<?xml version="1.0" encoding="UTF-8"?>
<?xml-stylesheet href="/rss.css" type="text/css"?>
<rdf:RDF xmlns="http://purl.org/rss/1.0/"
    xmlns:cc="http://web.resource.org/cc/"
    xmlns:dc="http://purl.org/dc/elements/1.1/"
    xmlns:extra="http://www.w3.org/1999/xhtml"
    xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/"
    xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#">
    <channel rdf:about="http://ccforum.com/feeds/latestarticles/journal?quantity=&amp;format=rss&amp;version=">
        <title>Critical Care - Latest Articles</title>
        <link>http://ccforum.com/</link>
        <description>The latest research articles published by Critical Care</description>
        <dc:date>2009-11-24T00:00:00Z</dc:date>
        <items>
            <rdf:Seq>
                                <rdf:li rdf:resource="http://ccforum.com/content/13/6/232" />
                                <rdf:li rdf:resource="http://ccforum.com/content/13/6/R186" />
                                <rdf:li rdf:resource="http://ccforum.com/content/13/6/R185" />
                                <rdf:li rdf:resource="http://ccforum.com/content/13/6/R184" />
                                <rdf:li rdf:resource="http://ccforum.com/content/13/6/426" />
                                <rdf:li rdf:resource="http://ccforum.com/content/13/6/425" />
                                <rdf:li rdf:resource="http://ccforum.com/content/13/6/R183" />
                                <rdf:li rdf:resource="http://ccforum.com/content/13/6/R182" />
                                <rdf:li rdf:resource="http://ccforum.com/content/13/6/R181" />
                                <rdf:li rdf:resource="http://ccforum.com/content/13/6/1005" />
                            </rdf:Seq>
        </items>
        <extra:info rdf:parseType="Literal">
            <html:div style="font:14px Verdana, Geneva, Arial, Helvetica, sans-serif" xmlns:html="http://www.w3.org/1999/xhtml">
                <html:span style="font-weight:bold">
                    This is an RSS newsfeed from BioMed Central
                </html:span>
                <html:br />
                <html:span style="font-size: 12px;">
                    It is intended to be used with an RSS reader. For more information about RSS newsfeeds from BioMed Central, visit
                    <html:br />
                    <html:a href="http://www.biomedcentral.com/info/about/rss/" style="color:#3333CC; font-size:12px;">
                        http://www.biomedcentral.com/info/about/rss/
                    </html:a>
                    <html:br />
                </html:span>
            </html:div>
        </extra:info>
        <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </channel>
        <item rdf:about="http://ccforum.com/content/13/6/232">
        <title>A Review and Analysis of Heart Rate Variability and the Diagnosis and Prognosis of Infection</title>
        <description>Bacterial infection leading to organ failure is the most common cause of death in critically ill patients. Early diagnosis and expeditious treatment is a cornerstone of therapy. Evaluating the systemic host response to infection as a complex system provides novel insights. However, bedside application with clinical value remains wanting. Providing an integrative measure of an altered host response, the patterns and character of heart rate fluctuations measured over intervals-in-time may be analysed with a panel of mathematical techniques that quantify overall fluctuation, spectral composition, scale-free variation, and degree of irregularity or complexity. Using these techniques, heart rate variability (HRV) has been documented to be both altered in the presence of systemic infection, and correlated with its severity. In this review and analysis, we evaluate the use of HRV monitoring to provide early diagnosis of infection, document the real-time prognostic implications of altered HRV in infection, identify current limitations, highlight future research challenges, and propose improvement strategies. Given existing evidence and potential for further technological advances, we believe that longitudinal, individualized, and comprehensive HRV monitoring in critically ill patients at risk for or with existing infection offers a means to harness the clinical potential of this bedside application of complex systems science.</description>
        <link>http://ccforum.com/content/13/6/232</link>
                <dc:creator>Saif Ahmad</dc:creator>
                <dc:creator>Anjali Tejuja</dc:creator>
                <dc:creator>Kimberley Newman</dc:creator>
                <dc:creator>Ryan Zarychanski</dc:creator>
                <dc:creator>Andrew Seely</dc:creator>
                <dc:source>Critical Care 2009, 13:232</dc:source>
        <dc:date>2009-11-24T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/cc8132</dc:identifier>
        <prism:publicationName>Critical Care</prism:publicationName>
        <prism:issn>1364-8535</prism:issn>
        <prism:volume>13</prism:volume>
        <prism:startingPage>232</prism:startingPage>
        <prism:publicationDate>2009-11-24T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://ccforum.com/content/13/6/R186">
        <title>Effect of fluid resuscitation on mortality and organ function in experimental sepsis models</title>
        <description>IntroductionSeveral recent studies have shown that a positive fluid balance in critical illness is associated with worse outcome. We tested the effects of moderate vs. high-volume resuscitation strategies on mortality, systemic and regional blood flows, mitochondrial respiration, and organ function in two experimental sepsis models.
