The shoulder consists of three bony structures, clavicle, scapula, and humerus, that articulate at four joints sternoclavicular, acromioclavicular, scapulothoracic, and glenohumeral. When evaluating the shoulder these structures are considered functionally as a single unit, the shoulder girdle. Motion of the shoulder girdle is a complex interaction of many muscles groups providing a smooth and efficient transfer of energy. Normal abduction of the shoulder requires a ratio of glenohumeral to scapulothoracic motion of approximately 2 to 1. There is also appreciable motion at the sternoclavicular and acromioclavicular joints to allow for normal movement. The rotator cuff is comprised of the tendinous insertions of the supscapularis, suprapinatus, infraspinatus, and teres minor muscles. The rotator cuff stabilizes the glenohumeral joint and assists in the abduction and rotation of the humerus. Because the glenohumeral joint is shallow, it lacks inherent stability. Pertinent to athletic injuries, the inferior glenohumeral ligament is the main stabilizing force that resists anterior and inferior translation of the humerus in the glenoid (Fig. 1) 2409.

Initial examination begins with inspection of the various shoulder muscle groups. Any asymmetry, hypertrophy, or atrophy should be noted, and rotation checked at both 0° and 90° of abduction, with documentation of both external and internal rotation at its maximum point. Overhead abduction is best measured from behind by asking the patients to raise the arms slowly directly over the head. Symmetrical muscle pull and range of motion can be ascertained. Palpation of the sternoclavicular and acromioclavicular joints may reveal point tenderness. The coracoacromial ligament as well as the supraspinatus tendon may be palpated with the arm in the extended position. The strength of the supraspinatus muscle is tested by resisted depression of the forward flexed, partially abducted, and internally rotated arm. With the arm fully adducted, and the elbow flexed to 90°, resisted internal rotation measures the subscapularis muscle strength, while resisted external rotation evaluates the infraspinatus and teres minor muscles.

Physical signs of impingement are the Neer impingement sign, performed with the arm brought overhead with forward flexion and internal rotation, and the Hawkins test, performed with forward flexion, adduction, and internal rotation of the glenohumeral joint. Anterior stability can be evaluated with the patient either sitting or lying supine. The patient's arm is placed in 90° of abduction and is externally rotated. An anterior apprehension test occurs with an anterior translation force applied to the glenohumeral joint from the back of the shoulder, which causes the patient to feel as if the shoulder is going out. The relocation test is performed after the apprehension test has been completed. A posterior force is applied to the front of the abducted, externally rotated shoulder resulting in reduction of the feeling of going out. Inferior glenohumeral stability can be tested by pulling straight down on the adducted arm while the patient is sitting. A sulcus can be seen just inferior to the lateral aspect of the acromion. Posterior instability is tested in the supine position by forcing the flexed arm posterior to reproduce symptoms.

Standard radiographic examination includes anterior/posterior views of the glenohumeral joint and internal/external rotation in adduction. A transaxillary view or a true axillary lateral view must be obtained. A lateral view of the scapula may demonstrate subacromial spurs indicative of impingement of the acromion or coracoacromial ligament on the insertion of the supraspinatus tendon into the greater tuberosity. Further studies are directed to the evaluation of the suspected underlying disease. Computed arthrotomography and magnetic resonance imaging (MRI) are helpful in evaluating anterior capsular laxity and glenoid rim labral tears. CT scanning is also helpful in evaluating bony glenoid and humeral lesions. The arthrogram has been the gold standard for evaluation of rotator cuff tears. MRI is now the best imaging study to evaluate the rotator cuff. MRI is preferred over arthrography, as it is non-invasive and is more sensitive than the arthrogram in revealing partial tears and tendinitis. Ultrasonography can define accurately a complete tear of the rotator cuff. If no diagnosis is reached, arthroscopy is beneficial in the valuation of intra-articular and subacromial shoulder pathology.

Impingement syndrome includes conditions formerly called painful arc syndrome, chronic rotator cuff tendinitis, and bursitis. There is an inflammatory process involving the subacromial bursa, coracoacromial ligament, the rotator cuff, the biceps tendon, and the acromioclavicular joint. It is most commonly seen in sports involving throwing. The arm is brought into an abducted, externally rotated position. The supraspinatus tendon is most commonly involved in impingement. Repetitive overhead use causes a gradual impingement of the rotator cuff against the anterior aspect of the acromion, and the coracoacromial ligament. Occasionally one may see osteophyte formation of the acromioclavicular joint, which also produces stress on the rotator cuff. With repetitive use an inflammatory process weakens the supraspinatus muscle. When weakness occurs, the rotator cuff is unable to depress the humeral head into the glenoid, and the more powerful deltoid muscle causes the head to ride up into the overlying subacromial space. The anterior tip of the acromion process impinges into the rotator cuff causing further injury to the inflamed tendon. This portion of the rotator cuff (supraspinatus tendon) is in a poorly vascularized area. Unfortunately, the reparative process is compromised. Pain can be reproduced by elevating the patient's arm with forward flexion and internal rotation (Neer test). Inflamed tissue near the greater tuberosity is pressed against the underside of the acromion and the coracoacromial ligament. This can also be performed with adduction, forward flexion, and internal rotation of the arm (Hawkins test). Patients often complain of pain with overhead activity and pain at night. Radiographic examinations are often unremarkable. Sclerosis of the greater tuberosity and narrowing of the subacromial space may indicate a chronic tendinitis.

The diagnosis of impingement syndrome is made by an appropriate history of shoulder pain, an increase in pain with overhead activity, a positive impingement sign on physical examination, and a positive impingement test. To perform an impingement test, the physician injects 10 ml of 1 per cent lidocaine into the subacromial space from the posterolateral approach. The test is considered positive if the pain from impingement is eliminated. It is important to examine specifically the acromioclavicular joint for pathology, because pain from this joint alone can be misinterpreted as impingement pain. The adduction test for acromioclavicular joint pain is performed by placing the patient's shoulder in 90° of forward flexion. With maximal adduction of the arm, the acromioclovicular joint is compressed and if diseased, will hurt.

Impingement syndrome has been divided into three phases. Stage one is characterized by inflammation and oedema of the rotator cuff. In stage two there is a degenerative fibrosis of the rotator cuff, while the final stage is characterized by partial or complete tear. The first step in treatment begins with the athlete decreasing the provocative activity: this often means giving up overhead activities such as throwing. Anti-inflammatory medication may also be given. Once the pain has decreased, an aggressive physical therapy programme is required to restore full motion: loss of internal rotation is common. As motion is regained, strengthening of the rotator cuff muscles is emphasized, but the abducted, externally rotated arm position should be avoided while performing muscle strengthening exercises. If the patient continues to have symptoms, steroid injection in the subacromial bursa should be considered. One common method is the introduction of 9 ml of lidocaine containing a corticosteroid preparation into the subacromial bursa from a lateral or posterior lateral approach. Lidocaine produces dramatic relief of symptoms and reconfirms the diagnosis within 15 min. Although this effect will wear off, the steroid may provide long-lasting pain relief.

When conservative treatment fails, an athlete may have to change the motions that cause pain. Even with complete abstinence of overhead motion pain may continue.

Prior to the consideration of surgery, the physician must evaluate the stability of the glenohumeral joint. Impingement may co-exist or be secondary to this instability; if unrecognized the operation will fail. The primary goal of surgery is to decompress the subacromial space. Classically, the coracoacromial ligament is resected, the anterior acromion is removed, and the bursa is debrided in an open procedure. In those with acromioclavicular joint arthritis the distal clavicle may also need to be resected. Currently subacromial decompression is performed arthroscopically. Arthroscopy provides the additional benefits of decreased tissue trauma and a shortened rehabilitation phase.

Injuries to the acromioclavicular joint are known as shoulder separations. This joint is stabilized by strong coracoclavicular ligaments and weaker acromioclavicular ligaments. Type one shoulder separation is an acromioclavicular ligament sprain with intact coracoclavicular ligaments. Type two separation results in a mild upward migration of the clavicle, disruption of the acromioclavicular ligaments, and sprain of the coracoclavicular ligaments. In a type three separation the acromioclavicular and coracoclavicular ligaments are disrupted and the acromioclavicular joint is dislocated. A type four dislocation is characterized by posterior and superior migration of the distal clavicle into or through the trapezius muscle; type five is upward disruption of the distal clavicle 100 to 300 per cent greater than the normal shoulder; and type six has anterior and inferior displacement of the clavicle. Separations of types 1, 2, and 3 are often treated by placing the arm at rest, with a sling for comfort. Once the pain is decreased a rehabilitation programme is begun. Patients should be warned of possible degenerative changes of the joint over time. In type 4, 5, and 6 separations attempts should be made to improve the position of the distal clavicle. This often requires operative intervention to reduce the clavicle and secure it in its reduced position. Chronic pain from a chronically disrupted acromioclovicular joint may be successfully treated with a distal clavicle resection.

Biceps tendinitis often presents itself as anterior shoulder pain. Physical findings include Speed's and Yergason's signs. Although biceps tendinitis may be a localized phenomenon, more often it is part of a more common disorder of impingement. Treatment should be directed towards reducing inflammation both within the subacromial space and along the biceps tendon itself. Range of motion and strengthening of the whole shoulder should also be achieved.

Athletes who participate in activities requiring overhead throwing are at risk for anterior subluxation of the shoulder. Subluxation can be difficult to diagnose as the athlete may be unaware of signs of instability at the glenohumeral joint; he complains only of a diffuse paralysing type of pain. A smaller proportion of patients are aware that their shoulders are ‘slipping out’: these patients often have a more unstable shoulder. The athlete may complain of a ‘dead arm syndrome’. Patients often have a history of a sudden forceful hyperextension injury to the arm in the abducted externally rotated position or a direct blow to the shoulder at the point of maximum effort. The inferior glenohumeral ligament is the most common site of ligamentous incompetency. The ligament may be pulled from the bone, or it may be stretched. The physical examination elicits a positive apprehension test: the patient avoids having his arm brought out into the abducted, externally rotated position with force, a relocation test is performed to confirm this, using anterior pressure over the humeral head to relocate it in the glenoid fossa. Radiological confirmation is either by CT arthrogram or MRI of the shoulder, which shows bony avulsion or capsular laxity.

Rest is essential to treatment. All throwing or overhead activity must be avoided, and anti-inflammatory medication is also given. When the patient is comfortable, physical therapy directed towards rehabilitation of both the rotator cuff and all the scapular rotators is begun. If conservative treatment fails an anterior capsular repair is indicated. All repairs attempt to reduce the excess volume of the anterior capsule, especially of the inferior glenohumeral ligament. This may take the form of a straight soft tissue repair, soft tissue to bone repair, or a capsular shift with tightening of the inferior capsular recess. Regardless of type of treatment used, the repair often decreases symptoms.

Both instability and impingement are inter-related as the most common causes of shoulder disorders in the overhand athlete. Injuries resulting in instability progress to have mild subluxation of the glenohumeral joint. Impingement causes further damage of the rotator cuff and weakens its already compromised state. With further activity the shoulder will further sublux. This cascade has been termed the instability complex: the inter-relationship between these two diseases means that both must be looked for individually.

Shoulder arthroscopy has gained acceptance as a valuable tool in the evaluation and treatment of various disorders affecting the shoulder. When used appropriately this technique may enhance the surgeon's diagnostic and therapeutic capabilities. Many abnormalities of the cervical spine or the upper extremity can cause pain in the shoulder. Intrathoracic and intra-abdominal disease may also cause pain radiating to the shoulder. Thus, before proceeding to diagnostic studies such as arthroscopy, a complete preliminary examination must be done.

Indications for shoulder arthroscopy include a definitive therapeutic treatment, a diagnostic procedure to confirm suspected diagnosis, and diagnostic procedure for the patient whose problem cannot be definitively diagnosed by any other means.

Although there have been rapid advancements associated with shoulder arthroscopy, simple diagnostic arthroscopy with general anaesthesia is a straightforward and easy procedure.

Patterns of instability often become more obvious under general anaesthesia. The patient may be positioned either in a lateral decubitus position with his arm suspended overhead or in a beach chair (sitting) position. The equipment is similar to that used in knee arthroscopy.

