May 1st 2014 I was fortunate to attend an APA lecture evening hosted by the MPA, with guest lecturer Dr Christian Barton @DRChrisBarton, who presented on patellofemoral pain. Dr Barton gave a captivating lecture explaining the current evidence regarding patellofemoral pain (PFP), with particular emphasis on the recent evidence gained from the Patellofemoral Consensus Statement 2013.
The structure of the lecture was to cover:
- The problem
- What causes the problem
- How to manage the problem.
- Patellofemoral pain (PFP) is generally associated with overuse and joint loading.
- It is a spectrum disorder ranging from pain in adolescents to OA.
- IT OFTEN GOES HAND IN HAND WITH FAT PAD IRRITATION.
- PFP is present in 25-40% of all knee injuries.
- Of those with PFP, 23% stop activity and 30-50% reduce activity as a result of injury.
- IT IS NOT A SELF LIMITING CONDITION.
The fat pad.... is a highly vascularised structure, thought to be the most painful structure in the knee, which only takes a small amount of provocation to become painful. The fat pad is aggravated in deep flexion and terminal extension i.e. < 20 and > 100 degrees flexion.
Pain can be caused by either increased joint stress or reduced joint contact area, both of which cause increased joint forces.
One point which Dr Barton emphasised is that exercises in terminal extension are likely to be counter productive, because the PFJ is less stable and there is more compression of the fat pad ... which causes more irritation during the acute phase of injury.
What causes the problem.
Common deficits based on research and seen in clinical practice:
- Often we see a laterally deviated tibial tuberosity, shallow trochlear, and patella alta (high riding).
- Q angle is not a risk factor (nor something we can change clinically).
- Things we can change include local and proximal influences, of which we need to consider which are a risk factor and which are a contributing factor, and what is modifiable.
- The line of pull of quads - not a contributing factor.
- Delayed muscle functioning (specifically VMO) - worse when pain is present but not a risk factor for developing pain.
- Delayed activation is dependent on the task being performed, but commonly occurs during stairs (therefore a good functional assessment).
- Atrophy exists in the affected leg... but... VMO doesn't have to be more wasted than VL ... there is a trend for global muscle atrophy more than isolated VMO atrophy.
- The level of degeneration is not associated with pain.
- Fear avoidance.... People often adopt a toe-out gait and walk with reduced knee flexion range... which can lead to disuse and atrophy.
- You can't look at the knee in isolation... often people present with:
- Decreased lateral trunk flexion.
- Pelvic drop (research remains inconsistent and the gait pattern varies between individuals).
- Maltracking.... probably caused more by the femur rolling under the patella more than the patella tracking poorly on the femur.
- Reduced control of hip adduction and internal rotation.
- Hip strength is a contributing factor for pain. There tends to be a decreased in ration hip ER:IR strength, and hip ER and ABD are always reduced in patients with PFP.
- There may be sex specific differences in biomechanics. Males are more likely to have greater pelvic drop while females have increased hip adduction movements. Females tend to have reduced abduction strength and tend to have to work harder to regain strength.
- At the foot: patients tend to land in more pronation and not have as much movement which may reduce shock absorption, however, this is probably not a risk factor.
In summary, deficits are multifactorial. Maltracking exists, we don't know the direct source of pain, Quad weakness is a risk factor, muscle function and altered movement patterns are contributing factors, as well as hip motion and muscle function, and the foot is inconclusive but orthotics may work short term to assist with hip motion and patterning.
How to manage the problem.
'Good clinical practice is an art guided by science.'
Guide to conservative management.
- Empower the patient, focus on staying active and not be passive.
- Educate them on the cause of the problem.
- Set expectations that it is a condition that is not easily cured and one they will need to manage for the rest of their life.
- Prioritise pain relief at the start of their treatment. Try reduce their pain, gain their trust and then take them on the path they need.
- Activity modification in the early stages is required but .... Always aim to get them back to the activity levels they want.
- Address psychosocial factors ... Fear avoidance needs to be addressed.
- Gradually increase load slowly while monitoring irritability and then gradually increase function.
Multimodal interventions are more successful long term but this isn't efficient ... therefore we need to tailer interventions. Exercise is required but... there is no clear evidence on what exercise i.e open kinetic chain or closed, weight-bearing or non-weight-bearing, isolated muscle function or functional exercise.
Supervision during the early stages of rehabilitation is best, with a max of 3-4 exercises to improve compliance. Mirrors are also great for feedback and education of movement patterns (something we know to be important but is still lacking in research).
Strengthening quads and gluteals (again lacking level 1 research) is known to be important and effective.
Stretching..... Consider hamstring length and it's impact on stresses through the PFJS, checking for calf length and ankle mobility.
Taping - most effective lasting pain relief and builds trust. Bracing is helpful when taping can't be used.
Inconsistent research for orthotics and massage but both have a place in clinical practice to optimise movement patterns and biomechanics.
Conflicting evidence for dry needling but can be used for pain relief.
In summary our management requires education, rehabilitation, specific exercises, pain reduction and optimise our patients biomechanics.
A special thanks to Dr Barton for this informative and invaluable lecture.