In this essay I would like to address a topic most of you have learned a little about during your training, and likely have not given much thought since then. And such abbreviated attention could be considered adequate for the establishment of competence. But with your indulgence, I will address my remarks about the lowly pelvic phlebolith, perhaps boosting its importance as a diagnostic marker, or at least, I will endeavor to supplement somewhat general knowledge about it. I will delve into history, putative pathogenesis, morphologic appearance, positional changes and differential diagnosis [1].

Phleboliths-stones in veins-were first recognized by Rokitansky in 1852. Thirty years later von Recklinghausen stated that they were harmless entities. Yet 20 years after that statement, some physicians maintained that they were actually the cause of pelvic pain. They were thought to be frequently associated with non-hemangiomatous tumors. Faced with this supposed risk, operations to remove them were fashionable at that time. Remember that in the early decades of the twentieth century, in Middle Europe at least, diverticula were rare, epiploic appendagitis was common, and sigmoid volvulus was a relatively frequent diagnosis in middle-aged individuals, even those lacking present-day risk factors for it.

Phleboliths were first described radiologically by Orton in 1908, and 1 year later Clark demonstrated that they were intact intravenous concretions, appearing at autopsy, as seen by x-ray after the pelvic veins were dissected.

Phleboliths are stones made up of thrombi attached to venous walls. They consist of closely congregated laminae of platelets within a netting of erythrocytes and fibrin. Calcium deposition takes place only after the clot has fully formed. Almost always their opacity is due to the accumulation of calcium carbonate, with lesser contributions made by ammonium phosphate and magnesium ammonium phosphate.

Why do they form and why especially in the pelvic veins when they are rare elsewhere in the body? In adults pelvic veins are valveless and poorly supported in loose connective tissue. It has been proposed that sudden, intermittent increases in intra-abdominal pressure, as with straining at defecation, can serve to damage the vessel wall and thereby predispose to thrombosis. From this notion, Burkitt found support in his grand theory of the pathogenesis of the so-called diseases of western civilization, all of them occasioned by the consumption of a low-fiber diet characteristic of developed countries in which residents shun cellulose-laden foods. This leads, he theorized, in addition to the precipitation of phleboliths, to the propensity for colonic diverticula whose formation is abetted by straining at stools and, by a similar mechanism, related to prolonged colonic transit time, to large intestinal polyps and colonic malignancies. Interestingly, phleboliths have not been described in veterinary radiology, presumably because horizontally-oriented four footed animals do not subject the pelvic veins to increased pressure with the passage of stool.