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Pleurisy

Pleurisy, also known as pleuritis, is a condition characterized by inflammation of the pleura, the two thin layers of tissue that separate the lungs from the chest wall, resulting in sharp chest pain that typically worsens with breathing, coughing, or sneezing.^[1]^[2] This inflammation causes the pleural surfaces to rub against each other, triggering pain through somatic nerve fibers, and may lead to additional symptoms such as shortness of breath, fever, or a dry cough depending on the underlying cause.^[2]^[3] The most common causes of pleurisy include viral infections, such as those from influenza or coxsackieviruses, which account for many cases, as well as bacterial infections like pneumonia or tuberculosis, autoimmune disorders such as systemic lupus erythematosus or rheumatoid arthritis, pulmonary embolism, malignancies, trauma, or certain medications.^[1]^[2] Approximately 30-40% of cases are idiopathic, meaning the cause remains unknown, while risk factors include recent respiratory infections, family history of autoimmune diseases, or conditions like sickle cell disease.^[2] Complications can arise, such as pleural effusion (fluid buildup in the pleural space), atelectasis (lung collapse), or empyema (pus accumulation), which may impair breathing and require intervention.^[1]^[3] Diagnosis typically involves a physical exam to detect a pleural friction rub, imaging like chest X-rays or CT scans to identify inflammation or effusion, blood tests for infection or autoimmune markers, and sometimes procedures such as thoracentesis to analyze fluid or thoracoscopy for biopsy if malignancy or tuberculosis is suspected.^[2]^[4] Treatment focuses on addressing the underlying cause—such as antibiotics for bacterial infections or supportive care for viral cases—along with pain management using nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen, rest, and avoiding irritants like smoking.^[4]^[3] Prognosis is generally favorable for acute cases, resolving within 2-4 weeks, though it worsens with associated conditions like cancer or pulmonary embolism.^[2]

Overview

Definition

Pleurisy, also known as pleuritis, is an inflammation of the pleura, the thin, double-layered serous membrane that envelops the surface of the lungs (visceral pleura) and lines the inner aspect of the thoracic cavity (parietal pleura).^[1]^[2] The pleural layers are separated by a small volume of fluid that acts as a lubricant, enabling the lungs to expand and contract smoothly during respiration while providing mechanical protection against friction and minor trauma.^[5]^[6] The condition was first systematically described in ancient Greek medical texts by Hippocrates around the 5th century BCE, where it was termed "pleuritis" and linked to imbalances in bodily humors, often presenting as a complication of respiratory infections.^[7] Understanding advanced significantly in the early 19th century through autopsy examinations conducted by French physician René Laënnec, who correlated auscultatory findings with postmortem observations of pleural inflammation, adhesions, and effusions, laying the groundwork for modern pathological classification.^[8]^[9] Pleural effusions, often associated with pleurisy, affect an estimated 1.5 million individuals annually in the United States.^[10] Globally, the incidence of pleural disease, which includes pleurisy, is approximately 360 cases per 100,000 population per year.^[11] It is classified as dry pleurisy, characterized by fibrinous inflammation without significant fluid accumulation, or wet pleurisy, involving exudative effusion in the pleural space.^[12]^[13]

Epidemiology

Pleurisy, an inflammation of the pleural membranes, exhibits varying prevalence globally as part of broader pleural disease, with an annual incidence of approximately 200-350 cases per 100,000 population, higher in regions burdened by infectious diseases.^[14] In developing countries, infectious etiologies such as tuberculosis contribute to elevated incidence, where tuberculous pleurisy accounts for 2.2% to 31.4% of all tuberculosis cases and up to 67% of extrapulmonary tuberculosis presentations.^[15] Demographically, pleurisy is more prevalent among adults over 50 years of age, reflecting age-related vulnerabilities to underlying conditions like pneumonia and autoimmune disorders.^[2] A slight male predominance is observed, particularly in tuberculous cases, with male-to-female ratios often exceeding 2:1 in high-burden settings.^[16] Incidence is markedly increased in immunocompromised populations, such as those with HIV, where pleural involvement in tuberculosis rises significantly due to impaired immune responses.^[15] Geographically, rates are highest in tuberculosis-endemic areas, including sub-Saharan Africa and South Asia, which together account for over 60% of global tuberculosis cases and correspondingly elevated pleurisy from infectious causes.^[17] Pleural effusions have been reported in 5-11% of COVID-19 cases.^[18] Key risk factors include smoking, which exacerbates chronic lung diseases like COPD that predispose to pleural inflammation, and occupational exposures such as asbestos, associated with asbestos-related pleurisy and malignancies.^[19] Autoimmune disorders, including systemic lupus erythematosus (affecting 40-60% of patients at some point) and rheumatoid arthritis (3-5% symptomatic cases), further elevate risk through inflammatory mechanisms.^[2] As of 2025, infectious pleurisy cases have declined in vaccinated populations, particularly for vaccine-preventable respiratory pathogens, though global tuberculosis control efforts show mixed progress with persistent high burdens in low-resource regions.^[20] Conversely, autoimmune-related pleurisy is rising amid aging demographics and post-COVID autoimmune sequelae, with studies noting increased interstitial lung involvement in older adults.^[21]

