Spinal Deformities: Idiopathic Scoliosis and Kyphoscoliosis

Chapter 24


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Spinal Deformities: Idiopathic Scoliosis and Kyphoscoliosis


Julian Allen, MD, FAAP


Introduction


Scoliosis is a structural lateral and rotational deformity of the spine (Figure 24-1).


Hyperkyphosis is an excessive degree of the normal thoracic anteroposterior curvature.


Surgical correction is indicated for risk of progression through adulthood or pain in the case of severe kyphosis.


Etiology/Epidemiology


Idiopathic scoliosis (IS) occurs in 1%–3% of adolescents and is usually defined by a Cobb angle >10°.


The incidence of scoliosis in children with cerebral palsy is generally accepted to be about 20%–25%.


The etiologic origin of IS is unclear. A genetic component is suggested by 75% concordance for the condition in monozygotic twins and 33% concordance in dizygotic twins. Family pedigrees suggest autosomal dominant inheritance, with incomplete penetrance.


Multiple gene candidates related to collagen, fibrillin, and heparin N-sulfotransferase, vitamin D, and estrogen) are implicated in but not definitively known to cause IS.


An imbalance of paravertebral muscles has been proposed and is also seen in the association of neuromuscular disease and scoliosis.


Isolated hyperkyphosis can also be familial, such as in Scheuermann kyphosis, usually beginning during the adolescent growth spurt.


Regarding epidemiology, juvenile IS starts in and progresses through adolescence; progression slows markedly or stops when growth stops. Adolescent patients with IS generally fare better than those with early-onset scoliosis, but lung function is still compromised as the severity of the curve increases (Figure 24-2). Curves >50° are associated with reduced vital capacity and dyspnea.


Early-onset scoliosis, which occurs before the age of 8 years, accounts for only 4% of all IS cases.


Isolated hyperkyphosis is rarely associated with cardiorespiratory sequelae but can be associated with obstructive lung diseases, such as cystic fibrosis, which leads to air trapping. Hypokyphosis can be associated with a tendency toward recurrent pneumothoraces (“straight back syndrome”).


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Figure 24-1. Posteroanterior radiograph shows the mid-lower thoracic curvature of scoliosis. From Dede O, Demirkiran G, Yazici M. Update on the ‘growing spine surgery’ for young children with scoliosis. Curr Opin Pediatr. 2014; 26(1):57–63. http://journals.lww.com/co-pediatrics/Abstract/2014/02000/2014_Update_on_the__growing_spine_surgery__for.10.aspx


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Figure 24-2. Forced vital capacity (FVC) as a function of scoliosis curve in degrees. MC = major curve, TC = thoracic curve. From Dreimann M, Hoffmann M, Kossow K, Hitzl W, Meier O, Koller H. Scoliosis and chest cage deformity measures predicting impairments in pulmonary function. Spine. 2014;39:2024–2033. http://journals.lww.com/spinejournal/Abstract/2014/11150/Scoliosis_and_Chest_Cage_Deformity_Measures.8.aspx


Pathophysiology


The scoliotic chest wall, and to a lesser extent the lungs, are less compliant (stiffer) than normal (compare the normal respiratory system pressure-volume black curve with the severe respiratory system scoliosis red curve in Figure 24-3), which can lead to smaller lung volumes.


Diaphragmatic function and strength may be diminished in scoliosis, probably as a result of a diminished area of apposition of the diaphragm to the inner chest wall. Flattening of the diaphragm due to the torsion on its fibers may make it less efficient. Patients with scoliosis have diminished maximal inspiratory (but not expiratory) pressures.


Mild degrees of kyphoscoliosis do not usually lead to respiratory impairment. Lung restriction usually begins with scoliotic curves of ≥40°.


Clinical Features


Pulmonary function tests (PFTs) in IS


The typical pattern of lung function abnormality is respiratory system restriction. There is some evidence that scoliosis can also lead to a subtle obstructive defect or unevenness of gas mixing (ventilation).


