FLP de Toekomst - HvA Kennisbank

Transcription

“FLP de Toekomst”
Wetenschappelijke artikelen FLP de toekomst
Hogeschool van Amsterdam 3e jaar studenten Fysiotherapie
Opdrachtgever:
Mark Rekers
Begeleider:
Edwin Bogaard
Extern adviseur:
Mariska van Zuidam
Leden beroepsopdracht:
Mark Brockhoff
Wesley van Dekken
Ramon van Diepen
Wetenschappelijke artikelen FLP de Toekomst
1
Inhoudsopgave
Het aanleggen van een enkeltape ............................................................................................3
Prophylactic Ankle Taping and Bracing: A Numbers-Needed-to-Treat and Cost-Benefit
Analysis ...............................................................................................................................14
Detecting and Treating Common Foot and Ankle Fractures: Part 1: The Ankle and Hindfoot
.............................................................................................................................................23
Detecting and Treating Common Fractures of the Foot and Ankle: Part 2: The Midfoot and
Forefoot................................................................................................................................32
Foot Injuries of the Recreational Athlete...............................................................................39
Fractures of the Fifth Metatarsal ...........................................................................................48
Anatomy and Healing in the Fifth Metatarsal........................................................................59
Hyperpronation and Foot Pain ...................................................................................61
Bij de diagnostiek van een enkelverstuiking kan worden volstaan met lichamelijk onderzoek
.............................................................................................................................................69
Ankle acute injuries..............................................................................................................74
Video Analysis of the Mechanisms.......................................................................................82
for Ankle Injuries in Football................................................................................................82
The Football Association Medical Research Programme: an audit of injuries in professional
football: an analysis of ankle sprains.....................................................................................91
Ankle Sprains: Expedient Assessment and Management.....................................................106
Evaluation and Treatment of Ankle Sprains........................................................................117
Meniscal Tears of the Knee ................................................................................................127
Patellofemoral Pain: Let the Physical Exam Define Treatment ...........................................135
Posterior Knee Pain and Its Causes.....................................................................................142
Valgus Knee Instability in an Adolescent............................................................................151
Hamstring Strains: Expediting Return to Play.....................................................................156
When Groin Pain Is More Than 'Just a Strain': Navigating a Broad Differential..................162
Case Study: A Surprising Cause of Groin Pain in a Female Runner ....................................173
Giving Injuries the Cold Treatment.....................................................................................175
2
HET AANLEGGEN VAN EEN
ENKELTAPE
Inleiding
In het voorgaande artikel heb ik enkelletsels besproken, en heb ik specifiek aandacht besteed aan
letsels van de buitenste enkelbanden. Eén van de behandelen preventiemethodes is het tapen
van de enkel. vaak wordt mij gevraagd uit te willen leggen hoe er het beste getaped kan worden.
In dit artikel zal ik, in de vorm van een instructie, een voorbeeld van een enkeltape behandelen.
Laat dit artikel vooral een inspiratiebron zijn om je in dit onderwerp te verdiepen, maar bedenk je
tegelijkertijd dat dit nooit een goede instructie of cursus kan vervangen.
Het is mogelijk dat de manier van tapen die ik in dit artikel uitleg anders is dan je misschien
gewend bent. Dat wil niet zeggen dat andere manieren niet goed zouden zijn. Er is niet één
bepaalde manier van tapen die de enige goede is. Naast het feit dat een tape uiteraard functioneel
moet zijn, zoekt iedereen die taped in de loop van de tijd ook een methode uit die het best bij hem
of haar past.
Over het tapen doen veel verhalen en mythes de ronde. Eén ervan is, dat door veel of langdurig
tapen de enkel(banden) slapper zouden worden. In zijn algemeenheid kunnen we stellen dat dit
niet zo is. Ter verduidelijking het volgende: we hebben het hier over een preventieve tape. Bij een
preventieve tape namelijk wordt de tape zo aangelegd dat er geen functie van de enkel wordt
overgenomen, er wordt als het ware een veiligheidsgordel óm de enkel heengelegd zodat, wanneer
dat nodig mocht zijn, de enkelbeweging niet te ver kan doorschieten. (Vergelijkbaar met een
veiligheidsgordel in de auto). Dit in tegenstelling tot een curatieve tape die vaak wordt gebruikt
direct aansluitend op een letsel. Hierbij wordt de enkel vaak in een iets (over)gecorrigeerde stand
getaped. Zou de tape -gedurende lange tijd- een deel van de enkelfunctie overnemen, dan zou dat
inderdaad gevolgen voor de enkel kunnen hebben. Bij de preventieve tape is daar echter, zoals
gezegd, geen sprake van. Hetzelfde geldt ten aanzien van braces. Een tape kan direct op de huid
worden aangelegd, of er kan eerst nog een elastische onderlaag (bijvoorbeeld elastoplast of
acrylastic) worden aangelegd.
Daarnaast bestaat er nog de therapeutische tape. Dit is een tapebandage, waarbij gebruik gemaakt
wordt van een elastische onderlaag met daar overheen een starre tape, waarbij bovendien het doel
specifiek is om het bewegingsverloop te beïnvloeden of te wijzigen. Soms wordt daarbij bewust
gebruik gemaakt van plooien of pelottes (kussentje of verdikking om extra druk te geven). Figuur 1
is hiervan een voorbeeld. In dit geval is een tape van de elleboog met een pelotte afgebeeld.
3
Kortweg kunnen we stellen dat de preventieve tapes dienen ter voorkoming van een (nieuw) letsel,
en er primair op gericht zijn een te grote bewegingsuitslag in een gewricht te voorkomen of te
beperken. De therapeutische tapes zijn erop gericht een invloed uit te oefenen op het
bewegingsverloop van een gewricht, en primair op het toelaten van al die bewegingen die pijnvrij
zijn.
We richten ons hier, met betrekking tot de enkel, op de preventieve tape.
Definitie
Een methode die het mogelijk maakt anatomische stresspunten te ontlasten,
gewrichten te stabiliseren en/of te ondersteunen en rek op pezen,
ligamenten (=banden) en andere weke delen te verminderen.
Werking
"Een tape steunt en ontlast selectief beschadigde of gestoorde delen van een functie eenheid,
geleidt bewegingen, staat functionele belasting in de vrije bewegingsruimte toe, en vermijdt
extreme bewegingen." (Definitie van tape fabrikant Beiersdorf).
Kortweg gezegd staat hier: de beweging toelaten die kan, en de beweging remmen die geremd
moet worden. De werking van een tape bandage is op een aantal manieren te verklaren:
1. Mechanisch. Er wordt door de tape als het ware een "immitatie"-band gevormd.
2. (Neuro)reflectoir. De tape stimuleerd bepaalde sensoren, die op er hun beurt voor zorgen dat de
spieren die in dat gebied liggen een hogere spierspanning krijgen, en zo meehelpen om de stabiliteit te
verhogen.
3. Psychologisch. De tape kan het gevoel van meer stevigheid geven. Dit gevoel van een vergrote
stabiliteit, heeft doorgaans een gunstige invloed op het bewegen en het bewegingspatroon. (In
negatieve zin kan het soms een schijnveiligheid geven en zo roekeloos gedrag in de hand werken.)
4. Een combinatie van de hiervoor genoemde drie punten.
Voorzorgen
Het is van belang een aantal punten goed in de gaten te houden. Hoewel deze instructie bedoeld is
om inzicht te geven in het hoe en waarom van het tapen, en wellicht een aanleiding zal zijn om er
mee aan de slag te gaan, is het ook hierbij van belang geen risico's aan te gaan. Weet waar je
beperkingen liggen, en raadpleeg bij twijfel altijd een deskundige. In een aantal gevallen is het
absoluut niet aan de orde om te tapen, en in deze gevallen moet altijd een deskundig arts of
sportfysiothertapeut worden ingeschakeld:
1. bij ernstige letsels, zoals bijvoorbeeld een fractuur,
2. bij huidafwijkingen,
3. bij allergie en/of eczeem,
4. bij (veel) zwelling of oedeem (=vocht).
5. bij open wonden / wondjes.
4
Voordat we gaan tapen is het ook altijd van belang om deze zaken na te vragen. Verder is het van
belang om de huid goed te inspecteren op wondjes e.d. Wanneer het mogelijk is, is het sterk aan
te raden om eventueel aanwezige beharing vooraf, zo mogelijke de dag ervoor, te scheren.
Anatomie
Het enkelgewricht is een gecompliceerd geheel, vooral omdat het een aaneenschakeling van
diverse gewrichten is, die op hun beurt weer noodzakelijk zijn om aan de voet zowel stabiliteit
alsook beweeglijkheid te kunnen geven. De enkel heeft zowel aan de buitenkant als aan de
binnenkant een aantal enkelbanden. Aan de binnenzijde zijn deze (drie) zo sterk met elkaar
verweven dat ze vaak als één band gezien worden. Deze heeft dan ook een aparte naam: het
ligamentum deltoïdeum (zie figuur 2). Het feit dat deze band zo sterk is, samen met de opbouw
van de voet -het binnenste voetgewelf is duidelijk hoger dan het buitenste voetgewelf- maakt dat
we bij een enkelband letsel meestal te maken hebben met een letsel van de buitenste
enkelbanden.
In figuur 3 zien we de rechter enkel vanaf de buitenkant. De lange botjes aan de voorzijde zijn de
middenvoetsbeentjes. De tenen, die daar nog weer voor zitten, zijn in deze figuur niet getekend. Aan de
buitenkant van de enkel zijn drie bandjes (ligamenten) het belangrijkst; zie figuur 3 en 4:
1. de voorste enkelband - ligamentum talofibulare anterius.
2. de middelste enkelband - ligamentum calcaneofibulare.
3. de achterste enkelband - ligamentum talofibulare posterius.
Over het algemeen is het de voorste enkelband (1) die bij het letsel betrokken is, de middelste- en
achterste enkelbanden zijn dat veel minder vaak. Wanneer dat wel het geval is, hebben we vaak
ook met een gecompliceerder letsel te maken.
5
Naast de banden spelen de spieren die rondom de enkel liggen een grote rol bij de stabiliteit van
het gewricht. (Zie hiervoor ook het artikel over enkel letsels.) Met name het samenspel tussen de
stand van de voet, de banden én de spieren speelt een grote rol. Juist door dit samenspel wordt er
een groot beroep gedaan op de coördinatie tussen de verschillende onderdelen.
Basis opbouw
De hoeveelheid stroken en de hoogte waarop de tape wordt aangebracht zijn van verschillende
factoren afhankelijk, zoals: de ernst en de "versheid" van het letsel, het stadium in het
revalidatieproces, de mate van (sport)belasting die weer zal gaan plaatsvinden, lengte en gewicht
van de persoon.
De opbouw van elke tapebandage kent een basispatroon van "ankerstroken", waarop a.h.w. de
tape wordt verankerd, en van "werkstroken", waarmee het gewricht, de band of de pees wordt
beïnvloed.
Verder is het van belang er bij het aanbrengen van de stroken tape op te letten dat de stroken met
een egale kracht en zonder plooien worden aangebracht. Veel mensen hebben de neiging om de
stroken een bepaalde richting op te trekken. Het enige resultaat wat je op die manier zult krijgen is
een tape met veel -ongewenste en soms storende- plooien. Laat de tape "met het lichaam
meelopen"!
Ik zal eerst het schema puntsgewijs weergeven, waarna ik dit dan per punt zal uitwerken.
1. anker op onderbeen - 2x.
2. anker op de voet.
3. stijgbeugel.
4. halve stijgbeugel.
5. anti-rotatiestrook (anti-draaistrook) - 2x.
6. heel-lock - binnen zijde en buitenzijde, elk 1x.
7. werkstroken, o.h.a. 4 tot 8
8. 1e knel-controle
9. anker op onderbeen herhalen - 2x.
10. anker op de voet herhalen 1 tot 4x.
11. 2e knel-controle.
De foto's laten steeds de bedoelde tapestroken zien. Ter wille van de duidelijkheid heb ik hier elke
keer de bedoelde stroken weer apart aangebracht. Normaal gesproken worden de diverse stroken
uiteraard over elkaar heen aangebracht.
De ankers(punt 1 en 2) Bij de enkel worden ankerstroken aangelegd op ongeveer 1/3 (tot evt. de
½) van het onderbeen. Het bovenste anker bestaat uit twee elkaar half overlappende stroken, die
aan de achterzijde van het been niet gesloten zijn. Circulair tapen is hier niet nodig en op deze
manier voorkomen we dat de doorbloeding belemmerd kan worden. Het lijkt misschien overbodig
6
om de tape zo hoog aan te leggen, maar het voordeel is dat het mechanische effect (hefboom) zo
groter is, terwijl ook het neuroreflectoire effect (groter oppervlak) groter is.
Het anker aan de onderzijde wordt aan de zijkant van c.q. rondom de voet aangelegd, vanaf de
grote teen, via de hak, tot aan de kleine teen. Zie de figuren 5, 6 en 7.
Met name onder de voet komt het, als gevolg van transpiratie, nog wel eens voor dat de tape niet
goed wil hechten. Het is dan aan te raden een kleefspray te gebruiken, zoals in figuur 6 is
weergegeven.Na de ankers komen de stijgbeugel (punt 3). Deze tapestrook dient, samen met de
halve stijgbeugel, vooral om het hielbeen (de hak) te stabiliseren. De stijgbeugel begint aan de
binnezijde van het been op het bovenste anker, loopt dan naar beneden, gaat onder de hak door,
loopt aan de buitenkant weer omhoog, en hecht vervolgens weer vast op het bovenste anker. Van
groot belang is hier dat de tape -zowel aan de binnenkant als aan de buitenkant- midden over de
uiteinden van resp. scheenbeen en kuitbeen (de enkel botten) heen loopt. Wanneer de tape te ver
naar voren ligt, zal de voet juist onhoog geduwd worden, en wanneer de tape te ver naar achteren
licht, zal de voet juist naar beneden worden geduwd. De eerste mogelijkheid kan door de
sportfysiotherapeut in het begin van de revalidatiefase soms bewust worden gebruikt om de enkel
nog extra te ontzien. De tweede mogelijkheid echter moet zeker vermeden worden. Zie de figuren
8 en 9.
7
De halve stijgbeugel (punt 4) is in de figuren 10 en 11 aangegeven met de stippellijn. Deze
strook begint aan de binnenkant van de enkel, net naast en onder de binnenste enkelknobbel (het
uiteinde van het scheenbeen). Vervolgens loopt deze strook bijna parallel (maar net niet helemaal)
aan de hele stijgbeugel, gaat onder de voet door en komt dan aan de buitenzijde weer omhoog.
Omdat de strook niet precies parallel loopt zal deze dan verder niet langs de hele stijgbeugel
omhoog lopen, maar schuin over de vooorzijde van het onderbeen heenlopen en eindigen op het
bovenste anker, of op de binnenpoot van de stijgbeugel.
De anti-rotatiestrook (punt 5).
Analyse van beelden waarbij iemand door zijn enkel zwikt laten zien dat dit meestal gebeurd
wanneer de voet iets naar binnen gedraaid, en het been naar voren geplaatst is. Vaak is dit de
positie van het been bij een sliding (voetbal, tennis). Op dat moment gebeuren er twee dingen
tegelijk, enerzijds kantelt het hielbeen (de hak) naar binnen, en bovendien maakt het onderbeen
een draaibeweging naar buiten, terwijl de voet stil blijft staan. Zie de pijl in figuur 12. Om nu bij
een nieuwe belasting deze beweging iets af te remmen kunnen we een tweetal stroken tape
aanbrengen, die in het verloop van de voorste enkelband (nummer 1 in figuur 3) en tegengesteld
8
aan deze draaibeweging lopen. De strook -aangegeven met een enkele lijn- begint op de voorvoet
en loopt licht schuin omhoog, draait dan achter het been langs, en stopt op of net over de
stijgbeugel. Een tweede strook -hier met een dubbele lijn aangegeven- begint vanaf het zelfde
punt, maar verloopt onder een iets andere hoek, waardoor hij iets hoger zal uitkomen, en loopt
vervolgens ook achter het been langs.
De heel-lock (punt 6) is een tape die met name het hielbeen stabiliseert., en bestaat uit twee
delen: één aan de binnenzijde, en één aan de buitenzijde. Het eenvoudigst is het om een strook
tape af te scheuren, en dan het midden van die strook op de zijkant van de hak te leggen. Het
hielbeen is voor te stellen als een rechthoekig blokje, en de strook tape maakt daarbij een hoek
van ongeveer 45o t.o.v. de hak.
De beide uiteinden zijn dan nog los, en deze worden dan één voor één aangebracht door ze met de hand vast te
strijken. Zie figuur 15 tot en met 19.
9
De werkstroken (punt 6) Alle stroken tot nu toe hebben hun functie in het stabiliseren en/of
ondersteunen van de enkel en de structuren rond de enkel. De werkstroken die nu komen hebben
daarnaast als functie de voet zelf te stabiliseren en te ondersteunen. De eerste strook begint aan
de binnenzijde van de voet, zo dicht mogelijk bij het begin van de grote teen. Het is het beste deze
strook niet recht naar beneden, maar iets schuin naar achteren te beginnen (zie de pijl in figuur
20). Daarna loopt de strook onder de voet door, komt aan de buitenzijde van de voet weer
omhoog, en loopt dan schuin over het onderbeen naar boven en hecht vast op het bovenste anker,
of zoals hier, iets meer naar de zijkant op de binnenpoot van de stijgbeugel.
 Zie figuur 20 en 21.
10
De volgende werkstrook loopt parallel en begint iets meer naar achteren (in de richting van de
hak). Ook het verdere verloop van de tape zal dan grotendeels parallel zijn aan de eerste
werkstrook. Zie figuur 22 en 23.
Zo leggen we nog een aantal stroken aan, waarbij het beginpunt zich steeds weer iets in de
richting van de hak verplaatst. Zie de pijl in figuur 22.
11
Wanneer de gehele voorzijde van het onderbeen bedekt is met tape (figuur 24), zijn we
aangekomen bij punt 8, de 1e knel-controle. De persoon die ingetaped is gaat nu op het been
staan -zonder te lopen!- om te zien of de tape ook ergens knelt. Wanneer dat niet het geval is, kan
de tape afgemaakt worden. Geeft de persoon wél aan dat het ergens knelt of onplezierig zit, dan
moet dat, om klachten of complicaties te voorkomen, eerst worden verholpen.
In figuur 24 is met de pijl de plaats aangegeven waar een kleine opening in de tape is
overgebleven. Deze open plekken mogen absoluut niet open blijven. Doordat het omliggende
weefsel door de tape een iets hogere druk heeft zal zich in die open plek namelijk vocht gaan
ophopen, met mogelijk vervelende gevolgen. Het probleem is heel simpel te ondervangen, door
een klein stukje tape af te scheuren en dat, zoals in figuur 25 met de pijl is aangegeven, over de
open plek heen te plakken. Let wel, bij kleine(re) openingen is dit een goede manier, is de plek
duidelijk groter, dan is het beter om gewoon een extra werkstrook aan te leggen.
Punt 9 en 10: herhalen van de ankers. Het bovenste anker, op het onderbeen, wordt weer
herhaald, waarbij de laatste strook deels weer op de huid wordt aangebracht. Ook het anker aan
de voet wordt herhaald, en in tegenstelling tot de eerste maal, wordt het anker nu twee, of evt.
drie, maal aangelegd, waarbij de beide ankers elkaar circa voor de helft overlappen. Zie figuur 26.
Figuur 27 laat de tape zien wanneer ook de laatste ankers zijn aangebracht. Dan blijft alleen nog
punt 11, de 2e knel-controle over. Dit is ook een goed moment om te controleren of de tape
inderdaad doet wat de bedoeling is, namelijk beweging toelaten daar waar het kan en remmen
daar waar het moet, zonder dat er pijn optreedt. Zie figuur 28.
Wanneer er zich verder geen problemen voordoen, kan de enkel en de tape normaal belast
worden. Over het algemeen kan de tape zonder problemen 3 tot 14 dagen blijven zitten. Een
belangrijk advies is echter altijd om goed op te letten of er zich geen irritaties, jeuk, o.i.d.
voordoen. In dat geval is het belangrijk om niet door te lopen maar de tape er af te (laten) halen.
12
Loop in zo'n geval niet door met het idee dat het wel over zal gaan! Ik leg liever een keer extra een
tape aan, zonder dat er problemen waren, dan dat er een probleem bij komt.
Nog een laatste tip: bij het verwijderen van de tape blijven er soms wat lijmresten op de huid
achter. Zeker wanneer er opnieuw een tape wordt aangelegd, moeten deze lijmresten goed
verwijderd worden, om huidirritaties te vermijden. In de jaren dat ik me nu met tapen bezighoud
heb ik mensen al van alles zien gebruiken, van verfverdunner en nagellakremover tot zelfs
schuurpapier. Het enige resultaat is een geïrriteerde huid. De oplossing is even simpel als
doeltreffend: smeer de plaatsen in met een beetje bodymilk, massage olie of boter, laat het even
inwerken en na een paar minuten zijn de lijmresten met een (ruwe) handdoek makkelijk te
verwijderen.
13
J Athl Train. 2004 March; 39(1): 95–100.
Copyright © by the National Athletic Trainers' Association, Inc.
Prophylactic Ankle Taping and Bracing: A
Numbers-Needed-to-Treat and Cost-Benefit
Analysis
Lauren C. Olmsted, Luzita I. Vela, Craig R. Denegar, and Jay Hertel
The Pennsylvania State University, University Park, PA
Corresponding author.
Lauren C. Olmsted, MEd, ATC, and Luzita I. Vela, MS, ATC, contributed to conception and
design; acquisition and analysis and interpretation of the data; and drafting, critical revision,
and final approval of the article. Craig R. Denegar, PhD, ATC, PT, and Jay Hertel, PhD,
ATC, contributed to analysis and interpretation of the data and critical revision and final
approval of the article.
Address correspondence to Lauren C. Olmsted, MEd, ATC, The Pennsylvania State
University, Department of Kinesiology, 266 Recreation Bldg, University Park, PA 16801.
Address e-mail to lco100@psu.edu.
ABSTRACT
Objective:
Taping and bracing are thought to decrease the incidence of ankle sprains; however, few
investigators have addressed the effect of preventive measures on the rate of ankle sprains.
Our purpose was to examine the effectiveness of ankle taping and bracing in reducing ankle
sprains by applying a numbers-needed-to-treat (NNT) analysis to previously published
studies.
Data Sources:
We searched PubMed, CINAHL, SPORT Discus, and PEDro for original research from 1966
to 2002 with key words ankle taping, ankle sprains, injury incidence, prevention, ankle
bracing, ankle prophylaxis, andnumbers needed to treat. We eliminated articles that did not
address the effects of ankle taping or bracing on ankle injury rates using an experimental
design.
Data Synthesis:
The search produced 8 articles, of which 3 permitted calculation of NNT, which addresses the
clinical usefulness of an intervention by providing estimates of the number of treatments
needed to prevent 1 injury occurrence. In a study of collegiate intramural basketball players,
the prevention of 1 ankle sprain required the taping of 26 athletes with a history of ankle
sprain and 143 without a prior history. In a military academy intramural basketball program,
prevention of 1 sprain required bracing of 18 athletes with a history of ankle sprain and 39
14
athletes with no history. A study of ankle bracing in competitive soccer players produced an
NNT of 5 athletes with a history of previous sprain and 57 without a prior injury. A costbenefit analysis of ankle taping versus bracing revealed taping to be approximately 3 times
more expensive than bracing.
Conclusions/Recommendations:
Greater benefit is achieved in applying prophylactic ankle taping or bracing to athletes with a
history of ankle sprain, compared with those without previous sprains. The generalizability of
these results to other physically active populations is unknown.
Keywords: ankle sprain, ankle prophylaxis, orthoses, injury incidence, injury prevention.
Ankle sprains are one of the most common injuries in sports1–5 and occur nearly 7 times more
frequently than all other ankle injuries. 6 The anterior talofibular ligament is injured most
often, followed by the calcaneofibular ligament.7,8 In the United Kingdom, 5000 ankle injuries
per day are treated, whereas in the United States, it is estimated that more than 25 000 ankle
sprains occur per day.9 Residual disability is found in 20% to 50% of those suffering an ankle
sprain.10–12 Symptoms related to residual disability after an ankle sprain, such as pain,
inflammation, and loss of motion may lead to increased treatment costs and time lost from
activity.
Ankle sprain incidence by specific sport has also been studied. The most common injury in
soccer is the lateral ankle sprain, accounting for up to 85% of all ankle sprains.13 In American
football, ankle sprains comprise 10% to 15% of all injuries. 4 Smith and Reischl11 reported that
70% of interscholastic varsity male basketball players have suffered at least 1 ankle sprain. In
field hockey, the most common type of injury is a ligament sprain; most ligament sprains are
at the ankle.14 Athletes most susceptible to ankle sprain are those with a previous history of an
ankle sprain.1,12,15–18
The combination of a high incidence of ankle sprain in sports and residual disability after
sprains has led to the implementation of prophylactic measures. Preventive interventions such
as taping and bracing are thought to decrease ankle sprain incidence by providing mechanical
support and enhanced proprioception to the ankle. Although investigators19,20 have assessed
the effect of taping and bracing, which may be associated with ankle injury, on factors such as
range-of-motion restriction and functional performance, few authors13,15,21–27 have evaluated
the effect of preventive measures on reducing the incidence of ankle sprains. Previous
researchers reported injury incidence and calculated relative risks or odds ratios to describe
the effects of a preventive measure. However, relative risks and odds ratios are not easy to
interpret and might give a biased view of the actual treatment effects. For instance, a measure
that reduces injury incidence from 1 to 0.5 has a relative risk of 2.0, but a measure that
reduces injury incidence from 0.2 to 0.1 has, in this regard, the same effect.
A novel analysis to determine the effect of an intervention that builds upon traditional
epidemiologic methods is the numbers needed to treat (NNT). The NNT is a useful statistic
when trying to ascertain the clinical benefit of a treatment.28–31 The NNT is presented as the
number of treatments necessary to prevent one injury occurrence28–31 and is therefore easier to
interpret than odds ratios and relative risks.30 Our purpose was to examine the efficacy of
ankle taping and bracing in preventing ankle sprains in athletes by applying an NNT analysis
to previous studies of ankle taping and bracing.
15
METHODS
We searched studies published between 1966 and 2002 on PubMed, CINAHL, SPORT
Discus, and PEDro using the key wordsankle taping, ankle sprains, injury incidence
prevention, ankle bracing, ankle prophylaxis, andnumbers needed to treat. We also reviewed
reference lists of the resulting articles to identify additional studies. We then eliminated those
articles that did not address the effects of ankle taping or bracing on injury rates using an
experimental design. We were left with 9 English-language articles that met these criteria and
excluded one article27 because the choice of activity (parachuting) was not considered
relevant to our purpose (Table 1).
QUALITY ASSESSMENT
A critical appraisal scale developed by Verhagen et al32 was used to rate the 8 articles for their
research-design quality on a scale from 0 to 14, with 14 being the highest. Five of the 8
articles were rated for quality by Verhagen et al,32 and these previously reported scores were
used. For the 3 articles21,22,26 not previously rated using this scale, 3 of the authors (L.C.O,
L.I.V, C.R.D.) individually rated them using the same scale, and these scores were then
averaged (see Table 1). Articles scoring above 8.4 (greater than 60% of possible points) on
the scale of Verhagen et al32 were then reviewed to determine whether the research design
was appropriate and sufficient information was provided to permit the calculation of the NNT.
Three articles15,23,25 scored above the cut-off value and met all the criteria to calculate NNT.
One article was eliminated because it scored below the cut-off value, and the remaining 4
were eliminated because they did not include a true control group that received no
intervention.
CALCULATION OF NUMBERS NEEDED TO TREAT
The NNT is calculated28,31 as the inverse of the absolute risk reduction and is expressed as
follows:
P1 is the event rate in the treatment group, and P2 is the event rate in the control group. In
addition to being easy to understand clinically, NNT can be used to determine the costbenefit of a treatment.28–31 To calculate the NNT, a number of criteria must be met. Injury
incidence, including the number of injuries in relation to the number of subjects or athleteexposures in each population, must be reported, and a control group must be available for
comparison. The NNT is a valid measure only when the comparison groups are similar at
baseline. In the case of ankle sprains, it has been documented that injury risk increases
substantially for athletes with a history of ankle sprain.1,15–18 For groups to be similar at
baseline, injury history must be reported so that the NNT can be calculated for each group.28,30
COST-BENEFIT ANALYSIS
We applied a cost-benefit analysis by using the calculated NNT values to examine the
advantages and disadvantages of bracing and taping. 29,33 In a cost-benefit analysis, both costs
and benefits are assigned a monetary value.33 The cost-benefit not only determines the least
cost but also places values on effectiveness because the known outcomes are not identical. 33
In doing so, we make the assumption that the preventive effects of taping and bracing are
equal between intramural basketball players and competitive soccer players previously
16
studied and athletes who practice 6 days per week. The following assumptions were made in
calculating the costs associated with taping and bracing.
Tape Cost
We defined the cost of tape as one roll of Johnson and Johnson Zonas tape (New Brunswick,
NJ). The cost of one case (32 rolls) of tape is $43.95; therefore, one roll of tape would cost
$1.37 (Medco, Tonawanda, NY, winter 2002). We assumed that it would take one roll of tape
to tape one ankle. The cost does not include prewrap, tape adherent, heel and lace pads, or the
salary of an athletic trainer.
Brace Cost
We defined the cost of bracing based on the cost of an Air Cast stirrup brace (Summit, NJ).
One Air Cast brace costs $35.00 (Medco, winter 2002). The Air Cast brace was chosen
because it was the brace used by Sitler et al25 and Surve et al.23
Taping Intervention
The number of interventions was based on a 13-week traditional competitive season (end of
preseason to beginning of postseason) with 6 practice and game sessions per week. An
individual athlete would thus have each ankle taped 78 times in a 13-week season.
Bracing Intervention
We assumed that one brace per ankle would be used during a 13-week season with 6 practice
and game sessions per week.
Cost per Ankle Sprain
The cost to prevent one ankle sprain was estimated by multiplying the cost of the prophylaxis
by the NNT for each condition in both studies.
Total Cost per Season
We calculated the total cost per season by multiplying the cost per ankle sprain by the number
of interventions per season. For taping, a season is 78 interventions, and for bracing, a season
is one intervention.
Ratio
We calculated a ratio of the cost of taping to bracing to better explain the relative cost of
taping and bracing.33
RESULTS
NUMBERS NEEDED TO TREAT
From the data of Garrick and Requa15 on collegiate intramural basketball players, we
determined that to prevent 1 ankle sprain per game in athletes with a history of sprain, a
clinician would need to tape 26 ankles (Table 2). In athletes without a history of ankle sprain,
to prevent 1 sprain, a clinician would need to tape 143 ankles. From the data of Sitler et al25
on military academy intramural basketball players, we calculated that to prevent 1 ankle
sprain during an intramural season (participants had a mean of 8.4 sessions per season) in
athletes with a history of sprain, a clinician would need to brace 18 ankles. In athletes without
a history of ankle sprain, to prevent sprain, a clinician would need to brace 39 ankles. From
the data of Surve et al23 on competitive soccer players over the course of 1 season
(participants averaged 278 hours of play per season), NNTs of 5 athletes with a history of
17
previous sprain and 57 of those without a prior injury were determined. Both taping and
bracing therefore appear to be more beneficial in preventing ankle sprains in athletes with a
history of ankle sprain.
COST-BENEFIT ANALYSIS
Our cost-benefit analysis determined that ankle taping would be 3.05 times as expensive as
ankle bracing over the course of a competitive season (Table 3). From the results of Garrick
and Requa,15 the cost of taping 26 athletes with a history of sprain all season would be $2778,
whereas bracing these athletes would cost $910. To tape 143 athletes with no history of ankle
sprain would cost $15 281, whereas bracing would cost $5005. From the results of Sitler et
al,25 the cost of taping 18 athletes with a history of sprain would be $1923, whereas bracing
these athletes would cost $630. To tape 39 athletes with no history of ankle sprain would cost
approximately $4168, whereas bracing these athletes would cost $1365. From the results of
Surve et al,23 the cost of taping 5 athletes with a history of sprain would be $4534, whereas
bracing these athletes would cost $175. To tape 57 athletes with no history of ankle sprain
would cost $6091, whereas bracing would cost $1995.
DISCUSSION
Ankle taping and bracing are among the most common interventions associated with athletic
trainers, yet very few authors have examined the effectiveness of taping and bracing on the
prevention of ankle sprains and have reported injury rates.13,15,21–26 Most published studies
related to ankle taping and bracing have focused on performance measures rather than injury
prevention. Although it is important to understand how taping and bracing affect measures of
ankle range of motion, strength, proprioception, and neuromuscular control, clinicians
ultimately need to know whether taping and bracing actually prevent ankle sprains.
Our literature search produced only 9 studies13,15,21–27 on the effectiveness of ankle taping or
bracing in reducing ankle sprains. What is startling is that very few of these researchers
included a true control group that did not receive any intervention.13,15,22,23,25 Still more
troubling is that a prospective study of the effectiveness of ankle taping using a control group
and tracking injury rates has not been conducted in 30 years. One would assume that
developments related to the quality of athletic tape, shoewear, playing surfaces, and playing
styles could affect the ability of ankle taping to reduce ankle sprains.
We were able to apply an NNT analysis to 3 of the 8 studies to determine how many ankles
would need to be taped or braced to prevent one sprain. The NNT analysis has not been used
previously in the athletic training literature but has been used most often in studies of
experimental treatments and procedures in cardiology and pharmacology. The NNT has
typically been used when a negative outcome resulted in high morbidity or death. The value
of NNT has been established in various disciplines, and it is now commonly taught in
epidemiology and evidence-based medicine as a clinically useful analysis.28,29 The analyses
may be applied to injury prevention in sports medicine to determine how many athletes must
be treated with a given intervention in order to prevent 1 injury. The results can then be used
to determine the cost-benefit of performing the intervention. The ideal NNT of an intervention
is 1 because this would indicate that for every patient treated, 1 pathologic event would be
prevented; however, this ideal is rarely achieved. Values between 2 and 5 are considered
effective in studies of treatment of pathologic conditions, and values of 20 or more may be
useful for studies of prophylaxis aimed at preventing pathologic conditions.34 Because this is
18
the first known NNT analysis assessing the effectiveness of an intervention at preventing
sports injuries, we are unable to compare our NNT results with others in similar contexts.
Using the quality assessment scale of Verhagen et al,32 the 3 studies we used for the NNT
analysis were 3 of the highest rated of the 8 studies we examined. The quality assessment
provides an indication of the robustness of the experimental design and the completeness in
the reporting of the methods and results of individual studies. The lack of universally accepted
standards for performing quality assessment of sports medicine research articles should be
noted, however. We found 3 previous systematic reviews involving quality assessment of
studies related to ankle-sprain prevention.32,35,36 All 3 groups used their own assessment
scales. We opted for that of Verhagen et al32 because we felt it was the easiest to use and
understand. The previous authors32,35,36 addressed ankle- sprain prevention methods, such as
shoewear and balance training, in addition to prophylactic taping and bracing.
Of the 3 studies subjected to NNT analysis, 2 studies were conducted on collegiate intramural
basketball players (one of bracing,25 one of taping15), and the third examined bracing in
competitive South African soccer players.23 Generalizing these results to other athletic
populations must be done cautiously. Although there is no minimum number of studies
necessary to perform an NNT analysis, more generalizable conclusions can be generated
when NNT results from a large number of studies are available. As stated previously, few
studies have addressed the effectiveness of ankle taping and bracing on the prevention of
ankle sprains.
Although it is more cost effective to tape an athlete 1 time than to brace the same athlete,
bracing is approximately 3 times more economical over the entire season. Our conclusion is
that bracing is less expensive and less time consuming for the athlete and athletic trainer over
the duration of a sports season. These clinical conclusions are supported by a body of
laboratory research literature demonstrating that bracing is superior to taping in restricting
ankle-inversion range of motion both before and after exercise.37 Semirigid braces, similar to
those used in the studies by Sitler et al25 and Surve et al,23 restrict inversion range of motion
more than tape and lace-up braces do.20,37 Ankle taping and bracing have also been
hypothesized to prevent ankle sprains via enhanced proprioception and neuromuscular
control; however, there is no clear evidence that one intervention is more effective than the
other in this regard.19,20
Even though bracing is more cost effective, is bracing superior to taping in preventing ankle
sprains? The comparison of NNT results across studies of different populations is difficult and
must be done with caution. Specifically, injury exposures and length of intervention are not
part of the NNT calculation. All the studies we examined used a different length of
intervention, and, thus, the NNT calculations are specific to the individual lengths of
intervention. The NNT results for Garrick and Requa15 indicate the number of ankles that
need to be taped to prevent 1 ankle sprain in one intramural basketball game. The results for
Sitler et al25 are specific to the number of ankles that need to be braced to prevent 1 sprain
over the course of 1 intramural basketball season. The results of Surve et al23 reflect the
number of ankles that need to be braced to prevent 1 sprain over the course of an entire
competitive soccer season. The NNT is affected by, and should be interpreted in the context
of, the duration of intervention.
Three previous groups23,24,26 directly examined the preventive effects of ankle taping versus
bracing. Ankle bracing was more effective than taping in preventing ankle sprains in
19
collegiate football players24 and female collegiate soccer players.23 The third group did not
identify significant differences between taping and bracing in preventing ankle sprains in
collegiate football players.26 Based on the results of these studies directly comparing taping
and bracing, it appears that bracing may be more effective in preventing ankle sprains.
Large-scale studies of the effectiveness of taping and bracing in male and female athletes of
various activity levels are clearly needed. Contemporary studies of ankle taping in this context
are especially lacking. In Simon's 1969 article26 comparing the effectiveness of taping and
bracing on ankle-sprain prevention in collegiate football players, he stated that “as the status
of the athletic trainer increases and the true value of his services are fully recognized, it
becomes essential that members of the profession recognize the paucity of scientific evidence
to support many of its traditional procedures. … Today's demands on an athletic trainer's time
and budget no longer warrant the retention of practices or procedures which fail to survive the
critical scrutiny of a controlled study.” Despite this apt call for clinically based research of the
most common interventions rendered by athletic trainers, no study of the effects of taping in
the prevention of ankle sprains in 30 years has included a control group. A well-designed,
prospective study of injury-prevention methods should have 3 components. First, large
numbers of athletes and exposures are needed. This may be best accomplished by conducting
the study across several institutions. Second, 2 groups that are similar at baseline are needed.
One group with no history of ankle injury and another group with a history of ankle injury
should be included. Random and concealed allocation to a control (no taping or bracing) or
treatment group (taping or bracing) is essential. Third, calculation of injury incidence is
essential for determining NNT.
CONCLUSIONS
Although ankle taping and bracing are commonplace in athletic training, the time and cost of
taping and bracing large numbers of athletes must be considered. Our first conclusion is that
taping and bracing appear to be more effective in preventing ankle sprains in athletes with a
history of ankle sprain than in those without a history of ankle sprain. Second, when deciding
whether athletes should be taped or braced, the increased cost and time of ankle taping,
compared with bracing. must be considered. Ankle bracing, therefore, may be a better way to
provide the support necessary to prevent ankle sprains. Lastly, our application of the NNT
statistic was limited by the number of studies that had both treatment and control groups as
well as documentation of injury rates. Even though we were able to calculate NNT for 3
studies, generalizing these results to all sports, ages, and skill levels is not possible. Further
proper prospective research is needed to evaluate the effectiveness of taping and bracing in
reducing ankle sprains in male and female athletes who participate in interscholastic,
collegiate, professional, and recreational sports.
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22
Detecting and Treating Common Foot and
Ankle Fractures: Part 1: The Ankle and
Hindfoot
David B. Thordarson, MD
THE PHYSICIAN AND SPORTSMEDICINE - VOL 24 - NO. 9 - SEPTEMBER 96
This is the first of two articles on fractures of the foot and ankle. The second article, on
midfoot and forefoot fractures, will appear in a subsequent issue.
In Brief: Some of the most common and potentially serious ankle and hindfoot fractures seen
in a primary care sports medicine practice are fractures of the tibial plafond, malleolus,
calcaneus, and talus (including osteochondral lesions). Making a careful physical exam to
detect for sites of tenderness and ordering the appropriate diagnostic images--usually plain
films--are important in pinpointing the diagnosis, but some injuries, like Maisonneuve
fractures, can be difficult to detect. Certain injuries, like many fractures of the lateral process
of the talus, can be managed conservatively with casting, but severe or displaced fractures
usually require surgery. Rehabilitation typically focuses on rest and proper strengthening and
stretching exercises.
Fractures of the foot and ankle immediately impair a recreational or elite athlete's ability to
perform competitively in virtually any sporting activity. Fractures of the ankle and hindfoot
usually occur acutely in a traumatic episode; chronic injuries like stress fractures are more
likely in the midfoot and forefoot. Some of the more common fractures heal well with
nonoperative care and some require surgical treatment, so an accurate diagnosis is essential.
Ankle Fractures
Ankle fractures have been classified in various ways. An important initial distinction is
whether a fracture is of a malleolus, or is a much more severe tibial plafond (pilon) intraarticular impaction fracture.
Tibial plafond. Tibial plafond fractures (figure 1) generally result from a high-energy axial
load, as can occur in a fall from a height or a motor vehicle accident. Patients experience
immediate pain and cannot walk. On exam, they generally have significant swelling with or
without deformity.
23
These fractures--in contrast to malleolus fractures--involve the weight-bearing surface of the
plafond and generally require open reduction and internal fixation. Results are frequently poor
despite operative intervention (1). Fortunately, tibial plafond fractures are uncommon in
athletes.
Malleolus. Fractures involving the malleolus are a much more common type of ankle
fracture. They can involve the lateral or medial malleolus, or both, and they usually result
from an external rotation injury to the ankle (figure 2). Ligament damage is typical, generally
of the deltoid ligament and of the anterior and posterior tibiofibular ligaments. Patients feel
immediate pain and have difficulty walking or cannot walk. Moderate-to-severe swelling and
bony tenderness exist over the fracture site(s), with or without a visible deformity.
24
Malleolus fractures are typically classified by one of two systems. The Lauge-Hansen fracture
classification relies on the position of the foot at the time of injury and includes four types:
1. supination-lateral rotation
2. supination-adduction
3. pronation-abduction, and
4. pronation-lateral rotation (2).
The Danis-Weber system is based on the level of the fibular fracture relative to the ankle joint
(3). It includes type A, fracture below the ankle joint; type B, fracture at the level of the joint,
in which the tibiofibular ligaments are most likely intact; and type C, which occurs above the
joint and disrupts the syndesmotic ligaments. In both the Lauge-Hansen and Danis-Weber
classifications, a fracture higher on the fibula indicates more instability and, therefore, a
greater likelihood of surgical intervention.
The initial treatment for all displaced malleolus fractures is closed reduction and casting
followed by ice and elevation. If an anatomic reduction is obtained, these fractures can be
managed with a cast. However, postreduction radiographs must show that the joint space is
symmetric on a mortise view (figure 3) because even 1 to 2 mm of displacement of the talus
within the mortise can cause dramatic changes in the contact area and pressures within the
ankle. One study (4) demonstrated a 40% decrease in contact area with a 1-mm lateral shift of
the talus.
Because of this potential for change in the contact area and pressure in the ankle with an intraarticular fracture, surgeons recommend open reduction and internal fixation of persistently
displaced malleolus fractures to guarantee an anatomic reduction. An added benefit of
operative treatment in an athlete is a more aggressive, early rehabilitation. Range-of-motion
exercises can be started after wound healing, but compliance with non-weight bearing must be
emphasized.
Most patients with a malleolus fracture require 6 weeks of immobilization. Patients with a
displaced ankle fracture that has undergone successful closed reduction will typically require
2 to 4 weeks in a long-leg cast and then an additional 2 to 4 weeks in a short-leg nonwalking
25
cast. Patients with an initially nondisplaced fracture or who were treated surgically will
generally require 4 weeks of non-weight bearing in a short-leg cast or removable walking
boot, followed by 2 weeks in a walking cast or boot. The removable boot will allow for earlier
range-of-motion exercises.
In patients treated nonoperatively, follow-up radiographs must be obtained weekly for the first
2 to 3 weeks following injury to rule out fracture displacement. Following fracture healing,
patients can begin physical therapy for range-of-motion and strengthening exercises. Most
patients who sustain a malleolus fracture will miss at least 3 months from most sports, and
frequently 6 months or more from cutting-type sports.
Maisonneuve. A Maisonneuve fracture--an external rotation injury of the ankle with an
associated fracture of the proximal third of the fibula--is a serious injury that can have
deceptively minor radiographic findings. Although less common than other types of ankle
fractures, it is often misdiagnosed and can result in long-term disability. The typical
mechanism and presentation are external rotation of the foot and medial ankle pain. On
examination, the patient will have tenderness over the deltoid ligament and over the fracture
site on the proximal fibula. Any patient who has proximal fibular tenderness after a twisting
injury to the ankle should have radiographs taken of both the ankle and the tibia and fibula.
Radiographs of the ankle generally reveal no fracture or only a small avulsion injury of the
medial malleolus with variable widening of the space between the tibia and fibula (figure 4a).
A radiograph of the whole tibia and fibula, however, will demonstrate a high fibula fracture
(figure 4b). These patients require open reduction and internal fixation with one or two screws
placed between the distal fibula and tibia to maintain the bones' normal relationship while
ligament healing occurs. The screws are generally removed 8 to 12 weeks after surgery.
Calcaneus Fractures
Like tibial plafond fractures, calcaneus fractures occur most commonly after high-energy
axial loads. They can also stem from an avulsion of the Achilles tendon. Approximately 75%
of calcaneus fractures extend into the subtalar joint (5). Both high-energy fractures and
avulsion are relatively uncommon in athletes because of the mechanism of injury, but either
26
can result in permanent disability. Following a fracture, patients have severe heel pain and
cannot walk. They have moderate-to-severe hindfoot swelling and tenderness on exam.
Intra-articular fractures that result from an axial load need to be carefully assessed for
displacement on lateral and axial radiographs (figure 5); any displacement warrants a
computed tomography (CT) scan. Initial treatment for displaced and nondisplaced intraarticular fractures includes immobilization in a bulky dressing and splint, with ice and
elevation to control edema. Most displaced fractures are managed operatively, but these
patients typically experience residual stiffness of their subtalar joint that will adversely affect
future athletic performance. For nondisplaced extra-articular calcaneus fractures, patients
wear a short-leg cast or walking boot for about 6 weeks.
Avulsion fractures occur during a violent contraction of the gastrocnemius and soleus. If not
displaced or if minimally displaced, they can be managed in a plantar-flexed short-leg cast for
6 weeks followed by physical therapy involving stretching. Most of these fractures, however,
are significantly displaced and frequently require immediate surgery to repair the fracture and
relieve the pressure on the skin overlying the bony fragment.
27
Talus Fractures
Talus fractures typically involve either the talar neck or lateral process, or an osteochondral
fracture of the talar dome.
Talar neck. Although talar neck fractures (figure 6) are relatively uncommon and represent
high-energy injuries involving hyperdorsiflexion of the ankle, they deserve mention because
of the potential devastating complication of avascular necrosis of the talus. A typical
mechanism of injury is a motor vehicle accident in which the ankle is hyperdorsiflexed by the
brake pedal. Patients experience severe hindfoot pain and moderate-to-severe edema,
tenderness, and ecchymosis. The body of the talus may be palpable in the posteromedial ankle
area.
Displaced talar neck fractures are true surgical emergencies. The fracture must be reduced
immediately to minimize the risk of avascular necrosis or skin slough. The talus has limited
vascularization; most of its blood supply enters the neck via an anastomotic sling and flows
posteriorly. A fracture, therefore, disrupts the intraosseous portion of the blood supply, and
the greater the displacement, the greater the disruption of the blood supply and likelihood of
necrosis. Avascular necrosis may lead to collapse of the body of the talus, resulting in arthritic
changes that necessitate ankle fusion. Even without avascular necrosis, many patients develop
a significant degree of subtalar arthrosis or arthritis, which leads to residual hindfoot stiffness
and pain. Treatment for patients who have a nondisplaced talar neck fracture typically
involves a short-leg nonwalking cast for 6 to 8 weeks followed by range-of-motion exercises.
Lateral process. Although fractures of the lateral process of the talus are relatively
uncommon, they can be a source of chronic lateral ankle pain following an inversion injury.
The typical mechanism of injury is acute hyperdorsiflexion with inversion (5). The patient
will experience lateral ankle pain and have edema and tenderness in this area. Radiographs
28
reveal a variable-sized fragment of the lateral process along the inferior aspect of the talus.
This defect is most easily identified on a lateral radiograph.
Nondisplaced fractures require 6 weeks in a short-leg cast. Large displaced fragments
(generally greater than 1 cm in diameter) should be treated with open reduction and internal
fixation. Small displaced fragments can be treated symptomatically and can be excised if
symptoms persist.
Osteochondral injury. A more common talus injury in sports is an osteochondral fracture of
the dome of the talus that results from an inversion injury. A related, chronic condition
probably caused by repetitive trauma is osteochondritis dissecans (OCD). A typical
posttraumatic osteochondral fracture or an OCD lesion occurs in the anterolateral aspect of
the talar dome. It is postulated that the corner of the talus fractures as the dome rotates
laterally through the mortise (5).
Patients who sustain an acute osteochondral fracture have pain with weight bearing. If the
fragment displaces, they will experience locking or clicking. On exam, they have tenderness
over the lateral aspect of the talar dome. Radiographs typically show a small flake of bone off
the lateral dome of the talus. Occasionally, plain radiographs will be negative, and magnetic
resonance imaging can establish the diagnosis and define the extent of the lesion.
An OCD lesion may appear as a cyst or loose piece of bone in either the anterolateral or
posteromedial dome of the talus (figure 7). Patients report a gradual onset of pain that is
generally activity related and, if the fragment displaces, mechanical symptoms such as
locking. If the fragment is nondisplaced and follows an acute injury, the patient can be treated
with a short-leg nonwalking cast for 6 weeks followed by range-of-motion exercises. In more
chronic cases, or if the fragment is displaced, the fragment can be removed arthroscopically
and the bony defect can be drilled to encourage fibrocartilage formation. These patients
should avoid weight bearing for 6 weeks while fibrocartilage is forming, but they can do
range-of-motion exercises at this time.
29
Dual Strategies
Although fractures of the foot and ankle can be a source of significant disability and require
surgery, many ankle and hindfoot fractures sustained in athletic activities are amenable to
nonoperative treatment. Primary care sports medicine physicians, therefore, must not only
make astute diagnoses, they must be well-versed in rehabilitation strategies for both
conservative and postoperative treatment.
References
1. Chapman MW: Fracture and fracture-dislocations of the ankle, in Mann RA, Coughlin MJ (eds): Surgery of the Foot and
Ankle, ed 6. St Louis, CV Mosby Co, 1993, pp 1439-1464
2. Lauge-Hansen N: Fractures of the ankle: combined experimental-surgical and experimental-roentgenologic investigations.
Arch Surg 1950;60(5):957-985
3. Muller ME, Allgower M, Schneider R, et al (eds): Manual of Internal Fixation: Techniques Recommended by the AOGroup, ed 2. New York City, Springer-Verlag, 1979, pp 282-299
4. Ramsey PL, Hamilton W: Changes in tibiotalar area of contact caused by lateral talar shift. J Bone Joint Surg (Am)
1976;58(3):356-357
5. De Lee JC: Fractures and dislocations of the foot, in Mann RA, Coughlin MJ (eds): Surgery of the Foot and Ankle, ed 6. St
Louis, CV Mosby Co, 1993, pp 1465-1703
30
Dr Thordarson is an assistant professor of orthopedic surgery and the chief of Foot and Ankle
Trauma and Reconstructive Surgery in the Department of Orthopaedic Surgery at the
University of Southern California in Los Angeles. Address correspondence to David B.
Thordarson, MD, 1200 N State St, GNH 3900, Los Angeles, CA 90033.
31
Detecting and Treating Common Fractures
of the Foot and Ankle: Part 2: The Midfoot
and Forefoot
David B. Thordarson, MD
THE PHYSICIAN AND SPORTSMEDICINE - VOL 24 - NO. 10 - OCTOBER 96
This is the second of two articles on fractures of the foot and ankle. The first article, on ankle
and hindfoot fractures, appeared in the September issue.
In Brief: Midfoot and forefoot fractures commonly seen in a primary care practice include
navicular and metatarsal stress fracture, tarsometatarsal fracture-dislocation, and acute
fracture of the metatarsals, sesamoid, great toe, or lesser toes. A careful history to determine
the mechanism of injury and a methodical physical exam to detect sites of tenderness are
essential. X-rays are usually required, but stress fractures may warrant bone scans. Compared
with ankle and hindfoot fractures, sports-related midfoot and forefoot fractures are more often
treated conservatively with casting or wooden shoes. Tarsometatarsal disruption and Jones
fractures are more likely to require surgery.
When a person sustains a foot or ankle fracture, his or her ability to perform virtually any
athletic activity is immediately impaired. Several types of sports-related ankle and foot
fractures occur in the midfoot and forefoot. These injuries are often acute, but stress fractures,
which are frequently due to improper technique, commonly occur in this region as well. Exact
diagnosis based on physical exam findings and diagnostic images will determine treatment,
whether conservative or surgical.
Navicular Stress Fracture
Traumatic fractures of the navicular require high energy and are thus uncommon in sports.
The navicular, however, is one of the more common locations of stress fractures in the foot
and ankle (figure 1). These fractures are frequently due to the repetitive trauma of running,
and patients will typically describe chronic activity-related pain localized to the region of the
navicular along the midmedial arch.
32
Radiographs are often negative, but in patients who have persistent tenderness in the navicular
region, a technetium bone scan will reveal increased activity at the site of the fracture.
Computed tomography or tomograms can then help to definitively diagnose the fracture.
Patients who sustain a navicular stress fracture should wear a short leg nonwalking cast for 6
to 8 weeks. An alternative is a short leg brace for the same period of non-weight-bearing to
allow for mobilization. A highly competitive athlete, however, may not comply with the
period of non-weight-bearing if placed in a removable brace. If immobilization does not lead
to healing, these patients can be treated surgically.
Lisfranc (Tarsometatarsal) Fracture-Dislocation
A Lisfranc injury (figure 2), which involves disruption of the tarsometatarsal joint with or
without associated fracture, can be a source of prolonged disability for an athlete. Most
Lisfranc injuries involve the first three metatarsals, but the intercuneiform or
naviculocuneiform joints may also be affected.
Although typically a high-energy injury, a Lisfranc fracture-dislocation can occur during
athletic activities. The typical mechanisms of injury include twisting of the forefoot, axial
33
load on the forefoot, and a crush injury (1). A twisting injury can occur, for example, when a
person falls from a horse and gets a foot caught in a stirrup, or when a person is thrown from a
sailboard while his or her feet are secured in the straps. A classic sports-related Lisfranc
injury occurs when a football player falls onto the heel of another player's plantar-flexed foot,
causing an axial load along the metatarsals.
A high index of suspicion is necessary to diagnose this injury. The patient will report severe
midfoot pain, and examination will reveal moderate-to-severe swelling along the midfoot
region with variable flattening of the arch or abduction of the forefoot. Severe tenderness will
be present along the midfoot. Passive plantar flexion and dorsiflexion of the toes should be
assessed to rule out a compartment syndrome of the foot.
Radiographic evaluation includes anteroposterior (AP), lateral, and oblique views of the foot.
A normal AP or oblique radiograph should reveal that the medial and lateral aspects of the
first three metatarsals align with the medial and lateral aspects of the cuneiforms with which
they articulate, and the medial aspect of the fourth metatarsal aligns with the medial aspect of
the cuboid on the oblique view. Any alteration of these normal relationships demonstrates the
site or sites of displacement. Other radiographic signs include diastasis or a fleck fracture
between the base of the first and second metatarsals on an AP radiograph or dorsal
displacement of the metatarsals on lateral view.
A nondisplaced Lisfranc injury can be treated conservatively in a short leg nonwalking cast
for 6 weeks followed by 6 weeks in a short leg walking cast. Most of these injuries, however,
will have some degree of displacement and require open reduction and internal fixation.
Metatarsal Fractures
With the exception of stress fractures and injuries of the fifth metatarsal, metatarsal fractures
typically result from a direct blow to the foot. Fractures are generally classified according to
their anatomic location as neck, shaft, or base fractures, and AP and lateral radiographs are
generally sufficient for assessment.
Acute fracture. A single, traumatic fracture of a metatarsal is usually minimally displaced
because of the restraining forces of the intermetatarsal ligaments. Patients describe pain with
weight bearing. On examination, they will have swelling and tenderness localized to the
fracture site. These fractures can generally be treated conservatively in a cast or wooden shoe
for 6 weeks with weight bearing as tolerated until the patient's pain and tenderness subside.
Stress fracture. Metatarsal stress fractures generally involve a single metatarsal, usually the
second or third (figure 3). They typically result from training errors such as too rapid an
increase in mileage in a runner. Patients will report activity-related pain that gradually
increases. They will generally have tenderness over the fracture site with minimal edema.
Poor shoes can also contribute. These fractures can be treated with a stiff-soled shoe or
wooden shoe, and the patient should cross-train in low-impact activities such as swimming or
stationary cycling until tenderness resolves.
34
Multiple fracture. Multiple fractures frequently require open reduction and internal fixation
because of significant displacement. Residual displacement of a metatarsal fracture can
predispose a patient to develop a callus. This is because a displaced metatarsal, whether
plantar or dorsally displaced, alters the pressure pattern in the forefoot, and a callus forms in
the area of increased pressure. The callus, or intractable plantar keratosis, will cause persistent
pain with weight bearing and will require an orthosis or possibly even surgical correction of
the underlying bony deformity.
Fifth-metatarsal fracture. The most common injury of the fifth metatarsal is an avulsion
fracture at the insertion of the peroneus brevis tendon, which occurs with an inversion injury
to the hindfoot (figure 4). Patients will say that they sprained their ankle, but the tenderness
will be localized over the base of the fifth metatarsal. These fractures heal reliably and can be
treated with a wooden shoe, tennis shoe for support, or other symptomatic treatment, provided
that no displacement of the intra-articular base of the metatarsal exists.
A much more serious fracture of the fifth metatarsal is the Jones fracture (figure 5). This
fracture occurs at the diaphyseal-metaphyseal junction of the base of the fifth metatarsal. A
35
watershed area of the blood supply of the fifth metatarsal exists in this region, thus
predisposing this area to delayed healing, nonunion, or stress fracture. Patients who sustain a
Jones fracture may experience a sudden onset of pain with trivial trauma, or they may develop
a gradual onset of pain in the midlateral border of the foot.
Traumatic or stress fractures in this area must be treated with 6 weeks in a nonwalking cast.
Despite this aggressive nonoperative treatment, a significant proportion of these patients will
develop a nonunion (1). Primary open reduction and internal fixation of this fracture may be
preferred in competitive athletes to compress the fracture site to facilitate healing and thus
minimize the period of disability.
Sesamoid Fracture
Fractures of the sesamoid bones can occur acutely as a result of direct trauma or indirectly
from hyperdorsiflexion of the hallux metatarsophalangeal joint, such as in a football player.
Because of their poor blood supply, the sesamoids are also prone to stress fractures.
With either an acute or a stress fracture, patients typically will have pain over the plantar
aspect of the first metatarsal head and localized tenderness over the affected sesamoid. The
medial sesamoid is usually involved--probably because it is located more directly beneath the
first metatarsal (1). These fractures can be very recalcitrant, and patients must be warned that
symptoms will frequently persist for 4 to 6 months. Radiographic evaluation includes AP and
lateral views of the foot and a sesamoid x-ray--a tangential view of the plantar aspect of the
first metatarsal with the toe extended.
For an acute fracture, most authors advocate a short leg walking cast for 3 to 6 weeks
followed by a stiff-soled shoe with a metatarsal pad to elevate the metatarsal head until
symptoms resolve. Stress fractures are more difficult to treat and require 6 to 12 weeks in a
short leg walking cast. Patients must avoid all high-impact activities until tenderness subsides.
Patients with pain persisting for 3 to 6 months despite adherence to the above regimen may
require partial or complete surgical excision of the sesamoid. However, sesamoid excision can
be complicated by hallux valgus (with a medial sesamoid excision), hallux varus (lateral
36
sesamoid excision) or stiffness, and thus should be avoided if possible. A few authors even
advocate bone grafting (1).
Great Toe Fracture
Fractures of the great toe generally result from a direct blow or an axial load. Pain and
tenderness will be localized over the fracture. Nondisplaced fractures can be treated with
either a walking cast with a toe plate or a wooden shoe and crutches as needed. A fracture
displaced into the metatarsophalangeal or interphalangeal joint should be surgically repaired
to prevent osteoarthritis. AP and lateral radiographs will demonstrate the fracture anatomy.
Lesser Toe Fracture
Lesser toe fractures (figure 6) are typically caused by an axial load or direct trauma. Even
displaced fractures or intra-articular fractures are generally amenable to nonoperative
treatment. These patients are able to walk despite the fracture but have problems with
footwear. Again, AP and lateral x-rays will help pinpoint the fracture.
Patients are instructed to tape the injured toe to an adjacent uninjured toe (buddy taping) and
to place a small piece of gauze between the toes to prevent maceration of the skin. A wooden
shoe can be used until tenderness subsides to the point where the patient can begin using
tennis shoes. Most fracture tenderness resolves in 3 to 4 weeks. Typically, follow-up
radiographs are unnecessary since they will not influence subsequent treatment decisions.
Attuned to Foot Fractures
Fractures of the midfoot and forefoot are similar to those of the ankle and hindfoot in that they
can often be treated nonoperatively. But each fracture has its own distinguishing
characteristics and treatment options, so physicians need to be attuned to both detection and
management of these injuries. Misdiagnosing a Jones fracture, for example, can have serious
consequences to an active patient.
References
1. De Lee JC: Fractures and dislocations of the foot, in Mann RA, Coughlin MJ (eds): Surgery of the Foot and Ankle, ed 6. St
Louis, Mosby, 1993, pp 1465-1703
37
Dr Thordarson is an assistant professor of orthopedic surgery and the chief of Foot and Ankle
Trauma and Reconstructive Surgery in the Department of Orthopaedic Surgery at the
University of Southern California in Los Angeles. Address correspondence to David B.
Thordarson, MD, 1200 N State St, GNH 3900, Los Angeles, CA 90033.
38
Foot Injuries of the Recreational Athlete
Stephen M. Simons, MD
The Recreational Athlete Series
Editor: James L. Moeller, MD
THE PHYSICIAN AND SPORTSMEDICINE - VOL 27 - NO. 1 - JANUARY 1999
In Brief: Adult recreational athletes, or 'weekend warriors,' are vulnerable to foot injuries
such as Achilles tendon ruptures, plantar fasciitis, retrocalcaneal bursitis, midfoot tendinitis,
metatarsal stress fractures, and interdigital neuroma. Physicians also need to be alert for less
common injuries such as Jones fractures and tarsal navicular stress fractures because of the
risk of delayed healing or nonunion. Many foot injuries can be treated conservatively, but
some Achilles tendon ruptures, Jones fractures, and tarsal navicular stress fractures may
require surgery.
The scenario is a common one: The "weekend warrior" hobbles into the workplace on a
Monday morning, injured in the pursuit of recreation or, ironically, health--only to endure
gentle ridicule from sedentary colleagues. Such adult recreational athletes contribute to the
3% to 15% of all athletic injuries that involve the foot. This incidence varies by sport, but
whether the activity is recreational or professional, organized or spontaneous, the level of play
makes little difference in the type or severity of foot injury (1).
The foot is a complex structure that provides the principal interface with the playing surface.
Though the foot is highly adaptable, vertical reaction forces--from 0.6 times body weight
during walking to 7.9 times body weight for a running jump--place it at risk for acute
traumatic and chronic overuse injuries (2). The weekend warrior typically lacks the
conditioning that would prepare the musculoskeletal structures for occasional heavy demand.
Without proper conditioning, aging tissues lack the flexibility, strength, and resilience to
withstand high stresses that are applied only sporadically. These factors pave the way for both
acute and overuse injuries of the foot.
Some of the injuries discussed here are fairly common in unconditioned recreational athletes.
Others are less common but need to be kept in mind because they are easily missed or heal
poorly.
Traumatic Injuries
Achilles tendon ruptures. The middle-aged recreational athlete who continues a youthful
passion for basketball, racquetball, soccer, or some other vigorous sport becomes a prime
candidate for Achilles tendon rupture. The older, occasional athlete may have had repeated
episodes of subclinical or overt Achilles tendinitis. This scarred tissue that has become less
flexible with age becomes vulnerable to rupture.
Rapid eccentric loading of the Achilles tendon can occur with an abrupt stop, landing from a
jump, running the bases, or other quick movements. A recent instance in my practice, for
example, occurred when the patient was playing badminton and landed from a jump.
Patients may report a "pop" at the back of the leg or may say they were struck from behind.
On examination, a palpable defect may be found in the tendon 2 to 6 cm from the calcaneus.
39
With the Thompson test, done with the patient prone, the absence of passive plantar flexion
when the calf is squeezed indicates total Achilles rupture. Inability to perform a weightbearing single-leg toe raise can also indicate total rupture. Active plantar flexion is possible
