12.20 Injuries to muscle–tendon units

Skeletal muscle is the human body’s largest single tissue by weight, comprising 40–45% of total body weight. Muscle’s main function is to generate power for movement and maintain posture. Other functions include storage of energy and blood volume and thermoregulation. Muscles have tendons at each end which insert into bone or fascia.

Muscle, the musculotendinous (or myotendinous) junctions, tendon, and bony insertion together form a muscle–tendon unit.

Acute injuries to muscle–tendon units are common and cause considerable morbidity due to the site of injury and the age of those affected. They can occasionally be life- or limb-threatening. Much clinical and research experience on these injuries is the result of work by sports medicine clinicians. Chronic injuries to muscle–tendon units are discussed in Chapters 4.6 and 8.9.

There are controversies and deficiencies regarding natural history, classification, and treatment of these injuries, particularly when one compares the literature on bony and articular surface injuries. An understanding of structure, pathology, and healing helps in understanding the basis of operative and surgical treatments.

Epidemiologic data regarding the incidence and prevalence of muscle–tendon unit injuries in the general population are poor. Some estimate a point prevalence of muscle injury of 1–2% of the population in industrialized countries.

These injuries are uncommon in young children, but the incidence increases in the second decade to peak and plateau in the third and fourth decades. There is then a decline in acute injuries, and chronic or acute-on-chronic problems increase in frequency. They are more common in males.

The most common type is the indirect minimal or partial muscle rupture. These are the most commonly occurring sports injuries, but are also frequent in the workplace and therefore have a significant economic impact. The economic cost in the of acute non-articular soft-tissue problems in the United Kingdom has been estimated at over £1 billion per year

The incidence of muscle–tendon unit injuries seems to be increasing, due to increasing awareness and demand for treatment and increased adult participation in regular sport and exercise.

Current classifications are mainly based on the site, cause, and severity of injury. Unfortunately there is continuing confusion over nomenclature and terminology, and controversy over indications and optimal modes of treatment.

Skeletal muscle consists of multinucleate myocytes or fibres containing myofibrils which provide its contractile properties. Groups of muscle fibres form fasciculi. Groups of fasciculi form the whole muscle. There are other cells within muscle, such as stellate cells, which have important functions in healing and regeneration. Layers of connective tissue around muscle are the endomysium, which provides the extracellular space, the perimysium, which surrounds the fasciculi, and the epimysium, which surrounds the whole muscle (Figure 12.20.1A). A rich nerve and blood supply runs within these layers. The circulation within muscle is nutritive or non-nutritive; the latter are impedance and storage channels. The connective tissue sheaths fuse at the musculotendinous junction with tendon connective tissue.

Tendons are mainly composed of type I collagen (70% by dry weight) and are relatively acellular. Bands of collagen fibrils form fasciculi, and groups of fasciculi form bundles. Fasciculi are surrounded by the endotenon, containing nerves and small blood vessels. The outer connective tissue layer is the epitenon, which lies in loose areolar tissue (paratenon) or within a tendon sheath (Figure 12.20.1B). Tendon sheaths and bursae occur where moving structures are in tight apposition. The nerve supply is mainly efferent and the blood supply is poor, running in plexi between fasciculi. Watershed areas where the tendon blood supply is poorest have been identified and are linked to tendon pathology and rupture.

The musculotendinous junction is the interface between muscle and tendon. There is an intimate relationship between muscle fibres and collagen fibrils but no direct continuity (Figure 12.20.1C). The sarcolemma has multiple finger-like invaginations, known as terminal interdigitations, providing a large contact area to which collagen fibrils adhere. Adhesion is aided by glycoproteins and type III collagen. The junction is densely packed with sarcoplasmic organelles, mitochondria, and satellite cells, indicating potential for growth, repair, and regeneration. There is a portal blood supply and a rich efferent nerve supply.

The osseotendinous junction is also known as the enthesis. Tendons attach to bone at the periosteum and cortical bone, where they intermingle with perforating fibres of Sharpey, thus firmly anchoring them. If the attachment to bone is smooth, it implies the presence of a fibrocartilaginous plate which has anchoring properties.

Muscle contraction, controlled by voluntary or reflex neural activity, produces a force depending on the number of muscle fibres available, muscle adaptation, muscle fibre type, muscle length, velocity of shortening, state of activation, and temperature.

