Indexed on: 01 Sep '38Published on: 01 Sep '38Published in: Digestive Diseases and Sciences
While examining the gall bladders from routine cholecystectomies during the past year or two several instances of partial obstruction of the cystic duct were encountered. A classification of the various types of lesions which are apt to produce partial obstruction has been discussed. Important lesions in this group are adhesions, kinks, an acute inflammatory process, anomalous folds of Heister, stone in the cystic duct and compression by extrinsic factors. Complete obstruction such as illustrated by hydrops and empyema is not discussed because the mechanisms of production and pathology are so clearly understood. It is obviously very difficult to prove that a given lesion of the cystic duct is producing an incomplete obstruction, but an analysis of the cases studied has led us to believe that on many occasions the lesion in the cystic duct represents perhaps the only significant lesion of the gall bladder and that on other occasions it may be the instigating factor of disease in the gall bladder. It is difficult to demonstrate the obstruction experimentally, not only because a criteria of the degree of obstruction based on the rapidity of flow of bile of a given viscosity through the cystic duct would be difficult to establish, but also because of the fact that accurate reading could only be obtained after cholecystectomy. Removal of the gall bladder would of necessity destroy the attachment of the cystic duct thereby altering the factors producing the obstruction, because fixation and adhesions are bound to be important factors in a great majority of the obstructions even though the primary lesion may be a congenital anomaly involving the folds of Heister.It should be emphasized that in a great majority of instances, an anatomical lesion may be present without exerting any obstructive influence until an acute inflammatory process is implanted upon it. There is very good evidence that acute inflammation of the cystic duct occurs commonly. The fact that adhesions about the cystic duct are so commonly encountered in gall bladder disease is in itself fairly good proof. The presence of severe clinical manifestations typical of gall bladder disease, with a demonstrable lesion of the duct in the absence of significant pathologic changes in the gall bladder wall, as was the case in most of the patients studied in this series, is also suggestive proof that the lesion in the cystic duct may be an important factor in the production of the manifestations. This is particularly true if cholecystectomy relieves thepatient’s symptoms. A consideration of some of the patients in this series suggests very decisively that at least in some instances the failure of the gall bladder to empty (as determined by cholecystographic study) following the fat meal is indicative of serious choleeystic disease. It is conceivable that the failure of emptying might be due to (1) obstructive lesions of the cystic duct; (2) inefficient muscular response on the part of the gall bladder (e.g. atony) or (3) spasm of the sphincter of Oddi. In this study, however, attention was directed only to mechanisms involved in the first group.