Fiona K Gibbons

Brigham and Women's Hospital , Boston, MA, United States

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Publications (29)182.32 Total impact

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    ABSTRACT: Objective: To investigate whether preadmission 25-hydroxyvitamin D (25(OH)D) levels are associated with the risk of hospital-acquired Clostridium difficile infection (HACDI). Materials and Methods: Our retrospective cohort study focused on 568 adult patients from 2 Boston teaching hospitals between August 1993 and November 2006. All patients had 25(OH)D levels measured before hospitalization and were at risk for HACDI (defined as the presence of C difficile toxin A or B in stool samples obtained >48 hours after hospitalization). We performed multivariable regression analyses to test the association of prehospital 25(OH)D levels with HACDI while adjusting for clinically relevant covariates. Results: In these 568 patients, mean (SD) 25(OH)D level was 19 (12) ng/mL, and 11% of patients met criteria for incident HACDI. Following adjustment for age, sex, race (nonwhite vs white), patient type (medical vs surgical), and Deyo-Charlson index, patients with 25(OH)D levels <10 ng/mL had higher odds of HACDI (odds ratio [OR], 2.90; 95% confidence interval [CI], 1.01-8.34) compared with patients with 25(OH)D levels ≥30 ng/mL. When patients with HACDI were analyzed relative to a larger patient cohort without HACDI (n = 5047), those with 25(OH)D levels <10 ng/mL (OR, 4.96; 95% CI, 1.84-13.38) and 10-19.9 ng/mL (OR, 3.36; 95% CI, 1.28-8.85) had higher adjusted odds of HACDI compared with patients with 25(OH)D levels ≥30 ng/mL. Conclusions: In our cohort of adult patients, vitamin D status before hospital admission was inversely associated with the risk of developing HACDI. These data support the need for randomized, controlled trials to test the role of vitamin D supplementation to prevent HACDI.
    Journal of Parenteral and Enteral Nutrition 02/2014; · 2.49 Impact Factor
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    ABSTRACT: 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. Two-center observational cohort study SETTING:: All medical and surgical ICUs at the Brigham and Women's Hospital and Massachusetts General Hospital. We studied 43,212 patients, who were 18 years old or older and received critical care between 1997 and 2007 and survived hospitalization. None. 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). 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.
    Critical care medicine 01/2014; · 6.37 Impact Factor
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    ABSTRACT: Objective: To examine the association between pre-hospital serum 25-hydroxyvitamin D and risk of mortality following hospital admission. Design: We performed a retrospective cohort study of adults hospitalized for acute care between 1993 and 2011. Setting: Two Boston teaching hospitals. Patients: 24,094 adult inpatients. Intervention: None. Measurements: All patients had serum 25(OH)D measured before hospitalization. The exposure of interest was 25(OH)D categorized as <10 ng/mL, 10-19.9 ng/mL, 20-29.9 ng/mL, 30-49.9 ng/mL, 50-59.9 ng/mL, 60-69.9 ng/mL, and ≥70 ng/mL. The main outcome measure was 90-day mortality. Adjusted odds ratios (OR) were estimated by multivariable logistic regression with inclusion of potential confounders. Results: After adjustment for age, gender, race (white vs. non-white), patient type (surgical vs. medical), season of 25(OH)D draw and Deyo-Charlson index, patients with 25(OH)D levels <30 ng/mL or ≥60 ng/mL had higher odds of 90-day mortality compared to patients with levels 30-49.9 ng/mL [adjusted OR(95% confidence interval) for 25(OH)D <10 ng/mL, 10-19.9 ng/mL, 20-29.9 ng/mL, 50-59.9 ng/mL, 60-69.9 ng/mL and ≥70 ng/mL was 2.01(1.68-2.40), 1.89(1.64-2.18), 1.34(1.16-1.56), 0.94(0.69-1.26), 1.52(1.03-2.25) and 1.69(1.09-2.61), respectively, compared to patients with 25(OH)D levels 30-49.9 ng/mL]. Limitations: A causal relationship between either low or high 25(OH)D levels and increased mortality can not necessarily be inferred from this observational study. Conclusions: Analysis of 24,094 adult patients showed that 25(OH)D levels <20 ng/mL and ≥60 ng/mL before hospitalization were associated with an increased odds of 90-day mortality. Though previous reports have suggested an association between low vitamin D status and mortality, these data raise the issue of potential harm from high serum 25(OH)D levels, provide a rationale for an upper limit to supplementation, and emphasize the need for caution in the use of extremely high doses of vitamin D among patients.
