Unraveling Compression Science
What to do when the standard of care does not work?
Have you ever had a patient who presents with what seems to be a garden-variety venous leg ulcer (VLU), but it just won’t heal?
Meet Joe. His self-reported past medical history was significant for hypertension (HTN), obesity, and diabetes mellitus. Joe presented to an outpatient clinic with a history of a nonhealing wound on his lower leg, which had progressively worsened over the last six weeks despite a round of oral antibiotics and topical antibiotic cream prescribed by his primary medical doctor. He had significant hemosiderin staining and moderate edema in both lower extremities.
All of the guidelines were followed, and it was established that there was adequate circulation. The wound bed was prepared with adequate debridement of devitalized tissue, a primary wound dressing was applied to promote moist wound healing, followed by the application of a boxed compression bandage marketed to provided therapeutic compression of 30 mm Hg to 40 mm Hg. Despite the gold standard approach, the patient returned five days later, and the wound was larger. The periwound was macerated, and the patient expressed discomfort, reporting that the bandage was too tight and was making his wound worse. After assuring the patient that compression was the key, additional absorptive dressings were applied and he was rewrapped in the same compression application and sent on his way with an appointment to return one week later. Thus began a seemingly endless cycle of recurring visits marked by switching out of primary wound dressings and continuing with the same approach to compression, with little to no progress in wound healing. For clinicians experiencing a similar cycle, they are left scratching their heads and asking, “Why won’t the wound heal?” Or, perhaps they are contemplating advanced wound dressings that will require additional copays for the patient, which he cannot afford. It would appear they are stuck in the VLU cyclical storm.
Before you, or your patient, lose hope, let us reexamine the current treatment plan to look for opportunities for treatment modification. This begins with our own knowledge of the etiology of VLUs and the basics of compression science.
What do we know?
Venous leg ulcers, defined as open skin lesions (typically arising on the medial side of the lower leg between the ankle and knee) that occur in the presence of venous disease, are one of the most prevalent wound types seen in wound centers.1 Characteristically, VLUs are shallow in depth, have irregular margins, are highly exudative, may be painful, and can be slow to heal.2 The etiology of VLUs is often mixed, potentially involving chronic venous insufficiency (CVI) related to venous reflux and obstruction, lymphedema, local trauma, and infection, among other conditions.1,2
What is the standard of care for VLUs?
Reducing venous hypertension and/or reflux is key to the management of VLUs. Compression therapy, in the form of compression bandages, wraps, or garments, is an essential component in the management of VLUs and is universally incorporated into established treatment pathways.3-5
How does compression work?
The main function of compression is to counteract effects of gravity, which is the key factor for the disturbance of the venous and lymphatic return from the lower extremity in patients with CVI and VLUs.6 In a healthy individual, the venous pressure in the lower leg is approximately 10 mm Hg in the supine position.7 In the standing position, the pressure increases up to 80 mm Hg to 100 mm Hg depending on the body height.7,8 With an intact calf muscle pump, the pressure is reduced to approximately 25 mm Hg.8 For patients with CVI, the ambulatory pressures consistently exceed 40 mm Hg, with some studies demonstrating venous pressure in excess of 90 mm Hg with exercise.9 The goal of compression is to restore the competence of the venous system, which involves promoting increased venous return, reducing venous HTN, and optimizing lymphatic function.
How much compression is appropriate?
Therapeutic compression levels for the management of VLUs are subjectively reported as30 mm Hg to 40 mm Hg in clinical practice. However, a thorough review of the literature provides conflicting messages to the reader. Cited in the literature, prominent compression specialists have highlighted the following key points: “high compression of 40 mm Hg should be considered for a person with an adequate vascular supply indicated by an ankle-brachial pressure index of 0.8 to 1.2”2; and “experimental studies in the past have demonstrated that an IP of 60 mm Hg in the upright position, together with the massaging effect at calf level, are required to reduce venous reflux.”10 To further complicate the understanding of compression science, many of the studies evaluating the effectiveness of compression applications in the clinical setting often do not provide IP measurements outside of the manufacturers’ stated values.
To best understand compression science, one must understand two basic facts. First, the goal of compression is not to squeeze the fluid out of the limb (ie, tighter is not better). Far too often, clinicians apply compression bandages with a mindset that they are engineering the compression dosage, or the effectiveness of the compression application, by how tightly the bandage is applied. However, one must remember that too much pressure applied at rest, or too high of a dosage, can result in localized tissue injury, pain, and possibly impairment of limb circulation. Yes, dosage, or resting pressure, is important, but it is not the sole determinant of the efficacy of a bandage. An analogy that patients may be able to relate to is the use of a knee brace to support a bad knee. If the brace is too loose, it does not offer any support. However, if it is too tight, it will not allow proper movement or function of the knee. Compression is a brace to support the veins and lymphatics so that they may work better, and it should be applied with the mindset to support—not hinder—circulation.
Second, compression pressure is not static. Pressures produced under a compression application fluctuates withchange in position (supine, sit, stand), movement (active or passive), and volume changes. It is this fluctuation in pressure from a lower pressure at rest, to a higher working pressure that provides the massaging effect often referenced in the literature.11 Elevated pressure created by movement intermittently blocks the venous reflux and increases the volume expelled, reducing the ambulatory venous HTN. The repetitive, temporary elevated pressure created by movement or a change in position provides the hemodynamic force to lower venous HTN, reduces venous reflux, and stimulates the lymphatic system. A stiff, inelastic compression application has been shown to be most therapeutic.12
Muldoon10 beautifully summarized this concept, stating “that although 40 mm Hg has been cited as being optimal therapeutic pressure, it is now known that variation in pressures in the lying and standing positions yield better clinical outcomes.” The take-home message is not that we should be looking for an exact number but rather the dynamic range afforded by the compression textile. If expected results are not observed, then we need to work up from there to modify compression to produce a stiffer compression application.