In general, lung volumes correlate inversely with the Cobb angle (Figure 24-2). This is probably a function of chest wall stiffness rather than respiratory muscle weakness, since (a) there is no correlation between lung volumes and measures of respiratory muscle strength and (b) there is positive correlation between chest wall compliance and lung volumes.


One difficulty in interpreting PFT results in children with IS is the choice of the predicted value used when calculating the child’s percentage of predicted value. The predicted value of PFTs in normally developing children is most closely predicted by using standing height. In children with scoliosis, predicted value can be determined by using standing height, sitting height × 2 (in children >7 years old), or arm span (equal to height in normally developing children). The percentage predicted value in children with scoliosis will thus depend on the height value used. The percentage predicted value is greatest if actual height is used and is lowest if arm span is used.


In severe disease with vertebral rotation, compression of central airways by anterior vertebral bodies described but extremely rare


Exercise tolerance


Children with IS have decreased maximal exercise capacity.


As with PFTs, exercise limitation seems to be related to the degree of curvature.


The 6-minute walk test result can also be diminished.


Respiratory failure


Respiratory failure is common in severe congenital scoliosis but rare in adolescent IS, at least during childhood and adolescence.


When it does occur, it tends to occur perioperatively and in subjects with the most severe curves.


Severe unrepaired scoliosis and kyphoscoliosis can cause both ventilatory defect leading to CO2 retention and ventilation-perfusion mismatch in compressed segments of lung, leading to hypoxemia.


Isolated kyphosis rarely leads to respiratory impairment.


Increased risk for atelectasis and/or pneumonia, especially in children with chronic comorbidities


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Figure 24-3. Pressure-volume curve of the respiratory system for normally developed subjects (black line) and subjects with severe scoliosis (red line). Respiratory system volume as a percentage of vital capacity (VC) on the y-axis is plotted against trans– respiratory system pressure (Prs) on the x-axis. The respiratory system compliance is the slope of the curves and is much lower than normal in the subjects with scoliosis. The data for normally developed subjects are from Rahn H, Otis AB, Chadwick LE and Fenn WO. Pressure-volume diagram of the thorax and lung. Amer J Physiol. 1946;146:161–178. The data for patients with scoliosis are adapted from Ting EY, Lyons HA. The relation of pressure and volume of the total respiratory system and its components in kyphoscoliosis. Am Rev Respir Dis. 1964;89:379–386.


Differential Diagnosis


The major differential is distinguishing idiopathic spinal deformity from other forms:


Congenital, such as hemivertebrae


Syndromic, with (eg, Jarcho-Levin and Jeune syndromes) or without (eg, VATER [vertebral defects, imperforate anus, tracheoesophageal fistula, radial and renal dysplasia], neurofibromatosis) thoracic insufficiency syndrome


Neuromuscular, such as muscular dystrophy and spinal muscular atrophies


Diagnostic Considerations


The normal spine has an anteroposterior curvature between 20° and 40° and a lateral curve of <10°. Hypokyphosis is a curvature <10°, and hyperkyphosis is a curve >40°.


Physical examination


Most scoliosis curves will be easily demonstrated at physical examination, except for the most mild cases.


While standing behind the patient, have him or her perform the forward-bending test to look for thoracic asymmetry. This can be conducted with or without the use of a scoliometer, which is now available and validated as a smart phone app, to help discern more mild curves (Figure 24-4).


Hyperkyphosis can be observed by standing at the patient’s side during forward bending.


PFTs can help indicate the severity of lung function involvement, as well as indicate whether surgery carries increased intra- and postoperative risk, while recognizing that only severe curves generally affect lung function.


Radiologic studies include spine series with measurement of the Cobb angle (Figure 24-1) and flexibility studies.


Computed tomography and unenhanced static or dynamic magnetic resonance imaging of the entire spine are becoming commonplace and can help better assess the rotational component.


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Figure 24-4. Forward bending performed with the use of a scoliometer. From Weinstein SL, Dolan LA, Cheng JCY, Danielsson A, Morcuende JA. Adolescent idiopathic scoliosis. Lancet. 2008;371:1527–1537. Copyright 2008, with permission from Elsevier.


