道路交通伤急性肾损伤发生及预后危险因素分析
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摘要
背景
道路交通伤(Road Traffic Injury RTI)遍及世界各地,是威胁人类生命和健康的“杀手”。据统计全世界每年约有120万人死于RTI,其中15-44岁的青壮年占一半以上。如果不采取有效措施预计到2020年全球RTI死亡人数将继续增加65%,其中低收入国家和中等收入国家占90%以上。我国是道路交通安全问题最严重的国家之一,2001年我国万辆车事故发生率和死亡率居世界之首,造成10.6万人死亡。1978年至2005年的27年间,我国RTI致死人数增长了4倍。毋庸置疑,RTI已经成为日趋严重的全球公共卫生问题。
近年来对RTI的研究多集中在预防和减少伤害发生方面,而围绕如何改善伤员预后展开的研究较少。临床工作者对一些有生命威胁的严重并发症在RTI中发生情况和预后影响知之甚少,这在很大程度上阻碍了RTI救治工作的发展。研究已经证实急性肾损伤(Acute Kidney Injury AKI)是创伤后严重并发症。根据AKI定义和研究对象不同(如ICU或非ICU病人),创伤后AKI发生率为0.098-31.0%,死亡率高达13-78%,是造成伤员院内死亡的重要原因。RTI是现代创伤最主要的组成部分,50-70%创伤是由于道路交通事故造成。然而多年来道路交通事故只是作为创伤后AKI的主要致伤原因出现在研究中,临床研究者并没有针对RTI人群展开独立深入的研究,迄今为止国内外均无文献报告大样本RTI后AKI发生率、临床转归(包括伤员预后和肾脏转归)及相关危险因素,使RTI人群AKI的临床防治工作缺乏依据和指导。众所周知,AKI缺乏有效的治疗手段,血液净化技术没能改善病人转归,预防和早期干预一直是AKI防治策略的关键。了解交通伤AKI发生危险因素和预后决定因素对于指导临床治疗、使病人获得最佳转归非常重要。因此,本研究回顾分析了4857例RTI伤员发生AKI的危险因素及预后不良因素,旨在通过预防AKI发生、改善AKI预后从而降低交通伤死亡率和致残率(遗留肾功能障碍)。
对象和方法
1.研究人群
采用回顾性临床研究。通过伤员出入院电子数据库筛选2002年1月到2006年12月住南方医院和珠江医院的所有道路交通伤(RTI)伤员。研究剔除以下伤员病历:伤前慢性透析者;住院时间小于24小时者;血清肌酐(Scr)和尿量记录均缺如者。最后4857例伤员纳入研究。
2.诊断标准
AKI诊断和分级根据RIFLE(Risk,Injury,Failure,Loss和End stage)标准。非慢性肾功能不全伤员基础肌酐值(baseline Cr)取伤后24小时内Scr最低值,无此数值者采用公式估算值。存在慢性肾功能不全(非透析)伤员基础肌酐值采用受伤前实测值。358例AKI伤员中269例(75.0%)使用实测值,89例(25.0%)使用估算值。基础肌酐值估算按急性透析质量倡议(Acute Dialysis Quality InitiativeADQI)工作组意见根据肾脏病膳食改良试验(Modification of Diet in Renal DiseaseMDRD)公式计算。根据伤后Scr最高值或尿量最低值,AKI由轻微至严重分为3级:Risk_(max),Injury_(max),Failure_(max)。AKI伤员临床转归包括伤员转归和肾脏转归:根据伤后第14d、28d和出院时状态分为存活或死亡;根据AKI后第28d肾功能情况分为完全恢复(Scr不超过基础肌酐增长50%后的数值,例如基础肌酐为88umol/L即1.0mg/dl,Scr降至133 umol/L即1.5mg/dl以下则诊断为完全恢复)、部分恢复不依赖透析(Scr未降至完全恢复标准但不依赖透析)或依赖透析。休克定义为收缩压＜90mmHg,或较原水平下降＞40mmHg持续1h以上,常规补液不能使血压恢复或需要使用多巴胺6ug/Kg/min。横纹肌溶解定义筋膜室综合征伴CK＞975 IU/L。脓毒症(Sepsis)参考1991年美国芝加哥会议和2001年美国华盛顿会议标准诊断。非肾脏器功能障碍(呼吸、心血管、肝脏、胃肠道、血液、神经系统功能障碍)参考Gods标准。
3.数据收集
从数据库中记录人口学数据,临床数据和实验室数据。此外,还计算了损伤严重评分(Injury Severity Score ISS)、急性生理和慢性健康评估系统Ⅱ(Acute Physiology and Chronic Health EvaluationⅡAPACHEⅡ)评分、Glascow昏迷评分(Glascow Coma Score GCS)。所有数据由专人用Epidata3.0软件双份录入,并进行一致性核查。资料去除所有身份信息以保护病人隐私。
4.统计学方法
连续性变量以均数±标准差或中位数表示,分类变量以百分比表示,所有变量使用Kolmogorov-Smirnov方法进行正态性检验。根据是否为正态分布,连续性变量两组比较采用独立样本t检验或Mann-Whitney U方法,多组比较采用one-way ANOVA或Kruskal-Wallis H方法;分类变量采用Fisher精确检验或卡方检验。采用多变量Logistic方法分析AKI发生危险因素及预后不良因素,纳入Logistic回归模型的变量为单变量分析有统计学意义的因素和重要的临床因素;Hosmer-Lemeshow用于确定Logistic回归模型的拟合优度,P＞0.05视为可接受模型。采用Ordinal回归方法分析影响AKI严重程度的因素,Pearson和Deviance卡方检验用于检验Ordinal回归模型的拟合优度,P＞0.05视为可接受模型。双侧P＜0.05视为有统计学意义,采用SPSS13.0软件进行统计分析。
结果
1.RTI伤员特征
数据库中共4857例病例符合入选标准。76.6%为男性(3719/4857),伤员平均年龄33.3±15.4岁(1.90岁),70.0%(3390/4857)伤员为15-44岁青壮年,79.4%(3856/4857)为弱势道路使用者(包括行人、骑自行车者、骑摩托车者及摩托车乘员),1166例(24.0%)使用防护措施,1468例(30.2%)得到医务人员现场救护,送达时间(事故发生到送至医院接受治疗的时间)中位数是20min(1.0-720.0min)。入院平均ISS、GCS分别为12.9±8.7(1-75)和13.1±3.5(3-15),1054例(21.7%)进入ICU观察。受伤部位以四肢伤(64.6%)和头面部伤(49.7%)最多见,其余依次为胸部伤(19.2%)、腹部伤(18.5%)和脊柱伤(15.6%)。321例(6.6%)伤员发生休克,288例(5.9%)合并脓毒症,911例(18.8%)伴有一个或多个脏器功能障碍。住院时间中位数为17d(2-367d)。院内总死亡率为8.4%(408/4857),伤后14d内和28d内死亡分别6.4%(313/4857)和7.2%(352/4857)。
2.RTI后发生AKI者临床转归
358例(7.3%)伤员发生AKI。发生AKI的RTI伤员死亡率明显增高,并且部分存活伤员在AKI发生后28d仍然遗留肾功能障碍。358例AKI伤员院内死亡率高达51.1%(183/358),其中伤后14d内、28d内死亡率分别为40.2%、46.4%,而非AKI伤员院内死亡率仅为5.0%,其中伤后14d内、28d内死亡率分别为3.8%、4.1%(P均＜0.001)。并且伤员死亡率随AKI加重而增高,Risk_(max)、Injury_(max)和Failure_(max)伤员院内死亡率分别为34.2%、46.8%、76.5%(P＜0.001),其中伤后14d内死亡率分别为29.5%、42.6%、66.1%(P＜0.001),伤后28d内死亡率分别为30.9%、45.7%、71.3%(P＜0.001)。Risk_(max)、Injury_(max)和Failure_(max)死亡者存活时间中位数逐渐下降,分别7d(2-169d)、4d(2-199d)和3d(2-164d)(P=0.045),表明AKI越重者存活时间越短。
175例存活AKI伤员中无依赖透析者,11例(6.3%)在AKI后第28d仍然遗留肾功能障碍(肾功能部分恢复但不依赖透析),并且遗留肾功能障碍发生率随AKI加重而增高,Risk_(max)Injury_(max)和Failure_(max)分别为1.3%(2/149)、4.3%(4/94)和7.0%(5/115)(P=0.019)。
3.RTI后AKI发生危险因素及影响AKI严重程度因素
AKI发生率为7.3%(358/4857),其中73.2%(262/358)发生在伤后72h内,89.1%(319/358)发生在伤后一周内。男性伤员292例(81.4%),平均年龄44.0±17.4岁(13-88岁),301例(84.6%)为弱势道路使用者,仅60人(24.0%)使用防护措施,153例(43.2%)得到医务人员现场救援,送达时间(事故发生到送至医院接受治疗的时间)中位数是30min(4.0-420.0min),10.7%(38/358)伤员伤前有慢性疾病。伤员入院平均ISS和APACHEII评分分别为24.3±9.4(1-75)、19.6±8.0(1-42),266例(74.3%)伤员进入ICU观察,平均ICU时间是3d(2-116d)。235例(65-6%)并发非肾脏器功能障碍,平均功能障碍脏器数为2.3±1.3个(1—7个)。233例(65.0%)伤员受伤后接受外科手术;15例(4.2%)接受肾替代治疗(RRT)。住院时间中位数为12d(2-367d)。
单因素分析显示,AKI伤员男性比例高于非AKI伤员(81.4%vs 76.2%,P=0.027),前者平均年龄大(44.0岁vs 32.6岁,P＜0.001)、患慢性疾病者多(10.7%vs 5.9%,P=0.001)、弱势道路使用者比例高(84.1%vs 79.0%,P=0.006)、而采取安全防护措施伤员少(16.8%vs 24.6%,P=0.002)。在AKI伤员与非AKI伤员受伤程度和受伤部位比较中,前者损伤程度更严重(平均ISS:24.3 vs 12.0,P＜0.001;平均GCS:7.9 vs 13.5,P＜0.001),严重头部伤(GCS≤8)发生率(67.8%vs14.4%,P＜0.001)、胸部脏器伤发生率(21.2%vs 8.3%,P＜0.001)、腹部脏器伤发生率(31.4%vs 6.7%,P＜0.001)、开放长骨骨折发生率(23.4%vs 3.5%,P＜0.001)、多发伤发生率高于后者(82.4%vs 25.4%,P＜0.001)。AKI伤员与非AKI伤员伤后并发症(发生在AKI之前)比较,前者休克发生率(23.2%vs 5.3%,P＜0.001)、横纹肌溶解发生率(19.2%vs 5.4%,P＜0.001)、脓毒症(脓毒症:10.7%vs 4.9%,P＜0.001)和非肾脏器功能障碍发生率高于后者(33.2%vs 8.6%,P＜0.001)。将单因素分析有统计学意义的变量(P＜0.05)纳入logistic回归模型进行多因素分析,结果进一步证实男性(OR=1.471,95%CI:1.068-2.200),年龄增加(10yrs)(OR=1.387,95%CI:1.287-1.607),慢性疾病(OR=2.312,95%CI:1.458-3.665),送达时间＞60min(OR=3.470,95%CI:1.565-7.696),ISS＞15(OR=3.569,95%CI:2.090-6.094),严重头部伤(OR=4.236,95%CI:2.967-14.068),腹部脏器伤(OR=2.411,95%CI:1.666-3498),开放长骨骨折(OR=2.011,95%CI:1.408-2.873),休克(OR=2.055,95%CI:1.424-2.967),横纹肌溶解(OR=2.579,95%CI:1.776-3.745),呼吸系统功能障碍(OR=2.547,95%CI:1.567-4.138)是RTI发生AKI的危险因素。其中,对发生AKI影响最强的因素是伤势重(ISS＞25:OR=8.032,95%CI 4.417-14.650)、严重头部伤(OR=4.236,95%CI2.967-14.068)和送达时间＞60min(OR=3.470,95%CI 1.565-7.696)。与送达时间＜10min者比较,送达时间11-60min者发生AKI危险增加22.5%,而＞60min者发生AKI危险急剧增加247%。Hosmer-Lemeshow检验x~2=5.843,df=8,P=0.665,表明logistic回归模型拟合度较好。
AKI由轻微至严重分为Risk_(max)、Injury_(max)和Failure_(max),3组伤员分别为149例(41.6%),94例(26.3%)和115例(32.1%)。单因素分析显示,随着伤员受伤程度加重(平均ISS分别为20.0、24.6、27.3,P＜0.001;平均APACHEⅡ分别为17.0、20.2、22.7,P＜0.001;平均GCS分别为8.7、7.6、6.8,P=0.004)、平均低血压持续时间延长(分别为3.0h、6.0h、7.3h,P=0.037),严重头部伤发生率增高(分别为61.1%、69.1%、76.5%,P=0.027)、腹部脏器伤发生率增高(分别为24.8%、27.7%、42.6%,P=0.006)、多发伤发生率增高(分别为76.5%、84.0%、87.8%,P=0.049),AKI程度加重。将上述变量纳入Ordinal回归模型进行多因素分析,结果进一步表明ISS、APACHEⅡ增高(per point)、GCS降低(perpoint)、低血压持续时间延长(per hour)是加重AKI程度的危险因素。Pearsonx~2=920.188,df=950,P=0.750.Deviance x~2=815.340,df=950,P=0.999,显示Ordinal回归模型拟合度较好。
4.发生AKI的RTI伤员死亡危险因素
单因素分析显示,死亡AKI伤员入院时伤情比存活者更严重(平均ISS:28.6vs 20.3,P＜0.001;平均APACHEⅡ:23.9 vs 16.2,P＜0.001;平均GCS:5.6 vs 10.2,P＜0.001),严重头部伤(87.7%vs 50.3%,P＜0.001,P＜0.001)、多发伤发生率高(94.0%vs 69.7%,P＜0.001),肾损伤程度重(Failure_(max):48.1%vs 15.4%,P=0.027),呼吸、心血管、血液、神经系统功能障碍发生率高(呼吸功能障碍:41.0%vs 17.1%,P＜0.001;心血管功能障碍:25.1%vs 2.9%,P＜0.001;血液功能障碍:57.9%vs 11.4%,P＜0.001;神经系统功能障碍:4.4%vs 0.6%,P＜0.001)。死亡AKI伤员接受RRT比例亦高于存活伤员,但无统计学差异(6.0%vs 2.8%,P=0.195)。将单因素分析中有统计学意义的变量(P＜0.05)和重要的临床因素,包括性别、入院ISS(0-15、16-25、＞25)、APACHEⅡ评分(0-17、18-27、＞27)、多发伤、严重头部伤、AKI(Risk_(max)、Injury_(max)和Failure_(max))、RRT、呼吸、心血管、血液、中枢神经系统功能障碍纳入logistic回归模型进行多因素分析。结果显示,入院ISS＞25(OR=6.309,95%CI:1.704-36.534)、严重头部伤(OR=2.707,95%CI:1.022-7.154)、AKI-Failure_(max)(OR=2.761,95%CI:1.123-7.148)、呼吸功能障碍(OR=1.852,95%CI:1.542-3.080)、心血管功能障碍(OR=22.245,95%CI:4.507-119.788)和血液系统功能障碍(OR=7.660,95%CI:3.098-19.532)是发生AKI的RTI伤员院内死亡危险因素。其中对AKI死亡影响最强的因素是心血管功能障碍。肾损伤严重是(Failure_(max))伤员死亡危险是肾损伤轻微(Risk_(max))者的2.761倍。Hosmer-Lemeshow检验x~2=3.592,df=8,P=0.892,表明logistic回归模型拟合度较好。
5.影响存活者28d肾脏转归的危险因素
单因素分析显示,肾功能部分恢复伤员肾损伤程度更严重(Injury_(max):36.4%vs 28.6%,P=0.034;Failure_(max):45.5%vs 11.8%,P=0.007),脓毒症(54.5%vs15.2%,P=0.005)、严重横纹肌溶解(CK≥10000IU/L)发生率高(27.3%vs 69.7%,P=0.023),接受RRT者比例高(18.2%vs 1.2%,P=0.020)。此外,肾功能部分恢复伤员平均年龄大(45.8 vs 41.3,P=0.430)、送达时间长(64.0 vs 47.0,P=0.198)、呼吸功能障碍发生率高(36.4%vs 15.5%,P=0.092),但两组比较无统计学差异。将单因素分析中有统计学意义的变量(P＜0.05)和重要的临床因素,包括年龄、性别、送达时间、脓毒症、严重横纹肌溶解(CK≥10000IU/L)、RRT、AKI(包括Risk_(max)、Injury_(max)和Failure_(max))、呼吸、心血管、肝脏、胃肠、血液及神经系统功能障碍纳入Logistic回归模型进行分析,结果显示年龄增长(10yrs)(OR=1.973,95%CI:1.075-3.765)、肾损伤程度重(Failure_(max):OR=140.414,95%CI 6.123-3220.148:Injury_(max):OR=26.709,95%CI 1.922-371.090)、合并脓毒症(OR=21.167,95%CI 1.808-247.828)、严重横纹肌溶解(OR=6.126,95%CI 1.243-34.345)及呼吸系统功能障碍(OR=12.995,95%CI 1.255-134.564)是影响28d肾功能完全恢复的危险因素。其中,肾损伤严重程度是对28d肾功能完全恢复影响最强的因素。Hosmer-Lemeshow检验x~2=6.012,df=8,P=0.646,表明logistic回归模型拟合度较好。
