No description available

Aneurysmal subarachnoid haemorrhage is a neurological syndrome with complex systemic complications. The rupture of an intracranial aneurysm leads to the acute extravasation of arterial blood under high pressure into the subarachnoid space and often into the brain parenchyma and ventricles. The haemorrhage triggers a cascade of complex events, which ultimately can result in early brain injury, delayed cerebral ischaemia, and systemic complications. Although patients with poor-grade subarachnoid haemorrhage (World Federation of Neurosurgical Societies 4 and 5) are at higher risk of early brain injury, delayed cerebral ischaemia, and systemic complications, the early and aggressive treatment of this patient population has decreased overall mortality from more than 50 % to 35 % in the last four decades. These management strategies include (1) transfer to a high-volume centre, (2) neurological and systemic support in a dedicated neurological intensive care unit, (3) early aneurysm repair, (4) use of multimodal neuromonitoring, (5) control of intracranial pressure and the optimisation of cerebral oxygen delivery, (6) prevention and treatment of medical complications, and (7) prevention, monitoring, and aggressive treatment of delayed cerebral ischaemia. The aim of this article is to provide a summary of critical care management strategies applied to the subarachnoid haemorrhage population, especially for patients in poor neurological condition, on the basis of the modern concepts of early brain injury and delayed cerebral ischaemia.

Critical care physicians have debated an appropriate term for the clinical phase preceding acute kidney injury (AKI). The recent development of cell cycle arrest biomarkers that signal the potential development of AKI is part of an evolution in the molecular diagnosis and understanding of AKI. It is proposed that the pre-injury phase that leads to AKI can be described as “acute kidney stress”. This term has the potential to expand horizons in regard to the early detection of situations that will lead to AKI and the early implementation of corrective measures.

Background: Assessment of pulmonary edema is a key factor in monitoring and guidance of therapy in critically ill patients. To date, methods available at the bedside for estimating the physiologic correlate of pulmonary edema, extravascular lung water, often are unreliable or require invasive measurements. The aim of the present study was to develop a novel approach to reliably assess extravascular lung water by making use of the functional imaging capabilities of electrical impedance tomography. Methods: Thirty domestic pigs were anesthetized and randomized to three different groups. Group 1 was a sham group with no lung injury. Group 2 had acute lung injury induced by saline lavage. Group 3 had vascular lung injury induced by intravenous injection of oleic acid. A novel, noninvasive technique using changes in thoracic electrical impedance with lateral body rotation was used to measure a new metric, the lung water ratio EIT , which reflects total extravascular lung water. The lung water ratio EIT was compared with postmortem gravimetric lung water analysis and transcardiopulmonary thermodilution measurements. Results: A significant correlation was found between extravascular lung water as measured by postmortem gravimetric analysis and electrical impedance tomography (r?=?0.80; p?<?0.05). Significant changes after lung injury were found in groups 2 and 3 in extravascular lung water derived from transcardiopulmonary thermodilution as well as in measurements derived by lung water ratio EIT . Conclusions: Extravascular lung water could be determined noninvasively by assessing characteristic changes observed on electrical impedance tomograms during lateral body rotation. The novel lung water ratio EIT holds promise to become a noninvasive bedside measure of pulmonary edema.

Background: Critical illness and the problems faced after ICU discharge do not only affect the patient, it also negatively impacts patients’ informal caregivers. There is no review which summarizes all types of burden reported in informal caregivers of ICU survivors. It is important that the burdens these informal caregivers suffer are systematically assessed so the caregivers can receive the professional care they need. We aimed to provide a complete overview of the types of burdens reported in informal caregivers of adult ICU survivors, to make recommendations on which burdens should be assessed in this population, and which tools should be used to assess them.MethodWe performed a systematic search in PubMed and CINAHL from database inception until June 2014. All articles reporting on burdens in informal caregivers of adult ICU survivors were included. Two independent reviewers used a standardized form to extract characteristics of informal caregivers, types of burdens and instruments used to assess these burdens. The quality of the included studies was assessed using the Newcastle-Ottawa and the PEDro scales. Results: The search yielded 2704 articles, of which we included 28 in our review. The most commonly reported outcomes were psychosocial burden. Six months after ICU discharge, the prevalence of anxiety was between 15 % and 24 %, depression between 4.7 % and 36.4 % and post-traumatic stress disorder (PTSD) between 35 % and 57.1 %. Loss of employment, financial burden, lifestyle interference and low health-related quality of life (HRQoL) were also frequently reported. The most commonly used tools were the Hospital Anxiety and Depression Scale (HADS), Centre for Epidemiological Studies-Depression questionnaire, and Impact of Event Scale (IES). The quality of observational studies was low and of randomized studies moderate to fair. Conclusions: Informal caregivers of ICU survivors suffer a substantial variety of burdens. Although the quality of the included studies was poor, there is evidence that burden in the psychosocial field is most prevalent. We suggest screening informal caregivers of ICU survivors for anxiety, depression, PTSD, and HRQoL using respectively the HADS, IES and Short Form 36 and recommend a follow-up period of at least 6 months.

