Parapneumonic Pleural Effusions and Empyema Thoracis – StatPearls

Continuing Education Activity

A parapneumonic effusion refers to the accumulation of exudative pleural fluid associated with an ipsilateral lung infection, mainly pneumonia. Parapneumonic effusions are mainly associated with bacterial infections. This activity reviews the pathophysiology and presentation of parapneumonic effusions and highlights the role of the interprofessional team in its management.

Objectives:

• Identify the etiology of parapneumonic effusions.

• Review the presentation of parapneumonic effusions.

• Outline the treatment and management options available for parapneumonic effusions.

• Describe interprofessional team strategies for improving care and outcomes in patients with parapneumonic effusions.

Access free multiple choice questions on this topic.

Introduction

A parapneumonic effusion refers to the accumulation of exudative pleural fluid associated with an ipsilateral lung infection, mainly pneumonia. Parapneumonic effusions are mainly associated with bacterial infections.[1]

Parapneumonic pleural effusions are classified into:

• Uncomplicated parapneumonic effusions, which are exudative,  neutrophilic effusion. Gram stain and culture are negative, glucose level greater than 60 mg/dl, pH above 7.20.

• Complicated parapneumonic effusions, resulting from a bacterial introduction into the pleura. In this type of parapneumonic effusion, there is a decreased glucose level, pleural fluid is below 7.20. Cultures of fluid from complicated parapneumonic effusions are negative and rapid bacterial clearance from the pleural space, or low bacterial count may explain this. The fluid termed as complicated because it necessitates drainage for resolution.

• Empyema thoracis in which there is frank pus in the pleural space, or there is evidence of bacterial infection of the pleural fluid by Gram stain or a positive culture.[2][3]

Pleural effusions are common in patients who develop pneumonia. At least 40-60% of patients with bacterial pneumonia will develop a pleural effusion of varying severity. Today, these parapneumonic effusions are not common because of prompt antibiotic therapy. However, in some patients the parapneumonic effusion becomes fibrinous and later develops an infection, resulting in an empyema.

Etiology

Pneumonia is the most frequent cause of parapneumonic effusions and empyema thoracis. Empyema may result as a complication of cardiothoracic surgery. Trauma can also lead to infection of the pleural space. The infecting organism may have spread from blood or other organs into the pleural space.[4][5]

Both viruses and bacteria can cause parapneumonic effusions, but it is the latter that is the most common cause of empyema thoracis.

Risk Factors

There are risk factors for empyema like age and comorbidities such as diabetes, alcoholism, GERD, advanced age and repeated hospitalization for pneumonia.[4]

Bacteriology

Streptococcus pneumoniae and Staphylococcus aureus are responsible for about 70% of aerobic gram-positive cultures. Klebsiella, Pseudomonas, and Haemophilus species are the commonest in gram-negative culture. Bacteroides and Peptostreptococcus species are the commonest anaerobic organisms. In empyema thoracis associated with aspiration pneumonia mixed bacterial florae containing aerobic and anaerobic bacteria are common. The common organism in cases of empyema thoracis complicating surgery is S. aureus.[4][6]

A very common cause of infection of the chest cavity is trauma. Any hemothorax that is not adequately evacuated can result in an empyema. Other causes include mediastinitis, ruptured esophagus, pericarditis, pancreatitis, and subdiaphragmatic abscesses.

Epidemiology

Parapneumonic effusion develops in about 20% to 40% of patients hospitalized with pneumonia. Approximately 1 million patients develop parapneumonic effusion annually in the United States.[2][7]

Despite a large number of parapneumonic effusions following pneumonia, less than 10% require aspiration.

Pathophysiology

 The stages of parapneumonic effusion are:

1. Exudative stage, in which there is an accumulation of fluid in the pleural space due to increased capillary permeability that results from proinflammatory cytokines, such as interleukin 8 (IL-8) and tumor necrosis factor-alpha (TNF-a). The pleural fluid in this early stage is usually clear exudative fluid with a predominance of neutrophils. Pleural fluid in this stage is simple parapneumonic effusion that usually resolves with adequate antibiotic treatment of pneumonia without the need for drainage. This stage takes approximately 2 to 5 days from the onset of pneumonia.

2. Fibrinopurulent stage, which can develop if adequate treatment is not provided. In this stage there is a deposition of fibrin clots and fibrin membranes in the pleural cavity, leading to fluid loculations. This stage takes about 5 to 10 days after pneumonia onset.

3. Organizing stage, in which fibrin membranes are transformed by fibroblast into a thick nonelastic pleural peel, resulting in the trapped lung with restrictive respiratory dysfunction. This stage may take about 2 to 3 weeks to develop.

The clinical course varies from spontaneous healing to chronic empyema and fibro-thorax with trapped restricted lung.[8]

History and Physical

The clinical manifestations of parapneumonic effusion or empyema are related to various factors like the presentation timing and the virulence of the causative organism. Common symptoms of bacterial pneumonia with parapneumonic effusion include a cough, expectoration, and a rise in body temperature, pleuritic chest pain, and difficulty breathing.

In most patients the following clinical signs are present in clinical examination and include:

• Fever, tachypnea, and tachycardia

• Pleural effusion (dullness to percussion decreased tactile fremitus and decreased or absent breath sounds)

• Adjacent pneumonia (rales or crackles and/or bronchial breath sounds)[9]

Evaluation

Radiographic Investigations

Plain chest x-ray: Pleural effusion can easily be detected by conventional radiographic. The consistency of these pleural-based densities suggests pleural fluid loculation.[1]

Chest ultrasound: Ultrasonography helps identify free or loculated pleural effusions and helps with thoracentesis guidance.[10]

Chest computed tomography (CT): For empyema or loculated effusion in adults, a CT scan with intravenous contrast is helpful. Radiographic contrast enhances the visualization of the pleural surfaces and helps identify pleural fluid loculations. Empyema is suggested by the presence of a split pleura sign in which there is a thickening of the visceral and parietal pleura with significant separation of the pleural surfaces. CT helps in detecting underlying parenchymal abnormalities.[11]

Thoracentesis

A diagnostic thoracentesis is needed for the management guidance of parapneumonic pleural effusion. In general, a parapneumonic effusion should be sampled if It is a free-flowing and layers greater than 10-mm on a lateral decubitus film. Radiological guidance of thoracentesis by ultrasound or chest computed tomography (CT) in some cases is helpful especially when the effusion is loculated.[12] The aspirated pleural fluid is subjected to:

• Microbiologic analysis: Gram stain with cultures and sensitivity (aerobic and anaerobic)

• Pleural fluid total and differential cell count

• Biochemical analysis: Total protein, lactate dehydrogenase, glucose) and  pH

• Pleural fluid biomarkers: Novel biomarkers of infection (e.g., C-reactive protein, procalcitonin, STREM-1) have been evaluated to help distinguish complicated parapneumonic pleural effusions from uncomplicated parapneumonic pleural effusions, but there is no proven superiority to traditional pleural biochemistries.[13][14]

More appropriate investigations should be performed to exclude other causes of pleural effusion when indicated.

Treatment / Management

Treatment of parapneumonic effusion includes appropriate antibiotic therapy together with drainage of pleural fluid as indicated.  

Parapneumonic effusion is classified into 4 groups based on risk for the poor outcome:

• Category 1 (very low risk): The effusion is small (less than 10-mm thickness on decubitus) and free-flowing. No thoracentesis is indicated.

