This review explores skin barrier restoration using skincare with gentle cleansers and moisturizers for CVI-related xerosis and VLD.
MATERIALS AND METHODS
The project used a modified Delphi process comprising structured literature searches and face-to-face discussions followed up online.20,21
Literature Review
The structured literature searches (01-November 2022) on PubMed and Google Scholar, as a secondary source, of the English-language literature (2010 - October 30, 2022) were performed by a dermatologist and a physician/scientist. They manually reviewed the selected literature for additional resources and prioritized studies on CVI, VLD and xerosis, SC barrier function, and skincare benefits using cleansers and moisturizers. The searches for CVI* VLD** and xerosis*** explored current clinical guidelines, treatment options, and therapeutic approaches using the following terms:
Group 1: CVI*, VLD**, xerosis*** AND pathophysiology OR inflammation OR cutaneous changes OR clinical signs OR clinical symptoms OR pruritus OR skin barrier physiology OR function OR dysfunction OR depletion of stratum corneum lipids
Group 2: CVI*, VLD**, xerosis*** AND compression therapy OR skincare OR cleansers OR moisturizers OR emollients OR ceramides OR ce¬ramide-containing skincare OR efficacy OR safety OR tolerability
The searches yielded 46 papers deemed clinically relevant to CVI, VLD, xerosis, and skin care to promote a healthy skin barrier and potential mitigation of xerosis and VLD using over-the-counter skincare and CER-containing cleansers and moisturizers.
Role of the Panel
The panel of six physicians (advisors) of various specialties (dermatology, vascular surgery, podiatry, and family medicine) involved in treating patients with CVI and resulting skin changes convened for a meeting. Prior to the meeting, a structured literature search yielded information on fourteen draft statements. During the meeting, the authors adopted five statements supported by the literature and the authors' clinical expertise.
RESULTS
Statement 1: Venous dermatitis is a common inflammatory dermatosis of the lower extremities occurring in patients with chronic venous insufficiency. Risk factors include age, deep vein thrombosis, heart failure, obesity, diabetes, and prolonged sitting/standing.
Clinical guidelines and pathways for patients with CVI-related VLD should include accurate diagnosis and the use of appropriate diagnostic tools.6 It is important to understand the individual patients' issues to achieve an optimal treatment outcome using a holistic approach.6,18 Compression is the standard treatment for lowering VH, decreasing edema and inflammation, and enhancing tissue vascularization.6,10-17 The underlying CVI should be treated with adequate compression that is appropriate and sustainable for the patient.25 Before applying compression, the ankle-brachial pressure index (ABPI) is to be measured to provide information if sufficient arterial circulation is present for leaving compression safely in place day and night.6,10-17,26 Lower extremity Doppler examination is recommended as the standard for patients with suspected peripheral arterial disease.11,26
CVI leads to sustained venous hypertension (VH) upon ambulation, which causes skin changes and inflammation.5,7-10 Dilated capillaries may trigger hemosiderin deposition in the dermis, producing hyperpigmentation (both hemosiderin and melanin), predominantly in the gaiter area.5,7-10 Chronic VH induces thinning of the epidermis, erythema, xerosis, and VLD.3-9 Patients with CVH frequently have pruritus, leading to scratching, skin markings, lichenification, and excoriations.5,7-10 Further changes occur through the proliferation of small vessels, edema, spongiosis, mixed inflammatory cell infiltrates, and structural alterations in the papillary dermis.5,7-10 Studies have shown that expression of matrix metalloproteinases (MMPs) 1, 2, and 13 is altered in the lesional skin of VLD in comparison with healthy skin, which could explain the spongiosis and structural abnormalities observed in the histology of VLD.24
Risk factors for developing VLD include advanced age, obesity, female gender, pregnancy, and prolonged standing.5 Further risk factors associated with VLD include inherited disorders (such as thrombophilia) and prolonged bed rest.1,5,6
Studies have supported that the pathophysiology of venous and arterial vascular disease are commonalities; however, population-based studies confirming the clinical implications are lacking.1,22,23 As many patients with leg ulcers never have venous studies, the advisors agreed that the term "venous leg ulcers" may not be appropriate, as the link to the venous system remains unproven in about 40% of leg ulcers.2,3,5,22,23 Publications and algorithms should distinguish between VLD and swelling leg dermatitis (SLD) as the approach to treatment may differ.7
Statement 2: Compression is the standard therapy for CVI; it has been shown to reduce edema and improve superficial skin lymphatic and venous function and transport.
Treatment of VLD consists of addressing the VH, usually with compression therapy.5,6-19
Clinical guidelines and pathways for patients with CVI-related VLD should include accurate diagnosis and the use of appropriate diagnostic tools.6 It is important to understand the individual patients' issues to achieve an optimal treatment outcome using a holistic approach.6,18 Compression is the standard treatment for lowering VH, decreasing edema and inflammation, and enhancing tissue vascularization.6,10-17 The underlying CVI should be treated with adequate compression that is appropriate and sustainable for the patient.25 Before applying compression, the ankle-brachial pressure index (ABPI) is to be measured to provide information if sufficient arterial circulation is present for leaving compression safely in place day and night.6,10-17,26 Lower extremity Doppler examination is recommended as the standard for patients with suspected peripheral arterial disease.11,26
