venous leg ulcersmanagement and prevention of venous leg ulcers: a literature- guided approach
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ABSTRACT
Managing venous leg ulcers involves management techniques
that are indicated both in the treatment of all chronic leg ulcers
and those that are specific to venous leg ulcers. The first step in
managing venous leg ulcers is performing a holistic assessment
of the patient. Once this is complete, any systemic or local fac-
tors that may affect wound healing should be addressed. This
approach to managing the whole patient is critically important
because if significant general wound healing factors are not
treated, other specific attempts at healing the venous ulcer will
be fruitless. This paper reviews nutritional supplementation,
wound bed preparation, antimicrobial therapy, venous insuffi-
ciency, compression therapy, different bandage systems, thera-
peutic adjuncts to compression therapy, and recent advances in
vascular surgery. Recurrence prevention also is discussed.
Ostomy/Wound Management 2001;47(6):3649
Because the population is aging and venous leg
ulcers are common in the elderly,1wound care
providers must have the skills to diagnose and
manage venous leg ulcers. Wound healing in generalmust first be optimized both in terms of the whole
patient and in terms of the wound itself. Only after such
issues are identified and treated can specific therapy be
directed at venous disease.
In preparing the patient for successful healing, several
aspects of holistic care must be considered. All too
often, these important issues are ignored, as caregivers
tend to focus only on treating the ulcer. For example, sys-
temic factors that may inhibit wound healing must be
corrected or the ulcer will not heal. Additionally, the
milieu of the wound bed must be optimized and debride-
ment may be necessary. If the bacterial load is thought to
be a significant problem, antibiotic therapy may be
required. Furthermore, the principle of moist wound
healing must be applied in the selection of ulcer dress-
ings. This paper reviews the above as well as the princi-
ples of medical and surgical management of venous dis-
ease and adjunctive medical and surgical therapy.
General Managementof Venous Leg Ulcers
Treating the whole patient.After careful holistic
assessment, all patients with suspected malnourishment
should be assessed by a nutritionist or dietitian. Protein
and vitamin deficiencies are not uncommon, particularly
in the elderly. Identifying and treating protein malnutri-
tion is the most important aspect of nutritional therapy.
Managing these deficiencies may make the differencebetween a healing and a nonhealing wound even in the
presence of best ulcer care.
Protein replacement, when deficiency exists, has been
shown to be beneficial. In the animal model, in the pres-
ence of protein malnutrition, parenteral nutrition has
36 OstomyWoundManagement
Management and
Prevention of Venous LegUlcers: A Literature-Guided Approach
Brian T. Kunimoto, MD
Dr. Kunimoto is Clinical Assistant Professor, Division of Dermatology, Department of Medicine, The University of British Columbia,Vancouver, British Columbia. Address correspondence to: Brian T. Kunimoto, MD, Division of Dermatology, Department ofMedicine, The University of British Columbia, 835 West 10th Avenue, Vancouver, British Columbia, V5Z 4E8, Canada.
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been demonstrated to improve fibroblast activity.2
Similarly, in malnourished humans, collagen synthesis
has been shown to be improved by enteral nutrition in
the immediate postoperative period.3 It also restores mal-
nutrition-induced impairment of immune responses.4
Vitamin A.Although, in one study, vitamin A supple-mentation in nondeficient animals and humans was
found to be beneficial,5 its use should be confined to
patients who are deficient. Theoretically, vitamin A may
benefit patients who are taking large doses of glucocorti-
costeroids6; however, high doses of vitamin A may be
required, which may be unsafe. In this situation, the
deleterious effects of high doses of glucocorticosteroids
may be reversed by the vitamin A supplementation. More
clinical study is needed before the use of vitamin A for
this particular indication can be recommended. Vitamin
A should be administered with caution because highdoses (more than 50,000 IU/day) can be associated with
hypervitaminosis A syndrome. Routine use of vitamin A
supplementation in the management of venous ulcera-
tion is not recommended. It should be used only in
patients who are vitamin A deficient.
Vitamin C. In the presence of vitamin C deficiency,
wound healing is significantly impaired in terms of speed
and tensile strength.7,8 In patients suffering from vitamin
C deficiency, supplementation is reasonable. The recom-
mended daily allowance for ascorbic acid is 60 mg.9 In
major burn injuries, up to 2 g per day may be required torestore adequate tissue levels.10 There is no evidence that
even higher doses of vitamin C may be toxic making sup-
plementation relatively safe.11
Few studies have examined vitamin C supplementa-
tion in nondeficiency states. No evidence shows that
large doses of vitamin C benefits human wound healing
unless a deficiency exists.12 One randomized double-blind
trial examined 88 patients with pressure ulcers and found
no significant benefit for healing when vitamin C was
given as an adjunct compared to placebo.13 On the other
hand, in severe acute wounds, such as large burns, body
stores of vitamin C may be rapidly depleted, making rou-
tine supplementation with large doses appropriate.12 The
routine use of vitamin C supplementation in the man-
agement of venous ulceration is not supported by the lit-
erature. Its use should be restricted to patients who are
deficient.
