LL pathologies Flashcards
aetiology of femoral acetabular impingement- 2 types
2 mechanisms- CAM type= extra bony growth of femoral head on anterior superior aspect of the femoral head-junction, cam impingement can become symptomatic in physical young males- extra growth plates
Pincer- result of excess acetabular coverage of femoral head,can be global (coxa profunda)-deep hip socket, or focal anteriorly (acetabular retroversions)- altered orientation of acetabilim, can occur in extreme ROM
symptoms of FAI
stiffness, hip pain worse during physical activity or after sitting, limping
diagnosing FAI
imaging tests- CAM- radiographyh- alpha angle- X ray hip at 90° flex and 20° abd, pincer- can be located on radiographic imaging by looking at lateral centre head angle- line from head of femur and second line going to rim of acetabulum- angle <40° is positive
impingement test- flex hip and rotate towards opposite shoulder
physio management of FAI
corticosteroids, NSAIDs, hip surgery, exercise to strengthen hip, stretch hip flexors, balance and proprioception exercise
aetiology- greater trochanteric pain syndrome
common cause of lat hip pain, attribute tendinopathy of glut med/min or bursal pathology. compressive forces cause impingement of these structures onto the greater trochanter by the ITB- puts pressure on tendons and structures, on bursa and glut med/min tendon
female 40-60 and post menopausal, lower femoral neck shaft angle and increase BMI
symptoms of GTPS
pain in the outer bottom/thigh/buttick area, worse pain when lying on side, pain increasing with exercise such as long periods of walking, standing or running. altered walking pattern, more noticeable pain when walking briskly, tenderness to touch, pain sitting with your legs crossed
test with FADER/FADER-R
treatment for GTPS
isometric abduction against wall, single leg stand, side lying abduction against pillow, wall squat, pelvic dips, bridge
pain relief, NSAIDs, cold
Meniscus vascularization- left
the blood supply to the meniscus, left- through fully vascularized birth, the blood vessels in the meniscus recede during maturity. in adulthood, the red region contains the overwhelming majority of blood vessels. Red-red region= blood supply, white- red region and white-white region are avascular.
meniscus vascularization- right
cells in outer, vascularized section of meniscus (red-red region) are spindle shaped, display cell process, and are more fibroblast like, while cells in the white-red region and inner section (white-white region) are morre chondrocyte like, though they are phenotypically distinct from chondrocyte. cells in the superficial layers of the meniscus are small and round
meniscal pathology
meniscus lesions most common intra-articular knee injury, medial injury more frequent, often associated with ACL tearsm can get degenerative meniscal tears
MOI- involves components of flex and rotational forces under compressions e.g. twisting/ squatting, manoeuvres, joint line tenderness/ effusion,
signs of MOI
most will not require MRI- pick up 95% of cases
apleys, McMurrys, thessalys
meniscal pathology- clinical presentation
symptoms are produced by instability of torn fragment. these symptoms can result in locking of knee, popping knee and clicking, medial and lateral knee pain, joint line tenderness, occurs mostly in 50 years of age, hyperflexion for long periods
meniscal pathology- treatment
PEACE & LOVE, strengthen exercises for quads and hamstrings- start with isometric, then progress to isotonic
joint mobs- superior tibiofibular, patellofemoral joint, tibiofemoral joint
plyrometrics
meniscal pathology- treatment
PEACE & LOVE, strengthen exercises for quads and hamstrings- start with isometric, then progress to isotonic
joint mobs- superior tibiofibular, patellofemoral joint, tibiofemoral joint
pylorometrics
MOI MCL
knee hit directly on lateral aspect- stretches ligament too far, commonly injured at similar time to ACL,
can also be injured through repeated stress
symptoms of tears in MCL
pain, stiffness, swelling, tenderness alongside inside knee, a feeling that knee may give way (instability) and locking/catching
diagnosis of MCL
valgus test
physio management MCL
good blood supply so responds well to treatment, lightweight cast initially to allow flex and ext but prevent rotation, restore strength and ROM, then complete proprioception work
PCL injury- MOI
posterior force to proximal tibia, if combined with rotational force injury to P-L complex, may occur in car crash- hit knee’s on dash board
S and S PCL
positive posterior draw test, often asymptomatic or may have vague symptoms of pain in posterior knee, pain on kneeling
LCL MOI
main cause of LCL injury is direct trauma to the inside of the knee. this puts pressure on the outside of the knee and causes the LCL to stretch and tear
symptoms of LCL
swelling of the knee, stiffness at the knee that can cause locking of the knee, pain or soreness on the outside of the knee, instability of the knee joint
diagnosis of LCL injury