Management


Nonsurgical approaches may be warranted.


Watchful waiting is usually advised for curves <25°.


Physical therapy is sometimes used to prevent progression of such curves, but there is no evidence that it circumvents the need for surgery. It is commonly used in Europe (eg, the Schroth method).


Bracing may be effective.


In adolescents with curves between 20° and 45°, bracing can be


used to prevent progression of the curve to 50°. In the Bracing in Adolescent Idiopathic Scoliosis Trial, or BRAIST, a randomized cohort arm had a success rate of 75% in the brace group and 42% in the observation group.


A positive association between hours of brace wear and the rate of treatment success was found; patients who wore the brace for >12.9 hours daily had success rates of 90%–93% versus 41% in patients who wore the brace for 0–6 hours daily.


Early casting may be performed for infantile forms of scoliosis.


Young children with milder curves demonstrate a higher rate of improvement with early casting.


Casts that derotate rather than just straighten the spine demonstrate a higher success rate.


Scoliosis surgery may be indicated in some cases.


Usually reserved for curves >45°


Spinal fusion


In adolescent IS, spinal fusion should be reserved for patients who have already undergone substantial spinal growth but not delayed until growth is nearly completed.


Since curves in adolescence progress until growth ceases, the timing of spinal curve repair also needs to have the current Cobb angle taken into account, as well as the rate of progression and projected severity of curvature.


Growing rods


With growing rods, the spine will continue to grow, even if fused at an earlier age, while controlling the scoliotic deformity, allowing for more prompt intervention (Figure 24-5).


New magnetically controlled growing rods are available and recently approved by the Food and Drug Administration for the treatment of early-onset scoliosis. They prevent the need for repeated surgical lengthening procedures and can be placed as an outpatient procedure in the office.


Management of respiratory failure


Patients with severe unrepaired kyphoscoliosis and respiratory failure are often successfully treated with nocturnal noninvasive ventilation.


Nocturnal noninvasive ventilation can reduce nocturnal and daytime CO2 retention, probably by increasing the thoracic cage flexibility and strength and resetting respiratory drive.


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Figure 24-5. Frontal radiograph demonstrates implanted growing rods. Lengthening is achieved by distraction through the telescopic connectors. From Dede O, Demirkiran G, Yazici M. Update on the ‘growing spine surgery’ for young children with scoliosis. Curr Opin Pediatr. 2014;26(1):57–63. http://journals.lww.com/co-pediatrics/Abstract/2014/02000/2014_Update_on_the__growing_spine_surgery__for.10.aspx


Expected Outcomes/Prognosis


IS can progress throughout duration of growth and then generally remains static.


The risk of progression is related to both degree of the curve at initial discovery and the amount of time left for growth. A curve of >40° discovered at age 12 has a nearly 100% chance of progression, while a curve of <30° discovered at age 16 has only a 10% chance of progression.


The main reason for spinal fusion is to prevent this progression to avoid the natural history reported in untreated patients with large curves who have increased pain and disability.


Long-term outcomes of scoliosis surgery on lung function vary with surgery performed, as well as the severity of the curve. The extent of actual correction of the spinal deformity varies markedly and appears to be related to the flexibility of the child’s spine.


Difficulties in interpreting the effects of surgery on lung function arise from whether absolute or percentage predicted values are used. Several studies have shown improvement in the former but not the latter. Furthermore, for percentage predicted value interpretation, it must be taken into account whether standing height or arm span is used.


Poor preoperative lung function need not be prohibitive. Experienced multidisciplinary teams that include pulmonologists, nutritionists, and anesthesiologists report positive outcomes of surgical treatment for pediatric patients with forced vital capacity <40%. Such severe cases may require pre- or postoperative noninvasive ventilation, or both.


Early-onset scoliosis, such as infantile and juvenile onset before the age of 8 years, has worse outcomes. Up to 40% of such patients die of respiratory failure if untreated, with a mean age of 54 years at death, although death in adolescence has been reported.


