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Empyema

Empyema, also known as empyema thoracis or pyothorax, is a serious infectious condition characterized by the accumulation of pus in the pleural space, the thin cavity between the lungs and the chest wall.^[1] This buildup typically results from bacteria invading the pleural cavity, most commonly as a complication of pneumonia, where 20-40% of cases develop a parapneumonic effusion that can progress to empyema in 5-10% of instances.^[1] The term derives from Greek, meaning "pus in the chest," and it represents a medical emergency that can lead to severe complications if not promptly treated.^[1] The primary cause of empyema is bacterial infection spreading from the lungs, often due to pathogens such as Streptococcus pneumoniae, Staphylococcus aureus, or anaerobes, though other sources include chest trauma, esophageal rupture, or post-surgical complications.^[1] Risk factors include extremes of age (such as younger than 60 or over 70), diabetes, chronic obstructive pulmonary disease (COPD), immunocompromise, and poor oral hygiene,^[2]^[1] with approximately 65,000 cases occurring annually in the United States (as of 2021).^[3] The condition evolves in three stages: an initial exudative phase with sterile fluid accumulation, a fibrinopurulent stage marked by bacterial proliferation and loculation (compartmentalization of pus), and a chronic organizational phase involving pleural fibrosis and thickening, which can restrict lung expansion.^[1] Epidemiologically, it affects approximately 6 per 100,000 people, with higher incidence in males (68%) and an average age of 58 years, and the incidence has been increasing in recent years; it carries a 30-day mortality rate of about 10.5%.^[1] Patients with empyema typically present with symptoms of the underlying infection, including fever, productive cough, pleuritic chest pain (worsening with breathing), shortness of breath, and chills, which may intensify as pus accumulates and impairs lung function.^[2] Diagnosis relies on clinical evaluation combined with imaging—such as chest X-rays (detecting fluid volumes over 175 mL), ultrasound for guiding procedures, or CT scans to differentiate from abscesses—and thoracentesis to analyze pleural fluid, which shows pus, low pH (<7.2), elevated lactate dehydrogenase (LDH), and low glucose levels.^[4] Blood tests often reveal leukocytosis and elevated inflammatory markers like C-reactive protein.^[2] Treatment focuses on source control through drainage of infected material and eradication of infection with antibiotics, typically administered for 2-6 weeks and tailored to culture results (e.g., broad-spectrum agents like amoxicillin-clavulanate initially).^[2] Drainage methods include tube thoracostomy (chest tube insertion), therapeutic thoracentesis for smaller collections, or intrapleural fibrinolytic therapy (e.g., tissue plasminogen activator and DNase) to break down loculations; surgical interventions like video-assisted thoracoscopic surgery (VATS) or open decortication are required in up to 20% of cases for advanced disease.^[1] Early intervention is critical, as delays can lead to complications such as sepsis, respiratory failure, bronchopleural fistula, or chronic pleural fibrosis.^[1] With prompt management, prognosis is favorable, with recovery in 2-6 weeks, though in-hospital mortality ranges from 5-15%, rising to 40% in immunocompromised patients; average hospital stays last 19 days, and the condition incurs significant costs of around $38,000 per case.^[1] Prevention emphasizes timely treatment of pneumonia and other thoracic infections, alongside vaccination against common pneumococcal strains.^[2]

Overview

Definition

Empyema derives its name from the Greek term empyein, meaning "to suppurate" or "pus-producing," reflecting the condition's hallmark of pus formation.^[5] Empyema is defined as the accumulation of pus—a thick, infected, purulent fluid composed of neutrophils (polymorphonuclear leukocytes), bacteria, cellular debris, and fibrin—in the pleural space, the potential cavity between the visceral pleura covering the lungs and the parietal pleura lining the thoracic wall.^[6]^[2]^[1] The pleural space normally contains only a small volume of serous fluid, approximately 0.3 mL per kg of body weight or about 10-20 mL total, which serves to lubricate lung movement during respiration; in empyema, this balance is disrupted by the influx of purulent material, resulting in pleural inflammation and potential lung entrapment through fibrin deposition and adhesions.^[7]^[8]^[1] This condition is distinct from a parapneumonic effusion, which involves sterile transudative or exudative fluid in the pleural space without pus or positive cultures, and from a pulmonary abscess, a localized collection of pus confined to the lung parenchyma rather than the extrapulmonary pleural cavity.^[9]^[2]^[10]