• Category 2 (low risk): The effusion is small to moderate (equal to 10 mm and less than half the hemithorax) and free-flowing with negative culture and Gram stain regardless of the prior use of antibiotics and pH equal to 7.20.

• Category 3 (moderate risk), in which one of the following criteria is present:  the fluid equal to half the hemithorax, loculated effusion, thicken pleura on contrast-enhanced CT scan, positive Gram stain or culture or pH less than 7.20.

• Category 4 (high risk): This is when pleural fluid is in the form of pure pus.

Patients with category 1 and category 2 may not require drainage. In patients with category 3 and 4, drainage is recommended. Fibrinolytics, VATS, and surgery may be indicated for managing patients with category 3 and category 4 parapneumonic effusion not responding to less invasive drainage methods.[12]

Antibiotic Therapy

It must cover the suggested causative organisms of pneumonia according to the clinical setting. The duration of antibiotic therapy depends on many factors, for example, the sensitivity of the organism, extent of pulmonary parenchymal and pleural disease, response to initial therapy and adequacy of drainage.[15]

Chest Tube Drainage

Chest tube drainage is generally preferred for patients with uninoculated effusions and free-flowing fluid. Chest tubes are ideally inserted under ultrasound or CT-guidance. The choice of a thoracostomy tube size is controversial. Imaging performed within 24 hours is essential for documenting the correct position of the chest tube. Chest tubes are left in place until the drainage rate is less than 50 ml per day and the empyema cavity has closed. [15]

Fibrinolytic Agents 

The intrapleural administration for fibrinolytic agents (for example, streptokinase and tissue plasminogen activator) or fibrinolytic plus mucolytic agents aiming for facilitating the drainage of the loculated parapneumonic effusion is controversial.[16][17]

Thoracoscopy

Thoracoscopy is an alternative therapy for loculated empyemas when antibiotics and tube thoracostomy fail for the drainage. Thoracoscopy disrupts the intrapleural adhesions and allows the drainage of the pleural fluid.[18] Previous studies showed that delay for referral for thoracoscopy more than two weeks was associated with failure of thoracoscopy and conversion to thoracotomy.[19]

Decortication 

Decortication is indicated when persistent (present after 6 months) pleural peel is formed, leading to significant pulmonary restriction.[20]

Rib Resection and Open Drainage of Pleural Space

A vertical incision through the chest wall with rib resection (1 to 3) is done to allow pleural fluid drainage. A chest tube is left in place (about 60 to 90 days). Open drainage of the pleural space may be considered when the previous methods fail, and when the patient is too ill to tolerate decortications.[20]

Differential Diagnosis

Prognosis

Most of the patients with parapneumonic pleural effusion recover, but the mortality rate still around 10%. Proper antibiotic therapy and pleural fluid drainage are vital for recovery.[1] Scoring systems have been studied (RAPID score) to determine which patients with parapneumonic effusions are at the highest risk for a poor outcome.[21]

Other factors that complicate treatment include patient age, cardiac and respiratory compromise, immunosuppression, and frailty. Overall, death rates are higher in older patients.

Complications

Complications of pleural empyema may include residual pleural thickening, extensive pleural fibrosis, bronchopleural fistula formation, and development of empyema necessitans.[22]

The surgery is also associated with numerous complications including pain, recurrence, prolonged hospital stay, injury to the chest organs, diaphragmatic paralysis and fractured ribs.

Pearls and Other Issues

Early diagnosis, appropriate antimicrobial therapy, and adequate drainage of parapneumonic effusion are essential for decreasing its morbidity and mortality.

Enhancing Healthcare Team Outcomes

The parapneumonic pleural effusion management requires interprofessional cooperation between physicians of the concerned specialties (e.g., pulmonary medicine, radiology, and microbiology and cardiothoracic surgery) for a good outcome. The interprofessional care provided to the patient must follow an evidence-based approach. [Level 3]

Review Questions

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Figure

CT Chest bliateral Plueral Effusions. Contributed by Scott Dulebohn, MD

Figure

Right Pleural Effusion, X-ray. Contributed by Steve Bhimji, MS, MD, PhD

Figure

CT scan of chest effusions. Image courtesy S Bhimji MD

Figure

Consolidation and Plueral Effusion. Contributed by Pranav Modi

Figure

Empyema chronic. Image courtesy Dr Chaigasame

References

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Light RW, Girard WM, Jenkinson SG, George RB. Parapneumonic effusions. Am J Med. 1980 Oct;69(4):507-12. [PubMed: 7424940]

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Tsang KY, Leung WS, Chan VL, Lin AW, Chu CM. Complicated parapneumonic effusion and empyema thoracis: microbiology and predictors of adverse outcomes. Hong Kong Med J. 2007 Jun;13(3):178-86. [PubMed: 17548905]

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Bartlett JG, Gorbach SL, Thadepalli H, Finegold SM. Bacteriology of empyema. Lancet. 1974 Mar 02;1(7853):338-40. [PubMed: 4131173]

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Jerng JS, Hsueh PR, Teng LJ, Lee LN, Yang PC, Luh KT. Empyema thoracis and lung abscess caused by viridans streptococci. Am J Respir Crit Care Med. 1997 Nov;156(5):1508-14. [PubMed: 9372668]

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Grijalva CG, Zhu Y, Nuorti JP, Griffin MR. Emergence of parapneumonic empyema in the USA. Thorax. 2011 Aug;66(8):663-8. [PMC free article: PMC4820002] [PubMed: 21617169]

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McCauley L, Dean N. Pneumonia and empyema: causal, casual or unknown. J Thorac Dis. 2015 Jun;7(6):992-8. [PMC free article: PMC4466426] [PubMed: 26150912]

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Dean NC, Griffith PP, Sorensen JS, McCauley L, Jones BE, Lee YC. Pleural Effusions at First ED Encounter Predict Worse Clinical Outcomes in Patients With Pneumonia. Chest. 2016 Jun;149(6):1509-15. [PMC free article: PMC6026265] [PubMed: 26836918]

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Svigals PZ, Chopra A, Ravenel JG, Nietert PJ, Huggins JT. The accuracy of pleural ultrasonography in diagnosing complicated parapneumonic pleural effusions. Thorax. 2017 Jan;72(1):94-95. [PMC free article: PMC5563972] [PubMed: 27613540]

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Waite RJ, Carbonneau RJ, Balikian JP, Umali CB, Pezzella AT, Nash G. Parietal pleural changes in empyema: appearances at CT. Radiology. 1990 Apr;175(1):145-50. [PubMed: 2315473]

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Colice GL, Curtis A, Deslauriers J, Heffner J, Light R, Littenberg B, Sahn S, Weinstein RA, Yusen RD. Medical and surgical treatment of parapneumonic effusions : an evidence-based guideline. Chest. 2000 Oct;118(4):1158-71. [PubMed: 11035692]

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Chung CL, Hsiao SH, Hsiao G, Sheu JR, Chen WL, Chang SC. Clinical importance of angiogenic cytokines, fibrinolytic activity and effusion size in parapneumonic effusions. PLoS One. 2013;8(1):e53169. [PMC free article: PMC3538784] [PubMed: 23308155]

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Porcel JM, Bielsa S, Esquerda A, Ruiz-González A, Falguera M. Pleural fluid C-reactive protein contributes to the diagnosis and assessment of severity of parapneumonic effusions. Eur J Intern Med. 2012 Jul;23(5):447-50. [PubMed: 22726374]

15.

