Partial and complete ruptures of the Achilles tendonand local corticosteroid injectionsF. Mahler MD, Dip Sports Med and D. Fritschy MD
IntroductionHench and co-workers first reported the spectaculareffects of a hormone of the adrenal cortex (17-OHdehydrocorticosterone on the rheumatoid joint'. Thiswon them the Nobel prize for medicine in 1950.
Unfortunately, the side effects of intramuscularinjections of cortisone were important and it was notuntil 1951 that Hollander et al. elucidated howsteroids could be used locally with reduction ofsystemic side effects2. They showed that hydrocorti-sone injected locally was much more effective thancortisone in suppressing synovial inflammation,confirming Mason's hypothesis that hydrocortisonerather than cortisone was the principal corticoid withanti-inflammatory activity at tissue level3.
This was the beginning of a new era in thetreatment of a wide variety of inflammatory patholo-gies. After an initial period of euphoria due to thespectacular effects of hydrocortisone on most inflam-matory conditions came the evidence that steroidsinjected locally also had adverse effects.Chandler and Wright reported ten cases of rapidly
progressive degenerative arthritis following intra-articular hydrocortisone injections4. Later, Mankinand Conger showed diminished synthesis of articularcartilage in the knees of rabbits treated withintra-articular steroids5. These initial reports werefollowed by many others condemning steroids,holding them responsible for conditions such assecondary osteoporosis, aseptic necrosis and tendonruptures. Since these initial reports, there has beenconflicting evidence as to the role of corticosteroids inthese pathologies, especially in tendon ruptures.At present there is still controversy as to whether
or not corticosteroids should be held responsiblewhen a tendon rupture occurs following local steroidtreatment. One of the commonest sites for tendonrupture is the Achilles tendon. The Achilles tendon(TA) has not been spared the increase in overuse
Address for correspondence: Dr Finn Mahler, 12 Chemin PontCeard, 1290 Versoix, SwitzerlandThis review is based on the author's dissertation for the diplomacourse in sports medicine of the London Hospital Medical Collegeand is reproduced by permission of J. B. King FRCS, coursedirector.
injuries in recent years and is often the site of acuteand chronic inflammation. This has led to the use oflocal corticosteroid injections into the tendon or to thesurrounding paratenon.Lee was the first to report a case of TA rupture
following local corticosteroid injection6.The aim of this dissertation is to analyse critically
the experimental and clinical knowledge availableconcerning corticosteroids and TA ruptures. The firstsection will relate to the fundamental researchconcerning the effect of corticosteroids on tendons.The second part will be a literature review relevant tothe role of local corticosteroid injections in thepathogenesis of TA ruptures.
Animal and human research related tocorticosteroids and tendon rupturesIntratendinous injectionsFerland's study on adult albino rabbit Achillestendons clearly demonstrates the consequences of aninjection of corticosteroid directly into the TA7. Thecomparison of two groups, one receiving an intraten-dinous injection of corticosteroid, the other aperitendinous injection, showed that 100% of thegroup with the intratendinous injection had localizedtendon necrosis at the site of the injection. On theother hand, the peritendinous injection groupshowed an intact structure in 95% of cases.To eliminate the hypothesis that the necrosis could
have been secondary to an increased intratendinouspressure, a third group was injected intratendinouslywith an identical volume of physiological serum(0.3ml). No necrosis occurred in this group, leavingthe corticosteroid solely responsible for the tendonnecrosis in the group receiving the intratendinousinjection.A similar study by Balasubramaniam, also on the
TA of rabbits and comparing an intratendinousinjection of hydrocortisone with an identical volumeof saline solution, showed no deleterious effect withthe saline injection and invariably a collagen necrosiswith the hydrocortisone8. Necrosis was seen as soonas 45 min after injection and after 8 weeks the healingprocess was still incomplete. Also, the tendonshaving received the injection into their central parthad poorer scar tissue at 8 weeks compared withthose where the corticosteroid had been peripherally
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Corticosteroids and Achilles tendon ruptures: F. Mahler
injected. This could be due to a comparatively poorerblood supply to the centre of the tendon.
