IntroductionArtificial stone is an increasingly popular material used to fabricate kitchen and bathroom benchtops. Cutting and grinding artificial stone is associated with generation of very high levels of respirable crystalline silica, and the frequency of cases of severe silicosis associated with this exposure is rapidly increasing.AimTo report the characteristics of a clinical series of Australian workers with artificial stone-associated silicosis.MethodsRespiratory physicians voluntarily reported cases of artificial stone-associated silicosis identified in their clinical practices. Physicians provided information including occupational histories, respiratory function tests, chest radiology and histopathology reports, when available.ResultsSeven male patients were identified with a median age of 44 years (range 26–61). All were employed in small kitchen and bathroom benchtop fabrication businesses with an average of eight employees (range 2–20). All workplaces primarily used artificial stone, and dust control measures were poor. All patients were involved in dry cutting artificial stone. The median duration of exposure prior to symptoms was 7 years (range 4–10). Six patients demonstrated radiological features of progressive massive fibrosis. These individuals followed up over a median follow-up period of 16 months (IQR 21 months) demonstrated rapid decline in prebronchodilator forced expiratory volume in 1 s of 386 mL/year (SD 204 mL) and forced vital capacity of 448 mL/year (SD 312 mL).ConclusionsThis series of silicosis in Australian workers further demonstrates the risk-associated high-silica content artificial stone. Effective dust control and health surveillance measures need to be stringently implemented and enforced in this industry.

An acute pulmonary embolism (aPE) is characterised by occlusion of one or more pulmonary arteries. Physiological disturbance may be minimal, but often cardiac output decreases as the right ventricle attempts to overcome increased afterload. Additionally, ventilation‐perfusion mismatches can develop in affected vascular beds, reducing systemic oxygenation. Incidence is reported at 50–75 per 100 000 in Australia and New Zealand, with 30‐day mortality rates ranging from 0.5% to over 20%. Incidence is likely to increase with the ageing population, increased survival of patients with comorbidities that are considered risk factors and improving sensitivity of imaging techniques. Use of clinical prediction scores, such as the Wells score, has assisted in clinical decision‐making and decreased unnecessary radiological investigations. However, imaging (i.e. computed tomography pulmonary angiography or ventilation‐perfusion scans) is still necessary for objective diagnosis. Anti‐coagulation remains the foundation of PE management. Haemodynamically unstable patients require thrombolysis unless absolutely contraindicated, while stable patients with right ventricular dysfunction or ischaemia should be aggressively anti‐coagulated. Stable patients with no right ventricular dysfunction can be discharged home early with anti‐coagulation and review. However, treatment should be case dependent with full consideration of the patient’s clinical state. Direct oral anti‐coagulants have become an alternative to vitamin K antagonists and are facilitating shorter hospital admissions. Additionally, duration of anti‐coagulation must be decided by considering any provoking factors, bleeding risk and comorbid state. Patients with truly unprovoked or idiopathic PE often require indefinite treatment, while in provoked cases it is typically 3 months with some patients requiring longer periods of 6–12 months.

In chronic obstructive pulmonary disease (COPD), loss of computed tomography (CT)-measured intercostal mass correlates with spirometric severity. Intercostal muscle ultrasound offers a repeatable and radiation-free alternative, however requires validation. We aimed to determine the reliability of parasternal intercostal muscle ultrasound, and the concurrent validity of parasternal ultrasound with clinicometric parameters. Twenty stable COPD patients underwent ultrasound measurement of thickness and echogenicity of 2nd and 3rd parasternal intercostal muscles, dominant pectoralis major and quadriceps, and diaphragm thickness; spirometry; and chest CT. Intra-rater intraclass correlation (ICC) for ultrasound intercostal thickness was 0.87–0.97 depending on site, with echogenicity ICC 0.63–0.91. Inter-rater ICC was fair to excellent. Ultrasound intercostal thickness moderately correlated with FEV1% predicted (r = 0.33) and quadriceps thickness (r = 0.31). Echogenicity correlated negatively with FEV1% predicted (r = −0.32). CT-measured lateral intercostal mass correlate negatively with parasternal ultrasound intercostal thickness. These data confirm ultrasound of parasternal intercostal musculature is reproducible. Lower intercostal muscle quantity and quality reflects greater COPD spirometric severity. This novel tool may have biomarker potential for both the systemic effects of COPD on muscle as well as local disruption of respiratory mechanics. The negative correlation between CT and ultrasound measurements may reflect complex site-dependent interactions between respiratory muscles and the chest wall.

