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I
njuries of the foot are commonly associated with edema, a concomitant of local
inflammationandmechanicalobstructiontolocalvenousbloodflow.Edemaalsocanresult
fromavarietyofsystemicconditions,someofwhicharepotentiallylifethreatening.However,
“swelling, likefever,isnotadisease itselfbutasign ofanunderlyingdisorder.”1 Therapy,
bothinitsformandurgency,mustbetargetedtothecausativeprocess,nottothephysicalsign.
The objective of this chapter is to review the pathophysiology of edema, differentiate the
pathophysiologiccharacteristicsassociatedwithlocalinjuryfromthoseassociatedwithother
diseases,andpresentthedifferentialdiagnosisofperipheraledema,withparticularreference
to the clinical signs and symptoms by which the edema of localized injury might be
differentiatedfromthatresultingfromothercauses.
Thischapterrepresentsanupdateofachapterwepublishedearlier(ShafferB,BorerJS.
Edemaandfootinjuries:pathophysiologyanddifferentialdiagnosis.In:RanawatCS,Positano
RG,eds.DisordersoftheHeel,Rearfoot,andAnkle.NewYork,NY:ChurchillLivingstone;
1999:116–124).Muchofthatmaterialisintegratedandincorporatedhereinbydirectquotation
or paraphrasing (with permission of the publisher), with addition of new material as
appropriate.
PATHOPHYSIOLOGYOFPERIPHERALEDEMA
Ultimately,edemaresultsfrom transudationoffluidacrossthe capillaryorproximalvenular
wall.Suchfluidmovementresultsfromanimbalancebetweencapillarypermeabilityandthe
flow of fluidthroughthecapillaries. Fluid flow is determinedby capillaryhydrostatic and
oncoticpressures
2–4
;capillarypermeabilityisafunctionoftheperformanceoftheendothelial
cells (throughwhichsolute andfluidcanmove)and size ofthe spaces betweenthesecells
(whichalsoserveaspathwaysforfluidandsoluteegress).
3,5
InterstitialandCapillaryHydrostaticPressure
The usual cause of abnormal capillary hydrostatic pressure is increased total intravascular
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volume.Concomitantwiththeincreasedintraluminalpressure,thepressuregradientbetween
the capillary lumen and the interstitium must rise, at least transiently, precipitating fluid
transudation through interendothelial interstices. Most commonly, intravascular volume
expansionresultsfromabnormalsodiumretention,asisfoundinthesettingofchronicheart
failure(CHF).InCHF,cardiacoutputissubnormal(low-outputCHF)orrelativelyinadequate
(high-outputCHF).Ineithercase,renalperfusioniscompromisedbyacombinationofneural
and humoral responses triggered by signals emanating from a series of baroreceptors and
chemoreceptors; these signals are influenced by cardiac output.
3,4,6–8
Subnormal renal
perfusion(plasmavolumedeficiency)increasesthereleaseofreninthroughstimulationofthe
β-adrenoceptorsinthejuxtaglomerularcellsoftherenalcortex,whichenhancestheproduction
of angiotensin I. In the bloodstream, angiotensin I is rapidly converted to angiotensin II.
AngiotensinIIcauses increasedsecretionofthe salt-retaininghormonealdosteronefrom the
adrenal cortex,renal vasoconstriction(specifically, constriction ofefferentrenalglomerular
arterioles), and sodium reabsorption from the proximal convoluted tubule. Angiotensinmediated vasoconstriction increases blood pressure and decreases renal perfusion, thus
increasing filtration fraction and proximal tubular reabsorption of water and sodium in the
kidney. Aldosterone acts on the distal convoluted tubule and collecting duct to reabsorb
sodium. Thus, theresultof activating therenin–angiotensin–aldosterone system is increased
plasmavolumepotentiatingthedevelopmentofedema.
