Critical Care Medicine (CRIT CARE MED )

Publisher: Society of Critical Care Medicine, Lippincott, Williams & Wilkins

Description

Critical Care Medicine publishes promising research and reports on clinical breakthroughs that lead to better care of patients in life-threatening situations. Each issue presents critical care practitioners with clinical breakthroughs that lead to better patient care, the latest news on promising research and advances in equipment and techniques.

  • Impact factor
    6.12
    Show impact factor history
     
    Impact factor
  • 5-year impact
    6.40
  • Cited half-life
    7.20
  • Immediacy index
    2.61
  • Eigenfactor
    0.07
  • Article influence
    2.04
  • Website
    Critical Care Medicine website
  • Other titles
    Critical care medicine
  • ISSN
    0090-3493
  • OCLC
    1789720
  • Material type
    Periodical, Internet resource
  • Document type
    Journal / Magazine / Newspaper, Internet Resource

Publisher details

Lippincott, Williams & Wilkins

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • Some journals have separate policies, please check with each journal directly
    • Pre-print must be removed upon acceptance for publication
    • Post-print may be deposited in personal website, university's institutional repository or employers intranet
    • Publisher's version/PDF cannot be used
    • Must include statement that it is not the final published version
    • Published source must be acknowledged with full citation
    • Must link to publisher version
    • NIH, Wellcome Trust and HHMI authors will have their accepted manuscripts transmitted to PubMed Central on their behalf (see policy for details)
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: 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/m2 (underweight), 18.5-24.9 kg/m2 (normal/referent), 25-29.9 kg/m2 (overweight), 30-39.9 kg/m2 (obesity class I and II), and more than or equal to 40.0 kg/m2 (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/m2. 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/m2. In a subset of patients with body mass index more than or equal to 30.0 kg/m2 (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/m2: 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.
    Critical Care Medicine 10/2014;
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    ABSTRACT: Objective: To determine the relationship between implementation of rapid response teams and improved mortality rate using a large, uniform dataset from one state in the United States. Design: This observational cohort study included 471,062 adult patients hospitalized between 2001 and 2009. Setting: Ten acute tertiary care hospitals in Washington State. Patients or Other Participants: Hospital abstract records on adult patients (18 years old or older) were examined (n = 471,062). Patients most likely to benefit from rapid response team interventions were included and other prognostic factors of severity of illness and comorbidities were controlled. Each participating hospital provided the implementation date of their rapid response team intervention. Mortality rates in 31 months before rapid response team implementation (pre–rapid response team time period) were compared with mortality rates in 31 months following rapid response team implementation (post–rapid response team time period). Intervention(s): Implementation of a rapid response team within each acute tertiary care hospital. Measurements and Main Results: In-hospital mortality. Relative risk for in-hospital mortality improved in the post-rapid response team time period compared with the pre- rapid response team time period (relative risk = 0.76; 95% CI = 0.72–0.80; p < 0.001). Conclusions: In-hospital mortality improved in six of 10 acute tertiary care hospitals in the post-rapid response team time period when compared with the pre-rapid response team time period. Because of a long-term trend of decline in hospital mortality, these decreases could not be unambiguously attributed to rapid response team implementation. Further research should examine additional objective outcomes and optimal configuration of rapid response teams to maximize intervention effectiveness. (Crit Care Med 2014; XX:00–00)
    Critical Care Medicine 09/2014;
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    ABSTRACT: Objective: To determine the relationship between implementation of rapid response teams and improved mortality rate using a large, uniform dataset from one state in the United States. Design: This observational cohort study included 471,062 adult patients hospitalized between 2001 and 2009. Setting: Ten acute tertiary care hospitals in Washington State. Patients or Other Participants: Hospital abstract records on adult patients (18 years old or older) were examined (n = 471,062). Patients most likely to benefit from rapid response team interventions were included and other prognostic factors of severity of illness and comorbidities were controlled. Each participating hospital provided the implementation date of their rapid response team intervention. Mortality rates in 31 months before rapid response team implementation (pre–rapid response team time period) were compared with mortality rates in 31 months following rapid response team implementation (post–rapid response team time