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superficialveins,whicharesufficienttocausesoft,pittingedemainadditiontothechronic,
brawnyedema.1Edemasecondarytochronicvenousstasiscausesbloodtopoolinthevenous
system, which activates inflammatory process and causes capillary damage. Furthermore,
venousstasisulcerstendtodemonstrateimpaired wound healingduetointracellularedema,
plateletaggregation,andleukocyteactivation.Venousstasisulcersarethemostcommonform
ofulcerationpresentonthelowerextremity. These ulcers tendtobesuperficial,bepainful,
and have irregular borders and are located over bony prominences. Ulcerations are an
important sequela of edema secondary to chronic venous insufficiency, accounting for
approximately80%oflowerextremityulcerations.
23
SuperficialThrombophlebitis
Historyofcausative/contributingfactors:temporallyrelateddevelopmentoftender,indurated
superficial“cord”extendingavariabledistancealongthepathofsuperficialvein,associated
with erythema, warmth, and tenderness during the acute stage; thrombus usually remains
palpable for days or weeks after diminution of the acute inflammation. Although systemic
symptomsusuallyareabsent,alow-grade fever maybepresent.
1,24
Physicalsigns: although
pitting, edema is not soft, because inflammatory process can be expected to alter
microvascularpermeability;importantly,edema usuallyisuniforminconsistencyinthearea
drainedbytheobstructedvein.
24
DeepVeinThrombosisand/orThrombophlebitis
History of causative/contributing factors: temporally related conditions associated with
enforced bed rest or physical inactivity, particularly if extremities are immobilized (e.g.,
orthopedicorabdominalsurgery,prolongedairplaneflight,childbirth,traumaticinjury,orany
particularlydebilitating illness). Diagnosis generallyrequiressupportfrom objective testing
(e.g., contrast venography, Doppler ultrasonography, radionuclide-based thrombus imaging)
and leads to chronic venous hypertension of the affected lower extremity when the leg is
dependent.2Historyoftemporalfactors:edema maydevelopgradually, overafew days,or
morerapidlyoverhours,dependingonthelocationandextentoftheunderlyingprocess.
1,2,24
Whenthrombosis isunusuallyextensive, edema can occurrelativelyabruptly, with massive
sudden swelling and intense cyanosis of extremity. The latter presumably results from
particularly complete oxygen extraction from blood flowing very slowly through the
capillaries, combined with compromise of arterial and arteriolar flow resulting from the
externalmechanicalpressureoftherapidlyaccumulatingedemaandengorgedveins.Indeed,in
thissetting,pulsesinthelimbaresubnormalorabsent;gangrenecanresultiftheobstructionto
the arterial flow is particularly severe,1 as inthe condition known as phlegmasia cerulean
dolens,whichcancauseshockbytrappingalargequantityofbloodintheswollenextremity.
Phlegmasia cerulean dolens primarily is associated with advanced or metastatic
malignancies.1Even insomewhatless severedeepvenous obstruction,fluidcanaccumulate
beneath thedeep fascia. Symptoms: deep venous thrombosis or thrombophlebitis cancause
localizeddull,achingpain,whichcanbequitesevere,particularlywhenlimbisdependent,
4
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butlackofpaindoesnotruleoutthiscause.Low-gradefevermaybecommon,butrigorsare
uncommonandlymphadenopathyandlymphangiticstreakingareabsent.1Physical signs:soft,
pittingedemaoftendevelopswithin 24 to48hours ofthethrombosisandcanbe extensive.
Associatedinflammationcancauselocalwarmth,tenderness,erythema,andevencyanosis;it
canoccurasinchronicvenousinsufficiency.
1,2
Superficialveinscanbeprominent1(asingle
“sentinel”veinmaybeobserved),andtendernessondeeppalpationcanbepresent.
