42759.pdf

“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

Wetenschappelijke artikelen FLP de Toekomst

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 behandel- en 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.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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 [email protected]. 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

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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. REFERENCES 1. Ekstrand J, Tropp H. The incidence of ankle sprains in soccer. Foot Ankle. 1990;11:41–44. [PubMed] 2. Garrick JG, Requa RK. The epidemiology of foot and ankle injuries in sports. Clin Sports Med. 1988;7:29–36. [PubMed] 3. Glick JM, Gordon RB, Nishimoto D. The prevention and treatment of ankle injuries. Am J Sports Med. 1976;4:136– 141. [PubMed] 4. Garrick JG. The frequency of injury, mechanism of injury, and epidemiology of ankle sprains. Am J Sports Med. 1977;5:241–242. [PubMed] 5. Barker HB, Beynnon BD, Renstrom PA. Ankle injury risk factors in sports. Sports Med. 1997;23:69–74. [PubMed]

Wetenschappelijke artikelen FLP de Toekomst

20

6. Garrick JG. Epidemiologic perspective. Clin Sports Med. 1982;1:13–18. [PubMed] 7. Broström L. Sprained ankles: I, anatomic lesions on recent sprains. Acta Chir Scand. 1964;128:483–495. [PubMed] 8. Staples OS. Ruptures of the fibular collateral ligaments of the ankle: result study of immediate surgical treatment. J Bone Joint Surg Am. 1975;57:101–107. [PubMed] 9. Kannus P, Renstrom P. Treatment for acute tears of the lateral ligaments of the ankle: operation, cast, or early controlled mobilization. J Bone Joint Surg Am. 1991;73:305–312. [PubMed] 10. Freeman MA, Dean MR, Hanham IW. The etiology and prevention of functional instability of the foot. J Bone Joint Surg Br. 1965;47:678–685. [PubMed] 11. Smith RW, Reischl SF. Treatment of ankle sprains in young athletes. Am J Sports Med. 1986;14:465–471. [PubMed] 12. Torg JS. Athletic footwear and orthotic appliances. Clin Sports Med. 1982;1:157–175. [PubMed] 13. Tropp H, Askling C, Gillquist J. Prevention of ankle sprains. Am J Sports Med. 1985;13:259–262. [PubMed] 14. Murtaugh K. Injury patterns among female field hockey players. Med Sci Sports Exerc. 2001;33:201–207. [PubMed] [Full Text] 15. Garrick JG, Requa RK. Role of external support in the prevention of ankle sprains. Med Sci Sports. 1973;5:200– 203. [PubMed] 16. Milgrom C, Shlamkovitch N, Finestone A, et al. Risk factors for lateral ankle sprain: a prospective study among military recruits. Foot Ankle. 1991;12:26–30. [PubMed] 17. Jones BH, Cowan JP, Tomlison JR, Robinson JR, Polly DW, Frykman PN. Epidemiology of injuries associated with physical training among young men in the Army. Med Sci Sports Exerc. 1993;25:197–203. [PubMed] 18. Yeung, Ms.; Chan, KM.; So, CH.; Yuan, WY. An epidemiological survey on ankle sprain. Br J Sports Med. 1994;28:112–116. [PubMed] 19. Wilkerson GB. Biomechanical and neuromuscular effects of ankle taping and bracing. J Athl Train. 2002;37:436– 445. [ Free Full text in PMC] 20. Cordova ML, Ingersoll CD, Palmieri RM. Efficacy of prophylactic ankle support: an experimental perspective. J Athl Train. 2002;37:446–457. [ Free Full text in PMC] 21. Quigley TB, Cox J, Murphy J. A protective wrapping for the ankle. JAMA. 1946;123:924. 22. Sharpe SR, Knapik J, Jones B. Ankle braces effectively reduce recurrence of ankle sprains in female soccer players. J Athl Train. 1997;32:21–24. 23. Surve I, Schwellnus MP, Noakes T, Lombard C. A fivefold reduction in the incidence of recurrent ankle sprains in soccer players using the Sport- Stirrup orthosis. Am J Sports Med. 1994;22:601–606. [PubMed] 24. Rovere GD, Clarke TJ, Yates CS, Burley K. Retrospective comparison of taping and ankle stabilizers in preventing ankle injuries. Am J Sports Med. 1988;16:228–233. [PubMed] 25. Sitler M, Ryan J, Wheeler B, et al. The efficacy of a semirigid ankle stabilizer to reduce acute ankle injuries in basketball: a randomized clinical study at West Point. Am J Sports Med. 1994;22:454–461. [PubMed] 26. Simon JE. Study of the comparative effectiveness of ankle taping and ankle wrapping on the prevention of ankle injuries. Athl Train J Nat Athl Train Assoc. 1969;4:6–7. 27. Amoroso PJ, Ryan JB, Bickley B, Leitschuh P, Taylor DC, Jones BH. Braced for impact: reducing military paratroopers' ankle sprains using outside-the-boot braces. J Trauma. 1998;45:575–580. [PubMed] [Full Text]