period). Intervention(s): Implementation of a rapid response team within each acute tertiary care hospital. Measurements and Main Results: In-hospital mortality. Relative risk for in-hospital mortality improved in the post-rapid response team time period compared with the pre-rapid response team time period (relative risk = 0.76; 95% CI = 0.72–0.80; p < 0.001). Conclusions: In-hospital mortality improved in six of 10 acute tertiary care hospitals in the post-rapid response team time period when compared with the pre-rapid response team time period. Because of a long-term trend of decline in hospital mortality, these decreases could not be unambiguously attributed to rapid response team implementation. Further research should examine additional objective outcomes and optimal configuration of rapid response teams to maximize intervention effectiveness.
    Critical Care Medicine 09/2014; 42(9):2001-2006.
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    ABSTRACT: Lung contusion is a major risk factor for the development of acute respiratory distress syndrome. Hypoxia-inducible factor-1α is the primary transcription factor that is responsible for regulating the cellular response to changes in oxygen tension. We set to determine if hypoxia-inducible factor-1α plays a role in the pathogenesis of acute inflammatory response and injury in lung contusion.
    Critical Care Medicine 07/2014;
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    ABSTRACT: To determine the epidemiology of death in PICUs at 5 geographically diverse teaching hospitals across the United States.
    Critical Care Medicine 06/2014;
  • Critical Care Medicine 06/2014; 42(6):e486-7.
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    ABSTRACT: OBJECTIVES: To evaluate the influence of genetic polymorphisms on the susceptibility to Candida colonization and intra-abdominal candidiasis, a blood culture-negative life-threatening infection in high-risk surgical ICU patients. DESIGN: Prospective observational cohort study. SETTING: Surgical ICUs from two University hospitals of the Fungal Infection Network of Switzerland. PATIENTS: Eighty-nine patients at high risk for intra-abdominal candidiasis (68 with recurrent gastrointestinal perforation and 21 with acute necrotizing pancreatitis). MEASUREMENTS AND MAIN RESULTS: Eighteen single-nucleotide polymorphisms in 16 genes previously associated with development of fungal infections were analyzed from patient's DNA by using an Illumina Veracode genotyping platform. Candida colonization was defined by recovery of Candida species from at least one nonsterile site by twice weekly monitoring of cultures from oropharynx, stools, urine, skin, and/or respiratory tract. A corrected colonization index greater than or equal to 0.4 defined "heavy" colonization. Intra-abdominal candidiasis was defined by the presence of clinical symptoms and signs of peritonitis or intra-abdominal abscess and isolation of Candida species either in pure or mixed culture from intraoperatively collected abdominal samples. Single-nucleotide polymorphisms in three innate immune genes were associated with development of a Candida corrected colonization index greater than or equal to 0.4 (Toll-like receptor rs4986790, hazard ratio = 3.39; 95% CI, 1.45-7.93; p = 0.005) or occurrence of intra-abdominal candidiasis (tumor necrosis factor-α rs1800629, hazard ratio = 4.31; 95% CI, 1.85-10.1; p= 0.0007; β-defensin 1 rs1800972, hazard ratio = 3.21; 95% CI, 1.36-7.59; p = 0.008). CONCLUSION: We report a strong association between the promoter rs1800629 single-nucleotide polymorphism in tumor necrosis factor-α and an increased susceptibility to intra-abdominal candidiasis in a homogenous prospective cohort of high-risk surgical ICU patients. This finding highlights the relevance of the tumor necrosis factor-α functional polymorphism in immune response to fungal pathogens. Immunogenetic profiling in patients at clinical high risk followed by targeted antifungal interventions may improve the prevention or preemptive management of this life-threatening infection.
    Critical Care Medicine 04/2014; 42(4).
  • Critical Care Medicine 01/2014; 42(1):9.
  • Critical Care Medicine 12/2013;
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    ABSTRACT: Objectives: To test the hypothesis that low bispectral index scores and low sedative requirements during therapeutic hypothermia predict poor neurologic outcome. Design: Observational study of a prospectively collected cohort. Setting: Cardiovascular ICU. Patients: One hundred sixty consecutive cardiac arrest patients treated with therapeutic hypothermia. Interventions: None. Measurements and Results: Eighty-four of the 141 subjects (60%) who survived hypothermia induction were discharged from the ICU with poor neurologic outcome, defined as a cerebral performance category score of 3, 4, or 5. These subjects had lower bispectral index (p < 0.001) and sedative requirements (p < 0.001) during hypothermia compared with the 57 subjects discharged with good outcome. Early prediction of neurologic recovery was best 7 hours after ICU admission, and median bispectral index scores at that time were 31 points lower in subjects discharged with poor outcome (11 [interquartile range, 4-29] vs 42 [37-49], p < 0.001). Median sedation requirements decreased by 17% (interquartile