Epidemiology

Ulcers of venous origin account for 70% of all leg ulcers. Chronic venous leg ulceration has an estimated prevalence of between 0.1% - 0.3% in the UK and increases with age. Venous insufficiency is the most common cause of lower-leg ulcers, accounting for nearly 80% of all cases (21).  

 

Aetiology

Causes include venous valve incompetence: failure of the calf muscle pump to work effectively, leading to oedema (pooling of fluid in the lower limb). This can lead to venous hypertension (high pressures in the lower limb on walking), which leads to hypoxia in the tissues and trapping of harmful substances such as growth factors and enzymes. This ultimately results in tissue breakdown precipitated by simple trauma such as knocking the leg. The calf muscle pump relies on adequate levels of mobility; therefore, anything that might affect this such as old age, obesity and trauma predisposes the individual to these events if they also have poor venous return. Risk factors associated with venous ulcers include deep vein thrombosis, varicose veins, or surgery/trauma to the leg (17). 

 

 

 

 

 

 

 

 

 

 

 

Clinical Signs

As a result of venous hypertension and fluid leakage, red blood cells are deposited in the tissues causing hemosiderin discolouration. This is often seen on the lower limb and may be coloured red or brown (Image 10). Varicose veins may also be visible as will oedema and a characteristic change known as lipodermatosclerosis (LDS) (image 11). Over time, the limb may develop a typical inverted ‘champagne bottle’ appearance (image 12). Venous ulcers are typically shallow and develop in the gaiter area  (between the knee and ankle) (17). 

 

 

 

 

 

 

 

 

 

 

 

 

Treatment 

The mainstay of treatment is graduated compression bandaging. Specific bandage systems apply external pressure, to aid venous return. The ABPI (ankle brachial pressure index) must be ≥ 0.8 for this treatment. The aim of most systems is to create pressures of 40 mmHg at the ankle decreasing up to the knee. As well as bandaging, the patient should keep mobile by doing ankle exercises to improve blood flow for example. Leg elevation and rest should also be incorporated in management. Other treatment options include antibiotics in systemic infection or topical antimicrobial dressings for local infection. Intermittent pneumatic compression, surgery, skin grafting, bioengineered skin and pharmacological treatments such as oxypentifylline have all been suggested as adjuvant therapies to compression therapy.

 

Gravitational eczema is common in patients with venous disease and is related to the changes caused by venous hypertension. The patient may complain of intense itching, and scratch marks may be visible on examination. It is vital to differentiate eczema from contact sensitivity and cellulitis as each are treated differently (17).

 

ARTERIAL LEG ULCERS

 

These are caused by reduced arterial blood flow and subsequently, reduced tissue perfusion. Arterial or arteriolar occlusion can result in ischemia and necrosis of the skin and subcutaneous tissues, potentially leading to ulceration. Peripheral vascular disease due to atherosclerosis, diabetes with microvascular or macrovascular disease, and/or vasculitis could lead to ischemic leg resulting in these ulcers. Ulcer development is often rapid with deep tissue destruction. The limb appears pale, and is noticeably hairless. This ulceration typically occurs over the toes, heels, and bony prominences of the foot. The ulcer appears “punched out” with well-demarcated edges and a pale, non-granulating, and non-necrotic base (21, 22).