Skin reaction

Our skin is very well adapted to receive pressure from outside and will thicken in response to pressure. A callus generally refers to a diffuse thickening of the skin (more common on the toes, but can occur under the ball of the foot) whereas a corn is a thicker more focal area area (more common on the toes). However when the skin receives pressure from inside, the opposite occures and the skin gets thinner with time, and eventually will atrophied.

The first sign of venous insufficiency is the formation of oedema which is an accumulation of fluid under the skin. This in return causes an additional local pressure increase accompanied by fluid retention, thus further intensifying the underlying metabolic problems. Oedema formation is followed by several perivascular activities including fibrosis, degeneration and inflammation along with trophic alterations of the skin. Additional obliterative inflammatory processes in the small veins and arteries eventually lead to the development of ulcus cruris, the now clearly apparent sign of decompensated venous hypertension, that first presents in areas with unfavourable venous hemodynamics.

The different clinical pictures of venous disease are determined by the severity, localisation, and history of the venous condition, as well as the degree and duration of stress acting on the venous system of the legs. They are all summarized under the generic term chronic venous insufficiency (CVI) and can generally be graded into three stages according to the severity of the dermal lesion. A stage I CVI is characterized by vein dilation along the sides of the foot with concomitant formation of oedema in the ankle region, stage II already involves hyper- and depigmentation of the skin, dermatoliposklerosis, or even atrophie blanche together with marked oedema formation on the lower legs. Stage III is the florid or healed ulcus cruris venosum that is preferentially located in the perimalleolar region (Bisgaard region), but can also be found at other sites of the low leg.

Ankle flare: distension of the small veins on the medial aspect of the foot caused by chronic venous hypertension

Dermatitis: chronic dryness of the skin with epithelial scaling

Hemosidirin Staining - also called hemosiderosis; a brown or rust discoloration of the skin resulting from the buildup of hemosiderin in the interstitial fluid. Venous hypertension results in the extravasation of red blood cells into the tissues. Over time, these red blood cells break down, and hemosiderin (a yellowish-brown, iron containing pigment) deposits result from the breakdown of hemoglobin.

Lipodermatosclerosis: is woody induration of the leg; when fibrous tissue replaces the fatty layer, edema remains above this area, making the leg look like an inverted champagne bottle. Occurs in long-standing venous disease, as the progressive deposition of fibrin in the deep dermis and fat results in the woody induration of the gaiter area and calf. This induration and fibrosis may result in the leg taking on the appearance of an inverted bottle. Lipodermatosclerosis has also been described as a bound down appearance with atrophy, telangiectasia, and hyperpigmentation or hypopigmentation.

Atrophie Blanche - refers to smooth, ivory-white plaques in the skin. These plaques are
avascular, sclerotic areas (may be speckled with telangiectases) that are prone to ulcer formation due to the relative lack of oxygen and nutrient flow to the area.

Treatment

The influence of compression on lymphatic drainage in CVI is a widely underestimated effect that can be assessed with lymphoscintigraphy, fluorescence microlymphography, and microlymphatic pressure measurements

Combined physical therapy (CPT) The first phase consists of skin care, light manual massage (manual lymph drainage), range of motion exercise and compression typically applied with multi-layered bandage-wrapping. Phase 2 aims to conserve and optimize the results obtained in Phase 1. It consists of compression by a low-stretch elastic stocking or sleeve, skin care, continued “remedial” exercise, and repeated light massage as needed.

Drug therapy

a. Diuretics. Some patients may derive benefit from a short course of diuretic drug treatment. Long-term administration of diuretics, however, is discouraged for it is of marginal benefit in treatment of peripheral lymphedema and potentially may induce fluid and electrolyte imbalance.

b. Benzopyrones. Oral benzopyrones, which are thought to hydrolyze tissue proteins and facilitate their absorption while stimulating lymphatic collectors, are neither an alternative nor substitute for CPT. The exact role for benzopyrones (and related rutin and bioflavonoid compounds) in lymphedema treatment is still not definitively determined.

c. Antimicrobials. Systemic antibiotics are not needed for wounds with clinical signs of local infection. Topical antibiotics effective against gram-negative, gram-positive, and anaerobic organisms should be considered (e.g. silver sulfadiazine, triple antibiotic). Always document the reason for using topical antibiotics (e.g., presence of redness, warmth, pain or lack of healing despite optimal management) and the response of the wound to treatment. Advancing cellulitis, osteomyelitis, and bacteremia do need to be treated with systemic antibiotics. In most instances, washing the skin using a mild disinfectant followed by antibiotic-antifungal cream is helpful.

d. Mesotherapy. The injection of hyaluronidase or similar agents to loosen the extracellular matrix is of unclear benefit.

e. Diet. No special diet has proved to be of therapeutic value for uncomplicated venous insufficiency. In an obese patient, however, reducing caloric intake combined with a supervised exercise program is of distinct value in decreasing limb bulk. Restricted fluid intake is not of demonstrated benefit.

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