结论
研究显示AKI是RTI严重并发症,发生AKI的RTI伤员死亡率明显增加,存活者可能因遗留肾功能障碍而致残。RIFLE标准能够预示发生AKI的RTI伤员预后和肾脏转归。延误院内救治时间(＞60min)、受伤程度(ISS＞15)和受伤部位(严重头部伤、腹部脏器伤)是RTI伤员发生AKI的重要因素;严重损伤(ISS＞25)、严重头部伤及非肾脏器功能障碍是发生AKI的RTI伤员预后危险因素。临床上针对这些因素加强防治可能降低AKI发生率、改善预后,从而降低RTI伤员死亡率和致残率。
Background
Road traffic injury(RTI) occurs on all continents,in every country of the world. Worldwide,an estimated 1.2 million people are killed in road crashes each year and more than half of these ones are young adults aged between 15 and 44 years. Projections of the World Health Organization(WHO) indicate that these figures will increase by about 65%by 2020,low-income and middle-income countries account for about 90%of the deaths unless there is new commitment to prevention.China is one of the most serious countries of road traffic safety problem.In 2001,China occupied the top of all countries in the rate of accident and mortality per ten thousand vehicles,which resulted in 106,000 deaths.The annual numbers of road traffic deaths rose sharply,and road traffic fatality rates rose by 4 times from 1978 to 2005. Without doubt,RTI is a growing worldwide public health problem of global. Acute kidney injury(AKI) is a clinical syndrome with high mortality in patients with severe trauma.The incidence of AKI ranged from 0.098 to 31%depending on the definition of AKI and studied populations.The mortality remained high(13 to 78%) and it was an important contributor to hospital mortality in post-traumatic population. However,we have known little so far concerning AKI after RTI though it was the most common cause of post-traumatic AKI.There is no large sample study to report the exact incidence of AKI,clinical outcome,and risk factors in patients with RTI.It is well known that prevention is better than cure for AKI,since there is no specific and effective management for the syndrome and blood purification do not improve patients' outcome.To promote clinical practice and further obtain the best outcomes for patients,it is important for clinicians to understand predictors of development and prognosis of AKI.Thus,the study was performed retrospectively in patients with RTI. In the study,we aimed to investigate independent risk factors for development and outcome of AKI in patients undergoing traffic,then offering a survival and health benefit for the patient suffered RTI.
Patients and Methods
1.Study population
A retrospective clinical study was performed.The NangFang Hospital and ZhuJiang Hospital is 2 academic medical centers affiliated with Sourthern Medical University.All patients with RTI admitted to both of hospitals between January 2002 and December 2006 were screened using the computerized hospital admissions and discharges database.Following patients were excluded from the study cohort:on chronic dialysis before traffic,staying in hospital less than 24 hrs,neither serum creatinine(Scr) value nor urine output record after the traffic.If a patient had more than one admission during the study period,only the first admission was included in the study.As a result,4857 records were analysed in the study.
2.Definitions
AKI was diagnosed and classified according to RIFLE criteria.The _(max)imum RIFLE stratum(class R_(max),class I_(max) or class F_(max)),which was based on the highest Scr level or the least urine output during hospital stay,was assigned to each patient for analysis.The clinical outcome of those with AKI included patient outcome and renal outcome.Complete renal recovery was defined by a convalescent Scr not more than 50%increased from baseline.e.g.if baseline Scr was 1.0 mg/dL(88 mcmol/L), complete recovery was said to occur if the new steady state SCrt was＜1.5 mg/dL (133 mcmol/L).Partial renal recovery was said to occur if the above condition for complete recovery was not met but the patient did not require chronic dialysis.
3.Data collection
The patients' information,including demographic data,clinical data and laboratory data were collected from the database.All data were inputted using Epidata3.0 software by a non-investigator data manager and repeated again,then double data were carried on consistency verification.All identifying information of patients was stripped of to preserve their anonymity.
4.Statistical analysis
In statistical data,continuous variables were presented as mean±standard deviation(SD) or median(range) and categorical variables were presented as percentages.All variables were tested for normal distribution using the Kolmogorov-Smimov test.One-way analysis of variance(one-way ANOVA) test or the Kruskal-Wallis H test for continuous variables according to their distribution; Fisher's exact test or the chi-square test were applied to assess categorical data associated with RIFLE classifications(including no AKI,class R_(max),class I_(max) and class F_(max)).To elucidate the impact of each category of RIFLE criterion on hospital mortality and find the risk factors for development of AKI,multiple-variable logistic regression analyses was conducted,variables at p＜0.05 in the univariate analysis and those considered clinically important were entered a multiple-variable logistic regression model.The Hosmer-Lemeshow test was employed to determine the goodness-of-fit of the model,P＞0.05 was regarded as an acceptable model.The results of multivariate logistic regression analysis were summarized by estimating odds ratios(OR) and respective 95%confidence interval(CI).We considered double-sided P＜0.05 as statistically significant.Data were analyzed using the SPSS version 13.0.
Results
1.Characteristic of patients with RTI
During the study period,4857 patients admitted for traffic trauma were evaluated.Of these patients,358 patients developed AKI.The number of male was 3719(76.6%),mean age was 33.3±15.4 yrs(1-90years).70.0%(3390/4857) patients were young adults aged between 15 and 44 years,and 79.4%(3856/4857) patients were vulnerable road users who had underlying probability of a crash for particular exposure.64.6%and 49.7%patients suffered extremity and head injury which were the most frequent injured location,followed by thoracic injury(19.2%),abdominal injury(18.5%) and spinal injury(15.6%).Mean ISS was 12.9±8.7(1-75) and mean GCS was 13.1±3.5(3-15) on admission,respectively.911(18.8%) patients had one or more than one organ dysfunctions.The median of length of hospital stay was 17d (2-367d).Overall mortality during hospitalization in population with RTI was 8.4% (408/4857).
2.Outcomes of patients who developed AKI after RTI
The mortality rate in patients who developed AKI was very high at 51.1% (183/358).This is in striking contrast to the mortality rate of only 5.0%(225/4499) in patients who did not develop AKI.There were significant differences in mortality rate between the population with AKI and those without AKI(P＜0.001).Of note,there was an increasing mortality with increasing severity of AKI.The mortality rate in patients of Risk_(max)、Injury_(max) or Failure_(max) were 29.5%、42.6%、66.1%within 14-day after injury,30.9%、45.7%、71.3%within 28-day after injury and 34.2%、46.8%、76.5%on discharge from hospital,respectively.
