By Steven E. Zimmet, MD, RVT, FACPh
Sponsored by an educational grant from Medi USA.
The prevalence of leg ulceration in adults, either active or healed, is 1% to 2%, and the majority have chronic venous insufficiency.1 Although CVI has received less attention than arterial insufficiency, estimates suggest it is 10 times more common. Despite the prevalence of venous ulcers, they are often neglected or managed inadequately.
Recognition
Venous leg ulcers are generally irregularly shaped partial thickness wounds with well-defined borders surrounded by erythematous
or hyperpigmented indurated skin (acute or chronic lipodermatosclerosis). A yellow-white exudate is common. Venous ulcers are usually located on the distal medial aspect of the lower leg. Varicose veins are often present and typically there are telangiectatic veins of the medial ankle, so-called corona phlebectatica. Edema of the ankle area is common.
Differential diagnoses—including arterial, metabolic, neuropathic, neoplastic, vasculitic, infectious, hematologic, and collagen vascular diseases and pyoderma gangrenosum—should be considered. However, if arterial insufficiency is ruled out and the patient has normal pinprick sensation in the presence of a typical appearing venous ulcer, then a venous etiology will be found in about 95% of cases.2
Macrocirculation
The calf muscle pump is the primary mechanism to return blood from the leg to the heart. The calf pump mechanism consists of the calf muscles (primarily the soleus and gastrocnemius); the deep venous compartment, or pump chamber; a superficial compartment con necting the superficial veins to the deep veins via perforators; and an outflow tract (popliteal vein).
In patients with chronic venous insufficiency, limbs with venous ulceration have been shown by air plethysmography to have significantly reduced ejection fractions and higher residual volume fractions than nonulcerated limbs.3 This substantiates the significant role calf pump dysfunction plays in venous ulceration.
Calf pump dysfunction may occur because of deep venous insufficiency (primary or post-thrombotic), deep venous obstruction, perforator insufficiency, superficial venous insufficiency, arteriovenous fistulas, neuromuscular dysfunction, or a combination of these. Calf pump dysfunction results in a failure to lower venous pressure in the distal veins of the leg, a condition called ambulatory venous hypertension.
Although any of the aforementioned factors may cause calf pump dysfunction, the main factor is usually venous insufficiency. A common misconception is that a venous leg ulcer is pathognomonic of a post-thrombotic syndrome. Superficial venous disease and perforator disease alone commonly cause venous ulceration.4 The common final pathway to venous ulceration is venous hypertension, whether the overload comes from superficial, perforator, deep vein, or combination disease.
An appropriate evaluation, including (but not limited to) directed history and physical exam and duplex ultrasound imaging, is essential in the evaluation of patients with leg ulcers.
History and physical
Clinicians should seek details relating to the ulcer, such as its duration and previous treatment, the presence and characteristics of exudate, the presence, description, and severity of pain, and factors that aggravate and alleviate the symptoms. A history of similar lesions and their course and management is also useful.
In addition, ask patients for their history of thromboembolic events, varicose veins, past vein treatment, tobacco use, arterial disease, diabetes, arthritis, ankle joint immobility, inflammatory bowel disease, and collagen vascular disease. Also note their occupation and social situation.
Physical examination should include a careful inspection and palpation of the legs, from the foot to the groin, for varicose veins. The suprapubic area should also be inspected for varicosities, which might represent collateral bypass of an old iliofemoral thrombosis. Percussion of veins helps trace the origin and extent of varices. Examine for signs of CVI, such as ankle flare, eczema, hyperpigmentation, induration, and atrophie blanche. Measure ankle and calf diameters for both legs and characterize edema as pitting or nonpitting.
Describe ulcer size, base, appearance, and location as well as the condition of the surrounding skin and note the presence and characteristics of exudate and signs of true tissue infection.
Acute lipodermatosclerosis, characterized by an erythematous tender area of induration, is commonly mistaken for cellulitis.5 However, lipodermatosclerosis is an inflammatory condition that results from venous insufficiency, does not cause fever, and is unresponsive to antibiotics. Note that both lipodermatosclerosis and cellulitis may be seen in the presence of venous ulcers.6
Signs of arterial insufficiency (cool skin, loss of extremity hair, shiny and atrophic skin, pallor on leg elevation) should be noted. Arterial pulses should be palpated. If there is suspicion of arterial insufficiency, measure the ankle brachial index (ABI=systolic pressure at the ankle divided by that at the brachial artery; normal ABI is >0.9).