1,2
Lymphedema
History of causative/contributing factors: any condition associated with obstruction of
lymphatics or incompetence of lymphatic valves, resulting in lymph stasis, increased
intralymphaticpressure,andinefficientdrainageoftheinterstitium(e.g.,femoralarterybypass
surgery, which appears to damage and interfere with surrounding lymphatics, or local
infection).1Lymphedemacanbesubclassifiedaccordingtothecause:(1)primarylymphedema
(idiopathic) can be congenital or acquired, commonly affects drainage of cutaneous or
subcutaneouslymphaticsinthelegs
1,2
;primarylymphedemacanbefurthersubclassifiedinto
(a) lymphedema tarda, whichbecomes apparent only after age 40, raising concern ofother
common causes (e.g., malignancy)1; (b) primary congenital lymphedema (either nonfamilial
[“simple”]orfamilial[Milroydisease]),presentatbirth,andusuallyinvolvingonlyonelower
extremitythatmanifests aplasia, hypoplasia, or varicose dilationofthelymphaticvessels
1,2
;
(c)primaryacquiredlymphedema(lymphedemapraecox),idiopathicbutapparentlyinvolving
asubnormallydevelopedlymphaticsystem,notseenbeforeadolescencebutusuallypresenting
beforeage30andpredominatelyaffectingwomen.2Characteristically,thisformisassociated
with a “hump” on the dorsum of thefoot, although upper extremities can be involved, and
edemadevelopment isslow,typicallyinvolvinganentirelimboverthe courseofmonthsto
years;althoughcommonlyunilateral,bothlimbsmaybeaffected.Inearlystages,edemaissoft
andpainlessanddisappearsovernight.Lymphangitisand/orcellulitisoccurswithinweeksto
months of edema ina minority of cases
1,2
;(2) secondary(obstructive) lymphedema maybe
inflammatory or noninflammatory1 and most commonly is secondary to malignancy. The
noninflammatory form almost always is unilateral and typically results from metastatic
carcinoma involving regional lymph nodes or after irradiation or surgical lymph node
resection,2butcanoccurwithretroperitonealfibrosisandotherconditions1;theinflammatory
form results from lymphangitis (sometimes recurrent) or cellulitis, commonly caused by
infection,localtraumaticinjury,filariasis,etc.,1andisoftenassociatedwithfever.Historyof
temporalfactors:allformsusuallydevelopslowlyovermonthsoryears.Symptoms:usually
painless.1 Physical signs: soonafter onset, edema is soft and pitting; in chronic stages, as
subcutaneousfibrosisdevelops,theskin thickens,andedemamayresistpittingandisfirmer
thanthatassociatedwithchronicvenousobstruction;superficialveinsarenotdilated,another
pointofdifferentiationfromchronicvenousobstruction.1Clinically,differentiationfromdeep
venousthrombosismaybedifficultunlesspainispresent(generallynotpresentwithlymphatic
obstruction); venograms can rule out venous obstruction,butlymphangiograms then may be
necessarytoconfirmlymphangiticabnormality.
1
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Lymphangitis
Likelymphedema,lymphangitisfeatureslymphaticobstruction,inthiscasebythrombosisand
fibrosis,whichoccurssecondarytolocalparasitic(dermatophytoses)andbacterialinfections,
typicallyintroduced inthe footandankle.The lymph stasis thatis producedpredisposes to
recurrentcellulitis, inturn causingrecurrentlymphangitis.Physical signs:although typically
restrictedtothefootandankle,inflammationandedemamayspreaduptheleg.
1,2
Infection
Although infection can cause lymphangitis and lymphedema, occasionally a particularly
virulent infection presents acutely with characteristics that justify a separate classification.
Historyofcausative/contributingfactors:traumabreakingtheskin(wound,cut,abrasion,ulcer,
contusion,scratch,hangnail,pinprick,orvesicle)allowsforinvasionofmicroorganisms;the
areabetweenthetoesisthemostcommonsite,becauseitisoftensoftenedfromchronictinea
pedis infection.
