Let`s Be Frank: Seeking Advice Can Be The Foundation of Optimal Wound Care

I purchased a rental home that needed an extensive renovation from the get-go 15 years ago. This same house recently required a complete re-renovation due to extensive moisture damage. I am someone who loves a good challenge, and so I gutted this property not only because it was necessary to make the home livable, but because I was in search of answers as to the “what,” “where,” “why,” and “how” everything came to be. As of this writing, my work on the house is (at least for the time being) finished, the result is better than I had expected, and I believe future problems will be prevented. During this long and physically, emotionally, and financially painful journey, which turned up everything from sluggish and corroded galvanized pipes to rain-damaged structures, many questions were raised in my mind that seemed all too familiar to the questions I ask myself while working as a healthcare clinician, such as: How often do we truly get to the underlying cause of our patients’ problems? How many of us are willing to make superficial “repairs” while forgoing the opportunity to “fix” the deeper, serious issues at large? Are we always willing to ask for help when we are unsure of what the best thing for a particular patient may be?

In my clinical experience, these questions can lead to likewise physical, emotional, and financial challenges, depending upon one’s answer. And in my recent home-improvement experiences, I continued to compare and contrast the work I was doing, the challenges I faced, and the questions I raised with my full-time wound care practice. In many instances, the same mentality that we should take with our patients applies to the same type of approach that we should take with our homes (or our cars for that matter): Do it right the first time by truly identifying the root cause and/or seek the services of a professional with proven experience if we need the help to do so.
In this column, I will discuss chronic venous insufficiency (CVI), a condition that’s cited as a commonly encountered problem that many clinicians fail to treat and seek out appropriate referral effectively, as it relates to lower extremity ulcers. 

GOOD CARE, COMPREHENSIVE PLAN

As healthcare providers, we should always have a care plan that contains measureable points (eg, comprehensive assessment and individualized treatments), fully understand the current and next steps (eg, wound care algorithm), and provide a strong foundation for justifying the “whys” behind the means we are taking to achieve an outcome (eg, wound bed preparation, controlling moisture levels). For any wound care patient, the “plumbing,” if you’ll allow me to use a rather convenient comparison, is the vascular system – the arterial/venous comorbidities inherent with any chronic wound. 

Now, if you were in my situation with the home renovation and knew there was an externally obvious problem (ie, moisture damage) that could have, at very least, internal root causes and/or future consequences, would you take shortcuts to move more quickly onto the next step or would you take the time to “get your hands dirty” and take into account everything from the inside out? Now, when it comes to, say, carpentry or any other manual labor, it can be said that in order to produce excellent work, you have to learn how to cover your mistakes. We should not be able to get away with this style of learning in healthcare, yet data continue to tell us that that we, as a wound care industry, have difficulty following established clinical practice guidelines. Ask yourself this: Do you think that every wound care patient who is ultimately healed was always given the right assessment, the right test, the right treatment, the right referral, the right product, and the right follow-up care all the time? Assuming that your answer is “no,” where does that leave those patients who don’t see their wounds healed? As it pertains to vascular health and CVI, let’s discuss some of the statistics found in the literature:

• 2-5% of all Americans have some changes associated with CVI.¹
• Approximately 1-2% of the adult population presents with lower limb ulceration, from which 70-90% of these ulcers are attributed to CVI.² 

Venous ulcers account for 80% of lower extremity ulcerations.³ 

• Compression therapy is the standard of care for venous ulcers and CVI.⁴

Surgery for venous insufficiency may be beneficial for severe or refractory cases associated with decreased rate of ulcer recurrence.⁵

• A 2010 study by the U.S. Wound Registry showed that < 17% of venous ulcer-related patients had adequate compression. More recent studies indicate an increase in this measure (> 70% for those reporting this measure compared to only 25% of venous leg ulcer visits for providers who do not report venous compression measure).
• A study to determine the effectiveness of a training workshop on compression bandaging for healthcare professionals with no prior experience in applying compression determined that, prior to training, only 5.4% of providers applied bandages in the optimal range compared to 58% after training and 37% post-training (six months). The conclusion was to have more practice over time to achieve optimal pressure range.⁶
• One study that included patients living with chronic venous ulcerations who were treated with weekly multilayered compressive dressings found that wounds < 5cm² with ulcerations present for < 6 months were more likely to heal by Week 24.⁷
• A wound that is < 10 cm² and < 12 months old at the first visit has a 29% chance of not healing by the 24th week of care, while a wound > 10 cm² and > 12 months old has a 78% chance of not healing. This can help the clinician determine whom should continue with standard of care and perhaps whom to treat with adjuvant therapies.⁸
• Compression treatment (Unna’s boot and graded elastic stocking) yielded a median heal time of 3.4 months. Normal venous refill time and patient compliance were associated with faster healing. Recurrent ulceration was 57%. Other factors associated with delayed healing included increased age, larger initial ulcer size, popliteal vein reflux, and poor response to the initial two weeks of compression treatment.⁹ 
• Approximately 15% of venous ulcers never heal and recurrence is 15-71%.¹⁰ 
• The VLU treatment algorithm recommends > 40% wound closure after four weeks of conventional therapy as a surrogate marker for the identification of patients who are likely to achieve complete wound closure with continued conservative treatment. Patients with < 40% closure at four weeks are unlikely to achieve complete wound healing and may benefit from alternative or advanced interventions.¹¹

