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FIGURE15-7.Palmardesquamationassociatedwithlate-stageCoxsackieA6virus–inducedhand,foot,andmouth
disease(borrowedfromtheMountSinaiCollectionphotographs).
FIGURE15-8.Blistersdevelopduringpregnancyorshortlyafterparturitioninherpesgestationis(borrowedfromthe
MountSinaiCollectionphotographs).
DiagnosticAidsandTreatment
There arefivebasic laboratorytests thatcanassistinmaking the correctdiagnosis: (a) the
Gramstain;(b)KOHprep;(c)Tzancksmear;(d)thepatchtest;andofcourse,(e)biopsy.In
additiontothestandardtests,therearecasesinwhichonemayneedtotestforyeast,acid-fast
bacilli, andother microorganisms. Darkfield microscopyforTreponema pallidum, VDRL,
enzymeimmunoassay,HIV,andgenetictestsmayalso playsignificantrolesinestablishinga
diagnosis.
7,8,39
Whenperformingthe Tzanck smear,anearly lesionshouldbeselected, its topremoved
withascalpel,andthefluidcontentsblottedawayinordertoavoidcontactwiththebaseof
thelesion.Thelesionisthenpinchedfirmlytopreventbleedingwhilethefloorisscrapedwith
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asharpcurette.Thesescrapingsarethenspreadonacleanglassslide,allowedtoairdry,and
then stained with Giemsa solution. In pemphigus patients, acantholytic cells with pyknotic
nuclei will be seen, whereas in cases of herpes zoster or simplex or in varicella,
multinucleatedgiantcellswillbenoted.
Thetraditionaltechniqueusedtobiopsyblistering lesionshas beenatwo-punchbiopsy
approach. It is recommended to first biopsy the perilesional skin for direct
immunofluorescence (DIF)andthenperform asecondarybiopsyfromlesionalskinforlight
microscopy using a hematoxylin and eosin (H&E) stain.40 Braswell et al.40 recommended
marking the blisters to ensure proper orientation, as well as to include at least 75% of
perilesionalskinattheedgeoftheblister.
Braswell et al.40 have also recommended an alternative approach for subepidermal
blisters.Thetechniqueinvolvesusingan8-mmunitbiopsytoolforasingle-punchbiopsyfor
bothDIFandlightmicroscopyusingH&Estain.Thefirstmethodusesan8-mmpunchbiopsy
centered over a 1 to 2 mm new lesion. This approach includes approximately 3 mm of
perilesional skin. Once the specimen is obtained, half of the specimen is placed in Zeus
medium for DIFand the remaining halfin formalinfor H&Estaining. Forlarger blisters, a
secondapproachisrecommended.Theysuggestmarkingtheroofoftheblisteralongwiththe
surrounding perilesional skin. An 8-mm punch biopsy unit is then used, creating a sample
comprised ofthree-fourths oftheperilesionalskinandone-fourthofthecenter ofthelesion.
Again,halfofthetissuewouldbesentforH&Estaining,whereastheremainingportionwould
be sent for DIF.40 With the larger blister, it is important to bisect the specimen from the
subcutaneoustissueusinga#15blade.41Thetechniquealsohelpstopreservebothepithelium
anddermisasspecimen.
There are two primary advantages to using a single-punch biopsytechnique; it is costeffectiveandalsoavoids havingtoperform a secondprocedure.Thelimitationofa singlebiopsyapproachisthatitwouldrequirethatthepathologistortechnicianbefamiliarwiththe
technique.40It isalso necessaryfor theportionthatincludes thecutedge ofeachhalftobe
included for DIF specimens and H&E staining. This technique is not recommended for
blisteringdisordersfoundtohaveapositiveNikolskysign.
40
Treatmentforallthevesiculobullousdiseasesthataffectthefootincludesthepreventionof
sepsis,soakingtodrythelesions,andincisionwithdrainageoflargebullaethatinterferewith
proper function.The entire roofof a vesicle or bulla should probablynever be completely
removed. General treatment will vary according to the specific disease. It is wise for the
podiatristtoseektheaidofa gooddermatologist,internist,oroncologist,depending onthe
underlyingdisorder.
Steroidsaresometimesusedtominimizetheinflammatorycomponentsofvesiculobullous
disease,whetherthefootaloneisinvolvedorotherbodysurfacesareaffected.
