Acute Charcot`s Arthropathy of the Foot and Ankle

Acute Charcot's Arthropathy of the Foot and Ankle
David G Armstrong and Lawrence A Lavery
PHYS THER. 1998; 78:74-80.
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Acute Charcot's Arthropathy of the
Foot and Ankle
harcot's joint (neuropathic osteoarthropathy) is a progressive condition affecting the musculoskeletal system and is characterized byjoint
dislocation, pathologic fractures, and often debilitating deformities
(Figs. 1 and 2).l The condition most commonly occurs in patients
with diabetes mellitus who have severe peripheral neuropathies. The prevalence of Charcot's joint is variable, ranging from 0.16% of all patients with
diabetes2 to as high as 13% of patients receiving care at a high-risk diabetic
foot clinic.' The frequency of diagnosis of this condition appears to be
increasing as a result of increased awareness of its signs and symptoms.
The Etiology of Neuropathic Osteoarthropathy (Charcot's Joint)
Neuropathic osteoarthropathy was first reported by Musgrave in 1703.We
described it as an arthralgia secondary to venereal disease. In 1868, the noted
French neurologist Jean-Martin Charcot became the first investigator to
.~
linked
concisely describe the neuropathic component of the d i ~ e a s eCharcot
the degenerative condition to syphilis, which was then a common malady.4
Syphilis was the disease most commonly associated with this type of arthropathy until 1936, when Jordan linked it to diabetes m e l l i t ~ s Since
.~
these first
descriptions, numerous theories on its etiology have been p r ~ m o t e d . ~ . " ~
Charcot believed that neuropathic osteoarthropathy was secondary to deficiencies in trophic centers in the spine.4 It was for this concept, along with his
brilliant description of the malady, that neuropathic osteoarthropathy was
subsequently renamed "Charcot's arthropathy." This spinal-centric view of
Charcot's arthropathy, however, was not shared by all of Charcot's contemporaries. Volkman, Virchow, and other members of the "German school"
vehemently opposed Charcot's theory, which they believed was based solely on
observation and assumption. They believed that the etiology of Charcot's
arthropathy was neurotraumatic in nature. That is, an insensate foot subjected
to trauma would fracture and heal with exuberant bone formation. In testing
this theory, Eloesser, in 1917, sectioned the posterior nerve roots to the
forelimbs in 38 cats.' Following a period of activity, Eloesser noted neuropathic
Key Words: Arthropathy, neurogenic;Joint diseases; Lowm extremity, ankle and foot.
[Armstrong DG, Lavery LA. Acute Charcot's arthropathy of the foot and ankle. Phys Thm.
1998;78:74- 80.1
David G Amtrung
Lawrence A Lavety
Physical Therapy . Volume 78 . Number 1
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.
January 1998
With the possible
exception of
bony changes in 71% of the animals. Six decades later,
Finsterbush and FriedmanQepeated Eloesser's experiments using a rabbit model. After sectioning the posterior nerve roots, the rabbits' hind limbs were casted. A
difference was noted in the response to immobilization
between normal and denervated groups. Finsterbush
and Friedman concluded that trauma was important but
not the primary factor leading to the deterioration of
insensate joints."
patient unaware of the
often profound osseous
Charcot's
arthropathy is
perhaps the most
debilitating
destruction taking place
with each step during
amb~lation.~-~"
Diagnosis of Acute
Charcot's
Arthropathy
The initial diagnosis of
acute Charcot's arthropathy is often based on i r e
found unilateral swelling,
Finsterbush and Friedman's work%pened the way for
further conjecture about the nature of Charcot's
arthropathy. Subsequent investigatorsI0 hypothesized
that trauma alone could not explain the sometimes
striking osteopenia seen in patients with Charcot's
arthropathy. This hypothesis led to the notion that
increased blood flow was at least partially responsible for
the arthropathy, causing a resorption of bone and a
subsequent weakening of the supporting structure.