It’s quite clear that having successful outcomes with these types of ulcers is somewhat challenging. First of all, compression is the standard of care for these ulcers, as long as no contraindications are noted. But compression is ineffective if not utilized or applied properly. Plus, the size and duration of a wound appear to affect outcomes and adjunctive interventions. The longer a patient has lived with CVI with ulceration, the greater the possibility of developing phlebolymphedema. Treatment for phlebolymphedema is different than treatment for CVI with ulceration alone. Finally, recurrence rate varies, but is that due to a patient’s nonadherence to a care plan or do we sometimes fail to properly educate all patients? Or do we not properly provide needed interventions? After all, once a wound heals the causative factor may still exist; therefore, does the patient need to continue using a compression device? If we compare lymphedema to CVI treatment, both of which share some similarities, both will progress if compression is not maintained.

When subcontracting jobs, I choose to hire individuals who are well versed in their field so that the job has the best chance of being conducted correctly, efficiently, and with fewer risks of further complications. This theory also applies to patients who are living with ulcers that limit their quality of life. As a patient advocate, when consulting or reviewing records, I frequently ask myself (or our physicians and nurses), “Why?”  If we can answer the “whys,” then we understand the purpose. If we don’t understand the “whys” and we continue to treat the patient, then that is the same as hiring the plumber to work on your house’s electrical system — except that a patient’s life hangs in the balance for the healthcare provider to consider. In my experience, the wound clinic’s collaboration with a vascular specialist for this patient population has always led to better outcomes.

COMPRESSION & CVI

To tie this back to an understanding of CVI, let’s consider a rather common occurrence: We have a patient who can develop hyperemia, congestion of the blood vessels. If we look at the capillary level, an increase of blood in this territory is attributed to the dilatation of the vessels. This is given the term “active hyperemia” when it involves dilation of the capillary arterial side. The vessels dilate due to a muscular activity, inflammation, etc., and increase the blood flow coming in. On the other hand, there’s passive hyperemia, which occurs on the venous side and is a result of venous reflux; an obstructed venous return such as compression; an obstruction of veins, clots, or heart failure as the veins, venules, and capillaries become passively dilated; or a combination of the aforementioned factors. The blood here accumulates because it can’t drain properly.

Passive hyperemia (congestion or stasis) increases the pressure in the veins. Venous hypertension, and increased inflammation of the veins and surrounding tissues, creates damage over time. Valvular incompetence is experienced and the skin may become darker or thickened. Ulcers will be difficult to heal without addressing the underlying cause. When a dysfunctional muscle pump exists, symptoms are aggravated. The venous anatomy is divided into a superficial and deep venous system in which perforator veins connect the two. Most of the blood will be located in the deep system as it makes its way back to the heart. The deep venous system is located underneath the fascia and in between the muscle. The superficial system, consisting of the great and small saphenous veins and their tributaries, is located above the fascia and superficially below the skin level. Blood returns to the heart against gravity as it collects into the superficial veins, draining into the deeper system as perforating veins piercing the fascia connect the two. This system has valves along the way to prevent retrograde blood flow. It has been reported that the main trunk of the great saphenous vein (superficial system) usually has at least six valves.¹² There are an average of five deep venous valves between the inguinal ligament and popliteal fossa, although the number varies from two to nine.¹³ There are an average of 64 perforating veins between the ankle and the groin.¹⁴ The major perforators of the medial calf and thigh have 1-3 valves that direct flow from the superficial to the deep veins.¹² These venous valves, along with the venous wall and the action of the calf muscle pump, prevent accumulation of blood in the lower extremity. When the calf muscle contracts, the veins empty blood and the valves promote a one-way directional flow back to the heart. This allows for low venous pressure post-muscle contraction.  When standing, venous pressure increases at the ankle to approximately 90 mm Hg as blood pools in the lower extremities. When walking, the pressure is reduced back to approximately 30 mm Hg, but when there’s also incompetent or damaged valves the pressure remains high and, therefore, there’s decreasing blood movement back to the heart. When laying down, the pressure is decreased to approximately 10 mm Hg. Damage to the valves, a faulty calf muscle pump, or deep vein thrombosis will yield failure to maintain low pressure in the venous system experiencing retrograde flow. Calf muscle pump ejection fraction has been measured to be approximately 65%, whereas this number decreases with active ulceration (35%), followed by limbs with healed ulcers (49%), and those without ulceration but with duplex evidence of reflux (53%).¹⁵ Decreased ankle range of motion, lack of exercise, and increasing disease process may contribute to a poor calf muscle pump. Graduated compression becomes the standard of care when treating ulcers related to venous insufficiency. It shall become part of the treatment while an active ulcer exists and for lifelong management of this disease. Surgical interventions are usually reserved when conservative measures do not produce improvements. The goal is to improve the activity of the calf muscle pump to move blood back to the heart and decrease reflux and high pressures in a low venous pressure system.

