Thoracic Empyema

Etiology

Empyema thoracis, meaning “pus in the chest” in Greek, occurs when infections from various parts of the body spread to the pleural space. The most common cause of empyema is bacterial pneumonia and its resulting parapneumonic effusion. Approximately 20% to 40% of patients admitted for pneumonia experience associated parapneumonic effusion. Among these, 5% to 10% will develop empyema; 30% of these patients require surgical drainage, and the mortality rate for these patients is 15%. Less frequently, empyema can arise from conditions such as bronchogenic carcinoma, esophageal rupture, blunt or penetrating chest trauma, infectious mediastinitis spreading to the pleurae, infection crossing the diaphragm from abdominal sources, spinal infections, or postsurgical complications.

The development of pleural space infections likely involves increased permeability of the mesothelial layer of the inflamed pleurae, allowing bacteria to invade the typically sterile space. Interestingly, up to 56% of community-acquired and 73% of hospital-acquired pleural space infections demonstrate no radiographic signs of pneumonia. This, along with differing microbial profiles between pneumonia and pleural infections, suggests that hematogenous spread might be a factor in some patients with empyema. Despite these varied mechanisms, the most common etiologic pathway involves the aspiration of organisms from the oropharynx, leading to pneumonia in the dependent lobes, which, if left untreated, can progress to parapneumonic effusion and, ultimately, empyema.[6]

Risk Factors

Many pleural space infections present as complications from community- or hospital-acquired pneumonia.[1] Other causes include penetrating chest trauma, thoracic surgery, esophageal rupture, pulmonary tuberculosis, lung abscess, bronchiectasis, subphrenic abscess, and osteomyelitis of ribs. Independent risk factors for empyema development include:

• Younger than 60 
• Poor oral hygiene
• Disorders with a predisposition to aspiration (seizure, alcohol use disorder, central nervous system disease)
• Intravenous drug misuse
• Diabetes
• Cardiovascular disease
• Liver cirrhosis
• Other immunocompromised states (eg, human immunodeficiency virus infection or malignancy)[7][8][9]

The results of a prospective observational study found 6 associated risk factors in patients admitted with community-acquired pneumonia who subsequently developed empyema, including albumin less than 30 g/L, sodium below 130 mmol/L, platelet count greater than 400 x 10⁹, C-reactive protein over 100 mg/L, and a history of alcohol use or intravenous drug use disorders.[10]

Bacteriology

Aerobic Staphylococcus and Streptococcus species and gram-negative bacteria, including Escherichia coli, Haemophilus influenzae, and Klebsiella pneumoniae, are the predominant microorganisms in community-acquired empyema.[11] However, recent literature suggests that anaerobes and staphylococcal species have replaced Streptococcus pneumoniae as the primary pathogen in surgically treated empyemas. Also, anaerobic isolates were found to have a higher incidence of community-acquired pneumonia than previously reported.[12][13] Methicillin-resistant Staphylococcus aureus and gram-negative organisms, including Pseudomonas and Enterobacteriaceae, are pathogens commonly seen in hospital-acquired empyema. Anaerobes are slow-growing organisms that notoriously yield negative culture media. Therefore, broad-spectrum antibiotic coverage with anaerobic coverage is warranted.

The microbiology of pleural infections plays a critical role in patient outcomes, with survival rates varying with the causative organisms. For instance, patients with streptococcal infections had an 83% survival rate, similar to the 87% in cases where no organism could be identified. This suggests that many culture-negative pleural infections may be streptococcal, with antibiotics quickly reducing bacterial load, leading to negative cultures. Anaerobic infections also had relatively favorable outcomes, with an 80% survival rate. In contrast, diseases caused by Staphylococcus, Enterobacteriaceae, and mixed aerobic organisms were associated with much higher mortality, with only 55% of patients surviving at 1 year.[13]