Tendon properties vary depending on functional requirement, balancing tensile strength with elasticity. Tendons have high tensile strength, similar to bone, with 1cm² supporting 600–1000kg. Tendons display viscoelastic properties of stress relaxation, hysteresis, and creep. Overloading causes permanent lengthening damage—plastic deformation. Ultimate tensile strength is reached when all fibrils have failed—complete rupture.

The musculotendinous junction is important in force transmission, particularly during eccentric muscle contractions which occur in lengthening muscle; for example, landing from a jump causes eccentric contraction of the quadriceps, putting severe demands on the musculotendinous junction.

In vitro studies have shown that muscles tested to failure do so in the region of the musculotendinous junction on the muscle side of the junctional membrane. Muscle fatigue, prior injury, poorly conditioned muscle, and denervation all predispose strongly to. In human lower limbs, proximal rupture occurs in the proximal lower limb and distal rupture occurs in the distal lower limb. In the first and second decades the enthesis is the weakest part of the unit, and is thus more prone to injury.

The pathology of injury and healing are intimately connected. Injury incites an acute inflammatory response, of lag phase, lasting for 2–10 days, in proportion to and dependent on the degree of cellular injury and cell death. The inflammatory process will usually resolve and a cellular phase will commence. If there has been no tissue destruction, there is rapid resolution of the inflammatory exudate and return to normal, i.e. a grade I muscle injury. In the relatively avascular tendons, phases are prolonged. Sepsis or continuing injury will cause continuing inflammation. At 3–4 weeks postinjury the cellular regenerative phase will give way to a remodelling phase, which may go on for months.

Local and systemic factors influencing muscle–tendon unit healing are shown in Box 12.20.5.

Traditionally it was thought that muscle mainly healed by scarring. However, the capacity for muscle to compensate and return to full function by regeneration and hypertrophy has been demonstrated. Soon after muscle fibre injury, the fibres at each end of the injury zone break into short cylinders back to the next intact Z-disc and hypercontract, restricting the injury, although there is fibre necrosis. Rupture of epimyseal vessels cause intermuscular haematomas with extensive ecchymosis and mild pain. Central ruptures cause intermuscular haematomas with more localized swelling, intense pain, muscle inhibition, and stiffness.

As well as necrosis and haemorrhage, there is acute inflammatory response with oedema and cellular infiltrate including macrophages which appear on days 1–2, ingesting debris but leaving the basal laminas. Muscle fibres from each end produce myotubes from their sarcolemmas, along which muscle fibres regrow. Satellite cells attach to the myotubes at day 3 and aid regeneration. Fibroblasts are also activated at this time. Regeneration occurs most rapidly and completely in clean muscle incisions, but has been noted after all muscle injuries. There is always some scar tissue formation proportional to the amount of muscle loss; thus healed muscle does not return to normal ultrastructurally. Remodelling follows. There is good evidence that mobilization may reduce the amount of scar tissue formation.

Events at the musculotendinous junction are similar to but slower than those in muscle, with a central core of necrosis and a zone of hypercontracted fibres. Myotube formation occurs at 7–14 days, new sarcoplasmic contents appear at 21–28 days, and the cellular phase continues for 5–7 weeks postinjury.

In tendon the inflammatory response takes over 14 days to settle. The tendon ends fill with fibrinous clot and granulation.

Repair occurs by proliferation of fibroblasts, either tenocytes from the tendon or from surrounding connective tissue layers, which synthesize collagen commencing on day 7 and continuing for several weeks. Fibroblast numbers and metabolism peak at day 14 and then slowly decline. Tendon strength increases as collagen fibrils are formed and reorientate. By week 4 the tendon has regained 70% of its pre-rupture stiffness and 40% of its strength.

Remodelling commences at week 4. Eight weeks postinjury, peritendinous adhesions break down and the tendon strength continues to increase. The collagen fibres are realigned fully at 9 months and remodelling continues for a year postinjury. In sutured tendons the lowest breaking strength is at day 7. It is doubled at 2–3 weeks and again at 4–12 weeks postinjury.

Experimentally, cyclical loading and early mobilization improve collagen fibril realignment, capillary ingrowth, time to normal strength, and viscoelasticity, and reduce stiffness. Immobilization of muscle–tendon units reduces tensile strength at the musculotendinous junction, increases risk of strain injury, and causes a 30% reduction in vascular density following 3 weeks of immobilization.