In infantile and early-onset IS, spinal fusion does not improve outcomes; because it can create thoracic insufficiency syndrome, it is not a good option in the young child. The rate of vertebral growth after spinal fusion is reduced by approximately half, and in adulthood, these patients have permanently shortened spines. Vital capacity <50% is seen in 40%–60% of subjects who undergo early fusion. Growth-friendly instrumentation (ie, vertical expandable titanium rib, growing rods, magnetically controlled growing rods) are indicated for the surgical treatment of early-onset scoliosis and may change these outcomes. Long-term studies of lung function are pending.


When to Refer


Prompt referral to an orthopedic surgeon is necessary when a spinal curve is first noticed, so that curve quantitation and progression can be assessed and followed up.


Prevention


There is little evidence that scoliosis can be prevented, although exercise programs have been undertaken to do so. Rotational exercises may be of temporizing value, and only in mild cases.


Resources for Families


Patients and Families (Scoliosis Research Society). www.srs.org/patients-and-families


What Is Scoliosis? (U.S. Department of Health and Human Services). www.niams.nih.gov/Health_Info/Scoliosis/scoliosis_ff.pdf



Part II Bibliography


CHAPTER 10: CHOANAL ATRESIA


Brown OE, Pownell P, Manning SC. Choanal atresia: a new anatomic classification and clinical management applications. Laryngoscope. 1996;106(1 Pt 1):97–101


Burrow TA, Saal HM, de Alarcon A, Martin LJ, Cotton RT, Hopkin RJ. Characterization of congenital anomalies in individuals with choanal atresia. Arch Otolaryngol Head Neck Surg. 2009;135(6):543–547


Corrales CE, Koltai PJ. Choanal atresia: current concepts and controversies. Curr Opin Otolaryngol Head Neck Surg. 2009;17(6):466–470


Gujrathi CS, Daniel SJ, James AL, Forte V. Management of bilateral choanal atresia in the neonate: an institutional review. Int J Pediatr Otorhinolaryngol. 2004;68(4):399–407


Kwong KM. Current updates on choanal atresia. Front Pediatr. 2015;3(52):52


Ramsden JD, Campisi P, Forte V. Choanal atresia and choanal stenosis. Otolaryngol Clin North Am. 2009;42(2):339–352


CHAPTER 11: LARYNGOMALACIA


Dobbie AM, White DR. Laryngomalacia. Pediatr Clin North Am. 2013;60(4):893–902


Thorne MC, Garetz SL. Laryngomalacia: review and summary of current clinical practice in 2015. Pediatr Respir Rev. 2015;28


Hartl TT, Chadha NK. A systematic review of laryngomalacia and acid reflux. Otolaryngol Head Neck Surg. 2012;147(4):619–626


Landry, AM, Thompson, DM. Laryngomalacia: disease presentation, spectrum and management. Int J Pediatr. 2012;753526


Ida JB, Thompson DM. Pediatric stridor. Otolaryngol Clin North Am. 2014;47(5): 795–819


Ayari S, Aubertin G, Girschig H, Van Den Abbeele T, Mondain M. Pathophysiology and diagnostic approach to laryngomalacia in infants. Eur Ann Otorhinolaryngol Head Neck Dis. 2012;129(5):257–263


Venkatesan NN, Pine HS, Underbrink M. Laryngopharyngeal reflux disease in children. Pediatr Clin North Am. 2013;60(4):865–878


Thompson DM. Laryngomalacia: factors that influence disease severity and outcomes of management. Curr Opin Otolaryngol Head Neck Surg. 2010;18(6):564–570


Cooper T, Benoit M, Erickson B, El-Hakim H. Primary presentations of laryngomalacia. JAMA Otolaryngol Head Neck Surg. 2014;140(6):521–526


CHAPTER 12: VOCAL FOLD PARALYSIS


King EF, Blumin JH. Vocal cord paralysis in children. Curr Opin Otolaryngol Head Neck Surg. 2009;17(6):483–487


Lesnik M, Thierry B, Blanchard M, et al. Idiopathic bilateral vocal cord paralysis in infants: Case series and literature review. Laryngoscope. 2015;125(7):1724–1728


