Subcutaneous rupture of the Achilles tendon - NCBI

BrJ Sports Med 1997;31:285-298

Subcutaneous rupture of the Achilles tendon:basic science and some aspects of clinical practice

Stuart William Waterston, Nicola Maffulli, StanleyW B Ewen

Achilles, the legendary warrior and hero ofHomer's Iliad, lends his name to the Achillestendon, the thickest and strongest tendon inthe human body.' Achilles' mother Thetisattempted to make her son invulnerable byimmersing him in the waters of the river Styxafter being told by a prophet that her son wasdestined to die in battle. However, the heel bywhich his mother held him remained un-touched by the water, and thus Achilles had avulnerable point. Achilles did go to battle, asthe leader of the forces of Myrmidons whosetask was to destroy Troy.' He killed Hector,leader of the Trojans, and Troy was subse-quently captured. However, Hector's death wasavenged by his brother Paris, who killed Achil-les by firing a poisoned arrow into his heel.

Hippocrates is credited with the first descrip-tion of injury to the Achilles tendon. He statedthat "this tendon, if bruised or cut, causes themost acute fevers, induces choking, derangesthe mind and at length brings death".3Ambroise Pare, the French military surgeonregarded as the father of modern surgery, iscredited with the first description of rupture ofthe Achilles tendon in 1575. Pare believed thatthe affected leg should be strapped with band-ages dipped in wine and spices, but he was nothopeful of a good result.4 The first descriptionof surgical repair of a ruptured Achilles tendonwas by Polaillon in 1888.4 Tendon suture wasnot a new idea, as it had been advocated asearly as the 10th century AD by an Arabianphysician. In the 12th century AD, William ofFalicet, an Italian surgeon, stated that naturewas unable to unite divided tendons, and thatsurgeons could make a much better job of it.Many researchers have attempted to elucidatethe aetiology ofAchilles tendon rupture, but itstrue nature still remains unclear. There is alsostill disagreement regarding the best method oftreatment for an acute Achilles tendon rupture.Some workers advocate surgical repair,whereas others insist that surgery is unneces-sary, and is an unacceptable risk.

MethodA computerised literature search of the entireMEDLINE database, covering the years 1966to the present, was conducted for this review.Table 1 lists the keywords used in the search.All articles that were relevant to the subjectwere retrieved, either locally, or by inter-libraryloan. The search was not limited to the Englishliterature, and articles in all journals were con-sidered. The authors own personal collectionof papers, and any relevant personal corre-spondence were also included. The references

that were selected were reviewed by all authors,and judged on their contribution to the body ofknowledge of this topic. The conduct andvalidity of any clinical studies was carefullyconsidered, and the outcomes of managementprotocols were carefully scrutinised. Casereports were excluded, unless they mentioned aspecific association with the condition that wasthought to be relevant to the discussion. Onlypapers that made a significant contribution tothe understanding of this condition wereincluded in the review. This left a total of 121publications, 87 of which were directly relatedto the Achilles tendon, and the remainder totendon or tendon structure in general.

The Achilles tendonThe Achilles tendon is formed by the mergingof the tendinous portions of the gastrocnemiusand soleus muscles, which constitute thetriceps surae muscle group in the leg. Theplantaris muscle, present in 93% of persons,5although related to the medial border of theAchilles tendon, does not participate in theformation of the Achilles tendon. The medialand lateral heads of the gastrocnemius musclearise posteriorly from the femoral condyles.5The soleus muscle originates from the poste-rior aspect of the tibia and fibula.6 The gastroc-nemius tendon originates as a broad aponeuro-sis at the lower margin of the muscle bellies.7The soleus tendon begins as a band high on theposterior surface of soleus. Both componentsof the tendon vary in length and extent offusion. The gastrocnemius component variesfrom 11 to 26 cm,7 the soleus component var-ies from 3 to 11 cm. From its origin, the Achil-les tendon becomes progressively rounded, to alevel of about 4 cm above the calcaneus.8 Thetendon inserts onto the calcaneus posterior tothe superior calcaneal tuberosity.9 The fibres ofthe Achilles tendon spiral through 900 duringits descent. Therefore fibres that lie mediallyproximally become posterior distally. Thisarrangement permits elongation and elasticrecoil within the tendon, and allows storedenergy to be released during the appropriatephase of locomotion.8 This stored energyallows the generation of higher shorteningvelocities and greater instantaneous musclepower than could be achieved by muscle fibresalone.'0 The region of the calcaneal insertion ofthe Achilles tendon is highly specialised."' Asubcutaneous bursa (located between tendonand skin) is variably present. A retrocalcanealbursa lies between tendon and the calcaneum.9These bursae reduce friction between tendonand the surrounding tissues.

Departments ofOrthopaedic Surgeryand Pathology,University ofAberdeenMedical School,Polwarth Building,Foresterhill, AberdeenAB25 2ZD, ScotlandStuart William WaterstonNicola MaffulliStanleyW B Ewen

Correspondence to:Dr Maffulli.

Accepted for publication5 August 1997

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Waterston, Maffulli, Ewen

Table 1 Keywords used to search the MEDLINE database

Keywords for main MEDLINE literature searchAchilles tendon Extracellular matrix TendinitisAthletic injuries Incidence TendonBiomechanics Postoperative complications Tendon injuriesCollagen Rupture

Subheadings usedfor MEDLINE literature searchAbnormalities Growth and development PhysiopathologyAnatomy and histology Injuries SurgeryBlood supply Innervation TransplantationChemistry Metabolism UltrasonographyCytology Pathology UltrastructureDrug effects Physiology

Tendon structureTendons act as transducers of force from mus-cle to bone. The basic constituent is collagen,which accounts for 70% of the dry weight of atendon.' Approximately 95% of tendon is col-lagen type I,`2 with elastin present in only verysmall amounts.'2 This is of functional signifi-cance, as elastin can undergo up to 200% strainbefore failure. If the elastin content of tendonwere high, there would be a decrease in themagnitude of force transmitted to bone. Colla-gen fibrils are bundled into fascicles thatcontain blood vessels, lymphatics, and nerves.'3Fascicles are grouped together, surrounded byepitenon, to form the gross structure of thetendon. The entire structure is further en-closed by paratenon. A thin layer of fluidpresent between the paratenon and the epi-tenon, permits tendon movement with reducedfriction.

Collagen typing experiments by Coombs etal,4 using material from normal and rupturedAchilles tendons demonstrated that the normalAchilles tendon consists almost entirely of typeI collagen, whereas ruptured Achilles tendonsalso contained a significant proportion of typeIII collagen. Fibroblasts cultured from rup-tured Achilles tendons were found to produceboth type I and type III collagen. The presenceof type III collagen may account for thedecreased resistance oftendon to tensile forces,and may therefore predispose to spontaneousrupture.

