Section 1 Epidemiology and aetiology
Restrictions in healthcare spending have led to a reduction in NHS treatment of VV, despite evidence that it may improve quality of life.2
The lower limb venous system consists of deep and superficial veins. The principal superficial veins, the long saphenous vein (LSV) and short saphenous vein (SSV), drain into deep veins at the saphenofemoral junction (SFJ) and saphenopopliteal junction (SPJ) respectively.
Additional perforating veins in the thigh and calf allow further communication between these systems. Unidirectional venous flow is maintained by the presence of venous valves and the calf muscle pump provided by the contraction of calf muscles.
Failure of valves within superficial veins or at the junction with deep veins can lead to reversed blood flow in veins (reflux or incompetence) and result in skin changes associated with chronic venous insufficiency (CVI).
The causes of venous incompetence are multifactorial,3,4 but most are due to failure of valves, due to degenerative or developmental weakness. Secondary VV can arise following DVT.
The Clinical impact, Etiology, Anatomy and Pathology (CEAP) classification system (table 1) allows objective stratification of patients with lower limb venous disease, which can be used to guide treatment.5
|Table 1: CEAP classification for lower limb venous disease5|
|No visible or palpable signs of venous disease
Telangiectasia or reticular veins
Changes in skin and subcutaneous tissue
Pigmentation or eczema
Lipodermatosclerosis or atrophie blanche
Healed venous ulcer
Active venous ulcer
No venous cause identified
No venous location identified
Reflux and obstruction
No venous pathophysiology identified
Section 2 Making the diagnosis
Patients with VV can be divided into 'uncomplicated' and 'complicated' groups.1 In uncomplicated patients, a functioning calf pump mechanism compensates for refluxing veins, allowing maintenance of normal ambulatory venous pressures (AVP).
This is absent in complicated patients, leading to high AVPs with consequential skin change.1
Uncomplicated varicose veins
Uncomplicated VV patients may present with cosmetic concerns, pain, heaviness, throbbing or cramps. Little concordance exists between symptoms and the presence and severity of VV.
Patients may have concerns that developing VV increases their risk of DVT or venous ulceration, and can be reassured that the presence of VV alone rarely leads to such complications.
Complicated varicose veins
Once AVPs become elevated, patients may develop CVI, with resultant skin changes (see table 2). These often appear in the gaiter area around the medial malleolus. All patients with complications should be investigated for VV and referred to a vascular surgeon for consideration of intervention.6
History-taking includes previous DVT, lower limb and pelvic trauma and malignancies, and any previous VV treatment.
Examination of the legs with the patient standing will determine distribution and sequelae VV.
If peripheral pulses are absent, an ankle brachial index pressure (ABPI) should be obtained.
Duplex ultrasound is the gold standard modality for evaluation of venous incompetence.
In addition to its non-invasive nature, its advantages include assessment of the deep system, accurate mapping of all refluxing veins and sites of reflux, determination of duplex systems, large tributaries and perforators (causes of possible recurrence), and determination of tortuosity, proximity to skin and diameter of veins which implicate options for endovenous ablation (EVA).
Section 3 Managing the condition
Wide regional variations exist in the management of VV across the UK, in part due to an inability to identify those patients who will benefit most from treatment, and there is at present no established NHS framework for the diagnosis and management of the condition.6
In addition to technical aspects, successful treatment depends on excellent communication and management of patients' expectations.
Asymptomatic patients should be reassured regarding misconceptions surrounding future deterioration, DVT or ulceration.
Patients presenting with cosmetic concerns about their veins are a more difficult group to manage in the NHS, and may be treated in the private sector. Weight loss and moderate exercise can improve symptoms in some patients.
Graduated compression hosiery (GCH) opposes the hydrostatic forces of venous hypertension and may provide symptomatic relief and prevent skin deterioration.
This is the treatment of choice in pregnancy, or in patients where intervention is inappropriate, but should not be used as a primary treatment, because evidence for its efficacy in improving patients' symptoms and quality of life is weak.6
In uncomplicated patients, class 1 GCH may be adequate, but class 2-3 is required for those who have complications.7
Most patients will only require below-knee stockings, which may improve compliance.
