Lecture 9 - Lower Limb Soft Tissue And Bone Disorders Flashcards

1
Q

Dysplasia of the hip: Pathophysiology

A
  • during childbirth
  • abnormality in size, shape, orientation or organization of the femoral head or acetabulum

RISK FACTORS: breech, female, Family Hx, Firstborne

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2
Q

Dysplasia of the hip: assessment

A
  • ortolani and barlow maneuvers
  • Galeazzi sign
  • Hip abduction range
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3
Q

Dysplasia of the hip: management

A
  • subluxation often corrects spontaneously
  • if subluxation persists: Pavlik harness
  • if dislocation persists: closed reduction and Hip Spica casting
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4
Q

Perthe’s disease pathophysiology

A
  • 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
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5
Q

Perthe’s disease: Assessment

A
  • low grade ache, male 4-10 yo
  • Limited abduction and internal rotation upon physical exam
  • XRAY: increased density and flattening of femoral capital epiphysis
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6
Q

Perthe’s disease: Management

A

Rest

  • exercise for range of motion
  • Brace
  • surgery
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7
Q

Avascular necrosis of the femoral head: pathophysiology

A
  • 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
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8
Q

Avascular necrosis of the femoral head: clinical assessment

A
  • 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
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9
Q

Avascular necrosis of the femoral head: management

A
  • if non traumatic: non-weight bearing activities, alter risk factors
  • older patient: hip replacement
  • younger patient: reconstructive procedure
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10
Q

Osgood Schlatter’s syndrome (aka: traction apophysitis)

A
  • 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
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11
Q

What is an apophysis

A

Secondary ossification centre, attachment of tendons

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12
Q

Osgood Schlatters: clinical presentation

A
  • 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
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13
Q

Osgood Schlatters management

A

PRICEM

  • gentle strecth of rectus femoris
  • orthotics
  • patellar tendon taping
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14
Q

Patellofemoral dislocation

A
  • Patella moves laterally
  • Predisposing factor: femoral anteversion, genu valgum, increased Q angle, Patella alta, ligament laxity, muscle weakness
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15
Q

Patellofemoral dislocation assessment

A

Physical exam: tenderness over medial patella, patellar apprehension test

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16
Q

Patellofemoral dislocation: management

A
  • relocate and assess for fracture
  • conservative
  • surgery sometimes required
17
Q

Patellofemoral pain syndrome

A
  • 12-35 years
  • activity dependent
  • aching pain
  • cause unknown

Contributing factors: abnormal biomechanics, tight structured, muscle imbalance, training/load

18
Q

Patelofemoral pain syndrome diagnosis

A
  • 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
19
Q

Management of Patellofemoral pain syndrome

A

Rest

  • McConnell taping: increased activation of vastus medialis
  • Address control and strength issues
  • stretch tight structures
  • orthotics
  • NSAIDS in acute phase only
20
Q

Achilles tendinosis

A

A degenerative mucoid condition characterised by an increase in ground substance and vascular tissue and an absence of inflammatory markers

21
Q

Achilles tendinosis presentation

A
  • pain localised to tendon
  • gradual onset
  • pain aggravated during or after activities
  • pain can disappear after warm up and return when cooling down
22
Q

Stage 1: reactive tendinopathy

A
  • acute tensile stress or compressive overload
  • tendon cells activated and proliferate
  • proteoglycans produced
  • tendon thickening
  • short term reduction in stress
23
Q

Stage 2 tendinopathies: tendon dysrepair

A
  • 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
24
Q

Stage 3 tendinopathies: degenerative

A
  • end stage of disease
  • matrix and cell changes progress
  • apoptosis
  • large areas of disorganised matrix, little collagen, vessels
25
Q

Pain in tendinopathy

A

Up to 65% of degenerative tendons which rupture were pain free

Where does pain originate:

  • biochemical substances
  • neurovascular in growth
26
Q

Management of stage 1 early stage 2 tendinopathy

A

PHARMACOLOGY

  • tenocyte inhibitor
  • affrecan inhibitor

PHYSICAL
- load management

27
Q

Late stage 2 or stage 3 tendinopathy management

A

PHARMACOLOGY

  • prolotherapy
  • aprotinin
  • sclerosing therapy
  • glyceryl trinitrate

PHYSICAL

  • exercise with eccentric component
  • Shock wave therapy, friction, ultrasound
28
Q

Exercises for tendinopathies: effect

A
  • increased collagen production in affected tendon
  • improve tendon structure
  • reduce tendon vessels
  • reduce pain
29
Q

Achilles tendinosis prsentation

A
  • common in sports involving running and jumping
  • tenderness and thickening in mid portion of achilles
  • crepitus or nodules
  • pain on heel rise test
30
Q

Management of achilles tendinosis

A

Eccentric exercise protocol by Alfredson and cook

31
Q

Plantar heel pain pathophysiology

A

Overuse of plantar ffascia at attachment of calcaneus

  • collagen disarray in ABSENCE of inflammatory cells
  • RISK FACTORS: pes planus/cavus, sports, excessive load
32
Q

Plantar heel pain assessment

A
  • pain with 1st step am, prolonged standing or running

- palation of medial calcaneal tuberosity is the definitive objective sign

33
Q

Plantar heel pain: management

A
  • offload the platar fascia: activity modification
  • NSAIDS
  • stretching
  • self massage
  • strengthening exercise
  • taping
  • corticosteroid injection