, Coleen Napolitano1, 2, Daniel Miller3 and Francis J. Rottier1, 2
(1)
Department of Orthopaedic Surgery and Rehabilitation, Loyola University Stritch School of Medicine, 2160 S. First Ave, Maywood, IL 60153, USA
(2)
Hines Veterans Administration Hospital, Hines, IL, USA
(3)
Podiatry, St. Joseph Medical Center, Kansas City, MO, USA
Keywords
Foot ulcerUlcer preventionWound careUlcer debridementOff-loading foot woundsThe number of cases of diabetes diagnosed internationally is rapidly growing and is expected to reach 366 million by the year 2025 [1]. The annual incidence for diabetic foot ulceration is between 1 and 7 % with a lifetime risk of 15–25 % in patients with diabetes. Diabetic foot ulcers (DFU) are thought to develop from atherosclerosis, peripheral neuropathy, or a combination of these two disorders [2, 3]. Additionally, problems such as foot deformity, callus formation, motor imbalance, and trauma play a role in ulcer formation [4, 5]. Approximately 15 % of diabetic foot ulcers result in amputation and contribute to more than 85 % of all diabetes-related amputations.
Patients with foot ulcerations perceive themselves as disabled as those patients with a lower limb amputation [6]. Several studies have shown a relationship of diabetic foot ulcers to mortality in patients with diabetes. Reportedly, the 5-year mortality rates for patients affected by diabetic foot ulcers are near 50 % [7]. Clearly, a diabetic foot ulcer is a marker of disease severity.
As this chapter evolves, wound assessment, vascularity/tissue nutrition, local care, compression and off-loading, debridement, advanced therapies, and surgical care will all be discussed.
Ulcer Evaluation and Classification
Finding the initial cause for ulceration is critical for the wound resolution . A history of recurrent wounds with prior difficulties, infection, and the impact on patient mobility is critical to providing care for the patient. Once vascularity and sensation have been assessed, the wound is evaluated for its relation to musculoskeletal deformity and local callus formation [6]. The ulceration is measured for size (including length, width, and depth) as well as inspection with a probe to evaluate for sinus tracts or a probe-to-bone finding. The wound margins are evaluated for undermining necrosis, purulence, and percent of granulation tissue. Pain and malodor are also assessed.
The clinician must also be aware of cellulitis and gangrene, osteomyelitis or related Charcot foot deformity. Ankle mobility is important to assess especially for chronic and recurrent forefoot ulcerations.
The most well-established diabetic foot ulcer rating systems are those developed by Wagner [8], Armstrong, and Lavery (University of Texas) [9] (Table 45.1). While the Wagner system is the most simplistic and easy to use, the University of Texas system better defines ulcer depth, infection, and ischemia (Table 45.2).
(The premise being that all feet up to a Grade 4 can be converted back to a Grade 0 foot.) | |
Foot grade | Lesion type |
0 | No open wound |
1 | Superficial ulceration in epidermis to dermis |
2 | Deep ulcer to tendon or joint capsule |
3 | Deep ulceration with abscess, osteomyelitis, or joint sepsis |
4 | Localized gangrene—forefoot or locally on heel |
5 | Gangrene of foot—unsalvageable state |
Table 45.2
University of Texas Diabetic Wound Classification -modified [9]—helps to differentiate infected and ischemic wounds
Wound grade | Depth | |||
|---|---|---|---|---|
0 | 1 | 2 | 3 | |
A | Pre-ulcer | Superficial wound | Tendon/capsule—no infection | Bone/joint—no infection |
B | Closed with cellulitis | Superficial wound, cellulitis | Tendon/capsule, cellulitis | Bone/joint—infected |
C | Closed with ischemia | Superficial wound, ischemic | Tendon/capsule, ischemic | Bone/joint, ischemic |
D | Closed, B + C | Superficial, B + C | Tendon/capsule, B + C | Bone/joint, B + C |
Treatment of foot ulcerations involves management of arterial disease, providing an appropriate wound healing environment, infection control, wound protection, and advanced wound therapies should the wound fail to improve.