Of 175 survived patients suffered from AKI,93.7%(164/175) patients had complete renal recovery,6.3%(11/175) had partial renal recovery and all the survived became independent of RRT at 28 days after AKI.An increasing trend was observed for the rate of left renal insufficiency in class Risk_(max),class Injury_(max) and class Failure_(max),which was 1.3%、4.3%and 7.0%respectively(P=0.019).
3.Risk predictors for development of AKI and deteriorated AKI
The incidence of AKI in patients with road trauma was 7.3%(358/4857) according to the RIFLE criteria.In such patients,73.2%(262/358) of AKI occurred at the first 72 hours after trauma and 89.1%(319/358) occurred in the initial week, 10.7%(38/358) patients have pre-existing disease.The number of male and female was 183(82.8%) and 38(17.2%) respectively,mean age was 39.2±16.4 yrs(13—80years).Mean ISS was 24.4±9.0(1—75) and mean APACHEⅡscores was 19.6±8.3(4—42) on admission.137(61.9%) patients had additional organ dysfunctions and the mean number of organ dysfunction was 2.3±1.3(1—6).65% (233/358) patients underwent surgical operations,15(4.2%) patients required renal replacement therapy.they have a longer ICU stay and hospital stay compared to patients with no AKI.In univariate analysis,the patients with AKI were older than the patients without AKI(P=0.002),their rescue time were longer and were more severe injury assessed by ISS,APACHEⅡscore and GCS,The occurrence of severe head injury,abdominal organ injury,thoracic organ injury and open long bone fracture were more frequent in population with AKI(P＜0.001),and the patients with AKI had higher frequencies of serious complicating morbidities including shock, rhabdomyolysis,sepsis and additional renal dysfunction than those ones without AKI (P＜0.05).We used a multivariate logistic regression model to further investigate interactions between all statistically significant factors contributing to AKI.The analysis showed that increasing age(10yrs),rescue time＞60min,severe head injury, abdominal organ injury,open long bone fracture,rhabdomyolysis,shock and respiration system dysfunction were associated with increased risk for occurrence of AKI(P＜0.05).Hosmer-Lemeshow goodness-of-fit test showed that the model was statistically significant without bias(x~2=5.843,df=8,P=0.665).
The patients were categorized Risk_(max)、Injury_(max) or Failure_(max) based on alterations in serum creatinine or urine output,which was 284(58.3%),97(19.9%) and 115(21.8%) respectively.In univariable analysis,multiple injury,severe injury assessed by ISS,APACHEⅡscore and GCS,severe head injury,abdominal organ injury,duration of hypotension and were statistically significant predictors for deteriorated renal dysfunction.Ordinal regression analysis showed that the deteriorated AKI followed the increasing APACHEⅡscore,ISS,decreasing GCS and prolonged time of hypotension duration(p＜0.05).Pearson test(x~2=920.188, df=950,P=0.750) and Deviance test(x~2=815.340,df=950,P=0.999)showed that the regression model was statistically significant without bias.
4.Risk factors for mortality in patients with AKI
Among the 358 patients with AKI,51.1%(183/358) died prior to hospital discharge.The 14-day and 28-day mortality rate were 44.7%(160/358),47.8% (171/358) respectively.Several factors were associated with death in univariate analysis,including severity degree of injury assessed by ISS,APACHEⅡscore and GCS,severe head injury and organ dysfunction syndrome including respiratory, cardiovascular,hematological,neurological and kidney.Factors not significantly associated with death in hospital included gender,age or RRT.A multivariable logistic regression model was developed to assess for independent factors associated with death in hospital for patients with AKI.The analysis showed that severe head injury,ISS＞25,RIFLE-Failure,and respiratory,cardiovascular,hematological system dysfunction were associated with poor prognosis.Hosmer-Lemeshow goodness-of-fit test showed that the model was statistically significant without bias(x~2=3.592,df=8, P=0.892).
5.Renal outcome in the survived and risk factors for left renal insufficiency
Compared to those that recovered completely renal function,patients that remained left renal insufficiency were more likely to be male,older age,severe AKI, required renal replacement therapy,complicated with ODS and sepsis,with a diagnosis of pre-existing disease and severe rhabdomyolysis(CK≥10000IU/L) in univariate analysis.Followed variables were associated independently with poor renal outcome on 28-day after AKI in a multivariate logistic regression analysis:sepsis, AKI-Injury_(max),AKI-Failure_(max) and respiration system dysfunction. Hosmer-Lemeshow goodness-of-fit test showed that the model was statistically significant without bias(x~2=6.012,df=8,P=0.646).
Conclusions
AKI was a severe complication in the population with RTI and associated with greatly increased mortality during hospitalization,and could incapacitate the survivors because of left renal insufficiency.RIFLE criteria could contribute to predict the patient at a moderate to high risk for mortality and left renal insufficiency. Certain independent predictors such as delayed hospital rescue,severe injury assessed by ISS and severe head injury could predict patients at a high risk for development of AKI.The latter two and additional organs dysfunction were also predictors of mortality in those with AKI.Such risk predictors could assist in implementing strategies to prevent AKI and improve prognosis in patients with AKI,which should offer better outcomes for patients suffered RTI.
道路交通伤(Road Traffic Injury RTI)遍及世界各地,是威胁人类生命和健康的“杀手”。据统计全世界每年约有120万人死于RTI,其中15-44岁的青壮年占一半以上。如果不采取有效措施预计到2020年全球RTI死亡人数将继续增加65%,其中低收入国家和中等收入国家占90%以上。我国是道路交通安全问题最严重的国家之一,2001年我国万辆车事故发生率和死亡率居世界之首,造成10.6万人死亡。1978年至2005年的27年间,我国RTI致死人数增长了4倍。毋庸置疑,RTI已经成为日趋严重的全球公共卫生问题。
近年来对RTI的研究多集中在预防和减少伤害发生方面,而围绕如何改善伤员预后展开的研究较少。临床工作者对一些有生命威胁的严重并发症在RTI中发生情况和预后影响知之甚少,这在很大程度上阻碍了RTI救治工作的发展。研究已经证实急性肾损伤(Acute Kidney Injury AKI)是创伤后严重并发症。根据AKI定义和研究对象不同(如ICU或非ICU病人),创伤后AKI发生率为0.098-31.0%,死亡率高达13-78%,是造成伤员院内死亡的重要原因。RTI是现代创伤最主要的组成部分,50-70%创伤是由于道路交通事故造成。然而多年来道路交通事故只是作为创伤后AKI的主要致伤原因出现在研究中,临床研究者并没有针对RTI人群展开独立深入的研究,迄今为止国内外均无文献报告大样本RTI后AKI发生率、临床转归(包括伤员预后和肾脏转归)及相关危险因素,使RTI人群AKI的临床防治工作缺乏依据和指导。众所周知,AKI缺乏有效的治疗手段,血液净化技术没能改善病人转归,预防和早期干预一直是AKI防治策略的关键。了解交通伤AKI发生危险因素和预后决定因素对于指导临床治疗、使病人获得最佳转归非常重要。因此,本研究回顾分析了4857例RTI伤员发生AKI的危险因素及预后不良因素,旨在通过预防AKI发生、改善AKI预后从而降低交通伤死亡率和致残率(遗留肾功能障碍)。
对象和方法
1.研究人群
采用回顾性临床研究。通过伤员出入院电子数据库筛选2002年1月到2006年12月住南方医院和珠江医院的所有道路交通伤(RTI)伤员。研究剔除以下伤员病历:伤前慢性透析者;住院时间小于24小时者;血清肌酐(Scr)和尿量记录均缺如者。最后4857例伤员纳入研究。
2.诊断标准
AKI诊断和分级根据RIFLE(Risk,Injury,Failure,Loss和End stage)标准。非慢性肾功能不全伤员基础肌酐值(baseline Cr)取伤后24小时内Scr最低值,无此数值者采用公式估算值。存在慢性肾功能不全(非透析)伤员基础肌酐值采用受伤前实测值。358例AKI伤员中269例(75.0%)使用实测值,89例(25.0%)使用估算值。基础肌酐值估算按急性透析质量倡议(Acute Dialysis Quality InitiativeADQI)工作组意见根据肾脏病膳食改良试验(Modification of Diet in Renal DiseaseMDRD)公式计算。根据伤后Scr最高值或尿量最低值,AKI由轻微至严重分为3级:Risk_(max),Injury_(max),Failure_(max)。AKI伤员临床转归包括伤员转归和肾脏转归:根据伤后第14d、28d和出院时状态分为存活或死亡;根据AKI后第28d肾功能情况分为完全恢复(Scr不超过基础肌酐增长50%后的数值,例如基础肌酐为88umol/L即1.0mg/dl,Scr降至133 umol/L即1.5mg/dl以下则诊断为完全恢复)、部分恢复不依赖透析(Scr未降至完全恢复标准但不依赖透析)或依赖透析。休克定义为收缩压＜90mmHg,或较原水平下降＞40mmHg持续1h以上,常规补液不能使血压恢复或需要使用多巴胺6ug/Kg/min。横纹肌溶解定义筋膜室综合征伴CK＞975 IU/L。脓毒症(Sepsis)参考1991年美国芝加哥会议和2001年美国华盛顿会议标准诊断。非肾脏器功能障碍(呼吸、心血管、肝脏、胃肠道、血液、神经系统功能障碍)参考Gods标准。
3.数据收集
从数据库中记录人口学数据,临床数据和实验室数据。此外,还计算了损伤严重评分(Injury Severity Score ISS)、急性生理和慢性健康评估系统Ⅱ(Acute Physiology and Chronic Health EvaluationⅡAPACHEⅡ)评分、Glascow昏迷评分(Glascow Coma Score GCS)。所有数据由专人用Epidata3.0软件双份录入,并进行一致性核查。资料去除所有身份信息以保护病人隐私。
4.统计学方法
连续性变量以均数±标准差或中位数表示,分类变量以百分比表示,所有变量使用Kolmogorov-Smirnov方法进行正态性检验。根据是否为正态分布,连续性变量两组比较采用独立样本t检验或Mann-Whitney U方法,多组比较采用one-way ANOVA或Kruskal-Wallis H方法;分类变量采用Fisher精确检验或卡方检验。采用多变量Logistic方法分析AKI发生危险因素及预后不良因素,纳入Logistic回归模型的变量为单变量分析有统计学意义的因素和重要的临床因素;Hosmer-Lemeshow用于确定Logistic回归模型的拟合优度,P＞0.05视为可接受模型。采用Ordinal回归方法分析影响AKI严重程度的因素,Pearson和Deviance卡方检验用于检验Ordinal回归模型的拟合优度,P＞0.05视为可接受模型。双侧P＜0.05视为有统计学意义,采用SPSS13.0软件进行统计分析。
