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What is involved? (including coding of cases) SABRE Case Studies and Information
| ii. Asbestosis (Pneumonconiosis due to asbestos exposure)Asbestosis is a chronic progressive disease that requires high exposures to asbestos over prolonged periods of time and is characterised pathologically by interstitial fibrosis and asbestos bodies. Changes in industrial hygiene and other asbestos related work practices has meant that the latency period for the development of asbestosis has lengthened. Optimal diagnosis depends on a combination of histo-pathological and mineralogical information, although in the absence of pathology the diagnoses is based on the following factors (Begin, 1998):
The first three points are essential in diagnosing asbestosis (Begin, 1998), whilst the remaining points are confirmatory. During the initial stages of asbestosis, inhaled asbestos fibre's pierce the epithelium of the alveolar ducts resulting in an almost immediate low grade inflammatory response. Initially, exposure results in a localised peribronchiolar fibrosing alveolitis but as the fibres migrate into the interstitium between the alveoli and towards the pleura, further inflammation follows causing more widespread interstitial fibrosis. Disease progression requires chronic exposure to asbestos leading to further inflammation and fibrosis. An inability to remove the fibre causes continued cellular responses by alveolar macrophages and neutrophils causing increased cytokine and growth factor production, and fibroblast proliferation, all of which elicits scar tissue production and causes irreversible damage to the lung structure. To assess the severity of asbestosis histologically, pathologists use a grading scheme to determine the extent of fibrosis and the degree of respiratory bronchiole involvement (Craighead et al.,1982). The scheme is as follows: Grade 0: No fibrosis is associated with bronchioles. Conjoined with this grading scheme are three additional grades which include the level of involvement of the respiratory bronchioles and are as follows: Grade A: Only occasional bronchioles are involved; most show no lesion Clinically, patients present with dyspnea, dry cough and non-specific chest discomfort. Dry-end inspiratory crackles are an important physical finding and as the disease worsens patients experience increasing breathlessness. Lung function shows a restrictive ventilatory defect, with a greater loss of (FVC) than FEV1. The fibrosis causes a loss of compliance and a fall in gas transfer. References:
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