Chronic venous insufficiency involves an abnormality within the venous system of the lower extremities. Veins within the lower extremities contain one way valves that, in conjunction with muscular contractions, promote the flow of blood back to the heart. When the valves within these veins fail to function normally, blood refluxes back into the legs resulting in venous congestion and high venous pressures. Once chronic venous insufficiency manifests itself, it can be relentlessly progressive .
The lower extremity venous system is composed of a superficial and a deep venous system which are interconnected by numerous perforating veins. The deep venous system is encased in muscle and is a relatively high pressure system that returns approximately 90% of the blood from the legs. The superficial system is encased in a fibrous sheath and is a relatively low pressure system that returns approximately 10% of the blood from the legs. The primary components of the superficial venous system are the great saphenous veins (GSV) and the small saphenous vein (SSV). The primary components of the deep venous system include 3 paired veins below the knee: the posterior tibial veins, the anterior tibial veins, and the peroneal veins. They coalesce into the popliteal vein located behind the knee.The popliteal vein then continues cephalad into the thigh as the femoral vein. The majority of chronic venous insufficiency arises in the low pressure superficial venous system but it can also arise in the high pressure deep venous system or, less frequently, in both systems simultaneously.
Valve failure within the superficial venous system is most commonly an inherited tendency but it can also result from prolonged standing and sitting, pregnancy, injury, or recurrent phlebitis. Most cases of superficial vein valve failure occur when leakage develops between the high pressure deep system and the low pressure superficial system . The most common site for the valve failure to occur is the saphenofemoral junction which is where the GSV connects to the femoral vein. The high pressure that is transmitted from the femoral vein into the GSV leads to progressive valve failure throughout the length of the GSV and subsequent venous hypertension. The venous hypertension leads to visibly dilated and tortuous veins at the skin surface which are recognized as varicose veins. The venous hypertension also initiates an inflammatory reaction that can lead to changes in the overlying skin. Valve failure that occurs within the deep venous system is most commonly due to a DVT. The presence of the clot within the deep veins damages their valves which eventually leads to venous hypertension. Valve failure can also occur within the interconnecting perforating veins which allows the high pressure within the deep venous system to be transmitted up into the low pressure superficial venous system. This occurrence commonly manifests itself at the skin surface as a “blow-out” varicosity just above the ankle. Venous ulcers are commonly associated with an incompetent perforating vein.
Progressive valve failure results in congestion of blood within the venous system of the lower extremities. Venous hypertension is the eventual result. Venous hypertension is the root cause of the signs and symptoms that are associated with chronic venous insufficiency: leg swelling, pruritus, eczema, recurrent cellulitis, leg pain, restless leg syndrome, muscle cramps, phlebitis, skin discoloration, skin thickening, varicose veins, and venous ulceration. The pruritus, eczema, and recurrent cellulitis are due to a combination of venous hypertension and reduced clearance of cellular metabolites caused by the venous congestion. The edema associated with chronic venous insufficiency usually spares the feet and toes, worsens throughout the day, resolves overnight, and does not involve JVD. Leg pain is caused by abnormally dilated veins compressing nearby nerves. The leg pain is worse with prolonged sitting and standing (which dilate the incompetent veins) and it is improved with ambulation and leg elevation (which decompress the incompetent veins). Muscle cramps are, in fact, a compensatory mechanism. Incompetent leg veins cause a progressive pooling of blood within the legs which activate pressure sensors and muscle cramps are the body’s attempt to decompress the incompetent leg veins by forcing the blood in a cephalad direction. Phlebitis is an inflammatory condition within incompetent veins caused by the presence of congested blood and its associated sluggish flow.
Venous hypertension transmitted into the branches of the superficial venous system causes them to progressively dilate. It is those dilated branches that are recognized as varicose veins at the skin surface. Increased venous pressures can also exist within the deep venous system because of valvular damage caused by a DVT (post thrombotic syndrome) or by partial occlusion of an iliac vein by an overlying iliac artery in the pelvis which is a condition known as May-Thurner’s Syndrome. The partial occlusion typically occurs in the left leg and manifests itself as persistent left leg swelling. A stent can be placed in the partially occluded vein to relieve the outflow obstruction.
