In addition to emphasizing the correlation between gait abnormalities and diabetic forefoot ulcerations, these authors discuss the impact of equinus and motor sensory neuropathy, how diabetes affects wound healing and keys to successful offloading.
There are currently 24 million people in the United States who suffer from diabetes mellitus.1 A recent study estimates that one out of three American adults will be diagnosed with diabetes mellitus by the year 2050.1
With many well documented medical conditions associated with diabetes mellitus, peripheral neuropathy remains the most significant causal factor for complications of the diabetic lower extremity.2 The diabetic population in the United States contributes to the highest percentage of non-traumatic lower extremity amputations, many of which are directly associated with the presence of diabetic forefoot ulcerations.3 The diabetic foot ulcer is among the most destructive complications associated with diabetes mellitus because of the physical, social and economic strains placed upon the patient. Many of these patients experience a considerably decreased quality of life.4,5
The most documented locations of forefoot ulcerations include: the plantar surface of metatarsal heads, digital tufts of the hallux and lesser digits, the dorsomedial aspect of the first metatarsophalangeal joint, and the dorsal aspect of the interphalangeal joints of the lesser digits.6 We strongly believe the incidence and location of diabetic forefoot ulcerations are in direct correlation to the gait abnormalities that occur in patients with diabetes.
Neuropathic gait pattern changes include significantly slower walking speeds, prolonged stance phase, decreased joint movement of the lower extremity (hip, knee, ankle) and higher ground reactive forces, which are most costly in the sagittal and frontal planes.7 Without proper gait analysis and evaluation during the comprehensive patient assessment, ulcer recurrence and treatment failure become more prevalent.
For the purposes of surgical planning and intervention, the podiatric surgeon must address the pathomechanical transformations that occur with neuropathic gait patterns in the presence of plantar forefoot ulcerations.
Johnson and Christensen have described equinus as the “the most profound causal agent in foot pathomechanics and frequently linked to common foot pathology.”8 Ankle equinus is defined as less than +5 degrees of dorsiflexion of the ankle joint with the subtalar joint in neutral position and the midtarsal joint locked with the knee extended.9 Lavery and colleagues determined that non-enzymatic glycation and significant abnormalities of fibrillar density and fibrillar diameter of the Achilles tendon lead to shortening of the gastrocsoleus complex.10,11 These dynamic pathomechanical changes increase peak forefoot plantar pressure in the patient with diabetes three times more than that of non-diabetic patients.10,11 This ultimately leads to the tissue breakdown and ulcer formation. Therefore, addressing the equinus deformity is a crucial component of the algorithm in resolving and healing diabetic foot ulcerations.
Conservative management of equinus includes a comprehensive regimen to reverse the contractures of the gastrocsoleus complex. This regimen may include stretching exercises, night splints and physical therapy. Several studies have demonstrated that using an appropriate stretching exercise routine as the primary treatment for equinus has a statistically significant improvement in ankle joint dorsiflexion in comparison to other modalities.12 As physicians, it is essential to document and demonstrate to patients the importance of adducting the foot 10-15 degrees to unlock the midtarsal joint during stretching exercises to allow for the greatest stretching benefit.11-13
Surgical management of the equinus deformity, of course, consists of the highly debated tendo-Achilles lengthening and gastrocnemius recession. Both procedures have well documented benefits.14 Several studies, however, support the gastrocnemius recession as superior because it provides better healing potential, controlled lengthening of the entire posterior complex and avoids potential over-correction.15 In comparison to a gastrocnemius recession, there may be over-correction with the tendo-Achilles lengthening if one has not addressed the influence of the gastrocnemius soleus complex.15
Diabetic peripheral neuropathy is a multifocal disease process. Treatment is often devoted toward strict glycemic control and symptomatic treatment of sensory neuropathy.16 Pharmaceutical companies spend millions of dollars annually on research and development for treatments of sensory neuropathy aimed at the diabetic population.17 Motor neuropathy, on the other hand, has a much more subtle presentation. It often goes unexamined and the effects on the lower extremity consistently go unrecognized.18