Once the patient has been prepared and draped the anatomical landmarks of the shoulder should be outlined. The posterior portal site is situated approximately 3 cm inferior and 2 cm medial to the posterolateral tip of the acromion. A 20 gauge spinal needle is used to gain entrance through the posterior capsule of the shoulder joint. The needle is connected to a 50 ml syringe, through which Ringer's lactate solution is infiltrated to distend the joint. A small amount of adrenaline may be added to control bleeding. The arthroscope is then introduced into the joint along a similar path. Both inflow and outflow may be established through the arthroscopic sleeve. If a second portal is needed, it is usually placed anteriorly and is directed through the intra-articular triangle. This portal may be used for inflow or for instrumentation. Both superior portals and lateral portals may be used as needed for further instrumentation. The biceps tendon is found first and provides orientation. From there the rotator cuff, the glenoid articular surface and glenoid labrum, the inferior recess, humeral head, and anterior capsule and bursa are seen and examined. At the completion of an arthroscopic evaluation of the glenohumeral joint, the arthroscope is withdrawn and is repositioned to evaluate the subacromial space. The anterior and lateral portal may be repositioned superiorly to assist in procedures such as a subacromial decompression.

Since the glenohumeral joint has thick muscle coverage, a blind stab may produce injury to nerves or vessels. The risk of such injury is reduced if the procedure is confined within bony landmarks.

Although often described as a simple hinge joint, motion of the elbow involves a complex combination of flexion and extension, pronation, and supination. Measurement of the extended arm discloses 10 to 15° valgus angulation (the carrying angle) in normal individual. The most common stress placed on the elbow during throwing sports is a valgus stress. The medial side of the joint is placed under tension, while the lateral side is placed under compression. The capitellum articulates with the radial head, serving as a buttress for lateral compression. The lateral collateral ligament complex is less developed than is the strong medial collateral ligament, which is composed of three bands. The strong anterior oblique band that functions throughout the entire elbow range of motion, is the primary constraint to valgus stress at the elbow. This band is augmented by a posterior band and a transverse ligament band.

Examination of the elbow is always included in a physical examination of the upper extremity. Palpation helps to isolate the source of discomfort. One should palpate the posterior aspect of the elbow with the elbow flexed 15 to 20° to unlock the olecranon from its fossa in the distal humerus. In athletes who throw the olecranon fossa is a common area of irritation. Collateral ligament stability is also tested in 15 to 20° of flexion to eliminate the stabilizing effect of the olecranon locking in its fossa. Instability is evaluated by the gravity stress test. The patient is placed supine and the shoulder is externally rotated with the elbow flexed at 20°. The weight of forearm and hand will create valgus force that opens the medial side of an unstable elbow joint. Radiographs can be taken in this position to document the degree of instability.

The young throwing athlete may present with vague lateral elbow discomfort and lack of complete extension at the elbow. In patients under the age of 12, radiographs may confirm the diagnosis of osteochrondrosis or Panner's disease. The capitellar ossification centre appears fragmented. Abstinence from repetitive loading is sufficient treatment. Throwing and racket sports can cause repetitive valgus overload of the radiocapitellar joint. The physician must have a high index of suspicion because initial radiographs may be negative. Bone scan, tomogram, CT scan, or MRI may be required to identify the lesion accurately.

Three stages of the disease have been identified. Conservative treatment measures such as rest and splinting are often successful, unless bony fragmentation results in intra-articular debris. If this occurs bone chips may need to be removed with either arthroscopy or open arthrotomy. It is important to inform the family and coaches of possible permanent damage that may result if continued athlete activity occurs.

The medial aspect of the elbow is placed under repeated tensile forces. This may result in injury or failure of the medial collateral ligament complex, tardy ulnar nerve palsy, or flexor muscle strains. Injuries to the flexor pronator muscle mass can be diagnosed by pain on resisted wrist flexion with the elbow extended. Tenderness on palpation of the medial collateral ligament, as well as instability to a valgus stress with the elbow flexed 20° is indicative of an injury to the medial collateral ligament. Rest, non-steroidal anti-inflammatory medication, and cold compresses help to reduce acute pain and swelling.

Acute ruptures of medial collateral ligament can occur. Conservative care and rehabilitation are usually successful. Patients should be warned that they may have a small degree of flexion contracture at the end of treatment. In a very unstable elbow and/or highly competitive athlete, the possibility of surgical repair and augmentation may be entertained.

Epicondylitis is the result of inflammation and breakdown of the extensor muscles at their origin on the lateral epicondylar ridge of the distal humerus. Tennis elbow may be caused by any racket sport. This lesion can also occur medially to the flexor muscle mass origin, but is much less common than is lateral epicondylitis. Repetitive minor trauma can result in soft tissue inflammation and eventual failure: this overuse injury often occurs as a result of a training error. An athlete has often increased the amount or intensity of training rapidly, or changed the size of the racket grip. Most patients are between 30 and 50 years of age. Physical examination with the elbow extended reveals pain on resisted wrist extension. There is a well-defined area of tenderness about the lateral elbow. Early recognition and treatment is essential, because the disease process may become irreversible and resistant to conservative care. Treatment consists of rest, anti-inflammatory medicines, cold compresses, and bracing. Once the pain has resolved, physical therapy is critical to re-establish full range of motion and strength.

Lateral epicondylitis resistant to conservative care requires surgical decompression. The pathoanatomy is localized breakdown of the extensor carpi radialis brevis origin. The portion of the tendon showing inflammation and necrosis is removed and the origin of the tendon is reattached. After appropriate rehabilitation, success can be anticipated in approximately 80 per cent of patients.

The most common neurological problem in the elbow is due to repetitive tensile stress to the ulnar nerve in the cubital tunnel. Athletes complain of diffuse paraesthesias in the fourth and fifth fingers related to athletic activity. With continued stress the injury may become more pronounced. The motor fibres may also be affected. Tinel's sign is demonstrated by tapping on the skin over the nerve along its course around the medial epicondyle. A positive Tinel's sign will reproduce the pathological nerve irritation symptoms, reproducing the patient's distal paraesthesias. Conservative care includes rest, non-steroidal anti-inflammatory medication, and physical therapy. Recalcitrant ulnar nerve entrapment requires surgical decompression. Electrodiagnostic studies should be used to determine the point of entrapment prior to any attempt at surgical release. The offending fascial sheath often has to be divided to relieve pressure on the nerve. If entrapment occurs at the cubital tunnel, anterior transposition of the nerve usually provides successful relief of symptoms. A medial epicondylectomy, with or without ulnar nerve transposition, is also used to treat this compressive neuropathy.

Although less common than extremity injury, spine injury may occur in athletes, with potentially devastating consequences. Spinal cord trauma can result from football, rugby, gymnastics, wrestling, trampolining, ice hockey, water sports, snow skiing, and weight lifting. Injuries may range from immediate quadriplegia, to transient neuropraxia, to no neurological deficit at all. Athletic spine injury covers a spectrum from acute trauma (fractures), to accentuation of congenital insufficiency (spondylolisthesis), to overuse syndromes (chronic low back pain). Most spine injuries in athletes occur in the cervical or lumbar spine regions. Athletic thoracic spine injury is rare; it usually occurs only in high velocity collisions.

Injury to the cervical region of the vertebral column is most common in contact sports such as North American football, ice hockey, rugby, and wrestling. North American football is the major cause of head and spine injury. Some non-contact sports, such as gymnastics, diving, trampolining, and horse riding, are also in the high-risk group. Data collected from the National Football Head and Neck Injury Registry in the United States disclosed an incidence of 4.14/100 000 cervical spine fractures or dislocation and a 1.58/100 000 incidence of traumatic cervical quadriplegia over a 4-year period. C5–C6 is the most frequently injured level in the cervical spine.

Two distinct types of neurological injury are seen in athletes. Cord damage, complete or incomplete, may accompany fractures, dislocations, or a varying combination of these documentable injuries. The lower portions of the cervical spinal cord are at increased risk for injury because the diameter of the spinal canal is smaller than that of the upper cervical spine. A second type of injury is transient neuropraxia in the absence of identifiable vertebral column injury. This type of injury, referred to as ‘burners’ or ‘stingers’ by athletes, represents localized momentary spinal cord compression or brachial plexus traction. Symptoms vary from single extremity paraesthesias to transient quadriplegia. Symptoms may last from minutes to as long as 48 h. The hallmark of this injury is a clinically and radiographically ‘normal’ spine. Congenital fusion, cervical instability demonstrated on flexion–extension analysis, and protrusion of an intervertebral disc may increase the risk of neurological injury of the cervical spinal cord.

Spinal stenosis, as determined by the ratio method, will also help predict which athletes are at risk. The ratio of the spinal canal width to the vertebral body width is measured at the third through the sixth cervical vertebral levels on a lateral radiograph. A ratio of less than 0.80 is indicative of major spinal stenosis. A complete analysis of the cervical spine should be made in athletes with transient neuropraxias and in those found to have radiographically identifiable changes that may restrict participation in high risk sports.

Immediate comprehensive protection and evaluation must be undertaken in any athlete with a suspected cervical spine injury. Complete and immediate immobilization of the spine at the time of injury is mandatory to prevent further injury during transport and evaluation. Standard cervical spine radiographs should be augmented by physician-assisted flexion–extension lateral radiographs, CT, or MRI.

Patients with spinal cord injury and no radiographic abnormality should be treated with 3 months of strict immobilization in a collar or brace. A 20 per cent incidence of recurrent neuropraxia has been seen in these patients. Contact sports should be curtailed if symptoms recur. Range of motion and neck strength assessment can be used as a monitor of full recovery in an injured athlete. Neck strengthening protocols to help minimize recurrent spinal cord injury are recommended; however the protective benefits of such protocols have yet to be proven in controlled studies. Prescreening is recommended for high-risk individuals preparing for participation in contact sports. With the expansion of Special Olympic programmes, individuals with Down's syndrome are now frequently participating in athletics. Such patients are at risk for C1–C2 instability secondary to ligamentous laxity. They should be evaluated with flexion–extension radiographs prior to participation. In the normal athlete, strict avoidance of high-risk manoeuvres such as spear-headed tackling or blind-sided checking in American football is important. Strict adherence to rules prohibiting such dangerous manoeuvres may reduce the incidence of spine injury and quadriplegia by more than 70 per cent.

Athletes with mild cervical sprains or minimal wedge compression fractures can return to full activity once pain has resolved and full motion and strength is regained. Spinous process avulsions may be seen as a component of severe cervical sprains, and these represent avulsions of the supraspinous or interspinous ligaments. Careful evaluation with flexion–extension radiographs and/or CT should be undertaken to evaluate cervical spine stability. Treatment of cervical sprains includes a collar, ice, and analgesics. Muscle relaxants and cervical traction may be helpful. A course of 6 to 8 weeks of soft collar immobilization should be followed by progressive rehabilitation and muscle strengthening exercises. Athletes who undergo single level anterior disectomy and fusion may also be returned to contact sports; however, the activities of those with multiple level disectomy and fusion should be restricted.

Eighty per cent of the population has low back pain at some time. A survey of the Men's Professional Tennis Tour showed that 38 per cent of players missed at least one tournament because of low back problems. The incidence of chronic low back pain was 30 per cent, and 29 per cent of the acute injuries during the tour occurred in the lumbosacral spine. Half of all gymnasts experience transient low back pain during their competitive careers. A lower than normal incidence of low back injury is seen in runners; power weight lifters have an increased incidence. Lumbar spine injury may present as acute bony or soft tissue trauma or as a chronic overuse degenerative process. In the teenage athlete with back pain the presence of a spinal tumour must be ruled out by bone scan or MRI study. Herniated discs, facet syndrome, and spinal fractures occur in athletes.

Sprains of the lumbar spine ligaments and strains of the muscles are commonly caused by sudden violent movements with significant loads on the spine. These soft tissue injuries can be extremely painful and acutely disabling. Chronic low back pain may result from repeated soft tissue injury secondary to poor body mechanics or technique. Usual presenting symptoms of soft tissue injury include paraspinal tenderness with a limited and painful range of motion. The patient may have a truncal list to the side of injury. Treatment consists of rest, cold compresses, non-steroidal anti-inflammatory medication, ultrasound and, in rare cases, bracing. Return to activity should be gradual and be preceded by an abdominal and paraspinal muscle conditioning programme.

