A 12 year old boy is brought to your office for evaluation of limping for one month. His parents cannot recall a specific episode of trauma. Further probing may correlate the limp to a fall from his scooter at home. His left distal thigh near his knee is sore with prolonged walking. He cannot run or jump without severe medial left knee pain. He has difficulty squatting or rising from a deep chair. Previous examinations of his knee by another physician were reportedly normal. He has been taking ibuprofen for a "bursitis" without improvement. His limp is getting worse.
PMH is significant for asthma, sleep apnea and severe obesity.
ROS: He denies any radiation of pain below the knee, paresthesias or tingling in the feet, back pain, morning stiffness, swollen joints, fevers, chills or recent infection. He has no symptoms of endocrine abnormalities or hypothyroidism.
FH: Significant for multiple individuals with severe obesity.
Exam: VS T36.8, P 80, RR 24, BP 130/76. He is extremely obese but in no significant distress. He has difficulty standing with both feet together and prefers to externally rotate his left foot. His gait is notable for his left foot turned outward. He has a truncal sway to the left side with the swing phase of his right foot. He cannot squat. His spine is straight. His neurological exam is intact. His knee examination is normal bilaterally. His left hip flexion is decreased to 40 degrees. He has obligate external rotation of the hip with attempted flexion. Internal rotation causes severe thigh pain. Internal rotation is essentially zero degrees. His pulses are full and symmetric.
Although his chief complaint relates to pain near his knee, your examination suggests that his problem is in his hip. AP pelvis and lateral views of both hips demonstrate a left slipped capital femoral epiphysis.
He is placed on crutches with toe touch weight bearing on the left side. He is referred immediately to an orthopedic specialist for consultation. The pediatric orthopedist admits him to the hospital for insertion of a screw to secure the unstable growth plate. He remains on crutches for six weeks after surgery. After six weeks, he is allowed to walk freely. Swimming is encouraged. Activity restrictions include no running or jumping (no sports) until the growth plate has closed radiographically. Complete closure can take six to eighteen months. Since the slip is mild, he has a good to excellent prognosis. Many years of productive activity can be expected. Due to the deformity, mild arthritis may occur in the fifth to sixth decade of life.
Limping in the child can be the result of a multitude of causes. A careful history is critical to narrowing the differential diagnosis. The physician must consider any information that may direct the investigation. Three questions to consider are: 1) Is it painful? 2) How old is the child? 3) What is the duration of symptoms?
Pain is not a specific complaint, but may help the examiner to localize the area of interest to a specific joint or limb. Absence of pain does not narrow the list of causes as infection and neoplasia can present with a painless limp.
The age of the child can narrow the differential diagnosis. Broad overlap can occur so one should not ignore a possible diagnosis just because it is not typical in a certain age group. Leg length discrepancy and neuromuscular conditions such as cerebral palsy can affect the gait pattern of a child at any age. In the toddler (age 1 to 4 years), primary consideration should be given to infectious causes such as septic joint or osteomyelitis. Non-infectious causes include transient synovitis, trauma, or a late presentation of developmental dysplasia of the hip (DDH). In the child/juvenile (age 4 to 10 years), infection and transient synovitis must be excluded. Trauma is common in this age group. Legg-Calve-Perthes disease (idiopathic avascular necrosis of the hip) or juvenile rheumatoid arthritis (JRA) may be first diagnosed at this age. Benign bone tumors can also cause limping in this age group. The adolescent (age 11-16 years) commonly limps due to trauma. Neoplasia may affect children in the second decade. Conditions affecting the growth plate such as slipped capital femoral epiphysis (SCFE) must be excluded in any adolescent presenting to the office with limp and hip, thigh or knee pain. It should be noted that hip pathology may deceptively present with thigh or knee pain. Thus, the hips must be thoroughly examined in patients presenting with thigh or knee pain.
Developmental dysplasia of the hip (DDH) may be diagnosed in any age group. The age of the child will determine the presenting signs and symptoms. In the newborn, DDH is identified by instability of the hip on initial examinations. In the ambulatory child, the dislocated or dysplastic hip will be evident by a limp, waddle, or leg-length difference on examination. Early recognition of the dysplastic or unstable hip is important so that treatment can be instituted before significant deformity occurs and at a time when sufficient growth remains to enhance hip development (1). If the diagnosis is missed, patients may present in late childhood or in their teen or adult years with severe degenerative damage to the hip.
