Chronic Venous Insufficiency 

Chronic venous insufficiency (CVI) is a common condition affecting 2-5% of Americans. Historically, CVI was known as postphlebitic syndrome and postthrombotic syndrome, both of which refer to the etiology of most cases. However, these names have been abandoned because they fail to recognize another common cause of the disease, the congenital absence of venous valves.

In 1914, Homans postulated that the relative hypoxia of static venous blood decreases the amount of oxygen reaching the skin, causing skin changes and ulcers characteristic of CVI.^[1]

In 1930, Landis et al demonstrated the direct relationship between venous hypertension in the legs and increased capillary intraluminal pressures.

In 1953, Piulacks et al theorized that arteriovenous fistulas in the skin of the lower extremities cause hypoxia, resulting in changes to the skin and tissues.^[2]

In 1982, Burnand et al presented the fibrin cuff hypothesis, which describes the primary problem as venous hypertension in the lower extremities causing leakage of plasma proteins, particularly fibrinogen.^[3] A fibrin cuff encircles affected capillaries, decreasing oxygen diffusion to surrounding tissues.

In 1988, Coleridge-Smith et al described the white-cell trapping theory, which hypothesizes that venous hypertension and resultant increased capillary pressures trap white blood cells in the capillaries, where they become activated and damage capillary beds.^[4] Increased capillary permeability allows seepage of plasma proteins and fibrinogen into the interstitium, where a fibrin cuff forms, thus decreasing oxygen diffusion to surrounding tissues.

In addition to poor cosmesis, CVI can lead to chronic life-threatening infections of the lower extremities. Pain, especially after ambulating, is a hallmark of the disease. CVI causes characteristic changes, called lipodermatosclerosis, to the skin of the lower extremities, which lead to eventual skin ulceration.^[5]

Frequency

CVI is a significant public health problem in the United States. Of all Americans, estimates indicate that 2-5% have some changes associated with CVI.

Approximately 24 million Americans have varicose veins. Approximately 6 million Americans have skin changes associated with CVI. Venous stasis ulcers affect approximately 500,000 people.

The mean incidence for hospital admission for CVI is 92 per 100,000 admissions.

Epidemiology:

Peak incidence occurs in women aged 40-49 years and in men aged 70-79 years.

Congenital absence of or damage to venous valves in the superficial and communicating systems can cause CVI. Venous incompetence due to thrombi and formation of thrombi favored by the Virchow triad (venous stasis, hypercoagulability, endothelial trauma^[6] ) also can cause CVI, as depicted in the image below. Varicose veins rarely are associated with the development of CVI.

Risk factors associated with chronic venous insufficiency

• Age: Incidence of CVI rises substantially with age.
• Family history: History of deep vein thrombosis (DVT), which renders venous valves incompetent, causing backflow and increased venous pressure, is a risk factor.
• Lifestyle: A sedentary lifestyle minimizes the pump action of calf muscles on venous return, causing higher venous pressure. CVI occurs more frequently in women who are obese. Vocations that involve standing for long periods predispose individuals to increased venous pressure in dependent lower extremities. A higher incidence of CVI is observed in men who smoke.

Two major mechanisms in the body prevent venous hypertension. First, bicuspid valves in the veins prevent backflow and venous pooling. DVTs commonly occur at these valves, causing irreversible damage to the valve. Second, during normal ambulation, calf muscles decrease venous pressures by approximately 70% in the lower extremities. With rest, pressures return to normal in approximately 30 seconds. In diseased veins, ambulation decreases venous pressures by only 20%. When ambulation is stopped, pressure in the vein lumen increases slowly, returning to normal over a period of minutes, as depicted in the image below.

Venous hypertension in diseased veins is thought to cause CVI by the following sequence of events. Increased venous pressure transcends the venules to the capillaries, impeding flow. Low-flow states within the capillaries cause leukocyte trapping. Trapped leukocytes release proteolytic enzymes and oxygen free radicals, which damage capillary basement membranes. Plasma proteins, such as fibrinogen, leak into the surrounding tissues, forming a fibrin cuff. Interstitial fibrin and resultant edema decrease oxygen delivery to the tissues, resulting in local hypoxia. Inflammation and tissue loss result.

Clinical manifestations include the following:^[7]

• Varicose veins: In addition to poor cosmesis, varicose veins serve as indicators of venous hypertension, the most common reason for patient complaints regarding CVI, as depicted in the image below.^[8] Picture of venous valve: Thrombosis can begin as blood flow becomes turbulent, permitting platelets to remain in the valve sinus. This forms the nidus of a thrombus.
• Leg discomfort: Venous hypertension in muscles and fascial compartments of the lower leg from exercise and prolonged standing results in the characteristic ache of CVI. The discomfort is described as pain, pressure, burning, itching, dull ache, or heaviness in affected calves or legs.
• Nonhealing ulcers: Typically, these lesions occur around the medial malleolus, where venous pressure is maximal due to the presence of large perforating veins, as depicted in the image below.^[5] Hemodynamic charting of (a) healthy patients, (b) patients with only varicose veins, (c) patients with incompetent perforator veins, and (d) patients with deep and perforator incompetence.
• Leg edema: Damage done to capillary basement membranes by white blood cells results in leg edema.
• Lipodermatosclerosis: These characteristic skin changes in the lower extremities include capillary proliferation, fat necrosis, and fibrosis of skin and subcutaneous tissues. Skin becomes reddish or brown because of the deposition of hemosiderin from red blood cells, as depicted in the image below.^[9] Perforator vein bulging into subcutaneous tissue.

Surgical treatment is reserved for those with discomfort or ulcers refractory to medical management.

Indications for vein ligation: This technique is reserved for cases of CVI that include reflux in the saphenous system causing severe symptoms.^[10] For this reason, a diagnosis of reflux must be established preoperatively, usually with photoplethysmography or duplex imaging.

The venous network in the lower extremities commonly affected by CVI is divided into 3 systems. The first is superficial veins, which include the lesser and greater saphenous veins and their tributaries, as depicted in the 1st image below. The second is deep veins, which include the anterior tibial, posterior tibial, peroneal, popliteal, deep femoral, superficial femoral, and iliac veins. The third is perforating or communicating veins, as depicted in the 2nd and 3rd image below.

In patients with symptomatic greater saphenous varicosities, the presence of an occluded deep system must be ruled out. Deep occlusion is an absolute contraindication to vein ligation. Obtaining venographic studies of the deep venous system prior to superficial vein ligation is imperative.