Epidemiology

Empyema exhibits a global incidence of approximately 5 to 20 cases per 100,000 population annually, with reported rates of about 11 per 100,000 in the United States as of 2016 and around 7-8 cases per 100,000 in Europe.^[1]^[11]^[12] Higher incidences are observed in developing countries, attributed to factors such as limited access to timely antibiotics and higher burdens of infectious diseases.^[13] In developed nations like England, the incidence per 100,000 population rose from 6.44 in 2008 to 8.38 in 2017, reflecting an upward trend.^[14] The condition complicates 2-5% of community-acquired pneumonias overall, primarily as a bacterial complication, and up to 10% of hospitalized pneumonia cases, with pleural effusions occurring in 20-40% of such admissions and 10% progressing to empyema.^[15]^[16] In pediatric populations, rates are elevated, occurring in approximately 2-7% of children hospitalized with community-acquired pneumonia.^[17]^[18] Demographically, empyema is more prevalent in children under 5 years, where it complicates a notable proportion of pneumonias, and in adults over 65 years; a male predominance exists with a ratio of 1.5:1 to 3:1.^[19]^[1] As of 2025, post-COVID-19 trends show rising incidence in some regions due to secondary bacterial infections following viral respiratory illnesses, particularly in children.^[20]^[21] Pneumococcal conjugate vaccines have reduced pediatric empyema cases by up to 50% in highly vaccinated populations by decreasing invasive pneumococcal disease.^[22] Geographic variations include elevated rates in areas with high tuberculosis prevalence, where tuberculous empyema contributes significantly to overall cases.^[23]

Etiology and Pathophysiology

Causes and Risk Factors

Empyema most commonly arises as a complication of bacterial pneumonia, which accounts for approximately 60% of cases. This occurs when a parapneumonic effusion becomes infected, leading to pus accumulation in the pleural space. The primary pathogens involved include Streptococcus pneumoniae, Staphylococcus aureus (including methicillin-resistant strains, MRSA), anaerobic bacteria such as Bacteroides species often associated with aspiration, and gram-negative organisms like Klebsiella pneumoniae.^[1]^[10] Secondary causes of empyema include rupture of a lung abscess into the pleural cavity, thoracic trauma or penetrating injuries, postoperative complications following procedures such as lobectomy, esophageal perforation that allows gastric contents to contaminate the pleural space, and subdiaphragmatic infections like appendicitis that spread upward. Esophageal perforation, in particular, leads to empyema through chemical mediastinitis and bacterial translocation, often involving polymicrobial flora. Rare infectious etiologies encompass fungal infections (e.g., Candida or Aspergillus species, typically in immunocompromised patients) and tuberculous empyema caused by Mycobacterium tuberculosis.^[1]^[10]^[24]^[1] Although true empyema requires an infectious process with pus formation, non-infectious conditions can mimic it by producing sterile pleural fluid collections, such as hemothorax (blood accumulation from trauma or iatrogenic injury) or chylothorax (chyle leakage from thoracic duct disruption). These mimics lack bacterial involvement and are distinguished by fluid analysis.^[1]^[25] Several risk factors predispose individuals to empyema development, particularly by impairing host defenses or facilitating bacterial spread to the pleura. Immunosuppressive states, including HIV infection, chemotherapy, and diabetes mellitus, increase susceptibility to severe infections. Chronic lung diseases such as chronic obstructive pulmonary disease (COPD) and bronchiectasis promote recurrent pneumonia and poor clearance of pleural effusions. Additional risks include alcohol abuse, intravenous drug use, and recent viral respiratory infections like influenza or COVID-19, which can lead to bacterial superinfection. In pediatric populations, congenital heart disease heightens vulnerability due to associated immune dysregulation and structural abnormalities.^[1]^[26]^[27]

