Purpose
To assess whether invasive and non-invasive blood pressure (BP) monitoring allows the identification of patients who have responded to a fluid challenge, i.e., who have increased their ...cardiac output (CO).
Methods
Patients with signs of circulatory failure were prospectively included. Before and after a fluid challenge, CO and the mean of four intra-arterial and oscillometric brachial cuff BP measurements were collected. Fluid responsiveness was defined by an increase in CO ≥10 or ≥15 % in case of regular rhythm or arrhythmia, respectively.
Results
In 130 patients, the correlation between a fluid-induced increase in pulse pressure (Δ
500ml
PP) and fluid-induced increase in CO was weak and was similar for invasive and non-invasive measurements of BP:
r
² = 0.31 and
r
² = 0.29, respectively (both
p
< 0.001). For the identification of responders,
invasive
Δ
500ml
PP was associated with an area under the receiver-operating curve (AUC) of 0.82 (0.74–0.88), similar (
p
= 0.80) to that of
non-invasive
Δ
500ml
PP AUC of 0.81 (0.73–0.87). Outside large gray zones of inconclusive values (5–23 % for
invasive
Δ
500ml
PP and 4–35 % for
non-invasive
Δ
500ml
PP, involving 35 and 48 % of patients, respectively), the detection of responsiveness or unresponsiveness to fluid was reliable. Cardiac arrhythmia did not impair the performance of
invasive
or
non-invasive
Δ
500ml
PP. Other BP-derived indices did not outperform Δ
500ml
PP.
Conclusions
As evidenced by large gray zones, BP-derived indices poorly reflected fluid responsiveness. However, in our deeply sedated population, a high increase in invasive pulse pressure (>23 %) or even in non-invasive pulse pressure (>35 %) reliably detected a response to fluid. In the absence of a marked increase in pulse pressure (<4–5 %), a response to fluid was unlikely.
Delaying renal replacement therapy (RRT) for some time in critically ill patients with severe acute kidney injury and no severe complication is safe and allows optimisation of the use of medical ...devices. Major uncertainty remains concerning the duration for which RRT can be postponed without risk. Our aim was to test the hypothesis that a more-delayed initiation strategy would result in more RRT-free days, compared with a delayed strategy.
This was an unmasked, multicentre, prospective, open-label, randomised, controlled trial done in 39 intensive care units in France. We monitored critically ill patients with severe acute kidney injury (defined as Kidney Disease: Improving Global Outcomes stage 3) until they had oliguria for more than 72 h or a blood urea nitrogen concentration higher than 112 mg/dL. Patients were then randomly assigned (1:1) to either a strategy (delayed strategy) in which RRT was started just after randomisation or to a more-delayed strategy. With the more-delayed strategy, RRT initiation was postponed until mandatory indication (noticeable hyperkalaemia or metabolic acidosis or pulmonary oedema) or until blood urea nitrogen concentration reached 140 mg/dL. The primary outcome was the number of days alive and free of RRT between randomisation and day 28 and was done in the intention-to-treat population. The study is registered with ClinicalTrial.gov, NCT03396757 and is completed.
Between May 7, 2018, and Oct 11, 2019, of 5336 patients assessed, 278 patients underwent randomisation; 137 were assigned to the delayed strategy and 141 to the more-delayed strategy. The number of complications potentially related to acute kidney injury or to RRT were similar between groups. The median number of RRT-free days was 12 days (IQR 0–25) in the delayed strategy and 10 days (IQR 0–24) in the more-delayed strategy (p=0·93). In a multivariable analysis, the hazard ratio for death at 60 days was 1·65 (95% CI 1·09–2·50, p=0·018) with the more-delayed versus the delayed strategy. The number of complications potentially related to acute kidney injury or renal replacement therapy did not differ between groups.
In severe acute kidney injury patients with oliguria for more than 72 h or blood urea nitrogen concentration higher than 112 mg/dL and no severe complication that would mandate immediate RRT, longer postponing of RRT initiation did not confer additional benefit and was associated with potential harm.
