The impact of development of acute lung injury on hospital mortality in critically ill trauma patients.
ABSTRACT The additional impact of development of acute lung injury on mortality in severely-injured trauma patients beyond baseline severity of illness has been questioned. We assessed the contribution of acute lung injury to in-hospital mortality in critically ill trauma patients.
Prospective cohort study. The contribution of acute lung injury to in-hospital mortality was evaluated in two ways. First, multivariable logistic regression models were used to test the independent association of acute lung injury with in-hospital mortality while adjusting for baseline confounding variables. Second, causal pathway models were used to estimate the amount of the overall association of baseline severity of illness with in-hospital mortality that is attributable to the interval development of acute lung injury.
Academic level 1 trauma center.
Two hundred eighty-three critically ill trauma patients without isolated head injury and with an Injury Severity Score > or = 16 were evaluated for development of acute lung injury in the first 5 days after trauma.
Of the 283 patients, 38 (13.4%) died. The unadjusted mortality rate was nearly three-fold greater in the acute lung injury group (23.9% vs. 8.4%; odds ratio = 3.36; 95% confidence interval 1.67-6.77; p = 0.001). Acute lung injury remained an independent risk factor for death after adjustment for age, baseline Acute Physiologic and Chronic Health Evaluation III score, Injury Severity Score, and blunt mechanism of injury (odds ratio = 2.87; 95% confidence interval 1.29-6.37; p = 0.010). Forty percent of the total association of the baseline Acute Physiologic and Chronic Health Evaluation III score with mortality occurred via an indirect association through acute lung injury, and the remaining 60% via a direct effect.
Development of acute lung injury in critically ill trauma patients without isolated head injury contributes independently to in-hospital mortality beyond baseline severity of illness measures. In addition, a significant portion of the association between baseline illness severity and risk of death in these patients might be explained by the interval development of acute lung injury.
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ABSTRACT: RATIONALE: Acute respiratory distress syndrome (ARDS) behaves as a complex genetic trait, yet knowledge of genetic susceptibility factors remains incomplete. OBJECTIVE: To identify genetic risk variants for ARDS using large scale genotyping. METHODS: Multistage genetic association study of 3 critically ill populations phenotyped for ARDS. Stage I, a trauma cohort study (n=224), was genotyped with a 50K gene-centric single nucleotide polymorphism (SNP) array. We tested SNPs associated with ARDS at p < 5 x 10-4 for replication in stage II, a trauma case-control population (n=778). SNPs replicating their association in stage II (p < 0.005) were tested in a stage III nested case-control population of mixed ICU subjects (n=2063). Logistic regression was used to adjust for potential clinical confounders. We performed ELISA to test for an association between ARDS-associated genotype and plasma protein levels. MEASUREMENTS AND MAIN RESULTS: 12 SNPs met the stage I threshold for an association with ARDS. rs315952 in the IL1RN gene encoding interleukin 1 receptor antagonist (IL1RA) replicated its association with reduced ARDS risk in stage II (p < 0.004) and III (p<0.02), and was robust to clinical adjustment (combined OR 0.81, p = 4.2 x 10-5). Plasma IL1RA level was associated with rs315952C in a subset of critically ill subjects. The effect of rs315952 was independent from the tandem repeat variant in IL1RN. CONCLUSIONS: The IL1RN SNP rs315952C is associated with decreased risk of ARDS in 3 populations with heterogeneous ARDS risk factors, and with increased plasma IL1RA response. IL1RA may attenuate ARDS risk.American Journal of Respiratory and Critical Care Medicine 02/2013; · 11.04 Impact Factor
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ABSTRACT: Acute respiratory distress syndrome (ARDS) is a serious complication of sepsis and sepsis-associated ARDS is associated with significant morbidity and mortality. To date, no study has directly examined the epidemiology of ARDS in severe sepsis from the earliest presentation to the health care system, the Emergency Department (ED). Single-center retrospective, observational cohort study of 778 adults with severe sepsis presenting to the ED. The primary outcome was the development of ARDS requiring mechanical ventilation during the first 5 hospital days. ARDS was defined using the Berlin definition. We used multivariable logistic regression to identify risk factors associated independently with ARDS development. The incidence of ARDS was 6.2% (48 of 778 patients) in the entire cohort. ARDS development varied across the continuum of care: 0.9% of patients fulfilled criteria for ARDS in the ED, 1.4% admitted to the ward developed ARDS, and 8.9% admitted to the ICU developed ARDS. ARDS developed a median of 1 day after admission and was associated with a four-fold higher risk of in-hospital mortality (14% vs. 60%, p<0.001). Independent risk factors associated with increased risk of ARDS development included: intermediate (2-3.9 mmol/L) (p=0.04) and high (≥ 4) serum lactate levels (p=0.008), lung injury prediction score (LIPS) (p<0.001) and microbiologically-proven infection (p=0.01). In patients presenting to the ED with severe sepsis, the rate of sepsis-associated ARDS development varied across the continuum of care. ARDS developed rapidly and was associated with significant mortality. Elevated serum lactate levels in the ED and a recently validated clinical prediction score were independently associated with the development of ARDS in severe sepsis.Shock (Augusta, Ga.) 07/2013; · 2.87 Impact Factor
- Critical care medicine 01/2014; 42(1):226-227. · 6.37 Impact Factor