In a study of 169 consecutive patients with diabetes, Ishpekova and colleagues showed that nearly 60 percent of the patients suffered from motor sensory neuropathy in comparison to 18.6 percent with pure sensory neuropathy without the presence of detectable motor deficits.19 The most common manifestations of motor neuropathy in the lower extremity consist of atrophy of the anterior leg extensor musculature; atrophy of the plantar intrinsic musculature; hammertoe deformities secondary to a prolapsed metatarsal head and fat pad displacement; hallux valgus deformity; neuropathic ulceration; and gait instability.19
With the culmination of all potential deformities and abnormalities stemming from motor sensory neuropathy, the risk of diabetic forefoot ulcerations increases exponentially. Additionally, Anderson and colleagues concluded in a previous study that “patients with diabetes have ankle weakness with a significant decrease in available dorsiflexion as a result of motor neuropathy associated with diabetes, and that the degree of weakness was related to the degree of neuropathy.”19,20
Conservative treatment to accommodate the associated manifestations of motor neuropathy includes: diabetic shoes with custom moldable insoles; extra depth shoes; bracing and orthotics; or physical therapy for gait and strength training. One should initiate adjunctive surgical intervention in combination with conservative care in the presence of rigid hammertoe deformities to minimize the risk of ulceration or amputation. The current surgical recommendations regarding digital deformities triggered by motor neuropathy are a primary phalangeal joint arthrodesis or digital flexor tendon transfer.18 Prior surgical approaches often consisted of a more traditional arthroplasty. However, due to the overwhelming evidence of digital instability caused by motor neuropathy, many surgeons have proven arthrodesis to be more favorable.18
Diabetes mellitus is a progressive metabolic disorder characterized by an abnormal hyperglycemic state, which often negatively affects wound healing by producing abnormal granulation tissue as a result of altered protein and lipid metabolism.21 As a result, wound healing phases are delayed, specifically re-epithelialization and remodeling, due to the predominately abnormal collagen metabolism and collagen cross-linking necessary for wound healing.22 These changes generate a highly inflexible wound bed and unstable framework prone for tissue breakdown and reulceration.22 The presence of diabetic autonomic neuropathy exacerbates these changes due to the patients’ loss of thermoregulatory abilities. Similar to the subtle changes that occur with motor neuropathy, indications of autonomic dysregulation are frequently disregarded during physical examination. Advanced testing such as the quantitative sudomotor axon reflex test (QSART) and the thermoregulatory sweat test (TST) are modalities clinicians can use to quantify the body’s sudomotor function and sweat response, and confirm the extent of autonomic neuropathy.23 These tests usually occur at a testing center under the supervision of a qualified neurologist.
The natural physiological process of wound healing consists of four phases: hemostasis, inflammation, proliferation and remodeling. This process is well orchestrated with overlapping between each phase. Hemostasis occurs within the first hour of injury and begins with vasoconstriction of blood vessels and the clotting of platelets. Inflammation may take up to seven days. This phase is mediated with neutrophils and monocytes that clear out bacteria, promote chemotactic factors and release growth factors at the site of injury. Proliferation begins early in the injury and will last for about 20 days. This development begins the process of angiogenesis in which macrophages, growth factors and angiotensin initiate the formation of granular tissue. The last phase, remodeling, involves extensive remodeling of collagen and epithelial tissues to organize the construct into a stronger, more rigid scar.24
The pathophysiology of wounds in the diabetic foot does not follow the aforementioned pattern.25 Instead, diabetic wound healing is significantly impacted and strongly influenced by two forces: intrinsic and extrinsic factors.26,27 Intrinsic factors include hyperglycemia, altered immune function, abnormal expression of growth factors, tissue remolding and cells undergoing phenotypic changes.26 Extrinsic factors consist of trauma and abnormal load forces to the foot. The insensitive, neuropathic foot falls casualty to recurring trauma, injury and mechanical stress. Thickening of the basement membrane impairs wound healing and increases the incidence of forefoot ulceration.27