Programme Hospitalier de Recherche Clinique.
Despite their usefulness in perioperative and acute care settings, factor-Xa inhibitor-specific assays are scarcely available, contrary to heparin anti-Xa assay. We assessed whether the heparin ...anti-Xa assay can (1) be used as a screening test to rule out apixaban, rivaroxaban, fondaparinux, and danaparoid levels that contraindicate invasive procedures according to current guidelines (>30 ng·mL-1, >30 ng·mL-1, >0.1 µg·mL-1, and >0.1 IU·mL-1, respectively), (2) quantify the anticoagulant level if found significant, that is, if it exceeded the abovementioned threshold.
In the derivation cohort then in the validation cohort, via receiver operating characteristics (ROC) curve analysis, we evaluated the ability of heparin anti-Xa assay to detect levels of factor-Xa inhibitors above or below the abovementioned safety thresholds recommended for an invasive procedure (screening test). Among samples with relevant levels of factor-Xa inhibitor, we determined the conversion factor linking the measured level and heparin anti-Xa activity in a derivation cohort. In a validation cohort, the estimated level of each factor-Xa inhibitor was thus inferred from heparin anti-Xa activity. The agreement between measured and estimated levels of factor-Xa inhibitors was assessed.
Among 989 (355 patients) and 756 blood samples (420 patients) in the derivation and validation cohort, there was a strong linear relationship between heparin anti-Xa activities and factor-Xa inhibitors measured level (r = 0.99 95% confidence interval {CI}, 0.99-0.99). In the derivation cohort, heparin anti-Xa activity ≤0.2, ≤0.3, <0.1, <0.1 IU·mL-1 reliably ruled out a relevant level of apixaban, rivaroxaban, fondaparinux, and danaparoid, respectively (area under the ROC curve ≥0.99). In the validation cohort, these cutoffs yielded excellent classification accuracy (≥96%). If this screening test indicated relevant level of factor-Xa inhibitor, estimated and measured levels closely agreed (Lin's correlation coefficient close to its maximal value: 95% CI, 0.99-0.99). More than 96% of the estimated levels fell into the predefined range of acceptability (ie, 80%-120% of the measured level).
A unique simple test already widely used to assay heparin was also useful for quantifying these 4 other anticoagulants. Both clinical and economic impacts of these findings should be assessed in a specific study.
Purpose
Critically ill patients, among whom acute kidney injury is common, are often considered particularly vulnerable to iodinated contrast medium nephrotoxicity. However, the attributable ...incidence remains uncertain given the paucity of observational studies including a control group. This study assessed acute kidney injury incidence attributable to iodinated contrast media in critically ill patients based on new data accounting for sample and effect size and including a control group.
Methods
Systematic review of studies measuring incidence of acute kidney injury in critically ill patients following contrast medium exposure compared to matched unexposed patients. Patient-level meta-analysis implementing a Bayesian nested mixed effects multiple logistic regression model.
Results
Ten studies were identified; only four took into account the baseline acute kidney injury risk, three by patient matching (560 patients). Objective meta-analysis of these three studies (vague and impartial a priori hypothesis concerning attributable acute kidney injury risk) did not find that iodinated contrast media increased the incidence of acute kidney injury (odds ratio 0.95, 95% highest posterior density interval 0.45–1.62). Bayesian analysis demonstrated that, to conclude in favor of a statistically significant incidence of acute kidney injury attributable to contrast media despite this observed lack of association, one’s a priori belief would have to be very strongly biased, assigning to previous uncontrolled reports 3–12 times the weight of evidence strength provided by the matched studies including a control group.
Conclusions
Meta-analysis of matched cohort studies of iodinated contrast medium exposure does not support a significant incidence of acute kidney injury attributable to iodinated contrast media in critically ill patients.
