Pneumatocele

Etiology

The primary mechanism of pneumatocele formation involves interstitial or alveolar air trapping, forming thin-walled, air-filled cysts. Pneumatoceles arise due to various underlying etiologies, most commonly due to lung injury, infection, or mechanical forces. These include: 

• Infections
  • Pneumatoceles frequently occur following bacterial infections, with Staphylococcus aureus being a leading pathogen, especially in children.
  • Other infectious agents include tuberculosis, Streptococcus pneumoniae, Proteus mirabilis, Escherichia coli, Acinetobacter calcoaceticus, Klebsiella pneumoniae, and Pneumocystis jirovecii.[2]
  • Notably, intravenous (heroin users are also at risk of developing infection-related pneumatoceles due to aspiration and associated lung damage.
  • Infections induce necrosis and airway damage, promoting air trapping.
• Trauma
  • Pneumatoceles can develop following blunt or penetrating chest trauma. In traumatic cases, they often result from pulmonary contusions, where the force of impact causes alveolar rupture, trapping air in the interstitial space. This may be seen with pneumothorax, pneumomediastinum, or pulmonary lacerations.
• Mechanical ventilation
  • Another common cause is mechanical ventilation, particularly in patients receiving high levels of positive-pressure ventilation.[3][4] Overdistension of alveoli, especially in acute respiratory distress syndrome, can lead to alveolar rupture, with subsequent air leakage and pneumatocele formation.
• Other causes
  • Underlying lung diseases
    • Desquamative interstitial pneumonia can lead to the formation of multiple cysts or pneumatoceles.
    • Persistent or diffuse interstitial pulmonary emphysema is another cause.
  • Congenital disorders
    • Cystic adenomatoid malformations may also be linked to the development of similar air-filled cysts.
  • Hydrocarbon inhalation [2][5]
  • Kerosene ingestion [6][7]
  • Burns [8][6][9] 
  • Endobronchial valve-related injuries
    • These also lead to pneumatocele formation.[9]

The etiology of pneumatoceles reflects underlying alveolar or interstitial damage, with varying severity and clinical implications based on the root cause.

Epidemiology

Pneumatoceles are air-filled cystic lesions in the lungs due to trauma, pneumonia, or certain infections. They are particularly common among infants, children, adolescents, and individuals with weakened immune systems, such as those with acquired immunodeficiency syndrome. Traumatic pneumatoceles, in particular, are most often seen in children and young adults and are generally the result of nonpenetrating chest trauma, such as motor vehicle accidents or falls. These rare lesions occur in less than 3% of patients with pulmonary parenchymal injuries. Results from a study in Milan, Italy, reported 10 cases over 9 years, and other reports indicate that about 85% of traumatic pneumatoceles occur in individuals aged younger than 30. Male patients are more commonly affected due to the higher rates of trauma in men.[10][11][12][13] Pneumonia complicated by pneumatoceles is seen in 2.4% to 8.3% of hospitalized children with pneumonia.[14]

The incidence of pneumatoceles is notably higher in certain regions. For instance, results from a study in Brazil found that 9.5% of hospitalized children with pneumonia developed pneumatoceles. This high incidence has been linked to malnutrition, which can delay the development of Kohn pores in the lungs, leading to the formation of pneumatoceles when there is valvular obstruction.[14] Traumatic pneumatoceles in children and adolescents occur due to the greater compressibility of their thoracic skeleton and the elastic recoil of their lungs, which increases the negative intrathoracic pressure and leads to laceration of the lung parenchyma. Only about 20% of these patients have associated rib fractures. The formed cavities filled with fluid, blood, or air continue to increase in size until lung pressures are balanced between the cavities and the surrounding tissue.[4][15][16] A survey of 10,229 trauma admissions found that 12.3% of children with pulmonary contusions developed a pneumatocele. The largest pneumatocele reported in this study was 3.7 cm in diameter, and most cases resolved spontaneously without intervention.[12]

Pneumatoceles are also reported in patients recovering from viral infections. For example, results from a study of H7N9 influenza survivors showed that 9.8% developed pneumatoceles; a similar occurrence was noted in 10% of those after COVID-19 infection.[17][18] Additionally, pneumatoceles have been observed in patients with pulmonary metastases treated with chemotherapy, such as paclitaxel, where pulmonary nodules regressed into multiple pneumatoceles.[19] These various causes highlight the diverse etiologies of pneumatoceles and their clinical significance in both infectious and traumatic settings.

Pathophysiology

Pneumatoceles are air-filled cavities within the lung parenchyma that can arise from various causes, including trauma, infection, and inflammatory processes. The pathogenesis of pneumatocele formation is complex and involves mechanical and inflammatory mechanisms. The formation of a pneumatocele is commonly attributed to an endobronchial check-valve mechanism. This process leads to air trapping and the subsequent development of cystic air space in the distal regions of the lung. Another theory involves inflammation and necrosis of an airway segment, resulting in direct communication between the airway and the bronchovascular interstitium. This communication allows air to travel through the bronchovascular connective tissue, accumulating beneath the pleura and forming a recognizable pneumatocele.[20]

Pneumatoceles are also associated with various infectious agents, including: 

