What to do When Varicose Veins Rupture?

Jerry Chen, MD, FRCSC
Assistant Professor,
Vancouver General Hospital,
University of British Columbia,
Vancouver, BC.

Introduction
Varicose veins are a common condition involving the lower extremity superficial venous system. It is estimated that 10 to 20% of the population has varicose veins with the incidence being higher in women. This is thought to be due to the effects of progesterone, which inhibits smooth muscle contraction and allows dilatation of the subcutaneous veins. Men are not immune to this condition, however, constituting approximately 30% of the patients. In the majority of patients, these veins are benign and do not warrant therapy. Treatment is required for varicose veins only when they cause symptoms or when complications arise.

Occasionally, varicose veins may be complicated by manifestations of chronic venous insufficiency such as leg swelling, skin discolouration, eczema, induration, venous ulcers and varicose vein rupture. Although varicose vein rupture and bleeding is an uncommon manifestation of varicose veins, massive bleeding and even fatal cases have been reported.

Pathophysiology
To understand the mechanism of varicose vein formation and venous rupture, one must first understand the venous physiology of the leg. The role of leg veins is, of course, to return the blood from the leg back to the heart. The mechanism for venous return in the leg is dependent on several factors, the relative importance of which varies with a change in body position. In the supine position, blood flows passively to the heart down a pressure gradient. The system is low-pressured and venous return is influenced by fluctuations in right atrial pressure, as well as changes in intra-abdominal pressure in relation to breathing. The varicosities are unlikely to rupture in this position.

In the upright position, the two vital factors for normal venous return are calf muscle contractions and competent venous valves. Gravity, in the form of hydrostatic pressure, is the major impeding force against venous return in this position. Periodically, calf muscles must contract and overcome this hydrostatic pressure in order to force blood back to the heart. Normally, blood flows from the superficial veins, through communicating veins to the deep veins and then back to the heart. The valves within these veins govern the direction of blood flow. These valves ensure the forward flow of blood by preventing reflux of blood during the relaxation phase of the calf muscles.

The major cause of varicose veins and chronic venous insufficiency is the failure of these valves with resulting reflux. When a valve develops reflux, the blood flows backward away from the heart and into the superficial system causing venous congestion and high pressures within the superficial veins. The venous hypertension caused by reflux is detrimental not only to the veins but also to the skin and subcutaneous tissue. The high venous pressure impedes the cutaneous microcirculation and this results in tissue hardening, atrophy and eventually ulceration. Varicose vein rupture is a manifestation of this process of tissue damage; as the overlying skin and subcutaneous tissue are eroded away the vein becomes exposed. The vein wall is weakened, making it susceptible to rupture with minor trauma. In fact, the high internal venous pressures may even force the exposed vein to rupture spontaneously.

Clinical Features
Patients who are at risk of varicose vein rupture usually describe diffuse aching pain in their lower leg varicose veins, which is aggravated by prolonged standing or sitting. Leg edema, night cramps and chronic itching from stasis dermatitis are common. Dermatological manifestations of venous insufficiency are associated with the highest risk for varicose vein rupture. In some patients,