The greatest nightmare an obstetrician is likely to face is shoulder dystocia. At an otherwise normal delivery, just after the baby's head has emerged, the neck suddenly retracts back against the mother's perineum causing the baby's cheeks to puff out. The experienced obstetrician knows at this point that the baby's anterior shoulder is caught on the mother's pubic bone and if he or she is unable to free up the shoulder within a few minutes the baby will suffer irreversible brain damage or death.

Shoulder dystocia occurs in approximately one half of one percent of all deliveries. Given that there are 4 million babies born each year in the United States, this delivery complication will be experienced by roughly 20,000 women a year. The larger the baby, the more likely it is to occur. However, even with very large babies shoulder dystocia occurs only occasionally and sporadically. Therefore a physician never knows when it will be encountered.

The most common serious complication following a shoulder dystocia delivery is brachial plexus injury. This is when the nerves in a baby's neck--the brachial plexus--are temporarily or permanently damaged. The nerves of the brachial plexus control the function of the arm and hand. Injury to the upper part of the brachial plexus is called Erb palsy while injury to the lower nerves of the plexus is called Klumpke palsy. Both can cause significant, lifelong disability.

Because of the gravity and unexpectedness of shoulder dystocia it has long been a major area of obstetrical concern. Yet despite the hundreds of published studies about shoulder dystocia there still are multiple, important unanswered questions:

Is shoulder dystocia predictable?

Can it be prevented?

Is there anything that can be done when it does occur to prevent brachial plexus nerve damage?

If there is an injury, was it caused by mismanagement on the part of the physician while attempting to resolve the shoulder dystocia or was it an inevitable consequence of the shoulder dystocia?

The interest obstetricians have in these questions has been heightened in the last two decades by the increasing influence of medical-legal issues on the practice of medicine. As regards shoulder dystocia, it is frequently the case that when a brachial plexus injury occurs, an obstetrician will be charged with negligence. Such claims are now so frequent that law suits related to shoulder dystocia deliveries result in the second largest category of indemnity payments in obstetrics, exceeded only by birth asphyxia.

In their defense, physicians contend that shoulder dystocia is a totally unpredictable event and that even with perfect management brachial plexus injuries will occur.

Where does the truth lie?

This web site represents an attempt to answer this and other questions about shoulder dystocia. By having thoroughly reviewed the published literature on shoulder dystocia and brachial plexus injury from 1965 to the present, it has been possible to frame comprehensive and consistent answers to the major questions that bedevil this area of obstetrics. It is the hope of the author that the information presented here about the cause, preventability, and culpability for shoulder dystocia and brachial plexus injuries will (1) aid in improving the care given to women and their babies and (2) will help adjudicate responsibility in medical liability cases in which a baby has been injured during a shoulder dystocia delivery.

The phenomenon of shoulder dystocia has long been recognized. Smellie, one of the earliest physicians specializing in obstetrics, described a situation he encountered in 1730 as follows:

Called to a gentlewoman in labor. The child's head delivered for a long time -- but even with horrid pulling from the midwife, the remarkably large shoulder prevented delivery. I have been called by midwives to many cases of this kind, in which the child was frequently lost.

Morris in 1955 gave what is now a classic description of shoulder dystocia:

The delivery of the head with or without forceps may have been quite easy, but more commonly there has been a little difficulty in completing the extension of the head. The hairy scalp slides out with reluctance. When the forehead has appeared it is necessary to press back the perineum to deliver the face. Fat cheeks eventually emerge. A double chin has to be hooked over the posterior vulvar commisure, to which it remains tightly opposed . . .

Time passes. The child's face becomes suffused. It endeavors unsuccessfully to breathe. Abdominal efforts by the mother and by her attendants produce no advance. Gentle head traction is equally unavailing. Usually equanimity forsakes the attendants -- they push, they pull. Alarm increases. Eventually, "by greater strength of muscle or by some infernal juggle," the difficulty appears to be overcome, and the shoulder and trunk of a goodly child are delivered. The pallor of its body contrasts with the plum-colored cyanosis of the face, and the small quantity of freshly expelled meconium about the buttocks. It dawns upon the attendants that their anxiety was not ill founded, the baby lies limp and voiceless, and only too often remains so despite all efforts at resuscitation.

Perhaps the most famous case of shoulder dystocia was that involving Prince William of Germany who subsequently became Kaiser Wilhelm II in 1888. It seems that William was in breech position at birth and was manipulated by several physicians and a midwife during delivery. Apparently the baby was not breathing when it emerged, but by "continuous rubbing . . . dousing in a hot bath, and a series of short, sharp slaps on his buttocks" the doctors managed to get the child to breathe. The third day after delivery the midwife noticed that William's left arm was slack. It was thought that the arm had been "wrenched out of the socket" and some of the muscle tissue torn. In addition it is suspected that there were several moments of asphyxia which might have caused slight brain damage. It has been postulated that this was the cause of William's later hyperactivity and emotional instability. He may also have suffered slight cerebral palsy. For the rest of his life, William's "withered" left arm was concealed from the public by careful posing for photographs.

Shoulder dystocia occurs when, after delivery of the fetal head, the baby's anterior shoulder gets stuck behind the mother's pubic bone. If this happens, the remainder of the baby does not follow the head easily out of the vagina as it usually does during vaginal deliveries.

This simple definition of shoulder dystocia, however, glosses over many complexities. For example, should a delivery be categorized as involving shoulder dystocia only when there is some time delay -- 60 seconds is often suggested in this context-between the delivery of a baby's head and shoulders? Or is shoulder dystocia present any time that a delivering physician finds that the shoulders cannot be delivered with the normal amount of downward traction on the fetal head? Some have suggested that the definition of true shoulder dystocia requires that an obstetrician had to perform special maneuvers in order to deliver the shoulders.

Exactly how shoulder dystocia is defined is more than just a semantic issue. It sets the parameters for the collection of statistics related to shoulder dystocia, a necessity for research aimed at decreasing shoulder dystocia related injuries. It also determines when a baby's injuries might be attributed to a physician's actions during labor and delivery.

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It is necessary to know something about the anatomy of the fetus and the maternal pelvis in order to understand how shoulder dystocia comes about and how it causes the injuries it does.

As the accompanying diagram shows, the maternal pelvis is composed of a series of bones forming a circle protecting the pelvic organs. The front-most bone is the symphysis pubis. It is on this structure that a baby's anterior shoulder gets caught during a delivery complicated by shoulder dystocia. The bone at the back of the maternal pelvis is the sacrum. Because of its shape, it generally serves as a slide over which a baby's posterior shoulder can descend freely during labor and delivery. The side walls of the maternal pelvis, although very important in determining the ease of the process of labor in general, usually do not contribute to shoulder dystocia.

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In normal vaginal deliveries the head of the baby, called the "vertex", emerges first. During labor, the soft, mobile bones of the fetal head can "mold"-alter their shape -- and, to a slight degree, overlap. This facilitates the fetal head fitting into and through the maternal pelvis. The baby's shoulders, likewise being flexible, usually follow the delivery of the baby's head quickly and easily. But for this to happen, the axis of the fetal shoulders must descend into the maternal pelvis at an angle oblique to the pelvis's anterior-posterior dimension. This position affords the shoulders the most room for their passage. If instead the shoulders line up in a straight front-to-back orientation as they are about to emerge from the mother's pelvis, there will often be insufficient room for them to squeeze through. The back of the mother's pubic bone then forms a shelf on which the baby's anterior shoulder can get caught. If this happens, the shoulders cannot deliver and a shoulder dystocia results.