Unverferth compared the TA tensile strength oftwo groups of rabbits9. One was injected withcorticosteroid and the other with saline solution. Theresults showed a significant decrease in tensilestrength in the group injected with corticosteroids.Microscopic analysis showed disruption of thecollagen bundles with deposits of a pale materialpresumed to be steroids. Unfortunately no histo-chemical analysis was done, leaving doubt as to thenature of the deposits. The routine staining withhaematoxylin and eosin took on an orange, granularappearance, compatible with tendon necrosis. Thetendons injected with a saline solution showedinsignificant alterations.Kennedy and Baxter Willis studied the effect of a
single injection of P-methasone into the TA of rabbitsand showed a decrease in tensile strength of 35%after 48 h and at 7 days'0. After 2 weeks, no differencewas found with controls. In their conclusion, theyproposed a period of at least 2 weeks' abstinencefrom vigorous exercise after a local injection ofcorticosteroids.
Phelps, in his study on the tensile strength of thepatellar tendon of rabbits after multiple injections ofmethylprednisolone, found no alterations in themechanical properties of the tendons injected withcorticosteroids". He concluded that tendon rupturein athletes could stem from some underlying patho-logical process and not to a destructive processinitiated by the steroid injection.One of the main problems with animal research is
its extrapolation to man. Noyes et al. were able to getcloser to the human situation with their study on theanterior cruciate ligament of 110 Rhesus monkeys'2.They compared tensile strength and histologicalmodifications at 6, 15 and 52 weeks between twogroups. One group received a direct intraligamentalinjection of methylprednisolone, the other an intra-articular injection of the same product. The resultsshowed that a single intraligament injection substan-tially decreased the tensile strength (between 27 and39%) up to 52 weeks after the injection. Histologicalexamination showed death and absence of fibrocytes.In the group which received an intra-articularinjection, there were no significant changes in tensilestrength or histology.
Peritendinous injectionsLocal corticosteroid injections around the tendon aremore controversial. Authors such as Goldie deny thatcorticosteroids should be held responsible for tendonruptures following local injections'3. Initial researchwas designed to find out if steroids could reduceadhesions after tendon surgery.Carstam showed that the tensile strength of dog
Achilles tendon was not altered by the presence ofcorticosteroids14. Gonzalez investigated the localeffect of hydrocortisone on tendons repaired withinthe flexor tunnels"5. He showed that the functionalresults and the tensile strength of the tendons bathedin hydrocortisone were no better than those repairedwithout the drug.
In a more recent study, Vogel showed a surprisingincrease in the tensile strength of tendons aftercorticosteroid administration16. However, the repeti-tion of injections progressively weakened the ten-dons, suggesting a relationship between cumulativedose and effect.The only study showing a decrease in the tensile
strength of tendons after corticotherapy is the workby Wrenn and co-workers17. They showed that thedaily administration to dogs of 10mgkg-1 body-weight of cortisone inhibited excessive formation ofperitendinous fibrous tissue. On the other hand, thebreaking point of the sutured tendons treated withcortisone was consistently lower than in the controlgroup (40%). It should be noted that the doses ofcortisone used far exceed the relative doses currentlyused in humans. Furthermore, the relevance of theseintramuscular injections remains uncertain.
In the light of these studies tending to show theabsence of any deleterious effect of peritendinousinjections, how can one explain the reigning con-troversy as to whether or not peritendinous injectionsenfeeble the tendon.
Different explanations are possible. First, there isthe extrapolation of animal research to humans.Second, all the studies were carried out on tendonswithout any underlying pathology which is not thecase when corticosteroids are used in humans. Thedefenders of corticosteroids can always claim that theunderlying pathological processes of the tendon forwhich the corticosteroid was used is responsible forrupture. Others remain persuaded that cortico-steroids have a direct enfeebling effect on the tendon.A third view claims that corticosteroids, by
reducing inflammation and thereby pain, permit theathlete to resume vigorous exercise, hence exposingthe already fragile tendon to rupture.
