Infantile Brachial Plexus Injury

Intro

Neonatal brachial plexus palsy (NBPP), defined as weakness or flaccid paralysis of the upper extremity diagnosed soon after birth, results from injury of one or more cervical and thoracic nerve roots (C5–T1) (1). The global incidence of NBPP ranges between 0.38 and 5.1/1,000 live births, with regional variations depending on study setting (e.g., single centre, select populations), population-based data, and the availability of maternal-fetal care (2–5). The incidence of NBPP in Canada, based on Canadian Institute for Health Information (CIHI) data, has been estimated at 1.24/1,000 live births, with rates remaining stable from 2004 to 2012 (6). NBPP is often a debilitating condition with long-term effects. Apart from physical and functional impairments, NBPP can impact family dynamics, a child’s global development, and quality of life (

Neonatal brachial plexus palsy (NBPP) is reported worldwidein 0.1 to 8.1 per 1000 live births.1–6Incidence rates vary withstudy type and the availability of maternal and fetal care.7–9NBPP is the result of a closed nerve stretch injury to the bra-chial plexus, mostly occurring during labour. The mecha-nisms of injury include maternal, obstetric, and infant factorsthat apply traction on the anatomically vulnerable plexu'

Risk factors

he incidence of NBPP is decreasing. Shoulder dystocia, macrosomia,maternal diabetes, instrumental delivery, and breech delivery are risk factors for NBPP.Caesarean section appears as a protective facto

Neonatal Brachial Plexus Palsy (NBPP) is caused by traction of the brachial plexus during birth and can limit the function of the affected arm in various ways. It is the most common form of peripheral neuropathy, with an incidence rate of 0.5–2 cases per 1000 newborns in developed countries [1,2,3].

The causes associated with NBPP are macrosomia, breech/pelvic birth, diabetes in pregnancy, shoulder dystocia, small stature/cephalopelvic disproportion, primiparity, or a prolonged expulsion phase [4,5].

The clinical classification of NBPP is based on body structures, namely the complex of nerves that controls the affected finger, hand, arm, and shoulder muscles. In this sense, brachial plexus lesions are classified as “severing of the upper trunk” when the affected nerves are C5 and C6; “severing of the middle trunk” when the affected nerve is C7; and “severing of the lower trunk” when the affected nerves are C8 and T1. Finally, complete severing is considered when affecting C5–T1 nerves [6].

NBPP, in addition to being classified by considering the affected nerve roots, is also categorized according to the degree of lesion that affects the nerve and also to the function of the injured limb. According to the degree of lesion of the nerve, we can describe preganglionic and postganglionic avulsion injury (tearing near the dorsal root ganglion o near the spinal cord at an intraforaminal level, and tearing of the postganglionic nerve distant from the dorsal root ganglion and the spinal cord, respectively); neurotmesis lesion, also considered to be a severe injury of the nerve as there is a complete tearing of the axon and the connective tissue [7,8]; axonotmesis lesion, when there is an anatomic interruption of the axon but with no interruption or partial interruption of the connective tissue and the myelin; and, finally, stretching neuropraxic lesion without nerve rupture, implying a momentaneous physiological blockage of the nerve-axon connection, with spontaneous recovery. We must also consider neuroma lesion, which implies an interference of the injured nerve scar tissue that, when healing, does not allow the nervous impulse to the muscle.

CLASSIFICATION, TYPE OF INJURY, AND CLINICAL PRESENTATION

NBPP is characterized by the type and patterns of nerve injury. Clinically, the Narakas classification system (16) is used to group severity of injury from I to IV (Table 1), with groups I and II associated with higher rates of spontaneous recovery. Types of nerve injury range from neuropraxia (a temporary conduction block due to interruption of the myelin sheath, with recovery of full function generally within weeks), to axonotmesis (disruption of the nerve fibers and, likely, the myelin sheath, with some function returning within months but incomplete recovery), to neurotmesis (nerve disruption and avulsion of the nerve roots from the spinal cord, with no chance of recovery). Clinical presentation can range from transient weakness to global paresis, with passive greater than active range of motion. Infants with total plexus injury (groups III and IV) who show no signs of recovery will need reconstructive microsurgery to repair the injured plexus and improve outcome. Infants with neuropraxic injury who fully recover by 1 month of age are managed conservatively. However, a ‘gray zone’, where optimal therapy (i.e., the decision whether to intervene surgically) is unclear, certainly exists for infants with NBPP. This gray zone includes infants with a deficit that has been managed conservatively but who may be considered for surgery based on select criteria, such as no recovery of biceps function at 3 months of age, or a failed cookie test at 9 months.

