Diabetes is a medical condition unfortunately characterized by many complications, including neuropathy and peripheral artery disease. Loss of sensation can lead to ulceration of the skin and accelerated degeneration of the joint (a condition known as Charcot arthropathy); and poor vascularity can impede healing.
Diabetic foot ulcers typically begin with neuropathy. The development of peripheral neuropathy in individuals with diabetes is attributed to a complex interaction of glycosylated hemoglobin with arterioles of both central and peripheral nerves, leading to conduction defects in sensory, motor, and autonomic function.
Prolonged exposure to even low pressure over a bony prominence (as may be seen with ill-fitting shoes) can cause skin breakdown. Ordinarily, pressure will cause pain, and the person will shift his or her weight. With a loss of such protective sensation, loading continues to the point that the skin breaks down and ulcers appear. Without adequate blood flow, ulcers can easily progress to gangrene.
Charcot arthropathy is characterized by joint destruction caused by a failure to stop painful (and ultimately destructive) loading. The condition is named after Jean Marie Charcot (1825-1893) who described the collapse of the bones of the foot in patients who had lost feeling in the feet from tertiary syphilis. The three commonly affected locations in the foot and ankle are the tarsal-metatarsal joints (midfoot), the transverse tarsal joint (hindfoot just in front of the ankle), and the ankle joint.
According to the neurotraumatic theory, Charcot arthropathy is caused by repetitive trauma. Ordinarily, a normal person will shift his or her weight such that no area is exposed to too much load; with neuropathy, this protective function is lost. The neurovascular theory holds that an autonomic peripheral neuropathy creates increased blow flow that leads to increased bone resorption. In a simplified version of this theory, increased blood flow “washes out” structural calcium from the bone, leading to localized osteopenia and structurally inferior bone that ultimately collapses. (A more detailed version posits that proinflammatory cytokines such as IL-1 and TNF alpha activate the RANK (Receptor Activator of Nuclear Factor κ B) ligand pathway, causing up-regulation of NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) which leads to increased osteoclastogenesis and osteolysis.) Most likely, a combination of both theories contributes to this condition.
Diabetic Foot Ulceration
Patients with diabetic foot ulcers present with swelling, discharge or a foul-smelling odor from the affected foot. Pain can be present, but not always: indeed, in patients with severe neuropathy, foot ulcers can be found incidentally by the patient or primary caregiver.
Physical examination should be focused on the location of the ulcer as well as the depth. The size of the wound, perfusion, loss of sensation, signs of inflammation, the presence of gangrenous tissue, and signs of infection such as exudate or odor should also be noted.
Typically, the ulcers will occur over a prominent area such as the metatarsal heads, although any area of the foot that is subject to a concentrated, repetitive force is at risk for developing a diabetic ulceration.
Diabetic Foot Charcot Arthropathy
Patients with Charcot arthropathy of the foot often present with unilateral swelling, redness, and increased skin temperature around the midfoot or ankle. Most patients present in their sixth or seventh decade and have peripheral neuropathy. Many are morbidly obese and have had diabetes for many years.
Charcot arthropathy can be painful, but not always: after all, it is caused by neuropathy. Charcot arthropathy is commonly mistaken for an infection (eg, osteomyelitis) especially when there is an ulcer present.
Diabetic foot ulcers should be characterized objectively by location and severity. There are multiple classification systems to grade ulcers. The Wagner system rates ulcers on a zero to 6 scale, from "0: skin intact" to "6: ulcer with extensive foot gangrene"; the Brodsky system considers both the extent to the ulcer (superficial, deep and exposed bone) as well as the extent of ischemia.
The vascular status of the foot should also be assessed objectively, noting the skin color and temperature, the quality of capillary refill and presence or absence of good pulses. The ankle-brachial index (ABI), namely the ratio of the blood pressure in the ankle relative to that in the arm can be assessed in the clinic, though calcification of the vessels may produce a falsely normal result.
In patients presenting with an ulcer, standard anteroposterior, lateral, and oblique radiographs of the affected foot should be obtained. These films can detect deformities of the foot in general, as well as bone changes such as periosteal reaction, lucencies or osteolysis that would be indicative of osteomyelitis.
