Compression Therapy for Foot Wounds: Overview and Case Reports

Author(s): 
Steven Miller, DPM

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.

Case 1

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).

Case 2

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).

References: 

References

1. Armstrong DG, Nguyen HC. Improvement in healing with aggressive edema reduction after debridement of foot infection in persons with diabetes. Arch Surg. 2000;135(12):1405–1409.
2. Wunderlich RP, Armstrong DG, Harkless LB. Is intermittent pulsatile pressure a valuable adjunct in healing the complicated diabetic wound? Ostomy Wound Manage. 1998;44(10):70–76.
3. Ghauri AS, Nyamekye I, Grabs AJ, Farndon JR, Poskitt KR. The diagnosis and management of mixed arterial/venous leg ulcers in community-based clinics. Eur J Vasc Endovasc Surg. 1998;16(4):350–355.
4. Treiman GS, Copland S, McNamara RM, et al. Factors influencing ulcer healing in patients with combined arterial and venous insufficiency. J Vasc Surg. 2001;33(6):1158–1164.
5. Callam MJ, Harper DR, Dale JJ, Ruckley CV. Arterial disease in chronic leg ulceration: an underestimated hazard? Lothian and Forth Valley leg ulcer study. Br Med J. 1987;294(6577):929–931.
6. Callam MJ, Ruckley CV, Dale JJ, Harper DR. Hazards of compression treatment of the leg: an estimate from Scottish surgeons. Br Med J. 1987;295(6610):1382.
7. Bowering CK. Use of layered compression bandages in diabetic patients. Experience in patients with lower leg ulceration, peripheral edema, and features of venous and arterial disease. Adv Wound Care. 1998;11(3):129–135.
8. Ramaswami G, D’Ayala M, Hollier LH, Deutsch R, McElhinney AJ. Rapid foot and calf compression increases walking distance in patients with intermittent claudication: results of a randomized study. J Vasc Surg. 2005;41(5):794–801.



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