Rickert SM, Childs LF, Carey BT, Murry T, Sulica L. Laryngeal electromyography for prognosis of vocal fold palsy: a meta-analysis. Laryngoscope. 2012;122(1):158–161


Setlur J, Hartnick CJ. Management of unilateral true vocal cord paralysis in children. Curr Opin Otolaryngol Head Neck Surg. 2012;20(6):497–501


Zur KB, Carroll LM. Recurrent laryngeal nerve reinnervation in children: Acoustic and endoscopic characteristics pre-intervention and post-intervention. A comparison of treatment options. Laryngoscope. 2015;125(Suppl 11):S1–S15


CHAPTER 13: SUBGLOTTIC STENOSIS


Al-Samri M, Mitchell I, Drummond DS, Bjornson C. Tracheostomy in children: a population-based experience over 17 years. Pediatr Pulmonol. 2010;45(5):487–493


Douglas CM, Poole-Cowley J, Morrissey S, Kubba H, Clement WA, Wynne D. Paediatric tracheostomy-An 11 year experience at a Scottish paediatric tertiary referral centre. Int J Pediatr Otorhinolaryngol. 2015;79(10):1673–1676


Myer CM III, O’Connor DM, Cotton RT. Proposed grading system for subglottic stenosis based on endotracheal tube sizes. Ann Otol Rhinol Laryngol. 1994;103(4 Pt 1):319–323


Pfleger A, Eber E. Assessment of causes of stridor. Paediatr Respir Rev. 2015;pii: S1526-0542(15)00114-1


Yellon RF, Goldberg H. Update on gastroesophageal reflux disease in pediatric airway disorders. Am J Med. 2001;111(Suppl 8A):78S–84S


Manica D, Schweiger C, Maróstica PJ, Kuhl G, Carvalho PR. Association between length of intubation and subglottic stenosis in children. Laryngoscope. 2013; 123(4):1049–1054


CHAPTER 14: TRACHEOMALACIA, VASCULAR RINGS AND SLINGS, AND BRONCHOMALACIA


Abel RM, Bush A, Chitty LS, Harcourt J, Nicholson AG. Congenital lung disease. In: Chernick V, Boat TF, Wilmott RW, Bush A, eds. Kendig’s Disorders of the Respiratory Tract in Children. 7th ed. Philadelphia, PA: Saunders; 2006:280–316


Noriega Aldave AP, William Saliski D. The clinical manifestations, diagnosis and management of Williams-Campbell syndrome. N Am J Med Sci. 2014;6(9):429–432


Amin RS, Rutter MJ. Airway disease and management in bronchopulmonary dysplasia. Clin Perinatol. 2015;42(4):857–870


Gonik N, Smith L. Congenital and acquired tracheal anomalies. In: Hartnick CJ, Sataloff RT, eds. Sataloff’s Comprehensive Textbook of Otolaryngology: Head & Neck Surgery. 6th ed. Philadelphia, PA: Jaypee Brothers; 2016:523–540


Hysinger EB, Panitch HB. Paediatric tracheomalacia. Paediatr Respir Rev. 2016;17:9–15


Krustins E, Kravale Z, Buls A. Mounier-Kuhn syndrome or congenital tracheobronchomegaly: a literature review. Respir Med. 2013;107(12):1822–1828


Licari A, Manca E, Rispoli GA, Mannarino S, Pelizzo G, Marseglia GL. Congenital vascular rings: a clinical challenge for the pediatrician. Pediatr Pulmonol. 2015; 50(5):511–524


CHAPTER 15: TRACHEOESOPHAGEAL FISTULAS


Spitz L. Oesophageal atresia. Orphanet J Rare Dis. 2007;2:24


Spitz L. Esophageal atresia. Lessons I have learned in a 40-year experience. J Pediatr Surg. 2006;41(10):1635–1640


Holland AJ, Fitzgerald DA. Oesophageal atresia and tracheo-oesophageal fistula: current management strategies and complications. Paediatr Respir Rev. 2010; 11(2):100–106, quiz 106–107


