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closeQuestions to the Authors
Posted by rha123 on 30 Sep 2014 at 19:54 GMT
I read the article by Iskender et. al. with interest and congratulate them on including clavicle fractures in a study on brachial plexus injuries and shoulder dystocia. This is not often done.
There are seven issues I would like some clarity on and would be grateful if the authors – or others – could comment.
ACOG and RCOG define shoulder dystocia as a cephalic delivery that requires additional obstetric maneuvers to deliver the fetus after the head has delivered and gentle traction has failed. Although Spong et al (1995) introduced a 60-second definition of shoulder dystocia as an alternative definition; no other study has included both criteria as a definition for shoulder dystocia.
1. Why did the authors create this definition?
One outcome of using this definition resulted in a 0.29% incidence of shoulder dystocia, which is among the lowest incidences ever reported. Indeed, in their prospective study, Spong et al reported a reported shoulder dystocia incidence of 7%, and 10.8% of deliveries involved use of auxiliary maneuvers. The higher incidence of shoulder dystocia in 2100 vaginal deliveries in other prospective studies proves that shoulder dystocia is under reported.
2. Why did the authors not at least acknowledge shoulder dystocia is likely underreported in some of the injured neonates?
Cohen and Otto in 1980 established that clavicle fractures occur without recorded shoulder dystocia. The mechanical mechanism of clavicle fracture most often is compression of the clavicle caused by the anterior shoulder slipping just under the symphysis pubis. This usually occurs in neonates who have larger birthweight.
3. If calculated, what were the average birth weights of neonates with clavicle fracture independent of the whether delivery was recorded as shoulder dystocia or not?
4. Similarly, what were the birth weights of the infants who suffered brachial plexus injury that lasted one year?
5. If there was follow-up beyond one year, are the injuries still manifest? The neurological literature reports that there can be recovery up to two years of age.
In their conclusion, the authors suggest investigating brachial plexus injuries using prospective studies. In fact, Mollberg et al [2007, 2008] conducted a prospective study of more than 31000 vaginal deliveries, which resulted in 18 permanent injuries. They found that shoulder dystocia was reported only 36% of time, yet in all of the children who had residual functional deficits at 18 months, the provider applied downward traction with substantial force.
6. In light of this study, and many others where shoulder dystocia is associated with permanent injury nearly 100% of the time, do the authors still conclude that brachial plexus injury lasting one year was associated with shoulder dystocia only 17% of the time, and that 83% were caused by intrapartum factors and not clinician traction?
7. Finally, and most importantly, what clinical benefit to patients does this study provide?
RE: Questions to the Authors
cantekin replied to rha123 on 01 Oct 2014 at 08:30 GMT
1. The first statement of the reader is not correct. Both definitions are actively being used. Here is the definition of SD made by gherman in their article in 2006: " Shoulder dystocia defined as a prolonged head-to-body delivery time of>60 seconds and/or the use of ancillary obstetric maneuvers"
2. The incidence of SD ranged between 0.2-3 % in most studies (gherman et al 2006). But I assume the reader wishes to know why we have such a low rate despite including fetal head to body delivery time as a diagnostic criteria. One possible explanation is higher cesarean rate at our institution especially for suspected fetal macrosomia. Underreporting is another possibility especially in cases with not apparently traumatic delivery but prolonged head to body delivery time. This was discussed in the text
3. The birth weight characteristics are available for patients with CF and permanent BPI
4. There has been a great deal of debate whether BPI is associated with shoulder dystocia almost all the time. The relationship between shoulder dystocia and BPI is more evident in macrosomic fetuses. But GILBERT et all in 1999 have analyzed 1611 cases of BPI and found that SD is associated with approximately 22 % of cases in neonates weighing between 2500-3500. Interestingly, malpresentations other than breech was another significant contributor for BPI. Thus the authors concluded that brachial plexus injury has causes in addition to shoulder dystocia and might result from an abnormality during the antepartum or intrapartum period. A similar conclusion was also reached by Sandmire in 2002 based on distinctive features of BPI not associated with SD such as a higher rate of permanent injury or involvement of posterior shoulder. There are many other studies that report BPI not associated with SD. Therefore I personally think that based on previous data is not possible to accept SD as the sole risk factor for BPI or for permanent BPI.
5. The reader asks "Finally, and most importantly, what clinical benefit to patients does this study provide?"
I am afraid I do not have a straight answer for this question. The primary question that led this work to arise was whether concurrent CF was a protective factor in neonates with traumatic delivery. A further question arose inspired by the work of sandmire. This was whether it was possible to characterize BPI injury not associated with BPI.
I hope the information provided is valuable (at least to readers).
Many thank for considering our paper worth commenting.
Dr cantekin iskender