JBJS | Current Concepts Review - Rupture of the Achilles Tendon*

The Journal of Bone & Joint Surgery, Volume 81, Issue 7

Current Concepts Review | July 01, 1999

Current Concepts Review - Rupture of the Achilles Tendon*

NICOLA MAFFULLI, M.D., M.S., PH.D., F.R.C.S.(ORTH)†, ABERDEEN, SCOTLAND

The Journal of Bone & Joint Surgery. 1999; 81:1019-36

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Introduction

Achilles, the warrior and hero of Homer's Iliad, lends his name to the Achilles tendon, the thickest and strongest tendon in the human body¹³⁸. Thetis, Achilles's mother, made him invulnerable to physical harm by immersing him in the river Styx after learning of a prophecy that Achilles would die in battle. However, the heel by which he was held remained untouched by the water and thus Achilles had a vulnerable point. Achilles led the Greek military forces, which captured and destroyed Troy after killing the Trojan prince Hector. However, Hector's brother Paris killed Achilles by firing a poisoned arrow into his heel¹⁶⁴.

Hippocrates, in the first recorded description of an injury to the Achilles tendon, stated that "this tendon, if bruised or cut, causes the most acute fevers, induces choking, deranges the mind and at length brings death."²⁶ Ambroise Paré, in 1575, recommended that a ruptured Achilles tendon be strapped with bandages dipped in wine and spices, but advised that the result was dubious²⁷. Operative repair of a ruptured Achilles tendon was advocated in 1888 by another Frenchman, Gustave Polaillon²⁷, although an Arabian physician performed such procedures as early as the tenth century A.D. In the twelfth century, an Italian surgeon, Guglielmo di Faliceto, believed that nature was unable to unite divided tendons and that operative treatment was necessary²⁷.

Much research has been performed to elucidate the etiology of a rupture of the Achilles tendon, but its true nature still remains unclear¹⁹⁰. Also, the best method of treatment is still fiercely debated. Some physicians advocate operative repair, whereas others insist that an operation is unnecessary and poses an unacceptable risk.

*No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. Funds were received in total or partial support of the research or clinical study presented in this article. The funding source was Wellcome Trust, London, England.

†Department of Orthopaedic Surgery, University of Aberdeen Medical School, Polwarth Building, Foresterhill, Aberdeen AB25 2ZD, Scotland. E-mail address: n.maffulli@abdn.ac.uk.

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Fig. 1 Graph showing the stress-strain curve for tendon. Wavy lines indicate the wavy configuration of the tendon at rest, straight unbroken lines indicate the effect of tensile stresses (at strain levels of less than 4 percent, the tendon can regain its original configuration on removal of the load), one or two broken lines indicate that the collagen fibers are starting to slide past one another as the intermolecular cross-links fail, and the set of completely broken lines indicate macroscopic rupture due to the tensile failure of the fibers and the interfibrillar shear failure. (Modified from: Kannus, P.: Tendon pathology: basic sciences and clinical applications. Sports Exerc. and Injury, 3: 62, 1997. Reprinted with permission.)

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Fig. 2 Photographs showing the appearance of the feet of an eighty-year-old woman who had bilateral rupture of the Achilles tendon; she had been managed with orally administered corticosteroids for twenty-eight years because of asthma. The ruptures had been undiagnosed for 7.5 months. At the time of referral, the patient walked with plantigrade feet, with no push-off. She refused any management, as she perceived that she had adapted well to the functional deficit originating from the ruptures of the tendons. A palpable gap in the substance of the Achilles tendon was evident bilaterally (arrows).

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Fig. 3 Photograph showing breakdown of the wound after operative repair of a rupture of the Achilles tendon. The patient had removed the cast against medical advice at four weeks after the operation and had returned to playing volleyball. At his first jump, the skin broke down.

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Fig. 4 Photograph showing a repeat rupture in a fifty-four-year-old man who was originally managed nonoperatively. The repeat rupture occurred when the patient stumbled on a step as he was going to work seven months after the original injury. Note the presence of the plantaris longus tendon.

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Fig. 5 Photograph showing a rupture that had been unrecognized for four months in a forty-seven-year-old male farmworker. Note the hypertrophic paratenon and the rounded-off tendon stump.

The Achilles Tendon

The tendinous portions of the gastrocnemius and soleus muscles merge to form the Achilles tendon. The plantaris muscle, which was present in 93 percent (752) of 810 lower extremities in one study³⁸, is medial to the Achilles tendon and is distinct from it. The gastrocnemius tendon originates as a broad aponeurosis at the distal margin of the muscle bellies³⁸, whereas the soleus tendon begins as a band proximally on the posterior surface of the soleus muscle. The length of the gastrocnemius component ranges from eleven to twenty-six centimeters³⁸ and that of the soleus component, from three to eleven centimeters. Distally, the Achilles tendon becomes progressively rounded in cross section, to a level four centimeters proximal to the calcaneus, where it can become relatively flatter³⁸, before inserting on the superior calcaneal tuberosity¹⁹¹. The fibers of the Achilles tendon spiral through 90 degrees during its descent, such that the fibers that lie medially in the proximal portion become posterior distally. In this way, elongation and elastic recoil within the tendon are possible, and stored energy can be released during the appropriate phase of locomotion². Also, this stored energy allows the generation of higher shortening velocities and greater instantaneous muscle power than could be achieved by contraction of the triceps surae alone². The calcaneal insertion of the Achilles tendon is highly specialized^157,158, as it is composed of the attachment of the tendon, a layer of hyaline cartilage, and an area of bone not covered by periosteum. A subcutaneous bursa may lie between the tendon and the skin to reduce friction between the tendon and the surrounding tissues. A retrocalcaneal bursa lies between the tendon and the calcaneus¹⁹¹.

Structure of the Tendon

Tendons act as transducers of the force produced by muscle contraction to bone. Collagen accounts for 70 percent of the dry weight of a tendon¹³⁸. Approximately 95 percent of tendon collagen is type-I collagen, with a very small amount of elastin^10,35. Elastin can undergo as much as 0 percent strain before failure¹⁵³. If it were present in the tendon in high proportions, there would be a decrease in the magnitude of force transmitted to bone¹⁵⁰.

Collagen fibrils are bundled into fascicles containing blood and lymphatic vessels as well as nerves¹⁵⁴. The fascicles are grouped together, surrounded by epitenon, and form the gross structure of the tendon, which is further enclosed by paratenon, separated from the epitenon by a thin layer of fluid to allow tendon movement with reduced friction.

Although the normal Achilles tendon consists almost entirely of type-I collagen, a ruptured Achilles tendon also contains a substantial proportion of type-III collagen³⁵. Fibroblasts from ruptured Achilles tendons produce both type-I and type-III collagen on culture¹⁸⁷. Type-III collagen is less resistant to tensile forces and may therefore predispose the tendon to spontaneous rupture.