Thus, fractures could be caused by even trivial stress. In
an attempt to lend more credence to this concept,
E:dmonds and coworkers,ll using scintigraphy, demonstrated that blood flow within bone was greater when
neuropathy was present. This neurovascular theory has
gained a great deal of favor among many clinicians
treating patients with this condition.
locally increased skin temperature, erythema, joint
effusion, and bone resorp
tion in an insensate foot.
These characteristics, in the presence of intact skin and
loss of protective sensation, are often pathognomonic of
acute Charcot's arthropathy. Armstrong et all have also
noted that there is some degree of pain in an otherwise
insensate extremity in over 75% of patients with acute
Charcot's arthropathy. Diagnosis is complicated by the
fact that 40% of patients with acute Charcot's arthropathy have a concomitant ulceration,' thus raising the issue
of whether there is contiguous o s t e ~ m y e l i t i s . ~ ~
The actual etiology of Charcot's arthropathy may lie
somewhere between these neurovascular and neurotraunlatic theories. The current theory suggests that, following the development of autonomic neuropathy, there is
an increased blood flow to the extremity, resulting in
osteopenia. Subsequently, motor neuropathies result in
muscle imbalance, which places abnormal stress on the
affected extremity, while sensory neuropathy renders the
When faced with a warm, edematous, erythematous,
insensate foot with a concomitant wound, clinicians may
find it difficult to differentiate between acute Charcot's
arthropathy and osteomyelitis solely on the basis of plain
radiographs. Additional laboratory studies may prove to
be useful in arriving at a correct diagnosis. The white
blood cell count will often be elevated, with a left shift,
on differential analysis in patients with acute osteomyeli-
of diabetes
mellifus.
DG Armstrong, DPM, is Assistant Professor, Department of Orthopaedics, University of Texas Health Science Center, 7703 Floyd Curl Dr, San
Antonio, TX 782847776 (USA) ([email protected]).Address all correspondence to Dr Armstrong.
L4 Lavery, DPM, is Associate Professor, Department of Orthopaedics, University of Texas Health Science Center.
Physical Therapy . Volume 78
. Number 1 .
January 1998
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Armstrong and Lavery . 75
tis. Generalized white blood cell count elevation with a
left shift is strongly indicative of the presence of an
infectious disease such as osteomyelitis. The term "left
shift" implies the premature release of immature polymorphonuclear leukocytes (band forms) into the circulation in response to overwhelming physiologic demand.
This premature release of immature polymorphonuclear
leukocytes into the circulation is also typical in infection.
Although the erythrocyte sedimentation rate may also be
elevated in the case of acute infection, the sedimentation
rate increases in response to any inflammatory process
and is therefore nonspecific. The white blood cell count
with white cell differential assay remains the most clinically useful hematologic means of detecting infection,
and a glaringly elevated white blood cell count or
substantial left shift should alert the clinician to the
possibility of sepsis. A white blood cell count or white cell
differential assay that is within normal limits should
not deter the clinician from instituting appropriate
treatment. l5-I7
Technetium bone scans are expensive and nonspecific
in assisting in the differentiation between osteomyelitis
and acute Charcot's arthropathy.18 We do not believe
that technetium scanning is very useful for the diagnosis
of acute pedal sequelae to peripheral neuropathy.
Indium scanning, although expensive, has been shown
to be far more specific.IYIndium-1 11 scintigraphy may
be used in two instances. First, indium-] 11 scin tigraphy
may be used to initially assist in differentiation between
osteomyelitis and Charcot's joint in the presence of a
pedal ulcer. Second, several weeks following debridement of osteomyelitic bone, indium-1 11 scanning may
provide some benefit in determining the adequacy of
bony resection. If an indium-111 scan is returned positive, a bone biopsy is indicated to confirm the diagnosis
of osteomyelitis and rule out Charcot's joint.' If a scan is
returned negative, the presumptive diagnosis is Charcot's joint until proven otherwise. Additional studies
currently used for assistance in differentiating Charcot's
joint from osteomyelitis include bone scans utilizing
white blood cells labeled with technetium hexamethyl
propylenamine oxime and magnetic resonance imaging.
