CHAPTER 3O

NEUROTROPHIC CHARCOT JOINTS FIE,AL FASTERTHAN NORMALJOINTS: Fact or Ficton?

A. Louis Jimenez, DPMNicbol Saluo, DPM

INTRODUCTION

Charcot neuroarthropathy was first described byJean-Martin Charcot in 1868. He detailed a conditioncharacterized by significant and progressive joint andbone breakdown, thought to be associated with tabesdorsalis. Despite the decline in tertiary syphilis, theincidence of Charcot joint disease did not decrease.Conditions that cause Charcot joint include diabetesmellitus, leprosy, syringomyelia, and poliomyelitis.Diabetes mellitus is the most cofiunon cause.

ETIOLOGY

The cause of destructive neuroarthropathy isunclear, but several theories have been proposed.Volkman and Virchow proposed that the cause isfrom an insensate extremity subjected to trauma,both acute trallma and microtrauma. The traumaleads to fractures secondary to abnormalbiomechanical stresses. In fhct, Fishco reported thattrauma can precipitate the development of Charcot,and this includes surgical traLlma. Subsequentinvestigators noted that osteopenia was oftenassociated with this conclition. Theory exists thatsympathetic denelation associated with autonomicneuropathy results in hyperemia wlth subsequentosteopenia and bone weakening. Increased bloodflow is also thought to increase osteoclastic activity.Gough et al measured pyridinilone cross linkedcarboxl, terminal peptide domain of Type I collagen,a marker of bone resorption. It was increased inpatients with acute Charcot, compared with non-Charcot control subjects. Selby et al. measuredurinary deoxypyridilone and alkaline phosphatase.Again, both are markers indicating increasedosteoclastic activity. It is likely that the real etiologyis a combination of all of these theories.

CLINICAL PRESENTATION

Charcot neuropathic arthropathy is clinicallycharacterized as a painless, progressive degenerationof peripheral joints. In the acute phase, the exlremityis eq,thematous, warm, and moderately to severelyedematous. The patient may or may not remember ahistory of trauma.

EICHENH OLT Z CLASSIFICATION

The most widely accepted staging classification isthe Eichenholtz Classification. Although this is aradiographic staging, clinical parameters have beendevised. (Table 1). The big disadvantage to theEichenholtz classification is that early staging isabsent. Schon, et al and Yu, et a1 describe a Stage 0,where radiographic changes are evident but subtle.Mild fracture and/or joint space widening maybe present with the clinical identifiers of ery4hema,edema and calor. Clinically, it is difficult todifferentiate from a Stage I. \fith such subtleradiographic changes, a diagnosis of StaS;e 0 mayonly be determined by ru1ing out other differentials(i.e., cellulitis, osteomyelitis, DVT).

Eichenholt: Glr:aifi cetionSaagt Z * Atil*"/fr€rckp*efi.bJ ,f - Ce.bczret {rl- fr?$ilde,i,,8

RadioghpLir DebG &rutir& boef6{mnt.tiol! ltbhBli!}

Oeblii dhsrylir\coeleseerca olilasretr1s, $r!8Esi,

B6n, &]y1osis,Efomlirr sfelitoate

Clnial Si$aiii.et .rytli.r&.d?B!,ral4r

R*gr?siinl of?.}ltlts&d,edamq calor

fusgbrd

Table 1. The Eichenholtz Classification

I54 CHAPTER 30

DIAGNOSIS

The diagnosis of Charcot is made with the aboveclescribed clinical and radiographic findings, andcan be confirmed with other studies. Technetium99 bone scans can be employed, which will revealincreased uptake in al1 3 phases. A synovial tap willreveal multiple shards of bone ancl cartilageembedded in layers of the synovium. This studywill also help to exclude osteomyelitis from thedifferential. Dermal thermometry can also be usedsimpiy to confirm any temperature change in theextremity. Murff et al studied reliability of manualdetection of temperature changes. They found thatphysicians could correctly detect a temperaturegradient using their hands 1 out of 10 times, thussLrggesting that it may be difficult to cletect subrlecalor associated with Charcot. Dermal thermometrymay be crucial in stage 0.

