Venous Eczema and Lipodermatosclerosis

Venous Eczema and Lipodermatosclerosis
Laurel M. Morton, MD, and Tania J. Phillips, MD, FRCPC
Cutaneous changes are a common feature of chronic venous insufficiency and include venous
eczema and lipodermatosclerosis. This review will address the presumed pathophysiology of
these conditions, their clinical findings, and important management strategies.
Semin Cutan Med Surg 32:169-176 © 2013 Frontline Medical Communications
KEYWORDS venous eczema, lipodermatosclerosis, chronic venous insufficiency
C
hronic venous disease is commonly encountered in both
the United States and Europe.1,2 The most common disorders within this spectrum of disease include lower extremity edema, varicosities, and venous leg ulcers. The cutaneous
manifestations of venous insufficiency are very common and
often require dermatologic expertise. This article will address
venous eczema and lipodermatosclerosis (LDS), which can
sometimes produce diagnostic dilemmas and treatment challenges.
Venous eczema (otherwise known as gravitational eczema,
varicose eczema and stasis dermatitis) affects the lower legs
and ankles. The skin becomes erythematous, scaly and pruritic. There are also often associated signs of venous disease,
such as varicose veins, edema, hemosiderin pigmentation,
atrophie blanche, and LDS. LDS is a progressive fibrotic process of the dermis and subcutaneous fat associated with
chronic venous insufficiency (CVI), resulting in hyperpigmentation and induration of the lower leg. The presence of
these cutaneous conditions is important for the classification
of venous disease (Table 1).
Unfortunately, there is scarce epidemiologic data regarding the prevalence of venous eczema and LDS. In fact, little
data exists for chronic venous disease in general, likely because it is rarely life-threatening and has multiple definitions.
However, up to 17% of men and 40% of women suffer from
CVI;1 and of the 23% of Americans with varicose veins, 2
million will develop skin changes.4
The pathophysiology of cutaneous changes seen in venous
disease remains unclear. It involves chronic ambulatory venous hypertension and resulting microangiopathic and inflammatory changes, which lead to classic clinical and histoDepartment of Dermatology, Boston University, Massachusetts.
Disclosures: The authors have completed and submitted the ICMJE Form for
Disclosure of Potential Conflicts of Interest and none were reported.
Correspondence: Laurel M. Morton, MD, Department of Dermatology, Boston
University 1 Devonshire Place #3804, Boston, MA 02109. E-mail:
[email protected]
1085-5629/13/$-see front matter © 2013 Frontline Medical Communications
DOI: 10.12788/j.sder.0026
pathologic findings. The management of venous eczema and
LDS requires treatment of underlying venous insufficiency
with consideration of other medical and surgical interventions, if appropriate.
Pathophysiology
The normal venous system consists of a high pressure deep
venous system and a superficial system, linked by communicating veins. One-way valves prevent retrograde blood flow.
During walking, the calf muscle pump contracts, raising the
deep venous pressure, emptying the deep veins, and propelling blood towards the heart. Once the deep veins empty, the
deep venous pressure falls, the valves open, and blood flows
from the superficial to the deep system.
CVI arises from failure of the calf muscle pump or abnormalities in the venous system, such as valve dysfunction,
venous outflow obstruction or a combination of these factors.
In these circumstances, venous pressure fails to decrease significantly during exercise, creating ambulatory venous hypertension.5 How these mechanical changes result in the skin
signs and symptoms of venous disease is not well understood. Microangiopathic and proinflammatory effects resulting from venous hypertension are thought to play a role.
The microcirculatory changes resulting from CVI encompass decreased capillary counts, increased capillary diameter,
permeability to proteins and erythrocytes, and increased subcutaneous fluid flow.6 Increased permeability of small vessels
leads to pericapillary fibrin cuff formation7 postulated to result in decreased oxygenation of involved skin.8,9 However,
fibrin deposition is not confluent, which may mitigate against
decreased oxygen diffusion. Fibrin may also impair tissue
healing by inhibiting new collagen formation, contributing to
the fibrosis seen in LDS.