TENDON CELLSThe cellular component of tendon tissue is thefibroblast. These are observed as stellate cellsin cross sections of tendon, and appear tooccupy rows when seen in longitudinal section(fig 1). '5 The orderly arrangement of fibro-blasts in tendon is probably a consequence ofthe uniform centrifugal secretion of collagenaround the column of cells.'6 Fibroblastsproduce both the fibrillar and the non-fibrillarcomponents of the extracellular matrix.'7Fibroblasts can also reabsorb collagen fibres,'8although this has been disputed by someauthors.'9 The normal Achilles tendon shows awell organised arrangement, contrasting withthe appearance of ruptured one (fig 2).

The blood supply oftendonsMayer20 described how tendons may receivetheir blood supply from three sources: themusculotendinous junction, vessels in sur-rounding connective tissue, and the tendo-osseus junction. Ha'stad et a12' injected radio-

Figure 1 Low magnification appearance of normalAchilles tendon. Fibroblast nuclei (F) can be clearly seen.Note the longitudinal arrangement offibroblasts intocolumns.

Figure 2 Low magnification appearance of rupturedAchilles tendon. Note the disorganised appearance of thetissue. Haemorrhage (H) into the tendon substance is alsopresent.

active sodium (24Na) into the Achilles tendonsof volunteers, and measured its clearance time.The "clearance constant" for 24Na was signifi-cantly higher in younger subjects, indicatingthat tendon blood flow was higher in youngerpeople, and decreased with age. Lagergren andLindholm22 demonstrated that the Achillestendon had a very small number of vessels,especially in the mid-portion of the tendon.More than three decades later, Schimdt-Rolfing et al'8 used epoxy resin injection intothe vascular system of the leg to show thatblood vessels ran from the paratenon into thesubstance of the Achilles tendon. They alsoshowed that no vessels ran directly from thebone into the tendon, and that blood vesseldensity in the middle part of the Achillestendon was small compared with the proximalpart. This contrasts with the findings ofAstromand Westlin in 1994.23 Using laser Dopplerflowmetry, they showed that blood flow wasevenly distributed throughout the Achilles ten-don. They did however acknowledge thattendon blood flow may vary according to age,sex, and loading conditions.

Tendon biomechanicsFukashiro et a!'4 have measured a peak force of2233 N within the human Achilles tendon bydirect in vivo measurement. Komi et al25 havedescribed the pattern of force generationwithin the human Achilles tendon usingbuckle-type force transducers attached to theankles of human volunteers. During walking,force builds up within the tendon before the

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Subcutaneous rupture of the Achilles tendon

Tendon rupture

Overuse injury>8%

Physiological3-5%

1-3%

0-1%/A

1 2 3 4 5 6 7 8

Strain (%)

Figure 3 Stress-strain curve for tendon. Adaptedfrom Leadbetter WB. "Cell-matrixresponse in tendon injury". Clin Sports Med 1992;2:573-8.

heel strikes the ground. The force is then sud-denly released for 10-20 ms during earlyimpact. Thereafter, force builds up relativelyfast until it reaches a peak at the end of thepush-off phase. A similar pattern is observedduring running. Ippolito et al'6 have observedactin and myosin in tenoblasts. They suggestedthat the tendon itselfmay have an active mech-anism of contraction-relaxation, which couldregulate the transmission of force from muscleto bone.A stress/strain curve can be produced for the

Achilles tendon. The curve has four regions(fig 3). In its resting state, a tendon has a wavy

configuration, which is a result of crimping ofthe collagen fibrils.' When tensile force isapplied, the tendon loses this wavy configura-tion. This accounts for the toe region of thestress/strain curve. Collagen fibres deform andrespond linearly to increasing tendon load.'Most loads that the Achilles tendon is sub-jected to cause a strain less than 4%." If thestrain placed on tendon remains at less than4%, the tendon will regain its original configu-ration when the load is removed. At strain lev-els between 4% and 8%, the collagen fibres willstart to slide past one another as cross links fail.At strain levels greater than 8%, macroscopicrupture of the tendon will occur because of thetensile failure of the fibres and shear failurebetween fibres.'

Epidemiology ofAchilles tendon ruptureRupture of the Achilles tendon is compara-

tively common. Its incidence in the generalpopulation is difficult to determine, butappears to have been increasing over the pastdecade."7 Recently, Leppilahti et al" estimatedthe incidence of Achilles tendon rupture in

1994 to be around 18 per 100 0 in the city ofOulu, Finland. Most Achilles tendon rupturesoccur during sport. A review of literaturediscussing the epidemiology of Achilles tendonrupture yielded a range of figures for patientsparticipation in sport, ranging from 44.4% to83%." " Badminton players seem to beparticularly vulnerable to Achilles tendon rup-

ture, as 52.3% of patients injured while playing

Table 2 Conditions associated with Achilles tendonrupture

Associated conditions

Hereditary Osteogenesis imperfecta"8Infective Syphillis, gonorrhoea, tuberculosis36Inflammatory Rheumatoid arthritis, SLE, gout37Iatrogenic Corticosteroid use, fluroquinolone

antibiotics404Others Back pain, sciatica*

SLE = systemic lupus erythematosus.* Irwin AS, Maffulli N, Porter RWP, Smith F. Tendo Achillesrupture and prolapsed intervertebral disc. A possible associ-ation? Read at the 13th meeting of the North East of ScotlandOrthopaedic Association, Aberdeen, 14 May 1994.

sports were playing badminton at the time ofinjury.'9 Achilles tendon rupture is more com-mon in men, with a male:female ratio varyingfrom 2:1 to 12: 1. 30 This probably reflects agreater prevalence of sports participation inmen, although there may be other as yet unrec-ognised factors. The left Achilles tendon ismore frequently ruptured than the right,6probably because of a higher prevalence ofright sided dominance resulting in peoplepushing off with their left legs.6 The typicalpatient presenting to hospital with an acutelyruptured Achilles tendon is a middle aged manworking in a white collar profession who playssport occasionally." Patients presenting withan Achilles tendon rupture are most commonlyin the third or fourth decade of life"2 with amean age of 40.4 years, ranging between 16and 87.32

Jozsa et al"3 3' noted an association betweenthe incidence of Achilles tendon rupture andblood group 0. The incidence of blood groupo within the study group was significantlyhigher than in the general Hungarian popula-tion. Kujala et aP! also noted a relation betweenABO blood groups and Achilles tendonrupture. The ABO blood group gene is locatedon chromosome 9, a chromosome where noknown collagen genes are located.

AetiologySpontaneous rupture of the Achilles tendonhas been associated with a multitude of condi-tions, which are listed in table 2. There hasbeen little agreement in the literature regardingthe aetiology of Achilles tendon rupture. Thereare a number of possible aetiologies, listed intable 3, and discussed below in more detail.