Unlike other injuries, immobilization is a prerequisite for healing to occur. Given the age of the patients with disruptions at this level, healing is rapid and occurs by fracture-type healing of the bony avulsion.

In these two conditions, muscle injuries can cause limb- or life-threatening problems.

Compartment syndrome is caused by swelling confined by osseofascial compartments, causing interruption of the normal capillary arteriolar circulation which can result in a vicious cycle of cell death and further swelling, eventually causing infarction of muscle, nerves, and other structures within the compartment. Management of compartment syndromes is discussed in Chapter 12.2.

Crush syndrome may occur after any blunt trauma, classically entrapment or prolonged ischaemic revascularization injury where there has been extensive rhabdomyolysis causing release of muscle proteins and waste products. This leads to intravascular activation, circulatory collapse, and acute renal failure, which is also caused by intrinsic nephron damage by the free muscle products, frequently exacerbated by inadequate resuscitation.

Complications can be classified by time of onset from injury or by cause—the injury itself or iatrogenic (see Box 12.20.4).

The type and severity of injury to muscle–tendon units is determined by a number of factors summarized in Box 12.20.5. There is no equivalent to the comprehensive classification system for fractures.

Muscle injury can be divided broadly into indirect and direct injury, in terms of the force transmission causing injury.

Indirect muscle injuries are most common and are also known as muscle strain injury, intrinsic muscle injury, pulled muscle, muscle sprain, or muscle tear. They occur when an abnormal force is applied to a muscle usually when it is activated and contracting, often eccentrically. Other factors associated with indirect injuries are muscle conditioning, fatigue, warm-up or muscle stretch, muscle temperature, anabolic steroid use, and previous injury.

Indirect muscle injury occurs most commonly at the musculotendinous junction in adults, the tendon in older patients, and the enthesis in young adults. In older patients there is often underlying degeneration within the tendon.

Muscles prone to indirect injury are those which cross two joints, contract eccentrically, and have a high proportion of type II fast-twitch fibres. Common sites of indirect injury are the medial head gastrocnemius (tennis leg), triceps surae, rectus femoris, adductor longus, semimembranosus, triceps brachii, and pectoralis major.

Indirect injuries form a spectrum from minor sprains to complete muscle ruptures, which have been graded as follows.

Direct muscle injuries are divided into open and closed injuries. Closed injuries generally occur as a direct blow or crush as the result of sports injury (also known as extrinsic injury), blunt assault, industrial accidents, or road traffic collisions. Open injuries are associated with a sharp laceration or tissue loss such as those caused by glass, open fracture, gunshot injury, or burn. Direct injuries also form a spectrum from minimal to severe, and the O’Donoghue grading can be applied.

Other causes of muscle cell injury are injuries to structures such as major blood vessels or nerves which result in muscle fibre death or dysfunction. Compartment syndromes can also cause muscle fibre death.

Definitive management of patients with muscle–tendon unit injuries involves diagnosis treatment and rehabilitation of the patient. (This is summarized later in Box 12.20.9.) The terms emergency, initial treatment, and definitive treatment are not mutually exclusive; initial treatment of an indirect muscle injury is often definitive as well.

The first aim is to ensure the patient does not have a life- or limb-threatening condition; if this is the case the patient should be resuscitated and treated appropriately.

Clinical assessment involves history and examination, which is sufficient to diagnose most isolated injuries to muscle–tendon units. Compartment and crush syndromes, other injuries, and comorbidity should be identified, and this guides the need for further investigation and treatment. Initial clinical assessment is also a baseline for monitoring progress. Thorough note taking is advisable, particularly if treatment is going to be prolonged and multidisciplinary.

A number of conditions can be mistaken for acute muscle–tendon unit injuries; some affect the muscle–tendon unit from within and some originate outside the unit, as summarized in Box 12.20.6.

The history should provide information regarding the injury and the patients to aid diagnosis and plan the extent of examination and investigation. Principle symptoms of muscle–tendon unit injuries are localized pain, swelling, and loss of function. Key points in the history are shown in Box 12.20.7.

The clinical examination should be sufficiently thorough to confirm or suggest one diagnosis and exclude others. The basic principles are to inspect, palpate, and move the affected limb passively and actively. The neurovascular status of the limb is examined and, where applicable, specific tests of muscle or tendon integrity should be performed. These are summarized in Box 12.20.8.