Pathophysiology

Anatomy of the Pleura

The pleura is a serous membrane that envelops the lungs and lines the thoracic cavity, consisting of two principal layers: the visceral pleura, which directly covers the lung parenchyma and extends into the fissures to delineate lung lobes, and the parietal pleura, which lines the inner surface of the chest wall, diaphragm, and mediastinum.^[22] These layers are separated by the pleural cavity, a potential space that normally contains a thin layer of lubricating fluid, approximately 10 to 20 mL in volume, which facilitates smooth movement during respiration.^[23] The right and left pleural cavities are entirely separate, with the right side accommodating a larger lung volume due to the heart's position on the left, resulting in slight anatomical asymmetries such as the presence of an additional horizontal fissure in the right lung.^[5] Both pleural layers are composed of a single layer of mesothelial cells overlying a submesothelial layer of connective tissue, which includes blood vessels, lymphatics, and nerves.^[22] The visceral pleura receives its blood supply from bronchial arteries, while the parietal pleura is supplied by systemic arteries such as the internal thoracic, intercostal, and phrenic arteries; lymphatic drainage from the visceral pleura directs to hilar nodes, whereas parietal lymphatics drain through stomata to various thoracic lymph node stations.^[22] Pleural fluid is produced primarily at the parietal pleura through filtration from systemic capillaries, governed by Starling's forces, where the net filtration pressure is determined by the equation:

\text{Net filtration pressure} = (P_c - P_i) - \sigma (\pi_c - \pi_i)

Here, P_c is capillary hydrostatic pressure, P_i is interstitial (pleural) hydrostatic pressure, \sigma is the reflection coefficient for proteins, \pi_c is capillary oncotic pressure, and \pi_i is interstitial oncotic pressure.^[24] The primary functions of the pleura include reducing friction between the lungs and chest wall during breathing, maintaining negative intrapleural pressure (typically -3 to -5 cmH₂O) to support lung expansion and prevent collapse, and serving as an immune barrier through lymphatic drainage of potential pathogens or debris.^[22] Innervation differs between layers: the visceral pleura lacks somatic sensory nerves and thus does not contribute to pain sensation, while the parietal pleura is innervated by the phrenic nerve for its central portions (mediastinal and diaphragmatic), leading to referred pain to the shoulder or upper abdomen via shared dermatomes, and by intercostal nerves for the peripheral costal region, causing localized chest wall pain.^[22]

Mechanisms of Inflammation

Pleurisy arises from an inflammatory cascade typically triggered by infection or injury to the pleural space, initiating a response where damaged mesothelial cells release pro-inflammatory cytokines such as interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-α).^[2] These cytokines activate adjacent mesothelial and endothelial cells, promoting the expression of adhesion molecules and chemokines like IL-8, which facilitate the rapid influx of neutrophils into the pleural cavity.^[25] This neutrophil recruitment amplifies the inflammatory process by releasing additional mediators, including reactive oxygen species and proteases, that further damage pleural tissues.^[26] The inflammation in pleurisy manifests in distinct types based on the exudate composition and severity. Fibrinous pleurisy involves dry inflammation with prominent fibrin deposition on pleural surfaces, leading to adhesions without significant fluid accumulation.^[2] Serous pleurisy results in a clear, exudative effusion due to inflammatory increases in vascular permeability or mild to moderate inflammation, while purulent pleurisy, often termed empyema, features pus-laden exudate from bacterial infection, with high levels of neutrophils and bacteria.^[26] Pathogenic steps progress from initial vascular changes to chronic sequelae. Cytokine-driven endothelial activation increases vascular permeability in the pleural microvasculature, allowing plasma proteins and fluid to leak into the pleural space and form an inflammatory exudate.^[25] This exudate promotes fibrin deposition by mesothelial cells expressing tissue factor, which can generate a friction rub during breathing and, if unresolved, lead to fibrous adhesions or pleural fibrosis through sustained fibroblast activation.^[26] The immune response plays a central role in perpetuating pleural inflammation. Complement activation, particularly the classical pathway via immune complexes, enhances opsonization and chemotaxis, drawing more inflammatory cells to the site.^[2] Pleural mesothelial cells actively contribute by producing pro-inflammatory mediators such as monocyte chemoattractant protein-1 (MCP-1) and IL-6, which recruit monocytes and sustain the cytokine milieu.^[25] As of 2025, emerging research highlights the NLRP3 inflammasome's involvement in sterile pleurisy, where non-infectious triggers like asbestos or autoimmunity activate this multiprotein complex in mesothelial cells, leading to IL-1β release and pyroptotic cell death that exacerbates effusion formation.^[27] Additionally, genetic factors such as HLA-DR4, HLA-DR3*01, and HLA-DR2 alleles are associated with increased susceptibility to drug-induced systemic lupus erythematosus, a condition that can lead to autoimmune-mediated pleurisy through immune dysregulation.^[2]

