THE CHARCOT FOOT

MANAGEMENT OF DIABETIC CHARCOT ARTHROPATHY


Other Pictures of Charcot Foot

Author: Bret M. Ribotsky, D.P.M.


Charcot's original description of neurogenic arthropathy in 1869 was limited to patients with syphilis. Since that time, conditions other than syphilis have been found to cause a "Charcot's joint." To date over twenty-four different diseases have been demonstrated to develop this condition. Today diabetes mellitus is the leading etiology for the development of a Charcot joint. The process is characterized by pathologic fractures with an exuberant repair mechanism and is associated with mixed peripheral neuropathies. The common denominator in these various conditions is that motor function is not as severely affected as are sensory modalities in the patient.

The Charcot foot in the diabetic patient is a progressive condition that is not confined to bones but affects all of the tissues in the lower extremity. It is often confused with osteomyelitis and massive infection of the foot necessitating early identification and management to prevent amputation of the lower extremity. With the advent of advanced surgical techniques and a better understanding, the physician may be optimistic with the treatment of this condition. By thoroughly understanding the etiologic factors and deforming forces, treatment can be planned for each specific patient. The etiology of Charcot joints has been argued by many authors.

Johnson in JBJS 1967 reported on 118 patients with Charcot joints throughout the body and animal studies and described three consistent stages in the development of a Charcot joint, irrespective of location, that occur after denervation of that joint. Stage I is the destructive phase, and is characterized by fracture as a result of repetitive trauma without splinting or allowing for repair. As the acute inflammatory response ensues, mechanical destruction progresses and continues with resultant hyperemia and bone resorption. This destructive phase can be halted, and healing generally occurs, if the inflammatory reaction is allowed to proceed naturally, without disturbance. If mechanical destruction continues, however, it will eventually outpace the process of repair, and then the area enters the hyperemic phase. Stage II is characterized by persistent hyperemia and chronic inflammation that leads to progressive loss of bone strength. Further mechanical destruction in the desensitized joint can result in a cycle of destruction and failed attempts at biological repair that characterizes the final Stage III. Johnson observed that for treatment to be successful, the destructive phase must be halted with immobilization. Healing can then occur in an orderly fashion.

Much has been written about sensory defects in the diabetic foot. The clinician must remember that diabetes does not selectively affect the sensory nerves. Motor and autonomic fibers also are involved, and the consequence of motor and autonomic neuropathy must be understood.

There are no para-sympathetic autonomic nerves within the lower extremity; therefore, all discussion regarding autonomic dysfunction will be related to the sympathetic nervous system. The sympathetic nerves in the lower extremity supply innervation to the small blood vessels, sweat glands, and arrectores pilorum muscles of the foot. When the normal constrictive tone normally produced by the sympathetic fibers is lost, vasodilatation occurs and an increased peripheral perfusion occurs. As a result the foot without sympathetic function tends to be warm, dry, anhidrotic and may possess neuropathic edema.

Archer et al, in Diabetologia in 1984 showed that the mean skin temperature increases approximately 7 degrees centigrade in the neuropathic foot as compared to a control foot. Venous occlusion plethysmography demonstrates that, on average, blood flow to the diabetic neuropathic foot is five times greater than in the control patient.

Boulton et al, in Diabetologia in 1982 showed that the pO2 of venous blood in patients with neuropathic feet was significantly higher than that in control subjects. It has been theorized that the site of pathology was within the arteriovenous shunts, which normally are under control of the sympathetic system. Loss of this function will result in blood being routed rapidly to the venous side of the capillary bed, increasing the local pO2, thereby decreasing the distal perfusion to the cells.

The loss of sympathetic function has showed to increase the evidence of vascular calcification demonstrated on x-ray. It is theorized that once an autosympathectomy has occurred, the muscle within the tunica media of the arteries and arterioles will atrophy and secondarily calcify. Edmonds et al, found that vascular calcification was not related to the age, severity, or duration of diabetes, but to the degree of neuropathy that was present. Noting the internal diameter of the vessel is unaffected by medial calcification, the blood flow is not diminished. This fact results in a loss of the flexibility of the vessels; therefore, increasing velocities of blood flow have been demonstrated.

Several experts have suggested that this altered circulatory pattern is responsible for the increased incidence of ulceration seen in the diabetic patient. Arteriovenous shunting and fast flow of blood was said to route nutrients to the venous bed quickly. The tissues were, consequently, deprived of adequate nourishment so even small insults to the integument could initiate ulceration. This theory was objectively and logically disproved. Abnormal pressures in the presence of sensory neuropathy were determined as being the most important factor leading to skin compromise in the Charcot foot. 