• Streptococcus pneumonia [21]
• Staphylococcus aureus
  • In cases involving this pathogen, 60% result in pneumatocele.
  • This bacteria is more commonly found in children.
  • In an analysis of burns patients, those who develop staphylococcal pneumonia also develop pneumatocele.[22][23] 
  • A case report of S aureus and candida colonization leading to multiple pneumatoceles is also reported. 
• Pneumocystis carinii in human immunodeficiency virus [23][24][25][26]
• Pseudomonas aeruginosa
• Group A streptococci
• Klebsiella pneumoniae [27]
• Adenovirus
• Mycobacterium tuberculosis
  • Pneumatoceles can develop during or after treatment of tuberculosis.[28]
• Proteus mirabilis and extended-spectrum beta-lactamase Proteus mirabilis [29][30]
• Escherichia coli 
  • Cavitary pneumonia from this pathogen has been associated with the formation of pneumatocele.[31]
• Acinetobacter calcoaceticus [32]
• Hemophilus influenzae B [33]
• Bacteroides species, Peptostreptococcus asaccharolyticus, and Fusobacterium species [34]

These pathogens can trigger airway inflammation and obstruction. The resulting inflammatory exudates can create the ball-valve effect, contributing to pneumatocele formation. In postpneumonia cases, inflammation and narrowing of the bronchus often lead to an endobronchial ball-valve mechanism, causing distal dilation of the bronchi and alveoli. Air enters the cystic space but cannot escape due to inflammatory exudates within the airway lumen or wall. This mechanism results in pneumatocele enlargement, combined with pressure exerted by adjacent pneumatoceles or accumulating exudates. 

After trauma, pseudocysts form due to shearing forces that cause pulmonary lacerations, leading to the escape of air or fluid into the surrounding tissue. The exact mechanisms underlying traumatic pneumatocele formation remain uncertain, but several theories have been proposed:

• Concussive waves and shearing forces
  • Blunt trauma generates concussive waves, which create shearing forces capable of tearing the lung parenchyma. The location and type of injury depend on the impact characteristics:
    • High-velocity impacts with minimal chest wall displacement produce peripheral pseudocysts.
    • Low-velocity impacts with significant chest wall displacement result in central pseudocysts.
  • Both scenarios involve intraparenchymal pulmonary lacerations, with airway disruptions allowing air to leak into the pulmonary parenchyma.[35]
• Explosive pressure and "bursting lesions"
  • Sudden, severe compression of a segment of the peripheral bronchial tree can obstruct the bronchus and transmit explosive pressure distally, creating "bursting lesions." This process occurs in 2 steps:
    • Step 1
      • Compressive forces increase intrapulmonary pressure, causing the lung parenchyma to rupture and form lacerations.
    • Step 2
      • Subsequent chest decompression and increased negative intrathoracic pressure allow the lung's elastic tissue to recoil, forming small cavities filled with air or fluid. These cavities expand until the internal pressure equilibrates with the surrounding parenchyma.
• Check-valve mechanism
  • In cases of penetrating trauma or airway injury, a one-way or check-valve effect may occur. This allows air to enter a laceration in the pulmonary parenchyma while the defect seals quickly, trapping the air and preventing its escape. Similar mechanisms have been observed in patients mechanically ventilated receiving continuous positive airway pressure.[4]

Traumatic pneumatoceles typically result from significant chest trauma involving a pliable chest wall, where kinetic energy is efficiently transmitted to the underlying pulmonary parenchyma. The condition is more common in young people and children due to the increased elasticity of their chest walls. Radiologically, traumatic pneumatoceles appear as pulmonary cavities devoid of epithelial lining and filled with air, fluid, or blood. They often coexist with other injuries, such as pneumothorax or pneumomediastinum. A pneumatocele indicates extensive tissue disruption, signifying a more severe injury than a simple pulmonary contusion.[10][36][37]

The location of the pneumatocele may not correspond to the site of the chest wall injury. In some cases, traumatic forces are transmitted in a contrecoup manner. The velocity and nature of the impact influence the lesion's location. High-velocity impacts tend to cause peripheral alveolar injuries. In contrast, low-velocity impacts with substantial chest wall displacement lead to central parenchymal injuries. In studies of high-speed accidents, results showed all traumatic pneumatoceles occurred peripherally.

Environmental exposures, such as hydrocarbons, can induce lung injuries characterized by rapid progression of respiratory difficulty without causative factors and the presence of ground-glass opacities, spontaneous air leak syndrome resulting in pneumatoceles, and consolidation with later diffuse centrilobular nodular opacity on chest computed tomography.[5] Hydrocarbons contain polyhexamethylene guanidine (PHMG), oligo (2-[2-ethoxy]ethoxyethyl) guanidinium chloride (PGH), 5-chloro-2-methyl-4-isothiazolin-3-one (CMIT), or 2-methyl-4-isothiazolin-3-one (MIT). PHMG and PGH are commonly thought to cause hydrocarbon-associated lung injuries. Animal study results have not established definitive links between exposure to hydrocarbons containing CMIT and/or MIT, even though patients exposed to hydrocarbons containing only CMIT and/or MIT showed clinically similar lung injury to that of hydrocarbons containing PHMG and/or PGH.[38][39]

Persistent interstitial pulmonary emphysema (PIPE), when diffuse, can be associated with pneumatocele formation. PIPE is a rare entity related to mechanical ventilation-induced lung damage in premature infants with respiratory distress syndrome. Although PIPE localized in 1 lobe has the potential for curative resection, diffuse PIPE affecting both lungs carries a poor prognosis. Rarely, extrathoracic pneumatocele formation has been documented, such as in untreated tuberculosis patients where old scars provide a pathway for air accumulation.[28][40][41]

