Feasibility of a standardized protocol for respiratory training with intermitted positive pressure breathing ventilator application in dysphonia and dysarthria.

BACKGROUND: Brain damage can affect several functions related to speech production leading to dysphonia and dysarthria. Most rehabilitation treatments focus on articulation training rather than on pneumophonic coordination and respiratory muscle strength. Respiratory training using an intermitted positive pressure breathing (IPPB) ventilator can be used for this last purpose; no agreement on a standard protocol has been reached to date. AIM: To evaluate the feasibility and the effectiveness of a standardized incremental protocol of respiratory training using IPPB to treat dysphonia and dysarthria. DESIGN: Case series study. SETTING: Neuropsychological Rehabilitation Unit in an Italian Neurorehabilitation Division. POPULATION: Thirty-two subjects with dysphonia and dysarthria resulting from neurological lesion. METHODS: Participants were assessed using clinical evaluation scales (GIRBAS scale of dysphonia, Robertson dysarthria profile), respiratory function test, and arterial blood gas analysis in air. The evaluations were performed at baseline and after 20 sessions of respiratory training with IPPB. The protocol provided a default increment of ventilator parameters. All subjects also underwent a standard speech and language therapy treatment. A satisfaction survey to assess acceptability and the Goal Attainment Scale were applied. RESULTS: All participants fulfilled the protocol. No complications or discomfort were reported. Subjects' satisfaction at survey was 97.7%. After respiratory training, all respiratory function parameters increased, but only maximal voluntary ventilation (MVV), maximum inspiratory pressure (MIP), and maximum expiratory pressure (MEP) were statistically significant (P<0.05). Clinical evaluation scales significantly improved (P<0.05). Correlation between respiratory function parameters and clinical evaluation scales showed a moderate correlation between MVV, MEP, MIP, and Robertson dysarthria profile (P<0.01). A weak correlation was found between MIP, MVV, and GIRBAS scale (P<0.05). CONCLUSIONS: Our protocol showed to be practical and well-tolerated. After respiratory training, MVV, MIP and MEP improved in significantly. Clinical scale scores improved in all participants. CLINICAL REHABILITATION IMPACT: Respiratory training using IPPB ventilator can be useful in implementing speech and language treatments in subjects with dysphonia and dysarthria linked to brain injury.

Comparative Efficacy of Angiotensin II Type 1 Receptor Blockers Against Ventilator-Induced Diaphragm Dysfunction in Rats.

Mechanical ventilation (MV) is a life-saving intervention for many critically ill patients. Unfortunately, prolonged MV results in the rapid development of inspiratory muscle weakness due to diaphragmatic atrophy and contractile dysfunction (termed ventilator-induced diaphragm dysfunction (VIDD)). Although VIDD is a major risk factor for problems in weaning patients from MV, a standard therapy to prevent VIDD does not exist. However, emerging evidence suggests that pharmacological blockade of angiotensin II type 1 receptors (AT1Rs) protects against VIDD. Nonetheless, the essential characteristics of AT1R blockers (ARBs) required to protect against VIDD remain unclear. To determine the traits of ARBs that are vital for protection against VIDD, we compared the efficacy of two clinically relevant ARBs, irbesartan and olmesartan; these ARBs differ in molecular structure and effects on AT1Rs. Specifically, olmesartan blocks both angiotensin II (AngII) binding and mechanical activation of AT1Rs, whereas irbesartan prevents only AngII binding to AT1Rs. Using a well-established preclinical model of prolonged MV, we tested the hypothesis that compared with irbesartan, olmesartan provides greater protection against VIDD. Our results reveal that irbesartan does not protect against VIDD whereas olmesartan defends against both MV-induced diaphragmatic atrophy and contractile dysfunction. These findings support the hypothesis that olmesartan is superior to irbesartan in protecting against VIDD and are consistent with the concept that blockade of mechanical activation of AT1Rs is a required property of ARBs to shield against VIDD. These important findings provide a foundation for future clinical trials to evaluate ARBs as a therapy to protect against VIDD.

Chest physiotherapy for the prevention of ventilator-associated pneumonia: A meta-analysis.

