The Diabetic Foot

David E. Oji

Lew C. Schon

INTRODUCTION

Far from being just a foot problem, the patient with diabetes mellitus requires an integrated multidisciplinary approach to address every problem that can arise from the many systemic manifestations. Management requires treatment from many providers such as orthotists, nurse educators, dietitians, and physical therapists as well as expertise from other disciplines such as vascular surgery, endocrinology, infectious diseases, and neurology. The foot is a complex target of this multisystem disease, with disastrous consequences if the labor-intensive treatments do not adequately resolve its manifestations and complications in the lower extremity. The spectrum of clinical manifestations can range from mild neuropathy to severe ulcerations, infections, vasculopathy, Charcot arthropathy, and neuropathic fractures.

PATHOGENESIS

Epidemiology

The number of individuals affected by diabetes and its cost to society are staggering. The Center for Disease Control estimates that 8.3% of the general population, or 25.8 million people in the United States, are affected by diabetes, costing the healthcare system close to $174 billion in direct and indirect costs. Amputations among patients with diabetes are the leading cause of nontraumatic amputations. In 2006 alone, close to 65,700 amputations were performed among patients with diabetes. Instituting a comprehensive foot care program comprising risk assessment, foot care education, preventative care, and referral to specialists is believed to be able to reduce amputation rates by 45% to 85%.¹ One study demonstrated an incidence of foot pathology among patients with diabetes in a medical clinic to be 68%, with manifestations ranging from callus formation, hammer toes, and peripheral and autonomic neuropathy.²

Pathophysiology

Neuropathy

The initiator of many foot complications in patients with diabetes is sensory neuropathy and to a lesser extent autonomic and motor neuropathies. Neuropathic changes result in the loss of myelinated and nonmyelinated nerve fibers owing to poor regulation of microcirculation and delivery of oxygen. Moreover, hyperglycemia and the vascular changes have been shown to result in accumulation of sorbitol and advanced products of glycosylation in the nerves.³ These changes are progressive and gradual and thought to cause slowed nerve conduction.⁴ Enzymic blocking of aldose reductase conversion to sorbitol has been developed to slow the accumulation of sorbitol; however, the efficacy is still unknown.⁵ Even though the exact cause of diabetic neuropathy is still unknown, poor glucose control, along with age and height, has been shown to increase the risk.⁶

Of the neuropathic consequences seen in patients with diabetes, sensory neuropathy, combined with excessive mechanical stress, is the primary initiating event in foot ulcerations and infections.⁷ Sensory changes occur in the usual stocking glove fashion, affecting the distal aspect of the extremities first and progressing proximally. Diminished light touch sensation, proprioception, temperature awareness, and pain perception all combine to make the patient more susceptible to tissue failure from repetitive microtrauma. However, the loss of sensation itself does not result in foot complications. Brand,⁸ in his review, emphasized that inflammation and tissues breakdown are the result of repetitive stress of a certain magnitude to a specific area with sensory deprivation. Ulcerations are the result of this combination of pressure or shearing forces from the ground, shoe, or even an adjacent toe to a given area, usually accentuated by a bony prominence that lacks the usual sensory protective mechanism.

Autonomic and motor neuropathies also play an important role in the pathogenesis of the diabetic foot. Autonomic dysfunction has been linked to foot ulcerations in patients with diabetes.⁹ Neuropathy of the autonomic nervous system results in loss of normal regulation of perspiration, skin temperature control, and vascular flow. These changes result in the loss of pliability of local tissues, forming thick callus that is more prone to fissuring and cracking. Moreover, loss of normal perspiration prevents rehydration of the area, causing further tissue destruction and making the area more susceptible to bacterial seeding of the deep tissue.⁴

Motor neuropathy also plays a role because of contractures of the intrinsic foot muscles, which result in the classic claw toe deformity. Hyperextension of the metatarsophalangeal (MTP) joint has been shown to increase pressure directly under the metatarsal (MT) heads, thereby making the area more susceptible to ulcerations.¹⁰ The flexed proximal interphalangeal joint leads to increased risk of dorsal ulcerations over the prominent knuckle and at the plantar tip of the toe.

