Late Reconstruction of Brachial Plexus Birth Palsy Sarah E. Sibbel, MD, Andrea S. Bauer, MD, and Michelle A. James, MD
Abstract: Brachial plexus birth palsy (BPBP) presents to the physician on a clinical spectrum, and may substantially impair the child. Potential interventions to improve function for the child with BPBP include physical therapy, microsurgical nerve reconstruction and nerve transfers, soft-tissue balancing and reconstruction with musculotendinous transfers, and osteotomies. Some interventions, such as nerve reconstruction, are best performed in infancy; others, such as muscle transfers and osteotomies, are performed to treat manifestations of this condition that appear later in childhood. Although controversy continues to exist regarding the natural history and surgical management of these patients, recent literature has improved our understanding of surgical indications, anticipated outcomes, and potential complications. On the basis of current evidence, we present here the recommendations for surgical intervention in the upper extremity of children with BPBP, and encourage early referral to a brachial plexus specialist to establish care. Key Words: brachial plexus birth palsy, late reconstruction for brachial plexus, microsurgery, tendon transfer, shoulder reconstruction (J Pediatr Orthop 2014;34:S57–S62)
OVERVIEW AND BACKGROUND The incidence of brachial plexus birth palsy (BPBP) is estimated to range from 0.4 to 4 per 1000 live births.1–3 BPBP is thought to be due to a mechanical traction injury to the brachial plexus during the birth process. Perinatal risk factors are often multifactorial and complex, including multiparous pregnancies, previous deliveries resulting in BPBP, prolonged labor, fetal macrosomia, shoulder dystocia, breech delivery, and delivery assisted by vacuum or forceps.2,3 Prognosis is dependent upon the extent of the injury, as well as the timing and type of intervention performed. The literature traditionally cites spontaneous recovery of BPBP as 75% to 95%.4–7 However, more recent reports have suggested a much lower spontaneous recovery rate of 66%, with 10% to 15% left with conFrom the Shriners Hospital for Children Northern California, Sacramento, CA. None of the authors received financial support for this study. The authors declare no conflicts of interest. Reprints: Michelle A. James, MD, Shriners Hospital for Children Northern California, 2425 Stockton Boulevard, Sacramento, CA 95817. E-mail: [email protected]. Copyright r 2014 by Lippincott Williams & Wilkins
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siderable permanent weakness.2,8,9 Narakas10 classified the severity of BPBP along a clinical continuum. Narakas’ type I refers to C5-C6 nerve root involvement, the classic Erb palsy. This is the most common type of BPBP and carries the most favorable prognosis. Type II is an injury to the C5, C6, and C7 nerve roots. This group is the second-most common injury and carries a worse prognosis than type I. Type III is a global plexopathy with injury to the C5, C6, C7, C8, and T1 nerve roots, and type IV is the most severe form, characterized by a global palsy with a flaccid arm combined with Horner syndrome. This indicates involvement of the sympathetic chain and probable avulsion injury.11 It is important to determine whether the level of the nerve injury is preganglionic or postganglionic. The degree and type of postganglionic neural injury is defined by Sunderland12 as neurapraxia, axonotmesis, and neurotmesis, as opposed to preganglionic nerve root avulsions. Neurapraxias are common and have full recovery in the first months of life. Axonotmesis recovery is dependent upon the degree of nerve injury and is more prolonged. Some children with this type of injury may have improved outcomes with surgery. Neurotmesis will not recover without nerve reconstruction. Preganglionic avulsion injuries cannot recover, as the nerve roots have completely disconnected from the spinal cord. On examination, preganglionic injuries are characterized by Horner syndrome (ptosis, miosis, anhidrosis, and enophthalmos), phrenic nerve palsy (elevated hemidiaphragm), and loss of scapular control. Initial evaluation of the infant with BPBP should consist of assessing passive range of motion and active muscle strength. Passive internal and external rotation of the shoulder is measured with the arm adducted, and also abducted to 90 degrees while stabilizing the scapula against the thorax. The measurement of muscle strength is inherently difficult due to the fact that the young infant cannot cooperate with commands given by the examiner. This has led to the development of multiple classification methods to standardize examinations. The British Medical Council system, Modified Mallet classification, Toronto Score Test, and Hospital for Sick Children Active Movement Scores grading systems have all been used, with the latter 3 tests demonstrating interobserver and intraobserver reliability in infants.13 The Toronto Score Test and the Active Movement Scale are especially useful for those children who are unable to follow commands, as they are performed through prompting and observing the child. Serial physical examination is necessary to predict neurological recovery and determine the need for additional intervention. Directed physical therapy should start
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early in infancy and is focused on maintaining passive shoulder range of motion, especially external rotation, with scapular stabilization to prevent muscle contracture and subsequent glenohumeral joint deformity.14 Early (below 3 mo of age) microsurgical intervention is recommended for those with Narakas type IV BPBP, due to the poor prognosis for natural recovery.3,15–17 Reconstruction is limited to nerve transfers, as grafting is not a viable option when the nerve root is avulsed from the spinal cord.18,19 More controversy exists over the management of intraplexus ruptures in which there are varying degrees of injury severity and recovery. Return of antigravity elbow flexion strength is the key factor in determining the need for brachial plexus exploration and nerve reconstruction. A longer delay in the return of biceps function predicts poorer shoulder outcomes at 5 years and an increased need for secondary procedures.16,17 However, controversy continues to exist regarding the exact timing of microsurgical intervention, with most recommending this procedure when antigravity elbow flexion has not returned by 3 to 9 months of age.20–22 Nerve reconstruction procedures are best performed in infancy to allow the greatest potential for recovery of muscle strength. Other interventions, such as muscle transfers and osteotomies, are performed to treat manifestations of BPBP that appear later in childhood.
SHOULDER EVALUATION The natural history of BPBP with incomplete neurological recovery is progressive glenohumeral joint deformity due to muscle imbalance.23 Contracture of the dually innervated internal rotators and adductors versus the weakened external rotators and abductors, primarily the infraspinatus and teres minor muscles,24–26 result in progressive internal rotation and adduction of the humeral head, placing increased stress along the posterior aspect of the glenoid. These deforming forces cause increased retroversion of the glenoid, as well as flattening and posterior subluxation of the humeral head.27,28 Various classification systems have been described to assess the severity of glenohumeral joint deformity that takes these factors into account.23,29 As the glenoid becomes increasingly retroverted, its posterior aspect forms a false articulation (pseudoglenoid) with the humeral head. Several different imaging modalities have been utilized to assess glenohumeral joint development in BPBP, including radiographs, arthrograms, ultrasound, computed tomography (CT) scans, and magnetic resonance imaging (MRI). Plain radiographs and CT scans in the infant with BPBP are of limited value as the glenohumeral joint is largely nonossified cartilage. They will, however, allow visualization of concomitant bony injuries that may be present, such as a humeral shaft or clavicle fractures. Arthrography is not commonly used, as it requires sedation.29 Ultrasonography is a useful tool for evaluating the infant shoulder, as it is a noninvasive technique that does not require sedation and provides images of the nonossified humeral head. Grissom and Harcke30 reported on
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Anterior
FIGURE 1. Ultrasound image of a right shoulder demonstrating infantile shoulder dislocation with pseudoglenoid formation and an a angle of 47 degrees.