Fungal empyema is a clinical entity that is rare but carries a high mortality. One single-center retrospective analysis isolated Candida and Aspergillus species from 65 critically ill patients with variable comorbidities, including malignancy. Most of these cases were nosocomial infections or had concomitant fungemia.[14]

Epidemiology

In the US, the incidence of parapneumonic empyema is estimated to be 6 cases per 100,000. In-hospital mortality in patients older than 65 is approximately 16.1%.[15] Between 2005 and 2014, 150,469 patients aged 18 and older were admitted to US hospitals for pleural infections. The average age of these patients was 58.3 years; 68% of patients were men. White patients accounted for 79.3% of the admissions, and 4.4% of patients presented with either severe sepsis (a classification that has since been replaced by the Third International Consensus Definitions for Sepsis and Septic Shock) or septic shock.[16] 

Pathophysiology

Approximately 60 years ago, the American Thoracic Society first described the evolution of empyema as a continuous process subdivided into 3 distinct but continuous stages or phases: exudative, fibrinopurulent and loculated, and chronic organizational. Specific pleural fluid characteristics, radiographic findings, and corresponding treatments distinguish these stages of parapneumonic effusion, pleural infection, and empyema.[6][17]

Exudative Stage 

The initial phase of empyema formation is an exudative effusion, where fluid rapidly accumulates in the pleural space. During this phase, pleural fluid is typically culture and Gram stain negative, with glucose levels exceeding 60 mg/dL and lactate dehydrogenase (LDH) levels less than 3 times the upper limit of normal for serum. Proinflammatory mediators like tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6), and IL-8 are believed to be vital in driving the inflammatory response at this stage.[6]

Fibrinopurulent and Loculated Stage 

The second phase is the fibrinopurulent stage, which follows the initial exudative phase and typically results if antibiotic treatment is inadequate or delayed. This phase is characterized by bacterial invasion into the pleural space. In this stage, the pleural fluid will generally have a glucose level below 60 mg/mL with a pH below 7.20 and a pleural fluid LDH greater than 3 times the upper limit of normal for serum. Increased plasminogen-activator inhibitors and TNF-α lead to fibrin deposition, which forms septations and loculations. Within these loculations, walled-off bacteria increase neutrophil phagocytic activity, a corresponding increase in LDH, and increased production of lactic acid and glucose consumption; this explains the changes observed in pleural fluid analysis.[6]

Chronic Organizational Stage

The final stage, known as the organizing phase, is marked by the growth of fibroblasts into the visceral and parietal pleurae. This is accompanied by the deposition of a collagen-rich fibrin matrix within the pleural space, resulting in pleural thickening. This phase often leads to developing an inelastic visceral pleural peel, which can cause lung entrapment. The proliferation of fibroblasts is believed to be driven by the release of transforming growth factor-beta and platelet-derived growth factor.

History and Physical

Thoracic empyema has a complex presentation that varies based on the stage of the disease. Obtaining a thorough medical history and performing a comprehensive physical examination is vital for prompt diagnosis and management, especially given the condition’s high morbidity and mortality rates.

History

Patients with thoracic empyema often present with symptoms that mimic other respiratory or infectious conditions, particularly pneumonia. A typical history may include preceding or concurrent pulmonary infections, with pleural infection occurring as a complication of bacterial pneumonia in about 60% of cases. Other risk factors include recent thoracic surgery, trauma, esophageal perforation, or immunocompromise. Symptoms tend to evolve as the empyema progresses through its stages:

• Exudative stage: Early symptoms are similar to pneumonia, with common complaints of fever, cough, and pleuritic chest pain. Dyspnea may be mild at this stage, and chest discomfort is often described as a deep, dull pain.
• Fibrinopurulent stage: As the infection progresses, patients often report worsening chest pain, increased dyspnea, and a productive cough with purulent sputum. Fever may become more pronounced, and constitutional symptoms like malaise, fatigue, and night sweats are often present. This stage is marked by the accumulation of fibrin and pus, leading to loculated fluid pockets within the pleural space.
• Organizing stage: In chronic or untreated empyema, fibrous septa form within the pleural cavity, encasing the lung and restricting its expansion. At this stage, symptoms are more persistent and may include marked weight loss, cachexia, and chronic pain. Chronic empyema may lead to further respiratory compromise, with severe dyspnea and decreased exercise tolerance.