Vascular Disease

Vasculopathy is common in patients with diabetes and affects the prognosis for all diabetic foot conditions and their treatments. In general, peripheral vascular diseases involving both large and small vessels are more extensive in patients with diabetes and can progressive more aggressively. Changes in basement membrane causing increased capillary pressure and decreased flow have been documented. The role of vascular disease leading to soft tissue breakdown is less compared to recurrent repetitive trauma combined with sensory neuropathy.³

DIAGNOSIS

Physical Examination and History

Clinical Features

A thorough examination of the lower extremities up to the level of the knee should be done on both sides; it should be conducted at least once a year and more frequently for high-risk individuals. Important features are as follows:

Gait abnormalities should be documented.
Footwear should be inspected for wear pattern and for foreign objects that may be protruding into the shoe.
Pulses, hair growth, warmth, and capillary refill should be examined for vascular disease.
Foot and heel abnormalities such as claw toes, hammer toes, bunions, skin breaks, ulcers, heel position (varus/valgus), or changes in foot shape, should all be documented thoroughly.
If ulcers are present, the location, size, and whether erythema or drainage is present (Fig. 5.1) should be documented.
The clinician should monitor for the presence of edema or signs of inflammation as early signs of neuroarthropathy or stress fractures.
Instability of joints should be tested.
Weakness in manual muscle testing may indicate tendon or neurologic dysfunctions.

In addition, a thorough neurologic examination should be done for reflexes, a motor examination, and a sensory examination, including the following:

Qualitative sensory examinations such as light touch, two-point discrimination, pin prick, and proprioception.
Quantitative sensory examination most commonly done using the Semmes-Weinstein monofilaments (Fig. 5.2). The monofilament is pressed onto the skin perpendicularly until it bends. The 5.07 monofilament is considered the standard for adequate sensation. However, it is important to keep in mind that 10% of patients who can feel the 5.07 monofilament can develop ulcerations.⁷

Figure 5.1 A: Dorsal toe ulcer; B: Plantar MT head ulcer; C: Heel ulcer; and D: midfoot ulcer secondary to rocker bottom deformity.

Figure 5.2 Examination of the patient’s foot with a 5.07/10-g monofilament.

Vascular Studies. Noninvasive vascular studies can be done to supplement the clinical physical examination findings; the most common study is the arterial Doppler ultrasound. The data are expressed as absolute pressures or part of the ankle-brachial index. An ankle-brachial index of 0.45 was initially considered to be a minimum value for
healing after amputations. However, the advent of toe pressure measurements has greatly improved the reliability of the ultrasound study. An absolute pressure of 40 mm Hg is considered the minimum toe pressure measurement needed for wound healing. However, falsely elevated values can be obtained in individuals with arteriosclerotic vessels. Other tests for assessing vascularity include the determination of skin-perfusion pressures and transcutaneous oxygen pressures. The former is a test to determine the minimum pressure needed to prevent reddening of the skin after blanching. The latter can be used to determine healing potential also after amputation.⁴ Pressures of less than 20 mm Hg have a high rate of wound infections, whereas readings higher than 30 mm Hg indicate adequate healing potential.

Laboratory Studies. Glycolic control is very important in diabetic foot care. Poor metabolic control of diabetes has been linked to a higher risk of developing ulcers.¹¹^,¹² Elevated hemoglobin A1C levels are linked to increased ulcer healing times and recurrent ulcers.¹³^,¹⁴ These levels should be monitored because they are indicative of patient compliance and healing optimization.

In addition, total serum protein, serum albumin level, and total lymphocyte count should be evaluated. Minimum values for optimized tissue healing are as follows¹⁵:

Total serum protein concentration greater than 6.2 g per dL
Serum albumin level greater than 3.5 g per dL
Total lymphocyte count greater than 1,500 per mm³

Radiographic Features

Radiographs. Radiographs should be obtained as a first line diagnostic workup to assess for changes that can result from a diabetic foot. These changes include stress fractures, fractures, osteolysis/bone destruction, dislocations, subluxations, and any change in the alignment of the foot and ankle bone structure. Specific changes seen in the Charcot foot will be discussed later in the chapter.

Computed Tomography. The use of computed tomography provides improved detail of osseous anatomy compared with conventional radiographs and magnetic resonance imaging (MRI). Computed tomography is the preferred method for evaluating cortical details and changes, as in assessing postoperative bone healing of fractures or fusions. Moreover, computed tomography can also be used to evaluate soft tissue disease such as an abscess. However, MRI is favored for this type of analysis because of its ability to differentiate many types of tissues and their processes.