Signs and Symptoms

Clinical Presentation

The primary symptom of pleurisy is sharp, stabbing chest pain that is typically unilateral and localized to the lower chest or side, worsening with inspiration, coughing, sneezing, or any movement that expands the chest wall.^[1]^[2] A characteristic physical sign is the pleural friction rub, a creaking or grating sound heard on auscultation over the affected area during breathing, resulting from inflamed pleural surfaces rubbing together.^[1]^[2] This pleuritic pain often eases or resolves temporarily when the patient holds their breath or lies on the affected side to minimize pleural friction.^[1]^[2] Associated symptoms commonly include dyspnea, which arises from the patient's instinctive shallow breathing to avoid exacerbating the pain, along with a dry, non-productive cough, fever, and tachypnea.^[1]^[2] The pain may radiate to the shoulder, neck, or back due to involvement of the phrenic or intercostal nerves.^[2] Pleurisy can present with acute onset, characterized by sudden severe pain often linked to infectious causes such as viral or bacterial pleuritis, typically resolving within 2-4 weeks with treatment of the underlying condition.^[2] In contrast, chronic pleurisy develops gradually and persists longer, frequently associated with autoimmune disorders like systemic lupus erythematosus or rheumatoid arthritis.^[2] In elderly patients, symptoms of pleurisy may be atypical due to comorbidities, sometimes presenting with confusion or altered mental status alongside respiratory infections.^[2] Pediatric cases are often tied to viral illnesses and may present with fever, cough, and tachypnea, though children may not clearly articulate localized pain.^[2] As of 2025, pleuritic chest pain and dyspnea are recognized symptoms in long COVID cohorts, with breathlessness severity often assessed using the Borg scale.^[28]^[29] In some instances, the development of a pleural effusion may temporarily relieve the pain by separating the inflamed pleural layers.^[1]

Associated Complications

Pleurisy, characterized by inflammation of the pleural membranes, frequently leads to pleural effusion, the abnormal accumulation of fluid in the pleural space, which can be either a transudate (due to systemic factors like heart failure) or an exudate (resulting from local pleural inflammation or infection).^[10] This complication often manifests with a reduction in the sharp pleuritic pain as the effusion separates the inflamed pleural layers, but it progressively causes dyspnea due to restricted lung expansion.^[1] Effusions are classified using Light's criteria, which identify an exudate if the pleural fluid protein-to-serum protein ratio exceeds 0.5, the pleural fluid lactate dehydrogenase (LDH)-to-serum LDH ratio surpasses 0.6, or the pleural fluid LDH exceeds two-thirds of the upper limit of normal serum LDH.^[10] In cases of pleurisy linked to pneumonia or other infections, exudative effusions predominate and occur in up to 40% of patients with underlying pulmonary embolism-associated pleurisy, though rates vary by etiology and are higher in bacterial forms.^[30] Pneumothorax, the presence of air in the pleural space leading to partial or complete lung collapse, can present with symptoms similar to pleurisy and may occur in association with underlying lung pathology like pneumonia, but is not typically a direct complication of pleural inflammation alone.^[2]^[31] This condition impairs ventilation and oxygenation, with tension pneumothorax representing a life-threatening variant characterized by increased intrathoracic pressure causing mediastinal shift, hypotension, and cardiovascular collapse, necessitating immediate decompression.^[31] Hemothorax, involving the accumulation of blood in the pleural space, may develop in pleurisy secondary to trauma, malignancy, or vascular rupture amid intense inflammation, potentially leading to hypovolemic shock from significant blood loss.^[32] Blood accumulation restricts lung function and increases infection risk, with pleural fluid hematocrit exceeding 50% of peripheral blood confirming the diagnosis.^[33] Other associated complications include empyema, a pus-filled pleural collection often evolving from an untreated exudative effusion in infectious pleurisy, which requires prompt drainage to prevent sepsis and chronic fibrosis.^[10] Trapped lung, resulting from fibrotic pleural adhesions that restrict lung re-expansion despite fluid removal, commonly follows prolonged inflammatory or infectious episodes and can lead to persistent dyspnea.^[34] Overall, pleural effusions complicate 30-50% of pleurisy cases, with higher rates and severity in bacterial etiologies, while other issues like empyema occur in about 5-10% of parapneumonic effusions.^[35] Management of these often involves drainage procedures, as detailed in interventional approaches.^[10]

