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	<title>Virtual Journal Club &#187; Am J Respir Crit Care Med</title>
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	<description>Division of Hospital Medicine Virtual Journal Club</description>
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		<title>Twenty-four-hour intensivist presence: a pilot study of effects on intensive care unit patients, families, doctors, and nurses.</title>
		<link>http://beckerinfo.net/JClub/2012/05/17/twenty-four-hour-intensivist-presence-a-pilot-study-of-effects-on-intensive-care-unit-patients-families-doctors-and-nurses/</link>
		<comments>http://beckerinfo.net/JClub/2012/05/17/twenty-four-hour-intensivist-presence-a-pilot-study-of-effects-on-intensive-care-unit-patients-families-doctors-and-nurses/#comments</comments>
		<pubDate>Thu, 17 May 2012 12:33:23 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Respir Crit Care Med]]></category>

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		<description><![CDATA[Twenty-four-hour intensivist presence: a pilot study of effects on intensive care unit pa...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Twenty-four-hour intensivist presence: a pilot study of effects on intensive care unit patients, families, doctors, and nurses.</b></p>
        <p>Am J Respir Crit Care Med. 2012 Apr 1;185(7):738-43</p>
        <p>Authors:  Garland A, Roberts D, Graff L</p>
        <p>Abstract<br/>
        RATIONALE: Around-the-clock intensivist presence in intensive care units (ICUs) has been promoted as necessary to optimize outcomes. Little data have addressed how it affects the multiple stakeholders in such care.<br/>
        OBJECTIVES: To assess effects of around-the-clock intensivist presence on intensivists, patients, families, housestaff, and nurses.<br/>
        METHODS: This 32-week, crossover pilot trial of two intensivist staffing models, performed in two Canadian ICUs, alternated 8-week blocks of two staffing models: the standard model, where one intensivist worked for 7 days, taking night call from home; and the shift work model, where one intensivist worked 7 day shifts, while other intensivists remained in the ICU at night.<br/>
        MEASUREMENTS AND MAIN RESULTS: Surveys scaled from 0-100 points assessed outcomes for 24 intensivists (primary outcome: burnout); 119 families (satisfaction); 74 nurses (satisfaction with collaboration and communications, role conflict); and 34 housestaff (autonomy, supervision, and learning opportunities). Outcomes for 501 patients included mortality, length of stay, and resource use. Intensivists doing shift work experienced less burnout (-6.9 points; P = 0.04). Adjusted hospital mortality (odds ratio, 1.22; P = 0.44), ICU length of stay (-6 h; P = 0.46), and family satisfaction (0.9 points; P = 0.79) did not differ between staffing models. Under shift work staffing, nurses reported more role conflict (9 points; P &lt; 0.001), whereas nighttime housestaff reported less autonomy, more supervision, but no difference in learning opportunities.<br/>
        CONCLUSIONS: Shiftwork staffing was better for intensivists and most were receptive once they had experienced it. Although there were no evident negative outcomes for patients or families, further evaluation is needed to clarify how around-the-clock intensivist staffing influences the various stakeholders in ICU care, given power considerations in this study. Clinical trial registered with www.clinicaltrials.gov (NCT 01146691).<br/></p><p>PMID: 22246176 [PubMed - indexed for MEDLINE]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
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		<item>
		<title>The use of nonphysician providers in adult intensive care units.</title>
		<link>http://beckerinfo.net/JClub/2012/05/16/the-use-of-nonphysician-providers-in-adult-intensive-care-units/</link>
		<comments>http://beckerinfo.net/JClub/2012/05/16/the-use-of-nonphysician-providers-in-adult-intensive-care-units/#comments</comments>
		<pubDate>Wed, 16 May 2012 18:31:11 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Respir Crit Care Med]]></category>

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		<description><![CDATA[The use of nonphysician providers in adult intensive care units.
        Am J Respir Crit...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>The use of nonphysician providers in adult intensive care units.</b></p>
        <p>Am J Respir Crit Care Med. 2012 Mar 15;185(6):600-5</p>
        <p>Authors:  Gershengorn HB, Johnson MP, Factor P</p>
        <p>Abstract<br/>
        In the United States there are not currently enough critical care-trained practitioners to provide care to all critically ill patients. With calls for "high-intensity" staffing and 24-hour coverage of our intensive care units, the board-certified intensivists we do have are being stretched ever more thin. Nonphysician providers (physician assistants and nurse practitioners) are being used with increasing frequency in critical care settings to provide care to critically ill patients. In this review, we explore the impact of introducing nonphysician providers into the adult intensive care unit.<br/></p><p>PMID: 22135345 [PubMed - indexed for MEDLINE]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
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		<item>
		<title>Combination Biomarkers to Diagnose Sepsis in the Critically Ill Patient.</title>
		<link>http://beckerinfo.net/JClub/2012/04/28/combination-biomarkers-to-diagnose-sepsis-in-the-critically-ill-patient/</link>
		<comments>http://beckerinfo.net/JClub/2012/04/28/combination-biomarkers-to-diagnose-sepsis-in-the-critically-ill-patient/#comments</comments>
		<pubDate>Sat, 28 Apr 2012 10:03:42 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Respir Crit Care Med]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=d505744e79a07d88c0cbc0128ee037a5</guid>
		<description><![CDATA[Combination Biomarkers to Diagnose Sepsis in the Critically Ill Patient.