the use of sonography to evaluate the shoulder in infants using the posterior approach. Vathana et al31 defined the a angle, which is the angle formed by the intersection of a line through the axis of the scapula and a line tangential to the posterior aspect of the humeral head at the posterior osseous lip of the glenoid. This measurement has high intraobserver and interobserver reliability and can be easily identified on posterior sonographic images (Fig. 1). MRI allows visualization of osseous and soft-tissue structures, as well as observation of glenohumeral joint deformities before complete ossification of the glenoid and humeral head. The glenoscapular angle32 and the percent of the humeral head anterior to the scapular line23 can be calculated on the MRI. The degree of glenohumeral deformity can also be classified as described by Waters et al,23 with type I indicating a normal glenoid; type II, increased glenoid retroversion; and type III, increased glenoid retroversion and posterior humeral head subluxation. Type IV indicates severe deformity with formation of a pseudoglenoid; type V, severe flattening of the humeral head and glenoid; and type VI, complete dislocation of the glenohumeral joint. The degree of deformity noted on the imaging studies can help guide the surgical management of the child with BPBP.
SHOULDER TREATMENT Secondary orthopaedic procedures are often indicated for children with BPBP, regardless of whether or not they have had microsurgical intervention. Although nerve reconstruction is best performed in infancy, other interventions, such as muscle transfers and osteotomies, are performed to treat manifestations of BPBP that appear later in childhood. Indications for surgery about the shoulder include infantile glenohumeral joint dislocation, persistent internal rotation contracture despite maximal nonoperative treatment, limitation of active external rotation and above shoulder-level function with plateauing of neurological recovery, progressive or marked glenohumeral deformity, or a combination of any or all of the r
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above.33 The age at intervention can vary from 6 months through adolescence and is dependent upon severity and when the child presents for care. The general principles that must be addressed in any affected child are muscle imbalance, soft-tissue contracture, and joint deformity. Botulinum toxin type A (off-label) may be used as an adjunct to surgical treatment of BPBP.34 It is used in the young child (up to 2 y of age) with reduced passive shoulder external rotation to prevent dysplastic joint deformity by reducing muscle tone, allowing increased passive range of motion and reduction of the glenohumeral joint. Botulinum toxin type A is injected with a nerve-stimulating needle under general anesthesia into the pectoralis major and subscapularis. Following the injection, the shoulder is placed into a spica cast abducted to 30 to 40 degrees and externally rotated to 60 degrees. The elbow is flexed, the forearm is supinated, and the cast is maintained for 4 to 6 weeks. After the cast is removed, physical therapy is reinitiated to maintain external rotation and joint reduction.33,34 This treatment may be utilized alone or in conjunction with microsurgical reconstruction. Surgeons have attempted to improve shoulder external rotation through anterior capsulotomy, tenotomy, or z-lengthening of the subscapularis and pectoralis major since the 1920s.35 The subscapularis muscle slide was described by Carlioz and Brahimi36 in 1971, and allows for improvement of passive external rotation with less risk of developing an external rotation contracture or losing internal rotation strength than subscapularis tenotomy. Carlioz described the release of the subscapularis muscle origin off of the anterior scapula utilizing a medial scapular incision until 60 to 80 degrees of external rotation in adduction is achieved, followed by application of a shoulder spica cast with the shoulder in external rotation. In 2003, Pearl37 introduced the use of the arthroscopic techniques to achieve the same goals as the above procedures. This intraarticular procedure consists of a subscapularis tenotomy combined with anterior capsular release until 40 to 60 degrees of passive external rotation and reduction of the humeral head is noted (Fig. 2). Care is taken to avoid overrelease of the joint and resultant external rotation contracture. These procedures may be performed in isolation if the young child (6 mo to 2 y) is still showing signs of neurological recovery, or combined with extra-articular tendon transfers in children with glenohumeral joint deformity, subluxation, or dislocation. Tendon transfers are often combined with the above anterior procedures as an adjunct to improve active shoulder external rotation and abduction. Hoffer and Phipps38 modified the L’Episcopo transfer of the latissimus dorsi and teres major by changing the location of the transfer recipient site from the humeral shaft to the posterosuperior aspect of the rotator cuff and was found to result in improved overhead function. If weakness is present, but there is no internal rotation contracture, then tendon transfer alone should restore function. Usually both contracture and weakness are present; in these cases, both an anterior release, either open or arthroscopically, and tendon transfers are performed. The Hoffer modr
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HH
PG
FIGURE 2. Intraoperative arthroscopic image of the patient in Figure 1 demonstrating reduction of the humeral head (HH) into the glenoid and formation of a pseudoglenoid (PG).
ification of the L’Episcopo tendon transfer is the most widely accepted transfer to restore external rotation of the shoulder (Fig. 3). Multiple studies have suggested that improved shoulder motion may be gained with extra-articular procedures, but little correction of underlying osseous deformity occurs without concurrent intra-articular procedures.24,25,39–41 Waters and Bae42 demonstrated an improvement in the grade of dysplasia measured by the glenoid version and percentage of humeral head anterior to the mid-scapular line in 83% of patients with combined intra-articular and extra-articular procedures. Pearl et al43 and Kozin et al44 have both also shown that release of the subscapularis tendon or anterior release of the glenohumeral joint capsule, either in isolation or in combination with extra-articular tendon transfer of the latissimus dorsi and teres major, leads to improved passive external rotation and remodeling of glenoid dysplasia. There are few studies in the literature that examine long-term outcomes for patients who have undergone isolated tendon transfer or tendon transfers in combination with musculotendinous lengthenings, open or arthroscopic joint reductions. Long-term loss of active shoulder range of motion and recurrence of contracture may occur. Preliminary results of recent studies seem to show long-term improvement with a more thorough subscapularis and anterior glenohumeral joint capsular release, such as that described with an arthroscopic approach, but this procedure risks losing internal rotation strength.44 However, the upper limit of dysplasia severity and patient age for the successful application of jointreducing procedures is not clear. Traditionally, in adolescent patients with Waters type V glenohumeral joint deformity, internal rotation contracture, and functional limitations, a humeral derotational osteotomy has been shown to lead to significant clinical improvement.45 This places the hand in a more functional position by reorienting the arc of shoulder motion, allowing improved abduction and external rotation45,46 (Fig. 4). www.pedorthopaedics.com |
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B FIGURE 3. Preoperative (A) and postoperative (B) photographs showing active external rotation in a patient who underwent right arthroscopic anterior release and tendon transfer for external rotation.
Recently, combined glenoid anteversion osteotomy and tendon transfers have been described47 in patients with Waters type III, IV, or V glenohumeral dysplasia. This study showed improvement in passive and active external rotation, Mallet scores, glenoid retroversion, and percentage of the humeral head anterior to the midscapular line in their early outcome data. While investigation continues, this may offer an option for those with more severe glenohumeral joint deformity before requiring humeral osteotomy.
