Brachial plexus injury causation in newborns debated

Key Points

Brachial plexus injury in newborns is commonly ascribed to the occurrence of head rotation with entrapment of the shoulders and subsequent downward traction by the accoucheur on the fetal head, resulting in avulsion of the brachial plexus nerve roots with permanent paralysis. A temporary loss of function may result from stretching and edema of the plexus without avulsion. In brachial plexus injury cases, plaintiff attorneys usually contend that damage to the brachial plexus is always caused by negligence of the birth attendant. However, a review of current literature reveals evidence that additional etiologies may underpin brachial plexus injury and raises questions regarding the level of responsibility of the birth attendant in connection with the injury.

Shoulder dystocia

Macrosomia is a major risk factor for shoulder dystocia. Attempts at predicting fetal weight include Leopold's maneuvers and ultrasound. However, both methods are known to have a large margin of error. Other risk factors for shoulder dystocia include maternal obesity, diabetes, and postterm pregnancy, all also linked to macrosomia, as well as labor induction and epidural anesthesia.¹ However, there is no accepted strategy for predicting shoulder dystocia. Varying maneuvers have been used to alleviate shoulder dystocia and therefore militate against injury to the brachial plexus. McRobert's maneuver, suprapubic pressure, rotational maneuvers, and delivery of the posterior arm have all been used with varying degrees of success in relieving shoulder dystocia.

As noted, the majority of permanent or temporary cases of brachial plexus paralysis (BPP) have been ascribed to stretching or tearing the brachial plexus because of excessive traction on the head during delivery after the occurrence of the shoulder dystocia. In contrast, contemporary literature defines multiple etiologies for BPP. Anatomic malformations of both mother and fetus can cause congenital BPP.^2,3 For example, BPP has been reported in conjunction with congenital malformations of the uterus and undue pressure placed on the fetal plexus during in utero development, as well as abnormal fetal development of the plexus.⁴ Jennett et al concluded that intrauterine maladaption might play a role in the injury because of the force of contractions during labor and the use of endogenous maternal mechanical forces that push the anterior shoulder against the maternal pubic bone.⁵

Brachial plexus impairment should not be prima facie evidence that the actual delivery process caused the injury. A search of 1 perinatal database of 39 cases found 22 instances of BPP without any mention of shoulder dystocia.⁵ Gurewitsch et al reported a case of temporary Erb-Duchenne palsy in the posterior arm of a fetus that had a normal labor and delivery without any shoulder dystocia or traction on the fetal head.⁶ Allen et al attempted to measure the clinician-applied peak force by a birth attendant during delivery.^7,8 They concluded that a wide variation of force was used on the basis of personal preference, body strength, gender, and other factors. The research showed that during a difficult delivery, the forces increased above the norm. The faster the force was applied, the greater the risk of injury to the fetus.⁹

Several variables must be considered in modeling shoulder dystocia, including measurement of the magnitude of force, direction of force, rate of force generation-whether increasing or decreasing-and the elasticity of the bones, nerves, and other relevant tissue. Applied force on the infant can come from both mother and clinician. The force that produces injury is the component vector along the brachial plexus. It varies in direct trigonometric proportion to the angle of applied force on the infant.

Thresholds for producing injury by clinician-applied force have been measured (greater than 30 lbs), but the direction of force in these studies and the component force vector along the brachial plexus have not been measured. This fact alone means that we have no quantitative way to know how this force actually contributes to BPP.

Maternal forces are likely several-fold greater than clinician-applied forces, especially when considering the delivery of the shoulders. This period in which the mother experiences episodic oxytocin surges has important consequences. It leads to increased uterine force, increased impulse (ie, rate of change of force), and an increase in the acute angle between the uterus force vector and the infant's brachial plexus-especially when the first shoulder is delivered.

Benjamin reported factors associated with BPP at birth or directly after birth.^10,11 These included maternal diabetes, uterine abnormalities, bicornuate uterus, and infants weighing more than 4,500 g. Other risk factors include the presence of a cervical rib in the fetus, a transverse lie, or poor tone of the fetus.

Benjamin states that multiple studies support endogenous labor forces as the etiology of BPP.¹⁰ Intrapartum events that may add to the risk of injuring the brachial plexus are mechanical forces of labor alone, vaginal breech deliveries, prolonged duration of labor, operative vaginal delivery, precipitous delivery, and prolonged head-to-body delivery interval. In rare cases, fetal neoplasm, infection and extrinsic compression, and edema have been found to be postdelivery causes of BPP. However, using some or all of theses risk factors to predict BPP has proven unreliable.