BACKGROUND: Ventilator-associated pneumonia (VAP) remains a frequent and severe complication in mechanically ventilated patients. We undertook a meta-analysis to evaluate the efficacy of chest physiotherapy (CPT) for the prevention of VAP. METHODS: A systematic literature search of PubMed and Embase databases were searched up until November 25, 2018 for published studies of mechanically ventilated patients comparing CPT with controls and reporting on the occurrence of VAP. Two authors independently selected studies and abstracted data on study quality and outcomes. We pooled data using random-effects models. RESULTS: A total of 6 randomized (n = 704) controlled trials were identified. CPT did not significantly reduce the incidence of VAP (risk ratio = 1.02; 95% confidence interval, 0.82-1.26; P = .87), but reduced hospital mortality (risk ratio = 0.68; 95% confidence interval, 0.48-0.95; P = .02). No significant differences were observed regarding intensive care unit mortality, length of intensive care unit stay, and duration of mechanical ventilation. CONCLUSIONS: CPT may not significantly reduce the incidence of VAP and alter other important clinical outcomes in adult patients receiving mechanical ventilation. However, the results should be interpreted cautiously owing to the heterogeneity and the limited trials. Further large-scale, well-designed randomized controlled trials are needed.

The clinical significance of pneumonia in patients with respiratory specimens harbouring multidrug-resistant Pseudomonas aeruginosa: a 5-year retrospective study following 5667 patients in four general ICUs.

Pseudomonas aeruginosa is the leading cause of pneumonia in intensive care units (ICUs), with multidrug-resistant (MDR) strains posing a serious threat. The aim of this study was to assess the clinical relevance of MDR Pseudomonas isolates in respiratory clinical specimens. A 5-year retrospective observational study in four medical-surgical ICUs from a referral hospital was carried out. Of 5667 adults admitted to the ICU, 69 had MDR-PA in respiratory samples: 31 were identified as having pneumonia (HAP/VAP): 21 ventilator-associated pneumonia (VAP) and ten hospital-acquired pneumonia (HAP). Twenty-one (67.7%) adults with MDR-PA HAP/VAP died after a median of 4 days (18 of the 21 deaths within 8 days), compared with one (2.6%) without pneumonia at day 8. In a Cox proportional regression model, MDR-PA pneumonia was an independent variable [adjusted hazard ratio (aHR) 5.92] associated with 30-day ICU mortality. Most strains (85.1%) were susceptible to amikacin and colistin. Resistance to beta-lactams (third-generation cephalosporins and piperacillin-tazobactam) ranged from 44.1% to 45.3%. Meropenem showed poor overall activity (MIC[50/90] 16/32 mg/dL), with 47.0% having a minimum inhibitory concentration (MIC) breakpoint >8 mg/L. Twenty-four (77.4%) HAP/VAP episodes received inappropriate empirical therapy. Although empirical combination therapy was associated with less inappropriate therapy than monotherapy (16.7% vs. 88.3%, p < 0.01), there was no difference in survival (30% vs. 33.3%, p = 0.8). Pneumonia was identified in one-third of adult ICU patients harbouring MDR-PA in respiratory clinical specimens. These patients have a 6-fold risk of (early) death compared to ventilator-associated tracheobronchitis (VAT) and respiratory colonisation. New antibiotics and adjuvant therapies are urgently needed to prevent and treat MDR-PA HAP/VAP.

Safety of hyperbaric oxygen therapy in mechanically ventilated patients.

BACKGROUND: To evaluate the epidemiology of patients who require mechanical ventilation during hyperbaric oxygen therapy. MATERIALS AND METHODS: One-hundred-fifty patients who required mechanical ventilation during hyperbaric oxygen therapy were prospectively studied during a 6-year period in a French university hyperbaric centre. We analysed the indication of hyperbaric oxygen therapy, agent used for sedation, presence of a chest tube, need for vasopressor agents and tolerance and appearance of side effects. Finally, we compared the outcomes of patients according to the presence or absence of acute respiratory distress syndrome (ARDS). RESULTS: Eleven children and 139 adult patients were included (n = 150) in the study. In both populations, carbon monoxide poisoning (51%) and iatrogenic gas embolism (33%) were the two main causes of intubation and mechanical ventilation. The combination of midazolam and sufentanil was used in 85 (67%) patients. All of the patients were given a bolus of a neuromuscular blocker during the hyperbaric session, despite the presence of ARDS in 35 patients. Patient-ventilator asynchrony was the most frequent side effect in 6 (5%) patients and was often the consequence of suboptimal sedation. Mortality was higher in the group with ARDS (23%). CONCLUSIONS: Carbon monoxide poisoning and iatrogenic gas embolism are the two main diseases of the patients who required mechanical ventilation during hyperbaric oxygen therapy in this study. Mechanical ventilation is a safe method for patients during hyperbaric oxygen therapy. Sedation needs to be perfected to avoid patient-ventilator asynchrony.