ELBOW DEFORMITY Elbow flexion contracture is a well-recognized sequelae of BPBP, which can impair upper extremity function. Up to 48% of patients with BPBP have an elbow flexion contracture of Z10 degrees, with more than one third of these patients having a contracture of Z30 degrees and up to 6% with a concomitant documented radial head dislocation.48 Contracture is thought to be due to overactivity of the long head of the biceps brachii muscle serving as an additional anterior stabilizer of an abnormal glenohumeral joint.49 Currently, the mainstays of treatment for elbow flexion contracture in children with BPBP are serial casting and nighttime splinting. A recently published treatment algorithm recommends serial casting for contractures of Z40 degrees and nighttime splinting for contractures of 20 to 40 degrees.50
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FOREARM, WRIST, AND HAND Late sequelae of BPBP manifest in the forearm most commonly as a supination contracture, and less frequently as a pronation contracture.51 Both contractures result from the unopposed action of the antagonist muscle. Initially, passive correction of the deformity is possible; however, as the skeleton matures, the deformity becomes fixed due to contracture of the interosseous membrane. These deformities cause a functional and cosmetic disability, leading to difficulties with activities of daily living such as eating, writing, and bimanual activities. In children with a flexible supination contracture, a biceps lengthening through z-plasty and rerouting is performed. This converts the biceps force from that of supination to pronation. When a fixed supination contracture is encountered, correction of the bony anatomy is necessary through osteoclasis or osteotomy.52 A technique recently described by Ezaki and Oishi53 takes advantage of the robust periosteum present in a child and utilizes closed reduction and casting. They create a periosteal tube in the radius and ulna, osteotomize a 2 cm portion of each bone, morselize the osteotomized piece, and place it back in the perosteal tube. A carefully applied, well-molded, long-arm cast holds the new position of the forearm. Extension deficit and ulnar deviation of the wrist results from the relative muscle imbalance due to weakness of the extensor carpi radialis longus and brevis, in comparison with the flexor carpi ulnaris (C8, T1).51 This r
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B FIGURE 4. Preoperative (A) and Postoperative (B) photographs showing active external rotation in a patient who underwent left humeral derotational osteotomy.
can be a difficult problem to address in those affected with BPBP due to lack of potential donor musculotendinous units, particularly in those with global palsy. Potential donors include the flexor carpi ulnaris and the brachioradialis to transfer to the extensor carpi radialis brevis, but are dependent upon the patient’s overall function and goals, as well as availability and strength of donor muscles. Utilizing the flexor carpi ulnaris allows for conversion of a flexion and ulnar deviation force to that of wrist extension. For those with limited or no viable donor muscles, wrist arthrodesis may be considered in an older child to place the hand in a more functional helper position. Absent extrinsic digital and thumb extension may also be found in those with incomplete neurological recovery. A staged approach to tendon transfer is taken in these cases, with priority being placed on wrist, then digital extensor function. This is due to the paucity of available motor donors. Tenodesis and/or arthrodesis may allow for sufficient passive digital motion to allow for use of the hand in activities of daily living.54 Infants and children with BPBP present on a wide clinical spectrum. The management and treatment of each child should be tailored to fit their specific needs. New developments in nerve, soft tissue, and osseous procedures have led to improved outcomes. Children should be referred to a brachial plexus specialist and assessed as early as possible, to follow their clinical improvement over time. Microsurgical procedures are best performed in infancy, whereas interventions such as muscle transfers and osteotomies are used to treat sequelae of BPBP that appear later in childhood. Surgical intervention may be necessary, and there are many options that are now available to the younger patient, which were not utilized in treating BPBP in the past. r
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REFERENCES 1. Foad SL, Mehlman CT, Ying J. The epidemiology of neonatal brachial plexus palsy in the United States. J Bone Joint Surg. 2008; 90A:1258–1264. 2. Hoeksma AF, ter Steeg AM, Nelissen RG, et al. Neurological recovery in obstetric brachial plexus injuries: an historical cohort study. Dev Med Child Neurol. 2004;46:76–83. 3. Waters PM. Obstetric brachial plexus injuries: evaluation and management. J Am Acad Orthop Surg. 1997;5:205–214. 4. Greenwald AG, Schute PC, Shiveley JL. Brachial plexus birth palsy: a 10-year report on the incidence and prognosis. J Pediatr Orthop. 1984;4:689–692. 5. Jackson ST, Hoffer MM, Parrish N. Brachial-plexus palsy in the newborn. J Bone Joint Surg. 1988;70:1217–1220. 6. Michelow BJ, Clarke HM, Curtis CG, et al. The natural history of obstetrical brachial plexus palsy. Plast Reconstr Surg. 1994;93: 675–680. 7. van Ouwerkerk WJR, van der Sluijs JA, Nollet F, et al. Management of obstetric brachial plexus lesions: state of the art and future developments. Childs Nerv Syst. 2000;16:638–644. 8. Noetzel MJ, Park TS, Robinson S, et al. Prospective study of recovery following neonatal brachial plexus injury. J Child Neurol. 2001;16:488–492. 9. Pondaag W, Malessy MJ, van Dijk JG, et al. Natural history of obstetric brachial plexus palsy: a systematic review. Dev Med Child Neurol. 2004;46:138–144. 10. Narakas AO. Obstetrical brachial plexus injuries. In: Lamb DW, ed. The Paralysed Hand, Volume 2. Edinburgh, Scotland: Churchill Livingstone; 1987:116–135. 11. Shenaq SM, Bullocks JM, Dhillon G, et al. Management of infant brachial plexus injuries. Clin Plast Surg. 2005;32:79–98. 12. Sunderland S. Nerves and Nerve Injuries. London, England: Churchill Livingstone; 1978. 13. Bae DS, Waters PM, Zurakowski D. Reliability of three classification systems measuring active motion in brachial plexus birth palsy. J Bone Joint Surg. 2003;85A:1733–1738. 14. Hale HB, Bae DS, Waters PM. Current concepts in the management of brachial plexus birth palsy. J Hand Surg. 2010;35A:322–331. 15. Laurent JP, Lee R, Shenaq S, et al. Neurosurgical correction of upper brachial plexus birth injuries. J Neurosurg. 1993;79:197–203.