Also termed Duchenne-Erb syndrome, upper brachial plexus palsy (C5–C6) is characterized by impaired abduction and external rotation of the shoulder and elbow flexion, while hand function is preserved. Also known as Dejerine-Klumpke syndrome, lower brachial plexus palsy (C7–T1) impairs hand and wrist function. In the case of a complete brachial plexus palsy (C5–T1), the function of the entire arm is impaired, presenting with a completely flaccid arm without sensitivity, and sometimes with ocular impairment. This combination of symptoms is known as Horner’s Syndrome [9,10,11,12,13].

With NBPP, prognosis and outcomes depend on the extent of the injury. The rehabilitation options depend on the type of injury and the regeneration evidenced by spontaneous recovery of the affected limb [12].

Rehabilitation treatment for neonatal brachial plexus palsy includes conservative treatment, started as soon as possible with passive movements, sensory stimuli and guidance to the child’s relatives, instead of surgical treatment, which implies surgical techniques, and is performed only after spontaneous recovery, usually at 3 months of age [

Assessment

HCPs experienced in newborn assessment should undertake a detailed review of maternal history and delivery details to identify risk factors for NBPP (e.g., shoulder dystocia or presence of humeral or clavicular fracture). They should perform a detailed physical musculoskeletal and neurological examination, including active and passive range of motion, and assess normal reflexes. This exam should include assessing for clavicular or humeral fracture, which can mimic NBPP due to pain limiting range of motion. When concern is raised for bony injury, a chest and humeral x-ray should be obtained. Assess respiratory status and check symmetry of chest movements promptly to assess for phrenic nerve injury. An elevated hemi-diaphragm may be seen on chest x-ray or detected on ultrasound. The presence of Horner’s syndrome and diaphragmatic paralysis suggest an avulsion injury, which is a persistent, definitive deficit. Detailed documentation should be part of the newborn record and included in the referral form (Table 2). Differential diagnoses to be considered include: pseudoparesis (i.e., pain secondary to humeral fracture or to an infection of the bone, joints, soft tissue, or vertebra); myotonia congenita (a form of arthrogryposis multiplex congenita); anterior horn cell injury (e.g., congenital cervical spinal atrophy, congenital varicella syndrome); and pyramidal tract or cerebellar lesions

REcommendations

• 1) Neonatal care providers should evaluate newborns for NBPP when delivery has been complicated by shoulder dystocia, a humeral or clavicular fracture, or when asymmetrical upper extremity movement is apparent.
• 2) All newborns with NBPP and incomplete recovery by 1 month of age should be referred immediately to a multidisciplinary health care team to optimize outcomes and minimize residual deficits. The referral should include detailed information on the risk factors, severity of injury, and course of recovery.
• 3) For infants receiving ongoing nonoperative therapy in their community, continuous dialogue among the child’s multidisciplinary health care team, community health care providers, and nonoperative therapists is required to identify issues of growth and development and facilitate specialized assessments.

Treatment

These professionals use rehabilitation techniques and resources in a complementary way, such as electrostimulation, botulinum toxin injection, immobilizing splints, and constraint induced movement therapy of the non-injured limb. Professionals and family members work jointly. Surgical treatment includes primary surgeries, indicated for children who do not present any type of spontaneous rehabilitation in the first three months of life; and secondary surgeries, recommended in children who after primary surgery have some limitation of injured limb function, or in children who have had some spontaneous recovery, yet still have significant functional deficits. Treatment options for NBPP are defined by clinical evaluation/type of injury, but regardless of the type of injury, it is unanimous that conservative treatment is always started as early as possible.

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