Lee MS, Oh JY, Kang CI, Kim ES, Park S, Rhee CK, Jung JY, Jo KW, Heo EY, Park DA, Suh GY, Kiem S. Guideline for Antibiotic Use in Adults with Community-acquired Pneumonia. Infect Chemother. 2018 Jun;50(2):160-198. [PMC free article: PMC6031596] [PubMed: 29968985]

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Jerjes-Sánchez C, Ramirez-Rivera A, Elizalde JJ, Delgado R, Cicero R, Ibarra-Perez C, Arroliga AC, Padua A, Portales A, Villarreal A, Perez-Romo A. Intrapleural fibrinolysis with streptokinase as an adjunctive treatment in hemothorax and empyema: a multicenter trial. Chest. 1996 Jun;109(6):1514-9. [PubMed: 8769503]

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Gilbert CR, Gorden JA. Use of intrapleural tissue plasminogen activator and deoxyribonuclease in pleural space infections: an update on alternative regimens. Curr Opin Pulm Med. 2017 Jul;23(4):371-375. [PubMed: 28399008]

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Cassina PC, Hauser M, Hillejan L, Greschuchna D, Stamatis G. Video-assisted thoracoscopy in the treatment of pleural empyema: stage-based management and outcome. J Thorac Cardiovasc Surg. 1999 Feb;117(2):234-8. [PubMed: 9918962]

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Pan H, He J, Shen J, Jiang L, Liang W, He J. A meta-analysis of video-assisted thoracoscopic decortication versus open thoracotomy decortication for patients with empyema. J Thorac Dis. 2017 Jul;9(7):2006-2014. [PMC free article: PMC5542928] [PubMed: 28840000]

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Ng CS, Wan S, Lee TW, Wan IY, Arifi AA, Yim AP. Post-pneumonectomy empyema: current management strategies. ANZ J Surg. 2005 Jul;75(7):597-602. [PubMed: 15972055]

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Rahman NM, Kahan BC, Miller RF, Gleeson FV, Nunn AJ, Maskell NA. A clinical score (RAPID) to identify those at risk for poor outcome at presentation in patients with pleural infection. Chest. 2014 Apr;145(4):848-855. [PubMed: 24264558]

22.

Martínez MA, Cordero PJ, Cases E, Sanchis JL, Sanchis F, Ferrando D, Perpiñá M. [Prognostic features of residual pleural thickening in metapneumonic pleural effusion]. Arch Bronconeumol. 1999 Mar;35(3):108-12. [PubMed: 10216741]

Disclosure: Eman Shebl declares no relevant financial relationships with ineligible companies.

Disclosure: Manju Paul declares no relevant financial relationships with ineligible companies.

Pneumonia and empyema: causal, casual or unknown

J Thorac Dis. 2015 Jun; 7(6): 992–998.

doi: 10.3978/j.issn.2072-1439.2015.04.36

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Author information Article notes Copyright and License information Disclaimer

Parapneumonic effusions complicating pneumonia are associated with increased morbidity and mortality. Along with increased mortality, complicated parapneumonic effusion and empyema often necessitate prolonged treatment, longer hospital stay and interventions. Parapneumonic effusions arise from inflammation in the lungs and pleural space from direct invasion of bacteria, cascade of inflammatory events and bacteriologic virulence features. Patient factors and comorbidities also contribute to the pathophysiology of parapneumonic effusion development. The evolution of parapneumonic effusion can be divided into three progressive stages: (I) exudative stage; (II) fibrinopurulent stage; and (III) organizing stage with pleural peel formation. These stages can help categorize effusions into groups in order to evaluate the risk of a complicated course requiring intervention. We recommend that clinical data be evaluated and a stepwise approach be taken in management of these patients. This review article discusses current understanding of the development and relationship of parapneumonic effusions with pneumonia.

Keywords: Parapneumonic effusion, pleural infection, empyema, pneumonia

Community acquired pneumonia results in significant morbidity and mortality, and is the 9^th leading cause of death in the United States when combined with influenza (1). About 6 million cases are reported annually in the United States population, resulting in 500,000 to 1. 1 million hospitalizations annually (2,3). Among pneumonia patients admitted to the hospital, 20% to 40% have pleural effusion, and 10% of these develop complicated parapneumonic effusion or empyema (4,5). There is considerable variation in the course and aggressiveness of parapneumonic effusions; therefore an understanding of its progression is important. Along with increased mortality, complicated parapneumonic effusion and empyema often necessitate prolonged treatment, longer hospital stay and interventions. Thus, identification of these patients and prompt management is critical.

This review article discusses current understanding of the development and relationship of parapneumonic effusions with pneumonia.

An Egyptian physician, Imhotep was most likely the first to describe pleural infections around 3000 BC, however Hippocrates is more often cited for its recognition in 500 BC. It was not until the 19^th century that open lung drainage was recommended for treatment, however mortality was as high as 70%, likely related to complications of surgery. Closed chest tube drainage was first described in 1876 and widely used during the influenza epidemic of 1917-1919, resulting in improved survival (6,7). The introduction of antibiotics has not only reduced the incidence of empyema, but also changed its bacteriology. In the pre-antibiotic era, 60-70% of empyemas were due to Streptococcus pneumoniae (S. pneumoniae), which now only accounts for about 10% (8-10). Staphylococcus aureus empyema has become more common, along with anaerobic and Gram-negative bacteria infections (7,8,10-14). With the advent of antibiotics, the incidence of empyema was dramatically reduced; however more recent studies indicate the incidence of pleural infection is increasing (15,16).

Parapneumonic effusion is defined as any pleural effusion secondary to viral or bacterial pneumonia or lung abscess. “Complicated” parapneumonic effusion is a paraneumonic effusion that requires an invasive procedure, such as tube thoracostomy, to resolve, often with positive pleural fluid cultures (5). Empyema is defined by the presence of bacteria or pus in the pleural space. Pus is thick, viscous fluid that appears purulent. About 60% of empyemas are related to a primary pneumonic process, therefore risk factors for pleural infection are similar to those for pneumonia (3,17). However, up to 40% of empyema may be secondary to a non-pneumonic process, such as systemic infection with hematogenous spread or abdominal etiology. Independent risk factors for the development of empyema include diabetes, immunosuppression, gastro-esophageal reflux disease, alcohol and intravenous drug abuse, aspiration, and poor oral hygiene (18). Other causes of empyema include complications after thoracic surgical procedures, trauma, esophageal perforation, thoracentesis and subdiaphragmatic infection (3,17).

In homeostatic conditions, pleural fluid arises from the systemic pleural vessels, traverses across leaky pleural membranes into the pleural space and exits via the parietal pleural lymphatics in the dependent part of the cavity (19,20). In healthy adults, the pleural space contains a small volume (1-20 mL) of low protein fluid that forms a lubricating film about 10 µm thick between the visceral and parietal pleural surfaces (6,19). A pressure gradient facilitates movement into, but not out of the pleural space, as intrapleural pressure is lower than interstitial pressure, and pleural membranes are leaky, offering little resistance to liquid or protein movement. The majority of pleural fluid exits the space by bulk flow, rather than diffusion or active transport, through the parietal lymphatics (20). Pleural fluid turnover is estimated to be ~0.15 mL/kg·h (19).