Joint movement is important in differentiating between intra- and extra-articular problems; for example, pain and reduced power on testing active external rotation of the shoulder implies an injury to the teres minor or infrapinatus components of the rotator cuff.

Thompson’s calf squeeze test for the ruptured Achilles tendon is an example of a specific test of muscle tendon integrity.

Investigations, summarized in Box 12.20.9, are not essential for all muscle–tendon unit injuries. There should be clear indications, which are to confirm a diagnosis prior to definitive treatment, to define which treatment option is optimal, to aid operative planning, to diagnose or exclude other pathologies, and/or to give prognostic information.

The investigation of choice for muscle–tendon unit injuries is magnetic resonance imaging (MRI), which gives excellent resolution of normal and pathological musculoskeletal and neurovascular structures shown in Figure 12.20.2. Ultrasound and computed tomography (CT) are also useful, particularly the former. Plain radiographs have a role, particularly in osseotendinous junction injuries and suspected fractures in conjunction with MRI are also useful.

Most muscle–tendon unit injuries are treated non-operatively. The aims of treatment are to restore the muscle–tendon unit to normal function as quickly as possible and to prevent complications (see Box 12.20.4). Return to normal function can be improved by prompt adequate treatment and rehabilitation. A small proportion of patients will require specialized non-operative or surgical treatment, and in the latter a delayed operation or not operating may result in significant long-term morbidity.

Immobilization of the injured extremity, using a splint if necessary, is analgesic and avoids worsening the injury. Fluid resuscitation diuretics, dopamine, and dialysis are used for crush syndrome. Diagnosis, monitoring, and treatment are detailed elsewhere (Chapter 12.10).

Painkillers, rest, ice, compression, and elevation (PRICE) form the initial treatment for a significant proportion of patients with muscle–tendon unit injuries. It is commonly used as a postoperative regimen as well. The regime minimizes the inflammatory process symptoms and therefore the formation of fibrous adhesions. It is adequate for most grade 1 and grade 2 acute muscle–tendon unit injuries. This type of treatment is usually indicated for the first 3 to 7 days post-injury.

PRICE is frequently the definitive treatment. A smaller proportion of patients, particularly those seen in a hospital or clinic may require additional non-operative treatments.

Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used for musculoskeletal problems and act by inhibiting arachidonic acid metabolism, reducing inflammation and platelet activation. They also have secondary analgesic properties. The exact mode of action of NSAIDs is unknown and qualitative proof of efficacy is poor. Inhibiting the cellular phase has theoretical risks of inhibition of healing.

Simple analgesics, such as paracetamol and opiate derivatives, have no direct effect on the injury, but are useful for symptom control. They can be used in conjunction with, or as an alternative to, NSAIDs.

Sedatives or muscle relaxants may be used to counter severe or painful muscle spasms, particularly in an anxious or agitated patient. They should be avoided in patients with head injury, if there is a specific contraindication, if there is a history of allergy or drug dependency, or if there is inadequate monitoring.

Local anaesthetics can be given proximal to a lesion as a regional block or epidural in lower-limb problems, for pain control, or for operative anaesthesia. In the acute situation there is a theoretical risk of masking a compartment syndrome, as blocks may cause sensory and motor deficits. Hyperbaric oxygen has been used in a few patients with muscle–tendon unit injuries.

There is no role for the use of corticosteroids in the acute phase of muscle–tendon unit injury.

Rest, ice, compression, and elevation are most important in the first 72h postinjury.

Splinting, casting, or other forms of immobilization can be important in early management to help reduce pain and muscle spasm. They are also indicated for the definitive management of non-operatively treated tendon ruptures, most commonly of the Achilles tendon, as well as following surgical repairs. Various materials are available, including fibreglass and thermoplastics plaster of Paris. Splints can be removable, allowing for wound and skin care, and hinged to allow controlled joint motion.

Movement and exercise: understanding the normal healing process will guide the balance between immobilization to prevent rerupture or commencing mobilization to encourage faster return of normal blood supply and better remodelling. Ideally, exercise should be supervised, preferably by a physiotherapist.

Massage and counter-irritation have analgesic and potentially beneficial effects after the early inflammatory phase, similarly to other physical therapy treatment modalities (see later).