In the light of these studies, it does not seemreasonable to condemn peritendinous injections byinvoking a direct deleterious effect on the tendonitself.
Partial and complete ruptures of theAchilles tendonThe first precise description of Achilles tendonpathology came from Ambroise Pare in 1575. Hedescribed the serious nature of an injury to thistendon, which invariably had an unfavourableoutcome. It was not until the end of the 19th centurythat surgery was performed to ruptured TAs. In 1882,Maydl described for the first time a rupture in asporting situation (mountaineering). Later, Albrecht(1924), Pirker (1934) and others reported the lesion inathletes, dancers and tennis players. In 1941,Silverskjold reported seven cases of people withacute ruptures of the TA, all of whom wereparticipating in a sporting activity'8.
IncidenceThe incidence of TA ruptures is often quoted as rare.In 1969 Goldman et al. retraced 33 cases of presumedor proven complete ruptures in a period of 20 years atthe Mayo Clinic'9.
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In 1954, Christensen found only 57 cases of TAruptures in the 70000 patients treated in theorthopaedic department of Aarhus Hospital inDenmark20. More recently, Barfred suggested thatthere was a substantial increase in the incidence ofthis lesion2l. Nillius confirmed this hypothesis byperforming a retrospective study on the incidence ofTA ruptures in the population of Malmo between1950 and 197322. He showed that the increase in theincidence of ruptures was significantly greater thanthe increase of the population itself.However, in the same period, there happened to
be a remarkable increase in the number of peopleparticipating in sports, which was characterized byan increase in the enrolment of members in varioussporting associations. In so far as enrolment reflectsparticipation in sporting activities, the increase in theincidence of ruptured TAs was proportional to theincreased participation in the sports most commonlycausing the injury. As to the incidence of ruptures innon-sporting situations, it had also proportionallyincreased over time. The author had no satisfactoryexplanation.Arner and Lindholm found that the incidence of
TA ruptures had doubled in their practice since theyhad actively sought them'8. This might explain tosome extent Barfred's epidemiological finding of anincrease in the incidence of TA ruptures.Concerning the possible influence of local injec-
tions of corticosteroids on the incidence of ruptures,there is to date no longitudinal study.
Diagnosis and pathogenesisAcute rupture of the TA is typically seen in amesomorphic, middle-aged man, participating in anintermittent sporting activity3. In Arner and Lind-holm's study of 92 cases (79 men and 13 women), theaverage age was 38.5 years and the male to femaleratio was 6:118. Male predominance was 10:1 in Leaand Smith's study24.There is a preceding history of achillodynia before
many TA ruptures. This could be a sign of anunderlying pathological process. In Ljungqvist'sseries of 24 cases of partial ruptures, 16 had a historyof achillodynia25. To understand the causes ofachillodynia better, it is important to get an insightinto all the different categories of TA pathology.There exist many classifications of injury-related TApathology. Williams' is probably the most completethat is presently available26. It recognizes four tendonpathologies with distinct clinical findings: completerupture; partial rupture; focal degeneration; andtendinitis. A separate category is made for paratenonlesions; peritendinitis (acute or chronic). The lastcategory constitutes mixed lesions.Not included in Williams' classification but often
used by authors, including Williams himself, is theterm 'tendinosis'. This term was introduced byPuddu to describe the situation of a grossly degenera-tive tendon in the absence of alterations to theparatenon .