Traumatic spondylolysis is fracture of the pars interarticularis. Spondylolisthesis is the displacement in the lateral plane of adjacent vertebrae permeated by the spondylolysis. Spondylolysis of L5–S1 is a classic cause of low back pain in young gymnasts. An increased incidence of L5–S1 spondylolysis has also been noted in pole vaulters, hurdlers, football linemen, and weight lifters. The normal incidence of a non-traumatic spondylolytic defect at L5–S1 is approximately 5 per cent.

The lumbar spine is vulnerable to injury with extension. Force applied to a hyperextended lumbar spine translates to shear and compression concentrated on the inferior lumbar facet and pars interarticularis. With repeated hyperextension loads, such as in gymnastics, the pars interarticularis may develop a stress fracture (pars stress reaction). A violent hyperextension force, such as a lineman in football may sustain, may cause a pars interarticularis fracture or spondylolysis. To visualize a pars defect evaluation of the teenage athlete with low back pain should include lumbar spine radiographs with oblique views. If the radiographs are negative, a bone scan should be obtained to assess a stress fracture. A positive bone scan with negative radiographs is diagnostic of the pars stress reaction. The patient has low lumbar tenderness, and pain on hyperextension. Symptoms are usually relieved by rest. Treatment consists of restriction of athletic activity and bracing.

Minimal pars stress reaction may progress to radiographic spondylolysis, but few of these patients have a displaced fracture or one that slips. The treatment of traumatic spondylolysis is bracing for 6 to 8 weeks. Bone scans may be used to follow healing of these lesions and radiographs should be utilized to assess for progressive slip.

Spondylolisthesis is classified into five grades. Spondylolisthesis may be seen with a intact and elongated pars interarticularis, as well as with true pars defects or fractures. Elongation or lysis of the pars may be bilateral or unilateral. The greatest slippage has been reported to occur between the ages of 9 and 14. Grade I slips associated with pain usually respond to rest. Once the pain has resolved athletes are allowed to resume vigorous sports including gymnastics. Grade II slips mark the onset of clinical signs such as a short torso, flat heart shaped buttocks, low set rib cage, hamstring tightness, and waddling gait. These patients are also managed conservatively; however, they are restricted from participation in vigorous sports. Close monitoring is indicated as the condition can progress and result in neurological compromise. Symptomatic patients with Grade III or higher slip are considered candidates for surgical intervention. Slips greater than Grade II usually preclude the athlete from participating at a competitive level.

Knee arthroscopy became an established surgical technique in the mid-1970s. A multitude of arthroscopic techniques is now available for the treatment of disorders of the menisci, synovial plicae, the cruciate ligaments, and articular cartilage surfaces. Arthroscopy is also occasionally used for the evaluation of the patient with a problematic total knee arthroplasty.

Arthroscopy should not be performed on the mildly symptomatic knee until a trial of conservative treatment has been attempted. Although the indications for knee arthroscopy are not absolute, they may include evaluation of traumatic haemarthrosis, evaluation of instability, recurrent episodes of swelling, inability to fully extend the knee, and joint line tenderness. Arthroscopy is recommended when lesions such as a meniscal tear, a painful synovial plica, or a loose body in the knee are suspected. Arthroscopy is not required to confirm the diagnosis of an anterior cruciate ligament tear, but is used if the patient has coexisting symptoms of a meniscal tear or when confirmation of a diagnosis is required before reconstruction. There are no special contraindications to knee arthroscopy; however, after severe rupture of the joint capsule secondary to a knee dislocation, arthroscopic surgery acutely may cause injury to surrounding tissues because of extravasation of fluid used to distend the joint and allow visualization. The skin of the knee where the entry portals are to be made should be intact.

Arthrosopic surgery is performed through multiple 1 cm skin incisions around the knee. The surgery can be performed under local anaesthesia, but spinal block or general anaesthesia is preferable and a tourniquet is often used. Once the patient is anaesthetized, a complete examination of ligamentous stability, including pivot shift testing and range of motion, is performed. Many patients have hamstring spasm after injury that precludes an accurate cruciate ligament examination while awake. Muscle relaxation while under anaesthesia permits an excellent examination of the ligamentous stability of the knee. This examination under anaesthesia is a very important part of the surgical evaluation.

For arthroscopy, the leg is placed in a rigid leg holder that allows varus/valgus stress to be applied to the knee. Antibiotic prophylaxis is not usually required. Most procedures require three portals, the accurate location of which is essential to gain optimal visualization and to perform therapeutic manoeuvres. The superomedial portal is used for the inflow of Ringer's lactate solution to distend the joint for visualization. Sufficient fluid inflow is important - a 5.5 mm inflow cannula is recommended.

The arthroscope is 4 or 5 mm in diameter, with a fibreoptic light source attached. A light source with automatic variable intensity adjustment is preferred. A miniature high-resolution video camera is attached to the end of the arthroscope and the surgeon views the intra-articular structures of the knee on a television monitor. The third portal is used to place a probe or an array of biting, grasping, or motorized shaving instruments into the joint to remove pieces of torn meniscus, loose bodies, or synovium. Adjustable suction is attached to both the arthroscope and motorized shaver and is used to remove tissue particles and to irrigate the joint.

Although the sequence of an arthroscopic examination is unimportant, it is important to examine the suprapatellar pouch, patellofemoral joint surfaces, the medial and lateral gutters, the medial and lateral compartments with their menisci, articular surfaces, and the intercondylar notch with anterior and posterior cruciate ligaments. The arthroscope can be placed through the intercondylar notch to view the posterior cruciate ligament or posterior aspects of the menisci.

The probe is the instrument of palpation for the arthroscopist and assists in evaluation of the posterior horns of both the medial and lateral menisci. Most meniscal tears are located in the posterior half of the C-shaped menisci. The probe is also crucial in evaluation of the anterior cruciate ligament. The ligament must be seen completely from its femoral origin to the tibial insertion. The anterior cruciate ligament often appears to be intact on visualization alone, but with careful probing the anterior cruciate ligament may be found to be completely ruptured, scarred to the posterior cruciate ligament, and incompetent. The use of the arthroscope in one hand and the probe or other instrument in the other hand inside the knee joint (triangulation) requires excellent three-dimensional spatial skills.

Although not as safe as once thought, the complications of arthroscopic surgery are few and infrequent. The infection rate is less than 1 in 2000 cases. The most frequent complication is iatrogenic injury to the articular cartilage surfaces. While a small amount of scuffing of the cartilage is inevitable and seemingly harmless, care must be taken not to cause severe injury to the articular surfaces; these do not heal. The anterior horns of the menisci can be severed if entry portals are too low on the joint line. An occasional patient develops a neuroma secondary to injury to a cutaneous nerve. Breakage of instruments can require arthrotomy for retrieval.

The meniscus was previously considered to be an expendable structure. Total menisectomies were performed, even when the knee pain was not definitely related to a damaged meniscus. We now know that the meniscus serves many functions in the knee and that degenerative changes in the knee occur after menisectomy. Loss of the weight-bearing function of the meniscus may result in osteophyte formation, flattening of the femoral condyle, and narrowing of the joint space. Autopsy studies have shown fragmentation of the articular cartilage in over 90 per cent of the portion of joint surface not protected by the menisci. Many long-term studies have shown degenerative changes in 20 to 80 per cent of menisectomized knees. Up to 50 per cent of patients have unsatisfactory results.

Knowledge about the status of the meniscus has increased rapidly and our appreciation of the significance of this structure has changed surgical handling of it. The medial and lateral menisci are C-shaped wedges of fibrocartilage placed between the condyles of the femur and tibia. Type 1 collagen accounts for approximately 90 per cent of the total collagen of the meniscus. These collagen fibres are primarily oriented in a circumferential fashion, which allows the menisci to resist the hoop stresses placed on them. The surface and midsubstance of the meniscus contains radially oriented collagen fibre bundles which provide increase structural rigidity. The vascular supply to the menisci comes predominantly from the medial and lateral geniculate arteries. There is a perimeniscal vascular plexus within the synovial capsular attachment of the meniscus. The degree of vascular penetration into the meniscus is approximately 10 to 30 per cent of the width of the meniscus at its peripheral attachment. The vascularity and integrity of the meniscus decline with age. Vascularity also dictates the part of the meniscus that receives direct nutrition from the vascular tree and that part which is dependent on diffusion for nutrition.

The menisci are important in the protection of articular cartilage because they act as shock absorbers. This shock absorption capacity is important to prevention of degeneration of hyaline articular cartilage. They transmit between 30 and 70 per cent of load across the knee joint. Meniscectomy profoundly alters the ability of the meniscus to distribute load in the knee: the intra-articular contact area can be reduced by as much as 50 per cent. Removal of part of the meniscus causes less decrease in weight transmitting capability than removal of the whole meniscus. The menisci also serve to aid in joint congruity, as the spheres of the distal femur must articulate with the relatively flat surface of the tibial plateau. By assisting in congruity of the joint, the menisci also provide an important stability to the knee. Of special importance to the athlete is the fact that the menisci have little effect on the anterior–posterior translation of a normal knee. An anterior cruciate ligament tear renders the knee susceptible to anterior-posterior translation. This motion is resisted by the intact menisci, especially medially. Removal of the medial meniscus of the knee removes an important secondary stabilizer. Nutrition to the articular surface is improved by the ability of the menisci ability to compress the synovial fluid into the underlining articular cartilage.

A history of a twisting injury with a catching sensation or pain along the joint line is often indicative of a meniscal tear. Patients may complain of significant locking or catching inside their knee. Physical examinations reveals tenderness directly on the effected joint line. Both the McMurray test and the Apley compression/distraction test elicit pain from a torn meniscus. However, patients with significant meniscal tears may not show such a clear-cut history or physical examination results. Confirmation may be provided by one of three methods. The most accurate method for meniscal detection is by arthroscopic examination. Repair or partial excision of the lesion can be undertaken at the same time. However, the patient is exposed to the risk of anaesthesia if the examination is negative. Arthrography allows the knee to be systematically examined. Spot films of each portion of the meniscus are obtained as it is rotated across a point tangential to the X-ray beam. A torn meniscus can be demonstrated by arthrography when the contrast agent enters into the tear.

MRI has the advantages of being safe and non-invasive. It can also provide information on surrounding bones, ligaments, and tendons and may identify extra-articular disease masquerading as meniscal pathology. Meniscal lesions of grade I show a small focus of intrameniscal degeneration without extension to the surface. A grade II lesion is a more advanced state of meniscal degeneration without extension to the articular surface. Grade III tears appear on MRI as linear high signal changes that extend to the articular surfaces of the meniscus (Fig. 11) 2419.

Arthroscopic partial menisectomy has replaced open menisectomy as the treatment of choice for unrepairable meniscal tears. The minimum amount of tissue should be removed to provide the patient with a remaining stable rim of functioning meniscal tissue.

The treatment of meniscal tears has progressed from complete menisectomies, through arthroscopically performed partial menisectomies, to the present standard of care, which involves repair of meniscal tears when they occur through the vascular region of the meniscus. The peripheral 10 to 30 per cent of the human meniscus has a vascular supply sufficient to allow healing. Tears in this region are now repaired rather than excised. Such repairs can be performed using either an open or an arthroscopically aided technique. Repair is undertaken with the aid of dissection at the level of the joint line corresponding to the tear. Closed repairs result in needles being driven out blindly through the meniscus and joint line, resulting in vascular or neurological injury and are contraindicated. General indications for meniscus repair include longitudinal acute tears and vascular peripheral tears of the meniscus in young athletes with stable knees. Long-term success rates for other types of meniscal tears repairs have yet to be determined. Recurrence rates are higher in knees with an anterior cruciate ligament deficiency: complete reconstruction of both the ligament and the meniscus should be undertaken. When observing the vascular appearance of the surfaces of the tear, a ‘red on red tear’ through the vascular portion of the meniscus has the best prognosis for healing. A ‘red on white tear’ with a meniscal rim that has a good vascular supply, compared to the inside torn rim, is less likely to heal well. Tears that are ‘white on white’, in which the meniscus tear is completely in the avascular zone, have the least healing potential. Regardless of the technique used the surfaces of the meniscus tear should be roughened to stimulate a new healing response.