Results from a Brazilian study proposed that the Kohn pores theory contributes to pneumatocele formation. Kohn pores, small interalveolar connections, play a critical role in equalizing pressure within the lung. According to this theory, delayed development of Kohn pores, often due to undernutrition, leaves the lungs of malnourished children functionally similar to those of newborns. In this scenario, when a valvular obstruction occurs, air enters a lung segment but cannot escape, forming a pneumatocele. The absence of well-developed Kohn pores in these patients allows air trapping, as there are no alternative pathways for air redistribution within the alveolar network. This mechanism might explain the higher prevalence of pneumatoceles in children compared to adults, in whom fully developed Kohn pores facilitate better intrapulmonary pressure equilibration.[35]

Histopathology

Pneumatoceles are air-filled cystic lesions that arise within the lung parenchyma, and their histopathological features are characterized by the lack of epithelial lining and varying degrees of surrounding inflammatory and fibrotic changes. The specific histopathology of pneumatoceles depends on the underlying etiology (eg, trauma, infection, or inflammatory conditions) but generally includes the following features:

• Lack of epithelial lining
  • The most distinguishing feature of pneumatoceles is that they are not lined by epithelium, distinguishing them from true cysts. The cavity is essentially a space within the lung parenchyma filled with air or fluid, but it lacks the typical epithelial lining seen in other types of cysts. This absence of epithelial lining is a key histological feature of pneumatoceles, especially when compared to congenital cysts or other cystic lesions that might have a well-developed epithelial or mesothelial lining.
• Air or fluid-filled cavities
  • The cystic spaces within pneumatoceles contain air, fluid, or blood, depending on the underlying cause. These spaces are often filled with purulent exudate or inflammatory debris in infectious cases. The fluid component may appear as a proteinaceous exudate; in some cases, it may contain cellular debris, inflammatory cells (such as neutrophils), and fibrotic material in chronic cases.
• Surrounding inflammatory infiltrate
  • In many cases, a marked inflammatory infiltrate will surround the pneumatocele, particularly those related to infection or inflammation (such as pneumonia). This infiltrate often includes neutrophils, lymphocytes, and macrophages, depending on the inflammation stage and the underlying condition's nature. In bacterial infections, the inflammatory response may be more acute, while in viral or chronic infections, the infiltrate may be more chronic and predominantly lymphocytic.
• Fibrotic changes and granulation tissue
  • Chronic pneumatoceles, especially those associated with trauma or long-standing inflammation, may show varying degrees of fibrosis surrounding the cystic space. This fibrosis is typically a response to the injury or inflammation and may be seen as dense collagen deposition or fibrous tissue around the pneumatocele. In cases of traumatic pneumatoceles, the fibrotic changes may be a result of the healing response to pulmonary laceration and tissue disruption. Granulation tissue may also be observed in the surrounding lung parenchyma, especially in the early stages after trauma or infection.
• Necrosis and hemorrhage
  • In some cases, particularly in traumatic pneumatoceles, hemorrhage may occur within the cyst or surrounding tissue. The cyst may contain blood or hemosiderin-laden macrophages, indicating previous bleeding. Necrotic tissue may also be present, particularly in severe trauma or infectious processes, where the injury or infection has resulted in tissue death.
• Absence of a bronchial lining
  • Pneumatoceles, particularly those caused by trauma, often lack the bronchial or airway structure that would be expected in other types of pulmonary cysts. The lesion typically represents an area of pulmonary parenchyma dissected by air, blood, or fluid following mechanical trauma, infection, or other pathologic processes without forming a discrete bronchial or ductal system inside the cyst.
• Presence of septations (in some cases)
  • Some pneumatoceles, particularly those of infectious or inflammatory origin, may develop internal septations. These septations are thin, fibrous partitions that can arise from the inflammatory or reparative processes occurring within the cyst. These partitions may be more prominent in cases of chronic or long-standing pneumatoceles.

A documented case of pneumonectomy performed for multiple pneumatoceles revealed findings consistent with cystic adenomatoid malformation in a patient with hyper-immunoglobulin (Ig)E syndrome. This malformation was characterized by multiple cysts of varying sizes, all lined by epithelium, within the affected lung tissue.[42] Hyper-IgE syndrome, a rare immunodeficiency disorder, is often associated with recurrent infections, chronic inflammation, and structural lung abnormalities, including pneumatocele formation. In this case, the coexistence of multiple pneumatoceles and cystic adenomatoid malformation highlights a potential link between the chronic inflammatory state, immune dysfunction, and the development of complex pulmonary abnormalities in such patients.

History and Physical

The history and physical examination findings of a patient with a pneumatocele vary based on the size, location, underlying etiology, and associated complications. Pneumatoceles are typically asymptomatic but may cause symptoms in cases of significant size or secondary complications such as infection, rupture, or compression of adjacent structures.

History

Pneumatoceles are thin-walled, air-filled cystic lesions within the lung parenchyma that arise from various causes, including bacterial pneumonia (notably Staphylococcus aureus and Streptococcus species), blunt chest trauma, chemical toxin exposure (eg, hydrocarbons), or positive-pressure ventilation. Although more commonly seen in infants, children, and adolescents, pneumatoceles are relatively uncommon in adults, with limited cases documented in this population.[43] Risk factors for their formation include young age, postinfectious or posttraumatic conditions, human immunodeficiency virus, intravenous drug use, and immune dysfunctions such as hyper-IgE syndrome.[14][44][45] The clinical presentation varies based on the size of the lesion, the underlying cause, and associated complications, ranging from asymptomatic findings to significant respiratory symptoms.