Sleep in the Intensive Care Unit: A Review.

Patients in the intensive care unit (ICU) are susceptible to sleep deprivation. Disrupted sleep is associated with increased morbidity and mortality in the critically ill patients. The etiology of sleep disruption is multifactorial. The article reviews the literature on sleep in the ICU, the effects of sleep deprivation, and strategies to promote sleep in the ICU. Until the impact of disrupted sleep is better explained, it is appropriate to provide critically ill patients with consolidated, restorative sleep.

[Diagnosis and antimicrobial therapy of pneumonia caused by continuous mechanical ventilation after cardiosurgery].

The paper gives an update on the incidence and etiological structure of mechanical ventilation (MV)-associated pneumonias. The specific features of their pathogenesis are considered; clinical and laboratory diagnostic methods are reviewed. It is shown that it is necessary to make a microbiological monitoring. An algorithm is proposed to choose the tactics of antimicrobial treatment for MV-associated pneumonia; recommendations for the rational choice of antibiotics are given.

Genetic and pharmacologic evidence links oxidative stress to ventilator-induced lung injury in mice.

RATIONALE: Mechanical ventilation (MV) is an indispensable therapy for critically ill patients with acute lung injury and the adult respiratory distress syndrome. However, the mechanisms by which conventional MV induces lung injury remain unclear. OBJECTIVES: We hypothesized that disruption of the gene encoding Nrf2, a transcription factor that regulates the induction of several antioxidant enzymes, enhances susceptibility to ventilator-induced lung injury (VILI) and that antioxidant supplementation attenuates this effect. METHODS: To test our hypothesis and to examine the relevance of oxidative stress in VILI, we assessed lung injury and inflammatory responses in Nrf2-deficient (Nrf2(-/-)) mice and wild-type (Nrf2(+/+)) mice after an acute (2-h) injurious model of MV with or without administration of antioxidant. MEASUREMENTS AND MAIN RESULTS: Nrf2(-/-) mice displayed greater levels of lung alveolar and vascular permeability and inflammatory responses to MV as compared with Nrf2(+/+) mice. Nrf2 deficiency enhances the levels of several proinflammatory cytokines implicated in the pathogenesis of VILI. We found diminished levels of critical antioxidant enzymes and redox imbalance by MV in the lungs of Nrf2(-/-) mice; however, antioxidant supplementation to Nrf2(-/-) mice remarkably attenuated VILI. When subjected to a clinically relevant prolong period of MV, Nrf2(-/-) mice displayed greater levels of VILI than Nrf2(+/+) mice. Expression profiling revealed lack of induction of several VILI genes, stress response and solute carrier proteins, and phosphatases in Nrf2(-/-) mice. CONCLUSIONS: Our data demonstrate for the first time a critical role for Nrf2 in VILI, which confers protection against cellular responses induced by MV by modulating oxidative stress.

Relationship of minimal inhibitory concentration and bactericidal activity to efficacy of antibiotics for treatment of ventilator-associated pneumonia.