The standard treatment for diabetic forefoot ulcerations involves a multifocal approach. These measures include a thorough history and physical, optimizing glycemic control, assessing vascular supply, aggressive wound debridement, infection control, maintaining wound moisture control, and appropriate offloading.28
Optimizing glycemic control is often a difficult task in patients with diabetes. Hyperglycemia leads to microvascular complications, retinopathy, renal disease and poor wound healing.29 Tight control of glucose levels is necessary to prevent diabetic complications that predispose the patient to neuropathy, ischemia and infection. Multiple authors have demonstrated that tight glycemic control decreases complications, lowers the HbA1c and decreases wound healing time.29,30 This in turn will decrease the portal of entry time for infection and increase a patient’s quality of life. Game and colleagues noted that “A patient with glycosylated hemoglobin of >8% and an average daily glucose of >250 mg/dL will experience prolonged wound healing.”31
In your clinical assessment, it is imperative to conduct a thorough vascular evaluation with palpation of all lower extremity pulses.32 One can also confirm these pulses with the use of a Doppler waveform. If there is suspicion of vascular insufficiency, a reproducible and quantitative vascular assessment would be appropriate by evaluating a patient’s ankle brachial index (ABI) as well as his or her toe brachial index (TBI).28 Clinicians should perform transcutaneous partial pressure of oxygen testing (TcPO2) if the patient has a chronic wound with palpable pedal pulses and no macrovascular disease. This microvascular analysis will help assess whether hyperbaric oxygen therapy (HBOT) will be beneficial.31
If you consider the patient to be at risk of significant vascular disease, consider a referral for therapeutic revascularization as vascular supply is essential to wound healing.28
Debridement is the first step in wound bed preparation and activating the healing process. Aggressive surgical debridement enables one to transform a chronic wound into an acute wound by removing all necrotic dysfunctional tissue, restoring normal moisture balances, controlling bacterial loads and resetting the healing cascade at the wound border to a surface that is primed for subsequent healing.33 Aggressive surgical debridement in acute wounds is equally important to remove necrotic damaged tissues as well as any foreign materials.
Many diabetic wounds are stuck in a chronic inflammatory state. The presence of infection in either the soft tissue or bone prolongs the inflammatory phase of wound healing. Steed noted that “Increased levels of bacterial proteases break down endogenous growth factors and membrane receptor sites on the surface of cells involved in the healing process.”34 Taking a simple culture or tissue specimen can determine the organism(s) responsible for infection. Once you have identified the organism, you can select the appropriate antibiotic coverage and secondary wound healing can proceed.35
The essential keys of offloading are to prevent repetitive stress and microtrauma, and reduce pressure to the ulceration site. Each patient will require a different offloading modality according to his or her physical activities.36 One can accomplish offloading through the use of crutches, walkers, wheelchairs, removable walking braces, rocker bottom soles, shoe cutouts, felt foam, patella tendon bearing braces or total contact casts (TCCs).37 The gold standard for offloading is TCC as this modality has proven to be extremely effective in reducing plantar pressure and successful in the promotion of healing foot ulcers.38 Researchers have shown that TCCs reduce pressure at the site of ulceration by 84 to 92 percent.39 Regardless of whether one uses a TCC or a controlled ankle motion (CAM) walker boot, offloading the wound site has proven to be beneficial in wound closure.28
Maintaining wound closure can be a very difficult task. Ghanassia and colleagues found the primary healing rate of diabetic foot ulcers to be 77.5 percent, but noted a high rate of ulcer recurrence (60.9 percent) within 6.5 years and that 43.8 percent of these ulcers ultimately lead to amputations.40 Clinicians can mitigate ulcer recurrence with regular office follow-up and comprehensive foot examinations for early detection. The most important markers of long-term prognosis are the identification of peripheral neuropathy and levels of mechanical foot pressure.41 The use of therapeutic shoes and intense educational training, including the education of the family, contribute to lowering the incidence of ulceration and major amputation.42
Clinicians often prescribe custom diabetic footwear to prevent ulceration, particularly for patients who have suffered prior ulceration and are at higher risk. The primary goal is to redistribute pressure on the plantar foot surface to relieve pressure at locations that are at risk. A deep toe box will help offload dorsal pressure to the interphalangeal joint and plantar tip pressure of contracted toes. Evaluating the therapeutic treatment in neuropathic patients can be difficult as there tends to be inadequate feedback due to the presence of neuropathy.43