Methods:
48 pigs were randomized to continuous endotoxin infusion, fecal peritonitis, and a control group (n = 16 each), and each group further to two different basal rates of volume supply for 24 hours [moderate-volume (10 ml/kg/h, Ringer&apos;s lactate, n = 8); high-volume (15 + 5 ml/kg/h, Ringer&apos;s lactate and hydroxyethyl starch (HES), n = 8)], both supplemented by additional volume boli, as guided by urinary output, filling pressures, and responses in stroke volume. Systemic and regional hemodynamics were measured and tissue specimens taken for mitochondrial function assessment and histological analysis.
Results:
Mortality in high-volume groups was 87% (peritonitis), 75% (endotoxemia), and 13% (controls). In moderate-volume groups mortality was 50% (peritonitis), 13% (endotoxemia) and 0% (controls). Both septic groups became hyperdynamic. While neither sepsis nor volume resuscitation strategy was associated with altered hepatic or muscle mitochondrial complex I- and II-dependent respiration, non-survivors had lower hepatic complex II-dependent respiratory control ratios (2.6 +/- 0.7, vs. 3.3 +/- 0.9 in survivors; P = 0.01). Histology revealed moderate damage in all organs, colloid plaques in lung tissue of high-volume groups, and severe kidney damage in endotoxin high-volume animals.
Conclusions:
High-volume resuscitation including HES in experimental peritonitis and endotoxemia increased mortality despite better initial hemodynamic stability. This suggests that the strategy of early fluid management influences outcome in sepsis. The high mortality was not associated with reduced mitochondrial complex I- or II-dependent muscle and hepatic respiration.</description>
        <link>http://ccforum.com/content/13/6/R186</link>
                <dc:creator>Sebastian Brandt</dc:creator>
                <dc:creator>Tomas Regueira</dc:creator>
                <dc:creator>Hendrik Bracht</dc:creator>
                <dc:creator>Francesca Porta</dc:creator>
                <dc:creator>Siamak Djafarzadeh</dc:creator>
                <dc:creator>Jukka Takala</dc:creator>
                <dc:creator>Jose Gorrasi</dc:creator>
                <dc:creator>Erika Borotto</dc:creator>
                <dc:creator>Vladimir Krejci</dc:creator>
                <dc:creator>Luzius Hiltebrand</dc:creator>
                <dc:creator>Lukas Bruegger</dc:creator>
                <dc:creator>Guido Beldi</dc:creator>
                <dc:creator>Ludwig Wilkens</dc:creator>
                <dc:creator>Philipp Lepper</dc:creator>
                <dc:creator>Ulf Kessler</dc:creator>
                <dc:creator>Stephan Jakob</dc:creator>
                <dc:source>Critical Care 2009, 13:R186</dc:source>
        <dc:date>2009-11-23T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/cc8179</dc:identifier>
        <prism:publicationName>Critical Care</prism:publicationName>
        <prism:issn>1364-8535</prism:issn>
        <prism:volume>13</prism:volume>
        <prism:startingPage>R186</prism:startingPage>
        <prism:publicationDate>2009-11-23T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://ccforum.com/content/13/6/R185">
        <title>Effects of unilateral decompressive craniectomy on patients with unilateral acute post-traumatic brain swelling after severe traumatic brain injury</title>
        <description>IntroductionAcute post-traumatic brain swelling (BS) is one of the pathological forms that need emergent treatment following traumatic brain injury. There is controversy about the effects of craniotomy on acute post-traumatic BS. The aim of the present clinical study was to assess the efficacy of unilateral decompressive craniectomy (DC) or unilateral routine temporoparietal craniectomy on patients with unilateral acute post-traumatic BS.
