Objectives To evaluate the efficacy and safety of intravenous iron, focusing primarily on its effects on haemoglobin, requirement for transfusion, and risk of infection.Design Systematic review and meta-analysis of randomised controlled trials investigating the safety and efficacy of intravenous iron therapy. Eligibility criteria for selecting studies Eligible trials were randomised controlled trials of intravenous iron compared with either no iron or oral iron. Crossover and observational studies were excluded. Data sources Main outcome measures Change in haemoglobin concentration and risk of allogeneic red blood cell transfusion (efficacy) and risk of infection (safety).Results Of the 75 trials meeting the inclusion criteria, 72 studies including 10 605 patients provided quantitative outcome data for meta-analysis. Intravenous iron was associated with an increase in haemoglobin concentration (standardised mean difference 6.5 g/L, 95% confidence interval 5.1 g/L to 7.9 g/L) and a reduced risk of requirement for red blood cell transfusion (risk ratio 0.74, 95% confidence interval 0.62 to 0.88), especially when intravenous iron was used with erythroid stimulating agents (ESAs) or in patients with a lower baseline plasma ferritin concentration. There were no significant interactions between the efficacy of intravenous iron and type or dose administered. Intravenous iron was, however, associated with a significant increase in risk of infection (relative risk 1.33, 95% confidence interval 1.10 to 1.64) compared with oral or no iron supplementation. The results remained similar when only high quality trials were analysed.Conclusions Intravenous iron therapy is effective in increasing haemoglobin concentration and reducing the risk of allogeneic red blood cell transfusion and could have broad applicability to a range of acute care settings. This potential benefit is counterbalanced by a potential increased risk of infection.

Perioperative outcomes favored a GD therapy rather than liberal fluid therapy without hemodynamic goals. Whether GD therapy is superior to a restrictive fluid strategy remains uncertain.

There is currently much interest in the use of decompressive craniectomy for intracranial hypertension. Though technically straightforward, the procedure is not without significant complications. A retrospective analysis was undertaken of 164 patients who had had a decompressive craniectomy for severe head injury in the years 2004 to 2009 at the two major hospitals in Western Australia. Eighty-six patients had a bifrontal decompression and seventy-eight had a unilateral decompression. Two patients died due to post-operative care issues. Complications attributable to the decompressive surgery were: herniation of the cortex through the bone defect (42 patients, 25.6%), subdural effusion (81 patients, 49.4%), seizures (36 patients, 22%), hydrocephalus (23 patients, 14%), and syndrome of the trephined (2 patients, 1.2%). Complications attributable to the subsequent cranioplasty included: sudden death due to massive cerebral swelling in 3 patients (2.2%), infection requiring removal of the bone flap in 16 patients (11.6%), and bone flap resorption requiring augmentation in 10 patients (7.2%). After excluding simple complications such as subdural effusion and brain herniation through the skull defect and some patients who died as a direct consequence of traumatic brain or extracranial injury, 81 patients (55.5%) had at least one complication after decompressive craniectomy. The occurrence of at least one complication after decompressive craniectomy was significantly associated with an increased risk of prolonged stay in the hospital or rehabilitation facility (odds ratio 2.54, 95%confidence interval 1.22,5.24, p=0.013), after adjusting for predicted risk of unfavorable outcome.

Background and objectives Excess fluid balance in acute kidney injury (AKI) may be harmful, and conversely, some patients may respond to fluid challenges. This study aimed to develop a prediction model that can be used to differentiate between volume-responsive (VR) and volume-unresponsive (VU) AKI. Methods AKI patients with urine output < 0.5 ml/kg/h for the first 6 h after ICU admission and fluid intake > 5 l in the following 6 h in the US-based critical care database (Medical Information Mart for Intensive Care (MIMIC-III)) were considered. Patients who received diuretics and renal replacement on day 1 were excluded. Two predictive models, using either machine learning extreme gradient boosting (XGBoost) or logistic regression, were developed to predict urine output > 0.65 ml/kg/h during 18 h succeeding the initial 6 h for assessing oliguria. Established models were assessed by using out-of-sample validation. The whole sample was split into training and testing samples by the ratio of 3:1. Main results Of the 6682 patients included in the analysis, 2456 (36.8%) patients were volume responsive with an increase in urine output after receiving > 5 l fluid. Urinary creatinine, blood urea nitrogen (BUN), age, and albumin were the important predictors of VR. The machine learning XGBoost model outperformed the traditional logistic regression model in differentiating between the VR and VU groups (AU-ROC, 0.860; 95% CI, 0.842 to 0.878 vs. 0.728; 95% CI 0.703 to 0.753, respectively). Conclusions The XGBoost model was able to differentiate between patients who would and would not respond to fluid intake in urine output better than a traditional logistic regression model. This result suggests that machine learning techniques have the potential to improve the development and validation of predictive modeling in critical care research.