Williams has tried to differentiate tendinitis from'tendinosis' by pointing out that the essential elementof tendinitis is the characteristic reversibility of the
Corticosteroids and Achilles tendon ruptures: F. Mahler
26Onhcprocess . On the contrary, 'tendinosis' is a degenera-tive condition and therefore should be considered asa typically irreversible process. One might suggestthat 'tendinosis' is a form of advanced focal degenera-tion. Going even further, one could imagine that anacute inflammatory process evolves progressivelyinto a chronic degenerative process if the repairmechanisms of the tendon are inadequate, or if thephysiopathological cause responsible for the initialinflammation is not stopped.To support this hypothesis, it is interesting to note
that, in Puddu's study, all the ruptures showedmacroscopic and microscopic degenerative lesions27.Their conclusion was that subcutaneous ruptures ofthe TA were secondary to the underlying degenera-tive process, in both symptomatic and asymptomaticpatients. To support this 'degenerative theory', onecan mention Williams' work on patients operated forachillodynia having resisted all conservative treat-ment28. Invariably, there was macroscopic evidenceof repeated attempts to form normal scar tissue whichhad been hindered by recurrent trauma or byinsufficient blood supply for the completion of thehealing process.Fox showed that out of 22 patients presenting TA
pathology, ten went on to have complete ruptures29.Histology showed diffuse degenerative signs in nineout of ten. It is interesting to note that none of theseten patients had received local steroid injections.
Williams showed that in 12 cases of post mortemmaterial of patients without any history of achillo-dynia, no modifications of the tendon could befound, suggesting that degenerative changes werenot part of a normal ageing process26. Ippolito et al.did not come to the same conclusion in their postmortem studies3o. They did find degenerative changesin some cases, but some of their patients hadsystemic inflammatory diseases which could havecaused the tendon lesions.Taking into consideration these different studies, is
it possible to say that all tendons that rupture have anunderlying degenerative process? The answer is no.Jacobs showed that only slightly more than 50% ofTA ruptures had degenerative modifications; the restwere normal3l. So there is little doubt that an acuterupture can happen in a tendon without anyunderlying disease. It is for this reason that Barfredproposed a purely mechanical theory to explain thepathogenesis of TA ruptures21.
Certain authors suggested that, in ageing athletes,there could be a series of microruptures in thecollagen fibres following repetitive stresses beyondthe elastic threshold of the tendon29 32. This wouldlead to repair processes but at an insufficient ratecompared with the repetitive microtraumas to thetendon. Burry suggested a disparity between themetabolic demands of the tendon and the existingblood supply, leading to an ischaemic degenera-tion33.Lagergren and Lindholm, in their study on the
vascular distribution in the TA, showed that thesegment of the tendon with the poorest vasculariza-tion was situated 4-5cm proximal to the calcanealinsertion and suggested that this contributed to itssusceptibility to rupturem.
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Corticosteroids and Achilles tendon ruptures: F. Mahler
The mechanical theory was brought forward byBarfred to challenge the degeneration theory2l. Theview that the healthy tendon never ruptures hadbeen supported by histology and by rupture experi-ments on animals. Barfred's study on the rat TAshowed that an external force (maximal electricalstimulation of the sciatic nerve) could rupture thetendon.
His experiments raised interesting observations:rupture incidence was highest after inactivity; rup-ture risk was increased when oblique force wasapplied; fatigued muscle predisposes the tendon torupture. Barfred concluded that experimental ruptureof healthy tendon was possible in rats and that it wasthe consequence of many non-pathological factorsthat did not necessarily all have to be present at thesame time.Amer and Lindholm distinguished between three
indirect mechanisms capable of provoking TA rup-ture in man18:1. Propulsive movement of the weight-bearing fore-
foot during a simultaneous extension of the kneejoint, e.g. sprinting.
2. Unexpected dorsiflexion of the ankle joint, e.g.missing a step.
3. Violent dorsiflexion of a plantar flexed foot, e.g.falling from a height on to the plantar flexed foot.
The pathogenesis of TA rupture is probablymultifactorial. The classical story suggests thatrupture is the sole consequence of a violent, unusual,purely mechanical indirect force. The less classicalstory suggests a multifactorial aetiology - degenera-tive, ischaemic and biomechanical.Mechanical and degenerative factors may coexist.