Shoulder dystocia can also occur if the posterior shoulder of a baby gets caught on its mother's sacrum. This is a far less common cause of shoulder dystocia. The sacrum, having no protrusions equivalent to that of the pubic bone, is far less likely to impede the descent of the baby's posterior shoulder.

As can be readily appreciated, it is the relative sizes of the fetal head, shoulders, and chest compared to the shape and size of the maternal pelvis that determine how smoothly a delivery will go. Usually it is the fetal head that has the largest dimensions. Thus if it can pass through the maternal pelvis without difficulty, the rest of the baby usually follows easily. However, when the dimensions of the fetal shoulders or chest rival those of its head, the chances of a shoulder dystocia occurring are much increased. Such situations occur more frequently both in large babies and in babies of diabetic mothers.

In large babies, much of the excess growth that occurs is in the chest and abdominal areas. In these babies the dimensions of the shoulders and chest tend to be disproportionately larger than those of the head. This trend is exaggerated in babies of diabetic mothers. Multiple studies have shown that babies of diabetic mothers more frequently have larger ratios of shoulder circumference to head circumference than do their peers born of nondiabetic mothers. Babies of diabetic mothers also have greater arm circumference, larger triceps folds, and a higher percentage of body fat. Since larger babies are more likely to "get stuck", much of the work in the field of shoulder dystocia has been targeted at attempting to predict which babies will be larger than normal, especially when their mothers are diabetic.

Except in extraordinary circumstances, once the fetal head and shoulders have been delivered the remainder of the fetal trunk and legs slide out easily. Such extraordinary circumstances preventing easy delivery of the fetal body might be when:

• A fetus has a large abdominal or lower back tumor,
• The umbilical cord is wrapped tightly around the baby's neck, or
• There is a severe constriction of the uterine muscle -- "contraction rings" -- trapping the baby in the uterus.

The above applies only to vertex or headfirst deliveries. Breech deliveries, where the fetal legs and buttocks emerge first from the vagina, can also result in injury to the fetal arms and neck, producing the brachial plexus injuries discussed above. However, since these and other sorts of injuries to babies from vaginal breech deliveries occur at a relatively high rate, most breech babies in the United States are now delivered by cesarean section.

The incidence of shoulder dystocia is generally reported to be between 0.5 % and 1.5% with scattered reports listing values both higher and lower. Those studies involving the largest number of deliveries have usually found the rate of shoulder dystocia in a general population to be 0.5% - 0.6%. The "true" incidence of shoulder dystocia, however, is very much dependent upon how it is defined, how it is reported, and the characteristics of the population being measured.

The accuracy of reporting is an important variable in shoulder dystocia statistics. Many obstetricians are reluctant to write down in their delivery notes that a shoulder dystocia has occurred for fear that this will be a red flag attracting a malpractice suit should it later turn out that the baby has suffered an injury. Some studies have shown that only 25% to 50% of shoulder dystocias -- as noted by objective observers in a delivery room -- are recorded by the delivering physician.

How one defines shoulder dystocia, of course, affects its reported incidence. Some obstetricians will only report a delivery as involving shoulder dystocia if they had to employ specific maneuvers to deliver the baby's anterior shoulder. Others will record shoulder dystocia if there is any delay in the emergence of the shoulder following delivery of the head. In some cases a physician will only record "shoulder dystocia" when a fetal injury has occurred.

Finally, the characteristics of the delivery group being measured will affect statistics on shoulder dystocia. A study evaluating the incidence of shoulder dystocia utilizing only large babies or only infants of diabetic mothers as subjects will have a much higher reported incidence of shoulder dystocia than if the population were a general one containing both small and large babies and the normal percentage of mothers having diabetes.

Several of the more recent studies have shown a slightly higher incidence of shoulder dystocia than has been recorded in the past, reaching just above 1% of all deliveries. The question has therefore been asked, "Is the rate of shoulder dystocia increasing?" While there is as yet no definitive answer to this question, several hypotheses have been given to explain this possible trend:

1. On average babies are significantly larger then in years past. The percentage of very large baby's (>4000gms) in one study has gone up 300% between 1970 and 1988.

2. Over the last several decades there has been a marked increase in average maternal weight, average maternal weight gain during pregnancy, and the number of diabetic women having babies. All of these factors could be expected to increase the incidence of shoulder dystocia.

3. The increased focus of attention among obstetricians about shoulder dystocia deliveries may have heightened awareness about it and increased reporting of it.

The question as to whether or not women who have had a shoulder dystocia in a previous delivery are more likely to have one again in a subsequent delivery is an extremely important one. This information will help guide how future deliveries in these women are managed.

It appears from the literature that the risk of recurrent shoulder dystocia is substantial: 10 to 15%. Moreover, women who have had a shoulder dystocia delivery that resulted in injury to the fetus have an even greater risk of having a recurrent shoulder dystocia and subsequent fetal injury.

Following shoulder dystocia deliveries, 20% of babies will suffer some sort of injury, either temporary or permanent. The most common of these injuries are damage to the brachial plexus nerves, fractured clavicles, fractured humeri, contusions and lacerations, and birth asphyxia.

Brachial plexus injury

The brachial plexus consists of the nerve roots of spinal cord segments C5, C6, C7, C8, and T1. (See accompanying diagram). These nerve roots form three trunks which divide into anterior and posterior divisions. The upper trunk is made up of nerves from C5 and C6, the middle trunk from undivided fibers of C7, and the lowermost trunk is made up of nerves from C8 and T1.

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There are two major types of brachial plexus injury: Erb palsy and Klumpke palsy.

Erb palsy, the more commonly occurring of the two forms of brachial plexus injury, involves the upper trunk of the brachial plexus (nerve roots C5 through C7). This palsy affects the muscles of the upper arm and causes abnormal positioning of the scapula called "winging". The supinator and extensor muscles of the wrist that are controlled by C6 may also be affected. Sensory deficits are usually limited to the distribution of the musculo-cutaneous nerve. Together, these injuries result in a child having a humerus that is pulled in towards the body (adducted) and internally rotated. The forearm extended. Some have described this as the "waiters tip" position.

Klumpke palsy involves lower trunk lesions from nerve roots C7, C8, and T1. In this injury the elbow becomes flexed and the forearm supinated (opened up, palm-upwards) with a characteristic clawlike deformity of the hand. Sensation in the palm of the hand is diminished.

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It has been traditionally thought that most brachial plexus injuries result from stretching of the nerves of the brachial plexus during delivery. While this likely accounts for many brachial plexus injuries, reports of such injuries following deliveries in which there was no shoulder dystocia has led investigators to question whether or not brachial plexus injuries might have other etiologies. Such etiologies might be intrauterine cerebrovascular accidents (strokes), overstretching of the brachial plexus from fetal movement during the pregnancy, or basic maldevelopment of the brachial plexus.