结果
1.RTI伤员特征
数据库中共4857例病例符合入选标准。76.6%为男性(3719/4857),伤员平均年龄33.3±15.4岁(1.90岁),70.0%(3390/4857)伤员为15-44岁青壮年,79.4%(3856/4857)为弱势道路使用者(包括行人、骑自行车者、骑摩托车者及摩托车乘员),1166例(24.0%)使用防护措施,1468例(30.2%)得到医务人员现场救护,送达时间(事故发生到送至医院接受治疗的时间)中位数是20min(1.0-720.0min)。入院平均ISS、GCS分别为12.9±8.7(1-75)和13.1±3.5(3-15),1054例(21.7%)进入ICU观察。受伤部位以四肢伤(64.6%)和头面部伤(49.7%)最多见,其余依次为胸部伤(19.2%)、腹部伤(18.5%)和脊柱伤(15.6%)。321例(6.6%)伤员发生休克,288例(5.9%)合并脓毒症,911例(18.8%)伴有一个或多个脏器功能障碍。住院时间中位数为17d(2-367d)。院内总死亡率为8.4%(408/4857),伤后14d内和28d内死亡分别6.4%(313/4857)和7.2%(352/4857)。
2.RTI后发生AKI者临床转归
358例(7.3%)伤员发生AKI。发生AKI的RTI伤员死亡率明显增高,并且部分存活伤员在AKI发生后28d仍然遗留肾功能障碍。358例AKI伤员院内死亡率高达51.1%(183/358),其中伤后14d内、28d内死亡率分别为40.2%、46.4%,而非AKI伤员院内死亡率仅为5.0%,其中伤后14d内、28d内死亡率分别为3.8%、4.1%(P均＜0.001)。并且伤员死亡率随AKI加重而增高,Risk_(max)、Injury_(max)和Failure_(max)伤员院内死亡率分别为34.2%、46.8%、76.5%(P＜0.001),其中伤后14d内死亡率分别为29.5%、42.6%、66.1%(P＜0.001),伤后28d内死亡率分别为30.9%、45.7%、71.3%(P＜0.001)。Risk_(max)、Injury_(max)和Failure_(max)死亡者存活时间中位数逐渐下降,分别7d(2-169d)、4d(2-199d)和3d(2-164d)(P=0.045),表明AKI越重者存活时间越短。
175例存活AKI伤员中无依赖透析者,11例(6.3%)在AKI后第28d仍然遗留肾功能障碍(肾功能部分恢复但不依赖透析),并且遗留肾功能障碍发生率随AKI加重而增高,Risk_(max)Injury_(max)和Failure_(max)分别为1.3%(2/149)、4.3%(4/94)和7.0%(5/115)(P=0.019)。
3.RTI后AKI发生危险因素及影响AKI严重程度因素
AKI发生率为7.3%(358/4857),其中73.2%(262/358)发生在伤后72h内,89.1%(319/358)发生在伤后一周内。男性伤员292例(81.4%),平均年龄44.0±17.4岁(13-88岁),301例(84.6%)为弱势道路使用者,仅60人(24.0%)使用防护措施,153例(43.2%)得到医务人员现场救援,送达时间(事故发生到送至医院接受治疗的时间)中位数是30min(4.0-420.0min),10.7%(38/358)伤员伤前有慢性疾病。伤员入院平均ISS和APACHEII评分分别为24.3±9.4(1-75)、19.6±8.0(1-42),266例(74.3%)伤员进入ICU观察,平均ICU时间是3d(2-116d)。235例(65-6%)并发非肾脏器功能障碍,平均功能障碍脏器数为2.3±1.3个(1—7个)。233例(65.0%)伤员受伤后接受外科手术;15例(4.2%)接受肾替代治疗(RRT)。住院时间中位数为12d(2-367d)。
单因素分析显示,AKI伤员男性比例高于非AKI伤员(81.4%vs 76.2%,P=0.027),前者平均年龄大(44.0岁vs 32.6岁,P＜0.001)、患慢性疾病者多(10.7%vs 5.9%,P=0.001)、弱势道路使用者比例高(84.1%vs 79.0%,P=0.006)、而采取安全防护措施伤员少(16.8%vs 24.6%,P=0.002)。在AKI伤员与非AKI伤员受伤程度和受伤部位比较中,前者损伤程度更严重(平均ISS:24.3 vs 12.0,P＜0.001;平均GCS:7.9 vs 13.5,P＜0.001),严重头部伤(GCS≤8)发生率(67.8%vs14.4%,P＜0.001)、胸部脏器伤发生率(21.2%vs 8.3%,P＜0.001)、腹部脏器伤发生率(31.4%vs 6.7%,P＜0.001)、开放长骨骨折发生率(23.4%vs 3.5%,P＜0.001)、多发伤发生率高于后者(82.4%vs 25.4%,P＜0.001)。AKI伤员与非AKI伤员伤后并发症(发生在AKI之前)比较,前者休克发生率(23.2%vs 5.3%,P＜0.001)、横纹肌溶解发生率(19.2%vs 5.4%,P＜0.001)、脓毒症(脓毒症:10.7%vs 4.9%,P＜0.001)和非肾脏器功能障碍发生率高于后者(33.2%vs 8.6%,P＜0.001)。将单因素分析有统计学意义的变量(P＜0.05)纳入logistic回归模型进行多因素分析,结果进一步证实男性(OR=1.471,95%CI:1.068-2.200),年龄增加(10yrs)(OR=1.387,95%CI:1.287-1.607),慢性疾病(OR=2.312,95%CI:1.458-3.665),送达时间＞60min(OR=3.470,95%CI:1.565-7.696),ISS＞15(OR=3.569,95%CI:2.090-6.094),严重头部伤(OR=4.236,95%CI:2.967-14.068),腹部脏器伤(OR=2.411,95%CI:1.666-3498),开放长骨骨折(OR=2.011,95%CI:1.408-2.873),休克(OR=2.055,95%CI:1.424-2.967),横纹肌溶解(OR=2.579,95%CI:1.776-3.745),呼吸系统功能障碍(OR=2.547,95%CI:1.567-4.138)是RTI发生AKI的危险因素。其中,对发生AKI影响最强的因素是伤势重(ISS＞25:OR=8.032,95%CI 4.417-14.650)、严重头部伤(OR=4.236,95%CI2.967-14.068)和送达时间＞60min(OR=3.470,95%CI 1.565-7.696)。与送达时间＜10min者比较,送达时间11-60min者发生AKI危险增加22.5%,而＞60min者发生AKI危险急剧增加247%。Hosmer-Lemeshow检验x~2=5.843,df=8,P=0.665,表明logistic回归模型拟合度较好。
AKI由轻微至严重分为Risk_(max)、Injury_(max)和Failure_(max),3组伤员分别为149例(41.6%),94例(26.3%)和115例(32.1%)。单因素分析显示,随着伤员受伤程度加重(平均ISS分别为20.0、24.6、27.3,P＜0.001;平均APACHEⅡ分别为17.0、20.2、22.7,P＜0.001;平均GCS分别为8.7、7.6、6.8,P=0.004)、平均低血压持续时间延长(分别为3.0h、6.0h、7.3h,P=0.037),严重头部伤发生率增高(分别为61.1%、69.1%、76.5%,P=0.027)、腹部脏器伤发生率增高(分别为24.8%、27.7%、42.6%,P=0.006)、多发伤发生率增高(分别为76.5%、84.0%、87.8%,P=0.049),AKI程度加重。将上述变量纳入Ordinal回归模型进行多因素分析,结果进一步表明ISS、APACHEⅡ增高(per point)、GCS降低(perpoint)、低血压持续时间延长(per hour)是加重AKI程度的危险因素。Pearsonx~2=920.188,df=950,P=0.750.Deviance x~2=815.340,df=950,P=0.999,显示Ordinal回归模型拟合度较好。
4.发生AKI的RTI伤员死亡危险因素
单因素分析显示,死亡AKI伤员入院时伤情比存活者更严重(平均ISS:28.6vs 20.3,P＜0.001;平均APACHEⅡ:23.9 vs 16.2,P＜0.001;平均GCS:5.6 vs 10.2,P＜0.001),严重头部伤(87.7%vs 50.3%,P＜0.001,P＜0.001)、多发伤发生率高(94.0%vs 69.7%,P＜0.001),肾损伤程度重(Failure_(max):48.1%vs 15.4%,P=0.027),呼吸、心血管、血液、神经系统功能障碍发生率高(呼吸功能障碍:41.0%vs 17.1%,P＜0.001;心血管功能障碍:25.1%vs 2.9%,P＜0.001;血液功能障碍:57.9%vs 11.4%,P＜0.001;神经系统功能障碍:4.4%vs 0.6%,P＜0.001)。死亡AKI伤员接受RRT比例亦高于存活伤员,但无统计学差异(6.0%vs 2.8%,P=0.195)。将单因素分析中有统计学意义的变量(P＜0.05)和重要的临床因素,包括性别、入院ISS(0-15、16-25、＞25)、APACHEⅡ评分(0-17、18-27、＞27)、多发伤、严重头部伤、AKI(Risk_(max)、Injury_(max)和Failure_(max))、RRT、呼吸、心血管、血液、中枢神经系统功能障碍纳入logistic回归模型进行多因素分析。结果显示,入院ISS＞25(OR=6.309,95%CI:1.704-36.534)、严重头部伤(OR=2.707,95%CI:1.022-7.154)、AKI-Failure_(max)(OR=2.761,95%CI:1.123-7.148)、呼吸功能障碍(OR=1.852,95%CI:1.542-3.080)、心血管功能障碍(OR=22.245,95%CI:4.507-119.788)和血液系统功能障碍(OR=7.660,95%CI:3.098-19.532)是发生AKI的RTI伤员院内死亡危险因素。其中对AKI死亡影响最强的因素是心血管功能障碍。肾损伤严重是(Failure_(max))伤员死亡危险是肾损伤轻微(Risk_(max))者的2.761倍。Hosmer-Lemeshow检验x~2=3.592,df=8,P=0.892,表明logistic回归模型拟合度较好。
5.影响存活者28d肾脏转归的危险因素
单因素分析显示,肾功能部分恢复伤员肾损伤程度更严重(Injury_(max):36.4%vs 28.6%,P=0.034;Failure_(max):45.5%vs 11.8%,P=0.007),脓毒症(54.5%vs15.2%,P=0.005)、严重横纹肌溶解(CK≥10000IU/L)发生率高(27.3%vs 69.7%,P=0.023),接受RRT者比例高(18.2%vs 1.2%,P=0.020)。此外,肾功能部分恢复伤员平均年龄大(45.8 vs 41.3,P=0.430)、送达时间长(64.0 vs 47.0,P=0.198)、呼吸功能障碍发生率高(36.4%vs 15.5%,P=0.092),但两组比较无统计学差异。将单因素分析中有统计学意义的变量(P＜0.05)和重要的临床因素,包括年龄、性别、送达时间、脓毒症、严重横纹肌溶解(CK≥10000IU/L)、RRT、AKI(包括Risk_(max)、Injury_(max)和Failure_(max))、呼吸、心血管、肝脏、胃肠、血液及神经系统功能障碍纳入Logistic回归模型进行分析,结果显示年龄增长(10yrs)(OR=1.973,95%CI:1.075-3.765)、肾损伤程度重(Failure_(max):OR=140.414,95%CI 6.123-3220.148:Injury_(max):OR=26.709,95%CI 1.922-371.090)、合并脓毒症(OR=21.167,95%CI 1.808-247.828)、严重横纹肌溶解(OR=6.126,95%CI 1.243-34.345)及呼吸系统功能障碍(OR=12.995,95%CI 1.255-134.564)是影响28d肾功能完全恢复的危险因素。其中,肾损伤严重程度是对28d肾功能完全恢复影响最强的因素。Hosmer-Lemeshow检验x~2=6.012,df=8,P=0.646,表明logistic回归模型拟合度较好。
结论
研究显示AKI是RTI严重并发症,发生AKI的RTI伤员死亡率明显增加,存活者可能因遗留肾功能障碍而致残。RIFLE标准能够预示发生AKI的RTI伤员预后和肾脏转归。延误院内救治时间(＞60min)、受伤程度(ISS＞15)和受伤部位(严重头部伤、腹部脏器伤)是RTI伤员发生AKI的重要因素;严重损伤(ISS＞25)、严重头部伤及非肾脏器功能障碍是发生AKI的RTI伤员预后危险因素。临床上针对这些因素加强防治可能降低AKI发生率、改善预后,从而降低RTI伤员死亡率和致残率。
Background
Road traffic injury(RTI) occurs on all continents,in every country of the world. Worldwide,an estimated 1.2 million people are killed in road crashes each year and more than half of these ones are young adults aged between 15 and 44 years. Projections of the World Health Organization(WHO) indicate that these figures will increase by about 65%by 2020,low-income and middle-income countries account for about 90%of the deaths unless there is new commitment to prevention.China is one of the most serious countries of road traffic safety problem.In 2001,China occupied the top of all countries in the rate of accident and mortality per ten thousand vehicles,which resulted in 106,000 deaths.The annual numbers of road traffic deaths rose sharply,and road traffic fatality rates rose by 4 times from 1978 to 2005. Without doubt,RTI is a growing worldwide public health problem of global. Acute kidney injury(AKI) is a clinical syndrome with high mortality in patients with severe trauma.The incidence of AKI ranged from 0.098 to 31%depending on the definition of AKI and studied populations.The mortality remained high(13 to 78%) and it was an important contributor to hospital mortality in post-traumatic population. However,we have known little so far concerning AKI after RTI though it was the most common cause of post-traumatic AKI.There is no large sample study to report the exact incidence of AKI,clinical outcome,and risk factors in patients with RTI.It is well known that prevention is better than cure for AKI,since there is no specific and effective management for the syndrome and blood purification do not improve patients' outcome.To promote clinical practice and further obtain the best outcomes for patients,it is important for clinicians to understand predictors of development and prognosis of AKI.Thus,the study was performed retrospectively in patients with RTI. In the study,we aimed to investigate independent risk factors for development and outcome of AKI in patients undergoing traffic,then offering a survival and health benefit for the patient suffered RTI.