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16. Bain JR, Dematteo C, Gjertsen D, et al. Navigating the gray zone: a guideline for surgical decision making in obstetrical brachial plexus injuries. J Neurosurg Pediatr. 2009;3:173–180. 17. Gilbert A, Tassin JL. Surgical repair of the brachial plexus in obstetric paralysis. Chirurgie. 1984;110:70–75. 18. Chuang DC, Mardini S, Ma HS. Surgical strategy for infant obstetrical brachial plexus palsy: experiences at Chang Gung Memorial Hospital. Plast Reconstr Surg. 2005;116:132–142. 19. Noaman HH, Shiha AE, Bahm J. Oberlin’s ulnar nerve transfer to the biceps motor nerve in obstetric brachial plexus palsy: Indications, and good and bad results. Microsurgery. 2004;24: 182–187. 20. Smith NC, Rowan P, Benson LJ, et al. Neonatal brachial plexus palsy: outcome of absent biceps function at three months of age. J Bone Joint Surg. 2004;86:2163–2170. 21. DiTaranto P, Campagna L, Price AE, et al. Outcome following nonoperative treatment of brachial plexus birth injuries. J Child Neurol. 2004;19:87–90. 22. Clarke HM, Curtis CG. An approach to obstetrical brachial plexus injuries. Hand Clin. 1995;11:563–580; discussion 580–581. 23. Waters PM, Smith GR, Jaramillo D. Glenohumeral deformity secondary to brachial plexus birth palsy. J Bone Joint Surg. 1998; 80A:668–677. 24. Kozin SH, Chafetz RS, Barus D, et al. Magnetic resonance imaging and clinical findings before and after tendon transfers about the shoulder in children with residual brachial plexus birth palsy. J Shoulder Elbow Surg. 2006;15:554–561. 25. Newman CJ, Morrison L, Lynch B, et al. Outcome of subscapularis muscle release for shoulder contracture secondary to brachial plexus palsy at birth. J Pediatr Orthop. 2006;26:647–651. 26. Waters PM, Monica JT, Earp BE, et al. Correlation of radiographic muscle cross-sectional area with glenohumeral deformity in children with brachial plexus birth palsy. J Bone Joint Surg. 2009;91A: 2367–2375. 27. Po¨yhia¨ TH, Nietosvaara YA, Remes VM, et al. MRI of rotator cuff muscle atrophy in relation to glenohumeral joint incongruence in brachial plexus birth injury. Pediatr Radiol. 2005;35:402– 409. 28. van Gelein Vitringa VM, van Kooten EO, Jaspers RT, et al. An MRI study on the relations between muscle atrophy, shoulder function and glenohumeral deformity in shoulders of children with obstetric brachial plexus injury. J Brachial Plex Peripher Nerve Inj. 2009;4:9. 29. Pearl ML, Edgerton BW. Glenoid deformity secondary to brachial plexus birth palsy. J Bone Joint Surg. 1998;80A:659–667. 30. Grissom LE, Harcke HT. Infant shoulder sonography: technique, anatomy, and pathology. Pediatr Radiol. 2001;31:863–868. 31. Vathana T, Rust S, Mills J, et al. Intraobserver and interobserver reliability of two ultrasound measures of humeral head position in infants with neonatal brachial plexus palsy. J Bone Joint Surg. 2007;89:1710–1715. 32. Friedman RJ, Hawthorne KB, Genez BM. The use of computerized tomography in the measurement of glenoid version. J Bone Joint Surg. 1992;74A:1032–1037. 33. Waters PM, Bae DS. Pediatric Hand and Upper Limb Surgery: A Practical Guide. Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins Print; 2012. Print. 34. Ezaki M, Malungpaishrope K, Harrison RJ, et al. OnabotulinumtoxinA injection as an adjunct in the treatment of posterior shoulder subluxation in neonatal brachial plexus palsy. J Bone Joint Surg. 2010;92:2171–2177.
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35. Sever JW. Obstetric paralysis: report of eleven hundred cases. JAMA. 1925;85:1862–1865. 36. Carlioz H, Brahimi L. Place of internal disinsertion of the subscapularis muscle in the treatment of obstetric paralysis of the upper limb in children. Ann Chir Infant. 1971;12:159–167. 37. Pearl ML. Arthroscopic release of shoulder contracture secondary to birth palsy: an early report on findings and surgical technique. Arthroscopy. 2003;19:577–582. 38. Hoffer MM, Phipps GJ. Closed reduction and tendon transfer for treatment of dislocation of the glenohumeral joint secondary to brachial plexus birth palsy. J Bone Joint Surg. 1998;80:997–1001. 39. Waters PM, Bae DS. Effect of tendon transfers and extra-articular soft-tissue balancing on glenohumeral development in brachial plexus birth palsy. J Bone Joint Surg. 2005;87A:320–325. 40. El-Gammal TA, Saleh WR, El-Sayed A, et al. Tendon transfer around the shoulder in obstetric brachial plexus paralysis: clinical and computed tomographic study. J Pediatr Orthop. 2006;26: 641–646. 41. Kozin SH, Chafetz RS, Shaffer A, et al. Magnetic resonance imaging and clinical findings before and after tendon transfers about the shoulder in children with residual brachial plexus birth palsy: a 3-year follow-up study. J Pediatr Orthop. 2010;30:154–160. 42. Waters PM, Bae DS. The early effects of tendon transfers and open capsulorrhaphy on glenohumeral deformity in brachial plexus birth palsy. J Bone Joint Surg. 2008;90:2171–2179. 43. Pearl ML, Edgerton BW, Kazimiroff PA, et al. Arthroscopic release and latissimus dorsi transfer for shoulder internal rotation contractures and glenohumeral deformity secondary to brachial plexus birth palsy. J Bone Joint Surg. 2006;88A:564–574. 44. Kozin SH, Boardman MJ, Chafetz RS, et al. Arthroscopic treatment of internal rotation contracture and glenohumeral dysplasia in children with brachial plexus birth palsy. J Shoulder Elbow Surg. 2010;19:102–110. 45. Waters PM, Bae DS. The effect of derotational humeral osteotomy on global shoulder function in brachial plexus birth palsy. J Bone Joint Surg. 2006;88A:1035–1042. 46. Kirkos JM, Kyrkos MJ, Kapetanos GA, et al. Brachial plexus palsy secondary to birth injuries. J Bone Joint Surg. 2005;87B:231–235. 47. Dodwell E, O’Callaghan J, Anthony A, et al. Combined glenoid anteversion osteotomy and tendon transfers for brachial plexus birth palsy. J Bone Joint Surg. 2012;94:2145–2152. 48. Sheffler LC, Lattanza L, Hagar Y, et al. The prevalence, rate of progression, and treatment of elbow flexion contracture in children with brachial plexus birth palsy. J Bone Joint Surg. 2012;94:403–409. 49. Sheffler LC, Lattanza L, Sison-Williamson M, et al. Biceps brachii long head overactivity associated with elbow flexion contracture in brachial plexus birth palsy. J Bone Joint Surg. 2012;94:289–297. 50. Ho ES, Roy T, Stephens D, et al. Serial casting and splinting of elbow contractures in children with obstetric brachial plexus palsy. J Hand Surg. 2010;35:84–91. 51. Zancolli EA, Zancolli ER. Palliative surgical procedures in sequelae of obstetric palsy. Hand Clin. 1988;4:643–669. 52. Sebastin SJ, Chung KC. Pathogenesis and management of deformities of the elbow, wrist, and hand in late neonatal brachial plexus palsy. J Pediar Rehabil Med. 2011;4:119–130. 53. Ezaki M, Oishi SN. Technique of forearm osteotomy for pediatric problems. J Hand Surg. 2012;37A:2400–2403. 54. Ruchelsman DE, Ramos LE, Price AE, et al. Outcome after tendon transfers to restore wrist extension in children with brachial plexus birth injuries. J Pediatr Orthop. 2011;31:455–457.
