To estimate the effect of restrictive fluid management on renal function and mortality in critically ill patients with acute kidney injury (AKI) at high risk of developing positive fluid balance. We conducted a target trial emulation using data from 12 intensive care units in Queensland, Australia (2015–2021). Adults with AKI within 72 h of intensive care unit (ICU) admission and an AKI-Fluid Balance Risk Score ≥ 32 were included. The intervention comprised conservative crystalloid administration, restricted nutritional fluid intake, and diuretic use for 72 h. We estimated per-protocol effects using a sequential doubly robust estimator for longitudinal modified treatment policies. The primary outcome was AKI Rank at day 7; secondary outcomes included 30-day mortality. Among 8,685 patients, the intervention was associated with substantial reduction in fluid balance (− 2,304 mL at 72 h; 95

PURPOSE:The impact of augmenting enteral protein delivery on nitrogen balance, urea generation, and kidney function in critically ill patients remains poorly defined. This study aimed to investigate these effects in a nested cohort within the TARGET Protein trial. METHODS:We conducted a single-center study nested within a cluster randomized crossover trial. Consecutive patients were enrolled during either the usual protein intake period (n = 52) or the augmented protein intake period (n = 55). Nitrogen balance, its components, plasma urea concentrations, and urea nitrogen accumulation were compared between groups. Multivariable analyses identified factors independently associated with nitrogen balance and incident acute kidney injury (AKI). A causal mediation analysis was performed to assess whether the effect of augmented protein delivery on urea concentrations was mediated through incident AKI. RESULTS:From day 1 to day 7, mean protein intake was 0.84 ± 0.73 g·kg-1·day-1 in the usual-protein group and 1.35 ± 0.94 g·kg-1·day-1 in the augmented-protein group. Patients receiving augmented protein achieved a less negative nitrogen balance than those receiving usual protein (mean difference, +5 g per day; 95% confidence interval [CI], 0.4 to 10; P = 0.033), driven by greater nitrogen intake (mean difference, +7 g per day; 95% CI, 5 to 10; P < 0.001). Independent predictors of nitrogen balance were ideal body weight (-0.18 g.kg-1; 95% CI, -0.35 to -0.01; P = 0.040), AKI at ICU admission (+4.7 g; 95% CI, 0.10 to 9.3; P = 0.046), and allocation to augmented protein therapy (+5.1 g; 95% CI, 0.43 to 9.7; P = 0.033). Compared with usual protein delivery, augmented protein delivery resulted in higher plasma urea concentrations (median, 14 vs. 11 mmol/L) and greater urea nitrogen accumulation (+3 g; 95% CI, 1.0 to 6.0; P = 0.035). Approximately 60% of the additional positive nitrogen balance was accounted for by urea generation. Among patients without AKI at ICU admission, augmented protein delivery was independently associated with incident AKI (odds ratio, 4.79; 95% CI, 1.14 to 26.4; P = 0.046). In mediation analyses, most of the increase in urea concentrations associated with augmented protein delivery was attributable to a direct effect rather than mediation through incident AKI. CONCLUSIONS:In critically ill patients, augmented protein delivery resulted in a less negative nitrogen balance but substantially increased urea generation and plasma urea concentrations. These findings suggest that a substantial proportion of additional protein intake may be directed toward nitrogen waste production rather than net anabolic utilization.

