Problems in the diagnosis of neonatal hip instability.
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Biomedical subjects
Publications and source records attributed to B K Foster.
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In 23 patients with growth plate injuries, magnetic resonance imaging (MRI) studies were performed a total of 31 times to evaluate the physis which showed plain radiographic evidence of possible damage. Fourteen patients clinically showed growth arrest, and 10 patients required a Langenskiold operation. In 3 patients who underwent this operation, subsequent premature total fusion of the physis adversely affected the postoperative results. We propose that the merging shape of the arrest line with calcification of the provisional zone of the metaphysis shown by MRI indicates poor viability of the physis. MRI provided useful information on the appearance of the growth plate and changes in the metaphysis, both of which affected the prognosis and the results of the surgical procedures.
Using laser confocal microscopy and 5-chloromethyl-fluoresceindiacetate (CMFDA) loading of chondrocytes we have investigated the structure of the ovine physis during late fetal development and its relationship to the structure observed in the primary spongiosa. Chondrocytes within the ovine growth plate form nests that together span the growth plate. We propose that all growth plates may be composed of nests of cells, but that the length of the individual nests changes between growth plates and with gestational age. The continuous column of cells seen within some growth plates is a nest of cells that is in the process of being absorbed by the invading metaphyseal front. Scanning electron microscopy of the mineralized portion of the primary spongiosa revealed structures that were consistent with the hypothesis that the cartilage surrounding the nest structure gives rise to the structure in the primary spongiosa. Although mineralization does not occur between cells within a nest, bands of mineral form between nests in the lower hypertrophic region and around the end of the nest as it reaches the hypertrophic region. This pattern of mineralization around and between nest termini yields the complex three-dimensional network of mineralized trabeculae observed in the primary spongosia.
Our hypothesis is that physiological mineralization within the mammalian growth plate is a consequence of communication between cartilage chondrocytes and cells within metaphyseal bone. To test this hypothesis, chondrocytes were isolated from the proliferative region of the fetal ovine physis and co-cultured with cells or conditioned medium from cells characteristic of those in metaphyseal bone. The mineralization potential of chondrocytes alone and in the presence of other cells or conditioned medium was determined by 45calcium incorporation. Co-culture of chondrocytes with a crude cell isolate from metaphyseal bone resulted in a stimulation of 45calcium incorporation of 93% above that observed in the individual cell populations alone. Conditioned medium from metaphyseal bone cultures also stimulated 45calcium incorporation. This response to conditioned medium was dose-dependent and stable to 90 degrees C. Vascular endothelial cells and conditioned medium from chondrocyte and osteoblast cultures did not stimulate 45calcium incorporation by physeal chondrocytes. Thus, cells found in the metaphyseal bone produce a soluble factor, which promote calcium incorporation by physeal chondrocytes. The source of this factor is not chondrocytic, osteoblastic, or endothelial in origin.
BACKGROUND: The Medical Research Council Working Party on Congenital Dislocation of the Hip have reported an ascertainment-adjusted incidence of a first operative procedure for congenital dislocation of the hip (CDH) of 0.78 per 1000 livebirths, which is similar to the incidence of CDH before the start of the UK screening programme. The report showed that CDH had not been detected by routine screening before age 3 months in 70% of children reported to the national orthopaedic surveillance scheme. This report raised concerns about the merit of screening at birth for CDH. We aimed to find out the incidence of an operative procedure for CDH in the first 5 years of life among children born in South Australia between 1988 and 1993, and the proportion of these patients that were detected at age 3 months or older. METHODS: The state's database for inpatient separations between January, 1988, and April, 1998 was searched. Case records were examined for the age and circumstances of diagnosis, and type of operative procedures. Prevalence rates of CDH were obtained from the South Australian Birth Defects Register, which receives notifications from a statutory perinatal data collection of birth defects detected at birth and subsequent voluntary notifications for children up to age 5 years. FINDINGS: Of the 55 children born in South Australia between 1988 and 1993 identified as having non-teratological CDH and operative procedures, only 22 (40%) had been diagnosed at age 3 months or older. 18 had an open reduction of the hip joint or osteotomy, or both, and the remainder had arthrograms, closed reductions, and/or tenotomy. The prevalence of non-teratological CDH in children was 7.74 per 1000 livebirths. The incidence of surgery for CDH in the first 5 years of life was 0.46 per 1000 livebirths (95% CI 0.34-0.59) and only 0.19 per 1000 livebirths (0.11-0.26) for those diagnosed late (age 3 months or older). These children diagnosed late represented 2.4% of all known cases of CDH. INTERPRETATION: Only 2.4% of known cases of CDH in children born in South Australia had been detected late and required surgery. These results show that a screening programme for CDH can be successful, contrary to the findings of the UK Medical Research Council Working Party.
