developing a comprehensive diagnostic and treatment plan ... · tibiotic treatment of the causative...

tion of bone and joints, disorgani-zation, and finally collapse of thefoot and ankle if weight bearingcontinues during this stage. Thecollapse is accentuated by the con-tinued pull of the conjoined tricepstendon. The final stage is character-

Continued on page 152

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Successful outcomes for this insidious conditionare dependent on a proper work-up.

FEBRUARY 2008 • PODIATRY MANAGEMENTwww.podiatrym.com 151

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GOALS and OBJECTIVES

1) The practitionerwill be able to discussthe main theoreticalcauses of neu-roarthropathy.

2) The practitionerwill be able to list thediagnostic options forneuroarthropathy andidentify the gold stan-dard option and imple-ment them in clinicalpractice.

3) The practitionerwill be able to classify acase of neuroarthropa-thy by both diseasestage and anatomic lo-cation based on radio-graphic and clinical ex-amination.

4) The practitionerwill be able to formu-late a conservative planfor treatment of a caseof neuroarthropathyand identify the goldstandard off-loadingtechnique.

arthropathy in syphilitic patients in1703.1-3 Charcot neuroarthropathybegins with a neuropathic foot thattypically suffers from some type oftrauma, sometimes very minor orunremembered. This incident is fol-lowed by an acute inflammatorystage with progressive fragmenta-

C L I N I C A L P O D I A T R YC L I N I C A L P O D I A T R Y

Developing aComprehensiveDiagnostic and Treatment Plan for CharcotNeuroarthropathy—Pt. 1

Authors: Brent Bernstein, DPM andJohn Motko, RN

What is Charcot foot?Jean Martin Charcot first pub-

lished a description of neuropathicarthropathy in 1868, althoughWilliam Musgrave first noted

cians have accepted a confluence ofthese two theories. Additionally, re-searchers have investigated the pos-sibility of a pre-existing “diabeticosteoporosis” in setting the stagefor neuroarthropathy.8-13 Jeffcoatehas also implicated the possibility

of a cycle of pro-inflammatorycytokine release that allows thevicious cycle of inflammationand osteopenia to continue. (14)Lastly, important work has alsoadded the theory of the glycosy-lated diabetic Achilles tendon tothe understanding of the overallpicture of the Charcot foot. 15-16

How is Charcot diagnosed?Diagnosing an early Charcot’s

neuro-arthropathic fracture ne-cessitates a high index of suspi-cion. A neuropathic patient atthe earliest stage (Stage 0) will

demonstrate subtle signs andsymptoms such as edema, painor very subtle radiographicchanges which can be easilymistaken for infection. (Table1) After quickly ruling out ashort list of differential diag-noses such as cellulitis, gout,and etc., (Table 2) one shouldimmediately assume that aneuropathic arthropathy is pre-sent and prophylactically im-mobilize and off-load the ex-tremity while awaiting defini-tive testing. Both triple-phasebone technitium scans andmagnetic resonance imaging

are useful to show activity out ofproportion to the subtle clinicalsigns of inflammation to assist indiagnosis.17-18 All diabetic footwounds should be carefully ex-plored with a blunt sterile probe.19

A presumptive diagnosis of os-teomyelitis can bemade when skeletalstructures are exposed,which is bolstered byan elevated erythro-cyte sedimentationrate and C-reactiveprotein.20-21

A follow-up bonebiopsy and culture willallow appropriate an-tibiotic treatment ofthe causative organismand is the gold stan-dard in subtle cases. Incases when the possi-bility of osteomyelitisversus neuroarthropa-thy exists, then thesynovium should beevaluated as well. (Fig-ure 1) Shards of bone


152 www.podiatrym.comPODIATRY MANAGEMENT • FEBRUARY 2008

ized by slow resolu-tion of the inflamma-

tion with permanent, andsometimes bizarre, deformi-

ties remaining that occurredduring the prior phase. Thesecan lead to a non-functional andmany times chronically ulcerat-ed foot. Synonyms for the disor-der are numerous, includingCharcot’s foot, Charcot’s joint,Charcot’s fracture, neuropathicosteoarthropathy, and neu-roarthropathy, to name a few.

The incidence of neu-rarthropathy in the insensate dia-betic population varies in the lit-erature but at specialty centerswhere the index of suspicion ismost accurate, rates can be ashigh as 13%.4 Once neu-roarthropathy is diagnosed, theincidence of contralateral in-volvement goes up to 30% eitherdue to some inherent predilec-tion for the process or due to in-creased pressures on the initiallyuninvolved extremity. A retro-spective analysis comparing mor-tality and major amputation be-tween Charcot patients and sim-ple diabetic foot ulcer patientswas published in 2004. This smallstudy did not show a significantdifference in mortality between thetwo groups, although the amputa-tion rate trend was higher in theCharcot group.5

What causes Charcot foot?The two classically

opposed theories arethe German neurotrau-matic theory and theFrench neurovasculartheory. The Germans(via Virchow and Volk-mann) believed thatthe insensitive jointsare subject to repetitivemicrotrauma and final-ly deterioration. TheFrench (via Charcot)believed that deficien-cies in the trophic cen-ters of the spine led toa vasodilatory “washingout” of the bony sub-stance of the extremity.Both theories havebeen bolstered by ani-mal experiments.6-7

More recently, clini-

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Figure 2: Infrared Dermal Thermometry

Figure 1: Slide Showing Shards of Bone Groundinto the Synovium

TABLE 1

Early Signs and Symptoms ofCharcot Neuroarthropathy

Dull, Deep, Unilateral Pain Despite Neuropathy

Crepitus

Sudden Change in Foot Shape

Unilateral Edema

Unilateral Erythema

Unilateral Warmth

Small Fleck Fractures on Plain Radiograph


the bone infection and are followedconcomitantly with our infectiousdisease specialists. Additionally, pa-tients diagnosed with neu-roarthropathy should be fully eval-uated for the underlying cause ofsensorium loss. We’ve included alist of possible causes of neu-roarthropathy in Table 3, althoughthe list is not exhaustive.

