Congenital Transient Tuberculosis Still's Infective Slipped Ankylosing Prolapsed Rheumatoid Primary dislocation synovitis of the hip Perthes' disease of the hip disease arthritis femoral spondylitis intervertebral arthritis
(juvenile epiphysis Reiter's disc Secondary rheumatoid syndrome 'Low back osteoarthritis arthritis) strain'
Table 9.1 Age distribution of common hip pathology
9.1. Inspection (1): Examine the standing patient from the front. Note (A) any pelvic tilting (e.g. from adduction or abduction deformity of the hip, short leg. scoliosis). (B) muscle wasting (e.g. secondary to infection, disuse, polio), (C) rotational deformity (common in osteoarthritis).
9.2. Inspection (2): Examine the patient from the side. Note any increased lumbar lordosis suggestive of fixed flexion deformity of the hip(s).
9.3. Inspection (3): Look at the patient from behind. Note (A) any scoliosis (possibly secondary to pelvic tilting from, for example, an adduction deformity of the hip). (B) gluteal muscle wasting (e.g. from disuse, infection), (C) sinus scars (e.g. secondary to tuberculosis).
9.4. Gait! Observe the gait from the front, sides and behind. Analysis grows from experience. Try to assess the stride and dwell time on each side, and the possible factors of pain, stiffness, shortening and gluteal insufficiency. Note that a shuffling gait (where each foot is dragged on the ground in the swing phase) or a stomping gait (where the foot hits the ground in a violent manner) may be seen in cases of posterior cord syndrome, and a broad-based gait in cases of spinal cord compression.
9.5. Shortening ( 1 ): It is important in the examination of the hip and the lower limb to determine the presence or absence of shortening. In true shortening, the affected limb is physically shorter than the other. This may be caused by pathology (A) above or proximal to the greater trochanter or (B) distal to the trochanters.
9.6. True shortening (2): True shortening from causes distal to the trochanters most frequently results from (A) old fractures of the tibia or (B) of the femur; (C) growth disturbance (e.g. from polio, bone or joint infections, epiphyseal trauma, or one of many hereditary bone diseases. (N) = normal side for comparison. (Note that in children, likely leg discrepancies at skeletal maturity may be predicted using a number of methods, including that of multiplier factors devised by Dror Paley et al.)
9.7. True shortening (3): Above the trochanter causes include (A) coxa vara (e.g. from femoral neck fractures, slipped upper femoral epiphysis, Perthes' disease, congenital coxa vara; (B) loss of articular cartilage (from infection, arthritis), (C) dislocation of the hip (e.g. secondary to developmental dislocation of the hip).
9.8. Shortening (4): Very rarely lengthening of the other limb gives relative true shortening. This may be due to (A) stimulation of bone growth from increased vascularity (e.g. after long bone fracture in children, or a bone tumour); (B) coxa valga (e.g. following polio).
9.9. Shortening (5): In apparent shortening the limb is not altered in length, but appears short as a result of an adduction contracture of the hip, which has to be compensated for by tilting of the pelvis.
9.10. Shortening (6): Limb shortening may be compensated by (A) plantarflexion of the foot on the affected side, or by (B) flexion of the knee on the other side. Most frequently the discrepancy is countered by pelvic tilting. The latter may in turn be compensated for by the development of a lumbar scoliosis.
9.11. Shortening: examination (1): The patient should be adjusted to lie squarely on the couch, with the trunk and legs parallel to its edge. The position of the pelvis should be observed (by the position of the anterior superior iliac spines) and adjusted where possible.
9.12. Shortening: examination (2): In the normal patient the heels should be level, and the plane of the anterior superior iliac spines at right-angles to the edge of the couch.
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