Effect of asbestos-related pleural fibrosis on excursion of the lower chest wall and diaphragm

Department of Pulmonary Physiology, Sir Charles Gairdner Hospital, Nedlands, Australia.
American Journal of Respiratory and Critical Care Medicine (Impact Factor: 13). 11/1999; 160(5 Pt 1):1507-15. DOI: 10.1164/ajrccm.160.5.9806135
Source: PubMed


To examine mechanisms responsible for reduced lung volumes (restriction) in asbestos-related pleural fibrosis (APF), we studied diaphragm function and lower rib-cage excursion in 26 subjects with previous asbestos exposure and no evidence of asbestosis. Using posteroanterior (PA) and lateral chest radiographs taken at residual volume and at 25%, 70%, and 100% vital capacity (VC) during a slow inspiratory maneuver, we measured fractional expansion of the lower rib cage (FErc), fractional shortening of the diaphragm (FSdi), and changes (Delta) in diaphragm dome height (Hdo) and subphrenic volume (Vdi). Vdi was estimated by measuring the major and minor axes of the subphrenic space at 1-cm intervals, assuming an elliptical cross-sectional shape, and correcting for the volume of spinal and paraspinal tissues. Seven subjects had no evidence of APF (control), 12 had pleural plaques (PP), and seven had diffuse pleural thickening with costophrenic obliteration (DPT). Over the range of VC, results (mean +/- SEM, normalized for height) in control subjects were VC = 101.2 +/- 4.0 % predicted and DeltaVdi = 326 +/- 8 ml/m(3), and for the right hemithorax and hemidiaphragm on the PA film, FErc = 0.07 +/- 0.02, FSdi = 0.32 +/- 0.02 and DeltaHdo = 0.8 +/- 0.2 cm/m. Relative to controls: DPT subjects had reduced VC (77.4 +/- 4.9%, p < 0.01), DeltaVdi (256 +/- 2 ml/m(3), p < 0.01), FErc (0.01 +/- 0.02, p < 0.01), FSdi (0.24 +/- 0.01, p < 0.001), and DeltaHdo (-0.9 +/- 0.06 cm/m, p < 0.01); PP subjects had reduced FSdi (0.25 +/- 0.01, p < 0.001) and DeltaVdi (233 +/- 47 ml/m(3), p < 0.01), and no difference in FErc, DeltaHdo, or VC. We conclude that restriction in DPT is due to obliteration of the zone of apposition, and that by limiting separation of the diaphragm from the rib cage during inspiration, this reduces volume contributed by motion of the diaphragm and lower rib cage. Reduction in the latter contribution was the main cause of restriction, because the reduction in volume contributed by the diaphragm was partly compensated by flattening of its dome.

