Seminars in respiratory and critical care medicine
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Semin Respir Crit Care Med · Apr 2022
New Insights in the Pathophysiology of Hospital- and Ventilator-Acquired Pneumonia: A Complex Interplay between Dysbiosis and Critical-Illness-Related Immunosuppression.
Both hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP) have long been considered as diseases resulting from the invasion by pathogens of a previously sterile lung environment. Based on this historical understanding of their pathophysiology, our approaches for the prevention and treatment have significantly improved the outcomes of patients, but treatment failures remain frequent. Recent studies have suggested that the all-antimicrobial therapy-based treatment of pneumonia has reached a glass ceiling. ⋯ We proposed that HAP and VAP should be considered as a state of dysbiosis, defined as the emergence of a dominant pathogen thriving at the same time from the catastrophic collapse of the fragile ecosystem of the lower respiratory tract and from the development of critical-illness-related immunosuppression. This multidimensional approach to the pathophysiology of HAP and VAP holds the potential to achieve future successes in research and critical care. Microbiome and mucosal immunity can indeed be manipulated and used as adjunctive therapies or targets to prevent or treat pneumonia.
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Semin Respir Crit Care Med · Apr 2022
Viral Ventilator-Associated Pneumonia/Hospital-Acquired Pneumonia.
Among the viruses possibly responsible for hospital-acquired and ventilator-associated pneumonia, herpes simplex virus (HSV) is probably the most often involved: HSV reactivation is frequent in intensive care unit patients, and lung parenchymal infection (HSV bronchopneumonitis) has been well described, either using cytological signs of parenchymal involvement in cells obtained during bronchoalveolar lavage or using HSV virus load in the lower respiratory tract. Although treating patients with HSV bronchopneumonitis may be recommended, based on expert opinion, prophylactic or preemptive treatment of HSV reactivation should be avoided. ⋯ No data exists on the impact of antiviral treatment on CMV pneumonia. The involvement of respiratory viruses has been described in patients with healthcare-associated pneumonia and hospital-acquired pneumonia, but their role in ventilator-associated pneumonia is not clear.
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Nosocomial pneumonia, including hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP), are the most common nosocomial infections occurring in critically ill patients requiring intensive care. However, challenges exist in making a timely and accurate diagnosis of HAP and VAP. Under diagnosis of HAP and VAP can result in greater mortality risk, especially if accompanied by delays in the administration of appropriate antimicrobial treatment. ⋯ Optimal diagnosis and management of HAP and VAP require a systematic approach that combines clinical and radiographic assessments along with proper microbiologic techniques. The use of more invasive sampling methods (bronchoalveolar lavage and protected specimen brush) may enhance specimen collection resulting in more specific diagnoses to limit unnecessary antibiotic exposure. Molecular techniques, currently in use and investigational technique, may improve the diagnosis of HAP and VAP by allowing more rapid identification of offending pathogens, if present, thus increasing both appropriate antibiotic treatment and avoiding unnecessary drug exposure.
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Semin Respir Crit Care Med · Apr 2022
Defining Clinical and Microbiological Nonresponse in Ventilator-Associated Pneumonia.
Ventilator-associated pneumonia (VAP) is a severe complication of mechanical ventilation, with mortality reduced most effectively by adequate early antibiotic treatment. The clinical and microbiologic response can be assessed easily from 72 hours after starting antibiotic treatment. Evidence of nonresponse is based on several factors: (1) lack of clinical improvement, (2) radiographic progression, (3) an impaired Sequential Organ Failure Assessment (SOFA) score, (4) no improvement by days 3 to 5 on the Clinical Pulmonary Infection Score (CPIS), (5) no decreased in biomarkers on day 3, and (6) isolation of a new pathogen on day 3. ⋯ Physicians must evaluate whether treatments are adequate in terms of sensitivity, dose, and route. Pharmacokinetically and pharmacodynamically optimized doses are recommended in these patients. Clinical stabilization of comorbidities or underlying conditions may be of benefit.