6–10
Intravascularvolumealsocanbeexpandediatrogenicallybyintakeoflargefluidvolumes
ataratethatexceedsrenalexcretorypotential.11Effectivecapillaryvolumecanbeincreased
even without an increase in total vascular volume by relaxation of precapillary arteriolar
muscular sphincters, as occurs iatrogenically byadministration ofcertainvasodilators, like
nifedipine.12Similarly,capillaryvolume,andconcomitantintracapillaryhydrostaticpressure,
canbeincreasedbyobstructiontovenousflow,asbyvenousthrombosis.Suchobstructioncan
prevent egressoffluidfrom thecapillarylumeninto thevenularlumenwhileforward flow
continuesfromtheprecapillaryarterioles,resultinginabnormalfillingofthecapillarylumen.
Similarly, in CHF, increased central venous pressure is reflected backward throughout the
venoussystem,andtheeffectsofrelativeobstructiontooutflowpotentiatethoseresultingfrom
theincreaseintotalvascularvolume.
6,11,13
InterstitialandCapillaryColloidOncotic(Osmotic)Pressure
Capillaryosmoticpressureprimarilyisafunctionofplasmaproteinconcentrationand,most
specifically,theconcentrationoftherelativelysmallprotein,albumin.Thus,capillaryosmotic
pressureisreasonablyapproximatedascapillaryoncoticpressure.Generally,plasmaproteins
do not pass through the capillary endothelial cells or the intercellular capillary pores.
Therefore, the osmotic effects of the intraluminal plasma albumin counteract the effects of
abnormalhydrostaticpressureandeventendtopromoteresorptionofinterstitialfluid.Plasma
oncoticpressureisdiminishedbyvarioussystemic,renal,andhepaticdiseases(e.g.,nephrotic
syndrome,malnutrition,cirrhosis,lossofproteininthegastrointestinaltract,severecatabolic
state).
6,11
Theeffectsofintravascularproteinsareopposedbytheinterstitialcolloidconcentration.
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Tissue colloid osmotic pressure can be altered byextravascular proteinaccumulation as a
result of abnormal capillary permeability or obstruction of flow within the lymphatic
system.
3,6,13
Physiologically, the lymphatics remove the fluid, which is filtered by normal
capillaries.Thus,normally,thereisaslightflowgradientfromthearterialtothevenousside
ofthecapillaries;thefluidandprotein,whichenterthecapillariesfromthearterioles,exceed
thecapacityofthecapillaries,whichfiltertheexcessintotheinterstitialspace.Someofthis
excess is resorbed into the capillary as this vessel communicates withthe more compliant
venule. However, the amount filtered generally exceeds the efficiency of the resorption
process.Theexcessisremoveddirectlybythelymphaticvessels,whichdraintheinterstitial
space,thusenablingtissuehomeostasistobemaintainedforwaterandsolute.
3–6,13
Thelymph
is returnedtothe venous system via anastomoses between lymphatic vessels andthe larger
centralveins.
Ifthelymphaticsystemisobstructed(asmayoccurwithcertainmalignanciesandcentral
venous obstruction), excess fluid and protein can accumulate in the extravascular space,
increasinginterstitialosmoticpressureandpotentiatingedemaformation.
3,5,6,13
CapillaryPermeability
Generally, onlynoncolloidsolutes permeatethe capillarywallfreely.Injurytothe capillary
wall from chemical, bacterial, immunologic, thermal, or mechanical sources (as is
characteristic of inflammation) can increase capillary transmural permeability to larger
molecules, like albumin and other plasma proteins.Thus, for example, inextreme cases of
capillaryendothelialcellhypoxia(asmightbeseenwiththeischemiaofarteriolarorarterial
obstruction or in the context of poison gas, burns, or allergic reactions), increases in
permeabilityofcapillariesandsmallvenulescanallowfluid,highinproteincontent,toenter
the extravascular space within the injured tissue. Such abnormalities in microvascular
permeability generally are not important factors in the pathophysiology of the common
generalizededematousstates,butcanbeimportantinthegenesisoflocalizededema.