A detailed history often reveals preceding acute illnesses or events contributing to pneumatocele development. Many cases follow prior infections, particularly Staphylococcus aureus pneumonia in children or necrotizing pneumonia caused by organisms such as Klebsiella pneumoniae, Streptococcus pneumoniae, or Pseudomonas aeruginosa.[14][46] Patients typically report a history of fever, cough, dyspnea, chest pain, or sputum production linked to the initial infectious episode. Viral pneumonia, including those caused by influenza or respiratory syncytial virus, may also precede pneumatocele formation.

In some cases, trauma or iatrogenic factors play a significant role. Blunt or penetrating chest trauma, barotrauma from mechanical ventilation, or postoperative thoracic procedures such as thoracentesis or biopsy may predispose patients to pneumatocele development. Toxic shock syndrome associated with Staphylococcus aureus can also lead to pneumatocele formation, presenting with rash, fever, chills, and mucositis. Traumatic pneumatoceles often appear within 24 to 48 hours after injury, with hemoptysis occurring in 56% of cases, alongside cough and chest pain due to pulmonary parenchymal injury.[47] However, acute respiratory failure in these scenarios typically stems from associated pulmonary contusion rather than the pneumatocele itself.[48]

Complications of pneumatoceles can lead to specific symptoms. Sudden-onset chest pain or acute respiratory distress may indicate rupture, resulting in pneumothorax or tension pneumothorax. Secondary infection of the pneumatocele may present with fever, worsening respiratory symptoms, or systemic signs like malaise or fatigue. Underlying medical conditions, including immunosuppressive states, cystic fibrosis, or chronic granulomatous disease, increase pneumatocele susceptibility. A history of recurrent infections or chronic respiratory symptoms may further suggest structural lung abnormalities predisposing to their formation.

Physical

On physical examination, findings in patients with pneumatoceles vary depending on complications or associated conditions. In uncomplicated cases, patients may appear well or show mild respiratory symptoms. At the same time, those with complications often present with respiratory distress characterized by tachypnea, hypoxia, or the use of accessory muscles. Vital signs provide essential diagnostic clues, with tachypnea, fever, and hypoxia pointing to infection, respiratory compromise, hypotension, and tachycardia suggesting tension pneumothorax or sepsis.

Inspection may reveal decreased chest wall movement on the affected side, especially in significant pneumatocele or pneumothorax cases, with cyanosis or labored breathing apparent in severe cases. Palpation findings include decreased tactile fremitus over large pneumatoceles or pneumothorax and subcutaneous emphysema in rare cases of rupture. Percussion may reveal hyperresonance over air-filled spaces, such as a pneumatocele or pneumothorax.

Auscultation findings include diminished or absent breath sounds over affected lung areas. Adventitious sounds such as crackles or rhonchi may occur when infection or inflammation surrounds the pneumatocele. In cases of rupture causing tension pneumothoraces, mediastinal shift, and muffled heart sounds may occur, indicating a critical need for immediate intervention.

Mild fever or leukocytosis appearing 12 to 36 hours after trauma often results from the absorption of damaged lung tissue or blood clots rather than infection and should not be misinterpreted.[10] Advanced cases or those with complications, such as secondary infection, may also present with systemic signs like fever, chills, and leukocytosis. Careful monitoring of pneumatoceles, whether caused by trauma or illness, is crucial to address potential complications, including rupture, secondary infection, or compression of adjacent structures.

Evaluation

Evaluating pneumatoceles involves integrating clinical history, physical examination, laboratory findings, and imaging studies to confirm the diagnosis, identify underlying causes, and assess complications. While typically nonspecific, laboratory investigations play a supportive role in evaluating pneumatoceles. Blood tests may reveal leukocytosis, abnormal liver function, anemia, and thrombocytopenia, indicating an underlying infection or systemic inflammatory response. Although often negative, blood cultures can be positive for anaerobic organisms such as Bacteroides fragilis when infection is present. Elevated markers like c-reactive protein and procalcitonin may further indicate the severity of inflammation or infection. In certain cases, specific serum markers like cancer antigen-125 can help predict disease severity, particularly in complicated infectious conditions.

Imaging studies are paramount in diagnosing pneumatoceles and assessing their characteristics. Chest radiographs are frequently the first imaging modality used, especially in children, with 90% of pneumatoceles visible on the first chest radiograph after pneumonia (see Image. Pneumatoceles on Chest Radiograph). Radiologic evidence typically appears on the fifth to sixth day of hospitalization. However, chest radiographs have a low sensitivity of around 24% for diagnosing traumatic pneumatoceles, especially when obtained in the supine position or when the lesion is smaller than 2 cm. Despite the yield of false-negative findings, they are still used as the first diagnostic modality in patients with thoracic trauma.[10] 

The diagnostic accuracy of chest radiography ranges from 24% to 50%; however, serial chest radiographs taken over several days can enhance detection, particularly after the fifth post-trauma day when pulmonary contusions begin to resolve and pneumatoceles become more apparent. The typical radiographic presentation of a traumatic pneumatocele includes a round or oval shadow usually surrounded by pulmonary contusion, with air-fluid levels often present due to bleeding into the pneumatocele.[49][50] Most traumatic pneumatoceles are found in the lower lobes.[10] 

Computed tomography (CT) is the gold standard for evaluating pneumatoceles, offering a much higher sensitivity of approximately 96% compared to radiography. CT scans provide detailed images that precisely define the pneumatocele's location, size, and extent and identify any associated complications, such as pulmonary contusions or abscess formation. The typical appearance of a traumatic pneumatocele on CT is a round or oval thin-walled cavitary lesion with air-fluid levels commonly found in the lower lobes. The main advantage

s of CT include earlier identification, visualization of small lesions, and the ability to detect pneumatoceles even in the presence of pulmonary contusion. Recent study results report an increased incidence of pneumatoceles due to the more widespread use of CT rather than an actual rise in occurrence.[51] Additionally, CT-guided aspiration can be performed to sample the abscess and place an indwelling drain, facilitating diagnosis and treatment.

