduce acute lung injury. Mice received a 30% total body surface area burn. Subgroups were treated with specific p38 MAPK inhibitor or vehicle, which was topically applied to wounds. Topical p38 MAPK inhibition significantly reduced burn wound inflammatory signaling and subsequent systemic expression of proinflammatory cytokines and chemokines. In vitro macrophage functional assays demonstrated a significant attenuation in serum inflammatory mediators from animals receiving the topical inhibitor. Topical p38 MAPK inhibition resulted in significantly less pulmonary inflammatory response via reduction of pulmonary neutrophil sequestration, pulmonary cytokine expression, and a significant reduction in pulmonary microvascular injury and edema formation. Although dermal activating transcription factor-2, a downstream p38 MAPK target, was significantly reduced, there was no reduction in pulmonary activating transcription factor-2 expression, arguing against significant systemic absorption of the topical inhibitor. These experiments demonstrate a strong interaction between dermal inflammation and systemic inflammatory response. Attenuating local inflammatory signaling appears effective in reducing SIRS and subsequent systemic complications after burn injury.

Animals↗
PubMed2006

Factors influencing pediatric Injury Severity Score and Glasgow Coma Scale in pediatric automobile crashes: results from the Crash Injury Research Engineering Network.

BACKGROUND/PURPOSE: Motor vehicle crashes account for more than 50% of pediatric injuries. Triage of pediatric patients to appropriate centers can be based on the crash/injury characteristics. Pediatric motor vehicle crash/injury characteristics can be determined from an in vitro laboratory using child crash dummies. However, to date, no detailed data with respect to outcomes and crash mechanism have been presented with a pediatric in vivo model. METHODS: The Crash Injury Research Engineering Network is comprised of 10 level 1 trauma centers. Crashes were examined with regard to age, crash severity (DeltaV), crash direction, restraint use, and airbag deployment. Multiple logistic regression analysis was performed with Injury Severity Score (ISS) and Glasgow Coma Scale (GCS) as outcomes. Standard age groupings (0-4, 5-9, 10-14, and 15-18) were used. The database is biases toward a survivor population with few fatalities. RESULTS: Four hundred sixty-one motor vehicle crashes with 2500 injuries were analyzed (242 boys, 219 girls). Irrespective of age, DeltaV > 30 mph resulted in increased ISS and decreased GCS (eg, for 0-4 years, DeltaV < 30: ISS = 10, GCS = 13.5 vs DeltaV > 30: ISS = 19.5, GCS = 10.6; P < .007, < .002, respectively). Controlling for DeltaV, children in lateral crashes had increased ISS and decreased GCS versus those in frontal crashes. Airbag deployment was protective for children 15 to 18 years old and resulted in a lower ISS and higher GCS (odds ratio, 2.1; 95% confidence interval, 0.9-4.6). Front-seat passengers suffered more severe (ISS > 15) injuries than did backseat passengers (odds ratio, 1.7; 95% confidence interval, 0.7-3.4). A trend was noted for children younger than 12 years sitting in the front seat to have increased ISS and decreased GCS with airbag deployment but was limited by case number. CONCLUSION: A reproducible pattern of increased ISS and lower GCS characterized by high severity, lateral crashes in children was noted. Further analysis of the specific injuries as a function and the crash characteristic can help guide management and prevention strategies.

Accidents, Traffic↗
PubMed2006

Cardiomyocyte function after burn injury and lipopolysaccharide exposure: single-cell contraction analysis and cytokine secretion profile.

A component of multiorgan dysfunction in burned patients is heart failure. Burn trauma induces cytokine synthesis of interleukin (IL) 1beta, IL-6, and tumor necrosis factor alpha (TNF-alpha) which can negatively impact cardiac function. Infectious complications are common following severe burn injury. We hypothesized that burn injury and lipopolysaccharide (LPS) exposure independently influence peak cardiomyocyte contraction and cytokine secretion. Rats underwent a full-thickness 30% total body surface area scald or sham burn. At 1, 6, 12, and 24 h after burn, cardiomyocytes were isolated and incubated with increasing LPS doses. Peak sarcomere shortening and contractile velocity parameters were recorded using a variable-rate video camera with sarcomere length detection software. Supernatants were assayed for IL-1beta, IL-6, and TNF-alpha by ELISA. Peak sarcomere shortening was decreased in the burn group at 1, 6, 12, and 24 h after burn. IL-1beta, IL-6, and TNF-alpha levels were increased in cardiomyocytes isolated 1 h after burn compared with sham controls, but returned to sham levels at 6, 12, and 24 h after burn. LPS exposure caused dose-dependent decreases in sarcomere shortening in sham and burn animals. LPS exposure did not produce increased cardiomyocyte cytokine expression. Burn injury diminished peak sarcomere shortening. Whereas exposure to LPS did not have an effect on cardiomyocyte cytokine expression, LPS significantly inhibited sarcomere shortening in a dose-dependent fashion. Combined burn and LPS exposure inhibited sarcomere shortening more than each alone. These results demonstrate that LPS exposure and burn injury independently decrease peak cardiac shortening. These decreases did not directly correlate with the levels of cytokines released in response to each stressor.