Objective:To evaluate critical care professionals' perceptions of the burden of metabolic acidosis (MA) in the intensive care unit (ICU), and assess agreement on indications, modalities, risks, and benefits of sodium bicarbonate therapy. Design:A multinational, web-based survey administered at different times to Chinese and international ICU practitioners. Main outcome measures:The survey comprised 20 items across four domains: 1) perceived epidemiology and research relevance of MA; 2) rationale, indications, and treatment modalities; 3) potential benefits of sodium bicarbonate; and 4) potential adverse effects of sodium bicarbonate. Responses were recorded on a 5-point Likert scale and classified as "Agreed", "Disagreed", or "Uncertain". Results:A total of 1279 responses from 20 countries were analysed. MA was widely recognised as common, clinically relevant, a frequent cause of ICU admission, and an area requiring further research. Most clinicians supported targeted therapy beyond treating underlying causes, though uncertainty remained regarding sodium bicarbonate. Chinese respondents favoured early correction and continuous infusion, while international opinions varied on timing and approach. Perceived benefits, such as reduced vasopressor use and respiratory workload, were supported by Chinese clinicians, whereas international ones remained uncertain. Opinions on adverse effects also diverged. Chinese physicians highlighted risks of hypernatraemia, severe alkalosis, and hypokalemia, while international respondents viewed sodium bicarbonate as safe regarding the risk of fluid overload or pulmonary oedema. Conclusions:This international survey shows broad agreement that MA is a clinically important and understudied condition in the ICU but reveals substantial variability and uncertainty in clinicians' perceptions of sodium bicarbonate therapy, with notable differences between Chinese and international respondents. These findings underscore key knowledge gaps and the need for well-designed clinical trials.

AIM:This study aimed to assess the characteristics, transfusion events, and clinical outcomes of cardiac surgery patients treated with three-factor prothrombin complex concentrate (3F-PCC). METHOD:A retrospective observational study was performed in three cardiac surgery centres in Australia. We studied sequential cardiac surgeries and collected data on 3F-PCC, fresh frozen plasma (FFP) and red blood cell (RBC) use from blood banks and clinical outcomes from the Australian Society of Cardiothoracic Surgery database. We compared 3F-PCC treated to PCC-untreated patients. RESULTS:For 1,698 patients, 254 (15%) received 3F-PCC, with a median dose of 2,000 IU (Interquartile range [IQR]: 1,000 to 2,000), administered almost exclusively in the operating theatre. After adjustment by overlap weighting, 3F-PCC was associated with a reduction in post-surgical FFP transfusions (Relative risk [RR]: 0.47; 95% confidence interval [CI] 0.29 to 0.77). Similarly, 14% of 3F-PCC patients needed ≥2 RBC units after surgery compared to 21% in controls (RR: 0.63; 95% CI 0.45 to 0.88). Both groups displayed similar safety profiles and clinical outcomes. However, pulmonary embolism occurred in 1.8% of 3F-PCC patients versus 0.8% of controls. CONCLUSIONS:In a multicentre study, 3F-PCC use during cardiac surgery was independently associated with a significantly reduction of postoperative FFP and RBC transfusions. A phase III trial of early PCC at 2,000 IU appears justified.

PURPOSE:In intensive care unit (ICU) patients receiving unfractionated heparin (UFH) infusion, activated partial thromboplastin time (aPTT) and anti-factor Xa (anti-Xa) levels have limited correlation and significant discordance. We aimed to test whether thromboelastographic-derived citrated kaolin reaction time (CKR) and/or the difference (R-difference) and/or ratio (R-ratio) between CKR and heparinase-corrected CKR might help resolve such discordance METHODS: We obtained simultaneous triple-paired samples for aPTT, anti-Xa and thromboelastography (TEG) in ICU patients receiving UFH infusion. We assessed correlation between UFH dose and R-difference and concordance for therapeutic ranges between aPTT, anti-Xa, and CKR or R-difference or R-ratio. On multivariate analysis, we assessed factors associated with TEG R-based measurements RESULTS: We studied 136 samples from 24 patients with a median APACHE III score of 50 and median UFH dose of 14.6 [10.5, 18.3] units/kg/h. for each 1 unit/kg increase in UFH dose, the R-difference increased by 2 min (95% C.I. 0.23-3.7, p < 0.05) but the correlation was weak (R2 = 0.1). The Cohen's kappa coefficient for agreement was 0.39 for CKR-aPTT and 0.17 for CKR-anti-Xa. Similar results were seen for R-difference and R-ratio. When aPTT and anti-Xa were discordant for therapeutic ranges, TEG did not resolve discordance. On multivariate analysis, CKR, R-difference and R-ratio were independently positively associated with UFH dose but also with APACHE III score and, negatively, with iCa CONCLUSIONS: In ICU patients receiving UFH infusion, TEG R-based measurements have limited correlation and concordance with anti-Xa and aPTT for defined therapeutic ranges and do not help resolve their discordance.

