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Swimming is one of the most popular sports in the UK, with huge participation at non-elite level. People swim for reasons that range from fun, relaxation and cardiovascular fitness to competition1. In contrast with other mass participation sports such as rugby and football, swimming is relatively safe, with a low risk of major musculo-skeletal injuries, even at top competitive level. Kennedy and Hawkins found the prevalence of orthopaedic complaints in 2,496 Canadian competitive swimmers to be approximately 11%.2
Musculo-skeletal injuries in swimmers may be traumatic or secondary to overuse. Acute traumatic injuries are rare, and are mainly seen in water sports such as diving, water polo or water skiing. Overuse injuries occur predominantly in elite swimmers and mainly affect the shoulder, although many also involve the knee, elbow, foot and ankle, and the back (see chart overleaf).
There are four recognised strokes in competitive swimming: the ‘freestyle’ or front crawl, the breaststroke, the back stroke and the butterfly stroke. Shoulder problems arise from freestyle and butterfly strokes, but may occasionally be associated with breaststroke. Although most knee problems are caused by breaststroke, they may also occur in all stroke types4.
Richardson estimated that the competitive swimmer makes 1.32 million strokes per arm per year5; hence the predisposition to overuse-related shoulder pain. Classically, ‘swimmer’s shoulder’ refers to the painful arc syndrome caused by impingement of the supraspinatus and biceps tendons against the overlying coraco-acromial arch. Although the pain is usually related to tendinopathy, instability or both, recent evidence from Weldon and Richardson6 shows that most shoulder pain is caused by instability, which in turn is related to the sport-specific demands of:
Neer and Welsh described a classification system for shoulder tendinitis7. Stage I, mostly seen before the age of 25, consists of oedema and haemorrhage of the supraspinatus and biceps tendons from overuse. Stage II consists of fibrosis and tendinitis, and usually occurs in those older than 25 years. In Stage III, seen mostly after 40 years of age, there is degeneration and rupture of the tendons, as well as changes in the bony structure.
Impingement tendinopathy comes about through overwork, subacromial loading and hypovascularity8. The shoulder is a relatively unstable joint, conferring a high degree of mobility and significantly relying on the rotator cuff muscles for stability. When competitive swimmers make repeated overhead movements, the muscles fatigue, superior migration of the humeral head occurs and subacromial loading is increased, contributing to tendinopathy.
The blood supply to the tendon of supraspinatus and long head of biceps is another factor. When the arm is held in adduction and internal rotation, the two tendons are stretched over the humeral head, reducing the blood supply near the musculo-tendinous junction, which predisposes to tendinopathy8.
Finally, the passage of the tendons under the coraco-acromial arch makes them vulnerable. When the arm is abducted, flexed and internally rotated during entry and the beginning of the pull phase, the tendons are impinged upon as the head of the humerus is forced superiorly8. This in turn leads to degenerative changes and tendinopathy.
Weldon and Richardson showed that shoulder stability depends on the interaction between the bony ana-tomy, capsulo-ligamentous complex, and rotator cuff muscles. Reduced stability in one area is often compensated for by increased stability in other areas, but when the stabilisers are pushed beyond their limits, subluxation (temporary, partial dislocation) can occur, leading to unusual stress and inflammation of the tissues about the shoulder6.
The diagnosis of tendinopathy is usually clinical. Patients complain of pain and occasional snapping, especially in circumduction at the overhead phase of the stroke. There may be tenderness at the coraco-acromial ligament and the apprehension test may be positive. The diagnosis may be confirmed with the aid of plain radiography, arthroscopy or MRI.
In the first instance, treatment of swimmer’s shoulder is symptomatic focusing on rest, ice packing and non-steroidal anti-inflammatory medications. Physiotherapy with muscle strengthening exercises, bracing and heat is usually helpful. Attention to stroke mechanics and patient education are also vital.
Local cortico-steroid injections should be used judiciously: this treatment is controversial, as corticosteroids can weaken collagenous tissues9. Surgery for resistant cases of tendinopathy includes decompression by excising the coraco-acromial ligament, or anterior acromioplasty, with or without distal clavicle excision.
To treat instability, there is normally a ladder of management methods of increasing complexity. This always begins with shoulder specific rehabilitation programmes aimed at muscle control and may necessitate training and stroke modifications. In a few cases surgery is required. The precise operation undertaken depends on the exact underlying pathology but in principle the weak shoulder capsule is either tightened or augmented to resist dislocation.