Animals↗
PubMed2006

Topical p38MAPK inhibition reduces dermal inflammation and epithelial apoptosis in burn wounds.

Thermal injury induces dermal inflammatory and proapoptotic signaling. These phenomena extend burn wound size and trigger a systemic inflammatory response, factors known to adversely affect outcomes. p38MAPK is known to trigger inflammatory responses and induce epithelial proapoptotic genes. We hypothesize that topical p38MAPK inhibition will attenuate excessive inflammatory and apoptotic signaling and reduce dermal tissue loss. Rats were given a 30% total body surface area partial thickness burn or sham injury. Some of the animals were treated with a p38MAPK inhibitor or vehicle, which was applied directly to the wound. Dermal inflammation was investigated with enzyme-linked immunosorbent assay, reverse transcriptase polymerase chain reaction, myeloperoxidase assay, and Evans blue extravasation. Apoptotic changes were detected using terminal deoxynucleotidyl transferase dUTP nick-end labeling assay and Caspase-3 in situ staining. Burn injury activated dermal p38MAPK and induced a significant rise in dermal IL-6, TNF-alpha, and IL-1beta expression. Neutrophil sequestration, microvascular damage, and hair follicle apoptosis were significantly elevated after injury. Topical p38MAPK inhibition significantly attenuated downstream dermal p38MAPK targets, proinflammatory cytokine expression, neutrophil sequestration, and microvascular injury. A significant reduction in hair follicle apoptosis was seen. This study demonstrates the attenuation of burn-induced cellular stress by topical application of p38MAPK inhibitors. Blunting early excessive inflammatory signaling may be an efficient strategy to improve patient outcomes after burn injury.

Administration, Topical↗
PubMed2006

Gene therapy with lipopolysaccharide binding protein for gram-negative pneumonia: respiratory physiology.

BACKGROUND: Lipopolysaccharide binding protein (LBP) plays an essential role in the pulmonary immune response to gram-negative bacterial infection. LBP knockout mice with gram-negative pneumonia have increased mortality compared with wild-type controls. This mortality difference can be abolished with systemic LBP gene therapy. We postulate that LBP knockout mice will develop derangements in lung physiology from gram-negative pneumonia and that these changes can be reversed with systemic LBP gene therapy. METHODS: Twelve- to 16-week-old C57BL/6 wild-type mice and/or sex, age, matched LBP knockout mice were administered 1 x 10(3) colony-forming units/mouse of Klebsiella pneumoniae by intratracheal inoculation. Treated mice were administered 5 x 10(9) plaque-forming units of recombinant adenovirus containing either the gene for LBP or the irrelevant control protein beta-galactosidase by intravenous injection 2 days before bacterial inoculation. Respiratory physiology parameters were measured preinoculation and 24 hours postbacterial inoculation. RESULTS: Administration of LBP by systemic gene therapy to LBP knockout mice improved 7-day survival from Klebsiella pneumonia to a level equivalent to wild-type mice exposed to the same dose of bacteria (42 vs. 43% survival). LBP knockout mice given the LBP gene therapy demonstrated increased 14-day survival from Klebsiella pneumonia when compared with controls treated with beta-galactosidase (28 vs. 0%, p < 0.001). LBP knockout mice developed significant differences in respiratory rate, minute ventilation, and enhanced pause (Penh), when compared with wild-type mice with Klebsiella pneumonia. These respiratory derangements were prevented with adenoviral delivery of the LBP gene before K. pneumoniae inoculation. CONCLUSIONS: Gram-negative pneumonia produces measurable changes in mortality and respiratory physiology between wild-type and LBP knockout mice. These changes can be prevented in LBP knockout mice by systemic gene therapy to restore innate immunity.