PURPURICERUPTIONS
Incontrasttoerythematousmacules,purpuriclesionsaretheresultofactualbleedingintothe
skin. Eventually,extravasatedredbloodcells breakdowntoformthepigment, hemosiderin,
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andlesionswillnotblanchupondiascopy.Purpurawillassumedifferentconfigurationsbased
onthedimensionofthepathologicvessels.Ruptureofsmallvessels(i.e.,arterioles,venules,
andcapillaries)willresultinpinpointor“petechial”hemorrhages,whereasdamagetolarger
vesselswillresultinecchymosis,hematoma,orhemarthrosis.Lastly,theclinicianshouldbear
inmindthatpurpuriceruptionsmayinfactrepresent microembolization,vasospasticdisease
(i.e.,pernio,Behçetdisease),etc.
LeukocytoclasticAngiitis
This autoimmune disease affects arterioles, capillaries, and venules in skin and internal
organs.Itdiffersfromotherformsofangiitis(i.e.,macroscopicpolyarteritisnodosa,Wegener
granulomatosis)bothhistologicallyandinitsbroaderclinicalmanifestations.Leukocytoclastic
angiitis(LCA)derivesitsnamefromthecharacteristicappearanceoftheleukocytesfoundin
involved segments. These cells exhibit nuclear fragmentation, or “nuclear dust,” hence the
designationleukocytoclasticangiitis.
ThecutaneouschangesofLCAaresecondarytoexudationandhemorrhageratherthanto
ischemia.Bloodvesselswithintheupperdermisareusuallyaffected,leadinginitiallytothe
formation of an erythematous macule, as described previously. Edema and subsequent
extravascular hemorrhage transform macules into papules and then purpuric papules,
respectively. The feet, ankles, and lower legsare characteristically involved ina bilateral
fashion(Fig.15-9).Progressionofdiseaseleadstothrombosisandthereforeulceration.
LCAmayappearintwoclinicalforms:(a)Henoch–Schönleinoranaphylactoidpurpuraor
(b) a cutaneous-systemic variant. The former affects mainlyyoungboys, is preceded by an
upper respiratoryinfectionwithmildconstitutionalsymptoms,andhasapredilectionforthe
latefallandearlyspringmonths.Inadditiontothecutaneousrash,thevasculitiscanaffectthe
kidney,gut,andjoints,leadingtocomplaintsreferabletotheseareas.
FIGURE15-9.Thepalpablepurpuraassociatedwithleukocytoclasticvasculitis(borrowedfromtheMountSinai
Collectionphotographs).
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Thecutaneous-systemicformmorecommonlyaffectsadults;thereisnosexpredilection.
Theformrepresentsaspectrumofdisease:Itmayrangefrompurecutaneoustopurelyvisceral
involvement,witha certainpercentageexhibiting bothcutaneous and visceral involvement.
Signsofcutaneousvasculitisareprecededbymildconstitutionalchanges,asintheHenoch–
Schönlein form. Death can result from vasculitis-induced renal failure. Fortunately, fatality
occurs in only a small percentage of patients (in contrast to the rapidly fatal course of
macroscopic polyarteritis nodosa). Early urinalysis in such patients can detect renal
involvement,permittingrapidinitiationoftherapydirectedathaltingtheprocess.
LCA can therefore exist in a relatively benign form, but it may develop serious
complications.Itcanalsooccur,forunknownreasons,inassociationwithpatientsafflictedby
rheumatoidarthritis,lupuserythematosus,leukemias,andlymphomas.
Diagnosisdependsuponrecognitionofcharacteristiclesionsandhistopathology.
BacterialEndocarditis
Bacterialendocarditisexistsinsubacuteandacuteclinicalforms,determinedbytheinfectious
organism and the presence of preexisting cardiac disease. The acute type with its rapidly
fulminating course results from invasion by true pathogens; a prior cardiopathy is not a
prerequisite.Conversely,subacutebacterialendocarditisoccursinpatientswithcongenitalor
rheumaticheartdiseasefollowinginfectionwithlesspathogenicbacterialspecies.
Ineithercase,vegetationscomposedoffibrinandplateletsdevelopatthesiteofinfection.
Smallfragmentsmaynowbreakfreeandembolizetoanytissue,producingavariableclinical
picture.Cutaneouslesionsoftheextremitiesaresecondarytosuchvascularchangeandmaybe
petechialorgangrenous.Inthecaseofpetechiallesions,histologicsectionrevealsthesetobe
secondarytoanimmunevasculitis,andthereforetheyareprobablynotembolicinnature.
