Pelvis and Hip 3 Flashcards
etiology of hypermobility at the hip
traumatic like fx, ligament tear, or labral tear
atraumatic from extreme motions in sports, labral tear with FAI/IPI, and systemic connective tissue disorders
if there is a bony abnormality, what factors may contribute to hypermobility of hip
shallow acetabulum
inferior acetabular insufficiency
excessive femoral torsion or version (only one we can pick up clinically)
excessive femoral neck angle
what is femoral torsion
in transverse plane
angle between femoral condyles and femoral head and neck
excessive anteversion = toeing in
excessive retroversion = toeing out
what is the femoral neck angle
in frontal plane the angle between the shaft and neck
what is coxa valga
larger inclincation angle
leads to genu vara or bow legged
what does valgus mean
distal segment moves laterally
i.e. coxa valga = bow legged stature
what is coxa vara
smaller inclination angle
leads to genus valga or knock kneed position
prevalence of hypermobility at the hip
inconsistent with gender differences
5-35% of those with hip pain
risk factors for hypermobility
genetics
injury
nature of pts activities
-running
-ballet
-golf
-hockey
-soccer
-excessive RT, FLX, and hyper EXT
symptoms of hypermobility of hip
like impingement due to hypermobility plus:
anterior groin or lateral hip pain
popping, locking, or snapping
feeling of instability, especially when squatting
signs of hip hypermobility
like impingement plus
ROM: hip IR>30 at 90 flx
combined motion: possibly inconsistent
special tests for hip
hip apprehension
abnormal femoral version or torsion
what is the hip apprehension test
in prone
move hip into ext and abd while applying anterior inferior force on femur
specific to pubofemoral ligament test
PT Rx for hypermobility of hip
primary focus on cartilage integrity and stabilization
predominant innervation to the L4-S1 Z joints
L4 dorsal Rami
predominant and most consistent innervation to the L4-S1 discs
L1, 2 dorsal root ganglia
L4 and L5 sinuvertebral nn
iliolumbar ligaments are innervated by
L1-4 spinal nn
if there is a instability at L4-S1, what muscle groups would be more likely to excessively recruit due to the predominance of L1-L4
hip flexors (L1/2)
hip adductors (L3)
knee extensors (L3/4)
Ankle DF (L4/5)
main function of iliopsoas and where does it attach
primarily a hip flexor and trunk stabilizer
attaches to iliocapsularis
functions of iliocapsularis and where does it attach
primarily a dynamic stabilizer for capsule
also a hip flexor
attaches to iliopsoas, anteromedial capsule, and rectus femoris
rectus femoris attaches to
the capsule
the capsule attaches to
the labrum
nerve roots for iliopsoas, iliocapsularis, and rectus femoris
iliopsoas= L1-4
iliocapsularis = L2-4
rectus femoris = L2-4
simplify the hip consequence of excessively recruited hip flexors
muscles are overrecruited and pull on attachment to capsule that ultimatley pulls on the labrum as well
etiology of L4-S1 regional interdependence
L4-S1 hypermobility instability
most common segments
pathomechanics of L4-S1 regional interdependence x5
1-excessively recruited hip flexors that attach to capsule/labrum
2-this causes excessive traction on anterior medial portion of capsule and labrum (3/9 oclock)
3-this can lead to labral attrition WITHOUT bony changes
4-also inhibited hip extensors and abductors
5-these things lead to imbalnce of optimal axis of motion and joint support as well as easily overworked muscles due to lowered recruitment so overuse/lower supply occurs
hypertonicity of hip extensors and abductirs is due to what
being overworked even without overuse
often reported as tightness that stretching helps short term but doesnt resolve
describe why L4-S1 regional interdependence is self perpetuating without address of lumbar stabilization
iliopsoas is a stabilizer of LORDOSIS in standing
iliopsoas maintains its size or grows in those with LBP indicating continued/excessive recruitment
excessive recruitment can further add to the anterior shearing most often occurring with lumbar hypermobility/instability
excessive recruitment = more pull = more anterior shear = more LBP = more recruitment (cycle)
what is iliopsoas impingement
impingement without dysplasia or bony changes