1,2
History of temporal factors: dramatic development of edema, with
subsequent complete disappearance, occasionally featuring similarly characterized
recurrences.2 Infections that commonly cause sudden, unilateral edema include filariasis,
particularly in tropical climates, clostridia infections causing gas gangrene, and agents
associated with chronic osteomyelitis.1 Symptoms and physical signs: pronounced fever,
rigors, malaise, other nonspecific systemic symptoms, and localized pain2 associated with
rapidandevenexplosivedevelopmentoflocalwarmth,tenderness,erythema,“lymphangitic”
streaks following the course of affected lymphatics from the infection site, and regional
lymphadenopathy.Dermatophytosisofthetoesmayenablerecurrentattacks,probablycaused
bysecondarybacterialinvaders;inflammationandedemaarerestrictedtothefootandankle
butcanspreaduptheleg.
2
Trauma
Mechanicalinjurycanaffectcharacteristicsofmicrovasculaturedirectlyresultinginedema.
1,2
Inaddition,traumaticinjurytoveinscanresultinvenousthrombosisandprovideaskinportal
forentryofinfectiousagents.
Position-RelatedEdema
SeeBilateralEdema.
2
VascularAnomalies
Arteriovenousfistulasmustbeconsideredinthedifferentialdiagnosisofedemabecausethey
cancause edema (e.g., bymechanical pressure or microvasculature) and canresultinlimb
enlargement, which can mimic edema. History of causative/contributing factors: traumatic
penetrating injury. Physical signs: thrill and bruit overlying the lesion, abnormal limb
circumference;hemangiomasorothervascularanomaliesandsevere,unilateral,varicose,or
dilatedveins in unusual places mayindicate a congenital fistula.1 Angiography andvenous
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oxygensaturationdeterminationscanconfirmthediagnosis.
2
Klippel–Trenaunay–WeberSyndrome
Presentationofmuscular, bony, and soft tissue hypertrophy, persistent nevus flammeus, and
varicose veins usually involving a singlelower limb may be associated with arteriovenous
fistulas.
1
Tumors
Lipomas, hemangiomas, hemangiolymphangiomas, sarcomas, neuroepitheliomas, and
osteosarcomascancauseunilaterallimbedema,usuallyrelativelylocalizedtotheproximityof
thetumor,
1,2
unlikethemoreextensiveanddiffuseedemaofseveralothercommonprocesses.
Tumorsalsocancausemoreextensiveedemabyextrinsicmechanicalcompressionofvascular
structures.
FactitiousEdema
Edemacausebyself-inflictedconstrictionofveins,aswithatourniquet.Whenreported,such
edemagenerallyfollowsnopatternsuggestiveofaknowncause;onexamination,theremaybe
a sharply defined region of edema consistent with the application of the constricting
apparatus.
2
GastrocnemiusRupture
Typicallytheresultofathleticeffort,gastrocnemiusruptureissudden,acutelypainful(usually
mid-calf),commonlyassociatedwithalargeecchymosisindependentareas(foot,ankle)from
internalhemorrhage.Theincreasedlimbcircumferencemustbedifferentiatedfromedemaand
also causes edema as vascular structures are compressed by the internal hemorrhage and
hematoma.
1,2
PoplitealCyst,PoplitealSyndrome
Mechanicalcompressionofvenousstructuresbycystoraneurysmcancauseedemalikethatof
venousthrombosis;differentialclueisthepalpationofthecysticstructureonexamination.
2
CompartmentSyndrome
Increased tissue pressure in the region of the anterior tibial artery as a result of trauma,
thrombosis,orembolismcancausesevereischemia,edema,andpainovertheanteriortibial
compartment.2Edemawithintheconfinedspacemaycompressarterialstructuressufficiently
to compromise viability of muscle and nerve structures within the compartment, requiring
fasciotomytopreventgangrene.1Compartmentsyndromewithinthefootandlowerlegcanbe
identified by four main symptoms: pain, paresthesia, paresis, and pain with stretch. Pulse
examinationandpinkskincolorcanalsoaidindiagnosis.Withinthefoot,intracompartmental
pressure should be correlated with the diastolic pressure. Today, indication for surgical
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intervention (fasciotomy) depends on a differential pressure betweencompartment pressure
and diastolic pressure of less than 30 mmHg.25 Certain injuries have a higher risk in
developing compartmentsyndrome;forexample, withinthe foot,ChopartandLisfrancjoint
dislocationsarefrequentlyassociatedwithcompartmentsyndromewhereasinisolatedmidfoot
fractures,compartmentsyndromeisrarelyobserved.