        Am J Res...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Combination Biomarkers to Diagnose Sepsis in the Critically Ill Patient.</b></p>
        <p>Am J Respir Crit Care Med. 2012 Apr 26;</p>
        <p>Authors:  Gibot S, Béné MC, Noel R, Massin F, Guy J, Cravoisy A, Barraud D, De Carvalho Bittencourt M, Quenot JP, Bollaert PE, Faure G, Charles PE</p>
        <p>Abstract<br/>
        RationaleAlthough the outcome of sepsis benefits from the prompt administration of appropriate antibiotics upon correct diagnosis, the assessment of infection in critically ill patients is often a challenge for clinicians. In this setting, simple biomarkers, especially when used in combination, could prove useful.ObjectiveTo determine the usefulness of combination biomarkers to diagnose sepsisMethodsThree-hundred consecutive patients were enrolled to construct a biological score that was next validated in an independent prospective cohort of 79 critically ill patients from another center.Measurement and main resultsPlasma concentrations of soluble Triggering Receptor Expressed on Myeloid cells-1 (sTREM-1) and procalcitonin (PCT) were assayed, and the expression of the high affinity immunoglobulin-Fc fragment receptor I (Fc?RI) CD64 on neutrophils (PMN CD64 index) in flow cytometry was measured. A "Bioscore" combining these biomarkers was constructed. Serum concentrations of PCT and sTREM-1 as well as the PMN CD64 index were higher in septic patients compared to all others (p&lt;0.001 for the three markers). These biomarkers were all independent predictors of infection, the best ROC curve being obtained for the PMN CD64 index. The performance of the Bioscore, better than that of each individual biomarker was externally confirmed in the validation cohort. ConclusionThis prospective study, including both inceptive and validation cohorts of unselected ICU patients demonstrates the high performance of a Bioscore combining the PMN CD64 index together with PCT and sTREM-1 serum levels in diagnosing sepsis in the critically ill patient.<br/></p><p>PMID: 22538802 [PubMed - as supplied by publisher]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
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		<title>A Clinical Algorithm to Diagnose Invasive Pulmonary Aspergillosis in Critically Ill Patients.</title>
		<link>http://beckerinfo.net/JClub/2012/04/22/a-clinical-algorithm-to-diagnose-invasive-pulmonary-aspergillosis-in-critically-ill-patients/</link>
		<comments>http://beckerinfo.net/JClub/2012/04/22/a-clinical-algorithm-to-diagnose-invasive-pulmonary-aspergillosis-in-critically-ill-patients/#comments</comments>
		<pubDate>Sun, 22 Apr 2012 05:31:08 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Respir Crit Care Med]]></category>

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		<description><![CDATA[A Clinical Algorithm to Diagnose Invasive Pulmonary Aspergillosis in Critically Ill Patie...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>A Clinical Algorithm to Diagnose Invasive Pulmonary Aspergillosis in Critically Ill Patients.</b></p>
        <p>Am J Respir Crit Care Med. 2012 Apr 19;</p>
        <p>Authors:  Blot SI, Taccone FS, Van den Abeele AM, Bulpa P, Meersseman W, Brusselaers N, Dimopoulos G, Paiva JA, Misset B, Rello J, Vandewoude K, Vogelaers D,  </p>
        <p>Abstract<br/>
        Rational &amp; Objective. The clinical relevance of Aspergillus-positive endotracheal aspirates in critically ill patients is difficult to assess. We externally validate a clinical algorithm to discriminate Aspergillus colonization from putative invasive pulmonary aspergillosis in this patient group. Methods. We performed a multicentre (n=30) observational study including critically ill patients with ?1 Aspergillus-positive endotracheal aspirate culture (n=524). The diagnostic accuracy of this algorithm was evaluated using 115 patients with histopathologic data, considered the gold standard. Subsequently the diagnostic workout of the algorithm was compared on the total cohort (n=524), with the categorization based on the diagnostic criteria of the European Organization for the Research and Treatment of Cancer/Mycoses Study Group (EORTC/MSG). Results. Among 115 histopathology-controlled patients, 79 had proven aspergillosis. The algorithm judged 86/115 cases to have putative aspergillosis. This diagnosis was confirmed in 72 and rejected in 14 patients. The algorithm judged 29 patients to have Aspergillus colonization. This was confirmed in 22 and rejected in 7 patients. The algorithm had a specificity of 61% and a sensitivity of 92%. The positive and negative predictive values were 61% and 92% respectively. In the total cohort (n=524), 79 patients had proven invasive pulmonary aspergillosis (15.1%). According to the EORTC/MSG criteria 32 patients had probable aspergillosis (6.1%) and 413 patients were not classifiable (78.8%). The algorithm judged 199 patients to have putative aspergillosis (38.0%) and 246 to have Aspergillus colonization (46.9%). Conclusions. The algorithm demonstrated favourable operating characteristics to discriminate Aspergillus respiratory tract colonization from invasive pulmonary aspergillosis in critically ill patients.<br/></p><p>PMID: 22517788 [PubMed - as supplied by publisher]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
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		<title>A review of ?1-antitrypsin deficiency.</title>
		<link>http://beckerinfo.net/JClub/2012/04/18/a-review-of-%ce%b11-antitrypsin-deficiency/</link>
		<comments>http://beckerinfo.net/JClub/2012/04/18/a-review-of-%ce%b11-antitrypsin-deficiency/#comments</comments>
		<pubDate>Wed, 18 Apr 2012 11:31:57 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Respir Crit Care Med]]></category>

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		<description><![CDATA[A review of ?1-antitrypsin deficiency.