DEGENERATIVE THEORYAccording to McMaster,4" a normal Achillestendon does not rupture even when subjectedto severe mechanical strain. He proposed thatdisease processes in tendons predisposed themto spontaneous rupture from apparently minortrauma. Hastad et a!" demonstrated thattendon blood flow decreased with increasingage, and other authors have stated that the seg-ment of the Achilles tendon that is clinically

Table 3 Possible aetiologies ofAchilles tendon rupture

Degeneration'8 21 22 364244Corticosteroids (intra-/peritendinous, oral)4' 47-2Fluoroquinolone antibiotics41'5 54Hyperthermia55-57Mechanical"7 39 42 5863

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prone to rupture is relatively avascular com-pared with the rest of the tendon.'8 22 Kuwada43proposed that "footstrike haemolysis" may alsocontribute to the supposed vascular impair-ment within the Achilles tendon. The impact ofthe foot striking the ground could destroy nor-mal red blood cells, and, in extreme cases, thiscould give rise to an anaemic state. If thisoccurred in people with chronic Achilles tend-initis, it might predispose to tendon degenera-tion and subsequent rupture. However, there isno scientific support for such a hypothesis.Arner et aPt6 reported a series of 74 cases of

Achilles tendon rupture. Histologically, all ten-dons exhibited degenerative changes. However,a significant number (62.1%) of their speci-mens were obtained more than two days afterrupture, thus making it difficult to say whetherdegeneration had taken place before rupture orbetween the rupture and the time of repair.Davidisson and Salo44 reported two cases ofAchilles tendon rupture that were repaired onthe day of rupture. Both these specimensdemonstrated degenerative changes. The au-thors concluded that these degenerativechanges must be regarded as primary changes,which had developed before the rupture. Theysuggested that the increased vascularisationseen in muscle in response to exercise alsooccurred in tendon, and that vascularisation ofthe tissue decreased with inactivity. Therefore,athletes who started training again after aperiod of rest were more likely to rupture theirAchilles tendon at this stage. Kvist-Kristiansenet at'5 also believed that exercise and subse-quent periods of inactivity were the mechanismresponsible for degenerative changes seen intendons. Fox et at'6 stated that athletic partici-pation in addition to daily activity placed addi-tional stress on the Achilles tendon, potentiallyleading to areas of microtrauma within the ten-don. The accumulation of such episodes ofmicrotrauma could lead to secondary degen-erative changes within the tendon.

CORTICOSTEROIDS AND TENDON RUPTURE

Corticosteroid administration has been widelyimplicated in the aetiology of tendon rupture.Corticosteroids are administered for a varietyof diseases. Balasubramaniam and Prathap47demonstrated that infiltration of hydrocorti-sone into rabbit calcaneal tendons causednecrosis at the site of injection as soon as 45minutes after injection. Corticosteroid injectedtendons showed a delayed healing responsecompared with control tendons into whichsaline was injected. Corticosteroids may beimplicated in the aetiology of Achilles tendonrupture to the extent that their anti-inflammatory properties mask symptoms oftendon damage,48 therefore permitting peopleto increase their activity even with a damagedtendon. The ability of corticosteroids to inter-fere with healing was also believed to beimportant. Unverfirth and Olix" reported onfive athletes who had been given corticosteroidinjections in the region of their Achillestendons for symptoms of tenosynovitis. All suf-fered ruptures of their Achilles tendons. Inter-estingly, residua of steroid were found at the

site of rupture in four of five cases. Kennedyand Willis50 demonstrated that physiologicaldoses of corticosteroid, injected directly intothe tendon, resulted in significant weakening ofthe tendon for up to 14 days after injection.The disruption was directly related to collagennecrosis, and restoration of tendon strengthwas attributable to the formation of anamorphous, acellular mass, which was thoughtto be a precursor of collagen. Vigorous activityshould be avoided for at least two weeks afterinjection of corticosteroid close to a tendon.50Oral corticosteroids have also been implicatedin the aetiology of tendon rupture. Newham etat" reported a series of 12 patients in 10 yearswho had Achilles tendon ruptures, and whowere taking long term oral corticosteroids forchronic obstructive airways disease. Four ofthese ruptures were bilateral.

Therefore, there is a significant amount ofevidence suggesting that corticosteroid admin-istration can be a causative factor in tendonrupture. However, not all studies on experi-ments on corticosteroids and tendon rupturehave reported deleterious effects of corticoster-oid treatment. McWhorter et alr stated thatinjection of hydrocortisone acetate into thetraumatised rat calcaneal tendon had nosignificant adverse effect, either biomechani-cally or histologically. In a review of cortico-steroid induced tendon abnormality, Mahlerand Fritschy'2 stated that despite all theexisting evidence regarding corticosteroids andtendon rupture, it was still impossible to sayexactly what the aetiological role of corticoster-oids was. They pointed out that some studiesreported patients who had other risk factors fortendon rupture. He also questioned why, ifcorticosteroids had such a harmful effect ontendons, was the incidence of tendon rupturenot much higher, because of the prevalence ofcorticosteroid consumption within the popula-tion.

FLUOROQUINOLONES AND TENDON RUPTURE

Fluoroquinolone (4-quinolone) antibioticssuch as ciprofloxacin have recently been impli-cated in the aetiology of tendon rupture. Royeret at' have reported from France a series of 100patients taking fluoroquinolones between 1985and 1992 who have suffered tendon disorders,including 31 ruptures. Many of these patientshad also received corticosteroid treatment,therefore making it difficult to solely implicatethe fluoroquinolones. The Food and DrugAdministration (FDA) have reported animalstudies using fluoroquinolone doses close tothose given to humans, and showed disruptionof the extracellular matrix of cartilage, anddepletion of collagen. The FDA subsequentlyrecommended updating the labelling on allfluoroquinolone packing to include a warningabout the possibility of tendon rupture.53 Theinfections section of the British NationalFormulary54 also contains a warning aboutfluoroquinolones. It states that "at the first signof pain or inflammation, patients taking4-quinolones should discontinue the treatmentand rest the affected limb until the tendonsymptoms have resolved". It is possible that

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Overpronation of foot on heelstrike,"9 poor gastrosoleus flexibility39Flared heels, heel tabs6'Muscle fatigue results in tendon elongation and tearing,39 torsionalischaemia resulting from unequal tensile forces'9

collagen degradation seen in animals alsooccurs in humans, and is responsible for thetendon ruptures in patients taking such drugs.

HYPERTHERMIA AND TENDON RUPTURE

Hyperthermia may damage tendons, and some5-10% of the elastic energy that is stored intendons may be released as heat.55 Wilson andGoodship56 conducted in vivo experiments onequine superficial digital flexor tendons toevaluate the temperatures generated within thetendon. A peak temperature of 45°C was

measured within the core of the tendon afterjust seven minutes of exercise. Previous experi-ments by Arancia et al57 have shown thatfibroblasts can be damaged at temperaturesabove 42°C. Exercise induced hyperthermiamay be a contributory factor in tendon degen-eration. A good blood supply to a tissue shouldhelp to cool overheating. Therefore, tissuessuch as the Achilles tendon that may havecomparatively avascular areas may be more

susceptible to the effects of hyperthermia.

