Deep Venous Insufficiency


Deep Venous Insufficiency (DVI) is a chronic disease that can result in significant morbidity. It is commonly caused by either deep vein thrombosis (DVT) or valvular insufficiency, and together with varicose veins it is part of chronic venous insufficiency.

Prevalence of DVI is poorly reported, with estimates ranging from 10-15%, and is more common in women.

Causes can be divided into:

  • Primary, whereby there is an underlying defect to the vein wall or valvular component
    • Includes congenital defects and connective tissue disorders
  • Secondary, whereby defects occur secondary to damage
    • including post-thrombotic disease, post-phlebitic disease, venous outflow obstruction, and trauma

Deep Venous Insufficiency occurs as a result of a failure of the venous system, characterised by valvular reflux, venous hypertension and obstruction*.

*The pathophysiology is similar to that of varicose veins but it affects the deep venous system, instead of superficial veins.

Risk Factors

Risk factors for DVI include increasing age, female gender, pregnancy, previous DVT or phlebitis, obesity, and smoking.

Those in jobs which involve long periods of standing or with a strong family history of venous disease are also at risk.

Clinical Features

Patients may report chronically swollen lower limbs, which can become aching, pruritic, and painful.

On examination, several signs can indicate underlying DVI, including varicose eczema (dry and scaly skin), thrombophlebitis, haemosiderin skin staining, lipodermatosclerosis*, or atrophie blanche**

Patients will have varying degree of dependent pedal oedema and may also have venous ulcers, which are typically found over the medial malleolus.

Figure 1 – (A) Haemosiderin deposition with lipodermatosclerosis (B) Pitting oedema with varicose eczema

Patients who have had a prior DVT may present with symptoms of Post Thrombotic Syndrome, including heaviness, cramps, pain, pruritic, and paraesthesia, and signs of pretibial oedema, skin induration, hyperpigmentation, venous ectasia, redness, and ulceration. In order to monitor the degree of post thrombotic syndrome, the Villalta scale which can be used to assess progression with treatment.

*A tapering of legs above ankles, an “inverted champagne bottle” appearance **Localised round, white atrophic regions surrounded by dilated capillaries


A standardised reporting method for the clinical manifestations of varicose veins has been described by the CEAP Classification

Clinical Features

C0 – No visible or palpable signs of venous disease
C1 – Telangiectasia or reticular veins
C2 – Varicose veins
C3 – Oedema
C4a – Pigmentation or eczema
C4b – Lipodermatosclerosis or athrophie blanche
C5 – Healed venous ulcer
C6 – Active venous ulcer


Ec: Congenital, Ep: Primary, Es: Secondary, En: no venous cause


As: Superficial veins, Ap: Perforating veins, Ad: Deep veins, An: no venous location identified


Pr: Reflux, Po: Obstruction, Pr,o: Reflux and Obstruction, Pn: no venous pathophysiology identifiable

Table 1 – The CEAP classification for the clinical manifestations of varicose veins

Differential Diagnosis

Differential diagnoses to consider in patients who present with leg swelling include renal, hepatic, or cardiac disease, all of which require thorough work-up and investigation before being excluded.

Any ulcers forming will need careful evaluation for underlying cause, as discussed here


The gold standard for diagnosing DVI is a Doppler ultrasound scan, allowing the assessment for the extent of venous reflux, any sites of stenosis, and the presence of a DVT or varicose veins.

Routine blood tests may be useful to further exclude other potential aetiologies, including FBC, U&Es, and LFTs, and an ECHO if any cardiac disease is suspected

An essential component of the investigations is documentation of foot pulses and ankle brachial pressure index as this will be required to determine suitability for compression therapy.


Figure 2 – Compression stockings used in the treatment of DVI

Identifying DVI early is essential, as early treatment may reduce long-term complications and prevent irreversible damage. Management can be either conservative or surgical.

Conservative management includes compression stockings (Fig. 2) and suitable analgesic control. If symptoms remain, elevating the feet above the level of the heart can reduce symptoms and disease progression.

Surgical management of DVI is less successful. A Cochrane review focusing on surgical management of DVI found poor levels of evidence, with little to no evidence of benefit for valvuloplasty, however there was some evidence that patients who had deteriorating symptoms had a mild clinical improvement.

Patients with severe post thrombotic syndrome with an occluded iliac vein may be suitable for deep venous stenting, which remains a novel intervention performed in an ever increasing number of vascular units.


Common long-term complications of DVI include swelling, recurrent cellulitis, chronic pain and ulceration.

More serious but less common complications include DVT, secondary lymphoedema, and varicose veins.

Key Points

  • Deep Venous Insufficiency is a common condition yet requires careful work-up for a diagnosis to be made
  • Gold standard investigation is via a Doppler US scan, which can also aid to exclude DVT
  • Management is primarily conservative, but surgical treatment is an option
  • Complications include ulcer formation, recurrent cellulitis, chronic pain, and DVT


Question 1 / 4
What is the current estimated prevalence of deep venous insufficiency?


Question 2 / 4
Which of the following is not a risk factor for developing deep venous insufficiency?


Question 3 / 4
What is the term used to describe the localised round atrophic regions surrounded by dilated capillaries, typically caused by deep venous insufficiency?


Question 4 / 4
What is the gold standard for diagnosing deep venous insufficiency?


Further Reading

Progression of varicose veins and chronic venous insufficiency in the general population in the Edinburgh Vein Study
Lee AJ et al., J Vasc Surg Venous Lymphat Disord

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