Skip to main content

Pneumatic Compression for Venous Stasis Ulcers and the Implications of Lymphedema On Delayed Wound Healing

  The hallmark for virtually all protocols of care for venous stasis ulcers is limb compression in one form or another.1 Compression therapy decreases capillary filtration, reduces venous reflux, and attempts to reverse the edema caused by venous valvular incompetence by aiding venous return to the circulatory system. Though numerous types of compression methods exist,1,2 multi-layered compression bandages, combined with limb elevation and appropriate wound dressings, have become the accepted standard of care for treating venous leg ulcers.1,3,4 An obvious limiting factor, however, is that patients have difficulty remaining compliant with standard leg ulcer therapy. Compliance is a multifaceted issue, but one overriding problem is that leg ulcer patients often fail to wear their compression bandages due to discomfort or difficulty with application. In many cases, the level of compression required for optimal effectiveness is greater than the patient can tolerate, either due to skin integrity issues or pain.6 Bandages either feel too tight or physical limitations impede the patient’s ability to don stockings of a sufficient level of compression.6 There is an ongoing struggle to balance the goals of patient compliance and comfort against the need for clinically effective levels of compression. This is but one reason to consider use of a pneumatic compression device (PCD) as an adjunctive treatment for venous stasis ulcers (VSUs), as they are easy to administer and provide supplemental active and dynamic compression treatment that patients can use comfortably and consistently at home.

  Research on the use of pneumatic medicine in the treatment of VSUs is not robust but studies that do exist have been analyzed in at least three systematic reviews.2,7,8 Although limitations in study design have been recognized, support exists for the use of PCDs in combination with standard compression treatment and local wound care to enhance healing of VSUs, especially chronic, nonhealing ulcers.6-11 Review papers by Kalodiki8 and Comerota & Aziz12 make compelling cases for pneumatic compression by summarizing the physiologic benefits that studies have shown. These include hemodynamic changes (such as decrease in venous stasis and increase in venous velocity) and hematological changes (such as enhanced fibrinolytic activity), in addition to decreased intravascular coagulation and improved healing rates of VSUs. One hypothesis suggests that PCDs work by:

  ... “collapsing the superficial venous system and forcing blood into the deep system and thus increasing subcutaneous pressure, thereby preventing the leakage of blood, fibrin, and protein from the skin capillaries.”13

  The improved fibrinolytic activity indicates that, in addition to circulatory benefits, the removal of potentially harmful toxic wastes occurs during treatment with pneumatic compression.12,13 Chen et al14 reviewed the physiological mechanisms of action with PCD use. They concluded that, despite the wide acceptance of PCD use in the treatment of venous disease, the exact mechanisms of action in venous ulcer healing are still unclear and there may be biochemical benefits that have yet to be determined. The mechanical shear and strain on vascular endothelial cells have been shown in animal and cell culture models to result in the release of biochemical mediators that may further create a physiological environment conducive to healing (ie, tPA: tissue plasminogen activator; NO: nitric oxide; TFPI: tissue factor pathway inhibitor).14 Several investigators have proposed that the increase in fibrinolytic activity was secondary to increased tPA release from endothelial cells. General consensus contends, however, that the improved healing rate of VSUs with PCD treatment likely results from a combination of increased interstitial pressure (which directs fluid back into circulation), improved cutaneous oxygenation, and the clearance of metabolic toxins.

  Some PCDs are specifically designed to stimulate lymphatic vasculature. It is believed that these devices provide a therapeutic impact on the lymphatic system that results in the movement of stagnant, protein-rich fluid away from the peri-wound area, thereby enhancing the healing environment. It is well established that the venous and lymphatic systems are closely related and that longstanding venous disease leads to lymphedema.15-17 Chronic venous insufficiency (CVI) leads to venous hypertension, resulting in high filtration pressure and increased fluid in the interstitium that requires drainage by the lymphatic system. The lymphatics compensate by working hard to fill and empty at an increased rate. Over time, however, the lymphatic vessels are unable to meet the demand of fluid removal and become mechanically damaged, resulting in lymphedema.18

  It is important to note that the venous and lymphatic vessels have specific roles in fluid movement and the role of each system cannot be ignored in wound healing. Tissue fluid that is drained by the veins includes mostly water and small- to medium-sized plasma proteins and other substances. The lymphatic vasculature, by contrast, drains large protein molecules, lipids, excess water the veins cannot uptake, and cellular debris (eg dead cells, bacteria, viruses, etc.). Lymph capillaries are able to resorb and transport the large protein molecules that the venous capillaries cannot. It is therefore the lymphatic system’s role to remove the bulk of protein and other macromolecules that would otherwise remain stagnant in the tissue, creating an environment conducive to repeat infection. “This aspect of lymphatic physiology is highly relevant to wound care. When the efficient and timely removal of macromolecules fails to occur, growth factors, proteases, pro-inflammatory and pro-algesic molecules accumulate. This results in dysregulation of interstitial homeostasis and, potentially, metaplasia or breakdown of the dermis and subcutaneous tissues.”18

  Lymphatic damage in CVI occurs due to chronic inflammation resulting from the increased fibrinogen-rich protein concentration in the tissues, which leads to macrophage, fibroblast, and lymphocyte cell proliferation with further development of edema and induration.15 Endothelial damage and dilatation of the lymph vessels follows. When this combined venous/lymphatic failure occurs, there are obvious barriers to wound healing, as oxygen and nutrients are unable to get to the wound site to enable repair and tissue regeneration.