Duncanin in JBJS in 1977 showed that bones are highly innervated by sympathetic fibers and that the loss of these fibers have showed an increase in blood flow causing osseous hyperemia.

All the work of the above authors and others have showed beyond a doubt that good peripheral circulation is a necessary prerequisite for the development of the Charcot process.

Motor neuropathy in the diabetic lower extremity tends to precipitate a weakness of muscle groups in the lower extremity, creating dynamic and functional imbalances that either initiate or compound deformities within the foot. The anterior thigh, anterior leg and foot intrinsic muscles are the groups most often affected.

The loss of the intrinsic muscles in the foot will cause the functional development of contraction deformities at the MPJ level. Digital contracture may contribute to loss of sensory or proprioceptive function resulting with the patient grasping the ground with the digits to compensate for lack of balance. This buckling of the toes into a hammertoe deformity will exacerbate the pressure beneath the metatarsal heads and can increase the likelihood of plantar ulceration in a sensory an proprioceptive deficient area.

Loss of strength in the anterior leg will allow a compensatory muscular advantage to the posterior muscles and eventually lead to an equinus deformity. An ankle equinus will result in pathologic stress being applied to the foot most specifically at the tarsometarsal joints.

The loss of strength in the anterior thigh may make it difficult for patients to function around the obstacles of life, going up or down stairs, rising from chairs, etc. As the weakness progresses, the hamstrings gain and maintain a functional advantage and tend to present with a contracture and relative knee flexion deformity. This will continue to perpetuate the posterior leg equinus and shorten the stride of gait, placing the center of gravity anteriorly and causing increased pressure to the forefoot.

The neurotraumatic theory of the Charcot foot is that excessive pressure (trauma) on a foot that does not have sensation can lead to fracture, microscopic or gross, and initiate an exuberant repair process. In testing this theory Eloesser in 1917 sectioned the posterior nerve roots to the lower extremity in 38 cats, he noted neuropathic joint changes in 27 of the animals. Finsterbush in 1975 repeated Eloesser's experiments with rabbits. After sectioning the posterior roots, the rabbits were immobilized in hip spica casts. A difference was noted in the response to immobilization between normal and denervated groups. Their conclusion was that trauma was important but not the primary factor leading to the deterioration of anesthetic joints.

The hypervascular theory is that increases in blood flow are responsible for the weakening and the osteopenia found in the Charcot foot. Edmonds demonstrated with bone scans that radionuclide uptake was greater in all three phases when neuropathy was present. The circulation was increased as a result of neuropathy and that a patient was predisposed to excessive bone resorption, fractures and the development of neuropathic osteoarthropathy.

Hence, the scenario is created. Autonomic neuropathy results in osteopenia and a weakened osseous structure. Pathologic forces caused by mechanical imbalances, which may be present with or without motor neuropathy, place undue stress on the foot which in turn may lead to osseous failure. Sensory neuropathy ensures that the aberrant mechanical forces may go unnoticed by the patient until an enormous amount of damage is done.
 
 

MANAGEMENT OF ACUTE CHARCOT FOOT

The classical appearance of the acute Charcot foot is a warm, grossly edematous, erythematous, grossly deformed foot with rearfoot in valgus and forefoot adducted and elevated yet relatively painless foot in which pulses usually are palpable (edema permitting). Hypermobility of the affected joints/fractures may be found. Ulcerations are often found which may complicate treatment as an infection must be considered until proven negative. 

Radiographs can demonstrate the area of collapse, although the initial episode may consist of microfractures in which joint effusion is the only identifiable finding. The bone may look sclerotic and osteoporotic with multiple shards of bone. This presentation needs to be thought of as osteomyelitis with a high suspicion of Charcot foot until proven otherwise.

Managing the acute stage and ruling out infection is paramount. Vitals, complete blood count with differential, glyco-hemoglobin, SMA-20, sed rate, x-ray of both feet should be ordered on initial visit. If a sign of active infection is noted then hospital admission is warranted. Advanced nuclear imaging may be necessary to differentiate between infection and Charcot process. If infected, intravenous antibiotics and possibly surgical debridement may be necessary. Debridement should be kept as minimal as possible. Biopsy of bone is the definitive test to rule out infection, while analysis of synovial tissue for shards of bone is diagnostic of a Charcot joint. Immediate immobilization and non-weight bearing is mandatory. The crumbled bone cannot be expected to consolidate and unite if the patient remains in a weight bearing attitude. A relative osteopenia exists in the Charcot foot and the acute reaction following the joint collapse acts to further increase the local hyperemia and will promote further resorption of bone. Therefore, continued weightbearing in the acute phase may prevent healing or encourage additional breakdown even at sites other than the initial area. A wheelchair is often needed as protection to the other foot is important to prevent the additional stress from causing an affliction in the other foot.