25
RetroperitonealFibrosis
Asnotedpreviously,thisentitycancausesecondarylymphedema.Inaddition,retroperitoneal
fibrosiscancompromisearterialflowtotheaffectedlimb.
1,2
AngioneuroticEdema(HereditaryAngioedema)
This isanoninflammatoryandhereditarydiseasecharacterizedbylocalized swelling ofthe
skin,internalorgans,andmucousmembranesandcausedbylackofC1esteraseinhibitorofthe
firstcomponentofcomplementC1esterase,resultinginincreasedcapillarypermeabilityand
precapillary arteriolar dilation.2 History of temporal factors: attacks are episodic, usually
begininadolescence,andareoftenprecededbyanxietyandtriggeredbytraumaorinfection,
althoughanidentifiabletriggermaynotexist.Initialsiteofedemamaybeoneofminortrauma
(e.g., athletic contact).26 Frequency of attacks varies, from weekly to yearly or longer.
Symptoms: abdominal pain, tightness, or tingling of skin, followed by a nonpruritic and
painlessrash.Symptomsareusuallyshortlived.27Attackscommonlyareprecededbybloating,
anorexia,vomiting,constipation,andnausea.26Signs:stridor(resultingfrompotentiallylethal
edematousairwayobstruction),edemainupperextremitiesandoropharynx(upperface,trunk,
extremities;lowertrunkandlowerextremitiesarerarelyswollen);lesionsarenonpittingand
erythematous.
26
PretibialMyxedema
Unlike the myxedema associatedwithhypothyroidism, which mayresultfrom alterations in
capillarypermeabilityandinthesynthesisanddegradationratesofplasmaproteins,pretibial
myxedema is an unusual manifestation of hyperthyroidism.
1,2,28
The pathogenesis may be
relatedtoanincreaseinosmoticallyactivemucopolysaccharideproductionintheinterstitium,
producing a brawny, nonpitting edema, often with plaque formation of the overlying skin,
affectingthepretibialregionanddorsumofthefoot.Thebasisfortherarityofthisfindingin
the hyperthyroid population is unclear. Pretibial myxedema is seen in combination with
exophthalmosandmaynotresolvewithtreatmentoftheunderlyingdisease.
29
ThermalInjuryandExposuretoExtremeHighTemperatures
SeeBilateralEdema.
2
BakerCyst
This synovial structure can rupture behindthe knee into the calf muscle, producing severe
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4.
5.
6.
7.
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20.
pain,2swelling,andtenderness,whichcanmimicthepresentationofthrombophlebitis.1Baker
cysts have been associated with rheumatoid arthritis, osteoarthritis, and internal knee
malfunction1;maybebilateral;andcanbeconfirmedbyarthrography.
2
CONCLUSION
Peripheraledemaresultsfromwell-definedpathophysiologicprocessesthatcanbevariously
combinedin many disease entities. Theclinicalpresentation,specifically, the character and
distribution of edema, depends on the pathophysiologic mechanisms involved ineach case.
The operative pathophysiology is at least partially inferable from the clinical evaluation.
Althoughbeyond thescope ofthischapter, such recognitionis important inselectionamong
therapeuticmodalitiesfortheconditionsofwhichedemaisafeature.
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andWaterRetention.Philadelphia,PA:WBSanders;1960:3–6.
JohnsonHD,PflugJ.TheSwollenLeg:CausesandTreatment.Philadelphia,PA:J.B.Lippincott;1975:70–86,134–146.
WitteCL,WitteMH,DumontAE.Pathophysiologyofchronicedema,lymphedema,andfibrosis.In:StaubNC,TaylorAE,
eds.Edema.NewYork,NY:RavenPress;1984:521–542.