Acute-Phase Proteins↗
PubMed2005

An essential role for complement C5a in the pathogenesis of septic cardiac dysfunction.

Defective cardiac function during sepsis has been referred to as "cardiomyopathy of sepsis." It is known that sepsis leads to intensive activation of the complement system. In the current study, cardiac function and cardiomyocyte contractility have been evaluated in rats after cecal ligation and puncture (CLP). Significant reductions in left ventricular pressures occurred in vivo and in cardiomyocyte contractility in vitro. These defects were prevented in CLP rats given blocking antibody to C5a. Both mRNA and protein for the C5a receptor (C5aR) were constitutively expressed on cardiomyocytes; both increased as a function of time after CLP. In vitro addition of recombinant rat C5a induced dramatic contractile dysfunction in both sham and CLP cardiomyocytes, but to a consistently greater degree in cells from CLP animals. These data suggest that CLP induces C5aR on cardiomyocytes and that in vivo generation of C5a causes C5a-C5aR interaction, causing dysfunction of cardiomyocytes, resulting in compromise of cardiac performance.

Animals↗
PubMed2005

Burn wounds infected with Pseudomonas aeruginosa triggers weight loss in rats.

BACKGROUND: Despite dramatic improvements in the management of burns, infection still remains a serious risk for the burn patient. The aim of this study was to shed light on the impact of acute burn injury with or without infection on cytokine profiles. METHODS: Sprague-Dawley rats (n = 21) were randomized into three groups: 1) burn only 2) burn and infection or 3) sham burn. Weight was monitored and blood was collected for cytokine ELISA, LPS quantification, and peripheral blood analysis. Animals were sacrificed either after 6 or 12 days. RESULTS: Infected animals showed substantial weight loss until day 6 post-burn as compared to burn alone. Endotoxin and TNF-alpha levels were elevated early in the infected burn group within 48 hours post-burn. In contrast, significant up-regulation of the anti-inflammatory cytokine IL-10 occurred later in the clinical course and was associated with the recovery from weight loss. CONCLUSION: Our results suggest that in the presence of infection, you get a SIRS response possibly due to transient endotoxemia that is only seen in the infection group. In contrast, both burn and infection get a late IL-10 (CARS) response, which is then associated with a return to normal weight in the infection group.

Animals↗
PubMed2005

Lipopolysaccharide-binding protein modulates acetaminophen-induced liver injury in mice.

Acetaminophen toxicity is the most common cause of acute liver failure in the United States and Europe. Although much is known about the metabolism of acetaminophen, many questions remain regarding the pathogenesis of liver injury. In this study, we examined the role of lipopolysaccharide-binding protein (LBP), a protein important in mediating cellular response to lipopolysaccharides, by using LBP wild-type and knockout (KO) mice. We found that LBP KO mice were protected from acetaminophen-induced hepatotoxicity. At 350 mg/kg of acetaminophen, LBP KO mice had significantly less liver injury and necrosis than wild-type mice. Repletion studies in LBP KO mice using an LBP-adenoviral construct resulted in significantly more hepatic injury and necrosis after acetaminophen exposure compared with mice receiving the control adenoviral construct. In conclusion, LBP KO mice are protected from toxicity with a decrease in hepatic necrosis following acetaminophen challenge. This suggests a novel role for LBP in modulating acetaminophen-induced liver injury. Supplementary material for this article can be found on the HEPATOLOGY website (http://interscience.wiley.com/jpages/O270-9139/suppmat/index.html).

Acetaminophen↗
PubMed2005

Altered Kupffer cell function in biliary obstruction.