        Am J Respir Crit Care Med. 2012 Feb 1;185(...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>A review of ?1-antitrypsin deficiency.</b></p>
        <p>Am J Respir Crit Care Med. 2012 Feb 1;185(3):246-59</p>
        <p>Authors:  Stoller JK, Aboussouan LS</p>
        <p>Abstract<br/>
        ?(1)-Antitrypsin (AAT) deficiency is an underrecognized genetic condition that affects approximately 1 in 2,000 to 1 in 5,000 individuals and predisposes to liver disease and early-onset emphysema. AAT is mainly produced in the liver and functions to protect the lung against proteolytic damage (e.g., from neutrophil elastase). Among the approximately 120 variant alleles described to date, the Z allele is most commonly responsible for severe deficiency and disease. Z-type AAT molecules polymerize within the hepatocyte, precluding secretion into the blood and causing low serum AAT levels (? 3-7 ?M with normal serum levels of 20-53 ?M). A serum AAT level of 11 ?M represents the protective threshold value below which the risk of emphysema is believed to increase. In addition to the usual treatments for emphysema, infusion of purified AAT from pooled human plasma-so-called "augmentation therapy"-represents a specific therapy for AAT deficiency and raises serum levels above the protective threshold. Although definitive evidence from randomized controlled trials of augmentation therapy is lacking and therapy is expensive, the available evidence suggests that this approach is safe and can slow the decline of lung function and emphysema progression. Promising novel therapies are under active investigation.<br/></p><p>PMID: 21960536 [PubMed - indexed for MEDLINE]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Blood Eosinophils to Direct Corticosteroid Treatment of Exacerbations of COPD: a Randomized Placebo Controlled Trial.</title>
		<link>http://beckerinfo.net/JClub/2012/03/28/blood-eosinophils-to-direct-corticosteroid-treatment-of-exacerbations-of-copd-a-randomized-placebo-controlled-trial/</link>
		<comments>http://beckerinfo.net/JClub/2012/03/28/blood-eosinophils-to-direct-corticosteroid-treatment-of-exacerbations-of-copd-a-randomized-placebo-controlled-trial/#comments</comments>
		<pubDate>Thu, 29 Mar 2012 00:30:39 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Respir Crit Care Med]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=e5fcdc8b5e3f8395d5a7d0c2e78e851f</guid>
		<description><![CDATA[Blood Eosinophils to Direct Corticosteroid Treatment of Exacerbations of COPD: a Randomiz...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Blood Eosinophils to Direct Corticosteroid Treatment of Exacerbations of COPD: a Randomized Placebo Controlled Trial.</b></p>
        <p>Am J Respir Crit Care Med. 2012 Mar 23;</p>
        <p>Authors:  Bafadhel M, McKenna S, Terry S, Mistry V, Pancholi M, Venge P, Lomas DA, Barer MR, Johnston SL, Pavord ID, Brightling CE</p>
        <p>Abstract<br/>
        RATIONALE: Exacerbations of chronic obstructive pulmonary disease (COPD) and responses to treatment are heterogeneous. OBJECTIVES: Investigate the utility of blood eosinophils to direct corticosteroid therapy during exacerbations. METHODS: Subjects with COPD exacerbations were entered into a randomized biomarker-directed double-blind corticosteroid versus standard therapy study. Subjects in the standard arm received prednisolone for 2 weeks, whilst in the biomarker-directed arm, prednisolone or matching placebo was given according to the blood eosinophil count biomarker. Both study groups received antibiotics. Blood eosinophils were measured in the biomarker-directed and standard therapy arms to define biomarker-positive and -negative exacerbations (blood eosinophil count &gt; and ? 2% respectively). The primary outcome was to determine non-inferiority in health status using the chronic respiratory questionnaire (CRQ) and in the proportion of exacerbations associated with a treatment failure between subjects allocated to the biomarker-directed and standard therapy arm. MEASUREMENTS AND MAIN RESULTS: There were 86 and 80 exacerbations in the biomarker-directed and standard treatment group. In the biomarker-directed group 49% of the exacerbations were not treated with prednisolone. CRQ improvement following treatment in the standard and biomarker-directed therapy group was similar (0.8 vs. 1.1, mean difference 0.3, 95% CI 0.0 to 0.6, p=0.05). There was a greater improvement in CRQ in biomarker-negative exacerbations given placebo compared to those given prednisolone (mean difference 0.45; 95% CI 0.01 to 0.90; p=0.04). In biomarker-negative exacerbations, treatment failures occurred in 15% given prednisolone and 2% of those given placebo (p=0.04). CONCLUSION: The peripheral blood eosinophil count is a promising biomarker to direct corticosteroid therapy during COPD exacerbations, but larger studies are required.Clinical trial registration available at www.controlled-trials.com/ISRCTN92422949.<br/></p><p>PMID: 22447964 [PubMed - as supplied by publisher]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
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		<item>
		<title>Inflammatory Biomarkers Improve Clinical Prediction of Mortality in Chronic Obstructive Pulmonary Disease.</title>
		<link>http://beckerinfo.net/JClub/2012/03/22/inflammatory-biomarkers-improve-clinical-prediction-of-mortality-in-chronic-obstructive-pulmonary-disease/</link>
		<comments>http://beckerinfo.net/JClub/2012/03/22/inflammatory-biomarkers-improve-clinical-prediction-of-mortality-in-chronic-obstructive-pulmonary-disease/#comments</comments>
		<pubDate>Thu, 22 Mar 2012 23:31:02 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Respir Crit Care Med]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=405cb437b37a9bef6b6a747efe333ed1</guid>
		<description><![CDATA[Inflammatory Biomarkers Improve Clinical Prediction of Mortality in Chronic Obstructive P...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Inflammatory Biomarkers Improve Clinical Prediction of Mortality in Chronic Obstructive Pulmonary Disease.</b></p>
