on this X-ray that allow one to determine the location of the femoral head as well as the degree of acetabular dysplasia. In addition, subsequent X-rays are important to monitor the progress of treatment.

The prognosis for DDH is very good when the diagnosis is made early, and treatment initi­ated in infancy. With delay in diagnosis and, therefore, in treatment, the prognosis worsens. The most dreaded complication, avascular necrosis, can occur at many points in the treat­ment algorithm despite the advances in treatment.

Idiopathic avascular necrosis of the femoral head in the child was originally described in 1909 by multiple authors: Legg in Boston, Calvé in France, and Perthes in Germany. Unfortunately, all authors interpreted that the observed changes were due to nontuberculous sepsis. Slowly, it has

been recognized that this femoral head ischemia is of unknown etiology, with genetic and environ­mental factors playing various roles. The changes cannot be produced by a single period of avascu­larity, but multiple episodes may cause the char­acteristic pathologic changes. The exact trigger for this vascular disruption has remained elusive.

and magnetic resonance imaging (MRI) scans. Initially, the stage of synovitis, which lasts 2–3 weeks, produces an irritable hip syndrome easily confused with toxic synovitis. The X-rays are negative at this time. Subsequently, the stage of avascularity onsets, lasting 2–3months, during which time the femoral head necrosis occurs. Fragmentation changes of the capital femoral epiphysis herald this stage. Once the avascular event has occurred, the femoral head will revas­cularize and the process will “heal,” resulting in the stage of revascularization. The critical issue is the degree of deformation of the normally spheri­cal femoral head before complete healing occurs. Eccentric mechanical loads applied to the soft­ened, diseased head frequently alter its spheric­ity. The healing phase lasts approximately 2years, at which time only the residual deformity remains as the permanent marker of the disease (Fig.7.23).

The treatment principles for this disease are really no more advanced than they were 30years ago. Nevertheless, certain facts seem generally accepted. The prognosis hinges on two basic features. First is the patient’s age at onset of the disease. Children under age 5 will do well left untreated, which is the current recommenda­tion. Those over age 8 do poorly, despite treat­ment. The other factor is the extent of head involvement. Obviously, the head that is com­pletely necrotic is more likely to sustain perma­nent deformation than a head only partially involved. For children of intermediate age, 5–8years, the principle of “containment” con­tinues to be accepted. Conceptually, the thought is to place the softened femoral head concentri­cally into the acetabulum, which will in turn act as a mold or template as the head revascularizes. This can be accomplished in the smaller child by using an abduction orthosis and in the larger child by using either a femoral or acetabular osteotomy to improve congruity prior to defor­mation. The treatment for the older child with an already deformed hip is highly controversial. In general, the prognosis is good for the younger children, whereas many of those diagnosed after age 9 require total hip replacement in early adulthood.

Many of these children have been limping for several months before they present for evaluation. Pathologically, the capital femoral epiphysis has “slipped” or translated posteriorly and medially relative to the femoral neck. It is actually the femo­ral neck that is moving anteriorly and laterally rela­tive to the head which remains located in the acetabulum. This displacement ultimately results in an irritated hip which is manifested by a limp, pain, and external rotational deformity of the leg. This deformity is usually readily apparent on phys­ical examination: as the hip is exed, the leg obli­gately externally rotates. Diagnosis is made with X-rays of the pelvis including an AP and frog-leg lateral of the hip. If one traces a line up the femoral neck, and line should does not intersect with the epiphysis, SCFE may be diagnosed (Fig.7.24).

There have been multiple suggestions as to the etiology of the slipped capital femoral epiphysis. Many authors feel that these children are hormonally predisposed and with the super­imposed stress of obesity, the perichondral ring is no longer able to “girdle” the physis; hence, the slip occurs. Typically, the slip is said to occur through the hypertrophic zone of the phy­sis, but the displacement may actually tran­scend the entire physis. Children have chronic slips if they had symptoms for over 3weeks. Acute SCFE was often considered the result of an acute injury and therefore, frequently con­sidered by some authors to be a fracture through the physis. When the child had a history of limping and then a superimposed acute injury, the resultant slip is referred to as an acute on chronic slip.

Clinically, such children are not sick; they remain active, eat well, and are afebrile. Their lab studies, including X-rays, are usually normal. On exam, the hip is irritable, with additional ndings of an antalgic limp, decreased range of motion, and pain with log rolling of the leg.

Unlike the hip, the affectations that one sees about the knee in a child are, for the most part, all benign and generally respond to simple treatment measures.

Similar to DDH, this deformity is multifactorial in origin. Environmental factors applied to a genetically predisposed individual result in this pathologic deformity. As with DDH, it is impor­tant to make it clear to the parents that this is NOT a postural deformity. Rather, there is an anatomic abnormality of the talus. Due to the abnormal medial and plantar deviation of the talar neck, there are a number of secondary defor­mities. The tarsal navicular is dislocated dorsally onto the talar neck; soft tissue contractures develop, and the resultant conguration is char­acteristic. The forefoot is adducted, the hindfoot

is in varus (inverted), and the entire foot is in equinus. The deformity can be remembered with the pneumonic “CAVE”—cavus, adductus, varus, and equinus.