BioMechanics
September 1999

Evaluation of diabetic neuroarthropathy guides treatment

By Mark S. Myerson, MD

Although the major cause of neuroarthropathy worldwide today is probably still leprosy, the most common cause of what is more commonly called “Charcot deformity” in the U.S. is peripheral neuropathy secondary to diabetes. Neuroarthropathy is frequently associated with gross and bizarre deformities, which often lead to ulceration, infection, and ultimately amputation. The goal of neuroarthropathy treatment should be to stabilize the foot so that it fits in a shoe or brace and does not develop recurrent infection. Although a plantigrade foot is generally not attainable, one that is stable can be achieved for most patients with the use of such nonoperative techniques as simple shoe modifications, casting, or long-term bracing. Selected patients with uncontrolled instability or major bony prominence causing recurrent ulceration require reconstructive surgery.

Although about 40% of the diabetic population has neuropathy,^1-4 only 2% of these patients will develop neuroarthropathy.^5-7 Interestingly, the incidence of neuroarthropathy in the contralateral foot is far greater, about 30%.⁸ This may represent an inherent increased predisposition to developing neuroarthropathy or may be the result of increased load-bearing on the uninvolved foot.⁹ All patients with active or chronic neuroarthropathy must therefore be monitored because the potential for developing deformity in the opposite foot or ankle is a very real concern.

Limited sensation combined with some form of activity is required to develop a neuropathic fracture because repetitive stresses to the foot must occur, similar to the pathogenesis of a stress fracture in the patient without neuropathy.^8,10 I have observed that patients with neuroarthropathy have reasonable (but rarely normal) circulation to the foot. This is understandable because it is likely that perfusion of the foot is in some way related to this disease process. Locally increased circulation as a result of autosympathectomy may also play a role because blood flow may increase locally, increasing the likelihood of bone resorption.¹¹

Although neuroarthropathy is thought of as a process associated with or caused by fracture, this feature is not always present in initial radiographs; in fact, extensive deformity may be present without evidence of fracture. In such patients, failure of the ligamentous support of the foot occurs before fracture, implying that an inherent ligamentous structural weakness increases susceptibility to this type of neuropathic dislocation. Subsequently, as healing takes place, large osteophytes, loose bodies, and periosteal new bone are formed.

The patient with acute neuroarthropathy presents with painless deformity of the foot, erythema, and swelling. Because neuropathy is invariably present to some degree in such patients, it is rare for them to present with pain. However, if pain is present, regardless of the extent or the time of presentation of the neuroarthropathy, the practitioner should suspect the possibility of associated infection, which may cause pain even in the presence of neuropathy.

In this acute phase, due to the associated erythema and swelling, such patients are often incorrectly treated for presumed infection. The differential diagnosis of acute neuroarthropathy, therefore, should include some inflammatory or infectious process, but in the absence of fever or an elevated white blood cell count, and with a normal blood glucose level, infection is highly unlikely. If the diagnosis of infection is still in doubt, two hours of bed rest and elevation of the limb may be helpful, because swelling associated with acute neuroarthropathy will decrease, whereas that associated with infection will not. Occasionally, an infection such as osteomyelitis and neuroarthropathy may coexist, associated with an ulcer or open wound on the foot. However, osteomyelitis is not that common,¹² and the presence of drainage from an ulcer is not, of itself, sufficient to establish the diagnosis, although the presence of pus is strongly indicative of a deep infection. Plain radiographs are not helpful because multiple areas of bone lucency, fragmentation, and periosteal new bone formation are present with both conditions. Magnetic resonance imaging can define the presence (or absence) of soft tissue infection, but it does not differentiate well between acute neuroarthropathy and osteomyelitis because both are associated with bone edema.^8,13-15 Concurrent indium-labeled white cell and technetium-labeled polyphosphate scans (dual window imaging^8,13,16-18) may also be helpful in diagnosing infection. These nuclear medicine studies are quite useful for the diagnosis of osteomyelitis in the presence of neuroarthropathy. The more standard Tc 99m MDP (methylene diphosphonate) triple-phase bone scan is useful only for differentiating bone and soft tissue infection. It is very sensitive for detecting osteomyelitis but lacks specificity and, therefore, should not be used alone to distinguish osteomyelitis and neuroarthropathy.

Staging and treatment

The goal of treatment should be to create or maintain a foot that is stable (i.e., has no tendency to subluxate or dislocate without support) and can fit in a shoe or brace without a tendency to recurrent ulceration and infection. Some patients will need a brace, particularly for the hindfoot and ankle deformities, to provide or maintain this stability. When planning treatment, injury patterns, the patient’s demographics, and the present and anticipated future condition of the injury should be considered.^12,20 We try to anticipate specific problems, such as ulceration and infection, that may develop based on the type and location of deformity.⁸ Most patients with neuroarthropathy should be treated nonoperatively, although surgery may be essential for some deformities in either the acute or chronic stages.

During the acute stage of neuroarthropathy, most of these feet can be satisfactorily managed with some form of prolonged immobilization.²¹ The principles of this approach are to decrease the swelling, stabilize the foot, and protect the soft tissues from ulceration. Healing takes place, but over an extended period of time, and the weight-bearing forces on the foot must be evenly distributed during the healing process.