In some brachial plexus injuries sympathetic nerve fibers that traverse T1 can be damaged. This can result in depression of the eyelid and drooping of the mouth on the affected side, a constellation of symptoms called Horner's Syndrome.

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Incidence of brachial plexus injury

Brachial plexus injury is the classic injury following shoulder dystocia. First described by Duchenne in 1872, it occurs following roughly 10% of all shoulder dystocia deliveries as reported in a variety of studies:

Gherman (1998) 16.8%

McFarland (1996) 8.5%

Bofill (1997) 9.5%

Baskett (1995) 13%

Stallings (2001) 12.7%

Nocon (1993) 15.1%

The incidence of shoulder dystocia rises with many factors, the most prominent of which are the size of the baby and maternal diabetes status. Given that roughly one half of 1% of all babies experience shoulder dystocia during delivery and that approximately 10% of shoulder dystocia deliveries result in brachial plexus injuries, the theoretical rate of brachial plexus injury following shoulder dystocia is roughly one in 2000 deliveries. This prediction is confirmed by observation.

Brachial plexus injuries can also occur without there having been a shoulder dystocia. There are multiple reports in the literature of brachial plexus injuries following vaginal deliveries without shoulder dystocia, subsequent to breech deliveries, and even after otherwise uncomplicated cesarean sections. In fact, the rate of brachial plexus injury in which no shoulder dystocia was reported has been quoted to be as high as 40% to 50%. These findings are discussed in detail on subsequent pages on this site.

The natural history of brachial plexus injury

Fortunately, most brachial plexus birth injuries are transient. The majority of such injuries resolve by three months, with a range of two weeks to 12 months. Only 4 to 15% result in some degree of permanent injury:

Rate of brachial plexus injuries that persist permanently

Eckert (1997) 5-22%

Johnson (1979) 7.8%

Graham (1997) 20%

Sandmire (1988) 11.8%

Nocon (1995) 4%

Average: ~10%

Patients with upper lesions -- Erb palsy -- have a better prognosis than those with lower brachial plexus injuries-Klumpke palsy. Whereas upwards of 90 to 95% of all Erb palsies totally resolve, only 60% of Klumpke palsies do. Interestingly, those brachial plexus injuries associated with non-shoulder dystocia deliveries persist more often than those occurring following deliveries in which a shoulder dystocia was documented.

Brachial plexus injuries can also produce secondary effects. Muscle imbalances produced in the hand, arm, and shoulder may result in osseous deformities of the shoulder and elbow and in dislocations of the radial head. The development of the affected arm may be compromised, resulting in its being as much as 10 cm shorter than the nonaffected arm.

Treatment options and prognosis

As mentioned, the majority of brachial plexus injuries will resolve spontaneously over the course of several months to a year. Physical therapy is usually employed within weeks of birth to help strengthen muscles whose nerve supply has been damaged. For those injuries that are permanent there are two modes of therapy.

First, physical therapy can strengthen muscles that are only partially denervated, strengthen surrounding muscles to compensate for functional loss, and improve the range of motion of the affected shoulder, arm, elbow, or hand.

Second, surgical therapy in the form of nerve grafting or muscle transposition may be undertaken. There is, however, great controversy about the efficacy of such surgical procedures in improving the outcome of those with brachial plexus injuries. Several orthopedic and neurosurgeons from around the country who do this sort of surgery frequently report various degrees of improvement in many of their patients. Others in the field, however, refute these claims and feel that there is little or no benefit to such surgery.

Other physical injuries following shoulder dystocia deliveries

Fractured clavicle

The second most common injury suffered by infants following shoulder dystocia deliveries is a fractured clavicle. The incidence of this injury following shoulder dystocia is 10%.

If the fetal shoulders and chest are relatively large in relation to the maternal pelvis, significant pressure may be placed on them as they pass through the birth canal following delivery of the fetal head. In some infants, this pressure causes the clavicle to fracture. The overlapping of the ends of the broken clavicle reduces the diameter of the fetal chest and intra-shoulder distance and allows them to be delivered. This "safety valve" effect may in fact help reduce the incidence of severe brachial plexus injury.

The baseline clavicular fracture rate for all deliveries appears to be about 0.3%. Despite the fact that shoulder dystocia increases the risk of clavicular fracture 30 fold, approximately 75% of clavicular fractures are not associated with shoulder dystocia. Interestingly, although there are multiple reports of brachial plexus injuries following cesarean sections, clavicular fractures following cesarean sections are extremely rare.

Fractured humerus

This occurs in approximately 4% of infants with shoulder dystocia deliveries. Such injuries heal rapidly and are rarely result in litigation.

Contusions

The force with which the infant's shoulder is compressed against the maternal pubic bone and the pressure of the deliverer's hands on the fetus while performing various maneuvers to effect delivery will often result in bruises on the baby's body. Such bruising has often been cited by plaintiff attorneys as evidence that a baby has been handled roughly at delivery despite the fact that such bruises are common even in routine deliveries not involving shoulder dystocia or fetal injury.

Fetal asphyxia

The most feared complication of shoulder dystocia is fetal asphyxia. It has been frequently demonstrated in both animal experiments and in retrospective analyses of babies born following dramatic cessation of umbilical blood flow (placental abruption, uterine rupture, etc.) that if babies are not delivered within five to 10 minutes they will suffer irreversible neurologic damage or death. Wood, in an often-quoted article from 1973, showed that in the time between delivery of the head and trunk of an infant, the umbilical artery pH declines at a rate of 0.04 units per minute. This means that at the five-minute mark following delivery of the fetal head, the baby's pH may have dropped from 7.2 -- a common level after several hours of pushing -- to 7.0, the level that defines asphyxia. By 10 minutes the pH would have dropped to 6.8. Ouzounian (1998) reported that of 39 babies whose deliveries involved shoulder dystocia, 15 who suffered brain injury averaged a head-to-shoulder delivery interval of 10.6 minutes while the 24 babies also born following shoulder dystocia but without brain injury had a head-to-shoulder delivery interval of only 4.3 minutes. Cerebral palsy and fetal death are rare but unfortunately not unheard of consequences of prolonged head-to-shoulder delivery intervals following shoulder dystocia deliveries.

The reason for the increasing acidosis and asphyxia that occurs during a shoulder dystocia delivery is that once the fetal head emerges from the mother, the baby's umbilical cord becomes tightly compressed between its body and that of the mother's birth canal. This significantly decreases or totally cuts off blood flow between the mother and infant. If the pressure on the cord is not rapidly relieved, the consequences of cessation of lack of umbilical flow -- decreased delivery of oxygen to the fetus -- will occur.

Maternal injuries

The mother, too, is at some risk when shoulder dystocia occurs. The most common complications she may suffer are excessive blood loss and vaginal and vulvar lacerations.

Significant blood loss, which occurs in one quarter of all shoulder dystocia deliveries, may be seen either during the delivery or in the postpartum period. Its usual causes are uterine atony or lacerations of the maternal birth canal and surrounding structures. Such lacerations may involve the vaginal wall, cervix, extensions of episiotomies, or tears into the rectum. Uterine rupture has also been reported.