The vast majority of varicose veins arise from a valvular abnormality within a component of the superficial venous system (most commonly the great saphenous vein). The location of varicose veins on the leg can often reveal their underlying source. As a general rule, varicose veins along the medial extent of the leg arise from the GSV, varicose veins along the lateral extent of the leg arise from the anterior accessory vein, and varicose veins located in the posterior calf arise from the SSV. The underlying source of varicose veins must be addressed to effectively treat them. Simply removing the varicose veins at the skin surface will result in their eventual recurrence. A duplex ultrasound exam is used to identify the underlying source of the varicose veins. The most effective means to definitively treat varicose veins is to destroy their underlying source. One means of doing this is with endovenous laser ablation. Laser energy is used to destroy the target vein’s endothelium which leads to its fibrosis. The ablated vein is not removed, it is left in place to be reabsorbed by the body. The endovenous laser procedure is done using tumescent anesthesia and involves little to no downtime. The existing varicose veins at the skin surface are then removed thru micro incisions which are simply closed using steri strips. Patient’s wear a thigh high grade 2 compression hose for 1 week following the procedure and they are able to return to work within 1 to 2 days. The risk of varicose vein recurrence following endovenous laser ablation and micro-phlebectomy is less than 1%.
It is important to treat varicose veins because as many as 50% of patients with untreated varicose veins will develop superficial thrombophlebitis at some time. This is significant because unrecognized DVT is present in as many as 45% of patients with what appears to be purely superficial phlebitis. Approximately one half of patients with DVT have detectable pulmonary embolism and the death rate in this group exceeds 1 in 3. The risk of DVT is 3 times higher in patients with superficial varicosities than in the general population.
Venous ulcers represent the most severe manifestation of chronic venous insufficiency. They occur when venous hypertension within the lower extremity venous system rises to such a level that both capillary inflow and venous outflow are diminished. Nutrient levels fall while waste levels rise and the stage is set for the formation of a chronic wound. The high venous hypertension initiates an inflammatory reaction which causes the skin to thicken and discolor. The skin thickening is caused by the presence of chronic inflammation within the skin. The discoloration is caused by RBC’s being forced from the venous circulation by the continually increasing venous hypertension. Once outside of the circulation, the RBC’s die and their iron content is deposited in the skin. The discoloration initially takes on an erythematous color but, with time, the discoloration becomes dark brown. The skin thickening is termed lipodermatosclerosis and the skin discoloration is termed hemosiderin staining.
Venous ulcerations are the most common chronic wound to involve the lower extremities. The ulcers are usually located just above the ankle. As a general rule, venous ulcers above the medial ankle are associated with an incompetent GSV and venous ulcers above the lateral ankle are associated with an incompetent SSV. Most venous ulcers are also associated with an incompetent perforating vein at the ulcer’s base. The goal of venous ulcer treatment is to decrease the venous hypertension to the extent that capillary inflow can resume bringing nutrient rich blood into the site and effective venous outflow can resume transporting waste products away from the site. The most effective way to heal a venous ulcer and decrease its potential recurrence is to treat the underlying venous hypertension. Once the venous hypertension is decreased beyond a threshold level, healing of the venous ulcer can begin. A duplex ultrasound exam is used to identify the underlying source of the venous ulceration. The source within the superficial system and or perforating system is then ablated using an endovenous laser and any associated varicose veins are removed by microphlebectomy. Ultrasound guided foam sclerotherapy is used to destroy any smaller abnormal veins that are directly associated with the ulcer. Venous ulcerations typically heal within 2 to 3 months once the venous hypertension is controlled. Patients are kept in compression hose until the venous ulcer is fully healed.
Compression hose alone can heal a venous ulcer. The hose work by speeding the flow of blood out of the legs which decreases the venous hypertension and improves the microcirculatory environment beneath the venous ulcer. High levels of compression are required to adequately decrease the venous hypertension and patient compliance with wearing compression hose is always problematic. There are numerous options for venous ulcer dressings. None have been shown to work better than the other with respect to wound healing. Cost and ease of use for the patient are the best criteria when choosing a dressing for a venous ulcer.
