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FIGURE21-10.Superiorandlateralviewsoftheintervertebraldiskshowingthenucleuspulposusandannulus
fibrosus.(FromOpenStaxCollege[CCBY3.0,http://creativecommons.org/licenses/by/3.0],viaWikimedia
Commons.)
The herniated disk leads to nerve dysfunction through one of two mechanisms. First,
compressiononthenerverootcausesmechanicaldysfunction.Becausespinalnerverootslack
the robust protective connective tissuesheaths that characterize peripheral nerves, they are
thought to be especially susceptible to mechanical compression. Second, release of disk
materialinthevicinityofthenerverootstriggersaninflammatorycascadethatalsoresultsin
biologicnerverootdysfunction.
14
DiagnosisandLowerExtremityFindings
Patientspresentingwithdiskherniationmayprovidealonghistoryofmildtomoderateback
painordescribeaspecificincidentthattriggeredtheonsetoftheirpain.Thepainincasesof
diskherniationistypicallydescribedaslegandbackpain.Thelegpainfollowsadermatomal
distribution(Fig.21-2).CommonsitesofdiskherniationincludetheL4-5andL5-S1levels.
Examples of events that may trigger the onset of pain may include heavy lifting, bending,
twisting, orafall.Mostpatientspresentingfor this complaint typicallyhaveacomplaintof
pain,althoughnumbnessandweaknessarealsopossible.Thepainistypicallydescribedasa
“radiating”painextendingtodifferentpartsofthelowerextremitydependingonthelocationof
theherniation.Forexample,aherniationatL2maypresentaspaininthemedialthigh,whereas
aherniationatL4–S1willtypicallypresentaspainthatradiatesbelowthekneeandintothe
foot.Theymustalsoelicitanycomplaintsofbowelorbladderdysfunction,progressiveweight
loss,fevers,chills,andhistoryofcancer.Particularattentionmustalsobepaidtoperipheral
causesofpainsuchasnerve(tumor,peripheralnervecompression,ordiabeticneuropathy)or
musculoskeletalcausesofpain.
Thephysicalexaminationofpatientswithspinalstenosisbeginswithobservationofgait.
PatientswithL5herniationsmayexhibitaTrendelenburggaitbecauseofweaknessofthehip
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abductors.Patientsmayalsoleanawayfromtheaffectedsideasthismaneuveristhoughtto
releasethemechanicalpressureofthenerverootfromtheherniateddisk.Inadvancedcases,
patients may have a foot drop and exhibit a steppage-type gait pattern. A thorough
neurovascular exam must be performed as well. Unlike lumbar stenosis, findings in disk
herniationaretypicallyunilateral.Asymmetricreflexes,weakness,orchangesinsensationare
allpotentialredflagsfordiskpathology.
Severalclinical testsexisttoconfirmthediagnosisofdiskherniation.Inthepresenceof
lumbar diskherniation(L3–S1), theaffectednerve roots canbetensedduringastraight leg
raisemaneuver.Inthistest,thelegisextendedandpassivelyraised(Fig.21-11).Inthearcof
motionbetweenapproximately30°and70°ofhipflexion,thenerve rootisdrapedoverthe
disk and tensed. The straight leg raise test is considered positive when this maneuver
reproducesthepatients’symptoms.Thephysicianmayalsoperformastraightlegraiseonthe
contralateral extremity. If this reproduces symptoms in the affected limb, it is thought to
increase thespecificity of thefinding15;however, estimates varyfrom 10% to 100%.
1,16
A
variationofthestraightlegraise,theslumptest,canbeperformedwiththepatientinaseated
position.Thepatientisaskedtoflextheirneckandthoracicspine(“slump”) andthefootis
dorsiflexedandthekneeextended.Thismaneuvercausesthespinalcordtoglidecephaladand
increases thetensiononthenerveroots;ithasbeenshowntobemore sensitive.Finally, in
cases of upper lumbar disk herniation, the femoral nerve stretch test may be used. In this
maneuver,thekneeis flexedandthe hipisextended with the patientinthe proneorlateral
decubitus position. Reproduction of the patients’ pain (usually thigh pain) is indicative of
upperlumbarrootpathology(L1–L2orL2–L3).
