Eventration of the diaphragm is a disorder in which all or part of the diaphragmatic muscle is replaced by fibroelastic tissue [1,2]. The diaphragm retains its continuity and attachments to the costal margin. However, the weakened hemidiaphragm is displaced into the thorax, which can compromise breathing. With diaphragmatic hernia, in contrast, this continuity between the diaphragm and the costal margin is disrupted.
The incidence of eventration is uncertain, although in one report, the condition was detected in 1 per 1400 patients who had chest radiographs . More males than females are affected. Congenital eventrations can be isolated, although they sometimes are associated with other developmental defects such as cleft palate, congenital heart disease, situs inversus, or undescended testicle .
Eventration of the diaphragm can be congenital or acquired [4-6]. Congenital eventration results from inadequate development of the muscle or absence of the phrenic nerves. The most common cause of acquired eventration is injury to the phrenic nerve, resulting from either a traumatic birth or thoracic surgery for congenital heart disease. The loss of contractility leads to muscle atrophy with elevation of the hemidiaphragm . (See "Diaphragmatic paralysis in the newborn".)
The defect in congenital eventration can be partial or diffuse [3,7]. In the former, the defect is localized; whereas, in the latter, the diaphragm consists of a thin, diaphanous membrane that is attached peripherally to normal muscle. In one series, partial defects, mostly affecting the right hemidiaphragm, occurred in 65 percent of children . Diffuse defects also tend to be unilateral but occur more commonly on the left side.
In the acquired form, the central tendon is normal and the diaphragm consists of normally developed muscle that is atrophic. The phrenic nerve typically is small. Both sides are affected equally.