Slow Infusion Intravenous Cholangiography

Abstract

A safe and effective intravenous Cholangiographie agent has been available to radiologists since the introduction in Europe of Biligrafin as a 20 per cent solution of sodium iodipamide in 1953 and its successor in this country, the methylglucamine salt Cholografin.2 Through the twelve-year period, 1953 to 1965, clinical investigators using the recommended 20 cc injection have published widely divergent results on the success of this contrast agent (1–6). In their review of the literature, Floch and Geffen (7) noted that the incidence of nonvisualization was as high as 34 per cent, but with improved patient selection and experience the degree of failure is generally in the 6 to 15 per cent range. The duct was satisfactorily visualized in 83.5 per cent of the 237 cases in their series. Wise (8) indicated in his monograph that, with proper patient selection based on preliminary liver function evaluation, successful visualization of the common duct in the cholecystectomized patient might be improved from his initial results of 89.1 per cent in 1,194 cases to almost 100 percent. Most recently, Edmunds (9) reported 81 per cent visualization in 139 cases. Attempts to improve visualization of the common bile duct in cholecystectomized patients by mechanical aids such as abdominal compression (10) or the induction of sphincter spasm with morphine (11) have been notably unsuccessful. Similarly, dosage increases have been of little value. Pahl (12) noted this in a clinical trial in 1954, and more recently Fischer (13) reported no significant increase in biliary iodine in experimental animals after the ad-ministration of higher doses of contrast agent. Normally, 6 to 18 per cent of the injected medium is excreted through the kidneys (14), and increased doses produce higher urinary rather than liver excretion values. Experimental and clinical attempts to alter mechanisms of excretion have also failed to improve visualization efficiency or radiopacity. Edling and Helander (15) maintained that duct opacification was improved by the renal tubular blocking agents, PAH and penditan, used separately or in combination, but this has not been substantiated (16), since iodipamide is excreted through the kidneys by glomerular filtration (14). Fischer (17) found no increase in biliary iodine in dogs by the blocking of renal tubular function with probenecid. He also noted no significant improvement in biliary iodine by stimulating liver excretion with cortisol, sodium dehydrocholate, and tri-iodothyronine. Dehydration or the combined use of oral and intravenous Cholangiographie agents also produced no quantitative improvement in bile duct iodine. Liver excretion of iodipamide is attributed to both its molecular structure and its albumin-binding affinity. Lasser et al. (18) were unable to improve biliary excretion of contrast medium in rabbits by priming with human serum albumin or lowering blood pH to increase protein-binding affmity.