In pediatric populations, lung ultrasound has emerged as a useful adjunct to chest radiographs, enhancing diagnostic accuracy without radiation exposure.[52] The size of traumatic pseudocysts reported in the literature ranges from 1 to 14 cm in diameter, with larger pseudocysts more frequently occurring in patients with multiple injuries, bilateral pulmonary contusions, or significant respiratory involvement. Serial imaging studies are often necessary to monitor changes in size, shape, and composition of pneumatoceles within days following trauma, helping to differentiate them from other lesions.[53]

Advanced diagnostic techniques, such as CT-guided needle aspiration and bronchoscopy, may be employed in cases where secondary infection or abscess formation is suspected. These procedures allow microbiological sampling and direct intervention, particularly in recurrent or antibiotic-resistant collections. Emerging technologies, like optical property measurements and methylene blue uptake for photodynamic therapy, are being explored to improve the management of refractory pneumatoceles.

Treatment / Management

Treating pneumatoceles involves various approaches tailored to their etiology, size, complications, and clinical presentation. Accurate diagnosis is crucial to avoid unnecessary interventions and potential complications. Misdiagnosing a pneumatocele as a different cavitary pulmonary lesion, such as a pulmonary abscess or pneumothorax, can lead to harmful procedures like thoracostomy tube placement or inappropriate drainage. Below is a comprehensive description of management strategies, incorporating national and international guidelines.

Conservative Management

Conservative management is the cornerstone of treatment for most cases of pneumatocele, emphasizing observation, appropriate antimicrobial therapy, and supportive care. Most pneumatoceles resolve spontaneously within weeks to 6 to 12 months, with larger lesions sometimes requiring up to 6 months or more for complete resolution. In children, spontaneous resolution occurs in up to 90% of cases without invasive intervention. Regular clinical evaluations and imaging are essential for monitoring the progression or resolution of these lesions, with the average radiological resolution time being approximately 3 months.

Ventilation strategies are vital in managing pneumatocele-associated respiratory compromise. High-frequency oscillatory ventilation and unilateral main bronchus ventilation are effective techniques for maintaining adequate respiratory function while minimizing the risk of pneumatocele enlargement.[3][54] Avoiding high-pressure ventilation is critical to preventing further expansion of the lesion. Additionally, decubitus positioning with the affected side down can alleviate symptoms and improve clinical outcomes in some cases.(B3)

Antimicrobial therapy plays a key role in managing infected pneumatoceles. Empiric antibiotic regimens are initiated for suspected infections and tailored based on culture results to address common pathogens such as Staphylococcus aureus, Streptococcus pneumoniae, and mixed anaerobic organisms. Routine prophylactic antibiotic use is discouraged unless indicated by concomitant injuries or surgical interventions, as it may promote resistant strains and unnecessary colonization.

While conservative management remains the first-line approach for uncomplicated cases, it is insufficient in patients with cardiorespiratory instability or extensive disease.[55][56][57] Early escalation to invasive or surgical intervention is crucial in such situations to stabilize the patient and effectively address underlying complications. Therefore, careful clinical judgment and ongoing monitoring are essential to achieving favorable outcomes.(B3)

Minimally Invasive Interventions

• Percutaneous drainage
  • Percutaneous needle decompression and drainage is a therapeutic option for managing pneumatocele in select cases where complications arise, or conservative management proves insufficient. This technique is indicated under the following circumstances:
    • When the pneumatocele occupies more than 50% of the hemithorax, leading to compression of adjacent structures.[58]
    • In cases of significant atelectasis caused by the pneumatocele's mass effect.
    • Development of bronchopleural fistulae, which can lead to persistent air leaks.
    • Presence of a tension pneumatocele, where intrathoracic pressure compromises cardiorespiratory function.[59]
    • Persistent signs of a chest infection or infection within the cyst that fails to respond to antibiotic therapy.
    • Difficulty in ensuring adequate outpatient follow-up, raising concerns about monitoring progression or complications.
    • Decompression by percutaneous pigtail catheter placement in children who develop pneumatoceles as a result of a complication of pulmonary interstitial emphysema with superimposing respiratory syncytial virus infection has been described in a preterm infant in a case report.[60][61][62][63]
  • While effective, percutaneous needle decompression carries risks, including the potential development of bronchopleural fistulae, which may complicate the clinical course and necessitate further intervention.[64] Careful patient selection and meticulous procedural techniques are critical to minimizing complications and optimizing outcomes.
  • In some cases, patients are not suitable for earlier intervention with percutaneous drainage of the pneumatoceles due to the extent of lung disease and the high risk of complications associated with full heparinization and extracorporeal membrane oxygenation support.
• Injection therapy
  • The management of pneumatocele can also involve minimally invasive interventions, such as injecting fibrin sealant via a pigtail catheter, particularly in cases with persistent air leaks.[65] Fibrin sealant, a biodegradable material, is favored for effectively sealing air leaks by promoting natural tissue adhesion. This surgical hemostatic and adhesive material has applications in cardiac, vascular, hepatic, and maxillofacial surgeries.
  • Sclerosants used in pleurodesis, such as talc, antibiotics, antineoplastic drugs, and autologous blood, can also help manage air leaks. A study by Andres et al demonstrated the efficacy of autologous blood infusion, reporting 100% success in treating persistent air leaks within 24 hours.
  • The use of fibrin sealant, guided by CT-fluoroscopy, allows for precise catheter manipulation and targeted closure of fistulas. This approach is both rapid and safe, reducing the duration of hospitalization and potentially avoiding more invasive surgical interventions. These techniques underscore the importance of tailored, patient-specific strategies in effectively managing complicated pneumatocele cases.
• Bronchoscopy
  • Diagnostic and therapeutic bronchoscopy are crucial in managing traumatic pneumatoceles, particularly in cases with specific complications or diagnostic uncertainties. The indications for bronchoscopy include:
    • Endobronchial bleeding
    • Thick sputum
    • Large air leak
    • Mediastinal emphysema
    • Lobar collapse
  • Bronchoscopy in these scenarios serves diagnostic and therapeutic purposes, aiding in accurately identifying underlying issues while enabling immediate intervention to stabilize the patient's respiratory status.
(B2)