Causes

Infectious Causes

Infectious causes of pleurisy primarily involve pathogens that directly invade the pleural space or trigger an inflammatory response in the pleura, often as a complication of adjacent lung infections like pneumonia.^[2] Viral infections represent the most common etiology, accounting for the majority of cases in otherwise healthy individuals. Common culprits include influenza viruses, adenoviruses, coxsackieviruses, respiratory syncytial virus (RSV), and parainfluenza viruses, which can lead to pleurisy through direct pleural invasion or secondary immune-mediated inflammation.^[2]^[36] More recently, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been associated with pleurisy, either during acute COVID-19 pneumonia or as a post-infectious manifestation in long COVID syndromes, where persistent pleural inflammation contributes to ongoing chest pain.^[37]^[38] Bacterial infections often arise as extensions from pneumonic processes and can progress to more severe complications like empyema, a pus-filled pleural effusion. Streptococcus pneumoniae is a leading cause, particularly in community-acquired pneumonia, though widespread pneumococcal vaccination has contributed to a decline in such cases among vaccinated populations.^[2]^[39] Other bacteria include Staphylococcus aureus, Streptococcus pyogenes, and Haemophilus influenzae, while Mycobacterium tuberculosis causes tuberculous pleurisy in approximately 3-30% of extrapulmonary tuberculosis cases, depending on regional prevalence, often presenting as a primary infection or reactivation with lymphocytic pleural effusion.^[40] As of 2025, Mycoplasma pneumoniae infections have shown a notable resurgence, with increased incidence reported in children and adolescents since late 2024, leading to atypical pneumonia and associated pleurisy, though cases appear to be decreasing nationally.^[41]^[42] Fungal and parasitic causes are uncommon and typically occur in immunocompromised hosts or in endemic regions. Fungal pathogens such as Aspergillus species, Candida, and endemic fungi like Coccidioides (causing coccidioidomycosis) or Histoplasma can invade the pleura, often complicating disseminated infections or chronic lung disease.^[2]^[43] Parasitic infections, such as those from Echinococcus granulosus leading to hydatid cysts, rarely cause pleurisy through cyst rupture into the pleural space or secondary compression, predominantly in areas with high livestock exposure.^[44] Post-infectious reactive pleurisy frequently follows resolution of primary respiratory infections, such as viral illnesses or bacterial pneumonia, where immune responses persist in the pleural lining without ongoing active infection.^[2] Diagnosis of these infectious etiologies often involves pleural fluid cultures, as detailed in laboratory investigations.^[2]

Noninfectious Causes

Noninfectious causes of pleurisy encompass a range of systemic, traumatic, and iatrogenic factors that lead to pleural inflammation without microbial involvement. These etiologies often manifest as sterile pleural effusions or direct irritation of the pleural surfaces, contributing significantly to cases where no infectious agent is identified. Common mechanisms include autoimmune-mediated damage, neoplastic invasion, vascular occlusion, and mechanical injury, each requiring targeted diagnostic evaluation to differentiate from infectious origins.^[2] Autoimmune and rheumatologic disorders are prominent noninfectious triggers, with rheumatoid arthritis affecting up to 5% of patients through synovial inflammation extending to the pleura, often presenting with exudative effusions rich in rheumatoid factor. Systemic lupus erythematosus (SLE) similarly involves pleurisy in 40-60% of cases, sometimes as an initial manifestation in about 10% of patients, driven by immune complex deposition and complement activation in pleural tissues. Hypersensitivity reactions, including those in Sjögren's syndrome or ankylosing spondylitis, account for approximately 2-3% of pleural biopsies, highlighting the role of chronic immune dysregulation in pleural pathology.^[2]^[2]^[2] Malignancy represents another key noninfectious cause, accounting for approximately 56% of pleural biopsy cases, including primary lung cancer (16%), mesothelioma (often linked to asbestos exposure; 23%), metastatic disease (such as from breast cancer), and lymphomas (2.5%), leading to malignant effusions and sharp pleuritic pain. Paraneoplastic syndromes occasionally mimic inflammatory pleurisy through remote immune effects. Median survival post-diagnosis is approximately 13 months, underscoring the prognostic implications.^[2]^[2]^[2] Thromboembolic events, particularly pulmonary embolism, provoke pleurisy in 5-20% of cases by causing pulmonary infarction and secondary pleural inflammation, with 75% of affected patients reporting pleuritic chest pain alongside effusions. This condition is a leading life-threatening noninfectious etiology, often requiring urgent anticoagulation to mitigate ongoing inflammation.^[2]^[2] Traumatic and iatrogenic factors directly injure pleural tissues, as seen in chest wall trauma or rib fractures that disrupt the pleural lining and incite localized inflammation. Post-surgical complications, such as after coronary artery bypass grafting (CABG), result in pleural effusions in up to 20-30% of patients due to surgical manipulation and inflammatory responses, potentially evolving into pleurisy. Pancreatitis, whether acute or chronic, extends inflammation to the left pleura via diaphragmatic irritation, leading to effusions in 4-17% of severe cases.^[2]^[45] Other noninfectious causes include uremia in chronic kidney disease, where up to 20% of patients develop persistent pleural effusions from uremic toxins irritating the pleura. Drug-induced pleurisy, exemplified by nitrofurantoin, occurs in roughly 1 in 5,000 users through hypersensitivity mechanisms, manifesting as acute reactions within days of initiation or chronic fibrosis after prolonged exposure. Idiopathic pleurisy, lacking identifiable etiology, comprises 30-40% of cases, often following a benign course with spontaneous resolution in most patients.^[2]^[46]^[47] As of 2025, increased recognition highlights vaping-associated lung injury (EVALI) as an emerging cause, with pleural effusions and pleuritic symptoms reported in cases involving vitamin E acetate-contaminated products, contributing to inflammatory pleural damage. Immunotherapy-related adverse events, particularly immune checkpoint inhibitors like pembrolizumab, induce sterile pneumonitis with pleural involvement in 3-5% of treated patients, necessitating prompt corticosteroid intervention. Treatment for these noninfectious causes is tailored to the underlying etiology, as detailed in etiology-specific therapies.^[48]^[49]^[50]