Because of the pressure directed upwards towards the bladder by the anterior shoulder in shoulder dystocia deliveries, post-partum bladder atony is frequently seen. Fortunately, it is almost always temporary. Occasionally the mother's symphyseal joint may become separated or the lateral femoral cutaneous nerve damaged, most likely the result of overaggressive hyperflexion of the maternal legs during attempts at resolving the shoulder dystocia.

Ramifications

Even though shoulder dystocia occurs in only 0.5% to 1.0% of all deliveries, the fact that there are approximately 4 million deliveries a year in United States means that many thousands of mothers and babies will experience this obstetrical complication. A little math tells the story:

--If the rate of occurrence of shoulder dystocia is approximately 0.5%, and

--If the rate of brachial plexus injury is 10% in these deliveries, and

--If the rate of permanent injury is 10% of all brachial plexus injuries,

then the rate of permanent brachial plexus injury will be one in 10,000 to one in 20,000 deliveries.

This means that there will be approximately 200 to 400 babies born each year in the United States with permanent brachial plexus injuries following shoulder dystocia deliveries. In addition, there will be babies who will suffer severe central neurologic injury such as cerebral palsy from asphyxia. There will even be babies who will die following severe shoulder dystocias. It is for these reasons that shoulder dystocia injuries have become an important area of medical -- and medical-legal -- concern.

The medical concern involves trying to find ways of preventing shoulder dystocia related injuries. The best way to do this, of course, would be to prevent shoulder dystocia from occurring. If this is not possible, then it is necessary to try to find ways to resolve shoulder dystocias with minimal fetal injury when they do occur. However, since many brachial plexus injuries are seen following deliveries where there was no shoulder dystocia, even perfect prediction and prevention of shoulder dystocias would not entirely eliminate the occurrence of brachial plexus birth injuries.

The medical-legal implications of the above are obvious: Given a severely injured infant, if it can be shown that a physician was negligent either in allowing a shoulder dystocia to occur or in his or her handling of the shoulder dystocia once it did occur, then according to our legal system, that physician will be held liable for damages to the injured baby and his or her family.

Up until 2006, the answer to this question by the vast majority of experts in obstetrics would have been a resounding “No!” In fact, the majority of the obstetrical literature still indicates that this is the case. However new work by several investigators (Gudmundsson 2005, Mazouni 2006) has confirmed a linkage between maternal size, fetal weight, and shoulder dystocia. Moreover, based on this principle, Dr. Emily Hamilton in Montréal appears to have developed a means by which the majority of those pregnant women destined to have a shoulder dystocia can be detected (Dyachenko, Hamilton 2006).

It must be emphasized that this predictive tool -- called the CALM Shoulder Screen^TM (patent pending) -- is currently undergoing its first clinical applications. It has not been available to obstetricians in the past, and is by no means the current standard of care. However, if the results thus far demonstrated by this predictive technique continue to be validated, the standard of care for the preventative management of shoulder dystocia may soon change.

First, however, let’s review the data that obstetricians have had up until now in attempting to predict which mothers and babies would experience shoulder dystocia.

In the past, there have been physicians who have claimed that shoulder dystocia could be predicted. Hassan (1988) stated,

"In the majority of cases shoulder dystocia can be anticipated. Risk factors include maternal obesity, diabetes, preeclampsia, prolonged gestation, and fetal macrosomia. A male infant is at a greater risk for macrosomia and dystocia."

O'Leary, in his 1992 book, Shoulder Dystocia and Birth Injuries, concurred.

However, this has been an overwhelmingly a minority opinion. The vast majority of obstetricians, including those who have done the most work on shoulder dystocia and brachial plexus injuries, up till now have concluded that it is impossible with any degree of certainty to predict in which deliveries shoulder dystocia will occur. The key issue involved is "certainty". As will be shown, there are multiple "risk" factors for shoulder dystocia. Mothers and babies having these risk factors are, in an absolute sense, more likely than mothers and babies without these factors to experience shoulder dystocia. But whether the predictive value of such factors as currently measured is high enough to be useful clinically, that is, to justify changes in labor management plans in hopes of avoiding shoulder dystocia, is what is at issue. Moreover, as with most statistical questions in medicine, the predictability of shoulder dystocia has to be looked at from two directions:

Sensitivity: Are the risk factors associated with shoulder dystocia able to accurately identify most babies who will have shoulder dystocia at birth?

Positive predictive value: What percentage of mothers and babies having these risk factors will, in fact, experience shoulder dystocia?

In the case of shoulder dystocia, its infrequent rate of occurrence (0.5%) and the low positive predictive value of risk factors for it have severely impeded the ability of obstetricians to utilize such information to advantageously alter clinical care.

The past medical literature has confirmed this overwhelmingly. Gherman (2002), among current leaders in the study of shoulder dystocia, has said the following:

Most of these preconceptions and prenatal risk factors have extremely poor positive predictive values and therefore do not allow the obstetrician to accurately and reliably predict the occurrence of shoulder dystocia.

Resnick (1988), discussing the ability of obstetricians to predict when shoulder dystocias will occur, stated that "the diagnosis [of shoulder dystocia] will often be made only after delivery of the fetal head."

Lewis (1998) noted that only 25% of shoulder dystocia cases had at least one significant risk factor.

Geary (1995) reported that when all antenatal risk factors for shoulder dystocia were taken into account, the positive predictive value was less than 2% for individual factors and less than 3% when multiple factors were combined.

The bottom line is this: In the past, nowhere in the literature were there studies that showed that the sensitivity or positive predictive value for predicting shoulder dystocia was high enough to justify obstetrical interventions in hopes of avoiding it.

Categories of risk factors

The risk factors for shoulder dystocia can generally be divided into three categories:

Preconceptual -- before pregnancy

Antepartum -- during pregnancy

Intrapartum -- during labor and delivery

Preconceptual risk factors for shoulder dystocia

1. Previous shoulder dystocia

Previous shoulder dystocia proves to be one of the most accurate predictors for recurrent shoulder dystocia. This makes perfect sense. The pelvic anatomy of a woman does not change in between pregnancies. Moreover, second and subsequent babies are likely to be larger than first or previous babies.

The risk of a woman having a repeat shoulder dystocia once having had one, as reported from various authors, is:

Smith (1994) 12%

Ginsburg (2001) 11%.

Gherman (2002) 11.9%

This compares with the baseline risk for shoulder dystocia of 0.5%. Because of this significant increase in risk -- approximately 20-fold -- some obstetricians have proposed "once a shoulder dystocia, always a cesarean".

2. Maternal obesity

A mother's weight, likewise, proves to be significantly correlated with shoulder dystocia. Emerson showed (1962) that in his series shoulder dystocia occurred twice as often in obese women as it did in normal weight women: 1.78% versus 0.81%. Sandmire (1988) estimated that the relative risk of shoulder dystocia in women with a prepregnancy weight of greater than 82 kg (181 lbs) was 2.3.

However whether this is a primary effect or merely reflects the fact that obese women tend to have large babies is not clear. To answer this question would require a study evaluating the rates of shoulder dystocia correlated with both maternal and fetal weight categories. Given the fact that more pregnant women than ever are obese, and that obesity has a marked correlation with fetal macrosomia, it is likely that the rate of shoulder dystocia will be seen to increase over the next decade.