No description available

Background: Despite appropriate therapy, Candida bloodstream infections are associated with a mortality rate of approximately 40 %. In animal models, impaired immunity due to T cell exhaustion has been implicated in fungal sepsis mortality. The purpose of this study was to determine potential mechanisms of fungal-induced immunosuppression via immunophenotyping of circulating T lymphocytes from patients with microbiologically documented Candida bloodstream infections. Methods: Patients with blood cultures positive for any Candida species were studied. Non-septic critically ill patients with no evidence of bacterial or fungal infection were controls. T cells were analyzed via flow cytometry for cellular activation and for expression of positive and negative co-stimulatory molecules. Both the percentages of cells expressing particular immunophenotypic markers as well as the geometric mean fluorescence intensity (GMFI), a measure of expression of the number of receptors or ligands per cell, were quantitated. Results: Twenty-seven patients with Candida bloodstream infections and 16 control patients were studied. Compared to control patients, CD8 T cells from patients with Candidemia had evidence of cellular activation as indicated by increased CD69 expression while CD4 T cells had decreased expression of the major positive co-stimulatory molecule CD28. CD4 and CD8 T cells from patients with Candidemia expressed markers typical of T cell exhaustion as indicated by either increased percentages of or increased MFI for programmed cell death 1 (PD-1) or its ligand (PD-L1). Conclusions: Circulating immune effector cells from patients with Candidemia display an immunophenotype consistent with immunosuppression as evidenced by T cell exhaustion and concomitant downregulation of positive co-stimulatory molecules. These findings may help explain why patients with fungal sepsis have a high mortality despite appropriate antifungal therapy. Development of immunoadjuvants that reverse T cell exhaustion and boost host immunity may offer one way to improve outcome in this highly lethal disorder.

No description available

Background: Patients with subarachnoid haemorrhage (SAH) frequently develop cardiac complications in the acute phase after the bleeding. Although a number of studies have shown that increased levels of cardiac biomarkers after SAH are associated with a worse short-term prognosis, no prospective, consecutive study has assessed the association between biomarker release and long-term outcome. We aimed to evaluate whether the cardiac biomarkers, high-sensitive troponin T (hsTnT) and N-terminal pro B-type natriuretic peptide (NTproBNP), were associated with poor 1-year neurological outcome and cerebral infarction due to delayed cerebral ischaemia (CI-DCI). Methods: In this single-centre prospective observational study, all consecutive patients admitted to our neurointensive care unit from January 2012 to December 2013 with suspected/verified SAH with an onset of symptoms <72 hours were enrolled. Blood samples for hsTnT and NTproBNP were collected during three consecutive days following admission. Patients were followed-up after 1 year using the Glasgow Outcome Scale Extended (GOSE). Poor neurological outcome was defined as GOSE ?4. Results: One hundred and seventy seven patients with suspected SAH were admitted during the study period; 143 fulfilled inclusion criteria and 126 fulfilled follow-up. Forty-one patients had poor 1-year outcome and 18 had CI-DCI. Levels of hsTnT and NTproBNP were higher in patients with poor outcome and CI-DCI. In multivariable logistic regression modelling age, poor neurological admission status, cerebral infarction of any cause and peak hsTnT were independently associated with poor late outcome. Both peak hsTnT and peak NTproBNP were independently associated with CI-DCI. Conclusion: Increased serum levels of the myocardial damage biomarker hsTnT, when measured early after onset of SAH, are independently associated with poor 1-year outcome. Furthermore, release of both hsTnT and NTproBNP are independently associated with CI-DCI. These findings render further support to the notion that troponin release after SAH is an ominous finding. Future studies should evaluate whether there is a causal relationship between early release of biomarkers of myocardial injury after SAH and neurological sequelae.

