By John C. Hobbins, MD

Professor, Department of Obstetrics and Gynecology, University of Colorado School of Medicine, Aurora

Dr. Hobbins reports no financial relationships relevant to this field of study.

Synopsis: Previous Alerts have touched on the relationship between big babies and big problems, such as birth injury, infant/childhood obesity, and diabetes. This special feature is designed to provide a more comprehensive look at the causes, risks, prediction, management, and prevention of macrosomia.

The terms large for gestational age (LGA) and macrosomia are interchangeable, but different thresholds have been used by different authors, including a birth weight or estimated fetal weight (EFW) of > 4000 g (8 lbs, 15 oz) or > 4500 g (9 lbs, 13 oz) at any time in pregnancy. Other definitions are based on gestational age, using the 95th or 97th percentile. As expected, many adverse perinatal outcomes correlate directly with the degree of macrosomia.


Genetic predisposition obviously plays a role in fetal/infant size, and it is common for parents of large stature, in the absence of other factors, to have large babies. However, the three major causes are obesity, diabetes, and post-term pregnancy — with the most likely culprit being obesity.

Obesity is a major rising problem. Overall, more than one-third of women in the United States are obese and more than half of pregnant women are either overweight (body mass index [BMI] 25-30 kg/m2) or obese (BMI > 30 kg/m2).1 Also, in addition to a predilection for their larger babies to have downstream birth injuries, the offspring of obese women have higher rates of childhood obesity and later cardiovascular abnormalities,2 with the dye being cast long before birth.

Maternal diabetes affects various fetal organs in different ways. Maternal /fetal hyperglycemia and insulin resistance force the fetal pancreas to produce more insulin, a growth stimulator, and to store the extra glucose as glycogen in their larger livers. Also, lipogenic dysfunction leads to over-accumulation of fat in the subcutaneous tissues. All these macrosomic factors can lead, through resulting body to head disproportion, to birth injury. Add glucose intolerance to a clinical mix of an obese woman of short stature (with an inherently small pelvis) and you have the “perfect storm” for shoulder dystocia (SD).

In post-term pregnancy, there is more time for further growth of the fetus. Interestingly, while there is some slowing of overall fetal weight at term and into post-term, the size of the fetal abdomen (and with it, the shoulders) continue to increase linearly — another setup for SD. Nevertheless, this is becoming a less frequent cause of macrosomia and SD, because the fear today of stillbirth has led to a greater tendency to intervene before patients can become post-term. Therefore, this special feature will focus mostly on obesity with a secondary look at diabetes.

The Risks of Macrosomia

Maternal risks of fetal macrosomia mostly are associated with delivery events. These include the risk to the pelvic floor after vaginal birth — resulting in later anal incontinence, stress urinary incontinence, and prolapse, with odds ratios for each of 2.2, 4.4, and 7.5, respectively.3 One prospective study showed that urinary stress incontinence was independently related to birth weight, episiotomy, and the size of the fetal head.4 Another study showed that in those with postpartum stress incontinence, 21% persisted after a vaginal delivery, while only 3% persisted in those having cesarean sections.5

Infant injury can be traumatic or asphyxic. The incidence of SD in the overall population is 1.4%, but when birth weight exceeds 4500 g, the rate is 9-24%.6 When adding vacuum/forceps delivery to the mix, the rate is 23%, and with birth weights > 4750 g, the rate is 29%.7

Shoulder dystocia can lead to brachial plexus injury, with a usual rate of 0.5-1.9 per thousand, rising 20-fold when infants weigh more than 4500 g.6 Permanent injury can occur in 10% of these infants.6 One retrospective study found a 20% risk of hypoxic central nervous system injuries at 6 months of age in infants with SD.8

Diagnosis of Fetal Macrosomia

It is somewhat understandable that ultrasound estimates of fetal weight have been maligned since the often stated standard error is about 10% — meaning that an EFW of 4000 g carries a splay of between 3600 g and 4400 g. One study even suggested that the patient’s own estimate of fetal weight was better than ultrasound.9

Although the literature is replete with formulas for EFW, the most commonly used one, plotted against gestational age, was constructed at sea level in 392 patients.10 It consists of measurements of the biparietal diameter (BPD), head circumference, abdominal circumference (AC), and femur length. Newer methods, adding 3-D reconstructions of the fetal thigh, have yielded better accuracy.11