Although imaging studies may be useful at many centers,
including our own, we prefer to use a sterile blunt probe.
Probing to bone, combined with radiographic and clinical evaluation, may be the most practical and costeffective means of diagnosing osteomyelitis prior to
surgical debridement and definitive bone biopsy. If a
wound is probed directly to bone, osteomyelitis is frequently assumed. This diagnosis may then be confirmed
with a bone
A bone biopsy is currently the
"gold standard" by which all other diagnostic modalities
are measured."' Bone biopsies have a very low complication profile and are less expensive than many advanced
76 . Armstrong and Lavery
Figure 1. Clinical presentation of acute Charcot's arthropathy.
imaging technique^.^^ A positive histologic diagnosis of
Charcot's joint is less clinically important than a negative
diagnosis of osteomyelitis because a prolonged course of
parenteral antibiotics or surgical ablation may be obviated by a negative diagnosis. Nonetheless, a biopsy
consisting of multiple shards of bone and soft tissue
embedded in the deep layers of synovium is pathogne
monic for neuropathic osteoarthropathy.2'
The Classification of Charcot's A~hropathy
The most common classification system used in the
treatment of patients with Charcot's arthropathy was
described by Eichenholz in 1966.Z3 This classification
system is primarily radiographic in nature and is divided
into developmental, coalescent, and reconstructive
stages. The developmental stage is characterized by
profound osseous destruction, with frequent dislocation.
The coalescent stage is marked by evidence of repair of
large fracture fragments. The reconstructive stage
denotes bony ankylosis and often large amounts of
hypertrophic proliferation. Although this system is very
descriptive, it is not very clinically useful.
Sanders and MrdjencovichZ4introduced a classification
system based on the location of arthropathy. Loosely
based on Harris and Brand's classic
this system is
highly descriptive, and, because it denotes the location
of the arthropathy, it is clinically useful. The reason that
Sanders and Mrdjencovich's system is more clinically
useful is that location is pivotal when considering potential complications and fracture healing. For instance,
midfoot fractures, which frequently lead to a "rockerbottom" foot type where the majority of the patient's
weight is on the midfoot, are often the most debilitating
and result in permanent deformity. Using Sanders and
Mrdjencovich's system for location of arthropathy, we
further classify Charcot's arthropathy, based on radiographic,23dermal therm0metric,2"~and clinical signs,z8
as consisting of two treatment-oriented phases: (1) an
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acute phase and (2) a postacute (quiescent) phase. The initial clinical diagnosis of acute Charcot's arthropathy (as
described earlier) is well documented
in the l i t e r a t ~ r eFollowing
.~
resolution
of acute neuropathic osteoarthropathy,
patients a.re converted to the postacute
phase, during which uncasted weight
bearing is introduced (Fig. 3) .l
Management of Acute Charcot's
Arthropathy
lmmobilization and reduction of stress
are essential in the treatment of
patients with acute Charcot's arthropath~.l.~
Many
'
investigators advocate no
weight bearing, through the use of
crutches or other assistive devices, during the acute phase of Charcot's
arthropathy. Although this is an ~i~~~~
2. ~ ~ nphic
d i presentation
~ ~ , of acute Charcot's arthropathy.
accepted form of treatment, a threepoint gait may increase pressure to the
return of skin lines to the foot. Radiographic signs of
contralateral limb, thus predisposing it to repetitive
quiescence are evidenced by trabecular bridging on
stress, ulceration, and neuropathic f r a c t ~ r e . ~Arm"
serial radiographs. Although the prevalence of bilatstrong et all reported that, through the use of approprieral arthropathy has been reported to be as high as
ately applied total contact casts (Fig. 4), most patients
two thirds of cases, our recent report of a large series
may ambulate during the entire period of treatment.
