Dr. Frykberg is podiatry chief and residency director and Dr. Banks is a research fellow, both at the Phoenix VA Health Care System in Arizona. Dr. Frykberg is a professor of practice at the University of Arizona College of Medicine in Phoenix. Dr. Banks is a professor at Grand Canyon University in Phoenix.
Author disclosures Dr. Frykberg has received research support from Osiris Therapeutics, Advanced BioHealing, AOTI, KCI, Smith & Nephew, Tissue Regenix, and ACell. All other authors report no actual or potential conflicts of interest with regard to this article.
Disclaimer The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc., the U.S. Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review the complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.
Peripheral arterial disease is directly linked to lower extremity disorders, such as intermittent claudication, pain on exertion, pain at rest, and, in severe cases, critical limb ischemia and gangrene.1 Bilateral lower extremity pulses should routinely be palpated. When dorsalis pedis or posterior tibial artery pulses are absent or diminished, Doppler segmental pressures to the toes, pulse volume recording, skin perfusion pressure, or transcutaneous oxygen evaluation is indicated, and vascular consultation should be sought.3 Ischemia is caused by peripheral arterial occlusive disease of larger vessels, not by microangiopathy.13 Poor arterial inflow is associated not only with impaired ulcer healing, but also subsequent infection, gangrene, and amputation.13
Diabetic peripheral neuropathy is characterized by loss of protective sensation, allowing ulceration in areas of high pressure. Peripheral sensory neuropathy as measured by vibration perception thresholds can impart a 3.4-fold to 32-fold risk of ulceration.19,21 Patients insensitive to a 10-g monofilament, commonly used to assess peripheral neuropathy, has been shown in several studies to convey a 2.2-fold to18-fold risk of ulceration.6,19,27,28 In the large, population-based North-West Diabetes Foot Care Study, loss of protective sensation to the 10-g monofilament increased the risk of ulceration 80%, whereas abnormal ankle reflexes increased this risk 55%.29
Peripheral neuropathy has been demonstrated as a strong risk factor for foot ulceration in many cross-sectional studies and is present in > 80% of affected patients.29 Recent studies suggested that impaired sensation makes the foot increasingly vulnerable to damage caused by mechanical, thermal, or pressure-related injury.30 Autonomic neuropathy by virtue of subsequent anhidrosis causes dryness of the skin and, therefore, vulnerability to fissuring.13
Unhealed cracks in the skin can easily lead to infection, especially in the presence of PAD. Neuropathy has an insidious and nonhomogeneous manifestation, making it difficult to identify its onset and a challenge for patients and clinicians.31,32
Sacco and colleagues reviewed current literature and the International Consensus on the Diabetic Foot recommendation and concluded that most attention is given to patients with imminent foot ulceration rather than attempting to develop and improve assessment techniques that detect early impairments.31,33 They propose that effort should be made that detect patients at risk of developing diabetic polyneuropathy. Although the 10-g monofilament pressure perception threshold is a common screening technique for early detection, tests of the vibration perception threshold may be more sensitive.
The authors propose that different monofilament sizes could probably better help determine the disease status, as the vibration tests do. In addition to the considerable subjectivity of both methods of assessing sensitivity, they are unquestionably clinical resources that can contribute to early detection of DPN. Future studies should focus on developing assessment strategies and tools that better detect early neuropathic changes. Early diagnosis of impending problems will aid in preventing further limb-threatening complications.
Treatment
The management of diabetic foot disease is focused primarily on avoiding lower extremity amputation and should be carried out through 3 main strategies: identification of the at risk foot, treatment of the acutely diseased foot, and prevention of further complications.34 The primary goal in the treatment of DFUs is to obtain wound closure. Prompt, aggressive treatment of DFUs can often prevent an exacerbation of the problem and the potential need for amputation. The aim of therapy, therefore, should be early intervention to allow prompt healing of the lesion and, once healed, prevent its recurrence.3,20,25,35
Management of the foot ulcer is largely determined by its severity (grade), vascularity, and presence of infection.3,14,36 A multidisciplinary team approach should be used due to the multifaceted nature of foot ulcers, as well as for managing the numerous comorbidities attendant with these patients. The choice of treatment methods is determined by patient and ulcer characteristics. Equally important is the ability of patients to comply with the treatment as well as with the location and severity of the ulcer.4
Rest, elevation, and removal of pressure (off-loading) are essential components of treatment and should be initiated at first presentation. Recent studies provided evidence that indicated proper off-loading promotes more rapid DFU healing.37,38 Ill-fitting footwear should be discarded and replaced with an appropriate off-loading device for mitigating pressure at the site of the ulceration. Although many off-loading modalities are currently in use, only a few studies describe the frequency and rate of wound healing associated with their use.
The total contact cast (TCC) is considered the superior standard therapy in management for neuropathic ulcers due to its proven ability to redistribute pressure, thereby promoting expeditious wound closure. Another inherent benefit is to ensure patient adherence with off-loading as well as reducing activity levels.24,39 Previous randomized controlled trials have demonstrated that patients treated with TCC healed a higher percentage of plantar ulcers at a faster rate than did patients in the control groups. One unique study demonstrated histologic evidence of more rapid angiogenesis with formation of granulation tissue in the casted group compared with the standard treatment group.40,41