Houben CH, Curry JI. Current status of prenatal diagnosis, operative management and outcome of esophageal atresia/tracheo-esophageal fistula. Prenat Diagn. 2008;28(7):667–675


Pinheiro PF, Simões e Silva AC, Pereira RM. Current knowledge on esophageal atresia. World J Gastroenterol. 2012;18(28):3662–3672


Yalçin Ş, Ciftci AO, Karnak I, Tanyel FC, Şenocak ME. Management of acquired tracheoesophageal fistula with various clinical presentations. J Pediatr Surg. 2011;46(10):1887–1892


CHAPTER 16: PULMONARY HYPOPLASIA


Delgado-Pena YP, Torrent-Vernetta A, Sacolo G, et al. Pulmonary hypoplasia: an analysis of cases over a 20 year period. An Pediatr (Barc). 2016;85(2):70–76


Ruchonnet-Metrailler I, Leroy-Terquem E, Stirnemann J, et al. Neonatal outcomes of prenatally diagnosed congenital pulmonary malformations. Pediatrics. 2014; 133(5):e1285–e1291


Krivchenya DU, Rudenko EO, Lysak SV, Dubrovin AG, Khursin VN, Krivchenya TD. Lung aplasia: anatomy, history, diagnosis and surgical management. Eur J Pediatr Surg. 2007;17(4):244–250


Vergani P. Prenatal diagnosis of pulmonary hypoplasia. Curr Opin Obstet Gynecol. 2012;24(2):89–94


Breeze AC, Lees CC. Antenatal diagnosis and management of life-limiting conditions. Semin Fetal Neonatal Med. 2013;18(2):68–75


Kayemba-Kay A, Couvral-Carcauzon V, Goua V, et al. Unilateral pulmonary agenesis: a report of 4 cases, two diagnosed antenatally and literature review. Pediatr Pulmonol. 2014;49(3):E96–E102


Grivell RM, Andersen C, Dodd JM. Prenatal interventions for congenital diaphragmatic hernia for improving outcomes. Cochrane Database Syst Rev. 2015;27(11): CD008925


CHAPTER 17: PULMONARY SEQUESTRATION


Savic B, Birtel FJ, Tholen W, Funke HD, Knoche R. Lung sequestration: report of seven cases and review of 540 published cases. Thorax. 1979;34(1):96–101


Corbett HJ, Humphrey GM. Pulmonary sequestration. Paediatr Respir Rev. 2004; 5(1):59–68


Wei Y, Li F. Pulmonary sequestration: a retrospective analysis of 2625 cases in China. Eur J Cardiothorac Surg. 2011;40(1):e39–e42


Yucel O, Gurkok S, Gozubuyuk A, et al. Diagnosis and surgical treatment of pulmonary sequestration. Thorac Cardiovasc Surg. 2008;56(3):154–157


Kang M, Khandelwal N, Ojili V, Rao KL, Rana SS. Multidetector CT angiography in pulmonary sequestration. J Comput Assist Tomogr. 2006;30(6):926–932


Caradonna P, Bellia M, Cannizzaro F, Regio S, Midiri M, Bellia V. Non-invasive diagnosis in a case of bronchopulmonary sequestration and proposal of diagnostic algorithm. Monaldi Arch Chest Dis. 2008;69(3):137–141


CHAPTER 18: OVERINFLATION AND CONGENITAL LOBAR EMPHYSEMA


Karnak I, Senocak ME, Ciftci AO, Büyükpamukçu N. Congenital lobar emphysema: diagnostic and therapeutic considerations. J Pediatr Surg. 1999;34(9):1347–1351


Mei-Zahav M, Konen O, Manson D, Langer JC. Is congenital lobar emphysema a surgical disease? J Pediatr Surg. 2006;41(6):1058–1061


Man DW, Hamdy MH, Hendry GM, Bisset WH, Forfar JO. Congenital lobar emphysema: problems in diagnosis and management. Arch Dis Child. 1983;58(9):709–712