Although minimal inhibitory concentration (MIC) and minimal bactericidal concentration (MBC) have been used as the most popular prediction tools for antimicrobial action, they have shortcomings. The MIC and MBC do not consider time-related antimicrobial effects, such as killing rate and postantibiotic effect. In this regard, the concept of pharmacokinetic and pharmacodynamic (PK/PD) modeling has been introduced to help interpret determinations of susceptibility breakpoints. Although area under the inhibitory concentration-time curve (AUIC) can be used as a universal PK/PD parameter, target magnitudes of the parameter have to be high enough to exert rapid bactericidal activity (> 250) and to prevent selection and induction of resistance (> 100). For vancomycin used in treatment of methicillin-resistant Staphylococcus aureus pneumonia, a much higher AUIC (400) is suggested to avoid treatment failure. For resistant gram-negative bacteria, such as Pseudomonas aeruginosa, the usual dosage of fourth-generation cephalosporins, carbapenems, and fluoroquinolones cannot achieve the target AUICs. Either combination therapy or higher dosage should be administered to achieve target AUICs and prevent the potential for failure. Unresolved issues, such as influence of protein binding, PK/PD at tissue sites versus blood, the impact of the immune system, should be addressed to refine the applicability of PK/PD in antibiotic treatment.

Effects of body temperature on ventilator-induced lung injury.

PURPOSE: To evaluate the effects of body temperature on ventilator-induced lung injury. MATERIAL AND METHODS: Thirty-four male Sprague-Dawley rats were randomized into 6 groups based on their body temperature (normothermia, 37 +/- 1 degrees C; hypothermia, 31 +/- 1 degrees C; hyperthermia, 41 +/- 1 degrees C). Ventilator-induced lung injury was achieved by ventilating for 1 hour with pressure-controlled ventilation mode set at peak inspiratory pressure (PIP) of 30 cmH2O (high pressure, or HP) and positive end-expiratory pressure (PEEP) of 0 cmH2O. In control subjects, PIP was set at 14 cmH2O (low pressure, or LP) and PEEP set at 0 cmH2O. Systemic chemokine and cytokine (tumor necrosis factor alpha , interleukin 1 beta , interleukin 6, and monocyte chemoattractant protein 1) levels were measured. The lungs were assessed for histological changes. RESULTS: Serum chemokines and cytokines were significantly elevated in the hyperthermia HP group compared with all 3 groups, LP (control), normothermia HP, and hypothermia HP. Oxygenation was better but not statistically significant in hypothermia HP compared with other HP groups. Cumulative mean histology scores were higher in hyperthermia HP and normothermia HP groups compared with control and normothermia HP groups. CONCLUSIONS: Concomitant hyperthermia increased systemic inflammatory response during HP ventilation. Although hypothermia decreased local inflammation in the lung, it did not completely attenuate systemic inflammatory response associated with HP ventilation.

Ventilator-associated pneumonia by Staphylococcus aureus. Comparison of methicillin-resistant and methicillin-sensitive episodes.

All episodes of ventilator-associated pneumonia (VAP) caused by Staphylococcus aureus were prospectively analyzed for a 30-mo period. Methicillin-sensitive S. aureus (MSSA) was isolated in 38 episodes and methicillin-resistant S. aureus (MRSA) in 11 others. The two groups were similar regarding sex, severity of underlying diseases, prior surgery, and presence of renal failure, diabetes, cardiopathy, and coma. MRSA-infected persons were more likely to have received steroids before developing infection (relative risk [RR] = 3.45, 95% confidence interval [CI] = 1.38-8.59), to have been ventilated > 6 d (RR = 2.03, 95% CI = 1.36-3.03), to have been older than 25 yr (RR = 1.50, 95% CI = 1.09-2.06), and to have had preceding chronic obstructive pulmonary disease (RR = 2.76, 95% CI = 0.89-8.56) than MSSA-infected patients. MSSA-infected persons were more likely than MRSA-infected patients to have cranioencephalic trauma (RR = 1.94, 95% CI = 1.22-3.09). All patients with MRSA VAP had previously received antibiotics, compared with only 21.1% of those with MSSA infection (p < 0.000001). The incidence of empyema was similar in both groups; nevertheless, the presence of bacteremia and septic shock was more frequent in the MRSA group. Finally, mortality directly related to pneumonia was significantly higher among patients with MRSA episodes (RR = 20.72, 95% CI = 2.78-154.35). This analysis was repeated for monomicrobial episodes, and the difference remained statistically significant. We conclude that MRSA and MSSA strains infect patients with different demographic profiles; previous antibiotic therapy is the most important risk factor for developing MRSA infection.(ABSTRACT TRUNCATED AT 250 WORDS)