One could imagine a continuum between the two; onone side a purely mechanical rupture and on theother a low energy rupture in a grossly degenerativetendon. In between, a wide variety of situationswhere the mechanical energy necessary to producethe rupture corresponds to the level of degenerationof the tendon.
Role of corticosteroids in TA rupturesLee first reported TA rupture in a runner injectedwith corticosteroids on three previous occasions35.He suggested that the corticosteroids could haveinfluenced the final stage of the rupture. In hiscommentary, he did not exclude the possibility thatthe corticosteroids could have been injected betweenthe superficial and deeper layers of the tendon andabsorbed slowly due to the relatively avascular natureof the tissue. He also suggested that the disruptioncould have been going on for some time, and thatsimultaneous repair may have been hindered by thehydrocortisone. He also noted that there was noexperimental evidence of a deleterious effect ofhydrocortisone on tendon healing.
Controversy still exists 30 years later. The majorityof Lee's questions are still unanswered. Despite thisuncertainty, most orthopaedic, rheumatology andsports medicine text books condemn local corticoster-oid injections around the tendon, holding them
responsible for secondary tendon ruptures. As proofof their deleterious effect, studies such as those of Leeare quoted. This is highly questionable consideringLee's own uncertainty. Even more astonishing arecertain publications dealing specifically with thematter. For example, Rappaport and Gerster, on localsteroid injections in rheumatology, stipulate thattendon ruptures follow abrupt movements in sportspeople and most commonly involve the Achilles orbicipital tendon36. It is also said that they arefavoured by local corticosteroid injections. This issupported by the work of d'Anglejan37. In this article,the author discusses the deterioration and rupturescaused by corticotherapy, stating that 'these acci-dents seem to be favoured by local or generalcortisone treatment, particularly amongst sportsmen,for whom many cases have been reported in theliterature. This is based on five references.The first reference concerns a 48-year-old patient
suffering from rheumatoid arthritis38. Following twolocal injections of corticosteroids for achillodynia, sheis victim of an acute TA rupture. No allusion to anysporting activity is to be found in this article. It issuggested by the author that the two injections wereprobably intratendinous, thereby slowing down thematuration of the fibrous tissue and maybe decreas-ing the tensile strength. The fact that the patient wassuffering from rheumatoid arthritis makes it impossi-ble to evaluate the responsibility of the corticosteroidswhen one takes into consideration that spontaneousrupture of tendons is an integral part of the featuresof rheumatoid arthritis.The second reference concerns a 73-year-old
patient with a rapidly destructive arthritis afterintra-articular injections of hydrocortisone39. There isno allusion to any tendon in this article.The third reference concerns a 52-year-old patient
with a 14-year history of chronic lupus erythemato-sus40. Six months after the initiation of oral triamcino-lone the patient developed a bilateral TA rupture.There is no mention of any sporting activity. As to therole of the corticosteroids, again it seems impossibleto dissociate it from the underlying inflammatoryprocess.The fourth reference relates to an experimental
study on the rabbit TA7. The last reference describesthe cases of an 84-year-old man and a 69-year-oldlady, both of whom developed TA ruptures after localcorticosteroid injections41. There is no allusion to anysporting activity.There is no objective evidence in any of these
references to suggest that TA ruptures are caused bycorticosteroids. Furthermore, no mention of anysporting activity is to be found in the references.Unfortunately, this is but one of the many examplesof affirmations concerning local corticosteroid injec-tions without supporting evidence. Very little litera-ture dealing specifically with the subject exists, andmost is anecdotal.To the author's knowledge, 19 articles exist which
specifically relate to this subject. Eight ofthese35'38'4045 relate to TA ruptures in patients takingoral corticosteroids. All except one were taking thesteroids because of a systemic inflammatory disease,making it impossible to differentiate the role of the
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underlying disease processes in the aetiology of therupture from that of the possible influence of thecorticosteroids.