But there are major problems with attempting to use obesity by itself as a predictor of shoulder dystocia. Although obese women do have an incidence of shoulder dystocia several fold higher than that of thinner women, even the most pessimistic reports -- such as that by Hernandez in 1990 -- show a rate of shoulder dystocia in women weighing over 250 lbs. of no more than 5%. Thus even in this high risk population, 95% of extremely obese women will not have a shoulder dystocia at delivery. Thus any intervention undertaken based solely on the relationship between maternal weight and macrosomia would be without justification for 19 of 20 of such women.

3. Maternal age

Some studies have claimed maternal age to be a risk factor for shoulder dystocia. But careful analysis reveals that maternal age is a risk factor for shoulder dystocia only in so far as maternal obesity, diabetes, excessive weight gain, and instrumental deliveries are all more common in older women. These, of course, are all themselves risk factors for shoulder dystocia. In one of the few studies looking at the correlation between maternal weight and shoulder dystocia in isolation, Bahar (1996) did not find any difference in shoulder dystocia based on maternal age alone.

4. Abnormal pelvis

O'Leary, in his book on shoulder dystocia, places great significance on the abnormal pelvis as a risk factor for shoulder dystocia -- but offers no data to support his claim. Although it would make sense that a decrease in certain pelvic dimensions would increase the possibility of a baby's anterior shoulder getting caught on the maternal pubic bone, there are no reports in the literature demonstrating a relationship between shoulder dystocia and objectively-measured pelvic shape.

Moreover, the use of pelvimetry -- x-ray or other measurement of pelvic dimensions -- in obstetrics was discarded years ago, for several reasons:

1. Except in the very most extreme cases of congenital or pathological pelvic deformity, there is poor correlation between pelvic size and a woman's capacity to delivery vaginally.

2. The ability to more accurately monitor babies in labor enables obstetricians to safely allow labor itself to be the test of whether or not a baby will "fit" into and through the maternal pelvis.

5. Multiparity

In a 10-year series collected from Boston's Beth Israel Hospital covering the years 1975 to 1985, Acker (1988) showed that there were more Erb palsies in babies born to multiparous women then to primigravida women. He attributed this to a marked increase in precipitous labors in such women. In his series he noted that 31.8% of all babies with Erb palsy had experienced a precipitous delivery.

But as with maternal age, by the time a woman becomes "multiparous", she is old enough to have an increased risk of having other risk factors for shoulder dystocia such as larger babies, obesity, and diabetes. Moreover, only multiparous women could have the very significant risk factor of having had a previous shoulder dystocia. Thus most experts feel any relationship between multiparity and shoulder dystocia is secondary to other, more primary, risk factors.

Summary of preconceptual risk factors

• Previous shoulder dystocia significantly increases the risk of repeat shoulder dystocia
• Shoulder dystocia is seen more commonly with increased maternal age, obesity, and multiparity -- but in reality these are only markers for the increased risk of more primary risk factors
• There is no evidence linking the "abnormal pelvis" to shoulder dystocia

B. Antepartum factors risk factors for shoulder dystocia

1. Macrosomia

Macrosomia is far and away the most significant risk factor for shoulder dystocia. It is the factor that has been most studied and most often proposed as a potential target for manipulation in hopes of reducing the number of shoulder dystocia deliveries. Some authors go so far as to claim that no other risk factor has any independent predictive value for the occurrence of shoulder dystocia.

The most obvious confirmation of this relationship consists of those studies measuring the percentage of babies in different weight groups that experienced shoulder dystocia. What is vitally important to keep in mind when considering such data, however, is that these are the weights ascertained after delivery. They were not available to the obstetrician before delivery in making his or her clinical decisions as to how the delivery should be conducted.

Acker (1985) found that babies weighing over 4500gms experienced shoulder dystocia 22.6% of the time. The shoulder dystocia rate in his general population was 2%. His report showed the following:

More than 70% of all shoulder dystocias in his study occurred in infants weighing more than 4000 g.

Kolderup (1997), in a review of 2924 macrosomic deliveries at UCSF, reported that macrosomic infants have a six fold increase in significant injury from shoulder dystocia deliveries compared with controls.

Jackson (1988) showed in his series of 8258 deliveries that the average birth weight of babies who suffered brachial plexus injuries was 4029 g., whereas the average birth weight of all deliveries was 3160 g,

Lazer (1986) reported that the shoulder dystocia rate for infants weighing more than 4500 g was 18.5% while for "smaller babies" in his series the rate was 0.2%.

Nisbet (1998) published a chart showing similar data:

Sandmire (1998) likewise showed that the incidence of shoulder dystocia significantly increased with birth weight:

What is macrosomia?

The definition of macrosomia has varied both through the years and according to the author writing about it. The various cutoff points used to define macrosomia have been 4000 g, 4500 g, and 5000 g. Often a distinction has been made between macrosomia in nondiabetic versus diabetic mothers, the bar being set lower for the fetuses of diabetic mothers. In general, in babies born to nondiabetic mothers 5% to 7% will weigh more than 4000 g; 1% will exceed 4500 g.

One of the most important factors about macrosomia is the differential rate of growth of the fetal head, chest, and trunk as gestation proceeds, both in the babies of diabetic and of nondiabetic mothers. Until 36-38 weeks, the fetal head generally remains larger than the trunk. Between 36 and 40 weeks, however, the relative growth of the abdomen, chest, and shoulders begins to exceed that of the fetal head. This is especially the case in babies of diabetic mothers where glucose substrate levels are higher in both the mother and fetus. Thus both in prolonged gestation and in babies of diabetic mothers the size of a baby's trunk is likely to increase, increasing its chances of shoulder dystocia.

How is fetal weight predicted and how accurate are these predictions?

Although the correlation between fetal weight and shoulder dystocia is of great interest to obstetricians, knowing about this relationship is of no use unless fetal weight -- and the corresponding increased risk of shoulder dystocia -- can be predicted prior to delivery. How good, therefore, are our current techniques for estimating fetal weight?

Traditionally, fetal weight has been estimated by measurement of uterine height and by Leopold maneuvers. "Leopold maneuvers" is the name given to palpation of the maternal abdominal wall a series of four specific steps in order to determine fetal position, fetal presentation, and an estimate of the size of the baby.

Such estimates, however, are notoriously inaccurate. Studies have shown grave discrepancies between estimation of fetal weight by experienced obstetricians and actual fetal weight at delivery. Moreover these studies show that the same obstetrician will make different estimates of fetal weight on the same maternal abdomen when repeatedly checked at close intervals.

With the advent of ultrasonic fetal evaluation in the 1970's, it was hoped that a more accurate means of assessing fetal weight was at hand. Many papers were published presenting various formulas for ultrasound estimation of fetal size. Most of these involved some combination of measurements of fetal head and abdominal dimensions and fetal femur length. However comprehensive analyses of these various ultrasound formulas have concluded that none are consistently more accurate than being within 10 to 15% of actual birth weights. Chauhan in 1995 went so far as to say that in more than half of the models for ultrasound prediction, clinical predictions by obstetricians were as or more accurate. This was found to be especially true in larger babies:

From these data it appears that sonographic models are not significantly superior to clinical examination in detecting newborns with birth weight's greater than or equal to 4000 g.