The human hip begins as a continuous structure in the embryo. A cleft forms at the 7th week of development and the gross structure of the joint is formed by the 11th week. Growth of the hip joint is dependent on mechanical and genetic factors. The development of the acetabulum and the femoral head is dependent upon concentric reduction of the round ball in the cup. Dislocation of the femoral head from the acetabulum will cause deformity of both parts of the hip. Growth of the depth and width of the cup is determined genetically by the acetabular cartilage and the triradiate cartilages (2).
DDH is found in 1.0-1.5 per 1000 live births. Risk factors include female gender, first born child, and breech lie in pregnancy (1). A history of DDH in the family is also very significant as the incidence of DDH in parents of affected children is approximately 10 fold greater than the general population (3). Although the etiology is unknown, idiopathic, capsular laxity, hormonal, genetic, crowding, and syndromic causes have been proposed. Support for genetic relationships are noted by the 25 to 50 fold increase rate of DDH in American Indian and Polynesian populations (4,5). DDH is rarely seen in certain African populations or ethnic Chinese (6,7). Evidence for the crowding phenomenon is noted by the relationship of torticollis, hip dysplasia, oligohydramnios, and metatarsus adductus (8). Certain syndromes (Larsen syndrome and arthrogryposis) contain DDH as part of their constellation of findings.
Clinical findings are age-dependent. The newborn may have marked instability of the hip (9). The Ortolani maneuver involves dislocation and relocation of the hip. The palpable clunk associated with the relocation of the femoral head is often called the Ortolani sign. This Ortolani finding disappears as the soft-tissues around the dislocated hip become contracted in the first two-weeks of life. Similarly, the Barlow sign is likely present in the first few weeks of life, but this sign gradually disappears soon thereafter, making it imperative that a thorough examination of the hips be performed and documented several times during the newborn period. In the older child, limited abduction of the hip is the sentinel finding. In addition, the dislocated hip effectively shortens the thigh length giving the appearance of limb length discrepancy or the Galeazzi sign. The apparent thigh shortening often leads to dramatic asymmetry of the gluteal skin folds. With regards to prognosis, hip stability (stable/unstable) and the resting position of the hip (dislocated/reduced) are important concepts to recognize. A newborn with an unstable but reduced hip requires treatment directed at maintenance of stability. More active intervention such as surgery is needed for the ambulatory child with a fixed dislocation (2).
Treatment must be directed in achieving a concentric reduction of the femoral head in the acetabulum, stability of the hip joint, and proper remodeling of the growth cartilages throughout childhood. Treatment algorithms are age dependent: birth to six months, six months to 18 months, and greater than 18 months. The risk of complications such as deformity, avascular necrosis, and arthritis increases directly with the complexity of the treatment regimen. In the infant (birth to six months), a flexible harness designed to hold the hips in a reduced position and allow some movement is the primary form of treatment. The Pavlik harness is the simplest and most commonly used harness in the United States. Success with the Pavlik harness can approach ninety-five percent. Pavlik failures are associated with bilateral dislocations, Ortolani negative hip, application of the harness after 7 weeks of age, and noncompliance (10,11). Although early success with the Pavlik harness can be expected to result in development of a normal hip in the majority of cases, late dysplasia can be found in 10-20% of adolescents or adults (12,13). Therefore, long-term radiographic monitoring must be maintained. For the child (six months to 18 months), closed manipulation and application of a body cast are often employed to reduce the dislocated hip. In the older child or juvenile, open surgical reduction of the hip with reconstruction of bone deformity of either side of the hip joint is often required. In the adult with untreated DDH, significant deformity of the hip will be present. The decision for reconstruction will depend on the magnitude of arthritis already present at the time of diagnosis. Whatever the age, the treatment algorithm for DDH should adhere to the following principles: avoid complications, obtain a concentric reduction, achieve a stable hip, and promote growth and remodeling of the hip joint.
Clinical Practice Guidelines for Early Detection of DDH (1)
Newborns:
All newborns are to be screened by physical exam.
Ultrasonography of all newborns is not recommended.
Use of triple diapers is not recommended.
If exam is positive, refer to an orthopedist (ultrasonography is unnecessary).
If exam is equivocal, repeat exam by pediatrician in 2 weeks.
2 week exam:
If positive, refer to orthopedist.
If suspicious, consider orthopedic referral or ultrasound at 4 weeks.
If negative, periodic exams with well baby visits.
Consider risk factors if suspicious or negative.
Risk factors and recommended actions:
Female: Follow periodicity schedule.
Positive family history (male): Follow periodicity schedule.