Inflammatory cells may be even more important in the
development of venous eczema and LDS. The ‘white blood
cell trapping theory proposes that due to decreased flow,
169
L.M. Morton and T.J. Phillips
170
Table 1 Classification System for Chronic Venous Disease
(CEAP)3
Grade
Description
C: Clinical Manifestations
No visible or palpable signs of venous
C0
disease
C1
Telangiectasias or reticular veins
C2
Varicose veins; distinguished from
reticular veins by a diameter of 3 mm
or greater
C3
Edema
C4
Changes in skin and subcutaneous tissue
secondary to chronic venous disease:
4a (pigmentation or eczema), 4b (LDS
or atrophie blanche)
C5
Healed venous ulcer
C6
Active venous ulcer
E: Etiologic Factors
EC
Congenital
EP
Primary
ES
Secondary (post-thrombotic)
EN
No venous cause identified
A: Anatomic Distribution of Disease
AS
Superficial veins
AP
Perforator veins
AD
Deep veins
AN
No venous location identified
P: Pathophysiologic Findings
PR
Reflux
PO
Obstruction
PR,O
Reflux and obstruction
PN
No venous pathophysiology identifiable
Abbreviation: LDS, lipodermatosclerosis.
white blood cells accumulate and release toxic oxygen metabolites and proteolytic enzymes resulting in capillary damage, increased permeability, and fibrin cuff formation.10 A
28.6% decrease in circulating white blood cells was shown in
patients with CVI.11 Histologic specimens of LDS reveal increased white blood cells in tissue.12 T lymphocytes and macrophages increase in patients with varicose veins. Patients
with severe LDS also show elevated interleukin-1␣ and interleukin-1␤, important proinflammatory cytokines.13
Neutrophils, mast cells and interleukin-8 are also important mediators of inflammation in CVI.14,15 Neutrophils exit
the circulation and transverse the endothelium to enter the
dermis. The cell-adhesion molecule L-selectin aids neutrophils in this process by adhering to endothelial cells to promote rolling along blood vessel walls. After leukocyte activation, L-selectin is shed and CD11b begins to allow similar
adhesion and eventual extravascular migration.16 In chronic
venous disease, plasma L-selectin increases and L-selectin
decreases on the surface of circulating neutrophils. Venous
hypertension possibly leads to this neutrophil activation and
migration into tissue with subsequent decreased presence in
circulation.16 Others have demonstrated increased adhesion
molecules ICAM-1 and VCAM-1 in inflamed liposclerotic
skin.17
Finally, it is clear that the architecture of skin must change
to account for the firm induration of LDS. Expression of
mRNA for matrix metalloproteinase (MMP) – 1 and 2 is increased in LDS as is active MMP2. This unrestrained activity
likely leads to extracellular matrix turnover18 and eventually
venous ulceration.18,19 Tissue hypoxia and white cell activation may also stimulate transforming growth factor (TGF)-␤1
production and accelerate fibrosis.19
Clinical Findings
and Disease Course
Early clinical findings of CVI include lower extremity edema,
a condition that frequently presents at the ankles, worsens
towards the end of the day, and improves overnight. Although not always present, varicosities range from thin telangiectasias to submalleolar venous flares to larger tortuous
vessels.20,21 Over months to years, as venous hypertension
continues, distal red-brown hyperpigmentation due to extravasated erythrocytes, hemosiderin-laden macrophages,
and melanin deposition occurs.22 These changes tend to be
localized to the gaiter area. At this stage of the disease, xerosis
and pruritus may appear and can develop into venous eczema. This very pruritic condition begins at the ankle, particularly over the medial malleolus.23,24 It is often, but not
always, bilateral. It may begin as sharply demarcated erythematous papules and vesicles; however, it eventually becomes diffuse, poorly defined, and may demonstrate serous
exudate and crust.23-25 It is less frequently warm to the touch
compared to cellulitis.25
In venous eczema, secondary infection can occur and
should be suspected when the skin barrier has broken down
and other signs of impetiginization exist. Contact dermatitis
is common in these patients. Inciting agents include topical
antibiotics such as neomycin and bacitracin, lanolin products,26 fragrances, parabens,27 corticosteroids,28 rubber components,29 and epoxy resin.30 A thorough history should be
procured and patch testing considered in patients with recalcitrant lower extremity dermatitis. Disseminated eczema (id
reaction) has also been reported in the context of contact
dermatitis seen in patients with chronic venous disease.23,31,32
There is a clinical continuum of LDS ranging from acute to
chronic disease.33 Acute LDS presents as painful, erythematous and purple, indurated plaques confined to the lower
extremity. White scale may be present and lesions are usually
well-demarcated from normal skin.7,19 LDS is often warm,
