Musculoskeletal problems and injuries - part 6 pdf

7. Musculoskeletal Problems of Children 173 BC E SEVERITY OF SPONDYLOLISTHESIS SLIP ANGLE D C B A 5 1 2 3 4 90Њ 31Њ Fig. 7.10. Spondylolysis, and spondylolisthesis (right). (A) Radiographic representation of an abnormal elongation (grey- hound sign) of the pars interarticularis, or the “neck” of a scotty dog (arrow). Other defects, such as sclerosis or lysis in the pars, are best visualized in this “neck.” (From Lillegard and Kruse, 50 with permission.) (B) “Scotty dog.” A ϭ superior articular process (ear); B ϭ pedicle (eye); C ϭ pars interarticularis (neck); D ϭ lam- ina (body); E ϭ inferior articular process (front leg). (C) Severity of spondylolisthesis and slip angle. interarticularis) of L5. Sclerosis of the opposite pars may be present. A standing spot lateral view of L5-S1 allows accurate assessment of a possible slip. Scoliosis is commonly associated with spondylolisthesis. Bone scans show increased activity on one or both sides in symptomatic spondylolysis but are not routinely required. If asymptomatic, no treatment is required, and there is no need to limit contact sports. For a mildly symptomatic patient, temporary reduction of activity is all that is needed. If symptoms are alleviated, progressive activity is permitted. Symptoms that are sudden in onset, traumatically induced, or do not resolve with rest do heal—much as any fracture would heal—after 10 to 12 weeks of immobilization in a plastic body jacket or a Boston-type spinal orthosis. In general, once symptoms resolve, the child can resume normal activities, although advice regarding return to rigorous spine-bending athletic events (gym- nastics, diving, downed lineman in football) is controversial (see Chapter 10). With spondylolisthesis, if slippage is less than 30% and symptoms are minimal, treatment is conservative. With persistent pain unre- sponsive to treatment or slippage more than 30% to 50%, spinal fusion is recommended. Such fusion is generally at the L5-S1 level and includes L4 if slippage is more than 50%. 44 Idiopathic Scoliosis Idiopathic scoliosis is defined as lateral deviation of the spine of more than 10 degrees (measured by the Cobb method), 45 with structural change and without congenital anomalies of the vertebrae. It is inher- ited in an autosomal-dominant manner with variable penetrance or a multifactorial condition. It occurs in approximately 2% of the popu- lation. Normally, only about one fifth to one sixth of this group require treatment. 46 Scoliosis is a painless condition usually identified by shoulder, scapular, or pelvic asymmetry during school screening or routine physical examination. Forward bending (Adam’s) testing is done with the child standing straight and bending forward with palms together and knees straight. Truncal asymmetry, most commonly right rib prominence, may be seen. Any limb length irregularity should be noted and corrected by placing blocks under the short leg and level- ing the pelvis prior to examination. Neurological examination is nor- mal. Initial radiological evaluation consists of standing PA and lateral spine films on a long cassette to include the pelvis. The curve is meas- ured using the Cobb method 45 (Fig. 7.11). If a structural curve of 10 174 Mark D. Bracker et al. to 20 degrees is identified, orthopedic referral is recommended. Painful scoliosis or an atypical curve pattern (apex left thoracic) is indicative of possible underlying neurological problems, such as syringomyelia or spinal cord lesion, and is probably not idiopathic scoliosis. The risk of curve progression is higher in young children, in those with large curves or double curves, and in girls. Bracing is usually ini- tiated for curves of more than 20 degrees with documented progres- sion and growth remaining or for curves initially 30 degrees or more. Curves of more than 45 to 50 degrees are usually not amenable to bracing, so surgery is recommended, as the risk of continued progres- sion after skeletal maturity is high in this group. 