FIGURE21-11.Pictureofastraightlegraise;painbetween30°and70°issuggestiveoflumbarpathology.(By
Davidjr74[CC0],viaWikimediaCommons.)
Treatment
Inpatientspresentingtotheclinicwithanacutediskherniation,thenaturalhistory hasbeen
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1.
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documentedinseveral studies with an observational arm. Thesestudies show that between
50%and60%ofpatientshaveimprovementintheirsymptomswithoutsurgery.1Onewidely
citedretrospectivetrial foundthat92%ofpatientsreturntoworkand90%ofpatientshave
goodtoexcellentoutcomesafterlumbardiskherniation.17However,criticsofthisstudyhave
raisedthepossibilityofsignificantselectionbias (thestudyinvestigatorswerenonoperative
practitionersandonlyselected58of347patientsreferredtothemforasecondopinion)and
point to a 10% dropout rate in the study cohort as evidence that the results may not be
generalizable.TheSPORTtrialalsofollowedacohortofpatientstreatednonoperativelyfor
lumbardiskherniation.Inthisgroup,51%reportedmajorimprovementat4-yearfollow-up.
18
Thisissimilartoothermorerecentliterature.
19,20
Most trials designed to investigate the benefits of operative versus nonoperative
intervention havesuffered from significantcrossover bias,andthereforelimitedconclusions
canbedrawnaboutthebenefitsofoperativeintervention.However,datafromtheSPORTtrial
(as-treated analysis) and Maine Lumbar Spine Study seem to suggest that operative
intervention seems to produce improved outcomes compared to the nonsurgically treated
group.
18,20
Thereisa15%rateofreoperationfollowingsurgeryforherniateddisks.21Given
this mixed data, there are few concrete operative indications for lumbar disk herniations
except for progressive neurologic deficit.1 Patientswith a neurologic deficit in whom disk
herniationissuspectedshouldbereferredtoaspinesurgeonexpediently.Surgicalintervention
typicallyinvolvesanopen diskectomyor microdiskectomy, thatis, enteringthe spinalcanal
after making an opening in the lamina and removing the offending disk material. Relative
indicationsforsurgeryvarybut,attheveryleast,requirecross-sectionalimagingfindingsthat
correlatewiththepatients’symptoms.
Nonsurgical treatment for disk herniation involves physical therapy and back school.
Epidural steroid injections are commonly used in patients with lumbar disk herniation,
especiallyifpainistooseveretoinitiatephysicaltherapy.
REFERENCES
CannadaLK.OrthopaedicKnowledgeUpdate11.Rosemont,IL:AmericanAcademyofOrthopaedicSurgeons;2014.
Fogel GR,Esses SI.Hipspinesyndrome: management of coexistingradiculopathy andarthritisof the lower extremity.
SpineJ.2003;3:238–241.
NolteJ.TheHumanBrain:AnIntroductiontoitsFunctionalAnatomy.MarylandHeights,MO:Mosby/Elsevier;2009.
BernhardtM,HynesRA,BlumeHW,etal.Cervicalspondyloticmyelopathy.JBoneJointSurgAm.1993;75:119–128.
EismontFJ, HerkowitzHN, Garfin SR, et al. Rothman-Simeone the Spine Online: Access to Continually Updated
OnlineReference.Philadelphia,PA:ElsevierScienceHealthScienceDivision;2006.
HarropJS,NarojiS,MaltenfortM,etal. Cervicalmyelopathy: aclinicalandradiographic evaluation and correlationto
cervicalspondyloticmyelopathy.Spine(PhilaPa1976).2010;35:620–624.