Once Diagnosed, How isCharcot Foot Monitored?

Historically, radiographs weremonitored as the means to assessthe slow consolidation of neu-

ground into the synovium is in-dicative of Charcot. Horowiczwrote the definitive paper on this—and every clinician treating Char-cot should be familiar with hispaper.22 It has been our experiencethat while many authors referencethis original paper, this gold stan-dard diagnostic test is underutilizedin actual clinical practice. Patientswho are diagnosed with both os-teomyelitis and Charcot have serialerythrocyte sedimentation ratesdrawn to monitor the treatment of

Neuroarthropy—Pt. 1... roarthropathy. A moreobjective and the currentstandard for serial monitoringis the quantification of inflam-matory activity in a neuroarthro-pathic joint through the use of der-mal infrared thermometry (Figure2) .On a week-to-week basis, tem-peratures are compared betweenthe affected and unaffected foot(the control) to judge the efficacyof treatment and readiness of thefoot for surgery or shoeing. A tem-perature change of more than twodegrees Celsius compared to thesurrounding skin or contralateralsite has been shown to be a positiveindicator of an underlying patho-logic condition of the plantarfoot.23-25

Skin temperatures of the affect-ed foot and contralateral foot aremeasured after allowing the skintemperature to equilibrate to roomtemperature for ten minutes afterremoving cast, brace or shoes. Mea-surements with a hand-held in-frared dermal thermometric probeare taken over the medial and later-al arch, medial and lateral malleoli,the dorsum of the foot and the tib-ial crest, with care to avoid directsunlight on the extremities whichcan raise surface temperatures false-ly. This technique has been well de-scribed in the literature.26-32

Markers of Bone MetabolismResearchers are on the hunt for

markers of bone resorption and for-mation in serum and urine thatwould allow clinicians to identifyCharcot neuroarthropathy at anearlier stage.33 Numerous markers ofbone metabolism have been evalu-ated. Selby, et al. measured urinarydeoxypridinoline (bone resorptionmarker) and bone specific alkalinephosphate (bone formation marker)in patients with acute Charcot neu-roarthropathy and non-Charcot pa-tients with diabetes. The authorsfound an increase in both markersin Charcot patients, indicating anongoing remodeling process ofbone resorption and formation.34

Ulianova, et al. found, however,that while both processes increasein neuroarthropathy, only resorp-tion increases in osteomyelitis,while other authors found thatbone turnover markers are not use-


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TABLE 2

Differential Diagnosis

Acute Traumatic Fracture or Dislocation Superficial Thrombophlebitis

Stress Fracture Cellulitis

Bone Tumor Necrotizing Fasciitis

Gout Abscess

Pseudogout Osteomyelitis

Degenerative Joint Disease Septic Arthritis

Plantar Fibroma Inflammatory Arthritis

Deep Vein Thrombosis Reflex Sympathetic Dystrophy

TABLE 3

Neuropathies Associated withCharcot Joints

Diabetes Hemochromatosis

Alcoholism Antiretroviral Therapy

Spina bifida Lyme Disease

Myelomeningocele Hansen’s Disease

Syringomyelia Amyloidosis

Syphilis Steroid Use

Pernicious Anemia Spinal Cord Compression

Charcot Marie Tooth Syndrome Multiple Sclerosis

cles to them that outlined the tech-niques (Figures 3 & 4 ).38-39 In addi-tion, at St. Luke’s, we are able totake advantage of the hospital’s re-lationship with General Electrictechnology to obtain some of thehighest resolution computerized to-mograms available. We are lucky inthat our hospital has a special rela-tionship with General Electric andthe latest in CT scanners and digitalimaging are available to our pa-tients. Three-dimensional modelinggives our surgeons the ability to vi-sualize these complex, multi-planarcorrections prior to making the in-cisions. (Figures 5a & b)

Pressure Mapping and ForceMeasurement

A computerized gait analysisplatformis main-tained atthe cen-ter andall pa-t i e n t sare eval-u a t e dwith ani n i t i a lbarefoots t a t i cand dy-n a m i ci m a g e .Any pa-t i e n twho un-dergoesa surgi-cal inter-vention

is re-evaluated when healed toevaluate the efficacy of the pro-cedure. In-shoe images can alsobe obtained to assist our pedor-thist in shoe and brace modifi-cations (Figure 6).

Classification SystemsNeuroarthropathy can be

classified according to both thestage of disease process and theanatomical location. We havenot considered the classicEichenholz and the later Sellaand Barrette radiographic stag-ing systems useful in clinicalpractice due to the lack of corre-lation with clinical findings andtherefore do not use them.40-41

We use a four-stage system which isa combination of the Armstrongand Lavery pragmatic acute-to-

chronic system with the addition ofthe “pre-Charcot” stage discussedby Yu, et al.42-43

Our system includes a post-sur-gical stage to identify those patientswho have post-surgical inflamma-tion but are surgically stabilized.(Table 5) The inactive Charcot pa-tients are split into two distinctivegroups: those with pathology suchas pain, significant deformity; andthe non-pathologic group who areready for shoeing. We believe oursystem captures those pre-clinicalcases of neuroarthropathy that canbe “nipped in the bud” and also al-lows for clear cut decision-makingregarding treatment in those pa-



ful in discriminationbetween the two enti-

ties.35-36

We have recently presenteddata from our own facility thatcalls into question the usefulnessof the markers listed in Table 4.37

We attempted to correlate abnor-mal values of the four markerswith abnormal infrared pedaltemperatures. While trends werepresent for some of the markers,the correlation was not statistical-ly significant. This, in conjunc-tion with the previously men-tioned study showing changes inbone markers in the presence ofosteomyelitis, have lead us toconsider markers “not ready forprime time.” They are currently uti-lized at our facility as a second-linediagnostic for decision-making inborderline cases, unusual cases or bi-lateral cases that make thermometryproblematic. We plan on correlationof additional markers with thermom-etry readings in the future.