Friedberg CK. Edema and pulmonary edema: pathologic physiology and differential diagnosis. Prog Cardiovasc Dis.
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HarrisP.Roleofarterialpressureintheoedemaofheartdisease.Lancet.1988;1:1036–1038.
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SchnitzerJE. Update onthecellularandmolecularbasisofcapillarypermeability.TrendsCariovasc Med. 1993;3:124–
130.
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Hyman DA, Cohen PR. Stasis dermatitis as a complication of recurrent levofloxacin-associated bilateral leg edema.
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S
Table8-1.
ignificantmorbidityandmortalityareassociatedwiththedevelopmentofthromboembolic
diseaseafterorthopedicsurgery.1Thromboembolicdiseaseencompassesthedevelopment
ofdeepvenousthrombosis(DVT)andpulmonaryembolism(PE).Bothofthesecomplications
are considered to be life threatening, and they are both associated with significant patient
morbidity andinfluence managementafter foot and ankle trauma and surgery.2 As a result,
knowledge about the etiology, risk factors, diagnosis, and management of thromboembolic
diseaseisessentialtoanysurgeonwhotreatspatientswithfootandankledisorders.
Althoughtheratesofthromboembolicdiseasehavebeenthoroughlystudiedaftertotaljoint
replacement,hipfracturesurgery,andorthopedictrauma,onlyrecentlyhaveauthorsbegunto
studythe ratesofthromboembolismafter footand ankle trauma and surgery.
3,4
Therates of
thromboembolicdiseaseafterfootandanklesurgeryareconsideredtobelowerthanthoseof
thromboembolism afterhip andkneesurgery.5 Thecurrentincidence of DVT after footand
ankle surgery ranges from 0.12% to 5.7%,
4–12
withhighest rates reported after surgery for
acuteAchillestendonruptureandhalluxvalgus.
8,11
ThecurrentincidenceofPEafterfootand
anklesurgeryrangesfrom0.15%to1.1%.
4–10,12
Generally,therateofthromboembolicdisease
afterfootandanklesurgeryisconsideredtobelessthan1%,butitmaybehigherinpatients
withcertainriskfactors.Thereportedincidenceratesfromthemostrecentstudiesinfootand
anklesurgeryarelistedinTable8-1.
5
In this chapter, we describe the etiology of thromboembolic disease and also its risk
factors, clinical presentation, diagnosis, and management. Since disease prevention is an
essential component ofpatientcare and animportant institutional measure, we also discuss
prophylacticstrategiesforpreventingthromboembolicdiseaseafterfootandankletraumaand
surgery.
ReportedIncidencesofVenousThromboembolism(VTE)
IncludingDeepVenousThromboembolism(DVT)and
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PulmonaryEmbolism(PE)FollowingFootandAnkleSurgery
Study
IncidenceofVTE
DVT PE
Griffithsetal.
6
0.27 0.15
Shibuyaetal.
7
0.28 0.21
SaragasandFerrao
8
5.7 1.1
WukichandWaters
5
0.4 0.3
Hanslowetal.
4
4 1.3
Mizeletal.
9
0.22 0.15
SolisandSaxby
13
3.5 0
Bargetal.
10
3.9 0
Radletal.
11
4 0
Jamesonetal.
12
0.1 0.1
THROMBOEMBOLICDISEASEOVERVIEW
Although Rudolf Virchow, a German pathologist and biologist, initially described the
phenomenonofvenousthromboembolism(VTE)in1856,itstruemorbidityandmortalitywas
notappreciateduntilmanyyearslater.Approximately90%ofclinicallysignificantPEsarise
fromproximalDVTofthelowerextremities,anditisestimatedthatPEsareassociatedwith
5%to10%ofallhospitaldeathsintheUnitedStatesannually.