The normal Achilles tendon shows a well organized cellular arrangement¹⁷⁴, in stark contrast to one that is ruptured. Tenocytes, which are specialized fibroblasts, appear in transverse sections as stellate cells and are arranged in rows in longitudinal sections¹⁵⁴. This orderly arrangement probably is due to the uniform centrifugal secretion of collagen around the column of tenocytes¹⁷⁰, which produce both the fibrillar and the nonfibrillar components of the extracellular matrix¹⁴⁵ and may also reabsorb collagen fibers^19,161.

Blood Supply

Tendons can receive their blood supply from vessels originating from three sources: the musculotendinous junction, the surrounding connective tissue, and the bone-tendon junction¹³². The blood flow of the Achilles tendon depends on age, with a higher blood flow in younger individuals⁶⁶. The Achilles tendon is poorly vascularized, especially in its midportion⁹², with blood vessels running from the paratenon into its substance^47,161. There is a dispute concerning the distribution of blood vessels in the tendon⁵⁶. Some investigations have shown that the density of blood vessels in the middle part of the Achilles tendon is low compared with that in the proximal part¹⁰¹. Others have shown, with use of laser Doppler flowmetry, that blood flow is evenly distributed throughout the Achilles tendon and may vary according to age, gender, and loading conditions⁹.

Biomechanics of the Tendon

Actin and myosin are present in tenocytes⁷⁶, and the tendon itself may have an active contraction-relaxation mechanism, which could regulate the transmission of force from muscle to bone⁵⁴. Fukashiro et al.⁵⁵ measured a peak force of 2233 newtons within the human Achilles tendon in vivo. Komi et al.⁹⁶ used buckle-type force-transducers attached to the ankles of volunteers to show that, during walking, force builds up within the tendon before the heel strikes the ground. The force is then suddenly released for ten to twenty milliseconds during early impact. Thereafter, force builds up relatively fast until it reaches a peak at the end of the push-off phase, in a pattern similar to that observed during running. More recently, Arndt et al.⁵ showed that the Achilles tendon can be subjected to nonuniform stresses through modifications of individual muscle contributions. An injury therefore can be produced by a discrepancy in individual muscle forces caused, for example, by asynchronous contraction of the various components of the triceps surae or by uncoordinated agonist-antagonist muscle contraction due to impaired transmission of peripheral sensory stimuli¹²⁵.

At rest, a tendon has a wavy configuration, a result of crimping of the collagen fibrils¹³⁸. Tensile stresses cause the loss of this wavy configuration, accounting for the toe-region of the stress-strain curve (Fig. 1). As collagen fibers deform, they respond linearly to increasing tendon loads⁹³. If the strain placed on the tendon remains at less than 4 percent—that is, within the limits of most physiological loads¹³⁸—the fibers regain their original configuration on removal of the load. At strain levels between 4 and 8 percent, the collagen fibers start to slide past one another as the intermolecular cross-links fail. At strain levels of greater than 8 percent, macroscopic rupture occurs because of the tensile failure of the fibers and interfibrillar shear failure¹³⁸.

The compliance of the tendon is dependent at least in part on intratendinous waviness²⁹, which may affect the ability of the gastrocnemius-soleus muscle complex to generate force at the extremes of joint motion⁶⁸. Ultimately, it may also influence the forces exerted by muscle contraction on the tendon and, hence, the propensity of the tendon to rupture.

Epidemiology

Although ruptures of the Achilles tendon are relatively common, the incidence in the general population is difficult to determine but has probably increased during the past decade¹⁰⁴. Leppilahti et al.¹⁰⁵ estimated that the incidence of ruptures of the Achilles tendon in the city of Oulu, Finland, in 1994, was approximately eighteen per 100,000. Most ruptures of the Achilles tendon (range, 44 percent [twelve of twenty-seven]¹⁴⁴ to 83 percent [ninety-two of 111]³¹) occur during sports activities. In the Scandinavian countries, badminton players appear to be at particular risk⁴⁹; in a large study, fifty-eight (52 percent) of 111 patients who had a rupture of the Achilles tendon were playing badminton at the time of the injury³¹. A rupture of the Achilles tendon is more common in males, with a male-to-female ratio ranging from 1.7:1 to 12:1^26,146,189, possibly reflecting the greater prevalence of males than females who are involved in sports, although there may be other as yet unrecognized factors. The left Achilles tendon is ruptured more frequently than the right^67,172,173, possibly because of a higher prevalence of individuals who are right-side-dominant and thus push off with the left lower limb. Typically, acute ruptures of the Achilles tendon occur in men who are in the third or fourth decade of life, work in a white-collar profession, and play a sport occasionally^22,67,82.

The prevalence of rupture of the Achilles tendon has been shown to be greater in patients who have blood group O, at least among Hungarians⁸⁰ and in some Finns⁹⁹. These findings have not been confirmed in other studies¹²⁸ even when the same ethnic groups were involved¹⁰⁵. We were not able to prove an association with blood group in our area of Scotland, which has a high incidence of rupture of the Achilles tendon¹⁵².

Etiology

Spontaneous rupture of the Achilles tendon has been associated with a multitude of disorders, such as inflammatory and autoimmune conditions⁴⁶, genetically determined collagen abnormalities⁴², infectious diseases⁷, and neurological conditions¹²⁶. However, there is little agreement with regard to its etiology.

A disease process may predispose the tendon to spontaneous rupture from minor trauma¹¹⁴. Blood flow in the tendon decreases with increasing age⁶⁶, and the area of the Achilles tendon that is typically prone to rupture is relatively avascular compared with the rest of the tendon^100,101,161.

Histological evidence of collagen degeneration was found in all seventy-four ruptured Achilles tendons described in a study by Arner et al.⁷. However, nearly two-thirds of the specimens were obtained more than two days after the rupture. Davidsson and Salo⁴⁰ reported marked degenerative changes in two patients with a rupture of the Achilles tendon who had an operation on the day of the injury. The changes, therefore, should be regarded as having developed before the rupture. In a study by Waterston¹⁸⁷, performed at our center, all tendons that were operated on within twenty-four hours after the injury showed marked degenerative changes and collagen disruption, in accordance with the findings in another recent study⁷⁸.

Alternating exercise with inactivity could produce the degenerative changes seen in tendons⁹⁷. Sports in addition to daily activity places additional stress on the Achilles tendon, leading to the accumulation of trauma, which, although below the threshold for frank rupture¹⁸⁸, could lead to secondary intratendinous degenerative changes⁵³.

