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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. 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. 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. 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. 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. [Display omitted] •Faster sodium correction rates may improve mortality in hypernatremia.•Patients with admission-related hypernatremia may benefit from faster correction.•Severe hypernatremia shows a trend towards lower mortality with faster correction.•Early faster correction within 24 h is associated with reduced mortality.•No major neurological complications with correction rates <1 mmol/L/h.

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). 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 %). 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). CI often, repeatedly, and markedly decreased during IHD. Such decreases were not detected by MAP monitoring and were extreme in some patients. [Display omitted] •Cardiac index decreases occur very often and are hemodynamically important.•Such decreases cannot be identified by blood pressure monitoring.•Cardiac index decrease might be associated with high fluid removal.•Recovery-phase intermittent hemodialysis is hemodynamically suboptimal.•Continuous cardiac output monitoring can help avoiding organs' hypoperfusion.

Background Mega-dose sodium ascorbate (NaAscorbate) appears beneficial in experimental sepsis. However, its physiological effects in patients with septic shock are unknown. Methods We conducted a pilot, single-dose, double-blind, randomized controlled trial. We enrolled patients with septic shock within 24 h of diagnosis. We randomly assigned them to receive a single mega-dose of NaAscorbate (30 g over 1 h followed by 30 g over 5 h) or placebo (vehicle). The primary outcome was the total 24 h urine output (UO) from the beginning of the study treatment. Secondary outcomes included the time course of the progressive cumulative UO, vasopressor dose, and sequential organ failure assessment (SOFA) score. Results We enrolled 30 patients (15 patients in each arm). The mean (95% confidence interval) total 24-h UO was 2056 (1520–2593) ml with placebo and 2948 (2181–3715) ml with NaAscorbate (mean difference 891.5, 95% confidence interval [− 2.1 to 1785.2], P  = 0.051). Moreover, the progressive cumulative UO was greater over time on linear mixed modelling with NaAscorbate ( P  < 0.001). Vasopressor dose and SOFA score changes over time showed faster reductions with NaAscorbate ( P  < 0.001 and P  = 0.042). The sodium level, however, increased more over time with NaAscorbate ( P  < 0.001). There was no statistical difference in other clinical outcomes. Conclusion In patients with septic shock, mega-dose NaAscorbate did not significantly increase cumulative 24-h UO. However, it induced a significantly greater increase in UO and a greater reduction in vasopressor dose and SOFA score over time. One episode of hypernatremia and one of hemolysis were observed in the NaAscorbate group. These findings support further cautious investigation of this novel intervention. Trial registration Australian New Zealand Clinical Trial Registry (ACTRN12620000651987), Date registered June/5/2020.

Angiotensin II is approved for catecholamine-refractory vasodilatory shock but the conversion dose ratio from norepinephrine to angiotensin II remains unclear. We conducted a post-hoc analysis of the Acute Renal effects of Angiotensin II Management in Shock (ARAMIS) trial involving patients with vasodilatory hypotension. We determined the norepinephrine equivalent dose immediately prior to angiotensin II initiation and calculated the conversion dose ratio between norepinephrine and angiotensin II. We performed subgroup analyses based on recent exposure to angiotensin receptor blockers (ARBs) and renin levels at baseline. In 37 patients, the median conversion dose ratio between norepinephrine equivalent and angiotensin II was to 10:1 for norepinephrine bitartrate (5:1 for norepinephrine base). The conversion ratio was not affected by the baseline renin, with a median ratio of 10 (7–21) in the high renin group versus 12 (5–22) in the low renin group. Finally, exposure to ARBs prior admission appeared to diminish the conversion ratio with a median ratio of 7 (4–13) in ARB patients vs. 12 (7–22) in non-ARB patients. The norepinephrine to angiotensin II conversion dose ratio is 10:1 in a vasodilatory hypotension population. These findings can guide clinicians and researchers in the use, dosing, and study of angiotensin II in critical care. •The conversion ratio was determined as 10:1 for norepinephrine equivalent dose prior to angiotensin II initiation.•The conversion ratio was not affected by the baseline renin levels.•Exposure to angiotensin receptor blockers prior to admission appeared to diminish the conversion ratio.

Furosemide is the most commonly used diuretic in intensive care units (ICU). We aimed to evaluate the physiological effects of adjunctive acetazolamide with furosemide on diuresis and the prevention of potential furosemide-induced metabolic alkalosis. We performed a two-center, pilot, open-label, randomized trial. Where the treating physicians planned intravenous diuretic therapy, we randomized ICU patients to a bolus of furosemide (40 mg) plus acetazolamide (500 mg) (n = 15) or furosemide alone (40 mg) (n = 15). Urine output, additional furosemide use, acid-base parameters, and electrolytes were compared following a Bayesian framework. Adjunctive acetazolamide didn't increase urine output in the first six hours (mean difference: −112 ml, credible interval: [−742, 514]). However, compared with furosemide alone, it maintained a greater urine output response to furosemide over 24 h, with 100 % probability. Acetazolamide also acidified plasma (pH difference: −0.045, [−0.081, −0.008]) while alkalinizing urine (1.10, [0.04, 2.11]) at six hours, compared to furosemide alone with >95 % probability. Finally, we didn't observe severe acidosis or electrolyte disturbances over 24 h. Adjunctive acetazolamide may increase diuretic efficacy and counterbalance furosemide-induced metabolic alkalosis without safety concerns. Larger trials are warranted to verify these findings and assess their impacts on clinical outcomes. ACTRN12623000624684. A pilot trial of single versus dual diuretic therapy in the intensive care unit. •Pathophysiologic effects of adjunctive acetazolamide were assessed in this pilot RCT.•Acetazolamide may have preserved urine output response to furosemide.•Acetazolamide may have counterbalanced furosemide-induced metabolic alkalosis.•Adjunctive acetazolamide may not result in severe acidosis or electrolyte disturbance.•Larger trials to evaluate the effect of adjunctive acetazolamide appear justified.