In addition to the torn edges, the synovial fringe should be abraded to promote a healing response. Research on the efficacy of a fibrin clot to augment healing continues. Arthroscopy of the knee allows confirmation of the configuration of the tear, after which a decision can be made as to whether the patient will benefit from a partial menisectomy with well fashioned edges or meniscal repair. If a meniscal repair is performed, a minidissection is performed on the outside of the knee and brought down through anatomical planes to the joint line. The needle used in an inside-out technique to repair the meniscus may be identified and safely brought out of the wound without risk of neurovascular injury. To repair a meniscus, a long cannula is used to direct the suture needle accurately through the meniscus for the placement of horizontal mattress sutures. At the completion of the placement of the sutures around the meniscal periphery, a stable meniscal rim should be obtained. Following open or arthroscopically aided meniscal repair the patient is protected in a brace for at least 4 to 6 weeks. Sport is not allowed for at least 4 months. A healing rate of more than 80 per cent can be expected.

Osteochondritis dissecans is a focal separation of a fragment of articular cartilage and underlying subchondral bone from the surrounding articular condyle. The fragment maybe partially or completely separated. The condition occurs in the elbow, ankle, hip, and shoulder, but is most common in the knee, particularly in the medial femoral condyle. It also occurs occasionally on the patella and lateral femoral condyle. The aetiology of ostochondritis dissecans remains speculative. Theories include focal avascular necrosis, endocrine abnormalities, anatomical variations, and trauma. The cause is probably multifactorial in most cases, but a single traumatic event or repetitive microtraumatic events are common threads in most theories. Osteochondritis dissecans of the medial femoral condyle may be due to repetitive collision of the lateral edge of the medial femoral condyle against the tibial spine. This injury occurs with rotatory forces applied to the knee and is typically seen in those playing racket sports. Osteochondritis dissecans is most common in the 10- to 20-year age group and the male/female ratio is 3:1. The incidence is approximately 1/2000 in the knee.

Presenting complaints are usually pain on athletic activity, swelling, or clicking. Some patients complain of ‘giving way’. Locking may occur in a patient with a completely separated fragment. The physical examination shows pain about the area of the lesion on palpation. The patient with osteochondritis dissecans frequently has evidence of instability of the knee or genu recurvatum. Wilson's sign is diagnostic of osteochondritis dissecans of the medial femoral condyle. With the patient supine, the affected knee is flexed to 90°, and is then fully internally rotated and extended. Pain over the medial femoral condyle occurs at approximately 30° to full extension. In this position the tibial spine compresses the lesion on the lateral wall of the medial femoral condyle. Pain is relieved by external rotation of the leg. Patients with osteochondritis dissecans of the medial femoral condyle usually stand with increased external rotation of the affected leg, to prevent the tibial spine from pressing on the lesion.

Radiographic assessment allows the location and displacement of the osteochondral fragment to be determined, although a normal anteroposterior radiograph of the knee frequently does not show a femoral condylar lesion. A tunnel view or a notch view should be part of the routine radiographic evaluation of the symptomatic knee. A lateral radiograph often shows the well circumscribed lesion. CT scanning is useful for the diagnosis of osteochondritis dissecans, and also helps in assessment of healing and attachment of the fragment. Radionuclide bone scans help to determine the vascularity of the fragment and the condyle, as well as healing progress. Magnetic resonance imaging is useful for the assessment of vascularity and healing but is expensive.

The initial treatment of an undisplaced attached osteochondritis dissecans fragment in the knee is immobilization with casting to allow the lesion to heal. This method is usually successful in the young teenager or child, but is less so in the adult. Lesions that are separated or which do not heal after a trial of immobilization require operative fixation. The chronically separated fragment that has been floating in the knee as a loose body for months requires excision; this can usually be performed arthroscopically. The defect in the condyle should be drilled or debrided to bleeding bone in an attempt to stimulate fibrocartilagenous healing by revascularization. A recently separated or partially detached fragment should undergo anatomical pin or articular screw fixation to the condyle of origin. This procedure can be done arthroscopically, but the bed of the fragment must be clean of fibrous or necrotic tissue and debrided to bleeding bone if there is to be a reasonable chance of healing. If the lesion is only partially separated multiple drill holes can be placed through the lesion into the condyle to stimulate a bony healing response.

Hypertrophic synovial plicae are a rare cause of knee pain. The knee is formed from the fusion of three compartments that are divided by synovium in the embryo. These compartments fuse during the fourth fetal month. The synovial membrane remnants are called plicae. In some knees these remnants or plicae are nearly completely resorbed, in others they are thick fibrotic bands. Three plicae are commonly seen: the infrapatellar plica or ligamentum mucosum, the suprapatella plica, and the medial patellar plica. The last is seen less often than the other two plicae, but is most likely to be symptomatic. This plica attaches to the medial capsular wall, at the level of the superior edge of the patella, and runs along the anteromedial wall of the capsule to insert on the infrapatellar fat pad.

The symptomatic medial patellar plica is called the ‘shelf syndrome’. This is characterized by complaints of pain, catching, and popping on the medial side of the knee. The patient frequently notes the development of symptoms after a direct blow to the medial side of the joint. After mild trauma, a plica that was asymptomatic can become inflamed, hypertrophied, and painful. Physical examination reveals tenderness over the plica, superior to the medial joint line. Patients typically have pain on extreme flexion of the knee. Snapping of the plica over the medial femoral condyle with flexion is frequently palpable. Patients may also have tenderness along the medial side of the patella or pain with patella compression and range of motion, because of entrapment of a fold of the plica. A patient with similar complaints and medial joint line tenderness may have a torn medial meniscus; careful examination is important.

The shelf syndrome should be treated with rest and non-steroidal medication for 3 to 4 weeks. Symptoms frequently resolve with time. If non-operative treatment fails, arthroscopic excision of the entire medial patellar plica is recommended. Simply dividing the plica can result in recurrent symptoms, with scarring. Care should be taken at the time of arthroscopic excision not to resect the capsular wall. Wide capsular resection can cause complications such as arterial bleeding or lateral subluxation of the patella. The results of arthroscopic excision of the medial patellar plica are good, with most patients being asymptomatic 3 months postoperatively. The diagnosis of shelf syndrome can be difficult and the syndrome is infrequent. Plica resection in the patient who does not have complaints and findings consistent with the diagnosis is unwarranted and not recommended.

Skeletal ligaments are tough flexible band or rope-like structures that connect bone to bone across and about joints and control motion at the articular surfaces of joints in the proper orientation. Ligamentous injury can result in abnormal motion of articular surfaces and result in abnormal damaging forces being transmitted to the articular cartilage.

Ligaments are composed primarily of Type I collagen and water. Type I collagen is a strong, linear collagen with a high tensile strength. Ligaments also contain small amounts of Type III collagen (immature collagen found in scar), elastin, and proteoglycans. Ligaments contain important neurosensory elements, such as mechanoreceptors and Golgi receptors for proprioception and spinal reflexes.

The four stages of ligament healing have been described from study of the rabbit medial collateral ligament. Phase I is represented by inflammation, Phase II by matrix and cellular proliferation, Phase III by remodelling, and Phase IV by maturation (Table 1) 616. After a midsubstance rupture of the medial collateral ligament, inflammation occurs, with the potential space formed by the slight retraction of the ruptured ligament ends becoming filled with blood. The haematoma becomes organized and inflammatory cells invade the area. Polymorphonuclear leucocytes and lymphocytes appear almost immediately; within 24 h monocytes predominate. Monocytes and macrophages then phagocytose necrotic tissue and cellular debris. The end of Phase I is heralded by the migration of fibroblasts into the injury site. As the fibroblasts begin to produce extracellular matrix the injured ligament enters Phase II. As the original blood clot becomes organized the fibroblasts divide and produce large amounts of extracellular matrix material, consisting primarily of Type III collagen. Vascular granulation tissue forms between the two frayed and resorbing ligament ends. Electron microscopy shows these fibroblasts to contain large amounts of rough endoplasmic reticulum, indicative of the intense matrix production occurring at this time. Fibroblasts predominate in the highly cellular scar. Vascular invasion occurs, with capillary buds forming in the wound. The concentration of collagen in extracellular matrix increases steadily, but the total collagen content is still less than that of a normal ligament. Electron microscopy shows the collagen fibres to be highly disorganized and not parallel, as they are in a normal uninjured ligament. Type III collagen is more predominant than Type I. A gradual transition occurs over several weeks, progressing into the remodelling phase. A decrease in the number of fibroblasts and macrophages is seen. The remaining fibroblasts change morphologically and appear flatter. Translucent bridging scar joins the ligament ends. The vascularity of the healing tissues decreases, and the endoplasmic reticulum and cytoplasm content of fibroblasts decreases. The collagen fibres become more densely packed and organized as type I collagen replaces the type III collagen. Phase III lasts several months. At the start of Phase IV the scar is still slightly disorganized and hypercellular. It becomes more organized and appears more normal as the collagen fibres are aligned and adopt the proper crimp frequency and morphological pattern. The maturation phase can last several years. The mechanical strength changes throughout the four stages, going from a low tensile strength in stage I, to near normal in phase IV. Most extra-articular ligament injuries heal well and become functional if allowed to heal without recurrent injury.

The anterior cruciate ligament does not heal or become functional after disruption. This ligament is complex and not a simple band of collagen fibres like the medial collateral ligament. The anterior cruciate ligament has no single isometric fibres; it is an isometric structure with a multiplicity of collagen fibre bundles oriented in a spiral fashion. It is difficult for such a complex spiral structure to heal functionally in the dynamic environment of the knee joint. The biomechanics of the anterior cruciate ligament are of importance in its inability to heal primarily. It is the primary restraint to anterior tibial translation on the femur. In normal gait and stair climbing, abnormal anterior tibial translation allowed by the lack of the anterior cruciate ligament pulls the injured ligament ends away from each other, allowing the femur to rotate and sublux posteriorly. In man the force required to obtain 5 mm of anterior tibial translation decreases from approximately 470 N down to 50 N by cutting the anterior cruciate ligament. The ruptured ends of the anterior cruciate ligament are pulled away from each other with normal everyday use, thereby disrupting any healing process.

The anterior cruciate ligament is unique in that it is intra-articular but extrasynovial. The synovial covering is usually torn when it is ruptured, and loss of this synovial membrane exposes the injured ligament ends to destructive enzymes released within the joint. Synovial fluid adversely affects fibroblasts of the anterior cruciate ligament in vitro. Occasionally, rapid degeneration of the anterior cruciate ligament stump occurs after acute rupture. Collagenase has been implicated in this degradation, and this may be one of the major causes of poor healing of the damaged anterior cruciate ligament. Knees with a deficient anterior cruciate ligament frequently develop meniscal tears secondary to instability. There is a correlation between anterior cruciate ligament tears, meniscal pathology, and degenerative joint disease.

Treatment of the knee with an anterior cruciate deficiencies remains controversial. A basic understanding of the function of the anterior cruciate ligament is important. Motion of the knee can be described as having six degrees of freedom. There is rotation around an internal–external rotation plane, an anterior–posterior or extension–flexion plane, and a medial–lateral or varus–valgus plane. Translation is described on an anterior posterior axis, a medial lateral axis, and a proximal distal axis. Motions are often coupled during the normal activity of the knee, and single-plane analysis does not allow true representation of function. A four-bar linkage system used to describe the anterior cruciate ligament and posterior cruciate ligament restraint on the knee joint helps to illustrate the simultaneous function of these ligaments. The anterior cruciate ligament remains taut to some degree throughout full flexion and extension, and allows the knee to produce the correct amount of rolling and gliding over a full arc of motion. Lack of this ligament results in abnormal motion, with the femur becoming pathologically posterior on the tibial plateau. Abnormal intra-articular motion can cause injury to both articular hyaline cartilage and meniscal fibrocartilage (Figs. 14, 15) 2422,2423. The anterior cruciate ligament also contains sensory organs that provide proprioception for the knee. This allows muscle contraction to assist the ligament in providing stability to the knee. The ultimate strength of the ligament is about 1730 N; most normal activities requires forces of under 450 N. There is, therefore, a significant amount of reserve in the ligament before failure occurs.

