eMedicine Specialties > Orthopedic Surgery > Pediatrics

Brachial Plexus Injuries, Obstetrical

Author: Susan E Mackinnon, MD, FRCSC, FACS, Program Director, Division of Plastic and Reconstructive Surgery, Shoenberg Professor and Chief, Department of Surgery, Division of Plastic and Reconstructive Surgery, Washington University School of Medicine
Coauthor(s): Christine B Novak, PT, MS, Clinical Coordinator, Division of Plastic and Reconstructive Surgery, Research Associate Professor, Department of Surgery, Division of Plastic and Reconstructive Surgery, Washington University School of Medicine; Mark E Baratz, MD, Professor, Department of Orthopaedics, Drexel University College of Medicine; Residency Director, Department of Orthopaedics, Allegheny General Hospital; Consulting Staff, Allegheny Orthopaedic Associates
Contributor Information and Disclosures

Updated: Jul 16, 2008

Introduction

History of the Procedure

In 1764, Smellie described bilateral arm paralysis in a newborn. In 1872, Duchenne de Boulogne coined the term obstetrical paralysis. In 1874, Erb described the upper C5-C6 paralysis, and in 1885, Klumpke described paralysis of the lower plexus. In modern times, Gilbert has popularized surgical reconstruction of obstetrical brachial plexus injuries.1

Problem

Obstetrical brachial plexus paralysis (OBPP) refers to injury to all or a portion of the brachial plexus noted at the time of delivery.2,3 Injuries associated with the upper brachial plexus are termed Erb palsies, and those associated with the lower brachial plexus are termed Klumpke palsies. Obstetrical brachial plexus injuries often are associated with large weight at birth and shoulder dystocia. Obstetrical brachial plexus injuries are rarely (1% of cases) noted in neonates born via cesarean delivery.

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Resource Center  Neonatal Medicine
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Related eMedicine topic:
Brachial Plexus Injuries, Traumatic

Frequency

With improvement in obstetrical care, the incidence of brachial plexus injuries has decreased significantly. In countries in which obstetrical care is poor, OBPP is noted more frequently. The incidence ranges globally from 0.2-4% of live births. According to the World Health Organization, prevalence is generally 1-2% worldwide, with the higher numbers being in underdeveloped countries. In the United States, the prevalence is approximately 0.2%.

Etiology

Factors associated with obstetrical brachial plexus paralysis (OBPP) include large birth weight, breech delivery, and shoulder dystocia.4,5 Some consider intrauterine pressure neuropathy to be a cause of OBPP, based on the high pressures exerted between the brachial plexus and the mother's pelvis with labor and on the occurrence of OBPP in uneventful cesarean deliveries and in vaginal delivery without significant mechanical difficulty. Vertex presentation accounts for most OBPP cases (94-97%); breech presentations account for 1-2% of cases; and cesarean deliveries account for 1% of cases. Mothers with diabetes and mothers who are multiparous and previously had large babies are also considered to be at some risk for delivering neonates with OBPP.

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Pregnancy, Breech Delivery
Diabetes Mellitus and Pregnancy

Pathophysiology

Obstetrical brachial plexus paralysis (OBPP) results from excessive lateral traction on the head away from the shoulder.6 This force on the brachial plexus can cause varying degrees of injury to the nerves, including rupture of the nerve roots or trunks, avulsion of the nerve roots from the spinal cord, and traction preserving the continuity of the nerve but causing excessive scarring. Injury to the brachial plexus may result from demyelination, axonal degeneration, or avulsion. Clinically, this injury results in disruption of the sensory and/or motor function of the injured nerve. Spontaneous recovery of function occurs with remyelination with or without axonal regeneration and reinnervation of the sensory receptors, muscle endplates, or both. However, in some cases of severe nerve injury and with avulsion injuries, spontaneous recovery does not occur and surgical intervention is warranted.

The neonate has tremendous susceptibility to nerve injuries, as compared with the older infant, child, or adult. A brachial plexus injury in the neonate results in a more proximal injury and even cell death, as opposed to the result in an older child with the same injury. Gonik et al have suggested that spontaneous endogenous uterine and maternal expulsive forces are 4-9 times greater than the force calculated for clinician-applied forces.7

Presentation

At birth, the upper extremity may be flail. Two days following birth, the neurologic examination findings are more reliable. With Erb palsy or upper plexopathy, the arm is internally rotated and pronated with no movement at the shoulder or elbow; hand and wrist flexion are noted. With complete brachial plexus paralysis, the entire arm and hand are flail with no movement. A Horner syndrome (eyelid ptosis and pupillary miosis) may be noted, suggesting avulsion of the lower brachial plexus. Phrenic nerve palsy suggests a very severe avulsion injury, and urgent plication of the diaphragm may be indicated in patients with pulmonary compromise.