In Lee's case report of a bilateral TA rupture in a61-year-old man taking prednisone for 4 years, it isinteresting to note the commentary of Mayer35. Hedescribes the case of a perfectly fit 46-year-old womanwho suffered a similar injury though she had nevertaken steroids.There is no doubt that spontaneous, indirect,
bilateral ruptures of the TA do exist in patients nottaking corticosteroids. The only case of a TA ruptureamong these eight articles, where there is no systemicunderlying inflammatory disease process, is that of a68-year-old man on methylprednisolone because ofchronic bronchitis. This is yet another anecdotal case,of little help in the analysis of the role of corticoster-oids in TA ruptures.
If corticosteroids really had such an obviousdeleterious effect on tendons, one would expect anepidemic of tendon ruptures, when one takes intoconsideration the many patients taking cortico-steroids.Among the articles concerned specifically with
local injections, four, including Lee's study, relate toanecdotal cases of ruptures following one or multiplelocal injections35. Chechick et al. reported the case ofa professional football player with Achilles peritendi-nitis, injected on three occasions with predniso-lone4'. Ten days after the last injection the patientwas back playing. He suffered TA rupture in a game.No mention is made of whether the injections wereintratendinous or peritendinous.Kleinmann and Gross reported the cases of three
TA ruptures in middle-aged people with chronicAchilles tendinitis, all treated with local corticosteroidinjections47. In two of the cases, it is specified that theinjections were given directly into the tendon.
In their discussion the authors firmly believe thecorticosteroids to have played a causative role,because the tendon ruptured within 2-6 weeks ofsteroid injection and after relatively minor trauma.Furthermore, in their experience rupture of the TA isusually a sudden traumatic event with the patienthaving no preceding history of chronic pain.Concerning this last point, there is evidence
asserting the contrary. Fox studied 19 cases of TAruptures surgically repaired29. About 50% of thecases had a history of achillodynia before the rupture.None of the patients had received local corticosteroidinjections.Halpern also reported a 34-year-old man with a TA
rupture who had had a 4-year history of achillodyniatreated on five occasions with intratendinous cortico-steroid injections48.
Little can be learnt as to the role of local injectionsof corticosteroids in TA rupture through theseanecdotal reports. The only comment one can make isthat the majority of the local injections are describedas being intratendinous. This has clearly been shownabove to have a directly deleterious effect on thetendon and should be unanimously condemned.Unfortunately, no relevant information as to the roleof peritendinous injections can be collected fromthese studies.
In his study on central degeneration of the TA, Burryrefers to the possible role of local injections ofcorticosteroids33. He suggests that an injection in theperitendinous region could provoke an increase ofpressure sufficient to interrupt blood flow and causeinfarction. This has been shown not to be the case inanimal studies. Ferland's comparative study on therabbit TA failed to show any localized tendon necrosisdue to an increase in tissue pressure7. Balasubrama-niam agreed and showed that the corticosteroids weredirectly responsible for tendon necrosis8.Skoech evaluated 16 partial TA ruptures, nine of
which were explored and repaired49. Seven of these16 tendons had previously received between one andfive injections of corticosteroids. During surgery, twoof the tendons showed signs of acute rupture, threeshowed granulated tissue or maturing scar tissuewithin the area of the defect, and the remaining fourtendons showed areas of pearly nodular degenera-tion within the area of defect, some containing areasof calcification.
Unfortunately the proportion of the nine surgicallyexplored tendons previously injected is not stated.This makes it impossible to analyse the role of thecorticosteroids in the pathogenesis of these tendonruptures.Denstad and Roaas analysed 58 cases of partial TA
ruptures that had undergone surgery50. In all, 32cases (55%) had had local corticosteroid injectionsbefore the rupture.