Vitamin E. The use of vitamin E in wound healing is
controversial. Animal studies have shown some benefit in
the healing of rat gingiva14 and myocardium in dogs.15
One uncontrolled human study showed that vitamin E
appeared to accelerate healing in venous leg ulceration.16
A recent literature review of the possible uses of topical
and systemic tocopherols in dermatology revealed only
weak and conflicting evidence that vitamin E is of valuein the management of leg ulcers and wound healing in
general.17 Little or no evidence supports the use of vita-
min E in chronic wounds despite its popularity in the lay
community. Controlled studies are needed.
Zinc. Traditionally, zinc supplementation has been
considered to be a useful adjunct to wound management.
Although zinc deficiency, which is quite uncommon, is
associated with delayed wound healing18 and reduced ten-
sile strength,19 no study has shown that zinc supplemen-
tation in nondeficiency states benefits wound healing.20A
more recent review of the literature as of 1998 could notidentify a clinical trial that showed a statistically signifi-
cant benefit of zinc sulfate for healing venous or arterial
leg ulcers.21 Zinc supplementation is indicated when defi-
ciency exists.
Arterial insufficiency. If the leg affected by the
venous leg ulcer is complicated by significant arterial
insufficiency, consultation with a vascular surgeon is rec-
ommended. Any wound, acute or chronic, affected by
ischemia as a result of severe arterial insufficiency, will
not heal no matter what local measures are employed. If
the arterial disease is considered uncorrectable or if thepatients general health precludes surgery, management
becomes palliative and expectations of healing should be
abandoned.
Wound bed preparation.Wound bed preparation
requires management in three areas: debridement (if sig-
nificant wound debris, including slough, eschar, and
crust, is present); antimicrobial therapy (if bacteria in the
June 2001 Vol. 47 Issue 6 37
KEY POINTS
t In this second of two review articles (see
Ostomy/Wound Management, 2001;47(5):3853, the
author reviews the research base of all commonly
used ulcer management and prevention strategies.
t In addition to providing a succinct guideline for care,
the author identifies several areas in need of addi-
tional research, including guidelines for wound cul-
tures and antibiotic treatment and the comparative
efficacy of different types of compression bandages.
Ostomy/Wound Management 2001;47(6):3649
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ulcer base exists); and dressings (to achieve the optimum
moist wound healing environment).
Debridement.When slough and wound debris obscurethe base of the ulcer, debridement becomes essential.2224
Necrotic tissue left in the ulcer contributes to reduced host
resistance to infection because it acts like a foreign body.
Dead cells also release substances that inhibit healing.
However, debridement is contraindicated in ulcers when
healing is complicated by severe arterial insufficiency.
The many ways to debride a wound (see Table 1) are
well covered in an excellent recent review article.25
Venous leg ulcers often have fibrin in the base, which
appears as a dark yellow to brown gel and is easily dis-
lodged by gentle swabbing with a cotton tip applicator.Alternatively, autolytic debridement easily and painlessly
can clear this fibrinous material. In general, ulcers com-
plicated by significant arterial ischemia have slough and,
sometimes, dry eschar in the base as opposed to typical
venous leg ulcers.
Antimicrobial therapy. If the bacterial load in the
ulcer is suspected of being sufficient to impair wound
healing, antimicrobial therapy must be considered.
Bacteria can potentially become successful competitors for
the natural resources for wound healing. If a sufficiently
large population of a pathogenic species of bacteria ismultiplying in the living tissue of the ulcer, healing will
be severely impaired. However, bacterial quantitation may
not tell the whole story. Bacterial virulence that varies
among different bacterial species in the wound also will
impair healing. Lastly, if host resistance is deficient, bacte-
ria will thrive and markedly impair the healing process.
Host resistance comprises systemic and local factors.
Systemic factors include immune defenses and wound
vascularity. Many systemic conditions such as diabetes
and malnutrition contribute to reduced immune respons-
es. Some examples of local factors include necrotic debrisand foreign bodies that may be present at the wound sur-
face. The combination of these three factors determines
the risk of significant bacterial influence on healing. If
this bacterial influence is considered sufficient to abolish
good healing, antimicrobial intervention is necessary.
