Conservative management forestalls Charcot surgery

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September 2005

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Conservative management forestalls Charcot surgery

Treating a Charcot joint before deformity has occurred may obviate

invasive techniques.

By: A. Sage, DPM

As the number of patients with diabetes in the U.S. continues to

climb past 18 million,1 the incidence of neuropathy and Charcot joint

deformity can be expected to increase. Up to 50% of patients who have

had diabetes longer than 15 years suffer from neuropathy.2 Estimates

of the prevalence of diabetic neuroarthropathy range from 0.15% of

all diabetic patients to 29% of all neuropathic diabetic patients.

The expectation that foot specialists will continue to see

significant numbers of patients with this condition demands that an

appropriate treatment protocol evolve for the diagnosis and

management of early joint disruption as well as severe late

destruction.

Considerable attention has been given to reconstructive Charcot joint

surgery for major deformity. New, advanced techniques of internal and

external fixation are being applied to the surgical treatment of the

advanced stages of this condition. However, when the condition is

diagnosed and managed early, severe destructive changes may be

minimized. Orthotic care can be applied in many cases without the

need for surgery. Some deformities can be treated with relatively

simple exostectomies, which can successfully reduce ulcer risk with

far less likelihood of complication than extensive reconstruction.

As with most complications of diabetes, early detection and

appropriate long-term follow-up may reduce the morbidity of Charcot

joint with significantly less invasive techniques than may be

required to manage the advanced stages of this condition.

Definition, etiology, and diagnosis

Neuropathic joint destruction was first described by J.M. Charcot in

Paris in 1868. A Charcot joint may be defined as progressive

destruction of pedal architecture arising from relatively minor

stress or injury closely associated with peripheral neuropathy. It is

seen in many types of peripheral neuropathy, including those

associated with syphilis or chronic alcoholism. However, the most

common form seen today is associated with diabetic peripheral

neuropathy.

Eichenholz3 has classified Charcot joint in three stages. Stage I

refers to the developmental, or early destructive phase. This may

present only as an unexplained unilateral swelling in the foot. As

the condition progresses, periarticular fractures and subluxations

begin to appear. Untreated, these fractures and subluxations may

progress to severe distortion and dislocation. Stage II refers to

coalescence, where loose fracture fragments are resorbed, swelling

decreases, and early consolidation and healing take place. Stage III,

as the fragments ankylose and stability returns, is known as the

reconstructive phase. Swelling resolves during this stage and the

foot assumes what will be its long-term appearance.

Several theories have evolved to explain the process.4 Some believe

that a sensory defect alone leads to bone loss and destruction under

minimal stress. Others have suggested that a defective autonomic

neurovascular reflex can predispose the foot to fracture and

dislocation. A third theory implicates a bone metabolic defect

expressed as increased osteoclastic activity, which leads to the

destructive changes observed in Charcot joint.

The sensory neurotraumatic theory claims that minor injury leads to

significant damage because protective reflexes that usually support a

joint under stress fail to fire the necessary musculature. This

failure is a result of the sensory loss of diabetic neuropathy.

Lacking support under stress from intrinsic or extrinsic musculature,

bone fracture and joint collapse may then occur.

The autonomic theory suggests that lost control of peripheral

vasodilation leads to hyperemia in periarticular structures. This

results in weakening of the bone surrounding the foot joints,

allowing collapse to occur under relatively minor strain.

A metabolic abnormality of bone associated with diabetes that leads

to increased osteoclastic activity, and therefore greater destruction

of bone damaged by low-grade stress, has been suspected in the

etiology of Charcot joint. It may well be that a combination of these

factors actually leads to the Charcot joint destruction that we

observe clinically, which is characteristically out of proportion to

the degree of stress or injury sustained.

Several patterns of injury have been observed that include the

metatarsophalangeal joints, Lisfranc's joint, the midtarsal or

subtalar joints, and the ankle. The most severe and limb-threatening

are those patterns affecting the more proximal joints.

In early stage I, diagnosis is based on a history of relatively minor

foot strain or injury, and otherwise unexplained unilateral swelling

in a diabetic neuropathic patient. X-rays may initially be negative,

in which case a bone scan may be helpful to identify early

periarticular bone damage or hyperemia. In stage II, x-rays

demonstrating destructive bone and joint changes confirm the

diagnosis. Ulceration tends to be associated with the more severe

deformity in any stage. Osteomyelitis may be a component of the

diagnosis if there is open ulceration down to bone, but severe

collapse of the arch is still to be considered part of the Charcot

process. If the diagnosis is made early and the foot is properly

rested, the severe destructive changes frequently seen in this

condition may be prevented or minimized. Stage III Charcot joints

present deformity with evidence of healed bone and joint injury.

