6 Hip Pathomechanics
I. Alterations of bony structures of the hip (femoroacetabular impingement, hip dysplasia) alter the equilibrium of forces and contact areas of the articular surfaces resulting in instability. 1 Joint contact pressures are significantly increased in abnormal osseous morphology and dysplastic conditions, causing early onset hip osteoarthritis. 2 , 3
II. Neck deformities:
Coxa valga: the neck shaft angle is increased (normal value: 125 degrees; valgus > 135 degrees) on imaging. 4 As greater trochanter migrates distally, the abductor moment arm is increased with resultant increase in the joint reaction force.
Coxa valga: the neck shaft angle is decreased (<120 degrees), the greater trochanter is at a higher level, and the abductor lever arm is reduced with resultant reduction in joint reaction force. 4
Femoral torsion: normal value is 10- to 15-degree anteversion in adults. Retroversion or anteversion greater than 15 degrees may result in changes in the position of the femoral head within the acetabulum, which may precipitate hip joint instability. Anteversion greater than 15 degrees results in greater internal rotation. 4 In-toeing is a compensatory gait mechanism seen in individuals with excessive anteversion, while out-toeing compensates for retroversion.
III. Pathomechanics and maneuvers of lower limb disorders:
Weight gain increases the total compressive forces applied to the hip joint. Abductor muscle forces increase in reaction to the increased body weight. The increase in the joint reaction force may contribute to joint degeneration along with other factors.
Limping reduces hip joint load by bringing the center of gravity closer to the moment arm of the femoral head. Limping entails lateral acceleration of body mass, deceleration during stance phase, and subsequent acceleration back to midline. Energy expenditure is increased and movement is less efficient.
Cane walking: the abductor muscles and walking cane together produce a moment that is equal to the moment of the body weight. Cane reduces the joint force reaction because the cane–ground reaction force acts at a much larger distance from the center of the hip.
IV. Pathomechanic patterns of structural hip disorders:
Hip dysplasia: individuals with hip dysplasia experience limitation in hip extension during walking, reduced net activity of the hip flexors in preswing phase, and compensatory increase in pelvic excursion.
Femoroacetabular impingement (FAIS): limitations in all planes of motion. Individuals with symptomatic FAIS have diminished squat depth, external moments during hip flexion and external rotation, hip abduction, and pelvic frontal plane motion during the swing phase of walking. Abductor moment arm is reduced and joint reaction force is increased. 5 , 6
V. Hip–spine syndrome: This refers to hip pathology in the setting of degenerative disease of the spine. Individuals with hip pathology show increased lumbar lordosis and sloping of the sacrum. Flexion contracture of the hip results in pelvic rotation and increases lumbar lordosis, consequently increasing loading of the lumbar facets and ligaments. 7 Individuals with unilateral degenerative disease of the hip have increased bend of the lumbar spine on the side of the joint disease and increased movement in the sagittal plane with decreased coronal plane movement. 8 Osseous deformities and soft-tissue pathology of the hip that limit hip motion can also increase compensatory lumbopelvic motion. 9
VI. Gait pathomechanics: abnormal gait patterns may be adopted in compensation for injury to the lower extremity.
Osteoarthritis: individuals show loss of hip range of motion during gait and sagittal plane reversal motion as the hip goes into extension. The muscle force output is reduced and the hip joint reaction force is increased.
Hip contracture: individuals flex the hip during the stance phase, with marked posterior pelvic tilt and reduced stride length.
Hip abductor weakness: During the one-leg stance, gluteal muscles normally abduct the contralateral limb, preventing the pelvis from tipping toward the swing leg. Injury to the superior gluteal or obturator nerves results in weakness of the abductor muscles. Weak gluteus medius is unable to stabilize the unaffected pelvis. During the stance phase, the trunk leans over the affected side, while the unaffected pelvis drops. This is clinically seen as the Trendelenburg sign (see Fig. 2.1 ).
Antalgic gait: a compensatory gait pattern reflective of intra-articular or extra-articular hip pain. The duration of the stance phase is reduced in the affected limb with decrease in the swing phase of the unaffected limb. Body weight is shifted laterally to the unaffected limb.
Hamstring weakness: Hamstring muscles function normally to slow down the swing phase. Weakness causes the knee to snap into extension during the swing phase.
Gluteus maximus gait: the trunk leans backward during early stance phase; the center of gravity shift posterior to the hip to reduce demand on the hip extensors.
Psoatic gait: psoatic limp in patients with the Legg–Calvés–Perthes disease may be caused by weakness or reflex inhibition of the psoas major muscle. The affected leg moves in external rotation, flexion, and adduction. The limp may be accompanied by exaggerated trunk and pelvic movement.
Weak hip flexors: the lower extremity is unable to shorten for proper foot clearance off the floor; the unaffected pelvis rises during the swing phase elongating the limb to provide extra clearance for the affected leg.
Leg length discrepancy results in compensatory tilting of the pelvis to the shorter limb.
Scissors gait is the abnormal gait from hip adductor spasticity. During the swing phase, the trunk leans over the stance leg.