Wetenschappelijke artikelen FLP de Toekomst

21

28. Cook RJ, Sackett DL. The number needed to treat: a clinically useful measure of treatment effect. BMJ. 1995;310:452–454. [PubMed] [Free Full Text] 29. Sackett, Dl.; Straus, SE.; Richardson, WS.; Rosenberg, W.; Haynes, RB. Evidence-Based Medicine: How to Practice and Teach EBM. 2nd ed. Edinburgh, Scotland: Churchill Livingstone; 2000. 30. Walter SD. Choice of effect measure for epidemiological data. J Clin Epidemiol. 2000;53:931–939. [PubMed] [Full Text]

31. Chattellier G, Zapletal E, Lemaitre D, Menard J, Degoulet P. The number needed to treat: a clinically useful nomogram in its proper context. BMJ. 1996;312:426–429. [PubMed] [Free Full Text] 32. Verhagen EA, van Mechelen W, de Vente W. The effect of preventative measures on the incidence of ankle sprains. Clin J Sport Med. 2000;10:291–296. [PubMed] [Full Text] 33. Chang WY, Henry BM. Methodologic principles of cost analyses in the nursing, medical, and health services literature, 1990–1996. Nurs Res. 1999;48:94–104. [PubMed] [Full Text] 34. Bandolier, Extra. Calculating and using NNTs. Available at: http://www.ebandolier.com. Accessed February 2003. 35. Handoll, HHG.; Rowe, BH.; Quinn, KM.; de Bie, R. The Cochrane Library. Chichester, UK: John Wiley & Sons; 2000. Interventions for preventing ankle ligament injuries (Cochrane Review); pp. 1–57. 36. Thacker SN, Stroup DF, Brache CM, Gilchrist J, Goodman RA, Weitman EA. The prevention of ankle sprains in sports: a systematic review of the literature. Am J Sports Med. 1999;27:753–760. [PubMed] [Full Text] 37. Cordova ML, Ingersoll CD, LeBlanc MJ. Influence of ankle support on joint range of motion before and after exercise: a meta-analysis. J Orthop Sport Phys Ther. 2000;30:170–182.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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 Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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 Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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. Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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 [email protected].

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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).

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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).

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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 Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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 [email protected].

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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 [email protected]. 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.

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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%.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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. Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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-

Wetenschappelijke artikelen FLP de Toekomst

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. REFERENCES 1. Andersen TE, Larsen O, Tenga A, et al: Football incident analysis (FIA):

Wetenschappelijke artikelen FLP de Toekomst

87

A new video-based method to describe injury mechanisms in professional football. Br J Sports Med 37: 226–232, 2003 2. Arnason A, Gudmundsson A, Dahl HA, et al: Football injuries in Iceland. Scand J Med Sci Sports 6: 40–45, 1996 3. Arnason A, Gudmundsson A, Holme I, et al: Risk factors for injuries in football. Am J Sports Med: in press 4. Bahr R, Karlsen R, Lian Ø, et al: Incidence and mechanisms of acute ankle inversion injuries in volleyball. Am J Sports Med 22: 595–600, 1994 5. Bahr R: Can we prevent ankle sprains? in MacAuley D, Best T (eds): Evidence-based Sports Medicine. London, BJM Books, 2002, pp 470–490 6. Bahr R, Kannus P, van Mechelen W: Epidemiology and prevention of sports injuries, in Kjaer M, Krogsgaard M, Magnusson P, et al (eds): Textbook of Sports Medicine: Basic Science and Clinical Aspects of Sports Injury and Physical Activity. Munksgaard, Copenhagen, 2003, pp 299–314 7. Bahr R, Pena F, Shine J, et al: Ligament force and joint motion in the intact ankle: A cadaveric study. Knee Surg Sports Traumatol Arthrosc 6: 115–121, 1998 8. Biedert R: Anterior ankle pain in sports medicine: Aetiology and indications for arthroscopy. Arch Orthop Trauma Surg 110: 293–297, 1991 9. Broström L: Sprained ankles I. Anatomic lesions in recent sprains. Acta Orthop Scand 128: 483–495, 1964 10. Cawley PW, France EP: Biomechanics of the lateral ligaments of the ankle: An evaluation of the effects of axial load and single plane motions on ligament strain patterns. Foot Ankle 12: 99, 1991 11. Chomiak J, Junge A, Peterson L, et al: Severe injuries in football players: Influencing factors. Am J Sports Med 28(suppl): S58–S68, 2000 12. Cordova ML, Ingersoll CD, LeBlanc MJ: Influence of ankle support on joint range of motion before and after exercise: A meta-analysis. J Orthop Sports Phys Ther 30: 170–177, 2000 13. Drawer S, Fuller CW: Evaluating the level of injury in English professional football using a risk based assessment process. Br J Sports Med 36: 446–451, 2002 14. Dvorak J, Junge A: Football injuries and physical symptoms: A review of the literature. Am J Sports Med 28(suppl): S3–S9, 2000 15. Ekblom B: Applied physiology of football. Sports Med 3: 50–60, 1986 16. Ekstrand J, Tropp H: The incidence of ankle sprains in football. Foot Ankle 11: 41–44, 1990 17. Ferkel RD, Scranton PE Jr: Arthroscopy of the ankle and foot: Current concepts review. J Bone Joint Surg [Br] 75A: 1233–1242, 1993 18. Garrick J: The frequency of injury, mechanism of injury, and epidemiology of ankle sprains. Am J Sports Med 5: 241–242, 1977 19. Gauffin H, Tropp H, Odenrick P: Effect of ankle disc training on postural control in patients with functional instability of the ankle joint. Int J Sports Med 9: 141–144, 1988 20. Hawkins RD, Fuller CW: A prospective epidemiological study of injuries in four English professional football clubs. Br J Sports Med 33: 196–203, 1999 21. Hawkins RD, Hulse MA, Wilkinson C, et al: The association football medical research programme: An audit of injuries in professional football. Br J Sports Med 35: 43–47, 2001 22. Hoy K, Lindblad BE, Terkelsen CJ, et al: European football injuries: A prospective epidemiologic and socioeconomic study. Am J Sports Med 20: 318–322, 1992 23. Inklaar H: Soccer injuries I: Incidence and severity. Sports Med 18: 55–73, 1994