Magnetic Resonance Imaging. MRI is very sensitive in detecting both soft tissue and bone changes resulting from various causes, changes such as stress fractures, abscess, osteomyelitis, or neuropathic arthropathy. However, the difficulty arises in differentiating between Charcot joint versus osteomyelitis. Both pathologies will result in increased bone marrow edema and erosions, as will be discussed more at length in later sections.

Bone Scans and Labeled White Blood Cell Scans. Nuclear technetium-99m (⁹⁹mTc) bone scans have been found to be more sensitive in detecting Charcot joint and osteomyelitis than conventional radiographs. However, when compared with MRI, bone scans has been found to be less sensitive.⁴ Even though a negative study is a good indicator that osteomyelitis or a neuropathic joint is not present, a positive study is highly nonspecific. Uptake on all three phases of a bone scan is suggestive of infection as well as Charcot. Although cellulitis and soft tissue inflammation can be seen on the second phase of the study, a positive scan in the third phase indicative of inflammation in the bone cannot in itself distinguish between Charcot joint and osteomyelitis.¹⁶

A gallium-67 scan can be helpful for soft tissue infection and for detecting osteomyelitis, especially a chronic process. The specificity is improved compared with a ⁹⁹mTc study. However, when compared with a labeled white blood cell scan, the specificity is lower, and its use is further limited by its long imaging time (>24 hours) and high radiation burden.¹⁷

Indium 111- (¹¹¹In) labeled white blood cell scans provide higher specificity and sensitivity for infection than technetium labeled bone scan alone, especially when combined with a ⁹⁹mTc study.¹⁸^,¹⁹ Theoretically, ¹¹¹In-labeled scans help in evaluating for osteomyelitis and distinguish the area of interest from soft tissue infection or Charcot arthropathy. However, clinically it may be difficult to distinguish between the two. The counts produced by indium are low compared with technetium, and recognizing spatial patterns may be difficult. Moreover, bone marrow activation can be observed in chronic Charcot arthropathy, leading to a fasle-positive scan. The clinician should be aware that if there is an ulcer with an overlying dressing, the indium pool can be misleading. Overall, if the ¹¹¹In and ⁹⁹mTc scans are positive in a clinically suspicious area, the likelihood of osteomyelitis is high.

ULCERATONS

INTRODUCTION

Ulcerations in the diabetic foot result from continued pressure in the setting of neuropathy. The long-term cost of ulceration care is high owing to the patient’s need for home care and social services in the setting of recurrent lesions and the need for new amputations.²⁰ Often ulcers are the precursor to subsequent infections, and therefore, they should be treated aggressively.

PATHOGENSIS

Epidemiology

The average annual incidence of new diabetic foot ulcerations was found to be 2.2%.²¹ Risk factors for the development of diabetic ulcerations are prior or current ulcerations; abnormal neuropathy disability score comprising changes
in vibratory, temperature, and pin prick perceptions; abnormal Achilles reflex; previous podiatric attendance; insensitivity to 10 g monofilament; reduced pulses; foot deformities; increased age; and abnormal ankle reflexes. Of these risk factors, prior or current ulcers, abnormal neuropathy disability score, and prior podiatric attendance were found to be highest risk factors for new foot ulcers. A combination of 10 g monofilament, neuropathy disability score, and palpation of foot pulses were recommended as a screening tool in general practice.²¹

Classification

Meggitt^21a and Wagner¹⁵^,^21b described six grades of lesions that are seen in diabetic foot lesions (Table 5.1). Another commonly used classification is the depth-ischemia classification²²— a modification of the original Meggitt-Wagner classification separating evaluation of the foot lesion and vascular perfusions (Table 5.2 and Figs. 5.3,Figs. 5.4,Figs. 5.5 and Figs. 5.6).

DIAGNOSIS

Physical Examination and History

Clinical Features

Most diabetic foot ulcerations occur in the forefoot followed by the heel and midfoot. Treatment of all foot ulcerations must focus on the ulcer depth and vascularity, and whether infection is present. These factors, along with the location of the ulcer and foot deformities, such as claw toes, should be carefully documented. The ulcer depth will determine whether surgical treatment is needed, and the vascularity will help assess whether adequate healing will occur. If there is concern for a vascular pathology, such as decreased pulses and lack of hair growth on the dorsum of the toes, a vascular consultation should be sought. It is
important to determine infection because surrounding erythema or purulent drainage with an ulcer will usually require inpatient hospital admission for intravenous antibiotics and surgical debridement.

