Introduction: The usual surgical treatment of valgus knee in Ellis van Creveld Syndrom (EVC), is high tibial osteotomy. However, this approach failed to achieve the expected goal of lasting correction. Based on Dr. Paley’s observations, and our previous unsuccessful treatment of valgus knee in EVC syndrome, we changed the surgical approach. The aim of the surgical treatment is to eradicate all the elements causing sever valgus knee: 1) dysplasic lateral tibial condyle, 2) progressive depression of the lateral tibial plateau, 3) short fibula, 4) short and contracted fascia lata, 5) short lateral collateral ligament and biceps femoris, 6) short lateral head of gastrocnemius, and 7) contracted lateral knee capsule and lateral retinaculum. In many aspects the pathology of Blount’s disease grade 5 or 6 is similar, but located at the medial tibia causing genu vara.

Materials and Methods: Three valgus knees of EVC syndrome and two varus knees of Blount’s disease grade 5 & 6 underwent surgical treatment by a unique surgical approach to address all pathologies which contribute to the deformity. In the cases of EVC syndrome the first stage operation included: 1) peroneal nerve release and soft tissue release including T.F.L., B.F., L.C.L., capsule and gastrocnemius, 2) arthrogram, 3) fibulectomy, 4) elevation of lateral tibial plateau with bone graft, 5) reconstruction of L.C.L. and B.F., 6) lateral release of retinacula and rerouting of patella, and 7)cast application. In the second stage operation of these cases a corrective high tibial osteotomy was performed. In the Blount’s disease knees the operative treatment was performed in one stage and included: 1) arthrogram, 2) elevation of the medial tibial plateau, 3) fibulotomy, 4) closing wedge tibial osteotomy based laterally, 5) transfer of the bony wedge under the elevated plateau and fixation.

Results: All deformities were corrected with no recurrence, and stability of the knees persisted. We had one common peroneal nerve neuropraxia that recovered and one wound dehiscence.

Conclusions: In both conditions, EVC syndrome and Blount’s disease, corrective high tibial osteotomy does not address the pathology, and recurrence is to be expected. The described surgical technique fulfills that target – eradication of the pathologic elements that lead to valgus or varus.

We tested the hypothesis that it is possible to accelerate fracture healing by changing the mechanical environment used in current methods i.e., from initial rigidity or micromovement followed by dynamisation to initial macromovement followed by rigidity (micro-movement).

It is accepted that callus formation requires movement at the fracture site and this callus response is limited to the first few weeks after fracture. Logically, early macromovement at the fracture site would be beneficial for callus formation. Additional callus is not produced by further movement. Indeed, it may be counter-productive, just as continuing movement around two ends of a wooden stick bonded with glue will retard and even prevent “union”. We postulate that continuing movement at the fracture site after the callus response has ceased will also delay union. As a result, rigidity rather than dynamisation is required in the later stage of fracture healing.

After testing an animal model, we built an external fixator which allowed 5 mm of axial movement without “self-locking” and could be compressed at a later date in order to prevent further movement.

A trial containing 15 patients with unilateral tibial shaft fractures (closed or grade 1 open) was undertaken after permission was obtained from the Helsinki Ethical Committee.

So far, 13 patients have been entered into the trial. They have completed therapy and are at least one year post-fracture (12 months to 22 months). Age range is from 20 to 49. The group is composed of nine males and one female.

Under general anaesthetic, an external fixator was applied and the fracture reduced. The patients started ankle exercises (active and passive) the following day, with as much weight-bearing on the fractured leg as possible on the day after. The patients were seen every two weeks and AP and lateral radiographs were taken. The fracture was compressed two to six weeks later. The percentage of body weight that the patient was able to tolerate through the fractured limb was measured by using the scales of Meggit’s step test. The fixators were removed when there was radiographic union and the patient could take at least 80% of body weight through the fractured limb. Mean time duration up to removal of the fixator was 10.8 weeks (range 7 to 15.4 weeks).

We conclude that it is possible to increase the speed of bone healing by changing the mechanical environment to initial macromovement followed by elimination of movement.