Since the precision of fetal weight estimates involves systematic error (the biometric formulas themselves) and random error (maternal variables and even altitude), some formulas have utilized a “customized” approach to take this into account.12 What is clear is that most formulas underestimate the EFW in LGA babies, and Melamed et al found that in 21 formulas studied, the average underestimation in large babies was -6.2%.13

Taking into account all of the above variables in LGA fetuses, especially, Lindell et al derived a formula incorporating head, abdomen, femur length, and 3-D volumes of the fetal abdomen and thigh that identified 93% of fetuses whose weights were above 4500 g (when rates of SD rise appreciably) by using an EFW threshold of 4300 g.14 This seeming triumph was at a false-positive rate of 38%.

Using Ultrasound to Detect Macrosomia

It is clear that with forewarning one can avoid possible macrosomic disasters at birth, so various approaches have been put into play.

The AC alone as a screening tool. Since corpulent fetuses all have big abdomens, the AC has been noted to be as accurate as more complicated ultrasound formulas. Screening at 30-34 weeks can capture 70% of fetuses destined to be > 4000 g, with a false-positive rate of 25%.15 Interestingly, a more cumbersome multi-parameter formula added only 3% to the predictive accuracy.

A two encounter approach. This is a concept suggested by Campbell in a comprehensive review of the subject.16 A screening test is done at 30-34 weeks, followed by a 2-D/3-D scan targeted to macrosomia at 39 weeks in those identified to be LGA by the earlier scan. After initial screening, the higher prevalence of LGAs improves the positive predictive value appreciably.

Prediction of macrosomia at term with a single earlier EFW. The rationale here is that a careful EFW by a standard formula at 34-37 weeks (when there are ideal conditions for scanning) can be used to extrapolate forward to predict the fetal weight at term. This assumes that the fetus will grow along the same trajectory (in percentile). Best et al found it to be especially effective in predicting macrosomia (> 4000 g) in diabetics with a positive predictive value of 87% and an absolute error of 6.8%.17

Methods to Predict Shoulder Dystocia

In 1982, Cohen et al tried to predict shoulder dystocia by the degree of discordance between the abdomen and the head.18 The authors found that in fetuses with EFW of
> 3800 g, if the difference in average abdominal diameter (AD) AC divided by 3.14, minus the BPD exceeded 2.5 cm, there was a 33% chance of SD. If < 2.5 cm, none of the patients had SD. This finding was validated later by another group who found almost identical results (SD in 25% of all patients and 38% in diabetics if the AD-BPD difference was > 2.5 cm and only 3.8% if < 2.5 cm).19

Management Options for Patients with an Ultrasound Diagnosis of Macrosomia

Cesarean section for those with EFW > 4500 g. Campbell makes the case for elective cesarean in this backdrop since a targeted scan at 39 weeks in high-risk pregnancies (obesity, diabetes, postdates, or earlier suggestion of macrosomia) will identify more than 90% of those fetuses weighing more than 4500 g if the EFW is > 4000 g.16 Choosing a cesarean section in this setting would virtually eliminate birth injury and reduce later maternal morbidity to < 3%. Although a cost/benefit analysis by Rouse et al20 strongly challenged this approach, another paper by Culligan et al in a urogynecology journal21 did suggest an economic benefit. Indeed, ACOG agrees with the approach of offering elective section, but only if the EFW is > 5000 g.6

Some authors are bullish on the use of elective cesarean section in macrosomia, based on increased rates of maternal and neonatal morbidity. An interesting slant is that a New Zealand survey showed that 21% of OB/GYNs and 42% of urogynecologists would choose elective cesarean section if their fetuses had EFWs > 4500 g.22 So, ask the proponents, why would our patients not be given the same opportunity?

A selective approach to route of delivery with macrosomia. Although proponents point to the risk of later maternal pelvic morbidity, they seem to slip over the immediate operative, and later repeat pregnancy complications, with cesarean section, which is not an innocuous procedure. My feeling is that if the EFW is between 4500 g and 5000 g in non-diabetics and there is no evidence of body to head disproportion, then the risk of SD is negligible if the patient labors spontaneously, has a normal labor curve, does not have a lengthened second stage, and does not need an instrumental delivery.