Background: High respiratory effort may be common in invasively ventilated patients receiving pressure support ventilation, but its epidemiologic characteristics are unclear. Research Question: What are the epidemiologic characteristics of high respiratory efforts in critically ill patients, does agreement exist between high respiratory drive and high respiratory effort, what are clinician responses during such events, and what is the relationship between those with clinical parameters and outcomes? Study Design and Methods: This clinician-masked, prospective, observational study in 2 centers measured the drop in airway pressure during the first 100 ms of an inspiratory effort with an occluded airway (P-0.1), a validated noninvasive measure of respiratory drive, in patients receiving pressure support ventilation for > 24 hours. We also measured estimated respiratory muscle pressure (P-e(musc)), a validated surrogate of inspiratory effort. We measured P-e(musc) and P-0.1 twice daily. Results: Of 528 ventilated patients, 80 patients received pressure support ventilation for > 24 hours. Among them, 33 patients (41%) exhibited high respiratory effort, which was more common in COVID-19 ARDS, with 19 of such patients (58%) reached the predefined threshold vs 14 patients (27%) in the non-COVID-19 cohort (OR, 5.0; 95% CI, 1.9-14.9; P = .001). Moreover, 36% of P-0.1 values were >= 4 cm H2O, indicating high respiratory drive. Moderate agreement was found between P-e(musc) and P-0.1 measurements (intraclass correlation coefficient, 0.65), suggesting significant discrepancies between those 2 parameters. Clinician-directed management based on usual clinical observations (but masked to P-0.1 and P-e(musc)) rarely changed in the presence of high respiratory effort. Higher P-e(musc) and its concomitant elevation with P-0.1 were associated with worse blood gas parameters and respiratory mechanics. A concomitant elevation of both P-e(musc) and P-0.1 was associated independently with a decreased likelihood of being alive and ventilator-free up to day 28 (OR, 0.26; 95% CI, 0.06-0.87; P = .037). Interpretation: In this study, many critical care patients receiving invasive pressure support ventilation exhibited high respiratory efforts. In these patients, adjustments to ventilator settings were uncommon, despite association with worse clinical parameters and outcomes.

Objective:Mean arterial pressure (MAP) management is a key aspect of treatment in critically ill patients receiving vasopressor therapy. Guidelines in different clinical subgroups have proposed various target MAP values. This study aimed to describe delivered MAP values and corresponding vasopressor doses in such patients. Design:Multicenter, retrospective cohort study of adult intensive care unit (ICU) admissions. Setting:12 ICUs in Queensland, Australia, from January 1, 2015, to December 31, 2021. Participants:Patients receiving vasopressors for at least six continuous hours in the ICU. We studied the delivered MAP values using hourly data based on averaging all validated values obtained from the ICU monitors and average hourly doses of vasopressors. Main Outcome Measure:The primary outcome was the mean MAP during the entire cohort's first 72 hours of ICU admission, whilst vasopressors were administered. Results:In 26,519 patients who received vasopressors for at least six continuous hours, the median age was 62 years, and 9,373 (35%) were admitted after elective surgery. The median time from ICU admission to vasopressor commencement was 2 hours, and the median duration of vasopressor therapy was 27 hours. At 72 hours, 6,627 (25.0%) patients remained on vasopressors. The mean hourly MAP was 72 mmHg in the first six hours, then steadily increased to ≈75 mmHg at 72 hours. In the first 72 hours, 11,032 (41.6%) patients had a mean MAP of 70-74 mmHg, and 5,914 (22.3%) had a mean MAP of 75-79 mmHg. For every clinical subgroup, a MAP of 70-74 mmHg was the most common mean MAP, and the proportion of patients with a mean MAP of 60-65mmHg was less than 5%. Conclusions:In a large, multicenter study of heterogeneous critically ill patients on vasopressors, the mean hourly MAP was > 70 mmHg. This mean hourly MAP was observed consistently over diverse clinical subgroups and is higher than recommended by guidelines.