Pleural fluid accumulates when the rate of formation exceeds the rate of absorption. The flow of pleural lymphatics can efficiently increase in response to an increase in pleural fluid filtration, acting as a negative feedback mechanism. The lymphatic flow is about 15 mL/day, as this is the typical amount of pleural fluid formed per day. However, the capacity of the lymphatics is about 300-700 mL/day. Due to the large lymphatic capacity, unless the lymphatic drainage is severely impaired, another factor must be present for pleural fluid to accumulate (3,19).

The most common cause of increased pleural fluid formation is increased interstitial edema. This can occur as a result of several processes and is the predominant mechanism for the formation of parapneumonic effusions along with pleural effusions related to congestive heart failure (CHF), pulmonary embolism and acute respiratory distress syndrome. Decreased pleural pressures can also contribute to pleural fluid accumulation, as in advanced empyema when the visceral pleura becomes coated with a collagenous peel and traps the lung. Increased capillary permeability, particularly when the pleura becomes inflamed, also contributes to pleural effusion formation. Lymphatic obstruction is a common mechanism contributing to malignant effusions (3,19).

The evolution of parapneumonic effusion is divided into three progressive stages: (I) exudative stage; (II) fibrinopurulent stage; and (III) organizing stage with pleural peel formation (21). In the early exudative stage there is a rapid outpouring of fluid and inflammatory cells into the pleural space due to increased capillary microvascular permeability. This directly results from proinflammatory cytokines, such as interleukin 8 (IL-8) and tumor necrosis factor α (TNF-α) (22,23). The inflammatory process of the pulmonary parenchyma extends to the visceral pleura causing changes to the mesothelial cells lining the pleura, allowing increased fluid movement. This causes a local pleuritic reaction, and the characteristic pleuritic chest pain described by patients (5,21). Researchers studying rabbits infected with intrapulmonary Pseudomonas found a dose dependent relationship between bacterial levels and extent of alveolar epithelial injury, which further facilitated entry of alveolar protein and bacteria into the pleural space. This occurred within hours of inoculation (24). See .

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Schema shows mechanism of pleural effusion development in pneumonia. Initial bacterial infection causes local inflammatory reaction resulting in increased capillary microvascular permeability and a rapid outpouring of fluid containing inflammatory cells into the pleural space. Comorbidities such as heart failure also further contribute to interstitial edema. IL-8, interleukin 8; TNF-α, tumor necrosis factor α; VEGF, vascular endothelial growth factor.

The pleural fluid in this early exudative stage is usually clear free-flowing exudative fluid with predominance of neutrophils, and characterized by negative bacterial cultures, glucose level greater than 60 mg/dL, pH above 7.20, lactic acid dehydrogenase (LDH) less than three times the upper limit of normal for serum (often <1,000 units/L) and low white cell count (4,5,25-31). Pleural fluid that develops during this stage is usually considered a “simple” parapneumonic effusion and treatment with antibiotics is often adequate, without the need for tube drainage (4,27,28).

Patients can progress to stage 2, the fibrinopurulent stage within hours if effective treatment is not provided. This next stage is characterized by deposition of fibrin clots and fibrin membranes in the pleural space, leading to loculations and isolated collections of fluid. Invasion of bacteria from the pulmonary parenchyma occurs across the damaged endothelium. This invasion accelerates the immune response and directly contributes to fluid loculation (25) by promoting further migration of neutrophils and activation of the coagulation cascade. This leads to increased pro-coagulant and decreased fibrinolytic activity, which encourages fibrin deposition and promotes formation of septations within the fluid. The inflammatory reaction is further fueled by neutrophil phagocytosis and bacterial death, which results in release of more bacteria cell wall derived fragments and proteases (22).

This process has been demonstrated in mice with empyema after being infected intranasally with S. pneumoniae. Researchers found rapid bacterial invasion and increased inflammatory markers in the pleural space, such as IL-8, vascular endothelial growth factor (VEGF), monocyte chemotactic protein 1 (MCP-1) and TNF-α, which caused significant neutrophilia and development of fibrinous pleural adhesions. The pleural cavity offered a protected compartment for the bacteria, as bacterial clearance from the pleural space was poor in this animal model (31).

The pleural fluid in the fibrinopurulent stage is often turbid and characterized by positive bacteria on Gram stain and culture. Cytology shows neutrophils and degenerated cells. The combination of bacterial invasion and increased inflammatory response leads to increased lactic acid and carbon dioxide production, resulting in a fall in pleural fluid pH, increased glucose metabolism and a rise in LDH, consistent with “complicated” parapneumonic effusion. Typical pleural fluid studies in this stage have a glucose level less than 60 mg/dL, pH below 7.20, and pleural LDH more than three times the upper limit normal for serum (often >1,000 units/L) (5,25).

If stage 2 pleural fluid is not drained in conjunction with effective antibiotic therapy, the effusion may progress to stage 3, the organizing stage. This final stage is characterized by fibroblasts that proliferate and invade the pleural fluid from both the visceral and parietal pleura, forming a thick pleural peel. Fibrin membranes are transformed by fibroblast into a web of thick nonelastic pleura. This can occasionally encase the lung, preventing re-expansion and resulting in “trapped lung”. This can functionally result in impaired gas exchange and produce a persistent pleural space, increasing risk for continued infection (6,25). Clinical course varies considerably, from spontaneous healing with persistent defects of lung function, to chronic forms of empyema with high risk of complications, such as bronchopleural fistula, trapped restricted lung, fibro-thorax or spontaneous perforation through the chest wall (25).

Classifying the prognosis of a patient with a parapneumonic effusion is a critical first step in management. In 2000, the American College of Chest Physicians developed a classification system based on the anatomic features (A), bacteriology (B), and chemistry of the pleural fluid (C) (32). The anatomy (A) of the pleural fluid is based on three features; size, whether it is free flowing and whether the parietal pleura are thickened. The bacteriology (B) of the effusion is based on whether pleural cultures or smears are positive. The chemistry (C) of the pleural fluid is based on pH measured with a blood gas machine. Pleural fluid glucose can be used as an alternative to pH with a cutoff level of 60 mg/dL. Based on the A, B, and C classification, the effusion is categorized. Risk of poor outcome is based on the category of the effusion, as are recommendations to drain the effusion () (5,32). Similarly, the British Thoracic Society has published a diagnostic algorithm for management of these patients (6).

Table 1

Parapneumonic effusion classification

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*, small <10 mm on lateral decubitus; moderate less than half hemithorax; large greater than or equal to half hemithorax. Risk of poor outcome is very low to low for category 1 and 2; however category 3 and 4 have moderate to high risk.

The infectious organisms of community-acquired pneumonia (CAP) vary according to patient population, host immunity and geographic region, with the most common pathogens including S. pneumoniae, Haemophilus influenzae and Staphylococcus aureus (25). However, despite the relationship with pneumonia, studies suggest the bacteriology of pleural infections differ from that of pneumonia and have been altered significantly with the institution of antibiotic treatment. In a study of 434 patients with pleural infections, approximately 50% of parapneumonic infections were due to Streptococcal species, with the most common being S. intermedius [S. anginosus (milleri) group], followed by S. pneumoniae. Staphylococcus species were also common and accounted for about 14% of the parapneumonic infections. In this series, another, 20% of parapneumonic effusions were due to anaerobic bacteria (24). Most other series report similar rates of anaerobes (12-24%). However when DNA amplification and research laboratories are used to identify organisms, anaerobes may be present in up to 76% of the cases (14,33-35).