One effective way to offload the forefoot is by using a lightweight, semi-rigid rocker bottom type of shoe. A rocker bottom sole will allow offloading of the forefoot during gait and standing, redistributing the plantar force to the leg. It is also important to have a wide base to the shoe to allow for bulky dressings.44 Custom-molded healing sandals are another consideration for the offloading of forefoot ulcers. They do provide less pressure than a boot and may be a better alternative to a CAM walker but can be very difficult to walk in. Research has shown that offloading with felt alone decreases pressure at the ulceration site by 4 to 50 percent.45
Reducing the duration of force and plantar pressure at the ulceration site is an important element in the ulcer prevention strategy. Once peripheral neuropathy is present, there is a reduced or absent protective sensation. This increases plantar loads and tissue stress.46 The goal is to decrease the entire plantar pressure and strain. The time duration of stress is important to determine the amount of stain. There is a linear relationship between shear stress and the rate of strain.47 Neuropathic diabetic patents can apply up to 2 to 2.5 times their body weight to a plantar ulcer during each step, exceeding the body’s skin elasticity by up to three times.48
Reducing plantar pressure and decreasing the strain rate improves wound healing. Decelerating the foot prior to contact and decreasing the time the foot is on the ground will decrease force over time.47 This can be a very difficult task if the proposed treatment does not properly offload and/or change the biomechanics of gait.
There are only a few devices that decelerate the foot prior to hitting the ground and decrease plantar weightbearing while walking. The literature supports the following devices: TCC, Charcot restraint orthotic walker (CROW), CAM boot, patellar tendon bearing brace, and ankle foot orthoses (AFOs).45,49 Not all patients may be candidates for these types of devices and reimbursement may at times pose problems. The key is to choose the best modality that can provide adequate offloading, allow for adequate padding in high-risk areas and facilitate a transfer of ground forces away from the wound site.
Unfortunately, due to the cumbersome nature of some of these devices, patient adherence has become a challenge. Patients often refuse the application of a non-removable cast or the costs associated with them. This leads to a less costly or removable less effective device to be chosen. Patents may be more tolerating and adherent with slight modifications to shoe gear, which they may already have some familiarity.50
Additionally, Wu and colleagues noted that the practical realities of daily practice can lead to the use of less effective offloading modalities. They found that “… although most specialists understand that amelioration of pressure, shear, and repetitive injury are principal tenets of diabetic foot ulcer care, the cost/benefit analysis, realities of maintaining a busy clinical practice, the available manpower, and reimbursement issues may influence clinicians to use less optimal pressure mitigation methods.”50
All providers should follow the same consensus recommendations for diabetic foot ulcerations when performing a comprehensive foot and ulcer evaluation. These fundamental components should include: history and physical examination, appropriate laboratory testing/screening, neuropathic and vascular assessment, and ascertaining nutritional status.28
Ulcer evaluation should consist of determining the duration, location and measurements of the wound as well as the presence of infection and previous treatment. Identifying the presence of infection and ischemia in the diabetic limb is vital in the algorithm to successfully treat diabetic forefoot ulcerations.
Dr. Hanft is the Director of Research for the Podiatric Residency Program and the Director of Podiatric Education at the South Miami Hospital in Miami. He is in private practice at the Foot and Ankle Institute of South Florida in Miami. Dr. Hanft is a Fellow of the American College of Foot and Ankle Surgeons.
Dr. Hall is a third-year resident at the South Miami Hospital at Baptist Health South Florida in Miami.
Dr. Jarman is a third-year senior resident at the South Miami Hospital at Baptist Health South Florida in Miami.
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Editor’s note: For further reading, see “Tendon Lengthening: Is It A Viable Option For Forefoot Ulcers?” in the July 2005 issue of Podiatry Today. To access the archives, visit www.podiatrytoday.com .