charcot foot?

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someone close to me has just been diagnosed with this and i am wondering if anyone else here has it too? He is going in this week to have a cast put on it, but has been told he will prob be wheelchair bound in long term, is it really that bad?

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What is a Charcot Foot (Charcot's joints; Charcot arthropathy; Neuroarthropathy)?
Charcot's foot is a complication of diabetes that almost always occurs in those with neuropathy (nerve damage). When neuropathy is present, the bones in the foot become weakened and can fracture easily, even without there being any major trauma. As the neuropathy is present, the pain goes unnoticed and the person continues to walk on it. This can lead to severe deformities of the foot. As this can be very disabling, early diagnosis and treatment is vitally important.

Another way to consider it - imagine spraining your ankle and not knowing you have done this. You will continue to walk on it - imagine the damage that this would do. This is what happens in a Charcot foot.

The Charcot's foot should not be confused with the foot deformity that can occur in those with Charcot-Marie-Tooth disease - they are very different conditions.

Charcot's foot or Charcot disease takes it name from Jean-Martin Charcot (1825-1893) who was the first to describe the disintegration the occurs to the ligaments and joints. In the medical literature it is often called Charcot's arthropathy or Charcot neuroarthropathy.

What causes Charcots Foot:
In those with Charcot's foot the ability to sense pain is usually lost or impaired (as a result of diabetic neuropathy). The muscles lose their ability to support the foot correctly. As a result of this, minor trauma (eg sprains; stress fractures) to the foot go undetected and do not get treated. This leads to a slackness of the ligaments (laxity), joints being dislocated, bone and cartilage being damaged and deformity to the foot.

What are the symptoms of Charcot Foot:
The most early signs of Charcot's foot include the foot or affected part of the foot being warmer than the other foot, there will be some swelling and there may be redness - this is often all that is initially present (this can come on quite suddenly). There will be no pain and the circulation is usually very good. A deformity then will start to develop (as a result of joint subluxation/dislocation) as the arch of the foot collapses if the midfoot of the foot is affected and is left untreated.

In most cases only one foot is affected, but both feet can be affected over time. Generally, the diabetes is usually long standing and diabetic neuropathy (loss of sensation) is always present and often severe. However, some people with Charcot's foot can develop a "deep" aching type pain, but it is as never as severe as what would be expected given the extent of the injury.

Calluses and diabetic foot ulcers may occur as a result of bony protrusions (due to the deformity that develops) causing pressure inside the shoes. The ulceration can become infected and spread to the bone (stoneflies) and joints (septic arthritis) - this can cause tiredness and a fever.

What is the treatment for Charcots Foot:
The prevention of further joint destruction and foot deformity is the primary initial aim in treatment of Charcot's foot. Rest and stabilization of the area are a key. Most cases should be put in a plaster or fiberglass cast ('total contact cast') to relieve pressure and to prevent further deformity. These need to be replaced periodically until there is no temperature difference between the two feet. This can take up to 6-9 months. Care needs to be taken of the other foot to prevent problems developing.

A drug (bisphosphonates) have been shown to be useful as an adjunct in the management of Charcot's foot.

After the Charcot foot has healed specialized footwear and foot orthoses may be needed to prevent it happening again (this may depend on the extent of deformity). If treatment was not started early enough and/or the foot is deformed, the possibility of an ulcer developing is high. Prevention with footwear and foot orthoses is then very important.

If the deformity is severe or ulcer recurrence is a problem, surgery can be used to reshape the deformity. This may vary from a simple removal of a bony prominence to a fusion of joints to realign the foot.

What can you do to help Charcot Foot:
If you have a Charcot's foot, following medical advice is important. Charcot's can be very disabling if not managed early and properly. Avoid weightbearing as much as possible.

If you do not have Charcot's but have diabetes and neuropathy (loss of sensation), the risk of developing it increases. Avoid putting yourself in situations that may lead to trauma. Check your feet frequently for any swelling. Do not wait, seek professional help urgently if you notice any. The 'wait a couple of days to see what happens' could mean the difference between a good and poor outcome.