The difference in the bacteriology between pneumonia and pleural infections may be related to the acidic and hypoxic environment of the infected pleural space and bacterial virulence factors favoring certain pathogens (18,24). Furthermore, the difference in bacterial species between pleural infections and pneumonia, along with lack of chest imaging evidence of pneumonia in some patients, have led some experts to question the conventional belief that empyema and pneumonia are inherently related. Hematogenous spread of bacteria from systemic infection or an abdominal process with rapid growth of bacterial in the pleural space, as observed in animal models, offers a plausible explanation (24,31).

Aside from inflammation in the lungs and pleural space from direct invasion of bacteria and bacteriologic virulence features contributing to parapneumonic effusion, patient factors and comorbidities also contribute to the pathophysiology of parapneumonic effusion development. A recent study (11), analyzed 4,715 patients with CAP and 882 (19%) had pleural effusions, of which 261 (30%) had empyema or complicated parapneumonic effusion. In a multivariable analysis, no single baseline patient characteristic distinguished patients without pleural effusion from those with uncomplicated parapneumonic effusion. However, five independent baseline characteristics could predict the development of empyema or complicated parapneumonic effusion in patients with pneumonia: age <60 years old, alcoholism, pleuritic pain, tachycardia and leukocytosis. These investigators, and others have found a reduced prevalence of clinical manifestations in older patients, suggesting possible age-related change in the immune response (11,13,36,37). In this cohort, researchers also found patients with a history of tobacco abuse had increased risk of developing a complicated parapneumonic effusion or empyema, whereas, chronic obstructive pulmonary disease and heart failure decreased risk. Diabetes, chronic renal disease and liver disease were not associated with risk of pleural infection in the cohort (11). Similar results have been found in other prospective observational studies of patients diagnosed with CAP (12,13).

Pneumonia is a leading cause of death and pleural infections complicating pneumonia has been established to have considerable morbidity and mortality, with mortality approximately 20% for patients with empyema (16,38,39). This may be related to something inherent about the parapneumonic effusion and/or a more robust inflammatory response. Underlying comorbidities or patient factors may not only contribute to the development of a parapneumonic effusion, but might be the cause of increased mortality.

In a prospective cohort study of 1,906 patients with CAP, Hasley et al. (36) found an overall 30-day mortality of 4.9%. Patients with associated pleural effusion had 30-day mortality of 14.7% and those with bilateral effusions had an even higher mortality of 26.0%. In multivariate analysis of radiographic features and clinical characteristics, the presences of bilateral pleural effusions were independently associated with mortality. Other radiographic characteristics including infiltrates involving two or more lobes, the presence of bronchopneumonia, bilateral infiltrates, air bronchograms, postobstructive pneumonia, or an aspiration pattern, had univariate associations with mortality. However, none of these factors were independently associated with death after controlling for confounding variables know to be associated with mortality. The most common comorbidities in this pneumonia cohort were coronary artery disease, chronic obstructive pulmonary disease, and CHF. Mortality rates were greatest for patients with both CHF and bilateral pleural effusions (25. 6%).

Why bilateral pleural effusions are associated with mortality in pneumonia is not clear nor is the observation that patients with bilateral effusions and CHF are at greatest risk of mortality. Bilateral effusions in pneumonia patients may be a marker of severe pneumonia or may be attributable to underlying comorbidities. The increased mortality in patients with comorbidities such as CHF may reflect overall health status and those who are more likely to die from co-existing heart disease rather than directly from the pneumonia. Further research is needed (5,12,36).

Management of parapneumonic effusions involves a stepwise approach in addition to appropriate and timely antibiotic treatment. The treatment options include: observation, therapeutic thoracentesis, tube thoracostomy, intrapleural instillation of fibrinolytics, thoracoscopy with breakdown of adhesions and/or decortication, and open drainage procedures (5,6,32). The details of these procedures go beyond the scope of this article.

Pneumonia can be complicated by the development of a parapneumonic effusion, which has increased morbidity and mortality. Complicated parapneumonic effusion and empyema often necessitate prolonged treatment, longer hospital stay and interventions. Parapneumonic effusions arise from inflammation in the lungs and pleural space from a cascade of inflammatory events including, direct invasion of bacteria and bacteriology virulence features. Patient factors and comorbid illnesses such as heart failure also contribute to the pathophysiology of parapneumonic effusion development.

The evolution of parapneumonic effusions can be divided into three progressive stages: (I) exudative; (II) fibrinopurulent; and (III) organizing stages. These stages can help categorize effusions into groups in order to evaluate risk of an uncomplicated or complicated course requiring intervention. Clinical data should be collected to classify patients and a stepwise approach be taken in the management.

Disclosure: The authors declare no conflict of interest.

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What is the name of the disease in which fluid accumulates in the lungs?

Contents

• 1 Pleural effusion: what is it and why does it occur in the lungs?
  • 1.1 What is fluid accumulation in the lungs?
  • 1.2 Causes of fluid in the lungs
  • 1.3 What are the symptoms of fluid in the lungs?
  • 1.4 Diagnosis of fluid accumulation in the lungs
  • 1.5 Complications of fluid accumulation in the lungs
  • 1. 6 Treatment of fluid accumulation in the lungs
  • 1.7 Methods of medical treatment of fluid accumulation in the lungs
  • 1.8 Rehabilitation procedures for fluid accumulation in the lungs
    • 1.8.1 Treating the problem through lung drainage
    • 1.8.2 Physiotherapy exercises to treat the problem
    • 1.8.3 Scaling the problem with drugs
  • 1.9 How to prevent fluid in the lungs?
  • 1.10 Home care for a person with fluid in the lungs
  • 1.11 Where can you get qualified medical help if you have fluid in your lungs?
  • 1.12 Related videos:
  • 1.13 Q&A:
    • • 1.13.0.1 What is fluid in the lungs?
      • 1.13.0.2 What type of disease causes fluid to accumulate in the lungs?
      • 1.13.0.3 What symptoms indicate the accumulation of fluid in the lungs?
      • 1.13.0.4 How is accumulation of fluid in the lungs diagnosed?
      • 1.13.0.5 How is fluid accumulation in the lungs treated?
      • 1. 13.0.6 What are the consequences of fluid accumulation in the lungs?

Find out what is a disease in which fluid accumulates in the lungs, what causes it and what symptoms accompany this pathology. What methods of treatment are used for such a disease and what preventive measures will help to avoid it.

In pathological processes in the body, illness can occur when fluid accumulates in the lungs. This condition is called pleural effusion. Such a disease can be caused by various causes and have different health consequences.

Pleural effusion is not an independent disease, but only a symptom of a pathological process in the body. A variety of reasons can lead to fluid buildup in the lungs, including chronic diseases, infections, injuries, and tumors.

In order to correctly diagnose and treat pleural effusion, the underlying cause must be identified. In this article, we will discuss the causes, symptoms, and treatments for pleural effusion.

What is fluid accumulation in the lungs?