tender, and clinically misdiagnosed as acute cellulitis, erythema nodosum, or inflammatory morphea. Two thirds of
patients with LDS demonstrate abnormal venous reflux
and/or ejection.34 In its more chronic form, LDS is associated
with a classic ‘inverted champagne bottle’ appearance of the
distal third of the lower leg. Skin changes are characterized by
hyperpigmentation and fibrosis of dermal and subcutaneous
tissue,19,33 which is bilateral in approximately half of the cases
(Figure 1).35 This morphology was first described as hypodermatitis sclerodermiformis by Huriez in 1955.36 Over time,
Venous eczema and lipodermatosclerosis
171
theories regarding its etiology have varied. Huriez and colleagues suspected cellulitis in the setting of venous insufficiency.36 Many years later, acid-fast microorganisms were
thought to be an inciting factor.37 Today, most authors agree
that LDS is either exclusive to, or highly associated with,
venous insufficiency.20 The lower extremities are most often
involved though it has been documented in other dependent
locations. One interesting report describes a 54-year-old female with congestive heart failure demonstrating clinical and
histologic findings supportive for LDS in a pendulous abdomen.38
Risks factors for the development of LDS include female
gender, elevated body mass index, and deep venous incompetence. One retrospective study of 97 LDS patients showed
that 87% were women and 67% had deep venous incompetence while the mean body mass index was 34.3.35
Pathology
In CVI, the dermis may demonstrate lobulated, thick-walled
small blood vessels in the papillary and reticular dermis,
extravasated erythrocytes, hemosiderin-laden macrophages,
lymphohistiocytic infiltrates, and fibrosis (Figure 2).39,40 Venous eczema also demonstrates parakeratosis, epithelial hyperkeratosis, and dermal edema, which can be pronounced
in the papillary dermis. Fibrosis is variable and a mononuclear cell inflammatory infiltrate is somewhat inconspicuous.41 These changes may be mild in acute LDS and more
prominent in chronic disease.39,40
In LDS, the pathology lies in the subcutaneous tissue and
broadly includes fat necrosis, a lymphohistiocytic infiltrate,
and septal fibrosis.40 Acute lesions demonstrate focally ex-
Figure 1 An example of bilateral chronic lipodermatosclerosis demonstrating hyperpigmented and indurated plaques at the lower, medial legs.
Figure 2 Histopathologic changes of chronic venous insufficiency at
low power showing lobules of small blood vessels, hemorrhage and
hemosiderin.
travasated erythrocytes, ischemic necrosis in fat lobules with
hyalinized fat, a sparse inflammatory infiltrate, and mild septal fibrosis. Lipomembranous fat necrosis and microcysts
may only be seen in limited areas.40 As lesions progress, inflammation is more prominent as is septal fibrosis and obliteration of fat lobules. Cyst-like cavities occur within the adipose tissue and pseudocysts more often possess the classic
lipomembranous scalloped, feathered lining. Foamy macrophages and lipogranulomas may also occur.40 Moth-eatenappearing elastic fibers, resembling those in pseudoxanthoma elasticum, may be present and help differentiate LDS
from other fibrosing entities (Figure 3).39
Figure 3 Lipodermatosclerosis histopathology at low power
showing deep-seated fibrosis and fat degeneration with microand macrocysts.
L.M. Morton and T.J. Phillips
172
Differential Diagnosis
and Diagnostic Measures
It is important to differentiate venous eczema and LDS from
other dermatologic conditions of the lower extremities. For
the experienced clinician, these entities are most frequently
diagnosed by physical examination.33,42
The differential diagnosis for venous eczema includes
other papulosquamous conditions such as nummular eczema and psoriasis. These conditions usually affect additional body sites with nail changes or joint complaints in the
case of psoriasis. Xerosis and eczema craquele can resemble
venous eczema but are frequently more diffuse and generally
improve with emollients and topical steroids alone. Venous
eczema is commonly misdiagnosed as cellulitis.43,44 Both entities can present with pitting edema, erythema, serous drainage, and even desquamation. However, cellulitis is usually
unilateral, tender, and may be associated with systemic
symptoms such as a fever. Venous eczema is commonly bilateral and tends to be itchy, nontender, and more chronic.44
Perhaps the most challenging condition to rule out is allergic
contact dermatitis since this may be seen in conjunction with
venous eczema, which is characterized by a decreased skin
barrier that may increase the rate of sensitization.45 In cases
where allergy is suspected, patch testing is a valuable diagnostic tool.46 Irritant contact dermatitis should also be considered and the patient closely questioned about topical applications to the skin.