Diagnosis

Medical History and Physical Examination

The diagnosis of pleurisy begins with a thorough medical history to elicit symptoms and risk factors. Patients typically report sharp, stabbing chest pain that worsens with inspiration, coughing, sneezing, or positional changes such as lying supine, often localized to one side of the chest and relieved by sitting upright or shallow breathing.^[4] Clinicians inquire about recent upper respiratory infections, travel to endemic areas for tuberculosis or other infections, history of autoimmune disorders like rheumatoid arthritis or systemic lupus erythematosus, recent trauma, smoking, and occupational exposures such as asbestos.^[2] Additional symptoms like fever, productive cough, shortness of breath, or unexplained weight loss are probed to identify potential underlying etiologies.^[51] An electrocardiogram (ECG) is often performed to exclude cardiac causes of chest pain, such as pericarditis or myocardial infarction.^[4] During the physical examination, vital signs are assessed first, revealing possible fever, tachycardia, tachypnea, or hypoxia indicative of systemic inflammation or associated infection.^[2] Inspection may show chest wall asymmetry, splinting, or use of accessory muscles due to pain-related guarding.^[51] Percussion of the chest can produce dullness if pleural effusion is present, while auscultation frequently detects a pleural friction rub—a characteristic creaking, grating, or squeaking sound heard during breathing as inflamed pleural surfaces rub together.^[2] Reduced breath sounds may also be appreciated over affected areas.^[51] These historical and exam findings provide clues for differential diagnosis; for instance, pleuritic pain exacerbated by supine position distinguishes it from musculoskeletal or cardiac sources, while associated arthralgias or rash may suggest autoimmune involvement.^[2]

Imaging Modalities

Chest X-ray serves as the initial imaging modality for diagnosing pleurisy, effectively identifying pleural effusions by demonstrating blunting of the costophrenic angle, pneumothorax through visualization of air in the pleural space, or parenchymal consolidation suggestive of underlying infection.^[4]^[52]^[53] This modality is widely accessible and provides a rapid assessment of lung expansion and potential complications such as atelectasis.^[51] Thoracic ultrasound is a valuable bedside technique for evaluating pleural abnormalities in pleurisy, particularly for confirming effusions, guiding diagnostic or therapeutic thoracentesis, and detecting septations indicative of empyema.^[4]^[54] It excels in identifying small effusions with a sensitivity greater than 90%, surpassing chest X-ray in detecting volumes as low as 20 mL, and offers real-time imaging without radiation exposure.^[55]^[56] Computed tomography (CT) scanning represents the gold standard for complex pleurisy cases, delineating underlying etiologies such as pleural masses, pulmonary embolism, or parenchymal lesions with high resolution.^[4]^[52] It is particularly useful when initial imaging is inconclusive, providing multiplanar views to assess loculations or mediastinal involvement. Low-dose CT protocols are used to reduce radiation while preserving diagnostic accuracy for pleural evaluations.^[57] Magnetic resonance imaging (MRI) is infrequently used in pleurisy but provides exceptional soft tissue characterization, aiding differentiation of malignant from benign pleural disease or evaluation of fibrosis.^[58]^[59] Its role is limited by longer scan times and availability, typically reserved for cases where CT findings are equivocal regarding tumor invasion or chronic changes.^[51] Artificial intelligence integration in imaging modalities has advanced pleural assessment, enabling automated detection of effusions on ultrasound and CT with sensitivities approaching 95% and supporting risk stratification for complications like empyema or malignancy.^[60]^[61] These AI tools enhance workflow efficiency and interobserver agreement, particularly in resource-limited settings.^[62]

Laboratory Investigations

Laboratory investigations play a crucial role in evaluating pleurisy by identifying signs of infection, inflammation, or underlying systemic conditions. Initial blood tests often include a complete blood count (CBC), which may reveal leukocytosis indicative of an infectious etiology.^[2] Inflammatory markers such as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) are commonly elevated in pleurisy due to pleural inflammation.^[4] Additionally, D-dimer levels are assessed to rule out pulmonary embolism as a cause, with values below 500 ng/mL typically excluding this condition in low-risk patients.^[2] Arterial blood gas (ABG) analysis is performed in cases of significant respiratory involvement to detect hypoxemia and respiratory alkalosis, which can occur in severe pleurisy with impaired gas exchange.^[2] Serologic testing targets potential autoimmune or infectious triggers; for instance, antinuclear antibodies (ANA) and anti-double-stranded DNA antibodies help diagnose systemic lupus erythematosus (SLE) as an underlying cause.^[2] Blood and sputum cultures are obtained to identify bacterial or tuberculous pathogens when infection is suspected.^[2] If pleural effusion is present, thoracentesis allows for fluid analysis, which is essential for characterizing the effusion. Pleural fluid pH below 7.2 suggests complicated infection or malignancy, while low glucose levels (<60 mg/dL) indicate bacterial empyema or rheumatoid involvement.^[2] Elevated amylase in the fluid points to pancreatic or esophageal sources.^[2] Light's criteria, established in 1972, differentiate exudative from transudative effusions based on pleural fluid protein exceeding 0.5 times the serum level, pleural fluid lactate dehydrogenase (LDH) surpassing 0.6 times the serum level, or pleural fluid LDH greater than two-thirds the upper limit of normal serum LDH. Advanced biomarker panels enhance diagnostic precision; procalcitonin levels can help distinguish bacterial from viral causes in infectious pleurisy. Point-of-care polymerase chain reaction (PCR) testing on pleural fluid or blood enables rapid identification of pathogens such as Mycobacterium tuberculosis, improving timeliness in resource-limited settings.^[2]

