The metabolic response to stress is part of the adaptive response to survive critical illness. Several mechanisms are well preserved during evolution, including the stimulation of the sympathetic nervous system, the release of pituitary hormones, a peripheral resistance to the effects of these and other anabolic factors, triggered to increase the provision of energy substrates to the vital tissues. The pathways of energy production are altered and alternative substrates are used as a result of the loss of control of energy substrate utilization by their availability. The clinical consequences of the metabolic response to stress include sequential changes in energy expenditure, stress hyperglycaemia, changes in body composition, and psychological and behavioural problems. The loss of muscle proteins and function is a major long-term consequence of stress metabolism. Specific therapeutic interventions, including hormone supplementation, enhanced protein intake, and early mobilization, are investigated. This review aims to summarize the pathophysiological mechanisms, the clinical consequences, and therapeutic implications of the metabolic response to stress.

The diagnostic use of procalcitonin for bacterial infections remains a matter of debate. Most studies have used ambiguous outcome measures such as sepsis instead of infection. We performed a systematic review and meta-analysis to investigate the diagnostic accuracy of procalcitonin for bacteraemia, a proven bloodstream infection. We searched all major databases from inception to June 2014 for original, English language, research articles that studied the diagnostic accuracy between procalcitonin and positive blood cultures in adult patients. We calculated the area under the summary receiver-operating characteristic (SROC) curves and pooled sensitivities and specificities. To minimize potential heterogeneity we performed subgroup analyses. In total, 58 of 1567 eligible studies were included in the meta-analysis and provided a total of 16,514 patients, of whom 3420 suffered from bacteraemia. In the overall analysis the area under the SROC curve was 0.79. The optimal and most widely used procalcitonin cut-off value was 0.5 ng/mL with a corresponding sensitivity of 76% and specificity of 69%. In subgroup analyses the lowest area under the SROC curve was found in immunocompromised/neutropenic patients (0.71), the highest area under the SROC curve was found in intensive-care patients (0.88), sensitivities ranging from 66 to 89% and specificities from 55 78%. In spite of study heterogeneity, procalcitonin had a fair diagnostic accuracy for bacteraemia in adult patients suspected of infection or sepsis. In particular low procalcitonin levels can be used to rule out the presence of bacteraemia. Further research is needed on the safety and efficacy of procalcitonin as a single diagnostic tool to avoid taking blood cultures.

IntroductionIn Europe, vitamin D deficiency is highly prevalent varying between 40% and 60% in the healthy general adult population. The consequences of vitamin D deficiency for sepsis and outcome in critically ill patients remain controversial. We therefore systematically reviewed observational cohort studies on vitamin D deficiency in the intensive care unit.MethodsFourteen observational reports published from January 2000 to March 2014, retrieved from Pubmed and Embase, involving 9,715 critically ill patients and serum 25-hydroxyvitamin D3 (25 (OH)-D) concentrations, were meta-analysed.ResultsLevels of 25 (OH)-D less than 50 nmol/L were associated with increased rates of infection (risk ratio (RR) 1.49, 95% (confidence interval (CI) 1.12 to 1.99), P = 0.007), sepsis (RR 1.46, 95% (CI 1.27 to 1.68), P <0.001), 30-day mortality (RR 1.42, 95% (CI 1.00 to 2.02), P = 0.05), and in-hospital mortality (RR 1.79, 95% (CI 1.49 to 2.16), P <0.001). In a subgroup analysis of adjusted data including vitamin D deficiency as a risk factor for 30-day mortality the pooled RR was 1.76 (95% CI 1.37 to 2.26, P <0.001).ConclusionsThis meta-analysis suggests that vitamin D deficiency increases susceptibility for severe infections and mortality of the critically ill.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-014-0660-4) contains supplementary material, which is available to authorized users.

IntroductionMechanical ventilation (MV) is commonly regarded as a risk factor for acute kidney injury (AKI) in the critically ill. We investigated the strength of this association and whether settings of tidal volume (Vt) and positive end-expiratory pressure (PEEP) affect the risk for AKI.MethodsWe performed a systematic review and meta-analysis using studies found by searching MEDLINE, EMBASE, and references in relevant reviews and articles. We included studies reporting on a relation between the use of invasive MV and subsequent onset of AKI, or comparing higher with lower Vt or PEEP and subsequent onset of AKI. All studies clearly stating that MV was initiated after onset of AKI were excluded. We extracted the proportion with and without MV and AKI. We included 31 studies on invasive MV.ResultsThe pooled odds ratio (OR) for the overall effect of MV on AKI was 3.16 (95% CI 2.32 to 4.28, P <0.001). Nearly all subgroups showed that MV increases the risk for AKI. The pooled OR for studies with a multivariate analysis including MV as a risk factor for AKI was 3.58 (95% CI 1.85 to 6.92; P <0.001). Different settings of Vt and PEEP showed no effect.ConclusionsInvasive MV is associated with a threefold increase in the odds of developing AKI and various Vt or PEEP settings do not modify this risk. The latter argues in favour of a haemodynamic origin of AKI during MV.

The factors predisposing to and complicating acute renal failure (ARF) in the medical intensive care unit (ICU), and their relative influence on outcome during ARF are unclear. We retrospectively evaluated the relative importance of age, prior chronic disease (including chronic renal failure), sepsis and organ system failure, for development and outcome of ARF in the medical ICU. Of 487 consecutively admitted patients, 78 (16%) had ARF, in 63% treated with renal replacement therapy. Mortality was 63%. Independently from each other, advancing age, prior chronic disease, and cardiovascular and pulmonary failure directly related to the development of ARF, while neurological failure related inversely. Sepsis only contributed to ARF prediction from these variables if cardiopulmonary failure was excluded. Advancing age, cardiovascular failure before and after onset of ARF, pulmonary failure before ARF and use of renal replacement therapy were the major independent factors directly related to ARF mortality, while prior chronic renal failure related inversely and sepsis did not contribute. Hence, the outcome of ARF in a medical ICU is largely dependent on factors predisposing to ARF, even though the severity and complications of ARF may partly contribute. Our results may help in deciding on the prevention and therapy of ARF in a medical ICU.