Primary care physicians involved in the management of patients with diabetes are likely to encounter the diagnostic and treatment challenges of pedal neuropathic joint disease, also known as Charcot foot. The acute Charcot foot is characterized by erythema, edema and elevated temperature of the foot that can clinically mimic cellulitis or gout. Plain film radiographic findings can be normal in the acute phase of Charcot foot. A diagnosis of Charcot syndrome should be considered in any neuropathic patient, even those with a minor increase of heat and swelling of the foot or ankle, especially after any injury. Early recognition of Charcot syndrome and immobilization (often with a total contact cast), even in the presence of normal radiographs, can minimize potential foot deformity, ulceration and loss of function. Orthopedic or podiatric foot and ankle specialists should be consulted when the disease process does not respond to treatment. (Am Fam Physician 2001;64:1591-8.)

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Charcot neuropathy is a progressive deterioration of weight-bearing joints, usually in the foot or ankle. Historically, neuropathy of the knee was most frequently caused by syphilis, and neuropathy of the shoulder was usually caused by syringomyelia. Today, the Charcot foot occurs most often in patients with diabetic neuropathy; other predisposing conditions include alcoholic neuropathy, sensory loss caused by cerebral palsy or leprosy, and congenital insensitivity to pain. In 1868, Charcot identified neuropathic joints with an unusual pattern of bone destruction in patients with tabes dorsalis. The first description of neuroarthropathy occurring with diabetes mellitus was published in 1936.

Charcot foot occurs most often in patients with diabetic neuropathy, and also in patients with other neuropathic predisposing conditions.

Pathogenesis
Two theories (neurotraumatic and neurovascular) explain the pathogenesis of Charcot foot.1 The neurotraumatic theory attributes bony destruction to the loss of pain sensation and proprioception combined with repetitive and mechanical trauma to the foot. The neurovascular theory suggests that joint destruction is secondary to an autonomically stimulated vascular reflex that causes hyperemia and periarticular osteopenia with contributory trauma. Intrinsic muscle imbalance with increased heel and plantar forces can produce eccentric loading of the foot, propagating microfractures, ligament laxity and progression to bony destruction.

As many as 50 percent of patients with Charcot foot remember a precipitating, minor traumatic event (such as an ankle sprain or previous foot procedure); however, multiple cases of spontaneous Charcot joint changes, including patients with foot infections, support hyperemia as the cause.2

FIGURE 1. Osteolysis of the second metatarsal.
Epidemiology
Neuropathic arthropathy is prevalent in 0.8 to 7.5 percent of diabetic patients with neuropathy; 9 to 35 percent of these affected patients have bilateral involvement.3,4 The higher prevalences occur in referral-based practices. Most patients with neuropathic arthropathy have had poorly controlled diabetes mellitus for 15 to 20 years.

The tarsometatarsal (Lisfranc's) joint is the most common site for arthropathy, with initial involvement usually occurring on the medial column of the foot. The distribution of neuropathic arthropathy is 70 percent at the midfoot and 15 percent at the forefoot or rearfoot; it is usually contained in one area. Nearly 50 percent of patients with neuropathy had an associated plantar ulcer.4

Classification
Neuropathic arthropathy is either atrophic or hypertrophic. The atrophic form is usually localized to the forefoot and causes osteolysis of the distal metatarsals. The metatarsal heads and shafts have a radiographic deformity that resembles a pencil point or "sucked candy cane" (Figure 1). The hypertrophic type usually occurs at the midfoot, rearfoot or ankle, and is traditionally defined according to the Eichenholtz classification system.5 The first stage is the developmental, or fragmentation, stage (acute Charcot) and is characterized by periarticular fracture and joint dislocation leading to an unstable, deformed foot (Figure 2). Patients in the coalescence stage (subacute Charcot) present with resorption of bone debris. The consolidation, or reparative, stage (chronic Charcot) is associated with re-stabilization of the foot with fusion of the involved fragments (Figure 3). This leads to the return of a stable, although deformed, foot (Figure 4). An updated version of the Eichenholtz classification system (Table 1)6 identifies a prefragmentation (or acute inflammatory) stage zero. This is the stage when early diagnosis and intervention are critical to prevent long-range sequelae.7-9 This updated version of the classification system also more closely relates clinical findings to treatment options.

