The Pathology of Hip Dysplasia by oyc99684


									The Pathology of Hip Dysplasia

Capsular laxity, from what ever cause, is the most common underlying pathology in the
development of hip dysplasia. This laxity may produce secondary changes in the hip which
may be well established at birth or develop in the post natal period if the laxity persists.

Capsular laxity leads to a number of pathological scenarios

Subluxation - this refers to the femoral head sliding within the acetabulum but without
completely loosing contact. This is felt as a gliding sensation and may at times be difficult to

Dislocation - is where the femoral head looses contact with the acetabulum. The femoral head
may be dislocatable - able to be pushed out of the socket, or dislocated - not in the socket.
Dislocations may be able to be put back in the socket- that is “reducible”, or remain stuck in
the dislocated position – that is “irreducible”.

In 65% of cases hip dysplasia affects the left hip which appears to be related to intrauterine
posture where the left side of the foetus lies against the mother’s sacrum thus adducting the
hip. Bilateral dysplasia occurs in 20% of cases so the examiner needs to be aware that
bilateral irreducible hip dislocations may appear normal with symmetrical limbs and no
feeling of instability. These types of hips are often only identified late.

Joint changes

As the unstable hip subluxates and then dislocates changes occur to the normal anatomical
structures. Understanding these changes helps with interpreting clinical signs.

Dysplasia leads to morphological changes to the shape of the femoral head. Loss of a
spherical socket means that the head is no longer moulded and it takes on a progressively
more ovoid or egg shape. As the hip dislocates the capsule stretches and ultimately becomes
“hour glass” in shape with a constricted waist. The psoas tendon lies stretched across this
waist and the ligamentum teres elongates and becomes loose.

With the head lying laterally on the acetabular rim, the labrum and acetabular margin
become flattened and the acetabular shape deteriorates. As the femoral head moves out of the
socket, the adductors become tight due to their natural line of pull being disturbed.

Initially these changes are mild and can be overcome by positioning the hip in an abducted
and flexed posture. With time the changes become progressively fixed and it may not be
possible to reduce or hold the hip in a satisfactory position within the joint. Later significant
adaptive changes occur and a missed dislocation will often form a false joint on the side of the
pelvis and the leg will be short and walking unstable.

Acetabular dysplasia specifically refers to incomplete or insufficient development of the hip
socket. Such dysplasia may be due to the effect of an unstable hip but on occasion is an
isolated condition resulting in a shallow socket that does not contain the femoral head
appropriately. This type of hip does not necessarily become unstable. Some hips
spontaneously improve whilst others are only identified in adult life with the development of
early arthritis due to a poor mechanical environment in the joint producing cartilage damage.

To top