46 Scheuermann’s Disease Scheuermann’s disease (juvenile kyphosis) is defined as an abnormal increase in thoracic kyphosis (normal 20–40 degrees) during puberty with at least 5 degrees of anterior wedging of at least three or more adjacent vertebrae. It is to be distinguished from postural round back, which is more flexible and lacks radiographical changes in the verte- brae. 47 The etiology is unclear, but a familial incidence is noted in 30% to 48% of cases. It occurs in about 1% of the population and is more common in boys. Clinically, it is possible to distinguish two forms of juvenile kypho- sis. Thoracic Scheuermann’s disease has an apex of the curve at T7–9, 7. Musculoskeletal Problems of Children 175 OBSERVATION COBB ANGLE 0 - 25Њ 25Њ - 45Њ > 45Њ BRACE SPINAL FUSION Fig. 7.11. Measuring the Cobb angle and treatment of idiopathic scoliosis. 176 Mark D. Bracker et al. and thoracolumbar Scheuermann’s disease has an apex at T11-12. Cosmetic deformity is often the chief complaint. Pain is usually aching and occurs more commonly with the thoracolumbar form. Radiographs should include standing posteroanterior and lateral scoliosis films. Hyperextension lateral films help to determine the flexibility of the curve. Radiographs show irregularity of the vertebral endplates, anterior wedging of 5 degrees or more of three or more adjacent vertebrae, Schmorl’s nodes, and increased kyphosis meas- ured between T4 and T12 by the Cobb method. Kyphosis may worsen during the growing period. Curves of 40 to 60 degrees may be treated by a trial of hyperextension exercises if the curve is supple and demonstrates active correction. Curves of 60 to 75 degrees are treated with a Milwaukee brace or underarm orthosis with a breastplate. Bracing is begun if the vertebral end plates are not fused to the vertebral body, with full-time wearing for 6 to 12 months and then part-time (about 16 hours/day) for 6 months or until the end plate fuses. Bracing is less effective for curves of more than 65 to 75 degrees or after skeletal maturity. Surgery may be indicated for cosmesis, progressive deformity despite bracing, or intractable pain. No long-term cardiopulmonary problems have been identified. 48,49 References 1. Karoll LA. Rotational deformities in the lower extremities. Curr Opin Pediatr 1997;9:77–90. 2. Engel FM, Staheli LT. The natural history of torsion and other factors influencing gait in early childhood. Clin Orthop 1974;99: 12–17. 3. Wells L. Common lower extremity problems in children, primary care. Clin Office Pract 1996;23(2):299–303. 4. Brink DS, Levitsky DR. Cuneiform and cuboid wedge osteotomies for correction of residual metatarsus adductus: a surgical review. J Foot Ankle Surg 1995;34:371–8. 5. Fabray G, MacEwen GD, Shands AR Jr. Torsion of the femur: a follow- up study in normal and abnormal conditions. J Bone Joint Surg 1973;55A:1726–38. 6. Kling TF, Hensinger RN. Angular and torsional deformities of the lower limbs in children. Clin Orthop 1983;176:136–47. 7. Bruce RW Jr. Torsional and angular deformities. Pediatr Clin North Am 1996;43(4):867–81. 8. Mielke CH, Stevens PM. Hemiepiphyseal stapling for knee deformities in children younger than 10 years: a preliminary report. J Pediatr Orthop 1996;16:423–9. 