The tarsometatarsal (Lisfranc's) joint is the most common site of arthropathy, with initial involvement usually occurring on the medial column of the foot.

Diagnosis
Approximately 50 percent of patients with Charcot foot remember a precipitating, minor traumatic event, and about 25 percent of patients ultimately develop similar changes on the contralateral foot.9 In patients with diabetes and neuropathy, Charcot joint can develop very rapidly after a minor trauma.

Because trauma is not a prerequisite for Charcot foot, a patient with diabetes and neuropathy, erythema, edema, increased temperature of the foot and normal radiographs most likely has an acute Charcot process. These patients are afebrile, have stable insulin requirements and normal white blood cell counts, and often have no break in skin integrity. These are all conditions that make infection unlikely.

FIGURE 2. (Left and right) Radiographs showing acute Charcot process with dislocation that results in an unstable rocker-bottom foot.

Brodsky7,10 described a test to distinguish a Charcot process from infection in patients with associated plantar ulcers. With the patient supine, the involved lower extremity is elevated for five to 10 minutes. If swelling and rubor dissipate, the diagnosis of a Charcot process is supported. If the swelling and rubor persist, an infectious process is likely.

FIGURE 3. Consolidation, or reparative, stage (chronic Charcot).
Evidence of neuropathy is determined by decreased or absent sensation to pin prick, light touch or vibration. Decreased or absent protective sensation of the foot can be confirmed quite quickly using a Semmes-Weinstein 10-g (also known as 5.07-gauge) monofilament wire (Figure 5). The 10-g monofilament correlates with the threshold of protective sensation. If the patient cannot feel the monofilament (when it is applied with just enough pressure to bend the monofilament) on at least four of 10 sites, the test is abnormal, and the patient is considered to be at risk for ulcer formation.11 Another study12 has shown that testing only four sites on each foot provides information as accurate as that obtained by using eight sites or more. The test can be performed quickly and is sensitive and specific for identifying loss of protective sensation.13

Evaluation
In evaluating the patient who presents with an apparent soft tissue infection or a plantar ulcer, the physician should first determine whether probing to bone is possible. A study14 showed that in patients with diabetes mellitus, probing to bone is strongly correlated with osteomyelitis. Comparison bilateral weight-bearing radiographs, which are critical in determining instability, should then be obtained; however, not all experts agree that comparison views are necessary.15 If there is no radiographic evidence of osteomyelitis but the patient is neuropathic, indium-111 leukocyte scanning or magnetic resonance imaging (MRI) is warranted (Figure 6).16 Indium scanning is highly specific for infection. MRI is extremely sensitive, but the presence of an osteoarthropathy can lead to false-positive results. A variety of other laboratory studies are also typically performed. A high erythrocyte sedimentation rate is frequently found in patients with osteomyelitis, but this test has an extremely low sensitivity. Measurement of the white blood cell count may not help distinguish Charcot changes from osteomyelitis.16 Thus, differentiating Charcot from Charcot with infection remains difficult. Synovial and bone biopsies might be necessary for a definitive diagnosis. After determining that bone changes are charcoid, the patient's deformity is staged. If a neuropathic ulcer is present, it is graded using the Wagner classification (Table 2)17 or an equivalent grading system.

FIGURE 4. Rocker-bottom foot deformity secondary to Charcot process.
FIGURE 5. Semmes-Weinstein 10-g (also known as 5.07-gauge) monofilament wire.