THE "MECHANICAL THEORYMcMaster42 proposed that a healthy tendonwould not rupture, even when subjected to themost severe strain. However, Barfred,5"0through several studies on experimental rup-ture of the Achilles tendon, demonstrated that,if straight traction was applied to a tendon, asin McMaster's experiments, then the risk ofrupture was distributed equally to all parts ofthe muscle-tendon-bone complex. If obliquetraction was applied, the risk of rupture was

concentrated on the tendon. He calculatedthat, if a human Achilles tendon 1.5 cm widewas subjected to traction with 300 of supina-tion on the calcaneus, the fibres on the convex

aspect of the tendon would be elongated by10% before the fibres on the concave side werestrained. He concluded that the greatestpossibility of tendon rupture was present whenthe tendon was obliquely loaded, when themuscle was in maximum contraction, andwhen the initial tendon length was short. Suchfactors are probably all present in movementsthat occur in sports that require rapid push-offmovements, such as squash and badminton.Barfred's theory is largely supported by Guilletet al (cited by Postacchini and Puddu)21 whoproposed a purely traumatic theory to accountfor tendon rupture in young healthy patients.They believed that a healthy tendon may

rupture after a violent muscular strain in thepresence of various functional and anatomicalfactors, including incomplete synergism ofagonist muscles, a discrepancy in the thicknessquotient between muscle and tendon, andinefficient action of the plantaris muscle actingas a tensor of the Achilles tendon.

Sports participation plays an important partin the development of Achilles tendon prob-lems, and training errors or poor equipment

are important factors (table 4). The flared heelthat is present on most sports shoes forces therear foot into pronation when the heel strikesthe ground,6" and "heel tabs" present on someshoes probably also play a part. Clement et al,39in a study on the aetiology of Achilles tendini-tis, noted that 56% ofthe athletes in their studygroup displayed a "functional overpronation"of the foot on heelstrike. Functional overprona-tion produced a whipping action of the Achillestendon, and exaggeration of this whippingaction may lead to the development ofmicrotears within the tendon. Poor flexibility ofthe gastrocnemius-soleus unit was also consid-ered to contribute to overpronation. Trainingerrors were noted in 75% of the study group,and it was suggested that, in fatigued muscles,the effect of the eccentric action of gastrocne-mius and soleus, together with the gravitationalelongation of the tendon occurring on foot-strike, subjected the tendon to extreme stress,which could lead to the development of micro-tears. Unequal tensile forces on different partsof the tendon may produce a "torsional ischae-mic effect"-that is, causing blanching ofvessels within the tendon-and perhaps there-fore contribute to the vascular impairmentalready existing within the Achilles tendon.39Inglis and Sculco6' proposed that malfunctionor suppression of the proprioceptive compo-nent of skeletal muscle predisposed an athleteto Achilles tendon rupture. They believed thatathletes who resumed training after a period ofrest were particularly susceptible to Achillestendon rupture as a result of this malfunction.Knorzer et at63 conducted experiments using xray diffraction spectra to study the behaviour ofthe structure of collagen during loading of ten-don. Tendons that rupture without previousdegenerative changes are initially damaged atthe sub-microscopic fibrillar level, because of aprocess of intrafibrillar sliding, which occurs afew seconds before macroscopic slippage ofcollagen fibres. Therefore, rupture of tendonsunaffected by degenerative changes may be theresult of the accumulation of fibrillar damage.Such findings support the theory that acomplete rupture is the consequence of multi-ple microruptures, and that tendon damagemust reach a critical point, after which failureoccurs.

Mechanism of ruptureArner and Lindholm64 classified the history oftrauma in their patients into three maincategories. These mechanisms were firstly,pushing off with the weightbearing forefootwhile extending the knee joint. This type ofmovement is seen in sprint starts, and in jump-ing in sports such as basketball. It accountedfor 53.3% of the ruptures in their series.Secondly, sudden, unexpected dorsiflexion ofthe ankle, such as slipping into a hole, or fallingon stairs. This mechanism accounted for17.4% of their cases. Lastly, violent dorsiflex-ion of a plantarflexed foot, such as may occurafter falling from a height. This mechanismaccounted for 9.8% of their cases. In the rest oftheir cases it was difficult to quantify the exactmechanism of the injury.

Table 4 Mechanicalfactors in the aetiology ofAchilles tendon rupture

Anatomical factorsSports equipmentTraining errors

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PathologyIn 1976 Puddu et al° proposed a system toreplace the American Medical Associationdefinitions for tendon pathology. The majorheadings were (1) pure peritendinitis, (2) peri-tendinitis with tendinosis, (3) pure tendinosis.Tendinosis describes the degenerative proc-esses occurring within tendon. Tendinosis is anumbrella term that includes a number ofpathological processes such as hyaline degen-eration with a decrease in the normal cellpopulation, mucoid degeneration with chon-droid metaplasia of tenocytes, fatty degenera-tion of tenocytes, lipomatous infiltration oflarge areas of tendon, an increase in matrixmucopolysaccharides, and fibrillation of colla-gen fibres. Rupture of a tendon can be second-ary to this process, and is the critical end pointof the degenerative process. Tendinosis issymptomless, and is disclosed only by ruptureof a tendon. Patients who experience symp-toms before rupture of a tendon commonlyhave a combination of peritendinitis and tendi-nosis. Kannus and Jozsa65 noted that only onethird of the patients in their study of 891 rup-tures had symptoms before the rupture. Arneret aP6 observed degenerative changes in 100%of the ruptured Achilles tendons that theyexamined histologically. Features of the degen-eration that they noted included oedematousdisintegration of tendon tissue, patches ofmucoid degeneration, and a severe inflamma-tory reaction. They also noted that around onequarter of the larger calibre arteries that wereobserved in the peritendinous tissue exhibitedpathological hypertrophy of the tunica mediaand narrowing ofthe vessel lumen. Kannus andJozsa65 studied 1336 tendons to try to deter-mine the histopathological changes that pre-ceded a rupture. Of the 891 ruptured tendonsfrom all sites studied, all had pathologicalchanges, 97% of which could be described asdegenerative changes. The most commondegenerative lesion observed was hypoxicdegenerative tendinopathy, characterised bychanges in the size and shape of mitochondria,abnormal tenocyte nuclei, and occasionalintracytoplasmic or mitochondrial calcifica-tion. If degeneration is advanced, then hypoxicor lipid vacuoles and necrosis may be observed.Aberrant collagen fibres can also be seen, withabnormal variations in fibre diameter, angula-tion, splitting and disintegration. Kannus andJozsa also noted vascular changes in vessels ofthe tendon and paratenon in 62% of the 891ruptures, which were mostly luminal narrowingcaused by hypertrophy of the arterial intimaand media. The available evidence suggeststhat changes in blood flow and subsequenthypoxia and impaired metabolism were keyfactors in the development of the degenerativechanges that were observed in rupturedtendons.65 Degenerative changes were apparentin all tendons that had a spontaneous rupture.The interval between time of rupture and timeof repair was short, thus suggesting that thedegenerative changes were pre-existing. Failureofthe cellular matrix has also been suggested tolead to degenerative changes within thetendon.66 Jozsa et a167 observed fibronectin on

Figure 4 Simmond's calf squeeze test. The examinergently squeezes the patient's calf muscles with the palm ofthe hand. If the Achilles tendon is intact, the ankle plantarflexes (left leg). If the Achilles tendon is torn, the ankleremains still, or plantarflexes minimally (right leg)

Figure 5 Matles'test. With the patient prone, the kneesare flexed to 90°, and the position of the ankles andfeetobserved. If the foot on the affected side falls into neutral ordorsiflexion, an Achilles tendon rupture is diagnosed (R).On the uninjured side, the foot remains in slight plantarflexion (N).

the tear surfaces of ruptured Achilles tendons.Fibronectin is a high molecular weight glyco-protein, normally located in basement mem-branes, and also present in a soluble form inplasma. Fibronectin binds more readily todenatured collagen than to normal collagen,68suggesting that the presence of fibronectin onthe surfaces of ruptured tendons may indicatepre-existing collagen denaturation.