Rhee JM, HeflinJA, Hamasaki T, et al. Prevalence ofphysical signs in cervicalmyelopathy: a prospective, controlled
study.Spine(PhilaPa1976).2009;34:890–895.
RheeJM,ShamjiMF, ErwinWM,etal.Nonoperative managementof cervicalmyelopathy: asystematic review.Spine
(PhilaPa1976).2013;38:S55–S67.
KaradimasSK,ErwinWM,ElyCG,etal.Pathophysiologyandnaturalhistoryofcervicalspondyloticmyelopathy.Spine
(PhilaPa1976).2013;38:S21–S36.
IssackPS,CunninghamME,PumbergerM,etal.Degenerativelumbarspinalstenosis:evaluationandmanagement.J Am
AcadOrthopSurg.2012;20:527–535.
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Kreiner DS, Shaffer WO, Baisden JL, et al. An evidence-based clinical guideline for the diagnosis and treatment of
degenerativelumbarspinalstenosis(update).SpineJ.2013;13:734–743.
Weinstein JN, Lurie JD, Tosteson TD,et al. Surgical compared with nonoperative treatmentfor lumbar degenerative
spondylolisthesis. Four-yearresults in the spine patientoutcomes research trial (SPORT) randomizedand observational
cohorts.JBoneJointSurgAm.2009;91:1295–1304.
LurieJD,TostesonTD,TostesonAN,etal.Surgicalversusnonoperativetreatmentforlumbardischerniation:eight-year
resultsforthespinepatientoutcomesresearchtrial.Spine(PhilaPa1976).2014;39:3–16.
MullemanD, MammouS,Griffoul I,et al. Pathophysiologyofdisk-related sciatica.I.—evidence supportinga chemical
component.JointBoneSpine.2006;73:151–158.
HudginsWR.Thecrossedstraightlegraisingtest:adiagnosticsignofherniateddisc.JOccupMed.1979;21:407–408.
vanderWindtDA,SimonsE,RiphagenII,etal.Physicalexaminationforlumbarradiculopathyduetodischerniationin
patientswithlow-backpain.CochraneDatabaseSystRev.2010;(2):CD007431.doi:10.1002/14651858.CD007431.pub2
SaalJA,SaalJS.Nonoperative treatmentof herniatedlumbar intervertebraldiscwithradiculopathy. Anoutcome study.
Spine(PhilaPa1976).1989;14:431–437.
Weinstein JN,LurieJD,TostesonTD,etal.Surgicalversusnonoperativetreatmentforlumbardischerniation:four-year
resultsforthespinepatientoutcomesresearchtrial(SPORT).Spine(PhilaPa1976).2008;33:2789–2800.
Peul WC, vandenHoutWB,BrandR,et al.Prolongedconservative care versusearlysurgeryinpatientswithsciatica
causedbylumbardischerniation:twoyearresultsofarandomisedcontrolledtrial.BMJ.2008;336:1355–1358.
AtlasSJ,KellerRB,WuYA,etal.Long-termoutcomesofsurgicalandnonsurgicalmanagementofsciaticasecondaryto
alumbardischerniation:10yearresultsfromthemainelumbarspinestudy.Spine(PhilaPa1976).2005;30:927–935.
LevenD, Passias PG,Errico TJ, etal. Riskfactorsforreoperation inpatients treatedsurgically forintervertebral disc
herniation:asubanalysisofeight-yearSPORTdata.JBoneJointSurgAm.2015;97:1316–1325.
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P
rimary disorders of tendons are common musculoskeletal problems that represent
diagnosticandtreatmentchallengesfororthopedicsurgeons,resultinginchronicandlong-
lasting morbidities. Recent studies have elucidated that tissue degeneration is the main
pathophysiologicprocess responsiblefortendon injuriesanddisorders, not inflammation.
