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atients’ feet can serve as a window to their general health. The foot is a unique and dynamic organ. With its synchronization of joints, soft tissues, and osseous structures, it moves the body forward in a complex, triplanar fashion while serving as the foundation to maintain our bodies in an erect position. The average American logs an amazing 75,000 miles by the time he or she reaches the age of 50. Each foot has 26 bones, 33 joints, 107 ligaments, 19 muscles, and numerous tendons and soft tissue structures—and skin that contains all of it. The anatomy of the foot and ankle is composed of an intricate structure, with many tendons and ligaments traversing in multiple planes. Therefore, one can conclude that a thorough understanding of the normal function and structure of the foot and ankle—and how it influences and is influenced by the forces of ambulation—is imperative prior to the evaluation and treatment of the wounded foot.
       There are multiple factors influencing the threshold for risk of structural breakdown and wounding of the foot. Even in the healthy individual, there are anatomical and structural influences that may predispose one to pathology. Occupational, surface, and environmental factors, including the foot’s immediate environment (eg, shoe gear), can aggravate or hasten foot pathology. If one factors in systemic complications, such as vascular disease, neuromuscular pathology, diabetes, malnutrition, or congenital abnormalities, the threshold for skin structure breakdown reduces even further.

Assessment

       A wound clinician must consider numerous factors when assessing a patient’s foot wounds. Ulcerations of the foot are most frequently a direct result of a combination of neuropathy, ischemia, and trauma.¹ Other authors have identified neuropathic deformity and minor trauma as the most common component risks.1 Thus, before we can consider treatment for foot wounds, the healthcare professional must perform a thorough, problem-directed history assessment and physical.
       Initially, a thorough social history is critical. Of importance are the patient’s gender; age; socioeconomic situation; availability of a caregiver, family member, or significant other; level of coherence to understand the impact of the situation; and capability to follow directions. Often, the wound clinician is faced with a patient who lacks any social or economic support systems. The presence or lack of self-sufficiency, social and economic support systems, and ability to understand the impact of one’s current health situation will influence the practitioner’s plans to integrate a successful care plan.
       It is also vitally important to discuss the use of addictive agents (eg, tobacco, alcohol, or illicit drugs). Patients with poor sleep patterns, an often-overlooked factor, may have a lower threshold for pain tolerance. Additionally, sleep deprivation robs the body of the opportunity to rebuild and heal, decreasing one’s immune defense system.²
The patient presenting with a foot wound must also be questioned about the frequency of wounds and which measures have been taken for their prevention. A strong risk factor for the development of an ulcer in a patient with diabetes is a history of a previous ulcer or amputation. One study revealed that persons who had been healed of an initial foot ulcer had a 70% risk of developing new lesions after 5 years.³ The prudent wound clinician will also want to know if the patient is currently under the regular care of a family physician, endocrinologist, or cardiologist while undergoing regular foot care by a podiatrist as part of his or her healthcare.
       Hygiene practices can be noted by determining how often patients bathe or change their shoes and socks. By asking if they are active or involved in an exercise program and what shoe gear is required for their occupation, clinicians can discover if their patients are using the appropriate shoe gear for each situation. This includes how often they purchase new shoes and whether they break them in properly. Caregivers often find that patients are wearing inappropriate, worn, or ill-fitting shoes. Patients should have their feet measured yearly, since changes in foot structure are common in this population.
       An additional aspect of the social history is a patient’s nutrition status. Does he or she understand sound nutritional concepts and what is required for healing? A nutrition-screening questionnaire would be appropriate at this time and could be discussed at a follow-up visit and/or a consultation with a nutritionist or registered dietitian if required.
       Finally, a prudent wound clinician will peer into his or her patient’s psyche regarding mind/body image issues. Inquiring as to the patient’s anxiety level due to preconceived notions or misinformation (eg, that all wounds lead to amputations) is paramount. It is important to ask how this wound may affect the patient’s social behavior, especially if the wound has an odor. If the dressing is cumbersome or constantly draining, causing discomfort, wound patients will often begin to isolate themselves and become depressed. Frykberg states, “Wounds create a great deal of consternation for patients,” and that, “Foot ulcers can become a major impediment to quality of life and activity.”3 Possessing a good grasp of the answers to these questions creates a framework in which to work. It will provide the first step in formulating expectations of the extent and complexity of one’s care plan.
       A thorough review of systems is required to find potential causes of immunocompromise when assessing foot wounds. One must realize that when treating a patient’s feet, we are treating the whole person. Having a realization of which systems are intact or compromised will impact the treatment direction. The most common associated disease for lower extremity wounds is diabetes. The diabetic foot ulcer is the leading risk factor preceding 85% of all diabetic lower extremity amputations.³ It is additionally important to know how long one’s patient has been diagnosed with diabetes, since at least 60% of the patients with long-term diabetes (ie, more than 5–10 years) have neuropathy at the time of diagnoses.³ Neurological diseases and issues to consider that may result in neuropathies other than diabetes can include lumbar radiculopathy, Guillain-Barré Syndrome, malnutrition, heavy metal exposure, B12 deficiency, Hansen’s disease, and alcoholism. Any of these states can cause an insensate foot, therefore leading to the sequelae of ulcerations.
       Other common disease states that can have deleterious effects on a lower extremity may include rheumatoid arthritis or other connective tissue diseases like systemic lupus erythematosus. One must also consider cardiac problems or hypertension along with other vascular arterial disease states (eg, intermittent claudication or pain at rest). Venous diseases like venous insufficiency can mimic cellulitis or lead to deep vein thrombosis. One should question any lymphatic disease caused by familial or traumatic conditions as well as dermatological conditions, such as bullous disease or carcinoma. Clinicians can consider these conditions when an ulcer’s presentation is in an atypical location of the foot (eg, the dorsum or arch). Other diseases that can result in an ulcerative state may include sexually transmitted disease (STD) sequelae, such such as syphilis or human immunodeficiency virus (HIV).