Surgical Interventions

Surgical intervention is generally reserved for patients with pneumatocele who do not respond to conservative or less invasive treatments. Indications for surgery include persistent air leaks, progressive enlargement of the pneumatocele, significant compression of adjacent lung parenchyma, recurrent infections, or cardiorespiratory instability. Additionally, failure of catheter drainage, bronchoscopy, or other minimally invasive approaches may necessitate surgical management. The extent of the disease determines the choice of procedure, the patient’s clinical stability, and the potential to preserve functional lung tissue.

Pneumatoceles larger than 6 cm or those unresponsive to conservative treatment are considered strong candidates for surgical resection. Procedures such as video-assisted thoracoscopic surgery (VATS) lobectomy or traditional lobectomy are generally associated with improved outcomes, particularly when performed early in refractory cases. However, pneumonectomy remains a last-resort option, reserved for extensive disease with no salvageable lung tissue, offering a potentially life-saving solution. Optimizing outcomes while minimizing complications requires careful, individualized decision-making based on the patient’s disease progression and overall clinical status.

• VATS
  • VATS is preferred for smaller, localized lesions and is associated with reduced postoperative morbidity compared to open thoracotomy. This minimally invasive approach avoids rib displacement, making it a favorable option in stable patients who can tolerate double-lumen tube placement for thoracic exploration. However, in unstable patients with massive chest wall disruption, significant air loss, or hemoptysis, open thoracotomy may be more appropriate.[66]
• Lobectomy
  • Lobectomy is a definitive surgical option for large, infected, or necrotic lesions not amenable to conservative management. This procedure is particularly effective in reducing the risks of infection, parenchymal necrosis, and the need for additional surgeries. Early lobectomy may be indicated in cases of:
    • Persistent air leaks
    • Progressive pneumatocele enlargement
    • Compression of functional lung parenchyma
    • Extensive lung abscess surrounded by necrotic tissue
    • Failure of conservative treatment or bronchoscopic interventions.
  • Despite its benefits, lobectomy is unsuitable if the amount of salvageable lung tissue is negligible or if retaining necrotic tissue poses risks.
• Pneumonectomy
  • Pneumonectomy is reserved for cases of extensive disease with no salvageable lung tissue or when less invasive approaches fail. This procedure aims to remove large pneumatoceles or necrotic lung tissue, improving ventilation and cardiorespiratory function. Pediatric pneumonectomy has been documented, with long-term outcomes generally favorable despite potential complications like scoliosis or mild spirometric changes.[67] Removing as little lung parenchyma as possible is ideal, although extensive disease may necessitate a more aggressive approach.
(B3)

Adjunctive Measures 

Surgical options may still be viable after stabilization in cases where patients are unsuitable for early intervention, such as those requiring extracorporeal membrane oxygenation (ECMO). ECMO can serve as a bridge to definitive treatments like pneumonectomy. Additionally, late thoracotomy has been reported up to 6 months after trauma due to pneumonic infiltration and persistent cavitary size. 