7. Musculoskeletal Problems of Children 177 9. Cummings RJ, Lovell WW. Operative treatment of congenital idiopathic club foot. J Bone Joint Surg 1988;70A:1108–12. 10. Ponseti IV. Congenital clubfoot, the results of treatment. J Bone Joint Surg 1963;45A:261–9. 11. Cowell H. Talocalcaneal coalition and new causes of peroneal spastic flatfoot. Clin Orthop 1972;85:16–22. 12. Hoffinger SA. Evaluation and management of pediatric foot deformities. Pediatr Clin North Am 1996;43:1091–111. 13. Paulos L, Samuelson KM. Pes cavovarus: review of a surgical approach using selective soft tissue procedures. J Bone Joint Surg 1980;62A: 942–53. 14. Wenger DR, Mauldin D, Speck G, Morgan D, Lieber R. Corrective shoes and inserts as treatment for flexible flatfoot in infants and children. J Bone Joint Surg 1989;71A:800–10. 15. Steward M. Miscellaneous afflictions of the foot. In: Campbell’s opera- tive orthopedics. St. Louis: Mosby, 1980;1703. 16. Salter RB, Zaltz C. Anatomic investigation of the mechanism of injury and pathologic anatomy of “pulled elbow” in young children. Clin Orthop 1971;77:134. 17. Southmayd W, Ehrlich MB. Idiopathic subluxation of the radial head. Clin Orthop 1976;121:271. 18. Hardinse K. The etiology of transient synovitis of the hip in childhood. J Bone Joint Surg 1970;52B:100–7. 19. Del Beccaro M, Champoux A, Bockers T, Mendelman P. Septic arthritis versus transient synovitis of the hip: The value of screening laboratory tests. Ann Emerg Med 1992;21(12):1418–22. 20. Roy DR. Current concepts in Legg-Calve-Perthes Disease. Pediatr Ann 1999;28(12):748–52. 21. Busch M, Morrisy R. Slipped capital femoral epiphysis. Orthop Clin North Am 1987;18:637–47. 22. Fahey JJ, O’Brien ET. Acute slipped capital femoral epiphysis: review of the literature and report of ten cases. J Bone Joint Surg 1965;47A: 1105–27. 23. Kallio PE, Paterson DC, Foster BK, Lequene GW. Classification in slipped capital femoral epiphysis. Clin Orthop 1993;294:196–203. 24. Loder RT, Richards BS, Shapiro PS, Reznick LR, Aronsson DD. Acute slipped capital femoral epiphysis: the importance of physical stability. J Bone Joint Surg 1993;75A:1134–40. 25. Loder RT, Aronson DD, Greenfield ML. The epidemiology of bilateral slipped capital femoral epiphysis. J Bone Joint Surg 1993;75A:1141–7. 26. Umas H, Liebling M, Moy L, Harmamati N, Macy N, Pritzker H. Slipped capital femoral epiphysis: a physeal lesion diagnosed by MRI, with radi- ographic and CT correlation. Skel Radiol 1998;27:139–44. 27. Committee on Quality Improvement and Subcommittee on Developmental Dysplasia of the Hip. American Academy of Pediatrics: clinical practice guideline: early detection of developmental dysplasia of the hip. Pediatrics 2000;105(4):896–905. 28. Gerscovich EO. Radiologists’ guide to the imaging in the diagnosis and treatment of developmental dysplasia of the hip. Skel Radiol 1997; 26:386–97. 178 Mark D. Bracker et al. 29. Rosendahl K, Markestad T, Lie RT. Ultrasound in the early diagnosis of congenital dislocation of the hip: the significance of hip stability versus acetabular morphology. Pediatr Radiol 1992;22:430–3. 30. Graf R. Hip semiography: how reliable? Sector scanning versus linear scanning? Dynamic versus static examination? Clin Orthop 1992;281: 18–21. 31. Weinstein SL. Congenital hip dislocation: long-range problems, residual signs and symptoms after successful treatment. Clin Orthop 1992; 281:69–74. 32. Harris IE, Dickens R, Menelaus MB. Use of the Pavlic harness for hip displacements: when to abandon treatment. Clin Orthop 1992; 281:29–33. 33. Gruppo R, Glueck CJ, Wall E, Roy D, Wang P. Legg-Perthes disease in three siblings, two heterozygous and one homozygous for the factor V Leiden mutation. J Pediatr 1998;132(5):885–8. 