Ultrasound and short-wave diathermy are the most frequently used electrotherapy modalities in the treatment of muscle injuries. Others include electrical field stimulation and cryotherapy. Therapeutic ultrasound produces local thermal and non-thermal effects which reduces the duration of the inflammatory response by increasing macrophage and fibroblast activity, accelerates oedema and haematoma resorption, and improves the strength of scar tissue.

Needle aspiration of a persistent or worsening haematoma causing pain and muscle inhibition can be performed in the clinic or the radiology department. It must be carried out under aseptic conditions and a firm pressure dressing should be applied to the affected area to prevent recurrence.

The decision to undertake operative treatment is based on a number of factors (Box 12.20.11). The potential benefits of surgery should outweigh the risks. The aims of surgery are as for treatment in general.

The timing of surgery is largely dependent on the pathology, although patient factors such as injury in top-class athletes are important. Acute compartment syndromes should be decompressed urgently as the warm ischaemic time to irreversible muscle damage is about 6h. After this period, and particularly after 10 days, there is marked adhesion formation and fibrosis, so that dissection and surgical trauma are more extensive, increasing the risks of complications and delayed healing.

The principles of the surgery of soft tissues are summarized in Box 12.20.12.

The main types of procedure are shown in Box 12.20.13. A combination of procedures may be needed.

The diagnosis of compartment syndrome and the surgical techniques used in its management are discussed elsewhere (Chapter 12.2).

Haematoma evacuation is only indicated as the sole procedure when a large intramuscular haematoma fails to resolve, increases in size, causes incipient skin and subcutaneous tissue necrosis, inhibits muscle activity or causes spasms, or is likely to progress to an ancient haematoma (commonly in thigh muscle groups). These types of haematomas are more common in patients with bleeding diatheses, and prompt correction of the clotting abnormality is the priority in such cases. Ultrasound guided biopsy is preferable in this group. Early haematoma evacuation may have a role in top-class athletes.

Direct suture or apposition is most readily used in fresh ruptures of the muscle–tendon unit at the mid-tendon, musculotendinous junction, or muscle belly. It can be a formally open technique or minimally invasive or percutaneous. Given the longitudinal alignment of the muscle fibres and tendon fibrils, simple suture techniques are not applicable and more complex sutures such as mattress, Kessler, or Strickland sutures are more applicable.

Lengthening with repair is sometimes necessary to gain length to allow tension-free apposition of ruptured ends. Separation is caused by tissue loss at the time of trauma, fraying of tendon ends, retraction and shortening of the ruptured muscle, underlying muscle pathology, or a combination of these factors. An example of this type of repair is the V–Y lengthening of muscle, as used in quadriceps and Achilles tendon repairs (Figure 12.20.3B). Another method is to turn down flaps of the affected tendon as in rotator cuff or Achilles tendon repairs (Figure 12.20.3C).

Avulsed bone at the enthesis or avulsion of the tendon nearby may require direct fixation to bone. The former can be repaired using a small plate or toothed washer (Figure 12.20.3G), and the latter by using sutures with drill holes through bone or specially designed anchor sutures (Figure 12.20.3F, H).

A muscle–tendon unit repair can be augmented by using neighbouring muscle–tendon units as direct supports or brought into apposition as a flap, free fascia lata strips, implants such as Dacron or Marlex wrapped around the repair, or wires to protect the repair (Figure 12.20.3D, E).

In the presence of an open contaminated wound, the priority is toilet and debridement to render the wound tidy, prior to definitive repair of the muscle–tendon unit and soft tissue cover.

The initial priority is for early wound healing without infection. Early immobilization facilitates wound healing in the early phase. The immobilization time depends on the strength of the repair, the vascularity, the preoperative condition of the muscle–tendon unit and integument, and the treating physician’s preference.

For the lower limb, a consensus period of immobilization would be 6 weeks, followed by increasing protected and supervised mobilization over the next 6–12 weeks, and a return to normal activity profile at 6–12 months depending on the injury, the strength of the repair, and the pre-injury level of function.

Rehabilitation is the third and final part of the management of a patient with a muscle–tendon unit injury, forming a continuum with diagnosis and treatment. It is frequently neglected by physicians.

Rehabilitation aims to restore to normal function, or as normal as pathology allows, the injured muscle–tendon unit, adjacent joints, the affected limb, and the whole patient. Additional aims are to reduce complications and prevent further injury both during the remodelling phase (reinjury) and in the longer term.