using only the long flexor, peroneal, and tibialis posterior muscles, but these muscles alone
are generally too weak to allow full weight bearing on the toes of one foot (3).
The decision regarding conservative vs surgical treatment for Achilles tendon rupture is a
case-by-case judgment that requires consideration of the patient's occupation and social
circumstances as well as expectations about future sports activity.
A recent report (4) reviewed 19 studies examining operative vs nonoperative management of
patients who had Achilles tendon ruptures. The average patient was 37.9 years old, and 83%
of the patients were male. The surgically treated patients more often returned to sport at the
same level, and 2.8% experienced reruptures, as compared with 11.7% of the conservatively
treated patients. But the average sick leave was 8.2 weeks for patients treated nonsurgically vs
10.5 weeks for those treated surgically, and fewer minor complications occurred in patients
who were treated nonsurgically (5).
Conservative treatment involves cast immobilization for 3 months, followed by use of
crutches and wearing of shoes that have a built-up heel.
Acute fractures. Acute fractures of the foot occur infrequently in nonmotor sports. However,
physicians should be alert for fractures of the proximal fifth metatarsal, including avulsion
fractures and Jones fractures.
Fifth metatarsal avulsion fractures. Because avulsion of the proximal tip of the fifth
metatarsal (figure 1) occurs occasionally as a complication of a lateral ankle sprain, palpating
the base of the metatarsal should be a routine part of the ankle sprain evaluation. Tenderness
at the site should prompt x-rays. In the setting of an acute injury, a vertical fracture to the
proximal 1.0 to 1.5 cm of the fifth metatarsal is most likely an avulsion at the insertion of the
peroneus brevis.
40
This fracture generally heals without complication. Acute care with ice, elevation, and
compression should be followed by wearing a stiff-soled shoe such as a hiking boot or briefly
using a short leg cast. A minimum of 3 to 4 weeks of rest from sports activity can be followed
by gradual pain-guided return to sport. The patient should be warned about returning to sports
activity too early. The risk includes not only reinjury at the fracture site, but also secondary
overuse injuries due to new stresses resulting from incomplete rehabilitation.
Jones fractures. A Jones fracture is an acute fracture of the base of the fifth metatarsal at the
metaphyseal-diaphyseal junction (figure 1). In my experience these injuries have occurred as
a result of a pivot in the direction opposite the planted foot. A Jones fracture is sometimes
associated with antecedent lateral foot pain that indicates a preexisting stress fracture. These
fractures are prone to delayed healing and also to nonunion.
Torg (6) proposed a classification system for Jones fractures to assist management decisions:
Type 1 fractures are acute without prior pain; x-rays reveal a clean fracture line without
sclerosis or cortex hypertrophy. Type 2 fractures involve prior symptoms or a known prior
stress fracture; x-rays show some medullary sclerosis and a widened fracture line. In type 3
fractures, x-rays demonstrate repeated trauma, a wide fracture line, and exuberant sclerosis
that suggests fracture nonunion.
Because of their poorer healing rate, Jones fractures need to be distinguished from simple
metaphyseal avulsion fractures. Type 1 fractures in nonathletes may heal in 6 to 8 weeks with
a non-weight-bearing cast, but most authors recommend surgical management for active
patients. Type 2 and type 3 fractures are best treated with surgical fixation.
41
Rearfoot Overuse Injuries
Overuse injuries are more common than traumatic injuries and are caused by the repetition of
loading forces that, if applied singly, would not cause damage. Overuse injuries affecting the
foot can be grouped by their location in the rearfoot, midfoot, or forefoot. Rearfoot injuries
that can befall the weekend warrior include plantar fasciitis, fat pad syndrome, and calcaneal
bursitis.
Plantar fasciitis. Plantar fasciitis, or subcalcaneal pain, is a common reason for physician
office visits. Pain is located distal and medial to the base of the calcaneus at the tuberosity.
The condition is characterized by an insidious onset of heel pain, which is worse on arising in
the morning or after a brief period of inactivity.
A change of sports activity, training regimen, shoes, or other biomechanical factors may
precipitate plantar fasciitis. Weekend warriors are particularly at risk for plantar fasciitis when
tremendous repetitive stress is applied to a plantar fascia otherwise accustomed only to the
strain of a flight or two of stairs.
Once the condition is established, it may resist many different treatments. Pain of a few days'
to a few weeks' duration may be eased by simply providing more supportive athletic shoes,
minimizing barefoot walking, and taking oral nonsteroidal anti-inflammatory drugs
(NSAIDs).
Heel cups may help some patients. These work by providing direct shock absorption or by
minimizing fat pad splay under the calcaneus. Heel cups force more fat to remain below the
heel (figure 2), which helps if the pain is from swelling around the plantar fascia.
However, the pain may be due to tensile forces on the plantar fascia or calcaneal periosteum.
Controlling arch collapse or excessive pronation with off-the-shelf or custom orthoses can
provide some relief of this tension. I also find that advising people to lace their shoes as
tightly as tolerable assists medial support by the shoe's heel counter, reducing pronation.
Attention to Achilles flexibility will also relieve some of the arch-collapsing forces.
Another helpful measure is the use of a tension night splint (see "Making a Tension Night
Splint for Plantar Fasciitis," June 1998, page 113). The splint holds the foot in a slightly
dorsiflexed position, providing a gentle stretch and reducing the swelling that accumulates in
the relaxed plantar fascia.
42
Corticosteroid injections can provide dramatic, though often temporary, relief. The possibility
of fat pad injury should be discussed with the patient before injecting this area. Surgical
plantar fascia release is rarely necessary.
Fat pad syndrome. A direct blow to the bottom of the heel that results in a bruise, such as a
forceful heel-first landing on a rock by a swimmer, can also injure the fat pad, causing
symptoms similar to plantar fasciitis. Examination of the heel usually reveals tenderness
directly under the weight-bearing part of the calcaneus rather than on the anterior distal
tuberosity.
A well-fitted heel cup cushions the heel and prevents the fat pad from splaying, thereby
improving the intrinsic cushioning of the calcaneus (figure 2) (7). Also helpful are shoes with
softer midsoles, which provide more cushioning for the fat pad.
Retrocalcaneal bursitis. The bursae between the skin and the Achilles tendon and between
the Achilles tendon and the calcaneus are subject to friction from tight shoes or a calcaneal
protuberance. This differs from Achilles tendinitis in that, with retrocalcaneal bursitis,
tenderness is present at the Achilles tendon insertion rather than at the narrowest part of the
tendon, 2 to 3 cm proximal to the insertion.
Treatment for retrocalcaneal bursitis is directed at reducing the friction. The simplest solution
is to rest the area by wearing a shoe with an open back. But if conventional shoes are a must,
a well-padded heel counter is necessary. The fit of the shoe is also very important. A shoe that
is too loose at the heel allows the heel to rise first in the shoe and the shoe to follow, causing
rubbing and friction. Minimizing this slippage will minimize heel irritation. If a shoe is too
tight, compression of the bursa will also cause irritation. Accommodative donut padding
around the inflamed tissue can provide pain relief.
Midfoot Overuse Injuries
Tendinitis. Tendinitis of the posterior tibial tendon on the medial side and the peroneus
longus tendon on the lateral side (figure 3) can easily occur in the adult recreational athlete
unaccustomed to hours of stress.
With inflammation of these tendons, pain and tenderness are usually present along the tendon
inferior and distal to the malleolus. This tendinitis does not usually cause pain until weight is
placed on the foot. Eccentrically stressing the suspect tendon by applying resistance force
43
with the hand on the actively contracting muscle of the patient's inverted or everted foot can
help identify the tendon as the source of pain. If this test is negative, pain could be originating
from injury to ligaments, tissue, bone, or the ankle joint. Weight-bearing stress as with a
standing toe raise is used to assess tendon integrity. A newly collapsed arch suggests the
rarely occurring posterior tibial tendon rupture.
Tendinitis usually responds to rest, NSAIDs, ice, and, occasionally, brief immobilization.
Supporting the medial arch with motion-control shoes and orthoses will reduce eccentric
forces to the posterior tibial tendon, and supporting the medial longitudinal arch may help
peroneus longus tendinitis simply by reducing late-phase pronation. A gradual return to
activity and some weekday conditioning will help the weekend warrior resume his or her
previous routine. Posterior tibial tendon rupture requires more aggressive management, such
as casting.
Tarsal navicular stress fractures. Tarsal navicular stress fractures are rare, but unfortunately
many go undiagnosed for months (8). Chronic dorsal medial midfoot pain that is mainly
activity-related suggests the possibility of this stress fracture, which mostly occurs in
repetitive activities such as running, soccer, and basketball. In my practice, two patients who
presented with ankle pain were diagnosed as having tarsal navicular stress fractures.
The navicular tuberosity is easily palpated about 3 to 4 cm inferior and distal to the malleolus.
The fracture site is usually at the apex of the bone, or "N" spot (figure 4) (9), and tenderness
usually is present just under the anterior tibial tendon. X-rays are often normal. A bone scan
or computed tomography (CT) scan is necessary to make a definitive diagnosis.
Like carpal navicular (scaphoid) fractures, fractures of the tarsal navicular are notorious for
poor healing. Nonsurgical treatment is the use of a non-weight-bearing cast for 6 to 8 weeks.
If the fracture is managed nonsurgically, the patient should be warned that it will take a long
time to heal. Return to sport may take 6 months. Following immobilization, the patient should
focus on gastrocnemius and Achilles flexibility, wear good shoes, and use care in sports
activity.
44
Painful fracture nonunion requires internal fixation.
Forefoot Overuse Injuries
Metatarsal stress fractures. These injuries were originally called march fractures. The
second, third, and fourth metatarsals account for 90% of these fractures (10). Second
metatarsal fractures are most common, followed by fractures of the third and fourth
metatarsals. These fractures can occur in sports that involve running, such as soccer,
basketball, or tennis.
Metatarsal stress fractures often cause a diffuse swelling of the forefoot, disguising the
focused nature of the injury. Careful palpation of each metatarsal helps identify one of the
bones as the source of pain. Calluses on the plantar skin can provide clues to a pattern of
inordinate stress on the metatarsal heads.
Chronic pain at the proximal metaphysis should alert the examiner to the possibility of a stress
fracture. Prompt conservative treatment for a stress fracture at this site may prevent the
eventual occurrence of an acute (Jones) fracture.
With metatarsal stress fractures, x-rays are normal for the first 2 to 3 weeks, but obvious bone
callus usually appears subsequently. The diagnosis can be made earlier with a bone scan.
Avoiding weight-bearing while cross-training for approximately 4 weeks will allow adequate
healing for most metatarsal stress fractures. Accommodative orthotic devices, which
incorporate a depression that reduces pressure at the fracture site, may help prevent recurrence
if signs of excessive stress to the fractured metatarsal are present.
Interdigital neuroma. The classic Morton's neuroma (figure 5) is an interdigital lesion
involving the digital nerve common to the third and fourth metatarsal heads. This is not a true
neuroma, but rather a perineural fibrosis where the nerve passes underneath the transverse
metatarsal ligament. Repetitive irritation at this location causes distal plantar pain and often
numbness in the interdigital web space supplied by this nerve. The condition can occur in
runners, and shoes with a tight toe box may contribute to the problem. Palpating the distal
plantar area while squeezing the metatarsal heads together can elicit the patient's symptoms.
45
A shoe with a wide toe box and a soft metatarsal pad can gently spread the metatarsals and
may provide symptomatic relief. For weekend exercisers, NSAIDs and rest during the week
may control the symptoms and forestall the need for further intervention. If these measures do
not suffice, corticosteroid injection with a dorsal approach just proximal to the metatarsal
heads also can produce clinical improvement.
Patients whose symptoms do not improve with these conservative measures require surgical
management (11).
Other Problems
Black toe. Subungual hematoma develops from tight-fitting shoes, repeated sliding of the foot
into the front of the toe box, or direct trauma. Pain can be relieved by draining the blood that
is under pressure. This is accomplished with cautery or the heated tip of a paper clip.
Attention to shoe fit and movement in the shoe prevents recurrence of subungual hematoma
(12).
Blisters. Blisters are probably the most common foot injury in weekend athletes. Infrequently
stressed skin that is not conditioned is subject to injury just as muscle, tendon, and bone are.
Shoes that are new, improperly fitted, or wet contribute to blister development.
Skin that is red but not yet blistered may be protected with 2nd Skin dressing (Spenco
Medical Corporation, Waco, Texas) or an adhesive bandage, allowing the athlete to continue
sports activity.
An established blister should be drained and covered and further skin injury should be
avoided until epidermal recovery (13). I have found that layering first antibiotic ointment,
then 2nd Skin dressing, next an adhesive bandage, and sometimes donut padding around the
blister allows sports participation with reduced pain. The patient should watch closely for
signs of infection.
Stress Conditioning
Physicians who inquire about the activity patterns of their foot-injured patients may discover a
weekend warrior. Such patients may need to be reminded to train during the week. This will
help them avoid some of the overuse foot injuries that could become chronic or even
debilitating.
References
1. Clanton TO: Etiology of injury to the foot and ankle, in DeLee JC, Drez D, Stanitski CL (eds): Orthopaedic Sports
Medicine: Principles and Practice. Philadelphia, WB Saunders, 1994, pp 1642-1704
2. Nigg BM: Biomechanics of Running Shoes. Champaign, IL, Human Kinetics, 1986, p 21
3. Soma CA, Mandelbaum BR: Achilles tendon disorders. Clin Sports Med 1994;13(4):811-823
4. Lo IK, Kirkley A, Nonweiler B, et al: Operative versus nonoperative treatment of acute Achilles tendon ruptures: a
quantitative review. Clin J Sport Med 1997;7(3):207-211
5. Cetti R, Christensen SE, Ejsted R, et al: Operative versus nonoperative treatment of Achilles tendon rupture: a prospective
randomized study and review of the literature. Am J Sports Med 1993;21(6):
791-799
6. Torg JS, Balduini FC, Zelko RR, et al: Fractures of the base of the fifth metatarsal distal to the tuberosity: classification
and guidelines for non-surgical and surgical management. J Bone Joint Surg (Am) 1984;
66(2):209-214
7. Wargon C: Common foot injuries, in Sallis RE, Massimino F: Essentials of Sports Medicine. St Louis, Mosby-Year Book,
1997, pp 463-478
46
8. Bojanic I, Pecina MM: Conservative treatment of stress fractures of the tarsal navicular in athletes. Rev Chir Orthop
Reparatice Appar Mot, 1997;83(2):133-138
9. Khan KM, Brukner PD, Kearney C, et al: Tarsal navicular stress fracture in athletes. Sports Med 1994;
17(1):65-76
10. Weinfeld SB, Haddad SL, Myerson MS: Metatarsal stress fractures. Clin Sports Med 1997;16(2):319-338
Mann RA: Entrapment neuropathies of the foot, in DeLee JC, Drez D, Stanitski CL (eds): Orthopaedic Sports Medicine:
Principles and Practice. Philadelphia, WB Saunders, 1994, pp 1838-1841
11. Petrizzi MJ: Foot injuries, in Birrer RB (ed): Sports Medicine for the Primary Care Physician, ed 2. Ann Arbor, MI, CRC
Press, 1994, p 580
12. Garrick JG, Webb DR: Sports Injuries: Diagnosis and Management. Philadelphia, WB Saunders, 1990, p 320
Dr Simons is associate director of the family practice residency at St Joseph's Medical Center
in South Bend, Indiana, a fellow of the American College of Sports Medicine (ACSM), and a
charter member of the American Medical Society for Sports Medicine (AMSSM). Dr Moeller
is an assistant residency director and director of sports medicine at the William Beaumont
Hospital Family Practice Residency Program in Troy, Michigan, a member of the ACSM and
the AMSSM, and a member of the editorial board of The Physician and Sportsmedicine.
Address correspondence to Stephen M. Simons, MD, 837 E Cedar, Ste 125, South Bend, IN
46637; address e-mail to simonss@sjcg.org.
47
Fractures of the Fifth Metatarsal
Warren D. Yu, MD; Matthew S. Shapiro, MD
THE PHYSICIAN AND SPORTSMEDICINE - VOL 26 - NO. 2 - FEBRUARY 98
In Brief: Fractures of the fifth metatarsal are common in active people. Proximal metaphyseal
and distal fractures are usually amenable to conservative treatment, but some proximal
fractures, such as Jones, stress, and acute-on-chronic fractures, are often associated with
nonunion or delayed union. Such fractures are often best treated by early operative
intervention. Correct identification of fifth metatarsal fractures is important because prompt
surgical treatment when indicated can shorten recovery and allow a quick return to sports
activity. Other causes of lateral foot pain, including accessory ossicles, neuromas,
osteoporosis, herniated disks, and osteoid osteoma, should be considered when suspected
fractures fail to show up on radiographs.
Fractures of the fifth metatarsal are commonly encountered by physicians treating active
people. Choosing correctly between conservative and surgical treatment of these patients is
particularly important because conservative treatment sometimes leads to an extremely slow
recovery or to long-term problems. Competitive and recreational athletes are geared for a
rapid return to activity, and prolonged recoveries are not well tolerated. In addition, long-term
immobilization and rest can lead to muscle atrophy and stiffness, further hampering the
patient's return to full athletic participation.
Fifth metatarsal fractures are of several varieties. Proximal fractures include acute fractures of
the tuberosity (metaphysis), or "dancer's fractures"; the classic Jones fracture; stress fractures
of the proximal diaphysis; and acute-on-chronic diaphyseal fractures. These proximal
fractures may look alike, and differentiating them is critical in making the correct treatment
decision. Tuberosity fractures and fractures in the midshaft, neck, and head of the metatarsal
are generally more likely to respond well to conservative treatment than the others mentioned.
Proximal Metaphyseal Fractures
A fracture of the base of the fifth metatarsal--the so-called dancer's fracture--typically occurs
with inversion injuries to the ankle and may accompany an ankle sprain. Because pain at the
base of the fifth metatarsal is not a common finding in an ankle sprain, tenderness in this area
should prompt the clinician to order whole foot--not just ankle--x-rays.
48
These fractures are almost always nondisplaced and involve the cancellous bone and thin
cortices of the metaphysis. Some may present as avulsion fractures (figure 1). In the past,
these avulsions were thought to be associated with tearing at the peroneus brevis tendon
insertion, but it is more likely that the fracture occurs as the plantar aponeurosis is pulled from
the bone (figure 2) (1,2). The prognosis for fractures in this area is excellent; they almost
always heal within 4 to 6 weeks with conservative treatment.
Certain conditions may mimic an avulsion fracture radiographically. In the skeletally
immature athlete the apophysis of the tuberosity may be confused with a nondisplaced
tuberosity fracture. Unlike a fracture, a normal apophysis has a smooth radiolucent line that
lies parallel to the shaft of the metatarsal. It may be seen in girls aged 9 to 11 and in boys aged
11 to 14 years (3). The radiolucent line typically disappears 2 to 3 years after it first appears.
49
In skeletally immature patients, radiographs of both feet should be obtained so comparisons
can be made.
Accessory ossicles may be confused with a displaced tuberosity fracture fragment. The os
peroneum is located next to the lateral border of the cuboid and found within the peroneus
longus tendon, whereas the rare os vesalianum is adjacent to the peroneus brevis insertion (3).
Fractures typically have a ragged border in contrast to the smooth corticated border of an
ossicle. Meticulous clinical exam ensures accurate diagnosis.
Symptomatic treatment for dancer's fractures--consisting of limited weight bearing, modified
activity, ice, and analgesics--is all that is necessary. Common treatments range from
immobilization in a walking cast or walking with crutches to simply wearing a wooden-soled
shoe. Any of these is acceptable, but our preference is to use a removable foot-ankle fracture
brace with a rocker bottom. This allows immediate discontinuation of crutches, good
mobility, and a quick return to daily (but not sports) activity, with relatively little pain.
Moreover, since the patient may remove the device to bathe, apply ice, do range-of-motion
exercises, and even sleep, it is very well tolerated.
After 3 to 4 weeks, when pain diminishes, the brace may be removed in favor of some type of
modified footwear (eg, a high-top sneaker or hiking boot, sometimes with a lightweight ankle
orthosis), and the patient may gradually return to more vigorous activities. In most cases the
patient will be back to sports within 6 to 8 weeks.
Operative treatment for metaphyseal fractures is rarely indicated. Some may involve the
articular alignment between the base of the fifth metatarsal and the cuboid. If there is
significant intra-articular or subchondral step-off at this joint (more than 2 to 3 mm), or if
there is a large intra-articular fragment involving more than 30% of the articular surface,
operative intervention may be indicated in order to minimize degenerative arthritis to the
cuboid-fifth metatarsal articulation (4). Nonunion is exceedingly rare, but if it occurs, it may
cause persistent pain requiring surgical treatment.
Jones Fractures
The term "Jones fracture" has been used indiscriminately to describe several different types of
fractures of the proximal fifth metatarsal. The true Jones fracture, originally described in 1902
by Sir Robert Jones (5), consists of a transverse fracture at the junction of the diaphysis and
metaphysis (figure 3). This trauma site corresponds to the area between the insertion of the
peroneus brevis and tertius tendons. An oblique radiograph is essential to accurately assess
this fracture. To prevent confusion, only acute fractures in this precise location should be
labeled Jones fractures.
50
The Jones fracture is an acute midfoot injury with no prodrome. The injury occurs when the
ankle is plantar flexed and a strong adduction force is applied to the forefoot (5,6); this can
happen in soccer, football, basketball, tennis, and other sports. Because of low vascularization
and high stresses at this site, Jones fractures are associated with a poor outcome (see
"Anatomy and Healing in the Fifth Metatarsal," below) (4,6-13). Nonunions and delayed
unions are common, particularly in patients who have received less-than-optimal
treatment(1,7,13-16). Radiographic recognition of this fracture pattern should alert the
physician that this injury requires special medical attention.
The optimal treatment is non-weight-bearing immobilization for a minimum of 4 weeks,
followed by the use of a walking cast or orthosis for an additional 4 weeks. Athletic activity
should be avoided until clinical and radiographic evidence of union appears, typically by 8 to
12 weeks. Noncompliance with treatment and an early return to athletic activities may result
in nonunion of the fracture, which will significantly delay the ultimate recovery.
With Jones fractures, failure to heal by 12 weeks is not uncommon, and at this point the
difficult decision must be made either to treat operatively or continue conservative treatment.
Continued non-weight-bearing immobilization may ultimately lead to union, but is often not
well tolerated by the athlete.
Stress and Acute-on-Chronic Fractures
Stress fractures. A stress-induced variant of a Jones fracture is commonly encountered in
athletes who do a lot of running. It is often seen in soccer players, and may have something to
do with their enormous amount of running, as well as their tendency to wear very narrow,
tight-fitting shoes that allow the fifth metatarsal to hang over the sole laterally.
Patients typically present with pain over the lateral aspect of the foot in the area of the fifth
metatarsal base, and report no significant episode of trauma (8,12,16). Radiographs typically
show evidence of a stress phenomenon at the metaphyseal-diaphyseal junction (the same site
as a Jones fracture) with severe intramedullary sclerosis, profound thickening of both the
medial and lateral cortices, and a lucency in the lateral cortex (figure 4).
51
In our experience, conservative treatment of these stress injuries has yielded uniformly poor
results. Healing is slow, and recurrence of the stress fracture is almost certain even if
radiographic improvement is seen in the interim.
Our current preference is to treat these patients operatively with the percutaneous insertion of
a cannulated screw, placed longitudinally down the intramedullary canal (figure 5). Active
patients typically recover from this surgery quickly, bear weight within days, begin aerobic
activities such as bicycling within the first week or two, and return to full activities within 6 to
8 weeks (8-11,16-18). The screw is well tolerated and may stay in place for the duration of the
patient's athletic career.
52
Acute-on-chronic fractures.Occasionally a patient will present with an acute injury that
results in pain at the base of the fifth metatarsal, and radiographs will appear atypical. A
fracture line at the same site as a Jones fracture is easily identified on the radiograph, but there
may also be features typical of a stress injury, such as cortical thickening and a lucency in the
lateral cortex (figure 6).
53
A careful history will often reveal that the patient has had a prodrome consisting of
intermittent pain in the region. This is an important distinguishing feature, for acute-onchronic stress fractures will behave more like stress fractures than they do acute Jones
fractures, and casting and immobilization will frequently fail. Attempted conservative
treatment may result in delayed union, the loss of months of competition, and significant
dysfunction from long periods of disuse, and surgery will frequently be required in the end.
It is our belief that if this fracture pattern is strongly suspected, the patient is best served by
early operative intervention similar to the procedure used for typical stress fractures.
Indications for Surgery
Once nonunion at the metaphyseal-diaphyseal junction is established, further conservative
treatment is not likely to result in union (1,4,7,9,10,13). Prolonged immobilization (3 to 6
months) has been recommended in the past, but with currently available surgical techniques is
probably not indicated. Patients who have difficulty healing after a Jones fracture, those who
present months after an injury with evidence of bony nonunion, those who have had poor or
inadequate treatment, and those who have stress injuries and acute-on-chronic injuries are all
candidates for surgical treatment.
Our preferred operative procedure, as described above, is intramedullary placement of a
cannulated screw, but other surgical procedures are commonly used (8). Open repair with
fixation and/or bone grafting yields good results. The minimal morbidity and excellent
outcome of percutaneous cannulated screw placement, however, makes it very appealing for
athletes.
54
Distal Fractures
Midshaft and neck fractures. With athletic activity, direct trauma to the fifth metatarsal
midshaft and neck may result in fractures. Most will be nondisplaced, but even significant
deformity may be well tolerated. The vast majority of these fractures can be treated
nonsurgically. The blood supply to this area is excellent, and healing is very predictable
(figure 7).
Lateral radiographs should be carefully evaluated for displacement in the sagittal plane. If a
fracture, particularly a more distal one, heals with a significant dorsal or plantar angulation, a
painful plantar keratosis may occur, accompanied by painful dorsal corns, irritation by shoes,
or pain in adjacent metatarsals. If significant deformity is suspected, referral to an orthopedic
foot specialist may be indicated. Displacement in other planes is well tolerated (17,19).
Nondisplaced or minimally displaced midshaft fractures can be managed with early weight
bearing in a rigid-soled device such as a cast, fracture brace, or wooden-soled cast shoe
(17,19). Fifth metatarsal shaft and neck fractures requiring reduction can be managed with a
hematoma block and gentle traction and manipulation. Follow with weight bearing as
tolerated in a cast for 4 to 6 weeks. Prolonged non-weight-bearing immobilization should be
avoided; it may lead to disuse atrophy, osteopenia, and, rarely, reflex sympathetic dystrophy.
There are no universally accepted guidelines for open reduction and internal fixation of
diaphyseal fractures. Generally, surgical intervention is considered if the fracture is
55
irreducible, has residual displacement of more than 3 to 4 mm, or has angulation of more than
10° in the sagittal plane (17). Screws, K-wires, or mini-fragment plates may be used to
maintain reduction.
Delayed unions and nonunions may occur, particularly in the distal metaphyseal-diaphyseal
area where vascularity may be compromised by the original injury. Symptomatic nonunions
may be treated with inlay bone grafting with or without internal fixation with good success
(17,19).
Intra-articular metatarsophalangeal fractures. In active people, metatarsal head fractures
may occasionally result from direct trauma, and these injuries require careful evaluation. The
intra-articular fragment is usually displaced in the plantar and lateral direction. A subtle
osteochondral fracture pattern can be noted secondary to shear injury from dorsal dislocation
of the metatarsophalangeal joint.
Gentle traction and manipulation typically effect stable reduction. Early weight bearing in a
rigid-soled device such as a sandal or a cast for 4 to 6 weeks is adequate for the majority of
these injuries. Unstable fractures may occur when the distal fragment lacks soft-tissue
attachments. These injuries may require open reduction and pinning. Stiffness and traumatic
arthritis of the metatarsophalangeal joint may complicate the final result, and patients should
be so advised to ensure appropriate expectations (17,19).
Other Causes of Lateral Foot Pain
When a suspected fracture is not evident on initial or follow-up radiographs, other causes of
lateral foot pain must be considered. These include accessory ossicles (os peroneum or os
vesalianum), neuromas, osteoporosis, herniated disks, and, rarely, an osteoid osteoma.
If other conditions have been ruled out, accessory ossicles may be the cause of a patient's
lateral foot pain and disability. These ossicles can be difficult to visualize on routine
radiographs, and oblique views may be needed (3). Initial treatment consists of conservative
measures including anti-inflammatory medications, ice, footwear modification, and/or
orthoses. A cortisone injection may be attempted in refractory cases, but if pain persists,
surgical excision remains as a last resort.
Neuromas of the superficial peroneal or sural nerve should be suspected if previous trauma
has occurred. Testing for Tinel's sign along the course of the nerve may reproduce the
symptoms, and sometimes a palpable mass is present on exam. A cortisone injection may be
attempted, but surgical excision is often required.
Osteoporosis is a common cause of foot pain in the older population but may present as lateral
foot pain in young active patients--particularly in female runners who have little body fat and
are not menstruating regularly. Leg injuries requiring periods of non-weight bearing, such as
fractures and surgery, can cause osteoporosis in the foot and ankle, often leading to pain. The
patient's bone quality should be evaluated on radiographs and a bone density scan obtained.
Symptomatic treatment along with nutritional and hormonal consultation should be sought.
A herniated disk should be considered in all cases of unexplained lateral foot pain. Careful
lumbosacral and neurologic examination should ensure correct diagnosis. If this condition is
suspected, magnetic resonance imaging should be performed to corroborate the clinical
findings. Typically, either the L-5 or S-1 nerve roots will be involved in the pathology.
56
Rarely, lateral foot pain can be caused by benign and malignant tumors. One of these is the
osteoid osteoma (figure 8), a benign bony tumor occurring in people between the ages of 5
and 30. Patients present with gradually increasing pain, particularly at night. The pain is
dramatically improved by nonsteroidal anti-inflammatory drugs. Radiographs typically reveal
intensely reactive bony sclerosis that mimics a healing stress fracture, with which it may be
confused. A radiolucent nidus, best seen on computed tomography scans, will confirm the
diagnosis.
Treatment for osteoid osteoma consists of round-the-clock anti-inflammatory medications
until the patient can undergo surgical excision. Several case reports of spontaneous involution
of the nidus exist, but in most cases the patient will require surgery.
Promoting a Quick Return
In fifth metatarsal fractures, correctly identifying the fracture type is essential for permitting
the earliest possible return to sports. Proximal metaphyseal fractures usually heal well with
conservative treatment, but other proximal fractures--Jones fractures, stress fractures, and
acute-on-chronic fractures--often lead to delayed union or nonunion, and are best treated by
early operative intervention. More distal fractures can almost always be treated
nonoperatively, except for unstable intra-articular fractures.
References
1. Heckman JD: Fractures and dislocations of the foot, in Rockwood CA Jr, Green DP, Bucholz RW (eds): Fractures in
Adults. Philadelphia, JB Lippincott Co, 1991, vol 2, pp 2041-2182
2. Richli WR, Rosenthal DI: Avulsion fracture of the fifth metatarsal: experimental study of pathomechanics. AJR Am J
Roentgenol 1984;143(4):889-891
3. Wilson DW: Fractures of foot, in Klenerman L (ed): The Foot and its Disorders. Boston, Blackwell Scientific Publications,
1991, pp 237-238
4. Hansen ST: Foot injuries, in Browner BD (ed): Skeletal Trauma. Philadelphia, WB Saunders, 1992, pp l984-1986
Jones R: Fractures of the base of the fifth metatarsal bone by indirect violence. Ann Surg 1902;35:697-700
5. Kavanaugh JH, Brower TD, Mann RV: The Jones fracture revisited. J Bone Joint Surg (Am) 1978;60(6):776-782
57
6. Acker JH, Drez D Jr: Nonoperative treatment of stress fractures of the proximal shaft of the fifth metatarsal (Jones'
fracture). Foot Ankle 1986;7(3):152-155
7. DeLee JC, Evans JP, Julian J: Stress fracture of the fifth metatarsal. Am J Sports Med 1983;11(5):349-353
Lawrence SJ, Botte MJ: Jones' fractures and related fractures of the proximal fifth metatarsal. Foot Ankle 1993;14(6):358365
8. Lehman RC, Torg JS, Pavlov H, et al: Fractures of the base of the fifth metatarsal distal to the tuberosity: a review. Foot
Ankle 1987;7(4):245-252
9. Sammarco GJ: The Jones fracture. Instr Course Lect 1993;42:201-205
10. Torg JS, Balduini FC, Zelko RR, et al: Fractures of the base of the fifth metatarsal distal to the tuberosity: classification
and guidelines for non-surgical and surgical management. J Bone Joint Surg (Am) 1984;66(2):209-214
11. Zogby RG, Baker BE: A review of nonoperative treatment of Jones' fracture. Am J Sports Med 1987;15(4):304-307
Glasgow MT, Naranja RJ Jr, Glasgow SG, et al: Analysis of failed surgical management of fractures of the base of the fifth
metatarsal distal to the tuberosity: the Jones fracture. Foot and Ankle Int 1996;17(8):449-457
12. Josefsson PO, Karlsson M, Redlund-Johnell I, et al: Jones fracture: surgical versus nonsurgical treatment. Clin Orthop
1994;(299):252-255
13. Zelko RR, Torg JS, Rachun A: Proximal diaphyseal fractures of the fifth metatarsal--treatment of the fractures and their
complications in athletes. Am J Sports Med 1979;7(2):95-101
14. Anderson RB: Injuries to the midfoot and forefoot, in Lutter LD, Mizel MS, Pfeffer GB (eds): Orthopaedic Knowledge
Update: Foot and Ankle. Rosemont, IL, American Academy of Orthopaedic Surgeons, American Orthopaedic Foot and
Ankle Society, 1994, pp 264-267
15. Mindrebo N, Shelbourne KD, Van Meter CD, et al: Outpatient percutaneous screw fixation of the acute Jones fracture.
Am J Sports Med 1993;21(5):720-723
16. Shereff MJ: Complex fractures of the metatarsals. Orthopedics 1990;13(8):875-882
58
Anatomy and Healing in the Fifth
Metatarsal
With an understanding of the anatomy of the fifth metatarsal (figure A), the clinician can
better understand the natural history of fractures to this area.
The base, or proximal metaphysis, of the fifth metatarsal consists mostly of cancellous bone
with extremely thin cortices. Being well-vascularized, this region heals promptly and
predictably.
Anatomic limitations, however, result in poor healing of Jones fractures and proximal
diaphyseal stress fractures (1,2). The cortex of the fifth metatarsal thickens considerably and
the medullary canal narrows at the junction of the proximal metaphysis and diaphysis (figure
B), marking a transition from mostly cancellous to relatively avascular cortical bone. This has
important implications for fracture healing, especially for active people, because the cortices
of the metaphyseal-diaphyseal junction can thicken even more when running focuses stress on
this weight-bearing area. This thickening causes the already poor blood supply to be further
diminished. The poor vascularity retards bone healing because the proteins and cells required
for bone healing and remodeling require adequate circulation.
59
Midshaft, neck, and head fractures generally heal well. The blood supply to this part of the
metatarsal, surrounded as it is by the soft tissues of the intermetatarsal and plantar areas, is
quite good, and healing is very predictable.
References
1. Shereff MJ, Yang WM, Kummer FJ, et al: Vascular anatomy of the fith metatarsal. Foot Ankle 1991;11(6):350-353
Smith JW, Arnoczky SP, Hersh A:The intraosseous blood supply of the fith metatarsal: Implications for proximal fracture
healing. Foot Ankle 1992;13(3)143-152
Dr Yu is a senior resident and Dr Shapiro is an associate professor, both in the department of
orthopedic surgery at the University of California School of Medicine in Los Angeles.
Address correspondence to Matthew S. Shapiro, MD, UCLA Center for Health Sciences,
Dept of Orthopedic Surgery, 10833 Le Conte Ave, Los Angeles, CA 90024-6902; e-mail to
mshapiro@ortho.medsch.ucla.edu.
60
Hyperpronation and Foot Pain
Steps Toward Pain-Free Feet
Steven D. Stovitz, MD; J. Chris Coetzee, MD
THE PHYSICIAN AND SPORTSMEDICINE - VOL 32 - NO. 8 - AUGUST 2004
In Brief: Primary care physicians often see patients who have foot pain. Although foot
disorders may have many diagnostic possibilities, the majority can be explained via the
pathologic biomechanics of hyperpronation and the resulting changes in the kinetic chain.
Four common problems often associated with hyperpronation are plantar fasciitis, posterior
tibial tendon dysfunction, metatarsalgia, and hallux valgus. Interventions that seek to reduce
hyperpronation and strengthen foot muscles are often recommended for treating foot pain.
Foot pain is an extremely common problem. Exact prevalence rates in the general population
are unknown, but various small studies in women report rates between 32% and 80%. 1
Evaluating and diagnosing foot pain can be daunting for physicians because of the wide array
of conditions that can cause discomfort. One article2 listed 49 different possible diagnoses for
subcalcaneal heel pain alone. Although diagnoses may differ, hyperpronation (ie, pronation
too early in the gait cycle) is likely an associated event. An understanding of the causes and
effects of hyperpronation will greatly assist the evaluation and treatment of patients who have
foot pain.
Defining the Problem
The discussion of foot disorders begins with an understanding of terminology and a review of
the gait cycle. Foot pronation and supination are active processes that must be distinguished
from pes planus and pes cavus, which are terms describing a static foot. Pronation entails
calcaneal eversion, a downward migration of the midfoot, then forefoot abduction and
dorsiflexion. With supination, the calcaneus inverts, and the forefoot adducts and plantar
flexes.
Pes planus signifies a flatfoot and pes cavus denotes a hollow foot. While pes planus is
typically described from visual observation alone, the actual definition depends on the
metatarsal bones losing their normal longitudinal arch. Thus, people with hypertrophied
muscles on the plantar surfaces of their feet, such as lifelong barefoot walkers, can be
mistakenly viewed as having flatfeet, when, in fact, their bones maintain a normal
longitudinal arch. The term "flexible flatfoot" describes an arch that is high when unloaded
but flattens with standing if weight bearing does not cause calcaneal eversion. Hyperpronation
occurs if weight bearing causes calcaneal eversion, in which case the static property of the
foot cannot be clinically specified. The bottom of a "fixed" flatfoot remains flat whether the
patient is sitting or standing.
The Gait Cycle
The normal gait cycle begins with a heel strike, and then very brief supination with force
moving forward. This action is followed by pronation of the foot, whereby the weight
becomes distributed over the midfoot, and finally a toe-off (figure 1). Toe-off is associated
61
with a brief supination (ie, calcaneal inversion) caused by the windlass mechanism of the
medial longitudinal arch. In normal ambulation, the force of the body is transmitted over the
toes with approximately one third of body weight going over the first toe, and one sixth of
body weight going over each of the lateral four toes.
Individuals who lack physiologic pronation are said to be supinators, and their feet have
difficulty absorbing the shock of weight bearing. The weight does not disseminate over the
middle part of the foot, but rather remains on the bony lateral side. Much more commonly,
people who have foot pain lack the initial supination, and thus pronate too early in the gait
cycle (ie, hyperpronate).
What Causes Hyperpronation?
With too-early pronation, the force is transmitted medially while the weight is still on the
hindfoot and proximal midfoot. The medial longitudinal arch loses height, and that may set up
a cascade of biomechanical problems related to the causes and effects of hyperpronation
(figure 2).
Biomechanically, the precipitating events in hyperpronation can be viewed in relation to the
position of the talus. Although kinetic chain reactions occur from the hip down to the foot, the
interdependent relationships of the talus, calcaneus, and navicular are especially important. A
key point is that the talus does not simply sit atop the calcaneus; rather, it is positioned
anteriorly and medially on the calcaneus (figure 3). The talus contacts the anterolateral edge
of the proximal navicular bone, the most superior bone of the medial longitudinal arch. The
talus has no tendinous attachments and thus depends on the static support of surrounding
ligaments and bones. Malposition of one bone affects the adjacent proximal or distal bone.
62
The position of the calcaneus is greatly determined by the Achilles tendon. The Achilles
tendon inserts onto the calcaneus slightly lateral to midline. A tight Achilles provides not only
plantar flexion, but also eversion to the calcaneus. Both of these actions translate force
medially on the talus and downward and medially on the navicular, possibly causing
subsequent loss of height of the medial longitudinal arch.
The position of the talus is supported distally by the navicular bone. In standing, the navicular
bone maintains its position high on the medial longitudinal arch through the static support of
surrounding bones and ligaments. A natural alignment between the talus and the navicular and
a spring ligament (ie, the calcaneonavicular ligament) adjoining these bones locks the foot in
place (figure 4). With ambulation, dynamic support from the posterior tibial tendon (PTT) is
needed to maintain the superior position of the navicular. A weak PTT is unable to support the
position of the navicular, and, once again, a loss of the medial longitudinal arch may occur.
63
Collapse of the medial longitudinal arch everts the calcaneus in relation to the talus; that is,
the foot pronates. This may stretch the soft-tissue structures located posterior to the medial
malleolus (namely, the PTT and the posterior tibial nerve), manifesting as posterior tibial
tendinopathy or posterior tibial nerve entrapment. A collapsed arch can also stretch the spring
ligament and plantar fascia, producing plantar fasciitis. With calcaneal eversion (pronation),
the forefoot abducts and increases force through the medial rays, which can result in problems
over the first ray, such as hallux valgus, and over the second ray, such as metatarsalgia.
Modern society, with our rising obesity and dependence on footwear, may contribute to more
people having hyperpronation and subsequent foot pain. Obese individuals have an altered
gait with more extensive rearfoot eversion.3 Heavier body weight results in higher plantar
pressures, with the largest effect under the longitudinal arch and metatarsal heads.4 Greater
foot pronation occurs when wearing shoes than when walking barefoot. Shoes elevate the
calcaneus, shorten the Achilles tendon, and effectively splint the foot, thereby limiting muscle
contraction during ambulation. Extensive observational data suggest that wearing shoes in
childhood is detrimental to the development of a normal longitudinal arch5,6 and that shoeless
populations have less chronic foot pain.7
Examining the Feet
When evaluating patients who have foot pain, it is essential to view their bare legs and feet
from at least the midcalf down. The feet are examined when patients are seated with their feet
off the ground, standing, and with ambulation. The "too many toes" sign (when the examiner
can see the lateral four toes as the patient walks away) is often attributed to hyperpronation
and forefoot abduction (figure 5). While this is generally the case, visualization of the lateral
four toes may also result from more proximal causes, such as external rotation of the hip (eg,
in the gait of classic dancers) without hyperpronation of the feet. More emphasis should be
placed on viewing the Achilles tendon and noting if calcaneal eversion occurs. With the
patient walking toward them, clinicians should observe if the medial longitudinal arch is
maintained or whether the navicular bone seems to drop toward the floor with midstance.
64
It is also essential to note the strength of the PTT and the flexibility of the Achilles tendon.
The PTT can be assessed by observing the patient while he or she does heel raises. Normally,
the calcaneus inverts and the foot supinates with heel raises. Calcaneal eversion is often a sign
of a weak PTT. Achilles tendon flexibility testing should be done with both a bent and a
straight knee to differentiate the soleus (evident when knee is bent) from the gastrocnemius.
The opposite foot can be used for comparison. It is important to place the subtalar joint in
neutral alignment, and then apply a laterally directed force to the talar neck while pushing the
forefoot medially to lock the foot (figure 6). Otherwise, calcaneal eversion or forefoot
dorsiflexion may give a false impression of Achilles flexibility.
Common Foot Disorders
The deleterious effects of hyperpronation have been implicated in four common disorders of
the feet. It is important to note that, while we discuss the physiologic plausibility whereby
hyperpronation may lead to foot pain, prospective data are lacking.
Plantar fasciitis. The most common cause of hindfoot pain, plantar fasciitis results from a
degeneration of the fibrous aponeurosis that courses the medial longitudinal arch. Patients
report pain, generally near the distal medial border of the calcaneus, that is most prominent
with the first step after a long rest. Plantar fasciitis is seen in patients who have a rigid cavus
foot and in those who hyperpronate, and either deformity may increase the stress on the
plantar fascia. Excessive body weight, genu valgus, and gastrocnemius-soleus contracture are
all associated with increased pronation of the feet and are known precipitants of plantar
fasciitis.3,8
65
Treatment options have historically included rest, physical therapy, ice, heat, heel cups, pads,
splints, shoe modification, orthoses, nonsteroidal anti-inflammatory medications, injections,
and surgery. Of all the treatment options, the most consistently positive results have come
from Achilles stretching programs, both active and passive, using night splints. 9,10 Exercises
to stretch and strengthen the Achilles tendon are an effective means of decreasing
hyperpronation, thus reducing pain. A large study8 found that the use of heel cups, which raise
the calcaneus (the opposite of Achilles tendon stretching), was the least effective of the
various treatments evaluated.
Posterior tibial tendinopathy. The main insertion for the PTT is on the medial navicular
bone. The PTT is essential for initiating inversion and thus counteracting the forces of tooearly pronation. Proper functioning of the PTT is necessary for dynamic stabilization of the
medial longitudinal arch. A weak PTT cannot maintain the usual talonavicular alignment. The
talonavicular joint capsule and plantar spring ligament will stretch out with time. With the
resulting dorsolateral subluxation around the talar head, the midfoot is "unlocked," taking
away the ability to push off. PTT dysfunction can cause compensatory forefoot supination,
leading to problems such as hallux valgus and metatarsalgia. Thus, a strong PTT is necessary
to protect against hyperpronation. Additionally, hyperpronation from other causes may result
in PTT weakness, because the tendon becomes overstretched.
PTT dysfunction, once considered a rare entity, is now recognized with increasing frequency,
perhaps because of increasing obesity and improvements in diagnostic techniques.11 Patients
who have PTT dysfunction may report pain along the tendon's course, or pain more distally
caused by changes in forefoot biomechanics. In the later stages, the lateral ankle may sustain
compressive forces.
Treatment in the early stages focuses on correcting the root cause of the hyperpronation, with
an emphasis on mitigating gastrocnemius-soleus tightness and strengthening the PTT.
Correcting PTT dysfunction early in its course may help avoid surgical intervention later.11,12
If attenuation occurs, it is exceedingly difficult to treat conservatively.
Hallux valgus. Lateral deviation of the proximal phalanx on the first metatarsal head often
leads to a painful medial eminence, or bunion. Most patients who have hallux valgus have a
genetic predisposition that combines with developmental changes to cause hyperpronation
and excessive force on the first ray. Hallux valgus is almost exclusively found in shoewearing societies.13 With rare exception, shoes elevate the heel in relation to the midfoot,
producing a downward and medial force on the talus. A tight Achilles tendon has also been
implicated.13 Conservative treatment options include digital splinting, wearing wide-toed
shoes, and stretching the Achilles tendon.
Metatarsalgia. Pain over the metatarsal heads without any other obvious diagnosis, such as a
fracture, corn, or infection, can be termed metatarsalgia. The second metatarsal head is most
frequently involved. Normally, weight is distributed over the toes in a fanlike pattern, with the
first toe taking one third of the weight and the rest of the toes equally dividing the remaining
two thirds. With hyperpronation, the forces move medially, and the second metatarsal may
assume an excessively large percentage of the force. Additionally, weak flexor tendons place
extra force on the metatarsal heads.14 General treatment recommendations include
strengthening the plantar muscles, wearing shoes with low heels and wide toe boxes, and,
occasionally, using orthoses.
66
Treating Foot Pain
Each patient needs to be assessed individually, but some general recommendations seem to
apply to many patients who have foot pain. Low-heeled shoes, Achilles tendon stretching,
wide-toed shoes, foot strengthening exercises, and weight loss (if needed) are common
suggestions for foot pain associated with hyperpronation.
Altering calcaneal position. High-heeled shoes increase force on the forefoot.15 Low-heeled
shoes and Achilles tendon stretching decrease the equinus force from an elevated calcaneus.
The talus sits both anteriorly and medially atop the calcaneus, and thus any forward tilt to the
calcaneus produces a medially directed downward force on the navicular, causing excessive
pressure on the medial longitudinal arch. This changes the forces through the midfoot and
forefoot, putting extra stress on the medial digits. A tight Achilles tendon enhances the medial
force, because it inserts on the lateral side of the calcaneus. For years, Achilles tendon
stretching has been a nearly ubiquitous recommendation in the treatment of foot pain, but a
recent study by DiGiovanni et al16 was the first to document that those with midfoot and
forefoot pain had a tighter gastrocnemius tendon than controls who did not have foot pain.
Increasing muscle strength. Weak foot muscles may contribute to foot pain. Wide-toed shoes
and foot-strengthening exercises are prescribed. Axial loading applied to cadaveric feet
without simulating the activity of the plantar flexors causes foot pronation and medial
longitudinal arch collapse.14 Wide-toed shoes allow the flexors to contract, and thereby
strengthen, the surrounding musculature. Foot- strengthening exercises, such as toe curls and
heel raises, strengthen the PTT, peroneus longus muscles, and the flexor tendons. Walking
barefoot, if acceptable to the patient, is a functional method to strengthen foot musculature. In
fact, less foot pronation occurs when running barefoot than when wearing shoes.
Foot strengthening and weight loss (for overweight and obese patients) may help prevent
chronic overload of the metatarsals that can lead to stress fractures and stress reactions. Foot
musculature decreases with normal aging, and this may add to the effects of obesity to cause
foot pain. Cadaveric studies have demonstrated that contraction of the flexor hallucis longus
and the flexor digitorum longus pedis each decrease force on the metatarsals and,
theoretically, prevent bony stress reactions.14 Strengthening exercises help to preserve the
strength of the contractions. Given that excessive body weight results in extra pressure and
hyperpronation, weight loss should be encouraged for overweight patients who have foot
pain.3,4
A Note of Caution
Not all foot pain stems from hyperpronation. We believe that most cases of foot pain in the
general population can be attributed to hyperpronation, but a lack of normal pronation has its
own set of problems, namely, difficulty in absorbing the shock of weight bearing. The concept
of hyperpronation may be novel to some medical providers, but it is frequently cited in
running magazines as the major cause of foot pain. It is not uncommon for us to see runners
who lack physiologic pronation and yet believe that their lower-leg or foot pain is caused by
hyperpronation. They often are wearing custom rigid orthoses meant for hyperpronators. We
recommend gently informing them that their rigid orthoses do not seem to be working and
encouraging a trial of increased foot flexibility and strength.
Linking the Kinetic Chain
Foot pain is an extremely common problem, and the incidence will likely increase as our
population ages and grows more obese. Although diagnoses may differ, hyperpronation is
implicated as a common cause, and treatment recommendations are generally geared toward
67
reducing hyperpronation. Helping patients understand the causes and effects of
hyperpronation will increase their compliance with treatment recommendations, such as
Achilles tendon stretching, foot strengthening, weight loss, and appropriate footwear.
References
1. Balint GP, Korda J, Hangody L, et al: Regional musculoskeletal conditions: foot and ankle disorders. Best Pract Res Clin
Rheumatol 2003;17(1):87-111
2. Karr SD: Subcalcaneal heel pain. Orthop Clin North Am 1994;25(1):161-175
3. Messier SP, Davies AB, Moore DT, et al: Severe obesity: effects on foot mechanics during walking. Foot Ankle Int
1994;15(1):29-34
4. Hills AP, Hennig EM, McDonald M, et al: Plantar pressure differences between obese and non-obese adults: a
biomechanical analysis. Int J Obes Relat Metab Disord 2001;25(11):1674-1679
5. Rao UB, Joseph B: The influence of footwear on the prevalence of flat foot: a survey of 2300 children. J Bone Joint Surg
Br 1992;74(4):525-527
6. Sachithanandam V, Joseph B: The influence of footwear on the prevalence of flat foot: a survey of 1846 skeletally mature
persons. J Bone Joint Surg Br 1995;77(2):254-257
7. Hoffmann P: Conclusions drawn from a comparative study of the feet of barefooted and shoe-wearing peoples. Amer J
Orthop Surg 1905;3(2):105-136
8. Gill LH: Plantar fasciitis: diagnosis and conservative management. J Am Acad Orthop Surg 1997;5(2):109-117
9. Powell M, Post WR, Keener J, et al: Effective treatment of chronic plantar fasciitis with dorsiflexion night splints: a
crossover prospective randomized outcome study. Foot Ankle Int 1998;19(1):10-18
10. Batt ME, Tanji JL, Skattum N: Plantar fasciitis: a prospective randomized clinical trial of the tension night splint. Clin J
Sport Med 1996;6(3):158-162
11. Churchill RS, Sferra JJ: Posterior tibial tendon insufficiency: its diagnosis, management, and treatment. Am J Orthop
1998;27(5):339-347
12. Coetzee JC, Hansen ST: Surgical management of severe deformity resulting from posterior tibial tendon dysfunction.
Foot Ankle Int 2001;22(12):944-949
13. DeLee JC, Drez D Jr, Miller MD: DeLee & Drez's Orthopaedic Sports Medicine: Principles and Practice, ed 2.
Philadelphia, Saunders, 2003
14. Sharkey NA, Ferris L, Smith TS, et al: Strain and loading of the second metatarsal during heel-lift. J Bone Joint Surg Am
1995;77(7):1050-1057
15. Snow RE, Williams KR: High heeled shoes: their effect on center of mass position, posture, three-dimensional
kinematics, rearfoot motion, and ground reaction forces. Arch Phys Med Rehabil 1994;75(5):568-576
16. DiGiovanni CW, Kuo R, Tejwani N, et al: Isolated gastrocnemius tightness. J Bone Joint Surg Am 2002;84(6):962-970
Dr Stovitz is an assistant professor in the department of family practice and community health
and director of sports medicine curriculum for family practice residency programs and Dr
Coetzee is an assistant professor and chief of the foot and ankle division in the department of
orthopedic surgery, both at the University of Minnesota in Minneapolis. Address
correspondence to Steven D. Stovitz, MD, Smiley's Clinic, 2615 E Franklin Ave,
Minneapolis, MN 55406; e-mail to stovi001@umn.edu.
Disclosure information: Drs Stovitz and Coetzee disclose no significant relationship with any
manufacturer of any commercial product mentioned in this article. No drug is mentioned in
this article for an unlabeled use.
68
Bij de diagnostiek van een enkelverstuiking
kan worden volstaan met lichamelijk
onderzoek
Physical examination is sufficient for the diagnosis of sprained ankles [Journal of Bone
and Joint Surgery 1996;78B:958-62][Verkorte weergave]
C.N. van Dijk, L.S.L. Lim, P.M.M. Bossuyt, R.K. Marti
Stimulus 16 (1997), p. 332-336
Trefwoorden: diagnostiek enkelverstuiking;verstuiking enkel;lichamelijk onderzoek
enkelverstuiking;
Inleiding
In verband met de onbetrouwbaarheid van lichamelijk onderzoek zijn er diverse beeldvormende
technieken ontwikkeld voor het diagnosticeren van een inversietrauma van de enkel. Aanvankelijk
werd gebruik gemaakt van stressfoto's plus behandeling met gipsimmobilisering; later werd dit
artrografie en operatieve behandeling. In de jaren tachtig werd aangetoond dat functionele
behandeling even goede resultaten had en dit werd vervolgens de voorkeursbehandeling (Kannus &
Renström, 1991).
Diagnostische artrografie en tenografie werden als kostbaar en onnodig beschouwd en stressfoto's
werden gezien als niet betrouwbaar.
Bij nalopen van de literatuur werd geen verschil gevonden in de resultaten van de behandeling van
enkelvoudige en meervoudige ligamentaire rupturen (Kannus & Renström, 1991). De diagnose
dient daarom te differentiëren tussen een verstuiking en een ligamentaire ruptuur, kosteneffectief
te zijn en ook kosteneffectieve functionele behandeling mogelijk te maken (Brooks, Potter en
Rainey, 1981).
Stiell et al. (1994) hebben aangetoond dat lichamelijk onderzoek niet betrouwbaar is voor een
goede diagnose van een enkelfractuur. Wij hebben daarom geprobeerd de betrouwbaarheid ervan
te verbeteren met behulp van de opsporing van rupturen van enkelligamenten. Wij opperden het
idee dat wanneer lichamelijk onderzoek een aantal dagen na het trauma zou worden uitgevoerd,
dit in verband met pijn- en zwellingsafname mogelijk een betere diagnostische kwaliteit zou
hebben.
Ons onderzoek naar de merites van het lichamelijke onderzoek na een inversietrauma van de enkel
betrof 160 patiënten. De proefpersonen -- 116 mannen en 44 vrouwen -- hadden een leeftijd die
varieerde van 18 tot 40 jaar en zij hadden nooit eerder hun enkel verstuikt.
De studie maakte deel uit van een willekeurig gecontroleerd onderzoek naar verschillende
behandelmethoden.
Methode
Binnen 48 uur na het trauma werd een lichamelijk onderzoek verricht, waarbij werd gelet op de
mate van zwelling, hematoomvorming en locatie van de pijn bij palpatie; tevens werd de voorsteschuifladetest uitgevoerd. Aanwijzingen voor een laterale ligamentaire ruptuur werden op een
standaardformulier genoteerd als positief, negatief of onduidelijk. Vier tot zeven dagen later
69
werden alle patiënten opnieuw onderzocht door een ervaren orthopedisch chirurg. Daarnaast
werden de patiënten zonder dat zij op de hoogte waren van het resultaat van het voorgaande
onderzoek, allen onafhankelijk onderzocht door één van een groep van vier onervaren, maar goed
geïnstrueerde artsen, die elk, met behulp van dezelfde criteria (fig. 1 en 2), de waarschijnlijkheid
van een ligamentaire laesie bepaalden. Wij maakten bij elke patiënt een artrogram, maar de
uitkomst daarvan werd noch aan de patiënt noch aan de onderzoeker onthuld; dat gebeurde pas na
het uitgestelde onderzoek.
Figuur 1 Onderzoek van de pijnlijke enkel, vijf dagen na het
inversietrauma. (LTFA = lig. talofibulare anterius; VST = voorsteschuifladetest; LR = ligamentaire ruptuur).
Figuur 2a De patiënt zit aan het voeteneinde van de behandelbank of ligt op de rug met het bovenbeen ondersteund door de bank en de knie
gebogen. De enkel wordt in 10 tot 15 graden plantaire flexie gehouden. De linkerhand van de onderzoeker omvat de hiel, terwijl de voet van de
patiënt op de ventrale onderarm van de onderzoeker rust.
Figuur 2b De hiel wordt heel voorzichtig naar voren getrokken. De talus, en daarmee de voet, draait voorwaarts uit de enkelvork. Het rotatiecentrum is
het intacte lig. deltoideum. Bij een ruptuur van het lig. talofibulare anterius kan men een kuiltje zien, net voor de top van de laterale malleolus. De
voorwaartse beweging van de talus resulteert in een negatieve druk, die de huid naar binnen trekt aan de kant van de ligamentaire ruptuur.
70
Patiënten van wie men dacht dat zij een laterale ligamentaire ruptuur hadden bij het uitgestelde
lichamelijke onderzoek, of die een positief artrogram hadden, ondergingen een kijkoperatie. Zo
nodig werd het ligament operatief gehecht, waarna vijf dagen immobilisering volgden en daarna
functionele behandeling met een bandage. Alle patiënten werden minstens zes maanden gevolgd.
De gegevensanalyse betrof de specificiteit, sensitiviteit en voorspeliende waarde van de positieve
en negatieve resultaten van het uitgestelde lichamelijke onderzoek. Ook gingen wij na wat de
resultaten waren indien de 'onduidelijke' beoordelingen als negatief respectievelijk als positief
werden beschouwd. Teneinde de interobservatorvariatie bij het uitgestelde lichamelijk onderzoek
na te gaan, bepaalden wij de kappawaarden voor de patiënten die waren onderzocht door een
hoofdonderzoeker en één van de andere onderzoekers.
Resultaten
Vijfentwintig patiënten hadden een negatief artrogram en vertoonden geen klinische tekenen van
een ligamentaire laesie. Van de overige 135 patiënten bleken er 122 bij operatie een ligamentaire
laesie te hebben; bij 55 was die meervoudig.
Lichamelijk onderzoek binnen 48 uur na het trauma
Er werden 46 patiënten onderzocht. In veel gevallen traden er moeilijkheden op. De
hematoomverkleuring ontbrak vaak, waardoor het onzeker was of de zwelling te wijten was aan
een bloeding of aan oedeem. Vaak was er diffuse pijn en de schuifladetest was veelal
onbetrouwbaar wegens pijn en zwelling. De door het uitvoeren van de schuifladetest opgewekte
pijn werd soms, onbewust, beschouwd als aanwijzing voor ligamentaire schade. Voor dit onderzoek
werd een sensitiviteit gevonden van 71% en een specificiteit van 33%.
71
Lichamelijk onderzoek vijf dagen na het trauma
Indien de 'onduidelijke' beoordelingen werden beschouwd als positief, waren de totaalresultaten
minder accuraat dan indien zij als negatief werden beschouwd. Voor het uitgestelde lichamelijke
onderzoek werd een sensitiviteit gevonden van 96% en een specificiteit van 84%.
Van de zes patiënten bij wie een fout-positieve diagnose werd gesteld, hadden er drie een laesie
van de syndesmose. Van de overige drie had één patiënt een oude ruptuur van het lig. talofibulare
anterius met een verlenging van het geheelde ligament en hadden twee patiënten alleen een
kapselscheur.
De interobservator-overeenkomst vijf dagen na het trauma
De invloed van de ervarenheid van de onderzoekers was beperkt en de interobservatorovereenkomst was goed. De kappawaarden (werkelijke overeenkomst, gecorrigeerd voor toeval,
gedeeld door de potentiële overeenkomst, gecorrigeerd voor toeval) waren respectievelijk 0,5; 0,6;
0,6 en 1,0.
Analyse van de lichamelijke bevindingen
Er was een onmiddellijke zwelling bij 78% van de patiënten met een ligamentaire laesie en bij 55%
van degenen zonder ligamentaire laesie (p = 0,02). Ten tijde van het uitgestelde lichamelijke
onderzoek was er bij de meeste patiënten van beide categorieën nog middelmatige zwelling
aanwezig.
Afwezigheid van de zwelling werd vaker gevonden bij patiënten zonder ligamentaire laesie, terwijl
bij patiënten met een laesie vaker duidelijke zwelling werd gezien (p < 0,01).
Alle patiënten met een bevestigde ligamentaire laesie hadden pijn bij palpatie van de regio van het
lig. talofibulare anterius, terwijl bij de groep zonder ligamentaire laesie 12 van de 38 patiënten
geen pijn bij palpatie van dit gebied hadden (p < 0,01). De specificiteit van de positieve
voorsteschuifladetest was 74% met een sensitiviteit van 86%.
De combinatie van pijn bij palpatie in het gebied van de lig. talofibulare anterius-laesie, laterale
verkleuring als gevolg van een hematoom, en een positieve voorste-schuifladetest, gaven een 95%
incidentie van een definitieve ligamentaire laesie. Als er geen zichtbare verkleuring was en de
voorsteschuifladetest negatief bevonden, werd altijd een intact lateraal ligament aangetroffen.
Slechts 36 van de 160 patiënten pasten niet in één van deze drie categorieën, maar de meeste
hiervan (33) werden correct gediagnosticeerd.
Conclusie
Vergeleken met het onderzoek binnen 48 uur produceerden de onderzoekers met een beperkte
klinische ervaring accuratere resultaten indien het lichamelijke onderzoek vijf dagen na het trauma
werd uitgevoerd.
Uitgesteld lichamelijk onderzoek geeft informatie met een diagnostische kwaliteit die gelijk is aan
die van artrografie en bezorgt de patiënt weinig ongemak.
Onze resultaten en de observaties van Stiel et al. (1994) doen veronderstellen dat bij een patiënt
met een pijnlijke enkel, eerst onderzoek moet worden gedaan om een fractuur uit te sluiten.
Patiënten zonder fractuur dienen dan het advies te krijgen het been hoog te leggen, intermitterend
ijs te gebruiken en zo min mogelijk te lopen. Eventueel kan een drukverband of elastische bandage
worden toegepast. Via lichamelijk onderzoek, vijf dagen later, kan men vervolgens nagaan of er
sprake is van een ligamentaire laesie.
72
Het uitstel van de diagnose, en daarmee van de definitieve behandeling, heeft geen nadelige
invloed op het uiteindelijke herstel, omdat de nu geldende voorkeursbehandeling, in de vorm van
functioneel tapen, kan worden gestart zodra de zwelling is afgenomen.
[97014 -- vert. L. Eenkhoorn]
Copyright 2005 Bohn Stafleu van Loghum, Houten
73
ANKLE ACUTE INJURIES
Karim Khan and Peter Bruker
Olympic Sports Medicine Clinic
Melbourne, Australia
Khan, K., & Bruker, P. (1998). Ankle acute injuries. In: Encyclopedia of Sports Medicine and Science,
T.D.Fahey (Editor). Internet Society for Sport Science: http://sportsci.org. 7 March 1998.
Ligamentous injuries around the ankle joint are among the most common sporting injuries
especially in jumping sports (e.g., basketball, volleyball). They are not always well managed.
Associated injuries are frequently not diagnosed and the rehabilitation of ligamentous injuries
is often inadequate leading to a high rate of recurrence.
Functional Anatomy
The ankle contains three joints. The talocrural or ankle joint is a hinge joint formed between
the inferior surface of the tibia and the superior surface of the talus. The medial and lateral
malleoli provide additional articulations and stability to the ankle joint. The movements at the
ankle joint are plantarflexion and dorsiflexion.
The inferior tibiofibular joint the articulation of the distal parts of the fibula and tibia. The
inferior tibiofibular joint is supported by the tibiofibular ligaments or syndesmosis. A small
amount of rotation is present at this joint. The subtalar joint between the talus and calcaneus is
divided into an anterior and posterior articulation separated by the sinus tarsi. The main roles
of the subtalar joint are to provide shock absorption, to permit the foot to adjust to uneven
ground and to allow the foot to remain flat on the ground when the leg is at an angle to the
surface.
The ligaments of the ankle joint are shown in Figure 1. The lateral ligament consists of three
parts: the anterior talofibular ligament (ATFL) which passes as a flat band from the tip of the
fibula anteriorly to the lateral talar neck; the calcaneofibular ligament (CFL), which is a cordlike structure directed somewhat posteriorly; and the posterior talofibular ligament (PTFL),
which runs posteriorly from the fibula to the talus. The medial or deltoid ligament of the ankle
(not shown) is a strong, fan shaped ligament extending from the medial malleolus anteriorly
to the navicular and talus, inferiorly to the calcaneus and posteriorly to the talus.
Figure 1: Lateral ligaments of the ankle joint.
74
Clinical Perspective
Inversion injuries are far more common than eversion injuries due to the relative instability of
the lateral joint and weakness of the lateral ligaments compared to the medial ligament.
Eversion injuries are seen occasionally. The strong medial ligament requires a greater force to
be injured, therefore, these sprains usually take longer to rehabilitate. Ankle injuries are listed
in Table 1.
Table 1: Ankle acute injuries.
Common