Acute LDS is also frequently misdiagnosed as cellulitis as it
presents with a very tender, well-circumscribed red plaque;
however it does not improve with antibiotics. LDS may be
confused with other panniculitidies such as erythema nodosum (usually presenting with multiple red tender nodules on
the shins), thrombophlebitis (presenting as redness and tenderness along the course of the vein, usually accompanied by
swelling), and fibrosing conditions such as inflammatory
morphea (presenting with indurated round or oval plaques
which may be red to purple on initial presentation).19,47 LDS
can be seen as a secondary diagnosis in patients with connective tissue disease; it should be considered prior to the use of
immunosuppressants in these patients with lower extremity
fibrosis.48 A rare but interesting case of sarcoidosis masquerading as LDS was reported where ulcerated plaques, morpheaform lesions, and lower extremity edema closely mimicked findings of CVI.49
Biopsy should be avoided in patients with LDS since up to
50% of biopsy sites fail to heal33 and may become chronic
ulcers. Furthermore, the histologic changes are not specific to
this entity.50 Duplex ultrasound should be performed to confirm the suspected diagnosis of venous insufficiency51,52 and
can specifically identify incompetent veins.53 Ultrasound indentometry may be a useful way to quantify fibrosis in LDS54
and the durometer can be used to assess skin hardness. It has
been reported that magnetic resonance imaging can be used
in the diagnosis of LDS, showing characteristic though not
pathognomonic fibrosclerotic septa and a honeycomb pattern in the subcutaneous tissue.42
Treatment Options
Management of venous eczema and LDS must address underlying venous insufficiency, primarily by compression therapy. Venous eczema may also be treated with topical interventions typically used for eczematous skin disease. There are several useful
adjunctive measures for LDS in Table 2.
Compression Therapy
Compression is a mainstay of treatment for CVI. A 2012
Cochrane Database review, including 48 randomized controlled trials, verified that compression increases venous ulcer healing rates compared to no compression. Furthermore,
multi-component compression containing an elastic bandage
is more effective than compression without an elastic component.55 Given that venous eczema and LDS also improve
with compression, this should be the first-line treatment recommendation for patients. In one study of 150 patients,
graduated compression alone effectively reduced the skin
changes seen in LDS.56 In particular, below-the-knee, opentoe, graded compression is ideal.33 Pressure at 20-30 mm Hg
may be sufficient for less severe cases; however, patients with
any history of ulcer disease should employ 30-40 mm Hg.4 It
is important to note that up to two thirds of patients may be
nonadherent in the use of compression stockings for reasons
including a binding sensation, presumed ineffectiveness, the
sensation that they are too hot to wear, limb soreness, poor
cosmesis, contact dermatitis, pruritus, and cost.57 Prior to
attempting more aggressive interventions, clinicians should
attempt to elicit an honest report from patients regarding
their compliance with compression. While not ideal,58 even
10-15 mm Hg pressure may improve symptoms of venous
insufficiency.59 In one small study of 11 patients, ultrasound
revealed that compression from 18-26 mm Hg is sufficient to
decrease dermal edema in LDS patients.58 Compression
wraps rather than stockings should be utilized in patients
with open venous leg ulcers.19
Other simple interventions focus on lifestyle changes such
as weight loss, increased leg elevation, and increased exercise
to improve calf muscle pump function.4,52
Topical Interventions for Dermatitis
In addition to treating underlying venous insufficiency with
compression, venous eczema is managed topically with
emollients and immunomodulators, including corticosteroids60 and calcineurin-inhibitors. There is scant data to support this approach. In one study of 19 patients with ‘stasis
dermatitis’, betamethasone valerate 0.12% foam led to improvement in erythema compared to vehicle alone.61 Dissemond et al also reported one case of dermatitis treated twice
daily for 5 days with topical 0.1% tacrolimus that resulted in
complete healing.60 For severe venous eczema, a short course
of oral corticosteroids can be helpful.