Fluid accumulation in the lungs, also known as pulmonary edema, is a pathological condition in which fluid begins to accumulate in the lung tissue. This can occur due to various diseases and conditions such as heart failure, bronchitis, pneumonia, pneumoconiosis, and others.

Treatment for fluid in the lungs depends on the cause. Doctors usually prescribe diuretics, drugs that help remove excess fluid from the body. In some cases, surgery or other treatments may be required.

• Advice: If you have symptoms of fluid in your lungs such as cough, shortness of breath, extreme fatigue, seek medical attention as soon as possible.

Causes of fluid accumulation in the lungs

China-like disease – this disease often causes fluid accumulation in the lungs. China-like disease is a rare genetic disorder that causes abnormal development of blood vessels in the lungs. Because of this, blood cannot pass freely through the vessels, and fluid begins to accumulate in the lungs.

Heart failure is a condition in which the heart is unable to pump enough blood. In addition, fluid accumulation in the lungs is often observed due to age-related changes in the heart and blood vessels, obesity, arterial hypertension and diabetes.

Acute and chronic bronchitis – Hypothermia and infections of the upper respiratory tract can lead to acute or chronic bronchitis, and increase the chance of fluid accumulation in the lungs.

Other possible causes of fluid in the lungs are: lung infections, chest trauma, alcohol, drug or substance abuse, allergic reactions, and some types of cancer.

What are the symptoms of fluid accumulation in the lungs?

One of the main symptoms of fluid accumulation in the lungs is a cough. Most often it is not accompanied by discharge, and experts describe it as drier. The cough may be worse at night and in the morning when the patient is lying down.

Another noticeable symptom of fluid accumulation in the lungs is fatigue. The patient may tire quickly with exertion, have difficulty moving, and exhale quickly. Shortness of breath, chest tightness, and noisy breathing may also occur.

Pay attention to changes in urine. If it has become less voluminous and more saturated in color, this may indicate the accumulation of fluid in the lungs. Patients may also experience leg swelling, chest pain, and excessive sweating.

If you notice one or more of these symptoms, contact your doctor. Treatment of fluid accumulation in the lungs requires an integrated approach and the appointment of individual therapy based on the causes of this condition.

Diagnosis of Fluid in the Lungs

Fluid in the lungs can lead to serious consequences, including respiratory failure and heart problems. For the timely detection of this disease, it is necessary to undergo regular medical examinations and monitor your health.

Blood tests for oxygen and carbon dioxide, as well as electrocardiography (ECG) and other additional studies, may be performed to further assess the patient’s condition.

When fluid buildup is detected in the lungs, doctors will prescribe appropriate therapy, which may include medications and lung drainage to remove the accumulated fluid. It is important to seek medical attention as soon as possible when the corresponding symptoms appear in order to avoid serious complications and maintain health.

Complications of fluid accumulation in the lungs

Pneumothorax is one of the possible complications in which air accumulates in the pleural cavity and leads to compression of the lungs, which can lead to their collapse.

Pleural empyema is a purulent inflammation of the pleural cavity that can develop as a result of fluid accumulation in the lungs. It is necessary to immediately begin treatment with antibiotics and, if necessary, drainage of the pleural cavity with the removal of purulent contents.

Pulmonary fibrosis – In some cases, fluid accumulation in the lungs can cause an extensive fibrotic reaction with connective tissue formation in the lungs. This can lead to a violation of the functions of the body and even to its complete unsuitability.

Hypoxia – When the areas of the lungs in close proximity to the fluid that accumulates do not receive enough oxygen, this can lead to hypoxia (decrease in the level of oxygen in the blood) and complicate the general condition of the patient.

Infected insect sting – fluid buildup in the lungs may increase the risk of infection by an infected insect, which can also lead to other illnesses.

Difficulty breathing – regardless of the cause of the accumulation of fluid, it can lead to breathing difficulties, a deterioration in the quality of life and a complication of the general condition of the patient.

Treatment of fluid accumulation in the lungs

A disease in which fluid accumulates in the lungs is called pneumophorax. Its treatment depends on the cause and degree of development of the disease.

In addition, it is important to monitor the patient’s respiratory function and, if necessary, prescribe oxygen therapy. In some cases, surgery may be required to remove excess fluid or regulate breathing function.

1. It is important to consult a doctor in time and not delay treatment.
2. Patients should follow their doctor’s orders, take their medications correctly, and control their breathing.
3. In the presence of chronic diseases and disorders in the functioning of the lungs, it is necessary to carefully monitor your health and undergo regular examinations.

With proper and timely treatment of fluid accumulation in the lungs, it is possible to achieve complete recovery and prevent complications.

Medical Treatments for Fluid in the Lungs

Fluid in the lungs can be caused by a variety of things, from heart failure to infections and cancer. The treatment for this condition depends on its cause.

One of the most common medical treatments for fluid in the lungs is diuretics. These drugs increase the excretion of fluid from the body by the kidneys, reducing its accumulation in the lungs. Depending on the severity of the condition and the individual patient, different types of diuretics may be used.

If fluid builds up in the lungs due to infection, antibiotics may be used. They will help destroy the infectious agent and reduce inflammation, which in turn will help reduce fluid buildup.

For more serious cases of lung cancer or drug abuse, treatment may include chemotherapy or surgery to remove fluid buildup.

• Diuretics – drugs that increase the excretion of fluid from the body.
• Medicines that improve heart function – medicines that improve blood circulation and reduce swelling.
• Antibiotics are drugs used to treat infectious diseases.
• Chemotherapy and surgery are treatments for more severe cases of fluid in the lungs.

Rehabilitation procedures for fluid accumulation in the lungs

Treating the problem with a lung drain

A lung drain is a procedure used to remove accumulated fluid in the lungs with a needle or tube inserted into the chest. This procedure helps to improve respiratory function and reduce the discomfort caused by the accumulation of fluid in the lungs. However, it is only performed in a hospital and may not be safe, so it must be prescribed by a doctor.

Physiotherapy exercises for the treatment of problem

Certain exercises to increase lung capacity and strengthen the muscles of the respiratory system can help with fluid buildup in the lungs. Warm-ups with specialized devices such as pulmonators are also considered effective in the treatment of such diseases. It is important that these exercises are prescribed by a specialist and monitored during execution to avoid possible complications.

Scaling the problem with drugs

Some medicines can help improve fluid buildup in the lungs, such as diuretics and bronchodilators. Diuretics are used to remove excess fluid from the body, and bronchodilators help open the bronchi and reduce associated diseases such as obstructive pulmonary disease. Certain medications can have side effects, so their use should be discussed with a healthcare professional.

How can I prevent fluid buildup in my lungs?

Fluid buildup in the lungs can result from a variety of conditions, including heart failure, pneumonia, and lung cancer. It is important to know that the main preventive measure is the prevention of the underlying disease.

However, there are a few additional steps you can take to help reduce the risk of fluid buildup in your lungs:

• Do not smoke. Smoking increases the risk of many diseases, including lung cancer and pneumonia.
• Maintain a healthy lifestyle. Eat nutritious foods, get regular exercise, maintain a healthy weight, and control your cholesterol and blood pressure.
• Maintain personal hygiene. Wash your hands, use a respirator if you have SARS, and avoid contact with people who have TB.

It is important to understand that if you have a high risk of developing a condition that can cause fluid to build up in your lungs, discuss this with your doctor. He may recommend additional prophylaxis or examination.