Positive family history (female): Optional future imaging.
Breech (male): Optional future imaging.
Breech (female): Recommend imaging (ultrasound/X-rays).
Legg-Calve-Perthes Disease (LCP disease) is commonly diagnosed in the juvenile patient (4-8 years old). The condition is characterized by limp, loss of hip internal rotation and abduction, and progressive deformity of the femoral head. The shape of the head, congruency of the hip joint, and range of motion of the hip at maturity determine long term prognosis.
LCP disease is more common in boys than in girls (5:1). The incidence of bilaterality is 10-15%. There is no evidence to suggest LCP disease is inherited. The disease is more common in certain geographical locations especially urban centers. Affected children are thought to manifest a specific psychological profile such as hyperactivity. In addition, 89% of those children affected have a delayed bone age. Ethnic variations show a higher risk in Japanese, Eskimos, and central Europeans while American Indians, Polynesians, and African Americans have a lower risk. Anthropometric studies document small stature in height and weight. Normalization of stature occurs in early adolescence. Growth abnormalities may represent alterations of growth hormone dependent somatomedin activity (14-16).
Although the etiology is unknown, most current theories involve vascular compromise to the femoral epiphysis. Two episodes of infarction are thought necessary to cause the changes consistent with LCP disease in humans. Increased blood viscosity, thrombophilia, and intraosseous venous hypertension have been proposed as mechanisms for vascular compromise (17-19).
The syndrome is typified by certain classic radiographic stages: initial, fragmentation, reossification, and residual phases (20). The femoral head deformity may occur in many ways. In general, softening of the femoral head marks the period of fragmentation. Synovitis and restricted hip motion lead to deforming forces that compress the femoral head. Deformity may also result from physeal arrest of the femoral epiphysis. Reossification of the deformed head fixes the abnormal shape. Potential for remodeling of the deformity is related to the age of onset as a younger child has more years of growth remaining to reshape the head. Therefore, age of disease onset is the second most important factor related to outcome, preceded only by residual deformity. In general, affected children younger than 8 years of age at onset have a better prognosis. Attempts to estimate risk of deformity and overall prognosis by radiographic criteria in the early stages of LCP disease have met with variable success (20-24).
The clinical presentation is most commonly an insidious limp. Although pain in the thigh or knee should prompt a thorough examination of the hip, pain is not a frequent finding in LCP. Physical examination is marked by limited abduction and internal rotation of the hip. Flexion contracture of the hip is an important finding. The Trendelenburg test, which tests gluteus medius strength, is often positive. It is done by standing behind the patient and checking that the pelvis is level. The patient is then asked to stand on one leg which should result in gluteus medius muscle contraction on the weight bearing side and the contralateral pelvis should elevate on the unsupported side, indicating that the gluteus medius muscle on the weight bearing side is working properly (negative Trendelenburg sign). A positive Trendelenburg sign is recognized if the pelvis on the unsupported side does not elevate.
Limb length should be measured as any significant discrepancy may predict a poor prognosis if due to head collapse. Imaging should begin with plain radiographs. Early in the disease course, the x-rays will show increased density of the femoral head. Progressive fragmentation of the epiphysis will follow. Weakness of the bone may lead to collapse. With reossification of the femoral head, the deformity will become fixed in the new bone (25). Other modalities such as magnetic resonance imaging (MRI) and bone scan may be helpful in diagnosis and to direct treatment. Arthrography is often used to document true head deformity in the younger child especially in early phases of the disease (26). The differential diagnosis may be broad and careful selection of laboratory and radiographic studies should make the diagnosis clear. Specific consideration should be given to the following: transient synovitis, septic joint, osteomyelitis, trauma, hypothyroidism, multiple epiphyseal dysplasia, chondrolysis, Gaucher disease, hemophilia, juvenile rheumatoid arthritis, neoplasia, mucopolysaccharidoses, Meyer's dysplasia, or residuals of congenital hip dysplasia (27).
Treatment protocols abound (19,22,25,28-32). The primary goals in the treatment are to prevent deformity, to minimize growth disturbance, and to prevent degenerative joint disease. The critical concept is the containment of the femoral head in the acetabulum through the period of risk of deformity (19). The treatment remains controversial. Non-operative and operative advocates abound. Non-operative treatment requires maintenance of sufficient range of motion through therapy and bracing protocols. Surgical treatment is oriented toward redirecting the softened femoral head into the acetabulum to cover the vulnerable regions and to provide a mold for femoral head remodeling (25,32). For the hip that cannot be contained in the socket, sophisticated surgical techniques are used to treat pain, length discrepancy, and restricted motion. Well controlled studies with uniform treatment protocols in patients matched for age, gender, degree of head involvement, and other factors are needed to determine direct management of this complex disease in the future.