Vascularity and Tissue Nutrition
As ischemia may be a factor in foot ulceration development and nonhealing, when pulses are absent, assessment of blood flow is pursued. Doppler ultrasonography is commonly utilized to determine whether adequate perfusion exists in the extremity to heal the foot ulceration. The ischemic index is a ratio of the systolic Doppler pressure at the ankle to the brachial systolic pressure. An ischemic index of 0.5 or greater is thought to be necessary to support wound healing. An ankle-brachial index of 0.45 in the patient with diabetes has been considered adequate for healing as long as the systolic pressure at the ankle was 70 mmHg or higher. These values are falsely elevated and non-predictive, in at least 15 % of patients with peripheral arterial disease. This is primarily due to the non-compressibility of calcified peripheral arteries. Other forms of noninvasive vascular testing can be considered when ABIs are unreliable. This would include the use of transcutaneous partial pressure of oxygen (TcPO2), measurement of skin perfusion pressure (SPP), and the toe brachial index (TBI) [10]. A vascular laboratory can measure toe pressures as an indicator of arterial inflow to the foot. The arteries of the hallux are less commonly found to be calcified than the vessels of the leg and at the level of the ankle [11–14]. The accepted threshold for toe pressure is at least 30 mmHg. Consultation with a vascular specialist should be obtained for patients who do not have adequate inflow demonstrated on these exams.
For nonhealing wounds , the review of nutritional status is obtained by measuring the serum albumin and the total lymphocyte count (TLC). The serum albumin should be at least 3.0 gm/dL and the total lymphocyte count should be greater than 1500. A serum albumin level of 3.5 g/dL or less indicates malnutrition. Serum prealbumin levels can also be considered when nutritional competence is border line. Prealbumin levels are thought to be a better measure when determining the effects of nutritional supplementation due to its short half-life. Normal prealbumin levels range from 6 to 35 mg/dL. The TLC is calculated by multiplying the white blood cell count by the percent of lymphocytes in the differential. When these values are suboptimal, consultation with a nutritionist is helpful to assist with optimizing the patient before definitive amputation. Surgery in stabilized patients with malnutrition or immunodeficiency should be delayed until these issues can adequately be addressed. When infection or gangrene requires urgent surgery, the goal should be to eradicate infection and eliminate necrotic tissue to viable margins. Deep tissue or bone cultures are taken to direct antibiotic therapy while the patient’s nutrition and vascularity are optimized [15–18]. Patients with severe renal disease may never achieve desirable nutritional parameters. Local wound care attempts may still be pursued, but at known higher risk for failure.
Poor glycemic control has been identified as a risk factor associated with a higher frequency of amputation [19, 20]. Hyperglycemia will deactivate macrophages and lymphocytes and may impair wound healing. There is also a higher risk of urinary tract and respiratory infections when glucose levels are uncontrolled. Ideal management involves maintenance of glucose levels below 200 mg/dL [18]. Caution must be taken in managing the ulcerated patient’s glucose with calorie reduction. This may lead to significant protein depletion and subsequent wound failure. If the patient’s BMI is normal, 25 cal/kg is required to maintain adequate nutrition and avoid negative nitrogen balance.
The combined wound healing parameters of vascular inflow and nutritional status have been shown to significantly affect healing rates for pedal wounds. Optimizing the patient’s nutritional parameters and achieving adequate tissue perfusion will limit the risk of wound complications and failure.
Local Wound Care
Acute vs Chronic Ulceration
Ulcers can be classified as acute or chronic. Acute ulcerations usually heal within a short period of time. A chronic ulcer is one that has failed to proceed through an orderly and timely process to produce anatomic and functional integrity or proceeded through the repair process without establishing or maintaining a sustained anatomic and functional result within 3 months [21]. The exact factors that contribute to producing a chronic wound are not known but likely involve both local and systemic factors. It is important to understand the normal healing process of Hemostasis/Inflammatory phase, Proliferative phase, and the Remodeling phase whether you are treating an acute or chronic wound. Factors that can adversely affect healing such as vascular disease, uncontrolled or poorly controlled metabolic disorders, malnutrition, pressure relief, and edema control have already been addressed and will not be repeated. Discussion here will focus on topical wound care management and topical wound care dressings.
Topical Therapies
The application of combining substances in the topical care of wounds has been recorded back to 2000 BCE. The Ancient Egyptians had specific details on how to clean the wound and prepare the wound for application of the topical compounding substance [22, 23]. Traditionally topical wound care had been directed at creating a dry wound. Winter is credited with recognizing the importance of a moist wound environment for more rapid wound healing [24, 25]. The primary goal of any wound care is to facilitate resolution of a wound by creating an environment ideal for wound healing. A wound dressing alone will not heal a wound. A wound dressing has ideal components which include the removal of excessive exudate, maintain a moist wound environment, protect against contaminants, cause no pain or trauma with dressing changes, leave no debris within the wound, and provide thermal insulation [24]. Wound characteristics should be evaluated and your choice of wound dressing should match the wound.