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Abstract: Brachial plexus birth palsy (BPBP) presents to the physician on a clinical spectrum, and may substantially impair the child. Potential interventions to improve function for the child with BPBP include physical therapy, microsurgical nerve reconstruction and nerve transfers, soft-tissue balancing and reconstruction with musculotendinous transfers, and osteotomies. Some interventions, such as nerve reconstruction, are best performed in infancy; others, such as muscle transfers and osteotomies, are performed to treat manifestations of this condition that appear later in childhood. Although controversy continues to exist regarding the natural history and surgical management of these patients, recent literature has improved our understanding of surgical indications, anticipated outcomes, and potential complications. On the basis of current evidence, we present here the recommendations for surgical intervention in the upper extremity of children with BPBP, and encourage early referral to a brachial plexus specialist to establish care. Key Words: brachial plexus birth palsy, late reconstruction for brachial plexus, microsurgery, tendon transfer, shoulder reconstruction (J Pediatr Orthop 2014;34:S57–S62)
OVERVIEW AND BACKGROUND The incidence of brachial plexus birth palsy (BPBP) is estimated to range from 0.4 to 4 per 1000 live births.1–3 BPBP is thought to be due to a mechanical traction injury to the brachial plexus during the birth process. Perinatal risk factors are often multifactorial and complex, including multiparous pregnancies, previous deliveries resulting in BPBP, prolonged labor, fetal macrosomia, shoulder dystocia, breech delivery, and delivery assisted by vacuum or forceps.2,3 Prognosis is dependent upon the extent of the injury, as well as the timing and type of intervention performed. The literature traditionally cites spontaneous recovery of BPBP as 75% to 95%.4–7 However, more recent reports have suggested a much lower spontaneous recovery rate of 66%, with 10% to 15% left with conFrom the Shriners Hospital for Children Northern California, Sacramento, CA. None of the authors received financial support for this study. The authors declare no conflicts of interest. Reprints: Michelle A. James, MD, Shriners Hospital for Children Northern California, 2425 Stockton Boulevard, Sacramento, CA 95817. E-mail: [email protected]. Copyright r 2014 by Lippincott Williams & Wilkins
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siderable permanent weakness.2,8,9 Narakas10 classified the severity of BPBP along a clinical continuum. Narakas’ type I refers to C5-C6 nerve root involvement, the classic Erb palsy. This is the most common type of BPBP and carries the most favorable prognosis. Type II is an injury to the C5, C6, and C7 nerve roots. This group is the second-most common injury and carries a worse prognosis than type I. Type III is a global plexopathy with injury to the C5, C6, C7, C8, and T1 nerve roots, and type IV is the most severe form, characterized by a global palsy with a flaccid arm combined with Horner syndrome. This indicates involvement of the sympathetic chain and probable avulsion injury.11 It is important to determine whether the level of the nerve injury is preganglionic or postganglionic. The degree and type of postganglionic neural injury is defined by Sunderland12 as neurapraxia, axonotmesis, and neurotmesis, as opposed to preganglionic nerve root avulsions. Neurapraxias are common and have full recovery in the first months of life. Axonotmesis recovery is dependent upon the degree of nerve injury and is more prolonged. Some children with this type of injury may have improved outcomes with surgery. Neurotmesis will not recover without nerve reconstruction. Preganglionic avulsion injuries cannot recover, as the nerve roots have completely disconnected from the spinal cord. On examination, preganglionic injuries are characterized by Horner syndrome (ptosis, miosis, anhidrosis, and enophthalmos), phrenic nerve palsy (elevated hemidiaphragm), and loss of scapular control. Initial evaluation of the infant with BPBP should consist of assessing passive range of motion and active muscle strength. Passive internal and external rotation of the shoulder is measured with the arm adducted, and also abducted to 90 degrees while stabilizing the scapula against the thorax. The measurement of muscle strength is inherently difficult due to the fact that the young infant cannot cooperate with commands given by the examiner. This has led to the development of multiple classification methods to standardize examinations. The British Medical Council system, Modified Mallet classification, Toronto Score Test, and Hospital for Sick Children Active Movement Scores grading systems have all been used, with the latter 3 tests demonstrating interobserver and intraobserver reliability in infants.13 The Toronto Score Test and the Active Movement Scale are especially useful for those children who are unable to follow commands, as they are performed through prompting and observing the child. Serial physical examination is necessary to predict neurological recovery and determine the need for additional intervention. Directed physical therapy should start
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early in infancy and is focused on maintaining passive shoulder range of motion, especially external rotation, with scapular stabilization to prevent muscle contracture and subsequent glenohumeral joint deformity.14 Early (below 3 mo of age) microsurgical intervention is recommended for those with Narakas type IV BPBP, due to the poor prognosis for natural recovery.3,15–17 Reconstruction is limited to nerve transfers, as grafting is not a viable option when the nerve root is avulsed from the spinal cord.18,19 More controversy exists over the management of intraplexus ruptures in which there are varying degrees of injury severity and recovery. Return of antigravity elbow flexion strength is the key factor in determining the need for brachial plexus exploration and nerve reconstruction. A longer delay in the return of biceps function predicts poorer shoulder outcomes at 5 years and an increased need for secondary procedures.16,17 However, controversy continues to exist regarding the exact timing of microsurgical intervention, with most recommending this procedure when antigravity elbow flexion has not returned by 3 to 9 months of age.20–22 Nerve reconstruction procedures are best performed in infancy to allow the greatest potential for recovery of muscle strength. Other interventions, such as muscle transfers and osteotomies, are performed to treat manifestations of BPBP that appear later in childhood.
SHOULDER EVALUATION The natural history of BPBP with incomplete neurological recovery is progressive glenohumeral joint deformity due to muscle imbalance.23 Contracture of the dually innervated internal rotators and adductors versus the weakened external rotators and abductors, primarily the infraspinatus and teres minor muscles,24–26 result in progressive internal rotation and adduction of the humeral head, placing increased stress along the posterior aspect of the glenoid. These deforming forces cause increased retroversion of the glenoid, as well as flattening and posterior subluxation of the humeral head.27,28 Various classification systems have been described to assess the severity of glenohumeral joint deformity that takes these factors into account.23,29 As the glenoid becomes increasingly retroverted, its posterior aspect forms a false articulation (pseudoglenoid) with the humeral head. Several different imaging modalities have been utilized to assess glenohumeral joint development in BPBP, including radiographs, arthrograms, ultrasound, computed tomography (CT) scans, and magnetic resonance imaging (MRI). Plain radiographs and CT scans in the infant with BPBP are of limited value as the glenohumeral joint is largely nonossified cartilage. They will, however, allow visualization of concomitant bony injuries that may be present, such as a humeral shaft or clavicle fractures. Arthrography is not commonly used, as it requires sedation.29 Ultrasonography is a useful tool for evaluating the infant shoulder, as it is a noninvasive technique that does not require sedation and provides images of the nonossified humeral head. Grissom and Harcke30 reported on
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Anterior
FIGURE 1. Ultrasound image of a right shoulder demonstrating infantile shoulder dislocation with pseudoglenoid formation and an a angle of 47 degrees.