Robertson R, James ES. Congenital lobar emphysema. Pediatrics. 1951;8(6):794–804


Wang CC, Wu ET, Chen SJ, et al. Scimitar syndrome: incidence, treatment, and prognosis. Eur J Pediatr. 2008;167(2):155–160


Bhide A, Murphy D, Thilaganathan B, Carvalho JS. Prenatal findings and differential diagnosis of scimitar syndrome and pulmonary sequestration. Ultrasound Obstet Gynecol. 2010;35(4):398–404


CHAPTER 19: CONGENITAL PULMONARY AIRWAY MALFORMATION


Adzick NS, Harrison MR. Management of the fetus with a cystic adenomatoid malformation. World J Surg. 1993;17(3):342–349


Durell J, Lakhoo K. Congenital cystic lesions of the lung. Early Hum Dev. 2014;90(12): 935–939


Ng C, Stanwell J, Burge DM, Stanton MP. Conservative management of antenatally diagnosed cystic lung malformations. Arch Dis Child. 2014;99(5):432–437


Pacharn P, Kline-Fath B, Calvo-Garcia M, et al. Congenital lung lesions: prenatal MRI and postnatal findings. Pediatr Radiol. 2013;43(9):1136–1143


Polites SF, Habermann EB, Zarroug AE, Thomsen KM, Potter DD. Thoracoscopic vs open resection of congenital cystic lung disease—utilization and outcomes in 1120 children in the United States. J Pediatr Surg. 2015;pii:S0022-3468(15)00821-0


Sfakianaki AK, Copel JA. Congenital cystic lesions of the lung: congenital cystic adenomatoid malformation and bronchopulmonary sequestration. Rev Obstet Gynecol. 2012;5(2):85–93


Stocker JT, Madewell JE, Drake RM. Congenital cystic adenomatoid malformation of the lung. Classification and morphologic spectrum. Hum Pathol . 1977;8(2):155–171


CHAPTER 20: BRONCHOGENIC CYSTS


Polites SF, Habermann EB, Zarroug AE, Thomsen KM, Potter DD. Thoracoscopic vs open resection of congenital cystic lung disease—utilization and outcomes in 1120 children in the United States. J Pediatr Surg. 2015;pii: S0022-3468(15)00821-0


Vimala LR, Sathya RK, Lionel AP, Kishore JS, Navamani K. Unilateral obstructive emphysema in infancy due to mediastinal bronchogenic cyst-diagnostic challenge and management. J Clin Diagn Res. 2015;9(5):TD03–TD05


Jiang JH, Yen SL, Lee SY, Chuang JH. Differences in the distribution and presentation of bronchogenic cysts between adults and children. J Pediatr Surg. 2015;50(3): 399–401


Durell J, Lakhoo K. Congenital cystic lesions of the lung. Early Hum Dev. 2014;90(12): 935–939


Rios LT, Araujo Júnior E, Nardozza LM, Moron AF, Martins Mda G. Prenatal diagnosis and postnatal findings of bronchogenic cyst. Case Rep Pulmonol. 2013;2013:483864


Maurin S, Hery G, Bourliere B, Potier A, Guys JM, Lagausie PD. Bronchogenic cyst: clinical course from antenatal diagnosis to postnatal thoracoscopic resection. J Minim Access Surg. 2013;9(1):25–28


Pacharn P, Kline-Fath B, Calvo-Garcia M, et al. Congenital lung lesions: prenatal MRI and postnatal findings. Pediatr Radiol. 2013;43(9):1136–1143


CHAPTER 21: PULMONARY ARTERIOVENOUS MALFORMATIONS


Al-Saleh S, Dragulescu A, Manson D, et al. Utility of contrast echocardiography for pulmonary arteriovenous malformation screening in pediatric hereditary hemorrhagic telangiectasia. J Pediatr. 2012;160(6):1039–1043


Faughnan ME, Palda VA, Garcia-Tsao G, et al; HHT Foundation International— Guidelines Working Group. International guidelines for the diagnosis and management of hereditary haemorrhagic telangiectasia. J Med Genet. 2011; 48(2):73–87


