VOLUME 2
SECTION 7 : Special Surgery Conditions
CHAPTER 38 Charcot Neuroarthropathy
● Most commonly cited etiology is DM, alcoholic, neuropathy, syringomyelia, injuries to
the spinal cord and syphilis.
● Multifactorial pathological mechanism, oxidative stress, mitochondrial dysfunction,
adipose toxicity, activation of the polyol pathway, elevation of inflammatory markers,
accumulation of advanced glycation end products.
● Neurotraumatic theory: German researcher, Volkman who hypothesized that in the
setting of peripheral neuropathy, there are significant sensory deficits resulting in
impaired pain perception allowing for repetitive acute minor injury or chronic injury to
the foot & ankle. Since the pt lacks inability to sense pain & prevent this from
happening, a response is initiated to the trauma in the form of microfracture or
microdislocation
● Neurovascular theory: autonomic neuropathy, results in impaired vascular reflexes with
arteriovenous (AV) shunting resulting in increased arterial perfusion. Increase in blood
flow to the foot has been implicated in an increased bone resorption with reduction of
bone mineral density predisposing these pts for fractures and collapse.
● In healthy pts, this ligand is expressed by osteoblasts and vital to osteoclast function in
bone resorptions. Osteoprotegerin is also secreted by osteoblasts and also plays an
important role in inhibition of bone resorption by actively inhibiting RANKL.
● Receptor activator of nuclear factor kappaB ligand or RANKL is produced by osteoblasts
and interacts with the RANK receptors on precursors and mature osteoclast cells
● DM with CN, increased expression of NF-kappaB. Cell injury initiates the process leading
to expression of RANKL receptors expressed on the surface of the osteoblasts and T
cells. As the transduction cascade continues, IK kinase is inducted resulting in the
phosphorylization of nuclear factor kappaB, which once activated acts as a transcription
factor promoting increasing osteoclast activity and generation.
Classification
● Clinical symptoms such as swelling, erythema and warmth along with joint effusion.
● Bone scans may be positive in all stages
, ● To monitor progression, serial imaging as well as protected WB should be initiated
● Stage I: development/fragmentation, radiographically there are signs of fragmentation,
dislocations, or jt subluxation as well as osteopenia. Clinically ligamentous laxity.
Protected WB in a total contact cast or pneumatic brace should be initiated. Bracing
utilized until there appears to be resolution on radiograph of fragmentation and
presence of normal skin temperature (up to 4 months)
● Stage II: coalescence phase, radiographically absorption of debris, sclerosis, and fusion
of larger fragments. Clinically decreased warmth, swelling, and erythema. Total contact
casting, pneumatic bracing, CROW, AFO
● Stage III: reconstruction phase, radiographically consolidation of deformity, jt arthrosis,
fibrous ankylosis, and rounding and smoothing of bone fragments. Clinically, absence of
warmth, swelling and erythema, as well as a stable jt with or without a fixed deformity.
Recommend: custom inlay shoes with a rigid shank and rocker bottom sole may be
made. On an ulceration foot surgical intervention in indicated in the form of
debridement, exostectomy, deformity correction, arthrodesis with internal/external
fixation
Sanders & Frykberg
● Classification based on involved areas of the foot and ankle.
● Pattern I: MPJ & IPJ affected, 15% charcot foot
● Pattern II: TMT or Lisfranc JT, 40% most common
● Pattern III: naviculocuneiform, talonavicular, CCJ or Chopart jt affected. 30% occurrence
● Pattern IV: ankle & STJ, occurrence 10%
● Pattern V: calcaneus & least common
Brodsky
● Describes the incidence of DM CN among different anatomical regions of the foot &
ankle
Schon
● Categorizes midfoot deformities
● 4 types: Lisfranc, neviculocuneiform, perinavicular, transverse tarsal patterns of
deformity
● Also stages of severity on the degree of collapse in the sagittal plane as shown on lateral
WB
, ● Stage A: least severe as the deformity does not collapse to the level of the plantar
surface of the foot
● Stage B: deformity collapse to the level of the plantar surface of the foot
● Stage C: represents the most severe deformity in which the midfoot is collapsed beneath
the level of the plantar foot. Deformity represents a rocker bottom foot and is often
associated with plantar ulceration
Physical Exam
● Diagnosis typically made from the appearance of the foot and ankle dislocation or
fracture dislocation on xr in combination with a lack of normal sensation. An equinus
contracture. Hyperemia.