Special considerations

• Traumatic pneumatoceles
  • The management of traumatic pneumatoceles is primarily conservative, as most resolve spontaneously over time, though complications may necessitate surgical intervention. Radiological resolution varies depending on lesion size and content, typically averaging 3 months but ranging from 4 weeks to 6 months. Larger lesions or those filled with blood may require significantly longer periods, with an average resolution time of 5 months for those exceeding 2 cm in diameter or containing blood, as reported by Chon et al.[11][68] Notably, some pneumatoceles may transiently enlarge during the first 2 weeks posttrauma, potentially prompting unnecessary diagnostic or therapeutic procedures that could increase the risk of complications.
  • Traumatic pneumatoceles complicated by secondary infection or associated with respiratory compromise demand more active management. Positive-pressure ventilation may exacerbate lesion enlargement, hypoxemia, and inadequate ventilation, necessitating surgical interventions such as VATS or open thoracotomy with tube decompression. In cases of secondary infection, antibiotic therapy tailored to sputum culture and sensitivity is the first step. Percutaneous drainage is indicated if an infected pneumatocele is larger than 2 cm or sepsis persists beyond 72 hours of antibiotics. Early CT-guided catheter drainage is recommended if no clinical improvement is observed, with escalation to thoracotomy or thoracoscopy for refractory cases.
  • Long-term follow-up with chest radiography or other imaging modalities is essential to ensure resolution.[11] While the prognosis for traumatic pneumatoceles is excellent in most cases, with lesions typically disappearing within 3 months, late thoracotomy may occasionally be required for persistent cavitary lesions or associated pneumonic infiltration up to 6 months posttrauma. Cases like the giant hemopneumatocele described by Romero et al, which resolved conservatively, underscore the importance of individualized treatment strategies, particularly in patients with multiple thoracic injuries who may not tolerate surgery.
• Pediatric pneumatoceles
  • Pneumatoceles in pediatric populations present unique challenges due to the distinct physiology and vulnerabilities of children compared to adults. Ventilator-induced pneumatoceles are a subset of intrathoracic air leaks commonly observed in premature neonates and are considered markers of ventilator-induced lung injury. These lesions arise from alveolar overdistension and rupture, often caused by high mean airway pressures during mechanical ventilation. The fragile and immature lung parenchyma of preterm neonates predisposes them to such complications, making this condition a significant concern in neonatal intensive care settings.
  • Historically, neonatal pneumatoceles were frequently described as complications of ventilator-induced air leak conditions, particularly during the 1970s and 1980s. During this era, high-pressure ventilation was more common, leading to increased incidence of such complications. However, advances in neonatal care, including the introduction of surfactant replacement therapy and the adoption of lung-protective ventilation strategies, have significantly reduced the incidence of all intrathoracic air leaks, including pneumatoceles, in neonates.
  • The clinical significance of ventilator-induced pneumatoceles lies in their association with increased morbidity and mortality in premature infants. Despite this, the condition typically responds well to conservative management. Reducing mean airway pressure is the cornerstone of treatment, as it minimizes further lung damage and promotes spontaneous resolution of the pneumatocele. Modern lung-protective strategies, such as permissive hypercapnia and high-frequency oscillatory ventilation, further enhance the outcomes by preventing overdistension and reducing ventilator-induced injury.
  • Surgical intervention is rarely necessary for ventilator-induced pneumatoceles, as most resolve with conservative measures.[4][16][69] The focus remains on optimizing ventilatory support to allow for natural healing while minimizing the risk of additional complications, such as pneumothorax or secondary infection.
  • Pediatric cases of pneumatoceles are often associated with infections, such as pneumonia, and may be complicated by conditions like bronchopulmonary fistulae. In severe cases involving extensive disease, management may require advanced interventions. For example, venovenous (V-V) ECMO can be employed as a salvage measure in children with extensive disease affecting multiple lobes.[67] In rare, refractory cases, pneumonectomy may be necessary to manage enlarging pneumatoceles or severe bronchopulmonary fistulae. While preoperative care in such cases has not been well-defined in the literature, outcomes following pneumonectomy are generally positive.[67]
  • Long-term complications after pediatric pneumonectomy are infrequent and typically mild. Reported issues include scoliosis and changes in spirometry values, likely attributable to the anatomical adaptations following lung resection. Despite these potential changes, most children demonstrate no significant impairments in respiratory function or exercise capacity. These outcomes underscore the resilience of pediatric patients and highlight the importance of tailoring management strategies to the unique needs of this population.
(B3)

Differential Diagnosis

Differential Diagnosis

The differential diagnosis for a pneumatocele includes a wide range of conditions that can mimic its radiological appearance or clinical presentation. These include:

• Infectious and inflammatory causes
  • Lung abscess
  • Postinflammatory pneumatocele
  • Tuberculosis
  • Mycosis
  • Coccidioidomycosis
  • Fungus ball
  • Aspergilloma
  • Empyema
  • Pneumonia
  • Tuberculoma
• Congenital and structural anomalies
  • Bronchial cyst
  • Pulmonary sequestration
  • Cystic adenomatoid malformation
  • Congenital cysts
• Cystic conditions
  • Cystic fibrosis
  • Primary ciliary dyskinesia
  • Primary immunodeficiencies
• Systemic and genetic disorders
  • Marfan syndrome
  • Proteus syndrome
  • Neurofibromatosis (pulmonary cystic changes, blebs, bullae, giant bulla)
• Neoplastic and granulomatous conditions
  • Granulomatosis with polyangiitis
  • Langerhans cell histiocytosis
  • Hydatid cysts
  • Lung cancer
  • Metastatic neoplasm
• Trauma and other structural conditions
  • Herniation of viscera
  • Esophageal rupture

Radiological and Pathological Considerations

Cysts are thin-walled spaces (<2 mm) that lack associated pulmonary emphysema on CT scans and are distinguished from bullae by their greater wall thickness and location. Bullae, in contrast, are airspaces larger than 1 cm with an imperceptibly thin wall (<1 mm) and are typically subpleural, often occurring in the context of emphysema. Cavitary lesions, on the other hand, are gas-filled spaces characterized by thick, irregular walls and are commonly seen within areas of pulmonary consolidation, masses, or nodules. These cavities are distinct from cysts due to their irregular shape and thicker walls and are frequently associated with infections, chronic systemic diseases, or malignancies.[70][71] A thorough clinical history, imaging studies, and microbiological or histopathological investigations are crucial to narrowing the differential diagnosis and guiding appropriate management.

Prognosis

The prognosis of pneumatoceles generally depends on the underlying cause, size, and complications. In most cases, pneumatoceles are self-limiting and resolve spontaneously without significant long-term effects. This is particularly true for small, traumatic pneumatoceles, which typically undergo spontaneous resolution within weeks to months, especially when associated with minor injuries. For instance, many children with traumatic pneumatoceles show complete resolution within 6 months without the need for invasive treatment. However, larger pneumatoceles or those associated with severe trauma or pneumonia may persist for longer periods and pose greater risks, such as rupture or infection.