Injury to the anterior cruciate ligament can occur following hyperextension or rotatory force. Injury forces are often a combination of rotation and translation, and are therefore accompanied by injuries to the menisci, capsule, and other intra-articular structures.

The injured athlete often hears or feels a pop as the kinetic energy stored within the anterior cruciate ligament is released. Usually, but not always, the knee becomes swollen and painful, and motion of the knee will be limited. The anterior Lachman test provides the highest sensitivity for the evaluation of the disrupted anterior cruciate ligament, and is most accurate soon after injury (Fig. 16) 2424. The knee anterior drawer test is also accurate (Fig. 17) 2425. The pivot shift test uses the iliotibial band to help reduce the anterolateral subluxation of the tibia back into the anatomical position. This is also consistent with an anterior cruciate ligament tear. A full and thorough physical examination is essential: anterior cruciate ligament tears are rarely an isolated lesion. Plain radiographs are the initial study required: the lateral capsular sign or Segond fracture is pathognomonic of disruption of the anterior cruciate ligament. Often, however, these radiographs are negative.

MRI has now become the test of choice for evaluation of these injuries. The accuracy remains at about 85 to 95 per cent and is highly dependent on the skill of the radiologist (Fig. 18) 2427. If an anterior cruciate ligament injury is suspected and the MRI is normal further evaluation is required. Mechanical devices such as the KT–1000 provide an objective measurement of the displacement of the tibia on the femur allowed by the injured ligament. The ‘gold standard’ for definitive diagnosis of an anterior cruciate ligament tear is an arthroscopic evaluation. The patient should be examined under anaesthesia for associated ligamentous injuries, and status of the anterior and posterior cruciate ligaments should be evaluated, as well as the articular surface of the joint and of both menisci. A good history and physical examination are highly accurate in evaluation of such injuries.

There are many variables to consider in the treatment of the anterior cruciate-deficient knee. Modification of lifestyle dictates withdrawal from all sporting activities that requires pivoting, twisting, or turning activity; the anterior cruciate deficient knee will not provide the stability needed. If the athlete is unwilling to make this modification, rehabilitation with an emphasis on strengthening the quadriceps and hamstring muscles, and bracing, is the other conservative option. Surgery provides the final option for a patient with an anterior cruciate deficient knee. An athlete with an anterior cruciate-deficient knee who remains active risks injury to the menisci: 50 to 70 per cent of such patients develop a torn meniscus.

Evolution of the surgical treatment of the anterior cruciate-deficient knee has defined basic concepts which will allow for successful repair. The concept of isometric graft replacement is critical for the reconstruction of any ligament injury. Surgical reconstruction should attempt to replace the ligament with a substitute that will function in a similar anatomical position, in the hope that normal biomechanical function will follow. An accepted standard procedure today is the intra-articular reconstruction of the anterior cruciate deficient knee with an autogenous substitute. The two most common autologous substitutes are the patella–patella tendon–tibial tubercle bone–tendon–bone graft, and the semitendinosis tendon graft. Grafts are placed in an isometric position, through the knee. Regardless of which substitute is used, certain concepts must be maintained. A notchplasty is usually required to allow the removal of any bone impinging on the replacement graft. Good visualization of the notch is also needed so that isometric placement of both the tibial and femoral tunnels can be guaranteed. Isometers can be used to assist in correct placement of guide pins to mark the position of the tibial and femoral bone tunnels. Once the graft has been placed within the knee secure fixation at both ends is necessary. Bone–tendon–bone repair has the advantage of allowing immediate interference screw fixation, and good bony healing is expected within 6 weeks. Although optimal graft strength may not be achieved for over 1 year, a graduated physical therapy programme of increasing stress to the healing graft is required for the maturation of the graft. Athletes usually return to their sport 6 months to 1 year after surgery. Braces may be used.

Posterior cruciate ligament injuries are less common than anterior cruciate ligament injuries. The posterior cruciate ligament is injured by forced posterior translation of the tibia on the femur, as occurs with a fall on a bent knee. The patient may hear a ‘pop’. Another mechanism of injury is deceleration, wherein the leg is impacted with another object. When evaluating the patient with a posterior cruciate ligament injury a globally unstable knee that may have dislocated during the injury and spontaneously reduced must be specifically looked for. Such a patient has a potentially disabling vascular injury that may lead to amputation. An emergency arteriogram is required. The posterior tibial sag test is diagnostic for posterior cruciate ligament disruption: if both legs are held at 90° with the hips flexed at 90°, the tibia on the damaged side is subluxed posteriorly on the femur compared to the contralateral side. The 90° quadriceps active test is another accurate diagnostic physical test. The knee is flexed to approximately 90° and the patient is asked to relax and then contract the quadriceps tendon. If contraction of the quadriceps causes the tibia to go from a subluxed to a reduced position, moving in the anterior direction secondary to the quadriceps pull through the patellar tendon, posterior cruciate ligament injury is indicated. Finally, if there is no tibial ridge with palpation of the anterior joint line sulcus in the injured knee, compared to the normal knee there is a posterior cruciate ligament tear.

Injury to the posterior cruciate ligament is associated with medial compartment articular cartilage injury. When the posterior cruciate ligament tears, the tibia subluxes posteriorly exposing articular cartilage to the femoral condyles. Disruptions of the posterior cruciate are not as disabling as injuries of the anterior cruciate, provided that the patient maintains a strong quadriceps muscle after injury.

Treatment of a posterior cruciate disruption is generally conservative, unless the ligament is avulsed with a bone fragment from either the femoral or tibial attachment. Such a bony attachment avulsion injury is amenable to surgical repair. Primary surgical repair of the posterior cruciate midsubstance often fails. Reconstruction of the ligament requires augmentation grafting with the patella tendon, semitendinosis, or gracilis tendon. Placement of the tibial and femoral tunnels for the ligament graft in an anatomical position is absolutely essential. Reconstruction is reserved for patients in whom conservative treatment and appropriate rehabilitation fails. Conservative treatment for posterior cruciate injury takes the form of approximately 6 weeks of immobilization in 15° of flexion with motion only to full extension in a brace or cylinder cast. Weight bearing is allowed. After this period of immobilization, the patient must undergo aggressive rehabilitation of the quadriceps muscle. There is a strong correlation between quadriceps strength and good results. Some patients develop patella femoral arthritis and tibial femoral arthritis after posterior cruciate ligament injury. In the best series of long-term results of non-operative treatment of isolated posterior cruciate ligament injuries in athletes approximately 80 per cent of patients were satisfied with the long-term outcome and returned to their previous sport.

The ‘isolated’ medial collateral ligament injury does not require surgical treatment. Generally, isolated grade 1 (0–5 mm of medial joint line opening), grade 2 (5–10 mm of medial joint line opening), and grade 3 (>10 mm of medial joint line opening) medial collateral ligament tears can be treated with knee immobilization or a cast brace with early protected mobilization. Basic science and clinical studies have shown the benefits of non-operative treatment of complete tears of the medial collateral ligament of the knees. It is important to exclude an anterior cruciate or posterior cruciate ligament injury as well as medial meniscal injury at the time of initial examination or on further diagnostic studies.

The medial collateral ligament is usually torn secondary to a valgus stress of the knee without rotatory movement. Patients with isolated ruptures of this ligament do not generally hear an audible ‘pop’. Tenderness along the medial collateral ligament either at midsubstance level, or over the femoral or tibial attachment is indicative of a tear. The patient's knee will open up on valgus stress with the knee flexed at 20 to 30°. This opening allows isolation of the medial collateral ligament. If the knee opens up to a valgus stress in full extension, the posterior cruciate ligament is also damaged. The Lachman test may be one plus positive in a patient with an isolated medial collateral ligament disruption, but there will be a firm end-point, indicating that the anterior cruciate ligament is intact.

Diagnostic studies are of limited value in assessing the ruptured medial collateral ligament. Stress radiographs obtained by placing a valgus stress across the knee may demonstrate incompetency of the medial collateral ligament. These are of only moderate help. MRI can be helpful in reaching the diagnosis, as well as helping the clinician assess possible associated injuries such as medial meniscal damage or cruciate ligament injury. Tenderness posterior to the medial collateral ligament in the posteromedial corner of the knee, should suggest additional injury to the posterior oblique capsular ligament. If the cruciate ligaments are intact, medial collateral ligament injuries can be treated with a hinged cast or brace for 3 to 6 weeks. Most patients are able to tolerate full weight bearing at approximately 1 week after injury, after the inflammation subsides. There may be a surprising amount of ligamentous laxity on valgus stress 3 to 6 weeks after injury. In most patients such valgus laxity resolves over the following 12 to 16 weeks. Mild laxity is well tolerated by most athletes, and grade I laxity at a repeat examination should not cause concern. There are minimal complications when medial collateral ligament ruptures are treated non-operatively, provided a tear of the anterior cruciate ligament, which may result in significant knee instability, is not missed.

Treatment of injury to the lateral collateral ligament, (also called the fibular collateral ligament) and the surrounding lateral joint capsule is controversial. This injury is much less common than injury to the anterior cruciate or medial collateral ligaments. Disruption of the lateral collateral ligament is highly associated with injury of the anterior or posterior cruciate ligaments. The lateral collateral ligament can be easily isolated for palpation by flexing the knee and externally rotating at the hip to cross the legs. An isolated injury to this ligament can be treated non-operatively with bracing of the knee with a 30 to 90° arc of motion for 4 weeks, followed by physical therapy with protected range of motion and strengthening. The management of the torn lateral collateral ligament and surrounding complex becomes controversial when it is accompanied by an anterior cruciate tear and rotatory instability. The surgical treatment of acute injury involves primary repair of the lateral collateral ligament with sutures, taking care to avoid injury to the nearby peroneal nerve. Surgical treatment of the chronic tear with instability involves dissection of the ligament and capsular attachment from the femoral side. This complex is then advanced proximally on the femur and reattached with a staple to tighten the ligament and thereby restore its function. Protection after surgery is required while the ligament heals in the new location.

There is a paucity of scientific documentation on the function of knee bracing, and poor clinical studies supporting their use. There are three categories of brace: prophylactic, rehabilitative, and functional. Prophylactic braces are used to prevent knee injuries, particularly to the collateral ligaments. Although such use of knee braces is increasing, no strong clinical studies have proved their efficacy. The rehabilitative brace is used in the postoperative period following ligament repairs. Since it is important that joints move through a protected range of motion after injury, these braces are very useful in controlling knee movement. Functional knee braces are used to provide functional stability to the unstable knee. These braces cannot be relied upon as the only protection for knees with a deficient anterior eruciate ligament. They must be used in conjunction with an effective rehabilitation programme and appropriate activity modification.

Documenting whether anterior knee pain is acute will lead to evaluation of traumatic events such as patellar dislocation or subluxation. Gradual onset is more common in inflammatory disorders such as tendinitis or synovial impingement. Pain during activities is often seen with specific structural abnormalities, whereas pain after activities is more typically inflammatory in nature. Provocative tests such as walking up and down stairs often place the patellofemoral mechanism under stress and should therefore be tested.

Physical examination should begin with evaluation of the overall alignment of the leg, with the patient both standing and sitting. The quadriceps angle (Q angle) is measured from the anterior superior iliac spine to the centre of the patella, then from the centre of the patella to the tibial tubercle (normal values are up to approximately 15°). While standing, the feet are examined: if pes planus or a severe pronation deformity is found, the resultant rotational and angular deformities on the knee may be the cause of anterior knee pain. The thigh circumference of the injured leg should be compared with that of the uninjured leg and the amount of atrophy recorded. The vastus medialis oblique muscle is examined for both development and angle of insertion into the patella. The height of the patella can be determined with the patient sitting and the legs hanging at 90°. Normal, patella alta (high), and patella baha (low) positions can be confirmed by a lateral radiograph of the knee. Patellofemoral stability can be determined by forcefully displacing the patella both medially and laterally with both the knees straight and flexed 40° and measuring percentage displacement from the neutral position. Patellar tilt is measured by estimating the amount the lateral patella can be everted. Patellar tracking is determined by bringing the knee actively and passively through a full range of motion. Palpation of the anterior aspect of the knee during an active range of motion often reveals significant patellofemoral crepitance. Tilting the inferior patella slightly upwards and palpating the insertion of the patella tendon may provide evidence of patellar tendinitis. The degree of hamstring tightness is noted on flexibility testing: tightness often aggravates any underlying patellofemoral problems.