Medications

       Wound patients commonly take multiple medications, some of which may interfere with treatments or make them less effective. Chronic antibiotic use can cause an increased resistance to organisms. Patients undergoing anticoagulant therapy can present with relative contraindications to surgical debridement. Excessive anticoagulant therapy can lead to hematomas, which can become secondarily infected. Prednisone and antineoplastic drugs are immunosuppressive and often need to be stopped or reduced when dealing with a foot wound.
       The role of analgesics, such as acetaminophen, nonsteroidal anti-inflammatory drugs (NSAIDs) and opioids, is important in the treatment of wound patients. A combination of smaller doses of NSAIDs and opioids can work at different sites along the pain pathway and improve analgesia with fewer opioid side effects.⁴

Allergies

       A wound clinician must determine whether the patient has allergies or sensitivities to: antibiotics, NSAIDs and aspirin products, latex, topical preparations or adhesives, and foams. One must discuss reported allergies that are actually sensitivities. This is especially true with some antibiotics that can cause patients gastrointestinal distress rather than anaphylaxis. Furthermore, securing dressings on the contours of the foot often requires use of an extra-wide adhesive that covers an area larger than the wound itself. Over time, this excessive coverage can cause a local skin reaction that is often an irritation and not an allergy. This can often be alleviated by applying a good skin barrier and rotating dressings and adhesives until the irritation subsides.

