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Respiratory weakness after mechanical ventilation is associated with one-year mortality - a prospective study.

ABSTRACT: Diaphragm dysfunction in mechanically ventilated patients is associated with poor outcome. Maximal inspiratory pressure (MIP) can be used to evaluate inspiratory muscle function. However, it is unclear whether respiratory weakness is independently associated with long-term mortality. The aim of this study was to determine if low MIP is independently associated with one-year mortality.We conducted a prospective observational cohort study in an 18-bed ICU. Adults requiring at least 24 hours of mechanical ventilation with scheduled extubation and no evidence of pre-existing muscle weakness underwent MIP evaluation just before extubation. Patients were divided into two groups: low MIP (MIP ?30 cmH2O) and high MIP (MIP >30 cmH2O). Mortality was recorded for one year after extubation. For the survival analysis, the effect of low MIP was assessed using the log-rank test. The independent effect of low MIP on post mechanical ventilation mortality was analyzed using a multivariable Cox regression model.One hundred and twenty-four patients underwent MIP evaluation (median age 66 years (25(th)-75(th) percentile 56-74), Simplified Acute Physiology Score (SAPS) 2?=?45 (33-57), duration of mechanical ventilation 7 days (4-10)). Fifty-four percent of patients had low MIP. One-year mortality was 31 % (95 % CI 0.21, 0.43) in the low MIP group and 7 % (95 % CI 0.02, 0.16) in the high MIP group. After adjustment for SAPS 2 score, body mass index and duration of mechanical ventilation, low MIP was independently associated with one-year mortality (hazard ratio 4.41, 95 % CI 1.5, 12.9, p?=?0.007). Extubation failure was also associated with low MIP (relative risk 3.0, 95 % CI 1, -9.6; p?=?0.03) but tracheostomy and ICU length of stay were not.Low MIP is frequent in patients on mechanical ventilation and is an independent risk factor for long-term mortality in ICU patients requiring mechanical ventilation. MIP is easily evaluated at the patient's bedside.This study was retrospectively registered in www.clinicaltrials.gov (NCT02363231) in February 2015.

SUBMITTER: Medrinal C

PROVIDER: S-EPMC4967510 | biostudies-literature | 2016 Jul

REPOSITORIES: biostudies-literature

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Respiratory weakness after mechanical ventilation is associated with one-year mortality - a prospective study.

Medrinal Clément C Prieur Guillaume G Frenoy Éric É Robledo Quesada Aurora A Poncet Antoine A Bonnevie Tristan T Gravier Francis-Edouard FE Lamia Bouchra B Contal Olivier O

Critical care (London, England) 20160731 1

<h4>Background</h4>Diaphragm dysfunction in mechanically ventilated patients is associated with poor outcome. Maximal inspiratory pressure (MIP) can be used to evaluate inspiratory muscle function. However, it is unclear whether respiratory weakness is independently associated with long-term mortality. The aim of this study was to determine if low MIP is independently associated with one-year mortality.<h4>Methods</h4>We conducted a prospective observational cohort study in an 18-bed ICU. Adults ...[more]

PMID: 27475524

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Project description:BackgroundHost-associated microbial communities have important roles in tissue homeostasis and overall health. Severe perturbations can occur within these microbial communities during critical illness due to underlying diseases and clinical interventions, potentially influencing patient outcomes. We sought to profile the microbial composition of critically ill mechanically ventilated patients, and to determine whether microbial diversity is associated with illness severity and mortality.MethodsWe conducted a prospective, observational study of mechanically ventilated critically ill patients with a high incidence of pneumonia in 2 intensive care units (ICUs) in Hamilton, Canada, nested within a randomized trial for the prevention of healthcare-associated infections. The microbial profiles of specimens from 3 anatomical sites (respiratory, and upper and lower gastrointestinal tracts) were characterized using 16S ribosomal RNA gene sequencing.ResultsWe collected 65 specimens from 34 ICU patients enrolled in the trial (29 endotracheal aspirates, 26 gastric aspirates and 10 stool specimens). Specimens were collected at a median time of 3 days (lower respiratory tract and gastric aspirates; interquartile range [IQR] 2-4) and 6 days (stool; IQR 4.25-6.75) following ICU admission. We observed a loss of biogeographical distinction between the lower respiratory tract and gastrointestinal tract microbiota during critical illness. Moreover, microbial diversity in the respiratory tract was inversely correlated with APACHE II score (r = - 0.46, p = 0.013) and was associated with hospital mortality (Median Shannon index: Discharged alive; 1.964 vs. Deceased; 1.348, p = 0.045).ConclusionsThe composition of the host-associated microbial communities is severely perturbed during critical illness. Reduced microbial diversity reflects high illness severity and is associated with mortality. Microbial diversity may be a biomarker of prognostic value in mechanically ventilated patients.Trial registrationClinicalTrials.gov ID NCT01782755 . Registered February 4 2013.