1–6
Besidesoveruse,anyprocess,intrinsicorextrinsic,thatalterstendonmorphologyordisrupts
the stepwise progressionoftendon healing(inflammatory, proliferative, andmaturationand
remodelingphases),hasthepotentialtocausetendoninjury.Thisincludessystemicdiseases
suchasdiabetesmellitus(DM),hypercholesterolemia,gout,rheumatoidarthritis,andgenetic
disorders that alter collagen form and function (i.e., Ehlers–Danlos syndrome, Marfan
syndrome,andochronosis).
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FIGURE22-1.Thebiologicresponsesoftendonfibroblaststorepetitivemechanicalloadingconditionsareshown.
Dependingonmechanicalloadingpositions,thecellularmechanobiologicresponsesmayleadtotendonphysiologic
remodelingorpathologicchangessuchastendinopathy.ECM,extracellularmatrix;MMP,matrixmetalloproteinase;
PG,prostaglandins;LT,leukotriene;IL,interleukin.(ReproducedfromWangJH,IosifidisMI,FuFH.Biomechanical
basisfortendinopathy.ClinOrthopRelatRes.2006;443:320–332.)
Newer theories concerning the pathogenesis of tendinopathies suggest that both
inflammatoryanddegenerativeprocessesplayrolesinthiscomplexdiseaseentity7(Fig.22-
1). The most common tendons affected by tendinopathy in the foot and ankle include the
Achilles,posteriortibial,peroneal,andflexorhallucislongus(FHL).Ithasbeenestimatedthat
11% ofrunnersare afflictedby Achilles tendinopathy.8However,notall tendinopathies are
associated with sporting activities, as it has been shown that approximately one-third of
patients with Achilles tendinopathy do not participate in vigorous activities.9 This is
exemplifiedbythefactthatthemajorityofpeoplewithradiographicevidenceoftendinosisare
asymptomatic.7 Tendinopathies of thefoot and ankle cause chronic pain and deformity and
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affect patients’ overall quality of lives. Treatment options depend on the specific tendon
involved,durationofsymptoms,previoustreatments,andpatientfactorsincludingage,activity
level,andmedicalcomorbidities.Bothnonsurgicalandoperativeinterventionscanbeusedon
acase-by-casebasis. Unfortunately, thereisapaucityintheliteratureofqualityrandomized
controlledstudiestohelpguidetreatment.
In this chapter, we review the pathophysiology of tendinopathy and the risk factors
predisposing patients to tendinopathy, particularly in the setting of systemic disorders, and
reviewtheevaluationandtreatmentofcommonfootandankletendinopathies.
DEFINITIONS
Intheliterature,thenomenclatureusedtodescribetendondisordershasbeenconfusing,and
multiple terms are often used to describe the same disease process. Traditionally, the term
tendonitis has been used to describe chronic pain or dysfunction of a tendon, with the
implication that an inflammatory process is the primary underlying pathology. However,
histologic review ofsurgical specimensfromchronictendinopathiesoftheAchilles, rotator
cuff, patella, and extensor carpi radialis brevis has shown either absent or minimal
inflammation.
1,2,4–6
Throughout this chapter,the term “tendinopathy” will be usedtodescribeaspectrum of
tendonoverusedisordersthatincludeparatendinitis,tendonitis,andtendinosis.Paratendinitis
isanacuteinflammatoryprocessaffectingtheparatenonandadjacentnontendinoustissues.In
isolation,thispathologicprocessdoesnotusuallycausetendonrupture,isreversible,andcan
betreatedwithtenolysisinrefractorycases.
Tendonitis is tendinopathy with the presence of a histologically proven inflammatory
process.Studieshavedemonstratedthatoverloaded equinesuperficialdigitalflexortendons
undergoanacutephaseoftendoninjurythatinvolvesinflammatorycellsearlyonintheinjury
process, which is followed by a degenerative process.