Patients and Methods
1.Study population
A retrospective clinical study was performed.The NangFang Hospital and ZhuJiang Hospital is 2 academic medical centers affiliated with Sourthern Medical University.All patients with RTI admitted to both of hospitals between January 2002 and December 2006 were screened using the computerized hospital admissions and discharges database.Following patients were excluded from the study cohort:on chronic dialysis before traffic,staying in hospital less than 24 hrs,neither serum creatinine(Scr) value nor urine output record after the traffic.If a patient had more than one admission during the study period,only the first admission was included in the study.As a result,4857 records were analysed in the study.
2.Definitions
AKI was diagnosed and classified according to RIFLE criteria.The _(max)imum RIFLE stratum(class R_(max),class I_(max) or class F_(max)),which was based on the highest Scr level or the least urine output during hospital stay,was assigned to each patient for analysis.The clinical outcome of those with AKI included patient outcome and renal outcome.Complete renal recovery was defined by a convalescent Scr not more than 50%increased from baseline.e.g.if baseline Scr was 1.0 mg/dL(88 mcmol/L), complete recovery was said to occur if the new steady state SCrt was＜1.5 mg/dL (133 mcmol/L).Partial renal recovery was said to occur if the above condition for complete recovery was not met but the patient did not require chronic dialysis.
3.Data collection
The patients' information,including demographic data,clinical data and laboratory data were collected from the database.All data were inputted using Epidata3.0 software by a non-investigator data manager and repeated again,then double data were carried on consistency verification.All identifying information of patients was stripped of to preserve their anonymity.
4.Statistical analysis
In statistical data,continuous variables were presented as mean±standard deviation(SD) or median(range) and categorical variables were presented as percentages.All variables were tested for normal distribution using the Kolmogorov-Smimov test.One-way analysis of variance(one-way ANOVA) test or the Kruskal-Wallis H test for continuous variables according to their distribution; Fisher's exact test or the chi-square test were applied to assess categorical data associated with RIFLE classifications(including no AKI,class R_(max),class I_(max) and class F_(max)).To elucidate the impact of each category of RIFLE criterion on hospital mortality and find the risk factors for development of AKI,multiple-variable logistic regression analyses was conducted,variables at p＜0.05 in the univariate analysis and those considered clinically important were entered a multiple-variable logistic regression model.The Hosmer-Lemeshow test was employed to determine the goodness-of-fit of the model,P＞0.05 was regarded as an acceptable model.The results of multivariate logistic regression analysis were summarized by estimating odds ratios(OR) and respective 95%confidence interval(CI).We considered double-sided P＜0.05 as statistically significant.Data were analyzed using the SPSS version 13.0.
Results
1.Characteristic of patients with RTI
During the study period,4857 patients admitted for traffic trauma were evaluated.Of these patients,358 patients developed AKI.The number of male was 3719(76.6%),mean age was 33.3±15.4 yrs(1-90years).70.0%(3390/4857) patients were young adults aged between 15 and 44 years,and 79.4%(3856/4857) patients were vulnerable road users who had underlying probability of a crash for particular exposure.64.6%and 49.7%patients suffered extremity and head injury which were the most frequent injured location,followed by thoracic injury(19.2%),abdominal injury(18.5%) and spinal injury(15.6%).Mean ISS was 12.9±8.7(1-75) and mean GCS was 13.1±3.5(3-15) on admission,respectively.911(18.8%) patients had one or more than one organ dysfunctions.The median of length of hospital stay was 17d (2-367d).Overall mortality during hospitalization in population with RTI was 8.4% (408/4857).
2.Outcomes of patients who developed AKI after RTI
The mortality rate in patients who developed AKI was very high at 51.1% (183/358).This is in striking contrast to the mortality rate of only 5.0%(225/4499) in patients who did not develop AKI.There were significant differences in mortality rate between the population with AKI and those without AKI(P＜0.001).Of note,there was an increasing mortality with increasing severity of AKI.The mortality rate in patients of Risk_(max)、Injury_(max) or Failure_(max) were 29.5%、42.6%、66.1%within 14-day after injury,30.9%、45.7%、71.3%within 28-day after injury and 34.2%、46.8%、76.5%on discharge from hospital,respectively.
Of 175 survived patients suffered from AKI,93.7%(164/175) patients had complete renal recovery,6.3%(11/175) had partial renal recovery and all the survived became independent of RRT at 28 days after AKI.An increasing trend was observed for the rate of left renal insufficiency in class Risk_(max),class Injury_(max) and class Failure_(max),which was 1.3%、4.3%and 7.0%respectively(P=0.019).
3.Risk predictors for development of AKI and deteriorated AKI
The incidence of AKI in patients with road trauma was 7.3%(358/4857) according to the RIFLE criteria.In such patients,73.2%(262/358) of AKI occurred at the first 72 hours after trauma and 89.1%(319/358) occurred in the initial week, 10.7%(38/358) patients have pre-existing disease.The number of male and female was 183(82.8%) and 38(17.2%) respectively,mean age was 39.2±16.4 yrs(13—80years).Mean ISS was 24.4±9.0(1—75) and mean APACHEⅡscores was 19.6±8.3(4—42) on admission.137(61.9%) patients had additional organ dysfunctions and the mean number of organ dysfunction was 2.3±1.3(1—6).65% (233/358) patients underwent surgical operations,15(4.2%) patients required renal replacement therapy.they have a longer ICU stay and hospital stay compared to patients with no AKI.In univariate analysis,the patients with AKI were older than the patients without AKI(P=0.002),their rescue time were longer and were more severe injury assessed by ISS,APACHEⅡscore and GCS,The occurrence of severe head injury,abdominal organ injury,thoracic organ injury and open long bone fracture were more frequent in population with AKI(P＜0.001),and the patients with AKI had higher frequencies of serious complicating morbidities including shock, rhabdomyolysis,sepsis and additional renal dysfunction than those ones without AKI (P＜0.05).We used a multivariate logistic regression model to further investigate interactions between all statistically significant factors contributing to AKI.The analysis showed that increasing age(10yrs),rescue time＞60min,severe head injury, abdominal organ injury,open long bone fracture,rhabdomyolysis,shock and respiration system dysfunction were associated with increased risk for occurrence of AKI(P＜0.05).Hosmer-Lemeshow goodness-of-fit test showed that the model was statistically significant without bias(x~2=5.843,df=8,P=0.665).
The patients were categorized Risk_(max)、Injury_(max) or Failure_(max) based on alterations in serum creatinine or urine output,which was 284(58.3%),97(19.9%) and 115(21.8%) respectively.In univariable analysis,multiple injury,severe injury assessed by ISS,APACHEⅡscore and GCS,severe head injury,abdominal organ injury,duration of hypotension and were statistically significant predictors for deteriorated renal dysfunction.Ordinal regression analysis showed that the deteriorated AKI followed the increasing APACHEⅡscore,ISS,decreasing GCS and prolonged time of hypotension duration(p＜0.05).Pearson test(x~2=920.188, df=950,P=0.750) and Deviance test(x~2=815.340,df=950,P=0.999)showed that the regression model was statistically significant without bias.
4.Risk factors for mortality in patients with AKI
Among the 358 patients with AKI,51.1%(183/358) died prior to hospital discharge.The 14-day and 28-day mortality rate were 44.7%(160/358),47.8% (171/358) respectively.Several factors were associated with death in univariate analysis,including severity degree of injury assessed by ISS,APACHEⅡscore and GCS,severe head injury and organ dysfunction syndrome including respiratory, cardiovascular,hematological,neurological and kidney.Factors not significantly associated with death in hospital included gender,age or RRT.A multivariable logistic regression model was developed to assess for independent factors associated with death in hospital for patients with AKI.The analysis showed that severe head injury,ISS＞25,RIFLE-Failure,and respiratory,cardiovascular,hematological system dysfunction were associated with poor prognosis.Hosmer-Lemeshow goodness-of-fit test showed that the model was statistically significant without bias(x~2=3.592,df=8, P=0.892).
5.Renal outcome in the survived and risk factors for left renal insufficiency
Compared to those that recovered completely renal function,patients that remained left renal insufficiency were more likely to be male,older age,severe AKI, required renal replacement therapy,complicated with ODS and sepsis,with a diagnosis of pre-existing disease and severe rhabdomyolysis(CK≥10000IU/L) in univariate analysis.Followed variables were associated independently with poor renal outcome on 28-day after AKI in a multivariate logistic regression analysis:sepsis, AKI-Injury_(max),AKI-Failure_(max) and respiration system dysfunction. Hosmer-Lemeshow goodness-of-fit test showed that the model was statistically significant without bias(x~2=6.012,df=8,P=0.646).
Conclusions
AKI was a severe complication in the population with RTI and associated with greatly increased mortality during hospitalization,and could incapacitate the survivors because of left renal insufficiency.RIFLE criteria could contribute to predict the patient at a moderate to high risk for mortality and left renal insufficiency. Certain independent predictors such as delayed hospital rescue,severe injury assessed by ISS and severe head injury could predict patients at a high risk for development of AKI.The latter two and additional organs dysfunction were also predictors of mortality in those with AKI.Such risk predictors could assist in implementing strategies to prevent AKI and improve prognosis in patients with AKI,which should offer better outcomes for patients suffered RTI.
引文
[1]Baker SP,O'Neill B,Haddon W et al.The Injury Severity Score:a method for describing patients with multiple injuries and evaluating emergency care.J Trauma.1988,14:187-196.
[2]简明损伤定级标准—1990修订版;1998更新本重庆出版社;2002.3
[3]Knaus WA,Draper EA,Wanger DP,et al.APACHE Ⅱ:a severity of disease classifiaction system.Crit Care Med 1985,13(3):818-819.
[4]Teasdale G,Jennet B.Assessment of coma and impaired consciousness.A practical scale.Lancet 1974,2:81-84.
[5]Bellomo R,Ronco C,Kellum JA,Mehta RL,Palevsky P,the ADQI workgroup:Acute renal failure-definition,outcome measures,animal models,fluid therapy and information technology needs:the Second International Consensus Conference of the Acute Dialysis Quality Initiative(ADQI) Group.Crit Care 2004,8:204-212.
[6]National Kidney Foundation.K/DOQI clinical practice guidelines for chronic kidney disease:evaluation,classification,and stratification.Am J Kidney Dis 2002,39:S1-266.
[7]Teasdale G,Jennet B.Assessment coma and impaired consciousness.A practical scale.Lancet 1974,2:81-84.
[8]Regel G,Lobenhoffer P,Grotz M,Treatment results of patients with multiple Trauma:an analysis of 3406 cases treated between 1972 and 1991 at German level I trauma center.J Trauma1995,38:70-77.
[9]Antonelli M,Moro ML,Capelli O.Risk factorsfor early and late onset pneumonia in trauma patients.Chest 1994,105:224-228.