Shields et al. evaluated the isokinetic force of themusculotendinous unit in 32 cases having undergonesurgery for complete TA rupture51. Ten had receivedprevious steroid injections, of whom eight (80%) hadreceived their local injection after the episode ofcomplete rupture, which had not been diagnosed. Inthis series, 18 of the 32 patients did not have thediagnosis established until late.Apart from showing that the repaired TAs had on
average a 16.5% loss of plantarflexion strength and a17.5% loss of plantarflexion power,- the authors'results demonstrated that the strength and powerratings of the injured leg were not influenced bycortisone injections. Only two patients out of 32 hadreceived corticosteroid injections before the rupture.The experimental part of Unverferth's study on the
effect of local steroid injections showed that intraten-dinous steroid injection decreases tensile strength9.The clinical part of this study reports the cases ofthree elite athletes with acute TA rupture followingsteroid injections. The delays between the lastinjection and the rupture were respectively 2, 4 and36 weeks. In two of the cases, it is clearly specifiedthat the injections were both intratendinous andperitendinous. No details are given concerning thethird case. In his discussion, the author adheres tothe hypothesis that local corticosteroid injectionsmask the symptoms, hence permitting the athlete toreturn to active competition prematurely.The author also suggests that local steroid injec-
tions diminish tensile strength, especially when theinjection enters the tendon itself. This statementpresupposes that peritendinous injections also de-crease tensile strength. In his conclusion it isproposed that all steroid injections are to be
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abandoned, not only because they give the patient afalse sense of security, but also because local injectionof steroid in and about the tendon decreases itstensile strength and predisposes it to completerupture. The numerous studies previously enumer-ated fully support the author's point of view onintratendinous injections. However, there are noarguments in the study permitting the conclusion, ashe suggests, that peritendinous injections alsodecrease tensile strength.The last study with a specific insight into local
corticosteroid injections is that of Ljungqvist25. In thechapter on the aetiology of partial rupture, steroidinjections are discussed. The material for the studycomprises 24 cases of partial ruptures of which sixhad been given intratendinous and peritendinouscorticosteroid injections before the rupture occurred.Four cases had injections before and after; eight caseshad been injected solely after the rupture; six patientswere never given injections. Accordingly, 14 patientshad not received any corticosteroid injection beforethe rupture. Among the ten patients injected beforethe rupture, two had a 1-year interval between theinjection and the rupture, making it hard for theauthor to believe that the injection in these casescould have had any particular significance.
Six other patients out of the ten had been given theinjections 2-4 months before the rupture. In four ofthese six, the local symptoms causing injection wereat a different site from that of the rupture. The lasttwo cases had been given their injections 5 and 6weeks before the rupture and were symptom-freeuntil they sustained the rupture.
Histology was performed on all surgical cases. Nodifference was shown between the group havingreceived local corticosteroid injections and thosewithout any history of corticosteroid injections.The author concludes that more than 50% of the
patients had never received injections before therupture. In the others, it was his opinion that the timerelationships, among other factors, argued againstthe possibility that the corticosteroids would havebeen of direct aetiological significance. However, theauthor formulates the hypothesis that the corticoster-oids 'might have played a part by relieving thepatient of the symptoms attending a small rupture orsome other injury of the Achilles tendon, and soallowed increased weight-bearing on the tendon,thus being involved in causing the clinically manifestrupture'.
In conclusion, one can say that in the light of all theexisting literature to date, it is still impossible todetermine with precision the role of local injections ofcorticosteroids in the pathogenesis of partial andcomplete ruptures of the TA.
Nevertheless, certain important points can bepostulated. First, on the basis of animal experimenta-tion and clinical observations it is clear that allintratendinous injections should be abandoned.Second, there exists no formal proof of any deleter-ious effects of peritendinous injections. Last, Ljung-qvist's hypothesis stipulating that local corticostleroidinjections could mask the symptomatology andtherefore expose the tendon to further trauma isplausible25.
ConclusionAnimal research has shown that intratendinouscorticosteroid injections result in collagen necrosis,followed by a decrease in tensile strength. On theother hand, the majority of studies dealing withperitendinous corticosteroid injections are unable toshow any direct deleterious effect to the tendon.