Background: The aim of the present study was to investigate the incidence of adverse events (AEs) during intra-hospital transport (IHT) of critically ill patients and evaluate the risk factors associated with these events. Methods: This prospective multicenter observational study was performed in 34 intensive care units in China during 20 consecutive days from 5 November to 25 November 2012. All consecutive patients who required IHT for diagnostic testing or therapeutic procedures during the study period were included. All AEs that occurred during IHT were recorded. The incidence of AEs was defined as the rate of transports with at least one AE. The statistical analysis included a description of demographic and clinical characteristics of the cohort as well as identification of risk factors for AEs during IHT by univariate and multivariate logistic regression analyses. Results: In total, 441 IHTs of 369 critically ill patients were analyzed. The overall incidence of AEs was 79.8 % (352 IHTs). The proportion of equipment- and staff-related adverse events was 7.9 % (35 IHTs). The rate of patient-related adverse events (P-AEs) was 79.4 % (349 IHTs). The rates of vital sign–related P-AEs and arterial blood gas analysis–related P-AEs were 57.1 % (252 IHTs) and 46.9 % (207 IHTs), respectively. The incidence of critical P-AEs was 33.1 % (146 IHTs). The rates of vital sign–related critical P-AEs and arterial blood gas analysis–related critical P-AEs were 22.9 % (101 IHTs) and 15.0 % (66 IHTs), respectively. All data collected in our study were considered potential risk factors. In the multivariate analysis, predictive factors for P-AEs were pH, partial pressure of carbon dioxide in arterial blood, lactate level, glucose level, and heart rate before IHT. Furthermore, the Acute Physiology and Chronic Health Evaluation II score, partial pressure of oxygen in arterial blood, lactate level, glucose level, heart rate, respiratory rate, pulse oximetry, and sedation before transport were independent influential factors for critical P-AEs during IHT. Conclusions: The incidence of P-AEs during IHT of critically ill patients was high. Risk factors for P-AEs during IHT were identified. Strategies are needed to reduce their frequency.Trial registrationChinese Clinical Trial Register identifier ChiCTR-OCS-12002661. Registered 5 November 2012.

No description available

Background: High serum lactate is associated with increased mortality in septic shock patients. Metformin alters lactate metabolism, and may affect its prognostic value. We compared, between metformin users and nonusers, the prognosis of extremely elevated plasma lactate levels in patients with septic shock. Methods: The electronic medical records (EMR) of patients admitted to the emergency room between January 2011 and June 2013 were reviewed. The study cohort comprised patients with an initial diagnosis of septic shock and blood lactate higher than 10 mmol/L. The selected population was divided into two groups: metformin users (exposed) and metformin nonusers (unexposed). The primary outcome measured was inhospital mortality. Results: The study included 44 metformin users and 118 nonusers. Metformin users were similar to nonusers with respect to levels of lactate, HCO 3 , and blood pH; however, they were older and had higher incidence rates of cardiovascular disease and acute kidney injury at admission, compared to nonusers. Inhospital mortality rates were significantly lower in the metformin-treated group, 56.8 % vs. 88.1 %, p <0.0001. Conclusions: Though high lactate concentration indicates poor prognosis in septic patients, mortality rate was found to be significantly lower in those who were treated with metformin. This finding may help clinicians in deciding treatment for these patients, who could otherwise be considered too ill for real treatment benefit.

