Association between blood alcohol concentration and mortality in critical illness.

OBJECTIVE: In animal models of renal, intestinal, liver, cardiac, and cerebral ischemia, alcohol exposure is shown to reduce ischemia-reperfusion injury. Inpatient mortality of trauma patients is shown to be decreased in a dose-dependent fashion relative to blood alcohol concentration (BAC) at hospital admission. In this study, we examined the association between BAC at hospital admission and risk of 30-day mortality in critically ill patients. DESIGN: We performed a 2-center observational study of patients treated in medical and surgical intensive care units in Boston, Massachusetts. SETTING: Medical and surgical intensive care units in 2 teaching hospitals in Boston, Massachusetts. PATIENTS: We studied 11850 patients, 18 years or older, who received critical care between 1997 and 2007. The exposure of interest was the BAC determined in the first 24 hours of hospital admission and categorized a priori as BAC less than 10 mg/dL (below level of detection), 10 to 80 mg/dL, 80 to 160 mg/dL, and greater than 160 mg/dL. The primary outcome was all-cause mortality in the 30 days after critical care initiation. Secondary outcomes included 90- and 365-day mortality after critical care initiation. Mortality was determined using the US Social Security Administration Death Master File, and 365-day follow-up was present in all cohort patients. Adjusted odds ratios (ORs) were estimated by multivariable logistic regression models with inclusion of covariate terms thought to plausibly interact with both BAC and mortality. Adjustment included age, sex, race (white or nonwhite), type (surgical vs medical), Deyo-Charlson index, sepsis, acute organ failure, trauma, and chronic liver disease. RESULTS: Thirty-day mortality of the cohort was 13.7%. Compared to patients with BAC levels less than 10 mg/dL, patients with levels greater than or equal to 10 mg/dL had lower odds of 30-day mortality; for BAC levels 10 to 79.9 mg/dL, the OR was 0.53 (95% confidence interval [CI], 0.40-0.70); for BAC levels 80 to 159.9 mg/dL, it was 0.36 (95% CI, 0.26-0.49); and for BAC levels greater than or equal to 160 mg/dL, it was 0.35 (95% CI, 0.27-0.44). After multivariable adjustment, the OR of 30-day mortality was 0.97 (0.72-1.31), 0.79 (0.57-1.10), and 0.69 (0.54-0.90), respectively. When the cohort was analyzed with sepsis as the outcome of interest, the multivariable adjusted odds of sepsis in patients with BAC 80 to 160 mg/dL or greater than 160 mg/dL were 0.72 (0.50-1.04) or 0.68 (0.51-0.90), respectively, compared to those with BAC less than 10 mg/dL. In a subset of patients with blood cultures drawn (n=4065), the multivariable adjusted odds of bloodstream infection in patients with BAC 80 to 160 mg/dL or greater than 160 mg/dL were 0.53 (0.27-1.01) or 0.49 (0.29-0.83), respectively, compared to those with BAC less than 10 mg/dL. CONCLUSIONS: Analysis of 11850 adult patients showed that having a detectable BAC at hospitalization was associated with significantly decreased odds of 30-day mortality after critical care. Furthermore, BAC greater than 160 mg/dL is associated with significantly decreased odds of developing sepsis and bloodstream infection.

The relationship among obesity, nutritional status, and mortality in the critically ill.