Wetenschappelijke artikelen FLP de Toekomst

88

24. Inklaar H, Bol E, Schmikli SL, et al: Injuries in male football players: Team risk analysis. Int J Sports Med 17: 229–234, 1996

25. Karlsson J, Peterson L, Andreasson G, et al: The unstable ankle: A combined EMG and biomechanical modeling study. Int J Sport Biomech 8: 129–144, 1992 26. Keller CS, Noyes FR, Buncher CR: The medical aspects of football injury epidemiology. Am J Sports Med 15: 230–237, 1987 27. Konradsen L, Olesen S, Hansen HM: Ankle sensorimotor control and eversion strength after acute ankle inversion injuries. Am J Sports Med 26: 72–77, 1998 28. Konradsen L, Ravn JB: Prolonged peroneal reaction time in ankle instability. Int J Sports Med 12: 290–292, 1991 29. Larson M, Pearl A, Jaffet R, et al: Soccer, in Caine DJ, Caine CG, Lindner KJ (eds): Epidemiology of Sports Injuries. Champaign, IL, Human Kinetics, 1994, pp 387–398 30. Lewin G: The incidence of injury in an English professional football club during one competitive season. Physiotherapy 75: 601–605, 1989 31. Luthje P, Nurmi I, Kataja M, et al: Epidemiology and traumatology of injuries in elite football: A prospective study in Finland. Scand J Med Sci Sports 6: 180–185, 1996 32. Massada JL: Ankle overuse injuries in football players: Morphological adaptation of the talus in the anterior impingement. J Sports Med Phys Fitness 31: 447–451, 1991 33. McMaster WC, Walter M: Injuries in football. Am J Sports Med 6: 354–357, 1978 34. McMurray T: Footballer’s ankle. J Bone Joint Surg [Br] 32B: 68–69, 1950 35. Morris L: Report of cases of athlete’s ankle. J Bone Joint Surg [Br] 25: 220, 1943 36. Nielsen AB, Yde J: Epidemiology and traumatology of injuries in football. Am J Sports Med 17: 803–807, 1989 37. Orchard J: Orchard Sports Injury Classification System (OSICS). Sports Health 11: 39–41, 1993 38. Parkes JCH, Hamilton WG, Patterson AH: The anterior impingement syndrome of the ankle. J Trauma 20: 895–898, 1980 39. Peterson L, Renstrom P: Ankle, in Peterson L, Renstrom P (eds): Sports Injuries: Their Prevention and Treatment. Singapore, Martin Dunitz, 2001, pp 361–392 40. Sitler M, Ryan J, Wheeler B: The efficacy of a semirigid ankle stabilizer to reduce acute ankle injuries in basketball: A randomized clinical study at West Point. Am J Sports Med 22: 454–461, 1994 41. Steinbruck K: Epidemiology of sports injuries: A 25–year-analysis of sports orthopedic-traumatologic ambulatory care. Sportverletz Sportschaden 13: 38–52, 1999 42. Surve I, Schwellnus MP, Noakes T, Lombard C: A fivefold reduction in the incidence of recurrent ankle sprains in football players using the Sport-Stirrup orthosis. Am J Sports Med 22: 601–606, 1994 43. Thacker SB, Stroup DF, Branche CM, et al: The prevention of ankle sprains in sports: A systematic review of the literature. Am J Sports Med 27: 753–760, 1999 44. Tol JL, Slim E, van Dijk CN: The relationship of the kicking action in football and anterior ankle impingement syndrome. Am J Sports Med 30: 45–50, 2002 45. Tropp H, Askling C, Gillquist J: Prevention of ankle sprains. Am J Sports Med 13: 259–262, 1985 46. Tropp H, Odenrick P, Gillquist J: Stabilometry recordings in functional and mechanical instability of the ankle joint. Int J Sports Med 6: 180–182, 1985

Wetenschappelijke artikelen FLP de Toekomst

89

47. Tucker AM: Common football injuries: Diagnosis, treatment and rehabilitation. Sports Med 23: 21–32, 1997 48. van der Ent FWC: Lateral ankle ligament injury. Thesis, Rotterdam University, 1984 49. van Dijk CN, Tol JL, Verheyen CCPM: A prospective study of prognostic factors concerning the outcome of arthroscopic surgery of anterior ankle impingement. Am J Sports Med 25: 737–745, 1997 50. Verhagen EA, van Mechelen W, de Vente W: The effect of preventive measures on the incidence of ankle sprains. Clin J Sport Med 10: 291–296, 2000 51. Verhagen EA, van Mechelen W, van der Beck AJ: The effect of tape, braces and shoes on ankle range of motion. Sports Med 31: 667–677, 2001 52.Woods C, Hawkins RD, Hulse M, et al: The Football Association Medical Research Programme: An audit of injuries in professional football: An analysis of ankle sprains. Br J Sports Med 37: 233–238,

2003

Wetenschappelijke artikelen FLP de Toekomst

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 [email protected] 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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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

*Percentage totals may be subject to rounding errors associated with individual 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 Wetenschappelijke artikelen FLP de Toekomst

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).