TABLE 5.1 WAGNER CLASSIFICATION FOR DIABETIC FOOT ULCERS

Grade	Definition	Description
0	Foot at risk	Thick callus, no break in skin, prominent bony lesion
1	Superficial ulcer	Total destruction full thickness of skin
2	Deep ulcer	Penetrates through skin, fat, and ligaments but not through bone
3	Abscessed deep ulcer	Localized osteomyelitis or abscess
4	Limited gangrene	Limited necrosis in toes or foot
5	Extensive gangrene	Necrosis of complete foot, with systemic effects

TABLE 5.2 DEPTH/ISCHEMIA CLASSIFICATION FOR ULCERS DEVELOPED BY WAGNER AND MODIFIED BY BRODSKY

Grade	Description
Depth Classification
0	At risk foot, no ulcer (Fig. 5.3)
1	Superficial ulcer, not infected (Fig. 5.4)
2	Deep ulceration exposing tendon or joint, with or without superficial infection (Fig. 5.5)
3	Extensive ulceration with exposed bone and deep infection (Fig. 5.6)
Ischemia Classification
A	Not ischemic
B	Ischemia without gangrene
C	Partial (forefoot) gangrene of the foot
D	Complete gangrene of the foot

Figure 5.3 Grade 0 ulcer: foot at risk for ulceration.

Figure 5.4 Grade 1 lesion: superficial uninfected ulceration.

Figure 5.5 Grade 2 lesion: exposed tendon.

Figure 5.6 Grade 3 lesion: extensive ulceration with exposed bone and deep infection or abscess.

TREATMENT

Grade 0 lesions with the foot at risk can be treated by shoe modifications, molded inserts or extra depth shoe, patient education, and regular examinations. Once skin breakdown occurs, it must be treated aggressively to prevent progression of the lesion. Options for external pressure relief of grade 1 lesions are postoperative shoes, ankle foot orthosis, prefabricated walking braces, and total contact casts. Of these options, the total contact cast was found to have both a higher rate of and shorter time to healing.²³ Healing rates of 90% were found at a mean of 5.5 weeks in grades 1 and 2 lesions. Of recurrent ulcers, 81% healed after 2 weeks in a second cast.²⁴

In addition to proper offloading of pressure areas, appropriate wound care of the ulcer is necessary to prevent tissue dehydration cell death, and to help accelerate wound healing. The correct dressing will help absorb exudates from the ulcer, act as a barrier to further contamination, prevent wound desiccation, and is easily removed.²⁵ An array of products is available to help with ulcer management that have different properties, including maintaining moisture, decreasing fluids/maceration, protection from pressure and shearing, absorbance of exudates, debridement of tissues, delivery of antibiotics, controlling odor, contouring to the appendage’s wound, and application of compression.

Furthermore, if the ulcer is recalcitrant to treatment or if vascular compromise is suspected, additional evaluation by vascular surgery should be sought. Vascular stents or reconstruction by the surgeon might be needed to allow optimal perfusion for tissue healing.

Surgical indications are when pressure modification fails or when higher-grade lesions are diagnosed. Grade 2 and 3 lesions require surgical intervention, with grade 3 lesions requiring antibiotics and possible amputation. Compared with ulcers in other areas, hindfoot ulcers are more likely to require surgical intervention because of the difficulty in unloading the tissues and the decreased perfusion in the area.

Techniques used in operative treatment comprise ulcer debridement, resection of bony prominences, and realignment of foot and ankle deformities. Correction of claw toes and hammer toes might also be considered to decrease occurrence or the recurrence of dorsal forefoot ulcers. Moreover, an Achilles tendon lengthening might also be considered to decrease forefoot or midfoot plantar pressures. One study found the recurrence of plantar ulcers decreased by 75% at 7 months and by 52% at 2 years in patients who underwent total contact cast with an Achilles tendon lengthening compared with patients with total contact cast alone.²⁶

Complications

Total contact cast application can result in new ulcerations over bony prominences, especially the malleoli,
fifth MT tuberosity, toes, and skin overlying the anterior tibia. To reduce these complications, a well-fitting cast covering the toes should be applied and checked regularly for loosening, which could lead to pistoning-induced rubbing. Moreover, placing the cast with the ankle in neutral will help to prevent increased pressure along the anterior

tibia.⁷

Nonhealing ulcers after surgical debridement and resection of high pressure areas can be secondary to avascularity, inadequate relief of pressure, residual infection, or poor nutrition.⁷ Although limb salvage is often preferred, amputation is a treatment option. Risk of amputation is considerably increased with a history of ulcerations. Five-year amputation rates in diabetic patients with ulcerations were found to be 19%.²⁷ Therefore, aggressive ulcer treatment is pivotal.