3,6,11
Severalmechanismsmayunderliepathologicalterationsincapillarypermeability.During
acuteandnon-necrotizinginjurytotheskin,releaseofendogenousautacoids(e.g.,histamine,
serotonin), presumablymost often from mast cells, can cause arterial constriction,possibly
associatedwithcapillaryinjury(itselfpotentiallyaffectingcapillaryendothelialfunctionand
integrity).Aperiodofconstrictiongenerallyisfollowedbyarterialdilation,whichincreases
flow into the capillaries. Release of autacoids appears tobe triggered by local release of
calciumionsfrominjuredcells.Theeffectsoftheautacoidsarehighlyselective,resultingin
separationofthelateralbordersonlyoftheendothelialcellsliningthepostcapillaryvenulesof
10to30µmindiameterandnot,strictlyspeaking,ofthecapillariesthemselves.Indeed,the
effect can be quite marked: the width of the intercellular clefts can be greatly enlarged,
sufficiently even to accommodate 7 to 10 µm of formed blood elements.14 Although the
microvascular basement membrane, which limits movement of colloidal particles (e.g.,
lipoproteins), is not affected by autacoid release, this barrier can be traversed by plasma
proteinsandsmallersolutes,allowingedemaformation.
14
Alterationinthefunction oftheendothelialcellsthemselvesalsocanbeimportantinthe
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1.
a.
b.
1.
2.
pathophysiology of edema formation. Endothelium lining the microvasculature forms the
critical barrier controlling the exchange of molecules between blood and interstitial fluid.
Interactionofbloodwiththeendothelialcellsurface(theglycocalyx)canrestrictorincrease
transendothelial transport of specific ligands. Excessive movement of osmotically active
moleculesintotheinterstitiumcanpromoteedemaformation,whereastheirtransportoutofthe
interstitialspacecanhavetheoppositeeffect.Becausetheseendothelialtransportmechanisms
depend on endothelial expression of cell surface glycoproteins, regional variations in
endothelial transportcanbeexpected andmaybe usefulindeveloping tissue-directed drug
therapies,whichmightlimitedemaformationincertainsettings.
15
The composition of the serum also can affect capillary permeability. This influence
depends on the capacity of serum components to affect the configuration of the electrical
chargeoftheglycocalyx.Normally, the netnegative chargeconfigurationatthecell surface
tends to restrict transcapillary transport of polyanionic molecules to a greater degree than
neutralorpolycationicmolecules.Endothelialcellsurfacebinding ofcertainplasmaanionic
macromolecules, such as albumin and orosomucoids, increases the charge negativity at the
glycocalyx, resulting in greater polyanion exclusion.15 In addition to its effects via surface
chargealteration,serumalbuminactsasastericmolecular“filter”thatcanresistthetransport
ofwater,smallsolutes,andmacromoleculesacrossthemicrovascularwall.15Thus,reduction
inserumproteinscanpromoteedemaformationbothbyreducingserumoncoticpressureand
minimizing theelectrostaticandphysical effectsthat retard movement ofosmoticallyactive
moleculesintotheextravascularspace.
DIFFERENTIALETIOLOGICDIAGNOSISOF
PERIPHERALEDEMA
The pathophysiologic processes described previously can occur in various combinations
amongthemanydiseaseprocessescharacterizedbyperipheraledema.Cluestotheunderlying
causecanbeinferredfromassociatedclinicalsymptomsandphysicalsigns.Inapproachingthe
differential diagnosis ofedema, a useful frameworkforseparating localizedprocessesfrom
systemicordiffusediseasescanbebasedonconsiderationofthefollowingcharacteristics:
History
Known potential causes or contributing factors (recent trauma, surgery, concurrent
illness,drugtherapy)
Temporalfactors
Rapidity of onset (gradual, more commonly associated with systemic diseases,
versussudden,morecommonlyassociatedwithlocalizedprocesses)
Temporalpattern(shortduration/firstepisode,chronic,recurrent,cyclic;notethat
variationsinedemaduring24-hourperiodshavelimiteddiagnosticvaluebecause,
irrespective of cause, peripheral edema is greatest in dependent regions and,
therefore,typicallyisgreater infeetandanklesduring thedaytime,whenupright
postureismostcommon)
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c.
