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FIGURE13-2.Clinicalphotographofbilateralclubfootdeformity.(CourtesyofGleesonRebello,MD,Boston,MA.)
Treatment for clubfoot consists of both operative and nonoperative management. The
consensusisforearlynonoperativeintervention,whichhasanoverallhighsuccessrate.Once
clubfootisidentified, treatment with longlegcasting toabovethekneeand moldingshould
begin.Castsareplacedweeklyforatotalofabout6to8weeks.Thereareseveraltechniques
forcasting; however,the Ponsetitechniqueis themostcommontechniqueusedcurrently by
pediatricorthopedicsurgeons.Thefirststepinthetreatmentalgorithmistocorrectthecavus.
Thisisfollowedbyaddressingforefootadductionandheelvarus.Theequinuscontractureis
dealtwithlastandrequirespercutaneoustendoachilleslengtheningat8weeksinover80%of
thecases.Aftercasting,treatmentincludesplacingthepatientinfootabductionorthosis(FAO)
(Denis-Brownbars)upuntiltheageof4.TheFAOiswornfor23hoursadayforthefirst3
monthsafterthecorrectionandthenonlyatnighttimeandnapsuntiltheageof4.Recurrenceof
theclubfoothasbeeninverselycorrelatedwithcomplianceofwearingthebrace;therefore,it
isessentialtodiscusswithparentstheimportanceofbracecompliance.ThePonsetimethod
with appropriate bracing compliance has been reported to have an over 90% success
rate.
35,36,41,43–45
Inuntreatedclubfootdeformity, thedeformitywill progressandleadtoseveredeformity
andpainwithambulation.Thesepatientswillneedalargesurgicalreconstruction involving
multiplesofttissueandbonyprocedurestocorrectthedeformity.
CongenitalVerticalTalus
CVTisarareconditionrepresentinglessthan1%ofallcongenitalfootdeformities.36CVTis
manifested at birth by a rigid rocker bottom foot deformity due to an irreducible dorsal
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■
■
dislocationofthenavicularonthetalus(Fig.13-3).CVTifuntreatedwillleadtorigidflatfoot
deformityassociatedwithpainandweakpush-offpower.
36,46
CVT is overall a rare foot deformity, but occurs more frequently in genetic and
neuromuscular conditions, representing 10% of foot deformities in patients with
myelomeningoceles.IsolatedCVThasbeenshowntobeinheritedinanautosomal dominant
patternwithvariableexpressionandincompletepenetrance.Apositivefamilyhistoryhasbeen
shown to occur in 20% of patients. Associated neuromuscular conditions included
myelodysplasia,chromosomalabnormalities,diastematomyelia,andarthrogryposis.
37,41
CVT clinicallypresents with rocker bottom foot deformity, with the calcaneus fixed in
equinusandvalgus,Achillestendoncontracture,andforefootabductionanddorsiflexion.The
pathoanatomyofCVThasbeenwelldefined.
Rigidhindfootequinus—BecauseofAchillescontracture.
Midfootdorsiflexion—Thereisdisplacementthroughthetransversetarsaljointwiththe
navicularmovingdorsalandlateralrelativetothetalus.Thelateralcolumnoffootcan
alsobeinvolvedandcausesdorsalsubluxationofthecuboidonthecalcaneus.
Forefootabductionanddorsiflexion—Contractureoftibialisanteriorandperoneals
FIGURE13-3.Clinicalphotographofcongenitalverticaltalusshowingrockerbottomdeformity.(Courtesyof
GleesonRebello,MD,Boston,MA.)
Afterathoroughexamandassessment,radiographicimagingisusedtoconfirmthediagnosis.
Standard3viewsofthefootshouldbeobtained.Anteroposterior(AP)radiographswillshow
anincreasedtalocalcanealangleusuallygreaterthan40°.Radiographsinthelateralposition
will show increased Meary angle usuallyover20°.Forced plantarflexionlateral viewsare
usedtoconfirmthediagnosis,whichwilldemonstrateanirreducibletalonavicularjoint.These
fully plantarflexed lateral radiographs differentiate CVT from congenital oblique talus.
Radiographically,thenavicularisassessedbythelocationofthefirstrayasthenaviculardoes
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notossifyuntilage3. ThefirstraywillremaindorsallydisplacedinCVTandreduceinan
obliquetalusontheplantarflexedlateralview.
36,38,47
Without treatment, CVT will develop into a painful rigid flatfoot deformity. Both
nonoperative and operative treatments have been described, but a combination is usually
necessarytoadequatelyaddressthiscondition.