Induction of labor near term to pre-empt further growth. This approach to macrosomia has been validated in diabetics,23 but not in non-diabetics when EFWs are < 5000 g,24 and an oft-quoted review showed that the cesarean section rate doubled in those having induction, with no difference in any other outcome variables.

Prevention of Macrosomia

First, it is important to point out that there is more to macrosomia than being big. The diagnosis is made simply by weight at birth or in utero EFW according to gestational age. Infant BMI and ponderal index give us an idea about weight distributed over length, but what is becoming clear is that anthropometric measurements of adiposity correlate best with childhood obesity, metabolic syndrome, and eventual diabetes. Work is in progress to use 3-D measurements of the abdomen and thigh as in-utero surrogates for adiposity.

Limiting Weight Gain in Pregnancy

For years, there has been a laissez-faire approach to weight gain in pregnancy until the Institute of Medicine (IOM) came out with some stringent guidelines in 200925 based on patients’ pre-pregnant BMIs. Succinctly, recommended weight gain is 15-20 pounds for women with BMI > 25 kg/m2, and 11-20 pounds for all obese women (BMI > 30 kg/m2). Studies conflict as to whether weight gain in pregnancy is more important than pre-pregnant weight, but it is clear that curtailing both will be of benefit to decrease adverse outcomes in children of obese mothers.

While one Florida study26 (previous Alert) suggested that weight gain in pregnancy had a greater effect on birth weight than pre-pregnant weight or diabetes, other studies have shown pre-pregnant weight to exert the greatest influence.27 Lifestyle interventions (diet and exercise) seem to have a less effect on birth weight in obese patients, while weight gain has its greatest effect in those mothers with normal starting weights.

Pre-pregnant Weight

Clearly, weight reduction in obesity and in diabetes prior to pregnancy can give the patient a leg up on a prospective pregnancy. However, this apparently is not so easy to do. A recent NIH study showed that in 774 women studied, average weight gained in pregnancy was 32 pounds.28 One year later, 75% were heavier than their previous pre-pregnant weight — 47% were > 10 pounds over and 24.2% were more than 20 pounds over. This is why BMIs tend to stair-step upward with each pregnancy. Interestingly, in the same issue of the journal, another study from British Columbia showed that there was a very worrisome linear relationship between adverse pregnancy outcomes and increasing pre-pregnant BMI.29 This, coupled with an earlier study relating pre-pregnancy weight directly to longer-term consequences of macrosomia,30 such as childhood obesity and metabolic dysfunction, should get our attention.

Pre-conceptual Counseling

This can have a major beneficial effect in the two conditions that can go hand in hand: diabetes (gestational and pre-gestational) and obesity. Peterson et al have calculated that by employing universal pre-conceptual counseling and screening for pre-gestational diabetes, and applying appropriate treatment and management, 8397 preterm deliveries, 3725 birth defects, and 1875 perinatal deaths could be averted per year.31 This would result in a saving of $4.3 billion over the lifetimes of the surviving children.

By applying (postpartum) the same principle in obese patients (again, representing at least one out of three women in the United States), huge health care savings could be accrued by optimizing conditions prior to their next pregnancies.