Project description:BACKGROUND:Most prognostic studies in acute stroke patients requiring invasive mechanical ventilation are outdated and have limitations such as single-center retrospective designs. We aimed to study the association of ICU admission factors, including the reason for intubation, with 1-year survival of acute stroke patients requiring mechanical ventilation. METHODS:We conducted a secondary data use analysis of a prospective multicenter database (14 ICUs) between 1997 and 2016 on consecutive ICU stroke patients requiring mechanical ventilation at admission. We excluded patients with stroke of traumatic origin, subdural hematoma or cerebral venous thrombosis. The primary outcome was survival 1 year after ICU admission. Factors associated with the primary outcome were identified using a multivariable Cox model stratified on inclusion center. RESULTS:We identified 419 patients (age 68 [58-76] years, males 60%) with a Glasgow coma score (GCS) of 4 [3-8] at admission. Stroke subtypes were acute ischemic stroke (AIS, 46%), intracranial hemorrhage (ICH, 42%) and subarachnoid hemorrhage (SAH, 12%). At 1 year, 96 (23%) patients were alive. Factors independently associated with decreased 1-year survival were ICH and SAH stroke subtypes, a lower GCS score at admission, a higher non-neurological SOFA score. Conversely, patients receiving acute-phase therapy had improved 1-year survival. Intubation for acute respiratory failure or coma was associated with comparable survival hazard ratios, whereas intubation for seizure was not associated with a worse prognosis than for elective procedure. Survival did not improve over the study period, but patients included in the most recent period had more comorbidities and presented higher severity scores at admission. CONCLUSIONS:In acute stroke patients requiring mechanical ventilation, the reason for intubation and the opportunity to receive acute-phase stroke therapy were independently associated with 1-year survival. These variables could assist in the decision process regarding the initiation of mechanical ventilation in acute stroke patients.

Project description:Background Mortality in acute respiratory failure remains high despite the use of lung-protective ventilation. Recent studies have shown an association between baseline ventilation parameters (driving pressure or mechanical power) and outcomes for patients with acute respiratory distress syndrome. Strategies focused on limiting these parameters have been proposed to further improve outcomes. However, it remains unknown whether driving pressure and mechanical power should be limited over the entire duration of mechanical ventilation and in all patients with acute respiratory failure. We aimed to estimate the association between exposure to different intensities of mechanical ventilation over time and intensive care unit (ICU) mortality in patients with acute respiratory failure.MethodsIn this registry-based, prospective cohort study, we obtained data from the Toronto Intensive Care Observational Registry, which includes all patients receiving mechanical ventilation for 4 h or more in nine ICUs that are affiliated with the University of Toronto (Toronto, ON, Canada). We included all adult (≥18 years) patients who received invasive mechanical ventilation between April 11, 2014, and June 5, 2019. Patients were excluded if they received treatment with extracorporeal life support. The primary outcome was ICU mortality. Bayesian joint models were used to estimate the strength of associations, accounting for informative censoring due to death during follow-up.FindingsOf 13 939 patients recorded in the registry, 13 408 (96·2%) were eligible for descriptive analysis. The primary analysis comprised 7876 (58·7%) patients with complete baseline characteristics, and a secondary analysis included all 13 408 patients after multiple imputation in the joint model analysis. 2409 (18·0%) of 13 408 patients died in the ICU. After adjustment for baseline characteristics, including age and severity of illness, a significant increase in the hazard of death was found to be associated with each daily increment in driving pressure (hazard ratio 1·064, 95% credible interval 1·057-1·071) or mechanical power (hazard ratio 1·060, 95% credible interval 1·053-1·066). These associations persisted over the duration of mechanical ventilation.InterpretationCumulative exposure to higher intensities of mechanical ventilation was harmful, even for short durations. Limiting exposure to driving pressure or mechanical power should be evaluated in further studies as promising ventilation strategies to reduce mortality in patients with acute respiratory failure.FundingCanadian Institutes of Health Research.