CHARCOT PERIOPERATTVECONSIDERATIONS

Several factors must be considered when deciding tooperate on a Charcot foot, including age, lifestyle,health, and physician and patient expectations. Onemust consider not only the physiologic status of thepatient and the involved extremity, but peripheralsabout the patient. For example, does the patienthave personal assistance and home settingrequirements that provide for a maximum healingenvironment postoperatively?

The following concerns must be consideredpre-operatively for any patient undergoing Charcotreconstruction.

Many diabetics have co-morbidities that neeclto be adclressed. Many are renally and visuallyimpaired, obesity is a concern and their nutritionalstatus must be assessed. The patient should beunder the best metabolic and nutritional control.

It must be determined whether the patient cantolerate general, spinal, or intravenous sedationanesthesia. \7ill lower extremity tor-rrniquets affectcardiopulmonary status? A decision must also bemade by the surgeon as to whether the entireprocedure can and should be performed wet.

Assessment of vascular status must be com-pleted. Of particular importance are the ABI, Dopplerwaveform, and transcutaneous oxTgen pressure.

One must consider an existing ulceration andthe ability to excise the lesion. Baravarian et alsuggested a 25o/o infection rate involving surgicalintervention with an existing ulceration.

Osteomyelitis must be ruled out. Ifosteomyelitis is present, surgical debridement andcomplete resolution prior to any reconstr-uction isrecommended. Large defects may remain postsurgical debridement. These defects will need to beaddressed before final reconstruction. Intravenousantibiotics, possible antibiotic beads, and bonegrafting may need to be used.

The region of collapse should be noted.Specifically, one should consider the level of laxity,joint stability, and the number of joints involvedbecause this may help to determine the amount ofsurgery required.

The quality of bone should be assessed. Asdiscussed earlieq many patients may present with asignificant amount of osteopenia, and this can havea dramatic effect on surgical olltcome, particulady ifthe surgery involves osteotomies and/or afihrodesis.The surgeon must be prepared to use internalfixation, external tkation, or combination methods tobest address each component of the deformity.

Most patients with Charcot joint breakdowndemonstrate a significant pes valgo planr:s deformityas a result of LisFranc, midtarsal and/or subtalar jointcollapse. An acquired triceps shofiage usually ensuesfurther wedging of the midfoot and rearfootworsening the deformity. Tendoachilles lengtheningmay be considered when total repair of thisdeformity is performed.

Another issue that may be considered, is theappropriate Eichenholtz stage for reconstructiveinteruention. Simon et al published a comprehensivearthrodesis study in 2000. The study involved 74patients who undemrent reconstruction involving afusion procedure at some 1evel. All patients were aStage I Charcot, and all had complete healing withno evidence of delay. \Wang et al followed the studyin 2002 involving 28 patients, all Stage I Charcot. Allunderwent an afihrodesis with the application of anexlernal f'Lrator ancl bone stimulator. All patientswent on to complete healing with no fufiher break-down. The significance of both of these studies isthat acute Charcot may no longer be a contraindica-tion to surgical intervention.

CHAPTER 30 r55

SI]RGICAL CONSIDERATIONS

The question often posed in ner,rropathic Charcotjoint reconstruction is, does a Charcot joint pose anychallenges (internal physiologic, neural, orcirculatory, etc.) that makes surgery in these patientsmore dangerous'? Is there some reason that makesthese bones more difficult to heal? And does thisphenomenon increase morbidity in these patients?There is very 1ittle information published on thissutrject, and these questions have never real1y beenanswered directly. But there are some factors thatmust be considered, u.hich may pafiially explain,and in fact, support some concerns of healing inCharcot foot surgery. \i7e will clemonstrate someclinical examples for the reader to considerregarcling this question later. Despite the idea thatstaging may be of litt1e consequence when perform-ing a reconstructive procedlrre, many of these casesgo on to delayed union, nonunion or malunion. Theremainder of this discussion will explore variablesthat may interfere will postoperative healing.

As mentioned previously, strict glucose controlis of extreme importance perioperatively. Loder andassociates reported that an overall union rate forfracture was 163a/o longer in diabetic patientscompared with healthy controls. Edelsonrecommended that bloocl glucose be maintained at200 mg/dl or lower perioperatively. Uncontrolleddiabetes meilitus causes polymorphonuclearIeukocl,te (PMN) imbalance, including but notlimited to decreased chemotaxis, phagocytosis, anddiapedesis. A1l of these abnormalities combined,directly results in impaired wound healing, impaireclcollagen formation and decre:rsed ability to fightinfection. Edelson reported that diabetics have a 40o/oincreased risk of developing a w-ound infectionfollowing surgical interv-ention.