BACKGROUND: An altered Kupffer cell (KC) response is thought to be responsible for the characteristic phenotype observed after biliary obstruction: a phenotype marked by a defect in the hepatic reticuloendothelial system and a hypersensitivity to endotoxin. Few studies, however, have directly examined KC function. We have sought to define the specific alterations in function and phenotype that occur in the KC after biliary obstruction. METHODS: KCs were isolated from female C57BL/6 mice 4 days after a sham or common bile duct ligation (CBDL) operation. Phagocytosis, oxidative burst potential, and intracellular bacterial killing were measured as markers of reticuloendothelial system function. The KC response to endotoxin was assessed by measuring tumor necrosis factor alpha and interleukin 6 levels in the media after stimulation with lipopolysaccharide (LPS) or with LPS plus LPS-binding protein (LBP). RESULTS: CBDL KCs demonstrated a significant increase in phagocytic ability and significantly decreased baseline oxidative stress, compared with Shams. The oxidative burst potential, however, was equivalent or higher for CBDL KCs. CBDL KCs also demonstrated increased numbers of viable intracellular bacteria after infection; however, it is unclear if this finding represents impaired intracellular bacterial killing or increased phagocytosis of bacteria. With respect to the KC response to endotoxin, CBDL KCs were found to be less sensitive to the stimulatory effects of LPS alone but were exquisitely sensitive to the effects of LBP. LBP levels were found to be significantly elevated in CBDL animals, and CBDL KCs demonstrated a dose-dependent, exaggerated tumor necrosis factor alpha and interleukin 6 response to LPS administered with LBP. CONCLUSIONS: KC function is clearly altered after biliary obstruction. Phagocytic ability is actually increased, although the ability of CBDL KCs to kill bacteria within the phagosome remains ill defined. CBDL KCs are exquisitely sensitive to the effects of LBP, and LBP levels are elevated after biliary obstruction. LBP may be responsible for the increased proinflammatory response observed after endotoxin challenge in animals with biliary obstruction.

Acute-Phase Proteins↗
PubMed2005

Improved survival in mice given systemic gene therapy in a gram negative pneumonia model.

BACKGROUND: We previously demonstrated an essential role for lipopolysaccharide binding protein (LBP) in the pulmonary immune response to Gram-negative bacterial infection. LBP knockout mice had significantly higher mortality, greater rates of bacteremia, and higher counts of viable bacteria in their lungs at sacrifice compared with wild-type controls. We postulate that systemic LBP gene therapy will reconstitute a protective innate immune response in LBP knockout mice and that overexpression of LBP in wild-type mice may offer a survival advantage. METHODS: 12-16 week old female C57BL/6 wild-type mice and age matched LBP knockout mice were given 5 x 10(9) PFU of recombinant adenovirus containing either the gene for LBP or the irrelevant control protein beta-galactosidase by tail vein injection. 72 hours later each mouse was administered 1 x 10(3) CFU of Klebsiella pneumoniae by intratracheal injection. RESULTS: Administration of LBP by systemic gene therapy to LBP knockout mice improved survival from Klebsiella pneumonia to a level equivalent or better than wild-type mice exposed to the same dose of bacteria (36 versus 25%). Wild-type mice given the LBP gene therapy demonstrated increased 7 day survival from Klebsiella pneumonia when compared with controls treated with beta-galactosidase (68 versus 30%, p = 0.03). CONCLUSIONS: Systemic gene therapy with intravenous adenoviral vector transfer of LBP significantly improves survival in LBP knockout mice. Overexpression of LBP in wild-type mice improves survival from Klebsiella pneumonia. Raising levels of LBP in the setting of Gram-negative pneumonia may be of therapeutic benefit.

Acute-Phase Proteins↗
PubMed2004

Pelvic ring fractures: implications of vehicle design, crash type, and occupant characteristics.

BACKGROUND: Pelvic ring fractures (PRFs) are a major cause of morbidity and mortality in motor vehicle collisions (MVCs). Understanding the factors leading to PRFs may help improve vehicle design and safety. This study sought to determine the vehicular, crash, and occupant characteristics that contribute to PRFs. METHODS: From 1997 to 2003, 240 adult patients involved in lateral or frontal crashes were prospectively studied. Comprehensive crash reconstructions, vehicle analysis, and occupant data were compiled and analyzed as part of the national Crash Injury Research Engineering Network project. RESULTS: Of 240 study patients, 38 had PRFs. The incidence of PRFs was significantly associated with female gender, lateral impact crashes, vehicle incompatibility, and severity of crash. Seat belts and airbags were not protective against PRFs in either lateral or frontal crashes. CONCLUSIONS: All vehicles in the current study were less than 6 years old at the time of the MVC and thus reflect newer safety designs. Compared with studies of PRFs in MVCs before the widespread adoption of modern safety standards, our series suggests there has been a modest decrease in the incidence of PRFs in newer vehicles. Current safety standards do not adequately protect against PRFs, especially in lateral MVCs involving incompatibility and female occupants. New technology needs to be developed and implemented. Our data suggest that side impact airbags, alteration of vehicle geometry, and increased reinforcement of side panels and doors may result in fewer PRFs.