    The Journal of Clinical Endocrinology and Metabolism 01/2014; · 6.31 Impact Factor
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    ABSTRACT: Community-acquired bloodstream infections have not been studied related to diabetes mellitus in the critically ill. 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. 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. 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. A diagnosis of diabetes mellitus and HbA1c of 6.5% or higher is associated with the risk of CA-BSI in the critically ill.
    Journal of critical care 09/2013; · 2.13 Impact Factor
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    ABSTRACT: The study objective was to investigate the association between primary language spoken and all-cause mortality in critically ill patients. 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. 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. 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.
    Journal of critical care 09/2013; · 2.13 Impact Factor
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    ABSTRACT: We hypothesized that deficiency in 25-hydroxyvitamin D prior to hospital admission would be associated with sepsis in the critically ill. Two-center observational study of patients treated in medical and surgical ICUs. Two hundred nine medical and surgical intensive care beds in two teaching hospitals in Boston, MA. Three thousand three hundred eighty-six patients, 18 years old or older, in whom 25-hydroxyvitamin D was measured prior to hospitalization between 1998 and 2011. None MEASUREMENTS AND MAIN RESULTS:: Preadmission 25-hydroxyvitamin D was categorized as deficiency in 25-hydroxyvitamin D (≤ 15 ng/mL), insufficiency (15-30 ng/mL), and sufficiency (≥ 30 ng/mL). The primary outcome was sepsis as defined by International Classification of Diseases, 9th Edition, Clinical Modification and validated by the 2001 Society of Critical Care Medicine/European Society of Intensive Care Medicine, American College of Chest Physicians, American Thoracic Society, and Surgical Infection Society international sepsis definitions conference guidelines. Logistic regression examined the presence of sepsis 3 days prior to critical care initiation to 7 days after critical care initiation. Adjusted odds ratios were estimated by multivariable logistic regression models. Preadmission 25-hydroxyvitamin D deficiency is predictive for the risk of sepsis. In the full cohort, 25-hydroxyvitamin D deficiency is a significant predictor for the risk of International Classification of Diseases, 9th Edition, Clinical Modification-defined sepsis following multivariable adjustment, including age, gender, race, type (surgical vs medical), and Deyo-Charlson index (adjusted odds ratio, 1.51 [95% CI, 1.17-1.94]; p = 0.001) relative to patients with 25-hydroxyvitamin D sufficiency. In a subset of cohort patients enriched for those with International Classification of Diseases, 9th Edition, Clinical Modification-diagnosed sepsis (n = 444), preadmission 25-hydroxyvitamin D deficiency is a significant predictor for the risk of conference guideline-defined sepsis following multivariable adjustment, including age, gender, race, type (surgical vs medical), and Acute Physiology and Chronic Health Evaluation II (adjusted odds ratio, 2.05 [95% CI, 1.19-3.52]; p = 0.009) relative to patients with 25-hydroxyvitamin D sufficiency. Furthermore, in cohort patients with International Classification of Diseases, 9th Edition, Clinical Modification-defined sepsis (n = 568), the multivariable adjusted risk of 90-day mortality was 1.6-fold higher in those with preadmission 25-hydroxyvitamin D values in the insufficient and deficient range, compared with those with preadmission vitamin D sufficiency (adjusted odds ratio, 1.63 [95% CI, 1.11-2.39]; p = 0.01). 25-hydroxyvitamin D deficiency prior to hospital admission is a significant predictor of sepsis in the critically ill. Additionally, patients with sepsis who are not vitamin D sufficient have an increased risk of mortality following critical care initiation.
