title: Effect of asbestos-related pleural fibrosis on excursion of the lower chest wall and diaphragm.
abstract: 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.
authors.affiliation: Department of Pulmonary Physiology, Sir Charles Gairdner Hospital, Nedlands, Australia. bsingh@cyllene.uwa.edu.au
authors.forename: B
authors.initials: B
authors.lastname: Singh
authors.forename: P R
authors.initials: PR
authors.lastname: Eastwood
authors.forename: K E
authors.initials: KE
authors.lastname: Finucane
authors.forename: J A
authors.initials: JA
authors.lastname: Panizza
authors.forename: A W
authors.initials: AW
authors.lastname: Musk
mesh_terms: D001194:Asbestos / Q000009:adverse effects*; D003964:Diaphragm / Q000503:physiopathology*; D005355:Fibrosis; D006801:Humans; D008297:Male; D008875:Middle Aged; D009068:Movement; D009784:Occupational Diseases / Q000503:physiopathology*; D010995:Pleural Diseases / Q000209:etiology / Q000503:physiopathology*; D013902:Radiography, Thoracic; D012115:Residual Volume; D015656:Respiratory Mechanics; D012272:Ribs / Q000503:physiopathology; D013909:Thorax / Q000503:physiopathology*; D014797:Vital Capacity
chemical_list: D001194:Asbestos