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28
Compression Therapy and Nursing Care
for Venous Leg Ulcers
Jill Robson
Freeman Hospital, Newcastle upon Tyne, U.K.
Hany Hafez
St. Richard’s Hospital, Chichester, U.K.
BACKGROUND
Patients with leg ulcers should expect to have a full assessment carried out by a competent
healthcare professional (1). In most cases the ulcer will be found to be due to venous
insufficiency, and should respond to treatment with sustained graduated compression,
which remains the preferred method of treatment worldwide (2). There are different ways
of applying this amount of compression, and healthcare professionals who carry out these
treatments should demonstrate their competence to do so. The choice of compression
method should be based on the patient’s condition, the patient’s preference and the
availability of suitable, evidence-based equipment. As with any intervention, patient
consent must be sought.
Most leg ulcers are due to venous incompetence. The incidence of venous ulceration
is in the region of 0.3% and is responsible for 90% of all leg ulcers. Venous ulceration can
result from superficial venous insufficiency, deep venous insufficiency, or both. “Stasis”
ulceration can also occur secondary to excessive obesity, immobility with prolonged leg
dependency, and poor calf muscle pump function. These ulcers often benefit from
treatment aimed at improving venous return. Compression therapy is currently the most
effective way of doing this (3). There are, however, other causes for leg ulceration
which, although less common, can have serious consequences if treated inappropriately.
These causes include arterial insufficiency, diabetes, skin malignancy, vasculitis, and
autoimmune disease such as rheumatoid arthritis. Every patient presenting with a leg ulcer
should therefore be carefully assessed to determine the etiology prior to proceeding with
compression therapy.
The Venous System in the Leg and Principles of Compression
Leg venous flow to the heart is mainly maintained by the combined action of the muscle
pump and venous valvular directional regulation. When the calf muscles contract, pressure
is exerted on the deep veins which are responsible for 75% of the venous return from the
leg. During relaxation, blood is prevented from gravitating in the veins by the action of
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competent valves. Failure of one or both components of this system, such as damaged
valves or poor muscle function or inability to move the ankle joint, can lead to venous
hypertension. Over a period of time venous hypertension can lead to skin devitalisation
and ulceration. The principle behind compression therapy for venous ulceration is to
counteract the venous hypertension effects on the skin. This is achieved by the direct
physical pressure of the dressing and by augmenting the calf muscle pump action (4).
The ideal levels of compression to reverse venous hypertension are 35–40 mmHg at the
ankle, graduating down to 17–20 mmHg under the knee.
Several methods of applying such pressure have been tried, these include:
1. Multilayer elastic compression bandage
2. Inelastic short stretch bandage
3. Two layer Vari-stretch
w
bandage (Proguide
w
)
4. Elastic compression hosiery
As the degree of compression is inversely proportional to the circumference of the
limb, i.e., more compression is exerted on a thinner part of the leg than on a wider part
(Laplace’s law), the effectiveness of any graduated compression method will rely on the
shape of the leg being conical. The leg should therefore be thinner at the ankle than it is
below the knee. If the leg is not naturally this shape, then the padding layer should be used
to reshape it before the compression is applied (Fig. 1).
It is important that none of these methods of compression are used if there is any
evidence of arterial insufficiency, as indicated by an ankle brachial pressure index of less
than .85. Reduced compression may, however, be appropriate for some patients with
mixed disease. All patients must be fully assessed and etiology determined before a plan
of care can be made (5).
ASSESSMENT
All patients require full assessment, preferably using a written pro forma. Particular
attention should be paid to the following issues (6).
Predisposing History for Venous Disease
Carefully question the patient and use medical records if available.
† Patients may already have history of venous disease and surgery. The type of
previous surgery should be sought. Similarly, patients may have had deep
venous thrombosis (DVT) in the past; details of this should also be sought.
Figure 1 Correct and incorrect appearance of leg before application of compression.
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† An undiagnosed DVT in the past should be investigated. Relevant history
includes history of major leg orthopedic trauma or surgery, known DVT risks
such as concurrent malignancy, thrombophilia, and morbid obesity.
† Any occupation that involves long periods of standing can aggravate or lead to
varicose veins and so an occupational history should be taken.
Predisposing History for Arterial Disease
† Smoking is the most significant risk factor for arterial disease and should always
be asked about.
† Arterial disease often affects other vessels such as coronary arteries, carotid or
renal arteries. Symptoms related to these vessels such as angina, myocardial
infarction, stroke or hypertension should be sought. Some patients may have
already been diagnosed with peripheral arterial disease.
† Diabetes can be associated with medium and small vessel disease.
† Rheumatoid arthritis and other autoimmune diseases can lead to
vasculitic changes.
Presenting Clinical Signs and Symptoms of Venous Disease
† Varicose veins, if present, are easily visible under the skin.
† Inverted champagne bottle shape is the characteristic shape of the leg, due to
long term venous insufficiency. This is due to gradual loss of muscle bulk
and lipodermatosclerosis.