Achilles lengthening can also have complications. Holstein et al.²⁸ found increased transfer lesions to the heel in patients with complete anesthesia of the area and with placement of the ankle in extreme dorsiflexion postoperatively. They was against Achilles lengthening in individuals with complete anesthesia of the heel pad and suggested that the procedure should be done in a setting where complications can be identified and treated. If a lengthening were performed, the patient had to be protected with splinting, bracing, or casting in neutral or plantar flexion.

INFECTIONS

PATHOGENESIS

Epidemiology

Diabetic foot infections are commonly polymicrobial, with various combinations of organisms, although single-source infection can occur. Common organisms include Grampositive cocci such as staphylococci, group B streptococci, and enterococci; Gram-negative aerobic rods (Escherichia coli, Enterobacter, Proteus, Pseudomonas); and anaerobes (Bacteroides fragilis, Clostridium, Bacteroides). Of the organisms listed, the most common is Staphylococcus aureus, Streptococcus species, and Enterococcus species. However, it is important to remember that one-third of diabetic foot infections test positive for anaerobes in addition to other organisms.⁴^,⁷

Pathophysiology

Patients with diabetes are prone to infections from various factors. Autonomic dysfunction makes them more susceptible to skin fissures and cracks that introduce organisms into the body. Fibroblast function decreases, resulting in less collagen production, and reduces soft tissue strength, making the patient more susceptible to soft tissue breakdown.⁴ Leukocytes respond less effectively because of altered chemotaxis.²⁹ Furthermore, hyperglycemia, decreased oxygen tension, and malnutrition all contribute to soft tissue edema, increased acidity, hypertonicity, and inefficient anaerobic metabolisms. These changes result in an environment favorable for bacterial growth and impaired leukocyte function.⁷ Moreover, vascular compromise can lead to decreased antibiotic delivery, which in turn leads to ineffective bacterial eradication.

DIAGNOSIS

Physical Examination and History

Clinical Features

Diagnostic cultures should be obtained to adjust antibiotics to specific organisms and their susceptibilities. As a result, proper culture technique is very important. Superficial swabs from the ulcers, sinus tracts, or outside layers from deep wounds have a poor correlation with organisms causing the deep tissue infection.³⁰^,³¹ ^and ³² The most reliable method is to obtain surgical deep tissue biopsies and bone biopsy if osteomyelitis is suspected. In the outpatient setting, curettage of the base ulcer will have better correlation with deep cultures than with superficial swabs. Specimens should be sent for aerobic and anaerobic cultures, as well as for pathologic examination, to document signs of inflammation in the tissues and bone. In situations where the patient was already on antibiotics, negative culture results can occur. It is reasonable to stop antibiotics for several days before the procedure to aid in obtaining positive surgical cultures.⁷

Radiographic Features

In addition to basic radiographs, MRI should be obtained to localize infections, assess areas of fluid collection and abscess, and to evaluate the extent and planes of infection. The role of MRI in evaluating infection has been found to be highly sensitive and specific.²⁵ On MRI, infections will show as increased T2 signal intensity. In osteomyelitis, infected bone marrow with increased T2 signal might be observed compared with normal areas. Although not required for every infection, MRI imaging when done early in the hospital course can be cost-effective by leading to quick and proper diagnosis.³³ However, it is important to remember that MRI does not distinguish Charcot arthropathy from osteomyelitis.

TREATMENT

General Considerations

Grossly infected wounds or any wound with an abscess should be aggressively debrided down to viable bleeding tissue; debridement should not be limited to the superficial dermal layer. However, a balance between stability and removal of infectious foci must be reached. When draining abscesses, longitudinal linear incisions should be made to provide increased flexibility and better healing potential.⁷ Established areas of osteomyelitis should also be debrided as much as possible while balancing foot stability with the removal of infectious foci. In addition to operative management, hospital admission for intravenous antibiotics is
often required for grossly infected wounds. The duration of therapy and choice of antibiotics will be based on culture data, extent of infection, and clinical response to treatment. Infectious disease consultation should also be considered.