Introduction: Angiotensin II may reduce muscle ischemia during intermittent hemodialysis and thereby decrease the incidence and/or intensity of intradialytic muscle cramps. We aimed to test whether angiotensin II infusion during intermittent hemodialysis is safe, feasible, and effective in the attenuation of muscle cramps. Methods: We performed a pilot, single-blinded, randomized crossover trial of patients receiving intermittent hemodialysis who frequently experience intradialytic muscle cramps. Patients were randomly allocated to receive either intravenous angiotensin II or placebo for the duration of their first dialysis session of the week. They crossed over to the alternate arm each week for four weeks. The primary outcome was safety. Secondary outcomes included cramp-related symptoms, hemodynamic parameters, dialysis prescription alterations, and biomarkers. Results: We studied 24 sessions in 6 patients. Intradialytic hypertension (systolic blood pressure >180mmHg) occurred more often with angiotensin II than with placebo (33% vs 17% sessions, P=0.64). There were no other adverse events. Compared with placebo, muscle cramps were less frequent (33% vs. 92% sessions, P=0.009) and of lower intensity with angiotensin II (median Brief Pain Inventory score 1.4 vs. 5.3; P<0.001; maximal Brief Pain Inventory score 1.2 vs. 6.0; P<0.001). Fluid bolus administration for cramps was less common during angiotensin II infusion than placebo (0% vs. 42% sessions, P=0.037). Conclusion: Angiotensin II increased blood pressure and heart rate but not cardiac output or levels of troponin, creatine kinase or renin. In conclusion, angiotensin II infusion during intermittent hemodialysis appears safe and effective at reducing intradialytic muscle cramps. These observations justify further investigation in larger controlled studies.

In septic shock, the optimal timing of adjunctive vasopressin initiation shock is unknown. We aimed to assess the effect of its early initiation for patients with septic shock. We conducted a multicenter target trial emulation to estimate the intensive care unit (ICU) mortality effect of early (≤ 6 h) adjunctive vasopressin compared with usual care. Eligible patients had septic shock diagnosed within 6 h of ICU admission. The primary outcome of this study was 30-day ICU mortality. Subgroup analyses were conducted to test the interaction of early vasopressin start with peak norepinephrine-equivalent dose (NED) at 6 h, APACHE score, peak lactate at 6 h and invasive mechanical ventilation. Secondary outcomes were the impact of delayed vasopressin introduction on 30-day ICU mortality and effect of NED at vasopressin start on 30-day ICU mortality. We used the parametric g-formula to emulate a target trial. Overall, 3,105 patients fulfilled the inclusion criteria. Mean age was 62 years and mean APACHE III score was 83. In the first six hours of vasopressor therapy, 1,864 (60

INTRODUCTION:Hypophosphataemia is common in acute liver failure (ALF) and may worsen during continuous renal replacement therapy (CRRT) with phosphate-free fluids. We aimed to evaluate the safety and efficacy of Phoxilium®, a phosphate-containing CRRT fluid. METHODS:We conducted a retrospective single-center cohort study of paracetamol-induced ALF patients treated with CRRT between January 2018 and May 2024 as our ICU transitioned from Accusol® to Phoxilium®. We obtained data on demographics, biochemistry, and outcomes. We compared biochemical variables every 6 h up to 48 h post-CRRT initiation and then every 12 h until 168 h. The primary outcome was the occurrence of severe hypophosphataemia (<0.32 mmol/L). RESULTS:In 38 ALF patients (Phoxilium® = 14 and Accusol® = 24), Phoxilium® was associated with a reduction in the incidence of severe hypophosphataemia (0% vs. 38%; p = 0.014), a reduction in its median burden (proportion of phosphate readings <0.81 mmol/L: 13% [interquartile range: 2-33%] vs. 44% [29-51%]; p = 0.001), and significantly lower phosphate supplementation requirements (median, 45 mmol [20-70 mmol] vs. 100 mmol [60-210 mmol]; p = 0.008). Phoxilium® patients experienced a small but significant decrease in median arterial pH and standard base excess, which remained within normal limits, but lower than with Accusol® (p = 0.018 and p = 0.046, respectively). No significant differences were observed in clinical outcomes. CONCLUSION:In paracetamol-induced ALF patients, Phoxilium® was associated with reduced incidence of severe hypophosphataemia, hypophosphataemia burden, and need of phosphate supplementation. Larger studies are needed to further assess its impact on ALF patient outcomes.