The evaluation of patellofemoral disorders includes standard radiographs of the knee. These comprise an anteroposterior projection, a lateral film with the knee flexed 40°, and a sunrise view of the patellofemoral joint. The anteroposterior view allows gross evaluation of the knee joint alignment and of articular congruity. It also helps in the evaluation of the centring of the patella within the femoral trochlea and with the possibility of a bipartite patella. An anteroposterior view with the knee flexed 40° and the patient weight bearing is particularly helpful in diagnosing early articular narrowing, as this first occurs in the posterior part of the femoral condyles. The lateral view, also at 40° of flexion, is helpful for determining the patella height. The length of the patella tendon from tibial tubercle to the inferior pole of the patella should be approximately 1.2 times the length of the patella itself on the lateral radiograph. The sunrise view demonstrates the patellofemoral articulation best. True centring of the patella in the femoral trochlea, and relative size of both the patella and of the lateral femoral condyle should be determined. A hypoplastic lateral condyle can be associated with lateral subluxation. The degree of lateral patella tilt is recorded. Osteochondral fracture fragments or defects can be seen, the presence of which is suggestive of a significant subluxation or dislocation. CT scanning, MRI, and radionuclide bone scans represent a second level of specialized patellofemoral evaluation.

Because of its normal valgus alignment, contraction of the quadriceps muscle will lead to a lateral displacement of the patella. An increased Q angle, hypoplastic vastus medialis oblique, patella alta, hypoplastic lateral femoral condyle, and lower extremity rotational disorders may place the patient at risk for subluxation or true dislocation. The patient often complains of a knee ‘going out’. This is often due to patellofemoral instability, with either subluxation or dislocation.

If the problem is patellofemoral instability, the patient should be asked if he actually saw the patella displace laterally. True dislocations are easily diagnosed, but accurate diagnosis of subluxation may be quite difficult. In an acute situation the lateral apprehension test, performed by forcefully pushing the patella laterally with the knee extended, may recreate the pain. This is often the only positive confirmation of subtle subluxation. Radiographs may show lateral tilting or lateral subluxation on a sunrise view, but these are often within normal limits. Patella alta and a hypoplastic lateral femoral condyle may also be seen on the sunrise view.

Physical therapy is often successful in the treatment of patellofemoral subluxation. Short arc quadriceps extension exercises from 30° of knee flexion to full extension are often helpful in building up quadriceps musculature, especially the vastus medialis oblique muscle. However, if even this small arc of motion causes pain the patient should be placed on a more restricted programme, comprising multiple sets of quadriceps setting exercises and straight leg raises. Strengthening of both the hip and the ankle musculature and stretching of all lower extremity muscles are also important. Once a safe physical therapy programme has commenced a patellofemoral antisubluxation brace may be used. The athlete's activity may need to be altered.

Patients with patellofemoral pain secondary to maltracking or with patellofemoral instability are candidates for a lateral retinacular release. However, a 6-month programme of non-operative treatment with an appropriate well supervised exercise programme, non-steroidal anti-inflammatory medication, and bracing is a prerequisite to lateral release. The knee should first be examined arthroscopically to identify areas of articular cartilage injury. Evidence of maltracking will often be found: failure of the median ridge of the patella to centre in the femoral notch with contact on both medial and lateral facets by 45° of flexion. The release can be performed with scissors through a small percutaneous approach or can be arthroscopically aided. Release should cause a marked increase in patella tilt compared to the preoperative evaluation, and this should be approximately the same as that obtained on the medial side. Good results are obtained in 80 per cent of selected patients following lateral retinacular release. The most common complication is a haemarthrosis, because the superior lateral geniculate artery runs through the zone of the release. The vessel can often be found and coagulated at the time surgery. Excessive release may result in medial subluxation of the patella, vastus lateralis atrophy, and unsatisfactory results after rehabilitation.

Patients with residual symptoms after lateral retinacular release are challenging because subsequent procedures are even less reliable. The surgeon must avoid the trap of further surgery and a downward spiral of worsening results. The first step is to re-evaluate the differential diagnosis and obtain further radiographic evaluation. A second extended course of physical therapy is also warranted. However, if the patient continues to have lateral instability of the patellofemoral joint, a good proximal and distal realignment, such as the Elmslie–Trillat procedure, gives good results. This procedure involves a more extensive lateral retinacular release and a reefing of the vastus medialis oblique to increase the pull on the patella in a medial direction. In addition, the patient with a high Q angle may benefit from a tibial tubercle osteotomy to rotate the point of insertion medially, thus reducing the lateral force vector on the patella. It is important to avoid any distal advancement of the tibial tubercule, because of the potential for making the patellofemoral pain worse.

Jumpers' knee occurs in athletes engaged in sports in which jumping is stressed. It includes all stress reactions of both the proximal and distal ends of the patella and has been called Sinding–Larsen–Johansonn syndrome, patella tendinitis, quadriceps tendinitis, and patella epiphysitis. Cyclists can also develop this overuse patella tendinitis problem. Blazina classified jumpers' knee into three phases. Phase I is pain only after activity, phase II is pain during and after activity, but the athlete is able to perform satisfactory, and phase III is associated prolonged pain during and after activity that results in an unsatisfactory level of performance. Phase I and II can often successfully be treated with strengthening of the quadriceps and hamstring muscles, with an aggressive hamstring stretching programme. Ice is used after activity. Non-steroidal anti-inflammatory medication is prescribed for 2 to 4 weeks. Patellofemoral restraining braces may help the end-stage of the disease. Prolonged rest and immobilization are often needed to bring the inflammation and accompanying pain under control. Surgery to debride the diseased patellar tendon may be required for end-stage patients.

Osgood-Schlatter's disease is a common and easily recognizable stress injury to the extensor mechanism in the adolescent. The resulting concentration of stress from the quadriceps muscle pull, through the patella tendon to tibial tubercle apophysis results in chondro-osseous failure and separation. Patients often present with an insidious onset of anterior knee pain that is directly related to their activity level. Pain is often bilateral, and patients will point directly to the tibial tubercle as the source of their pain; palpation elicits exquisite tenderness. The hamstring muscles are frequently tight. Radiographic evaluation shows fragmentation of the tibial tubercle apophysis.

Treatment is directed to the relief of stress to the extensor mechanism. Athletic activity usually has to be reduced or stopped. Cold compresses, non-steroidal anti-inflammatory medication, and hamstring stretching are important. With successful treatment and reduction in pain, the athlete can return to sports; however, the underlying pathophysiology must be discussed with the athlete so that they understand the need for activity modification. Completion of growth often renders the athlete asymptomatic. He or she will be left with the minor cosmetic deformity of an enlarged tibial tubercle. Some patients continue to have significant pain and tenderness over the tibial tubercle, with an ununited ossicle in the patella tendon. Resection of the ossicle and surrounding bursa is necessary to relieve symptoms (Fig. 20) 2428.

Compartment syndromes were described as early as the 1850s. Much research has centred on the aetiology, evaluation, and treatment of acute compartment syndromes related to trauma. Chronic compartment syndromes related to exercise may be confused with stress fractures and shin splints. The pain of compartment syndrome is associated with and increased with periods of exercise, and decreases or disappears with rest. Diffuse pain in the affected compartments of both legs is common. Physical findings are often unimpressive: at most there is mild soreness on palpation. The normal resting compartment pressures in the leg are between 4 and 15 mmHg. During exercise, the muscles contract and the bulk of the muscle increases significantly. The four compartments of the leg described classically are the anterior, lateral, superficial posterior, and deep posterior compartments. A fifth compartment, comprising the posterior tibial muscle separate from the deep compartment, has also been described (Fig. 21) 2429. A strong non-compliant fascia divides the muscles of the leg into these compartments. When the muscles contract, the tissue pressure increases inside the fascial compartment; if the pressure increases enough, muscle blood flow is compromised. The pathophysiology is centred around the fact that muscle microcirculation is compromised if tissue pressures increases above 30 to 40 mmHg. Capillary perfusion is inadequate to meet the metabolic demands of the intracompartmental tissue. Irreversible injury may be produced with pressures as low as 30 mmHg for only 6 to 8 h. The athlete feels ischaemic muscle pain and, occasionally, paraesthesias or neuropathic symptoms in the distal distribution of the nerve travelling through the ischaemic compartment.

Tissue pressures in patients with compartment syndrome are higher than normal, both at rest and during exercise. After the completion of exercise elevated pressure is maintained for prolonged periods of time: this prolonged maintenance of an elevated post-exercise compartment pressure is the hallmark of chronic compartment syndrome.

The differential diagnosis includes stress fractures, shin splints, and peripheral neuropathy. The athlete with complaints consistent with compartment syndrome should undergo compartment pressure monitoring. The most accurate technique is a system using a wick or slit catheter to allow dynamic pressure measurements in the patient before, during, and after exercise on a treadmill.

Non-operative treatment such as physical therapy, anti-inflammatory medication, changes in training regimen, or in shoe type may improve the symptoms. Most patients do not require surgical release, but if conservative treatment fails, a fasciotomy of the involved compartment generally relieves the discomfort. These athletes require a supervised physical therapy programme and need 2 to 3 months for rehabilitation.

Exercise-induced pain in the leg may be due to the medial tibial stress syndrome, commonly called shin splints. These are caused by repetitive traction and microinjury to the periosteal attachment of the soleus muscle, at the posteromedial corner of the midshaft of the tibia which causes a painful periostitis. It is not a compartment pressure-related phenomenon. The athlete with shin splints complains of pain of variable intensity brought on by running or jumping and relieved by rest. The posteromedial border of the tibia is tender and the patient usually has pronated feet, but is otherwise normal. Radiographs are usually negative, although in severe cases there may be some periosteal reaction along the posteromedial border of the lower tibia. A bone scan usually shows increased uptake on the medial side of the distal tibia.

Treatment of shin splints is non-operative, except in severely affected individuals if conservative treatment fails. Rest, non-steroidal anti-inflammatory medication, and treatment of the pronated foot deformity with orthotics are the usual treatments. Ice to the area of pain after all activity is helpful. Surgical treatment takes the form of fasciotomy of the soleus attachment to the posteromedial corner of the tibia.

Stress fractures, also described as fatigue fractures, insufficiency fractures, and march fractures, are common in athletes who submit the musculoskeletal system to cyclical stresses beyond which the bone is able to respond. Wolff's Law dictates that bone remodels in response to stress: in the normal state there is an equilibrium between the synthesis and degradation of bone.

Runners provide a classic example of the formation of stress fractures. Muscle fatigue may cause altered gait and decreased energy absorption, both of which result in an altered stress distribution with excessive elastic deformation of bone in response to stress. Local bone resorption can result in a relatively isolated osteoporosis. In response to the stress of running, the body attempts to increase the amount of bone laid down to stabilize the bony architecture. If however, stress continues beyond the body's ability to respond, there is an insufficiency of the reparative process; a stress fracture results. This is a localized incomplete lesion. Training techniques have come under closer scrutiny because of the cyclical loading incurred in most sports. The athlete must have regularly scheduled periods of rest to allow the bone to stabilize.

Eating disorders are not uncommon, especially among women athletes. Female athletes are therefore at an increased risk for stress injuries. A normal oestrogen/progesterone cycle is also important in maintaining bone mass. Unfortunately endurance sports such as running may render the female athlete amenorrhoeic and at an increased risk for stress fracture.

The physician has to maintain a high index of suspicion for non-traumatic injuries that present with gradual onset of symptoms. This often coincides with a change in the athlete's level of physical activity. If the stress fracture is located on an extremity such as the metatarsal or tibia the physical examination is highly diagnostic. However, if it is in the area of the pubic rami or femoral neck, the physical examination may be less helpful. Initial diagnostic studies include radiographs. However radiographically evident changes may not appear for 3 to 6 weeks: findings are often negative at the initial presentation. The bone scan is the standard examination used to evaluate stress fractures, the affected area shows increased uptake and false-negative results are rare. The bone scan must be correlated with radiographic results because false positive bone scans may occur. Bone cysts, osteomyelitis, osteoid osteoma, and other injuries must be considered.