Surgical Treatment for Osteomyelitis

Forefoot Osteomyelitis. Osteomyelitis of the toes must be treated by an ablative surgery that transects or disarticulates all or part of the toe. Because the infection can track along the flexor and extensor tendons, squeezing the forefoot after toe removal and observing for purulent material around the proximal remaining tendon is important. Regardless of the level of amputation, preservation of adequate skin and subcutaneous tissue to provide primary closure of the wound is critical. A common complication after complete toe amputation is the drifting of the adjacent toes owing to lack of support from the adjacent toes and pressure from footwear.

Osteomyelitis of the Metatarsals. The most common site for osteomyelitis is the MT heads because of the high frequency of ulcers in these bony prominences. If infec tion involves the level of the first MTP head, partial or complete first ray resection is usually needed. However, the infected MTP head can be resected if the infection is isolated to that area. It is important to remember that there is a high incidence of transfer lesions requiring further MTP head resections. If the corresponding toe is viable, attempts can be made to preserve the toe to prevent migration of adjacent toes. If local resection is not possible, then single or multiple ray resections might be warranted. This option is more favorable than trans-MT amputations because it allows better footwear fit after surgery.

Osteomyelitis of the Midfoot, Hindfoot, and Ankle. Midfoot osteomyelitis is usually the result of varus deformity of the hindfoot and subsequent ulcer and osteomyelitis of the base of the fifth MT. After aggressive debridement, the deformity can be worsened if the peroneus brevis tendon is resected or not reattached. If reattachment is not possible, then future triple arthrodeisis may be needed to treat the deformity.

Hindfoot osteomyelitis can be treated by partial or total calcanectomy. Typically, these are performed through longitudinal posterior and plantar incisions. However, published series demonstrate a high failure rate in partial calcanectomies.^33a^,^33b Negative pressure dressings can assist in achieving closure. Failure of calcanectomies are treated with a below-the-knee amputation.

Ankle osteomyelitis usually results from deformity secondary to Charcot arthropathy. If conservation management with casts, removable boots, or custom ankle foot orthosis fails, local debridement followed by realigning arthrodeisis should be considered. When osteomyelitis is the result of venous or arterial insufficiency or pressure ulcers, vascular intervention and resection of osteomyelitis are undertaken. The more challenging cases may ultimately require amputation.

CHARCOT ARTHROPATHY

INTRODUCTION

Charcot neuroarthropathy is a progressive disease associated with deterioration of weight-bearing joints that occurs most commonly in the foot and ankle. Charcot arthropathy was first described by Jean Martin Charcot³⁴ in 1868. Initially associated with tabes dorsalis infection, Jordan³⁵ recognized the association between Charcot and diabetes mellitus in 1936. In 1958, Jacobs³⁶ recognized that early and frequent radiographs are needed to follow the pathology closely in patients with diabetes, especially in those with concurrent ulcers. Currently, diabetes mellitus is the leading cause of the neuroarthropathy.

PATHOGENSIS

Epidemiology

The incidence of Charcot arthropathy has been estimated to be 1% to 37% among the diabetic population. A retrospective review of 456 patients with diabetes in 1997 noted radiographic changes of Charcot joint in 1.4% of patients.^36a However, it is important to note that the rate of Charcot arthropathy has been increasing compared with older studies, which could be attributed either to an actual increase in the incidence of the disease or to increased awareness among treating physicians. Rates among men and women are similar. Approximately 30% of patients have bilateral involvement.⁷

Pathophysiology

The exact mechanism of Charcot neuroarthropathy has not been elucidated. Two major theories have been proposed, although the pathogenesis is likely multifactorial. The first is the neurotraumatic theory, attributing bony destruction to repetitive mechanical trauma or a single traumatic event secondary to loss of pain sensation and proprioception. The abnormal sensory function prevents proper offloading of the area by the patient, thereby allowing continued stress and tissue failure. Animal models have supported this theory by showing the development of Charcot denervation and mechanical trauma. Some doubt has been cast on this theory by clinicians who observe Charcot changes in non-weight-bearing joints.

The second theory is the neurovascular theory. This theory proposes that bone resorption and weakening occurs secondary to autonomic dysfunction, leading to increased blood flow to the area. In turn, repetitive minor trauma results in bone fragmentations and instability. Markers of bone turnover and resorption have been found to be elevated in acute Charcot arthropathy, indicating possible increased osteoclastic activity. Moreover, bone density studies have indicated osteopenia and the increased risk for neuropathic fractures.

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