The rehabilitation phase should take into account the diagnoses, treatment, pre-injury level of activity, and expectations of recovery. Physical, social, ergonomic, and psychological factors should be considered in rehabilitation. Most rehabilitation is performed by the patient, guided by physiotherapists. Physicians commonly prescribe rehabilitation without supervising it. Less commonly, pain clinics, psychologists, and psychiatrists are involved.

The treatment options are similar to those used in the early treatment, although the emphasis is different. Mobilization and exercise, following splintage and immobilization, are the cornerstones of rehabilitation. Other treatment modalities include counselling and drugs.

The most common closed muscle–tendon unit injuries requiring repair, excluding open direct injuries, are listed in Box 12.20.14. They are generally complete ruptures due to indirect trauma. Ruptures and subsequent repair of almost every muscle–tendon unit have been described. Further details are given in this section and in the relevant chapters.

Complete ruptures of the Achilles tendon are the most commonly operated tendon ruptures. They occur most frequently in the fourth and fifth decades, and are twice as common in males. This is the most commonly occurring tendon rupture in sport.

The location of ruptures (2–4cm from the calcaneal insertion) is the watershed area of hypovascularity most prone to microtrauma and degenerative change, strongly associated with tendon ruptures.

The usual cause is sudden dorsiflexion of a plantarflexed foot, although it can be caused by direct sharp or blunt trauma. The classic symptom is of a feeling of being kicked above the heel. There is loss of active plantarflexion and no passive foot movement on squeezing the calf.

Partial ruptures do occur, but confirmation should be sought with ultrasound or MRI scanning, as the plantaris may continue to plantarflex the foot when the tendo-Achilles is ruptured. Musculotendinous junction injuries of the soleus or gastrocnemius are common, but rarely require surgery except in the case of high-class athletes.

Most authors agree that ruptures over a week old and reruptures should be treated operatively. More recently, non-operative treatment has been recommended if the gap that closes to less than 6mm in equines, as seen on ultrasound.

Developments in surgical technique include percutaneous repair (see Figure 12.20.3A) and the increasing use of a paramedian incision, which have reduced wound complication rates compared with earlier series. The immobilization time for both operatively and non-operatively treated patients is now 6–8 weeks.

In acute presentations the choice lies between the higher risk of rerupture if treated non-operatively (8–20%) and wound infection, breakdown, or rerupture (5–8%) if treated operatively.

Thus the optimal treatment for a fit athletic patient with an acute rupture is an early repair, which can be minimally invasive, followed by 4 weeks of cast immobilization or ‘minimal immobilization’ in a hinged cast, 2–4 weeks in a removable orthosis with passive ankle motion, 3 months with a heel raise and no running sports, and finally a graded return to full activity. Early weight bearing in an orthosis has not been found to be detrimental. Non-operative treatment would follow a similar course of immobilization, with a higher rerupture risk, and is a reasonable alternative.

Injuries to the rotator cuff cover the entire spectrum from minor strains to complete massive ruptures. There is a strong association with degenerative change within the cuff prior to injury in older adults. Acute-on-chronic ruptures in the middle-aged population make up the largest group of patients. Ruptures in young adults most commonly occur following a fall on the outstretched hand, injuring the supraspinatus. Full-thickness cuff tears are unusual in the younger age group (under 40), but the majority are acute and may be associated with fractures or dislocations. Definitive diagnosis may be difficult and is confirmed by arthrography, ultrasound, or MRI. Younger patients with ruptures make up a disproportionate group of those undergoing surgical repair. The epidemiology and specific management of rotator cuff injuries are discussed elsewhere (Chapter 4.3).

The majority of patients with full-thickness tears have fixation of the tendon to bone, possibly with intertendinous sutures, a transposition of subscapularis tendon, or a V–Y type repair. Other alternatives are Marlex, fascial autograft, or another tendon flap augmentation, with or without acromioplasty. Seventy to ninety per cent of patients undergoing surgery have reported good or excellent outcomes. Those who had surgery within 3 weeks of injury and no chronic radiological changes seemed to do best following acute injuries.

In a longer-term follow-up series younger women had slightly poorer outcomes than younger men, but at 4 years postsurgery there was an overall 94% satisfaction rate. There has been a move towards arthroscopic repair of some smaller acute tears over the past decade.

