Venous Insufficiency Clinical Presentation

Updated: Sep 25, 2020
  • Author: Robert Weiss, MD; Chief Editor: William D James, MD  more...
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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, whereas almost 50% complain of episodic symptoms.

In addition to poor cosmesis, varicose veins serve as indicators of venous hypertension, the most common reason for patient complaints regarding chronic venous insufficiency (CVI). [15] 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.

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 the severity of the pain.

Patients with deep system insufficiency are nearly always symptomatic. Leg aching, heaviness, and soreness are the most common subjective symptoms.

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 venous insufficiency is the opposite of that of the pain caused by arterial insufficiency. The pain of arterial insufficiency usually is worse with walking and worse when the legs are elevated. Cold tends to aggravate the symptoms of arterial insufficiency, 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.

Nonhealing ulcers are often noted around the medial malleolus, where venous pressure is maximal because of the presence of large perforating veins. [1] Leg edema, resulting from damage done to capillary basement membranes by white blood cells (WBCs), may be reported.

The characteristic skin changes of lipodermatosclerosis 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. [16]


Physical Examination

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

Swelling may result from acute venous obstruction (as in deep venous thrombosis [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 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 as a result of severe venous hypertension (a so-called venolymphatic syndrome).

Darkened, discolored, and stained skin may be a sign of venous stasis, arterial insufficiency, chronic infection, prior injury, or various other conditions (see the image below). Such discoloration is particularly likely to be a sign of chronic venous stasis 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 great saphenous vein (GSV) and all the attached perforating veins.

Superficial venous insufficiency with skin changes Superficial venous insufficiency with skin changes.

Normal veins are visibly distended at the foot and ankle and, occasionally, in the popliteal fossa; they usually are 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 (see the image below).

Perforator vein bulging into subcutaneous tissue. Perforator vein bulging into subcutaneous tissue.

Nonhealing ulcerations may be due to deep or superficial venous insufficiency (see the images below); other causes include arterial insufficiency, rheumatologic disorders, local trophic effects, unrecognized cancer, and various more exotic conditions. 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.

Ulcer due to venous insufficiency. Ulcer due to venous insufficiency.
Chronic venous stasis ulcer. Chronic venous stasis ulcer.
Venous stasis ulcer and surrounding dystrophic tis Venous stasis ulcer and surrounding dystrophic tissue.

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.

The visual appearance of the lower extremities is a useful but not always reliable guide to the peripheral venous condition. [17] Clinical findings in venous disease are also common to many other entities that affect the lower extremities. [18] 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.

Trendelenburg test

The Trendelenburg test is a traditional part of the physical examination that may help in distinguishing distal venous congestion caused by superficial venous reflux from that caused by incompetence of the valves in the deep venous system.

To perform this test, elevate the patient’s leg until all of the congested superficial veins collapse. Apply direct pressure to occlude the superficial veins below the point of suspected reflux from the deep system into the superficial varicosity. Most often, the GSV is manually occluded just below the saphenofemoral junction at the groin.

With the occlusion still in place, have the patient stand. If the distal varicosity remains empty or fills slowly, quickly remove the occluding hand or tourniquet. If the slow filling observed with occlusion is followed by rapid filling after the occlusion is removed, the principal high-pressure entry point into the superficial system is correctly identified.

Immediate refilling of the varicosity despite manual occlusion indicates that the principal entry point has not yet been identified or that more than 1 reflux pathway is involved. Extremely rapid refilling despite occlusion of the superficial reflux pathways suggests that the valves in the deep veins may be incompetent between the groin and the level at which the reflux escapes the deep system. The result is rapid filling of the superficial system.

If deep venous insufficiency is confirmed with results from further evaluations, the treatment options for the patient may be severely limited.



The local tissue sequelae of venous insufficiency are due to a combination of high venous pressures and reduced clearance of cellular metabolites from the lower extremity. Complications of untreated venous insufficiency include the following:

  • Recruitment of veins – High venous pressures may cause the recruitment of adjacent normal veins into refluxing circuits

  • DVT

  • Pulmonary embolism (PE)

  • Venous ulceration

  • Secondary lymphedema

Chronic pain, swelling, recurrent cellulitis, and chronic nonhealing leg ulcers (ulcer cruris) are the most common sequelae of venous insufficiency, but they are not the most severe.