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SU27.5-6 | Lower Limb Venous Disorders — SDL Guide (Part 2)
Principles of Management
Management follows the diagnosis. For varicose veins and chronic venous insufficiency, the foundation is conservative: leg elevation, exercise to engage the calf pump, weight loss, skin care, and graduated compression stockings (only after the ABPI has confirmed an adequate arterial supply). When symptoms persist or complications develop (skin changes, ulceration, bleeding, thrombophlebitis), the incompetent veins are treated by endovenous ablation (radiofrequency or laser, now the first-line interventions), ultrasound-guided foam sclerotherapy, or conventional surgery (sapheno-femoral junction ligation with stripping of the great saphenous vein and avulsion of varicosities). A venous ulcer is treated chiefly by graded compression bandaging (the mainstay, again after excluding arterial disease) with wound care, and by correcting the underlying superficial reflux. For deep vein thrombosis, the principle is prompt anticoagulation to prevent clot propagation and pulmonary embolism: a direct oral anticoagulant (DOAC), or low-molecular-weight heparin bridging to warfarin, is started, typically for at least three months (longer or indefinitely for unprovoked, recurrent or ongoing-risk thrombosis such as active cancer). An inferior vena cava (IVC) filter is reserved for patients in whom anticoagulation is contraindicated or who embolise despite it. Above all, prevention is paramount — early mobilisation, mechanical (graduated compression/intermittent pneumatic) and pharmacological (LMWH) thromboprophylaxis for surgical and immobile patients — because the cheapest treatment for a fatal PE is the DVT that never forms.
- Varicose veins: conservative (elevation, exercise, compression after ABPI); intervene with endovenous ablation (RFA/laser, first-line), foam sclerotherapy or surgery (SFJ ligation + stripping/avulsions).
- Venous ulcer: graded compression bandaging (after excluding arterial disease) + wound care + correct reflux.
- DVT: prompt anticoagulation (DOAC, or LMWH→warfarin) for ≥3 months (longer if unprovoked/recurrent/cancer); IVC filter if anticoagulation contraindicated.
- Prevention: early mobilisation + mechanical and pharmacological thromboprophylaxis in at-risk patients.
CLINICAL PEARL
Never apply compression to a leg before you have checked its arterial supply. Graduated compression stockings and compression bandaging are the mainstay of treating venous disease and venous ulcers — but if the leg is also arterially compromised, compression can cut off its remaining perfusion and precipitate ischaemic necrosis and gangrene. So measure the ABPI first: compression is safe with an adequate index, but is withheld or modified if significant arterial disease is present (and remember the ABPI can read falsely high in calcified diabetic vessels). Treating a mixed arterio-venous ulcer as if it were purely venous, with full compression, is a classic and dangerous error.
Check Your Understanding
Bring the threads together by reasoning back through the two patients in the hook. The 45-year-old shopkeeper with ropy medial-calf varicosities, evening aching, ankle pigmentation and a shallow medial-malleolar ulcer has chronic venous insufficiency from superficial valvular incompetence (great saphenous territory): she needs duplex mapping of the reflux, ABPI before any compression, then graded compression and ulcer care, with endovenous ablation of the incompetent vein to heal the ulcer and prevent recurrence. The 60-year-old post-operative, immobile, breathless man with a unilaterally swollen, warm, tender calf has a deep vein thrombosis with probable pulmonary embolism (Virchow's triad fully in play): he needs a Wells assessment, compression duplex (and investigation of the chest for PE), and prompt anticoagulation, while the whole episode is a reminder that thromboprophylaxis should have been in place. Use these to self-test the competencies this module covers. First, can you describe the applied venous anatomy — superficial versus deep systems, the sapheno-femoral and sapheno-popliteal junctions, perforators, valves and the calf pump? Second, can you explain the pathophysiology (valvular incompetence/reflux for varicose veins; Virchow's triad for DVT), the clinical features and the investigations (duplex, Wells + D-dimer, CEAP, ABPI)? Third, can you state the principles of management for both, including the absolute rule to exclude arterial disease before compression? The questions below check exactly these links.
SELF-CHECK
A patient with a swollen, tender calf is assessed with a Wells score and found to have LOW clinical probability of DVT. Which next step is most appropriate, and what drives clot formation in DVT?
A. Start lifelong warfarin immediately; clot forms from valvular reflux
B. Measure D-dimer — if negative, DVT is effectively excluded; clot forms via Virchow's triad (stasis, endothelial injury, hypercoagulability)
C. Apply tight compression bandaging at once; clot forms from arterial embolism
D. Perform venous stripping surgery; clot forms from lymphatic obstruction
Reveal Answer
Answer: B. Measure D-dimer — if negative, DVT is effectively excluded; clot forms via Virchow's triad (stasis, endothelial injury, hypercoagulability)
With a LOW Wells probability, a negative D-dimer effectively excludes DVT and avoids unnecessary imaging; a positive D-dimer (or a high Wells score) proceeds to compression duplex ultrasound. Deep vein thrombosis is driven by Virchow's triad — venous stasis, endothelial (vessel-wall) injury and hypercoagulability. Compression and venous stripping treat venous reflux, not acute DVT, and starting lifelong warfarin before confirming the diagnosis is inappropriate.