The two most common causes of diaphragmatic elevation are congenital eventration of the diaphragm and phrenic nerve palsy.1,2 Both may require plication of the diaphragm. This chapter specifically focuses on techniques to plicate the diaphragm from above (intrathoracic).
Congenital eventration is the lack of muscle or tendon within the diaphragm. It is a spectrum of disorders that share the underlying cause of impaired fetal myotome migration.1 Mild cases may only lack the central tendon, while severe cases may lack the central tendon as well as the entire muscular diaphragm. The area of congenitally missing muscle tissue is usually closed with a fused single membrane of pleura and peritoneum. This membrane is generally displaced within the ipsilateral hemithorax owing to the absence of muscle. If only a membrane is present, a patch may be more appropriate than plication.1 A rim of rudimentary diaphragmatic tissue can generally be found around the lateral contour of the chest with enough substance to hold sutures to anchor the patch. Along the medial side, the patch can be stitched to the pericardium and the anterior thoracic spinal ligaments.
Causes of acquired phrenic nerve paralysis include viral palsy, iatrogenic injury (typically following thoracic surgery or instrumentation around the phrenic nerve above the clavicle), fracture of the first rib and clavicle, or a traction injury to the phrenic nerve. This last mechanism can also be seen in infants following a forceps delivery. The muscle and tendon of the diaphragm are normal, and plication pulls the muscle taut and reduces the compression of the ipsilateral lung.
A flaccid diaphragm compresses the lower lobe of the ipsilateral lung. In addition, if there is a large displacement of abdominal components into the negative pressure thorax, this bulk mechanically shifts the mediastinum with compression of the contralateral lung. Thus, there is atelectasis of the ipsilateral lower lobe, compression of the left atrium, impairment of pulmonary venous blood flow, and contralateral lung compression with additional atelectasis.2
Adults with paralyzed diaphragms do not always need plication if they are asymptomatic during normal activity. If they have underlying pulmonary disease, or desire strenuous activity, then plication can offer palliation of dyspnea from a paralyzed diaphragm. If the phrenic nerve is believed to be intact, but injured with the possibility of recovery within 2 years, conservative management will eventually lead to recovery of function. Plication, however, remains a low-risk procedure which continues to be underutilized. The radial plication technique, in particular, is designed to palliate symptoms while providing the maximum probability that the phrenic nerve will recover.
A recent study of patients who underwent unilateral plication via VATS technique documented substantial increases in spirometry readings at 6 months postprocedure.3 The mechanism for improvement in these patients is the increased tension of the diaphragmatic barrier between the thorax and abdomen. This allows patients to generate a more negative intrapleural pressure than was possible with a floppy, paralytic diaphragm.