† Lipodermatosclerosis is the term given to the hard “woody,” scaly, appearance
of the skin due to gradual hardening of the dermis and fibrosis of the
subcutaneous fat, a side effect of long-term venous hypertension.
† Venous eczema also known as varicose eczema, is similar in appearance to
eczema. It is the term given to red, very itchy patches that weep clear fluid. This
is due to small splits in the skin, as it is unable to stretch and
accommodate edema.
† Ankle flare also known as telangiectasia, is often seen as a result of venous
insufficiency. As the veins and venules become more and more congested, they
become distended and visible as a crop of purple vessels under the skin on the
foot or ankle.
† Edema in venous disease is usually accompanied by one or more other
symptoms. It is not “pitting,” and care must be taken to ensure that it is not
a result of congestive cardiac failure.
† Atrophie blanche is another symptom of venous disease. It refers to the ivory
white patches of scarred looking skin, often stippled with the red dots of
distended capillary loops, due to a loss of the capillaries’ ability to transfer
oxygen to the tissues. This condition can be very painful and is often mistaken as
an arterial symptom.
† The skin pigmentation associated with venous insufficiency is due to
microhemorrhages leading to a build up of hemosiderin deposition. This causes
the skin to become brown or black in the area most affected. The gaiter area of
the leg is usually most affected (Fig. 2).
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Presenting Signs and Symptoms of Arterial Disease
† Intermittent claudication is the term given to a severe cramp-like pain usually in
the calf but sometimes in the thigh or buttock. The pain comes on during walking
or other exercise, and stops after a few minutes of rest. This is due to poor
perfusion of muscles and is an indicator of arterial disease.
† Ischemic rest pain also known as just “rest pain,” is usually in the foot or lower
part of the leg. It comes on whenever the limb is elevated. This is due to critical
foot arterial supply, which relies on gravity to draw the arterial blood into the
foot. The limb may also lose color on elevation. Patients with this condition
often have to sleep in a chair or hang their leg out of the bed. This is not to be
confused with night cramps, a benign condition suffered by many elderly people
with or without peripheral arterial disease.
† The location of the ulcer is important. Any ulcer on the toes or foot, below the
level of the malleolus, must be suspected of being arterial or diabetic in origin.
Occasionally, however, patients may present with pressure ulcers on the foot,
which have the appearance of arterial ulcers, so this should be eliminated as
a cause.
† Delayed capillary refilling, when combined with other features of arterial
disease, can be a useful sign. The perfusion of the skin is often poor in arterial
disease. To test capillary refill time, gently apply pressure to the toenail bed
until it blanches, then release the pressure and count the number of seconds
until the color returns. As a rule, refill time over 3 seconds may indicate
poor perfusion.
Figure 2 Patient with chronic venous insufficiency showing skin pigmentation, venous ulceration,
and patchy lipodermatosclerosis in the gaiter area.
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† Atrophic shiny skin, when combined with other signs and symptoms of arterial
disease, can add to the overall picture of long-term arterial insufficiency. This
sign can also occur with long-term steroid therapy.
† The appearance of the ulcer is important, as arterial ulcers are usually deeper,
have a “punched out” edge, and often have evidence of tissue necrosis such as
eschar or slough.
Mixed Arterial and Venous Disease
As previously mentioned, most patients with ulcers have venous insufficiency, and will
benefit from compression therapy. Careful history taking and physical examination can
determine those whose ulcers are due to arterial disease who must not have compression
therapy. There are, however, some patients who present with all the features of venous
disease, but who have underlying arterial disease not immediately apparent. It is therefore
imperative that further investigation is carried out to determine this, before potentially
dangerous bandaging is started.
Ankle to Brachial Pressure Index (ABPI)
This procedure is used widely to assess arterial blood flow in the arteries in the leg, and
must be done for all patients presenting with a leg ulcer, and have absent palpable ankle
pulses before any compression is used (7). Ankle to brachial pressure index (ABPI) is
a comparison of the ankle systolic arterial blood pressure with the brachial systolic arterial
blood pressure. The procedure should be explained to the patient and verbal consent
obtained. Make sure the patient is lying flat for at least 10 minutes before starting.
Prepare the equipment:
† Doppler machine
† Sphygmomanometer and suitably sized cuff
† Ultrasound gel or other water-based gel
† Tissues
† Light waterproof dressing to cover the ulcer
Secure the cuff around the arm as if taking a blood pressure reading in the normal
manner. Apply gel over the brachial pulse. Hold the Doppler probe over the brachial pulse,
at an angle of 608 to the skin, tucked into the gel. Move the probe carefully until a good
signal is obtained. Inflate the cuff until the signal disappears, then gradually inflate until
the signal returns. Note the pressure reading on the sphygmomanometer. Repeat on the
other arm. Make a note of the higher of the two readings. This is the brachial systolic
pressure.
Place a light dressing over the ulcer, look for foot pulses in the shown positions
(Fig. 3). Apply gel to the search area. Secure the cuff around the leg just above the ankle.
