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Pleural infection is a millennia-spanning condition that has proved challenging to treat over many years. Fourteen percent of cases of pneumonia are reported to present with a pleural effusion on chest X-ray (CXR), which rises to 44% on ultrasound but many will resolve with prompt antibiotic therapy. To guide treatment, parapneumonic effusions have been separated into distinct categories according to their biochemical, microbiological and radiological characteristics. There is wide variation in causative organisms according to geographical location and healthcare setting. Positive cultures are only obtained in 56% of cases; therefore, empirical antibiotics should provide Gram-positive, Gram-negative and anaerobic cover whilst providing adequate pleural penetrance. With the advent of next-generation sequencing techniques, yields are expected to improve. Complicated parapneumonic effusions and empyema necessitate prompt tube thoracostomy. It is reported that 16–27% treated in this way will fail on this therapy and require some form of escalation. The now seminal Multi-centre Intrapleural Sepsis Trials (MIST) demonstrated the use of combination fibrinolysin and DNase as more effective in the treatment of empyema compared to either agent alone or placebo, and success rates of 90% are reported with this technique. The focus is now on dose adjustments according to the patient’s specific ‘fibrinolytic potential’, in order to deliver personalised therapy. Surgery has remained a cornerstone in the management of pleural infection and is certainly required in late-stage manifestations of the disease. However, its role in early-stage disease and optimal patient selection is being re-explored. A number of adjunct and exploratory therapies are also discussed in this review, including the use of local anaesthetic thoracoscopy, indwelling pleural catheters, intrapleural antibiotics, pleural irrigation and steroid therapy.

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Pleural disease diagnostics represent a sprawling topic that has enjoyed a renaissance in recent years from humble beginnings. Whilst pleural patients are heterogeneous as a population and in the aetiology of the disease with which they present, we provide an overview of the typical diagnostic approach. Pleural fluid analysis is the cornerstone of the diagnostic pathway; however, it has many shortcomings. Strong cases have been made for more invasive upfront investigations, including image-guided biopsies or local anaesthetic thoracoscopy, in selected populations. Imaging can guide the diagnostic process as well as act as a vehicle to facilitate therapies, and this is never truer than with the recent advances in thoracic ultrasound.

Systemic inflammatory diseases are a heterogeneous family of autoimmune chronic inflammatory disorders that affect multiple systems within the human body. Connective tissue disease (CTD) is a large group within this family characterised by immune-mediated inflammation of the connective tissue. This group of disorders are often associated with pleural manifestations. CTD-induced pleuritis exhibits a wide variety of symptoms and signs including exudative pleural effusions and chest pain. Accurate estimation of prevalence for CTD-related pleuritis is challenging as small effusions are asymptomatic and remain undetected. Rheumatoid arthritis and systemic lupus erythematosus are frequent CTDs and present with pleural pathology in approximately 5–20% and 17–60% of cases, respectively. By contrast, pleural involvement in systemic sclerosis, eosinophilia–myalgia syndrome, mixed connective tissue disease, ankylosing spondylitis, polymyositis and dermatomyositis syndrome is rare. Clinical management depends on the severity of symptoms; however, most effusions resolve spontaneously. In this review we discuss the pathophysiological mechanisms and the clinical considerations of CTD-induced pleuritis.

Contributor statementEOB, NIK and NMR conceived and designed the study. JPC and EOB curated the PILOT database. EOB, NIK and YZ performed the laboratory processing and analyses. EOB and NMR analysed the data. MH, RA, RMM, AS and DNA contributed clinical data. EOB wrote the first draft of the manuscript. TD provided materials. RFM, TD and AMC provided expert knowledge. All authors reviewed and approved the final manuscript. EOB, NIK and NMR verified the underlying data and jointly act as guarantors.

Pleural effusions are a common respiratory condition with many etiologies. Nonmalignant etiologies explain most pleural effusions and despite being nonmalignant, they can be associated with poor survival; thus, it is important to understand their pathophysiology. Furthermore, diagnosing a benign pleural pathology always harbors the uncertainty of a false-negative diagnosis for physicians and pathologists, especially for the group of non-specific pleuritis. This review aims to present the role of the inflammation in the development of benign pleural effusions, with a special interest in their pathophysiology and their association with malignancy.

<b><i>Background:</i></b> Thoracoscopy is the “gold standard” diagnostic modality for investigation of suspected pleural malignancy. It is postulated that meticulous assessment of the pleural cavity may be adequate to indicate malignancy through the macroscopic findings of nodules, pleural thickening, and lymphangitis. We attempted to critically assess this practice, by precisely defining objective macroscopic criteria which might differentiate benign from malignant pleural diseases according to intrapleural pattern and anatomical location, and thereby to explore the predilection of abnormalities to specific sites on pleural surfaces. <b><i>Methods:</i></b> A structured review of recorded video footage from medical thoracoscopy procedures in 96 patients was conducted by 2 independent assessors. Abnormalities were scored on agreed, objective criteria for the presence of nodules, lymphangitis and inflammation on each of the costoparietal, visceral and diaphragmatic surfaces. The costoparietal pleura was divided into 6 levels (apical, middle, and inferior surfaces of the lateral and posterior parietal pleura). The anterior surface of the costoparietal pleura was excluded from analysis after interim review as this surface was rarely seen. <b><i>Results:</i></b> In the benign group, inflammation was the predominant finding in 65% (<i>n</i> = 33; costoparietal), 44% (<i>n</i> = 21; visceral), and 42% (<i>n</i> = 15; diaphragmatic). Nodules were detected in 24% (<i>n</i> = 12; costoparietal), 8% (<i>n</i> = 4; visceral), and 8% (<i>n</i> = 3; diaphragmatic). The most affected surfaces with inflammation were the middle lateral (60%) and the inferior lateral (57.8%) parts of the costoparietal pleura. In the malignant group, nodules were the predominant finding according to surface in 73% (<i>n</i> = 33; costoparietal), 32% (<i>n</i> = 13; visceral) and 48% (<i>n</i> = 17; diaphragmatic). Inflammation was detected in 44% (<i>n</i> = 20; costoparietal), 25% (<i>n</i> = 10; visceral), and 29% (<i>n</i> = 10; diaphragmatic). The most affected surfaces with nodules were the middle lateral (67.4%) and inferior lateral (66.7%) costoparietal pleural surfaces. <b><i>Conclusion:</i></b> This is the first detailed, anatomical description of abnormalities in the pleural space during thoracoscopy. While nodules were the predominant pattern in malignant pleural effusion, they were detected in 24% of benign diagnoses. Detection of nodules in &#x3e;1 area of the costoparietal pleura was in favor of a malignant diagnosis. Inflammation was the predominant pattern in benign pleural effusion. Our results suggest that macroscopic nodules in malignant diagnoses have a predilection for the middle and inferior surfaces of the lateral costoparietal pleura.