RadiologyAll patients who enter our pro-

gram undergo a plain radiographseries. In addition to standardviews, we obtain the long leg cal-caneal axial and hindfoot align-ment views on all patients. The use-fulness of these views in surgicalplanning is indispensable and ourradiology department was veryhelpful in modifying their tech-niques when we brought the arti-

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Figure 4: Long Leg Calcaneal Axial View

Figure 3: Technique for Long Leg ReconstructivePlain Radiographs

TABLE 4

Common Bone Markers

Tartrate-resitant acid phosphotase is a glycosylatedmonomeric metalloenzyme that is used as a bone resorptionmarker.

Osteocalcin is a protein secreted by osteoblast that is used asa biochemical marker for bone formation.

Bone alkaline phosphate is a hydrolase enzyme responsiblefor removing phosphate groups from many types ofmolecules and is used as a biochemical marker for boneformation.

Urinary excretion of deoxypridinoline crosslinks is abiochemical marker for bone resorption.


neuroarthropathy. 47-48 We alsoidentify distal absorptive osteopa-

thy that we see in the phalanges.Lastly, we differentiate betweenmedial and lateral midtarsus diseaseas the treatment differs for each.

Conservative TreatmentOptions:

Immobilization and Off-Loading

As long as patients do not havea deep infection re-quiring immediate de-bridement, all patientsinitially begin conser-vative treatment withthe goal of ulcerationhealing and conver-sion of the Charcotprocess from the activephase to the inactive

p h a s e ,w h i l em a i n -t a i n i n gthe bonyarchitec-ture ofthe foota n da n k l e .The key-stone oft r e a t -m e n t ,just asw h e ntreatingdiabeticfoot ul-c e r a -tions, is

tients with full-blown cases.Patients enrolled in the pro-

gram are classified according toboth disease stage and anatomic lo-cation. There are many anatomicsystems available to practitioners.44-

46 Our anatomic classification sys-tem is an expanded version of theSanders system that we have modi-fied to capture cases that we feelneed to be treated very differently.In addition to the five classic loca-tions described by Sanders, et al.,we separate cases of classic neu-roarthropathy from fresh fractures.(Table 6) We feel that this is impor-tant because, although these frac-tures may be treated with a similarprotocol as in non-neuropathicfractures initially, they more oftenthan not can trigger on full-blown

Neuroarthropy—Pt. 1... immobilization and off-loading. This can be ac-complished using awheelchair, which can createproblems with compliance inhomes without adequatewheelchair access. Crutches provideanother option, but are not easilyused by older or obese patents.

We have had success with aproduct called a Roll-a-bout ( Roll-A-Bout Corporation, Frederica, DE,USA) There are different modelsthat can accommodate patients upto 400 pounds and as tall as 6’10”.The gold standard, however, is cor-rect application of the classic rigid

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Figure 5a: Three Dimensional CT Scanwith Extrinsic Tendon Reconstruction

Figure 5b: Three Dimensional CT Scanwith Hardware Highlighting

TABLE 5

St. Luke’s CharcotStaging System

Stage 0—Pre-Charcot

Stage 1a—Active Charcot

Stage 1b—Post-Surgical Charcot

Stage 2a—Non-Pathologic, InactiveCharcot

Stage 2b—Pathologic, Inactive Charcot

TABLE 6

Modified SandersAnatomic

Classification System

Level I Forefoot (IPJ, MPJ)A. Absorptive Distal OsteopathyB. InsidiousC. Traumatic—Metatarsals

Level II Lisfranc’s Joint

Level III Midtarsal JointsA. Medial ColumnB. Lateral Column

Level IV Ankle and Subtalar JointsA. InsidiousB. Traumatic Ankle Fractures

Level V Calcaneal Insufficiency Fracture

* Modifications to the Sanders System in Italics

Figure 6: Example of Plantar PressureMapping to Assess Orthotic Un-Loadingof Ulceration


other authors as well.54 Pa-tients with open wounds re-ceive debridement and appli-cation of a slow-release an-timicrobial dressing at eachcast change. Of course, therewill be patients who cannottolerate the cast for reasonssuch as active infection, over-w h e l m i n gd r a i n a g e ,

obesity, andclaustrophobia,necessitating al-ternative off-load-ing devices andtechniques. (Table7). Once the footis stable, the pa-tient transitionsinto a removablecast walker orCharcot RestraintOrthotic Walker(CROW) (Figures8 & 9).55 Patientsprogress intoextra-depth foot-gear with custominserts after onemonth as long asdermal thermo-metric measurements remain with-in two degrees Celsius. Patients re-quiring tri-plane control will beprescribed ankle foot orthoses to beused within the footgear or a cus-tom-molded high-top shoe with ex-

tended shanks, rigid counters, andsupra-malleolar bracing. (Figure 10)

Adjunctive MedicalTreatments

In addition to mandatory off-loading, many times we will initi-ate treatment in patients with anextreme amount of inflammation

with a shortcourse of rest, ice,elevation, com-pression (Jonesboot, Unna’sboot, or pneu-matic compres-sion), and bed-rest. Once formalcasting begins, wewill always evalu-ate each patientfor adjunctivetherapy to short-en the diseaseprocess. Afterevaluating thebone markers andthe patient’srenal status, aug-mentation treat-ment with bis-p h o s p h o n a t e s

(oral or intravenous), salmon calci-tonin therapy, or non-invasivebone stimulation will be selected inan effort to attenuate the bone de-struction. Overall, the research be-hind these adjunctive treatments is

far from concrete andmany questions re-main. Our position,however, has been thatdue to the severe mor-bidity associated withneuroarthropathy, ad-junctive treatmentshould be offered aslong as the risks arelow.

