Altered Concepts of the Mechanism of Nonvisualization of the Gallbledder

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Abstract
Several observations made in the course of routine clinical cholecystography in recent months have rekindled an interest in our department in the basic mechanisms that determine whether or not visualization of the gallbladder will occur. The first such observation concerns the instance in which good opacification is apparent, but surgical extirpation reveals marked sclerosis of the gallbladder wall to an extent that suggests possible interference with the organ's ability to concentrate contrast material. The second observation is the instance in which initial examination with contrast material fails to reveal a gallbladder shadow, and yet repeat examination with a similar dose on the following day demonstrates good opacification (Fig. 1). In Rosenbaum's series of 450 consecutive patients examined by cholecystography (1), in 66 visualization was initially absent or inadequate without evidence of gallstones. Findings were normal in 10 per cent of those with initial nonvisualization and in 64 per cent of those with initially inadequate visualization on repeat examination with an additional dose of contrast material. In our experience in these circumstances, the density of the gallbladder after the second dose usually appears to be more than can be explained by a simple doubling of the quantity of contrast material in the gallbladder. Therefore, one must postulate a mechanism whereby a higher percentage of the second dose in comparison to the first can be retained within the organ. In an attempt to explain these and other related phenomena encountered in clinical cholecystography, we speculated on the possibility of reabsorption of cholecystographic material from the inflamed gallbladder. If such a phenomenon occurs and were of importance in terms of visualization or nonvisualization, one might have an explanation for the clinical circumstances just cited. The gallbladder with a very thick wall, for example, would opacify readily since the wall could absorb neither water nor the cholecystographic material. In this circumstance the gallbladder lumen might be considered as a dilated extension of the common bile duct. Opacification of the bile ducts in individuals with a previous cholecystectomy is not uncommon. Furthermore, if reabsorption of the contrast material proved to be significant, one might explain second-dose visualization by hypothesizing that with the first dose, a marginally inflamed gallbladder reabsorbs the contrast material at a rate that prevents sufficient concentration for visualization. With the second dose, however, many of the serum and tissue protein binding sites are occupied, leading to a more sustained elevation of available opaque material in the blood and to an inhibition of reabsorption of contrast material through the marginally in-flamed gallbladder wall.

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