Physical Examination

The physical examination findings in thoracic empyema are variable and depend on the amount of pleural fluid, the degree of lung compression, and the stage of the disease.

• Vital signs: Fever is common, although its severity varies. Tachycardia and tachypnea may indicate a more severe infection or systemic inflammatory response. Hypoxemia may present in patients with underlying respiratory compromise, particularly in advanced empyema.
• Inspection: Patients may appear acutely ill, especially in the fibrinopurulent or organizing stages. Signs of respiratory distress or accessory muscle use may indicate severe disease. In chronic cases, weight loss and cachexia may be evident.
• Palpation and percussion: Dullness to percussion over the affected hemithorax is a hallmark of pleural effusion, and in empyema, the dullness is often more pronounced and localized. Tactile fremitus is typically decreased or absent over areas with large fluid collections.
• Auscultation: Breath sounds are diminished or absent over fluid accumulation, especially in the fibrinopurulent and organizing stages. In some cases, crackles or bronchial breath sounds may be heard at the periphery of the empyema cavity, suggesting surrounding lung consolidation. Friction rubs, though uncommon, may be audible, especially in the earlier stages.

Evaluation

Imaging

Chest imaging is a cornerstone of empyema diagnosis and management as it provides critical information about pleural infections' presence, extent, and nature. While advancements in imaging modalities have enhanced diagnostic accuracy, plain radiography remains a valuable initial screening tool, particularly in patients with pneumonia. A unilateral, markedly asymmetric pleural effusion with costophrenic angle blunting is typically seen, and smaller effusions may be better visualized using a lateral view. Decubitus radiographs can further assess for layering and quantify fluid volume. However, the specificity of chest radiography is limited, particularly in the early stages of empyema, necessitating further imaging. However, ultrasonography and computed tomography (CT) have greater sensitivity for fluid detection and provide additional information for determining the extent and nature of the pleural infection.[18] 

Thoracic ultrasonography can differentiate simple effusions from complex ones, detect septations and loculations characteristic of empyema, and guide safe thoracentesis for fluid sampling. In a case series, ultrasonography demonstrated superior sensitivity to plain radiography for diagnosing pleural effusions, reinforcing its role as a preferred modality in suspected empyema cases.[19]

CT with intravenous contrast remains the most definitive imaging study for empyema and provides detailed visualization of pleural thickening, loculations, and enhancement of the pleurae, hallmark features of empyema. The “split pleura” sign, characterized by thickened visceral and parietal pleurae separated by fluid greater than 30 mm, is a highly specific finding suggesting complicated parapneumonic effusion requiring drainage.[20] CT is particularly useful for distinguishing empyema from lung abscess, which can present with overlapping clinical and radiographic findings but requires distinct management approaches. Additionally, CT helps evaluate the extent of disease, the involvement of adjacent structures, and the appropriateness of drainage procedures.

Thoracentesis

Diagnostic fluid sampling via thoracentesis is essential in evaluating pleural effusions associated with pneumonia, recent chest trauma, surgery, or ongoing sepsis, particularly when effusion depth exceeds 2 cm on lateral decubitus films or CT.[18][19] Frank pus in the pleural space necessitates surgical drainage. However, in cases where the fluid is turbid but not purulent, a pleural fluid pH of less than 7.2, measured using a blood gas analyzer, indicates the need for invasive drainage.[20] Additional biochemical and microbiological analyses provide critical diagnostic information.