Ligament Sprain
o lateral ligaments
Less Common





Ligament Injuries
o medial ligament
o AITFL sprain
Peroneal Dislocation
Fractures
o lateral / medial / posterior malleolus
o tibial plafond
o base of the 5th metatarsal
o anterior process of calcaneus
o lateral process of talus
o os trigonum
Dislocated Ankle (fracture/dislocation)
Tendon Rupture
o tibialis posterior
o peroneal tendons
Uncommon but not to be Missed



Reflex Sympathetic Dystrophy (post surgery)
Greenstick or Growth Plate Fractures (children)
Ruptured Syndesmosis
The most important component of the assessment of ligamentous injuries is to determine the
degree, if any, of instability present in the joint. This will determine the management of the
injury. A comprehensive rehabilitation program is required in athletes with ligamentous
injuries of the ankle if they are to return to their sport with full functional capacity and avoid
recurrence of the injury.
Occasionally, other structures are damaged in addition to the ligaments. If these are not
recognized and treated, prolonged pain and disability may result. These include fractures
around the ankle joint, osteochondral fractures of the dome of the talus and dislocation of the
peroneal tendons.
75
History
The mechanism of onset is an important clue to the diagnosis. An inversion injury suggests
lateral ligament damage, an eversion injury medial ligament damage. The presence of a
compressive component indicates the possibility of osteochondral injury.
At the time of the injury, the athlete may have heard a snap or tear. Unlike the significance of
a 'snap' or 'pop' in an acute knee injury, this sensation is not of diagnostic significance
The location of pain will give an indication as to the ligaments injured. The most common site
is over the anterolateral aspect of the ankle involving the ATFL. Occasionally in severe
injuries, both medial and lateral ligamentous structures will be damaged.
Most ankle joint injuries are accompanied by swelling. The site of the swelling may give an
indication of the location of the pathology, but the degree of swelling is usually, but not
always a reliable indication of severity.
The degree of disability, both immediately following the injury and subsequently, is an
important indicator of the severity of the injury. The initial management, the use of the RICE
regimen and the duration of restricted weight bearing after the injury should all be noted.
A previous history of ankle injury and an assessment of the quality of the post-injury
rehabilitation programme should be obtained. Subsequent use of protective tape and braces
should be noted.
Examination
Examination of the ankle requires assessment of the degree of instability present and the
grading of the ligamentous injury. Examination should detect functional disability such as loss
of range of motion, reduced strength and reduced proprioception. For illustration of clinical
examination the reader is directed to Clinical Sports Medicine pp 440-2
Investigations
X-ray including A-P, lateral and at least one oblique view should be performed after ankle
sprains in situations where instability is present or when acute bony tenderness is present on
the malleoli or the medial or lateral dome of the talus. X rays of the ankle joint must include
the base of the 5th metatarsal to exclude associated fracture.
An osteochondral fracture may not be apparent on initial X-ray. If significant pain and
disability are present despite appropriate treatment 4 - 6 weeks after an apparent 'routine'
ankle sprain, specialist sports physician or orthopedic surgeon referral is indicated. A
radioisotopic bone scan may be performed to exclude an osteochondral fracture.
Lateral Ligament Injuries
Lateral ligament injuries occur in activities involving rapid changes in direction, especially on
uneven surfaces. They are also seen when contact with another competitor's feet causes
imbalance in jumping or landing. They are one of the most common injuries seen in
basketball, volleyball, netball and most football codes.
76
In the typical inversion and plantarflexion injury, the three parts of the lateral ligament are
usually damaged in order depending on the severity of the sprain. The ATFL is the first
ligament damaged, followed by the CFL and finally the PTFL. Complete tear of all three
ligaments results in a dislocation of the ankle joint and is frequently associated with a
fracture.
In the assessment of lateral ligament injuries, each of the three components of the ligament
must be examined and the overall degree of instability determined. Lateral ligament injuries
are divided into three grades. Grade I corresponds to a minor tear with pain produced by
stressing the ligament, but no laxity. Grade 11 injuries are painful on stressing the ligament
and show some degree of laxity on examination, but have a firm end point. Grade 111 injuries
show gross laxity without a discernible endpoint. Grading of these injuries gives a guide to
prognosis and helps determine the rate of rehabilitation.
The usual mechanism of lateral ligament injury is inversion and plantarflexion. This may be
accompanied by an audible snap, crack or tear. Depending on the severity of the injury, the
athlete may have been able to continue activity immediately or have been forced to rest.
Swelling usually appears soon after the injury, although occasionally it may be delayed some
hours.
Treatment of lateral ligament injuries
The management of lateral ligament injuries of all three grades follows the same principles.
Initial Management
The initial management of lateral ligament injuries requires the RICE regimen. This is
probably the single most important factor in treatment, particularly with Grade I and Grade II
injuries. Many of the problems resulting from ankle sprains are due to the presence of blood
and edema in and around the joint. This restricts the range of motion of the joint and can act
as an irritant causing excessive synovial reaction. As well as ice, compression and elevation, it
is important for the injured athlete to avoid factors which will promote blood flow and
swelling, e.g. hot showers, heat rubs, alcohol, excessive weight bearing.
Reduction Of Pain And Swelling
Pain and swelling can be reduced with the use of electrotherapeutic modalities, e.g., TENS,
interferential, magnetic field therapy. Analgesics may be required. Gentle soft tissue therapy
and mobilization after the first 48 hours also may help to reduce pain. By reducing pain and
swelling, muscle inhibition around the joint is minimized enabling range of motion exercises
to be performed.
Restoration of Full Range Of Motion
The patient may be non weight bearing on crutches for the first 24 hours, but should then
commence partial weight bearing in normal heel-toe gait. It will be necessary from this stage
to protect the damaged joint with strapping or bracing. This will allow partial and ultimately
full weight bearing without danger of aggravating the injury. Accessory and physiological
mobilization of the ankle, subtalar and midtarsal joints should be commenced early in the
rehabilitation process. As soon as pain allows, active range of motion exercises, e.g.
stationary cycling, can be commenced.
77
Muscle Conditioning
Strengthening exercises should be commenced as soon as pain allows. Active exercises
should be performed initially with gradually increasing resistance. Exercises should include
plantar and dorsiflexion, inversion and eversion. Eversion strength is particularly important in
the prevention of future lateral ligament injuries. Weight bearing exercises should be
commenced as soon as possible.
Restoration Of Normal Proprioception
Proprioception is invariably impaired after ankle ligament injuries. Proprioceptive retraining
exercises can be commenced early in the rehabilitation stage and should be gradually
progressed from balancing on one leg to the use of the rockerboard or minitramp and
ultimately to functional activities while balancing.
Functional Exercises
Functional exercises, e.g., jumping, hopping, twisting, figure-of-eight running, should be
commenced when the athlete is pain-free, has full range of motion and adequate muscle
strength and proprioception.
Return To Sport
Return to sport is permitted when functional exercises can be performed without pain during
or after activity. While performing rehabilitation activities and upon return to sport, added
ankle protection is required. This can be provided either with taping or bracing. As both seem
equally effective, the choice of taping or bracing should be made on the grounds of patient
preference, cost, availability and expertise in tape application.
Any athlete who has had a significant lateral ligament injury should have protective taping or
bracing for all future sporting activities. There are a number of methods to protect against
inversion injuries. The three main methods of tape application are stirrups, heel lock and the
figure-of-six. Usually at least two of these methods are used.
Braces have the advantage of ease of fitting and adjustment, lack of skin irritation and
reduced cost compared to taping over a lengthy period. There are a number of different ankle
braces available. The lace-up brace is an effective ankle brace.
Treatment of Grade III Injuries
Treatment of grade III ankle injuries requires initial conservative management over a 6 week
period. If the patient continues to make good progress and is able to perform sporting activity
with the aid of taping or bracing and without persistent problems during or following activity,
surgery may not be required. If however, despite appropriate rehabilitation and protection, the
patient complains of recurrent episodes of instability or persistent pain, then surgical
reconstruction of the lateral ligament, using one of the peroneal tendons or a fibular periosteal
flap, is recommended. Following surgery, it is extremely important to undertake a
comprehensive rehabilitation programme to restore full joint range of motion, strength and
proprioception.
78
The indications for use of nonsteroidal anti-inflammatory drugs in ankle injuries is unclear.
The majority of practitioners tend to prescribe these drugs in all cases of lateral ligament
sprains although evidence of their efficacy in this condition is not convincing. However, it
may be appropriate to commence medication 2-3 days following injury because of the risk of
developing synovitis on resumption of weight bearing.
Medial Ligament Injuries
Medial ligament injuries do not occur as frequently as lateral ligament injuries because the
deltoid ligament requires considerable force to be damaged. Occasionally they may be seen in
conjunction with a lateral ligament injury. Medial ligament injuries may occur with fracture
of the medial malleolus, talar dome or damage to articular surfaces. Medial ligament sprains
should be treated in the same manner as lateral ligament sprains, although return to activity
may be prolonged.
Pott's Fracture
A fracture affecting one or more of the malleoli (lateral, medial, posterior) is known as a
Pott's fracture. It can be difficult to distinguish clinically between a fracture and a moderate to
severe ligament sprain. Both conditions may result from inversion injuries, with severe pain
and varying degrees of swelling and disability.
The management of these fractures involves restoration of the normal relationship between
the superior surface of the talus and the ankle mortise (inferior margins of tibia and fibula). If
this relationship has been disrupted, internal fixation is required.
Isolated spiral fractures of the lateral malleolus (without medial ligament instability) and
posterior malleolar fractures involving less than 25% of the articular surface are very stable.
These fractures can be treated symptomatically with immobilization and crutches in the early
stages for pain relief only.
Lateral malleolar fractures associated with medial instability, hairline medial malleolar
fractures or larger undisplaced posterior malleolar fractures are potentially unstable, but may
be treated conservatively. This involves a below knee cast extending to include the metatarsal
heads. A walking heel may be applied after swelling has subsided (3-5 days). The cast should
be worn for 6 weeks.
Displaced medial malleolar, large posterior malleolar, bimalleolar or trimalleolar fractures, or
any displaced fracture which involves the ankle mortise, should be internally fixed. A
comprehensive rehabilitation program should be undertaken following surgical fixation or
removal of cast. The aims of the rehabilitation program are to restore full range of motion,
strengthen the surrounding muscles and improve proprioception.
Persistent Pain After Ankle Sprain: the "Difficult Ankle"
In most cases of ligament sprain, the patient progresses satisfactorily through the
rehabilitation process with reduction in pain and swelling and improvement in function.
However, there is a significant group of patients who do not progress well and complain of
persistent pain, swelling and impaired function without any indication of improvement 3-6
79
weeks after their injury. In these cases, it is important to consider the presence of one of the
conditions listed in Table 2.
Table 2: Causes of persistent ankle pain following acute injury.











Inadequate rehabilitation
Osteochondral fracture of the dome of the talus
Chronic synovitis of the ankle joint
Chronic ligamentous instability
Sinus tarsi syndrome
Antero-inferior tibiofibular ligament (AITFL) injury
Anterior impingement syndrome
Posterior impingement syndrome
Anterolateral impingement
Dislocation of the peroneal tendons
Other fractures
o Avulsion fracture of the base of the 5th metatarsal
o Fracture of the lateral process of the talus
o Fracture of the anterior process of the calcaneus
o Fracture of the tibial plafond
o Fracture of the posterior process of the talus / os Trigonum
o Reflex sympathetic dystrophy (RSD)
An ankle ligament injury which is inadequately rehabilitated may present with persistent pain
and loss of function. This usually occurs with increased activity levels. The common
problems associated with inadequate rehabilitation are a loss of range of motion in the ankle
joint (especially dorsiflexion), weakness of the peroneal muscles and impaired proprioception.
Management involves restoration of full dorsiflexion by mobilization of the ankle joint, a
programme of strengthening exercises for the peroneal muscles and proprioceptive exercises.
If rehabilitation has been appropriate and symptoms persist, it is necessary to consider the
presence of other pathology. Symptoms of intra-articular pathology include clicking, locking
and joint swelling. Examination may reveal effusion, bony tenderness or swelling at the sinus
tarsi or peroneal tendons. The ankle should be re-assessed for evidence of chronic
ligamentous instability.
Osteochondral Fractures of the Talar Dome
Osteochondral fractures of the dome of the talus which occur in association with ankle sprains
are commonly overlooked. These fractures may occur when there is a compressive component
to the inversion injury, especially with landing from a jump. The dome of the talus is
compressed by the tibial plafond causing damage of the osteochondral surface. The fractures
occur most commonly in the superomedial and the superolateral corners of the talus.
If large, these fractures may be recognized at the time of injury. The fracture site will be
tender and may be evident on X-ray. Usually the fracture is not detected initially and the
patient presents some time later complaining of an unremitting ache in the ankle, despite
80
appropriate treatment for a ankle sprain. The patient often presents with a history of
progressing well following a sprain, but then developing symptoms of increasing pain and
swelling, stiffness and perhaps catching or locking as activity is increased.
References
Anderson, I.F., Crichton, J.K., Grattan-Smith, T., et al. Osteochondral fractures of the dome of the
talus. J. Bone Joint Surg. 71A: 143-52, 1989.
Brukner, P. and K. Khan. Clinical sports medicine. Sydney: McGraw Hill, 1993.
Kannus, P. and P. Renstrom. Treatment for acute tears of the lateral ligaments of the ankle. J. Bone
Joint Surg. 73A: 305-12, 1991.
Vegso, J.J., and E. Harman. Nonoperative management of athletic ankle injuries. Clin. Sports Med. 1:
85-98, 1982.
81
Video Analysis of the Mechanisms
for Ankle Injuries in Football
Thor Einar Andersen,* MD, Tonje Waale Floerenes, stud med, Arni Arnason, MSc,
PT, and Roald
Bahr, MD, PhD
From the Oslo Sports Trauma Research Center, University of Sports and Physical
Education,
Oslo, Norway
Background: Although ankle sprains are frequent in football, little is known about their mechanisms.
Purpose: To describe the injury mechanisms for ankle injuries in male elite football.
Study Design: Prospective cohort study.
Methods: Videotapes and injury information were collected for 313 of 409 matches from Norwegian and Icelandic
elite football during the 1999 to 2000 seasons. Video recordings of incidents that resulted in ankle injuries were
analyzed and cross-referenced with injury reports from the team medical staff.
Results: A total 46 acute ankle injuries were reported to have occurred, that is, 4.5 injuries per 1000 match hours.
Of these, 26 (57%) were identified on the videotapes. Two mechanisms thought to be specific to football were
found: 1) player-to-player contact with impact by an opponent on the medial aspect of the leg just before or at foot
strike, resulting in a laterally directed force causing the player to land with the ankle in a vulnerable, inverted
position; and 2) forced plantar flexion where the injured player hit the opponent’s foot when attempting to shoot or
clear the ball.
Conclusions: Systematic video analysis provides detailed information on the mechanisms for ankle injuries in
football—for lateral ligament sprains and for the condition dubbed “footballer’s ankle.”
Keywords: biomechanics; video recording; footballer's ankle; incidence; ligament injury; anterior ankle
impingement syndrome
Football is responsible for between one-fourth and one-half of all sports-related injuries in Europe.6,22,24,26 A direct
comparison between studies is difficult because of differences in study design and injury definitions, but the risk of
injury is undoubtedly high. The injury incidence among adult male players is estimated to 10 to 35 injuries per
1000 match hours.14,23 Injury severity is also a concern. In fact, in a recent study, Drawer and Fuller13 concluded
that the risk of acute injury in professional football is unacceptably high when evaluated against accepted
occupational health criteria. Thus, attention needs to be directed at how to prevent injuries in football.
Ankle injuries are common among football players, accounting for 11% to 25% of all acute injuries.11,16,21,29,33,41,52
Despite this, to our knowledge no study has examined the mechanisms for ankle injuries in football in detail.
Since football is a contact sport requiring a variety of skills, including running, jumping, passing, shooting, kicking,
dribbling, turning, heading, and tackling, 15,23 the mechanisms may differ from the inversion injuries typically seen
among runners.18
Although the lateral ligament complex is the most commonly injured structure, an injury type thought to be specific
to football has also been described. Morris35 and later McMurray34 originally described a condition referred to as
“athlete’s ankle” and “footballer’s ankle” with talotibial osteophyte formation at the anterior joint capsule. Although
this condition—later also referred to as “anterior ankle impingement syndrome”—is a common cause of anterior
ankle pain,17,38,44 the exact cause is unknown. Three different hypotheses have been suggested to explain the
formation of osteophytes. First, recurrent maximal plantar flexion and stretching of the joint capsule from repetitive
kicking has been suggested to result in traction spurs.8,32,34 Second, repetitive kicking of the football ball is
hypothesized to cause direct damage to the rim of the anterior ankle cartilage, resulting in inflammation, scar
tissue formation, and calcification.49 Finally, repetitive forced dorsiflexion causing minor fractures due to impacts
between the bone surfaces of the anterior tibia and the talus has been suggested to cause exostoses to develop
on the anterior edge of the tibia and talus.39
82
A limitation with epidemiological studies is that the injury information is based on postinjury player interviews or
medical staff reports.2,21,22,36,42 However, determining the injury mechanism based on reports from the injured
player or their medical staff is difficult. This approach may result in recall bias, and since injuries happen quickly,
the player may not even be able to provide an accurate description
of how the injury occurred. Since two players can be expected to be involved in the injury situation, at least in
many cases, the injured player may not always be fully aware of what actually caused the injury.
A more revealing approach may be to examine videotapes of actual ankle injury situations to describe the
mechanisms leading to injury. Thus, the objective of this study was to describe the specific injury mechanisms for
ankle injuries in elite male football using video recordings.
METHODS
Videotapes and injury information were collected prospectively from the Norwegian professional football league
during the 2000 season and from the elite division in Iceland during the 1999 and 2000 seasons.
The Norwegian Broadcasting Corporation (NRK) and TV2 Norway secured a weekly delivery of DVC pro or Beta
SP–quality videotapes from the Norwegian professional football league, and Beta SP–quality videotapes were in
the same way made available from the Sports Department of the Icelandic National Broadcasting Service–
Television. National or regional television-production teams with one to three cameras were responsible for all
recordings in Iceland and most of the recordings in Norway, although 20 matches from Norway were live
broadcasts covered with six cameras.
Video recordings from 313 of 409 regular matches (77%), 174 of 182 (league matches only) in Norway (96%),
and 139 of 227 (121 league and 18 cup matches) in Iceland (61%) were made available from the television
companies. Of these, 296 covered the match in full, whereas for 17 matches the tapes covered 73 minutes on
average (range, 36 to 87 minutes). This corresponds to 464.5 match hours, that is, 10,219 player hours. The
tapes were reviewed to identify incidents, that is, all situations where the match was interrupted by the referee,
one or more players laid down on the pitch for more than 15 seconds, and the player(s) appeared to be in pain or
received medical treatment.1 The incidents, including the play leading up to each of them, were transferred to a
master videotape for further analysis.
Figure 1. Case 3. A, overview of the playing situation; B, close-up of the injured player (in red) dribbling the ball
prior to the tackle; C, the opponent player hits the injured player on the medial side of the right leg, whereupon the
injured player transfers his weight fully to his right ankle while it is in an inverted
position; D, the moment just after the ankle injury.
A
The medical staff of each club collected the injury information on all acute injuries that occurred during the
season. An injury was recorded if the player was unable to participate in training or match play for at least 1 day
following the incident. The incidence of injuries has been expressed as the number of injuries per 1000 match
hours. Injuries were classified as minor when the player could not practice football normally or play matches for 1
to 7 days, moderate if absent for 8 to 21 days, and serious if absent for
more than 21 days.23,30 All players with an A-squad contract were covered by the injury registration. A
standardized injury questionnaire was used, and reports were collected on a monthly basis. The form included
information on the date of injury as well as the time during the match when the injury occurred. Furthermore, the
injury location was registered, and injuries were classified as contusions, sprains, strains, fractures, or lacerations.
Finally, each injury received a specific diagnosis using Orchard codes.37
Each incident identified on the videotapes was crossreferenced with the injury reports from the team medical staff.
In addition, the original tapes were reexamined to find incidents that had not been identified in the first video
review. The recordings of all ankle injuries were transferred to a separate master videotape. Each recording was
edited to include three sequences, that is, the entire playing situation including the play leading up to the injury at
normal speed, one repetition of the injury, and a slowmotion close-up repeat of the injury.
A specific ankle questionnaire was developed to describe the injury mechanism and the events leading up to the
injury. The questionnaire included the case number and the side injured in each case. The variables used in the
questionnaire were defined as follows: 1) the primary injury mechanism: tackling with the foot on the ground,
tackling with the foot in the air, clearing or shooting, running, landing after jump, or other; 2) the movement
intensity of the player at the moment of injury: high intensity (that is, sprinting and moderate intensity running) or
low intensity (that is, jogging, walking, and standing); 3) whether the injured player was actively tackling an
opponent (active) or whether he was being tackled by an opponent (passive); 4) the tackling types used by the
injured player and the opponent: sliding tackle, locking tackle of the foot or leg, stepping, kicking, dribbling, or
other; 5) whether it was a late tackle (that is, whether the tackle occurred after the ball had been passed by the
injured player); 6) contact with another player: before the injury, at the time of injury, after the injury, or no contact;
7) the main
Figure 2. Case 6. A, overview of the playing situation. B, close-up from a slightly different view. The injured player
(in white) has passed the ball and the opponent player makes a sliding tackle and hits the
injured player on the medial side of the left leg (late tackle). C, the injured player transfers his weight fully
to his ankle while this is in an inverted position. D, the moment just after the ankle injury.
A
83
direction of ankle motion: eversion (pronation, external rotation, dorsiflexion), inversion (supination, internal
rotation, plantar flexion), forced plantar flexion, or could not be evaluated; 8) point of impact on the injured player:
medial side of the ankle or leg, lateral side of the ankle or leg, forefoot of the injured player, or other; 9) position of
the injured foot at the time of injury: on the ground or in the air; 10) degree of weightbearing at the time of injury:
full, moderate, or minimal; and 11) decision made by the match referee: no foul, free kick for or against the injured
player, and whether the free kick resulted in a yellow or red card.
The master videotape was analyzed independently by two experienced specialists in sports medicine (TEA and
RB). Disagreements were discussed in a consensus meeting, where the video recordings were reevaluated and a
final decision was made.
RESULTS
Incidents and Injuries
During the 313 matches available on videotape (174 from the Norwegian professional league and 139 from the
Icelandic elite division), 712 incidents were recorded (425 from Norway and 287 from Iceland), that is, 69.5
incidents per 1000 match hours (75.5 per 1000 match hours in Norway and 62.5 in Iceland). A total of 297 acute
injuries were reported to have occurred during the same matches by the
team medical staff (121 from Norway and 176 from Iceland). This corresponds to an incidence of 29.1 injuries per
1000 match hours (21.5 per 1000 match hours in Norway and 38.4 in Iceland). Of the 297 acute injuries reported,
46 (15%) were ankle injuries (18 from Norway and 28 from Iceland), which corresponds to an incidence of ankle
injuries of 4.5 per 1000 match hours (3.2 per 1000 hours in Norway and 6.1 in Iceland). Of these ankle injuries, 26
(57%) were identified on the videotapes (10
from Norway and 16 from Iceland).
Of the 26 ankle injuries, 23 were classified as sprains and 3 as contusions (cases 8, 15, and 19; see Table 1).
Video Analysis
The video analysis of the 26 ankle injuries showed that 14 occurred during tackling, 4 during clearing or shooting,
4 during running, and 2 during landing after heading, whereas 2 were classified as other injury mechanisms
Figure 3. Case 4. A, overview of the playing situation. B, close-up of the situation. The injured player
(in red) tries to avoid a tackle with the opponent player by jumping over him. C, opponent player hits the injured
player on the medial side of the right leg at the moment the foot hits the ground. He tries to
avoid the ankle injury by outwardly rotating the knee. D, the ankle is forced into an inverted position, the knee
position can no longer compensate, and the player puts his full weight on it.
TABLE 1
Results From Video Analysis of the Mechanisms for Ankle Injuries in Elite Footballa
Case
numb
er
Primary
mechani
sm
Injured
player
Late
tack
le
Action of
injured
player
Timing of
contact
Injury
mechani
sm
Contact
Location
of contact
Foot
location
1
2
3
4
5
6
7
8
9
10
Tackling
Tackling
Tackling
Tackling
Tackling
Tackling
Tackling
Tackling
Tackling
Tackling
Passive
Passive
Passive
Passive
Passive
Passive
Passive
Passive
Passive
Passive
Yes
Yes
Yes
Yes
Yes
Yes
No
No
No
No
Dribbling
Dribbling
Dribbling
Dribbling
Dribbling
Passing
Dribbling
Dribbling
Receiving
Receiving
Before
During
During
During
During
During
During
During
During
During
Invers.
Invers.
Invers.
Invers.
Invers.
Invers.
Invers.
Invers.
Invers.
Evers.
Foot/leg
Foot/leg
Foot/leg
Foot/leg
Foot/leg
Foot/leg
Foot/leg
Foot/leg
Foot/leg
Foot/leg
Medially
Medially
Medially
Medially
Medially
Medially
Medially
Medially
Forefoot
Forefoot
11
12
13
14
15
16
17
18
Tackling
Tackling
Tackling
Tackling
Shooting
Shooting
Shooting
Shooting
Active
Active
Active
Active
Active
Active
Active
Active
Yes
No
No
Yes
Yes
Yes
Yes
No
Tackling
Tackling
Tackling
Tackling
Kick
Kick
Kick
Kick
During
During
During
During
During
During
During
During
Invers.
Invers.
Invers.
Invers.
Cannot
be seen
Forced
plantar
flexion
Forced
plantar
flexion
Forced
plantar
flexion
Foot/leg
Foot/leg
Foot/leg
Foot/leg
Foot/leg
Foot/leg
Foot/leg
Foot/leg
Medially
Medially
Medially
Other
Medially
Forefoot
Forefoot
Forefoot
Severity
of injury
Ground
Ground
Ground
Ground
Ground
Ground
Ground
Ground
Ground
Ground
Decision
made by
the
referee
No foul
Yellow
Yellow
No foul
No foul
Foul for
Yellow
Yellow
No foul
No foul
Ground
Ground
Ground
Ground
Air
Air
Air
Air
No foul
No foul
No foul
Yellow
No foul
Yellow
No foul
No foul
Normal
Minor
Minor
Normal
Minor
Severe
normal
Severe
84
Minor
Normal
Normal
Normal
Minor
Minor
Minor
Minor
Severe
Minor
19
20
21
22
23
24
Running
Running
Running
Running
Landing
Landing
Passing
Running
Running
Running
Heading
Heading
None
Before
During
None
Before
Before
25
26
Other
Other
Dribbling
Running
None
During
Invers.
Invers.
Invers.
Invers.
Invers.
Cannot
be seen
Invers.
Cannot
be seen
Ground
Ground
Ground
Ground
Ground
Ground
Ground
Ground
No foul
Red
No foul
No foul
Foul
against
No foul
No foul
No foul
The horizontal lines indicate the grouping of the injuries into tackling situations, situations in which the injured player was
clearing or shooting the ball, running, landing, and
other situations.
a
(Table 1). Midfielders were injured in 14 cases, strikers in 4, and defenders in 7. The referee awarded no foul in
17 cases, whereas 6 incidents led to a free kick and yellow card, 1 to a free kick and red card, and 1 to a free kick
only for the injured player. In 1 incident, a free kick was awarded against the injured player. Of the 11 incidents
classified as late tackles (Table 1), a foul was called in 5 incidents.
Four of these led to a yellow card.
Tackling Injuries. In 10 of the 14 tackling incidents, the injured player was tackled by an opponent. Of these, 6
were classified as a late tackle; that is, the player was tackled after the injured player had passed the ball. The
injured player was dribbling the ball in 7 cases and receiving a pass or passing the ball in 3 cases. In 4 of the
tackling incidents, the injured player was actively tackling; 2 of them were classified as late tackles. Of the 14
incidents, all except 1 involved contact between the injured player and the opponent at the moment of injury. Of
the 14 tackling injuries, all except 1 were the result of an inversion mechanism. They occurred with the foot of the
injured player touching the ground and with contact between the foot of the opponent and the leg of the injured
player. In 11 cases, the injured player was hit on the medial side of the foot, whereupon the injured player
transferred his weight fully to his ankle while it was in an inverted position (Figs. 1 to 4). In 11 of the 14 incidents,
the injured player was moving at high intensity, whereas in 3 he was moving at low intensity. In all cases, the
injured player had some part of the injured foot on the ground, and all of the injured players except one were
transferring all of their weight to the injured foot at the moment of injury.
Kicking Injuries. Four injuries occurred when the player was attempting to clear the ball or shoot while an
opponent tried to block the ball (Fig. 5). In all cases, the injured player was the active part, hitting the opponent’s
leg while kicking with the foot in an equinus position, resulting in a forced plantar flexion in three cases. The foot
position of the final case could not be assessed from the video. All except from one were classified as late
tackles. In all case incidents, the injured player was moving with high intensity.
None of the players was disturbed at the time of injury.
Running Injuries. Four injuries occurred while the player was running: two while involved with an opponent player
and two while alone. All injuries happened when the injured player placed his foot on the ground while it was in an
inverted position. The injured player was moving with high intensity at the moment of injury in all four cases.
Other Injuries. Two injuries occurred during landing after a heading duel with an opponent. The final two incidents
resulted from other mechanisms. In one case, the
Figure 4. Case 7. A, overview of the playing situation; B, injured player (in blue) is trying to shield the ball from
the opponent; C, opponent hits the ball; D, injured player is hit on the medial side of his right leg,
forcing it into inversion before bearing weight on it.
A
player was alone and appeared to simply stumble after having received the ball, perhaps resulting from an
uneven pitch. The other incident occurred after the injured player was kicked unintentionally in the foot by a
teammate.
DISCUSSION
The aim of this study was to describe the mechanisms of ankle injuries in football based on an analysis of video
recordings of injuries from Norwegian and Icelandic elite football. A main finding was—as expected—that most
injuries resulted from inversion trauma. However, in most cases involving player-to-player contact, accounting for
about half of all injuries, the indirect cause of injury appeared to be contact to the medial aspect of the lower leg or
ankle. Most likely, this laterally directed force did not produce the injury itself but caused the player to land with
the ankle in a vulnerable, inverted position. The other
main finding was that we observed four cases in which the injured player hit the opponent’s foot with a full-force
kick, resulting in forced plantar flexion of the ankle. This mechanism may explain the condition dubbed footballer’s
ankle.
Methodological Considerations
When interpreting the results of the present study, some obvious limitations must be considered. First, although
we had information on the approximate time during the match each ankle injury occurred, we were able to identify
85
Severe
Normal
Minor
Minor
Severe
Normal
Normal
Normal
only 57% of the acute ankle injuries that were reported by team medical staff to have occurred, even after close
scrutiny of the tapes. This leads us to believe that the remaining 43%
of the injuries resulted from minor trauma and mechanisms that may have been different from those identified on
tape. At least they were more difficult to detect, possibly because they did not result from player-to-player contact
or because they occurred outside camera view.
Second, the video recordings used in this study were from matches only. Therefore, only mechanisms for ankle
injuries in match play could be evaluated. However, previous studies2,14,16,20,23,31,36 have shown that most football
injuries in elite players occur during match play, as was the case in the present study (data not shown). Whether
the mechanisms for training and match injuries differ is unknown, although we would expect there to be fewer late
tackles and less foul play during training than in match play.
Figure 5. Case 18. A, overview of the playing situation. B, close-up of the situation prior to the contact.
Player to be injured (in white) prepares to hit the ball with a forceful kick while opponent comes in
with a sliding tackle. C, opponent player hits the ball before the injured player kicks maximally with his
right foot, hitting the opponent’s foot, and gets injured. D, moment just after the injury.
Another limitation is that the assessment was subjective and qualitative and in some cases based on tapes with
less than optimal quality and a limited number of views available. Nevertheless, the main mechanism for tackling
injuries appeared to be remarkably consistent between cases, and it was easy to agree on the description and
classification of mechanisms. Even keeping the limitations mentioned in mind, a systematic analysis of injury
situations from video would seem to be the obvious approach
toward a more detailed understanding of the mechanisms for sports injuries, providing more reliable information
than retrospective player interviews.
However, it should be noted that this study was conducted on elite male football players. There may be
differences in injury mechanisms between these players and other player populations (for example, younger
players, female players) that warrant attention in future studies.
Injury Mechanisms
The majority (88%) of the ankle injuries we were able to identify on video resulted from contact with an opponent.
This is in contrast to a study among youth and adult players participating at various competition levels in one
football club in Denmark.36 Based on reports from the coaches, they found that ankle sprains occurred equally
during tackling and running. However, Chomiak et al.11 in a similar
study in the Czech Republic found that 68% of the ankle injuries were due to body contact, and in a recent study
among professional English football players 59% of the ankle injuries were reported to be caused by contact
mechanisms. 52 Although a direct comparison of the results is difficult, it seems reasonable to conclude that
challenging ball possession is a situation with a high risk for ankle injuries.
An inversion mechanism was found in all but one of the tackling injuries, all running injuries, and in one of two
after landing after a heading duel. Based on questionnaire data, inversion of the ankle has been described to be
the most frequent injury mechanism for ankle sprains in football11,47 and among runners.18 Studies of ankle
sprains in volleyball have shown the main mechanism to be landing on the foot of an opponent or teammate after
blocking or attacking at the net.4 From the present study, it appears
that there is a specific mechanism for football injuries as well. The injured player received a laterally directed hit
on the medial side of the ankle or lower leg, whereupon landing in a supinated position led to an inversion injury
(Fig. 6). In some cases, it appeared that the players tried to avoid the ankle injury by flexing their knee and
externally rotating their thigh to avoid putting weight on the ankle joint. However, when he no longer could
compensate, the player had to put weight on the ankle and an injury occurred.
Ankle inversion torques that result in lateral ligament lesions are thought to arise primarily in situations in which
the ankle goes through a transition from an unloaded to a loaded condition.46 Other biomechanical studies have
shown that the anterior talofibular ligament (ATFL) is the first ligament to be tensed and so the first to rupture
when forced inversion of the ankle occurs. 7,10
Broström9 and van der Ent48 have presented data from surgery showing that half of all ankle sprains were isolated
ATFL tears and about 25% were combined ATFL and calcaneofibular ligament tears. In other words, the findings
from clinical studies, biomechanical research, and surgical findings correspond well with the present findings,
suggesting that the typical football mechanism is an inversion sprain after a laterally directed hit on the medial
side of the ankle or lower leg.
In three of the four incidences classified as “clearing or shooting,” the injured player was actively kicking with the
foot placed in a forced plantar flexion. It may be hypothesized that this is the mechanism whereby footballer’s
ankle occurs, even if the number of cases is small in this study. McMurray,34 after Morris35 first had described this
specific condition, suggested that kicking the ball with the foot usually
in a position of full extension leads to strain on the anterior capsule of the ankle joint, eventually giving rise to
osteophyte formation. The mechanism for footballer’s ankle is controversial, and three theories exist to explain the
formation of osteophytes. Recurrent maximal plantar flexion and stretching of the joint capsule from repetitive
kicking is suggested to result in traction spurs.8,32,34 Van Dijk et al.49 suggested that repetitive kicking of the
football ball caused direct damage to the anterior joint cartilage, resulting in inflammation, scar tissue formation,
and calcifica-
86
Figure 6. Typical mechanism for lateral ligament injury in football: opponent contact to the medial side of the leg,
causing the player to put weight on an inverted ankle. Illustration reproduced with permission by ©Oslo Sports
Trauma Research Center/T. Bolic.
tion. Finally, repetitive forced dorsiflexion causing minor fractures due to impacts between the bone surfaces of
the anterior tibia and the talus has been suggested to cause exostoses to develop on the anterior edge of the tibia
and talus.39 The present video analysis suggests that the first theory, with forced plantar flexion, may be the cause
of footballer’s ankle (Fig. 7).
Perspectives for Injury Prevention
Ankle sprains can be prevented.5,43,51 The protective effects of taping and bracing have been shown persuasively
in football, although only for players with previous ankle injury.42,45 The most important risk factor for ankle injuries
is history of a previous sprain.3 Neuromuscular function is reduced in athletes with persistent instability complaints
after injury25,28,46 and even in the immediate recovery period
after an acute injury.27 How tape and orthoses work is uncertain, but they may simply enhance neuromuscular
control of the ankle joint. This view is corroborated by the fact that their effect is limited to players with previous
injury,40,42,45 where proprioceptive function is reduced,25,28,45 and that orthoses do not seem to restrict inversion
enough to substantiate their prophylactic effect.12,50 If the protective effect were mechanical, one would expect an
effect in healthy ankles as well. It is also important to note that neuromuscular control in chronically unstable
ankles can be restored with a balance board training program19 and that such a program appears to reduce the
risk of reinjury at the same level as healthy
ankles.45
The present study shows that a significant proportion of ankle injuries are contact injuries resulting from a medial
blow to the ankle or lower leg, a mechanism where neither balance training nor ankle support would be expected
to have a protective effect. However, as mentioned above, it may be that the laterally directed blow is not the
direct cause of injury but merely serves to put the ankle in a vulnerable
position when landing or running. Thus, increased neuromuscular control through training or bracing could aid the
player in correcting foot position before putting weight on the ankle, at least in some cases.
The role of fair play and proper refereeing is frequently discussed in injury prevention. Based on our assessment
of the videotapes, there were a number of cases in which injuries resulted from late tackles without penalty to the
offender. In some cases, our impression was that these were intentional, professional fouls. Although we
acknowledge that the task of enforcing the laws of the game is difficult—
the match referee not having the benefit of video replay— we would argue that the present findings show that
there is a need for stricter enforcement of the laws of the game in tackling situations. A number of measures can
potentially be effective, including improved referee training focusing on situations with injury potential, immediate
or delayed video review by the match referee in such cases, more specific
wording of the laws of the games regarding late tackles, and stricter penalties for this type of rule violation. It
appears that free kicks or even yellow cards do not have the desired deterrent effect on player behavior, and we
therefore suggest that the introduction of timed suspensions (for example, 10 minutes for dangerous play) be
considered. Such suspensions would—unlike free kicks or yellow cards—in many cases directly influence match
outcome and may be a more effective disincentive on dangerous foul play.
CONCLUSION
This study showed that a thorough video analysis seems to give detailed information about mechanisms of ankle
injuries in football. The most frequent injury mechanism found was player-to-player contact with impact on the
medial aspect of the lower leg or ankle of the injured player. Most likely, this laterally directed force caused the
player to land with the ankle in a vulnerable, inverted position. In addition, we observed four cases in which the
injured player hit his opponent’s foot, resulting in forced plantar flexion of the ankle. This mechanism may explain
the condition dubbed footballer’s ankle.
Figure 7. Probable mechanism for development of footballer’s ankle. Illustration reproduced with permission by
©Oslo Sports Trauma Research Center/T. Bolic.
ACKNOWLEDGMENT
We are indebted to Albin Tenga, MSc, and Lasse Nettum for video analysis and editing and to the team physical
therapists and physicians in Iceland and Norway for collecting the injury information. We appreciate the
assistance of NRK, TV2 and Icelandic Television in making the videotapes from league matches available for
analysis. Oslo Sports Trauma Research Center has been established through generous grants from the Royal
Norwegian Ministry of Culture, the Norwegian Olympic Committee and Confederation of Sport, Norsk Tipping AS,
and Pfizer.
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90
The Football Association Medical Research
Programme: an audit of injuries in
professional football: an analysis of ankle
sprains
C Woods, R Hawkins, M Hulse and A Hodson
The Football Association, Medical and Exercise Department, Lilleshall National Sports
Centre, Shropshire, UK
Correspondence to:
Caroline Woods, Lilleshall National Sports Centre, Nr Newport, Shropshire TF10 9AT, UK;
The FA.com
caroline.woods@TheFA.com
Accepted 23 August 2002
ABSTRACT
Aim: To conduct a detailed analysis of ankle sprains sustained in English professional
football over two competitive seasons.
Methods: Club medical staff at 91 professional football clubs annotated player injuries. A
specific injury audit questionnaire was used together with a weekly form that documented
each club’s current injury status.
Results: Completed injury records for the two competitive seasons were obtained from 87%
and 76% of the participating clubs. Ankle ligament sprains accounted for 11% of the total
injuries over the two seasons, with over three quarters (77%) of sprains involving the lateral
ligament complex. A total of 12 138 days and 2033 matches were missed because of ankle
sprains. More sprains were caused by contact mechanisms than non-contact mechanisms (59%
v 39%) except in goalkeepers who sustained more non-contact sprains (21% v 79%, p<0.01).
Ankle sprains were most often observed during tackles (54%). More ankle sprains were
sustained in matches than in training (66% v 33%), with nearly half (48%) observed during the
last third of each half of matches. A total of 44% of sprains occurred during the first three
months of the season. A high number of players (32%) who sustained ankle sprains were
wearing some form of external support. The recurrence rate for ankle sprains was 9% (see
methodology for definition of reinjury).
Conclusion: Ankle ligament sprains are common in football usually involving the lateral
ligament complex. The high rate of occurrence and recurrence indicates that prevention is of
paramount importance.
Keywords: ankle; football; injury; sprain
91
Abbreviations: ATFL, anterior talofibular ligament; CFL, calcaneofibular ligament
Ankle sprains (especially those involving the lateral ligament complex) have often been
reported as the most common injuries in sport.1–6 It has been suggested that such injuries are
usually sustained in sports involving running,2 cutting,2 jumping,2,7 and contact with other
players,8,9 and this partly explains the high incidence of ankle sprains in football.10–12 Ankle
sprains in this population have been reported to have a high recurrence rate.11,13–15
The findings of the initial Football Association Audit of Injuries study were consistent with
these findings.16 Over two seasons, the authors observed that 17% of all injuries were to the
ankle, the same figure being reported by Ekstrand and Gillquist.11 Ekstrand and Tropp13 found
that ankle sprains comprised 19% of all injuries. Sandelin et al17 observed that 75% of ankle
injuries were ligament sprains (mostly lateral ligament complex), whereas Hawkins et al16
reported this figure to be 67% (80% being to the lateral ligament complex). Hawkins et al16
found that a total of 76% of ligament sprains that recurred during the same season were to the
ankle. Given the high incidence of ankle sprains, the authors suggested that prevention and
rehabilitation of ligament sprains warranted further investigation.
As a follow up to the initial study, the aim of this study was to undertake a detailed analysis of
the data on ankle sprains. Information on incidence, time lost, mechanism of injury, use of
external support, and timing of ankle sprains could help to suggest the best methods of
preventing and rehabilitating such injuries.
METHODS
Player injuries were prospectively reported from July 1997 through to the end of May 1999
inclusive. A total of 91 of the 92 football clubs from the English football leagues (Premier and
Football League) committed themselves to the project. Injuries were recorded by club
physiotherapists and/or doctors on a specific player injury audit questionnaire designed for
this study. Injury audit questionnaires for players who had returned to full
training/competition during a particular week were returned weekly together, with a form
indicating which players had been absent and the number of days and competitive matches
each had missed that week. Before the study, medical staff from clubs attended a briefing day
and were issued with guidance notes on how to complete the questionnaires. Only
professional players with a squad number were involved in the study. Participants were asked
to complete a consent form, and each club provided details of their squad at the beginning of
each season. Table 1 presents the information obtained. New players who joined the club
were included, and players leaving clubs were omitted from the study if they did not stay
within one of the four English leagues.
Table 1 Division, playing position, and age distribution of the cohort at the beginning of the
study
No
%
618
26
Division
Premier
92
1st
712
30
2nd
550
23
3rd
496
21
Total*
2376
100
Goalkeeper
223
9
Defender
817
34
Midfielder
739
31
Forward
597
25
Total*
2376
99
17–22
970
41
23–28
817
34
29–34
508
21
35+
81
3
Total*
2376
99
Playing position
Age distribution
*Percentage totals may be subject to rounding errors associated with individual
components.
A recordable injury was defined as one sustained during training or competition and which
prevented the injured player from participating in normal training or competition for more
than 48 hours (not including the day of the injury). Injuries unrelated to football were not
included, nor was any absence resulting from illness. Injuries acquired during international
duty were included because details of such injuries were generally reported back to club
medical staff. The severity of each injury was defined as slight, minor, moderate, or major
depending on whether the player was absent from training or competition for two to three
days, four to seven days, one to four weeks, or more than four weeks, respectively. Reinjury
was defined as an injury of the same nature and location involving the same player in the
same season. The dominant foot was defined as the predominant foot used for kicking a ball.
Data were analysed using SPSS (Chicago, Illinois, USA). Descriptive and comparative data
are presented. The 2 significance test was used to investigate differences, and significance
was accepted at p<0.05 level. All players agreed to participate in the study, and there were no
drop outs during the study period.
RESULTS
93
Of the 91 clubs starting the study, completed injury records for the entirety of the 1997/1998
and 1998/1999 competitive seasons were attained from 87% and 76% respectively. During the
study period, 1011 ankle injuries were documented, comprising 17% of the 6030 total number
of injuries sustained over the two seasons
Table 2 displays the nature of all ankle injuries. Ankle ligament injuries (sprains) accounted
for 11% of the total injuries sustained over the two seasons. There was no significant
difference between the incidence of dominant and non-dominant ankle sprains based on
expected values (56% v 42%). No significant differences in the incidence of ankle sprains
between Premier, 1st, 2nd, and 3rd divisions were observed.
Table 2 Nature of ankle injuries
Nature
No
%
Sprain and rupture
677
67
Tissue bruising
79
8
Tendonitis and paratendonitis
65
6
Inflammatory synovitis
31
3
Fracture
25
3
Capsular tear
21
2
Strain
21
2
Other*
74
7
Not specified
18
2
Total
1011
100
*Other includes periostitis, dislocation, chondral lesion, muscular contusion, tendon
rupture, cut, overuse, and bursitis.
Table 3 shows the medical classification of ankle sprains. Most involved injury to some
portion of the lateral ligament complex, that is the anterior talofibular, calcaneofibular, and
posterior talofibular ligaments (77%).
Table 3 Medical classification of ankle ligament injuries
Name of ligament
No
%
Anterior talofibular
493
73
Medial
97
14
94
Unspecified
28
4
Anterior tibiofibular
23
3
Calcaneofibular
14
2
Posterior talofibular
13
2
Other*
5
1
Missing
4
1
Total
677
100
*Other includes interosseous membrane and posterior tibiofibular ligament.
Table 4 shows the diagnostic investigations performed on ankle sprains. Only six players
underwent some form of surgery, and 19 players had injections.
Table 4 Diagnostic investigation of ankle sprains
Nature
No
%
x Ray
59
9
MRI
12
2
x Ra+MRI
3
0.4
Ultrasound
1
0.1
Arthroscopy
1
0.1
x Ray+ultrasound
1
0.1
None
600
89
Total*
77
101
components.
One third of ankle sprains were sustained during training and two thirds during matches; there
was no significant difference between the observed and expected incidence of ankle sprains
based on the percentage of total match and training injuries reported. Player to player contact
was responsible for 59% of injuries, and 39% were non-contact injuries. Tackling (36%) and
being tackled (18%) were the most common mechanisms of sustaining an ankle sprain. Figure
1 displays the non-contact mechanisms of ankle sprains: 77% of non-contact sprains were
caused during landing, twisting and turning, and running. Ankle sprains in goalkeepers were
95
the result of significantly more non-contact mechanisms of injury than contact mechanisms
(79% v 21%, p<0.01). The most common mechanisms of injury for this position were landing
(36%), twisting/turning (21%), and diving (10%).
Figure 1 Mechanism of non-contact ankle sprains.
The total number of days that players were absent over the two seasons was 12 138, and a
total of 2033 matches were missed. A total of 83% of the ankle sprains required players to
miss one month or less.
Figure 2 shows the timing of match injuries. A total of 48% of injuries were sustained during
the last third of the first and second halves of the match. There was no significant difference
between the number of ankle sprains sustained in the first and second halves of matches.
There was no significant difference between the timing of contact and non-contact ankle
sprains during matches or training.
Figure 2 Timing of ankle sprains sustained during match play.
Figure 3 shows the number of ankle sprains during each month of the season. During the first
three months of the season, 44% of ankle injuries were sustained (p<0.01).
96
Figure 3 Month in which injury occurred: ankle sprains and all injuries.
Table 5 shows the number of players wearing external support to the ankle. In 32% of
injuries, players had been wearing some form of external support.
Table 5 Type of external support worn by players who sustained ankle sprains
No
%
No support
336
50
Taping
167
25
Joint support
46
7
Missing
128
19
Total*
677
101
components.
The reinjury rate for ankle sprains was 9%, whereas the average reinjury rate for all injuries
was 7%. Although not significant, there were more non-contact reinjuries than initial injuries
(47% v 39%). The average number of training days missed and the average number of
matches missed per ankle sprain for reinjuries and initial injuries did not differ significantly
(19 days and four matches v 18 days and three matches).
DISCUSSION
Of all the injuries sustained over the two seasons, ankle injuries were responsible for 11%.
This figure is lower than most other studies, with figures of 15%,18 22%,12 and 32%19 being
reported. The differences in injury definition and methodology18,20,21 makes comparison
97
between studies difficult and may help explain differences in the results. For example, some
studies record injury rate per 1000 hours. However, in this study, the exposure of players to
training and matches was not measured, therefore injury rate could only be reported in
absolute terms. Also, we did not include any injuries where players missed training for less
than 48 hours, whereas other studies have used the definition that an injury is any incident that
causes a player to miss the next scheduled game or practice.11–13 On consultation with doctors
and physiotherapists working in professional football, it was felt that the definition used in the
present study was more appropriate. It should also be noted that the results of this study are
based on the diagnoses of individual club medical personnel, which may vary from
practitioner to practitioner.
We found that a sprain was, by far, the most common type of injury to the ankle (67%). Ankle
sprains most often involved the lateral ligament complex (77%). Lewin12 also found the lateral
ligament to be the most commonly injured structure (67%). This may be because of the
relative shortness of the medial malleolus and the natural tendency for the ankle to go into
inversion rather than eversion.5 We observed involvement of the anterior talofibular ligament
(ATFL) in 73% of cases. Other authors have also found the ATFL to be the most commonly
sprained ligament,6 with Sitler et al22 reporting that 66% of the ligamentous injuries of the
ankle were to the ATFL. A possible reason for the high incidence of injury to the ATFL could
be that it has a lower load to failure than the calcaneofibular ligament (CFL). 2 Clanton and
Porter23 quoted values of 138 N and 345 N for the ATFL and CFL respectively. Secondly, in
plantarflexion, the ATFL is relatively taut, whereas the CFL is relatively loose; in
dorsiflexion, the converse is true.23 This would fit with the common mechanism of injury to
the lateral ligament, which typically involves the foot and ankle just at the moment of loading
with a plantarflexion and inversion force.23–27
Injuries to the medial or deltoid complex accounted for only 14% of ankle sprains. Clanton
and Porter23 stated that medial ligament complex injuries occur in 10% of all ankle sprains;
however, their review of ankle sprains included many different sports. It is hardly surprising
that the incidence of medial ligament complex sprains in our study was higher than 10% given
that the demands of soccer include kicking with the inside of the foot and ankle as well as
receiving tackles to this area.
This study shows that the anterior and posterior tibiofibular ligament and interosseous
membrane were injured in 4% of sprains. These structures generally constitute the
syndesmosis of the ankle making this value comparable to that of Renström and Konradsen,27
who reported a 3% incidence for isolated syndesmosis injuries.
In our study, 11% (77) of ankle sprains were diagnostically investigated, mostly by x ray
examinations (59). According to the Ottawa strategy for ankle injuries,28 radiographs should
be taken if there is bone tenderness at the tip or posterior aspect of the lateral malleolus, at the
tip or posterior aspect of the medial malleolus, at the navicular tuberosity or base of the fifth
metatarsal, or if the patient is unable to weight bear immediately after the injury and at the
initial examination. This system can then be used to reduce the use of radiographs.
A low number of players (6) had surgery for their ankle sprains. This may be because
functional non-operative treatment is the accepted choice for grade I and grade II ankle
sprains.27 In the case of grade III sprains, the treatment is less clear—that is, whether to
immobilise in a cast, to operate, or to allow early controlled mobilisation. Kuwada9 stated that,
98
when conservative measures have been exhausted and the patient is not satisfied with his or
her condition, surgical correction is a reliable and viable treatment.
Our results show that more ankle injuries were sustained to the dominant side than the nondominant side, although the difference was not significant based on expected incidence. Other
studies have shown significant differences.11,29,30 It could be expected that most sprains would
be to the dominant side, as the main mechanisms of injury discussed previously generally
involve the dominant leg.
More contact than non-contact mechanisms of injury were observed (59% v 39%). Árnason et
al18 also found contact ankle sprains to be more common than non-contact (69% v 31%).
Similarly they found that "tacklings", which presumably includes tackling and being tackled,
to be the major mechanism of injury (62%); in comparison, we observed this value to be 54%.
Non-contact mechanisms were most commonly landing, twisting and turning, and running.
The only positional variation in mechanism of injury was that goalkeepers sustained
significantly more non-contact injuries (namely twisting and turning, landing, and diving).
This would correlate with the functional profile of a goalkeeper as they are regularly
performing these activities as part of their positional requirements. The mechanism of injury is
vital from the point of view of functional rehabilitation programmes and in devising strategies
for the prevention of reinjury. It has been suggested that athletes be trained and rehabilitated in
potential positions of injury.26,31 If this principle is applied to football, activities involving
jumping, landing, cutting and turning, and running could be performed during late stage
rehabilitation and preventive protocols to maximise ankle stability during such manoeuvres.
Contact positions of injury can also be used, but as this generally involves tackling, it may be
more difficult to simulate and control safely. Laskowski et al32 stated that sport specific
training is crucial in regaining proprioception to "hard wire the proprioceptive pathways and
solidify a neuromuscular engram specific to these activities."
According to Hawkins et al,16 the impact of an injury on a club can be considered in relation
to its severity and the number of potential competitive matches missed. We observed that 12
138 days and 2033 matches were missed because of ankle sprains, which equates to an
average of 18 days and three games missed per sprain. Ekstrand and Gillquist30 reported that
players were absent from practice on average for four weeks after an ankle sprain, but the
number of players in their study was much smaller than in the present one. In this study, 83%
of ankle sprains had a rehabilitation period of less than one month. This suggests that most
ankle sprains are not severe, and it is the incidence rather than severity of ankle sprains that
makes them problematic injuries. It also suggests that the rehabilitation period was rather
short, which may explain the higher than expected reinjury rate for ankle sprains compared
with total injuries (9% v 7%), as the injury may not have had enough time to heal completely.
Houglum33 stressed the importance of understanding the phases and timing of healing for
appropriate, efficient, and effective rehabilitation. There is no uniform consensus on how long
injured ligaments take to reach normal tensile strength; figures range from 16 weeks to 40–50
weeks for a return to 85–95% of normal tensile strength.33 With periods of rehabilitation being
much shorter than the duration of ligament healing, players may have returned to full function
without full tensile strength of the ligament. Applying stress to collagen in the maturation
phase helps to organise the collagen fibres, enhancing the strength of the scar.33 This may
present a case for continuing treatment of the ligament during the maturation and remodelling
stage even when the player has returned to full training. This would ensure that the ligament
regains as much strength and organisation as possible.
99
Konradsen et al34 monitored changes in ankle eversion strength and sensorimotor control
functions after acute ankle inversion injury. They found that 12 weeks after the injury, an
increased error in accuracy of ankle position was still present compared with the healthy
ankle. It took six weeks for normalisation of eversion strength. These findings justify
continued proprioceptive and strength type training even after players have returned to play.
Tropp et al35 recommended wobble board training after return to play to prevent reinjury. This
training may also help to avoid the development of chronic ankle joint instability (especially
functional instability), ankle instability being common among athletes.2,4,35
More injuries were sustained during matches than in training (66% v 33%). Árnason et al18
also reported a higher injury rate for matches, but the difference was much greater (4.4 v 0.1
per 1000 hours equating to 98% v 2%). This correlates with the increased number of contact
mechanisms, as more contact injuries would be expected during games.18 Nearly half (48%) of
ankle sprains sustained during games occurred during the last one third of each half. This
pattern was observed by Hawkins et al16 for all injuries, with the authors citing Gleeson et al36
who suggested that the risk of ligamentous injury may be increased by increases in
electromechanical delay and anterior tibiofemoral displacement. This emphasises the
importance of endurance training in ankle rehabilitation to avoid fatigue at the end of each
half. It may also present a case for preventive training programmes when players are more
fatigued—that is, at the end of training sessions. However, this requires further research, as
other studies have found ankle injuries to be evenly distributed throughout games.11,37
The timing of injuries throughout the season is also important; 44% of ankle injuries were
sustained during the first three months of the season, considerably more than expected. The
importance of structured neuromuscular coordination and proprioceptive training during the
closed season and preseason months is emphasised, as the number of ankle sprains peak in
August and September. In their systematic review on the prevention of ankle sprains, Thacker
et al20 emphasised the importance of conditioning of the ankle before the competitive season
and during the course of the season, with emphasis on ankle strength and proprioception.
According to Gauffin et al38 postural sway and the pattern for postural correction were
improved by wobble board training.
Ankle sprains are commonly known as recurrent injuries, with 56%,19 75%,39 and 69%18 of
sprains involving players with a previous history of ankle sprain. The problem with comparing
these data with our own is that this study only recorded injuries over two seasons and
therefore the past medical history of the players is not known—that is, if they sustained an
ankle sprain in previous years. Also, the studies cited above have not recorded how they
defined and measured previous injury. Of the 677 injuries recorded over the two seasons in
this study, 57 were reinjuries, (9%). Although not significant, it was found that those players
sustaining recurrent injuries missed on average more training days and matches than those
with first time injuries (18 v 19 days, three v four matches). Missing four matches instead of
three may not be significant in terms of statistics, but in terms of football, it is crucial that
players, especially "first choice" ones, miss as few matches possible.
More non-contact mechanisms were responsible for reinjuries than initial injuries (47% v
39%). Nielsen and Yde19 described a characteristic pattern of major trauma causing the initial
injury, with minor trauma (for instance during running) being responsible for the reinjury.
Ekstrand and Gillquist39 reported that many major injuries were preceded by minor injuries;
they suggested that this may be due to impairment of timing and neuromuscular coordination.
Árnason et al37 suggested that reinjuries were caused by lack of preventive measures and
100
inadequate rehabilitation. Controlled rehabilitation and strict adherence to directions for
resumption of play should therefore be insisted upon. It may also help to have preinjury or
normative measures of ankle strength and proprioception as a component of player functional
profiles. The objective measures could then be used to help decide when the player is fully fit.
Waddington and Shepherd26 suggested measuring postural sway as a prediction of injury risk.
Athletes in the "higher injury incidence zone" would then carry out a specifically designed
functional training programme to potentially reduce the risk of ankle injury.
Our study showed that 32% of players were wearing some form of ankle support when they
sustained an injury. This appears remarkably high given that this is often considered to be a
form of prevention of ankle sprains.14,29,31,40 The question must be posed as to why so many
players were wearing an ankle support. Perhaps it was for prophylactic reasons to prevent
initial injury or because of mechanical and or functional instability from a previous injury.
The high number of injuries in taped ankles may be explained if the players involved had a
history of ankle sprain, because the risk of reinjuring a previously sprained ankle is high.
Some players are keen to return to training without reaching full fitness and may request to
have their ankle strapped in the hope that this will provide extra support and protection from
reinjury. This may also help to explain the high number of players sustaining injury even with
an ankle support. This study did not record how many players were wearing an ankle support
and who did not sustain an injury. This, along with more detail on the ankle supports used (for
example the method of application, skill of applicant, and the type of joint support used),
would be required to draw further conclusions. A discussion on the effectiveness of joint
support for the ankle joint as a preventive tool in football is beyond the scope of this paper,
although it is an issue that undoubtedly requires further investigation.
As the lateral ligament ankle sprain is so common in football, prevention of initial and
recurrent injuries is of paramount importance. Methods of preventing contact ankle sprains
have previously been suggested. These include rules to control and minimise unnecessary or
hazardous contact with other players and appropriate officiating to ensure compliance with
event rules.20 These may in practice be very difficult to implement, and so more practical
interventions such as the education of coaches and players to minimise contact in training
sessions and the wearing of an ankle guard component of shin guards are recommended. None
of these factors have been subject to rigorous scientific review, but common sense suggests
that they would be useful in the prevention of such injuries. Ekstrand and Gillquist39
recommended that coaches emphasise injury prevention and that athletes be taught basic
principles of injury prevention. Other suggestions for the prevention of ankle sprains include
adequate maintenance of pitches and training surfaces. 39 This is a plausible suggestion because
it has been reported that one of the risk factors for ankle injury is an uneven surface. 5
Complete rehabilitation and preseason ankle conditioning (involving functional stimulus to
both proprioceptive and muscular control systems closely related to the action that overloads
the system in the first instance) have already been suggested. The use of external support in
the prevention of ankle sprains has yet to be validated. However, both taping and braces have
been shown to prevent ankle sprains in football players.14,29,41 The design selected for some of
these studies may form a basis for questioning the validity of the results.7
Take home message
101
Ankle sprains are common in football and usually involve the lateral ligament. Their frequent
occurrence and recurrence indicates that preventive strategies such as functional profiles
(including normative and preinjury measures of ankle stability), effective rehabilitation,
preseason conditioning of the ankle, and education of coaches and players are of paramount
importance.
As a component of long term planning of athlete development, Bayli42 emphasised the
importance of mastering eye-foot coordination and balance at an early age (6–10 years). If
such fundamentals are not mastered early in an athlete’s career, his or her ability to move to a
higher level of sporting achievement will be limited. This so called "window of opportunity"
could also be used as a long term injury prevention strategy by educating coaches to introduce
proprioceptive and coordination activities at this early age.
Ankle sprains (especially those involving the lateral ligament) are common injuries in
football. It is the frequency and risk of reinjury rather than severity (time missed) that makes
these injuries problematic. Emphasis is therefore on prevention through the use of functional
profiles (including normative and preinjury measures of ankle stability), adequate
rehabilitation, preseason conditioning of the ankle, and education of coaches and players.
ACKNOWLEDGEMENTS
We acknowledge the financial support given by The Professional Footballers’ Association
together with the support of The League Managers Association, The Premier League, and The
Football League, and the commitment of the medical practitioners working at professional
football clubs in England and Wales. We also gratefully acknowledge the contributions made
by the members of the Project Consultative Committee Working Group, namely Mr R Myles
Gibson (Chairman), Dr C Cowie, Dr M Waller, Mr G Lewin, and Mr A Jones.
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105
Ankle Sprains: Expedient Assessment and
Management
Thomas H. Trojian, MD, MMB; Douglas B. McKeag, MD, MS
Emergencies Series Editor: Warren B. Howe, MD
THE PHYSICIAN AND SPORTSMEDICINE - VOL 26 - NO. 10 - OCTOBER 98
In Brief: Most ankle injuries occur from excessive inversion, but it is important to be able to
differentiate a simple inversion sprain from a potentially disabling injury. Expedient diagnosis
includes first screening for deformities and then performing specific tests like the anterior drawer
and side-to-side test. To optimize assessment, the examiner needs to take advantage of the
preswelling period on the sidelines. Physicians can treat most ankle injuries nonoperatively, taking
steps to ensure a quick return to play. Fracture signs and treatment are covered in a
comprehensive table.
Ankle sprains are the most common athletic injury (1). Most involve injury to the lateral
supporting ligaments from an inversion incident (2). The risk of ankle injuries varies by sport; they
make up 45% of all injuries in basketball, 31% in soccer, and 25% in volleyball (1). In
professional, college, and high school football, ankle sprains account for 10% to 15% of all time
lost to injury. Yet these injuries are often minimized.
In addition to common ankle sprains, primary care physicians will see uncommon ankle injuries
that need urgent care. Appropriate treatment can help patients avoid chronic ankle pain, laxity, or
arthritis (3). Keeping a high index of suspicion for subtle, unusual injuries around the ankle will
increase patients' quality of care.
Detail of Two Joints
The ankle consists of two joints: the talar mortise and the subtalar joint (4,5). The mortise is
shaped like an inverted "U" bounded by the distal fibula and tibia (figure 1) and allows plantar
flexion and dorsiflexion. Inside the "U" is the trapezoid-shaped talar dome; its greater anterior
width gives the ankle more stability in dorsiflexion. The subtalar joint allows for inversion, eversion,
and internal and external rotation.
106
The ligamentous structures of the ankle can be divided into three groups: tibiofibular, medial, and
lateral complexes. The tibiofibular ligament stabilizes the ankle mortise and allows little movement
between tibia and fibula.
The medial complex (figure 2) consists of the strong, fan-shaped deltoid ligament, which limits
eversion of the ankle and lateral displacement of the talus. The medial malleolus will often fracture
before this ligament tears.
The lateral complex (figure 3) consists of three ligaments: anterior talofibular, calcaneofibular, and
posterior talofibular, which resist internal rotation, anterior displacement, and inversion. The
anterior talofibular ligament is the most frequently injured in the ankle.
107
Muscles and tendons act as secondary stabilizers and are often injured. The peroneus longus is the
main everter of the ankle. The anterior tibialis acts in dorsiflexion. The posterior tibialis inverts and
plantar flexes the foot, and the Achilles tendon also acts in plantar flexion.
Initial On-Field Management
All ankle injuries need immediate on-the-field assessment by the athletic trainer or team physician.
The goal is to evaluate the athlete quickly and identify any serious injury. Mechanism and position
of the ankle at the time of injury are important. If the injury is minor, a full evaluation can be
completed on the sideline. The initial survey needs to screen for any deformities. The athlete with
no deformity can try to bear weight, which will help in grading the injury. (Inability to bear weight
tends to indicate instability and thus a more serious injury.)
The physician needs to be prepared to stabilize any fracture or dislocation and transport the
patient. If an athlete has an ankle deformity, axial traction and relocation should be attempted only
once. Neurovascular assessment and documentation and urgent transport are essential after
relocation or if relocation is not possible. When an ambulance is not available, transport in a large
vehicle such as a station wagon is needed so the patient can lie supine.
Sideline or Office Evaluation
When the athlete's ankle is not deformed, the best opportunity for accurate diagnosis often comes
on the sideline. Initially, palpation for crepitus and ligament testing will be difficult with an anxious
athlete and global pain.
After the athlete relaxes, however, the initial pain decreases and what we like to call the "golden
period" begins. During this period, there is no swelling, the initial pain has subsided, and guarding
is not yet present--all of which facilitate a fruitful physical exam. (If a physician is not on site, the
athletic trainer can take advantage of this period.) One caveat regarding the "golden period" is that
a stable fracture may produce crepitus over the fracture site without causing initial tenderness.
History. A well-thought-out history can lead to the proper diagnosis most of the time. Mechanism
of injury is very helpful (3), but if the injury occurred rapidly, the athlete may not know the
mechanism. Important questions to ask are:





How did it happen (inversion, eversion, dorsiflexion, etc)?
Where does it hurt (table 1)?
Did the intensity of pain make you stop playing (ruptured ligament, fracture)?
Were you able to bear any weight right away (fracture, severity of injury)?
Have you injured this or the other ankle before (to identify recurrent sprain, fractures,
normal contralateral ankle)?
108
Table 1. Useful Tests for Various Ankle Injuries
Injury
Location
Specific Injury
Useful Test
Lateral
Inversion sprain
Lateral malleolus fracture
Osteochondritis dissecans
Peroneal tendon
subluxation
Bifurcate ligament avulsion
Anterior drawer, talar tilt
X-ray as per Ottawa ankle rules
Mortise view ankle x-rays
Resisted dorsiflexion and eversion
X-rays
Medial
Medial ankle sprain
Medial malleolus fracture
Posterior tibialis tendon
injury
Flexor hallucis longus
tendinitis
Eversion stress
X-ray as per Ottawa ankle rules
Single heel-rise test
Resisted first-toe flexion
Posterior
Achilles tendon rupture
Os trigonum fracture
Thompson's
Weight-bearing lateral x-ray, tenderness on passive
plantar flexion
Anterior
Syndesmosis sprain
Dorsiflexion injuries
Anterior tibialis tendon
injury
"Squeeze," external rotation
Side-to-side
Resisted dorsiflexion
Other
Avulsion fracture, 5th
metatarsal
Maisonneuve fracture
Palpation tenderness, foot x-rays
Palpation tenderness, fibula x-rays
Physical exam. Examining the athlete's uninjured ankle provides a useful reference point and
helps reduce anxiety for examination of the injured ankle. Shoe and sock removal is important for
performing a proper examination and evaluating neurovascular status.
Any swelling or ecchymosis should be noted (5). The athlete should move the joint through all
directions, then the physician should move the ankle through the six ranges of motion: plantar
flexion, dorsiflexion, and inversion and eversion in plantar flexion and dorsiflexion. Results are
compared with the uninjured side. The examiner also palpates the ligaments, tendons, and bones,
paying close attention to any feeling of crepitus, tenderness, or swelling.
Strength testing is the last piece in the general exam. The physician should test inversion and
eversion in plantar flexion and dorsiflexion by resisting active range of motion and comparing with
the other ankle. Special tests for joint stability are also important.
Specific tests. The anterior drawer test (figure 4) assesses the integrity of the anterior talofibular
ligament (5). However, initially its reliability may be suspect: A positive anterior drawer test within
48 hours of injury suggests a tear of the anterior talofibular ligament, but the test has a large
number of false-negatives. If the test is performed 4 to 5 days postinjury, however, it has a
sensitivity of 86% and specificity of 74% (6).
109
Talar tilt can be used to assess the deltoid ligament and the calcaneofibular ligament by eversion
and inversion stressing, respectively. However, this is an unreliable test for ligamentous rupture
with poor interrater reliability (6).
The side-to-side test (7) (figure 5) assesses widening of the ankle mortise caused by instability of
the tibiofibular ligament. It is important in dorsiflexion injuries.
Thompson's test (figure 6) evaluates Achilles tendon continuity. It has a sensitivity of 96% and
specificity of 93%.
The squeeze test (figure 7) and external rotation stress test (figure 8) help diagnose syndesmosis
injuries (8).
110
Radiographs. The Ottawa ankle rules help guide ordering of radiographs for acute ankle and
midfoot injuries. The rules cannot be applied if the examiner cannot palpate the bone because of
excessive swelling.
The rules state that an ankle x-ray series is necessary only if there is pain on or superficial to the
malleoli and any of these findings: (1) the inability to bear weight either immediately or in the
emergency department (patient cannot take four steps) or (2) bone tenderness from 0 to 6 cm up
the posterior edge or on the tip of either malleolus (9,10). These rules, however, were derived
from the emergency department experience--an athlete at the field may initially have no
tenderness at the site of fracture, only crepitus.
A foot x-ray series is necessary only for midfoot pain and any of these findings: (1) an inability to
bear weight, both immediately and in the emergency department or (2) bone tenderness at the
navicular or the base of the fifth metatarsal. These rules, if properly applied, will have about 100%
sensitivity.
Ankle Injury Differential
On-site primary care physicians must be knowledgeable about a variety of soft-tissue and bony
ankle injuries.
Lateral inversion sprain. The lateral sprain--the most common ankle injury--accounts for 85% of
all ankle sprains (2). After an inversion injury, the lateral ligaments are stretched or torn, usually
from anterior to posterior. Grading the injury (table 2) (11) can help with prognosis.
Table 2. Grading of Lateral Ankle Sprains and Return to Play (11)
Grade
Anterior
Drawer Test
Talar Tilt
Test
Return to
Play
111
1
Negative
Negative
1-10 dy
2
Increased laxity
Negative
2-4 wk
3
Positive
Positive
5-8 wk with optimal rehab
All lateral sprains can be treated conservatively with protection, rest, ice, compression, and
elevation (PRICEMMM, table 3). Crutches may be beneficial until pain-free weight bearing is
achieved. A felt horseshoe, taped with an open basket weave technique or secured with elastic
bandage, around the ankle initially will decrease swelling and aid in recovery. Ankle taping or
bracing and proprioception retraining are often needed.
Table 3. 'PRICEMMM' Mnemonic for Treating Ankle Sprains
Protection with ankle bracing to prevent reinjury while ligament
heals
Rest for injured ankle until normal heel-toe gait is restored
Ice on ankle to decrease swelling and relieve pain
Compression as soon as possible to decrease swelling
Elevation: the initial step for reducing swelling
Medication: NSAIDs or acetominophen for pain relief
Mobilization early on when pain free to expedite return to play
Modalities: exercise and proprioception training to prevent reinjury
Medial eversion sprain. Medial sprains are commonly seen in wrestlers. The tibia and strong
deltoid ligament make eversion sprains less likely than lateral sprains (10% versus 85%) (7).
However, 75% of ankle fractures occur on the medial side. Tears of the deltoid ligament can be
detected by laxity or tenderness on eversion stress testing. Deltoid ligament tears point to other
injuries that may require surgery, like a Maisonneuve fracture (see below), syndesmosis injury,
distal fibular fracture, or avulsion fracture of the medial malleolus. Medial sprains otherwise can be
treated like inversion sprains.
Syndesmosis sprain. The syndesmosis is stabilized by the interosseous membrane and the
anterior and posterior inferior tibiofibular, transverse tibiofibular, and interosseous ligaments. The
mechanism of syndesmosis (high ankle) sprains is uncertain but is postulated to be external
rotation and hyperdorsiflexion (8). Syndesmosis sprains range from 1% to 11% of all ankle
sprains, with the higher rate of injury occurring in contact sports. This injury, unlike the lateral
sprain, has little swelling and lacks recurrence. Patients typically have tenderness over the anterior
inferior tibiofibular ligament and proximally along the interosseous membrane. The squeeze,
external rotation stress, and side-to-side tests are important in the diagnosis.
If a serious ligament tear is suspected, external rotation stress radiographs should be obtained.
More than 5 mm of widening of the tibiofibular clear space indicates a complete rupture.
Delayed healing of syndesmosis sprains is typical, with recovery time of 55 days as compared with
35 days for a grade 3 lateral sprain. Treatment should involve non-weight bearing with
advancement to a walking boot.
Bifurcate ligament injury. Because the bifurcate ligament is taut with plantar flexion and
inversion, injury to it usually occurs with violent dorsiflexion, forceful plantar flexion, or direct
trauma. It is associated with up to 19% of ankle inversion sprains. This mechanism can avulse the
anterior process of the calcaneus.
112
A bifurcate sprain or avulsion fracture is often mistaken for a lateral ankle sprain because pain and
swelling are near the lateral malleolus. The point of maximal tenderness is found midway on a line
connecting the tuberosity of the fifth metatarsal and the distal tip of the lateral malleolus.
Treatment of an avulsion fracture of the calcaneus should include a non-weight-bearing cast for 4
weeks. These injuries can produce pain for many months.
Achilles tendon rupture. Rupture of the Achilles tendon is often seen in older, deconditioned
athletes (7). It is also seen in the younger athlete who has had prolonged inactivity because of
another injury. Mechanism of action is rapid plantar flexion as in turning to sprint up court in
basketball. The site of rupture is in the area of poor circulation 2 to 6 cm above the os calcis.
Patients will feel a sharp pain in the Achilles and often state that it sounded like someone shot
them.
Treatment is controversial. Casting is a reasonable option, especially if the tear is more than 2 cm
from the calcaneal attachment. Surgery should be considered for the elite athlete to minimize the
chance of rerupture.
Peroneal tendon subluxation or dislocation. The peroneus longus and brevis tendons lie in the
shallow groove posterior to the fibula. Subluxation or dislocation of these tendons is not common
but can happen with an inversion sprain. Disruption of the retinaculum or a fracture of the
posterior edge of the fibula can cause dislocation of the tendon (12). This can be detected by
palpating over the tendon with active dorsiflexion and eversion of the foot and ankle. The examiner
will feel the tendon sublux, or the maneuver will elicit pain. Patients typically report pain with
walking and with walking on the balls of the feet.
Conservative treatment consists of a U-shaped felt pad with ankle taping for primary dislocation.
Surgical referral is warranted for lateral pain and a lack of stability. Postsurgical recovery time is at
least 8 weeks.
Flexor hallucis longus injury. The flexor hallucis longus passes through a fibro-osseous tunnel
behind the medial malleolus (13). Injury to this ligament is seen in dancers or other athletes who
stand on tiptoe or on the balls of their feet. It is not typically associated with other injuries and can
be misdiagnosed as Achilles tendinitis or as posterior tibialis tendinitis (14). Palpation of the sheath
with active and passive ranges of motion of the hallux will reproduce symptoms. Treatment is
conservative with rest, ice, nonsteroidal anti-inflammatory drugs, and an inflexible shoe.
Lateral periostitis. Lateral periostitis, or jumper's ankle, can occur in high-jumpers prior to
takeoff in the planted foot (5). The foot is dorsiflexed and everted suddenly, thereby causing
trauma to the talus from the distal fibula. Diagnosis can be difficult. Symptoms are similar to those
of a lateral sprain but without anterior talofibular ligament tenderness. Palpation of the lateral talus
with the foot in plantar flexion and inversion elicits pain. Treatment is rest and a G-in. medial heel
wedge to prevent trauma.
Os trigonum injury. In this injury, severe plantar flexion (15) causes lateral posterior triangle
pain. Resisted eversion will be pain-free, but forceful passive plantar flexion should reproduce
symptoms. A bone scan or MRI can aid diagnosis. Treatment involves a short leg cast in 15°
plantar flexion for 1 to 3 weeks. Steroid injection into the posterior triangle can be helpful.
Anterior tibialis tendon injury. The anterior tibialis tendon accounts for 80% of the dorsiflexion
power of the ankle. It is rarely injured acutely, most often in elderly people, and produces pain on
the dorsum of the foot. It can rupture or avulse from its site of insertion. Foot drop is common, and
resisted dorsiflexion will be weak or tender. Typical treatment is surgery.
Fractures. Fractures constitute about 15% of ankle injuries and can coexist with ligament injuries.
A complete discussion is not possible here, but some of the fractures associated with ankle sprains
are covered in table 4 (15-18).
Table 4. Diagnosing and Managing Ankle Fractures
113
Site or Type
Malleolus
Characteristics and
Findings
Treatment
Injuries that extend across
an imaginary line drawn
through the top of talar
dome on AP x-ray
considered unstable
Referral for unstable
fxs; closed reduction,
postreduction x-rays,
casting and non-weight
bearing for stable fxs
Comments
Epiphysis of
tibia
Be wary of "ankle sprain"
in prepubescent patients
since ligaments are
stronger than physis at
this age. Good to
excellent healing for
types 1-3; poor
prognosis for types 4 and
five.
Type 1 (SalterHarris)
Localized swelling or minimal Casting for 2-4 wk
widening on x-ray
Type 2
Metaphyseal fx into physis
on x-ray
Closed reduction, long
leg cast
Type 3
Epiphyseal fx into physis on
x-ray
Referral to surgeon
Type 4
Fx through both metaphysis
and epiphysis on x-ray
Referral to surgeon
Type 5
Narrowing of physis on x-ray Referral to surgeon
Osteochondral
Weak ankles, crepitus,
Casting if fragment not
locking, deep pain, recurrent avulsed from talar
swelling
dome; otherwise,
surgical intervention
Often missed initially;
may follow compression
injury of talar dome.
Posterior
tubercle of
talus and os
trigonum
Mechanism is severe plantar
flexion of foot; patient has
lateral posterior triangle
pain; resisted eversion pain
free; passive plantar flexion
mimics symptoms
Short leg cast in 15° of
plantar flexion for 4
wk; surgical excision
occasionally
Occur in dancers,
runners, soccer players.
Avulsion of fifth Inversion injury can avulse
metatarsal
plantar aponeurosis from
proximal tuberosity;
produces tenderness at base
of 5th metatarsal
Symptomatic care in
cast shoe or hard shoe
Jones fracture
Tenderness at base of 5th
metatarsal
Surgical screw fixation
followed by nonweight-bearing cast
Common in basketball
players and ballroom
dancers
Lateral process
of talus
Inversion injury; seen on
mortise view but difficult to
see on lateral view; bone
scan or CT scan may help
identify
Nondisplaced fxs: short
leg cast for 6 wk, 4 wk
non-weight bearing;
displaced fxs: surgical
intervention
Often missed for months
because of proximity to
lateral ligaments.
Common in
snowboarders.
114
Maisonneuve
fracture
Eversion injury often
associated with deltoid
ligament sprain; pain and xray findings on proximal
third of fibula; involves
interosseus membrane
Referral for internal
fixation
Often misdiagnosed;
important to palpate
entire fibula with
eversion injuries.
Calcaneus
Extra-articular fx often from
twisting forces; intraarticular fx often from fall
from height; both involve
pain with walking or inability
to bear weight; CT can
delineate two types
Extra-articular: nonweight-bearing cast;
intra-articular: surgical
referral
Extra-articular fxs often
heal well.
Subluxation
Occurs during pronation;
pain over lateral side of foot,
often along sinus tarsi; pain
is elicited by pressing on
plantar aspect of cuboid in
dorsal direction; running,
cutting, jumping markedly
increase pain
Repositioning cuboid by Mostly seen in classical
holding the forefoot
ballet dancers and
with thumbs over
distance runners.
plantar surface of
cuboid and 'whipping'
the foot into plantar
flexion while thumbs
push cuboid dorsally
Fracture
Uncommon but can occur
with inversion and plantar
flexion; mimics severe
sprain or fx of anterior
process of calcaneus
Short leg cast for
nondisplaced fx;
displaced fx requires
surgery
Subtalar
dislocation
Violent plantar flexion and
inversion of foot produce
medial dislocation;
dorsiflexion and eversion
lead to lateral dislocation;
foot is deformed in both
types
Reduction under
general anesthesia
Cuboid
85% are medial.
Neurovascular
assessment is critical.
AP = anteroposterior, fx = fracture
Safe Return to Play
Many ankle injuries will not prevent an immediate return to action, but return to play is a casespecific decision. A few guidelines will help with this complex decision:



A patient who has a stable injury should not return to play if that injury may become
unstable.
Pain-free range of motion is important.
The athlete needs to complete functional testing pain free. Example: walking, jogging
(forward and backward), figure eights, zigzags, and one-foot hops.
115
Using these guidelines and knowing the differential diagnosis, the team physician will be able to
return a player to competition safely.
Widespread Knowledge
Primary care physicians need to be familiar not only with acute assessment and management of
ankle sprains, but also with the many other injuries in the differential diagnosis, for they will see
most of them over time.
References
1. Garrick JG: The frequency of injury, mechanism of injury, and epidemiology of ankle
sprains. Am J Sports Med 1977;5(6):241-242
2. Tropp H, Askling C, Gillquist J: Prevention of ankle sprains. Am J Sports Med
1985;13(4):259-262
3. Trevino SG, Davis P, Hecht PJ: Management of acute and chronic lateral ligament injuries
of the ankle. Orthop Clin North Am 1994;25(1):1-16
4. Netter FH: The CIBA Collection of Medical Illustrations, vol 8: Musculoskeletal System, Part
1: Anatomy, Physiology, and Metabolic Disorders. West Caldwell, NJ, CIBA-GEIGY Corp,
1991, pp 106-110
5. Renström PA, Konradsen L: Ankle ligament injuries. Br J Sports Med 1997;31(1):11-20
6. van Dijk CN, Lim LS, Bossuyt PM, et al: Physical examination is sufficient for the diagnosis
of sprained ankles. J Bone Joint Surg (Br) 1996;78(6):958-962
7. McKeag DB, Hough DO: Common sports-related injuries and illnesses: pelvis and lower
extremity. Section E: ankle, in McKeag DB, Hough DO: Primary Care Sports Medicine.
Dubuque, IA, 1993, Brown & Benchmark, pp 433-448
8. Boytim MJ, Fischer DA, Neumann L: Syndesmotic ankle sprains. Am J Sports Med
1991;19(3):294-298
9. Stiell IG, Greenberg GH, McKnight RD, et al: Decision rules for the use of radiography in
acute ankle injuries: refinement and prospective validation. JAMA 1993;269(9):1127-1132
10. Chande VT: Decision rules for roentgenography of children with acute ankle injuries. Arch
Pediatr Adolesc Med 1995;149(3):255-258
11. Chorley JN, Hergenroeder AC: Management of ankle sprains. Pediatr Ann 1997;26(1):5664
12. Sammarco GJ: Peroneal tendon injuries. Orthop Clin North Am 1994;25(1):135-145
13. Frey CC, Shereff MJ: Tendon injuries about the ankle in athletes. Clin Sports Med
1988;7(1):103-118
14. Conti SF: Posterior tibial tendon problems in athletes. Orthop Clin North Am
1994;25(1):109-122
15. Thordarson DB: Detecting and treating common foot and ankle fractures. Part 1: the ankle
and hindfoot. Phys Sportsmed 1996;24(9):29-38
16. Baumhauer JF, Alvarez RG: Controversies in treating talus fractures. Orthop Clin North Am
1995;26(2):335-351
17. Waler JF Jr, Maddalo AV: The foot and ankle linkage system, in Nicholas JA, Hershman EB
(eds): The Lower Extremity and Spine in Sports Medicine, ed 2. St Louis, CV Mosby Co,
1995
18. Quill GE Jr: Fractures of the proximal fifth metatarsal. Orthop Clin North Am
1995;26(2):353-361
Dr Trojian is an assistant professor of family medicine at UConn Health System, St Francis Hospital
and Medical Center, Department of Family Medicine in Hartford, Connecticut. He is also a team
physician at the University of Connecticut in Hartford and a member of the American Medical
Society for Sports Medicine (AMSSM). Dr McKeag is the Arthur J. Rooney chair of sports medicine,
a professor of family medicine and orthopedics, and the director of primary care sports medicine at
the University of Pittsburgh. He is past president of the AMSSM and an editorial board member of
The Physician and Sportsmedicine. Dr Howe is the team physician at Western Washington
University in Bellingham and an editorial board member of The Physician and Sportsmedicine.
Address correspondence to Douglas B. McKeag, MD, MS, Primary Care Sports Medicine, Room 215
School of Nursing, UPMC-Shadyside, 5230 Centre Ave, Pittsburgh, PA 15262.
116
Evaluation and Treatment of Ankle Sprains
Clinical Recommendations for a Positive Outcome
R. Todd Hockenbury, MD; G. James Sammarco, MD
THE PHYSICIAN AND SPORTSMEDICINE - VOL 29 - NO. 2 - FEBRUARY 2001
In Brief: Ankle sprains usually involve damage to lateral ankle ligaments and syndesmotic
ligaments. A detailed examination that focuses on physical examination techniques is important
because other injuries may mimic ankle sprains, and hands-on grading of ankle sprains dictates
treatment and forecasts recovery time. Most ankle sprains can be successfully treated
nonsurgically with PRICE (protection, rest, ice, compression, and elevation). When patients
experience chronic pain or instability from an ankle sprain, a directed approach will help physicians
fine-tune nonsurgical treatments or suggest a surgical referral.
Sprain of the lateral ankle ligaments is the most common injury seen by healthcare providers who
treat sports injuries to the lower extremity (1,2). Ankle injuries constitute 25% of all sports-related
injuries (3), including 21% to 53% of basketball injuries and 17% to 29% of all soccer injuries
(4,5). One third of all West Point cadets sustain an ankle sprain during their 4-year tenure (6).
Anatomy and Biomechanics
The ankle is a simple hinge joint. The stability of the talocrural joint depends on both joint
congruency and the supporting ligamentous structures. The lateral ankle ligaments (figure 1A),
responsible for resistance against inversion and internal rotation stress, are the anterior talofibular
ligament (ATFL), the calcaneofibular ligament (CFL) and the posterior talofibular ligament (PTFL).
The medial supporting ligaments are the superficial and deep deltoid ligaments, which are
responsible for resistance to eversion and external rotation stress and are less commonly injured.
The ATFL resists ankle inversion in plantar flexion, and the CFL resists ankle inversion during
dorsiflexion (7-10). The accessory functions of the ATFL are resistance to anterior talar
displacement from the mortise, clinically referred to as the anterior drawer, and resistance to
internal rotation of the talus within the mortise. The CFL spans both the lateral ankle joint and
lateral subtalar joint, thus contributing to both ankle and subtalar joint stability (11). The PTFL is
under greatest strain in ankle dorsiflexion and acts to limit posterior talar displacement within the
mortise as well as talar external rotation (12).
117
Clinically, the most commonly sprained ankle ligament is the ATFL, followed by the CFL. The PTFL
is rarely injured. The incidence of ligamentous injury tends to match both the mechanism of injury
and relative ligamentous strength. The strength of the ankle ligaments from weakest to strongest
is the ATFL, PTFL, CFL, and deltoid ligament (13).
Lateral ankle sprains occur as a result of landing on a plantar flexed and inverted foot. These
injuries occur while running on uneven terrain, stepping in a hole, stepping on another athlete's
foot during play, or landing from a jump in an unbalanced position. During periods of ankle
unloading, the ankle rests in a position of plantar flexion and inversion. If the ground or another
object is met unexpectedly by the unloaded foot, lateral ligament injury may occur.
The subtalar joint lies inferior to the ankle joint and is responsible for inversion and eversion of the
hindfoot. The subtalar joint controls foot supination and pronation in close conjunction with the
transverse tarsal joints of the middle foot. The CFL provides stability to inversion and torsional
stresses to both the ankle and subtalar joints. Up to 50% of apparent ankle inversion observed
actually comes from the subtalar joint (11). The structures that contribute to stability of the
subtalar joint are the CFL, the cervical ligament, the interosseous ligament, the lateral
talocalcaneal ligament, the fibulotalocalcaneal ligament (ligament of Rouviere), and the extensor
retinaculum (14).
The syndesmotic ligaments, responsible for maintaining stability between the distal fibula and tibia,
consist of the anterior tibiofibular ligament, the posterior tibiofibular ligament, the transverse
tibiofibular ligament, the interosseous ligament, and the interosseous membrane (figure 1B).
Injuries to the ankle syndesmosis occur as a result of forced external rotation of the foot or during
internal rotation of the tibia on a planted foot. A common mechanism is a direct blow to the back of
the ankle while the patient is lying prone with the foot externally rotated. These injuries more
commonly occur in contact sports and skiing (15). Among 96 ankle sprains reported at West Point,
17% were sprains of the syndesmosis (16).
Physical Examination
A detailed, complete examination is essential to avoid misdiagnosis or overlooking associated
injuries. The ATFL, CFL, distal tibiofibular syndesmotic ligaments, deltoid ligament, lateral
malleolus, and medial malleolus should be carefully palpated with one finger. The fifth metatarsal
base, anterior process of the calcaneus, Achilles tendon, peroneal tendons, and posterior tibial
tendon should also be palpated, because injuries to these structures may mimic ankle sprains.
Swelling is usually seen laterally but may be diffuse. Ecchymosis is also frequently found laterally,
but it may settle into the lateral or medial heel. A careful neurologic examination is essential to rule
out loss of sensation or motor weakness, as peroneal nerve and tibial nerve injuries are sometimes
seen with severe lateral ankle sprains (17).
Provocative tests for lateral ankle instability include the anterior drawer test, inversion stress test,
and the suction sign (figure 2). Two provocative tests for syndesmotic ligament injury are the
squeeze test and the external rotation stress test (figure 3).
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Radiologic Evaluation
Every swollen, painful, twisted ankle does not require a radiograph to rule out fracture. The
decision to obtain postinjury radiographs is based on the Ottawa ankle rules (18). These guidelines
state that an ankle radiographic series (anteroposterior, oblique, and lateral views) should be
119
obtained if bone tenderness is present over the lateral or medial malleolus, or if the patient is
unable to bear weight for four steps both immediately postinjury and in the emergency
department. Exclusions for use of the Ottawa ankle rules are age younger than 18 years,
intoxication, multiple painful injuries, pregnancy, head injury, or diminished sensation due to
neurologic deficit. These criteria have been found to be 100% sensitive for detecting fracture while
decreasing the incidence of unneeded radiographs (18).
Radiographs. If radiographs are warranted, they should be examined for fractures of the medial,
lateral or posterior malleoli, talar dome, lateral talar process, and anterior calcaneal process.
Injuries to the distal syndesmotic ligaments and deltoid ligament will produce widening of the ankle
mortise that is manifested by increased medial clear space and lateral talar subluxation. A fracture
of the posterior rim of the distal fibula, known as a "flake fracture," may be associated with a tear
of the superior peroneal retinaculum that occurs during dislocation of the peroneal tendons (19).
Foot radiographs should also be obtained if the physical examination demonstrates tenderness in
the hindfoot, middle foot, or forefoot.
Stress radiographs. Stress radiographs help document lateral ligamentous ankle injury but are
not required to make the diagnosis of an acute ankle sprain. Talar tilt stress radiographs and
anterior drawer stress radiographs are primarily used to document mechanical instability as a
cause of chronic lateral ankle instability. Either test may be performed with or without a mechanical
testing apparatus. Local or nerve block anesthesia is recommended by some authors (7,20) to
prevent muscle guarding, relax muscles, and decrease pain during stress testing. We feel that
injecting 5 mL of local anesthetic (usually 1% xylocaine) near the lateral ankle ligaments and sinus
tarsi promotes peroneal muscle relaxation and yields a more reliable test.
Talar tilt testing is performed by taking an anteroposterior or mortise view of the ankle while
applying inversion stress to the slightly plantar flexed ankle. The angle between the superior aspect
of the talar dome and the tibial plafond is measured to yield the talar tilt angle.
The true stress radiologic criteria for diagnosing mechanical lateral ankle instability are
controversial. Normal talar tilt values have been reported to range from 0° to 23° (21,22). Because
of the wide variance of normal values, some authors feel that this test is not a reliable indicator of
ankle instability (22). Others argue that anteroposterior and lateral stress views do not take into
account the rotational instability that is occurring at the ankle and subtalar joint (23). This may
explain the complaints of subjective ankle instability in the face of normal radiographic stress tests
("functional instability"). One study (24) demonstrated that a 10° difference in talar tilt between
the injured and uninjured ankle was diagnostic of a sprain of both lateral ankle ligaments in 97% of
cases. Most authors agree that a difference of 5° to 15° between the injured and uninjured side is
diagnostic of mechanical ankle instability (25).
Anterior drawer stress radiographs are obtained by taking a lateral view of the ankle while
attempting to translate the talus anteriorly within the mortise, as in the clinical anterior drawer
test. The anterior drawer is measured as the shortest distance between a point on the posterior
aspect of the distal tibial articular surface and a point on the posterior aspect of the talar dome. A
difference of more than 3 mm between injured and uninjured ankles is thought to be diagnostic of
anterior talofibular ligament laxity (26).
Other stress tests include a view of the subtalar joint (a stress Broden's view) obtained by
internally rotating the leg 45° and angling the radiographic tube 45° cephalad. This test has been
used by some authors (27), but recent studies (28,29) have questioned its validity in diagnosing
subtalar instability.
A mortise stress radiograph of the ankle syndesmosis can be obtained by placing an external
rotation force on the ankle while stabilizing the proximal tibia with the knee flexed 90°. Abnormal
widening of the mortise and lateral talar shift indicate distal syndesmotic instability. A lateral
radiograph during external rotation stress will show posterior distal fibular translation and is
reported to be a more accurate way to diagnose instability of the syndesmosis (30).
Magnetic resonance imaging. Magnetic resonance imaging (MRI) will confirm acute injuries to
the ATFL or CFL, but it is not required to make the diagnosis (31). MRI is most useful for the
120
evaluation of causes of chronic ankle pain following ankle ligament injury. MRI can diagnose talar
dome injuries, peroneal tendon tears, bone bruises, or other occult fractures.
Grading Is a Useful Tool
Grading of ankle sprains guides treatment, rehabilitation, and prognosis. The West Point ankle
sprain grading system is a useful tool (table 1) (16). The time to return to sporting activities
averages 11 days for grade 1 sprains, 2 to 6 weeks for grade 2 sprains, and 4 to 26 weeks for
grade 3 sprains (32-34).
TABLE 1. West Point Ankle Sprain Grading System
Criterion
Grade 1
Grade 2
Grade 3
Location of
tenderness
ATFL
ATFL, CFL
ATFL, CFL, PTFL
Edema, ecchymosis
Slight local
Moderate local
Significant diffuse
Weight-bearing ability Full or
partial
Difficult without
crutches
Impossible without significant
pain
Ligament damage
Stretched
Partial tear
Complete tear
Instability
None
None or slight
Definite
Emphasis on Early Treatment
Ligamentous injuries undergo a series of phases during the healing process: hemorrhage and
inflammation, fibroblastic proliferation, collagen protein formation, and collagen maturation
(35,36). The more severe the ligament injury, the greater the time required to progress through
the stages of healing. Early mobilization of joints following ligamentous injury actually stimulates
collagen bundle orientation and promotes healing, although full ligamentous strength is not
reestablished for several months (25,37-40). Therefore, early treatment focuses on regaining
range of motion while protecting the injured ligaments against reinjury. Limiting soft-tissue
effusion speeds healing (25,34,41).
The standard early treatment following an acute ankle sprain is PRICE (protection, rest, ice,
compression, and elevation). Cryotherapy, compression, and elevation are essential to limit initial
swelling from hematoma and edema around the ankle and speed ligamentous healing. Early use of
cryotherapy, applied in the form of ice bags, a cold whirlpool, or a commercially available
compressive cuff filled with circulating coolant, has been shown to enable patients to return to full
activity more quickly (42). Compression can be applied by means of an elastic bandage, felt
doughnut, neoprene or elastic orthosis, or pneumatic device.
Early mobilization. Protected weight bearing with an orthosis is allowed, with weight bearing to
tolerance as soon as possible following injury. Crutches are used until pain-free weight bearing is
achieved. Generally, the higher the grade of sprain, the longer it takes to achieve pain-free weight
bearing.
Bracing. Protection of the ankle during initial healing is essential. This may be accomplished with
taping, a lace-up splint, a thermoplastic ankle stirrup splint, a functional walking orthosis, or a
short leg cast. Flexible and semiflexible braces have been shown to effectively limit ankle inversion
and to resist passive torque (43). More severe injuries usually require longer immobilization.
Generally, protected range of motion is superior to rigid immobilization with a cast. Early protected
range of motion in a flexible or semirigid orthosis is superior to rigid cast immobilization in terms of
patient satisfaction, return of motion and strength, and earlier return to function (44,45).
121
Rehabilitation. Physical therapy of the injured ankle is divided into five phases: acute, subacute,
rehabilitative, functional, and prophylactic (46). The exact timing of each phase varies with the
severity of the sprain. The acute phase is based on PRICE with goals to limit effusion, reduce pain,
and protect from further injury. The subacute phase focuses on decreasing and eliminating pain,
increasing pain-free range of motion, continuing protection against reinjury with bracing, limiting
loss of strength with isometric exercises, and continuing modalities to decrease effusion. The
rehabilitative phase emphasizes regaining full pain-free motion with joint mobilization and
stretching, increasing strength with isotonic and isokinetic exercises, and employing proprioceptive
training. The functional phase focuses on sports-specific exercises with a goal of returning the
patient to sports participation. The prophylactic phase seeks to prevent recurrence of injury
through preventive strengthening, functional proprioceptive drills, and prophylactic support as
needed (46).
Nonsurgical Treatment Results
Primary surgical repair of the torn lateral ankle ligaments has been advocated by some (47-50) as
treatment for elite athletes and young adults, assuming that anatomic repair will speed healing and
improve long-term outcome. However, primary ligamentous repair has not been supported in
comparative studies (51-53) that recommend early nonoperative functional treatment of ankle
ligament injuries. Satisfactory healing of the lateral ankle ligaments with the use of a functional
ankle brace has been documented by MRI (31).
Numerous studies (31,54-57) have documented that satisfactory subjective and clinical stability
have been restored with nonoperative treatments such as casting, taping, bracing, and early
physical therapy. A prospective study (56) of 146 patients with grade 3 ankle sprains who were
randomized into operative or nonoperative groups found that the group treated with an ankle
orthosis for 6 weeks returned to work faster. No difference in joint laxity between the groups was
found on stress radiographs performed 2 years postinjury.
Syndesmotic ligamentous injuries without fracture or gross widening of the ankle mortise are
treated nonoperatively with a short leg cast or brace, followed by physical therapy. The patient
should be advised that these injuries result in longer periods of disability than injuries to the lateral
collateral ligaments. In one study (16), only 44% of 16 patients had an acceptable outcome at 6
months. Heterotopic ossification of the distal syndesmosis has been reported in up to 25% of
patients, though no correlation between ossification and functional outcome has been found (58). If
diastasis of the syndesmosis is evident on plain radiographs, operative stabilization of the ankle
mortise is accomplished with a syndesmotic screw.
Evaluating Chronic Symptoms
Chronic pain following ankle injury is common. In a retrospective study (8) of 457 patients treated
with immobilization or bracing, 72.6% reported residual symptoms at 6 to 18 months. A study (16)
of 96 ankle sprains in West Point cadets noted residual symptoms in 40% of ankles at 6 months
postinjury.
Pain. Initial workup should center on whether the patient's chief chronic ankle complaint is pain or
instability (figure 4). If the primary problem is ankle pain, a concentrated effort should be made to
rule out occult fracture of the foot or ankle. A technetium bone scan is an excellent screening test
to rule out occult fractures and to guide further treatment. If the bone scan reveals increased
uptake in a discrete area, a spot radiograph or computed tomography scan is useful to further
identify the exact location of fracture. Occult or associated injuries to the tendons of the foot and
ankle should also be considered, and MRI is the most useful exam to identify and confirm them.
Table 2 lists some commonly missed occult fractures and tendon pathologies.
122
TABLE 2. Commonly Missed Diagnoses in Patients Who Have Chronic Ankle
Pain
Fractures
Talar dome osteochondral
Lateral talar process
Anterior process calcaneal
Lateral malleolar
Posterolateral distal fibular flake
Fifth metatarsal base
Navicular
Tendon Injuries
Achilles rupture
Peroneal tendon rupture
Peroneal tendon subluxation/dislocation
123
Posterior tibial tendon rupture
Anterior tibial tendon rupture
Flexor hallucis longus tendon rupture
Other soft-tissue causes of chronic ankle pain include anterolateral ankle impingement (meniscoid
lesion), anteroinferior tibiofibular ligament impingement (Basset's ligament), and anomalous
peroneal pathology. Injury to the lateral ankle ligaments may produce scarring of the ATFL and
joint capsule, leading to the formation of "meniscoid tissue" in the anterolateral ankle.
Anterolateral impingement can develop when inflamed tissue is pinched between the talus, fibula,
and tibia (59). The distal fascicle of the anteroinferior tibiofibular ligament may abrade the
anterolateral surface of the talus when the ankle is dorsiflexed during abnormal anterior translation
of the talus (60). An anomalous or accessory peroneal tendon may also cause chronic
posterolateral ankle pain (61).
Instability. If the primary problem is ankle instability, the patient will experience feelings of
"giving way" of the ankle on uneven ground, inability to play cutting or jumping sports, loss of
confidence in ankle support, reliance on braces, and a history of multiple ankle sprains. If, on
further evaluation, stress radiographs are positive for mechanical lateral ligamentous laxity,
surgery is indicated to reconstruct the loose ligaments.
If stress radiographs are nondiagnostic for mechanical laxity, the patient may have functional ankle
instability due to deficient neuromuscular control of the ankle, impaired proprioception, and
peroneal weakness (62,63). Treatment in this case should be directed toward restoring peroneal
tendon strength and ankle motion and improving ankle proprioception with physical therapy. Other
causes of instability, not demonstrated by stress radiographs, include rotational instability of the
talus, subtalar instability, distal syndesmotic (tibiofibular) instability, and hindfoot varus
malalignment (23).
When to Consider Surgery
Surgical treatment of lateral ligamentous ankle laxity should be considered after a full course of
physical therapy and a trial of bracing have been attempted, the patient continues to experience
multiple episodes of lateral ankle instability, and mechanical problems are documented by stress
radiographs. Most procedures are designed to tighten or reconstruct the ATFL and CFL.
Following lateral ankle ligamentous reconstruction, most postoperative regimens immobilize the
ankle in a cast for 4 weeks followed by an orthosis for an additional 4 weeks. Physical therapy with
an emphasis on peroneal strengthening and propioceptive training is instituted 6 to 8 weeks after
surgery. Return to sports occurs at about 3 months postsurgery.
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peroneus brevis tendon graft. Foot Ankle Int 1999;20(2):97-103
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Dr Hockenbury is an orthopedic surgeon at River City Orthopedic Surgeons in Louisville,
Kentucky, and a clinical professor at the University of Louisville. Dr Sammarco is an orthopedic
surgeon at the Center for Orthopedic Care in Cincinnati and a volunteer professor at the University
of Cincinnati. Address correspondence to R. Todd Hockenbury, MD, University of Louisville, River
City Orthopedic Surgeons, PSC, Old Third Street Rd, Suite 105, Louisville, KY 40272.
126
Meniscal Tears of the Knee
Diagnosis and Individualized Treatment
Joseph Bernstein, MD, MS
THE PHYSICIAN AND SPORTSMEDICINE - VOL 28 - NO. 3 - MARCH 2000
In Brief: Meniscal tears are very common sports injuries. Typical symptoms include pain, catching,
and buckling. Signs on physical exam include joint-line tenderness, effusion, and, possibly, a click
when the knee is taken through full range of motion. MRI is often needed to confirm tears and
differentiate pain from that caused by other injuries such as articular cartilage damage. Treatment
comprises physical therapy and rest, partial meniscectomy, or, in special instances, surgical repair.
Therapeutic goals, which are often achieved, are to restore a high level of pain-free function and to
prevent premature joint degeneration.
Knee meniscal tears are among the most common injuries seen in sports medicine. Twisting
motions with the knee flexed, which are common in sports, place high stresses on the menisci.
Many times the injury occurs when the athlete attempts a pivot; contact with another player
typically does not occur, nor does lunging or landing awkwardly. A single "wrong step" is sufficient.
Meniscal tears among active patients are clinically significant on two counts. First, they cause pain,
mechanical symptoms such as catching or locking, and effusion. Even if athletes can continue to
play, they are rarely at top form with a tear. Second, healthy menisci are needed to prevent
damage and degeneration of the joint. Thus, even if the patients are able to ignore symptoms,
they should be dissuaded from doing so, especially if the tear is repairable.
Meniscus Anatomy and Function
Gross anatomy. The shape of the meniscus (figure 1) and its microanatomy are tailored to
absorbing shock, distributing load, and stabilizing the joint (1). The meniscus consists of cartilage,
but its composition is slightly different from the articular cartilage that lines the ends of bone.
Meniscal cartilage is configured to be springy and resist shearing. Each knee has a medial and
lateral meniscus that are attached by ligaments to the proximal tibia. The word meniscus means
"little moon" in Greek--when viewed from above, the meniscus has a crescent shape. The meniscal
ring is thickest at the periphery and tapers off centrally, creating a shallow cup to hold the round
condyles of the femur. In cross-section, the meniscus has a triangular wedge shape.
127
Function. For many years, it was thought that the meniscus had no function. Accordingly, painful
tears were treated by open meniscectomy (complete removal); however, this practice was
abandoned after Fairbank (2) noted that x-rays in a large percentage of patients who had
meniscectomies showed progressive flattening of the femur, narrowing of the joint space, and
formation of bone spurs, some of the cardinal signs of osteoarthritis. These radiographic findings
after meniscectomy are now known as Fairbank's changes (2).
The menisci play important roles in the biomechanics of the knee (3). The tapered-ring geometry
of the meniscus promotes the "mating" of the rounded edge of the femur and the flat edge of the
tibia. Without a meniscus, weight transmitted by the femur would concentrate on a single contact
point on the tibia, under high pressure. (Pressure is defined as force divided by area; thus, a
constant force on a smaller area creates higher pressure.) The meniscus allows the femur to rest
effectively on nearly the entire tibial plateau, distributing the force and preventing excess stress on
any single area. In addition, the meniscus functions as a shock absorber, dampening the forces
that the femur may apply to the tibia under high-load activities such as jumping or running.
The meniscus also helps the anterior cruciate ligament (ACL) to stabilize the knee. Just as a block
placed behind the wheel of a car prevents it from rolling, the body of the meniscus prevents the
femur from gliding too far off the tibia. The posterior oblique ligament on the medial side of the
knee tethers the posterior horn of the meniscus to ensure that this stabilizing wedge is kept in
place. Patients who tear the posterior meniscal horn may feel instability--even if their cruciate
ligament is intact--because this stabilizing effect is lost (4).
Differing Presentations
Tears of the menisci occur in two distinct settings. The first occurs when a healthy meniscus is
traumatized and is characteristic of the young athlete. The mechanism of injury is commonly a
twisting motion with the knee bent, and such tears can be found either within the body of the
meniscus or at the junction of the meniscus and the inner lining of the knee, an area known as the
joint capsule. When a large piece of the meniscus tears from the capsule, it can flip over within the
joint creating a so-called a "bucket-handle" tear: attached at two ends, with the middle flipped
upward in the center. The movable flap of meniscus can block motion and is one of the rare causes
of a truly "locked" knee.
A different injury is seen in older patients. Because the tissue is no longer as strong or resilient,
less force is needed to tear the meniscus. Accordingly, the older patient may not even recall when
the injury occurred. Rather, the symptoms may appear gradually. Finally, since a degenerative tear
cannot be repaired in the older patient, the urgency for treatment is much lower than that required
when treating a bucket-handle tear in a young person, in which the objective is to prevent damage
to potentially repairable tissue.
Diagnosing Tears
History and physical. Diagnosis of meniscal tears can often be made clinically (table 1). In the
young athlete, there is usually a history of twisting injury that prevented continuation of play. An
older athlete may note a more gradual onset of symptoms. If no other structures were damaged,
pain localizes at the joint line and worsens with hyperflexion. In the early course, patients may
limp as they find full weight bearing too painful. An effusion is common but may be absent if the
tear occurs as an isolated injury.
TABLE 1. Primary Care Diagnosis and Management of Suspected Meniscal Tears
Task
How
Why
Localize the symptoms
to the joint line
- Palpate the joint line
- Ask the patient to squat
Although not a specific
finding, a meniscal tear is
128
- Stress the collaterals
almost always associated with
joint-line signs and symptoms
Determine if there is a
bloody effusion
Have the patient lie supine, compress
the area above the patella with your
hand closest the patient's head, and
hold your other hand just below and
alongside the patella. If an effusion is
present, a fluid wave will move to the
distal hand; aspirate this fluid with a
16-gauge needle.
Bloody effusions, in the
absence of overt fracture, are
associated with ACL
disruption, patellar
dislocation, osteochondral
fracture, and red-zone
meniscal tear. All need
orthopedic care.
Rule out other injury
(especially those
associated with
twisting)
- Test the ACL (Lachman test), MCL
(valgus stress), and patellar stability
(patellar apprehension test--if the
patient remains calm as the examiner
attempts to push the patella laterally,
the test is negative)
- Obtain x-rays
- Other injuries, with or
without a meniscus tear, are
possible
- Do not miss a fracture
Determine if there is
pre-existing arthritis
Obtain weight-bearing x-rays
If the patient has arthritis, it,
rather than the meniscal tear,
may be the cause of
symptoms; results of
arthroscopic surgery on the
meniscus are much worse
when arthritis is present
Assess whether the
tear is repairable
- Assume that all patients younger than
age 35 have potentially repairable tears
- Tears associated with bloody effusions
may be repairable
Repairable tears should be
fixed to prevent arthritis
Unless signs warrant
orthopedic consultation,
begin a program of
physical therapy (antiinflammatory drugs
may be added)
Regimen should include range-ofmotion exercises and gentle hamstring
and quadriceps strengthening
Prevents atrophy while
awaiting symptomatic
recovery
Reassess
Unless the patient is referred to an
orthopedic surgeon, reassess at least
once a month to ensure that symptoms
are improving and to continue to rule
out other injury
Pain and swelling at the time
of injury may cause guarding
and thus compromise the
accuracy of the physical exam
ACL= anterior cruciate ligament; MCL= medial collateral ligament
129
Specific tests. An aspiration may help identify the underlying cause of the effusion. Blood in the
knee is an ominous sign: Since the meniscus itself is avascular, hemarthrosis should not be
attributed to a meniscal tear. Rather, the physician should assume that other structures in addition
to the meniscus (such as the ACL) may have been injured (5). The lone exception to this rule is
when the meniscus is torn from the capsule, a vascularized structure. Such an injury will produce
blood in the joint. The presence of blood in this situation is a significant finding, but for beneficial
reasons; it implies that the meniscus may be repairable. Accordingly, all patients with a bloody
effusion after trauma should be referred to an orthopedic surgeon.
Special diagnostic maneuvers exist for identifying meniscal tears on physical examination, but they
are not particularly sensitive. For example, the McMurray test, which attempts to detect a click as a
torn meniscus is moved with knee extension, will miss at least 40% of all meniscal tears (6,7).
Thus, the best diagnostic steps are general ones: Establish a history consistent with the injury,
localize the symptoms to the joint line, and exclude other injuries such as cruciate or collateral
ligament tears. If the clinician suspects a meniscal tear and determines that it needs to be treated,
magnetic resonance imaging (MRI) can confirm the diagnosis.
MRI. The use of MRI is a hotly debated topic. The clinician should be aware of the strengths and
limitations of MRI, and use it when the technique can be helpful. The advantages of MRI are that it
involves minimal risk to the patient (since no ionizing radiation is used) and that it paints a fairly
accurate picture of soft tissues of the knee (figure 2). MRI is both sensitive and specific for
meniscal tears--accuracy is approximately 90% (8). Finally, MRI may reveal abnormalities that
were not suspected on the clinical exam and thus may influence treatment.
One disadvantage of MRI is its high cost. In addition, patients may insist on treatment for a lesion
discovered on MRI, even if the clinician is certain that such a lesion is not the source of the
patient's symptoms. Although MRI is very helpful for discovering abnormalities (9), it cannot
differentiate lesions responsible for the patient's symptoms from incidental lesions. As such, MRI is
not always helpful for determining a treatment plan.
The important clinical factors to consider in management include the severity and location of
symptoms, the patient's preferences, and the overall impact of the tear on the function of the
patient's knee. None of these is reflected on the MRI. As such, MRI cannot replace the history and
physical and does not supplant medical judgment.
Clearly, an MRI is not necessary for all patients. Consider, for example, an athlete who has a
locked knee after a twisting injury, medial joint-line tenderness, and bloody effusion. These
findings strongly suggest a bucket-handle tear of the medial meniscus. This tear needs to be
reduced and repaired, if possible. Urgent arthroscopy, without MRI, is warranted. On the other
hand, if the patient had known osteoarthritis and was not, accordingly, a good candidate for
arthroscopy, using MRI for diagnosing a tear is unnecessary because it would not influence the
immediate treatment plan.
Radiographs. Omitting an MRI does not mean that all imaging studies should be skipped. Athletes
who have had an injury and cannot fully bear weight or have tenderness along the tibia, femur, or
patella should be sent for plain radiographs to rule out a fracture. Because x-rays show only bone,
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plain radiographs cannot detect a meniscal tear; however, they can often exclude other problems
such as a fracture or an osteochondral defect. In addition, weight-bearing x-rays can help detect
degenerative arthritis, a finding that may affect treatment.
Treatment Options
Nonoperative therapy. Current treatment for meniscal tears can be grouped into three
categories (table 2): nonoperative, partial meniscectomy, and meniscal repair. Nonoperative
treatment includes the use of anti-inflammatory medications as well as physical therapy to prevent
quadriceps weakness, stiffness, and other consequences of disuse. Conservative treatment is
appropriate even when there is a documented meniscal tear as long as the tear is not repairable
and the patient is willing to wait and monitor symptom progression. In older patients, symptoms
may simply abate with time. In Europe, where some national health insurance plans require a long
wait for surgery, many patients cancel their operations because they have recovered sufficiently
(10,11).
TABLE 2. Comparison of Treatment Options for Meniscal Tears
Treatment
Advantages
Disadvantages
Comments
Nonoperative
- Surgery and its risks
are avoided
- Small peripheral tears
may heal on their own
- Preferable in patients
whose chief complaints
are caused by arthritis,
rather than a meniscal
tear
- May not relieve all
symptoms, especially
catching and clicking
- Potentially repairable
tear may become
irrepairable
- Does not mean no
therapy
- Requires an exercise
program and some physical
therapy to prevent
quadriceps weakness
Partial
meniscectomy
- Often relieves
symptoms very well
- Rapid return to joint
function
- Yields poor results if
articular cartilage is
already damaged
Meniscal tissue is lost,
creating some risk for
degeneration
Only for patients who are
sufficiently bothered by
their tear, and for whom
meniscal repair is not
possible
Meniscal repair
- Provides reliable shortterm relief from pain
- Helps long-term
preservation of joint
- Not all tears are
repairable
- The risk of
complications is higher
than for simple
meniscectomy
- Longer recovery than
for meniscectomy
This surgery is not as
simple as a meniscectomy
and should be performed
by a sports medicine
specialist
Open
meniscectomy
None
Excessive dissection,
causing a slower
functional recovery
Rare now, but physicians
may see patients who had
this surgery years ago;
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arthritis likely
Small tears are especially good candidates for nonoperative therapy (12). If the tear is small and
peripheral, it may heal without intervention (13). The risk of neglecting a tear is that a second,
perhaps trivial, injury may lengthen the original tear. This risk, however, is small. Nonoperative
treatment should always include an exercise program as well as physical therapy to prevent muscle
atrophy. There is no formal role for knee braces, but some patients report a subjective
improvement wearing a wrap or sleeve, perhaps because of the retained body warmth or increased
proprioception from skin stimulation.
Nonoperative treatment also can produce complications. The patient's function may deteriorate
until the meniscus is removed. Muscles may atrophy from disuse, and the meniscal fragment can
detach and block knee motion or injure the adjacent articular cartilage. Blocked motion, especially
if it persists after the pain improves, indicates a need for specialist referral. Finally, a potentially
repairable tear can be pulverized by the articular surfaces and become irrepairable.
Partial meniscectomy. Typically, meniscectomies are performed arthroscopically, as are most
repairs (figures 3 and 4). This minimally invasive approach lessens the disruption of normal tissue
and allows for rapid rehabilitation. Arthroscopy leads to less postoperative swelling, faster
achievement of full flexion, quicker return to work and sports, and lower hospital costs compared
with open surgery (14,15). Meniscectomy reliably treats the acute symptoms of the tear (16). In
the absence of a second intra-articular problem, excellent results are the norm (17-19). Still, most
patients will need supervised postoperative physical therapy to regain full muscle strength (20,21).
One disadvantage of partial meniscectomy relative to repair is that it eliminates some of the
benefits provided by the cartilage in that area; eg, arthroscopic partial meniscectomy may lead to
Fairbank's changes if a large fragment is removed (22). Repairable tears should thus be fixed and
132
not removed. Also, meniscectomy is not appropriate in all patients: If there is extensive articular
damage, simply removing the meniscus will not revitalize the joint (23-25).
Meniscal repair. Meniscal repair, on the other hand, may prevent Fairbank's changes (26). In this
surgery, the torn edges of the meniscus are sutured to preserve the form and function of the
cartilage. Short-term follow-up shows that approximately 90% of sutured peripheral meniscal tears
do, in fact, heal (27,28). Better still, some evidence suggests that repaired menisci can prevent
articular degeneration (29).
In one 10-year study (30) of 50 arthroscopically repaired meniscal tears, only 8% of surgically
treated knees had minimal joint changes, as compared with 3% in the uninjured knee. This finding
represents a dramatic improvement over that noted by Fairbank (2) and suggests that the repaired
cartilage can prevent degenerative changes. This potential benefit prompts some surgeons to
advocate attempted repair of even those tears that have a fairly low chance of healing (31).
Not all patients are candidates for meniscal repair (32). Sometimes the tissue is too damaged to
save. Also, since the meniscus itself is avascular, only tears at the periphery of the meniscus,
adjacent to the synovial blood supply and capsule, are likely to heal. This region near the capsule is
called the "red zone" because of its proximity to the capillaries of the synovium. The more central
area is called the "white zone." It may be possible to repair a tear in the white zone under special
circumstances. For instance, if a repair were undertaken at the same time as a ligament
reconstruction, a white-zone tear may heal (33). It is thought that the intra-articular bleeding
caused by drilling tunnels for ligament reconstruction provides the biological factors that can
stimulate healing. When the tear is not quite in the red zone and no ligament surgery is done,
creating vascular channels or placing a fibrin clot in the tear may increase the healing potential
(34-36).
Rehabilitation and Education
If none of the signs that warrant orthopedic consultation are present, the primary care physician
should recommend a program of physical therapy and perhaps medication for pain such as an antiinflammatory drug or acetaminophen. Relative rest, but not complete inactivity, may also be
helpful. It is also important to reassess the patient after a few days. At this point, the acute pain
should have subsided, and a more accurate physical examination will be possible. Rehabilitative
exercises, including stretching, flexion and extension strengthening, and stamina building can
speed the patient's return to function, both as a primary treatment modality and as part of the
postoperative regimen.
The final consideration is to educate patients about their injury. Some older patients may be very
hampered initially by their symptoms, but they need to know that recovery is possible without
surgery. On the other hand, a young athlete may be inclined to persevere despite the injury, which
may damage a potentially repairable meniscal tear. Remember that an anatomic diagnosis does
not define the treatment. Rather, the unique features of each patient's case--age, activity,
symptom severity, etc--dictate the care required.
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meniscectomy. Arthroscopy 1997;13(6):673-679
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extensor and flexor muscles after arthroscopic meniscectomy: a pilot study. Clin Orthop
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partial meniscectomy. J Rheumatol 1992;19(12):1938-1942
25. Matsusue Y, Thomson NL: Arthroscopic partial medial meniscectomy in patients over 40
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26. DeHaven KE: Decision-making factors in the treatment of meniscus lesions. Clin Orthop
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27. Warren RF: Meniscectomy and repair in the anterior cruciate ligament-deficient patient.
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29. Muellner T, Egkher A, Nikolic A, et al: Open meniscal repair: clinical and magnetic
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30. Johnson MJ, Lucas GL, Dusek JK, et al: Isolated arthroscopic meniscal repair: a long-term
outcome study (more than 10 years). Am J Sports Med 1999;27(1):44-49
31. Rubman MH, Noyes FR, Barber-Westin SD: Arthroscopic repair of meniscal tears that
extend into the avascular zone: a review of 198 single and complex tears. Am J Sports Med
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32. Eggli S, Wegmüller H, Kosina J, et al: Long-term results of arthroscopic meniscal repair: an
analysis of isolated repairs. Am J Sports Med 1995;23(6):715-720
33. Cannon WD, Vittori JM: The incidence of healing in arthroscopic meniscal repairs in anterior
cruciate ligament-reconstructed knees versus stable knees. Am J Sports Med
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34. Henning CE, Lynch MA, Yearout KM, et al: Arthroscopic meniscal repair using an exogenous
fibrin clot. Clin Orthop 1990;252(Mar):64-72
35. Van Trommel MF, Simonian PT, Potter HG, et al: Arthroscopic meniscal repair with fibrin
clot of complete radial tears of the lateral meniscus in the avascular zone. Arthroscopy
1998;14(14):360-365
Patellofemoral Pain: Let the Physical Exam
Define Treatment
William R. Post, MD
THE PHYSICIAN AND SPORTSMEDICINE - VOL 26 - NO. 1 - JANUARY 98
In Brief: The complex causes of patellofemoral disorders are most effectively identified through a
systematic evaluation of a patient's lower-extremity alignment, patellar mobility, muscle flexibility,
strength, and coordination as well as an assessment of soft-tissue and articular pain. By combining
information from such an exam with a careful history and appropriate radiographic studies, the
physician can make a specific diagnosis. This sets the stage for an optimal rehabilitation
prescription, which usually will involve some combination of muscle flexibility and strength training,
taping, orthoses, analgesics, and therapy with heat and ice.
Primary care and specialist physicians often treat patients who have patellofemoral disorders.
These conditions generally respond to nonoperative treatment, but the chance of a satisfactory
outcome is best if the treatment is planned in accord with a careful history and a systematic
physical exam. The exam should include assessment of alignment, soft-tissue flexibility, muscle
strength and coordination, and the location of pain sites. Such an approach will permit the
physician to prescribe an exam-directed rehabilitation program that can increase the efficiency and
success of nonoperative treatment.
Clues From the History
The first goal in taking a history is to discern whether a patient has complaints of pain and/or
instability and to determine the mechanism of injury, if any. Most patients complain of pain or
instability, but some have both. An attentive examiner can glean important diagnostic information
from patients' descriptions of the location of their pain (see "Pain Diagrams Aid Diagnosis," below).
Patients often report anterior knee pain, which is typically activity related and worsens when a
patient negotiates stairs or runs over hilly terrain. It usually increases after the prolonged knee
flexion that occurs during long car rides or sitting in class or a movie theater. Patients who have
symptoms of patellar instability have had a dislocation or recurrent subluxation. True patellar
subluxation occurs when the patella slips laterally out of the trochlear groove during a twisting
injury. This action is different from a "giving way" or "buckling" of the knee, which more commonly
represents reflex inhibition of the quadriceps from painful stimulus. Medial dislocation or
subluxation is very rare and almost always is a result of failed patellofemoral realignment surgery.
The mechanism of injury is another important diagnostic clue. Patients who are injured by highimpact blunt trauma are much more likely to have suffered articular cartilage damage, particularly
if the patient's flexed knee received a direct impact from, for example, the dashboard in a motor
vehicle accident. If the impact occurred over the proximal tibia, the posterior cruciate ligament
may have been injured, and the physical examination should include the posterior drawer test.
Patellar injuries due to relatively low-energy trauma such as may occur during walking, twisting, or
dancing should raise suspicion of anatomic malalignment or flexibility deficits that may predispose
the patient to instability. Similarly, insidious onset of patellofemoral complaints can be related to
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an anatomic predisposition or training errors that may cause soft-tissue inflammation such as
patellar tendinitis. Understanding training errors or overuse patterns is essential for nonoperative
management of patellofemoral disorders, since rehabilitation may include exercise and/or activity
modification (see "Why Rehabilitation Requires Exercise," below).
Physical Examination: The Key Step
The key to providing a rational diagnosis and sound nonoperative treatment is the physical exam.
The objectives of the exam are to confirm that the pain is patellofemoral in origin, reproduce the
complaint, evaluate anatomic alignment and flexibility, and locate painful structures (1). Once the
sequence is mastered, these tasks can generally be accomplished in a concise, directed exam that
takes approximately 5 minutes. In patients who have unilateral complaints, comparison with the
asymptomatic knee is critical, since "normal" values for physical exam variables are lacking.
Note that anterior knee pain may be referred. Particularly in children and adolescents, screening
physical examination of the hip joint is important. Disorders such as Perthes disease and slipped
capital femoral epiphysis can cause anterior knee pain in this age-group. In patients of all ages,
lumbar radiculopathy and peripheral nerve entrapment are possible causes of anterior knee pain
that can be diagnosed by a careful examiner. Examination of hip range of motion and straight leg
raising should generally exclude lumbar and hip disorders.
In attempting to discern the source of the patient's pain, an important question is whether it
primarily involves the soft tissues or the patellofemoral articulation itself. The examiner should
consider the retinacular and synovial tissues, since they are densely innervated structures. The
paratenon and the subcutaneous nerves in the patellofemoral joint area can also cause pain.
Subchondral bone contains nerve fibers that may cause pain by responding to overload or
increased interosseous pressure. Articular cartilage does not contain nerve endings; therefore,
chondromalacia cannot be considered the true anatomic cause of anterior knee pain (2).
(Chondromalacia is a surgical finding that may represent areas of hyaline cartilage trauma or
aberrant loading but is not the cause of pain. For this reason physicians should abandon the use of
"chondromalacia" to mean a cause of anterior knee pain and use the term only to refer to actual
articular cartilage softening when it is described at surgery.) In investigating the cause of pain in
patients who carry a diagnosis of chondromalacia, careful examination will usually reproduce the
patient's complaints by uncovering multiple areas of tenderness in the peripatellar soft tissues.
Is There Malalignment?
To assess alignment, first observe the patient while he or she stands barefoot facing you. Observe
the standing Q-angle (ie, the valgus angle) acting across the knee; angles greater than 25° in
females and 20° in males are considered abnormal. Watch for torsional deformities as well as
significant hindfoot pronation. If excessive pronation is present, ask the patient to turn around and
stand on tiptoe; if the heel inverts, the pronation is supple. Excessive hindfoot pronation results in
prolonged internal tibial rotation during gait, adversely affecting patellar mechanics. Orthoses can
sometimes help control overpronation, though they are not routinely prescribed (see "Putting It All
Together: The Rehab Prescription," below).
Next, observe the patient squat and stand. Note how difficult this is for the patient, as this helps
determine the severity of functional deficit.
Tubercle sulcus angle and crepitus. With the patient sitting on the examining table facing you,
observe whether the tibial tubercles are directly below the patellae or are displaced laterally more
than 10°, indicating an increased tubercle sulcus angle (3). Lateral displacement of the tubercle
suggests bony patellofemoral malalignment that may indicate an underlying predisposition to
lateral patellar tracking. Next ask the patient to actively flex and extend the knee and observe the
dynamic patellar tracking. Palpate and listen for crepitus as the patient moves his or her leg. Be
sure to compare any crepitus with the contralateral knee, because crepitus is common in
asymptomatic knees. If crepitus is clearly greater in the symptomatic knee, there may be articular