range, -50 to 0%) 7 hours after ICU admission in subjects with poor outcome but increased by 50% (interquartile range, 0-142%) in subjects with good outcome (p < 0.001). Each 10-point decrease in bispectral index was independently associated with a 59% increase in the odds of poor outcome (95% CI, 32-76%; p < 0.001). The model including bispectral index and sedative requirement correctly reclassified 15% of subjects from good to poor outcome and 1% of subjects from poor to good outcome. The model incorrectly reclassified 1% of subjects from poor to good outcome but did not incorrectly reclassify any from good to poor outcome. Conclusions: Bispectral index scores and sedative requirements early in the course of therapeutic hypothermia improve the identification of patients who will not recover from brain anoxia. The ability to accurately predict nonrecovery after cardiac arrest could facilitate discussions with families, reduce patient suffering, and limit use of ICU resources in futile cases.
    Critical Care Medicine 12/2013; EPUB.
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    ABSTRACT: Introduction: Endotracheal tube (ETT) cuff pressure must be kept less than 30 cm H2O to prevent tracheal wall pressure necrosis, but must maintain an adequate seal for ventilation. Manometry and a minimal leak test (MLT) are both well-described methods for measuring cuff pressure. Methods: During a 2 month period, we used a manometer to obtain initial ETT cuff pressure measurements on all mechanically ventilated patients in a surgery ICU. Two different physicians then separately performed a MLT for each patient and measured the corresponding cuff pressure; these were compared between the two physicians. The VAP rate per ventilator days were calculated for the two months during the study period and compared to the two months immediately prior to the study. Results: Twenty-eight patients were included for a total of 50 events. The post-MLT measured cuff pressures by the two physicians were highly consistent, with an intraclass correlation coefficient of 0.872 (95% CI). The post-MLT measured cuff pressures were greater than 30 cm H2O in only 2 cases (4%; avg 32 cm H2O). During the first half of the study, the incidence of starting cuff pressures elevated above 30 cm H2O was not significantly different than the second month (19% vs 31%, p = 0.38); however, of the patients with elevated cuff pressures, the mean and elevation above the norm were both higher (47.5 +/- 7.724 vs 38.89 +/- 5.302 cm H20 and 17.5 +/- 7.724 vs 8.89 +/- 5.302 cm H20, p = 0.037). There was no difference in VAP rate during the study compared to historical controls (2.79 vs 2.99 VAPs per 1000 ventilator days, p = 0.961). Conclusions: The incidence of ventilator-associated pneumonia is not significantly increased due to the performance of a daily MLT. The MLT is a reliable indicator of endotracheal cuff pressure, does not undergo significant inter-observer subjective variation, and produces cuff pressures consistently within the acceptable range of less than 30 cm H2O. Additionally, we suspect that by emphasizing safe cuff pressures and daily cuff measurements during the course of our study we were able to decrease unacceptably high starting endotracheal cuff pressures.(C) 2013 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins
    Critical Care Medicine 12/2013; 41(12):A92 (abstract).
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    ABSTRACT: Introduction: Patients in the ICU often experience a stress-related reduction in insulin sensitivity, necessitating insulin therapy (INSiv) to avoid hyperglycemia. Methods: We measured the plasma concentrations of C-peptide, insulin (INSpl) and blood glucose (BG) in blood samples from 9 mechanically ventilated, hyperglycemic ICU patients (ICU day 3-10, age 58 +/- 13 yrs). 7 patients were treated with INSiv including 2 type II diabetes patients. Measurements were steady-state, i.e. when nutrition and INSiv were unchanged for >1 hour up to the test. A population model of C-peptide kinetics was used to convert plasma C-peptide to C-peptide secretion rate and thereby also to pancreatic insulin secretion rate (INSpa). Results: INSpa correlated positively, but not significantly, with BG (r=0.62, p=0.08), indicating that BG drives pancreatic production of insulin. However, the correlation was moderate, and INSpa varied considerably. Even for 3 patients all with a BG of 8 mmol/l, INSpa varied 8-fold, from 11.5 mU/min to 93.5 mU/min. This implies that the patients' endogenous insulin production differ substantially independent of BG. Interestingly the insulin production (11.6 +/- 8.4 mU/min) was significantly lower (p<0.004) in the diabetes patients and in two patients over 70 years, relative to the other patients (48.5 +/- 15.2 mU/min). BG (7.9 +/- 0.9 mmol/l) was not correlated with INSpl, indicating a substantial variation in the patients' insulin sensitivity. A negative correlation (r=-0.66, p=0.05) was found between INSiv and INSpa, indicating that exogenous insulin therapy is primarily used to compensate for inadequate insulin production. Conclusions: It was confirmed that the patients had different insulin sensitivities. It was also found that BG drives the endogenous insulin production, but that there are large differences between the insulin production independent of BG. It appears that reduced insulin sensitivity and production both contribute to the need for exogenous insulin and that insulin infusions are largely used to compensate for the reduced insulin production. Possibly diabetes and high age dispose for the inability to secret endogenous insulin at adequate amounts.
