RFA has become the major treatment for HCC, especially HCC with liver cirrhosis. Therefore, it can be speculated that the incidence of rare complications, such as DH as a result of RFA, will inevitably increase.
DH following RFA can be categorized as diaphragmatic injury (DI). Complications within 30 days after RFA are classified as early DI, and complications that occur more than 30 days after RFA are classified as delayed DI [6]. Delayed DI can result in a poorer prognosis compared with early DI. The incidence of death is 30% with delayed DI and 7.1% with early DI [7]. Pekmezci et al. reported that thoracoscopy is an effective tool for diagnosis and subsequent surgical repair of DI [8]. Furthermore, thoracoscopy can eliminate pleural collections, which can cause pyothorax. Therefore, when the diagnosis is uncertain, thoracoscopy is recommended.
The mechanism of DH after RFA has not been clarified. Nagasu et al. reported three causative factors of DH after RFA [9], including the location of the targeted lesions, collateral thermal injury during RFA, and the advanced cirrhosis status had listed. Collateral thermal damage to the diaphragm during RFA to target areas adjacent to the diaphragm is common. In this case, all tumors that were treated with RFA were located adjacent to the diaphragm. Thermal damage to the diaphragm may result in an inflammatory response, leading to fibrosis that could ultimately weaken the muscle fibers of the diaphragm and cause late-onset defects [10]. Poor liver function might prevent the injured tissue from healing adequately, with complications such as ascites and pleural effusion, thereby contributing to further tissue damage [11]. According to past DH reports, most previous patients had a history of RFA treatment for HCCs with right dome lesions of segments 7 or 8 and showed a right-sided DH [12]. This patient had previously undergone S8 resection and had an enlarged medial segment to the right side. It was suggested that this may be the cause of DH at the scar of RFA to medial segment.
Furthermore, Chilaiditi’s syndrome is a condition that is caused by a deterioration in liver function. Moaven et al. reported that the incidence of Chilaiditi’s syndrome inevitably increases in patients with cirrhosis due to liver atrophy or relative atrophy in the medial segment of the left lobe of the liver, which creates space between the diaphragm and liver [13]. Therefore, it is plausible that liver atrophy contributes to perforation and herniation of the diaphragm. In our case, CT 6 months before the onset of DH showed no findings suggestive of Chilaiditi’s syndrome (Fig. 5a, b).
We have previously performed thoracoscopic RFA for HCC under the diaphragm, which is difficult to approach percutaneously [14]. With thoracoscopic RFA, the tumor can be directly confirmed by cutting the diaphragm. We usually cut the diaphragm and puncture the tumor directly using thoracoscopy. The reason we cut the diaphragm is to avoid heat injury. In this case, we did not cut the diaphragm because it was expected that adhesion peeling would be difficult due to repeated treatment.
To avoid damage to the diaphragm, it has been reported that ablation for HCC with artificial pleural effusion or ascites treatment is useful [15, 16]. It will be necessary to consider treatment with pleural effusion or ascites for lesions directly under the dome.