Knee pain ranks second after shoulder pain as a common com-plaint in competitive swimmers. It mostly affects breaststrokers, but may occur in any stroke4.
Injuries to the knee were originally described as being isolated to the medial collateral ligament (MCL). However, Stulberg et al later documented abnormalities of both the MCL and the medial patellar facet10. On the other hand only one case of medial synovitis was reported in a study of breaststrokers with knee pain by Keskinen et al11. The medial side of the knee is the main site of problems because the ‘whip kick’ – a prominent feature of the breaststroke – applies high valgus loads on the joint.
Clinically, the diagnosis of MCL strain is suggested by point tenderness along the course of the ligament, especially at its origin and insertion. Applying a valgus external rotation force to the knee flexed at 20 to 30 degrees will often reproduce the pain1. With the patello-femoral syndrome, abnormal lower extremity alignment may be present, with or without hypermobility or instability of the patellofemoral joint. Tenderness is usually found on palpating the patellar facets, and pain may be reproduced with the patello-femoral compression test1.
Clinical findings in medial synovitis are local tenderness and a palpable thickened syno-vium as it crosses the medial femoral condyle. Confirmation of the diagnosis may require plain radiography, MRI and/or arthroscopy.
Most swimmers’ knee pain responds well to conservative treatment. This involves rest, activity modification, proper warm-up and physiotherapy. Acute symptoms are treated with rest, ice and NSAIDs. Local corticosteroid injections should be used with caution.
Surgery for knee pain is reserved for patients not respon-ding to conservative measures. Options include arthroscopic debridement of medial patellar facet chondral lesions, re-section of fibrotic and thickened synovial plica, and lateral retinacular release.4
Competitive swimmers aim for maximal ankle plantarflexion and, among breaststrokers, maximal dorsiflexion. They gain the extra range of movement by stretching the anterior compartment muscles of the leg during the stroke action. Repetitive actions of this sort may inflame the extensor tendons2.
A diagnosis of extensor tendonitis around the ankle is usually straightforward. There is pain and crepitus over the tendons during flexion and extension. Treatment is rest, ice and heat. NSAIDs are often effective. In resistant cases, local corticosteroid injections may prove effective, but should be used with caution2.
Swimming-related problems around the elbow stem from the arm pull in the butterfly stroke and breaststroke, and, less frequently, in freestyle1. Most competitive swimmers use a form of ‘elbow-up’ pull, which involves bending the elbow and holding it higher than the hand throughout the first part of the pull. This creates the most efficient angle for the swimmer to pull the water backward, giving maximal thrust of the hand3. As the elbow is bent, the upper arm rotates internally and the forearm pronates. Repeated movement of this type can provoke lateral epicondylitis (tennis elbow).
The diagnosis of lateral epicondylitis is clinical, and treatment is conservative. Ice, NSAIDs and physiotherapy, plus stroke alteration, are usually effective. Surgery, in the form of excision of the degenerative lesion usually found in extensor carpi radialis brevis, is rarely required.
Recent changes in stroke mechanics have encouraged swimmers to maintain the ‘elbow-up’ position for longer in order to propel their upper body above the water. This tends to force an exaggerated lumbar lordosis, potentially causing lower back problems, including mechanical low back pain from posterior facet irritation, spondylolisthesis, and, less frequently, stress fractures of the pars interarticularis1.
The ‘adolescent swimmer’s back’ is a term originally described by Wilson and Lindseth in three adolescent butterfly swimmers12. These patients were diagnosed with Scheuermann’s kyphosis or vertebral osteochondritis, a disease that must be borne in mind as it occurs most frequently in the age group common to competitive swimmers.
The diagnosis of back problems relies on clinical assessment and plain radiography. Examination may reveal a step deformity in the lumbar spine, or an abnormal gait with posterior tilt of the pelvis. An isotope bone scan may be indicated to diagnose a pars stress fracture.
Treatment depends on the diagnosis, and is usually conservative; options including: rest, physiotherapy, transcutaneous electrical nerve stimulation (TENS), and steroid injections into the inflamed facet. Patients should also be encouraged to swim as an exercise. Surgery, in the form of laminectomies and vertebral fusions, is reserved for severe and resistant cases.
Wael Dandachli