3
VTE is the third most common vascular disease, following acute ischemic attacks and
cerebrovascular accidents.3 A DVT occurs when one or more of the calf veins become
obstructedtovenousbloodflow.TheformationofDVTismultifactorialandbestdescribedby
Virchow.14Infact,Virchow’striadofhypercoagulability,endothelialinjury,andvenousstasis
provides thefoundation for understanding thepathogenesis of DVT formationafter footand
ankle surgery and trauma.15 For example, orthopedic surgery causes the release of
thromboplastinsthatcanactivatethecoagulationcascadeandresultinahypercoagulablestate.
Similarly,endothelialinjuryiscommoninsurgery,andvenousstasisoccurswiththeuseofa
tourniquetorpostoperativeimmobilizationafterfootandanklesurgery.Postoperativeswelling
andlimitedambulationfurthercontributetovenousstasis,andprovide anidealenvironment
forclotformation.
3
The majority of these thrombi occur in the deep veins of the calf; however, clot
propagationtomoreproximalveinsisknowntooccuraswell.Morespecifically,therateof
propagation after total knee replacement surgery has been documented at 23%,16 which
underscorestheimportanceoflongitudinalfollow-up.APEoccurswhenaDVTinthepelvis
or lower extremity embolizes through the right heart and gets lodged in the pulmonary
vasculature. This event results in an obstruction of pulmonary perfusion and subsequent
oxygenation of blood. Although themajorityof PEs are asymptomatic, theseevents maybe
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Table8-2.
fatal.ThesizeandlocationofthePEdeterminetheassociatedmorbidity andmortality,with
largesaddle-typePEsbeingthemostfataltype.
3
RISKFACTORSFORTHROMBOEMBOLICDISEASE
Multiple risk factors have been identified as increasing a patient’s predisposition to
thromboembolic disease. Given the multifactorial nature of thromboembolic disease, it is
importanttorecognizethepresenceofmultipleriskfactorsineachpatientandtostratifythe
riskofthromboembolicdiseaseineachpatientaccordingly.Afewstudieshavelookedatthe
mostimportantriskfactorsforthromboembolicdiseaseinpatientsundergoinglowerextremity
surgery, some of which are listed in Table 8-2. For example, Barg et al.10 concluded that
obesity,historyofpreviousthromboembolicdisease,andabsenceoffullweight-bearingstatus
postoperativelyareindependentriskfactorsfordevelopingsymptomaticDVTaftertotalankle
replacement.Similarly, Jameson et al.12 foundincreasing age andmultiple comorbidities as
beingriskfactorsforthromboemboliceventsafterfootandankletraumasurgeryinaBritish
NationalHealthServiceregistry.Morerecently,Shibuyaetal.7foundthatolderage,obesity,
andhigherinjuryseverityscorearesignificantlyassociatedwiththedevelopmentofDVTand
PEafterfootandankletrauma.Otherknownriskfactorsforthromboembolicdiseaseinclude
rheumatoidarthritis,recentairtravel,malignancy,hypercoagulablestates,pregnancy,andoral
contraceptiveuse.
3,4
ReportedRelativeRisk(RR)orOddsRatio(OR)ofVTERisk
Factors
Study VTERiskFactors RRorOR
Shibuyaetal.
7
Olderage 1.02(ORforDVT);1.02(ORforPE)
Obesity 2.35(ORforDVT);3.06(ORforPE)
Higherinjuryseverityscore 1.22(ORforDVT);1.21(ORforPE)
WukichandWaters
5
Manylisted NoRRorORprovided
Mayleetal.
17
Manylisted NoRRorORprovided
Hanslowetal.
4
Historyofrheumatoidarthritis NoRRorORprovided
Recenthistoryofairtravel NoRRorORprovided
PreviousDVTorPE NoRRorORprovided
Limbimmobilization NoRRorORprovided
Wangetal.
2
Anticoagulantprophylaxisnotprescribed NoRRorORprovided
Immobilizationwithacastorsplint NoRRorORprovided
Ageover40y NoRRorORprovided
Obesity NoRRorORprovided
Mizeletal.
9
Postoperativenonweightbearingand
immobilization
0.4%increaseinRRforVTE
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