Invasive Diagnostic Procedures

Invasive diagnostic procedures for pleurisy are employed when noninvasive tests, such as imaging and laboratory analyses, fail to provide a definitive diagnosis, particularly in cases of unexplained pleural effusions requiring direct sampling for cytology to detect cancer cells or histology to identify tuberculosis or malignancy.^[63] These interventions allow for targeted fluid aspiration or tissue retrieval to guide etiology-specific management.^[64] Thoracentesis involves ultrasound-guided needle aspiration of pleural fluid, serving both diagnostic and therapeutic purposes by alleviating symptoms like dyspnea while enabling fluid analysis for cellular composition, as referenced in laboratory investigations.^[65] The procedure is indicated for moderate to large effusions in pleurisy, with a pneumothorax risk of approximately 6%, reduced further by ultrasound guidance.^[66] Pleural biopsy obtains tissue samples for histopathological examination, crucial in suspected malignancy or tuberculosis when fluid cytology is nondiagnostic. Closed needle biopsy, performed percutaneously under imaging guidance, uses a specialized needle to sample the parietal pleura and is suitable for outpatient settings, though its diagnostic yield is lower (around 50-60%) compared to more invasive methods.^[67] Risks include pneumothorax and bleeding, occurring in less than 1% of cases.^[68] Open pleural biopsy via thoracoscopy provides direct visualization and higher diagnostic accuracy (over 90%), allowing biopsy of suspicious lesions.^[69] Bronchoscopy is indicated if endobronchial involvement, such as obstruction or primary lung pathology contributing to pleurisy, is suspected based on imaging or history. Flexible fiberoptic bronchoscopy permits visualization of airways and sampling via brushings or lavage, though its yield in isolated pleural effusions is low (less than 10%).^[70] Complications are rare, primarily including transient hypoxia or minor bleeding.^[71] Video-assisted thoracoscopic surgery (VATS) provides direct visualization and a diagnostic yield over 90% for pleural biopsy in complex cases like loculated effusions.^[63]

Treatment

Symptomatic Management

Symptomatic management of pleurisy focuses on alleviating sharp chest pain and respiratory discomfort caused by pleural inflammation, enabling patients to breathe more comfortably without targeting the etiology. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen at doses of 400–800 mg every 6–8 hours, serve as first-line therapy to reduce both pain and pleural inflammation, often providing significant relief within hours.^[2]^[72] In severe cases where NSAIDs prove insufficient, short courses of opioids like codeine or morphine may be used for breakthrough pain, though monitoring for respiratory side effects is essential.^[73]^[74] To support respiration and prevent complications from pain-induced shallow breathing, supplemental oxygen therapy is recommended if hypoxemia develops, typically delivered via nasal cannula at 2–4 L/min to maintain saturation above 92%.^[75] Incentive spirometry, involving sustained deep inspirations against resistance, promotes lung expansion and helps avert atelectasis by countering reduced tidal volumes.^[76] Patients are encouraged to perform 10–15 breaths hourly while awake to sustain this benefit.^[77] Optimal positioning minimizes pleural rubbing during movement. A semi-upright posture, such as sitting at 45–60 degrees or propped with pillows, reduces gravitational stress on the pleura and eases breathing; alternatively, lying on the affected side can limit lung expansion on the painful side, thereby decreasing friction.^[4]^[78]^[79] Non-pharmacologic strategies further aid symptom control. Heat or cold packs applied to the chest for 15–20 minutes several times daily can relax muscles and numb nociceptors, offering adjunctive pain relief alongside rest to avoid exacerbating inflammation.^[80]^[79] Additionally, virtual reality (VR)-based breathing exercises, involving guided diaphragmatic and pursed-lip techniques in immersive environments, enhance pain tolerance and adherence to respiratory training in patients with pleuritic discomfort from various respiratory disorders.^[81]^[82] These approaches complement traditional measures while etiology-specific therapies address the root cause.