cartilage damage on the patella and/or trochlea.
Is patellar mobility restricted? Before palpating for tenderness--which might make the patient
uncomfortable and apprehensive, thereby making the rest of the examination more difficult--
136
evaluate the patient's patellar mobility and lower-extremity flexibility. With the patient supine on
the examination table, perform the patellar tilt test (figure 1: not shown) as a first step in
evaluating patellar mobility. Compare the results with those of the contralateral knee and note any
asymmetry that can be addressed during rehabilitation.
While holding the patella in corrected or neutral position of patellar tilt, attempt to displace the
patella first medially and then laterally. Medial glide of one quarter or less of the patellar width
suggests an abnormally tight lateral retinaculum, while medial glide of three quarters or more of its
width suggests hypermobility (4). If lateral displacement produces apprehension of impending
patellar subluxation or reproduces symptoms, the test is considered positive and strongly suggests
patellar instability. Comparing superior and inferior patellar glide can sometimes reveal side-to-side
differences as well, especially in patients who have undergone surgery.
What's Tight?
Flexibility deficits in the hip external rotators, hamstrings, quadriceps, and gastrocnemius-soleus
muscle group may contribute to abnormal patellofemoral biomechanics. Diagnosing asymmetry
that results from such deficits is a critical part of managing patellofemoral disorders, because
asymmetry should be addressed in a treatment plan that uses stretching exercises to focus on
specific muscle groups.
Hamstring and gastrocnemius flexibility. Hamstring flexibility may be estimated by measuring
the popliteal angle while the patient is supine. Flex the hip to 90° and then extend the knee. Keep
the patient's pelvis flat on the examination table and measure the angle created by the thigh and
lower leg. While the hip and knee are flexed 90°, also check the amount of ankle dorsiflexion.
When the patient's leg is brought down to the exam table, check the ankle dorsiflexion again in
extension. Commonly, it will be less when the knee is extended, indicating gastrocnemius
tightness.
Quadriceps flexibility. Checking quadriceps flexibility while the patient is prone (figure 2: not
shown) is a crucial part of the examination. Because the rectus femoris muscle crosses the hip
knee joints, prone examination is necessary to keep the hip extended during evaluation of
quadriceps flexibility. Significant prone quadriceps flexibility deficits are common, especially in
patients with chronic pain. If a deficit exists, a home program of quadriceps stretching can produce
dramatic improvement.
Iliotibial band flexibility. The iliotibial band (ITB) connects the iliac crest to Gerdy's tubercle on
the anterolateral proximal tibia and has strong attachments to the lateral patella through the
lateral retinaculum. It is often tight in patients who have patellofemoral symptoms, especially in
those whose patellar tilt does not correct to neutral. Ober's test assesses ITB flexibility (figure 3).
While performing Ober's test, palpation of the ITB just proximal to the lateral femoral condyle
during maximal stretch (ie, at the end of the test) frequently causes severe pain in patients who
have excessive ITB and lateral retinacular tightness. When this is found, ITB stretches are an
indispensable component of treatment. We have found that Ober's position (figure 3c) is
consistently effective for treatment as well as diagnosis. Flexibility assessment is a critical part of
the patellofemoral examination, because asymmetry should be addressed in the treatment plan by
gearing stretching exercises to tight muscle groups.
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What's Tender?
Careful palpation of all soft tissues in the peripatellar area is essential. Begin at the quadriceps
tendon and work around the patella, palpating the central quadriceps tendon insertion, the vastus
lateralis insertion, the lateral patellar retinaculum, the patellar tendon (origin, midsubstance, and
tibial insertion), the medial retinaculum, the medial parapatellar plica between the medial border of
the patella and the medial femoral epicondyle, and the vastus medialis obliquus muscle insertion.
Note areas of tenderness and ask if the elicited tenderness reproduces the patient's pain.
To assess articular pain due to irritation of subchondral bone, the patella must be compressed into
the trochlea at various degrees of flexion (figure 4: not shown). Normally the patella enters the
trochlea at 10° to 15° of knee flexion, so pressure applied in full extension does not directly
produce articular compression between the patella and the trochlea. As the patella enters the
trochlea in early flexion, the distal portion of the patella is articulating; pain with compression in
this range suggests a lesion in the distal patellar or proximal trochlear area. Conversely, as knee
flexion increases, the patella is drawn distally into the trochlea, causing the area of articulation to
be more proximal on the patella; pain with articular compression in flexion suggests a more
proximal patellar lesion.
Other authors have described direct palpation of the lateral facet of the patella. Any tenderness
noted, however, cannot necessarily be ascribed specifically to the bone, since such palpation
involves the highly innervated lateral patellar retinaculum and synovial tissue as well.
Muscle Strength and Coordination
Office evaluation of quadriceps strength and motor control can only provide a rough estimate.
However, measurements of thigh girth at set distances above the superior pole of the patella allow
side-to-side comparison and meaningful data for follow-up evaluations.
It is also helpful to ask the patient to contract the quadriceps and to observe the timing of the
vastus medialis obliquus and vastus lateralis contractions. Normally they fire simultaneously,
balancing the quadriceps moment acting on the patella. In patients with anterior knee pain and
patellofemoral malalignment, it is not unusual to see the vastus lateralis fire before the vastus
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medialis obliquus. When patients have unbalanced quadriceps contraction, treatment should
include methods to improve coordination, such as biofeedback.
Radiographic Studies
Initial evaluation of patients who have patellofemoral complaints usually involves plain radiographic
studies. Anteroposterior and lateral views can rule out associated and potentially serious bony
conditions such as tumors, infection, or bony loose bodies. Plain radiographic patellar axial views-the sunrise or Merchant view--can demonstrate patellofemoral malalignment, but plain radiographs
are less sensitive than computed tomography or magnetic resonance imaging studies in this
regard. However, until thorough nonoperative management has failed, radiographic studies beyond
standard plain x-rays are not indicated. Detailed radiographic measurements are not necessary to
refine the nonoperative treatment of patellofemoral disorders.
Putting It All Together: The Rehab Prescription
In a busy clinical practice, the information gathered from the physical exam and radiographic
studies becomes the basis for a rehabilitation prescription. For example, when the physician has
observed and documented flexibility deficits and retinacular and ITB limitations that contribute to
the patient's patellofemoral symptoms, the prescription should include specific stretches such as
Ober's stretch--performed in the same manner as Ober's test--for ITB tightness. Physical therapists
should be fully informed about the patient's condition and the rehabilitation prescription so that
treatment proceeds effectively.
Taping. A rehabilitation prescription for patients with soft-tissue tightness, especially lateral
patellar tilt and soft-tissue pain, can include patellar taping, which frequently reduces pain during
exercise (3) and, in some patients, even allows pain-free exercise, a key to progress in
patellofemoral disorders. How taping relieves pain is uncertain, but the improvement may result
from alterations in local soft-tissue tensions or decompression of synovial tissue that can be
pinched during motion. Some patellar braces may offer similar advantages.
Quadriceps strengthening. Quadriceps strengthening is a universal recommendation for patients
with patellofemoral problems. A quadriceps strengthening program should initially avoid exercise in
the arcs of motion found to be painful during articular compression and should gradually increase
the range of resisted activities as the patient improves.
Although rehabilitation has traditionally begun with open-chain terminal knee extension exercise
with low weight, the advantages of closed- versus open-chain exercise have been debated.
Recently, Steinkamp et al (5) evaluated patellofemoral joint reaction (PFJR) force and
patellofemoral joint stress (force per unit area) for leg press and leg extension exercise at
intensities producing equal quadriceps tension demands. They found that closed-chain knee
extension (leg press) generated less PFJR force than open-chain knee extension from
approximately 45° to full extension. Conversely, at greater degrees of flexion, PFJR force was less
with open-chain knee extension exercise. Thus, in some patients leg press exercise may be better
tolerated than traditional open-chain knee extension exercises.
In my experience, the cocontractions and weight-bearing loads associated with closed-chain
activities tend to be tolerated better than open-chain exercise in most patients with patellofemoral
disorders. However, biomechanical arguments can be made in favor of open-chain exercise at
different points in the range of motion, and often a trial-and-error approach works best in
determining which exercises are best tolerated by individual patients.
When specific areas of tendinitis have been identified, eccentric exercise of the involved muscle
group should be included (6). For example, patients with patellar tendinitis should include eccentric
quadriceps strengthening. As rehabilitation progresses and pain decreases, the patient should also
include sport- or work-specific exercise in his or her program.
Biofeedback. If a patient has been diagnosed as having unbalanced quadriceps contraction,
biofeedback should be part of the rehabilitation prescription. This can be as simple as asking the
patient to palpate the quadriceps during contraction in order to voluntarily correct the
139
asynchronous contraction. More complex biofeedback techniques can provide visual and auditory
feedback on muscle contraction and aid in quadriceps retraining.
Orthoses. The routine use of orthoses in patients with flexible hindfoot pronation and
patellofemoral problems remains controversial. Because of this controversy and the cost of orthotic
devices, I avoid their routine prescription initially. Use of orthoses is reasonably reserved for
patients who have not responded to flexibility and strengthening routines.
Analgesics. The use of analgesics, including nonsteroidal anti-inflammatory drugs (NSAIDs), can
be an important adjunct to the flexibility and strengthening prescription, because analgesics reduce
pain and allow patients to pursue meaningful and successful rehabilitation. Since analgesic use
does not resolve the strength and flexibility problems that underlie patellofemoral disorders,
patients who are treated only with NSAIDs and rest have a high rate of recurrent symptoms.
Heat and cold. The use of heat before exercise increases soft-tissue flexibility. Ice application
after exercise should be a routine part of treatment. In particular, ice massage over the areas
found to be most tender on physical examination is frequently effective. Ice massage is particularly
helpful where painful tissues are superficial, such as the vastus lateralis tendon insertion, the
patellar tendon, and pathologic hypertrophic medial parapatellar plicae. Such localized areas of
inflammation may also respond to anti-inflammatory modalities such as phonophoresis with
hydrocortisone.
Patient Education and Follow-up
With the advent of limits on the number of therapy visits covered by insurance, we need to assist
our patients in making the most of their visits. One way to assist is to let patients know what you
expect for their therapy and also what they can expect. For example, patients who have restricted
patellar mobility and iliotibial band tightness should expect hands-on stretching by therapy
personnel for at least 15 to 20 minutes of each session. In addition, since data on patients'
progress is increasingly important to managed-care providers, we need to document change to
provide objective measures that may justify ongoing treatment. Although these steps may take
time, they are worthwhile because they improve treatment specificity and quantify progress.
Physicians can and should do better than simply sending patients to therapy for "quadriceps
strengthening." By doing a careful clinical evaluation of our patients' patellofemoral problems, we
can provide a more scientific and rational diagnosis than "chondromalacia" or "patellofemoral pain
syndrome." Improved diagnoses will foster clearer thinking and problem solving for the therapist
involved and will ensure that patients who are referred to different therapists will receive consistent
and appropriate rehabilitation. Such an approach will be efficient for patients, cost-effective for
medical insurance carriers, and rewarding for healthcare providers.
References
1. Post WR: Physical examination of the patellofemoral joint, in Fulkerson JP (ed): Disorders
of the Patellofemoral Joint, ed 3. Baltimore, Williams and Wilkins, 1997
2. Radin EL: A rational approach to the treatment of patellofemoral pain. Clin Orthop
1979;144(Oct):107-109
3. McConnell J: The management of chondromalacia patellae: a long term solution. Austr J
Physiother 1986;32:215-223
4. Kolowich PA, Paulos LE, Rosenberg TD, et al: Lateral release of the patella: indications and
contraindications. Am J Sports Med 1990;18(4):359-365
5. Steinkamp LA, Dillingham MF, Markel MD, et al: Biomechanical considerations in
patellofemoral joint rehabilitation. Am J Sports Med 1993;21(3):438-444
6. Stanish WD, Rubinovich RM, Curwin S: Eccentric exercise in chronic tendinitis. Clin Orthop
1986;208(Jul):65-68
Pain Diagrams Aid Diagnosis
140
The use of a simple, patient-drawn pain diagram may help clarify a vague, frustrating, and
complicated history in a patient with patellofemoral pain. One study (1) used a standard knee
diagram divided into nine zones to correlate areas of pain noted by patients with areas of
tenderness found by physicians on physical examination. Patients who complained of anterior knee
pain marked areas of pain on the diagram before being evaluated. After the physical exam, the
physician marked areas of tenderness on a separate, identical diagram. The patient-drawn
diagrams correlated fully or partially with the physician-drawn diagrams in 88% of cases. The
association of pain and tenderness in the nine anatomic zones was very consistent. Even more
clinically relevant was the finding that 86% of the sites where the patient did not indicate pain
correctly predicted the absence of tenderness.
These findings are important because they show that a focused physical exam can reproducibly
distinguish anatomic sites likely to be involved in generating the patient's pain. Identifying these
tender structures and associated strength and flexibility imbalances forms the basis of a thorough,
rational nonoperative rehabilitation program.
Reference
1. Post WR, Fulkerson J: Knee pain diagrams: correlation with physical examination findings
in patients with anterior knee pain. Arthroscopy 1994;10(6):618-623
Why Rehabilitation Requires Exercise
Tissues in the anterior knee most often become painful as a result of tissue overload. This overload
may be acute--as in blunt anterior knee trauma or a high-energy patellar dislocation--or may be
the result of repetitive overuse. Overuse may result from training errors and underlying
malalignment, which lead to soft-tissue microinjury. If a training schedule does not permit time to
heal such microinjury, continued strenuous activity can result in overload and microfailure. Though
the exact mechanism by which overload produces pain is uncertain, strength and flexibility
imbalances are almost always clinically important features of this cycle.
For patients and athletes to return to their desired activity level, their rehabilitated strength and
flexibility must often exceed the preinjury level, since that level was inadequate to support the
original loads imposed. The patient must temporarily decrease and/or modify the loading conditions
of the knee and work toward restoration of adequate strength and flexibility to reach his or her
goals safely. Rest and medication can certainly decrease pain, but they cannot improve the ability
to perform at the desired level. Thus, when treatment features only rest and medication,
recurrence is likely when patients resume their activities.
141
Posterior Knee Pain and Its Causes
A Clinician's Guide to Expediting Diagnosis
In Brief: Because posterior knee pain is a relatively uncommon patient complaint, its etiology
is challenging and often elusive. The differential diagnosis for posterior knee pain can be vast,
so clues for distinguishing causes are important. Many clinicians are unfamiliar with this
complicated anatomic area and may not have a standard clinical evaluation to establish a
cause of the patient's pain. Review of several known causes of knee pain can provide the
examiner with a more comprehensive list of potential disorders to consider as differential
diagnoses when patients present with posterior knee pain.
It is critical that the examiner obtain a good history when evaluating patients who have
posterior knee pain. Information regarding the onset, duration, location and quality of pain
(using the visual analogue scale), aggravating and alleviating factors, past injuries, operations,
and other treatments, including medications, procedures, rehabilitation, and orthotic use, can
aid with diagnosis. Also significant is knowing whether the pain truly arises from a local source
or is being referred from a more distant source, such as in sacroiliac dysfunction or radicular
pain.
Soft-tissue and tendon injuries are perhaps more common causes of posterior knee pain than
are vascular, neurologic, and iatrogenic injuries, but these less common origins should not be
overlooked in patients who present with posterior knee pain (table 1).
TABLE 1. Characteristics of Disorders That Exhibit Posterior Knee Pain
Diagnosis
Support Structures and
Tumors
Baker's cyst
Soft-tissue or bone tumor
Meniscal tear
Tendons
Hamstring injury
Distinguishing Symptoms
Physical Findings
May be asymptomatic; patient
may have feeling of fullness in
the popliteal fossa
Crescent sign; may simulate
venous thrombosis
Knee locking; palpable
mass; pain without weight
bearing
Limited knee flexion; may
mimic a meniscal tear
Increasing pain with deep knee
flexion
Point joint-line tenderness;
positive McMurray's test;
effusion
Posterior knee pain with sudden
acceleration or deceleration
Tenderness at distal biceps
femoris tendon; pain with
knee flexion
Gastrocnemius tendon
calcification
Posterior knee pain with knee
extension and ankle dorsiflexion
Popliteus tendon injury
Pain with running, especially
downhill
Ligaments
Posterolateral corner injury
Varus thrust in stance or with
ambulation; hyperextension,
external rotation; peroneal
Patient may have tenderness
over areas of CPPD deposition
Knee flexion with internal
rotation of the tibia in prone
position may cause pain
Varus thrust; positive external
recurvatum test; positive
dial test
142
external rotation; peroneal
nerve may also be injured
Blood Vessels
Popliteal artery entrapment
syndrome
Nerves
Common peroneal nerve
entrapment
Tibial nerve entrapment
Iatrogenic
Postsurgical arthrofibrosis
Bioabsorbable tacks
Other
Degenerative joint disease
Hypertrophy of calf muscles;
claudication; paresthesias below
the knee
Tenderness over area of
entrapment; pain may increase
with exertion
Tenderness over area of
entrapment; pain may increase
with exertion
Distal pulses may disappear
with hyperextension and
active plantar flexion or
passive dorsiflexion; trophic
changes below the knee
Local tenderness over area
of entrapment
Local tenderness over area
of entrapment
Limited knee extension
Limited range of motion;
stiffness
Sharp posterior knee pain
exacerbated with knee extension
Pain increases with loading;
morning stiffness
Focal tenderness over points
of
tack placement; stable knee
Crepitus; limited range of
motion; change in
structural alignment
CPPD = calcium pyrophosphate dihydrate
Baker's Cyst and Tumors
Clinicians should be cognizant of soft-tissue disorders and tumors when examining patients
who report posterior knee pain.
Baker's cyst (popliteal synovial cyst). The popliteal synovial cyst, more commonly known
as Baker's cyst, is a frequently documented source of posterior knee pain. The condition is
caused by a posterior herniation of the synovial membrane or by a communicating
semimembranous bursa into the popliteal space and usually indicates underlying pathology.
This cyst is seen in disorders such as osteoarthritis, rheumatoid arthritis, and internal
derangement of the knee, including meniscal tears.1 However, degenerative arthritis or
meniscal pathology alone may be a potential source of posterior knee pain. In fact, posterior
horn meniscal tears often present with ill-defined posterior knee pain, especially during deep
flexion. Thus, clinicians should examine patients who have posterior knee pain for meniscal
pathology.
Magnetic resonance imaging (MRI) or ultrasound can aid the diagnosis of Baker's cyst. MRI is
advantageous, because it may identify the underlying cause, such as a concomitant meniscal
tear. Focus should be in the most common area for Baker's cyst--along the medial aspect of
the popliteal fossa beneath the medial head of the gastrocnemius.
Even though Baker's cysts are often asymptomatic, they can enlarge or dissect and become
symptomatic, producing joint swelling, pain, or a feeling of fullness in the popliteal fossa.
Occasionally, dissection or rupture may lead to lower-limb swelling, simulating venous
thrombosis. A ruptured cyst usually displays a "crescent sign"--an ecchymotic area around the
malleoli--that may help distinguish this disorder from venous thrombosis.2 Venography or
ultrasonography should be performed if any doubt persists about the diagnosis.
Treatment should address the precluding problem, such as associated meniscal tear or
inflammatory arthritis, but if the cause is unknown, conservative management with the RICE
protocol (rest, ice, compression, and elevation) and nonsteroidal anti-inflammatory medication
143
can be helpful. Although the cyst may disappear without intervention, some rare cases may
require excision. Unfortunately, surgery may not always provide a cure, because the cyst can
recur and refill, particularly if the underlying derangement is not addressed.
Tumors. Both benign and malignant soft-tissue and bone tumors can also cause posterior
knee pain. Diagnosis of soft-tissue tumors is often delayed, because patients may not come in,
especially in the early stages of tumor growth, and the tumors are difficult to diagnose.
Presenting symptoms of tumors in the posterior knee include pain from pressure of the mass
on adjacent nerves,3 limitation of knee flexion,4 and knee locking with an effusion.5 Some
tumors that cause posterior knee pain include osteochondromas, endochondromas,
chondroblastomas, osteosarcomas, pigmented villonodular synovitis, and synovial
chondromatosis.
Anteroposterior and lateral knee radiographs may show gross formation of a mass. However, if
suspicion for a tumor is high, an MRI with contrast should be obtained for further diagnostic
workup and management. MRI is a useful imaging study, because it can help clinicians
distinguish location, expansion, and characteristics of the tumor. For example, in pigmented
villonodular synovitis, the tumor may clinically mimic a meniscal tear, but MRI can be used to
distinguish between these two entities.6 Similarly, another advantage of a contrast-enhanced
MRI is that one can differentiate a solid tumor from a ganglion cyst, which will only have rim
enhancement.7 MRI can also aid with preoperative staging and planning as well as
postoperative follow-up. In addition, angiography may reveal further anatomic information
about the content of the mass and show any meaningful displacement of nearby vascular
structures. Treatment options may include resection, amputation, radiation, and
chemotherapy, depending on the stage and grade of the lesion.
Affected Tendons
Posterior knee pain can arise from acute tendon strain or chronic injury resulting in tendinitis
of any of the musculotendinous structures in or about the popliteal fossa. Ganglion cysts in the
presence of tendon injury may also contribute to the pain. Some of the more commonly
injured structures posterolaterally include the biceps femoris and the popliteus tendons.
Posteromedially, injuries to the semitendinosus and semimembranosus tendons are more
common. Although they are unusual occurrences, strains or ruptures of the plantaris muscle
may cause posterior knee pain.
Hamstring injury. Although the hamstring tendons consist of the semitendinosus,
semimembranosus, and the long and short heads of the biceps femoris, the most commonly
injured of these is the short head of the biceps femoris. Most hamstring injuries occur around
the musculotendinous junction. However, injury to the tendon itself near the posterolateral
corner of the knee may occur during rapid bursts of running or jumping or during sudden
deceleration. Increased susceptibility to this injury may be from inadequate stretching during
warm-up exercises, decreased flexibility, and muscle fatigue. Endurance sports, such as
running or cycling, are also associated with injury to the biceps femoris tendon.
Physical examination may reveal tenderness at the distal aspect of the biceps femoris tendon
as well as pain during knee extension. If the clinical diagnosis is in doubt, an ultrasound or MRI
may be done. If peripheral neurologic symptoms are present, advanced imaging modalities
may help to rule out a concomitant hematoma that may externally compress adjacent
structures, such as the tibial nerve. MRI may also help physicians determine the prognosis for
return to sport. If more than 50% of cross-sectional muscle or distal myotendinous tears
occur, athletes usually require more than 6 weeks before they may return to sports-specific
programs.8 An earlier return to play may be associated with subtle muscle strength
abnormalities, which can lead to a recurrence of symptoms and possibly worsen the original
tear.9
Gastrocnemius tendon calcification. A rare cause of tendon injury accompanied by
posterior knee pain is calcification of the gastrocnemius tendon as calcium pyrophosphate
dihydrate (CPPD) becomes deposited.10,11 Anteroposterior and lateral knee radiographs may
reveal this phenomenon. CPPD deposition may be seen more often among the elderly; the
144
involvement of the gastrocnemius tendon is relatively rare in younger patients.12
Popliteus injury. The examiner should also test the popliteus tendon as a possible pain
generator. The popliteus muscle and tendon (figure 1) stabilize the posterolateral corner of the
knee and prevent anterior translation, especially during downhill running. Injury to the
popliteus tendon, therefore, is most commonly seen in athletes who run. The posterolateral
corner is a complex area that is often misunderstood and underrepresented as a cause of
posterior knee pain.
On examination, the popliteus muscle may be tender in the posterolateral corner of the knee.
However, a provocative maneuver that typically provokes pain involves examining the patient
in the prone position with internal rotation of the tibia. The patient then flexes the knee against
resistance. Reproduction of symptoms during flexion suggests injury to the popliteus tendon.
Treatment of a popliteus tendon injury consists of the RICE protocol, gradual stretching
exercises in multiple planes, closed–kinetic-chain eccentric strengthening exercises, such as
slow, multidirectional lunges that patients progress to doing on nonlevel surfaces, and gradual
return to athletic participation. Since these muscle fibers have a rotational component,
rehabilitation should emphasize exercises with rotation.
Other Posterolateral Corner Components
Although the popliteus may be a frequently injured part of the posterolateral corner, other
components include the lateral collateral ligament, the posterolateral capsule, and the
popliteofibular ligament. During the initial 30° of knee flexion, these posterolateral structures
in combination with the posterior cruciate ligament (PCL) are important in resisting excessive
varus orientation, external rotation, and posterior translation of the knee.
145
Injury mechanism and exam. The most common mechanisms of posterolateral corner injury
involve athletic trauma, motor vehicle collisions, and falls. Isolated injury to this complex
usually derives from a posterolaterally directed force when the knee is in full extension.
Although a patient's initial clinical presentation may involve minimal symptoms, a
compromised posterolateral corner can lead to worsening local symptoms. Patients typically
complain of knee pain while walking and may even develop a varus thrust. Examination may
reveal swelling, abrasion, or ecchymosis. Point tenderness may occur over the fibular head as
well as diffusely in the posterolateral corner. In chronic cases, there may be a varus thrust
seen in stance (figure 2) or during ambulation.
Tests, accompanying injuries, and treatment. The external rotation recurvatum test
(figure 3) can help confirm posterolateral rotary instability. The examiner performs the test by
holding the patient by each great toe and observing any side-to-side differences in
hyperextension, varus, and tibial external rotation.
146
The dial test also assesses posterolateral rotation of the tibia on the femur to detect
posterolateral knee instability. The patient is supine with 30° of knee flexion and with the foot
extended over the side of the examining table. The examiner externally rotates the foot while
stabilizing the thigh and observes the amount of rotation of the tibial tubercles. Increased
external rotation on the injured side indicates a posterolateral corner injury. If this maneuver
is performed with the knee flexed to 90° and less rotation is seen than when performed at 30°,
then an isolated posterolateral corner injury is probable. If the injured knee rotates more at
90°, then a concomitant PCL injury is likely. Since isolated posterolateral corner injuries are
relatively uncommon and exam maneuvers are often negative, this injury is frequently missed.
The posterior drawer test is more sensitive for detecting PCL-only injury.
Paresthesia and weakness from common peroneal nerve injury may also be present with a
posterolateral corner injury. Researchers have documented that 15% of patients with a
posterolateral knee injury also have a common peroneal nerve injury.13 In their review, Veltri
and Warren14 noted that hemorrhage can be a contributing factor to peroneal nerve palsy in
acute posterolateral corner injury despite an intact nerve. They also noted that in some cases
of lateral and posterolateral corner knee injury, the concomitant varus thrust may lead to
direct injury of the peroneal nerve.
Radiographs taken while the patient is standing may illustrate abnormal widening of the lateral
joint space and arthritis. However, MRI is superior at delineating injury to the structures of the
posterolateral corner.
Nonoperative treatment includes early mobilization with gait retraining and hip girdle
strengthening. The focus should be on quadriceps strengthening, since the quadriceps are
most likely to atrophy in chronic posterolateral instability. Some acute ligamentous injuries
warrant operative repair in the first 3 weeks after injury to provide the optimal result.
Vascular and Nerve Injuries
147
Injuries to vessels and nerves should not be overlooked in patients with posterior knee pain.
Popliteal artery entrapment syndrome (PAES). This condition arises from hypertrophy of
the medial gastrocnemius, soleus, plantaris, or semimembranosus muscles that compresses
the popliteal artery as it courses through the popliteal fossa. Although the symptoms are most
common in athletes, other cases have been reported in truck drivers, because the same
mechanism causes direct arterial compression. Individuals with rheumatoid arthritis and
associated knee pathology can also present with PAES.15
Symptoms include posterior knee pain and progressive lower-extremity arterial insufficiency
causing claudication of the calf with ambulation or other exertion. Leg swelling, cramping,
coldness, paresthesias, trophic changes, and blanching below the knee may also be present.
On exam, distal pulses decrease or disappear when the knee is in hyperextension with active
plantar flexion or passive dorsiflexion. Other conditions that can mimic PAES include
accelerated atherosclerosis, thromboangiitis obliterans, adventitial cystic disease, adductor
canal outlet syndrome, acute popliteal artery occlusion, microemboli, collagen vascular
disease, Takayasu's arteritis, and coagulopathy.
Several imaging studies can help determine this unusual diagnosis. Duplex ultrasonography
can be used for detection; however, because it is operator dependent, the technique may yield
a high rate of false positives.16 The single most useful study is MRI, since it can illustrate the
area of entrapment as well as determine the patency of the artery if the scan is combined with
special imaging sequences. Although angiography with digital subtraction can be useful in
determining the severity of stenosis, it cannot detect the source of extrinsic compression, and
it is also an invasive study.
Functional stretching can treat the condition, but if that is unsuccessful, then surgical
intervention may be necessary. Surgery usually involves resection of the hypertrophied muscle
to liberate the popliteal artery.
Nerve entrapment. Although rare, common peroneal and tibial nerve injury in the popliteal
space should be suspected in patients who have unrelenting posterior knee pain. In a case
report, Ekelund17 described idiopathic nerve entrapment in the popliteal space that caused
posterior knee pain in a young patient during walking and running. The patient had a tender
lateral popliteal space that was surgically explored, exposing a fibrous band that was
compressing the common peroneal nerve. Decompression was performed, and 2 weeks later,
the patient was asymptomatic. The same patient later returned to the clinic with complaints of
pain and had tenderness in the central aspect of the popliteal space in the opposite knee. This
area was also explored operatively, and fibers from the medial gastrocnemius were found to be
the cause of tibial nerve entrapment. This area was also decompressed, and in 2 weeks, the
patient was asymptomatic. In a case series, Saal et al18 also reported nine patients who had
tibial nerve lesions in the popliteal space with local tenderness over the area of entrapment.
Iatrogenic Injuries
Traumatic injuries or soft-tissue injuries that have been surgically repaired may provoke
posterior knee pain.
Postsurgical arthrofibrosis. Posterior knee pain can arise from posttraumatic arthrofibrosis,
a condition in which scar tissue proliferates after trauma. Occasionally, patients with a history
of injury or surgery may experience arthrofibrosis, and it usually produces limited range of
motion, stiffness, and pain. Affected patients experience posterior knee pain that becomes
worse with knee extension. A typical example may occur after an acute anterior cruciate
ligament (ACL)–deficient knee is reconstructed before the patient regains adequate range of
motion. In such cases, hypertrophic tissue may adhere to the ACL graft site or graft itself. This
additional scar tissue contributes to posterior knee pain, because it can prevent the patient
from regaining full range of motion postoperatively, particularly the terminal 5° of extension.19
Therefore, delaying the operation approximately 3 weeks after ACL injury should decrease the
likelihood of arthrofibrosis and reduce the overall incidence of posterior knee pain. Aggressive,
accelerated rehabilitation programs that emphasize passive extension, muscle reeducation,
cryotherapy, and functional rehabilitation may decrease the incidence of this disabling
148
condition.20
Bioabsorbable tacks. Another potentiator of postoperative posterior knee pain is placement
of bioabsorbable tacks. Because the menisci are important for weight bearing within the knee,
new systems of repair, such as bioabsorbable tacks, to prevent future degenerative joint
disease have been employed in arthroscopy. Bioabsorbable tacks are T-shaped fasteners with
barbed shafts. The tacks generally maintain structural integrity for approximately 4 to 6
months and fully resorb in 3 years. In one retrospective case series,21 a relatively high
incidence (31%) of focal posterior knee pain was referred from the site of tack placement,
despite a stable knee 6 weeks after surgery. However, pain resolved between 4 and 6 months
postoperatively, about the time the tacks begin to resorb. The tack length, number used, and
meniscal tear type were irrelevant to symptoms.
Knowledge of this transient phenomenon is important to the examiner evaluating patients who
have postarthroscopic posterior knee pain. Symptoms may include tenderness of the posterior
knee and sharp posterior knee pain that is exacerbated by knee extension. Physical therapy
protocols should not be altered, as there is no difference in knee stability or return to activity
in these patients. Reassurance is important during patient evaluation, since symptoms typically
resolve as the tacks resorb.
Thoughts About Diagnosis
With these descriptions and diagnostic tips (see table 1), examiners should have a more
comprehensive understanding of potential pain generators about the posterior knee. While
many different sources can cause posterior knee pain, review of potential causes should give
providers a firm understanding of disorders to consider in their diagnostic workup.
References
1. Baylis WJ, Rzonca EC: Common sports injuries to the knee. Clin Podiatr Med Surg
1988;5(3):571-589
2. Kraag G, Thevathasan EM, Gordon DA, et al: The hemorrhagic crescent sign of acute
synovial rupture. Ann Intern Med 1976;85(4):477-478
3. Helfet AJ: Disorders of the Knee, ed 2. Philadelphia, Lippincott, 1982, p 478
4. Dienst M, Schneider G, Pahl S, et al: Intra-articular osteochondroma of the posterior
cavity of the knee. Arch Orthop Trauma Surg 2002;122(8):462-465
5. Ogata K, Ushijima M: Tenosynovial fibroma arising from the posterior cruciate
ligament. Clin Orthop 1987;215 (Feb):153-155
6. Muscolo DL, Makino A, Costa-Paz M, et al: Localized pigmented villonodular synovitis of
the posterior compartment of the knee: diagnosis with magnetic resonance imaging.
Arthroscopy 1995;11(4):482-485
7. Helms CA: Fundamentals of Skeletal Radiology, ed 2. Philadelphia, WB Saunders,
1995, p 55
8. Clanton TO, Coupe KJ: Hamstring strains in athletes: diagnosis and treatment. J Am
Acad Orthop Surg 1998;6(4):237-248
9. Croisier JL, Forthomme B, Namurois MH, et al: Hamstring muscle strain recurrence and
strength performance disorders. Am J Sports Med 2002;30(2):199-203
10. Yang BY, Sartoris DJ, Resnick D, et al: Calcium pyrophosphate dihydrate crystal
deposition disease: frequency of tendon calcification about the knee. J Rheumatol
1996;23(5):883-888
11. Foldes K, Lenchik L, Jaovisidha S, et al: Association of gastrocnemius tendon
calcification with chondrocalcinosis of the knee. Skeletal Radiol 1996;25(7):621-624
12. Iguchi Y, Ihara N, Hijioka A, et al: Calcifying tendonitis of the gastrocnemius: a report
of three cases. J Bone Joint Surg Br 2002;84(3):431-432
13. LaPrade RF, Wentorf F: Diagnosis and treatment of posterolateral knee injuries. Clin
Orthop 2002;402(Sep):110-121
14. Veltri DM, Warren RF: Anatomy, biomechanics, and physical findings in posterolateral
knee instability. Clin Sports Med 1994;13(3):599-614
15. Akiyama K, Maeda T, Taniyasu N, et al: An unusual popliteal entrapment in a patient
with rheumatoid knee. J Cardiovasc Surg (Torino) 2001;42(2):281-284
16. Lambert AW, Wilkins DC: Popliteal artery entrapment syndrome. Br J Surg
149
1999;86(11):1365-1370
17. Ekelund AL: Bilateral nerve entrapment in the popliteal space. Am J Sports Med
1990;18(1):108
18. Saal JA, Dillingham MF, Gamburd RS, et al: The pseudoradicular syndrome: lower
extremity peripheral nerve entrapment masquerading as lumbar radiculopathy. Spine
1988;13(8):926-930
19. Shelbourne KD, Wilckens JH, Mollabashy A, et al: Arthrofibrosis in acute anterior
cruciate ligament reconstruction: the effect of timing of reconstruction and
rehabilitation. Am J Sports Med 1991;19(4):332-336
20. Shelbourne KD, Nitz P: Accelerated rehabilitation after anterior cruciate ligament
reconstruction. Am J Sports Med 1990;18(3):292-299
21. Whitman TL, Diduch DR: Transient posterior knee pain with the meniscal arrow.
Arthroscopy 1998;14(7):762-76
150
Valgus Knee Instability in an Adolescent
Ligament Sprain or Physeal Fracture?
Kenneth R. Veenema, MD
In Brief: A 15-year-old boy was hit on the lateral aspect of his left knee while playing football. The
injury was initially diagnosed as a medial collateral ligament sprain, and radiographs were
negative. Stress views, however, demonstrated medial widening of the physis consistent with a
Salter-Harris type 1 injury to the distal femur, and magnetic resonance imaging (MRI)
demonstrated a type 3 injury extending through the epiphysis. Stress radiographic views or MRI is
diagnostic of distal femoral physeal fracture, and a positive diagnosis should prompt referral.
Valgus loading from a lateral blow is a common mechanism of knee injury in sports activity and
often results in an isolated injury to the medial collateral ligament (MCL), but, among children and
adolescents, fracture of the distal femoral physis is also a possibility. These fractures, though
uncommon, are frequently associated with significant morbidity, including fracture displacement,
joint motion loss, and growth-plate arrest with subsequent angular deformity and limb-length
discrepancy. Complications can occur even with nondisplaced fractures.
The typical treatment for an MCL injury--aggressive functional rehabilitation emphasizing early
motion, strength maintenance, and early return to activity with protective bracing--could cause
displacement or impair healing if a distal femoral physeal fracture has occurred. Thus it is
important to exclude this fracture before starting treatment. The following case report emphasizes
the importance of considering distal femoral physeal fracture in any skeletally immature athlete
who presents with posttraumatic valgus knee instability and tenderness at the distal femoral
growth plate.
Case Report
A 15-year-old high school football player sustained a valgus injury to his left knee when, with his
leg extended, he was struck laterally by another player during a game. He described immediate
disability and swelling but was able to limp off the field. He denied hearing a pop and had no
history of earlier knee injury. He was evaluated on the sidelines and held out for the remainder of
the game.
Subsequent training-room evaluation demonstrated an effusion, medial tenderness, and valgus
instability. He was placed in a knee immobilizer, given crutches, and instructed to see his physician
the next day for treatment of an MCL injury.
The following day he was evaluated by his primary care physician, who referred him to our sports
medicine clinic for management and functional rehabilitation of his presumed MCL sprain.
Physical exam. On examination, the patient had a 3+ effusion of the left knee, a flexion range of
10° to 90°, and tenderness of the distal femur at the origin of the MCL. This pain increased with
valgus stress. A 6- to 8-mm increase in medial joint-line opening was present with valgus stress at
both the limit of extension and at 30° of flexion, but a firm end point was felt. Varus stress caused
no lateral tenderness, pain, or instability.
Lachman and anterior drawer tests demonstrated mildly increased translation, but a ligamentous
end point was difficult to assess because of guarding by the patient. A posterior drawer test was
negative. No patellar tenderness, patellar instability, or apprehension was present. The patient was
151
able to do a straight-leg raise from the supine position without difficulty. His neurovascular exam
was normal.
Imaging studies. Initial anteroposterior (AP) and lateral plain radiographs were unremarkable
(figure 1). The distal femoral physis appeared close to maturity but was still open. A subsequent AP
valgus stress view demonstrated widening of the medial aspect of the distal femoral physis, but no
epiphyseal or metaphyseal extension of the fracture line was evident (figure 2).
The patient was presumptively diagnosed as having a Salter-Harris type 1 fracture of the distal
femoral physis (a type 1 fracture follows the physeal line). However, magnetic resonance imaging
(MRI) was obtained to exclude an accompanying anterior cruciate ligament (ACL) injury. The MRI
demonstrated an intact ACL, but there was clear evidence of fracture-line extension through the
epiphysis to the intra-articular surface of the distal femur, indicating a type 3 injury (figure 3). No
joint surface incongruity or MCL injury was evident.
152
Treatment. A long leg cast was applied and strict non-weight-bearing with crutches for 4 weeks
was prescribed. The patient's progress was followed with weekly plain radiographs to assess for
any fracture displacement.
After 4 weeks there was good radiographic evidence of periosteal bone formation along the distal
femoral metaphysis and physis. The cast was subsequently removed, and no pain was present at
the fracture site. The patient was placed in an adjustable hinged brace allowing protected range of
motion and was told to start joint motion exercises, but to avoid weight-bearing for an additional 4
weeks.
At the 8-week point he had regained full motion. He gradually began to resume bearing weight and
also started a quadriceps and hamstring restrengthening program.
After 12 weeks he demonstrated 80% of full strength in the quadriceps and hamstrings as
compared with the opposite side and was bearing his full weight without pain. A functional
progression of impact and pivot activities was begun, but he was withheld from any contact
activity.
At 16 weeks, he demonstrated full strength in the quadriceps and hamstring muscles as compared
with the uninjured side and was participating in noncontact activities without difficulty. He was
therefore allowed to return to unrestricted activities. Plain radiographs at the 16-week visit
demonstrated closure of the medial aspect of the distal femoral physis and near-closure of the
lateral physis. Limb lengths and valgus carrying angles of the femur relative to the tibia and pelvic
bones (Q-angles) were equal bilaterally.
Follow-up clinical and radiographic examinations were planned for 6-month and 1-year intervals to
assess for growth-plate closure and evidence of limb-length discrepancy or angular deformity.
Discussion
Any time valgus instability is present in a skeletally immature individual, a distal femoral physeal
fracture should be considered. As with this patient, this injury may not be suspected, because
ligament injuries are the more common result of lateral knee trauma and because fractures of this
physis are relatively uncommon. In a recent report of a series of pediatric patients (1), fractures of
the distal femoral physis accounted for 7% of lower-extremity physeal fractures, while those to the
distal tibial physis made up 72%.
Early detection of distal femoral physeal fractures is important because this physis accounts for
70% of the femur's longitudinal growth and 40% of the lower extremity's (2). Fractures of the
distal femoral physis have been shown to result in a significant incidence of limb-length
discrepancy and angular deformity, either of which may be more severe than predicted by the
initial Salter-Harris classification (3). It should be noted, however, that although distal femoral
153
physeal fractures are more frequent in adolescents than in younger children, complications in
adolescents are less common because growth-plate closure is imminent (4).
Besides age, factors that affect growth deformity following distal femoral physeal fractures are
initial displacement of the fracture and the ability to maintain an anatomic reduction (3,5).
Anatomic factors. The placement of ligamentous attachments about the distal femoral physis
makes it vulnerable to injury (figure 4). The posterior capsule, MCL, and cruciate ligaments all
attach to the distal femoral epiphysis, leaving the physis fully exposed to valgus loads applied to
the extended knee. In contrast, the MCL attaches at a site distal to the proximal tibial metaphysis,
making the proximal tibial physis less vulnerable to damage from valgus loads.
Because of growth-related anatomic factors, distal femoral physeal fractures are more frequent in
adolescents than in younger children and more likely to result from relatively minor trauma, such
as from sports activities. During adolescence, the periosteum overlying the physis is thin and
relatively weak compared with the strong metaphyseal bone. Also, at this time the MCL remains
stronger than the cartilaginous physis. This makes the distal femoral physis particularly prone to
injury. Furthermore, the knee is subjected to increasing forces during athletic activities in
adolescence. In younger children, fractures of the distal femoral physis are often a result of more
severe trauma, such as car-pedestrian accidents.
Appropriate imaging. This case also illustrates the importance of appropriate imaging studies.
Displaced physeal fractures are obvious both clinically and radiographically, but nondisplaced
physeal injuries may look normal on initial radiographs. Further imaging studies are essential if this
fracture is suspected.
Stress views. Before the advent of MRI, stress views were traditionally recommended if a skeletally
immature individual's initial films were negative but the clinical exam suggested valgus instability
with distal femoral tenderness. This recommendation was supported by reports (6,7) of
adolescents who had sports-related Salter-Harris type 1 and type 3 distal femoral physeal fractures
that were not evident on initial radiographs but were demonstrated by stress films.
154
To avoid further injury when obtaining stress views, the knee should be carefully flexed to 30° and
subjected to gentle valgus stress while slight traction is applied to the leg. Conscious sedation with
intravenous narcotics and benzodiazepines may facilitate the exam and prevent further physeal
injury if muscle spasm and/or pain prevents adequate relaxation.
Magnetic resonance imaging. The advent of MRI is redefining diagnosis of distal femoral physeal
fractures. In two recent series (8,9), early MRI raised the Salter-Harris classification to a higher
grade than was initially apparent on plain radiographs in more than 50% of cases.
In a skeletally immature patient, MRI should be considered in lieu of stress films if plain
radiographs are negative, a nondisplaced distal femoral physeal fracture is suspected, and the
patient has an acute hemarthrosis. Use of MRI in this situation protects the physis from further
injury and potential fracture displacement.
MRI is also helpful in diagnosing ligamentous injury (such as to the ACL), which, in one study (10),
occured in 38% of patients (6 of 16) who had femoral physeal fractures. MRI provides excellent
visualization of the knee ligaments and may help confirm the extent of these associated injuries
when physical exam findings are equivocal.
Treatment. Treatment for a nondisplaced distal femoral physeal fracture should include
immobilizing the knee in a long leg cast, prescribing non-weight-bearing use of crutches, and
following up with weekly radiographs to assess for fracture displacement. If displacement is
suspected or diagnosed, the patient should be referred to an orthopedic specialist.
References
1. Mann DC, Rajmaira S: Distribution of physeal and nonphyseal fractures in 2,650 long-bone
fractures in children aged 0-16 years. J Pediatr Orthop 1990;10(6):713-716
2. Pritchett JW: Longitudinal growth and growth-plate activity in the lower extremity. Clin
Orthop 1992;Feb(275):274-279
3. Lombardo SJ, Harvey JP Jr: Fractures of the distal femoral epiphyses. Factors influencing
prognosis: a review of 34 cases. J Bone Joint Surg (Am) 1977;59(6):742-751
4. Beaty JH, Kumar A: Fractures about the knee in children. J Bone Joint Surg (Am)
1994;76(12):1870-1880
5. Thomson JD, Stricker SJ, Williams MM: Fractures of the distal femoral epiphyseal plate. J
Pediatr Orthop 1995;15(4):474-478
6. Simpson WC Jr, Fardon DF: Obscure distal femoral epiphyseal injury. South Med J
1976;69(10):1338-1340
7. Torg JS, Pavlov H, Morris VB: Salter-Harris type-III fracture of the medial femoral condyle
occurring in the adolescent athlete. J Bone Joint Surg (Am) 1981;63(4):586-591
8. Smith BG, Rand F, Jaramillo D, et al: Early MR imaging of lower-extremity physeal
fracture-separations: a preliminary report. J Pediatr Orthop 1994;14(4):526-533
9. Jaramillo D, Hoffer FA, Shapiro F, et al: MR imaging of fractures of the growth plate. AJR
Am J Roentgenol 1990;155(6):1261-1265
10. Bertin KC, Goble EM: Ligament injuries associated with physeal fractures about the knee.
Clin Orthop 1983;Jul(177):188-195
Dr Veenema is an assistant professor of emergency medicine and orthopedics in the department of
orthopedics, division of athletic medicine, at the University of Rochester School of Medicine in
Rochester, New York. He is a member of the American Medical Society for Sports Medicine and the
American Board of Emergency Medicine and holds a certificate of added qualifications in sports
medicine. Address correspondence to Kenneth R. Veenema, MD, University Sports Medicine, 2180
South Clinton Avenue, Rochester, New York 14618.
155
Hamstring Strains: Expediting Return to
Play
Thomas M. Best, MD, PhD; William E. Garrett Jr, MD, PhD
In Brief: Strains to the hamstring muscle group are prevalent and, unfortunately, often recurrent,
with prolonged rehabilitation and persistent disability. Most hamstring injuries are of a single
muscle near the muscle-tendon junction. Rarely, the hamstring muscle group may avulse from the
ischial tuberosity. The diagnosis can usually be made by history and physical exam, but MRI can be
used to help pinpoint the extent and location of the injury. Initial treatment typically consists of
rest, ice, compression, elevation, and pain relief. There is no consensus on optimal rehabilitation,