Evaluation and Treatment

       Vital signs must be assessed along with pain, using a validated pain scale.⁵ Pulse and respiration are often increased in patients with infected wounds, as is pain level. It should be noted that patients in an immunocompromised state like diabetes might have a normal temperature despite an infection.
       The vascular exam should be initially performed by palpating for the presence or absence of the dorsalis pedis and posterior tibialis pulses of the foot as well as pulses of the popliteal arteries behind the knee. Testing the capillary fill time by elevating limbs and looking for the return of blood flow to the digits in less than 5 seconds is normal.⁶ One also can test for elevation pallor, which is a reliable indicator of vascular disease. Conversely, dependent rubor reveals a hyperemic response that causes partial deoxygenation of the blood by the vascular system. Dependent rubor usually presents as a cool limb and disappears with elevation. Presence of cyanosis results from venous insufficiency and deoxygenation of the blood; this is often associated with pulmonary disease. As mentioned earlier, skin temperature usually increases in the presence of infection and should be assessed relative to the opposing limb. Edema is often nonspecific and, when seen with an infected wound, usually increases in proximity to the wound. One must also look for hemosiderin deposits, which are often seen with venous insufficiency. This can, however, be confused with cellulitis and even mask cellulitis. If it is a chronic condition, suspect venous insufficiency. Deep vein thrombosis must always be considered in the lower limb when pain and cellulitis are present. This is especially true if the cellulitis is not in close proximity to the digital or foot ulcer.⁶
       A neurological exam is usually conducted to assess for presence or absence of protective sensation. This is conducted using a Semmes-Weinstein 5.07/10g monofilament test in several areas of the plantar and dorsal foot, with the patient’s eyes closed. If the patient is unable to perceive the monofilament test, one can surmise that a neuropathic process is present, in which case patient education must be strongly emphasized. Patients with insensitive feet tend to be less likely to offload them due to a lack of pain response. Daily visual inspection, rather than reliance on a pain response, is crucial for these patients. Patients with diabetes may possess more than peripheral sensory neuropathy. Patients with diabetes can also develop motor neuropathy and autoimmune neuropathy.

Figure 1

The inactivity and atrophy of muscle groups secondary to motor neuropathy leads to foot deformities (eg, clawed toes and high pressure to the forefoot). Autoimmune neuropathy can lead to microneurovascular basal motor disturbances and endothelial dysfunction, resulting in lack of sweating. This anhydrous state contributes to cracked skin that bleeds and creates a potential for open wounds (see Figure 1).³ Quality skin care products, especially moisturizers with advanced nutritional capabilities, can prevent dry, cracked feet and minimize excessive transepidermal water loss (e-TEWL). Harsh soaps and detergents should be avoided. Patients with diabetes should not use moisturizers between their toes, as it can encourage the development of fungus. Mild, soap-free, pH-balanced cleansers should be used to bathe the feet.
       Conversely, other patients may suffer from a localized hyperhydrosis (ie, excessive sweating to the feet). The excessive moisture can lead to fungal infections, viral wart infections, or maceration of the plantar skin. This state potentiates growth of bacteria and places the skin at risk for infection and breakdown. This patient can also present a challenge when attempting to adhere a wound dressing to an open wound. Over-the-counter and prescription-strength antiperspirant preparations should be applied before bedtime 3 or 4 times per week. Although not a cure, these products can control perspiration.
       The musculoskeletal orthopedic/biomechanical exam is very important to obtain a picture of potential risks and treatments for the patient. Deformities and faults in the anatomical structure of the feet are often direct causes of ulceration, and the risk is markedly increased in the neuropathic patient. Additionally, complexities or delays in healing the vascularly compromised patient can be seen. Deformities should be identified early and treated immediately and over the long term. About 30% of the ulcers in patients with diabetics are secondary to a callus over a bony prominence.³ These biomechanical protuberances of osseous structures cause increased pressure to the skin structures, forming an area of hypertrophy of the keratin layer of the epidermis, or callus, often associated with an underlying wound. In other words, the bony deformities cause ulcerations due to direct pressure on the skin. These secondary calluses have a characteristically dry subepidermal hemorrhage and often possess a macerated periphery. These areas frequently require decisive surgical intervention. This may be preventative or emergent. Abnormal gait patterns caused by these deformities can also cause shear-type lesions. These forces can be rectified through modifications in shoe gear, such as the use of functional orthoses or accommodative, shear-reducing inserts. There are numerous deformities, too many to list in this article, of the foot and ankle that can cause skin structure breakdown. Some of the more common structural abnormalities that cause an increased risk for ulcers include rigid hammer toes, claw and mallet toes, overlapping digits, bunions to the first and fifth metatarsals, forefoot plantar fat pad atrophy, hypertrophic bone formation secondary to gait abnormalities (eg, retrocalcaneal exostosis), hypertrophic sesmoids, and accessory bones. Also, there are several joint and osseous adaptations that can occur in these conditions, such as flat feet, cavus feet, diabetic neuroosteoarthropathy (Charcot Foot), or Charcot-Marie-Tooth (CMT) disease. Frequently, tendon ruptures causing adaptive changes with protrusion of the navicular or cuboid are noted, placing patients’ feet at further risk for ulceration.
       Digital deformities, hammer toes, claw toes, and mallet toes are caused by an imbalance of the dorsal and plantar digital tendons. They can be flexible or rigid in nature. When they are rigid, they present the highest risk for breakdown. Hammer toes often develop secondary corns, dorsally, over the proximal phalanx head from the excess friction caused by shoe gear. Due to the digits’ intimate relationship to the metatarsal, a retrograde pressure often forms on the metatarsal, causing plantar-grade pressure, resulting in the plantar forefoot callus. Claw toes are those that have contracture at both the proximal and distal interphalangeal joint. A mallet toe occurs when the distal interphalangeal joint is rigid and contracture at the proximal interphalangeal joint cannot be straightened. These usually present with pressure at the most distal aspect of the digit, and a plantar or distal interphalangeal ulceration will ensue.
       Digital contracture deformities tend to get gradually worse with time, and flexible deformities become rigid. The development of these digital deformities results from a muscle imbalance that causes the ligaments and tendons to become excessively tight.