Etiology-Specific Therapies

Etiology-specific therapies for pleurisy target the underlying cause to resolve inflammation and prevent recurrence, contrasting with general symptomatic approaches.^[2] For infectious etiologies, treatment selection depends on the pathogen identified through diagnostic evaluation. Bacterial pleurisy, often secondary to pneumonia, is managed with antibiotics such as ceftriaxone, which provides broad-spectrum coverage against common respiratory pathogens like Streptococcus pneumoniae.^[83] Viral pleurisy, such as that associated with influenza, may benefit from antivirals like oseltamivir, particularly when initiated early to reduce complications including lower respiratory involvement.^[84] Tuberculosis-related pleurisy requires a standard anti-TB regimen known as RIPE therapy, consisting of rifampin, isoniazid, pyrazinamide, and ethambutol, administered for 6 to 9 months to eradicate Mycobacterium tuberculosis and resolve pleural inflammation.^[85] In autoimmune conditions like systemic lupus erythematosus (SLE) or rheumatoid arthritis, immunosuppressive therapies form the cornerstone of management. Corticosteroids such as prednisone are commonly used to suppress inflammation and alleviate pleural involvement, often starting at moderate doses with gradual tapering.^[4] For refractory cases, immunosuppressants like methotrexate are employed as steroid-sparing agents to control disease activity.^[86] Biologics, including rituximab, have shown efficacy in severe or refractory SLE-associated pleurisy by depleting B cells and inducing remission of pulmonary manifestations.^[87] Malignancy-induced pleurisy, frequently from lung cancer or metastases, is addressed through oncologic interventions tailored to the tumor type. Chemotherapy regimens, such as platinum-based combinations, target systemic disease and reduce pleural involvement.^[88] Radiation therapy may be applied for localized control, particularly in non-small cell lung cancer, to shrink tumors impinging on the pleura.^[89] Targeted therapies like EGFR inhibitors (e.g., erlotinib or osimertinib) are effective in EGFR-mutated lung adenocarcinomas with pleural effusions, improving survival and symptom control.^[90] Thromboembolic causes, such as pulmonary embolism, necessitate anticoagulation to prevent clot propagation and resolve associated pleural inflammation. Initial therapy typically involves unfractionated heparin or low-molecular-weight heparin, followed by oral anticoagulants for extended management.^[91] For autoimmune pleurisy, Janus kinase (JAK) inhibitors, such as tofacitinib or upadacitinib, represent an emerging targeted option, particularly in rheumatoid arthritis-associated cases, by modulating inflammatory pathways and improving interstitial lung disease outcomes.^[92] In cases with significant effusion complicating these etiologies, drainage may be briefly considered alongside cause-directed therapy.^[93]

Interventional Procedures

Interventional procedures for pleurisy primarily address complications involving the pleural space, such as effusions, pneumothorax, hemothorax, or empyema, by providing mechanical drainage or facilitating adhesion formation to prevent recurrence.^[94] These approaches are indicated when conservative measures fail to alleviate symptoms like dyspnea or when diagnostic sampling is required, often guided by imaging to confirm the need for intervention.^[4] Thoracentesis involves the percutaneous insertion of a needle or small catheter into the pleural space, typically under ultrasound guidance, to aspirate fluid for both diagnostic analysis and therapeutic relief of symptoms caused by pleural effusions associated with pleurisy.^[94] The procedure is performed after local anesthesia, with the patient in a sitting or supine position, targeting the 6th to 8th intercostal space in the midaxillary line to minimize risks like pneumothorax.^[94] For symptomatic relief, up to 1 to 1.5 liters of fluid can be safely removed in a single session, particularly when monitored to avoid reexpansion pulmonary edema, though larger volumes may be drained with pleural manometry to ensure pressures remain above -20 cm H₂O.^[95] This intervention is especially useful in infectious or inflammatory pleurisy where effusion contributes to pain and respiratory compromise.^[4] Chest tube insertion, or tube thoracostomy, is employed for more persistent or complicated pleural space issues in pleurisy, such as large effusions, pneumothorax, or hemothorax, allowing continuous drainage of air, blood, or fluid.^[96] The tube, often small-bore (≤14 French) for effusions, is placed through a chest wall incision under local anesthesia and sterile conditions, directed posteriorly for fluid or anteriorly for air, connected to a drainage system with suction if needed.^[97] For recurrent effusions, sclerotherapy via talc pleurodesis can be performed through the indwelling tube; talc slurry or poudrage induces inflammation and adhesion of pleural layers, achieving success rates of approximately 77% in preventing reaccumulation, particularly in malignant or persistent cases.^[98] This method is preferred over repeated aspirations for patients with better prognoses, balancing efficacy against risks like pain or infection.^[99] Video-assisted thoracoscopic surgery (VATS) or open thoracotomy serves as a minimally invasive or surgical option for pleurisy-related conditions requiring direct visualization, such as pleural biopsy for undiagnosed effusions or decortication to remove restrictive peel in empyema.^[100] VATS involves small incisions (typically 3-4) for inserting a thoracoscope and instruments, allowing evacuation of loculated fluid, division of septations, and tissue sampling with lower morbidity than thoracotomy, which is reserved for complex cases like extensive empyema or VATS failure.^[101] Conversion from VATS to thoracotomy occurs in 18-59% of empyema procedures, but VATS reduces hospital stays and postoperative pain while enabling effective management of infectious complications.^[100] Intrapleural fibrinolytics, combining tissue plasminogen activator (tPA) and deoxyribonuclease (DNase), are administered via chest tube for loculated effusions in pleurisy, particularly those resistant to simple drainage, to lyse fibrin septations and reduce pus viscosity.^[102] A typical regimen involves 10 mg tPA and 5 mg DNase instilled twice daily for 3 days, achieving surgical avoidance in over 90% of cases and shortening hospital stays by about 7 days, as demonstrated in randomized trials like MIST-2.^[102] This therapy is recommended for stage II empyema or complicated parapneumonic effusions with loculations, though it carries risks of chest pain (20%) or bleeding (2%), and is contraindicated in active hemorrhage.^[102] As of 2025, indwelling pleural catheters (IPCs) have become a standard outpatient option for managing recurrent malignant pleural effusions linked to pleurisy, allowing intermittent self-drainage to control symptoms without hospitalization.^[98] Inserted tunneled under local anesthesia, IPCs facilitate fluid removal every 1-2 days, with success in symptom palliation for 70-90% of patients and potential for auto-pleurodesis in 30-50% over time, per updated guidelines favoring them over repeated thoracentesis for trapped lung or poor surgical candidates. Complications like infection occur in 5-10%, but overall, IPCs improve quality of life in advanced malignancy.^[103]