Pneumatoceles resulting from pneumonia, especially when complicated by bacterial infections like Streptococcus pneumoniae or Staphylococcus aureus, can have a more guarded prognosis. Infected pneumatoceles are at a higher risk of leading to more severe complications, including lung abscess, empyema, and pyopneumothorax, which can increase morbidity and mortality rates. These cases may require surgical intervention, including drainage or resection and extended antibiotic therapy. Additionally, pneumatoceles associated with conditions such as cystic fibrosis or immunocompromised states (eg, acquired immunodeficiency syndrome) may have a more complicated course due to the underlying disease process and the risk of recurrent infections.

For patients with pneumatoceles caused by mechanical ventilation, such as in premature infants or those with acute respiratiry distress syndrome, the prognosis is influenced by the severity of the lung injury and the effectiveness of ventilation management. In these cases, the development of a pneumatocele can be indicative of significant pulmonary trauma, which may lead to ongoing respiratory issues or the need for long-term respiratory support. The overall prognosis of pneumatoceles is more favorable in young, otherwise healthy individuals, particularly if the pneumatocele is small, noninfected, and does not lead to significant complications.

However, in the presence of large pneumatoceles, secondary infections, or complications like pneumothorax, the prognosis can be more serious and may require more intensive management. Follow-up care with imaging and clinical monitoring is essential, as unresolved or enlarging pneumatoceles may require surgical intervention to prevent further complications. In general, with appropriate management, most patients experience a good outcome, although severe cases can result in long-term respiratory issues or, in rare instances, death.

Complications

Pneumatoceles, though often self-limited and generally resolving without the need for invasive treatment, can lead to a range of complications. These complications can arise from the nature of the pneumatocele itself or from errors in diagnosis and subsequent intervention, which can exacerbate the condition. Below are the key complications associated with pneumatoceles:

• Infection
  • Infected pneumatoceles are one of the most common complications, particularly in traumatic or post-pneumonia cases. Infection may lead to the development of empyema or lung abscess. Infected traumatic pulmonary pneumatoceles have higher mortality rates compared to typical lung abscesses. Pulmonary contusion impairs bacterial clearance and can increase the risk of secondary infections. The treatment for infected traumatic pulmonary pneumatoceles is similar to that of lung abscesses and typically includes antibiotics, drainage of pus if necessary, and supportive care.[72]
• Rupture
  • Rupture of a pneumatocele is a critical complication that may result in pneumothorax or even tension pneumothorax. In this life-threatening condition, the pressure from trapped air compresses the lung and mediastinal structures, leading to severe respiratory distress and cardiovascular instability. The rupture may occur spontaneously or due to external trauma. Tension pneumothorax requires emergency treatment, typically with conventional tube thoracostomy (chest tube placement) to relieve the trapped air and reexpand the lung. If left untreated, this can lead to a mediastinal shift and severe hemodynamic instability. 
• Pneumomediastinum
  • Pneumomediastinum, the presence of air in the mediastinum, is another potential complication. This can occur due to pneumatocele rupture or air leakage from the cystic space into the surrounding tissues. Pneumomediastinum may lead to chest pain, dyspnea, and subcutaneous emphysema. In some cases, it can progress to life-threatening complications such as tension pneumomediastinum.[73]
• Pyopneumothorax
  • Pyopneumothorax, a combination of pneumothorax and infection (pus accumulation in the pleural space), can develop when a pneumatocele becomes infected. The accumulation of pus and air in the pleural space can cause further respiratory distress and necessitate drainage. This condition is also associated with a higher mortality rate compared to a simple pneumothorax, making early detection and intervention crucial.
• Hemothorax and hemopneumothorax
  • Trauma-related pneumatoceles may also be complicated by hemothorax (blood in the pleural space) or hemopneumothorax (air and blood in the pleural space). These conditions often result from pulmonary laceration and the escape of blood into the pleural cavity. Both conditions can cause significant respiratory distress and require urgent treatment, typically in the form of chest tube placement or surgical intervention, depending on the severity of the bleeding.
• Fistulous pleural-extrathoracic communication
  • In untreated or inadequately treated tuberculosis cases, pneumatoceles may develop a fistulous communication between the pleura and the extrathoracic environment. This is more likely to occur in patients who have not completed anti tuberculosis treatment. Such fistulas may cause persistent air leaks or fluid drainage from the pleural cavity to the outside of the body, necessitating surgical intervention for closure.
• Continuous positive airway pressure complications
  • In those who are mechanically ventilated, particularly those on continuous positive airway pressure, pneumatocele enlargement can occur, leading to compression of adjacent lung tissue. This increased compression can lead to worsening hypoxemia, which may result in cardiopulmonary instability.[11] Monitoring pneumatocele size and managing ventilation settings is essential to avoid these complications, especially in critically ill individuals.
• Obstruction of adjacent airway
  • Large pneumatoceles can exert pressure on nearby bronchial structures, potentially leading to airway obstruction. This can result in atelectasis (collapse of a part of the lung) or impaired ventilation, further compromising respiratory function. Airway obstruction also increases the risk of infection, as secretions become trapped in the obstructed region of the lung.
• Fibrosis and scarring
  • Chronic pneumatoceles, especially those that result from repeated infections or trauma, can lead to fibrosis or scarring of the lung tissue. This process may reduce lung compliance and capacity, leading to chronic respiratory insufficiency. If left untreated, this could result in restrictive lung disease, which would require ongoing medical management.
• Chronic respiratory symptoms
  • Chronic respiratory symptoms such as cough, dyspnea, and wheezing may develop in some cases, especially those with multiple or large pneumatoceles. These persistent symptoms can impair quality of life and may require long-term monitoring or surgical intervention if the symptoms worsen or lung function deteriorates.