        <p>Am J Respir Crit Care Med. 2012 Mar 15;</p>
        <p>Authors:  Celli BR, Locantore N, Yates J, Tal-Singer R, Miller BE, Bakke P, Calverley P, Coxson H, Crim C, Edwards LD, Lomas DA, Duvoix A, Macnee W, Rennard S, Silverman E, Vestbo J, Wouters E, Agusti AA,  </p>
        <p>Abstract<br/>
        Rationale Accurate prediction of mortality helps select patients for interventions aimed at improving outcome. Objectives Because chronic obstructive pulmonary disease is characterized by low-grade systemic inflammation, we hypothesized that addition of inflammatory biomarkers to established predictive factors will improve accuracy. Methods 1843 patients enrolled in the ECLIPSE study were followed for 3 years. Kaplan-Meier curves, log rank analysis and Cox proportional hazards analyses determined the predictive value for mortality of clinical variables, while C-statistics assessed the added discriminative power offered by addition of biomarkers. Measurements At recruitment we measured anthropometrics, spirometry, 6 minute walk distance, dyspnea, BODE index, history of hospitalization, co-morbidities and CT scan emphysema. White blood cell and neutrophil counts, serum or plasma levels of fibrinogen, chemokine ligand 18, surfactant protein D, C-reactive protein , Clara cell secretory protein-16, Interleukin-6 and -8 and tumor necrosis factor alpha were determined at recruitment and subsequent visits.. Main Results 168 of the 1843 patients (9•1 %) died. Non-survivors were older, had more severe airflow limitation, increased dyspnea, higher BODE score, more emphysema, and higher rates of co-morbidities and history of hospitalizations. The best predictive model for mortality using clinical variables included age, BODE and hospitalization history (C-statistic of 0•686, p&lt;0•001). One single biomarker (Interleukin-6) significantly improved the C statistic to 0.708, but this was further improved to 0•726, (p=0•003) by the addition of all biomarkers. Conclusions The addition of a panel of selected biomarkers improves the ability of established clinical variables to predict mortality in COPD.<br/></p><p>PMID: 22427534 [PubMed - as supplied by publisher]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
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		<title>The implications of long-term acute care hospital transfer practices for measures of in-hospital mortality and length of stay.</title>
		<link>http://beckerinfo.net/JClub/2012/03/06/the-implications-of-long-term-acute-care-hospital-transfer-practices-for-measures-of-in-hospital-mortality-and-length-of-stay-2/</link>
		<comments>http://beckerinfo.net/JClub/2012/03/06/the-implications-of-long-term-acute-care-hospital-transfer-practices-for-measures-of-in-hospital-mortality-and-length-of-stay-2/#comments</comments>
		<pubDate>Tue, 06 Mar 2012 13:31:01 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Respir Crit Care Med]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=f5268532ebd8d8162973cea2d698d975</guid>
		<description><![CDATA[The implications of long-term acute care hospital transfer practices for measures of in-h...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>The implications of long-term acute care hospital transfer practices for measures of in-hospital mortality and length of stay.</b></p>
        <p>Am J Respir Crit Care Med. 2012 Jan 1;185(1):53-7</p>
        <p>Authors:  Hall WB, Willis LE, Medvedev S, Carson SS</p>
        <p>Abstract<br/>
        RATIONALE: The National Quality Forum recently endorsed in-hospital mortality and intensive care unit length of stay (LOS) as quality indicators for patients in the intensive care unit. These measures may be affected by transferring patients to long-term acute care hospitals (LTACs).<br/>
        OBJECTIVES: To quantify the implications of LTAC transfer practices on variation in mortality index and LOS index for patients in academic medical centers.<br/>
        METHODS: We used a cross-sectional study design using data reported to the University HealthSystem Consortium from 2008-2009. Data were from patients who were mechanically ventilated for more than 96 hours.<br/>
        MEASUREMENTS AND MAIN RESULTS: Using linear regression, we measured the association between mortality index and LTAC transfer rate, with the hospital as the unit of analysis. Similar analyses were conducted for LOS index and cost index. A total of 137 hospitals were analyzed, averaging 534 transfers to LTAC per hospital during the study period. Mean±SD in-hospital mortality was 24±6.4%, and observed LOS was 30.4±8.2 days. The mean LTAC transfer rate was 15.7±13.7%. Linear regression demonstrated a significant correlation between transfer rate and mortality index (R2=0.14; P&lt;0.0001) and LOS index (R2=0.43; P&lt;0.0001).<br/>
        CONCLUSIONS: LTAC hospital transfer rate has a significant impact on reported mortality and LOS indices for patients requiring prolonged acute mechanical ventilation. This is an example of factors unrelated to quality of medical care or illness severity that must be considered when interpreting mortality and LOS as quality indicators.<br/></p><p>PMID: 21940788 [PubMed - indexed for MEDLINE]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
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		<title>Refusal of ICU Admission Due to a Full Unit: Impact on Mortality.</title>
		<link>http://beckerinfo.net/JClub/2012/02/22/refusal-of-icu-admission-due-to-a-full-unit-impact-on-mortality/</link>
		<comments>http://beckerinfo.net/JClub/2012/02/22/refusal-of-icu-admission-due-to-a-full-unit-impact-on-mortality/#comments</comments>
		<pubDate>Wed, 22 Feb 2012 15:03:38 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Respir Crit Care Med]]></category>

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		<description><![CDATA[Refusal of ICU Admission Due to a Full Unit: Impact on Mortality.