Presentation and diagnosisThe typical patient with an Achilles tendonrupture generally presents to hospital with aclassic history of sudden pain in the affectedleg, often reporting that, at the time of injury,they thought that they had been struck by anobject or kicked by a fellow sportsman. Somepatients report an audible snap. They are oftenunable to weightbear and notice weakness orstiffness of the affected ankle.69 If they wereplaying sport, the injury tends to occur late in agame when they are fully warmed up. Indeed,Achilles tendon rupture is rarely associatedwith insufficient warm up.70 Patients withchronically ruptured Achilles tendons also tendto give a fairly typical history, often recallingonly very minor or perhaps no trauma, and firstnoticing the injury as an inability to completeeveryday tasks such as climbing stairs."On examination, there may be diffuse

oedema and bruising,69 and a palpable gap maybe felt along the course of the tendon69 unlessthe swelling is severe. The site of rupture is

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B

Linear array transducerStandoff pad

AT C

Figure 6 Comparison of sector-type and linear array ultrasound probes for imaging of theAchilles tendon. (AT = Achilles tendon, C = calcaneus).

usually 2-6 cm proximal to the insertion of thetendon,2' the average distance measured intra-operatively being 4.78 cm in a recent largestudy.7'

Diagnosis of Achilles tendon rupture shouldbe straightforward. However, up to 25% aremissed by the first examining doctor.72 Thereare a number of diagnostic signs and tests, bothclinical and radiological, that the examiner mayuse to aid diagnosis.

SIMMOND 'S TESTAlso known as the "calf squeeze test", it entailsplacing the patients prone on the examinationcouch, with their ankles clear of the couch, andsqueezing the fleshy part of the calf. If themusculotendinous unit is intact, plantarflexionof the foot should occur. If the Achilles tendonis ruptured, plantarflexion does not occur (fig4). The affected leg should be compared withthe opposite leg.73 A false positive may occur inthe presence of an intact plantaris, althoughthis has not been scientifically proved. TheSimmond's test works because of posteriorbowing of the tendons of the calf muscles and,to a lesser extent, proximal displacement of thebelly of gastrocnemius.7'The Simmond's test is often wrongly accred-

ited to Thompson, who described the testjointly with Doherty in 1962,75 five years afterSimmond's paper was published in 1957. Laterin 1962, Thomson described the test again inActa Orthopaedica Scandinavica,76 this timewithout the aid of Doherty.77

MATLES' TESTThis test entails placing the patients prone onthe examination couch, with their ankles clearof the end of the couch, and asking them toactively flex their knee to 900. During flexion,the position of the ankle and feet should beobserved. If the foot on the affected side fallsinto neutral or dorsiflexion, then an Achillestendon rupture can be diagnosed (fig 5).78

NEEDLE TESTThis test entails inserting a hypodermic needlethrough the skin of the calf, medial to the mid-line and approximately 10 cm proximal to theinsertion of the tendon. The needle is inserteduntil its tip is just within the substance of thetendon. The ankle is then alternately plantar-flexed and dorsiflexed. If, when the ankle isdorsiflexed, the needle points distally, thetendon is intact in the portion distal to the

needle. If the needle points proximally whenthe ankle is dorsiflexed, there is a loss of conti-nuity between the needle and the tendoninsertion.79

COPELAND TEST

This test entails inflating a sphygmomano-meter cuff around the mid-calf of the affectedleg while the patient is lying prone. The cuff isinflated to 100 mm Hg with the foot inplantarflexion. The foot is then dorsiflexed,and if the pressure rises to approximately 140mm Hg then the musculotendinous unit isintact. If, however, the pressure stays at around100 mm Hg then an Achilles tendon rupturemay be diagnosed.80

Recent work in our unit, with a large groupof patients with Achilles tendon ruptures,ascertained that there was no statisticallysignificant difference in predictive value be-tween the above mentioned tests (Maffulli N,unpublished data ). The diagnosis of Achillestendon rupture is certain if the result of at leasttwo of these tests were positive.

Tendon imaging in diagnosisPLAIN RADIOGRAPHYSome signs that may be observed on lateralradiographs of the ankle are said to indicate thatthe Achilles tendon has been ruptured. The firstsuch sign involves the contours of Kager'striangle,8' the fat filled space bounded by themargins of the Achilles tendon, calcaneus, anddeep toe flexors. When the Achilles tendon isruptured, this triangle loses its regular configu-ration. Toygar's sign82 entails measuring theangle of the posterior skin surface curve seen onplain radiographs. An angle of 130° to 1500would indicate Achilles tendon rupture. Toygarhimself considered an angle of 1300 to 1500accompanied by displacement of Kager's tri-angle to be so characteristic of Achilles tendonrupture as virtually suffice for diagnosis. Arnerand Lindholm83 studied the plain radiographicchanges seen with Achilles tendon rupture.They stated that "a curving away from the boneof the posterior tendon contour between itsinsertion and the upper margin of the calcaneuscombined with unimpaired contour, and for-ward deviation of the anterior tendon contourproximal to the calcaneus" were the radio-graphic changes most likely to be associatedwith Achilles tendon rupture.83

Clinical diagnosis is usually sufficient foracute ruptures ofthe Achilles tendon. Rupturesthat are more longstanding may be harder todiagnose because of associated tissue swelling,etc. Magnetic resonance imaging (MRI) andreal time high resolution ultrasonography (US)provide an adjunct to clinical diagnosis, andthey are more sensitive than soft tissue radio-graphy or xeroradiography.8'

MRI

On MRI, the normal Achilles tendon is seen asan area of low signal intensity on all pulsesequences used. The tendon is well delineatedby the high signal intensity of the fat padof Kager's triangle.85 Any increase in signalintensity within the tendon should be regarded

