A pulmonary cavity is defined in the radiology literature as lucency surrounded by a thickened wall (at least 5 mm) within a parenchymal consolidation, mass or nodule.1,2 Cavitary pulmonary lesions are due to a various congenital and acquired diseases such as infectious (bacterial, fungal or parasitic), inflammatory/autoimmune disorders and neoplasms (primary or metastatic tumors). Other reported common cavitary pulmonary disorders in adults are rheumatologic diseases (eg, Wegener granulomatosis, sarcoidosis), trauma and pulmonary embolism.1–3 Infectious diseases including pneumonia, empyema and tuberculosis (TB) have the highest prevalence in adults and children.4–7 There is limited information regarding the etiology of nontuberculous cavitary pulmonary lesions in children.8–10 We investigated retrospectively the causes of these lesions in our patients.
MATERIALS AND METHODS
Children included in the study group were those who met the criteria for cavitary lesions detected by chest computerized tomography: loss of lung architecture, decreased enhancement and cavities with thin, nonenhancing walls (at least 5 mm). None of the patients had TB contact, tuberculin skin test positivity or positive microbiologic results for Mycobacterium tuberculosis. The patients analyzed were treated between November 2010 and December 2013 and evaluated retrospectively. Demographic, clinic and radiologic features of the patients were investigated. This study was conducted at Bezmialem Vakif University Hospital, an urban city hospital where malnutrition is not common at that area.
Forty-two patients (23 females and 19 males; mean age of 91.1 ± 6.8 months, range 3 months to 15 years) were enrolled in the study. Common symptoms of patients were cough (77%), fever (31%), sputum (23%) and hemoptysis (11%). There was recurrent pneumonia in 5 and failure to thrive in 3 patients. Mean duration of symptoms and signs was 22.8 ± 4.6 months. Physical examination was normal in 22% of the patients while 35% had ronchi. Median follow-up period was 10 months (4–14 months, 25–75 interquartile range).
Computerized tomography localization of the pulmonary lesions was 47% (n = 20) in the left lung [left upper lobe, n = 11 (26%); left lower lobe, n = 9 (21%)] and 34% (n = 14) in the right lung [right upper lobe, n = 3 (7%); right middle lobe, n = 3 (7%); right lower lobe, n = 8 (19%)] and 19% (n = 8) bilaterally. One cavity was diagnosed in 20 patients (48%), 2 cavities in 4 patients (10%) and 3 or more cavities in 18 patients (42%).
The most common cause of cavitary pulmonary lesions was necrotizing pneumonia (Table 1). Four patients with infectious disease had immunodeficiency [hyper IgE syndrome (n = 2) and severe immunodeficiency (n = 2)] and 2 patients had malignancy [acute myeloid leukemia (n = 1), Hodgkin disease (n = 1)]. Microbiologic culture was positive in 14 (33%) patients. Isolated bacteria were Haemophilus influenzae (n = 3), Streptococcus pyogenes (n = 2), Pseudomonas aeruginosa (n = 2), methicillin-resistant Staphyloccus aureus (n = 1), Streptococcus pneumoniae (n = 1), Moraxella catarrhalis (n = 1), Nocardia (n = 1) and Fusobacterium (n = 1). Aspergillus fumigatus was obtained from 2 patients with malignancy. HIV screening was done in all the patients. None were identified.
Twenty-one patients (50%) underwent flexible bronchoscopy for evaluation of localized or recurrent infection. Three patients had endobronchial lesions (later diagnosed as lung abscess with Fusobacterium, nocardiosis and cystic hydatid disease), 1 patient was diagnosed with foreign body aspiration, 1 patient endobronchial tumor (later diagnosed as carcinoid by pathology) and 7 patients had purulent secretions.
Surgery was performed in 11 (26%) patients [ruptured hydatid cyst (n = 3), lung abscess (n = 3), cystic adenomatoid malformation (n = 2), foreign body aspiration (n = 1), carcinoid tumor (n = 1) and thymic cyst (n = 1)].
The etiology of lung cavitary lesions exhibits a broad spectrum, ranging from benign to malignant pulmonary diseases of acquired or congenital origin, including various infectious diseases.1–3 A number of pathologic processes can lead to lung cavity formation including suppurative necrosis (eg, pyogenic lung abscess), caseous necrosis (eg, TB), ischemic necrosis (eg, pulmonary infarction), cystic dilatation of lung structures (eg, ball valve obstruction) or displacement of lung tissue by cystic structures (eg, Echinococcus). In addition, malignant processes can cavitate because of treatment-related necrosis, internal cyst formation or internal desquamation of tumor cells with subsequent liquefaction.1,2 The likelihood that a given process will cavitate depends on host factors and the nature of the underlying pathogenic process. The most common reported causes of cavitary lesions are malignancy and infection in adults. Other less common causes include bronchiectasis, rheumatologic diseases (eg, Wegener granulomatosis, sarcoidosis), autoimmune diseases (rheumatoid arthritis, primary amyloidosis), bronchiolitis obliterans organizing pneumonia, trauma and pulmonary embolism.1–3
M. tuberculosis cavity formation has the highest etiologic prevalence in adults and children, particularly in endemic areas.1,2,4 There have been few reports of children with non-tuberculous cavitary pulmonary lesions. Ramphul et al7 investigated 75 cases presenting with empyema or parapneumonic effusion. A cavitary lesion was detected in 15 cases (20%). S. pneumoniae was the most common isolated bacterium (in 13 of 15 cases). Necrotizing pneumonia is a severe complication of community-acquired pneumonia characterized by liquefaction and cavitation of lung tissue. It has increasingly been identified as a complication of pediatric pneumonia.5,6 Similarly, in this series we established that necrotizing pneumonia was the commonest etiology of nontuberculous cavitary lesions. Other reports of cavitary lesions in children are usually only in the form of case reports with various causes including infectious, bronchiectasis, malignancy, immunodeficiency, rheumatologic diseases or congenital lung abnormalities.8–10
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