the use of sonography to evaluate the shoulder in infants using the posterior approach. Vathana et al31 defined the a angle, which is the angle formed by the intersection of a line through the axis of the scapula and a line tangential to the posterior aspect of the humeral head at the posterior osseous lip of the glenoid. This measurement has high intraobserver and interobserver reliability and can be easily identified on posterior sonographic images (Fig. 1). MRI allows visualization of osseous and soft-tissue structures, as well as observation of glenohumeral joint deformities before complete ossification of the glenoid and humeral head. The glenoscapular angle32 and the percent of the humeral head anterior to the scapular line23 can be calculated on the MRI. The degree of glenohumeral deformity can also be classified as described by Waters et al,23 with type I indicating a normal glenoid; type II, increased glenoid retroversion; and type III, increased glenoid retroversion and posterior humeral head subluxation. Type IV indicates severe deformity with formation of a pseudoglenoid; type V, severe flattening of the humeral head and glenoid; and type VI, complete dislocation of the glenohumeral joint. The degree of deformity noted on the imaging studies can help guide the surgical management of the child with BPBP.
SHOULDER TREATMENT Secondary orthopaedic procedures are often indicated for children with BPBP, regardless of whether or not they have had microsurgical intervention. Although nerve reconstruction is best performed in infancy, other interventions, such as muscle transfers and osteotomies, are performed to treat manifestations of BPBP that appear later in childhood. Indications for surgery about the shoulder include infantile glenohumeral joint dislocation, persistent internal rotation contracture despite maximal nonoperative treatment, limitation of active external rotation and above shoulder-level function with plateauing of neurological recovery, progressive or marked glenohumeral deformity, or a combination of any or all of the r
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above.33 The age at intervention can vary from 6 months through adolescence and is dependent upon severity and when the child presents for care. The general principles that must be addressed in any affected child are muscle imbalance, soft-tissue contracture, and joint deformity. Botulinum toxin type A (off-label) may be used as an adjunct to surgical treatment of BPBP.34 It is used in the young child (up to 2 y of age) with reduced passive shoulder external rotation to prevent dysplastic joint deformity by reducing muscle tone, allowing increased passive range of motion and reduction of the glenohumeral joint. Botulinum toxin type A is injected with a nerve-stimulating needle under general anesthesia into the pectoralis major and subscapularis. Following the injection, the shoulder is placed into a spica cast abducted to 30 to 40 degrees and externally rotated to 60 degrees. The elbow is flexed, the forearm is supinated, and the cast is maintained for 4 to 6 weeks. After the cast is removed, physical therapy is reinitiated to maintain external rotation and joint reduction.33,34 This treatment may be utilized alone or in conjunction with microsurgical reconstruction. Surgeons have attempted to improve shoulder external rotation through anterior capsulotomy, tenotomy, or z-lengthening of the subscapularis and pectoralis major since the 1920s.35 The subscapularis muscle slide was described by Carlioz and Brahimi36 in 1971, and allows for improvement of passive external rotation with less risk of developing an external rotation contracture or losing internal rotation strength than subscapularis tenotomy. Carlioz described the release of the subscapularis muscle origin off of the anterior scapula utilizing a medial scapular incision until 60 to 80 degrees of external rotation in adduction is achieved, followed by application of a shoulder spica cast with the shoulder in external rotation. In 2003, Pearl37 introduced the use of the arthroscopic techniques to achieve the same goals as the above procedures. This intraarticular procedure consists of a subscapularis tenotomy combined with anterior capsular release until 40 to 60 degrees of passive external rotation and reduction of the humeral head is noted (Fig. 2). Care is taken to avoid overrelease of the joint and resultant external rotation contracture. These procedures may be performed in isolation if the young child (6 mo to 2 y) is still showing signs of neurological recovery, or combined with extra-articular tendon transfers in children with glenohumeral joint deformity, subluxation, or dislocation. Tendon transfers are often combined with the above anterior procedures as an adjunct to improve active shoulder external rotation and abduction. Hoffer and Phipps38 modified the L’Episcopo transfer of the latissimus dorsi and teres major by changing the location of the transfer recipient site from the humeral shaft to the posterosuperior aspect of the rotator cuff and was found to result in improved overhead function. If weakness is present, but there is no internal rotation contracture, then tendon transfer alone should restore function. Usually both contracture and weakness are present; in these cases, both an anterior release, either open or arthroscopically, and tendon transfers are performed. The Hoffer modr
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HH
PG
FIGURE 2. Intraoperative arthroscopic image of the patient in Figure 1 demonstrating reduction of the humeral head (HH) into the glenoid and formation of a pseudoglenoid (PG).
ification of the L’Episcopo tendon transfer is the most widely accepted transfer to restore external rotation of the shoulder (Fig. 3). Multiple studies have suggested that improved shoulder motion may be gained with extra-articular procedures, but little correction of underlying osseous deformity occurs without concurrent intra-articular procedures.24,25,39–41 Waters and Bae42 demonstrated an improvement in the grade of dysplasia measured by the glenoid version and percentage of humeral head anterior to the mid-scapular line in 83% of patients with combined intra-articular and extra-articular procedures. Pearl et al43 and Kozin et al44 have both also shown that release of the subscapularis tendon or anterior release of the glenohumeral joint capsule, either in isolation or in combination with extra-articular tendon transfer of the latissimus dorsi and teres major, leads to improved passive external rotation and remodeling of glenoid dysplasia. There are few studies in the literature that examine long-term outcomes for patients who have undergone isolated tendon transfer or tendon transfers in combination with musculotendinous lengthenings, open or arthroscopic joint reductions. Long-term loss of active shoulder range of motion and recurrence of contracture may occur. Preliminary results of recent studies seem to show long-term improvement with a more thorough subscapularis and anterior glenohumeral joint capsular release, such as that described with an arthroscopic approach, but this procedure risks losing internal rotation strength.44 However, the upper limit of dysplasia severity and patient age for the successful application of jointreducing procedures is not clear. Traditionally, in adolescent patients with Waters type V glenohumeral joint deformity, internal rotation contracture, and functional limitations, a humeral derotational osteotomy has been shown to lead to significant clinical improvement.45 This places the hand in a more functional position by reorienting the arc of shoulder motion, allowing improved abduction and external rotation45,46 (Fig. 4). www.pedorthopaedics.com |
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A
B FIGURE 3. Preoperative (A) and postoperative (B) photographs showing active external rotation in a patient who underwent right arthroscopic anterior release and tendon transfer for external rotation.
Recently, combined glenoid anteversion osteotomy and tendon transfers have been described47 in patients with Waters type III, IV, or V glenohumeral dysplasia. This study showed improvement in passive and active external rotation, Mallet scores, glenoid retroversion, and percentage of the humeral head anterior to the midscapular line in their early outcome data. While investigation continues, this may offer an option for those with more severe glenohumeral joint deformity before requiring humeral osteotomy.