        Am J Respir Cri...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Refusal of ICU Admission Due to a Full Unit: Impact on Mortality.</b></p>
        <p>Am J Respir Crit Care Med. 2012 Feb 16;</p>
        <p>Authors:  Robert R, Reignier J, Tournoux-Facon C, Boulain T, Lesieur O, Gissot V, Souday V, Hamrouni M, Chapon C, Gouello JP,  </p>
        <p>Abstract<br/>
        RATIONALE: Intensive-care-unit (ICU) beds are a scarce resource, and patients denied intensive care only because the unit is full may be at increased risk of death. OBJECTIVE: To compare mortality after first ICU referral in admitted patients and in patients denied admission because the unit was full. METHODS: Prospective observational multicenter cohort study of consecutive patients referred for ICU admission during two 45-day periods, conducted in 10 ICUs. MEASUREMENTS AND MAIN RESULTS: Of 1762 patients, 430 were excluded from the study, 116 with previously denied admission to another ICU and 270 because they were deemed too sick or too well to benefit from ICU admission. Of the remaining 1332 patients, 1139 were admitted and 193 were denied admission because the unit was full (65 were never admitted, 39 were admitted after bumping of another patient, and 89 were admitted upon subsequent referral). Crude day-28 and day-60 mortality rates in the nonadmitted and admitted groups were 30.1% vs. 24.3%, p=0.07 and 33.3% vs. 27.2%, p=0.06, respectively. Day-28 mortality adjusted on age, previous disease, Glasgow scale score ?8, shock, creatinine level ?250 µmol/L, and prothrombin time ?30 sec was nonsignificantly higher in patients refused ICU admission only because of a full unit, compared to patients admitted immediately. Patients admitted after subsequent referral had higher mortality rates on day 28 (p=0.05) and day 60 (p=0.04) compared to directly admitted patients. CONCLUSIONS: Delayed ICU admission due to a full unit at first referral is associated with increased mortality.<br/></p><p>PMID: 22345582 [PubMed - as supplied by publisher]</p></body>]]></content:encoded>
			<wfw:commentRss>http://beckerinfo.net/JClub/2012/02/22/refusal-of-icu-admission-due-to-a-full-unit-impact-on-mortality/feed/</wfw:commentRss>
		<slash:comments>1</slash:comments>
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		<title>Surgical Face Masks Worn By Multidrug-Resistant Tuberculosis Patients: Impact on Infectivity of Air on a Hospital Ward.</title>
		<link>http://beckerinfo.net/JClub/2012/02/11/surgical-face-masks-worn-by-multidrug-resistant-tuberculosis-patients-impact-on-infectivity-of-air-on-a-hospital-ward/</link>
		<comments>http://beckerinfo.net/JClub/2012/02/11/surgical-face-masks-worn-by-multidrug-resistant-tuberculosis-patients-impact-on-infectivity-of-air-on-a-hospital-ward/#comments</comments>
		<pubDate>Sat, 11 Feb 2012 19:31:25 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Respir Crit Care Med]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=d3052af2b47fb9cc7c993d8dd4acb587</guid>
		<description><![CDATA[Surgical Face Masks Worn By Multidrug-Resistant Tuberculosis Patients: Impact on Infectiv...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Surgical Face Masks Worn By Multidrug-Resistant Tuberculosis Patients: Impact on Infectivity of Air on a Hospital Ward.</b></p>
        <p>Am J Respir Crit Care Med. 2012 Feb 9;</p>
        <p>Authors:  Dharmadhikari AS, Mphahlele M, Stoltz A, Venter K, Mathebula R, Masotla T, Lubbe W, Pagano M, First M, Jensen PA, van der Walt M, Nardell EA</p>
        <p>Abstract<br/>
        RATIONALE AND OBJECTIVES:  Drug-resistant tuberculosis transmission in hospitals threatens staff and patient health.  Surgical face masks used by TB patients are believed to reduce transmission, but have not been rigorously tested. We sought to quantify their efficacy when worn by multidrug resistant tuberculosis (MDR-TB) patients. METHODS:  Over 3 months, 17 pulmonary MDR-TB patients occupied an MDR-TB ward in South Africa and wore face masks on alternate days.  Ward air was exhausted to two identical chambers each housing 90 pathogen-free guinea pigs that breathed ward air either when patients wore surgical face masks (intervention group) or when patients did not wear masks (control group). Efficacy was based on differences in guinea pig infections in each chamber.  MEASUREMENTS AND  MAIN RESULTS:   69/90 control guinea pigs (76.6%; 95% CI: 68 - 85%) became infected, compared to 36/90 intervention guinea pigs (40%; 95% CI: 31 - 51%), representing a 56% (95% CI: 33% - 70.5%) decreased risk of tuberculosis transmission when patients used masks.   CONCLUSIONS:  Surgical face masks on MDR-TB patients significantly reduced transmission and offer an adjunct measure for reducing TB transmission from infectious patients.<br/></p><p>PMID: 22323300 [PubMed - as supplied by publisher]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
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		<title>Screening and prevention of venous thromboembolism in critically ill patients: a decision analysis and economic evaluation.</title>