Aftercare of surgically repaired cuffs follows a regime of passive movements building slowly to active resisted motiown over 12 weeks.

Groin strain injury encompasses a number of muscle–tendon unit injuries around the inguinal and anterior hip area. The most common injury sites are the proximal adductor origin at the enthesis or tendon, the distal iliopsoas enthesis, the proximal insertion of the rectus femoris at the anterior superior iliac spine, or disruption of muscles inserting into or near the inguinal ligament. The last of these injuries, in the absence of a hernia, is sometimes termed ‘the groin disruption syndrome’ or ‘sportsman’s hernia’.

These injuries commonly occur acutely in athletes who sprint, and are commonly reported in the sports literature. MRI scanning, ultrasound, and herniography are valuable in confirming the diagnosis and the need for treatment.

Treatment for the majority of the injuries is non-operative. A large avulsion from the ischium or iliac spine can be fixed using a screw or small plate and screws. The groin disruption syndrome (‘Gilmore groin’) can be treated operatively with direct or augmented repair of disrupted parts with a reported 90% success rate, i.e. a return to sport.

Acute indirect injury commonly occurs in the rectus femoris muscle. The quadriceps muscles are also commonly affected by direct injury in sport, with the risk of a painful intramuscular haematoma, and in association with femur fractures. The most common cause of indirect injury is a fall or stumble against resistance, causing eccentric contraction.

The mean age of injury is about 45 years, more commonly in males. In patients over 40 the site of rupture is in the distal mid-tendon, while in patients under 40, rupture is more likely to occur near the distal enthesis. In middle-aged and elderly patients there is a strong association with chronic systemic diseases, such as gout, diabetes, or renal failure, or long-term steroid therapy.

Case reports and small series demonstrate good or excellent functional outcomes in over 90% of patients who receive early repair, followed by 6 weeks of immobilization in extension and rehabilitation for 3 months.

Injury to the muscle belly is more difficult to repair surgically and in most cases the treatment is non-operative, with splinting for 6 weeks followed by rehabilitation. A delayed presentation mid-belly rupture may mimic a soft-tissue tumour, which should be excluded by investigations.

Ruptures occur distally in the adolescent or proximally in the athlete aged over 20 years. There may be a history of a recent previous injury or chronic pain around the patellar tendon (jumper’s knee). Compared with other muscle–tendon units, particularly the quadriceps, there is a lower association with chronic disease states or tendinopathy in older adults.

Repair often involves opposing the tendon to bone using drill holes and multiple sutures, or a tension band wire around the patellar tendon mechanism, or both. Bony avulsions can be fixed back using screws.

Partial injuries to the hamstrings are very common, particularly in activities involving sprinting. Complete ruptures are rarer, but occur most commonly in sprinting athletes. The most common site is the proximal enthesis and the rupture is often an avulsion injury, seen on radiography. The distal musculotendinous junction is the next most common site.

Isolated hamstring ruptures are being diagnosed with increased frequency using ultrasound and MRI.

Surgical repairs of bony avulsions and musculotendinous junctions with good results have been reported in a small series.

Most ruptures are due to sudden forced flexion of the arm against resistance. The most common site of rupture is the long head tendon proximally in the bicipital groove, followed by the proximal musculotendinous junction, the short head tendon, the muscle belly, and most rarely the distal enthesis. Rupture is generally well tolerated in terms of function and cosmesis.

Surgery may be indicated in athletes and heavy manual workers, if the symptoms persist, or if there is a cosmetic defect. Reattachment procedures using anchor sutures, drill holes, and sutures have been described, with good functional outcomes in up to 80%.

This rarely occurs as an acute event, and is usually an acute-on-chronic rupture in a middle-aged or elderly patient who notes pain posterior to the medial malleolus, followed by an acute correctable flat foot. In younger patients it occurs following a sharp laceration, usually due to glass.

Surgery involves exploration at the level of or proximal to the medial malleolus. Direct repair is not usually possible. A tenodesis to the flexor digitorum longus is used, followed by distal transfer of the latter into the navicular. Use of the flexor hallucis longus is a more complex procedure.

This rupture occurs rarely in young adults lifting heavy weights. Considerable pain, bruising, and blood loss is associated with the injury. Scanning will differentiate partial from complete ruptures, and direct repairs have been reported with good or excellent functional outcomes.