Treatment
TOTAL CONTACT CAST
Most cases of acute Charcot foot can be treated nonsurgically with pressure-relieving methods such as total contact casting (TCC), which is believed to be the gold standard of treatment. TCC was developed in the 1950s. Most of the cast padding is eliminated for exact conformity to the lower extremity, with the goal of evenly distributing forces across the plantar surface of the foot. A tubular stockinette with low-density foam or one-quarter inch felt is applied over the tibial crest and malleoli, and around the metarsal heads with one layer of synthetic padding. A three-layer inner plaster shell is followed by a fiberglass outer shell13 (Figure 7).

TABLE 1
Classification, Characteristics and Treatment Strategies for Charcot Foot
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Stage Characteristics Treatment*
0 Clinical stage Erythema, edema, increased temperature to foot Limited weight bearing (possibly TCC or PPWB), close observation
1 Fragmentation stage Periarticular fractures, joint dislocation, instability, deformed foot TCC, limited weight bearing
2 Coalescence stage Reabsorption of bone debris TCC followed by CROW
3 Reparative stage Stable foot Possible surgical intervention for removal of bony prominences associated with ulceration

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TCC = total contact cast; PPWB = prefabricated pneumatic walking brace; CROW = Charcot restraint orthotic walker.
*--Extra-depth shoes and pressure-relieving orthoses also may be needed.
Adapted with permission from Kelikian AS. Operative treatment of the foot and ankle. Stamford, Conn.: Appleton & Lange, 1999:153.

The first cast is changed after one week because of the rapid reduction of edema that occurs as a result of TCC and restricted, protected weight bearing. Changing the cast prevents shearing between cast and skin. Follow-up casts are changed at two- to four-week intervals until erythema and edema have resolved, the temperature of the affected limb has decreased and is similar to that of the contralateral limb, and stabilization has been established on radiographic findings.

The presence of a Wagner grade 3 (or higher) ulcer necessitates incision, drainage and antibiotic therapy, with resolution of any abscess before application of the TCC. Periodic ulcer evaluation should be performed along with debridement at the time of cast changes.

After the initial radiographs, surveillance films should be taken at four- to six-week intervals (or more often if there is an acute change). It is quite common for the lower extremity to be confined in a TCC for up to four months, with conversion to a Charcot restraint orthotic walker (CROW) after the active phase of the condition is complete, as evidenced by temperature normalization and radiographic stability. Protective foot gear with orthotics will later be needed.

An updated version of the Eichenholtz classification system identifies a prefragmentation (acute inflammatory) stage, when early diagnosis and intervention are critical to prevent long-range sequelae.

TCC with guarded ambulation will lower the risk of developing a contralateral Charcot process compared with strict nonweight-bearing with crutches. Sella and Barrette8 found that 25 percent of patients in the early stages of Charcot with joint diastasis and subluxation who were treated with TCC did not develop foot deformity (severe fragmentation and collapse). TCC also has been associated with improved ulcer healing in noninfected plantar ulcers in patients with diabetes.18

PREFABRICATED PNEUMATIC WALKING BRACE
An alternative to TCC is a prefabricated pneumatic walking brace (PPWB), which has been found to decrease forefoot and midfoot plantar pressure in the treatment of neuropathic plantar ulceration.19 Benefits include easier wound surveillance, ease of application and the ability to use several types of dressings. Use of the PPWB is limited in patients who have severe foot deformity or who are noncompliant.

Distinguishing Charcot Foot from Osteomyelitis

FIGURE 6. An algorithmic approach to distinguishing Charcot foot from osteomyelitis. (MRI = magnetic resonance imaging)
Adapted with permission from Lipsky BA. Osteomyelitis of the foot in diabetic patients. Clin Infect Dis 1997;25:1321.