Slipped Capital Femoral Epiphysis (SCFE) remains one of the most common disorders affecting the hip in adolescence (33). This condition is characterized by a displacement of the femoral head through the physeal plate. Since the femoral head is held securely in the acetabulum, the femoral neck displaces anteriorly causing an apparent varus deformity of the proximal femur. Weakening of the perichondral ring associated with puberty leads to a separation of the physis through the widened zone of hypertrophy.
SCFE has been reported in 2 to 10 per 100, 000 population. Children with SCFE tend to be obese because this excess weight places excessive downward stress on the femoral epiphysis. Lower rates are seen in eastern Japan. Higher rates have been reported in African Americans and Polynesians (34,35). SCFE is more common in boys than girls (3:1). Boys are commonly affected between ages 9-16 years and girls are affected between 8-15 years of age.
Children with SCFE are usually obese. An antalgic gait or painful limp (Trendelenburg gait) with the foot turned outward is commonly seen. Knee pain is reported in 25-50% (36). Whenever knee or thigh pain is the chief complaint, the hip must be thoroughly evaluated since the pathology may be originating from the hip. Hip examination is notable for limited true flexion. Due to the deformity of the femoral head, the hip will turn in external rotation to prevent impingement of the femoral neck on the acetabulum with hip flexion (obligate hip external rotation with flexion). The hip has little or no internal rotation. For the acute slip, ability to bear weight may be limited.
The differential diagnosis includes trauma, infection, neoplasia, rheumatoid disease, avascular necrosis, congenital hip dysplasia or dislocation.
The goal of treatment is to prevent further displacement. The child should be restricted in his/her activity immediately after recognition of the problem. The child should remain non-ambulatory until the hip is stabilized. Preferably the child will be placed on bed rest or restricted to a wheelchair. A single screw is placed percutaneously to fix the slipped epiphysis in situ. Screw placement is guided by fluoroscopic imaging under anesthesia. A single screw is adequate fixation if properly placed (37). The patient is restricted to crutch assisted ambulation for 6-12 weeks after surgery. Corrective osteotomy may be planned for severe deformity. Due to the excellent long term prognosis for the hip, osteotomy should be delayed at least 2 years to allow bone remodeling (28).
Long term follow up data of patients with SCFE are available (28,29). In general, the prognosis is good to excellent. Mean hip activity scores were related to the severity of the slip. Degenerative arthritis is seen in almost all hips with moderate to severe slips. Two-thirds of mild slips had degenerative changes on radiographs at 41 years average follow up. Only one hip replacement surgery had been performed for this group over 41 years. Hips that were pinned in situ had less complications and higher activity scores than hips that underwent corrective surgery (29).
Complications such as avascular necrosis and chondrolysis can adversely affect outcome. Bilateral slipped capital femoral epiphysis can occur simultaneously or sequentially. Identifying those patients at risk for a slip on the contralateral asymptomatic hip is difficult. Children with endocrine disease (thyroid deficiency), renal failure, and previous radiation of the femoral epiphysis are at highest risk of bilateral slip (16,38).
Questions
1. What three questions should be considered in the limping child? Why?
2. What are three common causes for limping in the toddler? Juvenile? Adolescent?
3. What physical findings are noted in a newborn with DDH?
4. What physical findings are found in the toddler with hip dislocation?
5. What three factors are required for normal hip development to guide treatment for DDH?
6. What is the proposed etiology of LCP?
7. What are the four radiographic stages of LCP?
8. What factors influence the long-term prognosis most significantly for LCP?
9. What is the typical body habitus for a patient with SCFE?
10. What physical findings are present in SCFE?
11. What is the overall prognosis with proper treatment for SCFE?
Related x-rays
SCFE: Yamamoto LG. Thigh and Knee Pain in an Obese 10-Year Old. In: Yamamoto LG, Inaba AS, DiMauro R. Radiology Cases In Pediatric Emergency Medicine, 1995, volume 2, case 10. Available online at: www.hawaii.edu/medicine/pediatrics/pemxray/v2c10.html
Challenging hip case: Yamamoto LG. Vomiting Following Reduction of Intussusception. In: Yamamoto LG, Inaba AS, DiMauro R. Radiology Cases In Pediatric Emergency Medicine, 1995, volume 2, case 13. Available online at: www.hawaii.edu/medicine/pediatrics/pemxray/v2c13.html
Avascular necrosis: Herman MI. A Limping 6-Year Old. In: Yamamoto LG, Inaba AS, DiMauro R. Radiology Cases In Pediatric Emergency Medicine, 1996, volume 4, case 16. Available online at: www.hawaii.edu/medicine/pediatrics/pemxray/v4c16.html
References
1. Lehmann HP, et al, Committee on Quality Improvement, and Subcommittee on Developmental Dysplasia of the Hip. Developmental dysplasia of the hip practice guideline: Technical report. Pediatrics, 2000;105(4):E57.