Patients with venous ulcers are typically treated with four-layer compression bandaging to achieve ulcer healing, before any contemplated intervention.8
Surgery for LSV VV typically involves ligation of the SFJ ('high tie'), stripping of the LSV to below the knee and multiple stab avulsions.
Treatment is similar for the SSV, but without stripping, because of its close proximity to the sural nerve.
Subfascial endoscopic perforator surgery allows ligation of incompetent perforators,9 but its effect on recurrence rates is unproven.
EVA is now the primary treatment. This involves passing a catheter into the vein, with various methods used to damage the vein wall, causing fibrotic occlusion.
Thermoablative (laser, radiofrequency), mechanochemical (Clarivein) or sclerotherapy (liquid, foam) techniques can all be used.10-12 These are comparable to surgery for primary failure and recurrence, but are associated with less haematoma, infection and pain, with quicker return to normal activities.13,14
NICE guidelines suggest referral to the vascular service if patients have any of the following:
- Bleeding VV
- Symptomatic primary or recurrent VV
- Skin changes thought to be caused by chronic venous insufficiency
- Superficial vein thrombosis and suspected venous incompetence
- Venous leg ulcer
- Healed venous leg ulcer
Section 4 Prognosis and follow-up
There is good evidence that quality of life is improved in patients with uncomplicated and complicated VV following surgery.2,15
Patients are usually offered outpatient follow-up, and a postoperative duplex following EVA, to ensure adequate occlusion of veins.
VV recurrence following surgery has been reported at 20-60% and may be due to inaccurate initial diagnosis or surgery, disease progression, altered venous dynamics or neovascularisation.16,17
Although it has been estimated that only 3-6% of patients with untreated VV go on to develop ulceration, there is a lack of evidence regarding the progression of VV from stage C2 or C3 to more serious stages.6
Section 5 Case study
A previously fit and well 34-year-old female hairdresser presented to her GP with left leg VV.
They had been present since the birth of her first child 10 years ago and were associated with dull aching pain, particularly at the end of the day and around the time of her menstrual period.
On examination, VV were found in the LSV distribution, with a patch of dry, itchy skin around the left medial malleolus.
The GP offered the patient a referral to the vascular outpatient clinic for further evaluation and consideration of intervention. However, she declined as she did not want to take any time off work. She was therefore fitted with a class 2, below-knee, graduated compression stocking.
She wore this daily, with good symptomatic relief.
She presented 12 years later with a small ulcer at the site of the previous venous eczema. There was now haemosiderin deposition, with associated lipodermatosclerosis.
The patient was referred to the vascular clinic, where a venous duplex demonstrated a patent and competent deep system, with an incompetent left SFJ and LSV, associated with grossly dilated incompetent calf varicose veins.
She had easily palpable foot pulses and an ABPI of one, and was therefore put into four-layer compression bandaging.
This was changed on a weekly basis by the district nurses and after four months, her ulcer had healed and she was offered surgery to treat her incompetent superficial veins.
Her previous venous duplex demonstrated a markedly tortuous and large LSV, precluding endovenous intervention, and she therefore underwent open surgery, with a high tie, LSV strip and multiple stab avulsions.
Postoperatively, she had some minor residual veins, with bruising and numbness at the site of surgery, which she had been warned about beforehand. All of these settled down after several weeks and she continued to wear a compression stocking thereafter.
Section 6 Evidence base
- Barwell JR, Davies CE, Deacon J et al. Comparison of surgery and compression with compression alone in chronic venous ulceration (ESCHAR study): randomised controlled trial. Lancet 2004; 363(9424): 1854-9
This study demonstrated that ulcer healing time was not improved by venous surgery, but surgery did significantly reduce the rate of venous ulcer recurrence following healing.
- Biemans AA, Kockaert M, Akkersdijk GP et al. Comparing endovenous laser ablation, foam sclerotherapy, and conventional surgery for great saphenous varicose veins. J Vasc Surg 2013; 58(3): 727-34
An RCT of laser EVA, injection foam sclerotherapy and surgical high ligation and stripping. The study demonstrated EVA and surgery to be equally effective at obliterating the LSV (88.5% and 88.2% respectively), and superior to injection foam sclerotherapy (72.2%) at the 12-month venous duplex follow-up.