Depending on the degree of nerve injury, recovery may be noted within a few days. In most cases, some degree of spontaneous recovery occurs within 1 month, although in some injuries, evidence of full recovery may not appear for up to 3 months.8 Seddon and Sunderland each described a classification for nerve injuries.9,10 The classification of nerve injury described by Seddon consisted of neurapraxia, axonotmesis, and neurotmesis. Sunderland expanded the classification system into 5 degrees of nerve injury, as follows:

  • A first-degree injury, or neurapraxia, involves a temporary conduction block with demyelination of the nerve at the site of injury. Electrodiagnostic studies elicit normal results above and below the level of injury, and no denervation muscle changes are present. No Tinel sign is present. Once the nerve has remyelinated at that area, complete recovery occurs. Recovery may take up to 12 weeks.
  • A second-degree injury, or axonotmesis, results from a more severe trauma or compression. This causes Wallerian degeneration distal to the level of injury and proximal axonal degeneration to at least the next node of Ranvier. In more severe traumatic injuries, the proximal degeneration may extend beyond the next node of Ranvier. Electrodiagnostic studies demonstrate denervation changes in the affected muscles, and in cases of reinnervation, motor unit potentials (MUPs) are present. Axonal regeneration occurs at a rate of 1 mm/d or 1 in/mo and can be followed with an advancing Tinel sign. The endoneurial tubes remain intact, and the recovery, therefore, is complete with axons reinnervating their original motor and sensory targets.
  • A third-degree injury, more severe than a second-degree injury, was introduced by Sunderland. Similar to a second-degree injury, Wallerian degeneration occurs, and electrodiagnostic studies demonstrate denervation changes with fibrillations in the affected muscles. In cases of reinnervation, MUPs are present. Regeneration occurs at a rate of 1 mm/d, and progress may be followed with an advancing Tinel sign. However, with the increased severity of the injury, the endoneurial tubes are not intact. Therefore, the regenerating axons may not reinnervate their original motor and sensory targets. The pattern of recovery is mixed and incomplete. Reinnervation occurs only if sensory fibers reach their sensory end organs and motor fibers reach their muscle targets. Even within a sensory nerve, recovery can be mismatched if sensory fibers reinnervate a different sensory area within the nerve's sensory distribution. If the muscle target is a long distance from the site of injury, nerve regeneration may occur, but the muscle may not be reinnervated completely, due to the long period of denervation.
  • A fourth-degree injury results in a large area of scar at the site of nerve injury and precludes any axons from advancing distal to the level of nerve injury. Electrodiagnostic studies reveal denervation changes in the affected muscles, and no MUPs are present. A Tinel sign is noted at the level of the injury, but it does not advance beyond that level. No improvement in function is noted, and the patient requires surgery to restore neural continuity, thus permitting axonal regeneration and motor and sensory reinnervation.
  • A fifth-degree injury is a complete transection of the nerve. Similar to a fourth-degree injury, surgery is required to restore neural continuity. Electrodiagnostic findings are the same as those for a fourth-degree injury.

Mackinnon introduced a sixth-degree injury classification to describe a mixed-nerve injury with a combination of the other degrees of injury in one patient.11 This commonly occurs when some fascicles of the nerve are working normally while other fascicles may be recovering. Other fascicles may require surgical intervention to permit axonal regeneration.

Motor evaluation of patients with obstetrical brachial plexus paralysis (OBPP) is difficult, due to the young age of the child and the variability of presentation. Several classification systems have been described to categorize motor function and particularly OBPP. The Medical Research Council (MRC) uses a grading scale of 0-5, with 0 representing no muscle contraction and 5 representing normal muscle power through full range of motion, as follows:

  • M0 - No contraction
  • M1 - Flicker contraction
  • M2 - Muscle contraction with active motion with gravity eliminated
  • M3 - Full range of motion against gravity
  • M4 - Full range of motion against gravity with some resistance
  • M5 - Full range of motion against gravity with maximum resistance for that muscle

This classification system requires active contraction and movement of the muscle through full range of motion, which is extremely difficult to assess in neonates and infants.

Gilbert and Tassin introduced a modification of the MRC scale to be used in children, as follows12 :

  • M0 - No contraction
  • M1 - Muscle contraction
  • M2 - Movement with gravity eliminated
  • M3 - Full movement against weight of extremity

However, this classification system lacks sensitivity.

The Active Movement Scale introduced by Clarke and Curtis is based on overall joint motion rather than individual muscle testing.13 The 7-point scale ranges from no contraction to full motion with gravity eliminated and against gravity. Motions assessed include shoulder flexion, abduction, adduction, internal rotation, and external rotation; elbow flexion and extension; wrist flexion and extension; and finger flexion and extension.

Mallet introduced a classification system (grade 0-5) based on voluntary upper extremity movements, including active abduction, external rotation, hand to nape of neck, hand to back, and hand to mouth.

