Pulmonary pneumatoceles are thin-walled, air-filled cysts that develop within the lung parenchyma. They can be single emphysematous lesions but are more often multiple, thin-walled, air-filled, cystlike cavities. Most often, they occur as a sequela to acute pneumonia, commonly caused by Staphylococcus aureus. However, pneumatocele formation also occurs with other agents, including Streptococcus pneumoniae, Haemophilus influenzae, Escherichia coli, group A streptococci, Serratia marcescens, Klebsiella pneumoniae, adenovirus, and tuberculosis. Pneumatoceles are generally observed soon after the development of pneumonia but can be observed on the initial chest radiograph.
Noninfectious etiologies include hydrocarbon ingestion, trauma, and positive pressure ventilation.
In most circumstances, pneumatoceles are asymptomatic and do not require surgical intervention.  Treatment of the underlying pneumonia with antibiotics is the first-line therapy. Close observation in the early stages of the infection and periodic follow-up care until resolution of the pneumatocele is usually adequate treatment. The natural course of a pneumatocele is slow resolution with no further clinical sequelae. Invasive approaches should only be reserved for patients who develop complications.
Since the 1950s, multiple theories have been proposed as to the exact mechanism of pneumatocele formation; however, the exact mechanism remains controversial.
Carrey suggested that the initial event is inflammation and narrowing of the bronchus, leading to the formation of an endobronchial ball valve.  Ultimately, this bronchial obstruction leads to distal dilatation of the bronchi and alveoli. In 1951, Conway proposed that a peribronchial abscess forms and subsequently ruptures its contents into the bronchial lumen.  This also acts similarly to a ball-valve obstruction in the bronchus and leads to distal dilatation. In 1972, Boisset concluded that pneumatoceles are caused by bronchial inflammation that ruptures the bronchiolar walls and causes the formation of "air corridors."  Air dissects down these corridors to the pleura and forms pneumatoceles, a form of subpleural emphysema.
Traumatic pneumatocele has a different pathophysiology from the infectious type,  developing in a 2-step process. Initially, the lung is compressed by the external force of the trauma, followed by rapid decompression from increased negative intrathoracic pressure. A "bursting lesion" of the lung occurs and leads to pneumatocele formation.
Incidence of postinfectious pneumatocele formation ranges from 2-8% of all cases of pneumonia in children.  However, the frequency can be as high as 85% in staphylococcal pneumonias.
Although mortality from the initial pneumonia can be significant, mortality associated with pneumatoceles is quite low. Complete resolution without long-term sequelae is typical; however, rare complications can occur, including the following:
Secondarily infected pneumatocele
No specific racial predilection is observed for pneumatocele formation. Because pneumatoceles are usually a complication of pneumonia, the predilection is based on susceptibility for infection.
No sex predilection is known.
Infants younger than 1 year account for three fourths of the cases of staphylococcal pneumonia. Because pneumatoceles commonly develop as a complication of staphylococcal pneumonia, pneumatoceles are found more frequently in infants and young children. One study reported that 70% of pneumatoceles occurred in children younger than 3 years. 
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