Compression Therapy for Foot Wounds: Overview and Case Reports
I nterstitial edema can impair wound healing, and while the exact mechanism is unknown, healing may be impaired by increased distance for diapedesis from capillary bed to cell, restricted ability to remove metabolites and cell debris, deposition of fibrin around the capillary bed, and plugging of capillaries by leukocytes. Armstrong1,2 demonstrated that edema reduction by intermittent mechanical compression improved the healing of foot wounds. The author presents 2 cases where multilayer compression bandages were utilized as an adjunctive measure in the treatment of foot wounds.
A 67-year-old black man developed bilateral posterior heel pressure ulcers following right knee replacement. The same complication also occurred after a left hip replacement performed 18 months earlier and a right hip replacement 6 months earlier. Each of the previous ulcerations healed in 4 months. The patient’s past medical history included type 2 diabetes mellitus, peripheral neuropathy, bilateral femoral-popliteal bypass, hypertension, and spinal stenosis.
Upon initial presentation of the most recent ulcerations, the wound base consisted of dry, black eschar (Figure 1). Arterial Doppler examination confirmed patent lower-extremity bypasses. After 8 months, the patient still had a 1-cm diameter, full-thickness skin loss at the posterior aspect of the right heel. There was red granulation tissue at the base and minimally hyperkeratotic borders (Figure 2). The patient utilized a surgical shoe for walking and a heel suspension boot when sleeping. He remained homebound except for doctor appointments. The patient took a 10-day course of trimethoprim-sulfamethoxazole 160 mg/800 mg for light growth of methicillin-resistant Staphylococcus aureus (MRSA). The wound failed to close despite 4 weeks of a collagen wound dressing (Fibracol Plus, Johnson & Johnson, New Brunswick, NJ), followed by 4 weeks of cadexomer iodine gel (Iodosorb, Healthpoint, Fort Worth, Tex), and then 4 weeks of autologous platelet-derived growth factors (Autologel, Cytomedix, Rockville, Md).
Wide excision was performed, and tissue culture again confirmed the presence of MRSA. As a result, the patient was prescribed a 10-day course of oral linezolid (Zyvox, Pfizer, New York, NY). Negative pressure wound therapy (V.A.C.Freedom®, KCI, San Antonio, Tex) was applied at a continuous pressure of 125 mmHg with a polyurethane foam. The ulcer diminished in size but became dormant again at 1.5 cm x 1 cm (Figure 3). The wound finally healed after 6 weekly applications of cadexomer iodine gel and 3-layer compression dressings (Profore Lite, Smith & Nephew, Largo, Fla).
A 75-year-old black woman with a past medical history of hypertension, chronic obstructive pulmonary disease, meningioma, and a 60 pack-year history of cigarette smoking was diagnosed with a nonhealing left foot wound. In a single surgical session, the patient underwent iliac angioplasty, common femoral to popliteal bypass, and partial third, fourth, and fifth ray resection.
One week after surgery, the lateral left foot wound measured 7.5 cm x 7.5 cm x 1.5 cm. The 2 remaining toes were affected with dry gangrene (Figure 4). The patient’s albumin level was 2.6 g/dL, and although there was no history of diabetes mellitus, alcohol abuse, or illegal drug use, the patient could not feel a Semmes-Weinstein 5.07 monofilament applied to the left foot. The progress notes on the patient stated “unlikely foot will heel.”
Nutritional deficits were evaluated and amended by a certified nutritionist. The patient was restricted to non-weightbearing on her left lower extremity. Negative pressure wound therapy was utilized for 3 weeks but discontinued due to periwound maceration. During the next month, cadexomer iodine gel and intravenous imipenem/cilastatin (Primaxin, Merck, Whitehouse Station, NJ) was used to counterPseudomonas aeruginosa (Figure 5). Approximately 2 1/2 months after bypass surgery, the patient’s foot wound was thoroughly debrided and a bilayered skin substitute (Apligraf, Organogenesis, Canton, Mass) was applied. Additionally, the 2 remaining toes were amputated, and the hallux site was closed by primary intention. One month later, the bilayered skin substitute sloughed and the hallux site partially dehisced. Culture and sensitivity identified Pseudomonas aeruginosa resistant to all antibiotics except tobramycin. Negative pressure wound therapy was resumed, and a 10-day course of tobramycin was initiated and adjusted based on peak and trough levels.
Approximately 2 1/2 months after the toe amputations and hallux closure, the left foot wound, which now included the deficit of the amputated second toe, measured 9 cm x 5 cm x 0.3 cm. Confirmation of patent bypass was achieved via Doppler ultrasound. Three-layer compression therapy was instituted due to presence of sustained, generalized lower-extremity edema. This dressing was reapplied 2 to 3 times weekly because of heavy drainage. A silver-impregnated primary dressing (Acticoat Absorbent, Smith & Nephew) was incorporated to facilitate antibiosis except when hypergranulation tissue was present, for which hypertonic sodium chloride-impregnated gauze (Mesalt, Molnlycke, Newtown, Pa) was utilized. Upon the patient’s last visit, after 3 months of compression therapy, the hallux site was closed, and the lateral foot wound measured 5 cm x 1 cm x 0.1 cm.
These 2 cases presented a unique challenge that has been reflected in previous studies— edema control in the presence of arterial disease.3,4 Callum et al.5 noted that compression bandages are dangerous when applied to limbs with arterial insufficiency. In their initial review of 600 patient records, application of compression precipitated amputation in 8 cases.5 The authors also surveyed 157 Scottish general surgery consultants.6 In the survey, the authors questioned the surgeons about the incidence of ulceration or necrosis specifically induced or aggravated by compression bandages, elastic stockings, or anti-thromboembolism stockings encountered in the past 5 years. Based on the surgeons’ responses, the authors concluded that necrosis induced by compression is common in Scotland.6 These reports may reflect improper application of compression bandages or inappropriate patient selection.
Various modifications have been utilized to combat edema in the presence of arterial disease. In the treatment of venous ulcers with relatively normal arterial perfusion, Ghauri et al.3 utilized a 4-layer compression bandage with a 50% stretch to provide 40 mmHg at the ankle. For patients with ankle brachial indices (ABIs) between 0.50 and 0.85, they applied the bandage with 25% stretch to achieve 30 mmHg. None of the patients suffered any major adverse effects with this reduced compression.3 Bowering7 utilized a 3-layer compression bandage in patients with compromised peripheral arterial circulation, as determined by the presence of any of the following: absence of pedal pulses, great toe capillary refill time greater than 2 seconds, and/or ABI 1.2. Acute progression of distal ischemia did not occur while reduced compression therapy was in place.7
In the 2 cases presented here, a 3-layer compression bandage was applied distal to lower-extremity bypass. The reduced compression level the 3-layer multilayer bandage provided was both safe and effective. Furthermore, despite the various advanced treatments implemented, compression therapy was essential in healing these foot wounds.
The benefits associated with multilayer compression bandages are low cost, easy accessibility, unrestricted mobility, and minimal effort from the patient. The benefit of intermittent pneumatic compression is a reduced risk of arterial compromise. Indeed, rapid foot and ankle compression may assist arterial perfusion in addition to assisting with edema reduction;8 however, lack of compliance is a greater concern with pneumatic compression than with multilayer compression.
As it is difficult to draw broad conclusions from the cases presented, additional research in aggressive edema reduction in pedal wounds is needed, particularly with patients with arterial insufficiency. Future research could also address whether similar results would have been achieved with use of an intermittent vasopneumatic compression device.