Pathophysiology. The top of the femur, known as the capital femoral epiphysis, serves as the ball of the hip joint when the acetabulum is the socket. In SCFE, the acetabulum holds the femoral head in place. This act contributes to the shearing off of the femoral neck through the cartilage growth zone (physis), especially if there is thick, soft cartilage and if the forces are high, such as in a relatively large or heavy person. As a result of these forces, which cause a slip, a child or adolescent can develop a limp and may experience mild to moderate pain in the hip. This pain can be referred to the thigh and/or knee.
Diagnosis. In many SCFE cases, symptomatology develops gradually during adolescence and may consist of pain in the groin, upper thigh, or knee. If a patient comes in with knee pain but radiographs of the knee are normal, the clinician should order hip films as well, as many of these individuals will have referred knee pain. The patient may complain of a limp or leg weakness. Exercising, walking, or just standing for an extended length of time can exacerbate these symptoms. Conversely, the onset of a slip may be acute, with symptoms arising more suddenly—within a two-week period; this is often due to a trauma.
A proper physical examination is imperative when a slip is suspected. When SCFE is present, the exam will often reveal obligatory external rotation of the hip when the person is lying supine and the examiner attempts to flex the hip up. In addition, the patient may have a leg-length discrepancy as well as pain upon attempted internal rotation of the hip while in a supine position.
Definitive diagnosis of SCFE involves x-rays of the hip, including anterior/posterior and frog lateral radiographs. Radiographs typically show the “ice cream falling off the cone” phenomenon, which is the proximal epiphysis slipping off the metaphysis through the proximal femoral physis on the hip, often indicative of SCFE. In some instances, x-rays do not allow for precise enough imaging; other advanced radiographic modalities—for example, MRI, bone scan, or CT scan—can aid in the diagnosis of SCFE and help prevent complications.18,19,20
Treatment. The primary goal of SCFE treatment is to prevent further slipping or displacement in the head of the femur. In situ pinning, the gold standard for treating SCFE, a screw is inserted into the hip through a percutaneous incision. The screw is placed so as to extend up the length of the femoral neck and into the femoral head, thereby stabilizing the previously displaceable epiphysis. In rare severe cases, a more significant surgery may be warranted to attempt to correct a deformity that results from SCFE.
In situ pinning yields excellent results with low complication rates. After undergoing the procedure, the patient’s return to physical activity will be gradual. He or she will need to be on crutches and gradually increase weight bearing for six weeks. The patient must also abstain from any high-collision, high-impact sports for six months.
Follow-up. Approximately 40% of people with SCFE will develop the condition bilaterally, either at the same time or, less commonly, at different times in adolescence.15 Be sure your SCFE patients know that if they experience any pain in the contralateral hip, thigh, or knee (assuming an in situ pinning unilaterally), or groin, they must cease activity and weight bearing on that extremity and consult the orthopedic surgeon immediately.
Legg-Calvé-Perthes disease (Figure 3), often referred to simply as Perthes disease, affects growing children, most commonly boys aged 5 to 7 years. The condition was described independently by three physicians around 1910.21
In Perthes disease, reduced blood flow to the head of the femur makes the femoral head susceptible to collapse and small fractures, flattening its spherical shape.1,22 This is also known as avascular necrosis (AVN) of the femoral head.
Specific risk factors that increase a person’s likelihood of developing Perthes disease include:1,22
Male gender. Males are up to five times more likely than females to develop Perthes.
Caucasian heritage. Perthes is predominantly seen in white males.
Short stature and delayed growth. Perthes is commonly seen in males who grow later and are smaller than their peers.
Family history. Roughly 10% of people with Perthes will have a positive family history for the disease.
The etiology of Perthes disease is unknown, but the most likely theories center on a disruption in blood flow to the capital femoral epiphysis.22,23,24 Children with Perthes have increased blood viscosity, abnormal venous drainage from the femoral head and neck, a tendency toward thrombophelia, and low concentration of certain blood factors, such as factor V Leiden mutation, protein C and/or protein S deficiencies, and lupus anticoagulant—all of which may lead to AVN of the femoral head.22,23,25,26 (Chronic use of steroids and amphetamines has been linked to avascular hips; however, this is different than the AVN seen in Perthes disease.) Trauma, prior transient synovitis, smoke inhalation, and infection have all been proposed as etiological sources, but all remain unsubstantiated.21