In addition to PMN firnction, diabetic patientshave an increased incidence of microvasculardisease. Chronic hyperglycemia has a toxic effecton vascular and endothelial cells, as it promotesgiycosylation of blood vessel wal1s resulting incapi11ary basement membrane thickening. Edelsonspeculated that microvascular disease of the skinand subcutaneous tissues may impair woundhealing through decreased clelivery of glucose,oxTgen, and other nutrients to the site of injury.Vhile the macrovascular system often remainsnormal or increased (hyperemia secondary toautonomic deneruation), Pham and associatesreported decreased vasodilation within the

microvasculature system of patients with diabeticneuropathy and Charcot neuroarthropathy.

Diabetes mellitus is also associated withinsulin resistance. Chronic insulin resistance leadsto altered lipid and protein metabolism.Insulinemia has an anabolic effect on protein,which results in impaired neovasculaization,fibroblastic activity and poor PMN bactericidalcapacity. Insulinemia also prevents the productionof fiee fatty acids, which are necessary for celimembrane synthesis needed for wound healing.

Another risk factor for poor surgical healing issuboptimal patient compliance. This may includepoor weight-bearing compliancei poor bloodglucose control, noncompliance with physicaltherapy and external fixation adjustments, poorhygiene with pin sites, and impaired antibioticand/or medication regimen. Edelson reported thatpatient noncompliance is a direct contraindicationfor surgery. The patient truly is the rate limitingfactor, and lf a patient is noncompliant withdiabetes manallement or ulcer management, thenthat behavior will most likely continue throughpostoperative recovery.

It is important that the length of time requiredfor immobilization is not underestimated. Baravartanand associates suggested that diabetics beimmobilized twice as long as the nondiabeticpatient. Surgical planning must be complete.Hamilton and associates remind the surgeon thataggressive bone resection of a plantar and/orrnidfoot prominence can create afi unstablestfticture, which can fufiher progress to a rockerbottom deformity and ulcer formation. Compressionand stability are also impofiant, particularly witharthroclesis procedures. Baker et al advocateexternal fixation to allow for early weightbearingand retardation of disuse osteoporosis, muscleatrophy and joint stiffening. They sugS;est internalbeaming of the medial column with short, Iarge-diameter screws to provide support in conjunctionwith a frame. Recent advances in locking platemechanics and design have improved bone-plateinterface such that an internal constfl-lct is createdwith rigidiry simrlar to an external fkator.

Althoup;h we use clltting-edge technology,instrLrmentation and surgical techniques, often lesssurgery is the better sr:rgical choice, particularly forhigh risk Charcot patients. The goal of surrgery is tocreate a stable and fr-rnctional foot, which may beachieved with a "less is more" approach.

I56 CHAPTER 30

CASE PRESENIATIONS

The first case is a 73-year-ctld neuropathic, type IIcliabetic female who presented to the office with aJones compression dressing after being treatecl atEastside Medical Center for a right ankle fiactureexperienced while she was descending stairs.Clinical evaluation revealed moderate edema of theright ankle, lateral displacement of the foot on theankle, and very mild discomfort inferior to themedial malleoh-rs. Neurological examinationrevealed absent protective response to Semmes-\Weinstein monofilament testing. Radiographicexamination revealed a PER IV ankle fracture withshortening of the fibula and increased medial clearspace (Figure 1). The patient was taken for ORIFand repair consisting of fibular interfragmental screwancl neutralization plate fixation and a transfixionsyndesmotic screw to protect the interosseousmembrane (Figure 2). The patient was kept non-weight-bearing for 6 weeks. This was followed byuse of a fracture boot and physical therapy.Thirleen-week postoperative radiographs revealedloss of correction as a result of transvndesmotic

Figtrre 1. Preoper:ltive radiograpl'ric view reveals PER IV ankle fr:rcture

screw loosening. The fibular fracture had not yetconsolidated and the medial clear space hadincreased (Figure 3). It was felt that because thepatient was a neuropathic diabetic, the absence ofthe protective proprioceptive and kinestheticresponses were absent and pafily responsible forredr:ction failure. The patient was returned tosurgery for exchange of the distal syndesmotic screwand addition of another proximal transfkion screwto provide a rrore rigid construct (Figure 4). Asrecommended by Barav'trian et al the patient waskept nonweightbearing for an additional 12 weeks.One year postoperatively, the ankle was clinicallystable with radiographs revealing complete mainte-nance of reduction and osseous healing (Figure 5).