Ignoring the early warning signs of a stress fracture may lead to a complete cortical break. Once a stress fracture is suspected the athlete's activities must be modified: elimination of repetitive use is essential. Rest of the injured bone will usually allow normal healing. Casting is rarely required unless the athlete has significant symptoms. Medications are rarely indicated. Any metabolic deficiency should be treated. Surgery is rarely indicated for these injuries unless a displaced fracture or an impending fracture such as in a femoral neck develops. In a patient treated appropriately in a conservative manner symptoms often last 4 to 6 weeks. The patient should continue to exercise to maintain cardiovascular fitness which unloading forces across the stress fracture site. This goal can often be achieved with aquatic rehabilitation: in a pool the athlete is in a stress-free environment and can maintain his or her level of muscle tone. Athletes should not return to sports for an average of 3 to 8 weeks, depending on the progress of fracture healing. The athlete must be pain free and have undergone a rehabilitation programme prior to returning to athletics.

Prevention is the best treatment for stress fractures. Sports that require a high amount of running or jumping place athletes at special risk, and training regimens that provide for rest during the season are most appropriate. Proper equipment, including shoes and running surfaces, are also important. Coaches and nutritionists must help their athletes maintain adequate levels of nutritional support. Women with hormonal irregularities should be evaluated by a gynaecologist.

The lateral ligament complex ankle sprain is the most frequent injury sustained by athletes and it accounts for the greatest loss of time from training and competition. The ankle joint owes its stability to its bony architecture as well as to its ligamentous support. The distal tibia (plafond), the medial malleolus, and distal fibula (lateral malleolus) form a bony mortise in which the talus articulates. This joint is further stabilized by the superficial and deep layers of the deltoid ligament medially, the syndesmotic ligament between tibia and fibula, and by the lateral ligament complex. The lateral ligament complex is composed of the anterior talofibular ligament, the calcaneofibular ligament, and the posterior talofibular ligament. The syndesmosis between the distal tibia and fibula comprises a coalition of the interosseous ligament, the anterior inferior tibiofibular ligament, and the posterior inferior tibiofibular ligament. The articular surface of the talus resembles a section of a cone. That bony architecture lends itself to rotatory instabilities of the ankle (Fig. 22) 2430.

The most common mechanism of injury for an ankle sprain is plantar flexion of the foot with inversion and internal rotation. The anterior talofibular ligament is the primary restraint for talar internal rotation, plantar flexion, and anterolateral subluxation. The deltoid ligament also provides significant resistance to plantar flexion and internal rotation. When the pathological motion consists primarily of inversion, the calcaneofibular ligament becomes the primary stabilizer. In eversion injuries, which are uncommon, the deltoid ligament represents over 80 per cent of the resistance to the pathological motion. In considering ankle sprains it is also important to consider the physiological loading across the articular surface. The articular surface of the ankle joint provides approximately 100 per cent of stability in both inversion and eversion and approximately 30 per cent of stability in rotation.

The aetiology of ‘weak ankles’ continues to be examined. Cadaver studies have shown that as the angle between the anterior talofibular ligament and the calcaneofibular ligament increases above 125° there is a corresponding decrease in the stability of the ankle joint to an inversion stress. This is theoretically due to the absence of a ligament in the line of stress along the deforming force. Athletes with a high arch and a plantar flexed first metatarsal are at risk for repeated ankle sprains since the normal resting position of their foot results in an inversion attitude.

The standard grading of ankle injuries is similar to that of other ligament injuries about the body. A grade 1 sprain is a mild stretch with partial ligamentous tear but with overall structural integrity maintained. A grade 2 sprain is a moderate sprain with a greater degree of ligamentous disruption but with overall continuity maintained. A grade 3 ankle sprain is a severe sprain resulting in complete loss of ligamentous continuity. Although this grading system has been generally accepted, it often does not help fully identify the pattern and degree of ligamentous injury.

Since initial radiographs are often normal, assessment of the sprained ankle relies heavily on clinical examination. Stability can be considered in three planes. The injured ankle is always compared to the uninjured or normal side. The coronal plane is evaluated by a forced adduction tilting of the talus. Sagittal plane stability is evaluated by the anterior tibiotalar drawer test. The horizontal plane is evaluated by the amount of anterolateral rotatory instability. The syndesmosis can be evaluated by the squeeze test. Compression of the tibia and fibula above the mortise is painful if there is a disruption of the syndesmotic ligaments.

Since ankle pain and ankle sprains are a common presenting complaint to sports medicine physicians, an accurate differential diagnosis must be entertained. Tarsal coalition (fusion of hindfoot bones) has been described as common in patients with ankle sprains, and should be looked for in the initial radiographs. Special angled plain films or CT scan may be needed for positive identification. Patients may present with occult fractures or a stress fracture which may not be apparent on initial radiographs. Occasionally, a rupture of a tendon will present as an ankle sprain. Osteochondritis dissecans of the talar dome should be apparent on initial radiographs.

Comparison stress radiographs are helpful in understanding which ligaments are injured. Stress examinations are performed in an anterior plane to evaluate the function of the anterior talofibular ligament. Medial talar tilt views in the adduction plane help evaluate the calcaneofibular ligament. The literature does not establish the exact amount of displacement needed to establish definite ligamentous disruption.

Initial treatment of grade 1 and 2 ankle sprains takes the form of rest, immobilization, ice, compression, and elevation. Patients then require an aggressive rehabilitation programme that emphasizes peroneal and lower leg muscle strengthening, proprioceptive retraining, and functional splinting. There is some controversy over treatment of grade 3 ankle sprains. Clinical outcome studies indicate that a great majority of these patients can be initially casted with the foot in slight dorsiflexion and eversion to allow the disrupted ligament ends to approach one another and heal in a normal anatomical length. At the end of the immobilization period, a rehabilitation programme is begun.

Occasionally, an athlete has continuing instability of the ankle in spite of appropriate conservative care. Surgical reconstruction of the ruptured lateral ankle ligaments is then required. Several procedures have been described which attempt to reconstruct one, two, or all three of the lateral ligaments. For optimal success exact documentation of the ligamentous injury is required. The most common repairs require a section of the peroneal brevis tendon to be woven from the base of the fifth metatarsal through the fibula, and occasionally through the calcaneus, to provide lateral stability. Newer concepts of ligament reconstruction include attempts to reef the original lateral ligament complex to provide isomeric reconstruction without affecting joints distal to the ankle joint. The literature reports satisfactory results in about 85 per cent of patients, irrespective of technique used.

Specific indications for use of the arthroscope in the ankle are still being developed. The arthroscope is useful for removal of loose bodies and osteophytes, evaluation and treatment of osteochondral defects, lysis of post-traumatic adhesions, synovectomy, and evaluation of post-traumatic pain. Lateral ankle impingement disorder is seen in patients with chronic lateral ankle pain, not related to instability, occurring months to years after an ankle sprain. The patient complains of pain in the anterolateral corner of the ankle joint with activity. Physical examination discloses tenderness on palpation over the joint line at the distal tibiofibular syndesmosis. This pain is increased with dorsiflexion. The distal band of the anterior inferior tibiofibular ligament subluxes into the joint and impinges on the talus as the talus swings up in dorsiflexion. This subluxed band of ligament can be removed arthroscopically without a loss of ankle stability. Arthroscopic techniques can also be used for ankle fusion and lateral ligamentous reconstructions.

Ankle arthroscopy is usually an outpatient procedure performed under general anaesthesia, although local or regional blocks can be used. Because of the multiple tendons and neurovascular structures in close proximity to the ankle joint, the surgeon needs to palpate and identify the locations for the portals prior to inflation of the tourniquet. After the neurovascular structures and the tendons have been marked, the tibiotalar joint is identified. A spinal needle is placed in the joint and used to distend the joint with saline or lactated Ringer's solution. The anterolateral portal is then made using a scalpel to incise the skin and then sharp and dull trochars to pierce the capsule. The intermediate dorsal cutaneous nerve can be injured while developing this portal. A diagnostic arthroscopy can be performed through this portal alone using a 2.7 mm or 4.0 mm arthroscope. The anteromedial portal is made at the anteromedial corner of the ankle joint, taking care to avoid the saphenous vein, which should be medial to the preferred location of the portal on the medial side of the tibialis anterior tendon. Most procedures can be performed through these two portals. Occasionally a device such as an external fixator is needed to distract the talus away from the tibia, thus increasing the joint space for improved visualization. The anterolateral and anteromedial portals are the most commonly used and safest portals, but others have been described. The ankle may be a more difficult joint to arthroscope than the knee or shoulder because of its limited intra-articular space; however it is effective and associated with low morbidity and a rapid recovery and return to activity when used for appropriate indications.

Tendinitis, or inflammation of a tendon and its surrounding tissue or sheath, is a frequent cause of pain about the foot in athletes. The Achilles, posterior tibial, and peroneal tendons are the most frequently involved. Tendinitis about the foot is usually due to repetitive stress to the tendon; irritation from an external source or bony prominence can contribute to its formation. Poor training habits or a training error, such as marked increase in distance or speed in runners, can result in tendinitis. Tendinitis about the foot usually occurs in endurance athletes or those using long distance running training techniques. There is an insidious onset of pain that is increased by performing activity that stresses the inflamed tendon. Palpation usually quickly localizes the involved tendon and the area is frequently indurated and crepitant. Care should be taken to ensure the tenderness is not of a bony origin, indicative of a stress fracture. The evaluation should rule out other diseases, such as rheumatoid arthritis or gout.

Treatment of tendinitis consists of rest, ice, and non-steroidal anti-inflammatory medication. Rest for 3 weeks is usually needed for the inflammation to resolve. Immobilization with splinting or casting is helpful in refractory or non-compliant athletes. A 5- to 8-mm heel lift is useful for treating Achilles tendinitis: the tendon is rested by avoiding stretch. The patient's shoes should be examined for poor fit or edges that rub against the inflamed tendon. Proper shoe wear is very important in runners to prevent recurrence of tendinitis. The formation of a protruding painful bursa along the Achilles tendon, called Haglund's syndrome, is due to irritation by rigid low-back shoes. The running shoe should have adequate padding, midfoot support and a heel counter or lift. Although local corticosteroid injection can relieve pain and inflammation, it is not recommended because it does not treat the cause of the inflammation and may actually weaken the tendon. It is important to relieve the inflammation of tendinitis; chronic inflammation can lead to tendon necrosis and rupture. After resolution of tendinitis stretching exercises and a graduated return to athletic activity are important to avoid recurrence. Surgery is rarely indicated, but paratenon release with debridement of inflammatory tissue can be useful for intractable Achilles tendinitis.

Plantar fasciitis is inflammation of the plantar fascia and presents with moderate pain of insidious onset about the plantar surface of the foot near the calcaneus. The pain and inflammation are secondary to repeated traction on the plantar fascia, causing microtears and injury. The calcaneal insertion of the plantar fascia is tender. The patient may have a pronated foot, which contributes to the traction injury of the plantar fascia, and often has a tight gastrocnemius soleus complex, causing increased stress concentration on the plantar fascia. This overuse injury is typically seen in long-distance runners or walkers. Hill or toe running, running on soft terrain, and sudden increases in activity are contributory factors to plantar fasciitis.

Treatment is much the same as for tendinitis with rest, ice, and non-steroidal medication. Corticosteroid injection can be useful. Heel pads and arch supports give relief and emphasize the importance of adequate shoe wear in these athletes. Athletes with a tight gastrocnemius soleus complex should be taught stretching exercises to avoid recurrent symptoms.

Excessive pronation of the foot can be asymptomatic or can frequently accompany many disorders in running athletes. Severe pronation causes malalignment of the foot with the subtalar joint, the ankle joint, and the knee joint. Pronation deformity is a contributory factor to overuse injuries, such as plantar fasciitis, posterior tibial and Achilles tendinitis, and chondromalacia patellae. Pronation of the foot permits excessive internal rotation of the leg, allowing lateral displacement of the patella. This abnormal lateral displacement results in increased force on the lateral articular facet of the patella and causes pain and articular damage called chondromalacia or ‘runner's knee’.

