General Information about Activity Related (Sports) Injuries
Activity related injuries can be categorised into sports trauma, overuse injuries, wear and tear conditions related to activity and compression syndromes of nerve muscle or tendon. Biomechanical conditions (the way your own body shape functions in sport), training errors and age can all have an effect on the frequency, type and severity of activity related injuries.
Diagnosis, Treatments and Rehabilitation
At CSIS we take a holistic approach to the diagnosis and treatment of activity related disorders. We take into account:
Adolescent athletes have greater recovery potential but also a much longer sporting career that has to be considered. More mature sports men and women may suffer with wear and tear problems that are aggravated by sports participation.
The strains on the body tissue of a 6’4” premiership goalkeeper is very different to the injuries produced in a national level martial arts athlete. Being very flexible (double jointed) can self select an athlete to achieve high standards in sports such as dancing or gymnastics. Hyperlaxity of the ligaments can of course also make the same athletes prone to joint instability with minimal trauma.
The frequency and rate of a training program may exploit a weakness in an athlete. Training footwear and surface conditions may create injuries such as stress fractures in an athlete without a weakness.
The recovery from sports injury is faster and more complete if the correct diagnosis is made early. Examination in the outpatient clinic by a Sports Orthopaedic Surgeon with twenty years experience as a Consultant in treating elite athletes is complimented by an array of diagnostic aides such as Ultrasound (US), Computerised Tomography (CT) and Magnetic Resonance Imaging (MRI) by radiologists respected and renowned for their expertise in the field of sports injury diagnostics.
Anatomy of Knee Arthritis
Osteoarthritis produces pain with swelling. Other symptoms include locking, catching sensations and a feeling of grinding (also called crepitus)
In the past we used to divide osteoarthritis into idiopathic (that means we don’t know why) and post-traumatic types. We now know old age is not the only cause of what was called idiopathic osteoarthritis. Genetic factors on both a cellular and morphological (how you are built) level play the major role in the development of this type of arthritis. I can highly commend the paper by Professor Michael Doherty on the subject that is available in full online. 1
The other factor that plays a powerful role in the development of premature ‘idiopathic osteoarthritis’ is the shape of the leg. Genu varus (bowed legs) and genu valgus (knocked knees) can both cause and accelerate wear changes in the inside and outside knee compartments respectively.
Osteoarthritis is caused by the combination of biological failure of cartilage and meniscus on the one hand, and overload in one or more areas of the knee. The simple model of the knee in the erect patient has a medial and lateral compartment made up by cartilage and a medial and lateral meniscus supported by the bone of the femur and tibia. The menisci make the relatively flat surface of the tibia into a cupped or concave structure matching the convex shape of the femoral condyles.
The principle accelerator of osteoarthritis is overload. Magnitude of overload is dictated by the weight of the patient and alignment of the whole leg.
In osteoarthritis the meniscus and cartilage loose their relationship by the meniscus or the cartilage failing together or the one after the other. Once the meniscus fails it gets extruded from the joint causing all the weight bearing force to pass through either the medial (most common) or the lateral compartment producing either a varus or valgus deformity of the knee.
Cartilage is made up of:
- Cells (chondrocytes)
Collagen and proteoglycan combined make up the matrix that the chondrocytes nest in. The cocooned chondrocyte is not very active and become less so as the patient gets older. The matrix behaves like steel reinforced concrete with the collagen being the ‘steel’ and the proteoglycan being the ‘concrete’.
Chondrocyte and proteoglycan quality is very similar in all patients. The big variable is the collagen. The main fibres (type II) are bound by crosslinks to their fellows by ‘lesser’ collagen molecules that are variable based on inheritance. When these ‘lesser’ collagen molecules are in short supply the main (type II) collagen structure fails. The proteoglycan, imbedded in the collagen superstructure, is extremely hydrophilic (loves water) and cannot help itself from absorbing water to the point of literally bursting. Once free fluid gets into the blistered cartilage surface he damage is relentless.