- Siribumrungwong B, Noorit P, Wilasrusmee C et al. A systematic review and meta-analysis of randomised controlled trials comparing endovenous ablation and surgical intervention in patients with varicose veins. Eur J Vasc Endovasc Surg 2012; 44(2): 214-23
This meta-analysis of 27 RCTs comparing EVA to surgery found EVA similar to surgery with respect to primary failure and recurrence, but significantly better regarding haematoma formation, wound infection, pain and return to normal activities.
- NICE. Varicose veins in the legs (CG168). July 2013 (updated January 2014). http://guidance.nice.org.uk/CG168
- SIGN. Management of chronic venous leg ulcers (SG120). September 2013. www.sign.ac.uk/
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2. Sam RC, Darvall KA, Adam DJ et al. A comparison of the changes in generic quality of life after superficial venous surgery with those after laparoscopic cholecystectomy. J Vasc Surg 2006; 44: 606-10.
3. Raffetto JD, Eberhardt RT. Chronic venous disorders: general considerations. In: Cronenwett JL (ed). Rutherford's Vascular Surgery. Maryland Heights, WB Saunders, 2010.
4. Sharma AK, Drumsta D, Lee AE. Duplex ultrasonography in the management of varicose veins. Ultrasound Clinics 2013; 8: 227-35.
5. Eklof B, Rutherford RB, Bergan JJ et al. Revision of the CEAP classification for chronic venous disorders: consensus statement. J Vasc Surg 2004; 40(6): 1248-52.
6. NICE. Varicose veins in the legs (CG168). July 2013 (updated January 2014). http://guidance.nice.org.uk/CG168
7. Lattimer CR, Kalodiki E, Kafeza M et al. Quantifying the degree graduated elastic compression stockings enhance venous emptying. Eur J Vasc Endovasc Surg 2014; 47(1): 75-80.
8. Barwell JR, Davies CE, Deacon J et al. Comparison of surgery and compression with compression alone in chronic venous ulceration (ESCHAR study): randomised controlled trial. Lancet 2004; 363(9424): 1854-9.
9. Gloviczki P, Bergan JJ, Menawat SS et al. Safety, feasibility, and early efficacy of subfascial endoscopic perforator surgery: a preliminary report from the North American registry. J Vasc Surg 1997; 25(1): 94-105.
10. McCoppin HH, Hovenic WW, Wheeland RG. Laser treatment of superficial leg veins: a review. Dermatol Surg 2011; 37(6): 729-41.
11. Merchant RF, Pichot O. Long-term outcomes of endovenous radiofrequency obliteration of saphenous reflux as a treatment for superficial venous insufficiency. J Vasc Surg 2005; 42(3): 502-9.
12. Bishawi M, Bernstein R, Boter M et al. Mechanochemical ablation in patients with chronic venous disease: a prospective multicenter report. Phlebology 2013 (Epub ahead of print).
13. Siribumrungwong B, Noorit P, Wilasrusmee C et al. A systematic review and meta-analysis of randomised controlled trials comparing endovenous ablation and surgical intervention in patients with varicose veins. Eur J Vasc Endovasc Surg 2012; 44(2): 214-23.
14. Biemans AA, Kockaert M, Akkersdijk GP et al. Comparing endovenous laser ablation, foam sclerotherapy, and conventional surgery for great saphenous varicose veins. J Vasc Surg 2013; 58(3): 727-34.
15. Jull A, Parag V, Walker N et al. Responsiveness of generic and disease-specific health-related quality of life instruments to venous ulcer healing. Wound Repair Regen 2010; 18(1): 26-30.
16. Gad MA, Saber A, Hokkam EN. Assessment of causes and patterns of recurrent varicose veins after surgery. N Am J Med Sci 2012; 4(1): 45-8.
17. Caggiati A, Bergan J, Gloviczki P et al. Nomenclature of the veins of the lower limb: extensions, refinements, and clinical application. J Vasc Surg 2005; 41(4): 719-24.
- By Mr Abe Chandra, vascular registrar, and Mr Joe Dawson, vascular surgeon, department of vascular surgery, University of Adelaide Discipline of Surgery, The Queen Elizabeth Hospital, Adelaide, South Australia.