Swelling is reduced by limb elevation and activity modification, by the use of an Unna bandage, or with an intermittent compression foot pump device. The foot pump rapidly decreases the swelling and will accelerate the initial phase of recovery,²² although due to neuropathy, this should be done in a monitored setting as skin necrosis can occur. Weight-bearing is not permitted during the acute phase, and either a total contact cast ^8,12 or a commercially available removable boot can be used for selected patients. Once the subacute stage is reached and weight-bearing is initiated, a removable boot is used.²³ For the midfoot, six weeks of nonweight-bearing are followed by a cast or boot for an additional four to six months. For the hindfoot and ankle, three months of restricted activity are followed by six to 12 months in a cast.

The goal of treatment for chronic neuroarthropathy should be to evenly distribute the forces of weight-bearing across the foot surface with a custom orthotic arch support in an accommodative shoe or a protective brace, such as an ankle foot orthosis. Generally, midfoot neuroarthropathy can be successfully managed with an extra-depth shoe and an orthotic arch support, whereas deformity of the hindfoot or ankle requires an ankle foot orthosis.

Reconstructive surgery

For acute neuroarthropathy, surgery is indicated if skin necrosis secondary to pressure of a dislocated bone is imminent or if other skin problems are likely to occur as a result of cast or boot treatment. Surgery is also indicated for marked dislocation of the foot that is likely to cause problems with footwear at a later date. Surgery should be performed only during the acute stage because the bone must be of sufficient quality to support the internal fixation. We do not recommend operating on the foot if more than eight weeks have elapsed since the onset of the acute process, or if periosteal new bone formation and bone healing is already present. It is generally far easier to perform surgery when there is a dislocation without fracture. I have found that open reduction and internal fixation alone is not sufficient treatment, and primary arthrodesis is required to adequately stabilize the foot.¹²

After surgery, the foot is protected and, typically, a cast is used for two months with no weight-bearing, and then a weight-bearing cast or a cast brace is used for four months for the midfoot, six to nine months for the hindfoot, and 12 to 24 months for the ankle. However, these times are variable because it is not easy to determine the onset of arthrodesis in such feet. Although arthrodesis, and therefore stability, is the goal of these reconstructive procedures, this may also be provided if a stable pseudoarthrosis of the foot is present.

The problems encountered with chronic midfoot neuroarthropathy are different. Such feet are often unstable and prone to recurrent ulceration and infection despite adequate protection of the foot with an orthosis. This is particularly applicable to the unstable midfoot because a rocker-bottom deformity occurs, with secondary hindfoot equinus and a marked contracture of the Achilles tendon. This type of deformity is extremely difficult to manage because dorsiflexion occurs not through the ankle but through the midfoot at the apex of the rocker deformity. If recurrent ulceration occurs despite adequate protective footwear, it may be caused by prominent deformed bone that will require surgical correction.

If the midfoot is quite stable, the simplest procedure may be to remove the offending bone by exostectomy.^8,12,25 However, an exostectomy will succeed only if the foot is rigid because after this procedure a stable rocker-bottom deformity can become quite unstable. Exostectomy is therefore not my preferred method of treatment, particularly if the prominent bone is in any way supportive of the midfoot.

Generally, if the midfoot has a prominent area of bone causing recurrent ulceration, realignment and arthrodesis are performed. In such feet, realignment is accomplished by resecting a biplanar wedge from the midfoot with a closing wedge osteotomy, and arthrodesis with a screw or plate fixation (Figure 1).^12,20,26

Neuroarthropathy of the hindfoot or ankle is particularly difficult to manage, regardless of the stage of presentation, because the forces of weight-bearing tend to increase the deformity despite adequate immobilization. The goal of treatment should be to maintain the weight-bearing axis of the lower extremity centered over the ankle and subtalar joints. If bone fragmentation and deformity occur, this weight-bearing axis will be medial or lateral to the ankle and subtalar joints, and pressure from the prominent bone will cause ulceration. I have not encountered as much difficulty with anteroposterior deformity as with varus/valgus malalignment. The former, which usually leads to anterior subluxation of the talus anteriorly under the tibia, can be held securely in a brace, unless gross instability is present. The indications for operative intervention include marked instability, fixed deformity or recurrent ulceration, and infection not manageable with a total contact brace (Figure 2). In such patients, open reduction and arthrodesis of the involved joints (such as a triple, tibiotalar, tibiotalocalcaneal, tibiocalcaneal, or pantalar arthrodesis) are performed. I use large, partially threaded, cannulated screws; an intramedullary rod; a blade plate; or a ring fixator, depending on the extent of deformity, bone loss, and the presence of infection (Figure 3).

In the presence of acute or chronic infection or circulatory impairment, the practitioner(s) must decide whether an amputation or a prolonged effort at salvage and reconstruction would be better for the patient. If the patient is unlikely to tolerate the prolonged period of convalescence and rehabilitation intrinsic to salvage and reconstruction, amputation may be the better choice. For those with infection who undergo salvage and reconstruction, I stage the reconstructive process, first with a ring fixator and then, if necessary, using some form of internal fixation for a second stage.

Conclusion

Mark S. Myerson, MD, is director of the foot and ankle service in the department of orthopedic surgery at The Union Memorial Hospital in Baltimore.

References