Acute kidney injury (AKI) after cardiac surgery is a common and serious complication. Protein loading appears nephroprotective; thus, continuous hyperoncotic albumin infusion may impact AKI following high-risk cardiac surgery. To evaluate the effect of postoperative 20% albumin infusion compared with usual care on the occurrence of AKI in high-risk cardiac surgery patients. This was an investigator-initiated randomized multicenter open-label pragmatic clinical trial. Participants were stratified by site and estimated glomerular filtration rate (eGFR) above and below 60 mL/min/1.73 m2. The study was conducted at 7 cardiac centers in Australia and Italy between July 2019 and August 2024. Patients undergoing on-pump cardiac surgery with a preoperative eGFR of greater than 15 mL/min/1.73 m2 and less than 60 mL/min/1.73 m2 or undergoing a combined cardiac surgical procedure or major aortic surgery were included, excluding those who were in intensive care for longer than 6 hours following the index surgery, had a serum albumin level less than 20 g/L, were dialysis dependent, had a previous kidney transplant, were receiving extracorporeal life support or ventricular assist device, or had an objection to receiving albumin or blood products. Participants were randomized 1:1 within 6 hours after surgery to receive a 300-mL infusion of 20% albumin over 15 hours or usual care, as per clinician discretion. All patients received volume resuscitation and hemodynamic treatment according to participating centers’ protocols. The primary outcome was stage 1-3 AKI according to the creatinine-based Kidney Disease Improving Global Outcomes definition. The main secondary outcomes included major adverse kidney events and mortality at hospital discharge or day 28 following randomization. The primary analysis included 307 patients randomized to the 20% albumin group and 304 to usual care. The mean (SD) age was 69 (10.8) years, and 281 patients (45.8%) had an eGFR less than 60 mL/min/1.73 m2. The median (IQR) European System for Cardiac Operative Risk Evaluation score-II was 3.23 (1.91-5.30). AKI occurred in 150 of 307 patients in the albumin group (48.9%) vs 132 of 304 in usual care (43.4%) (unadjusted relative risk, 1.13; 95% CI, 0.95-1.34; P = .18; strata-adjusted relative risk, 1.12; 95% CI, 1.04-1.21; P = .003). This effect was more pronounced in patients with an eGFR of <60 mL/min/1.73 m2 (adjusted relative risk, 1.14; 95% CI; 1.07-1.22; P < .001). There were more blood transfusions given in the albumin group (116 [37.8%] vs 91 [29.9%]; P = .04) but no other significant differences in secondary outcomes. In this study of cardiac surgery patients at high risk of AKI, an infusion of 20% albumin increased the risk of AKI. These findings do not support the routine use of hyperoncotic albumin infusion in patients undergoing high-risk cardiac surgery. Anzctr.org.au Identifier: ACTRN12619001355167

In the context of tumor lysis syndrome (TLS), the optimal timing and criteria for initiating kidney replacement therapy (KRT) remain unclear. This study aims to assess the effect of initiating KRT at various phosphatemia thresholds on Major Adverse Kidney Events at day 30 (MAKE30). We retrospectively emulated a pragmatic clinical trial comparing the effect of KRT initiation at various phosphatemia thresholds versus a conventional approach during TLS on MAKE30. All consecutive patients admitted to the ICU at Saint-Louis University hospital in Paris and Angers University hospital between January 2007 and June 2020, presenting with laboratory TLS were included. The design criteria of a clinical trial were mimicked by using the cloning, censoring and weighting method. The primary outcome was the MAKE30 composite outcome, considering only KRT requirement between day 7 and day 30 for the dialysis criteria. We evaluated multiple phosphatemia thresholds to guide KRT initiation, ranging from 6.20 mg.dL-1 to 9.30 mg.dL-1. Among the initial population of 220 patients, 192 were included in the emulated trial (median age 60 years old, with non-Hodgkin Lymphoma and Acute Leukemia being the most frequent hematological malignancies). TLS-related AKI occurred in 140 patients, and 75 patients met the criteria for MAKE30. Regardless of the phosphate threshold considered, KRT initiation based on phosphate level was not associated with a significant difference in the MAKE30 rate. KRT requirement during the first 7 days (Odd Ratio [OR] 4.01 [1.65–4.86], p = 0.003) and non-renal SOFA (OR 1.39 per 1 point increment [1.25–1.57], p < 0.001) were identified as factors associated with MAKE30 (multivariable analysis). Our results do not support the strategy of KRT initiation based on a sole critical phosphatemia level in TLS patients.