The large cartilage proteoglycan, aggrecan, was found to vary throughout the ovine physis corresponding to the maturational state of the resident chondrocytes. Two populations of proteoglycan monomer were observed in articular, epiphyseal, and in the resting zone of growth plate cartilage. These proteoglycans contained chondroitin sulfate glycosaminoglycan chains sulfated predominantly in the 4 position along with lesser amounts of chondroitin-6-sulfate and keratan sulfate. In the proliferative zone of the growth plate, chondrocytes synthesize one population of proteoglycan monomer which was significantly larger than monomer populations in articular, epiphyseal, or resting zone and this size increase could be attributed to an increase in its constituent chondroitin sulfate side chains. As these chondrocytes progress through their life cycle they continue to modify the structural characteristics of the aggrecan molecule they synthesize. Thus, in the hypertrophic region of the growth plate, the proteoglycan monomer is larger again than in the proliferative region. Variation in sulfation pattern on aggrecan chondroitin sulfate side chains is also observed in the hypertrophic region with an increasing proportion of unsulfated residues present, which may play a role in the initiation of mineralization. In addition, increasing amounts of the carbohydrate sequence recognized by monoclonal antibody 7-D-4 are observed in the hypertrophic zone.
The continued diagnosis of cases of late developmental dysplasia of the hip reaffirms the failure of initial clinical neonatal screening programs. Even the identification of an "at risk" patient profile will not eliminate the late diagnoses, but referral of these patients will ensure that up to 50% of late diagnoses can be eliminated. The role of ultrasound as a screening diagnostic tool has not, at this time, been confirmed to eliminate late diagnoses. Its use, however, has led to an increased incidence of treatment with the recognition of the sonographic "immature hip." This, in turn, will increase the number of complications of treatment with iatrogenic avascular necrosis. Therefore, the ideal elimination of all late developmental dysplasia of the hip referrals remains the unattained goal.
BACKGROUND: The effect on subsequent respiratory function of spinal stabilisation for scoliosis in Duchenne muscular dystrophy is unclear. In order to clarify this clinical problem, changes in the forced vital capacity of a group of children with Duchenne muscular dystrophy who had undergone spinal surgery were measured and compared with a group of children with Duchenne muscular dystrophy who had not had surgery. METHODS: In this retrospective study 17 boys with Duchenne muscular dystrophy who underwent spinal stabilisation at a mean age of 14.9 years (surgical group) were compared with 21 boys with Duchenne muscular dystrophy who had not had surgery (non-surgical group). The mean (SD) Cobb angle of the surgical group at 14.9 years was 57 (16.4) degrees, and of the non-surgical group at 15 years was 45 (29.9) degrees. Forced vital capacity expressed as percentage predicted (% FVC) was measured in total over a seven year period in the surgical group and over 6.5 years in the non-surgical group, and regression equations were calculated. Survival curves for both groups were also constructed. RESULTS: No difference was found between spinal stabilisation (surgical group) and the non-surgical group in the rate of deterioration of % FVC which was 3-5% per year. There was no difference in survival in either group. CONCLUSIONS: Spinal stabilisation in Duchenne muscular dystrophy does not alter the decline in pulmonary function, nor does it improve survival.
In an unselected series of 55 cases of slipped capital femoral epiphysis (SCFE) we observed an incidence of 25% of epiphyseal reduction, mostly unintentional. Reduction indicated physeal instability and was associated with an effusion, detected by sonography on admission, and inability to bear weight. The true prevalence of instability may be higher since an effusion was noted in 33 cases (60%) on the initial sonographic assessment. Serial radiographs showed reduction in 12 (22%), with an average change of 15.1 degrees in the head-neck angle. Serial sonography showed reduction in 7 out of 20 cases (35%), with an average change of 3.7 mm in displacement. In two cases reduction was seen on sonography but not on radiography. Of the hips which showed subsequent reduction, 12 had had a bone scan on admission; three showed initial epiphyseal avascularity but only one progressed to symptomatic avascular necrosis. All stable hips had normal epiphyseal vascularity on the initial bone scan. This indicates the importance of injury from the initial displacement in causing avascular necrosis, rather than effusion, vascular compromise or iatrogenic injury from gentle repositioning. Physeal instability in SCFE is common and should be assessed clinically on admission. It is indicated by joint effusion or inability to bear weight. A slip is very unlikely to be unstable in a child able to bear weight and with no sonographic effusion.