etiology of iliopsoas impingement
not fully clear
conditions that lead to excessive hip flexor recruitment
lumbar hypermobility/instability with regional interdependence
symptoms of iliopsoas impingement
like FAI
possible lumbar hypermobility/instability symptoms if aggravated
signs of iliopsoas impingement
(PROM, tracking, inhibited muscles, neuro, palpation, and thoracolumbar scan/BE)
like FAI plus:
-IR limited at 90 flexion with elastic end feel
-hip maltracking at 90 flx (hip deviated into abd while passively flexing)
-possible hip ER inhibition at 90 with RST
-possible inhibition of extensors and abductors
-possible hypersensitivity with neuro
-TTP over ant hip (3/9 oclock)
-thoracolumbar scan/BE findings for lumbar hypermobility
explain why IR is lost in PROM at 90 flexion
because of the inhibition and hypertonicity of extensors; primarily glut max inhibition which is also the main external rotator at 90 flexion
explain why jip maltracking at 90 flx occurs with iliopsoas impingement
due to inhibition and hypertonicity of piriformis that is an abductor at 90 flx; draws hip out and wont let it stay in line
elastic end feel into flexion if deviation is not allowed
why might there be inhibited ER at 90 flx with iliopsoas impingement
due to glut max inhibition bc it is the main ER at 90 flx
if a pt has iliopsoas impingement and you ask them to squat what might you see
quad dominant squat pattern
knees over toes
due to inhibited hip ext and excessive knee ext
PT Rx for iliopsoas impingement
“culprit Rx” for lumbar hypermobility/instability
“victim Rx” like FAI Rx
MD Rx for iliopsoas impingement
iliopsoas surgical release
Describe gluteal tendinopathy
lateral hip P!
usually diagnosed as greater trochanteric bursitis
called tendinopathy b/c usually there are already structural changes (more accurate description)
aka GTPS
prevalence of gluteal tendinopathy
most prevalent in LE
women > men
> 40
sedentary > athletic
risk factors for gluteal tendinopathy
female
BMI
excessive hip ADD
weak hip ABD
coxa vara
plyometric overuse
structures involved with gluteal tendinopathy
primarily greater trochanteric bursa
primary muscle = glut med
secondary muscle = TFL/IT band
describe insertions in releation to the R greater trochanter
12 oclock = Gmed
11= piriformis
10 = GOGOs
9 = QF
etiology and pathomechanics of gluteal tendinopathy
abnormal mechanical loading is the primary driver
excessive loads may be applied longitudinally or perpindicularly
excess loads can also occur with impaired LE control including but not limited to excessive femoral ADD
when do tensile loads occur
with concentric loads
when do tensile and compressive loads occur
with eccentric loads
particularly in lengthened ranges
how does L4-S1 rehional interdependence play a role with gluteal tendinopathy
TFL/IT band overrecruitment
known to hypertrophy indicating excessive recruitment
symptoms of gluteal tendinopathy
gradual and unknown onset but possible overuse/lower supply
increasing lateral hip pain and maybe lateral thigh
decreased pain with rest
possible lumbar hypermobility/instability symptoms if aggravated
when are symptoms increased with gluteal tendinopathy
walking, running, stairs, any single leg loading
prolonged sitting, especially crossing legs as IT band tension increases thru Gmax lengthening, particularly in lower seat and then first few steps
lying on involved side
observation/functional tests for gluteal tendinopathy
possible antalgic and or trendelenburg gait
impaired LE control
-pain/weak with 30 sec SLS
-may need to assess higher level ADLs like jumping/running
ROM signs with gluteal tendinopathy
possible lateral hip pain and limitation with add and IR in neutral (lengthening fibers of glut med)
ER (glut med and min lengthening) and H. ADD (piriformis) in 90 flexion
resisted/MMT for gluteal tendinopathy
possible weakness and pain with
-ABD (especially in ADD position)
-ER in neutral
-IR and H Abd in 90 hip flx
-ABD and ERs weak and atrophied
special tests for gluteal tendinopathy
+ ER (G med and min lengthened) and H add (piriformis lengthened)
possible + Obers
palpation findings for gluteal tendinopathy
TTP over bursa (hallmark sign) > Glut Med
PT Rx for gluteal tendinopathy aside from MET
victim vs culprit?