The decision to use antibiotics for clinically infected
ulcers is an easy one. The patient who develops periulcer
erythema, swelling, cellulitis, purulence, tenderness and
38 OstomyWoundManagement
TABLE 1ADVANTAGES AND DISADVANTAGES OF DEBRIDEMENT25
Method Advantages Disadvantages
Easy to use Utilizes moist occlusion
Painless
Effective when minimal debris
present
Easy to apply
Painless
May be combined with surgical
debridement
Easy to perform
Immediate results
Can be used with local
anesthesia
Any debris may be debrided
Very selective
Slow method (may require weeks)
May irritate surrounding skin
May be slow if slough or eschar is thick
May be expensive
Requires equipment (hydrotherapy, irrigation)
May remove viable tissue especially with
wet-to-dry dressings Painful
Requires training
May be painful and may need anesthesia
Maggots must be cultured and ordered
Autolytic (Moistocclusive dressings)
Chemical (Enzymatic)
Mechanical
(Hydrotherapy, wet-
to-dry dressings,
irrigation,dextra-
nomer)
Surgical (Sharp
debridement)
Biological (Maggots)
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pain, and sometimes fever and toxicity, is a good candi-
date for systemic antibiotic therapy. In this situation, tak-
ing a culture swab of the wound base after cleansing and
debriding taking care not to sample the normal flora of
the wound edge is justified. Although the patient will
likely be started on an antibiotic before results are avail-able, changes can be made later if sensitivity results are
not favorable and the wound is not responding. Careful
interpretation of culture results is necessary because mul-
tiple organisms frequently are identified. Determining
which of the bacteria is the pathogen is difficult.26Also,
caution must be exercised in interpreting laboratory
attempts to quantify the results. Further research is need-
ed to correlate swab techniques and quantitative results
with healing rates. Large studies have not been published
to verify correlation between swab sampling and quanti-
tative biopsy.26
Infection is only one cause of periulcer inflammation;
therefore, cellulitis must be differentiated from these
other causes. Venous dermatitis (stasis dermatitis is a mis-
nomer) occurs much more frequently than wound infec-
tion and is also more common in the summer months.
This form of eczema presents with erythema, scaling,
erosion, and excoriation. Deep swelling characteristic of
cellulitis is not seen. Another noninfective cause of peri-
ulcer eczema is the irritant dermatitis that occurs under
the wound dressing if excessive moisture is draining from
the ulcer. Wound fluid contains many proteolyticenzymes that can be very irritating to the surrounding
skin. Again, deep swelling is absent. One other cause of
peri-ulcer eczema is allergic contact dermatitis.
Once a venous leg ulcer is considered clinically infect-
ed, systemic antibiotic therapy is indicated. In most cases
oral antibiotic therapy is adequate. The use of topical
antibiotics in this situation is not established as standard
therapy,26 and although common in practice, remains to
be clarified by clinical study. In cases where the infection
is thought to have resulted in septicemia, intravenous
therapy is necessary.
The choice of antibiotic is most often empirical and
occurs before the bacterial species is identified. In the
case of venous leg ulcers, Gram-negative organisms are
common colonizers, although, in general, chronic ulcers
of less than 1-month duration are usually colonized by
Gram-positive organisms.27 Staphylococcus aureusand
Group A Streptococcus are important to consider. In
these settings, cephalexin would be an ideal choice,
although cloxacillin is often used as well. If moist, occlu-
sive wound dressings are used, the bacterial flora gradual-
ly changes to favor Gram-negative and anaerobic organ-
isms.28After 1 month of therapy, the empirical choice of
antibiotic therapy must accommodate these changes. For
milder infections, clindamycin and cotrimoxazole wouldbe a good combination.26 More severe, potentially life-
threatening infections may require intravenous clin-
damycin and a third-generation cephalosporin agent such
as cefotaxime.26
Distinguishing the rapidly healing wound from the
clinically infected one is not difficult. However, between
these two extremes lies a gray area where the wound
stops healing because of significant bacterial numbers,
but as yet shows no obvious signs of inflammation. In
these cases, despite optimal management of venous insuf-
ficiency, using appropriate dressings, and debridement,the wound will show no improvement for several weeks.
Furthermore, wound deterioration may be noted as
healthy-looking granulation tissue turns into dusky, dark
red, friable tissue or is replaced by yellow necrotic slough.
In both of these situations, the signs and symptoms of
infection may be absent. The existence of this gray area
between noninfection and clinical infection needs to be
clarified, possibly by developing diagnostic criteria. In
this situation, considering an empirical trial of oral
antibiotics is justified in the authors opinion. However,
prospective studies are needed to confirm this approach.The role of nonantibiotic antimicrobials such as cadex-
omer iodine and silver-coated membranes in this situa-
tion also remains to be defined.
Wound bacterial culturing. The routine use of wound
bacterial culturing should be discouraged. Sampling of
the wound for bacteria should be reserved for instances
when nonhealing or deterioration of the wound is con-
sidered to be due to bacterial influence.
