In my recent WoundSource webinar on management strategies of venous leg ulcers (VLU), I discussed the complex pathophysiology of VLUs and procedural interventions that can help them reach closure. VLUs comprise the majority of lower extremity ulcers. These wounds are costly to treat and have a high rate of recurrence. Sequelae of VLUs include infection or sepsis risk, pain, loss of mobility, and possible amputation. Healing of VLUs requires an understanding of their multifactorial etiology, consideration of patient-specific risk factors, careful assessment, and best practice management for optimal clinical outcomes. The following categories of VLU prevention, management and treatment can help to answer some of the most frequently asked questions about VLUs.
A crucial thing to remember as we treat our patients’ leg ulcers is that they do not occur in a vacuum. Most of the time, leg ulcers have a multifactorial etiology. It is important to determine the main causative factor and address it while looking at other factors. For instance, a VLU can be distal to the malleolus in a diabetic patient and still be mainly secondary to an engorged varicose vein or venous disease. Diabetes then becomes a factor in non-healing, but there is a distinct venous cause of the ulcer.
There are many ways to differentiate VLUs from atypical causes of leg ulcers. First, it is very important to take a thorough history. Does the patient have a history of sickle cell disease? Is there a history of hepatitis B or C or rheumatoid arthritis (vasculitis)? What symptoms accompany the leg ulceration? If the patient is also experiencing joint pain, muscle weakness, finger or toe pain, “purple” areas on the skin (petechiae or purpura), or other systemic symptoms, it is time to think outside of the box.
Vasculitic ulcers are typically very painful. They may appear more inflamed than a chronic VLU, but this is not always the case. Sickle cell ulcerations generally occur near the medial and lateral malleolus and are also often very painful. The classic sign of pyoderma gangrenosum is that the ulcer generally worsens with trauma, sharp debridement, or any insult to the ulcerated or surrounding area. Pain, history, clinical examination, and symptoms are your best cues. If you are uncertain about whether you are looking at a VLU or a “zebra” ulcer of atypical etiology, you can also use your diagnostic tools. Sickle cell ulcers are caused primarily by micro-ischemia rather than by venous insufficiency, but the two may happen concurrently. A venous reflux study result may be negative in a patient with either vasculitis or sickle cell–related ulcerations, although this does not fully rule out a venous component.
Remember to check the ankle-brachial index (ABI) on nearly all patients with VLUs to help rule in or rule out an arterial component, and look at toe pressures in your diabetic patients. Mildly compressive garments are not optimal, but they can be a good way to obtain some compression in our patients who do not tolerate more aggressive therapy. These lightly compressive garments are usually acceptable in patients with concurrent peripheral arterial disease, unless the ABI is less than 0.5. For more specific ABI and compression guidelines, fast-forward to 39:40 in my recent webinar on VLUs.
Venous Reflux Studies
We all practice in different environments, and sometimes access to diagnostic studies is limited. I reserve venous reflux studies for patients who are likely good candidates for procedural intervention: usually at least somewhat ambulatory, able to get to a clinic or facility where the procedure can be done, and fairly adherent to other recommended therapies. Venous reflux studies should also be considered a priority in patients with non-healing ulcerations when all other factors have been addressed. If a patient is tolerating compression and/or the ulcer is closing at an acceptable trajectory, these studies can be reserved in patients who have difficulty obtaining them.
Prevention of post-thrombotic syndrome (PTS) is a hot topic right now! Previous studies recommended that compression therapy be consistently utilized for two years after deep vein thrombosis (DVT) to prevent PTS. However, current research recommends that compression therapy be used only in the management of PTS and not for prevention. I typically teach patients to employ the tactics we use for prevention of chronic venous insufficiency (CVI) in general. Avoidance of prolonged standing without rest or calf muscle exercises, leg elevation when possible, healthy diet, smoking cessation, and diabetes management will help prevent CVI. If a patient has DVT with subsequent edema, varicose veins, or other signs or symptoms of CVI, compression therapy will be indicated.
Some is better than none. I feel that the best kind of compression is the one that our patients will utilize—within guideline recommendations, of course. When considering compression, one of the most important things to consider is safety. Remember to check those ABIs! Compressive elastic (ACE) wraps are generally not an optimal option in the treatment of VLUs both because of their elasticity and because it is difficult to control the amount of pressure exerted by an ACE wrap. I never say never, but ACE wraps are not something I use in my everyday practice. One of the other things we need to be aware of is the patient’s cardiac status. Compression therapy can be absolutely safe to use in a patient with congestive heart failure (CHF). Here is that history piece again! How regularly does the patient weigh in? How often does he or she see a cardiologist or primary provider for CHF? How is the patient’s breathing?
In the case of CHF, I auscultate lung sounds and assess the patient’s overall status. I work closely with the patient’s cardiologist or treating provider, usually by telephone. If a patient is not weighing himself or herself regularly, or is dyspneic or has signs of CHF exacerbation, I will hold off on aggressive compression and talk with the patient’s provider. I sometimes check laboratory data and always try to play an active part in helping the patient follow—or see a provider to obtain—their CHF self-management principles. Very rarely will I alter a patient’s diuretic therapy without first talking with the treating provider. In cases where the patient’s CHF is stable, I begin unilateral compression and instruct the patient and caregivers on warning signs and when to call the office.
If a patient follows up with their provider regularly, does not have signs or symptoms of worsening CHF, and is taking medications as prescribed, I will institute compression. Another frequent question with compression is utilization in active cellulitis. Studies have shown that compression therapy in patients with cellulitis can help speed recovery and prevent venous complications down the line. In the case of severe cellulitis, I typically encourage leg elevation until appropriate antibiotics have been initiated and then begin compression. In cases of mild cellulitis, compression can be utilized. If I have any concerns about antibiotic therapy or the patient’s status, I see the patient in clinic more quickly (three to four days) than I might in the absence of cellulitis, or I engage the patient’s home health team to help ensure improvement with compression. It used to be that compression therapy was recommended after DVT to prevent PTS.