Corticosteroids and Rupture of the Tendon

Corticosteroids are administered for a variety of diseases and have been widely implicated in tendon ruptures. Injection of hydrocortisone into the calcaneal tendons of rabbits caused necrosis at the site of injection forty-five minutes after the injection, and the tendons that had been given an injection of corticosteroids showed a delayed healing response compared with those that had received an injection of saline solution¹¹. The anti-inflammatory and analgesic properties of corticosteroids may mask the symptoms of tendon damage⁴⁵, inducing individuals to maintain high levels of activity even when the tendon is damaged. Corticosteroids interfere with healing, and intratendinous injection of corticosteroids results in weakening of the tendon for as many as fourteen days⁹¹. The disruption is directly related to collagen necrosis, and restoration of the strength of the tendon is attributable to the formation of an acellular amorphous mass of collagen. For these reasons, vigorous activity should be avoided for at least two weeks after injection of corticosteroids in the vicinity of a tendon⁹¹. Unverferth and Olix¹⁸³ reported a subcutaneous rupture in five athletes who had been given injections of corticosteroids in the region of the Achilles tendon for the treatment of tendinopathy. Residua of the corticosteroids were found at the site of the rupture in four of the five patients. A meta-analysis recently has shown that corticosteroid injections do not seem to play a beneficial role in the treatment of Achilles tendinopathy¹⁶⁵.

Orally administered corticosteroids also have been implicated in the etiology of tendon rupture. At our center, twelve patients who were managed with long-term oral therapy with corticosteroids for the treatment of chronic obstructive small airways disease were diagnosed with a rupture of the Achilles tendon during a ten-year period. Four of them sustained a bilateral injury¹³⁶ (Fig. 2).

It still is not possible to pinpoint the etiological role of corticosteroids¹²⁷, and some studies have not demonstrated deleterious effects of these agents. For example, McWhorter et al.¹¹⁵ demonstrated that a single injection of hydrocortisone acetate in a traumatized calcaneal tendon of a rat had no important biomechanical or histological adverse effect. However, given the present evidence, prolonged oral administration and repeated peritendinous injection of corticosteroids probably should be avoided.

Fluoroquinolones and Rupture of the Tendon

Fluoroquinolone (4-quinolone) antibiotics such as ciprofloxacin recently have been implicated in the etiology of rupture of the tendon. In France, between 1985 and 1992, 100 patients who were being managed with fluoroquinolones had tendon disorders, which included thirty-one ruptures¹⁵⁶. Many of these patients also had received corticosteroids, so it is difficult to implicate only the fluoroquinolones. Szarfman et al.¹⁷⁶ noted that studies have shown that animals that received fluoroquinolone in doses close to those administered to humans had disruption of the extracellular matrix of cartilage, which exhibited as fissuration and chondrocyte necrosis, as well as depletion of collagen. The abnormalities seen in animals might also occur in humans. Szarfman et al. recommended that the labeling on packaging for fluoroquinolone be updated to include a warning about the possibility of tendon rupture. In its recommendations on the use of this class of antibiotics, the British National Formulary suggested that "at the first sign of pain or inflammation, patients should discontinue the treatment and rest the affected limb until the tendon symptoms have resolved."²⁴

Recently, Bernard-Beaubois et al.¹⁶ found laboratory evidence of direct deleterious effects of fluoroquinolones on tenocytes. They suggested that pefloxacin, a fluoroquinolone, does not affect transcription of type-I collagen but decreases the transcription of decorin at a concentration of only 10^-4 millimoles. The resulting decrease of decorin may modify the architecture of the tendon, altering its biomechanical properties, and produce increased fragility.

Hyperthermia and Rupture of the Tendon

As much as 10 percent of the elastic energy stored in tendons may be released as heat⁹². Wilson and Goodship¹⁹² evaluated the temperatures generated in vivo within equine superficial digital flexor tendons during exercise. A peak temperature of 45 degrees Celsius (a temperature at which tenocytes can be damaged⁴) was measured within the core of the tendon after just seven minutes of trotting. Exercise-induced hyperthermia therefore may contribute to tendon degeneration. As good blood supply to tissues should help to cool overheating, tissues such as the Achilles tendon, which has relatively avascular areas, may be more susceptible to the effects of hyperthermia.

The Mechanical Theory

McMaster¹¹⁴ proposed that a healthy tendon would not rupture, even when subjected to severe strain. However, Barfred^13-15 demonstrated that, if straight traction were applied to a tendon, as in McMaster's experiments, the risk of rupture would be distributed equally to all parts of the muscle-tendon-bone complex. If oblique traction were applied, the risk of rupture would be concentrated on the tendon. He calculated that, if a 1.5-centimeter-wide Achilles tendon in a human were subjected to traction with 30 degrees of supination on the calcaneus, the fibers on the convex aspect of the tendon would be elongated by 10 percent before the fibers on the concave side would be strained. Therefore, the risk of rupture would be greatest when the tendon was obliquely loaded, when the muscle was in maximum contraction, and when the initial length of the tendon was short. Such factors are probably all present in movements occurring in many sports that require rapid push-off. Barfred's theory is largely supported by that of Guillet et al. (reported in a study by Postacchini and Puddu¹⁴⁴), who proposed a purely traumatic theory for rupture of the tendon in young healthy patients. A healthy tendon may rupture after a violent muscular strain in the presence of certain functional and anatomical conditions. These include incomplete synergism of agonist muscle contractions, a discrepancy in the thickness quotient between muscle and tendon, and inefficient action of the plantaris muscle acting as a tensor of the Achilles tendon.

Participation in sports plays a major role in the development of problems with the Achilles tendon, and training errors are a major factor^33,39,62,69. The flared heel on most sport shoes forces the hindfoot into pronation when the heel strikes the ground¹³⁶, and the heel tabs on some shoes may play a similar role. Clement et al.³⁴, in a study on the etiology of Achilles tendinopathy, found that sixty-one (56 percent) of 109 athletes displayed a so-called functional overpronation of the foot on heel-strike, with a whipping action of the Achilles tendon. Exaggeration of this whipping action may lead to intratendinous microtears. Poor flexibility of the gastrocnemius-soleus unit was also considered to contribute to overpronation^33,39. Unequal tensile forces on different parts of the tendon may produce a so-called torsional ischemic effect—that is, transient vasoconstriction of the intratendinous vessels—and therefore contribute to the vascular impairment already present within the Achilles tendon³⁴.

Inglis and Sculco⁷⁵ proposed that malfunction or suppression of the proprioceptive component of skeletal muscle predisposes athletes to rupture of the Achilles tendon. They believed that athletes who resume training after a period of rest are particularly susceptible to rupture of the Achilles tendon as a result of this malfunction.

Knörzer et al.⁹⁵ used x-ray diffraction spectra to study the behavior of the structure of collagen during tendon-loading. Tendons that rupture without previous degenerative changes are damaged initially at the submicroscopic fibrillar level because of a process of intrafibrillar sliding, which occurs a few seconds before macroscopic slippage of collagen fibers. Therefore, rupture of tendons unaffected by degenerative changes may result from the accumulation of fibrillar damage. Such findings support the theory that a complete rupture is the consequence of multiple microruptures and that tendon damage must reach a critical point, after which failure occurs.