ELBOW DEFORMITY Elbow flexion contracture is a well-recognized sequelae of BPBP, which can impair upper extremity function. Up to 48% of patients with BPBP have an elbow flexion contracture of Z10 degrees, with more than one third of these patients having a contracture of Z30 degrees and up to 6% with a concomitant documented radial head dislocation.48 Contracture is thought to be due to overactivity of the long head of the biceps brachii muscle serving as an additional anterior stabilizer of an abnormal glenohumeral joint.49 Currently, the mainstays of treatment for elbow flexion contracture in children with BPBP are serial casting and nighttime splinting. A recently published treatment algorithm recommends serial casting for contractures of Z40 degrees and nighttime splinting for contractures of 20 to 40 degrees.50
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FOREARM, WRIST, AND HAND Late sequelae of BPBP manifest in the forearm most commonly as a supination contracture, and less frequently as a pronation contracture.51 Both contractures result from the unopposed action of the antagonist muscle. Initially, passive correction of the deformity is possible; however, as the skeleton matures, the deformity becomes fixed due to contracture of the interosseous membrane. These deformities cause a functional and cosmetic disability, leading to difficulties with activities of daily living such as eating, writing, and bimanual activities. In children with a flexible supination contracture, a biceps lengthening through z-plasty and rerouting is performed. This converts the biceps force from that of supination to pronation. When a fixed supination contracture is encountered, correction of the bony anatomy is necessary through osteoclasis or osteotomy.52 A technique recently described by Ezaki and Oishi53 takes advantage of the robust periosteum present in a child and utilizes closed reduction and casting. They create a periosteal tube in the radius and ulna, osteotomize a 2 cm portion of each bone, morselize the osteotomized piece, and place it back in the perosteal tube. A carefully applied, well-molded, long-arm cast holds the new position of the forearm. Extension deficit and ulnar deviation of the wrist results from the relative muscle imbalance due to weakness of the extensor carpi radialis longus and brevis, in comparison with the flexor carpi ulnaris (C8, T1).51 This r
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B FIGURE 4. Preoperative (A) and Postoperative (B) photographs showing active external rotation in a patient who underwent left humeral derotational osteotomy.
can be a difficult problem to address in those affected with BPBP due to lack of potential donor musculotendinous units, particularly in those with global palsy. Potential donors include the flexor carpi ulnaris and the brachioradialis to transfer to the extensor carpi radialis brevis, but are dependent upon the patient’s overall function and goals, as well as availability and strength of donor muscles. Utilizing the flexor carpi ulnaris allows for conversion of a flexion and ulnar deviation force to that of wrist extension. For those with limited or no viable donor muscles, wrist arthrodesis may be considered in an older child to place the hand in a more functional helper position. Absent extrinsic digital and thumb extension may also be found in those with incomplete neurological recovery. A staged approach to tendon transfer is taken in these cases, with priority being placed on wrist, then digital extensor function. This is due to the paucity of available motor donors. Tenodesis and/or arthrodesis may allow for sufficient passive digital motion to allow for use of the hand in activities of daily living.54 Infants and children with BPBP present on a wide clinical spectrum. The management and treatment of each child should be tailored to fit their specific needs. New developments in nerve, soft tissue, and osseous procedures have led to improved outcomes. Children should be referred to a brachial plexus specialist and assessed as early as possible, to follow their clinical improvement over time. Microsurgical procedures are best performed in infancy, whereas interventions such as muscle transfers and osteotomies are used to treat sequelae of BPBP that appear later in childhood. Surgical intervention may be necessary, and there are many options that are now available to the younger patient, which were not utilized in treating BPBP in the past. r
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REFERENCES 1. Foad SL, Mehlman CT, Ying J. The epidemiology of neonatal brachial plexus palsy in the United States. J Bone Joint Surg. 2008; 90A:1258–1264. 2. Hoeksma AF, ter Steeg AM, Nelissen RG, et al. Neurological recovery in obstetric brachial plexus injuries: an historical cohort study. Dev Med Child Neurol. 2004;46:76–83. 3. Waters PM. Obstetric brachial plexus injuries: evaluation and management. J Am Acad Orthop Surg. 1997;5:205–214. 4. Greenwald AG, Schute PC, Shiveley JL. Brachial plexus birth palsy: a 10-year report on the incidence and prognosis. J Pediatr Orthop. 1984;4:689–692. 5. Jackson ST, Hoffer MM, Parrish N. Brachial-plexus palsy in the newborn. J Bone Joint Surg. 1988;70:1217–1220. 6. Michelow BJ, Clarke HM, Curtis CG, et al. The natural history of obstetrical brachial plexus palsy. Plast Reconstr Surg. 1994;93: 675–680. 7. van Ouwerkerk WJR, van der Sluijs JA, Nollet F, et al. Management of obstetric brachial plexus lesions: state of the art and future developments. Childs Nerv Syst. 2000;16:638–644. 8. Noetzel MJ, Park TS, Robinson S, et al. Prospective study of recovery following neonatal brachial plexus injury. J Child Neurol. 2001;16:488–492. 9. Pondaag W, Malessy MJ, van Dijk JG, et al. Natural history of obstetric brachial plexus palsy: a systematic review. Dev Med Child Neurol. 2004;46:138–144. 10. Narakas AO. Obstetrical brachial plexus injuries. In: Lamb DW, ed. The Paralysed Hand, Volume 2. Edinburgh, Scotland: Churchill Livingstone; 1987:116–135. 11. Shenaq SM, Bullocks JM, Dhillon G, et al. Management of infant brachial plexus injuries. Clin Plast Surg. 2005;32:79–98. 12. Sunderland S. Nerves and Nerve Injuries. London, England: Churchill Livingstone; 1978. 13. Bae DS, Waters PM, Zurakowski D. Reliability of three classification systems measuring active motion in brachial plexus birth palsy. J Bone Joint Surg. 2003;85A:1733–1738. 14. Hale HB, Bae DS, Waters PM. Current concepts in the management of brachial plexus birth palsy. J Hand Surg. 2010;35A:322–331. 15. Laurent JP, Lee R, Shenaq S, et al. Neurosurgical correction of upper brachial plexus birth injuries. J Neurosurg. 1993;79:197–203.