Swelling is decreased or absent at this point. The deformity is

unlikely to progress further.

Initial treatment

Treatment depends on the severity of the deformity and the presence

or absence of ulceration or infection. Ulceration to bone with

evidence of osteomyelitis or deep abscess requires surgical

debridement. Likewise, if the condition was not recognized early on

and the patient has walked extensively, severe instability or

ulcerative deformity may develop. Severe deformity, gross

instability, and dislocation are indications for major surgical

reconstruction or amputation if serious infection complicates the

Charcot joint. If the diagnosis can be made on the basis of minor

injury, unexplained unilateral swelling, and minimal deformity,

nonoperative intervention will suffice. In his recent review of 147

feet with midfoot disease, Pinzur noted that fewer than half required

surgical intervention to achieve the end point of community

ambulation in a depth-inlay shoe with a custom-fabricated orthosis.5

When minimal deformity is noted and the foot appears plantigrade

(even if dislocation is present), early treatment is directed at

protection and edema reduction. If there is suspicion of deep venous

thrombosis, this should be ruled out with a venous Doppler exam.

According to the protocol I follow, a compressive dressing, similar

to a dressing, is then applied to the lower leg with the foot

in a neutral position. This involves application of multiple layers

of cast padding, followed by application of a posterior splint,

followed again by more cast padding, which is then covered with an

elastic bandage. The patient is provided with a cast shoe, an

assistive device, such as a walker, crutches, or cane, and advised to

minimize his or her walking and standing activity. Work restrictions

are provided, if necessary. Wheelchair use is encouraged if the

patient cannot otherwise protect the affected foot.

The splint is changed weekly and continued until there is significant

reduction in the acute edema. Once this has occurred, the patient is

placed in a removable diabetic cam walker with pneumatic support and

continued in this device until most of the edema has subsided. Knee-

length compression stockings are also helpful in controlling edema.

Some coalescence of the fractures starts to occur in stage II.

The foot will need to be protected from further deformity until

consolidation in stage III has occurred. In my experience, this may

take anywhere from three to 12 months. Once the edema is controlled,

a custom-molded thermoplastic ankle foot orthosis with a cushioned

liner may be prescribed. The AFO should be fabricated in a neutral,

slightly plantar-flexed position to avoid a dorsiflexion stress that

might actually break down the midfoot further instead of protecting

it from damage. A slight 1/8- to 1/4-inch heel may be applied (Figure

1). This orthosis is worn full-time until consolidation is complete

and a physical exam reveals no instability, indicating that stage III

has been reached.

Ulcer care and off-loading

If deformity and ulceration have occurred, the basic principles of

wound care management need to be applied. Most cases of Charcot joint

have adequate circulation for healing. If this is in doubt, however,

a peripheral vascular consultation should be obtained. Diabetes

control and nutritional status need to be optimized. Infection needs

to be controlled. If osteomyelitis is suspected, debridement and long-

term antibiotics will be required. Most important to achieving

healing, however, is off-loading. Several devices may be used for

this purpose.6

Total contact casting has many proponents and will effectively off-

load an ulcerated foot. Application of wound dressings and a

posterior splint as described above has been effective in my

experience, with less risk of cast complications. Likewise, wound

care combined with a pneumatic diabetic cam walker is an effective

method of off-loading.

Two different custom-fabricated devices can be used to off-load and

immobilize the ulcerated Charcot joint. The first is the Charcot

restraint orthotic walker (CROW). This is a removable clamshell-type

brace that is lined with a cushioned material and may have a patellar-

tendon-bearing component. It is bulky and heavy, but effective in off-

loading an ulcerated deformity.4 Our studies have indicated that a

thermoplastic, soft-lined AFO may also reduce pressure adequately to

heal plantar ulceration.7 Figure 2 demonstrates pressure mapping of a

foot with an ulcerated Charcot joint in an unprotected condition and

in a custom AFO. The pressure reduction is dramatic as weight-bearing

stress is dispersed throughout the foot and no longer concentrated in

the ulcerated area.

The use of a cane, crutches, walker, or wheelchair is encouraged

throughout the management of all acute Charcot joints, and especially

those with ulceration. If the patient works on his or her feet,

modifications, work restrictions, or temporary disability may be

required. The more aggressive the early protection and off-loading

are, the less likely there will be severe destructive changes

requiring surgical reconstruction or amputation.