Figure 2

These deformities cause foot movement to become more restricted, leading to extra stress at the distal and plantar surfaces of the increasingly curled digits and forefoot. Due to the dynamics of the ever-accommodating foot to deforming forces, these conditions can also lead to overlapping of any of the digits. Arthritis can also contribute to these different forefoot deformities (see Figure 2). The increased risk for ulceration involved with these conditions creates a need for precise treatment.
       The clinician can perform preventative measures with extra-depth or custom-molded shoe gear and padding, symptomatic treatment with padding, analgesics, and anti-inflamatories. Curative treatment using surgical correction, such as digital arthroplasties/arthrodesis, tendon lengthening of the extensor tendons, or tenotomies of the flexor tendons, is recommended. Consultation with a podiatrist is imperative.
       Likewise, bunions present a magnified risk to the insensate or vascularly compromised patient. They can occur at the first metatarsal phalangeal joint or fifth metatarsal phalangeal joint (a condition known as Tailor’s bunion), representing deviation of the metatarsal with an overgrowth of bone on the metatarsal head. The digit then progresses to deviate toward the second or fourth digit. Developed as a result of an abnormal foot structure and mechanics, such as excess pronation or flat foot, the soft tissue structures are stretched excessively, and the joint capsule and ligaments adapt. This results in a gradual drifting outward of the metatarsal. Accommodation by the adjacent digits with contracture or under/overlapping is often seen. These deformities can be treated conservatively, as mentioned above, or surgically with the repositioning of the metatarsal to decrease the deforming forces and make the joint more functional. Bunions often present with full-thickness or subcutaneous-depth ulcerations, mostly due to ill-fitting shoe gear. Debridement and advanced wound care techniques are futile unless the etiology and cause of the pressure is addressed.