		<link>http://beckerinfo.net/JClub/2012/02/03/screening-and-prevention-of-venous-thromboembolism-in-critically-ill-patients-a-decision-analysis-and-economic-evaluation/</link>
		<comments>http://beckerinfo.net/JClub/2012/02/03/screening-and-prevention-of-venous-thromboembolism-in-critically-ill-patients-a-decision-analysis-and-economic-evaluation/#comments</comments>
		<pubDate>Fri, 03 Feb 2012 23:32:23 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Respir Crit Care Med]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=687514ab11e8c6c4dcfc1a6eabeef045</guid>
		<description><![CDATA[Screening and prevention of venous thromboembolism in critically ill patients: a decision...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Screening and prevention of venous thromboembolism in critically ill patients: a decision analysis and economic evaluation.</b></p>
        <p>Am J Respir Crit Care Med. 2011 Dec 1;184(11):1289-98</p>
        <p>Authors:  Sud S, Mittmann N, Cook DJ, Geerts W, Chan B, Dodek P, Gould MK, Guyatt G, Arabi Y, Fowler RA</p>
        <p>Abstract<br/>
        RATIONALE: Venous thromboembolism is difficult to diagnose in critically ill patients and may increase morbidity and mortality.<br/>
        OBJECTIVES: To evaluate the cost-effectiveness of strategies to reduce morbidity from venous thromboembolism in critically ill patients.<br/>
        METHODS: A Markov decision analytic model to compare weekly compression ultrasound screening (screening) plus investigation for clinically suspected deep vein thrombosis (DVT) (case finding) versus case finding alone; and a hypothetical program to increase adherence to DVT prevention. Probabilities were derived from a systematic review of venous thromboembolism in medical-surgical intensive care unit patients. Costs (in 2010 $US) were obtained from hospitals in Canada, Australia, and the United States, and the medical literature. Analyses were conducted from a societal perspective over a lifetime horizon. Outcomes included costs, quality-adjusted life-years (QALY), and incremental cost-effectiveness ratios.<br/>
        MEASUREMENTS AND MAIN RESULTS: In the base case, the rate of proximal DVT was 85 per 1,000 patients. Screening resulted in three fewer pulmonary emboli than case-finding alone but also two additional bleeding episodes, and cost $223,801 per QALY gained. In sensitivity analyses, screening cost less than $50,000 per QALY only if the probability of proximal DVT increased from a baseline of 8.5-16%. By comparison, increasing adherence to appropriate pharmacologic thromboprophylaxis by 10% resulted in 16 fewer DVTs, one fewer pulmonary emboli, and one additional heparin-induced thrombocytopenia and bleeding event, and cost $27,953 per QALY gained. Programs achieving increased adherence to best-practice venous thromboembolism prevention were cost-effective over a wide range of program costs and were robust in probabilistic sensitivity analyses.<br/>
        CONCLUSIONS: Appropriate prophylaxis provides better value in terms of costs and health gains than routine screening for DVT. Resources should be targeted at optimizing thromboprophylaxis.<br/></p><p>PMID: 21868500 [PubMed - indexed for MEDLINE]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
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		<title>Utility of the COPD Assessment Test&trade; (CAT) to Evaluate Severity of COPD Exacerbations.</title>
		<link>http://beckerinfo.net/JClub/2012/01/30/utility-of-the-copd-assessment-testtrade-cat-to-evaluate-severity-of-copd-exacerbations/</link>
		<comments>http://beckerinfo.net/JClub/2012/01/30/utility-of-the-copd-assessment-testtrade-cat-to-evaluate-severity-of-copd-exacerbations/#comments</comments>
		<pubDate>Mon, 30 Jan 2012 07:09:01 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Respir Crit Care Med]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=a0dc4f80c1dddf7a660428c5ed9c56df</guid>
		<description><![CDATA[Utility of the COPD Assessment Test&#038;trade; (CAT) to Evaluate Severity of COPD Exacerb...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Utility of the COPD Assessment Test&amp;trade; (CAT) to Evaluate Severity of COPD Exacerbations.</b></p>
        <p>Am J Respir Crit Care Med. 2012 Jan 26;</p>
        <p>Authors:  Mackay AJ, Donaldson GC, Patel AR, Jones PW, Hurst JR, Wedzicha JA</p>
        <p>Abstract<br/>
