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| Journal of the New Zealand Medical Association,
04-April-2003, Vol 116 No 1171
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An uncommon clinical presentation of asbestos-related
disease
Chris Walls, Margaret Wilsher and Bill Glass
A 55-year-old European fitter and turner required admission
to hospital with acute shortness of breath. The diagnoses of transient
pericarditis and mild left ventricular impairment (echocardiogram) suggestive of
a previous infero-postero-lateral myocardial infarct were made. There was no
clinical or biochemical evidence of a recent infarct.
Chest X-ray demonstrated a large left pleural effusion,
which on CT scan was loculated. Pleural plaques and significant pleural
thickening, 14 mm on the right and 11 mm on the left side, were noted. A biopsy
of the pleura was negative for malignant mesothelioma and did not show
ferruginuous (asbestos) bodies (nor did a subsequent pericardial
biopsy).
Lung function testing
showed severely reduced total lung
capacity of 3.95 litres (predicted 6.72) and a residual volume of 1.33 litres
(predicted 2.3) consistent with restriction. A DLCO (diffusing capacity of the
lung for carbon monoxide) was at the lower limit of normal (75%
predicted).
The shortness of breath increased and a repeat CT scan
demonstrated marked pericardial thickening and both pleural and pericardial
calcification (Figure 1). Constrictive pericarditis was diagnosed.
 Figure 1. CT scan displaying pleural thickening and
pericardial calcification
At pericardectomy the pericardium was noted to be
significantly thickened and in some areas calcified, and the parietal pleura
showed significant thickening. Post-operatively there was a good relief of
symptoms.
The patient had worked for 22 years as a fitter and turner
in various employers’ maintenance departments, including working for more
than eight years at Auckland’s largest asbestos products manufacturing
plant. His screening chest X-rays over this employment period deteriorated from
normal (at the commencement of employment) to a report of ‘pleural
thickening, probably pleural fat collections’, to ‘pleural
plaques’ on an exit chest X-ray. There had been no leisure-time asbestos
exposure.
An ACC claim was declined because constrictive pericarditis
was not thought to be a complication of asbestos exposure, because of the
uncertainty of the diagnosis (his original claim was for asbestosis), and the
lack of asbestos bodies on pleural and pericardial biopsy.
DiscussionThe patient suffered from diffuse
pleural thickening identified by plain X-ray, CT scan, operative findings and
histological diagnosis. Rudd describes pleural disease as ‘a less common
manifestation of exposure to asbestos than plaque formation. The incidence
increases with increasing time after first exposure. Its occurrence is dose
related although less clearly so than asbestosis or the malignant
diseases.’1
The formation of asbestos bodies is dependent on the type
and length of fibre and individual patient
factors.2–4 Indeed, Churg and Green state
‘There are also limitations to examining asbestos bodies. Some patients
and some sizes/types of fibre appear to form bodies poorly, thus this type of
analysis may miss real exposure.’4 Parkes
notes that ‘Low counts may be encountered in those known to have previous
exposure.’2 The presence (and degree of
presence) or absence of bodies is subject to sampling error and
technique.
Both Parkes2 and
Parker3 observe that the presence of asbestos
bodies is used to quantify the degree of exposure, unnecessary in this case.
This patient’s exposure had been quantified by his occupational history,
the deterioration of screening chest X-rays while working at an asbestos
manufacturing plant, and an abnormal CT scan of the lung.
Rudd also notes that ‘exposure to asbestos
occasionally causes benign pericardial effusion, thickening and
calcification’,1 an observation supported
by other reports.5 Review of the hospital notes
of this patient uncovered an amended pericardial biopsy report showing the
presence of ‘numerous ferruginous (asbestos) bodies, some of which have
the finely beaded appearance suggestive of asbestos’.
This case presents two relatively uncommon but accepted
consequences of asbestos exposure. The key to assessing the likelihood of
causation in this and many occupational medicine cases is not histological
sampling but an accurate exposure history and a proper interpretation of
workplace biological monitoring (chest X-rays).
Author information:
Chris Walls, Occupational Physician, OSH Departmental Medical
Practitioner; Margaret Wilsher, Respiratory Physician, Greenlane Hospital; Bill
Glass, Occupational Physician, Convenor, OSH Asbestos Disease Panel,
Auckland
Correspondence: Dr C
Walls, OSH, Manakau Branch, Department of Labour, P O Box 63010, Papatoetoe
South, Auckland. Fax: (09) 262 5301; email: chris.walls@osh.dol.govt.nz
References:
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