Edmonds Rebecca D, Cuschieri Joseph, Minei Joseph P, Rosengart Matthew R, Maier Ronald V, Harbrecht Brian G, Billiar Timothy R, Peitzman Andrew B, Moore Ernest E, Sperry Jason L
Division of General Surgery and Trauma, Department of Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15213, USA.
J Trauma. 2011 Feb;70(2):292-8. doi: 10.1097/TA.0b013e31820b5f69.
Obesity defined by a body mass index (BMI) >30 kg/m is associated with increased morbidity and mortality following trauma. Evidence suggests that obesity represents a state of chronic inflammation and that the adipose tissue content may affect the intensity and resolution of inflammatory response. We sought to avoid the confounding effects attributable to obesity and determine the association of BMI and outcomes following injury in nonobese patients.
Data were obtained from a multicenter prospective cohort study evaluating outcomes in blunt-injured adults with hemorrhagic shock. Only patients with a BMI≥18.5 and<30 were analyzed. Those with isolated traumatic brain injury and cervical cord injury and those who survived<24 hours were excluded. Logistic regression was used to evaluate the effects of BMI on mortality, multiple organ failure (MOF, multiple organs dysfunction score [MODS]>5), and nosocomial infection (NI) after adjusting for differences in demographics, injury severity, early resuscitation needs, shock parameters, and comorbidities.
Overall mortality, MOF, and NI rates for the study cohort (n=820) were 13%, 37%, and 46%, respectively. Median Injury Severity Score was 33 (interquartile range, 22-41). Median BMI for the study cohort was 25 (interquartile range, 23-27). As BMI increased, maximum organ dysfunction scores also significantly increased for cardiac, respiratory, and renal systems. Logistic regression revealed no significant association with mortality (odds ratio [OR]=0.95; 95% confidence interval [CI], 0.9-1.0); however, BMI was independently associated with a higher risk of MOF (OR=1.09; 95% CI, 1.02-1.06) and NI (OR=1.07; 95% CI, 1.01-1.13). For every single-point increase in BMI, the risk of MOF and NI increase by 9% and 7%, respectively.
The risk of MOF and NI increases as BMI increases in the nonobese injured patient. These results suggest that body adipose content may be associated with the magnitude of or extent of the inflammatory response postinjury. Further studies are needed to elucidate the mechanism responsible for this association.
体重指数（BMI）>30 kg/m²所定义的肥胖与创伤后发病率和死亡率增加相关。有证据表明，肥胖代表一种慢性炎症状态，且脂肪组织含量可能影响炎症反应的强度和消退。我们试图避免肥胖造成的混杂效应，并确定非肥胖患者中BMI与损伤后结局之间的关联。
数据来自一项多中心前瞻性队列研究，该研究评估钝性损伤并伴有失血性休克的成年患者的结局。仅分析BMI≥18.5且<30的患者。排除孤立性创伤性脑损伤和颈髓损伤患者以及存活时间<24小时的患者。在对人口统计学、损伤严重程度、早期复苏需求、休克参数和合并症的差异进行校正后，使用逻辑回归评估BMI对死亡率、多器官功能衰竭（MOF，多器官功能障碍评分[MODS]>5）和医院感染（NI）的影响。
研究队列（n = 820）的总体死亡率、MOF和NI发生率分别为13%、37%和46%。损伤严重程度评分中位数为33（四分位间距，22 - 41）。研究队列的BMI中位数为25（四分位间距，23 - 27）。随着BMI增加，心脏、呼吸和肾脏系统的最大器官功能障碍评分也显著增加。逻辑回归显示与死亡率无显著关联（比值比[OR]=0.95；95%置信区间[CI]，0.9 - 1.0）；然而，BMI与MOF风险较高独立相关（OR = 1.09；95% CI，1.02 - 1.06）以及NI（OR = 1.07；95% CI，1.01 - 1.13）。BMI每增加一个单位，MOF和NI的风险分别增加9%和7%。
在非肥胖损伤患者中，MOF和NI的风险随着BMI增加而增加。这些结果表明，身体脂肪含量可能与损伤后炎症反应的程度或范围相关。需要进一步研究以阐明这种关联的机制。