Accidents, Traffic↗
PubMed2004

Impaired hepatocyte regeneration in toll-like receptor 4 mutant mice.

Multiple lines of evidence suggest a role for endogenous lipopolysaccharides in toxin-induced liver injury. Toll-like receptor 4 has recently been implicated as a cell surface receptor important for lipopolysaccharide responsiveness. In these experiments, we sought to determine the role of toll-like receptor 4 in acute liver injury by carbon tetrachloride by utilizing the naturally occurring toll-like receptor 4 mutant and wild-type mice strains. Mice were injected with either carbon tetrachloride or the carrier. Serum transaminase levels peaked at 24 hr after carbon tetrachloride administration for both wild-type and mutant mice, with no significant histological difference in initial liver injury between the two groups. However, an overall decrease in hepatocyte proliferation was found in the mutant mice. Examination of the liver tissue revealed significant decreases in intrahepatic expressions of proinflammatory mediators. In conclusion, our results suggest that toll-like receptor 4 is important in the hepatic regenerative response to CCl4 liver injury via its role in modulating the inflammatory response to hepatic injury.

Animals↗
PubMed2004

Delayed repair for blunt thoracic aortic injury: is it really equivalent to early repair?

BACKGROUND: Blunt thoracic aortic injury (BTAI) is a severe injury that traditionally has mandated immediate surgical repair. Delaying operative intervention for BTAI can allow other life-threatening injuries to be managed first, but potentially increases the risk of aortic rupture and death. The objective of this study was to evaluate the outcome of delayed repair (DR) compared with early repair (ER) for BTAI and to assess the effectiveness of a protocol for medical control of systolic blood pressure and heart rate in those patients whose repairs were delayed. METHODS: This study is a retrospective review of University of Michigan Health System (UMHS) data from January 1, 1992, through March 1, 2003. ER was defined as operative repair within 16 hours from the time of injury. A similar analysis was conducted for patients with BTAI selected from the National Trauma Data Bank. RESULTS: For the UMHS data, there were 45 patients in the DR group and 33 patients in the ER group. Mortality in the ER group versus the DR group was 9% versus 20%. Multivariate analysis adjusting for age, Injury Severity Score, abdominal Abbreviated Injury Scale score, Glasgow Coma Scale score, and intubation status demonstrated an odds ratio for death from ER compared with DR of 1.72 (p = 0.57). Patients undergoing DR had an absolute increase in hospital length of stay (33.1 vs. 20.9 days) and complication rate (2.1 vs. 1.5 incidents per patient). A similar result was obtained for multivariate analysis of the National Trauma Data Bank data, with an odds ratio of 1.40 (p = 0.51) for death from ER versus DR. UMHS patients whose repairs were delayed achieved target systolic blood pressure and heart rate for 76% and 74% of the hourly measurements recorded, respectively. CONCLUSION: Patients with BTAI can safely undergo delayed aortic repair if other injuries warrant a higher treatment priority without increasing their overall risk of mortality. Delayed repair is, however, associated with a higher complication rate.

Adult↗
PubMed2004

Beta-blocker use is associated with improved outcomes in adult burn patients.