Another study by Chauhan (1992) showed that pregnant women themselves were more accurate than either ultrasound or physician clinical estimates in determining the birth weights of their infants.

There are many studies that confirm the inability of any current diagnostic technique to determine fetal weight prior to birth to any better than 10-15% above or below the true weight:

Delpapa (1991): Only 48% of estimates of fetal weight as determined by ultrasound within three days of birth were within 500 g of the final fetal weight.

Benson (1987): The use of ultrasound formulas to predict macrosomia was correct in only 47% of infants.

Jazayeri (1999): Using a formula based on ultrasound abdominal circumference in an attempt to determine which babies would weigh over 4500gmshe obtained a positive predictive value of only 9%.

Shoulder/chest/abdomen ratios

As discussed above, post term growth and maternal diabetes result in the fetal trunk growing larger relative to the fetal head. The same pattern of disproportionate growth occurs with babies that are large for any reason, including inherent genetic predisposition. This is why macrosomic babies have a higher incidence of shoulder dystocia. In a normally proportioned baby, once the head is delivered the fetal shoulders and body usually deliver easily. With shoulders and trunk bigger than the fetal head, it is much more likely that they will get stuck.

Several investigators have sought to measure the differences in size between fetal shoulders, trunks, and head circumferences to see if there existed a certain ratio at which the risk of shoulder dystocia became prohibitively high. Hopewood (1982) proposed that when the transthoracic diameter is 1.5 cm larger than the biparietal diameter, shoulder dystocia would be significantly increased. Kitzmiller in 1987 developed a formula involving a CT scan of fetal shoulders by which he was able to predict fetal weight with good accuracy: a positive predictive value of 78% for predicting birth weights over 4200 g. with a negative predictive value of 100%.

However, several authors have refuted the utility of using the relationship between measurements of different anatomic structures to predict shoulder dystocia. Benson (1986), while acknowledging that femur length/abdominal circumference ratios differ in macrosomic vs. nonmacrosomic fetuses, claimed that there is too much overlap between the larger and smaller groups in any formula protocol to be clinically useful. He states in his paper that "for no cutoff value of these measurements is there a high sensitivity and high specificity."

Thus the question: Can shoulder dystocia be reliably predicted by estimating fetal weight?

The problems with attempting to estimate which fetuses will be macrosomic and using this information as a tool for predicting shoulder dystocia are twofold:

In the first place, it is the general conclusion of most obstetrical experts who have studied this issue that predicting macrosomia is unreliable. If macrosomia cannot be reliably determined, it is hard to try to use it to predict shoulder dystocia.

Secondly, only a very small percentage of babies, even of those who have macrosomia, go on to develop shoulder dystocia. This presents a significant obstacle to the use of estimates of fetal weight as a tool for deciding when to change clinical management in hopes of preventing shoulder dystocia deliveries.

These difficulties are highlighted in the data presented below:

Resnick (1980) found that shoulder dystocia occurred in only 1.7% of 1409 infants born at Johns Hopkins Hospital weighing more than 4000 g.

Acker (1986) pointed out that although the relative frequency of shoulder dystocia varied directly with increasing birth weight, almost half of the shoulder dystocias occurred in deliveries involving average and smaller babies. This is because there were so many more of them. Forty-seven percent of all shoulder dystocias at the Beth Israel hospital during the time of his study occurred in babies weighing less than 4000 g, a weight category which encompassed 91.2% of his total delivery population. Thus any attempt to use estimates of fetal weight as an isolated factor to reduce the incidence of shoulder dystocia would miss half of all shoulder dystocias -- even if macrosomia could be accurately measured.

Gonen (2000) evaluated 17 babies with brachial plexus injuries from a population of 16,416 deliveries. Only three of these injured babies were macrosomic.

Geary (1995) found that the positive predictive value of a birth weight of more than 4000 g for predicting shoulder dystocia was only 3.3%.

Delpapa's 1991 study showed that, at his institution, 50% of babies estimated to weigh more than 4000gm in fact had birth weights below 4000gm -- a false positive rate for predicting macrosomia of 50%!

Levine in 1992 showed that if macrosomia was defined as the 90th percentile of fetal weight for a given gestational age, then sonographic prediction of macrosomic was wrong 50% of the time both in underestimating and overestimating fetal weight. Similar unsuccessful attempts to accurately ascertain fetal birth weight during the antenatal or intrapartum period have been published by:

Sandmire (1993)

Sacks DA (2000)

Boyd (1983)

Chauhan (1992)

Levine (1992)

The American College of Obstetricians and Gynecologists bulletin on shoulder dystocia states that ultrasound has a sensitivity of only 22 to 44% and a positive predictive value of only 30 to 44% in predicting macrosomia.

Thus up until now, as has been shown, it has been the general consensus of obstetricians who have done research in the area of shoulder dystocia that the occurrence of shoulder dystocia based on estimations of fetal weight could not be reliably predicted.

El Madany sums up this issue well in his 1990 paper:

"Even if certain combinations of risk factors exist which could with high likelihood isolate which babies experienced shoulder dystocia, the inability to predict macrosomia with the requisite degree of certainty on which such a clinical suspicion is based precludes making active action protocols. Until the macrosomic infant can be accurately identified, no reasonable risk factor profile can be established."

Sandmire, in his 1993 article, concludes:

"Any approach using ultrasound would have to demonstrate that its use improves newborn or maternal outcome without disproportionate increases in morbidity and mortality. A barrier to achieving this goal is the inaccuracy associated with ultrasonic estimations of fetal weight. The current ultrasonic procedures for estimation of fetal weight are not accurate enough for detecting macrosomia defined by weight criteria. And even if clinicians could determine fetal weight accurately, the frequency of persistent fetal injuries associated with vaginal birth of the macrosomic fetus is so low that induction of labor or cesarean birth is not justified on that basis. Delivery decisions based on inaccurate estimated fetal weight should be avoided."

Thus, while macrosomia is a major risk factor for shoulder dystocia, it has not been possible to accurately predict shoulder dystocia by attempting prediction of macrosomia.

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2. Diabetes

Next to macrosomia, the factor most closely associated with shoulder dystocia is maternal diabetes in pregnancy. One of the first clear-cut demonstrations of this was Acker's 1985 paper showing the following:

As can be seen, babies of diabetic mothers had a three to fourfold increase in the risk of shoulder dystocia compared to babies of nondiabetic mothers in each weight category.

Although diabetic mothers accounted for only 1.4% of the birth population in this study, they accounted for 4.9% of shoulder dystocias. Acker also showed that although the general rate of Erb palsy following shoulder dystocia is roughly 10%, 17% of babies born to diabetic mothers developed Erb palsy.

Other investigators have shown similar or larger correlations between diabetes and shoulder dystocia. In Al-Najashi's study (1989), the rate of shoulder dystocia in babies weighing over 4000gm born of diabetic mothers was 15.7%. Babies born to nondiabetic mothers had a shoulder dystocia rate of 1.6%.

Casey (1997), in a study of over 62,000 patients, found the shoulder dystocia rate in his general obstetrical population to be 0.9% while in his patients with gestational diabetes it was 3%.

