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Pengelolaan Kasus:

Cutaneous Changes in Venous and Lymphatic Insufficiency

Chronic Venous Disease: chronic disease of the peripheral veins includes a spectrum of diseases from edema and
tenderness to venous ulceration.

Risk factors for chronic venous disease include heredity, age, female sex, obesity, pregnancy, prolonged standing
and greater height.

Etiology and Pathogenesis

Venous ulcers occur after failure of the calf muscle pump. The heart pumps blood down to the foot; the calf muscle
pump (when standing) returns venous blood to the heart. Venous blood from the skin and subcutis collects in the
superficial venous systems including the greater and lesser saphenous veins and its tributaries, moves through the
fascia in a series of perforating or communicating veins and fills the muscle enveloped deep vein system.
With muscle contraction, the deep veins are compressed; one way valves in the deep system allow the now high
pressure flow to move against gravity and one way valves in the perforators close to prevent pressure injury in the
skin. In all patients with venous disease there is failure of these one way valves and this can result in vericose veins.
The severity of venous disease is influenced by the number and distribution of incompetent valves and is worsened
by any impairment of leg muscle function.

Any obstruction to venous return (thrombosis, radiation fibrosis, etc) or elevation of tight artrial pressure
(pulmonary hypertension, heart failure) further compromises venous return. The most commmon cause of valvular
failure is thrombosis. The nidus for venous thrombosis is typically the valve cusp, and when the thrombus is lysed by
plasmin, valve function is often lost as well. Calf muscle pump failure after deep venous thrombosis (DVT) is often
referred to as post phlebitic syndrome.

Once valves fail, especially those in the perforators, high pressure blood in the deep system reflexes into the
unsupported veins of the skin, leading to soft tissue injury, inflammation and eventually fibrosis as the subcutaneous
fat is replaced by scsar in a processed described by the term lipodermatosclerosis.

Cutaneous lesions: Once there is venous valvular failure, a rather predictable series of changes occur in the skin. The
earliest physical finding is soft tissue tenderness, even of normal appearing skin, discovered when checking for the
presence of edema by palpation. Its association with other cutaneous signs of chronic venous disease is common.

The soft tissue injury that precedes ulceration begins in the subcutis and visible changes may not appear for some
time. Frequently one notes the appearence of petechial lesions, which have the appearence of cayenne pepper
sprinkled about. As the hemoglobin in the petechial lesions breaks down, the iron remains in the skin as hemosiderin
and may lead to visible discoloration.

Stasis dermatitis: characterized by erythema, scaling, pruritus, erosions, oozing, crusting and occasional vesicles may
occur during any stage of chronic venous insufficiency. It typically occurs in the medial supramaleolar region where
microangiopathy is most intense. Over time, the lesions will lichenify.

In lipodermatosclerosis pliable subcutaneous fat is gradually replaced by fibrosis, and the skin begins to feel
indurated. This is a fibrosing panniculitis characterized by a bound down, indurated plaque that begins at the medial
ankle and extends around the entire leg. As the fibrosis increases, it may constrict and strangle the lower leg further,
impending venous and lymphatic flow and leading to brawny edema above and below the fibrosis. These late
changes resemble an inverted champagne bottle (bottle neck appearence).

Varicose veins are more noticeable when the patient is standing. Although they are usually asymptomatic, patients
may complain of symptoms of aching, cramping, itching, fatigue and swelling that are worse with prolonged
standing.

Atrophy blanche (livedo vasculitis, semental hyalinizing vasculitis) refers to skin overlying areas of fibrosis that often
appears porcelain white and atrophic. Fully established lesions of this consist of irregular, smooth, atrophic plaques
with surrounding hyperpigmentation and telangiectasis. Although mostly related to venous stasis, it may also be
associated with an underlying disorder of coagulation (coagulopathies) or autoimmune disease.

Each pharmaceutical therapy targets a specific clinical aspect of chronic venous insufficiency. Diuretics may be used
in the short term for treating severe edema. Aspirin (300-325 mg/day) and pentoxifylline may improve healing of
chronic venous ulcers. Finally, tpical steroids and emolients aid resolution of stasis dermatitis. Although all wounds
have potential for pathogens, there is no evidence that routine use of antibiotics is helpful in patients with venous
ulcers. If cellulitis is suspected, empiric therapy with coverage for S. Aureus and Streptococci is warrented. Topical
antibiotics especially mupirocin are useful for folliculitis due to these bacteria.

Pentoxifylline is a methyl-xanthine derivative with many anti inflammatory effects. There are many hypotheses
regarding the mechanism of action of pentoxifylline and its cellular and molecular effects based on human and
animal studies. It has been found to have effects on immune modulation, anti TNF alpha effects, hemorheological
effects, antifibrinolytic effects along with effects on endothelial cells and adhesion molecules.
Other venous diseases: DVT is important because the thrombosed veins are the sources of pulmonary embolisms
and the thrombosed leg may progress to chronic venous disease.

Deep Vein Thormbosis:


Clinical didagnosis of DVT is unreliable. Swelling, pain, discoloration, warmth and/or superficial venous dilation may
be seen in the involved extremity: less than one third of patients of having a DVT on clinical grounds have hte
disease.

Superficial venous thrombosis and Phlebitis:


Superficial phlebitis is the clinical finding of pain, tenderness, induration and/or erythema in a superficial vein often
associated with a palpable cord. These signs may be due to inflammation, infection and/or thrombosis. Clinically, a
thrombus is suggested by superficial phlebitis with a palpable cord that persists after a limb is raised.
Due to the possibility of co existing DVT in patients with superficial venous thrombosis, some experts recommend
compression ultrasound for all patients with lower extremity superfical venous thrombosis.