BisphosphonatesBisphosphonates

are potent inhibitors ofosteoclast activation.There have been trialsshowing significant re-duction in symptomsand bone turnovermarkers compared tocontrol groups. Theyhave also been shownto normalize skin tem-



total contact castas described by

Brand.49-51 (Figure 7)While clinicians have

made several modifications tothe original technique overthe years, such as use of syn-thetic casting material ratherthan plaster, the basic deviceremains the same.52-53 The castreduces edema, applies exter-nal stabilization of fracture frag-ments, prevents further injury, en-forces compliance; and most im-portantly, negates the damaging ef-fect of the triceps surae while thefoot is in the weakened status of ac-tive-phase Charcot. Safe applicationof a total contact cast requires sim-ple training in either doctoral orpost-doctoral programs, or atten-dance at a casting lab, or proctoringby a specialist familiar with thetechnique.

We are amazed at the amountof dogma surrounding the tech-nique. The literature has many ref-erences by clinicians who note con-straints such as application time,material costs, and risks inherent inthe technique. It has been our ex-perience that clinicians make themajority of these statements witheither limited clinical contact withpatients, or have never actually ap-plied a total contact cast. This sin-gle example of “diabetic footdogma” has limited availability ofthe best treatment forpatients, and possiblycost thousands of dia-betic amputations. Tothis day, however, wesee patients with tightAchilles tendons andinflamed, edematousCharcot feet being am-bulated in diabeticshoes, Unna boots, ornon-custom walkingboots. This virtuallyguarantees gross defor-mity and failure.

At our program, atotal contact cast is ap-plied in approximately15 minutes. The cost ofmaterials is well underthe third-party reim-bursement. The effi-cient application oftotal contact casts hasbeen discussed by

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Figure 7:Rigid TotalContact Cast

TABLE 7

Alternative to the Rigid TotalContact Cast

Non-Removable Cast Brace (“Instant Total Contact Cast”)

Removable Cast Brace

Patellar Tendon Bearing Brace (“PTB”)

Charcot Restraining Orthotic Walker (“CROW”)

Crutches

Wheelchair

Bedrest

Knee-Bearing Scooter (“Roll-A-Bout”)

Hands- free crutch device (“iWALKFree”)

A temperature change

of more than two

degrees Celsius

compared to the

surrounding skin or

contralateral site has

been shown to be a

positive indicator of

an underlying

pathologic condition

of the plantar foot.


Pamidronate sparingly.We now require a fulldental examinationprior to consideringbisphosphonate thera-py. The majority of ourpatients are now pre-scribed calcitonin-salmon spray daily, al-ternating nostrils eachday. Researchers haveshown this treatmentto be beneficial in driv-ing down the markersof bone metabolism.64

Calc i tonin-salmonnasal spray has beenused to increase verte-bral bone mass in post-menopausalosteoporosis and to decrease the inci-dence of vertebral fractures.

The treatment adverse reactionsare mild to moderate in severity(mostly local nasal complaints).We’ve noted an anecdotal decreasein pain in the involved extremitywhen utilizing this therapy. It canbe used at any time of the daywithout regard to food restrictionsor supplementation. The previousresearch with calcitonin-salmonspray did not, however, drive downthe skin temperature faster thanthe control, and questions remain.

We hope to addto the data beinggathered on thisadjunct.

Electrical BoneStimulation

Harshorne re-ported the use ofelectrical energyto directly stimu-late bone healingin 1841.65 Yasuda,et al.66 studiedelectrical fieldsand bone forma-tion in the early1950’s. They wereable to demon-strate the devel-

opment of subperiosteal callus inbones under mechanical stress. Thecallus was formed as a result of theelectrical potentials induced by themechanical stress (piezoelectricity).Electronegative potentials are gen-erated in areas of compression andelectropositive potentials are gener-ated in areas of tension. They were

perature differential between af-fected and non-affected feet.56-60

However, it has been shown thatbisphosphonates decrease boneremodeling and are contraindi-cated in patients with renal in-sufficiency.61

Due to recent questions regard-ing bisphosphonate-associated os-teonecrosis in patients undergoingdental surgery, we have taken theapproach that any patient whomay possiblyneed bone surgeryon the affectedfoot will be treat-ed with salmoncalcitonin prefer-entially at thepresent time.62-63

Due to the slowclearance of thesedrugs from bone,these drugs arenot given if sur-gery is being con-templated. Thedental literature isbeing followedclosely. We stillutilize bone oraland intravenousbisphosphonates in those patientswith limited deformity in the acutephase of Charcot when the goal isto arrest the process without any re-construction.

We initially used oral bisphos-phonates such as Fosamax, Boniva,and Actonel exclusively in the acutephase of CN. We have used IV

Neuroarthropy—Pt. 1... then ableto show thatpassing 10 µAof continuous cur-rent along the bonecould result in similarcallus formation. In-creased osteoblastic(bone formation) ac-tivity would be seenon the concave sideof the bone, whichhas an electronega-tive potential. This iswhy the cathode neg-atively-charged elec-trode is placed at thesite of nonunion or at

the fracture site.67 The amount ofcurrent is dose specific; currentsless than 5 µA do not cause boneformation, currents of 5 to 20 µAproduce progressively increasingamounts of bone formation, cur-rents over 20 µA produce necro-sis.68-69

Current can be delivered to thebone by either direct current or byintermittent pulsed electromagnet-ic fields. Direct current devices aresurgically implanted where as inter-mittent pulsed electromagneticfield devices are noninvasive anddeliver current by means of two op-posing coils of wires mounted on acast or skin. The coils face eachother at 180 degrees.68-69

Research has shown some bene-fit in the use of stimulation of bonehealing through electrostimulation,magnetic fields, and low intensityultrasound when treating neu-roarthropathy.70-74 We typically uti-lize this adjunct when traumaticfractures that morph into neu-roarthropathy, long bone fractures,or high risk fusions exist in theclinical picture. We utilize pulsedelectromagnetic field stimulators(EBI Medical Inc, Parsippany, NJ,USA) to speed up bone formation.Direct current devices have beenused with success in a few surgicalpatients with high risk tibiocal-caneal fusions implanted directlyinto the fusion site.