34. Catterall A. The natural history of Perthes’ disease. J Bone Joint Surg 1971;53B:37–53. 35. Gershuni DH. Preliminary evaluation and prognosis in Legg-Calvé- Perthes disease. Clin Orthop 1980;150:16–22. 36. Herring JA. The treatment of Legg-Calve-Perthes disease. J Bone Joint Surg 1994;76A(3):448–57. 37. McAndrew MP. Weinstein SL. A long-term follow-up of Legg-Calve- Perthes disease. J Bone Joint Surg 1984;66A(6):860–9. 38. Osgood RB. Lesions of the tibial tubercle occurring during adolescence. Boston Med J 1903;148:114–17. 39. Sever JW. Apophysitis of the os calcis. NY Med J 1912;95: 1025–9. 40. Obedian RS, Grelsamer RP. Osteochondritis dissecans of the distal femur and patella. Clin Sports Med 1997;16:157–74. 41. De Smet AA. Omer AI, Graf BK. Untreated osteochondritis dissecans of the femoral condyles: prediction of patient outcome using radiographic and MR findings. Skel Radiol 1997;26:463–7. 42. Wiltse LL, Newman PH, Macnab I. Classification of spondylolysis and spondylolisthesis. Clin Orthop 1976;117:23–9. 43. Hensinger RN. Spondylolysis and spondylolisthesis in children and ado- lescents. J Bone Joint Surg 1989;71A:1098–107. 44. Boxall D, Bradford DS, Winter RB, Moe JH. Management of severe spondylolisthesis in children and adolescents. J Bone Joint Surg 1979;61:479–95. 45. Sorensen KH. Scheuermann’s juvenile kyphosis. Copenhagen: Munksgaard, 1964. 46. Hensinger RN, Greene TL, Hunter LY. Back pain and vertebral changes simulating Scheuermann’s kyphosis. Spine 1982;6:341–2. 47. Bradford DS. Juvenile kyphosis. In: Bradford DS, Lonstein JE, Moe JH, et al, eds. Moe’s textbook of scoliosis and other spinal deformities, 2nd ed. Philadelphia: WB Saunders, 1987;347–68. 48. Cobb J. Outline for study of scoliosis. AAOS Instruct Course Lect 1948;5:261–275, Ann Arbor: J. W. Edwards. 49. Moe JH, Byrd JA III. Idiopathic scoliosis. In: Bradford DS, Lonstein JH, Moe JH, et al, eds. Moe’s textbook of scoliosis and other spinal deformi- ties, 2nd ed. Philadelphia: WB Saunders, 1987;191–232. 50. Lillegard W, Kruse R. In Taylor RB, eds. Family medicine: principles and practice, 4th ed. New York: Springer-Verlag, 1993. 51. Taylor RB. Family medicine: principles and practice, 6 th ed. New York: Springer-Verlag, 2003. 52. Gerberg LF, Micheli LJ, Nontraumatic hip pain in active children: a crit- ical differential. Phys Sports Med 1996;24:69–74. 53. Peck DM. Apophyseal injuries in the young athlete. Am Fam phys 1995;51:1891–5. 7. Musculoskeletal Problems of Children 179 [...]... predicts the risk of osteoporotic fractures in postmenopausal women. 26 These markers include indices of bone resorption such as serum and urine levels of C- and N-telopeptide, and indices of bone formation such as osteocalcin and bone-specific alkaline phosphatase These markers of bone turnover may be particularly 1 86 Paula Cifuentes Henderson and Richard P Usatine Table 8.2 Indications for Bone Mineral Density... Engl J Med 1998;339:292–9 16 Bassey EJ, Rothwell MC, Littlewood JJ Pre- and post-menopausal women have different bone mineral density responses to the same high impact exercise J Bone Miner Res 1998;13:1805–13 17 Dawson B, Harris SS, Krall EA Effect of calcium and vitamin D supplementation on bone density in men and women 65 years of age or older N Engl J Med 1997;337 :67 0 6 18 NIH Consensus Development... body weight history in the occurrence and recovery of osteoporosis in patients with anorexia nervosa: evaluation by dual x-ray absorptiometry and bone metabolic markers Eur J Endocrinol 1998;139:2 76 83 20 Consensus Development Conference