Wetenschappelijke artikelen FLP de Toekomst

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

*Percentage totals may be subject to rounding errors associated with individual 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 Wetenschappelijke artikelen FLP de Toekomst

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,

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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.

REFERENCES 1. Robbins S, Waked E, Rappel R. Ankle taping improves proprioception before and after exercise in young men. Br J Sports Med 1995;29:242–7.[Abstract] 2. Barrett J, Bilisko T. The role of shoes in the prevention of ankle sprains. Sports Med 1995;20:277–80.[Medline] 3. Ogilvie-Harris DJ, Gilbart M. Treatment modalities for soft tissue injuries of the ankle: a critical review. Clin J Sport Med 1995;5:175–86.[Medline] 4. Karlsson J, Swärd L, Andréasson GO. The effect of taping on ankle stability. Sports Med 1993;16:210–15.[Medline] 5. Garrick JG. The frequency of injury, mechanism of injury, and epidemiology of ankle sprains. Am J Sports Med 1977;5:241–2.[Medline]

Wetenschappelijke artikelen FLP de Toekomst

102

6. Orteza LC, Vogelbach WD, Denegar CR. The effect of molded and unmolded orthotics on balance and pain while jogging following inversion ankle sprain. Journal of Athletic Training 1992;27:80–4. 7. Callaghan MJ. Role of ankle taping and bracing in the athlete. Br J Sports Med 1997;31:102–8.[Abstract] 8. Garrick JG, Requa RK. The epidemiology of foot and ankle injuries in sports. Clinics in Podiatric and Medical Surgery 1989;6:629–37. 9. Kuwada GT. Current concepts in the diagnosis and treatment of ankle sprains. Clinics in Podiatric Medicine and Surgery 1995;12:653–65.[Medline] 10. Pardon ET. Lower extremities are site of most common soccer injuries. Physician and Sports Medicine 1977;6:43–8. 11. Ekstrand J, Gillquist J. Soccer injuries and their mechanisms: a prospective study. Med Sci Sports Exerc 1983;15:367–70. 12. Lewin G. The incidence of injury in an English professional soccer club during one competitive season. Physiotherapy 1989;75:601–5. 13. Ekstrand J, Tropp H. The incidence of ankle sprains in soccer. Foot Ankle Int 1990;11:41–4. 14. Tropp H, Askling C, Gillquist J. Prevention of ankle sprains. Am J Sports Med 1985;13:259–62.[Abstract] 15. Putukian M, Knowles WK, Swere S, et al. Injuries in indoor soccer: The Lake Placid Dawn to Dark Soccer Tournament. Am J Sports Med 1996;24:317–22.[Abstract] 16. Hawkins RD, Hulse MA, Wilkinson C, et al. The association football medical research programme: an audit of injuries in professional football. Br J Sports Med 2000;34:0–4. 17. Sandelin J, Santavirta S, Kiviluoto O. Acute soccer injuries in Finland in 1980. Br J Sports Med 1985;19:30–3.[Abstract] 18. Arnason Á, Gudmundsson Á, Dahl HA, et al. Soccer injuries in Iceland. Scand J Med Sci Sports 1996;6:40–5.[Medline] 19. Nielsen AB, Yde, J. Epidemiology and traumatology of injuries in soccer. Am J Sports Med 1989;17:803–7.[Abstract] 20. Thacker SB, Stroup DF, Branche CM, et al. The prevention of ankle sprains in sports. A systematic review of the literature. Am J Sports Med 1999;27:753–60.[Abstract/Free Full Text]