of patients showed a prevalence of only 9%.1,",33
All patients at our center were initially treated with total
Perhaps more interesting than the prevalence of bilatcontact casting.30The total contact cast consists of an
eral acute Charcot's arthropathy is whether contralateral
inner layer of plaster with thin felt applied to the
Charcot's joint events occur during treatment. We have
malleoli and tibia1 crest and foam applied to the digits
observed no contralateral events during treatment of
for protection. The outer splints and remaining layers
patients with unilateral acute Charcot's arthropathy.
are made of fiberglass, with an optional rubber cast plug
Patients whose lower limbs are placed in these casts are
secured to the plantar aspect of the cast to increase
able to ambulate freely during the majority of treatment.
durability. Casts are routinely checked weekly and evalWe believe that the resultant reduced stride length and
uated for proper fit. Casts of patients with concomitant
decreased cadence expose the contralateral extremity to
ulceration (Fig. 5 ) are changed weekly for ulcer evalualess repetitive trauma than might occur if a patient
tion and debridement. Cast change intervals for patients
walked with crutches. These factors, combined with
w~thout ulcers are dependent on cast comfort and
frequent monitoring and appropriate prescription of
integrity ( 3 weeks maximum). Casting is discontinued
footwear (eg, depth-inlay shoes versus custom-molded
based on clinical, radiographic, and dermal thermometshoes), may reduce the risk of precipitating a bilateral
ric signs of quiescence. Skin temperatures are monitored
episode of acute Charcot's arthropathy.
using a portable infrared thermometric probe. Use of
dermal thermometry in the diabetic foot has been well
de~cribed.Z~,~~
Until recently, there were no reports concisely detailing
treatment of patients with acute Charcot's arthropathy
through the postacute period. The mean time of immoPatients with bilateral acute Charcot's arthropathy
bilization (casting followed by removable cast walker)
present a unique dilemma. Because of increased
inflammation (and subsequent increase in temperaprior to return to permanent footwear was approximately 6 months in our study of 55 patients.l Patients
ture) on both sides, dermal thermometry is less effecreceiving arthrodeses and patients who had bilateral
tive in providing clinically useful information. These
Charcot's arthropathy were casted for longer periods of
patients' lower limbs, therefore, remain in bilateral
time (approximately 6 months versus 4 months) and
total contact casts until both feet and ankles normalize
took longer to return to permanent footwear (approxiclinically and radiographically. Clinical signs of quiesmately 11 months versus 6 months).' Myerson and
cence include reduction of edema and erythema and
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January 1998
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Armstrong and Lavery . 77
Charcot's
Figure 3. Charcot's arthropathy treatment algorithm. Reprinted
with permission from Armstrong et 01.1
coworkersmreported that, following open reduction and
internal fixation of acute Charcot's fractures or dislocations in eight patients, the mean time of casting was 5
months. This report, however, did not discuss when
patients returned to permanent prescription footwear
and fully ambulaton functional status.
Figure 4. The ambulatory total contact cast.
Following casting until quiescence, the patients move
into the postacute phase of treatment. Patients may, as
required, then progress from casting to removable cast
walkers to accommodative footwear with ankle-foot
orthoses. Removable cast walkers or braces may be used
to ease the transition from total contact casting to full,
unprotected weight bearing in prescription footwear.