but functional exercises with stretching and strengthening have been emphasized.
Hamstring strains are among the most common injuries in sports, and they often frustrate
physician and athlete alike with a long recovery and high rate of recurrence. But by diagnosing the
extent of the injury accurately and taking appropriate therapeutic steps, clinicians can improve the
odds.
Case 1: Acute Hamstring Injury
A 34-year-old male recreational bicyclist and tennis player felt a painful "pop" in his left posterior
thigh while playing tennis but continued to play despite pain. Over the next few days, he
experienced mild pain in his midposterior thigh when playing tennis. Ten days after the initial
injury, he experienced a similar "pop" with his hip flexed and knee extended, but the pain was
worse. He was unable to continue play and had difficulty sleeping that night because of pain.
On physical exam the next day, the patient walked with a limp. He had a subcutaneous ecchymosis
and palpable tenderness over the left semimembranosus muscle 4 cm distal to the ischial
tuberosity. When he performed an isometric contraction with knee flexion, his hamstring muscles
were felt to be in continuity. He had full range of motion of both hips. When he touched his
fingertips to his ankles while standing, he had moderate tenderness at the left hamstring origin.
Strength and sensation were intact except for 4-/5 strength in the left hamstrings. Straight-leg
raise was 90° on the right and 75° on the left. Knee and ankle jerk reflexes were symmetric.
The patient was diagnosed as having an acute left hamstring strain and started on a physical
therapy program of passive stretching and isometric strengthening. He maintained aerobic
conditioning initially with swimming pool and stationary bicycle activities as tolerated. Ice and
electrical stimulation were used before and after workouts. Nonsteroidal anti-inflammatory drugs
(NSAIDs) were prescribed for pain control.
One week later the patient was walking without a limp and began concentric strengthening and
more aggressive hamstring stretching. He began a jogging program when he was able to walk
without hamstring discomfort for 20 to 30 minutes. He gradually advanced to sport-specific skills
over the next 2 weeks and also started eccentric strengthening. He was discharged from physical
therapy about 1 month after starting rehab and was advised that he could play tennis. The patient
has not had further problems, although he notes that the muscle periodically is "a little stiff."
Case 2: Chronic Hamstring Pain
A 23-year-old professional football player was referred for persistent left hamstring pain of 4
months' duration. Four months prior to initial consultation he had injured the hamstring when
diving for a loose ball and had felt a pop. He also noticed that he felt painful nervelike sensations
down the lateral aspect of his leg. Six weeks after the initial injury he was subjectively better,
156
although he still had a large ecchymosis in the midbelly of his
hamstring with occasional pain radiating from the popliteal fossa
into the foot. Magnetic resonance imaging (MRI) showed significant
changes within the belly of the muscle. Two weeks later, the
patient was able to jog lightly but could not sprint and had not
returned to play. One month later, repeat MRI was obtained by
another consulting physician and showed no interval change.
Electromyography (EMG) studies were normal.
On presentation to our clinic 2 months later (4 months after the
initial injury), physical exam revealed a well-muscled individual
with a normal gait. He had no appreciable quadriceps atrophy. An
obvious asymmetry of the hamstring muscles was visible with
distal retraction of the muscle belly, and a defect was palpated immediately distal to the ischial
tuberosity on the left side. When the patient attempted to contract the muscle, the hamstrings
could be felt retracting at the mid and distal thigh. It was easy to feel the ischial tuberosity on the
patient's left side, in contrast to the uninjured leg, where the hamstring origin prevented palpation
of this bony landmark.
Despite an aggressive 4-month rehabilitation program of eccentric strengthening and stretching,
isokinetic testing showed a 50% strength reduction in the left hamstring. The clinical diagnosis at
this time was complete avulsion of the hamstring muscle complex from the ischial tuberosity. An
MRI confirmed this injury and showed significant distal retraction of the muscle complex into the
midthigh (figure 1).
Treatment options at this point included continued rehabilitation or surgical exploration of the
avulsed hamstring. Findings at surgery included a complete avulsion of the hamstring complex with
a retracted and scarred distal muscle belly. A delayed primary repair was performed with a
fractional release of the muscle belly distally. He was back training for football 6 months later but
still had symptoms. Other injuries prevented his return to football.
Hamstring Anatomy and Function
The hamstrings consist of three muscles that run from the hip to the knee and assist with hip
extension and knee flexion: the semitendinosus, the semimembranosus, and the biceps femoris
(figure 2). The semimembranosus muscle forms the bulk of the mass of the muscle group. Both
the semimembranosus and semitendinosus are innervated by the tibial portion of the sciatic nerve.
The biceps femoris has a dual innervation: The long head is supplied by the tibial part of the
sciatic, and the short head is supplied by the common peroneal part of the sciatic. As with other
frequently injured muscles, the hamstrings span two joints and are therefore subject to stretching
at more than one point.
157
During walking and running, the hamstrings probably function primarily to decelerate the extending
knee prior to foot strike and to assist with hip extension after foot strike (1). In the first half of the
swing phase of the running cycle, the hip rapidly flexes. Knee flexion is passive during this period
and results from the rapid forward acceleration of the thigh during hip flexion. Midway through the
swing phase, however, while hip flexion continues, the knee begins to rapidly extend. During the
latter part of the swing phase of gait, or float phase of running, the hamstring muscles decelerate
the forward swing of the tibia, thus opposing the activity of the quadriceps.
Efforts have been made to correlate EMG data and time of maximum muscle activity with time of
injury during the gait cycle (2). On the basis of conflicting results, it appears that there is probably
a complex, poorly understood neuromuscular coordination pattern that may help explain why the
hamstrings are injured.
Possible Risk Factors
Hamstring injuries are common in sports that require bursts of speed or rapid acceleration, such as
soccer, track and field, football, and rugby. Improper warm-up, fatigue, previous injury, strength
imbalance, and poor flexibility have been correlated with injury, but evidence showing a causeand-effect relationship is sparse. These ideas have largely been based on results from small patient
samples. For example, Burkett (3) correctly predicted 4 of 6 hamstring muscle injuries in
professional football players based on strength imbalances between the quadriceps and
hamstrings. In each of the injured players, hamstring strength was less than 60% of quadriceps
strength. Furthermore, hamstring injuries were more likely to occur if the isometric strength of the
right and left knee flexors differed by more than 10%. Despite these data, we are unaware of a
published study that identifies athletes at risk because of strength imbalance and attempts to
correct the imbalance to determine if this reduces the risk for injury.
Dorman (4) reported on 140 hamstring injuries and found that they usually occurred either quite
early or in the latter stages of practices or matches and concluded that improper warm-up and
fatigue are risk factors for injury.
158
What appears clear from the literature is the tendency for hamstring injuries to recur. Ekstrand and
Gillquist (5) prospectively studied male Swedish soccer players and found hamstrings to be the
muscle group most often injured. Perhaps more important, they noted that minor injuries doubled
the risk of having a more severe injury within 2 months. Others (6) have noted a recurrence rate
of 25% for hamstring injuries in intercollegiate football players. Despite such observations, it is not
well understood why these injuries tend to recur so frequently.
History and Physical Findings
Hamstring strains can usually be diagnosed from history and physical exam findings. The patient
will often describe pain in the posterior thigh, particularly during and following activities during
which the hamstring is eccentrically activated, like running. On physical examination, tenderness
and swelling can exist at the location of the injury, which is most often the muscle-tendon junction.
A careful physical exam can also usually help in detecting an avulsion of the hamstring complex
from its bony origin. The patient often has a palpable defect extending from the retracted muscle
belly proximally to the ischium.
When Imaging Is Warranted
Imaging studies, including x-rays, are probably not routinely warranted when evaluating hamstring
strains. The clinician must always keep in mind, however, the high incidence of bony avulsions in
children with open epiphyseal plates and rule this out by x-ray if indicated.
Recently, computed tomography (CT) has been used to accurately define the anatomy of injuries,
which may aide in choosing between surgical and conservative measures (7,8). CT scanning of
acute hamstring injuries has shown that the site of injury in running athletes is most often the
muscle-tendon junction of the long head of the biceps femoris. Images taken 1 to 2 days after
injury show areas of hypodensity consistent with inflammation and edema (high-density images
suggest hemorrhage). Follow-up scans on patients with chronic injury often show calcifications at
the muscle-tendon junction where the injury occurred, but their significance is unknown.
On T2-weighted MRI images, acute lesions appear as increased signal densities because of the
increase of free water in traumatized muscle tissue (8,9) Acute hemorrhage is difficult to detect by
MRI; the hemoglobin must become methemoglobin before it shows up.
MRI has shown some promise in predicting recovery following hamstring injuries. In a retrospective
study (9) of 14 professional athletes, recovery was delayed in those who had complete muscle
transection or had greater than a 50% cross-sectional muscle involvement. We use two possible
indications for MRI: a suspected total proximal avulsion of the hamstring muscle complex from the
ischial tuberosity, and a suspected complete muscle transection. In both cases, surgical referral
may be warranted.
Conservative Treatment vs Surgical Care
As is true of most strains in general, the vast majority of injuries to the hamstrings can be
managed without surgery. Initial treatment typically consists of rest, ice, compression, elevation,
and pain relief. Compression of the affected area with elastic wrap may help reduce swelling. For
pain relief, NSAIDs or acetaminophen can be used for 7 to 10 days. However, no optimal treatment
regimen has been developed based on carefully designed clinical trials.
There is likewise no consensus on optimal rehabilitation following initial treatment, but functional
rehabilitation that includes stretching and strengthening has been emphasized. A complete rehab
program should also address the cardiovascular demands of the patient's sport.
One exception to the general preference for nonsurgical treatment may be avulsion of the
hamstring complex at or near the proximal bone-tendon junction. This lesion often leads to chronic
pain and functional deficits. Sallay et al (10) reported that it took 12 patients an average of 7
weeks to walk without a limp after sustaining an avulsion-type injury while water skiing. Three of
159
the 12 patients went on to surgery because of persistent functional limitations and chronic pain.
Complete rupture of the hamstring muscles may also require surgical repair (10,11).
Based on these small anecdotal patient samples, we believe that surgical referral may be indicated
in individuals with total avulsion of the hamstring complex from the ischial tuberosity. The exact
timing of surgery is debatable given the infrequent reporting of this injury. Prospective, randomized
studies would need to be done to provide clear guidelines and indications for surgical referral. It is
our opinion that acute primary repair is preferable so that the risk of scar formation and loss of
function is minimized.
Preventive Measures
Most clinicians prescribe warm-up and stretching to help reduce the incidence and severity of
muscle strains. The evidence supporting these ideas is sketchy at best and largely based on
retrospective studies. For example, following hamstring injury, the affected extremity and muscle
group are significantly less flexible than the uninjured side, but there are no differences in
isokinetic strength (12) Jonhagen et al (13) found decreased flexibility and lower eccentric
hamstring torques in runners who sustained a hamstring strain when compared with uninjured
subjects matched for age and speed.
It may well be that stretching and warm-up do more to improve performance than to prevent
injury. A recent study (12) showed that hamstring stretching and increased flexibility were
effective for improving hamstring muscle performance as measured by peak torque values. The
role of stretching and warm-up in injury prevention needs to be better understood so that optimal
strategies can be developed.
Emphasizing Nonoperative Steps
Hamstring strains continue to be a challenging and often frustrating problem for professionals who
care for athletes. The often long convalescence and high recurrence suggest the need for a better
understanding of the mechanism and pathophysiology of these injuries. Fortunately, most patients
can be treated nonoperatively. Surgical consultation is probably required for patients with
hamstring avulsion from the ischial tuberosity and distal muscle retraction, scarring, and functional
limitation. The role of stretching, strengthening, and warm-up in injury prevention is unclear at this
time.
References
1. Inman VT, Ralston HJ, Todd F: Human Walking. Baltimore, Williams & Wilkins, 1981
2. Mann RA, Hagy JL: Running, jogging, and walking: a comparative electromyographic and
biomechanical study, in Bateman JE, Trott AW (eds): The Foot and Ankle. New York City,
Thieme-Stratton, 1980
3. Burkett LN: Causative factors of hamstring strains. Med Sci Sports Exerc 1970;2(1):39-42
4. Dorman P: A report of 140 hamstring injuries. Aust J Sports Med 1971;4:30-36
5. Ekstrand J, Gillquist J: Soccer injuries and their mechanisms: a prospective study. Med Sci
Sports Exerc 1983;15(3):267-270
6. Heiser TM, Weber J, Sullivan G, et al: Prophylaxis and management of hamstring muscle
injuries in intercollegiate football players. Am J Sports Med 1984;12(5):368-370
7. Garrett WE Jr, Rich FR, Nikolaou PK, et al: Computed tomography of hamstring muscle
strains. Med Sci Sports Exerc 1989;21(5):506-514
8. Speer KP, Lohnes J, Garrett WE Jr: Radiographic imaging of muscle strain injury. Am J
Sports Med 1993;21(1):89-96
9. Pomeranz SJ, Heidt RS Jr: MR imaging in the prognostication of hamstring injury: work in
progress. Radiology 1993;189(3):897-900
10. Sallay PI, Friedman RL, Coogan PG, et al: Hamstring injuries among water skiers:
functional outcome and prevention. Am J Sports Med 1996;24(2):130-136
11. Blasier RB, Morawa LG: Complete rupture of the hamstring origin from a water skiing
injury. Am J Sports Med 1990;18(4):435-437
12. Worrell TW, Smith TL, Winegardner J: Effect of hamstring stretching on hamstring muscle
performance. J Orthop Sports Phys Ther 1994;20(3):154-159
160
13. Jonhagen S, Nemeth G, Eriksson E: Hamstring injuries in sprinters: the role of concentric
and eccentric hamstring muscle strength and flexibility. Am J Sports Med 1994;22(2):262266
Suggested Readings
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Christensen C, Wiseman D: Strength: the common variable in hamstring strain. Athletic
Training 1972;7:36-40
Ekstrand J, Gillquist J, Moller M, et al: Incidence of soccer injuries and their relation to
training and team success. Am J Sports Med 1983;11(2):63-67
Liemohn W: Factors related to hamstring strains. J Sports Med Phys Fitness
1978;18(1):71-76
Morris A, Lussier L, Bell G, et al: Hamstring/quadriceps strength ratios in collegiate middledistance and distance runners. Phys Sportsmed 1983;11(10):71-77
Stanton P, Purdam C: Hamstring injuries in sprinting: the role of eccentric exercise. J
Orthop Sport Phys Ther 1989;10(9):343-349
Worrell TW: Factors associated with hamstring injuries: an approach to treatment and
preventative measures. Sports Med 1994;17(5):338-345
Worrell TW, Perrin DH, Gansneder BM, et al: Comparison of isokinetic strength and
flexibility measures between hamstring injured and noninjured athletes. J Orthop Sport
Phys Ther 1991;13(3):118-125
Yamamoto T: Relationship between hamstring strains and leg muscle strength: a follow-up
study of collegiate track and field athletes. J Sports Med Phys Fitness 1993;33(2):194-199
Dr Best is an assistant professor of family medicine and orthopedic surgery at the University of
Wisconsin in Madison and an associate editor of Medicine and Science in Sports and Exercise. Dr
Garrett is a professor of orthopedic surgery at Duke University in Durham, North Carolina, and an
editorial board member of The Physician and Sportsmedicine. Address correspondence to
Thomas M. Best, MD, PhD, Research Park, 621 Science Dr, Madison, WI 53711; e-mail to
tm.best@hosp.wisc.edu.
161
When Groin Pain Is More Than 'Just a
Strain': Navigating a Broad Differential
Joseph J. Ruane, DO; Thomas A. Rossi, MD
THE PHYSICIAN AND SPORTSMEDICINE - VOL 26 - NO. 4 - APRIL 98
In Brief: Most groin pain results from musculotendinous injuries, but not all groin pain signifies
simply a pulled muscle. The pain can stem from one or more musculoskeletal or
nonmusculoskeletal origins, such as avulsion fracture, osteitis pubis, or hernia. While acute causes
are often readily identified, chronic groin pain can present a diagnostic challenge. Paying close
attention to the history can help identify acute causes such as strains and avulsion fractures;
determining the location and nature of the pain can also help with diagnosis. Conservative
treatment is often effective for treatment of acute injuries such as strains and avulsion fractures.
W
hile the most common cause of groin pain in active patients may be a garden-variety muscle
strain, less common causes add up to a wide differential. Broadly considered, the pain can be
thought of in terms of onset and chronicity (acute vs chronic), and in terms of its musculoskeletal
or nonmusculoskeletal origin (table 1).
Table 1. Differential Diagnosis of Groin Pain: Key Features and Treatments
Musculoskeletal
Causes
Key Features
Treatment Options
Abdominal muscle tear
Localized tenderness to palpation;
pain with activation of rectus
abdominis
Relative rest, analgesics
Adductor tendinitis
Tenderness over involved tendon,
pain with resisted adduction of lower
extremity
NSAIDs, rest, physical therapy
Avascular necrosis of
the femoral head
Inguinal pain with internal rotation of Mild: conservative measures;
hip; decreased hip range of motion
severe: total hip replacement
Avulsion fracture
Pain on palpation of injury site; pain
with stretch of involved muscle
Relative rest; ice; NSAIDs;
possibly crutches
Bursitis
Pain over site of bursa
Injection of cortisone, anesthetic,
or both
Conjoined tendon
Pain with Valsalva's maneuver
Surgical referral
162
dehiscence
Herniated nucleus
pulposus
Positive dural or sciatic tension signs
Physical therapy or appropriate
referral
Muscle strain
Acute pain over proximal muscles of
medial thigh region; swelling;
occasionally, bruising
Rest; avoidance of aggravating
activities; initial ice, with heat
after 48 hours; hip spica wrap;
NSAIDs for 7 to 10 days
Myositis ossificans
Pain and decreased range of motion
in involved muscle; palpable mass
within substance of muscle
Moderately aggressive active or
passive range-of-motion
exercises; wrap thigh with knee in
maximum flexion for first 24
hours; NSAIDs used sparingly for
2 days after trauma
Nerve entrapment
Burning or shooting pain in
distribution of nerve; altered light
touch sensation in medial groin; pain
exacerbated by hyperextension at
hip joint, possibly radiating;
tenderness near superior iliac spine
Infiltration of site with local
anesthetic; topical cream (eg,
capsaicin)
Osteitis pubis
Pain around abdomen, groin, hip, or
thigh, increased by resisted
adduction of thigh
Relative rest; initial ice and
NSAIDs; possibly crutches; later,
stretching exercises
Osteoarthritis
Inguinal pain with hip motion,
especially internal rotation
Nonnarcotic analgesics or
NSAIDs; hip replacement for
intractable pain
Pubic instability
Excess motion at pubic symphysis;
pain in pubis, groin, or lower
abdomen
Physical therapy, NSAIDs,
compression shorts
Referred pain from
knee or spine
Hip range of motion and palpation
response normal
Identify true source
Seronegative
spondyloarthropathy
Signs of systemic illness, other joint
involvement
Refer to rheumatologist
Slipped capital femoral
epiphysis
Inguinal pain with hip movement;
insidious development in ages 8 to
15; walking with limp, holding leg in
external rotation
Discontinue athletic activity; refer
to orthopedic surgeon
163
Stress fracture
Pubic ramus
Chronic ache or pain in the groin,
buttock, and thighs
Relative rest; avoid aggravating
activities
Femoral neck
Chronic ache or pain in the groin,
buttock, and thighs, or pain with
decreased hip range of motion
(internal rotation in flexion)
Refer to orthopedist if radiographs
show lesion; for nonoperative
fractures, strict non-weight
bearing until pain free, with
gradual return to activity
Key Features
Treatment Options
Epididymitis
Tenderness over superior aspect of
testes
Antibiotics if appropriate, or refer
to urologist
Hydrocele
Pain in lower spermatic cord region
Refer to urologist
Varicocele
Rubbery, elongated mass around
spermatic cord
Refer to urologist
Hernia
Recurrent episodes of pain; palpable
mass made more prominent with
coughing or straining; discomfort
elicited by abdominal wall tension
Refer for surgical treatment
Lymphadenopathy
Palpable lymph nodes just below
inguinal ligaments; fever, chills,
discharge
Antibiotics
Ovarian cyst
Groin or perineal pain
Refer to gynecologist
Pelvic inflammatory
disease
Fever, chills, purulent discharge
Refer to gynecologist
Postpartum symphysis
separation
Recent vaginal delivery with no prior
history of groin pain
Physical therapy, relative rest,
analgesics
Prostatitis
Dysuria, purulent discharge
Antibiotics, NSAIDs
Nonmusculoskeletal
Causes
Genital swelling or
inflammation
164
Renal lithiasis
Intense pain that radiates to scrotum Pain control, increased fluids until
stone passes; hospitalization
sometimes necessary
Testicular neoplasm
Hard mass palpated on the testicle;
may not be tender
Refer to urologist
Testicular torsion or
rupture
Severe pain in the scrotum; nausea,
vomiting; testes hard on palpation or
not palpable
Refer immediately to urologist
Urinary tract infection
Burning with urination; itching;
frequent urination
Short course of antibiotics
NSAIDs = nonsteroidal anti-inflammatory drugs
Acute groin pain is a common result of musculoskeletal injuries that can occur with the sharp,
cutting movements of kicking and running sports. These injuries are especially common in soccer
but are also seen in racket sports, basketball, hockey, volleyball, football, and other sports.
Chronic groin pain, in contrast, may suggest nonmusculoskeletal causes such as hernias,
lymphadenopathy, infections, sexually transmitted diseases, or even cancer.
Directions for Diagnosis
As in all medicine, the diagnosis of groin pain begins with a good history. Paying close attention to
subtle clues in the patient's history often leads to the correct diagnosis. With a sudden change of
direction while running, a forceful eccentric contraction of a muscle can occur instead of the
intended concentric contraction, causing the most common groin injury--a muscle strain.
Overstretching a muscle can also induce a strain (1,2). A forceful muscle contraction in an adult
might strain the muscle unit, while in an adolescent the same action can cause an avulsion fracture
(3). Symptoms that occur with a change of training regimen suggest a stress fracture. A detailed
history of injury or trauma to the area can lead you to the source of pain (see "Case Study: A
Surprising Cause of Groin Pain in a Female Runner," below).
Determining the site of pain will further assist in the diagnosis. Is it localized--such as in the medial
thigh, over the pubis, over an apophysis, or in the testes--or is it diffuse? Is there a referral pattern
such as into the scrotum, into the knee, or along a specific dermatomal area; or is the pain
nonradiating? Movements that reproduce or intensify the pain should also be sought.
Perhaps the most important task in diagnosis is delineating whether the injury is acute or chronic.
While acute causes are often readily identified, chronic groin pain may suggest myriad diagnoses,
many with vague and overlapping signs and symptoms.
For chronic groin pain, the physician needs to inquire about urinary symptoms, night pain,
rheumatologic components, or systemic symptoms. Chronic, insidious groin pain can indicate a
nonmusculoskeletal cause and requires a more complex diagnostic approach.
If groin pain persists despite treatment, other diagnoses must be entertained. A multidisciplinary
strategy may be required, and secondary diagnoses are not uncommon (4-6).
Following are musculoskeletal and nonmusculoskeletal causes of groin pain, with clinical features
and treatments described.
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Primary Musculoskeletal Causes
Active people who incur an acute injury with a sharp, cutting motion usually experience pain in the
proximal medial thigh and, possibly, swelling. Such patients usually have only minor discomfort
with walking, but their pain increases with running or cutting. Musculotendinous injuries most often
involve the adductor longus muscle but can also include the iliopsoas, rectus femoris, sartorius, or
gracilis muscle (figure 1) (1,2,4,7).
Most groin injuries in active people are musculotendinous (5).
Strains. The most common musculoskeletal cause of groin pain is a muscle strain, which occurs
when a muscle is stretched beyond its normal capability or encounters an unexpected opposing
force. Signs and symptoms include acute pain over the proximal muscles of the medial thigh,
swelling, and, occasionally, bruising. Also present will be the classic musculotendinous injury triad:
tenderness to palpation, pain with resistance, and pain with passive stretching.
Imaging procedures are usually unnecessary in simple muscle strains. If obtained, they are usually
done to rule out concomitant or more severe injuries (8). Ultrasound should be used with caution
because it can promote bleeding in the acute injury and mutagenesis, and the treatment area is
often close to reproductive organs.
The treatment of muscle strains consists of rest from aggravating activities for the first 1 to 2
weeks (7). Ice is used initially, and heat can be used after the first 48 hours. Compression shorts
can provide symptomatic relief and expedite return to play. If compression shorts are not available,
a hip spica wrap can provide both warmth and support. We like to use nonsteroidal antiinflammatory drugs (NSAIDs) for the first 7 to 10 days to limit inflammation and control pain in
order to facilitate rehabilitation.
When inflammation subsides, patients can start a stretching program. During the stretching phase
of rehabilitation, patients are encouraged to maintain cardiovascular fitness with aerobic exercises
that do not exacerbate their pain. A strengthening program consisting initially of low-intensity
isotonic exercises can follow the stretching phase (7). Surgical repair for musculotendinous injuries
166
has been tried with varied success, and should be the decision of an orthopedist familiar with the
techniques (9,10).
Adductor tendinitis. Tendititis is often caused by chronic overloading of a musculotendinous unit,
resulting in microscopic tears in the tissue substance. If this happens in the adductor muscle, the
patient experiences pain and stiffness in the groin region that is often worse after an exercise bout.
There is local tenderness to palpation, and adductor tendinitis is often difficult to differentiate from
an adductor strain on physical exam. Pain may at times radiate along the medial thigh or toward
the rectus abdominis. Treatment centers on allowing the tendon unit to heal without further
overload.
Avulsion fractures. Avulsion fractures occur in adolescents, especially teenagers, and are more
common in the mid to late teens when muscles significantly increase in contractile strength. These
fractures occur in one of several apophyses in the hip area (figure 2) (11). Avulsions are usually
caused by an unexpected, explosive contraction of the muscle. Direct trauma is a much rarer cause
(3).
A typical history is that of a hurdler or sprinter who experienced a "pop" and acute pain while
"kicking it out" at the end of a race. A limp with an avulsion fracture is a clue that it is severe (3).
The patient will have pain on palpation at the site of the injury and with stretching of the involved
muscle.
Plain radiographs are usually diagnostic (1,3,7). A small piece of bone is observed near the
attachment site of the tendon. This should not be confused with calcification in the tendon unless a
chronic process has been elucidated in the history.
Most avulsion fractures are treated conservatively, beginning with relative rest. Ice and NSAIDs are
used to control pain and swelling, and crutches may be needed for the first several days. Return to
sports is allowed when the patient is pain free, which can take 4 to 6 weeks depending on the site
of the avulsion.
Stress fractures. Repetitive forces on the long bones can lead to stress fractures. The most
common sites causing groin pain include the pubic ramus and femoral neck. These injuries usually
occur in long-distance runners, whose sport subjects these bones to repetitive stresses. They can
occur when there is a change in equipment, especially running shoes. Sudden increases in training
intensity or duration can also overwhelm the natural physiologic response to stress and weaken
167
bony architecture. Changing to a harder training surface such as pavement has also been
associated with stress fractures (12).
The active patient who has a chronic ache or pain in the groin, buttock, and thigh can have a pubic
ramus stress fracture (8); a similar ache or pain with decreased range of hip motion (specifically
internal rotation in flexion) may indicate a femoral neck stress fracture. Plain radiographs are
initially negative, but a bone scan can show increased isotope uptake at the site of the stress
fracture early on (4-8,13). Serious complications can arise if a femoral neck stress fracture is not
recognized and the athlete continues to train despite pain. Avascular necrosis of the femoral head,
nonunion, and varus deformity of displaced fractures have all been reported. Several classification
protocols exist; all are based on defining the femoral neck stress fracture as compressive or
distracted in nature, with the latter posing a greater likelihood of disability.
If suspicion is high, thorough investigation is mandatory. Patients with negative radiographs should
be treated with complete non-weight-bearing until a bone scan can be completed. If there is
radiographic evidence of a stress fracture, then magnetic resonance imaging (MRI) or computed
tomography (CT) scans should be obtained to determine its extent and type. Involvement of an
orthopedist is prudent early on if plain radiographs show a lesion (12).
Femoral neck stress fractures that are nonoperative in nature are treated with strict non-weight
bearing until the patient is pain free. Rehabilitation and return to sport must be gradual, allowing
for adequate remodeling of the femoral neck. Water exercise is excellent for rehabilitation, and
various pool running progressions have been described. A progression from water to cycling to a
walk-run program is advised (12).
Treatment for other stress fractures consists of relative rest and avoidance of aggravating
activities. Six to 8 weeks away from running is often needed for these fractures to heal.
Secondary Musculoskeletal Causes
Pubic instability. Pubic instability results in excess motion at the pubic symphysis. Trauma to the
pelvis or significant unilateral axial loads to the lower extremity can lead to instability. Pain is felt in
the pubis, groin, or lower abdomen and is sometimes accompanied by a clicking sensation with
certain lower-extremity movements. A flamingo view radiograph confirms the diagnosis and is
considered positive when alternating weight-bearing views show a shift of 2 mm or more in the
pubic symphysis.
Treatment includes traditional conservative measures to relieve symptoms, such as physical
therapy, NSAIDs, and compression shorts. In refractory cases, surgical intervention including bone
grafts and plating have been described (14).
Osteitis pubis. Some believe osteitis pubis to be a self-limiting disease of the pubic symphysis
(13). It is believed that repetitive twisting and cutting motions initiate a lytic response caused by
traction of the adductor and gracilis muscles.
Symptoms include pain over the pubic symphysis or medial groin region that is increased with
resisted adduction of the thigh. Because pain can be diffuse around the abdomen, groin, hip, or
thigh (15), this entity can be confused with other musculoskeletal conditions.
Plain radiographs may show irregularity, sclerosis, and widening of the pubis consistent with
osteolysis, although they often do not provide good correlation with the clinical exam (3,15,16). A
bone scan typically shows increased uptake unilaterally or bilaterally at the pubic bones
(13,15,16).
Treatment consists of relative rest with ice and NSAIDs initially, followed by stretching exercises.
If symptoms persist, a treatment regimen described by Batt et al (15) may be undertaken,
consisting of betamethasone injection into and around the pubic symphysis, followed by NSAIDs.
With injections, utmost care must be taken with needle placement as bladder perforation or
168
injection into the abdominal cavity is possible. A repeat injection can be done 2 weeks later, if
needed, when a stretching program is begun.
The patient can return to play gradually when pain free. Osteitis pubis can sometimes take as long
as 9 months to resolve with conservative care. Reported rates of recurrence and failure to return to
previous levels of competition have been as high as 25%, and may be higher in men (16).
Bursitis. Bursitis usually develops acutely from trauma or can be chronic when overuse of the
overlying muscles leads to inflammation.
Symptoms include pain over the site of the bursa. (Iliopsoas tendinitis or bursitis may cause pain in
the lower abdomen, anterior thigh, or groin, making it tricky to diagnose.) Diagnosis is usually
clinical, but is best confirmed when anesthetic infiltration relieves the symptoms.
Treatment can consist of an injection of cortisone, an anesthetic, or both.
Avascular necrosis. Groin pain can be caused by avascular necrosis of the femoral head following
hip trauma. Medications (especially corticosteroids), alcohol abuse, and systemic disease can also
cause avascular necrosis. Avascular necrosis of the femoral head that occurs in children 5 to 8
years old, especially boys, is called Legg-Calvé-Perthes disease. Symptoms include inguinal pain on
internal rotation of the hip and decreased hip range of motion.
Plain radiographs show subchondral lucency around the superolateral femoral head (the crescent
sign) (8). Other early radiographs may reveal increased density at the femoral epiphysis, and later,
a mottled, moth-eaten appearance of the femoral head may be seen. MRI can aid in diagnosis
(13), and in the elderly population should include a view of the opposite hip, as avascular necrosis
is more likely to occur bilaterally in this population.
Treatment ranges from conservative measures focused on pain relief to total hip replacement.
Regardless of severity, referral to an orthopedic surgeon is warranted.
Myositis ossificans. A direct blow to a muscle or significant muscle strain can lead to the
development over several months of myositis ossificans. Initial bleeding leads to hematoma
formation that later calcifies within the substance of the muscle, restricting its extensibility.
Symptoms and signs include pain and decreased range of motion in the involved muscle. A
palpable mass is often detected within the substance of the muscle once calcification has begun.
Radiographs can be negative up to 5 weeks after trauma and before calcific changes are seen in
the soft tissues. A discrete margin between the cortex of the involved bone and the calcified area
helps distinguish heterotopic bone formation from other pathologic entities. Osteogenic sarcoma is
sometimes difficult to differentiate from heterotopic bone on radiographs. However, it is contiguous
with, rather than distinct from, the adjacent cortices. Heterotopic bone and osteogenic sarcoma
biopsy specimens share similar histologic features, which can further confound the diagnosis. A
triple-phase bone scan can help to make the diagnosis earlier by revealing increased uptake within
soft tissues adjacent to the bones.
Treatment consists of moderately aggressive active or passive range-of-motion exercises. Care
must be taken not to overstretch the muscle and cause further bleeding. Keeping the muscle in a
lengthened position in the early phase can help decrease the incidence of heterotopic bone
formation. For the quadriceps muscles, this can be accomplished by wrapping the affected area in
an elastic bandage with the knee in maximum flexion for the first 24 hours after the trauma.
NSAIDs are avoided or used sparingly in the first 2 days to limit hematoma formation but are the
drugs of choice to limit calcification later on. Indomethacin has historically been associated with
treating myositis, but it is not necessarily any more effective than other NSAIDs.
Nerve entrapment. Nerve entrapments in the inguinal region, including genitofemoral,
ilioinguinal, and obturator nerves, have all been described as causes of chronic groin pain.
Mechanisms of entrapment or injury include local hernia into the nerve tunnel, nearby
inflammatory or infectious processes, or trauma or scarring from surgery or nearby injuries. Thick
169
fascial bundles causing stenotic canals have also been described as a mechanism (17). The
ilioinguinal, genitofemoral, iliofemoral, or lateral cutaneous nerves are most commonly involved.
The patient describes a burning or shooting pain in the distribution of the nerve. Light touch
sensation in the medial groin can be altered, or pain can be exacerbated by hyperextension at the
hip joint. Occasionally, there is tenderness near the anterior superior iliac spine where the
ilioinguinal nerve pierces the fascia and is subject to entrapment. An electrodiagnostic study can
help in the diagnosis.
Treatment consists of infiltration around the nerve site with a local anesthetic (4). Topical creams
such as capsaicin can also be used in the treatment of painful dysesthesias. After several weeks,
the medicine can be discontinued to see if the dysesthesias have subsided.
Musculoskeletal Causes in Youth and Elderly
Slipped capital femoral epiphysis. Insidious groin pain that develops in the 8- to 15-year-old
child or adolescent should make the physician suspect slipped capital femoral epiphysis (see "Case
Study: Hip Pain in a Young Football Player," below). The typical adolescent will be an obese or
rapidly growing boy who has not yet begun puberty.
The patient has inguinal pain with hip motion, and pain made worse with physical activity. He or
she usually walks with a limp and holds the leg in external rotation. Plain radiographs, especially
frog-leg lateral views, are usually diagnostic (13).
Treatment involves discontinuing all athletic activity and referring the patient to an orthopedic
surgeon.
Osteoarthritis. Osteoarthritis of the femoral head is a degenerative disease that occurs most
often in elderly patients. Complaints include inguinal pain with hip movement, especially internal
rotation. Plain films are usually diagnostic (4).
Treatment can be conservative with nonnarcotic analgesics or NSAIDs for pain relief. If intractable
pain affects the patient's quality of life, a total hip replacement can be considered.
General Nonmusculoskeletal Causes
Hernia. The recent literature shows hernia to be an often-overlooked cause of chronic groin pain
(4-6,13,18,19). In his review of chronic groin pain in 189 athletes, Lovell (4) noted that over 50%
had incipient hernias. The debate continues over the significance of clinically undetectable hernias,
but surgical repair is producing excellent results in cases of recalcitrant groin pain.
The most common type of hernia is a direct inguinal hernia, which is the result of a tear or
weakness of the posterior wall of the inguinal canal. This produces chronic episodic pain just above
the pubic tubercle. Initially the pain occurs after activity, but it increases and occurs during activity
as the problem progresses. Pain can be unanticipated and sharp, with abrupt increases in
abdominal pressure (18). The pain can also radiate into the proximal medial thigh or the scrotum
in males.
A palpable mass may or may not be detected. Patients can be asked to perform maneuvers such as
coughing or tensing muscles to increase intra-abdominal pressure and make a mass more
prominent (18). In males, the scrotum should be invaginated so that the inguinal rings are
palpated. Tension on the abdominal wall may also elicit discomfort. A tear or strain of the
conjoined tendon--the fused aponeurosis of the internal oblique and transversus abdominis--can
cause pain at the external inguinal ring or at the pubic crest area (4). The pain from hernias
responds poorly to traditional measures, including prolonged rest, and it usually resurges soon
after return to activity.
Herniography, a procedure that has been used in Europe with success, can be an option when a
hernia is the suspected cause of chronic groin pain and surgical treatment is being considered (1,4-
170
6,18). The procedure involves injecting a contrast medium into the pelvic cavity, obtaining
radiographs, and looking for anterior extension of the dye into the inguinal area (4,13).
Lymphadenopathy. Lymphadenopathy can be caused by an infection in the trunk or lower
extremities, or by a sexually transmitted disease. The physician can find palpable lymph nodes just
below the patient's inguinal ligaments. Lymphadenopathy may be associated with fever, chills, or
discharge, depending on the specific cause of the lymphadenopathy.
Treatment usually consists of antibiotics for the underlying infection. If lymphadenopathy persists
despite acute treatment, an underlying neoplasm should be suspected, although it is not as
common. A rule of thumb is that tender lymph nodes suggest infection and nontender nodes a
neoplasm.
Nonmusculoskeletal Causes in Males
Genital swelling or inflammation. Epididymitis, hydroceles, and varicoceles may cause groin
pain in males.
Epididymitis is caused by sexually transmitted diseases in younger active patients, and usually by
gram-negative organisms in older patients. The inflamed epididymis is often exquisitely tender over
the superior aspect of the testes.
A hydrocele is a fluid-filled mass around the testes, and symptoms usually involve pain in the lower
spermatic cord region. Transilluminating the scrotum with a penlight can facilitate diagnosis of a
hydrocele.
A varicocele is usually located on the left and is a rubbery, elongated mass around the spermatic
cord (13). This painful dilation of the venous plexus can cause infertility.
If infection is identified, treatment consists of appropriate antibiotics. Otherwise, referral to a
urologist is prudent.
Testicular torsion or rupture. Testicular torsion or rupture is considered a medical emergency. It
has an acute onset and, in the case of a rupture, is usually preceded by trauma. Signs and
symptoms include swelling and severe pain in the scrotum, often accompanied by nausea and
vomiting. The testes may be hard on palpation or may not be palpable at all.
The patient should be referred to a urologist immediately if torsion or rupture is suspected.
Prostatitis. Prostatitis can cause dysuria as well as a purulent discharge in male patients. Both
urinalysis and a culture of the prostatic secretion will demonstrate infection and/or inflammation
and aid diagnosis. A rectal exam will reveal a tender, soft, and irregular prostate (6). Prostatitis
has been correlated with symphysitis, and it must be considered in an older man who has chronic
symptoms. The belief is that the infection in the prostate can trigger a reactive arthritis (20).
Prostatitis can also mimic adductor longus tendinitis, which is differentiated by the rectal exam.
Treatment consists of appropriate antibiotics to treat the infection and NSAIDs to reduce pain and
inflammation.
Testicular cancer and other neoplasms. Testicular cancer has an insidious onset in men aged
18 to 36. Signs and symptoms include palpation of a hard mass on the testis and, possibly, a
tender testis.
Ultrasound can aid in the diagnosis, and patients should be referred to a urologist. The suspicion of
neoplasm must always lurk when obvious causes are becoming less likely.
Nonmusculoskeletal Causes in Females
171
Ovarian cysts. Active female patients with no obvious cause for perineal or groin pain should have
a pelvic exam. Ovarian cysts have an insidious onset and produce groin or perineal pain.
An adnexal mass can sometimes be palpated on exam. Ultrasonography can help make the
diagnosis (13), and treatment consists of referral to a gynecologist.
Urinary tract infections. Urinary tract infections can occur, especially in female athletes who do
not maintain adequate hydration. Symptoms include burning with urination, itching, and frequent
urination. Urinalysis with culture and drug sensitivity will confirm the diagnosis (6,13), and
treatment consists of a short course of appropriate antibiotics.
Pelvic inflammatory disease. Pelvic inflammatory disease is most often the result of a sexually
transmitted disease. A patient can become gravely ill if treatment is delayed. The patient may have
fever, chills, and purulent discharge in additon to groin pain.
A pelvic exam with cultures can help to make the diagnosis. Treatment usually consists of
intravenous antibiotics and referral to a gynecologist.
Meeting the Challenge
Diagnosis and treatment of an active patient who has groin pain can often offer a much deeper
challenge than meets the eye. Referral to a specialist is often helpful, and it may take more than
one referral or specialist. Finding the right treatment not only will help active patients return to
their sport, but can also help them avoid long-term pain.
References
1. Hasselman CT, Best TM, Garrett WE Jr: When groin pain signals an adductor strain. Phys
Sportsmed 1995;23(7):53-60
2. Estwanik JJ, Sloane B, Rosenberg MA: Groin strain and other possible causes of groin pain.
Phys Sportsmed 1990;18(2):54-65
3. Combs JA: Hip and pelvis avulsion fractures in adolescents: proper diagnosis improves
compliance. Phys Sportsmed 1994;22(7):41-49
4. Lovell G: The diagnosis of chronic groin pain in athletes: a review of 189 cases. Aust J Sci
Med Sport 1995;27(3):76-79
5. Karlsson J, Swärd L, Kälebo P, et al: Chronic groin injuries in athletes: recommendations
for treatment and rehabilitation. Sports Med 1994;17(2):141-148
6. Ekberg O, Persson NH, Abrahamsson PA, et al: Longstanding groin pain in athletes: a
multidisciplinary approach. Sports Med 1988;6(1):56-61
7. Balduini FC: Abdominal and groin injuries in tennis. Clin Sports Med 1988;7(2):349-357
8. Pavlov H: Roentgen examination of groin and hip pain in the athlete. Clin Sports Med
1987;6(4):829-843
9. Akermark C, Johansson C: Tenotomy of the adductor longus tendon in the treatment of
chronic groin pain in athletes. Am J Sports Med 1992;20(6):640-643
10. Peterson L, Stener B: Old total rupture of the adductor longus muscle: a report of seven
cases. Acta Orthop Scand 1976;47(6):653-657
11. Ogden JA: Skeletal Injury in the Child, ed 2. Philadelphia, WB Saunders Co, 1990, pp 651657
12. Gross ML, Nassar S, Finerman GAM: Hip and pelvis, in DeLee JC, Drez D (eds), Orthopaedic
Sports Medicine: Principles and Practice. Philadelphia, WB Saunders, 1994, vol 2, pp 10631085
13. Swain R, Snodgrass S: Managing groin pain: even when the cause is not obvious. Phys
Sportsmed 1995;23(11):55-66
14. Delaunay C, Roman F, Validire J: Pubic osteoarthropathy caused by symphyseal instability
or chronic painful symphysiolysis: treatment by symphysiodesis. Apropos of a case and
review of the literature (French). Rev Chir Orthop 1986;72(8):573-577
15. Batt ME, McShane JM, Dillingham MF: Osteitis pubis in collegiate football players. Med Sci
Sports Exerc 1995;27(5):629-633
16. Fricker PA, Taunton JE, Ammann W: Osteitis pubis in athletes: infection, inflammation, or
injury? Sports Med 1991;12(4):266-279
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17. Bradshaw C, McCrory P, Bell S, et al: Obturator nerve entrapment: a cause of groin pain in
athletes. Am J Sports Med 1997;25(3):402-408
18. Hackney RG: The sports hernia: a cause of chronic groin pain. Br J Sports Med
1993;27(1):58-62
19. Taylor DC, Meyers WC, Moylan JA, et al: Abdominal musculature abnormalities as a cause
of groin pain in athletes: inguinal hernias and pubalgia. Am J Sports Med 1991;19(3):239242
20. Abrahamsson PA, Westlin N: Symphysitis and prostatitis in athletes. Scand J Urol Nephrol
1985;19(suppl 93):42
Case Study: A Surprising Cause of Groin
Pain in a Female Runner
A 33-year-old woman presented with right groin pain. Three weeks earlier she had had a dirt bike
accident but did not recall any significant impact to the pelvic region. She was an avid runner and
was having difficulty returning to her sport. She was treating her "bad groin pull" with heat and
over-the-counter analgesics. She also had right-side sacroiliac pain, and discomfort in the right
anterior thigh with running.
Clinical examination revealed tenderness and spasm of the proximal adductor mass on the right,
with significant tenderness at the insertion. There was pain and weakness with activation of that
adductor muscle group. The right sacroiliac joint was tender, with tenderness extending a few
centimeters into the sacrum.
An anteroposterior pelvis radiograph was obtained (figure A), mostly to inspect the sacrum and
sacroiliac joint. A minimally displaced transverse fracture of the right superior pubic ramus was
discovered, which likely resulted from the trauma at the time of the dirt bike accident. As the
patient had already been ambulatory for 3 weeks, treatment consisted of continued protected
weight bearing. At 8 weeks postinjury she was pain free with ambulation, and she gradually
returned to running with no further incident.
Case Study: Hip Pain in a Young Football Player
A 14-year-old boy had right hip pain for 2 months. Radiographs (figure B) taken 1 month earlier
had been interpreted as negative; he had then begun 3 weeks of physical therapy for a "chronic
groin pull." He was removed from football just prior to his visit because he was unable to run.
173
The radiographs demonstrate a chronic grade 1 slip of the capital femoral epiphysis. This patient
was a slightly overweight prepubescent male who walked into our office with the classic antalgic
gait, holding his leg in external rotation. While it was probably not so obvious in the early stages,
this case demonstrates why it is important to keep a broad differential in mind, especially in
adolescents.
The patient was referred immediately to an orthopedic surgeon, and open reduction with screw
fixation was performed the following day. At 2 weeks postsurgery the patient was healing well with
no evidence of recurrence.
Dr Ruane is a family physician specializing in the diagnosis and treatment of sports-related injuries
at SportsMedicine Grant in Columbus, Ohio. Dr Rossi is a physiatrist at Physical Medicine
Associates, Inc, and has completed a fellowship in primary care sports medicine at SportsMedicine
Grant, both in Columbus. Drs Ruane and Rossi are members of the American College of Sports
Medicine. Address correspondence to Joseph J. Ruane, DO, SportsMedicine Grant, 323 East Town
St, Columbus, OH 43215; e-mail to josport@ix.netcom.com.
174
Giving Injuries the Cold Treatment
Bryant Stamford, PhD
When you sprain your ankle or have a similar injury, tissue is stretched and torn, and swelling
occurs. Swelling interferes with healing, so anything that will prevent or reduce swelling should
help you recover from a minor injury more quickly.
The sooner you attend to swelling after an injury the better, and the best approach is to apply cold
directly to the injured area right away. (See "A Time for Cold, a Time for Heat") Cold shrinks the
blood vessels, which reduces bleeding in the area and helps to prevent swelling. It also helps
prevent the muscles from going into spasm (involuntary contractions) and relieves pain.
The use of cold as a treatment is as old as the practice of medicine, dating back to Hippocrates.
Today, methods of applying cold are more advanced than they were in 400 BC, but the principles
and the need for precautions are the same. When you apply cold, the skin will initially feel cold,
often followed by relief of pain from the injury. As icing progresses, you will feel a burning
sensation, then pain in the skin, and finally numbness.
To avoid skin damage, stop when the skin begins to feel numb. (This is different, though, from the
"numbness" you feel early on as the cold relieves injury pain. Keep icing after this pain subsides.)
Applying too much cold for too long can cause frostbite or even nerve damage. Also, cold
treatment is not for everyone (see "When to Avoid Cold Therapy").
The length of time you apply cold will vary depending on the method and location of the injury (see
specifics below). Areas with little body fat (like the knee, ankle, and elbow) do not tolerate cold as
well as fatty areas (like the thigh and buttocks). So, for bonier areas, keep to the low end of the
recommended application ranges listed below.
For best results, apply cold at regular intervals throughout the waking hours of the day, allowing a
few hours between treatments. Time off will keep cooling effects from accumulating and will allow
the skin to return to normal temperature. An ice bag remains--for good reason--the cool treatment
of choice for most people, but several options exist:
Ice Bags