Objective: The combination of catecholamine-resistant vasodilatory shock and acute kidney injury (AKI) is associated with high morbidity and mortality. The role of angiotensin II (ANGII) in this setting is unclear. Methods: We conducted a post hoc analysis of the Angiotensin II for the Treatment of High-Output Shock (ATHOS) 3 trial which assessed the effect of Intravenous ANG II or placebo in patients with refractory vasodilatory shock in 75 intensive care units across nine countries in North America, Australasia, and Europe. We included patients with all stages AKI at initiation of ANG II or placebo and assessed 28-day mortality as primary outcome. We studied mean arterial pressure (MAP) response and days alive and free from renal replacement therapy (RRT) up to day 7 as secondary outcome. Results: Of 321 ATHOS-3 patients, 203 (63%) had AKI at randomization, with stage 3 AKI being dominant (67%). Median age was 63 years and median APACHE II score was 30. By day 28, overall, 118 (58%) of patients had died (53% with ANGII vs. 63% with placebo, hazard ratio = 0.75, 95% CI [0.52-1.08], P = 0.121). Among AKI stage 3 patients, however, ANGII was associated with significantly lower mortality (48% vs. 67%, hazard ratio = 0.57, 95% CI [0.36-0.91], P = 0.024). Additionally, in this subgroup, compared with placebo, patients receiving ANGII were more likely to achieve a MAP response (P < 0.001) and had more days alive and free from RRT (P < 0.001). Conclusions: Compared with placebo, in patients with catecholamine-resistant vasodilatory shock and stage 3 AKI, ANGII is associated with lower 28-day, greater likelihood of MAP response, and more days alive and free from RRT. These findings support the conduct of future ANGII trials in patients with stage 3 AKI.

BACKGROUND:Hypernatremia is relatively common in acutely ill patients and associated with mortality. Guidelines recommend a slow rate of correction (≤ 0.5 mmol/L per hour). However, a faster correction rate may be safe and improve outcomes. OBJECTIVES:To evaluate the impact of sodium correction rates on mortality and hospital length of stay and to assess types of hypernatremia treatment and treatment side effects. METHODS:We conducted a systematic review and meta-analysis according to PRISMA guidelines, searching Ovid MEDLINE, Embase, and CENTRAL databases from inception to August 2024. Studies reporting sodium correction rates and clinical outcomes in hospitalized adults were included. A random-effects meta-analysis assessed mortality and hospital length of stay, with subgroup analyses exploring correction timing and severity. Treatment method and side effects were analyzed qualitatively. RESULTS:We reviewed 4445 articles and included 12 studies. Faster correction rates (> 0.5 mmol/L/h) overall showed no significant change in mortality and a high level of heterogeneity (OR 0.68, 95 % CI: 0.38-1.24, I2 = 95 %). However, subgroup analyses found significantly lower mortality with faster correction of hypernatremia at the time of hospital admission (OR 0.48, 95 % CI: 0.35-0.68, I2 = 2 %), with fast correction within the first 24 h of diagnosis (OR 0.48, 95 % CI: 0.31-0.73, I2 = 65 %), and for severe hypernatremia (OR 0.55, 95 % CI: 0.33-0.92, I2 = 79 %). There was no significant different in hospital length of stay by correction rate. No major neurological complications were reported when the correction rate was < 1 mmol/L/h. CONCLUSION:Faster sodium correction appears safe and may benefit patients with severe admission-related hypernatremia, particularly within the first 24 h. Further studies are needed to refine correction protocols.