FURTHER TREATMENTS
After swelling and erythema resolve and radiographic stability has been achieved, the TCC is changed to either a CROW, an ankle foot orthosis or a patellar tendon-bearing brace, depending on residual anterior edema. If anterior edema persists, the CROW full-enclosure system is used (Figure 8). This device is used for six months to two years, until a stable foot is obtained. Patients can then be fitted for extra-depth shoes with custom insoles or orthotics to accommodate any residual deformity. Return to conventional foot gear may not be possible in all cases.

TABLE 2
Wagner Ulcer Classification
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Grade Description
1 Superficial diabetic ulcer
2 Ulcer extension to ligament, tendon, joint capsule or deep fascia without abscess or osteomyelitis
3 Deep ulcer with abscess or osteomyelitis
4 Gangrene to portion of forefoot
5 Extensive gangrenous involvement of the foot

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Adapted with permission from Wagner FW. The diabetic foot. Orthopedics 1987;10:163-72.

The primary care physician may be the first to evaluate minor lower extremity trauma in a neuropathic patient. If the radiographic findings are normal, a one- to two-month period of immobilization with protected weight bearing, followed by supportive shoe wear, is advisable.9 This treatment can usually prevent breakdown of the foot. Diagnosis of a charcoid process is delayed in as many as 25 percent of patients,10 but early recognition can prevent amputation.

SURGICAL TREATMENT
Patients with a consolidated (stable chronic) Charcot foot with a residual exostosis or recurrent or nonhealing ulcer may require an exostosectomy. In patients whose subluxation produces a markedly unstable extremity, a joint stabilization procedure performed by a foot and ankle specialist may be required.

FIGURE 7. Total contact cast for Charcot foot.
FIGURE 8. Charcot restraint orthotic walker (CROW).

PROPOSED TREATMENTS
Other treatments for the Charcot process have included electrical bone stimulation or low-intensity ultrasonography during the acute phase to enhance healing. Although pilot studies of electrical bone stimulation show promise, it has not been labeled by the U.S. Food and Drug Administration for the treatment of Charcot foot.20 Another study found that use of a bisphosphonate (pamidronate) resulted in decreased erythema, decreased temperature and decreased Charcot activity.21 Additional controlled studies are needed to further evaluate the effectiveness of these treatments.

Most cases of acute Charcot foot can be treated nonsurgically with pressure-relieving methods such as total contact casting.

Final Comment
Primary care physicians must consider the diagnosis of Charcot syndrome in any neuropathic patient with erythema, edema and elevated temperature regardless of local or systemic signs of infection. In the patient with diabetes and lower extremity neuropathy, any minor injury requires careful observation because of the tendency of the limb to proceed to a Charcot process. Early identification and treatment of the Charcot process helps prevent deformity and decreased function of the lower extremity, as well as possible subsequent amputation. Physicians should continually educate their patients about the proper care of a neuropathic foot and the use of orthotic devices or custom footwear. The patient with a history of a Charcot process should be seen regularly, with close attention given to erythema, edema or increased temperature in the foot or ankle.

The authors indicate that they do not have any conflicts of interest. Sources of funding: none reported.

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The Authors
TODD C. SOMMER, D.O., D.P.M., has a family medicine/podiatry practice with Prevea Health System, Green Bay, Wis. Dr. Sommer graduated from the University of Osteopathic Medicine and Health Sciences in Des Moines, Iowa. He completed a residency in family medicine at Mayo Clinic, Rochester, Minn. He earned a degree in podiatry from the Illinois College of Podiatric Medicine, Chicago, and completed a residency in podiatric surgery at Henrotin Hospital, also in Chicago.

THOMAS H. LEE, M.D., is director of the division of foot and ankle surgery at Ohio State University College of Medicine, Columbus, and is affiliated with the Orthopedic Foot and Ankle Center, also in Columbus. Dr. Lee received his medical degree from Columbia University College of Physicians and Surgeons, New York City. He completed a residency in orthopedic surgery at the New York Orthopaedic Hospital at Columbia-Presbyterian Medical Center, New York, and a fellowship in foot and ankle surgery at Thomas Jefferson University Hospital, Philadelphia.