Helpful Hints

Home care for a person with fluid accumulation in the lungs

Fluid accumulation in the lungs is a serious disease that requires complex treatment and constant medical supervision.

However, some patient care measures can be taken at home to alleviate the patient’s condition and make the treatment process more effective.

• Monitor the patient’s condition: regularly measure temperature, pressure, pulse, record the results and report to the doctor.
• Provide comfortable conditions: maintain optimal room temperature and humidity, provide fresh air, provide a comfortable bed and pillows for a comfortable sleep of the patient.
• Maintain drinking habits: Give the patient water or other liquids regularly as recommended by the physician.
• Monitor nutrition: provide the patient with a diet appropriate for his condition and doctor’s recommendations.
• Breathing exercises: Regular breathing exercises to improve lung function.

Do not forget that it is important not only to support and help the patient, but also to follow the doctor’s instructions and not make any independent decisions in the treatment of the disease.

Where can you get qualified medical help if you have fluid in your lungs?

Fluid buildup in the lungs can be a dangerous condition requiring immediate medical attention. If you notice coughing, difficulty breathing, chest pain, or other signs associated with fluid in your lungs, contact your healthcare provider right away.

If you cannot get advice from your doctor, consult a neurologist or a general practitioner. These professionals can make recommendations or make appointments to help you manage your condition.

If you have acute symptoms such as difficulty breathing or chest pain, you may need emergency care. In this case, contact an ambulance or call an ambulance.

In any case, if fluid builds up in the lungs, professional medical attention should be sought to diagnose and treat the problem. Don’t put off seeing a doctor until tomorrow because your health and life may depend on it.

Related videos:

Q&A:

What is fluid in the lungs?

Fluid in the lungs is a medical condition where fluid builds up in the lungs. It can cause various diseases.

What type of disease causes accumulation of fluid in the lungs?

The accumulation of fluid in the lungs can be caused by various diseases such as tuberculosis, pneumonia, cancer, cardiovascular disease, and others.

What symptoms indicate the accumulation of fluid in the lungs?

Symptoms can range from mild to severe, including cough, difficulty breathing, leg swelling, frequent urination and chest pain.

How is accumulation of fluid in the lungs diagnosed?

Diagnosis may include physical examination, X-ray, computed tomography, bronchoscopy, and other tests.

How is fluid accumulation in the lungs treated?

Treatment may include drugs, surgery, radiation, or a combination of these.

What are the consequences of fluid accumulation in the lungs?

Effects may vary depending on the cause of fluid accumulation and the degree of lung involvement. Complications such as respiratory failure, infections and even death are possible.

Pleural effusion – causes, diagnosis and treatment

Classification

In terms of composition, pleural effusions are divided into 2 large groups:

• Exudative is an effusion of inflammatory origin. It occurs in infectious, autoimmune, oncological diseases.
• Transudative – effusion resulting from a violation of capillary hydrostatic or colloid osmotic pressure. It is observed in congestive heart failure, kidney pathology with proteinuria, cirrhosis of the liver.

The presence of transudative effusion is called hydrothorax. The nature of the exudate, in turn, can be:

• Serous.
• Purulent (pyothorax).
• Hemorrhagic (hemothorax).
• Chylous (chylothorax): accumulation of lymph in the pleural cavity.

The location of the effusion may be unilateral or bilateral.

Causes of pleural effusion

Infectious diseases

The most common etiology of pleural effusion is infection of the pleura (pleurisy). Pleurisy can occur as an independent disease, for example, tuberculous pleurisy, but in the vast majority of cases it develops as a complication of the inflammatory process in the lung tissue (pneumonia). The pathogenetic mechanism of the formation of pleural effusion is quite simple.

Penetration of an infectious agent into the pleural cavity causes inflammation, accompanied by the release of biologically active substances (cytokines, interleukins), which induces an increase in the permeability of the vascular wall, the migration of neutrophils to the focus of inflammation, and cell infiltration. The volume of pleural effusion depends on the severity of the inflammatory process.

Pleural effusions of bacterial and viral origin occur acutely. The exception is tuberculous pleurisy, which often has a chronic relapsing character. Effusions of a parasitic nature develop gradually. The main infectious agents leading to pleural effusion:

• Pneumococcus.
• Beta-hemolytic streptococcus.
• Staphylococcus aureus.
• Influenza and ARVI viruses.
• SARS-CoV-2.
• Klebsiella.
• Escherichia coli.
• Mycobacterium tuberculosis.
• Alveococcus.
• Aspergillus.

Chronic heart failure

In patients with decompensated CHF, pleural effusion is often observed. Due to a pronounced decrease in the contractility of the heart muscle, blood stagnation occurs in the systemic circulation (with right ventricular and biventricular CHF). Due to the accumulation of blood, hydrostatic pressure in the capillaries increases, which leads to plasma leakage into the pleural cavity (hydrothorax). The effusion is bilateral. It is worth noting that in addition to pleural effusion, BCC blood stasis is also often accompanied by the presence of fluid in the abdominal cavity (ascites).

Hypoalbuminemia

One of the main functions of the plasma protein albumin is to maintain colloid-osmotic (oncotic) blood pressure, which allows water to be retained in the bloodstream. With a pronounced decrease in the concentration of albumin, oncotic pressure decreases, which leads to pathological diffusion of water from blood vessels into the interstitial tissue.

Clinically, this is manifested by swelling of the face, upper and especially lower extremities, as well as accumulation of fluid in the cavities – abdominal and pleural. The following are diseases and pathological conditions that cause hypoalbuminemia and pleural effusion:

• Liver failure : cirrhosis of the liver, viral hepatitis.
• Kidney diseases with nephrotic syndrome : glomerulonephritis, various nephropathies in systemic diseases (collagenoses, monoclonal gammopathy, amyloidosis).
• Malabsorption: chronic pancreatitis with severe exocrine insufficiency, celiac disease (celiac disease).
• Protein starvation.

Pleural effusion on x-ray

Autoimmune pathology

Quite often, in autoimmune conditions, lung tissue and pleura are involved in the inflammatory process. For systemic diseases of the connective tissue, this occurs within the framework of the so-called extra-articular manifestations. The defeat of the bronchopulmonary system is mainly interstitial in nature (in the form of pneumonitis or fibrosis), exudative pleurisy is less often observed.

The effusion may be unilateral or bilateral. The following are autoimmune pathological conditions in which pleural effusion can occur:

• Systemic lupus erythematosus. According to various sources, pleurisy as a manifestation of lupus polyserositis develops in 50-90% of patients with SLE, but the prevalence of effusion pleurisy is unknown.
• Rheumatoid arthritis. Pleural effusion occurs in approximately 25% of patients. The main predictor is a high level of antibodies to cyclic citrullinated peptide (ACCP).
• Sjögren’s syndrome. Pleural effusion may occur in association with lymphocytic pneumonitis.
• Dressler’s syndrome. Is an autoimmune complication of myocardial infarction. It develops on days 7-10 in 10% of patients. Accompanied by pleurisy (both dry and effusion), pericarditis, fever and joint pain.