Cartilage has no ability to repair, as it has no blood supply to allow an inflammatory response to initiate the repair process. It also has no nerve supply and therefore the initial phase of damage may not be noticed. The initial breakup of cartilage does however release inflammatory and pain producing enzymes (IL1 and TNF) that causes the synovial membrane to react. When this process moves from a microscopic to macroscopic level the synovium becomes ‘sick’ causing it to loose balance between synovial fluid production and absorption. The knee now swells (develops effusion) in response to activity.
With the loss of cartilage and meniscus in either the medial or lateral knee compartment the distance between bone of the femoral condyle and tibial plateau gets less. The leg starts deforming. This results in the mechanical axis (line of force passing from hip to ankle) shifting from the middle of the knee into the compartment where the cartilage is breaking down. The process of cartilage fragmentation is thus accelerated and the forces passing to the supporting bone is increased (compartment overload).
Bone in the human body is unique in its response to load. In accordance with Volkmann’s Law it actually grows to become thicker and stiffer to resist the load increase. The circulation through this thicker bone is slower than through bone with normal density and as with most body tissue oedema ensues as water leaks from the sinusoids (vascular channels in bone). This is called bone oedema that can be clearly seen on a MRI scan. It also results in the dull gnawing rest pain of osteoarthritis.
- Pain sources in OA are torn menisci, synovial inflammation and bone oedema.
- Joint space loss produces deformity (varus, valgus or fixed flexion) that alters the mechanical axis of the limb resulting in overload in one or more areas of the knee.
Weight loss: Neither non-operative nor operative management of osteoarthritis will succeed in the presence of obesity. A Body Mass Index (BMI=Weight in kg/Height2) in excess of 33 will cause knee pain even in the absence of pathology. In the presence of meniscus tear or cartilage damage obesity will accelerate disease progression. Non-operative treatments will be less successful and complication rates with operative treatments will be higher.Physiotherapy: Deformity, in the early stages, will be very minor and can be counteracted by addressing overall body posture as well as improving muscle strength and balance. Core strength and proprioception will aid in postural control. Hip abductor strength rapidly diminishes especially when joint space is lost in the medial knee compartment. The involvement of an interested and able physiotherapist is therefore crucial in the treatment of early knee arthritis.
Braces and insoles: When deformity has exceeded what the patient and therapist can achieve though exercise, deformity control/correction can be achieved through external bracing or support. Physics dictate that the more remote such a brace or support is from the deformity it’s trying to correct the less effective it’ll be. Shoe insoles may therefore have a limited role to play in the very early form of the disease.
The length of the lever and surface area over which the brace is working can reduce the forces required by an external brace to control deformity. To that end I prefer to use a brace such as the Össur Unloader brace that has a good lever length and silicone thigh and calf lining over a big surface area.
Painkillers: The use of analgesia in combination with Non-Steroidal Anti-Inflammatory Drugs (NSAID’s) is fairly straightforward and algorithms for escalation by your GP are well established. The natural history of the disease will however dictate that with disease progression analgesia will become less effective. Therefore when the end stage of the disease is reached and the ‘pills don’t work anymore’, consideration is given to manage your knee arthritis with surgery.
Surgery: Arthroscopy will not help the pain of arthritis. It may have a role to play your main symptom is that of locking or catching of the knee.
The only effective surgery for arthritis is osteotomy and knee joint replacement surgery. I don’t offer knee replacement surgery as it falls out with the scope of my practice of joint reconstruction in active, younger patients with earlier stages of arthritis. Joint replacement is generally reserved for the older patient with end stage knee arthritis. It is done by most lower limb orthopaedic surgeons
Osteotomy changes leg alignment to shift the mechanical axis (the line where the load from the hip to the ankle passes through the knee) from an arthritic part of the knee to a healthy part. Tibial osteotomy is conventionally done for medial compartment OA (varus knee) and femoral osteotomy for lateral compartment OA (valgus knee).
- Weight loss together with shifting load from the site of maximum damage is the most effective way of treating OA of the knee.
- Painkillers and NSAID may be required during this process to achieve objectives.