Pathophysiological Stages

Empyema develops through a progressive series of pathophysiological stages following an initial pleural infection, typically arising from pneumonia or other thoracic insults. These stages reflect the evolving inflammatory response in the pleural space, transitioning from a simple effusion to a complex, organized process that can entrap the lung if untreated. The classification into three stages—exudative, fibrinopurulent, and organizing—guides therapeutic decisions based on the fluid's biochemical and structural changes.^[11]^[6] In the exudative stage (stage 1, typically 0-7 days after onset), infection increases vascular permeability in the pleural capillaries, leading to the accumulation of sterile, protein-rich fluid without significant bacterial invasion. This clear exudate has a pH greater than 7.2, glucose levels above 60 mg/dL, and lactate dehydrogenase (LDH) below 1000 IU/L, reflecting an acute inflammatory response that often resolves with systemic antibiotics alone, without the need for drainage.^[28]^[11]^[29] The fibrinopurulent stage (stage 2, approximately 7-14 days) marks bacterial proliferation within the pleural space, resulting in pus formation characterized by neutrophil influx, fibrin deposition, and the development of loculations that compartmentalize the fluid. The pleural fluid becomes turbid with a decreased pH below 7.2, glucose less than 40 mg/dL, and LDH exceeding 1000 IU/L, indicating ongoing tissue degradation and impaired clearance; intervention with drainage is essential to prevent progression.^[28]^[11]^[29] During the organizing stage (stage 3, beyond 14 days), persistent inflammation triggers fibroblast proliferation and collagen deposition, forming a thickened pleural "peel" that restricts lung expansion and leads to restrictive physiology. The pus turns viscous and adherent, trapping the lung and potentially causing atelectasis; this stage often necessitates more aggressive interventions to disrupt the fibrotic barriers.^[28]^[11]^[29] Underlying these stages are key inflammatory mechanisms, including the release of cytokines such as interleukin-8 (IL-8) and tumor necrosis factor-alpha (TNF-α), which chemotactically attract neutrophils into the pleural space and amplify the local immune response. Bacterial toxins and enzymes further contribute by degrading pleural tissue, promoting excessive fibrin deposition, and fostering adhesions that exacerbate loculation and organization. Common pathogens like Streptococcus pneumoniae drive this process through direct invasion following pneumonia.^[15]^[30]^[31]

Clinical Presentation

Signs and Symptoms

Patients with empyema typically present with a combination of systemic and local symptoms reflecting the infectious and inflammatory process in the pleural space. These manifestations often develop in the context of an underlying pneumonia, where bacterial invasion leads to pus accumulation.^[1] Systemic symptoms are prominent and include persistent fever often exceeding 38.5°C, night sweats, profound fatigue, unintentional weight loss, and leukocytosis with white blood cell counts greater than 15,000/μL, predominantly neutrophils. These signs indicate ongoing infection and systemic inflammatory response.^[1]^[2] Local symptoms primarily affect the chest and respiratory function, featuring sharp pleuritic chest pain that intensifies with breathing or coughing, dyspnea due to compression of the lung by the accumulating effusion, and a non-productive cough in early stages. In advanced cases with tissue necrosis, hemoptysis may occur, though it is less common.^[1]^[32] On physical examination, key findings include decreased or absent breath sounds over the affected side, dullness to percussion indicating fluid presence, and reduced chest wall expansion due to restricted lung movement; additionally, tachycardia and tachypnea are frequently observed as compensatory responses to hypoxia and infection.^[1]^[32] Symptom variations occur across age groups. In children, particularly infants, presentations may include irritability, feeding difficulties, tachypnea, and severe respiratory distress alongside fever and malaise, rather than clearly articulated chest pain. In the elderly, symptoms can be atypical, with confusion, minimal or absent fever, and generalized weakness predominating over classic respiratory complaints.^[33]^[34] If untreated, symptoms progressively worsen over weeks, evolving through stages of effusion accumulation and organization, potentially leading to sepsis and increased risk of multi-organ failure.^[1]^[35]

