Entries Tagged as 'Proc Am Thorac Soc'
Computed tomography-detected noncalcified pulmonary nodules: a review of evidence for significance and management.
Proc Am Thorac Soc. 2008 Dec 15;5(9):900-4
Authors: McWilliams A, Mayo J
Our purpose was to review the reported behavior and malignant risk of small noncalcified pulmonary nodules detected by computed tomography (CT). A review of published clinical guidelines and studies using CT scan for lung cancer screening was performed. Small pulmonary nodules are found in 5 to 60% of patients in published CT screening studies. The detection rate is influenced by the CT scan technique used, definition of a significant nodule, and the population of subjects screened. There is limited published systematic longitudinal observation of all nodules of any size. The malignancy rate of small nodules detected in smokers is likely less than 1 to 2%, and predictors of malignancy include semisolid appearance, diameter greater than or equal to 10 mm or persistent growth on greater than or equal to two CT scans. There is a wide variation in the performance of positron emission tomography (PET) scan in screening detected lung cancers. In summary, multidetector row CT detects greater than or equal to 1 nodule in most high-risk patients. The risk of malignancy for a single nodule appears to be low, but is increased by serial growth, diameter greater than or equal to 10 mm, and semisolid appearance. The role of PET in evaluating these nodules needs further exploration. Serial follow-up for 24 months in a high-risk cohort appears reasonable based on present data, but further longitudinal information is required.
PMID: 19056713 [PubMed - indexed for MEDLINE]
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Cardiac disease in chronic obstructive pulmonary disease.
Proc Am Thorac Soc. 2008 May 1;5(4):543-8
Authors: Falk JA, Kadiev S, Criner GJ, Scharf SM, Minai OA, Diaz P
The cardiac manifestations of chronic obstructive pulmonary disease (COPD) are numerous. Impairments of right ventricular dysfunction and pulmonary vascular disease are well known to complicate the clinical course of COPD and correlate inversely with survival. The pathogenesis of pulmonary vascular disease in COPD is likely multifactorial and related to alterations in gas exchange and vascular biology, as well as structural changes of the pulmonary vasculature and mechanical factors. Several modalities currently exist for the assessment of pulmonary vascular disease in COPD, but right heart catheterization remains the gold standard. Although no specific therapy other than oxygen has been generally accepted for the treatment of pulmonary hypertension in this population, there has been renewed interest in specific pulmonary vasodilators. The coexistence of COPD and coronary artery disease occurs frequently. This association is likely related to shared risk factors as well as similar pathogenic mechanisms, such as systemic inflammation. Management strategies for the care of patients with COPD and coronary artery disease are similar to those without COPD, but care must be given to address their respiratory limitations. Arrhythmias occur frequently in patients with COPD, but are rarely fatal and can generally be treated medically. Use of beta-blockers in the management of cardiac disease, while a theoretical concern in patients with increased airway resistance, is generally safe with the use of cardioselective agents.
PMID: 18453369 [PubMed - indexed for MEDLINE]
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Acute exacerbations and respiratory failure in chronic obstructive pulmonary disease.
Proc Am Thorac Soc. 2008 May 1;5(4):530-5
Authors: MacIntyre N, Huang YC
Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) describe the phenomenon of sudden worsening in airway function and respiratory symptoms in patients with COPD. These exacerbations can range from self-limited diseases to episodes of florid respiratory failure requiring mechanical ventilation. The average patient with COPD experiences two such episodes annually, and they account for significant consumption of health care resources. Although bacterial infections are the most common causes of AECOPD, viral infections and environmental stresses are also implicated. AECOPD episodes can be triggered or complicated by other comorbidities, such as heart disease, other lung diseases (e.g., pulmonary emboli, aspiration, pneumothorax), or systemic processes. Pharmacologic management includes bronchodilators, corticosteroids, and antibiotics in most patients. Oxygen, physical therapy, mucolytics, and airway clearance devices may be useful in selected patients. In hypercapneic respiratory failure, noninvasive positive pressure ventilation may allow time for other therapies to work and thus avoid endotracheal intubation. If the patient requires invasive mechanical ventilation, the focus should be on avoiding ventilator-induced lung injury and minimizing intrinsic positive end-expiratory pressure. These may require limiting ventilation and “permissive hypercapnia.” Although mild episodes of AECOPD are generally reversible, more severe forms of respiratory failure are associated with a substantial mortality and a prolonged period of disability in survivors.
PMID: 18453367 [PubMed - indexed for MEDLINE]
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