Silicosis


Epidemiology


Etiology


Physiology


Pathologic Patterns


Diagnosis

PFT’s:
-Acute silicosis:
-Chronic silicosis: usually obstruction or combined obstruction-restriction (decreased flow rates/ decreased VC, TLC, RV/ usually normal FRC/ variable DLCO)
-Accelerated silicosis:

FOB:
-BAL: silica detected suggests diagnosis/
-TBB: silica dust detected

OLB: may be necessary in some cases

CXR/Chest CT patterns:
1) Acute silicosis: alveolar (or interstitial) infiltrates
2) Chronic silicosis: small, rounded opacities (SRO)
-“Eggshell” calcifications of mediastinal/ hilar lymph nodes: strongly suggestive of silicosis
-Pleural plaques: occur but are not common in silicosis
3) Accelerated silicosis: irregular upper zone fibrosis with nodular component

Hypergammaglobulinemia: may be seen

Serum autoantibodies: may be seen

ACE level: may be elevated


Clinical

Clinical Patterns:
1) Acute Silicosis:
-Exposure: usually intense exposure to fine dust (usually with high quartz content) for months
-Absence of clubbing
-Course: rapid progression to ALI/ARDS
-Complications: fulminating TB (common)

2) Chronic Silicosis:
-Exposure: occurs after >20 years of exposure to respirable dust (usually with <30% quartz)
-Impaired pulmonary function may occur (not always)/ absence of clubbing
-Course: not necessarily associated with increased morbidity or mortality
-Complications: progressive massive fibrosis (PMF)/ TB (especially in high-prevalence areas)

3) Accelerated Silicosis:
-Exposure: usually occurs after 5-15 year of heavy exposure (usually higher quartz content fiber dust)
-Symptomatic with pulmonary impairment / absence of clubbing
-Course: progression to respiratory failure and death
-Complications: PMF with cavitation (this usually indicates infection by atypical TB)


Treatment


References