Executive Summary Introduction Methodology Used to Prepare the Guideline Epidemiology Incidence Etiology Major Epidemiologic Points Pathogenesis Major Points for Pathogenesis Modifiable Risk Factors Intubation and Mechanical Ventilation Aspiration, Body Position, and Enteral Feeding Modulation of Colonization: Oral Antiseptics and Antibiotics Stress Bleeding Prophylaxis, Transfusion, and Glucose Control Major Points and Recommendations for Modifiable Risk Factors Diagnostic Testing Major Points and Recommendations for Diagnosis Diagnostic Strategies and Approaches Clinical Strategy Bacteriologic Strategy Recommended Diagnostic Strategy Major Points and Recommendations for Comparing Diagnostic Strategies Antibiotic Treatment of Hospital-acquired Pneumonia General Approach Initial Empiric Antibiotic Therapy Appropriate Antibiotic Selection and Adequate Dosing Local Instillation and Aerosolized Antibiotics Combination versus Monotherapy Duration of Therapy Major Points and Recommendations for Optimal Antibiotic Therapy Specific Antibiotic Regimens Antibiotic Heterogeneity and Antibiotic Cycling Response to Therapy Modification of Empiric Antibiotic Regimens Defining the Normal Pattern of Resolution Reasons for Deterioration or Nonresolution Evaluation of the Nonresponding Patient Major Points and Recommendations for Assessing Response to Therapy Suggested Performance Indicators

Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia the official statement of the American Thoracic Society and the Infectious Disease Society of America (特集 救急診療ガイドライン) -- (海外のガイドライン)

Ventilator-associated pneumonia (VAP) continues to complicate the course of 8 to 28% of patients receiving mechanical ventilation (MV). In contrast to infections of more frequently involved organs (e.g., urinary tract and skin), for which mortality is low, ranging from 1 to 4%, the mortality rate for VAP ranges from 24 to 50% and can reach 76% in some specific settings or when lung infection is caused by high-risk pathogens. The predominant organisms responsible for infection are Staphylococcus aureus, Pseudomonas aeruginosa, and Enterobacteriaceae, but etiologic agents widely differ according to the population of patients in an intensive care unit, duration of hospital stay, and prior antimicrobial therapy. Because appropriate antimicrobial treatment of patients with VAP significantly improves outcome, more rapid identification of infected patients and accurate selection of antimicrobial agents represent important clinical goals. Our personal bias is that using bronchoscopic techniques to obtain protected brush and bronchoalveolar lavage specimens from the affected area in the lung permits physicians to devise a therapeutic strategy that is superior to one based only on clinical evaluation. When fiberoptic bronchoscopy is not available to physicians treating patients clinically suspected of having VAP, we recommend using either a simplified nonbronchoscopic diagnostic procedure or following a strategy in which decisions regarding antibiotic therapy are based on a clinical score constructed from seven variables. Selection of the initial antimicrobial therapy should be based on predominant flora responsible for VAP at each institution, clinical setting, information provided by direct examination of pulmonary secretions, and intrinsic antibacterial activities of antimicrobial agents and their pharmacokinetic characteristics. Further trials will be needed to clarify the optimal duration of treatment and the circumstances in which monotherapy can be safely used.

Ventilator-associated pneumonia.

Linda Nici, Claudio Donner, Emiel Wouters, Richard Zuwallack, Nicolino Ambrosino, Jean Bourbeau, Mauro Carone, Bartolome Celli, Marielle Engelen, Bonnie Fahy, Chris Garvey, Roger Goldstein, Rik Gosselink, Suzanne Lareau, Neil MacIntyre, Francois Maltais, Mike Morgan, Denis O’Donnell, Christian Prefault, Jane Reardon, Carolyn Rochester, Annemie Schols, Sally Singh, and Thierry Troosters, on behalf of the ATS/ERS Pulmonary Rehabilitation Writing Committee

/pdf/american-thoracic-society-european-respiratory-society-fshcxcru7i.pdf

American Thoracic Society/European Respiratory Society Statement on Pulmonary Rehabilitation

Inadequate Antimicrobial Treatment of Infections: A Risk Factor for Hospital Mortality Among Critically Ill Patients

http://www.zirkin.com/em/articles/General%20Critical%20Care/Theinfluenceofinadequateantimicrobialtreatmentofbloodstreami.pdf

The influence of inadequate antimicrobial treatment of bloodstream infections on patient outcomes in the ICU setting

Impact of BAL data on the therapy and outcome of ventilator-associated pneumonia

Effects of Supplemental Oxygen During Activity in Patients With Advanced COPD Without Severe Resting Hypoxemia

Pulmonary lymphangiomyomatosis associated with tuberous sclerosis. Treatment with tamoxifen and tetracycline-pleurodesis.

Effect of Tracheal Dilatation and Rupture on Mechanical Ventilation Using a Low-Pressure Cuff Tube

Benzodiazepines are known to cause muscle hypotonia, but their effects on respiratory muscle function, particularly on diaphragm, have not yet been studied. Our aim was to look for any effect of lorazepam on respiratory muscle function in patients with chronic obstructive pulmonary disease (COPD). Nine stable COPD patients (mean +/- SD forced expiratory volume in one second (FEV1) 0.91 +/- 0.31 l) were included in the study. The following measurements were performed before and 1 hour after lorazepam administration (doses: 1.5 to 2 mg) by sublingual route: forced vital capacity (FVC), FEV1, maximal voluntary ventilation (MVV), arterial oxygen tension (PaO2), arterial carbon dioxide tension (PaCO2), minute ventilation (Ve), tidal volume (Vt), respiratory rate (f), inspiratory time/inspiratory plus expiratory time (Ti/Ttot)-, mean inspiratory flow (Vi), maximal inspiratory (MIP) and expiratory (MEP) pressures, maximal pleural pressure (Pplmax), transdiaphragmatic pressures (Pdi) and skeletal muscle strength and endurance. As expected, no change was noted in FVC, FEV1, FEV1/FVC (Table-1). Besides stability of expiratory flows, this denotes no change in collaboration in spite of the sedative effects of lorazepam. There was a 20% decrease in Ve, due to a Vt reduction and a small increase in PaCO2. These could be explained by the central effects of benzodiazepines. Skeletal muscle strength and endurance decreased significantly (22 and 50% respectively-Table 2), in accordance with the previously reported muscular actions of this pharmacological group. Respiratory muscle function parameters, MIP, MEP, MVV and Ppl showed significant reductions (10 to 20 per cent), as was the case with diaphragmatic function measured by Pdi (Muller maneuver with abdominal protrussion and maximal open-glottis expulsive maneuver) (Table 3). This study demonstrates that a single lorazepam dose reduces strength and endurance of respiratory muscle in chronic stable COPD patients.

Enrique C. Jolly

Papers

Impact of BAL data on the therapy and outcome of ventilator-associated pneumonia

Effects of Supplemental Oxygen During Activity in Patients With Advanced COPD Without Severe Resting Hypoxemia

Pulmonary lymphangiomyomatosis associated with tuberous sclerosis. Treatment with tamoxifen and tetracycline-pleurodesis.

Effect of Tracheal Dilatation and Rupture on Mechanical Ventilation Using a Low-Pressure Cuff Tube

Acute effect of lorazepam on respiratory muscles in stable patients with chronic obstructive pulmonary disease