2.
a.
b.
c.
d.
Symptoms (painless, more common in systemic diseases, versus painful, very
uncommoninmostsystemicdiseases)
1,2,4,6,11
Physicalsigns
Laterality (unilateral, more common in localized processes, versus bilateral, more
commoninsystemicdiseases)
Conditionof overlying skin(taut, thick,fibrotic skin generallyis associated witha
chronicprocess,morelikelyaresultofsystemicdiseaseorvenousinsufficiencythan
musculoskeletalcondition)
Density of edema (edema that is relatively low in protein commonly is soft and
“pitting,”typicalofCHForhypoproteinemia;edemathatisrelativelyhighinprotein
content or involves extensive subcutaneous fibrosis generally is nonpitting, as in
pretibialmyxedema)
Location (anasarca, edema plus ascites, simultaneous upper and lower extremity
edema, and other generalized patterns suggest systemic diseases; localized edema,
evenifbilateral,maybemorecloselyassociatedwithalocalizedprocess)
1,2,4,6,11
Laterality ofedema isperhapsthemostefficientinitialdiscriminator ofsystemicversus
localized processes. Therefore, the etiologic differential diagnosis of peripheral edema,
presentednext,iskeyedtothischaracteristic,asmodifiedfromtheclassificationschemesof
RuschhauptandGraor2andYoung.
1
BilateralEdema
Bilateraledemacommonlybeginssimultaneouslyinbothlegsatfeetandanklesandproceeds
symmetricallyupthelegs.2Possiblecausesincludethefollowing:
ChronicHeartFailure
Historyofpotentialcauses/contributingfactors:hypertension,angina,ormyocardialinfarction;
valvular diseases; cardiomyopathy; etc. Symptoms: dyspnea on exertion, orthopnea,
paroxysmal nocturnal dyspnea; associated signs: tachypnea, rales, rhonchi, distended neck
veins, tachycardia, hepatomegaly, ventricular gallop, heart murmur, etc.
1,2,11
Edema of CHF
typically is soft and easily pitting, occurs predominantly in dependent parts of body, and,
therefore, diminishes in legs after a period of recumbency.
1,2,11
CHF edema can be
distinguishedfromotherformsofdependentedemabythepresenceofengorgedcervicalveins,
particularlyifevidence ofdiffusely elevatedsystemic venous pressure(e.g.,hepatomegaly)
alsoispresent.
6
PulmonaryHypertension
Causesofpulmonaryhypertensionareleft-sidedheartfailure,chronicobstructivepulmonary
disease(COPD),andsleep apnea.16Sleepapneais anunderrecognizedcauseofedemaand
can cause hypertension due to sympathetic nervous system overactivity secondary to
intermittenthypoxia.17Pulmonaryhypertensionhasbeenreportedtobecommoninthosewith
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obstructivesleepapnea,andpretibialedemaisacommonsignofpulmonaryhypertensionin
those with sleep apnea.18 Studies suggest that patients who are at risk for pulmonary
hypertension and over the age of 45 with nonspecific leg edema should undergo
echocardiograminordertoruleoutobstructivesleepapnea.
16
NephroticSyndrome
Historyofcausative/contributingfactors:renaldisease/uremia,proteinuria,hypoalbuminemia,
hypercholesterolemia;symptoms:polyuria/polydipsia,nocturia.Renalbiopsycanconfirmthe
diagnosis.
1,2,6
AcuteGlomerulonephritis
Historyofcausative/contributing factors: historyconsistentwith recent groupA β-hemolytic
streptococcal infection; proteinuria, hematuria, markedly subnormal creatinine clearance,
recent-onsethypertension.