Surgical care

Even if significant off-loading efforts are provided and accepted by

the patient, some Charcot joint deformities create extreme plantar

prominences that require excision if the patient is to remain ulcer-

free. Plantar ostectomy or even partial tarsectomy are relatively

simple procedures that can be used to eliminate ulcerative plantar or

medial bone deformity in an otherwise plantigrade foot.8

If the ulcer can be healed before surgery, exostectomy is performed

and primary closure may be obtained. The clinical protocol in my

practice, if ulceration is present, calls for wide excision of the

ulcer and removal of the underlying bone with an osteotome, bone-

cutting forceps, or ronguer. Then I resect bone until there is no

plantar prominence palpable. If bone biopsies and deep cultures

indicate osteomyelitis, long-term, culture-driven antibiotics are

initiated. In ulcerated cases, especially where there may be

underlying infection, I do not attempt primary wound closure, but

implement local wound care or vacuum-assisted closure, along with off-

loading efforts, until healing is obtained (Figure 3).

Long-term management

Even after the patient has reached stage III, ulcerations have been

closed, and no significant bony prominences remain, I have found that

the foot is still at risk for further ulcerations. AFO use can

usually be discontinued after consolidation has been achieved and all

ulcers are closed. If any instability is noted on physical exam, it

may be wise to continue the AFO use, follow the patient regularly,

and monitor him or her and the device for changes or excessive wear

that may require a new prescription.

It is rare for the stage III Charcot joint to break down further once

consolidation has been achieved. However, focal pressure points at

any residual deformity, hammertoe, or metatarsal head are risk

factors for new ulceration. It is essential that Charcot joint

patients be considered at high risk for further foot ulcers. The

patient should be seen at frequent intervals for evaluation and

management of any keratotic lesions that may develop. Prescription

shoes and orthoses should be obtained, and inspected regularly for

excessive wear. The shoes or orthoses will need replacement at least

annually. With a conscientious program of frequent evaluation and

management that includes keratosis control and orthotic care combined

with patient education, those with these high-risk feet can remain

ulcer-free community ambulators (Figure 4).

Conclusion

Charcot joint is a serious complication of diabetes that can result

in ulceration, infection, and amputation. Severe deformities

frequently require extensive and complicated surgical reconstruction.

Such procedures carry significant risk of failure. However, if

diagnosed early, conservative management may prevent progression of

the condition to the point where amputation or high-risk

reconstructive procedures are necessary.

Compression dressings, splinting, total contact casts, and other off-

loading methods are appropriate early interventions. Custom AFOs,

CROW walkers, and pneumatic cam walkers may be used to protect the

Charcot joint until consolidation is achieved. Simple surgical

debridements and exostectomies may resolve ulcerative deformity

without the need for major reconstruction in many cases.

Once the Charcot joint has become stable in stage III, diligent long-

term care is necessary to reduce the risk of further ulceration. This

care should include the evaluation and management of focal pressure

points, prescription of appropriate shoes and orthoses, and patient

education.

A. Sage, DPM, is a professor and section chief of podiatry in

the department of orthopedic surgery and rehabilitation at Loyola

University's Stritch School of Medicine in Maywood, IL.

References

1. National Diabetes Information Clearinghouse. National diabetes

statistics. diabetes.niddk.nih.gov/ dm/pubs/statistics/#7, accessed

July 26, 2005.

2. Mayfield JA, Reiber GE, LJ, et al. Preventive foot care in

people with diabetes. Diabetes Care 1998;21(12):2161-2177.

3. Eichenholz SN. Charcot joints. Springfield, IL: C. ,

1966.

4. Frykberg RG. Charcot changes in the diabetic foot. In: Veves A,

Giurini JM, LoGerfo FW. The diabetic foot: medical and surgical

management. Totowa, NJ: Humana Press, 2002.

5. Pinzur M. Surgical versus accommodative treatment for Charcot

arthropathy of the midfoot. Foot Ankle Int 2004;25(4):545-549.

6. Armstrong DG, Lavery LA, Wu S, Boulton AJ. Evaluation of removable

and irremovable cast walkers in the healing of diabetic foot wounds.

Diabetes Care 2005;28(3):551-554.

7. Landsman AS, Sage R. Off-loading neuropathic wounds associated

with diabetes using an ankle foot orthosis. J Am Podiatr Med Assoc

1997;87(8):349-357.

8. Pinzur MS, Sage R, Stuck R, et al. A treatment algorithm for

neuropathic (Charcot) midfoot deformity. Foot Ankle 1993;14(4):189-

197.