A

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Figure 7 (A) An 8 to 10 cm longitudinal incision is placedjust medial to the medial border of the tendon, centred on thepalpable gap. (B) The subcutaneous fat is divided by sharp dissection, with no undermining of the skin edges. Theparatenon is visualised, then incised longitudinally. If the paratenon remains viable then it may be attached to thesubcutaneous fat with temporary sutures so that it does not interfere with the tendon itself during the procedure. (C) Theruptured tendon is exposed, demonstrating the typical horse tail appearance. Frayed ends are not routinely freshened, butthis may be necessary in patients presenting later. Two self retaining retractors are positioned to expose the tendon. (D) Theankle is plantarfiexed to aid apposition of tendon ends. A single Kessler suture is passed through the proximal and distalstumps of the tendon. A running circumferential suture is then inserted using a finer material. The repair is often too thickto facilitate closure of the paratenon, in which case it is simply laid over the repair. (E) Interrupted fine reabsorbable suturesare used to close the subcutaneous fat, and the skin is closed with fine reabsorbable sutures inserted into the subcuticularlayer. (F) The wound is supported with steristrips, and a routine gauze and wool dressing is applied. A below knee cast ingravity equinus is then applied.

as abnormal.86 Axial and saggital plane T1 andT2 weighted images should be used to evaluatesuspected Achilles tendon ruptures. Tiweighted images show complete ruptures oftheAchilles tendon as disruptions of the signalwithin the tendon. T2 weighted images are themethod of choice for MRI diagnosis ofAchillestendon ruptures. The rupture is demonstratedas a generalised increase in signal intensity, andthe oedema and haemorrhage at the site ofrupture is seen as an area of high signalintensity.85

ULTRASOUNDUS of the Achilles tendon using linear probesproduces a dynamic and panoramic image ofthe tendon.85 The appearance of the tendonvaries with the type of transducer used and the

angle of the ultrasound beam with respect tothe tendon.87 High frequency probes of 7.5-10MHz provide the best resolution but arelimited by a short focusing distance, usually notexceeding 3-4 cm.88 The Achilles tendon iscomposed of longitudinally arranged collagenbundles, which act as reflectors of the ultra-sound beam. The US probe should be held atright angles to the tendon to ensure that anoptimal amount of ultrasonic energy is re-turned to the transducer87 and to avoidartefacts.88 Linear array transducers are there-fore better suited than sector-type transducers,which produce excess obliquity ofthe US beamat the edges (fig 6). It may also be necessary touse a synthetic gel spacer or standoff pad,increasing the definition of the surface echoesand permitting a suitable support.89

292

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Table S Surgical repair ofAchilles tendon rupture: complications and re-ruptures (note:re-rupture rate is included in complication rate)

Number (%) of Number (%/6) ofAuthors Cases complications re-ruptures

Arner and Lindholm 195964 86 21 (24.4) 4 (4.6)Gilles and Chalmers 1970102 6 1 (16.7) 0 (0)Kvist and Andersen 197245 37 7 (18.9) 1 (2.7)Inglis et al 1976'" 44 2 (4.5) 0 (0)Jacobs et al 1978'2' 26 5 (19.2) 0 (0)Quigley and Scheller 1980'23 40 7 (17.5) 2 (5)Nistor 1981104 45 4 (8.9) 2 (4.4)Kellam et al 1985'22 68 9 (13.2) 2 (2.9)Carden et al 1987' 56 6 (10.7) 2 (3.6)Aldam 1989'08 41 2 (4.9) 1 (2.4)Sejberg et al 1990'24 81 17(21.1) 3 (3.7)Cetti etal 199329 56 15 (26.8) 3 (5.4)Saw et al 1993"° 19 4 (21.1) 0 (0)Krueger-Franke et al 199571 365 55 (15.1) 9 (2.5)Soldatis et al 1997106 23 2 (8.7) 0 (0)Total 993 157 (15.8) 29 (2.9)

A normal Achilles tendon appears sono-

graphically as a hypoechogenic, ribbon-likeimage within two hyperechogenic bands. Ten-don fascicles can be observed as alternatehypo- and hyper-echogenic bands, which are

separated when the tendon is relaxed and morecompact when it is under strain.89 Sonographi-cally, there are no differences between the leftand right Achilles tendons, nor any differencesbetween sexes, except that tendons in men are

slightly thicker than those in women.90 Ruptureof the Achilles tendon is seen on US as anacoustic vacuum with thick, irregular edges.89Campani et al9' conducted 170 US examina-tions for various lower limb traumas. The high-est percentage of positive findings was in theAchilles tendon (75%), compared with only38% for lesions in the thigh. Maffulli et al2 haveshown that US is a suitable tool for assessingtendon structure after surgical repair. US can-not only give a morphological picture of a ten-don, but can be used to study its biomechanicalproperties.93

TreatmentMany techniques and procedures have beendescribed for the treatment of a rupturedAchilles tendon. Such techniques can begrouped under three headings: surgical, percu-taneous, and non-surgical. Controversyabounds regarding which is the best method oftreatment as there is no agreed protocol, andthe choice of treatment regimens still lieslargely with the preference of the surgeon andthe patient.

SURGICAL TREATMENTVarious surgical techniques have been used torepair ruptured Achilles tendons. These range

from simple end to end suturing by Bunnell or

Kessler type sutures (fig 7), to more complexrepairs using fascial reinforcement or tendongrafts.94 Artificial tendon implants have alsobeen performed, using material such as absorb-able polymer-carbon fibre composite,95 Marlexmesh,96 97 and a collagen tendon prosthesis.98Simple end to end suturing techniques havebeen modified by the use of materials such as

Dacron vascular graft, which is passed throughthe tendon in a Bunnell-type fashion.99 Canineexperiments have shown that Dacron supportsthe growth of fibrous tissue."'0 It also facilitates

the approximation of tendon ends but causesless tension of the repair site than standardsutures.99 However, as maturation of collagenmay be dependent on a tensional stimulus,'01lack of tension on the repair site may not beadvantageous.The main opponents of surgical repair cite

the high complication rate as the maindisadvantage.3 6 102-105 Arner and Lindholm64reported a series of 86 operative repairs ofAchilles tendon ruptures in which there were21 complications (24.4%), including two casesof deep vein thrombosis, one of which resultedin pulmonary embolism and death, threewound infections, 11 cases of wound necrosis,and four re-ruptures. More recent reports havehad a much lower complication rate. Soldatis etal'06 reported a series of 23 surgically treatedpatients, in which the only complications weretwo cases of delayed wound healing. It is prob-able that the complication rate has fallenbecause of greater surgical experience, andimproved surgical technique. Wound problemsshould not be unexpected when surgical repairis used, as the classic longitudinal incisionpasses through poorly perfused skin.'07Aldham'08 used a transverse incision just distalto the gap in the tendon. In his 41 patientsthere was only one case of wound breakdown.After surgical repair, the leg is immobilised in acast for four to six weeks.29 Some workers haveadvocated the use of a functional orthosis afterjust several days of cast immobilisation. Thispermits unlimited plantarflexion, but restrictsdorsiflexion, and is designed to help preventatrophy of the triceps surae.'09 110 Table 5outlines some of the studies on surgical repair,and shows the comparatively high overall com-plication rate, and low re-rupture rate.