-itis vs osis
-regional interdependence
pt edu
-soreness rule
-load management
-avoid provoking symptoms (i.e. lying on side/crossed legs)
-pillow between knees when on uninvolved side
POLICED
stretching not recommended (maximally lengthening and compressing structure)
shockwave effectiveness with gluteal tendinopathy
shock wave therapy proposed but not substantiated in research
primary MET focus for gluteal tendinopathy
tendon proliferation and stabilization (hip and lumbar)
MET parameters for gluteal tendinopathy
isometric without compression from lengthening
isotonic without compression from lengthening
isotonic with compression from lengthening
isometric loading in WB (best place to start doing closed chain; should be able to do above first)
plyometric loading
MD Rx for gluteal tendinopathy
corticosteroid injections
-inflammation not primary issue
-mainly acts as a analgesic
-may hinder tendon from responding to optimal loading
-may hinder response to optimal loading
platelet rich and other “regenerative” injections lack sufficient support for all soft tissue injuries
describe hamstring tendinopathy
glute pain that is more often a tendinopathy
common in athletes; rare in general public
risk factors for hamstring tendinopathy
prior injury
regional interdependence from L4-S1 lumbar hypermobility/instability
weak Gmax, Gmed, and or adductors
explain how regional interdependence from L4-S1 can affect hamstring tendinopathy
excessive hip flexor recruitment leads to anterior pelvic tilt and adds to excessive tension/compression
inadequate ham/quad ratio
-excessive quad recruitment
-overuse/lower supply with hamstring inhibition
advanced age means less pliable tissue = greater tension/compression
structures involved with hamstring tendinopathy
hamstring proximal tendon
adductor magnus = shared origin and fascial connections with hamstrings
ischial bursa
rarely sciatic n; possibly adhered if tendinosis
etiology of hamstring tendinopathy
abnormal mechanical loading
-repetitive hamstring action with hip flexion (running, jumping, training errors)
-excessive prolonged stretching
-sedentary lifestyle
-muscle imbalances
-prior injury
deceleration - hamstrings eccentrically control knee ext
heel strike and foot flat - after lengthening hamstrings act in a lengthened position with hip in flexion
symptoms of hamstring tendinopathy
posterior hip/butt pain (deep ache)
less symptomatic with warm up
worsened with activities that lengthen hamstring with or without m action
stiffness after prolonged position, particularly sitting
signs of hamstring tendinopathy
observation = possible atrophy if long standing
functional tests = pain with activoty involving lengthening with muscle action (i.e. lunge, running, squat, etc)
ROM = possible limits/pain with hip flexion and knee extension especially if combined
RST/MMT = possible weakness/pain with hip ext and knee flex especially with lengthened position
neuro = possible dural mobility limits if sciatic involved
TTP over proximal tendon and bursa at ischial tuberosity
special test = bent knee test and shortened muscle length test
describe the bent knee stretch test
hip and knee flexed
PT slowly straightens knee
mod to high reliability
PT Rx for hamstring tendinopathy
follow general prinicples of gluteal tendinopathy and tendinosis Rx plus
pt edu to stand more than sit and avoid low seats/prolonged sitting
dry needling has limited support
neural mobs for sciatic involvement
MET for hamstring tendinopathy
eccentric training to reduce pain and injury
lumbopelvic stabilization to improve hamstring activity that supports regional interdependence
prognosis for hamstring tendinopathy
good out to at least 6 months with 8-10 weeks if PT
MD Rx for hamstring tendinopathy
corticosteroid injections
-mainly act as a analgesic
-may hinder tendon from responding to normal loading
platelet rich other “regenerative” injections (lack support for ALL soft tissue injuries)