Patient Education, Lifestyleand Disease Modification

One of the main reasons thatwe have excellent salvage rates andfunctional extremities is due to the


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Figure 8: Charcot Restraining OrthoticWalker

Both triple-phase bone

technitium scans and

magnetic resonance

imaging are useful to

show activity out of

proportion to the

subtle clinical signs of

inflammation to assist

in diagnosis.

Figure 9: Cast Walker Immobi-lization with External BoneGrowth Stimulator

then evaluated for chronic pain, in-stability, equinus or bony deformi-ty that would preclude safe andcomfortable ambulation withshoes. If any of these exist, thensurgery is contemplated. From theoutset, we know that any patientwith a history of neuroarthropathyhas high risk for re-activation of theprocess in the same foot as well as a30% chance of developing similarproblems in the contra-lateral foot.We educate the patient on this aswell as review the signs and symp-toms of the process. We also edu-cate the patient on risk factors par-ticular to their neuro-arthropathy.(Table 9) Lastly, we make sure thatwe make an appointment for thepatient to go to his/her podiatristfor regular high-risk foot care. ■

Editor’s Note: Part 2 will ap-pear next month.

References1 Sanders LJ. Jean-Martin Charcot

(1825-1893) The Man Behind theJoint Disease. JAPMA. Vol 92 No7.375-380, 2002.

2 Charcot JM. Sur quelquesarthropathies qui paraissent dependre

d’une lesion due cerveau ou de lamoelle epiniere. Arch Physiol. NormPath 1868; 1: 161-71 Kelly M.William Musgrave’s De arthritidesymptomatica (1703): his descriptionof neuropathic arthritis. Bull HistMed; 37: 372-6, 1963.

3 Armstrong DG, Peters E: Char-cot’s arthropathy of the foot. JAPMA92: 390, 2002.

4 Gazis A, Pound N, Macfarlane R,et al. Mortality in patients with dia-betic neuropathic osteoarthropathy(Charcot foot). Diabet Med 21, 1243-1246, 2004.

5 Eloesser L. On the nature of neu-ropathic affections of the joint. AnnSurg 191; 66: 201-207, 1917.

6 Finsterbush A, Friedman B. Theeffect of sensory denervation on rab-bits’ knee joints. J Bone Jt Surg 57A:949-57, 1975.

7 Petrova NL, Foster AV, EdmondsME. Difference in presentation ofcharcot osteoarthropathy in type 1compared with type 2 diabetes. Dia-betes Care. May 27 (5):1235-6, 2004.

8 Fleischli JG, Laughlin TJ,Athanasiou K, et al. Effect of diabetesmellitus on the material properties ofthe distal tibia. JAPMA 96(2): 91-95,2006.

9 Brown SA, Sharpless JL. Osteo-porosis: An Under-appreciated com-

plication of diabetes. Clini-cal Diabetes 22:10-20, 2004.

10 Herbst SA, Jones KB,Saltzman CL. Pattern of dia-betic neuropathic arthropa-thy associated with the pe-ripheral bone mineral densi-ty. J Bone Joint Surg (Br); 86-B: 378-83, 2004.

11 Childs M, ArmstrongDG, Edelson GW. Is Charcotarthropathy a late sequela ofosteoporosis in patients withdiabetes mellitus? Journal ofFoot and Ankle Surgery. Sep-Oct;37(5):437-9, 1998.

12 Young MJ, Marshall A,Adams JE, et al: Osteopenia,neurological dysfunction,and the development ofCharcot neuroarthropathy,Diabetes Care 18: 34, 1995.

13 Jeffcoate WJ. Abnormali-ties of Vasomotor Regulationin the Pathogenesis of theAcute Charcot Foot of Dia-betes Mellitus. The Interna-tional Journal of Lower Ex-tremity Wounds. Vol. 4, No.3, 133-137,2005.

14 Grant WP, Foreman EJ,Wilson S, et al. Evaluation ofYoung’s Modulus in AchillesTendons with Diabetic Neu-



“whole picture” ap-proach that we take with

these patients. Applying atotal contact cast and prescrib-

ing a bisphosphonate in a patientwho is blind, with poor dentition,

in chronic renal failure, has glyco-sylated hemoglobin of 10, andmust drive himself to andfrom doctors’ visits isdoomed to failure andcomplications. At the ini-tial enrollment of thesepatients, we look at manyfactors that will enhancethe treatment of the neu-ropathic joint as well asdecrease overall morbidityin the patient (Table 8).We have developed pa-tient education sheets onCharcot and casting, aswell. While the cast appli-cation is simple andstraightforward, these lastcomponents of our con-servative treatment pro-gram are certainly themost challenging and uti-lize the most time and re-sources.

Prevention ofRecurrence?

A patient with twoconsecutive visits withequal and symmetricalfoot temperatures is con-sidered to be in the inac-tive phase. Patients are

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Figure 10: Molded Foot and Ankle Or-thosis

TABLE 8

Patient Education

Charcot Neuro-arthropathy disease process

Treatment options

The Necessity of Off-loading

Compliance with treatment plan

Diagnostics

Blood glucose control (HBgA1c)

Hand controls for car

Residential Modifications (Ramps, Grab Bars, etc.)

Weight Management and Conditioning

Dilated Eye Examinations

Dental Examination if Bisphosphonates Are Planned

Smoking Cessation

Pain Management

Depression Management


teomyelitis (OM) of metatarsals andproximally in the infected diabeticfoot (DF).

21 Horwitz T. Bone and cartilagedebris in the synovial membrane. Itssignificance in the early diagnosis ofneuroarthropathy. J Bone Jt Surg1948; 30A: 579-88.