10,11
Tendinosis describes a
degenerativeprocessthatlacksinflammation.Thesetendonshaveintrasubstancedegeneration,
whichcanbeappreciatedclinicallybynoduleswithinthetendon.
PATHOPHYSIOLOGY
Tendons are composed mainly of collagen fibrils, which are encased by an endotenon.
Multiplecollagenfibrilsgroupedtogetheraresurroundedbyan epitenonthatdemarcatesthe
actualtendon.Inordertoprovideprotectionandlubricationandpreventfriction,sometendons
haveatrueenvelopingsynovialsheath(i.e.,tibialisposteriorandperonealtendons),whereas
other tendons are encased solely by a peritenon (i.e., Achilles). The extracellular matrix
consistsofcollagen(65% to80%ofdryweight),mostofwhichisTypeI,whichprovides
tendons with tensile strength. The mechanical behavior oftendons, whichis viscoelastic in
nature,issecondarytothecross-sectionalareaandlengthofthetendon.Thelargeratendon’s
cross-sectional area, the greater theload to failure rate.12 Tendons with longer fibers have
decreasedstiffness,equivalentloadtofailurerates,butincreasedelongationtofailurerates.
13
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Therestoftheextracellularmatrixismadeupof1%to2%elastinandagroundsubstancethat
consistsof 60% to 80% water, proteoglycans,and glycoproteins.7 Tenoblasts andtenocytes
form parallel rows between collagen fibers, making up 90% to 95% of tendons’ cellular
components.7 Tendons carry their function through the musculotendinous junction, a richly
innervated transitional area between the muscle and the tendon that experiences high
mechanical forces, therefore making this region susceptible to injury. The enthesis, or
osteotendinousjunction,isanorganizedtransitionzonefromtendontoboneallowingmuscles
toeffectivelytransmitforcetobone.
To date, the etiology and pathophysiology of tendinopathy are not well understood. As
previouslystated,tendinopathywasoncebelievedtobetheresultofinflammation.However,
throughclinicalpractice,ithasbecomerecognizedthatanti-inflammatorymedicationsdonot
relieve the painassociatedwithtendinopathy. In addition,using microdialysis,Alfredson et
al.14demonstratedalackoftheinflammatorymediatorprostaglandinE2inchronicallyaffected
Achilles tendons. However, clinical and basic science research often involves chronically
affected tendons, making it possible that inflammation plays a role in the initial insult to
chronicallydiseasedtendons.
Histologically, chronic tendinopathy is characterized by degenerative changes, which
include decreased cellularity and calcific, hypoxic, hyaline, mucoid, myxoid, fibrinoid, and
fattydegenerations
2,4,15
(Fig.22-2).Chronictendinopathyisalsocharacterizedbyanincrease
inType III collagen, which hasless cross-links thanType I collagen, conferring decreased
tensilestrength,aswellasdegenerationandlossoforganizationofcollagenfibersmainlydue
to increased activity of matrix metalloproteinases.16 Studies have shown that degenerative
areas of tendons experience neovascularization.
17,18
Interestingly, using in vivo powered
Doppler ultrasonography, various studieshave demonstrated thatneovascularizationis often
associatedwithpatientswhoaresymptomaticandexperiencingpain.
17,19
Lastly,degenerative
changescharacterizedby adhesionsand increased numberoffibroblasts andmyofibroblasts
arefoundinperitendinoustissues,mostcommonlyoccurringintendonswithsynovialsheaths
(posterior tibial and peroneal tendons).20 Grossly, chronically diseased tendons have a
disorganized appearanceillustratedby ayellowishor browncolor,palpable thickenings or
nodulesintheareasofchronicdiseaseanddegenerationthatcanbecalcified.
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FIGURE22-2.Asummaryofthepathologicfindingsassociatedwithtendinopathy.(ReproducedfromUpToDate,
WoltersKluwerHealth.)
