Uremia (see Uremic Pleurisy, [[Uremic Pleurisy]]): unilateral
Asbestos Exposure-Related Pleural Plaques (see Pleural Plaques, [[Pleural Plaques]]): bilateral
Deposition is mainly on the parietal pleural surface
Predisposed by occurrence of pleural effusion after asbestos exposure
Physiology
Hypoventilation with acidosis and hypoxia -> pulmonary vasoconstriction
Pulmonary hypertension due to chest wall disease (due to development of thick visceral pleural fibrous peel/parietal surface in asbestos exposure)
On the side of the pleural peel, blood flow is decreased out of proportion to ventilation
Progression of fibrothorax leads to restriction of chest wall movement, narrowing of intercostal spaces, decreased size of hemithorax, and displacement of medistinum to the affected side
Diagnosis
ABG: hypoxemia/hypercapnia may be seen in bilateral cases (associated with asbestos exposure)
PFT’s: mild-severe restrictive pattern
CXR/Chest CT: pleural plaques may be seen and are often calcified (on the inner aspect of the peel)
Clinical
Dyspnea: depends on extent of disease
Pulmonary Hypertension/Cor Pulmonale (see Pulmonary Hypertension, [[Pulmonary Hypertension]])
Respiratory failure may be seen in bilateral cases associated with asbestos exposure
Treatment
Surgical Decortication: only available treatment
Degree of success depends on integrity of unerlying lung (bilateral fibrothoraces do not respond well to surgery, probably due to underlying parenchymal lung disease)
VC may improve >50% after surgery if underlying lung is normal (VC may decrease in some cases where underlying lung is abnormal)
Duration of fibrothorax: does not affect surgical success
Timing of surgery: improve-ment occurs in first 3-6 months after acute insult that produced fibrothorax (sur-gery should be delayed until later to observe for any spontaneous improvement)