The only reason to take a swab of a wound for bacte-
ria is to obtain information to make the antibiotic deci-
sion-making process more accurate. Patients often are
managed with antibiotics as adjunctive therapy even
though significant infection is not suspected. In many
cases, antibiotics are prescribed on the basis of a positive
culture swab result. However, the literature does not sup-
port this approach. One randomized, controlled trial
compared the use of elastic support bandages to the same
treatment plus systemic antibiotics.29 No significant dif-
ferences were noted in terms of healing rates or changes
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in bacterial flora. The routine use of systemic antibiotics
is ineffective, costly, and will only facilitate the emer-
gence of yet more drug-resistant bacteria.
Topical antibiotics. The use of topical antibiotics as
routine adjuncts to venous ulcer therapy should be dis-
couraged.26,30 Further research is needed to conclusively
define the use of topical antibiotics in wound healing.
Evidence is lacking that shows that topical antibiotics are
capable of eliminating bacterial colonization.Concentrating on proper wound bed preparation to
reduce bacterial burden and improve host resistance
would be far more effective.
Topical agents.Avoiding the use of potentially aller-
genic materials is important. Contact eczema is always a
risk when patients or caregivers use a multitude of topical
agents in chronic wound healing. Evidence demonstrates
that, on the legs, patients with venous insufficiency are
more susceptible to allergic contact dermatitis from topi-
cal agents.3133 One study30 showed that 50% of leg ulcer
patients demonstrated allergic contact sensitization in the
absence of concomitant or past history of eczema. For
these reasons, topical agents containing such substances
as neomycin and related antibiotics, fragrance, lanolin,
and preservatives such as benzalkonium chloride and
parabens32 should be avoided.
Dressings. Chronic ulcer management requires the
use of wound dressings that provide the optimal moist
environment for healing. Moist occlusive dressings
should be utilized when-
ever possible.
Moist wound healing.
In 1958, Odland demon-
strated that blister
wounds healed faster ifleft intact.34 Then in the
early 1960s, a study
reported that occluded
porcine wounds healed
faster than dry ones.35At
that time, the concept of
moist wound healing
originated. Over the last
20 years, an explosion in
the number of new dress-
ings that incorporate theadvantages of moist occlu-
sion has occurred.
Moisture is required for the survival of cells involved in
healing and preserves the activity of growth factors and
enzymes important in the wound healing process. Many
of these enzymes are proteolytic and are important in the
process of autolytic debridement. Occlusive dressings also
provide a physical barrier to invasion by bacteria from
the surrounding skin. This is likely the reason infection
rates are lower for occlusive dressings when compared to
nonocclusive dry dressings.36 In fact, the use of hydrocol-loid dressings is associated with the lowest infection rates
of 1.3% compared to 7.6% for dry dressings.35 In addi-
tion, re-epithelialization rates are also increased by 30%
to 50% under moist occlusion.35An exhaustive review of
wound dressings is covered in three excellent current
reviews3739 (see Table 2).
With respect to venous leg ulcers, specific issues must
be addressed. For example, an edematous leg ulcer will
produce a great deal of drainage, which can be copious
for the first few weeks of treatment. This means that the
initial wound dressing should have considerable
absorbency. Also, during this early stage of ulcer manage-
ment, the absorbent dressing may have to be changed
frequently to avoid the development of irritant dermatitis
of the surrounding skin. This also reduces the annoying
odor that accompanies treatment, particularly with
hydrocolloid dressings. Appropriate dressing types for
this situation include absorbent foam dressings and calci-
um alginates.
TABLE 2CLASSIFICATION OF WOUND DRESSINGS
Dressing Type Main Uses Contraindications
Epithelialization
Granulation tissue formation
Absorption of exudate
Infected wounds
Absorption of exudate
Hemostasis
Infected wounds
Hydration of dry wounds
Donor sites (grafts)
Epithelialization
Difficult cases
Draining wounds Infected ulcers
Poorly granulated ulcers
Infected wounds
Excessively draining ulcers
Superficial wounds
Epithelializing wounds
Superficial wounds
Epithelializing wounds
Infected wounds
Excessively draining ulcers
Infected ulcers
Plastic films
Hydrocolloid dressings
Absorbent dressings
Calcium alginates
Hydrogels
Biological dressings
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Once the initial edema is under
control, switching to a hydrocolloid
dressing that still retains some
absorbency is often useful. This
dressing can potentially be left on for
up to 1 week and may be combinedwith compression bandaging.
After the granulation tissue has filled the defect, facili-
tating re-epithelialization is important. At this time,
dressing changes should be kept to a minimum, as ker-
atinocytes beginning to migrate across the wound do not
anchor to the wound bed until it is covered. Too frequent
dressing changes at this point tend to tear off the neoep-
ithelium before it has a chance to establish itself.