Therearecurrentlythreemaintheoriesdescribingtheetiologyoftendondegenerationthat
can progress to chronic tendinopathy and potential rupture: the mechanical, vascular, and
neuraltheories.
The mechanical theory of tendinopathy describes how chronic repetitive damage to
tendons over time could lead to a state of degeneration as opposed to inflammation. This
theory states that repetitive loading of a tendon under physiologic loads progresses to
degenerationandultimatetendonfailure.Atrest,tendoncollagenfibersaredisorganizedina
wave-likeformation.Asatendonisloaded,thesefibersbegintoorganizeinaparallelmanner.
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This occurs in thetoe region ofthestress–strain curve. Once thecollagen fibers align and
experiencecontinuedforce,thetendonenterstheelasticpartofthestress–straincurve,which
ischaracterizedbyalinearrelationshipbetweenloadandstrain.Ithasbeenshownthatnormal
physiologicloadingofatendonoccursbetween4%and8%strain.
21–26
Atthehigher endof
thephysiologicloading,tendonsexperiencemicroscopictrauma,leadingtodegenerationand
failure with repetitive stress. This repetitive microtrauma can lead to the alteration of
mechanicalpropertiesoftendonsaswellasasymptomatictendon.
21,27–29
Thistheoryfailsto
accountforwhyspecificareasoftendonshaveapredilectionforinjuryanddoesnotexplain
whysomepatientsaresymptomaticandothersarenot.
The vascular theory of tendinopathy is formed on the basis that tendons are metabolic
structures with metabolic demandsrequiring an adequatevascular supply. Thetheory states
that in the absence of an adequate blood supply, tendons undergo degeneration. Certain
tendons,includingtheAchilles30andposteriortibial31tendons,havebeenshowntohaveareas
ofhypovascularity.Forexample,thewatershedareaoftheAchillestendonhasbeenshownto
occur in the midportion of the tendon as compared to areas closer to the proximal
musculotendinous junction and distal enthesis.32 However, using laser Doppler flowmetry,
AstromandWestlin32demonstratedthattheAchillestendonhasuniformbloodsupply,except
atthedistalinsertion.
Theneuraltheoryoftendinopathyisbasedonmultipleobservationsfromvariousstudies
trying to connect the role of tendon degeneration and neural-mediated causes. Tendons are
highlyinnervatedstructuresthathavenerve endings closelyassociatedwithmastcells.Itis
theorizedthattendonoverusecausesoverstimulationofnervesandsubsequentdegranulationof
mast cells with the release of neuromodulators such as substance P, a nociceptive
neurotransmitterandproinflammatorymediator,33andacalcitonin-relatedpeptide.34Increased
levelsofsubstancePhavebeenfoundinrotatorcufftendinopathy,35and theneurotransmitter
glutamate has been found in Achilles tendinopathy.14 Lastly, Maffulli et al.36 discovered a
relationship between sciatica and Achilles tendinopathy, suggesting a connection between
tendinopathyand a neural-mediatedcause.Further researchis neededtounderstandthefull
significanceandroleofrelationshipbetweennervestimulationandtendinopathy.
Itislikelythatthecombinationofearlyinflammationandlaterdegenerationplaysarolein
thepathogenesisofchronictendoninjuryandtendinopathy.Noonetheorycompletelyexplains
theetiologyoftendinopathy;rather,itislikelyacombinationofthemechanical,vascular,and
neural theories that best explains the pathogenesis. Further studies are needed to better
understandtheinterconnectednessofthesetheories.
RISKFACTORS
Theriskfactorsimplicatedinthedevelopmentoftendinopathycanbestratifiedintotwolarge
categories: extrinsic andintrinsic (Table 22-1). Extrinsic riskfactors, suchas overuse, are
those most commonly implicated. However, other extrinsic factors that must be recognized
include training errors, fatigue, environmental conditions, footwear, equipment, and
medications/nutritionalsupplementation.Intrinsicriskfactorsareinnatetoagivenindividual,
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