RUPTURE OF THE CALCANEAL TENDON

Surprising as it may seem, a ruptured calcaneal tendon (tendo Achillis) is often overlooked, the symptoms being wrongly ascribed to a strain or to a ruptured plantaris tendon.

Pathology. The rupture is nearly always complete. It occurs about 5 cm above the insertion of the tendon. If it is left untreated the tendon unites spontaneously, but with lengthening and loss of function.

Clinical features. While running or jumping, the patient feels a sudden agonising pain at the back of the ankle. He may believe that something has struck him. He is able to walk, but only with a bad limp. On examination of the back of the heel there is tenderness at the site of rupture. There is general thickening from effusion of blood and from oedema of the paratenon, but a gap can usually be felt in the course of the tendon. The power of plantarflexion at the ankle is greatly weakened, though some power remains through the action of the tibialis posterior, the peronei, and the toe flexors. A useful test, to be carried out with the patient prone, is to squeeze the bulk of the calf muscles from side to side. Normally this causes a slight plantarflexion movement of the foot, but not if the tendon is ruptured.

Diagnosis. The retention of some power of plantarflexion may deflect the unwary from the correct diagnosis. The crucial test is to ask the patient to lift the heel from the ground while standing only upon the affected leg (Fig. 19.5). This is impossible if the tendon is ruptured. In cases of doubt the gap in the tendon may be well demonstrated by ultrasound or MRI scanning (Fig. 19.6).

Fig. 19.6 A Ultrasound of normal Achilles tendon. Patient’s foot on right. Normal appearance of tendon seen above the word ‘Tendon’. B Compare with this ultrasound of a ruptured tendon.

Treatment. Non-operative treatment may be used in selected cases, usually older and more sedentary patients who make less demands on their ankle function. The method is only applicable where passive ankle flexion can bring the torn ends of the tendon into apposition. The ankle is then immobilised in a below-knee plaster for 5 weeks, with the foot in slight equinus to relax the tendon and thus help to prevent lengthening.

In the majority of younger patients, particularly those who wish to continue athletic pursuits after healing, operative treatment is preferable. It entails repair of the tendon, using non-absorbable sutures of synthetic material, tension on the suture line being relaxed by immobilising the limb with right-angled knee flexion and moderate ankle plantarflexion for 2 weeks. For the next four weeks a below-knee plaster with the ankle at 90° is worn. Certain protocols allow earlier mobilisation of the ankle under close supervision of a physiotherapist.

Whether treatment is by plaster alone or by operation, it must be completed after removal of the plaster by increasingly vigorous exercises for the calf muscles, practised under the supervision of a physiotherapist until full strength is restored.

ACUTE OSTEOMYELITIS (General description of acute osteomyelitis, p. 85)

The tibia is one of the commonest sites of haematogenous osteomyelitis. Because of its liability to open (compound) fracture it is also the commonest site of osteomyelitis from direct contamination. The fibula is less often affected.

The pathological and clinical features and treatment conform to the general description on page 89.

CHRONIC OSTEOMYELITIS (General description of chronic osteomyelitis, p. 90)

Chronic osteomyelitis in the lower leg, as elsewhere, is nearly always a sequel of acute osteomyelitis. It may follow either the haematogenous type of infection or an infected open fracture.

Brodie’s abscess. This rather uncommon lesion was described on page 92. It is a special form of chronic osteomyelitis which arises insidiously, without a recognised acute infection preceding it. The tibia is the commonest site (see Fig. 7.7, p. 93).

SYPHILITIC INFECTION OF THE TIBIA (General description of syphilitic osteitis, p. 95)

Although skeletal syphilis is now rare in Western countries, it still occurs in other parts of the world, and when it does occur the tibia is often the bone affected. The infection may take the form of a localised gumma or of diffuse osteoperiostitis (see Fig. 7.11A&B, p. 96). There is a gradually enlarging swelling, with moderate pain. It is important to bear the possibility of syphilis in mind, because the swelling is easily mistaken for a tumour.

TUMOURS OF BONE

INTERMITTENT CLAUDICATION

Intermittent claudication is a symptom of arterial insufficiency in the lower limb. In its typical form it is characterised by cramp-like pain in the calf, induced by walking and relieved by rest.

Cause. The usual underlying cause is arteriosclerosis with consequent partial or total obstruction of the main limb vessel. Thrombo-angiitis obliterans and arterial embolism are less common causes. Tobacco smoking is a major contributory factor.

Pathology. The basic disturbance is ischaemia of muscle, in consequence of which metabolites cannot be removed speedily enough when the muscle is exercised. The accumulation of metabolites is believed to be responsible for the pain, which subsides within a few minutes when the muscle is rested. The muscles usually affected are those of the calf, but in some instances other muscle groups are involved, according to the site of the arterial obstruction. The vascular lesion is usually a complete occlusion of the femoral or the popliteal artery. In claudication affecting the buttock the aortic bifurcation or the iliac artery may be occluded.

Clinical features. Intermittent claudication is much more common in men than in women. In the usual arteriosclerotic type the patient is past middle life, but in cases due to thrombo-angiitis obliterans or embolism the symptoms may develop in early adult life. The patient is usually a regular smoker.