Mortality is often assessed during ICU stay and early after, but rarely at later stage. We aimed to compare the long-term mortality between TBI and ICH patients.
From an observational cohort, we ...studied 580 TBI patients and 435 ICH patients, admitted from January 2013 to February 2021 in 3 ICUs and alive at 7-days post-ICU discharge. We performed a Lasso-penalized Cox survival analysis.
We estimated 7-year survival rates at 72.8% (95%CI from 67.3% to 78.7%) for ICH patients and at 84.9% (95%CI from 80.9% to 89.1%) for TBI patients: ICH patients presenting a higher mortality risk than TBI patients. Additionally, we identified variables associated with higher mortality risk (age, ICU length of stay, tracheostomy, low GCS, absence of intracranial pressure monitoring). We also observed anisocoria related with the mortality risk in the early stage after ICU stay.
In this ICU survivor population with a prolonged follow-up, we highlight an acute risk of death after ICU stay, which seems to last longer in ICH patients. Several variables characteristic of disease severity appeared associated with long-term mortality, raising the hypothesis that the most severe patients deserve closer follow-up after ICU stay.
•Comparing the long-term mortality between TBI and ICH patients after post-ICU discharge.•From the French cohort AtlanREA, we observed a poorer long-term survival for patients admitted for an ICH.•We highlighted an acute risk of death after ICU stay, which seems to last longer in ICH patients.•Disease severity variables appeared associated with long-term mortality.
Continuous and intermittent noninvasive measurements of arterial blood pressure (BP) have not been compared in the same population. In a large panel of intensive care unit patients, we assessed the ...agreement between CNAP™ (Continuous Noninvasive Arterial Pressure) finger cuff beat-to-beat monitoring of BP and reference intraarterial measurements. Two automated oscillometric brachial cuff devices were also tested: CNAP brachial cuff (used for CNAP finger cuff calibration) and an alternative device. The performance for detecting hypotension (intraarterial mean BP <65 mm Hg or systolic BP <90 mm Hg), response to therapy (therapy-induced increase in mean BP >10%), and hypertension (intraarterial systolic BP >140 mm Hg) was evaluated. We also assessed the between-calibration drift of CNAP finger cuff BP in specific situations: cardiovascular intervention or no intervention.
With each device, 3 pairs of noninvasive and intraarterial measurements were prospectively collected and analyzed according to current guidelines, the International Organization for Standardization (ISO) standard. The trending ability and drift of the CNAP finger cuff BP were assessed over a 15-minute observation period.
In 182 patients, CNAP finger cuff and CNAP brachial cuff readings did not conform to ISO standard requirements (mean bias ± SD exceeding the maximum tolerated 5 ± 8 mm Hg), whereas the alternative automated brachial cuff succeeded for mean and diastolic BP. CNAP finger cuff trending ability was poor (concordance rate <70% over a 15-minute period) owing to a significant drift since calibration, especially if a cardiovascular intervention was performed (n = 75, -7.5 ± 10.2 mm Hg at the 14th minute, ie, before recalibration, versus -2.9 ± 7.9 mm Hg if no cardiovascular intervention occurred, n = 103, P = 0.0008). However, a similar and reliable performance was observed for the detection of hypotension with the CNAP finger cuff (within 4 minutes after calibration) and with the 2 automated brachial cuffs (area under the receiver operating characteristic curve ≥0.91, positive and negative likelihood ratios ≥5 and ≤0.20, respectively). The performance for the detection of response to therapy or of hypertension was slightly lower.
In a large population of intensive care unit patients, CNAP did not fulfill the ISO criteria and exhibited a relevant between-calibration drift. However, CNAP measurements collected within 4 minutes after calibration were reliable for detecting hypotension, as were oscillometric devices, while providing beat-to-beat measurements. Interestingly, an alternative automated brachial cuff was more reliable than the native one, used for calibration. This information is important to clinicians using those devices and for further development of the CNAP technology.
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