Critical Care and Resuscitation最新文献

Objective: To describe pain assessment and analgesic management practices in patients in intensive care units (ICUs) in Australia and New Zealand.

Design, setting and participants: Prospective, observational, multicentre, single-day point prevalence study conducted in Australian and New Zealand ICUs. Observational data were recorded for all adult patients admitted to an ICU without a neurological, neurosurgical or postoperative cardiac diagnosis. Demographic characteristics and data on pain assessment and analgesic management for a 24-hour period were collected.

Main outcome measures: Types of pain assessment tools used and frequency of their use, use of opioid analgesia, use of adjuvant analgesia, and differences in pain assessment and analgesic management between postoperative and non-operative patients.

Results: From the 499 patients enrolled from 45 ICUs, pain assessment was performed at least every 4 hours in 56% of patients (277/499), most commonly with a numerical rating scale. Overall, 286 patients (57%) received an opioid on the study day. Of the 181 mechanically ventilated patients, 135 (75%) received an intravenous opioid, with the predominant opioid infusion being fentanyl. The median dose of opioid infusion for ventilated patients was 140 mg oral morphine equivalents. Of the 318 non-ventilated patients, 41 (13%) received patient-controlled analgesia and 76 (24%) received an oral opioid, with the predominant opioid being oxycodone. Paracetamol was administered to 63 ventilated patients (35%) and 164 non-ventilated patients (52%), while 2% of all patients (11/499) received a non-steroidal anti-inflammatory drug. Ketamine infusion and regional analgesia were used in 15 patients (3%) and 17 patients (3%), respectively. Antineuropathic agents (predominantly gabapentinoids) were used in 53 patients (11%).

Conclusions: Although a majority of ICU patients were frequently assessed for pain with a validated pain assessment tool, cumulative daily doses of opioids were high, and the use of multimodal adjuvant analgesia was low. Our data on current pain assessment and analgesic management practices may inform further research in this area.

Objectives: To investigate the prevalence and features of self-reported burnout among intensivists working in Australia and New Zealand, and evaluate potentially modifiable workplace stressors associated with increased risk of self-reported burnout.

Methods: We performed an electronic survey among registered intensivists in Australia and New Zealand. Burnout and professional quality of life were measured using the Professional Quality of Life Scale version 5 (ProQOL-5). Socio-organisational factors were defined a priori and assessed using a five-point Likert scale. Thematic analysis was conducted on an open-ended question on workplace stressors.

Results: 261 of 921 estimated intensivists responded (response rate, 28.3%). Overall, few participants (0.8%) demonstrated high scores (> 75th centile) for burnout, and 70.9% of participants scored in the average range for burnout. Of note, 98.1% of participants scored in the average to high range for compassion satisfaction. No association was found between sex, age, or years of practice with the level of burnout or compassion satisfaction. Seven themes emerged regarding intensivists' most stressful aspects of work: interpersonal interactions and workplace relationships (25.5%), workload and its impact (24.9%), resources and capacity (22.6%), health systems leadership and bureaucracy (16.1%), end-of-life issues and moral distress (8.4%), clinical management (4.9%), and job security and future uncertainty (1.3%).

Conclusion: Fewer Australian and New Zealand intensivists experienced burnout than previously reported. Many self-reported work stressors do not relate to clinical work and are due to interpersonal interactions with other colleges and hospital administrators. Such factors are potentially modifiable and could be the focus of future interventions.

Background and objectives: The effect of initiating continuous renal replacement therapy (CRRT) on urine output, fluid balance and mean arterial pressure (MAP) in adult intensive care unit (ICU) patients is unclear. We aimed to evaluate the impact of CRRT on urine output, MAP, vasopressor requirements and fluid balance, and to identify factors affecting urine output during CRRT.

Design: Retrospective cohort study using data from existing databases and CRRT machines.

Setting: Medical and surgical ICUs at a single university-associated centre.

Participants: Patients undergoing CRRT between 2015 and 2018.

Main outcome measures: Hourly urine output, fluid balance, MAP and vasopressor dose 24 hours before and after CRRT commencement. Missing values were estimated via Kaplan smoothing univariate time-series imputation. Mixed linear modelling was performed with noradrenaline equivalent dose and urine output as outcomes.

Results: In 215 patients, CRRT initiation was associated with a reduction in urine output. Multivariate analysis confirmed an immediate urine output decrease (–0.092 mL/kg/h; 95% confidence interval [CI], –0.150 to –0.034 mL/kg/h) and subsequent progressive urine output decline (effect estimate, –0.01 mL/kg/h; 95% CI, –0.02 to –0.01 mL/kg/h). Age and greater vasopressor dose were associated with lower post-CRRT urine output. Higher MAP and lower rates of net ultrafiltration were associated with higher post-CRRT urine output. With MAP unchanged, vasopressor dose increased in the 24 hours before CRRT, then plateaued and declined in the 24 hours thereafter (effect estimate, –0.004 μg/kg/ min per hour; 95% CI, –0.005 to –0.004 μg/kg/min per hour). Fluid balance remained positive but declined towards neutrality following CRRT implementation.

Conclusions: CRRT was associated with decreased urine output despite a gradual decline in vasopressor and a positive fluid balance. The mechanisms behind the reduction in urine output associated with commencement of CRRT requires further investigation.

Objective: Pregnancy is a risk factor for acute respiratory failure (ARF) following severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. We hypothesised that SARS-CoV-2 viral load in the respiratory tract might be higher in pregnant intensive care unit (ICU) patients with ARF than in non-pregnant ICU patients with ARF as a consequence of immunological adaptation during pregnancy.

