Chest
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Dyspnea is an uncomfortable sensation with the potential to cause psychological trauma. Patients presenting with acute respiratory failure, particularly when tidal volume is restricted during mechanical ventilation, may experience the most distressing form of dyspnea known as air hunger. Air hunger activates brain pathways known to be involved in posttraumatic stress disorder (PTSD), anxiety, and depression. ⋯ We suggest such efforts will be more successful if they are directed at the known mechanisms of air hunger. Investigation of the antidyspnea effects of sedative and analgesic drugs commonly used in the ICU and their impact on post-ARDS PTSD symptoms is a logical next step. Although in practice we often accept negative consequences of life-saving therapies as unavoidable, we must understand the negative sequelae of our therapies and work to minimize them under our primary directive to "first, do no harm" to patients.
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Review Case Reports
How I Do It: Approach to Eosinophilia Presenting with Pulmonary Symptoms.
Eosinophilia with pulmonary involvement is characterized by the presence of peripheral blood eosinophilia, typically ≥500 cells/mm3, by pulmonary symptoms and physical examination findings that are nonspecific, and by radiographic evidence of pulmonary disease and is further supported by histopathologic evidence of tissue eosinophilia in a lung or pleura biopsy specimen and/or increased eosinophils in BAL fluid, usually >10%. Considering that there are a variety of underlying causes of eosinophilia with pulmonary manifestations and overlapping clinical, laboratory, and radiologic features, it is essential to approach the evaluation of eosinophilia with pulmonary findings systematically. ⋯ Overall, optimal management of eosinophilic lung disease presentations are directed at the underlying cause when identifiable, and the urgency of treatment may be guided by the presence of severe end-organ involvement or life-threatening complications. When an underlying cause is not easily attributable, management of eosinophilia with pulmonary involvement largely relies on eosinophil-directed interventions, for which biologic therapies are increasingly being used.
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A right heart catheterization with measurements of pulmonary artery wedge pressure (PAWP) may be necessary for the diagnosis of left heart failure as a cause of pulmonary hypertension or unexplained dyspnea. Diagnostic cutoff values are a PAWP of ≥ 15 mm Hg at rest or a PAWP of ≥ 25 mm Hg during exercise. However, accurate measurement of PAWP can be challenging and heart failure may be occult. ⋯ The procedure is simple and does not take much catheterization laboratory time. Combining echocardiography with invasive measurements may increase the diagnostic accuracy of diastolic dysfunction. Cardiac output after a fluid challenge may be of prognostic relevance.
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Multicenter Study
Lung-Protective Ventilation and Associated Outcomes and Costs Among Patients Receiving Invasive Mechanical Ventilation in the Emergency Department.
Invasive mechanical ventilation is often initiated in the ED, and mechanically ventilated patients may be kept in the ED for hours before ICU transfer. Although lung-protective ventilation is beneficial, particularly in ARDS, it remains uncertain how often lung-protective tidal volumes are used in the ED, and whether lung-protective ventilation in this setting impacts patient outcomes. ⋯ Use of lung-protective ventilation in the ED was associated with important patient- and system-centered outcomes, including lower hospital mortality, decreased incidence of ARDS, lower hospital length of stay, and decreased total costs. Protocol development promoting the regular use of lung-protective ventilation in the ED may be of value.
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Case Reports
Acute Tracheal Necrosis After Intubation in a Childhood Onset Systemic Lupus Erythematosus.
Upper airway involvement in systemic lupus erythematosus (SLE) disease process is uncommon. A 15-year-old girl, a known patient with class IVA lupus nephritis, presented in acute renal failure due to flare-up of SLE. ⋯ After 36 hours of extubation, she developed biphasic stridor and severe shortness of breath that was unresponsive to multiple medications. Prompt airway evaluation by laryngoscopy and confirmation of acute tracheal necrosis by histopathology along with reintubation and high-dose steroid therapy resulted in good outcome and recovery.