Orthotic devices that support the arch of the pronated foot are useful to treat and prevent the sequelae of the pronation deformity. Custom-made orthotic devices are expensive, and their construction and fitting require special expertise. Off-the-shelf orthotic shoe inserts can be used to see whether such treatment will relieve the condition. If relief is obtained with an inexpensive orthotic, soft custom orthotics should be fabricated for the patient's athletic shoes and hard plastic orthotics for street shoes. If no relief is obtained from the inexpensive off-the-shelf orthotic, no investment in the custom-made orthotics is required.

Rupture of the Achilles tendon or tendocalcaneus is common in middle-aged amateur athletes. Typically, a basketball player in suboptimal physical condition jumps and feels immediate pain in the posterior aspect of the leg. For the younger person the ruptures usually occurs near the musculotendinous junction (‘tennis leg’), and in the middle-aged person the rupture affects the midsubstance of the tendon closer to the calcaneus. Physical examination can be misleading, because the patient is often able to plantarflex the foot actively. The Thompson test aids diagnosis of an acute Achilles tendon rupture. With the patient prone, and the knee flexed 90°, the gastrocnemius-soleus muscle complex is squeezed. If the Achilles tendon is intact the foot will plantarflex. If the tendon is ruptured the foot will not plantarflex (Fig. 24) 2433. A defect in the tendon may be palpable if the patient is seen very early after injury.

Treatment of Achilles tendon ruptures is controversial. Non-operative treatment comprises immobilization of the leg with the foot in equinus for 6 weeks, followed by progressive weight bearing and range of motion rehabilitation. Surgical options vary from percutaneous repair techniques to open procedures with primary sutures and fascial turndown flaps. A period of postoperative immobilization is required with most techniques. Open surgical repair gives excellent results with minimal complications in healthy athletes. Debilitated patients or those with significant surgical risk are treated non-operatively with immobilization in equinus.

The medial and lateral sesamoid bones of the foot are contained in the tendon of the flexor hallucis brevis. The sesamoids are usually fractured by a fall from height or hyperextension injury of the great toe. This is seen in ballet dancers, who also suffer other deforming abnormalities of the great toe, and athletes involved in other jumping activities. Physical examination discloses tenderness on palpation of the sesamoid bones, increased with dorsiflexion of the great toe. The injury can be very painful and debilitating. Anteroposterior and lateral radiographs of the foot usually reveal the fracture; however, a tangential sesamoid view may be required. Treatment of the non-displaced or minimally displaced fracture consists of casting for approximately 3 weeks. If pain is still present after 3 months of rest and immobilization, surgical excision can be performed with repair of the flexor hallucis brevis tendon. This fracture must not be confused with a bipartite sesamoid, a normal variant with a similar radiographic appearance.

Turf toe is another injury caused by forced hyperextension of the great toe. This injury is seen in football players and occurs most frequently in players wearing lightweight shoes on an artificial playing surface. Injuries range from fractured sesamoid bones, through phalangeal fractures, to dislocation of the first metatarsophalangeal joint and can cause symptoms ranging from minor nuisance to total disability requiring surgical reconstruction. The injury usually results when a player standing on his toes with his heels off the ground is hit by another player, causing the metatarsophalangeal joint to sustain a forced hyperextension.

Physical examination and radiographs are important to define the injury and rule out more severe conditions. Most turf toe injuries can be treated non-operatively. Dislocation of the metatarsophalangeal joint should be reduced and immobilized for 3 to 4 weeks. Fractures of the phalanges can usually be treated with taping and a hard sole shoe. Intra-articular fractures may need reduction and internal fixation. If the athlete has chronic instability or other difficulty after a trial of non-operative treatment, surgery for capsular repair or sesamoid excision may be required. Thin steel inserts made especially for athletic shoes can decrease the incidence of turf toe.

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Ligaments

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Bartlett EC. Arthroscopic repair and augmentation of the anterior cruciate ligament in cadaver knees. Clin Orthop 1983; 172: 107–11.

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Clancy WG, Shelbourne KD, Zoellner GB, Keene JS, Reider B, Rosenberg TD. Treatment of knee joint instability secondary to rupture of the posterior cruciate ligament. J Bone Joint Surg 1983; 65A: 310–22.

DeHaven KE. Diagnosis of acute knee injuries with hemarthrosis. Am J Sports Med 1980; 8: 9–14.

DeLee JC, Riley MB, Rockwood CA Jr. Acute straight lateral instability of the knee. Am J Sports Med 1983; 11: 404–11.

Fischer SP, Fox JM, Del Pizzo W, Friedman MJ, Synder SJ, Ferkel RD. Accuracy of diagnoses from magnetic resonance imaging of the knee. J Bone Joint Surg 1991; 73A: 2–10.

Garrick JG, Requa RK. Prophylactic knee bracing. Am J Sports Med 1987; 15: 471–6.

Gillquist J, Odensten M. Arthroscopic reconstruction of the anterior cruciate ligament. Arthroscopy 1988; 4: 5–9.

Hughston JC, Bowden JA, Andrews JR, Norwood LA. Acute tears of the posterior cruciate ligament: results of operative treatment. J Bone Joint Surg 1980; 62A: 438–50.

Levy IM, Torzilli PA, Warren RF. The effect of medial meniscectomy on anterior-posterior motion of the knee. J Bone Joint Surg 1982; 64A: 883–8.

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Paulos LE, Butler DL, Noyes FR, Grood ES. Intra-articular cruciate reconstruction. II: Replacement with vascularized patellar tendon. Clin Orthop 1983; 172: 78–84.

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Wojtys EM, Loubert PV, Serafin YS, Viviano DM. Use of a knee-brace for control of tibial translation and rotation. J Bone Joint Surg 1990; 72A: 1323–9.

Woods GW, Stanley RF, Tullos HS. Lateral capsular sign: X-ray clue to a significant knee instability. Am J Sports Med 1979; 7: 27–33.

Patellofemoral

Blazina ME, Kerlan RK, Jobe FW, Carter VS, Carlson GJ. Jumper's knee. Orthop Clin N Am 1973; 4: 665–78.

Bowers K. Patellar avulsion as a complication of Osgood-Schlatter disease. Am J Sports Med 1981; 9: 356–9.

Cash JD, Hughston JC. Treatment of acute patellar dislocation. Am J Sports Med 1988; 16: 244–9.

Cerullo G, et al. Evaluation of the results of extensor mechanism reconstruction. Am J Sports Med 1988; 16: 93–6.

Huberti HH, Hayes WC. Contact pressures in chondromalacia patellae and the effects of capsular reconstructive procedures. J Orthop Res 1988; 6: 499–508.

Hughston JC, Deese M. Medial subluxation of the patella as a complication of lateral retinacular release. Am J Sports Med 1988; 16: 383–8.

Hughston JC, Walsh WM. Proximal and distal reconstruction of the extensor mechanism for patellar subluxation. Clin Orthop 1979; 144: 36–42.

Inoue M, et al. Subluxation of the patella: computed tomography analysis of patellofemoral congruence. J Bone Joint Surg 1988; 70A: 1331–7.

Jensen CM, Roosen JU. Acute traumatic dislocations of the patella. J Trauma 1985; 25: 160–2.

Medlar RC, Lyne ED. Sinding-Larsen-Johansson disease. Its etiology and natural history. J Bone Joint Surg 1978; 60A: 1113–16.

Ogilvie-Harris DJ, Jackson RW. The arthroscopic treatment of chondromalacia patellae. J Bone Joint Surg 1984; 66B: 660–5.

Osborne AH, Fulford PC. Lateral release for chondromalacia patella. J Bone Joint Surg 1982; 64B: 202–5.

Simpson LA, Barrett JP Jr. Factors associated with poor results following arthroscopic subcutaneous lateral retinacular release. Clin Orthop 1984; 186: 165–71.

Leg

Matheson GO, Clement DB, McKenzie DC, Taunton JE, Lloyd-Smith DR, Macintyre JG. Stress fracture in athletes: a study of 320 cases. Am J Sports Med 1987; 15: 46–58.

Mubarak SJ, et al. The medial tibial stress syndrome (a cause of shin splints). Am J Sports Med 1982; 10: 201–5.

Puranen J, Alavaikko A. Intracompartmental pressure increase on exertion in patients with chronic compartment syndrome in the leg. J Bone Joint Surg 1981; 63A: 1304–9.

Rorabeck CH, Fowler PJ, Nott L. The results of fasciotomy in the management of chronic exertional compartment syndrome. Am J Sports Med 1988; 16: 224–7.

Rorabeck CH. The diagnosis and management of chronic compartment syndrome. In: Barr JS Jr, eds. Instructional Course Lectures. Chicago: American Academy of Orthopedic Surgery. 1989: 466–471.

Torg JS, Pavlov H, Cooley LH, Bryant MH, Arnoczky SP, Bergfeld J, Hunter LY. Stress fractures of the tarsal navicular: a retrospective review. J Bone Joint Surg 1982; 64A: 700–12.

Ankle

Attarian DE, et al. Biomechanical characteristics of human ankle ligaments. Foot Ankle 1985; 6: 54–8.

Bassett FH, Gates HS, Bills JB, Morris HB, Nikolaou PK. Talar impingement by the anteroinferior tibiofibular ligament. J Bone Joint Surg 1990; 72A: 55–9.

Black HM, Brand RL, Eichelberger MR. An improved technique for the evaluation of ligamentous injury in severe ankle sprains. Am J Sports Med 1978; 6: 276.

Carson WG, Andrews JR. Arthroscopy of the ankle. Clin Sports Med 1987; 6: 503–12.

Chapman MW. Sprains of the ankle. American Association of Orthopedic Surgeons Instructional Course Lectures, Vol XXIV. St Louis: CV Mosby, 1975; 24: 294–308.

Chrisman OD, Snook GA. Reconstruction of lateral ligament tears of the ankle. J Bone Joint Surg 1969; 51A: 904–12.

Cox JS. Surgical and nonsurgical treatment of acute ankle sprains. Clin Orthop 1985; 198: 118.

Evans GA, Hardcastle P, Frenyo SD. Acute rupture of the lateral ligament of the ankle: to suture or not to suture? J Bone Joint Surg 1984; 66B: 209–12.

Gillespie HS, Boucher P. Watson-Jones repair of lateral instability the ankle. J Bone Joint Surg 1971; 53A: 920–31.

Grace DL. Lateral ankle ligament injuries: inversion and anterior stress radiography. Clin Orthop 1984; 183: 153–9.

Kannus P, Renström P. Treatment for acute tears of the lateral ligaments of the ankle. Operation, cast or early controlled mobilization. J Bone Joint Surg 1991; 73A: 305–12.

Sefton GK, George J, Fitton JM, McMullen H. Reconstruction of the anterior talofibular ligament for the treatment of the unstable ankle. J Bone Joint Surg 1979; 61B: 352–4.

Foot

Andrews JR. Overuse syndromes of the lower extremity. Clin Sports Med 1983; 2(1): 137–48.

Barnes MJ, Hardy AE. Delayed reconstruction of the calcaneal tendon. J Bone Joint Surg 1986; 68B: 121–4.

Carden DG, Noble J, Chalmers J, Lunn P, Ellis J. Rupture of the calcaneal tendon. The early and late management. J Bone Joint Surg 1987; 69B: 416–20.

Coker TP, Arnold JA. Sports injuries to the foot and ankle. In: Jahss MH, ed. Disorders of the Foot. Philadelphia: WB Saunders 1982: 1578–604.

James SL, Bates BT, Osterng LR. Injuries to runners. Am J Sports Med 1978; 6: 40.

Ma GWC, Griffith TG. Percutaneous repair of acute closed ruptured Achilles tendon. Clin Orthop 1977; 128: 247–55.

Nistor L. Surgical and non-surgical treatment of Achilles tendon. J Bone Joint Surg 1981; 63A: 394–9.

Rubin BD, Wilson HJ Jr. Surgical repair of the interrupted Achilles tendon. J Trauma 1980; 20: 248.

Schepsis AA, Leach RE. Surgical management of Achilles tendinitis. Am J Sports Med 1987; 15: 308–15.

Torg JS, Paulov H, Torg E. Overuse injuries in sport: the foot. Clin Sports Med 1987; 6(2): 291–4.