varus test, or MRI scan
treatment for all ligament injuries
PEACE and LOVE, pain relief, strengthening and ROM exercise, proprioception work
train breaks- ACL= hamstrings, PCL- quads, LLS- evertors
anterior knee pain
indicates no individual structures can be isolated for pain, could be tightness of muscles infront or behind knee- altered biomechanics at PF joint, altered alignment, could be due to high or low riding patella
S and S of anterior knee pain
adolescent people generally, triggered by overuse, aching infront of knee, aggravated by deep flexion- going up stairs, rest receives symptoms
clinical presentation- anterior knee pain
functional deficits, crepitus and/or instability, pain when walking down stairs/ squatting/ depressing the clutch pedal in car/ wearing high-heeled shoes, sitting for long periods with knees in a flexed position, instability when walking on stairs,
differential diagnosis- Anterior knee pain
symptoms- pain (location and type) or instability problems, alignment of the entire LL (squinting patella, high Q-angle), patellar position, muscle and soft tissue (hypertrophy-VMO, muscle imbalance between VL and VM, weakness of knee extensors, hip flexors or hip abductors), knee function- during functional activities
physical therapy anterior knee pain
knee taping and exercise for mal alignment, proprioceptive training, shoe inserts, improve eccentric muscle control, improve knee ext strength,
ankle lateral ligament- MOI
usually after a traumatic event/acute presentation, excessive inversion/PF movements,
risk factors- BMI, slow eccentric inversion strength, fast concentric PF, passive inversion joint position sense, reaction time of peroneus brevis were associated with increased risk
assessment of the joint- ankle lateral ligament
amount of instability present by assessing the grade of the sprain, loss of ROM, loss of muscle strength, levels of reduced proprioception
special tests, anterior draw (ATFL and CFL), talar tilt (ATFL and CFL), proprioception
ankle lat ligament- reduce pain and swelling (early treatment)
initial management (within first 48-72 hours)- PEACE and LOVE, if weight bearing painful start with NWB, but quickly progress to PWB
physio management- ankle lat ligament
ROM- AROM, strength- eversion is particularly important, proprioception, plyometrics- twisting, jumping, hoping on one leg, running, figure 8 running
achilles tendinopathy-
is an overuse injury caused by repetitive energy storage and releases with excessive compression. this can lead to sudden injury, or rupture. risk factors- lack of flexibility or stiffness Achilles tendon
2 types:
insertional- transition between tendon and bone, mid-portion- within tendon body
achilles tendinopathy- first stage
is non-inflammatory proliferative response in the cell matrix, this is as. result of compressive or tensile load, straining the tendon during physical activity can cause repetitive micro traumas, these are linked with a non-uniform tension between the gastroc and soleus, causing frictional forces between the fibres and abnormal concentrations of loading in the tendon
consequences of micro traumas
inflammation of the tendon sheath, degeneration, or a combination of both. without the minimum time for recovery, this can lead to tendinopathy.
possible factors that lead to chronic tendon overuse injuries
decreased arterial blood flow, local hypoxia, decreased metabolic activity, nutrition, and persistent inflammatory response
acute stage of Achilles tendinopathy
caused by acute overload, blunt trauma or acute muscle fatigued, and is characterised by an inflammatory reaction and oedema formation. if the treatment is overlooked, it can cause a fibrin and form adhesions off the tendon
progression of achilles tendinpathy
the progression of the reactive tendinopathy to tendon disrepair can occur if the tendon is not offloaded and allowed to regress back to normal state. During this phase, there is the continuation of increased protein production which has been shown to result in seperation of the collagen and disorganisation within the cell matrix. this is the attempt of tendon healing
degenerative Achilles tendinopathy
the final stage of the continuum and it is suggested that at this stage there is a poor prognosis for the tendon and change is now irreversible. often, tendon degeneration is found in combination with peri-tendinous adhesions, but this does not mean one condition causes the other one
risk factors of achilles tendinopathy
obesity, high blood pressure, rapid changed to load, type 2 diabetes, prolonged steroid use, family history of tendinopathy, inappropriate footwear
clinical presentation
morning pain, swelling and pain are less common, the tendon may appear thicker in M-L and A-P outline
anterior knee pain
clarkes test (reproduction in symptoms), see biomechanics changes- changes in Q angle, knee more medially causes patella to be forced laterally, treat- sort biomechanics out, ER hip resisted straightening leg- step forward into it, quad strength