INTRODUCTION: The association between obesity and mortality in critically ill patients is unclear based on the current literature. To clarify this relationship, we analyzed the association between obesity and mortality in a large population of critically ill patients and hypothesized that mortality would be impacted by nutritional status. METHODS: We performed a single-center observational study of 6,518 adult patients treated in medical and surgical ICUs between 2004 and 2011. All patients received a formal, in-person, and standardized evaluation by a registered dietitian. Body mass index was determined at the time of dietitian consultation from the estimated dry weight or hospital admission weight and categorized a priori as less than 18.5 kg/m (underweight), 18.5-24.9 kg/m (normal/referent), 25-29.9 kg/m (overweight), 30-39.9 kg/m (obesity class I and II), and more than or equal to 40.0 kg/m (obesity class III). Malnutrition diagnoses were categorized as nonspecific malnutrition, protein-energy malnutrition, or well nourished. The primary outcome was all-cause 30-day mortality determined by the Social Security Death Master File. Associations between body mass index groups and mortality were estimated by bivariable and multivariable logistic regression models. Adjusted odds ratios were estimated with inclusion of covariate terms thought to plausibly interact with both body mass index and mortality. We utilized propensity score matching on baseline characteristics and nutrition status to reduce residual confounding of the body mass index category assignment. RESULTS: In the cohort, 5% were underweight, 36% were normal weight, 31% were overweight, 23% had class I/II obesity, and 5% had class III obesity. Nonspecific malnutrition was present in 56%, protein-energy malnutrition was present in 12%, and 32% were well nourished. The 30-day and 90-day mortality rate for the cohort was 19.1 and 26.6%, respectively. Obesity is a significant predictor of improved 30-day mortality following adjustment for age, gender, race, medical versus surgical patient type, Deyo-Charlson index, acute organ failure, vasopressor use, and sepsis: underweight odds ratio 30-day mortality is 1.09 (95% CI, 0.80-1.48), overweight 30-day mortality odds ratio is 0.93 (95% CI, 0.80-1.09), class I/II obesity 30-day mortality odds ratio is 0.80 (95% CI, 0.67-0.96), and class III obesity 30-day mortality odds ratio is 0.69 (95% CI, 0.49-0.97), all relative to patients with body mass index 18.5-24.9 kg/m. Importantly, there is confounding of the obesity-mortality association on the basis of malnutrition. Adjustment for only nutrition status attenuates the obesity-30-day mortality association: underweight odds ratio is 0.74 (95% CI, 0.54-1.00), overweight odds ratio is 1.05 (95% CI, 0.90-1.23), class I/II obesity odds ratio is 0.96 (95% CI, 0.81-1.15), and class III obesity odds ratio is 0.81 (95% CI, 0.59-1.12), all relative to patients with body mass index 18.5-24.9 kg/m. In a subset of patients with body mass index more than or equal to 30.0 kg/m (n = 1,799), those with either nonspecific or protein-energy malnutrition have increased mortality relative to well-nourished patients with body mass index more than or equal to 30.0 kg/m: odds ratio of 90-day mortality is 1.67 (95% CI, 1.29-2.15; p < 0.0001), fully adjusted. In a cohort of propensity score matched patients (n = 3,554), the body mass index-mortality association was not statistically significant, likely from matching on nutrition status. CONCLUSIONS: In a large population of critically ill adults, the association between improved mortality and obesity is confounded by malnutrition status. Critically ill obese patients with malnutrition have worse outcomes than obese patients without malnutrition.

The association of red cell distribution width at hospital discharge and out-of-hospital mortality following critical illness*.

OBJECTIVES: Red cell distribution width is associated with mortality and bloodstream infection risk in the critically ill. In hospitalized patients with critical illness, it is not known if red cell distribution width can predict subsequent risk of all-cause mortality following hospital discharge. We hypothesized that an increase in red cell distribution width at hospital discharge in patients who survived to discharge following critical care would be associated with increased postdischarge mortality. DESIGN: Two-center observational cohort study SETTING: : All medical and surgical ICUs at the Brigham and Women's Hospital and Massachusetts General Hospital. PATIENTS: We studied 43,212 patients, who were 18 years old or older and received critical care between 1997 and 2007 and survived hospitalization. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The exposure of interest was red cell distribution width within 24 hours of hospital discharge and categorized a priori in quintiles as less than or equal to 13.3%, 13.3-14.0%, 14.0-14.7%, 14.7-15.8%, and more than 15.8%. The primary outcome was all-cause mortality in the 30 days following hospital discharge. Secondary outcomes included 90-day and 365-day mortality following hospital discharge. Mortality was determined using the U.S. Social Security Administration Death Master File, and 365-day follow-up was present in all cohort patients. Adjusted odds ratios were estimated by multivariable logistic regression models with inclusion of covariate terms thought to plausibly interact with both red cell distribution width and mortality. Adjustment included age, race, gender, Deyo-Charlson Index, patient type (medical vs surgical), sepsis, and number of organs with acute failure. In patients who received critical care and survived hospitalization, the discharge red cell distribution width was a robust predictor of all-cause mortality and remained so following multivariable adjustment. Patients with a discharge red cell distribution width of 14.0-14.7%, 14.7-15.8%, and more than 15.8% have an odds ratio for mortality in the 30 days following hospital discharge of 2.86 (95% CI, 2.25-3.62), 4.57 (95% CI, 3.66-5.72), and 8.80 (95% CI, 7.15-10.83), respectively, all relative to patients with a discharge red cell distribution width less than or equal to 13.3%. Following multivariable adjustment, patients with a discharge red cell distribution width of 14.0-14.7%, 14.7-15.8%, and more than 15.8% have an odds ratio for mortality in the 30 days following hospital discharge of 1.63 (95% CI, 1.27-2.07), 2.36 (95% CI, 1.87-2.97), and 4.18 (95% CI, 3.36-5.20), respectively, all relative to patients with a discharge red cell distribution width less than or equal to 13.3%. Similar significant robust associations post multivariable adjustments are seen with death by days 90 and 365 postdischarge. Estimating the receiver-operating characteristic area under the curve shows that discharge red cell distribution width has moderate discriminative power for mortality 30 days following hospital discharge (area under the curve = 0.70; SE 0.006; 95% CI, 0.69-0.71; p < 0.0001). CONCLUSION: In patients treated with critical care who survive hospitalization, an elevated red cell distribution width at the time of discharge is a robust predictor of subsequent all-cause patient mortality. Increased discharge red cell distribution width likely reflects the presence of proinflammatory state, oxidative stress, arterial underfilling, or a combination, thereof which may explain the observed impact on patient survival following discharge. Elevated red cell distribution width at hospital discharge may identify ICU survivors who are at risk for adverse outcomes following hospital discharge.