In 2012, Maroo et al suggested treating venous eczema
with a combination of oral doxycycline and topical tacrolimus. The authors cite the anticollagenase, anti-inflammatory
and immunomodulatory effects of doxycycline and the T-cell
Venous eczema and lipodermatosclerosis
173
Table 2 Treatment Recommendations for Lipodermatosclerosis
Treatment
Recommended Dosing
Adverse Effects
Monitoring
30-40 mm Hg graduated compression
(20-30 mm Hg may be effective in
patients without history of venous
leg ulcer)
Stanozolol 2-5 mg by mouth twice
daily
Danazol 100-200 mg by mouth twice
daily
Oxandralone 100 mg by mouth twice
daily
Limb soreness
Contact dermatitis
Pruritus
Prior to initiation, rule out
arterial disease by palpating
for pulses; ABI
Edema and hypertension
Abnormal liver function tests
Lipid abnormalities
Virilization
Dysmenorrhea
Exacerbation of prostatic
hypertrophy
Peliosis hepatitis
Hepatocellular carcinoma
Blood pressure, liver function
tests, lipid panel, prostatespecific antigen, complete
blood count and renal
function tests at baseline
Blood pressure monitoring
weekly for up to one month
and then every 3-4 weeks
Liver function tests every 3-4
weeks
Uncontrolled hypertension,
congestive heart failure,
history of prostate
adenocarcinoma and benign
prostatic hypertrophy are
contraindications
Pentoxifylline
400-800 mg by mouth 3 times daily
Intralesional
Triamcinolone
5-10 mg/ml intradermal (dose varies
based on area of involvement)
Topical Capsaicin
0.075% cream
Nausea
Dizziness
Heartburn
Vomiting
Pain with injection
Cutaneous atrophy and
dyspigmentation
Burning sensation and/or pain
Dermatitis
Compression
Anabolic Agents
Abbreviation: ABI, ankle brachial index.
inhibitory effects of tacrolimus as important mechanisms for
disease modification. Of 15 patients that completed the study
with CVI, 13 showed improvement with 6 patients achieving
0-15% improvement of the involved area, 6 patients achieving 15-35% improvement, and one patient achieving greater
than 35% improvement. The study showed statistically significant improvement in pain, edema, erythema, pigmentation, pruritus, and exudate.62
Anabolic Agents for Lipodermatosclerosis
If tolerated, compression should be used to treat LDS. It is
important to remember that patients with LDS often do not
tolerate compression due to extreme skin tenderness.
In addition to compression therapy, multiple publications
have supported the use of stanozolol, an anabolic steroid
with fibrinolytic properties.19 In a 6-month trial with 23 patients, Burnand et al showed an increased rate of LDS healing
(based on involved area) with stanozolol 5 mg twice daily
with compression compared to placebo with compression.63
In 1991, McMullin and colleagues showed similar results in a
larger double-blind randomized controlled trial with 60 patients. After 6 months, those treated with graduated compression stockings (30-40 mm Hg) plus stanozolol 5 mg
twice daily showed a 28% reduction of the involved area
compared to a 14% reduction in patients treated with com-
pression alone.64 The authors postulated that perivascular
fibrin deposition in LDS created local hypoxia and eventually
ulceration.64 They also suggested that stanozolol may improve oxygenation due to its fibrinolytic properties; however,
transcutaneous oxygen measurements were not affected.64
Lower doses of 2 mg twice daily may also be successful in
acute LDS with decreased pain in 3 weeks and decreased
induration at 8-10 weeks.33 Stanozolol might even be considered as monotherapy when patients absolutely cannot tolerate compression due to pain. In an open trial of 17 patients,
stanozolol 2 mg twice daily alone reduced dermal thickness
(as measured by high resolution ultrasound) and pain after 8
weeks and all participants tolerated compression at the end of
treatment.65
Stanozolol has reversible anabolic and androgenic effects,66 including sodium retention with edema and hypertension, hirsuitism, acne, liver function, lipid abnormalities,
and dysmenorrhea. Patients on this medication should have
their blood pressure closely monitored and undergo liver
function tests every 3-4 weeks. If the latter become elevated,
the dose should be reduced.19 This intervention is best
avoided in patients with uncontrolled hypertension or congestive heart failure.33
Danazol, a weak androgen with fibrinolytic properties
used for endometriosis and acquired angioedema, has been
L.M. Morton and T.J. Phillips
174
reported in several cases to improve pain and induration of
LDS at doses between 200 mg-400 mg (in divided twice daily
dosing).67,68 However, the virilizing side effects can be
marked.67 Unfortunately, manufacturers in the United States
no longer distribute danazol due to its abuse among weight
lifters.19 Oxandrolone, another anabolic agent with less androgenicity, has also been used. Because it undergoes less
metabolism by the liver compared to the aforementioned
agents, Segal and colleagues chose this medication in a patient with LDS and elevated liver enzymes. After 2 weeks of
100mg twice daily dosing, the patient experienced pain reduction and subjective softening of the skin.66
Pentoxifylline
An alternative for patients who cannot tolerate or safely take
stanozolol is pentoxifylline, a demethylxanthine derivative
that increases red blood cell flexibility, alters fibroblast physiology, and stimulates fibrinolysis. Pentoxifylline is generally
given in doses of 400 mg 3 times daily. A 2012 Cochrane
Database review states that this agent improves venous ulcer
healing when combined with compression or when used
alone.69 A retrospective study published in 2012 supported
the use of pentoxifylline 1200 mg daily in combination with
hydroxychloroquine in dosages up to 6.5 mg/kg/day in the
treatment of LDS. Without compression, 13 of 30 patients
experienced complete remission of pain, edema resolution
occurred in 14 of 15 patients, and erythema resolution occurred in 24 of 28 patients. Induration was significantly improved in 17 patients.70
For difficult cases, the dose of pentoxifylline may be increased to 800 mg 3 times daily. Side effects include nausea,
dizziness, heartburn, and occasional vomiting.