Diagnosis, prophylaxis and treatment of osteoporosis Am J Med 1993;94 :64 6–50 21 Nattiv A Osteoporosis: its prevention, recognition, and management Family Pract Recert... Osteoporosis Prevention Study Maturitas 2000; 36( 3):181–93 32 Komulainen MH, Kroger H, Tuppurainen MT, et al HRT and Vit D in prevention of non-vertebral fractures in postmenopausal women; a 5 year randomized trial Maturitas 1998;31(1):45–54 33 Torgerson DJ, Bell-Syer SEM Hormone replacement therapy and prevention of nonvertebral fractures: a meta-analysis of randomized trials JAMA 2001;285:2891–7 34 Ettinger... women with osteoporosis treated with raloxifene: results from a 3-year randomized clinical trial JAMA 1999;282 :63 7–45 35 Karpf DB, Shapiro DR, Seeman E Prevention of nonvertebral fractures by alendronate: a meta-analysis JAMA 1997;277:1159 64 36 Saag KG, Emkey R, Schnitzer TJ, et al Alendronate for the prevention and treatment of glucocorticoid-induced osteoporosis GlucocorticoidInduced Osteoporosis Intervention... decrease of the bone density.25 The ultimate goal is to prevent vertebral and hip fractures The most thoroughly studied and most widely used technique to measure BMD is the dual-energy x-ray absortiometry (DEXA) scan This is considered to be the gold standard screening test to measure the BMD of the hip and spine It is less expensive and involves less radiation exposure than the quantitative computed tomography... enough vegetables and fruits, and have a high intake of low-calcium/high-phosphorus beverages like sodas These beverages have a negative effect on calcium balance Laboratory Assessment If the history and physical exam suggests secondary causes of osteoporosis, the physician should consider tests such as thyroid-stimulating hormone (TSH), parathyroid hormone (PTH), calcium, vitamin D, urine N-teloptide, complete... assessment Prevention and Treatment Nonpharmacological Nonpharmacological therapy for prevention and treatment of osteoporosis includes adequate dietary intake of calcium and vitamin D, weight-bearing exercise, fall precautions, no smoking, and avoidance of excessive alcohol intake These steps should be started early in life and continued through menopause because BMD peaks at about age 35 and then begins... women and will reduce the risk of fractures.27 The effect is not strong enough to recommend calcium alone for osteoporosis prevention Table 8.3 Optimal Calcium Intake Population Infants, children, and young adults 0 6 Months 6 12 Months 1–10 years 11–24 years Adult women Pregnant and lactating Ͻ24 years Ͼ24 years Premenopausal 25–49 years Postmenopausal 50 64 years On estrogen Not on estrogen 65 years... prevention and treatment of postmenopausal osteoporosis Endocrinol Pract 19 96; 2(2):157–71 useful if obtained prior to starting treatment and then repeated in 3 to 6 months to measure the response Despite the fact that these markers may identify changes in bone remodeling, they do not predict fracture risk These tests are very expensive and are not recommended for screening or as the first-line studies . evaluation and prognosis in Legg-Calv - Perthes disease. Clin Orthop 1980;150: 16 22. 36. Herring JA. The treatment of Legg-Calve-Perthes disease. J Bone Joint Surg 1994;76A(3):448–57. 37. McAndrew. women. 26 These markers include indices of bone resorption such as serum and urine levels of C- and N-telopeptide, and indices of bone formation such as osteocalcin and bone-specific alka- line. 1994;76A(3):448–57. 37. McAndrew MP. Weinstein SL. A long-term follow-up of Legg-Calve- Perthes disease. J Bone Joint Surg 1984 ;66 A (6) : 860 –9. 38. Osgood RB. Lesions of the tibial tubercle occurring