Background: Leukocyte-mediated pulmonary inflammation is a key pathophysiological mechanism involved in acute respiratory distress syndrome (ARDS). Massive sequestration of leukocytes in the pulmonary microvasculature is a major triggering event of the syndrome. We therefore investigated the potential role of leukocyte stiffness and adhesiveness in the sequestration of leukocytes in microvessels.  Methods: This study was based on in vitro microfluidic assays using patient sera. Cell stiffness was assessed by measuring the entry time (ET) of a single cell into a microchannel with a 6 × 9–?m cross-section under a constant pressure drop (?P = 160 Pa). Primary neutrophils and monocytes, as well as the monocytic THP-1 cell line, were used. Cellular adhesiveness to human umbilical vein endothelial cells was examined using the laminar flow chamber method. We compared the properties of cells incubated with the sera of healthy volunteers (n = 5), patients presenting with acute cardiogenic pulmonary edema (ACPE; n = 6), and patients with ARDS (n = 22), of whom 13 were classified as having moderate to severe disease and the remaining 9 as having mild disease.  Results: Rapid and strong stiffening of primary neutrophils and monocytes was induced within 30 minutes (mean ET >50 seconds) by sera from the ARDS group compared with both the healthy subjects and the ACPE groups (mean ET <1 second) (p < 0.05). Systematic measurements with the THP-1 cell line allowed for the establishment of a strong correlation between stiffening and the severity of respiratory status (mean ET 0.82 ± 0.08 seconds for healthy subjects, 1.6 ± 1.0 seconds for ACPE groups, 10.5 ± 6.1 seconds for mild ARDS, and 20.0 ± 8.1 seconds for moderate to severe ARDS; p < 0.05). Stiffening correlated with the cytokines interleukin IL-1?, IL-8, tumor necrosis factor TNF-?, and IL-10 but not with interferon-?, transforming growth factor-?, IL-6, or IL-17. Strong stiffening was induced by IL-1?, IL-8, and TNF-? but not by IL-10, and incubations with sera and blocking antibodies against IL-1?, IL-8, or TNF-? significantly diminished the stiffening effect of serum. In contrast, the measurements of integrin expression (CD11b, CD11a, CD18, CD49d) and leukocyte–endothelium adhesion showed a weak and slow response after incubation with the sera of patients with ARDS (several hours), suggesting a lesser role of leukocyte adhesiveness compared with leukocyte stiffness in early ARDS.  Conclusions: The leukocyte stiffening induced by cytokines in the sera of patients might play a role in the sequestration of leukocytes in the lung capillary beds during early ARDS. The inhibition of leukocyte stiffening with blocking antibodies might inspire future therapeutic strategies.

Background: Evidence suggests that EMS-physician-guided cardiopulmonary resuscitation (CPR) in out-of-hospital cardiac arrest (OOHCA) may be associated with improved outcomes, yet randomized controlled trials are not available. The goal of this meta-analysis was to determine the association between EMS-physician- versus paramedic-guided CPR and survival after OOHCA.Methods and ResultsStudies that compared EMS-physician- versus paramedic-guided CPR in OOHCA published until June 2014 were systematically searched in MEDLINE, EMBASE and Cochrane databases. All studies were required to contain survival data. Data on study characteristics, methods, and as well as survival outcomes were extracted. A random-effects model was used for the meta-analysis due to a high degree of heterogeneity among the studies (I 2 ?=?44 %). Return of spontaneous circulation [ROSC], survival to hospital admission, and survival to hospital discharge were the outcome measures.Out of 3,385 potentially eligible studies, 14 met the inclusion criteria. In the pooled analysis (n?=?126,829), EMS-physician-guided CPR was associated with significantly improved outcomes compared to paramedic-guided CPR: ROSC 36.2 % (95 % confidence interval [CI] 31.0 – 41.7 %) vs. 23.4 % (95 % CI 18.5 – 29.2 %) (pooled odds ratio [OR] 1.89, 95 % CI 1.36 – 2.63, p?<?0.001); survival to hospital admission 30.1 % (95 % CI 24.2 – 36.7 %) vs. 19.2 % (95 % CI 12.7 – 28.1 %) (pooled OR 1.78, 95 % CI 0.97 – 3.28, p?=?0.06); and survival to discharge 15.1 % (95 % CI 14.6 – 15.7 %) vs. 8.4 % (95 % CI 8.2 – 8.5 %) (pooled OR 2.03, 95 % CI 1.48 – 2.79, p?<?0.001). Conclusions: This systematic review suggests that EMS-physician-guided CPR in out-of-hospital cardiac arrest is associated with improved survival outcomes.

Glutamine is one of the conditionally essential free amino acids with multiple biological functions. Its supplementation to parenteral nutrition has been widely used for the management of complications in intensive care. However, controversial clinical reports have generated reluctance in the use of this pharmaco-nutrient. In this commentary, we address the impact of four studies that influenced the recommendations on glutamine supplementation by the Canadian Clinical Practice Guide 2015. Because of the importance of this guideline in clinical practice, we strongly believe that a more rigorous and critical evaluation is required to support recommendations in future guidelines.