Figure 3

       Plantar fat and heel fat pad atrophy are problems that place the insensate or vascularly compromised patient at risk for ulcerative breakdown. (See Figure 3 for a clinical example of a plantar surface wound). Serving as the body’s natural shock absorber, the fat pad in the heel has a columnar arrangement that allows for great impact and near-perfect memory, accepting shear and torsional forces without deforming. This is repeated at each heel strike during ambulation. Aging and systemic conditions affect the fat pad’s integrity, as does obesity. This is especially noted in collagen diseases.⁷ The forefoot fat pad will often be seen to atrophy or displace anteriorly as well. This thinning—which often is associated with aging, ill-fitting high-heel shoes, a narrow toe box, and/or a high cavus foot type (ie, high arch)—leads a patient to be much more susceptible to pain in the second, third, and fourth metatarsals. Many patients also have a hypertrophic tibial (medial) sesmoid located just plantar to the first metatarsal. Certain foot types will cause increased plantar and shear force to this area, especially if they have residual muscular weakness causing a spinning or abductory twist in this area. This may also be seen at the medial plantar interphalangeal joint of the hallux. These areas repeatedly form callus and secondary ulcerations. With the decreased fat pad, an ever-increasing risk for plantar forefoot ulcerations is noted; it is a very common area for diabetic neuropathic ulcerations.
       Finally, other deformities that lower the risk threshold are bony spurs of the foot, such as retrocalcaneal exostosis, Haglund’s deformity, and a tight heel cord or Achilles tendon. This area will recurrently develop a bursae as the body attempts to protect and respond to forces of friction. The exostosis often forms secondarily to a tight Achilles tendon, causing decreased range of motion at the ankle and heel during heel strike and propulsion. These areas are at risk not only in the ambulatory patient but also the bedfast patient, serving as a pressure source from the shoe or the bed. Achilles tendon tightness also places more pressure on the forefoot and healed ulcer sites in patients who have neuropathy and the resultant decreased ankle dorsiflexion. It has been found that tendo-achilles lengthening procedures promote healing of chronic foot ulcers in patients with neuropathy, with less recurrence, and that surgical intervention will prevent recurrence of forefoot ulcerations, which are caused by excess pressure on the forefoot caused due to the lack of dorsiflexion at the ankle.⁸ A retrocalcaneal exostectomy may also be concurrently performed to remove the osseous protuberance and decrease the risk for pressure phenomena.

Skin

       The dermatological exam must assess not only the overall skin health but also the toenails. As mentioned earlier, calluses and corns are the body’s natural response to pressure or friction. Not all areas of thickened skin are corns or calluses, however. Plantar warts, inclusion cysts, and porokeratoses also cause a discreet thickening of the skin that resembles corns and calluses. Often, these structures must be treated with excision, topical medications, or padding, and their impact on creating risk for further breakdown of skin structures cannot be overlooked. Blisters result from heat moisture and friction. They can also result from fungal infections of the skin, allergic reactions, or burns.

Figure 4

Chemical burns often occur when a high-risk patient soaks his or her feet in a bleach solution (see Figure 4) or cannot determine the temperature of the water when it is too hot. Therefore, soaking should not be permitted. Blisters that occur due to fungal infection or allergic reactions generally occur in clusters and are smaller than blisters caused by friction (or occur in areas that are free from friction sources). Blisters should be drained, leaving the cover intact and placing a protective, light-compression, non-stick dressing over it. Attention to the type of sock gear (eg, avoiding 100% cotton and often wearing 2 socks) can be useful prevention methods that allow friction to be absorbed and reduce friction to the skin. Cotton socks can often become wet from perspiration and can actually stick to the skin, creating increased friction.
       Athlete’s foot (tinea pedis) is common, interdigitally and in a moccasin distribution, in the immunocompromised or diabetic population.

Figure 5

An interdigital fissure can be devastating in that a secondary bacterial infection can occur, creating ulceration in the very thin tissue of the inner space (see Figure 5). This can cause the formation of a sinus tract into the intermetatarsal space. Athlete’s foot is most commonly caused by the dermatophyte Trichophyton rubrum and is associated with fungal infections of the nail as well (see Figure 6).
       The recurrent form of Athlete’s foot is associated with fungal nail infections.