    Critical care medicine 08/2013; · 6.37 Impact Factor
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    ABSTRACT: Alterations in immune function can predispose patients to nosocomial infections. Few studies have explored potentially modifiable host factors that may improve immune function and decrease risk of hospital-acquired bloodstream infection (HABSI). Vitamin D is a key regulator of innate and adaptive immune systems that may influence host susceptibility to infections. We investigated the association between prehospital serum 25-hydroxyvitamin D [25(OH)D] concentrations and risk of HABSI. We performed a retrospective cohort study of 2135 adult patients from 2 Boston teaching hospitals. All patients had 25(OH)D concentrations measured before hospitalization between 1993 and 2010. The main outcome measure was HABSI, which was defined as positive blood cultures from samples drawn 48 h after hospital admission. Coagulase-negative Staphylococcus isolates were not considered to be bloodstream infections. Associations between 25(OH)D groups and HABSI were estimated by using bivariable and multivariable logistic regression models. Adjusted ORs were estimated with the inclusion of covariate terms thought to plausibly interact with both 25(OH)D concentration and HABSI. Compared with patients with 25(OH)D concentrations ≥30 ng/mL, patients with concentrations <30 ng/mL had higher odds of HABSI. For 25(OH)D concentrations <10 ng/mL, the OR was 2.33 (95% CI: 1.45, 3.74); for 25(OH)D concentrations from 10 to 19.9 ng/mL, the OR was 1.60 (95% CI: 1.04, 2.46); and for 25(OH)D concentrations from 20 to 29.9 ng/mL, the OR was 1.13 (95% CI: 0.69, 1.84). After adjustment for age, sex, race (nonwhite compared with white), patient type (medical compared with surgical), and Deyo-Charlson index, the ORs of HABSI were 1.95 (95% CI: 1.22, 3.12), 1.36 (95% CI: 0.89, 2.07), and 0.98 (95% CI: 0.60, 1.62), respectively. The analysis of 2135 adult patients showed that 25(OH)D concentrations <10 ng/mL before hospitalization were associated with significantly increased odds of developing HABSI. These data support the initiation of randomized trials to test the role of vitamin D supplementation in HABSI prevention.
    American Journal of Clinical Nutrition 08/2013; · 6.50 Impact Factor
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    ABSTRACT: The study objective was to examine the association between pre-hospital serum vitamin D concentration and mortality after hospitalization. We performed a retrospective cohort study in 2 tertiary hospitals in Boston, Mass, on 23,603 patients aged ≥18 years in whom 25(OH)D was measured before hospitalization between 1993 and 2010. The main outcome measures were all-cause mortality by day 30 post-hospital admission, in-hospital mortality, and community-acquired bloodstream infection. Compared with patients with pre-hospital 25(OH)D ≥30 ng/mL, patients with pre-hospital 25(OH)D ≤15 ng/mL or 15 to 30 ng/mL have higher odds of mortality 30 days after hospital admission. After adjustment for age, gender, race, Deyo-Charlson index, season, type (surgical vs medical), creatinine, blood urea nitrogen, hematocrit, and time between 25(OH)D draw and hospital admission, the adjusted odds ratio (OR) of 30-day mortality in patients with 25(OH)D ≤15 ng/mL is 1.45 (95% confidence interval [CI], 1.21-1.74; P<.0001) and the adjusted OR of 30-day mortality in patients with 25(OH)D 15 to 30 ng/mL is 1.30 (95% CI, 1.10-1.54; P = .003) both compared with patients with pre-hospital 25(OH)D ≥30 ng/mL. In a subgroup analysis of patients who had blood cultures drawn (n = 5628), pre-hospital serum 25(OH)D ≤15 ng/mL was associated with increased odds of community-acquired bloodstream infection (adjusted OR, 1.29; 95% CI, 1.06-1.57; P = .01) relative to patients with 25(OH)D ≥30 ng/mL. Analysis of 23,603 hospitalized patients identified both 25(OH)D ≤15 ng/mL and 25(OH)D 15 to 30 ng/mL before hospital admission as associated with the odds of all-cause patient mortality at 30 days after hospitalization. In addition, pre-hospital serum 25(OH)D ≤15 ng/mL is significantly associated with the odds of community-acquired bloodstream infection.