Wetenschappelijke artikelen FLP de Toekomst

103

21. Lüthje P, Nurmi I, Kataja M, et al. Epidemiology and traumatology of injuries in elite soccer: a prospective study in Finland. Scand J Med Sci Sports 1996;6:180– 5.[Medline] 22. Sitler M, Ryan J, Wheeler B, et al. The efficacy of a semirigid ankle stabilizer to reduce acute ankle injuries in basketball. Am J Sports Med 1994;22:454–61.[Abstract] 23. Clanton TO, Porter DA. Primary care of foot and ankle injuries in the athlete. Clin Sports Med 1997;16:435–66.[Medline] 24. Robbins S, Waked E. Factors associated with ankle injuries. Sports Med 1998;25:63– 72.[Medline] 25. Liu SH, Jason WJ. Lateral ankle sprains and instability problems. Foot and Ankle Injuries 1994;13:793–809. 26. Waddington GS, Shepherd RB. Ankle injury in sports: role of motor control systems and implications for prevention and rehabilitation. Physical Therapy Review 1996;1:79–87. 27. Renström AFH, Konradsen L. Ankle ligament injuries. Br J Sports Med 1997;31:11– 20.[Medline] 28. Stiell IG, McKnight RD, Greenberg GH, et al. Implementation of the Ottawa ankle rules. JAMA 1994;271:827–32.[Abstract] 29. Surve I, Schwellnus MP, Noakes T, et al. A fivefold reduction in the incidence of recurrent ankle sprains in soccer players using the sport-stirrup orthosis. Am J Sports Med 1994;22:601–6.[Abstract] 30. Ekstrand J, Gillquist J. The frequency of muscle tightness and injuries in soccer players. Am J Sports Med 1982;10:75–8.[Abstract] 31. Safran MR, Zachazewski JE, Benedetti RS, et al. Lateral ankle sprains: a comprehensive review. Part 2: treatment and rehabilitation with an emphasis on the athlete. Med Sci Sports Exerc 1999;31:S438–47.[Medline] 32. Laskowski ER, Newcomer-Aney K, Smith J. Refining rehabilitation with proprioception training. Physician and Sports Medicine 1997;25:89–102. 33. Houglum PA. Soft tissue healing and its impact on rehabilitation. Journal of Sport Rehabilitation 1992;1:19–39. 34. Konradsen L, Olesen S, Hansen HM. Ankle sensorimotor control and eversion strength after acute ankle inversion injuries. Am J Sports Med 1998;26:72– 7.[Abstract/Free Full Text] 35. Tropp H, Odenrick P, Gillquist J. Stabilometry recordings in functional and mechanical instability of the ankle joint. Int J Sports Med 1985;6:180–2.[Medline]

Wetenschappelijke artikelen FLP de Toekomst

104

36. Gleeson NP, Reily T, Mercer T, et al. Influence of acute endurance activity on leg neuromuscular and musculoskeletal performance. Med Sci Sports Exerc 1998;30:596– 608.[Medline] 37. Árnason Á, Jóhannsson E, Gudmundsson Á, et al. Strains, sprains and contusions in Icelandic elite soccer players. Med Sci Sports Exerc 1994;26:s17. 38. Gauffin H, Tropp H, Odenrick P. Effect of ankle disk training on postural control in patients with functional instability of the ankle joint. Int J Sports Med 1988;9:141– 4.[Medline] 39. Ekstrand J, Gillquist J. The avoidability of soccer injuries. Int J Sports Med 1983;2:120–8. 40. Hume PA, Gerrard DF. Effectiveness of external ankle support. Sports Med 1998;25:285–312.[Medline] 41. Ekstrand J, Gillquist J, Liljedahl S. Prevention of soccer injuries. Am J Sports Med 1983;11:116–20.[Abstract] 42. Bayli I. Long-term planning of athlete development: the training to train phase. Faster Higher Stronger 1998;1:8–11.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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)?

Wetenschappelijke artikelen FLP de Toekomst

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).

Wetenschappelijke artikelen FLP de Toekomst

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).

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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).

Wetenschappelijke artikelen FLP de Toekomst

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).

Wetenschappelijke artikelen FLP de Toekomst

118

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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).

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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.

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. Garrick JG, Requa RK: The epidemiology of foot and ankle injuries in sports. Clin Sports Med 1988;7(1):29-36 3. Mack RP: Ankle injuries in athletics. Clin Sports Med 1982;1(1):71-84 4. Ekstrand J, Tropp H: The incidence of ankle sprains in soccer. Foot Ankle 1990;11(1):41-44 5. Garrick JG, Requa RK: Role of external support in the prevention of ankle sprains. Med Sci Sport 1973;5(3):200-203 6. Jackson DW, Ashley RL, Powell JW: Ankle sprains in young athletes: relation of severity and disability. Clin Orthop 1974; 101(1):201-215 7. Becker HP, Komischke A, Danz B, et al: Stress diagnostics of the sprained ankle: evaluation of the anterior drawer test with and without anesthesia. Foot Ankle 1993;14(8):459-464 8. Braun BL: Effects of ankle sprain in a general clinic population 6 to 18 months after medical evaluation. Arch Fam Med 1999; 8(2):143-148 9. Brostrom L: Sprained ankles VI: Surgical treatment of "chronic" ligament ruptures. Acta Chir Scand 1966;132(5):551-565