Figure 6

A Candida albicans yeast infection is also common among this population. Fungal and yeast infections usually progress slowly and can overtake all of the nails. This presents a risk factor in that the thickness of the nail becomes a pressure source aggravated by the shoes. This places a resultant pressure on the nail bed and can lead to infection or ulceration. Add to this the problem of subungual exostosis, which is a spurring of the distal phalanx. Usually caused from long-term pressure on the toe from the shoe, trauma, or thickened nail, it further increases the risk for ulceration or bleeding under the nail (ie, subungual hematoma).
       The most effective treatment for fungal infections is prevention. Instructing patients to keep their feet clean and dry between the digits and applying antifungal powder between their toes and in their socks are good first steps to prevent this troublesome condition. Once infected, the skin structures can often be treated by an antifungal cream, gel, or spray. Fungal nails have been treated successfully with prescription oral agents and/or topical solutions. These prescription treatments must, however, be concurrently treated with debridement or removal of the fungal nail on a regular basis. It can take up to a year to see clinical results. Often, the painful nail that presents with a subungual exostosis must be surgically excised.
       Finally, ingrown toenails generally result in infection. The cause is often congenital, although they can also be caused by improper trimming by the patient or a family member or by tight-fitting hosiery (eg, prescription compression stockings). The nail borders will become irritated and red from the offending nail border and, if left untreated, result in an infection with bacterial spread. At-risk patients will often develop localized or ascending cellulitis and must be treated immediately to prevent formation of sinus tracking and osteomylitis. This occurs because the ingrown nail is in a moist, warm, bacteria-rich environment, and it should be treated with sterile instrumentation to remove the offending nail border and any denuded tissue resulting from the infection. The condition normally responds to topical antimicrobials within a week, after cleansing with a safe, noncytotoxic wound cleanser or flushing with saline and covering with a bandage daily. Oral antibiotics are rarely indicated if the condition is caught early enough. In the high-risk patient with a long-standing infection, a plain X-ray may be ordered to rule out osteomylitis.

The Whole Picture

       Ancillary blood work, X-rays, bone scans, or magnetic resonance imaging (MRI) must be performed once the clinician has assessed the patient, to complete the picture for treatment. The extent of infection can be determined with the presence of occult soft tissue or osseous abscess, as can structural deformities that place the patient at risk for nonhealing. As with any patient who requires aggressive, sharp debridement or surgical intervention, a complete vascular examination or consultation would be warranted. Baseline dopplers, noninvasive vascular studies, transcutaneous oxygen or magnetic resonance arteriography, and/or ultrasound may aid in developing a strategy for treatment. Offloading principles are essential for patients with foot wounds. This may be as simple as using a plantar metatarsal pad, a surgical shoe, an immobilizing walking boot, a total contact cast (TCC), a walker, crutches, or a wheelchair. The emphasis is on offloading and knowing anatomical landmarks and structures that influence ambulation. These often require a lifestyle change for the patient.
       With the advent of negative pressure wound therapy (NPWT) and numerous other advanced wound therapies, many of the wounds that were once the most difficult to heal and led to amputation can now be healed successfully by controlling exudate and infecton and stimulating granulation tissue. Often, split-thickness skin grafts are warranted once the wounds granulate to surface. This can be hastened with the use of biologically engineered skin, NPWT, or the patient’s own skin. Use of advanced wound healing products and dressings to manipulate the wound microenvironment and create a more physiological situation are as applicable in the foot wound as any other part of the body. These therapies should be used as early as possible in the course of wound care to increase the overall outcome. Because diabetic/neuropathic wounds tend to be highly contaminated with increased levels of bioburden, the use of broad-spectrum antimicrobials with ionic silver and polyhexamethylene (PHMB) are safe and often warranted early in the treatment process for prophylaxis of infection.
       With foot wounds, the challenge is innovating or creating dressings that are designed for more linear parts of the body. The foot has many contours and offloading issues that one may not have to deal with in a wound of an upper extremity or the pelvis.
       Regardless of whether the cause of foot wounds is diabetes, poor circulation, or immunocompromised states, treatment must include an extensive evaluation of the patient’s general health. Treating the wound in relation to the patient’s overall health helps clinicians to determine the best course toward reaching the goal of healing and closure—putting the clinician’s and the patient’s best foot forward.