Critical Care Medicine (CRIT CARE MED)

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

Journal 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.

Current impact factor: 6.15

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 6.147
2012 Impact Factor 6.124
2011 Impact Factor 6.33
2010 Impact Factor 6.254
2009 Impact Factor 6.373
2008 Impact Factor 6.594
2007 Impact Factor 6.283
2006 Impact Factor 6.599
2005 Impact Factor 5.077
2004 Impact Factor 4.182
2003 Impact Factor 4.195
2002 Impact Factor 3.361
2001 Impact Factor 3.486
2000 Impact Factor 3.824
1999 Impact Factor 3.98
1998 Impact Factor 3.745
1997 Impact Factor 3.639
1996 Impact Factor 4.26
1995 Impact Factor 3.172
1994 Impact Factor 2.807
1993 Impact Factor 2.431
1992 Impact Factor 1.79

Impact factor over time

Impact factor

Additional details

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 or institutional repository
    • 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
    • Set statement to accompany deposit
    • Must link to publisher version
    • NIH authors will have their accepted manuscripts transmitted to PubMed Central on their behalf after a 12 months embargo (see policy for details)
    • Wellcome Trust and HHMI authors will have their accepted manuscripts transmitted to PubMed Central on their behalf after a 6 months embargo (see policy for details)
    • Publisher last reviewed on 19/03/2015
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: OBJECTIVES: A novel stomach-derived peptide, ghrelin, is down-regulated in sepsis and its IV administration decreases proinflammatory cytokines and mitigates organ injury. In this study, we wanted to investigate the effects of ghrelin on proinflammatory responses and cognitive impairment in septic rats. DESIGN: Prospective, randomized, controlled experiment. SETTING: Animal basic science laboratory. SUBJECTS: Sprague-Dawley rats, weighing 250-300 g. INTERVENTIONS: Sepsis was induced by cecal ligation and puncture. Animals were randomly divided into four groups: sham, sham + ghrelin, cecal ligation and puncture, and cecal ligation and puncture + ghrelin. Saline was given subcutaneously (30 mL/kg) at 4 and 16 hours after surgery for all rats. Septic rats were treated with ceftriaxone (30 mg/kg) and clindamycin (25 mg/kg) subcutaneously at 4 and 16 hours after surgery. Ghrelin (80 μg/kg) was administrated intraperitoneally 4 and 16 hours after surgery in sham + ghrelin group and cecal ligation and puncture + ghrelin group. MEASUREMENTS AND MAIN RESULTS: The levels of proinflammatory cytokines in hippocampus were measured by enzyme-linked immunosorbent assay, and cleaved caspase-3 was detected by Western blot 24 hours after surgery. Neuronal apoptosis was determined by terminal deoxynucleotidyl transferase dUTP nick-end labeling staining 48 hours after surgery. Additional animals were monitored to record survival and body weight changes for 10 days after surgery. Survival animals underwent behavioral tasks 10 days after surgery: open-field, novel object recognition, and continuous multiple-trial step-down inhibitory avoidance task. Ghrelin significantly decreased the levels of proinflammatory cytokines and inhibited the activation of caspase-3 in the hippocampus after cecal ligation and puncture. The density of terminal deoxynucleotidyl transferase dUTP nick-end labeling-positive apoptotic neurons was significantly lowered by ghrelin. In addition, ghrelin improved the survival rates after cecal ligation and puncture. There were no differences in the distance and move time between groups in open-field task. However, the survivors after cecal ligation and puncture were unable to recognize the novel object and required more training trials to reach the acquisition criterion. All these long-term impairments were prevented by ghrelin. CONCLUSIONS: Ghrelin inhibited proinflammatory responses, improved the survival rate, and prevented cognitive impairment in septic rats.
    Critical Care Medicine 05/2015; 43(5):143-50.
  • Critical Care Medicine 04/2015; DOI:10.1097/CCM..0000000000001066
  • Critical Care Medicine 04/2015; 43(4):911-912. DOI:10.1097/CCM.0000000000000847
  • Critical Care Medicine 04/2015; 43(4):924-925. DOI:10.1097/CCM.0000000000000844
  • [Show abstract] [Hide abstract]
    ABSTRACT: Although metabolic syndrome is associated with increased sympathetic activity that chronically stimulates β-adrenoceptors, the β-adrenoceptor signaling pathway has been poorly studied in this situation. We studied the β-adrenoceptor signaling pathway in Zucker lean, obese, and obese diabetic rats. Experimental, prospective study. University medical research laboratory. Adult male Zucker lean (control), obese, and obese diabetic rats. The effects of β-adrenoceptor stimulation were investigated in vitro in isolated left ventricular papillary muscles in control, obese, and obese diabetic rats. β1-, β2-, and β3-adrenoceptors and multidrug resistance-associated protein 4 were quantified by Western Blotting. Triglyceride, cholesterol, leptin, adiponectin, and C-peptide plasma concentrations were measured. Data are mean ± SD. Hyperlipidemia, high leptin, and C-peptide concentrations were observed in obese and obese diabetic strains, whereas hyperglycemia occurred only in the diabetic strain. The positive inotropic effect of isoproterenol was slightly reduced in obese rats (183% ± 11% of baseline; p = 0.003; n = 7) and markedly reduced in obese diabetic rats (137% ± 18% of baseline; p < 0.001; n = 10) when compared with control rats (210% ± 17% of baseline; n = 9). β1-adrenoceptors were down-regulated in obese (-41%; p = 0.02) and diabetic (-54%; p = 0.003) when compared with control rats, whereas β3-adrenoceptors and multidrug resistance-associated protein expression remained unchanged. Direct stimulation of adenylate cyclase with forskolin or administration of 3',5'-cyclic adenosine monophosphate suggests that subtle impairments also occurred beside the down-regulation of β1-adrenoceptor. The positive inotropic effect of β-adrenoceptor stimulation is slightly decreased in Zucker obese rats and was more markedly decreased in Zucker diabetic rats. These decreases are mainly related to β1-adrenoceptor down-regulation.
    Critical Care Medicine 04/2015; 43(7). DOI:10.1097/CCM.0000000000000999
  • [Show abstract] [Hide abstract]
    ABSTRACT: Objective: Prior research indicates that off-label use is common in the ICU; however, the safety of off-label use has not been assessed. The study objective was to determine the prevalence of adverse drug reactions associated with off-label use and evaluate off-label use as a risk factor for the development of adverse drug reactions in an adult ICU population. Design: Multicenter, observational study Setting: Medical ICUs at three academic medical centers. Patients: Adult patients (age >= 18 yr old) receiving medication therapy. Interventions: All administered medications were evaluated for Food and Drug Administration-approved or off-label use. Patients were assessed daily for the development of an adverse drug reaction through active surveillance. Three adverse drug reaction assessment instruments were used to determine the probability of an adverse drug reaction resulting from drug therapy. Severity and harm of the adverse drug reaction were also assessed. Cox proportional hazard regression was used to identify a set of covariates that influenced the rate of adverse drug reactions. Measurements and Main Results: Overall, 1,654 patient-days (327 patients) and 16,391 medications were evaluated, with 43% of medications being used off-label. One hundred and sixteen adverse drug reactions were categorized dichotomously (Food and Drug Administration or off-label), with 56% and 44% being associated with Food and Drug Administration-approved and off-label use, respectively. The number of adverse drug reactions for medications administered and the number of harmful and severe adverse drug reactions did not differ for medications used for Food and Drug Administration-approved or off-label use (0.74% vs 0.67%; p = 0.336; 33 vs 31 events, p = 0.567; 24 vs 24 events, p = 0.276). Age, sex, number of high-risk medications, number of off-label medications, and severity of illness score were included in the Cox proportional hazard regression. It was found that the rate of adverse drug reactions increases by 8% for every one additional off-label medication (hazard ratio = 1.08; 95% CI, 1.018-1.154). Conclusion: Although adverse drug reactions do not occur more frequently with off-label use, adverse drug reaction risk increases with each additional off-label medication used. Copyright (C) by 2015 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.
    Critical Care Medicine 04/2015; DOI:10.1097/CCM.0000000000001022
  • [Show abstract] [Hide abstract]
    ABSTRACT: Objective: Recent interest has arisen in airway driving pressure (DPAW), the quotient of tidal volume (VT), and respiratory system compliance (CRS), which could serve as a direct and easily measured marker for ventilator-induced lung injury risk. We aimed to test the correspondence between DPAW and transpulmonary driving pressure (DPTP)-the quotient of VT and lung compliance (CL), in response to intra-abdominal hypertension and changes in positive end-expiratory pressure during different models of lung pathology. Design: Well-controlled experimental setting that allowed reversible modification of chest wall compliance (CCW) in a variety of models of lung pathology. Setting: Large animal laboratory of a university-affiliated hospital. Subjects: Ten deeply anesthetized swine. Interventions: Application of intra-abdominal pressures of 0 and 20 cm H2O at positive end-expiratory pressure of 1 and 10 cm H2O, under volume-controlled mechanical ventilation in the settings of normal lungs (baseline), unilateral whole-lung atelectasis, and unilateral and bilateral lung injuries caused by saline lavage. Measurements and Main Results: Pulmonary mechanics including esophageal pressure and calculations of DPAW, DPTP, CRS, CL, and CCW. When compared with normal intra-abdominal pressures, intra-abdominal hypertension increased DPAW, during both "normal lung conditions" (p < 0.0001) and "unilateral atelectasis" (p = 0.0026). In contrast, DPTP remained virtually unaffected by changes in positive end-expiratory pressure or intra-abdominal pressures in both conditions. During unilateral lung injury, both DPAW and DPTP were increased by the presence of intra-abdominal hypertension (p < 0.0001 and p = 0.0222, respectively). During bilateral lung injury, intra-abdominal hypertension increased both DPAW (at positive end-expiratory pressure of 1 cm H2O, p < 0.0001; and at positive end-expiratory pressure of 10 cm H2O, p = 0.0091) and DPTP (at positive end-expiratory pressure of 1 cm H2O, p = 0.0510; and at positive end-expiratory pressure of 10 cm H2O, p = 0.0335). Conclusions: Our data indicate that DPAW is influenced by reductions in chest wall compliance and by underlying lung properties. As with other measures of pulmonary mechanics that are based on unmodified PAW, caution is advised in attempting to attribute hazard or safety to any specific absolute value of DPAW.