BACKGROUND:Globally, managing critically ill adults with acute brain injuries (ABIs) in specialised neurocritical units (NCCUs) is associated with improved survival, but this has not been assessed in Australia. This study aims to determine in adults with an ABI if admission to a general intensive care unit (ICU) or a NCCU was associated with a difference in outcomes. METHODS:Australian ICUs were surveyed regarding NCCU capabilities via the Australian and New Zealand Intensive Care Society (ANZICS). Linked patient-level outcomes were extracted from the ANZICS Adult Patient Database for a retrospective observational cohort study. Adults with an ABI (intracerebral haemorrhage, acute ischaemic stroke, subarachnoid haemorrhage or traumatic brain injury) admitted to ICU between January 2016 and December 2022 were included. Readmissions within the same hospital, transfers from another ICU and admissions for end-of-life care or organ donation were excluded. The primary outcome was in-hospital mortality. Secondary outcomes were ICU mortality, ICU length of stay (LOS), hospital LOS and discharge destination other than home. RESULTS:Responses were received from 78 out of 192 surveyed ICUs. Amongst these, 41 reported routinely caring for ABI patients, of which 8 were specialist NCCUs. There were 14,740 index admissions to participating ICUs over the study period, with 7,402 NCCU and 7,338 general ICU admissions respectively. Crude in-hospital mortality was 18% (1,356/7,402) in NCCUs and 21% (1,514/7,338) in general ICUs. The adjusted odds ratio (OR) for in-hospital mortality was 0.88 (95% confidence interval [CI] 0.81-0.96, p-value 0.003), favouring those cared for in a NCCU. In survivors, those admitted to NCCUs were more likely to remain in hospital longer (relative change in geometric mean = 20.5%, 95% CI 16.2-25.1, p-value < 0.001) and less likely to be discharged home (OR = 2.01, 95% CI 1.83-2.21). CONCLUSION:In Australian adult ABI patients admitted to ICU, admission to a NCCU was independently associated with lower hospital mortality. However, in survivors, this was associated with a lower likelihood of being discharged home and a longer stay in hospital. Variable intensive care capabilities for neurocritical care may impact key patient-centred outcomes. Future research is required to assess long-term functional outcomes.

Hypernatremia of critical illness is an common and important complication that affects close to 7% of intensive care unit (ICU) patients. The term describes the development of hypernatremia that is not present at admission but occurs during the patient’s illness in the ICU. Given that hypernatremia appears preventable by the administration of electrolyte-free water, either enterally or intravenously, it is surprising that this condition should develop in the ICU where monitoring of serum sodium is universal and frequent. In this article, we review the epidemiology of this condition, the pathophysiological background behind the development of such ICU-acquired hypernatremia and the risk factors that predispose to its development. In particular, we focus on the role of urinary free water losses associated with the catabolic state of patients and the large amounts of urea excreted in the urine. We further discuss the role of diarrhea and fever in exacerbating such free water losses. We identify the importance of diuretics in this setting, where they often fail to achieve natriuresis and further increase free water losses. We highlight the importance of estimating urinary free water losses by measurement of urinary sodium and potassium. We explain the misleading nature of urinary osmolarity measurements in a setting where osmolarity and tonicity are dissociated by the presence of urea in urine. Finally, we discuss the importance of prevention or rapid correction of hypernatremia and the evidence supporting particular rates of correction.

PURPOSE:To detect changes in cardiac output and blood pressure during intermittent hemodialysis (IHD) in patients recovering from severe acute kidney injury (AKI) after transition from continuous renal replacement therapy (CRRT). MATERIAL AND METHODS:In this single-center pilot feasibility study, we applied continuous hemodynamic monitoring (ClearSight System™) before and during IHD sessions in patients recovering from severe AKI. We also measured relative blood volume (BV; CRIT-LINE®IV) and Net Ultrafiltration Rate (NUF). CI changes were categorized as follows: Increase (>5 %), Stable (-5 % to 5 %), Mild Decrease (-5 % to -15 %), Moderate Decrease (-15 % to -25 %), and Severe Decrease (<-25 %). RESULTS:We enrolled 10 AKI patients. Overall, there were 119 episodes of severe and 286 episodes of moderate reductions in cardiac index (CI). The median time spent with severe and moderate intradialytic reductions in CI was 8.2 min [2.1-115.8] and 49.5 min [21.6-57.5], respectively. Severe CI reductions happened in nine patients out of 10, and in three patients, they lasted more than 2 h. During IHD, mean arterial pressure increased or remained stable in >78 % of measurements, regardless of changes in CI. Overall, CI decreased by -1.14 L/min/m2 during a moderate BV decrease (p < 0.001) and by -0.57 L/min/m2 when NUF rate was high (p < 0.001). CONCLUSIONS:CI often, repeatedly, and markedly decreased during IHD. Such decreases were not detected by MAP monitoring and were extreme in some patients.