PERCUTANEOUS REPAIRThe percutaneous technique for repair of rup-tured Achilles tendons was first described byMa and Griffith."' They developed thistechnique because of their dissatisfaction withthe complications of surgical and non-surgicaltechniques and stated that this technique mini-mised many of the complications of surgicalrepair, while restoring tendon continuity andlength. The technique entails producing sixsmall stab incisions along the medial andlateral borders of the tendon, then passing asuture through the tendon via these incisions(fig 8). Ma and Griffith reported on a smallseries of 18 patients treated by this technique,in which there were only two minor, non-infectious skin complications and no re-ruptures. Rowley and Scotland"2 described 24cases of rupture of the Achilles tendon, 14treated by equinus cast alone, and 10 treated bythe percutaneous technique described above.There was one case on entrapment of the suralnerve in the sutured group, but no other com-plications were encountered. Plantar flexionstrength was measured in both groups accord-ing to a method described by Gilles andChalmers.'02 It was noted that patients in thesutured group were more likely to have a returnto near normal plantar flexion strength, andpatients in this group were also perceived to

293


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Figure 8 (A) Gap in tendon is identified by palpation. (B) 1% Lignocaine with adrenaline 1:100 000 is infiltrated alongthe medial and lateral borders of the tendo Achilles. (C) Creating the stab incisions along the medial and lateral borders ofthe tendon, through which the sutures will be passed. (D) Suture passed into the proximal lateral stab incision and throughthe proximal portion of the ruptured tendon. (E) Suture passed into distal lateral stab incision and through the distalportion of the ruptured tendon. (F) Suture is tied and cut short, then pushed subcutaneously. The stab incisions may beclosed with steristrips, or simply covered with gauze. A routine gauze and wool bandage is applied, then the leg is cast in abelow knee gravity equinus cast.

return to activity sooner the group treated bycast alone. Other authors have not had so muchsuccess with this technique. Klein et al'13reported on a series of 38 patients in whichsural nerve entrapment occurred in 13%. An invitro comparison of surgical and percutaneoustechniques by Hockenbury and Johns"4showed that repair of Achilles tendons by apercutaneous technique was up to 50% weakerthan surgical end to end suturing. They alsonoted that there was a high risk of sural nerveentrapment using this technique, and that thetendons ends were not anatomically juxta-posed. Bradley and Tibonel5 found that thethickness of percutaneously repaired Achillestendons was significantly less than that of sur-gically repaired ones. Patients who had theirAchilles tendons repaired percutaneously weremuch less likely to complain of heel pain."15Table 6 shows some of the results of studiesusing the percutaneous technique. The figuresdemonstrate the higher re-rupture rate associ-ated with percutaneous repair.

NON-SURGICAL TREATMENTThere are two forms of non-surgical treatmentfor rupture of the Achilles tendon. The firstconsists essentially of supervised neglect. Thisis used for elderly patients with longstandingruptures discovered by chance. These patientsare warned that, if the symptoms caused bytheir Achilles tendon rupture worsen, they mayrequire an operation. They are reviewed atregular intervals, but will usually require nofurther treatment (Maffulli N, unpublisheddata).The second form of non-surgical treatment

is by plaster cast immobilisation, usually for aperiod of six to eight weeks.29 Some workershave advocated that immobilisation alone pro-duces a similar, if not better result thansurgery.3 6 102-105 Lea and Smith'03 reported on aseries of 55 spontaneously ruptured Achillestendons that were treated by eight weeks ofimmobilisation. They had seven re-ruptures(12.7%), and 52 of the 55 patients weresatisfied with the result. Lea and Smith

294


Table 6 Percutaneous repair ofAchilles tendon rupture: complications and re-ruptures(note: re-rupture rate is included in complication rate)

Number (%) of Number (%o) ofAuthors Cases complications re-ruptures

Ma and Griffiths 1977"' 18 2 (11.1) 0 (0)Rowley and Scotland 1982"12 10 1 (10) 0 (0)Bradley and Tibone 1990"5 12 2 (16.7) 2 (16.7)Klein etal 1991 "' 38 8 (21.1) 3 (7.9)Total 78 13 (16.7) 5 (6.4)

Table 7 Non-surgical repair ofAchilles tendon rupture: complications and re-ruptures(note: re-rupture rate is included in complication rate)

Number (%/o) of Number (%/o) ofAuthors Cases complications re-ruptures

Gilles and Chalmers 1970102 7 1 (14.3) 1 (14.3)Lea and Smith 1972'°3 55 7 (12.7) 7 (12.7)Inglis et al 197672 23 9 (39) 9 (39)Persson and Wredmark 1979"' 20 9 (45) 7 (35)Carden etal 1987' 76 3 (3.9) 1 (1.3)Total 181 29 (16.0) 25 (13.8)

believed that these results indicated that surgi-cal treatment was not necessary. They statedthat "the success of this method (non-surgicaltreatment) evolves from the fact that the Achil-les tendon, when ruptured, sectioned or

removed, will regenerate itself".'03 This state-ment totally ignores the fact the one of themain goals of treatment of Achilles tendonrupture is to prevent tendon lengthening. Non-surgical treatment cannot usually achieve thisgoal.94 Persson and Wredmark"6 reported on a

series of 20 patients with Achilles tendon rup-tures treated non-surgically. There were seven

re-ruptures in this group (35%), and only 13 ofthe patients (65%) were satisfied with theresult. They concluded that, although thefunction after non-surgical repair was generallygood, the high incidence of re-rupture was

unacceptable. Stein and Luekensl'05 stated that,when Achilles tendon rupture occurs, theparatenon remains intact. They found experi-mentally that stripping of the paratenon duringsurgery reduced the amount of reactive tissuethat was later seen at the site of injury. Theysuggested that surgical repair of rupturedAchilles tendons should be avoided as theparatenon provided a valuable blood supply tothe damaged tendon. Table 7 shows the highcomplication and re-rupture rate associatedwith non-surgical management of Achilles ten-don rupture.Work by Haggmark and Eriksson" 7 shows

that long immobilisation, such as that occur-

ring during non-surgical treatment for Achillestendon rupture, results in a significant decreasein calf circumference. As the cross sectionalarea of a muscle is directly related to the forcethat the muscle can develop,"8 long periods ofimmobilisation will result in a significant loss ofcalf muscle strength. The soleus muscle seemsto be particularly susceptible to immobilisa-tion, while the gastrocnemius is less affectedbeing a biarticular muscle, and therefore is stillstretched to a certain extent, even when the legis immobilised below the knee. Human soleuscontains a high proportion of type I musclefibres."17 Type I muscle fibres are particularlysusceptible to atrophy if the muscle is immobi-lised, as they are responsible for postural tone,

and are continually activated while standing."'9When the leg is immobilised, the muscle spin-dle relaxes, and afferent impulses to type Ifibres cease, thus causing them to atrophy.Obviously, problems resulting from immobili-sation occur after surgical and percutaneousrepair too, but not to the same extent.Haggmark et al'20 compared the degree ofdecrease in calf circumference after surgicaland non-surgical repair of Achilles tendonruptures. They found that, while there was asignificant decrease in the non-surgicallytreated group, the surgically treated groupshowed no significant decrease. Patients withsurgical or percutaneous repairs spend lesstime in plaster,29 and on the whole are oftenmore serious athletes who will comply wellwith treatment regimens. The lack of tensionon the immobilised musculotendinous unit isan important factor in the development of calfatrophy, and, if optimal results are requiredfrom a repair of a ruptured Achilles tendon,then the repair should be put under as muchtension as possible,"7 and the casts should bechanged regularly, decreasing the angle ofplantarflexion as much as possible each time.