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    • "Quite possibly, the proprioception of breathing arises mostly in the intercostal muscles (Sant'Ambrogio and Widdicombe, 1965). In a healthy body, the diaphragm's excursion will always be dictated by the motion of the ribcage, and its healthy shape always tends to be an expiratory, high dome and an inspiratory, low dome moving in the posterior direction with increasing lung volume (Singh et al., 1999). However, the muscular pattern of breathing can vary dramatically from conscious control or the effect of disease. "
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    ABSTRACT: Buddhist statues may provide kinesthetic lessons relating the human body's actions and the spiritual life. This two-part paper presents a descriptive analysis of a statue of a meditating Buddha sitting in lotus pose. The statue, from the ancient Javanese monument, Borobudur, is correlated with Iyengar yoga and therapeutic soft-tissue manipulation. In addition, discussion is presented of the statue as a history of Hindu pranayama and Buddhist meditation practices. The three-dimensional modeling of the Buddha's torso is evaluated from the perspective of anatomy and the movement arts. A resulting somatic vocabulary presents Asian art without emphasizing textual discourse and analysis of esthetic motifs so that the art presents a kinesthetic lesson on the ideal connection between the human body's actions and the spiritual life. Central to this paper is the presumption that sculpture depicts the kinesthetics of breathing but must be carefully teased apart from historical anachronism.
    Journal of Bodywork and Movement Therapies 07/2007; 11(3):214-222. DOI:10.1016/j.jbmt.2007.04.004
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    • "Dysfunction of the diaphragm can cause breathlessness, reduced exercise tolerance, respiratory failure, and death. Singh et al. [14] have recently developed a fluoroscopic method for quantifying excursion of the diaphragm during each breath that may provide clinicians with valuable information about diaphragm function [13] [15] [16]. Use of this method has been facilitated by computerized analysis [12] and would be further automated by the ability to track the contour of the diaphragm during respiration [6] "
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    ABSTRACT: A semi-automatic method is described for tracking the contour of the diaphragm in lateral X-ray image sequences. It is part of a method being developed to quantify diaphragm function non-invasively. Initialization is achieved by interactive segmentation of the diaphragm contour and identification of landmarks. The method relies on modelling the contour using an augmented active contour model incorporating anatomical constraints. The contour is then tracked iteratively across successive frames using reduced-search space dynamic programming. The method has been tested on several image sequences and preliminary results are promising with an 85.3 % tracking accuracy for one such sequence.
    Digital Image Computing: Techniques and Applications, 2005. DICTA '05. Proceedings 2005; 01/2006
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    • "Pro Milliliter Volumenzunahme der Pleurafibrose kam es in dieser Studie zu einem Abfall der TLC von 5 ml [18]. Inwieweit Pleuraveränderungen die Atemmechanik beeinflussen, untersuchten Singh et al. [20]. Sie fanden heraus, dass es bei diffusen Pleuraverdickungen zu einer Verringerung sowohl der Verkürzung des Diaphragmas, als auch der Ausdehnung des unteren Brustkorbes bei der Inspiration kommt. "
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    ABSTRACT: Diese Studie beschreibt den Einfluss von im HRCT diagnostizierten asbestassoziierten Pleuraplaques und der kumulativen Asbestexposition, unabhängig von pleuralen oder parenchymalen Veränderungen, auf die Lungenfunktion. Ebenfalls wurde der Unterschied zwischen den Korrelationen der Lungenfunktion zu entweder durch HRCT oder durch konventionelles Röntgen diagnostizierten Pleuraplaques ermittelt. Das Untersuchungskollektiv umfasste 319 asbestexponierte Personen, bei denen durch HRCT parenchymale Veränderungen ausgeschlossen worden waren. Weder die Ausdehnung, die Dicke und die Verkalkung asbestassoziierter Pleuraplaques noch die kumulative Asbestexposition, unabhängig von pleuralen oder parenchymalen Veränderungen, zeigten einen Einfluss auf die Lungenfunktion. Die statistischen Auffälligkeiten, die sich bei der Untersuchung der Lokalisation bei ventral gelegenen verkalkten Plaques für das RV und den Quotienten RV/TLC und bei kranial gelegenen für die VCIN und die FVC ergaben, lassen sich am ehesten durch Zufall erklären. Ein Unterschied zwischen den Korrelationen von durch HRCT und durch konventionelles Röntgen diagnostizierten Plaques zur Lungenfunktion konnte nicht nachgewiesen werden; beide Korrelationen waren äußerst gering. This study describes the influence of HRCT-diagnosed asbestos related pleural plaques and cumulative asbestos exposure, independently of pleural and parenchymal variances, on lung function. Furthermore the difference between the correlations of lung function to pleural plaques, diagnosed either by HRCT or conventional radiographs was investigated. The collective of study objects consisted of 319 asbestos exposed people with no HRCT-verifiable parenchymal variances. Neither extension, thickness and calcification of asbestos related pleural plaques, nor the cumulative asbestos exposure, independent of pleural and parenchymal variances, had any influence on lung function. All statistical distinctive features, which appeared during investigation of localisation of ventral calcified plaques in RV and the quotient RV/TLC and of cranial ones in VCIN and FVC, are best explained by chance. A difference between the correlations of HRCT-diagnosed plaques and those diagnosed by conventional radiographs to lung function could not be verified; both correlations were very small.
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