Methods:
Seventy-four patients of unilateral acute post-traumatic BS with midline shifting more than 5 mm were divided randomly into two groups: unilateral DC group (n = 37) and unilateral routine temporoparietal craniectomy group (control group, n = 37). The vital signs, the intracranial pressure (ICP), the Glasgow outcome scale (GOS), the mortality rate and the complications were prospectively analysed.
Results:
The mean ICP values of patients in the unilateral DC group at hour 24, hour 48, hour 72 and hour 96 after injury were much lower than those of the control group (15.19+/-2.18 mmHg, 16.53+/-1.53 mmHg, 15.98+/-2.24 mmHg and 13.518+/-2.33 mmHg versus 19.95+/-2.24 mmHg, 18.32+/-1.77 mmHg, 21.05+/-2.23 mmHg and 17.68+/-1.40 mmHg, respectively). The mortality rates at 1 month after treatment were 27% in the unilateral DC group and 57% in the control group (p=0.010). Good neurological outcome (GOS Score of 4 to 5) rates 1 year after injury for the groups were 56.8% and 32.4%, respectively (p=0.035). The incidences of delayed intracranial hematoma and subdural effusion were 21.6% and 10.8% versus 5.4% and 0, respectively (p=0.041 and 0.040).
Conclusions:
Our data suggest that unilateral DC has superiority in lowering ICP, reducing the mortality rate and improving neurological outcomes over unilateral routine temporoparietal craniectomy. However, it increases the incidence of delayed intracranial hematomas and subdural effusion, some of which need secondary surgical intervention. These results provide information important for further large and multicenter clinical trials on the effects of DC in patients with acute post-traumatic BS.Trial registration: ISRCTN14110527</description>
        <link>http://ccforum.com/content/13/6/R185</link>
                <dc:creator>Wusi Qiu</dc:creator>
                <dc:creator>Chenchen Guo</dc:creator>
                <dc:creator>Hong Shen</dc:creator>
                <dc:creator>Keyong Chen</dc:creator>
                <dc:creator>Liang Wen</dc:creator>
                <dc:creator>Hongjie Huang</dc:creator>
                <dc:creator>Min Ding</dc:creator>
                <dc:creator>Li Sun</dc:creator>
                <dc:creator>Qizhou Jiang</dc:creator>
                <dc:creator>Weiming Wang</dc:creator>
                <dc:source>Critical Care 2009, 13:R185</dc:source>
        <dc:date>2009-11-20T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/cc8178</dc:identifier>
        <prism:publicationName>Critical Care</prism:publicationName>
        <prism:issn>1364-8535</prism:issn>
        <prism:volume>13</prism:volume>
        <prism:startingPage>R185</prism:startingPage>
        <prism:publicationDate>2009-11-20T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://ccforum.com/content/13/6/R184">
        <title>Complications of continuous renal replacement therapy in critically ill children: a prospective observational evaluation study</title>
        <description>IntroductionContinuous renal replacement therapy (CRRT) frequently gives rise to complications in critically ill children. However, no studies have analyzed these complications prospectively. The purpose of this study was to analyze the complications of CRRT in children and to study the associated risk factors.
Methods:
A prospective, single-centre, observational study was performed in all critically ill children treated using CRRT in order to determine the incidence of complications related to the technique (problems of catheterization, hypotension at the time of connection to the CRRT, hemorrhage, electrolyte disturbances) and their relationship with patient characteristics, clinical severity, need for vasoactive drugs and mechanical ventilation, and the characteristics of the filtration techniques.
Results:
Of 174 children treated with CRRT, 13 (7.4%) presented problems of venous catheterization; this complication was significantly more common in children under 12 months of age and in those weighing less than 10 kg. Hypotension on connection to CRRT was detected in 53 patients (30.4%). Hypotension was not associated with any patient or CRRT characteristics.  Clinically significant hemorrhage occurred in 18 patients (10.3%); this complication was not related to any of the variables studied. The sodium, chloride, and phosphate levels fell during the first 72 hours of CRRT; the changes in electrolyte levels during the course of treatment were not found to be related to any of the variables analyzed, nor were they associated with mortality.
