Management of Pleural Infection

Abstract

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.

Inflammation of the Pleural Cavity: A Review on Pathogenesis, Diagnosis and Implications in Tumor Pathophysiology

“…It is, however, worth reiterating that pleural fluid culture is positive in only about half of the cases [20]. One intriguing question is if the indwelling pleural catheter which can be used for the management of recurrent (mainly malignant) effusions can be compli- The incidence of pleural infection is 6.7-9.9 cases/100,000 population [18].…”

“…It is, however, worth reiterating that pleural fluid culture is positive in only about half of the cases [20]. One intriguing question is if the indwelling pleural catheter which can be used for the management of recurrent (mainly malignant) effusions can be complicated by pleural infection; the reported frequency varies from 2 to 12% and they are predominantly represented by Staphylococcus aureus and gram-negative organisms [21].…”

“…In addition, mesothelial cells contain tissue plasminogen activator (tPA) and urokinase plasminogen activator (uPA), but no fibrinolytic activity probably due to release of plasminogen activator inhibitors-1 and -2 (PAI-l and PAI-2) as well as antiplasmins [58]. The use of fibrinolytic agents (such as streptokinase, urokinase, tPA, PAI-1-neutralisisng antibodies, single-chain urokinase plasminogen activator), and DNAase are the basis of intrapleural fibrinolytic therapies aiming to disrupt the fibrine adhesions via activation of the plasminogen and to reduce the viscosity of the fluid through breakdown of extracellular DNA [20]. Intrapleural fibrinolytic therapy is associated with subsequent production of large effusions-this helps by may having a somewhat lavage effect [20]-probably mediated by the MCP-1 [59].…”

“…All these steps of pleural inflammation resemble the proposed mechanisms following pleurodesis, a condition that could serve as an example of pleura inflammation/fibro- In addition, mesothelial cells contain tissue plasminogen activator (tPA) and urokinase plasminogen activator (uPA), but no fibrinolytic activity probably due to release of plasminogen activator inhibitors-1 and -2 (PAI-l and PAI-2) as well as antiplasmins [58]. The use of fibrinolytic agents (such as streptokinase, urokinase, tPA, PAI-1-neutralisisng antibodies, single-chain urokinase plasminogen activator), and DNAase are the basis of intrapleural fibrinolytic therapies aiming to disrupt the fibrine adhesions via activation of the plasminogen and to reduce the viscosity of the fluid through breakdown of extracellular DNA [20]. Intrapleural fibrinolytic therapy is associated with subsequent production of large effusions-this helps by may having a somewhat lavage effect [20]-probably mediated by the MCP-1 [59].…”

Reduced survival in patients requiring chest tubes with COVID-19 acute respiratory distress syndrome

“…7 There have been numerous reports of tube thoracostomy in COVID-19 for pneumothorax and pleural effusion, yet these populations have been limited in size and included noncritically ill patients. [6][7][8][9][10][11][12][13][14][15][16][17] Furthermore, there has been scant evidence regarding incidence and postprocedure outcomes for critically ill patients with COVID-19 with tube thoracostomy. Among other globally important respiratory illnesses, one series of H1N1 pandemic influenza ICU patients reported a 14% tube thoracostomy rate and 1 small series of patients with SARS reported that 3 out of 6 patients with pneumothorax received tube thoracostomy.…”