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

Our plain-English summary of Effect of asbestos-related pleural fibrosis on excursion of the lower chest wall and diaphragm, by B. Singh, P.R. Eastwood, K.E. Finucane, et al (American Journal of Respiratory and Critical Care Medicine, 1999).

The study

• Authors: B. Singh, P.R. Eastwood, K.E. Finucane, J.A. Panizza, A.W. Musk
• Journal: American Journal of Respiratory and Critical Care Medicine
• Published: 1999;160(5 Pt 1):1507-15
• Cited by: 23 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

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.

In plain English

This study, from Sir Charles Gairdner Hospital in Nedlands, Australia, looked at why asbestos-related pleural fibrosis can reduce lung volumes. The authors studied 26 men with previous asbestos exposure and no evidence of asbestosis. Seven had no pleural disease and served as controls, 12 had pleural plaques, and 7 had diffuse pleural thickening with obliteration of the costophrenic angle. Chest X-rays taken at several points during a slow, full breath in were used to measure movement of the diaphragm and lower rib cage. Men with diffuse pleural thickening had a lower vital capacity (77.4% of predicted, against 101.2% in controls). They also had less diaphragm shortening and much less expansion of the lower right rib cage, and their diaphragm dome flattened as they breathed in. Men with plaques also had less diaphragm shortening, but normal rib-cage expansion and normal vital capacity. The authors concluded that diffuse pleural thickening restricts breathing mainly by limiting lower rib-cage expansion. They noted that their measurements were estimates from X-rays that relied on several assumptions.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Cross-sectional physiological study comparing three groups of asbestos-exposed men, using lung function tests, exercise testing, and chest radiographs taken at set lung volumes during a slow inspiration
• Who was studied: 26 men recruited from outpatients seen between October 1994 and September 1995 at Sir Charles Gairdner Hospital, Nedlands, Australia, because of previous asbestos exposure. People with asbestosis or other interstitial lung disease, asthma, emphysema, lung cancer, pleural effusion or neuromuscular disorders were excluded. The groups were 7 controls with no pleural disease, 12 with pleural plaques, and 7 with diffuse pleural thickening with costophrenic angle obliteration.
• Exposure: Previous asbestos exposure (fiber type, job and dose not specified for the subjects). The comparison was by type of pleural disease on chest X-ray: none, pleural plaques, or diffuse pleural thickening with costophrenic obliteration.
• Main results:
  • Total lung capacity and vital capacity were lower in the diffuse pleural thickening group than in controls: vital capacity 77.4% predicted versus 101.2% (p less than 0.01), and total lung capacity 75.2% versus 93.6% (p less than 0.05). These volumes were not reduced in the plaque group (vital capacity 98.0% predicted).
  • In the diffuse pleural thickening group, vital capacity was 900 ml less than predicted.
  • Diaphragm shortening was reduced in both pleural disease groups compared with controls. Fractional shortening of the right hemidiaphragm was 0.316 in controls, 0.247 with plaques and 0.239 with diffuse pleural thickening (each p less than 0.001 versus controls).
  • The height of the diaphragm dome increased during inspiration in controls and in the plaque group, but decreased in the diffuse pleural thickening group. The authors took this to mean relative flattening of the dome.
  • Lower rib-cage expansion was reduced in the diffuse pleural thickening group on the lateral film and on the right side of the front-view film. Fractional expansion on the right was 0.011, against 0.071 in controls (p less than 0.01). Plaques caused no significant change (0.072).
  • Compared with controls, the volume displaced by the diaphragm over the vital capacity range was reduced by 93 ml/m3 (457 ml) in the plaque group and by 70 ml/m3 (356 ml) in the diffuse pleural thickening group.
  • Using a model of the lower thorax, the authors estimated that the volume contributed by the lower rib cage was 773 ml less in the diffuse pleural thickening group than in controls. Of this, 534 ml was attributed to differences in chest wall expansion and 239 ml to differences in the height of the lower rib cage.
  • Gas transfer and respiratory muscle strength were normal in all groups, and exercise capacity was similar across groups.
  • Vital capacity could not be predicted from the radiographic pleural severity scores. Giving a score of 15 for each obliterated costophrenic angle significantly improved the correlation with vital capacity (r2 = 0.36, p less than 0.01).
• The authors' conclusion: The authors concluded that restriction in diffuse pleural thickening is due to obliteration of the zone where the diaphragm lies against the rib cage. This reduces the volume contributed by the diaphragm and the lower rib cage. Reduced lower rib-cage expansion was the main cause, because flattening of the dome partly compensated for the diaphragm's reduced contribution. They also concluded that costophrenic fibrosis is more likely to cause restriction than pleural plaques, and that both limit the diaphragm's volume contribution to inspiration.
• Limitations the authors state:
  • Diaphragm length and shortening were estimated from the diaphragm outline on chest X-rays using several assumptions. These measurements may not represent the whole diaphragm and would tend to be underestimates.
  • The volume calculations assumed elliptical cross-sections. Because the thorax expands more front-to-back than side-to-side, this could underestimate the volume contributed by the diaphragm and lower thorax.
  • Inspired volume during the X-ray sequence was lower than vital capacity measured in formal lung function testing, likely because of posture and arm elevation. The authors judged this unlikely to have influenced the results, because it was reduced to the same extent in all groups.
  • Because of film size, the whole thorax could not be imaged in nine subjects (two control, six plaque, one diffuse pleural thickening). These subjects were excluded from left-sided measurements and from estimates of diaphragm volume displacement.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Pleural plaques and thickening.

Medical terms in this study, explained in our Lexicon: Fibrosis, Diaphragm, Asbestos Exposure, Chest X-Ray, Pleural Plaques, Diffuse Pleural Thickening, Hemithorax.

Related studies

• Asbestos-induced pleural fibrosis and impaired exercise physiology — J.F. Shih, J.S. Wilson, et al. (1994)
• Efficacy of intra-operative unilateral diaphragm plication for patients undergoing unilateral phrenicotomy during extended surgery — T. Tokunaga, N. Sawabata, et al. (2010)
• The management of the diaphragm during radical surgery for malignant pleural mesothelioma — A.J. Sharkey, R. Bilancia, et al. (2016)
• Cardiorespiratory responses to incremental exercise in patients with asbestos-related pleural thickening and normal or slightly abnormal lung function — A. Miller, A. Bhuptani, et al. (1993)
• Long-term Survival and Propensity Score Matched Outcomes of Bilateral vs. Unilateral Diaphragm Interventions in Cytoreductive Surgery plus Intra-peritoneal Chemotherapy — B. Singh, G. Singh, et al. (2018)
• Exercise impairment in asbestos-induced pleural fibrosis. Is it really just interstitial fibrosis? — E.T. Mannix, W.J. Martin (1994)

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