A Clinical Guide to Pediatric Weight Management and Obesity, 1st Edition
Slipped capital femoral epiphysis (SCFE) and Blount's disease (tibia vara) are becoming more prevalent as the rates of obesity and morbid obesity increase.
Skeletal maturation is a feature of adolescent development, with closure of the growth plate signaling the attainment of adult height. Obese children are susceptible to unique orthopedic problems, which occur during growth.
SCFE is the most common hip disorder of adolescence. Prevalence rates as high as 10.08 per 100,000 have been reported in the 1970s in the northeast United States (1). In data from the National Inpatient Sample from 1993 to 2000 (data collected from 1,000 hospitals to approximate a 20% sample of U.S. hospital discharges), 4,924 patients were treated for SCFE from ages 7 to 17 years (2). It has also been observed that 70% of children having SCFE had weights above the 80th percentile for age (3). In children from 8 to 18 years of age who had radiologic studies to rule out SCFE, a retrospective review of charts from 1994 to 2004 found that more children were obese or at risk for obesity (95.3%) who were diagnosed with SCFE than children with symptoms due to other causes (41.3%) (4).
The incidence of SCFE is highest during puberty, with the peak in incidence in boys from 12 to 15 years and in girls 10 to 13 years (5). In an international study of SCFE, relative risk of disease (compared with the Caucasian population) was highest in the Polynesian population, relative risk (RR) 4.5, followed by 2.2 for black, 1.05 for American Indian, 0.5 for Indonesian-Malay, and 0.1 for Indo-Mediterranean children (6). Long-term consequences of SCFE can include the following (4):
- Degenerative hip disease
- Gait abnormalities
- Avascular osteonecrosis
Idiopathic SCFE is associated with obesity.
Atypical SCFE can be caused by the following:
- Renal osteodystrophy
- Radiation therapy
Adolescent tibia vara, or Blount's disease, is also more common in obese than in normal weight adolescents; up to two thirds of patients with Blount's disease are obese (7).
Slipped Capital Femoral Epiphysis
- Slipped capital femoral epiphysis—Posterior and inferior slip of the proximal femoral epiphysis on the metaphysis (femoral neck) occurring through the zone of hypertrophic cartilage (physeal plate) (8).
- Chondrolysis—A process of progressive cartilage degeneration resulting in joint space narrowing and loss of motion, most frequently observed as a complication of SCFE (9).
The pathology of SCFE involves a slip through the hypertrophic zone of the femoral growth plate. The growth plate includes undifferentiated or reserve cartilage cells, proliferating cartilage cells, and hypertrophic or maturing cartilage cells. In the undifferentiated zone, cartilage cells are in a resting state immediately adjacent to the epiphysis. Germinal cells from this layer supply the developing cartilage cells to increase the width of the growth plate.
The proliferative zone is where chondrocytes are actively growing and being aligned in columns to increase bone length. The hypertrophic or maturational zone is where chondrocytes terminally differentiate and mineralization begins. This is the weakest part of the growth plate (10,11) (Fig. 9.1).
The preferential site of slipping within the epiphysis is a zone of hypertrophic cartilage cells under the influence of both gonadal hormones and growth hormone (12). The exact cause of SCFE is unknown. SCFE often occurs at peak height velocity during puberty (13). The most common form of SCFE is seen in obese adolescents, who in some series have been slightly taller than their peers and have undergone slower than average skeletal maturation (5). Additional studies have shown that the age of onset of SCFE is younger with greater degrees of obesity (6).
Growth hormone stimulates the production of insulin-like growth factors (IGFs), which stimulate chondrocyte proliferation in the growth plate (13). Growth hormone has been found to stimulate local synthesis of IGFs by chondrocytes in rats (14). Futami (15) described features on magnetic resonance imaging (MRI) of a “preslip” that involved physeal widening. Lalaji et al. (16) described similar changes in two patients presenting with hip pain prior to the progression to a slip. Pathologically, chondrocyte degeneration and death have been noted throughout the hypertrophic
and proliferative zones of SCFE growth plates (10,11). Adamczyck et al. (17) found a high incidence of apoptosis in SCFE growth plates from chronic slips when compared with normal growth plates. The reason for this is unknown, but they hypothesized that apoptosis occurred prior to the slip, weakening the growth plate and making it more susceptible to increased stress. In a review of patients with SCFE, 25% of those tested had low triiodothyronine levels, 76% of those tested had low testosterone levels, and 87% in this group also had low growth hormone levels, possibly reflecting subtle hormonal influences in this population (3).