The combination of fever, cardiac murmurs, and cutaneous lesions of the type to be
discussed is a certain indicator of bacterial endocarditis. In the subacute type, subungual
splinterhemorrhagesareoftenfound.Digitalpulpsmayexhibittender,purple,orerythematous
subcutaneouspapulesknownasOslernodes.Largernodules,probablyembolicinorigin,may
develop on the palms and soles. These are known as Janeway lesions. Emboli to larger
arteriesmaycreateclaudicationorfrankgangrene.
Incontrast,acutebacterialendocarditisdemonstratesmanypetechialandembolicchanges,
butOslernodesandJanewaylesionsareabsent.
Early diagnosis of bacterial endocarditis is imperative and known to improve clinical
outcomeanddecreasepatientmortalityrate.Althoughnewdiagnosticbiomarkersareemerging
and show promise, definitive diagnosis of bacterial endocarditis continues to remain a
challenge. The most important diagnostic tools continue to involve high clinical suspicion,
blood cultures, andechocardiology.42 Mestres et al.43 discuss the importance of preventive
measurestoavoidinfectionthroughproperhandwashingtechniques,alongwithanemphasis
on patient education. This involves the patient’s understanding of the disease process,
procedures that may ultimately cause bacteremia, as well as the prophylactic antibiotics
involvedtopreventthedisease.
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Papular-Purpuric“GlovesandSocks”Syndrome
Thepapular-purpuric“glovesandsocks”syndrome(PPGSS)isadermatosisofacuteonsetin
adults,characterizedbypruritic,erythematous,papulopurpuriclesionsonthehandsandfeetin
a gloves and socks distribution. Oral aphthoid lesions and fever are concomitant findings.
PPGSSpatientsoftendemonstratecytomegalovirusorparvovirusinfection.
4,12,23,40
Meningococcemia, leukemia, and rickettsial disease may also manifest with palpable
purpura,asdescribedearlier.
NODULARDISEASES
Nodulesrepresentmasseslocatedbeneaththeskin.Whentheyapproachlargedimension,they
may be called tumors. Nodules may be either soft or firm, solitary or multiple, tender or
nontender,andfixedornonfixedtotheoverlyingskin.
LeukocytoclasticAngiitis
Theidenticalpathologicprocessmayaffectvesselsmoredeeplyplacedwithinthedermis.In
thislocation,nodulesdevelop,ratherthanpurpuricpapules.Thesenodulesareinflammatoryin
nature, and tender topalpation.When vessels in this cutaneous location are affected, other
presentationsincludelivedoreticularisandatrophieblanche.
Churg–StraussSyndrome
The histologic examination of erythematous nodules occurring on the feet rendered a final
diagnosis in a patient with acutely developed bilateral pulmonary infiltrates and marked
eosinophilia. Even a transbronchial biopsy did not reveal the necrotizing extravascular
granulomasanddermaleosinophilicinfiltrateswitnessedinthepedallesions.
25
Lesionstypicallypresentonthehead,trunk,andextremities.Theyrangefromapalpable
purpura,ornodular lesionsalongwitherythematousmaculopapularorpustularinformation.
Patients with Churg–Strauss syndrome will present with specific histopathologic
characteristics,includingeosinophilsandflamefigureswithdiffusenecrotizingvasculitis.
44
There are six criteria in the classification of Churg–Strauss syndrome according to the
AmericanCollegeofRheumatology.Fourofthesixhaveasensitivityof85%andspecificity
of99.7%forChurg–Strausssyndrome:asthmabronchiale,peripheraleosinophilia,paranasal
sinusitis, pulmonary infiltration, vasculitis proven by histology, and mononeuropathy.44 The
lesionswill often resolve with the useofsystemicsteroids thatwill result initspermanent
clearing.
32
Once the diagnosis of Churg–Strauss syndrome has been established, patients usually
respond well to corticosteroid therapy. However, for those who fail to respond to
corticosteroids or thosewhopresent with fulminantmultisystem disease, cyclophosphamide
canbeadded,dependingontheseverityofthedisease.41Topicalcorticosteroidsmayalsobe
addedtotheregimentobeappliedtotheskinofthelesions.
45
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BacterialEndocarditis
ThereadershouldrecallthatOslernodesandJanewaylesionsmayoccurinthesepatients.