Conclusions:
CRRT-related complications are common in children and some are potentially serious. The most common are hypotension at the time of connection and electrolyte disturbances. Strict control and continuous monitoring of the technique are therefore necessary in children on CRRT.</description>
        <link>http://ccforum.com/content/13/6/R184</link>
                <dc:creator>Maria Santiago</dc:creator>
                <dc:creator>Jesus Lopez-Herce</dc:creator>
                <dc:creator>Javier Urbano</dc:creator>
                <dc:creator>Maria Solana</dc:creator>
                <dc:creator>Jimena Del Castillo</dc:creator>
                <dc:creator>Yolanda Ballestero</dc:creator>
                <dc:creator>Marta Botran</dc:creator>
                <dc:creator>Jose Bellon</dc:creator>
                <dc:source>Critical Care 2009, 13:R184</dc:source>
        <dc:date>2009-11-19T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/cc8172</dc:identifier>
        <prism:publicationName>Critical Care</prism:publicationName>
        <prism:issn>1364-8535</prism:issn>
        <prism:volume>13</prism:volume>
        <prism:startingPage>R184</prism:startingPage>
        <prism:publicationDate>2009-11-19T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://ccforum.com/content/13/6/426">
        <title>Presentation and management of critically ill patients with Influenza A (H1N1) influenza - a UK perspective</title>
        <description>A report of the demographics, presentation and management of patients with influenza A (H1N1) in a general adult intensive care unit in the United Kingdom.</description>
        <link>http://ccforum.com/content/13/6/426</link>
                <dc:creator>Joyce Yeung</dc:creator>
                <dc:creator>Mark Bailey</dc:creator>
                <dc:creator>Gavin Perkins</dc:creator>
                <dc:creator>Fang Gao Smith</dc:creator>
                <dc:source>Critical Care 2009, 13:426</dc:source>
        <dc:date>2009-11-19T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/cc8151</dc:identifier>
        <prism:publicationName>Critical Care</prism:publicationName>
        <prism:issn>1364-8535</prism:issn>
        <prism:volume>13</prism:volume>
        <prism:startingPage>426</prism:startingPage>
        <prism:publicationDate>2009-11-19T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://ccforum.com/content/13/6/425">
        <title>Severe Influenza A (H1N1)v in patients without any known risk factor</title>
        <description>In Rello et al work 15 out of 32 critical pandemic flu patients did not have any risk factor. A further analysis in this subgroup of patients is needed. Antiviral treatment delay or any other management event differences perhaps were responsible for progressive illness. This data may help management in initial care of pandemic flu patients.</description>
        <link>http://ccforum.com/content/13/6/425</link>
                <dc:creator>Carles Alonso-Tarres</dc:creator>
                <dc:creator>Cristina Cortes-Lletget</dc:creator>
                <dc:creator>Sara Pintado</dc:creator>
                <dc:creator>Assumpta Ricart</dc:creator>
                <dc:source>Critical Care 2009, 13:425</dc:source>
        <dc:date>2009-11-19T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/cc8150</dc:identifier>
        <prism:publicationName>Critical Care</prism:publicationName>
        <prism:issn>1364-8535</prism:issn>
        <prism:volume>13</prism:volume>
        <prism:startingPage>425</prism:startingPage>
        <prism:publicationDate>2009-11-19T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://ccforum.com/content/13/6/R183">
        <title>The leading causes of death after burn injury in a single pediatric burn center</title>
        <description>IntroductionSevere thermal injury is characterized by profound morbidity and mortality. Advances in burn and critical care, including early excision and grafting, aggressive resuscitation and advances in antimicrobial therapy have made substantial contributions to decrease morbidity and mortality. Despite these advances, death still occurs. Our aim was to determine the predominant causes of death in burned pediatric patients in order to develop new treatment avenues and future trajectories associated with increased survival.
Methods:
Primary causes of death were reviewed from 144 pediatric autopsy reports. Percentages of patients that died from anoxic brain injuries, sepsis, or multi-organ failure were calculated by comparing to the total number of deaths. Data was stratified by time (from 1989 to 1999, and 1999 to 2009), and gender. Statistical analysis was done by chi-squared, Student&apos;s t-test and Kaplan-Meier for survival where applicable. Significance was accepted as p&lt;0.05.
Results:
Five-thousand two-hundred-sixty patients were admitted after burn injury from July 1989 to June 2009, and of those, 145 patients died after burn injury. Of these patients, 144 patients had an autopsy. The leading causes of death over 20 years were sepsis (47%), respiratory failure (29%), anoxic brain injury (16%), and shock (8%). From 1989 to 1999, sepsis accounted for 35% of deaths but increased to 54% from 1999 to 2009, with a significant increase in the proportion due to antibiotic resistant organisms (p&lt;0.05).