This experimental study reports the results of implantation of cartilaginous and periosteal tissues into growth plate defects in the tibiae of sheep. When no material was used, the defect rapidly filled with marrow-like tissue. When cartilage from the margin of the secondary centre of ossification was implanted, endochondral ossification continued and no shortening or deformity resulted. Implantation of periosteum with or without reconstructed peripheral tissues resulted in the formation of a bony bridge which led to a 32% inhibition of longitudinal growth and a 12 degrees varus deformity in the absence of peripheral connective tissues. After reconstruction with these tissues, the inhibition of longitudinal growth was 47% with a 28 degrees varus deformity. The chondroprogenitor cells in the implanted tissues cannot change phenotypic expression. Periosteum has a strong potential for bone formation after it has been implanted.
Significant advances in the management of hip and pelvic disorders have occurred during 1992. Developmental dysplasia of the hip or congenital dislocation of the hip has continued to provoke innovative thinking regarding preoperative planning for hip and pelvic reconstruction. "New" osteotomies are proposed but will require long-term follow-up to confirm their appropriateness. A new classification for Perthes' disease has been proposed, and further clues for the basic understanding of the etiology of Perthes' disease add to the already voluminous literature on the subject. For chronic slipped capital femoral epiphysis, there has been confirmation of single-pin in situ fixation as being safe treatment for the disorder. However, the management of acute slipped capital femoral epiphysis remains unresolved.
AIM: To characterise the distribution of major growth plate proteoglycans in a group of infants who died of SIDS. METHODS: Nine such infants and eight age matched controls were selected from the necropsy files at the Adelaide Children's Hospital. Sections of rib and adjacent costal cartilage were stained for chondroitin-4-sulphate, chondroitin-6-sulphate, and keratan sulphate with antibodies 2-B-6, 3-B-3, and 5-D-4, respectively, using standard techniques. RESULTS: The distribution of proteoglycans within the extracellular matrix of the costochondral junction in the group of SIDS infants was identical with that found in control infants. CONCLUSION: Any changes present in the growth plate in cases of SIDS are most likely caused by secondary phenomena.
In a prospective study of 26 hips in 21 patients with slipped capital femoral epiphyses (SCFEs), serial sonography was more sensitive than radiography in showing epiphyseal displacement and reduction. Reductions were associated with grossly visible hip joint effusions. The initial slips were reduced by treatment in seven of 11 hips with effusion. The 15 hips without effusion were unreduced. After stabilization and pinning, the effusion did not recur in any case. Sonography is sensitive and free from projectional errors in the assessment of metaphyseal remodeling. If any remodeling is present, the SCFE is at least three weeks in duration. A new classification into acute, acute-on-chronic, and chronic SCFEs is proposed, based on the objective sonographic data. Joint effusion represents physeal instability or recent progression, and remodeling is a sign of chronicity. An acute SCFE is characterized by effusion, whereas a slip without effusion but with remodeling is designated as chronic. An acute-on-chronic SCFE is associated with both effusion and remodeling. Joint effusion suggests that SCFEs should be operatively fixed and that displacement may diminish with traction or intraoperative positioning of the hip.