Acute vs Chronic Charcot
● Stage I Eichenholtz: grossly swollen, warm, painless foot (occasional complains of mild
to moderate discomfort) in a long standing diabetic
● 5th or 6th decade of life and are overweight
● Temperature difference between the contralateral extremity with the affected limb, area
2 C warmer
● Pulses 4/4 bounding in nature
● Classic rocker bottom foot, continued WB may result in plantar ulceration
● Acute Charcot jt: erythema, edema, increased warmth. Sometimes misdiagnosed as
gout, cellulitis, or DVT. To r/u cellulitis, perform the a rubor of dependency test by
elevating the affected limb above the level of the heart for a few minutes, erythema
stops is Charcot, erythema remains is cellulitis. Several degrees warmer than the
contralateral foot. Rocker bottom foot in which the talus is PF and medially deviated
with a collapse of the midfoot. It can also present in other jts & lead to medial arch
collapse, bony prominence, ligamentous laxity. Suspicion pts age 40 or over, DM
diagnosis >10 yrs, obesity, peripheral neuropathy. Pts may describe “crunching”
sensation with ambulation.
Imaging
● WB xrays, CT images of the foot and ankle may be negative in the early stages of the dz,
they can be useful in ID chronic pathologic changes.
● XR low sensitivity, specificity <50% in detection, early stages show focal demineralization
and degenerative changes can mimic OA or septic arthritis
● MRI can detect changes earlier than XR
● MRI: very useful detecting early changes of acute Charcot in the form of soft tissue
edema, cortical fx, joint effusion, subchondral bone marrow edema
● MRI lacks utility in distinguishing between OM & Charcot. Anatomically Charcot
primarily affects jts, whereas OM is typically an extension from a skin ulcer. Bone biopsy
is GOLD STANDARD for diagnosis of OM, its sensitivity and specificity are 95% and 99%.
● Three phase bone scans: ineffective in distinguishing between OM and
Neuroarthropathy due to bone remodeling present in both conditions. Uninfected
Charcot jt may have increased activity on bone scan due to hematopoietically active
, marrow, rather than inflammation. With combined technetium-99m sulfur colloid
imaging, OM can be determined when there is accumulation of leukocytes in bone.
● PET: can distinguish between inflammatory and infectious soft tissue and between OM &
neuroarthropathy.
● FDG PET scan to be 100% sensitive and 93.8% specific & MRI to be 76.9% sensitive and
75% specific
Diagnostic Studies
● Pt presents with a red, hot, swollen foot with no skin breakdown, the WBC is within
normal limits, ESR and C-reactive protein are normal or slightly raised. ESR that is
significantly elevated >70mm/h, without other probable cause, is likely a diabetic foot
infection.
● Charcot and OM can be concurrently
● If in fact OM is present, infection needs to be addressed and more importantly
eliminated prior to addressing the Charcot if reconstruction is to be considered and
successful.
● Workup- ESR, CRP, bone biopsy and advanced imaging as needed
Treatment
● TCC non-op treatment of choice when dealing with stage o or stage I of CN
● Plantigrade foot, NON- WB below knee cast or TCC is acceptable for 8-12 weeks during
the acute phase. If TCC is used, then it should be changed every 1-2 weeks while in acute
stage, until edema and warmth stabilize (around 2-4 months). If ulcer present the case
change should be done weekly
● Xr must be take monthly to monitor progression
● For pts with moderate to severe Charcot collapse, custom-made footwear with
custom-made orthosis is recommended
● TCC has been the gold standard in the tx of neuropathic diabetic plantar foot ulcers
● Brodsky type II averages 18 months of NWB
● Ulceration occurs, exostectomy of bony prominence can be considered
● Exostectomy performed for TMT deformity (Brodsky type 1), Achilles tendon lengthening
should be considered for the pt with concomitant recurrent plantar ulceration and
severe equinus contracture.
● TAL or Gastroc recession can decrease the forefoot pressures and improve the alignment
of the ankle and hindfoot to the midfoot and forefoot
Surgical
● Test for vasculature
● DM pt can have falsely elevated ABIs because of Monckeberg medial calcific sclerosis.
Digital vessels are spared from these calcifications, therefore, the digital pressures may
provide more accurate reflection of the perfusion to the pt given extremity.
● When condition is chronic, deformity is more severe and there is more severe
malalignment with fixed deformities
● Address charcot foot as soon as possible