Fenestrated, nonadherent plastic film dressings may be
best at this stage of healing.
One interesting recent advance in managing venous legulcers has been the development of biological skin equiva-
lents. In 1997, a cultured, allogeneic, bilayered human
skin equivalent, Apligraf (Organogenesis, Canton, Mass.;
Novartis Pharmaceuticals Canada Inc., Dorval, Quebec,
Canada), was first released in Canada. This has made
treating nonhealing venous and other difficult-to-treat
ulcers possible.40 By 1999, considerable Canadian experi-
ence had accumulated resulting in a consensus paper,39
which recommended that healthcare providers consider
using the human skin equivalent if the venous ulcer does
not show significant healing after 1 month of optimaltherapy. The pivotal study that confirmed the efficacy of
the human skin equivalent, Apligraf, was a randomized,
multicentered, prospective study involving 275 patients
with venous leg ulcers.41 The researchers found that treat-
ment with human skin equivalent was more effective than
compression therapy alone in the percentage of patients
healed at 6 months (63% vs 49%). Also, the median time
to complete wound closure was 61 days for the human
skin equivalent group compared to 181 days for those
receiving compression therapy alone. Both results were
considered statistically significant. Although this dressing
is expensive and must be delivered by courier for use
within a short time, human skin equivalent may provide
an alternative treatment for nonhealing wounds.
In the past decade, a great deal of research also has
been conducted in the field of growth factors. However,
the use of growth factors has been more successful in
treating diabetic and pressure ulcers than in the treat-
ment of venous leg ulcers.
Regarding venous leg ulcers and dressings, the author
believes that a wound covered by new epidermis should be
protected for about 2 months because the new skin cover-
ing the wound is fragile. In fact, the process of matrix-
remodeling continues for several months after the ulcer has
grown skin cover. Any protective dressing may be used for
this purpose. Thin hydrocolloid dressings are a good
choice because they can be applied under elastic stockings.
Specific Venous Ulcer ManagementCompression therapy. The cornerstone of managing
venous leg ulcers is treating the underlying disease:
Venous insufficiency. In the vast majority of patients, this
involves some form of compression therapy.
Venous hypertension underlies the development of
venous ulceration. In a way, the venous leg ulcer is sim-
ply a complication of this underlying disease. The final
insult to the skin before the development of the ulcer is
cutaneous ischemia as a result of the venous disease.
Without correction of the underlying disease, this
ischemia persists, resulting in a chronic wound that will
not respond to general measures. Compression therapywith a number of different bandaging systems corrects
this problem, giving the ulcer a chance to heal using the
proper techniques of wound bed preparation.
All ambulatory patients with venous leg ulcers require
compression therapy. A recent systematic review of the
literature was conducted restricting the search to ran-
domized controlled trials.42 The authors concluded that
compression systems improve the healing of venous leg
ulcers and should be used routinely in uncomplicated
venous ulcers. Many caregivers are unaware of this fact
and rely on topical treatments such as creams and the lat-
est wound dressings.43 Part of the reason for this may be
that only over the past decade has the mechanism of how
external compression works been elucidated. Many care-
givers are faced with a confusing array of different com-
pression bandage systems, making treatment decisions
unnecessarily difficult.
Compression pressures. Compression pressures of at least
30 mm Hg to 40 mm Hg at the ankle should be utilized
Compression = N (number of bandage layers) x T (bandage tension)
R (radius of the leg)
Figure 1Law of Laplace (modified).
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in the management of venous leg ulcers. All compression
bandage systems must create a pressure gradient from
ankle to knee. According to the Law of Laplace (see
Figure 1), which mathematically relates bandage tension,
compression pressure, and limb girth, the shape of the leg
will create this gradient. Thus, if the bandage tension isconstant as the healthcare provider winds the bandage up
the leg, a compression gradient will naturally develop
because the smallest limb radius is found at the level of
the gaiter area, just proximal to the ankle joint. As the
bandage is wrapped up the leg, progressively larger radii
are encountered, resulting in lesser degrees of compression
given the constant bandage tension. This pressure gradi-
ent provides support against venous hypertension, which
is greatest at the ankles when the patient is standing.
Correcting venous hypertension requires that the com-
pression system be capable of exerting at least 30 mm Hgof pressure at the level of the ankle.4446 One study44
demonstrated that after 15 minutes of motionless stand-
ing, the transcutaneous oxygen tension around the ankle
drops to very low values. After examining the effects of
different degrees of compression using a pneumatic pump
device, the researchers found that 30 mm Hg to 40 mm
Hg at the ankle area abolished this response.