Mechanism of Rupture

Arner and Lindholm⁸ classified the trauma resulting in the rupture in ninety-two patients into three main categories. The first category was pushing off with the weight-bearing forefoot while extending the knee. This movement is seen in sprint starts and in jumping in sports such as basketball. This mechanism accounted for 53 percent of the ruptures in their series. The second category was sudden, unexpected dorsiflexion of the ankle, such as that occurring when the foot slips into a hole or the individual falls down stairs. This mechanism accounted for 17 percent of the ruptures. The third category was violent dorsiflexion of a plantar flexed foot, such as may occur after a fall from a height. This mechanism was reported by 10 percent of their patients. The exact mechanism of injury could not be identified for the rest of their patients.

Pathological Characteristics

In 1976, Puddu et al.¹⁴⁶ proposed a system to classify abnormalities of the tendon. The major categories were paratendinitis, paratendinitis with tendinosis, and pure tendinosis. The term tendinosis describes the degenerative processes occurring within the tendon. Tendinosis includes a number of pathological processes, such as hyaline degeneration with a decrease in the normal cell population, mucoid degeneration with chondroid metaplasia or fatty degeneration of tenocytes, lipomatous infiltration of large areas of tendon, an increase in matrix mucopolysaccharides, and fibrillation of collagen fibers. A rupture of a tendon may be the result of this process. In the opinion of Puddu et al., tendinosis is symptomless and is discovered only on rupture of a tendon. Patients who have symptoms before the rupture of a tendon commonly have a combination of peritendinitis and tendinosis, and it is possible that a patient who has tendinosis may become symptomatic because of paratendinopathy, which may accompany tendinosis. Kannus and Józsa⁸⁷ noted that only one-third of the 891 patients in their study had symptoms before rupture of the tendon. We found that only nine (5 percent) of the 176 patients managed because of a rupture of the Achilles tendon at our center between January 1990 and December 1995 had had previous symptoms^151,187.

Arner and Lindholm⁸ reported that all ninety-two ruptured Achilles tendons that they examined histologically had degenerative changes, including edematous disintegration of tendon tissue, patches of mucoid degeneration, and a marked inflammatory reaction. They also noted that approximately one-quarter of the larger-caliber arteries in the peritendinous tissue exhibited pathological hypertrophy of the tunica media and narrowing of the lumen.

Kannus and Józsa⁸⁷ noted pathological alterations, 97 percent of which were degenerative changes, in all of the 891 spontaneously ruptured tendons from all of the sites that they studied. The most common degenerative lesion was hypoxic degeneration, with alterations in the size and shape of mitochondria, abnormal tenocyte nuclei, and occasional intracytoplasmic or mitochondrial calcium deposition. In advanced degeneration, hypoxic or lipid vacuoles and necrosis may be observed. Aberrant collagen fibers also can be seen, with abnormal variations in the diameter, angulation, splitting, and disintegration of the fibers. Kannus and Józsa also noted vascular changes, mostly luminal narrowing due to hypertrophy of the arterial intima and media, in vessels of the tendon and paratenon in 62 percent of the 891 ruptures. Alterations in blood flow, subsequent hypoxia, and impaired metabolism may have been factors in the development of the degenerative changes observed in the ruptured tendons⁸⁷. The interval between the rupture and the repair was short enough to suggest that the degenerative changes were preexisting.

Failure of the cellular matrix also may lead to intratendinous degeneration¹⁰³. Józsa et al.⁸² observed fibronectin on the torn surfaces of ruptured Achilles tendons. Fibronectin normally is located in basement membranes, is present in a soluble form in plasma, and binds more readily to denatured collagen than to normal collagen⁴⁸, indicating preexisting denaturation of collagen.

Presentation and Diagnosis

Patients who have a rupture of the Achilles tendon typically are first seen with a history of sudden pain in the affected leg, and they often report that, at the time of the injury, they thought that they had been struck by an object or kicked in the posterior aspect of the distal part of the leg. Some patients report an audible snap. They often are unable to bear weight and notice weakness or stiffness of the affected ankle⁴⁴. Rupture of the Achilles tendon may be associated with insufficient warm-up exercises before sports⁶¹, with the injury occurring late in a game. Patients who have a chronically ruptured Achilles tendon also tend to have a fairly typical history; they often recall only very minor or perhaps no trauma and that they first noticed the injury because of an inability to complete everyday tasks such as climbing stairs⁶⁷.

Examination may reveal diffuse edema and bruising⁴⁴, and, unless the swelling is severe, a palpable gap may be felt along the course of the tendon⁴⁴. The site of the rupture is usually two to six centimeters proximal to the insertion of the tendon⁴⁴. Krueger-Franke et al.⁹⁸ measured the location of the rupture intraoperatively in 303 patients and ascertained that, on the average, it was 4.78 centimeters proximal to the insertion of the tendon on the calcaneus.

In general, rupture of the Achilles tendon does not pose diagnostic problems¹²⁴. However, even in teaching centers, it is not uncommon to find that more than 20 percent of such injuries (sixteen of seventy-three in one study⁷⁴) are missed by the first doctor to examine the patient. There are a number of diagnostic signs and tests, both clinical and radiographic, that the examiner may use to aid in diagnosis.

Clinical Tests

Calf-squeeze test: The description of the calf-squeeze test is often credited to Thompson^120,122,123, who described the test in 1962^179,180, five years after Simmonds¹⁶⁶. With the patient prone on the examining table and the ankles clear of the table, the examiner squeezes the fleshy part of the calf. Squeezing the calf deforms the soleus muscle, causing the overlying Achilles tendon to bow away from the tibia, resulting in plantar flexion of the ankle if the tendon is intact¹⁶². The affected leg should always be compared with the contralateral leg¹⁶⁶. A false-positive finding may occur in the presence of an intact plantaris tendon, although this has not been proved scientifically.

Knee-flexion test: The patient is asked to actively flex the knees to 90 degrees while lying prone on the examining table. During this movement, if the foot on the affected side falls into neutral or dorsiflexion, a rupture of the Achilles tendon can be diagnosed¹³⁰.

Needle test: A hypodermic needle is inserted through the skin of the calf, just medial to the midline and ten centimeters proximal to the insertion of the tendon. The needle is inserted until its tip is just within the substance of the tendon. The ankle is then alternately placed in plantar flexion and dorsiflexion. If, on dorsiflexion, the needle points distally, the portion of the tendon distal to the needle is presumed to be intact. If the needle points proximally, there is presumed to be a loss of continuity between the needle and the site of the insertion of the tendon¹³⁹.