Oncological diseases

Pleural effusion is not uncommon in oncological diseases. The pathogenesis consists in mechanical obstruction of the lymph nodes, lymphatic vessels (in some cases, obstruction of the thoracic duct), which makes it difficult for the outflow of lymph from the pleural cavity. Therefore, in oncology, the effusion has a chylous character. All cases of pleural effusion in neoplasms can be divided into 3 groups:

• Metastases in the pleura. Metastatic pleurisy often occurs with lung cancer (24-50%), breast cancer (48%), as well as with oncohematological diseases – lymphomas, leukemias (26%).
• Pleural mesothelioma. It is a malignant tumor of the mesothelial cells that make up the pleura. The main provoking factor of development is constant contact with asbestos.
• Meigs syndrome. A special type of paraneoplastic polyserositis in ovarian tumors. Accompanied by ascites and pleural effusion. The exact pathogenetic mechanism of development is unknown.

Pathology of the gastrointestinal tract

The occurrence of pleural effusion in pathologies of the organs of the gastrointestinal tract is associated with the formed fistula (fistula) between the pleural cavity and the organs of the gastrointestinal tract or the abdominal cavity. For example, a subdiaphragmatic abscess that develops as a complication after surgical treatment of abdominal organs (cholecystitis, appendicitis, perforated gastric ulcer or duodenal ulcer) is accompanied by pleural effusion in 80% of cases.

Due to the formation of a pancreatic-pleural fistula, effusion pleurisy occurs in approximately 20% of cases of acute pancreatitis (enzymatic, pancreatogenic pleurisy). Perforation of the esophagus in 60% of patients leads to pleural effusion. As a rule, with the above pathologies, the effusion is unilateral.

Other causes

• PE (hemorrhagic pleural effusion is noted in half of the cases of pulmonary embolism).
• Injuries of the chest.
• Overdose of anticoagulants or thrombolytic drugs.
• Allergic reaction to drugs.
• Sarcoidosis.
• Periodic illness.
• Chronic renal failure (uremic pleurisy).
• Endocrine disorders: hypothyroidism (due to increased capillary permeability).
• Pulmonary fibrosis.

Diagnosis

The presence of pleural effusion requires a visit to a pulmonologist or general practitioner. Based on the findings of the physical examination, it can be suspected that there is fluid in the pleural cavity. Such signs include weakening of voice trembling, dullness of percussion sound, weakening of breath sounds during auscultation. It should be noted that these symptoms can only be detected if the volume of the effusion exceeds 300 ml.

During the interview and examination, the doctor may identify signs that are characteristic of a particular disease that could cause the development of pleural effusion. For example, fever and a wet cough are most typical of pneumonia, persistent pain in the joints is observed in rheumatological patients, generalized swelling may suggest a pathology of the liver or kidneys.

An important place is occupied by anamnestic data – what chronic diseases the patient suffers from, what medications he takes, whether he underwent surgical interventions, which specialists he is registered with, etc. One of the key roles in the search for an etiological factor is the direct examination of the pleural fluid obtained using diagnostic thoracocentesis:

• Physical and chemical properties. The color, transparency of the pleural fluid, its pH is assessed. The concentration of protein, glucose, LDH activity is determined. A high content of amylase is characteristic of pancreatogenic pleurisy. If tuberculous pleurisy is suspected, the level of adenosine deaminase is measured.
• Cytological examination. Microscopy of the punctate is carried out, the cellular composition is studied (erythrocytes, lymphocytes, neutrophils).
• Microbiological examination. Bacterial culture is mandatory (including culture studies for Mycobacterium tuberculosis) with the determination of sensitivity to antibacterial drugs.

Previously, Rivalta’s test was used in clinical practice to differentiate between transudate and exudate. If turbidity appeared when acetic acid was added to the pleural fluid (PJ), the fluid was considered exudate. However, this technique has a number of disadvantages. First, the visual control of the cloudiness of the solution is a very subjective assessment of the results of the sample. Secondly, the test reflects only the presence of protein in the punctate, which can be both in the transudate and in the exudate. Therefore, it is recommended to use Light’s special criteria. If at least one of them is present, the fluid is an exudate:

• The ratio of pancreatic protein to total serum protein is more than 0.5;
• The ratio of the concentration of LDH in the pancreas to LDH serum more than 0.6;
• LDH of pleural fluid exceeds 2/3 of the upper limit of normal for serum LDH.

Also, to establish an accurate diagnosis, additional tests are prescribed:

• Complete blood count. In persons with infectious pleurisy, there are signs of a pronounced inflammatory process – leukocytosis with a shift of the formula to the left, an increase in ESR. In rheumatological and oncological diseases, normochromic normocytic anemia is often observed.
• Biochemical blood test. The level of total protein and albumin, urea, creatinine, LDH activity is determined.
• Urinalysis. Nephrotic syndrome is characterized by a high concentration of protein in the urine.
• Detection of autoantibodies . For the diagnosis of rheumatological pathology, tests are carried out for specific antibodies – aCCP, antibodies to DNA, to extractable nuclear antigens, etc.
• Chest Imaging . To determine the presence and volume of effusion, an X-ray of the chest cavity and an ultrasound examination of the pleural cavities are performed. To assess the condition of the lung tissue (infiltrates, fibrosis), CT is recommended.
• Histological examination . To diagnose mesothelioma or metastases to the pleura, a transthoracic pleural biopsy is performed.

Pleural ultrasound

Treatment of pleural effusion

Elimination of effusion

In the course of treatment, a therapeutic pleural puncture (thoracocentesis) should be performed first to evacuate the pleural effusion, which reduces chest excursion and makes breathing difficult. In the presence of a massive pleural effusion (at the level of II-III ribs), thoracocentesis is performed on an emergency basis immediately after the patient’s hospitalization.

It is recommended to remove no more than 1.5 liters per procedure to avoid sudden expansion of the lung, which can lead to mediastinal reversal. For the subsequent gradual removal of fluid, a drainage tube is installed. With pleural effusion caused by congestive CHF, in the case of a positive response to conservative diuretic therapy, puncture is not performed, even if the volume of fluid exceeds 1 liter.

For various pathologies, drugs can be administered intrapleurally – antibiotics, cytostatics, enzyme inhibitors. In patients with recurrent exudative pleurisy, pleurodesis is performed to avoid recurrence. This procedure consists in the introduction of sclerosing substances (for example, talc) into the pleura. They cause obliteration of the visceral and parietal pleura (chemical serositis), which further prevents the appearance of effusion.

Etiopathogenetic therapy

Depending on the etiological factor that caused the pleural effusion, the following types of therapy are used:

• Oxygen therapy. Patients with severe pneumonia with respiratory failure are inhaled with oxygen through a mask or nasal cannula. When saturation is less than 90%, connection to a ventilator is indicated.
• Antibacterial therapy. In pleurisy of bacterial etiology, extended-spectrum antibiotics are used – cephalosporins, fluoroquinolones. In the case of tuberculous pleurisy, a combination of anti-tuberculous chemotherapy drugs is prescribed.
• CHF control . Patients with CHF should follow a salt-restricted diet of up to 3 g per day. To eliminate decompensation and stimulate the excretion of excess fluid, loop diuretics are prescribed. Standard treatment on an ongoing basis includes ACE inhibitors, beta-blockers, aldosterone receptor antagonists.
• Correction of hypoalbuminemia. Used intravenous albumin, antiviral therapy for hepatitis, hormonal treatment of nephrotic syndrome.
• Anti-inflammatory therapy. In order to suppress autoimmune inflammation, glucocorticoids, cytostatics, synthetic antimalarials are used.