Hold the Doppler probe in the gel over the dorsalis pedis area at an angle of 608, and
look for a signal. Once a signal is found, keep the probe in position and inflate the cuff
until the signal disappears. Deflate gradually until the signal returns. Note the pressure
reading on the sphygmomanometer. Repeat the procedure for the posterior tibial signal.
Make a note of the higher of the two readings. This is the ankle systolic pressure. Use the
tissues to remove gel from patient’s skin. To work out the ABPI, divide the ankle
systolic pressure by the brachial systolic pressure. If the ankle pressure is the same as the
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brachial, the ABPI will be 1.0. If the ankle pressure is lower than the brachial, then the
ABPI will be less than 1.0. To allow for a small margin of error, any reading of between
0.85 and 1.2, where all the assessment criteria point to there being no arterial disease, is
considered normal and compression can be used (8).
In patients with diabetes, renal disease or severe arteriosclerosis, the ankle pressure
reading may be significantly higher than the brachial systolic pressure. These conditions
can lead to calcification of the arterial walls, making them impossible to occlude with the
sphygmomanometer cuff. It is therefore important that all readings are interpreted
with care.
An ABPI of between 0.6 and 0.85 indicates a moderate degree of arterial
insufficiency. It is not considered safe to apply full compression, but in some
circumstances light compression can be applied. It is advisable to seek advice from a
specialist practitioner before doing so.
An ABPI of less than 0.6 usually indicates more severe arterial disease; no
compression should be applied to these patients under any circumstances. They will
require referral to the vascular service for further investigations.
Recognizing Rare Causes for Leg Ulceration
There are several unusual causes for ulcers that will be difficult for less experienced
practitioners to recognize. Some are listed here:
† Neuropathic diabetic foot ulcers will need to be referred to the diabetic podiatry
service. Initial treatment will be centered on relief of pressure, and prevention
and treatment of infection. Compression is not advised.
† Pyoderma gangrenosum can occur anywhere on the body, but particularly on the
leg. It is due to a vasculitic response to a systemic autoimmune disease such as
Crohn’s disease or ulcerative colitis. The ulcer often has a necrotic appearance
and may have a purple border around it. Treatment is usually offered though the
dermatology unit.
† Rheumatoid ulcers often have a punched out appearance with tissue necrosis.
Treatment of the underlying rheumatoid disease along with local wound care
is advised. Malignancy can occur on the skin of the leg or develop within an
existing ulcer. If malignancy is suspected then the patient should be referred
urgently to the dermatology department.
† Factitious ulcers are those caused by the patient self-harming. This is a complex
problem requiring sensitive management. Psychological support may
be required.
Figure 3 Sites of dorsalis pedis and posterior tibial arteries.
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† Tropical ulcers are due to infection with any one of a number of tropical
organisms, causing tissue necrosis. The infection should be treated and help
should be sought from microbiology or the department of tropical diseases.
If any of these unusual causes is suspected, the patient should be referred to the
appropriate specialist and simple local wound care continued.
Assessing the Ulcer and Surrounding Skin
The size of the ulcer should be documented either with a ruler or tape measure, making a
tracing, or taking a photograph. Remember that the patient’s consent is required before
photographs may be taken, and this must be documented.
As with other chronic wounds, good wound bed preparation is important. The
wound should be assessed to determine the presence of necrotic material or slough, the
bacterial burden on the wound surface and the level and type of exudate. Patients with leg
ulceration often develop skin sensitivities to various preparations used to treat their ulcers
or their dry scaly skin. If skin sensitivity or allergy is suspected, then the preparation
should be discontinued and referral to dermatology considered so that the source of the
sensitivity can be determined. A pain assessment form should also be completed for all
patients. As with all patients suffering from chronic illness, it is important that they are
adequately nourished. Obesity can also be a contributing factor to the leg ulceration and
should be treated. Dietetic referral may be appropriate in these circumstances.
TREATMENT
The leg should be washed in warm tap water and the ulcer and surrounding skin treated
before dressings are applied. The type of primary dressing should be chosen according to
the nature of the wound bed. As a general rule it is best to choose the simplest dressing,
such as non-adherent knitted viscose. There may be circumstances where the wound bed
requires modification.
1. An anti-microbial dressing may help to reduce the bacterial burden
2. An odor control dressing may be used if odor is a problem
Hydrogels and other dressings with high water content are not usually appropriate
under a compression bandage as they can cause maceration of the surrounding skin.
Where there is a large amount of exudate, it is important to get the compression
profile correct, so padded dressings are to be avoided. These can alter the shape of the limb
and make the problem worse (Fig. 1). A simple absorbent pad can be applied on top of the
bandage if “strike through” occurs.
COMPRESSION
The first graduated compression stockings were introduced by Conrad Jobst more than
40 years ago and now bandaging systems and hosiery of various types are available. The
common forms of compression used today are:
1. Multi-layer elastic compression bandages; e.g., Profore
w
, K four
w
, Ultra four
w
,
System 4
w
, Hospifour
w
2. Short stretch inelastic bandages; e.g., Comprilan
w
, Rosidal K
w
, Actiban
w
,
Silkolan
w
, Varex
w
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