With gradual arterial occlusion the onset is insidious and the symptoms are slowly progressive; but in cases precipitated by thrombosis or embolism the onset may be sudden. In a typical case the patient complains that after walking a certain distance – perhaps a hundred metres or so – he is forced to stop by severe cramp-like pain in the calf, or occasionally in another muscle group, such as the buttock. After a few minutes’ rest the pain disappears and he is able to walk on again for a similar distance.

On examination there is objective evidence of impaired arterial circulation in the lower limb (p. 421). The posterior tibial, dorsalis pedis, and popliteal pulses are absent. There may be ischaemic changes in the skin of the foot. Evidence of widespread arterial or cardiac disease is nearly always found on general examination.

For further details on the investigation, diagnosis and treatment of this condition readers should refer to a textbook of vascular surgery.

PYOGENIC ARTHRITIS OF THE ANKLE (General description of pyogenic arthritis, p. 96)

Pyogenic arthritis of the ankle is uncommon. The organisms reach the joint through the blood stream or through a penetrating wound; local spread from a focus of osteomyelitis of the tibia or fibula is rare because the bony metaphyses are entirely extra-capsular (see Fig. 7.2, p. 87).

TUBERCULOUS ARTHRITIS OF THE ANKLE (General description of tuberculous arthritis, p. 98)

Tuberculosis is much less common in the ankle than it is in the hip and knee. In Britain it is now seen very seldom. When it is seen, it is often in an immigrant from a developing country.

The clinical features correspond to those of tuberculous arthritis of other superficial joints, with pain, swelling, increased warmth of the overlying skin, restriction of movement, and limp.

Treatment. Early conservative treatment (p. 102) may restore a mobile ankle, but if in a resistant case articular cartilage is badly eroded or destroyed arthrodesis may have to be undertaken.

RHEUMATOID ARTHRITIS OF THE ANKLE (General description of rheumatoid arthritis, p. 134)

One or both ankles are often affected by rheumatoid arthritis in common with other joints in the lower limb, particularly the foot. There may be marked destruction of the articular cartilage and subchondral bone with pain, stiffness, and deformity (Fig. 19.7).

Fig. 19.7 Radiographs of the ankle with advanced rheumatoid arthritis showing loss of joint space and erosion of the articular surfaces of the tibia and talus.

Treatment. Medical treatment is along the lines suggested for the disease as a whole (p. 137). Local treatment: In the active phase rest in a plaster is sometimes required, but in most cases the patient should be encouraged to remain active as far as possible, with such help as may be gained from local support by a moulded polypropylene splint. Operation is advised mainly when destruction of articular cartilage has led to intractable pain with marked impairment of capacity for walking. Arthrodesis and replacement arthroplasty are the methods available. Arthrodesis is usually the operation of choice because it gives permanent relief of pain with good function. If the subtalar and midtarsal joints are also severely affected they should be included in the fusion. Replacement arthroplasty of the ankle is appropriate in some patients (Fig. 19.8). The operation is technically demanding because of the limited surgical access to the joint, while the long-term results are much less satisfactory than with the hip or knee because poor bone support may lead to early implant loosening.

Fig. 19.8 A and B Radiographs of a Scandinavian total ankle replacement arthroplasty inserted for the treatment of advanced rheumatoid arthritis. Metal prostheses have been used to resurface the dome of the talus and the distal tibia and both articulate with a mobile polyethylene meniscal prosthesis placed between them (position shown by wire marker).

OSTEOARTHRITIS OF THE ANKLE (General description of osteoarthritis, p. 140)

Degenerative destruction of the articular cartilage is less common in the ankle than in the knee or hip. There is nearly always a known predisposing factor which causes the joint to wear out prematurely. The commonest is irregularity or mal-alignment of the joint surfaces after a fracture. Sometimes articular disease such as previous rheumatoid arthritis or osteochondromatosis is the primary factor.

Clinical features. The symptoms are pain which slowly increases over months and years, and limp. On examination the joint is a little thickened from hypertrophy of bone (osteophyte formation) at the joint margins. Movements are restricted slightly or severely according to the degree of arthritis.

Radiographs show the typical features of osteoarthritis – narrowing of the cartilage space, a tendency to sclerosis of the bone adjacent to the joint, and osteophyte formation at the joint margins (Fig. 19.9).

Fig. 19.9 Osteoarthritis of the ankle complicating fracture-subluxation 10 years before. Note the marked narrowing of the cartilage space and the prominent osteophytes.

Treatment. In mild cases treatment is often unnecessary, because the patient may be willing to accept the disability when the nature of the trouble has been explained. When treatment is called for, conservative measures should be tried first if the disability is only moderate. Physiotherapy by short-wave diathermy, and active exercises are usually advised. Sometimes local splintage by a moulded polypropylene support will provide relief while allowing the patient to continue to walk. Such treatment, however, is only palliative, and if the disability increases to the extent of becoming a serious handicap operation should be undertaken.