The occasional venous ulcer patient is nonambulatory
or absolutely cannot or will not tolerate compression
therapy. Most experts recommend these patients utilize
leg elevation (at least 2 hours per day) as an alternative.This requires positioning the ankle at the level of the
heart. Sometimes this can be achieved by placing 6-inch
wooden blocks under the foot of the bed. Asking the
patient to keep a legs-up chart can benefit compliance.
Compression systems may be classified into three
groups: short-stretch bandages (SSB), long-stretch ban-
dages (LSB), and stockings. If the limb affected by the
ulcer is edematous, most experts recommend using an
SSB system.45,47,48 Because SSB, by definition, provides lit-
tle or no elasticity against the contracting calf muscle, the
highest working pressures are attained. This working
pressure drives blood in the deep femoral vein upward.
For the same reason, when the calf muscle relaxes, the
bandage does not continue to exert pressure. This low
resting pressure facilitates deep venous filling.45
Short-stretch bandage systems require patients to be
ambulatory. Without a calf muscle capable of contract-
ing, the inelastic bandage becomes ineffective. Thus,
patients who tend to shuffle around need to be trained to
walk properly, making sure they push off with their toes.
Similarly, those patients with ankle joints stiffened by
arthritis or old injury may not be good candidates for
SSB systems.
Despite expert opinion that supports the use of SSB
while managing edema, only a few studies compare themto LSB and the results have been far from conclusive.
One recent controlled, nonrandomized study found that
inelastic compression was better than elastic compression
for reducing deep venous reflux.49Another study, which
looked at venous pressure in the dorsal vein of the foot
during treadmill walking, found that only the short-
stretch system was able to reduce the elevated venous
pressure seen in venous insufficiency.50 One recent
prospective, randomized, observer-blind, parallel group
study compared both systems in 32 patients with 39
ulcers. After 15 weeks, using complete healing as theendpoint, the study found no statistically significant dif-
ference.51A prospective, randomized trial comparing the
four-layer bandage system with an inelastic bandage in
53 patients revealed no significant differences in healing
after 12 weeks.52 Other comparison trials are currently
under way.
Long-stretch bandages are more commonly used than
SSB systems in North America and the United Kingdom.
The four-layer bandage is popular because it is capable of
maintaining high compression for several days and up to
a week. This reduces the frequency of dressing changes, agreat advantage for home healthcare nursing. The four-
layer bandage must be applied by trained personnel.
Because of elasticity, the four-layer bandage and other
LSBs continue to exert compression even when the leg is
elevated. This can be a problem if the patient has signifi-
cant arterial insufficiency. Therefore, the four-layer ban-
dage should not be used in patients with an ankle-
brachial index (ABI) of less than 0.8.
Other LSB systems are capable of lower levels of com-
pression. These systems are relatively safe in the presence
of moderate arterial insufficiency. They may be used if
the ABI is greater than 0.5 and require only a minor
degree of training. Like the four-layer bandage, they may
be left on for 1 week at a time. In the presence of severe
arterial disease (ABI less than 0.5), even these lower com-
pression systems are contraindicated.
Surgery. In some cases, the wound stubbornly refuses
to heal even after systemic factors have been managed,
the wound bed has been optimized, and compression
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therapy has been instituted. In this situation, venous vas-
cular surgery should be considered.
Venous incompetence in the deep system cannot be
corrected surgically. On the other hand, perforator
incompetence and disease of the superficial venous sys-
tem can be managed using new surgical techniques thatare associated with only mild morbidity. Significant per-
forator incompetence may cause localized venous hyper-
tension that may not be adequately managed by the use
of a compression bandage system.
Chronic venous insufficiency is caused by vascular dis-
ease affecting the deep, perforator, or superficial veins.
Historically, the first theories on venous insufficiency
postulated that the primary problem with the post-
thrombotic leg was that of deep-vein obstruction.
Obstruction of the deep veins was thought to cause
venous hypertension. Later, a small minority of patientswas found to have isolated venous outflow obstruction,
and in 90% to 95% of cases, valvular incompetence is
the cause of venous hypertension.53 Deep vein valvular
incompetence is believed to be of greatest importance in
pathogenesis. Despite Hippocrates observation correlat-
ing leg ulceration with the presence of varicose veins,
superficial venous disease has been considered to be
much less significant. Recently, duplex ultrasound scan-
ning has improved the measurement of reflux in deep,
superficial, and perforator veins. Of interest is the finding
that a lesser but significant proportion of venous ulcerpatients has competent deep veins and isolated superficial
venous reflux.54 Many of these patients have isolated
incompetence of great or lesser saphenous veins and may
benefit from saphenectomy.