2
HepaticCirrhosis
Historyofcausative/contributingfactors:historyofcontinuingjaundiceorabdominalswelling,
hepatosplenomegaly, gynecomastia, ascites, spider angiomas, palmar erythema2; abnormal
fecallossofalbumin,6diagnosticliverbiopsyorscan,abnormalserumliverenzymes,etc.
1
Hypoproteinemia
History of causative/contributing factors: malnutrition, diarrhea, known malabsorption
syndromeofanycause.
1,2
IdiopathicCyclicEdema
Historyoftemporalfactors:onsetisquickandmarkedanddisappearanceiscomplete,with
recurrences of a similar pattern; edema affects hands, face, legs, abdomen, and lower
extremities. Itoften is relatedto themenstrual cycleand is limitedalmostentirelytoobese
womenaged 20 to 40 years; maycause a 3- to 4-lb weightgain from morningto evening,
reversedbybedrest;syndromemaybeself-limited,sometimesdisappearingafterafewcycles
(months). More commonly, it recurs during 1 to 20 years after initial episode. Associated
symptoms:headache,irritability,anxiety,anddepression.
1,2,19
Position-RelatedEdema
Historyofcausative/contributingfactors: any conditionthatseverelylimitsambulation(e.g.,
various arthritides2). History of temporal factors: temporal association with sitting and
standingforlongperiodswithoutuseofcalfandlegmuscles(increasingcapillaryhydrostatic
pressure by relative obstruction to capillary outflow because of gravity-mediated venous
pressureelevationinlowerextremities).Symptoms:generallypainless,butifpainexistsfor
otherreasons(e.g.,musculoskeletalinjury),hangingaffectedfootoverbedatnighttorelieve
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painmayresultinunilateraledema2;sitting (torelieveischemicpain)canresultinbilateral
edema.2 Physical signs: skin generally increasingly compliant with age, resulting in
diminishing interstitial fluid pressureand enabling considerable fluid accumulation2;edema
can be unilateral if arterial insufficiency coexists with dependency or if dependency is
systematicallyunilateral.
Lipedema
Historyofcausative/contributingfactors:bilateralsymmetricdistributionoffatconfinedtoor
predominantly present in thelower extremities, characteristically sparing thefeet (andthus
distinguishable from lymphedema
1,2
), occurring only in women, often familial. Symptoms:
generally painless,1 although if complicated by exogenous obesity can be painful. Physical
signs: thisis nottrueedema and is not associated with pittingunless a comorbidcondition
causeswaterretention.1Supporthose,oftenusefulinotherformsofedema,doesnotprovide
benefitandcanpotentiatepain;avoidanceofabnormalweightgainmaybeuseful,butintensive
weight loss generally is not effective therapy because site of abnormal fat accumulation
(buttocksandlegs)generallydoesnotrespondtodietaryalteration.
1
DrugEffects
History of causative/contributing factors: temporally related use of nonsteroidal antiinflammatory medications (e.g., phenylbutazone, oxyphenbutazone, ibuprofen2), certain
vasodilating andantihypertensive drugs(e.g.,dihydropyridinecalcium channelblockerslike
nifedipine,α-methyldopa,guanethidinesulfate,hydrazaline,diazoxide, rauwolfiaalkaloids),
1
hormone therapy (e.g., progesterone, estrogen, testosterone, corticosteroids,
adrenocorticotropins),monoamineoxidaseinhibitorantidepressantdrugs,etc.Physicalsigns:
edemaissoftandpitting,similartothatobservedwithcyclicedemaorhypoproteinemia.
1
Inrareinstances,theantibioticclassoffluoroquinoloneshasbeenassociatedwithcausing
peripheral leg edema. Levofloxacin, which is commonly prescribed for treatments of the
respiratorytract,urinarytract,andskin/softtissueinfections,hasbeenassociatedwithacute
leg edema and stasis dermatitis.20 Furthermore, antibiotics that are excreted through the
kidneysneedtobemonitored,aslegedemacouldbeasignofkidneypathologysecondaryto
antibiotic regimen. Antibiotics that have been associated with acute renal failure are
aminoglycosides,amphotericinB,vancomycin,andβ-lactamantibiotics.