Newer research has shown that this may not be effective, however, and compression therapy is now recommended for the management, but not prevention, of PTS. In active or acute DVT, as long as the patient is being treated with anticoagulation or has undergone procedural intervention and is anticoagulated, compression therapy is recommended when there is concurrent CVI. I recommend working closely with the patient’s vascular medicine team in these cases, however, because each case is unique. Intermittent pneumatic compression pumps are generally not as effective as consistent application of multilayer compression bandages, but they can offer an adjunctive option for patients who do not tolerate multilayer bandaging. These pumps are also a viable option for bedridden patients. Thromboembolic deterrent (TED) stockings are utilized for DVT prevention in bed-bound patients and should not be used in the treatment of VLU. Although we value inelastic bandages in compression therapy for VLUs, the question has been raised whether such rigid bandaging limits ankle mobility enough to compromise calf muscle pump activity. At this point, while ankle mobility may be slightly compromised, this is not thought to contribute enough to alter the recommendation for multilayer wraps.
The patient’s location also plays a role in treatment. If a patient is in a long-term care or acute care setting, unique challenges are presented. If a patient remains ambulatory and the facility already has staff members trained in compression wrapping or is willing to train them, this is a viable option. I typically work closely with the facility’s clinical and administrative leadership in determining the best products to utilize in these settings. In the acute care setting, I generally prefer iodine-based dressings over silver according to the guidelines, but this is not always a possibility. It is appropriate to continue a patient’s compression bandaging while in these locations. First-line therapy for VLUs should always involve compression (depending on the presence of peripheral arterial disease) and follow moist wound healing principles.
Physical therapists (PTs) are crucial not only to the field of wound management in general, but especially in the management of VLUs. If you have access to PTs, especially wound-trained PTs, utilize them. PTs can help with ankle mobility and calf muscle pump action, patient positioning, leg elevation, compression wrapping, management of lymphedema, strengthening, and, in many cases, dressing management and more.
Topical Steroids and Hydrochlorous Acid
There is a role for topical steroids in CVI-associated dermatitis. The key with topical steroids is to use caution because chronic inflammation of the skin can increase systemic absorption of the steroid and cause skin atrophy, thus risking ulceration. A short course of topical steroids can improve stasis dermatitis. There is also a role for hypochlorous acid in the treatment of VLUs, especially if bioburden is of concern.
There is also a definite role for autolytic debridement in treatment of VLUs. Although sharp debridement is preferred for necrotic ulcerations, autolytic debridement is important also. There are hypertonic products, an enzymatic product, and others that can be useful in assisting the autolytic process.
Insurance coverage of radiofrequency ablation (RFA) or endovenous laser ablation (EVLA) can often be difficult. I recommend documenting the medical necessity from day one on seeing the patient to help with this quest. If we document pain, pruritus, edema, ulceration, infection, leg fatigue, and failure of aggressive and consistent compression therapy, this has helped in our practice. I often do peer-to-peer appeals for these procedures. If we cannot obtain coverage for RFA or EVLA for greater saphenous vein reflux, we often look at treating underlying perforators or varicose veins and consider sclerotherapy or phlebectomy if appropriate. Some studies have shown EVLA to be more effective than RFA for the treatment of saphenous veins larger than 10mm in diameter with quicker return to function.
Venous ulceration is a complex medical condition that requires knowledge of underlying causes, pathological features, and treatment strategies. Management often focuses on local wound care and compression therapy, but for best outcomes, we must take into account the whole patient, including comorbidities, risk factors, treatment setting, and mobility issues.
Lim CS, Davies AH. Graduated compression stockings. CMAJ. 2014;186(10):E391–8. Mese B, Bozoglan O, Eroglu E, et al. A comparison of 1,470-nm endovenous laser ablation the treatment of great saphenous veins of 10 mm or more in size. Ann Vasc Surg. 2015;29(7):1368–72.
Minniti CP, Eckman J, Sebastiani P, Steinberg MH, Ballas SK. Leg ulcers in sickle cell disease. Am J Hematol. 2010;85(10):831–3.
Roaldsen KS, Elfving B, Stanghelle JK, Mattsson E. Effect of multilayer high-compression bandaging on ankle range of motion and oxygen cost of walking. Phlebology. 2012;27(1):5–12.
Treadwell TA. Demystifying compression: answers that may surprise you. Online continuing education webinar. 2011. https ://www.slideshare.net/3MSkinWoundCare/3m-health-care-compression-webcast.
About the Author
Karen Bauer is a certified Nurse Practitioner. She graduated with a BA in Sociology from the University of Toledo and an MS from the Ohio State University. She has been practicing as a nurse practitioner for 12 years, with 10 of those years being in the field of wound management and vascular medicine. She currently practices at the University of Toledo Medical Center as well as multiple outreach sites encompassing ambulatory clinics, long-term care, and acute care centers. She is certified as a wound specialist through the American Board of Wound Management and currently serves as both the Director of Wound Services at the University of Toledo and the Program Director at the Fulton County Wound and Hyperbaric Center. She is a nurse board member of the Association for the Advancement of Wound Care and serves on the editorial board of Ostomy Wound Management. She is a published researcher and is currently projected to graduate with her Doctorate of Nursing Practice in the Spring of 2019. She loves dogs, yoga, and watching her daughter play soccer.
The views and opinions expressed in this blog are solely those of the author, and do not represent the views of WoundSource, HMP Global, its affiliates, or subsidiary companies.