The acute phase is over when the following conditions are met: The foot returns to normal temperature, a resolution of the edema, an elimination of the redness, and no longer any presence of any hypermobility exists. During this phase rebuilding and reconsolidation of the bony fragments are progressing to bony union. This can vary from months to well over a year and the use of pulsed electromagnetic field units have been found to be extremely beneficial. It has been shown that regions of bone under compression exhibit negative electric potentials while areas under tension showed positive potentials. Basset reported that
an induced voltage of 1.0 to 1.5 Volts/cm of bone is required to trigger calcification of the blocking fibrocartilage found at un-united sites. This allows the final phase of fracture healing to follow. This process is similar in many respects to enchondral ossification.

Careful attention is necessary to recognize and neutralize the deforming forces on the foot and leg. Physical therapy is often helpful in correcting the muscular imbalances by increasing the strength and decreasing the rate of contractures of the specific muscles involved. Muscle imbalances are not benign and sometimes need surgical intervention. Molded shoes, custom orthotics and ankle foot orthotics (AFO) are usually necessary in some aspect at some time in the treatment process.

Surgical intervention is often needed in some capacity in the long term management of the Charcot foot. Biopsy is the definitive test for the diagnosis of Charcot joints. The specimen will demonstrate the presence of multiple shards of bone and cartilage embedded within the deeper layers of the synovium. If osteomyelitis is of concern then a bone biopsy is essential for diagnosis. A skin graft is often helpful to decrease the size of an open wound and the resulting chance for bacterial infection. Even if less than a fifty percent reduction in the size of the wound is accomplished the resulting chance for contamination or infection is significantly reduced. Exostectomy is used when an offending osseous prominence is directly responsible for an ulceration. This is best done through an incision site remote from the ulceration to minimize bacterial contamination of the bone. It is widely felt that exostectomy may be applicable in some instances, however, it appears at best a temporary means by which one can alleviate an ulceration problem. Tendon surgery is often necessary to remove the deforming force that is unable to be eliminated through therapy or to restore muscle balance to a joint. Elective reconstruction may result in the creation of a functional part and prevent amputation in the select patient. Procedural selection is very important. Where joint replacement is very helpful in the patient with osteoarthritis, motion and specifically excessive motion is common in the neuropathic joint and therefore joint replacement and arthroplastic type procedures leave the patient with a grossly unstable joint, and are doomed to failure. Arthrodesis has become the procedure of choice as it provides for the correction and realignment of the deformities, elimination of the instability, improvement in function as well as maintenance of correction.
 

PREVENTION

While it is still unknown why some patients with diabetes develop a Charcot process and others do not, and more interestingly why some patients only develop this condition in one of their feet, an introspective review is necessary. This author's observation that all patients with a mid-foot Charcot collapse have some degree of ankle equinus. It has been theorized by McGlamary and others that this equinus in the Charcot foot begins as a gastrocnemius equinus and progresses onto a gastro-soleus equinus and/or bony ankle equinus. With this in mind, the author believes that patients with neuropathic feet consistent with developing a Charcot foot be thoroughly evaluated for a muscular imbalance.

An equinus deformity has been reported in classic orthopaedic literature as any limitation of passive ankle dorsiflexion to less than a right angle of the foot on the leg. The podiatric literature additionally takes into account the sagittal plane contribution of the subtalar joint into the equation. Dr. Gregg Young of Salt Lake City, has gone one step further and defines equinus as the limitation of dorsiflexion at the ankle to less than 10 with the knee extended and the subtalar joint in its neutral position, when the patient is in their normal shoe gear (compensating for heel height).

In these patients a surgical prophylactic gastrocnemius resection is recommended. It is felt that the risks involved with gastro-resection far undershadow the treatment of a Charcot foot. 
 

SUMMARY

Ideally the goal in treating the Charcot deformity would be to prevent the initial breakdown within the foot. By each physician having a better understanding of the role of the autonomic and motor neuropathy in conjunction with sensory deficits, the Charcot process can be identified earlier and treatment begun sooner. It should be kept in mind that in some patients, conservative care is not in the best interest of the patient.

In the past, surgical intervention has not been considered seriously. This is most likely because of a grave misunderstanding of the vascular factor and the healing capacity of such individuals. Consequently, many patients eventually succumb to amputation following infection or severe deformity that resulted from the progression of the Charcot process. 

With proper planning, timing and knowledge of all facets of diabetic neuropathy, manypatients may retain their foot and benefit from its' function.

BIBLIOGRAPHY

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Reprinted from

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Copyright 1996, Keith R. Reber, DPM ABPS, All Rights Reserved