BackgroundLong-term survival outcome of critically ill patients is important in assessing effectiveness of new treatments and making treatment decisions. We developed a prognostic model for estimation of long-term survival of critically ill patients.Methodology and Principal FindingsThis was a retrospective linked data cohort study involving 11,930 critically ill patients who survived more than 5 days in a university teaching hospital in Western Australia. Older age, male gender, co-morbidities, severe acute illness as measured by Acute Physiology and Chronic Health Evaluation II predicted mortality, and more days of vasopressor or inotropic support, mechanical ventilation, and hemofiltration within the first 5 days of intensive care unit admission were associated with a worse long-term survival up to 15 years after the onset of critical illness. Among these seven pre-selected predictors, age (explained 50% of the variability of the model, hazard ratio [HR] between 80 and 60 years old = 1.95) and co-morbidity (explained 27% of the variability, HR between Charlson co-morbidity index 5 and 0 = 2.15) were the most important determinants. A nomogram based on the pre-selected predictors is provided to allow estimation of the median survival time and also the 1-year, 3-year, 5-year, 10-year, and 15-year survival probabilities for a patient. The discrimination (adjusted c-index = 0.757, 95% confidence interval 0.745–0.769) and calibration of this prognostic model were acceptable.SignificanceAge, gender, co-morbidities, severity of acute illness, and the intensity and duration of intensive care therapy can be used to estimate long-term survival of critically ill patients. Age and co-morbidity are the most important determinants of long-term prognosis of critically ill patients.

Complications after using titanium plate for primary or secondary cranioplasty were common (29%) and associated with an increased length of hospital stay. Infection was a major complication (16%), and this suggested that more vigorous perioperative infection prophylaxis is needed for titanium plate cranioplasty.

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There continues to be a considerable interest in decompressive craniectomy in the management of severe traumatic brain injury (TBI). Though technically straightforward, the procedure is not without significant complications. In this study we assessed the incidence and risk factors for the development of subdural hygroma and hydrocephalus after decompressive craniectomy. A total of 195 patients who had had a decompressive craniectomy for severe TBI between 2004 and 2010 at the two major trauma centers in Western Australia were considered. Of the 166 patients who survived after the acute hospital stay, 93 (56%; 95% confidence interval [CI] 48,63%) developed subdural hygroma; 45 patients (48%) had unilateral and 48 patients (52%) had bilateral subdural hygromas. Of the 159 patients who survived more than 6 months after surgery, 72 (45%; 95% CI 38,53%) developed radiological evidence of ventriculomegaly, and 26 of these 72 patients (36%; 95% CI 26,48%) developed clinical evidence of hydrocephalus and required a ventriculoperitoneal (VP) shunt. Maximum intracranial pressure prior to decompression (p=0.005), subdural hygroma (p=0.012), and a lower admission Glasgow Coma Scale score (p=0.009), were significant risk factors for hydrocephalus after decompressive craniectomy. Hydrocephalus requiring a VP shunt was associated with a higher risk of unfavorable neurological outcomes at 18 months (odds ratio 7.46; 95%CI 1.17,47.4; p=0.033), after adjusting for other factors. Our results showed a clear association between injury severity, subdural hygroma, and hydrocephalus, suggesting that damage to the cerebrospinal fluid drainage pathways contributes to the primary brain injury rather than the margin of the craniectomy as the factor responsible for these complications.