Diabetes mellitus and community-acquired bloodstream infections in the critically ill.

INTRODUCTION: Community-acquired bloodstream infections have not been studied related to diabetes mellitus in the critically ill. HYPOTHESIS: We hypothesized that the diagnosis of diabetes mellitus and poor chronic glycemic control would increase the risk of community-acquired bloodstream infections (CA-BSIs) in the critically ill. METHODS: We performed an observational cohort study between 1998 and 2007 in 2 teaching hospitals in Boston, Massachusetts. We studied 2551 patients 18 years or older, who received critical care within 48 hours of admission and had blood cultures obtained within 48 hours of admission. The exposure of interest was diabetes mellitus defined by International Classification of Diseases, Ninth Revision, Clinical Modification, code 250.xx in outpatient or inpatient records. The primary end point was CA-BSI (<48 hours of hospital admission). Patients with a single coagulase-negative Staphylococcus positive blood culture were not considered to have bloodstream infection. Associations between diabetes groups and bloodstream infection were estimated by bivariable and multivariable logistic regression models. Subanalyses included evaluation of the association between hemoglobin A1c (HbA1c) and bloodstream infection, diabetes and risk of sepsis, and the proportion of the association between diabetes and CA-BSI that was mediated by acute glycemic control. RESULTS: Diabetes is a predictor of CA-BSI. After adjustment for age, sex, race, patient type (medical vs surgical), and acute organ failure, the risk of bloodstream infection was significantly higher in patients with diabetes (odds ratio [OR], 1.42; 95% confidence interval [CI], 1.10-1.82; P = .006) relative to patients without diabetes. The adjusted risk of bloodstream infection was increased in patients with HbA1c of 6.5% or higher (OR, 1.31; 95% CI, 1.04-1.65; P = .02) relative to patients with HbA1c less than 6.5%. Furthermore, the adjusted risk of sepsis was significantly higher in patients with diabetes (OR, 1.26; 95% CI, 1.04-1.54; P = .02) relative to patients without diabetes. Maximum glucose did not significantly mediate the relationship between diabetes mellitus diagnosis and CA-BSI. CONCLUSIONS: A diagnosis of diabetes mellitus and HbA1c of 6.5% or higher is associated with the risk of CA-BSI in the critically ill.

The association between primary language spoken and all-cause mortality in critically ill patients.

PURPOSE: The study objective was to investigate the association between primary language spoken and all-cause mortality in critically ill patients. MATERIALS AND METHODS: We performed a cohort study on 48 581 patients 18 years or older who received critical care between 1997 and 2007 in 2 Boston hospitals. The exposure of interest was primary language spoken determined by the patient or family members who interacted with administrative staff during hospital registration. The primary outcome was 30-day mortality. Associations between language and mortality were estimated by bivariable and multivariable logistic regression models with inclusion of covariate terms thought to plausibly interact with both language and mortality. Adjustment included age, race, sex, Deyo-Charlson index, patient type (medical vs surgical), sepsis, creatinine, hematocrit, white blood count, and number of organs with acute failure. RESULTS: Validation showed that primary language spoken was highly accurate for a statement in the medical record noting the language spoken that matched the assigned language. Patients whose primary language spoken was not English had improved outcomes (odds ratio 30-day mortality, 0.69 [95% confidence interval, 0.60-0.81; P < .001), relative to patients with English as the primary language spoken, fully adjusted. Similar significant associations are seen with death by days 90 and 365 as well as in-hospital mortality. The improved survival in patients with a non-English primary language spoken is not confounded by indicators of severity of disease and is independent of the specific language spoken and neighborhood poverty rate, a proxy for socioeconomic status. There are significant limitations inherent to large database studies that we have acknowledged and addressed with controlling for measured confounding and evaluation of effect modification. CONCLUSIONS: In a regional cohort, not speaking English as a primary language is associated with improved outcomes after critical care. Our observations may have clinical relevance and illustrate the intersection of several factors in critical illness outcome including severity of illness, comorbidity, and social and economic factors.