Tumour type is an important determinant of pleural fluid cytology diagnostic yield. Cytology has good sensitivity and specificity for the diagnosis of adenocarcinoma, but if another tumour type is suspected, particularly mesothelioma, clinicians should be aware of the limitations.

Pulmonary infarction results from occlusion of the distal pulmonary arteries leading to ischemia, hemorrhage and ultimately necrosis of the lung parenchyma. It is most commonly caused by acute pulmonary embolism (PE), with a reported incidence of around 30%. Following an occlusion of the pulmonary artery, the bronchial arteries are recruited as primary source of perfusion of the pulmonary capillaries. The relatively higher blood pressure in the bronchial circulation causes an increase in the capillary blood flow, leading to extravasation of erythrocytes (i.e. alveolar hemorrhage). If this hemorrhage cannot be resorbed, it results in tissue necrosis and infarction. Different definitions of pulmonary infarction are used in literature (clinical, radiological and histological), although the diagnosis is nowadays mostly based on radiological characteristics. Notably, the infarcted area is only replaced by a fibrotic scar over a period of months. Hence and formally, the diagnosis of pulmonary infarction cannot be confirmed upon diagnosis of acute PE. Little is known of the impact and relevance of pulmonary infarction in acute PE, and whether specific management strategies should be applied to prevent and/ or treat complications such as pain, pneumonia or post-PE syndrome. In this review we will summarize current knowledge on the pathophysiology, epidemiology, diagnosis and prognosis of pulmonary infarction in the setting of acute PE. We highlight the need for dedicated studies to overcome the current knowledge gaps.

The FOBT was applied in clinically inappropriate settings without consideration to confounding issues, and often led to inappropriate clinical decisions with considerable cost to hospital and patient. There is no place for FOBT in an acute hospital setting.

Incidental pulmonary nodules are common in the general population. This has implications for possible lung cancer screening recommendations in the Australian population. Referral and/or review systems are essential to ensure adequate follow up of incidental findings, as it is likely some patients are not receiving adequate follow up at present.

Objectives: To assess the prevalence of sleep disorder(s) in males with Fabry disease and explore possible association with disease phenotype.Background: Fabry disease, an X-linked lysosomal storage disease caused by deficiency in a-galactosidase, results in intracellular accumulation of globotriaosylceramide. It causes organ dysfunction, most significantly affecting renal, cerebrovascular and cardiovascular systems. Respiratory involvement may include obstructive lung disease, reduced diffusing capacity and thickened soft and hard palates. Patients commonly develop small-fibre sensory peripheral neuropathy manifested by acroparaesthesia and pain crises. Combined with self-reported sleep disturbance and snoring, these features suggest an increased risk of sleep disorders.Methods: In-laboratory polysomnography (PSG) studies and sleep inventory assessments, including Epworth Sleepiness Scale (ESS), were performed in a cohort of male Fabry patients. PSGs were reviewed by a sleep physician. Sleep-disordered breathing and periodic leg movements were targeted for analysis. Associations with renal, cardiovascular and cerebrovascular function were sought.Results: Twenty males underwent overnight PSG. Patient baseline characteristics included age 43.9 AE 10.7 years, BMI 24.3 AE 3.8 kg/m 2 , neck circumference 39.7 AE 3.3 cm and ESS 9.8 AE 5.1 (7/20, abnormal ESS >10). Abnormal periodic leg movement index (PLMI) was present in 95% (mean frequency 42.4 AE 28.5/min) and sleep-disordered breathing in 50% patients. Periodic leg movements were associated with pain and depression but not with increased cortical arousal.Conclusions: Sleep-disordered breathing and abnormal PLMI are highly prevalent in patients with FD.