Good intertester reliability has been reported for the Active Movement Scale and the Mallet Classification.14

Related eMedicine topic:
Horner Syndrome

Indications

Reports vary regarding the timing for surgical intervention for obstetrical brachial plexus injuries. The recovery of biceps function appears to be a significant criterion for deciding whether surgical intervention is necessary. Gilbert recommends surgery if biceps recovery is not evident by 3 months; Hentz recommends waiting 3.5 months; and Waters suggests waiting until 4 months.15,16,17 Clarke has developed an active movement scale and scores recovery to determine the need for surgery.18 At 9 months, the infant is assessed with the cookie test, which requires the child to put a cookie to his or her mouth with limited neck flexion. If the infant does not pass the cookie test, then surgery is recommended. Shenaq et al reports that at Texas Children's Hospital, surgery is recommended if the infant does not show improvement in deltoid, triceps, and biceps muscle function within 4 months.19 Because of the short distance required for nerve regeneration to the target muscle in babies,the authors believe that it is prudent towait 4 months. If recovery of biceps muscle function is not evident by 4 months, then the prognosis for spontaneous recovery is poor, so surgery is indicated.

Relevant Anatomy

A very detailed knowledge of the brachial plexus is necessary to localize the level of the injury within the brachial plexus. During surgery, knowledge of motor and sensory fascicular topography is critical to ensure correct alignment of the motor and sensory fascicles.

Contraindications

Patients with brachial plexus injury whose functional recovery continues to improve are not candidates for surgery. Note that each nerve must be evaluated separately (for instance, recovery of hand function without function of shoulder or elbow function is an indication for surgery to reconstruct the upper plexus palsy).

More on Brachial Plexus Injuries, Obstetrical

Overview: Brachial Plexus Injuries, Obstetrical
Workup: Brachial Plexus Injuries, Obstetrical
Treatment: Brachial Plexus Injuries, Obstetrical
Follow-up: Brachial Plexus Injuries, Obstetrical
References

References

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Further Reading

Keywords

brachial plexus injuries, spinal nerve injuries, obstetrical brachial plexus injuries, obstetrical brachial plexus palsy, OBPP, obstetrical paralysis, C5-C6 paralysis, lower plexus paralysis, Erb palsy, Klumpke palsy, Horner syndrome, neurapraxia, axonotmesis, wallerian degeneration, node of Ranvier

Contributor Information and Disclosures

Author

Susan E Mackinnon, MD, FRCSC, FACS, Program Director, Division of Plastic and Reconstructive Surgery, Shoenberg Professor and Chief, Department of Surgery, Division of Plastic and Reconstructive Surgery, Washington University School of Medicine
Susan E Mackinnon, MD, FRCSC, FACS is a member of the following medical societies: American Association for Hand Surgery, American Association of Plastic Surgeons, American College of Surgeons, American Society for Surgery of the Hand, American Surgical Association, Canadian Medical Association, and Canadian Society of Plastic Surgeons
Disclosure: Nuerotube Honoraria Consulting

Coauthor(s)

Christine B Novak, PT, MS, Clinical Coordinator, Division of Plastic and Reconstructive Surgery, Research Associate Professor, Department of Surgery, Division of Plastic and Reconstructive Surgery, Washington University School of Medicine
Christine B Novak, PT, MS is a member of the following medical societies: American Association for Hand Surgery
Disclosure: Nothing to disclose.

Mark E Baratz, MD, Professor, Department of Orthopaedics, Drexel University College of Medicine; Residency Director, Department of Orthopaedics, Allegheny General Hospital; Consulting Staff, Allegheny Orthopaedic Associates
Mark E Baratz, MD is a member of the following medical societies: Allegheny County Medical Society, American Academy of Orthopaedic Surgeons, American Association for Hand Surgery, American Orthopaedic Association, American Society for Surgery of the Hand, Orthopaedic Research Society, and Pennsylvania Orthopaedic Society
Disclosure: Nothing to disclose.

Medical Editor

Mininder S Kocher, MD, MPH, Associate Professor of Orthopedic Surgery, Harvard Medical School/Harvard School of Public Health; Associate Director, Division of Sports Medicine, Department of Orthopedic Surgery, Children's Hospital Boston
Mininder S Kocher, MD, MPH is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Association for the History of Medicine, American Medical Association, American Orthopaedic Society for Sports Medicine, and Massachusetts Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

George H Thompson, MD, Director, Pediatric Orthopedics, Rainbow Babies and Children's Hospital
George H Thompson, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Association, Pediatric Orthopaedic Society of North America, and Scoliosis Research Society
Disclosure: Nothing to disclose.

CME Editor

Dinesh Patel, MD, FACS, Associate Clinical Professor of Orthopedic Surgery, Harvard Medical School; Chief of Arthroscopic Surgery, Department of Orthopedic Surgery, Massachusetts General Hospital
Dinesh Patel, MD, FACS is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Association of Physicians of Indian Origin, American College of International Physicians, and American College of Surgeons
Disclosure: Nothing to disclose.

Chief Editor

Dennis P Grogan, MD, Clinical Professor, Department of Orthopedic Surgery, University of South Florida College of Medicine; Chief of Staff, Department of Orthopedic Surgery, Shriners Hospital for Children of Tampa
Dennis P Grogan, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Medical Association, American Orthopaedic Association, American Orthopaedic Foot and Ankle Society, Eastern Orthopaedic Association, Irish American Orthopaedic Society, Pediatric Orthopaedic Society of North America, and Scoliosis Research Society
Disclosure: Nothing to disclose.

 
 
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