    The American journal of medicine 07/2013; 126(7):640.e19-640.e27. · 5.30 Impact Factor
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    ABSTRACT: OBJECTIVE:: We hypothesized that the delta anion gap defined as difference between critical care initiation standard anion gap and prehospital admission standard anion gap is associated with all cause mortality in the critically ill. DESIGN:: Observational cohort study. SETTING:: Two hundred nine medical and surgical intensive care beds in two hospitals in Boston, MA. PATIENTS:: Eighteen thousand nine hundred eighty-five patients, age ≥18 yrs, who received critical care between 1997 and 2007. MEASUREMENTS:: The exposure of interest was delta anion gap and categorized a priori as <0, 0-5, 5-10, and >10 mEq/L. Logistic regression examined death by days 30, 90, and 365 postcritical care initiation and in-hospital mortality. Adjusted odds ratios were estimated by multivariable logistic regression models. The discrimination of delta anion gap for 30-day mortality was evaluated using receiver operator characteristic curves performed for a subset of patients with all laboratory data required to analyze the data via physical chemical principles (n = 664). INTERVENTIONS:: None. RESULTS:: Delta anion gap was a particularly strong predictor of 30-day mortality with a significant risk gradient across delta anion gap quartiles following multivariable adjustment: delta anion gap <0 mEq/L odds ratio 0.75 (95% confidence interval 0.67-0.81; p < 0.0001); delta anion gap 5-10 mEq/L odds ratio 1.56 (95% confidence interval 1.35-1.81; p < 0.0001); delta anion gap >10 mEq/L odds ratio 2.18 (95% confidence interval 1.76-2.71; p < 0.0001); and all relative to patients with delta anion gap 0-5 mEq/L. Similar significant robust associations post multivariable adjustments are seen with death by days 90 and 365 as well as in-hospital mortality. Correcting for albumin or limiting the cohort to patients with standard anion gap at critical care initiation of 10-18 mEq/L did not materially change the delta anion gap-mortality association. Delta anion gap has similarly moderate discriminative ability for 30-day mortality in comparison to standard base excess and strong ion gap. CONCLUSION:: An increase in standard anion gap at critical care initiation relative to prehospital admission standard anion gap is a predictor of the risk of all cause patient mortality in the critically ill.
    Critical care medicine 11/2012; · 6.37 Impact Factor
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    ABSTRACT: OBJECTIVE:: Given the importance of inflammation in acute kidney injury and the relationship between vitamin D and inflammation, we sought to elucidate the effect of vitamin D on acute kidney injury. We hypothesized that deficiency in 25-hydroxyvitamin D prior to hospital admission would be associated with acute kidney injury in the critically ill. DESIGN:: Two-center observational study of patients treated in medical and surgical intensive care units. SETTING:: Two hundred nine medical and surgical intensive care beds in two teaching hospitals in Boston, Massachusetts. PATIENTS:: Two thousand seventy-five patients, aged ≥18 yrs, in whom serum 25-hydroxyvitamin D was measured prior to hospitalization between 1998 and 2009. INTERVENTIONS:: None. MEASUREMENTS AND MAIN RESULTS:: The exposure of interest was preadmission serum 25-hydroxyvitamin D and categorized a priori as deficiency (25-hydroxyvitamin D ≤15ng/mL), insufficiency (25-hydroxyvitamin D 15-30ng/mL), or sufficiency (25-hydroxyvitamin D ≥30ng/mL). The primary outcome was acute kidney injury defined as meeting Risk, Injury, Failure, Loss, and End-stage kidney disease (RIFLE) Injury or Failure criteria. Logistic regression examined the RIFLE criteria outcome. Adjusted odds ratios were estimated by multivariate logistic regression models. Preadmission 25-hydroxyvitamin D deficiency is predictive of acute kidney injury. Patients with 25-hydroxyvitamin D deficiency have an odds ratio for acute kidney injury of 1.73 (95% confidence interval 1.30-2.30; p < .0001) relative to patients with 25-hydroxyvitamin D sufficiency. 25-Hydroxyvitamin D deficiency remains a significant predictor of acute kidney injury following multivariable adjustment (adjusted odds ratio 1.50; 95% confidence interval 1.42-2.24; p < .0001). Patients with 25-hydroxyvitamin D insufficiency have an odds ratio for acute kidney injury of 1.49 (95% confidence interval 1.15-1.94; p = .003) and an adjusted odds ratio of 1.23 (95% confidence interval 1.12-1.72; p = .003) relative to patients with 25-hydroxyvitamin D sufficiency. In addition, preadmission 25-hydroxyvitamin D deficiency is predictive of mortality. Patients with 25-hydroxyvitamin D insufficiency have an odds ratio for 30-day mortality of 1.60 (95% confidence interval 1.18-2.17; p = .003) and an adjusted odds ratio of 1.61 (95% confidence interval 1.06-1.57; p = .004) relative to patients with 25-hydroxyvitamin D sufficiency. CONCLUSION:: Deficiency of 25-hydroxyvitamin D prior to hospital admission is a significant predictor of acute kidney injury and mortality in a critically ill patient population.