Pleural fluid analysis begins with assessing appearance, as grossly purulent fluid strongly suggests empyema. Biochemical markers are also crucial, with empyema typically characterized by low pH (<7.2), low glucose (<60 mg/dL), and elevated LDH (>1000 IU/L), reflecting the acidic, metabolically active environment of infection. A leukocytosis with neutrophilic predominance indicates acute inflammation, further supporting the diagnosis.

Microbiological evaluation includes Gram staining for immediate organism identification and pleural fluid cultures for definitive diagnosis. Pathogens frequently associated with empyema include Streptococcus species, Staphylococcus aureus, and anaerobes. Pleural fluid culture yield can be significantly improved by injecting pleural fluid into blood culture bottles immediately after aspiration.[21] These cultures are vital for guiding targeted antimicrobial therapy and determining the need for additional interventions, such as mechanical drainage or surgery.

In certain cases, additional testing may be necessary. For example, pleural fluid should be analyzed in patients with suspected tuberculosis using acid-fast bacilli stain, culture, and polymerase chain reaction testing, especially in high-risk populations or regions with a high tuberculosis prevalence. This comprehensive diagnostic approach ensures accurate identification of the underlying cause and informs the optimal therapeutic strategy.

Blood Cultures

Blood cultures are necessary for any patient with empyema. Although generally nondiagnostic, they can help identify causative pathogens and bacteremia if the results are positive.

Advanced Diagnostic Techniques

Advanced diagnostic techniques may be necessary when initial fluid analysis and imaging fail to provide a definitive diagnosis. Pleural biopsy is particularly valuable in suspected tuberculosis or malignancy cases when pleural fluid studies are nondiagnostic. Thoracoscopic biopsy offers the advantage of direct visualization of the pleurae, allowing for targeted tissue sampling for histopathology and culture. Although not routinely used to evaluate empyema, bronchoscopy can be helpful in specific scenarios and is particularly useful in identifying bronchopleural fistulas, endobronchial obstructions, or other intrathoracic pathologies that may contribute to the infection.

Treatment / Management

The treatment and management of thoracic empyema involve a combination of medical and surgical interventions aimed at eradicating infection, achieving adequate drainage of the pleural space, and restoring lung function. Early and aggressive management is critical to improving outcomes and minimizing complications. In 2000, the American College of Chest Clinicians published clinical practice guidelines emphasizing the importance of pleural space anatomy, fluid bacteriology, and fluid chemistry in determining the risk of poor outcomes in empyema.

Categories 1 and 2 represent free-flowing exudative-stage effusions with the lowest risk for adverse outcomes. Category 3 refers to complicated effusions in the fibrinopurulent stage, which may be larger, loculated, or free-flowing, with a moderate risk of poor outcomes.[22] Empyema, categorized as stage 4, carries the highest risk of adverse outcomes. Management aims to eradicate infection through antimicrobials and achieve adequate pleural drainage using tube thoracostomy, with or without intrapleural therapies, video-assisted thoracoscopic surgery (VATS), or open thoracotomy with decortication.(A1)

Data from 2005 to 2014 reveal trends in empyema management, revealing that 76.3% of patients underwent interventions such as tube thoracostomy, VATS, or thoracotomy. Tube thoracostomy as a first-line treatment increased from 21.7% to 29.6%, while VATS rose from 11.2% to 14.9%, reflecting its growing acceptance. Thoracotomy decreased from 22.6% to 18.9%, likely due to the less invasive nature of VATS. Notably, 64.9% of patients treated with initial tube thoracostomy did not require further surgical intervention, underscoring its effectiveness in many cases.[16]

Medical Management

Antimicrobials

Empiric broad-spectrum antibiotics are necessary for most patients with suspected or confirmed empyema. Initiation of therapy should not delay diagnostic procedures. Antimicrobials should be tailored to target pathogens based on geographic epidemiology, antibiotic resistance patterns, mode of acquisition (aspiration, trauma), and whether the affected patient presents from a community versus a healthcare setting.