Background: Electrical impedance tomography (EIT) is a non-invasive bedside tool which allows an individualized ventilator strategy by monitoring tidal ventilation and lung aeration. EIT can be performed at different cranio-caudal thoracic levels, but data are missing about the optimal belt position. The main goal of this prospective observational study was to evaluate the impact of different electrode layers on tidal impedance variation in relation to global volume changes in order to propose a proper belt position for EIT measurements. Methods: EIT measurements were performed in 15 mechanically ventilated intensive care patients with the electrode belt at different thoracic layers (L1-L7). All respiratory and hemodynamic parameters were recorded. Blood gas analyses were obtained once at the beginning of EIT examination. Off-line tidal impedance variation/tidal volume (TV/VT) ratio was calculated, and specific patterns of impedance distribution due to automatic and user-defined adjustment of the colour scale for EIT images were identified. Results: TV/VT ratio is the highest at L1. It decreases in caudal direction. At L5, the decrease of TV/VT ratio is significant. We could identify patterns of diaphragmatic interference with ventilation-related impedance changes, which owing to the automatically adjusted colour scales are not obvious in the regularly displayed EIT images. Conclusions: The clinical usability and plausibility of EIT measurements depend on proper belt position, proper impedance visualisation, correct analysis and data interpretation. When EIT is used to estimate global parameters like VT or changes in end-expiratory lung volume, the best electrode plane is between the 4th and 5th intercostal space. The specific colour coding occasionally suppresses user-relevant information, and manual rescaling of images is necessary to visualise this information.

Background: Critical illness following head injury is associated with a hypermetabolic state but there are insufficient epidemiological data describing acute nutrition delivery to this group of patients. Furthermore, there is little information describing relationships between nutrition and clinical outcomes in this population. Methods: We undertook an analysis of observational data, collected prospectively as part of International Nutrition Surveys 2007-2013, and extracted data obtained from critically ill patients with head trauma. Our objective was to describe global nutrition support practices in the first 12 days of hospital admission after head trauma, and to explore relationships between energy and protein intake and clinical outcomes. Data are presented as mean (SD), median (IQR), or percentages. Results: Data for 1045 patients from 341 ICUs were analyzed. The age of patients was 44.5 (19.7) years, 78 % were male, and median ICU length of stay was 13.1 (IQR 7.9-21.6) days. Most patients (94 %) were enterally fed but received only 58 % of estimated energy and 53 % of estimated protein requirements. Patients from an ICU with a feeding protocol had greater energy and protein intakes (p?<0.001, 0.002 respectively) and were more likely to survive (OR 0.65; 95 % CI 0.42-0.99; p?=?0.043) than those without. Energy or protein intakes were not associated with mortality. However, a greater energy and protein deficit was associated with longer times until discharge alive from both ICU and hospital (all p?<0.001). Conclusion: Nutritional deficits are commonplace in critically ill head-injured patients and these deficits are associated with a delay to discharge alive.

Background: Bleeding after cardiac surgery requiring surgical reexploration and blood component transfusion is associated with increased morbidity and mortality. Although prothrombin complex concentrate (PCC) has been used satisfactorily in bleeding disorders, studies on its efficacy and safety after cardiopulmonary bypass are limited. Methods: Between January 2005 and December 2013, 3454 consecutive cardiac surgery patients were included in an observational study aimed at investigating the efficacy and safety of PCC as first-line coagulopathy treatment as a replacement for fresh frozen plasma (FFP). Starting in January 2012, PCC was introduced as solely first-line treatment for bleeding following cardiac surgery. Results: After one-to-one propensity score–matched analysis, 225 pairs of patients receiving PCC (median dose 1500 IU) and FFP (median dose 2 U) were included. The use of PCC was associated with significantly decreased 24-h post-operative blood loss (836?±?1226 vs. 935?±?583 ml, p?<?0.0001). Propensity score–adjusted multivariate analysis showed that PCC was associated with significantly lower risk of red blood cell (RBC) transfusions (odds ratio [OR] 0.50; 95 % confidence interval [CI] 0.31–0.80), decreased amount of RBC units (? unstandardised coefficient ?1.42, 95 % CI ?2.06 to ?0.77) and decreased risk of transfusion of more than 2 RBC units (OR 0.53, 95 % CI 0.38–0.73). Patients receiving PCC had an increased risk of post-operative acute kidney injury (AKI) (OR 1.44, 95 % CI 1.02–2.05) and renal replacement therapy (OR 3.35, 95 % CI 1.13–9.90). Hospital mortality was unaffected by PCC (OR 1.51, 95 % CI 0.84–2.72). Conclusions: In the cardiac surgery setting, the use of PCC compared with FFP was associated with decreased post-operative blood loss and RBC transfusion requirements. However, PCC administration may be associated with a higher risk of post-operative AKI.