        RATIONALE:  The COPD Assessment Test™ (CAT) is an 8-item questionnaire designed to assess and quantify the impact of COPD symptoms on health status. COPD exacerbations impair quality of life and are characterized by worsening respiratory symptoms from the stable state. We hypothesized that CAT scores at exacerbation relate to exacerbation severity as measured by exacerbation duration, lung function impairment and systemic inflammation.  OBJECTIVES:  To evaluate the utility of the CAT to assess exacerbation severity. METHODS:  161 patients enrolled in the London COPD cohort completed the CAT at baseline (stable state), exacerbation and during recovery between April 2010 and June 2011. MEASUREMENTS AND  MAIN RESULTS:   Frequent exacerbators had significantly higher baseline CAT scores than infrequent exacerbators (19.5±6.6 vs. 16.8±8.0, p=0.025). In 152 exacerbations, CAT scores rose from an average baseline value of 19.4±6.8 to 24.1±7.3 (p&lt;0.001) at exacerbation. Change in CAT score from baseline to exacerbation onset was significantly but weakly related to change in CRP (rho=0.26; p=0.008) but not to change in fibrinogen (rho=0.09, p=0.351) from baseline to exacerbation. At exacerbation, rises in CAT score were significantly associated with falls in FEV1 (rho=-0.20, p=0.032). Median recovery time as judged by symptom diary cards was significantly related to the time taken for the CAT score to return to baseline (rho=0.42; p=0.012). CONCLUSIONS:  The CAT provides a reliable score of exacerbation severity. Baseline CAT scores are elevated in frequent exacerbators. CAT scores increase at exacerbation and reflect severity as determined by lung function and exacerbation duration.<br/></p><p>PMID: 22281834 [PubMed - as supplied by publisher]</p></body>]]></content:encoded>
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		<title>Matrix elastin: a promising biomarker for chronic obstructive pulmonary disease.</title>
		<link>http://beckerinfo.net/JClub/2012/01/06/matrix-elastin-a-promising-biomarker-for-chronic-obstructive-pulmonary-disease/</link>
		<comments>http://beckerinfo.net/JClub/2012/01/06/matrix-elastin-a-promising-biomarker-for-chronic-obstructive-pulmonary-disease/#comments</comments>
		<pubDate>Fri, 06 Jan 2012 18:00:36 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Respir Crit Care Med]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=b5fd198c235e85435bab211dba675ab0</guid>
		<description><![CDATA[Matrix elastin: a promising biomarker for chronic obstructive pulmonary disease.
        ...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Matrix elastin: a promising biomarker for chronic obstructive pulmonary disease.</b></p>
        <p>Am J Respir Crit Care Med. 2011 Sep 15;184(6):637-41</p>
        <p>Authors:  Turino GM, Ma S, Lin YY, Cantor JO, Luisetti M</p>
        <p>Abstract<br/>
        Chronic obstructive pulmonary disease (COPD) is a major health problem worldwide and is now the third leading cause of death in the United States. There is a lack of therapies that can stop progression of the disease and improve survival. New drug discovery can be aided by the development of biomarkers, which can act as indicators of severity in the course of the disease and responses to therapy. This perspective brings together the laboratory and clinical evidence, which suggest that elastin degradation products can fulfill the need for such a biomarker. Elastin is a recognized target for injury in COPD. The amino acids desmosine and isodesmosine exist only in matrix elastin; can be measured specifically and sensitively in plasma, urine, and sputum; and indicate changes in the systemic balance between elastase activity and elastase inhibition brought on by the systemic inflammatory state. The biomarker levels in sputum reflect the state of elastin degradation in the lung specifically. Clinical data accumulated over several decades indicate correlations of desmosine and isodesmosine levels with COPD of varying severity and responses to therapy.<br/></p><p>PMID: 21757624 [PubMed - indexed for MEDLINE]</p></body>]]></content:encoded>
			<wfw:commentRss>http://beckerinfo.net/JClub/2012/01/06/matrix-elastin-a-promising-biomarker-for-chronic-obstructive-pulmonary-disease/feed/</wfw:commentRss>
		<slash:comments>0</slash:comments>
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		<title>Acute exacerbations of chronic obstructive pulmonary disease: identification of biologic clusters and their biomarkers.</title>
		<link>http://beckerinfo.net/JClub/2012/01/06/acute-exacerbations-of-chronic-obstructive-pulmonary-disease-identification-of-biologic-clusters-and-their-biomarkers/</link>
		<comments>http://beckerinfo.net/JClub/2012/01/06/acute-exacerbations-of-chronic-obstructive-pulmonary-disease-identification-of-biologic-clusters-and-their-biomarkers/#comments</comments>
		<pubDate>Fri, 06 Jan 2012 18:00:36 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Respir Crit Care Med]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=c94ba3f1e807fd947def4506333979b7</guid>
		<description><![CDATA[Acute exacerbations of chronic obstructive pulmonary disease: identification of biologic ...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Acute exacerbations of chronic obstructive pulmonary disease: identification of biologic clusters and their biomarkers.</b></p>
        <p>Am J Respir Crit Care Med. 2011 Sep 15;184(6):662-71</p>
