Deep Venous Insufficiency

Introduction

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 (in the superficial venous system) it is part of chronic venous insufficiency.

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

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

*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. They may also report venous claudication, characterised by a bursting pain and tightness on walking which resolves on leg elevation.

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 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

Classification

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

aEtiology

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

Anatomical

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

Pathophysiology

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


Investigations

The primary investigation 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.

*If there is evidence of a venous occlusion or reflux in the pelvis as characterised by poor flow wave forms in the femoral veins or varicosities over the buttocks/perineum, then an MR Venogram may be performed.


Management

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 the patient has a venous ulcer then they should be started in full compression treatment such as a 4 layer bandage. 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.

Venous Stenting

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.

As the long-term outcomes of this intervention remain unknown this procedure is reserved for patients with the most severe symptoms despite maximal conservative therapy, and as with any vascular procedure a good inflow and outflow from the stent is required.

The procedure typically involves puncturing the popliteal or femoral vein in the thigh, and crossing the occluded segment of vein with a wire up into the IVC. A balloon is then used to dilate the iliac vein prior to placement of a venous stent.


Complications

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

Quiz

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

Quiz

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

Quiz

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?

Quiz

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

Results

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

Rate This Article

4

Average Rating: