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Neonatal brachial plexus palsy

Barry Russman, MD
Section Editors
Marc C Patterson, MD, FRACP
Jeremy M Shefner, MD, PhD
Deputy Editor
John F Dashe, MD, PhD


The brachial plexus (figure 1) is a network of nerve fusions and divisions that originate from cervical and upper thoracic nerve roots and terminate as named nerves that innervate muscles and skin of the shoulder and arm. The first clinical description of neonatal brachial plexus palsy (NBPP) was reported in the 1760s [1]. In the late 1800s, the different types of NBPP were defined; Duchenne and Erb in separate reports described upper trunk nerve injury to the C5 and C6 nerve roots, now called Erb palsy or Duchenne-Erb palsy [2,3], and Klumpke described lower trunk injury involving the C8 and T1 nerve roots [4]. Subsequently, palsy of all the nerve roots from C5 to T1 was reported.

The major controversies about NBPP revolve around the etiologies and the management. Once the diagnosis is established, what studies should be performed? How often does shoulder dystocia or obstetrical intervention contribute to the etiology? What is the role of rehabilitation therapies? When should nerve surgery be considered? When is orthopedic intervention needed? What is the prognosis for complete or partial recovery? Unfortunately, the literature provides a variety of different answers to the questions posed and controversy remains. In addition, the quality of the published evidence about NBPP is suboptimal; high-quality population-based studies with prospective analysis, sufficient follow-up, and clear assessment are scarce [5].

This topic will review the etiology, epidemiology, clinical features, diagnosis, management, and prognosis of NBPP, which is also known as obstetric brachial plexus palsy and birth-related brachial plexus palsy. Other brachial plexopathies are discussed separately. (See "Brachial plexus syndromes".)


Potential mechanisms of neonatal brachial plexus palsy (NBPP) include stretching/traction, compression, infiltration, and oxygen deprivation [6]. Of these, stretching is considered the most common mechanism. In addition, stretching may contribute to brachial plexus injury in cases where the principal cause is one of the other mechanisms. The etiology of NBPP traditionally has been attributed to iatrogenic lateral traction on the fetal head, typically when shoulder dystocia impedes delivery [7-9]. Downward lateral traction (ie, bending the neck away from the anterior shoulder and toward the posterior shoulder) causes increased stretching of the brachial plexus compared with downward axial traction (ie, applying force parallel to the fetal spine) [10].

However, NBPP can occur even when axial traction is properly applied; the occurrence of NBPP following birth does not automatically indicate that the practitioner applied forces or maneuvers that caused the nerve injury [10]. The forces of uterine contraction and maternal pushing alone are probably sufficient to cause excessive traction on the brachial plexus [10,11]. In addition, antepartum factors may predispose to NBPP, including uterine abnormalities such as Müllerian anomalies and fibroids that can result in fetal malpositioning and compression [12].


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Literature review current through: Sep 2016. | This topic last updated: Jul 15, 2016.
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