Despite this difference, all the retrospective clinicalstudies in humans dealing with corticosteroid injec-tions and TA ruptures never attempt to differentiatebetween these two fundamentally different types ofinjections. This having been said, one might ask if itis really so easy to distinguish between an intratendi-nous and a peritendinous injection. Theoretically, theresistance to the injection of the product in anintratendinous injection is said to be much greaterthan in a purely peritendinous injection. Practically,the distinction might not be that obvious. Further-more, in the presence of a tendinosis or a partialrupture, it is most probable that the resistance to theinjection is altered, thereby giving a false impressionas to the exact location of the injection.We need to identify separately the effects of
corticosteroid injections in each distinct group of TApathologies. If there is a risk in giving corticosteroidinjections, is it the same in treating a pure peritendi-nitis, compared with a tendinitis or a focal degenera-tion? This brings up the vast issue that is beyond thescope of this dissertation of the actual indications forcorticosteroid injections.There is probably as big a controversy on this
subject as there is on the role of corticosteroidinjections in tendon ruptures! Hamilton's point ofview is that corticosteroids should never be used neara tendon52. Renstrom thinks that they should only beused in chronic situations and that the injectionshould be given into the paratenon53. In Da Cruz'sprospective, randomized, double-blind study toevaluate the role of peritendinous injection ofmethylprednisolone in the treatment of Achillesperitendinitis, the author concludes that cortico-steroids have no role to play in the management ofthis pathology'. There are as many points of view asauthors on this controversial subject, and again it israre that any distinction is made between thedifferent categories of TA pathology.Another important fact that has led to the
controversy on corticosteroid injections and TAruptures is improper diagnosis. As cited before, it isastounding to note that in Shields' study on completeruptures of the TA, 25% of the patients were givencorticosteroid injections after the acute rupture . It isabsolutely clear that corticosteroid injections have noplace in the management of acute ruptures of the TA,but their use in these situations by ignorance orincompetence has probably contributed to our confu-sion on the subject.
It is only through the selection of rigorouslyhomogeneous groups that one will be able toaccomplish the prospective studies necessary toelucidate the fundamental questions remaining un-answered. With the appearance of new imagingtechniques, it should be possible to distinguishbetween the different categories of TA pathology and
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Corticosteroids and Achilles tendon ruptures: F. Mahler
thereby differentiate between degenerative and in-flammatory conditions. These two conditions areoften sources of confusion when it comes to theevaluation of the role of corticosteroid injections. Thisis due to the fact that degenerative pathologies areprobably intrinsically a risk factor for ruptures. Thisintrinsic risk is hard to differentiate from the potentialadded risk of a local corticosteroid injection.What sort of studies are necessary for a better
comprehension of the subject? First, the differencebetween a peritendinous and an intratendinouscorticosteroid injection should be precisely defined.One could imagine a study comparing the tensilestrengths of two groups of animals, one receiving anintratendinous corticosteroid injection, the other aperitendinous injection. The ideal model would bethe study of Noyes12 on the Rhesus monkey, butinstead of using the anterior cruciate ligament, onewould use the TA.Another interesting study would be to see if one
can produce a cartilaginous and osseous metaplasiain a tendon merely by injecting it with cortico-steroids. This is important because the histologicalexamination of material taken from the site ofruptures often describes this modification without itbeing possible to know if it is a degenerative processof the tendon itself, or if it is the consequence of thelocal corticosteroid injection.As to the studies in man, the ethical restrictions are
definitely a limiting factor. This is why one isgenerally obliged to conduct retrospective studies onnon-homogenous groups, which unfortunatelymakes a precise analysis difficult. This having beensaid, it is surprising that no longitudinal study on therole of corticosteroid injections in partial and com-plete ruptures has ever been done. Such a study,comparing the long-term evolution of patients treatedwith local corticosteroid injections and those havingnever been injected, should be a priority in thefuture.
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