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Charcot Foot: The Diagnostic Dilemma
TODD C. SOMMER, D.O., D.P.M.,
Prevea Health System, Green Bay, Wisconsin
THOMAS H. LEE, M.D.,
Ohio State University College of Medicine, Columbus, Ohio
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.
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| Charcot foot
occurs most often in patients with diabetic neuropathy, and also
in patients with other neuropathic predisposing conditions. |
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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.
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| The
tarsometatarsal (Lisfranc's) joint is the most common site of
arthropathy, with initial involvement usually occurring on the
medial column of the foot. |
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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 stockinet with low-density foam or one-quarter
inch felt is applied over the tibial crest and malleoli, and around the
metatarsal
heads with one layer of synthetic padding. A three-layer inner plaster shell is
followed by a fiberglass outer shell13 (Figure 7).
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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 |
|
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.
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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.
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| 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. |
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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.
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.
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 exostectomy. 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 ultrasonographer 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.
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| Most cases of
acute Charcot foot can be treated nonsurgically with
pressure-relieving methods such as total contact casting. |
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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.
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.
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- 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.
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the diabetic foot. Instr Course Lect 1993;42:121-39.
- Sella EJ, Barrette C. Staging of Charcot
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patient. J Foot Ankle Surg 1999; 38:34-40.
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- Myerson M, Papa J, Eaton K, Wilson K. The
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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
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North Am 1995;26:375-92.
- Lipsky BA. Osteomyelitis of the foot in
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- Wagner FW. The diabetic foot. Orthopedics
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- 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.
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