Regular bone survey radiographs have allowed identification of limb deformity and metaphyseal changes in several patients with thalassaemia major treated at the Adelaide Children's Hospital. Following the progression of limb deformity in five of these patients who were receiving human growth hormone therapy, the records of 25 thalassaemia patients were reviewed. Six patients had evidence of limb deformity, four of whom also had metaphyseal changes. Three additional patients had metaphyseal changes alone. Patients with either type of skeletal change shared similar characteristics, including younger age, earlier commencement of desferrioxamine therapy, better compliance and, in general, lower levels of ferritin. Females predominated in both groups. The frequency of sensorineural hearing loss was similar in affected and nonaffected groups and biochemical parameters, especially plasma calcium, phosphate, alkaline phosphatase, and zinc, which were normal in all patients. The cause of these skeletal changes is not clear; however, several potential factors need to be considered. Among these are focal marrow expansion in the metaphyseal region due to incomplete suppression of erythropoiesis and possible effects of desferrioxamine, including direct interference with bone growth, altered response of bone to inflammation or infection, and altered bone metabolism related to chelation of trace metals. While we can only speculate on aetiological factors, it is clear that human growth hormone therapy has resulted in exaggeration of deformity due to an increased rate of bone growth or decreased rate of mineralization of physeal cartilage. We believe that bone survey radiographs are useful in early identification of skeletal changes.(ABSTRACT TRUNCATED AT 250 WORDS)
Monoclonal antibodies were used in this study to immunolocate glycosaminoglycans throughout the human growth plate. Chondroitin-4-sulfate, chondroitin-6-sulfate, and keratan sulfate were observed in the extracellular matrix of all zones of the growth plate and persisted into the cartilage trabeculae of newly formed metaphyseal bone. Also present in the extracellular matrix was an oversulfated chondroitin/dermatan sulfate glycosaminoglycan which appeared to be specific to the proliferative and hypertrophic zones of the growth plate. As with the other extracellular matrix molecules, this epitope persisted into the cartilage trabeculae of the metaphyseal bone. Zonal differences between the extracellular and pericellular or lacunae matrix were also observed. The hypertrophic chondrocytes appeared to synthesize chondroitin sulfate chains containing a non-reducing terminal 6-sulfated disaccharide, which were located in areas immediately adjacent to the cells. This epitope was not found to any significant extent in the other zones. The pericellular region around hypertrophic chondrocytes also contained a keratan sulfate epitope which was also observed in the resting zone but not in the proliferative zone. These cell-associated glycosaminoglycans were not found in the cartilage trabeculae of metaphyseal bone, indicating their removal as the terminal hypertrophic chondrocytes and their lacunae are removed by invading blood vessels. These changes in matrix glycosaminoglycan content, both in the different zones and within zones, indicate constant subtle alterations in chondrocyte metabolic products as they proceed through their life cycle of proliferation, maturation, and hypertrophy.
After treatment with two lateral percutaneous pins, 80 children with grade II-III supracondylar elbow fractures were reviewed. The result was good in 55 patients (68%) and was the same for extension- and flexion-type injuries. These patients had less than 10 degrees change in carrying angle and less than 20 degrees total change in range of motion. This method eliminates risk of iatrogenic injury to the ulnar nerve but is technically very demanding. Redisplacement, joint penetration, and damage to the capitellar side of growth plate can be avoided only by positioning the pins divergently.
Direct comparison of type X collagen synthesized by human, sheep and chick growth-plate cartilage has shown that the human type X collagen is similar to the chick in both its molecular mass, containing component alpha-chains of 59 kDa with helical regions of 45 kDa, and apparent absence of disulphide-stabilized aggregates, whereas the sheep type X collagen has slightly larger alpha-chains (63 kDa) accounted for by a longer helical region (49 kDa) that contains cystine residues essential for the formation of the high-molecular-mass aggregates found with this species. Type X collagen from all three species showed heterogeneity in primary collagen structure as revealed by Staphylococcus aureus V8 proteinase-generated peptide maps. Collagen synthesis by growth-plate cartilage in culture, particularly synthesis of type IX and X collagen, was shown to be very sensitive to prior storage and suggests caution in the interpretation of changes detected when examining collagen synthesis by growth plates in culture.
We used ultrasonography to study 26 hips with slipped capital femoral epiphyses. In recently slipped epiphyses the ultrasound image revealed a step at the anterior physeal outline (mean 6.4 mm), diminished distance between the anterior acetabular rim and the femoral metaphysis (mean 4.3 mm) and an effusion. As metaphyseal remodelling progressed the physeal step decreased. The femoral neck appeared straighter in hips which had been symptomatic for longer than three weeks. It was possible to measure posterior epiphyseal displacement without projectional errors and the method was accurate in diagnosing minimal slip and in staging displacement. The suggested criteria are, less than 7 mm for a mild slip, 7 to 11 mm for a moderate slip and more than 11 mm for a severe slip. We recommend ultrasonography for the diagnosis, staging and follow-up management of slipped upper femoral epiphysis.