Background: Prolonged controlled mechanical ventilation depresses diaphragmatic efficiency. Assisted modes of ventilation should improve it. We assessed the impact of pressure support ventilation versus neurally adjusted ventilator assist on diaphragmatic efficiency.MethodPatients previously ventilated with controlled mechanical ventilation for 72 hours or more were randomized to be ventilated for 48 hours with pressure support ventilation (n =12) or neurally adjusted ventilatory assist (n?=?13). Neuro-ventilatory efficiency (tidal volume/diaphragmatic electrical activity) and neuro-mechanical efficiency (pressure generated against the occluded airways/diaphragmatic electrical activity) were measured during three spontaneous breathing trials (0, 24 and 48 hours). Breathing pattern, diaphragmatic electrical activity and pressure time product of the diaphragm were assessed every 4 hours. Results: In patients randomized to neurally adjusted ventilator assist, neuro-ventilatory efficiency increased from 27?±?19 ml/?V at baseline to 62?±?30 ml/?V at 48 hours (p?<0.0001) and neuro-mechanical efficiency increased from 1?±?0.6 to 2.6?±?1.1 cmH 2 O/?V (p?=?0.033). In patients randomized to pressure support ventilation, these did not change. Electrical activity of the diaphragm, neural inspiratory time, pressure time product of the diaphragm and variability of the breathing pattern were significantly higher in patients ventilated with neurally adjusted ventilatory assist. The asynchrony index was 9.48 [6.38– 21.73] in patients ventilated with pressure support ventilation and 5.39 [3.78– 8.36] in patients ventilated with neurally adjusted ventilatory assist (p?=?0.04). Conclusion: After prolonged controlled mechanical ventilation, neurally adjusted ventilator assist improves diaphragm efficiency whereas pressure support ventilation does not.Trial registrationClinicalTrials.gov study registration: NCT0247317, 06/11/2015.

Background: The aim of extracorporeal albumin dialysis (ECAD) is to reduce endogenous toxins accumulating in liver failure. To date, ECAD is conducted mainly with the Molecular Adsorbents Recirculating System (MARS). However, single-pass albumin dialysis (SPAD) has been proposed as an alternative. The aim of this study was to compare the two devices with a prospective, single-centre, non-inferiority crossover study design with particular focus on reduction of bilirubin levels (primary endpoint) and influence on paraclinical and clinical parameters (secondary endpoints) associated with liver failure. Methods: Patients presenting with liver failure were screened for eligibility and after inclusion were randomly assigned to be started on either conventional MARS or SPAD (with 4 % albumin and a dialysis flow rate of 700 ml/h). Statistical analyses were based on a linear mixed-effects model. Results: Sixty-nine crossover cycles of ECAD in 32 patients were completed. Both systems significantly reduced plasma bilirubin levels to a similar extent (MARS: median ?68 ?mol/L, interquartile range [IQR] ?107.5 to ?33.5, p?=?0.001; SPAD: ?59 ?mol/L, ?84.5 to +36.5, p?=?0.001). However, bile acids (MARS: ?39 ?mol/L, ?105.6 to ?8.3, p?<?0.001; SPAD: ?9 ?mol/L, ?36.9 to +11.4, p?=?0.131), creatinine (MARS: ?24 ?mol/L, ?46.5 to ?8.0, p?<?0.001; SPAD: ?2 ?mol/L, ?9.0 to +7.0/L, p?=?0.314) and urea (MARS: ?0.9 mmol/L, ?1.93 to ?0.10, p?=?0.024; SPAD: ?0.1 mmol/L, ?1.0 to +0.68, p?=?0.523) were reduced and albumin-binding capacity was increased (MARS: +10 %, ?0.8 to +20.9 %, p?<?0.001; SPAD: +7 %, ?7.5 to +15.5 %, p?=?0.137) only by MARS. Cytokine levels of interleukin (IL)-6 and IL-8 and hepatic encephalopathy were altered by neither MARS nor SPAD. Conclusions: Both procedures were safe for temporary extracorporeal liver support. While in clinical practice routinely assessed plasma bilirubin levels were reduced by both systems, only MARS affected other paraclinical parameters (i.e., serum bile acids, albumin-binding capacity, and creatinine and urea levels). Caution should be taken with regard to metabolic derangements and electrolyte disturbances, particularly in SPAD using regional citrate anti-coagulation.Trial registrationGerman Clinical Trials Register (www.drks.de) DRKS00000371. Registered 8 April 2010.