2. Weinstein S. Developmental Hip Dysplasia and Dislocation. In: Morrissy RT, Weinstein SL (eds). Lovell and Winters's Pediatric Orthopaedics, 5th edition. 2001, Philadelphia: Lippincott-Raven, pp. 905-956.
3. Wynne-Davies R. Acetabular dysplasia and familial joint laxity: Two etiological factors in congenital dislocations of the hip. J Med Genet 1970;7:315.
4. Coleman SS. Congenital dysplasia of the hip in the Navajo infant. Clin Orthop 1968;56:179-193.
5. Woolf CM, Koehn JH, Coleman SS. Congenital hip disease in Utah: The influence of genetic and nongenetic factors. Am J Hum Genet 1968;20(5):430-439.
6. Skirving AP, Scadden WJ. The African neonatal hip and its immunity from congenital dislocation. J Bone Joint Surg [Br] 1979;61-B(3):339-341.
7. Hoaglund FT, Yau AC, Wong WL. Osteoarthritis of the hip and other joints in southern Chinese in Hong Kong. J Bone Joint Surg [Am] 1973;55(3):545-557.
8. Dunn PM. Perinatal observations on the etiology of congenital dislocation of the hip. Clin Orthop 1976;119:11-22.
9. Ortolani M. Congenital hip dysplasia in the light of early and very early diagnosis. Clin Orthop 1976;119:6-10.
10. Mubarak S, et al. Pitfalls in the use of the Pavlik harness for treatment of congenital dysplasia, subluxation, and dislocation of the hip. J Bone Joint Surg [Am] 1981;63(8):1239-1248.
11. Viere RG, et al. Use of the Pavlik harness in congenital dislocation of the hip. An analysis of failures of treatment [see comments]. J Bone Joint Surg [Am] 1990;72(2):238-244.
12. Tucci JJ, et al. Late acetabular dysplasia following early successful Pavlik harness treatment of congenital dislocation of the hip. J Pediatr Orthop 1991;11(4):502-505.
13. Rachbauer F, et al. Acetabular development following early treatment of hip dysplasia by Pavlik harness. Arch Orthop Trauma Surg 1994;113(5):281-214.
14. Wynne-Davies R, Gormley J. The aetiology of Perthes' disease. Genetic, epidemiological and growth factors in 310 Edinburgh and Glasgow patients. J Bone Joint Surg [Br] 1978;60(1):6-14.
15. Hall DJ. Genetic aspects of Perthes' disease. A critical review. Clin Orthop 1986;209:100-114.
16. Blethen SL, Rundle AC. Slipped capital femoral epiphysis in children treated with growth hormone. A summary of the National Cooperative Growth Study experience. Horm Res 1996;46(3):113-116.
17. Chung SM. The arterial supply of the developing proximal end of the human femur. J Bone Joint Surg [Am] 1976;58(7):961-970.
18. Kleinman RG, Bleck EE. Increased blood viscosity in patients with Legg-Perthes disease: A preliminary report. J Pediatr Orthop 1981;1(2):131-136.
19. Salter RB. Legg-Perthes disease: The scientific basis for the methods of treatment and their indications. Clin Orthop 1980;150:8-11.
20. Catterall A. The natural history of Perthes' disease. J Bone Joint Surg [Br] 1971;53(1):37-53.
21. Stulberg SD, Cooperman DR, Wallensten R. The natural history of Legg-Calve-Perthes disease. J Bone Joint Surg [Am] 1981;63(7):1095-1108.
22. Ippolito E, Tudisco C, Farsetti P. The long-term prognosis of unilateral Perthes' disease. J Bone Joint Surg [Br] 1987;69(2):243-250.
23. Herring, JA, et al., The lateral pillar classification of Legg-Calve-Perthes disease. J Pediatr Orthop 1992;12(2):143-150.
