ABSTRACT
We present a case of a combination of primary and secondary diaphragmatic hernia in a 63-year male patient. For progressive dyspnea and palpitations caused by a large and symptomatic Morgagni hernia resulting in a right-sided enterothorax, an open tension-free mesh repair was performed. The postoperative course was complicated by a secondary hepatothorax through a spontaneous rupture of the right diaphragm. Primary mesh repair of the Morgagni hernia, however, proved to be sufficient. This recurrent herniation might be a consequence of (1) preexisting atrophy of the right diaphragm caused by disposition and/or long-term diaphragmatic dysfunction due to the large hernia, combined with (2) further thinning out of the diaphragm by intraoperative hernia sac resection, and (3) postoperative increase of intra-abdominal pressure.
Subject(s)
Diaphragm/surgery , Hernia, Diaphragmatic/surgery , Hernias, Diaphragmatic, Congenital/surgery , Herniorrhaphy/methods , Diaphragm/diagnostic imaging , Hernia, Diaphragmatic/diagnostic imaging , Hernia, Diaphragmatic/etiology , Hernias, Diaphragmatic, Congenital/diagnostic imaging , Humans , Male , Middle Aged , Radiography , Recurrence , Reoperation , Surgical MeshABSTRACT
We present a case of a combination of primary and secondary diaphragmatic hernia in a 63-year male patient. For progressive dyspnea and palpitations caused by a large and symptomatic Morgagni hernia resulting in a right-sided enterothorax, an open tension-free mesh repair was performed. The postoperative course was complicated by a secondary hepatothorax through a spontaneous rupture of the right diaphragm. Primary mesh repair of the Morgagni hernia, however, proved to be sufficient. This recurrent herniation might be a consequence of (1) preexisting atrophy of the right diaphragm caused by disposition and/or long-term diaphragmatic dysfunction due to the large hernia, combined with (2) further thinning out of the diaphragm by intraoperative hernia sac resection, and (3) postoperative increase of intra-abdominal pressure.
ABSTRACT
We report a 63-year-old lady with Cronkhite-Canada syndrome, who developed colorectal cancer. A hemicolectomy was performed, and the tumor specimen was prepared for DNA-analysis and immunohistochemical screening. We found a mutation of p53 gene without APC- and ras-gene alteration and expression of erbB2-protooncogen. The polyps in non-hereditary Cronkhite-Canada-syndrom are neither adenomatous nor hyperplastic, but patients often develop colorectal cancers. The steps of mutation do not follow the adenoma-carcinoma sequence, first described by Vogelstein 1988. This and previous observations suggest that carcinogenesis in Cronkhite-Canada syndrome follows another independent sequence.