    Critical Care Medicine 12/2013; 41(12):A245.
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    ABSTRACT: Introduction: Hypotension during sedation with propofol is very common and well reported. The hypotension that results often leads to major interventions, which may prolong the sedation time and sometime force the procedure to be aborted.Ways to prevent the hypotension would be helpful in avoiding these complications. Methods: The study was a retrospective chart review comparing a cohort of children undergoing sedation with Propofol receiving 2XMIVF (n=100) with a prior cohort with no IVF during sedation (n=100). Study data included patient characteristics (gender, age, and weight), propofol bolus dose and infusion rate, and hemodynamic parameter measured at baseline and 5 minute intervals for the procedure duration as dictated by the sedation monitoring guidelines. Total and percent maximum decrease in systolic blood pressure (SBP) and mean arterial pressure (MAP) relative to baseline were calculated. MaxSBP and MAP decreases were also dichotomized at 25 SBP units (SBPdrop25) and 20% MAP (pctMAPdrop20). Group differences in baseline and blood pressure changes during the procedure were explored with Chi square analyses, t-tests and linear correlations. Interventions (adjusting Propofol infusion rate or administration fluid boluses) in response to decreases in arterial blood pressure and other indications during the procedure were also recorded. Results: Small but significant associations between groups were noted in procedure duration, propofol infusion and bolus. Only duration among these was also significantly associated with max SBP and MAP drops (r = -.18, p = .01). Differences in the rates of SBPdrop25 and pctMAPdrop20 were not significant comparing the IVF Group and No IVF Groups in bivariate analyses (46% versus 42% and 86% versus 83%, respectively). Logistic regression models adjusting for procedure duration. (A.O.R. 1.18, 95% CI 0.67-2.08) or pctMAPdrop20 (A.O.R. 1.12, 95% CI 0.51-2.45).A total of 22 interventions, in response to decreases in arterial blood pressure and other indications, were recorded in the No IVF group, compared to 6 in the IVF group. This difference was statistically significant (p = .001). Conclusions: The use of 2XMIVF during sedation with propofol did not show a statistically significant difference in SBP and MAP changes. However, the patients in the IVF group had less procedure interrupting interventions, including adjusting the Propofol infusion rate, and the need to give fluid boluses. The use of IVF during Propofol sedation may be justified because it results in a more efficient sedation process.
    Critical Care Medicine 12/2013; 41(12):B1-B16,A1-A377.
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    ABSTRACT: Introduction: There are concerns that fluid abstinence prior to sedation may put patients at risk for hypotension during sedation. This risk may be increased in children. Methods: This study is a retrospective chart review of 263 children who received intravenous (IV) Propofol by bolus then continuous infusion to complete magnetic resonance imaging from June 2011 through May 2013. All patients were instructed to take nothing by mouth as directed by the American Society of Anesthesiologists preoperative fasting guideline. Actual time of abstinence was documented prior to initiation of sedation. Study data included patient characteristics (gender, age, and weight), propofol bolus dose and infusion rate and hemodynamic parameters were measured at baseline and 5 minute intervals for the sedation duration which is routine per policy. IV fluid received was also recorded. Total and percent maximum decrease in systolic blood pressure (SBP) and mean arterial pressure (MAP) relative to baseline were calculated. Max SBP and MAP decreases were also dichotomized at 25 SBP units (SBPdrop25) and 20% MAP (pctMAPdrop20). Associations of hemodynamic changes with fluid abstinence and other patient characteristics were explored with linear correlation and logistic regression analyses. Results: Mean fluid abstinence time was 538.4 +/- 294.0 minutes, propofol bolus dose 2.4 +/- 0.9 mg/kg, propofol infusion rate dose 160.1 +/- 29.3 g/kg/min, and duration 51.6 +/- 24.8 minutes. Duration of procedure, baseline SBP and MAP were significantly correlated with blood pressure decreases but not with fluid abstinences time. Fluid abstinence time was not significantly correlated with maximum SBP decrease (r = 0.02, p = .727) or maximum percent MAP decrease (r = 0.08, p = .20). Logistic regression showed no significant relationships between fluid abstinence time and SBPdrop25 (O.R. 1.0, 95% C.I. 1.00 – 1.01) or pctMAPdrop20 (O.R. 1.0, 95% C.I. 1.00 – 1.01). Conclusions: In our study duration of fluid abstinence prior to sedation with Propofol is not independently associated with hemodynamic changes in children.
    Critical Care Medicine 12/2013; 41(12):B1-B16,A1-A377.
  • Critical Care Medicine 12/2013;