Objective To assess the characteristics, treatments and outcomes of paediatric and adult intensive care unit (ICU) patients with respiratory syncytial virus (RSV) infection, and compare these with coronavirus disease (COVID-19) during the same period. Design, setting, and participants We conducted a multicenter, prospective, observational study using data from the short period incidence study of severe acute respiratory infection (SPRINT SARI) Australia, in 38 Australian ICUs from 1 June 2022 to 1 September 2024. Demographic, treatment, and outcome data were analysed for patients with confirmed RSV or COVID-19. The primary outcome was in-hospital mortality. Results Of 4693 patients were recorded in the SPRINT-SARI database, 2540 met inclusion criteria. RSV was more common in paediatric patients (410/620, 62%) than in adults (249/1920, 13%). Adult with RSV had more chronic pulmonary conditions than those with COVID-19. Paediatric patients with RSV had fewer comorbidities and less invasive mechanical ventilation (IMV) compared to those with COVID-19 (P < 0.05), but required longer duration of IMV once intubated. In-hospital mortality was similar for both adult RSV and COVID-19 (36/249, 14.5%) vs (260/1671, 15.6%), and paediatric RSV(3/410 [0.7%] vs 7/210 [3.3%] P = 0.07). Mortality in adults was associated with male sex, older age, comorbidities, and IMV. Mortality in children was associated with IMV only. Conclusions RSV infection can result in an attributable number of ICU admission in Australia, especially in specific populations including young children and older adults with respiratory comorbidities. Mortality in patients admitted to ICU is similar to COVID-19.

BACKGROUND:Feeding-associated hypophosphataemia in critically ill patients is a well-recognised phenomenon that has been associated with adverse outcomes. However, the research has been limited by various definitions and small sample sizes. METHODS:A multicentre retrospective cohort study of critically ill patients from six intensive care units in Queensland, Australia. Feeding-associated hypophosphataemia was defined as a decrease of >0.16 mmol.L-1 and a phosphate nadir of 0.80 ≤ mmol.L-1 within 24 h of nutrition commencement. RESULTS:A total of 10,672 patients, with a mean age of 56 ± 17 years and a mean Acute Physiology and Chronic Health Evaluation III score of 63 ± 27, were included. On the day of nutrition commencement, 7801 (73 %) patients were invasively ventilated, and 7053 (66 %) were on vasopressor support. Within 24 h of nutrition, 1298 (13 %) developed moderate to severe feeding-associated hypophosphataemia. Crude hospital mortality was higher in the moderate/severe feeding-associated hypophosphatemia group compared to the control group (18 % vs. 14 %, p < 0.001). Caloric quantity (aOR = 1.06; 95 %CI [1.02, 1.10]), feeding commenced within 48 h of admission (aOR = 1.56; 95 %CI [1.28, 1.91]) and receiving insulin on the day of feeding start (aOR = 1.22; 95 %CI [1.07, 1.40]) were independently associated with developing feeding-associated hypophosphataemia. After adjustment for confounders, moderate-severe feeding-associated hypophosphataemia was independently associated with an increased risk of 30-day hospital mortality (HR = 1.30; 95 %CI [1.08 to 1.56]). CONCLUSION:In a large group of critically ill patients, almost one in seven patients experienced moderate to severe hypophosphatemia after starting to consume calories. The dose of caloric intake and early nutrition initiation were linked to its development. Additionally, moderate to severe hypophosphatemia was independently associated with a higher risk of 30-day hospital mortality.