The second case is a 78-year-o1d IDDMneuropathic female who underwent midfoot andrearfoot Charcot reconstruction of the right foot(Figure 6). Postoperatively, against instructions, thepatient walked out of bed, applying weight to theoperated foot. The patient did not ask forassistance and while trying to sit back on the bed,slipped on the floor, falling ancl traumatizing theleft contralateral ankle. Ankle racliographs revealed

Figtire 2. Irostoperative ankle raciiographs demonstrating recluction ofclcar space, neutralization pl.Lte fixation of lateral malleolus andtransfixion 5s1gv,r plotcctiflg the interosseous membrane.

Figure J. Racliographsmedial clear space as a

3.5 months postoperativelyresult of transtlxion screw

Figure 4. Improvelnent of medial clearankle '.rfter exchange of harchvare ancltransfirion scrern,.

space :Lnd restabilization ofaddition of second proximal

Note s.,icleningloosening.

CHAPTER 30 157

Figule 5. Onc year I'olloning hatchvare exchange anclcolnplete healing of ell osseor,rs se€lnents hrs occurrcclr-cmained completelv stable.

Figure 11. Coniplete fi.rsion of ankle notcclfiamc external fr-ration of left ankle.

Figure 6. Postoper:rtive racliographs of right tirot fbllou'ing reconstrttction of Chalcot foot.

restabilization.'l'he rnkle hrs

Figure 7. Posbperative reduction of fibnlar fi:rcture

Fignre !. Four month postoperativc ankle :rrtlrrodesis laclioglaphicviervs iclentifying loose cannlrlutecl screws. FigLrrc 10. Refusion of ankle ancl stabilization rvith Ilizarov fr:rme

Figure 8. Ankle instabiliry* as aof tlbulal fr:rcture and broken

result of harcl*,are loosening. non unionlr'3 semitr-rbular plate.

2 ye:rrs follou'ing Ilizarov

T58 CHAPTER 30

an SER IV fracture. The patient was taken tosurElery the following clay nhere repair wasaccomplished using an interfragmental screw and aone-third tubr-r1ar neutralization plate (Figure 7).Unfortunately, the patient was very non-compliantwith maintzrining a nonweight-bearing statlls of theleft ank1e. This resultecl in hardware failure,nonunion of the fibula ancl plate breakage (FigureB). One year 1ater, the patient was taken to surgeryfor hardware removal and ankle fusion using 2cannulated screws. Again, the patient ambulatedtoo soon on the operated ankle, causing looseningof the cannulated screws later resulting innonunion of the ankle (Figure 9). The patient wastaken to sllrgery for hardware removal and refilsionof tlre ankle using an Ilizarov external fixationframe (Figure 10). The ankle was healed and stableafter 6-and-a-half months and the external fixatorwas removed. The last office visit 2 years laterrevealed excellent consolidation and stability of theankle (Figure 11).

SUMMARY

In summary, neuropathic patients with autonomicneuropathy, lack sympathetic control of their bloodvessels and therefore, vasoconstriction cannot bezrccomplished. As a result of chronic arterialvasodilation, arthrodesed joints wili consoliclateearlier than in the sensate patient. Yet, because oflack of proprioception ancl lack of muscle andkinesthetic control, these patients are at a higher riskfor loss of intraoperatively acquired alignment.Fractures and osseous procedures, such asarthrodeses, mllst be augmented with aclded formsof fixation and nonweightbearing continuecl 70 to 72weeks longer than the sensate patient. Twenty yearszgo, surgical reconstruction of the diabeticneuropathic Charcot foot was rare. However, usingadvances in medical and surgical knowledge, andcutting edge instrumentation and techniques,Charcot foot reconstruction is now a dailv event.

Multiple morbidities can occur with treatment of theneuropathic Charcot patient. Vhen a mr-rltidiscipli-nary approach is used, the podiatric surgeon cancontinue to achieve very acceptable outcomes inthese patients.

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