Wetenschappelijke artikelen FLP de Toekomst

124

10. Cawley PW, France EP: Biomechanics of the lateral ligaments of the ankle: an evaluation of the effects of axial load and single plane motion on ligament strain patterns. Foot Ankle 1991;12(2):92-99 11. Stephens MM, Sammarco GJ: The stabilizing role of the lateral ligament complex around the ankle and subtalar joints. Foot Ankle 1992;13(3):130-136 12. Sarrafian SK: Anatomy of the Foot and Ankle, ed 2. Philadelphia, Lippincott, 1993, pp 137149 13. Attarian DE, McCrackin HJ, Devito DP, et al: Biomechanical characteristics of human ankle ligaments. Foot Ankle 1985;6(2):54-58 14. Harper MC: The lateral ligamentous support of the subtalar joint. Foot Ankle 1991;11(6):354-358 15. Wuest TK: Injuries to the distal lower extremity syndesmosis. J Am Acad Orthop Surg 1997;5(3):172-181 16. Gerber JP, Williams GN, Scoville CR, et al: Persistent disability associated with ankle sprains: a prospective examination of an athletic population. Foot Ankle Int 1998;19(10):653-660 17. Nitz AJ, Dobner JJ, Kersey D: Nerve injury and grades II and III ankle sprains. Am J Sports Med 1985;13(3):177-182 18. 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 19. Earle AS, Moritz JR, Tapper EM: Dislocation of the peroneal tendons at the ankle: an analysis of 25 ski injuries. Northwest Med 1972;71(2):108-110 20. Sammarco GJ, Idusuyi O: Reconstruction of the lateral ankle ligaments using a split peroneus brevis tendon graft. Foot Ankle Int 1999;20(2):97-103 21. Rubin G, Witten M: The talar tilt angle and the fibular collateral ligaments: a method for the determination of talar tilt. J Bone Joint Surg 1960;42A:311-326 22. Seligson D, Gassman J, Pope M: Ankle instability: evaluation of the lateral ankle ligaments. Am J Sports Med 1980;8(1):39-42 23. Hintermann B: Biomechanics of the unstable ankle joint and clinical implications. Med Sci Sports Exerc 1999;31(7 Suppl):S459-S469 24. Chrisman OD, Snook GA: Reconstruction of lateral ligament tears of the ankle: an experimental study and clinical evaluation of seven patients treated by a new modification of the Elmslie procedure. J Bone Joint Surg Am 1969;51(5):904-912 25. Safran MR, Benedetti RS, Bartolozzi AR 3rd, et al: Lateral ankle sprains: a comprehensive review. Part 1: etilology, pathoanatomy, histopathogenesis, and diagnosis. Med Sci Sports Exerc 1999;31(7 Suppl):S429-S437 26. Anderson KJ and Lecocq JF: Operative treatment of injury to the fibular collateral ligaments of the ankle. J Bone Joint Surg 1954;36A:825-832 27. Clanton TO: Instability of the subtalar joint. Orthop Clin North Am 1989;20(4):583-592 28. Harper MC: Stress radiographs in the diagnosis of lateral instability of the ankle and hindfoot. Foot Ankle 1992;13(8):435-438 29. van Hellemondt FJ, Louwerens JWK, Sijbrandij ES, et al: Stress radiography and stress examination of the talocrural and subtalar joint on helical computed tomography. Foot Ankle Int 1997;18(8):482-488 30. Xenos JS, Hopkinson WJ, Mulligan ME, et al: The tibiofibular syndesmosis: Evaluation of the ligamentous structures, methods of fixation, and radiographic assessment. J Bone Joint Surg Am 1995;77(6):847-856 31. De Simoni C, Wetz HH, Zanetti M, et al: Clinical examination and magnetic resonance imaging in the assessment of ankle sprains treated with an orthosis. Foot Ankle Int 1996;17(3):177-182 32. Inman VT: Sprains of the ankle, in Chapman MW (ed):AAOS Instructional Course Lectures, 1975;24:294-308 33. Iverson LD, Clawson DK: Manual of acute orthopaedic therapeutics. Boston, Little, Brown, and Company, 1982, pp 231-236 34. Thorndike, A: Athletic Injuries: prevention, diagnosis, and treatment, ed 5. Philadelphia, Lea & Febiger, 1962 35. Akeson WH, Woo SLY, Amiel D, et al: The chemical basis for tissue repair, in Hunter LH and Funk FJ (eds): Rehabilitation of the Injured Knee, St. Louis, CV Mosby, 1984, pp 93-147 36. Chvapil, M: Physiology of Connective Tissue. London, Butterworths Ltd., 1967, pp 246-285 37. Noyes FR, Torvik PJ, Hyde WB, et al: Biomechanics of ligament failure: II. An analysis of immobilization, exercise, and reconditioning effects in primates. J Bone Joint Surg Am 1974;56A(7):1406-1418 38. Tipton CM, James SL, Mergner W, et al: Influence of exercise on strength of medial collateral ligaments in dogs. Am J Physiol 1970;218(3):894-902