Antimicrobial topical agents have been utilized to reduce the microbial bioburden of the wound. Iodine, honey, and/or silver has been the most commonly utilized antimicrobial products and has been used topically or incorporated into various wound dressing products. Iodine has been used for over 100 years without any bacteria resistance. Free iodine combines irreversibly with tyrosine residues of protein to result in oxidase reaction that adversely affected normal cellular metabolism. The use of iodine has declined due to the potential for toxic effects to human fibroblast. Newer versions of iodine-containing products have a sustained delivery of bactericidal concentrations to moist wounds without apparent tissue damage [26]. The newer products also have properties that can absorb up to seven times its weight in exudate. Iodine-containing products are not recommended if there is an allergy to iodine or if the patient is on lithium.
Honey has beneficial antimicrobial effects related to the osmotic effect produced by the high sugar content and the presence of an enzyme that produces hydrogen peroxide. Different honeys have not exhibited the same antimicrobial effect. Medical-grade honey is recommended and has unidentified non-peroxide factors that exert an even higher antimicrobial activity. Medical-grade honey is resistant to denaturing by heat or light and still be effective if diluted [27]. Honey products should not be used if there is an allergy to bee venom.
Topical agents with silver have been utilized in wound care for over 100 years. The effectiveness of silver products varies from bacteriostatic to bactericidal. The bactericidal effect of silver is directly proportional to the silver ions in the wound exudate. The mechanism of action includes the ability of the positively charged silver ion to attract the negatively charge cell wall and enter the bacterial cell. The interaction of the silver ion and bacterial thiol damages/blocks the cell wall, membranes, respiratory enzymes, and ribonucleoproteins [28]. Silver dressing should not be used in persons who may have an allergic reaction to metal and should not be used with enzymatic debriding agents. Prolonged use of silver is not recommended as it may be toxic to keratinocytes and fibroblasts. Although silver dressings have been the subject of case series, there have no reported results from a well-designed clinical trial [26]. Bergin and Wright failed to locate any clinical study pertaining to the use of silver dressing for the treatment of foot ulcers that would qualify for the Cochrane systematic review criteria [29].
Topical antimicrobial agents have a potential role in wound care but do not replace the need for sharp debridement of a wound bed to remove necrotic tissue and bacteria/biofilm. Steed et al. found that wounds without debridement had a 75 % nonhealing rate, while wounds treated with debridement had a 20 % nonhealing rate [30]. Moist to dry dressings for wound coverage and debridement is no longer universally accepted as a gold standard for diabetic wound care. The use of moist to dry dressings should be reserved for grossly contaminated wounds and when removal of necrotic tissue must be performed faster than use of autolytic or enzymatic measures . A moist to dry dressing does not permit selective debridement of only necrotic tissue as it can leave gauze fibers within the wound and can be painful when changed, and the moisture of the dressing may evaporate too quickly to maintain a moist wound environment [24, 31].
Enzymatic agents have been utilized for wound debridement. Collagenase is an exopeptidase and is derived from Clostridium histolyticum. Collagenase specifically digests the denatured collagen on the wound base [32]. This enzymatic agent can be deactivated by such elements as pH, heat, silver, peroxide, and some antibiotics.
A biological debriding agent is medicinal maggots. Maggot therapy is regulated by the FDA for the debridement of wounds. Maggots are applied to the wound bed, 5–10 larva/cm2, in a maggot-confined dressing which secures the maggots within the wound bed. The dressing has a porous net overlying the maggots and then an absorptive out layer for exudate. Medicinal maggots are left on the wound for up to 72 h. Although maggot therapy has been proven effective in wound debridement of necrotic tissue, pain can be associated with this debridement method. Contraindications for the use of maggots include bleeding disorders, deep tunneling wounds, and ischemia [33].
Other debriding methods include autolytic debridement. The autolytic debriding agents are used to help address the moisture imbalances, allowing the enzymes within the wound to digest damaged extracellular matrix and necrotic tissue. The debridement process by the use of autolytic agents is a slow process. Hydrogels and hydrocolloids are examples of autolytic debriding agents. (Surgical debridement will be addressed later in this chapter.)
The hydrogels are an insoluble hydrophilic polymer, a three-dimensional structure containing either polyethylene oxide or carboxymethyl cellulose and 90 % water. The high water content permits the hydrogel to donate moisture [22, 25, 34]. Hydrogel products come in sheets, gels, or gauzes. The use of hydrogels should be reserved for a noninfected wound since most have no antimicrobial properties. Hydrogels should be used on wounds with minimal exudate.