Classification

Empyema is classified etiologically into primary, secondary, and iatrogenic forms. Primary empyema arises from direct infection of the pleural space without underlying pulmonary disease and is rare, often resulting from conditions such as esophageal perforation or subdiaphragmatic abscess.^[1] Secondary empyema, which accounts for the majority of cases (approximately 60-80%), develops as a complication of pneumonia or other pulmonary infections, with bacterial spread from the lung parenchyma to the pleura.^[36] Iatrogenic empyema occurs following medical procedures, such as thoracic surgery, central line placement, or thoracentesis, and represents a smaller but significant proportion of cases.^[1] Anatomically, empyema is categorized based on the extent and nature of pleural involvement. Free-flowing empyema involves pus that lacks significant loculations, allowing for easier drainage.^[11] In contrast, complicated empyema involves loculated collections of pus, often with multiloculated compartments formed by fibrinous adhesions that complicate therapeutic intervention.^[1] Stage-based classification, originally proposed by Light, delineates the progression of empyema into three phases. Stage 1, the simple or exudative stage, involves thin, free-flowing pleural fluid with minimal fibrin deposition and negative cultures in most cases.^[37] Stage 2, the complicated or fibrinopurulent stage, is characterized by viscous pus, loculation due to fibrin strands, and positive bacterial cultures, often with low pH and glucose levels.^[1] Stage 3, the chronic or organizing stage, features thick pleural peels from fibroblast proliferation and collagen deposition, leading to lung entrapment.^[37] Microbiologically, empyema is classified according to the causative organisms isolated from pleural fluid. Aerobic bacteria, such as Streptococcus pneumoniae and Staphylococcus aureus, predominate in community-acquired cases.^[38] Anaerobic bacteria, including Bacteroides species, are common in aspiration-related empyema and often coexist with aerobes.^[36] Polymicrobial infections occur in approximately 13% of cases overall, rising to about 23% in culture-positive samples, particularly in hospitalized patients.^[38] Fungal empyema, such as that caused by Aspergillus species, is rare and typically affects immunocompromised individuals, while tuberculous empyema results from Mycobacterium tuberculosis and is more prevalent in endemic regions.^[1] The British Thoracic Society (BTS) guidelines integrate these elements into a practical scheme for parapneumonic effusions and empyema. Uncomplicated effusions are small and sterile, requiring no drainage; simple parapneumonic effusions are larger but uninfected; complicated parapneumonic effusions show signs of infection with pH <7.2 or positive cultures; and empyema denotes frank pus in the pleural space, necessitating drainage.

Diagnosis

Clinical Assessment

The clinical assessment of suspected empyema begins with a detailed history to identify potential etiologies and risk factors. Clinicians should inquire about recent episodes of pneumonia, the most common cause (accounting for approximately 50% of cases), as well as penetrating chest trauma, recent thoracic or abdominal surgery, and conditions leading to immunosuppression such as HIV infection, malignancy, diabetes, or corticosteroid use.^[1]^[39] Additional relevant history includes travel to regions endemic for tuberculosis to assess TB-related risk, and vaccination status, particularly for pneumococcal and influenza vaccines, to evaluate preventive measures against common precipitating infections.^[1]^[9] Physical examination focuses on systemic and localized findings to support suspicion of pleural space involvement. Vital signs often reveal fever (typically below 102°F), tachypnea, tachycardia, and hypoxemia in more advanced cases, reflecting the inflammatory and respiratory burden.^[39]^[9] Chest inspection may show asymmetry due to pleural effusion, while palpation can detect decreased tactile fremitus over the affected area. Auscultation typically demonstrates reduced or absent breath sounds, egophony, and dullness to percussion on the involved side; rales or bronchial breath sounds may indicate underlying pneumonia.^[40]^[39] An abdominal examination is essential to exclude subdiaphragmatic sources, such as abscesses from prior surgery or pancreatitis, which can extend to the pleural space via transdiaphragmatic spread.^[41]^[1] To gauge severity, especially when empyema complicates pneumonia or leads to sepsis, validated scoring systems are applied. The CURB-65 score, which assesses confusion, urea level, respiratory rate, blood pressure, and age ≥65 years, helps predict mortality and guide hospitalization needs in associated community-acquired pneumonia.^[42]^[1] Similarly, the quick Sequential Organ Failure Assessment (qSOFA) evaluates altered mentation, respiratory rate ≥22 breaths/min, and systolic blood pressure ≤100 mmHg to identify sepsis risk and prompt intensive care consideration.^[1]^[43] Red flags warranting urgent evaluation include rapid symptom progression, prominent unilateral chest findings suggesting loculated effusion, or lack of improvement after initial antibiotics for presumed pneumonia, indicating potential complicated parapneumonic evolution to empyema.^[40]^[9] Initial differential diagnosis relies on the clinical picture, distinguishing empyema from uncomplicated pleural effusions, lung abscesses, or tuberculosis based on history of acute infection versus chronicity and risk factors, prior to confirmatory testing; common associated symptoms such as chest pain and dyspnea further heighten suspicion when combined with these elements.^[1]^[39]

Diagnostic Tests

Diagnostic confirmation of empyema requires a combination of laboratory analysis, imaging, and microbiological evaluation, with thoracentesis serving as the cornerstone procedure for pleural fluid sampling.^[1] Pleural fluid obtained via thoracentesis, preferably under ultrasound guidance, is mandatory in suspected cases to differentiate empyema from uncomplicated parapneumonic effusions.^[44] The fluid typically appears grossly purulent, with characteristic biochemical parameters including a pH less than 7.2, glucose below 60 mg/dL, and lactate dehydrogenase (LDH) exceeding 1000 IU/L or three times the upper limit of normal serum LDH, indicating an exudative and complicated process.^[1] Additional laboratory findings may include complete blood count (CBC) revealing leukocytosis and anemia of chronic disease, alongside blood cultures to identify concurrent bacteremia.^[1] Light's criteria are employed to classify the effusion as exudative, supporting the diagnosis of empyema; these include a pleural-to-serum LDH ratio greater than 0.6, pleural LDH greater than two-thirds of the upper normal serum limit, or a pleural-to-serum protein ratio exceeding 0.5, with near 100% sensitivity for exudates.^[44] These parameters also contribute to staging empyema, such as identifying the fibrinopurulent stage when pH and glucose are markedly reduced.^[1] Imaging begins with chest X-ray, which detects pleural effusion through blunting of the costophrenic angle or a meniscus sign, particularly when the effusion exceeds 10 mm in depth on lateral views.^[44] Thoracic ultrasound enhances detection of small or loculated effusions, identifies septations indicative of organization, and safely guides thoracentesis with superior sensitivity compared to plain radiography.^[1] Contrast-enhanced chest computed tomography (CT) is the gold standard for delineating the extent of disease, revealing complications such as abscesses or the "split pleura" sign (pleural enhancement and thickening greater than 3 mm), with a pooled specificity of 90% for empyema diagnosis.^[1]^[45] Microbiological evaluation of pleural fluid involves Gram stain and cultures for aerobic (e.g., Streptococcus, Staphylococcus) and anaerobic organisms, with yields of 40-60% in empyema cases, improved by immediate inoculation into blood culture bottles; acid-fast bacilli (AFB) smears and fungal studies are pursued if tuberculosis or fungal infection is suspected.^[1] Polymerase chain reaction (PCR) assays on pleural fluid enable rapid pathogen identification, particularly in culture-negative cases.^[46] In select cases, positron emission tomography-computed tomography (PET-CT) with 18F-fluorodeoxyglucose is rarely utilized to differentiate chronic empyema from associated malignancy, leveraging maximum standardized uptake values exceeding 10.8 for high specificity in detecting tumor infiltration.^[47]

