Abstract and Introduction
Abstract
Management of VLUs can be challenging, depending on wound complexity, and may require the use of several treatment modalities to achieve complete wound closure or significant wound area reduction. This review presents a systematic approach to management of VLUs based on previous literature and the authors' clinical experience, with consideration given to wound size, etiology, and responses to prior treatment. Techniques described include debridement (autolytic, enzymatic, sharp/surgical), compression therapy, physical therapy, medical adjuncts, and cellular- and tissue-based therapy. The algorithm of care for VLUs is multimodal. Appropriate diagnostic studies must be performed, including venous duplex and appropriate pathophysiology to confirm the diagnosis of VLU. After the correct diagnosis is confirmed, appropriate treatment may commence. All patients should undergo appropriate wound debridement; the exact modality used is dependent on wound characteristics. Patients must also adhere to consistent compression therapy. Any underlying venous disease that is amenable to surgical intervention should be addressed. Treatment with a medical adjunct and physical therapy are recommended. For patients who do not achieve significant wound area reduction, the addition of CTP is recommended. Use of these methods should result in substantial wound area reduction and/or wound closure.
Introduction
The first priority when managing a VLU is making the appropriate diagnosis. A clinical history and physical examination are paramount. Appropriate noninvasive imaging is also necessary, along with measurement of ABI. VLUs are open lesions between the knee and ankle joint that occur in the presence of venous disease.[1] Such wounds are not necessarily the result of venous hypertension. Thus, there is somewhat of a disconnect between the diagnosis of an ulcer that occurs in the leg with underlying venous disease and an ulcer that occurs secondary to underlying venous disease. A large number of studies do not make a distinction between these 2 very distinct wound types.[2]
The development of venous ulcers is a debilitating consequence of CVI. Tissue breakdown and ulceration results from chronic dermal inflammation, leading to dermatitis. The inflammatory response stimulated by venous hypertension causes extravasation of macromolecules and red blood cell products into the dermal interstitium and alterations in the extracellular matrix that deposits disorganized collagen, which allows for persistent and sustained dermal injury.[3] The characteristic skin changes seen are brawny induration, thickening, edema, and eventual tissue breakdown. The Clinical-Etiology-Anatomy-Pathophysiology classification system is often used to aid in identifying CVI clinically. This descriptive classification is composed of 7 stages, from C0 (no venous disease) to C6 (open and active ulcer).[4] This system takes into account clinical signs including the presence of varicose veins, reticular veins, telangiectasia, edema, pigmentation, skin changes, and presence of ulcers. Although the diagnosis of CVI is primarily clinical, it is important to confirm with imaging studies. However, there is a role for other dermatologic evaluation. A comprehensive history is also necessary, including evaluation for other skin manifestations of inflammatory conditions, such as rheumatoid arthritis, systemic lupus, and scleroderma. Other atypical diseases and hematologic disorders such as sickle cell anemia, thalassemia, hemochromatosis, and protein S and protein C deficiency may also manifest as chronic skin conditions. Although these diseases can occur in the setting of venous disease, they are not caused by venous disease. Therefore, treatment in these cases is aimed at the primary underlying pathophysiology.
A study published in 2018 in France followed the French health authorities' guidelines that if there is no clinical improvement after 6 months and/or atypical clinical signs persist, biopsy should be performed.[5] In that study, biopsy findings were positive in 5% of the lower extremity ulcers that fit these criteria. In patients without a clear etiology of leg ulceration, however, early biopsy is indicated because waiting 6 months could potentially delay diagnosis.
Although the majority of lower extremity ulcers are attributed to CVI, a significant number of lower extremity ulcers are the result of both arterial and venous disease. These so-called mixed ulcers account for up to 26% of lower extremity ulcers, and they are defined by the absence of pedal pulses, reduced ABI (<0.90), inflow stenosis greater than 50%, superficial or deep venous insufficiency, and/or deep venous thrombosis at ultrasound.[6] As previously mentioned, physical examination and noninvasive imaging studies are important in determining the etiology of the wound. Without a correct diagnosis, a patient may undergo weeks or months of treatment without obtaining the desired results.
Another potential contributor to nonhealing lower extremity ulceration is the relationship between the venous system and the lymphatic system. In patients with CVI, the lymphatic systems can be overloaded, leading to phlebolymphedema—that is, combined venous and lymphatic insufficiency.[7] When lymphatic channels become overloaded, increased fibrosis of interstitial tissue is observed with large protein concentration in the tissue, which ultimately results in skin infections and ulceration.
Wounds. 2022;34(12):288-296. © 2022 HMP Communications, LLC