MRI may be helpful to determine the extent of bony and soft-tissue disruption, but MRI cannot differentiate between Charcot arthropathy and osteomyelitis with high specificity. Occasionally, a bone scan is indicated, although very often the results of the bone scan will not change the management and may not reveal any information that cannot be obtained from a detailed physical examination.
Figure. Anteroposterior (top) and lateral (bottom) radiographs of the patient in figure 3 demonstrating subcutaneous gas extension down to bone with cortical disruption.
In cases of suspected infection, aerobic and anaerobic cultures of the wound should be obtained to help direct antibiotic therapy. Osteomyelitis is present in approximately 70% of ulcers that extend down to bone.
Laboratory tests such as white blood cell counts, sedimentation rate, and C-reactive protein levels may be used to establish the diagnosis of osteomyelitis, though a a bone biopsy is the most specific method. A biopsy of multiple shards of bone and soft tissue embedded in deep layers of synovium is a hallmark of Charcot arthropathy.
CT scans can be helpful to look at a more detailed picture of the collapse, but is not often necessary unless surgery is planned.
Diabetic foot disorders are common because diabetes itself is common. The prevalence of diabetes in the US is approximately 10% of the adult population, and in turn, about 10% of patients with diabetes will develop a lower extremity ulcer during the course of their disease and about 1% will develop Charcot arthropathy.
The rate of lower extremity amputations is at least 50% higher in men versus women. Mexican (Hispanic) Americans, Native Americans, and African Americans each have at least a 1.5- to 2-fold greater risk for diabetes related amputations than age-matched diabetic Caucasians.
When a patient presents with a foot ulcer, the main diagnostic question is What caused it? It is thus critical to evaluate for previous ulcerations, medical comorbidities, level of diabetic control and monitoring, and tobacco and intravenous drug use.
The presence of sensory neuropathy should be assessed. Granted, a sensory exam is not objective, but it can be (in a cooperative patient) at least standardized. For example, a Semmes-Weinstein 5.07 monofilament nylon wire can be used to exert a consistent force (If the wire bow into a C shape when pressed against the skin for 1 second, 10g of force is applied). This is an important threshold: Patients who can’t a 10-g force have lost protective sensation.
Figure 2. Semmes-Weinstein 5.07 monofilament used to evaluate peripheral neuropathy
There are many potential causes for peripheral neuropathy besides diabetes that can be responsible: alcoholism, vitamin B1 and B12 deficiencies heavy metal poisoning, among others. A focused history and appropriate laboratory studies can rule out other causes besides diabetes.
In the absence of diabetes, foot ulcers can be caused by atherosclerosis involving the lower extremities, vascular lesions, and even severe Raynaud’s phenomenon (vasospastic attacks in digits). A squamous cell carcinoma may also be responsible.
Charcot arthropathy may have a similar presentation as gout, cellulitis, osteomyelitis, and septic arthritis. Diabetic neuropathy is the most common cause of Charcot arthropathy, but other less common causes include spina bifida, cerebral palsy, meningomyelocoele, syringomyelia, leprosy and alcohol abuse. Last, advanced syphilis, the condition in which the disease was first described, is still a possible etiology.
Figure. Semmes-Weinstein 5.07 monofilament used to evaluate peripheral neuropathy
In all patients with diabetes, breaks in the skin are a red flag: infection may be present or looming. Indeed, any sign of increased pressure on focal areas of the foot (such as erythema or skin changes), as a precursor to worse problems, is best considered a red flag too.
The primary goal for treatment of diabetic ulcers is to get the wound to close without infection. Often, the best first step to offload the affected area, giving it an opportunity to heal. This is typically done with a total contact cast or removable diabetic walker boot.
Total contact casting has been shown to significantly increase the healing rate of neuropathic plantar foot ulcers at 12 weeks compared to removable cast walkers and half-shoes so it is the preferred method of treatment. It can take anywhere from 6 weeks to a year for an ulcer to heal depending on the size, depth, and duration of the ulcer. A patient should not return to unmodified shoes until the ulcer has completely healed. Unfortunately, obtaining successful healing of a diabetic ulcer often does not remove the underlying etiologies (neuropathy and pressure points) so recurrence of the ulcer over time is often high.