Address correspondence to Todd C. Sommer, D.O., D.P.M., Prevea Health System, P.O. Box 19070, Green Bay, WI 54307 (e-mail: todds@prevea.com). Reprints are not available from the authors.

REFERENCES
Brower AC, Allman RM. Pathogenesis of the neurotrophic joint: neurotraumatic vs. neurovascular. Radiology 1981;139:349-54.
Schon LC, Easley ME, Weinfeld SB. Charcot neuroarthropathy of the foot and ankle. Clin Orthop 1998;349:116-31.
Armstrong DG, Todd WF, Lavery LA, Harkless LB, Bushman TR. The natural history of acute Charcot's arthropathy in the diabetic foot specialty clinic. Diabet Med 1997;14:357-63.
Harrelson JM. The diabetic foot: Charcot arthropathy. Instr Course Lect 1993;42:141-6.
Eichenholtz SN. Charcot joints. Springfield, Ill.: Thomas, 1966.
Kelikian AS. Operative treatment of the foot and ankle. Stamford, Conn.: Appleton & Lange, 1999: 153.
Brodsky JW. Outpatient diagnosis and care of the diabetic foot. Instr Course Lect 1993;42:121-39.
Sella EJ, Barrette C. Staging of Charcot neuroarthropathy along the medial column of the foot in the diabetic patient. J Foot Ankle Surg 1999; 38:34-40.
Caputo GM, Ulbrecht J, Cavanagh PR, Juliano P. The Charcot foot in diabetes: six key points. Am Fam Physician 1998;57:2705-10.
Brodsky JW. The diabetic foot. In: Mann RA, Coughlin MJ, eds. Surgery of the foot and ankle. 6th ed. St. Louis: Mosby, 1993.
Armstrong DG, Lavery LA, Vela SA, Quebedeaux TL, Fleischli JG. Choosing a practical screening instrument to identify patients at risk for diabetic foot ulceration. Arch Intern Med 1998;158:289-92.
Smieja M, Hunt DL, Edelman D, Etchells E, Cornuz J, Simel DL. Clinical examination for the detection of protective sensation in the feet of diabetic patients. International Cooperative Group for Clinical Examination Research. J Gen Intern Med 1999; 14:418-24.
Myerson M, Papa J, Eaton K, Wilson K. The total-contact cast for management of neuropathic plantar ulceration of the foot. J Bone Joint Surg [Am] 1992;74:261-9.
Grayson ML, Gibbons GW, Balogh K, Levin E, Karchmer AW. Probing to bone in infected pedal ulcers. A clinical sign of underlying osteomyelitis in diabetic patients. JAMA 1995;273:721-3.
Schon LC, Marks RM. The management of neuroarthropathic fracture-dislocations in the diabetic patient. Orthop Clin North Am 1995;26:375-92.
Lipsky BA. Osteomyelitis of the foot in diabetic patients. Clin Infect Dis 1997;25:1318-26.
Wagner FW. The diabetic foot. Orthopedics 1987;10:163-72.
Mason J, O'Keeffe C, Hutchinson A, McIntosh A, Young R, Booth A. A systematic review of foot ulcer in patients with type 2 diabetes mellitus. II: treatment. Diabet Med 1999;16:889-909.
Baumhauer JF, Wervey R, McWilliams J, Harris GF, Shereff MJ. A comparison study of plantar foot pressure in a standardized shoe, total contact cast, and prefabricated pneumatic walking brace. Foot Ankle Int 1997;18:26-33.
Strauss E, Gonya G. Adjunct low intensity ultrasound in Charcot neuroarthropathy. Clin Orthop 1998;349:132-8.
Selby PL, Young MJ, Boulton AJ. Bisphosphonates: a new treatment for diabetic Charcot neuroarthropathy. Diabet Med 1994;11:28-31.

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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.

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