Nonoperativemanagementbeginswithserialcastingtoplacethefootinplantarflexionand
inversiontostretchoutthedorsalsofttissues.Despitepossiblelargeimprovementswithserial
casting,however,completecorrectionisrarelyobtained.48Afterserialcasting,manyauthors
recommendminimallyinvasivesingle-stagesurgicalcorrectiontoreduceandtemporarilyfix
the talonavicular joint and if needed the calcaneocuboid joint. Extensive release of the
dorsolateral tendons was historically performed but associated with major complications.
Achilles tendonlengtheningisalso performed. Surgical treatmentisusuallydoneat6 to18
months of age. Commoncomplicationsinclude wound breakdown, stiffness, talar avascular
necrosis,andrecurrence.
37,46
CalcaneovalgusFoot
Calcaneovalgusfootdeformityisacommoncongenitalfootdeformityandoccursatarateof1
in 1,000 live births.49 It is often caused by intrauterine packaging and is unrelated to
neuromuscular or genetic disorders. Itis more common in females andthe breechposition.
Calcaneovalgus deformityshould be differentiated from posteromedial tibial bowing, CVT,
andparalyticfootdeformities,whichcanhavesimilarpresentations.
38,47,50
On exam, thefootis dorsiflexedandlyingontheanterior tibia.UnlikeCVT,the footis
passivelycorrectedtoneutralandthereisnoAchillescontracture(Fig.13-4).41Completeand
thorough neurovascular exam must be performed as a L5 myelomeningocele, with intact
dorsiflexorsandevertorsandweakplantarflexorsandinverterscanproducethesameclinical
deformity. Radiographsare obtained to rule out CVT, andon forced plantar flexionviews,
thereisnoevidenceofdislocationofthenavicularonthetalus.Atthis age,theossification
nucleus isnotseen, but thefirstraywill be in linewiththe talusin a calcaneovalgus foot,
rulingoutaCVT.Oftentimes,calcaneovalgusisassociatedwithposteromedialbowing,which
canbeseenonradiographs.Also,patientswithcalcaneovalgusdeformityaremore likelyto
haveassociateddevelopmentaldysplasiaofthehip,soathoroughexamofthehipsandpelvis
isneeded.
36,37,41
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FIGURE13-4.Clinicalphotographsshowingflexibilityofcalcaneovalgusdeformity.(CourtesyofGleesonRebello,
MD,Boston,MA.)
Treatment is usually observation and passive stretching bythe parents as the condition
usually resolves spontaneously at 3 to 6 months of age. In severe cases, casting in
plantarflexionandinversioncanbedone.
37,51
TarsalCoalitions
Tarsalcoalitionsarefusionsbetweenthetarsalbonesresultinginrigidflatfootdeformity.The
coalitioncanbe abony,cartilaginous,orfibrousconnectionandisanoftenisolatedfinding.
Conditions that have been associated with tarsal coalitions, however, include fibular
hemimelia,ApertsyndromeandNievergelt–Pearlmansyndrome.
36,52
Tarsalcoalitionresultsfromfailureofmesenchymalsegmentationinthedevelopingfetus.
Themostcommonformsarecalcaneonavicularandtalocalcanealcoalitionsusuallypresenting
in8-to12-year-oldsand12-to15-year-olds.
52,53
Thesecoalitionsarecongenitalbutpresent
laterinlifeasfurtherossificationofthetarsalbonesoccur.
Patientsoften presentintheirearlyteenswith lateralanklepain,recurrentanklesprains,
calfpain,andrigidflatfootdeformity.Thecoalitionleadstoarigidflatfootdeformitycausing
tight Achilles andperoneal spasticity. Physical examinationshowshindfootvalgus, forefoot
abduction,limitedsubtalarmotion,positiveSilfverskioldtest,andnoinversionoftheheelor
reconstitution of the foot arch on toe rise. Radiographs are necessary but may not fully
visualizethecoalitions.Oneshouldobtainweight-bearingAP,lateral,45°obliqueviews,and
Harrisheelviews.The45°obliqueviewisveryhelpfultoseecalcaneonavicularcoalitions,
whichmaydemonstrateelongationoftheanteriorprocessofthecalcaneusoftenreferredtoas
the “anteater” sign(Fig. 13-5). Talonavicular coalitions may show talar beaking on lateral
radiographsaswellasanabnormalmedialfacetontheHarrisheelview.CTscanshouldbe
performedtoassess thesizeof the coalitionas well asassess foradditional coalitionsfor
surgicalplanning.AnMRIcanbeperformedtoassessforfibrousorcartilaginouscoalitionsif
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theCTscanisnondiagnostic.