What does this mean for Joe?
Let us go back to the patient and look a little closer. In order to optimize healing, a few details were integral to planning therapeutic compression for Joe.
Joe is 6’4” tall and weighs approximately 395 lbs. The circumference of his ankle is 35 cm. He has obstructive sleep apnea and prefers to sleep in his recliner.
Why is this information important?
Standard compression applications are engineered to provide 30 mm Hg to 40 mm Hg at the ankle in order to address the anticipated elevated hydrostatic pressure of an individual of average height, weight, and ankle circumference. Joe’s tall stature and large ankle circumference were not accommodated by standard compression applications. His elevated stature and weight predisposed his venous system to hydrostatic pressure that was significantly higher. As noted by A. Hopkins, in the presence of height greater than 180 cm (5’9”), traditional compression applications act as reduced or light compression13; this explains the onset of the destructive cycle of uncontrolled edema, excessive exudate, progressive erosion of the periwound, and increased pain.
How can we engineer the bandage to provide therapeutic compression?
Joe needed a compression application that could produce higher working pressures to outmatch his underlying venous hypertension. This was achieved with a stiffer bandage. Stiffness of a bandage is determined by the number of layers, including the degree of overlap and friction between the layers, and the elastic property of the textile itself.14 Additionally, different forms of padding can be used to provide distribution of the pressure evenly across the skin/wound surface in areas of concavities (ie, medial malleoli) or excessive skin folds. In Joe’s case, progressively increased stiffness, moving from a two-layer to a four-layer bandage to, finally, a multi-component lymphedema bandage, was utilized in order to build in a stiffness profile to optimize healing.
What did we learn?
The wound care mantra is to look beyond the hole in the leg to the whole patient. Similarly, we must think beyond the box, as not every patient will fit into the box. As healthcare clinicians, we must be prepared to utilize our knowledge of compression science to optimize compression selection and applications to match our patients’ needs. Finally, we cannot forget what happens when the patient leaves the clinic. Where do they sleep? How do they walk? Are they activating their calf muscle pumps? Do they routinely and properly take their medications? If we do not ask, we do not know.
Suzie Ehmann, PT, DPT, CWS, CLT-LANA, is Certified Lymphedema Therapist at Atrium Health Stanly and a member of the Wound Care Learning Network Editorial Board.
References
1. Harding K, Dowsett C, Fias L, et al. Challenging passivity in venous leg ulcer care - the ABC model of management. Int Wound J. 2016;13(6):1378–1384. doi:10.1111/iwj.1260
2. Alavi A, Sibbald RG, Phillips TJ, et al. What's new: management of venous leg ulcers: treating venous leg ulcers. J Am Acad Dermatol. 2016;74(4):643–666. doi:10.1016/j.jaad.2015.03.059
3. O'Donnell TF Jr., Passman MA, Marston WA, et al. Management of venous leg ulcers: clinical practice guidelines of the Society for Vascular Surgery and the American Venous Forum. J Vasc Surg. 2014;60(2 Suppl):3S–59S. doi:10.1016/j.jvs.2014.04.049
4. Harding K, Dowsett C, Fias L. Simplifying venous leg ulcer mangement: consensus recommendations. Wounds Int. May 8, 2015. https://www.woundsinternational.com/resources/details/simplifying-venous-leg-ulcer-management-consensus-recommendations
5. Ratliff CR, Yates S, McNichol L, Gray M. Compression for primary prevention, treatment, and prevention of recurrence of venous leg ulcers: an evidence-and consensus-based algorithm for care across the continuum. J Wound Ostomy Continence Nurs. 2016;43(4):347–364. doi:10.1097/WON.0000000000000242
6. Partsch H. Compression therapy: clinical and experimental evidence. Ann Vasc Dis. 2012;5(4):416–422. doi:10.3400/avd.ra.12.00068
7. Hettrick H. The science of compression therapy for chronic venous insufficiency edema. J Am Col Certif Wound Spec. 2009;1(1):20–24.
8. Recek C. Calf pump activity influencing venous hemodynamics in the lower extremity. Int J Angiol. 2013;22(1):23–30.
9. Nicolaides MS, Hussein MK, Szendro G, Christopoulos D, Vasdekis S, Clarke H. The relation of venous ulceration with ambulatory venous pressure measurments. J Vasc Surg. 1993;17(2):414–419. doi:10.1067/mva.1993.37694
10. Muldoon J. Interface pressures with compression systems: relevance to clinical practice. Br J Community Nurs. 2019;24(Sup10):S32–S35. doi:10.12968/bjcn.2019.24.Sup10.S32
11. Partsch H. Compression heals leg ulcers due to abolishment of venous reflux. J Wound Care. 2019;28(7):427. doi:10.12968/jowc.2019.28.7.427.
12. Mosti G, Mattaliano V, Partsch H. Inelastic compression increases venous ejection fraction more than elastic bandages in patients with superficial venous reflux. Phlebology. 2008;23(6):287–294. doi:10.1258/phleb.2008.008009
13. Hopkins A, Bull R, Worboys F. Needing more: the case for extra high comprssion for tall men in UK leg ulcer management. Veins Lymphat. 2017;6(1). doi:10.4081/vl.2017.6630
14. Partsch H, Mortimer P. Compression for leg wounds. Br J Dermatol. 2015;173(2):359–369. doi:10.1111/bjd.13851