Conclusions:
Sepsis is the leading cause of death after burn injury. Multiple antibiotic resistant bacteria now account for the bulk of deaths due to sepsis. Further improvement in survival may require improved strategies to deal with this problem.</description>
        <link>http://ccforum.com/content/13/6/R183</link>
                <dc:creator>Felicia Williams</dc:creator>
                <dc:creator>David Herndon</dc:creator>
                <dc:creator>Hal Hawkins</dc:creator>
                <dc:creator>Jong Lee</dc:creator>
                <dc:creator>Robert Cox</dc:creator>
                <dc:creator>Gabriela Kulp</dc:creator>
                <dc:creator>Celeste Finnerty</dc:creator>
                <dc:creator>David Chinkes</dc:creator>
                <dc:creator>Marc Jeschke</dc:creator>
                <dc:source>Critical Care 2009, 13:R183</dc:source>
        <dc:date>2009-11-17T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/cc8170</dc:identifier>
        <prism:publicationName>Critical Care</prism:publicationName>
        <prism:issn>1364-8535</prism:issn>
        <prism:volume>13</prism:volume>
        <prism:startingPage>R183</prism:startingPage>
        <prism:publicationDate>2009-11-17T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://ccforum.com/content/13/6/R182">
        <title>Ventilator-induced endothelial activation and inflammation in the lung and distal organs</title>
        <description>IntroductionResults from clinical studies have provided evidence for the importance of leukocyte-endothelial interactions in the pathogenesis of pulmonary diseases such as acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), as well as in systemic events like sepsis and multiple organ failure (MOF). The present study was designed to investigate whether alveolar stretch due to mechanical ventilation (MV) may evoke endothelial activation and inflammation in healthy mice, not only in the lung but also in organs distal to the lung.
Methods:
Healthy male C3H/HeN mice were anesthetized, tracheotomized and mechanically ventilated for either 1, 2 or 4 hours. To study the effects of alveolar stretch in vivo, we applied a MV strategy that causes overstretch of pulmonary tissue i.e. 20 cmH2O peak inspiratory pressure (PIP) and 0 cmH20 positive end expiratory pressure (PEEP). Non-ventilated, sham-operated animals served as a reference group (non-ventilated controls, NVC).
Results:
Alveolar stretch imposed by MV did not only induce de novo synthesis of adhesion molecules in the lung but also in organs distal to the lung, like liver and kidney. No activation was observed in the brain. In addition, we demonstrated elevated cytokine and chemokine expression in pulmonary, hepatic and renal tissue after MV which was accompanied by enhanced recruitment of granulocytes to these organs.
Conclusions:
Our data implicate that MV causes endothelial activation and inflammation in mice without pre-existing pulmonary injury, both in the lung and distal organs.</description>
        <link>http://ccforum.com/content/13/6/R182</link>
                <dc:creator>Maria Hegeman</dc:creator>
                <dc:creator>Marije Hennus</dc:creator>
                <dc:creator>Cobi Heijnen</dc:creator>
                <dc:creator>Patricia Specht</dc:creator>
                <dc:creator>Burkhard Lachmann</dc:creator>
                <dc:creator>Nicolaas Jansen</dc:creator>
                <dc:creator>Adrianus van Vught</dc:creator>
                <dc:creator>Pieter Cobelens</dc:creator>
                <dc:source>Critical Care 2009, 13:R182</dc:source>
        <dc:date>2009-11-16T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/cc8168</dc:identifier>
        <prism:publicationName>Critical Care</prism:publicationName>
        <prism:issn>1364-8535</prism:issn>
        <prism:volume>13</prism:volume>
        <prism:startingPage>R182</prism:startingPage>
        <prism:publicationDate>2009-11-16T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://ccforum.com/content/13/6/R181">
        <title>Association of arterial blood pressure and vasopressor load 
with septic shock mortality: a post hoc analysis of a multicenter trial</title>
        <description>IntroductionIt is unclear to which level mean arterial blood pressure (MAP) should be increased during septic shock in order to improve outcome. In this study we investigated the association between MAP values of 70 mmHg or higher, vasopressor load, 28-day mortality and disease-related events in septic shock.