22 Bergtholdt HT, Temperature as-sessment of the insensitive foot. PhysTher 59: 18, 1979.

23 Armstrong DG, Lavery LA,Wunderlich RP, ET AL: Skin tempera-tures as a one- time screening tool donot predict future diabetic foot com-plications. JAPMA 93: 443, 2003.

24 Brand PW: Repetitive stress onthe insensitive feet: The pathologyand management of Public HealthService, Carville, LA, 1975.

25 DG Armstrong, LA Lavery, PJLiswood, WF Todd, and JA Tredwell J:Infrared dermal thermometry for thehigh-risk diabetic foot. Physical Ther-apy 1997; 77: 169-177.

26 Armstrong DG, Lavery LA:Monitoring healing of acute charcot’sarthropathy with infrared dermalthermometry. J Foot Ankle Surg 1996;35:335-338.

27 McGill M, Molyneaux L, BoltonT et al. Response of Charcot’sarthropathy to contact casting: assess-ment by quantitative techniques. Dia-

roarthropathy. JAPMA. Vol. 95. No.3,May/June 2005. 242-246.

15 D’Ambrogi E, D’Agostino M, Gi-acomozzi C, Macellari V, Caselli A,Uccioli L. Contribution of plantar fas-cia to the increased forefoot pressuresin diabetic patients. Diabetes Care.May;26 (5):1525-9, 2003.

16 Edmonds ME, Clarke MB, New-ton S, ET AL: Increased uptake ofbone radiopharmaceutical in diabeticneuropathy. QJM 57: 843, 1985.

17 Edmonds ME. The neuropathicfoot in diabetes. Part 1: blood flow.Diabetic Med 1986; 3: 111-115. All di-abetic foot wounds should be careful-ly explored with a blunt sterile probe.

18 Grayson ML, Balaugh K, Levin I,Karchmer AW. Probing to bone in-fected pedal ulcers. A clinical sign ofunderlying osteomyelitis in diabeticpatients. J Am Med Assoc: 273(9):721-23, 1995.

19 Judge MS. Using serologicscreening to identify and monitor at-risk Charcot patients. Podiatry Today.1045-7860—Volume 17—Issue 8—August 2004.

20 Katsaros TF, Makras P, KoutmosS, et al. Simple laboratory and clinicaltests may be of use as indicators of in-creased suspicion of underlying os-

Neuroarthropy—Pt. 1... betologia 2000; 43(4):481-4.

28 Armstrong DG, LaveryLA. Monitoring healing of acuteCharcot’s arthropathy with infrareddermal thermometry. J Rehabil ResDev; 34: 317-21, 1997.

29 Nube VL, McGill M, MolyneauxL, et al. From Acute to Chronic—Monitoring the Progress of Charcot’sArthropathy. JAPMA 92(7): 384-389,2002.

30 Bharara M, Covv JE, ClaremontDJ, et al. Thermography and Ther-mometry in the Assessment of Dia-betic Neuropathic Foot: A Case forFurthering the Role of Thermal Tech-niques. Lower Extremity Wounds5(4); 2006 250-260.

31 Foto JG, Brasseaux D, Birke JA.Essential Features of a Handheld In-frared Thermometer Used to Guidethe Treatment of Neuropathic Feet.JAPMA 97(5): 360-365, 2007.

32 Piaggesi A, Rizzo L, Golia F, etal. Biochemical and ultrasound testsfor the early diagnosis of active neu-roosteoarthropathy (NOA) of the dia-betic foot. Diabetes Res Clin Pract;58:1-9, 2002.

33 Selby PL, Jude EB, Burgess J, etal: Bone turnover markers in acuteCharcot Neuroarthropathy. Dia-betologia 41 (suppl 1): A275, (1998).

34 Ulianova I, Tokmakova A,Antsiferov M. Biochemical markers ofbone remodeling in diagnosis ofacute Charcot osteoarthropathy andosteomyelitis. Diabetes, National Re-search Centre for Endocrinology,Moscow, Russian Federation.http://87.234.226.93/easd/custofiles/easd/38th/abstracts/PS89.html

35 Jude EB, Selby PL, Mawer EB, etal. Inflammatory and bone turnovermarkers in Charcot arthropathy andosteomyelitis of the feet in diabeticpatients. Horm Metab Res 2006; 38:361-367.

36 Bernstein BH, Acor CL,Williams A. Limitations of Markers ofBone Metabolism in Staging CharcotNeuroarthropathy”, Poster Presenta-tion, The 2007 National APMA An-nual Scientific Meeting, August 2007.

37 Mendicino RW, Catanzariti AR,Reeves CL, et al. A systematic ap-proach to evaluation of the rearfoot,ankle and leg in reconstructive sur-gery. JAPMA Vol 95 No 1 2005 2-12.

38 Lamm BM, Mendicino RW,Catanzariti AR, et al. Static RearfootAlignment: a comparison of clinicaland radiographic measures. JAPMAVol 95 No 1 2005 26-33.

39 Eichenholtz SN: Charcot Joints,Charles C Thomas, Springfield, IL,1966.

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TABLE 9

Risk Factors for Neuroarthropathy

Clinical Signs of Peripheral Neuropathy:75

Insensate to MonofilamentDecreased Vibratory SensationDecreased Deep Tendon Reflexes

Patient History of:RetinopathyNephropathyPrevious Foot UlcerNeuro-arthropathy

Activities / Events including: (112)Use of Ladders or Digging Tools (i.e., Shovels)ObesityLifting Heavy ObjectsSudden Change in Activity LevelImpact Sports/Activities (Jogging, Stair-Climber, Dance)OsteopeniaFoot or Ankle Surgery of any kindTraumatic Fractures of the Foot or AnkleMinor Trauma (sprains, contusions, etc.)


et al.: Measurements of markers of os-teoclastic and osteoblastic activity inpatients with acute and chronic dia-betic Charcot neuroarthropathy. Dia-betes Med 14:517-531, 1997.