Wetenschappelijke artikelen FLP de Toekomst

125

39. Tipton CM, Matthes RD, Maynard JA, et al: The influence of physical activity on ligaments and tendons. Med Sci Sports 1975;7(3):165-175 40. Vailas AC, Tipton CM, Mathes RD, et al: Physical activity and its influence on the repair process of medial collateral ligaments. Connect Tissue Res 1981; 9(1):25-31 41. Hettinga DL: Inflammatory response of synovial joint structures, in Gould JA 3rd, Davies GJ (eds): Orthopaedic and Sports Physical Therapy. St. Louis, Mosby, 1985, pp 87-117 42. Hocutt JE Jr, Jaffe R, Rylander CR, et al: Cryotherapy in ankle sprains. Am J Sports Med 1982;10(5):316-319 43. Hartsell HD, Spaulding SJ: Effectiveness of external orthotic support on passive soft tissue resistance of the chronically unstable ankle. Foot Ankle Int 1997;18(3):144-150 44. Klein J, Hoher J, Tiling T: Comparative study of therapies for fibular ligament rupture of the lateral ankle joint in competitive basketball players. Foot Ankle 1993;14(6):320-324 45. Regis D, Montanari M, Magnon B, et al: Dynamic orthopedic brace in the treatment of ankle sprains. Foot Ankle Int 1995;16(7):422-426 46. Safran MR, Zachazewski JE, Benedetti, RS et al: Lateral ankle sprains: a comprehensive review. Part 2: treatment and rehabilitation with an emphasis on the athlete. Med Sci Sports Exerc 1999;31(7 Suppl):S438-S447 47. Eggert A, Gruber J, Darda L: Zur Therapie von Aussenknoecheldbandverletzungen. Randomstudie zur postoperativen Therapie und fruehfunktionellen Behandlungssatktik. Unfallchirurg 1986;89(7):316-320 48. Jaskulka R, Fischer G, Schedl R: Injuries of the lateral ligaments of the ankle joint. Operative treatment and long-term results. Arch Orthop Trauma Surg 1988;107(4):217221 49. Krahl H: Kommentar zum Thema operative vs konservative Therapie der fibularen Bandruptur. Orthopaedie 1989; 18:341-344 50. Neumann K: Ist die konservativ funktionelle Behandlung frischer Aussenbandruptur am OSG gerechtfertigt? Teil 2. Hefte Unfallheilkunde 1987;189:1018-1019 51. Sommer HM, Arza D: Functional treatment of recent ruptures of the fibular ligament of the ankle. Int Orthop 1989;13(2):157-160 52. Weise K, Rupf G, Weinelt J: Die laterale Bandverletzung des OSG beim Sport. Aktuelle Traumatol 1988;18 Suppl 1:54-66 53. Zwipp H, Hoffmann R, Wippermann B, et al: Fibulare Bandruptur am oberen Sprunggelenk. Orthopade 1989;18(4):336-341 54. Balduini FC, Tetzlaff J: Historical perspectives on injuries of the ligaments of the ankle. Clin Sports Med 1982;1(1):3-12 55. Kannus P, Renstrom P: Treatment for acute tears of the lateral ligaments of the ankle: operation, cast, or early controlled mobilization. J Bone Joint Surg Am 1991;73(2):305-312 56. Povacz P, Unger SF, Miller WK, et al: A randomnized, prospective study of operative and non-operative treatment of injuries of the fibular collateral ligaments of the ankle. J Bone Joint Surg Am 1998;80(3):345-351 57. Sammarco GJ, Idusuyi O: Reconstruction of the lateral ankle ligaments using a split peroneus brevis tendon graft. Foot Ankle Int 1999;20(2):97-103 58. Taylor DC, Englehardt DL, Basset FH 3rd: Syndesmosis sprains of the ankle: The influence of heterotopic ossification. Am J Sports Med 1992;20(2):146-150 59. Wolin I, Glassman F, Sideman S et al: Internal derangement of the talofibular component of the ankle. Surg Gynechol 1950; 91:193-200 60. Bassett FH 3d, Gates HS 3d, Billys JB, et al: Talar impingement by the anteroinferior tibiofibular ligament: a cause of chronic pain in the ankle after inversion sprain. J Bone Joint Surg Am 1990;72(1):55-59 61. Trono M, Tueche S, Quintart C, et al: Peroneus quartus muscle: a case report and review of the literature. Foot Ankle Int 1999;20(10):659-662 62. Freeman MA, Dean MR, Hanham IW: The etiology and prevention of functional instability of the foot. J Bone Joint Surg Br 1965;47(4):678-685 63. Gauffin H, Tropp H, Odenrick P: Effect of ankle disk training on postural control in patients with functional instability of the ankle. Int J Sports Med 1988;9(2):141-144 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.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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,

Wetenschappelijke artikelen FLP de Toekomst

130

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;

Wetenschappelijke artikelen FLP de Toekomst

131

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

Wetenschappelijke artikelen FLP de Toekomst

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.

References 1. Messner K, Gao J: The menisci of the knee joint: anatomical and functional characteristics, and a rationale for clinical treatment. J Anat 1998;193(pt 2):161-178 2. Fairbank TJ: Knee joint changes after meniscectomy. J Bone Joint Surg Br 1948;30(4):664670 3. Fithian DC, Kelly MA, Mow VC: Material properties and structure-function relationships in the menisci. Clin Orthop 1990; 252(Mar):19-31 4. McConville OR, Kipnis JM, Richmond JC, et al: The effect of meniscal status on knee stability and function after anterior cruciate ligament reconstruction. Arthroscopy 1993;9(4):431-439 5. Maffulli N, Binfield PM, King JB, et al: Acute haemarthrosis of the knee in athletes: a prospective study of 106 cases. J Bone Joint Surg (Br) 1993;75(6):945-949 6. Corea JR, Moussa M, al Othman A: McMurray's test tested. Knee Surg Sports Traumatol Arthrosc 1994;2(2):70-72