Gill SS, Roddie ME, Shovlin CL, Jackson JE. Pulmonary arteriovenous malformations and their mimics. Clin Radiol. 2015;70(1):96–110


Giordano P, Lenato GM, Suppressa P, et al. Hereditary hemorrhagic telangiectasia: arteriovenous malformations in children. J Pediatr. 2013;163(1):179–186 y Grace JA, Angus PW. Hepatopulmonary syndrome: update on recent advances in pathophysiology, investigation, and treatment. J Gastroenterol Hepatol. 2013; 28(2):213–219


Wong HH, Chan RP, Klatt R, Faughnan ME. Idiopathic pulmonary arteriovenous malformations: clinical and imaging characteristics. Eur Respir J. 2011;38(2):368–375


CHAPTER 22: CHEST WALL DEFORMITIES: THORACIC INSUFFICIENCY SYNDROME


Campbell RM Jr, Smith MD, Mayes TC, et al. The characteristics of thoracic insufficiency syndrome associated with fused ribs and congenital scoliosis. J Bone Joint Surg Am. 2003;85-A(3):399–408


Campbell RM Jr, Smith MD. Thoracic insufficiency syndrome and exotic scoliosis. J Bone Joint Surg Am. 2007;89(Suppl 1):108–122


Campbell RM Jr. VEPTR: past experience and the future of VEPTR principles. Eur Spine J. 2013;22(Suppl 2):S106–S117


Mayer OH. Management of thoracic insufficiency syndrome. Curr Opin Pediatr. 2009; 21(3):333–343


Mayer OH. Chest wall hypoplasia—principles and treatment. Paediatr Respir Rev. 2015;16(1):30–34


Redding GJ. Primary thoraco-spinal disorders of childhood. Paediatr Respir Rev. 2015;16(1):25–29


CHAPTER 23: PECTUS DEFORMITIES: PECTUS EXCAVATUM AND PECTUS CARINATUM


Koumbourlis AC. Pectus deformities and their impact on pulmonary physiology. Paediatr Respir Rev. 2015;16(1):18–24


Redding GJ, Kuo W, Swanson JO, et al. Upper thoracic shape in children with pectus excavatum: impact on lung function. Pediatr Pulmonol. 2013;48(8):817–823


Lawson ML, Mellins RB, Paulson JF, et al. Increasing severity of pectus excavatum is associated with reduced pulmonary function. J Pediatr . 2011;159(2):256–261


Fokin AA, Steuerwald NM, Ahrens WA, Allen KE. Anatomical, histologic, and genetic characteristics of congenital chest wall deformities. Semin Thorac Cardiovasc Surg. 2009;21(1):44–57


Fonkalsrud EW. Current management of pectus excavatum. World J Surg. 2003;27(5): 502–508


CHAPTER 24: SPINAL DEFORMITIES: IDIOPATHIC SCOLIOSIS AND KYPHOSCOLIOSIS


Koumbourlis AC. Scoliosis and the respiratory system. Paediatr Respir Rev. 2006;7(2):152–160


Weinstein SL, Dolan LA, Cheng JCY, Danielsson A, Morcuende JA. Adolescent idiopathic scoliosis. Lancet. 2008;371(9623):1527–1537


Weinstein SL, Dolan LA, Wright JG, Dobbs MB. Effects of bracing in adolescents with idiopathic scoliosis. N Engl J Med. 2013;369(16):1512–1521


Gomez JA, Hresko MT, Glotzbecker MP. Nonsurgical management of adolescent idiopathic scoliosis. J Am Acad Orthop Surg. 2016;24(8):555–564


Gomez JA, Lee JK, Kim PD, Roye DP, Vitale MG. “Growth friendly” spine surgery: management options for the young child with scoliosis. J Am Acad Orthop Surg. 2011;19(12):722–727

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Aug 22, 2019 | Posted by in PEDIATRICS | Comments Off on Spinal Deformities: Idiopathic Scoliosis and Kyphoscoliosis

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