Obviously, there are various types of compression. The standard for treating venous insufficiency among patients living with ulcers has been the use of multilayer compression, but literature states that other forms of compression are better than no compression at all. The aim is to provide 30-40 mm Hg at the ankle, with a gradual decrease in pressure to the proximal leg. Additional recommendations are for patients to elevate their legs and to engage in appropriate exercise. Physical therapists are crucial in providing patients with appropriate exercise programs while wearing compression (eg, diaphragmatic breathing, improving calf muscle pump and flexibility). Selecting the appropriate form of compression for each patient and providing effective education is important to improve compliance and to decrease ulcer recurrence. Venous insufficiency may progress if treatment is not targeted to correcting the underlying problem. Progression of this disease may include skin changes such as stasis dermatitis, lipodermatosclerosis, and ulceration.  

Whether there’s collaboration across the continuum or not, it is the wound care clinician’s responsibility to understand the root of the problem for any chronic wound and to develop an effective treatment plan for any wound care patient. Be sure to be honest with your patient (and yourself) when assessing the need to consult a vascular specialist — or any specialist, for that matter. 

Frank Aviles Jr. is wound care service line director at Natchitoches (LA) Regional Medical Center; wound care and lymphedema instructor at the Academy of Lymphatic Studies, Sebastian, FL; physical therapist/wound care consultant at Louisiana Extended Care Hospital, Lafayette; and physical therapist/wound care consultant at Cane River Therapy Services LLC, Natchitoches.

References

1. Acton A. Venous insufficiency: new insights for the healthcare professional: 2013 edition. Atlanta, GA. ScholarlyEditions;2013.

2. Matic M, Matic A, Djuran V, Gajinov Z, Prcic S, Golusin Z. Frequency of peripheral arterial disease in patients with chronic venous insufficiency. Iran Red Crescent Med J. 2016;18(1):e20781.

3. O’Meara S, Al-Kurdi D, Ologun Y, Ovington LG. Antibiotics and antiseptics for venous leg ulcers. Cochrane Database Syst Rev. 2010;20(1):CD003557.

4. O’Meara S, Cullum NA, Nelson EA. Compression for venous leg ulcers. Cochrane Database Syst Rev. 2009;21(1):CD000265.

5. Barwell JR, Davies CE, Deacon J, et al. Comparison of surgery and compression with compression alone in chronic venous ulceration (ESCHAR study): randomised controlled trial. Lancet. 2004;363(9424):1854-9.

6. Tidhar D, Keren E, Brandin G, Yogev M, Armer, JM. Effectiveness of compression bandaging education for wound care nurses. J Wound Care. 2017;26(11):625-31. 

7. Margolis DJ, Berlin JA, Strom BL. Which venous leg ulcers will heal with limb compression bandages? Am J Med. 2000;109(1):15-9.

8. Quan SY, Lazarus GS, Kohli AR, Kapoor R, Margolis DJ. Digital imaging of wounds: are measurements reproducible among observers? Int J Low Extrem Wounds. 2007;6(4):245-8.

9. Erickson CA, Lanza DJ, Karp DL. Healing of venous ulcers in an ambulatory care program: the roles of chronic venous insufficiency and patient compliance. J Vasc Surg. 1995;22(5):629-36.

10. Kimmel HM, Robin AL. An evidence-based algorithm for treating venous leg ulcers utilizing the cochrane database of systematic reviews. Wounds. 2013;25(9):242-50. 

11. Phillips TJ, Machado F, Trout R, Porter J, Olin J, Falanga V. Prognostic indicators in venous ulcers. J Am Acad Dermatol. 2000;43(4):627-30.

12. Mozes G, Carmichael SW, Gloviczki P. In: Gloviczki P, Yao JST, ed. Handbook of Venous Disorders: Guidelines of the American Venous Forum. 2nd ed. London: Arnold;2001. 

13. Negus D. In: Dodd H, Cockett FB, ed. The Pathology and Surgery of the Veins of the Lower Limb. 2nd ed. Edinburgh: Churchill Livingstone;1976. 

14. Thomson H. The surgical anatomy of the superficial and perforating veins of the lower limb. Ann R Coll Surg Engl. 1979;61(3):198-205.

15. Araki CT, Back TL, Padberg FT, et al. The significance of calf muscle pump function in venous ulceration. J Vasc Surg. 1994;20(6):872–7.