SCIENTIFIC BASES IN ACCELERATED PHYSIOTHERAPY IN THE RECONSTRUCTION OF LCA WITH PLASTIA H-T-H. SECTION II

AUTHOR: José Manuel Sánchez PhDs
FC Barcelona High Performance Senior Teacher
Phone: 656935516
e-mail : chema632@hotmail.com

• REGARDING MOBILITY: Consequences of Immobilisation:

1 ) ON THE CARTILAGE:

-Experimentally, joint immobilisation produces different modifications on the cartilage:
1) Cartilage softening (chondromalacia)
2) Joint space reduction.
3) Irregularities on the joint surface.
-There will also exist a reduction in glicosaminoglicanes (up to a 48%, mostly on the articular surface) Kiviranta,1987.
-Troyer,1975 : has demonstrated that there are modifications on the cartilage hydration.
-Evans,1960 : Demonstrated the existance of subchondral osteoporosis.
-These changes start quickly and become permanent after 8 weeks of immobilisation.
-It has also been confirmed that there are necrotic areas on the cartilage-cartilage contact points when an axial compression is applied (Soltem,1960).
-After some time, fibro-adiposity aherences are confirmed on the cartilage surface.
-Salter,1982 : he verified with rabits that the cartilage defects scar better when the joint is applied to a Passive Continuous Mobilisation  (MPC). The worst results were obtained when the joint was immolibilised.

2 ) ON THE SYNOVIAL :

-The continuous immobilisation favours the increasing of the fibro-adipose tissue in the joint and, therefore, the creation of adherences in the bottom of the synovial sac (Evans,1960).
-He verified also that Force Mobilisation produces superficial abrassions at cartilage level in animals.
-Paulos,1987 : He has described an infrapatelar contracture syndrome related to fibrosis on the knee´s front side (Patella infera syndrome due to arthrofibrosis), and comes along with flexion and extension loss.

3 ) ON THE TRANSPLANT :

-Immobilisation doesn´t garantee a normal movement of synovial fluid which is essential for the neoligament nutrition, specially during the revascularisation stage along the first post-operatory weeks (Mc. Donough).
-Amiel,1983 : He demonstrated that there exists knee peripheral ligament atrophy besides the fact that the collagen degradation increased. If immobilisation goes from 9 to 12 weeks, collagen degradation is respectively from 14 to 28%, more elevated that the NON immobilised rabbit group. An exponential degradation continues as long as immobilisation persists.
-Akeson,1984 : He confirms a collagen cellular and fibrilar lack of organization. The immobilised ligament becomes less rigid and less resistant. For a same weight, the ligament shows an increased deformation
-The resistance to side ligament or LCA rupture shows a clear reduction of resistance around 1/3 in the immobilised group, besides the energy which has been absorbed before the rupture (Noyes,1977).
-The phenomenon is increased by the fact that there is a weekess on the bone anchorage, which becomes osteoporotic (Woo,1984), and he verifies besides that the recovering after a long immobilisation is slow and incomplete.
-Hart,1987 : in a study with animals, he shows that active mobilisation encourages a more solid mechanically.The immobilisation seems to generate neosynthesized collagen which organises itself in such a way to resist better traction forces (following the force lines)
-Woo,1984. This author points the effect of capsule injuries. When the capsule is intact, mobilisation has a positive effect on the ligament scarring. But if the capsule is broken, mobilisation will have a negative effect.

• HOW SHOULD YOU TREAT MOBILITY PROTECTING THE PLASTY:

-First, you should fight the joint effusion: drainage, ice, antiinflammatories, compressive cryotherapy.
-Noyes,1987 : In a prospective study, he demonstrated that early mobilisation does NOT increase the joint effusion percentage.
The hyperextension produces tension or overload in the transplant. For Markolf, these overload goes from 50 to 500N for 5º of hyperextension. This value is less than the transplant mechanical value and the fixation systems. Tensions on LCA increase after 120º  flexion, but staying beneath the reasonable limits. FIG-1:
-Wascher : He demonstrated on 18 cadavers that there is a medium tension of 180N for a 10Nm in hyperextension on LCA.
-At LCP level, tensions during mobilisations are less important. In this case, there is LCP tension starting from a flexion of 60º.
-Knee mobilisation is another key in the recovering joint amplitudes in the immediate postoperatory stage. If there is a lack of knee mobility on the front and vertical plane due to a quadriceps retraction, it will slow down the flexion and extension recovery, producing femur-patelar pain.
-The complete extension recovery and the fight against flexum are a priority without danger for LCA neoplasty. The passive flexium recovery beneath the pain threshold is also very important.
-The 0º extension must be achieved before the 14th postoperatory day and a flexion of 120º in 6 weeks time.
-Lerat,1982 : He foresights that an early passive mobilisation beneath the pain threshold from 0-120º. Monitoring apparatus play an important role (MPC).