The Jaipur foot was developed for barefoot amputees by Professor P. K. Sethi. He used local artisans and readily available materials. The prosthesis was cheap and could be made in one hour. It enabled amputees to work in rural conditions, muddy and wet fields and to climb trees. It has been widely used in India, South East Asia and Africa, where local variations to the design have now been made.

This paper describes how we came to understand the pathophysiology of Volkmann’s ischaemic contracture with references to relevant papers in this Journal, and the investigation and management of acute compartment syndrome is briefly discussed.

Osteomyelitis is one of the oldest diseases known. It took many years before the acute infection could be brought under control with antibiotics and chronic osteomyelitis remains difficult to manage. The modern history of the disease is reflected in the pages of the

We have previously shown that prior exposure of rat hind limbs to ischaemia for five minutes and reperfusion for five minutes reduced the structural damage to skeletal muscle which followed a subsequent period of ischaemia for four hours and reperfusion for one hour. We have now examined the potential mechanisms by which this ischaemic preconditioning protocol may be effective in reducing damage to skeletal muscle induced by prolonged ischaemia and reperfusion. Prior exposure of the hindlimb to ischaemia for five minutes and reperfusion for five minutes did not prevent the fall in the ATP content of tibialis anterior which occurred after a subsequent period of ischaemia for four hours and reperfusion for one hour. Similarly, no effect of the preconditioning protocol was seen on the elevated muscle myeloperoxidase, indicative of an elevated neutrophil content, or abnormal muscle cation content. Reperfused ischaemic muscle was also found to have an increased content of heat-shock protein (HSP) 72, but the preconditioning protocol did not further increase the content of this or other HSPs indicating that it was not acting by increasing the expression of these cytoprotective proteins. The protective effects of preconditioning appeared to be mimicked by the infusion of adenosine to animals immediately before exposure to the four-hour period, indicating a potential mechanism by which skeletal muscle may be preconditioned to maintain structural viability.

Ischaemic preconditioning is a process by which exposure of a tissue to a short period of non-damaging ischaemic stress leads to resistance to the deleterious effects of a subsequent prolonged ischaemic stress. It has been extensively described in the heart, but few studies have examined the possibility that it can occur in skeletal muscle. We have used a rat model of ischaemia of one limb to examine this possibility. Exposure of the hind limb to a period of ischaemia of five minutes and reperfusion for five minutes significantly protected the tibialis anterior muscle against the structural damage induced by a subsequent period of limb ischaemia for four hours and reperfusion for one hour. This protection was evident on examination of the muscle by both light and electron microscopy. Longer or shorter times of prior ischaemia had no effect.

We reviewed all patients with a clinically infected foot ulcer attending a specialised neuropathic foot clinic. Neuropathy was confirmed by the inability to feel a 5.07 Semmes-Weinstein hair, areflexia and impaired vibration sense, as measured by a biothesiometer.

Of 40 patients who attended the clinic over a two-year period, six with ischaemic ulcers were excluded. The remaining 34 had plain radiographs of the foot followed by a ^99mTc-MDP bone scan. If the latter was positive, an ¹¹¹In-labelled WBC scan was performed with planar and/or tomographic dual-isotope studies where appropriate. Bone and WBC scans were performed in 31 patients. In ten, isotope imaging showed infection localised to the soft tissues only and conservative treatment was successful in them all. Eighteen patients were treated surgically with excision of the involved bone, which was sent for culture and histological examination.

Dual-isotope scans had a sensitivity of 93% and a specificity of 83%. ^99mTc-MDP bone scans with the appropriate ¹¹¹In-labelled WBC scans can reliably determine the site and extent of osteomyelitis in the neuropathic diabetic foot.

There is some evidence that the anterior tibial vascular tree is poorly developed in children with club foot. We have found a significantly greater prevalence of absence of the dorsalis pedis pulse in the parents of such children. We also found significantly more tobacco smokers among the club-foot parents than in the control group.

We describe three cases of traumatic myositis ossificans in which fractures occurred through a mature, quiescent ossification mass. None of the fractures reactivated the original pathological process, no callus was formed and union did not occur. The nonunion became painless over a period of months. This unusual late complication of myositis ossificans seems to require only symptomatic treatment by temporary splintage and subsequent mobilisation. We could find no previous report of a similar case.

In the 1950s Frederick Dwyer evolved the concept of treating resistant and relapsed clubfoot by osteotomy of the calcaneum. He published the results of his medial opening wedge procedure in 1963 with a mean follow-up of five years. We present the structured, radiographic and functional results at a mean elapsed time of 27 years of 36 feet (26 patients) all operated on by Dwyer. Their mean Laaveg and Ponseti (1980) grading was 83.7%. In 94% the heel was in neutral or valgus and 86% of the feet were plantigrade. A good range of movement was present in the ankle and subtalar joints in 83%.

Ulceration of the insensitive foot continues to cause great morbidity in diabetic patients. We treated 46 patients with neuropathic ulceration by applying total contact casts. Most neuropathic ulcers healed within six weeks but ischaemic ulcers did not heal. One patient developed gangrene and required partial amputation of the foot.

Thirty-three patients with reflex sympathetic dystrophy were studied prospectively to ascertain the pressure-pain threshold of affected and unaffected limbs. The affected side had a lower threshold which was found to be statistically significant. In all 18 patients with upper limb involvement, the pain threshold was reduced on the affected side, but this applied to only 11 of the 15 with leg involvement. This difference may be because patients with lower limb symptoms had been referred later in the course of the syndrome. We showed by repeated tests that after an average of 49 days there was a slow return to normality. The estimation of pressure-pain thresholds may help in the earlier diagnosis of reflex sympathetic dystrophy.

The importance of well-functioning toes has long been recognised but has not previously been assessed in biomechanical studies. We have examined the weight-bearing function of the foot in 160 normal subjects by use of the pedobarograph. The function of the toes was assessed by reference to the time they were in contact with the ground and the peak pressures they exerted individually in comparison with other parts of the foot. The toes were in contact for about three-quarters of the stance phase of gait and exerted peak pressures similar to those of the metatarsal region. When the foot was bearing the second peak of total force, the area in contact with the ground (the metatarsal heads and toes) was decreasing.