• Community-acquired empyema: The antibiotic regimen should target common pathogens of the oropharynx, including aerobic Staphylococcus and Streptococcus species and anaerobes. Appropriate antibiotics include third-generation cephalosporins, metronidazole, or a beta-lactam/beta-lactamase inhibitor combination.[23]
• Hospital-acquired empyema: Antimicrobial therapy should cover methicillin-resistant S aureus, Pseudomonas, and typical organisms and anaerobes. Reasonable options include vancomycin plus metronidazole and an antipseudomonal cephalosporin. Vancomycin plus piperacillin/tazobactam, a broad-spectrum beta-lactam/beta-lactamase inhibitor, provides both anaerobic and antipseudomonal activity.
(B3)

Caution should be taken with aminoglycosides due to poor pleural penetration; this antimicrobial class is not recommended for treating empyema.[24] The duration of antibiotics is generally recommended to be 2 to 6 weeks (intravenous followed by oral), depending on the degree of infection and clinical response to therapy.[25][26]

Surgical and Procedural Interventions

Tube thoracostomy and intrapleural therapies

Chest tube placement under radiologic guidance remains the cornerstone nonsurgical intervention for empyema. Optimal thoracostomy tube size has been a controversial topic amongst chest physicians. Traditionally, large-bore (>22F) tubes were preferred for draining viscous purulent fluid; recent evidence suggests no significant advantage over small-bore (<20F) tubes regarding mortality or surgical delays.[27][28] Clinical success depends more on accurate placement, as malpositioning is a common cause of treatment failure. Radiographic confirmation of tube location within 24 hours is essential. Typically, chest tubes are removed when drainage falls below 50 mL in 24 hours or when imaging confirms lung reexpansion.(A1)

The use of adjunctive intrapleural therapies has varied outcomes. Isolated fibrinolytic agents such as streptokinase, urokinase, or tissue-type plasminogen activator (tPA) have demonstrated limited benefit. However, combination therapy with tPA and deoxyribonuclease (DNase) significantly improves fluid drainage, reduces surgical referrals, and shortens hospital stays without impacting mortality. Emerging approaches, such as saline lavage, have shown promise. The Pleural Irrigation Trial's results showed a radiographic improvement after 3 days in empyema patients receiving saline irrigation via tube thoracostomy vs standard of care.[29] Results from a smaller retrospective study comparing saline flushes plus urokinase versus saline alone found decreased chest tube duration and use of fibrinolytic. Although researchers noted no mortality benefit, more extensive randomized studies are needed to confirm the benefits of this inexpensive, well-tolerated therapy.[28] (A1)

Intrapleural enzyme therapy (IET) is an adjunctive approach, particularly for complicated parapneumonic effusions and empyema. This therapy involves administering fibrinolytic agents, such as tPA, and enzymatic agents, like DNase, directly into the pleural space. tPA dissolves fibrin clots, reducing septations, while DNase targets extracellular deoxyribonucleic acid in pus, lowering fluid viscosity. The combination enhances fluid drainage, improves pleural clearance, and minimizes the need for surgical intervention.[29](A1)

Since the publication of the results from the Multicenter Intrapleural Sepsis Trial study, IET has significantly transformed the medical management of pleural infections. Although the MIST-2 trial had a limited number of patients in the IET group (n= 52) and primarily measured radiographic clearance, subsequent reports involving over 600 patients have demonstrated reduced surgical intervention rates and shorter hospital stays. Additionally, a multicenter retrospective study of 1850 patients treated with IET reported a low incidence of bleeding complications (4.2%) and no significant adverse events.[30](A1)

IET is particularly indicated for patients with loculated effusions unresponsive to tube thoracostomy, those at high surgical risk, or as a bridge to surgery for preoperative optimization. The standard regimen includes 10 mg of tPA and 5 mg of DNase in sterile saline, instilled via a chest tube every 12 hours for 3 days, with a 1-hour dwell time per dose. While generally safe, IET can cause fever, pain, and rarely systemic bleeding, requiring careful patient selection, especially in those with coagulopathies. Though not universally effective in advanced cases with dense fibrous organization, IET offers a minimally invasive option that enhances drainage, reduces surgical interventions, and optimizes patient outcomes when integrated into a multidisciplinary care strategy.

