Venous Insufficiency Clinical Presentation

Patients with venous insufficiency often report subjective symptoms that are typically bothersome early in the disease, become less severe in the middle phases, and then worsen again with advancing age.

• Even small telangiectasias are often symptomatic. More than one half of patients who present with telangiectasias smaller than 1 mm in diameter report symptoms that abate after treatment. Common symptoms include the following:

  • Burning
  • Swelling
  • Throbbing
  • Cramping
  • Aching
  • Heaviness
  • Restless legs
  • Leg fatigue
• Subjective complaints are also common in patients with truncal varices; 18% of patients with varicosities report frequent or continuous symptoms, while almost 50% complain of episodic symptoms.
• Patients with deep system insufficiency nearly always are symptomatic. Leg aching, heaviness, and soreness are the most common subjective symptoms.
• Episodic pain and other symptoms associated with superficial venous disease may be temporally related to hormonal changes, both physiologic and pharmacologic.
• One half of all pregnant women with varicose veins complain of pain, and 17% are unable to remain upright for more than 1-2 hours at a time because of its severity.
• Pain caused by venous insufficiency often is improved by walking or by elevating the legs.

  • Warmth tends to aggravate the symptoms of venous insufficiency, and cold tends to relieve them.
  • Compression stockings usually ameliorate or prevent the pain of venous insufficiency.
• In many ways, the behavior of the pain caused by arterial insufficiency is the opposite to the behavior of the pain caused by venous insufficiency.

  • The pain of arterial insufficiency usually is worse with walking and worse when the legs are elevated.
  • Cold tends to aggravate the symptoms, whereas warmth tends to relieve them.
  • Compression stockings usually aggravate the pain of arterial insufficiency.
• The pain of venous obstruction is worse with walking or warmth but better with elevation of the legs. Compression stockings usually improve the pain of venous obstruction.

The visual appearance of the lower extremities is a useful but not always reliable guide to the peripheral venous condition.^[4] Clinical findings in venous disease are also common to many other entities that affect the lower extremities. Physical examination alone is not a reliable means of assessing the venous system. Diagnostic testing nearly always is necessary to rule out deep venous obstruction, to assess the paths of reflux, and to guide treatment planning. The Trendelenburg test is traditionally part of the physical examination and may be helpful in making the differential diagnosis (see Procedures).

• Swelling may result from acute venous obstruction (as in DVT) or deep or superficial venous reflux. Alternatively, swelling may be completely unrelated to the venous system.

  • Lower-extremity pitting edema is common in patients with venous insufficiency.
  • Hepatic insufficiency, renal failure, cardiac decompensation, infection, trauma, and environmental effects can also cause lower-extremity pitting edema that may be indistinguishable from the edema due to venous obstruction or venous insufficiency.
  • Lymphatic edema may be a sign of primary lymphatic outflow obstruction, or it may be secondary to the overproduction of lymph due to severe venous hypertension (a so-called venolymphatic syndrome).
• Skin discoloration may be a sign of venous stasis, arterial insufficiency, chronic infection, prior injury, or a host of other conditions (see the image below). Superficial venous insufficiency with skin changes.
• Nonhealing ulcerations (see the image below) may be due to deep or superficial venous insufficiency. Other causes include arterial insufficiency, rheumatologic disorders, local trophic effects, unrecognized cancer, or other more exotic causes. Ulcer due to venous insufficiency.
• The most common physical signs of venous insufficiency are those attributed to the progressive syndromes of chronic venous stasis and chronic venous hypertension. These signs include the following:

  • Edema
  • Hyperpigmentation
  • Venous dermatitis
  • Chronic cellulitis
  • Cutaneous infarction (atrophie blanche)
  • Ulceration
• A long-standing venous ulcer rarely converts to a basal cell carcinoma or squamous cell carcinoma. The venous ulcer may develop collision lesions (eg, basal cell carcinoma and stasis ulceration) at the same site.
• Normal veins are visibly distended at the foot and ankle and, occasionally, in the popliteal fossa.

  • Normal veins are usually not visibly distended in the rest of the leg. Translucent skin may cause the normal veins to become visible in a bluish subdermal reticular pattern.
  • A dilated vein above the ankle is usually evidence of venous pathology.
• Darkened, discolored, and stained skin is often a sign of chronic venous stasis, particularly if it is localized along the medial part of the ankle or the medial aspect of the lower leg.

  • These areas are especially prone to venous hypertension because their drainage largely depends on the competence and patency of the entire length of the greater saphenous vein and all of the perforating veins attached to it.
  • Nonhealing ulcers on the medial part of the ankle are most likely due to underlying venous stasis.
• Skin changes or ulcerations that are localized to the lateral aspect of the ankle are more likely to be related to prior trauma or arterial insufficiency than to pure venous insufficiency.

The sequelae of venous insufficiency are caused by reflux through superficial or deep veins or by venous outflow obstruction. Most cases of venous insufficiency are related to reflux through the superficial veins.

• Superficial venous insufficiency is most often caused by the failure of a valve in the superficial venous system. Greater than 80% of varicose veins seen on the leg are caused by venous insufficiency or a leaky valve in the great saphenous vein, which terminates near the inguinal ligament as it joins the common femoral vein.

  • The initial valve failure may occur at any level between the groin and the ankle, but the saphenofemoral junction is the high point of reflux in most patients with severe superficial venous insufficiency.
  • Valve failure can be spontaneous in patients with congenitally weak valves.
  • Congenitally normal valves can fail due to direct trauma, thrombosis, hormonal changes, or chronic environmental insult (eg, prolonged standing).
• Deep venous insufficiency can be due to congenital valve or vessel abnormalities, but DVT is the most common cause of deep system valve injury.
• A less common cause of venous insufficiency is Klippel-Trenaunay-Weber (KTW) syndrome, which involves port-wine stains, varicose veins, and bony or soft-tissue hypertrophy. Patients with pure Klippel-Trenaunay syndrome have only venous involvement, whereas those with the Parkes Weber variant also have arteriovenous malformations.

  • Like those of other forms of venous insufficiency, the capillary hemangiomas (port-wine stains) of KTW syndrome can lead to local skin breakdown and ulceration, bleeding, and secondary infection. This can occur in any organ system of the body.
  • The KT, or sciatic vein, is a large superficial vessel that is present during fetal development, but it usually does not persist. In patients with KTW syndrome, this vein may be noticed at birth, or it may become apparent later in life. The vein extends along the posterolateral aspect of the leg from the foot to the gluteal region. When present, it is invariably a reflux pathway rather than a pathway for antegrade flow.
  • Patients with KTW syndrome may have atresia of the deep veins as well as many abnormal venous pathways involving the deep and superficial venous systems.
  • Surgical attempts to treat the abnormal refluxing veins in KTW syndrome are fraught with peril because postoperative worsening of venous abnormalities is common.
  • KTW syndrome can produce such severe venous insufficiency that the otherwise normal lymphatic system becomes overwhelmed by the amount of lymph production, which leads to secondary lymphedema.