Certain modcls of removable cast walkers (eg, EasyStep
Walker*) have been shown to be as effective as total
contact casts for reducing vertical plantar pressures."4
Several models of removable cast walkers, however, have
poor off-loading characteristics. Therefore, care must be
taken in using a removable cast walker that will not
off-load effectively. The transition to a removable cast
walker should be made when skin temperature gradients
are within 1"C for 2 consecutive weeks at the affected site
compared with the corresponding site on the contralatera1 extremity.' The transition from a removable cast
walker to prescription footwear is based on 1 month of
* Kendall Health Care, 1.5 Hampshire St, Mansfield, MA 02048
7 8 . Armstrong and lavery
skin temperature equilibrium (21°C) at the affected site
compared with the corresponding site on the cantralatera1 ext~wnity.This period of protected weight bearing
provides the pedorthic shoe specialist time in which to
fabricate and appropriately fir prescription footwear.
Reconstructive surgery should be performed if a deformity places the foot at risk for ulceration and if the
deformity cannot be safely accommodated in prescription footwear. If the arthropathy is identified in its early
stages, surgery is often unnecessary. Only 25% of the
patients in the recent study by Armstrong et all ultimately required any form of surgical intervention, with
about two thirds of those patients requiring an exostosectomy to remove a bony prominence and about one
third of the patients needing an arthrodesis. The goal of
any surgery for patients with Charcot's arthropathy is to
create a stable, plantigrade foot that may be appropriately shod and that can support an ambulatory adult.
Surgery is generally undertaken only after radiographic,
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. January
1998
to be of some assistance as an adjunctive modality.77We
refer the reader to the references in this report to
thoroughly investigate this complex neuropathic sequela
of diabetes mellitus.
Summary
With the possible exception of osteomyelitis, Charcot's
arthropathy is perhaps the most debilitating orthopedic
sequela of diabetes mellitus. For this reason, early diagnosis and aggressive, noncompromising immobilization,
pressure reduction, and consistent follow-through are
paramount to effecting an acceptable result.
References
1 i\rmstrong DG, Todd WF, Lavery LA, Harkless LB. The natural
history of acute Charcot's arthropathy in a diabetic foot specialty clinic.
D~abetMed. 1997;14:357-363.
2 Sinha S, Munichoodapa CS, Kozak GP. Neurnarthropathy (Charcot
joints) in diabetes mellitus. Medicine. 1972;51:191-210.
3 Kelly M. William Musgrave's De Al-thrilide Symptomatica (1703): his
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4 Charcot JM. Sur quelaques arthropathies qui paraissent depender
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joint quiescence. After surgery, the patient's lower limb
is inlmobilized until skin temperatures and postoperative edema normalize. Following immobilization, the
patient is progressed to a removable cast walker, followed by prescription of permanent footwear.
Limitations of This Review
The focus of this update is to provide current information regarding the etiology, diagnosis, and treatment of
neuropathic osteoarthropathy. Most of the literature on
this topic has focused on surgical treatment for neuropathic osteoarthropathy, often neglecting the nonsurgical aspects of the treatment protocol. We believe (and
we have reported1) that the majority of patients with
Charcot's arthropathy do not require surgical intervention. For this reason, we have concentrated on outlining
this important aspect of care. There have been brief
disc~lssionsof pharmacologic augmentation to current
treatments, using bisphosphonates to retard bone
resorption,-l5." but this is in need of further investigation. Additionally, electrical bone stimulation may prove
10 Brower AC, Allman RM. The neuropathic joint: a neurovascular
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ulcers associated with midfoot fracture due to Charcot's arthropathy.
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poor indicator of acute osteomyelitis of the foot in diabetes mellitus.
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count with diffeer-entialin the acute diabetic foot infection. J Am Podiatr
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Med. 1996;101:521-525.
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Armstrong and Lavery . 79
18 Keenen AM, Tindel NL, Alavi A. Diagnosis of pedal osteomyelitis in
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35 Selby PL, Young MJ, Boulton AJ. Bisphosphonates: a new treatment
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80 . Armstrong and Lavery
Physical Therapy.
Volume 78
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1 . January 1998
Acute Charcot's Arthropathy of the Foot and Ankle
David G Armstrong and Lawrence A Lavery
PHYS THER. 1998; 78:74-80.
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