Other Nonsurgical Interventions
Campbell and Miller have shown that intralesional triamcinolone at concentrations of 5-10 mg/ml effectively improves
pain, edema, induration, and erythema of LDS.71 In their
study of 28 patients, compression was also utilized and multiple treatments were required for lasting improvement.71
Intralesional therapy with platelet-rich plasma was used to
treat a 76 year old man with LDS who failed multiple interventions including compression, anabolic steroids, pentoxifylline, antibiotics, nonsteroidal anti-inflammatory drugs,
and surgery. He was given autologous platelet-rich plasma
subcutaneously at 2-week intervals. Five treatments resulted
in decreased pain, hyperpigmentation, induration, and eventual epithelialization of an associated leg ulcer. Platelet-richplasma may work by stimulating adipose tissue regeneration
and angiogenesis.72
Topical capsaicin, frequently employed to treat localized
pruritus, improved LDS in 2 patients who failed more conventional therapy. The topical 0.075% capsaicin cream was
used for 3 weeks and the authors postulate that the cream
may have fibrinolytic and antithrombotic effects.73
The least-invasive intervention utilized for LDS is ultrasound. In 2009, Damian et al reported 11 patients with longstanding LDS treated with 3 MHz of continuous ultrasound
for 8 minutes 3 times weekly for 4-8 weeks. Patients also used
compression stockings. A durometer was used to measure
skin hardness; erythema was monitored by a reflectance erythema meter. This intervention improved pain and tenderness within 2 weeks. A total of 10 of 13 legs showed a reduction in hardness (averaging 60%) and 7 of 9 legs showed
decreased erythema. No adverse events were reported.74
There is little evidence for this modality; however, it is certainly a safe intervention in recalcitrant disease and in patients unable to proceed with other therapeutic options.
Surgical Intervention
The best published data supporting venous ablation in CVI
more specifically references venous leg ulcers. The 2004
ESCHAR study evaluated 500 patients with active or recently
healed venous leg ulcers. Patients were randomly assigned to
receive ablative superficial vein surgery with compression or
compression alone. Data revealed that 24-week healing rates
were similar between groups. Ulcer recurrence at 12 months
was significantly reduced in the patients that also received
surgery (12% vs 28%). For this reason, patients with documented superficial venous disease and a history of leg ulcers
are generally referred for ablative surgery.75
Many studies of surgical intervention for venous insufficiency do not provide specific descriptions regarding improvement of LDS. In patients treated with saphenofemoral
junction ligation and ultrasound-guided foam sclerotherapy,
Figueiredo et al reported improved venous clinical severity
scores, taking LDS into account.76
Conclusion
Cutaneous disease is frequent in CVI. It is imperative that
clinicians identify conditions such as venous eczema and
LDS, differentiating them from similar appearing disorders
with a thorough history and physical exam. While the most
important aspect of management is compression therapy,
this spectrum of disease offers an exciting avenue for further
research since much of the literature to date focuses on the
management of venous leg ulcers rather than venous eczema
and LDS.
Acknowledgements
Thank you to Dr. Daniel Miller and Dr. Meera Mahalingam at
Skin Pathology Laboratory at Boston University Medical Center for assisting with the acquisition of histopathologic images.
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