SURGICAL VERSUS NON-SURGICAL TREATMENT

Although there are a number of reports thatcompare the results of surgical treatment ofAchilles tendon rupture with that of non-surgical treatment, only a few well controlled,prospective randomised trials have been con-ducted (table 8). Gilles and Chalmers'02 objec-tively measured the plantarflexion strength ofpatients with Achilles tendon ruptures treatedsurgically and non-surgically. They found thatthere was little difference between the twogroups, and concluded that the results ofsurgery were not sufficiently superior towarrant the extra risk that accompanies a gen-eral anaesthetic. Inglis et af2 followed up agroup of 67 patients, 44 of whom were treatedsurgically and 23 non-surgically. There were nore-ruptures in the surgically treated group, butnine re-ruptures (39%) occurred in the non-surgically treated group. Strength testingshowed that surgically treated patients hadsuperior strength, power, and endurance. Theauthors concluded that surgery was the treat-ment option of choice. Nistor'04 conducted aprospective randomised trial along similarlines. He had a group of 105 patients, 45 ofwhom had surgical treatment, and 60 who hadnon-surgical treatment. The re-rupture rate ofNistor's surgical group was 4.4% comparedwith 8.3% for the non-surgical group. How-ever, there were a large number of secondarycomplications in the surgical group. Patientstreated non-surgically were found to have lessabsence from work, less ankle stiffness, andsimilar strength to the surgical group. Nistorconcluded that, because there were only minordifferences between the two groups, non-surgical treatment was the method of choice.Carden et al' compared the results of surgicaland non-surgical treatment in patients present-ing to hospital less than 48 hours after injurywith those presenting greater than 48 hours. Intotal, they treated 76 patients non-surgically,

295

296 Waterston, Maffulli, Ewen

Table 8 Randomised controlled trials of repair ofAchilles tendon rupture (note: re-rupturerate is included in complication rate)

Number (%/6) of Number (%/6) ofCases complications re-ruptures

Surgically managed patientsNistor 1981'°4 45 4 (8.9) 2 (4.4)Cetti etal 199329 56 5(9) 3(5)Total 101 9 (8.9) 5 (5.0)

Non-surgically managed patientsNistor 1981 '04 60 5 (8.3) 5 (8.3)Cetti et al 199329 55 9 (16.3) 7 (12.7)Total 115 14 (12.2) 12 (10.4)

and 56 surgically. The overall complication ratein the non-surgical group was 3.9% comparedwith 16.6% for the surgical group. Subjectiveresults were also better in the non-surgicallytreated group. They concluded that patientspresenting less than 48 hours after injuryshould be treated non-surgically by eight weeksof cast immobilisation, whereas patients pre-senting greater than one week after injuryshould be treated surgically. Cetti et at9 alsoconducted a prospective randomised trial ofsurgical versus non-surgical treatment Theirstudy group consisted of 111 patients, 56 withoperative repairs and 55 with non-operativerepairs. They compared complication rates andre-rupture rates between the two groups.Surgical treatment had a complication rate of9% and a re-rupture rate of 5% compared with16% and 15% respectively for non-surgicaltreatment. These results, however, were notstatistically significant. They also conducted areview of Achilles tendon rupture literature,and identified 4597 ruptures. Making the samecomparisons as above, surgical treatment wasfound to have significantly lower complicationrates and re-rupture rates than non-surgicaltreatment. They concluded that surgical treat-ment was the method of choice, but non-surgical treatment was an acceptable alterna-tive. In summary, if optimal performance isrequired of the ruptured Achilles tendon, thensurgery is the treatment of choice. It should beused in athletes and in patients who areparticularly active. Percutaneous repair isuseful for patients who do not wish to undergoan open surgical repair, possibly for cosmeticreasons, or perhaps because they view an opensurgical repair as a more serious procedure.Many patients undergo percutaneous repairwith only a local anaesthetic, and are able toreturn home the same day."0 Conservativetreatment should be reserved for older patientswho are unlikely to achieve any major benefitfrom a surgical procedure, or for those patientswho view surgery as an unnecessary risk.

ConclusionsIt is perhaps surprising to people who are notinvolved in this field that the aetiology of whatwould seem to be a simple condition is, in fact,rather complicated. Despite extensive investi-gation, few answers about the aetiology ofAchilles tendon rupture have been found. Thelack of study of human tissue is an obviousproblem, but it is difficult to see how this couldbe overcome.The type of treatment for acute Achilles ten-

don ruptures remains largely with the prefer-

ence of individual surgeons. It is evident thatopen surgical repair produces superior func-tional results, but may have significant post-operative complications. Non-surgical treat-ment may result in a poorer functional result,but the problems of postoperative complica-tions are avoided.

If the studies that report increasing incidenceof Achilles tendon rupture are correct, then thefield of Achilles tendon surgery will become anincreasingly important one. Future develop-ments may include the routine use of adhesivesin tendon surgery. An understanding of the rolethat cytokines play in tendon healing may leadto the advent ofnew treatments. However, suchnovel treatments are unlikely to be in routineclinical use for some time.

Part of this work was supported by the Wellcome Trust.

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Thirty years ago we dissected frogs for mus-cle and heart experiments and used kymo-graphs and stethographs. Heart rate andECG were measured using an old Devesesmachine and oxygen uptake was analysed bya Haldane gas analysis apparatus. If youturned the wrong tap you were in trouble.Then we used Douglas bags and Beckmanoxygen analysers and in the 1 980s we devel-oped an online system. Because studentslearn more by doing it themselves were areback to Douglas bags and 02/CO2 analysers.

Initially anthropometric measurementswere limited. Skin folds and somatotypemeasurements were often taken, but my firstattempt to measure body composition in thelab was by volumetric displacement using awooden tank painted liberally with yachtvarnish. I even got the engineers at BrightonPolytechnic to make a helium dilutionapparatus, which looked like a coffin andstill leaked gases. Now we have a speciallaboratory and a large plastic tank for

underwater weighing that takes over a tonof water without any leaks! When will weget DXA, magnetic resonance imaging orcomputed tomography?When I started teaching we had a small

fourth year BEd group. Most of the lecturerswho taught physiology especially to physicaleducation students, were PE teachers withan interest in physiology and anatomy. Therewas no sports science. It was remarkable tosee the evolution of our discipline through-out my own career during which time I wentthrough four changes of establishment andhad to apply for my post three times. Nodoubt there will be as many changes-anddifferent colleges in the next 30 years-but Ishall not experience them. I retired inSeptember.

PETER BALEChelsea School ofPhysical Education,

Sports Science, Dance and LeisureTrevin TowersGaudick Road

Eastbourne BN20 7SP

Subcutaneous rupture of the Achilles tendon - NCBI

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