MacroscopicPolyarteritisNodosa
Becauseofthelarger-sizedvesselsafflicted,thisautoimmunediseasedoesnotprimarilyaffect
theskin.Theonlyvalidcutaneoussignsinclude5-to10-mmsubcutaneousnodules(whichare
in actuality small aneurysms). These nodules follow the course ofarteries, ulcerations that
resultfrominfarction,inadditiontogangreneoffingersandtoes,andecchymosessecondaryto
ruptureofaneurysmsandweakenedarterialwalls.AsinLCA,visceralbloodvesselsarealso
affected.Asaresult,macroscopicpolyarteritisnodosafrequentlyfollowsafatalcourse.
ThePanniculitides
Thepanniculitidesrepresentagroupofpainfuldisordersinvolvingsubcutaneousfat.Factitial
andpurulenttypes resultfrom readilyidentifiable etiologies. Theremainingtypes form the
“nodularnonsuppurative”variety.
Nodular nonsuppurativepanniculitismaybe associatedwithfeverandasynovitis ofthe
distal articulations, including the metatarsophalangeal joints. Females in the third to fourth
decade of life appear to be most commonly affected, although an infant form does exist.
Occasionallysingle,butmoreoftenmultiple,tendersubcutaneousnodulesdevelopinrecurrent
crops,whichischaracteristicofthesedisorders.Necrosisanddrainageofthenodulesrarely
occurs. Histologically, these nodules form secondary to leukocytic invasion. The
postinflammatory healing and fibrosis lead to localized fat atrophy, which is manifest
clinicallyashyperpigmenteddepressionsinthepreviouslynodularareas.Althoughtheyoccur
mostcommonlyovertheshins,dorsal footnodules havebeenreportedinboththeadultand
infantforms.
Nodularnonsuppurativepanniculitisisincludedbecauseofitsassociationwithpancreatic
diseases, including carcinoma ofthepancreas (particularly thatofthe body and tail). Such
patients usuallypresentwithmultiple panniculitic areas of the lower extremities, which in
theoryaretheresultofcirculatinglipasesreleasedbythediseasedpancreas.
Nodularnonsuppurativepanniculitishasbeenfoundtobeassociatedwithtrauma,halogen
compounds or other drug ingestions, and infections, especially of a tuberculous nature.
Associationwithhistoplasmosis,dermatomyositis,systemiclupuserythematosus,andsteroid
withdrawalcanoccur.Otherconditions,suchasulcerativecolitis,jejunoilealbypasssurgery,
erythemanodosum, sarcoidosis, Hodgkin disease,glomerulonephritis, diabetesmellitus, and
α1-antitrypsin deficiency, have been implicated. This last occurrence, with α1-antitrypsin
deficiency patients, has resulted in terminal disease. These disorders are generally not
immediatelylife-threateningconditions,however.
CONCLUSION
Spacelimitationsandexpandingmedicalknowledgeprecludethe“all-encompassing”chapter.
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Nevertheless, it is hoped thatthe treatment of thematerial presentedis consistent withthe
algorithm described in the introductory sections.Commonsenseand experiencedictatethat
histologic diagnosis (i.e., biopsy) be performed in the patient with a pedal dermatosis
nonresponsivetostandardtherapies.
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T
1.
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4.
he clinical laboratory can be of great help in the diagnosis of disorders of the foot.
Although laboratory testsare often informative, they are rarelydefinitive ordiagnostic.
Laboratoryexaminationsmustbe usedinconjunctionwithacompletehistory, physical, and
radiographic examinations. Over the past few years, many new testshave been developed,
someofwhichwillbediscussedlater.
Laboratorytestsmaybeusedinanumberofdifferentways.Forexample,theymaybeused
to diagnose a specific illness involving the foot. Examples of this include detecting the
presenceofintracellularmonosodiumuratecrystalsinsynovialfluidaspiratedfromanacutely
inflamed joint. Thisfinding is diagnostic of gout. A positive Gram stain or culture from an
acutelyinflamedjointisdiagnosticofinfection.Laboratorytestsmayalsobeusedtodiagnose
asystemicillness(e.g.,acompletebloodcellcount[CBC]andbonemarrowexaminationmay
be diagnostic of leukemia in a patient with bone painor a low platelet count or abnormal
coagulationprofilewithsuddenfootswellingmayreflecthemarthrosisorahighwhitecount
mayreflect septic arthritis). Thelaboratoryshouldalways be used with a goal in mind: to
arriveataspecificdiagnosis;toprovidefurtherevidenceofasuspecteddiagnosis,suchasa
positiverheumatoidfactor(RF)inapatientwithasystemicpolyarthritis;toruleoutcompeting
diagnoses; to guide therapy; or to assess prognosis or response to treatment. Treatment
decisionsarerarelybasedononetestalone.Cliniciansshouldalsobeawareaboutvariability
betweendifferentlaboratoriesanddifferenttestingapproaches.