  Though physiology and pathophysiology provide a basis of understanding the various mechanisms of action of pneumatic medicine, the literature is limited and does not provide solid guidance with regard to appropriate device selection when treating VSUs. While there seems to be a clear benefit in using pneumatic medicine for VSU treatment, no comparative studies have been published that definitively establish the most effective type of device, optimal pressure levels, or appropriate treatment times. Seen throughout the literature are fairly broad statements about PCD use. This lack of device specificity fails to distinguish pump types or delineate how various devices deliver the therapy. Generally, however, the literature suggests that use of multi-chamber, gradient, programmable devices may yield better outcomes than simpler devices, and those with rapid-inflation and short cycle times facilitate quicker healing.8 Although no studies directly compared single-chamber devices with multi-chamber devices, there is evidence that use of a single-chamber device leads to trapping of venous blood in the distal veins, while their more sophisticated, sequential, gradient counterparts result in more complete emptying of the deep veins.8 It has also been emphasized that single-chamber devices apply pressure in all directions, thereby distributing fluid laterally and distally as well as proximally.12

  One of the initial barriers in clarifying appropriate PCD usage in the literature and current practice is that clinicians and professional societies are not aware of how PCDs are classified and then reimbursed by third-party payers, nor are they aware of the distinctions in mechanisms of action among varying PCD types. PCDs are classified by the Centers for Medicare & Medicaid Services (CMS) using the Healthcare Common Procedure Coding System (HCPCS) into three distinct groups—from mechanically simple to technically sophisticated devices:

  E0650 – A non-segmental pneumatic compressor that has a single outflow port (ie, one chambered garment that inflates all at once and then deflates all at once).

  E0651- A segmental pneumatic compressor without calibrated gradient pressure, which has multiple outflow ports leading to distinct segments on the garment (ie, chambers inflate sequentially but have the same level of pressure in each segment or have a predetermined pressure gradient in successive segments but no ability to set or adjust pressures individually in each segment for customized treatment).

  E0652- A segmental pneumatic compressor with calibrated gradient pressure and manual control on at least three outflow ports to deliver an individually determined pressure to each segmental unit (ie, multi-chambered with ability to customize programming of pressures and often treatment sequences to address unique clinical needs).

  Note: There are also separate codes for each garment (referred to as an “appliance” by CMS) used in treatment of specified areas of the body. They too are classified based on whether they are non-segmented or segmented, and, furthermore, whether they apply gradient pressure.

  To further complicate the choice of appropriate PCD, the use of traditional, non-programmable PCDs has been denounced in recent years by clinicians well versed in the anatomy and micro-physiology of the lymphatics and their interplay with the vascular system, in light of risks associated with these devices. The detrimental effects of some types of PCDs, although reported scarcely in the literature, have been observed consistently in clinical practice. Many of the older and simpler PCDs apply higher static compression than is deemed clinically suitable and that is intolerable to patients, resulting in decreased compliance and poor clinical outcomes. Limited reports have indicated that the higher levels of pressure may potentially damage fragile lymphatic vessels.19,20 Other negative outcomes attributed to use of non-programmable PCDs include the development of a fibrotic cuff at the limb root and onset or worsening of edema in other areas of the body such as the genitals, trunk and chest.21

  When evaluating the appropriate PCD for a complex vascular or lymphedema patient, treating clinicians tend to distinguish between PCDs by what a specific device type can safely and effectively treat, rather than by HCPCS coding terms. For instance, a device chosen for a patient with swelling confined to the ankle and foot may differ from the device chosen to treat CVI with VSU and co-morbid lymphedema with significant pain, or edema extending proximally to the thighs and trunk. Conversely, payers rely on codes associated with technical descriptions of devices with little or no acknowledgement of the known physiology and clinical symptoms that may dictate a specific mechanism of action. When asked about PCD use, clinicians are often unaware of the coding and technical descriptions, but tend to be quite aware of risks associated with the home use of many simpler devices.

