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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 80-
85% 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 limb-
threatening injuries. Motor neuropathy leads to a gradual denervation of the intrinsic musclesof 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].
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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
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* 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
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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 80-
90% 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.
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