    Critical care medicine 09/2012; · 6.37 Impact Factor
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    ABSTRACT: To investigate the association between potassium concentration at the initiation of critical care and all-cause mortality. We performed a retrospective observational study on 39,705 patients, age ≥18 years, who received critical care between 1997 and 2007 in two tertiary care hospitals in Boston, Massachusetts. The exposure of interest was the highest potassium concentration on the day of critical care initiation and categorized a priori as 4.0-4.5, 4.5-5.0, 5.0-5.5, 5.5-6.0, 6.0-6.5, or ≥6.5 mEq/l. Logistic regression examined death by days 30, 90, and 365 post-critical care initiation, and in-hospital mortality. Adjusted odds ratios were estimated by multivariable logistic regression models. The potassium concentration was a strong predictor of all-cause mortality 30 days following critical care initiation with a significant risk gradient across potassium groups following multivariable adjustment: K = 4.5-5.0 mEq/l OR 1.25 (95 % CI, 1.16-1.35; P < 0.0001); K = 5.0-5.5 mEq/l OR 1.42 (95 % CI, 1.29-1.56; P < 0.0001); K = 5.5-6.0 mEq/l OR 1.67 (95 % CI, 1.47-1.89; P < 0.0001); K = 6.0-6.5 mEq/l OR 1.63 (95 % CI, 1.36-1.95; P < 0.0001); K > 6.5 mEq/l OR 1.72 (95 % CI, 1.49-1.99; P < 0.0001); all relative to patients with K = 4.0-4.5 mEq/l. Similar significant associations post multivariable adjustments are seen with in-hospital mortality and death by days 90 and 365 post-critical care initiation. In patients whose hyperkalemia decreases ≥1 mEq/l in 48 h post-critical care initiation, the association between high potassium levels and mortality is no longer significant. Our study demonstrates that a patient's potassium level at critical care initiation is robustly associated with the risk of death even at moderate increases above normal.
    European Journal of Intensive Care Medicine 07/2012; 38(11):1834-42. · 5.17 Impact Factor
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    ABSTRACT: Poverty is associated with increased risk of chronic illness, but its contribution to bloodstream infections is not well-defined. We performed a multicenter observational study of 14,657 patients, aged 18 yrs or older, who received critical care and had blood cultures drawn between 1997 and 2007 in two hospitals in Boston, Massachusetts. Data sources included 1990 U.S. Census and hospital administrative data. Census tracts were used as the geographic units of analysis. The exposure of interest was neighborhood poverty rate categorized as <5%, 5%-10%, 10%-20%, 20%-40%, and >40%. Neighborhood poverty rate is the percentage of residents with income below the federal poverty line. The primary end point was bloodstream infection occurring 48 hrs before critical care initiation to 48 hrs after. Associations between neighborhood poverty rate and bloodstream infection were estimated by logistic regression models. Adjusted odds ratios were estimated by multivariable logistic regression models. Two thousand four-hundred thirty-five patients had bloodstream infections. Neighborhood poverty rate was a strong predictor of risk of bloodstream infection, with a significant risk gradient across neighborhood poverty rate quintiles. After multivariable analysis, neighborhood poverty rate in the highest quintiles (20%-40% and >40%) were associated with a 26% and 49% increase in bloodstream infection risk, respectively, relative to patients with neighborhood poverty rate of <5%. Within the limitations of our study design, increased neighborhood poverty rate, a proxy for decreased socioeconomic status, appears to be associated with risk of bloodstream infection among patients who receive critical care.