        <p>Authors:  Bafadhel M, McKenna S, Terry S, Mistry V, Reid C, Haldar P, McCormick M, Haldar K, Kebadze T, Duvoix A, Lindblad K, Patel H, Rugman P, Dodson P, Jenkins M, Saunders M, Newbold P, Green RH, Venge P, Lomas DA, Barer MR, Johnston SL, Pavord ID, Brightling CE</p>
        <p>Abstract<br/>
        RATIONALE: Exacerbations of chronic obstructive pulmonary disease (COPD) are heterogeneous with respect to inflammation and etiology.<br/>
        OBJECTIVES: Investigate biomarker expression in COPD exacerbations to identify biologic clusters and determine biomarkers that recognize clinical COPD exacerbation phenotypes, namely those associated with bacteria, viruses, or eosinophilic airway inflammation.<br/>
        METHODS: Patients with COPD were observed for 1 year at stable and exacerbation visits. Biomarkers were measured in sputum and serum. Viruses and selected bacteria were assessed in sputum by polymerase chain reaction and routine diagnostic bacterial culture. Biologic phenotypes were explored using unbiased cluster analysis and biomarkers that differentiated clinical exacerbation phenotypes were investigated. Measurements and Main Results: A total of 145 patients (101 men and 44 women) entered the study. A total of 182 exacerbations were captured from 86 patients. Four distinct biologic exacerbation clusters were identified. These were bacterial-, viral-, or eosinophilic-predominant, and a fourth associated with limited changes in the inflammatory profile termed “pauciinflammatory.” Of all exacerbations, 55%, 29%, and 28% were associated with bacteria, virus, or a sputum eosinophilia. The biomarkers that best identified these clinical phenotypes were sputum IL-1?, 0.89 (area under receiver operating characteristic curve) (95% confidence interval [CI], 0.83–0.95); serum CXCL10, 0.83 (95% CI, 0.70–0.96); and percentage peripheral eosinophils, 0.85 (95% CI, 0.78–0.93), respectively.<br/>
        CONCLUSIONS: The heterogeneity of the biologic response of COPD exacerbations can be defined. Sputum IL-1?, serum CXCL10, and peripheral eosinophils are biomarkers of bacteria-, virus-, or eosinophil-associated exacerbations of COPD. Whether phenotype-specific biomarkers can be applied to direct therapy warrants further investigation.<br/></p><p>PMID: 21680942 [PubMed - indexed for MEDLINE]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
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		<title>Intensive care unit management of patients with severe pulmonary hypertension and right heart failure.</title>
		<link>http://beckerinfo.net/JClub/2012/01/06/intensive-care-unit-management-of-patients-with-severe-pulmonary-hypertension-and-right-heart-failure/</link>
		<comments>http://beckerinfo.net/JClub/2012/01/06/intensive-care-unit-management-of-patients-with-severe-pulmonary-hypertension-and-right-heart-failure/#comments</comments>
		<pubDate>Fri, 06 Jan 2012 17:34:06 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Respir Crit Care Med]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=054ca043e1307eb372299a87bd362139</guid>
		<description><![CDATA[Intensive care unit management of patients with severe pulmonary hypertension and right h...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Intensive care unit management of patients with severe pulmonary hypertension and right heart failure.</b></p>
        <p>Am J Respir Crit Care Med. 2011 Nov 15;184(10):1114-24</p>
        <p>Authors:  Hoeper MM, Granton J</p>
        <p>Abstract<br/>
        Despite advances in medical therapies, pulmonary arterial hypertension (PAH) continues to cause significant morbidity and mortality. Although the right ventricle (RV) can adapt to an increase in afterload, progression of the pulmonary vasculopathy that characterizes PAH causes many patients to develop progressive right ventricular failure. Furthermore, acute right ventricular decompensation may develop from disorders that lead to either an acute increase in cardiac demand, such as sepsis, or to an increase in ventricular afterload, including interruptions in medical therapy, arrhythmia, or pulmonary embolism. The poor reserve of the right ventricle, RV ischemia, and adverse right ventricular influence on left ventricular filling may lead to a global reduction in oxygen delivery and multiorgan failure. There is a paucity of data to guide clinicians caring for acute right heart failure in PAH. Treatment recommendations are frequently based on animal models of acute right heart failure or case series in humans with other causes of pulmonary hypertension. Successful treatment often requires that invasive hemodynamics be used to monitor the effect of strategies that are based primarily on biological plausibility. Herein we have developed an approach based on the current understanding of RV failure in PAH and have attempted to develop a treatment paradigm based on physiological principles and available evidence.<br/></p><p>PMID: 21700906 [PubMed - indexed for MEDLINE]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
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