57 Selby PL, Jude EB, Burgess J, etal.: Bone turnover markers in acuteCharcot Neuroarthropathy. Dia-betologia. 41 (suppl 1): A275, 1998.

58 Jude EB, Selby PL, Burgess J, etal.: Bisphosphonates in the treatmentof Charcot Neuroarthropathy: a dou-ble- blind randomized controlled trial.Diabetologia. 44:2032-2037, 2001.

59 Pitocco D, Ruololo V, Caputo S,et al.: Six-month treatment with alen-dronate in acute Charcot neu-roarthropathy: a randomized con-trolled trial. Diabetes Care. May;28(5): 1214-1215, 2005.

60 Anderson J, Woelffer KE, Holtz-man JJ, et al.: Bisphosphonates forthe treatment of Charcot neu-roarthropathy. Journal of Foot andAnkle Surgery. 43(5): 285-289, 2004.

61 Stepan JJ, Alenfeld F, Boivan G,et al.: Mechanisms of action of anti-resortive therapies of postmenopausalosteoporosis. Endocr Regul. 37:227-240, 2003.

62 Dental Management of PatientsReceiving Oral Bisphosphonate Thera-py: Expert Panel, Journal of the Ameri-can Dental Association, August 2006.

63 Osteonecrosis of the Jaw andOral Bisphosphonate Treatment, Jour-nal of the American Dental Associa-tion, August 2006.

64 Bem R, Jirkovska A, Fejfarova V,et al.: Intranasal calcitonin in thetreatment of acute Charcot neu-roarthropathy—a randomized con-trolled trial. Diabetes Care. June;29(6): 1992-1994, 2006 .

65 Harshorne E: On the causes andtreatment of psuedoarthrodesis andespecially that form of it sometimescalled supernumerary joint. Am JMed Sci.1:121, 1841.

66 Yasuda I, Noguchi K, Sata T: Dy-namic callus and electric callus. JBone Joint Surg Am. 37:1292, 1995.

67 Cohen M, Roman A, Lovins JE:Totally implanted direct current stimu-lator as treatment for a nonunion in thefoot. J Foot Ankle Surg. 32: 375, 1993.

68 Basset CA: The developmentand application of pulsed electromag-netic fields (PEMF’s) for ununitedfractures and arthrodeses. OrthropClin North Am. 15: 61, 1984.

69 Nerubay J, Marganit B, Bubis J,et al.: Stimulation of bone formationby electrical current on spinal fusion.Spine. 11: 167, 1986.

70 Grady JF, O’Connor KJ, Axe TM,et al.: Use of electrostimulation in thetreatment of diabetic neuroarthropa-thy, JAPMA 90: 287, 2000.

71 Hanft JR, Goggin JP, LandsmanA, et al: The role of combined mag-netic field bone growth stimulationas an adjunct in the treatment of neu-roarthropathy/Charcot joint: an ex-panded pilot study. J Foot Ankle Surg.37: 510, 1998.

72 Strauss E, Gonya G. AdjunctLow Intensity Ultrasound in CharcotNeuroarthropathy. Clinical Or-thopaedics and Related Research. 349April; 132-135,1998.

73 Wang Z, Glark C, Brighton CT.Up-regulation of bone morphogeneticproteins in cultured murine bonecells with use of specific electricfields. J Bone Joint Surg Am. May;88(5): 1053-1065, 2006.

74 Petrisor B, Lau JTC. Electricalbone stimulation: an overview and itsuse in high risk and Charcot foot andankle reconstructions. Foot AnkleClin. Dec; 10(4):609-620, 2005.


Neuroarthropy—Pt. 1...40 Sella EJ, Barrette C:

Staging of Charcot Neu-roarthropathy along the medial

column of the foot in the diabeticpatient. J Foot Ankle Surg. Jan-

Feb;38(1):34-40, 1999.41 Armstrong DG, Lavery LA. Acute

Charcot’s arthropathy of the foot andankle. Phys Ther 1998; 78: 74-80.

42 Yu GV, Hudson JR: Evaluationand Treatment of Stage 0 Charcot’sNeuroarthropathy of the Foot andAnkle. JAPMA 92: 210, 2002.

43 Harris JR, Brand PW. Patterns ofdisintegration of the tarsus in theanesthetic foot. J Bone Joint Surg48A:14-16, 1966.

44 Schon LC, Easley ME, Cohen I,et al. The acquired midtarsus deformi-ty classification system—interobserverreliability and intraobserver repro-ducibility. Foot and Ankle Internation-al. Vol. 23. No.1 January 2002. 30-36.

45 Sanders LJ, Frykberg RG: “Char-cot Neuroarthropathy of the Foot,” inLevin and O’Neal’s The Diabetic Foot,6th Ed, ed by JH Bowker, MA Pfeifer,p 439, CV Mosby, St Louis, 2001.

46 Bibbo C, Lin SL, Bean HA, et al.Complications of ankle fractures indiabetic patients. Orthop Clin NorthAm 2001; 32(1):113-33.

47 Brand P, Yancy P. The Gift ofPain, Zondervan Publishing House,Grand Rapids, Michigan. 1997.

48 Finsterbush A, Friedman B. Theeffect of sensory denervation on rab-bits’ knee joints. J Bone Jt Surg 1975;57A: 949-57.49 Kominsky SJ. The ambulatory totalcontact cast. In: Frykberg, RG, ed. Thehigh risk foot in diabetes mellitus.New York: Churchill Livingstone,1991; 449-55.

50 Pinzur MS, Lio T, Posner M.Treatment of Eichenholtz stage ICharcot foot arthropathy with aweight-bearing total contact cast.Foot and Ankle International.May;27(5):324-9, 2006.

51 Armstrong DG, Todd WF, Lav-ery LA, et al.: The natural history ofacute Charcot’s arthropathy in a dia-betic foot specialty clinic. Diabet Med14: 357, 1997.