    Critical care medicine 05/2012; 40(5):1427-36. · 6.37 Impact Factor
  • Critical Care 03/2012; 16(1). · 4.93 Impact Factor
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    ABSTRACT: We hypothesized that deficiency in 25-hydroxyvitamin D at critical care initiation would be associated with all-cause mortalities. Two-center observational study. Two teaching hospitals in Boston, MA. The study included 1,325 patients, age ≥ 18 yrs, in whom 25-hydroxyvitamin D was measured 7 days before or after critical care initiation between 1998 and 2009. 25-hydroxyvitamin D was categorized as deficiency in 25-hydroxyvitamin D (≤ 15 ng/mL), insufficiency (16-29 ng/mL), and sufficiency (≥ 30 ng/mL). Logistic regression examined death by days 30, 90, and 365 postcritical care initiation and in-hospital mortality. Adjusted odds ratios were estimated by multivariable logistic regression models. None. 25-hydroxyvitamin D deficiency is predictive for short-term and long-term mortality. Thirty days following critical care initiation, patients with 25-hydroxyvitamin D deficiency have an odds ratio for mortality of 1.85 (95% confidence interval 1.15-2.98; p = .01) relative to patients with 25-hydroxyvitamin D sufficiency. 25-hydroxyvitamin D deficiency remains a significant predictor of mortality at 30 days following critical care initiation following multivariable adjustment for age, gender, race, Deyo-Charlson index, sepsis, season, and surgical vs. medical patient type (adjusted odds ratio 1.94; 95% confidence interval 1.18-3.20; p = .01). Results were similarly significant at 90 and 365 days following critical care initiation and for in-hospital mortality. The association between vitamin D and mortality was not modified by sepsis, race, or neighborhood poverty rate, a proxy for socioeconomic status. Deficiency of 25-hydroxyvitamin D at the time of critical care initiation is a significant predictor of all-cause patient mortality in a critically ill patient population.
    Critical care medicine 09/2011; 40(1):63-72. · 6.37 Impact Factor
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    ABSTRACT: Red cell distribution width is a predictor of mortality in the general population. The prevalence of increased red cell distribution width and its significance in the intensive care unit are unknown. The objective of this study was to investigate the association between red cell distribution width at the initiation of critical care and all cause mortality. Multicenter observational study. Two tertiary academic hospitals in Boston, MA. A total of 51,413 patients, aged ≥ 18 yrs, who received critical care between 1997 and 2007. None. The exposure of interest was red cell distribution width as a predictor of mortality in the general population. The prevalence of increased red cell distribution width and its significance in the intensive care unit are unknown and categorized a priori in quintiles as ≤ 13.3%, 13.3% to 14.0%, 14.0% to 14.7%, 14.7% to 15.8%, and >15.8%. Logistic regression examined death by days 30, 90, and 365 postcritical care initiation, inhospital mortality, and bloodstream infection. Adjusted odds ratios were estimated by multivariable logistic regression models. Adjustment included age, sex, race, Deyo-Charlson index, coronary artery bypass grafting, myocardial infarction, congestive heart failure, hematocrit, white blood cell count, mean corpuscular volume, blood urea nitrogen, red blood cell transfusion, sepsis, and creatinine. Red cell distribution width was a particularly strong predictor of all-cause mortality 30 days after critical care initiation with a significant risk gradient across red cell distribution width quintiles after multivariable adjustment: red cell distribution width 13.3% to 14.0% (odds ratio [OR], 1.19; 95% confidence interval [CI], 1.08-1.30; p <.001); red cell distribution width 14.0% to 14.7% (OR, 1.28; 95% CI, 1.16-1.42; p <.001); red cell distribution width 14.7% to 15.8% (OR, 1.69; 95% CI, 1.52-1.86; p <.001); red cell distribution width >15.8% (OR, 2.61; 95% CI, 2.37-2.86; p <.001), all relative to patients with red cell distribution width ≤ 13.3%. Similar significant robust associations postmultivariable adjustments are seen with death by days 90 and 365 postcritical care initiation as well as inhospital mortality. In a subanalysis of patients with blood cultures drawn (n = 18,525), red cell distribution width at critical care initiation was associated with the risk of bloodstream infection and remained significant after multivariable adjustment. The adjusted risk of bloodstream infection was 1.40- and 1.44-fold higher in patients with red cell distribution width values in the 14.7% to 15.8% and >15.8% quintiles, respectively, compared with those with red cell distribution width ≤ 13.3%. Estimating the receiver operating characteristic area under the curve shows that red cell distribution width has moderate discriminative power for 30-day mortality (area under the curve = 0.67). Red cell distribution width is a robust predictor of the risk of all-cause patient mortality and bloodstream infection in the critically ill. Red cell distribution width is commonly measured, inexpensive, and widely available and may reflect overall inflammation, oxidative stress, or arterial underfilling in the critically ill.