Sphygmomanometer test: For this test, a sphygmomanometer cuff is wrapped around the midpart of the calf while the patient is lying prone. The cuff is inflated to 100 millimeters of mercury (13.33 kilopascals) with the foot in plantar flexion. The foot is then dorsiflexed. If the pressure rises to approximately 140 millimeters of mercury (18.66 kilopascals), the musculotendinous unit is presumed to be intact. If, however, the pressure remains at around 100 millimeters of mercury (13.33 kilopascals), then a rupture of the Achilles tendon may be diagnosed³⁶.

A recent study of 174 patients managed at our institution because of a rupture of the Achilles tendon demonstrated little or no difference in the predictive values among the just described tests¹²⁵. The diagnosis of complete rupture of the Achilles tendon was certain if the results of at least two of these clinical tests were positive¹²⁵.

Imaging

Plain radiography: Lateral radiographs of the ankle have been used to diagnose a rupture of the Achilles tendon. When the Achilles tendon is ruptured, Kager's triangle⁸⁵, the fat-filled triangular space anterior to the Achilles tendon and between the posterior aspect of the tibia and the superior aspect of the calcaneus, loses its regular configuration. Toygar's sign¹⁸¹ involves measurement of the angle of the posterior skin-surface curve seen on plain radiographs, as the ends of the tendon are displaced anteriorly after a complete tear. The posterior aspect of Kager's triangle then approaches the anterior aspect, and the triangle decreases or disappears. An angle of 130 to 150 degrees indicates a rupture of the Achilles tendon. Arner et al.⁶ found that deformation of the contours of the distal segment of the tendon resulting from loss of tone was the radiographic change most likely to be associated with rupture of the Achilles tendon.

In general, clinical examination is sufficient for a diagnosis of acute rupture of the Achilles tendon. Ruptures that are more long-standing may be harder to diagnose because of associated tissue swelling. Real-time high-resolution ultrasonography and magnetic resonance imaging provide an adjunct to clinical diagnosis, and they are more sensitive and less invasive than soft-tissue radiography or xeroradiography^122,123.

Ultrasonography: Ultrasonography of the Achilles tendon with linear probes produces a dynamic and panoramic image of the tendon³⁷, the appearance of which varies with the type of transducer that is used and the angle of the ultrasound beam with respect to the tendon¹¹⁷. High-frequency probes of 7.5 to 10.0 megahertz provide the best resolution, but they have a short focusing distance⁵¹. The Achilles tendon is composed of longitudinally arranged collagen bundles, which reflect the ultrasound beam. The probe should be held at right angles to the tendon to ensure that an optimum amount of ultrasonic energy is returned to the transducer³⁷, avoiding the production of artifacts⁵¹. Linear-array transducers, therefore, are better suited than sector-type transducers, which produce excess obliquity of the ultrasound beam at the edges. It also may be necessary to use a synthetic gel spacer or stand-off pad, which increases the definition of the surface echoes and allows a suitable support¹². A normal Achilles tendon appears as a hypoechogenic, ribbon-like image that is contained within two hyperechogenic bands. Tendon fascicles appear as alternate hypoechogenic and hyperechogenic bands that are separated when the tendon is relaxed and are more compact when the tendon is strained¹². Men have slightly thicker tendons than women⁸⁶. Rupture of the Achilles tendon is seen on ultrasonography scans as an acoustic vacuum with thick, irregular edges^10,118. Campani et al.²⁵ conducted 170 ultrasonographic examinations for various types of traumatic injury of the lower limb. The Achilles tendon had the highest percentage of positive findings (75 percent); in comparison, only 38 percent of the findings in the thigh were positive for a lesion. In a study that I did with two colleagues, we showed that ultrasonography is a suitable tool for assessing the structure of the tendon after operative repair¹¹⁹. Ultrasonography also can be used to study the elastic properties of the tendon; this is done by measuring the distance between an intratendinous hypoechogenic or hyperechogenic point and the calcaneus and by assessing how this distance changes with different forces exerted by the gastrocnemius-soleus complex⁵⁵.

Magnetic resonance imaging: The normal Achilles tendon is seen as an area of low signal intensity on all pulse sequences. The tendon is well delineated by the high signal intensity of the fat pad of Kager's triangle⁸⁵. Any increase in intratendinous signal intensity should be regarded as abnormal⁴³. T1 and T2-weighted images in the axial and sagittal planes should be used to evaluate suspected ruptures of the Achilles tendon. On T1-weighted images, a complete rupture of the Achilles tendon is identified as a disruption of the signal within the tendon. On T2-weighted images, the rupture is demonstrated as a generalized increase in signal intensity and the edema and hemorrhage at the site of the rupture is seen as an area of high signal intensity⁸⁴.

Treatment of Acute Rupture of the Achilles Tendon

The many techniques and procedures described for the treatment of an acutely ruptured Achilles tendon can be grouped under three headings: open operative, percutaneous operative, and nonoperative. As there is no agreed-on protocol, the choice of treatment regimen is still based largely on the preference of the surgeon and the patient¹⁰⁸. Nonoperative treatment has its supporters, but operative treatment has been the method of choice in the last two decades for athletes and young people and for patients who have a rupture for which treatment has been delayed. Acute ruptures in nonathletes may be treated nonoperatively. For example, in a prospective, randomized trial, forty patients who had an acute complete rupture of the Achilles tendon were allocated either to immobilization in a cast for eight weeks or to immobilization in a cast for three weeks followed by controlled early mobilization in a Sheffield splint, which is an ankle-foot orthosis that holds the ankle in 15 degrees of plantar flexion but allows some movement at the metatarsophalangeal joints¹⁵⁹. The splint allows controlled motion of the ankle during physiotherapy. Patients managed with the splint regained mobility notably faster and preferred the splint to the plaster cast. The range of dorsiflexion of the ankle improved more rapidly after treatment with the splint, and patients were able to return to normal activities sooner. Recovery of plantar flexion power was similar in the two groups, and no patient had excessive lengthening of the tendon. One repeat rupture occurred in each group¹⁵⁹.

Open Operative Repair

The many operative techniques used to repair ruptured Achilles tendons range from simple end-to-end suturing, with Bunnell or Kessler-type sutures, to more complex repairs with use of fascial reinforcement or tendon grafts¹⁶⁹. Artificial tendon implants, with use of materials such as absorbable polymer-carbon fiber composites¹⁴¹, Marlex mesh (monofilament knitted polypropylene)^72,140, and collagen tendon prostheses⁸⁹, have been used. End-to-end suturing, which can be performed with local anesthesia¹⁶³, has been modified by use of materials such as Dacron vascular graft, which is passed through the tendon in a Bunnell-type fashion¹⁰⁹. Studies of dogs have shown that Dacron supports the growth of fibrous tissue¹³³ and facilitates the approximation of the ends of the tendon, causing less tension at the repair site than standard sutures¹⁰⁹. However, maturation of collagen may be favorably influenced by cyclical tensional stimuli¹³¹. Therefore, lack of tension on the repair site may not be advantageous.

