Shoulder Dystocia










 

 

 


 


Can shoulder dystocia be anticipated accurately?

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 ScreenTM (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:

Infant weight in Nondiabetic women

Percent shoulder dystocia

Less than 4000 g 1.1%
4000g - 4499 g 10.0%
Greater than 4500 g 22.6%

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:

Weight

Percent shoulder dystocia

4000-4250 5.2
4250-4500 9.1
4500-4750 14.3
4750-5000 21.1

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

Infant weight Rate of shoulder dystocia
Less than 4000g 0.3%
4000-4500 g 4.7%
Greater than 4500 g 9.4%

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:

Estimated fetal wt. Nondiabetic mothers
% shoulder dystocia
Diabetic mothers
% shoulder dystocia
< 4000 g 1.1% 3.7%
4000-4499 g 10.0% 30.6%
> 4500 g 22.6% 50%

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:

Weight (g) SD % in unassisted births SD % in instrumental deliveries
4000-4250 8.4% 12.2%
4250-4500 12.3% 16.7%
4500-4750 19.9% 27.3%
>4750 23.5% 34.8%

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

  SD BPI
SVD 0.3% 0.04%
Low forceps deliveries 0.9% 0.06%
Midforceps delivery 2.8% 0.5%

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 woman in whom the perineal tissues are lax enough to allow these maneuvers to be performed, the automatic making of an episiotomy will not facilitate delivery and would be unnecessary.

Thus the almost universal recommendation that an episiotomy be made during a shoulder dystocia delivery is not only without literature support, but is theoretically unsupportable as well.

So, can shoulder dystocia be reliably predicted?

Up until this year, both the short and the long answer to this question would have been: "No". 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 interventions. While macrosomia, diabetes, prolonged second stage of labor, instrumental delivery, and other factors do indicate a statistically increased risk of having a shoulder dystocia, their low positive predictive value and high false positive rate make them clinically useless as tools for predicting -- and hence trying to prevent -- shoulder dystocia.

Below are the thoughts of various shoulder dystocia investigators on the predictability of this entity based on evidence that had been available up until this year (2006):

Basket (1995):
The profile of risk for shoulder dystocia -- prolonged pregnancy, prolonged second stage of labor, macrosomia, and assisted mid pelvic delivery -- were not clinically useful because the large majority of cases of shoulder dystocia occur in patients without these risk factors.

Resnick (1980):
Most babies with shoulder dystocia do not have risk factors.

German (2002):
Most of these preconception 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.

Lewis (1998):
Only 25% of shoulder dystocia cases had at least 1 significant risk factor . . . the positive predictive value of pre-partum risk factors for shoulder dystocia is less than 2% individually, 3% when combined.

Hope for the future

As mentioned above, there is new research that has linked maternal size and fetal weight to the risk of shoulder dystocia. In addition, Dr. Emily Hamilton and her team of researchers in Montreal have developed a tool, based on sophisticated statistical and mathematical analysis of large numbers of shoulder dystocia cases, that can identify the majority of those mothers and fetuses destined to experience a shoulder dystocia.

The factors involved in this analysis of risk are maternal height, maternal weight, parity, gestational age, baby’s estimated weight, and maternal history of gestational diabetes or previous shoulder dystocia. Dr. Hamilton’s formula has been tested against several large independent samples of patients who had experienced shoulder dystocia with permanent injury. The data—some already published, some in the process of submission—shows that it is possible to consistently identify 50-70% of patients destined to have a shoulder dystocia with a false positive rate (rate of additional cesarean sections) of only 2.7%. (Dyachenko, Hamilton 2006)

Dr. Hamilton’s shoulder dystocia risk prediction tool has been commercialized into a web-based application by LMS Medical Systems and labeled CALM Shoulder ScreenTM (patent pending -- see http://www.lmsmedical.com).

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Copyright © 2006 Henry Lerner
 

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