Four characteristics of diagnostic tests help determine their usefulness in evaluating
patients:
Sensitivity,orthelikelihoodthatatestwillbepositiveinapersonwiththedisease.
Specificity,orthelikelihoodthatatestwillbenegativeinapersonwithoutthedisease.
Positivepredictivevalue,orthelikelihoodthatadiseasewillbepresentinapersonwith
apositivetestresult.
Negativepredictivevalue,orthelikelihoodthatadiseasewillbeabsentinapatientwith
anegativetestresult.
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TESTSASSOCIATEDWITHINFLAMMATION—ACUTE
PHASEREACTANTS
Whendiagnosingadisorder,oneofthemostimportantconsiderationsistodeterminewhether
the cause is inflammatory (and frequently systemic) or noninflammatory. Many metabolic
changes occur in thesetting of inflammatory processes. Together, theyare called the acute
phase response. The acute phase response occurs after many events, including infections,
trauma,immunediseases,crystallinediseases,andmalignancy.
C-ReactiveProtein
C-reactiveprotein(CRP)iscomposedoffiveidenticalsubunitsthatarelinkedtogether.This
proteinispresentinanimals thattrace their evolutionaryoriginsforhundredsofmillionsof
years(suchasthehorseshoecrab).CRPisnormallypresentinplasmainonlytraceamounts:
approximately 0.2 mg per dL. Levels increase dramatically and quickly after a stimulus.
Moderateelevationsoccurinmostconnectivetissuediseases(1to10mgperdL).Veryhigh
levelsareseeninbacterialinfectionsandsystemicvasculitis(15to20mgperdL).Diabetes,
obesity,andcigarettesmokingcanincreaseCRPlevelsinvariableamounts.CRPisnotthought
tobealteredbyageorgender.TheCRPlevelscanincreasewithin4to6hoursandnormalize
within1weekinresponsetoastimulus.Thesechangesoccurmuchmorequicklycomparedto
the erythrocyte sedimentation rate (ESR). CRP levels fall when inflammation subsides.
BecauseasubstantialstimulusisrequiredforCRPelevation,anormalvaluedoesnotexclude
aninflammatory process. Many clinicians prefer sending ESR concomitantly withCRP. Of
interest, in systemic lupus erythematosus (SLE) and other connective tissue diseases, CRP
levels are lower than one would expect for theamount of inflammation present. CRP was
initially identified by its ability to form a precipitin reaction with pneumococcal
polysaccharide.Itisnowmeasuredbyeitherlatexagglutinationorrocketelectrophoresis.In
contrasttotheESR,CRPcanbeassayedonspecimensthathavebeenstoredbyfreezing.This
isanadvantagecomparedwithESR,whichmustbeperformedonfreshblood.Generallyfor
CRP, the upper limit of the reference range is age/50 in men and age/50 +0.6 in women.
Recently,high-sensitivityCRPhasbecomeavailable.Thistestismuchmoresensitive,andcan
detect slight elevations of CRP that are technically within the normal range, but may have
clinicalrelevancewithrespecttocoronary arterydisease.However,ithasnotbeenproven
cost-effectiveorhavingadditionalbenefitinroutinemonitoringofrheumatologicdiseases.
ErythrocyteSedimentationRate
Although an elevated CRPis highly associated with inflammation, ESR has been the most
widelyused indicator ofinflammation andthe acute phase response.ESRis performed by
placinganticoagulatedbloodinaverticalglasstubeandmeasuringtherateofredbloodcell
(RBC)settling.Normally,RBCsrepeleachotherbecausetheelectricalchargesonthesurface
of all RBCs are the same. When inflammation is present, there is an increase in the
concentrationofasymmetricallychargedproteinsthatbindtotheRBCsandthuspreventthis
repulsion. The RBCs, therefore, tend to aggregate. Aggregated clumps of cells settle more
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