Several authors have opposed operative repair, noting that the high rate of complications is the main disadvantage^{26,59,102,137,172,173}. Arner and Lindholm⁸, in a series of eighty-six operative repairs of ruptured Achilles tendons, reported a 24 percent rate of complications, including two instances of deep-vein thrombosis, one of which resulted in pulmonary embolism and death; three wound infections; eleven instances of wound necrosis; and four repeat ruptures. More recent studies have demonstrated a much lower rate of complications. Soldatis et al.¹⁶⁷, in a study of twenty-three patients who had operative repair, reported only two complications, both delayed wound-healing. The explanation for this low rate of complications may be greater operative experience combined with improved technique. However, wound problems should not be unexpected when open repair is used, as the most commonly used longitudinal incision passes through poorly vascularized skin⁶³ (Fig. 3). In a study of forty patients, Aldam¹ used a transverse incision just distal to the gap in the tendon and reported only one wound breakdown.

Several authors have proposed primary augmentation of the repair¹⁷⁷ with the plantaris tendon^112,148, the peroneus tendon¹⁴², a single central gastrocnemius fascial turndown flap²¹, or two such flaps (one medial and one lateral)¹¹⁰. However, there is no evidence that primary augmentation of a repair of an acute rupture of the Achilles tendon is any better than nonaugmented end-to-end repair⁷⁹. I prefer to use augmentation in delayed repairs and in the treatment of repeat ruptures.

After the operation, the leg is immobilized in a cast for four to six weeks^31,175. Some surgeons have advocated the use of a functional orthosis after several days of immobilization in a cast. This orthosis allows plantar flexion but restricts dorsiflexion and is designed to help to prevent atrophy of the triceps surae^28,160. Some surgeons allow free motion of the ankle but no weight-bearing after operative repair^134,168.

There is a never-ending controversy regarding the use of open operative techniques to manage subcutaneous ruptures of the Achilles tendon, with some investigators reporting a high overall rate of complications^20,58,77 and others noting few complications^30,60,71 and a low rate of repeat rupture^17,41,75.

Percutaneous Repair

Ma and Griffith¹¹⁶ developed a method for percutaneous repair as a compromise between open operative methods and nonoperative treatment. The technique involves producing six small stab incisions along the medial and lateral borders of the tendon and then passing a suture through the tendon with use of these incisions. In a small series of eighteen patients managed with this technique, Ma and Griffith reported only two minor, noninfectious skin complications and no repeat ruptures. Rowley and Scotland¹⁵⁵ described twenty-four patients at our center who had a rupture of the Achilles tendon; fourteen were managed with immobilization in a cast alone, with the ankle in the equinus position, and ten were managed with percutaneous repair. One patient who had percutaneous repair had entrapment of the sural nerve, but no other complications were encountered. The patients who were managed with sutures were more likely to regain nearly normal plantar flexion strength, and they also returned to activity sooner than the group managed with a cast alone. Other authors have reported a much lower success rate with this technique. Klein et al.⁹⁴ reported sural nerve entrapment in 13 percent of thirty-eight patients. Hockenbury and Johns⁷⁰ compared in vitro percutaneous repair of the Achilles tendon and open repair of the Achilles tendon with use of a transverse tenotomy of the Achilles tendon in ten fresh-frozen below-the-knee specimens from cadavera. The specimens were divided into two groups of five specimens each; one group had open repair of the Achilles tendon with use of the Bunnell suture technique, and the other had percutaneous repair with use of the technique of Ma and Griffith¹¹⁶. The tendons that were repaired with an open technique were able to resist almost twice the amount of ankle dorsiflexion before a ten-millimeter gap appeared in the repaired tendon compared with those that were repaired with a percutaneous technique (a mean of 27.6 degrees compared with a mean of 14.4 degrees; p < 0.05). Entrapment of the sural nerve occurred in three of the five specimens that had percutaneous repair. The tendon stumps sutured with use of the percutaneous technique were malaligned in four of the five specimens. On the basis of the findings in that study, it appears that percutaneous repair of a ruptured Achilles tendon provides approximately 50 percent of the initial strength afforded by open repair and places the sural nerve at risk for injury.

Percutaneously repaired Achilles tendons are less thick than are those repaired with open procedures, and some patients may prefer the better appearance that this may afford²³. Overall, most studies have demonstrated that the rate of repeat rupture after percutaneous repair is higher than that after open operative repair^3,23. Also, disturbingly high rates of transfixion of the sural nerve have been reported^70,155,171, with persistent paresthesias and the necessity of a formal operative exploration to remove the suture and free the nerve^50,94.

Nonoperative Treatment

The most commonly used form of nonoperative treatment is immobilization in a plaster cast, usually for a period of six to eight weeks³¹. Immobilization has been advocated by those who think that it produces results similar to those achieved with operative treatment^{26,59,102,137,172,173}. When the Achilles tendon ruptures, the paratenon generally remains intact¹⁷². Stripping of the paratenon during an operation reduces the amount of reactive tissue that is produced later at the site of the injury¹⁷². Those authors have therefore suggested that operative repair of a ruptured Achilles tendon should be avoided, as the paratenon provides a valuable blood supply to the damaged tendon. Lea and Smith¹⁰², in a study of fifty-five spontaneously ruptured Achilles tendons treated with eight weeks of immobilization in a plaster cast, reported that seven (13 percent) of the patients had a repeat rupture and only three patients were dissatisfied with the result. These results contrast sharply with those of Persson and Wredmark¹⁴³, who reported on twenty patients who were managed nonoperatively. Seven patients had a repeat rupture, and seven patients—not necessarily those who had a repeat rupture—were not satisfied with the result. Although function after nonoperative repair is generally good, the high prevalence of repeat rupture is considered unacceptable. A primary goal of the treatment of a rupture of the Achilles tendon is to avoid lengthening of the tendon, and this cannot be achieved with nonoperative treatment¹⁶⁹.

Recently, on the basis of results reported with use of functional postoperative bracing²⁸, McComis et al.¹¹³ managed fifteen patients nonoperatively with a functional bracing protocol to repair a rupture of the Achilles tendon. They achieved good functional results, proving that, for selected patients, nonoperative functional bracing may be a viable alternative to operative intervention or to use of a plaster cast for the treatment of an acute rupture of the Achilles tendon.

Some patients, especially those who are elderly, may be seen with a long-standing rupture that has been discovered by chance. These patients often adapt well to the disability, but they are warned that an operation may be necessary if the symptoms caused by the rupture of the Achilles tendon worsen. Such patients are followed at regular intervals, but they usually do not need additional treatment¹²⁵.

