LOWER LIMB ULCERATION

There are a number of causes which lead to ulcers on the lower limb, especially on the foot. Venous ulcers are the commonest type of leg ulcer in the western world accounting for 8085% of all lower limb ulcers. Apart from venous ulcers, other causes of lower limb ulcers include arterial disease leading to arterial ulcers, diabetes and peripheral neuropathy leading to neuropathic ulcers, ulcers due to vasculitic conditions such as systemic lupus erythematosus and rheumatoid arthritis, ulcers due to haematological causes such as polycythaemia and sickle cell anaemia, and ulcers due to trauma, neoplasia, sarcoidosis and pyoderma gangrenosum. In this section we will look at the pathogenesis,clinical features,investigation and management of venous, arterial and neuropathic ulcers, the three most common types of ulcer encountered in the western world.

Pathogenesis

* Venous ulcers (Fig 10) * These occur due to sustained venous hypertension or chronic venous insufficiency secondary to venous disease (such as varicose veins or venous valve malfunction due to previous DVT), impaired function of the calf muscle pump (due to immobility, arthritis, paralysis or severe obesity limiting mobility) or congestive cardiac failure. This leads to repetitive ischaemic reperfusion injury which in turn results in the formation of ulcers.

* Arterial ulcers (Fig 11) * These are the result of artherosclerosis within the large and medium sized arteries of the lower limb. The significant ischaemia results in the formation of ulcers.

* Neuropathic ulcers (Fig 12) * These occur in diabetic patients who have peripheral neuropathy. Peripheral neuropathy encompasses sensory, motor and autonomic nerve malfunction. Sensory neuropathy leads to neglect of minor injuries or infections which may progress to ulcers and eventually limbthreatening injuries. Motor neuropathy leads to a gradual denervation of the intrinsic muscles of the foot which in turn lead to loss of the transverse and longitudinal arches of the foot and the foot adopting a characteristic claw-like shape. Autonomic neuropathy results in opening of arterio-venous shunts allowing blood to bypass the skin capillary bed and resulting in an increased flow of blood through bone, which promotes osteoclastic activity. This in turn increases the susceptibility of the foot to fracture with minor trauma and Charcot foot collapse. There are several theories regarding the pathological mechanisms leading to nerve malfunction in peripheral nueropathy, this is however beyond the scope of this article.

Fig 10. A venous ulcer in the gaiter area of the lower limb, [13].

Fig 11. An arterial ulcer on the dorsal aspect of the foot.

These ulcers are extremely painful and usually give out a pungent odour, [15].

Fig 12. A neuropathic ulcer at a pressure point on the foot.

The lateral edge of the foot has inward pressure exerted on it by footwear such as shoes which may contribute to the ulceration, [14].

Clinical features

* Venous Ulcers * These are usually located in the gaiter area just proximal to the medial or lateral malleous within an area of lipodermatosclerosis or haemosiderosis. They are usually painless and it maybe possible to notice varicose veins proximal to the area of ulceration.

* Arterial ulcers * These are usually located distally over and between the toes or in pressure points such as the heels or malleoli. They are usually very painful and have a pungent smell. The limb maybe appear pale. Palpation of pulses will usually reveal a diminished pulse and the capillary refill maybe prolonged >2 seconds.

* Neuropathic ulcers * These are characteristically associated with a warm foot with palpable pulses. Ulcers maybe located at points of repetitive trauma. Looking at how ones shoe fits onto the foot and the contact points between the foot and footwear may reveal the mechanism of injury. In certain situations there maybe concomitant arterial insufficiency leading to absent/reduced pulses.

Examination & Investigations

Management

* Venous ulcers * Pure superficial venous incompetence based ulcers maybe treated with varicose vein stripping. These ulcers respond well to surgery and may heal within 4 weeks of the operation. On the other hand patients who are unfit for surgery or who have deep venous incompetence are best treated conservatively with occlusive dressings covered by compression bandages worn from the foot to the knee. These patients require weekly

dressing change and sometimes ulcer debridement. Topical applications such as antibiotic and antiseptic creams have not shown to reduce ulcer healing time. Treated in this way 8090% of ulcers heal by 1 year. It is recommended that patients wear compression stockings for life to prevent recurrence.

* Arterial ulcers * As these ulcers are usually very painful they require analgesia. They need to be dressed, but compression should be avoided as this may worsen tissue ischaemia. In diabetic patients, good glycaemic control should be advocated. Smokers should be advised to stop smoking. The ulcers should be debrided of necrotic tissue. If there is significant arterial disease revascularization should be considered.

* Nueropathic ulcers * X-rays to assess the bones of the foot and to rule out foreign bodies, osteomyelitis, fractures, gas or bone collapse. The patient should be adivsed to regularly visit the chiropodist to aid early recognition of problems with regular debridement of ulcers if already present. Ulcers in pressure areas that are not infected may be treated with pressure relieving footwear such as a total-contact cast which distributes pressure on ambulation over the entire surface area of the foot. The cast needs to be changed every 48 hours to ensure a snug fit, and then weekly for 8-10 weeks until the ulcer is healed. Any infected or gangrenous ulcers should be treated promptly with surgical debridement if necessary and broadspectrum IV antibiotic therapy. If an ischaemic component is suspected, revascularization should be considered as the ulcers are unlikely to heal in this circumstance.