VATS

Surgical consultation should be a consideration when drainage via tube thoracostomy fails or for patients with multiloculated empyema. VATS is a minimally invasive surgical technique that allows for direct visualization and evacuation of the infected pleural space. Although the appropriate timing of VATS is unclear, it has been documented to have superior outcomes when compared to tube thoracostomy for the treatment of advanced-stage empyema in terms of postoperative morbidity, complications, and length of hospital stay.[31](A1)

Open thoracostomy and decortication

Persistent empyema refractory to standard therapies, including VATS, should be considered for open window thoracostomy with prolonged chest tube drainage or decortication. Acute empyema can have long-term consequences despite adequate therapeutic interventions. Pleural scarring and fibrosis can lead to adhesions, decreased lung compliance, and a restrictive lung disease pattern. Decortication is an option for lung reexpansion if symptoms persist 6 months after empyema resolution.

Supportive care

Supportive care is crucial in managing thoracic empyema and promoting patient recovery. Nutritional support is essential for enhancing immune function and overall recovery, as patients with empyema often experience significant systemic inflammation and metabolic demands. Pulmonary rehabilitation, including breathing exercises and physiotherapy, is equally important to encourage lung expansion, prevent atelectasis, and restore respiratory function. Additionally, regular imaging and clinical evaluations are necessary to monitor the resolution of the infection and ensure proper lung re-expansion, enabling early detection and management of any complications or recurrence.

Collaborative approach

Effective management requires an interdisciplinary team of healthcare professionals involving pulmonologists, thoracic surgeons, infectious disease specialists, radiologists, and nursing staff. Coordination ensures timely diagnosis, proper drainage procedures, and individualized treatment plans. This collaborative effort minimizes morbidity, improves patient outcomes, and reduces healthcare costs.

Differential Diagnosis

The differential diagnosis of thoracic empyema includes several other causes of pleural effusion and thoracic infections and conditions that mimic empyema clinically and radiographically. Differentiating empyema from these conditions is essential to ensure appropriate treatment. Key considerations include:

• Uncomplicated parapneumonic effusion
• Complicated parapneumonic effusion
• Lung abscess
• Tuberculosis pleuritis
• Malignant pleural effusion
• Chylothorax
• Hemothorax
• Fungal pleural infection
• Autoimmune pleuritis (eg, rheumatoid arthritis, lupus)
• Heart failure-related effusion
• Pulmonary infarct

Prognosis

Empyema has a generally poor prognosis if not treated promptly and aggressively, as untreated or inadequately managed cases can lead to high morbidity and mortality. Although most patients recover, outcomes remain challenging, with approximately 20% requiring surgery and a 1-year mortality rate nearing 20%. Frail, older adults, and immunocompromised individuals have a 1.5-fold increase in adverse outcomes, highlighting the importance of early, individualized intervention for these vulnerable groups. The in-hospital mortality rate for empyema ranges from 5% to 15%, influenced by factors such as age, delayed diagnosis, advanced disease stage, and underlying health conditions.

Empyema risks recurrence and long-term complications, including chronic fibrothorax and restrictive lung disease, especially in cases of insufficient drainage or persistent infection. These chronic changes can impair lung function, reduce exercise tolerance, cause chronic cough, and decrease quality of life. The average hospital stay for empyema is approximately 19 days due to the need for prolonged drainage, antibiotics, and sometimes surgical intervention, with prolonged recovery impacting functional outcomes, especially in older individuals.

