China
Africa
Explore chapters and articles related to this topic
Pulmonary Function Testing
Published in Pudupakkam K Vedanthan, Harold S Nelson, Shripad N Agashe, PA Mahesh, Rohit Katial, Textbook of Allergy for the Clinician, 2021
Ekta Kakkar, Flavia CL Hoyte, Devasahayam J Christopher, Rohit K Katial
Pulmonary function testing helps to differentiate between obstructive and restrictive lung disease. Obstructive lung disease is characterized by obstruction or narrowing of the airways. This is often due to excessive smooth muscle contraction. Examples of obstructive lung disease include asthma, Chronic Obstructive Pulmonary Disease (COPD) and bronchiectasis. Restrictive lung disease is characterized by the inability to fully expand the lungs. This results in decreased lung volume and increased work of breathing. Restrictive lung disease can be due to occupational exposures, medications, neuromuscular disorders or pulmonary fibrosis. Extrinsic diseases can also restrict expansion of the lung. For a comprehensive list of etiologies of restrictive lung disease see Table 16.1 (Johnson et al. 2014).
Case 46
Published in Edward Schwarz, Tomos Richards, Cases of a Hollywood Doctor, 2019
Edward Schwarz, Tomos Richards
The causes of an obstructive pattern include: asthma, COPD, bronchiectasis and cystic fibrosis. The conditions causing restrictive lung disease include: pulmonary fibrosis, sarcoidosis, obesity, kyphoscoliosis, asbestosis and neuromuscular disease.
Dyspnea in Asthma and Restrictive Lung Disease
Published in Donald A. Mahler, Denis E. O’Donnell, Dyspnea, 2014
Pierantonio Laveneziana, Giorgio Scano
Restrictive lung disease is a broad term encompassing several conditions in which lung volumes are reduced. Interstitial lung disease (ILD) is the prototypical restrictive disease. Dyspnea is a common clinical manifestation of ILD. Activity-related dyspnea appears to be the earliest and dominant symptom limiting exercise in the majority of patients afflicted by ILD. This symptom progresses relentlessly with time leading invariably to avoidance of activity with consequent skeletal muscle deconditioning and poor perceived quality of life. Effective management of this symptom awaits a better understanding of its underlying physiology.
Indwelling tunneled pleural catheters in patients with hepatic hydrothorax: A single-center analysis for outcomes and complications
Published in Canadian Journal of Respiratory, Critical Care, and Sleep Medicine, 2023
Fatmah F. Alhabeeb, Katia Carle-Talbot, Natalie Rakocevic, Tinghua Zhang, Michael Mitchell, Kayvan Amjadi, Chanel Kwok
Analysis of the chest x-ray scores demonstrate that the majority of patients had a large pleural effusion at the time of insertion, and many failed to completely expand despite the insertion of a catheter. We think that this is likely due to the development of trapped lung, as demonstrated by the radiographic evidence of volume loss, premature cessation of drainage due to pain (1 patient), and residual effusion post-drainage (2 patients with persistent moderate effusion, 1 patient with hydro-pneumothorax). However, given the lack of manometry data, we can use the term “non-expanding lung” instead. This highlights the possibility of developing progressive volume loss and parenchymal stiffening as a result of chronic effusion, even if the underlying etiology is benign. The current fear surrounding pleural interventions in HH may result in unnecessary delays in facilitating lung expansion and may contribute to the development of non-expanding lung. Perhaps earlier intervention with an IPC could prevent the development of this permanent, restrictive lung disease in some patients.
Using quantitative computed tomography to predict mortality in patients with interstitial lung disease related to systemic sclerosis: implications for personalized medicine
Published in Expert Review of Precision Medicine and Drug Development, 2021
Alarico Ariani, Nicola Sverzellati, Andrea Becciolni, Gianluca Milanese, Mario Silva
There are reservations about the reliability of this approach. First, it appears to be too complicated and time-consuming to be implemented in clinical practice [62]. Furthermore, the judgment of progression of restrictive lung disease must be considered with extreme caution [64]. In fact, volumes (normal vs fibrotic lung) and their relationship are altered by the morphological changes that reduce the geometry of the lung. These areas and volumes can be modified in an unpredictable way by fibrotic lesions, resulting in an overall reduction of the lung section (if the restrictive fibrotic evolution prevails) [65] or an increase for the coexistence of emphysema or bronchiectasis, related to the traction suffered by the lung parenchyma [66]. Furthermore, the segmentation of lung volumes requires a correction by the operator who must eliminate from the ROI, structures not belonging to the lung [67].
Features of Marfan syndrome not listed in the Ghent nosology – the dark side of the disease
Published in Expert Review of Cardiovascular Therapy, 2019
Yskert von Kodolitsch, Anthony Demolder, Evaldas Girdauskas, Harald Kaemmerer, Katharina Kornhuber, Laura Muino Mosquera, Shaine Morris, Enid Neptune, Reed Pyeritz, Svend Rand-Hendriksen, Alexander Rahman, Nina Riise, Leema Robert, Ingmar Staufenbiel, Katalin Szöcs, Thy Thy Vanem, Stephan J. Linke, Marina Vogler, Anji Yetman, Julie De Backer
The lung manifestations of Marfan syndrome are burdensome and complex [169]. More importantly, they can lead to substantial disability and reduced quality of life. Scoliosis, pectus deformities and respiratory muscle weakness contribute to restrictive lung disease. Parenchymal lung disease, often developmental in origin, leads to upper lobe blebs, pneumothoraces and, especially in the setting of neonatal Marfan syndrome, overt emphysema. Both chest wall deformities and airway wall defects can manifest disorders such as asthma and bronchiectasis. Finally, soft tissue laxity and a predilection for upper airway obstruction confer the high prevalence of sleep-disordered breathing. This spectrum of lung disorders is challenging for care providers who often have to evaluate dyspnea, chest pain and reduced exercise capacity in the context of the known risks of highly morbid and fatal cardiac and aortic disease. Unfortunately, no reliable contemporary (post-Ghent 2010) assessment of lung disease prevalence is available given that screening for pulmonary impairment is inconsistent across centers and mostly symptom- or finding-triggered [170]. However, even small, single-center retrospective studies confirm a high burden of respiratory disease in Marfan syndrome [171].