36,52–54
Treatment consists of both nonoperative and operative management. For asymptomatic
coalitions, observation is appropriate. Initial treatment for painful coalitions involves
immobilizationinashortlegcastfor4weeksororthotics,suchasaUniversityofCalifornia
BiomechanicsLaboratoryorthosis,whichareusefultolimiteversionandinversionstress.54In
patients with persistent pain after casting or trial of orthotics, surgical management is
recommended.Insubtalarcoalitionsthatinvolvelessthan50%ofthemiddlefacetoronlyan
isolatedbar,resectionwithfatinterpositionisperformed.Iftherearemultiplebarsormore
than50%jointinvolvement,thensubtalarfusionisusuallyperformed.55Forcalcaneonavicular
coalitions, resection with extensor digitorum brevis or fat interposition is the preferred
treatment.
56,57
FIGURE13-5.45°obliqueradiographofthefootshowingcalcaneonavicularcoalitionswithelongationoftheanterior
processofthecalcaneus,oftenreferredtoasthe“anteater”sign.
CONGENITALTOECONDITIONS
Syndactyly
Syndactylyisaconditioncharacterizedbyfusionofthe bonesorthe softtissue ofthetoes.
Syndactyly occurs in 1 in 2,000 births and is most common between the second and third
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digits. Syndactyly is often inherited in an autosomal dominant pattern and is because of
incompleteorabsentapoptosisduringgestation.Syndactylycanbeisolatedorassociatedwith
syndromessuchas Klippel–Feilsyndrome,Apert syndrome, andDown syndrome.Itoccurs
bilaterallyin50%ofthecases.
35
Syndactylycanbecharacterizedaseithersimpleorcomplex.Simplesyndactylydoesnot
involve bony or nail structures, whereas complex syndactyly does. Differentiation generally
requiresradiographs.
36,37
Simple syndactyly in the foot does not often cause footwear problems or pain, and
therefore,surgicalmanagementisnotrecommendedunlesssymptomatic.Complexsyndactyly
cancauseproblemswithshoewearandpainasthefootgrows;therefore,itshouldbetreated
surgically.Inthesesituations,surgicalmanagementshouldbeperformedat9to12monthsof
age.
35–37
Polydactyly
Polydactyly occurs in approximately 2 in 1,000 newborns, and there is usually a strong
positive familyhistory,withreportsashigh as 30% withinthefamily.Eightypercentofthe
cases have a postaxial (lateral border of foot) duplicationofthe fifth digit, and itis more
common in African Americans. Preaxial polydactyly occurs in 15% of the patients, with
central duplication occurring inthe remaining 5%.35 Inheritance is thought to be autosomal
dominantwithvariablepenetrance.Polydactylyiscausedby failure ofdifferentiation inthe
apicalectodermalridgeduringthefirsttrimesterofpregnancyandusuallyoccursinisolation
but can be associated with Down syndrome, Apert syndrome, tibial hemimelia, or trisomy
13.
36,41
Examination reveals whether digits are well-formed articulated digits or rudimentary
digits. Radiographs should be obtained to identify the degree of involvement of the bony
structures. Duplications can involve all levels from the metatarsal to the distal phalanx.
Polydactyly can cause problems with shoe wear and angular deformity of the toes and
thereforeusuallyrequiressurgicalremoval.
Options for treatment include both nonoperative and operative management. In patients
with centralorpostaxialpolydactylywithgood alignmentand anarrowfoot,observationis
reasonable.Surgicalresection,however,shouldbeconsideredifshoewearisaproblemor
the extra digit causes angular deformity. There are several guiding principles in resection
includingsaving thedigitwiththebestaxial alignment,resecting theprojectingsymptomatic
toe, repairing the capsule, balancing the soft tissues, and removing any metatarsal
prominence.36Rudimentarydigitscanoftenbeligatedinthenewbornnursery,whereasmore
complexformswillberemovedaround9to12monthsofage.Mostoften,theborderdigitand
metatarsal should be removed in order to narrow the forefoot. If the outer toes are better
developed than the inner toes,however,theinner toes should be removed.Withoutsurgical
treatment,75%ofpatientswillexperienceshoefittingproblemsand25%willhavepersistent
pain.
36,37,58
Oligodactyly
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Oligodactylyisafailureofformationandusuallyresults inloss ofoneormoreraysofthe
foot.Thelateralraysare more often affected than thehallux. Theremaybeastrong family
history,butmostcasesoccursporadically.Oligodactylyresultsfromimproperdifferentiation
inthe apical ectodermal ridgeand canbe caused byteratogenic agents, amniotic bands,or
impaired blood flow. Oligodactyly can be associated with many other musculoskeletal or
systemic conditions including fibular hemimelia, proximal femoral focal deficiency, tarsal
coalition,polydactyly,syndactyly,constrictionrings,brachydactyly,VACTERLsyndrome,and
Fanconianemia.