In patients with combined deep and superficial dis-
ease, the removal of varicose superficial veins has been
feared to eliminate an important venous outflow tract for
occluded or hypertensive deep veins. This may not be
true in the majority of cases. One study found that less
than 10% of patients with deep vein obstruction had sig-
nificant reduction of venous outflow when the superficial
veins were occluded.55A recent study demonstrated that
in patients with combined disease, ablation of superficial
and perforator veins reduced deep venous reflux.56
Another study showed that preoperative femoral vein
reflux could be abolished by greater saphenous vein strip-
ping in 27 of 29 limbs.57Although more research is need-
ed, lesser saphenous vein reflux might be a significant
contributor to venous ulceration. One recent study
showed that incompetence of the lesser saphenous vein
may contribute to venous insufficiency and ulcers of the
lateral aspect of the leg.58 However, a significant propor-
tion of these patients have associated deep venous incom-
petence, making lesser saphenous vein ablation ineffec-
tive in improving long-term outcome.53
The role of perforator vein incompetence in chronic
venous insufficiency requires more study as well.
Perforator vein incompetence is accepted as important in
the development of venous ulcers. In 1949, Linton
described a technique for dissecting incompetent perfora-
tors using a long paratibial incision.59 This procedure
causes significant morbidity and prolonged hospitaliza-
tion. Since the mid-1990s, subfascial endoscopic perfora-
tor surgery (SEPS) has been studied.60 Its major advan-
tage over the Linton procedure is the greatly reduced
postoperative morbidity. One study examined the use ofSEPS in 19 patients with venous ulcers.61 The ulcers had
been present an average of 4.4 years. After treatment, all
ulcers healed within 90 days. A more recent study from
the Mayo Clinic reported an ulcer recurrence rate of
12% after SEPS compared to their population average of
28%.62 Contrasting these good results, another study
reported failure of healing or ulcer recurrence after SEPS
ranging from 2.5% to 22%.63 This study stated that one
limitation of SEPS is that perimalleolar perforators are
difficult to access.
Currently, surgical ablation of incompetent superficialveins and SEPS cannot be recommended as routine pro-
cedures. Certainly, if an ulcer shows no sign of healing
after 3 months using best practices, vascular surgery
should be considered. However, more research is needed
over the next few years to establish the role of vein
surgery in the treatment of nonhealing venous leg ulcers.
Adjunctive TherapyPhysical therapy for the ankle joint.A physical ther-
apist should be consulted for patients who possess little
ankle mobility if any potential for improvement of joint
flexion and extension exists. The ankle joint is equivalent
to the hinge component of the calf muscle pump. A
mobile ankle joint is essential for the pump to function.
If the joint in a patient with chronic venous insufficiency
is ankylosed, venous congestion is exacerbated. Patients
with this problem tend to shuffle around, barely lifting
their feet off the floor. Furthermore, the ability of com-
pression bandages such as the SSB system to enhance
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venous return is compromised in the presence of the
frozen ankle. Chronic venous insufficiency itself may
contribute to ankle immobility through the deposition of
fibrotic tissue.
If ankle joint mobility is present, and an SSB system is
being used, the patient should be encouraged to raiseboth heels off the ground while in a standing position.
The shuffling gait that is so common among the elderly
should be discouraged.
If joint mobility is reduced, yet potential for improve-
ment exists, a physical therapist may be able to loosen
soft-tissue contractures through the use of physiotherapy.
Intermittent pneumatic compression. One means of
intermittently increasing compression to relieve edema is
to use the intermittent pneumatic compression (IPC)
device. Because some patients require higher levels of
compression than is tolerated, noncompliance with thebandage system becomes an issue. The IPC device can be
used as an adjunct to compression bandaging. It also may
be used as an alternative to compression bandaging in
patients who are relatively immobile and, therefore,
unable to activate the calf muscle pump.
The IPC device comprises a series of balloons that are
inflated by a pump. The timing of balloon inflation in
sequence moves edema fluid toward the inguinal region.
This device may be used to quickly reduce the volume of
the leg before compression bandages or graduated com-
pression stockings are applied. The device is also useful asan alternative to compression bandages in patients who
lack good mobility and cannot walk around to activate
the calf muscle pump and in those with lymphedema.
IPC therapy is contraindicated in the presence of signifi-
cant arterial insufficiency, and edema due to congestive
heart failure.
One randomized, controlled study compared healing
rates for 24 patients using moist occlusive dressings and
graduated compression stockings (30 mm Hg to 40 mm
Hg) with 21 patients using the same treatment plus IPC
for a total of 4 hours per day. The treatment period last-
ed 3 months. Only one patient in the control group
completely healed compared to 10 of the 21 in the IPC
group (P= 0.009, Fischers exact probability test).64
Another randomized, prospective controlled study exam-
ined 22 patients. Both groups received local wound care
and Unnas boot. The experimental group used IPC twice
weekly for 1 hour each session and achieved statistically
significant better healing rates.65
Intermittent pneumatic compression may be a useful
adjunct that complements compression bandage or stock-
ing therapy in the treatment of venous leg ulcers and
may be used in difficult cases.66
Medication therapy: Edema-preventive drugs.