  Making a distinction between VSU patients with lymphedema and ulcer patients without accompanying lymphedema may be a useful decision-making criterion in selecting the appropriate device. Peri-wound edema and specifically lymphedema have been identified as significant impediments to venous ulcer healing, though it has not been clearly defined exactly how lymphedema inhibits wound healing. Experts agree that long-standing CVI will generally result in lymphatic damage and eventually lymphedema,15-17 and research has shown that lymphatic function was reduced in ulcerated limbs compared with normal limbs, and in edematous legs compared with nonedematous legs.22 Lymphedema in the VSU patient has significant negative implications for wound healing including: 1) inhibited delivery of oxygen and nutrients; 2) impaired removal of toxins and inflammatory proteins; 3) increase in wound exudates with consequent skin maceration; 4) increased risk of infection. Use of a PCD designed to enhance lymphatic drainage—thereby removing proteins and waste that the venous system cannot absorb—may be the appropriate option for a patient with chronic, non-healing VSU.

  In recent years a new group of “advanced” or “new generation” PCDs have become available to address the shortcomings of older generation PCDs. These advanced devices, still classified as E0652s, were designed to stimulate lymphatic drainage. Similar to the principles applied by therapists in manual lymph drainage, these devices generally use gentler, dynamic pressures intended to mobilize high-protein lymph fluid out of the compromised limb, rather than “squeezing” fluid into the venous system. These advanced devices incorporate truncal treatment and begin with proximal treatment that progresses distally, with subsequent repetitive distal-to-proximal treatment. The need for truncal treatment is necessary in patients whose VSU is complicated by lymphedema because protein accumulation in the interstitial space creates osmotic pressure strong enough to congest the full lymphatic contributory region. This requires decongestion of not only the distal extremity, but also the full extremity and adjacent truncal quadrant as well.23 The lymph vessel system is divided into lymphatic drainage territories governed by lymph nodes and divided by watersheds which delineate the direction of flow. When a patient with intact lymph nodes still presents with chronic swelling, both the venous and lymphatic systems are working at maximum capacity yet are still overwhelmed. Sufficiently treating the full territory is important because the limb and the adjacent truncal quadrant both drain to the same lymph node group, which requires that the fluid be manually or mechanically redirected to a healthy, functioning region.

  Simpler, non-calibrated PCDs that lack programmability and trunk appliances are ineffective if the proximal circulation is also congested, as is often the case in patients with long standing CVI and non-healing VSUs that are complicated by uncontrolled edema.23 Initial lymph vessel capillaries are just 2mm beneath the skin. Occlusion of the vital and delicate lymph capillary structure by using a simpler “squeeze and hold” type compression pump occludes resorption by the initial lymph capillaries, setting the stage for perpetual and progressive swelling. Left behind is a protein-rich edema in the tissue, perpetuating the continual attraction of water, owing to the hydrophilic nature of proteins. Therefore, CVI patients with chronic VSUs that have additionally developed lymphedema will likely demonstrate optimal outcomes with a device that employs a mechanism of action conducive to stimulating the lymphatics, in addition to providing treatment of the truncal quadrant. Efficacy of at least one of these advanced systems has been demonstrated for lymphedema treatment,24-26 and preliminary work suggests the capability of the device to enhance healing of a variety of wound types, including venous leg ulcers.27 Although to date there have been no published randomized controlled trials on the use of these advanced PCDs in the treatment of VSUs, increasing clinical practice has supported their use.

  Clinicians must be guided by their best assessment of the patient’s pathophysiology and expected ability to tolerate the level and type of pneumatic compression. For example, a programmable device is invaluable to patients with marked pain at the ulcer site, while patients who do not have significant pain may be able to tolerate non-programmable devices. In addition to efficacy, tolerance and comfort are also essential to achieve compliance.

  PCDs that employ a pressure profile compatible with the principles of MLD may offer a more complete treatment for patients who have phlebolymphedema28 and VSUs because the mechanism of action stimulates lymphatic transport.26 These new generation devices that purport to be compatible with lymphatic stimulation employ various mechanisms of action, however, and must be assessed independently from one another, as there are differences among the devices in the applied levels of pressure and the inflation/deflation cycle times.29 Clinicians need to understand the desired physiological effects and take into account the various mechanisms of action each device employs to choose the most appropriate device for optimal treatment of VSU and lymphedema. Training and education of clinicians on coding, selection, and appropriate use of PCD is needed to facilitate more robust and comprehensive studies on use of PCDs as adjunctive treatment of VSUs and chronic wound healing (with or without associated lymphedema), which in turn will help establish clear guidelines and protocols.

  Cecilia M. Cervantes, MD, CWS, CLT is currently the Medical Director, at HealthSouth, The Center for Wound Care and Hyperbaric Medicine in Austin, TX.

  Sharon Orphey, PT, FACCWS, CLT, in the Physical Medicine Department at Baylor Medical Center at Irving, in Irving, TX.

  For the complete list of references for this article please visit

Cecilia M. Cervantes, MD, CWS, CLT and Sharon Orphey, PT, FACCWS, CLT
Back to Top