Treatment of the ulceration may involve surgical debridement of the callus or necrotic tissue with scalpels and curved scissors. Usually, this can be done in the clinic, although sometimes it may need to be done in the operating room if the infection involves the bone and there is some need to remove part of the infected bone. Keeping the wound moist without excess fluids can accelerate re-epithelialization of the wound. Various topical agents and dressings may expedite healing. Hyperbaric oxygen therapy, ultrasonic therapy, negative pressure wound therapy, and electric stimulation are all being tested for treatment of diabetic foot ulcers.
The vascular status of the affected extremity is critical in determining the healing potential of foot ulcers and the need for possible surgical intervention. More than 60% of diabetic foot ulcers have decreased arterial blood flow due to concurrent peripheral vascular disease. Formal vascular studies are often needed to determine status of the posterior tibial and dorsalis pedis arteries and the need for surgical or endovascular procedures to perfuse the foot.
Because gastrocnemius contractures cause plantarflexion and thus increased forefoot pressures, patients with such a contracture may benefit from a tendon release. A percutaneous Achilles tendon lengthening prior to total contact casting markedly decreases the rate of recurrence of plantar ulcers.
Diabetic foot ulcers if not treated (or if they do not respond to treatment) can lead to gangrene, abscesses and osteomyelitis. Amputation of the lower extremity may be needed. The need for this procedure, it should noted, is a marker for severe disease, as the 5-year mortality rate following an amputation is approximately 66%.
Charcot arthropathy is resistant to easy treatment. The best approach is to detect it early and prevent it from getting worse. When detected early, treatment involves a period of non-weight bearing or limited weight-bearing in either a total contact cast or a diabetic removable boot. Swelling and redness will usually resolve or improve with elevation. Later in the process, when the bones have started to stabilize, the patient can walk more and put increasingly more weight on the leg. Rolling knee walkers can help keep the weight off the bad foot while allowing patients to be mobile and not over-loading the better foot. The treatment of Charcot arthropathy is a particularly frustrating not only because it can take 6-12 months or more for the involved joints to stabilize, but because it may resolve with a gross deformity of the foot that places patient at risk for developing an ulcer over newly prominent bony areas.
Some studies suggest that inhibitors of osteoclasts (as would be used to treat osteoporosis) may be helpful in treating Charcot arthropathy, by limiting osteolysis, though good clinical results have not yet been attained. Electrical bone growth stimulation to promote rapid healing of fractures has been suggested as a supplement to the treatment of acute Charcot arthropathy. Similar to bisphosphonate therapy, there is no conclusive data for its efficacy.
Surgery may be recommended as a treatment if a severe deformity has occurred or the foot or ankle has become unstable and cannot be corrected through immobilization and off-loading. Surgery ranges from exostectomy (removal of prominent bone) to reconstruction of the foot including fusion of the unstable joints after the deformity has been corrected. The goal of surgery is a foot that is stable, can bear weight, and can fit in a shoe or brace without ulcers developing over prominent areas of bone. Surgery for Charcot arthropathy, because of the patient’s baseline ill-health, is associated with significant risks of infection, problems with wound healing, and non-union.
Because diabetic foot disorders are caused by diabetes, all factors that increase the risk of the underlying condition increase the risk of resultant foot problems. Among patients with diabetes, cigarette smoking and poor glycemic control is associated with more diabetic neuropathy, peripheral artery disease, and in turn more foot disease. In addition, inappropriate footwear and poor toenail grooming increases the risk for ulcerations.
Previous ulcerations or amputations are associated with a higher risk of developing another ulcer.
A tight calf muscle (equinus contracture) causes the patient to place more weight on the forefoot and increases the risk of ulcers there.
There are reports of high complication rates associated with simple ankle fractures in the population of patients with diabetes, especially those with peripheral neuropathy. Many patients who present with Charcot arthropathy of the ankle initiated their disease process with an ankle fracture. Many experts recommend augmented internal fixation with prolonged non-weight-bearing to treat these ankle fractures.
Diabetic foot ulcer, Charcot arthropathy, neurotraumatic theory, neurovascular theory, neuropathy, infection, amputation
Thorough physical exam of feet in diabetic population
Classify ulcers to treat accordingly
Distinguish infection from Charcot arthropathy
Provide basic patient education information to diabetic patients