Methods:
This is a post hoc analysis of data of the control group of a multicenter trial and includes 290 septic shock patients in whom a mean MAP [greater than or equal to] 70 mmHg could be maintained during shock. Demographic and clinical data, MAP, vasopressor requirements during the shock period, disease-related events and 28-day mortality were documented. Logistic regression models adjusted for the geographic region of the study center, age, presence of chronic arterial hypertension, simplified acute physiology score (SAPS) II and the mean vasopressor load during the shock period was calculated to investigate the association between MAP or MAP quartiles [greater than or equal to] 70 mmHg and mortality or the frequency and occurrence of disease-related events.
Results:
There was no association between MAP or MAP quartiles and mortality or the occurrence of disease-related events. These associations were not influenced by age or pre-existent arterial hypertension (all P&gt;0.05). The mean vasopressor load was associated with mortality (relative risk (RR), 1.83; confidence interval (CI) 95%, 1.4-2.38; P&lt;0.001), the number of disease-related events (P&lt;0.001) and the occurrence of acute circulatory failure (RR, 1.64; CI 95%, 1.28-2.11; P&lt;0.001), metabolic acidosis (RR, 1.79; CI 95%, 1.38-2.32; P&lt;0.001), renal failure (RR, 1.49; CI 95%, 1.17-1.89; P=0.001) and thrombocytopenia (RR, 1.33; CI 95%, 1.06-1.68; P=0.01).
Conclusions:
MAP levels of 70 mmHg or higher do not appear to be associated with improved survival in septic shock. Elevating MAP &gt;70 mmHg by augmenting vasopressor dosages may increase mortality. Future trials are needed to identify the lowest acceptable MAP level to ensure tissue perfusion and avoid unnecessary high catecholamine infusions.</description>
        <link>http://ccforum.com/content/13/6/R181</link>
                <dc:creator>Martin Dunser</dc:creator>
                <dc:creator>Esko Ruokonen</dc:creator>
                <dc:creator>Ville Pettila</dc:creator>
                <dc:creator>Hanno Ulmer</dc:creator>
                <dc:creator>Christian Torgersen</dc:creator>
                <dc:creator>Christian Schmittinger</dc:creator>
                <dc:creator>Stephan Jakob</dc:creator>
                <dc:creator>Jukka Takala</dc:creator>
                <dc:source>Critical Care 2009, 13:R181</dc:source>
        <dc:date>2009-11-16T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/cc8167</dc:identifier>
        <prism:publicationName>Critical Care</prism:publicationName>
        <prism:issn>1364-8535</prism:issn>
        <prism:volume>13</prism:volume>
        <prism:startingPage>R181</prism:startingPage>
        <prism:publicationDate>2009-11-16T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://ccforum.com/content/13/6/1005">
        <title>The Value of a Risk Model for Early-onset Candidemia</title>
        <description>Blood stream infections from Candida species are associated with an increased length of stay, increased hospital costs, and higher mortality when compared to bacterial blood stream infections.  Delayed or inappropriate therapy in candidemia leads to increased mortality, thus early recognition becomes paramount.  With biomarkers showing promise, blood cultures  still remain the gold standard but require 24-72 hours for growth.  Thus, the reliance on epidemilogic risk factors for the initiation of empiric antifungal therapy provides the best method for early appropriate therapy.  Shorr and colleagues have devised a risk score to identify patients with early onset candidemia as defined by positive blood cultures within 2 days of admission, thus allowing for the initiation of early appropriate antifungal therapy.</description>
        <link>http://ccforum.com/content/13/6/1005</link>
                <dc:creator>Christian Sandrock</dc:creator>
                <dc:creator>Javeed Siddqui</dc:creator>
                <dc:source>Critical Care 2009, 13:1005</dc:source>
        <dc:date>2009-11-16T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/cc8127</dc:identifier>
        <prism:publicationName>Critical Care</prism:publicationName>
        <prism:issn>1364-8535</prism:issn>
        <prism:volume>13</prism:volume>
        <prism:startingPage>1005</prism:startingPage>
        <prism:publicationDate>2009-11-16T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <cc:License rdf:about="http://creativecommons.org/licenses/by/2.0/">
        <cc:permits rdf:resource="http://creativecommons.org/ns#Reproduction" />
        <cc:permits rdf:resource="http://creativecommons.org/ns#Distribution" />
        <cc:permits rdf:resource="http://creativecommons.org/ns#DerivativeWorks" />
    </cc:License>
</rdf:RDF>