36
A thorough musculoskeletal exam along with cardiovascular, gastrointestinal, and
genitourinaryassessmentsiscrucial.Radiographsofthefoot,leg,andhipshouldbeobtained.
IfFanconianemiaissuspected,acompletebloodcountshouldbedone.
Surgical treatment is rarely indicated unlike with polydactyly and syndactyly as this
condition usually does not cause problems with shoe wear or function. Shoe inserts or
modifications may be needed to accommodate a narrowed foot. If there are several rays
absent, however,thena shoeable balancedfootmaynotbe achievable and amputationmay
needtobeconsidered.
36
Brachymetatarsia
Brachymetatarsia is a congenital hypoplasia or shorteningof oneor more metatarsals. This
conditionis often bilateral, occursina female:male ratio of25:1, andthe4thmetatarsal is
most commonly involved. It occurs because of premature closure of the epiphysis of the
metatarsalordissolutionoftheapicalectodermalridge.Brachymetatarsiaisoftenisolatedbut
canbeassociatedwithmanyothersyndromesincludingDownsyndrome,multiplehereditary
exostoses, diastrophic dwarfism, Albright osteodystrophy, Turner syndrome, and Larsen
disease.
36,41
Onexam,thereisashortrayrelativetotheothersaswellasalossofthenormalcascade
ofthetoes.Sometimes,theinvolvedtoeresidesonthedorsumofthefootduetoextensionat
the metatarsal phalangeal joint. Weight-bearing AP andlateral views of the feetshould be
obtained.
Treatment consists of both operative and nonoperative management. Depending on the
extentofthedisease, nonoperativeinterventionsusuallyinvolveextradepth andextra width
shoes to accommodate the deformity. This usually is successful to help manage symptoms.
Tapingand/orsplintingisusuallyineffective.Inpatientswithrecalcitrantsymptoms,surgeryis
indicated.There are several surgicalprocedures described including extensortenotomy and
capsulotomy,metatarsallengthening,andamputation.
35,36,41
CONCLUSION
Congenital disorders of the lower extremity span the spectrum from easily managed with
conservative stretching and bracing to possibly benefiting from complex surgical
reconstructions.Almostalldiagnosescanbemadebyexaminationandbasicradiographs.The
detailed diagnosisandmanagementofthe more complexconditions islikelybestleft tothe
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purviewofdedicatedpediatricorthopedicsurgeons.Anyclinicianwhocaresforpatientswith
lowerextremitycomplaints,however,shouldbefamiliarwiththegeneralspectrumofdisease
andassociatedsystemicconditions.
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A
lthough hormone secretion is necessarily systemic in nature, many of the effects of
hormones extend to the lower extremities. This becomes especially true during
derangementsoftheendocrinesystem.
GROWTHHORMONEDISORDERS
Criticalfornormalgrowthtoadultstature,growthhormone(GH)is secretedbytheanterior
pituitaryundertheinfluenceofhypothalamichormones.1Growthhormone–releasinghormone
and somatostatin secreted by the hypothalamus stimulate and inhibit GH secretion,
respectively,atthelevelofthepituitarygland.GHinturnactsperipherally,eitherdirectlyon
itstargettissuesorthroughitsintermediarysomatomedins(insulin-likegrowthfactors),whose
production it induces in the liver. The normal response to GH includes accelerated linear
growth,increasedleanbodymass,andincreasedorgansize.
GH hypersecretion occurs in the context of somatotropic adenomas, the second most
common pituitary tumor after prolactinomas.2 If such an adenoma develops before physeal
closure,itresultsinexcesslineargrowthknownasgigantism.Morecommonly,however,such
adenomasoccurafterphysealclosure,leadingtoacromegalywhoseconstellationofsymptoms
includes expansion of the jaw and brow, enlargement of the hand and feet, and internal
derangements such as organ swelling, hyperglycemia, hypertension, and osteoporosis.3 In
additiontotheincreasedsizeofthehandsandfeet,patientsalsofrequentlynoteanassociated
sponginessinthefeet,especiallyintheheelpad,andmaydescribeerythematousspotsonthe
skinoftheextremities.
4
CUSHINGSYNDROME
Cushing syndrome refers to elevated levels of glucocorticoids, primarily cortisol. Most
commonly, this isbecauseofexogenousadministrationofsteroids, butotheretiologiesalso
exist.
5,6
Cortisol is normally produced by the adrenal cortex under the influence of
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