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Why and how venous collateralization occurs is not clear, but the existence of a subgroup of postthrombotic limbs with noncollateralizing obstruction and diffuse iliac vein narrowing has not been emphasized before. The 11 limbs identified in this study presented no specific symptomatology and did not differ hemodynamically from collateralizing obstructed limbs. Their venographic appearance is easily mistaken as normal unless compared to the contralateral side. At surgery, these veins also display significant resistance to dilation. The lack of collateralization and increased stiffness could result from postthrombotic periphlebitis, which can produce scarring and a fibrous sheath surrounding the vein (phlebosclerosis), preventing distension and collateral formation. Although there is no focal obstruction, the decreased compliance due to the encompassing sheath results in outflow obstruction when flow increases.

Int Angiol. 2011 Jun;30(3):212-20.

Distribution and clinical impact of phlebosclerosis.

Tzogias L, Labropoulos N, Amaral SI, Antoniou GA, Giannoukas AD.

Department of Vascular Surgery, University Hospital of Larissa, University of Thessaly, Larissa, Greece.

Abstract

Sclerosis of the vessels has been extensively described in arteries but rarely in veins. Phlebosclerosis refers to the thickening and hardening of the venous wall. Despite its morphological similarities with arteriosclerosis and potential morbid consequences phlebosclerosis has gained only little attention. This is a narrative review based on a MEDLINE search (1949 to February 2009) of articles in English, German and Japanese (with English abstracts). References in retrieved articles were searched for further potentially relevant articles. Controversy about the definition, etiology, pathogenesis and histological aspects of phlebosclerosis exists. Phlebosclerosis constitutes a fibrous degeneration of the venous wall, predominantly the intima, with or without calcification. It has been described to affect almost the entire venous system with variable clinical consequences. The exact pathophysiologic mechanisms are unknown. Despite the confusing terminology and limited scientific data, we conclude that phlebosclerosis should be regarded as a distinct clinical entity. Its prevalence and clinical significance may be underestimated. Future research towards the better definition of the term and recognition of its true prevalence, distribution and clinical significance is warranted.

Vasa. 1991;20(3):230-6.

Phlebosclerosis: disorder or disease?

Leu HJ, Vogt M, Pfrunder H, Odermatt BF.

Institute of Pathology, University of Zürich, Switzerland.

Abstract

Morphological examinations were performed in a total of 318 subjects (168 men and 150 women). Electron microscopic and immunohistological examinations were added in selected cases. Phlebosclerosis is a fibrotic degeneration of the venous wall that is regularly found in non-varicose veins of aged persons. Although its incidence is age-related, no correlation exists between degree and age. Marked degrees may occasionally occur already below the age of twenty. Both sexes and all the superficial leg veins (various levels of the long saphenous vein and minor venous branches) are likewise affected. The intima of the superficial leg veins is predominately involved, but media and adventitia may also be affected. Although the morphological appearance is similar to that of arteriosclerosis, localization, progression and clinical consequences are different. Phlebosclerosis of superficial leg veins is a disorder of little direct clinical consequence, but may have an indirect influence on the wall contractility. In the deep leg veins, however, a distinct phlebosclerosis of the intimal layer may be responsible for the development of thrombosis. As a secondary alteration, phlebosclerosis may complicate varicose veins (fibrous degeneration of wall areas with tortuosity, ectasia and smooth muscle atrophy). These lesions may further impair the already deficient reflux function. However, phlebosclerosis is no prerequisite but a late sequel of varicosis.

As a secondary alteration, phlebosclerosis may complicate varicose veins (fibrous degeneration of wall areas with tortuosity, ectasia and smooth muscle atrophy). These lesions may further impair the already deficient reflux function. However, phlebosclerosis is no prerequisite but a late sequel of varicosis.