Venous ulcerations may also occur because of venous hypertension within the deep venous system. T he vast majority of venous ulcers are caused by venous reflux that is purely or largely confined to the superficial venous system. Only a minority (<10%) are caused by valvular insufficiency that involves the deep venous system alone . This situation is most commonly caused by recurrent DVT’s . Endovenous laser ablation is not an option to treat incompetent deep veins. Aggressive compression therapy is the treatment of choice when an abnormality within the deep venous system of the lower leg is the primary cause of a venous ulceration. If venous outflow obstruction is the source of the venous hypertension, a deep vein stent may be helpful.
Venous ulcers are generally differentiated from arterial ulcers by their heavy exudate, irregular borders, and their prominent association with hemosiderin staining and lipodermatosclerosis. The symptoms of venous insufficiency are differentiated from arterial symptoms by their improvement with ambulation, leg elevation, and use of compression hose. An important exception to this generality is the symptom of leg pain associated with venous obstruction. In the case of leg pain caused by venous outflow obstruction, the leg pain increases with ambulation just like the pain from arterial obstruction. However, the leg pain from venous outflow obstruction is often improved by wearing compression hose while the leg pain from arterial obstruction is worsened by it. The edema associated with chronic venous insufficiency is differentiated from that associated with lymphedema by its sparing the toes and by its resolution overnight. Edema caused by chronic venous insuficiency is pitting while that associated with lymphedema is not. There is a condition called phlebolymphedema (secondary lymphedema) that involves both chronic venous insufficiency and lymphedema coexisting together. The edema associated with chronic venous insufficiency overloads the lymphatics which results in the formation of lymphedema. Patients with phlebolymphedema have clinical findings that are a combination of both chronic venous insufficiency and lymphedema (hemosiderin staining, lipodermatosclerosis, and persistent edema that involves the entire foot). The edema may be associated with recurrent bouts of cellulitis and lymphangitis. In these cases, treating the underlying cause of the chronic venous insufficiency with endovenous laser ablation will often improve the associated lymphedema.
Compression therapy is the most conservative option for the management of chronic venous insufficiency. Graduated compression hose work by increasing the flow of blood out of the legs, clearing out the venous congestion, reducing the venous hypertension, and improving symptoms. The compression is greatest at the ankle and progressively decreases as it ascends the leg. A hose with 20 to 30 mm Hg compression is usually well tolerated by the patient but a 30 to 40 mm Hg compression hose may be necessary in cases that involve venous ulcerations. The problem with compression hose is that the level of compliance needed for them to be effective is often difficult for patients to be compliant with, especially during the heat of a Mississippi summer. Also, getting the compression hose on can be very difficult for the elderly and those with significant arthritis. Other conservative options include exercise, weight loss, and leg elevation. Strengthening the calf muscle is particularly important since it is the primary muscle pump responsible for propelling blood up and out of the lower extremities.
The prevalence of venous insufficiency increases with age. Peak incidence occurs in women aged 40-49 years and in men aged 70-79 years. A history of DVT, which renders venous valves incompetent and increases venous pressures within the deep venous system, is also a risk factor. A sedentary lifestyle minimizes the pump action of the calf muscle on venous return which leads to higher venous pressures. CVI occurs more frequently in those who are obese. Vocations that involve standing for long periods of time predispose individuals to increased venous pressure in dependent lower extremities. A higher incidence of CVI is observed in patients who smoke. Pregnancy is an important causative factor in the development of peripheral venous insufficiency. CVI is a significant public health problem in the United States. It has been estimated that 2-5% of all Americans have some changes associated with CVI. Published estimates of the prevalence of varicosities range from 7% to 60% in the adult population, with most studies demonstrating clinical varicose reflux in about 40% of the adult population. Venous stasis ulcers affect approximately 500,000 Americans per year.
Chronic venous insufficiency is a serious problem for a large number of Americans. It is a relentlessly progressive disease that, if left unchecked, can result in severe morbidity and even death. Treating the underlying source of venous hypertension is the key to an effective and long lasting treatment.