[10]Melli G,Chaudhry V,Cornblath DR.Rhabdomyolysis:an evaluation of 475 hospitalized patients.Medicine (Baltimore). 2005 Nov;84(6):377-385.
[11] American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference. Definitions for sepsis and organ failure and guidelines for the use of innovation therapies in sepsis. Critical Care Medicine 1992,20:864-872.
[12] Goris RJ, te Boekhorst TP, Nuytinck JK, Gimbrere JS. Multiple-organ failure. Generalized autodestructive inflammation? Arch Surg 1985,120(10): 1109-1115.
[13] Mangano CM, Diamondstone LS, Ramsay JG, Aggarwal A, Herskowitz A,Mangano DT: Renal dysfunction following myocardial revascularization: risk factors, adverse outcomes and hospital resource utilization. The Multicenter Study of Perioperative Ischemia Research Group. Ann Intern Med 1998; 128:194-203.
[14] Nash K, Hafeez A, Hou S: Hospital-acquired renal insufficiency. Am J Kidney Dis 2002; 39: 936 Pruchnicki MC, Dasta JF: Acute renal failure in hospitalized patients: part I. Ann Pharmacother 2002; 36: 1261-1267.
[15] Pruchnicki MC, Dasta JF: Acute renal failure in hospitalized patients: part II.Ann Pharmacother 2002; 36: 1430-42 Parfrey PS, Griffiths SM, Barrett BJ:Contrast material-induced renal failure in pts with diabetes.
[16] mellitus, renal insufficiency, or both. A prospective controlled study. N Engl J Med 1989; 320:143-9 Schmekal B, Pichler R, Biesenbach G: Causes and prognosis of nontraumatic acute renal failure.
[17] requiring dialysis in adult pts with and without diabetes. Ren Fail 2004; 26: 43
[18] Peden M, McGee K, Sharma G. The injury chart book: a graphical overview of the global burden of injuries. Geneva, World Health Organization, 2002.
[19] Carlos VR Brown, MD, FACS, Joseph J Dubose.Natural History and Outcomes of Renal Failure after Trauma. J Am Coll Surg 2008;206:426-431.
[20]Plurad D,Brown C,Chan L,et al.Emergency department hypotension is not an independent risk factor for post-traumatic renal dysfunction.J Trauma 2006;61:1120-1127,discussion 1127-1128.
[21]Morris JA Jr,Mucha P Jr,Ross SE,et al.Acute posttraumatic renal failure:A multicenter perspective.J Trauma 1991;31:1584.
[22]Nadvi SS,Mokoena T,Gouws E,Haffajee AA.Prognosis in post-traumatic acute renal failure is adversely influenced by hypotension and hyperkalemia.Eur J Surg 1996;162:121-124.
[23]Mendonca A,Vincent JL,Suter PM,et al.Acute renal failure in the ICU:risk factors and outcome evaluated by the SOFA score.Int Care Med 2000;26:915-921.
[24]Gettings LG,Reynolds HN,Sea.lea T.Outcome in posttraumatic acute renal failure when continous renal replacement is applied early vs.late.Int Care Med 1999;25:805-813.
[25]Champion H,Saco W,Long W,et al.Indications for early haemodialysis in multiple trauma.Lancet 1974;I:1125-1127.of the larger constellation of multiorgan failure.
[26]张文贤,张训,侯凡凡.创伤后急性肾衰竭临床分析.解放军医学杂志,2002,27(7):641-642.
[27]Regel G,Lobenhoffer P,Grotz M,et al.Treatment results of patients with multiple trauma,an analysis of 3406 cases treated between 1972 and 1991 at German level I trauma center.J Trauma 1995.38.70-77.
[28]Mehta RL,PascualMT,Soroko S,et al.Diuretics,mortality,and nonrecovery of renal function in acute renal failure.JAMA 2002;288:2547-2553.
[29]Vivino G,Antonelli M,Moro ML,et al.Risk factors for acute renal failure in trauma patients.Int CareMed 1998;24:808-814.
[30]Guly UM, Turney JH. Post-traumatic renal failure, 1956_1988. Clin Nephrol 1990;34:79-83.
[31] Ympa YP, Sakr Y, Reinhart K, Vincent J. Has mortality from acute renal failure decreased? A systematic review of the literature. Am J Med 2005;118:827-832.
[32] Thurman D. The epidemiology and economics of head trauma. In. Miller L,Hayes R, eds. Head trauma. basic, preclinical, and clinical directions. New York,NY, Wiley and Sons, 2001.327-347.
[33] Baldo V. Epidemiological aspect of traumatic brain injury in Northeast Italy.European Journal of Epidemiology, 2003,18.1059.1063.
[34] Nikoli S, Mici J, Mihailovi Z. Correlation between survival time and severity of injuries in fatal injuries in traffic accidents. Srp Arh Celok Lek. 2001 Nov-Dec;129(11-12):291-5.
[35] Teasdale G, Jennet B. Assessment coma and impaired consciousness. A practical scale. Lancet 1974, 2: 81-84.
[36] Tran DD, Cuesta MA. Acute renal failure in patients with severe civilian trauma.Nephrol Dial Transplant. 1994; 9.121-125.
[37] Menashe PI, Ross SA, Gottlieb JE. Acquired renal insufficiency incritically ill patients. Crit Care Med 1988; 16.1106-1109.
[38] Stene JK. Renal failure in trauma patients. Crit Care Clin 1990;6. 111.
[39] Zager RA. Studies of mechanisms and protective maneuvers in myoglobinuric acute renal injury. Lab Invest 1989; 60. 619-29.
[40] Rabb H, Wang Z, Nemoto T. Acute renal failure leads to dysregulation of lung salt and water channels. Kidney Int 2003; 63. 600-6.
[41] Rasmussen HH, Ibel LS. Acute renal failure. Multivariate analysis of causes and risk factors. Am J Med 1982; 73. 211-8.Mangano CM, Diamondstone LS, Ramsay JG, et al, Renal dysfunction following myocardial revascularization.risk factors, adverse outcomes and hospital resource utilization. The Multicenter Study of Perioperative Ischemia Research Group. Ann Intern Med 1998; 128.194-203.
[42] Nash K, Hafeez A, Hou S. Hospital-acquired renal insufficiency. Am J Kidney Dis 2002; 39. 936.
[43] Pruchnicki MC, Dasta JF. Acute renal failure in hospitalized patients. part I. Ann Pharmacother 2002; 36. 1261-7.
[44] Pruchnicki MC, Dasta JF. Acute renal failure in hospitalized patients. part II.Ann Pharmacother 2002; 36. 1430-42.
[45] Parfrey PS, Griffiths SM, Barrett BJ. Contrast material-induced renal failure in pts with diabetes mellitus, renal insufficiency, or both. A prospective controlled study. N Engl J Med 1989; 320. 143-9.
[46] Schmekal B, Pichler R, Biesenbach G. Causes and prognosis of nontraumatic acute renal failure requiring dialysis in adult pts with and without diabetes. Ren Fail 2004; 26. 43,
[47] Mehta RL, Pascual M, Grata CG, et al. Refining predictive models in critically ill patients with acute renal failure. J Am Soc Neprhol 2002; 13. 1350-7.
[48] Meuller C, Buerkle G, Perruchoud AP, et al. Female sex and risk of contrast nephropathy after percutaneous coronary interventions. Can J Cardiol 2004; 20.505-509.
[49] Athanasiou T, Al-Ruzzeh S, DelStanbridge R, et al. Is the female gender an independent predictor of adverse outcome after off-pump coronary artery bypass grafting? Ann Thorac Surg 2003; 75. 1153-60.
[50] Thakar CV, Arrigain S, Worley S, et al. A clinical score to predict acute renal failure after cardiac surgery. Journal of the American Society of Nephrology 2005; 16.162-8.
[51] Sever MS, Erek E, Vanholder R, Lameire N. Effect of gender on various parameters of crush syndrome victims of the Marmara earthquake. J Nephrol.2004 May-Jun;17(3):399-404.
[52] Regaller MJR, Theilen H, Koch T. Volume replacement in criticallyill patients with acute renal failure. J Am Soc Nephrol.
[53]2001;12:S33-S39.Abernathy VE, Lieberthal W. Acute Renal Failure in the critically illpatient. Crit Care Clin. 2002;18:203-222.
[54] Brady H, Singer GG. Acute renal failure. Lancet.
[55] 1995;346:1533-1540.Holmes CL, Walley KR. The evaluation and management of shock. Clin Chest Med. 2003;24:775-789.
[56] Kohli HS, Bhaskaran MC, Muthukumar T et al. Treatment-related acute renal failure in the elderly: a hospital=based prospective study. Neprhol Dial Transplant 2000; 15: 212-217.
[57] Dziedzic T, Bartus S, Klimkowicz A, et al . Intracerebral hemorrhage triggers interleukin- 6 and interleukin- 10 re -lease in blood [J]. Stroke, 2002, 33. 2334-2335.
[58] Breen D ,Bihari D. Acute renal failure as a part of multiple organ failure .The slippery slope of critical illness. Kidney Int ,1998 ,53 (Suppl 66) .S25.
[59] Brown C, Rhee P, Chan L .Preventing renal failure in patients with rhabomyolysis: dobicarbonate and mannitol make a difference? J Trauma.2004;56:1191-1196.
[60] Lee KH, Hwang SO, Cho JH, Moon JB, Kang GH, Kim SH. 179 predicting factors for acute renal failure induced by rhabdomyolysis at the early stage of multiple trauma. American College ofEmergency Physicians 2000 Research Forum. 36: S47.
[61] Fine DM, Gelber AC, Melamed ML, Lin JC, Zhang L, Eustace JA.Risk factors for renal failure among 72 consecutive patients withrhabdomyolysis related to illicit drug use. Am J Med. 2004;l 17:607-610.
[62] McGonigal MD. The effects of treatment of renal trauma on renalfunction. J Trauma. 1987;27:471-476.
[63] Better OS, Rubinstein I, Reis DN. Muscle crush compartment syndrome.fulminant local edema with threatening systemic effects. Kidney Int 2003; 63.1155-7.
[64] Menashe PI, Ross SA, Gottlieb JE. Acquired renal insufficiency incritically ill patients. Crit Care Med 1988; 16.1106-1109.
[65] Stene JK. Renal failure in trauma patients. Crit Care Clin 1990;6. 111.
[66] Baliga R, Ueda N, Walker PD, et al. Oxidant mechanisms in toxic acute renal failure. Drug Metab Rev. 1999; 31. 971-97.
[67] Homsi E, Barreiro MF, Orlando JM, et al. Prophylaxis of acute renal failure in patients with rhabdomyolysis. Renal Failure 1997; 19. 283-8.
[68] Better OS, Stein JH. Early management of shock and prophylaxis of acute renal failure in traumatic rhabdomyolysis. N Engl J Med 1990; 322. 825-9.
[69] Hojs R, Ekart R, Sinkovic A, et al. Rhabdomyolysis and acute renal failure in intensive care unit. Ren Fail 1999; 21. 675-84.
[70] Solomon R, Werner C, Mann D, D'Elia J, Silva P: Effects of saline, mannitol,and furosemide to prevent acute decreases in renal function induced by radiocontrast agents [see comments]. New England Journal of Medicine 1994;331:1416-20.
[71] Trivedi HS, Moore H, Nasr S: A randomized prospective trial to assess the role of saline hydration on the development of contrast nephrotoxicity. Nephron Clin Pract 2003;93:C29-C34.
[72] Stevens MA, McCullough PA, Tobin KJ: A prospective randomized trial of prevention measures in patients at high risk for contrast nephropathy. Results of the P. R. I. N. C. E. study. J Am Coll Cardiol 1999; 33: 403-11.
[73] Leehey DJ, Braun BI, Tholl DA, Chung LS, Gross CA, Roback JA, Lentino JR:Can pharmacokinetic dosing decrease nephrotoxicity associated with aminoglycoside therapy. Journal of the American Society of Nephrology 1993; 4:81-90.
