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Purpose To evaluate the daily values and trends over time of relevant clinical, ventilatory and laboratory parameters during the intensive care unit (ICU) stay and their association with outcome in critically ill patients with coronavirus disease 19 (COVID-19). Methods In this retrospective–prospective multicentric study, we enrolled COVID-19 patients admitted to Italian ICUs from February 22 to May 31, 2020. Clinical data were daily recorded. The time course of 18 clinical parameters was evaluated by a polynomial maximum likelihood multilevel linear regression model, while a full joint modeling was fit to study the association with ICU outcome. Results 1260 consecutive critically ill patients with COVID-19 admitted in 24 ICUs were enrolled. 78% were male with a median age of 63 [55–69] years. At ICU admission, the median ratio of arterial oxygen partial pressure to fractional inspired oxygen (PaO 2 /FiO 2 ) was 122 [89–175] mmHg. 79% of patients underwent invasive mechanical ventilation. The overall mortality was 34%. Both the daily values and trends of respiratory system compliance, PaO 2 /FiO 2 , driving pressure, arterial carbon dioxide partial pressure, creatinine, C-reactive protein, ferritin, neutrophil, neutrophil–lymphocyte ratio, and platelets were associated with survival, while for lactate, pH, bilirubin, lymphocyte, and urea only the daily values were associated with survival. The trends of PaO 2 /FiO 2 , respiratory system compliance, driving pressure, creatinine, ferritin, and C-reactive protein showed a higher association with survival compared to the daily values. Conclusion Daily values or trends over time of parameters associated with acute organ dysfunction, acid–base derangement, coagulation impairment, or systemic inflammation were associated with patient survival.

Background: Sepsis is one of the major causes of in-hospital death, and is frequent in patients presenting to the emergency department (ED). Early identification of high-risk septic patients is critical. Machine learning (ML) techniques have been proposed for identification and prognostication of ED septic patients, but these models often lack pre-hospital data and lack validation against early sepsis identification scores (such as qSOFA) and scores for critically ill patients (SOFA, APACHE II). Methods We conducted an electronic health record (EHR) study to test whether interpretable and scalable ML models predict mortality in septic ED patients and compared their performance with clinical scores. Consecutive adult septic patients admitted to ED over 18 months were included. We built ML models, ranging from a simple-classifier model, to unbalanced and balanced logistic regression, and random forest, and compared their performance to qSOFA, SOFA, and APACHE II scores. Results: We included 425 sepsis patients after screening 38,500 EHR for sepsis criteria. Overall mortality was 15.2% and peaked in patients coming from retirement homes (38%). Random forest, like balanced (0.811) and unbalanced logistic regression (0.863), identified patients at risk of mortality (0.813). All ML models outperformed qSOFA, APACHE II, and SOFA scores. Age, mean arterial pressure, and serum sodium were major mortality predictors. Conclusions: We confirmed that random forest models outperform previous models, including qSOFA, SOFA, and APACHE II, in identifying septic patients at higher mortality risk, while maintaining good interpretability. Machine learning models may gain further adoption in the future with increasing diffusion and granularity of EHR data, yielding the advantage of increased scalability compared to standard statistical techniques.

Background: Acute kidney injury (AKI) is highly prevalent in critical COVID-19 patients. The diagnosis and staging of AKI are based on serum creatinine (sCr) and urinary output criteria, with limitations in the functional markers. New cell-cycle arrest biomarkers [TIMP2]*[IGFBP7] have been proposed for early detection of AKI, but their role in critically ill COVID-19 patients is poorly understood. Methods: We conducted an observational study to assess the performance of [TIMP2]*[IGFBP7] for the detection of AKI in critical COVID-19 patients admitted to our intensive care unit (ICU). We sampled urinary [TIMP2]*[IGFBP7] levels at ICU admission, 12 h, 24 h, and 48 h, and compared the results to the development of AKI, as well as baseline and laboratory data. Results: Forty-one patients were enrolled. The median age was 66 years [57–72] and most were males (85%). Thirteen patients (31.7%) developed no/mild stage AKI, 19 patients (46.3%) moderate AKI, and nine patients (22.0%) severe AKI. The ICU mortality was 29.3%. sCr levels in the Emergency Department or at ICU admission were not significantly different according to AKI stage. [TIMP-2]*[IGFBP-7] urinary levels were elevated in severe AKI at 12 h after ICU admission, but not at ICU admission or 24 h or 48 h after ICU admission. Conclusion: Urinary biomarkers [TIMP-2]*[IGFBP-7] were generally increased in this population with a high prevalence of AKI, and were higher in patients with severe AKI measured at 12 h from ICU admission. Further studies are needed to evaluate the best timing of these biomarkers in this population.

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.