Project description:BackgroundMechanical ventilation is a life-saving intervention used to provide adequate pulmonary ventilation in patients suffering from respiratory failure. However, prolonged mechanical ventilation is associated with significant diaphragmatic weakness resulting from both myofiber atrophy and contractile dysfunction. Although several signaling pathways contribute to diaphragm weakness during mechanical ventilation, it is established that oxidative stress is required for diaphragmatic weakness to occur. Therefore, identifying the site(s) of mechanical ventilation- induced reactive oxygen species production in the diaphragm is important.ObjectiveThese experiments tested the hypothesis that elevated mitochondrial reactive oxygen species emission is required for mechanical ventilation-induced oxidative stress, atrophy, and contractile dysfunction in the diaphragm.DesignCause and effect was determined by preventing mechanical ventilation-induced mitochondrial reactive oxygen species emission in the diaphragm of rats using a novel mitochondria-targeted antioxidant (SS-31).InterventionsNone.Measurements and main resultsCompared to mechanically ventilated animals treated with saline, animals treated with SS-31 were protected against mechanical ventilation-induced mitochondrial dysfunction, oxidative stress, and protease activation in the diaphragm. Importantly, treatment of animals with the mitochondrial antioxidant also protected the diaphragm against mechanical ventilation-induced myofiber atrophy and contractile dysfunction.ConclusionsThese results reveal that prevention of mechanical ventilation-induced increases in diaphragmatic mitochondrial reactive oxygen species emission protects the diaphragm from mechanical ventilation-induced diaphragmatic weakness. This important new finding indicates that mitochondria are a primary source of reactive oxygen species production in the diaphragm during prolonged mechanical ventilation. These results could lead to the development of a therapeutic intervention to impede mechanical ventilation-induced diaphragmatic weakness.

Project description:ObjectivesAlthough mechanical ventilation is a life-saving measure for patients in respiratory failure, prolonged mechanical ventilation results in diaphragmatic weakness attributable to fiber atrophy and contractile dysfunction. Therefore, identifying the signaling pathways responsible for mechanical ventilation-induced diaphragmatic weakness is important. In this context, it is established that oxidative stress is required for mechanical ventilation-induced diaphragmatic weakness to occur. Numerous redox-sensitive signaling pathways exist in muscle including the transcription factor nuclear factor-κB. Although it has been suggested that nuclear factor-κB contributes to proteolytic signaling in inactivity-induced atrophy in locomotor muscles, the role that nuclear factor-κB plays in mechanical ventilation-induced diaphragmatic weakness is unknown. We tested the hypothesis that nuclear factor-κB activation plays a key signaling role in mechanical ventilation-induced diaphragmatic weakness and that oxidative stress is required for nuclear factor-κB activation.DesignCause and effect was determined by independently treating mechanically ventilated animals with either a specific nuclear factor-κB inhibitor (SN50) or a clinically relevant antioxidant (curcumin).Measurements and main resultsInhibition of nuclear factor-κB activity partially attenuated both mechanical ventilation-induced diaphragmatic atrophy and contractile dysfunction. Further, treatment with the antioxidant curcumin prevented mechanical ventilation-induced activation of nuclear factor-κB in the diaphragm and rescued the diaphragm from both mechanical ventilation-induced atrophy and contractile dysfunction.ConclusionsCollectively, these findings support the hypothesis that nuclear factor-κB activation plays a significant signaling role in mechanical ventilation-induced diaphragmatic weakness and that oxidative stress is an upstream activator of nuclear factor-κB. Finally, our results suggest that prevention of mechanical ventilation-induced oxidative stress in the diaphragm could be a useful clinical strategy to prevent or delay mechanical ventilation-induced diaphragmatic weakness.

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Respiratory weakness after mechanical ventilation is associated with one-year mortality - a prospective study.

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Respiratory weakness after mechanical ventilation is associated with one-year mortality - a prospective study.

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