    Critical care medicine 04/2011; 39(8):1913-21. · 6.37 Impact Factor
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    ABSTRACT: Poverty is associated with increased risk of chronic illness but its contribution to critical care outcome is not well defined. We performed a multicenter observational study of 38,917 patients, aged ≥ 18 years, who received critical care between 1997 and 2007. The patients were treated in two academic medical centers in Boston, Massachusetts. Data sources included 1990 US census and hospital administrative data. The exposure of interest was neighborhood poverty rate, categorized as < 5%, 5% to 10%, 10% to 20%, 20% to 40% and > 40%. Neighborhood poverty rate is the percentage of residents below the federal poverty line. Census tracts were used as the geographic units of analysis. Logistic regression examined death by days 30, 90, and 365 post-critical care initiation and in-hospital mortality. Adjusted ORs were estimated by multivariable logistic regression models. Sensitivity analysis was performed for 1-year postdischarge mortality among patients discharged to home. Following multivariable adjustment, neighborhood poverty rate was not associated with all-cause 30-day mortality: 5% to 10% OR, 1.05 (95% CI, 0.98-1.14; P = .2); 10% to 20% OR, 0.96 (95% CI, 0.87-1.06; P = .5); 20% to 40% OR, 1.08 (95% CI, 0.96-1.22; P = .2); > 40% OR, 1.20 (95% CI, 0.90-1.60; P = .2); referent in each is < 5%. Similar nonsignificant associations were noted at 90-day and 365-day mortality post-critical care initiation and in-hospital mortality. Among patients discharged to home, neighborhood poverty rate was not associated with 1-year-postdischarge mortality. Our study suggests that there is no relationship between the neighborhood poverty rate and mortality up to 1 year following critical care at academic medical centers.
    Chest 03/2011; 139(6):1368-79. · 7.13 Impact Factor
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    ABSTRACT: We hypothesized that elevated blood urea nitrogen can be associated with all-cause mortality independent of creatinine in a heterogeneous critically ill population. Multicenter observational study of patients treated in medical and surgical intensive care units. Twenty intensive care units in two teaching hospitals in Boston, MA. A total of 26,288 patients, age ≥ 18 yrs, hospitalized between 1997 and 2007 with creatinine of 0.80-1.30 mg/dL. None. Blood urea nitrogen at intensive care unit admission was categorized as 10-20, 20-40, and >40 mg/dL. Logistic regression examined death at days 30, 90, and 365 after intensive care unit admission as well as in-hospital mortality. Adjusted odds ratios were estimated by multivariable logistic regression models. Blood urea nitrogen at intensive care unit admission was predictive for short- and long-term mortality independent of creatinine. Thirty days following intensive care unit admission, patients with blood urea nitrogen of >40 mg/dL had an odds ratio for mortality of 5.12 (95% confidence interval, 4.30-6.09; p < .0001) relative to patients with blood urea nitrogen of 10-20 mg/dL. Blood urea nitrogen remained a significant predictor of mortality at 30 days after intensive care unit admission following multivariable adjustment for confounders; patients with blood urea nitrogen of >40 mg/dL had an odds ratio for mortality of 2.78 (95% confidence interval, 2.27-3.39; p < .0001) relative to patients with blood urea nitrogen of 10-20 mg/dL. Thirty days following intensive care unit admission, patients with blood urea nitrogen of 20-40 mg/dL had an odds ratio of 2.15 (95% confidence interval, 1.98-2.33; <.0001) and a multivariable odds ratio of 1.53 (95% confidence interval, 1.40-1.68; p < .0001) relative to patients with blood urea nitrogen of 10-20 mg/dL. Results were similar at 90 and 365 days following intensive care unit admission as well as for in-hospital mortality. A subanalysis of patients with blood cultures (n = 7,482) demonstrated that blood urea nitrogen at intensive care unit admission was associated with the risk of blood culture positivity. Among critically ill patients with creatinine of 0.8-1.3 mg/dL, an elevated blood urea nitrogen was associated with increased mortality, independent of serum creatinine.
