Phlebomalacia and Phlebosclerosis

PHLEBOMALACIA, softening or weakening of the vein wall. Phlebomalacia is a specific instance of angiomalacia in general. It may be based on various pathological processes leading to changes in the physical properties of the vein wall. Phlebomalacia can result from necrosis, degeneration, inflammation, atrophy, etc. Among the theories explaining the development of phlebosclerosis and phlebectasia is Thoma's theory, which treats their origin as the result of preceding phlebomalacia, possibly of a vasomotor nature, i.e., the same viewpoint as regarding the origin of atherosclerosis (see Arteriosclerosis). PHLEBOSCLEROSIS, sclerosis of the vein, a concept encompassing all cases of connective tissue proliferation in the venous wall within any of its layers. The etiology and pathogenesis of phlebosclerosis can be highly diverse. Phlebosclerosis may result from hypertrophy of the venous wall on the basis of prolonged venous hyperemia. Phlebomalacia can result from senile atrophy of the muscular part of the venous wall followed by its replacement with connective tissue. Often, phlebosclerosis is the result of phlebitis, and among inflammatory phleboscleroses, according to literature data, those associated with syphilitic infection predominate. Phlebosclerosis may be of traumatic origin: bruises, tears of the venous wall followed by scarring. Phlebomalacia is often associated with thrombosis, being either a consequence of thrombosis and developing along the course of thrombus organization or preceding thrombosis, which further enhances phlebomalacia. The fundamental issue in the doctrine of phlebosclerosis is whether any variety of phlebosclerosis exists that would be an analogue to atherosclerosis as a general disease and what the relationship is between phlebosclerosis and arterial atherosclerosis. At present, this question must be answered in the negative. We know of no general phlebosclerosis analogous to general atherosclerosis from a pathogenetic, morphological, or clinical standpoint. That phlebosclerosis with lipid accumulation and even calcification, which is extremely rarely observed in the portal vein system, has fundamentally nothing in common with atherosclerosis. This variety of phlebosclerosis is a local disease associated with some other process, most often syphilis, and consequently is not connected with a primary disturbance of lipoid metabolism. The lipid infiltration and calcification observed in this condition represent a local dystrophic process. Morphological diagnosis of phlebosclerosis presents no difficulties, especially if special connective tissue staining of the van Gieson type is used. The clinical significance of phlebosclerosis is determined by its localization and the extent of the lesion. Phlebosclerosis is a serious precondition for thrombosis. Traumas to sclerosed veins present a great danger in terms of subsequent hemorrhage.