Prognosis and Prevention

Prognosis

The prognosis of pleurisy varies significantly based on the underlying cause, with most cases resolving fully when promptly identified and managed. For uncomplicated viral pleurisy, the most common etiology, symptoms typically improve within 3 to 5 days and resolve completely in 2 to 4 weeks with supportive care alone, as the condition is self-limited.^[2]^[104] In contrast, pleurisy linked to malignancy carries a guarded outlook, with median survival after diagnosis ranging from 4 to 9 months, influenced by the primary tumor type and stage; for instance, lung cancer patients with malignant pleural involvement have a 5-year survival rate of approximately 3%.^[105]^[88] Untreated tuberculous pleurisy often leads to spontaneous resolution of the effusion but carries a substantial risk of progression to active pulmonary tuberculosis, with overall mortality for untreated TB approaching 50%.^[106]^[107] Key factors affecting recovery include the timeliness of diagnosis, effectiveness of etiology-specific treatment, and the patient's baseline health, such as comorbidities or immune status; early intervention can prevent complications and improve outcomes across etiologies.^[4]^[2] In autoimmune-associated cases, like those in rheumatoid arthritis or systemic lupus erythematosus, recurrence rates range from 10% to 20%, often tied to disease flares, though pleural involvement resolves in up to two-thirds of patients within 4 months with appropriate management.^[2]^[108] Long-term sequelae are uncommon in resolved cases but may include chronic pleuritic pain, pleural fibrosis leading to lung restriction, or, in instances of severe untreated effusions, cor pulmonale from resultant pulmonary hypertension and right heart strain.^[2] Overall survival exceeds 95% for uncomplicated pleurisy without effusion or systemic involvement, reflecting low mortality from benign causes like viral infections.^[109] As of 2025, biologic therapies for systemic lupus erythematosus have improved overall outcomes and quality of life, though evidence for specific benefits in pleural involvement remains limited, per recent reviews. The 2025 American College of Rheumatology guideline for SLE emphasizes early introduction of biologics like belimumab or anifrolumab for active disease, which may benefit pleural manifestations.^[110]^[111]

Prevention Strategies

Preventing pleurisy involves addressing its common underlying causes, such as infections, autoimmune conditions, and environmental exposures, through targeted strategies that reduce risk factors.^[2] Vaccination plays a key role in mitigating infectious causes of pleurisy. Annual influenza vaccination is recommended for all adults to prevent viral infections like flu that can lead to pleurisy as a complication.^[112] Similarly, pneumococcal vaccines, such as PCV20 or PPSV23, are advised for adults aged 65 and older or those with chronic conditions to reduce the risk of bacterial pneumonia, a frequent trigger for pleurisy.^[75] COVID-19 vaccination, including updated formulations, helps prevent severe respiratory illness that may result in pleural inflammation. In high-risk areas for tuberculosis, the BCG vaccine is used to lower the incidence of TB-related pleurisy, particularly in children and vulnerable populations.^[113] Lifestyle modifications target modifiable risk factors associated with pleurisy. Smoking cessation is crucial, as tobacco use increases susceptibility to respiratory infections and irritates the pleura, heightening pleurisy risk; quitting can significantly lower this vulnerability.^[2] Avoiding exposure to asbestos and other occupational irritants is essential, since asbestos fibers can cause chronic pleural inflammation leading to pleurisy; adherence to exposure limits prevents such damage.^[114] Prompt diagnosis and treatment of respiratory infections, such as with antibiotics for bacterial cases, are vital to avert progression to pleurisy or related complications.^[2] For individuals at elevated risk, tailored interventions can prevent pleurisy onset. In those with hypercoagulable states, prophylactic anticoagulants like low-molecular-weight heparin reduce the likelihood of pulmonary embolism, a known cause of pleurisy, by inhibiting clot formation.^[115] Family members of individuals with autoimmune diseases, such as rheumatoid arthritis or lupus, may benefit from targeted screening for autoantibodies to enable early detection and management of underlying conditions that predispose to pleural involvement.^[116] General infection control measures further decrease transmission of pathogens that cause pleurisy. Regular hand hygiene, including washing with soap for at least 20 seconds, effectively reduces the spread of respiratory viruses and bacteria.^[117] During pandemics or outbreaks, wearing masks in crowded settings helps prevent droplet transmission of infectious agents responsible for pleurisy-inducing illnesses.^[118] As of 2025, advancements in vaccination and regulatory frameworks enhance prevention efforts. Updated mRNA-based COVID-19 boosters demonstrate efficacy in reducing severe post-viral respiratory complications, including those involving the pleura, by bolstering immune responses against variants.^[119] Strengthened workplace regulations, such as OSHA standards limiting exposure to airborne irritants like asbestos, continue to protect against environmental triggers of pleural disease.^[120] Smoking remains a key risk factor, as detailed in epidemiology discussions.^[121]

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