24. Salter RB, Thompson GH. Legg-Calve-Perthes disease: The prognostic significance of the subchondral fracture and a two-group classification of the femoral head involvement. J Bone Joint Surg [Am], 1984;66(4):479-489.
25. Catterall A. Legg-Calve-Perthes disease. Instr Course Lect, 1989;38:297-303.
26. Kaniklides C, et al. Legg-Calve-Perthes disease: Comparison of conventional radiography, MR imaging, bone scintigraphy and arthrography. Acta Radiol 1995;36(4):434-439.
27. Andersen PE, Jr., et al. Bilateral femoral head dysplasia and osteochondritis: Multiple epiphyseal dysplasia tarda, spondylo-epiphyseal dysplasia tarda, and bilateral Legg-Perthes disease. Acta Radiol 1988;29(6):705-709.
28. Bellemans J, et al. Slipped capital femoral epiphysis: A long-term follow-up, with special emphasis on the capacities for remodeling. J Pediatr Orthop B, 1996;5(3):151-157.
29. Carney BT, Weinstein SL. Natural history of untreated chronic slipped capital femoral epiphysis. Clin Orthop 1996;322:43-47.
30. Herring JA. The treatment of Legg-Calve-Perthes disease: A critical review of the literature. J Bone Joint Surg Am 1994;76(3):448-458.
31. Perpich M, McBeath A,Kruse D. Long-term follow-up of Perthes disease treated with spica casts. J Pediatr Orthop 1983;3(2):160-165.
32. Wenger DR, Ward WT, Herring JA. Legg-Calve-Perthes disease. J Bone Joint Surg [Am], 1991;73(5):778-788.
33. Kehl D. Slipped Capital Femoral Epiphysis. In: Morrissy RT, Weinstein SL (eds). Lovell and Winters's Pediatric Orthopaedics, 5th edition. 2001, Philadelphia: Lippincott-Raven, pp. 999-1033.
34. Aronson DD, Loder RT. Slipped capital femoral epiphysis in black children. J Pediatr Orthop 1992;12(1):74-79.
35. Spero CR, et al. Slipped capital femoral epiphysis in black children: Incidence of chondrolysis. J Pediatr Orthop 1992;12(4):444-448.
36. Matava MJ, et al. Knee pain as the initial symptom of slipped capital femoral epiphysis: An analysis of initial presentation and treatment. J Pediatr Orthop 1999;19(4):455-460.
37. Kibiloski LJ, et al. Biomechanical analysis of single- versus double-screw fixation in slipped capital femoral epiphysis at physiological load levels. J Pediatr Orthop 1994;14(5): 627-630.
38. Loder RT, Wittenberg B, DeSilva G. Slipped capital femoral epiphysis associated with endocrine disorders. J Pediatr Orthop 199515(3):349-356.
Answers to questions
1. Is it painful? How old is the child? What is the duration of symptoms? These three questions will help to narrow the differential diagnostic possibilities.
2. Toddler: transient synovitis, infection, trauma. Juvenile: trauma, transient synovitis/infection, Legg-Calve-Perthes disease. Adolescent: slipped epiphysis, trauma, neoplasia
3. Hip instability - Ortolani sign. Asymmetric gluteal skin folds.
4. Leg length discrepancy, Galeazzi sign (apparent thigh length difference), waddling gait.
5. Concentric reduction of femoral head, stability, remodeling and growth of acetabular cartilage.
6. Although the etiology is unknown (commonly stated as idiopathic), most current theories involve vascular compromise of the femoral epiphysis. Two episodes of infarction are thought necessary to cause the changes consistent with LCP disease in humans. Increased blood viscosity, thrombophilia, and intraosseous venous hypertension have been proposed as mechanisms for vascular compromise.
7. 1. Initial, 2. Fragmentation, 3. Reossification, 4. Residual.
8. Age of patient at onset and proportion of femoral head involvement. Children who have LCP disease before age eight have a better prognosis over children greater than eight years of age at time of onset. The proportion of head involvement forms the foundation for several classification schemes. Maintenance of the height of the lateral column of the femoral epiphysis appears to have the most prognostic significance in children in any age group. Whole head involvement or collapse of the lateral column by more than fifty percent carries a poor prognosis.
9. Obese, delayed maturation of skeletal age.
10. Trendelenburg gait or antalgic limp, obligate external rotation of the hip with flexion, limited internal rotation of the hip.
11. Good to excellent. High activity level. Slow degenerative process of the hip with few cases requiring prosthetic hip replacement.