Chronic Venous Insufficiency, Superficial Thrombophlebitis & Leg Ulcers
Where the ulcer sits, how the swelling pits, and when a tender cord needs anticoagulation
Chronic venous insufficiency: mechanism and findings
Mechanism. Walking normally empties the leg veins through the calf-muscle pump, and competent valves keep blood from falling back. When valves fail — from primary degeneration or damage after DVT — or the outflow is obstructed, venous pressure stays high during standing and walking (ambulatory venous hypertension). Capillaries leak fluid, red cells and fibrinogen, leukocytes are trapped and activated, and the resulting inflammation produces edema, pigment, fibrosis and eventually ulceration. Risk factors include older age, female sex, pregnancy, obesity, prolonged standing, prior DVT and family history.
Clinical findings.
- Edema and aching heaviness that worsen by evening and after standing and improve with elevation or overnight
- Varicose veins, spider and reticular veins
- Red-brown hemosiderin staining and itchy, scaly stasis dermatitis
- Lipodermatosclerosis: indurated, fibrotic skin that narrows the lower leg (the inverted champagne bottle)
- Atrophie blanche: white stellate scars; ulcers in the gaiter area above the medial malleolus
Bilateral red, scaly, itchy, non-tender legs in an afebrile patient are stasis dermatitis; true cellulitis is almost always unilateral, warm and tender.
Evaluation. Venous duplex ultrasound confirms reflux — retrograde flow longer than 0.5 s in superficial veins or 1 s in the femoral and popliteal veins — identifies obstruction, excludes DVT and maps veins for ablation. Severity is graded with the CEAP clinical classes: C1 spider or reticular veins, C2 varicose veins, C3 edema, C4 skin changes (pigmentation, eczema, lipodermatosclerosis, atrophie blanche), C5 healed ulcer and C6 active ulcer.
Managing venous disease and venous ulcers
- Conservative measuresLeg elevation above heart level, walking and calf exercises, weight loss.
- Measure the ABICompression over significant arterial disease can cause ischemic necrosis: avoid it if the ABI is below 0.5 and use reduced compression at 0.5–0.8.
- CompressionGraduated stockings of 20–30 mmHg (up to 30–40 mmHg); multilayer compression bandaging for an open ulcer.
- Ulcer careMoist dressings, debridement, pentoxifylline as an adjunct; antibiotics only for clinical infection.
- Treat the refluxEndovenous thermal ablation (radiofrequency or laser) for symptomatic saphenous reflux; foam sclerotherapy for tributaries and spider veins; phlebectomy for bulky varicosities.
Ablation. Endothermal ablation has largely replaced ligation and stripping. Early ablation of superficial reflux speeds healing of venous ulcers and lowers their recurrence. A follow-up duplex looks for thrombus extending from the treated vein into the deep system (heat-induced thrombosis).
A chronic leg ulcer that will not heal or develops heaped, rolled edges needs a biopsy to exclude squamous cell carcinoma (Marjolin ulcer).
Telling leg ulcers apart
| Feature | Venous | Arterial | Neuropathic |
|---|---|---|---|
| Location | Gaiter area, above the medial malleolus | Toes, heel, lateral malleolus, pressure points | Plantar pressure points (metatarsal heads, heel) |
| Appearance | Shallow, irregular, exudative, red granulating base | Punched-out, pale or necrotic dry base | Deep, surrounded by callus |
| Pain | Moderate, eased by elevation | Severe, worse elevated, eased by dangling | Painless (sensory loss) |
| Surrounding leg | Edema, hemosiderin, dermatitis; pulses present | Shiny hairless skin, absent pulses, low ABI | Loss of monofilament sensation; pulses may be present |
| Key treatment | Multilayer compression, reflux ablation | Revascularization; no compression | Off-loading, glucose control; probe to bone for osteomyelitis |
Superficial thrombophlebitis
Presentation. A tender, warm, erythematous, palpable cord follows a superficial vein, most often a varicose great saphenous vein or an infusion site. Up to about a quarter of patients have a concurrent DVT, so venous duplex is the first test: it excludes DVT and measures the thrombus length and its distance from the saphenofemoral junction. Infusion-related phlebitis resolves after the catheter is removed; fever and pus at the site suggest suppurative thrombophlebitis, which needs antibiotics and sometimes excision of the vein.
Treatment by extent. A short thrombus (less than 5 cm) far from the junction is treated with warm compresses, NSAIDs, elevation and compression, with repeat duplex if symptoms progress. A thrombus ≥5 cm long warrants fondaparinux 2.5 mg subcutaneously daily for about 45 days, with prophylactic-dose LMWH as an alternative. A thrombus within 3 cm of the saphenofemoral junction is anticoagulated, and many clinicians treat it as a DVT with full therapeutic dosing.
When to look further. Recurrent migratory thrombophlebitis, especially at unusual sites such as the arms or chest or in nonvaricose veins, is Trousseau syndrome and should prompt a search for occult adenocarcinoma — pancreatic classically, also lung and stomach. Other causes of unprovoked or recurrent superficial thrombosis include inherited thrombophilia, Buerger disease in young smokers and Behçet disease.
Post-thrombotic syndrome and lymphedema
Post-thrombotic syndrome. In 20–50% of patients after DVT, usually within 2 years, valve damage and residual obstruction produce chronic pain, heaviness, swelling, venous claudication, skin changes and ulcers in the affected leg. Risk is highest after proximal (iliofemoral) DVT, with ipsilateral recurrence, and with subtherapeutic anticoagulation. Routine compression stockings do not prevent it, but compression and exercise relieve symptoms; the most reliable prevention is avoiding the first DVT and its recurrence.
Lymphedema. Protein-rich fluid accumulates when lymphatic drainage fails. Swelling pits early but becomes firm and nonpitting, involves the dorsum of the foot with squared toes, and brings peau d'orange skin and hyperkeratosis. A positive Stemmer sign — inability to pinch the skin at the base of the second toe — is characteristic. Secondary causes are lymph node dissection or radiation (arm lymphedema after breast cancer treatment), tumor obstruction, recurrent cellulitis and filariasis (Wuchereria bancrofti, the leading cause worldwide); primary forms include congenital Milroy disease. Treatment is complete decongestive therapy — manual lymphatic drainage, multilayer compression, exercise and meticulous skin care; diuretics do not mobilize protein-rich lymph.
Lipedema differs from both: symmetric fat deposition in the legs of women that spares the feet, does not pit and has a negative Stemmer sign.