Management

Medical Treatment

The cornerstone of medical treatment for empyema involves prompt administration of intravenous antibiotics to eradicate the underlying infection, combined with supportive measures to stabilize the patient and address complications such as hypoxia and pleural loculations.^[1] Empirical antibiotic therapy is initiated immediately upon suspicion of empyema, typically within 1 hour in cases with signs of sepsis, to prevent progression and improve outcomes, as emphasized in updated infectious disease guidelines.^[48] For community-acquired empyema, broad-spectrum regimens such as ceftriaxone combined with metronidazole are recommended to cover common pathogens including Streptococcus pneumoniae, anaerobes, and Staphylococcus aureus.^[49] In hospital-acquired or healthcare-associated cases, where risks of methicillin-resistant S. aureus (MRSA) or Pseudomonas are higher, vancomycin plus piperacillin-tazobactam provides appropriate coverage.^[49] These intravenous therapies are continued for 3-6 weeks, transitioning to oral agents once clinically stable, with duration guided by culture results, clinical response, and source control.^[1] Once microbiological cultures and sensitivities are available, antibiotic therapy is de-escalated to targeted agents to minimize resistance and toxicity; for example, high-dose penicillin G is preferred for sensitive S. pneumoniae isolates.^[49] In loculated empyema, adjunctive intrapleural instillation of fibrinolytic agents such as tissue plasminogen activator (tPA) combined with deoxyribonuclease (DNase) via chest tube can facilitate drainage by breaking down fibrin and viscous pus, administered as tPA 10 mg plus DNase 5 mg every 12 hours for 3 days.^[1] Evidence from randomized trials supports this approach in reducing the need for surgery in stage II (fibrinopurulent) empyema, though older fibrinolytics like streptokinase have shown mixed results and are less commonly used today.^[1] Supportive care plays a vital role in optimizing recovery, including supplemental oxygen to correct hypoxemia, pain management with nonsteroidal anti-inflammatory drugs (NSAIDs) or opioids as needed, and nutritional support to bolster immune function, particularly in malnourished patients.^[1] Addressing the underlying etiology is essential; for instance, antiviral therapy may be added if empyema complicates influenza pneumonia.^[1] Guidelines, including the IDSA/ATS 2025 guidelines for community-acquired pneumonia (which address complications like empyema) and the AATS consensus guidelines for empyema, recommend de-escalation of broad-spectrum antibiotics as soon as culture data are available (typically within 48-72 hours after initiation) to promote antimicrobial stewardship, while extending total duration for complicated cases such as empyema.^[48]^[50]^[49] In complicated cases with persistent infection, medical therapy is often combined with drainage procedures to achieve full resolution.^[49]

Surgical Interventions

Surgical interventions are indicated for complicated empyema, particularly in stages 2 (fibrinopurulent) and 3 (organizing), when medical therapy with antibiotics and initial drainage fails, or when loculations prevent adequate pus evacuation.^[49]^[51] These procedures aim to mechanically drain infected material, debride necrotic tissue, and facilitate lung re-expansion to resolve infection and prevent chronic sequelae.^[1] Chest tube thoracostomy serves as the initial surgical approach for free-flowing pus in early-stage empyema, involving insertion of a 12- to 28-French tube under local anesthesia or sedation, positioned in the pleural space and connected to underwater seal drainage with suction to promote evacuation.^[49] This method achieves success in approximately 70% of uncomplicated cases by allowing continuous drainage and monitoring of output, though failure rates increase to 30-60% in the presence of loculations or thick pus, often necessitating escalation to more invasive techniques.^[52]^[53] For persistent infection in the fibrinopurulent stage, video-assisted thoracoscopic surgery (VATS) is preferred as a minimally invasive option for debridement and partial decortication, involving small incisions for camera and instrument insertion to break down septations, aspirate pus, and remove fibrinous deposits.^[49] VATS demonstrates success rates of 85-95% in resolving empyema, with reduced postoperative pain, shorter hospital stays (typically 4-8 days compared to 10-14 days for open procedures), and lower morbidity than traditional surgery.^[53]^[54] In advanced organizing-stage empyema or when VATS fails due to extensive pleural peel entrapment, open thoracotomy with full decortication is employed to excise the restrictive fibrous rind from both parietal and visceral pleura, enabling complete lung re-expansion and thorough irrigation of the cavity.^[55] This approach is reserved for complex cases, such as trapped lungs or multiloculated infections unresponsive to less invasive methods, and remains the gold standard for stage 3 disease despite higher risks of prolonged recovery.^[56] Emerging techniques as of 2025 include robotic-assisted VATS, which enhances precision in debridement through three-dimensional visualization and articulated instruments, potentially reducing conversion rates to open surgery in challenging anatomies, though widespread adoption is still evolving.^[57] Additionally, intrapleural catheters, such as tunneled small-bore devices, are gaining use for prolonged outpatient drainage in selected chronic or residual empyema cases post-initial intervention.^[49] Postoperative care involves continued systemic antibiotics guided by culture results alongside mechanical drainage, combined with chest physiotherapy and early mobilization to promote lung expansion and prevent atelectasis.^[49] Regular imaging and clinical monitoring ensure resolution, with most patients achieving full recovery within weeks when interventions are timely.^[53]