Sandmire (1988) found a relative risk for shoulder dystocia in the babies of diabetic mothers of 6.5 compared to nondiabetic mothers.

There are two main reasons for this correlation between diabetes and shoulder dystocia. In the first place, diabetes in pregnancy shows a very strong correlation with macrosomia. The growth of diabetic babies represents not only their genetic potential for growth but also reflects the laying down of extra glucose substrates present in both the mother and baby. Secondly, as previously mentioned, the nature of the fetal growth differs in diabetic babies. Growth is not as evenly distributed between the head and trunk as it is in nondiabetic babies. Rather, babies of diabetic mothers show a pattern of greater shoulder, chest, and abdominal growth. As Ellis summarized in 1982:

"The infant of a diabetic mother has a different body configuration than the infant of a nondiabetic mother. Increased deposition of fat in various organs may be due to increased insulin secretion in response to hyperglycemia."

Can shoulder dystocia be predicted in babies of diabetic mothers?

In the 1980s several authors published studies purporting to show that they could predict which babies of diabetic mothers would be at high risk for shoulder dystocia.

Elliott (1982) claimed that by evaluating the chest-biparietal diameter in infants of diabetic mothers weighing more than 4000 g, he could reduce the incidence of traumatic morbidity at delivery from 27% to 9%.

Tamura (1986) found that in diabetic women fetal abdominal circumference values greater than the 90 percentile correctly predicted macrosomia in 78% of cases. In his study, when both the abdominal circumference and the estimated fetal weight exceeded the 90th percentile in pregnant women with diabetes, macrosomia was correctly diagnosed 88.8% of the time.

Mintz, in a promising study from 1989, published data showing that in his hands a combination of fetal abdominal circumference > the 90th percentile for gestational age and shoulder soft tissue width greater than 12 mm was the best predictor of macrosomia. His data reported a sensitivity of 96%, specificity of 89%, and "accuracy" -- positive predictive value -- of 93%. He also found a significant correlation between shoulder width and a high HgA1C, a blood test that measures blood sugar control over the preceding three months.

Unfortunately, these results have not been supported or replicated by other investigators. Multiple experts in the field of shoulder dystocia have published data from very large series that absolutely contradict the conclusions listed above. In addition, the results of these studies are not as powerful as might first be assumed.

In Elliott's study, for instance, although he was able to show that a large number of babies meeting certain chest-biparietal diameter criteria were macrosomic, 39% of babies with these same parameters -- chest/biparietal diameter ratio of > 1.4 -- were not larger than 4000 g. In Tamura's steady, although he was able to predict macrosomia in babies meeting certain abdominal circumference criteria, he still was unable to identify the vast bulk of macrosomic fetuses. As for Mintz's study, no one has yet been able to duplicate his results.

In fact, most past studies have found that neither macrosomia nor shoulder dystocia can be reliably predicted in the babies of diabetic mothers. Acker (1985) showed that by using the criteria of large baby and diabetic mother he could predict 54.7% of shoulder dystocias -- but would miss 45.3% of them (false negatives). Delpapa (1991) stated that the predictive value of estimated fetal weight in babies of diabetic mothers for predicting shoulder dystocia was not sufficient to reliably identify them.

Moreover, most diabetic mothers do not have macrosomic babies and the overwhelming majority of macrosomic infants are not babies of diabetic mothers. The bottom line is that macrosomia is as difficult to predict in diabetic mothers as it is in the nondiabetic population.

There are two other studies of interest relating to this question.

Coen (1980) showed that although HgbA1C is a good marker for long-term monitoring of blood sugars in diabetic patients, it is not a good predictor of large-for-gestational age infants. The average HgA1C in mothers of large-for-gestational age infants in his study was 6.7; for mothers delivering normal sized babies the average HgA1C was 6.5 -- too close to be clinically useful.

Casey (1997) reported that although the rate of shoulder dystocia was in fact increased in mothers with gestational diabetes, this was not manifest in an increase in the rate of Erb palsy.

The bottom line: Predicting macrosomia and shoulder dystocia in diabetic mothers has been as difficult as predicting these factors in the nondiabetic population.

3. Maternal weight gain

The data linking maternal weight gain and fetal birth weight are controversial.

Abrams (1995) and Langhoff-Roos (1987) both showed that total maternal weight gain was significantly correlated with infant birth weight. Dawes (1991), however, was not able to confirm this:

There was no apparent difference in correlation between maternal weight gain and birth weight between women giving birth to average for gestation or large for gestational age infants

Moreover, several investigators have reported conflicting information as to the effect of patterns of maternal weight gain on ultimate fetal weight. Some studies have found second trimester weight gain to be the major determinate whereas others have found that the weight gain in the last trimester was the most important factor. Given the contradictory and confusing data on this subject, Dawes' (1991) closing statement is probably the most apt:

"The variations in total (maternal) weight gain and incremental weight gain are so wide that these measurements are unlikely to be clinically useful."

4.. Fetal sex

There is little data correlating fetal sex with macrosomia and shoulder dystocia. Although on average male babies do weigh slightly more than females, there is no data showing a significantly higher number of macrosomic male infants than female infants.

Resnick in his classic 1980 paper mentions fetal sex as a potential factor but does not supply data to substantiate his claim. El Madany (1990) showed that 59.2% of babies experiencing shoulder dystocia in his study were male -- statistically significant but not of much value as a clinical predictor.

5. Multiparity

Any relationship thus far observed between multiparity and either macrosomia or shoulder dystocia has been linked to the fact that multiparous women are, on average, older and heavier than primigravida women. They are therefore more likely to have larger babies and are more likely to have or develop diabetes, both of which would increase the risk of shoulder dystocia. In addition, by definition multiparous women have already had one or more babies. Thus they may already have experienced a shoulder dystocia which of course would place them at greater risk for recurrent shoulder dystocia.

The only primary association between multiparity and shoulder dystocia is the fact that multiparous women are more likely than primiparous women to have precipitous labors. This has been linked by several investigators (Gonen [2000], Acker [1988]) to an increased risk of shoulder dystocia.

6. Post-dates

Even though fetal growth slows in the last several weeks of pregnancy, there is still some growth as long as pregnancy continues. Thus the longer the baby remains in utero, the larger the baby will be -- and the greater the risk of shoulder dystocia. Acker (1985) was one of the first to demonstrate this association. Chervenak confirmed this in 1989 when he reported that 25.5% of babies delivering at 41 weeks gestation were macrosomic while only 6% (risk ratio 4.2) were macrosomic in a group delivering between 38 and 40 weeks gestation. Hernandez (1990), too, found a direct correlation between post date babies and an increased risk of shoulder dystocia. He attributed this entirely to the increased tendency of post-date babies to be macrosomic.

Multiple risk factors

The greatest risk for shoulder dystocia occurs in those groups of women who have multiple risk factors. An obese woman with a large pregnancy weight gain and gestational diabetes will have a significantly greater likelihood of having a macrosomic baby and shoulder dystocia than will a woman who has just one of these risk factors. The worst possible combination of risk factors would be a mother with diabetes, an estimated large-for-gestational-age fetus, a prolonged second stage of labor, and a forceps delivery (to be discussed below). The rate of shoulder dystocia in such a situation approaches 40%.