52 Shaw JE, Boulton AJM: TheCharcot foot. Foot 5: 65, 1995.

53 Morgan JM, Beihl WC 3rd,Wagner FW JR: Management of neu-ropathic arthropathy with the Char-cot Restraint Orthotic Walker. ClinOrthop 296:58, 1993.

54 Jensen J, Jaakola E. Physicianand staff time efficiency in total con-tact cast application: proper tech-nique results in time savings for thisuseful procedure. Podiatry Manage-ment, June-July, 2004. .

56 Gough A, Abraha H, Purewal TS,

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Dr. Bernstein isboard certifiedby the AmericanBoard of Podia-tric Surgery andis a Fellow of theAmerican Col-lege of Foot andAnkle Surgeons.He graduatedfrom TempleUniversity School of Podiatric Medicineand completed both a residency in footsurgery and a fellowship in limb salvagesurgery with Dr. Stanley Kalish in At-lanta, Georgia. He currently practices inthe Lehigh Valley and is program direc-tor of the Charcot and ReconstructiveFoot Program at St. Luke’s Hospital andHealth Network, Quakertown Campus.Dr. Bernstein participates in missiontrips to impoverished regions to per-form pediatric deformity surgery on ayearly basis.

John Motko is a registered nursewho works at the Wound Management

Center St. Luke’sHealth Network,Q u a k e r t o w nCampus. He hasa BS in Nursingfrom MoravianCollege/ St.Luke’s School ofNursing. He iscertified inwound care from

both the American Academy of WoundManagement and the Wound, Ostomyand Continence Nurses Society. He isalso a Certified Hyperbaric RegisteredNurse. He has over seven years of clini-cal experience in caring for patientswith chronic non-healing wounds andCharcot neuroarthropathy.


acterized by the following:A) Marked DeformityB) Edema and WarmthC) Massive Disorganization ofOsseous Structures on Plain RadiographD) Fever, elevated white count, high erythrocyte sedi -mentation rate

5) Achilles tendon contracture isassociated with Charcot Neu-roarthropathy:

A) OccasionallyB) Only in insulin-dependent patientsC) OftenD) Never

6) Acceptable means of immobi-lization of an acute Charcot footare:

A) Custom diabetic shoesB) Total Contact CastC) Unna Boot, Post-OperativeShoe and Partial Weightbearing with CaneD) Extra-Depth Shoes

7) The german theory of neu-roarthropathy links Charcotwith:

A) Repetitive microtraumaB) VasodilationC) Pro-inflammatory cy-tokinesD) Nephropathy

8) What is the gold standard testfor diagnosis of neuroarthropa-thy?

A) bone cultureB) sedimentation rateC) Synovial biopsyD) Serum bone markers

1) Urinary excretion of de-oxypyridinoline crosslinks is abiochemical marker for boneformation.

a) Trueb) Falsec) only when patient is dia-beticd) only when patient is a non-diabetic

2) Infrared dermal thermome-try should be completed:

a) immediately after the cast, shoe or brace is removed to ensure accurate skin temperatures.b) 24 hours after cast re-movalc) 10-20 minutes after cast removald) directly through the cast-ing material

3) When obtaining infrared dermal temperatures to track the activity of a neuro-pathic fracture, one should:

a) Compare the affected foot temperatures to other areas on the affected footb) Compare the affected foot temperatures to corresponding areas on the unaffected footc) Compare the affected foot temperatures to the patient’s oral temperatured) Compare the affected temperatures to a non-Charcot patient’s tempera-tures

4) Stage 0 Charcot Neu-roarthropathy is typically char-

9) The following are possible un-derlying causes of neroarthropa-thy:

A) alcoholic neuropathyB) Psoriatic arthritisC) Peripheral vascular diseaseD) Raynaud’s phenomenon

10) Bisphosphonate therapyshould not be offered when thepatient is suffering from:

A) Dental pathologyB) herpes zosterC) peripheral vascular diseaseD) xerosis of the skin

11) The Sanders classificationsystem involves:

A) disease stageB) anatomic locationC) diabetes controlD) ulcer depth

12) The Eichenholz classificationsystem involves:

A) disease stageB) anatomic locationC) diabetes controlD) ulcer depth

13) The Eichenholz classificationsystem utilizes:

A) patient pain profilingB) radiographic presentationC) infrared dermal thermo-metryD) all of the above

14) A prerequisite for neu-roarthropathy is:

A) traumaB) obesityC) poor glucose controlD) peripheral neuropathy

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E X A M I N A T I O N

See answer sheet on page 163.


162 PODIATRY MANAGEMENT

15) Patients with Charcot neuroarthropathy have blood flow that is:

A) Always excessive compared to normal baselineB) Varies based on comorbidities, family history and ageC) NormalD) Generally decreased compared to nor-mal baseline

16) Contralateral neuroarthropathy occurs:A) 5% of the timeB) 30% of the timeC) 80% of the timeD) Never

17) The differential diagnosis of Charcotshould include:

A) cellulitisB) necrobiosis lipoidica diabeticorumC) diabetic dermapathyD) diabetic bullosis

18) Contracture of the Achilles tendon existsin Charcot patients:

A) NeverB) RarelyC) Some of the timeD) Most of the time

19) Patient should not transition from totalcontact cast to shoegear until:

A) Infrared temperatures are within 2 degrees Celcius bilaterallyB) Bone markers are normalizedC) Three months have elapsed from first castD) The patient promises not to walk too much

20) Patients should be transitioned fromtotal contact cast to shoegear after tempera-tures are equal and symmetrical:

A) ImmediatelyB) Gradually while temporizing with a

transitional device such as a CROW or castboot

C) NeverD) When glucose is under control

E X A M I N A T I O N

(cont’d)

See answer sheet on page 163.

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LESSON EVALUATION

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Circle:

EXAM #2/08Developing a Comprehensive Diagnostic

and Treatment Plan for CharcotNeuroarthropathy–Pt. 1(Bernstein and Motko)

developing a comprehensive diagnostic and treatment plan ... · tibiotic treatment of the causative...

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