BACKGROUND: There is no direct evidence that beta-blockers improve mortality in burn victims. Beta-blockers attenuate hypermetabolic states in burned children, and perioperative use in elective adult cases has beneficial effects, which suggests that beta-blockers may also improve burn outcomes. However, beta-blockers decrease cardiac output and may decrease oxygen delivery, and theoretically may increase mortality. What is the effect of beta-blockers on healing time and mortality in burn patients? METHODS: This was a retrospective cohort study. We identified three cohorts of adult burn patients between 1996 and 2001: all who were on beta-blockers (BB) before their injury (PMH BB); all who were initiated on BB during their hospitalization for management of hypertension or tachyarrhythmia (HOSP BB); and control, who were never treated with beta-blockers. For each patient in the PMH BB and HOSP BB groups, two patients were placed in the control cohort by matching age and total body surface area burn. Premorbid conditions such as diabetes, hypertension, cardiac disease, renal insufficiency, and diuretic and calcium channel blocker use were analyzed. Multivariate regression models were used to identify independent modifiers. RESULTS: There were 21 PMH BB, 22 HOSP BB, and 86 control patients. All PMH BB patients remained on their BB regimen in the hospital. HOSP BB patients were initiated on beta-blockers at a mean of 8.8 days postinjury. There were no differences in age (mean, 58 +/- 17 years), total body surface area burned (mean, 14 +/- 12%), or mechanism of injury among the cohorts. The mortality rate was 5% for the PMH BB cohort, 27% for the HOSP BB cohort, and 13% for controls. The mean healing times were 51 +/- 29 days for PMH BB patients, 79 +/- 54 days for HOSP BB patients, and 60 +/- 39 for controls. In multivariate analyses, PMH BB was associated with a significant decrease in fatal outcome and healing time (p < or = 0.05 compared with control). CONCLUSION: Beta-blockers have the potential to improve adult burn outcomes. Postinjury treatment should be studied in a randomized, clinical trial.

Adrenergic beta-Antagonists↗
PubMed2004

Computed tomographic scanning reduces cost and time of complete spine evaluation.

BACKGROUND: We hypothesize that data collected from computed tomographic (CT) scans obtained for workup of chest or abdominal injuries provide data that are sufficient to screen for spinal fractures and will decrease the cost and time of spine evaluation after trauma. METHODS: We reviewed plain radiographs from 55 selected trauma patients who also underwent CT scanning of the chest, abdomen, and pelvis. We also timed the radiologic workup of 50 consecutive trauma patients to determine the time required to complete radiographic spine evaluation. RESULTS: Forty-seven patients had thoracolumbar fractures. Thirteen patients were found to have 33 thoracolumbar spine fractures identified by CT scan but not plain radiography. Fractures were found on initial trauma CT scans of the chest, abdomen, and pelvis obtained to evaluate for visceral injuries. No injuries seen on plain film were missed on CT scan. CONCLUSION: We recommend using the data acquired from CT scans to evaluate the spine, supplementing them with additional studies only when needed for further clarification.

Accidental Falls↗
PubMed2004

Gender differences in hip anatomy: possible implications for injury tolerance in frontal collisions.

Male occupants in frontal motor vehicle collisions have reduced tolerance for hip fractures than females in similar crashes. We studied 92 adult pelvic CT scans and found significant gender differences in bony pelvic geometry, including acetabular socket depth and femoral head width. Significant differences were also noted in the presentation angle of the acetabular socket to frontal loading. The observed differences provide biomechanical insight into why hip injury tolerance may differ with gender. These findings have implications for the future design of vehicle countermeasures as well as finite element models capable of more accurately predicting body tolerances to injury.

Accidents, Traffic↗
PubMed2003

The cushion effect.

BACKGROUND: The pattern and severity of crash injury depends on a complex interaction of biomechanical factors such as deceleration velocity at impact (delta-V), seat-belt and airbag use, and type of impact. Human body characteristics such as height and weight may play an important role. We hypothesized that body mass index (BMI) will influence crash injury patterns. METHODS: The University of Michigan Program for Injury Research and Education database was queried. Three cohorts were analyzed, lean (BMI </= 25 kg/m2), overweight (BMI 25-30 kg/m2), and obese (BMI > 30 kg/m2) RESULTS: There were 189 detailed crash cases, with 22 fatalities. There was an increased risk of fatal outcome associated with the obese cohort (adjusted odds ratio, 4.2 compared with lean; p = 0.04). Age, delta-V, seat-belt use, and type of impact were independent predictors of Injury Severity Score (ISS). After adjusting for other modifiers, being overweight was associated with decreased ISS (p = 0.03) and abdominal maximal Abbreviated Injury Scale (mAIS) score (p = 0.008) when compared with the lean cohort. However, the lower extremity mAIS score increased when overweight (p = 0.03) and obese cohorts (p = 0.001) were compared with the lean cohort. CONCLUSION: Although no difference in ISS was identified between the lean and obese cohorts, there was an increase in mortality with the obese cohort. The severity of lower extremity injuries increased with increasing BMI. The overweight cohort was associated with lower ISS and abdominal mAIS score compared with the lean cohort. This protection may be attributable to an increase in insulating tissue, or a "cushion effect," without a significant increase in mass and momentum.

Accidents, Traffic↗