Faster Healing and a Lower Rate of Recurrence of Venous Ulcers Treated With Intermittent Pneumatic Compression

Results of a Randomized Controlled Trial

Oscar M. Alvarez, PhD; Lee Markowitz, DPM; Rachelle Parker, MD; Martin E. Wendelken, DPM, RN


ePlasty. 2020;20(e6) 

In This Article

Abstract and Introduction


Objective: Fifty-two subjects with chronic venous insufficiency and hard-to-heal lower leg ulceration (>1-year-old and >20-cm2 surface area) were treated with either intermittent, gradient, pneumatic compression (n = 27) plus standard compression therapy or compression therapy alone (control).

Methods: Compression therapy consisted of a nonadherent primary wound dressing plus a 4-layer compression bandage (n = 25). The mean age and size of the ulcers were 1.4 years and 31 cm2, respectively, and did not differ significantly between groups. Intermittent pneumatic compression was performed using a 4-chamber pneumatic leg sleeve and gradient, sequential pump. All pumps were calibrated to a pressure setting of 50 mm Hg on each subject, and treatments were for 1 hour twice daily. Evaluations were performed weekly to measure edema, local pain, granulation, and wound healing.

Results: The median time to wound closure by 9 months was 141 days for the intermittent pneumatic compression–treated group and 211 days for the control group (P = .031). The rate of healing was 0.8 ± 0.4 mm/d for the control group and 2.1 ± 0.8 mm/d for the group treated with intermittent pneumatic compression (P < .05). When compared with subjects treated with standard care, the group treated with intermittent pneumatic compression reported less pain at each evaluation point for the first 6 weeks of the trial. At weeks 1, 2, and 3, the visual analog pain scores were significantly lower for the intermittent pneumatic compression–treated group (P < .05).

Conclusion: These results suggest that intermittent pneumatic compression is a valuable adjunct to compression therapy in the management of large or painful venous ulcers.


Venous leg ulcers (VLUs) are the most common type of leg ulcers. VLUs, caused by chronic venous insufficiency (CVI) and venous hypertension, affect approximately 1% of the population and 3% of people older than 80 years.[1] VLUs most often occur in the gaiter region of the lower leg, from just below the ankle up to mid-calf. In the United States, more than 7 million people have CVI.[1,2] Normally, calf muscle contraction promotes venous return by squeezing blood in the deep veins; this pressure is prevented from reaching the superficial circulatory system by one-way valves within the perforating veins. In patients with CVI, venous pressure builds up in the superficial veins and is transmitted to the capillaries of the skin.[3] In most cases, this venous incompetence is secondary to thrombophilia, which often damages valves.[4] Three hypotheses have been proposed to explain how venous insufficiency leads to ulceration:

  1. The fibrin cuff theory proposes that fibrin gets excessively deposited around capillary beds, leading to elevated intravascular pressure. This causes enlargement of endothelial pores, resulting in further increased fibrinogen deposition in the interstitium. The "fibrin cuff," which surrounds the capillaries in the dermis, decreases oxygen permeability 20-fold. This permeability barrier inhibits diffusion of oxygen and other nutrients, leading to tissue hypoxia causing impaired wound healing.[5,6]

  2. The inflammatory trap theory, which proposes that various growth factors and inflammatory cells that get trapped in the fibrin cuff, promote severe uncontrolled inflammation in surrounding tissue, preventing proper regeneration of wounds.[7]

  3. The white cell entrapment hypothesis proposes that leukocytes trapped in the diseased vessels by reduced shear stress become activated on the endothelial surface. These leukocytes then release inflammatory mediators, leading to tissue destruction and blockage of small capillaries causing localized tissue ischemia.[8]

The hallmark to the diagnosis of CVI is hemosiderosis (staining of the skin from leaking red blood cells) in the gaiter area of the leg. The presence of microvericosoities (along the medial or lateral aspects of the mid-foot), interstitial edema, lipodermatosclerosis, stasis dermatitis, and superficial skin erosion combined with burning pain is another criterion that helps identify CVI. Frequently, patients develop CVI as a result of decreased ambulation or a gait abnormality. Therefore, they are more common with increasing age or in those with arthritis or other musculoskeletal conditions affecting normal gait.[9] Although venous ulcers are not generally prone to acute infection,[10] long-standing, untreated CVI can lead to secondary lymphedema and increased risk of cellulitis.[11] In a recent study[11] of 440 patients with lower extremity lymphedema, the most common cause was CVI or phlebolymphedema (41.8%).

The cornerstone of treatment of VLUs is compression therapy. Compression forces the fluid that has leaked into the perivascular space back into circulation. Ideal compression pressures for these patients remain unknown.

Intermittent pneumatic compression (IPC) devices have also been proven effective, but compliance and reimbursement (especially for Medicaid patients) are major hurdles. A distinct advantage of IPC therapy is that it can be done by the patient or other family member in the home with little or no training. Compression alone with multilayer or short stretch bandage systems is helpful but requires application by a skilled (trained) nurse or technician; a dedicated family member may be trained to appropriately apply the multilayer short stretch bandage system.

Venous ulcers in patients with secondary lymphedema pose a significant challenge, as these wounds are one of the most difficult to heal. These patients have significant brawny edema, fibrosis, and very large legs, making bandaging difficult as gradient compression pressures are often not achieved. IPC has been shown to accelerate the healing of venous ulcers in several randomized trials.[12–16] However, it has never been shown to be more effective than standard compression provided with short stretch or multilayered bandage systems.[13] Our goal was to investigate whether intermittent compression (IPC) assisted the healing of venous ulcers in patients with lymphedema who were already receiving standard compression with short stretch or multilayered compression therapy.