Results from a retrospective cohort analysis by Wilshire et al found no significant mortality advantage between initial surgery and fibrinolytic therapy but highlighted that initial surgical intervention was linked to shorter hospital stays, reduced duration of chest tube placement, and fewer subsequent treatments or readmissions.[32] These findings align with other studies' results, indicating that early surgical intervention may optimize outcomes by reducing treatment failure rates and minimizing healthcare resource utilization.

The economic impact of empyema is considerable, with an estimated treatment cost of $38,000 per case and annual US healthcare costs nearing $500 million. Costs are driven by extended hospitalizations, advanced pharmacologic interventions, and procedural requirements, emphasizing the need for timely diagnosis and management to reduce financial and healthcare burdens.

Complications

If untreated or inadequately managed, empyema can lead to serious complications affecting the respiratory system and overall patient health. These complications contribute to prolonged hospital stays, increased healthcare costs, and significant morbidity and mortality. Key complications associated with empyema include:

Pleural fibrosis and fibrothorax: Chronic empyema can lead to fibrosis of the pleural membranes, resulting in a condition known as fibrothorax, where the pleural space becomes thickened and scarred. This restricts lung expansion, causes restrictive lung disease, and results in persistent dyspnea, reduced exercise tolerance, and diminished quality of life. Fibrothorax may require surgical decortication to release the lung from the fibrous encasement.

Bronchopleural fistulae: A bronchopleural fistula, an abnormal connection between the bronchial tree and pleural space, can occur due to lung necrosis or after surgical intervention, particularly lobectomy or pneumonectomy. Bronchopleural fistulae can lead to persistent air leaks, pneumothorax, and impaired lung function, complicating the treatment and drainage of empyema. Bronchopleural fistulae increase the risk of severe, recurrent infection and are challenging to manage, often requiring surgical repair or prolonged chest tube placement.

Sepsis and septic shock: If empyema is not adequately contained, the infection can spread into the bloodstream, leading to sepsis, a life-threatening systemic response to infection. This complication significantly increases mortality and is particularly common in those who are immunocompromised, older, or frail. Sepsis due to empyema requires intensive care and aggressive antibiotic therapy, often alongside respiratory support and hemodynamic monitoring.

Respiratory failure: Empyema compromises lung function by compressing the underlying lung, impairing ventilation, and causing hypoxemia. If left untreated, this compression can progress to respiratory failure, particularly in patients with underlying pulmonary diseases like chronic obstructive pulmonary disease or asthma. In severe cases, patients may require mechanical ventilation, and the prognosis is generally poorer when empyema leads to respiratory decompensation.

Recurrent empyema: Inadequate drainage or incomplete resolution of infection may lead to recurrent empyema, which can occur weeks or even months after the initial episode. Recurrent empyema increases the risk of pleural thickening, longer hospital stays, and the need for more aggressive surgical interventions. This condition is often seen in cases where conservative management alone was insufficient or in patients with a history of pleural disease.

Empyema necessitans: In rare cases, empyema can erode through the chest wall, leading to an external draining sinus—a condition known as empyema necessitans.[33] This unusual complication typically occurs in patients with tuberculosis or chronic infections and can lead to chest wall deformity and severe scarring. Empyema necessitans often require surgical debridement and may necessitate prolonged antibiotic therapy.

Reduced quality of life and functional impairment: Chronic empyema is associated with long-term functional limitations and reduced quality of life, especially in patients who develop fibrothorax. Persistent dyspnea, chest pain, and fatigue are common, especially in patients who are older or those with preexisting lung disease. Patients may experience limited physical activity, dependence on supplemental oxygen, and chronic respiratory symptoms, which impact their daily lives.

Cardiovascular complications: The inflammation and infection associated with empyema can strain the cardiovascular system, especially in large effusions that compress the heart and great vessels. Patients may experience hemodynamic instability, including hypotension and tachycardia, which can be exacerbated by sepsis or a systemic inflammatory response. This strain is particularly dangerous for patients with preexisting cardiac conditions.