Wetenschappelijke artikelen FLP de Toekomst

133

7. Stratford PW, Binkley J: A review of the McMurray test. J Orthop Sports Phys Ther 1995;22(3):116-120 8. Fischer SP, Fox JM, Del Pizzo W, et al: Accuracy of diagnoses from magnetic resonance imaging of the knee: a multicenter analysis of one thousand and fourteen patients. J Bone Joint Surg (Am) 1991;73(1):2-10 9. Boden SD, Davis DO, Dina TS, et al: A prospective and blinded investigation of magnetic resonance imaging of the knee: abnormal findings in asymptomatic patients. Clin Orthop 1992;282(Sep):177-185 10. Noble J, Erat K: In defence of the meniscus: a prospective study of 200 meniscectomy patients. J Bone Joint Surg (Br) 1980;62(1):7-11 11. Hede A, Hempel-Poulsen S, Jensen JS: Symptoms and level of sports activity in patients awaiting arthroscopy for meniscal lesions of the knee. J Bone Joint Surg (Am) 1990;72(4):550-552 12. Weiss CB, Lundberg M, Hamberg P, et al: Nonoperative treatment of meniscal tears. J Bone Joint Surg (Am) 1989;71(6):811-822 13. DeHaven KE, Lohrer WA, Lovelock JE: Long-term results of open meniscal repair. Am J Sports Med 1995;23(5):524-530 14. Martens MA, Backaert M, Heyman E, et al: Partial arthroscopic meniscectomy versus total open meniscectomy. Arch Orthop Trauma Surg 1986;105(1):31-35 15. Pettrone FA: Meniscectomy: arthrotomy versus arthroscopy. Am J Sports Med 1982;10(6):355-359 16. Schimmer RC, Brülhart KB, Duff C, et al: Arthroscopic partial meniscectomy: a 12-year follow-up and two-step evaluation of the long-term course. Arthroscopy 1998;14(2):136142 17. Whipple TL, Caspari RB, Meyers JF: Arthroscopic meniscectomy: an interim report at three to four years after operation. Clin Orthop 1984;183(Mar):105-114 18. Bolano LE, Grana WA: Isolated arthroscopic partial meniscectomy: functional radiographic evaluation at five years. Am J Sports Med 1993;21(3):432-437 19. Burks RT, Metcalf MH, Metcalf RW: Fifteen-year follow-up of arthroscopic partial meniscectomy. Arthroscopy 1997;13(6):673-679 20. Durand A, Richards CL, Malouin F: Strength recovery and muscle activation of the knee extensor and flexor muscles after arthroscopic meniscectomy: a pilot study. Clin Orthop 1991;262(Jan):210-226 21. Durand A, Richards CL, Malouin F, et al: Motor recovery after arthroscopic partial meniscectomy: analyses of gait and the ascent and descent of stairs. J Bone Joint Surg (Am) 1993;75(2):202-214 22. Hede A, Larsen E, Sandberg H: The long term outcome of open total and partial meniscectomy related to the quantity and site of the meniscus removed. Int Orthop 1992;16(2):122-125 23. Lotke PA, Lefkoe RT, Ecker ML: Late results following medial meniscectomy in an older population. J Bone Joint Surg (Am) 1981;63(1):115-119 24. Katz JN, Harris TM, Larson MG, et al: Predictors of functional outcomes after arthroscopic partial meniscectomy. J Rheumatol 1992;19(12):1938-1942 25. Matsusue Y, Thomson NL: Arthroscopic partial medial meniscectomy in patients over 40 years old: a 5- to 11-year follow-up study. Arthroscopy 1996;12(1):39-44 26. DeHaven KE: Decision-making factors in the treatment of meniscus lesions. Clin Orthop 1990;252(Mar):49-54 27. Warren RF: Meniscectomy and repair in the anterior cruciate ligament-deficient patient. Clin Orthop 1990;252(Mar):55-63 28. Morgan CD, Wojtys EM, Casscells CD, et al: Arthroscopic meniscal repair evaluated by second-look arthroscopy. Am J Sports Med 1991;19(6):632-638 29. Muellner T, Egkher A, Nikolic A, et al: Open meniscal repair: clinical and magnetic resonance imaging findings after twelve years. Am J Sports Med 1999;27(1):16-20 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 1998;26(1):87-95 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 1992;20(2):176-181

Wetenschappelijke artikelen FLP de Toekomst

134

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

Wetenschappelijke artikelen FLP de Toekomst

135

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--

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

137

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

Wetenschappelijke artikelen FLP de Toekomst

138

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

141

Posterior Knee Pain and Its Causes A Clinician's Guide to Expediting Diagnosis THE PHYSICIAN AND SPORTSMEDICINE - VOL 32 - NO. 3 - MARCH 2004

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

150

Valgus Knee Instability in an Adolescent Ligament Sprain or Physeal Fracture? Kenneth R. Veenema, MD THE PHYSICIAN AND SPORTSMEDICINE - VOL 27 - NO. 8 - AUGUST 99

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

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

155

Hamstring Strains: Expediting Return to Play Thomas M. Best, MD, PhD; William E. Garrett Jr, MD, PhD THE PHYSICIAN AND SPORTSMEDICINE - VOL 24 - NO. 8 - AUGUST 96

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,

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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        

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 [email protected].

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

165

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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-

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

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

Wetenschappelijke artikelen FLP de Toekomst

172

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.

Wetenschappelijke artikelen FLP de Toekomst

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 [email protected].

Wetenschappelijke artikelen FLP de Toekomst

174

Giving Injuries the Cold Treatment Bryant Stamford, PhD THE PHYSICIAN AND SPORTSMEDICINE - VOL 24 - NO. 3 - MARCH 96

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

Wetenschappelijke artikelen FLP de Toekomst

175

  

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   

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

Wetenschappelijke artikelen FLP de Toekomst

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.

Wetenschappelijke artikelen FLP de Toekomst

177