    Critical Care Medicine 04/2015; DOI:10.1097/CCM.0000000000001036
  • Critical Care Medicine 04/2015; 43(4):e120-e121. DOI:10.1097/CCM.0000000000000873
  • Critical Care Medicine 04/2015; 43(4):929-930. DOI:10.1097/CCM.0000000000000846
  • [Show abstract] [Hide abstract]
    ABSTRACT: Objective: To investigate bilirubin-induced lung alveolar epithelial cell injury together with the protection afforded by dexmedetomidine. Design: Prospective, randomized, controlled study. Setting: Research laboratory. Subjects: Sprague Dawley rats. Interventions: Alveolar epithelial A549 cell lines were cultured and received bilirubin (from 0 to 160 [mu]M) to explore the protective pathway of dexmedetomidine on bilirubin-induced alveolar epithelial cell injury assessed by immunochemistry and flow cytometry. Sprague-Dawley rats were subjected to common bile duct ligation surgery to explore the protective effect of dexmedetomidine on hyperbilirubinemia-induced alveolar epithelial cell injury and respiratory failure in comparison with the Sham (subjected to the surgery procedure but without bile duct ligation) or dexmedetomidine control (only received intraperitoneal injection of dexmedetomidine). Measurements and Main Results: In vitro, dexmedetomidine reversed the collapse of mitochondrial membrane potential ([DELTA][psi]m), upregulation of cytochrome C, B cell leukemia 2 associated X protein, and cleaved-caspase 3 and 9 in A549 epithelial cells with bilirubin challenge. Furthermore, dexmedetomidine reversed the arrest of cell cycle and the downregulation of the transforming growth factor[beta], phosphorylated mammalian target of rapamycin, and p42/44 mitogen-activated protein kinase induced by bilirubin. In vivo, pulmonary edema and inflammation were found after common bile duct ligation. Bilirubin and PaCO2 were significantly increased, and oxygen (PaO2) was significantly decreased in the blood of common bile duct ligation rats from the postsurgery day 7 to day 21 when compared with those in the sham controls, respectively (p < 0.01). Daily intraperitoneal injection of dexmedetomidine significantly alleviated the lung edema and injury and prevented respiratory failure. Conclusion: Our data both in vitro and in vivo demonstrated that dexmedetomidine protected alveolar epithelial cell from bilirubin-induced injury. Dexmedetomidine may be a good choice of anesthetic/sedative for patients with chronic liver disease during the perioperative period.
    Critical Care Medicine 04/2015; DOI:10.1097/CCM.0000000000001035
  • [Show abstract] [Hide abstract]
    ABSTRACT: Objective: We performed a systematic review of the published evidence regarding nonpharmacologic antishivering interventions in various clinical settings. Data Sources: Studies through November 2014 were identified using predefined search terms in electronic databases, including PubMed, the Cochrane Library, EMBASE: Excerpta Medica (Ovid), and Web of Science. Study Selection: All identified articles were critically analyzed by applying prespecified criteria. We included experimental trials with comparable baseline data investigating the antishivering efficacy of nonpharmacological interventions in subjects without underlying thermoregulatory dysfunction. Data Extraction: Sixty-five publications (3,361 subjects) were analyzed by the type of clinical setting, intervention, comparison, and study design. In addition, each study underwent a standardized study quality assessment. Data Synthesis: Nonpharmacological interventions consisted of active cutaneous warming (forced-air warming, electric heating pad/blanket, radiant heating, and water-circulating mattress), body core warming (fluid or gas warming system), passive cutaneous warming (space blankets or towels), and electroacupuncture. Identified clinical settings included perioperative settings without induced hypothermia (60 of 77 comparisons), perioperative settings with induced hypothermia (8 of 77), and induced hypothermia without anesthesia (9 of 77). Active cutaneous warming was the most commonly studied intervention, and it was associated with the highest prevalence of positive results when compared with controls in all three clinical settings. In contrast, passive cutaneous warming and body core warming showed conflicting efficacy. Comparison evaluations among different antishivering interventions were limited due to the paucity and heterogeneity of studies directly comparing different interventions against one another. Conclusion: This systematic review of the effectiveness of nonpharmacological antishivering methods delineates active cutaneous warming as the most effective nonpharmacologic antishivering intervention in the perioperative and induced hypothermia settings.
    Critical Care Medicine 04/2015; DOI:10.1097/CCM.0000000000001014
  • Critical Care Medicine 04/2015; 43(4):913-914. DOI:10.1097/CCM.0000000000000832
  • Critical Care Medicine 04/2015; 43(4):916-917. DOI:10.1097/CCM.0000000000000835