Summary of antepartum risk factors

• Macrosomia and maternal diabetes are the main risk factors for shoulder dystocia
• Predicting fetal weight is extremely unreliable
• Other factors -- maternal weight gain, fetal sex, and post dates -- are secondary risk factors. They do indicate an increased risk for shoulder dystocia but they are only relevant to the degree that they increase risk of fetal macrosomia
• Since multiparity increases the number of precipitous labors it may be a primary risk factor for shoulder dystocia

Intrapartum risk factors

Various characteristics of labor and delivery have been claimed to be useful in predicting whether or not a given mother-baby pair will end up with a shoulder dystocia and possible brachial plexus injury.

1. Instrumental delivery

Several studies have clearly shown that labors that end in instrumental vaginal deliveries -- vacuum or forceps -- show a higher rate of shoulder dystocia in each fetal weight group.

Nesbitit (1998), for example, reported the following data:

Baskett (1995) similarly showed a tenfold increase of shoulder dystocia and a fivefold increase in brachial plexus injury (BPI) with mid-forceps deliveries

Benedetti reported that in deliveries with the combination of a prolonged second stage of labor and a mid pelvic delivery there was a 4.6% rate of shoulder dystocia -- compared to 0.4% when there was neither prolonged second stage nor mid pelvic delivery.

McFarland (1986) showed that the relative risk of brachial plexus injury was 18.3 for midforceps deliveries and 17.2 for vacuum deliveries when compared to unassisted vaginal deliveries.

Thus it is clear that deliveries requiring instrumental assistance have a higher risk of shoulder dystocia and brachial plexus injury. It is not clear, however, that it is the instrumental deliveries themselves that are to blame for these shoulder dystocias. It may well be that the mother's inability to push the baby out without assistance is due to fetal macrosomia or an altered distribution of fat between the fetal head, chest, shoulders, and abdomen -- themselves major risk factors for shoulder dystocia.

2. Experience of the deliverer

Since the safe resolution of a shoulder dystocia involves specific obstetrical maneuvers and since shoulder dystocias occur relatively infrequently, it would seem that more experienced practitioners would have better outcomes in these situations merely by virtue of having seen more of them. Such an opinion would surely be voiced by most obstetricians and experienced labor and delivery nurses. However the data does not support this belief.

In the only study that has looked at the experience of the deliverer in relation to shoulder dystocia, that by Acker in 1988, the number of Erb palsies following shoulder dystocia deliveries did not vary with either the number of years a physician had been in practice or the number of deliveries that physician performed. As Acker stated,

Most clinicians hardly gain expertise and confidence in the difficult

manipulations required to resolve shoulder dystocia due to the rarity of the condition.

3. Labor abnormalities

Several studies have shown a higher incidence of shoulder dystocia in labors in which the second stage of labor is prolonged. Nevertheless -- and paradoxically -- shoulder dystocias are not infrequently seen during labors with very rapid second stages.

Al-Natasha (1989) found that a delay in the second stage of labor and slowed descent of the fetal head in an obese multiparous woman greatly increased the possibility that a shoulder dystocia would occur.

Hopewood (1982) found that there was a deceleration phase of active labor from eight to 10 cm in 58% of shoulder dystocia deliveries.

Acker (1985) showed that arrest disorders significantly increase the chance of shoulder dystocia with larger babies

But the literature has sometimes contradicted itself on this issue.

Acker, in that same 1985 article referenced above, states:

No particular labor abnormality was predictive of an increased incidence of shoulder dystocia relative to that encountered with a normal labor pattern, a spontaneous delivery, or both.

Lurie (1995) also found no correlation between length of the stages of labor and shoulder dystocia. He showed that there was no difference in (1) the mean rate of dilatation, (2) the percentage of protracted labors, or (3) the mean duration of the second stage of labor in a group of mothers who experienced shoulder dystocia deliveries versus a group that delivered without complication. His conclusion was that protracted labor did not seem to be a risk factor for shoulder dystocia. As he says in his paper,

One could not identify shoulder dystocia in advance while analyzing the rate of cervical dilation or duration of the second stage of labor.

Hernandez (1990) reported that although there is a relationship between the length of various stages of labor and shoulder dystocia, 70% of patients who experienced shoulder dystocia had normal labor patterns.

McFarland (1975) likewise reported the same rate of labor abnormalities of the active phase of labor and of the second stage of labor in both shoulder dystocia and control groups. He concluded that labor abnormalities could not serve as clinical predictors for the subsequent development of shoulder dystocia.

Even if disorders of labor were found to be correlated with shoulder dystocia, it is not clear whether this would represent an independent risk factor. It might merely confirm that labor disorders are more common with macrosomic babies and that macrosomic babies more commonly experience shoulder dystocia. To date there has been no major study evaluating the length of various stages of labor broken down by weight category in relationship to shoulder dystocia deliveries.

To further complicate the issue, it is well known that shoulder dystocias and brachial plexus injuries are often seen with short second stages of labor:

Gonen (2000) reported that 7 of 17 patients (41%) with brachial plexus injury had second stages of labor shorter than 10 minutes

Acker (1988) found that 31.8% of all babies with Erb palsy were born after precipitate second stages of labor. As he explains,

The rapidity of descent may prohibit the fetal shoulders from entering the inlet in an oblique diameter, preclude adequate preparation for delivery, and add to nerve root trauma.

This phenomenon of shoulder dystocias with rapid second stages of labor will be discussed in further detail below.

4. Oxytocin and anesthesia

There does not appear to be any independent correlation between the use of either oxytocin or anesthesia and shoulder dystocia deliveries.

Oxytocin is generally used to increase the strength of uterine contractions. To the extent that oxytocin is used more frequently with macrosomic infants, it might have a secondary correlation with shoulder dystocia deliveries. But there is no published data linking oxytocin use with the incidence of shoulder dystocia independent of fetal weight.

Likewise with anesthesia, there is no reported increase in shoulder dystocia deliveries in labors in which conduction anesthesia is employed.

5. Episiotomy

There is no statistically significant relationship between the absence of episiotomy, the frequency of shoulder dystocia, and any subsequent neonatal injury. That this is the case is perplexing given that almost all protocols for the resolution of shoulder dystocia advocate making a "generous episiotomy". This recommendation appears to be without support in the literature.

There are two possible reasons one might make an episiotomy in the case of a shoulder dystocia.

The first would be to make more room for the baby to emerge. In this situation the indications for making an episiotomy would be the same as in any delivery: alleviating soft tissue dystocia of the perineum. If the perineal tissue were tight, then an episiotomy might be helpful in delivering the baby. However, if the soft tissue is pliable and stretches easily, as in most multiparous women, then an episiotomy will not make it any easier to free the anterior shoulder from behind the pubic bone.

The second possible indication for an episiotomy during a shoulder dystocia would be to allow more room for the obstetrician's hand to move inside the pelvis in performing the Wood screw maneuver or in attempting to deliver the baby's posterior arm. An episiotomy might be helpful in accomplishing these maneuvers in a woman whose perineal tissues impede access to the fetal shoulders. However, in a