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16. Bain JR, Dematteo C, Gjertsen D, et al. Navigating the gray zone: a guideline for surgical decision making in obstetrical brachial plexus injuries. J Neurosurg Pediatr. 2009;3:173–180. 17. Gilbert A, Tassin JL. Surgical repair of the brachial plexus in obstetric paralysis. Chirurgie. 1984;110:70–75. 18. Chuang DC, Mardini S, Ma HS. Surgical strategy for infant obstetrical brachial plexus palsy: experiences at Chang Gung Memorial Hospital. Plast Reconstr Surg. 2005;116:132–142. 19. Noaman HH, Shiha AE, Bahm J. Oberlin’s ulnar nerve transfer to the biceps motor nerve in obstetric brachial plexus palsy: Indications, and good and bad results. Microsurgery. 2004;24: 182–187. 20. Smith NC, Rowan P, Benson LJ, et al. Neonatal brachial plexus palsy: outcome of absent biceps function at three months of age. J Bone Joint Surg. 2004;86:2163–2170. 21. DiTaranto P, Campagna L, Price AE, et al. Outcome following nonoperative treatment of brachial plexus birth injuries. J Child Neurol. 2004;19:87–90. 22. Clarke HM, Curtis CG. An approach to obstetrical brachial plexus injuries. Hand Clin. 1995;11:563–580; discussion 580–581. 23. Waters PM, Smith GR, Jaramillo D. Glenohumeral deformity secondary to brachial plexus birth palsy. J Bone Joint Surg. 1998; 80A:668–677. 24. Kozin SH, Chafetz RS, Barus D, et al. Magnetic resonance imaging and clinical findings before and after tendon transfers about the shoulder in children with residual brachial plexus birth palsy. J Shoulder Elbow Surg. 2006;15:554–561. 25. Newman CJ, Morrison L, Lynch B, et al. Outcome of subscapularis muscle release for shoulder contracture secondary to brachial plexus palsy at birth. J Pediatr Orthop. 2006;26:647–651. 26. Waters PM, Monica JT, Earp BE, et al. Correlation of radiographic muscle cross-sectional area with glenohumeral deformity in children with brachial plexus birth palsy. J Bone Joint Surg. 2009;91A: 2367–2375. 27. Po¨yhia¨ TH, Nietosvaara YA, Remes VM, et al. MRI of rotator cuff muscle atrophy in relation to glenohumeral joint incongruence in brachial plexus birth injury. Pediatr Radiol. 2005;35:402– 409. 28. van Gelein Vitringa VM, van Kooten EO, Jaspers RT, et al. An MRI study on the relations between muscle atrophy, shoulder function and glenohumeral deformity in shoulders of children with obstetric brachial plexus injury. J Brachial Plex Peripher Nerve Inj. 2009;4:9. 29. Pearl ML, Edgerton BW. Glenoid deformity secondary to brachial plexus birth palsy. J Bone Joint Surg. 1998;80A:659–667. 30. Grissom LE, Harcke HT. Infant shoulder sonography: technique, anatomy, and pathology. Pediatr Radiol. 2001;31:863–868. 31. Vathana T, Rust S, Mills J, et al. Intraobserver and interobserver reliability of two ultrasound measures of humeral head position in infants with neonatal brachial plexus palsy. J Bone Joint Surg. 2007;89:1710–1715. 32. Friedman RJ, Hawthorne KB, Genez BM. The use of computerized tomography in the measurement of glenoid version. J Bone Joint Surg. 1992;74A:1032–1037. 33. Waters PM, Bae DS. Pediatric Hand and Upper Limb Surgery: A Practical Guide. Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins Print; 2012. Print. 34. Ezaki M, Malungpaishrope K, Harrison RJ, et al. OnabotulinumtoxinA injection as an adjunct in the treatment of posterior shoulder subluxation in neonatal brachial plexus palsy. J Bone Joint Surg. 2010;92:2171–2177.
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35. Sever JW. Obstetric paralysis: report of eleven hundred cases. JAMA. 1925;85:1862–1865. 36. Carlioz H, Brahimi L. Place of internal disinsertion of the subscapularis muscle in the treatment of obstetric paralysis of the upper limb in children. Ann Chir Infant. 1971;12:159–167. 37. Pearl ML. Arthroscopic release of shoulder contracture secondary to birth palsy: an early report on findings and surgical technique. Arthroscopy. 2003;19:577–582. 38. Hoffer MM, Phipps GJ. Closed reduction and tendon transfer for treatment of dislocation of the glenohumeral joint secondary to brachial plexus birth palsy. J Bone Joint Surg. 1998;80:997–1001. 39. Waters PM, Bae DS. Effect of tendon transfers and extra-articular soft-tissue balancing on glenohumeral development in brachial plexus birth palsy. J Bone Joint Surg. 2005;87A:320–325. 40. El-Gammal TA, Saleh WR, El-Sayed A, et al. Tendon transfer around the shoulder in obstetric brachial plexus paralysis: clinical and computed tomographic study. J Pediatr Orthop. 2006;26: 641–646. 41. Kozin SH, Chafetz RS, Shaffer A, et al. Magnetic resonance imaging and clinical findings before and after tendon transfers about the shoulder in children with residual brachial plexus birth palsy: a 3-year follow-up study. J Pediatr Orthop. 2010;30:154–160. 42. Waters PM, Bae DS. The early effects of tendon transfers and open capsulorrhaphy on glenohumeral deformity in brachial plexus birth palsy. J Bone Joint Surg. 2008;90:2171–2179. 43. Pearl ML, Edgerton BW, Kazimiroff PA, et al. Arthroscopic release and latissimus dorsi transfer for shoulder internal rotation contractures and glenohumeral deformity secondary to brachial plexus birth palsy. J Bone Joint Surg. 2006;88A:564–574. 44. Kozin SH, Boardman MJ, Chafetz RS, et al. Arthroscopic treatment of internal rotation contracture and glenohumeral dysplasia in children with brachial plexus birth palsy. J Shoulder Elbow Surg. 2010;19:102–110. 45. Waters PM, Bae DS. The effect of derotational humeral osteotomy on global shoulder function in brachial plexus birth palsy. J Bone Joint Surg. 2006;88A:1035–1042. 46. Kirkos JM, Kyrkos MJ, Kapetanos GA, et al. Brachial plexus palsy secondary to birth injuries. J Bone Joint Surg. 2005;87B:231–235. 47. Dodwell E, O’Callaghan J, Anthony A, et al. Combined glenoid anteversion osteotomy and tendon transfers for brachial plexus birth palsy. J Bone Joint Surg. 2012;94:2145–2152. 48. Sheffler LC, Lattanza L, Hagar Y, et al. The prevalence, rate of progression, and treatment of elbow flexion contracture in children with brachial plexus birth palsy. J Bone Joint Surg. 2012;94:403–409. 49. Sheffler LC, Lattanza L, Sison-Williamson M, et al. Biceps brachii long head overactivity associated with elbow flexion contracture in brachial plexus birth palsy. J Bone Joint Surg. 2012;94:289–297. 50. Ho ES, Roy T, Stephens D, et al. Serial casting and splinting of elbow contractures in children with obstetric brachial plexus palsy. J Hand Surg. 2010;35:84–91. 51. Zancolli EA, Zancolli ER. Palliative surgical procedures in sequelae of obstetric palsy. Hand Clin. 1988;4:643–669. 52. Sebastin SJ, Chung KC. Pathogenesis and management of deformities of the elbow, wrist, and hand in late neonatal brachial plexus palsy. J Pediar Rehabil Med. 2011;4:119–130. 53. Ezaki M, Oishi SN. Technique of forearm osteotomy for pediatric problems. J Hand Surg. 2012;37A:2400–2403. 54. Ruchelsman DE, Ramos LE, Price AE, et al. Outcome after tendon transfers to restore wrist extension in children with brachial plexus birth injuries. J Pediatr Orthop. 2011;31:455–457.
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