Академический Документы
Профессиональный Документы
Культура Документы
CASE REPORT
Abstract Silicosis, caused by inhaling dust containing free crystalline silica, typically has a chronic course, with
the numbers of silicosis patients declining globally. Much rarer are the acute and subacute forms.
Presented is a case of severe subacute (accelerated) silicosis. The condition resulted from ~2 years
of very intense exposure without appropriate personal protective equipment while sandblasting. The
patient’s initial symptoms were progressive cough, dyspnoea and weight loss. Given his occupational
history, typical clinical manifestations and radiological findings, an initial diagnosis of accelerated
silicosis was proposed and histologically confirmed. The patient was a candidate for lung transplant-
ation. The case demonstrates a rare but largely preventable disease with serious health effects and a
poor prognosis.
Key words Accelerated silicosis; crystalline silica; lung transplantation; pneumoconiosis.
Introduction with lack of appetite. His job was to repair old car bodies
by pressure blasting with silica sand (98% SiO2) in a sheet
Silicosis is most commonly a chronic condition. However, metal container. The only personal protective equipment
rarely the course may be subacute (accelerated) or acute he used was a balaclava helmet. There was no dust extrac-
[1]. These have been described as single case reports or tion system. Based on his contract with the employer, he
small case series in the literature. We have previously only worked informally from early 2012 to early 2014.
reported a case of a sandblaster with silicosis who died During the initial examination, an anteroposterior
during lung transplantation (LT) <5 years from diagno- chest radiograph showed diffuse, bilateral, nearly sym-
sis and 10 years after the initial exposure [2]. metrically confluent, ill-defined opacities with honey-
While acute silicosis develops within only a few years comb emphysema. The diaphragm was slightly blurred,
after the usually short but intense exposure, accelerated with adhesions and the costophrenic angles slightly
silicosis (AS) mostly occurs 5–10 years from the initial blunted by pleural fluid (Figure 1A). A high-resolution
exposure to dust with high concentrations of silica par- computed tomography scan of the lungs showed large,
ticles [3]. AS both resembles acute silicosis, by accumu- almost symmetrical consolidations, particularly in the
lation of granular lipoproteinaceous material in alveolar upper and middle lung fields.
spaces, and has features of chronic silicosis with nodules Initial spirometry and body plethysmography showed
and a more rapid progression [1,3]. a combined respiratory defect: forced vital capacity
(FVC) 2940 ml (55% predicted); forced expiratory vol-
Case report ume in the first second (FEV1) 1860 ml (41%); total lung
capacity 5020 ml (68%); residual volume (RV) 1860 ml
In early 2017, a 28-year-old male with interstitial lung (106%); FEV1/FVC ratio 63%. Moderately reduced car-
disease and a 2-year history of sandblasting was referred bon monoxide diffusing capacity (DLCO) was detected
to a department of occupational medicine. The patient (55% predicted).
who had smoked 20 cigarettes a day since being a teen- Laboratory tests showed positive results for antineu-
ager reported progressive exertional dyspnoea, morning trophil cytoplasmic antibodies (ANCAs), borderline
cough and weight loss (10 kg over the previous month) positive results for antinuclear antibodies (ANAs), mild
© The Author(s) 2018. Published by Oxford University Press on behalf of the Society of Occupational Medicine.
All rights reserved. For Permissions, please email: journals.permissions@oup.com
M. NAKLÁDALOVÁ ET AL.: A CASE OF ACCELERATED SILICOSIS 483
leucocytosis (13.34 × 109/L), elevated C-reactive protein Bronchoscopy revealed diffuse mucosal hyperaemia
(8.7 mg/L), soluble interleukin-2 receptor (1349 kU/L), with disperse flaky mucus. Cytological analysis of bron-
IgA (4.77 g/L), IgG (17.2 g/L), circulating immune choalveolar lavage fluid (BALF) showed mixed, lym-
complexes (CICs, 82 U) and lactate dehydrogenase phocytic and neutrophilic, alveolitis with demonstrated
(12.32 µkat/L). Rheumatological examination showed erythrocytes, multinucleated cells and pigment-laden
no evidence of systemic disease. macrophages.
The other biochemical tests were normal. Further Lung tissue biopsy showed fibrosing histiocytic infil-
laboratory tests detected elevated tumour markers, namely trates (Figure 2A) with a tiny hyaline silicotic nodule and
Discussion
AS is a severe condition with multiple manifestations.
Published cases indicate an association between silico-
sis (not only accelerated) and increased levels of some
Figure 1. (A) Chest radiograph—bilateral, nearly symmetrically con- Figure 2. (A) Alveolar septa thickened with lymphohistiocytic infil-
fluent, ill-defined opacities. (B) Chest positron emission tomography/ trates and early fibrosis; haematoxylin–eosin stain, scale bar = 200 µm.
computed tomography—glucose hypermetabolism in irregular con- (B) Optically active crystals in both the interstitium and the alveolar
densations in both lungs and mediastinal lymph nodes. lumen; polarized light microscopy, scale bar = 100 µm.
484 OCCUPATIONAL MEDICINE