Physiological Effects of Immobilization After a Rupture of the Achilles Tendon

The cross-sectional area of a muscle is directly related to the muscle force that the muscle can develop^64,73, and immobilization results in a profound alteration of the morphological and physiological characteristics of a muscle¹⁴⁷. The soleus muscle appears to be particularly susceptible to the effects of immobilization, whereas the gastrocnemius, a biarticular muscle, is able to move when a below-the-knee cast is used and thus is less affected. The human soleus contains a high proportion of type-I muscle fibers⁶⁴, which are particularly susceptible to atrophy if immobilized, as they are responsible for postural tone and are continually activated while the person is standing¹⁸⁴. When the leg is immobilized, the muscle spindle relaxes and afferent impulses to type-I fibers cease, causing them to atrophy. The Achilles tendon is susceptible to the effects of prolonged immobilization⁸⁸. Problems due to immobilization occur after open operative repair as well as after percutaneous repair, but not to the same extent. Häggmark et al.⁶⁵ reported on fifteen subcutaneous ruptures of the Achilles tendon that were treated operatively and eight that were treated nonoperatively. They found a significant decrease in the circumference of the calf in the group that was treated nonoperatively (p < 0.01), whereas the group that was treated operatively showed no significant difference between the injured and the uninjured calf. Patients who have an open operative or percutaneous repair wear a plaster cast for less time³¹ than do those managed nonoperatively and on the whole are often more serious athletes who comply well with postoperative management regimens. The lack of tension on the immobilized musculotendinous unit is a major factor in the development of atrophy in the calf³¹. If optimum results from a repair of a ruptured Achilles tendon are necessary, the site of the repair should be put under as much tension as possible as early as possible⁶⁴ and the cast should be changed regularly, decreasing the angle of plantar flexion as much as possible each time.

A viable alternative is immobilization of the foot and ankle in a plantigrade position¹⁴⁹. This minimizes the number of changes of the plaster cast as well as the discomfort at the time of the changes when the ankle must be progressively dorsiflexed. It requires a sufficiently strong repair that can be subjected to early tensile stresses.

Operative Compared with Nonoperative Treatment

The results after operative treatment of ruptured Achilles tendons often have been compared with those after nonoperative treatment, but only a few well controlled, prospective, randomized trials have been conducted^31,137,193. A major problem is the lack of a valid, reliable, reproducible protocol for subjective and objective evaluation of the results of repair of a ruptured Achilles tendon¹⁰⁷.

Gillies and Chalmers⁵⁹ measured plantar flexion strength after operative and nonoperative treatment of a rupture of the Achilles tendon. Little difference was found between the two groups, and the results of the operation were not sufficiently superior to warrant the risk associated with use of anesthesia and an operation. Inglis et al.⁷⁴ followed forty-four patients who had been managed operatively and twenty-three who had been managed nonoperatively. No repeat ruptures occurred in the patients who had been managed operatively, but nine (39 percent) of the patients managed nonoperatively had a repeat rupture. Strength-testing revealed superior strength, power, and endurance after operative treatment, and the authors advocated the use of this type of management. Nistor¹³⁷ conducted a prospective, randomized trial that included 105 patients; forty-five had operative management, and sixty had nonoperative management. The rate of repeat rupture in the group managed operatively was 4 percent compared with 8 percent in the group managed nonoperatively. However, there were a large number of secondary complications in the group that had an operation. The patients who were managed nonoperatively were found to have less absence from work, less ankle stiffness, and similar strength compared with the operatively managed group. Nistor recommended nonoperative management, as there were only minor functional differences between the two groups and the operation caused more complications. In a study by Carden et al.²⁶, seventy-six patients were managed nonoperatively and fifty-six were managed operatively. The patients who were seen less than forty-eight hours after the injury were compared with those who were seen more than forty-eight hours after the injury. The overall rate of complications was 4 percent in the group managed nonoperatively compared with 17 percent in the group managed operatively. The subjective results were also better in the group managed nonoperatively. The authors concluded that patients who are seen less than forty-eight hours after the injury should be managed nonoperatively, with eight weeks of immobilization in a cast, whereas patients who are seen one week or more after the injury should be managed operatively.

In a randomized trial, twenty-two patients who had operative management were compared with twenty-eight who had nonoperative management; both groups had functional treatment with a newly developed boot¹⁷⁸. No significant differences were found between the groups with respect to either the functional results or the course of healing. The functional treatment in both groups allowed shorter periods of rehabilitation.

Kellam et al.⁹⁰ performed a review of the literature and identified 609 patients who had been managed operatively and 208 who had been managed nonoperatively. The rate of repeat rupture was 1 percent for the patients who had had an operation compared with 18 percent for the patients who had had nonoperative management. Also, 83 percent of the patients managed operatively and 69 percent of those managed with immobilization in a cast returned to the preinjury level of activity. In addition, 93 percent of the patients managed operatively and 66 percent of those managed nonoperatively were satisfied with the result of treatment.

Cetti et al.³¹, in a prospective, randomized study, reported on fifty-six patients who were managed operatively and fifty-five who were managed nonoperatively. The rates of complications and repeat ruptures were 9 and 5 percent, respectively, for the patients managed operatively compared with 16 and 15 percent, respectively, for the patients who were managed nonoperatively. The differences between the groups, however, were not found to be significant. The authors also conducted a review of the literature and identified 4597 ruptures of the Achilles tendon. Operative treatment of the ruptures was associated with lower rates of complications and repeat ruptures than was nonoperative treatment. Cetti et al. concluded that operative treatment was the method of choice, but nonoperative treatment was an acceptable alternative.

Recently, Lo et al.¹¹¹ performed a quantitative review of all of the studies on the treatment of rupture of the Achilles tendon in the English-language literature published between 1959 and 1997 to determine the optimum treatment of acute ruptures. All of the identified articles were reviewed independently by at least three of the four authors to decide the eligibility of each study on the basis of predetermined criteria. Eligible studies were reviewed independently, and the data were extracted with use of standardized coding forms. Inconsistencies in data extraction were settled by discussion and majority vote. The main outcomes extracted were strength, time until the patient returned to work, frequency of return to sports, rate of repeat rupture, and complications. Complications were classified as major, moderate, or minor. Lo et al. identified a total of 742 patients who were managed operatively and 248 patients who were managed nonoperatively. The overall rate of repeat rupture was 3 percent for those managed operatively and 12 percent for those managed nonoperatively (p < 0.001). Although the rate of repeat rupture after operative treatment was lower than that after nonoperative treatment, the rate of minor and moderate complications associated with operative treatment was twenty times greater in some reports (Fig. 4).

In summary, treatment should be individualized according to the concerns and health of the patient. If optimum performance is necessary, operative management is probably the treatment of choice. Operative management should be used in athletes and in patients who have a high level of physical activity. Percutaneous repair should be considered for patients who do not wish to have open repair, possibly for cosmetic reasons or perhaps because they view an open operative repair as a more serious procedure¹⁶⁰. Nonoperative treatment should be reserved for older patients who are unlikely to derive any major benefit from an operative procedure and for patients who view an operation as an unnecessary risk.