PurposeAngiotensin II is approved for catecholamine-refractory vasodilatory shock but the conversion dose ratio from norepinephrine to angiotensin II remains unclear.MethodsWe conducted a post-hoc analysis of the Acute Renal effects of Angiotensin II Management in Shock (ARAMIS) trial involving patients with vasodilatory hypotension. We determined the norepinephrine equivalent dose immediately prior to angiotensin II initiation and calculated the conversion dose ratio between norepinephrine and angiotensin II. We performed subgroup analyses based on recent exposure to angiotensin receptor blockers (ARBs) and renin levels at baseline.ResultsIn 37 patients, the median conversion dose ratio between norepinephrine equivalent and angiotensin II was to 10:1 for norepinephrine bitartrate (5:1 for norepinephrine base). The conversion ratio was not affected by the baseline renin, with a median ratio of 10 (7–21) in the high renin group versus 12 (5–22) in the low renin group. Finally, exposure to ARBs prior admission appeared to diminish the conversion ratio with a median ratio of 7 (4–13) in ARB patients vs. 12 (7–22) in non-ARB patients.ConclusionsThe norepinephrine to angiotensin II conversion dose ratio is 10:1 in a vasodilatory hypotension population. These findings can guide clinicians and researchers in the use, dosing, and study of angiotensin II in critical care.

Background 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. Methods 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. Results 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%) patients were invasively ventilated. Estimated 30-day ICU mortality was 19.34% (95%CI, 17.0 to 21.68) in the no vasopressin group and 18.45% (95%CI, 16.26 to 20.63) in the early vasopressin group; relative risk 0.95 (95%CI, 0.93 to 0.98). The estimated 30-day ICU mortality effect of starting vasopressin was particularly strong at lower norepinephrine doses (< 0.25 µg.kg −1 .min −1 ) and significant at lower norepinephrine doses than recommended by the Surviving Sepsis Campaign Guidelines. Vasopressin administration progressively increased over the study period, from 35.2% (95%CI, 30.0 to 40.5) in 2015 to 45.1% (95%CI, 40.7 to 49.6) in 2021 (ß =  + 1.3% per year; 95%CI, + 0.46 to + 2.16, p  = 0.011). Patients had progressively lower norepinephrine equivalent dose (ß = − 0.05 µg.kg −1 .min −1 per year; 95%CI, − 0.09 to − 0.002, p  = 0.038) and lower total SOFA score (ß = − 0.1 point per year; 95%CI, − 0.18 to − 0.07, p  < 0.001) at vasopressin start. Conclusions In this emulation of a hypothetical target trial, patients with septic shock benefited from early vasopressin administration. These findings can help design prospective randomised-control trials of early adjunctive vasopressin use in septic shock.

The impact of blood pressure targets and surgical approach (laparoscopic or open) on continuous urinary oxygenation (PuO2), a validated surrogate of renal medullary PO2, during general surgery, is unclear. We aimed to assess the effects of different blood pressure targets and surgical procedures on PuO2. We randomized patients receiving either laparoscopic or open surgery into two mean arterial pressure (MAP) target groups: usual MAP or a high MAP. We measured PuO2 in real-time and analyzed it according to the type of surgery and blood pressure target. The study was retrospectively registered on the 5th of July 2023 (ACTRN12623000726651). We included 43 participants who underwent either laparoscopic (n = 20) or open surgery (n = 23). We found that PuO2 significantly decreased during both laparoscopic and open surgery under a usual blood pressure target (− 51% and − 49%, respectively). However, there was a sharper fall with laparoscopic surgery resulting in a higher PuO2 with open surgery (mean difference: 11 ± 1 mmHg higher; p < 0.001). Targeting a higher MAP resulted in a higher PuO2 over time during laparoscopic surgery (mean difference: 7 ± 1 mmHg, p < 0.001). In contrast, targeting a usual MAP resulted in a higher PuO2 during open surgery (mean difference: 7 ± 1 mmHg, p < 0.001). Surgical approach and intraoperative blood pressure targets significantly impact urinary oxygenation. Further studies with larger sample sizes are needed to confirm these findings and understand their potential clinical implications.Registration number: ACTRN12623000726651; Date of registration: 05/07/2023 (retrospectively registered).