FIG. 9.1. Anatomy of the growth (epiphyseal) plate. A: Normal growing epiphyseal plate. The epiphysis is separated from the epiphyseal plate by transverse plates of bone that seal the plate so that it grows only toward the metaphysis. The various zones of cartilage are illustrated. As the calcified cartilage migrates toward the metaphysis, the chondrocytes die, and the lacunae are empty. At the interface of the epiphyseal plate and the metaphysis, osteoclasts bore into the calcified cartilage, accompanied by a capillary loop from the metaphyseal vessels. Osteoblasts follow the osteoclasts and lay down osteoid on the cartilage core, thereby forming the primary spongiosum, or primary trabeculae. B: Normal closure. The epiphyseal cartilage has ceased to grow, and metaphyseal vessels penetrate the cartilage plate. Transverse bars of bone separate the plate from the metaphysis. (From
Rubin E, Farber JL. Pathology Image Collection. Philadelphia: Lippincott Williams & Wilkins; 2000: Figure 26.9
Additional risk factors for SCFE include the following:
- Renal failure
- History of radiation therapy
- Primary hypothyroidism (18)
- Use of gonadotropin-releasing hormone agonists
- Growth hormone deficiency (treated or untreated) (9,19,20)
One study also found that levels of midportion parathyroid hormone (M-PTH) and 1,25-dihydroxy vitamin D (1,25-(OH) 2D), which are involved in growth-plate chondrogenesis and matrix mineralization, were significantly lower in patients with SCFE than in controls. In patients with initially low levels of M-PTH and 1,25-(OH) 2D, all levels returned to normal within a year after the onset of disease (21).
Most risk factors have been found to play a role in either decreasing the strength of the epiphyseal plate or increasing the amount of shearing stress to which the plate is subjected at the time it is most vulnerable (5). There have been cases of familial SCFE; Rennie (22) observed 12 adolescents with SCFE who also had an affected family member.
Obesity is clearly a predisposing factor in SCFE. In a study of 106 children presenting with SCFE, those affected had a mean body mass index (BMI) of 29.2, at an average age of 11.7 years. Ninety-five percent of children were greater than the 85th percentile for BMI and 81% were greater than the 95th percentile for BMI for age and gender (23). Obesity has been associated with a younger age at diagnosis. In a study from Michigan, 67% of patients diagnosed with SCFE were obese. The obese children were significantly younger at the time of the diagnosis of the slip (12 ± 1.6 years) than were the nonobese children (13 ± 1.6 years) (24). Bilateral slips may also be more common in obese children. In the same study, half the children had bilateral involvement on diagnosis, and half had only one hip affected. The children who went on to have a slip of the contralateral hip were more likely to be obese. The average time between diagnosis of the first and second slip was 1 ± 0.9 years (range 1–5 years). The diagnosis of the contralateral slip was made in 88% of the children within 18 months of the first slips (24).
In a study of bone maturation in children with SCFE, more than 82% of whom were greater than 1 SD above average weight and 54% greater than 3 SD above average weight, bone ages were found to be advanced in younger children and delayed in
older children. In this study the average chronologic age was 13.6 ± 1.7 years for boys and 12.0 ± 1.4 years for girls, with 42% having a bone age corresponding to chronologic age (± 6 months). In 28%, bone age was advanced more than 6 months, and 30% had delay in mean bone age of more than 6 months (25). There is also a suggestion that chronic weight gain can increase the likelihood of a slip. In a study of BMI and SCFE, BMI values were increased starting from age 2 through age 14 in children with SCFE (26).
Increased repetitive stress and stress from injury have also been proposed as etiologic factors for SCFE. In a study from Japan, a history of injury was reported for 31.8% of children with SCFE. Seasonal variations in numbers of patients have been noted in relation to sports participation (27).
Endocrine disorders, particularly hypothyroidism and growth hormone deficiency, may alter age of onset of SCFE. In children with endocrine disorders, the average age at diagnosis of SCFE was 15.3 ± 5.3 years. This group of children was also noted to have discrepant bone/chronologic age, 11.6 ± 3.0 versus 16.5 ± 6.5 years, with a wider range of age at presentation (7–35 years) and a greater rate of bilateral involvement (61%) (28).
Slips can be either stable or unstable. A slip is considered stable if walking and weight bearing are still possible and unstable if walking is impossible regardless of the duration of symptoms (29). An unstable slip may present acutely, sometimes after a sports injury or fall, and it behaves more like a fracture. Unstable SCFE cases make up about 10% to 15% of the total cases of SCFE. Management of unstable SCFE is associated with most of the complications, including avascular necrosis and chondrolysis (29).
Early signs and symptoms of SCFE may be mild, with only vague complaints of pain and slight loss of internal rotation.
It is extremely important to ask about knee, groin, thigh, or hip pain in the history because children with early slips may not be reported.