Treatment of an Older Rupture of the Achilles Tendon

When patients are operated on within seventy-two hours after the injury, it is usually possible to suture the stumps of the tendon in an end-to-end fashion¹²¹. However, more than 20 percent of patients who have a rupture of the Achilles tendon may be diagnosed late¹²². In these instances, young and middle-aged patients generally are first seen with a limp and severe impairment in the performance of day-to-day activities. When, after trimming, the tendon stumps cannot be approximated without undue tension (Fig. 5), the gap can be bridged with a single central gastrocnemius fascial turndown flap²¹ or with two such flaps (one medial and one lateral)¹¹⁰. If it is available, the tendon of the plantaris longus can be used as a reinforcing membrane¹¹².

When a patient has an extreme rupture, in which the gap resulting from the rupture of degenerated tissue does not allow direct suture, the tendons of the tibialis posterior and peroneus brevis can be split longitudinally and used as pedicled transplants. The plantaris tendon is used as reinforcement, and the construct is augmented by a turndown flap of the superficial aponeurosis of the gastrocnemius⁵².

More recently, Wapner et al.^185,186 used a transfer of the flexor hallucis longus muscle and tendon to provide a dynamic repair. The procedure was performed on seven patients with a mean age of fifty-two years. After a mean of seventeen months (range, three to thirty months), there were no postoperative infections, loss of skin, or repeat ruptures. Each patient had a small loss in the range of motion of the involved ankle and hallux, but it was of no functional importance. All patients were satisfied with the functional result, although one needed a molded foot-ankle orthosis for prolonged walking¹⁸⁵.

When the gap between the ends of the tendon is such that the ends cannot be juxtaposed, the gap can be bridged by Marlex (monofilament knitted polypropylene) or Dexon (polyglycolic acid) mesh^72,140, and tendon graft can be used to cover the mesh. Postoperatively, the patients should be managed more conservatively, with restricted weight-bearing and immobilization in a plaster cast for eight weeks instead of six weeks.

Postoperative Care

Normally, patients are discharged on the day of the operation or the next day, after an orthopaedic physiotherapist has instructed them regarding the use of crutches^111,125. Patients are allowed to bear weight on the involved leg as tolerated, but they should be told to keep the affected leg elevated for as long as possible to prevent postoperative swelling¹²¹. Patients are followed on an outpatient basis at two-week intervals, and the cast is removed six weeks after the operation^119,121,125. If the cast has been applied with the ankle in the equinus position, the cast is changed at two and four weeks, with the ankle placed in gradually increasing dorsiflexion until a plantigrade position is reached. The cast is removed altogether six weeks after the operation¹¹⁹.

Patients are allowed partial weight-bearing and gradual stretching and strengthening exercises, increasing the frequency as tolerated, only after removal of the cast¹¹⁹. Gradually, patients proceed to full weight-bearing at eight to ten weeks after the operation.

During the period of immobilization in the cast, patients are instructed to perform gentle isometric contractions of the gastrocnemius-soleus complex after weight-bearing has become comfortable¹¹⁹. After removal of the cast, patients mobilize the ankle under the guidance of the physiotherapist. Two weeks after removal of the cast, cycling and swimming are started and the mobilization exercises of the ankle are continued. Patients are prompted to increase the frequency of the self-administered exercise program. Patients are normally able to return to sports activities in the third or fourth postoperative month.

Postoperative Management of Athletes

Treatment that avoids immobilization of the ankle should be considered for athletes and well motivated, reliable patients. These patients are managed with an anterior below-the-knee plaster-of-Paris slab applied with the ankle in gravity equinus²⁸. Patients are discharged on the day of the operation or the day after, and they are allowed toe-touch weight-bearing on the involved limb as tolerated. They are instructed to keep the involved leg elevated for as long as possible. At forty-eight to seventy-two hours after the operation, by which time the postoperative swelling (if any) has substantially decreased, the anterior below-the-knee plaster-of-Paris slab is changed to an anterior below-the-knee synthetic slab with the ankle in gravity equinus. The slab is kept in place by an elastic bandage, which allows plantar flexion of the ankle, while dorsiflexion is limited by the foot-piece of the slab²⁸. Patients are allowed weight-bearing as tolerated, with use of crutches. The slab is changed at the second and fourth postoperative weeks, so that the ankle can dorsiflex to neutral by the fourth postoperative week. The limitation of dorsiflexion is continued for a total of six weeks, at which time the slab is removed. High-level, well motivated athletes who comply with the postoperative protocol normally are able to return to sports activities six to eight weeks after the removal of the anterior slab. A hinged orthosis could be used as an alternative to the anterior slab¹²⁹. However, it is more expensive than a simple synthetic cast, although it is reusable.

Solveborn and Moberg¹⁶⁸ prospectively studied seventeen consecutively managed patients (fifteen men and two women) who had operative repair of a subcutaneous, complete acute rupture of the Achilles tendon. The patients were managed with a new postoperative regimen that allowed free motion of the ankle in a patellar ligament-bearing cast that had a protective frame under the foot to permit weight-bearing immediately after the operation. Early free motion of the ankle after repair of a ruptured Achilles tendon proved to be safe, with satisfactory clinical results.

Overview

The etiology of what would appear to be a simple condition still has not been completely clarified. Despite extensive investigation, few definitive answers have been found. The lack of study of human tissue is an important problem, but it is difficult to see how this could be overcome. It is notable that animal models of rupture of the Achilles tendon have relied mostly on tenotomy^18,83,135. The model developed by Barfred^13-15 hardly reflects clinical practice and has not found wide application.

The treatment of acute rupture of the Achilles tendon depends on the preference of the individual surgeon. Open operative repair probably produces better functional results than nonoperative management does, but it may lead to a higher rate of postoperative complications. Nonoperative management may result in a poorer functional result, but the problems of postoperative complications are avoided.

A major problem has been the lack of a universally accepted system for scoring results of treatment of a ruptured Achilles tendon. Leppilahti et al.^106,107 proposed a scoring scale that included subjective assessment of clinical factors and isokinetic evaluation of strength. However, it has been used only by those authors¹⁰⁷, and isokinetic dynamometry is time-consuming, expensive, and not widely available.

If the reports that have described a rising incidence of rupture of the Achilles tendon are accurate, the field of operative repair of the Achilles tendon will become an increasingly important one for orthopaedic surgeons. Future developments may include the use of adhesives in operations on the tendon¹⁸². An understanding of the role that cytokines play in tendon-healing³² also may lead to new treatments, possibly based on gene therapy⁵⁷. However, such novel interventions are unlikely to be in routine clinical use for some time.

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