Brachial plexus palsy is a potentially serious complication of child birth, with a reported incidence of 0.4 to 5.1 cases per 1,000 live births.1 With brachial plexus palsy, nerve roots may undergo stretching, tearing, and, in some cases, complete avulsion during labor or delivery. Most cases of brachial plexus palsy are transient, but permanent damage can occur in up to 10% of cases. Although many cases of brachial plexus palsy occur in relation to shoulder dystocia, other cases have been reported to occur with spontaneous vaginal delivery,2–4 with cesarean delivery,5 and in the posterior shoulder of neonates delivered with an anterior shoulder dystocia.6,7
Even though many of the risk factors that predispose patients to have shoulder dystocia (eg, fetal macrosomia, maternal diabetes, and intrauterine maladaption) may also predispose patients to have neonatal brachial plexus palsy, such an association should not be equated as a tacit description of unequivocal causation.1,8 With shoulder dystocia or brachial plexus palsy, historic obstetric risk factors typically have demonstrated low sensitivity and positive predictive values in predicting the occurrence of the events.1,9,10 Here, we present eight cases of severe brachial plexus palsy that occurred in the absence of shoulder dystocia.
PATIENTS AND METHODS
We included cases of severe brachial plexus palsy occurring at Los Angeles County and University of Southern California Medical Center identified from our neonatal intensive care unit database from 1993 to 2006. During this time period, there were 43,337 births, with 477 cases of shoulder dystocia (1.1%) and 91 cases (0.2%) of brachial plexus palsy. The study was approved by the Institutional Review Board and complied with all patient protection criteria set forth therein.
Severe brachial plexus palsy was defined as the presence of severe brachial plexus injury requiring neonatal intensive care unit admission. All the neonates had documented evidence of brachial plexus impairment with limitations in range of motion and arm movement requiring neonatal intensive care unit observation. Shoulder dystocia was considered to have occurred if obstetric maneuvers other than gentle downward traction were required for delivery. Cases of severe brachial plexus palsy without shoulder dystocia were reviewed and analyzed. All maternal and neonatal records were reviewed systematically by a chief resident in obstetrics and gynecology at our institution (Dr. Torki).
Maternal demographics are summarized in Table 1. The brachial plexus palsy cases are summarized in Table 2. All cases were vaginal deliveries except for case 5. In this case, the patient was a 23-year-old multiparous woman with estimated fetal weight of 4,800 g by ultrasound examination. She had an elective primary cesarean delivery without labor and delivered a viable neonate weighing 4,940 g with severe brachial plexus palsy.
Case 3 presented at 30 weeks of gestation in active labor with a twin gestation complicated by one anencephalic fetus. She delivered both twins vaginally, with the anencephalic twin having no signs of life and the living twin having Apgar scores of 6 at 1 minute and 5 at 5 minutes and severe brachial plexus palsy. The delivery itself was otherwise uncomplicated and no shoulder dystocia was noted.
Other than case 5, all patients presented with spontaneous active labor and had uncomplicated vaginal deliveries without shoulder dystocia. None of the patients had any significant medical history, previous shoulder dystocia, previous macrosomia, or maternal diabetes.
Note that the mean second stage of labor was normal (2.15±1.93 hours), as was the mean birth weight (3,514±1,043 g). These are detailed in Table 2. All of the infants had persistent severe neonatal brachial plexus palsy at their 1-month follow-up assessments. Longer-term follow-up was not available.
In this series, severe brachial plexus palsy occurred in women without shoulder dystocia and without any clinical risk factors. Of note, both the mean estimated fetal weight and the actual birth weights were less than 4,500 g, and six of eight (75%) neonates weighed less than 4,000 g. Only one of the neonates weighed more than 4,500 g, and that child was delivered by cesarean.
Unlike previous studies,7,11–14 these cases are unique in that they describe patients without any antepartum or intrapartum historic risk factors. Moreover, they corroborate that factors other than traction applied at delivery (eg, fetal shoulders remaining in a persistent antero-posterior orientation at the pelvic brim, the propulsive forces of labor, intrauterine maladaptation, in utero compression, and others) had to have been responsible for the severe brachial plexus palsy noted at birth.
Some authors have suggested that, in some cases of brachial plexus palsy, shoulder dystocia may have occurred but was unrecognized at the time of delivery.13,14 In the present study, maternal medical records were reviewed thoroughly, including all nursing documentation and standardized delivery summaries. As such, we submit that nonrecognition of shoulder dystocia at delivery would be unlikely.
In one case, a patient with severe brachial plexus palsy was delivered by cesarean delivery. Other reports have shown that brachial plexus palsy can occur with abdominal delivery.1,5 Interestingly, despite the continuous increase in cesarean deliveries in the United States15 and the increasing use of obstetric simulation and shoulder dystocia drills,16 the incidence of brachial plexus palsy has remained constant over the past several decades. Taken together, and in conjunction with the results of the current study, this further supports the in utero injury mechanisms noted.
In summary, these cases demonstrate that severe brachial plexus palsy occurs without shoulder dystocia and without identifiable risk factors. Shoulder dystocia and brachial plexus palsy remain unpredictable clinical events.
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