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Factors leading
to venous ulceration:
1. Impairment of the
muscle pumping mechanism of the leg due to disease of the
superficial venous system secondary to varicose veins (20-50% of
venous ulcers) or due to incompetence of valves of the deep system
(previous DVT or primary failure). Such patients cannot reduce foot
vein pressure below the resting level. This leads to venous
hypertension, setting the scene for other factors to cause venous
ulceration.
2. Browse and Burnard
proposed that a cuff of fibrin formed around capillaries in patients
with venous disease, which reduced oxygen diffusion into the skin.
However, this has never been conclusively proved.
3. White cell trapping.
Coleridge-Smith and others have suggested that in patients with
venous disease, there is reduced venous flow on standing, leading to
white cell margination and activation with release of free radicals,
proteolytic enzymes and cytokines that cause local tissue injury.
4. Vascular
proliferation in liposclerotic skin. Whether this makes an active
contribution to ulceration is unclear.
5. Development of a type
of peripheral naturopathy with loss of neuronal
regulation of the microcirculation in the skin. This
probably acts
together with the mechanism described in 3.
6.
Venous disease damages
lymphatics in the skin eventually
destroying them. This may account for the
swelling of the legs
often seen with venous
ulcers.
Leg ulcer healing
and recurrence
In
the Skaraborg study of
the natural history of leg ulcers, the overall long term healing was
poor. Only about half were free of ulceration at the end of 54
months. 45% still had open ulcers or had undergone amputation. The
subgroup that did the worst in this study was the one with venous
ulcers and deep venous insufficiency (DVI). Recurrence of venous
ulcers after compression bandaging varies between 30and 57%.
Diagnosis
To label every leg ulcer
as a venous ulcer would be to oversimplify the problem and result in
the wrong treatment being chosen. The classification by Nelzen gives
a good idea what should be kept in mind when dealing with leg
ulcers.
i.
Venous ulcer - due to venous insufficiency without another
cause. Forms
55% of all leg ulcers and 70% of ulcers
above the foot.
ii. Mixed
venous/arterial ulcers - predominately venous but
some arterial
impairment; ABI 0.7 - 0.9.
iii. Mixed arterial/
venous ulcers - predominantly venous due
to superficial
vein incompetence with ABI of < 0.7.
iv. Arterial ulcer - no venous factors. ABI
< 0.7; usually
painful.
v. Arterial and diabetic
ulcers - combination of arterial insufficiency
and diabetic neuropathy.
vi. Diabetic ulcers - due to diabetic
neuropathy. Usually deep
and painless and usually on the foot.
vii. Traumatic ulcers -
obvious history of trauma. Normal ABI
and no obvious
venous disease.
viii. Pressure ulcers - usually buttocks or feet.
No obvious
venous or
arterial disease. Associated with prolonged confinement to
bed.
Clinical diagnosis
should be supplemented with a hand held Doppler examination to
detect arterial and venous insufficiency. Failure to do this means a
wrong diagnosis in I in 4 patients. In more complex cases, a
duplex Doppler examination should be obtained.
Treatment
1. Compression
Bandaging
(CB)
In our Trust we have a main
hospital based ulcer clinic, which takes referrals from hospital
consultants, OP surgeries, and fronl3 community clinics. These
clinics are run by nurses with training in tissue viability and
compression bandaging. Patients presenting with leg ulcers have a
venous and arterial assessment. This may often include an arterial
and venous duplex and a biopsy. Our first line of treatment is a
course of compression bandaging. If the ABI is 0,8 or more, this
will be 4-layer compression. If ABI is 0.6-0.7, a 3-layer bandage
will be applied and the patient referred for a vascular opinion.
Healing rates
for CB are:
Venous
ulcers 66% - 12 weeks
89% - 24 weeks
Mixed
ulcers 42% - 12 weeks
Indications for
referral of leg ulcer patients to a vascular surgeon:
2. Surgery
Ninety percent of all ulcers
are associated with a detectable deficiencies, arterial or venous
and 40% can be cured with surgical procedures. Half of all venous
ulcers are due to superficial/perforating venous insufficiency,
which is eminently dealt with surgically. Venous ulcers treated
surgically have a less than 10% recurrence rate. There is no
evidence to support continual conservative treatment of venous
ulcers once they have been healed with compression bandaging. In
fact there is evidence that long standing superficial or perforated
vein incompetence may progress through the venous system, which may
then become no longer amenable to surgical cure.
The normal venous procedure
for such patients is the high tie and strip of the long and/or short
saphenous veins with multiple phlebectomies. More recently
endovenous laser ablation or VNUS ablation of incompetent
superficial veins is being used. Subfacial Endoscopic Perforation
Surgery (SEPS) can be used to clip incompetent perforations through
an endoscope inserted via a small incision in the calf into the
subfascial space.
Arterial ulcers should be
treated with bypass surgery or angioplasty. Mixed arterial/venous
ulcers are a difficult group to treat. We normally try modified
3-layer compression to heal the ulcers. If this does not work we
would do an angiogram and venous duplex ultrasound. If the arterial
component could be treated with angioplasty, we would do this and
assess the result. If this were not possible, then an acceptable
alternative would be to perform a bypass using the incompetent
superficial vein as a conduit thus dealing with both problems at
once.
References:
Venous Disease: Epidemiology, Management and Delivery of Care.
Ed Ruckley CV, Fowkes FER and Bradbury AW.
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