Prognosis and Complications

Prognosis

The prognosis of empyema has improved with modern management, but outcomes vary based on timely intervention and patient factors. With prompt treatment, including early drainage and antibiotics, the in-hospital mortality rate ranges from 5% to 15%.^[1] This rate increases to 20% or higher in cases of delayed diagnosis, elderly patients, or polymicrobial infections, where comorbidities and advanced disease contribute to poorer survival.^[58]^[59]^[60] Most patients achieve resolution with early drainage, though some may experience residual pleural changes.^[1] Key prognostic factors include early intervention within 7 days, which is associated with better outcomes, as is the simple (exudative) stage and infection with aerobic bacteria.^[61] In contrast, the organizing stage, anaerobic or polymicrobial infections, and comorbidities such as diabetes (which roughly doubles mortality risk) predict unfavorable prognosis.^[1]^[62]^[63] Long-term, survivors may develop chronic pain or restrictive lung disease due to pleural scarring, though many achieve stable function.^[1] In pediatric cases, long-term sequelae are minimal, with low rates of persistent issues.^[64] Pediatric cases generally have a better prognosis, with mortality rates under 5%.^[65] Video-assisted thoracoscopic surgery (VATS) is associated with improved outcomes, including shorter hospital stays of around 9-12 days compared to longer durations for open surgery.^[66]^[67]^[1]

Complications

Empyema, if untreated or inadequately managed, can lead to a range of acute complications that exacerbate the infection and threaten systemic stability. Sepsis can develop due to bacterial dissemination from the pleural space, often progressing to septic shock with high mortality risk.^[1] Acute respiratory distress syndrome (ARDS) may arise from severe inflammatory response and lung compression by the effusion, impairing gas exchange and necessitating mechanical ventilation. Empyema necessitans occurs when pus erodes through the parietal pleura into the chest wall or subcutaneous tissues, presenting as a subcutaneous abscess or fistula, though it remains uncommon. Bronchopleural fistula formation, resulting from pleural inflammation extending to bronchial tissue, leads to persistent air leaks, pneumothorax, and challenges in effective drainage. In chronic stages, particularly with delayed intervention, fibrothorax develops as organized fibrin and fibrous tissue entrap the lung, causing restrictive ventilatory defects and often requiring surgical decortication for release. Recurrent infections can occur, stemming from incomplete source control or persistent nidi of infection within the pleural space, with rates around 5% after surgical treatment.^[62] Osteomyelitis of the ribs can occur via direct extension of the empyema. In pediatric patients, chronic pleural effusions from empyema have been associated with scoliosis in some cases, attributed to mechanical distortion from the effusion or fibrotic changes. Systemic sequelae from prolonged empyema are less frequent but severe. Secondary amyloidosis, a rare outcome of chronic inflammation, can manifest as AA-type amyloid deposition in organs due to sustained infection, leading to multiorgan dysfunction. Metastatic infections, such as brain abscess via hematogenous spread, can occur in chronic empyema cases, highlighting the potential for distant seeding of pathogens. Treatment-related complications arise primarily from invasive procedures like video-assisted thoracoscopic surgery (VATS). Postoperative bleeding, wound infections, and prolonged air leaks (persisting beyond 5-7 days) are recognized complications of VATS and decortication, potentially prolonging recovery and hospital stays.^[1] Prevention of these complications hinges on early diagnosis and intervention, as delayed management increases the likelihood of requiring surgical intervention, with overall surgical rates around 30%.^[1] Recent guidelines emphasize multidisciplinary care involving pulmonologists, thoracic surgeons, and infectious disease specialists to optimize outcomes and reduce complication incidence in advanced-stage presentations. As of 2025, in-hospital mortality remains around 10.5% in some cohorts.^[68]

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