Hydrocolloid products are autolytic debriding agents. Hydrocolloids have a hydrophilic polymer inner layer and a water-resistant outer layer. Unlike hydrogels, the hydrocolloid dressing absorbs the exudate. The wound exudate interacts with the inner layer as it is absorbed and forms a gel that conforms to the wound base. The gel prevents the disruption of the wound base with dressing changes. The gel material that forms over the wound can vary in color from yellow to light brown and should not be mistaken for pus. The hydrocolloids are to be used in wounds with low to moderate exudate. Dressing changes can vary depending on the wound exudate but may be left in place up to 7 days or when fluid leaks. The wound environment under the hydrocolloid dressing is acidic (pH 5). This acidic environment has been shown to inhibit Pseudomonas aeruginosa and Staphylococcus aureus [35]. Some hydrocolloid products have odor-controlling properties. The hydrocolloid dressing can also assist in shear/friction protection.
Foam dressings assist in shear protection and cushioning over boney prominences while providing thermal insulation. Foam dressings are for wounds with moderate to heavy exudate. The foam dressings have a highly absorptive hydrophilic polyurethane or silastic inner membrane and a hydrophobic outer film layer [36, 37]. The outer film of the dressing provides a barrier to water and bacteria. Some foam products have adhesive borders but most require a secondary dressing. Variations of the foam products include cavity filling or spreadable versions. Caution should be used not to fill cavity more than 50 % with foam as expansion of the foam may prevent wound from contracting.
A very highly absorptive wound care product is the calcium alginates . A calcium alginate product is a biodegradable dressing that is derived from brown seaweed. Alginate products may be used on high exudating wounds. The alginates can absorb 20 times its weight in exudate. The interaction of the calcium ions of the alginate and sodium ions from the exudate forms a soluble gel that provides the moist wound environment. The absorptive ability of the alginate across the entire wound, “lateral wicking,” can lead to periwound maceration if the alginate overlaps the adjacent skin [38]. Active release of the calcium ion of the alginate can assist with hemostasis. Alginates may assist in antimicrobial activity by bacteria from the wound exudate becoming trapped in the dense fibers of the alginate [39]. Alginates are available in sheet and rope versions and can be used in wound sinus or tunneling wounds. The alginates do require a secondary dressing. The time frame for dressing changes would be directly proportional to the amount of exudate. Although alginate dressing product is reported to be biodegradable, residual product in a wound can result in inflammation and pain.
Bioengineered products have been developed to assist in the healing of chronic wounds. Delay in the proliferative and remodeling phase is when the use of these products is traditionally warranted. Included in the advanced bioengineered products are the collagen products. Collagen is the major protein of the extracellular matrix. The collagen dressings absorb excess matrix metalloproteinases (MMPs) that can lead to a chronic wound, to degrade the collagen of the product thus protecting the patient’s collagen within the wound. The degradation process of the collagen in the wound dressing also protects other growth factors from degradation. The different collagen products have various types of collagen, denatured (gelatin) and/or native (Type 1) [40]. The collagen difference determines which of the MMP the product is targeting. Collagen products are usually derived from ovine, bovine, porcine, or equine so allergic reactions are possible (Fig. 45.1).
Fig. 45.1
Application of ovine forestomach dressing to lateral ray amputation wound. Note non-adherent dressing over this with Steri-Strip application for stability. This type of dressing is changed every 3–5 days. This product is a collagen base that will absorb MMPs to promote healing
Other advances in bioengineered wound care have been the production and use of skin substitutes and biologic cellular therapies and membranes [41]. These products are developed to facilitate wound healing with as many key features of skin as possible including but not limited to growth factors, cytokines, and human keratinocytes. Products vary as to whether they have inductive or conductive properties. These products are effective in providing a wound environment to facilitate healing, but these products are also associated with high manufacturing costs.
A wound care product does not heal a wound. There is no single wound care product designed to be utilized from wound origin to complete wound repair. The wound care provider needs to understand that wound healing is a dynamic process. The wound care specialist must be prepared to adapt the wound care plan to accommodate the changing wound needs.
Compression Therapy
Compression therapy is widely considered a first-line efficacious treatment in the managemen t of ulceration of the lower extremity. Multiple studies have indicated the superiority of compression therapy versus standard wound care in the treatment of foot and leg ulceration, provided the etiology of the wound is clear and that confounding factors such as nutrition and various comorbidities are properly addressed by the clinician. Compression therapy relieves edema and stasis of the lower extremity by reducing distention of the superficial venous system and assisting the calf muscle pump. Compression may also help stimulate healthier granulation tissues within wounds and decrease presence of pro-inflammatory cytokines in wound exudates [24, 42]. Prior to the initiation of compression therapy, baseline noninvasive vascular studies should be considered to ensure adequate circulation to the involved limb with interventional cardiology or vascular surgery consultation if needed.
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