Lymphedema may result in patients who have long-standing venous edema. This type of edema may respond
to coumarin drugs, which may be recommended as
adjunct therapy. The benzopyrones (coumarin) have been
shown to be efficacious in the management of chronic
lymphedema.67 Long-standing venous hypertension often
develops into chronic lymphatic insufficiency, especially
in obese patients.
Diuretics should not be used in the management of
edema caused by venous insufficiency. The edema associ-
ated with venous disease is caused by pump failure,
which causes venous hypertension and leakage of fluidfrom the intravascular compartment into the interstitial
space. None of this can be corrected with diuretics.
However, diuretics may be required during edema man-
agement using compression bandaging in patients who
suffer from congestive left-sided heart failure. Here, sig-
nificant increases in effective arterial blood volume may
be evident; these are caused by the improvement in calf
muscle pump function afforded by bandaging. This sud-
den shift of fluid from the interstitial space into the
blood may exacerbate left ventricular function, resulting
in the appearance of pulmonary edema. This should be aconsideration in the elderly with fragile cardiac function.
Hemorheologic agents. The routine use of hemorhe-
ologic agents, such as pentoxifylline, in the treatment of
venous leg ulcers is not recommended at this time.
Pentoxifylline increases the deformability of red blood
cells, improving blood supply to ischemic tissues. It also
has been found to reduce white blood cell trapping, mak-
ing it an attractive therapeutic agent in venous ulcer
management.68A review of the literature does not
unequivocally endorse the use of pentoxifylline.
One of the original studies was a prospective, random-
ized, double-blind, placebo-controlled trial involving 80
consecutive venous leg ulcer patients for 6 months.69
Complete healing was seen in the pentoxifylline group in
23 of 38 patients, compared to 12 of 42 patients in the
placebo group. This was found to be statistically signifi-
cant. A more recent double blind, placebo-controlled trial
involved only 12 patients.70 Drug or placebo was adminis-
tered for 60 days. In the active drug group, complete
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healing was seen in 4 of 6 patients compared to 1 of 6 in
the placebo group. This was considered statistically sig-
nificant; however, the study size was small. The most
recent randomized double blind, placebo-controlled trial
involved 200 patients.71 Complete healing was seen in 65
of 101 (64%) patients receiving active drug compared to52 of 99 (53%) patients on placebo drug. This result did
not reach statistical significance.
Management of obesity. In many patients with
venous ulceration, morbid obesity is a problem that must
be managed concomitantly with specific venous ulcer
therapy. Morbid obesity directly causes deep venous
insufficiency. If obesity is not managed, it is the authors
opinion that compression therapy will be difficult if not
impossible. Morbidly obese patients usually do not toler-
ate compression therapy.
Obesity is a risk factor for the development of venoushypertension. Patients who are severely obese may not be
able to lie down in bed at night as a result of restrictive
respiratory failure. However, sleeping in a chair can have
disastrous consequences on venous hypertension.
Lymphatic insufficiency is not unusual among these
patients and ulceration presents a major therapeutic chal-
lenge. After venous ulcer healing, continued morbid obe-
sity will predispose patients to ulcer recurrence. Obesity
management requires the skills of a dietitian or weight-
loss expert.
Prevention of Venous Leg UlcersGraduated compression stockings. Once the venous
leg ulcer has healed, prevention must be the main objec-
tive. In all ambulatory patients, graduated compression
stockings (GCS) should be recommended. Graduated
compression stockings are of proven value in the manage-
ment of venous hypertension.7274 The issue of ulcer pre-
vention was illustrated in a study that examined ulcer
recurrence rates both with and without the regular use of
GCS rated at 30 mm Hg to 40 mm Hg.75 Fifty-three
patients with venous leg ulcers were healed using GCS.
They were followed for the next 6 months and compli-
ance with stocking use was evaluated. Among the 25
patients who demonstrated good compliance, one ulcer
recurred. Of the 28 patients who were either poorly or
noncompliant, 22 had at least one ulcer recurrence. One
15-year retrospective study examined the efficacy of GCS
in the management of venous ulcers.76 Of 113 patients,
105 (93%) achieved 100% healing after an average of 5.3
months. One hundred two patients were compliant in
the use of GCS and 11 patients were not. Of those who
were compliant, 99 of 102 (97%) patients healed com-
pared to 6 of 11 (55%) patients who were not (P