Design: Single-centre, retrospective observational case–control study.

Setting: Adult level 3 ICU in a French university hospital.

Participants: Eligible participants were adults with ARF associated with coronavirus disease 2019 (COVID-19) pneumonia.

Main outcome measure: The primary endpoint of the study was viral load in pregnant and non-pregnant patients.

Results: 251 patients were included in the study, including 17 pregnant patients. Median gestational age at ICU admission amounted to 28 + 3/7 weeks (interquartile range [IQR], 26 + 1/7 to 31 + 5/7 weeks). Twelve patients (71%) had an emergency caesarean delivery due to maternal respiratory failure. Pregnancy was independently associated with higher viral load (-4.6 ± 1.9 cycle threshold; P < 0.05). No clustering or over-represented mutations were noted regarding SARS-CoV-2 sequences of pregnant women. Emergency caesarean delivery was independently associated with a modest but significant improvement in arterial oxygenation, amounting to 32 ± 12 mmHg in patients needing invasive mechanical ventilation. ICU mortality was significantly lower in pregnant patients (0 v 35%; P < 0.05). Age, Simplified Acute Physiology Score (SAPS) II score, and acute respiratory distress syndrome were independent risk factors for ICU mortality, while pregnancy status and virological variables were not.

Conclusions: Viral load was substantially higher in pregnant ICU patients with COVID-19 and ARF compared with non-pregnant ICU patients with COVID-19 and ARF. Pregnancy was not independently associated with ICU mortality after adjustment for age and disease severity.

Objective: A 1-hour plasma glucose level ≥ 8.6 mmol/L in a 75 g oral glucose tolerance test has been strongly associated with increased morbidity and mortality in outpatients without diabetes. Our primary aim was to evaluate the 1-hour plasma glucose level in a 75 g glucose tolerance test in survivors of critical illness with stress hyperglycaemia at 3 months after intensive care unit (ICU) discharge, with the secondary aims to evaluate the 2-hour plasma glucose level, glycated haemoglobin (HbA_1c), and gastric emptying.

Design:Post hoc analysis of a single-centre, prospective cohort study.

Setting: Single-centre, tertiary referral, mixed medical-surgical ICU.

Participants: Consecutively admitted patients aged ≥ 18 years who developed stress hyperglycaemia and survived to hospital discharge were eligible.

Interventions: Participants returned at 3 months after ICU discharge and underwent a 75 g oral glucose tolerance test.

Main outcome measures: One- and 2-hour post load plasma glucose level, HbA_1c, and assessment of gastric emptying via an isotope breath test.

Results: Thirty-five patients (12 females; mean age, 58.5 years [SD, 10.5]; mean HbA_1c, 37.4 mmol/mol [SD, 7.0]) attended the followup. In 32/35 patients (91%) the 1-hour post load plasma glucose level was ≥ 8.6 mmol/L. There was a positive correlation between the plasma glucose level at 1 hour (r² = 0.21; P = 0.006), but no correlation between the 2-hour glucose level (r² = 0.006; P = 0.63) and gastric emptying.

Conclusion: Glucose intolerance, when defined as 1-hour glucose level ≥ 8.6 mmol/L following a 75 g oral glucose load, persists at 3 months in most survivors of stress hyperglycaemia and is dependent on the rate of gastric emptying. Longitudinal studies to characterise mechanisms underlying dysglycaemia and progression to diabetes in individuals with stress hyperglycaemia are indicated.

Objective: To evaluate the performance of cystatin C as a prognostic and predictive marker in a trial of patients with acute respiratory distress syndrome (ARDS).

Design, patients and setting: A retrospective analysis was performed on plasma samples from patients included in the HARP-2 (hydroxymethylglutaryl-CoA reductase inhibition with simvastatin in acute lung injury to reduce pulmonary dysfunction) trial — a multicentre, phase 2b trial carried out in general intensive care units across 40 hospitals in the United Kingdom and Ireland. Cystatin C concentrations in plasma obtained from 466 patients with ARDS (before they were randomly assigned in the trial) were quantified by ELISA (enzyme-linked immunosorbent assay).

Results: In a univariate analysis, plasma cystatin C concentrations were significantly higher in patients with ARDS who did not survive past 28 days (odds ratio [OR], 1.39 [95% CI, 1.12–1.72]; P = 0.002). In a multivariate model adjusted for selected covariates, cystatin C concentrations remained higher among patients with ARDS who did not survive, although this did not reach statistical significance (OR, 1.28 [95% CI, 0.96–1.71]; P = 0.090). Cystatin C concentration was also significantly associated with hyperinflammatory ARDS (OR, 2.64 [95% CI, 1.83–3.89]; P < 0.001). In multivariate models adjusted for both cystatin C concentration and ARDS subphenotype, hyperinflammatory ARDS was prognostic for mortality (OR, 2.06 [95% CI, 1.16–3.64]; P = 0.013) but cystatin C concentration was not (OR, 1.16 [95% CI, 0.85–1.57]; P = 0.346). In a multivariate analysis, hyperinflammatory ARDS was predictive of a beneficial effect of simvastatin on mortality (OR, 2.05 [95% CI, 1.16–3.62]; P = 0.014) but cystatin C concentration was not (OR, 1.10 [95% CI, 0.77–1.56]; P = 0.614).

Conclusion: The association between cystatin C concentration and mortality in ARDS may be dependent on inflammatory subphenotype. Cystatin C concentration does not appear to add to existing prognostic or predictive approaches.