Review Skin Changes Are One of the Earliest Signs of Venous a R T I C L E Hypertension

pp 11 - 19 ABSTRACT Review Skin changes are one of the earliest signs of venous A R T I C L E hypertension. Some of these changes such as venous eczema are common and easily identified whereas DERMATOLOGICAL other changes such as acroangiodermatitis are less common and more difficult to diagnose. Other vein MANIFESTATIONS OF VENOUS related and vascular disorders can also present with specific skin signs. Correct identification of these DISEASE: PART I skin changes can aid in making the right diagnosis and an appropriate plan of management. Given KUROSH PARSI, MBBS, MSc(Med), FACD, FACP the significant overlap between phlebology and Departments of Dermatology, St. Vincent’s Hospital and dermatology, it is essential for phlebologists to be Sydney Children’s Hospital familiar with skin manifestations of venous disease. Sydney Skin & Vein Clinic, This paper is the first installment in a series of 3 Bondi Junction, NSW, Australia and discusses the dermatological manifestations of venous insufficiency as well as other forms of vascular ectasias that may present in a similar Introduction fashion to venous incompetence. atients with venous disease often exhibit dermatological Pchanges. Sometimes these skin changes are the only clue to an appropriate list of differential diagnoses. Venous ulceration. Less common manifestations include pigmented insufficiency is the most common venous disease which purpuric dermatoses, and acroangiodermatitis. Superficial presents with a range of skin changes. Most people are thrombophlebitis (STP) can also occur in association with familiar with venous eczema, lipodermatosclerosis and venous incompetence but will be discussed in the second venous ulcers as manifestations of long-term venous instalment of this paper (Figure 2). insufficiency. The less familiar are changes such as Venous hypertension is responsible for many acroangiodermatitis and pigmented purpuric dermatoses. manifestations of chronic venous insufficiency (CVI) Dilatation of venous structures is not always due to including oedema, red cell extravasation, perivascular venous incompetence and could be primary or secondary fibrin deposition, impaired arterial inflow, and other to systemic disease, or environmental influences such as locally mediated disturbances. The local tissue sequelae of actinic damage and radiation. This paper will discuss the CVI are due to impaired clearance of cellular metabolites dermatological manifestations of venous insufficiency as secondary to concurrent damage to the lymphatic system. well as other forms of vascular ectasias that may present One of the earliest manifestations of venous hypertension in a similar fashion to venous incompetence. The second is lower limb oedema. Oedema is defined as a clinically instalment will focus on dermatological manifestations apparent increase in the interstitial fluid volume. Oedema of haematologic disease and in particular thrombo- that retains an indentation when pressed with a finger is inflammatory conditions. The third instalment will discuss called pitting oedema. Systemic causes of oedema include vascular anomalies. congestive cardiac failure, hepatic insufficiency, renal failure, pretibial oedema in myxoedema, hypoproteinemia, Skin Manifestations Of Venous Insufficiency and other systemic disorders. Lymphoedema may be a sign of primary lymphatic outflow obstruction, or it may be Common Manifestations secondary to the overproduction of lymph due to severe Common manifestations of venous insufficiency include oedema, corona phlebectasia paraplantaris (Figure Address Correspondence to: Kurosh Parsi, Sydney Skin and Vein Clinic, Suite 2102, Westfield Tower 1, 520 Oxford Street, Bondi 1), stasis dermatitis, pigmentary changes (hyper- and Junction NSW 2022, Australia Telephone: +612 9386 0211 hypo-), atrophie blanche, lipodermatosclerosis, and skin Facsimile: +612 9386 0258 Email: [email protected] A USTR A LI A N & N EW Z E A L A ND J OURN A L OF P HLEBOLOGY V OLUME 1 0 ( 1 ) : J A NU A RY 2 0 0 7 11 K.Parsi venous hypertension (the so-called phlebolymphoedema). venous eczema.1 Contact dermatitis should be considered Usually, lower leg oedema is symmetrical in patients with when venous eczema becomes clinically worse or does systemic disorders. not improve despite appropriate topical treatment. Patch testing will be indicated. Topical antibiotics such as Oedema of venous insufficiency is quite often associated neomycin and popular preparations such as Kenocomb with skin changes. Venous eczema (Figure 3) is usually the should never be used on open venous ulcers. earliest cutaneous manifestation of venous insufficiency, and it may be a precursor to hyperpigmentation and Venous hypertension leads to red cell extravasation. lipodermatosclerosis. The