  1. Flegal KM, et al. Prevalence of obesity and trends in the distribution of body mass index among US adults 1999-2010. JAMA 2012;307:491-497.
  2. Salsberry PJ, Reagan PB. Taking the long view: The prenatal environment and early adolescent overweight. Res Nurs Health 2007;30:297-307.
  3. Handa VL, et al. Pelvic floor disorders 5-10 years after vaginal or cesarean childbirth. Obstet Gynecol 2011;118:777-784.
  4. Viktrup L, et al. The symptom of stress incontinence caused by pregnancy or delivery in primiparas. Obstet Gynecol 1992;79:945-949.
  5. Meyer S, et al. Birth trauma: Short and long-term effects of forceps delivery compared with spontaneous delivery on pelvic floor parameters. BJOG 2000;107:1360-1365.
  6. American College of Obstetricians and Gynecologists. Fetal macrosomia. ACOG practice bulletin number 22. ACOG: Washington, DC; 2000.
  7. Nesbitt TS, et al. Shoulder dystocia and associated risk factors with macrosomic infants born in California. Am J Obstet Gynecol 1998;179:476 480.
  8. Iffy L, et al. The risk of shoulder dystocia related permanent fetal injury in relation to birth weight. Eur J Obstet Gynecol Reprod Biol 2008;136:53-60.
  9. Chauhan SP, et al. Intrapartum clinical, sonographic, and parous patients’ estimates of the newborn birth weight. Obstet Gynecol 1992;79:956-958.
  10. Hadlock FP, et al. In utero analysis of fetal growth: A sonographic weight standard. Radiology 1991;181:129-133.
  11. Lee W, et al. New fetal weight estimation models using fractional limb volume. Ultrasound Obstet Gynecol 2009;34:556-565.
  12. Gardosi J, et al. An adjustable fetal weight standard. Ultrasound Obstet Gynecol 1995;6:168-174.
  13. Malamed N, et al. Sonographic weight estimation: Which model should be used? J Ultrasound Med 2009;28:617-629.
  14. Lindell G, et al. Ultrasound weight estimation of large fetuses. Acta Obstet Gynecol Scand 2012;91:1218-1225.
  15. Jazayeri A, et al. Macrosomia prediction using ultrasound fetal abdominal circumference of 35 cm or more. Obstet Gynecol 1999;93:523-526.
  16. Campbell S. Fetal macrosomia: A problem in need of a policy. Ultrasound Obstet Gynecol 2014;43:3-10.
  17. Best G, Pressman ER. Ultrasonographic prediction of birth weight in diabetic pregnancies. Obstet Gynecol 2002;99(5 Pt 1):740-744.
  18. Cohen B, et al. Sonographic predictions of shoulder dystocia in infants of diabetic women. Obstet Gynecol 1982;60:159.
  19. Miller RS, et al. Sonographic fetal asymmetry predicts shoulder dystocia. J Ultrasound Med 2007;26:1523-28.
  20. Rouse DJ, et al. The effectiveness and costs of elective cesarean delivery for fetal macrosomia diagnosed by ultrasound. JAMA 1996;276:1480-1486.
  21. Culligan PJ, et al. Elective cesarean section to prevent fetal incontinence and brachial plexus injuries associated with macrosomia — a decision and analysis. Int Urogynecol J Pelvic Floor Dysfunct 2005;16:19-28.
  22. Turner CE, et al. Vaginal delivery compared with cesarean section: The views of pregnant women and clinicians. BJOG 2008;115:1494-1502.
  23. Boulvain M, et al. Elective delivery in diabetic pregnant women. Cochrane Database Syst Rev 2001;2:CD001997.
  24. Sanchez-Ramos L, et al. Expectant management versus labor induction for suspected fetal macrosomia: A systematic review. Obstet Gynecol 2002;100(5 Pt 1): 997-1002.
  25. Weight gain during pregnancy: Re-examining the guidelines. Washington, DC: National Academic Press; 2009.
  26. Kim SW, Sharma AJ, Sappenfield W, et al. Association of maternal body mass index, excessive weight gain, and gestational diabetes mellitus with large-for-gestational-age births. Obstet Gynecol 2014;123:737-744.
  27. Waters TP, et al. Neonatal body composition according to the revised Institute of Medicine recommendations for maternal weight gain. J Clin Endocrinol Metab 2012;97:3648-3654.
  28. Endres LK, et al. Postpartum weight retention risk factors in relationship to obesity at 1 year. Obstet Gynecol 2015;125:144-152.
  29. Schummers L, et al. Risk of adverse pregnancy outcomes by pre-pregnancy body mass index: A population-based study to inform prepregnancy weight loss counseling. Obstet Gynecol 2015;125:133-143.
  30. Catalano P, et al. Perinatal risk factors for childhood obesity and metabolic dysregulation. Am J Clin Nutr 2009;5:1303-1313.
  31. Peterson C, et al. Preventable health and cost burden of adverse birth outcomes associated with pre-gestational diabetes in the United States. Am J Obstet Gynecol 2015;212:74.e1-9.