[74] Moore RD, Smith CR, Lipsky JJ, Mellits ED, Lietman PS: Risk factors for nephrotoxicity in patients treated with aminoglycosides. Ann Intern Med 1984;100: 352-7.
[75] Kaufman J, Dhakal M, Patel B, Hamburger R: Community-acquired acute renal failure. Am J Kidney Dis 1991; 17: 191-8.
[76] Malinoski DJ, Slater MS, Mullins RJ. Crush injury and rhabdomyolysis. Crit Care Clin. 2004 Jan;20(1).171-92.
[77] Gunal AI, Celiker H, Dogukan A, et al. Early and vigorous resuscitation prevents acute renal failure in the crush victims of catastrophic earthquakes. J Am Soc Nephrol 2004; 15. 1862-1867
[78] Bell M, Liljestam E, Granath F, et al. Optimal follow-up time after continuous renal replacement therapy in actual renal failure patients stratified with the RIFLE criteria. Nephrol Dial Transplant 2005; 20.354-360.
[79] Abosaif NY, Tolba YA, Heap M, et al. The outcome of acute renal failure in theintensive care unit according to RIFLE. model application, sensitivity, and predictability. Am J Kidney Dis 2005; 46.1038-1048.
[80] Kuitunen A, Vento A, Suojaranta-Ylinen R, et al. Acute renal failure aftercardiac surgery. evaluation of the RIFLE classification. Ann Thorac Surg 2006;81.542-546.
[81] Guitard J, Cointault O, Kamar N, et al. Acute renal failure following liver transplantation with induction therapy. Clin Nephrol 2006; 65.103-112.
[82] Hoste EA, Clermont G, Kersten A, et al. RIFLE criteria for acute kidney injury are associated with hospital mortality in critically ill patients. a cohort analysis.Crit Care 2006; 10.R73.
[83] Uchino S, Bellomo R, Goldsmith D, et al. An assessment of the RIFLE criteria for acute renal failure in hospitalized patients. Crit Care Med 2006;34.1913-1917.
[84] Lin C-Y, Chen Y-C, Tsai F-C, et al. RIFLE classification is predictive of shoRTIerm prognosis in critically ill patients with acute renal failure supported by extracorporeal membrane oxygenation. Nephrol Dial Transplant 2006;doi.10.1093/ndt/gfl326.
[85] Heringlake M, Knappe M, Vargas HeinO, et al. Renal dysfunction according to the ADQI-RIFLE system and clinical practice patterns after cardiac surgery in Germany. Minerva Anestesiol 2006; 72.645-654.
[86] Lopes JA, Jorge S, Neves FC, et al. An assessment of the RIFLE criteria for acute renal failure in the severely burned patients.Nephrol Dial Transplant 2006;doi.10.1093/ndt/gfl468.
[87]A Akcan-Arikan, M Zappitelli, LL Loftis, et al.Modified RIFLE criteria in critically ill children with acute kidney injury. International Society of Nephrology 2007; 71(10).1028-35.
[88] Jose Antonio Lopes, Joana Fernandes, Sofia Jorge, et al. An assessment of the RIFLE criteria for acute renal failure in critically ill HIV-infected patients.Critical Care 2007,11.401 (doi.10.1186/cc5121).
[89] Perrone RD, Madias NE, Levey AS. Serum creatinine as an index of renal function: new insights into old concepts. Clin Chem,1992,38:1933-1953.
[90] Mehta RL, Kellum JA, Shah SV, et al. Acute kidney injury network: report of an initiative to improve outcomes in acute kidney injury. Crit Care (2007) 11 :R31.
[91] Durham RM, Moran JJ, Mazuski JE, Multiple organ failure in trauma patients.J Trauma. 2003 Oct;55(4):608-616.
[92] Barie P, Hydro L, Fischer E. A prospective comparison of two multiple dysfunction/failure scoring systems for prediction of mortality in critical surgical illness. J Trauma. 1994;37:660-666.
[93] Van Biesen W, Yegenaga I, Vanholder R, et al:Relationship between fluid status and its management on acute renal failure (ARF) in intensive care unit (ICU) patients with sepsis:A prospective analysis. J Nephrol 2005; 18: 54-60.
[94] Rabb H, Wang Z, Nemoto T, et al: Acute renal failure leads to dysregulation of lung salt and water channels. Kidney Int 2003; 63:600-606.
[95] Kelly KJ: Distant effects of experimental renal ischemia/reperfusion injury. J Am SocNephrol 2003; 14:1549-1558.
[96] Hoke TS, Douglas IS, Klein CL, Acute renal failure after bilateral nephrectomy is associated withcytokine-mediated pulmonary injury. J Am Soc Nephrol. 2007 Jan;18(1).155-64..
[97] Himmelfarb J, McMonagle E, Freedman S, et al: Oxidative stress is increased in critically ill patients with acute renal failure. J Am Soc Nephrol 2004;15:2449-2456.
[98] Kjellstrand CM,Gornick C,DavinT. Recovery from acute renal failure. Clin Exp Dial Apheresis 1981 ;5:143-161.
[99] Sean M. Bagshaw. MD, MSc, Garth Mortis, MD. Christopher J. Doig. MD, MSc,Tomas Godinez-Luna, MD. One-Year Mortality in Critically Ill Patients by Severity of Kidney Dysfunction: A Population-Based Assessment. Am J Kidney Dis 48:402-409.
[2]简明损伤定级标准—1990修订版;1998更新本重庆出版社;2002.3
[3]Knaus WA,Draper EA,Wanger DP,et al.APACHE Ⅱ:a severity of disease classifiaction system.Crit Care Med 1985,13(3):818-819.
[4]Teasdale G,Jennet B.Assessment of coma and impaired consciousness.A practical scale.Lancet 1974,2:81-84.
[5]Bellomo R,Ronco C,Kellum JA,Mehta RL,Palevsky P,the ADQI workgroup:Acute renal failure-definition,outcome measures,animal models,fluid therapy and information technology needs:the Second International Consensus Conference of the Acute Dialysis Quality Initiative(ADQI) Group.Crit Care 2004,8:204-212.
[6]National Kidney Foundation.K/DOQI clinical practice guidelines for chronic kidney disease:evaluation,classification,and stratification.Am J Kidney Dis 2002,39:S1-266.
[7]Teasdale G,Jennet B.Assessment coma and impaired consciousness.A practical scale.Lancet 1974,2:81-84.
[8]Regel G,Lobenhoffer P,Grotz M,Treatment results of patients with multiple Trauma:an analysis of 3406 cases treated between 1972 and 1991 at German level I trauma center.J Trauma1995,38:70-77.
[9]Antonelli M,Moro ML,Capelli O.Risk factorsfor early and late onset pneumonia in trauma patients.Chest 1994,105:224-228.
[10]Melli G,Chaudhry V,Cornblath DR.Rhabdomyolysis:an evaluation of 475 hospitalized patients.Medicine (Baltimore). 2005 Nov;84(6):377-385.
[11] American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference. Definitions for sepsis and organ failure and guidelines for the use of innovation therapies in sepsis. Critical Care Medicine 1992,20:864-872.
[12] Goris RJ, te Boekhorst TP, Nuytinck JK, Gimbrere JS. Multiple-organ failure. Generalized autodestructive inflammation? Arch Surg 1985,120(10): 1109-1115.
[13] Mangano CM, Diamondstone LS, Ramsay JG, Aggarwal A, Herskowitz A,Mangano DT: Renal dysfunction following myocardial revascularization: risk factors, adverse outcomes and hospital resource utilization. The Multicenter Study of Perioperative Ischemia Research Group. Ann Intern Med 1998; 128:194-203.
[14] Nash K, Hafeez A, Hou S: Hospital-acquired renal insufficiency. Am J Kidney Dis 2002; 39: 936 Pruchnicki MC, Dasta JF: Acute renal failure in hospitalized patients: part I. Ann Pharmacother 2002; 36: 1261-1267.
[15] Pruchnicki MC, Dasta JF: Acute renal failure in hospitalized patients: part II.Ann Pharmacother 2002; 36: 1430-42 Parfrey PS, Griffiths SM, Barrett BJ:Contrast material-induced renal failure in pts with diabetes.
[16] mellitus, renal insufficiency, or both. A prospective controlled study. N Engl J Med 1989; 320:143-9 Schmekal B, Pichler R, Biesenbach G: Causes and prognosis of nontraumatic acute renal failure.
[17] requiring dialysis in adult pts with and without diabetes. Ren Fail 2004; 26: 43
[18] Peden M, McGee K, Sharma G. The injury chart book: a graphical overview of the global burden of injuries. Geneva, World Health Organization, 2002.
[19] Carlos VR Brown, MD, FACS, Joseph J Dubose.Natural History and Outcomes of Renal Failure after Trauma. J Am Coll Surg 2008;206:426-431.
[20]Plurad D,Brown C,Chan L,et al.Emergency department hypotension is not an independent risk factor for post-traumatic renal dysfunction.J Trauma 2006;61:1120-1127,discussion 1127-1128.
[21]Morris JA Jr,Mucha P Jr,Ross SE,et al.Acute posttraumatic renal failure:A multicenter perspective.J Trauma 1991;31:1584.
[22]Nadvi SS,Mokoena T,Gouws E,Haffajee AA.Prognosis in post-traumatic acute renal failure is adversely influenced by hypotension and hyperkalemia.Eur J Surg 1996;162:121-124.
[23]Mendonca A,Vincent JL,Suter PM,et al.Acute renal failure in the ICU:risk factors and outcome evaluated by the SOFA score.Int Care Med 2000;26:915-921.
[24]Gettings LG,Reynolds HN,Sea.lea T.Outcome in posttraumatic acute renal failure when continous renal replacement is applied early vs.late.Int Care Med 1999;25:805-813.
[25]Champion H,Saco W,Long W,et al.Indications for early haemodialysis in multiple trauma.Lancet 1974;I:1125-1127.of the larger constellation of multiorgan failure.
[26]张文贤,张训,侯凡凡.创伤后急性肾衰竭临床分析.解放军医学杂志,2002,27(7):641-642.
[27]Regel G,Lobenhoffer P,Grotz M,et al.Treatment results of patients with multiple trauma,an analysis of 3406 cases treated between 1972 and 1991 at German level I trauma center.J Trauma 1995.38.70-77.
[28]Mehta RL,PascualMT,Soroko S,et al.Diuretics,mortality,and nonrecovery of renal function in acute renal failure.JAMA 2002;288:2547-2553.
[29]Vivino G,Antonelli M,Moro ML,et al.Risk factors for acute renal failure in trauma patients.Int CareMed 1998;24:808-814.
[30]Guly UM, Turney JH. Post-traumatic renal failure, 1956_1988. Clin Nephrol 1990;34:79-83.
[31] Ympa YP, Sakr Y, Reinhart K, Vincent J. Has mortality from acute renal failure decreased? A systematic review of the literature. Am J Med 2005;118:827-832.
[32] Thurman D. The epidemiology and economics of head trauma. In. Miller L,Hayes R, eds. Head trauma. basic, preclinical, and clinical directions. New York,NY, Wiley and Sons, 2001.327-347.
[33] Baldo V. Epidemiological aspect of traumatic brain injury in Northeast Italy.European Journal of Epidemiology, 2003,18.1059.1063.
[34] Nikoli S, Mici J, Mihailovi Z. Correlation between survival time and severity of injuries in fatal injuries in traffic accidents. Srp Arh Celok Lek. 2001 Nov-Dec;129(11-12):291-5.
[35] Teasdale G, Jennet B. Assessment coma and impaired consciousness. A practical scale. Lancet 1974, 2: 81-84.
[36] Tran DD, Cuesta MA. Acute renal failure in patients with severe civilian trauma.Nephrol Dial Transplant. 1994; 9.121-125.
[37] Menashe PI, Ross SA, Gottlieb JE. Acquired renal insufficiency incritically ill patients. Crit Care Med 1988; 16.1106-1109.
[38] Stene JK. Renal failure in trauma patients. Crit Care Clin 1990;6. 111.