21
PrimaryLymphedema
History of temporal factors: onset gradual, over days, weeks, or months2 (and thus
distinguishable from idiopathiccyclic edema) and is chronic.Symptoms: generallypainless
unlessaconcurrentpainfulprocessisextant.Physicalsigns:oftenaccompaniedbyabnormal
epidermalproliferationanddermalsubcutaneousfibrosis22butrarelybyskinulceration;often
notbilateraland,inanyevent,generallylessuniformlydistributedandextensivethanedema
caused by lymphatic or venous obstruction.1 A positive Kaposi-Stemmer’s sign is
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pathognomonic lymphedema andan acceptedwaytodifferentiatefromlipidema. Apositive
outcomeofthisclinicalevaluationiswhenthereisfailureoftheskinoverlyingthedorsumof
thesecondtoetotentwhena“pincergrasp”isapplied.
23
ExtremeHigh-TemperatureExposure
History of causative/contributing factors: temporally related exposure to high temperatures
(which cause peripheral vasodilation, increasing flow through, and hydrostatic pressure in
affected capillary beds), typically occurring in healthy individuals.2 History of temporal
factors: moderately rapid onset (many minutes to hours depending on temperatures,
dependency of limbs, etc.), moderately rapid resolution (again depending on temperature
change,aswellasintercurrentambulation).
UnilateralEdema
Thecausesofunilateraledemaaremorenumerousthanbilateraledemaand,mostcommonly,
arebecauseoflocalratherthansystemicconditions.
2
ChronicVenousInsufficiency
Thisisthemostcommoncauseofunilateraledema,
1,2
occasionallyresultingfromcongenitally
absent or abnormal valves of thedeep veins butmore commonlycaused by acquired deep
venousvalvulardysfunction;ineithercase,valvularinsufficiencyresultsinabnormalvenous
pressure when affected body parts are dependent, with associated relative obstruction to
capillary outflow.History ofcausative/contributing factors: remote deep venous thrombosis
(veins subjected to engorgement distal to thrombi often are permanently dilated because of
damageandremodelingvascularwall,commonlyrenderingvalvesincompetent;additionally,
venous valves often are damaged or destroyed during the healing process1). Deep venous
thrombophlebitis can be symptomatic, but often is asymptomatic and must be detected by
objective testing. A specific “subacute” form of this syndrome regularly is observed after
coronary artery bypass grafting in which a venous bypass conduit is used; removal of the
saphenousveinleadstotransientvolumeoverloadoftheremainingveinsintheipsilateralleg,
withresultingsoft,pittingedemathatresolvesoverseveralmonthsasthedeepveinsremodel
tohandle their newload.Chronicstasis changes(seelater) seldom occurunlessadditional,
preexistingvenousdiseaseispresent.Physicalsigns:inearlystages, edematypicallyissoft
and pitting, consisting mainly of fluid transudation resulting from excessive microvascular
hydrostatic pressure
1,2
; with time, inefficient capillary inflow and abnormal interstitial
pressureleadtochronicskinchanges,includingpigmentation(irondepositioncanoccurasa
resultofextravasationofredbloodcells),dermatitis,andfibrosis,occasionallyaccompanied
byinduratedcellulitis andulceration.1Theresultis so-calledbrawnyedema,whichcan be
contrastedwiththesoft,easilypittingedemaofhypoproteinemia.Thesechangescommonlyare
associatedwithvenousstasis.Prominentsuperficialveinsmayappearshortlyafteranattackof
phlebitisandmaybecomevaricoseinthechronicstageofvenousinsufficiency.Intheverylate
stages, chronic venous insufficiency can result in secondary hemodynamic stresses in the
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