Strengths: Ice bags are the old standby for applying deep, penetrating cold. Fill a bag
made of thick plastic, rubber, or moisture-proof fabric with ice and apply it directly to the
skin. The cooling effect of ice bags lasts long and is more effective than some of the
superficial methods like ice massage. If you use a regular plastic food bag, place a thin
towel (like a dish towel) between the bag and your skin.
Weaknesses: A shortcoming is getting the bag to contour to the curves of the body for
maximum application. The bag will mold better if you don't fill it completely with ice or if
you use crushed ice. An alternative is to use a bag of frozen peas or corn. The bag will
conform nicely to the injured part of the body. Place a thin towel between the bag and the
skin.
Application time: 10 to 30 minutes, depending on the body part and comfort.
Gel Packs
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Strengths: Cold gel packs contain a special gel that can be frozen and refrozen. Just store
the packs in the freezer until needed. The gel remains flexible when frozen, allowing it to
contour to the injured body part.
Weaknesses: Cold gel packs will cool the skin faster than ice bags and so deserve greater
caution. Never apply them directly to the skin--always wrap them in a towel.
Application time: No more than 10 minutes at a time.
Chemical Cold Bags

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Strengths: Chemical cold bags stay at air temperature until squeezing the bag and mixing
the chemicals produces cold. They work well on the field or in the wilderness.
Weaknesses: The degree of cold produced by the chemical reaction is not great. Even so,
the bags provide a good first-aid approach.
Application time: Because the temperature is not that low, a 30-minute application
should not be a problem, and the bag can be applied directly to the skin.
Immersion



Strengths: Immersion entails placing the foot, hand, or elbow in icy water filled with
crushed ice or ice cubes. This technique provides very complete and concentrated cold
exposure to the entire injured area.
Weaknesses: Body parts besides the foot, hand, and elbow do not lend themselves to
immersion, because too much of the uninjured area is exposed to the cold.
Application time: 10 to 20 minutes. Let comfort be your guide.
Ice Massage



Strengths: Ice massage involves rubbing ice on the skin with a circular motion. It is easy
to apply and focuses the cold on the injured area. A useful approach is to fill a paper or
foam cup with water and freeze it until needed. Then peel away the top to reveal the ice
and hold the bottom of the cup to apply. Ice cubes or chunks can also be used.
Weaknesses: The cold tends not to penetrate as deeply nor last as long as the methods
listed above.
Application time: When applying to bony areas such as the ankle, apply for only 7 to 10
minutes. Double the time when applying to fatty areas such as the thigh or buttocks.
Combination Treatment
To maximize the benefits of cold therapy, think RICE: rest, ice, compression, and elevation. So in
addition to cold therapy, rest your injury, apply elastic wrap snugly, and keep the injured area
raised. New technologies combine RICE aspects. Cold tape, for example, compresses and-because
of a chemical reaction-applies cold to an injured part.
Putting Injuries on Ice
Whichever method you choose, remember to ice early, ice often. But not too often. To avoid
harmful effects like frostbite, let your skin recover between cold applications, and listen to your
body.
A Time for Cold, a Time for Heat
There has been controversy over the years as to when to apply cold and when to apply heat.
Because heat stimulates blood flow, it promotes healing just as cold does. It can also relax muscles
and ease pain.
But heat can make swelling worse. That's why cold is best right after an injury and heat is
176
recommended for later, when swelling abates. As a rule of thumb, use ice for at least 48 hours
after injury. Then, when the swelling is gone, you can apply heat. (Back to article)
When to Avoid Cold Therapy
Using cold therapy may not be a good idea for some people. Those who are very sensitive to cold
will not be able to tolerate icing long enough to do any good. Conversely, those who have a high
tolerance to cold-or who pride themselves on being "tough"-open themselves to injury by
applying cold therapy too long.
People with problems in the blood vessels near the skin should avoid cold therapy, especially
those with Raynaud's phenomenon (a condition in which the blood vessels in the fingers, toes,
ears, and nose constrict dramatically when exposed to cold and other stimuli). If you suspect you
may be at risk because of diabetes or another condition that can diminish blood flow, check with
your doctor before applying cold to an injury. (Back to article)
Remember: This information is not intended as a substitute for medical treatment.
Before starting an exercise program, consult a physician.
Dr Stamford is director of the Health Promotion and Wellness Center and professor of exercise
physiology in the School of Education at the University of Louisville, Kentucky. He is also an
editorial board member of The Physician and Sportsmedicine.
177

FLP de Toekomst - HvA Kennisbank

Transcription

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