[39] Zager RA. Studies of mechanisms and protective maneuvers in myoglobinuric acute renal injury. Lab Invest 1989; 60. 619-29.
[40] Rabb H, Wang Z, Nemoto T. Acute renal failure leads to dysregulation of lung salt and water channels. Kidney Int 2003; 63. 600-6.
[41] Rasmussen HH, Ibel LS. Acute renal failure. Multivariate analysis of causes and risk factors. Am J Med 1982; 73. 211-8.Mangano CM, Diamondstone LS, Ramsay JG, et al, Renal dysfunction following myocardial revascularization.risk factors, adverse outcomes and hospital resource utilization. The Multicenter Study of Perioperative Ischemia Research Group. Ann Intern Med 1998; 128.194-203.
[42] Nash K, Hafeez A, Hou S. Hospital-acquired renal insufficiency. Am J Kidney Dis 2002; 39. 936.
[43] Pruchnicki MC, Dasta JF. Acute renal failure in hospitalized patients. part I. Ann Pharmacother 2002; 36. 1261-7.
[44] Pruchnicki MC, Dasta JF. Acute renal failure in hospitalized patients. part II.Ann Pharmacother 2002; 36. 1430-42.
[45] Parfrey PS, Griffiths SM, Barrett BJ. Contrast material-induced renal failure in pts with diabetes mellitus, renal insufficiency, or both. A prospective controlled study. N Engl J Med 1989; 320. 143-9.
[46] Schmekal B, Pichler R, Biesenbach G. Causes and prognosis of nontraumatic acute renal failure requiring dialysis in adult pts with and without diabetes. Ren Fail 2004; 26. 43,
[47] Mehta RL, Pascual M, Grata CG, et al. Refining predictive models in critically ill patients with acute renal failure. J Am Soc Neprhol 2002; 13. 1350-7.
[48] Meuller C, Buerkle G, Perruchoud AP, et al. Female sex and risk of contrast nephropathy after percutaneous coronary interventions. Can J Cardiol 2004; 20.505-509.
[49] Athanasiou T, Al-Ruzzeh S, DelStanbridge R, et al. Is the female gender an independent predictor of adverse outcome after off-pump coronary artery bypass grafting? Ann Thorac Surg 2003; 75. 1153-60.
[50] Thakar CV, Arrigain S, Worley S, et al. A clinical score to predict acute renal failure after cardiac surgery. Journal of the American Society of Nephrology 2005; 16.162-8.
[51] Sever MS, Erek E, Vanholder R, Lameire N. Effect of gender on various parameters of crush syndrome victims of the Marmara earthquake. J Nephrol.2004 May-Jun;17(3):399-404.
[52] Regaller MJR, Theilen H, Koch T. Volume replacement in criticallyill patients with acute renal failure. J Am Soc Nephrol.
[53]2001;12:S33-S39.Abernathy VE, Lieberthal W. Acute Renal Failure in the critically illpatient. Crit Care Clin. 2002;18:203-222.
[54] Brady H, Singer GG. Acute renal failure. Lancet.
[55] 1995;346:1533-1540.Holmes CL, Walley KR. The evaluation and management of shock. Clin Chest Med. 2003;24:775-789.
[56] Kohli HS, Bhaskaran MC, Muthukumar T et al. Treatment-related acute renal failure in the elderly: a hospital=based prospective study. Neprhol Dial Transplant 2000; 15: 212-217.
[57] Dziedzic T, Bartus S, Klimkowicz A, et al . Intracerebral hemorrhage triggers interleukin- 6 and interleukin- 10 re -lease in blood [J]. Stroke, 2002, 33. 2334-2335.
[58] Breen D ,Bihari D. Acute renal failure as a part of multiple organ failure .The slippery slope of critical illness. Kidney Int ,1998 ,53 (Suppl 66) .S25.
[59] Brown C, Rhee P, Chan L .Preventing renal failure in patients with rhabomyolysis: dobicarbonate and mannitol make a difference? J Trauma.2004;56:1191-1196.
[60] Lee KH, Hwang SO, Cho JH, Moon JB, Kang GH, Kim SH. 179 predicting factors for acute renal failure induced by rhabdomyolysis at the early stage of multiple trauma. American College ofEmergency Physicians 2000 Research Forum. 36: S47.
[61] Fine DM, Gelber AC, Melamed ML, Lin JC, Zhang L, Eustace JA.Risk factors for renal failure among 72 consecutive patients withrhabdomyolysis related to illicit drug use. Am J Med. 2004;l 17:607-610.
[62] McGonigal MD. The effects of treatment of renal trauma on renalfunction. J Trauma. 1987;27:471-476.
[63] Better OS, Rubinstein I, Reis DN. Muscle crush compartment syndrome.fulminant local edema with threatening systemic effects. Kidney Int 2003; 63.1155-7.
[64] Menashe PI, Ross SA, Gottlieb JE. Acquired renal insufficiency incritically ill patients. Crit Care Med 1988; 16.1106-1109.
[65] Stene JK. Renal failure in trauma patients. Crit Care Clin 1990;6. 111.
[66] Baliga R, Ueda N, Walker PD, et al. Oxidant mechanisms in toxic acute renal failure. Drug Metab Rev. 1999; 31. 971-97.
[67] Homsi E, Barreiro MF, Orlando JM, et al. Prophylaxis of acute renal failure in patients with rhabdomyolysis. Renal Failure 1997; 19. 283-8.
[68] Better OS, Stein JH. Early management of shock and prophylaxis of acute renal failure in traumatic rhabdomyolysis. N Engl J Med 1990; 322. 825-9.
[69] Hojs R, Ekart R, Sinkovic A, et al. Rhabdomyolysis and acute renal failure in intensive care unit. Ren Fail 1999; 21. 675-84.
[70] Solomon R, Werner C, Mann D, D'Elia J, Silva P: Effects of saline, mannitol,and furosemide to prevent acute decreases in renal function induced by radiocontrast agents [see comments]. New England Journal of Medicine 1994;331:1416-20.
[71] Trivedi HS, Moore H, Nasr S: A randomized prospective trial to assess the role of saline hydration on the development of contrast nephrotoxicity. Nephron Clin Pract 2003;93:C29-C34.
[72] Stevens MA, McCullough PA, Tobin KJ: A prospective randomized trial of prevention measures in patients at high risk for contrast nephropathy. Results of the P. R. I. N. C. E. study. J Am Coll Cardiol 1999; 33: 403-11.
[73] Leehey DJ, Braun BI, Tholl DA, Chung LS, Gross CA, Roback JA, Lentino JR:Can pharmacokinetic dosing decrease nephrotoxicity associated with aminoglycoside therapy. Journal of the American Society of Nephrology 1993; 4:81-90.
[74] Moore RD, Smith CR, Lipsky JJ, Mellits ED, Lietman PS: Risk factors for nephrotoxicity in patients treated with aminoglycosides. Ann Intern Med 1984;100: 352-7.
[75] Kaufman J, Dhakal M, Patel B, Hamburger R: Community-acquired acute renal failure. Am J Kidney Dis 1991; 17: 191-8.
[76] Malinoski DJ, Slater MS, Mullins RJ. Crush injury and rhabdomyolysis. Crit Care Clin. 2004 Jan;20(1).171-92.
[77] Gunal AI, Celiker H, Dogukan A, et al. Early and vigorous resuscitation prevents acute renal failure in the crush victims of catastrophic earthquakes. J Am Soc Nephrol 2004; 15. 1862-1867
[78] Bell M, Liljestam E, Granath F, et al. Optimal follow-up time after continuous renal replacement therapy in actual renal failure patients stratified with the RIFLE criteria. Nephrol Dial Transplant 2005; 20.354-360.
[79] Abosaif NY, Tolba YA, Heap M, et al. The outcome of acute renal failure in theintensive care unit according to RIFLE. model application, sensitivity, and predictability. Am J Kidney Dis 2005; 46.1038-1048.
[80] Kuitunen A, Vento A, Suojaranta-Ylinen R, et al. Acute renal failure aftercardiac surgery. evaluation of the RIFLE classification. Ann Thorac Surg 2006;81.542-546.
[81] Guitard J, Cointault O, Kamar N, et al. Acute renal failure following liver transplantation with induction therapy. Clin Nephrol 2006; 65.103-112.
[82] Hoste EA, Clermont G, Kersten A, et al. RIFLE criteria for acute kidney injury are associated with hospital mortality in critically ill patients. a cohort analysis.Crit Care 2006; 10.R73.
[83] Uchino S, Bellomo R, Goldsmith D, et al. An assessment of the RIFLE criteria for acute renal failure in hospitalized patients. Crit Care Med 2006;34.1913-1917.
[84] Lin C-Y, Chen Y-C, Tsai F-C, et al. RIFLE classification is predictive of shoRTIerm prognosis in critically ill patients with acute renal failure supported by extracorporeal membrane oxygenation. Nephrol Dial Transplant 2006;doi.10.1093/ndt/gfl326.
[85] Heringlake M, Knappe M, Vargas HeinO, et al. Renal dysfunction according to the ADQI-RIFLE system and clinical practice patterns after cardiac surgery in Germany. Minerva Anestesiol 2006; 72.645-654.
[86] Lopes JA, Jorge S, Neves FC, et al. An assessment of the RIFLE criteria for acute renal failure in the severely burned patients.Nephrol Dial Transplant 2006;doi.10.1093/ndt/gfl468.
[87]A Akcan-Arikan, M Zappitelli, LL Loftis, et al.Modified RIFLE criteria in critically ill children with acute kidney injury. International Society of Nephrology 2007; 71(10).1028-35.
[88] Jose Antonio Lopes, Joana Fernandes, Sofia Jorge, et al. An assessment of the RIFLE criteria for acute renal failure in critically ill HIV-infected patients.Critical Care 2007,11.401 (doi.10.1186/cc5121).
[89] Perrone RD, Madias NE, Levey AS. Serum creatinine as an index of renal function: new insights into old concepts. Clin Chem,1992,38:1933-1953.
[90] Mehta RL, Kellum JA, Shah SV, et al. Acute kidney injury network: report of an initiative to improve outcomes in acute kidney injury. Crit Care (2007) 11 :R31.
[91] Durham RM, Moran JJ, Mazuski JE, Multiple organ failure in trauma patients.J Trauma. 2003 Oct;55(4):608-616.
[92] Barie P, Hydro L, Fischer E. A prospective comparison of two multiple dysfunction/failure scoring systems for prediction of mortality in critical surgical illness. J Trauma. 1994;37:660-666.
[93] Van Biesen W, Yegenaga I, Vanholder R, et al:Relationship between fluid status and its management on acute renal failure (ARF) in intensive care unit (ICU) patients with sepsis:A prospective analysis. J Nephrol 2005; 18: 54-60.
[94] Rabb H, Wang Z, Nemoto T, et al: Acute renal failure leads to dysregulation of lung salt and water channels. Kidney Int 2003; 63:600-606.
[95] Kelly KJ: Distant effects of experimental renal ischemia/reperfusion injury. J Am SocNephrol 2003; 14:1549-1558.
[96] Hoke TS, Douglas IS, Klein CL, Acute renal failure after bilateral nephrectomy is associated withcytokine-mediated pulmonary injury. J Am Soc Nephrol. 2007 Jan;18(1).155-64..
[97] Himmelfarb J, McMonagle E, Freedman S, et al: Oxidative stress is increased in critically ill patients with acute renal failure. J Am Soc Nephrol 2004;15:2449-2456.
[98] Kjellstrand CM,Gornick C,DavinT. Recovery from acute renal failure. Clin Exp Dial Apheresis 1981 ;5:143-161.
[99] Sean M. Bagshaw. MD, MSc, Garth Mortis, MD. Christopher J. Doig. MD, MSc,Tomas Godinez-Luna, MD. One-Year Mortality in Critically Ill Patients by Severity of Kidney Dysfunction: A Population-Based Assessment. Am J Kidney Dis 48:402-409.