The word atelectasis is of Greek origin and means lack of stretch; in current medical usage, the term refers to collapse or loss of lung volume. Atelectasis is also defined as collapse of alveolar spaces, generally of a magnitude severe enough to appear on a plain chest radiograph. Atelectasis is a common problem in pediatric patients. The three main types of atelectasis noted in children include obstructive atelectasis, resorptive atelectasis, and compressive atelectasis. In almost all cases, atelectasis is acquired and referred to as secondary; rarely, primary atelectasis caused by congenital abnormalities may be present from birth. An overview of atelectasis in children is presented here. The radiographic appearance of atelectasis and an overview of atelectasis in adults are discussed separately. (See "Radiologic patterns of lobar atelectasis" and "Atelectasis: Types and pathogenesis in adults".)
In order to understand the pathophysiology of atelectasis, a review of the normal mechanisms that prevent lung collapse is required. Elastin fibers within alveolar walls result in a tendency for the alveoli to recoil inwards. This is balanced by the outward recoil of the chest wall and the interaction between the parietal and visceral pleura. In addition, the primary mechanism that keeps the lung from collapsing at low volumes is surfactant.
Surfactant is a complex phospholipid and protein mixture produced by type II alveolar epithelial cells. It functions to lower surface tension, which is defined by the law of Laplace:
Pressure = 2 x (surface tension) / radius
As alveolar volume decreases with expiration, surface tension increases to the degree that, without surfactant, the alveolus would collapse completely. This adhesive atelectasis becomes clinically relevant in diseases that result in absent or deficient surfactant production and homeostasis, including neonatal respiratory distress syndrome, congenital surfactant protein B deficiency, and pulmonary alveolar proteinosis. (See "Overview of neonatal respiratory distress: Disorders of transition" and "Clinical manifestations and etiology of pulmonary alveolar proteinosis in adults".)