Lecture 9 - Lower Limb Soft Tissue And Bone Disorders Flashcards
Dysplasia of the hip: Pathophysiology
- during childbirth
- abnormality in size, shape, orientation or organization of the femoral head or acetabulum
RISK FACTORS: breech, female, Family Hx, Firstborne
Dysplasia of the hip: assessment
- ortolani and barlow maneuvers
- Galeazzi sign
- Hip abduction range
Dysplasia of the hip: management
- subluxation often corrects spontaneously
- if subluxation persists: Pavlik harness
- if dislocation persists: closed reduction and Hip Spica casting
Perthe’s disease pathophysiology
- osteochondrosis of capital epiphysis of femoral head: disruption of blood supplu
- cessatin of endochondral ossification
- Vascular invasion of cartilage
- necrosis of marrow space and trabecular bone
Perthe’s disease: Assessment
- low grade ache, male 4-10 yo
- Limited abduction and internal rotation upon physical exam
- XRAY: increased density and flattening of femoral capital epiphysis
Perthe’s disease: Management
Rest
- exercise for range of motion
- Brace
- surgery
Avascular necrosis of the femoral head: pathophysiology
- damage to deep branch of medial femoral circumflex artery leading to necrosis of femoral head
- follows femoral fracture in high energy trauma
- can have non traumatic causes: anything that compromises blood supply in artery
Avascular necrosis of the femoral head: clinical assessment
- history of hip pain progressively worse over time
- located in groin, proximal thigh, buttock
- aggravates with weight bearing and eases with rest
- antalgic gait
- passive movement elicits pain
- limitation in motion in capsular pattern
- MRI
Avascular necrosis of the femoral head: management
- if non traumatic: non-weight bearing activities, alter risk factors
- older patient: hip replacement
- younger patient: reconstructive procedure
Osgood Schlatter’s syndrome (aka: traction apophysitis)
- apophysis biomechanically weak during growth spurt: at danger in young athletes
- resultant traction causes irritation, inflammation, microtrauma
- Osgood Shlatters: tibial tuberosity
- Sinding Larsen Johansson: inferior angle of patella
What is an apophysis
Secondary ossification centre, attachment of tendons
Osgood Schlatters: clinical presentation
- in very active younf children aged 10-15 during growth spurt
- more often boys cause growth spurt later
- often unilateral
- inflammed, swollen and tender on palpation
- child may have poor lower limb alignment
Osgood Schlatters management
PRICEM
- gentle strecth of rectus femoris
- orthotics
- patellar tendon taping
Patellofemoral dislocation
- Patella moves laterally
- Predisposing factor: femoral anteversion, genu valgum, increased Q angle, Patella alta, ligament laxity, muscle weakness
Patellofemoral dislocation assessment
Physical exam: tenderness over medial patella, patellar apprehension test
Patellofemoral dislocation: management
- relocate and assess for fracture
- conservative
- surgery sometimes required
Patellofemoral pain syndrome
- 12-35 years
- activity dependent
- aching pain
- cause unknown
Contributing factors: abnormal biomechanics, tight structured, muscle imbalance, training/load
Patelofemoral pain syndrome diagnosis
- history : area of pain, aggrevating activities, crepitus
- Physical: alignment abnormalities, single leg step down (less pain if glide patella medially), isometric muscle test
- no imaging required
Management of Patellofemoral pain syndrome
Rest
- McConnell taping: increased activation of vastus medialis
- Address control and strength issues
- stretch tight structures
- orthotics
- NSAIDS in acute phase only
Achilles tendinosis
A degenerative mucoid condition characterised by an increase in ground substance and vascular tissue and an absence of inflammatory markers
Achilles tendinosis presentation
- pain localised to tendon
- gradual onset
- pain aggravated during or after activities
- pain can disappear after warm up and return when cooling down
Stage 1: reactive tendinopathy
- acute tensile stress or compressive overload
- tendon cells activated and proliferate
- proteoglycans produced
- tendon thickening
- short term reduction in stress
Stage 2 tendinopathies: tendon dysrepair
- worsening pathology with greater matrix breakdown
- tendon cells more prominant
- myofibroblasts appear
- increased production of proteoglycans and collagen
- collagen separation and disruption of matrix
- growth of vessels and nerves
Stage 3 tendinopathies: degenerative
- end stage of disease
- matrix and cell changes progress
- apoptosis
- large areas of disorganised matrix, little collagen, vessels
Pain in tendinopathy
Up to 65% of degenerative tendons which rupture were pain free
Where does pain originate:
- biochemical substances
- neurovascular in growth
Management of stage 1 early stage 2 tendinopathy
PHARMACOLOGY
- tenocyte inhibitor
- affrecan inhibitor
PHYSICAL
- load management
Late stage 2 or stage 3 tendinopathy management
PHARMACOLOGY
- prolotherapy
- aprotinin
- sclerosing therapy
- glyceryl trinitrate
PHYSICAL
- exercise with eccentric component
- Shock wave therapy, friction, ultrasound
Exercises for tendinopathies: effect
- increased collagen production in affected tendon
- improve tendon structure
- reduce tendon vessels
- reduce pain
Achilles tendinosis prsentation
- common in sports involving running and jumping
- tenderness and thickening in mid portion of achilles
- crepitus or nodules
- pain on heel rise test
Management of achilles tendinosis
Eccentric exercise protocol by Alfredson and cook
Plantar heel pain pathophysiology
Overuse of plantar ffascia at attachment of calcaneus
- collagen disarray in ABSENCE of inflammatory cells
- RISK FACTORS: pes planus/cavus, sports, excessive load
Plantar heel pain assessment
- pain with 1st step am, prolonged standing or running
- palation of medial calcaneal tuberosity is the definitive objective sign
Plantar heel pain: management
- offload the platar fascia: activity modification
- NSAIDS
- stretching
- self massage
- strengthening exercise
- taping
- corticosteroid injection