Surgical treatment should usually be by arthrodesis, which provides a painless stable joint for many years. A number of different methods are available to produce reliable bony fusion and with the introduction of arthroscopic techniques to remove the degenerate cartilage, combined with rigid internal fixation across the opposed bone surfaces, the post-operative rehabilitation is rapid. Unfortunately, after 10–15 years more than 50% of these patients develop further disability from hindfoot pain because of the accelerated onset of arthritis in the adjacent sub-talar and talo-navicular joints. In an attempt to overcome this problem in younger patients, replacement arthroplasty with resurfacing prostheses has been explored as a possible alternative (see Fig. 19.8). As with arthroplasty for rheumatoid arthritis, the long-term results are still uncertain because of bone resorption and implant loosening and it is not yet widely recommended.

NEUROPATHIC ARTHRITIS OF THE ANKLE (General description of neuropathic arthritis, p. 147)

Neuropathic arthritis is uncommon but nevertheless well recognised in the ankle. The underlying neurological disease is diabetic neuropathy, syringomyelia, cauda equina lesion, tabes dorsalis, or, where it is prevalent, leprosy.

Treatment. In many cases protection by a firm surgical boot, reinforced if necessary by a below-knee brace, is all that is required. Occasionally arthrodesis of the ankle may have to be considered. Appropriate treatment must be given for the underlying neurological disorder.

RECURRENT SUBLUXATION OF THE ANKLE

When the lateral ligament of the ankle is torn and fails to heal there may be persistent instability with recurrent attacks of giving way in which the talus tilts medially in the ankle mortise. Anterior displacement relative to the tibial articular surface may also occur. The causative injury is always a severe inversion force.

Clinical features. The patient complains that the ankle ‘goes over’ at frequent intervals, often causing him to fall. Each incident is accompanied by pain at the lateral side of the ankle. There is always a history of previous severe injury, followed by much swelling and extensive bruising at the lateral side of the joint.

On examination there is often some oedema about the ankle. There is tenderness over the site of the lateral ligament. The normal ankle movements – dorsiflexion and plantarflexion – are unchanged, but abnormal mobility is present as shown by the fact that the heel can be inverted passively beyond the normal range permitted at the subtalar joint. Moreover, when the heel is fully inverted a dimple or depression of the skin may be visible in front of the lateral malleolus, where the soft tissues have been ‘sucked’ into the gap created between tibia and talus.

Radiographic features. Routine radiographs do not show any abnormality. Antero-posterior films must be taken while the heel is held fully inverted. If the lateral ligament is torn or lax the talus will then be shown tilted away from the tibio-fibular mortise at the lateral side through 20 or 30° or more (Fig. 19.10). Anterior displacement of the talus relative to the tibial articular surface may sometimes also be demonstrated in lateral radiographs taken while the foot is pushed forwards.

Fig. 19.10 Tilting of the talus in the ankle mortise under adduction stress; an indication of torn lateral ligament.

Diagnosis. Chronic strain of the lateral ligament may cause similar symptoms, but in that condition radiographs will not show the talus tilted significantly on forced inversion. (It should be noted that the talus may tilt up to 10° or even 15° in a normal ankle. Tilting beyond that amount is demonstrated only when the ligament is torn.)

Treatment. If the disability is slight it may be sufficient to strengthen the evertor muscles (mainly the peronei) by exercises, to enable them to control the ankle more efficiently. Stability may also be enhanced by broadening and ‘floating out’ the heel of the shoe. If the disability is severe operation is required. A new lateral ligament may be constructed either from the peroneus brevis tendon or from the peroneus tertius. Trials are also proceeding with the use of artificial ligaments, either as substitutes or as a means of promoting the growth of new ligamentous tissue.

CONGENITAL CLUB FOOT (Talipes equino-varus)

The rather vague term ‘club foot’ has come to be synonymous in the minds of most surgeons with the commonest and most important congenital deformity of the foot—talipes equino-varus (Fig. 19.11). The less common, and usually less serious, form of club foot, talipes calcaneo-valgus, will be considered later under that title.

Fig. 19.11 Bilateral club foot (talipes equino-varus) in an infant boy. Note the poor development of the calf muscles.

Cause. This is still under debate. In most cases a defect of fetal development is responsible, with imbalance between the invertor-plantarflexor muscles and the evertor-dorsiflexor muscles. A neuromuscular defect is possibly relevant. Minor degrees of the deformity may possibly be explained by prolonged mal-position of the foetal foot in the uterus, but this cannot be accepted as the usual cause.

Pathology. The crucial component of the deformity is subluxation of the talo-navicular joint, so that the navicular bone lies partly on the medial aspect of the head of the talus instead of on its distal aspect (Fig. 19.12). The soft tissues at the medial side of the foot are under-developed and shorter than normal. The foot is adducted and inverted at the subtalar, midtarsal, and anterior tarsal joints, and is held in equinus (plantarflexion) at the ankle. In most cases under-development of the calf and peroneal muscles is a striking feature. Thus if only one foot is affected there is a marked discrepancy in the girth of the calf between the two sides.

Fig. 19.12

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