Note that the ABI is unreliable in assessing arterial insufficiency in patients with diabetes or other conditions in which there may be arterial calcification.7 In such cases metatarsal or toe pressures are more reliable. Evaluate ankle mobility and gait and check peripheral sensation.
Compression
There is wide agreement on the importance of compression in treating venous ulcers.8,9 Compression therapy may be done in the context of complex (or complete) decongestive therapy (CDT), which, in addition to compression therapy, consists of patient instruction in meticulous skin care, manual lymphatic drainage, and exercise.10
There are two compression phases to CDT, an initial decongestive phase followed by a maintenance phase.10-11 Generally, the adage that compression bandaging obtains a result and compression stockings maintain the result is true. However, several multilayer compression stocking options have been designed specifically to heal venous ulcers. If those options are not available, compression bandaging during the decongestive phase is done with inelastic short-stretch bandages.
Expertise in applying a short-stretch bandage is required. In the presence of concomitant arterial insufficiency, one must exercise considerable caution; it is imperative that any compression exert a low resting pressure (inelastic compression) in order not to compromise arterial flow.12 If arterial insufficiency is severe, compression of any type may be contraindicated.
Physical limitations notwithstanding, prescription compression stockings should be used in the maintenance phase of treatment. Generally a calf-length stocking with 30 mm Hg to 40 mm Hg is used, but another option is to superimpose two 20 mm Hg to 30 mm Hg stockings (yielding 40-plus mm Hg).13 Velcro-based bandages can also be useful in patients with arthritis who have a difficult time donning stockings.
Compression leads to increased venous flow, decreased pathological reflux while walking, and increased ejection volume with activation of the calf pump.14-18 Tissue pressure is increased, which favors resorption of edema fluid. Proinflammatory cytokine protein levels are elevated in ulcer tissue, and compression therapy significantly reduces these levels.19 Noncompliance with stocking use is an independent risk factor for progression of chronic venous disease.20
Ablate superficial venous disease
If a patient has hemodynamically significant superficial venous disease, either isolated or in combination with perforator or deep vein disease, important hemodynamic improvement will be obtained by treating the varicose veins. A randomized controlled trial found that treatment of underlying reflux in combination with compression therapy reduced recurrence rate compared to compression alone.21 Minimally invasive endovenous ablation modalities, such as endovenous laser, radiofrequency ablation, and foam sclerotherapy, are largely replacing stripping in the treatment of saphenous incompetence.
The hemodynamic significance of perforators in CVI remains controversial.22 Deep venous reconstruction should only be done as a last resort and probably only as part of an appropriately designed clinical study.
Ancillary measures
A detailed review of wound care is beyond the scope of this article. Note that local wound care is a matter of clinical judgment, and even optimal wound care is no substitute for compression and other measures that address the underlying pathophysiology.
Patients should be instructed to maintain a normal weight and avoid smoking and educated about physical therapy, which can improve ankle joint mobility.23 Encourage patients to take regular brisk walks. It’s helpful to have a patient periodically elevate his or her leg above heart level and to raise the foot of their bed with 6-inch blocks.
Manual lymphatic drainage performed by trained therapists can reduce edema associated with CVI. Research has shown that pentoxifylline, a drug that improves blood flow, facilitates venous leg ulcer healing when used as an adjunct to compression and may also be effective on its own.24
If a patient doesn’t respond to appropriate therapy within two to three months, the practitioner should review the adequacy of compression as well as patient compliance. The diagnosis also needs to be reconsidered.25 In particular, one should consider obtaining a biopsy of the ulcer edge to rule out malignancy.26
Conclusion
Newer methods of investigation have led to an improvement in our understanding of the pathophysiology and management of venous disease. Compression should serve as the cornerstone of treatment in patients with venous ulcers. However, one must define the basic underlying abnormality of the venous system and any associated diseases to establish a rational, individualized management plan for patients with venous ulceration.
Steven E. Zimmet, MD, is in private practice in Austin, Texas. His practice focus is phlebology and procedural dermatology.
References
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