As the slip progresses, loss of internal rotation, flexion, and abduction becomes even more apparent on examination and the gait becomes more painful. Obligate external rotation of the lower extremity is observed when the involved hip is flexed and can occur early in the course when radiologic changes are minimal (30). A child with a stable SCFE may give a history of intermittent pain and limping over weeks or even months. Pain may be localized to the thigh, groin, or knee because of the passage of sensory cutaneous nerves close to the hip capsule (31).
Delay in diagnosis has been correlated with the occurrence of knee and/or distal thigh pain, Medicaid coverage, and stable slips (31). In the same study, the median
delay in diagnosis was 8 weeks, with a range of 0 to 111 weeks. There was a significant relationship between a longer delay in diagnosis and greater slip severity. There were no significant associations between diagnostic delay and age, gender, side of slip, or weight (31).
If a slip is suspected, no passive motion should be attempted, to avoid displacing the epiphysis (32). The child should be made non–weight-bearing right away and referred to an orthopedic surgeon for immediate correction. Diagnosis is made using an anteroposterior radiograph of the pelvis which includes both hips (Fig. 9.2). Findings of a widened growth plate and posterior slipping of the epiphysis are diagnostic. A line drawn along the anterior femoral neck should intersect the epiphysis in a normal hip (33). In a recent study, a lateral radiograph was also used to further define a subtle slip or examine the contralateral hip and was found to be more sensitive than the anteroposterior view in detecting an abnormality of the slipping angle (34).
MRI can be used to diagnose SCFE and to detect a widened growth plate and edema in preslip conditions (35). Clinical suspicion is paramount in making the diagnosis of SCFE, with radiologic studies used as confirmatory tests.
The first aim of treatment is to prevent further slipping of the epiphysis. Suspicion of a slip is an orthopedic emergency, so consultation should be immediate. Pinning of the hip or hips results in good functional improvement. The risk of degenerative arthritis increases with the severity of the slip, making early diagnosis and treatment crucial. Avascular necrosis is the most serious complication, hastening the deterioration of the hip and requiring hip reconstruction or replacement (36).
FIG. 9.2. Left hip shows medial and posterior displacement of the femoral epiphysis through the growth plate relative to the femoral neck. (Courtesy of Dr. Richard Bowen, Wilmington, Delaware.)
Chondrolysis is a process of progressive cartilage degeneration resulting in joint space narrowing and loss of motion, most frequently observed as a complication of SCFE (37). Higher immunoglobulin and C3 complement levels have been noted in SCFE patients who developed chondrolysis (38). A correlation has been found between “persistent” pin penetration of the femoral head after SCFE pinning and chondrolysis (39).
Avascular necrosis is an uncommon but serious complication of SCFE and may result in osteoarthritis (39a).
Blount's Disease (Tibia Vara)
- Blount's disease—Medial bowing of the tibia (tibia vara) resulting from overgrowth of the proximal tibial metaphysis.
There are four types of tibia vara: (a) infantile tibia vara occurs between the ages of 1 and 4 years, (b) juvenile tibia vara is caused by partial closure of the growth plate due to trauma or infection between the ages of 6 and 13, (c) adolescent-onset tibia vara due to obesity, and (d) tibia vara from other causes (40) (personal communication, R. Bowen, Orthopedics Department, A.I. duPont Hospital for Children, Wilmington, Delaware, May 2006). The exact mechanism of adolescent tibia vara due to obesity is not known. In a study of gait abnormalities in obese children, it was found that the gait deviation developed to compensate for increased thigh circumference could result in increased loading of the medial compartment of the knee, generating pathologic compressive forces during ambulation (41).
Patients present with medial bowing of the tibia. Clinical presentation can include pain and tenderness over the medial prominence of the proximal tibia, abnormal gait, and leg length discrepancy with shortening of the affected leg. X-ray studies confirm the findings (Fig. 9.3). Histologically, the usual columnar organization of the cartilage cells is disrupted with areas of acellular fibrous cartilage and abnormal groups of capillary vessels.
Surgical osteotomy corrects the deformity.
FIG. 9.3. Radiograph showing collapsed medial epiphysis and beaking of tibia in Blount's disease. (Courtesy of Dr. Richard Bowen, Wilmington, Delaware.)
Impact on Weight Management
Even common orthopedic injuries can become more complex for obese children and adolescents. They have been found to have a greater rate of persistent symptoms after ankle sprain than normal weight children. Symptoms include persistent pain, swelling, or weakness at 6 weeks and 6 months postinjury.
For every unit increase of BMI, the risk of having long-term morbidity increases 0.66% (42).
Gait abnormalities can be present following SCFE and further impair a patient's ability to participate in exercise. More severe slips have a higher correlation with abnormal gait. However, children with slip angles less than 30 degrees do not have any significant difference in gait than age- and weight-matched controls (43), further emphasizing the importance of early diagnosis and treatment.
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