    Critical care medicine 02/2011; 39(2):305-13. · 6.37 Impact Factor
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    ABSTRACT: We hypothesized that deficiency in 25-hydroxyvitamin D before hospital admission would be associated with all-cause mortality in the critically ill. Multicenter observational study of patients treated in medical and surgical intensive care units. A total of 209 medical and surgical intensive care beds in two teaching hospitals in Boston, MA. A total of 2399 patients, age ≥ 18 yrs, in whom 25-hydroxyvitamin D was measured before hospitalization between 1998 and 2009. None. Preadmission 25-hydroxyvitamin D was categorized as deficiency in 25-hydroxyvitamin D (≤ 15 ng/mL), insufficiency (16-29 ng/mL), and sufficiency (≥ 30 ng/mL). Logistic regression examined death by days 30, 90, and 365 post-intensive care unit admission, in-hospital mortality, and blood culture positivity. Adjusted odds ratios were estimated by multivariable logistic regression models. Preadmission 25-hydroxyvitamin D deficiency is predictive for short-term and long-term mortality. At 30 days following intensive care unit admission, patients with 25-hydroxyvitamin D deficiency have an odds ratio for mortality of 1.69 (95% confidence interval of 1.28-2.23, p < .0001) relative to patients with 25-hydroxyvitamin D sufficiency. 25-Hydroxyvitamin D deficiency remains a significant predictor of mortality at 30 days following intensive care unit admission following multivariable adjustment (adjusted odds ratio of 1.69, 95% confidence interval of 1.26-2.26, p < .0001). At 30 days following intensive care unit admission, patients with 25-hydroxyvitamin D insufficiency have an odds ratio of 1.32 (95% confidence interval of 1.02-1.72, p = .036) and an adjusted odds ratio of 1.36 (95% confidence interval of 1.03-1.79, p = .029) relative to patients with 25-hydroxyvitamin D sufficiency. Results were similar at 90 and 365 days following intensive care unit admission and for in-hospital mortality. In a subgroup analysis of patients who had blood cultures drawn (n = 1160), 25-hydroxyvitamin D deficiency was associated with increased risk of blood culture positivity. Patients with 25-hydroxyvitamin D insufficiency have an odds ratio for blood culture positivity of 1.64 (95% confidence interval of 1.05-2.55, p = .03) relative to patients with 25-hydroxyvitamin D sufficiency, which remains significant following multivariable adjustment (odds ratio of 1.58, 95% confidence interval of 1.01-2.49, p = .048). Deficiency of 25-hydroxyvitamin D before hospital admission is a significant predictor of short- and long-term all-cause patient mortality and blood culture positivity in a critically ill patient population.
    Critical care medicine 01/2011; 39(4):671-7. · 6.37 Impact Factor
  • American Journal of Kidney Diseases - AMER J KIDNEY DIS. 01/2011; 57(4).
  • American Journal of Kidney Diseases - AMER J KIDNEY DIS. 01/2010; 55(4).

Publication Stats

244 Citations
182.32 Total Impact Points

Institutions

  • 2004–2013
    • Brigham and Women's Hospital
      • • Department of Medicine
      • • Division of Renal Medicine
      Boston, MA, United States
  • 2005–2011
    • Massachusetts General Hospital
      • Division of Pulmonary & Critical Care Medicine
      Boston, Massachusetts, United States
  • 2002–2011
    • Harvard Medical School
      • • Department of Genetics
      • • Department of Medicine
      Boston, MA, United States