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Abstract Background in COVID-19 acute respiratory failure, the effects of CPAP and FiO2 on respiratory effort and lung stress are unclear. We hypothesize that, in the compliant lungs of early Sars-CoV-2 pneumonia, the application of positive pressure through Helmet-CPAP may not decrease respiratory effort, and rather worsen lung stress and oxygenation when compared to higher FiO2 delivered via oxygen masks. Methods In this single-center (S.Luigi Gonzaga University-Hospital, Turin, Italy), randomized, crossover study, we included patients receiving Helmet-CPAP for early (

Abstract Background Data on the prevalence and clinical impact of extrapulmonary findings at screening computed tomography (CT) on initiation of veno-venous extracorporeal membrane oxygenation (V-V ECMO) are limited. We aimed to identify the prevalence of extrapulmonary findings on screening CT following V-V ECMO initiation. We hypothesized that extrapulmonary findings would influence clinical management and outcome. Methods Retrospective analysis (2011–2021) of admission screening CT including head, abdomen and pelvis with contrast of consecutive patients on initiation of V-V ECMO. CT findings identified by the attending consultant radiologist were extracted. Demographics, admission physiological and laboratory data, clinical decision-making following CT and ECMO ICU mortality were recorded from the electronic medical record. We used multivariable logistic regression and Kaplan–Meier curves to evaluate associations between extrapulmonary findings and ECMO ICU mortality. Results Of the 833 patients receiving V-V ECMO, 761 underwent routine admission CT (91.4%). ECMO ICU length of stay was 19 days (IQR 12–23); ICU mortality at the ECMO centre was 18.9%. An incidental extrapulmonary finding was reported in 227 patients (29.8%), leading to an invasive procedure in 12/227 cases (5.3%) and a change in medical management (mainly in anticoagulation strategy) in 119/227 (52.4%). Extrapulmonary findings associated with mortality were intracranial haemorrhage (OR 2.34 (95% CI 1.31–4.12), cerebral infarction (OR 3.59 (95% CI 1.26–9.86) and colitis (OR 2.80 (95% CI 1.35–5.67). Conclusions Screening CT frequently identifies extrapulmonary findings of clinical significance. Newly detected intracranial haemorrhage, cerebral infarction and colitis were associated with increased ICU mortality.

Take home message Successful weaning from veno-venous ECMO requires understanding and consideration of the complex physiological interactions between the native and the extracorporeal lung. We describe our understanding of the physiological adaptations of the patient as extracorporeal support is weaned and outline the implications for clinical practice.

Abstract The extent of ventilator‐induced lung injury may be related to the intensity of mechanical ventilation––expressed as mechanical power. In the present study, we investigated whether there is a safe threshold, below which lung damage is absent. Three groups of six healthy pigs (29.5 ± 2.5 kg) were ventilated prone for 48 h at mechanical power of 3, 7, or 12 J/min. Strain never exceeded 1.0. PEEP was set at 4 cmH2O. Lung volumes were measured every 12 h; respiratory, hemodynamics, and gas exchange variables every 6. End‐experiment histological findings were compared with a control group of eight pigs which did not undergo mechanical ventilation. Functional residual capacity decreased by 10.4% ± 10.6% and 8.1% ± 12.1% in the 7 J and 12 J groups (p = 0.017, p

Inflammation and oxidative stress characterize sepsis and determine its severity. In this study, we investigated the relationship between albumin oxidation and sepsis severity in a selected cohort of patients from the Albumin Italian Outcome Study (ALBIOS). A retrospective analysis was conducted on the oxidation forms of human albumin [human mercapto-albumin (HMA), human non-mercapto-albumin form 1 (HNA1) and human non-mercapto-albumin form 2 (HNA2)] in 60 patients with severe sepsis or septic shock and 21 healthy controls. The sepsis patients were randomized (1:1) to treatment with 20% albumin and crystalloid solution or crystalloid solution alone. The albumin oxidation forms were measured at day 1 and day 7. To assess the albumin oxidation forms as a function of oxidative stress, the 60 sepsis patients, regardless of the treatment, were grouped based on baseline sequential organ failure assessment (SOFA) score as surrogate marker of oxidative stress. At day 1, septic patients had significantly lower levels of HMA and higher levels of HNA1 and HNA2 than healthy controls. HMA and HNA1 concentrations were similar in patients treated with albumin or crystalloids at day 1, while HNA2 concentration was significantly greater in albumin-treated patients (p < 0.001). On day 7, HMA was significantly higher in albumin-treated patients, while HNA2 significantly increased only in the crystalloids-treated group, reaching values comparable with the albumin group. When pooling the septic patients regardless of treatment, albumin oxidation was similar across all SOFA groups at day 1, but at day 7 HMA was lower at higher SOFA scores. Mortality rate was independently associated with albumin oxidation levels measured at day 7 (HMA log-rank = 0.027 and HNA2 log-rank = 0.002), irrespective of treatment group. In adjusted regression analyses for 90-day mortality, this effect remained significant for HMA and HNA2. Our data suggest that the oxidation status of albumin is modified according to the time of exposure to oxidative stress (differences between day 1 and day 7). After 7 days of treatment, lower SOFA scores correlate with higher albumin antioxidant capacity. The trend toward a positive effect of albumin treatment, while not statistically significant, warrants further investigation.

Abstract Background Mechanical power is a summary variable including all the components which can possibly cause VILI (pressures, volume, flow, respiratory rate). Since the complexity of its mathematical computation is one of the major factors that delay its clinical use, we propose here a simple and easy to remember equation to estimate mechanical power under volume-controlled ventilation: Mechanical Power=VE×Peak Pressure+PEEP+F/620 $$ \mathrm{Mechanical}\ \mathrm{Power}=\frac{\mathrm{VE}\times \left(\mathrm{Peak}\ \mathrm{Pressure}+\mathrm{PEEP}+F/6\right)}{20} $$ where the mechanical power is expressed in Joules/minute, the minute ventilation (VE) in liters/minute, the inspiratory flow (F) in liters/minute, and peak pressure and positive end-expiratory pressure (PEEP) in centimeter of water. All the components of this equation are continuously displayed by any ventilator under volume-controlled ventilation without the need for clinician intervention. To test the accuracy of this new equation, we compared it with the reference formula of mechanical power that we proposed for volume-controlled ventilation in the past. The comparisons were made in a cohort of mechanically ventilated pigs (485 observations) and in a cohort of ICU patients (265 observations). Results Both in pigs and in ICU patients, the correlation between our equation and the reference one was close to the identity. Indeed, the R 2 ranged from 0.97 to 0.99 and the Bland-Altman showed small biases (ranging from + 0.35 to − 0.53 J/min) and proportional errors (ranging from + 0.02 to − 0.05). Conclusions Our new equation of mechanical power for volume-controlled ventilation represents a simple and accurate alternative to the more complex ones available to date. This equation does not need any clinical intervention on the ventilator (such as an inspiratory hold) and could be easily implemented in the software of any ventilator in volume-controlled mode. This would allow the clinician to have an estimation of mechanical power at a simple glance and thus increase the clinical consciousness of this variable which is still far from being used at the bedside. Our equation carries the same limitations of all other formulas of mechanical power, the most important of which, as far as it concerns VILI prevention, are the lack of normalization and its application to the whole respiratory system (including the chest wall) and not only to the lung parenchyma.