medial ankle is most frequently Breakdown of red cells leads to haemosiderin involved revealing erythematous, scaling, and sometimes deposition and cutaneous pigmentation (Figure 5). exudative, weeping patches and plaques (Figure 4). Hyperpigmentation secondary to red cell extravasation Secondary bacterial infection with staphylococcus aureus is difficult to treat and not responsive to hydroquinone can cause typical crusting. Pseudomonal colonisation or other standard bleaching agents used to treat is a common complication. In long-standing cases, hypermelanosis. Treatment of the underlying venous lichenification may occur as a consequence of chronic hypertension can help in lightening the pigmentation but scratching and rubbing. in general once haemosiderin pigmentation is present, it is mostly irreversible. Post-inflammatory hypopigmentation The development of contact dermatitis is especially may occur which can even result in depigmentation. This problematic in the treatment of patients with venous should be differentiated from atrophie blanche. eczema. Topical treatments, including neomycin, bacitracin and some topical corticosteroids, have been Atrophie blanche is a specific type of dermal scarring reported to cause contact sensitization in patients with usually presenting as a small reticulated porcelain white Figure 1: Corona phlebectatica Figure 2: Superficial Figure 3: Venous eczema over Figure 4: Discoid para-plantaris. Thrombophlebitis (STP) the dorsum of the foot. Venous eczema associated of a great saphenous hyperpigmentation over the lateral with venous vein tributary. aspect of the foot. hypertension. Figure 5: Typical Figure 6: Porcelain white scars Figure 7: Diagram demonstrating Figure 8: Close-up image of venous hyper- of atrophie blanche in an area of the arteriolar supply of the skin atrophie blanche, interspersed pigmentation of the lipodermatosclerosis. corresponding with cutaneous punctate telangiectasias and medial gaiter area. infarcts of atrophie blanche. underlying varicose veins. 12 V OLUME 1 0 ( 1 ) : J A NU A RY 2 0 0 7 A USTR A LI A N & N EW Z E A L A ND J OURN A L OF P HLEBOLOGY Dermatological Manifestations of Venous Disease: Part 1 patch. Dermoscopic examination of atrophie blanche sclerosis of the overlying skin.3 A less-known form is the demonstrates dilated capillary loops interspersed within so called ‘acute lipodermatosclerosis’ which is primarily the dermal scars. Atrophie blanche is not specific for an acute panniculitis. Acute lipodermatosclerosis can venous hypertension and can be a manifestation of livedoid be confused with acute cellulitis or even acute venous vasculopathy as discussed below. Atrophie blanche is eczema. Eventual induration of skin and the underlying caused by obstruction of dermal arterioles and infarction adipose tissue leads to the more familiar clinical picture of the skin supplied by these vessels (Figures 6-8). This of chronic lipodermatosclerosis. Progression of disease obstruction can be secondary to venous hypertension or leads to the classic inverted champagne bottle appearance. thrombo-occlusive vasculitis involving dermal arterioles. The induration and lack of perfusion of the tissue makes Skin in this condition is avascular and prone to ulceration it prone to ulceration. and necrosis. Vasculitis can also lead to identical white Most chronic lower leg ulcers have a venous aetiology.3 scars of atrophie blanche on the legs. Other systemic Most venous ulcers are caused by superficial venous diseases, such as systemic lupus erythematosis (SLE), incompetence.4 Only a minority are caused by deep vein rheumatoid arthritis, and Klinefelter syndrome can result incompetence or obstruction. Non-healing ulcers of the in skin ulcerations that heal with atrophie blanche-like lesions.2 medial ankle are most likely due to underlying venous hypertension. These areas are especially prone to venous Lipodermatosclerosis (LDS) is the induration of skin and hypertension because their drainage largely depends on the underlying fat in the lower legs (Figure 9). It usually the competence of the great saphenous system and its extends from the ankles to the lower border of the calf associated perforating veins. The incompetent Cockett muscle. Histologically, there is a septal panniculitis and perforators along the posterior arch tributary of the great Figure 9: Lipodermatosclerosis Figure 10: Advanced venous ulcers causing fixed Figure 11: Livedoid vasculopathy associated with atrophie blanche. foot deformity. This patient received ultrasound secondary to protein S deficiency. guided sclerotherapy and all ulcers healed. However, she eventually required a left below knee amputation to facilitate mobility. Figure 12: Acroangio- Figure 13: Hyperpigmentation Figure 14:

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